Imaging of the Musculoskeletal System [1] 141602963X, 9781416029632

Table of contents :
Cover
Introduction and General P rinciples
John H. Harris, Jr.
PURPOSE OF THE IMAGING REPORT
BONE TYPES
GEOGRAPHIC ANATOMY OF LONG AND SHORT BONES
T YPES OF MUSCULOSKELETAL INJURIES Ligamentous Injuries (Selected Examples)
SKELETAL INJURY
FRACTURES
MUSCULOSKELETAL INJURIES COMMONLY ASSOCIATED WITH NONLIGAMENTOUS SOFT TISSUE
SPINAL INJURIES WITH INHERENT SPINAL CORD INJURY
Cervical Spine
Thoracic and Lumbar Spine
SPINAL INJURIES WITH POTENTIAL SPINAL CORD INJURY
BENDING FRACTURES
MUSCULOSKELETAL INJURIES WITH ASSOCIATED CLINICALLY SIGNIFICANT LIGAMENTOUS
W rist
Hand
P elvis A vulsion Injuries
Ankle
F oot
SUGGESTED READINGS
Imaging of Facial and Skull Trauma
Lorne Rosenbloom, Bradley N. Delman, and Peter M. Som
PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS
ANATOMY AND BIOMECHANICS
CLINICAL PRESENTATION Nasal Fractures
Orbital Fractures
Internal Orbital Fractures
Orbital Rim Fractures
N aso-Orbito-Ethmoid Fractures
Zygomaticomaxillary Complex Fractures
Le Fort Fractures
F rontal Sinus Fractures
T emporal Bone Fractures
Skull Base Fractures
Cranial Vault Fractures
Mandibular Fractures
MANIFESTATIONS OF THE DISEASE Radiography
Multidetector Computed Tomography
Magnetic Resonance Imaging
DIFFERENTIAL DIAGNOSIS
REFERENCES
T emporomandibular Joint
Vijay M. Rao and Steven Finden
PREVALENCE AND EPIDEMIOLOGY
P A THOPHYSIOLOGY Anatomy
P athology
Plain Radiography
Arthrography
Computed Tomography
Magnetic Resonance Imaging
MANIFESTATIONS OF THE DISEASE
COMPLICATIONS OF INTERNAL DERANGEMENT
Surgical Management
REFERENCES
Cervical Spine Injuries
Donna G. Blankenbaker, Kirkland W. Davis, and Richard H. Daffner
PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS
ANATOMY
BIOMECHANICS
P A THOLOGY
Flexion
Extension
R otation
Shearing
IMAGING TECHNIQUES
Indications for Imaging
MANIFESTATIONS OF THE DISEASE Radiography
Flexion-Extension Radiographs
Multidetector Computed Tomography
Obtunded Patients
Recommendations
Imaging Findings Radiologic Evaluation
Computed Tomographic Evaluation
Magnetic Resonance Imaging Evaluation
Radiographic Stability versus Instability
Normal Variants
SPECIFIC CERVICAL SPINE INJURIES C0-C1
A tlanto-occipital Dissociation
Occipital Condyle Fractures
C1-C2
Lower Cervical Spine
Burst Fracture
Flexion Teardrop Fracture
Extension Teardrop Fracture
V ertical Split Fracture
F acet Dislocation
Hyperflexion Sprain
Hyperextension Sprain
P osterior Element Fractures
Spinous Process Fractures
Articular Pillar/Facet/Laminar/Transverse Process Fractures
Whiplash Injuries
SCIWORA
Associated Neurologic Injuries
SYNOPSIS OF TREATMENT OPTIONS
What the Referring Physician Needs to Know
SUGGESTED READINGS
Injury to the Thoracic Cage and Thoracolumbar Spine
Cornelis van Kuijk and Digna R. Kool
ANATOMY
BIOMECHANICS
MANIFESTATIONS OF THE DISEASE Rib Fractures
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Nuclear Medicine
Classic Sign
Sternal Fractures Radiography
Multidetector Computed Tomography
F ractures to the Thoracic and Lumbar Spine
Magnetic Resonance Imaging
Multidetector Computed Tomography
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
What the Referring Physician Needs to Know
SUGGESTED READINGS
REFERENCES
Normal Shoulder
Qi Chen, Theodore T. Miller, Mario Pardon, and Javier Beltran
TECHNICAL ASPECTS Conventional Radiography (Table 6-1, F ig. 6-1)
Rationale and Indications
A dvantages
Computed Tomography (Table 6-2) Rationale and Indications
CT Arthrography (Fig. 6-2) Rationale and Indications
A dvantages
Limitations
Method
Conventional Magnetic Resonance Imaging (Table 6-3; Fig. 6-3; Table 6-4)
Rationale and Indications
A dvantages
Limitations
Method
Indirect MR Arthrography (Table 6-5; Fig. 6-4) Rationale and Indications
T echnical Aspects
A dvantages
Direct MR Arthrography (Table 6-6; Fig. 6-5) Rationale and Indications
T echnical Aspects
A dvantages
Ultrasonography Rationale and Indications
A dvantages
Limitations
T echnical Aspects
NORMAL ANATOMY Osseous Structures
The Labrum
The Joint Capsule
The Ligaments
The Long Head of the Bicipital Tendon
The Rotator Cuf f
The Deltoid Muscle
The Bursae
The Neurovascular Bundles
MOST SIGNIFICANT NORMAL VARIANTS Shape of the Undersurface of the Acromion
Os Acromiale
Sublabral Foramen and Sublabral Recess
V ariations of the Glenohumeral Ligaments
Anterior Capsular Insertion
Insertion of the Long Head of the Biceps Tendon
B ASIC BIOMECHANICS Normal Biomechanics
The Overhead Throwing Mechanism
Joint Stability
REFERENCES
Osseous Injuries of the Shoulder Girdle
Joseph S. Yu
Anatomy
MANIFESTATIONS OF THE DISEASE
Acute Osseous Injuries of the Clavicle
Radiography
Multidetector Computed Tomography
Acute Osseous Injuries of the Acromioclavicular Joint
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Acute Osseous Injuries of the Sternoclavicular Joint
Radiography
Acute Osseous Injuries of the Glenohumeral Joint
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Classic Signs
Acute Osseous Injuries of the Scapula
Radiography
Multidetector Computed Tomography
Acute Osseous Injuries of the Proximal Humerus
Multidetector Computed Tomography
DIFFERENTIAL DIAGNOSIS
Classic Signs
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
What the Referring Physician Needs to Know
REFERENCES
Shoulder Impingement S y ndromes
George C. Nomikos and Mahvash Rafii
PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS
DEFINITIONS
CLASSIFICATION
P A THOPHYSIOLOGY Anatomy
Biomechanics
P athology
Magnetic Resonance Imaging
T echnical Aspects
Rotator Cuff Tendinosis
F ull-Thickness Rotator Cuff Tears
P artial-Thickness Rotator Cuff Tears
C y s t i c Lesions
Muscle Atrophy
Acromial Morpholog y
Pitfalls in Magnetic Resonance Imaging of the Rotator Cuff
Multidetector Computed Tomography
Ultrasonography
Arthroscopy
Classic Signs
Subcoracoid Impingement and Subscapularis Tendon Tears Radiography
Magnetic Resonance Imaging
Ultrasonography
Arthroscopy
Classic Signs
Internal (Posterosuperior) Impingement Magnetic Resonance Imaging
Anterosuperior (Anterior Internal) Impingement and the Rotator Inter v al Ar
DIFFERENTIAL DIAGNOSIS
Classic Signs
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
What the Referring Physician Needs to Know
SUGGESTED READINGS
Glenohumeral Instability
Michael J. Tuite
ANATOMY
Normal Variations
BIOMECHANICS Anterior Instability
P osterior Instability
Multidirectional Instability
Microinstability and Superior Labrum Anterior to Posterior Tears
P osterosuperior Labral Tears
P A THOLOGY Anterior
P osterior
Multidirectional
Microinstability
SLAP Tears
P osterosuperior Labral Tears
MANIFESTATIONS OF THE DISEASE Anterior Instability
Radiography
Conventional Magnetic Resonance Imaging versus Magnetic Resonance Arthrograph
Magnetic Resonance Imaging Findings
Multidetector Computed Tomography
Arthroscopy
P osterior Instability Radiography
Magnetic Resonance Imaging
Classic Signs
Multidetector Computed Tomography
Arthroscopy
Multidirectional Instability Radiography
Multidetector Computed Tomography
Arthroscopy
Classic Signs
Microinstability Radiography
Magnetic Resonance Imaging
Superior Labrum Anterior to Posterior T ears
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Arthroscopy
P osterosuperior Labral Tears and P aralabral Cysts
Magnetic Resonance Imaging
Multidetector Computed Tomography
Arthroscopy
F rom Supportive Diagnostic Techniques
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
Classic Sign
What the Referring Physician Needs to Know
SUGGESTED READINGS
REFERENCES
Normal Elbow
Emad Yacoub, Javier Beltran, and Theodore T. Miller
TECHNICAL ASPECTS Conventional Radiography 1, 2
Rationale and Indications
Projections
Computed Tomography (Fig. 10-2) Rationale and Indications
CT Arthrography Indications
A dvantages
Disadvantages
Conventional Magnetic Resonance Imaging (Fig. 10-3)
Rationale and Indications
A dvantages
Limitations
T echnical Aspects (Table 10-4)
MR Arthrography (Fig. 10-4; Table 10-5) Rationale and Indications
Indirect Arthrography
Direct Arthrography
Ultrasonography 4 Rationale and Indications
A dvantages and Limitations
T echnical Aspects
NORMAL ANATOMY Bones
Elbow Joint
Ligaments
Muscles
Cubital Fossa
Neurovascular Structures
Normal Ultrasonographic Anatomy
B ASIC BIOMECHANICS
A cute Osseous Injury of the Elbow and Forearm
Steven Shankman and Brandon Liu
ANATOMY (INCLUDING GROSS ANATOMY AND NORMAL VARIANTS)
F at Pads
Normal Variants
MANIFESTATIONS OF THE DISEASE Radiography
Imaging Techniques
Imaging Findings
Radial Head/Neck
Olecranon
Dislocation
Coronoid Process
Distal Humerus
Capitellum
Monteggia Lesion
Chronic Injury
Magnetic Resonance Imaging Imaging Techniques
Multidetector Computed Tomography Imaging Techniques
SYNOPSIS OF TREATMENT OPTIONS Medical
Radial Head and Neck Fracture
Olecranon Fracture
Elbow Dislocation
Coronoid Fracture
Distal Humeral Fracture
Capitellum Fracture
Monteggia Lesion
SUGGESTED READINGS
Soft Tissue Injury t o the Elbow
Jenny T. Bencardino and Javier Beltran
Lateral Epicondylitis
Medial Epicondylitis
K E Y P O I N T S
Biceps Tendon Injuries
T riceps Tendon Injuries
Ligamentous Injuries and Elbow Instability
Ulnar Collateral Ligament Complex
Radial Collateral Ligament Complex
Elbow Dislocation
Entrapment Neuropathy
BIOMECHANICS T endons
Ligaments
Ner v es
P A THOLOGY Lateral Epicondylitis
Medial Epicondylitis
Biceps Tendon Injuries
T riceps Tendon Injuries
Elbow Instability
MANIFESTATIONS OF THE DISEASE Lateral Epicondylitis
Radiography
Magnetic Resonance Imaging
Ultrasonography
Medial Epicondylitis
Radiography
Magnetic Resonance Imaging
Ultrasonography
Biceps Tendon Injuries
Radiography
Magnetic Resonance Imaging
Nuclear Medicine
T riceps Tendon Injuries
Radiography
Ultrasonography
Elbow Instability
Radiography
Magnetic Resonance Imaging
Ulnar Collateral Ligament Complex
Radial Collateral Ligament Complex
Ultrasonography
SYNOPSIS OF TREATMENT OPTIONS Lateral Epicondylitis
Medical Treatment
Surgical Treatment
Medial Epicondylitis Medical Treatment
Biceps Tendon Injur y Medical Treatment
T riceps Tendon Injur y Surgical Treatment
Elbow Instability Medical Treatment
SUGGESTED READINGS
REFERENCES
The Normal Wrist
Punita Gupta and Louis A. Gilula
THE NORMAL WRIST T echnical Aspects
Conventional Radiography
Fluoroscopy
Fluoroscopic Arthrography
Computed Tomography
K E Y P O I N T
T echnical Aspects
Computed Tomographic Arthrography
Rationale and Indications
T echnical Aspects
Magnetic Resonance Arthrography (Direct)
Magnetic Resonance Imaging
T echnical Aspects
Magnetic Resonance Arthrography (Indirect—with I n t r a v e n o u s Infusio
T echnical Aspects
Ultrasonography
NORMAL ANATOMY OF THE WRIST AND HAND
Osseous Structures
Carpal Bones
Metacarpals
Phalanges
Synovial Compartments
Joint Anatomy
Metacarpophalangeal Joints
Metacarpophalangeal Joint of the Thumb
Metacarpophalangeal Joints of the Fingers
Interphalangeal Joints
Interphalangeal Joint of the Thumb
Proximal Interphalangeal Joint
Distal Interphalangeal Joint
Carpal Ligaments
Muscles and Tendons Extensor Tendons
Flexor Tendons
Lumbricals
Interosseous Muscles
Thenar Muscles
Hypothenar Muscles
Digital Extensor Hood Mechanism
Extrinsic Digital Extensor Mechanism
Intrinsic Digital Extensor Mechanism
Intrinsic Muscles
Extensor Mechanism of the Thumb
Extrinsic Extensor Mechanism
Intrinsic Extensor Mechanism
Digital Flexor Tendon Sheath
Flexor Tendon Sheath
Fibro-osseous Tunnels
Fibro-osseous Tunnels of the Fingers
Fibro-osseous Tunnel of the Thumb
The Distal Phalanges
The Middle and Proximal Phalanges
The Metacarpals
The Short Hand Bones
The Scaphoid
PRACTICAL NORMAL VARIANTS Development
The Long Hand Bones
The Lunate
The Triquetrum
The Trapezium
The Trapezoid
The Capitate
The Pisiform
The Hamate
The Distal Forearm
Sesamoid Bones
BIOMECHANICS
W rist Motion
Carpal Bone Motion
A cute Osseous Injury t o the Wrist
Nisha Rao, Peter Hrehorovich, and Manesh Mathew
BIOMECHANICS
Special Anatomic Considerations
ANATOMY (INCLUDING GROSS ANATOMY AND NORMAL VARIANTS)
K E Y P O I N T S
Scapholunate Angle and the Capitolunate Angle
V ariants
IMAGING TECHNIQUES
MANIFESTATIONS OF THE DISEASE Distal Radius/Ulna
Carpal Fractures
Dislocations
SYNOPSIS OF TREATMENT OPTIONS Surgical Treatment
Tr a p e z i u m a n d t r a p e z o i d f r a c t u r e s : Cast i m mobi
Per i lunate i n st a bi l ity t reat ment : See references 1 1 and
REFERENCES
Internal Derangement o f the Wrist
T ravis Snyder and Andrew Haims
ANATOMY
T riangular Fibrocartilage Complex
V ascular Supply
Central Disc or Triangular Fibrocartilage
Dorsal and Volar Radioulnar Ligaments
Ulnocarpal Ligaments
Ulnar Collateral Ligament Complex
Scapholunate Ligament
Lunotriquetral Ligament
Extrinsic Ligaments
BIOMECHANICS
Scapholunate Ligament
Lunotriquetral Ligament
Carpal Instability
P A THOLOGY
T riangular Fibrocartilage Complex
Scapholunate Ligament
Lunotriquetral Ligament
Scapholunate Dissociation and Rotatory Subluxation of the Scaphoid
Dorsif lexed Intercalated Segment Instability
V olarf lexed Intercalated Segment Instability
MANIFESTATIONS OF THE DISEASE Radiography
Ulnar Impaction Syndrome
Scapholunate Ligament
W rist Arthrography
Magnetic Resonance Imaging Class 1: Traumatic Lesions of the TFCC
Class 2: Degenerative Lesions of the TFCC
Articular Cartilage Evaluation
Ulnar Impaction Syndrome
Scapholunate Ligament
Lunotriquetral Ligament
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS Ulnar Impaction Syndrome
Scapholunate Ligament
P artial Tears
Complete Tears
Lunotriquetral Ligament
What the Referring Physician Needs to Know
A cute Osseous Trauma t o the Hand
Joshua Owen, Richard Oh, Peter Hrehorovich, and Manesh Mathew
PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS
P A THOLOGY R outine Imaging
Additional Imaging
MANIFESTATIONS OF THE DISEASE F ractures of the Thumb
Radiography
Bennett’s Fracture
Rolando’s Fracture
Ulnar Collateral Ligament Avulsion (Skier’s Thumb)
Extra-articular Fractures of Thumb
Second through Fifth Metacarpal F ractures
Metacarpal Neck Fractures (Boxer’s Fracture)
M e t a c a rpal Diaphyseal Fractures
Intra-articular Basilar Fractures of Metacarpals
T raumatic Injuries to the Proximal Phalanx
T raumatic Injury to the Middle Phalanx Radiography
V olar Base Fractures
Dorsal Base Fractures
Comminuted or “Pilon” Fractures of the Base
T raumatic Injury to the Distal Phalanx Radiography
Dorsal Base Fracture (Baseball or Mallet Finger)
V olar Base Fractures
Epiphyseal Fractures
Dislocations Involving the Metacarpals Radiography
Dislocations of the Interphalangeal Joints Radiography
Proximal Interphalangeal Joint
Distal Interphalangeal Joint
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
SUGGESTED READINGS
REFERENCES
Soft Tissue Injuries of the Hand and Wrist
Luis Cerezal, Eva Llopis, Ana Canga, Faustino Abascal, and Alejandro Rolón
ULNAR-SIDED IMPACTION SYNDROMES
K E Y P O I N T S : U L N A R - S I D E D I M PAC T I O
Ulnar Impingement Syndrome Prevalence, Epidemiology, and Definitions
P athology
Manifestations of the Disease
Radiography
Computed Tomography
N u c l e a r Medicine
Magnetic Resonance Imaging
Differential Diagnosis
Synopsis of Treatment Options
Ulnar Styloid Impaction Syndrome Prevalence, Epidemiology, and Definitions
Anatomy
P athology
Manifestations of the Disease
Multidetector Computed Tomography
N u c l e a r Medicine
Magnetic Resonance Imaging
Arthroscopy
Differential Diagnosis
Synopsis of Treatment Options
Hamatolunate Impaction Syndrome Prevalence, Epidemiology, and Definitions
Anatomy
P athology
Manifestations of the Disease
Radiography
Multidetector Computed Tomography
N u c l e a r Medicine
Magnetic Resonance Imaging
Differential Diagnosis
Synopsis of Treatment Options
What the Referring Physician Needs to Know: Ulnar-Sided Impaction Syndromes
WRIST INSTABILIT Y
Prevalence, Epidemiology, and Definitions
P athology
Classification
Manifestations of the Disease
Additional Views
M e a s u r e m e n t of Carpal Bone Alignment
Fluoroscopy
S t r e s s Views
Cineradiography or Fluoroscopy with Videotape
Arthrography
Multidetector Computed Tomography
N u c l e a r Medicine
Magnetic Resonance Imaging
Magnetic Resonance Arthrography
Arthroscopy
Differential Diagnosis
What the Referring Physician Needs to Know: Wrist Instability
P athology
Synopsis of Treatment Options
LESIONS OF THE LIGAMENTS OF
THE FINGERS
Metacarpophalangeal Joint of the Thumb
Prevalence, Epidemiology, and Definitions
Manifestations of the Disease
Radiography
Ultrasonography
Multidetector Computed Tomography
Magnetic Resonance Imaging
Differential Diagnosis
Synopsis of Treatment Options
Medical Treatment
Basal Joint of the Thumb Prevalence, Epidemiology, and Definitions
Anatomy
P athology
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
Synopsis of Treatment Options
Proximal Interphalangeal Joint Prevalence, Epidemiology, and Definitions
P athology
Manifestations of the Disease
Multidetector Computed Tomography
Magnetic Resonance Imaging
Synopsis of Treatment Options
Metacarpophalangeal Joint Prevalence, Epidemiology, and Definitions
K E Y P O I N T S : L I G A M E N T L E S I O N S
Anatomy
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
Synopsis of Treatment Options
EXTENSOR TENDON INJURIES
Anatomy
First Extensor Compartment (de Quer v ain’s Disease)
Prevalence, Epidemiology, and Definitions
Manifestations of the Disease
Ultrasonography
Magnetic Resonance Imaging
Differential Diagnosis
Synopsis of Treatment Options
Medical Treatment
Surgical Treatment
Second Extensor Compartment (Intersection Syndrome)
Prevalence, Epidemiology, and Definitions
P athology
Manifestations of the Disease
Ultrasonography and Magnetic Resonance Imaging
Differential Diagnosis
Synopsis of Treatment Options
Medical Treatment
Surgical Treatment
Third Extensor Compartment Prevalence, Epidemiology, and Definitions
Manifestations of the Disease
Ultrasonography and Magnetic Resonance Imaging
Synopsis of Treatment Options
F ourth and Fifth Extensor Compartments: Lacerations
Ultrasonography and Magnetic Resonance Imaging
Synopsis of Treatment Options
Mallet Finger
Prevalence, Epidemiology, and Definitions
Manifestations of the Disease
Ultrasonography and Magnetic Resonance Imaging
Synopsis of Treatment Options
Boutonnière Deformity
Prevalence, Epidemiology, and Definitions
Manifestations of the Disease
Magnetic Resonance Imaging
Synopsis of Treatment Options
Medical Treatment
Surgical Treatment
Metacarpophalangeal (Zone V)
Subluxation or Dislocation Prevalence, Epidemiology, and Definitions
Manifestations of the Disease
Magnetic Resonance Imaging
Synopsis of Treatment Options
Sixth Extensor Compartment Prevalence, Epidemiology, and Definitions
P athology
Manifestations of the Disease
Ultrasonography and Magnetic Resonance Imaging
Synopsis of Treatment Options
FLEXOR TENDON INJURIES
Open Injuries
Manifestations of the Disease
Magnetic Resonance Imaging
Synopsis of Treatment Options
Closed Injuries
Manifestations of the Disease
Ultrasonography and Magnetic Resonance Imaging
Synopsis of Treatment Options
Digital Flexors
Flexor Pollicis Longus
Flexor Carpi Radialis
Flexor Carpi Ulnaris
Pulley System Injuries
Prevalence, Epidemiology, and Definitions
Manifestations of the Disease
Ultrasonography and Magnetic Resonance Imaging
K E Y P O I N T S : T E N D O N I N J U R I E S
Synopsis of Treatment Options
What the Referring Physician Needs to Know: T endon Injuries
GANGLION CYST
Prevalence, Epidemiology, and Definitions
P athology
Manifestations of the Disease
Radiography
Ultrasonography
Magnetic Resonance Imaging
Arthroscopy
Differential Diagnosis
Synopsis of Treatment Options
F OREIGN BODIES
Prevalence, Epidemiology, and Definitions
P athology
Manifestations of the Disease
K E Y P O I N T S : G A N G L I O N C YS T
Radiography
Ultrasonography
Multidetector Computed Tomography
K E Y P O I N T S : FO R E I G N B O D I E S
Magnetic Resonance Imaging
Differential Diagnosis
Synopsis of Treatment Options
What the Referring Physician Needs to Know: F oreign Bodies
REFERENCES
P elvis-Hip: Technical A spects, Normal Anatomy, Common Variants, and Basic Biomechanics
Eva Llopis, Pilar Ferrêr, and Francisco Aparisi
TECHNICAL ASPECTS T echniques and Relevant Aspects
Conventional Radiography
Measurements from an Anteroposterior View 1,2 Acetabular Measurements
Femoral Head
Proximal Head
Multidetector Computed Tomography
Rationale and Indications (Fig. 18-8)
T echnical Aspects See Table 18 - 2. 3,4
Computed Tomographic Arthrography 6
Magnetic Resonance Imaging: Conventional P elvis Imaging
Limitations Expensive
T echnical Aspects
Dedicated Hip Magnetic Resonance Imaging
Rationale and Indications
Advantages
Measurements
Indirect Magnetic Resonance Arthrography
Limitations
Direct Magnetic Resonance Arthrography
Rationale and Indications
Advantages
Ultrasonography
Advantages
NORMAL ANATOMY Osseous Structures
F emoral Head
P elvis and Acetabulum
Bone Marrow
Cartilage
Labrum
Joint Capsule
Ligaments
Muscles and Tendons
Anterior Quadrant
Lateral Quadrant
P osterior Quadrant
Bursae
Neurovascular Bundles
COMMON VARIANTS
Cystic Changes in the Femoral Neck, Herniation Pits
Labral Signal
Sublabral Sulcus
V ariations of the Labrum
T rabecular Bars
Iliopsoas Bursa Communication
Anterior Capsule Variants
Os Acetabuli
Otto Pelvis, Protrusio Acetabuli
B ASIC BIOMECHANICS
SUGGESTED READINGS
A cute Osseous Injury to the P elvis and Acetabulum
Eva Llopis, Victoria Higueras, Pilar Aparisi, José M. Mellado, and Francisco A
PELVIC RING INJURIES Prevalence, Epidemiology, and Def initions
Anatomy
Biomechanics
Imaging Techniques
Radiography
Anteroposterior Radiographs of the Pelvis
Inlet Radiographs of the Pelvis
Outlet Radiographs of the Pelvis
Lateral Projection
Ultrasonography
Computed Tomography
Angiography
Manifestations of the Disease
Anteroposterior Compression Injury
Lateral Compression Injury
V ertical Shear Injury
Complex Injury
Synopsis of Treatment Options
K E Y P O I N T S : P E L V I C R I N G I N J U R I E S
Provisional Stabilization
Definitive Stabilization
Anteroposterior Compression Injuries
Lateral Compression Injuries
A CETABULAR FRACTURES Prevalence, Epidemiology, and Def initions
Anatomy
Imaging Techniques Radiography
P osterior Wall Fracture
T r ansverse Fracture
Anterior Column
P osterior Column
Anterior Wall
Associated Fractures
T r ansverse and Posterior Wall Fractures
F r actures of Both Columns
T -Shaped Fractures
Anterior Wall or Anterior Column with T r ansverse Fracture
P osterior Column and Posterior Wall Fracture
Synopsis of Treatment Options
K E Y P O I N T S : A C E T A B U L A R F R AC T U R E S
BONE STRESS FRACTURES OF THE PELVIS
Prevalence, Epidemiology, and Def initions
Biomechanics and Pathology
Manifestations of the Disease
Radiography
Computed Tomography
Magnetic Resonance Imaging
Nuclear Medicine
Differential Diagnosis
Synopsis of Treatment Options
A VULSION FRACTURES Prevalence, Epidemiology, and Def initions
Anatomy
Biomechanics
Imaging Techniques
Manifestations of the Disease
Radiography
A vulsion Fractures of the Ischial Tuberosity
A vulsion Fractures of the Anterior-Inferior Iliac Spine
A vulsion Fractures of the Anterior-Superior Iliac Spine
A vulsion Fractures of the Pubic Bones
A vulsion Fractures of the Iliac Crest
Differential Diagnosis
Surgical Treatment
A cute Osseous Injury to the Hip and Proximal Femur
José M. Mellado, Ana M. Hualde, Jorge Albareda, and Eva Llopis
TRAUMATIC HIP DISLOCATIONS AND FEMORAL HEAD FRACTURES Prevalence, Epidemiolo
Anatomy
Biomechanics
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
Computed Tomography
Classic Signs: Hip Dislocation
Nuclear Medicine
Differential Diagnosis
Synopsis of Treatment Options Medical Treatment
Surgical Treatment
SUBCHONDRAL INSUFFICIENCY FRACTURES OF THE FEMORAL HEAD Prevalence, Epidemio
Anatomy
Biomechanics
P athology
Manifestations of the Disease
Magnetic Resonance Imaging
Nuclear Medicine
Classic Signs: Subchondral Insufficiency Fractures o f the Femoral Head
Differential Diagnosis
Synopsis of Treatment Options Medical Treatment
Surgical Treatment
TRAUMATIC FRACTURES OF THE FEMORAL NECK Prevalence, Epidemiology, and Def i
Anatomy
Biomechanics
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
Computed Tomography
Nuclear Medicine
Classic Signs: Traumatic Fractures of the Femoral Neck
Differential Diagnosis
K E Y P O I N T S : T R A U M A T I C F R A C T U R E
Synopsis of Treatment Options Medical Treatment
Surgical Treatment
STRESS FRACTURES OF THE FEMORAL NECK
Prevalence, Epidemiology, and Def initions
Anatomy
Biomechanics
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
Differential Diagnosis
Classic Signs: Stress Fractures of the Femoral Neck
Synopsis of Treatment Options Medical Treatment
Surgical Treatment
ISOL A TED FRACTURES OF THE GREATER AND LESSER TROCHANTERS Prevalence, Epide
Radiography
Magnetic Resonance Imaging
K E Y P O I N T S : S T R E S S F R A C T U R E S
Differential Diagnosis
Synopsis of Treatment Options Medical Treatment
Surgical Treatment
INTERTROCHANTERIC FRACTURES Prevalence, Epidemiology, and Def initions
K E Y P O I N T S : I S O L A T E D
F R A C T U R E S O F T H E G R E A T E R A N D L E S S
Biomechanics
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
K E Y P O I N T S : I N T E R T RO C H A N T E R I C F R AC T U R E
Computed Tomography
Differential Diagnosis
Synopsis of Treatment Options Medical Treatment
Classic Signs: Intertrochanteric Fractures
Surgical Treatment
SUBTROCHANTERIC FRACTURES Prevalence, Epidemiology, and Def initions
Biomechanics
Manifestations of the Disease
Radiography
K E Y P O I N T S : S U B T R O C H A N T E R I C F
Classic Signs: Subtrochanteric Fractures
Synopsis of Treatment Options Medical Treatment
Surgical Treatment
SUGGESTED READINGS
Internal Derangements o f the Hip and Proximal F emur (Including Intra- and
Josef Kramer, Christian Czerny, Christian W. Pfirrmann,
Sigfried Hofmann, and Anna Scheurecker
ANATOMY OF THE HIP JOINT
RADIOLOGIC METHODS
Magnetic Resonance Arthrography of the Hip
K E Y P O I N T S
OSTEONECROSIS OF THE HIP Prevalence, Epidemiology, and Def initions
P A THOLOGY
Imaging Findings by Stage
S tage 0
S tage I
Radiography and Computed Tomography
N u c l e a r Medicine
Magnetic Resonance Imaging
S tage II
Radiography and Computed Tomography
S tages III and IV
Radiography and Computed Tomography
Magnetic Resonance Imaging
Synopsis of Treatment Options
N u c l e a r Medicine
Magnetic Resonance Imaging
LEGG-CALVÉ-PERTHES DISEASE Prevalence, Epidemiology, and Def initions
P athology
Imaging Findings by Catterall Classif ication
Radiology
Grade I
Grade II
Grade III
Grade IV
Magnetic Resonance Imaging
TRANSIENT OSTEOPOROSIS
OF THE HIP (BONE MARROW EDEMA SYNDROME)
Prevalence, Epidemiology, and Def initions
P athology
Imaging Findings
Radiography and Computed Tomography
Nuclear Medicine
Synopsis of Treatment Options
BONE CONTUSION/MICROFRACTURES Prevalence, Epidemiology, and Def initions
P athology
Radiography and Computed Tomography
Nuclear Medicine
Magnetic Resonance Imaging
STRESS/INSUFFICIENCY FRACTURES
Prevalence, Epidemiology, and Def initions
Imaging Findings
LESIONS OF THE ACETABULAR L ABRUM Anatomy
P athology
Imaging Findings
Radiography and Computed Tomography
Magnetic Resonance Imaging
Synopsis of Treatment Options
FEMOROACETABULAR IMPINGEMENT Prevalence, Epidemiology, and Def initions
Biomechanics
Imaging Findings
Radiography
Magnetic Resonance Imaging and Computed T omography
Synopsis of Treatment Options
SYNOVIAL OSTEOCHONDROMATOSIS Prevalence, Epidemiology, and Def initions
Anatomy
Computed Tomography
Magnetic Resonance Imaging
ILIOPSOAS BURSITIS Prevalence, Epidemiology, and Def initions
Synopsis of Treatment Options
SNAPPING (EXTERNAL) HIP Prevalence, Epidemiology, and Def initions
Synopsis of Treatment Options
SEPTIC ARTHRITIS
RAPID DESTRUCTIVE HIP DISEASE
REFERENCES
Knee: Technical Aspects, Normal Anatomy, Common
V ariants, and Basic Biomechanics
Michel O. De Maeseneer and Maryam Shahabpour
IMAGING TECHNIQUES T echnical Aspects
Controversies
NORMAL ANATOMY
BIOMECHANICS
A cute Osseous Injury t o the Knee
Adam C. Zoga and David Karasick
P A THOPHYSIOLOGY Anatomy
P athology
Radiographic Diagnosis of Fractures
Radiographic Findings That Warrant A dditional Imaging
Internal Derangement of the Knee: Meniscal Injuries
Linda J. Probyn and Lawrence M. White
NORMAL ANATOMY
K E Y P O I N T S
BIOMECHANICS Meniscal Function
IMAGING TECHNIQUES
MANIFESTATIONS OF THE DISEASE Magnetic Resonance Imaging
Meniscal Tears
Oblique or Horizontal Tears
V ertical Longitudinal Tears and Bucket Handle Tears
Radial and Parrot Beak Tears
P eripheral Tears
Meniscal Extrusion/Meniscal Root Tears
Complex Tears
S y m p t o m a t i c versus Asymptomatic Meniscal Tears
Errors and Pitfalls of Interpretation
Anterior Horn of the Lateral Meniscus
Meniscal Flounce
Meniscofemoral Ligament
T r ansverse Meniscal Ligament
P opliteus Tendon
V olume Averaging
Chondrocalcinosis
Magic-Angle Phenomenon
Computed Tomography Arthrography
Ultrasonography
Miscellaneous Meniscal Conditions Meniscal Cysts
Meniscal Contusion
Discoid Meniscus
Meniscocapsular Separation
Meniscal Ossicle
SYNOPSIS OF TREATMENT OPTIONS Surgical Treatment
P ostoperative Meniscus
What the Referring Physician Needs to Know
REFERENCES
Internal Derangement of the Knee: Ligament Injuries
Eugene G. McNally
THE ANTERIOR CRUCIATE LIGAMENT Prevalence, Epidemiology, and Def initions
Biomechanics
P athology
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
Primary Signs
Secondary Signs
Bony Injuries Associated with Anterior Cruciate Ligament Rupture
Soft Tissue Secondary Signs
Secondary Signs due to Tibial Translation
Computed Tomography
Ultrasonography
Nuclear Medicine
Synopsis of Treatment Options
Classic Signs
THE POSTERIOR CRUCIATE LIGAMENT Prevalence, Epidemiology, and Def initions
Anatomy
Biomechanics
P athology
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
OTHER INTRA-ARTICULAR LIGAMENTS Prevalence, Epidemiology, and Def initions
Anatomy Intermeniscal Ligaments
Computed Tomography
Ultrasonography
Classic Sign
The Meniscofemoral Ligaments
Miscellaneous Intra-articular Minor Ligaments
L A TERAL SUPPORTING STRUCTURES Prevalence, Epidemiology, and Def initions
Anatomy
Classic Signs
Biomechanics
Manifestations of the Disease
Classic Signs
MEDIAL SUPPORTING STRUCTURES Prevalence, Epidemiology, and Def initions
Biomechanics
P athology
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
Ultrasonography
Synopsis of Treatment Options
A CKNOWLEDGMENT
REFERENCES
Internal Derangement of the Knee: Tendon Injuries
Theodore T. Miller
THE EXTENSOR APPARATUS
Quadriceps Tendon Rupture Anatomy
Prevalence
Biomechanics
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
Ultrasonography
Synopsis of Treatment Options
What the Referring Physician Needs to Know
K E Y P O I N T S : T H E E X T E N S O R A P PA R AT
P atellar Tendinosis and Tear
Anatomy
Prevalence and Epidemiology
Biomechanics
P athology
Clinical Presentation
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
Jumper ’ s Knee (Patellar Tendinitis)
Prevalence
Biomechanics
P athology
Manifestations of the Disease
Magnetic Resonance Imaging
Ultrasonography
Synopsis of Treatment Options
Osgood-Schlatter Disease, Sinding- Larsen-Johansson Syndrome, and Patellar S
Prevalence and Epidemiology
Biomechanics
P athology
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
Ultrasonography
Differential Diagnosis
P atellar Tendon/Lateral Femoral Condyle F riction Syndrome
Prevalence
Biomechanics
Manifestations of the Disease
Magnetic Resonance Imaging
Infrapatellar Fat Pad Impingement (Hoffa’s Disease)
Anatomy
Biomechanics
P athology
Manifestations of the Disease
Magnetic Resonance Imaging
Differential Diagnosis
P atellar Position and Maltracking Anatomy
Prevalence
Biomechanics
Manifestations of the Disease
Magnetic Resonance Imaging
Excessive Lateral Pressure Syndrome and the Patellofemoral Pain Syndrome Pre
Biomechanics
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
Differential Diagnosis
Synopsis of Treatment Options
Medical Treatment
Surgical Treatment
P atellar Dislocation Biomechanics
P athology
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging 54,55
Ultrasonography
Biomechanics
Clinical Presentation
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
Synopsis of Treatment Options
ILIOTIBIAL BAND Anatomy
What the Referring Physician Needs to Know
Bipartite Patella and Dorsal Defect of the Patella
Prevalence
POPLITEUS AND BICEPS FEMORIS MUSCLES AND TENDONS (THE POSTEROL A TERAL CORNE
Anatomy
Prevalence
Biomechanics
Biomechanics
Ultrasonography
Differential Diagnosis
Synopsis of Treatment Options
K E Y P O I N T: H A M S T R I N G S
What the Referring Physician Needs to Know
HAMSTRINGS Anatomy
Prevalence
Biomechanics
P athology
Manifestations of the Disease
Magnetic Resonance Imaging
Ultrasonography
Synopsis of Treatment Options
What the Referring Physician Needs to Know
CALF Anatomy
K E Y P O I N T: C A L F
Biomechanics
Prevalence
P athology
Manifestations of the Disease
Magnetic Resonance Imaging
K E Y P O I N T : S E M I M E M B R A N O S U S A N
Differential Diagnosis
Synopsis of Treatment Options
SEMIMEMBRANOSUS AND PES ANSERINUS TENDONS (THE POSTEROMEDIAL CORNER)
Anatomy
Biomechanics
What the Referring Physician Needs to Know
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
BURSAE Anatomy
Prevalence
K E Y P O I N T: B U R SA E
Biomechanics
Manifestations of the Disease
Ultrasonography
Differential Diagnosis
Synopsis of Treatment Options
PLICAE Anatomy
Prevalence
Biomechanics
K E Y P O I N T S : P L I C A E
Differential Diagnosis
Synopsis of Treatment Options
What the Referring Physician Needs to Know
REFERENCES
Internal Derangement of the Knee: Cartilage and
Osteochondral Injuries
K oenraad L. Verstraete and Wouter C. J. Huysse
K E Y P O I N T S
T raumatic Chondral or Osteochondral Lesions
Osteochondritis Dissecans
Subchondral Insuf f iciency Fractures
ANATOMY
BIOMECHANICS
Reaction of Cartilage to Loading
Reaction of Cartilage to Injur y
MANIFESTATIONS OF THE DISEASE T raumatic Chondral or Osteochondral Lesions a
Grading of Cartilage Lesions
Magnetic Resonance Imaging
Multidetector Computed Tomography
Ultrasonography
Nuclear Medicine
P ositron Emission Tomography/Computed T omography
Arthroscopy
Osteochondritis Dissecans of the Knee
Grading of Osteochondritis Dissecans
Radiography
Classic Signs
Multidetector Computed Tomography
Nuclear Medicine
Arthroscopy
Classic Signs
Subchondral Insuf f iciency Fracture Associated with Spontaneous Osteonecros
Grading of Subchondral Insufficiency Fractures
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Nuclear Medicine
Arthroscopy
DIFFERENTIAL DIAGNOSIS
F rom Clinical Data
F rom Supportive Diagnostic Techniques
Medical Treatment
Surgical Treatment
SUGGESTED READINGS
REFERENCES
Ankle/Foot: Technical A spects, Normal Anatomy, Common Variants, and Basic
Lisa O. Ballehr
TECHNICAL ASPECTS
Conventional Radiography (Table 28-1)
Indication
A dvantages
Disadvantages
T echnical Aspects
Computed Tomography (Table 28-2)
Indications
A dvantages
Disadvantages
A dvantages
Disadvantages
T echnical Aspects
Magnetic Resonance Imaging (Table 28-3)
Indications
Ultrasonography
A dvantages
Disadvantage
T echnical Aspects
NORMAL ANATOMY
T alocrural Joint
Medial Ankle Mortise (Figs. 28-1 to 28-4)
M e d i a l C o l l a t e r a l L i g a m e n t C o m p l e x
Central Ankle Mortise and Joint Capsule
Syndesmotic Ligament Complex (see Figs. 28-3 to 28-6)
Lateral Collateral Ligament Complex
Anterior Subtalar Joint
P osterior Subtalar Joint
Spring Ligament Complex
T alocalcaneonavicular Ligament Complex
Lisfranc Ligament (see Fig. 28-10)
Lesser Digit Metatarsophalangeal Joints, Plantar Plates (Phalangeal Apparatus
Muscles, Tendons, and Retinacula about the Ankle
Muscles, Tendons, and Retinacula about the Foot
Hallux Sesamoid Complex and Third Plantar M u s c l e Layer (see Figs. 28-1
Fourth Plantar Muscle Layer (see Figs. 28-12 and 28-14)
COMMON VARIANT ANATOMY
Accessory Ossicles (Fig. 28-20)
P osterior Intermalleolar Ligament
L o w - L y i n g Peroneus Brevis Muscle
P eroneus Quartus Muscle (Fig. 28-22)
P eroneus Calcaneus Internus (Fig. 28-23)
Accessory Soleus (Fig. 28-24)
Accessory Flexor Digitorum Longus Muscle (Fig. 28-25)
B ASIC BIOMECHANICS
A cute Osseous Injury t o the Ankle
A. Bassem Elaini and William E. Palmer
ANATOMY
BIOMECHANICS
MANIFESTATIONS OF THE DISEASE Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
DIFFERENTIAL DIAGNOSIS F rom Clinical Data
F rom Supportive Diagnostic Techniques
Surgical Treatment
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
REFERENCES
Soft Tissue Injury to the Ankle: Ligaments
Y v o n n e Y. Cheung and Zehava S. Rosenberg
GENERAL CONSIDERATIONS Prevalence, Epidemiology, and Def initions
Anatomy
Biomechanics
P athology
K E Y P O I N T S : G E N E R A L C O N S I D E R AT I O N
Manifestations of the Disease Radiography
Magnetic Resonance Imaging
Classif ication of Ligamentous Sprain
Multidetector Computed Tomography
Ultrasonography
Nuclear Medicine
Differential Diagnosis
L A TERAL LIGAMENT INJURY Prevalence, Epidemiology, and Def initions
K E Y P O I N T S : L A T E R A L
L I G A M E N T I N J U RY
Anatomy
Biomechanics
P athology
Magnetic Resonance Imaging
Manifestations of the Disease
Radiography
Ultrasonography
SYNDESMOTIC SPRAIN Prevalence, Epidemiology, and Def initions
K E Y P O I N T S : S Y N D E S M O T I C S P R A I N
Anatomy
Biomechanics
P athology
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Classic Signs
DELTOID LIGAMENT INJURY Prevalence, Epidemiology, and Def initions
Synopsis of Treatment Options
Medical Treatment
Biomechanics
K E Y P O I N T S : D E L T O I D
L I G A M E N T I N J U RY
Anatomy
P athology
Manifestations of the Disease
Radiography
Arthroscopy
Synopsis of Treatment Options
Medical Treatment
Surgical Treatment
SINUS TARSI
Prevalence, Epidemiology, and Definitions
Biomechanics
P athology
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
Replacement of Normal Fat Signal in the Sinus Tarsi
A bnormal Sinus Tarsi Ligaments
Associated Findings
Multidetector Computed Tomography
Classic Signs: Sinus Tarsi Syndrome
Arthroscopy
Synopsis of Treatment Options
SPRING LIGAMENT Prevalence, Epidemiology, and Def initions
Anatomy
Biomechanics
P athology
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
Synopsis of Treatment Options
LISFRANC LIGAMENT COMPLEX Prevalence, Epidemiology, and Def initions
Anatomy
K E Y P O I N T S : L I S F R A N C
L I G A M E N T C O M P L E X
Biomechanics
P athology
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Nuclear Medicine
Synopsis of Treatment Options Medical Treatment
Surgical Treatment
Classic Sign: Lisfrance Ligament Complex
SUGGESTED READINGS
REFERENCES
Soft Tissue Injury to the Ankle: Tendons
Alison R. Spouge and Kevin R. Willits
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY
Anatomy
K E Y P O I N T S
P osterior Ankle Tendons (Achilles, Plantaris)
Achilles Tendon
Achilles Tendon Variants
Plantaris Tendon
Medial Ankle Tendons (Tibialis Posterior, Flexor Hallucis Longus, and Flexor
Tibialis Posterior
Flexor Hallucis Longus
Flexor Digitorum Longus
Lateral Tendons (Peroneus Brevis and Peroneus Longus)
Anatomic Variants of the Peroneal Tendons
Anterior Ankle Tendons (Tibialis Anterior)
Extensor Digitorum Longus
Extensor Hallucis Longus
BIOMECHANICS
Achilles Tendon
Medial Tendons
Lateral Tendons
Anterior Tendons
IMAGING TECHNIQUES
Radiography
Magnetic Resonance Imaging
Multidetector Row Computed To m o g r a p h y
Ultrasonography
Nuclear Medicine
P ositron Emission Tomography/
Computed Tomography
Te n o g r a p h y
MANIFESTATIONS OF THE DISEASE
Anterior Tendons
General Features
Tibialis Anterior
Radiography
Ultrasonography
Classic Sign
Medial Tendons
General Features
Tibialis Posterior
Flexor Hallucis Longus
Radiography
Magnetic Resonance Imaging
Tibialis Posterior
Flexor Hallucis Longus Tendon
Lateral Tendons
General Features
P eroneal Tendons
Classic Signs
Radiography
Magnetic Resonance Imaging
Lateral Tendons
Ultrasonography
P osterior Tendons
General Features
Achilles Tendon
Classic Signs
Plantaris Tendon
Radiography
Magnetic Resonance Imaging
Achilles Tendon
Classic Signs
Ultrasonography
DIFFERENTIAL DIAGNOSIS
P osterior Ankle Pain
Heel Pain
Lateral Ankle Pain
P eroneal Tendons
Medial Ankle Pain
Tibialis Posterior Tendon Dysfunction
Anterior Ankle Pain
Tibialis Anterior Disorders
Medical Treatment
P eroneus Brevis
Tibialis Posterior Tendon
A chilles Tendon
Surgical Treatment
Tibialis Posterior Tendon
P eroneal Tendon
What the Referring Physician Needs to Know
Soft Tissue Injury to the Ankle: Osteochondral Injury and Impingement
Luis Cerezal
P athology
ANTEROL A TERAL IMPINGEMENT SYNDROME
Prevalence, Epidemiology, and Def initions
Anatomy
Manifestations of the Disease
Radiography
Multidetector Computed Tomography
Nuclear Medicine
Magnetic Resonance Imaging
Arthroscopy
Classic Signs
Synopsis of Treatment Options Medical Treatment
Surgical Treatment
ANTERIOR IMPINGEMENT SYNDROME Prevalence, Epidemiology, and Def initions
Anatomy
What the Referring Physician Needs to Know
Manifestations of the Disease Radiography
Ultrasonography
Multidetector Computed Tomography
Nuclear Medicine
Magnetic Resonance Imaging
Arthroscopy
Classic Signs
Differential Diagnosis
Synopsis of Treatment Options Medical Treatment
Surgical Treatment
What the Referring Physician Needs to Know
MEDIAL IMPINGEMENT SYNDROME Prevalence, Epidemiology, and Def initions
Anatomy
Biomechanics and Pathology
K E Y P O I N T S
Manifestations of the Disease
Radiography and Multidetector Computed T omography
Ultrasonography
Magnetic Resonance Imaging
Arthroscopy
Classic Signs
POSTERIOR IMPINGEMENT SYNDROME Prevalence, Epidemiology, and Def initions
Anatomy
Differential Diagnosis
Synopsis of Treatment Options Medical Treatment
Surgical Treatment
What the Referring Physician Needs to Know
Biomechanics and Pathology
Manifestations of the Disease
Radiography
Ultrasonography
Arthroscopy
Classic Signs
Differential Diagnosis
Synopsis of Treatment Options Medical Treatment
Surgical Treatment
OSTEOCHONDRAL LESION OF THE TALUS
Prevalence, Epidemiology, and Def initions
Anatomy
Biomechanics and Pathology
What the Referring Physician Needs to Know
Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Nuclear Medicine
Arthroscopy
Classic Signs
Differential Diagnosis
Synopsis of Treatment Options
Medical Treatment
Surgical Treatment
SUGGESTED READINGS
A cute Osseous Injury t o the Foot
Thomas H. Berquist
PREVALENCE, EPIDEMIOLOGY, DEFINITIONS, AND ANATOMY
Hindfoot
T alus
T alar Neck Fractures
K E Y P O I N T S
T alar Body Fractures
Lateral Process Fractures
P osterior Process Fractures
Comminuted Talar Body Fractures
T alar Head Fractures
T alar Dislocations
Calcaneus
Calcaneal Fracture-Dislocations
Intra-articular Fractures
Extra-articular Fractures
Calcaneal Dislocations
Midfoot
Midfoot Fracture-Dislocations
N a vicular Fractures
Cuboid Fractures
Cuneiform Fractures
T arsometatarsal Fracture-Dislocations
Forefoot
Metatarsal Fractures
Phalangeal Fractures
Metatarsophalangeal and Interphalangeal Dislocations
MANIFESTATIONS OF THE DISEASE Radiography
Sesamoid Fractures
Multidetector Computed Tomography
Nuclear Medicine
Imaging of Specif ic Structures
T alar Fracture-Dislocations
Calcaneal Fracture-Dislocations
Midfoot Fracture-Dislocations
Forefoot Fracture-Dislocations
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS
T alar Fracture-Dislocations
Calcaneal Fracture-Dislocations
Midfoot Fracture-Dislocations
Forefoot Fracture-Dislocations
REFERENCES
Imaging of the Forefoot
Hilary Umans
IMAGING TECHNIQUES
MANIFESTATIONS OF THE DISEASE
Disorders of the First Metatarsophalangeal Joint
K E Y P O I N T S
Sesamoiditis
T urf Toe
Plantar Plate Anatomy
Metatarsalgia
Plantar Plate Rupture
Morton’s Neuroma
SUMMARY
Upper Extremity Injuries in Children (Including Sports Injuries)
Ann M. Johnson and Matthew A. Marcus
ANATOMY
K E Y P O I N T S
Remodeling
BIOMECHANICS
P A THOLOGY
MANIFESTATIONS OF THE DISEASE
Injuries of the Clavicle
Lateral Clavicular Physis and Acromioclavicular Joint
Medial Clavicular Physis and Sternoclavicular Joint
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Ultrasonography
Scapular Fractures
Radiography
Computed Tomography
Injuries of the Glenohumeral Joint, R otator Cuff, and Proximal Humerus
Glenohumeral Dislocation
Rotator Cuff Injuries
Proximal Humeral Fractures
Computed Tomography
Ultrasonography
Injuries of the Elbow
Supracondylar Fractures
Lateral Condyle Fractures
Medial Epicondyle Fractures
Distal Humerus Fracture Separation
F r actures of the Proximal Radius
Lateral Epicondyle Fractures
Olecranon Fractures
Radial Head Subluxation
Elbow Dislocation
Sports Injuries about the Elbow
Magnetic Resonance Imaging
Multidetector Computed Tomography
Classic Signs: Elbow Injuries
Ultrasonography
Injuries of the Forearm, Wrist, and Carpus
D i a p h y s e a l Injuries of Radius and Ulna
Monteggia Fracture-Dislocations
F r actures of the Distal Forearm and Wrist
Carpal Fractures
Radiography
Magnetic Resonance Imaging
Classic Signs
Metacarpal and Phalangeal Fractures
Metacarpal and Phalangeal Injuries
Magnetic Resonance Imaging
Multidetector Computed Tomography
Ultrasonography
SUGGESTED READINGS
REFERENCES
L o w er Extremity Injuries in Children (Including Sports Injuries)
D . Barron, J. Farrant, and Philip O’Connor
PREVALENCE AND EPIDEMIOLOGY
DEFINITIONS AND ANATOMY
BIOMECHANICS
DIAPHYSEAL AND METAPHYSEAL INJURIES
Manifestations of the Disease
T oddler’s Fracture
F r a c t u r e of the Tibial Metaphysis
F r actures with Nonossifying Fibromas
U nicameral Bone Cyst
F r actures of the Femoral Neck
Hip Fractures and Dislocations
F r actures of the Femoral Shaft
Bone Scintigraphy
Magnetic Resonance Imaging
Computed Tomography
Synopsis of Treatment Options Medical Treatment
Hip and Femoral Shaft
Hip Dislocation
Femoral Shaft Fracture
PHYSEAL INJURIES Manifestations of the Disease
Radiography
What the Referring Physician Needs to Know
BOX 36-1 Salter-Harris Classification
Hip
Magnetic Resonance Imaging
P elvis
Computed Tomography
Magnetic Resonance Imaging
Differential Diagnosis N o naccidental injur y
Synopsis of Treatment Options
A CUTE APOPHYSEAL INJURY
Manifestations of the Disease
Computed Tomography
Magnetic Resonance Imaging
Differential Diagnosis
Synopsis of Treatment Options
Ischial Tuberosity Avulsion
CHRONIC APOPHYSEAL INJURY: OSGOOD-SCHL A TTER DISEASE Manifestations of the
What the Referring Physician Needs to Know
Ultrasonography
Synopsis of Treatment Options Medical Treatment
Surgical Treatment
What the Referring Physician Needs to Know
CHRONIC APOPHYSEAL DISEASE: SINDING-LARSEN-JOHANSSON DISEASE Manifestations
Radiography
Ultrasonography
Synopsis of Treatment Options
THE PATELLAR SLEEVE FRACTURE Manifestations of the Disease
Ultrasonography
Magnetic Resonance Imaging
Differential Diagnosis J umper’s knee
Synopsis of Treatment Options
Medical Treatment
Surgical Treatment
A CUTE OSTEOCHONDRAL INJURIES Manifestations of the Disease
Ultrasonography
Magnetic Resonance Imaging
Arthroscopy
Synopsis of Treatment Options
OSTEOCHONDRITIS DISSECANS Manifestations of the Disease
Radiography
Ultrasonography
Computed Tomography
Bone Scintigraphy
Differential Diagnosis Stress fracture
Synopsis of Treatment Options
OTHER OSTECHONDROSES Manifestations of the Disease
Radiography
STRESS FRACTURES
Manifestations of the Disease
Nuclear Medicine
Magnetic Resonance Imaging
Ultrasonography
Computed Tomography
Differential Diagnosis
Synopsis of Treatment Options
THE PATELLAR TENDON Manifestations of the Disease
Radiography
Magnetic Resonance Imaging
Ultrasonography
Synopsis of Treatment Options
Medical Treatment
MYOTENDINOUS INJURY Manifestations of the Disease
Magnetic Resonance Imaging
Classification of Myotendinous Strains
MRI Appearances
Ultrasonography
Synopsis of Treatment Options
A CCESSORY OSSICLES Manifestations of the Disease
Scintigraphy
Differential Diagnosis
Synopsis of Treatment Options Medical Treatment
Surgical Treatment
REFERENCES
Skeletal Manifestations o f Child Abuse
Susanne Lardenoye-Broker and Alan Sprigg
ANATOMY
BIOMECHANICS
P A THOLOGY Radiographic Evaluation
Dating of Fractures
MANIFESTATIONS OF THE DISEASE F ractures of the Extremities
Classic Metaphyseal Lesion/Metaphyseal Fracture
Diaphyseal Fractures (Fig. 37-3)
Epiphyseal Injuries (Fig. 37-5)
F r actures of the Hands and Feet (Fig. 37-6)
F r actures of the Shoulder Girdle and Sternum
Spinal Fractures (Fig. 37-9)
Craniofacial Fractures (Fig. 37-10)
Thoracic Trauma
Rib Fractures (Fig. 37-7)
DIFFERENTIAL DIAGNOSIS
Diseases Simulating Abuse
Rickets and Metabolic Disease of Prematurity (Fig. 37-11)
Osteogenesis Imperfecta (Fig. 37-12)
Osteomyelitis (Fig. 37-13)
Other Diseases
A ccidental Trauma
Obstetric Injury
N o r m a l Variants
Stress Injury
Joong Mo Ahn and Georges Y. El-Khoury
K E Y P O I N T S
ANATOMY
BIOMECHANICS
P A THOLOGY
MANIFESTATIONS OF THE DISEASE
Radiography
Magnetic Resonance Imaging
Ultrasonography
Nuclear Medicine
SPECIFIC ANATOMIC SITES FOR STRESS INJURIES
F emur
Tibia
Calcaneus
T alus
T arsal Navicular
Stress Fractures in the Metatarsal and Sesamoid Bones
Other Sites of Lower Extremity
Sacrum
P elvis
P ars Interarticularis Stress Fracture (Spondylolysis)
Upper Extremity
Stress Injuries of the Physis
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS
Medical Therapy
Surgical Therapy
What the Referring Physician Needs to Know
R adiation Effects in the M usculoskeletal System
T amara Miner Haygood and William A. Murphy, Jr.
HISTORY AND RADIATION SOURCES
ANATOMY
P A THOLOGY
MANIFESTATIONS OF THE DISEASE Benef icial Effects
Side Effects in Sof t Tissue Radiography
Magnetic Resonance Imaging
Non-neoplastic Side Effects in Bone Radiography
R adiation-Induced Neoplasms
Computed Tomography
T umor Induction Radiography
Magnetic Resonance Imaging
Benign Side-Effects in Bone
REFERENCES
Complications of Osseous T r auma
Dechen Tshering and Suzanne Anderson
PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS
MANIFESTATIONS OF THE DISEASE Delayed Union, Pseudarthroses, or Nonunion of
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Arthroscopy
Growth Disturbances due to Physeal Injuries
Malunion, Cartilage Damage, and Early Degenerative Changes
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
P ost-traumatic Osteomyelitis
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Ultrasonography
Nuclear Medicine
P ositron Emission Tomography
A v ascular Necrosis
Magnetic Resonance Imaging
Multidetector Computed Tomography
Nuclear Medicine
P ost-traumatic Osteoporosis and Osteolysis
Sudeck’s Atrophy
Re-fracture
P ost-traumatic Cysts and Pseudotumors
DIFFERENTIAL DIAGNOSIS
What the Referring Physician Needs to Know
REFERENCES
M uscle Injury and Sequelae
Donald J. Flemming and Robert D. Boutin
PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS
ANATOMY
BIOMECHANICS
P A THOLOGY
MANIFESTATIONS OF THE DISEASE Muscle Strain or Tear
Magnetic Resonance Imaging
Ultrasonography
Hematoma
Radiography
Magnetic Resonance Imaging
Myositis Ossif icans
Magnetic Resonance Imaging
Multidetector Computed Tomography
Nuclear Medicine
Delayed-Onset Muscle Soreness
Magnetic Resonance Imaging
Ultrasonography
Muscle Herniation
Magnetic Resonance Imaging
Multidetector Computed Tomography
Compartment Syndrome
Magnetic Resonance Imaging
Diabetic Muscle Infarction
Ultrasonography
Dener v ation
Multidetector Computed Tomography
What the Referring Physician Needs to Know
SUGGESTED READINGS
Complex Regional Pain S y ndrome
Conrado F. Cavalcanti and Mark E. Schweitzer
PREVALENCE AND EPIDEMIOLOGY
K E Y P O I N T S
CLINICAL PRESENTATION
CLINICAL STAGING
MANIFESTATIONS OF THE DISEASE
Radiography
Scintigraphy
Single Photon Emission Computed T omography of the Brain
Doppler Ultrasonography
Magnetic Resonance Imaging
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS
What the Referring Physician Needs to Know
Degenerative Disorders o f the Spine
Iain McCall
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY Anatomy
P athology
MANIFESTATIONS OF THE DISEASE
Inter v ertebral Disc Degeneration
Magnetic Resonance Imaging
Discography
P osterior Annular Tears
Magnetic Resonance Imaging and Computed T omographic Discography
Herniation of the Nucleus Pulposus
Radiography
Computed Tomography
V ertebral End Plate
Radiography
Magnetic Resonance Imaging
Osteoarthritis of the Facet Joints
Radiography
Computed Tomography
Magnetic Resonance Imaging
P ain Testing
Cysts of the Inter v ertebral Facet Joints
Computed Tomography
Degenerative Spondylolisthesis
Radiography
Magnetic Resonance Imaging
Spinal Stenosis
Radiography
Computed Tomography
DIFFERENTIAL DIAGNOSIS
Correlation between Clinical and Imaging Findings
SYNOPSIS OF TREATMENT OPTIONS
What the Referring Physician Needs to Know
SUGGESTED READINGS
REFERENCES
A ging
WHAT IS AGING?
K E Y P O I N T S
MECHANISMS OF AGING
THE AGING MUSCULOSKELETAL SYSTEM
Within the Joint Organ as a Whole
A ge-Related Changes within Bone
A ge-Related Changes in Hyaline Cartilage
A ge-Related Changes in Skeletal Muscle
A ge-Related Changes in Ligaments and Tendons
Other Age-Related Changes in the Spine
A ge-Related Changes in the Whole Joint Organ
Degenerative Disease: Cartilage Anatomy, Physiology, and A dvanced Imaging
Timothy J. Mosher
ETIOLOGY
P A THOPHYSIOLOGY Anatomy
BIOMECHANICS
T echniques and Relevant Aspects
MANIFESTATIONS OF THE DISEASE
Grade I Lesions
Magnetic Resonance Imaging
Grade II Lesions Magnetic Resonance Imaging
Grade III Lesions Magnetic Resonance Imaging
Grade IV Lesions Magnetic Resonance Imaging
Bone Marrow Lesions Associated with Cartilage Injur y
Magnetic Resonance Imaging
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
What the Referring Physician Needs to Know
SUGGESTED READINGS
Rheumatoid Arthritis
Marcy B. Bolster and Johnny U. V. Monu
CLINICAL PRESENTATION
IMAGING TECHNIQUES
General Radiographic Obser v ations Joint Swelling
Subluxations
Osteopenia
Loss of Joint Space
Erosions
Osteolysis
Osteitis
Subchondral Cysts
Osteonecrosis
Selected Joints Hands and Feet
Spine
MANIFESTATIONS OF THE DISEASE Extra-articular Manifestations
Radiography
Magnetic Resonance Imaging
Ultrasonography
Nuclear Medicine
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS
SUGGESTED READINGS
REFERENCES
Psoriatic Arthritis and Psoriatic Spondylarthropathy
Karsten Jablonka and Jürgen Freyschmidt
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
IMAGING TECHNIQUES T echniques and Relevant Aspects
Pros and Cons
MANIFESTATIONS OF THE DISEASE P eripheral Skeleton
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Ultrasonography
Nuclear Medicine
Axial Skeleton
Radiography
Classic Signs
Multidetector Computed Tomography
Ultrasonography
Nuclear Medicine
Entheses
Radiography
Multidetector Computed Tomography
Nuclear Medicine
DIFFERENTIAL DIAGNOSIS
Classic Signs
What the Referring Physician Needs to Know
REFERENCES
R eactive Arthritis
Daniel Nissman and Thomas L. Pope
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
Musculoskeletal Manifestations
Extra-articular Manifestations
Natural History and Prognosis
P A THOLOGY
IMAGING TECHNIQUES
MANIFESTATIONS OF THE DISEASE Spondylitis
Magnetic Resonance Imaging
Multidetector Computed Tomography
Nuclear Medicine
Sacroiliitis
Classic Signs
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Nuclear Medicine
Erosive Arthritis and Proliferative New Bone Formation
Magnetic Resonance Imaging
Radiography
Magnetic Resonance Imaging
Ultrasonography
Multidetector Computed Tomography
Ultrasonography
Nuclear Medicine
Enthesitis
Dactylitis
Ultrasonography
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
What the Referring Physician Needs to Know
SUGGESTED READINGS
Ankylosing Spondylitis
Corinna Schorn and Gerwin Lingg
PREVALENCE AND EPIDEMIOLOGY
K E Y P O I N T S
L ABORATORY FINDINGS
DIAGNOSIS
P athology
BIOMECHANICS
IMAGING TECHNIQUES T echniques and Relevant Aspects
Pros and Cons
Controversies
MANIFESTATIONS OF THE DISEASE Sacroiliitis
Radiography
Erosions
Sclerosis
Bony Bridges and Ankylosis
Magnetic Resonance Imaging
Multidetector Computed Tomography
Ultrasonography
Nuclear Medicine
P ositron Emission Tomography/Computed T omography
Arthroscopy
VERTEBRAL MANIFESTATIONS
Radiography
Classic Signs
Magnetic Resonance Imaging
Multidetector Computed Tomography
Nuclear Medicine
Extravertebral Skeletal Manifestations
Magnetic Resonance Imaging
Computed Tomography
Ultrasonography
Nuclear Medicine
P ositron Emissions Tomography/Computed T omography
Arthroscopy
Classic Signs
Osteoporosis
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS Physiotherapy
Medical Treatment
Surgical Treatment
What the Referring Physician Needs to Know
SUGGESTED READINGS
REFERENCES
P r ogressive Scleroderma
Karsten Jablonka and Jürgen Freyschmidt
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
K E Y P O I N T S
IMAGING TECHNIQUES
MANIFESTATIONS OF THE DISEASE Radiography
Computed Tomography
Magnetic Resonance Imaging
Classic Signs
DIFFERENTIAL DIAGNOSIS
Surgical Treatment
SUGGESTED READINGS
REFERENCES
S y s t emic Lupus Erythematosus
Corinna Schorn and Gerwin Lingg
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOLOGY
BIOMECHANICS
IMAGING TECHNIQUES
Musculoskeletal Manifestations
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Ultrasonography
Nuclear Medicine
Classic Signs
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS
Medical Treatment
N o n s t e r o i d a l Anti-inflammatory Drugs
Corticosteroids
Antimalarial Agents
Immunosuppressive Agents
Azathioprine
Methotrexate
Surgical Treatment
What the Referring Physician Needs to Know
M ixed Connective T issue Disease
Corinna Schorn and Gerwin Lingg
ETIOLOGY, EPIDEMIOLOGY, AND PREVALENCE
CLINICAL PRESENTATION
MANIFESTATIONS OF THE DISEASE
RADIOGRAPHY
SYNOPSIS OF TREATMENT OPTIONS
Classic Signs
SUGGESTED READINGS
REFERENCES
Juvenile Idiopathic Arthritis
Karl Johnson
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY Anatomy
P athology
IMAGING TECHNIQUES T echniques and Relevant Aspects
K E Y P O I N T S
Pros and Cons
MANIFESTATIONS OF THE DISEASE Appendicular Skeleton Involvement
Radiography
Multidetector Computed Tomography
Ultrasonography
MANIFESTATIONS OF THE DISEASE Axial Skeleton Involvement
Radiography
Magnetic Resonance Imaging
Classic Signs
SYNOPSIS OF TREATMENT OPTIONS
DIFFERENTIAL DIAGNOSIS
What the Referring Physician Needs to Know
SUGGESTED READINGS
REFERENCES
Idiopathic Inflammatory
M y opathy
Lawrence Yao and Lisa G. Rider
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY Anatomy
P athology
IMAGING TECHNIQUES Magnetic Resonance Imaging
T echniques and Relevant Aspects
Pitfalls (Pros and Cons)
Controversies
MANIFESTATIONS OF THE DISEASE Myositis
Magnetic Resonance Imaging
Computed Tomography
Ultrasonography
Magnetic Resonance Spectroscopy
Nuclear Medicine
F asciitis
Magnetic Resonance Imaging
Calcinosis
Computed Tomography
DIFFERENTIAL DIAGNOSIS
Surgical Treatment
What the Referring Physician Needs to Know
SUGGESTED READINGS
REFERENCES
Hemochromatosis
Mini N. Pathria
PREVALENCE AND EPIDEMIOLOGY
MANIFESTATIONS OF THE DISEASE
K E Y P O I N T S
Radiography
Magnetic Resonance Imaging
What the Referring Physician Needs to Know
REFERENCES
Ochronosis
Claire Coggins and Curtis Hayes
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY
BIOMECHANICS
IMAGING TECHNIQUES
K E Y P O I N T S
Magnetic Resonance Imaging
Arthroscopy
DIFFERENTIAL DIAGNOSIS
Classic Signs
What the Referring Physician Needs to Know
Surgical Treatment
SUGGESTED READINGS
REFERENCES
Diffuse Idiopathic Skeletal Hyperostosis and Ossification of the Posterior L ongitudinal Ligament
Curtis Hayes and Claire Coggins
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY
IMAGING TECHNIQUES
MANIFESTATIONS OF THE DISEASE Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
DIFFERENTIAL DIAGNOSIS
Classic Signs
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
SUGGESTED READINGS
REFERENCES
Gout
Lee F. Rogers and Sachin Dheer
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
K E Y P O I N T S
P A THOPHYSIOLOGY Anatomy
P athology
MANIFESTATIONS OF THE DISEASE
P eriarticular Erosions and Tophi
Magnetic Resonance Imaging
Multidetector Computed Tomography
Nuclear Medicine
P ositron Emission Tomography/Computed T omography
Arthroscopy
DIFFERENTIAL DIAGNOSIS
Classic Signs
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
What the Referring Physician Needs to Know
Surgical Treatment
SUGGESTED READINGS
Crystal-Related Arthritis
CALCIUM PYROPHOSPHATE DIHYDRATE DEPOSITION Etiology
Prevalence and Epidemiology
Clinical Presentation
P athology
Manifestations of the Disease
Radiography
Articular and Periarticular Calcification—Chondrocalcinosis
S tructural Changes in Joints—“Pyrophosphate Arthropathy”
Other Radiologic Findings
Multidetector Computed Tomography
Ultrasonography
Prevalence and Epidemiology
Clinical Presentation
Synopsis of Treatment Options
What the Referring Physician Needs to Know
HYDROXYAPATITE AND BASIC CALCIUM PHOSPHATE
Etiology
K E Y P O I N T S
Manifestations of the Disease Radiography
Calcification in Ligaments and Tendons
Episodes of Acute Transient Synovitis
Calcification due to HA in Soft Tissues Other Than Joints
Rapidly Progressive Osteoarthritis
Magnetic Resonance Imaging
Multidetector Computed Tomography
Nuclear Medicine
Differential Diagnosis
Cholesterol
Corticosteroids
Calcium Oxalate (Oxalosis)
Synopsis of Treatment Options Medical Treatment
Surgical Treatment
What the Referring Physician Needs to Know
SUGGESTED READINGS
Neuropathic Osteoarthropathy
Sandra Moore
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
Diabetic Pedal Neuropathy
P A THOPHYSIOLOGY
Anatomy
BIOMECHANICS
Controversies
MANIFESTATIONS OF THE DISEASE Radiography
Magnetic Resonance Imaging
IMAGING TECHNIQUES T echniques and Relevant Aspects
Multidetector Computed Tomography
Nuclear Medicine
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Soft Tissue Disease: Cellulitis, Pyomyositis, Abscess, Septic Arthritis
David Wilson and Bridget Atkins
P A THOLOGY
IMAGING TECHNIQUES
Soft Tissue Swelling with Er ythema
Unexplained Pain with or without Fever
MANIFESTATIONS OF THE DISEASE Cellulitis
Abscess
Impetigo
Acute Septic Arthritis
Chronic Septic Arthritis
Pyomyositis
Necrotizing Fasciitis
T uberculosis
F ungal Infections
MANIFESTATIONS OF THE DISEASE
Ultrasonography
Magnetic Resonance Imaging
Image-Guided Biopsy
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
SUGGESTED READINGS
Infection in the Appendicular Skeleton (Including Chronic Osteomyelitis)
Shah H. M. Khan and Hans L. Bloem
ETIOLOGY
CLINICAL PRESENTATION
Anatomy
BOX 62-1 Definitions
P athology
BIOMECHANICS
T echniques and Relevant Aspects
Pro and Cons (Table 62-2)
MANIFESTATIONS OF THE DISEASE
Radiography
Computed Tomography
Ultrasonography
Nuclear Medicine
P ositron Emission Tomography
DIFFERENTIAL DIAGNOSIS (Table 62-3)
Classic Signs
SYNOPSIS OF TREATMENT OPTIONS
Medical Treatment
Surgical Treatment
What the Referring Physician Needs to Know
A CKNOWLEDGMENT
SUGGESTED READINGS
REFERENCES
63 Spinal Infection
B e r n h a r d Tins and Victor Cassar-Pullicino
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY Anatomy
P athology
IMAGING TECHNIQUES T echniques and Relevant Aspects
Magnetic Resonance Imaging
Diffusion-Weighted Imaging
Computed Tomography
Ultrasonography
Nuclear Medicine
Pros and Cons
Controversies
MANIFESTATIONS OF THE DISEASE I n fection with Mycobacter ium tuberculosis
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Nuclear Medicine
P ositron Emission Tomography/ Computed Tomography
Classic Signs: Tuberculosis of the Spine
Pyogenic Infection
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Nuclear Medicine
P ositron Emission Tomography/Computed T omography
DIFFERENTIAL DIAGNOSIS
Classic Signs: Pyogenic Spine Infection
Collapsed Vertebral Body
Single Vertebral Body Edema
Disc and End-Plate Changes
Destructive Soft Tissue Mass
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
What the Referring Physician Needs to Know
SUGGESTED READINGS
Complications of Infection
Francesca Beaman and Laura Bancroft
IMAGING TECHNIQUES
MANIFESTATIONS OF THE DISEASE Infection Requiring Percutaneous/
Surgical Drainage
Infection Resulting in Tendon Failure
Infection Resulting in Joint Destruction/Ankylosis/Deformity
Infectious Hardware Failure Requiring Revision Arthroplasty
Infectious Complications Requiring a Myocutaneous Flap
Infectious Complications Requiring Amputation
Surgical
SUGGESTED READINGS
Diabetic Pedal Infection
William Morrison and H. P. Ledermann
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
ANATOMY
IMAGING TECHNIQUES T echniques and Relevant Aspects
Pros and Cons
Controversies
MANIFESTATIONS OF THE DISEASE Radiography
Magnetic Resonance Imaging (Table 65-2)
Devitalization
Evaluation of Extent of Involvement
Multidetector Computed Tomography
Ultrasonography
Nuclear Medicine
Three-Phase Bone Scintigraphy
Labeled White Blood Cell Scan
Gallium Scanning
P ositron Emission Tomography/
Computed Tomography
DIFFERENTIAL DIAGNOSIS
Neuropathic Osteoarthropathy
Gout and Other Inf lammatory Arthropathies
SYNOPSIS OF TREATMENT OPTIONS
Medical Treatment
Classic Signs
Surgical Treatment
What the Referring Physician Needs to Know
REFERENCES
P ediatric Infections
Helen Williams
SOFT TISSUE INFECTION
Cellulitis
Necrotizing Fasciitis
Pyomyositis
Osteomyelitis
A cute Osteomyelitis
Subacute and Chronic Osteomyelitis
Chronic Recurrent Multifocal Osteomyelitis
ORTHOPEDIC COMPLICATIONS OF MENINGOCOCCAL SEPTICEMIA
SEPTIC ARTHRITIS
VERTEBRAL OSTEOMYELITIS AND DISCITIS
CONGENITAL INFECTION
Human Immunodeficiency V irus Infection and Acquired Immunodeficiency Syndro
Sandra Moore and Theodoros Katsivas
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY
Anatomy
P athology
IMAGING TECHNIQUES
T echniques and Relevant Aspects
Radiography
Cross-Sectional Imaging
Nuclear Scintigraphy
P ositron Emission Tomography
Pros and Cons
Controversies
MANIFESTATIONS OF THE DISEASE
Musculoskeletal Infection
A bscesses, Bursitis, Tenosynovitis
Necrotizing Fasciitis
Pyomyositis
Septic Arthritis
O s t e o m y e l i t i s (Nontuberculous)
T uberculous Osteomyelitis, Spondylitis, Spondylodiscitis
Related Inf lammatory Conditions: Arthritides, Polymyopathies
Psoriatic Arthritis
Reactive Arthritis
A cute Symmetric Polyarthritis
N o n s p e c i fic Arthralgias
Inflammatory Conditions of Muscle
Related Musculoskeletal Neoplasms
Musculoskeletal Complications of Antiretroviral Therapy
Miscellaneous Musculoskeletal Manifestations
A v ascular Necrosis
Osteopenia and Osteoporosis
Hypertrophic Osteoarthropathy
Myositis Ossificans Circumscripta
What the Referring Physician Needs to Know
A CKNOWLEDGMENT
SUGGESTED READINGS
A typical Mycobacterial Infection
Mihra S. Taljanovic
M y c obacterial Infection
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
K E Y P O I N T S
P A THOPHYSIOLOGY
IMAGING TECHNIQUES
MANIFESTATIONS OF THE DISEASE
Magnetic Resonance Imaging
Multidetector Computed Tomography
Ultrasonography
Nuclear Medicine
P ositron Emission Tomography/
Computed Tomography
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
Brucellosis
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY
Magnetic Resonance Imaging
Ultrasonography
Nuclear Medicine
SYNOPSIS OF TREATMENT OPTIONS
Medical Treatment
Surgical Treatment
SUGGESTED READING
REFERENCES
Cat-Scratch Disease
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY
K E Y P O I N T S
MANIFESTATIONS OF THE DISEASE
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Ultrasonography
P ositron Emission Tomography/
Computed Tomography
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
Classic Signs
What the Referring Physician Needs to Know
REFERENCES
F ungal and Higher Bacterial Infections
ETIOLOGY, PATHOPHYSIOLOGY, PREVALENCE AND EPIDEMIOLOGY, CLINICAL PRESENTATIO
North American Blastomycosis
South American Blastomycosis
Cryptococcosis
Sporotrichosis
Histoplasmosis
Aspergillosis
Candidiasis
Mucormycosis
Maduromycosis
Actinomycosis
Nocardiosis
MANIFESTATIONS OF THE DISEASE Radiography
Coccidioidomycosis
N o rth American Blastomycosis
Cryptococcosis
Sporotrichosis
Histoplasmosis
Aspergillosis
Candidiasis
Mucormycosis
Maduromycosis
A ctinomycosis
Nocardiosis
Magnetic Resonance Imaging Coccidioidomycosis
N o rth American Blastomycosis
Cryptococcosis
Sporotrichosis
Histoplasmosis
Aspergillosis
Candidiasis
Mucormycosis
Maduromycosis
A ctinomycosis
Nocardiosis
Multidetector Computed Tomography Coccidioidomycosis
N o rth American Blastomycosis
Cryptococcosis
Sporotrichosis
Histoplasmosis
Aspergillosis
Candidiasis
Mucormycosis
Maduromycosis
A ctinomycosis
Nocardiosis
Ultrasonography
Nuclear Medicine Coccidioidomycosis
N o rth American Blastomycosis
Cryptococcosis
Sporotrichosis
Histoplasmosis
Aspergillosis
Candidiasis
Mucormycosis
Maduromycosis
A ctinomycosis
Nocardiosis
P ositron Emission Tomography/
Computed Tomography
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Coccidioidomycosis
Blastomycosis
Cryptococcosis
Sporotrichosis
Histoplasmosis
Aspergillosis
Candidiasis
Mucormycosis
Maduromycosis
A ctinomycosis
Nocardiosis
SUGGESTED READING
REFERENCES
H y datid Disease (Echinococcosis)
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY
IMAGING TECHNIQUES
Ultrasonography
Nuclear Medicine
P ositron Emission Tomography/
Computed Tomography
DIFFERENTIAL DIAGNOSIS
SUGGESTED READINGS
REFERENCES
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
L eprosy
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY
MANIFESTATIONS OF THE DISEASE Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Ultrasonography
Nuclear Medicine
SYNOPSIS OF TREATMENT OPTIONS
Medical Treatment
Surgical Treatment
SUGGESTED READING
REFERENCES
L y me Disease
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY
IMAGING TECHNIQUES
MANIFESTATIONS OF THE DISEASE
Radiography
Multidetector Computed Tomography
Ultrasonography
Nuclear Medicine
P ositron Emission Tomography/
Computed Tomography
DIFFERENTIAL DIAGNOSIS
Medical Treatment
Surgical Treatment
S yphilis
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
SUGGESTED READINGS
REFERENCES
P A THOPHYSIOLOGY
Congenital Syphilis
Acquired Syphilis
MANIFESTATIONS OF THE DISEASE
Radiography
Early Congenital Syphilis
Osteochondritis
Osteitis (Diaphyseal Osteomyelitis)
P eriostitis
Miscellaneous Findings
Late Congenital Syphilis
Clutton’s Joints
Secondary Syphilis
T ertiary Syphilis
Nuclear Medicine
SYNOPSIS OF TREATMENT OPTIONS
Medical Treatment
Surgical Treatment
What the Referring Physician Needs to Know
SUGGESTED READING
REFERENCES
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
T uberculosis
ETIOLOGY
K E Y P O I N T S
P A THOPHYSIOLOGY
IMAGING TECHNIQUES
MANIFESTATIONS OF THE DISEASE
Magnetic Resonance Imaging
Ultrasonography
Nuclear Medicine
P ositron Emission Tomography/
Computed Tomography
Classic Signs
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
What the Referring Physician Needs to Know
REFERENCES
General Principles of Magnetic R esonance Imaging of the Bone Marrow
Bruno Vande Berg
ANATOMY AND PHYSIOLOGY OF NORMAL BONE MARROW
MAGNETIC RESONANCE IMAGING TECHNIQUES
T1-Weighted Spin-Echo Sequence
Intermediate-Weighted Spin-Echo Sequence
T2-Weighted Fast Spin-Echo Sequence
F at-Saturated Spin-Echo Sequences
Gradient-Echo Sequences
Gadolinium-Enhanced Sequences
Other Sequences
NORMAL ANATOMY
Magnetic Resonance Appearance of the Normal Marrow
MAGNETIC RESONANCE IMAGING P A TTERNS OF MARROW LESIONS
Marrow Depletion
Marrow Inf iltration
Marrow Replacement
WHAT THE RADIOLOGIST NEEDS T O KNOW
How Does One Increase Sensitivity of Bone Marrow Magnetic Resonance Imaging?
How Does One Increase Specif icity of Bone Marrow Magnetic Resonance Imaging
With or Without Fat Suppression?
Is This a Normal Variant?
Islands of Fatty Marrow
V ertebral Hemangioma
Enostosis
Islands of Red Marrow
Hematopoietic Marrow Hyperplasia
SUGGESTED READINGS
REFERENCES
Ischemic Bone Lesions
Bruno Vande Berg
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
P A THOPHYSIOLOGY
Histopathology
IMAGING TECHNIQUES
Magnetic Resonance Imaging
P ost-traumatic Osteonecrosis
Overuse Epiphyseal Osteonecrosis
Multidetector Computed Tomography
Nuclear Medicine
P ositron Emission Tomography/
Computed Tomography
Classif ication Systems
Natural History of Ischemic Bone Lesions
Magnetic Resonance Imaging
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
SUMMARY OF MAGNETIC RESONANCE IMAGING FINDINGS
REFERENCES
Hemophilia and Related Disorders
G. M. Allen, C. J. Fang, and D. J. Wilson
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION Acute Hemarthrosis
Recurrent Hemarthrosis
Chronic Joint Pain and Dysfunction
Acute Soft Tissue Hemorrhage
Recurrent Soft Tissue Hemorrhage
Chronic Mass Lesion/Pseudotumor
Life-Threatening Blood Loss
F racture
P A THOPHYSIOLOGY
MANIFESTATIONS OF THE DISEASE
Acute Hemarthrosis
Magnetic Resonance Imaging
Multidetector Computed Tomography
Ultrasonography
Chronic Joint Changes
Radiography
Hyperemia
Synovial Hypertrophy
Hemosiderin Deposition
Articular Surface Damage
Intraosseous Cyst Formation
Multidetector Computed Tomography
Acute Soft Tissue Changes
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Chronic Soft Tissue Changes Magnetic Resonance Imaging
Recurrent Hemorrhage Magnetic Resonance Imaging
Multidetector Computed Tomography
Ultrasonography
Pseudotumor
Multidetector Computed Tomography
Ultrasonography
DIFFERENTIAL DIAGNOSIS
Sickle Cell Anemia
Hilary R. Umans and Thomas L. Pope
PREVALENCE AND EPIDEMIOLOGY
K E Y P O I N T S
IMAGING TECHNIQUES
MANIFESTATIONS OF THE DISEASE
Bone Marrow Changes (Marrow Hyperplasia)
Magnetic Resonance Imaging
Multidetector Computed Tomography
Ultrasonography
N u c l e a r Medicine
P ositron Emission Tomography/Computed Tomography
V ascular Occlusion
Sickle Cell Dactylitis (Hand-Foot Syndrome, Aseptic Dactylitis)
Classic Signs
Magnetic Resonance Imaging
Multidetector Computed Tomography
Ultrasonography
Epiphyseal Infarction and Osteonecrosis Diaphyseal Infarction
Miscellaneous Findings
Imaging Features
Magnetic Resonance Imaging
Multidetector Computed Tomography
Infection (Osteomyelitis and Septic Arthritis)
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Classic Signs
Ultrasonography
N u c l e a r Medicine
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
Thalassemia
Apostolos Karantanas
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY AND IMAGING TECHNIQUES
Bone Disease in Untreated or Undertreated Thalassemia Major
Skull
Thorax
Spine
T ubular Bones
Bone and Joint Disease after Optimal T ransfusion and Iron Chelation
Osteoporosis-Bone Mineral Densitometr y
Bone Marrow and Magnetic Resonance Imaging
DIFFERENTIAL DIAGNOSIS
Surgical Treatment
What the Referring Physician Needs to Know
74 M y elofibrosis
Eoin Carl Kavanagh
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
K E Y P O I N T S
IMAGING TECHNIQUES T echniques and Relevant Aspects
Pros and Cons
MANIFESTATIONS OF THE DISEASE
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Ultrasonography
P ositron Emission Tomography/
Computed Tomography
Dual-Energy X-ray Absorptiometr y
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
DIFFERENTIAL DIAGNOSIS
What the Referring Physician Needs to Know
SUGGESTED READING
REFERENCES
Osteoporosis
Judith Adams
Bone Turnover
Generalized Osteoporosis
Primary Osteoporosis
Osteogenesis Imperfecta
Secondary Osteoporosis
Regional Osteopenia
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY Anatomy
P athology Regional Osteoporosis
Generalized Osteoporosis
IMAGING TECHNIQUES
Radiographic Morphometr y
Bone Densitometr y
Dual-Energy X-ray Absorptiometry
Quantitative Computed Tomography
Radiation Dose in Bone Densitometry (Table 75-6)
Other Research Methods
DIFFERENTIAL DIAGNOSIS
Surgical Treatment
What the Referring Physician Needs to Know
SUGGESTED READINGS
H yperparathyroidism, R enal Osteodystrophy, Osteomalacia and Rickets
Murali Sundaram and Jean Schils
H yperparathyroidism
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
P A THOPHYSIOLOGY
IMAGING TECHNIQUES
MANIFESTATIONS OF THE DISEASE
DIFFERENTIAL DIAGNOSIS
R enal Osteodystrophy
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
P A THOPHYSIOLOGY
What the Referring Physician Needs to Know
SUGGESTED READING
REFERENCES
MANIFESTATIONS OF THE DISEASE
Soft Tissue Calcif ication
In Children
Osteoarticular Manifestations and Chronic Dialysis
Magnetic Resonance Imaging
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
REFERENCES
R ickets and Osteomalacia
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY
K E Y P O I N T S
IMAGING TECHNIQUES
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS
What the Referring Physician Needs to Know
REFERENCES
Amyloidosis
Bryan T. Jennings, Michael S. Gibson, Mark D. Murphey, and Rogerich T. Paylor
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Ultrasonography
Nuclear Medicine
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS
What the Referring Physician Needs to Know
A CKNOWLEDGMENT
SUGGESTED READINGS
P ituitary and Thyroid Disorders
Calvin Ma, Paul Marten, and Rodrigo Dominguez
A cromegaly and Pituitary Gigantism
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
K E Y P O I N T S
P A THOPHYSIOLOGY Anatomy
P athology
IMAGING TECHNIQUES T echniques and Relevant Aspects
Pros and Cons
MANIFESTATIONS OF THE DISEASE Radiography
Soft Tissue
Skull
Hand
F oot
Spine
P eripheral Joints
Bony Excrescences
Bone Mineral Density
Pituitary Gigantism
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
What the Referring Physician Needs to Know
H ypopituitarism
ETIOLOGY
P A THOPHYSIOLOGY Anatomy
SUGGESTED READINGS
REFERENCES
P athology
IMAGING TECHNIQUES T echniques and Relevant Aspects
Pros and Cons
MANIFESTATIONS OF THE DISEASE Radiography
DIFFERENTIAL DIAGNOSIS
Surgical Treatment
SUGGESTED READINGS
REFERENCES
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
H yperthyroidism
What the Referring Physician Needs to Know
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY Anatomy
P athology
IMAGING TECHNIQUES
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
H ypothyroidism
ETIOLOGY
What the Referring Physician Needs to Know
SUGGESTED READINGS
REFERENCES
CLINICAL PRESENTATION
P A THOPHYSIOLOGY Anatomy
P athology
IMAGING TECHNIQUES
MANIFESTATIONS OF THE DISEASE Radiography
DIFFERENTIAL DIAGNOSIS
SUGGESTED READINGS
REFERENCES
Gaucher Disease
Daniel Rosenthal
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY Anatomy
Nonskeletal
Skeletal Features
P athology
IMAGING TECHNIQUES T echniques and Relevant Aspects
Pros and Cons
MANIFESTATIONS OF THE DISEASE Radiography
Bone Densitometr y
Magnetic Resonance Imaging
Computed Tomography
Ultrasonography
Nuclear Medicine
Enzyme Replacement
Enzyme Replacement Therapy in Children
Monitoring the Effects of Treatment
Costs
Surgical Treatment
What the Referring Physician Needs to Know
SUGGESTED READINGS
Storage Diseases (Mucopolysaccharidoses/ Glycogenoses)
Calvin Ma and Rodrigo Dominguez
ETIOLOGY Mucopolysaccharidoses
Glycogenoses
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION Mucopolysaccharidoses 6–11
Hurler Syndrome (MPS I H)
Scheie Syndrome (MPS I S)
Hurler-Scheie Syndrome (MPS I H/S)
Hunter Syndrome (MPS II)
Sanfilippo Syndrome (MPS III)
Morquio Syndrome (MPS IV)
Maroteaux-Lamy Syndrome (MPS VI)
Sly Syndrome (MPS VII)
N atowicz Syndrome (MPS IX)
Glycogenoses
v on Gierke Disease (GSD I)
P ompe Disease (GSD II)
F orbes-Cori Disease (GSD III)
Andersen Disease (GSD IV)
McArdle Disease (GSD V)
Hers Disease (GSD VI)
T arui Disease (GSD VII)
GSD IX
P A THOPHYSIOLOGY
MANIFESTATIONS OF THE DISEASE: MUCOPOLYSACCHARIDOSES
Radiography
Hurler Syndrome (MPS I H)
Skull
Chest
Spine
P elvis
Hand
Long Bones
The Other Mucopolysaccharidoses (Except Morquio Syndrome)
Morquio Syndrome (MPS IV)
Magnetic Resonance Imaging
Multidetector Computed Tomography
MANIFESTATONS OF THE DISEASE: GLYCOGENOSES
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS
Medical Treatment
Surgical Treatment
What the Referring Physician Needs to Know
Osteogenesis Imperfecta
James Teh and Roger Smith
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION AND P A THOPHYSIOLOGY
T ype I
T ype II
T ype III
T ype IV
Other Forms of Osteogenesis Imperfecta
IMAGING FINDINGS T ype I
T ype II
T ype III
T ype IV
MANIFESTATIONS OF THE DISEASE Radiography
Magnetic Resonance Imaging
Classic Signs
Multidetector Computed Tomography
Ultrasonography
Bone Mineral Densitometr y
Differentiation from Nonaccidental Injur y
DNA Testing
Collagen Analysis
SYNOPSIS OF TREATMENT OPTIONS
Medical Treatment
What the Referring Physician Needs to Know
Surgical Treatment
M arfan Syndrome
Filip M. Vanhoenacker, A. Snoeckx, and M. Biervliet
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY
IMAGING TECHNIQUES
MANIFESTATIONS OF THE DISEASE
K E Y P O I N T S
Chest Deformity
Spine
Radiography
Magnetic Resonance Imaging and Multidetector Computed Tomography
P elvis
Radiography
Bone Mineral Density
Elongation of the Extremities and Arachnodactyly
F eet Radiography
Skull Radiography
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
What the Referring Physician Needs to Know
SUGGESTED READINGS
P aget’s Disease
Iain Watt
PREVALENCE
ETIOLOGY
P A THOPHYSIOLOGY
CLINICAL PRESENTATION
MANIFESTATIONS OF THE DISEASE Laboratory Investigations
BOX 83-1 Clinical Features of Paget’s Disease
Skeletal Scintigraphy
Computed Tomography and Magnetic Resonance Imaging
COMPLICATIONS Benign
Bone Softening
F r acture
Associated Arthritis
Neurologic Complications
Neoplastic
Metastasis
Soft Tissue Masses
H ypertrophic Osteoarthropathy
Michael S. Gibson, Bryan T. Jennings, and Mark D. Murphey
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY
K E Y P O I N T S
BOX 84-1 Diseas Associated with Secondary Hypertrophic Osteoarthropathy
MANIFESTATIONS OF THE DISEASE Radiography
Nuclear Medicine
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
A CKNOWLEDGMENT
REFERENCES
Sarcoidosis
Hakan Ilaslan and Murali Sundaram
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
MANIFESTATIONS OF THE DISEASE Radiography
Magnetic Resonance Imaging
Nuclear Medicine
P ositron Emission Tomography/
Computed Tomography
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS
What the Referring Physician Needs to Know
SUGGESTED READINGS
REFERENCES
T uberous Sclerosis
Luis Beltran
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
IMAGING TECHNIQUES
K E Y P O I N T S
MANIFESTATIONS OF THE DISEASE Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
SUGGESTED READINGS
Drug-Related Bone and Soft T issue Disorders
Natalie Zelenko, Romulo Baltazar, and Javier Beltran
CORTICOSTEROIDS
Osteoporosis and Pathologic Fractures
Osteonecrosis
K E Y P O I N T S
Neuropathic-Like Articular Destruction
Osteomyelitis and Septic Arthritis
Other Disorders
OTHER DRUGS ASSOCIATED WITH OSTEOPOROSIS
PHENY T OIN AND PHENOBARBITAL
ALUMINUM
DEFEROXAMINE
DIPHOSPHONATES
IFOSFAMIDE
OTHER DRUGS ASSOCIATED WITH RICKETS AND OSTEOMAL A CIA
VITAMIN A
RETINOIDS
VITAMIN D
FLUOROSIS
PROSTAGLANDIN E
V ASOCONSTRICTORS, CALCIUM GLUCONATE, AND MILK-ALKALI SYNDROME
POLYVINYL CHLORIDE
BISMUTH POISONING
METHOTREXATE
TERATOGENS
Vitamin A and Retinoids
Alcohol
Thalidomide
Cocaine
W arfarin
DISORDERS ASSOCIATED WITH NUTRITIONAL DEFICIENCIES Hypovitaminosis C (Scurvy
Infantile Scurvy
A dult Scurvy
Def iciencies of Zinc and Other Elements
SUGGESTED READINGS
REFERENCES
The Patient with a Tumor or T umor-like Lesion of Bone
Hans L. Bloem and Herman M. Kroon
K E Y P O I N T S
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY
IMAGING TECHNIQUES
T echniques and Relevant Aspects
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Nuclear Medicine
Classic Signs: Signs in Favor of Malignancy
What the Referring Physician Needs to Know
SUGGESTED READINGS
REFERENCES
The Patient with a Soft T issue Lump
Gina Allen
IMAGING TECHNIQUES Recognition
Ultrasonography
Magnetic Resonance Imaging
Computed Tomography
MANIFESTATIONS OF THE DISEASE Def ining the Shape and Structure of a Lesion
V ascularity
Calcif ication
Muscle Injur y
Ultrasonography of Muscle Trauma Hematomas
Nerve-Related Lesions
Lesions According to Site
SUMMARY
Locating Spread
The Decision to Biopsy
What the Referring Physician Needs to Know
REFERENCES
P rimary Bone Tumors
A. Mark Davies
MANIFESTATIONS OF DISEASE Osteoid-Producing Tumors
Osteoma
Osteoid Osteoma and Osteoblastoma
Osteosarcoma
Conventional (High-Grade Intramedullary) Osteosarcoma
Multicentric Osteosarcoma
T elangiectatic Osteosarcoma
Low-Grade Central Osteosarcoma
Surface Osteosarcoma
P a r o s t e a l Osteosarcoma
P e r i o s t e a l Osteosarcoma
H i g h - G r a d e Surface Osteosarcoma
Secondary Osteosarcoma
Cartilage-Producing Tumors
Osteochondroma
Chondroma
Chondroblastoma
Chondromyxoid Fibroma
Chondrosarcoma
Central Chondrosarcoma
Surface Chondrosarcoma
Dedifferentiated Chondrosarcoma
Clear Cell Chondrosarcoma
Mesenchymal Chondrosarcoma
Fibrogenic and Fibrohistiocytic Tumors
Desmoplastic Fibroma
Benign Fibrous Histiocytoma
Fibrosarcoma and Malignant Fibrous Histiocytoma
R ound Cell Tumors
Hematopoietic (Myeloproliferative) T umors
L ymphoma
Giant Cell Tumor
Notochordal Tumors
V ascular Tumors
Hemangioma
Glomus Tumor
Cystic Angiomatosis, Lymphangiomatosis, and Gorham’s Disease
Angiosarcoma and Hemangioendothelioma
Smooth Muscle Tumors
Lipogenic Tumors
MISCELLANEOUS TUMORS
SUGGESTED READINGS
M y eloma
Andrea Baur-Melnyk
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY
IMAGING TECHNIQUES T echniques and Relevant Aspects
Pros and Cons
Radiography versus Magnetic Resonance Imaging
Computed Tomography versus Radiography
Multidetector Computed Tomography versus Magnetic Resonance Imaging
MANIFESTATIONS OF THE DISEASE
Magnetic Resonance Imaging
Prognosis
DIFFERENTIAL DIAGNOSIS
Monoclonal Gammopathy of Unknown Signif icance, Smoldering Myeloma
Classic Signs
Nuclear Medicine Studies
P ositron Emission Tomography/
Computed Tomography
Solitary Plasmacytoma
V ertebral Fractures
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
Evaluation of Relapse/Response to Therapy
What the Referring Physicians Needs to Know
REFERENCES
C H A P T E R
T umor-like Lesions of Bone
A. Mark Davies
CYSTIC LESIONS Simple Bone Cyst
Aneur y smal Bone Cyst
Epidermal Inclusion Cyst
Intraosseous Ganglion
FIBROUS LESIONS
Fibrous Cortical Defect/Nonossifying Fibroma
Fibrous Dysplasia
Osteof ibrous Dysplasia
Liposclerosing Myxof ibrous Tumor
L ANGERHANS CELL HISTIOCY T OSIS
METABOLIC DISORDERS
NORMAL VARIANTS
POST-TRAUMATIC DISORDERS Stress Fractures
A vulsion Injuries
Subperiosteal Hemorrhage and Hyperplastic Callus
P ost-traumatic Bone Cysts
INFECTION
SUGGESTED READINGS
REFERENCES
Soft Tissue Tumors
Arthur de Schepper
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
IMAGING TECHNIQUES
T umors of Connective Tissue
N o d u l a r Fasciitis
Elastofibroma Dorsi
Fibromatoses
P almar Fibromatosis
Plantar Fibromatosis
Extra-abdominal Desmoid Tumors (Aggressive Fibromatosis)
A bdominal Fibromatosis
Solitary Fibrous Tumor
A dult Fibrosarcoma
Myxofibrosarcoma
Fibrohistiocytic Tumors
Giant Cell Tumor of Tendon Sheath
Pigmented Villonodular Synovitis
Xanthoma
Dermatofibrosarcoma Protuberans
Malignant Fibrous Histiocytoma
Lipomatous Tumors Lipoma
Chondroid Lipoma
Lipoblastoma
Lipoma of Tendon Sheath and Joint
Lipomatosis of Nerve (Fibrolipomatous Hamartoma)
Diffuse Lipomatosis
Hibernoma
Malignant Lipomatous Tumors
A typical Lipomatous Tumor, Well-Differentiated Liposarcoma, or Lipoma-like L
Myxoid Liposarcoma
Pleomorphic and Round Cell Liposarcoma
Dedifferentiated Liposarcoma
T umors of Vascular Origin
Benign Vascular Tumors
V ascular Tumors of Intermediate Malignancy Grade
T umors of Lymphatic Origin
T umors of Muscular Origin
Synovial Tumors
T umors of Peripheral Ner v es
Extraskeletal Cartilaginous and Osseous T umors
Synovial Osteochondromatosis
Extraskeletal Chondrosarcoma
Extraskeletal Osteosarcoma
Primitive Neuroectodermal Tumors
T umors of Uncertain Differentiation
Soft Tissue Metastases
P ediatric Soft Tissue Tumors
DIFFERENTIAL DIAGNOSIS Cytogenetics and Molecular Genetics of Soft Tissue Tu
SYNOPSIS OF TREATMENT OPTIONS
What the Referring Physicians Needs to Know
REFERENCES
T umor-like Soft Tissue Lesions
Rodrigo Salgado and Arthur de Schepper
NORMAL ANATOMIC VARIATIONS AND MUSCULAR ANOMALIES
INFLAMMATORY AND INFECTIOUS LESIONS
Necrotizing Fasciitis
Abscess
Pyomyositis
Hydatid Cystic Disease
F ocal Myositis
Diabetic Muscle Infarction
Bursitis
Sarcoidosis
Cat-Scratch Disease
Actinomycosis
TRAUMATIC LESIONS
Hematoma and Contusion
F oreign Body Reactions
Calcif ic Myonecrosis
Hypothenar Hammer Syndrome
Muscle Herniations
Myositis Ossif icans
Injection Granulomas
SKIN LESIONS
Pilomatricoma
Granuloma Annulare
Epidermal Inclusion Cyst (Infundibular Cyst)
CRYSTAL DEPOSITIONS
Gout and Pseudogout
Calcif ic Tendinosis
OTHER VASCULAR LESIONS
MISCELLANEOUS T umoral Calcinosis
Amyloid Tumor of Soft Tissue
SUGGESTED READINGS
T umoral Calcinosis
Bryan T. Jennings, Michael S. Gibson, and Mark D. Murphey
ETIOLOGY
PREVALENCE AND EPIDEMIOLOGY
CLINICAL PRESENTATION
P A THOPHYSIOLOGY
MANIFESTATIONS OF THE DISEASE
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
What the Referring Physician Needs to Know
Nuclear Medicine
DIFFERENTIAL DIAGNOSIS
SYNOPSIS OF TREATMENT OPTIONS
A CKNOWLEDGMENT
SUGGESTED READING
REFERENCES
M e t astatic Disease
Michael Mulligan, Donald Flemming, and Mark D. Murphey
PREVALENCE AND EPIDEMIOLOGY
K E Y P O I N T S
CLINICAL PRESENTATION
Anatomy
P athology
T echnical Aspects
Radiography
Magnetic Resonance Imaging
Multidetector Computed Tomography
Ultrasonography
Nuclear Medicine
P ositron Emission Tomography/
Computed Tomography
Pros and Cons
Controversies
Which Whole-Body Imaging Technique is Best for Initial Staging and Subsequent
Does Magnetic Field Strength Matter?
A r e Intravenous Contrast Agents Needed?
MANIFESTATIONS OF THE DISEASE
Spinal Involvement
Magnetic Resonance Imaging
Multidetector Computed Tomography
Nuclear Medicine
Ivory Vertebra
Hypertrophic Osteoarthropathy
Radiography
Nuclear Medicine
F ocal Periosteal Reaction
Cortical Metastases
Soft Tissue Mass
Multidetector Computed Tomography
Ultrasonography
Synovial Involvement
Magnetic Resonance Imaging
P athologic Fracture
Radiography
Magnetic Resonance Imaging
DIFFERENTIAL DIAGNOSIS
Medical Treatment
Surgical Treatment
What the Referring Physician Needs to Know
REFERENCES
T r eatment Strategies f or Musculoskeletal Tumors and Tumor-like Lesions
Davide Donati
FUNCTIONALIT Y
DIAGNOSIS
P atient Histor y
Physical Examination
Laboratory Tests
Imaging
Biopsy
PRINCIPLES OF TREATMENT
Staging and Compartments
Systemic Control
Local Control
Surgery
(Neo)-adjuvant Therapies
Antiblastic Chemotherapy
Isolating Limb Perfusion
Radiation Therapy
Arterial Embolization
Surgical Treatment
Benign Bone and Soft Tissue Tumors
Malignant Bone and Soft Tissue Tumor
Bone Metastases
Surgical Techniques
Amputation
Limb Salvage
Prosthetic Device
Bone Allograft
Allograft Prosthetic Composite
Bone Transplant
Choosing a Type of Reconstruction
The Patient’s Choice
A CKNOWLEDGMENT
REFERENCES
Staging Bone and Sof t Tissue T umors
Hans L. Bloem and Herman M. Kroon
IMAGING TECHNIQUES Magnetic Resonance Imaging
K E Y P O I N T S
Computed Tomography
P ositron Emission Tomography/
Computed Tomography
Controversies
Bone Scintigraphy
MANIFESTATIONS OF THE DISEASE
Bone Marrow Involvement
Cortex
P eriosteum
Muscular Compartments
Neurovascular Bundle
Joints
REFERENCES
M onitoring Therapy in Bone and Sof t T issue Tumors
Catharina S. P. van Rijswijk and Hans L. Bloem
P A THOPHYSIOLOGY
Dynamic Contrast-Enhanced Magnetic Resonance Imaging
Diffusion-Weighted Magnetic Resonance Imaging
MONITORING THERAPY Conventional Radiography
Unenhanced Magnetic Resonance Imaging
Contrast-Enhanced Magnetic Resonance Imaging
Ultrasonography
P ositron Emission Tomography
IMAGING POST-THERAPEUTIC CHANGES AND RECURRENCES Benign Bone Tumors
Sarcomas
P ositron Emission Tomography in Detection of Recurrence
IMAGING AS SURVEILLANCE STRATEGY
What the Referring Physician Needs to Know
SUGGESTED READINGS
REFERENCES
F ocal Growth Disturbances
F . M. Vanhoenacker, W. Courtens, and A. Snoeckx
Prevalence and Epidemiology
Clinical Presentation
P athophysiology
IMAGING TECHNIQUES
T echniques and Relevant Aspects
MANIFESTATIONS OF THE DISEASE
Absent or Hypoplastic Bones (Def iciency)
Glenoid Hypoplasia
Radiographic Findings
MRI Arthrography
R a d i a l or Ulnar Ray Deficiency
Amputations of Limbs
Proximal Femoral Focal Def iciency
Radiographic Findings
Ultrasonography and MRI
Tibial and Fibular Deficiency
N ail-Patella Syndrome
Radiographic Findings
Hands and Feet Anomalies
Extra Bones
F usion Anomalies and Segmentation Deformities
Congenital Pseudarthrosis
Synostosis
Syndactyly and Symphalangism
Bowing Deformities
What the Referring Physician Needs to Know
SYNOPSIS OF TREATMENT OPTIONS
Medical Treatment
REFERENCES
Developmental D y splasia of the Hip
David Wilson
ETIOLOGY AND PREVALENCE
MANIFESTATIONS OF THE DISEASE
Radiography
Computed Tomography
Magnetic Resonance Imaging
Ultrasonography
SYNOPSIS OF TREATMENT OPTIONS
Clinical Examination
Ultrasound Techniques
Anatomic (Morphology) Measurement
Dynamic Stability Testing
Combined Clinical and Ultrasound Examination
Late Presentation
Screening Strategies
Follow-Up
T rue Dislocation
P ostoperative Imaging
SUMMARY
REFERENCES
Coalitions
Michele Calleja and Simon Ostlere
CLINICAL PRESENTATION T arsal Coalition
Carpal Coalition
MANIFESTATIONS OF THE DISEASE T arsal Coalition
Calcaneonavicular Coalition
Radiography
T alocalcaneal Coalition
Computed Tomography
Magnetic Resonance Imaging
T alonavicular Coalition
Radiography
Other Coalitions
CARPAL COALITIONS
Lunotriquetral Coalition
Capitate-Hamate Fusion
Pisiform-Hamate Fusion
SYNOPSIS OF TREATMENT OPTIONS Medical Treatment
Surgical Treatment
REFERENCES
D y splasias
Amaka Off i ah
HYPOCHONDROPLASIA
A CHONDROPLASIA
Classic Signs
THANATOPHORIC DYSPLASIA
ASPHYXIATING THORACIC DYSTROPHY
ELLIS-VAN CREVELD SYNDROME
KNIEST’S DYSPLASIA
SPONDYLOEPIPHYSEAL DYSPLASIA CONGENITA
STICKLER’S SYNDROME
X -LINKED SPONDYLOEPIPHYSEAL D Y SPLASIA TARDA
MULTIPLE EPIPHYSEAL DYSPLASIA
PSEUDOACHONDROPLASIA
CHONDRODYSPLASIA PUNCTATA
SCHMID METAPHYSEAL CHONDRODYSPLASIA
D Y SCHONDROSTEOSIS
CAMPTODACTYLY-ARTHROPATHY COXA VARA-PERICARDITIS (CACP) SYNDROME
CLEIDOCRANIAL DYSPLASIA
CAMPOMELIC DYSPLASIA
MUCOPOLYSACCHARIDOSES
OSTEOGENESIS IMPERFECTA
OSTEOPETROSIS
PYKNODYSOSTOSIS
DIAPHYSEAL DYSPLASIA
INFANTILE CORTICAL HYPEROSTOSIS
HEREDITARY MULTIPLE EXOSTOSES
MULTIPLE ENCHONDROMATOSIS
FIBROUS DYSPLASIA
APERT’S SYNDROME
TREACHER COLLINS SYNDROME
TURNER’S SYNDROME
TRISOMY 21 (DOWN SYNDROME)
Spinal Deformity
James J. Rankine
CLASSIFICATION AND DEFINITIONS
K E Y P O I N T S
SCOLIOSIS
CONGENITAL SPINAL DEFORMIT Y
Cur v e Characteristics
ETIOLOGY, CLINICAL PRESENTATION, AND IMAGING TECHNIQUES
Idiopathic Scoliosis
Early-Onset Idiopathic Scoliosis
Late-Onset Idiopathic Scoliosis—Adolescent Scoliosis
Congenital Spinal Deformities
Spinal Dysraphism
Neuromuscular Scoliosis
Scoliosis Associated with Neurof ibromatosis
K yphosis
Scheuermann’s Disease
Congenital Kyphosis
General Principles of F ixation, Fusion, and Joint R eplacement
Kirkland W. Davis
PL A TES AND SCREWS
Cortical Plates
Locked Plates
SCREWS
K E Y P O I N T S
INTRAMEDULLARY DEVICES
PEDIATRIC FIXATION
F ractures
External Fixators
ARTHROPLAST Y AND ARTHRODESIS
Osteotomies and Epiphysiodesis
SPINE HARDWARE
BIOLOGIC IMPLANTS
Bone Graft Substitutes
K E Y P O I N T S
Bioabsorbable Hardware
POSTOPERATIVE IMAGING AND COMPLICATIONS
P ostoperative Imaging
K E Y P O I N T S
Infection
Loosening
Catastrophic Failure
Complications of Joint Replacements
Implant-Related Sarcoma
SUGGESTED READINGS
P ostoperative Imaging o f the Shoulder
Babu Paruchuri and Michael Zlatkin
IMAGING TECHNIQUES
Subacromial Decompression
Description
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P o tential Complications and Radiologic Appearance
R otator Cuff Repair or Débridement
Description
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P o tential Complications and Radiologic Appearance
Repairs for Glenohumeral Instability
Description
Indications, Contraindications, Purpose, and U nderlying Mechanics
Expected Appearance on Relevant Modalities
P o tential Complications and Radiologic Appearance
SUGGESTED READINGS
REFERENCES
The Postoperative Elbow, Wrist, and Hand
L ynne S. Steinbach and Christine B. Chung
Ulnar Collateral Ligament of the Elbow Reconstruction
DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS
Figure-of-Eight Repair
Muscle-Splitting Modif ication
American Sports Medicine Institute (ASMI) Modif ication
Suture Anchor Method
Docking Technique
Interference Technique
EXPECTED APPEARANCE ON IMAGING
SUGGESTED READINGS
POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE
REFERENCES
L a t eral Collateral Ligament of the Elbow Reconstruction
DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS
Presentation and Indications for Operative Treatment
Primary Ligament Repair
Lateral Collateral Ligament Complex Reconstruction
EXPECTED APPEARANCE ON IMAGING
POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE
SUGGESTED READINGS
REFERENCES
Indications for Operative Ulnar Ner v e T reatment
Surgical Therapy for Ulnar Ner v e Decompression
Simple Decompression of the Ulnar Nerve
Ulnar Nerve Decompression
DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS
Ulnar Nerve Transposition
EXPECTED APPEARANCE ON IMAGING
POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE
SUGGESTED READINGS
REFERENCES
Epicondylitis
DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS
K E Y P O I N T S
POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE
Biceps Tendon
DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS
EXPECTED APPEARANCE ON IMAGING
POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE
SUGGESTED READINGS
REFERENCES
T riceps Tendon
DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS
EXPECTED APPEARANCE ON IMAGING
POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE
SUGGESTED READINGS
K E Y P O I N T S
REFERENCES
Olecranon Bursitis
EXPECTED APPEARANCE ON IMAGING
DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS
POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE
Common Elbow Fractures
DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS
SUGGESTED READINGS
REFERENCES
POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE
SUGGESTED READINGS
Distal Forearm Fractures a t the Wrist
DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS
EXPECTED APPEARANCE ON IMAGING
POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE
SUGGESTED READINGS
REFERENCES
Carpal Tunnel Syndrome
DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS
EXPECTED APPEARANCE ON IMAGING
POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE
SUGGESTED READINGS
REFERENCES
Scaphoid Fractures
DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS
EXPECTED APPEARANCE ON IMAGING
POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE
P ostoperative Evaluation of Carpometacarpal, Metacarpal, and Phalangeal Tra
DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS
SUGGESTED READINGS
REFERENCES
EXPECTED APPEARANCE ON IMAGING
POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE
The Postoperative Hip
Derek R. Armfield, Jon K. Sekiya, Marc J. Philippon, Eoin C. Kavanagh, and Ge
P ostoperative Imaging in Arthroscopic Hip Surgery
K E Y P O I N T S
L ABRAL INJURY
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearances
CARTIL A GE INJURY
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P o tential Complications and Radiologic Appearances
CAPSULAR INJURY
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearances
FEMOROACETABULAR IMPINGEMENT
Indications, Contraindications, Purpose, and Underlying Mechanics
LIGAMENTUM TERES INJURY
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearances
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearances
SUGGESTED READINGS
REFERENCES
P ostoperative Imaging in Arthroplastic Hip Surgery
Eoin C. Kavanagh and George Koulouris
Indications, Contraindications, Purpose, and Underlying Biomechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
L OOSENING
DISLOCATION
INFECTION
PERIPROSTHETIC FRACTURE
A CETABULAR LINER WEAR
P ARTICLE DISEASE
HETEROTOPIC BONE FORMATION
PSEUDOBURSAE
ILIOPSOAS IMPINGEMENT
The Postoperative Knee
Douglas Mintz
ARTHROSCOPY Description
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
ARTHROTOMY Description
Indications, Contraindications, Purpose, and Underlying Mechanics
P otential Complications and Radiologic Appearance
ANTERIOR CRUCIATE LIGAMENT RECONSTRUCTION
Description
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P osition
Signal
Harvest Site
P otential Complications and Radiologic Appearance
POSTERIOR CRUCIATE LIGAMENT RECONSTRUCTION
Description
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
MEDIAL COLL A TERAL LIGAMENT RECONSTRUCTION
Description
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
POSTEROL A TERAL CORNER RECONSTRUCTION Description
Indications, Contraindications, Purpose, and Underlying Mechanics
P otential Complications and Radiologic Appearance
MULTIPLE LIGAMENT RECONSTRUCTION Description
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
MENISCECTOMY Description
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
MENISCAL REPAIR Description
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
MENISCAL TRANSPLANT Description
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
CHONDRAL STIMUL A TION Description
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
MOSAICPLAST Y/OATS Description
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
A UTOLOGOUS CHONDROCYTE IMPLANTATION
Description
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
OSTEOCHONDRAL ALLOGRAFT Description
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
OSTEOCHONDRITIS DISSECANS REPAIR Description
Indications, Contraindications, Purpose, and Underlying Mechanics
P otential Complications and Radiologic Appearance
ARTHROPLAST Y Description
Indications, Contraindications, Purpose, and Underlying Mechanics
P otential Complications and Radiologic Appearance
QUADRICEPS REPAIR Description
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
PROXIMAL PATELLAR REALIGNMENT Description
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
DISTAL PATELLAR REALIGNMENT Description
Indications, Contraindications, Purpose, and Underlying Mechanics
P otential Complications and Radiologic Appearance
TIBIAL PL A TEAU FRACTURE FIXATION Description
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
P A TELLAR FRACTURE TREATMENT Description
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
TUMOR RESECTION WITHOUT INSTRUMENTATION
Description
Expected Appearance on Relevant Modalities
Soft Tissue Tumors
Bone Tumors
P otential Complications and Radiologic Appearance
Soft Tissue
Bone
TUMOR RESECTION WITH INSTRUMENTATION/ALLOGRAFT Description
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
TIBIAL OSTEOTOMY Description
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
SUGGESTED READINGS
The Postoperative Ankle and Foot
David Rubin
OSTEOSYNTHESIS Description
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
INSTABILITY OPERATIONS Description
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
TENDON PROCEDURES Description
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
PLANTAR FASCIA SURGERY Description
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
NERVE DECOMPRESSION Description
Indications, Contraindications, Purpose, and Underlying Mechanics
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
REFERENCES
Imaging of the Residual Limb a f t e r Amputation
Laura M. Fayad
AMPUTATION SURGERY Description
INDICATIONS, CONTRAINDICATIONS, PURPOSE, AND UNDERLYING MECHANICS
Indications
Contraindications
Expected Appearance on Relevant Modalities
P otential Complications and Radiologic Appearance
REFERENCES
Dental Imaging
See the full chapter by Michael Pharoah on CD.
Normal Variants
See the full chapter by Thomas Pope, Theodore E. Keats, and Mark W. Anderson
Biopsy: Soft Tissue
See the full chapter by Patrick T. Liu and Catherine C. Roberts on CD.
P ercutaneous Biopsy of the Appendicular Skeleton
See the full chapter by Raphaëlle Souillard, Patrick Chastanet, and Anne Cott
P ercutaneous Biopsy of the Spine
See the full chapter by Patrick Chastanet, Anne Cotten, and Raphaëlle Souilla
T umor Ablation
See the full chapter by Willem Obermann on CD.
Spinal Injections
See the full chapter by Michelle S. Barr on CD.
Discography
See the full chapter by Peyman Borghei, Arash Anavim, and Jamshid Tehranzadeh
V ertebroplasty and Kyphoplasty
P ercutaneous Intradiscal Therapies
See the full chapter by Patrick A. Brouwer and Barry Schenk on CD.
Ultrasound Procedures
A P P E N D I X 1
M easurements Most Frequently Used in Orthopedic Imaging
See the full chapter by José Luis del Cura on CD.
Orthopedic Devices
See the full chapter by Angela Gopez and Aaron Cho on CD.
Fractures with Names
See the full chapter by José Martel and Ángel Bueno on CD.
Diseases with Names
See the full chapter by Oleg Opsha and Steven Shankman on CD.
A P P E N D I X 5
Classic Signs and Findings in M usculoskeletal Radiology
See the full chapter by Imran Omar on CD.
Compressive and Entrapment Neuropathies of the Upper and L o w er Extremitie
See the full chapter by Luis Beltran, Calvin Ma, and Javier Beltran on CD.
Case Studies
See full text on CD
Chapter 38 S tress Injury
Chapter 49 Ankylosing Spondylitis
Chapter 51 S ystemic Lupus Erythematosus
Chapter 52 M ixed Connective Tissue Disease
Chapter 95 T umoral Calcinosis
Index
I-i
I-ii I N D E X
I N D E X I-iii
I-iv I N D E X
I N D E X I-v
I-vi I N D E X
I N D E X I-vii
I-viii I N D E X
I N D E X I-ix
I-x I N D E X
I N D E X I-xi
I-xii I N D E X
I N D E X I-xiii
I-xiv I N D E X
I N D E X I-xv
I-xvi I N D E X
I N D E X I-xvii
I-xviii I N D E X
I N D E X I-xix
I-xx I N D E X
I N D E X I-xxi
I-xxii I N D E X
I N D E X I-xxiii
I-xxiv I N D E X
I N D E X I-xxv
I-xxvi I N D E X
I N D E X I-xxvii
I-xxviii I N D E X
I N D E X I-xxix
I-xxx I N D E X
I N D E X I-xxxi
I-xxxii I N D E X
I N D E X I-xxxiii
I-xxxiv I N D E X
I N D E X I-xxxv
I-xxxvi I N D E X
I N D E X I-xxxvii
I-xxxviii I N D E X
I N D E X I-xxxix
I-xl I N D E X
I N D E X I-xli
I-xlii I N D E X
I N D E X I-xliii
I-xliv I N D E X
I N D E X I-xlv
I-xlvi I N D E X
I N D E X I-xlvii
I-xlviii I N D E X
I N D E X I-xlix
I-l I N D E X
I N D E X I-li
I-lii I N D E X
I N D E X I-liii
I-liv I N D E X
I N D E X I-lv
I-lvi I N D E X
I N D E X I-lvii
I-lviii I N D E X
I N D E X I-lix
I-lx I N D E X
I N D E X I-lxi
I-lxii I N D E X
I N D E X I-lxiii
I-lxiv I N D E X
I N D E X I-lxv
I-lxvi I N D E X
I N D E X I-lxvii
I-lxviii I N D E X

Citation preview

Imaging of the Musculoskeletal System Volume 1 Thomas Lee Pope, Jr, MD, FACR Professor of Radiology and Orthopaedics Medical University of South Carolina Charleston, South Carolina

Hans L. Bloem, MD, PhD Chairman and Professor of Radiology Leiden University Medical Center Leiden,The Netherlands

Javier Beltran, MD, FACR Clinical Professor of Radiology Mount Sinai School of Medicine Chairman, Department of Radiology Maimonides Medical Center New York, New York Director of Medical Education Franklin & Seidelmann, Inc., Subspecialty Radiology Beachwood, Ohio

William Brian Morrison, MD Associate Professor of Radiology Thomas Jefferson University Director, Division of Musculoskeletal and General Diagnostic Radiology Thomas Jefferson University Hospital Philadelphia, Pennsylvania

David John Wilson, MBBS, FRCP, FRCR, MFSEM Consultant Musculoskeletal Radiologist Nuffield Orthopaedic Centre and Oxford Radcliffe Hospital Senior Clinical Lecturer University of Oxford Oxford, United Kingdom

1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899

Imaging of the Musculoskeletal System

ISBN: 978-1-4160-2963-2

Copyright © 2008 by Saunders, an imprint of Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Permissions may be sought directly from Elsevier’s Rights Department: phone: (+1) 215 239 3804 (US) or (+44) 1865 843830 (UK); fax: (+44) 1865 853333; e-mail: [email protected] may also complete your request on-line via the Elsevier website at http://www.elsevier.com/permissions.

Notice Knowledge and best practice in this field are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on their own experience and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions.To the fullest extent of the law, neither the Publisher nor the Editors assume any liability for any injury and/or damage to persons or property arising out of or related to any use of the material contained in this book. The Publisher

Library of Congress Cataloging-in-Publication Data Imaging of the musculoskeletal system / [edited by] Thomas Lee Pope Jr., [et al.]. 1st ed. p. ; cm. ISBN 978-1-4160-2963-2 1. Musculoskeletal system—Imaging. I. Pope,Thomas Lee. [DNLM: 1. Musculoskeletal Diseases—diagnosis. 2. Diagnostic Imaging—methods. 3. Musculoskeletal System—injuries. WE 141 I305 2008] RC925.7.I4356 2008 616.7 0754—dc22

Acquisitions Editor: Judith Fletcher Developmental Editor: Jennifer Shreiner Publishing Services Manager: Tina Rebane Project Manager: Norm Stellander Design Direction: Steve Stave

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C H A P T E R

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C H A P T E R

Introduction and General Principles John H. Harris, Jr.

In this chapter concepts are identified and described that are intrinsic to musculoskeletal trauma, such as the purpose of the imaging report, vector forces causing musculoskeletal injury, musculoskeletal injury terminology, and fractures and dislocations in which the associated soft tissue component—not routinely delineated by conventional radiography—is the principal element of the injury. Because most of the musculoskeletal injuries described in this chapter are discussed and illustrated in greater detail in the chapters on specific anatomic regions, this chapter can also serve as a quick synoptic reference.

PURPOSE OF THE IMAGING REPORT The imaging report is not only the formal transmittal of the findings of the examination but also serves as the basis of patient management, the source of comparison with subsequent examinations, a historic record, and a source of possible research data. For all these reasons, all musculoskeletal injury imaging reports must be as accurate and thorough as possible. The report must be dictated after critical observation, analysis, and synthesis of the data present on the examination. Timely transmission of information derived from the musculoskeletal injury imaging examination to the attending physician is essential for proper patient management. The initial examination (conventional radiography, CT, or MRI) may be requested in acute or emergent circumstances, in which event the radiologist should communicate the findings directly to the attending physician or designated representative. In less acute or urgent circumstances, the information may be transmitted in the form of a written report. When the attending physician does not request a “stat” report, the radiologist should determine

whether the injury should be considered emergent or urgent based on the findings of the examination and reasonable medical judgment. Follow-up musculoskeletal injury examination information may be considered as “routine” and the information transmitted by written report. Should the follow-up study show related but unexpected findings, such as infection or change in position of fragments, the radiologist should transmit the findings directly to the attending physician or designee. In every instance, all deviations from normal, including artifacts, recorded on the examination must be included in the report. All appropriate negative observations must be included as well. With respect to CT and MRI, the technical factors and imaging sequences, respectively, must be appropriate to the indications for the examination and should be included in the body of the report.

KEY POINTS Timely transfer of information obtained on a musculoskeletal imaging study to the appropriate referring physician is the primary responsibility of the interpreting radiologist. ■ Emergent or serious unsuspected findings should be transmitted immediately and directly to the referring physician. ■ General knowledge of the fundamental principles of trauma imaging as outlined in this chapter are of utmost importance for the adequate interpretation of musculoskeletal imaging studies. ■

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P A R T O N E ● Injury

Digital imaging and electronic communication should preclude informal, “curb-side” verbal communication between the radiologist and attending physician. Informal verbal communication may lead to misinterpretation, misunderstanding of the transmitted information, or even misdiagnosis, with resultant patient mismanagement and the potential for medical liability. When the radiologist and attending physician do consult directly, the consultation must be supported by a formal written report. The Practice Guidelines of the American College of Radiology recommend that the radiologist’s initial report consist of two parts: a heading called “Impression,” “Diagnosis,” or “Conclusion” and a descriptive portion (body) frequently designated as “Comment.”1 The body of the report should describe the findings that prompted the impression, diagnosis, or conclusion. If a single diagnosis is not possible, the impression, diagnosis, or conclusion should be expanded to include a reasonable differential diagnosis with the possibilities listed in the order of likely probability. The body or “comment” portion of the study should indicate the part or anatomic region examined and the views (projections) obtained (e.g., “the cervical spine was examined in anteroposterior, lateral, and open-mouth projections”). Follow-up examinations need not contain a “Diagnosis” or “Impression”; however, they should indicate the views

and projections constituting the examination and always include the phrase, “In comparison with the previous examination of the (part or anatomic area) dated____, etc.”All changes between the previous and current examination must be carefully and accurately described.

BONE TYPES The different types of bone include the following2: Long: length greater than width (e.g., femur, phalanx) Short: cuboid shape (e.g., carpal and tarsal bones) Flat: two layers of compact bone separated by a thin marrow space; usually preformed in a membrane (e.g., sternum, ribs, scapula) Irregular: mixed shape (e.g., vertebra, pelvis) Sesamoid: small, usually round or oval bones that develop in tendons. Sesamoid bones are usually flat on the side adjacent to the neighboring bone (Fig. 1-1). Accessory (supernumerary): arise from separate centers of ossification located adjacent to a parent bone and found most frequently in the foot (e.g., os intermetatarseum (Fig. 1-2).

■ FIGURE 1-1

Sesamoid bones. The sesamoid bones on the plantar surface of the head of the first metatarsal (arrows) are located in the tendons of the adductor hallucis and the lateral head of the flexor hallucis brevis and the abductor hallucis and medial head of the flexor hallucis brevis muscles. Other sesamoid bones include the patella and the pisiform bone of the wrist.

■ FIGURE 1-2

Os intermetatarseum (arrow) between the base of the first and second metatarsal bones.

CHAPTER

1

● Introduction and General Principles

5

GEOGRAPHIC ANATOMY OF LONG AND SHORT BONES Long and short bones have their origin from primary and secondary ossification centers (Fig. 1-3).The primary ossification originates in the mid shaft of the bone, with ossification progressing proximally and distally from that center. Secondary ossification centers develop in the proximal and distal epiphyses, which unite with the metaphysis of the shaft at the physis to provide longitudinal growth of the bone (Fig. 1-4). Other secondary centers arise in cartilage and form apophyses, which develop into tuberosities or exostoses from, or to which, tendons and ligaments arise or insert (see Fig. 1-4). Portions of long and short bones are designated as “diaphysis” (shaft),“metaphysis” (transitional area between the diaphysis and the epiphysis), and “epiphysis,” which is the proximal and distal fused growth center (see Fig. 1-4).

TYPES OF MUSCULOSKELETAL INJURIES Ligamentous Injuries (Selected Examples) ●

●

■ FIGURE 1-3

Endochondral ossification.

Anterior subluxation (hyperflexion sprain) of the cervical spine. This is caused by a primary hyperflexion mechanism of injury of the cervical spine resulting in the disruption of the posterior ligament complex (Fig. 1-5). Soft tissue Chance injury. This is a hyperflexion injury of the thoracolumbar (T10-L2) spine in which the vertebra at the level of the injury remains intact but all ligamentous structures including the intervertebral disk and the anterior and posterior longitudinal ligaments are disrupted (Fig. 1-6). This injury, like the

■ FIGURE 1-5

■ FIGURE 1-4

Geographic anatomy, humerus.

Disruption of the posterior ligament complex. Anterior subluxation of C4 on C5 is characterized by widening of the interspinous space (arrowhead), subluxation of the C4-C5 interfacetal joints (arrows), and anterior rotation of the C4 vertebra relative to C5.

6

A

P A R T O N E ● Injury

B ■ FIGURE 1-6

A to F, Soft tissue Chance injury of T12. A, Anteroposterior radiograph of the thoracolumbar spine shows rotation of T12 to the patient’s left side. B, Lateral radiograph shows anterior rotation of T12 with subluxation of the T12-L1 apophyseal joints (arrow). C, Axial CT images of T12-L1 show subluxation of the right T12-L1 apophyseal joint (arrow) and the “naked” left T12 facet (open arrow).

(Continued)

C

CHAPTER

■ FIGURE 1-6—Cont’d

D, Axial CT of the T12-L1 area shows the complete left T12-L1 interfacetal dislocation (open arrow). E, Sagittal reformatted CT image shows T12-L1 right interfacetal joint subluxation (arrow). F, Sagittal reformatted CT image shows left interfacetal joint dislocation (open arrow).

E

D

F

1

● Introduction and General Principles

7

8

P A R T O N E ● Injury

■ FIGURE 1-7

Pelvic ring disruption with separation of the pubic symphysis (arrow) and each sacroiliac joint (open arrow) without associated fracture.

●

●

Chance fracture, is associated with an approximate 20% incidence of intra-abdominal injury, such as to the pancreas. Pelvic ring disruption. The pubic symphysis and one or both of the sacroiliac joints are disrupted without associated fracture (Fig. 1-7). Rupture of the Achilles tendon.

Skeletal Injuries ● ● ● ●

Subluxation: partial disruption of a joint (Fig. 1-8). Dislocation (luxation): complete disruption of a joint (Fig. 1-9). Fracture: break in the continuity of a bone (Fig. 1-10). Fracture-dislocation: a musculoskeletal injury in which both disruption of a bone and complete dislocation of a joint occur simultaneously (Fig. 1-11).

SKELETAL INJURY Skeletal injuries are the result of the effect of the major injury vector force on the involved bone.The major injury vectors include axial load (compression), distraction, bending, torsion, and traction (avulsion).The effect of each major injury vector on a long or short bone is schematically illustrated in Figure 1-12. The same vector forces may be applied to the pediatric skeleton. Injuries peculiar to the pediatric age group

■ FIGURE 1-8

Subluxation of the radial head. The frontal radiograph of the right elbow shows lateral subluxation (arrow) of the radial head with respect to the capitellum as one component of a Bado type III Monteggia fracture-dislocation of the elbow.

CHAPTER

■ FIGURE 1-9

Posterior dislocation of the right femoral head with respect to the acetabulum.

■ FIGURE 1-11

1

● Introduction and General Principles

■ FIGURE 1-10

Comminuted fracture of the os calcis.

Fracture-dislocation. The lateral radiograph of the foot and ankle shows a complete fracture through the neck of the talus (arrows) with posterior dislocation of the separate proximal fragment (asterisk).

9

10

P A R T O N E ● Injury

■ FIGURE 1-12

Mechanism of injury/fracture types.

involve the physis (growth plate, epiphyseal plate), the epiphysis, and the metaphysis (see Fig. 1-4) alone or in combination. These injuries are defined by the SalterHarris classification and are described and illustrated in Section 3, Pediatric Injuries. Three injuries involving the distal end of the pediatric tibia—the biplanar fracture of Tillaux, the triplanar fracture, and the Rang type VI physeal injury—are not included in the Salter-Harris classification. The biplanar fracture of Tillaux (Fig. 1-13), sometimes erroneously called a lateral Salter-Harris type III injury, is actually an avulsion fracture of the lateral aspect of the distal tibial epiphysis pulled off by the intact distal tibiofibular ligaments. The biplanar fracture occurs in the 10- to 14-year age group and involves the lateral aspect of the epiphysis because the distal tibial physis

fuses from medial to lateral, allowing the separate fragment to be laterally retracted. In contradistinction, the Salter-Harris type III injury is caused by axial loading, with the vertical fracture typically in the midsagittal plane of the epiphysis (Fig. 1-14). The triplanar fracture consists of a sagittally oriented fracture of the distal tibial epiphysis, a horizontal (axial) fracture through the adjacent physis, and a coronally oriented fracture of the posterior aspect of the adjacent metaphysis. The triplanar fracture may be either two part (Fig. 1-15), in which the component parts constitute a single fragment, or three part, in which each component is a separate fragment.3 The Rang type VI physeal injury is rare and reportedly caused by a direct blow to the periosteum or perichondral ring. It is characterized by a tiny fragment arising

CHAPTER

■ FIGURE 1-13

Biplanar fracture of Tillaux. The mortise view of the right ankle shows a vertical fracture through the lateral aspect of the distal right tibial epiphysis (arrow), disruption of the lateral aspect of the physis (open arrow) and lateral distraction of the separate fragment (asterisk) by the intact distal tibiofibular ligaments. Compare with Figure 1-14.

A ■ FIGURE 1-15

1

● Introduction and General Principles

11

■ FIGURE 1-14

Salter-Harris type III physeal injury. The fracture to the distal tibial epiphysis (arrow) and separation of the medial aspect of the physis (open arrow) result in medial displacement of the medial epiphyseal fragment (asterisk). The medial malleolar styloid process is an ununited secondary ossification center (arrowhead).

B

Triplanar fracture of the distal left tibia. The frontal projection (A) shows a sagittal plane fracture through the epiphysis (arrow) and disruption of the lateral aspect of the physis in the axial plane (open arrows). The lateral radiograph (B) shows the coronally oriented fracture of the posterior aspect of the tibia (arrowheads). In this instance, the epiphyseal, physeal, and metaphyseal components constitute a single fragment. Hence, this is an example of a two-part triplanar fracture.

12

P A R T O N E ● Injury

■ FIGURE 1-16

Inside-out open fracturedislocation. The skin of the proximal forearm has been penetrated by the displaced, distracted proximal radius (R) and the proximal end of the distal ulnar fragment (arrow). Air (open arrows) is diffusely present in the soft tissues of the elbow.

■ FIGURE 1-17

Open fracture of the right foot caused by a crush injury. Subcutaneous emphysema is extensive (curved arrows).

■ FIGURE 1-18

Transverse fracture at the junction of the middle and distal thirds of the humerus (arrow). The open arrow indicates a concomitant Salter-Harris I physeal injury with displacement of the metaphysis relative to the humeral head epiphysis.

from either the epiphysis or the metaphysis and located in the periphery of the physis. The presence of the tiny fragment distinguishes the Rang type VI injury from the Salter-Harris type I physeal injury.

FRACTURES Fractures may be classified by the causative force as either “direct” or “indirect.” Direct forces include gunshot, explosion, stabbing, and crushing injuries. Direct fractures occur in random patterns, whereas most indirect fractures occur in reasonably predictable patterns. Fractures may also be classified as being “closed” (intact skin of the involved body part) or “open,” in which the skin of the involved body part is disrupted. The “open” fracture may be caused from inside out, as when the overlying skin is lacerated by the jagged edge of a displaced fracture fragment (Fig. 1-16). An “open” fracture also may be the result of a penetrating or crushing injury (outside in) (Fig. 1-17).4 Fractures may be classified by the orientation of the fracture line, such as transverse (Fig. 1-18), distracted (Fig. 1-19), oblique (Fig. 1-20), spiral (Fig. 1-21), or impacted (Fig. 1-22); by the orientation of the fracture fragments,

■ FIGURE 1-19

Displaced, angulated, distracted fracture of the proximal ulna (open arrow). The ulnar fracture is a component of the Bado type IV Monteggia injury. The straight arrow indicates the radial head-neck component.

■ FIGURE 1-20

fibula.

Oblique fracture (arrows) in the distal third of the left

■ FIGURE 1-21

Spiral fracture. The fracture line, with its sharply pointed edges, makes a complete rotation around the shaft of a long bone, the tibia in this instance (white arrowheads). The vertical component (black arrowheads), acting as a hinge, causes the fragments on the back side of the fracture to separate. (From May DA, Disler DG: Trauma: generalizations. In Manaster BJ, Disler DG, May DA [eds]: Musculoskeletal Imaging, 2nd ed. The Requisites Series. Philadelphia, Mosby, 2002.)

■ FIGURE 1-22

Axial loading (impacted) fracture of C5. Impaction, or compression, of the body of C5 resulted in bilateral separation of the C5 body fragments as evidenced by the widening of the C4-5 (open arrows) and narrowing (arrows) of the C5-6 Luschka joints (A). The lateral radiograph (B) shows a burst (bursting) fracture of C5 (arrows).

A

B 13

14

P A R T O N E ● Injury

■ FIGURE 1-23

Stress fracture. Oblique radiograph (A) of the left foot shows very minimal callus formation (arrow) at the distal diaphysis of the second metatarsal. A similar projection of the left foot taken 3 months later (B) clearly demonstrates circumferential callus formation (arrows) of the healed stress fracture.

A

B

such as nondisplaced (Fig. 1-23) (stress fracture), displaced (Fig. 1-24), angulated (Fig. 1-25), displaced and angulated (Fig. 1-26), and bayonet (overlapped) (Fig. 1-27); or as “simple” (two fragments) (see Fig. 1-24), “comminuted” (more than two fragments) (see Fig. 1-10),“segmental” (two fracture sites in the same bone resulting in three separate fragments) (Fig. 1-28), and “complete” (circumferential cortical disruption) (see Fig. 1-18) and “incomplete” or “greenstick” (partial cortical disruption) (Fig. 1-29). Insufficiency fractures may occur in areas of bone demineralization (osteoporosis) (Fig. 1-30) or areas of skeletal neoplasia (pathologic fracture) (Fig. 1-31). Axial loading may cause impaction (Fig. 1-32) or separation of fragments (see Fig. 1-22). Fractures may be caused by forceful abrupt (Fig. 1-33) or repetitive less forceful (Fig. 1-34) ligamentous traction (“little leaguer’s elbow”).

■ FIGURE 1-24

Displaced fracture. The frontal radiograph of the wrist shows the distal ulnar fragment laterally displaced with respect to the proximal fragment.

CHAPTER

■ FIGURE 1-25

Angulated fracture. The lateral radiograph of a Galeazzi fracture shows volar angulation of the distal radial fragment with respect to its proximal fragment.

■ FIGURE 1-26

Displaced, angulated fracture. The lateral radiograph of the forearm and wrist shows the distal radial fragment to be both angulated (broken lines indicate long axis of each radial fragment) and displaced (arrowheads indicate the volar cortex of the proximal fragment and the arrow the volar cortex of the distal fragment).

■ FIGURE 1-27

1

● Introduction and General Principles

Bayonet, or overriding, fracture as indicated by the position of the distal femoral fragment with respect to its proximal fragment.

■ FIGURE 1-28

15

Segmental fracture. The anteroposterior radiograph of the leg shows two fracture sites in the tibia (open arrows) resulting in three distinct fracture fragments (1–3).

16

P A R T O N E ● Injury

■ FIGURE 1-29

Greenstick (incomplete) fracture of the radius (arrow). Note bowing of the ulna.

■ FIGURE 1-31

Pathologic fracture (arrows) through a benign cortical defect (arrowheads) of the distal femur.

■ FIGURE 1-30

Insufficiency fractures of the pubic symphysis (arrows).

CHAPTER

■ FIGURE 1-32

1

● Introduction and General Principles

17

Impacted, subcapital fracture (arrow) of the left femur.

■ FIGURE 1-34

Little leaguer’s elbow. Avulsion and displacement of the medial epicondylar apophysis (asterisk) is due to repeated contractions of the flexor muscles of the forearm.

■ FIGURE 1-33

“Beak” fracture of the os calcis. The separate fragment (asterisk) is avulsed by abrupt, forceful contraction of the Achilles tendon. Metallic rings indicate sites of concomitant skin laceration.

Displaced, angulated, or comminuted fractures of the femoral diaphysis should always raise the possibility of superficial femoral artery injury. Dislocation of the knee (Fig. 1-38) always places the popliteal artery at risk and is considered to be an acute surgical or orthopedic emergency.

MUSCULOSKELETAL INJURIES COMMONLY ASSOCIATED WITH NONLIGAMENTOUS SOFT TISSUE INJURY Posterior sternoclavicular subluxation/dislocation places the subclavian vein at risk. Supracondylar fracture or posterior dislocation (Fig. 1-35) of the elbow places the median nerve and brachial artery at risk. All pelvic ring disruptions must be assessed for lower urinary tract injury and/or intrapelvic hemorrhage (Fig. 1-36) regardless of the degree of pubic symphysis separation or fracture fragment displacement. Subcapital fracture of the femoral neck (Fig. 1-37) carries about an 80% incidence of avascular necrosis of the femoral head secondary to disruption of the blood supply from the lateral and medial circumflex arteries.

■ FIGURE 1-35

Posterior dislocation of the elbow.

18

P A R T O N E ● Injury

■ FIGURE 1-36

Pelvic ring disruption with intrapelvic hematoma compressing and distorting the urinary bladder.

■ FIGURE 1-38

Anterior dislocation of the knee.

■ FIGURE 1-37

■ FIGURE 1-39

Subcapital femoral neck fracture (arrows).

“Bumper” fracture of the proximal tibia (arrow) with occlusion of the distal popliteal artery (stemmed arrow).

CHAPTER

1

● Introduction and General Principles

The “bumper” fracture of the proximal tibia (Fig. 1-39) must always raise the possibility of injury to the distal popliteal artery or its branches. The Chance fracture, dislocation (see Fig. 1-6), or fracture-dislocation has an approximate 20% incidence of intra-abdominal injury (e.g., the pancreas).

SPINAL INJURIES WITH INHERENT SPINAL CORD INJURY Cervical Spine ● ● ● ●

Type III traumatic spondylolisthesis (Fig. 1-40) Bilateral interfacetal dislocation or fracture-dislocation (Fig. 1-41) Flexion teardrop fracture (Fig. 1-42) Hyperextension dislocation (Fig. 1-43)

Thoracic and Lumbar Spine ●

Displaced fracture or fracture-dislocation

■ FIGURE 1-41

Bilateral interfacetal fracture-dislocation of C6. Bilateral laminar fractures of C6 (open arrow) result in the C6 spinous process (arrow) being a separate fragment.

■ FIGURE 1-40

Effendi type III traumatic spondylolisthesis.

■ FIGURE 1-42

Flexion teardrop fracture of C4.

19

20

P A R T O N E ● Injury

■ FIGURE 1-44

Type III dens fracture (arrows). The fracture line breaks the axis ring.8 The rostral axis fragment, together with C1 and the head, are anteriorly displaced.

■ FIGURE 1-43

Hyperextension dislocation of the cervical spine characterized radiographically by the diffuse prevertebral soft tissue swelling (asterisk) and normally aligned, intact vertebrae. This injury is clinically evidenced by the acute central cervical cord syndrome and signs of injury to the face.7

SPINAL INJURIES WITH POTENTIAL SPINAL CORD INJURY Cervical Spine ● ● ●

Type III dens fracture (Fig. 1-44) Extension teardrop fracture (Fig. 1-45) Burst (bursting, axial load) fracture (see Fig. 1-22)

Thoracolumbar Spine ●

Burst (bursting, axial load) fracture

■ FIGURE 1-45

Extension teardrop fracture of C5. The diffuse, marked prevertebral soft tissue (asterisk) swelling indicates a severe hyperextension mechanism of injury with probable spinal cord injury. The extension teardrop fragment (arrow) typically involves the anteroinferior corner of the vertebral body with its vertical height being equal to the horizontal width of its base.

CHAPTER

BENDING FRACTURES Bending fractures deserve special mention because of the spectrum of injuries that the bending major injury vector produces, the location of microfractures in pediatric patients, and, when present, the location and significance of the butterfly fragment in adult patients. To understand the skeletal manifestations of bending forces, it is necessary to understand the bending mechanism of injury. Bending fractures are most common in long bones. Bending loads cause the bone to bend along its neutral, typically longitudinal, axis. Bending subjects the bone to tensile stresses along the convex and compression stresses along the opposite (concave) side of the bone. In adults, the tensile (convex) side is weaker than the compression (concave) side; consequently, the bone fails initially on the convex side. The fracture propagates through the bone to merge with the fracture on the compression side. When present, the butterfly fragment is the result of two oblique compression side fractures merging both with each other and with the transverse fracture from the convex side, forming the butterfly fragment

■ FIGURE 1-46

(asterisk).

Butterfly fragment

■ FIGURE 1-47

(arrow).

1

● Introduction and General Principles

21

(Fig. 1-46). Therefore, the butterfly fracture always indicates a bending mechanism of injury and also the side of compression.5,6 In pediatric patients, bending may result in a cortical-buckling fracture of the compression (concave) side (Fig. 1-47) or a greenstick fracture that is commonly associated with a bowing fracture of the paired long bone (see Fig. 1-29). The latter constellation of fractures, with healing, shows callus formation along the concave side of the long bone, indicating the side of the microfractures of a bowing fracture (Fig. 1-48). Fracture fragments consisting of both cartilage and underlying bone are called osteochondral fragments, seen most commonly in the shoulder and less commonly in the knee (Fig. 1-49). Osteochondral fragments are difficult to recognize radiographically because the separate fragment is primarily chondral with only an attached thin segment of underlying cortical bone. Intra-articular fractures are those occurring within a joint capsule such as a compression fracture of a tibial plateau (Fig. 1-50). Intra-articular fractures heal without radiographically visible cortical callous formation.

Cortical buckling fracture

■ FIGURE 1-48

An anteroposterior follow-up radiograph of the leg of a child who suffered a transverse fracture of the mid tibia (arrow) and a bowing fracture of the fibula. Fibular callus formation (arrowheads) along the concave side of the fibula indicates the location of the bowing microfractures, which are typically not visible on the initial radiograph.

22

P A R T O N E ● Injury

■ FIGURE 1-49

Osteochondral fracture fragment (arrow).

MUSCULOSKELETAL INJURIES WITH ASSOCIATED CLINICALLY SIGNIFICANT LIGAMENTOUS COMPONENT The fractures in this category of musculoskeletal injury are typically obvious by conventional radiography, whereas the ligamentous component typically is not. In addition to identifying the fracture, it is the responsibility of the radiologist to emphasize, and delineate, the integral ligamentous component, which typically is not visible by conventional radiography, in the report to the referring physician. In this section, the injuries will either be defined or illustrated, from proximal to distal, in the upper extremity, the pelvis, and from proximal to distal in the lower extremity. Because many of these injuries are described and illustrated in the appropriate anatomic region chapter, only those uncommon skeletal injuries with a significant ligamentous or soft tissue component are mentioned here.

■ FIGURE 1-50

Interarticular compression (depression) fracture of the right lateral tibial plateau (arrows).

● ●

Wrist ● ●

●

● ●

Types III, IV, V, and VI acromioclavicular separation Glenohumeral dislocation Scapulothoracic dissociation (Fig. 1-51), which is associated with brachial plexus and axillary artery injury

Elbow ●

Transverse fracture of the olecranon process, which may be caused by a triceps tendon avulsion mechanism of injury

The carpal instabilities Isolated rotatory subluxation of the scaphoid (Fig. 1-52), which indicates disruption of the scapholunate ligament Distal radioulnar subluxation-dislocation, as in the Galezzia (see Fig. 1-25) fracture or any fracture that causes shortening of either the radius or the ulna and results in disruption of the triangular fibrocartilage

Hand ●

Shoulder ●

Monteggia fractures Avulsion fracture of the medial epicondylar apophysis. In this injury, the forearm flexor muscles are detached from the humerus (see Fig. 1-34).

●

●

Skier’s (gamekeeper’s) thumb (Fig. 1-53), which is disruption of the ulnar collateral ligament of the thumb metacarpophalangeal joint caused by forceful abduction of the thumb Bennett fracture of the thumb (Fig. 1-54), in which the large distal fragment is retracted by the adductor pollicis tendon attached to the base of the distal fragment Volar plate fracture (Fig. 1-55). The tiny fracture fragment from the volar aspect of the base of the phalanx indicates that the volar plate of the involved joint is intact but is no longer attached to its distal phalanx. Volar plate fracture must not be considered a “chip” fracture and of no clinical significance.

CHAPTER

1

● Introduction and General Principles

■ FIGURE 1-51

Scapulothoracic dissociation. The scapula and humerus are severely laterally displaced secondary to the distracted clavicular fracture (arrow) and the disrupted acromioclavicular joint (open arrow). The soft tissue density extending from the axilla to the supraclavicular area (two asterisks) represents a major hematoma.

■ FIGURE 1-52

Isolated rotatory subluxation of the scaphoid. The abnormally wide space between the scaphoid and lunate bones (open arrow) is the “Terry Thomas” sign. The “ring” sign of the rotated scaphoid is indicated by the arrows.

■ FIGURE 1-53

Gamekeeper’s thumb. The proximal thumb phalanx (asterisk) is severely abducted with respect to the first metacarpal.

23

24

P A R T O N E ● Injury

■ FIGURE 1-54

Bennett fracture (arrows) of the first metacarpal. The proximal extent of the fracture line of a Bennett fracture must involve the proximal articulating surface of the first metacarpal.

■ FIGURE 1-55

Volar plate fracture. The site of avulsion of the tiny fragment of the volar surface of the middle phalanx (arrow) indicates the origin of the avulsed fragment by the intact volar plate.

Pelvis Avulsion Injuries ● ● ●

Anterior superior iliac spine apophysis avulsion (Fig. 1-56) indicates the sartorius muscle is no longer attached. Anterior inferior iliac spine apophysis avulsion (Fig. 1-57) indicates the rectus femoris muscle is detached. Ischial tuberosity apophysis avulsion (Fig. 1-58) indicates separation of all, or a portion, of the hamstring muscles of the posterior thigh.

Knee ● ● ●

Intercondylar spine fracture (Fig. 1-59) indicates detachment of the anterior cruciate ligament. High-riding patella (Fig. 1-60) with history of knee trauma indicates tear of the infrapatellar ligament. Fracture/epiphyseal separation of the anterior tibial tubercle (Fig. 1-61) indicates detachment of the infrapatellar ligament.

Ankle Ligamentous injuries associated with ankle fractures and/ or dislocations are indicated by the position of the ankle mortis components and are described and illustrated in detail in Chapter 30. In Figure 1-62, the medial collateral

■ FIGURE 1-56

Avulsion of the anterior superior iliac spine apophysis (arrow) indicates detachment of the sartorius muscle.

CHAPTER

■ FIGURE 1-57

Avulsion of the anterior inferior iliac spine apophysis (arrow) indicates detachment of the rectus femoris muscle.

A ■ FIGURE 1-59

1

● Introduction and General Principles

■ FIGURE 1-58

Avulsion of the ischial tuberosity apophysis (arrows) indicates detachment of the hamstring muscles.

B Femoral intercondylar spine fracture (arrows, A and B) indicate detachment of the anterior cruciate ligament.

25

26

P A R T O N E ● Injury

■ FIGURE 1-60

Torn inferior patellar tendon is indicated by a highriding patella (asterisk).

■ FIGURE 1-62

Fracture-dislocation of the left ankle with disruption of the medial collateral ligament (arrow) and the tibiofibular ligament (open arrow). The lateral collateral ligament (curved arrow) is intact. The interosseus membrane (asterisk) is torn to the level of the fibular fracture.

and the anterior and posterior distal tibiofibular ligaments are disrupted, whereas the lateral collateral ligament remains intact. The interosseous membrane is torn to the level of the fibular fracture.

Foot ● ● ●

■ FIGURE 1-61

Fracture-avulsion of the anterior tibial tubercle (arrow) indicates detachment of the infrapatellar tendon.

Beak fracture of the calcaneus (see Fig. 1-33) indicates the Achilles tendon is detached from the calcaneus. Fracture of the base of the fifth metatarsal (Fig. 1-63) indicates detachment of the peroneus brevis muscle. Lisfranc injury (Fig. 1-64) indicates disruption or detachment of the Lisfranc ligament, which extends from the distal lateral corner of the first cuneiform bone to the medial aspect of the base of the second metatarsal (in Fig. 1-64, the fracture of the first cuneiform is not a component of the classic Lisfranc injury).

CHAPTER

1

● Introduction and General Principles

27

■ FIGURE 1-64 ■ FIGURE 1-63

Fracture of base of the fifth metatarsal (arrow) indicates that the peroneus brevis muscle is no longer attached.

Homolateral Lisfranc injury with disruption of the Lisfranc ligament (arrow). The first metatarsal bone remains in its normal position with respect to the first cuneiform bone. The lateral four metatarsal bones are laterally subluxated. The fractures of the first cuneiform (asterisk) are not a component of the pure Lisfranc injury.

SUGGESTED READINGS Chew FS. Musculoskeletal Imaging. Philadelphia, Lippincott Williams & Wilkins, 2003. Chew FS, Roberts CE. Musculoskeletal Imaging, A Teaching File, 2nd ed. Philadelphia, Lippincott Williams & Wilkins, 2003. Harris JH Jr, Harris WH. The Radiology of Emergency Medicine, 4th ed. Philadelphia, Lippincott Williams & Wilkins, 2000. Johnson TR, Steinbach LS (eds). Essentials of Musculoskeletal Imaging, 2nd ed. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2004. Koval KJ, Zuckerman JD. Handbook of Fractures, 2nd ed. Philadelphia, Lippincott Williams & Wilkins, 2002. Manaster BJ. Handbook of Skeletal Radiology, 2nd ed. St. Louis, Mosby, 1997.

Manaster BJ, Disler DG, May DA. Musculoskeletal Imaging: The Requisites, 3rd ed. St. Louis, Mosby, 2002. Miller TT, Schweitzer ME. Diagnostic Musculoskeletal Imaging. New York, McGraw-Hill Medical Publishing, 2005. Nordin M, Frankel VH. Basic Biomechanics of Musculoskeletal System, 3rd ed. Philadelphia, Lippincott Williams & Wilkins, 2001. Rogers LF. Radiology of Skeletal Trauma, 3rd ed. Philadelphia, Churchill Livingstone, 2002. Salter RB.Textbook of Disorders and Injury of the Musculoskeletal System, 3rd ed. Philadelphia, Lippincott Williams & Wilkins, 1999. Stern EJ (ed). Trauma Radiology Companion. Philadelphia, LippincottRaven, 1997.

REFERENCES 1. ACR Practice Guidelines for Communication: Diagnostic Radiology. Practice Guidelines and Technical Standards. Reston, VA, American College of Radiology, 2003, pp 5-7. 2. Schultz RJ. The Language of Fractures, 2nd ed. Baltimore, Williams & Wilkins, 1990. 3. Brown SD, Kassar JR, Zurakowski D, Jaramillo D. Analysis of fifty-one tibial triplane fractures using CT with multiplanar reconstruction. AJR Am J Roentgenol 2004; 183:1489–1495. 4. Behrens FF. Fractures with soft tissue injuries. In Browner BD, Jupiter JB, Levine AM,Trafton PG (eds). Skeletal Trauma. Philadelphia, WB Saunders, 1998, pp 391–448.

5. Chew FS, Roberts CC. Musculoskeletal Imaging: A Teaching File. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 450–451. 6. Harris JH Jr,Yeakley JW. Hyperextension-dislocation of the cervical spine. J Bone Joint Surg Br 1992; 74:567–570. 7. Nordin M, Frankel VH. Basic Biomechanics of the Musculoskeletal System. Philadelphia, Lippincott Williams & Wilkins, 2001, pp 40–42. 8. Harris JH Jr, Burke JT, Ray RD, et al. Low (type III) odontoid fracture: a new radiographic sign. Radiology 1984;153:353–356.

C H A P T E R

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Imaging of Facial and Skull Trauma Lorne Rosenbloom, Bradley N. Delman, and Peter M. Som

The craniofacial vault has the formidable task of protecting the brain, the soft tissues that form the proximal airways, and the tissues vital to the special senses of vision, smell, taste, and hearing. Injury to the craniofacial region may therefore have devastating implications to the traumatized patient. Prompt and accurate diagnosis of craniofacial injuries is necessary for appropriate treatment to minimize both functional and aesthetic sequelae.

PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS The epidemiology of craniomaxillofacial trauma varies greatly with the population being studied.1 Differences are best explained by rates of motor vehicle usage, seat-belt laws, violent crime, and different kinds of leisure activities between groups in various geographic locations. However, certain epidemiologic principles regarding craniomaxillofacial trauma are relatively constant across most studied groups. Taken as a group, males sustain skull or facial trauma considerably more frequently than females, and the incidence of facial trauma tends to be higher in the mid-teenage years through the end of the second decade.1 The major causes of injury in these patients include motor vehicle accidents, violent assault, falls, and sports-related injuries.2 Beyond the third decade the incidence of injury declines until the elderly years, when strokes and age-related reductions in coordination lead to a second peak predominantly due to falls. Workrelated trauma and animal attacks account for a relatively small percentage of cases of facial trauma worldwide.

ANATOMY AND BIOMECHANICS A comprehensive discussion of the anatomy of the skull and facial vault is beyond the scope of this overview. However, when considering facial trauma, it is useful to review the concept of the facial buttresses. The support system of the facial skeleton can be thought of as a lattice

of crisscrossing structures. Each individual structure is relatively weak, but together they offer significant resistance to compression and shearing forces. Failure of the lattice (i.e., a fracture) results in significant absorption and redistribution of mechanical energy, largely shielding the airway and brain from transmitted force in all but the most severe cases. The horizontal (axial) struts of the face include (1) the orbital roof, including the frontal bar (the thickened segment of frontal bone between the two zygomaticofrontal sutures forming the superior orbital rims); (2) the orbital floors, including the more robust inferior orbital rims; and (3) the hard palate and the more robust maxillary alveolus anteriorly. The mandibular symphysis and parasymphysis are occasionally considered segments of a fourth caudal horizontal strut, but the relatively independent motion of the mandible renders it susceptible to trauma even in the absence of midfacial injury. The vertical (sagittal) struts are nearly parallel, although they converge slightly at their superior aspects. The lateral (zygomaticomaxillary) buttress extends from the lateral maxillary alveolus along the zygoma to the lateral orbital rim at the zygomaticofrontal suture. The medial (nasomaxillary) facial buttress runs from the anterior maxillary alveolus along the piriform aperture of the nose and frontal process of the maxilla to the glabella of the frontal bone. The midline nasal septum is regarded by some as representing the third vertical component, but this is ordinarily thin and is frequently deformed or deviated so that it likely contributes little to overall facial stability. The struts in the coronal plane offer the least resistance to facial compression, although they do aid in integrating or distributing force between two or more of the perpendicular struts to which they articulate. Anterior walls of the maxillary sinuses, which are frequently fractured in moderate to severe facial trauma, transmit secondary force to the zygomaticomaxillary, nasomaxillary, and orbital floor structures. The posterior buttress runs from the posterior 31

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KEY POINTS The struts that comprise the face are relatively weak individually; however, the intertwined lattice they form offers significant resistance to compression and shearing forces. ■ Most facial trauma imaging can be performed adequately using thin-collimation, thin-section overlapping CT images with reconstruction in orthogonal or arbitrary oblique planes. However, because of fine submillimeter structures in the temporal bones, many institutions still use dedicated axial and coronal imaging to offer supreme visualization of this region. ■ Orbital blowout injuries occur in two phases. The primary wave, which propagates through the bone itself, shatters the thin orbital floor and/or lamina papyracea. A secondary wave, which propagates through soft tissue, displaces the resulting fragments medially or inferiorly into the maxillary sinus toward regions of least resistance. ■ Essentially all Le Fort fractures involve the pterygoid plates, and almost all fractures that involve the pterygoid plates will be of the Le Fort variety. Therefore, presence or absence of pterygoid plate fracture correlates highly with presence or absence of Le Fort type injury. ■ Pterygoid fracture with inferior orbital rim fracture usually reflects a Le Fort II pattern. ■ Pterygoid fracture with lateral orbital rim fracture and, in particular, zygomatic arch fracture is most compatible with a Le Fort III pattern. ■ Most temporal bone fractures contain elements of transverse and longitudinal fracture lines. Therefore, use of these terms alone, without description of the course of the fractures, is discouraged. ■ Because of limited mobility of the temporomandibular joint, if injured the mandible can fracture in one or multiple sites. Subluxation of one or both joints can absorb some of the impact and limit the extent of osseous injury. ■

The paired nasal bones join at the midline. The thicker upper portion of the nasal bone, which articulates with the frontal bone and frontal processes of the maxillae, is more resistant to fracture than is the thinner, broader inferior portion (Fig. 2-1).4 The quadrangular cartilaginous nasal septum, which attaches to the perpendicular plate of the ethmoid bone posterosuperiorly and vomer posteroinferiorly, may also fracture, being more prone to injury in its thinner dorsal aspect. Although the diagnosis of nasal fracture can be made with both conventional lateral radiography of the nose and CT, multiple studies have demonstrated that nasal imaging is of little use in simple nasal fracture, because diagnosis can usually be made on clinical grounds.4 Soft tissue swelling over a nasal fracture might make the fracture less conspicuous to the clinician, particularly in those fractures that are minimally displaced. Thus, what may be interpreted as swelling may mask a nasal fracture of minimal significance clinically, and when this possibility is detected the clinician should be alerted.

Orbital Fractures Four categories of orbital fracture are recognized: internal (blowout) fractures, orbital rim fractures, naso-orbito-ethmoid (NOE) fractures, and zygomatico-orbital (zygomaticomaxillary complex) fractures.

Internal Orbital Fractures Orbital blowout fractures, by definition, involve the orbital walls and grossly spare the more robust orbital rims.5 When an object larger than the diameter of the orbital rim strikes

maxillary alveolus along the posterior wall of the maxillary sinus to the pterygoid processes of the sphenoid bone; injury to this segment is ordinarily associated with other severe midfacial injury, for which the interpreter should search if more anterior structures appear spared initially. Some authors will also include the ascending ramus of the mandible as a fourth vertical buttress as well.3 The integrity of the buttress system is of great importance in the structural support of the face. Accordingly, a primary goal of maxillofacial surgery in facial trauma is the restoration of proper alignment and adequate fixation of the significantly displaced facial buttresses. However, repair may be delayed or deferred if strut injury has little or no functional or cosmetic deficit.

CLINICAL PRESENTATION Nasal Fractures Nasal fractures are the most common of all facial fractures, in part because of the central prominent location of the nose, as well as the relatively small force required to fracture it. The pattern of nasal fracture is highly dependent on the vector of force applied to the nose.4 Fracture may involve the bony or cartilaginous elements of the nose and often involves both.

■ FIGURE 2-1 Bilateral nasal fractures. There is severe comminution on the right (straight arrows) and an overriding nasal bone fragment on the left (hatched arrow). Note how the smooth skin contour, although displaced slightly by soft tissue swelling underneath, is so symmetric that it may obscure the degree of osseous injury on clinical inspection. The generalized swelling effaces the anterior nasal lumen. In addition, the presence of gas in the soft tissues seen in the setting of acute trauma suggests some laceration of nearby soft tissues.

CHAPTER

the orbit, forces are absorbed by bone as well as the globe itself. Direct force to the osseous rim propagates rapidly in the first wave, resulting in subtle fragmentation of the struts to which it articulates. Of these struts, the inferior and medial orbital walls appear to be the weakest, given the frequency with which they are involved. Thus, fracture of these struts results in significant dissipation of force, but this initial wave fails to significantly displace these fracture fragments. The delayed recoil of the compressed globe, also vulnerable because it protrudes slightly beyond the orbital rim, causes a second pressure wave. This force is transmitted through the periphery of the globe into the adjacent fat and to the bone, ultimately causing the displacement of the fracture fragments that is characteristically noted on imaging (Fig. 2-2). Characteristic points of weakness include the portion of the floor formed by the orbital plate of the maxilla near the infraorbital groove, as well as the medial wall, which is formed by the thin lamina papyracea.6 In some series, the orbital floor variety is reported as the most common type6; whereas, in others, the medial wall variety is more frequent.7 Orbital roof and lateral orbital wall fractures are uncommon. Intraorbital fat and extraocular muscle (typically the inferior rectus) may herniate through the fracture defect, clinically resulting in diplopia. It is important to note that muscle itself need not herniate to cause entrapment; there exist significant fibrous septations running between fat and muscle, and therefore herniation of the tethered fat alone can lead to significantly restricted motion of the adjacent muscle. Periorbital emphysema likely results not simply in disruption of the common sinus/orbital wall but rather in sinus wall fracture combined with the increased intranasal pressure the patient effects by blowing the nose to clear epistaxis (Fig. 2-3). This increased pressure secondarily forces air into the adjacent fat. Such air may compensate for the orbital volume lost with fat herniation, so its detection is important in planning for surgery to prevent delayed enophthalmos in those patients without orbital dysfunction in whom surgery may not have been considered initially. Optimal assessment of blowout fractures includes axial CT with either true coronal scans or high-quality reformatted images in the coronal and possibly oblique sagittal planes.8 Blowout fractures may be treated operatively or conservatively.The goal of surgical intervention is to release entrapment, when present, as well as to restore normal orbital volume.5 In addition, because most patients with orbital floor blowout injuries develop some degree of inferior orbital and superior alveolar nerve hypesthesia, early nerve decompression may also be crucial if the neural canal is compromised. Dehiscence of the lamina papyracea may simulate a medial blowout fracture (Fig. 2-4). In this variant a segment of the medial orbital wall is bowed toward the ethmoid complex, with the medial extraconal fat (and sometimes a thickened medial rectus) herniating through the defect. While the posterior margin of dehiscence is typically the basal lamella, the anterior extent may vary. Unlike in acute fractures, in which one may see density in sinuses reflecting hemorrhage, in dehiscence there is ordinarily no opacification of adjacent cells; however, since mucosal disease can opacify any of the sinuses with variably dense material, radiologic distinction of sinus inflammation from acute trauma may be difficult in cases of dehiscence. Furthermore, because ancillary soft

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■ FIGURE 2-2

Illustration of mechanism of orbital blowout fracture. Forces are transmitted to the orbital region in two waves. First, the relatively smaller orbital rim absorbs the impact of an object and forces propagate posteriorly in an osseous wave. This leads to fragmentation of the weak inferior and/or medial walls of the orbit, apparently the weakest aspects of the orbit. A separate pressure wave results from forces that are initially absorbed by compression of the orbit, then released into the soft tissues after orbital recoil. This soft tissue wave causes displacement of the fragments that had been created by the osseous wave.

■ FIGURE 2-3 Orbital floor blowout fracture. Note the disruption of the left orbital floor in a “trap-door” configuration, hinged along the medial fracture line near the osteomeatal infundibulum and deflected more inferiorly on the lateral aspect (arrow). The latter may permit a one-way extension of extraconal fat, or fat with muscle, much like a child’s “Chinese finger trap” toy; either configuration may lead to the clinical diagnosis of “entrapment.” Note the orbital emphysema (hatched arrows), predominantly extraconal in this case. There is also extensive soft tissue emphysema (asterisks) that presumably spreads from the fracture site, through the orbit, and then superficially.

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■ FIGURE 2-4 Developmental dehiscence of the lamina papyracea. The posterior margin sits at the basal lamella (hatched arrow), while in this case the dehiscence extends through almost the entire ethmoid complex (arrow). The medial extraconal fat extends into the dehiscent region, and there is broadening of the medial rectus muscle. No inflammatory changes are noted within the orbital fat or adjacent ethmoid cells to indicate recent trauma.

tissue findings are lacking in chronic medial wall fractures, distinction of chronic injury from dehiscence may also be problematic. Although not reliably seen, the presence of an extra layer of bone just medial to the orbital fat would suggest prior fracture rather than dehiscence.

Orbital Rim Fractures Orbital rim fractures typically result from direct impact to the orbital rim by a blunt object traveling at high velocity. Fractures may involve the superior, lateral, or inferior

A ■ FIGURE 2-5

rims. In a superior rim fracture (the most common) the globe is displaced inferiorly and frequently anteriorly as well; associated edema and orbital or subperiosteal hemorrhage may exacerbate globe displacement (Fig. 2-5). Deep projection of an osseous fragment into the orbit may cause frank rupture of the globe; because imaging studies may not detect mild scleral disruption, the determination of globe rupture is best made by direct ophthalmologic evaluation. In cases in which there has been subperiosteal bleeding, failure to drain a hematoma early may allow it to organize and ossify, resulting in permanent displacement of the globe with diplopia. Because fracturing the orbital rim requires great force, other osseous and soft tissue injuries are common. In particular, the studies must be carefully searched for contusions or shearing injury to the brain, epidural hematomas, or cerebrospinal fluid leaks. These leaks, which result from tearing of arachnoid and dura and which may appear days to years after the trauma, are important to identify because they increase the risk for meningitis.

Naso-Orbito-Ethmoid Fractures The naso-orbito-ethmoid (NOE) complex is an area of intricate anatomy at the confluence of the nasal, lacrimal, ethmoid, maxillary, and frontal bones. A force directed at the central midface may cause an inward telescoping and consequent foreshortening of the nasoethmoid complex.9 The hallmark of the naso-orbito-ethmoid fracture is the creation of the so-called central fragment, an unstable portion of the medial orbital rim to which the medial canthal tendon attaches.10 This tendon, along with the lateral canthal tendon and tarsal plates (to which the medial tendon runs in continuity), provides a suspensory sling for the eye globe. NOE complex fractures may also involve the nasolacrimal duct, and one should pay particular attention to the bony contours of the duct to ensure its integrity. Compromise of the duct can lead to epiphora, the sense of excessive tearing, and early repair is crucial to

B

Fracture of the lateral orbital roof with subperiosteal hematoma. A, Bone windows show a displaced fracture fragment from the left superolateral orbital rim (arrow). B, Soft tissue windows show a soft tissue density indistinguishable from the superior muscle complex, representing subperiosteal hematoma (SPH). Note the thin cleft of fat (arrowheads) between the hematoma and otherwise normal-appearing optic nerve (asterisk). The superior rectus and superior oblique muscles are not independently identified. Such a hematoma can result in downward displacement of the conal structures and associated diplopia. If not evacuated, this hematoma may eventually ossify.

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Zygomaticomaxillary Complex Fractures

■ FIGURE 2-6 Fractures involving the right nasal bone with involvement of the right nasolacrimal canal. The diameter of the canal, and therefore the lumen of the nasolacrimal duct, is markedly compromised by the overriding fracture fragments (arrow); the contralateral nasolacrimal canal (hatched arrow), which contains a focus of air density that may be seen normally, is intact. Other post-traumatic features include soft tissue swelling that effaces the anterior right nasal cavity.

avoid scarring and the more difficult reconstruction associated with it (Fig. 2-6). Overall, treatment of NOE complex fractures usually involves early open reduction and fixation, with particular attention devoted to management of the central fragment and medial canthal tendon.10

The zygomaticomaxillary complex (ZMC) fracture is one of the most common injuries to the facial skeleton, second only to nasal fractures. The zygoma is prone to fracture because of its prominent exposed location in the midfacial skeleton. It forms the zygomatic arch (malar eminence), which plays a major role in defining the contours of the cheek, and forms a portion of the orbital floor and lateral orbital wall. The zygoma has three principal attachments to the remainder of the midface: it attaches to (1) the frontal bone and greater wing of the sphenoid bone via its orbital process at the lateral orbital wall and rim; (2) the maxilla via its maxillary process; and (3) the temporal squamosa via its temporal process. A blow to the cheek tends to fracture the zygoma in predictable locations at or near all three of its midfacial attachments (Fig. 2-7). The ZMC fracture has thus been termed the tripod or trimalar fracture. Alternatively, because such an injury involves four sutures (including the adjacent zygomaticofrontal and zygomaticosphenoid sutures), it has also been called the tetrapod fracture by some investigators. Isolated fractures of the zygomatic arch are less common than ZMC complex fractures, usually resulting from focal blunt force to the arch alone. Displaced fragments may impinge on the coronoid process of the mandible or the temporalis muscle and result clinically in trismus.11 In some instances, zygomaticotemporal sutural diastasis may be seen in lieu of frank arch fracture.

Le Fort Fractures In 1901, the French army surgeon Réné Le Fort published his now classic findings of predictable patterns of midfacial fracture after high-impact trauma. The Le Fort I, Le Fort II,

■ FIGURE 2-7 Trimalar fractures. A, Axial CT image demonstrates fractures through the anterior and posterolateral walls of the maxillary sinus (arrows), as well as a fracture of the zygomatic process of the temporal bone (hatched arrow). Related diffuse soft tissue swelling is seen centered over the right malar eminence. Vascular grooves with sclerotic margins should not be confused with fracture lines (arrowhead). B, Different patient. Three-dimensional surface rendering demonstrates fractures through the attachments of the left zygoma: zygomatic arch (comminuted, arrow), zygomaticomaxillary region (single-hatch arrows), and zygomaticofrontal region of the orbital rim (double-hatch arrows). In this instance, a fracture line extends posterosuperiorly into the frontal bone (arrowheads) and there are comminuted nasal fractures as well.

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■ FIGURE 2-8

Classic Le Fort I–III fracture lines. A, Anterolateral diagram. B, Lateral diagram. See text for description.

and Le Fort III fractures all involve the pterygoid plates, and all result in a clinically mobile fragment separated from the remainder of the midface (Fig. 2-8). The Le Fort I fracture is a horizontal fracture of the maxilla, above the apices of the maxillary teeth, that results in a mobile or “floating” maxillary alveolus and hard palate (Fig. 2-9). The Le Fort II fracture is a pyramidal-shaped fracture that involves the nasal bridge, frontal process of the maxilla, inferior orbital rim, and wall of the maxillary sinus, resulting clinically in a

A ■ FIGURE 2-9

mobile pyramid-shaped maxillary fragment (Fig. 2-10). The Le Fort III is a transverse fracture that involves, from medial to lateral, the nasofrontal junction, medial orbital wall, orbital floor, lateral orbital wall, and zygoma, resulting clinically in craniofacial separation (Fig. 2-11). Le Fort fractures may be unilateral or bilateral and may be roughly symmetric or asymmetric. Thus, two different Le Fort patterns may coexist on opposite sides of the face and attributes of two patterns may even coexist on the same side.

B

Le Fort I fractures. A, Note the horizontal fracture through the inferior pyriform aperture (arrows). B, There are fractures of the pterygoid processes bilaterally (arrows). The pterygoid processes rarely fracture in the absence of a Le Fort-type injury and, conversely, pterygoid fractures are essential in the diagnosis of all classic Le Fort fractures.

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37

If the anterolateral margins of the nasal fossa are fractured, a Le Fort I injury is most likely present. If the inferior orbital rim is fractured, a Le Fort II injury is likely present; and if the zygomatic arch is fractured, a Le Fort III injury is likely present. Conversely, the absence of fracture in the three structures strongly argues against the presence of Le Fort injury.

Frontal Sinus Fractures

■ FIGURE 2-10 Le Fort II fractures. There are oblique fracture lines (arrows) extending up the medial maxillary regions through the orbital floors, in this case involving the nasolacrimal ducts on both sides. A component of a Le Fort I fracture is also seen on the left (hatched arrow). Combinations of Le Fort varieties, either simultaneously on one side or differing from one side to the other, are common.

A simplified technique for the radiologic identification of Le Fort fractures has been suggested.12 Because the pterygoid plates are rarely fractured in the absence of a Le Forttype injury, the involvement of the pterygoids should prompt a diligent search for associated fractures. Close attention should be directed at the anterolateral margins of the nasal fossa, inferior orbital rim, and zygomatic arch.

Frontal sinus fractures account for 5% to 15% of craniofacial fractures. The vast majority occurs in male patients, with motor vehicle collisions the most common reported etiology.13 Fractures of the frontal sinus may be displaced (by definition > 2 mm) or nondisplaced and can involve the anterior table only, the posterior table only, or extend through both tables (Fig. 2-12). Because the posterior frontal sinus table is in intimate association with dura, fractures involving the posterior table are associated with a higher incidence of complications, including cerebrospinal fluid (CSF) rhinorrhea, meningitis, encephalitis, and post-traumatic meningoencephalocele (Fig. 2-13). In addition, because of the close anatomic relationship of the anterior skull base with the orbital and sinonasal regions, frontal sinus fractures are often associated with naso-orbito-ethmoid injuries.14 Fractures that involve the nasofrontal ducts are associated with impairment of frontal sinus drainage and may thus be complicated by delayed mucocele or mucopyocele formation. Although frontal sinus fractures may be treated conservatively in some patients, surgical intervention may be needed to reconstruct the anterior sinus table for aesthetic purposes, to explore and possibly repair the dura if larger posterior table fractures are present, or to provide adequate sinus drainage if the nasofrontal duct has been compromised.

■ FIGURE 2-11 Le Fort III fractures. A, Anterior coronal image demonstrates fractures through the orbital aspect of both frontal sinuses. Partial opacification of the sinuses (asterisks) in the acute setting usually represents blood. Also note the paired nasal fractures (hatched arrows), which do not comprise a Le Fort II complex because they neither extend to meet the Le Fort III complex nor do they extend back to the pterygoids directly. B, Coronal image, slightly more posterior to A. Classic fracture lines extend through the lateral orbital walls (arrows).

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■ FIGURE 2-12 Frontal sinus fracture. A, There is disruption of both the anterior and posterior sinus tables (arrows). Fluid is seen within the sinus. B, Slightly superiorly there is a gas bubble deep to the left frontal bone inner table, suggesting communication of the sinus with the intracranial compartment. These patients are at markedly increased risk for infectious meningitis.

If adequate frontal sinus drainage cannot be achieved, sinus cranialization, mucosal stripping, or obliteration may be necessary.13

Temporal Bone Fractures Unlike other facial and skull regions, in which thin-section overlapping datasets can be reformatted into adequate coronal images, optimal assessment of temporal bone fractures may still include thin-section CT images acquired in both the axial and coronal planes. Plain radiographs are relatively insensitive in the detection of temporal bone fractures, demonstrated in only 17% to 30% in one series; thus, if there is concern for a fracture, a CT should be obtained.15 Patients with injury to the petrous portion of the temporal bone may exhibit CSF otorrhea, hemotympanum, postauricular hematoma (Battle sign), or cranial nerve palsies.16 Middle skull base fractures may also injure the

A ■ FIGURE 2-13

internal carotid artery and result in dissection or carotidcavernous fistula. The traditional classification of temporal bone fractures is based on the orientation of the fracture line in relation to the long axis of the petrous pyramid; thus, longitudinal fractures are oriented parallel to the long axis of the petrous pyramid and transverse fractures perpendicular (Fig. 2-14). In reality, many temporal bone fractures defy classification using the traditional system because they follow an oblique, multiplanar, or comminuted course.15,17 With this in mind, longitudinal fractures have been reported as up to four times as common as transverse fractures. Longitudinal fractures are often due to impact in the temporal or parietal areas18 and classically were said to involve the external auditory canal, tympanic membrane, middle ear cavity and ossicles, jugular fossa, facial canal, and carotid canal. Middle ear cavity involvement may result in conductive hearing loss due to disruption of the critical ossicular articulation or frank ossicular subluxation.

B

Post-traumatic encephalocele. A, Coronal T2-weighted MR image demonstrates intermediate intensity material (E) within the frontal sinus, partially surrounded by higher intensity fluid (asterisk) representing accumulated postobstructive secretions. The defect in the posterior wall of the frontal sinus, through which the encephalocele herniates, is also indicated (arrow). B, Sagittal T2-weighted MR image. The herniated encephalocele (E) is so entrapped that the adjacent brain appears gathered and stretched (arrowheads) toward the defect in the posterior wall of the frontal sinus (asterisk).

CHAPTER

■ FIGURE 2-14 Temporal bone fracture, essentially transverse. The fracture line is indicated by the arrows and runs through the basal turn of the cochlea. The tympanic and epitympanic spaces are filled with fluid, with loss of the normally lucent air space around the ossicles. Fluid in mastoid cells (asterisk) suggests that the fracture is recent.

Transverse fractures are more often due to occipital or frontal impact and classically were said to involve the otic capsule, internal auditory canal, and petrous apex.18 Because of this, they have been associated with sensorineural hearing loss and vestibular dysfunction. Recently, several authors have described a poor correlation between fracture type using the traditional classification of temporal bone fractures with associated complications such as hearing loss,facial nerve injury,and cerebrospinal fluid leak. Accordingly, various other classification systems have been devised, including one based on involvement versus sparing of the otic capsule17 and another based on a petrous versus nonpetrous location of fracture,18 which reportedly show a stronger correlation with associated sequelae.

Skull Base Fractures Fractures of the anterior skull base are typically limited to episodes of severe trauma; lesser forces tend to be absorbed by the relatively thin facial bones anteriorly, leaving the skull base either intact or with only mild trauma. Anterior skull base fractures may extend through the frontal sinuses, cribriform plates, and orbits and may clinically present as CSF rhinorrhea, epistaxis, or anosmia. In addition to these osseous considerations, there are numerous soft tissue structures that are at risk for disruption with anterior skull base trauma.14 Specifically, the medial canthal ligaments, lacrimal sac, and, in particular, the nasofrontal duct (which connects frontal and ethmoidal sinuses and obstruction of which may lead to frontal mucocele) may all be injured with blunt or penetrating trauma. CSF leak may develop in any skull base injury that permits communication of the CSF with the nasopharynx, paranasal sinuses, or tympanomastoid complexes. In these cases the risk for meningitis (either acute or delayed) warrants surgical repair in virtually all instances. Fractures not abutting a pharyngeal or sinus lumen would initially be more likely to

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39

develop a pseudomeningocele than a frank leak, although larger pseudomeningoceles can also eventually erode into lumina causing CSF leakage as well. Because fluid representing either CSF or blood often accumulates around a fracture line, opacification of mastoid or ethmoid air cells, or even air-fluid levels in the larger paranasal sinus cavities, should prompt a diligent search for a fracture line on imaging. Because of the force required to fracture the sphenoid bone, injuries to the sphenoid are usually associated with fractures at other sites. These fractures also carry a high association with brain parenchymal injury, although usually not due to a direct effect of the fracture; thus, contusion and shearing due to generalized head trauma are commonly seen with sphenoid injury. Concomitant orbital injury is commonly seen with fracture of the greater sphenoid wing. Carotid artery disruption may be seen when fractures extend from the sphenoid body into the adjacent temporal bone; in these instances the threshold for evaluation of the internal carotid artery angiographically should be low.14 The clivus is the most central of skull base structures, sitting at the junction of the anterior, middle, and posterior fossae. Because of the relatively protected location of the clivus, a fracture is usually associated with severe head trauma and portends a very poor prognosis.9 Fractures extending into the cavernous sinuses may lead to unilateral or bilateral cavernous-carotid fistula. If the fracture extends through the sella, the patient may develop pituitary insufficiency, particularly if the stalk has been avulsed, transected, or sheared by the diaphragma sella. Clival fractures may also lead to functional compromise of the specific mid and lower cranial nerves, even if they do not appear to be frankly transected.

Cranial Vault Fractures Whereas radiographs still had a role in the diagnosis and characterization of minimally displaced cranial vault fractures before the advent of multidetector CT, current scanners can demonstrate virtually any fracture regardless of its orientation relative to the actual plane of scanning. As a result, emergency departments in most major trauma centers choose to entirely forgo craniofacial radiographs on trauma patients, which only delay the inevitable CT, ultimately prolong treatment, and provide little or no additional information over CT.19 Depressed and/or penetrating fractures may require more aggressive treatment than nondepressed fractures. Some neurosurgeons will opt to elevate a fragment depressed as little as one-half a calvarial width, whereas others consider a full-width depression of a fragment to be convincing surgical indication. Associated conditions such as epidural or subdural hemorrhage or cerebral edema may also necessitate rapid intervention. Fractures that tear dura and allow arachnoid or pia to extend into the skull defect may ultimately prevent proper skull healing. Over time, chronic CSF pulsations may encourage these pseudomeningoceles to grow, eroding bone along the fracture line to form a so-called leptomeningeal cyst. Sutural diastasis may be seen in younger patients in whom the sutures have not yet fused. These may exist with or without associated fractures, but their significance should not be overlooked because of the relative risk for hemorrhage

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(especially intracranial) or parenchymal contusion or shearing injury. Occasionally, adjacent sutures may also impact one another, resulting in a band of apparent increased density related to bony infraction. In addition, when a fracture line approaches a dural sinus, the risk for subsequent thrombosis increases; and with any significant change in mental status one should consider contrast CT or preferably an MRI to evaluate the dural sinuses further.

Mandibular Fractures The epidemiology of mandibular fractures varies substantially with the population being studied. Motor vehicle accidents and assault are listed as the most frequent causes.20 The mandible is a U-shaped bone consisting of a horizontally oriented body flanked by two vertically oriented rami. Because of its curved or ring-like shape, the mandible has a tendency to fracture in multiple places, with roughly one half of mandibular fractures being multiple (Fig. 2-15). When solitary, the most common fracture site is the body, and when multiple, a combination of the parasymphysis and mandibular angle is the most common pattern.20 Fractures of the ramus and coronoid process are less common. When the patient has sustained any mandibular trauma of significance, the condylar heads should be scrutinized for both osseous integrity and proper articulation within the glenoid fossae. If a mandibular fracture surfaces at the root of a tooth, the fracture is considered compound (open) and the risk for developing osteomyelitis increases. Because

A ■ FIGURE 2-15

the mandible is such a substantial bone, its fracture may be often diagnosed by radiographs (including Towne view or Panorex) or by CT.

MANIFESTATIONS OF THE DISEASE Radiography The standard radiographic series for the evaluation of facial trauma may consist of the Caldwell (posteroanterior), Waters (occipitomental), and lateral views, and occasionally the Towne and submentovertex views as well as nasal radiographs. These are described here largely because of their historical significance, because most trauma centers will bypass radiographs and instead rely on CT for diagnosis. Radiographs may still be obtained in cases of particularly severe trauma, when a patient’s condition is too unstable to travel for CT, but in these instances, if the airway can be maintained, evaluation of the facial bones is often deferred until more definitive imaging may safely be performed. The Caldwell projection is a posteroanterior view with slight craniocaudal angulation, which clearly demonstrates the superior orbital rims, greater sphenoid wing (seen tangentially as the oblique orbital or innominate line), lesser sphenoid wing, anterolateral walls of the maxillary antra, and the planum sphenoidale. The Waters view provides the most comprehensive evaluation of skeletal structures, including superior and inferior orbital rims, hard palate, lateral walls of the maxillary antra, and portions of the zygomatic arches; this view is also useful for demonstrating the

B

Mandibular fractures. A, Coronal image showing fractures of the arch (arrows) posterior to the mental foramen, which is usually found in the vicinity of the canine-premolar gap. Fractures that involve the inferior alveolar canal, particularly displaced fractures, are associated with high risk of mandibular (V3) nerve dysfunction with lower facial numbness. B, Coronal reformatted images in a different patient demonstrating bilateral upper ramus fractures with angulation (arrows). A fracture through this level rarely involves the mandibular nerve, although angulation of one or both condyles can predispose to arthritic changes in the temporomandibular joints if satisfactory surgical alignment of the fragments is not achieved.

CHAPTER

degree of pneumatization of the maxillary sinuses. The submentovertex radiograph may be acquired to better assess the zygomatic arches, the margins of which can easily be traced from zygomatic bone back to temporal bone in the normal patient. The Towne view provides additional information about the mandibular rami and subcondylar region, as well as visualization of the occipital bones and foramen magnum. The lateral view demonstrates the orbital roofs, planum sphenoidale, and hard palate and allows assessment of the pterygoid processes of the sphenoid bone. Conventional radiographic signs of fracture include cortical disruption manifest as interruption in bony continuity, abnormal bony overlap (seen as double-density of the bone), and abnormal linear densities created by rotation of fracture fragments.21 Less direct signs suggestive of fracture include sinus opacification (either complete or with an airfluid level), soft tissue swelling, and abnormal collections of gas within soft tissues.

Multidetector Computed Tomography Computed tomography has largely supplanted conventional radiographs in the diagnosis of facial fractures. Indeed, in most centers CT is the primary modality in assessment of facial trauma in the emergency department. CT does not suffer from the limitations of overlapping of complex structures when compared with conventional radiographs. CT also provides additional information concerning soft tissue structures, including the optic globes and nasal air passages. Furthermore, a CT examination performed on a modern multidetector scanner will be performed significantly faster than a conventional series of radiographs, allowing for more rapid imaging in potentially unstable trauma patients.11 The ideal CT evaluation of facial trauma includes visualization in the axial and coronal planes. Before the development of multidetector scanners, most centers had performed dedicated axial and coronal scans at 3-mm thickness or less in both soft tissue and bone algorithms. However, this approach does require repositioning of the patient between acquisitions into a hyperextended configuration of the cervical spine that could potentially threaten the spinal alignment in those patients with spinal injury. Many larger institutions now use multidetector scanners to acquire a volumetric dataset in the axial plane with the thinnest detector collimation possible and reconstructed at the thinnest slice thickness available with 30% to 50% reconstruction overlap. From these data high-quality coronal, sagittal, or even oblique planes may be reformatted for accurate diagnosis. This method allows the patient to return to the emergency department as quickly as possible and reduces radiation exposure, and elimination of the dedicated coronal set frees the technologist to perform relatively quick reformats in any plane necessary.22 Three-dimensional images of the facial skeleton may be created from thin axial images by employing volumerendering techniques.These images may be preferred over 2D CT images or plain radiographs by clinicians, who are more accustomed to visualizing 3D spatial orientations of fracture fragments clinically.23,24 However, overreliance on surface renderings may lead the interpreter to overlook

2

● Imaging of Facial and Skull Trauma

41

subtle fractures, or normal variations in bony density may be interpreted as fractures if the surface renderings are processed with voxels in too narrow a density range. Still, many surgeons have come to rely on three-dimensional data to help plan the approach and preoperatively simulate the procedure; this helps to minimize operative time and reduce associated patient morbidity.

Magnetic Resonance Imaging Magnetic resonance imaging currently has no significant role in the assessment of most instances of craniofacial trauma in the acute setting. However, in severe trauma MRI may be considered to assess soft tissue structures when fat planes are so obscured by hemorrhage or edema that structures cannot reliably be defined by CT alone. For example, in cases of orbital floor injury MRI may document the degree of herniation of extraocular muscle and surrounding fat; the actual determination of entrapment must be made on clinical grounds. Acute vascular injury, primarily involving the internal carotid artery, may be assessed with MRI as well, to screen for dissection, carotid-cavernous fistula, or frank thrombosis. When vascular injury is strongly suspected, however, the supreme resolution of catheter angiography renders it the imaging modality of choice. If there has been compromise of the intracranial compartment, MRI would offer unparalleled visualization of associated contusions or shearing injury to the brain and in many instances may demonstrate post-traumatic herniation of the meninges and brain better than CT.

DIFFERENTIAL DIAGNOSIS Once a fracture is identified on a radiograph or with CT, the diagnosis is relatively straightforward, especially when the context of craniofacial trauma is known. However, normal anatomic structures may occasionally be mistaken for fracture.25 Although a comprehensive review of such “pseudofractures” is beyond the scope of this discussion, a general overview deserves some mention. Familiarity with the anatomy of the various suture lines of the facial skeleton and skull base is essential to avoid the misinterpretation of a normal suture line as a fracture. Similarly, familiarity with the locations of common channels for various emissary veins may prevent mistaking a normal vascular groove for a fracture. Still, canals and neural foramina may be imaged nearly tangentially, especially when they run in the axial plane, and mistaken for fractures. In general, a lucency that has somewhat sclerotic margins is unlikely to represent acute fracture; this sclerosis may suggest at least partial healing about a nonacute fracture or more likely normal margins of a neural foramen, vascular groove, or interosseous suture. If sclerosis is not seen or remains questionable, one may fairly reliably compare the area of questionable abnormality with the corresponding normal region on the contralateral side. All patients are somewhat asymmetric, however, so one must be conscientious not to implicate any mere asymmetry without more imaging when abnormality is suggested.

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What the Referring Physician Needs to Know ■

■

■

■

Facial fractures tend to be related to motor vehicle accidents or violence in the second through fourth decades, whereas falls are the most common cause in the elderly. The possibility that facial trauma is related to abuse, at any age, should not be overlooked. Although radiography may still be requested for nasal fracture evaluation, CT has replaced radiography in the evaluation of most other varieties of facial fractures. Soft tissue swelling, or soft tissue emphysema (particularly with blowout injuries), may mask asymmetries in the underlying facial contour. Careful examination of osseous structures on CT is necessary to determine whether open repair will be necessary to avoid delayed cosmetic deficit when edema or gas subsides. Extraocular muscle entrapment is a clinical diagnosis. In many instances, fibrous adhesions between muscle and herniated fat may impair muscle mobility more than would be expected by imaging alone.

■

■

■

Le Fort injuries are commonly asymmetric or compound, with disparate grades of injury from one side to another or multiple patterns of involvement simultaneously on the same side. At some point during the mechanism of trauma, foraminal compromise may have been more severe than it appears at the time of CT, and the affected vessel or nerve may be injured more than expected on imaging alone. CT angiography can be obtained acutely to evaluate vessel integrity, and fat-saturated T2-weighted imaging may identify subtle areas of edema involving nerves that might otherwise go overlooked. Fracture lines that run from the margin of a lumen (e.g., sinus, pharynx, nasal cavity) to dura may be associated with CSF leak if dura and arachnoid are also disrupted. In these cases, meningitis can be seen soon after the trauma or after a latency of months to years, with or without active CSF leak. CSF cisternography, with iodinated contrast infusion, can help to determine the exact point of leakage for surgical planning.

SUGGESTED READINGS Linnau KF, Stanley RB, Hallam DK, et al. Imaging of high-energy midfacial trauma: what the surgeon needs to know. Eur J Radiol 2003; 48:17–32. McRae M, Frodel J. Midface fractures. Facial Plast Surg 2000; 16:2.

Rhea JT, Rao PM, Novelline RA. Helical CT and three-dimensional CT of facial and orbital injury. Radiol Clin North Am 1999; 37:3. Schuknecht B, Graetz K. Radiologic assessment of maxillofacial, mandibular, and skull base trauma. Eur Radiol 2005; 15:560–568.

REFERENCES 1. Gassner R,Tuli T, Hächl R, et al. Cranio-maxillofacial trauma: A 10-year review of 9,543 cases with 21,067 injuries. J Cranio-Maxillofacial Surg 2003; 31:51–61. 2. Iida S, Kogo M, Sugiura T, et al. Retrospective analysis of 1502 patients with facial fractures. Int J Oral Maxillofac Surg 2001; 30:286–290. 3. Linnau KF, Stanley RB, Hallam DK, et al. Imaging of high-energy midfacial trauma: what the surgeon needs to know. Eur J Radiol 2003; 48:17–32. 4. Mondin V, Rinaldo A, Ferlito A. Management of nasal bone fractures. Am J Otolaryngol 2005; 26:181–185. 5. Cruz AA, Eichenberger GC. Epidemiology and management of orbital fractures. Curr Opin Ophthalmol 2004; 15:416–421. 6. Lee HJ, Jilani M, Frohman L, Baker S. CT of orbital trauma. Emerg Radiol 2004; 10:168–172. 7. Burm JS, Chung CH, Oh SJ. Pure orbital blowout fracture: new concepts and importance of medial orbital blowout fracture. Plast Reconstructr Surg 1999; 103:1839–1849. 8. Ball JB. Direct oblique sagittal CT of orbital wall fractures. AJR Am J Roentgenol 1987; 148:601–608. 9. Schuknecht B, Graetz K. Radiologic assessment of maxillofacial, mandibular, and skull base trauma. Eur Radiol 2005; 15:560–568. 10. Markowitz MD, Manson PN, Sargent L, et al. Management of the medial canthal tendon in nasoethmoid orbital fractures: the importance of the central fragment in classification and treatment. Plast Reconstructr Surg 1991; 87:843–853. 11. Rhea JT, Rao PM, Novelline RA. Helical CT and three-dimensional CT of facial and orbital injury. Radiol Clin North Am 1999; 37:489–513. 12. Rhea JT, Novelline RA. How to simplify the CT diagnosis of Le Fort fractures. AJR Am J Roentgenol 2005; 184:1700–1705. 13. Metzinger SE, Guerra AB, Garcia RE. Frontal sinus fractures: management guidelines. Facial Plast Surg 2005; 21:199–206.

14. Kienstra MA, Van Loveren H. Anterior skull base fractures. Facial Plast Surg 2005; 21:180–186. 15. Holland BA, Brant-Zawadzki M. High-resolution CT of temporal bone trauma. AJR Am J Roentgenol 1984; 143:391–395. 16. Samii M,Tatagiba M. Skull base trauma: diagnosis and management. Neurol Res 2002; 24:147–156. 17. Dahiya R, Keller JD, Litofsky NS, et al.Temporal bone fractures: otic capsule sparing versus otic capsule violating clinical and radiographic considerations. J Trauma 1999; 47:1079–1083. 18. Ishman SL, Friedland DR.Temporal bone fractures: traditional classification and clinical relevance. Laryngoscope 2004; 114:1734–1741. 19. Parizel PM, Van Goethem JW, Ozsarlak O, et al. New developments in the neuroradiological diagnosis of craniocerebral trauma. Eur Radiol 2005; 15:569–581. 20. Copcu E, Sisman N, Oztan Y. Trauma and fracture of the mandible. Eur J Trauma 2004; 30(2):110. 21. Dolan KD, Jacoby CG, Smoker WK.The radiology of facial fractures. Radiographics 1984; 4:575–663. 22. Novelline RA, Rhea JT, Rao PM, Stuk JL. Helical CT in emergency radiology. Radiology 1999; 213:321–329. 23. Saigal K, Winokur RS, Finden S, et al. Use of three-dimensional computerized tomography reconstruction in complex facial trauma. Facial Plast Surg 2005; 21:214–220. 24. Reuben AD, Watt-Smith R, Dobson D, Golding SJ. A comparative study of evaluation of radiographs, CT and reformatted CT in facial trauma: what is the role of 3D? Br J Radiol 2005; 78:198–201. 25. Connor SEJ,Tan G, Fernando R, Chaudhury N. Computed tomography pseudofractures of the midface and skull base. Clin Radiol 2005; 60:1268–1279.

C H A P T E R

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C H A P T E R

Temporomandibular Joint Vijay M. Rao and Steven Finden

ETIOLOGY Internal derangement is defined as an abnormal relationship of the temporomandibular joint (TMJ) disc to the mandibular condyle, articular eminence, and glenoid fossa and may affect up to 28% of the population. The exact etiology of internal derangement remains a subject of debate, although a recent trauma history can sometimes be elicited. It is important to recognize that early stages of disc derangement can be identified in up to 30% of the asymptomatic population.1–3 Iatrogenic causes may account for approximately 30% of trauma-induced internal derangement. Procedures that necessitate jaw hyperextension, such as tonsillectomy, endoscopy, and molar tooth extraction, are the most frequently implicated.

PREVALENCE AND EPIDEMIOLOGY Clinical symptoms of internal derangement are three to five times more common in women and typically appear in the second to fourth decades.4,5 Although there is a peak incidence of TMJ disc displacement reported during puberty for both genders, the female-to-male ratio for all age groups is approximately 3:1.6 The clinical signs and symptoms described collectively as TMJ syndrome are frequently confused with another clinically similar condition, myofascial pain dysfunction (MPD). Whereas TMJ syndrome refers to an abnormality or disorder involving the joint itself, MPD syndrome is primarily a stress-related psychophysiologic disorder involving the extracapsular muscles of mastication. MRI plays a major role in establishing a definitive diagnosis of internal derangement, thereby facilitating appropriate treatment.

and include craniofacial pain, joint clicking or popping, and limited range of motion. The syndrome demonstrates a complex pathophysiology, with a variable correlation of the patient’s clinical signs and symptoms with the degree of anatomic derangement within the joint.1–3

PATHOPHYSIOLOGY Anatomy The TMJ is a diarthrodial joint bounded by the glenoid fossa and articular eminence of the temporal bone above and the mandibular condyle below. A joint capsule extends from the posterior portion of the temporal bone, glenoid fossa, and the articular eminence superiorly to the neck of the mandibular condyle inferiorly in the form of an inverted pyramid. The joint is divided into a superior joint space and a smaller inferior joint space by a concave, fibrous structure called the TMJ disc. The TMJ disc has three distinct segments: an anterior band, an intermediate zone, and a posterior band. Both the anterior and posterior bands are triangular and are connected by a thin intermediate zone. The articular surfaces of the condylar head and articular eminence are lined with fibrocartilage. Dynamic stability is provided to the disc by several ligamentous attachments. The main stabilizing force for the TMJ is the posterior ligament or bilaminar zone, consisting of elastic tissue fibers that extend from the posterior band of the disc to the condylar neck and the temporal

KEY POINTS

CLINICAL PRESENTATION TMJ syndrome is a term commonly used to signify an internal derangement within the TMJ. In internal derangement there is an abnormal anatomic relationship of the fibrous disc with the condylar head. It is considered to be a progressive disorder.7 Clinical symptoms of internal derangement typically appear in the second to fourth decades

TMJ syndrome with internal derangement has similar signs and symptoms as other clinical entities such as myofascial pain dysfunction. ■ MRI is the most accurate means to diagnose internal derangement of the TMJ. ■ Conservative bite splint and pharmacologic therapy frequently provide significant relief of symptoms. ■

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bone, allowing for mobility of the disc. The bilaminar zone has a rich neurovascular supply and is the source of joint proprioception. Katzberg and colleagues have further defined the anatomy of the posterior ligament into three zones: the temporal zone, visible on MRI as a thin dark line arching posteriorly; an intermediate zone; and a condylar zone that is generally not visible on MRI.8 Anteriorly, fibers from the superior head of the lateral pterygoid muscle attach to the joint capsule and the anterior band of the disc. Additionally, lateral and medial ligaments have also been described. Normal TMJ function requires synchronized and coordinated motion of the disc, condylar head, and the muscles of mastication. The lateral pterygoid, medial pterygoid, temporalis, and masseter muscles form the muscles of mastication. Of these, the lateral pterygoid muscle is the only major contributor to jaw opening and the remainder help in repositioning the jaw during mouth closing. The lateral pterygoid muscle consists of a superior and an inferior head. Fibers of the superior head insert onto the joint capsule and the condylar neck. Some of the fibers from the tendinous portion extend through the joint capsule and blend with and attach directly to the anterior band of the disc. The inferior head inserts onto the anterior aspect of the condylar neck. Jaw opening occurs in two phases. The first, short phase is rotation of the condylar head within the glenoid fossa. At about 10 degrees of opening, the condylar head/disc complex translates anteroinferiorly along the slope of the glenoid fossa to assume a position directly inferior or slightly anterior to the articular eminence. In the maximal open-mouth position, the disc assumes a bow-tie configuration, with the thin intermediate zone normally situated between the

articulating surfaces of the mandibular condyle and the articular eminence (Fig. 3-1).

Pathology In an ideal physiologic situation there is perfect harmony within the masticatory system. That is, when the jaw closes, the dentition fits perfectly together and the bilateral condylar heads along with their respective discs are normally situated within the glenoid fossa. In contradistinction to this ideal setting, when the patient with an occlusal disorder bites together, it is proposed that premature contacts of the teeth will cause the jaw to unconsciously and automatically seek a more comfortable position to rest in. This causes activation of the muscles of mastication, including the lateral pterygoid. There has been extensive investigation into the anatomic relationship of the lateral pterygoid muscle to the condylar head, disc, and capsule, with multiple electromyographic studies looking at the contraction patterns of the muscles of mastication during both rest and motion.9–13 Wang and coworkers demonstrated maximal activity of the superior head of the lateral pterygoid muscle during clenching, with its major function as a stabilizer of the disc and condylar head, whereas the inferior head of the lateral pterygoid muscle demonstrates maximal activity during opening. The superior head of the lateral pterygoid muscle, which has been shown to frequently insert on the capsule of the TMJ and therefore the anterior edge of the disc, has been postulated to undergo spasm, which results in contraction of the muscle. This prolonged contraction places forward traction on the disc, which can result in anterior displacement.14

■ FIGURE 3-1 MRI of the normal TMJ. Sagittal proton density–weighted images of the TMJ in the closed- and open-mouth positions. A, The closedmouth image demonstrates the posterior band normally positioned at the apex of the condylar head (arrow). B, The open-mouth image shows normal translation of the disc and mandibular condyle with the thin intermediate zone (arrow) positioned between the articular eminence and the condylar head.

CHAPTER

IMAGING TECHNIQUES Techniques and Relevant Aspects Historically, imaging of the TMJ included plain radiographs, conventional tomography, CT, as well as direct arthrography. Currently, MRI is the study of choice in the evaluation of the TMJ.5 The development of MRI techniques allowing for the acquisition of high-resolution multiplanar images provides detailed evaluation of the soft tissues as well as the osseous structures that form this important joint. More importantly, it allows us to evaluate the joint in various degrees of opening, which provides an opportunity to evaluate the joint for one of the more debilitating as well as the most common abnormality affecting the joint—internal derangement. It is reported to be 95% accurate in assessing the position and configuration of the disc and 93% accurate in assessing osseous changes.15 Whereas MRI is now considered the study of choice in evaluation of the TMJ, other imaging modalities may be used on a complementary basis when MRI may be inconclusive.

Plain Radiography Plain film examination of the TMJ consists of transcranial views of the TMJ in both the closed- and open-mouth positions. Plain films routinely demonstrate the glenoid fossa, the articular eminence, the mandibular condyle, and the relationship of these structures to each other. Positive plain film findings include decreased translation, spurring and eburnation indicative of degenerative osteoarthritis, and, less frequently, calcified loose bodies. The obvious disadvantage of plain film radiography is its inability to demonstrate internal joint architecture.

Arthrography Arthrography was the standard in the evaluation of internal derangement of the TMJ before the advent of MRI. Although Norgaard pioneered this procedure in the mid 1940s, it became popular much later in the 1970s. Through the years, several TMJ arthrographic procedures using single-contrast or double-contrast techniques have been developed and described. In general, the procedure is performed under fluoroscopic guidance with the use of local anesthesia. A preauricular approach is used, and the posterior recess of the lower synovial compartment is punctured and opacified with approximately 0.5 mL of water-soluble contrast medium. Some radiologists advocate dual joint space injection (both lower and upper compartments), which improves assessment of the disc position. Static images, tomography, and videofluoroscopy may be utilized to examine the joint. The accuracy of information about disc position and morphology as provided by arthrography is very high and quite comparable to that of MRI. Arthrography is superior to MRI in the detection of discal and posterior ligament perforation.16 Disadvantages of arthrography include exposure to ionizing radiation, its invasive nature, indirect disc assessment, and the expertise required to perform the study.

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Computed Tomography Before the advent of MRI, the literature was replete with the use of CT in the evaluation of TMJ dysfunction. Highresolution multidetector CT is preferable to plain film and pluridirectional tomography because it allows better bone and soft tissue detail. Direct sagittal CT images of the TMJ are obtained by positioning the patient’s head on a 45degree lumbar sponge in a semisupine position. However, with the advent of multidetector CT, submillimeter highresolution axial images may be obtained and reformatted in sagittal and coronal planes. The main advantage of CT is the ability to display exquisite bony detail. Disadvantages include exposure to ionizing radiation and suboptimal resolution of the disc.

Magnetic Resonance Imaging MRI is the modality of choice in imaging of the TMJ. Optimal MRI of the TMJ requires the use of a surface coil, which allows for a small field of view and provides a high signal-tonoise ratio. A dual 3-inch surface coil allows simultaneous imaging of both TMJs, significantly decreasing the examination time. The imaging protocol currently used at our institution includes T1-weighted axial localizer images that allow identification of the condylar heads and mandibular rami. Proton density–weighted images in a sagittal oblique plane, perpendicular to the condylar head, are obtained in both closed- and open-mouth positions.17 T2-weighted fast spin-echo sagittal oblique images are obtained in the closed-mouth position to evaluate for joint effusions, and coronal T1-weighted images are obtained to evaluate the joint for a component of medial or lateral disc displacement. For the open-mouth images, the Burnett opening device is used and is placed between the upper and lower incisors, allowing 1-mm incremental opening. It is controlled by the patient to provide maximal tolerable opening.

MANIFESTATIONS OF THE DISEASE In the early stages of internal derangement, patients usually complain of pain and clicking that is often audible, as the displaced disc shifts in and out of its normal position within the joint. With progression of internal derangement, the displaced disc may become deformed and the stretched posterior ligament may lose its elasticity, resulting in failure of the disc to shift back into the joint. As a result, patients frequently experience pain along with limited range of motion and/or intermittent closed lock. In the more advanced stage of internal derangement, the posterior ligament may undergo fibrosis or perforation, allowing the displaced disc to migrate anterior to the articular eminence, resulting in paradoxical improvement of the patient’s symptoms. However, bone-to-bone contact between the condylar head and glenoid fossa and articular eminence promotes the development of osteoarthritic degenerative changes within the joint. MRI evaluation of the TMJ begins with the determination of disc position in the sagittal plane with the mouth closed. When the posterior band of the disc is positioned anterior to the apex of the condylar head, it is said to be anteriorly displaced (Fig. 3-2A). The next step in the evaluation is to

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■ FIGURE 3-2

Anterior disc displacement with reduction (recapture). Sagittal T2- and proton density–weighted images of the TMJ in the closedand open-mouth positions. A, The closed-mouth image demonstrates anterior displacement of the disc with altered disc morphology. B, The openmouth image demonstrates a normal relationship of the disc to the condylar head indicating reduction (recapture) of the disc on opening.

determine the position of the disc on the coronal images. If the disc material is noted extending beyond the medial or lateral pole of the condylar head, it is said to have a rotational component. Displaced discs with a rotational component are described as anteromedial or anterolateral displacement. Less frequently, coronal images may reveal pure sideways displacement of the disc, a finding that may or may not be suspected based on the sagittal images (Fig. 3-3).18 The next

■ FIGURE 3-3

Sideways displacement of the disc. Coronal proton density–weighted image in the closed-mouth position demonstrates lateral displacement of the disc (arrows).

step in the evaluation is to determine the disc position with the mouth open. If the disc is seen in its expected position relative to the condylar head and articular eminence, it is said to be recaptured, or reduced (see Fig. 3-2B). However, if the disc remains anteriorly positioned, it is said to have failed to recapture or reduce (Fig. 3-4). It is noted that although disc displacement is the most common finding in patients with symptoms suggestive of TMJ internal derangement, it can be seen in up to 20% of the asymptomatic population. Evaluation of the T2-weighted images is then performed to look for joint effusions as well as marrow signal alteration. Increased T2-weighted signal intensity and enhancement in the retrodiscal tissues has been described in patients with internal derangement with painful joints, attributed to increased vascularity within the retrodiscal tissues.19,20 Decreased T1-weighted signal intensity of retrodiscal tissues has been described in pain-free patients with advanced stages of internal derangement. This has been attributed to decreased vascularity and fibrosis of the retrodiscal tissues.21,22 T2-weighted images provide information regarding the presence of joint fluid. Small amounts of fluid may be seen in normal and abnormal joints. Moderate to large joint effusions, however, are seen only in abnormal joints (Fig. 3-5). Association between large joint effusion with internal derangement and degree of pain is described.23 It has been shown that T2-weighted imaging has a role in evaluation of the lateral pterygoid muscle. Finden and colleagues demonstrated a measurable difference in T2-weighted signal intensity involving the superior head of the lateral pterygoid muscle when compared with the inferior head of the lateral pterygoid muscle in patients with internal derangement. This finding is postulated to represent edema as well as possibly fatty atrophic changes within the superior head of the muscle, whose increase in signal intensity correlates in a nearly linear fashion with the severity of internal derangement.24

CHAPTER

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■ FIGURE 3-4

Anterior disc displacement without reduction (recapture). Sagittal proton density–weighted images of the TMJ in the closed- and open-mouth positions. A, The closed-mouth image demonstrates anterior displacement of the disc. B, The open-mouth image demonstrates persistent anterior displacement of the disc.

TMJ function and range of motion can be compromised as well by formation of intracapsular adhesions. This can result in a fixed or “stuck” disc, which may be in either a normal or a displaced position (Fig. 3-6). These adhesions can be subdivided by direct visualization with arthroscopy into fine synovial adhesions or

thicker fibrotic adhesions. While the significance of the fine adhesions is less clear, the thicker fibrotic adhesions directly affect the mobility of the disc and range of motion of the mandible. Although these adhesions are not directly visualized with MRI, the lack of discal mobility is highly suggestive.25 Frequently over time, the TMJ with internal derangement undergoes the progressive changes described earlier. However, there are longitudinal epidemiologic studies that bring into question the inevitability of progression. In one study in which 293 subjects with clicking were observed, the 5-year followup demonstrated no progression of clicking to locking in any of the subjects.26 After 10 years, intermittent locking was reported by just 1 subject.27 This study also reported that of the patients who exhibited clicking at age 15, half that group demonstrated no clicking 5 years later. Also noted in this study is that approximately half of those 15-year-olds with no clicking developed clicking within 5 years. The natural course of anterior disc displacement without reduction has been studied, and the findings suggest that the signs and symptoms of anterior disc displacement without reduction tend to be alleviated during the natural course of the condition, although morphologic changes to the disc/condylar head complex may continue.28,29

COMPLICATIONS OF INTERNAL DERANGEMENT

■ FIGURE 3-5

Joint effusion. Sagittal T2-weighted image of the TMJ in the closed-mouth position. A large effusion is identified in the superior joint space (arrow).

Osteoarthritis in the TMJ is not necessarily a disease of the aging process. It is well recognized that many cases of TMJ osteoarthritis are the result of internal derangement. As many as 20% of patients with internal derangement have osteoarthritis at the time of initial presentation.30,31

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■ FIGURE 3-6

Stuck TMJ disc in normal position. Sagittal T1-weighted MRI of the TMJ in the closed- and open-mouth positions. A, In the closed-mouth position, the TMJ disc is in normal position. B, With jaw opening, the disc remains fixed in position while the condyle shows limited anterior translation. The position of the posterior and anterior bands relative to the glenoid fossa is unchanged, indicating that the disc is “stuck” or fixed in position.

Osteoarthritis becomes more common with increasing duration of internal derangement and is closely associated with disc displacement. Some investigators have reported no major difference in the degree of pain experienced by patients with internal derangement and osteoarthritis from those patients with only internal derangement. In the older population with osteoarthritis of the TMJ, they may be completely asymptomatic.32 It remains controversial whether TMJ disc displacement, osteoarthritis, or both can be directly correlated with the onset, progression, or cessation of TMJ related signs and symptoms. A group of investigators have reported a poor correlation between the presence of TMJ pain and the imaging diagnosis of internal derangement, osteoarthritis, or both.33 MRI is therefore warranted in patients with TMJ pain to establish the presence or absence of internal derangement. Osteoarthritis may result in narrowing of the joint space, articular erosion, eburnation, and osteophytosis (Fig. 3-7). Osteophytes typically develop at the margins of the articular surfaces of the mandibular condyle and the articular eminence. Alternatively, regressive remodeling of the condyle is reported in association with internal derangement.34,35 Abnormal bone marrow signal and avascular necrosis (AVN) may be seen in less than 10% of the patients with TMJ disorders.20,36 The various risk factors associated with AVN of the hip and shoulder joints have not been

implicated in AVN of the TMJ. This is further substantiated by the fact that AVN of the TMJ is usually unilateral. In many cases of AVN of the TMJ, a prior history of trauma, surgery, or inflammatory arthropathy may be elicited. MRI has been established as a highly sensitive and accurate procedure for the diagnosis of early AVN. The appearance of acute AVN on MRI is related to vascular congestion with resultant fluid transudation into the medullary space. This causes decreased T1-weighted signal intensity and increased T2-weighted signal intensity. MRI is more accurate than nuclear scintigraphy in detecting these early changes of AVN.37 With chronic AVN, the normal fat-containing marrow is replaced by hypointense fibrous tissue and sclerotic bone. This change results in the loss of normal marrow signal. CT in AVN is characterized by irregularity and flattening of the mandibular condyle (Fig. 3-8). Increased sclerosis and subchondral cyst formation may be apparent.

SYNOPSIS OF TREATMENT OPTIONS Medical Management The mainstay of therapy for TMJ internal derangement continues to be conservative treatment. This consists largely of occlusal splint therapy, which is frequently

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■ FIGURE 3-7

Advanced osteoarthritic changes of the TMJ. Sagittal and coronal CT reformatted images demonstrate marked deformity of the condylar head and articular eminence with flattening, hypertrophic spurring, and loss of the normal joint space.

■ FIGURE 3-8

Avascular necrosis of the TMJ condyle. A, Sagittal T1-weighted MRI of the TMJ. The condylar head is flattened. There is loss of normal marrow signal in the mandibular condyle. B, Coronal CT image of the TMJ. The corresponding CT image shows marked flattening and irregularity of the condylar head.

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combined with muscle relaxation techniques, including physical and pharmacologic therapy. Occlusal splint therapy has a good success rate and alleviates the premature occlusal contacts postulated to cause spasm of the lateral pterygoid muscle leading to anterior disc displacement. By providing a flat surface for the teeth to glide on, there is no longer a premature occlusal contact to act as an activator of the musculature. Many patients report instant relief of symptoms. Another approach is to actually reshape the occlusal surfaces so that when the disc/condylar head complex is in a normal relationship, the occlusal contacts are repositioned so that all teeth contact simultaneously. This procedure has a similar success rate with resolution or significant reduction in pain as well as clicking.

Surgical Management In cases refractory to conservative therapy, surgical intervention may at times be performed. Therapy for a stuck disc may consist of conservative arthroplasty with joint lavage and lysis of adhesions, frequently leading to improved mobility of the disc. In patients with anterior displacement of the disc, it may be returned to a normal position by performing a discal plication, which consists of partial resection of the posterior ligament with posterior repositioning of the disc. Discal plication may be performed either through an arthroscopic approach or by open surgery. In patients with chronically displaced, shrunken and calcified discs, simple discectomy with or without the placement of a discal implant may become necessary. A variety of alloplastic and autogenous implants have been utilized. Alloplastic materials include nonporous Teflon (Proplast) and silicone (Silastic). Autogenous implants include fascial, dermal, and rib grafts. The synthetic implants are diamagnetic substances and therefore demonstrate absent signal on all MR pulse sequences (Fig. 3-9). In more advanced cases of internal derangement, condylectomy and articular eminence reduction osteotomy may be necessary.38 MRI provides direct and noninvasive evaluation of the postoperative TMJ. In patients who have undergone discal plication, the postoperative disc may show central high signal intensity on both T1- and T2-weighted sequences, likely representing mucoid degeneration. The disc may not show change in position compared with the preoperative MRI study, but patients often report remarkable improvement in their symptoms.39 This may be secondary to joint lavage with lysis of the intracapsular adhesions. MRI allows assessment of postoperative granulation tissue, joint fluid, adhesions, or displaced implants. Foreign body destructive reactive changes have been described with a variety of implant materials and are characterized by erosions that are similar in appearance to those seen in infection and rheumatoid arthropathies. CT may be helpful as an adjunctive study in distinguishing joint calcification from hypointense scar tissue. Other complications such as hypertrophic bone formation and fibrous or bony ankylosis may also be better assessed with CT (Fig. 3-10).

■ FIGURE 3-9

Silastic implant. Sagittal T1-weighted MRI of the TMJ. A Silastic TMJ implant is typically identified as a thin band of low signal intensity along the glenoid fossa (arrows).

■ FIGURE 3-10

Postsurgical changes. New bone formation and ankylosis in a patient with history of severe TMJ trauma submitted to surgery. Coronal CT scan through the TMJ. Extensive bone formation and ankylosis involving the bony constituents of the right TMJ condylar head and glenoid fossa are seen. The patient has undergone a ramus osteotomy in an attempt to regain some range of motion.

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What the Referring Physician Needs to Know ■

■

Disc position: normal or anteriorly displaced? Is there a sideways component to the displacement? Does it recapture (reduce) on open-mouth view? Disc morphology: normal or altered? Is there signal abnormality in the posterior band?

■ ■ ■ ■

Disc mobility: normal or fixed (stuck disc) Condylar translation: none, limited, or normal Osseous changes: normal, osteoarthritis, regressive remodeling, avascular necrosis either acute or chronic Joint effusion: present or not and amount

REFERENCES 1. Katzberg RW, Westesson PL,Tallents RH, Drake CM. Anatomic disorders of the temporomandibular joint disc in asymptomatic subjects. J Oral Maxillofac Surg 1996; 54:147–153; discussion 153–155. 2. Larheim TA, Westesson P, Sano T.Temporomandibular joint disk displacement: comparison in asymptomatic volunteers and patients. Radiology 2001; 218:428–432. 3. Tasaki MM, Westesson PL, Isberg AM, et al. Classification and prevalence of temporomandibular joint disk displacement in patients and symptom-free volunteers. Am J Orthod Dentofacial Orthop 1996; 109:249–262. 4. Katzberg RW.Temporomandibular joint imaging. Radiology 1989; 170:297–307. 5. Helms CA, Kaplan P. Diagnostic imaging of the temporomandibular joint: recommendations for use of the various techniques. Am J Roentgenol 1990; 154:319–322. 6. Isberg A, Hagglund M, Paesani D.The effect of age and gender on the onset of symptomatic temporomandibular joint disk displacement. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998; 85:252–257. 7. Manzione JV, Katzberg RW, Manzione TJ. Internal derangements of the temporomandibular joint. I. Normal anatomy, physiology, and pathophysiology. Int J Periodont Restor Dent 1984; 4:8–15. 8. Katzberg RW,Tallents RH. Normal and abnormal temporomandibular joint disc and posterior attachment as depicted by magnetic resonance imaging in symptomatic and asymptomatic subjects. J Oral Maxillofac Surg 2005; 63:1155–1161. 9. Wang MQ,Yan CY,Yuan YP. Is the superior belly of the lateral pterygoid primarily a stabilizer? An EMG study. J Oral Rehabil 2001; 28:507–510. 10. Carpentier P,Yung JP, Marguelles-Bonnet R, Meunissier M. Insertions of the lateral pterygoid muscle: an anatomic study of the human temporomandibular joint. J Oral Maxillofac Surg 1988; 46:477–482. 11. Christo JE, Bennett S,Wilkinson TM,Townsend GC. Discal attachments of the human temporomandibular joint. Aust Dent J 2005; 50:152–160. 12. Fujita S, Iizuka T, Dauber W. Variation of heads of lateral pterygoid muscle and morphology of articular disc of human temporomandibular joint—anatomical and histological analysis. J Oral Rehabil 2001; 28:560–571. 13. Hiraba K, Hibino K, Hiranuma K, Negoro T. EMG activities of two heads of the human lateral pterygoid muscle in relation to mandibular condyle movement and biting force. J Neurophysiol 2000; 83:2120–2137. 14. Wongwatana S, Kronman JH, Clark RE, et al. Anatomic basis for disk displacement in temporomandibular joint (TMJ) dysfunction. Am J Orthod Dentofacial Orthop 1994; 105:257–264. 15. Tasaki MM, Westesson PL.Temporomandibular joint: diagnostic accuracy with sagittal and coronal MR imaging. Radiology 1993; 186:723–729. 16. Rao VM, Farole A, Karasick D.Temporomandibular joint dysfunction: correlation of MR imaging, arthrography, and arthroscopy. Radiology 1990; 174:663–667. 17. Musgrave MT, Westesson PL,Tallents RH, et al. Improved magnetic resonance imaging of the temporomandibular joint by oblique scanning planes. Oral Surg Oral Med Oral Pathol 1991; 71:525–528. 18. Katzberg RW, Westesson PL,Tallents RH, et al.Temporomandibular joint: MR assessment of rotational and sideways disk displacements. Radiology 1988; 169:741–748. 19. Sano T, Westesson PL. Magnetic resonance imaging of the temporomandibular joint. Increased T2 signal in the retrodiskal tissue of painful joints. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1995; 79:511–516. 20. Sano T, Westesson PL, Larheim TA,Takagi R.The association of temporomandibular joint pain with abnormal bone marrow in

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37. 38. 39.

the mandibular condyle. J Oral Maxillofac Surg 2000; 58:254–257; discussion 258–259. Westesson PL, Paesani D. MR imaging of the TMJ: decreased signal from the retrodiskal tissue. Oral Surg Oral Med Oral Pathol 1993; 76:631–635. Sakuma K, Sano T,Yamamoto M, et al. Does decreased T1 signal intensity in the retrodiscal tissue of the temporomandibular joint reflect increased density of collagen fibres? Dentomaxillofac Radiol 2003; 32:222–228. Finden SG, Enochs W, Rao V. Pathologic changes of the lateral pterygoid muscle in patients with temporomandibular joint disk derangement: objective measures at MR imaging. Proceedings of the ASNR 43rd annual meeting, May 21–27, 2005, Chicago, ASNR, 2005. Rao VM, Liem MD, Farole A, Razek AA. Elusive “stuck” disk in the temporomandibular joint: diagnosis with MR imaging. Radiology 1993; 189:823–827. Westesson PL, Brooks SL.Temporomandibular joint: relationship between MR evidence of effusion and the presence of pain and disk displacement. AJR Am J Roentgenol 1992; 159:559–563. Magnusson T. Five-year longitudinal study of signs and symptoms of mandibular dysfunction in adolescents. Cranio 1986; 4:338–344. Magnusson T, Carlsson GE, Egermark I. Changes in subjective symptoms of craniomandibular disorders in children and adolescents during a 10-year period. J Orofac Pain 1993; 7:76–82. Kurita K, Westesson PL,Yuasa H, et al. Natural course of untreated symptomatic temporomandibular joint disc displacement without reduction. J Dent Res 1998; 77:361–365. Kurita H, Uehara S,Yokochi M, et al. A long-term follow-up study of radiographically evident degenerative changes in the temporomandibular joint with different conditions of disk displacement. Int J Oral Maxillofac Surg 2006; 35:49–54. Westesson PL. Structural hard-tissue changes in temporomandibular joints with internal derangement. Oral Surg Oral Med Oral Pathol 1985; 59:220–224. Katzberg RW, Keith DA, Guralnick WC, et al. Internal derangements and arthritis of the temporomandibular joint. Radiology 1983; 146:107–112. Sano T. Recent developments in understanding temporomandibular joint disorders: I. Bone marrow abnormalities of the mandibular condyle. Dentomaxillofac Radiol 2000; 29:7–10. Bertram S, Rudisch A, Innerhofer K, et al. Diagnosing TMJ internal derangement and osteoarthritis with magnetic resonance imaging. J Am Dent Assoc 2001; 132:753–761. Rao VM, Babaria A, Manoharan A, et al. Altered condylar morphology associated with disc displacement in TMJ dysfunction: observations by MRI. Magn Reson Imaging 1990; 8:231–235. Schellhas KP, Piper MA, Omlie MR. Facial skeleton remodeling due to temporomandibular joint degeneration: an imaging study of 100 patients. AJR Am J Roentgenol 1990; 155:373–383. Lieberman JM, Gardner CL, Motta AO, Schwartz RD. Prevalence of bone marrow signal abnormalities observed in the temporomandibular joint using magnetic resonance imaging. J Oral Maxillofac Surg 1996; 54:434–439; discussion 439–440. Mitchell DG, Rao VM, Dalinka MK, et al. Femoral head avascular necrosis: correlation of MR imaging, radiographic staging, radionuclide imaging, and clinical findings. Radiology 1987; 162:709–715. Youssefzadeh S. Postoperative imaging of the temporomandibular joint.Top Magn Reson Imaging 1999; 10:193–202. Conway WF, Hayes CW, Campbell RL, et al.Temporomandibular joint after meniscoplasty: appearance at MR imaging. Radiology 1991; 180:749–753.

C H A P T E R C H A P T E R

4

Cervical Spine Injuries Donna G. Blankenbaker, Kirkland W. Davis, and Richard H. Daffner

The exclusion of cervical spine injuries in patients with blunt trauma is one of the major challenges facing traumatologists and emergency department physicians. “Clearing” the cervical spine is a complex interdisciplinary process and has two major components. The first is the radiologic evaluation for exclusion of fracture and to determine normal alignment of the cervical spine. Second, even with a normal radiologic study, assessment for ligamentous injuries is paramount. In many cases this can be accomplished clinically by a thorough physical examination. Absence of ligamentous injury may be confirmed in patients with no neurologic symptoms and no focal pain or tenderness over the cervical ligaments. For the trauma team to be able to properly diagnose and treat patients with cervical spine injuries, all parties, including radiologists, emergency physicians, and trauma surgeons, must understand the normal and the injured cervical spine. In this chapter we review the following regarding the cervical spine: normal anatomy and physiology, epidemiology of injuries, injury types and patterns, imaging techniques, and radiologic findings in patients with injuries.

PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS In the United States, an estimated 10,000 persons sustain cervical spinal injuries each year, an incidence of 15 to 30 injuries per million persons. The majority of these injuries are the result of motor vehicle crashes or falls. Among the elderly, especially those older than 65 years, low energy impacts, such as falls from seated or standing heights, are the most common cause of clinically unstable spine injuries. Fracture frequency and distribution vary with patient age. The three common locations for all spine fractures are C1-C2, C5-C7, and T12-L2. However, cervical spine injuries are less common in children than in adults. The anatomy of the developing cervical spine predisposes children to injury of the upper cervical spine. The younger the child, the more likely an upper cervical injury will occur. Typically, in this younger patient 52

population, injuries are located from the occiput (C0) to C2-C3. These injuries are associated with a high risk of neurologic injury. In children older than 14, injuries are similar to those of adults. Cervical spinal injuries are often multifocal. Published studies suggest that patients with at least one cervical spine fracture or subluxation have multiple injuries 9% to 20% of the time. However, these studies were based solely on radiographs. The use of CT for evaluating the entire spine in trauma patients has shown the incidence of noncontiguous multiple fractures to be around 25%. Noncontiguous spine fractures are more common in the lower cervical and upper thoracic regions. Therefore, it should be emphasized that not only the entire cervical spine and the cervicothoracic junction must be completely examined in any patient with suspected neck injury but also that the thoracic and lumbar spine regions should be studied when the cervical spine is injured. Injuries of the cervical spine produce neurologic damage in 40% of cases. The incidence of neurologic injury increases to 60% when fractures involve the vertebral

KEY POINTS There are four major mechanisms of injury: flexion, extension, rotation, and shearing. ■ Major cervical spine injuries include injuries that have radiographic and/or CT evidence of instability, that are associated with neurologic findings, or that have the potential to produce those findings. ■ Minor injuries include injuries with no evidence for instability, that are not associated with neurologic findings, or that do not have any potential to produce those findings. ■ There is no role for flexion-extension radiographs in the obtunded patient. ■ MRI is the preferred technique to visualize spinal cord lesions in trauma patients, to diagnose if they are hemorrhagic, to detect and determine the cause of spinal cord compression, and to monitor the evolution of these lesions after the acute injury. ■

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53

bodies and posterior elements, especially if there is malalignment. The majority (85%) of spinal cord injuries occur at the time of trauma. Late complications occur in 5% to 10% in the immediate postinjury period. Late complications are likely secondary to mishandling of the patient.

ANATOMY The spine can be divided into anterior and posterior components. The anterior component consists of the vertebral bodies, intervertebral discs, and anterior and posterior longitudinal ligaments. The anterior longitudinal ligament is a broad taut structure that runs from the anterior arch of the atlas to the sacrum and is important in maintaining vertebral alignment. It is closely attached to the vertebral bodies and the annulus of the intervertebral discs. Similarly, the posterior longitudinal ligament is closely applied to the posterior aspect of the vertebral bodies and intervertebral discs. Although it is thinner overall than the anterior longitudinal ligament, it flares laterally at each disc level. The posterior component of the spine, known as the neural arch, consists of the pedicles, articular masses, apophyseal joints, laminae, spinous processes, and all intervening ligaments. The ligamentum flavum lines the dorsal aspect of the vertebral canal and is closely attached to the laminae. The interspinous ligaments interconnect the spinous processes. The supraspinous ligament connects the dorsal tips of the spinous processes contiguously from occiput to sacrum. Congenital malformations are common and should not be confused with injuries. These vary from minor defects such as failure of fusion of the anterior or posterior arches of the atlas to severe malformations such as vertebral fusion and hemivertebrae. In children, normal physes and ring apophyses may be mistaken for fractures; lax ligaments may produce a picture suggesting subluxation.

BIOMECHANICS Most physicians who assess and treat spine injuries accept Denis’s three-column concept of vertebral stability (Fig. 4-1). The three-column concept is helpful in understanding the biomechanics of injury, and it is useful in the diagnosis and treatment of spine fractures and dislocations. This concept was originally described for the classification of thoracolumbar injuries but was also found to be useful in understanding cervical spine injuries. The anterior column comprises the anterior longitudinal ligament, the anterior annulus fibrosis, and the anterior two thirds of the vertebral body and intervertebral disc. The middle column consists of the posterior third of the vertebral body and intervertebral disc, the posterior annulus fibrosus, and the posterior longitudinal ligament. The posterior column consists of every structure posterior to the posterior longitudinal ligament—the posterior osseous elements (posterior arch) and posterior ligamentous complex (supraspinous ligament, interspinous ligament, facet capsule, and ligamentum flavum). The middle column is the most important and acts like a hinge or pivot between the anterior and posterior columns during flexion and extension. The presence or absence of middle column failure helps determine the type of spinal fracture

■ FIGURE 4-1 Biomechanically the spine is divided into three columns (A = anterior, B = middle, C = posterior). The middle column functions as a fulcrum between two adjacent vertebrae.

and predicts neurologic injury. Generally, spinal injuries in which the middle column remains intact are considered stable and those in which the middle column is disrupted are unstable injuries. The vertebral column is further divided into functional spinal units or motion segments, defined as two contiguous vertebrae and their connecting disc and ligaments. This concept is based on the biomechanical principle that motion of any single vertebra produces some element of motion in the immediate adjacent vertebra that it shares in the motion segment. In addition, each motion segment is endowed with a certain allowable range of motion, measured in degrees in flexion, extension, and rotation about the X, Y, and Z axes of the body. At the atlantoaxial level there is limited flexion and extension. However, up to 45 degrees of total rotation is permitted (22.5 degrees right and left). From C3 downward there is marked limitation of rotation but normal flexion and extension is greater. Spine injuries result when these allowable limits of motion are exceeded.

PATHOLOGY Cervical spine injuries occur primarily from indirect forces generated by the movement of the head and trunk and are only rarely the result of a direct blow. The forces are typically multiple and complex, representing flexion, extension, compression, rotation, shearing, or distraction or a combination of several motion vectors. These mechanisms produce injuries that can be categorized as flexion, extension, rotation, or shearing injuries. These

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Flexion is the most common force vector that causes spinal injury. In flexion the spine bends anteriorly, pivoting about the fulcrum of the middle column. This results in compression of the vertebral body and tension (posterior distraction) within the neural arch posterior to the fulcrum. It is these tensile forces that may produce ligamentous injuries and fractures of the posterior elements. The forces may be directed anteriorly or laterally. Anterior flexion forces typically involve the anterior superior vertebral body, whereas lateral forces involve the superior lateral vertebral body. This mechanism produces four distinct subtypes of injury: simple compression, burst, distraction, and dislocation. Simple compression injuries involve compression of the vertebral body end plates without involvement of the posterior elements (Fig. 4-2).

Burst fractures are the result of severe compression forces applied to the vertebrae typically during flexion. As the spine is compressed, the vertebral body explodes, creating a comminuted fracture with involvement of the posterior wall. There is a characteristic retropulsion of bone fragments into the spinal canal that encroaches on the thecal sac and cord. In addition, the posterior elements are typically fractured, usually in sagittal cleavage fractures. In the cervical spine, a special variety of this type of fracture has been called a flexion teardrop fracture because of the characteristic appearance of the fragment at the anterior inferior corner of the vertebral body (Fig. 4-3). Distraction injuries refer to forces that are pulling objects apart. There are two types of distraction injuries: ligamentous/soft tissue injuries and horizontal osseous fractures. With distraction, pure ligamentous and soft tissue injury is referred to as a hyperflexion-sprain. When fractures occur with this injury, they are typically small avulsion fractures. The posterior ligaments are torn along with the posterior longitudinal ligament and posterior portions of the intervertebral disc. This injury produces widening of the interlaminar and interspinous spaces, widening of the facets, and anterolisthesis (Fig. 4-4). The

■ FIGURE 4-2 Simple compression fracture in a 72-year-old woman involved in a motor vehicle accident. Reformatted sagittal CT shows the C7 vertebral body compression fracture (arrow) with loss of vertebral body height anteriorly.

■ FIGURE 4-3 Flexion teardrop fracture fragment of C6 in a 40-yearold man. There is a triangular fracture fragment (arrow) arising from the anterior inferior margin of C6. The vertebral body demonstrates overall height loss and there is a retropulsed fragment.

main injury patterns are discussed separately because each of these mechanisms generates a relatively specific pattern of injuries that is important to recognize. In general, compression forces create fractures and rotational and shearing forces disrupt ligaments.

Flexion

CHAPTER

■ FIGURE 4-4

4

● Cervical Spine Injuries

Hyperflexion sprain in a 32-year-old man after a motor vehicle accident. A, Lateral radiograph shows kyphotic angulation, slight anterolisthesis of C4 on C5, and widening of the interspinous space at C4 (asterisk). B, Anteroposterior radiograph shows widening of the interspinous space (arrow). C and D, T1- and T2-weighted MR images, respectively, show rupture of the posterior longitudinal ligament and a central disc herniation at C4. Hyperflexion sprains are significant injuries that result in spinal instability.

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spinolaminar line is typically disrupted. A horizontal vertebral body fracture may occur with a distraction injury and may extend out through the posterior elements. These injuries have been termed the Chance-type injuries, are the result of forward flexion, and occur in the thoracolumbar region. Chance-type fractures do not occur in the cervical spine. Finally, flexion-dislocation types of injuries are the result of severe distractive forces. In the cervical spine this results in a unilateral or bilateral jumped facets (Fig. 4-5), depending on whether there is associated rotation (unilateral) or not (bilateral). These injuries almost always produce severe neurologic deficits.

Extension Extension is the opposite of flexion, with backward bending of the spine; the fulcrum of motion is at the level of the articular pillars. The anterior column is in tension and the posterior column is in compression. The radiographic hallmark of extension injuries is the widening of the disc space below the level of injury. This force results in tension of the anterior longitudinal ligament, which may tear

at the intervertebral disc space or at the margin of the vertebral body and avulse a small fragment from the anterior superior or anterior inferior margin of the vertebral body (Fig. 4-6). The compression force on the posterior elements may result in fractures of the spinous processes, facets, or laminae. The spinolaminar line, however, usually remains intact. Extension forces are more common in the cervical region owing to the greater mobility of the cervical spine. There are three subtypes of extension injury: simple, distraction, and dislocation. In simple extension injuries an avulsion fracture occurs off of the anterosuperior portion of the vertebral body with or without minimal disc space widening. In the distraction type of extension injury, there is widening of the disc space with or without a fracture of the vertebral body. The more severe injury is the hyperextension sprain. This injury produces widening of the disc space and retrolisthesis. This injury is common in elderly patients and is associated with severe neurologic deficits, usually a central cord syndrome. Extension dislocations can occur but are rare. These injuries result in anterolisthesis and fractured articular pillars without disruption of the spinolaminar line.

■ FIGURE 4-5 A 38-year-old man presented with hyperflexion injury. Midline (A), right (B), and left (C) sagittal reconstructed CT images show anterolisthesis of C6 on C7 (thin arrow, A) with bilateral facet lock (thick arrows, B and C). Note the loss of imbrication of the facets.

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■ FIGURE 4-6 Lateral radiograph (A) and sagittal fat-suppressed T2 MR image (B) in this elderly patient after trauma. A, There is retrolisthesis of C4 on C5 with widening of the anterior disc space (arrow) and narrowing of the posterior disc space. B, Arrow points to high T2 signal within the anterior disc space and injury of the anterior longitudinal ligament in this patient with a hyperextension sprain injury.

Rotation Rotary injuries, with one exception, do not involve the cervical spine. They typically occur at the thoracolumbar junction, where there is severe restriction to rotary motion by the facet joints. In the cervical region, rotary injuries are found as atlantoaxial rotary subluxation and rotary fixation. Rotational forces disrupt the interspinous ligaments and fracture the posterior elements. It is this force that plays a major role in fracture-dislocations of the spine. In rotational injuries, the posterior vertebral line is disrupted. An avulsion fracture can also occur from the anterior superior margin of the adjacent vertebra. Other fractures that occur include transverse processes and ribs. At CT, fragmentation and disruption of facets are common findings. In the thoracolumbar region it is important to recognize and distinguish these injuries from burst fractures, because treatment for each injury is different.

Shearing Shearing injuries are also more common in the thoracolumbar junction region. In the cervical region, they most often occur at the craniocervical junction as occipital condyle fractures. Shear injuries are produced by a horizontal force applied to one portion of the spine relative

to the other. This force may occur in an anterior, posterior, and/or lateral direction. Shear injuries occur when patients are struck by large objects or are ejected from motor vehicles. Shearing injuries frequently result in fracture-dislocations of the spine and usually disrupt multiple ligaments. Typically, both shearing and rotational forces occur together. Such injuries have a high association with severe neurologic damage. Similar to rotational injuries, shearing injuries need to be distinguished from burst fractures, because treatment differs for each injury.

IMAGING TECHNIQUES The imaging options for evaluating patients with suspected vertebral trauma include radiography, CT, and MRI. Radiography is generally the first imaging study performed. However, in many large medical centers within the United States, multidetector (or multislice) CT is the preferred primary imaging modality in blunt spinal trauma and is rapidly replacing conventional radiography. Victims of trauma must be studied to determine whether they have an injured or uninjured spine. A missed cervical spine injury can result in devastating neurologic injury. Therefore, those patients with spine injuries must be correctly identified and accurately characterized to guide treatment planning and management and to determine prognosis.

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● Injury: Axial Skeleton

Indications for Imaging Should we image the cervical spine in all patients after trauma? Criteria for imaging the cervical spine in trauma continue to evolve. In 1990, Vandemark defined 10 criteria that would identify patients at high risk for cervical spine injury (Table 4-1). Only one of the indications needs

TABLE 4-1 High-Risk Criteria for Cervical Spine Injury High-velocity blunt trauma Multiple fractures Cervical pain, spasm, or deformity Altered mental status Drowning or diving accident Fall greater than 10 feet Head or facial injury Thoracic or lumbar fractures Rigid vertebral disease Paresthesias or burning in extremities

Data from Vandemark RM. Radiology of the cervical spine in trauma patients: practice pitfalls and recommendations for improving efficiency and communication. AJR Am J Roentgenol 1990; 155:465–472.

■ FIGURE 4-7

to be present to indicate the patient is at high risk for cervical injury and thus requires cervical spine imaging (Fig. 4-7). Hanson and colleagues published a different set of indications for patients to undergo helical CT using clinical parameters that would indicate a high risk for cervical injury (Table 4-2). The presence of any one of these indications places the patient in a high-risk category for cervical spine injury, mandating CT of the cervical spine. There are two studies that were designed to identify factors that would indicate a low probability for cervical spine injury. The first was the National Emergency X-Radiography Utilization Study (NEXUS). This study determined that one could forego cervical imaging in patients with no midline tenderness, no focal neurologic deficits, normal alertness, no intoxication, and no painful distracting injuries. We refer to their results as the “5 NOs”. The second study led to the formulation of the “Canadian Rules,” applying to patients who are alert, oriented, and stable (Table 4-3). These rules differentiate high-risk from low-risk factors for cervical spine injury. If a high-risk factor is present, imaging is recommended. If low-risk factors are present, assessment is done for

A 47-year-old man presented with ankylosing spondylitis after a motor vehicle accident. A, Initial lateral radiograph of the cervical spine demonstrates prior anterior and posterior spinal fusion hardware and diffuse syndesmophytes related to the patient’s ankylosing spondylitis. No definite fracture was seen on this initial view. B, Sagittal CT of the cervical spine depicts a fracture line through the anterior syndesmophyte at C4-C5 and extension through the C5 vertebral body (arrows). Fractures in these patients can be difficult to visualize on radiographs; therefore, CT should be obtained in all patients with ankylosing spondylitis after trauma.

CHAPTER

TABLE 4-2 Six High-Risk Criteria for Cervical Spine Injury Mechanism Parameters 1. High speed (>35 mph) motor vehicle accident 2. Survivor at a deadly crash scene 3. Fall from height greater than 10 feet Clinical Parameters 4. Closed-head injury or intracranial hemorrhage seen on CT 5. Neurologic symptoms or signs referred to the cervical spine 6. Pelvis or multiple extremity fractures

Data from Hanson JA, Blackmore CC, Mann FA, Wilson AJ. Cervical spine injury: a clinical decision rule to identify high-risk patients for helical CT screening. AJR Am J Roentgenol 2000; 174:713–717.

TABLE 4-3 “Canadian Rules” for Cervical Spine Injury High-Risk Factors Age older than 65 years “Dangerous” mechanism Fall greater than 3 feet/five stairs Axial load to head (diving) High speed (>100 km/hr), rollover, ejection Motorized recreational vehicles Bicycle collision Paresthesias in extremities Low-Risk Factors Simple rear-end motor vehicle crash Not pushed into oncoming traffic Not hit by bus or large truck No rollover Not hit by high-speed vehicle Sitting position in emergency department Ambulatory at any time Delayed onset of neck pain No midline cervical tenderness

motion (flexion, extension, and 45-degree rotation to either side). If motion is normal, then no imaging is recommended; otherwise, imaging is advised. If no high- or low-risk factors are present, then no imaging is recommended. In Canada, imaging would typically consist of radiography; in the United States, CT is the recommended imaging modality.

MANIFESTATIONS OF THE DISEASE Radiography The major question in the trauma setting is, “Is the cervical spine cleared?” Until a few years ago, radiography was the universal initial imaging procedure in the evaluation of the cervical spine in trauma patients. Radiographic examination of a possible spinal injury must be tailored to the patient’s clinical signs and symptoms. The patient who has an obvious neurologic deficit may only require a lateral view to define a fracture or fracture-dislocation before undergoing CT or MRI. Careful examination of an adequate lateral cervical radiograph alone can eliminate the presence of an unstable cervical spine injury in a high percentage of patients.

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Asymptomatic trauma patients do not require radiographic assessment of the cervical spine. These patients must be neurologically intact, not intoxicated, without neck pain or midline tenderness, and with no associated severe injury, such as a pelvic or major long bone fracture, that could distract the patient. Avoidance of radiographic assessment in this patient population will result in a decrease in unnecessary radiation exposure, immobilization time, and cost. A three-view cervical spine series, including anteroposterior, lateral, and open-mouth odontoid views, is recommended for radiographic evaluation of the cervical spine in patients who are symptomatic after traumatic injury. If the cervicothoracic junction cannot be evaluated, a swimmer’s view should be obtained to complete the study. The single most common cause of missed cervical spine injury is the failure to adequately visualize the region of injury. This typically occurs at the extremes of the cervical spine, both at the cervicocranium (occiput to C2) and at the C7-T1 levels. The negative predictive value of a normal three-view cervical spine series has been reported to range from 85% to 100%. Although the negative predictive value is high, the sensitivity is lower, in the range of 62.5% to 84%. Studies also have shown that the three-view cervical spine series will also be normal in 15% to 17% of patients who have cervical spine injuries. Although some have advocated obtaining oblique views of the cervical spine to complement the three-view series, this practice has fallen out of favor at most centers. In many centers, more recent practice has been to obtain a single lateral view to assess for gross fracture and malalignment before CT. Most radiographically occult fractures involve the transverse processes and the posterolateral elements of the vertebrae. In the study by Nunez and colleagues, 32 of 88 trauma patients had cervical spine fractures that were either not seen or were incompletely demonstrated on radiographs. Of these patients, one third with missed fractures had either clinically significant or unstable injuries. Of the undetected fractures, 42% were located at C1-C2, 30% at the midcervical spine (C3-C5), and 28% at C6-C7. These investigators found fractures in this group have at least one additional unsuspected fracture. Because trauma patients require rapid evaluation and treatment and because cervical spine radiography is less accurate than originally thought and is often time consuming, many centers now forego radiographs and begin the radiologic evaluation of the cervical spine with CT while the patient is in the scanner for a cranial scan.

Flexion-Extension Radiographs What is the role for flexion-extension radiographs? Flexionextension radiographs have been used to rule out ligamentous or osseous injury to the cervical spine in patients with negative or nondiagnostic radiographs in the past. These views also may be obtained in the patient with persistent pain or tenderness in the presence of a normal three-view radiographic series or CT scan. However, after acute injury to the neck, the presence of muscle spasm results in an extremely limited examination. Therefore, flexion-extension radiographs are typically of little benefit in the acutely injured patient. Certainly, they should never be performed

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in the unconscious patient. When there is concern for ligamentous instability and a need for prompt diagnosis, such as in a patient with a head injury, MRI is preferred, whereas occult fractures are better assessed with CT. The role of flexion- extension radiographs in the trauma patient is mostly limited to follow-up of patients with persistent pain but normal initial radiographs or CT scan.

Multidetector Computed Tomography Computed tomography detects more cervical spine fractures than radiographs do. Studies have shown that, compared with CT, three-view radiography “misses” cervical spine fractures at rates of 40% to 53%, including up to one third of potentially unstable injuries. CT is far superior to radiography for identifying fractures, especially of the pedicles, pillars, and neural arches. For instance, Hanson and colleagues performed CT scans on 20 patients with cervical spine fractures seen on radiographs. CT demonstrated additional occult fractures in 50% of these patients. Besides the higher sensitivity for fractures, CT better depicts some soft tissue abnormalities such as disc herniations, soft tissue hematoma, and, occasionally, ligamentous injuries. In those trauma patients who do undergo an initial radiographic examination of the cervical spine first, CT is indicated whenever there is suboptimal visualization of the entire cervical spine, unexplained soft tissue swelling, or positive radiographic abnormalities. Where available (generally on all scanners installed since 2001), multidetector CT with 1.25-mm slice thickness is used to examine the entire cervical spine in patients with known or suspected cervical spine injury based on clinical history. With multidetector technology, the entire cervical spine can be imaged in 11 seconds. The short scan time usually eliminates the chance of motion artifacts from swallowing, moving, or breathing. Reformatted, 2D sagittal and coronal images at 2- or 3-mm intervals using a smooth enhancing algorithm help in assessing cortical detail, fractures, and alignment and should complement any trauma CT of the cervical spine. CT should be used as the primary screening tool in high-risk patients. Eliminating the radiographic series saves valuable time, especially if the patient is already undergoing a cranial or body CT. The appropriate use of CT may improve patient outcome by rendering more accurate diagnosis; judicious initial CT also may save money during diagnosis and treatment planning in the long run. Although CT does increase radiation exposure to some patients, other patients may require numerous repeat radiographs to complete the cervical spine series, diminishing the overall increased radiation burden from CT. CT is rapidly becoming the screening tool of choice for the evaluation of patients with suspected cervical injury. Along these lines, CT often detects clinically insignificant fractures that may only require minimal symptomatic and supportive treatment. Therefore, a new classification system has been devised to distinguish between those injuries requiring stabilization or other intervention and those that do not. The two categories are classified as “major” and “minor” injuries. Major injuries are defined as having either radiographic or CT evidence of instability, with or without associated localized or central neurologic

findings; included are those injuries that have the potential to produce neurologic compromise. The majority of major injuries require operative treatment. Minor injuries, on the other hand, have no radiographic or CT evidence of instability and are not associated with neurologic findings or the potential to produce neurologic compromise. Cervical injury should be classified as “major” if one of the following radiographic and/or CT criteria is present: displacement more than 2 mm in any plane, wide vertebral body in any plane, wide interspinous or interlaminar space, wide facet joint, disrupted posterior vertebral body line, wide disc space, burst fracture, jumped or perched facets (unilateral or bilateral), hangman’s fracture, and type III occipital condyle fracture (displacement of bone into the foramen magnum). All other types of fractures may be considered minor. Tables 4-4 and 4-5 show the classification of “major” and “minor” injuries.

TABLE 4-4 “Major” Cervical Injuries Hyperflexion Hyperflexion sprain Hyperflexion dislocation Without facet lock With unilateral or bilateral facet lock Comminuted (teardrop) body fracture Burst fracture Hyperflexion fracture-dislocation Occipitoatlantal dislocation/subluxation Atlantoaxial dislocation Anterior fracture-dislocation of dens Lateral fracture-dislocation of dens Hyperextension Hangman’s fracture Hyperextension sprain Posterior fracture-dislocation of dens Posterior atlantoaxial dislocation Rotary Rotary atlantoaxial dislocation (fixed) Rotary atlantoaxial subluxation Axial Compression Burst fracture Jefferson fracture Vertical and oblique fractures of axis body Occipital condyle type III fracture

TABLE 4-5 “Minor” Cervical Injuries Hyperflexion Spinous process fracture Wedge fracture Transverse process fracture (isolated) Uncinate process fracture (isolated) Articular pillar fracture (isolated) Laminar fracture Lateral wedge vertebral body fracture Hyperextension Horizontal fracture of anterior arch of atlas Anterior inferior margin of C2 (“teardrop”) Spinous process fracture Posterior arch of atlas fracture (isolated) Rotary None Axial Compression Lateral mass of atlas (isolated) Occipital condyle type I and type II fractures

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Magnetic Resonance Imaging Clinical indications for MRI include signs of radiculopathy, progressive neurologic deficit, and spinal cord injury. Patients with negative radiographs but suspected cervical ligamentous injury should also be evaluated with MRI.

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MRI demonstrates acute disc herniation (Fig. 4-8), cord edema, hemorrhage, and ligamentous injuries (Fig. 4-9) well. Myelomalacia, cord contusion, and transections can also be shown. Currently, MRI imaging is the method of choice for identifying and characterizing the causes of

■ FIGURE 4-8 Acute disc protrusion in a 38-year-old patient after a motor vehicle accident. A, Sagittal T2-weighted MR image shows a disc protrusion at C5-C6 (arrow). B, Axial T2* gradient-recalled-echo MR image shows a left-central disc protrusion (arrow).

■ FIGURE 4-9 Anterior longitudinal ligament injury in a 51-year-old woman involved in a rollover motor vehicle crash. A, Axial CT demonstrates left articular pillar fractures of C5 entering the transverse foramen (arrow). T2-weighted (B) and STIR (C) sagittal MR images demonstrate discontinuity of the anterior longitudinal ligament (long arrow) and disc extrusion (thick arrow). Note the mild prevertebral fluid (small arrow).

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cord compression. MRI imaging is also recommended in patients with severe cervical spine spondylitic changes or patients with “rigid spine disease” (ankylosing spondylitis, diffuse idiopathic skeletal hyperostosis) who experience hyperextension injuries and may present with neurologic deficits (central cord syndrome) despite “negative” radiographs (Fig. 4-10). In these patients, MRI is invaluable for demonstrating spinal cord injury and compression. Characterization of spinal cord injury is important because accurate imaging correlates with improved neurologic function at discharge after spinal cord injury. Also, MRI is more reliable than flexion-extension radiographs at demonstrating acute posterior ligamentous injury, providing a definitive confirmation of hyperflexion sprain. The optimal time frame for ordering an MRI after acute traumatic injury to the cervical spine is limited. MRI studies should be obtained within the first 48 hours after injury. MRI is also useful to follow up spinal cord injuries by evaluating for the development of cord atrophy and syringomyelia. A limited MRI examination consisting of fast spinecho T1-weighted and STIR sagittal images of the cervical spine can be obtained if only ligamentous injury is to be ruled out. In patients with neurologic signs and symptoms, MRI examination should include sagittal fast spin-echo T1, T2, STIR and axial T2*2D gradient-echo and T1-weighted images through the entire cervical spine.

Obtunded Patients In the obtunded, unconscious, or unreliable patient who has sustained trauma, performing the appropriate examination for assessment of cervical spine injury is difficult and controversial. Several methods have been suggested for “clearing” the cervical spine in these patients, including flexion-extension dynamic fluoroscopy, lateral traction radiographs, CT, and MRI. Prior management guidelines have stated that the cervical spine can be considered stable in patients who remain unconscious after 24 hours, after normal plain radiographs and CT images of the cervical spine are obtained. Revision of these guidelines a decade later included dynamic fluoroscopic evaluation and did not recommend removal of the cervical collar after routine cervical spine imaging. However, recent guidelines have shown dynamic fluoroscopy not to be necessary to clear the cervical spine in the unconscious patient. At many level I trauma centers, MRI is utilized for evaluation of the obtunded patient. Depending on one’s institution, a negative lateral radiograph of the cervical spine with a negative CT with reconstructed images may be considered sufficient to clear the cervical spine. If there are any equivocal findings at CT, an MRI is performed. However, in other centers an MRI examination is performed within the first 48 hours of injury, in addition to normal radiographs and CT, to clear the cervical spine in the unresponsive patient.

Recommendations The optimal imaging evaluation for cervical spine injury can be determined by using the following imaging indications. In the absence of cervical pain, the alert and oriented patient who has never lost consciousness and is not under the influence of alcohol and/or drugs does not need

cervical spine imaging. These patients also should have no distracting injuries or neurologic findings. The cooperative patient with cervical tenderness alone should undergo a three-view radiographic series unless there are high-risk factors. The patients who do not fall into one of these categories should undergo a CT examination supplemented by a single lateral radiograph. Flexion and extension views are not helpful in acute injury except for evaluating minor degrees of anterolisthesis or retrolisthesis in the patient with degenerative disc disease. MRI should be used to evaluate the patient with neurologic findings and may help “clear” the spine in the obtunded patient.

Imaging Findings Radiologic Evaluation Using a simplified approach referred to as the “ABCS” method for analyzing the cervical spine may be helpful: A1: Anatomy—extent to include from the occiput to T1, penetration, rotation/projection A2: Alignment—anterior aspect of vertebral bodies, posterior aspect of the vertebral bodies, spinolaminar line B: Bone integrity abnormalities C: Cartilage or joint space abnormalities S: Soft tissue abnormalities A technically adequate lateral cervical spine radiograph should include down to the first thoracic vertebral body (Fig. 4-11). Normal alignment should be evaluated and be confirmed on all radiographs as well as on MR and reconstructed CT images. On the lateral view, three separate lines are useful in determining the presence or absence of normal alignment (Fig. 4-12). These lines are drawn along the anterior and posterior margins of the vertebral bodies and the spinolaminar line. They should be uninterrupted and will be concave dorsally (lordosis) in the normal patient. Any abrupt reversal in angulation or disruption of these lines suggests an underlying injury. In older patients with spur formation and other degenerative changes, it may be difficult to draw the anterior line. In this case, the alignment of the cervical spine is better assessed by using the posterior vertebral body line. In a normal patient, there is less than 2 mm of anterior displacement of successive vertebrae; greater than 2 mm or an 11-degree angle between adjacent end plates indicates instability, whether traumatic or degenerative. Similarly, on the anteroposterior view, lines joining the lateral margins of the lateral cortex or lateral margins of the articular pillars on each side should be smooth and undulating and another line joining the spinous processes in the midline should form a relatively straight line. The normal lordotic curvature of the cervical spine depends on the status of contraction of the paravertebral muscles and the position of the head. With muscle spasm, the curve is straightened. Positioning in a cervical collar may also produce straightening (“military posture”). An exception to these smooth lines may occur in young children, in whom pseudosubluxation occurs due to the differences in growth rates and cartilage ossification between various portions of the vertebral column. This is typically located at C2-C3 and, to a lesser extent, at C3-C4. Pseudosubluxation appears as offset of the posterior vertebral line with a normal spinolaminar line (Fig. 4-13).

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■ FIGURE 4-10 Hyperextension sprain. A, Drawing showing mechanism and injury. In this diagram there is a small avulsion from the anterosuperior margin of the vertebra immediately below the affected level. Note the retrolisthesis and wide disc space as the consequence of the injury. The spinal cord is frequently injured in this setting. B, Lateral radiograph of a 72-year-old man who fell and struck his chin shows widening of the C4 disc space (asterisk). There are no fractures. Note the degenerative changes present. C, T2-weighted sagittal MR image shows cord compression and edema (asterisk).

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■ FIGURE 4-11

Missed C7-T1 fracture-dislocation. The lateral view must include the top of T1 to clear the cervical spine. A, Lateral cervical spine radiograph in this 25-year-old male after a motor vehicle crash shows no fracture or malalignment. The C7-T1 junction is not visualized. B, Sagittal CT shows fracture-dislocation of C7-T1 (arrow). C, Axial CT image shows the dislocation of both facets (arrows) with central canal and right neural foramen compromise.

■ FIGURE 4-12 Convex lines of the cervical spine. The anterior vertebral line (A) is formed by joining the anterior margin of all the cervical vertebral bodies. The posterior vertebral line (P) joins the posterior cortical margin of the vertebral bodies. The spinolaminar line (S) connects the junction of the laminae and spinous processes.

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■ FIGURE 4-13 Pseudosubluxation of C2 on C3 in this 5 year-old patient. Lateral radiograph demonstrates the classic offset of the vertebral bodies at the C2-C3 level. This is normal but can be misconstrued as a dislocation. The spinolaminar line is normal.

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The facet joints are obliquely oriented. In a perfect lateral projection, they nearly completely superimpose. However, minor degrees of rotation produce double-facet images. This change is typically gradual. An abrupt duplication of the image, causing a “bow tie” appearance, indicates a unilateral facet jump (Fig. 4-14). Other alignment abnormalities commonly seen are focal kyphotic angulation, loss of lordosis, and torticollis. These abnormalities are usually combined with other findings and are never the sole manifestation of an injury. The lateral cervical radiograph should also be scrutinized in regard to alignment at the craniocervical junction. The anterior atlantodental interval (AADI), the space between the posterior margin of the anterior arch of C1 and the anterior margin of the odontoid process, is less than or equal to 3 mm in adults. It may be up to 5 mm in a child owing to incomplete ossification. Measurements above these are indicative of an atlantoaxial subluxation. When the transverse ligament is intact, the AADI should not change with flexion or extension. However, atlantoaxial subluxation is rarely the result of trauma but instead is usually due to one of a number of chronic conditions, such as rheumatoid arthritis. On the anteroposterior view, the joint spaces between the lateral masses of C1 and C2 are symmetric, as is the distance from C1 to the odontoid. The lateral margins of the lateral masses of C1 exactly overlie the lateral margins of C2. The most common cause of offset of the lateral masses of C1 and C2 is positional, as part of the normal rotation or tilting of the head; when this occurs, both lateral masses of C1 should move in the same direction.

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The normal relationship of the dens and clivus can be assessed on the lateral radiograph. The dens-basion line describes the shortest distance from the basion, which is the inferior tip of the clivus, to a vertical line drawn up the back of the dens and extended cephalad. This distance should be 6 to 12 mm (Fig. 4-15). The vertical distance between the basion and the tip of the dens should not exceed 12 mm. Any deviation from these distances may indicate occipitoatlantal dissociation. The distance between adjacent laminae/spinous processes is an important indicator for ligamentous injuries. This distance should not vary by more than 2 mm from one level to the next. Similarly, on a frontal radiograph the distance between the pedicles should not exceed 2 mm. The space between the posterior arch of C1 and the spinous process of C2 should not exceed 18 mm. Alignment abnormalities are summarized in Table 4-6. Abnormalities of bone integrity include both direct and indirect signs. Vertebral body height, articular pillars, laminae, and spinous processes should be assessed. C4 and C5 normally may be shorter in the craniocaudal dimension than the adjacent third and sixth vertebral bodies, as long as there is no wedging. If the anterior height of a vertebral body measures 3 mm or more less than the posterior height, a fracture of the vertebral body should be assumed. On a true lateral view, one should identify Harris ring of C2; this is a ring-like structure consisting of the cortex of the junction of the pedicle and body anteriorly, the cortex at the junction of the dens and body superiorly, and the posterior cortex of the axis body posteriorly (Fig. 4-16). The posteroinferior ring

■ FIGURE 4-14

Unilateral jumped facet at C5-C6 in an 18-year-old young man involved in a motor vehicle rollover. A, Anteroposterior radiograph shows offset of the spinous processes at C5-C6 (arrows). B, Lateral radiograph shows anterior displacement of C5 on C6 approximating 25% (thin arrow). The rotated facets above C5 are seen in an oblique profile (thick arrow), giving them the characteristic “bow tie” appearance.

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■ FIGURE 4-15 Normal dens-basion interval drawn directly on this lateral radiograph of the cervicocranium. Posterior axial line is drawn along the posterior cortex of the body of the axis. The distance between upward extension (line) and tip of the basion (arrow) normally should not exceed 12 mm.

TABLE 4-6 Anatomy and Alignment Abnormalities Disruption of anterior or posterior vertebral body lines Disruption of spinolaminar line Jumped and/or locked facets Rotation of spinous processes Wide interpedicle distance Wide predental space Wide facet joints Kyphotic angulation Loss of lordosis Torticollis

has been found to be incomplete half of the time in normal patients. Disruption of Harris ring may frequently be the only visible sign of a fractured C2. The “fat C2 sign” (Fig. 4-17) indicates a fracture of the body of C2 with displaced fracture fragments. In these cases, the anteroposterior diameter of the C2 vertebral body is larger than the anteroposterior diameter of the adjacent normal C3 vertebral body, hence the term fat C2. Frequently, the posterior arch of the atlas is also displaced anteriorly. Other abnormalities to assess for osseous integrity of the cervical spine include an obvious fracture and disrupted posterior vertebral body line.

■ FIGURE 4-16 the C2 ring.

Harris ring. Arrows depict the normal appearance of

Abnormalities of osseous integrity are summarized in Table 4-7. Abnormalities of the cartilage or joint spaces occur frequently with cervical injuries. Disc spaces should be evaluated for narrowing or widening. Flexion injuries produce narrowing of the disc space above the level of compression, whereas extension injuries typically widen the disc space below, especially anteriorly. A narrow disc space is a less specific sign because this also can be a manifestation of degenerative disc disease. Widening of the facet joint and “naked” facets is a common manifestation of flexion injuries (Fig. 4-18). If posterior distraction occurs, the interlaminar distance may be increased. Cartilage or joint space abnormalities are summarized in Table 4-8. Soft tissue abnormalities are seen in some patients with cervical spine fractures. On radiographs, the prevertebral soft tissues should be assessed in all trauma patients. An increase in the retropharyngeal soft tissues caused by hemorrhage/edema indicates likely adjacent fracture or ligament disruption. The retropharyngeal space is measured from the anterior inferior margin of the body of C2 to the pharyngeal air column. The retrotracheal space is measured from the anterior inferior margin of the body of C6 to the tracheal air column. As a rule of

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■ FIGURE 4-17

“Fat C2 sign” (type III fracture of the odontoid). A, Lateral radiograph shows the body of C2 to be significantly widened. B, CT image shows the fracture through the body of C2 with displacement.

TABLE 4-7 Abnormalities of Osseous Integrity Obvious fracture Disrupted “ring” of C2 “Fat” body of C2 Wide interpedicle distance Disrupted posterior vertebral body line

thumb, an abnormally wide retropharyngeal space measures over 7 mm in adults and children and an abnormally wide retrotracheal space measures over 22 mm in adults and 14 mm in children. However, an abnormal contour of the soft tissues is a more important finding than the width of the soft tissues. Swelling of the nasopharyngeal soft tissues may be a clue to injury of C1 and C2 or facial fractures. Adenoidal tissue is often prominent in children, making this assessment especially difficult in the younger population. Cervical emphysema with distortion of the laryngeal air column suggests laryngeal fracture, whereas retropharyngeal and mediastinal gas should suggest injury to the esophagus. Massive prevertebral soft tissue swelling rarely occurs in cervical injuries and is more often due to an aortic injury or a severe facial injury in a trauma patient. Soft tissue abnormalities are summarized in Table 4-9.

Computed Tomographic Evaluation Normal alignment and fracture assessment on CT follow the same principles and are similar to those criteria used for radiographic assessment. Findings of cervical spine

imaging at CT include cervical spine fracture, marked prevertebral edema, cervical spine malalignment (including the anterior spinal, posterior spinal, or spinolaminar line), widening of the normal interspinous or intervertebral disc spaces, and loss of normal facet coverage. One notable exception is the relationship of the facet joints. On CT the normal facet joint has the appearance of a hamburger bun, with the inferior facet of the upper vertebra facing convexly anteriorly and the superior facet of the lower vertebra facing convexly posteriorly. The common articular surface is flat. The determination of whether a fracture is a “major” or “minor” injury should be determined by using both radiographs and CT.

Magnetic Resonance Imaging Evaluation Magnetic resonance imaging assesses alignment and osseous structures in a similar fashion to radiography. In addition, the paravertebral soft tissues, discs, ligaments, joints, cervical cord, nerve roots, and presence of hematoma can be assessed better with MRI. At MRI of the cervical spine, visualization of ligament discontinuity, whether partial or complete, indicates ligament injury. The presence or absence of prevertebral, interspinous, or posterior neck soft tissue edema, adjacent intervertebral disc edema or injury, and bone injury will allow differentiation between acute and old findings. A systematic inspection of the cervical spine with MRI after trauma should include spinal cord, epidural space, spinal column, ligaments, and vascular assessment. The cervical cord should be assessed for edema, swelling, hemorrhage, and compression. The epidural space evaluation

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■ FIGURE 4-18 Widened facet in flexion injury. Axial (A) and sagittal (B) reconstructed CT images show the widened left facet joint (arrows). Unilateral widening can be difficult to detect on radiographs. This is an unstable injury.

TABLE 4-8 Cartilage (Joint Space) Abnormalities Wide predental space Wide or narrow disc space Wide facet joints “Naked” facets Locked facets Wide interlaminar (interspinous) space Disrupted dens-basion line

TABLE 4-9 Soft Tissue Abnormalities Wide retropharyngeal space Wide retrotracheal space Displaced prevertebral fat stripe Craniocervical soft tissue “mass” Tracheal or laryngeal deviation

should be scrutinized for a disc herniation, bone fragment extending into the central spinal canal, and hematoma. The spinal column assessment should include evaluation for vertebral body fracture, posterior element fracture, marrow edema, and spondylosis. The ligaments that need to be assessed are the anterior and posterior longitudinal ligaments, the ligamenta flava, and the interspinous

and supraspinous ligaments. Finally, the vertebral artery flow voids should be confirmed to exclude post-traumatic dissection.

Radiographic Stability versus Instability A critical role of imaging in acute spinal injuries is to detect instability. Clinical instability is definitely present when an acute neurologic deficit is correlated to a structural vertebral column abnormality, regardless of the appearance on imaging. Clinical instability also may be inferred when structural abnormalities are sufficient to disrupt the protective biomechanical integrity of the vertebral bodies or their soft tissue bindings and therefore pose risk of new or further neurologic injury. There is no universally accepted definition of instability. As already discussed, some employ a classification of “major” and “minor” injuries to determine whether a spine injury is stable. The following types of fractures are considered unstable: bilateral interfacetal dislocation, flexion teardrop fracture, extension teardrop fracture (unstable in extension), hangman’s fracture, Jefferson fracture, and hyperextension fracture-dislocation (see Table 4-4). Other findings that strongly suggest instability include loss of anterior or posterior structural integrity, subluxation greater than 3.5 mm, kyphosis greater than 11 degrees, and traumatic disc space widening or narrowing.

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Normal Variants There are a large number of normal variants in the cervical spine. In the context of trauma, these may cause a degree of anxiety for the radiologist or emergency physician. Familiarity with these anomalies can make interpretation easier. Most cervical spine variants occur at the craniocervical junction. Various stages of fusion of the atlas to the basiocciput and atlantoaxial fusion can be seen. These range from partial fusion, either anterior or posterior, to complete occipitoatlantal fusion. On the other hand, any portion of the C1 or C2 ring may be hypoplastic or aplastic and may simulate a fracture on radiographs. Smooth, sclerotic margins at a ring anomaly should suggest the diagnosis of a normal variant (Fig. 4-19), whereas fractures have irregular, uncorticated margins. Posterior arch anomalies typically are associated with hyperplasia of the anterior arch of the atlas. Occasionally, CT may be necessary for evaluation. The dens may be completely absent, hypoplastic, or incompletely fused to the body of C2 (os odontoideum). The os odontoideum (Fig. 4-20) is smaller than the normal dens and is fixed to the anterior ring of C1. There is usually compensatory hyperplasia of the anterior arch of C1, because the two move as one unit. Subluxation and instability are common. Another variant is anterior or posterior tilting of the dens, occurring in approximately 15% of people.

■ FIGURE 4-20 Os odontoideum. Sagittal (A) and coronal (B) reconstructed CT images show the rounded, corticated ossicle superior to the dens, a congenital os odontoideum. Note the hyperplasia of the anterior arch of the atlas. Typically this variant is more widely separated from the base of the odontoid than a fracture. C, Treatment consists of C1-C2 stabilization.

A

B

■ FIGURE 4-19 Abnormalities of the neural arch of C1. Bilateral congenital absence of a segment of neural arch is present in this 22-yearold woman. Note the smooth tapered cortical surface on the anterior aspect of the posterior segment. The posterior segment is in normal position.

C

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In the lower cervical spine, fusion of the vertebral bodies or fusion of the posterior elements is an easily recognized anomaly. In a patient with incomplete ossification of the posterior elements, the smooth sclerotic margins help to differentiate this normal variant from fracture.

SPECIFIC CERVICAL SPINE INJURIES C0-C1 Atlanto-occipital Dissociation Atlanto-occipital dislocations are usually fatal, although there has been an increase in survival secondary to improved immediate supportive care. The diagnosis is established on the lateral radiograph with gross dislocation of the skull with respect to C1 (Fig. 4-21). The dens-basion line will be abnormal in these patients. Atlanto-occipital subluxation is rare and not usually fatal, may not be associated with neurologic deficits, and is recognized on the lateral radiograph or CT of the cervicocranium by abnormal relationship between the basion and C2 (Fig. 4-22).

Occipital Condyle Fractures With increased utilization of CT, it is apparent that fractures of the occipital condyles are more common than once thought. These injuries are best defined on sagittal or coronal reformatted images (Fig. 4-23). The fractures are typically avulsion injuries of the alar ligaments.

■ FIGURE 4-21

C1

tures house the vertebral arteries within the transverse foramina. The most common fracture of C1 is a bilateral fracture through the neural arch. This type of fracture is caused by hyperextension of the head on the neck, which compresses the neural arch of C1 between the occiput and the neural

The C1 ring, or atlas, is a ring structure consisting of two lateral articular masses jointed by thin anterior and posterior arches. The lateral articular masses consist of the facets and thin transverse processes. These latter struc-

■ FIGURE 4-22 A 40-year-old woman presented with atlantooccipital dissociation. A, Lateral radiograph shows abnormal alignment of the craniocervical relationships. This was initially missed. B, CT better demonstrates subluxation of the occipital condyles from C1.

Atlanto-occipital dislocation. Lateral radiograph depicts the obvious dislocation of the cervical spine relative to the skull base.

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■ FIGURE 4-23 Occipital condyle fracture in an 18 year-old young man. Initial radiographs were interpreted as normal. Coronal (A) and axial (B) CT images show the left occipital condyle fracture with 4-mm anteromedial displacement without compromise of the foramen magnum.

arch of C2. Unilateral fractures of the neural arch are also occasionally encountered. Also reported is an isolated fracture of the medial portion of the lateral mass of the atlas and horizontal fractures of the anterior arch. These fractures are more commonly found in elderly patients. The Jefferson fracture is a comminuted fracture of the C1 ring involving both the anterior and posterior arches (Fig. 4-24). The Jefferson fracture results from a blow to the vertex with an axial load. The force is transmitted from the cranium to the cervical spine through the occipital condyles. The lateral masses of C1 are compressed between the occipital condyles and the superior articular facets of C2. Based on the shape of the lateral masses, this creates a centrifugal force on them, resulting in a burst fracture of C1. The open-mouth odontoid view or coronal reconstructed CT images should be scrutinized for bilateral offset of the lateral articular masses of C1 and C2. The fracture can sometimes be difficult to see, although the presence of a fracture can be implied from lateral displacement of the lateral masses of C1 relative to the superior facet of C2.

C1-C2 Atlantoaxial dissociation is usually associated with rheumatoid arthritis or Down syndrome (Fig. 4-25). It can also be found in patients with severe infections of the head and neck resulting in ligamentous laxity. Atlantoaxial dissociation is less commonly traumatic, occurring from rupture of the transverse atlantal ligament or detachment of the

ligament from the lateral mass of C1, producing an avulsion fracture. Traumatic atlantoaxial dissociation is usually the result of a longitudinal distraction. The diagnosis is made on the lateral radiograph obtained in flexion. It is also shown on both axial and sagittal reconstructed CT images. Rotary atlantoaxial abnormalities occur in two forms: torticollis or acute trauma. Torticollis is an atlantoaxial rotary displacement (subluxation) encountered in childhood or early adolescence, which may occur spontaneously or in association with acute infections of the upper respiratory tract. Rotary dislocation, or fixation, produces a fixed “lock” of C1 on C2. Both types are characterized by a tilting of the head in one direction and simultaneous rotation of the head in the opposite direction. The radiographic findings include asymmetry of the space between the dens and the articular masses of the axis, increase in the transverse diameter of the anteriorly rotated articular mass of the atlas, decrease in the width of the posteriorly rotated articular mass, and displacement of the spinous process of the axis from the midline in the direction opposite that toward which the head is rotated. On the lateral view, the normal relationships of C1 and C2 are distorted. CT better depicts the obvious rotary displacement of C1 on C2 (Fig. 4-26).

C2 Hangman’s fractures are bilateral fractures of the pars interarticularis of C2, also referred to as traumatic spondylolisthesis (Fig. 4-27). Hangman’s fractures are usually the

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■ FIGURE 4-24 Jefferson fracture in a 26-year-old woman. A, Lateral radiograph shows the fracture line of the posterior neural arch of C1 (arrow). B, Open-mouth odontoid view demonstrates the offset of C1 lateral masses relative to C2 (arrows). C and D, Axial CT images show the fractures through the anterior and posterior ring of C1 (arrows). E, Coronal CT image shows a small avulsion fracture from the alar ligament (arrow). Note is also made of offset of C1 on C2 on this image.

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■ FIGURE 4-25 Atlantoaxial dissociation in a 60-year-old man with rheumatoid arthritis. A, Flexion radiograph shows widening of the distance between the dens and anterior arch of C1 (arrow) measuring 8 mm, which reduces on the extension view (B). The patient went on to have posterior fusion of C1-C2.

■ FIGURE 4-26 C1-C2 rotary fixation (dislocation). A 25-year-old man presented with neck pain after awaking from a drunken stupor. Lateral (A) and open-mouth (B) radiographs show rotation of the head to the left.

(Continued)

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C

● Injury: Axial Skeleton

D

■ FIGURE 4-26—Cont’d

C, CT image of C1 shows the atlas to be rotated nearly 45 degrees to the left. D, CT image of C2 shows the axis to be midline. E, Sagittal reconstructed image shows the dislocated articular facet of the lateral mass of C1 on the left (arrow).

E

■ FIGURE 4-27 Hangman’s fracture in this 38-year-old man injured in a motor vehicle accident. Lateral radiograph shows the bilateral fractures of the neural arch of C2 (arrow) with anterior displacement of C2 on C3. Diffuse prevertebral soft tissue swelling is present (arrowheads), related to disc disruption and anterior longitudinal ligament avulsion. C1 neural arch fractures are also present.

result of acute hyperextension of the head on the neck, but some of these fractures may be due to hyperflexion and axial compression. These fractures are typically not associated with a neurologic deficit because of the favorable cord-canal ratio at the C2 level and also the bilateral pars fracture produces decompression of the canal. Classification of hangman’s fractures proposed by Effendi consists of type I, II, and III. Type I is classified as “isolated hairline fractures” of the axis ring with minimal displacement of the C2 body. Type II is characterized by displacement of the anterior segment and an abnormal C2-C3 disc. In type III fractures, there is anterior displacement of the body of C2 in the flexion position associated with disruption of the facet joints of C2-C3. Type I fractures are most common. Fractures of the dens can be difficult to visualize. Most fractures are transverse or oblique and located at the base of the dens. The dens may be displaced anteriorly in the setting of a flexion injury or posteriorly as a result of an extension injury. The degree of lateral offset is variable. The Anderson and d’Alonzo dens classification of fractures consists of three types: type I is an oblique fracture limited to the tip of the dens; type II is a transverse fracture at the base of the dens (Fig. 4-28); and type III is an oblique fracture extending into the body of C2 (Fig. 4-29). The most common is the type II fracture. Nonunion is a complication of type II fractures at the base of the dens, whereas type III fractures heal without difficulty. It has been suggested that the type I fracture may not really exist and may represent either an unfused terminal ossicle

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A

B

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C

■ FIGURE 4-28

Type 2 odontoid fracture in an 85-year-old man after a fall. A to C, CT reformatted images show the oblique fracture at the base of the odontoid (arrows).

A ■ FIGURE 4-29

B

C

Type III odontoid fracture in a 53-year-old woman from a fall down a flight of stairs. A, Subtle odontoid fracture is not seen well on the lateral radiograph. B, Sagittal CT image shows the mildly displaced type 3 odontoid process fracture (arrow). C, Coronal CT image demonstrates the extension of the fracture of the odontoid into the C2 vertebral body (arrows). There has been prior anterior spinal fusion of C3-C4.

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C ■ FIGURE 4-30 Burst fracture in a 23-year-old man who dived off a boat into a riverbed. A, Sagittal CT shows a C4 vertebral body comminuted fracture (arrow) with retropulsion into the central canal and associated kyphosis. B, Associated unilateral facet lock with facet fractures (arrow). C, Axial image showing the burst C4.

A

B

of the dens or a Mach band caused by overlap of the image of the skull base on the tip of the dens. Isolated C2 body fractures without associated dens fracture are uncommon. The fragments often separate, increasing the anteroposterior diameter of the body of C2. This creates the appearance of C2 being wider than C3, causing the “fat” C2 sign described earlier.

Lower Cervical Spine The cervicocranium, which consists of the occiput, C1, and C2, demonstrates a specific set of injuries, as described previously. Injury patterns differ in the lower cervical spine and are described next.

Burst Fracture The vertical compression injury of the lower cervical spine is referred to as the “burst” fracture (Fig. 4-30). Vertebral body fragments are displaced in all directions with posterior fragments retropulsed a variable distance into the central canal, impinging or penetrating the ventral surface of the cord. Typically, the posterior arch of the vertebra is fractured also. On the anteroposterior radiograph, widening of the vertebral body and facet joints can be seen. A vertical fracture line also may be seen on the frontal projection. On the lateral view, the burst fracture is characterized by comminution of the vertebral body with varying degrees of retropulsion of fracture fragments with loss of the normal posterior vertebral body line. Straightening or only mild reversal of the normal cervical lordosis is typically present. CT should

be performed to assess the degree of central canal narrowing and evaluate for concomitant injuries. MRI may be needed to assess for cord injury.

Flexion Teardrop Fracture The flexion teardrop fracture is a specific form of the burst fracture in which there is a characteristic triangular fragment from the anterior inferior margin of the vertebral body, almost always associated with spinal cord injury. The flexion teardrop fracture is the most devastating injury of the cervical spine (Fig. 4-31). This injury is due to a combination of severe flexion force and axial loading and clinically is characterized by the acute anterior cervical cord syndrome or permanent quadriplegia. In this injury, the anterior longitudinal ligament, the intervertebral disc, and the posterior longitudinal ligament are all disrupted. The distractive force on the posterior column results in disruption of the posterior ligament complex and either subluxation or dislocation of the facet joints. The cervical spine assumes a flexed appearance (kyphotic angulation) above the site of injury.

Extension Teardrop Fracture The extension teardrop fracture (Fig. 4-32) involves the anterior inferior corner of the axis. Similar to a flexion teardrop fracture, this injury also results in a triangular fracture fragment at the anterior inferior corner of the vertebra. In extension teardrop fractures, however, this fragment is avulsed by a hyperextension force. This fracture type is more common in older patients with osteoporosis

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■ FIGURE 4-31 Flexion teardrop fracture of C3 in a 27-year-old man. Characteristic teardrop fracture (arrow) is manifested by posterior dislocation at C3-C4 with a triangular fragment arising from the anterior inferior C3 vertebral body. Flexion deformity is only mild because cervical stabilization with tongs has already been applied.

■ FIGURE 4-32 Extension teardrop fracture in a 22-year-old woman. There is a large triangular fragment arising from the anterior inferior margin of C2 vertebral body (arrow). There is the suggestion of minimal posterior subluxation of C2 on C3 and widening of the anterior disc space. Arrowheads show the diffuse prevertebral soft tissue swelling.

and degenerative changes of the spine. Characteristically, the vertical height of a teardrop fragment, whether extension or flexion type, equals or exceeds its horizontal width. Typically, the hyperextension teardrop involves only C2 but occasionally may involve more than one segment or only a lower cervical segment.

Facet Dislocation

Vertical Split Fracture Occasionally a vertical split of the vertebral body occurs, typically due to compressive forces in the sagittal plane. Usually more than two contiguous vertebral bodies will be fractured. The fracture is more obvious as a vertical linear lucency on the anteroposterior radiograph; the lateral radiograph may demonstrate this fracture as a very slight anterior wedge compression without definitive vertebral body deformity. Most of these fractures will involve fractures of the posterior arch also. CT easily demonstrates the findings.

Bilateral facet dislocation (Fig. 4-33) results from a flexion injury combined with distraction and rotational forces. The apophyseal joints at the affected level are completely disrupted, causing the superior vertebra to displace anteriorly to such a degree that the facets dislocate (“jump”) anterior to the facets of the vertebral body below. The superior vertebral body is displaced anteriorly by 50% or more over the vertebral body below. Lesser degrees of displacement, in the range of 25% and 4 to 5 mm anterior displacement of one vertebra on the other, are usually due to a unilateral facet lock (Fig. 4-34). CT will demonstrate facet dislocation and facet fractures (Fig. 4-35). Recognition of the inferior facet located anterior to the superior facet confirms facet dislocation. As mentioned previously, the superior facet is rounded anteriorly and straight posteriorly, the opposite of the inferior facet, which is flat anteriorly at the joint surface

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■ FIGURE 4-33 Bilateral facet dislocations in two different patients. A, Lateral radiograph demonstrates bilateral severe facet dislocations at C2-C3. B, Lateral radiograph demonstrates less severe bilateral facet dislocations at C4-5. Note greater than 50% anterior displacement of C4 on C5 and abnormal alignment of the facets (arrow). Both of these patients became quadriplegic.

and rounded posteriorly. As a result, the joint resembles a hamburger bun. The jumping of the facets causes rotation of one vertebra anterior to the other with disruption of the facet joint on the affected side(s). This produces the “reverse hamburger bun sign,” in which the rounded ends of the facets touch (see Fig. 4-34). Perched facets can also be visualized at CT, in which they are appreciated best on the sagittal reconstructions (Fig. 4-36).

Hyperflexion Sprain This injury occurs due to a combination of distraction and flexion that disrupts the ligamentous structures between two adjacent vertebrae. All of the posterior ligaments are disrupted with the anterior longitudinal ligament remaining intact. Anterior subluxation occurs with a hyperkyphotic angulation of the cervical spine at the level of the ligamentous disruption (Fig. 4-37). This injury may not be noted on initial supine radiographs and is more obvious when the patient is placed in some degree of flexion, such as with an upright film. These injuries are highly unstable despite typically subtle radiographic findings; eventually they may lead to complete dislocation. When this injury is found, surgical stabilization is required, typically consisting of posterior fusion.

Hyperextension Sprain Hyperextension dislocation, also known as hyperextension sprain, typically occurs in older individuals, but it also can occur in the younger population after a high-speed motor vehicle accident. These injuries are associated with facial injuries and have signs and symptoms of acute central spinal cord syndrome. The anterior longitudinal ligament is disrupted and avulses the intervertebral disc from the superior vertebral body at the level of injury. A tiny avulsion fracture at the insertion of Sharpey’s fibers of the annulus fibrosus is often present. Posterior displacement of the vertebral body results in stripping of the posterior longitudinal ligament from the adjacent inferior vertebral body. The cervical cord is pinched between the posteriorly displaced vertebra and the infolding of the ligamentum flavum or impaled by osteophytes; this impingement results in central hematomyelia and central cord syndrome. The radiographic signs can be subtle, with normal alignment but extensive prevertebral soft tissue swelling. An avulsion fracture of the anterior aspect of the inferior end plate on one cervical vertebra occurs in two thirds of patients. The horizontal width of the avulsion fragment exceeds its vertical height (Fig. 4-38), distinguishing this fracture from the extension teardrop fracture of the axis, in which the vertical height equals or exceeds the horizontal width (Fig. 4-39).

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■ FIGURE 4-34

Unilateral facet lock in a 27-year-old woman after a motor vehicle accident. A, Lateral radiograph shows anterolisthesis of C4 on C5 (arrow). Note the “bow tie” appearance of the articular pillars from C4 and above. There is minimal widening of the interlaminar space. B, Frontal radiograph shows rotation of the spinous process of C4 to the right, compared with the levels below. Note the wide interspinous distance between C4 and C5, compared with the other levels. The rotation of the spinous processes is to the side of the locked facet. C, CT image shows the point of locking on the right (arrow). There is a fracture of the posterior body of C4. D, CT image slightly higher shows the rotated spinous process of C4 to the right. Note the epidural hematoma (asterisk).

(Continued)

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■ FIGURE4-34—Cont’d

E, Sagittal reconstructed CT image shows the point of locking (arrow). F, Axial STIR MR image shows absence of the normal flow void of the right vertebral artery (arrow), indicating occlusion. G, Sagittal T1-weighted image shows the locked facet on the right (arrow). Note absence of the signal void from the vertebral artery. H, MR image of the opposite side shows the normal vertebral artery flow void.

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■ FIGURE 4-35

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A 40-year-old woman involved in a motor vehicle accident sustained a fracture-dislocation at C5-C6. A to C, Sagittal CT images show greater than 80% anterior displacement of C5 on C6 (long arrow) with small fracture fragments. There is bilateral facet dislocation with the superior facet anterior to the inferior facet (small arrows). D, Axial CT image shows two vertebral bodies with the right superior facet anterior to the inferior facet (arrow). E, Sagittal T2-weighted, fat-suppressed MR image shows near-complete cord transection at C5-C6 (arrow). There has been a previous anterior spinal fusion of C5-C6. Note how well the MR image shows the abnormality despite the proximity of surgical hardware.

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■ FIGURE 4-36 Unilateral perched facet in this 25-year-old patient after trauma. A, Lateral radiograph demonstrates mild anterolisthesis of C6 on C7 (arrow). B, CT sagittal reformatted image shows a small fracture fragment off the anterior C7 vertebral body. There is approximately 25% of anterior displacement of C6 on C7 (arrow). C, A unilateral perched facet (arrow) was present with (D) fractures of the opposite facets (arrow).

CHAPTER

■ FIGURE 4-37 Hyperflexion injuries. A, Hyperflexion sprain. Lateral view in a teenager after trauma shows loss of the normal cervical lordosis with kyphosis centered at C5-C6 (arrow). Widening of the interspinous distance is also present. A small avulsion fracture is noted off the C3 spinous process. B, Hyperflexion fracturedislocation. Lateral radiograph in a different patient shows a C6-C7 fracture dislocation. The C7 vertebral body resides behind the C6 vertebral body. Spinous process fractures of C5 and C6 are superiorly displaced. The disrupted spinolaminar line differentiates this injury from a hyperextension fracture-dislocation. C, Axial CT image of the same patient in B shows complete anterior dislocation with C6 anterior to C7. Note the fractures of the posterior elements (arrow).

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■ FIGURE 4-38 The typical hyperextension fracture fragment has a greater horizontal width compared with the vertical height.

■ FIGURE 4-39

Hyperextension injury in this elderly man after trauma. Lateral view of the cervical spine shows an extension teardrop fracture (arrow) off of the anterior inferior C6 vertebral body. The C6-C7 disc space is widened anteriorly and narrowed posteriorly.

Posterior Element Fractures Spinous Process Fractures Clay shoveler’s fracture represents an isolated fracture of the spinous process of the lower cervical and upper thoracic spine (Fig. 4-40). These fractures occur as a result of forced flexion of the upper cervical segments against an opposing force of the interspinous and supraspinous ligaments, producing an avulsion fracture. These fractures also may occur as a result of extension when the spinous processes are compressed against each other.

Articular Pillar/Facet/Laminar/Transverse Process Fractures

■ FIGURE 4-40 Clay shoveler’s fracture in a 32-year-old woman involved in a motorcycle accident. Sagittal CT image shows the fractures of the C7 spinous process (arrow).

Fractures of the facets and articular pillars are the result of compressive forces of hyperextension or shearing and compression forces associated with hyperflexion. Unilateral fractures may result from lateral bending. Most of the fractures of the articular pillars or facets are not visualized on radiographs but are typically seen at CT (Fig. 4-41). These fractures are common, occurring in 20%

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■ FIGURE 4-41 Articular pillar and facet fractures in different patients not seen on radiographs. A, CT axial image shows a nondisplaced fracture of C7 (arrow). B and C, Axial CT sequential images show fractures of the pedicle (in front) and lamina (back) resulting in a “floating pillar” (white arrows) with extension into the transverse foramen (black arrow). Some advocate MR angiography to assess the vertebral artery. D and E, Sagittal and axial images show a nondisplaced fracture of the C6-C7 facets (arrows).

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of all patients with cervical spine fractures. The fractures are variable in appearance. There may be a vertical or horizontal fracture line, compression with flattening, or wedging of the articular pillar. An acute radiculopathy is an important clue to the presence of an articular pillar fracture. Fractures of the laminae rarely occur in isolation. Instead, they are typically associated with other fractures involving the vertebral body or posterior elements. With the increasing use of CT, transverse process fractures are frequently recognized. These fractures can extend into the transverse foramen, potentially causing nerve root and vertebral artery injuries.

SCIWORA

Whiplash Injuries

Associated Neurologic Injuries

Whiplash injuries are typically a result of automobile accidents. They have been described as hyperextension/ hyperflexion injuries, although recent studies indicate that a whiplash injury is the result of a combined axial loading and rotation around an abnormal center of rotation, resulting in anterior discal distraction injuries and posterior facet compression lesion. The role of imaging in whiplash injuries remains to be determined. CT will likely be performed to exclude fracture with certainty. MRI is able to detect different soft tissue injuries and is especially useful in the evaluation of the intervertebral discs, cervical ligaments, and spinal cord.

Spinal cord injuries are commonly associated with fracture-dislocations of the spine, bilateral facet lock, teardrop and severe crush-type fractures, and unilateral lock of the facets. MRI detects spinal cord compression and/ or the presence of intraspinal hematoma. MRI is helpful in determining long-term prognosis by demonstrating intrinsic spinal cord injury, including edema, swelling, and hemorrhage. Early detection of spinal cord damage is possible with diffusion-weighted imaging. Those patients with hemorrhagic cord contusion have an extremely poor prognosis compared with those with nonhemorrhagic contusions. Late findings after spinal cord injury include

A ■ FIGURE 4-42

Spinal cord injury in children often occurs without evidence of fracture or dislocation. Children younger than 8 years old sustain more serious neurologic damage and suffer a larger number of upper cervical cord lesions than children older than age 8. Spinal cord injury without radiographic abnormality (SCIWORA) is secondary to the inherent elasticity of the vertebral column in infants and young children that makes the pediatric spine vulnerable to deforming forces (Fig. 4-42). The long-term prognosis in cases of SCIWORA is grim.

B

SCIWORA in a 3-year old struck by an automobile. A, Lateral radiograph is normal. B, T2-weighted sagittal MR image shows central cord hemorrhage (asterisk). Note the epidural hematoma anterior to the cord. (Courtesy of Leonard E. Swischuk, MD, Galveston, TX.)

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■ FIGURE 4-43 Bilateral C4-C5 facet lock in this young patient after a motor vehicle accident. A, Anterior displacement of C4 on C5 by greater than 75% with abnormal alignment of the facets. B, Anterior spinal fusion was performed for stabilization of C4-C5 after restoration of normal cervical alignment.

progressive enlargement of an intramedullary or extramedullary cyst (syringomyelia), progressive myelomalacia, tethering and adhesion, and/or cord atrophy.

Various surgical procedures are performed depending on the injury type (Fig. 4-43).

What the Referring Physician Needs to Know

SYNOPSIS OF TREATMENT OPTIONS The treatment of individuals with suspected cervical spine injury consists of immediate immobilization, physical and neurologic examination, and radiographic evaluation. If the injury is unstable, tongs are applied for skeletal traction. The presence of spinal shock may make it difficult to initially determine the extent of neural injury. Once spinal shock has resolved (in 24 to 48 hours), the deficit can be more accurately assessed.

■ ■

■

CT is rapidly replacing conventional radiography for evaluation of suspected cervical injury. CT is far superior to radiography for identifying fractures, especially for fractures of the pedicles, pillars, and neural arches. MRI should be used to evaluate the patients with neurologic abnormalities and to “clear” the cervical spine in the obtunded patient.

SUGGESTED READINGS Al-Khateeb H, Oussedik S. The management and treatment of cervical spine injuries. Hosp Med 2005; 66:389–395. Anderson LD, d’Alonzo RT. Fractures of the odontoid process of the axis. J Bone Joint Surg Am 1974; 56:1663–1674. Blackmore CC. Clinical prediction rules in trauma imaging: who, how, and why? Radiology 2005; 235:371–374. Blackmore CC, Mann FA, Wilson AJ. Helical CT in the primary trauma evaluation of the cervical spine: an evidence-based approach. Skeletal Radiol 2000; 29:632–639.

Blackmore CC, Ramsey SD, Mann FA, Deyo RA. Cervical spine screening with CT in trauma patients: a cost-effectiveness analysis. Radiology 1999; 212:117–125. Brohi K, Healy M, Frotheringham T, et al. Helical computed tomographic scanning for the evaluation of the cervical spine in the unconscious, intubated trauma patient. J Trauma 2005; 58:897–901. Bub LD, Blackmore CG, Mann FA, Lomoschitz FM. Cervical spine fractures in patients 65 years and older: a clinical prediction rule for blunt trauma. Radiology 2005; 234:143–149.

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Daffner RH. Cervical radiography for trauma patients: a time-effective technique? AJR Am J Roentgenol 2000; 175:1309–1311. Daffner RH. Helical CT of the cervical spine for trauma patients: a time study. AJR Am J Roentgenol 2001; 177:677–679. Daffner RH. Controversies in cervical spine imaging in trauma patients. Semin Musculoskeletal Radiol 2005; 9:105–115. Daffner RH, Brown RR, Goldberg AL. A new classification for cervical vertebral injuries: influence of CT. Skeletal Radiol 2000; 29:125–132. Daffner RH, Daffner SD. Vertebral injuries: detection and implications. Eur J Radiol 2002; 42:100–116. Davis JW, Kaups KL, Cunningham MA. Routine evaluation of the cervical spine in head-injured patients with dynamic fluoroscopy: a reappraisal. J Trauma 2001; 50:1044–1047. Davis JW, Phreaner DL, Hoyt DB, Mackersie RC. The etiology of missed cervical spine injuries. J Trauma 1993; 34:342–346. Denis F. The three column spine and its significance in the classification of acute thoracolumbar spinal injuries. Spine 1983; 8:817–831. Effendi B, Roy D, Cornish B, et al. Fractures of the ring of the axis: a classification based on the analysis of 131 cases. J Bone Joint Surg Br 1981; 63:319–327. Eismont FJ, Currier BL, McGuire RA. Cervical spine and spinal cord injuries: recognition and treatment. Instr Course Lect 2004; 53:341–358. El-Khoury GY, Kathol MH, Daniel WW. Imaging of acute injuries of the cervical spine: value of plain radiography, CT, and MR imaging. AJR Am J Roentgenol 1995; 164:43–50. Emery SE, Pathria MN, Wilber RG, et al. Magnetic resonance imaging of posttraumatic spinal ligament injury. J Spinal Disord 1989; 2:229–233. Griffiths HJ, Wagner J, Anglen J, et al. The use of forced flexion/extension views in the obtunded trauma patient. Skeletal Radiol 2002; 31:587–591. Hanson JA, Blackmore CC, Mann FA, Wilson AJ. Cervical spine injury: a clinical decision rule to identify high-risk patients for helical CT screening. AJR Am J Roentgenol 2000; 174:713–717. Harris JH Jr, Carson GC, Wagner LK. Radiologic diagnosis of traumatic occipitovertebral dissociation: I. Normal occipitovertebral relationships on lateral radiographs of supine subjects. AJR Am J Roentgenol 1994;162:881–886. Harris JH Jr, Carson JT, Wagner LK, Kerr N. Radiologic diagnosis of traumatic occipitovertebral dissociation: II. Comparison of three methods of detecting occipitovertebral relationships on lateral radiographs of supine subjects. AJR Am J Roentgenol 1994;162:887–892. Harris JH Jr, Edeiken-Monroe B, Kopaniky DR. A practical classification of acute cervical spine injuries. Orthop Clin North Am 1986; 17:15–30. Harris JH Jr, Mirvis SE. The Radiology of Acute Cervical Spine Trauma, 3rd ed. Baltimore, Williams & Wilkins, 1996. Hoffman JR, Mower WR, Wolfson AB, et al. Validity of a set of clinical criteria to rule out injury to the cervical spine in patients with blunt trauma. National Emergency X-Radiography Utilization Study Group. N Engl J Med 2000; 343:94–99.

Hogan GJ, Mirvis SE, Shanmuganathan K, Scalea TM. Exclusion of unstable cervical spine injury in obtunded patients with blunt trauma: is MR imaging needed when multi-detector row CT findings are normal? Radiology 2005; 237:106–113. Li AE, Fishman EK. Cervical spine trauma: evaluation by multidetector CT and three-dimensional volume rendering. Emerg Radiol 2003;10:34–39. Lustrin ES, Karakas SP, Oritz AO, et al. Pediatric cervical spine: normal anatomy, variants, and trauma. Radiographics 2003; 23:539–560. Mann FA, Cohen WA, Linnau KF, et al. Evidence-based approach to using CT in spinal trauma. Eur J Radiol 2003; 48:39–48. Mirvis SE, Diaconis JN, Chirico PA, et al. Protocol-driven radiologic evaluation of suspected cervical spine injury: efficacy study. Radiology 1989; 170:831–834. Morris CG, Mullan B. Clearing the cervical spine after polytrauma: implementing unified management for unconscious victims in the intensive care unit. Anesthesia 2004; 59:755–761. Nuñez DB, Quencer RM. The role of helical CT in the assessment of cervical spine injuries. AJR Am J Roentgenol 1998; 171:951–957. Nuñez DB, Zuluaga A, Fuentes-Bernardo DA, et al. Cervical spine trauma: how much more do we learn by routinely using helical CT? Radiographics 1996; 16:1307–1318. Patel RV, DeLong W Jr, Vresilovic EJ. Evaluation and treatment of spinal injuries in the patient with polytrauma. Clin Orthop Relat Res 2004; 422:43–54. Pollack CV Jr, Hendey GW, Martin DR, et al. Use of flexion-extension radiographs of the cervical spine in blunt trauma. Ann Emerg Med 2001; 38:8–11. Richards PJ. Cervical spine clearance: a review. Injury 2005; 36:248– 269; discussion 270. Rogers LF. Radiology of Skeletal Trauma, 3rd ed. Philadelphia, Churchill Livingstone, 2002. Sees DW, Rodriguez Cruz LR, Flaherty SF, Ciceri DP. The use of bedside fluoroscopy to evaluate the cervical spine in obtunded trauma patients. J Trauma 1998; 45:768–771. Sliker CW, Mirvis SE, Shanmuganathan K. Assessing cervical spine stability in obtunded blunt trauma patients: review of medical literature. Radiology 2005; 234:733–739. Stiell IG, Wells GA, Vandemheen KL, et al. The Canadian C-spine rule for radiography in alert and stable trauma patients. JAMA 2001; 286:1841–1848. Takhtani D, Melhem ER. MR imaging in cervical spine trauma. Magn Reson Imaging Clin North Am 2000; 8:615–634. Tins BJ, Cassar-Pullicino VN. Imaging of acute cervical spine injuries: review and outlook. Clin Radiol 2004; 59:865–880. Van Goethem JWM, Maes M, Ozsarlak O, et al. Imaging in spinal trauma. Eur Radiol 2005; 15:582–590. Vandemark RM. Radiology of the cervical spine in trauma patients: practice pitfalls and recommendations for improving efficiency and communication. AJR Am J Roentgenol 1990; 155:465–472.

C H A P T E R

5

Injury to the Thoracic Cage and Thoracolumbar Spine Cornelis van Kuijk and Digna R. Kool

PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS Injury to the thoracic cage and the spine is common in severe traumatic injury. These patients are usually transported to level 1 trauma centers because these injuries are seldom isolated and usually part of a multiple-injury syndrome. Isolated rib fractures are very common with less severe injury and often seen in osteoporotic patients with only minor trauma. Sternal fractures, however, only occur after significant force to the anterior chest wall. Similarly, severe impact is needed before fractures of the spine occur, although, again, in osteoporotic patients vertebral body fractures can occur with only minor trauma. These latter fractures are usually confined to the end plates of the vertebral bodies. In this chapter the discussion is restricted to that of acute injuries of the thoracic cage and the thoracolumbar spine.

ANATOMY The thoracic cage consists of the sternum anteriorly; the ribs anteriorly, laterally, and posteriorly; and the thoracic spine as an anchor point posteriorly. The cage protects the lungs, heart, and great vessels that are situated in the thoracic cavity and also protects the liver and the spleen situated in the upper abdominal cavity. Usually there are 12 ribs on both sides; however, anatomic variants occur often with dysplastic ribs at T12 or extra ribs at L1. The ribs have an osseous part and a cartilaginous part. All the thoracic vertebrae articulate with two ribs. Each rib has two articulations with the vertebrae: one with the vertebra itself at the level of the facet joint, the other with the transverse process. The cartilaginous part of the first 10 ribs also articulates with the sternum anteriorly. The surrounding rib cage adds to the stability of the thoracic spine. The sternum consists of three parts: the manubrium, the body (corpus), and the xiphoid process.

The thoracic spinal column usually has 12 vertebrae, consisting of the vertebral body anterior to the spinal canal, the pedicles, and the transverse processes at both lateral sides and the lamina and spinous processes posterior to the spinal canal. The spinal canal holds the myelin. The thoracic spine is curved (kyphosis), which leads to the fact that the upper thoracic vertebral bodies are anterior to the middle thoracic bodies. The lumbar spine usually has five vertebrae, although anatomic variants at the lumbosacral junction are quite common. The curve of the lumbar spine is lordotic. Because of the difference in curves of the thoracic and lumbar spine the thoracolumbar spine has an S-shaped curve. Between the vertebral bodies are the intervertebral disks; they act as cushions between the bony structures and together with the facet joints provide for range of motion of the spine. The bones are attached to each other by strong ligamentous structures. It is these structures that together with the muscles support the body. The bones are anchor points that along with the ligaments, joints, and muscles compose the structure of the human body. As such, injury to a bone is usually accompanied by damage to the other

KEY POINTS In the Denis classification, involvement of two or three columns represents an unstable fracture. ■ MDCT is essential for diagnosis and characterization of spinal injury. ■ Status of the posterior interspinous ligaments is critical for determining surgical management. ■ MRI is the evaluation of choice for detection of spinal ligament disruption as well as traumatic disk herniation, hematoma, and spinal cord injury. ■

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structures. It is usually the damage to the latter that is disabling for a patient. Bones heal remarkably well, whereas destruction of ligamentous structures and joints can cause considerable instability and loss of integrity with poor outcome.

BIOMECHANICS The fracture mechanism and the biomechanics of injury determine the type of damage that occurs to the bones and supporting structures. A direct blow to the sternum anteriorly will displace the sternum posteriorly, potentially fracturing the sternum and causing a contusion of the heart. A direct blow to a rib will displace the rib inwardly, potentially fracturing the rib and causing a pneumothorax and/or lung contusion. The spine can be damaged by a direct or indirect force. A jumper (by parachute or otherwise) can land hard on the feet, transmitting the force through the entire axial skeleton; in this case multiple fractures can be observed, often at noncontiguous levels. Flexion and extension injuries occur as the spine is bent forcefully either forward or backward. All these mechanisms exert different forces to the spine, leading to specific types of injuries.1,2 Some injury patterns indicate mechanisms that should suggest another pathologic process; for example, a flexion-distraction mechanism resulting from seatbelt injury is commonly associated with abdominal visceral injury.3,4 Similarly, seemingly innocuous transverse process fractures can be associated with visceral injury.5 Axial load injury can be associated with spinal fractures at multiple sites (often noncontiguous) as well as lower extremity injuries.6 Dural tears are also commonly associated with spinal fracture.7 Because the human body has the tendency to retain and regain its optimal form and structure, it is not always clear which trauma mechanism was present when the injury occurred. The severity of the trauma cannot always be determined by the damage to the bones themselves, which may have been grossly displaced during the traumatic event but subsequently reduced. The bones may look more or less normal and perfectly aligned, but the damage to the soft tissues could be extensive and extremely disabling. For example, a patient could be completely paraplegic due to a traumatic event that resulted in forceful herniation of the intervertebral disk into the spinal canal. With or without a disk herniation, a traumatic spinal cord lesion can occur due to transient displacement of the vertebrae during impact, with normal alignment at the time of imaging. It is necessary to realize that when injury to the skeletal system is evaluated there will be additional and accompanying damage to the soft tissues even if one sees only the damage to the bones on radiography or CT. Injury to the thoracic and lumbar spine is usually classified according to the so-called anatomic column concept.8–12 Holdsworth identified two columns in the spine to classify spinal injury: the anterior column and the posterior column. In this concept osseous as well as ligamentous injury was considered. Denis introduced the concept of middle column or middle osteoligamentous complex between the traditionally recognized posterior ligamentous complex and the anterior longitudinal

ligament.9 The anterior column consists of the anterior vertebral body, anterior annulus fibrosus, and anterior longitudinal ligament. The middle column is formed by the posterior wall of the vertebral body, the posterior longitudinal ligament, and the posterior annulus fibrosus. The posterior column consists of the pedicles, lamina, facet joints, and transverse and spinous processes. The middle column is crucial, because the mode of its failure correlates both with the type of spinal fracture and with its neurologic injury. When the three-column concept of Denis is used, the general idea is that single-column (usually anterior) injuries are stable injuries, whereas two- or three-column injuries are unstable (see Fig. 4-1 in Chapter 4, Cervical Spine Injuries, for further discussion of the Denis classification). Because stability of the thoracic spine is partially provided by the thoracic cage, the presence of rib fractures at the levels around the spinal fracture should be included in the consideration of stability of thoracic spinal injury.13,14 Fracture classifications according to the biomechanics of injury are used frequently by traumatologists, orthopedic surgeons, and spine surgeons. For the spine the distinction is made between flexion-compression, vertical-compression (burst), flexion-distraction, and fracturedislocation (lateral, shear, torsion-flexion) injuries. The most common fractures are flexion-compression injuries, with damage to the anterior column and possible damage to the other columns. Because rotation is prevented by the rib cage, most thoracic spine injuries are caused by flexion and compression.

MANIFESTATIONS OF THE DISEASE Rib Fractures Radiography Rib fractures are usually detected first on chest radiographs that are acquired routinely in patients with severe trauma. The chest examination is directed toward a rapid overview of the airway system, more specifically the lungs, to gauge damage that may influence oxygenation and circulation. In the Advanced Trauma Life Support (ATLS) concept the airway (A) and breathing (B) are investigated first, rapidly followed by investigation of the circulatory system (C)—the ABCs. The number and location of rib fractures can be an indication of a significant traumatic event for the patient (Fig. 5-1). Single rib fractures usually have little clinical consequence, and diagnosing the fracture itself is not essential to management. However, rib fractures can lead to complications, including laceration of the pleura, lung, or intercostal arteries, causing pneumothorax or hemothorax. A flail chest is present when the bony continuity of the chest wall is disrupted by fractures of two or more ribs in two or more places. This instability of a segment of the thoracic cage leads to paradoxical movement during respiration, which can cause respiratory insufficiency and can lead to atelectasis and diminished oxygenation. Furthermore, almost invariably there is significant injury to the underlying lung. Instability of the chest wall can also be caused by a combination of rib fractures or costochondral fractures and a sternal fracture.

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■ FIGURE 5-1 Rib fractures and apical capping on standard chest radiograph in a trauma setting. Arrows show multiple rib fractures.

Rib fractures can lead to hemothorax and extrapleural hematoma. The differentiation between the two is important when a chest tube is placed. Drainage of an extrapleural hematoma leads to an extrapleural localization of the chest tube that will not protect against a tension pneumothorax and will not drain a pneumothorax and a hemothorax. An extrapleural hematoma gives a focal impression of the lung and does not change in location with positioning of the patient, contrary to a hemothorax in which blood between the parietal and visceral pleura changes location with different positions of the patient. When an extrapleural hematoma is located at the apex of the lung, it is called an apical/pleural cap and can be caused by rib fractures of the first three ribs, but it can also be the result of injury to the subclavian artery or extrapleural extension of a mediastinal hematoma. Therefore, it is an indication to perform a CT angiogram of the thorax to exclude traumatic vascular injury. In the supine patient an apical cap and apically dependent hemothorax are difficult to differentiate. Isolated fractures of the ribs occur due to a direct force and less commonly to a squeezing injury; in children and adults quite some force is needed to break a rib; in the elderly with progressive osteopenia minor trauma can lead to rib fractures. Young patients have more flexible ribs and can present with a pneumothorax or lung contusion without fractured ribs.

Magnetic Resonance Imaging Magnetic resonance imaging does not play a role in the detection of rib fractures but is very useful for detection of suspected costal cartilage injury as well as occult sternomanubrial and sternoclavicular separation.

Multidetector Computed Tomography In the setting of multiple trauma MDCT is the standard of care in the workup of severely injured patients. Many more rib fractures are seen on CT scans than are detected by radiography.15–17 The circular structure of the thoracic cage and the many places where rib fractures occur make it unlikely that ribs can be imaged such that the fracture is always perpendicular to the radiographic beam on radiographs, and thus rib fractures will often be missed. Fractures through the cartilaginous part of the ribs are never visible on radiography but can be identified with CT or MRI (Figs. 5-2 and 5-3).

■ FIGURE 5-2

Rib fracture (arrow) on CT not seen by radiography.

Ultrasonography Ultrasonography is excellent for detection of rib fractures but is not commonly used in clinical practice.

Nuclear Medicine Rib fractures are often detected on bone scintigraphy in patients with suspected skeletal metastasis originating from several types of tumors. In these cases these pathologic fractures are not injury related. Classically, benign trauma-related rib fractures are multiple and aligned vertically.

Classic Sign ■ ■

Traumatic rib fractures are typically multiple and vertically aligned; look for associated pneumothorax/hemothorax. Apical cap (curvilinear nondependent opacity with mass effect on the lung apex) can be associated with upper rib fractures and is a sign of significant traumatic force; angiography is indicated to exclude injury to the great vessels.

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■ FIGURE 5-3 A, Fracture through the cartilaginous aspect of a rib at the sternal junction with dislocation (arrow). B, Coronal STIR image of a different patient shows costochondral disruption (arrows). C, Sagittal STIR image of a third patient shows seperation of the manubrium (M) from the sternum (S) with offset and disruption of the fibrous capsule (arrow) and surrounding edema.

Sternal Fractures Radiography Sternal fractures are difficult or impossible to diagnose on anteroposterior chest views, especially in the setting of multiple trauma; targeted sternal views with dedicated exposure parameters can be made as well as additional lateral sternal views. However, the patient with multiple trauma with extensive damage to the chest will get a CT scan, which facilitates the detection of these fractures. Usually these patients, if still alert, have localized pain on the sternum and when the area is palpated the fracture and its crepitations can be felt. Sternal fractures can be accompanied by lung contusion and myocardial contusion. Major injury to the heart and great vessels in patients with an isolated sternal fracture is uncommon.

■ FIGURE 5-4

Direct trauma to the sternum, such as anteroposterior compression from steering wheel or seat belt injuries, leads to posterior displacement of the distal fracture fragment. Indirect trauma to the sternum, such as severe flexion and axial compression, leads to posterior displacement of the proximal fracture fragment. This type of injury is associated with thoracic spinal injury. Most patients with a sternal fracture were involved in a motor vehicle accident (83%) and were restrained with a seat belt (92%). Only 1% of patients do not complain of pain. Most fractures are located at the sternal body. More than half are nondisplaced. In 56%, concomitant injuries to the chest and spine are diagnosed. Most frequently, these are rib fractures, followed by lung contusion or laceration and cardiac contusion. In 13% of patients one or more spinal fractures are diagnosed. In nondisplaced fracture the frequency of concomitant injury is less than in displaced fractures (Fig. 5-4).

(A), Sternal fracture on lateral sternal view (arrows); cardiac contusion should be excluded. Coronal reformatted CT image (B) and sagittal STIR image (C) of a different patient show a fracture through the sternum (arrows). The fracture line is better appreciated on CT, whereas the soft tissue and marrow injury is evident on MRI.

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■ FIGURE 5-5

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Sternal fracture (arrow) detected by CT.

Magnetic Resonance Imaging Magnetic resonance imaging is excellent for diagnosis of sternal injury and associated hematoma. In particular, soft tissue injury such as manubrial-sternal and sternoclavicular injury is easily diagnosed using MRI. However, CT performed in a trauma setting is often diagnostic of sternal and peristernal injury; MRI can be acquired in cases with symptoms and negative CT or when MDCT is not available.

Multidetector Computed Tomography Multidetector CT is ideal in detecting and describing sternal fractures.15–17 Because the spatial resolution is high in MDCT, the reconstructions yield high-quality images of the broken sternum. Furthermore, sternal fractures can cause mediastinal hemorrhage if vascular structures behind the sternum are damaged. With contrast medium– enhanced MDCT these hemorrhages can be detected as high density on a noncontrast examination or as blushes of contrast medium, especially when scanned in a late (venous) phase (Fig. 5-5).

Ultrasonography Ultrasonography can be used to detect sternal fractures but is not typically used in clinical practice.

Fractures to the Thoracic and Lumbar Spine Radiography Radiographs are routinely performed in injured patients to detect spinal fractures.18–22 Lateral and anteroposterior views of the thoracic spine and lumbar spine are acquired. It is important to note that on the lateral thoracic views the upper vertebral bodies (T1-T3/T4) cannot be assessed due to overlying shoulder density. A swimmer’s view can be attempted to image these upper thoracic vertebrae. However, in severely injured patients this view can be impossible to obtain.

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Upper thoracic spine fractures are also easily missed in patients with multiple injuries due to concomitant lifethreatening injuries. Most patients in whom the injury is initially missed have a widened paravertebral line and loss of height of the vertebrae with or without malalignment. When a vertebral fracture is diagnosed in a patient with a widened paravertebral line, one should not assume that the mediastinal abnormality is strictly caused by the spinal injury. A traumatic vascular injury should still be excluded. When, on a high-quality contrast-enhanced CT of the chest, the paravertebral hematoma surrounds the fractured vertebra and displaces the aorta, which is otherwise normal without a concomitant perivascular hematoma, a traumatic aortic injury can be excluded. On the anteroposterior and lateral views, loss of vertebral height and cortical disruption with or without displacement, search for fracture fragments. When the paravertebral soft tissue line is widened, it can be an indirect sign of vertebral fracture. On the anteroposterior view an increased distance between the pedicles is highly indicative of vertebral damage (Figs. 5-6 and 5-7). The differential diagnosis when vertebral deformities are detected is extensive. In addition to traumatic lesions the vertebral bodies can have an altered appearance due to congenital disorders, metastasis, myeloma, infection, or degenerative disease. Furthermore, osteoporotic deformities are common in the elderly. When trying to determine the cause of a vertebral deformity, it is helpful to have access to the medical history of the patient, which is generally not the case in the trauma setting. When viewing the images, some features can be helpful. Avulsion and dislocation of fragments is almost always caused by trauma. One can view the difference between traumatic lesions and osteoporotic lesions as the difference between an explosion (traumatic force causing displacement of fragments and cortical disruptions) and an implosion (the vertebral body deforms into itself due to weakness of the trabecular network within the vertebral body). The distinction between a traumatic lesion and a metastatic lesion or a lesion due to myeloma can be facilitated by studying the bone architecture. In trauma the bony structures are broken but are present; in malignant diseases they have been eaten away and thus absent and replaced by malignant tissue. Congenital deformities can often be ruled out by careful investigation of bone morphology, especially on the anteroposterior views of the spine. Clefts and fusion defects can then be found (Figs. 5-8 and 5-9). Degenerative disease and remodeling can cause a wedge-shaped appearance of the vertebral bodies. However, there is no cortical or trabecular damage. Infectious spondylodiskitis can cause vertebral deformities; however, usually the damage to the intervertebral disk space and the adjacent vertebral end-plate damage as well as the reactive sclerosis of the vertebral bodies help in making the correct differential diagnosis. Furthermore, Scheuermann’s disease causes end-plate deformities that are acquired in adolescence due to a juvenile spondyloepiphyseal growth disturbance. Multiple vertebrae show short, broad morphology with irregular end plates and usually several Schmorl’s nodes (disk impressions) (Fig. 5-10).

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■ FIGURE 5-6

L2 (arrows).

Burst fracture of

■ FIGURE 5-7 Fracture of thoracic spine with dislocation.

CHAPTER

■ FIGURE 5-8 Pathologic deformity at L3 on radiograph (left) with multiple metastases on the MR image (right).

■ FIGURE 5-9 Congenital deformity of the thoracic spine (arrows).

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■ FIGURE 5-10

Scheuermann’s disease.

Most thoracolumbar spinal injuries involve the thoracolumbar junction.

Magnetic Resonance Imaging Magnetic resonance imaging is indicated when spinal cord damage is anticipated and needs to be evaluated and when there is neurologic damage without clear damage to the osseous spinal column. In that case the differential diagnosis is a traumatic herniated disk or an epidural hematoma, which both can give pressure on the spinal cord and need immediate surgery. MRI is also indicated to evaluate spinal ligament integrity because disruption of the stabilizing ligaments can alter prognosis and treatment options; for example, a solitary fracture of the anterior column on CT that is considered stable but with coexistent disruption of the posterior interspinous ligament, equivalent to posterior column injury, upgrades the diagnosis to an unstable spine.23–27

Multidetector Computed Tomography Multidetector CT is the ultimate imaging technique to detect osseous damage to the spinal column.28–34 Because the current spiral multidetector scanners can produce isotropic voxels in a large volume, the spinal column can be viewed in any reconstruction with high resolution. The images of the spinal column should be reconstructed in axial, coronal, and sagittal views, providing the ultimate possibilities in the assessment of the osseous structures. Images should be reconstructed with the appropriate bone kernel or filter and displayed in a bone window and level setting (Figs. 5-11 and 5-12).

■ FIGURE 5-11

Axial CT slice showing fracture of vertebral body (arrow).

In the patient with multiple trauma, an MDCT of the chest and the abdomen is often performed to detect damage to the inner organs. These datasets can easily be used to produce excellent images of the spine when reconstructed in the appropriate manner. When abdominal CT data are available, radiographs of the lumbar spine have no additional value. Furthermore, dedicated CT of the lumbar spine is not required. Abdominal CT data with multiplanar reformatted images show more fractures than radiography and miss no fractures compared with dedicated CT of the lumbar spine. Interpretation of the multiplanar reconstructions alone is a feasible approach for assessment of vertebral fractures and classifying them into stable/unstable categories. Transverse images must be analyzed in patients with complex fractures or with uncertain findings. Accurate evaluation of the thoracolumbar spine is possible with targeted reconstructions based on a standardized MDCT trauma protocol of the chest and abdomen: a 4 × 1-mm collimation has the same sensitivity and specificity as a 4 × 2.5-mm protocol but results in a higher diagnostic confidence.

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment Whereas nonsurgical treatment is standard for osteoporotic compression fractures, many traumatic fractures require surgical fixation. Simple posterior element or transverse process fractures are treated conservatively.

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■ FIGURE 5-12 Coronal (A) and sagittal (B) reconstructions of the vertebral fracture shown in Figure 5-11. Sagittal T2-weighted fat-suppressed image (C) shows a burst fracture with retropulsion.

Bracing in extension can be applied to treat mechanically stable fractures such as anterior wedge compression fractures with intact posterior ligaments. Studies have also shown that traction can improve retropulsion because the retropulsed fragment is often attached to the posterior longitudinal ligament. Some mechanically unstable but neurologically stable (i.e., no neurologic symptoms or impending compromise of neural structures) fractures may also be treated conservatively, depending on a number of factors including type of fracture (i.e., osseous Chance fracture), patient condition (i.e., poor surgical candidate or osteoporosis), and location (i.e., based on size of the spinal canal). There has been a suggestion that acute traumatic fractures may be treated with cement augmentation, but this is not standard practice.35–39

Surgical Treatment The mainstay of treatment for acute unstable spinal fracture is decompression and fixation/fusion.40–45 Various devices used for this purpose are summarized in the appendices on the CD.

What the Referring Physician Needs to Know ■ ■ ■

Fracture type implies mechanism, which is useful for treatment and to predict other injuries. Middle column and/or posterior interspinous ligament disruption usually necessitates surgical fixation. There may be an associated visceral injury.

SUGGESTED READINGS Bagley LJ. Imaging of spinal trauma. Radiol Clin North Am 2006;44:1–12. Heinemann U, Freund M. Diagnostic strategies in spinal trauma. Eur J Radiol 2006;58:76–88. Miller LA. Chest wall, lung, and pleural space trauma. Radiol Clin North Am 2006;44:213–224, viii.

Mirvis SE. Diagnostic imaging of acute thoracic injury. Semin Ultrasound CT MR 2004;25:156–179. Rivas LA, Fishman JE, Munera F, Bajayo DE. Multislice CT in thoracic trauma. Radiol Clin North Am 2003;41:599–616.

REFERENCES 1. Denis F, Burkus JK. Shear fracture-dislocations of the thoracic and lumbar spine associated with forceful hyperextension (lumberjack paraplegia). Spine 1992; 17:156–161. 2. Ferguson RL, Allen BL. A mechanistic classification of thoracolumbar spine fractures. Clin Orthop Relat Res 1984; 189:77–88. 3. Ball ST, Vaccaro AR, Albert TJ, et al. Injuries of the thoracolumbar spine associated with restraint use in head-on motor vehicle accidents. J Spinal Disord 2000; 13:297–304. 4. Liu YJ, Chang MC, Wang ST, et al. Flexion-distraction injury of the thoracolumbar spine. Injury 2003; 34:920–923.

5. Miller CD, Blyth P, Civil ID. Lumbar transverse process fractures—a sentinel marker of abdominal organ injuries. Injury 2000; 31:773–776. 6. Keenen TL, Antony J, Benson DR. Noncontiguous spinal fractures. J Trauma 1990; 30:489–491. 7. Keenen TL, Antony J, Benson DR. Dural tears associated with lumbar burst fractures. J Orthop Trauma 1990; 4:243–245. 8. Mirza SK, Mirza AJ, Chapman JR, et al. Classifications of thoracic and lumbar fractures: rationale and supporting data. J Am Acad Orthop Surg 2002; 10:364–377.

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9. Denis F. The three column spine and its significance in the classification of acute thoracolumbar spinal injuries. Spine 1983; 8:817–831. 10. Denis F. Spinal instability as defined by the three-column spine concept in acute spinal trauma. Clin Orthop Relat Res 1984; 189:65–76. 11. Panjabi MM, Oxland TR, Kifune M, et al. Validity of the threecolumn theory of thoracolumbar fractures: a biomechanic investigation. Spine 1995; 20:1122–1127. 12. Magerl F, Aebi M, Gertzbein SD, et al. A comprehensive classification of thoracic and lumbar injuries. Eur Spine J 1994; 3:184–201. 13. White AA III, Panjabi MM. In: Clinical Biomechanics of the Spine, 2nd ed. Baltimore, Lippincott Williams & Wilkins, 1990, p 352. 14. James KS, Wenger KH, Schlegel JD, et al. Biomechanical evaluation of the stability of thoracolumbar burst fractures. Spine 1994; 19:1731–1740. 15. Mirvis SE. Imaging of acute thoracic injury: the advent of MDCT screening. Semin Ultrasound CT MR. 2005; 26:305–331. 16. Trupka A, Waydhas C, Hallfeldt KK, et al. Value of thoracic computed tomography in the first assessment of severely injured patients with blunt chest trauma: results of a prospective study. J Trauma 1997; 43:405–411. 17. Alkadhi H, Wildermuth S, Marincek B, Boehm T. Accuracy and time efficiency for the detection of thoracic cage fractures: volume rendering compared with transverse computed tomography images. J Comput Assist Tomogr 2004; 28:378–385. 18. Daffner RH. Thoracic and lumbar vertebral trauma. Orthop Clin North Am 1990; 21:463–482. 19. Daffner RH, Deeb ZL, Goldberg AL, et al. The radiologic assessment of post-traumatic vertebral stability. Skeletal Radiol 1990; 19:103–108. 20. Petersilge CA, Emery SE. Thoracolumbar burst fracture: evaluating stability. Semin Ultrasound CT MR 1996; 17:105–113. 21. Daffner RH, Deeb ZL, Rothfus WE. The posterior vertebral body line: importance in the detection of burst fractures. AJR Am J Roentgenol 1987; 148:93–96. 22. Ballock RT, Mackersie R, Abitbol JJ, et al. Can burst fractures be predicted from plain radiographs? J Bone Joint Surg Br 1992; 74:147–150. 23. Oner FC, van Gils AP, Dhert WJ, et al. MRI findings of thoracolumbar spine fractures: a categorisation based on MRI examinations of 100 fractures. Skeletal Radiol 1999; 28:433–443. 24. Petersilge CA, Pathria MN, Emery SE, et al. Thoracolumbar burst fractures: evaluation with MR imaging. Radiology 1995; 194:49–54. 25. Brightman RP, Miller CA, Rea GL, et al. Magnetic resonance imaging of trauma to the thoracic and lumbar spine. The importance of the posterior longitudinal ligament. Spine 1992; 17:541–550. 26. Haba H, Taneichi H, Kotani Y, et al. Diagnostic accuracy of magnetic resonance imaging for detecting posterior ligamentous complex injury associated with thoracic and lumbar fractures. J Neurosurg Spine 2003; 99:20–26. 27. Terk MR, Hume-Neal M, Fraipont M, et al. Injury of the posterior ligament complex in patients with acute spinal trauma: evaluation by MR imaging. AJR Am J Roentgenol 1997; 168:1481–1486. 28. McAfee PC, Yuan HA, Fredrickson BE, et al. The value of computed tomography in thoracolumbar fractures: an analysis of one hundred consecutive cases and a new classification. J Bone Joint Surg Am 1983; 65:461–473.

29. Guerra J Jr, Garfin SR, Resnick D. Vertebral burst fractures: CT analysis of the retropulsed fragment. Radiology 1984; 153:769–772. 30. Campbell SE, Phillips CD, Dubovsky E, et al. The value of CT in determining potential instability of simple wedge-compression fractures of the lumbar spine. AJNR Am J Neuroradiol 1995; 16:1385–1392. 31. Wintermark M, Mouhsine E, Theumann N, et al. Thoracolumbar spine fractures in patients who have sustained severe trauma: depiction with multi-detector row CT. Radiology 2003; 227:681–689. 32. Herzog C, Ahle H, Mack MG, et al. Traumatic injuries of the pelvis and thoracic and lumbar spine: does thin-slice multidetector-row CT increase diagnostic accuracy? Eur Radiol 2004; 14:1751–1760. 33. Begemann PG, Kemper J, Gatzka C, et al. Value of multiplanar reformations (MPR) in multidetector CT (MDCT) of acute vertebral fractures: do we still have to read the transverse images? J Comput Assist Tomogr 2004; 28:572–580. 34. Roos JE, Hilfiker P, Platz A, et al. MDCT in emergency radiology: is a standardized chest or abdominal protocol sufficient for evaluation of thoracic and lumbar spine trauma? AJR Am J Roentgenol 2004; 183:959–968. 35. Kinoshita H, Nagata Y, Ueda H, et al. Conservative treatment of burst fractures of the thoracolumbar and lumbar spine. Paraplegia 1993; 31:58–67. 36. Celebi L, Muratli HH, Dogan O, et al. The efficacy of nonoperative treatment of burst fractures of the thoracolumbar vertebrae. Acta Orthop Traumatol Turc 2004; 38:16–22. 37. Aligizakis A, Katonis P, Stergiopoulos K, et al. Functional outcome of burst fractures of the thoracolumbar spine managed nonoperatively, with early ambulation, evaluated using the load sharing classification. Acta Orthop Belg 2002; 68:279–287. 38. Tropiano P, Huang RC, Louis CA, et al. Functional and radiographic outcome of thoracolumbar and lumbar burst fractures managed by closed orthopaedic reduction and casting. Spine 2003; 28:2459–2465. 39. Kim NH, Lee HM, Chun IM. Neurological injury and recovery in patients with burst fracture of the thoracolumbar spine. Spine 1999; 24:290–294. 40. Vaccaro AR, Kim DH, Brodke DS, et al. Diagnosis and management of thoracolumbar spine fractures. Instr Course Lect 2004; 53:359–373. 41. Vollmer DG, Gegg C. Classification and acute management of thoracolumbar fractures. Neurosurg Clin North Am 1997; 8:499–507. 42. Dai LY, Yao WF, Cui YM, et al. Thoracolumbar fractures in patients with multiple injuries: diagnosis and treatment—a review of 147 cases. J Trauma 2004; 56:348–355. 43. Jeanneret B, Holdener HJ. Vertebral fractures and abdominal trauma: a retrospective study based on 415 documented vertebral fractures. Unfallchirurg 1992; 95:603–607. 44. Rabinovici R, Ovadia P, Mathiak G, et al. Abdominal injuries associated with lumbar spine fractures in blunt trauma. Injury 1999; 30:471–474. 45. Tyroch AH, McGuire EL, McLean SF, et al. The association between Chance fractures and intra-abdominal injuries revisited: a multicenter review. Am Surg 2005; 71:434–438.

C H A P T E R

6

C H A P T E R

Normal Shoulder

Qi Chen, Theodore T. Miller, Mario Pardon, and Javier Beltran

TECHNICAL ASPECTS Conventional Radiography (Table 6-1,

Limitations ●

Fig. 6-1)

●

Rationale and Indications

●

● ●

Visualization of osseous anatomy and pathology, bone contours, and joint alignment Recommended for any primary evaluation of suspected shoulder pathology, including fractures, dislocations, bone tumors, and infection

Advantages ● ●

Computed Tomography (Table 6-2) Rationale and Indications ●

●

Readily available Inexpensive

Limited soft tissue evaluation Patient position may be difficult if there is limited motion for any reason (e.g., pain, fracture, ankylosis) Ionizing radiation, although minimal

Provides multiplanar and surface rendering of the osseous anatomy with multiple reconstruction algorithms, including disarticulation. Rotation of surface-reconstructed model in infinite projections for visualization of complex osseous anatomy and pathology

TABLE 6-1 Conventional Radiography of the Shoulder Projections

Main Visualized Anatomy and Pathology

Anteroposterior (neutral arm position)

Anterior dislocation Fracture of proximal humerus, clavicle, and scapula (i.e., Bankart lesion) Fat-fluid level (erect position) Hill-Sacks lesion (posterolateral humeral head impacted fracture) Trough sign (anteromedial humeral head compression fracture) in posterior dislocation Fracture of scapular body, acromion, coracoid process, proximal humerus Humeral head to glenoid fossa relationship Humeral head to glenoid relationship Anterior and posterior dislocation Anteroinferior rim of glenoid (West Point view) Acromial fracture and morphology Rotator cuff outlet Glenohumeral joint space (obliterated in posterior dislocation) Acromioclavicular joint separation Bicipital groove Proximal humeral fracture Humeral head to glenoid relationship

Anteroposterior—internal rotation* Anteroposterior—external rotation* Scapula “Y” (true lateral of scapula)* Axillary (superoinferior view)* Lawrence (no full abduction required) West Point (minimal arm abduction) Outlet (oblique) Grashey (posterior oblique with glenoid in profile) Acromioclavicular (without/with stress) Bicipital groove (tangent, humeral head) Lateral transthoracic (true lateral of proximal humerus)

*Standard shoulder series (see Fig. 6-1).

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C

A

B ■ FIGURE 6-1 Conventional radiographic series of the shoulder. A, Exterior rotation; B, interior rotation; C, axillary view (arrowheads, acromioclavicular joint; short arrows, acromion; long arrow, coracoid process); D, scapular “Y” view.

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● ● ●

Evaluation of complex fractures and dislocations and degree of healing (callus formation, partial union, nonunion, adequate reduction, joint congruity) Evaluation of matrix calcification (osteoid, cartilage) in some bone tumors Evaluation of poorly visualized or suspected bone abnormality on conventional radiography Assessment of soft tissue calcifications TABLE 6-2 Technical Aspects of 16-Slice Multidetector CT of the Shoulder

Slice thickness Collimation Kernel Pitch Reconstruction

3 mm × 3 mm 0.75 mm × 16 slices B31 soft tissue, B70 bone 0.5 Multiplanar, surface rendering

D

CT Arthrography (Fig. 6-2) Rationale and Indications ●

● ●

Intra-articular injection of iodine contrast material allows visualization of the internal capsular anatomy and pathology Main indication: assessment of suspected labral tears Indicated when there is a contraindication to MRI or in patients with claustrophobia

Advantages ● ● ● ●

Excellent depiction of osseous structures and calcified tissues Multiplanar and surface rendering capabilities Nonclaustrophobic Availability

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● Normal Shoulder

103

B

■ FIGURE 6-2

CT arthrography of the shoulder. A, Axial image. Single arrowheads, glenoid labrum; short arrows, distended joint capsule; long arrow, long biceps tendon; double arrowheads, within a rotator cuff tear. B, Coronal reformatted image. C, Sagittal reformatted image. Short arrows in B and C indicate subacromial subdeltoid bursa with contrast material.

C

Limitations ● ● ● ●

Limited visualization of soft tissues, although better than conventional radiography Ionizing radiation, expensive Beam-hardening artifact from metal (improved with recent multidetector technology) Invasive when using with arthrography

●

●

●

Method ●

A conventional single- or double-contrast arthrogram is performed first (as described under MR arthrography) using diluted iodinated contrast material (3 to 5:1) with or without air for a total of 13 to 15 mL.

●

The CT examination is performed without delay (to avoid extravasation and dilution of contrast and, thus, avoid loss of capsular expansion). Patient position: supine, injected arm in neutral position; contralateral arm is elevated and flexed at elbow to decrease shoulder girdle girth and allow the injected shoulder to be moved closer to gantry center. Scanning in multiple patient positions is not routinely performed owing to the added radiation exposure. However, there are specific indications or benefits for scanning in different patient positions. Caution: arm rotation changes capsulolabral complex morphology (i.e., glenohumeral ligament position change may mimic a labral tear anteriorly).

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Injected shoulder position External rotation: improved visualization of anterior and posterior labral tear Prone: improved visualization of posterior labrum

TABLE 6-3 Conventional MRI of the Shoulder Imaging Planes

First-line Oblique coronal Fast spin-echo proton density,T2 fat saturated Oblique sagittal Fast spin-echo proton density,T2 fat saturated Axial T1 fast spin-echo,T2 Additional and Optional Oblique coronal T1, short tau inversion recovery Oblique sagittal T1, short tau inversion recovery Axial Gradient recalled echo

Conventional Magnetic Resonance Imaging (Table 6-3; Fig. 6-3;Table 6-4) Rationale and Indications ●

Visualization and assessment of soft tissue anatomy and pathology including rotator cuff, capsulolabral and neurovascular structures, and osseous pathology

Advantages ● ●

Multiplanar Nonionizing

Pulse Sequences

Limitations ● ● ● ●

Expensive Claustrophobic in closed magnets Long examination time Patient motion and respiratory motion artifacts

A

B ■ FIGURE 6-3 Conventional MRI of the shoulder. A, Oblique coronal proton-density image. B, Oblique coronal T2-weighted image. C, Oblique coronal proton-density image.

(Continued)

C

CHAPTER

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● Normal Shoulder

105

E

F

G

■ FIGURE 6-3—Cont’d

D to F, Oblique sagittal proton-density images. G, Axial gradient-recalled-echo image.

TABLE 6-4 Abbreviations Used in Illustrations A ArC AxR C CAL CAP CHL CL DM GT GHL IGHL Ant Band IGHL Post Band

Acromion Articular cartilage Axillary recess Coracoid process Coracoacromial ligament Joint capsule Coracohumeral ligament Clavicle Deltoid muscle Greater tuberosity Inferior glenohumeral ligament Anterior band inferior glenohumeral ligament Posterior band inferior glenohumeral ligament

IL ISM ISN IST L LBT LT MGHL PL QS RCI SASDB SCB

Inferior labrum Infraspinatus muscle Infraspinatus nerve Infraspinatus tendon Glenoid labrum Long head biceps tendon Lesser tuberosity Middle glenohumeral ligament Posterior labrum Quadrilateral space Rotator cuff interval Subacromial subdeltoid bursa Subcoracoid bursa

SGHL SGL SL SScapL SScapM SScapN SScapT SSCN SSM SSN SST TM TMaj TMT TrM

Superior glenohumeral ligament Spinoglenoid ligament Superior labrum Suprascapular ligament Subscapularis muscle Suprascapular nerve Subscapularis tendon Suprascapular notch Supraspinatus muscle Supraspinatus nerve Supraspinatus tendon Teres minor muscle Teres major muscle Teres minor tendon Triceps muscle

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Technical Aspects ● ● ● ● ●

Suggested parameters use a 1.5-Tesla magnet. Phase-array surface coil Slice thickness: 3 to 4 mm Matrix: 512 × 512 Field of view: 14 to 16 cm

Indirect MR Arthrography (Table 6-5; Fig. 6-4) Rationale and Indications ●

Method ●

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●

Axial sections from the superior aspect of the acromioclavicular joint through the proximal humeral shaft including the insertion of the pectoralis muscle Oblique coronal sections from the coracoid process to the infraspinatus muscle oriented following the longitudinal plane of the scapula Oblique sagittal sections from the neck of the glenoid through the deltoid muscle oriented following a plane perpendicular to the oblique coronal sections

TABLE 6-5 Indirect MR Arthrography of the Shoulder

A

B

C

D

■ FIGURE 6-4

Takes advantage of bulk flow and diffusion of contrast material from the vascular supply into the synovial tissue lining the bursae, joint capsule, and tendon sheaths to ultimately pool into the joint space. Gadopentetate dimeglumine–based contrast

Imaging Plane

Pulse Sequences

Oblique coronal Oblique sagittal Axial ABER

T1 fat saturated, fast spin-echo T2 fat saturated T1 fat saturated T1 fat saturated T1 fat saturated

Indirect MR arthrography of the shoulder. A, Oblique coronal T1-weighted image with fat saturation. Short arrow, normal enhancement of the subacromial subdeltoid bursa; arrowhead, magic angle artifact in the distal supraspinatus tendon; long arrow, normal distention of the axillary recess. B, Axial T1-weighted image with fat saturation. Long arrow, anterior labrum. C, Oblique sagittal T1-weighted image with fat saturation. Short arrow, normal enhancement of the subacromial subdeltoid bursa; arrowhead, magic angle artifact in the distal supraspinatus tendon. D, Abducted and externally rotated projection. Long arrow, normal distention of the joint anteriorly by contrast.

CHAPTER

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agents shorten the T1 relaxation time of tissues, which can be utilized to produce arthrographic T1-weighted fat-suppressed images. This technique enables an anatomic and physiologic assessment of joint pathology. Indicated in suspected capsulolabral lesions

Technical Aspects ●

● ●

●

Intravenous injection of a 15-mL solution of 0.1 mmol/ kg gadopentetate dimeglumine. Greater concentrations of gadopentetate dimeglumine including 0.2 and 0.4 mmol/kg have not been shown to derive greater arthrographic benefit.1 Ten to 20 minutes of gentle active exercise before imaging Oblique coronal fast spin-echo T2-weighted fat saturation is included for the identification of preexisting extra-articular fluid collections (bursitis) and to evaluate possible magic angle artifact in the distal rotator cuff and labrum. The use of the abducted externally rotated (ABER) position in which the palm of the hand is positioned against the dorsal aspect of the craniocervical junction allows for a static assessment of stress placed on the anterior glenoid.2 Coronal scout images of the patient in the ABER position are performed, from which sagittal images are prescribed along the longitudinal axis of the humerus, resulting in oblique sagittal series of sections from the anteroinferior labrum through the posterior superior labrum. It is recommended to obtain the ABER plane as the first sequence to ensure patient compliance with the entire examination.

● ● ●

Allows assessment of both intra- and extra-articular soft tissues.3,4 It is based on the concept that the synovial membrane is vascular and injected intravenous contrast medium will diffuse to the joint over time. This property is advantageous when diagnosing inflammatory arthropathies such as rheumatoid arthritis that result in synovial hyperplasia. The contrast agent enhances this intermediate signal synovial tissue, a finding that is conspicuous during indirect arthrographic imaging. Less costly than direct MR arthrography Provides more data regarding physiologic state as well as assessment of intra-articular surface anatomy Does not require fluoroscopic guidance or joint injection and is superior to conventional MRI in delineating the labrum when there is minimal joint fluid4

Limitations ●

●

Inability to control the volume of the contrast that diffuses into the joint. There is insignificant joint distention, unless there is preexisting effusion. Enhancement of subacromial bursa can obscure a rotator cuff tear. This potential pitfall may be avoided by comparing pre- and postcontrast images.4

● Normal Shoulder

107

Direct MR Arthrography (Table 6-6; Fig. 6-5) Rationale and Indications ●

Distention of the joint capsule to demonstrate to best advantage the intracapsular structures (i.e., glenoid labrum, glenohumeral ligaments, articular surface of the rotator cuff)

Technical Aspects ●

●

Advantages ●

6

●

Direct MR arthrography is a two-phase procedure in which the intra-articular injection of contrast material is performed under fluoroscopic visualization and then the patient is transferred to the MR scanner for diagnostic imaging. The technique of intra-articular injection must avoid the cartilage, labrum, and capsular attachments to yield diagnostic utility.5-8 Although multiple techniques have been described, the anterior approach is most common and has been modified over time.5,6 Utilizing the anterior approach to glenohumeral joint injection requires supine positioning of the patient with the shoulder in external rotation. External rotation exposes more of the articular surface of the humeral head anteriorly and increases the intra-articular area available for needle insertion. The first step requires localization of the desired needle position, which is medial to the superior third of the humeral head that is covered by the joint capsule. The area then is prepped and draped in a sterile fashion, and the subcutaneous tissue is anesthetized. Needle size may vary, but commonly a 20- to 22-gauge 3.5-inch spinal needle is used.7 The needle tip is then advanced in an anteroposterior direction to the humeral head, avoiding contact with the glenoid labrum. In the posterior approach to shoulder arthrography, the patient is positioned prone with the ipsilateral shoulder raised off the table with a pad.7 The needle is directed toward the inferomedial aspect of the humeral head. After local anesthetic is used, a 21-gauge spinal needle is advanced vertically under fluoroscopic guidance toward the cartilage of the humeral head.9 Chung and coworkers have demonstrated that an anterior approach may result in penetration of the anterior stabilizing structures of the glenohumeral joint, which has a tendency for anterior instability.6 The study included six shoulders from a fresh cadaver using an 18-gauge needle with markers in the anterior and posterior approaches. The marker for the anterior approach has traversed through the subscapularis muscle or tendon in all cases, the inferior

TABLE 6-6 Direct MR Arthrography of the Shoulder Imaging Plane

Pulse Sequences

Oblique coronal Oblique sagittal Axial ABER

T1 fat saturated, fast spin-echo T2 fat saturated T1 fat saturated T1 fat saturated T1 fat saturated

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A

B ■ FIGURE 6-5 Direct MR arthrography of the shoulder. A, Oblique coronal T1-weighted fat-saturated image. B and C, Oblique sagittal T1-weighted fat-saturated images.

(Continued)

C

●

glenohumeral ligament in two cases, and the anterior inferior labrum. On the other hand, the marker for the posterior approach has traversed the posterior inferior labrum in a single case without violation of the anterior structures. Thus, it has been recommended to use the posterior approach if the patient presented with anterior instability or anterior symptoms.6,7 The posterior approach will decrease the likelihood of injecting into the subscapularis tendon or inferior glenohumeral ligament.10 On confirming intra-articular location using the least iodinated contrast agent possible (2 to 3 mL), approximately 15 mL of a 0.1-mmol/kg solution of gadopentetate dimeglumine is injected and the patient is taken to the MR scanner for sequence acquisition. The volume of the injection ranges between 10 and 20 mL.5

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●

Injections of less than 15 mL decrease the likelihood of extra-articular leak, which may be mistaken for a full-thickness rotator cuff tear. Exercise after shoulder arthrography has no beneficial or detrimental effect on MRI quality or on the depiction of rotator cuff tear.11 Ideally, MRI should begin within 30 minutes of joint injection to minimize absorption of contrast. Additional maneuvers such as arm traction using 1- to 3-kg weights applied to the wrist combined with external rotation improve the sensitivity and specificity for detection of a superior labral anteroposterior lesion than if no arm traction is used.12 Alternatively, the intra-articular position of the needle can be performed using ultrasound guidance, open MRI guidance, and even blindly, resulting in considerable time savings and scheduling coordination.13

CHAPTER

D

6

● Normal Shoulder

109

E

F ■ FIGURE 6-5—Cont’d

D to F, Axial gradient-recalled-echo images. G, Abducted and externally rotated projection, T1-weighted image.

G

Advantages ●

Ability to detect capsulolabral pathology and partialthickness and vertical rotator cuff tendon tears. Better distention of the joint capsule, particularly the labral-ligamentous complex, allows easier depiction of irregular tears versus more smoothly delineated anatomic variants such as sublabral sulci and foramina.

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Limitations ●

Patient’s adversity to procedure, safety, cost, extra time and labor hours per procedure, scheduling, and coordinating use of both fluoroscopy and MRI and the direct involvement of the radiologist. Postprocedure assessment of pain and discomfort shows that direct arthrography is better tolerated than the MRI itself.14

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Ionizing radiation The potential for contrast reaction is considerably greater for the iodinated agents. Although the overall risk of complications with a minimally invasive intra-articular needle arthrography is very low, the potential complications are considerable. An introduced infection to the joint can result in septic arthritis, osteomyelitis, or fasciitis. Arthrography may cause direct damage to the nerves, capsule, or ligaments. The expense of the fluoroscopy suite, nursing, and MRI time add to decrease the efficiency when evaluating patient throughput. Cost of the radiologist’s time for a direct arthrogram is considerably greater than utilizing a nurse or technologist to administer an intravenous injection.

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Leak of contrast through the capsular puncture site can cause spread of contrast along the fascial planes into the subdeltoid space, causing a “bursogram,” which can be misinterpreted as a full-thickness rotator cuff tear. Accidental injection of gas can lead to an incorrect diagnosis of loose bodies from the magnetic susceptibility artifact. However, attributing the exact cause of a susceptibility artifact should be based on its location (i.e., joint bodies are typically located in the more dependent portions and gas bubbles rise to the nondependent portions of the joint).

●

Technical Aspects ●

Ultrasonography Rationale and Indications ●

Rapid performance, low cost, and preference by patients.15-18 Middleton and colleagues19 surveyed 118 patients who underwent both ultrasonography and MRI of the shoulder for suspected rotator cuff disease and found that 79% of them preferred ultrasonography. Even if MRI remains the primary modality for suspected rotator cuff disease, ultrasonography rather than conventional arthrography should be considered the alternative modality for patients with contraindications to MRI, because ultrasonography is noninvasive, is more rapidly performed than arthrography, and can demonstrate tendinosis, bursal surface tears, and subdeltoid bursitis, none of which can be diagnosed arthrographically.

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Advantages ● ●

●

Greater resolution than MRI.20 Allows “dynamic” scanning of tendons in motion. Thus, a subluxing biceps tendon may be demonstrated during internal and external rotation of the humerus, and entrapment of the supraspinatus tendon and subdeltoid bursa between the greater tuberosity and the acromion may be demonstrated during abduction of the arm. Facilitates face-to-face communication between the patient and examiner, thus providing more information than garnered from a “patient information” form.

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Limitations ●

●

●

●

It is more operator dependent than MRI, analogous to ultrasonography of the abdomen compared with CT of the abdomen. It has a long learning curve both for performing the examination and interpreting it. The long learning curve is because the images are not anatomically intuitive as they are with MRI or CT and that diagnostic images are dependent on proper patient positioning and transducer placement. It cannot assess the joint space as well as MRI, and it cannot demonstrate the deep surface of the acromioclavicular joint for capsular hypertrophy or spur formation, either of which may narrow the supraspinatus outlet and cause clinical impingement. It cannot demonstrate a torn supraspinatus tendon that has retracted more than 3 cm,21 but this is a relative

limitation because nonvisualization of the tendon edge indicates retraction at least beyond the top of the humeral head (i.e., beyond the 12 o’clock position). Although fatty atrophy of the supraspinatus muscle can be demonstrated as echogenic replacement of the muscle,22 a qualitative grading system of mild, moderate, or severe atrophy has yet to be developed.

●

A high frequency (5 to 12 MHz) transducer is used because the structures of interest are superficial and the transducer needs to be linear because tendons are highly ordered, linear structures. Tissue harmonic imaging, if used, may increase the conspicuity of tears but does not increase the diagnostic accuracy.23 The ultrasound beam must be perpendicular to the tendon, because angulation can create artifactual hypoechogenicity, simulating a tear. This artifact is called anisotropy, a sonographic phenomenon created when the highly organized parallel tendon fibers are not 90 degrees to the insonating beam (Fig. 6-6). To perform the sonographic examination, the patient is seated and the examiner may stand or sit and may face, be at the side, or be behind the patient. Unlike the sonographic evaluation of other joints in the body, which focuses on the specific tendon or ligament of clinical suspicion, the examination of the shoulder should encompass all four muscles and tendons of the rotator cuff, the tendon of the long head of the biceps, subdeltoid bursa, and acromioclavicular joint, because all of these structures may be involved in rotator cuff dysfunction. The posterior joint capsule, posterior labrum, and spinoglenoid notch can also be visualized and therefore should also be evaluated. To evaluate the biceps tendon, the forearm is supinated and placed on the thigh, bringing the bicipital groove anteriorly. By placing the transducer transversely across the humeral head, the long tendon of the biceps will be seen in cross section in the bicipital groove (Fig. 6-7). By turning the transducer longitudinally, the biceps tendon will appear as an echogenic fibrillar structure between the deltoid and humerus (Fig. 6-8). The tendon can be followed distally from its musculotendinous junction to its proximal aspect around the humeral head. The patient’s arm is then externally rotated, making sure to keep the elbow as close to the body as possible, thus bringing the subscapularis tendon into view in cross section, analogous to an oblique sagittal MR image (Fig. 6-9). By turning the transducer 90 degrees so that it is transverse to the arm, the longitudinal extent of the subscapularis tendon is seen as it inserts on the lesser tuberosity (Fig. 6-10). Some fibers extend across the bicipital groove, forming the transverse humeral ligament. To visualize the supraspinatus tendon, the patient’s hand is placed behind the back (the “Crass” position24) or on the buttock with the elbow pointed back (the “modified Crass” position). These maneuvers bring into view the distal aspect of the supraspinatus tendon, which would otherwise be obscured by the acromion. Either of these positions is accurate for diagnosis of

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● Normal Shoulder

111

B

■ FIGURE 6-6

Anisotropy. A, When the insonating sound beam (long arrows) is perpendicular to a linear structure, the sound waves are reflected back to the transducer (T). In this case, the beam is perpendicular to the biceps tendon (short solid arrows), thus demonstrating the echogenic fibrillar appearance of the biceps tendon. The echogenic cortex of the humerus is also visualized (striped-tail arrows). B, When the insonating beam is not perpendicular to the structure, the sound beams (long white arrows) are reflected away from the transducer (T), thus giving a hypoechoic or anechoic appearance to the tendon (short solid arrows). The cortex of the humerus is still seen (striped-tail arrows).

A ■ FIGURE 6-7

B

Biceps tendon in cross-section. A, An axial gradient-echo MR image shows the tendon of the long head of the biceps in crosssection (solid arrow). The subscapularis tendon is also seen (striped-tail arrow). The black box indicates the field of view that is visualized in the corresponding ultrasound image. B, Corresponding transverse sonographic image shows the echogenic biceps tendon (white arrow) within the bicipital groove. The distal aspect of the subscapularis tendon (striped-tail arrow) is hypoechoic due to anisotropy.

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A

B

■ FIGURE 6-8

Longitudinal view of the biceps tendon. A, Sagittal fat-suppressed T2-weighted MR image shows the tendon of the long head of the biceps (solid arrow). The cortex of the humerus is also seen (striped-tail arrow). The box indicates the field of view that is visualized in the corresponding ultrasound image. B, Corresponding longitudinal sonographic image of the biceps shows the echogenic fibrillar appearance (solid arrows). The underlying cortex of the humerus is also seen (striped-tail arrows).

A ■ FIGURE 6-9

B

Subscapularis tendon in cross-section. A, Oblique sagittal fat-suppressed T2-weighted MR image shows tendon slips of the subscapularis tendon (arrows). The box indicates the visualized field of view in the corresponding ultrasound image. B, Corresponding longitudinal ultrasound image shows the tendon slips of the subscapularis in cross-section (white arrows).

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● Normal Shoulder

113

B

■ FIGURE 6-10

Subscapularis tendon in longitudinal extent. A, Axial proton density MR image shows the subscapularis tendon (striped-tail arrow). The biceps tendon is located within the bicipital groove (solid arrow). The box indicates the visualized field of view in the corresponding sonographic image. B, Corresponding transverse sonographic image. The patient’s arm is mildly externally rotated, thus bringing the subscapularis tendon perpendicular to the insonating beam, thus allowing visualization of its fibrillary appearance (striped-tail arrows). The biceps tendon is still visualized within the groove (black arrow). Notice that the position of the bicipital groove indicates that the arm is externally rotated compared to Figure 6-7B.

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full-thickness tear of the supraspinatus tendon, but the modified Crass position overestimates the size of the tear in the transverse plane.25 The transducer should be oriented 45 degrees or approximately midway between the transverse and longitudinal planes to visualize the longitudinal course of the supraspinatus, analogous to the oblique coronal plane on MRI (Fig. 6-11). The transducer is then rotated 90 degrees to visualize the tendon in the transverse plane, analogous to an oblique sagittal MR image. In this plane, the deltoid muscle, which is hypoechoic with hyperechoic fascial planes, is just deep to the subcutaneous fat. Underneath the deltoid is the normally thin anechoic subacromial-subdeltoid bursa surrounded by thin hyperechoic peribursal fat. The supraspinatus tendon appears echogenic and sits directly on the humerus. A thin anechoic rim of cartilage covers the hyperechoic cortex (Fig. 6-12). As the transducer is moved anteriorly around the curvature of the humeral head in this oblique transverse plane, the biceps tendon will be seen in cross section. The biceps tendon is used as a reference point for measuring the location of tears or other abnormalities. The 2 cm of cuff tissue immediately posterior to the biceps tendon is the supraspinatus. Posterior to that is the infraspinatus. Finally, the posterior aspect of the shoulder is evaluated. The arm is brought forward again, and the

forearm is either placed on the thigh or the patient can be asked to reach across his or her chest to the contralateral arm. The transducer is positioned just inferior to and parallel to the spine of the scapula. The infraspinatus muscle is followed laterally as it crosses the joint and becomes the tendon, to its insertion on the greater tuberosity (Fig. 6-13). By sliding the transducer medially, the posterior aspects of the humeral head and glenohumeral joint will be seen. The posterior glenoid labrum appears as a homogeneous hyperechoic triangle (Fig. 6-14). Sliding the transducer even more medially will bring the spinoglenoid notch into view (Fig. 6-15).

NORMAL ANATOMY Osseous Structures The osseous structures forming the shoulder joints include the scapula, the clavicle, and the proximal humerus. The articular surface of the glenoid articulates with the humeral head. The acromion process along with the coracoid process and the coracoacromial ligament form the acromial arch under which the supraspinatus and infraspinatus muscles and tendons glide during abduction and adduction of the arm.

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A

B

■ FIGURE 6-11

Supraspinatus tendon longitudinally. A, Oblique coronal proton density MR image shows the longitudinal extent of the supraspinatus tendon (solid arrow) inserting on the greater tuberosity (striped-tail arrow). The box indicates the visualized field of view in the corresponding sonographic image. B, Corresponding longitudinal sonographic image shows the fibrillar echogenic appearance of the supraspinatus tendon (solid white arrows) inserting on the greater tuberosity (striped-tail black arrow). The focal area of hypoechogenicity within the supraspinatus tendon (A) is due to anisotropy. Notice the thin stripes of echogenic peribursal fat (striped-tail white arrows).

A ■ FIGURE 6-12

B

Supraspinatus tendon in cross-section. A, Oblique sagittal fat-suppressed T2-weighted MR image shows the supraspinatus tendon (S) in cross-section. The supraspinatus tendon overlies the bright stripe of articular cartilage (solid black arrow). The thin peribursal fat overlies the supraspinatus tendon (white arrow). The biceps tendon is seen in cross section anteriorly (striped-tail black arrow). The box indicates the field of view visualized in the corresponding sonographic image. B, Corresponding transverse sonographic image shows the supraspinatus tendon (S) overlying the thin hypoechoic stripe of articular cartilage (black arrow). The overlying echogenic peribursal fat is visualized (solid white arrow). The echogenic biceps tendon in cross section is also seen anteriorly (striped-tail white arrow).

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115

B

■ FIGURE 6-13

Infraspinatus tendon longitudinally. A, Oblique coronal proton density MR image shows the infraspinatus tendon (arrow) inserting on the posterior aspect of the greater tuberosity. The box indicates the field of view visualized in the corresponding ultrasound image. B, Corresponding transverse ultrasound image shows the longitudinal extent of the infraspinatus tendon (solid white arrows). The overlying peribursal fat is seen (striped-tail arrows).

A ■ FIGURE 6-14

B

Posterior labrum. A, Axial proton density MR image shows the low signal intensity posterior labrum (white arrow). The posterior aspect of the humeral head is also seen (black arrow). The box indicates the field of view visualized in the corresponding sonographic image. B, Corresponding transverse sonographic image shows the echogenic triangular-shaped posterior labrum (striped-tail arrow) lying adjacent to the thin echogenic cortex of the humeral head (solid arrow).

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A

B

■ FIGURE 6-15

Spinoglenoid notch. A, Transverse proton density MR image shows the spinoglenoid notch (striped-tail arrow) filled with fibrofatty tissue. The posterior labrum (solid white arrow) and posterior aspect of the humeral head are visualized (black arrow). The box indicates the field of view visualized in the corresponding sonographic image. B, Corresponding transverse sonographic image shows the spinoglenoid notch (striped-tail arrow) filled with echogenic fibrofatty tissue. The echogenic posterior labrum (solid short white arrow) and cortex of the posterior aspect of the humeral head (long white arrow) are visualized.

The Labrum The glenoid labrum is a fibrous structure surrounding the edge of the osseous glenoid. It increases the depth of the glenoid fossa and hence the stability of the glenohumeral joint. However, its more important function is to serve as the anchoring structure for the glenohumeral ligaments and the long head of the biceps tendon, superiorly (Fig. 6-16). The normal labrum is firmly attached to the glenoid margin of the scapula and the scapular periosteum.

The Joint Capsule The joint capsule inserts in the glenoid margin of the scapula and in the anatomic neck of the humerus. There are two main recesses of the capsule: the subscapularis recess and the axillary recess. The subscapularis recess is located between the coracoid process superiorly and the superior margin of the subscapularis tendon. The axillary recess is located between the anterior and posterior bands of the inferior glenohumeral ligament. The capsular mechanism provides the most important contribution to the stabilization of the glenohumeral joint. The anterior capsular mechanism includes the fibrous capsule, the glenohumeral ligaments, the synovial

■ FIGURE 6-16

The glenoid labrum (see Table 6-4).

CHAPTER

membrane and its recesses, the fibrous glenoid labrum, the subscapularis muscle and tendon, and the scapular periosteum. The posterior capsular mechanism is formed by the posterior capsule, the synovial membrane, the glenoid labrum and periosteum, and the posterosuperior tendinous cuff and associated muscles (supraspinatus, infraspinatus, and teres minor). The long head of the biceps tendon inserting in the superior aspect of the labrum and the triceps tendon inserting in the infraglenoid tubercle inferiorly constitute additional supportive structures of the glenohumeral joint.

The Ligaments The glenohumeral ligaments are infoldings of the capsule (see Fig. 6-16). The superior glenohumeral ligament is a fairly constant structure that arises in the shoulder capsule just anterior to the insertion of the long head of the biceps tendon and inserts into the fovea capitis line just superior to the lesser tuberosity. The middle glenohumeral ligament has been described arthroscopically as being attached to the anterior surface of the scapula, medial to the articular margin. It then lies obliquely, posterior to the superior margin of the subscapularis muscle, and blends with the anterior capsule. Distally it is attached to the anterior aspect of the proximal humerus, below the attachment of the superior glenohumeral ligament.26,27 With the use of MR arthrography, the scapular insertion of the middle glenohumeral ligament is seen more often at the level of the superior anterior labrum than at the level of the scapula as was suggested arthroscopically.26,27 The inferior glenohumeral ligament is composed of an anterior band, a posterior band, and the axillary recess of the capsule located in between the two bands. It inserts in a collar-like fashion in the inferior aspect of the anatomic neck of the humerus. The coracohumeral ligament is an extracapsular structure located superior to the long head of the biceps tendon. Additional ligamentous structures include the coracoclavicular ligaments and the spinoglenoid ligament.

The Long Head of the Bicipital Tendon The long head of the biceps tendon has an intracapsular portion and an extracapsular portion. The intracapsular portion extends from its insertion into the superior labrum to the bicipital groove. There are four components to the origin of the long head of the biceps. These include fibers from the supraglenoid tubercle, superior posterior labrum, and superior anterior labrum and a final set of fibers that becomes extra-articular curves medially and attaches to the lateral edge of the base of the coracoid process.

The Rotator Cuff The rotator cuff is composed of the supraspinatus, the infraspinatus, the subscapularis, and the teres minor muscles and their corresponding tendons (see Figs. 6-3 to 6-5). The supraspinatus muscle has two tendon slips that

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become a single tendon 7 to 10 cm proximal to its insertion in the greater tuberosity of the humerus. A hypovascular zone called the critical zone is present at 3 to 4 cm proximal to its insertion. The orientation of the tendons of the supraspinatus muscle does not follow the longitudinal axis of the muscle, but they are at an angle of 5 to 7 degrees. Just below the acromial arch, the supraspinatus tendon turns downward about 55 degrees, to insert in the greater tuberosity. The infraspinatus muscle has three to five tendon slips that join into a single tendon near its insertion just below the insertion of the supraspinatus tendon. The teres minor muscle has a single tendon. Between the supraspinatus and infraspinatus muscles there is a fat plane that allows easy identification of the two muscle groups. There is no fat plane between the infraspinatus and the teres minor muscles. The subscapularis muscle has multiple tendon slips that merge into a broad tendon inserting in the lesser tuberosity of the humerus. The distal fibers of the subscapularis tendon merge with the transverse ligament that serves as the roof for the bicipital groove, occupied by the long head of the biceps tendon.The short head of the biceps tendon inserts in the tip of the coracoid process along with the tendons of the pectoralis minor and the coracobrachialis muscles. The space between the anterior margin of the supraspinatus muscle and the superior margin of the subscapularis muscle is called the rotator cuff interval. The joint capsule covers this space, and it contains the long head of the biceps tendon, the coracohumeral ligament, and the superior glenohumeral ligament.

The Deltoid Muscle The deltoid is triangular with anterior, middle, and posterior fibers converging to insert into the midhumeral shaft laterally (deltoid tuberosity). The stronger multipennate middle fibers arise from the lateral border of the acromion. The anterior fibers arise from the lateral third of the anterior border of the clavicle. The posterior fibers arise from the lower border of the spine of the scapula.

The Bursae There are several synovial bursae around the shoulder, the most important being the subacromial subdeltoid bursa, located between the rotator cuff and the acromion and deltoid muscle. Under normal circumstances this bursa does not communicate with the joint space and is not seen on MRI unless it is distended by fluid. The subcoracoid bursa, located in the subcoracoid space, is normally bordered by the coracoid process and combined tendon of the coracobrachialis and short head of the biceps anterosuperiorly and by the subscapularis tendon posteroinferiorly. Differentiation from the superior subscapularis recess, the other structure in the subcoracoid space, can be made on MRI on the basis of their anatomic relationships. The subcoracoid bursa is located between the subscapularis muscle and the coracoid process, whereas the superior subscapularis recess, also

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■ FIGURE 6-17

Neurovascular branches for the infraspinatus muscle.

known as the subscapularis bursa, is located between the anterior surface of the scapula and the subscapularis muscle. The subcoracoid bursa does not communicate with the glenohumeral joint and is separated from the subscapularis recess by an identifiable fibrous septum. However, the subcoracoid bursa may communicate with the subacromial/subdeltoid bursa in about 20% of people. The normal subcoracoid bursa is usually not identified on MRI unless distended by fluid.28

The Neurovascular Bundles The suprascapular nerve and vessels run under the suprascapular ligament of the scapula, at the level of the suprascapular notch. At this point they divide in branches for the supraspinatus and infraspinatus muscles. The branches for the infraspinatus muscle run under the spinoglenoid ligament in the posterior aspect of the scapula, near the posterior glenoid margin (Fig. 6-17). The teres minor and deltoid muscles are innervated by branches of the axillary nerve passing through the quadrilateral space created between the humeral shaft, the triceps muscle, and the teres major and minor muscles (Fig. 6-18).

MOST SIGNIFICANT NORMAL VARIANTS Shape of the Undersurface of the Acromion The shape of the undersurface of the acromion has been classified in three types (Fig. 6-19).46 Type I acromion has a flat undersurface (see Fig. 6-19A). Type II has a curved undersurface (see Fig. 6-19B), and type III has a hooked

■ FIGURE 6-18

Innervation of the teres minor and deltoid muscles.

anterior undersurface (see Fig. 6-19C). A type IV acromion, convex inferiorly, has also been described (see Fig. 6-19D). Although still controversial, it has been stated that the type III hooked acromion is associated with a high incidence of rotator cuff pathology.

Os Acromiale The os acromiale results from failure of fusion of an acromial accessory ossification center. This failure of fusion can occur at one of three separate sites (different from that of a normal fusing apophysis) on the anterior aspect of the acromion, resulting in a preacromion, mesoacromion, or metacromion.29 Historically, the diagnosis is usually not made until after age 25. However, the frequency of os acromiale ranges from 1.3% to 15% with bilateral involvement ranging from 33% to 62%.30 It occurs with a higher frequency in males and blacks.31 Identification of an os acromiale is important because it has been implicated as a cause of rotator cuff tear and impingement symptoms (Fig. 6-20).

Sublabral Foramen and Sublabral Recess The anterior superior labrum is frequently partially detached, creating a space between the glenoid and the labrum called the sublabral foramen or sublabral hole, not to be confused with an anterosuperior labral tear when performing arthroscopy or MRI (Fig. 6-21). A second potential space or recess may exist between the superior labrum and the glenoid, and it is termed the sublabral recess or sublabral sulcus, often confused with a superior labral tear (Fig. 6-22).

CHAPTER

A

B

C

D

■ FIGURE 6-19

■ FIGURE 6-20

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Normal variants of acromion shape: type I (A), type II (B), type III (C), and type IV (D).

Os acromiale (arrows).

■ FIGURE 6-21 The sublabral foramen. Long arrow, sublabral foramen; single arrowhead, anterior superior labrum; short arrow, anterior glenoid margin; double short arrows, middle glenohumeral ligament.

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study, the ligament was absent in 30% of the specimens.32 In Chandnani’s series27 the middle glenohumeral ligament was identified with MR arthrography in 85% of their cases. Other frequent variants include the common origin of the middle glenohumeral ligament with the superior glenohumeral ligament; the common origin with the superior glenohumeral ligament and long biceps tendon; the common origin with the inferior glenohumeral ligament; cord-like thickening, with or without associated absence of the anterior superior portion of the labrum (Buford complex) (Fig. 6-23); and split or duplicate ligament.33,34

Anterior Capsular Insertion The anterior capsular insertion can be divided into three types depending on the proximity of the capsular insertion to the glenoid margin (Fig. 6-24). In general, the further the anterior capsular insertion from the glenoid margin (type III), the more unstable will be the glenohumeral joint. However, the MRI appearance of the anterior capsular insertion may vary with the arm in external or internal rotation. In internal rotation the capsular insertion may appear more medial (type III), and with the arm in external rotation it may appear more lateral (type I).

■ FIGURE 6-22 The sublabral recess (sublabral sulcus) (long arrow). Short arrows show articular cartilage in the glenoid fossa.

Variations of the Glenohumeral Ligaments

Insertion of the Long Head of the Biceps Tendon

Significant anatomic variations of the glenohumeral ligaments are recognized. The superior glenohumeral ligament varies in thickness, and it is present 90% to 97% of the time in cadaveric dissections. The middle glenohumeral ligament presents the largest multiplicity of normal variants. In one anatomic

The insertion of the long head of the biceps tendon may be in a broad base or in a thin area. It may have a predominant anterior or predominant posterior insertion. The predominant posterior insertion is prone to superior labral tears with posterior extension of the tear in the throwing athlete.

A ■ FIGURE 6-23

B A and B, Buford complex. Note the absent anterior superior labrum and the thick middle glenohumeral ligament (arrows).

CHAPTER

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BASIC BIOMECHANICS Normal Biomechanics

A

B

The function of the shoulder requires the coordinated motion of five joints: the scapuloclavicular, acromioclavicular, glenohumeral, and scapulothoracic joints. Almost 30 muscles contribute to the motion of this joint complex. Most of the motion occurs at the level of the glenohumeral and scapulothoracic joints. The glenohumeral joint is the joint of the human body with the greatest range of motion: 0 to 180 degrees in elevation, internal and external rotation of 150 degrees, and anterior and posterior rotation in the horizontal plane of approximately 170 degrees. The relatively large articular surface of the humeral head compared with the small articular surface of the glenoid cavity explains the extended mobility of the joint. Because of its wide range of motion, the glenohumeral joint is also more susceptible to dislocations, subluxations, and lesions related to chronic stress in the surrounding soft tissues. With the arm at 90 degrees of abduction, a normal range of 90 to 110 degrees of internal and external rotation is easily achieved in the normal individual. During internal and external rotation, the humeral head rotates within the glenoid fossa centered in one point located in the fovea. During external rotation with the arm in abduction, the greater tuberosity of the humerus describes an arc from anterior to posterior.

The Overhead Throwing Mechanism

C ■ FIGURE 6-24 A to C, Normal variants of the anterior capsular insertion, differentiated by the proximity to the glenoid margin.

The overhead throwing action places high stress loads on the capsulolabral complex and rotator cuff, and even minor degrees of injury to these structures can become symptomatic and produce significant functional impairment. Joint laxity may develop as a consequence of the injury to the tissues, leading to even more damage and further instability. It is now understood that in the throwing athlete these injuries are not the consequence of a single event of dislocation but are the result of multiple episodes of microtrauma producing gradual increase of shoulder pain at some point in the throwing position. To understand the pathophysiology of the glenohumeral instability in the throwing athlete it is important to know the normal joint motion during the action of throwing. With minor differences, overhead throwing, the volleyball spike, the golf swing, and the tennis serve all have similar throwing mechanics.35,36 There are six phases in the overhead throwing motion (Fig. 6-25): wind-up, early cocking, late cocking, acceleration, deceleration, and follow-through. During the wind-up phase there is minimal stress loading and muscular activity of the shoulder. At the end of this phase the shoulder is in minimal internal rotation and slight abduction (positions 1 and 2, see Fig. 6-25A and B). During the second phase of early cocking the shoulder reaches 90 degrees of abduction and 15 degrees of horizontal abduction (elbow posterior to the coronal plane of the torso) (position 3, see Fig. 6-25C). During this phase there is early activation of the deltoid muscle and late activation of the rotator cuff muscles, with the exception of the subscapularis muscle. During the third phase of late cocking the shoulder ends in maximum external rotation of 170 to 180 degrees, main-

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A

D ■ FIGURE 6-25

follow-through.

C

B

F

E

A to F, The six phases in the overhead throwing motion: wind-up, early cocking, late cocking, acceleration, deceleration, and

CHAPTER

taining 90 to 100 degrees of abduction. The 15 degrees of horizontal abduction changes to 15 degrees of horizontal adduction (position 4, see Fig. 6-25D). The scapula retracts to facilitate this position and provide a stable base for the humeral head.The combination of abduction and external rotation forces posterior translation of the humeral head on the glenoid. The activity of the deltoid muscle decreases while that of the rotator cuff muscles reaches its peak. During the terminal portion of the late cocking phase, the subscapularis, latissimus dorsi, pectoralis major, and serratus anterior muscles increase their activity. During the fourth phase of acceleration, abduction is maintained while the shoulder rotates to the ball release (position 5, see Fig. 6-25E). The scapula protracts as the body moves forward and the humeral head re-centers in the glenoid fossa, decreasing the stress on the anterior capsule. During the early acceleration phase the triceps muscle shows marked activity, whereas the latissimus dorsi, pectoralis major, and serratus anterior muscles increase their activity during the late acceleration phase. During the fifth phase of deceleration the energy not imparted to the ball is dissipated. It begins at the moment of ball release, and it ends with cessation of humeral rotation to 0 degrees. Abduction is maintained at 100 degrees, and horizontal adduction increases to 35 degrees. All muscle groups contract violently, with eccentric contraction, allowing the arm to slow down. During this phase joint loads are very high posteriorly and inferiorly. Additional compressive forces are generated through strong contraction of the bicep muscle. During the sixth phase of follow-through the body moves forward with the arm until the motion ceases. Shoulder rotation decreases to 30 degrees, horizontal adduction increases to 60 degrees, and abduction is maintained at 100 degrees while joint loads decrease, ending in adduction (position 6, see Fig. 6-25F).

Joint Stability The stability of the glenohumeral joint is maintained by the presence of active and passive mechanisms depending on whether muscle energy is used. Active mechanisms include the biceps tendon and the rotator cuff muscles and tendons. Passive mechanisms include the labrum, the joint capsule, and the superior, middle, and inferior glenohumeral ligaments, which reinforce the joint capsule anteriorly. The relative contribution of each of the glenohumeral ligaments to joint stability has been the subject of debate. Matsen and colleagues37 and Caspari and associates38 indicated that the superior and middle glenohumeral ligaments are absent in a high percentage of individuals; therefore, they must not be important structures in maintaining joint stability. Turkel and associates39 studied the contribution of each one of the glenohumeral ligaments by means of selectively cutting these structures in cadavers and then assessing the stability of the joint at different degrees of abduction and external rotation. They concluded that the

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inferior glenohumeral ligament is the most important structure in the prevention of dislocation with the arm at 90 degrees of abduction and external rotation. In another classic experiment, O’Connell and coworkers40 measured the tension of the glenohumeral ligaments in cadavers after application of a controlled external torque. They concluded that at 90 degrees of arm abduction, the inferior and middle glenohumeral ligaments developed the most strain, whereas with the arm at 45 degrees of abduction, the most strain was also developed by the inferior and middle glenohumeral ligaments, but some strain also occurred at the superior glenohumeral ligament. The inferior glenohumeral ligament is considered the most important stabilizer of the glenohumeral joint, especially with the arm in abduction and external rotation (the throwing position). In this position the anterior band is under tension. If the arm is placed in abduction and internal rotation, the posterior band is in more tension than the anterior band. The long head of the biceps tendon and the coracohumeral and coracoacromial ligaments are also important structures contributing in different ways to the normal biomechanics of the joint. The coracohumeral ligament helps in maintaining the stability of the long head of the biceps tendon, and the acromion humeral ligament is an important part of the acromial arch.The long head of the biceps tendon has an intracapsular portion and an extracapsular portion. The intracapsular portion extends from its insertion into the superior labrum to the bicipital groove. The insertion of the tendon may be in a broad base or in a thin area. The muscles around the shoulder are important contributors to the stability of the shoulder joint. The rotator cuff muscles provide internal and external rotation and some degree of abduction and, along the long bicipital tendon, provide dynamic compression of the humeral head into the glenoid fossa, centering the humeral head and countering the oblique translational forces generated during the act of throwing.41,42 It has been demonstrated by Warner and colleagues43 that this concavity-compression mechanism provides greater stability to the glenohumeral joint in the inferior direction than negative intra-articular pressure or ligament tension in all degrees of abduction and rotation. Another significant factor contributing to the stability of the glenohumeral joint is the scapulothoracic coordination during throwing. This is achieved mainly through synchronization with the latissimus dorsi, pectoralis major, and serratus anterior muscles.35 There is a 2:1 ratio of glenohumeral to scapulothoracic motion during abduction. More recent studies indicate that this ratio is even higher and that it is more significant during the early degrees of abduction.36 Failure of the scapulothoracic coordination may place additional stress on the capsulolabral complex, hence increasing the risk for soft tissue damage. It has been shown that patients with shoulder instability have increased scapulothoracic asymmetry.

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SUGGESTED READINGS Beltrán J, Bencardino J, Mellado J, et al. MR arthrography of the shoulder: variations and pitfalls. Radiographics 1997; 17:1403–1412. Bitzer M, Nasko M, Krackhardt T, et al. Direct CT-arthrography versus direct MR-arthrography in chronic shoulder instability: comparison of modalities after the introduction of multidetector-CT technology. Rofo 2004; 176:1770–1775. De Maeseneer M, Van Roy F, Lenchik L, et al. CT and MR arthrography of the normal and pathologic anterosuperior labrum and labralbicipital complex. Radiographics 2000; 20(spec no):S67–S81. Kopka L, Funke M, Fischer U, et al. MR arthrography of the shoulder with gadopentetate dimeglumine: influence of concentration,

iodinated contrast material, and time on signal intensity. AJR Am J Roentgenol 1994; 163:621–623. Matsen FA III, Thomas SC, Rockwood CA Jr. Anterior glenohumeral instability. In Rockwood CA, Marsen FA III (eds). The Shoulder. Philadelphia, WB Saunders, 1990 pp 526–622. Rafii M. The shoulder. In Firooznia H, et al (eds). MRI and CT of Musculoskeletal System. St. Louis, Mosby-Year Book, 1991, pp 465–549. Steinbach LS, Palmer WE, Schweitzer ME. Special focus session: MR arthrography. Radiographics 2002; 22:1223–1246.

REFERENCES 1. Vahlensieck M, Peterfl CG, Wischer T, et al. Indirect MR arthrography: optimization and clinical applications. Radiology 1996; 200:249–254. 2. Lee SY, Lee JK. Horizontal component of partial thickness tears of rotator cuff: imaging characteristics and comparison of ABER view with oblique coronal view at MR arthrography —initial results. Radiology 2002; 224:470–476. 3. Farmer KD, Hughes PM. MR arthrography of the shoulder: fluoroscopically guided technique using a posterior approach. AJR Am J Roentgenol 2002; 178:433–434. 4. Bergin D, Schweitzer ME. Indirect magnetic resonance arthrography. Skeletal Radiol 2003; 32:551–558. 5. Jacobson JA, Lin J, Jamadar D, et al. Aids to successful shoulder arthrography performed with a fluoroscopically guided anterior approach. Radiographics 2004; 23:373–379. 6. Chung CB, Dwek JR, Feng S, et al. MR arthrography of the glenohumeral joint: a tailored approach. AJR Am J Roentgenol 2001; 177:217–219. 7. Helgason JW, Chandanani VP, Yu JS. MR arthrography: a review of current technique and applications. AJR Am J Roentgenol 1997; 168:1473–1479. 8. Hajek PC, Baker LL, Sartoris DJ, et al. MR arthrography: anatomicpathologic investigation. Radiology 1987; 163:141–147. 9. Kopka L, Funke M, Fischer U, et al. MR arthrography of the shoulder with gadopentetate dimeglumine: influence of concentration, iodinated contrast material, and time on signal intensity. AJR Am J Roentgenol 1994; 163:621–623. 10. Matsuzaki S, Yoneda M, Kobayashi Y, et al. Dynamic enhanced MRI of the subacromial bursa: correlation with arthroscopic and histologic findings. Skeletal Radiol 2003; 32:510–520. 11. Brenner ML, Morrison WB, Carrino JA, et al. Direct MR arthrography of the shoulder: is exercise prior to imaging beneficial or detrimental? Radiology 2000; 215:491–496. 12. Chan KK, Muldoon KA, Yeh L, et al. Superior labral anteroposterior lesions: MR arthrography with arm traction. AJR Am J Roentgenol 1999; 173:1117–1122. 13. Adler RS, Sofka CM. Percutaneous ultrasound-guided injections in the musculoskeletal system. Ultrasound Q 2003; 19:3–12. 14. Binkert CA, Zanetti M, Holder J. Patient’s assessment of discomfort during MR arthrography of the shoulder. Radiology 2001; 221:775–778. 15. Schydlowsky P, Strandberg P, Galbo H, et al. The value of ultrasonography in the diagnosis of labral lesions in patients with anterior shoulder dislocations. Eur J Ultrasound 1998; 8:107–113. 16. Taljanovic MS, Carlson KL, Juhn JE, et al. Sonography of the glenoid labrum: a cadaveric study with arthroscopic correlation. AJR Am J Roentgenol 2000; 174:1717–1722. 17. Hammar MV, Wintzell GB, Astrom KG, et al. Role of US in the preoperative evaluation of patients with anterior shoulder instability. Radiology 2001; 219:29–34. 18. Sugimoto K. Ultrasonographic evaluation of the Bankart lesion. J Shoulder Elbow Surg 2004; 13:286–290.

19. Middleton WD, Payne WT, Teefey SA, et al. Sonography and MRI of the shoulder: comparison of patient satisfaction. AJR Am J Roentgenol 2004; 183:1449–1452. 20. Erickson SJ. High-resolution imaging of the musculoskeletal system. Radiology 1997; 205:593–618. 21. Kluger R, Mayrhofer R, Kroner A, et al. Sonographic versus magnetic resonance arthrographic evaluation of full-thickness rotator cuff tears in millimeters. J Shoulder Elbow Surg 2003; 12:110–116. 22. Sofka CM, Haddad ZK, Adler RS. Detection of muscle atrophy on routine sonography of the shoulder. J Ultrasound Med 2004; 23:1031–1034. 23. Strobel K, Zanetti M, Nagy L, Hodler JH. Suspected rotator cuff lesions: tissue harmonic imaging versus conventional US of the shoulder. Radiology 2004; 230:243–249. 24. Crass JR, Craig EV, Feinberg SB. The hyperextended internal rotation view in rotator cuff ultrasonography. J Clin Ultrasound 1987; 15:416–420. 25. Ferri M, Finlay K, Popowich T, et al. Sonography of full-thickness supraspinatus tears: comparison of patient positioning technique with surgical correlation. AJR 2005; 184:180–184. 26. Caspari RB, Geissler WB. Arthroscopic manifestations of shoulder subluxation and dislocation. Clin Orthop Relat Res 1993; 291:54–66. 27. Chandnani VP, Gagliardi JA, Murnane TG, et al. Glenohumeral ligaments and shoulder capsular mechanism: evaluation with MR arthrography. Radiology 1995; 196:27–32. 28. Grainger AJ, Tirman PF, Elliott JM, et al. MR anatomy of the subcoracoid bursa and the association of subcoracoid effusion with tears of the anterior rotator cuff and the rotator interval. AJR Am J Roentgenol 2000; 174:1377–1380. 29. Sammarco VJ. Os acromiale: frequency, anatomy, and clinical implications. J Bone Joint Surg Am 2000; 82:394–400. 30. Park JG, Lee JK, Phelps CT. Os acromiale associated with rotator cuff impingement: MR imaging of the shoulder. Radiology 1994; 193:255–257. 31. Macalister A. Notes on the acromion. J Anat Physiol 1893; 27:245–251. 32. Moseley HF, Overgaard B. The anterior capsular mechanism in recurrent anterior dislocation of the shoulder. J Bone Joint Surg Br 1962; 44:913–927. 33. Tirman PFJ, Feller JF, Palmer WE, et al. The Buford complex—a variation of normal shoulder anatomy: MR arthrographic imaging features. AJR Am J Roentgenol 1996; 166:869–873. 34. Williams MM, Snyder SJ, Buford D. The Buford complex—the cordlike middle glenohumeral ligament and absent anterosuperior labrum complex: a normal anatomic capsulolabral variant. Arthroscopy 1994; 10:241–247. 35. Meister K. Injuries to the shoulder in the throwing athlete: I. Biomechanics/pathophysiology/classification. Am J Sports Med 2000; 2:265–275. 36. Pink M, Jobe FW, Perry J. Electromyographic analysis of the shoulder during the golf swing. Am J Sports Med 1990; 18:137–140. 37. Matsen FA, Harryman DT, Sidles JA. Mechanics of glenohumeral instability. Clin Sports Med 1991; 10:783–788.

CHAPTER 38. Caspari RB, Geissler WB. Arthroscopic manifestations of shoulder subluxation and dislocation. Clin Orthop Relat Res 1993; 291:54–66. 39. Turkel SJ, Panio MW, Marshall JL, et al. Stabilizing mechanisms preventing anterior dislocations of the glenohumeral joint. J Bone Joint Surg Am 1981; 63:1208–1217. 40. O’Connell PW, Nuber GW, Mileski RA, et al. The contribution of the glenohumeral ligaments to anterior stability of the shoulder joint. Am J Sports Med 1990; 18:579–584.

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41. Itoi E, Keuchle DK, Newman SR, et al. Stabilizing function of the biceps in stable and unstable shoulders. J Bone Joint Surg Br 1993; 75:546–550. 42. Pagnani MJ, Deng XH, Warren RF, et al. Role of the long head of the biceps brachii in glenohumeral stability: a biomechanical study in cadavera. J Shoulder Elbow Surg 1996; 5:255–262. 43. Warner J, Bowen M, Deng X, et al. Effect of joint compression on inferior stability of the glenohumeral joint. J Shoulder Elbow Surg 1999; 8:31–36.

C H A P T E R

7

Osseous Injuries of the Shoulder Girdle Joseph S. Yu

PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS Osseous injuries that affect the shoulder girdle are common in adults. The acromioclavicular joint is the primary connection between the arm and the thorax, and the glenohumeral joint is inherently unstable, owing to the disproportionate size of the articular surfaces of this spheroidal joint. The majority of injuries occur from either a direct impact on a focal point on the shoulder or from a fall on an outstretched hand, resulting in both fractures and dislocations in this area of the skeleton. Shoulder injuries have no particular predilection to the sex of the patient but do appear to be somewhat age dependent.1 For instance, glenohumeral joint dislocation and acromioclavicular joint separation occur in young people, whereas fractures of the surgical neck of the humerus most frequently occur in the elderly or those with osteoporosis.2 Fractures of the scapula are uncommon, owing to the protective covering of the adjacent musculature. In this chapter, a review of the osseous injuries of the shoulder that affect the acromioclavicular, sternoclavicular, and glenohumeral joints is presented along with some of the more commonly used classification systems that describe related injury patterns.

Anatomy The anatomic configuration of the shoulder is complex because it incorporates three bones with strikingly different shapes into three different articulations.3 The clavicle is slightly S shaped and has a unique purpose in serving as the only osseous connection between the arm and the trunk. It is one of the first bones to ossify, although the medial epiphysis does not fuse until the second decade of life. Medially, it is broad and articulates with the manubrium at the sternoclavicular joint and the first rib. The sternoclavicular joint is a gliding synovial joint with an 126

KEY POINTS Osseous injuries of the shoulder girdle are common. They often coexist with ligamentous injuries or muscle tears. ■ The shoulder is the most unstable joint in the skeleton and thus most frequently dislocated. ■ The clavicle is the only osseous connection between the arm and the trunk. ■ The most common location of clavicle fracture is the middle one third of the bone, but lateral and medial fractures have higher morbidity. ■ Acromioclavicular joint separations may be subtle. Weight-bearing views are not necessary if there is asymmetric widening of the joint space or coracoclavicular distance. ■ Sternoclavicular joint dislocation often requires CT for further evaluation. Although anterior dislocations are much more common, posterior dislocations are associated with more potentially severe complications. ■ Anterior glenohumeral joint dislocations often require further evaluation by MRI to evaluate the labrocapsular integrity. However, CT should be considered when an osseous Bankart lesion is small. ■ Trough lesions and posterior glenoid rim fractures are more optimally evaluated with CT. ■ Scapular fractures are difficult to evaluate radiographically. CT is advocated if there is concern for extension into the glenoid or suprascapular notch. ■ Comminuted fractures of the proximal humerus should be evaluated with CT because the number of fragments and the severity of displacement affect the treatment regimen. ■ The majority of shoulder injuries are treated conservatively, but it is important to understand when a lesion requires surgical management, because many of these injuries have to be promptly addressed to avoid future complications. ■

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articular disc that divides the joint into a medial and lateral compartment. It is supported by the interclavicular, costoclavicular, anterior sternoclavicular, and posterior sternoclavicular ligaments. Laterally, the clavicle is relatively flat and articulates with the acromion process of the scapula at the acromioclavicular joint and occasionally the coracoid process. The acromioclavicular joint is a synovial joint that also serves as a gliding joint. Development of an intra-articular disc is variable. The capsule is supported by the superior and inferior acromioclavicular ligaments and the coracoclavicular ligaments. The scapula is a large, flat triangular bone dorsal to the thoracic cage and is almost entirely surrounded by muscles. It develops from several ossification centers that fuse by the second decade of life, giving rise to the tubercles and processes that serve as attachments to the muscles and connective tissues. The glenohumeral joint of the shoulder is the most mobile joint in the body. The glenoid fossa is small and shallow, articulating at any one time with a small area of the humeral head, which is disproportionately large.4 The glenoid joint surface is perpendicularly oriented to the axis of the axial skeleton, therefore providing no inferior osseous support. Furthermore, because the scapula is anteverted, there is also minimal osseous support anteriorly. Stability is enhanced by soft tissue constraints such as the rotator cuff tendons, capsule, and the intra-articular glenohumeral ligaments and coracohumeral ligament.

MANIFESTATIONS OF THE DISEASE Appropriately, evaluation of the shoulder girdle begins with a radiographic inspection of the osseous structures and joints. A conventional radiographic examination allows for adequate depiction of the clavicle and proximal humerus and is useful in giving an impression of the alignment of the acromioclavicular and glenohumeral joints. But there are limitations associated with the radiographic evaluation. An important limitation of radiographs is often an inadequate assessment of the scapula. Nondisplaced fractures of the humerus and glenoid rim in cases of shoulder dislocation may not be conspicuous, and these findings can be an important indicator of instability. Additionally, complex fractures or fracture-dislocation complexes are difficult to characterize radiographically, owing to the displacement of osseous fragments. In these situations, CT assumes an important role. The availability of multidetector CT has enabled rapid and accurate evaluation of osseous injuries of the shoulder, and the depiction of acute osseous abnormalities in an infinite number of imaging planes has rendered CT an indispensable modality for assessment of bone integrity and joint configuration.5 Although CT is an excellent imaging tool for demonstrating the integrity of the osseous cortex, it does not depict the connective and cartilaginous tissues of the shoulder girdle as well as MRI, even in the setting of arthrography. The main advantage of MRI is the ability to directly visualize the joint capsule, labrum, articular cartilage, tendons, and supporting ligamentous structures. MR arthrography has further improved our ability to assess the components

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of the glenohumeral joint, including the attachment of the capsule and labrum, the glenohumeral ligaments, and the articular side of the rotator cuff. MRI is outstanding for assessing shoulder instability, but in the setting of acute trauma it is also useful for depicting marrow edema associated with contusions and occult fractures.4,6–8

Acute Osseous Injuries of the Clavicle The clavicle has a unique purpose in serving as the only osseous bridge between the arm and the thorax. As such, it is a vulnerable bone in trauma, particularly in childhood and adolescence, accounting for nearly 50% of fractures in children younger than 10 years of age.9 A fall directly on the shoulder during play or as a result of an athletic activity is the etiology of the fracture in over 90% of cases.10 A small percentage of fractures occur from a direct blow to the clavicle, such as those occurring in a motor vehicle–related trauma or assault and rarely from a fall on an outstretched hand. A clavicular fracture is also a common fracture of childbirth (Fig. 7-1).11 The delivery of the child through the birth canal may place excessive pressure of the anterior shoulder against the maternal symphysis pubis, producing failure of the bone that characteristically occurs between the middle and lateral one third of the clavicle.12

Radiography In general, 80% of fractures of the clavicle occur in the middle one third of the bone (Fig. 7-2).13 Typically, these fractures are simple and transversely oriented but are occasionally comminuted. Displacement is common, owing to the pull of the sternocleidomastoid muscle on the medial fragment and the depression of the lateral fragment from the weight of the arm, and sometimes these two fragments can overlap each other.2,14 When the fracture is severe or is caused by direct impaction against the bone, an injury to the subclavian artery, subclavian vein, and/or

■ FIGURE 7-1 Clavicle fracture occurring during childbirth. The fracture of the clavicle (arrow) occurred from excessive pressure against the anterior shoulder when it passed through the pubic symphysis.

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■ FIGURE 7-2 Fractures involving the middle third of the clavicle. A, Anteroposterior radiograph of the left shoulder in a 34-year-old man shows an acute fracture of the mid shaft of the left clavicle with slight superior displacement of the lateral fragment. B, The left midclavicle fracture in this 13-year-old boy shows superior angulation but no significant displacement. The acromioclavicular joint appeared intact in both patients.

brachial plexus may complicate the fracture.10 An arterial injury may be accompanied by a large hematoma that protrudes above the clavicle superiorly or into the axilla inferiorly. About 15% of clavicular fractures involve the lateral third of the bone (Fig. 7-3).15,16 An injury that drives the humerus and scapula downward causes these fractures. Neer describes three types.15 In a type 1 fracture the break occurs lateral to the coracoclavicular ligaments. The fracture may extend to the articular surface of the acromioclavicular joint. These fractures are stable and treated with a sling. A type 2 fracture is complex with an intact acromioclavicular joint and distal clavicle but with disruption of the coracoclavicular ligament through an oblique fracture. Sometimes a small fragment of bone is left attached to the coracoclavicular ligaments, avulsed from the clavicle; and when the deformity is marked, it should be treated with surgical fixation. A type 3 fracture is an intra-articular fracture of the distal clavicle at the acromioclavicular joint, where it may produce arthritic changes in the joint. Only 5% of fractures involve the medial third of the clavicle, but these may be difficult to visualize, owing to the overlap of the spine and ribs, and may require additional imaging by CT, particularly if there is a concomitant question of sternoclavicular joint subluxation or dislocation (Fig. 7-4).13 The majority of these fractures are the result of direct trauma and also are divided into two types: transverse and intra-articular fractures. Preservation of the costoclavicular ligament prevents fracture displacement.13 However, when these fractures violate the sternoclavicular joint, it can result in a painful articulation as well as a displaced fracture.

Multidetector Computed Tomography Congenital pseudarthrosis of the clavicle is a rare entity.17 It presents on the right side in 90% of the patients and bilaterally in up to 10%. Radiographic evaluation in the majority of cases is sufficient, but, occasionally, CT with

multiplanar reconstruction allows optimal assessment of the pseudarthrosis of the clavicle and is conclusive in excluding a neoplastic, infective, or traumatic origin.

Acute Osseous Injuries of the Acromioclavicular Joint The acromioclavicular joint is a common site for dislocations, accounting for about 12% of shoulder dislocations.18,19 The mechanism of injury is either a direct fall on the point of the shoulder or a fall on an outstretched hand. The force applied to the shoulder girdle during the fall determines the spectrum of pathology that develops within and around the joint. Generally, it is an injury of young people between 15 and 40 years old.

Radiography The normal distance between the superior surface of the coracoid process and the inferior aspect of the clavicle is 1.1 to 1.3 cm.11 The inferior cortical margin of the acromion and the clavicle are aligned and, more importantly, symmetric with the opposite side. The width of the normal acromioclavicular joint is 3 to 5 mm and decreases with age.20 A discrepancy of the coracoclavicular distance of 3 to 4 mm or more or asymmetry of the acromioclavicular joint space greater than 2 mm may indicate a rupture of the coracoclavicular ligaments.21 When the acromioclavicular joint separates, the initial injury is a strain of the acromioclavicular ligament. An increase in force that ruptures the acromioclavicular ligament may then strain the trapezoid and conoid ligaments. With complete rupture of the coracoclavicular ligaments, the clavicle is allowed to detach, resulting in injuries to the insertion of the deltoid and trapezius muscles. A variation that occurs in young people is preservation of the coracoclavicular ligaments with avulsion of the coracoid process at its base.22–25 This injury typically occurs in patients younger than 25 years, because fusion of the coracoid ossification center can occur as late as 21 to 25 years of age.23

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A ■ FIGURE 7-3 Fractures involving the distal third of the clavicle. A, Anteroposterior radiograph of the right shoulder in a 24-year-old man shows a vertically oriented, extra-articular fracture of the distal clavicle (arrow) that is lateral to the coracoclavicular ligaments. A good indicator of rupture of the coracoclavicular ligaments is elevation of the medial clavicle fragment. B, This 53-year-old patient has a comminuted distal clavicle fracture, but the principal fracture lines remain lateral to the coracoclavicular ligaments. C, A right clavicle fracture in a 23-year-old man extended to the articular surface. There is superior displacement of part of the lateral fragment (arrow). When a distal clavicular fracture extends to the articular surface, it can increase the potential for development of secondary osteoarthritis.

C

A ■ FIGURE 7-4

Fracture of the medial third of the clavicle. A, Proton-density–weighted transaxial MR image through the medial clavicle in a 60-year-old woman shows an intra-articular fracture of the head of clavicle (arrow). There is soft tissue swelling in the surrounding interstitial soft tissues and the pectoralis muscle. Radiographs of the shoulder were unrevealing. B, The corresponding T2-weighted image shows edema manifested as high T2 signal intensity in the marrow surrounding the fracture.

The classification proposed by Tossy and colleagues and later reclassified by Allman is the most widely used classification describing injuries to the acromioclavicular joint.12 In a type 1 separation, conventional radiographs appear normal or may show some soft tissue swelling over the

joint (Fig. 7-5). In a type 2 injury there is disruption of the acromioclavicular ligament and partial disruption of the coracoclavicular ligaments, so that the clavicle is allowed to migrate superiorly. Displacement measures less than 5 mm or 50% of the width of the clavicle on weight-bearing

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A

B

■ FIGURE 7-5

Grade 1 acromioclavicular joint separation. A, Close-up of an anteroposterior radiograph of the right shoulder in a 21-year-old football player who sustained a direct impaction injury shows soft tissue swelling over the acromioclavicular joint. The only finding is soft tissue swelling over the joint (arrow). B, Coronal T2-weighted image through the acromioclavicular joint shows marked thickening of the superior acromioclavicular ligament associated with interstitial edema (arrow) and overlying soft tissue swelling within the adjacent subcutaneous fat.

views. In type 3 injuries the acromioclavicular and coracoclavicular ligaments are completely disrupted and there is clavicular migration exceeding 5 mm or 50% of the bone width. Rockwood and coworkers proposed three additional grades to the classification.26 In type 4 injuries the clavicle is displaced posteriorly into or through the trapezius muscle. In type 5 injuries superior clavicle migration is more pronounced than in a type 3 separation. In type 6 injuries the clavicle dislocates inferiorly below the coracoid or acromion process, an injury that may also be associated with rib fractures. Types 4 to 6 are extremely rare injury patterns and are usually discovered at the time of surgical exploration and may not be necessarily detected radiographically.

Magnetic Resonance Imaging Occasionally, further evaluation of an acromioclavicular joint separation by MRI is required. The strength of MRI is in the ability to directly visualize the joint capsule, interstitial soft tissues, and integrity of the superior acromioclavicular ligament as well as the coracoclavicular ligaments.27 In type 1 and 2 separations, soft tissue swelling about the joint indicates a strain of the acromioclavicular ligament but there is no or minimal discontinuity of the coracoclavicular ligaments. Disruption of the coracoclavicular ligaments indicates the presence of a type 3 separation and is a conspicuous finding on fluid-sensitive images of the shoulder manifested by loss of fiber continuity accompanied by the presence of edema and hemorrhage (Fig. 7-6). Additional findings of marrow edema in the clavicle and acromion process as well as fluid in the joint and subacromial/subdeltoid bursa are important indicators of acute trauma. In severe dislocations, it is useful to evaluate the surrounding musculature, particularly the trapezius muscle, for the presence of a tear.

Multidetector Computed Tomography Computed tomography is an important adjunct imaging modality in patients with acromioclavicular separation when a concomitant fracture of the acromion process or coracoid process is suspected, because these bony protuberances are difficult to evaluate radiographically.25

Acute Osseous Injuries of the Sternoclavicular Joint The sternoclavicular joint is considered the primary articulation between the arm and the trunk. It is freely movable and functions almost like a ball-and-socket joint with motion in almost all planes, including rotation.28 It is infrequently dislocated, accounting for only 2% to 3% of all dislocations of the shoulder girdle.29 The majority of dislocations of this joint occur in people younger than 25 years of age. When it dislocates, the clavicle can dislocate anteriorly or posteriorly.30 The majority of dislocations are anterior, with a frequency 2 to 20 times that of posterior dislocations.29,30 The most common mechanism of injury to the sternoclavicular joint is indirect trauma. As such, the costoclavicular or rhomboid ligament, which connects the inferior margin of the proximal clavicle to the superior margin of the proximal first rib, acts as a fulcrum when there is a blow against the anterior or posterior aspect of the shoulder. Occasionally, a direct impaction to the medial clavicle can cause a posterior dislocation. Rarely, a dislocation can occur spontaneously.31 In the pediatric patient, a fracture through the physeal plate of the medial clavicle is more likely than a true dislocation of the sternoclavicular joint.32 Infrequently, a complete disruption of the sternoclavicular joint may result in scapulothoracic dissociation.

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A

B ■ FIGURE 7-6 Grade 3 acromioclavicular joint separation. A, Anteroposterior view of the left clavicle obtained after a 25-yearold skateboarder fell on his left shoulder shows superior displacement of the distal clavicle with widening of the coracoclavicular distance (arrow). The articular surface of the clavicle projects completely above articular surface of the acromion process producing widening of the acromioclavicular joint. B, Coronal T1-weighted image shows abnormal morphology and signal intensity of both components of the coracoclavicular ligaments (arrow) indicating fiber disruption. C, Sagittal T2-weighted image shows complete disruption of the superior acromioclavicular ligament (arrow), swelling in the adjacent soft tissues, and marrow edema in the distal clavicle.

C

Radiography

Multidetector Computed Tomography

The diagnosis of a sternoclavicular joint dislocation is difficult radiographically. Detection requires asymmetry of the position of the medial ends of the clavicle on a frontal radiograph, but the limitation of radiographs is that anterior and posterior subluxation is impossible to identify in many instances (Fig. 7-7).

The imaging modality of choice is CT for the diagnosis of a sternoclavicular joint dislocation.33 Posterior sternoclavicular dislocations are relatively uncommon injuries. Nevertheless, these dislocations are associated with potentially fatal injuries to the mediastinum and the great vessels. Medial clavicle physeal injury with

A ■ FIGURE 7-7

B

Sternoclavicular joint dislocation. A, Close-up view of a frontal chest radiograph in a 41-year-old man after an automobile accident shows asymmetry of the sternoclavicular joints. Note that the head of the right clavicle resides more superiorly than the left (arrow). B, Bone-windowed axial CT image shows that the head of the right clavicle is dislocated posteriorly (arrow). It is important to image potential sternoclavicular joint dislocations because posterior dislocations may injure the adjacent vascular structures residing posterior to the sternum.

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posterior dislocation may present as a similar clinical picture in younger patients. CT has the ability to depict the direction of the dislocation and degree of displacement but also any potential complication to the adjacent structures, such as an injury to the great vessels, trachea, or esophagus. The most common classification for sternoclavicular dislocation was described by Allman.12 In a type 1 dislocation there is minimal disruption of the sternoclavicular ligament. In a type 2 dislocation the sternoclavicular ligament is torn. In a type 3 dislocation both the sternoclavicular and costoclavicular ligaments are torn, resulting in either a complete anterior or posterior dislocation.

Acute Osseous Injuries of the Glenohumeral Joint The glenohumeral joint of the shoulder is the most mobile and, thus, most commonly dislocated articulation in the body. Approximately 50% of all dislocations in the human body involve this articulation.32 This spheroidal joint is inherently unstable. The glenoid fossa is disproportionately small and shallow, compared with the humeral head. Reportedly, shoulder dislocations occur at a rate of 1% to 2% in the general population and have an incidence as high as 7% in selected groups of athletes.34,35 Certain congenital conditions such as glenoid hypoplasia predispose

the shoulder to multidirectional instability.36 Posterior glenoid rim deficiency and glenoid retroversion contribute to posterior instability.37,38 Posterior dislocations are much less common than anterior dislocations but are more devastating because they frequently are occult and go undetected for months. The most common mechanism of injury is indirect trauma to the shoulder, although repetitive microtrauma or an underlying congenital deformity may be contributing factors in some people. The majority of anterior dislocations are caused by abduction with forced external rotation of the arm.32 Occasionally, a direct blow to the back of the shoulder may result in a dislocation. Posterior dislocations are caused by adduction, flexion, and internal rotation. Inferior dislocations, referred to as luxation erecta, are caused by either hyperabduction of the arm or by a direct blow against the length of the arm with the shoulder maximally abducted.39 Superior dislocation is rare and is caused by a force directed cephalad along the arm with the shoulder adducted and is associated with rupture of the rotator cuff.39 Seizures and electrocution are common causes of bilateral dislocations.

Radiography The most common type of shoulder dislocation is an anterior dislocation, accounting for about 95% of all glenohumeral joint dislocations (Fig. 7-8). Radiographic diagnosis

B ■ FIGURE 7-8

Anterior glenohumeral joint dislocation. A, Frontal radiograph of the left shoulder in a 20-year-old hockey player shows that the humeral head is positioned inferior to the coracoid process. The articular surface of the humeral head does not articulate with the glenoid fossa. B, Scapular Y-view shows that the humeral head has become displaced anteriorly and inferiorly. This subcoracoid dislocation is the most common type of glenohumeral joint dislocation.

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of an anterior dislocation is not difficult with standard internal and external rotation views. However, detection of associated osseous abnormalities of the shoulder girdle is usually best obtained with additional axillary, Grashey, or apical oblique views. Four types of anterior dislocations have been described depending on the location of the humeral head after it has become dislocated: subcoracoid (the most common type), subclavicular, subacromial, and intrathoracic. The shoulder must be closely scrutinized for associated injuries after an anterior dislocation. An impaction fracture of the posterolateral aspect of the humeral head, or Hill-Sachs lesion, occurs when the humeral head lodges against the anteroinferior aspect of the glenoid rim.40–42 This abnormality is best detected on the internal rotation view of the humerus and is present in 75% of patients who develop chronic anterior instability (Fig. 7-9).43 It is

A ■ FIGURE 7-9 Anterior dislocation with Hill-Sachs defect. A, Postreduction radiograph of a left shoulder in a 25-year-old man who had his shoulder relocated after sustaining a dislocation. There is a defect in the posterolateral aspect of the humeral head that produces a vertically oriented, linear deformity (arrow) and a change in the contour of the articular surface. B, Bone-windowed axial CT image of the shoulder while dislocated shows a large wedge-like defect in the humeral head produced by its impaction against the anterior glenoid. C, Transaxial gradient axial MR image shows that the defect in the humeral head conforms to the shape of the area of the glenoid rim. The defect begins in the superiormost aspect of the humeral head, whereas the physiologic trough of the humerus begins 1 cm below the superior articular surface.

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often associated with an avulsion of the labrum from the glenoid rim or Bankart lesion. In 5% to 8% of patients, a fracture of the glenoid rim (osseous Bankart lesion) occurs and may require operative fixation (Fig. 7-10).44 Fifteen to 25 percent of anterior dislocations are associated with a fracture of the greater tuberosity (Fig. 7-11).44,45 Another 2% of dislocations are associated with a fracture of the surgical neck of the humerus, scapular body, acromion process, and the clavicle. A posterior dislocation is an unusual injury, accounting for 2% to 4% of all shoulder dislocations, although more than 50% of posterior shoulder dislocations may be initially missed or misdiagnosed.46–49 Indirect forces, such as seizures and electric shock, are the most common mechanisms of injury.50 The strong internal rotators of the arm, such as the latissimus dorsi, pectoralis major, and subscapularis muscles, overwhelm the external rotators, resulting in

A

B

■ FIGURE 7-10

Anterior dislocation with osseous Bankart fracture. A, Anteroposterior radiograph of the shoulder in a 22-year-old athlete after reduction of an anterior dislocation shows a density in the anteroinferior aspect of the glenoid fossa (arrow). B, A reformatted CT coronal image shows that the density represents an osseous Bankart fracture, a sliver of bone that broke off the inferior aspect of the anterior glenoid rim. C, A transaxial gradient-recalled-echo MR image shows the ossific fragment anterior and inferior to the glenoid rim (arrow). CT is considered a preferred technique for assessing the osseous injuries, whereas MRI is more optimal for evaluating the soft tissue restraints.

C

A ■ FIGURE 7-11

B

Anterior dislocation with a fracture of the greater tuberosity. A, Anteroposterior radiograph of the left shoulder in a 29-year-old man after a fall shows an anterior glenohumeral joint dislocation associated with a slightly distracted fracture (arrow) of the greater tuberosity. B, Coronal T1-weighted MR image shows that there is retraction of the greater tuberosity fragment (arrow) from the pull of the supraspinatus tendon. If allowed to heal in this position, the rotator cuff may become insufficient.

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flexion, adduction, and internal rotation of the humerus.51 A fall on an outstretched hand or direct blow to the anterior shoulder is a less common injury mechanism. Because posterior dislocations do not spontaneously reduce in the majority of cases, the longer the diagnosis is delayed, the more likely it is for that shoulder to become unstable. There are three types of posterior shoulder dislocations. Nearly all, about 98%, are the subacromial type. The posterior subglenoid and subspinous types are uncommon.

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When the humeral head dislocates posteriorly, it is immediately pulled back toward its anatomic position by the overstretched anterior musculature. This forces the humeral head to impact against the posterior glenoid rim, creating a wedge defect in the anteromedial aspect of the humeral head in a similar fashion to a Hill-Sachs lesion (Fig. 7-12).52 Radiographically, it is apparent as a dense linear abnormality that parallels the medial cortex of the humeral head when the arm is internally rotated.53 The incidence of a

A

D ■ FIGURE 7-12

Posterior glenohumeral joint dislocation with trough line. A, Anteroposterior-oblique radiograph of a left shoulder in a 29-year-old man after a seizure. There is a vertically oriented, linear density (arrows) in the humeral head consistent with an impaction fracture. The articular surface of the humeral head overlaps the glenoid rim. B, Scapular Y-view of the shoulder shows that the humeral head is located posterior to the glenoid rim and inferior to the acromion process. C, Axillary view shows impaction of the humeral head against the posterior rim of the glenoid. D, Axial CT image after reduction shows the corresponding impaction fracture in the anterior and medial aspect of the humeral head (arrow).

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trough lesion has been estimated to occur in 29% to 75% of all dislocations.52,54 Although the linear defect may be difficult to detect radiographically if the position of the humeral head is not optimal, the trough fracture is easily detected on cross-sectional studies. The reverse Bankart lesion represents damage to the posterior labrum that occurs either when the humeral head displaces posteriorly, stripping the posterior capsule and scapular periosteum, or when it impacts on the posterior glenoid rim.55 The labrum may appear detached, fragmented, frayed, or eroded. This abnormality has been estimated to accompany as many as 88% of shoulders with posterior unidirectional instability.54 Twenty percent of patients with prior posterior shoulder dislocations demonstrate a focus of capsular calcification or erosion in the posterior aspect of the glenoid rim (Fig. 7-13).51,56 Concomitant fractures of the lesser tuberosity occur in 25% of posterior dislocations, and humeral head fractures occur in another 10% of dislocations (Fig. 7-14).52 Numerous additional radiographic signs have been reported, thus reflecting the difficulty of diagnosing a posterior shoulder dislocation (Fig. 7-15). Some of these

radiographic observations include the rim sign (widening of the joint beyond 6 mm), disruption of the scapulohumeral arch, absent half-moon sign (loss of humeral head/glenoid rim overlap), and Velpeau sign (superior humeral head subluxation). The most common complication of a posterior dislocation, recurrence, is much less frequent than in anterior dislocations and is estimated to occur in about one third of patients. The patient’s age at the time of initial dislocation again appears to be a main determining factor.57 Inferior dislocations of the shoulder are rare. In this type of dislocation, the arm is abducted, elevated, and fixed with the forearm resting on top of the patient’s head and is an unmistakable clinical diagnosis. It is caused by hyperabduction, which levers the humeral head from the glenoid fossa and into a position below the coracoid process. Radiographically, the arm is hyperabducted and parallels the scapular spine and may be associated with a fracture of the acromion, greater tuberosity of the humerus, or the inferior glenoid rim.39 A superior dislocation of the shoulder is the rarest dislocation of the shoulder. A force directed in a cephalad direction on an adducted arm drives the humeral head

B

A ■ FIGURE 7-13 Posterior dislocation with posterior glenoid rim fracture. A, Axial CT image of the left shoulder in a 27-year-old man shows posterior dislocation of the humerus, impaction of the anteromedial surface of the humeral head, and a posterior glenoid rim fracture fragment (arrow) consistent with a reverse osseous Bankart lesion. B, Axillary view of the shoulder after reduction of a posterior dislocation shows the displaced bone fragment in the posterior soft tissues (arrow). The impaction fracture of the anterior surface of the humeral head is depicted by an area of diminished density (curved arrow). C, Transaxial gradient-recalled-echo MR image 2 years later shows a deformity of the posterior aspect of the glenoid rim (arrow) and slight posterior subluxation of the humeral head.

C

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B

■ FIGURE 7-14

Posterior dislocation with lesser tuberosity fracture. A, Anteroposterior radiograph of the left shoulder in a 42-year-old man who presented with a posterior dislocation shows an abnormal density in the medial aspect of the humeral head (arrow). B, Axillary view after reduction shows a fracture (arrows) through the lesser tuberosity. Any patient who presents with a lesser tuberosity fracture should be evaluated for a possible posterior shoulder dislocation.

through the rotator cuff into the acromion. Associated osseous abnormalities include a fracture of the acromion, clavicle, coracoid, or greater tuberosity of the humerus in addition to the rotator cuff tear.39

Magnetic Resonance Imaging Magnetic resonance imaging techniques, particularly those performed with intra-articular contrast agents, have been shown to be more accurate than radiography for diagnosis of injuries to the labroperiosteal complex and for depiction of unsuspected fractures of the humeral head and glenoid.58–60 An osteochondral defect of the glenoid has been associated with anterior shoulder dislocations.61 It represents a focal abnormality in the subchondral region of the glenoid fossa with an overlying cartilage defect, manifested as either fibrillation or a chondral flap. Other associated soft tissue injuries that are depicted well with MRI include erosion of the labrum, stripping of the anterior capsular, and rupture of the subscapularis tendon (Fig. 7-16). Posterior labral tears and capsular ruptures associated with posterior dislocations are well depicted on MRI.

Multidetector Computed Tomography Computed tomography is the optimal modality for depicting an osseous Bankart lesion since the fragment may vary considerably in size. The advantage of CT over MRI in the acute setting of trauma is that thin-section images can be acquired rapidly in a patient with a painful shoulder, and reformatted into the plane that best depicts the osseous abnormality. Multiplanar reconstruction images allow the surgeon to evaluate the anatomic relationship quickly before planning any surgical management. In patients with recurrent anterior shoulder dislocation, the degree of glenoid bone loss may predispose the patient to further

dislocation and failure of a Bankart repair. CT has been shown to accurately depict the severity of anterior glenoid flattening, decreased glenoid width, and decreased width-to-length glenoid ratio.62 In patients with a posterior dislocation, CT has been efficacious in better demonstrating the trough impaction fracture, particularly when they are smaller lesions. Lesser tuberosity fractures are also well depicted on CT.

Classic Signs ANTERIOR DISLOCATION ■ Hill-Sachs lesion ■ Osseous Bankart lesion POSTERIOR DISLOCATION ■ Trough lesion ■ Reverse osseous Bankart lesion ■ Rim sign ■ Scapulohumeral arch disruption ■ Absent half-moon sign ■ Velpeau sign

Acute Osseous Injuries of the Scapula Fractures of the scapula are uncommon because of the inherent protection provided by surrounding muscles.63,64 For a fracture to occur, major trauma with a direct force to the scapula in the form of falls, crush injuries, or motor vehicle accidents is required. Indirect impaction forces transmitted through the humeral shaft can also fracture the scapula. Scapular fractures occur in about 4% of patients who experience polytrauma from motor vehicle collisions.65

C ■ FIGURE 7-15 Radiographic signs associated with posterior dislocation. A, Rim sign—the glenohumeral joint space exceeds 6 mm. In this case, it measured 12 mm. B, Absent half-moon sign—absence of a normal overlap between the humeral head and glenoid rim. C, Broken arch sign—the scapulohumeral arch should have a smooth and continuous contour. In this patient, the arch is too angulated. Note that there is a fracture of the lesser tuberosity (arrow).

■ FIGURE 7-16 Soft tissue injuries associated with anterior dislocation. Sagittal T2-weighted MR image shows intense interstitial edema within the posterior deltoid, infraspinatus, and subscapularis muscles and a complete rotator cuff tear of the supraspinatus and infraspinatus tendon insertions. There is a focus of marrow edema in the posterosuperior portion of the humeral head (arrow). The defect in the rotator cuff allowed communication between the joint space and the subacromial bursa, which contained fluid (curved arrow).

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Radiography At present there is no standardized classification system for scapular fracture, although several have been popularized. The majority of classifications describe fractures based on the anatomic location and on the involvement of the coracoid, glenoid, and scapular body.64,66 One third of fractures of the scapula involve the body, one fourth of fractures involve the scapular neck, and the remainder of fractures has a similar frequency involving the scapular spine, glenoid, and acromion process.67 Fractures of the body, the most common fracture of the scapula, occur with either a vertical or horizontal orientation and are often comminuted. They are best detected with either the Grashey or transscapular-Y projections. These fractures, however, seldom require more than symptomatic treatment and heal well. Fractures of the scapular neck can be either an avulsion from the glenoid rim

A ■ FIGURE 7-17 Acromion process fracture. A, Anteroposterior radiograph of the right shoulder in a 33-year-old woman involved in a motor vehicle accident is unrevealing except for subtle irregularity of the undersurface of the acromion process that could easily pass for a subacromial spur (arrow). Coronal (B) and sagittal (C) T2-weighted MR images show marrow edema in the area of the fracture manifested as high T2 signal intensity in the posterior aspect of the acromion process.

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when the humeral head dislocates or a transverse extension of a scapular body fracture.68 Frequently, these fractures are displaced but are considered stable if the coracoclavicular joint and the clavicle remain intact. Fractures of the glenoid may also occur from impaction of the humeral head against the glenoid fossa.66 A fracture of the acromion process usually occurs at the junction of the spine and the acromion (Figs. 7-17 and 7-18).69 It is typically oriented vertically and associated with little displacement. It is most commonly caused by a direct impaction on the point of the shoulder, but rarely it may be the result of a superior glenohumeral joint dislocation. It should not be mistaken for an os acromiale, which has sclerotic and well-corticated margins and is frequently bilateral (Fig. 7-19). Coracoid process fractures characteristically are transversely oriented and extend through its base (Fig. 7-20). It may be caused by a direct

A

■ FIGURE 7-18

Pediatric acromion process fracture. A, Anteroposterior radiograph of the right shoulder in a 13-year-old boy with anterior shoulder pain after falling. The skeleton is immature, and there is a slight stepoff in the apophysis with the native scapula (arrow). B, Axillary view shows that there are two ossification centers in the acromion process. C, Transaxial gradient-recalled-echo MR image shows edema in the anterior apophysis (arrow).

C

A ■ FIGURE 7-19

B

Shoulder with an os acromiale. A, Anteroposterior radiograph of the right shoulder shows a lucency (arrow) in the region of the acromion process that mimics a fracture. B, Axillary view depicts a normal-appearing os acromiale with a transversely oriented lucency across the acromion process (arrows). It is important to note this normal variant because the pseudarthrosis may be injured in trauma and become symptomatic.

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B

■ FIGURE 7-20

Fracture near the base of the coracoid process. A, Anteroposterior radiographs of the right shoulder in a 30-year-old man with pain shows a faint lucency near the base of the coracoid process (arrow). B, Axillary view shows a transverse subacute fracture of the coracoid process (arrow) near its base with some callus formation. A fracture of this process often is radiographically occult if the axillary view is not performed routinely.

impaction against the tip of the coracoid, by an anterior glenohumeral joint dislocation, and occasionally by a dislocation of the acromioclavicular joint.70–74 Fractures of the acromion and coracoid processes are difficult to visualize with conventional radiographs. Axillary views and transscapular Y-views are considered essential projections for depicting fractures of either bony tubercle. When a coracoid process fracture is not detected, it may result in a nonunion (Fig. 7-21).

Multidetector Computed Tomography Reportedly, 25% to 43% of scapular fractures are initially missed on radiographic inspection, often because attention is diverted to other life-threatening injuries or because the symptoms of the fracture are masked by injuries to adjacent structures (Figs. 7-22 and 7-23).66,69 CT is an optimal modality for evaluating fractures of the scapula because it allows unimpeded inspection of this bone (Fig. 7-24). Scapular neck fracture displacement, angulation, and anatomic classification can be further enhanced by CT, but CT is superior in identifying associated injuries to the superior shoulder suspensory complex, which can be missed by radiographic evaluation alone.75 MRI allows simultaneous inspection of the bone marrow and the ligamentous structures of the shoulder girdle but is best reserved as a follow-up examination after the osseous injuries have been ascertained acutely.

Acute Osseous Injuries of the Proximal Humerus Fractures of the proximal humerus are common in older women and are prevalent in the sixth and seventh decades of life.76–78 These fractures may involve the surgical or anatomic neck of the humerus, the greater or lesser tuberosities, or the articular surface or may occur with

■ FIGURE 7-21 Nonunion of a fracture of the coracoid process. Axillary view of the left shoulder in a 45-year-old woman shows a fracture of the coracoid process. There is lamellar bone on both sides (arrows) of the distracted fracture indicating a nonunion. She had sustained an injury 3 years earlier from an all-terrain vehicular accident.

various combinations of these structures. The majority of proximal humerus fractures result from a fall on an outstretched hand, whereas those affecting younger patients are caused by more severe trauma. The importance of muscular insertions is noteworthy in proximal humeral fractures, because the actions of the muscles of the rotator cuff and the pectoralis, latissimus dorsi, and teres

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A ■ FIGURE 7-22 Horizontal fracture of the scapula. A, Anteroposterior radiograph of the left shoulder in a 38-year-old man shows a fracture (arrows) traversing through the superior portion of the scapula extending into the glenoid fossa. B, Scapular Y-view shows that the fracture (arrow) also extends through the base of the coracoid process.

B

A ■ FIGURE 7-23

B

Vertical fracture of the scapula. A, Anteroposterior radiograph of the left shoulder in a 31-year-old man shows a vertical fracture (arrow) extending from the lateral scapular margin below the glenoid fossa to the suprascapular notch (curved arrow). B, Transaxial gradient-recalledecho MR image shows that the fracture is displaced at the level of the suprascapular notch (arrow). The patient presented with a rotator cuff palsy from an injury to the suprascapular nerve.

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A ■ FIGURE 7-24

Comminuted fracture of the scapula. A, Anteroposterior radiograph of the left shoulder shows a comminuted fracture of the scapula involving the infraglenoid region, suprascapular notch, and scapular spine. There is also a fracture of the clavicle (arrow) and numerous rib fractures. B, Sagittal reformatted CT image shows the complexity of the fractures and their relative relationships. The fracture has resulted in numerous fragments within the body, many of which are rotated and displaced. CT is useful for identifying displaced fragments in the suprascapular notch and glenoid fossa.

major muscles can influence the degree of displacement of osseous fragments.

Radiography The surgical neck of the humerus is the most common location of fracture in the proximal humerus (Fig. 7-25). Fractures of the surgical neck are frequently impacted and often extend to the adjacent tuberosities. Although the majority of these fractures are not significantly displaced and treated conservatively, 15% to 20% of patients will have sufficiently displaced fractures requiring open reduction and internal fixation.78 Isolated fractures of the anatomic neck of the humerus are rare but can be complicated by osteonecrosis if displaced, owing to disruption of the blood supply to the articular surface. Greater tuberosity fractures are uncommon in isolation and are most commonly associated with surgical neck fractures.78 Lesser tuberosity fractures are rare and most commonly associated with posterior shoulder dislocations.52,79 The Neer classification of fractures of the proximal humerus is the most widely applied classification because it provides predictive value to the treatment plan.78,80 The classification roughly follows the anatomic lines of epiphyseal union and is based on the presence or absence of displacement of the components of the proximal humerus, namely, the head, greater tuberosity, lesser tuberosity,

and shaft. A fragment is defined as displaced if it is either removed more than 1 cm from its anatomic position or angulated more than 45 degrees. Even if a fracture fragment is comminuted, it is considered one fragment because it is held in place by soft tissue continuity. The majority of fractures under this classification, or 80% of fractures, are one-part fractures without significant displacement of any fragments. About 10% are two-part fractures with displacement of one fragment with respect to the other three anatomically aligned fragments. Three-part fractures constitute about 3% of fractures, and as long as one of the tuberosities remains attached to the humeral head, the blood supply to the head should be intact (Fig. 7-26).80 About 4% of fractures are four-part fractures and because the vascular integrity to the head is violated, osteonecrosis is a common occurrence (Fig. 7-27). Displaced tuberosity fractures are typically associated with a tear of the rotator cuff (Fig. 7-28). Humeral head fractures account for 2% to 5% of proximal humeral fractures.78 These fractures are either articular fractures that bisect the head or compression fractures that impact the articular surface when the head dislocates either anteriorly or posteriorly. Humeral head–splitting fractures are caused by a direct blow to the lateral aspect of the shoulder that drives the humeral head into the glenoid, and these require treatment with a prosthetic implant.78 Compression fractures are graded by

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B ■ FIGURE 7-25 Fracture of the surgical neck of the left humerus. A, Anteroposterior radiograph of the right shoulder in a 65-year-old woman after she fell shows a minimally displaced, transverse fracture below the head of the humerus (arrow). B, Axial CT shows that the fracture was more comminuted posteriorly (arrow) and displaced than initially suspected on the radiographs. This is a Neer two-part fracture.

A

A ■ FIGURE 7-26

Neer three-part fracture of the proximal humerus. A, Anteroposterior radiograph of the right shoulder in a 74-year-old woman shows fractures of the anatomic neck, surgical neck, and greater tuberosity. The articular surface of the humeral head is inferiorly subluxed, whereas the greater tuberosity remains in position owing to the pull of the rotator cuff. B, Coronally reformatted CT image depicts the three fragments of bone separated by the fracture lines.

CHAPTER

■ FIGURE 7-27 Neer four-part fractures of the proximal humerus. Anteroposterior radiograph of the right shoulder in a 68-year-old woman shows a comminuted fracture of the proximal humerus with a transverse fracture of the surgical neck and fractures through greater and lesser tuberosities, both of which are displaced.

the percentage of the surface that is involved. Generally, if less than 20% to 25% of the articular surface is involved, the injury can be treated conservatively. Fractures that involve 25% to 50% of the articular surface require operative correction, and those that exceed 50% of the articular surface will likely require replacement with an implant.

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■ FIGURE 7-28

Neer four-part fracture. Anteroposterior projection of the shoulder in a 62-year-old man shows widening of the joint space from marked rotation of the humeral head and fractures through the surgical neck and both tuberosities. Both tuberosities are fragmented, and there is an impaction fracture of the articular surface of the humeral head (arrow). The greater tuberosity is superiorly displaced, whereas the lesser tuberosity is medially displaced from the pull of the respective rotator cuff tendons.

Classic Signs Neer classification (articular head, surgical neck, greater tuberosity, lesser tuberosity) ■

Multidetector Computed Tomography

■

Computed tomography of the shoulder is of great value in delineating the extent of complex or comminuted fractures of the proximal humerus, particularly when associated with dislocations.81 The relation of the glenoid to the humeral head fragments is more optimally depicted on CT than on radiographs, as well as orientation, displacement, and entrapment of fragments.82 Furthermore, CT allows accurate characterization of specific types of fractures that may not be evident, such as impaction fractures, split fractures of the humeral head, and glenoid rim fractures. Multiplanar reconstructions of three-dimensional CT images have been shown to improve the reliability of complex fracture classification and characterization, although not necessarily the accuracy over radiographic and two-dimensional CT images.83,84

■

■

1-part: No segment displaced 2-part: One segment displaced relative to other three segments 3-part: Two segments displaced relative to other two segments 4-part: All segments displaced

DIFFERENTIAL DIAGNOSIS The clavicle is at risk when young people sustain a fall or have a direct force impacting on their shoulder. Characteristically, fractures of the clavicle are readily apparent clinically and radiographically. Occasionally, a fracture of the clavicle in a newborn may mimic unilateral clavicular pseudarthrosis, which often is associated with cleidocranial dysostosis.85 In pseudarthrosis, the right side is more frequently involved and the patient presents with a prominent supraclavicular bump but notable absence

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of pain, swelling, and ecchymosis and lack of periosteal bone or callus formation. The diagnosis of an acromioclavicular separation is not problematic. However, it may be a diagnostic dilemma to differentiate between the different types of acromioclavicular joint separations. In mild separations, weightbearing views may be beneficial in identifying the type of separation. In more severe injuries, cross-sectional imaging techniques have additive value to the diagnostic algorithm. Anterior sternoclavicular joint dislocations are clinically palpable lesions. Posterior dislocations are more difficult to diagnose because soft tissue swelling may obscure the findings.86 The majority of complications associated with sternoclavicular dislocations occur with posterior dislocations.87 Approximately 25% of these dislocations are associated with a laceration of the superior vena cava, thoracic outlet syndrome from venous compression, compression of the recurrent laryngeal nerve, rupture or compression of the trachea, pneumothorax, esophageal rupture, or injury to the subclavian or carotid artery.33 Anterior glenohumeral joint dislocations are injuries that are obvious radiographically and clinically. The important observation should be made on reduction. The most common complication of an anterior dislocation is recurrence of the dislocation. The principal factor that influences the risk of recurrence is reported to be the age of the person at the time of the initial dislocation.68,88 Sixty to 90 percent of people who have anterior glenohumeral dislocation before 20 years of age experience a recurrence.68,89 Nearly 90% of recurrent dislocations occur in the first 2 years after the initial injury.90 The incidence decreases with increasing age. When the initial dislocation occurs between 20 and 40 years, the rate of recurrence has ranged between 40% and 74%; and when the initial dislocation occurs after age 40 years, the rate of recurrence decreases to 10% to 25%.68,88,91 Recurrence is considered rare when the first dislocation occurs beyond the age of 50 years. MR arthrography has been purported to be predictive of the frequency of recurrence based on the severity of injury to the anterior band of the inferior glenohumeral ligament.92 In anterior shoulder dislocations the position of the humerus and the presence of associated fractures dictate the ease of reduction. Interposition of the tendon of the long head of the biceps may impede reduction altogether. A dislocated tendon should be considered if there is a large greater tuberosity fracture.93 Although an uncommon injury, over one half of posterior shoulder dislocations go undetected.49 Several factors contribute to the difficulty of recognizing this injury.49,52 A posterior dislocation itself is an unusual injury, accounting for 2% to 4% of all shoulder dislocations.46–48 The clinical findings may be masked by a hematoma or prominent shoulder musculature, or the physical signs may suggest another diagnosis such as a rotator cuff tear or a frozen shoulder. A fracture of the humeral head may distract the clinician and radiologist from the diagnosis of a dislocation.52 Finally, the radiographic findings may be subtle or the radiographic series may be compromised due to patient discomfort. The incidence of recurrence is much lower with posterior dislocations.94

The importance of diagnosing a scapular fracture is that the majority of acute fractures are associated with other injuries, including fractures of the rib, clavicle, spine, and extremities, contusion of the lung, vascular injuries, and injuries of either the brachial plexus or central nervous system.69 These concomitant injuries are common and have been reported in 81% to 98% of scapular fractures.63,64,66 A complication to consider in fractures that involve the proximal humerus is an injury to the neurovascular bundle, which lies inferior to the glenohumeral joint. Anterior glenohumeral joint dislocation and displaced surgical neck fractures have been associated with injuries to the axillary nerve, artery, and vein and the ulnar, median, and radial nerves of the brachial plexus because these structures are located adjacent to the coracoid process, the anterior glenoid rim, the anterior humeral head, and the surgical neck of the humerus.80,95 Reported injuries of the axillary artery include transection, avulsion of one of its branches, or thrombosis secondary to an intimal tear.95,96 Other complications that often occur with fractures of the proximal humerus include decreased range of motion secondary to osteoarthritis or a frozen shoulder, chronic pain, and osteonecrosis of the humeral head.

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment The majority of clavicular fractures are treated conservatively with a sling. Displaced fractures are often treated with a figure-of-eight bandage to depress the medial fragment into anatomic alignment. Most clavicular fractures heal without complication, although nonunion has been reported in 1% to 4% of cases, usually after marked fracture comminution or from re-fracture through a previous fracture. The ends of the bone in a clavicular nonunion may be either hypertrophic or atrophic.97 Malunion and hypertrophic callus formation in a fracture that has healed could be a cause of delayed compression of the subclavian vessels, carotid artery, or brachial plexus.2 The treatment of acromioclavicular joint separations depends on the severity and type of separation. In general, types 1 through 3 are treated conservatively. Type 1 and 2 separations may be treated with a swathe and sling with early motion based on symptoms, whereas a type 3 separation, when treated conservatively, is best treated with a Kenny-Howard sling.98,99 The majority of sternoclavicular joint dislocations are treated with closed reduction and immobilization of the arm with a sling.29,86 There is a high likelihood of persistent instability with both conservative and surgical treatment of dislocations.100 Surgical management carries a risk for infection, pin fracture, and migration of pins or wires and is considered only when conservative measures fail.101,102 Patients with uncomplicated anterior glenohumeral joint dislocations can be treated with closed reduction. Posterior dislocations also are generally treated with closed reduction.103 Complications related to scapular fractures are dictated by the location of the fracture and the number and displacement of fragments. Generally, all fractures unite.

CHAPTER

Nonunion rarely occurs, even in severely displaced scapular body fractures. These fractures usually heal without significant dysfunction. Pain and loss of function are problematic, however, with displaced scapular neck and spine fractures. Disability related to weakness of shoulder abduction is common as well as generalized decreased range of motion. Fractures of the humeral head are treated conservatively when small (less than 20% of the articular surface). When larger, they require surgical management.79

Surgical Treatment The indications for surgery in patients with fractures of the clavicle include (1) neurovascular compromise due to posterior displacement and impingement of the bone fragments on the brachial plexus, subclavian vessels, and even the common carotid artery; (2) fracture of the distal third of the clavicle with disruption of the coracoclavicular ligament; (3) severe angulation or comminution of a fracture in the middle third of the clavicle; (4) the patient’s inability to tolerate prolonged immobilization (required by closed treatment) because of Parkinson’s disease, a seizure disorder, or other neuromuscular disease; and (5) symptomatic nonunion after treatment by closed methods.104,105 Acromioclavicular joint injuries that are classified as type 3 separations are frequently treated with internal fixation.29 Rockwood type 4 to 6 injuries, which constitute 10% to 15% of the total number of acromioclavicular joint separations, are generally managed surgically. Patients who have an anterior glenohumeral joint dislocation that is complicated by interposition of soft tissue, displaced greater tuberosity fractures, or large glenoid rim fractures generally are considered candidates for surgical fixation because the risk for either post-traumatic osteoarthritis or re-dislocation is high.29,44 Patients with large Hill-Sachs lesions often have persistent instability even after repair of the anterior capsulolabral structures. Humeral head plasty after elevation of the depressed area using allograft cancellous bone chips impacted into the

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defect has been reported, which elevates and supports the subchondral surface.106 In patients who have had traumatic posterior shoulder dislocations with posterior lesions of the labrum (“reverse Bankart”), articular cartilage, and/or capsule, surgical treatment addressing these lesions is advocated utilizing suture anchor repair with capsular plication.56 Humeral head fractures that involve 20% to 45% of the articular surface generally require operative fixation.79 If they exceed 50% of the articular surface, a prosthetic replacement may be the optimal treatment of choice. Fractures that involve both the lesser and greater tuberosity have a high likelihood of developing osteonecrosis and are treated with a humeral head prosthesis as well.

What the Referring Physician Needs to Know ■

■

■

■

The site of injury is somewhat dependent on the patient’s age. Clavicular fractures and subluxation/dislocations of the acromioclavicular and glenohumeral joints occur in young people, whereas fracture of the proximal humerus is an injury common in elderly patients. In patients with glenohumeral joint dislocations, further evaluation with MRI can be a valuable step in the assessment of instability. MR arthrography is becoming a preferred technique for evaluating the glenoid labrum, glenohumeral ligaments, and joint capsule owing to exquisite depiction of these anatomic tissues, which are difficult to discern in the absence of joint fluid. Scapular injuries tend to be related to high-velocity or highimpact trauma and are frequently associated with other injuries of the thorax. The shoulder girdle should be closely inspected if thoracic CT is performed for chest trauma. On the other hand, the thoracic contents should be closely inspected if a shoulder CT demonstrates a fracture of the scapula. CT is advocated for assessment of complex humeral head fractures because the severity of fragmentation and displacement has a direct impact on the management of the injury.

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Neer CS II. Displaced proximal humeral fractures: II. Treatment of three-part and four-part displacement. J Bone Joint Surg Am 1970; 52:1090–1103. Rafii M, Hossein F, Golimbu C. MR imaging of glenohumeral instability. MR Clin North Am 1997; 5:787–809. Ridpath CA, Wilson AJ. Shoulder and humerus trauma. Semin Musculoskelet Radiol 2000; 4:151–170. Robinson CM, Aderinto J. Posterior shoulder dislocations and fracturedislocations. J Bone Joint Surg Am 2005; 87:639–650.

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6. Rafii M, Hossein F, Golimbu C. MR imaging of glenohumeral instability. MR Clin North Am 1997; 5:787–809. 7. Shankman S, Bencardino J, Beltran J. Glenohumeral instability: evaluation using MR arthrography of the shoulder. Skeletal Radiol 1999; 28:365–382. 8. Rogers LF, Lenchik L. The shoulder and humeral shaft. In Rogers LF (ed). Radiology of Skeletal Trauma, 3rd ed. New York, Churchill Livingstone, 2002, pp 593–682. 9. Sankarankutty M, Turner BW. Fractures of the clavicle. Injury 1975; 7:101–106. 10. Pavlov H, Freiberger RH. Fractures and dislocations about the shoulder. Semin Roentgenol 1978; 13:85–96. 11. Madsen ET. Fractures of the extremities in the newborn. Acta Obstet Gynecol Scand 1955; 34:41–47. 12. Allman FL. Fractures and ligamentous injuries of the clavicle and its articulations. J Bone Joint Surg Am 1967; 49:774–784. 13. Ridpath CA, Wilson AJ. Shoulder and humerus trauma. Semin Musculoskelet Radiol 2000; 4:151–170. 14. Rowe CR. An atlas of anatomy and treatment of midclavicular fractures. Clin Orthop Relat Res 1968; 58:29–42. 15. Neer CS II. Fracture of the distal clavicle with detachment of the coracoclavicular ligaments in adults. J Trauma 1963; 3:99–110. 16. Neer CS II. Fractures of the distal third of the clavicle. Clin Orthop Relat Res 1968; 58:43–50. 17. Sloan A, Paton R. Congenital pseudoarthrosis of the clavicle: the role of CT scanning. Acta Orthop Belg 2006; 72:356–358. 18. Neviaser RJ. Injuries to the clavicle and acromioclavicular joint. Orthop Clin North Am 1987; 18:433–438. 19. Smith MJ, Stewart MJ. Acute acromioclavicular separations: a 20-year study. Am J Sports Med 1979; 7:62–71. 20. Petersson CJ, Redlund-Johnell I. Radiographic joint space in normal acromioclavicular joint. Acta Orthop Scand 1983; 54:431–433. 21. Resnick D. Physical injury: extraspinal sites. In Resnick D (ed). Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, 2002, pp 2783–2933. 22. Protass JJ, Stampfli FW, Osmer JC. Coracoid process fracture diagnosis in acromioclavicular separation. Radiology 1975; 116:61–64. 23. Montgomery SP, Loyd RD. Avulsion fracture of the coracoid epiphysis with acromioclavicular separation: report of two cases and review of the literature. J Bone Joint Surg Am 1977; 59:963–965. 24. Lasda NA, Murray DG. Fracture separation of the coracoid process associated with acromioclavicular dislocation: conservative treatment—a case report and review of the literature. Clin Orthop Relat Res 1978; 134:222–224. 25. Holst AK, Christiansen JV. Epiphyseal separation of the coracoid process without acromioclavicular dislocation. Skeletal Radiol 1998; 27:461–462. 26. Rockwood CA, Williams GR, Young DC. Injuries to the acromioclavicular joint. In Rockwood CA, Green GP, Bucholz RW (eds). Fractures in Adults, 3rd ed. Philadelphia, JB Lippincott, 1991, pp 1181–1251. 27. Yu JS, Dardani M, Fischer RA. MR observations of posttraumatic osteolysis of the distal clavicle after traumatic separation of the acromioclavicular joint. J Comput Assist Tomogr 2000; 24:159–164. 28. Booth CM, Roper BA. Chronic dislocation of the sternoclavicular joint: an operative repair. Clin Orthop Relat Res 1979; 140:17–20. 29. Neer CS II, Rockwood CA Jr. Fractures and dislocations of the shoulder. In Rockwood CA Jr, Green GP (eds). Fractures. Philadelphia, JB Lippincott, 1975, pp 585–815. 30. Nettles JL, Linscheid RL. Sternoclavicular dislocations. J Trauma 1968; 8:158–164. 31. Rockwood CA Jr, Odor JM. Spontaneous atraumatic anterior subluxation of the sternoclavicular joint. J Bone Joint Surg Am 1989; 71:1280–1288. 32. Rockwood CA, Thomas SC, Matsen FA III. Subluxation and dislocations about the glenohumeral joint. In Rockwood CA, Green DP, Bucholz RW (eds). Fractures in Adults, 3rd ed. Philadelphia, JB Lippincott, 1991, pp 1021–1179. 33. Gove N, Ebraheim NA, Glass E. Posterior sternoclavicular dislocations: a review of management and complications. Am J Orthop 2006; 35:132–136. 34. Hovelius L. Incidence of shoulder dislocation in Sweden. Clin Orthop 1982; 166:127–131.

35. Hovelius L. Shoulder dislocation in Swedish ice hockey players. Am J Sports Med 1978; 6:373–377. 36. Curranino G, Sheffield E, Twickler D. Congenital glenoid dysplasia. Pediatr Radiol 1998; 28:30–37. 37. Weishaupt D, Zanetti M, Nyffeler RW, et al. Posterior glenoid rim deficiency in recurrent (atraumatic) posterior shoulder instability. Skeletal Radiol 2000; 29:204–210. 38. Brewer JB, Wubben RC, Carrera GF. Excessive retroversion of the glenoid cavity: a cause of non-traumatic posterior instability of the shoulder. J Bone Joint Surg Am 1986; 68:724–731. 39. Downey EF Jr, Curtis DJ, Brower AC. Unusual dislocations of the shoulder. AJR Am J Roentgenol 1983; 140:1207–1210. 40. Hill HA, Sachs MD. The grooved defect of the humeral head: a frequently unrecognized complication of dislocations of the shoulder joint. Radiology 1940; 35:690–700. 41. Rowe CR. Prognosis in dislocations of the shoulder. J Bone Joint Surg Am 1956; 38:957–977. 42. Danzig LA, Greenway G, Resnick D. The Hill-Sachs lesion: an experimental study. Am J Sports Med 1980; 8:328–332. 43. Edwards TB, Boulahia A, Walch G. Radiographic analysis of bone defects in chronic anterior shoulder instability. Arthroscopy 2003; 19:732–739. 44. Kummel BM. Fractures of the glenoid causing chronic dislocation of the shoulder. Clin Orthop Relat Res 1970; 69:189–191. 45. Edmond M, Le Sage N, Lavoie A, Rochette L. Clinical factors predicting fractures associated with an anterior shoulder dislocation. Acad Emerg Med 2004; 11:853–858. 46. Neviaser JS. Posterior dislocations of the shoulder: diagnosis and treatment. Surg Clin North Am 1963; 43:1623–1630. 47. McLaughlin HL. Posterior dislocation of the shoulder. J Bone Joint Surg Am 1952; 34:584–590. 48. Wilson JC, McKeener FM. Traumatic posterior (retroglenoid) dislocation of the humerus. J Bone Joint Surg Am 1949; 31:160–172. 49. Arndt JH, Sears AD. Posterior dislocation of the shoulder. AJR Am J Roentgenol 1965; 94:639–645. 50. Robinson CM, Aderinto J. Posterior shoulder dislocations and fracture-dislocations. J Bone Joint Surg Am 2005; 87:639–650. 51. Schwartz E, Warren RF, O’Brien SJ, Fronek J. Posterior shoulder instability. Orthop Clin North Am 1987; 18:409–419. 52. Cisternino SJ, Rogers LF, Stufflebam BC, Kruglik GD. The trough line: a radiographic sign of posterior shoulder dislocation. AJR Am J Roentgenol 1978; 130:951–954. 53. Wadlington VR, Hendrix RW, Rogers LF. Computed tomography of posterior fracture-dislocations of the shoulder: case reports. J Trauma 1992; 32:113–115. 54. Mok DWH, Fogg AJB, Hokan R, Bayley JIL. The diagnostic value of arthroscopy in glenohumeral instability. J Bone Joint Surg Br 1990; 72:698–700. 55. Nobel W. Posterior traumatic dislocation of the shoulder. J Bone Joint Surg 1962; 44:523–537. 56. Bottoni CR, Franks BR, Moore JH, et al. Operative stabilization of posterior shoulder instability. Am J Sports Med 2005; 33:996–1002. 57. Roberts A, Wickstrom J. Prognosis of posterior dislocation of the shoulder. Acta Orthop Scand 1971; 42:328–337. 58. Danzig L, Resnick D, Greenway G. Evaluation of unstable shoulders by computed tomography: a preliminary study. Am J Sports Med 1982; 10:138–141. 59. Richards RD, Sartoris DJ, Pathria MN, Resnick D. Hill-Sachs lesion and normal humeral groove: MR imaging features allowing their differentiation. Radiology 1994; 190:665–668. 60. Workman TL, Burkhard TK, Resnick D, et al. Hill-Sachs lesion: comparison of detection with MR imaging, radiography, and arthroscopy. Radiology 1992; 185:847–852. 61. Yu JS, Greenway G, Resnick D. Osteochondral defect of the glenoid fossa: cross-sectional imaging features. Radiology 1998; 206:35–40. 62. Griffith JF, Antonio GE, Tong CW, Ming CK. Anterior shoulder dislocation: quantification of glenoid bone loss with CT. AJR Am J Roentgenol 2003; 180:1423–1430. 63. Imatani RJ. Fractures of the scapula: a review of 53 fractures. J Trauma 1975; 15:473–478. 64. Armstrong CP, Van Der Spuy J. The fractured scapula: importance and management based on a series of 62 patients. Injury 1984; 15:324–329.

CHAPTER 65. Weening B, Walton C, Cole PA, et al. Lower mortality in patients with scapular fractures. J Trauma 2005; 59:1477–1481. 66. Thompson DA, Flynn TC, Miller PW, Fischer RP. The significance of scapular fractures. J Trauma 1985; 25:974–977. 67. McGahan JP, Rab GT, Dublin A. Fractures of the scapula. J Trauma 1980; 20:880–883. 68. Rowe CR. Prognosis in dislocations of the shoulder. J Bone Joint Surg Am 1956; 38:957–977. 69. Harris RD, Harris JH. The prevalence and significance of missed scapular fractures in blunt chest trauma. AJR Am J Roentgenol 1988; 151:747–750. 70. Froimson AI. Fracture of the coracoid process of the scapula. J Bone Joint Surg Am 1978; 60:710–711. 71. Benchetrit E, Friedman B. Fracture of the coracoid process associated with subglenoid dislocation of the shoulder. J Bone Joint Surg Am 1979; 61:295–296. 72. Wong-Pack WK, Bobeehko PE, Becker EJ. Fracture of the coracoid with anterior shoulder dislocation. J Can Assoc Radiol 1980; 31:278–279. 73. Garcia-Elias M, Salo JM. Non-union of a fractured coracoid process after dislocation of the shoulder. J Bone Joint Surg Br 1985; 67:722–723. 74. Smith DM. Coracoid fracture associated with acromioclavicular dislocation: a case report. Clin Orthop Relat Res 1975; 108:165–167. 75. McAdams TR, Blevins FT, Martin TP, DeCoster TA. The role of plain films and computed tomography in the evaluation of scapular neck fractures. J Orthop Trauma 2002; 15:7–11. 76. Horak J, Nilsson BE. Epidemiology of fracture of the upper end of the humerus. Clin Orthop Relat Res 1975; 112:250–253. 77. Lind T, Kroner K, Jensen J. The epidemiology of fractures of the proximal humerus. Arch Orthop Trauma Surg 1998; 108:285–287. 78. Neer CS II. Displaced proximal humeral fractures: I. Classification and evaluation. J Bone Joint Surg Am 1970; 52:1077–1089. 79. Neer CS II. Displaced proximal humeral fractures: II. Treatment of three-part and four-part displacement. J Bone Joint Surg Am 1970; 52:1090–1103. 80. Ross GJ, Love MD. Isolated avulsion fractures of the lesser tuberosity of the humerus: report of two cases. Radiology 1989; 172:833–834. 81. Castagno AA, Shuman WP, Kilcoyne RF, et al. Complex fractures of the proximal humerus: role of CT in treatment. Radiology 1987; 165:759–762. 82. Mora Guix JM, Gonzalez AS, Brugalla JV, et al. Proposed protocol for reading images of humeral head fractures. Clin Orthop Relat Res 2006; 448:225–233. 83. Doornberg J, Lindenhovius A, Kloen P, et al. Two- and threedimensional computed tomography for the classification and management of distal humeral fractures: evaluation of reliability and diagnostic accuracy. J Bone Joint Surg Am 2006; 88:1795–1801. 84. Harness NG, Ring D, Zurakowski D, et al. The influence of three-dimensional computed tomography reconstructions on the characterization and treatment of distal radial fractures. J Bone Joint Surg Am 2006; 88:1315–1323. 85. Manashil G, Laufer S. Congenital pseudoarthrosis of the clavicle: report of three cases. AJR Am J Roentgenol 1979; 132:678–679.

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86. Buckerfield CT, Castle ME. Acute traumatic retrosternal dislocation of the clavicle. J Bone Joint Surg Am 1984; 66:379–384. 87. McKenzie JMM. Retrosternal dislocation of the clavicle. J Bone Joint Surg Br 1963; 45:138–141. 88. McLaughlin HL, Cavallaro WU. Primary anterior dislocation of the shoulder. Am J Surg 1950; 80:615–621. 89. te Slaa, Wijffels MP, Brand R, Marti RK. The prognosis following acute primary glenohumeral dislocation. J Bone Joint Surg Br 2004; 86:58–64. 90. Robinson CM, Howes J, Murdoch H, et al. Functional outcome and risk of recurrent instability after primary traumatic anterior shoulder dislocation in young patients. J Bone Joint Surg Am 2006; 88:2326–2336. 91. Simonet WT, Cofield RH. Prognosis in anterior shoulder dislocation. Am J Sports Med 1984; 12:19–24. 92. Takase K, Yamamoto K. Intraarticular lesions in traumatic anterior shoulder instability: a study based on the results of diagnostic imaging. Acta Orthop 2005; 76:854–857. 93. Janecki CJ, Barnett DC. Fracture-dislocation of the shoulder with biceps tendon interposition. J Bone Joint Surg Am 1979; 61:141–143. 94. Hawkins RJ, Koppert G, Johnston G. Recurrent posterior instability (subluxation) of the shoulder. J Bone Joint Surg Am 1984; 66:169–174. 95. Hayes JM, VanWinkle GN. Axillary artery injury with minimally displaced fracture of the neck of the humerus. J Trauma 1983; 23:431–433. 96. Lim EVA, Day LJ. Thrombosis of the axillary artery complicating proximal humeral fractures. J Bone Joint Surg Am 1987; 69:778–780. 97. Barger WL, Marcus RE, Ittleman FP. Late thoracic outlet syndrome secondary to pseudoarthrosis of the clavicle. J Trauma 1984; 24:847–859. 98. Bjernneld H, Hovelius JT, Thorling J. Acromioclavicular separations treated conservatively: A 5-year follow-up study. Acta Orthop Scand 1983; 54:743–745. 99. Larsen E, Bjerg-Nielsen A, Christensen P. Conservative or surgical treatment of acromioclavicular dislocation: a prospective, controlled, randomized study. J Bone Joint Surg Am 1986; 68:552–555. 100. Bicos J, Nicholson GP. Treatment and results of sternoclavicular joint injuries. Clin Sports Med 2003; 22:359–370. 101. Omer GE. Osteotomy of the clavicle in surgical reduction of anterior sternoclavicular dislocation. J Trauma 1967; 7:584–590. 102. Lemos MJ, Tolo ET. Complications of the treatment of the acromioclavicular and sternoclavicular joint injuries, including instability. Clin Sports Med 2003; 22:371–385. 103. Fronek J, Warren RF, Bowin M. Posterior subluxation of the glenohumeral joint. J Bone Joint Surg 1989; 71:205–216. 104. Hessmann M, Kirchner R, Baumgaertel F, et al. Treatment of unstable distal clavicular fractures with and without lesions of the acromioclavicular joint. Injury 1996; 27:47–52. 105. Zenni EJ Jr, Krieg JK, Rosen MJ. Open reduction and internal fixation of clavicular fractures. J Bone Joint Surg Am 1981; 63:147–151. 106. Re P, Gallo RA, Richmond JC. Transhumeral head plasty for large Hill-Sachs lesions. Arthroscopy 2006; 22:798:e1–e4.

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C H A PP T T EE RR

Shoulder Impingement Syndromes George C. Nomikos and Mahvash Rafii

PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS The etiology of rotator cuff tendinosis and tears is likely multifactorial, involving both intrinsic and extrinsic factors. Multiple causal factors have been described in association with rotator cuff pathology, including vascular, degenerative, traumatic, and anatomic/mechanical factors.1 The diagnosis is based on the patient’s history and findings on physical examination, supplemented by imaging findings. The modern understanding of shoulder impingement owes much to the description and classification described by Neer.2 He popularized the theory that extrinsic mechanical factors primarily related to the anterior one third of the acromion process, the coracoacromial ligament, and sometimes the acromioclavicular joint are responsible for impingement (predominantly of the supraspinatus tendon and long head of the biceps tendon), which he believed was, in turn, responsible for 95% of rotator cuff tears.3 This is known as primary mechanical impingement (Fig. 8-1).3 He postulated that the development of rotator cuff tears was best explained by the shape and slope of the anterior acromion.3 Patients with a “prominent” anterior edge of the acromion should be more susceptible to impingement and, by implication, rotator cuff tears (Fig. 8-2).3 Neer described three stages of impingement lesions.3 In stage I there is edema and hemorrhage of the rotator cuff.3 Stage I lesions tend to be seen in patients younger than 25 years old, although they may be seen in patients of any age, and may heal with only conservative treatment.3 Clinical symptoms of these lesions may be the same as stage III lesions, making clinical differentiation difficult.3 With repeated mechanical irritation, there is inflammation and fibrosis of the subacromial/subdeltoid bursa and “tendinitis,” which tends to be exacerbated by activities performed with the arm over the head (stage II).3 This stage of disease is typically seen in patients aged 25 to 40, according to Neer.3 150

Stage III is characterized by partial or full-thickness rotator cuff tears, biceps tendon rupture, and osseous changes.3 Ogawa and colleagues studied the relationship between subacromial enthesophyte formation and rotator cuff abnormalities in a series of 1029 shoulders.4 In their control group, small enthesophyte formation (less than 5 mm) was associated with advancing age; however, the presence of a small enthesophyte had no significant association with rotator cuff tears. This study demonstrated a high association between enthesophytes of 5 mm or greater in size and bursal surface rotator cuff tears, full-thickness supraspinatus tears, and massive rotator cuff tears.

■ FIGURE 8-1 This anterior view of the shoulder demonstrates the site of primary mechanical impingement on the rotator cuff (green shaded area) by the anterior one third of the acromion process and coracoacromial ligament, as postulated by Neer.

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KEY POINTS The etiology of rotator cuff tendinosis and tears is likely multifactorial. ■ Neer suggested that subacromial impingement, due to a “prominent” anterior edge of the acromion, accounts for 95% of all rotator cuff tears. ■ Codman postulated an area of hypovascularity (critical zone) in the rotator cuff that may be a site of tendon degeneration. ■ Risk factors predisposing to subacromial impingement include a subacromial enthesophyte, a type III acromion, and an os acromiale. ■ The cable and crescent model has been proposed to explain the biomechanics of rotator cuff tears. ■ MRI is excellent in the diagnosis of full-thickness rotator cuff tears but is less accurate in the diagnosis of partial-thickness tears. ■ In experienced hands, ultrasonography has an accuracy similar to MRI in the diagnosis of both full-thickness and partial-thickness rotator cuff tears and a greater patient satisfaction rate. ■ The phenomenon of subcoracoid impingement has been suggested as a potential etiology of some subscapularis tendon tears. ■ Narrowing of the coracohumeral space and partial tearing of the articular surface fibers of the subscapularis tendon are suggestive of subcoracoid impingement. ■ The “roller-wringer” effect has been proposed as a potential mechanism of subcoracoid impingement. ■ Internal (posterosuperior) impingement has been described predominantly in throwing athletes. ■ Classic findings of internal impingement include articular surface fraying and tearing of the rotator cuff, fraying and tearing of the posterosuperior glenoid labrum, and subchondral cyst formation in the humeral head deep to the infraspinatus tendon insertion. ■ Anterosuperior (anterior internal) impingement syndrome has been proposed as a potential mechanism of unexplained anterior shoulder pain not due to subacromial impingement. ■ Findings associated with anterosuperior impingement include lesions of the biceps pulley, medial subluxation of the long head of the biceps tendon, and partial articular surface tears of the cranial fibers of the subscapularis tendon. ■ Imaging of the rotator interval is best accomplished with MR arthrography. ■ A period of conservative treatment is appropriate initially in most cases of impingement and rotator cuff tears. ■ Early surgical intervention is suggested in patients with a full-thickness rotator cuff tear who demonstrate weakness and functional impairment of the rotator cuff. ■ Operative treatment of rotator cuff tears is indicated if conservative treatment fails. ■ Traditionally, rotator cuff repair has been performed using an open approach; however, the current trend is toward arthroscopic repair (which has shown promising results in the literature). ■ Rotator cuff arthropathy is a serious potential complication of chronic untreated massive rotator cuff tears. ■

■ FIGURE 8-2 An oblique sagittal fat-suppressed proton density– weighted MR image of the shoulder demonstrates a “prominent” anterior edge of the acromion (arrow) caused by an anterior acromial enthesophyte.

Secondary extrinsic impingement is most commonly seen in throwing athletes younger than 35 years old and is likely a result of glenohumeral or scapular instability.5 It is thought to be a much less common cause of rotator cuff abnormality related to a decrease in the supraspinatus outlet due to instability of the glenohumeral joint.5 With repetitive stress, as is often seen in athletes who throw overhand or over their head, there is damage to the glenohumeral ligaments, leading to mild instability.5 This instability leads to increased stress on the rotator cuff (dynamic stabilizers) and subsequent fatigue.5 This allows anterior translation of the humeral head and secondary mechanical impingement of the rotator cuff on the coracoacromial arch.5 Scapulothoracic muscle weakness or inflexibility (especially of the trapezius, rhomboids, and serratus anterior muscles) may lead to scapular instability, which may, in turn, lead to impingement of the rotator cuff by the coracoacromial arch during throwing.5 Intrinsic factors have also been implicated in the development of rotator cuff tears. Multiple studies have shown that abnormalities may occur in the rotator cuff without associated abnormalities of the undersurface of the acromion. Contrary to Neer’s hypothesis that mechanical impingement is the leading cause of rotator cuff tears, many authors have postulated that tendon degeneration is the primary cause. Tendon degeneration is thought to be associated with aging, and virtually all ruptured tendons demonstrate evidence of degeneration.1 In their anatomic and radiologic study of 76 shoulders, Ogata and Uhthoff concluded that the majority of rotator cuff tears are caused by intrinsic degenerative tendinopathy, not by impingement.6 This view was supported by the finding

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■ FIGURE 8-3 This diagram shows “wringing out” of the vessels in the critical zone of the rotator cuff with the arm in adduction. The changes of avascularity may precede tendon degeneration.

of increasing incidence and severity of rotator cuff tears with age and by the lack of correlation between aging and degenerative changes of the undersurface of the acromion (with the exception of very advanced degenerative changes).6 Furthermore, Kjellin and coworkers showed that isolated histologic abnormalities, which may lead to tendon tears, may occur on the articular surface of the supraspinatus tendon.7 This suggests that impingement, which would be expected to cause predominantly bursal surface abnormalities, may not be the primary or even most common cause of rotator cuff tears.7 Codman initially described a region of relative hypovascularity in the rotator cuff 5 to 20 mm from its insertion on the greater tuberosity, the critical portion or zone.8 Rathbun and Macnab’s cadaveric study also showed a consistent zone of relative avascularity in the supraspinatus tendon varying in location between 1 cm from the point of tendon insertion up to the point of tendon insertion.9 They also postulated that pressure exerted by the head of the humerus on the supraspinatus tendon with the arm adducted may “wring out” the vessels in this area of relative avascularity (Fig. 8-3).9 They demonstrated a similar area of avascularity in the intracapsular portion of the biceps tendon where it is stretched out over the humeral head near its point of insertion.9 These authors also showed that the changes of tendinitis, calcification, and tearing of the supraspinatus tendon occur in this region of relative avascularity and that the changes of avascularity precede the degenerative changes in the tendon.9 Lohr and Uhthoff demonstrated that while the bursal surface of the supraspinatus tendon in the critical zone does show abundant blood supply, the articular surface is deficient in blood supply, likely making it more susceptible to degeneration and tearing than the bursal surface.10 Although many authors have suggested that there is decreased vascularity to the critical zone of the rotator cuff, it must be noted that other authors disagree. Whereas cadaveric studies have suggested relative avascularity in the critical zone, other studies in symptomatic patients have revealed hyperemia or neovascularization in the critical zone in symptomatic patients.11 This is supported by the fact that hyperemia and marginal bleeding is commonly observed at the margins of rotator

cuff tears at the time of surgery.11 Some have suggested that symptomatic lesions may be due to mechanical impingement, leading to hypervascularity in the critical zone, and that the tears seen in association with hypovascularity in the cadaveric studies likely represent predominantly asymptomatic lesions.11 Furthermore, after their study of 32 cadaveric shoulders, Clark and Harryman concluded that while the vessels in the deeper portion of the supraspinatus tendon are relatively small compared with those in the more superficial layers, the blood supply to this portion of the tendon is sufficient for the metabolic needs of the tissue.12 A recent prospective study of 66 patients with partialthickness tears of the rotator cuff by Ko and colleagues suggests that articular surface tears are predominantly associated with intrinsic pathology and degeneration of the rotator cuff and that bursal surface tears are predominantly associated with subacromial impingement superimposed on less severe degenerative changes of the rotator cuff.13 Their results also indicate that the acromial insertion of the coracoacromial ligament is the primary area where impingement of the rotator cuff occurs, although the acromioclavicular joint can become the area of impingement in some circumstances.13 Trauma may also play a role in the development of rotator cuff tears. The presence of a displaced fracture of the greater tuberosity implies a rupture of the rotator cuff by definition (Fig. 8-4).1 Acute trauma to the shoulder with or without associated dislocation may be responsible for tears of the rotator cuff, especially in older individuals (who likely have underlying degeneration) (Fig. 8-5).1 Recurrent multidirectional and anterior instability as well as sports that require repetitive motions in an abducted, extended, and externally rotated position (throwing or serving motion) have also been implicated as traumatic causes of rotator cuff tears.1 Clinically, patients usually present with a history of slowly developing anterior shoulder pain increasing over a period of weeks to months that may radiate to the lateral humerus.14 The pain is often related to activities performed with the arm over the head.14 Patients typically experience pain with abduction and external rota-

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■ FIGURE 8-4

Proton density–weighted (A) and fat-suppressed proton density–weighted (B) oblique coronal MR images demonstrate a minimally displaced fracture of the greater tuberosity of the humerus (arrows).

■ FIGURE 8-5 Sequential oblique coronal fat-suppressed proton density–weighted MR images (A and B) demonstrate a traumatic partial tear of the infraspinatus tendon at the myotendinous junction (arrows).

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tion or elevation and internal rotation but usually retain a full range of shoulder motion.15 Neer described the “impingement test” to help distinguish shoulder impingement from other causes of shoulder pain. To perform this test, the scapula is stabilized with one hand while the examiner’s other hand raises the patient’s arm in forced forward elevation to impinge against the acromion. If the shoulder pain produced by this maneuver is relieved by a subacromial injection of 10 mL of 1.0% lidocaine (Xylocaine), then according to Neer, the cause of the shoulder pain can be attributed to (primary mechanical extrinsic) impingement. Several uncommon impingement syndromes deserve special mention. These include subcoracoid impingement and internal (posterosuperior) impingement. Subcoracoid impingement is an uncommon type of shoulder impingement in which there is narrowing of the coracohumeral space and resultant impingement of the subscapularis tendon. Patients complain of pain in the anterior aspect of the shoulder that is caused by adduction, internal rotation, and forward flexion, because this position decreases the coracohumeral space (space between the tip of the coracoid process and the lesser tuberosity).16 Internal impingement is classically, but not exclusively, associated with throwing overhand or over the head and occurs when the shoulder is placed in marked abduction and external rotation, at which time there may be impingement of the posterior supraspinatus and anterior infraspinatus tendons between the humeral head and glenoid.17 Findings in this type of impingement include posterosuperior labral lesions, superior labral tears (SLAP tears), humeral head articular cartilage lesions, humeral head cystic changes, and rotator cuff abnormalities of the infraspinatus and, less commonly, supraspinatus tendons.18 Anterosuperior impingement is a more recently described form of impingement thought to be a cause of anterior shoulder pain in some patients. Findings associated with this form of impingement include lesions of the biceps pulley, medial subluxation of the long head of the biceps tendon, and partial tears of the cranial fibers of the subscapularis tendon.

DEFINITIONS Several definitions should be established before proceeding to a review of rotator cuff pathology. Partial-thickness rotator cuff tears do not produce a communication between the glenohumeral joint and the subacromial/subdeltoid bursa, and full-thickness tears do produce such a communication. The former can be subdivided into articular and bursal surface tears depending on which side of the rotator cuff is involved. Rim-rent tears, initially described by Codman, are partial insertional articular surface tears of the anterior leading margin of the supraspinatus tendon (Fig. 8-6).19 Interstitial or intrasubstance tears are partial-thickness tears that are confined to the substance of the tendon and do not contact either the bursal or articular surface of the tendon. Small full-thickness tears are defined as those that measure less than 1 cm in longest diameter, medium-sized tears measure less than 3 cm, large tears measure less than 5 cm, and massive tears measure greater than 5 cm in longest diameter.20

■ FIGURE 8-6

Oblique coronal, fat-suppressed, proton density– weighted MR image demonstrates a partial articular surface insertional tear of the anterior supraspinatus tendon, also known as a rim-rent tear (arrow).

CLASSIFICATION Patte has proposed a classification system for rotator cuff tears based on the following criteria: extent of tear, topography of the tear in the sagittal plane, topography of the tear in the frontal plane, quality of the muscle, and state of the long head of the biceps.21 He defined the extent of the tear in centimeters measured at the level of the osseous insertion and divided it into four possible categories: group I lesions are defined as partial tears or full-thickness tears measuring 1 cm in sagittal diameter at the level of the osseous detachment, group II lesions represent full-thickness tears of the entire supraspinatus tendon, group III lesions are full-thickness tears involving more than one tendon, and group IV lesions are massive tears with secondary osteoarthritis.21 In the sagittal plane lesions are divided into six segments: segment 1 represents an isolated subscapularis tear; segment 2 represents an isolated coracohumeral ligament tear (usually traumatic in etiology); segment 3 includes isolated supraspinatus tears; segment 4 includes tears involving the supraspinatus and upper half of the infraspinatus tendon; segment 5 lesions involve the supraspinatus and entire infraspinatus tendons; and segment 6 lesions involve the entire cuff, including the subscapularis, supraspinatus, and infraspinatus tendons (Fig. 8-7) 21 This system does not address the teres minor, because tears of the teres minor tendon are extremely uncommon.21 In the coronal plane, tears are divided into three stages: stage 1 tears show little retraction of the proximal tendon stump, stage 2 lesions demonstrate retraction of the stump to the level of the humeral head, and stage 3 lesions demonstrate retraction of the tendon to the level of the glenoid (Fig. 8-8).21 Fatty atrophy in Patte’s system is divided into four stages and is based on

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ing the rotator cuff.21 In the setting of extensive tears, abnormalities of the biceps tendon contribute to elevation of the humeral head and may adversely affect the results of rotator cuff repair.21

PATHOPHYSIOLOGY Anatomy

■ FIGURE 8-7 This diagram shows the division of rotator cuff tears in the sagittal plane as defined by Patte. See text for details.

CT assessment.21 Currently, however, MRI is predominantly used for determination of the degree of muscle atrophy (see later). Determination of muscle atrophy is important because functional outcome in rotator cuff repair is strongly associated with the recovery of muscle strength.21 The status of the biceps tendon, including dislocation and tearing, is also important when assess-

■ FIGURE 8-8

Clark and Harryman studied the structure of the rotator cuff tendons in 32 cadavers and demonstrated that all four of the tendons of the rotator cuff fuse to form a common insertion on the humeral tuberosities.12 There is merging between the fibers of the subscapularis and supraspinatus anteriorly and between the fibers of the infraspinatus and supraspinatus posteriorly (Fig. 8-9).12 The superficial fibers of the tendons appear to pass along lines parallel to the orientation of the individual muscles, and the coalescence of the tendon fibers appears to occur primarily in the deep layers (see later discussion).12 Tendinous slips extend from the supraspinatus and subscapularis tendons to form a sheath around the biceps tendon (see later discussion). The deep portion of the sheath is formed by fibers from the subscapularis (primarily) and supraspinatus tendons, and the roof of the sheath over the biceps tendon is formed by fibers from the supraspinatus tendon (Fig. 8-10).12 Histologic examination demonstrated that the cuffcapsule complex of the supraspinatus and infraspinatus tendons is composed of five layers: layer 1 (most superficial) is a thin layer composed of obliquely oriented fibers that represent an extension of the coracohumeral ligament and that pass to the greater tuberosity in the rotator interval between the supraspinatus and subscapularis tendons; layer 2 is formed by tightly packed tendon fibers in large bundles that extend from their respective muscles to the humerus; layer 3 is composed of tendon bundles that are smaller and less tightly packed than those in layer 2 and run at a 45-degree orientation to one another; layer 4 is composed of loose connective tissue as well as thick collagen bands (which merge with fibers from the coracohumeral ligament and form a ligamentous

This diagram shows the division of rotator cuff tears in the coronal plane as defined by Patte. There is little tendon retraction in stage 1 lesions, retraction of the tendon stump to the humeral head in stage 2 lesions, and retraction of the tendon stump to the level of the glenoid in stage 3 lesions.

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■ FIGURE 8-9 Anatomy of the rotator cuff insertion. Note the merging of the subscapularis and supraspinatus tendon fibers anteriorly and of the supraspinatus and infraspinatus tendon fibers posteriorly. Fibers from the supraspinatus and subscapularis tendons form part of the sheath around the biceps tendon, only the deep part of which is shown in this figure. BG, bicipital groove; BT, biceps tendon; GT, lesser tuberosity; IS, infraspinatus tendon; LT, lesser tuberosity; SC, subscapularis tendon; SP, supraspinatus tendon.

■ FIGURE 8-10 Fibers from the supraspinatus and subscapularis tendons form a sheath around the biceps tendon as shown here in sagittal cross section through the proximal bicipital groove. The deep portion of the sheath is predominantly formed by fibers from the subscapularis tendon and the roof of the sheath is formed by fibers from the supraspinatus tendon. B, biceps tendon; R, roof of sheath, SC, subscapularis tendon; SP, supraspinatus tendon.

sleeve around the anterior portion of the supraspinatus tendon); and layer 5 is composed of a contiguous layer of interwoven collagen fibrils and forms the capsule of the glenohumeral joint (Fig. 8-11).12 The subscapularis tendon is formed by four to six thick parallel collagen fascicles that pass from the muscle of the subscapularis to the lesser tuberosity where they fan out before inserting on the bone.12 The collagen bundles are tightly packed in the superficial portion of the tendon and are more loosely packed in the deeper portion of the tendon where the tendon fibers are separated by loose connective tissue.12

■ FIGURE 8-11 The cuff-capsule complex of the supraspinatus and infraspinatus tendons is composed of five layers, which are shown here in cross section. See text for details. CHL, coracohumeral ligament; IS, infraspinatus tendon; SP, supraspinatus tendon.

Several anatomic variants have been implicated in the etiology of shoulder impingement and rotator cuff tears. Among primary extrinsic factors responsible for impingement, acromial shape has received much attention. Bigliani and Morrison described three different acromial morphologies: type I flat (17%), type II curved (43%), and type III hooked (39%) (Fig. 8-12). In their study, 70% of rotator cuff tears were seen in patients with a type III acromion, whereas only 3% of tears were seen in patients with a type I acromion. In addition, 70% of the patients with an anterior subacromial enthesophyte also demonstrated rotator cuff tears.22 These data suggest a high degree of correlation between anterior acromial morphology and rotator cuff pathology. A type IV acromion, which is thought to be relatively uncommon, has also been described. This type of acromion demonstrates a convex distal undersurface and has not been associated with rotator cuff tears.23 Although sometimes implicated as a cause of impingement, at least one study has suggested that lateral downsloping of the acromion is not significantly associated with extrinsic impingement.24 The presence of an os acromiale has also been implicated by some as a potential factor leading to impingement.25,26 The acromial apophysis forms from four individual ossification centers (preacromion, mesacromion, meta-acromion, and basiacromion). Failure of fusion between the acromial apophysis and the spine of the scapula, which should occur by age 22 to 25, results in an os acromiale, the type depending on which ossification centers fail to fuse (Fig. 8-13).25,27 The os acromiale may lead to shoulder pain due to instability at the site of nonunion or may be displaced inferiorly into the rotator cuff by the pull of the deltoid muscle, leading to impingement (Fig. 8-14).25

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■ FIGURE 8-13 View of the shoulder from above demonstrating the different types of os acromiale that may result depending on which of the acromial ossification centers fails to fuse. PA, preacromion; MSA, mesacromion; MTA, meta-acromion.

■ FIGURE 8-12 The three types of acromion as described by Bigliani and Morrison: type 1 (flat), type 2 (smoothly curved), and type 3 (angular curved or hooked).

is seen more commonly in younger patients. It has been suggested that with aging there is a transition from the crescent-dominant to the cable-dominant pattern, as the crescent begins to thin and the cable must assume increasing loads.28 It has also been postulated, based on arthroscopic observations, that the crescent is not under tension in cable-dominant shoulders.28 Therefore, tears of the crescent in cable-dominant shoulders may not be biomechanically significant, whereas tears in the cable likely are biomechanically important.28 In addition, Burkhart and colleagues’ biomechanical data suggest that tears in the crescent will not propagate solely on a mechanical basis but also require underlying biologic weakening.28

Biomechanics

Pathology

Burkhart and colleagues have described a biomechanical model of the rotator cuff similar to the appearance of a suspension bridge that they have termed the rotator crescent and rotator cable.28 The rotator crescent has been defined as the relatively avascular distal portion of the supraspinatus and infraspinatus tendons and the rotator cable as a thick bundle of fibers running perpendicular to the axis of the supraspinatus tendon that attaches anteriorly and posteriorly to the humerus (Fig. 8-15)28 This configuration has been compared to the appearance of a suspension bridge.28 The cable, which may represent a deep fibrous extension of the coracohumeral ligament, is approximately 2.6 times thicker than the crescent (Fig. 8-16).28 Most rotator cuff tears, both partial and full-thickness, have been noted to occur in the crescent.28 These authors postulated two different types of functional classes of shoulders: cable dominant and crescent dominant.28 In the former, which is most commonly seen in older patients, there is stress shielding of the crescent by the cable.28 The crescent-dominant pattern, in which there is no stress shielding of the crescent by the cable,

In their examination of the rotator cuff tendons, Clark and Harryman did not observe extensive pathologic changes; however, their specimens were chosen because they did not demonstrate tears.12 They did note that the rotator cuffs in the specimens greater than 50 years old were usually thinner than those in the younger specimens but the appearance of the collagen fibers and blood vessels in all specimens was relatively similar.12 They also noted that evidence of degeneration, such as hyaline necrosis of collagen, microtears, calcification, and abnormalities of the intima of the arterioles, did not appear to be age related.12 They concluded that aging alone was not responsible for degeneration of the rotator cuff.12 An early report by Kieft and colleagues suggested that increased signal intensity in the rotator cuff on MRI was due to tendon degeneration and inflammation.29 Kjellin and coworkers showed that the predominant changes in the rotator cuff corresponding to signal abnormality on MRI represent tendon degeneration and not inflammation, however.7 In their study, histologic evaluation of areas of abnormal signal intensity demonstrated three

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■ FIGURE 8-14 Axial proton density–weighted (A) and oblique coronal fat-suppressed proton density–weighted (B) MR images demonstrate a mesacromion type os acromiale (A, arrow). Note the increased signal intensity in the bone marrow on the fat-suppressed image in the os acromiale (B, arrow) representing marrow edema and suggesting motion and instability of the os acromiale. There is also tendinosis of the supraspinatus tendon (B, arrowhead).

■ FIGURE 8-15 Superior (left) and posterior (right) projections of the shoulder demonstrate the rotator cable (CA) and crescent (CR). The cable is a thick bundle of fibers that runs perpendicular to the axis of the supraspinatus tendon and extends from the level of the biceps tendon anteriorly to the inferior margin of the infraspinatus tendon posteriorly. The crescent is the thinner, relatively avascular distal portion of the supraspinatus and infraspinatus tendons. BT, biceps tendon; I, infraspinatus muscle; S, supraspinatus muscle; TM, teres minor muscle.

different types of tendon degeneration: eosinophilic, fibrillar, and mucoid.7 Microscopic calcium deposits were also commonly identified.7 The histologic findings seen in the rotator cuff in this study were not findings suggestive of acute inflammation and, therefore, they suggested that the terms tendinosis or tendinopathy are preferable to tendinitis to describe the signal alterations seen in the rotator cuff on MRI.7 Examination of the rotator cuff tendons in a small number of cadavers by Rafii and colleagues also demonstrated that the predominant changes corresponding to abnormal signal intensity without associated tear were those of tendon degeneration and repair, including cellular infiltration and disorganization of tendon fibers.30

Kannus and Jozsa evaluated 891 spontaneously ruptured tendons removed at the time of tendon repair.31 This study was not tailored to evaluate the rotator cuff but instead to evaluate ruptured tendons in general.31 None of the ruptured tendons in their study demonstrated a normal structure.31 Ninety-seven percent of the tendons in their series demonstrated signs of degeneration, including hypoxic degenerative tendinopathy, mucoid degeneration, tendolipomatosis, and/or calcifying tendinopathy.31 Such changes were identified in only 34% of the control tendons.31 They confirmed that spontaneous rupture of a tendon is virtually always associated with preexisting degeneration.31 In addition, they found no signs of infiltration or inflammation in the tendons that they evaluated.31

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MANIFESTATIONS OF THE DISEASE Subacromial Impingement and Rotator Cuff Tears Radiography

■ FIGURE 8-16 A coronal section through the shoulder demonstrates the thickened area of the rotator cable and the thinner rotator crescent. The inset image again demonstrates the thickened area (T) representing the cable and the thinner area of the crescent (t).

They concluded that many factors likely lead to tendon degeneration, which, in turn, leads to a reduction in the tensile strength of the tendon and the possibility for rupture.31 While the rotator cuff tendons were not specifically targeted for examination in this study, the findings of this study are nonetheless instructive.

■ FIGURE 8-17

Radiographs are essential in evaluation of the rotator cuff. Radiographs are important to evaluate for other pathologic processes that may simulate rotator cuff tears, such as fractures or calcific tendinitis (Fig. 8-17).32 Calcific tendin itis may coexist with underlying rotator cuff tears, especially in older patients and in those with small calcium deposits.33 Subacromial enthesophyte formation, as discussed earlier, is significantly associated with shoulder impingement and has been shown to be presumptive evidence of shoulder impingement.15 The anterior portion of the acromion is often difficult to see on conventional views of the shoulder secondary to superimposition on the body of the acromion.34 An impingement view has been described in which the x-ray beam is angled 22 to 25 degrees caudad from the anteroposterior projection in an attempt to see the anterior portion of the acromion, the area that Neer believed to be responsible for the vast majority of impingement lesions, to better advantage.34 In a study of 523 patients with chronic shoulder pain, the impingement view demonstrated 100 subacromial enthesophytes whereas only 18 were visible on the routine views.34 The supraspinatus outlet view, originally described by Neer and Poppen, is a lateral scapular view with caudal angulation of the x-ray beam that, when properly performed, allows evaluation of the shape and slope of the acromion, prominence of the acromioclavicular joint, thickness of the acromion, presence of subacromial enthesophyte formation, and adequacy of subacromial decompression (Fig. 8-18).35 Osteophyte formation on the undersurface of the acromioclavicular joint has also been associated with impinge-

External rotation (A) and transscapular lateral (B) views of the left shoulder demonstrate calcium hydroxyapatite deposition in the supraspinatus (large arrows) and infraspinatus (small arrows) tendons consistent with calcific tendonitis.

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■ FIGURE 8-18 Supraspinatus outlet radiograph of the shoulder demonstrates an enthesophyte on the anterior margin of the acromion process (arrow).

■ FIGURE 8-19 Anteroposterior radiograph of the right shoulder demonstrates severe narrowing of the acromiohumeral space, consistent with a full-thickness rotator cuff tear, as well as impingement of the greater tuberosity against the acromion.

ment.15,36 Impingement due to large acromioclavicular osteophytes likely occurs with greater degrees of shoulder abduction than subacromial impingement.15 Cone and colleagues did not observe impingement by acromioclavicular joint osteophytes as an isolated form of impingement but noted that large acromioclavicular osteophytes commonly coexisted with subacromial enthesophytes.15 An acromiohumeral interval of greater than 6 to 7 mm is considered to be normal, and narrowing of this space to less than this is highly suggestive of a rotator cuff tear (Figs. 8-19 and 8-20).36 Concavity of the undersurface of the acromion (acetabulization) due to articulation between the humeral head and acromion is an additional radiographic sign of a large chronic rotator cuff tear (Fig. 8-21).36 Obliteration of the peribursal fat plane around the subacromial bursa, which is normally best seen on the internal rotation view of the shoulder, is a sensitive but not a specific sign of rotator cuff tears and may be seen in association with other inflammatory processes, such as a calcific tendinitis and rheumatoid arthritis.37 Other radiographic findings associated with rotator cuff tears include sclerosis and flattening of the greater tuberosity, subchondral cyst formation and periosteal reaction, enthesophyte formation involving the greater tuberosity, narrowing of the glenohumeral joint space, and anterior subluxation of the humeral head (Fig. 8-22).15,36

be tailored to the available equipment and to the reader’s experience. It is generally agreed that imaging should be performed in multiple planes, provide good spatial and contrast resolution, and be able to be performed in a reasonable amount of time.39 Coronal oblique and sagittal oblique imaging planes plotted relative to the long axis of the supraspinatus tendon have proved to be the most useful planes for evaluation of the rotator cuff. Several studies have shown that fast spin-echo techniques are equivalent to conventional spin-echo techniques in evaluation of the rotator cuff.38,40 Sonin and colleagues demonstrated 100% correlation between T2-weighted spin-echo and turbo spin-echo sequences in evaluation of the integrity of the rotator cuff and an improved signal-to-noise ratio on the turbo spin-echo images.40 They also demonstrated an overall sensitivity of 89%, specificity of 94%, and accuracy of 92% for the diagnosis of full-thickness rotator cuff tears.40 Carrino and coworkers reported that T2-weighted fast spin-echo sequences yielded diagnostic results similar to conventional spin-echo sequences.38 Reviewers in this study also subjectively preferred the fast spin-echo images to the conventional spin-echo images because of the smaller slice thickness that was possible with the fast spin-echo sequences, and also likely due to decreased motion artifact on the fast spin-echo sequences.38 Fast spin-echo sequences provide a significant decrease in imaging time over conventional spin-echo sequences as well.38 Fast spin-echo sequences are also useful for minimizing artifact in the postoperative shoulder. Fat suppression is useful in improving soft tissue contrast because it allows an expansion in the dynamic range of image display, eliminates chemical shift misregistration artifacts that occur at fat-water interfaces, and reduces artifacts from respiratory motion.41 Singson and coworkers demonstrated that T2-weighted fast spin-echo

Magnetic Resonance Imaging Technical Aspects Magnetic resonance imaging has become the imaging study of choice for evaluation of the rotator cuff because of its ability to detect reliably full-thickness tears of this structure.38 There is no ideal imaging protocol for evaluation of the rotator cuff, and imaging protocols should

■ FIGURE 8-20 Oblique coronal fat-suppressed proton density– weighted (A), oblique coronal proton density–weighted (B), and oblique sagittal fat-suppressed T2-weighted (C) MR images demonstrate a massive full-thickness rotator cuff tear. Note the retraction of the myotendinous junction to the level of the glenoid (A and B, arrows). There is involvement of the entire supraspinatus and infraspinatus tendons as demonstrated by the complete stripping of the tendons from the greater tuberosity (C, arrowheads). Also note the markedly narrowed acromiohumeral interval.

■ FIGURE 8-21 Anteroposterior radiograph of the shoulder demonstrates narrowing of the acromiohumeral distance as well as concavity (acetabulization) of the undersurface of the acromion process, consistent with a full-thickness rotator cuff tear.

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■ FIGURE 8-22 A, AP radiograph of the shoulder demonstrating enthesophyte formation on the greater tuberosity of the humerus, indicating shoulder impingement (arrowhead). B, An oblique coronal T2-weighted MR image of the same shoulder demonstrates an associated full-thickness rotator cuff tear (arrow). C, An oblique coronal MR image of the shoulder in a different patient demonstrates the MR appearance of enthesophyte formation on the greater tuberosity (arrowhead).

images with and without fat suppression were both excellent for the diagnosis of full-thickness tears but that partial-thickness tears were better demonstrated with the use of fat suppression because of increased lesion conspicuity.42 Reinus and colleagues demonstrated improved detection of both full-thickness and partial-thickness tears with the use of fat suppression, although the overall detection of partial-thickness tears in their study was poor (35% detection rate with fat suppression and 15% detection rate without fat suppression).43 Fat-suppression techniques with fast spin-echo T2-weighted sequences employ chemical fat saturation techniques, which rely on the differences in the different resonance frequencies between the protons in fat and water and are subject to several limitations.44 These limitations include lower signal-to-noise ratios than non–fat-suppressed images, uneven fat suppression because of inhomogeneity in the static and radiofrequency magnetic fields, complete failure of fat suppression, and limited use on systems with

low magnetic field strength due to the closer resonance frequencies of fat and water.44 Some authors have therefore advocated a modified inversion recovery sequence (modified short tau inversion recovery [STIR] sequence with an inversion time decreased from 150 to 110 ms) to provide more homogeneous fat suppression.44 The shortening of the inversion time improves the relatively low signal-to-noise ratios seen with typical STIR sequences.44 Kijowski and colleagues showed relatively similar results for this modified STIR sequence relative to fat-suppressed T2-weighted fast spin-echo sequence regarding integrity of the rotator cuff.44

Rotator Cuff Tendinosis Tendinosis is diagnosed on MRI by increased intratendinous signal intensity on proton density– and/or T2-weighted images without tendon disruption.30 The increased signal intensity seen in the setting of tendinosis may be

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homogeneous or heterogeneous and may be focal or diffuse.30 Other MRI findings associated with tendinosis include enlargement of the tendon, a longitudinal intratendinous band of increased signal intensity, or a focal intratendinous zone of increased signal proximal to the tendon insertion on the greater tuberosity (Fig. 8-23).30 Total or partial loss of the peribursal fat plane was present in over half of the patients with tendinosis in a study by Rafii and colleagues (Fig. 8-24).30 A small amount of fluid is also not

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uncommon in the subacromial/subdeltoid bursa in the setting of tendinosis.30

Full-Thickness Rotator Cuff Tears MRI has been shown to be both sensitive and specific for diagnosis of rotator cuff tears in numerous studies. Rafii and colleagues evaluated 80 consecutive patients who had MRI of the rotator cuff and subsequent sur-

■ FIGURE 8-23 Oblique coronal fat-suppressed proton density–weighted (A) and oblique coronal proton density–weighted (B) MR images demonstrate mild thickening and heterogeneously increased signal intensity in the supraspinatus tendon consistent with tendinosis (arrows). Oblique coronal fat-suppressed proton density–weighted (C) and oblique coronal proton density–weighted (D) MR images in another patient demonstrate more severe tendinosis. Note the marked thickening and increased signal intensity in the distal portion of the supraspinatus tendon without evidence of tendon discontinuity.

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■ FIGURE 8-24 A, Oblique coronal proton density–weighted MR image of the shoulder demonstrates a normal peribursal fat plane (arrowheads). B and C, Oblique coronal proton density–weighted MR images from two different patients. Both images demonstrate obscuration of the peribursal fat plane due to adjacent rotator cuff tendinosis (B, arrow; C, arrowheads).

gery and showed an accuracy of 95% for full-thickness tears.30 Zlatkin and coworkers reported an overall sensitivity of 91% and specificity of 88% for rotator cuff tears, whereas the sensitivity and specificity of routine arthography were 88% and 71%, respectively.45 Other investigators have also shown excellent results for diagnosis of full-thickness tears, including Robertson and colleagues, who demonstrated high sensitivity and specificity, as well as low interobserver variability, in the diagnosis of full-thickness tears; Reinus and coworkers, who demonstrated 100% sensitivity for detection of full-thickness tears using fat-suppressed T2-weighted sequences; and Singson and colleagues, who demonstrated 100% sensitivity for full-thickness tears using T2-weighted spin-echo sequences either with or without fat suppression.42,43,46 In their early work on 31 shoulders with surgically confirmed rotator cuff tears, Farley and colleagues described the MRI findings associated with full-thickness rotator cuff tears.47 These findings include fluid

in the subacromial/subdeltoid bursa, discontinuity of the tendon, focal fluid signal intensity in the tendon, thinning of the rotator cuff, muscular atrophy, and retraction of the myotendinous junction (Figs. 8-25 to 8-28; see Fig. 8-20).47 In their study, the most specific finding for rotator cuff tear was supraspinatus muscle atrophy (97% specificity) (see Fig. 8-28), the most sensitive finding was fluid in the subacromial/subdeltoid bursa (93% sensitivity) (see Figs. 8-26 to 8-28), and the most accurate predictor of a full-thickness tear was a gap in the tendon (89% accuracy).47 Carrino and colleagues defined the MRI criteria for a full-thickness tear as fluid or near-fluid signal intensity extending from the articular surface to the bursal surface of the tendon (supraspinatus tendon for the purposes of their work).38 They further divided full-thickness tears into those in which some of the supraspinatus tendon fibers remained intact (incomplete tears) and those in which the entire supraspinatus tendon was disrupted and no supraspinatus tendon fibers were

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the glenohumeral joint, it should be noted that full-thickness tears may sometimes be present in the absence of an apparent tendon defect or fluid extending through the tendon.30 Some full-thickness tears may appear as areas of low or intermediate signal intensity on proton density– weighted and T2-weighted images, representing a severely degenerated tendon, a low signal intensity intact bursal or synovial surface, and granulation/scar tissue.30 These low-to-intermediate signal elements may fill the tear and replace the torn tendinous fibers and may maintain the continuity of the margins of the tendon.30 Tendon retraction is also often associated with full-thickness rotator cuff tears and is well assessed on MRI. Retraction is defined as medial migration of the myotendinous junction of the tendon away from its normal position (see Figs. 8-8, 8-20, and 8-28).38 Normally, the myotendinous junction of the supraspinatus tendon lies over the region of the middle third of the articular surface of the humeral head.38 ■ FIGURE 8-25 This oblique coronal fat-suppressed proton density– weighted MR image demonstrates a full-thickness insertional rotator cuff tear (arrow). There is discontinuity of the tendon and fluid extending from the articular surface to the bursal surface of the tendon. There is only minimal tendon retraction (see Fig. 8-8).

identified extending completely across from the muscle to the greater tuberosity (complete tears).38 Whereas in the setting of full-thickness tears the intense signal on the T2-weighted images may bridge the entire tendon, extending from the subacromial/subdeltoid bursa into

■ FIGURE 8-26

Partial-Thickness Rotator Cuff Tears The majority of partial-thickness rotator cuff tears appear to involve the supraspinatus tendon.48 Ellman has divided partial-thickness tears into articular surface, bursal surface, and interstitial (intrasubstance), indicating which portion of the tendon is involved.49 Partial-thickness tears can also be divided using size criteria: grade 1 is 3 mm deep, grade 2 is 3 to 6 mm deep, and grade 3 is 6 mm deep.49 Grade 3 lesions imply involvement of 50% of the thickness of the cuff and are significant lesions.49 Superficial fraying does not constitute a tear in this classification system.49

Oblique coronal fat-suppressed proton density–weighted (A) and oblique sagittal T2-weighted (B) MR images demonstrate an insertional full-thickness rotator cuff tear. There is fluid extension from the bursal to the articular surface of the tendon as well as tendon discontinuity (A, arrow). Note the subacromial/subdeltoid bursal fluid (A, arrowheads). There is also more tendon retraction than in Figure 8-25. The sagittal image demonstrates the anterior to posterior extent of the tear well (arrowheads). Note that a portion of the rotator cuff remains attached to the greater tuberosity posteriorly (B, arrow).

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■ FIGURE 8-27

Oblique coronal proton density–weighted (A), oblique coronal fat-suppressed, proton density–weighted (B), and oblique sagittal fat-suppressed proton density–weighted (C) MR images demonstrate a full-thickness rotator cuff tear proximal to the tendon insertion on the greater tuberosity. Note the fluid extension from the articular surface to the bursal surface of the tendon and the tendon discontinuity (arrows). The distal portion of the tendon remains attached to the greater tuberosity (A, arrowheads). There is also fluid in the subacromial/subdeltoid bursa (B and C, arrowheads). Note the acromioclavicular joint osteoarthrosis.

Clinically, it is thought that the majority of partial-thickness tears involve the articular surface of the tendon, but at least one cadaveric study has suggested that intrasubstance tears are actually the most common type of partial tear.48 The MRI criteria for partial tears of the rotator cuff were defined by Carrino and colleagues as focal fluid or near-fluid signal intensity on T2-weighted images that extends into the superior or inferior surface of the tendon (again, supraspinatus tendon for their purposes) but that does not extend entirely from one surface to the

other (Figs. 8-29 to 8-32).38 The results of MRI of partialthickness tears of the rotator cuff have been less favorable than have the results for full-thickness tears. Rafii and colleagues reported a sensitivity of 89%, specificity of 84%, and an accuracy of 85% for partial-thickness tears, but other authors have had less success.30 Reinus and coworkers demonstrated a poor detection rate for partial-thickness tears of 35% with T2-weighted fat-saturated images.43 Robertson and associates reported poor sensitivity for all readers in their study for the diagnosis of partialthickness tears (19% to 57%).46 They also demonstrated

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■ FIGURE 8-28 Oblique coronal fat-suppressed proton density– weighted (A) and sagittal T2-weighted (B) MR images through the shoulder demonstrate a massive full-thickness rotator cuff tear. There is prominent subacromial/subdeltoid bursal fluid (A, arrowheads). Note the severe tendon retraction (A, arrow) and the extensive stripping of the supraspinatus and infraspinatus tendons from the greater tuberosity (B, arrowheads). C, The oblique sagittal T2-weighted MR image demonstrates associated fatty atrophy of the supraspinatus and infraspinatus muscles in the same patient. SS, supraspinatus muscle; IS, infraspinatus muscle; SSc, subscapularis muscle.

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■ FIGURE 8-29 This oblique coronal fat-suppressed proton density–weighted MR image of the shoulder demonstrates a partial bursal surface tear of the supraspinatus tendon (arrow). There is fluid extending into the bursal surface of the tendon that does not pass entirely through the tendon. Some of the articular surface fibers of the tendon remain intact (arrowhead).

poor interobserver agreement in the diagnosis of partial tears or tendinosis.46 Tuite and colleagues studied 110 patients with a diagnosis of partial-thickness or small full-thickness rotator cuff tears and found an overall MRI sensitivity of 67%.19 They also evaluated the distribution

■ FIGURE 8-30

of these small tears in their study into anterior and posterior and noted that overall 85% of the tears in their patient group were centered in the anterior half of the cuff (79% of the tears in patients younger than 36 years old and 89% of the tears in patients 36 years old or older).19 It is also interesting to observe that these authors had only a single isolated infraspinatus tear.19 The varied results in detection of partial tears on MRI may, in part, reflect the varied criteria used in these studies. Tuite and colleagues also noted the difficulty of diagnosing rim-rent tears on MRI.19 These are articular surface tears of the supraspinatus tendon at its insertion on the greater tuberosity.19 The tendon is thought to be susceptible to tears in this area because of the abrupt 90-degree curvature of the fibers as they insert on the tuberosity.19 These investigators noted that these tears may easily be confused with the increased intrasubstance signal that is often seen in this area in older patients.19 Use of the oblique sagittal images in addition to the oblique coronal images may aid in detection of these tears (Fig. 8-33). Rim-rent tears appear to be more common in young adults, accounting for 25% of tears in patients younger than 36 years old in their study, and are thought to be an overlooked cause of shoulder pain in young adults.19 Sano and coworkers investigated the initial observations by Codman regarding widening of the sulcus between the edge of the articular cartilage and the insertion of the supraspinatus tendon (rim-rents).50 They confirmed his hypothesis that widening of this sulcus indicates an incomplete tear of the articular surface of the supraspinatus tendon (Fig. 8-34).50 This finding is often associated with craters at the junction of the articular cartilage and the tendon insertion and erosions of the tendinous insertion and articular cartilage, findings that indicate weakening of the tensile strength of the supraspinatus tendon insertion.50

Proton density-weighted (A) and fat-suppressed proton density-weighted oblique coronal (B) MR images demonstrate a partial bursal surface supraspinatus tendon tear (large arrows in A and B). There is discontinuity of, and fluid extension into, the bursal surface fibers of the tendon. The articular surface fibers remain intact. Note the associated subacromial enthesophyte (small arrows in A and B).

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■ FIGURE 8-31

Oblique coronal (A) and oblique sagittal fat-suppressed proton density–weighted MR images of the shoulder demonstrate a partial insertional articular surface tear of the supraspinatus tendon (arrows in A and B). There is also fraying of the more proximal articular surface of the supraspinatus tendon in A.

Although the etiology of the poor results of MRI for partial-thickness tears is not entirely clear, these results likely reflect the relative inability of MRI to distinguish areas of increased signal intensity associated with tendinosis from partial tears.46 Rafii and colleagues remarked

■ FIGURE 8-32 This oblique coronal fat-suppressed proton density– weighted MR image of the shoulder demonstrates a small partial articular surface tear of the supraspinatus tendon. Note the small gap in the articular surface fibers of the tendon with fluid extension into the tendon defect (arrow).

that 50% of the partial-thickness tears in their study lacked the finding of intense T2 signal intensity at the site of the defect.30 They noted that small bursal surface tears were often shallow lesions that could be interpreted as a partial tear or tendon degeneration and that partial tears of the substance of the tendon might appear as clefts within a degenerated tendon or as areas infiltrated or replaced by connective tissue, demonstrating intermediate, not high, signal intensity.30 Several studies have shown improved accuracy in diagnosis of partial-thickness rotator cuff tears with MR arthrography using intra-articular injection of a dilute solution of gadopentetate dimeglumine.51–53 After the intra-articular injection of the contrast material, imaging can be performed using T1-weighted sequences, taking advantage of the favorable signal-to-noise ratio and reduced motion artifacts provided by these sequences.51 Hodler and coworkers demonstrated that MR arthrography significantly improved the accuracy of diagnosis of partial-thickness tears of the articular surface of the rotator cuff, although arthrography did not aid in detection of very small superficial articular surface tears or of bursal surface tears.51 Palmer and colleagues prospectively examined 37 shoulders and demonstrated the utility of fat-suppression techniques in the setting of MR arthrography.52 With the use of fat-suppressed T1-weighted sequences, they were able to depict all tears in their series and to differentiate partial-thickness from full-thickness tears (note that all partial tears in their series were articular surface).52 Meister and colleagues conducted a retrospective review of 76 patients and demonstrated an 84% sensitivity and 96% specificity for diagnosis of partial undersurface tears of the rotator cuff with MR arthrography.53 They determined that the best diagnostic sequence was the coronal fat-suppressed T1-weighted sequence (Fig. 8-35).53

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■ FIGURE 8-33 Oblique coronal (A) and oblique sagittal (B) fat-suppressed MR images demonstrate a rim-rent tear of the supraspinatus tendon. Note that the tear (arrowheads) is better demonstrated on the oblique sagittal image than on the oblique coronal image.

Lee and Lee demonstrated the ability of MR arthrography to depict the horizontal component (also known as the intratendinous or laminated component) of partial-thickness tears.54 These tears can be classified based on the involvement of the articular surface: type A demonstrate no abnormality of the articular surface, type B demonstrate irregularity of the articular surface, and type C demonstrate an associated flap tear of the articular surface (Fig. 8-36).54 In their study, these tears were seen in patients with anterior instability, internal impingement (see later discussion), and acute trauma, suggesting that these tears may be related to both degeneration and a traumatic shearing type injury (Fig. 8-37).54 Shear injury occurs when parallel forces are applied across the tendon in opposite directions and may lead to injury of the rotator cuff at one of the interfaces between the different layers of the cuff.55 Lee and Lee were able to detect 100% of these lesions using MR arthrography and the abduction/ external rotation position (ABER position), whereas they

were only able to detect 21% on standard coronal oblique images (Fig. 8-38; see also Fig. 8-63B).54 Information regarding the horizontal component of a partial-thickness tear may be useful in determining the extent of the tear and in planning surgery.54

Cystic Lesions Several different types of periarticular cysts have been described in association with shoulder abnormalities,

■ FIGURE 8-35 ■ FIGURE 8-34 This diagram demonstrates widening of the sulcus between the edge of the articular cartilage and the supraspinatus tendon insertion, representing an incomplete articular surface (rim-rent) tear of the supraspinatus tendon.

A single oblique coronal fat-suppressed T1-weighted MR image of the shoulder from an MR arthrogram after the intra-articular injection of a dilute solution of gadopentetate dimeglumine into the glenohumeral joint demonstrates a subtle area of contrast medium extension into the articular surface fibers of the supraspinatus tendon consistent with a small articular surface tear (arrow).

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■ FIGURE 8-36 Four images of the shoulder in the abductionexternal rotation (ABER) position demonstrate the normal appearance of the supraspinatus tendon and the classification of horizontal partial-thickness tears as described by Lee and Lee. The normal appearance of the supraspinatus tendon is depicted in A. In B there is an intratendinous horizontal tear but no abnormality of the articular surface of the tendon (type A horizontal tear). In C note the irregularity/tearing of the articular surface of the tendon in association with a horizontal tear (type B horizontal tear), and in D there is a flap tear of the articular surface of the tendon in association with a horizontal tear (type C horizontal tear). A, acromion; C, intraarticular contrast; G, glenoid; H, humeral head.

■ FIGURE 8-37

Oblique coronal fat-suppressed T2-weighted (A) and proton density–weighted (B) MR images demonstrate a delamination type partial tear of the articular surface fibers of the supraspinatus tendon. There is a partial articular surface tear of the supraspinatus tendon with associated retraction of some of the articular surface fibers due to delamination between different layers of the supraspinatus tendon. The articular surface fibers are retracted (arrowheads) while the bursal surface fibers remain attached to the greater tuberosity (arrows).

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■ FIGURE 8-38 An oblique coronal fat-suppressed T1-weighted MR image (A) and an axial fat-suppressed T1-weighted MR image with the arm in the abduction/external rotation (ABER) position (B) of the shoulder after the intra-articular injection of a dilute solution of gadopentetate dimeglumine into the glenohumeral joint (MR arthrogram) are shown. The oblique coronal image demonstrates a small area of contrast medium extension into the articular surface of the supraspinatus tendon suggesting a small partial-thickness tear (A, arrowhead). The axial image obtained in the ABER position demonstrates that this is a delamination type partial articular surface tear with a flap component (B, arrow).

including paralabral cysts in association with labral tears, acromioclavicular joint cysts in association with fullthickness rotator cuff tears (Fig. 8-39), and intramuscular cysts in association with both partial-thickness (Fig. 8-40) and full-thickness rotator cuff tears.56–60 Cysts of the acromioclavicular joint, also known as geysers, are produced

■ FIGURE 8-39

when fluid extends from the glenohumeral joint through a full-thickness rotator cuff tear (often massive) and an interruption in the thin inferior capsule of the acromioclavicular joint into the acromioclavicular joint.57,58 There may be eventual distention of the superior portion of the joint capsule and formation of a supraclavicular mass

Oblique coronal fat-suppressed proton density–weighted (A) and axial T1-weighted (B) MR images of the shoulder demonstrate a large subcutaneous mass superficial to the acromioclavicular joint consistent with a geyser (arrowheads). This mass is fluid signal intensity on both of the images. A connection is demonstrated between this mass and the acromioclavicular joint on the axial image (B, arrow) and there is also a large associated retracted full-thickness rotator cuff tear (A, arrow).

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cysts were identified in all of the rotator cuff muscles.59 They concluded that the presence of an intramuscular cyst is strong evidence that there is an underlying rotator cuff tear, often a partial-thickness tear.59

Muscle Atrophy

■ FIGURE 8-40 An oblique coronal fat-suppressed proton density– weighted MR image of the shoulder demonstrates a large intramuscular cyst in the posterosuperior portion of the rotator cuff (arrowheads). There is also linear fluid signal intensity in the infraspinatus tendon consistent with an intrasubstance tear (arrow).

evident on physical examination.58,59 Excision or aspiration of the cyst without treatment of the underlying rotator cuff pathology usually leads to cyst recurrence.58 Sanders and associates analyzed 13 intramuscular cysts, all of which were either contained by the fascial sheath or substance of the rotator cuff muscles.60 The cysts in their study followed fluid signal intensity on all pulse sequences, were either unilocular or multilocular, were oval, and were parallel to the long axis of the involved muscle.60 There were associated rotator cuff tears, both small full-thickness and partial articular surface, in all 13 of the cases in their study.60 They postulated that fluid extends through the rotator cuff tear and then passes in a laminar fashion through the rotator cuff tendon and muscle, producing a cyst either in the muscle itself or under the fascial sheath.60 Unlike the geysers, these lesions are not obvious clinically.60 Kassarjian and colleagues reviewed 32 cases of intramuscular cysts that were located in the sheath or substance of the rotator cuff muscles and found that all but one of these cysts were associated with an underlying rotator cuff tear, 16 of which were partial-thickness tears.59 They noted that fluid entering at the site of a tear in one tendon may dissect into an adjacent tendon or muscle, likely owing to the interdigitation of the rotator cuff tendons as they insert on the humerus and a delaminating component of the tear that extends from one tendon into the adjacent muscle.59 In seven of the cases of cysts in their study the tendon of the muscle containing the cyst was intact, but a tear was identified in an adjacent tendon in six of these cases.59 Most of the cysts in their study were located in the supraspinatus muscle, and most were associated with tears of the supraspinatus tendon; however,

Another important role for MRI is in the assessment of the degree of muscle atrophy seen in association with rotator cuff tears. It has been shown in the rabbit model that interruption of the supraspinatus tendon leads to muscle atrophy relatively rapidly.61 In the rabbit model, atrophy was seen as early as 4 weeks after the tendon was severed and the histologic changes were most pronounced at 6 weeks.61 Muscle atrophy, in turn, correlates with muscle weakness, which has been shown to be an important prognostic indicator for rotator cuff repair.62 Itoi and Tabata demonstrated good results with conservative treatment of rotator cuff tears in patients who had preserved range of motion and strength on initial examination, regardless of the degree of pain.63 Bartolozzi and colleagues demonstrated excellent or good results in the majority of patients after treatment of rotator cuff pathology in those patients without weakness or with only mild weakness.64 Only 13% of patients with severe weakness and 33% of patients with moderate weakness in their study demonstrated an excellent or good outcome.64 Therefore, the degree of rotator cuff atrophy is important prognostic information for the referring physician. Several authors have investigated the role of MRI in the determination of the degree of muscle atrophy. Thomazeau and coworkers quantified the degree of supraspinatus muscle atrophy into three grades using the occupation ratio (R) of the supraspinatus fossa by the supraspinatus muscle with analysis performed on the parasagittal image where the scapula has a Y-shaped appearance due to the junction of the spine of the scapula with the base of the coracoid process.65 Grade 1 reflected no atrophy, and grade 3 reflected severe atrophy (Fig. 8-41).65 In their study, the degree of atrophy increased with increasing anteroposterior extent of the tear and with increasing tendon retraction in the coronal plane.65 They found that preoperative atrophy of the supraspinatus muscle was the most important anatomic predictor for postoperative re-tear.65 Zanetti and colleagues used quantitative measurements of cross-sectional area to assess the degree of muscle atrophy but also described a quick qualitative assessment of the degree of muscle atrophy: the tangent sign.62 The tangent sign is positive (abnormal) if a line drawn from the superior margin of the scapular spine to the superior margin of the coracoid process does not intersect the supraspinatus muscle (Figs. 8-42 to 8-44).62 This line is drawn on the most lateral image on which the spine of the scapula is still in contact with the remainder of the scapula.62 They also evaluated the degree of fatty infiltration of the rotator cuff muscles using mean signal intensities of the rotator cuff muscles.62 They found that cross-sectional area measurements and the qualitative tangent sign were useful in distinguishing medium and large rotator cuff tears from the asymptomatic population.62 They determined, however, that signal intensities were not useful in distinguishing asymptomatic patients from those with even large tears.62

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■ FIGURE 8-41 This image demonstrates the three grades of supraspinatus muscle atrophy as described by Thomazeau and colleagues using the occupation ratio (R). R is equal to the cross-sectional area of the muscle divided by the cross-sectional area of the supraspinatus fossa. Grade I is normal, grade II is mild-to-moderate muscle atrophy, and grade III is severe muscle atrophy.

■ FIGURE 8-42

■ FIGURE 8-43 Oblique sagittal proton density–weighted MR image demonstrates the normal appearance of the supraspinatus (SS), infraspinatus (IS), subscapularis (SSc), and teres minor (TM) muscles.

These images demonstrate a normal tangent sign (indicating no muscle atrophy) in A and a positive tangent sign (indicating the presence of muscle atrophy) in B.

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■ FIGURE 8-44 Oblique sagittal T2-weighted (A and C) and oblique coronal fat-suppressed proton density–weighted (B) MR images of the shoulder. In A note the disproportionate atrophy of the supraspinatus muscle (positive tangent sign). In B there is an associated full-thickness tear of the supraspinatus tendon including a fluid-filled tendon gap (arrowheads) and retraction of the myotendinous junction of the supraspinatus tendon to the level of the humeral head (arrow) in the same patient. The large full-thickness supraspinatus tendon tear is also well-shown in the oblique sagittal plane (C, arrowheads). IS, infraspinatus; SS, supraspinatus; SSc, subscapularis; TM, teres minor.

This is likely because linear fatty stranding may be present in the asymptomatic population, early fatty infiltration may not comprise enough tissue to affect the signal intensity measurements significantly, and in advanced muscle atrophy thin low signal intensity bands, likely representing fibrous tissue, may be present in the muscle.62 Schaefer and colleagues used the occupation ratio (R) and the tangent sign to assess supraspinatus atrophy.66 They found a sensitivity and specificity of 75% and 85%, respectively, for the occupation ratio (R).66 They also found a sensitivity and specificity of 100% and 85%, respectively, for the tangent sign, as well as a positive predictive value of 67% and a negative predictive value of 100%.66 There was also significant correlation between

the occupation ratio (R), tangent sign, and improvement in strength and mobility at 12 months postoperatively.66 They noted that even patients who demonstrated large tears and significant atrophy benefited from surgical repair and physical therapy.66 Lehtinen and colleagues have suggested a variation on the methods used by Thomazeau and Zanetti and their associates to obtain more accurate measurements of the true volume of the rotator cuff muscles, using not only the Y-shaped parasagittal image but also an additional image obtained more medially.67 They reported improved accuracy in determination of muscle volumes over the method of Thomazeau and associates, especially for the subscapularis muscle.67

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Yao and Mehta have noted that infraspinatus muscle atrophy may occur in the absence of a tear of the infraspinatus tendon.68 They determined that infraspinatus muscle atrophy is commonly associated with full-thickness tears of the supraspinatus or supraspinatus and subscapularis tendons and that there is often associated atrophy of the supraspinatus or supraspinatus and subscapularis muscles.68 Associated infraspinatus tears were present in only 53% of their cases; thus 47% of patients with infraspinatus atrophy had no associated infraspinatus tear.68 In addition, they also found that isolated infraspinatus muscle atrophy (without associated anterior cuff muscle atrophy) could occur even with an intact infraspinatus tendon.68 They found that improvement in muscle strength and atrophy in the supraspinatus tendon was greater than that seen in the infraspinatus tendon postoperatively.68 No cases of infraspinatus atrophy as a result of compression of the suprascapular nerve were identified in their series, suggesting that this is an uncommon cause of infraspinatus atrophy.68 In addition, the teres minor muscle was spared of atrophy in all cases.68

Acromial Morphology Assessment of acromial morphology (see Fig. 8-12) on MRI can be problematic. Whereas supraspinatus outlet radiographs have long been the standard for determination of acromial morphology, mild variations in technique may negatively affect correlation between apparent acromial shape and rotator cuff pathology.69 Peh and associates demonstrated that there is significant variation in acromial morphology on the oblique sagittal MRI images depending on the site chosen for review.69 Their study showed poor correlation between acromial morphology on MRI, as determined on an oblique sagittal image obtained 4 mm from the lateral acromial edge, and outlet radiographs as well as poor correlation between acromial morphology as determined on MRI and supraspinatus tendon pathology.69 Epstein and colleagues evaluated acromial morphology on the oblique sagittal image obtained just lateral to the acromioclavicular joint and demonstrated better correlation with rotator cuff pathology.70 They demonstrated hooked acromions more than two times as frequently in patients with impingement and more than four times as frequently in patients with full-thickness rotator cuff tears.70 Mayerhoefer and coworkers compared the diagnostic value of three different MRI slice positions to determine which provided the best diagnostic information.71 They evaluated three different parasagittal sections that were obtained (1) 4 mm from the lateral margin of the acromion (lateral section), (2) just lateral to the acromioclavicular joint (middle section), and (3) through the lateral portion of the acromioclavicular joint (medial section). Their results showed significant variation in acromial morphology depending on the slice selected, as was also shown by Peh and coworkers. They concluded that outlet radiographs are a better determinant of acromial morphology than is any single MRI section. The best prediction of acromial morphology in their study was provided by a mathematical combination of the undersurface angles obtained on the most lateral and middle MRI sections. They determined that the middle section (obtained just lateral to the acromioclavicular joint and

similar to the section used by Epstein and colleagues) was the single best section for determination of the acromial morphology and that the most lateral section (obtained 4 mm from the lateral acromial margin and similar to the section used by Peh and coworkers) was the most specific for a hooked acromion (type III).

Pitfalls in Magnetic Resonance Imaging of the Rotator Cuff Before concluding the discussion of MRI findings associated with primary mechanical extrinsic impingement and rotator cuff pathology, certain potential pitfalls in the MRI diagnosis of rotator cuff pathology should be reviewed. Many authors have noted the presence of increased signal intensity in the distal supraspinatus tendon in asymptomatic patients.41,72–74 Mirowitz reported the presence of a discrete area of relatively increased signal intensity in the distal supraspinatus tendon corresponding to the region of the critical zone.41 Kaplan and colleagues reported a similar finding in all patients in their study of 30 normal shoulders.72 This area was noted to be isointense to muscle on all pulse sequences in Kaplan and colleagues’ study, and they referred to this as pseudotendinopathy.72 Although it has been postulated that this area of increased signal intensity may be related to the anomalous blood supply in this area or to subclinical tendon degeneration, most would now attribute this finding to the magic angle phenomenon produced when the tendon fibers are oriented at 55 degrees to the static magnetic field on short echo time pulse sequences.41,75 Moderately increased signal intensity in this region should not be regarded as evidence of significant pathology unless the signal intensity in this area is greater than that of the surrounding muscle and similar to fluid or unless there is a focal change in the caliber or focal irregularity of the tendon in this area (Fig. 8-45).41,72 In a review of 15 asymptomatic volunteers with a mean age of 31.5 years, Mirowitz noted that the supraspinatus myotendinous junction is not a sharp transition from completely muscular to completely tendinous fibers.41 The transition is gradual and it is common to see muscle fibers of the supraspinatus extending along the undersurface of the supraspinatus tendon to within 1 cm of the greater tuberosity.41 These muscle fibers may create apparent increased signal intensity in the supraspinatus tendon but should be distinguishable from significant pathology because of their lack of focality (Fig. 8-46).41 Similarly, Neumann and coworkers postulated that connective tissue between the layers of muscle and tendon in the supraspinatus could contribute to the variable signal intensity observed in the distal supraspinatus tendon.74 Focal loss of the peribursal fat plane on MRI anteriorly adjacent to the greater tuberosity has been reported in normal shoulders, possibly due to the extremely thin nature of the fat plane in this area.41,72 Needell and colleagues noted a normal peribursal fat plane in 96% of patients with normal tendons but diffuse loss of this fat plane in 40% of patients with tendinopathy and in 95% of patients with partial or complete tears.76 Some researchers have reported small amounts of fluid in the subacromial/ subdeltoid bursa in normal patients, whereas others have

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■ FIGURE 8-45 Spin-echo proton density–weighted (A) and T2-weighted (B) oblique coronal MR images of the shoulder. Note the focal area of increased signal intensity in the supraspinatus tendon on the proton density (short echo time) sequence as the tendon changes course just prior to its insertion on the greater tuberosity (A, arrow). No corresponding signal abnormality is identified in this area on the T2-weighted image in B. This area of increased signal intensity in the supraspinatus tendon on the proton density sequence is likely due to the magic angle phenomenon (see text).

■ FIGURE 8-46 Oblique coronal proton density–weighted MR image of the shoulder demonstrates increased signal intensity in the distal supraspinatus tendon likely due to distal extension of muscle and/or connective tissue fibers (arrowheads).

not confirmed this finding. Mirowitz found small amounts of fluid in the glenohumeral joint space, biceps tendon sheath, and subacromial/subdeltoid bursa in asymptomatic patients and stated that the quantity of bursal fluid and not simply the presence of a small film-like layer of bursal fluid was more important for defining pathology.41 Kaplan and colleagues reported that none of the normal shoulders in their series demonstrated bursal fluid, and Needell and colleagues reported that subacromial/subdeltoid bursal fluid was rarely apparent in patients with normal rotator cuff tendons.72,76 Neumann and coworkers reported small amounts of bursal fluid in 20% of the asymptomatic patients in their series, however.74 Kaplan and colleagues noted a small low signal intensity structure projecting inferolaterally from the lateral aspect of the acromion corresponding to a tendon slip of the deltoid muscle at its attachment on the acromion that can be confused with a subacromial enthesophyte.72 They suggested that a true subacromial enthesophyte should demonstrate marrow extending into it, even when it is small, helping to distinguish it from the purely low signal intensity structure laterally representing the deltoid insertion.72 Acromioclavicular joint osteoarthritis, which has been shown to be directly related to the age of the subject, or mild impingement of the myotendinous junction of the rotator cuff by overlying bone from the acromion, acromioclavicular joint, or distal clavicle is not

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■ FIGURE 8-47

Internal rotation (A) and external rotation (B) views from a normal conventional single-contrast shoulder arthrogram. There is filling of the axillary recess (short black arrows), subscapularis recess (long black arrows), and biceps tendon sheath (arrowheads). There is no evidence of contrast extension into the subacromial/subdeltoid bursa or over the greater tuberosity (gray arrows).

a reliable indicator of pathology.41,73,74,76 Cystic change in the humeral head adjacent to the rotator cuff insertion may also be seen in asymptomatic patients and does not necessarily imply a pathologic process.41 Needell and colleagues identified humeral head cysts in approximately 25% of their asymptomatic patients but noted an increasing incidence of these cysts in association with increasingly severe rotator cuff abnormalities and concluded that these cysts may therefore be a useful marker of rotator cuff disease.76

Multidetector Computed Tomography

arthrography using upright tomography to improve the detection of the size of the tear and to better demonstrate the thickness of the remaining tissue, information that is important for the surgeon contemplating cuff repair.81 Digital subtraction arthrography has also been advocated by some to improve visualization of the cuff.82 Articular surface tears may be diagnosed by the extension of contrast material into, but not entirely across, the cuff or by an ulcer-like lesion in the synovial surface of the cuff.77,78,83 Intrasubstance tears of the rotator cuff may also be demonstrated by arthrography as long as the tear communicates with the articular cavity.77 Intrasubstance

The use of arthrography, alone or in conjunction with routine or computed tomography, and bursography to diagnosis disorders of the rotator cuff has been well described in the literature. On routine single- and double-contrast arthrography, the extension of contrast material into the subacromial/subdeltoid bursa after an intra-articular injection is diagnostic of a full-thickness rotator cuff tear (Figs. 8-47 to 8-49).77 In a study of 49 shoulders, Paavolainen and Ahovuo demonstrated a sensitivity of 93%, a specificity of 95%, an accuracy of 94%, and a positive predictive value of 96% for singlecontrast arthrography in the detection of full-thickness rotator cuff tears.78 The double-contrast technique, usually employing 4 mL of positive contrast agent, 0.3 mL of 1:1000 epinephrine, and 12 mL of room air, has been shown to be superior to the single-contrast technique because it not only demonstrates the presence of a tear but also provides additional information regarding the width of the tear and degree of tendon degeneration.77,79 Additional techniques to improve evaluation of the rotator cuff at the time of arthrography have also been described. The application of weight to the wrist at the time of arthrography has been described to increase the space between the humeral head and acromion and to separate the long head of the biceps tendon from the rotator cuff.80 Others have advocated double-contrast

■ FIGURE 8-48 A single anteroposterior view of the shoulder from a conventional arthrogram demonstrates a full-thickness rotator cuff tear. There is free extension of the intra-articular contrast material into the subacromial/subdeltoid bursa and over the greater tuberosity (arrows). There is also marked narrowing of the acromiohumeral distance (arrowheads). These findings are consistent with a full-thickness rotator cuff tear.

CHAPTER

■ FIGURE 8-49 A single image from a conventional single-contrast shoulder arthrogram demonstrates contrast medium extension from the glenohumeral joint into the subacromial/subdeltoid bursa (arrowheads) through a large full-thickness rotator cuff tear (arrow).

tears that do not communicate with the articular cavity and bursal sided partial-thickness tears will not be demonstrated by arthrography.77 Subacromial/subdeltoid bursography, although not commonly performed in most clinical practices, has been shown to be approximately 67% accurate in demonstrating partial-thickness bursal surface tears by the visualization of contrast material pooling in the torn portion of the tendon.84

■ FIGURE 8-50

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Whereas the major application of CT arthrography of the shoulder is in the evaluation of the capsulolabral complex, it has also been shown to be effective in the evaluation of the rotator cuff.77 Intra-articular injection of the joint with positive contrast material, a small amount of epinephrine (1:1000 dilution), and room air is performed in a manner similar to routine double-contrast arthrography, although a smaller amount of positive contrast material (1 to 3 mL) is often required to coat the joint.77 Farin and colleagues demonstrated identical sensitivities for routine double- contrast arthrography and CT arthrography in the detection of partial-thickness rotator cuff tears.83 CT arthrography had a slightly higher sensitivity for detection of full-thickness tears in their study (95% for CT arthrography vs. 90% for routine double-contrast arthrography).83 Evaluation of the size of the tear was more accurate with CT arthrography than with routine double-contrast arthrography (76% vs. 30%), as was determination of the location of the tear.83 A more recent study in the orthopedic literature demonstrated 99% sensitivity and 100% specificity for single-contrast CT arthrography in the diagnosis of supraspinatus tears.85 Sensitivity and specificity for infraspinatus tears in their study were 97% and 88%, respectively.85 This study also demonstrated good correlation between the degree of tendon retraction identified in the frontal plane at CT arthrography (presumably based on the oblique coronal reformatted images) and at arthroscopy (78% for the supraspinatus tendon and 71% for the infraspinatus tendon) (Fig. 850).85 This information is very important to the surgeon in determining the feasibility of arthroscopic versus open cuff repair.85 In this study, CT arthrography demonstrated deep, but not superficial, partial-thickness tears well.85 Previously, direct sagittal and direct coronal images have

Oblique coronal reformatted CT arthrogram images of the shoulder in two different patients. Part A (single-contrast arthrogram) demonstrates a full-thickness supraspinatus tendon tear. There is a large gap (long arrow) with extension of contrast material from the glenohumeral joint into the subacromial/subdeltoid bursa (arrowheads). Note the tendon retraction to the level of the humeral head (short arrow). Part B (double-contrast arthrogram) in a different patient demonstrates contrast extension into the substance of the supraspinatus tendon from the articular cavity (arrows in B) and irregularity of the articular surface of the supraspinatus tendon. There is no evidence of contrast medium extension into the subacromial/subdeltoid bursa to suggest a full-thickness rotator cuff tear. Only a small amount of air remains in the glenohumeral joint (arrowhead in B).

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■ FIGURE 8-51 Oblique coronal (A) and oblique sagittal (B) reformatted CT images of the shoulder after a single contrast arthrogram in a patient who had undergone rotator cuff repair 1 year previously. Just before this examination the patient had experienced a repeat injury. These images demonstrate contrast medium extension from the glenohumeral joint into the subacromial/subdeltoid bursa and over the greater tuberosity (arrowheads) through a full-thickness re-tear of the rotator cuff. Note the retracted tendon (A, arrow). The tear is also well demonstrated in the oblique sagittal plane (B, arrow). A metallic suture anchor from the prior rotator cuff repair is seen in the humeral head.

been advocated to improve accuracy of CT arthrography in the detection and characterization of rotator cuff tears over axial CT arthrography alone, but similar information can presumably be obtained from the multiplanar reformatted images available on current multidetector CT scanners (Figs. 8-50 and 8-51).86,87 CT has also been used to assess the degree of fatty atrophy present in the rotator cuff muscles.88 It has been shown that the infraspinatus muscle may demonstrate fatty degeneration in the presence of large anterosuperior rotator cuff tears, even when the infraspinatus tendon is not involved in the tear.88 Fatty degeneration of the infraspinatus has been shown to correlate with impairment of active external rotation and to have a negative impact on the success of supraspinatus tendon repairs.88

Ultrasonography Although ultrasonography is a popular method for the evaluation of the rotator cuff in certain practices, it is not as widely accepted in the evaluation of rotator cuff pathology as is MRI.89 Patient satisfaction with ultrasonography to evaluate the painful shoulder has been shown to be greater than that of MRI, but that is possibly related to the longer examination time of MRI relative to ultrasonography (although MR scan times have decreased with the development of newer technology) and the anxiety produced by the MRI examination.90 Ultrasonography has been shown to be equally accurate to CT arthrography in the diagnosis of the size and site of rotator cuff tears.83 Ultrasonography has also been shown to be highly accurate in the detection of full-thickness tears of the rotator cuff and has an accuracy similar to MRI in the detection and evaluation of the size of both full-thickness and partial-thickness rotator cuff tears.89,91 Although some authors have found limited success in the detection of partial-thickness tears, others have demonstrated high sensitivity and specificity in the diagnosis of these tears.89,92,93 In their review of 71 patients with shoulder pain, Teefey and coworkers reported only

five missed tears on ultrasonography, all of which were small partial-thickness tears.94 The accuracy of ultrasound examination of the shoulder is dependent on multiple factors, including image resolution, good scanning technique, adherence to the established diagnostic criteria, and the experience and ability of the operator.89,95 In experienced hands, however, interobserver variability for detection, classification, and localization of rotator cuff tears has been shown to be low. A detailed description of the technique of shoulder sonography is beyond the scope of this text but has been well described in the literature.39,96,97 Several technical points should be emphasized, however. Shoulder evaluation is best performed using a high-frequency linear transducer (10 to 12 MHz) placed perpendicular to the tendon being evaluated to avoid artifactual hypoechoic or anechoic areas that may mimic tears.96 This artifact is referred to as anisotropy and describes the hypoechoic or anechoic appearance of a structure composed of a highly ordered parallel pattern of collagen fibers (e.g., a tendon or ligament) when the insonation angle is not perpendicular or very near perpendicular to the collagen fibers (due to the absence of specular reflectors).39,96,98 Two positions have been advocated for evaluation of the supraspinatus tendon: (1) the Crass position in which the patient is seated and the shoulder is extended, adducted, and internally rotated with the elbow flexed, the palm facing out, and the fingers projecting toward the opposite scapula and (2) the modified Crass position in which the shoulder is extended, the elbow is flexed, and the palm of the hand is placed against the back pocket.99 The modified Crass position is useful in evaluation of the anteromedial portion of the tendon.99 Both of these positions have been shown to reflect the true size of full-thickness supraspinatus tears in the transverse plane.99 The Crass plane has also been shown to reflect accurately the size of a tear in the sagittal plane, whereas the modified Crass position may overestimate the tear size in the sagittal plane.99 Dynamic ultrasonography has been advocated by some

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to assess the relationship between the anterior acromion, subacromial/subdeltoid bursa, supraspinatus tendon, and greater tuberosity during active shoulder motion.100 Normal shoulders will demonstrate smooth passage of the greater tuberosity below the acromion.100 Findings of impingement on dynamic examination include pain, encroachment of the soft tissues between the greater tuberosity, and acromion, as well as upward migration of the humeral head.100 Tissue harmonic imaging has been shown to improve visualization of joint and tendon surfaces and to improve diagnostic accuracy in the detection of subscapularis tendon tears.101 In their early work on ultrasonography of the rotator cuff, Middleton and colleagues established four criteria for the diagnosis of a rotator cuff tear: (1) focal thinning of the cuff, (2) complete nonvisualization of the cuff, (3) focal discontinuity in the homogeneous echogenicity of the cuff without thinning, and (4) a central echogenic band in the region of the rotator cuff.102 Using these criteria, in their study of 106 patients they demonstrated a sensitivity and specificity of 91% in the detection of a rotator cuff tear (using double- contrast arthrography as the comparison standard).102 In this study the positive predictive value for a tear in patients with nonvisualization of the rotator cuff or focal thinning was 100% (Fig. 8-52). They found that the other two criteria, tendon discontinuity and a central echogenic band, were not as reliable in the prediction of a tear.102 In their study of 225 patients with surgical correlation, Weiner and Seitz attempted to subdivide rotator cuff tears into partial-thickness, small full-thickness, large full-thickness, and massive.92 Their criteria for a partial-thickness tear included a focal hypoechoic area within the rotator cuff, small hypoechoic areas of discontinuity in the bursal or articular surface of the cuff, or a large echogenic area in the cuff with or without associated thinning (Figs. 8-53 and 8-54).92 The criteria for a full-thickness tear in this study included a hypoechoic

area extending through the entire cuff or loss of the substance of the rotator cuff (focal or complete) and identification of tear margins.92 Massive tears were diagnosed in the absence of visualization of any rotator cuff tissue and “approximation” of the deltoid muscle to the humeral head.92 Using these criteria, they demonstrated an overall sensitivity and specificity in the detection of rotator cuff tears of 95% and 94%, respectively, and a sensitivity and specificity in the staging of tears of 91% and 94%, respectively.92 Jacobson and coworkers evaluated multiple primary and secondary ultrasonographic signs of rotator cuff tear.103 Similar to the results of Middleton and colleagues, Jacobson and associates showed that tendon nonvisualization on ultrasonography is the single best primary indicator of a full-thickness rotator cuff tear.103 In this study, other primary signs proved to be less reliable.103 For example, they determined that abnormal echogenicity of the tendon (hypoechoic or anechoic areas) was of limited value in predicting a tear because patients both with and without tears demonstrated areas of abnormal echogenicity.103 In patients without a tendon tear this signal heterogeneity may be related to tendinosis.103 In this study, tendon thinning was seen in 71% of patients with full-thickness tears, 40% of patients with bursal surface partial tears, 30% of patients with articular surface partial tears, and 14% of patients without a tear.103 Loss of the normal convex contour of the peribursal fat over the site of a hypoechoic defect in the rotator cuff tendon with compression has also been described as a sign of a full-thickness rotator cuff tear.96 This finding may also be identified without compression if there is no fluid at the site of the torn and retracted tendon, and the overlying hyperechoic peribursal fat becomes displaced into the tendon gap.96 This is referred to as the “sagging peribursal fat sign.”96 Among secondary signs, Jacobson and colleagues found that a combination of cortical irregularity of the greater

■ FIGURE 8-52 Oblique coronal ultrasound image through the shoulder demonstrates a full-thickness tear of the supraspinatus tendon. There is nonvisualization of the supraspinatus tendon and approximation of the deltoid muscle to the humeral head. Note the irregularity of the greater tuberosity (arrowheads). The hypoechoic area adjacent to the humeral head (arrows) likely represents fluid and/or synovitis. GT, greater tuberosity; D, deltoid muscle; HH, humeral head. (Courtesy of D. Petrover, MD, Paris, France.)

■ FIGURE 8-53 Oblique coronal ultrasound image of the shoulder demonstrates focal hypoechoic areas in the supraspinatus tendon consistent with a partial tear. Note the subacromial/subdeltoid bursal effusion (arrowheads). Compare with the normal appearance of the supraspinatus tendon and subacromial/subdeltoid bursa in Figure 9-54A. D, deltoid muscle; GT, greater tuberosity. (Courtesy of D. Petrover, MD, Paris, France.)

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■ FIGURE 8-54 Oblique coronal ultrasound images of the left (A) and right (B) supraspinatus tendons in the same patient. The left supraspinatus tendon is normal, whereas the right supraspinatus tendon demonstrates focal hypoechoic areas consistent with partial tearing. Note the calcification at the tendon insertion on the right side (B, arrow). (Courtesy of D. Petrover, MD, Paris, France.)

tuberosity and the presence of glenohumeral joint fluid is the most useful sign of a full-thickness supraspinatus tear (sensitivity of 60%, specificity of 100%, and accuracy of 84%).103 The cartilage interface sign has a high specificity but low sensitivity for the detection of a full-thickness supraspinatus tear.103 This sign, also called the “double-cortex sign,” refers to a thin, markedly echogenic line at the junction of the hypoechoic hyaline cartilage of the humeral head and the rotator cuff.96,103 It is best seen when there is fluid overlying the articular cartilage of the humeral head.103 Van Holsbeeck and colleagues demonstrated 93% sensitivity and 94% specificity in the detection of partial-thickness rotator cuff tears using two criteria: (1) a mixed hyperechoic and hypoechoic area in the critical zone of the supraspinatus tendon or (2) a hypoechoic area showing either bursal or articular extension identified in two orthogonal planes.93 In their study, the mixed pattern was the most common pattern seen in association with partial-thickness tears.93 They postulated that the mixed echogenicity pattern was due to fluid penetrating and surrounding the torn tendon edge.93 Similarly, Yen and colleagues evaluated six sonographic criteria for the evaluation of rotator cuff tear and determined that only the presence of focal heterogeneous hypoechogenicity (mixed hyperechoic, hypoechoic, and anechoic areas without the presence of an anechoic cleft) was suggestive of a partial-thickness tear.104 Van Holsbeeck also identified pits and irregularity of the greater tuberosity (see Fig. 8-52) on ultrasonography in patients with both partial-thickness and full-thickness rotator cuff tears but not in normal shoulders.93 Ultrasound imaging has also been used to assess rotator cuff muscle atrophy. Using the criteria of increased muscle echogenicity and decreased muscle bulk as indicative of atrophy, Sofka and associates identified fatty atrophy of at least one muscle in approximately one fourth of their study group of 199 shoulders (Fig. 8-55).105 With the exception of teres minor atrophy, most cases of muscle atrophy in this study were associated with full-thickness

rotator cuff tears.105 As noted previously, the presence of muscle atrophy is important information because it has negative prognostic implications for tendon repair and functional recovery.105,106 Atrophy of both the supraspinatus and infraspinatus muscles should raise the possibility of a lesion in the suprascapular notch compressing the suprascapular nerve.105 In comparison with MRI, Strobel and colleagues demonstrated 75% accuracy in demonstrating atrophy of the supraspinatus muscle and 72% accuracy for depicting atrophy of the infraspinatus muscle using ultrasound.106 Loss of visualization of the central tendon and loss of the typical pennate pattern of the muscle, as well as increased muscle echogenicity, were all suggestive of muscle atrophy.106 In addition to anisotropy, several other potential pitfalls in ultrasonography of the rotator cuff deserve mention. Calcific tendinitis of the rotator cuff will produce a focal hypoechoic area with associated acoustical shadowing, an appearance that may be misinterpreted as a rotator cuff tear.39 Failure to recognize the location of the normal rotator interval may also lead to the incorrect diagnosis of a tear because of the (normal) nonvisualization of rotator cuff tissue in this area.39 Furthermore, the normal hypoechoic interface between the biceps tendon and the supraspinatus tendon may mimic a longitudinal tear.39 It should also be noted that the normal rotator cuff may demonstrate heterogeneous echotexture due to the normal mingling of fibers from different components of the cuff.39

Arthroscopy Arthroscopy is extremely useful in both the diagnosis and treatment of shoulder disorders and currently represents the “gold standard” for rotator cuff evaluation.107 Endoscopic evaluation of the rotator cuff involves a detailed evaluation of the glenohumeral joint, including the articular surfaces of the rotator cuff tendons, as well as systematic bursography, including evaluation of the bursal surface of the rotator cuff.107 Rotator cuff

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■ FIGURE 8-55

Bilateral oblique sagittal ultrasound images of the suprapinatus fossa. Note the increased echogenicity of the supraspinatus muscle in A, due to fatty infiltration, relative to the normal appearance of the supraspinatus muscle on the contralateral side (B). SS, supraspinatus muscle; D, deltoid muscle; S, scapula. (Courtesy of D. Petrover, MD, Paris, France.)

abnormalities are classified arthroscopically based on the location of the tear (A for articular surface, B for bursal surface, and C for a complete or full-thickness tear) and the severity of the tear (from 0 to 4, with 0 indicating a normal tendon, 1 indicating minimal localized fraying, 2 indicating fraying or failure of the tendon less than 2 cm, 3 indicating more severe injury often involving the entire tendon surface but less than 3 cm, and 4 indicating the most severe partial tear which usually demonstrates a flap component in addition to the tendon fraying and fragmentation, and usually involves more than one tendon).107 Arthroscopy, like ultrasonography, is operator dependent and there is a technical learning curve in the successful performance of this procedure.108,109 Although arthroscopy is as accurate as open surgery in the diagnosis of the presence or absence of a supraspinatus tear, it has been shown to be less reliable than open surgery in the evaluation of the coronal and sagittal extents of rotator cuff tears, especially in assessing tear extension into the infraspinatus tendon.108 Arthroscopy has also been shown to underestimate the degree of reducibility of the torn and retracted supraspinatus tendon relative to the results obtained at open surgery.108 Arthroscopic repair of rotator cuff tears remains a controversial topic in the literature. Snyder and associates reported satisfactory results in 84% of patients treated arthroscopically for partial-thickness rotator cuff tears (with or without associated arthroscopic subacromial decompression, which they suggested should be reserved for patients with a bursal surface tear).110 Warner and colleagues reported excellent results with arthroscopic rotator cuff repair using strict preoperative and intraoperative selection criteria to ensure that they had a nonretracted, mobile, healthy tendon to repair.111 In this study, tendons

that were nonmobile at the time of arthroscopy were converted to an open procedure.111 Galatz and colleagues demonstrated a high percentage of recurrent defects (in 17 of 18 patients as diagnosed by ultrasound) after arthroscopically repaired large and massive rotator cuff tears, but two thirds of the patients in their study demonstrated significant improvement with a minimal follow-up of 2 years and an American Shoulder and Elbow Surgeons score of greater than or equal to 80.112 Re-tear after open rotator cuff repair is reported in the literature to be between 20% and 35%.65 Galatz and colleagues concluded that whereas an arthroscopic repair may not be the most appropriate repair for a young patient with a massive tear in whom restoration of strength in the long term is most important, it may play a significant role in transforming symptomatic tears to asymptomatic tears in the older population.112 Murray and colleagues reported good to excellent results with arthroscopic rotator cuff repair of tears greater than 1 cm in the sagittal plane in 95% of patients at between 2 and 6 year follow-up.109 Burkhart reported overall results for arthroscopically repaired rotator cuff tears equal to, or better than, reported results for open repair in the literature and also reported that patients with arthroscopic repair of massive rotator cuff tears had results equal to those who underwent arthroscopic repair of smaller tears.113 Bishop and colleagues demonstrated similar clinical outcomes for arthroscopic and open rotator cuff repair overall and similar cuff integrity for small tears repaired using both techniques 1 year postoperatively.114 They also showed, however, a re-tear rate for large tears repaired arthroscopically of almost twice that of large tears repaired by open techniques.114 Most massive tears of the rotator cuff can be classified into three different types: crescent shaped, U shaped, or

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■ FIGURE 8-56 Massive rotator cuff tears can be classified into three major different types. The appearance of each of these major types of tear both before and after repair is illustrated here. The U-shaped tear is illustrated in A (before repair) and B (after repair); the crescent-shaped tear is depicted in C (before repair) and D (after repair), and the L-shaped tear is shown in E (before repair) and F (after repair).

L shaped (Fig. 8-56).115,116 Crescent-shaped tears can usually be easily reduced to the bone at the time of arthroscopy, facilitating a tension-free repair to the bone.115 The apex of U-shaped tears may extend to the level of the glenoid and are often very immobile in the mediolateral plane.115 These tears may be more mobile in the anteroposterior dimension, allowing suturing of the anterior and posterior portions of the tendon progressing from medial to lateral.115 The lateral free edge of the tendon can then be attached to the bone without tension.115 This is known as marginal convergence, and it facilitates repair of tears that may initially appear irreparable with minimal tension at the site of bone attachment.115 L-shaped tears demonstrate an extended

longitudinal component along the long axis of the tendon as well as a transverse component at the cuff insertion.115 Repair of L-shaped tears can be performed in a manner similar to that of U-shaped tears.115 Either the anterior or the posterior portion of the torn tendon is usually much more mobile and can be approximated to the other portion of the tendon.115 The longitudinal portion of the tear is then sutured, and afterward the free edge can be repaired to the bone with minimal tension using this marginal convergence technique.115 Lo and Burkhart have also reported on an arthroscopic technique allowing mobilization of massive, severely contracted, immobile rotator cuff tears in which the tissue between the rotator interval and supra-

Classic Signs ■

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■

Findings on radiography suggestive of subacromial impingement and rotator cuff tear include subacromial enthesophyte formation, narrowing of the acromiohumeral interval to less than 6 to 7 mm, acetabulization of the acromion, sclerosis and flattening of the greater tuberosity, and subchondral cyst formation in the greater tuberosity. Increased intratendinous signal and tendon enlargement on MRI are suggestive of rotator cuff tendinosis. MRI is both sensitive and specific for detection of full-thickness rotator cuff tears. MRI findings of a full-thickness rotator cuff tear include a gap in the tendon, fluid or near-fluid signal intensity on T2weighted images extending across the tendon, and subacromial/subdeltoid bursal fluid. Partial-thickness tears, which may be more difficult to detect on MRI, are diagnosed by the presence of fluid or near-fluid signal intensity on T2-weighted images extending into the substance of the tendon (either bursal or articular surface) without extending across the entire tendon.

■ ■

■

■

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■

Detection of partial-thickness tears, especially of articular surface and laminated tears, may be improved with MR arthrography. Additional findings seen on MRI in association with rotator cuff tears include geyser formation, intramuscular cysts, and muscle atrophy. At arthrography and CT arthrography, extension of intraarticular contrast material into the subacromial/subdeltoid bursa is diagnostic of a full-thickness rotator cuff tear. On ultrasonography, nonvisualization of the tendon has been shown to be strong evidence of a full-thickness rotator cuff tear, whereas the finding of tendon thinning has been associated with both full-thickness and partial-thickness tears. Secondary signs of rotator cuff tear on ultrasonography include irregularity of the greater tuberosity, the presence of glenohumeral joint fluid, and the cartilage interface sign. Ultrasonographic findings suggestive of a partial-thickness rotator cuff tear include a mixed hyperechoic and hypoechoic area in the critical zone and a hypoechoic area in the tendon, visualized in two orthogonal planes, showing either bursal or articular surface extension.

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spinatus tendon is released (single interval slide) or both the tissue between the rotator interval and supraspinatus tendon as well as the tissue between the supraspinatus and infraspinatus tendons is released (double interval slide), depending on the type of tear.115 Multiple surgical alternatives have been described for the arthroscopic repair of partial-thickness tears of the rotator cuff.117–120 These are usually suggested for partial-thickness tears involving more than 50% of the tendon thickness, and surgical intervention often involves completion of the tear and subsequent repair.118–120 Waibl and Buess have suggested, however, that the intact bursal surface fibers in a common subgroup of partial-thickness tears, the so-called partial articular supraspinatus tendon avulsions (PASTA) lesions, may protect the repair and should be preserved.120 They have advocated an arthroscopic repair of these tears using a transtendon suture technique that allows reattachment of the tendon to its osseous footprint.120

Subcoracoid Impingement and Subscapularis Tendon Tears Radiography Routine radiography has not been shown to be useful in the diagnosis of subcoracoid impingement.121

Magnetic Resonance Imaging The etiology of tears of the subscapularis tendon is controversial. They may be isolated or found in association with tears involving other portions of the rotator cuff or with lesser tuberosity fractures and they may be partial or complete.122–126 Isolated traumatic subscapularis tears, usually due to traumatic hyperextension or external rotation of the abducted arm, have also been reported in the litera-

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ture.123,125 Tears of the subscapularis tendon in association with tears of the supraspinatus tendon are significantly more common than are isolated subscapularis tears, and incomplete tears of the subscapularis tendon are much more common than are complete ruptures.123 Sakurai and colleagues demonstrated that tears of the subscapularis tendon are relatively common in older patients, are often associated with tears of the supraspinatus tendon, are usually partial-thickness articular-sided tears, and are often associated with lesions of the long head of the biceps tendon (LHB).127 They also demonstrated that the majority of the pathologic changes that occur in the subscapularis tendon (either torn or intact) occur on the articular, not bursal, side of the tendon.127 They concluded, therefore, that subscapularis tears are due to a degenerative phenomenon involving the articular side of the tendon in older patients, which likely predisposes the tendon to tearing.127 Subscapularis tendon tears and degeneration most commonly involve the cranial portion of the tendon, and the caudal portion of the tendon is usually only involved in large subscapularis tears (Fig. 8-57).128 In addition, however, the phenomenon of subcoracoid impingement syndrome has received attention in the orthopedic literature as a cause of anterior shoulder pain and as a possible cause of tears of the subscapularis tendon.121,126,129–133 This diagnosis should be considered especially in patients with persistent symptoms after previous surgery for subacromial impingement.134 The etiology of this type of impingement may be a decrease in the size of the coracohumeral space or an increase in the contents of this space.121,129 Patients complain of anterior shoulder pain that is exacerbated by forward flexion, internal rotation, and horizontal adduction.121 Potential causes of a decrease in the size of this space include fractures of the coracoid process or lesser tuberosity, abnormal glenoid morphology secondary to prior osteotomy, and promi-

■ FIGURE 8-57 Transaxial proton density–weighted (A) and gradient-echo (B) MR images of the shoulder demonstrate a full-thickness tear of the subscapularis tendon with tendon retraction (arrows). Note the medial shift of the biceps tendon against the medial wall of the intertubercular sulcus (arrowheads). The biceps tendon is not frankly dislocated, however.

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nence of the coracoid process.121,129 Potential causes of an increase in the contents of this space include a traumatic tear of the subscapularis tendon with LHB dislocation, scar formation after a tear of the coracohumeral ligament, and calcific tendinitis of the subscapularis tendon.121,129 Subcoracoid impingement has also been implicated as a potential cause of failed anterior acromioplasty.134 Anterior acromioplasty leads to anterosuperior subluxation of the humeral head, which, in a patient who has abnormal rotator cuff function and a narrowed coracohumeral space, may produce subcoracoid impingement.134 Different measurements have been proposed to evaluate and assess the degree of narrowing of the coracohumeral space in an objective fashion. Dines and coworkers measured the lateral projection of the coracoid process beyond a line drawn tangent to the articular surface of the glenoid on CT in 67 normal shoulders (coracoid index) and found an average value of 8.2 mm.121 Tan and colleagues obtained multiple different measurements on 100 shoulders using MRI.130 These measurements, obtained with the arm in adduction and internal rotation, included the coracoid index as defined by Dines and coworkers and a measurement of the distance between the humeral head and posterior aspect of the tip of the coracoid process (coracohumeral distance).130 The normal values for the coracoid index in their study were 8.7 mm for men and 6.5 mm for women, and the reported normal values for the coracoid distance were 9.3 mm in men and 7.9 mm in women.130 Based on the high degree of correlation between their study and prior studies, they concluded that both CT and MRI were equally reliable in evaluating the coracohumeral space.130 Friedman and associates used cine MRI to evaluate 50 normal patients and 75 patients with clinical evidence of subcoracoid impingement.131 They found an average coracohumeral distance of 11 mm in maximal internal rotation in asymptomatic patients and of 5.5 mm in symptomatic patients.131 Richards and coworkers also found a significant relationship between narrowing of the coracohumeral distance and subcoracoid impingement.132 Using the measurement method of Tan and colleagues for the coracohumeral distance, they found an average value of 5.0 mm in the group with a tear of the subscapularis tendon and an average value of 10.0 mm in the control group.132 Some of the radiology literature has been less supportive of the role of subcoracoid impingement in the development of subscapularis tendon pathology.16,135 Giaroli and coworkers concluded that MRI of the shoulder with the shoulder placed in the routine neutral or external rotation position is poorly predictive of the diagnosis of subcoracoid impingement based on the size of the coracohumeral distance.16 In this study, a coracohumeral distance of 10.5 mm had a sensitivity of 79% but a specificity of only 59% for subcoracoid impingement.16 Similarly, Bergin and colleagues found no significant association between narrowing of the coracohumeral distance and degree of abnormality of the subscapularis tendon.135 They demonstrated a significant relationship between the presence of bone marrow edema and cyst formation in the lesser tuberosity with the severity of subscapularis pathology and the chronicity of the associated supraspinatus tendon tear.135 They postulated that in the setting of

chronic supraspinatus tendon tears the anterior humeral head subluxation leads to abnormal mechanical stress on the undersurface fibers of the subscapularis tendon, which leads to subsequent tendinosis and tearing.135 The importance of axial MR images in evaluation of the subscapularis tendon has been emphasized in the literature because these images allow assessment of the anatomic course of the subscapularis tendon and analysis of its insertion on the lesser tuberosity, as well as evaluation of the course of the LHB.125,128 Abnormalities of the LHB (including subluxation, dislocation, and rupture) are commonly associated with subscapularis tendon tears (Fig. 8-58).123,125,128 Pfirrmann and colleagues demonstrated high sensitivity for detection of subscapularis tendon tears using a combination of the axial and oblique sagittal imaging planes with MR arthrography.128 The results of their investigation demonstrated a higher specificity on the oblique sagittal images than on the axial images for subscapularis tendon pathology as well.128 Extension of contrast material onto the lesser tuberosity on CT or MR arthrography is a specific, but not sensitive, indicator of a subscapularis tendon tear.128 The poor sensitivity of this finding may be related to the formation of scar tissue that inhibits extension of contrast material into the subscapularis tendon.128 Fatty atrophy of the subscapularis muscle (especially of the upper half) and medial subluxation or dislocation of the LHB are also specific but insensitive MRI signs of tears of the subscapularis tendon.128 In a review of 16 patients with surgically confirmed subscapularis tendon tears, Tung and associates reported that only 31% were diagnosed prospectively on MRI, although 94% of cases demonstrated primary signs of a subscapularis tendon tear on retrospective review.136 In two thirds of the cases in their study, the subscapularis tendon tear involved the cranial one third of the tendon and there was preservation of the caudal two thirds of the tendon.136 As also observed by Pfirrmann and colleagues, Tung and associates remarked that scar tissue medially may cover the lesser tuberosity and obscure a subscapularis tendon tear.128,136 They also detected medial displacement of the LHB in 44% of the patients with subscapularis tendon tears; complete tears of the LHB and biceps tendinosis were identified less commonly.136 Other findings described in association with subscapularis tendon tears in this study included superior labral (SLAP) tears in 38% of patients and both subcoracoid bursal and subscapularis recess effusions.136 They identified an associated tear of the supraspinatus tendon in 69% of the cases of a subscapularis tendon tear; only 31% of the tears in this study were isolated to the subscapularis tendon alone.136

Ultrasonography Ultrasonography is also useful in the diagnosis of tears of the subscapularis tendon. Examination with maximal external rotation has been shown to improve visualization of tears that predominantly involve the subscapularis tendon.137,138 Farin and Jaroma demonstrated a detection rate of 86% for full-thickness subscapularis tendon tears (Fig. 8-59) and of 67% for partial-thickness subscapularis tendon tears by ultrasonography.138 Teefey and colleagues suggested that small (5 mm) partial-thickness subscapularis tendon tears may be difficult to diagnose with

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■ FIGURE 8-58

Transaxial (A), oblique sagittal (B), and oblique coronal (C) fat-suppressed proton density–weighted MR images of the shoulder demonstrate a tear of the subscapularis tendon (A and B, long arrows) and associated intratendinous dislocation of the long head of the biceps tendon (A, short arrow; B, arrowhead). In C, note the associated full-thickness supraspinatus tendon tear and supraspinatus tendon retraction (arrow).

ultrasound but that full-thickness tears should be readily identifiable.94 Tissue harmonic ultrasound imaging has been shown to improve detection of subscapularis tendon tears as well.101

Arthroscopy Arthroscopy is very useful in diagnosis of tears of the subscapularis tendon, especially in the setting of an undersurface tear of the subscapularis tendon, which may be missed on open surgery, because it allows direct exami-

nation of the deep surface of the tendon.125 Arthroscopy is also useful in cases in which scar tissue covers the lesser tuberosity and is effective in detecting LHB instability associated with subscapularis tendon tears.125 Based on their observations at arthroscopy, Lo and Burkhart have proposed a potential mechanism for subscapularis tears as a result of a “roller-wringer” effect on the subscapularis tendon in the setting of subcoracoid impingement.133 They have observed that, in patients with subcoracoid impingement, the subscapularis tendon “bowstrings” across the coracoid process (Fig. 8-60).133

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■ FIGURE 8-59 This transverse ultrasound image through the shoulder demonstrates a full-thickness subscapularis tendon tear with tendon retraction (large arrow) as well as intra-articular dislocation of the long head of the biceps tendon (arrowhead). Note the empty intertubercular sulcus (small arrow). LT, lesser tuberosity. (Courtesy of D. Petrover, MD, Paris, France.)

■ FIGURE 8-61 Lo and Burkhart proposed that the passage of the subscapularis tendon between the lesser tuberosity and the coracoid process is analogous to an old-fashioned clothes wringer in which the clothes pass between the rollers. The rollers create increased tension (T) on the convex surface of the clothes (larger arrows) relative to the concave surface of the clothes (smaller arrows). In the case of subcoracoid impingement, the increased tension on the articular (convex) surface of the subscapularis tendon leads to articular surface fiber tearing.

Classic Signs ■ ■ ■

■ ■ ■ ■ ■ FIGURE 8-60 This axial schematic diagram of the shoulder demonstrates the potential mechanism of subcoracoid impingement as proposed by Lo and Burkhart. In patients with subcoracoid impingement, the subscapularis tendon “bowstrings” across the prominent coracoid process. This “bowstring” effect is thought to create increased tensile load on the articular surface (undersurface or convex surface) of the subscapularis tendon (inset) and lead to tensile undersurface fiber failure (TUFF lesion). C, coracoid process; H, humeral head.

As the arm is internally rotated, the subscapularis tendon must pass between the prominent coracoid process and the lesser tuberosity (analogous to an old-fashioned clothes wringer) (Fig. 8-61).133 This effect creates high tensile load along the articular surface (undersurface) of the subscapularis tendon.133 This increased tensile load may, in turn, lead to tendon degeneration and partial articular surface

■

Patients complain of anterior shoulder pain exacerbated by forward flexion, internal rotation, and adduction. Diagnosis should especially be considered in patients with persistent pain after prior surgery for subacromial impingement. Narrowing of the coracohumeral space and partial tearing of the articular surface fibers of the subscapularis tendon are suggestive of this diagnosis. “Roller-wringer” effect has been proposed as a potential mechanism for this form of impingement (see Figs. 8-60 and 8-61). Subscapularis tendon tears are usually incomplete and usually involve the cranial fibers of the tendon. Subscapularis tendon tears are often seen in association with tears of the supraspinatus tendon. There is a significant relationship between the presence of cysts and marrow edema in the lesser tuberosity of the humerus and the severity of subscapularis tendon pathology. On MRI, extension of contrast material onto the lesser tuberosity (MR arthrography), subscapularis muscle atrophy, and medial subluxation or dislocation of the LHB have a high specificity but low sensitivity for detection of subscapularis tendon tears.

tearing. The location of subscapularis tendon abnormality described in this study corresponds to the area of pathologic change identified in the subscapularis tendon by Sakurai and colleagues.133 Lo and Burkhart described this phenomenon as a tensile undersurface fiber failure (TUFF) lesion, in which load is concentrated on the degenerated articular surface fibers, leading to tendon tearing.133

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Internal (Posterosuperior) Impingement Magnetic Resonance Imaging The concept of internal or posterosuperior impingement has been described predominantly in throwing athletes.139–142 This form of impingement has been proposed as a potential cause of shoulder pain occurring in the late cocking phase of throwing, when the arm is maximally abducted and externally rotated, but has also been reported as a cause of shoulder pain in patients who are not throwers.141,140 During the late cocking phase of throwing, the shoulder is abducted 90 degrees and in maximum external rotation (ABER position).141 This position produces contact of the undersurface of the rotator cuff and the posterosuperior glenoid and labrum (Fig. 8-62)141 This contact has been shown to occur in both throwing and nonthrowing shoulders of athletes and in patients who are not throwing athletes at all, suggesting that this contact is physiologic.141,143 It has been proposed, however, that repetitive contact of these structures, as is seen in the late cocking phase of throwing, may lead to pathology of the involved structures over time.139,141,142 The

■ FIGURE 8-62 This schematic diagram demonstrates the proposed mechanism of internal impingement. When the shoulder is in maximum abduction and external rotation (red arrow), as in the late cocking phase of throwing, there is contact between the undersurface of the rotator cuff and the posterior superior glenoid and labrum (black arrow on main figure). Repetitive contact between these structures may lead to tearing of the posterior superior labrum (arrowhead on inset) and of the articular surface of the rotator cuff (black arrow on inset).

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vulnerable structures in this form of impingement include (1) the inferior glenohumeral ligament and labrum, (2) the articular surface of the rotator cuff, (3) the posterosuperior labrum, (4) the greater tuberosity, and (5) the bone of the superior glenoid.140 Injuries to more than one of these vulnerable structures may coexist.140 In addition, some investigators have suggested that anterior shoulder instability also plays a role in the development of posterosuperior impingement.142,144,145 Jobe has suggested that stretching of the inferior glenohumeral ligament as it passes over the humeral head in the position of impingement may eventually lead to anterior translation and subluxation of the humeral head.140 Paley and colleagues suggested that repetitive microtrauma to the anterior static restraints or fatigue and dyssynchrony of the dynamic stabilizers of the shoulder may permit anterior translation of the humeral head during late cocking, which, in turn, may result in impingement of the posterosuperior structures.142 They also cited the high percentage of professional baseball pitchers who are able to return to preinjury levels of performance after anterior capsulolabral reconstruction as evidence that anterior instability plays an important causative role in the development of this form of impingement.142 Six of eight patients in the study by Tirman and associates demonstrated anterior instability, and four of six patients with internal impingement studied by Giaroli and colleagues demonstrated anterior instability.17,144 Liu and Boynton reported a patient with posterosuperior impingement and evidence of anterior instability and postulated that in the overhand or overhead throwing athlete excessive eccentric loading and muscular fatigue may lead to soft tissue imbalance in the shoulder, which in turn may lead to abnormal glenohumeral translation.145 This glenohumeral translation may then lead to stretching of the secondary stabilizers of the glenohumeral joint.145 One of the two cases of posterosuperior impingement reported by Davidson and coworkers revealed anterior instability, and these authors concluded that anterior instability accentuates internal impingement in the ABER position.146 Other investigators, including Walch and colleagues and Halbrecht and associates, have not found definite evidence of a connection between posterosuperior impingement and anterior instability.139,141 McFarland and coworkers also failed to demonstrate a definite relationship between instability and contact between the rotator cuff and the superior glenoid in the ABER position.143 Although the concept of internal impingement has gained popularity as an explanation for the coexistence of partial undersurface rotator cuff tears and superior labral fraying, these conditions have been shown to coexist frequently in the nonathletic population and they may be caused by mechanisms other than internal impingement.147 Tirman and colleagues reported bone marrow abnormalities in the humerus deep to the infraspinatus tendon on MRI in all of the patients with internal impingement in their study of eight shoulders.144 These abnormalities consisted of subcortical cysts in six of the eight patients and bone marrow edema in two of the patients.144 In this study, MR arthrography was superior to routine MRI in the detection of other findings associated with internal impingement, including associated rotator cuff tears (which were

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■ FIGURE 8-63 An oblique sagittal T1-weighted fat-suppressed MR image (A) and two transaxial T1-weighted fat-suppressed MR images with the arm in the ABER position (B and C) all obtained after the intra-articular injection of a dilute solution of gadopentetate dimeglumine (MR arthrogram) demonstrate the MR findings of internal impingement. Note that the image in B is inferior to the image in C. Subcortical cysts, which fill with intra-articular contrast material, are seen in the posterior portion of the humeral head (A, arrow). There is a partial articular surface tear of the infraspinatus tendon with a flap (B, arrow) as well as fraying of the posterosuperior portion of the glenoid labrum (C, arrowhead).

partial thickness in six patients and full thickness in only two patients) and tears of the anterior band of the inferior glenohumeral ligament.144 These authors also noted improved evaluation of the rotator cuff on MR arthrography with the use of the ABER position.144 This position was also useful to demonstrate contact between the undersurface of the rotator cuff and the glenoid labrum.144 All six of the patients with clinically and surgically proved internal impingement in a study by Giaroli and colleagues demonstrated irregularity/partial tearing in the undersurface of the supraspinatus and/or infraspinatus tendon(s), cystic changes in the posterosuperior aspect of the humeral head near the attachment of posterior supraspinatus and infraspinatus tendons, and fraying or tearing of the posterosu-

perior labrum on MRI.17 Common MRI findings associated with internal impingement in a study of nine patients by Kaplan and colleagues included posterosuperior labral lesions (in all patients), tendinopathy involving the infraspinatus tendon in all cases and of the supraspinatus tendon in three cases, sclerosis of the posterosuperior glenoid, and subchondral cyst formation in the humeral head below the infraspinatus tendon insertion (Fig. 8-63).18

Arthroscopy Arthroscopic findings of internal impingement are similar to the findings seen on MRI. Common arthroscopic findings include abnormalities of the posterosuperior

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Classic Signs ■

■ ■ ■

Interior (posterosuperior) impingement should be suspected especially in overhand or overhead throwing athletes who present with a history of posterior shoulder pain. Articular surface fraying and tearing of the rotator cuff occur. Fraying and tearing of the posterosuperior glenoid labrum occur. Subchondral cyst formation in the humeral head deep to the infraspinatus tendon insertion is also identified in patients with this form of impingement.

glenoid labrum, including labral fraying and tearing.18,142,144 Articular surface rotator cuff fraying or tearing are also commonly identified at arthroscopy in patients with posterosuperior impingement.18,142,144 Tearing of the anterior infraspinatus tendon has been reported to be more common than tearing of the supraspinatus tendon alone in this form of impingement.144 Full-thickness rotator cuff tears have also been reported.144 “Kissing” articular cartilage lesions on the glenoid and humeral head when the shoulder is placed in the ABER position or osteochondral lesions of the humeral head have been described, as have SLAP and Bankart lesions and biceps tendinopathy, but these lesions appear to be less common.18,142,145,148

Anterosuperior (Anterior Internal) Impingement and the Rotator Interval Arthroscopy A new form of shoulder impingement involving the anterosuperior portion of the glenohumeral joint, including the structures of the rotator interval, has recently received attention in the arthroscopy literature.149–151 Before undertaking an explanation of this form of impingement, however, a review of the complex anatomy in this area, and especially of the structures of the rotator interval, must be undertaken. The rotator interval is a triangular space (discontinuity in the rotator cuff) between the anterior margin of the supraspinatus tendon and the superior margin of the subscapularis tendon that has the coracoid process at its base and the intertubercular sulcus at its apex.152 The bursal surface of the capsule investing the rotator interval is predominantly formed by the coracohumeral ligament, and the articular surface of the investing capsule is predominantly formed by the superior glenohumeral ligament.152 The interval is produced due to the penetration of the rotator cuff by the coracoid process.152 Anatomically, the biceps (or reflection) pulley forms an important part of the rotator interval.150 The pulley is created by the contributions from four structures: (1) the coracohumeral ligament (CHL), (2) the superior glenohumeral ligament (SGHL), (3) fibers from the supraspinatus tendon, and (4) fibers from the subscapularis tendon.150 After arising from the coracoid process, the CHL separates into two bands, one that attaches to the anterior edge of the supraspinatus tendon and greater tuberosity and the other that attaches to the superior margin of the

■ FIGURE 8-64 This is a schematic representation of the rotator interval. A round portion of the rotator cuff has been cut away to allow better visualization of these structures. Note the biceps pulley, formed by contributions from the coracohumeral ligament (CHL, divided), superior glenohumeral ligament (SGHL, divided), and fibers from the supraspinatus and infraspinatus tendons. Laterally the SGHL forms a U-shaped sling deep to the long head of the biceps tendon before inserting on the lesser tuberosity.

subscapularis tendon, transverse humeral ligament, and lesser tuberosity.150,153 After arising from the anterosuperior portion of the glenoid labrum, near the supraglenoid tubercle, medially the SGHL forms a fold parallel to the LHB.150,153 As it passes more laterally, it forms a U-shaped sling deep to the LHB before inserting on the proximal aspect of the lesser tuberosity.150,153 At the proximal portion of the intertubercular sulcus, the CHL and SGHL ligament merge together and form the reflection pulley around the LHB (Fig. 8-64).150 The SGHL appears to function to resist shearing forces on the intra-articular portion of the LHB in the area of the rotator interval and to prevent anterior instability of the tendon.150,153 Werner and colleagues also observed that fibers from the transverse band of the rotator cuff (fasciculus obliquus) also contribute to the roof of this sling.153 In addition, fibers from the supraspinatus tendon reinforce the posterior portion of the roof of the sling at the proximal entrance to the bicipital groove.150 The subscapularis tendon does not appear to contribute to the suspensory mechanism of this sling but does appear to send fibers posteriorly deep to the LHB at

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the level of the proximal aspect of the bicipital groove.153 These findings correlate with the findings of Clark and Harryman, who reported the presence of sheath around the LHB, the roof of which is predominantly formed by fibers of the supraspinatus tendon and the deep portion of which is predominantly formed by fibers from the subscapularis tendon (see Fig. 8-10).12,153 Gerber and Sebesta evaluated 16 patients with unexplained anterior shoulder pain that was exacerbated by anterior elevation and internal rotation and that was not relieved by subacromial anesthetic injection.149 This position of the arm is commonly encountered in racquet sports such as tennis and in occupations such as bricklaying.149 At arthroscopy they observed isolated pulley lesions (lesions of the humeral insertion of the superior glenohumeral ligament and coracohumeral ligament) in 3 patients, isolated partial-thickness tears of the superolateral portion of the subscapularis tendon in 3 patients, and abnormalities involving both of these areas in 10 patients.149 Furthermore, they were able to demonstrate mechanical impingement between the biceps pulley/ subscapularis tendon and the anterosuperior portion of the glenoid in all cases.149 At greater than 90 degrees of elevation they demonstrated an area of mechanical contact between the region of the LHB/biceps pulley and the superior aspect of the glenoid labrum.149 With less elevation, mechanical contact was demonstrated between the subscapularis tendon insertion and the anterior glenoid labrum and glenoid rim.149 Habermeyer and associates evaluated 89 patients with pulley lesions and proposed that anterosuperior impingement is related to a cascade of events, of which a partial

■ FIGURE 8-65

articular surface tear of the subscapularis tendon is critical.150 The initial insult appears to be a tear of the reflection pulley, which may be caused by multiple factors, including trauma and degeneration.150 With disruption of the pulley, the LHB becomes unstable and medially subluxed.150 The displaced LHB is unable to perform its role of anterior stabilization of the humeral head, leading to anterior humeral translation and subsequent partial articular surface tears of the subscapularis tendon (Fig. 8-65A).150 A very strong association between subluxation of the LHB and subscapularis lesions is well known.154 In the presence of this partial tearing of the subscapularis tendon there is further anterosuperior subluxation of the humeral head, leading to anterosuperior impingement (see Fig. 8-65B).150 Struhl reported 10 patients who had clinical symptoms suggestive of subacromial impingement and who also had partial-thickness rotator cuff tears but did not have evidence of subacromial impingement or subacromial/ subdeltoid bursitis on arthroscopy.151 Contact between the torn rotator cuff and anterosuperior labrum could be clearly demonstrated in these patients at the time of arthroscopy, consistent with the diagnosis of anterosuperior impingement.151 He noted the importance of recognizing this as a potential cause of unresolved anterior shoulder pain, especially in the younger population.151 Of note, only 20% of the partial-thickness rotator cuff tears were correctly identified prospectively on MRI.151

Magnetic Resonance Imaging Reports of imaging findings associated with anterosuperior impingement are rare. In the review of 16 patients with

A and B, The mechanism of anterosuperior impingement as proposed by Habermeyer and colleagues. In the presence of a tear of the reflection pulley, when the arm is adducted and internally rotated (curved red arrows) there is medial subluxation of the biceps tendon (A, black arrow). This, in turn, leads to anterior humeral translation and partial articular surface tearing of the subscapularis tendon. Subscapularis tendon tearing leads to further anterior translation of the humeral head (B, straight red arrow) and anterosuperior impingement (B, black arrow).

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■ FIGURE 8-66 Oblique coronal T2-weighted (A) and oblique sagittal fat-suppressed proton density–weighted (B) MR images in a patient with abnormality of the rotator interval in association with a partial supraspinatus tendon tear. In A, a partial articular surface insertional tear of the supraspinatus tendon is demonstrated (arrow). In B, there is fluid in and irregularity of the rotator interval (arrow), compatible with an associated rotator interval tear or disruption.

anterosuperior impingement by Gerber and Sebesta, 13 patients underwent MR arthrography.149 Imaging findings seen in these patients included LHB signal abnormalities (7 cases), suspicion of a SLAP tear (2 cases), and LHB subluxation (1 case).149 Lesions of the superior margin of the subscapularis tendon near its insertion on the humerus were seen in 6 of the 13 cases in which MRI was available.149 Both partial-thickness and full-thickness supraspinatus tendon tears (most commonly partial articular surface tears), abnormalities in the region of the pulley, and acromioclavicular joint arthritis were also identified.149 Although their study was not specifically tailored to the evaluation of anterosuperior impingement, Chung and colleagues have studied the normal and abnormal appearance of the rotator interval using MRI.155 They determined that the rotator interval is best evaluated on MR arthrography in the sagittal plane and that MR arthrography is superior to routine MRI in demonstrating the structures of the rotator interval, including the coracohumeral ligament and superior glenohumeral ligament.155 They also suggested that using an imaging plane along the longitudinal axis of the long head of the biceps tendon may be useful in evaluating the anatomy of this area.155 Normally the rotator interval should demonstrate a smooth contour throughout its course and should have a thickness of approximately 2 mm as measured on sagittal sections just lateral to the coracoid process.152 Tears of the rotator interval usually appear as thinning, irregularity, or focal discontinuity in the interval and not as complete disruption.152 Demonstration of fluid extension across the rotator interval on routine MRI indicates rotator interval disruption, but this finding usually requires the presence of an associated glenohumeral joint effusion (Fig. 8-66).152 In the absence of a full-thickness rotator cuff tear, contrast extension from the glenohumeral joint through the rotator interval and into the subacromial/subdeltoid

Classic Signs ■

■ ■ ■ ■

Anterosuperior impingement should be considered in patients with a history of anterior shoulder pain that is not relieved by subacromial anesthetic injection. Reflection pulley lesions are noted. Medial subluxation of the LHB occurs. Partial articular surface tears of the cranial fibers of the subscapularis tendon occur. There is mechanical contact between the area of the LHB/ biceps pulley and the anterosuperior aspect of the glenoid labrum.

bursa on MR arthrography is indicative of a rotator interval tear.152 More subtle findings on MR arthrography of a rotator interval tear include thinning or discontinuity of the rotator interval structures without demonstration of communication between the glenohumeral joint and subacromial/subdeltoid bursa.152 Although tears of the rotator interval may occur alone, they are often associated with rotator cuff tears, especially with tears of the anterior fibers of the supraspinatus tendon and superior fibers of the subscapularis tendon.152

DIFFERENTIAL DIAGNOSIS Although shoulder impingement and rotator cuff tears are a common cause of shoulder pain and weakness, there are other shoulder pathologic processes that may produce similar symptoms.96 Other common conditions that may mimic impingement and rotator cuff tears clinically include calcific tendinitis or bursitis (Figs. 8-67 and

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8-68), subacromial/subdeltoid bursitis, fractures of the greater tuberosity, and adhesive capsulitis.96 Laboratory studies do not play a significant role in the diagnosis of shoulder impingement syndromes.

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment

■ FIGURE 8-67 This single anteroposterior radiograph of the shoulder demonstrates prominent soft tissue mineralization, likely representing calcium hydroxyapatite, adjacent to the greater tuberosity of the humerus in the region of the supraspinatus tendon that is consistent with calcific tendinitis.

Most cases of shoulder impingement and many cases of rotator cuff tear can be managed nonoperatively.116,156 Treatment programs should be tailored to the individual patient and to the patient’s goals, including improvement in pain level, range of motion, and functional status.116,156 Acute symptoms may be treated with rest, activity modification, ice, and nonsteroidal anti-inflammatory medications; however, nonsteroidal anti-inflammatory medications are less useful to treat chronic symptoms.156 Selective corticosteroid injections, in association with physical therapy, have been shown to be effective in the short-term treatment of impingement, although no more than two injections should be given because of the potential complications related to corticosteroid injection.157 Physical therapy is considered to be the cornerstone of nonoperative management.156 Important considerations in the design of a physical therapy program include (1) strengthening the proximal musculature, (2) working individual muscles, (3) working muscles in patterns, and (4) developing proper shoulder girdle mechanics and abilities.156 Additional local treatment measures may be

■ FIGURE 8-68 Oblique coronal fat-suppressed proton density–weighted (A) and oblique coronal proton density–weighted (B) MR images of the shoulder demonstrate globular low signal intensity material (presumably calcium hydroxyapatite) in the subacromial/subdeltoid bursa (arrowheads) consistent with calcific bursitis. Note the small area of erosion of this material into the underlying bone (A, arrow). Also note the high signal intensity in the bursa, representing bursal fluid and synovitis.

CHAPTER

used, including moist heat to increase vascular supply and to stimulate sympathetic nerve fibers, ice to decrease inflammation after exercise, ultrasound to increase local blood flow and the permeability of cell membranes (improving exchange of metabolic products), high- or low-voltage electric stimulation, transverse friction massage to remove metabolic waste products and prevent scarring, and selective rest.156 Success rates for conservative treatment in the literature are variable (50% to 90%), likely due to differences in operative criteria.158 Itoi and Tabata demonstrated good results (82% at a mean follow-up of 3.4 years) for conservative treatment in patients with preserved range of motion and muscle strength in the short term and mid term but noted that in the long term (more than 6-year follow-up) results deteriorated.158 Bokor and colleagues reported significant improvement in pain, function, and range of motion in their selective group of 53 patients treated conservatively for arthrographically proved full-thickness rotator cuff tears.159 Bartolozzi and coworkers demonstrated an unfavorable outcome for conservative treatment in patients with a rotator cuff tear greater than or equal to 1 cm, pretreatment symptoms longer than 12 months in duration, and severe functional impairment.64 They recommended that the period of conservative treatment should be shorter and the threshold for operative treatment should be lower in these patients than in other patients.64 They also found, however, that 85% of patients with impingement but without an associated rotator cuff tear will ultimately demonstrate good or excellent results with conservative treatment of at least 18 months’ duration.64

Surgical Treatment The goals for surgical repair of the rotator cuff are to relieve pain and to restore rotator cuff function.114 Recently, Oh and coworkers conducted a systematic review of the literature in an attempt to provide guidelines for surgical treatment of full-thickness rotator cuff tears.160 They concluded that early surgical treatment was indicated in patients with weakness and functional impairment of the rotator cuff.160 In their review of the literature they did not find that older chronologic age indicated a worse outcome; however, pending workers’ compensation actions do appear to influence outcomes negatively.160 These authors believed it is reasonable to start almost all patients with symptomatic full-thickness tears on nonoperative treatment for 6 weeks to 3 months.160 Operative treatment is indicated,

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however, if nonoperative treatment fails.160 They also concluded that early operative repair of a traumatic tear may improve outcome.160 In addition, they suggested that surgical repair may be required in very active patients to reestablish their previous levels of strength and motion.160 Surgical rotator cuff repair is usually combined with subacromial or outlet decompression.156 Neer first described the procedure of anterior acromioplasty and resection of the coracoacromial ligament (with or without resection of the distal clavicle and osseous excrescences on the undersurface of the acromioclavicular joint) for treatment of subacromial impingement and as a replacement for complete acromionectomy and lateral acromionectomy, which had demonstrated disappointing results.2 Although subacromial decompression and rotator cuff repair have traditionally been performed via an open approach, arthroscopic methods for both of these procedures have increased in popularity recently.156 Finally, it should be noted that patients with untreated massive rotator cuff tears are at risk for development of rotator cuff arthropathy.36,116 This condition, associated with chronic massive rotator cuff tears, consists of weakening of the subchondral bone around the glenohumeral joint, progressive impaction of the humeral head against the undersurface of the acromion process and acromioclavicular joint, osseous erosion, and eventually humeral head collapse.36,116

What the Referring Physician Needs to Know ■ ■ ■ ■ ■ ■ ■

■

Size of a full-thickness tear Depth of a partial-thickness tear Tear morphology Degree of tendon retraction Extension of tear into multiple tendons, rotator interval, or biceps tendon Degree of associated muscle atrophy Morphology of the coracoacromial arch including acromion type and presence of a subacromial enthesophyte, os acromiale, or large acromioclavicular joint osteophytes Narrowing of the coracohumeral space in the setting of subscapularis tendon tears

SUGGESTED READINGS Bergman A. Rotator cuff impingement: pathogenesis, MR imaging characteristics, and early dynamic MR results. MRI Clin North Am 1997; 5:705–719. Bigoni B, Chung C. MR imaging of the rotator cuff interval. Radiol Clin North Am 2006; 44:525–536. Fritz R, Stoller D. MR imaging of the rotator cuff. MRI Clin North Am 1997; 5:735–754. Fu F, Harner C, Klein A. Shoulder impingement syndrome: a critical review. Clin Orthop Relat Res 1991; 269:162–173. Lyons R, Green A. Subscapularis tendon tears. J Am Acad Orthop Surg 2005; 13:353–363.

Moosikasuwan J, Miller T, Burke B. Rotator cuff tears: clinical, radiographic, and US findings. Radiographics 2005; 25:1591–1607. Morag Y, Jacobson J, Miller B, et al. MR imaging of rotator cuff injury: what the clinician needs to know. Radiographics 2006; 26:1045–1065. Neer C. Impingement lesions. Clin Orthop Relat Res 1983;73:70–77. Oh L, Wolf B, Hall M, et al. Indications for rotator cuff repair. Clin Orthop Relat Res 2007; 455:52–63. Seibold C, Mallisee T, Erikson S, et al. Rotator cuff: evaluation with US and MR imaging. Radiographics 1999; 19:685–705. Sherman O. MR imaging of impingement and rotator cuff disorders. MRI Clin North Am 1997; 5:721–734.

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C H A P T E R

9

C H A P T E R

Glenohumeral Instability Michael J. Tuite

PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS Shoulder instability and labral tears are a common cause of shoulder complaints, particularly in young athletic individuals. The symptoms can be quite debilitating, and surgery is often required to reduce the pain or stabilize the shoulder. Imaging plays an important role in helping determine who might benefit from surgery. The glenoid labrum has several normal anatomic variants, however, that are crucial to recognize to accurately interpret imaging studies of the shoulder. The glenohumeral joint is the most commonly dislocated major joint in the body, accounting for 45% of all dislocations.1 The incidence of shoulder dislocation is about 1 per 10,000 people per year.2 After a dislocation, up to 90% of patients will have chronic symptoms of either pain or instability.1 The glenohumeral joint is designed for a wide range of motion, and thus the glenoid fossa is fairly shallow. As a consequence, the glenohumeral joint relies on the surrounding dynamic and static soft tissue structures to maintain stability. The main static stabilizer is the labroligamentous complex, composed of the glenoid labrum, capsule, and glenohumeral ligaments (GHLs). These structures often heal poorly, with residual laxity or a chronic tear after they are injured, which leaves the shoulder unstable. Shoulder instability is defined as recurrent subluxation or dislocation at the glenohumeral joint. Instability can be divided into four main types: anterior, posterior, multidirectional, and microinstability. Surgeons have also described “functional instability,” in which the patient has the sensation of shoulder instability but there is none on clinical examination. Functional instability is typically due to an isolated labral tear.3 Anterior instability is the most common type of symptomatic shoulder instability. Anterior dislocations account for 85% to 90% of all dislocations.1 Posterior instability makes up only 2% to 4% of patients with instability.4 Multidirectional instability is defined as shoulder joint

laxity in more than one direction. It is relatively common, although many of these patients are treated conservatively and are never imaged. Microinstability refers to a family of disorders in which there is mild instability in a predominantly superoinferior direction.5 In addition, there are some labral tears that are typically not associated with instability, such as superior labrum anterior to posterior (SLAP) tears and posterosuperior labral tears associated with spinoglenoid notch cysts. SLAP tears are seen in about 5% of patients in a typical orthopedic practice, whereas spinoglenoid notch cysts are a cause of shoulder pain in young adults.6–8 Other types of dislocations, such as inferior (luxatio erecti) and superior dislocation, are rare. Imaging plays an important role in the evaluation of patients with dislocations and chronic instability, as well as pain from suspected labral tears. In this chapter we discuss the imaging of the major types of instability and labral tears.

ANATOMY The anatomy and normal variants of the shoulder have already been discussed in Chapter 6. There are some specific anatomic features that are important to remember when imaging the shoulder with instability. The humeral head is held within the glenoid fossa by a number of forces, including adhesion-cohesion, the

KEY POINTS Start with radiographs; they can confirm a prior dislocation in patients with instability. ■ Conventional nonarthrographic MR images currently detect about 70% of chronic labral tears. ■ Direct MR arthrography with ABER images is the best technique for showing anterior labral tears. ■ Remember the normal variations and anatomic variants of the labrum when interpreting shoulder images. ■

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suction cup effect, and various dynamic and static stabilizers.1 The dynamic stabilizers are the muscles and tendons that cross the joint and include the rotator cuff and long head of the biceps tendon. The static stabilizers are the labrum and joint capsule, especially the focal thickenings of the capsule termed the glenohumeral ligament. The glenoid labrum is one of the most important shoulder stabilizers because it is the site that typically tears during a dislocation.1 The labrum is a triangular structure attached to the hyaline cartilage circumferentially around the glenoid rim. It is mostly fibrous tissue with a small fibrocartilage zone at the base, and the collagen fibers of the labrum blend with those of the GHLs and long head of the biceps tendon. The vascular supply to the labrum is fairly poor, with vessels mainly located near the capsular attachment, with decreased vascularity along the inner aspect and at the free edge.9 Because of this poor vascularity, labral tears often do not heal well on their own, particularly in active individuals who continually stress the shoulder.10 There are three main GHLs: the superior, middle, and inferior. The most important of these for maintaining stability is the inferior GHL. The inferior GHL is the thickened joint capsule of the axillary recess, but its important features are the focal thickenings along the anterior and posterior margins. These focal thickenings of the inferior GHL are termed the anterior band and the posterior band. These ligaments extend from the humerus to attach to the rim of the glenoid fossa via the labrum. The anterior band of the inferior GHL inserts into the anterior labrum at about the 4 o’clock position of the glenoid rim, whereas the posterior band of the inferior GHL forms the posterior aspect of the axillary recess and attaches near the 8 o’clock position of the labrum (Fig. 9-1). The anterior band of the

inferior GHL plays an important role in preventing anterior instability of the shoulder.

Normal Variations There are several normal variations to the labrum that can mimic a tear on MR images. The first is normal variation in the shape of the labrum. The periphery of the labrum is made of fibrous tissue and therefore is flexible. Several studies have shown that the labrum can assume a variety of appearances on MRI, including a notched or blunted shape.11–13 Diffuse increased signal intensity can be seen in a normal labrum due to the “magic angle” effect, or angular anisotropy. The magic angle effect occurs because the collagen fibers of the labrum are oriented circumferentially around the glenoid rim and are therefore oriented at 55 degrees to the main magnetic field in four places. MR images with short echo times through any of these four regions may have diffuse increased signal intensity in the labrum. Labral tears can usually be distinguished from magic angle effects because the high signal intensity of tears is more linear and can still be seen on images with an echo time above 30 to 40 ms. Part of the normal aging process of the labrum is myxoid degeneration within the substance of the labrum. This myxoid change is seen on MRI as globular increased signal intensity within the substance of the labrum, although low signal intensity is usually preserved at the periphery of the labrum.13–15 The labrum is usually normal at arthroscopy in patients with only mild myxoid changes on MRI. There are also three normal anatomic variants that can involve the labrum. The superior recess is seen in about 75% of people, the sublabral foramen in about 10%, and the Buford complex in 1.5% of people.13,15 The location on the glenoid rim where the labral high signal intensity is seen can be helpful; the superior recess occurs between the 11:00 and 1:00 o’clock positions, whereas the sublabral foramen and Buford complex occur between the 1:00 and 3:00 o’clock positions. The high signal intensity in a superior recess or sublabral foramen is at the junction of the labrum and articular cartilage and has smooth margins. There are two additional features of the normal labrum to remember. First, the normal anterior labrum is slightly larger than the posterior labrum. Second, there is normal variation in the size of the subscapularis recess and the apparent site of attachment of the capsule to the glenoid neck.16,17 Although capsular attachment site may correlate with instability,18 the presence of a tear of the labroligamentous complex, particularly the labrum, is the finding of most concern to the orthopedic surgeon.17

BIOMECHANICS Anterior Instability

■ FIGURE 9-1 Oblique sagittal MR arthrogram with the superior labrum defined as the 12 o’clock position and the anterior labrum defined as the 3 o’clock position. Note the middle (arrow) and anterior band inferior (arrowhead) glenohumeral ligaments.

Glenohumeral instability typically occurs after a traumatic dislocation with an injury to the labroligamentous complex or adjacent bone. For anterior instability, the classic mechanism for the initial dislocation is a blow to the upper arm with the humerus in abduction and external rotation. The anterior dislocation direction is usually

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actually anteroinferior because the humeral head has to slide under the coracoid process as it dislocates away from the glenoid fossa. When the humeral head dislocates, the most common site of failure of the anterior labroligamentous complex is the anterior labrum.3 Seventy-four percent of anterior dislocations in patients younger than age 40 will have a torn anterior labrum at surgery.19 If the labrum becomes completely detached from the adjacent glenoid rim, this is termed a Bankart lesion. Although in some people the humeral head dislocates with the arm under traction so that the Bankart lesion results from avulsion, in most young individuals the humeral head impacts against the glenoid rim when it dislocates. This can result in either a Bankart lesion or a fracture of the anterior glenoid rim, which is called a Bankart fracture. A Bankart fracture occurs in 15% of patients after an initial dislocation.20 The site on the humerus that impacts against the glenoid rim is typically the posterosuperolateral aspect of the humeral head. This can cause either a bone bruise of the humerus or a fracture called a Hill-Sachs lesion. A Hill-Sachs lesion occurs in 80% of individuals after an anterior dislocation.21 The likelihood of recurrent instability after an initial dislocation depends on age and occurs in a third to a half of individuals younger than age 20 but only in 10% of patients older than age 40.1 Many patients develop instability not only because labral tears rarely heal but also because the anterior capsule is stretched and remains lax, which allows the humeral head to sublux more easily.22 Additional dislocation episodes also deepen the Hill-Sachs fracture and cause mechanical attrition of the anterior glenoid rim, both of which increase the symptoms of instability and the susceptibility to redislocate. Dislocation can also overstretch the subscapularis tendon, causing it to tear. In many patients the subscapularis tendon becomes thinned and lengthened with repeated dislocations.23 Anterior dislocation is less common in older people, and labral tears and subsequent instability are also more rare.3 It is postulated that the anterior capsule becomes relatively weaker compared with the labrum as we age, and therefore it is the structure more likely to tear. Older people who have anterior dislocation do have a higher incidence of either a rotator cuff tear or greater tuberosity avulsion fracture. The rotator cuff tendons weaken with age so the cuff may tear more easily under the traction of dislocation. In addition, older patients may have osteoporosis and the supraspinatus can instead avulse a portion of the greater tuberosity. There are some anterior labral tears that occur in patients without anterior instability, and these should not be called a Bankart tear or Bankart variant. Many of these tears are partial tears of the anterior labrum and are probably degenerative or from a nondislocation injury.

epileptic seizure. In seizures, the strong internal rotators contract more forcefully than the weaker external rotators and the humeral head is pulled posteriorly. The humeral head is often fixed in internal rotation when the patient arrives in the emergency department.1 Posterior labral tears often are found in patients who have not had a posterior dislocation. Many of these tears are partial labral tears. Posterior tears can result from repetitive posteriorly directed forces applied to the shoulder, such as seen in athletes.3 Other posterior labral tears occur without any trauma. These have been shown to be particularly common in patients with a hypoplastic glenoid fossa when the posterior glenoid rim provides insufficient support against normal shearing forces on the posterior labrum.24,25 Posterior labral tears can also be seen in patients who have had an anterior stabilization surgical procedure.26 Finally, some patients with multidirectional instability have a labral tear only in the posterior labrum.25

Posterior Instability

The classic type of microinstability is due to a tear involving the anterosuperior labrum and the insertion of the superior GHL.5 It is called microinstability because, although there is slight subluxation, the humeral head is prevented from dislocating by the acromion and coracoid processes. These patients may also have associated tears

Posterior dislocations are much less common than anterior dislocations, and recurrence (i.e., instability) is even more rare.3 Posterior dislocations classically occur after a blow to the adducted and internally rotated arm, or during an

Multidirectional Instability Multidirectional instability can be divided into three main types: psychiatric, atraumatic, and traumatic.1 Psychiatric multidirectional instability is not a result of trauma and cannot be cured with surgery. It is seen in patients in whom the shoulder symptoms are a physical manifestation of the underlying psychiatric disorder. Even in patients who can actually dislocate their shoulder, surgical stabilization typically fails to eliminate the symptoms of pain and apprehension. Atraumatic multidirectional instability usually occurs in patients with diffuse joint laxity, many of whom have family members with the disorder. Some of these patients probably have congenitally “weaker”’ collagen fibers, sometimes due to less cross-linking of a collagen protein.1 Other patients with atraumatic instability participate in sports such as swimming in which the capsule is repetitively stretched. Once the dynamic stabilizers also weaken or become imbalanced, instability can develop. The classic presentation is bilateral laxity with symptoms during activities of daily living or while trying to sleep.1 The treatment of atraumatic instability usually begins with rehabilitation and strengthening exercises. If these fail, a capsular shift (capsulorrhaphy) or tightening procedure may be necessary. Traumatic multidirectional instability is usually due to injuries of the labroligamentous complex that involve more than a single segment. This can be a posterior labral tear in a patient with mild but previously asymptomatic anterior laxity or an extensive labral tear involving more than 180 degrees around the glenoid rim.27,28

Microinstability and Superior Labrum Anterior to Posterior Tears

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of the anterior rotator interval or anterior supraspinatus tendon.29 These tears can occur after acute trauma or from repetitive activities such as overhead throwing. The biceps tendon may sublux or dislocate as a result of tears to the anterior interval and biceps pulley, reducing the tendon’s ability to help maintain the stability of the glenohumeral joint. Although there is some controversy, several authors report that microinstability also can be due to a SLAP tear, although most patients with a SLAP tear present with pain without symptomatic subluxation. The mechanism for developing a SLAP tear is either a fall on an outstretched arm with impaction of the humeral head into the superior glenoid rim or acute or repetitive avulsion by the long head of the biceps tendon. Some authors prefer to use the term pseudolaxity for the mild, particularly posterosuperior instability that results from the posterior SLAP tears seen in athletes who throw overhead.30 These athletes develop posterior SLAP tears from a “peel-back mechanism” that occurs during the cocking phase of throwing. This labral tear between the 11 and 12 o’clock positions on the glenoid rim results from twisting of the long head of the biceps tendon at its insertion onto the labrum.30 Although the humeral head does not sublux posterosuperiorly in the direction of the labral tear, the break in the “labral ring” allows excessive translation of the humeral head in the opposite anteroinferior direction. There is overlap of these posterior SLAP tears with the labral fraying and tears that occur with internal impingement, and some authors believe the mechanism is the same.30,31

Posterosuperior Labral Tears There are two main injury mechanisms that can result in tears to the posterosuperior labrum: internal impingement and acute trauma. Internal impingement refers to painful compression of the posterior cuff between the humeral head and the posterosuperior glenoid rim.32–35 This is most commonly seen in athletes who throw overhead and occurs when the arm is in the cocking phase of the throwing motion. Although there is some controversy, many authors believe that it is this impingement against the posterosuperior glenoid rim that leads to tears or fraying of the labrum in this region. Many of these patients also have cuff tears involving the adjacent posterior supraspinatus tendon or superior infraspinatus tendon. The mechanism for these cuff tears is also controversial, with some authors believing that they instead result from shearing forces in throwers with reduced internal rotation.30,31 Traumatic tears of the posterosuperior labrum are, like SLAP tears, usually not associated with instability. These tears typically result from a fall on an outstretched hand, this time with the humeral head forces directed more posterosuperiorly. There is some overlap in the MR appearance of these labral tears with the posterior SLAP tears seen in overhead throwers. Paralabral ganglion cysts often develop adjacent to these traumatic posterosuperior labral tears when the tear extends completely through the labrum. The mechanism for developing a paralabral ganglion cyst is presumably

leakage of fluid into the paralabral soft tissues through the labral tear. Although paralabral ganglion cysts can occur anywhere around the glenoid rim, they are most common adjacent to the posterosuperior labrum.36 Cysts in this region form adjacent to the glenoid neck in the fatty tissue in the spinoglenoid notch between the supraspinatus and infraspinatus muscles.36 Although the cysts probably result from leaking joint fluid, by the time the patient presents to a physician the cyst fluid is usually thick and gelatinous.

PATHOLOGY Anterior The most common injury after an anterior dislocation, and the most common lesion seen in patients with anterior instability, is the Bankart lesion or anteroinferior labral tear.37 This tear occurs between the 3 o’clock and 6 o’clock positions of the glenoid rim. A true Bankart lesion is a detached segment of labrum with the tear extending across the labrum including the tough outer fibers that are an extension of the scapular periosteum. There are other anatomic pathologies that can be seen after a dislocation. A Bankart fracture is a fracture of the anterior glenoid rim, whereas a Hill-Sachs lesion is an impaction fracture of the lateral humeral head. In addition to these lesions there are other pathologic processes that can be seen with anterior instability. A not uncommon injury is an incomplete tear of the anteroinferior labrum, and these can be divided into three types. A partial Bankart tear is when the tear only extends partway across the labrum, leaving some intact labral tissue attached to the adjacent glenoid rim. If the labrum remains attached to the glenoid neck only by periosteum fibers, then the injury is called Perthe’s lesion if the labrum is nondisplaced or an anterior labrum periosteal sleeve avulsion (ALPSA) lesion if the labrum is displaced away from the glenoid rim.38,39 In a chronic ALPSA lesion, the labral fragment can become adherent to the anterior glenoid neck and be covered with epithelium. MRI is particularly helpful in the presurgical planning of these chronic ALPSA lesions because the labrum itself can be difficult for the surgeon to see. The surgeon must incise the epithelial covering to free up the labrum before reattaching it to the glenoid rim during the labral repair. Some dislocations with impaction of the humeral head on the anterior glenoid rim result in a chondral defect along with a labral tear. This injury is called a glenoid labral articular defect (GLAD) lesion.40 Bankart fractures can go on to nonunion, or the fragment can be resorbed leaving only a defect in the anterior glenoid rim. Alternatively, with multiple dislocations there can be mechanical attrition of the glenoid rim, also resulting in a defect of the bone. Hill-Sachs impaction fractures also routinely persist as a chronic Hill-Sachs defect in the humeral head. If the defect becomes too large as a result of multiple dislocations, bone grafting may be indicated to help prevent future dislocations. Not all dislocations result in injuries to the anterior labrum or glenoid rim. The anterior capsule and anterior band of the inferior GHL can tear at any point along

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its course between the anterior labrum and its humeral insertion. Capsular tears or stretching are more common in older individuals, although some laxity is seen in most patients after a dislocation.1,22 If the anterior band of the inferior GHL tears at the humeral attachment, it is called a humeral avulsion of the glenohumeral ligament (HAGL) lesion.41 This injury is present in about 9% of patients with an anterior dislocation.19 If the anterior band of the inferior GHL avulses a piece of bone from the humerus, it is called a bony humeral avulsion of the glenohumeral ligament (BHAGL) lesion.42 If the anterior labroligamentous complex tears in two locations, such as a HAGL and Bankart tear, this is called a floating GHL.43 Rotator cuff tears are more common in older patients after an anterior dislocation and involve either the supraspinatus or the subscapularis tendon.1 Alternatively, some patients fracture the greater tuberosity instead of tearing the supraspinatus tendon. These avulsion fractures involve the superior facet of the tuberosity at the supraspinatus tendon insertion. Some partial tears of the anterior labrum are not associated with instability or prior dislocation. A helpful imaging sign in these patients is that they do not have a Hill-Sachs lesion. These should be called anterior labral tears and not “Bankart” tears, although they may be débrided at surgery if believed to be a potential cause of pain. A paralabral cyst may be seen adjacent to some anterior labral tears.36 These cysts can be a helpful secondary sign of a labral tear when they are more obvious than the tear itself, particularly on conventional MR images. The paralabral cyst adjacent to a Bankart type tear usually by itself is not symptomatic, although if large it can compress the axillary nerve and cause symptoms.

Posterior Posterior dislocations and instability are associated with posterior labral tears or posterior glenoid rim fractures. The labral tear or reverse Bankart lesion is defined as a tear through the labrum that occurs between the 10 o’clock and 6 o’clock positions of the glenoid rim. The reverse Bankart fracture occurs in a similar location to the labral tear. Patients can also have an impaction injury of the anteromedial humeral head called a reverse Hill-Sachs lesion or “trough” sign. Posterior dislocations can cause an injury to the posterior labroligamentous structures other than a posterior labral tear.44 Similar to an ALPSA ligament, the labrum may be displaced but still attached to the glenoid rim by intact fibers from the periosteum, the posterior labrocapsular periosteal sleeve avulsion (POLPSA) lesion.45 If the posterior band of the inferior GHL is torn near the humeral insertion, the lesion has been called a posterior humeral avulsion of the glenohumeral ligament (PHAGL) lesion.46 With posterior instability, the posterior glenoid rim is often blunted or rounded. This can be due to mechanical attrition from recurrent dislocations or can represent a hypoplastic glenoid in a patient who then develops a labral tear and instability.24,25 Although posterior instability accounts for only 2% to 4% of patients with shoulder instability, posterior labral tears are seen in up to 18% of patients undergoing MRI.25

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Another posterior labroligamentous injury is the Bennett lesion, which is seen mainly in throwing athletes.47 This calcification adjacent to the posterior glenoid rim is presumably from repetitive traction and is typically not associated with a posterior labral tear. A similar process can sometimes instead lead simply to a stiffening of the posterior labrum and adjacent capsule. This is termed glenohumeral internal rotation deficit (GIRD).30 On MRI there is thickening of the posterior labrum and adjacent capsule, and on MR arthrography there is loss of the normal posterior labrocapsular recess.

Multidirectional The most common abnormality seen with atraumatic multidirectional instability is a lax capsule with stretched GHLs. In patients with traumatic multidirectional instability there may be a labral tear involving more than 180 degrees around the circumference of the glenoid rim. Some patients with multidirectional instability on clinical examination have a hypoplastic glenoid fossa and a posterior labral tear.25

Microinstability The classic lesion seen with microinstability is a tear of the anterosuperior labrum between the 12 and 2 o’clock positions involving the origin of the superior GHL.5 These patients may have associated tears of the anterior interval or anterior supraspinatus tendon as well. In overhead throwers with “pseudolaxity,” the typical lesion is a posterior SLAP tear that results from the “peel-back mechanism” during throwing.30

SLAP Tears A SLAP tear is a tear of the labrum between the 11 o’clock and 1 o’clock positions. SLAP tears were originally divided into four types.48 A type 1 SLAP tear is degenerative fraying of the superior labrum and is usually not a surgical lesion or a major cause of shoulder pain. The type 2 to 4 SLAP tears do cause shoulder pain and often must be treated surgically to give pain relief. The type 2 SLAP tear extends only partially through the superior labrum. When the tear extends completely from the inferior to superior surface of the labrum, the detached labrum will appear as a bucket handle at arthroscopy and is called a type 3 SLAP tear. The type 4 SLAP tear also extends into the long head of the biceps tendon. Several authors have described additional types (type 5 and above) of SLAP tears.49 These higher-number SLAP tears are basically type 2 to 4 tears associated with tearing of other portions of the labrum or other structures in the shoulder. For example, a type 9 SLAP tear is a tear that involves the entire labrum except for a small portion of intact labrum around the 6 o’clock position. Type 9 SLAP tears tend to occur in muscular athletic individuals who present with shoulder pain. Although a type 9 SLAP tear is extensive, it usually extends only partially across the labrum and therefore causes only mild instability.27,28

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Posterosuperior Labral Tears Posterosuperior labral tears can be seen either in internal impingement or after trauma in a patient with an adjacent paralabral cyst. Internal impingement labral lesions are usually small tears or fraying of the posterosuperior labrum.32–35,50 They occur almost exclusively in overhead throwing athletes, and there may be an associated articular surface partial-thickness cuff tear involving the posterior supraspinatus tendon or superior infraspinatus tendon. Traumatic tears of the posterosuperior labrum can be either partial or extend across the entire labrum. The tears through the entire labrum are often associated with a paralabral spinoglenoid notch ganglion cyst.36,51–53 Paralabral cysts in this region can occur with isolated posterosuperior labral tears or with SLAP tears that extend posteriorly to the region adjacent to the spinoglenoid notch. The labral tear itself may cause only minimal symptoms, but the cyst is often quite symptomatic. These cysts cause pain because they compress the sensory branch of the suprascapular nerve in the spinoglenoid notch. The cyst can also compress the motor branch to the infraspinatus muscle. This initially causes denervation edema but, if chronic, can lead to atrophy of the infraspinatus muscle. If the cyst becomes large enough, it may extend superiorly toward the suprascapular notch and compress the more proximal suprascapular nerve, causing atrophy of the supraspinatus muscle.

MANIFESTATIONS OF THE DISEASE Anterior Instability Radiography Imaging of a patient with anterior dislocation or instability should start with radiographs. If the patient has an acute dislocation, radiographs can confirm that the dislocation

A ■ FIGURE 9-2

is anterior and will show any fractures that may affect the reduction. On an anteroposterior radiograph of a shoulder that is anteriorly dislocated, the humeral head is usually located under the coracoid process slightly medial and inferior to the glenoid fossa (Fig. 9-2). The axillary or scapular-Y view will show that the humeral head is dislocated anterior to the glenoid fossa. Radiographs also show the fractures that can occur with a dislocation. The Bankart fracture appears as a crescent of bone off the anteroinferior glenoid rim (Fig. 9-3). On routine radiographs, the Hill-Sachs fracture is best seen with the arm internally rotated to profile the posterolateral aspect of the humeral head. A Hill-Sachs fracture appears as a flattening or indentation in the superior aspect of the humeral head (Fig. 9-4). Older patients may have a supraspinatus tendon avulsion fracture that appears as a fracture at the base of the greater tuberosity (Fig. 9-5). After a shoulder is reduced, radiographs are often obtained to confirm the reduction and document any residual displacement of the fracture fragments. Displaced fracture fragments may go on to nonunion or heal with unsatisfactory residual deformity, so radiographs can help the surgeon determine if a closed or open fracture reduction is necessary. Also, many small Bankart fractures are better seen on the postreduction radiographs. Radiographs are also helpful in evaluating patients with anterior instability who do not have a documented anterior dislocation. Some of these patients will have Bankart or Hill-Sachs fractures that can confirm that a dislocation has occurred in the past. Our usual instability radiographic views are the (1) Neer anteroposterior or Grashey view, (2) axillary view, and (3) West Point view. The West point view is an oblique axillary view that profiles the anteroinferior glenoid rim in the 4 to 5 o’clock region.20,54,55 The West Point view may show small Bankart fractures that are difficult to see on the standard radiographic views (see Fig. 9-3). Many imaging centers also

B

Anteroposterior (A) and axillary (B) radiographs of an anteriorly dislocated left shoulder show the humeral head (arrows) in the typical subcoracoid location anterior to the glenoid fossa (arrowhead).

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■ FIGURE 9-3 Axillary (A) and West Point (B) views in a patient with a prior anterior dislocation now with anterior instability. The Bankart fracture fragment (arrow) is best seen on the West Point view.

■ FIGURE 9-4 Anteroposterior radiograph with the humerus in internal rotation shows a Hill-Sachs defect (arrow) in the humeral head.

obtain a radiograph with the humerus in internal rotation to better demonstrate a Hill-Sachs impaction fracture. The Stryker notch view is a radiographic view that also profiles the posterolateral humeral head and shows Hill-Sachs lesions well.

■ FIGURE 9-5

Anteroposterior radiograph in a 69-year-old woman with an anterior dislocation of the humeral head and a greater tuberosity fracture (arrow).

Magnetic Resonance Imaging MRI has become the main modality for imaging patients with anterior instability. Not all patients need MRI before surgery or rehabilitation treatment, however. For example, a patient younger than the age of 40 who has

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had a documented anterior dislocation and persistent instability symptoms has a high probability of having a Bankart tear, and many surgeons are comfortable taking the patient straight to arthroscopy.

Conventional Magnetic Resonance Imaging versus Magnetic Resonance Arthrography Magnetic resonance imaging of the labrum can be done in one of three ways. It can be imaged using conventional noncontrast MRI, intravenous contrast-enhanced indirect MR arthrography, or direct MR arthrography in which the joint is injected with saline or dilute gadolinium. The main advantage of conventional MRI is that it is noninvasive, and it is very good at showing labral tears after a recent dislocation where there is also a joint effusion. Conventional MRI is not as sensitive for labral tears in patients with chronic instability without a recent dislocation.56–58 Many of these tears are at least partially filled with fibrovascular tissue that is similar in signal intensity to the surrounding labrum, and there may be little joint fluid within the tear to make it noticeable.38 A wide range of accuracies have been reported, but many authors believe that conventional MRI is about 70% sensitive for chronic labral tears.59–68 Although indirect MR arthrography has the advantage of requiring only an intravenous injection, there is little published in the literature and most centers that have fluoroscopy or ultrasound available prefer direct MR arthrography.69 Direct MR arthrography with dilute gadolinium for contrast is considered the most accurate technique for diagnosing tears of the anterior labrocapsular complex, with a sensitivity over 90% for even old labral tears.17,57,59,70,71 By adding images with the arm in abduction and external rotation (ABER position), the sensitivity is improved even further.72 The distention by the injected fluid not only separates and outlines the normal structures within

■ FIGURE 9-6

the glenohumeral joint, but the fluid also disrupts the fibrovascular tissue and therefore extends into the tear. T1-weighted images with their high signal-to-noise ratio can be used, and the gadolinium has excellent contrast with the adjacent structures on fat-suppressed images. The ABER position images place tension on the anterior band of the inferior GHL and anteroinferior capsule, opening up even small partial Bankart and Perthe’s tears to contrast so that they are seen more easily (Fig. 9-6). The ABER images are also perpendicular to the anteroinferior glenoid rim, so there is less partial averaging of the signal intensity within small tears.

Magnetic Resonance Imaging Findings Bankart tears appear on both conventional MRI and MR arthrography as linear increased signal intensity extending from the joint to the anteromedial surface of the anterior labrum (Fig. 9-7). A Bankart tear where the labrum is displaced or resorbed appears as fluid directly up against the glenoid rim. In partial tears and Perthe’s lesions, the linear increased signal intensity will only extend partly across the labrum (Fig. 9-8). In an ALPSA lesion, the labrum will be displaced medially from the glenoid rim and lie next to the anterior glenoid neck (Fig. 9-9). In the GLAD lesion there is also focal high signal intensity in an articular cartilage defect near the labral tear (Fig. 9-10). In acute tears of the capsule and anterior band of the inferior GHL there is edema in the superficial soft tissues adjacent to the tear on T2-weighted images. On MR arthrography, joint fluid may extravasate through the tear into the adjacent soft tissues (Fig. 9-11). The HAGL lesion is often best diagnosed on oblique coronal images where the anterior band of the inferior GHL and axillary recess capsule does not extend up to its normal insertion onto the humeral metaphysis (Fig. 9-12). This has been described as the J sign because the point where the capsule is apposed to the humerus is much lower than its

Axial (A) and ABER position (B) MR arthrograms show a labral tear (arrows). Perthe’s lesion was confirmed at surgery.

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■ FIGURE 9-7 Two axial fat-suppressed intermediate-weighted conventional MR images show a Bankart labral tear (arrows) and a Hill-Sachs fracture (arrowhead) with adjacent bone bruise (curved arrow). Axial section shown in B is cephalad to image in A.

■ FIGURE 9-8 Axial MR arthrogram shows a partial Bankart tear (arrow) with the labrum still partially attached (arrowhead) to the glenoid rim.

■ FIGURE 9-9 Axial MR arthrogram of an anterior labrum periosteal sleeve avulsion shows the medially displaced labral fragment (arrow) and the bare articular cartilage at the anterior rim of the glenoid fossa (arrowhead).

origin off the inferior glenoid rim, and on a right shoulder oblique coronal image the capsule looks like a letter J.41 A BHAGL lesion will show low signal intensity from an avulsion fracture fragment from the humerus attached to the anterior band of the inferior GHL. It is also helpful to look for a Hill-Sachs impaction injury on the MR images. In recent dislocations, this will appear as edema in the posterolateral portion of the superior humeral head on fluid-sensitive images (see Fig. 9-7). If the impaction force is great enough, an impaction fracture will be seen as a depression in this area

of the humeral head. It is important not to confuse a Hill-Sachs fracture with the normal anatomic groove that occurs slightly more inferiorly in the posterolateral humeral head.73

Multidetector Computed Tomography Routine nonarthrographic CT has a limited role in patients with instability but can be used to assess the size of a Bankart or Hill-Sachs fracture.74 CT arthrography is very helpful in evaluating patients who have instability but

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■ FIGURE 9-10 MR arthrogram with the arm in the ABER position shows a glenoid labral articular defect (arrow), and Perthe’s lesion of the labrum (arrowhead).

■ FIGURE 9-11 Axial MR arthrogram shows capsular elongation (arrowhead) with contrast medium extravasated into the anterior soft tissues (arrow). The tear in the wavy capsule was present on a more superior image (not shown).

■ FIGURE 9-12 Coronal MR T1-weighted (A) arthrogram anterior to a T2-weighted (B) image shows the humeral avulsion of the anterior band of the inferior glenohumeral ligament (arrowhead). The attachment of the axillary recess capsule to the humerus is too distal, the so-called J sign (arrows).

cannot undergo MR arthrography.75–80 CT arthrography can also be helpful in patients with prior shoulder surgery when metal artifact obscures the adjacent labrum. A CT arthrogram is done by injecting 12 to 15 mL of a mixture of iodinated contrast and lidocaine into the glenohumeral joint and scanning with thin sections in both neutral adducted and ABER positions. In addition to the neutral

axial images, 2D reformatted images are obtained similar to the slice orientation used for MR arthrography. Tears will appear as linear increased density contrast extending into the low density labrum or GHL (Fig. 9-13). There are a few recent studies comparing thin-section multidetector CT arthrography with MRI for imaging the anterior labrum.76,81 The sensitivity for the tears

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■ FIGURE 9-13 Axial CT arthrogram (A) and ABER position (B) image of a patient with a metal screw from prior surgery for a Bankart tear. The labrum is healed to the glenoid neck (arrows) similar to a chronic anterior labrum periosteal sleeve avulsion, and there is exposed bone at the anterior glenoid rim (arrowhead).

themselves is fairly similar for CT and MR arthrography. MR arthrography with its better soft tissue contrast is overall superior because it gives significant additional information concerning ligaments, muscle, and tendons, especially on the T2-weighted images. Several old studies reported that conventional MRI was as good or better than CT arthrography for depicting labral tears.59,80,82,83 A concern with these studies is that the reported sensitivity of CT arthrography is much lower (0.33–0.73) than the generally accepted sensitivity (0.94–1.00) published in many earlier and subsequent articles.75–81 The accuracy of CT arthrography is probably better than conventional MRI for chronic labral tears in patients without a joint effusion.

Arthroscopy At arthroscopy, the Bankart tear and its variants appear as detached labral tissue with irregular margins. Small Perthe’s lesions may require probing by the surgeon to locate, so MR arthrography with ABER images is helpful for presurgical planning. MRI is also helpful in chronic ALPSA lesions when the labral fragment is covered with epithelium and difficult for the surgeon to identify. In these patients, the surgeon must incise the epithelial

Classic Signs ■ ■

Radiography: Acute dislocations—humeral head located below the coracoid process; Bankart and Hill-Sachs fractures MRI: Linear high signal intensity in the anterior labrum; HAGL lesion: J sign.

covering to free up the labrum before reattaching it to the glenoid rim during the Bankart repair.

Posterior Instability Radiography In posterior dislocations, the humeral head often dislocates directly posteriorly so the abnormal position of the humeral head can be subtle on an anteroposterior radiograph (Fig. 9-14). The joint width may appear wide or incongruent. The humeral head is typically fixed in internal rotation, so the proximal humerus has a “light bulb” appearance. The posterior dislocation is usually obvious on an axillary or scapular-Y view. Similar to anterior dislocations, any fractures resulting from the dislocation are typically best seen on a postreduction radiograph (Fig. 9-15). The reverse Bankart fracture appears as a crescent of bone adjacent to the posterior glenoid rim on an axillary view. The lateral edge of the reverse Hill-Sachs fracture appears as a vertical sclerotic line in the medial anterior humeral head and is called the “trough” sign (Fig. 9-16). In patients with atraumatic posterior labral tears, the glenoid fossa may be hypoplastic and appear shallow with a deficient posterior glenoid rim.

Magnetic Resonance Imaging Posterior labral tears appear as linear increased signal intensity in the posterior labrum (Fig. 9-17). The tears can be either partial tears or true posterior Bankart tears in which the labrum on one or more axial sections is detached from the adjacent glenoid rim. In atraumatic posterior instability, there may be a posterior labral tear

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■ FIGURE 9-14 Anteroposterior (A) radiograph of a posterior dislocation shows the humeral head in fixed internal rotation giving the “light bulb” sign (arrowheads). The scapular-Y view (B) confirms the posterior location of the humeral head (arrowhead) relative to the glenoid fossa (arrows).

■ FIGURE 9-15 Axillary view after reduction of a posterior dislocation shows a posterior Bankart fracture (arrow) and the fracture donor site from the posterior glenoid rim (arrowheads).

■ FIGURE 9-17

Axial MR arthrogram shows a posterior labral tear (arrow).

and a hypoplastic glenoid fossa (Fig. 9-18). In the POLPSA lesion the posterior labral fragment is torn from the glenoid rim but still attached to the more medial glenoid neck by a periosteal sleeve. Acute tears of the posterior band of the inferior GHL will appear as high signal intensity through the ligament and capsule on fluid sensitive sequences or as a leakage of contrast on MR arthrography. The PHAGL lesion will have a tear of high signal intensity near the humerus and may have a torn insertion of the teres minor tendon (Fig. 9-19).44

Multidetector Computed Tomography ■ FIGURE 9-16

Anteroposterior radiograph shows a reverse Hill-Sachs lesion or “trough” sign (arrowheads) in the medial anterior humeral head.

As in anterior instability, CT arthrography can be helpful in evaluating for a labral tear when MR is contraindicated or there is extensive metal artifact. Posterior labral tears

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Classic Signs ■ ■

Radiography: Light-bulb sign, reverse Bankart fracture, and trough sign MRI: Linear high signal intensity in the posterior labrum; hypoplastic glenoid fossa.

consistently good results as those reported for anterior instability.84

Multidirectional Instability Radiography

■ FIGURE 9-18 Intermediate-weighted conventional MR image shows a hypoplastic glenoid fossa (arrowheads) with a posterior labral tear (arrow). There is also posterior subluxation of the humeral head and myxoid changes in the anterior labrum.

will appear as linear contrast extending into the labrum or between the labrum and the adjacent glenoid rim and articular cartilage.

Arthroscopy The arthroscopic appearance of posterior labral tears is similar to that of anterior tears, except for location. The surgical treatment of posterior instability has not had as

Radiographs in patients with multidirectional instability are usually normal.1 Some patients with traumatic multidirectional instability can have anterior and posterior labral tears, although Bankart and/or reverse Bankart fractures are uncommon.

Magnetic Resonance Imaging The most common appearance of the labrum in patients with multidirectional instability is a normal labrum. With the joint distended, some patients have a capacious capsule with a large communication with the subscapularis recess (Fig. 9-20). The GHLs and capsule may insert onto the glenoid neck more medially than normal. Some patients with clinical multidirectional instability will have anterior or, more commonly, posterior labral tears as well. These tears will often be partial tears without actual detachment of the labrum.

■ FIGURE 9-19 T1-weighted MR arthrograms of a posterior humeral avulsion of the glenohumeral ligament or PHAGL lesion. On axial (A) and oblique sagittal (B) images the posterior capsule near the humeral insertion is indistinct (arrow), and contrast agent extravasates through the capsular tear into the adjacent soft tissues (arrowhead) and around the posterior cuff (curved arrows).

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middle GHL. The Buford complex, and often the sublabral foramen, are associated with a thick, cord-like middle GHL.15

Superior Labrum Anterior to Posterior Tears Radiography Radiographs are usually normal.

Magnetic Resonance Imaging

■ FIGURE 9-20 MR arthrogram of a patient with multidirectional instability shows a capacious joint without a labral tear.

Multidetector Computed Tomography With CT arthrography, the labrum is usually normal but the joint may appear capacious with a lax capsule.

Arthroscopy The labrum is usually normal in patients with multidirectional instability, but the joint is capacious when it is distended with saline during the arthroscopic procedure. The arthroscopic treatment is usually capsulorrhaphy or capsular tightening.

Classic Signs ■

There are several MR signs of a SLAP tear.7,37,49,64,65,70,71,85–92 These signs attempt to distinguish a SLAP tear from the normal superior recess that occurs in the same region of the superior labrum.93 The superior recess is a partial unattachment of the superior labrum from the superior glenoid rim, resulting in a blind-ending pouch that curves smoothly medially at the labral-glenoid junction. There are four main appearances of a SLAP tear that help distinguish it from a normal variant superior recess: 1. SLAP tears typically extend laterally into the substance of the labrum curving away from the glenoid rim (Fig. 9-21). The linear high signal intensity tear is also often irregular or jagged. 2. The high signal intensity may extend across the entire labrum so that it is detached from the glenoid rim, which is a type 3 SLAP tear (Fig. 9-22). The superior recess is only a recess, so the labrum is always still attached at the top of the glenoid rim. 3. There may be two high signal intensity lines in the superior labrum that extend to the inferior articular surface of the labrum (Fig. 9-23). The medial line represents the superior recess, whereas the more lateral line within the substance of the labrum is the SLAP tear. This has been called the “double Oreo” sign.

MR arthrography: Elongated, lax capsule

Microinstability Radiography Radiographs are usually normal.

Magnetic Resonance Imaging The classic MR finding is a tear of the anterosuperior labrum.5 This can be a difficult diagnosis to make on imaging because three normal variants—the superior recess, sublabral foramen, and Buford complex—also occur between the 11 and 3 o’clock positions of the labrum. There are a couple of features that can help distinguish a tear from one of the normal variants. Tears are often jagged or irregular, whereas the margins of the unattached labrum in a sublabral foramen are smooth. Labral tears can occur in the substance of the labrum, whereas the superior recess and sublabral foramen always occur at the labral-glenoid junction. Labral tears are usually seen along with a normal-appearing

■ FIGURE 9-21 MR arthrogram of a SLAP tear with the high signal intensity tear curving laterally (arrow) in the superior labrum.

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B

■ FIGURE 9-22

Two adjacent MR arthrograms of a type 3 SLAP tear (arrows) with contrast agent extravasated into the superior paralabral soft tissues (arrowheads). This type of SLAP tear with a long-segment, detached superior labrum will often “bucket-handle” during arthroscopy.

4. The high signal intensity extending into the superior labrum may be abnormally wide on an oblique coronal image, even if the orientation and margins of the high signal intensity otherwise mimic a superior recess (Fig. 9-24). A normal superior recess should be less than

■ FIGURE 9-23

T2-weighted image of a SLAP tear (arrow). Note the more medial high signal intensity line from the normal superior recess and undercutting articular cartilage (arrowhead).

2 mm wide on conventional MR images and less than 2.5 mm wide on MR arthrographic images. Another sign of a SLAP tear that is more controversial is when the line of high signal intensity extends posterior to the back of the biceps attachment. Some authors have

■ FIGURE 9-24 MR arthrogram of a SLAP tear (arrow) where the high signal intensity within the superior labrum is too wide (arrowheads) to be a normal superior recess.

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■ FIGURE 9-25 Oblique coronal (A) and axial (B) MR arthrograms of a labral tear involving almost the entire circumference of the labrum in an athlete with pain and mild instability. This type 9 SLAP tear (arrow) extends to involve the anterior, posterior, and a portion of the inferior labrum as well (arrowheads).

reported that a normal superior recess does not extend posterior to the attachment site on the labrum of the long head biceps tendon.71,93 Other authors have found that, particularly on MR arthrographic images, the superior recess can appear to extend posterior to the attachment.7,88,91,94 This sign should probably not be used in isolation for diagnosing a SLAP tear. The structures adjacent to the labrum should also be evaluated to classify correctly the type of SLAP tear. Type 4 SLAP tears will have increased signal intensity on T2-weighted images within the long head of the biceps tendon near its origin. The type 5 and higher SLAP tears will have associated tears of adjacent portions of the labrum or other structures (Fig. 9-25).49 Patients with pain and multidirectional instability may have a tear with high signal intensity extending from the superior labrum to involve more than 180 degrees around the glenoid rim. Some SLAP tears may be seen only in the posterior portion of the superior labrum in throwers with a “peel-back” mechanism or only in the anterior portion of the superior labrum in patients with microinstability.

Multidetector Computed Tomography With thin-section multidetector CT, SLAP tears can be well demonstrated on CT arthrographic images.94 The tear is best seen on oblique coronal reformatted images. SLAP tears usually appear as an irregular, laterally curved, increased density line of contrast medium in the superior labrum.

Arthroscopy SLAP tears appear as a partial or complete detachment of the superior labrum at the biceps anchor, with irregular margins. It is usually easy at arthroscopy to distinguish a SLAP tear from a normal variant superior recess, which has smooth white margins. There is some debate among

Classic Signs ■

MRI: Laterally curved high signal intensity; “double Oreo” sign

orthopedists whether a partial lack of attachment of the superior labrum to the glenoid rim that extends posterior to the biceps tendon, if otherwise normal, is by itself an absolute criterion for a SLAP tear.91

Posterosuperior Labral Tears and Paralabral Cysts Radiography Radiographs are usually normal in patients with a spinoglenoid notch cyst and in throwers with internal impingement. If the cyst becomes large enough, it can cause a smooth erosion of the posterior scapula.

Magnetic Resonance Imaging Posterosuperior paralabral cysts appear as a rounded, homogeneous mass of high signal intensity on T2-weighted images adjacent to the labrum (Fig. 9-26). Moderate-sized cysts usually extend medially into the fatty space between the supraspinatus and infraspinatus tendons lateral to the scapular spine, the spinoglenoid notch. Because the cyst can compress the branch of the suprascapular nerve that innervates the infraspinatus muscle, the patient may have mild increased T2-weighted signal intensity in the infraspinatus muscle as a result of denervation muscle edema. If the cyst gets larger, it can extend cephalad into the region of the suprascapular notch. These large cysts can then also compress the suprascapular nerve branch to the supraspinatus muscle and give denervation edema of the supraspinatus muscle as well. If the nerve compression

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■ FIGURE 9-26

Oblique coronal (A) and axial (B) T2-weighted images of a spinoglenoid notch paralabral cyst (arrows). There is a posterosuperior labral tear (arrowhead) and infraspinatus muscle edema (curved arrows).

is chronic, there may be fatty atrophy of one or both muscles that appears as small muscles with areas of intramuscular stranding with fat of increased T1-weighted signal intensity. Eighty-five percent of spinoglenoid notch ganglion cysts have an adjacent tear of the posterosuperior labrum.51 These appear as linear high signal intensity within the posterosuperior labrum. At MR arthrography there is often communication of the intra-articular contrast into the cyst, although it may be slow and delayed (Fig. 9-27). Finally, some posterosuperior paralabral cysts are associated with SLAP tears that extend posteriorly.

A ■ FIGURE 9-27

Throwers with internal impingement can have either linear high signal intensity tears of the posterosuperior labrum (Fig. 9-28) or fraying with an irregular free edge of the labrum.32–34 The tears and fraying of the labrum may be seen better on the ABER images than on the standard adducted axial images. On ABER images, the sections are perpendicular to the posterosuperior labrum so there is less partial averaging of the high signal intensity of the tear with the adjacent low signal intensity labrum. Athletes with internal impingement can have additional abnormalities visible on MR images.35 They may have large and numerous subchondral cysts of high T2-weighted

B

Matching oblique coronal T1-weighted (A) and T2-weighted (B) MR arthrograms show contrast agent (arrow) extending into a paralabral cyst (arrowheads).

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■ FIGURE 9-28 MR arthrogram in ABER position of a baseball pitcher with internal impingement shows a labral tear in the posterosuperior labrum (arrow).

signal intensity within the humeral head near the insertion of the posterior cuff. They may also have articular surface partial-thickness tears of the posterior cuff that appear as increased signal intensity disrupting the low signal intensity of the articular surface of the posterior supraspinatus or superior infraspinatus tendons.

Multidetector Computed Tomography Spinoglenoid notch cysts are not as easy to see on routine CT images as on T2-weighted MR images. With CT arthrography, the labral tear will appear as linear increased-density contrast medium extending into the labrum, while some contrast medium may also extravasate into the cyst.

Arthroscopy Posterosuperior labral tears appear as detachments of the labrum with an irregular margin. Larger spinoglenoid notch ganglion cysts are sometimes visible through the arthroscope as a bluish bulge in the posterior capsule. Internal impingement patients will have either fraying or tears of the posterosuperior labrum in conjunction with the other clinical and arthroscopic findings seen in the throwing athlete’s painful shoulder.

Classic Sign ■

MRI: Infraspinatus muscle edema

DIFFERENTIAL DIAGNOSIS From Clinical Data Before imaging, the main differential diagnosis consideration in a patient with a shoulder dislocation is a fracture.

These can sometimes be difficult to distinguish without a radiograph, although a characteristic history and a palpable displaced humerus may allow the correct diagnosis. In patients with instability or a labral tear, the main initial considerations are other causes of shoulder pain, such as impingement syndrome or rotator cuff tears. Most patients with impingement syndrome are older, and there are several impingement tests that can help make the diagnosis clinically. Most patients with rotator cuff tears are also older than the typical instability patient, and many will have rotator cuff muscle weakness on examination. Other common causes of shoulder pain are radiculopathy from cervical spine disk disease or biceps tendon pathology. The hallmark of instability on physical examination is laxity or pain when the clinician attempts to sublux the humeral head. Instability is usually divided into one of three types: psychogenic, atraumatic, and traumatic.1 A careful history can usually determine if the patient voluntarily subluxes the shoulder, either by habit or due to psychiatric issues. Atraumatic instability is usually bilateral, and the tests of joint laxity such as the drawer or push-pull tests are positive. Patients with traumatic instability will often give a history of a prior dislocation and will have pain or apprehension when the humeral head is gently forced in the direction of the previous dislocation. Patients with labral tears without instability can be more difficult to sort out clinically. Patients with SLAP tears may have a positive O’Brien test.1

From Supportive Diagnostic Techniques There are few diagnostic techniques other than imaging that can be used in addition to the clinical tests in the evaluation of a patient with instability or a labral tear. There are several radiographic findings that it is good to be aware of because they can mimic those seen in instability injuries. One of these is the normal anatomic groove of the humeral head that occurs near the site of a Hill-Sachs fracture but, unlike the fracture, does not involve the top of the humeral head.73 Ossicles can also be seen adjacent to the glenoid rim in patients without instability, either from old heterotopic ossification or degenerative disease. The Bennett lesion of heterotopic ossification adjacent to the posterior glenoid rim can also appear similar to a reverse Bankart fracture.47,95

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment Medical treatment for instability is usually composed of two parts. First, exercises are done to help strengthen the deltoid, rotator cuff, and scapular muscles that act as active shoulder stabilizers. Second, the patient is taught to avoid those arm positions that cause the shoulder to sublux. Medical treatment is particularly effective in multidirectional and posterior instability.1

Surgical Treatment Surgical treatment for multidirectional instability or a lax capsule without a labral tear is usually a capsular shift procedure. In this surgical procedure, the capsule and GHLs

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■ FIGURE 9-29 Neer anteroposterior (A) and scapular-Y (B) views of a shoulder after a repair of a Bankart labral tear. There are three suture anchors in the anterior glenoid rim (arrows).

are tightened by placing a series of sutures in the lateral capsule and suturing it to the more medial capsule. For traumatic instability, the treatment options are tailored to the site of the tear in the labrocapsular complex. There are several surgical treatments used to repair a Bankart tear. One of the more common repairs is to place three anchoring sutures in the anterior glenoid near the rim and suture the labrum and capsule down to the glenoid rim so as to close the tear (Fig. 9-29). Posterior labral repairs are done similarly but to the posterior glenoid rim.

■ FIGURE 9-30

SLAP tears are often treated with surgical débridement, although if they are large or a type 3 they may need to be repaired (Fig. 9-30). Posterosuperior labral tears with ganglion cysts are treated in one of two ways. The cyst can be drained, such as percutaneously under ultrasound guidance, and the labral tear débrided or repaired. Alternatively, the cyst can be “marsupialized” through the paralabral capsule so that it communicates with the glenohumeral joint that causes it to decompress and take pressure off the nerve.

Anteroposterior (A) and arch (B) views of a SLAP tear repair using a suture anchor (arrows).

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What the Referring Physician Needs to Know ■ ■ ■

Radiographs should be obtained first in patients with instability. Posterior dislocation is often missed on an anteroposterior radiograph. Direct MR arthrography is the most accurate imaging technique for diagnosing glenoid labral tears.

SUGGESTED READINGS Beltran J, Bencardino J, Mellado J, et al. MR arthrography: variants and pitfalls. Radiographics 1997; 17:1403–1412. Beltran J, Rosenberg ZS, Chandnani VP, et al. Glenohumeral instability: evaluation with MR arthrography. Radiographics 1997; 17:657–673. Ly JQ, Beall DP, Sanders TG. MR imaging of glenohumeral instability. AJR Am J Roentgenol 2003; 181:203–213. Matsen FA, Thomas SC, Rockwood CA, Wirth MA. Glenohumeral instability. In Rockwood CA, Matsen FA (eds). The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998, pp 611–754. Mohana-Borges A, Chung C, Resnick D. Superior labral anteroposterior tear: classification and diagnosis on MRI and MR arthrography. AJR Am J Roentgenol 2003; 181:1449–1462.

Park YH, Lee JY, Moon SH, et al. MR arthrography of the labral capsular ligamentous complex in the shoulder: imaging variations and pitfalls. AJR Am J Roentgenol 2000; 175:667–672. Rafii M. Non-contrast MR imaging of the glenohumeral joint: II. Glenohumeral instability and labrum tears. Skeletal Radiol 2004; 33:617–626. Tirman PFJ, Smith ED, Stoller DW, Fritz RC. Shoulder imaging in athletes. Semin Musculoskelet Radiol 2004; 8:29–40. Tuite MJ, Rubin D. CT and MR arthrography of the glenoid labroligamentous complex. Semin Musculoskelet Radiol 1998; 2:363–375.

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CHAPTER 29. Morag Y, Jacobson JA, Shields G, et al. MR arthrography of rotator interval, long head of the biceps brachii, and biceps pulley of the shoulder. Radiology 2005; 235:21–30. 30. Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology: I. Pathoanatomy and biomechanics. Arthroscopy 2003; 19:404–420. 31. Morgan CD, Burkhart SS, Palmeri M, Gillespie M. Type II SLAP lesions: three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy 1998; 14:553–565. 32. Jobe CM. Posterior superior glenoid impingement: expanded spectrum. Arthroscopy 1995; 11:530–536. 33. Jobe CM. Superior glenoid impingement. Orthop Clin North Am 1997; 28:137–143. 34. Walch G, Boileau P, Noel E, Donnell ST. Impingement of the deep surface of the supraspinatus tendon on the posterosuperior glenoid rim: an arthroscopic study. J Shoulder Elbow Surg 1992; 1:238–245. 35. Giaroli EL, Major NM, Higgins LD. MRI of internal impingement of the shoulder. AJR Am J Roentgenol 2005; 185:925–929. 36. Tung GA, Entzian D, Stern JB, Green A. MR imaging and MR arthrography of paraglenoid labral cysts. AJR Am J Roentgenol 2000; 174:1707–1715. 37. Beltran J, Rosenberg ZS, Chandnani VP, et al. Glenohumeral instability: evaluation with MR arthrography. Radiographics 1997; 17:657–673. 38. Neviaser TJ. The anterior labroligamentous periosteal sleeve avulsion lesion: a cause of anterior instability of the shoulder. Arthroscopy 1993; 9:17–21. 39. Wischer TK, Bredella MA, Genant HK, et al. Perthes lesion (a variant of the Bankart lesion): MR imaging and MR arthrographic findings with surgical correlation. AJR Am J Roentgenol 2002; 178:233–237. 40. Sanders TG, Tirman P, Linares R, et al. The glenolabral articular disruption lesion: MR arthrography with arthroscopic correlation. AJR Am J Roentgenol 1999; 172:171–175. 41. Bui-Mansfield LT, Taylor DC, Uhorchak JM, Tenuta JJ. Humeral avulsions of the glenohumeral ligament: imaging features and a review of the literature. AJR Am J Roentgenol 2002; 179:649–655. 42. Oberlander MA, Morgan BE, Visotsky JL. The BHAGL lesion: a new variant of anterior shoulder instability. Arthroscopy 1996; 12:627–633. 43. Homan BM, Gittins ME, Herzog RJ. Preoperative magnetic resonance imaging diagnosis of the floating anterior inferior glenohumeral ligament. Arthroscopy 2002; 18:542–546. 44. Hottya GA, Tirman PFJ, Bost FW, et al. Tear of the posterior shoulder stabilizers after posterior dislocation: MR imaging and MR arthrographic findings with arthroscopic correlation. AJR Am J Roentgenol 1998; 171:763–768. 45. Yu JS, Ashman CJ, Jones G. The POLPSA lesion: MR imaging findings with arthroscopic correlation in patients with posterior instability. Skeletal Radiol 2002; 31:396–399. 46. Chung CB, Sorenson S, Dwek JR, Resnick D. Humeral avulsion of the posterior band of the inferior glenohumeral ligament: MR arthrography and clinical correlation in 17 patients. AJR Am J Roentgenol 2004; 183:355–359. 47. Ferrari JD, Ferrari DA, Coumas J, Pappas AM. Posterior ossification of the shoulder: the Bennett lesion. Etiology, diagnosis, and treatment. Am J Sports Med 1994; 22:171–175. 48. Snyder S, Banas M, Karzel R. An analysis of 140 injuries to the superior glenoid labrum. J Shoulder Elbow Surg 1995; 4:243–248. 49. Mohana-Borges A, Chung C, Resnick D. Superior labral anteroposterior tear: classification and diagnosis on MRI and MR arthrography. AJR Am J Roentgenol 2003; 181:1449–1462. 50. Tirman PF, Bost FW, Garvin GJ, et al. Posterosuperior glenoid impingement of the shoulder: findings at MR imaging and MR arthrography with arthroscopic correlation. Radiology 1994; 193:431–436. 51. Tirman PF, Feller JF, Janzen DL, et al. Association of glenoid labral cysts with labral tears and glenohumeral instability: radiologic findings and clinical significance. Radiology 1994; 190:653–658. 52. Elsayes KM, Shariff A, Staveteig PT, et al. Value of magnetic resonance imaging for muscle denervation syndromes of the shoulder girdle. J Comput Assist Tomogr 2005; 29:326–329.

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53. Sallomi D, Janzen DL, Munk PL, et al. Muscle denervation patterns in upper limb nerve injuries: MR imaging findings and anatomic basis. AJR Am J Roentgenol 1998; 171:779–784. 54. Engebretsen L, Craig EV. Radiologic features of shoulder instability. Clin Orthop Relat Res 1993; (291):29–44. 55. Rokous JR, Feagin JA, Abbott HG. Modified axillary roentgenogram. Clin Orthop Relat Res 1972; 82:84–86. 56. Flannigan B, Kursunoglu-Brahme S, Snyder S, et al. MR arthrography of the shoulder: comparison with conventional MR imaging. AJR Am J Roentgenol 1990; 155:829–832. 57. Applegate GR, Hewitt M, Snyder S, et al. Chronic labral tears: value of magnetic resonance arthrography in evaluating the glenoid labrum and labral-bicipital complex. Arthroscopy 2004; 20:959–963. 58. Tuite MJ, De Smet AA, Norris MA, Orwin JF. Anteroinferior tears of the glenoid labrum: fat-suppressed fast spin-echo T2 versus gradient-recalled echo MR images. Skeletal Radiol 1997; 26:293–297. 59. Chandnani VP, Yeager TD, DeBerardino T, et al. Glenoid labral tears: prospective evaluation with MRI imaging, MR arthrography, and CT arthrography. AJR Am J Roentgenol 1993; 161:1229–1235. 60. Garneau RA, Renfrew DL, Moore TE, et al. Glenoid labrum: evaluation with MR imaging. Radiology 1991; 179:519–522. 61. Green MR, Christensen KP. Magnetic resonance imaging of the glenoid labrum in anterior shoulder instability. Am J Sports Med 1994; 22:493–498. 62. Gross ML, Seeger LL, Smith JB, et al. Magnetic resonance imaging of the glenoid labrum. Am J Sports Med 1990; 18:229–234. 63. Gusmer P, Potter H, O’Brien S, et al. Accuracy of high-resolution, unenhanced shoulder MR imaging in the detection of labral injuries. Radiology 1995; 197(P):397. 64. Gusmer PB, Potter HG, Schatz JA, et al. Labral injuries: accuracy of detection with unenhanced MR imaging of the shoulder. Radiology 1996; 200:519–524. 65. Legan JM, Burkhard TK, Goff WB, et al. Tears of the glenoid labrum: MR imaging of 88 arthroscopically confirmed cases. Radiology 1991; 179:241–246. 66. Liu SH, Henry MH, Nuccion S, et al. Diagnosis of glenoid labral tears: a comparison between magnetic resonance imaging and clinical examinations. Am J Sports Med 1996; 24:149–154. 67. Tuite MJ, Shinners TJ, Hollister MC, Orwin JF. Fat-suppressed fast spin-echo mid-TE (TE[effective] = 34) MR images: comparison with fast spin-echo T2-weighted images for the diagnosis of tears and anatomic variants of the glenoid labrum. Skeletal Radiol 1999; 28:685–690. 68. Torstensen E, Hollinshead R. Comparison of magnetic resonance imaging and arthroscopy in the evaluation of shoulder pathology. J Shoulder Elbow Surg 1999; 8:42–45. 69. Bergin D, Schweitzer ME. Indirect magnetic resonance arthrography. Skeletal Radiol 2003; 32:551–558. 70. Palmer WE, Brown JH, Rosenthal DI. Labral-ligamentous complex of the shoulder: evaluation with MR arthrography. Radiology 1994; 190:645–651. 71. Waldt S, Burkart A, Lange P, et al. Diagnostic performance of MR arthrography in the assessment of superior labral anterosposterior lesions of the shoulder. AJR Am J Roentgenol 2004; 182:1271–1278. 72. Cvitanic O, Tirman PF, Feller JF, et al. Using abduction and external rotation of the shoulder to increase the sensitivity of MR arthrography in revealing tears of the anterior labrum. AJR Am J Roentgenol 1997; 169:837–844. 73. Richards RD, Sartoris DJ, Pathria MN, Resnick D. Hill-Sachs lesion and normal humeral groove: MR imaging features allowing their differentiation. Radiology 1994; 190:665–668. 74. Griffith J, Antonio G, Tong C, Ming C. Anterior shoulder dislocation: quantification of glenoid bone loss with CT. AJR 2003; 180:1423–1430. 75. Deutsch A, Resnick D, Mink J, et al. Computed and conventional arthrotomography of the glenohumeral joint: normal anatomy and clinical experience. Radiology 1984; 153:603–609. 76. Feller JF, Carroll KW, Tirman PF, et al. Prospective comparison of MR imaging, MR arthrography, and helical CT arthrography for the evaluation of glenohumeral instability [Abstract]. Radiology 1997; 205P:541–542.

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77. Rafii M, Firooznia H, Golimbu C, et al. CT arthrography of capsular structures of the shoulder. AJR Am J Roentgenol 1986; 146:361–367. 78. Singson RD, Feldman F, Bigliani L. CT arthrographic patterns in recurrent glenohumeral instability. AJR Am J Roentgenol 1987; 149:749–753. 79. Wilson AJ. Computed arthrotomography of glenohumeral instability. Topics Magn Reson Imaging 1994; 6:139–146. 80. Jahnke AH Jr, Petersen SA, Neumann C, et al. A prospective comparison of computerized arthrotomography and magnetic resonance imaging of the glenohumeral joint. Am J Sports Med 1992; 20:695–700. 81. Bitzer M, Nasko M, Krackhardt T, et al. Direct CT arthrography versus direct MR arthrography in chronic shoulder instability: comparison of modalities after the introduction of multidetector CT technology. Rofo 2004; 176:1770–1775. 82. Habibian A, Stauffer A, Resnick D, et al. Comparison of conventional and computed arthrotomography with MR imaging in the evaluation of the shoulder. J Comput Assist Tomogr 1989; 13:968–975. 83. Kieft G, Bloem J, Rozing P, Obermann W. MR imaging of recurrent anterior dislocation of the shoulder: comparison with CT arthrography. AJR Am J Roentgenol 1988; 150:1083–1087. 84. McIntyre L, Caspari R, Savoie F. The arthroscopic treatment of posterior instability: two-year results of a multiple suture technique. Arthroscopy 1997; 13:426–432. 85. Bencardino JT, Beltran J, Rosenberg ZS, et al. Superior labrum anterior-posterior lesions: diagnosis with MR arthrography of the shoulder. Radiology 2000; 214:267–271. 86. Chan K, Muldoon K, Yeh L, et al. Superior labral anteroposterior lesions: MR arthrography with arm traction. AJR Am J Roentgenol 1999; 173:1117–1122.

87. Connell D, Potter H, Wickiewicz T, et al. Noncontrast magnetic resonance imaging of superior labral lesions: 102 cases confirmed at arthroscopic surgery. Am J Sports Med 1999; 27:208–213. 88. Kreitner K, Botchen K, Rude J, et al. Superior labrum and labral-bicipital complex: MR imaging with pathologic-anatomic and histologic correlation. AJR Am J Roentgenol 1998; 170:599–605. 89. Smith AM, McCauley TR, Jokl P. SLAP lesions of the glenoid labrum diagnosed with MR imaging. Skeletal Radiol 1993; 22:507–510. 90. Tuite MJ, Cirillo RL, De Smet AA, Orwin JF. Superior labrum anterior-posterior (SLAP) tears: evaluation of three MR signs on T2-weighted images. Radiology 2000; 215:841–845. 91. Tuite MJ, Rutkowski A, Enright T, et al. Width of high signal and extension posterior to biceps tendon as signs of superior labrum anterior to posterior tears on MRI and MR arthrography. AJR Am J Roentgenol 2005; 185:1422–1428. 92. Yoneda M, Izawa K, Hirooka A, et al. Indicators of superior glenoid labral detachment on magnetic resonance imaging and computed tomography arthrography. J Shoulder Elbow Surg 1998; 7:2–12. 93. Smith DK, Chopp TM, Aufdemorte TB, et al. Sublabral recess of the superior glenoid labrum: study of cadavers with conventional nonenhanced MR imaging, MR arthrography, anatomic dissection, and limited histologic examination. Radiology 1996; 201:251–256. 94. Waldt S, Metz S, Burkart A, et al. Variants of the superior labrum and labro-bicipital complex: a comparative study of shoulder specimens using MR arthrography, multi-slice CT arthrography and anatomical dissection. Eur Radiol 2006; 16:451–458. 95. De Maeseneer M, Jaovisidha S, Jacobson JA, et al. The Bennett lesion of the shoulder. J Comput Assist Tomogr 1998; 22:31–34.

C H A P T E R

10

C H A P T E R

Normal Elbow

Emad Yacoub, Javier Beltran, and Theodore T. Miller

TECHNICAL ASPECTS Conventional Radiography1,2

Limitations ● ●

Rationale and Indications ● ●

Used to visualize osseous anatomy and pathology and evaluate bone contours and joints, including fat pads Recommended for any primary evaluation of suspected elbow pathology, including fractures, dislocations, bone tumors, and infection

●

Provides limited soft tissue evaluation Requires difficult patient positioning if there is limited motion for any reason (e.g., pain, fracture, ankylosis) Allows exposure to ionizing radiation, although minimal

Projections See Table 10-1 and Figure 10-1.

TABLE 10-1 Conventional Radiography of the Elbow Projections

Notes

Main Visualized Anatomy

Anteroposterior

Supine forearm, extended elbow, slight flexion of the fingers. Beam is perpendicular to the elbow joint. Take two views if there is contracture, one perpendicular to the humerus and one perpendicular to the forearm.

Lateral

Forearm flexed to 90 degrees. Trochlea and capitellum should overlap.There should be a space between the humerus and radial head. Beam is directed vertically toward the radial head.

Fractures of: Intercondylar notch of distal humerus Epicondyles Lateral capitellum Medial trochlea Lateral radial head Valgus and varus deformities Secondary ossification centers of the distal humerus Fat pad evaluation Fractures of: Supracondylar humerus Anterior radial head Olecranon process Complex elbow joint dislocations Fractures of: Medial epicondyle Coronoid process of ulna Evaluation of ulnar trochlear notch and tip of olecranon process Fractures of: Lateral epicondyle Head of radius Proximal radioulnar joint abnormalities Capitellar abnormalities Fractures of: Radial head Capitellum Coronoid process Humeroradial articulation Humeroulnar articulation

Internal oblique

External oblique

Radial head/capitellum3

Lateral view with the beam angulated toward the patient’s shoulder.

221

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B

C

D

Computed Tomography (Fig. 10-2) Rationale and Indications ●

●

●

●

■ FIGURE 10-1 Plain film series. A, Anteroposterior projection. B, Lateral projection. C, Anteroposterior projection in pronation. D, Radiocapitellar projection.

Provides multiplanar and surface rendering of the osseous anatomy with multiple reconstruction algorithms Allows visualization of complex osseous anatomy and pathology by rotation of surface-reconstructed model in infinite projections Evaluates complex fractures, dislocations, and degree of healing (callus formation, partial union, nonunion, adequate reduction and joint congruity, infection) Evaluates matrix calcification (osteoid, cartilage) in some bone tumors

● ●

Evaluates poorly visualized or suspected bone abnormality on conventional radiography Assesses soft tissue calcifications

CT Arthrography Indications ● ● ● ● ● ●

Shows subtle abnormalities of articular cartilage Shows capsular rupture Evaluates synovial abnormalities Shows chondral and osteochondral fractures Osteochondritis dissecans Loose osteochondral bodies

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223

■ FIGURE 10-2

CT series obtained with 64-slice multidetector CT. A, Axial section through the olecranon and trochlea. B, Axial section through the radioulnar joint. C, Coronal reconstruction through the head of the radius and coronoid process. D, Sagittal reconstruction through the trochlea and ulna. E, Sagittal reconstruction through the radiocapitellar joint. F, 3D surface rendering of the antecubital fossa. Note the biceps tendon (long arrow) and the median nerve (short arrows).

● ● ● ●

Single-contrast method preferred in:

●

Chondral fractures Osteochondritis dissecans Juxta-articular cyst evaluation Intra-articular loose bodies

●

Double-contrast method preferred in2: ● ●

Synovial abnormalities Capsular abnormalities

Advantages ●

Provides excellent depiction of osseous structures and calcified tissues

Has multiplanar and multisurface rendering capabilities Can be used for claustrophobic patients

Disadvantages ●

● ● ●

●

Has only limited visualization of soft tissues with conventional arthrography, although better than conventional radiography Uses ionizing radiation Expensive Has beam-hardening artifact from metal in CT arthrography (improved with recent multidetector technology) Is invasive

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Conventional Magnetic Resonance Imaging (Fig. 10-3) Rationale and Indications

Technical Aspects See Tables 10-2 and 10-3.

●

TABLE 10-2 16-Slice Multidetector CT of Elbow Attribute

Value

KV/effective mAs/rotation time Collimation Slice thickness Kernel Reconstruction

120/200/0.5 1.5 mm 3 mm B30s Multiplanar

●

Can visualize and assess soft tissue anatomy and pathology Can evaluate osseous pathology

Advantages ● ●

Provides multiplanar imaging Is nonionizing

Limitations ● ● ●

Is expensive Can be claustrophobic Has long examination time Results in motion artifacts

TABLE 10-3 64-Slice Multidetector CT of Elbow

●

Attribute

Value

Technical Aspects (Table 10-4)

KV/effective mAs/rotation time Slice thickness

120/200/0.5 0.75 mm (thin) 3 mm (thick) 0.6 mm B30f medium smooth (thick, ST) B60f bone (thick) B20f smooth (thin) 0.55 Multiplanar

Collimation Kernel Pitch Reconstruction

● ● ● ● ●

Uses routine elbow-supine position with the elbow by the side and the forearm fully supinated Uses flex coil Axial sequence is done first. Coronal sequence should be along the axis of the epicondyles. Sagittal sequence should be perpendicular to the epicondylar axis.

■ FIGURE 10-3 Normal MRI anatomy. A, Normal coronal anatomy. Coronal gradient-recalled-echo MR image illustrating the ulnar collateral ligament (UCL), radial collateral ligament (RCL), common flexor tendon (CFT), and common extensor tendon (CET). B, Normal axial anatomy. Axial T1-weighted image illustrating the muscle groups of the anterior and posterior compartments of the elbow, the radial (RN), ulnar (UN), and median (MN) nerves and the biceps tendon (BT) with the lacertus fibrosus (LF). BM, brachialis muscle; FDSM, flexor digitorum superficialis muscle; T, trochlea; O, olecranon; C, coronoid; AM, anconeus muscle; ECRL, extensor carpi radialis longus tendon; ECRB, extensor carpi radialis brevis tendon; BRM, brachioradialis muscle.

(Continued)

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225

■ FIGURE 10-3—Cont’d C, Normal sagittal anatomy. Sagittal gradient-recalled-echo MR image at the level of the radiocapitellar joint. R, radius; C, capitellum. D, Normal lateral ulnar collateral ligament. Coronal T1-weighted MR image illustrating the lateral ulnar collateral ligament (LUCL) extending from its humeral origin at the level of the lateral epicondyle to its insertion in the lateral aspect of the proximal ulna. E, Pseudodefect of the capitellum (PDC). Coronal T2weighted MR image demonstrating a small indentation in the posterior aspect of the capitellum (arrow). R, radius; T, trochlea.

TABLE 10-4 Technical Aspects of Conventional MRI of Elbow Sequence

FOV

Matrix/Nex

Slice

TR

ETL

BW

Axial PD FSE Non FatSat Axial T2 FSE FatSat Coronal T1 SE Non FatSat Coronal STIR Sagittal T2 FSE FatSat

10

512 × 256 2

4/0.5

3000

40

8

16

10

256 × 256 2

4/0.5

>2000

70–80

8

16

16–18

256 × 256 1

3/0.5

400–800

min

8

16

16–18

256 × 192 3 256 × 256 2

3/0.5

>1500

40

8

16

3/0.5

>1500

70–80

8

16

16

TE

TI

120

Flip

90

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MR Arthrography (Fig. 10-4; Table 10-5) Rationale and Indications ● ●

Evaluates intra-articular bodies Evaluates collateral ligaments

■ FIGURE 10-4

Indirect Arthrography ● ●

Gadopentetate dimeglumine–based contrast agents (15 mL of 0.1 mmol/kg) 20 minutes of prescan exercise

Normal MR arthrography. T1-weighted fat-saturated images after intra-articular injection of contrast material. A, Coronal image at the level of the ulnar collateral ligament (UCL) demonstrating its ulnar insertion at the level of the sublime tubercle (ST). B, Coronal image at the level of the radial collateral ligament (RCL), illustrating the common flexor tendon (CFT) and the synovial fringe or fold (SF). C, Sagittal image at the level of the radiocapitellar joint demonstrating the synovial fold (SF) and the pseudodefect of the capitellum (PDC). D, Sagittal image at the level of the medial epicondyle (ME) demonstrating the ulnar nerve (UN) and the common flexor tendon (CFT).

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227

■ FIGURE 10-4—Cont’d E, Sagittal image demonstrating the distal triceps tendon (TT). O, olecranon; CP, coronoid process. F, Sagittal image demonstrating the triceps (TT), brachialis (BrT), and the biceps (BT) tendons. T, trochlea.

TABLE 10-5 Technical Aspects of MR Arthrography of Elbow Sequence

FOV

Matrix/Nex

Slice

Axial T1 SE Non FatSat Axial T2 FSE FatSat Coronal T1 SE FatSat Coronal T2 FSE FatSat Sagittal T1 SE FatSat

TR

12–14

256 × 192

4/1

400–800

min

12–14

256 × 256

4/1

>1500

70–80

12–14

256 × 192

4/1

400–800

min

12–14

256 × 256

4/1

>1500

70–80

12–14

256 × 192

4/1

400–800

min

Advantages ● ● ●

Evaluates intra-articular and extra-articular pathology simultaneously Is noninvasive Is less expensive than direct arthrogram

Disadvantages ● ●

Enhancement of normal vascular tissues may cause confusion. Diagnosis is dependent on joint space distention in the absence of an effusion.

Direct Arthrography ●

Lateral approach is over the radial head under fluoroscopic guidance.

● ● ● ● ●

TE

TI

Flip

ETL

BW 16

8

16 16

8

16 16

Posterolateral approach is between the olecranon, humerus, and radial head. Distention of joint capsule is done to best evaluate intra-capsular structures. Use saline solution with or without iodinated contrast material or gadolinium. Recommend mixture of 3 mL of iodinated contrast material in 7 mL of saline solution May be good for evaluation of synovium and collateral ligament tears

Ultrasonography4 Rationale and Indications The clinical indications for elbow ultrasonography (US) involve suspected disorders of the biceps, triceps, common

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extensor and flexor tendons, medial collateral ligament, ulnar nerve, joint space, and bursae. Thus, typical candidates are the patient with focal pain and/or with weakness of a particular motion governed by a specific tendon, such as weakness of flexion and supination in the case of a torn biceps; the tennis player or golfer with lateral or medial elbow pain, respectively, when performing his or her activity; the baseball pitcher with medial pain and decreased power or accuracy of the throw; the patient with an elbow that locks, has crepitus, or lacks full range of extension and flexion; and the patient with clinical ulnar neuropathy. Unlike the US evaluation of the shoulder, which follows a standard protocol for the evaluation of the entire region, the US evaluation of the elbow is limited to the focused evaluation of the specific clinical question. Thus, for example, one would not evaluate the medial, lateral, and posterior aspects of the elbow as part of the evaluation of suspected distal biceps tendon rupture, nor would one evaluate the biceps and triceps tendons in a case of clinically suspected lateral epicondylitis.

Advantages and Limitations The elbow is well suited to US evaluation because it is a small joint with 360-degree accessibility by the transducer and is easily manipulated by the examiner. Moreover, most of the structures of clinical interest are superficial and linear (e.g., ligaments and tendons), and joint effusions and loose bodies are easily evaluated by scanning over the coronoid and olecranon fossae. US is more rapidly performed than MRI and allows dynamic scanning. Limitations of US are its operator dependence and long learning curve. In addition, US cannot assess the deep joint space and articular surfaces.

Technical Aspects

muscle along with some forearm extensors also originate from this structure. The medial epicondyle is the distal end of the medial pillar. It is the site of attachment of the ulnar collateral ligament of the elbow joint. The pronator teres muscle along with some forearm flexors also originates from this structure. The ulnar nerve runs in a groove on the back of the medial epicondyle. The epicondyles are continuous with the supracondylar ridges. The most distal surface of the humerus is complex and forms the articular surface. The capitellum is an anteriorly directed rounded eminence that makes up the lateral half of the articular surface. It articulates with the fovea of the radial head. A shallow groove in its medial border articulates with the medial margin of the head of the radius. Medial to this groove is the trochlea. The junction between the smooth capitellum and the rough, nonarticular surface of the lateral epicondyle is abrupt. It is accentuated by a trough-like undermining. The lateral capitellar margin overhangs this trough. The appearance of this on MR images may simulate a lesion.9 The trochlea is an anteriorly directed complex surface that articulates with the semilunar notch of the ulnar bone. It is convex from front to back and concave from side to side. The trochlea has articular cartilage over a 300-degree arc.5 The medial ridge is more prominent than the lateral, creating approximately 8 degrees of valgus tilt.10 This contributes to the normal carrying angle of the elbow. One percent of patients have a supracondylar spur. It is a hook-like bony spine of variable size that projects distally from the anteromedial surface of the humerus (Fig. 10-5). It is joined to the epicondyle by a fibrous band called the ligament of Struthers, which may ossify. The process, band, and shaft of the humerus form a ring or canal through which the median nerve and the brachial artery are transmitted. The nerve and/or artery may become compressed, causing clinical symptoms.11,12

A high-frequency (5–12 MHz) linear transducer is used because the ligaments and tendons of interest are superficial, highly ordered linear structures. However, the same limitations of anisotropy apply to elbow imaging as they do for shoulder imaging. To perform the US examination, the patient is seated and the examiner sits facing the patient. The patient’s forearm may be resting on a table or the patient’s lap (Finlay) or may be held by the examiner with his or her nonscanning hand to better control the patient’s elbow.

NORMAL ANATOMY Bones The bones that comprise the region of the elbow are the distal humerus, proximal radius, and proximal ulna. The distal humerus ends in a broad articular surface. It is divided into two parts by a slight ridge. These two pillars form a triangle with the distal articular surface. This triangular formation provides strength to the distal humerus.7 In distal humeral fractures, all three limbs of this triangle must be stabilized to have adequate reduction.8 The lateral epicondyle, a small tuberculated eminence, is the distal end of the lateral pillar. It is the site of attachment of the radial collateral ligament of the elbow joint. The supinator

■ FIGURE 10-5

Supracondylar process (arrow).

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■ FIGURE 10-6 Normal anatomy. Schematics of the elbow joint demonstrating the normal articular relationships in a coronal section (A), sagittal section at the level of the radiocapitellar joint (B), and sagittal section at the level of the ulnar trochlear joint (C). C, capitellum; CP, coronoid process; EM, extensor muscle; FM, flexor muscle; O, olecranon; R, radius; T, trochlea.

The radial fossa, a synovially lined anterior impression immediately superior to the capitellum, articulates with the anterior border of the head of the radius when the forearm is flexed (Fig. 10-6). The coronoid fossa, a synovially lined anterior impression immediately superior to the trochlea, is a small depression that articulates with the coronoid process of the ulna during flexion of the forearm. The olecranon fossa, a synovially lined posterior impression immediately superior to the trochlea, receives the olecranon process during forearm extension. The ulna contributes more to the elbow joint than does the radius. Important structures in its proximal portion are the olecranon, the coronoid process, and the semilunar notch. The olecranon is a curved eminence at the superior posterior ulna. In extension, it becomes situated in the olecranon fossa of the distal humerus (see Fig. 10-6). Its triangular posterior surface is smooth and lies directly under the skin. It is covered by a bursa. Its superior surface is where the triceps brachii tendon inserts. The posterior ligament of the elbow joint attaches at its anterosuperior margin. Its anterior surface is concave and forms the upper part of the semilunar notch. The ulnar collateral ligament and the posterior ligament insert on its medial and lateral borders, respectively. The coronoid process forms the lower part of the semilunar notch. It is continuous with the body of the ulnar bone. Its tip is slightly curved upward. In flexion of the forearm, it is situated in the coronoid fossa of the distal humerus. The brachialis muscle inserts at its anteroinferior surface, where it imparts a rough impression on the surface of the bone. The brachialis also inserts onto the ulnar tuberosity, which is slightly inferior to the coronoid

process. The ulnar collateral ligament attaches to the lateral surface of the coronoid process. The flexor digitorum sublimis originates from a small rounded eminence in the front aspect of the coronoid process. Behind this eminence is a depression for part of the origin of the flexor digitorum profundus. The pronator teres originates from a ridge that runs inferior to this eminence. Lateral to the coronoid process there is an articular depression called the radial notch that articulates with the radial head. It has prominent ridges that serve to attach the annular ligament. The semilunar notch articulates with the trochlea of the humerus. It is formed by the olecranon and the coronoid process. The notch is concave from top to bottom, forming an arc of approximately 190 degrees.13 Its medial half is slightly concave transversely, whereas the lateral half is slightly convex transversely in the superior half and slightly concave transversely in the inferior half. The proximal radius contributes less to the elbow than the ulna. Important structures in its proximal portion are the head, the neck, and the radial tuberosity. The radial head is round and smooth with a fovea at its most proximal end for articulation with the capitellum of the humerus. Medially, it articulates with the radial notch of the ulna. It has an articular surface over 280 degrees of its circumference.14 It is supported in place by the annular ligament. The radial neck is round and smooth. It is smaller in diameter than the radial head. The supinator inserts on its posterior surface. The radial tuberosity is inferior to the radial neck. This is where the biceps brachii inserts.

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Elbow Joint

Ligaments

The elbow joint is a hinge joint. It consists of three separate joints. These are the ulnotrochlear, radiocapitellar, and proximal radioulnar joints (see Fig. 10-6). All are synovial joints. A joint capsule surrounds these joints. Thickening of the capsule anteriorly, posteriorly, medially, and laterally forms the ligaments that stabilize and support the elbow joint. These ligaments are, respectively, called the anterior ligament, posterior ligament, ulnar collateral ligament, and radial collateral ligament. The synovial membrane is very extensive, extending from the articular surface of the humerus, the coronoid, and the radial and olecranon fossae. It is reflected over the deep surface of the capsule. It forms a pouch between the radial notch, the deep surface of the annular ligament, and the circumference of the head of the radius. Three focal areas of fat intervene between the capsule and synovial membrane. The first and most prominent of these, also known as the posterior fat pad, resides in the olecranon fossa. The second and third are found in the coronoid and radial fossae. These make up the anterior fat pad.6 The anterior fat pad is normally seen on a lateral projection, whereas the posterior fat pad is not usually seen unless displaced by fluid in the joint space.2

The ulnar collateral ligament, also known as the medial collateral ligament, is stronger and thicker than the radial collateral ligament. It is divided into anterior, transverse, and posterior bundles (Fig. 10-7). The anterior bundle extends from its apex at the anteroinferior aspect of the medial epicondyle to its fan-shaped base at the medial coronoid margin.15 It is the primary restraint to valgus stress.14 The posterior bundle also extends in a fan-like fashion from the posteroinferior aspect of the medial epicondyle to the medial olecranon. The transverse bundle extends from the coronoid process to the olecranon. It blends in with transverse fibers of the posterior longitudinal ligament. The ulnar collateral ligament is the primary stabilizer to valgus stress at the elbow.16 This tendon is closely associated with the common flexor tendon and ulnar nerve. Inflammation of the ulnar collateral ligament may also result in inflammation of these adjacent structures.17 The lateral collateral ligament is formed by the radial collateral ligament anteriorly and the lateral ulnar collateral ligament posteriorly (Fig. 10-8). The radial collateral ligament is variable and not well understood.8 It is less commonly injured than the ulnar collateral ligament.17 It extends from the lateral epicondyle to the annular

■ FIGURE 10-7 Schematic rendering of the medial aspect of the elbow illustrating the three components of the ulnar collateral ligament. AB, anterior bundle; PB, posterior bundle; TB, transverse bundle; AL, annular ligament.

■ FIGURE 10-8 Schematic rendering of the lateral aspect of the elbow illustrating the radial collateral ligament (RCL), annular ligament (AL), and lateral ulnar collateral ligament (LUCL).

CHAPTER

ligament. The annular ligament encircles the radial head and keeps it articulated at the proximal radioulnar joint. It attaches to the anterior and posterior margins of the radial notch of the ulna. The lateral ulnar collateral ligament provides ligamentous constraint to varus stress.18 The anterior ligament is a broad and thin fibrous covering of the anterior surface of the joint. It is attached to the anterior portion of the medial epicondyle, the anterior portion of the distal humerus, the anterior surface of the coronoid process of the ulna, and the annular ligament. Three sets of fibers comprise this ligament. The superficial fibers pass obliquely from the medial epicondyle of the humerus to the annular ligament. The middle fibers pass from the upper part of the coronoid depression and become partly blended with the superficial fibers. They insert mainly into the anterior surface of the coronoid process. The deep fibers intersect these at right angles. The anterior ligament contributes to varus-valgus stability when the elbow is extended.6 The posterior ligament is also thin and membranous. It consists of transverse and oblique fibers. It attaches to the humerus behind the capitellum and near the medial margin of the trochlea, to the margins of the olecranon fossa, and to the back of the lateral epicondyle. Below, it is fixed to the upper and lateral margins of the olecranon,

■ FIGURE 10-9 Schematic rendering of the anterior aspect of the elbow illustrating the biceps (BT) and brachialis (BrT) tendons, the lacertus fibrosus (LF), and the brachioradialis bursa (BRB).

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to the posterior part of the annular ligament, and to the ulna behind the radial notch. The transverse fibers of this ligament span across the olecranon fossa.

Muscles There are three arm muscles that influence elbow joint motion. Two of these are flexors in the anterior fascial compartment of the arm, and one is an extensor in the posterior fascial compartment. The most superficial muscle of the anterior arm compartment is the biceps brachii muscle (Fig. 10-9). The short head originates at the tip of the coracoid process of the scapula. The long head originates at the supraglenoid tubercle of the scapula proximally. Both fuse at the midlevel of the arm and insert on the tuberosity of the radius. The distal biceps tendon averages 7 cm in length and rotates laterally about 90 degrees before inserting on the radial tuberosity.8,19 The bicipitoradial bursa separates it from the anterior part of the tuberosity.8 It also attaches the fascia covering the forearm flexors via the bicipital aponeurosis. The biceps aponeurosis (lacertus fibrosus) (Fig. 10-10; see Fig. 10-9) is a membranous band that serves to protect underlying neurovascular structures in the cubital fossa and to lessen the burden on the radial tuberosity

■ FIGURE 10-10 Schematic rendering of the medial anterior of the elbow illustrating the common flexor tendon (CFT) and its components. BcM, biceps muscle; BRM, brachioradialis muscle; BT, biceps tendon; PT, pronator teres muscle; FCR, flexor carpi radialis muscle; LF, lacertus fibrosus; PL, palmaris longus muscle; FCU, flexor carpi ulnaris muscle.

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during flexion by dispersing some of the pressure to the fascia of the forearm. The biceps brachii is innervated by the musculocutaneous nerve, which includes some fibers from C5 and the majority from C6. The biceps brachii is the main flexor of the forearm when the elbow is extended. It is also a powerful supinator of the forearm when the forearm is flexed. It plays a very minor role in flexion of the pronated forearm. The brachialis muscle is deep to the biceps brachii (see Fig. 10-9). It originates from the anterior distal half of the humeral surface and inserts in the coronoid process and ulnar tuberosity. The brachialis muscle is the main flexor of the forearm. It maintains flexion for extended periods of time. The brachialis muscle is innervated by the musculocutaneous nerve, which includes some fibers from C5 and the majority from C6. The triceps brachii muscle (Fig. 10-11) is in the posterior fascial compartment of the arm and contains three parts. The long head originates from the infraglenoid tubercle of the scapula. The lateral head originates from the posterior surface of the humerus superior to the radial groove. The medial head originates from the posterior surface of the humerus but is inferior to the radial groove. All three heads insert into the proximal end of the olecranon process of the ulna and forearm fascia. It is the main extensor of the forearm. It is innervated by the radial nerve, which includes some fibers from C6 and the majority from C7 and C8.

■ FIGURE 10-11 Schematic rendering of the posterior aspect of the elbow illustrating the triceps tendon (TT).

The anconeus muscle is a small triangular muscle that blends in with the medial head of the triceps brachii. Thus, it is part of the posterior fascial compartment. It originates from the lateral epicondyle of the humerus and inserts into the lateral surface of the olecranon and superior part of the posterior surface of the ulna. Its functions include extension of the forearm and abduction of the ulna during pronation of the forearm. The anconeus derives its innervation from the radial nerve in equal distribution from C7, C8, and T1. The forearm muscles can be classified into two groups: the flexor/pronator group and the extensor/supinator group.20 The flexor/pronator group originates from the medial epicondyle of the humerus. This common origin is called the common flexor attachment (see Fig. 10-10). The muscles in this category belong to the superficial (pronator teres, flexor carpi radialis, palmaris longus and flexor carpi ulnaris) and intermediate (flexor digitorum superficialis) layers of the anterior compartment of the forearm. The deep layer (flexor digitorum profundus, flexor pollicis longus and pronator quadratus) originates distal to the elbow joint and is not discussed here. The pronator teres muscle is composed of a superficial portion that originates from the common flexor attachment and a deep portion that originates from the coronoid process of the ulna. Both portions join and insert on the middle of the lateral surface of the radius. The superficial portion is involved in flexion of the elbow joint. Both portions are involved in pronation of the forearm. This muscle is innervated by the median nerve with some fibers from C6 and the majority from C7. The flexor carpi radialis muscle is medial to the pronator teres. It originates from the common flexor attachment and inserts in the base of the second metacarpal bone. This muscle is innervated by the median nerve with some fibers from C6 and the majority from C7. Its primary function is hand flexion and abduction. It has no significant effect on elbow motion. The palmaris longus muscle is a variable muscle. It may be duplicated or even absent in 11% to 12% of patients.21 Left-sided absence predominates. When the muscle is present, it originates from the common flexor attachment and inserts in the distal half of the flexor retinaculum and palmar aponeurosis. It is innervated by the median nerve with fibers from C7 and C8. Its main function is hand flexion. It has no significant effect on elbow motion. The flexor carpi ulnaris muscle is composed of two heads. The humeral head originates from the common flexor attachment. The ulnar head originates from the olecranon and posterior border of the ulna. Both heads join distally and insert onto the pisiform, hook of hamate, and fifth metacarpal bones. The main function of this muscle is hand flexion and adduction. It has no significant effect on elbow motion. It is innervated by the ulnar nerve with some fibers from C7 and the majority from C8. The flexor digitorum superficialis is composed of two heads. The humeroulnar head originates from the common flexor attachment, ulnar collateral ligament, and coronoid process of the ulna. The radial head originates from the superior half of the anterior border of the radius. Both heads join distally and insert onto the bodies of the middle phalanges of the medial four digits. The function of this muscle is

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■ FIGURE 10-12 Schematic rendering of the posterior aspect of the elbow illustrating the common extensor tendon and its components. TT, triceps tendon; O, olecranon; AM, anconeus muscle; ECRL, extensor carpi radialis longus tendon; FCU, flexor carpi ulnari muscle; ED, extensor digitorum; ECU, extensor carpi ulnaris muscle.

■ FIGURE 10-13

primarily flexion of the middle phalanges, but it also plays a role in flexion of the proximal phalanges and the hand. It is innervated by the ulnar nerve with some fibers from C7 and T1 and the majority from C8. It is closely apposed to the anterior ligament of the ulnar collateral ligament.16 Four of the extensor/supinator group muscles originate from the lateral epicondyle of the humerus (Figs. 10-12 and 10-13). This common origin is called the common extensor attachment. These are the extensor carpi radialis brevis, extensor digitorum, extensor digiti minimi, and extensor carpi ulnaris. They are part of the superficial group of extensors in the posterior forearm compartment. The other muscles in this compartment, the brachioradialis and extensor carpi radialis longus muscles, originate slightly more superiorly from the lateral supracondylar ridge. The extensor carpi radialis brevis muscle originates from the common extensor attachment and inserts onto the base of the third metacarpal bone. It is innervated by the deep branch of the radial nerve, with the majority of fibers coming from C7 and some from C8. The main function of this muscle is extension and abduction of the hand. The extensor digitorum muscle originates from the common extensor attachment and inserts onto the extensor expansions of the medial four digits. Its main function

is extension of the medial four digits at the metacarpophalangeal and interphalangeal joints. It derives its innervation from the posterior interosseous nerve through some fibers from C8 but mostly fibers from C7. The digiti minimi muscle originates from the common extensor attachment and inserts onto the extensor expansion of the fifth digit. Its main function is extension of the fifth digit at the metacarpophalangeal and interphalangeal joints. It derives its innervation from the posterior interosseous nerve through some fibers from C8 and mostly C7. In some individuals, the extensor digiti minimi is not completely separated from the extensor digitorum.8 The extensor carpi ulnaris muscle originates from the common extensor attachment and inserts onto the base of the fifth metacarpal bone. Its main function is extension and adduction of the hand. It derives its innervation from the posterior interosseous nerve through some fibers from C8 but mostly fibers from C7. The brachioradialis muscle originates from the proximal two thirds of the lateral supracondylar ridge of the humerus and inserts onto the lateral surface of the distal end of the radius. Unlike the other muscles of the forearm, this muscle plays an important role in elbow joint mechanics. It functions to flex the forearm. It becomes the main

Schematic rendering of the posterior aspect of the elbow illustrating the common extensor tendon and the origin of its components in the distal humerus. BRM, brachioradialis muscle; ECRL, extensor carpi radialis longus tendon; ECRB, extensor carpi radialis brevis tendon; FDPM, flexor digitorum profundus muscle; SM, supinator muscle.

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flexor of the forearm in patients with denervation of the musculocutaneous nerve. This is because it derives its innervation from the radial nerve through some fibers from C5 and C7 but mostly fibers from C7. The extensor carpi radialis longus muscle originates from the lateral supracondylar ridge of the humerus and inserts onto the base of the second metacarpal bone. It is innervated by the radial nerve with fibers coming from C6 and C7. The main function of this muscle is extension and abduction of the hand.

Cubital Fossa The cubital fossa is a triangular space that is delineated by a line connecting the humeral epicondyles superiorly, the pronator teres medially, and the brachioradialis laterally. The brachialis and supinator muscles form the floor of the cubital fossa. Its roof is formed by the bicipital aponeurosis and the superficial and deep fascial layers. In this fossa run the brachial artery and veins and the median and radial nerves.

Neurovascular Structures The brachial artery has numerous branches in the arm, resulting in a rich collateral circulation around the elbow. Because of this, laceration or disruption of the brachial artery at the elbow often does not cause ischemia distally.6 The brachial artery is medial to the biceps brachii in the region of the elbow. Here, the median nerve can be seen coursing medial to it. Before reaching the cubital fossa, the brachial artery gives off two named branches to the elbow region: the superior and inferior ulnar collateral arteries. The superior ulnar collateral artery courses along with the ulnar nerve posterior to the medial epicondyle of the humerus. The inferior ulnar collateral artery courses more anteriorly. The lateral elbow receives blood supply from anterior and posterior branches of the profunda brachii artery. All these arteries anastomose at the elbow with the recurrent arteries from the ulnar, radial, and interosseous arteries, giving the elbow a rich redundant blood supply. At the level of the radial neck, the brachial artery divides under the bicipital aponeurosis into the radial and ulnar arteries. The radial artery is smaller than the ulnar artery. It emerges from under the bicipital aponeurosis between the pronator teres and the brachioradialis.6 The radial recurrent artery is the first to branch off after the origin of the radial artery. It ascends over the supinator to anastomose with the radial collateral artery. The radial artery continues in the forearm under the brachioradialis. The ulnar artery runs medially under the two heads of the pronator teres and travels in the forearm under the flexor digitorum profundus. It is accompanied by the ulnar nerve.6 The brachial artery is accompanied by two deep brachial veins. These are formed from the veins that follow the ulnar and radial arteries. The basilic, cephalic, and median cubital veins are superficial veins of the elbow. The first of these courses medially in the superficial fascia. The cephalic vein is lateral to the biceps brachii in the region of the elbow. Both of these veins communicate via the median cubital vein. This vein is superficial to the

bicipital aponeurosis and is often visible under the skin in the region of the cubital fossa. The median nerve initially runs lateral to the brachial artery in the arm (Fig. 10-14). Then, it passes anterior to the brachial artery at the midbrachium and runs medial to it in the cubital fossa.6 It courses under the bicipital aponeurosis and median cubital vein alongside the brachial artery. Here, an accessory bicipital aponeurosis may result in entrapment.8 The nerve enters the forearm between the two heads of the pronator teres muscle, which if hypertrophied may also cause entrapment.8 In addition to supplying most of the flexors in the forearm, it also sends articular branches to the elbow joint. The presence of a supracondylar spur in 1% of patients can be another source of compression for the median nerve.12 The ulnar nerve is posteromedial at the level of the elbow (Fig. 10-15). It courses along with the superior ulnar collateral artery posterior to the medial humeral epicondyle in the cubital tunnel, where it is well depicted on axial MRI.22 The roof of the cubital tunnel is formed by the deep fibers of the flexor carpi ulnaris aponeurosis distally and the cubital tunnel retinaculum proximally.23 The retinaculum is a thin fibrous structure that extends from the medial epicondyle to the olecranon.8 Anatomic variations of the cubital tunnel retinaculum may contribute to ulnar neuropathy.23 The retinaculum is absent in 10% of the population, allowing anterior dislocation of the nerve over the medial epicondyle during flexion.24 The floor of the cubital tunnel is formed from the capsule and the posterior and transverse portions of the ulnar collateral ligament. The ulnar nerve enters the forearm between the two heads of the flexor carpi ulnaris muscle. In addition to innervating some forearm muscles, it also sends articular branches to the elbow joint. The radial nerve spirals around the humeral shaft, sending branches to the triceps and anconeus (Fig. 10-16). It pierces the lateral intermuscular septum in the distal arm.6 The radial nerve courses between the brachialis and brachioradialis at the level of the elbow until it reaches the lateral humeral epicondyle. Here, it divides into deep and superficial branches. The deep branch continues deep to the supinator and supplies forearm extensors. Thickening of the arcade of Frohse along the proximal edge of the supinator muscle may cause compression of this nerve.8 The superficial branch is a sensory branch that continues superficial to the supinator and deep to the brachioradialis muscle. The lateral antebrachial cutaneous nerve is the continuation of the musculocutaneous nerve at the level of the elbow. It emerges between the biceps brachii and brachioradialis. It pierces the superficial fascia in the distal arm to become subcutaneous. It continues into the forearm to supply the lateral skin of the forearm. It can be injured in surgical approaches to the lateral forearm.6 The medial antebrachial cutaneous nerve accompanies the brachial vein in the arm. Distally it penetrates the fascia to become subcutaneous. It is anterior to the medial epicondyle, superficial and medial to the median nerve. In the proximal forearm, it gives off posterior sensory nerves that may be injured in elbow surgery.6 The posterior antebrachial cutaneous nerve branches from the radial nerve and becomes subcutaneous in the distal arm. It passes posterior to the lateral epicondyle and over the forearm extensors.

CHAPTER

■ FIGURE 10-14

Schematic rendering of the anterior aspect of the elbow illustrating the median nerve (MN). Note its distal course between the ulnar (PTuh) and humeral heads (PThh) of the pronator teres muscle. CFT, common flexor tendon; FDSM, flexor digitorum superficialis muscle.

■ FIGURE 10-15 Schematic rendering of the posterior aspect of the elbow illustrating the ulnar nerve (UN). Note its entrance into the cubital tunnel, under the flexor carpi ulnaris muscle (FCU).

Normal Ultrasonographic Anatomy Tendons and ligaments have an echogenic “snakeskin” appearance owing to the many echogenic interfaces between the collagen bundles that make up these structures. By placing the transducer longitudinally over the lateral aspect of the elbow, one can identify the radiocapitellar articulation, the radial collateral ligament, and the overlying thin long common extensor tendon (Fig. 10-17). The underlying bony anatomy can be used to help guide one to the correct location of the ligaments and tendons. Thus, when placing the transducer longitudinally over the medial aspect of the elbow to evaluate the medial collateral ligament and common flexor tendon, one should first look for the ulnohumeral articulation and the rounded appearance of the medial epicondyle and then it will be easy to identify the echogenic fan-shaped medial collateral ligament and the overlying short, broad common flexor tendon (Fig. 10-18). By sliding the transducer posterior to the medial epicondyle the ulnar nerve comes into view; this structure has a coarse echogenic appearance (Fig. 10-19). Rotating the transducer 90 degrees over the ulnar nerve will display the nerve in cross section as

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■ FIGURE 10-16

Schematic rendering of the anterior aspect of the elbow illustrating the radial nerve (RN). Note the distal course of the deep branch (RNdb) into the arcade of Frohse (AF) at the level of the supinator muscle (SM). RNsb, superficial branch of radial nerve.

a hypoechoic round structure surrounded by echogenic fat (Fig. 10-20). The triceps tendon is evaluated by placing the transducer longitudinally over the posterior aspect of the elbow and appears as a short, broad echogenic structure inserting on the echogenic cortex of the olecranon (Fig. 10-21). By flexing the elbow while scanning posteriorly, the olecranon will move distally and reveal the underlying olecranon fossa of the elbow, which can be assessed for effusion or loose bodies. The distal biceps tendon is evaluated by placing the transducer longitudinally over the antecubital fossa. The echogenic outline of the radial head, radial neck, and radial tuberosity should first be identified to help find the tendon. The tendon dives deep and therefore often appears hypoechoic, due to anisotropy. This can be compensated for by using compound imaging and by heeltoeing the transducer edge into the interosseous space of the forearm. The distal biceps tendon does not lie in a true sagittal plane, which is why its full longitudinal profile is often not well seen on sagittal MR images; by slightly rotating the transducer and maximally supinating the patient’s forearm, the full longitudinal profile can

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■ FIGURE 10-17

Normal lateral side of the elbow. A, Coronal T2-weighted MR image shows the radial head (RH), the lateral condyle (LC), the radial collateral ligament (white arrow), and the overlying thin long common extensor tendon (black arrows). The box delineates the field of view seen in the corresponding sonographic image. B, Longitudinal ultrasound of a different patient shows the outlines of the radial head (RH) and lateral condyle (LC). The echogenic radial collateral ligament is identified (white arrow). The common extensor mass (CEM) tapers to the common extensor tendon (small black arrows). This patient has a small focus of calcification at the insertion of the common extensor tendon (long black arrow).

■ FIGURE 10-18 Normal medial side of the elbow. A, Coronal T1-weighted MR sequence shows the coronoid process (C) and medial condyle (MC). The fan-shaped medial collateral ligament is identified (black arrows) as is the overlying common flexor mass (CFM) and the short broad common flexor tendon (white arrow). The box delineates the field of view seen in the corresponding sonographic image. B, Longitudinal ultrasound shows the echogenic outline of the coronoid process (C) and medial condyle (MC). The medial collateral ligament (black arrows), common flexor mass (CFM), and short broad common flexor tendon (white arrow) are identified.

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■ FIGURE 10-19

Normal ulnar nerve in profile. A, Sagittal T1-weighted MR image shows the medial condyle (MC) with the profile of the overlying ulnar nerve (white arrows). B, Longitudinal ultrasound shows the outline of the medial condyle (MC) and the coarse echogenic appearance of the ulnar nerve (black arrows).

■ FIGURE 10-20

Normal ulnar nerve in cross section. A, Axial T1-weighted MR image shows the low signal intensity ulnar nerve (arrow) surrounded by high signal intensity fat, located posterior to the medial condyle (MC). The box delineates the field of view seen in the corresponding sonographic image. B, Transverse sonographic image shows the hypoechoic ulnar nerve (arrow) surrounded by echogenic fat, located posterior to the outline of the medial condyle (MC).

be displayed sonographically (Fig. 10-22). An alternative method of scanning uses a more medial location of the transducer on the forearm with the beam angled laterally and obliquely25 (Fig. 10-23). Rotating the transducer 90 degrees will display the tendon insertion in cross section.

Ultrasonography is not as sensitive as MRI for epicondylitis.26 Because ultrasonography is more rapidly performed than MRI, it allows dynamic scanning such as for the evaluation of a subluxing ulnar nerve27 and the evaluation of ligamentous laxity during provocative stress maneuvers.28

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■ FIGURE 10-21 Normal triceps muscle and tendon. A, Sagittal T1-weighted MR image shows the triceps muscle (M) and its tendon (white arrows) inserting on the olecranon (O). Fat (F) is present in the olecranon fossa. The box delineates the field of view in the corresponding sonographic image. B, Longitudinal ultrasound shows the triceps muscle (M) and tendon (white arrows) inserting on the olecranon (O). Echogenic fat is present in the olecranon fossa (F).

■ FIGURE 10-22 Normal biceps tendon. A, Sagittal T1-weighted MR image shows the brachialis muscle (Br) and the overlying distal biceps tendon (arrows). Notice that the radius and actual insertion on the radial tuberosity are not in the plane of this standard sagittal image. B, Longitudinal ultrasound shows the biceps tendon (white arrows) inserting on the radial tuberosity (RT). The tendon is mildly hypoechoic due to anisotropy. The radial head (RH) and radial neck (RN) are also well seen.

CHAPTER

■ FIGURE 10-23 The alternative method of longitudinal scanning of the biceps shows only the outline of the radial tuberosity (RT) but shows the echogenic fibrillar appearance of the biceps tendon better than the conventional method (arrows) because of the ability to oblique the transducer and decrease the effects of anisotropy.

BASIC BIOMECHANICS The elbow is a complex joint that acts as a link between the shoulder and the hand, enhancing the flexibility of hand motion and transmitting generated forces.29 Approximately 150 degrees of forearm flexion occurs at the elbow when the ulna, trochlear, and radiocapitellar joints are acted on by the flexors in the arm. Ninety degrees of pronation/ supination occurs as the head of the radius rotates within

10

● Normal Elbow

the radial notch of the ulna. In full extension and supination, the forearm is angled slightly away from the long axis of the humerus. This angle is called the “carrying angle.” It is 10 to 20 degrees with no difference between the sexes.30 Because so many muscles originate or insert near the elbow, it is a common site for injury. The elbow is used in many different activities, such as throwing, tennis and golf swings, and volleyball, and therefore the majority of elbow complaints are related to sports. Although most elbow injuries are a result of repetitive use,31 traumatic injuries such as fractures are also common from falls in sports such as snowboarding. The elbow can also be affected by repetitive motions on the job and at home. Ensuing muscle weakness or ligament injury leads to abnormal forces on the elbow. Over time these abnormal forces can cause the articular cartilage of the elbow to wear out prematurely. Two situations briefly highlight this. Tennis elbow refers to a condition involving tenderness at the lateral epicondyle. It is due to repetitive or excessive wrist extension and forearm supination against resistance, causing damage to the common lateral forearm extensor tendon. The extensor carpi radialis brevis is the muscle most commonly involved.8,17 The condition becomes chronic with repeated damage to the tissues before sufficient healing can occur. It only rarely involves osseous changes.17 Tennis elbow is the most common source of elbow pain in the general population.32 Golfer’s elbow, a less common condition, refers to tenderness at the medial epicondyle. It is due to repetitive excessive stress to the common medial forearm flexor tendon seen with activities involving wrist flexion and pronation against resistance.8

TABLE 10-6 Table of Abbreviations AB AF AL AM BcM BM BRB BRM BrT BT C CET CFT CP ECRB ECRL ECU ED EM FCR FCU FDPM FDSM FM

Anterior bundle of ulnar collateral ligament Arcade of Frohse Annular ligament Anconeus muscle Biceps muscle Brachialis muscle Bicipitoradialis bursa Brachioradialis muscle Brachialis tendon Biceps tendon Capitellum Common extensor tendon Common flexor tendon Coronoid process Extensor carpi radialis brevis tendon Extensor carpi radialis longus tendon Extensor carpi ulnaris muscle Extensor digitorum muscle Extensor muscles Flexor carpi radialis muscle Flexor carpi ulnaris muscle Flexor digitorum profundus muscle Flexor digitorum superficialis muscle Flexor muscles

239

LF LUCL ME MN O PB PDC PL PT PThh PTuh R RCL RN RNdb RNsb SF SM ST T TB TT UCL UN

Lacertus fibrosus Lateral ulnar collateral ligament Medial epicondyle Median nerve Olecranon Posterior bundle of ulnar collateral ligament Pseudodefect of the capitellum Palmaris longus muscle Pronator teres muscle Pronator teres muscle humeral head Pronator teres muscle ulnar head Radius Radial collateral ligament Radial nerve Radial nerve deep branch Radial nerve superficial branch Synovial fold Supinator muscle Sublime tubercle Trochlea Transverse bundle of ulnar collateral ligament Triceps tendon Ulnar collateral ligament Ulnar nerve

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SUGGESTED READINGS Berquist T. Elbow and forearm. In Berquist T (ed). MRI of the Musculoskeletal System, 3rd ed. Philadelphia, Lippincott-Raven, 1996, pp 609–672. Finlay K, Ferri M, Friedman L. Ultrasound of the elbow. Skeletal Radiol 2004; 33:63–79.

Greenspan A. Upper limb II: Elbow. In Orthopedic Imaging, a Practical Approach, 4th ed. Philadelphia, Lippincott Williams & Wilkins, 2004, pp 135–145. Morrey BF. Anatomy of the elbow joint. In Morrey BF (ed). The Elbow and Its Disorders, 2nd ed. Philadelphia, WB Saunders, 1993, pp 16–52. Resnick D. Bone and Joint Imaging. Philadelphia, WB Saunders, 1996.

REFERENCES 1. Kerr R. Diagnostic imaging of upper extremity trauma. Radiol Clin North Am 1989; 27:891–908. 2. Singson RD, Feldman F, Rosenberg ZS. Elbow joint: assessment with double contrast CT arthrography. Radiology 1986; 160:167–173. 3. Greenspan A, Norman A. The radial head-capitellum view: useful technique in elbow trauma. AJR Am J Roentgenol 1982; 138:1186–1188. 4. Ferrara MA, Marcelis S. Ultrasound of the elbow. J Belge Radiol 1997; 8:122–123. 5. Angelo RL, Soffer SR. Elbow anatomy relative to arthroscopy. In Andrews JR, Soffer SR (eds). Elbow Arthroscopy. St. Louis, Mosby, 1994, pp 11–32. 6. Miyasaka KC. Anatomy of the elbow. Orthop Clin North Am 1999; 30:1–13 7. Mehne DK, Jupiter JB. Fractures of the distal humerus. In Browner BD, Jupiter JB, Levine AM, et al (eds). Skeletal Trauma. Philadelphia, WB Saunders, 1992, pp 1146–1176. 8. Fritz RC, Steinback LS, Tirman PF, Martinez S. MR imaging of the elbow: an update. Radiol Clin North Am 1997; 35:117–144. 9. Rosenberg ZS, Beltran J, Cheung YY. Pseudodefect of the capitellum: potential MR imaging pitfall. Radiology 1994; 191:821–822. 10. Steinberg BD, Plancher KD. Clinical anatomy of the wrist and elbow. Clin Sports Med 1995; 14:299–313. 11. Al-Naib I. Humeral supracondylar spur and Struthers’ ligament: a rare cause of neurovascular entrapment in the upper limb. Int Orthop 1994; 18:393–394. 12. Morrey BF. Nerve entrapment syndromes. In Spinner M, Linscheid RL (eds). The Elbow and Its Disorders, 2nd ed. Philadelphia, WB Saunders, 1993, pp 813–832. 13. Bass RL, Stern PJ. Elbow anatomy and surgical approaches. Hand Clin 1994; 10:343–356. 14. Morrey BF, An KN. Articular and ligamentous contributions to the stability of the elbow joint. Am J Sports Med 1983; 11:315–319. 15. O’Driscoll SW, Morrey BF, Jaloszynski R. Origin of the medial ulnar collateral ligament. J Hand Surg [Am] 1992; 17:164–168. 16. Munshi M, Pretterkleiber M, Chung C, et al: Anterior bundle of ulnar collateral ligament: evaluation of anatomic relationships by using MR imaging, MR arthrography, and gross anatomic and histologic analysis. Radiology 2004; 231:797–803.

17. Hornton MG, Timins ME. MR imaging of injuries to the small joints. Radiol Clin North Am 1997; 35:671–700. 18. O’Driscoll SW, Morrey BF, Korinek S, et al. Elbow subluxation and dislocation: a spectrum of instability. Clin Orthop 1992; 280:186–197. 19. Seiler JG, Parker LM, Chamberland PDC, et al. The distal biceps tendon: two potential mechanisms involved in its rupture: arterial supply and mechanical impingement. J Should Elbow Surg 1995; 4:149–156. 20. An KN, Hui FC, Morrey BF, et al. Muscles across the elbow joint: a biomechanical analysis. J Biomech 1981; 14:659–669. 21. Kaplan EB. Functional and Surgical Anatomy of the Hand. Philadelphia, JB Lippincott, 1953. 22. Rosenberg ZS, Beltran J, Cheung YY, et al. The elbow: MR features of nerve disorders. Radiology 1993; 188:235–240. 23. O’Driscoll SW, Horii E, Carmichael SW, et al. The cubital tunnel and ulnar neuropathy. J Bone Joint Surg Br 1991; 73:613–617. 24. Morrey BF. Applied anatomy and biomechanics of the elbow joint. Instr Course Lect 1986; 35:59–68. 25. Giuffre BM, Lisle DA. Tear of the distal biceps branchii tendon: a new method of ultrasound evaluation. Australas Radiol 2005; 49:404–406. 26. Miller TT, Shapiro MA, Schultz E, Kalish PE. Comparison of sonography and MRI for diagnosing epicondylitis. J Clin Ultrasound 2002; 30:193–202. 27. Jacobson JA, Jebson PJ, Jeffers AW, et al. Ulnar nerve dislocation and snapping triceps syndrome: diagnosis with dynamic sonography—report of three cases. Radiology 2001; 220:601–605. 28. Nazarian LN, McShane JM, Ciccotti MG, et al. Dynamic US of the anterior band of the ulnar collateral ligament of the elbow in asymptomatic major league baseball pitchers. Radiology 2003; 227:149–154. 29. Larson S. Phylogeny: the elbow and its disorders. In Morrey BF. Phylogeny, 2nd ed. Philadelphia, WB Saunders, 1993, p 6. 30. Beals RK. The normal carrying angle of the elbow: radiographic study of 422 patients. Clin Orthop Relat Res 1976; 119:194–196. 31. Field LD, Altchek DW. Elbow injuries. Clin Sports Med 1995; 14:59–78. 32. Schenk M, Dalinka MK. Imaging of the elbow. Orthop Clin North Am 1997; 28:517–535.

C H A P T E R

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C H A P T E R

Acute Osseous Injury of the Elbow and Forearm Steven Shankman and Brandon Liu

ANATOMY (INCLUDING GROSS ANATOMY AND NORMAL VARIANTS) Fat Pads The anterior fat pad is anterior to the olecranon fossa and is routinely seen on the normal lateral view, extending inferior, from the anterior humeral cortex, obliquely.1 The posterior fat pad lies in the olecranon fossa and is not visible on the normal lateral view (Fig. 11-1).1 Both fat pads are within the joint, intra-articular, extrasynovial, and therefore sensitive to any space-occupying lesion. Fluid, blood, or mass will displace the anterior fat pad superiorly and the posterior fat pad posteriorly. The anterior fat pad is displaced with small volumes of fluid that would not displace the posterior fat pad and, therefore, is more sensitive to an intra-articular pathologic process (Figs. 11-2 and 11-3).1 Very large effusions may obliterate the anterior fat pad, in which case the displacement of the posterior fat pad is more sensitive.1

MANIFESTATIONS OF THE DISEASE Radiography Imaging Techniques The routine radiographic examination of the elbow consists of anteroposterior and lateral views. The anteroposterior view is obtained with the forearm in supination and the elbow fully extended. The lateral view is obtained with the forearm in neutral position, midway between supination and pronation, and the elbow flexed 90 degrees. On the routine lateral view, three cortical arcs can be appreciated representing the capitellum and lateral and medial trochlea ridge. Anteroposterior internal and external oblique views may also be obtained in a search for occult fracture. The radiocapitellum view is a lateral view obtained by angling the x-ray tube 45 degrees cephalad. This projects the radiocapitellum joint compartment superior to the ulna-trochlea compartment, negating the superimposition of these anatomic structures.

Normal Variants The supracondylar spur, a normal variant seen in approximately 1% of the population, may be seen on the lateral view.2 Unlike an exostosis, it does not point away from the joint. This may be associated with compressive neuropathy.2 Often there is a projection or bony flange at the lateral aspect of the supracondylar humerus, which should not be confused with periosteal reaction. The radial tuberosity often appears as a relative area of radiolucency when seen en face on the lateral view. When the tuberosity is prominent, this radiolucency should not be confused with a true lytic lesion. The inferior aspect of the olecranon apophysis and the far medial and lateral aspect of the distal humeral epiphysis or condyles do not always unite with skeletal maturity and should not be confused with fracture.

KEY POINTS In the setting of recent trauma, elevated fat pads indicate fracture until proven otherwise. Additional views or MRI may be necessary to demonstrate the fracture. ■ Comminuted radial head fracture may be associated with dislocation at the distal radioulnar joint. Views of the wrist are necessary. ■ Coronoid fractures, which are difficult to detect, may appear isolated but are a clue to spontaneously reduced elbow dislocation. ■ A bone fragment above the radial head on the lateral view may indicate a fractured capitellum. ■ An isolated fracture of the ulna, with displacement and/ or angulation, indicates dislocation of the radial head. ■

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■ FIGURE 11-1 A and B, Anteroposterior and lateral radiographs of the elbow show normal anterior fat pad.

■ FIGURE 11-2 The fat pads of the elbow without (A) and with (B) joint distention. (Redrawn from Murphy W, Siegel MJ. Elbow fat pads with new signs and extended differential diagnosis. Radiology 1977; 124:659–665.)

■ FIGURE 11-3 Lateral radiograph of the elbow reveals displacement of both anterior and posterior fat pads.

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Imaging Findings Radial Head/Neck The most common elbow fracture in the adult involves the radial head and neck, accounting for about 50% of all such injuries.3 Most occur in young adults, are nondisplaced, and result from a fall on the outstretched hand. The Mason classification describes three types (Fig. 11-4).4 Type I fractures are nondisplaced and may be difficult to visualize with radiographic examination. The

■ FIGURE 11-4 Mason classification of radial head/neck fractures.

■ FIGURE 11-5 A and B, Anteroposterior and lateral radiographs of the elbow reveal displacement of the anterior and posterior fat pads, with cortical step-off at the lateral aspect of the head/neck junction: Mason type I fracture.

243

radiographic appearances include vertical lucency, cortical disruption, cortical step-off or abrupt angulation, and double cortical line (Fig. 11-5).3 Type II consists of a displaced split fragment. Type III is a comminuted fracture. A fourth type has an associated elbow dislocation. Complex fractures of the radial head and neck are those associated with other injuries (Fig. 11-6). Markedly comminuted radial head fractures may be associated with subluxation or proximal migration at the distal radioulnar joint.5 This combination of injuries is referred to as the Essex-Lopresti fracture, named after its first descriptor.

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■ FIGURE 11-6

A and B, Anteroposterior and lateral radiographs of the elbow reveal a complex fracture with comminution of the radial head and proximal ulna with diastasis.

Radiographic examination of the wrist is essential in such situations.3 Other associated injuries include proximal ulna fracture, capitellum fracture, and elbow dislocation.2

Olecranon The second most common elbow fracture in the adult involves the olecranon, accounting for about 20% of all such injuries.2 Most occur in older adults, are transverse fractures with diastasis, and result from either a fall on the outstretched hand with the elbow flexed or direct trauma.4 The transverse fracture at the trochlear notch extends obliquely to the posterior cortex. Triceps retraction results in diastasis. Comminuted fractures result from direct trauma. Oblique fractures, relative to the long axis of the ulna, may be nondisplaced and difficult to see radiographically.3 The Mayo classification system (Fig. 11-7) for olecranon fractures addresses issues of comminution, displacement, stability, treatment, and prognosis.3 Type I, or nondisplaced, fractures account for 5% of olecranon fractures (Fig. 11-8). Displaced fractures with an intact anterior bundle of the medial collateral ligament (type II) are stable and account for 85% of olecranon fractures (Fig. 11-9). Type III, or displaced, unstable fractures are usually comminuted and associated with radial head fracture (Fig. 11-10).

Dislocation The third most common adult elbow injury is dislocation, accounting for about 15% of acute adult elbow trauma.3 The elbow is, in fact, the third most common site of dislocation in the adult. Dislocations of the shoulder and of the interphalangeal joints of the hand are more common. Most elbow dislocations occur in young adults, are posterior or

■ FIGURE 11-7

The Mayo classification system for olecranon fractures.

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245

■ FIGURE 11-8 A and B, Anteroposterior and lateral radiographs of the elbow reveal linear lucency at the posterior aspect of the olecranon, with displacement of the anterior and posterior fat pads. There is no comminution or displacement: Mayo type I fracture.

■ FIGURE 11-9 A lateral radiograph of the elbow reveals displacement of the anterior fat pad, with a transverse fracture through the olecranon, with diastasis: Mayo type II fracture.

posterolateral, and result from a fall on the outstretched hand with the elbow hyperextended. The classification of elbow dislocations refers to the direction of displacement (Fig. 11-11). Most (85% to 90%) are posterior or posterolateral (Fig. 11-12). The remaining types are equally unusual: anterior, lateral, medial, or posteromedial. The divergent type, whereby the radius and ulna dislocate, is extremely rare. Posterior elbow dislocation proceeds through four stages, as described by O’Driscoll. Stage I occurs when there is disruption of the ulnar band of the lateral collateral ligament that allows for posterolateral rotatory subluxation, which may reduce spontaneously.6 Disruption anteriorly and posteriorly with partial dislocation constitutes stage II, with the medial ulna perched on the trochlea.6 In stage IIIA there is complete dislocation with all the soft tissues disrupted except the anterior bundle of the medial collateral ligament.6 If the entire medial collateral ligament is injured, varus and valgus instability are present after reduction.7 About 25% of elbow dislocations are associated with fracture, mostly radial head and neck fractures. Coronoid

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■ FIGURE 11-10 A and B, Anteroposterior and lateral radiographs of the elbow reveal comminuted fracture of the olecranon, with diastasis of a proximal fragment: Mayo type III fracture.

fractures are common, resulting from trochlear impaction during posterior dislocation/relocation (Fig. 11-13). Isolated coronoid fractures should always suggest previous dislocation.7 Such fractures may result in joint body and joint incongruity.

Coronoid Process Fractures of the coronoid process are almost always secondary to impaction with the trochlea, occurring in 33% of patients after elbow dislocation.8 Coronoid fractures may result from brachialis avulsion. These fractures are often difficult to visualize, owing to the superimposition of bony structures. Oblique views are often necessary. The classification system of Reagan and Morrey is based on the degree of coronoid involvement and resulting instability (Fig. 11-14).8 Type I fractures are frequently associated with elbow dislocation. Type II fractures involve less than half of the coronoid process and have varying degrees of stability. Type III fractures involve greater than 50% of the coronoid and are almost always unstable. Type I and type II fractures may be comminuted or noncomminuted.

Distal Humerus

■ FIGURE 11-11 Patterns of elbow dislocation. (Redrawn from Jupiter JB. Part 1. Trauma to the adult elbow and fractures of the distal humerus. In Browner BD, Jupiter JB, Levine AM, et al [eds]. Skeletal Trauma. Philadelphia, WB Saunders, 1992, p 1142.)

Intracapsular fractures of the adult distal humerus may or may not involve the articular surface. Most occur in the elderly. Transcondylar fractures traverse both condyles in a horizontal direction and do not involve the articular surface.2 There are extension and flexion types.2 Most fractures of the adult distal humerus involve the articular surface. These are intercondylar fractures and are T or Y shaped.2 They result from direct impact with the elbow flexed.2 The ulna-trochlea ridge splits the humeral

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■ FIGURE 11-12

A and B, Anteroposterior and lateral radiographs of the elbow show posterior elbow dislocation with no associated fracture.

■ FIGURE 11-13 A and B, Anteroposterior and lateral radiographs of the elbow reveal posterior dislocation with fracture of the coronoid process and radial head.

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■ FIGURE 11-14 fractures.

Reagan and Morrey classification of coronoid

trochlea groove, resulting in a vertical fracture extending proximally and dividing horizontally or obliquely separating the condyles. These fractures, in turn, may rotate and displace, owing to their respective muscle attachments. Marked comminution is common. Fractures of the medial and lateral condyles are unusual. A direct blow to the flexed elbow with an angular component may separate either condyle.4 Stable fractures are those that do not involve the lateral surface of the trochlea, thereby maintaining the integrity of the trochlea-ulna articulation. Therefore, lateral condylar fractures are stable if they do not extend medial to the capitotrochlear sulcus.9 Medial condylar fractures are stable if they do not extend lateral to the trochlear groove.10 Riseborough and Radin’s classification categorizes distal humeral fractures into four types based on displacement, comminution, and the presence or absence of rotation of either the trochlea or capitellum (Fig. 11-15).11 Type I describes no displacement of fragments. Type II is a T-shaped intercondylar fracture with the trochlear and

■ FIGURE 11-16

Muller classification of distal humeral fractures.

capitellar fragments separated but not appreciably rotated in the frontal plane. Type III is a T-shaped intercondylar fracture with separation of the fragments and significant rotatory deformity. Type IV is a T-shaped intercondylar fracture with severe comminution of the articular surface and wide separation of the humeral condyles. Muller and associates developed a more comprehensive classification that divides fractures of the distal humerus into nonarticular type A fractures, partial articular type B fractures, and total articular type C fractures (Fig. 11-16).3 All of these are subdivided into 3 subtypes, which are again divided into 3 subtypes, making 27 different subtypes of distal humeral fractures (Figs. 11-17 and 11-18).12

■ FIGURE 11-15 Riseborough and Radin classification of distal humerus fractures.

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■ FIGURE 11-17 A and B, Anteroposterior and lateral radiographs of the elbow reveal a minimally displaced transcondylar fracture: Muller type A2.

■ FIGURE 11-18

A and B, Anteroposterior and lateral radiographs of the elbow reveal an impacted, intercondylar fracture of the distal humerus: Muller type C.

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Milch contributed by describing condylar fractures into two types: type I is a simple compression fracture of either condyle, with upward displacement of the fractured fragment following a transverse or longitudinal force directed against the fractured condyle; type II is a fracture-dislocation of either condyle with upward displacement of the affected condyle and dislocation of the forearm toward the side of the fracture when the outer wall of the trochlea is disrupted (Fig. 11-19).10 Of importance is the integrity of the lateral wall of the trochlea.9

Capitellum Fractures of the capitellum are rare, resulting from shearing forces transmitted by the radial head after a fall on the outstretched hand. The fragment is displaced proximally and is seen above the radial head and coronoid process on the lateral view. It is typically rotated 90 degrees, with the convex articular surface facing ventral. It is difficult to appreciate on the anteroposterior view where a poorly defined articular cortex may be the only clue. At times, the superimposition of the fracture fragment will be evident. When the capitellum fracture is associated with radial head fracture, the capitellar fragment is usually smaller. When the fracture is comminuted, the radial head fragments rarely migrate proximally, above the radial head and coronoid process. Therefore, the capitellar fracture fragment should not be confused with a radial head fragment in the setting of a comminuted radial head fracture. Type I (Hahn-Steinthal) fractures have a large osseous component, with the fracture hinging anteriorly between the radial head and the radial fossa, limiting the range of motion (Figs. 11-20 and 11-21).3 Type II (Kocher-Lorenz)

■ FIGURE 11-19 Milch classification of abduction lateral condylar fractures. Note that the lateral ridge of the trochlea is intact in the type I fracture but is disrupted in the type II fracture-dislocation.

■ FIGURE 11-20

Fracture of capitellum, types I and II.

fractures are sleeve fractures of the articular surface with little osseous component.3

Monteggia Lesion In 1814, Giovanni Battista Monteggia described “a traumatic lesion distinguished by a fracture of the proximal third of the ulna and an anterior dislocation of the proximal epiphysis of the radius.” In 1967, Bado coined the term Monteggia lesion, which also includes fractures at the mid and distal ulna and all directions of radial dislocation (Fig. 11-22).13 Eighty-nine percent of such fractures occur at the proximal third, 10% at the middle third, and 1% at the distal third.3 The four main types refer to the shared angulation of the ulna fracture apex and the direction of the dislocation.13 In all cases, the proximal radioulnar joint is disrupted with injury to the orbicular and annular ligaments. This distinguishes such lesions from anterior elbow dislocation with olecranon fracture. Here, there is dislocation of the radius and most of the distal ulna connected proximally by an intact proximal radioulnar joint. These injuries usually occur in young adults secondary to direct trauma or fall on the outstretched hand with the elbow flexed and the forearm pronated. The most common type, type I, involves anterior angulation of the ulnar fracture apex and anterior dislocation of the radius, the lesion originally described by Monteggia, comprising 65% of the cases.3 Type II, 18% of cases, involves the opposite, posterior fracture angulation and dislocation (Fig. 11-23). Type III is unique to the pediatric population, with fracture of the ulnar metaphysis with lateral or anterolateral dislocation of the radial head. Type IV is rare and is characterized by fracture at the proximal radius at the same level along with the ulna.

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251

■ FIGURE 11-21

A and B, Anteroposterior and lateral radiographs of the elbow reveal a type I fracture of the capitellum.

■ FIGURE 11-22 Bado classification of Monteggia fracture-dislocations.

Radiographic diagnosis is dependent on recognizing the radial head dislocation that may be overshadowed by the more obvious ulna fracture. As stated previously, a line bisecting the proximal radial shaft (the radiocapitellar line) will pass through the capitellum on any view. Proximal ulna fractures may complicate matters when forearm films are ordered and the elbow is barely included in the field of view. Any angulated fracture of the radius or ulna must be accompanied by fracture or dislocation of the other. When there is an angulated fracture of the ulna, there must be a concomitant fracture of the radius or dislocation, almost always, at the elbow. Isolated fracture of the ulna, the nightstick fracture, is

more common at the distal shaft. They are neither displaced nor angulated.

Chronic Injury Chronic injury to the elbow may be sports related or occupational. Different types of stress on the athletic elbow have been described. Diffuse generalized stress may result in cortical thickening and premature osteoarthritis.2 Bony hypertrophy and irritation of the synovium may result in synovial metaplasia and incongruity of the articulation. Subsequent joint bodies may block full extension and flexion.

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■ FIGURE 11-23

A and B, Anteroposterior and lateral radiographs of the elbow reveal fracture of the proximal ulna with anterior angulation and posteromedial dislocation of the radial head: Monteggia type II lesion.

Rotational forces on the humeral shaft may lead to spiral fractures in the less-seasoned athlete before the development of cortical thickening.2 Valgus strain results in medial tension stress whereby increased pull of the ulnar collateral ligament at the coronoid process leads to traction spur formation. Compressive forces are generated at the lateral joint compartment where chronic osteochondral fracture of the capitellum, osteochondritis dissecans, may develop.2 These injuries usually occur in the adolescent athlete. Panner disease, on the other hand, is a capitellar osteochondrosis. Although the radiographic findings are similar, this is a self-limited disorder of young children, 4 to 8 years of age, that resolves with rest.2 Abrupt, excessive, repetitive elbow extension creates extension stress. Traction of the triceps muscle at the olecranon may result in traction spurs, stress, or avulsion fracture. Traction of the biceps tendon at the bicipital tuberosity may result in hypertrophy, spurring, and cubital bursitis. A rapidly induced, eccentrically applied load to such an elbow in the flexed position may result in tendon avulsion. Biceps tendon avulsion at the bicipital tuberosity is much more common than injury at the musculotendinous junction or the tendon itself. Post-traumatic myositis ossificans usually results from a direct blow to the involved soft tissues.2 About 3 to 4 weeks after the injury, wispy soft tissue calcification and periosteal reaction may be seen on conventional radiographs and should not be mistaken for malignancy. In the following weeks, the lesion will mature with organized

new bone formation, progressing from the periphery toward the center.

Magnetic Resonance Imaging Imaging Techniques Magnetic resonance examination best depicts occult fracture, bone contusion, and ligament and tendon injury.

Multidetector Computed Tomography Imaging Techniques Multidetector computed tomography best depicts calcified structures, including cortical and trabecular bone and joint bodies. This capacity is more recently enhanced with helical and multirow detector technology, allowing for higher-quality multiplanar reformats and three-dimensional volume renderings that are useful for demonstrating complex fracture morphology. The search for joint bodies and the origin of certain fracture fragments is also made easier.

SYNOPSIS OF TREATMENT OPTIONS Medical Radial Head and Neck Fracture ●

Mason type I: nondisplaced fracture requires conservative management consisting of brief period of splinting followed by early mobilization.4

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Mason type II: displaced fracture of at least 2 mm may be treated conservatively4 or by open reduction and internal fixation, including possible excision of fracture fragment or, less commonly, the radial head.3 Mason type III: comminuted fracture involving the entire head requires radial head excision. Essex-Lopresti lesions require surgical management.4

Distal Humeral Fracture ●

●

Olecranon Fracture ● ●

●

Nondisplaced fractures are managed conservatively. Displaced fractures with an intact anterior bundle of the medial collateral ligament are treated with open reduction and internal fixation or by excision with triceps reinsertion.4 Displaced, unstable fractures are usually comminuted and associated with radial head fracture. Rigid fixation is required to stabilize the joint.

●

●

Most elbow dislocations are treated conservatively with splint, cast, or brace application. Surgical intervention is rarely indicated and usually only if there are associated fractures.

●

Coronoid Fracture ●

● ●

Reagan and Morrey type I fracture is frequently associated with elbow dislocation and is treated as such. Reagan and Morrey type II fracture may have varying degrees of instability, and, therefore, treatment varies. Reagan and Morrey type III fracture is almost always unstable and requires external fixation.8

The management is complex. Factors to take into consideration include the location of the horizontal fracture plane, the presence of separate fractures of the epicondyles, and comminution between the trochlear and capitellar fragments.4 The majority of cases are best treated with open reduction and internal fixation.14 Conservative management may be indicated with nondisplaced single fractures of the humeral condyle.4 Other indications include supracondylar fractures that are minimally displaced, comminution or osteopenia for which successful internal fixation and early range of motion is not possible, and when a major surgical approach is not feasible.4

Capitellum Fracture

Elbow Dislocation ●

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Nondisplaced capitellar fracture requires conservative management with splinting for several weeks.4 Displaced capitellar fractures may be treated with closed reduction.4 Open reduction and internal fixation is applicable to type I fractures in which the fragment is large. Excision of the fractured fragment is another viable option with good results.4 Type II fractures often require excision when there is inadequate subchondral bone to act as support for internal fixation.

Monteggia Lesion ●

The recommended treatment for Monteggia lesions is open reduction and internal fixation of the ulna fracture and closed or open reduction of the radial head fracture.3 Comminuted fractures are best treated with bone grafting.4

SUGGESTED READINGS Kuntz DG Jr, Baratz ME. Fractures of the elbow. Orthop Clin North Am 1999; 30:37–61. Rettig AC. Traumatic elbow injuries in the athlete. Orthop Clin North Am 2002; 33:509–522. Ring D, Jupiter JB. Fracture-dislocation of the elbow. Hand Clin 2002; 18:55–63.

Sofka CM. Imaging of elbow injuries in the child and adult athlete. Radiol Clin North Am 2002; 40:251–265. Watson JT. Fractures of the forearm and elbow. Clin Sports Med 1990; 9:59–83.

REFERENCES 1. Murphy W, Siegel MJ: Elbow fat pads with new signs and extended differential diagnosis. Radiology 1977; 124:659–665. 2. Resnick D. Bone and Joint Imaging. Philadelphia, WB Saunders, 1996. 3. Rogers LF. Radiology of Skeletal Trauma, 3rd ed. New York, Churchill Livingstone, 2002. 4. Spivak JM, DiCesare PE, Feldman DS, et al. Orthopaedics, A Study Guide. New York, McGraw-Hill, 1999. 5. Essex-Lopresti P. Fractures of the radial head with distal radioulnar dislocation. J Bone Joint Surg Br 1951; 33:244–247. 6. O’Driscoll SW, Morrey BF, Korinek S, An KN. Elbow subluxation and dislocation: a spectrum of instability. Clin Orthop Relat Res 1992; 280:186–197. 7. Pacelli LL, Guzman M, Botte MJ. Elbow instability: the orthopedic approach. Semin Musculoskelet Radiol 2005; 9:56–66.

8. Regan W, Morrey B. Fractures of the coronoid process of the ulna. J Bone Joint Surg Am 1989; 71:1348–1354. 9. Milch H. Fractures and fracture dislocations of the humeral condyles. J Trauma 1964; 15:592–607. 10. Milch H. Fractures of the external humeral condyle. JAMA 1956; 160:641–646. 11. Riseborough EJ, Radin EL. Intercondylar T fractures of the humerus in the adult. J Bone Joint Surg Am 1969; 51:130–141. 12. Miller WE. Comminuted fractures of the distal end of the humerus in the adult. J Bone Joint Surg Am 1964; 46:644–657. 13. Bado LJ. The Monteggia lesion. Clin Orthop 1967; 50:71–86. 14. Bickel WE, Perry RE. Comminuted fractures of the distal humerus. JAMA 1963; 184:553–557.

12

C H A PP T T EE RR

Soft Tissue Injury to the Elbow Jenny T. Bencardino and Javier Beltran

PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS Myotendinous Injury Traumatic injury to the myotendinous structures of the elbow may result from acute trauma or repetitive microtrauma. Furthermore, acute trauma is frequently superimposed on tendinopathy or other chronic injuries. MRI can be highly valuable in the assessment of elbow pain, owing to its super soft tissue resolution. Even in those patients with clear clinical diagnosis of myotendinous pathology, MRI can better establish the severity of injury as well as the presence of associated conditions. Three stages of myotendinous injury have been defined based on pathologic changes. Acute injury is typically characterized by disruption of the muscle fibers and bleeding at the myotendinous junction or tendinous avulsion from the osseous attachment. In the setting of recurrent injury, microtearing of the tendinous fibers and/or myotendinous junction may result in scarring with decreased flexibility of the tendon, making it susceptible to reinjury. Chronic injury, or tendinosis, is defined as progressive myotendinous mucoid degeneration and angiofibrotic hyperplasia.

Lateral Epicondylitis Lateral epicondylitis is an overuse injury involving the extensor/supinator muscles that originate on the lateral epicondylar region of the humerus (Fig. 12-1). It is the most commonly encountered sports-related injury to the elbow. The condition is highly prevalent among tennis players, hence the term “tennis elbow.”1 The risk of overuse injury is increased two to three times in players with more than 2 hours of play per week and two to four times in players older than age 40 years.2 Although originally described in a tennis player, lateral epicondylitis is not limited to tennis players, and it is commonly seen in the general population as a result of repetitive work-related activities.3,4 254

Medial Epicondylitis Medial epicondylitis is defined as a flexor pronator tendinopathy at its origin from the medial epicondyle. The tendon origins of the flexor carpi radialis muscle and pronator teres muscle are more commonly involved.5 Medial epicondylitis is similar to the more common lateral epicondylitis in many respects. Both conditions are overuse tendinopathies that can be associated with racquet sports. Sports activities that involve repetitive valgus and flexion stress at the elbow such as golfing, bowling, arching, weightlifting, and throwing sports have been associated with medial epicondylitis.6 Some authors have considered Little Leaguer’s elbow a variant of medial epicondylitis. This condition, however, is a traction apophysitis of the medial epicondyle, which requires a different treatment course.

KEY POINTS Lateral epicondylitis is the most commonly encountered sports-related injury at the elbow. ■ The extensor carpi radialis brevis is the most commonly affected tendon in lateral epicondylitis. ■ Medial epicondylitis is much less common than lateral epicondylitis. ■ Medial epicondylitis and ulnar neuritis often present together. ■ A torn bicipital aponeurosis may allow retraction of the distal biceps tendon into the arm. ■ Triceps tendon injury is very rare. ■ MRI has proven to be useful for differentiating partial versus complete biceps and triceps tendon rupture. ■ Ulnar collateral complex injuries are often seen in association with elbow dislocation. ■ Posterolateral rotatory instability is often secondary to proximal tear of the radial collateral ligament and lateral ulnar collateral ligament. ■

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■ FIGURE 12-1

Common extensor tendinosis. Coronal STIR MR image demonstrates thickening and increased intrasubstance signal affecting the common extensor tendon at its origin from the lateral epicondyle (arrow).

Medial epicondylitis is much less common than lateral epicondylitis, accounting for only 10% to 20% of all epicondylitis diagnoses. Medial epicondylitis is often found in the dominant elbow of a golfer.7 Tennis players who hit their forehand with heavy topspin are also at increased risk for developing medial epicondylitis. On the other hand, the annual incidence estimate of medial epicondylitis among workers was 1.5% in a recent study. The association of forceful work and the presence of other work-related upper limb musculoskeletal disorders with medial epicondylitis was found to be statistically significant.8 In this same study, repetitive work was not found to be a risk factor. Acute rupture of the flexor pronator myotendinous unit can occur in association with ulnar collateral injuries particularly after trauma during forceful extension of the elbow and pronation of the forearm by the throwing athlete9 (Fig. 12-2).

Biceps Tendon Injuries Distal biceps tendon injuries most frequently affect the dominant extremity of middle-aged men. The spectrum of biceps tendon injury ranges from tendinosis to partial and complete tears. The vast majority of cases is the result of acute injury and often involves complete rupture. Distal rupture of the biceps tendon is at least 10 times less common than rupture of the proximal long head of the biceps tendon.10–12

Triceps Tendon Injuries Triceps tendon rupture is a rather uncommon entity. Acute posterior elbow pain after a single traumatic episode is

■ FIGURE 12-2

Common flexor tendon avulsion. Coronal STIR MR image demonstrates avulsion of the common flexor tendon (arrows) associated with a high-grade partial tear of the ulnar collateral ligament anterior band (arrowhead).

most often related to avulsion of the triceps tendon at or adjacent to its insertion on the olecranon.10,13 Triceps tendinosis as well as partial intrasubstance, myotendinous, and intramuscular tears may occur, although rarely.14–16 Although triceps tendon avulsion may affect both males and females in a wide range of age presentation, it is most common in weightlifters, bowlers, baseball pitchers, and football players. Disruption occurs at the site of distal attachment of the triceps tendon onto the olecranon process. Predisposing conditions for triceps tendon avulsion include hyperparathyroidism, chronic renal failure, diabetes mellitus, corticosteroid use, cortisone injections, total elbow arthroplasty, olecranon bursitis, subluxation of the ulnar nerve, and radial head fracture.17 Another cause of posterior elbow pain has been referred to as the snapping triceps syndrome. This relates to transient subluxation of the medial head of the triceps over the medial epicondyle during elbow flexion.18 Several etiologic factors have been implicated and may include congenital, developmental, and post-traumatic causes. It has also been described in weightlifters in relation to triceps muscle hypertrophy.19 This condition often coexists with ulnar nerve dislocation.

Ligamentous Injuries and Elbow Instability The elbow joint has three primary stabilizing mechanisms, including (1) the ulnohumeral articulation, which provides 33% of valgus stability; (2) the anterior bundle

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of the ulnar collateral ligament, which provides 54% of valgus stability; and (3) the ulnar band of the radial collateral ligament.20 Clinical experience suggests that greater than 50% integrity of the coronoid process of the ulna is required for elbow stability with or without ligamentous integrity. Also, greater than 30% of the articular surface of the olecranon is needed for stability. The secondary stabilizers include the radiohumeral articulation, the joint capsule, and the elbow musculature.

Ulnar Collateral Ligament Complex Injury to the ulnar collateral ligament complex occurs in overhead throwing athletes as a result of chronic repetitive valgus stress or, less frequently, acute trauma.21 The former may be an isolated finding or seen as a component of the so-called valgus extension overload syndrome. The latter can result from falling on an outstretched arm or may be secondary to posterior dislocation of the elbow. When injured as a result of repetitive microtrauma, such as seen in the overhead athlete, the anterior oblique ligament is usually injured in its mid substance (Fig. 12-3). In the setting of acute macrotrauma, rupture occurs most commonly in the proximal aspect of the anterior oblique ligament of the ulnar collateral ligament complex.22 Avulsion of the sublime tubercle fills out the spectrum of possible injury involving the ulnar collateral ligament complex (see later). Chronic repetitive valgus stress results in a collection of microtraumatic injuries that occur when the elbow is repeatedly subjected to the considerable valgus stress intrinsic to overhead throwing.23–25 In particular, the late

cocking (phase 3) and early acceleration (phase 4) phases of overhead throwing cause medial distraction (tensile forces) and lateral impaction (compressive forces) with the elbow flexed and the forearm supinated.23,26 Athletes involved in baseball, tennis, football, volleyball, ice hockey, and water polo can be affected. Medially, the distraction forces, if excessive, outmatch the tensile strength of the ulnar collateral ligament complex. In the absence of the required period of recovery after this insult, the functional integrity of the ulnar collateral ligament complex is compromised. The end result can include (1) sprain of the ulnar collateral ligament complex, (2) medial epicondylitis, (3) ulnar nerve traction injury, and (4) avulsion injury to the medial epicondyle in the skeletally immature. Laterally, the compressive forces can result in chondral or osteochondral injury within the radiocapitellar joint with possible loose body formation.27,28 In this setting, valgus subluxation may also occur due to laxity of the ulnar collateral ligament complex.

Radial Collateral Ligament Complex Injury to the lateral ulnar collateral ligament results (1) from chronic varus stress overload due to work, sports-related activity, or cubitus varus; (2) from an acute elbow injury such as posterior dislocation, hyperextension, or acute varus stress; or (3) as a complication of aggressive surgical treatment for lateral epicondylitis or radial head excision (Fig. 12-4). Patients with insufficiency of the lateral ulnar collateral ligament experience laxity of the ulnotrochlear joint and secondary subluxation/dislocation of the radiocapitellar joint, while the proximal radioulnar joint

■ FIGURE 12-3

Partial tear of the ulnar collateral ligament (UCL) anterior band. There is intrasubstance linear fluid-like signal involving the origin of the anterior band of the UCL at its origin from the medial humerus (arrow) noted on this coronal fat-suppressed T2-weighted MR image.

■ FIGURE 12-4

Tear of the radial collateral ligament. Coronal T2weighted MR image demonstrates a tear of the radial collateral ligament involving its proximal humeral insertional fibers (arrow).

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retains its normal relationship. As discussed earlier, injury to the lateral collateral ligament may accompany lateral epicondylitis.

Elbow Dislocation Elbow dislocation is the second most common major joint dislocation. The condition affects patients usually between the ages of 5 and 25 years. Dislocations are classified based on the direction of dislocation, namely, posterior, posterolateral, posteromedial, lateral, medial, or divergent. Eighty to 90 percent of all elbow dislocations are posterior or posterolateral, affecting both the radius and the ulna, which are displaced in a posterior direction in relation to the distal humerus.29 Isolated dislocations of the ulna and radial head without associated fracture are rather rare in adults. Elbow dislocation is also classified into simple or complex depending on the presence of associated fractures. The most common complex dislocation is that associated with radial head fracture. Elbow dislocation is usually closed and posterior. Fall onto an extended elbow is a frequent mechanism of trauma.

Entrapment Neuropathy Alteration of nerve function secondary to compression by mechanical or dynamic forces may be a cause of upper extremity pain and weakness. Anatomically narrow passages predispose individual nerves to entrapment neuropathies. More often, the compression is related to space-occupying lesions, such as tumors, cysts, inflammatory processes, or post-traumatic conditions, such as hematoma, myositis ossificans, and callous formation. Dynamic changes within a narrow space or tunnel during repetitive activity can result in entrapment of a nerve with only minimal anatomic variations.30 Ulnar nerve compression is the most common neuropathy at the elbow, and the second most common neuropathy in the upper extremity, only exceeded by carpal tunnel syndrome. The cubital tunnel syndrome can be classified into physiologic and compressive syndromes, with the latter subdivided into acute, subacute, and chronic presentations. Normal loss in volume and increased pressure within the tunnel during elbow flexion may result in physiologic cubital tunnel syndrome. This can be seen in “sleep palsy” as the arm is held in flexion for prolonged periods of time. Blunt trauma to the cubital tunnel is a typical cause of acute external compression syndrome of the ulnar nerve. Subacute compression syndrome has been described in hospitalized bedridden or wheelchair-bound patients and after surgery. The anconeus epitrochlearis muscle has also been implicated as a cause of ulnar neuropathy and external compression syndrome31 (Fig. 12-5). Other causes include callus formation from distal humeral and supracondylar fractures, elbow dislocation, avulsed medial epicondylar apophysis, and masses such as tumors, distended bursae, ganglions, hematoma, inflammatory pannus, gouty tophi, loose bodies, and osteophytes can result in chronic tunnel syndrome. In athletes, a frequent cause of chronic cubital tunnel syndrome is lateral shift of the ulna, commonly associated with chronic laxity of the ulnar collateral ligament.

■ FIGURE 12-5

Anconeus epitrochlearis. Axial T1-weighted MR image through the medial epicondyle demonstrates an anconeus epitrochlearis (arrow) roofing the cubital tunnel and ulnar nerve, which is markedly enlarged (arrowheads).

The pronator syndrome is the most common cause of median nerve entrapment at the elbow. Other causes include elbow fractures and dislocations,32 accessory muscles such as the Gantzer muscle (the accessory head of the flexor pollicis longus muscle), soft tissue masses, and dynamic forces at the elbow. Radial nerve compression at the elbow occurs infrequently and is often misdiagnosed.33 It can be subdivided into two major categories, both involving compression of the posterior interosseous nerve: radial tunnel syndrome, in which pain is present without motor deficits, and posterior interosseous nerve syndrome, which is a motor neuropathy.

BIOMECHANICS Tendons The wrist extensor tendons assist in stabilizing the elbow against varus stress. On repetitive varus stress, the musculotendinous complex may be subjected to eccentric loading and potential overuse as in lateral epicondylitis. The flexor pronator group serves as a secondary stabilizer of the elbow joint, assisting the ulnar collateral ligament against valgus stress. Valgus stress is placed on the elbow by activities such as throwing and golfing. Valgus stress is particularly high during the late cocking and acceleration phases of the throw. Golfers place this area under stress during their swing: from the top of the backswing to just before ball impact.34 The biceps is the most powerful supinator of the forearm, while also assisting in elbow flexion. Therefore, flexion or flexion-supination motions most often aggravate pain related to distal biceps tendinopathy. Rupture of the distal biceps tendon is most often secondary to sudden, forceful extension overload of the arm with the elbow in mid flexion. This mechanism of trauma is most common in weightlifters and rugby players.11 Distal biceps

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musculotendinous ruptures are typically associated with trauma occurring on glenohumeral elevation with the elbow extended and the forearm in supination.35 Triceps tendon avulsion is most often secondary to acute trauma. The mechanisms of injury include (1) decelerating counterforce during active extension as in a fall with an outstretched hand; (2) direct blow to the tendon; and (3) forceful eccentric contraction of the triceps muscle with the elbow flexed. Relocation of the medial head of triceps tendon during elbow extension from the flexed position is responsible for the painful snapping sensation typical of snapping triceps syndrome.

Ligaments The ulnar collateral ligament arises from the medial humeral epicondyle, slightly posterior to the central axis of elbow rotation. Therefore, it is under greatest tension with elbow flexion.36 The radial collateral ligament emanates from the lateral epicondyle at the central axis of rotation. Consequently, this ligament is constantly under tension regardless of elbow position.36 Ligamentous injuries of the elbow may be related to a single traumatic event, as in elbow dislocation or varus extension stress injury to the radial collateral ligament or to chronic repetitive trauma with valgus stress to the medial collateral ligament. Injury to the ulnar band of the radial collateral ligament has also been reported as a complication of common extensor tendon release for treatment of lateral epicondylitis.1,37 Elbow instability can be divided into three stages.38 In stage I there is posterolateral rotational subluxation of the ulna on the humerus associated with supination or external rotation of the ulna related to disruption of the radial ulnar collateral ligament. In stage II there is incomplete elbow dislocation with the coronoid process of the ulna perched on the humeral trochlea. This stage of injury implies tearing of the lateral ulnar collateral ligament and radial collateral ligament as well as anterior and posterior capsular disruption. In stage III the coronoid process of the ulna is located behind the humerus. This stage is subdivided into A and B if the posterior band of the ulnar collateral ligament is disrupted and the anterior band of the ulnar collateral ligament is involved, respectively.

Nerves At the distal arm and elbow there are several potential sites of compression of the ulnar nerve. Compression at the cubital tunnel is the most common. In this location, the ulnar nerve is quite superficial and can be easily injured by direct trauma. The cubital tunnel experiences dynamic changes during flexion and extension of the elbow. The cubital tunnel is reduced in size during elbow flexion, as the overlying arcuate ligament becomes progressively taut.39 At 90 degrees of elbow flexion, the greatest tightness of the arcuate ligament is achieved. Further decrease in the volume of the cubital tunnel and medial displacement of the elbow nerve during elbow flexion are secondary to medial bulging of the ulnar collateral ligament and the medial head of the triceps. Increased cubital tunnel pressure with flexion has also been described.

The pronator syndrome is the most common cause of median nerve entrapment at the elbow. The four potential sites of compression that constitute the pronator syndrome from proximal to distal are as follows: (1) the supracondylar process/ligament of Struthers; (2) the lacertus fibrosus; (3) the pronator teres muscle; and (4) the proximal arch of the flexor digitorum superficialis muscle.40 Dynamic compression of the median nerve between the superficial (humeral) and deep (ulnar) heads of the pronator teres muscle is the most frequent cause for the pronator syndrome.41 Fibrous bands can be found in up to 50% of anatomic specimens located dorsal to the humeral head or to the nerve itself. These bands can produce nerve compression, particularly in pronation and elbow extension, when the distance between the two heads of the pronator teres is decreased. Radial tunnel syndrome refers to compression of the posterior interosseous nerve within the radial tunnel without motor deficit.42 Potential compression sites of the posterior interosseous nerve within the radial tunnel include, from proximal to distal: (1) fibrous bands extending from the radiocapitellar joint; (2) the tendinous edge of the extensor carpi radialis brevis muscle; (3) the radial recurrent artery and branches (leash of Henry); (4) the arcade of Fröhse at the proximal edge of the supinator muscle43; and (5) a fibrous band at the distal end of the supinator muscle. Repeated pronation and supination or forceful extension of the forearm may result in dynamic compression within the radial tunnel. Tennis players, swimmers, housewives, welders, conductors, and violinists are frequently affected by this disorder. The posterior interosseous nerve syndrome is defined as a motor neuropathy. Trauma, space-occupying lesions, and inflammatory processes have been implicated as potential etiologic factors. Compression sites for posterior interosseous nerve syndrome are the same as those for the radial tunnel syndrome (see earlier).

PATHOLOGY Lateral Epicondylitis Nirschl and Petrone44 attributed the cause of lateral epicondylitis to microscopic tearing with formation of reparative tissue (angiofibroblastic hyperplasia) in the origin of the extensor carpi radialis brevis muscle from the lateral epicondyle (Fig. 12-6). Increased signal intensity on T1weighted and T2-weighted MR sequences is likely related to intratendinous mucoid degeneration and neovascularization. Over time, this microtearing and repair response can result in macroscopic tearing and structural failure of the origin of the extensor carpi radialis brevis muscle. The origins of the extensor digitorum communis and extensor carpi radialis longus tendons may also be involved.1,45 Furthermore, a large proportion of patients with moderate to severe lateral epicondylitis have associated lateral collateral ligamentous injury.46

Medial Epicondylitis The pathologic findings of medial epicondylitis parallel those described for those of a disorder that affects the

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Elbow Instability Elbow dislocation without associated fractures (simple) often involves rupture of the capsule, ulnar collateral ligament, flexor pronator muscle mass, and, less commonly, brachialis muscle injury. Closed posterior dislocations are rarely associated with vascular injury, whereas open and/ or anterior dislocations often have associated brachial artery and median nerve injuries.

MANIFESTATIONS OF THE DISEASE Lateral Epicondylitis

■ FIGURE 12-6

Partial tear of the common extensor tendon. Coronal gradient echo T2*-weighted MR image demonstrates a focal fluid-filled gap (arrow) within the proximal fibers of the common extensor tendon at its origin from the lateral epicondyle.

common extensor tendon, ranging from tendinosis to partial and complete tears. However, unlike with the common extensor tendon, the common flexor tendon is more susceptible to acute disruption.17 The close spatial and functional relationship of the common flexor tendon to the ulnar collateral ligament renders the two susceptible to concomitant injury.47,48 Injury to the ulnar nerve is also commonly seen in this context.47,49

Biceps Tendon Injuries The most common site of distal biceps tendon injury is a few millimeters proximal to the osseous insertion into the radial tuberosity. Intrasubstance and myotendinous tears are rare.35 The distal biceps tendon has an area of relative hypovascularity just proximal to its insertion onto the radial tuberosity.50 This explains the increased susceptibility of the distal biceps tendon to injury, placing it as the most commonly torn tendon in the elbow. The bicipital aponeurosis is of particular importance in the pathophysiology of distal biceps tendon rupture. Preservation of the bicipital aponeurosis will prevent proximal retraction of the distal biceps tendon. If compromised, the bicipital aponeurosis may allow retraction of the distal biceps tendon into the arm.

Triceps Tendon Injuries The typical site of acute traumatic triceps tendon injury is at, or adjacent to, its insertion on the olecranon. Anabolic steroid abuse and local corticosteroid injections have been associated with detrimental effects on the mechanical properties of connective tissue, thus acting as predisposing factors for triceps tendon rupture.51 Spontaneous rupture of the triceps tendon has also been reported in patients with underlying chronic renal failure, secondary hyperparathyroidism, rheumatoid arthritis, and collagen vascular disorders.52

Clinically, patients complain of insidious and often progressive lateral elbow and forearm pain exacerbated by use. The condition typically presents in a middle-aged individual who either is a professional/recreational athlete or engages in rigorous daily activities. On examination, the point of maximal tenderness is often found 5 to 10 mm distal to the lateral epicondyle. Wrist extension or supination against resistance with the elbow extended should elicit symptomatology. The diagnosis of lateral epicondylitis is often made based on clinical grounds but can be confused with radial neuropathy. Therefore, if the clinical examination indicates a possible neural etiology for the patient’s symptoms, electromyographic studies can be helpful in excluding posterior interosseous nerve compression syndrome as the diagnosis.

Radiography Conventional anteroposterior, oblique, and lateral radiographs of the elbow may help exclude intra-articular pathologic processes, including lateral elbow osteoarthritis, posterior osteophytes, and intra-articular bodies. Dystrophic calcification of the origin of the extensor carpi radialis brevis can be seen in chronic cases.

Magnetic Resonance Imaging Magnetic resonance imaging can help confirm the presence of lateral epicondylitis; however, this is rarely needed because most injuries are diagnosed based on clinical grounds. In those cases refractory to conservative therapy, MRI may help determine the severity of the condition and the presence of a concomitant pathologic process and exclude other causes of lateral elbow pain.53 MRI features of lateral epicondylitis include thickening/ thinning of the common extensor tendon and intratendinous signal hyperintensity. Increased signal intensity on T1-weighted and T2-weighted sequences is likely related to intratendinous mucoid degeneration and neovascularization. Nevertheless, focal areas of hyperintensity and even thickening of the common extensor tendon have been reported in asymptomatic individuals. The presence of fluid-like signal intensity areas may reflect areas of focal or complete disruption of the tendon fibers (Fig. 12-7). However, fluid-like signal may also be related to recent injection of corticosteroids (3 mm) on plain radiographs or fluid signal extending through the scapholunate interval on T2-weighted sequences is characteristic of a scapholunate ligament tear. Dorsiflexion of the lunate with a capitate lunate angle of greater than 30 degrees is suggestive of DISI. Palmar flexion of the lunate with a capitate lunate angle of greater than 30 degrees is suggestive of VISI.

DIFFERENTIAL DIAGNOSIS Ulnar-sided wrist pain can be seen with extensor carpi ulnaris tenosynovitis, TFC injuries and ulnar impaction, wrist ganglion, ulnar nerve sheath tumors, and direct trauma with bone bruises and fractures.

SYNOPSIS OF TREATMENT OPTIONS Ulnar Impaction Syndrome Initial treatment of ulnar impaction is conservative with splinting, nonsteroidal anti-inflammatory agents, and modification in activity. If conservative therapy fails, surgical management becomes a consideration. Many options exist for treatment, and ultimately the choice lies with the surgeon. In patients with underlying ulnar-positive variance, débridement has been proposed for traumatic tears or degenerative perforations along with ulnar shortening in some manner to unload the ulnocarpal joint.13,40,49 Ulnar shortening has been found to relieve ulnar-sided wrist pain in both traumatic tears of the TFC and degenerative perforations. There are two basic means to shorten the ulna: osteotomy and wafer resection. Osteotomy is an open technique in which the surgeon performs an osteotomy of the distal ulnar diaphysis and shortens the ulnar length with an end goal of an ulnar-neutral or mild ulnar-minus variance. The osteotomy has been described using either a transverse or oblique cut across the bone. The osteotomy site is then traversed by a dynamic compression plate with screws for healing. Complications include reflex sympathetic dystrophy, nonunion, ulnar nerve damage with numbness, and irritation of the skin caused by the bulk of the side plate. Most patients experience improvement in their ulnar-sided wrist pain. Factors sited for failure to improve include underlying carpal instability and malunion of a Colles fracture when excess dorsal tilt of the radiocarpal joint results. Osteotomy can be performed with or without arthroscopy of the ulnocarpal joint to evaluate the

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TFCC. Because osteotomy is performed away from the ulnocarpal joint, a second arthroscopic procedure would be required to débride or repair TFCC tears and perforations. Arthroscopy also allows the opportunity to evaluate the lunotriquetral ligament, because it is often abnormal in degenerative perforations of the TFC. The second common method for shortening ulnar length is wafer resection. The procedure is accomplished using a bur grinder. This shortening process can be accomplished entirely by arthroscopy. The wrist joint is distracted, and the bur grinder is used to remove articular cartilage and subchondral bone of the ulnar head. Because the arthroscopic portals used for wafer resection are the same as those used for TFCC surgeries, TFCC lesions can be débrided or repaired concomitantly with wafer resection. A contraindication for the wafer procedure is an ulnar-positive variance exceeding 4 mm. These cases are better treated with open osteotomy.41 Patients are not considered surgical candidates if they have several preexisting conditions. Arthritis or instability of the DRUJ is considered an exclusion criterion by many because ulnar shortening is thought to speed the development of DRUJ arthritis. However, some claim that ulnar shortening actually improves DRUJ stability.40 Preexisting carpal instabilities, including VISI and DISI abnormalities, are reasons for exclusion from surgical management. These populations have wrist pain for a multitude of reasons, and correction of ulnocarpal loading may not improve the patients’ symptoms. Acute fractures that result in ulnarpositive variance require correction of the fracture acutely to try to prevent a post-traumatic ulnar-positive variance. Ulnar styloid impaction is also a contraindication for ulnar shortening. Finally, if the patient has other diagnoses that could lead to ulnar-sided wrist pain, those are treated first. For example, if a patient with ulnar-positive variance has an extensor carpi ulnaris tenosynovitis and ulnar-sided wrist pain, the extensor carpi ulnaris tendon sheath could be injected with corticosteroids before surgery should be considered. Partial or complete tears of the lunotriquetral ligament are not a contraindication for surgery. Often, after correction of ulnar-positive variance in ulnar impaction syndrome, MR signal changes in the ulnar aspect of the lunate and the radial aspect of the triquetrum may remain but they often show complete resolution.49

Scapholunate Ligament The treatment of scapholunate tears is a very difficult problem with many surgical options. The goals of treatment are relief of pain, restoration of function, and halting the progression of degenerative changes seen with a SLAC wrist. The treatment of partial tears and of complete tears with instability is considered separately because the treatments are very different.

Partial Tears As previously stated, the membranous and volar portions of the scapholunate ligament are less important biomechanically and functionally than those of the dorsal portion. Nonetheless, tears in these regions can cause significant pain and mechanical symptoms. These tears are typically treated with débridement with synovial

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resection, occasionally combined with thermal shrinkage. The healing effects are attributed to scar formation, and the pain relief is thought to be related to partial denervation. Satisfaction is high, with patients reporting good pain relief and improved wrist function.60 The natural history of partial scapholunate ligament tears does not typically include progression to a SLAC wrist as is seen with complete tears.

Complete Tears Many hand surgeons consider early treatment of acute complete scapholunate ligament tears the most effective way to prevent the development of wrist instability and degeneration. Surgical treatment within 3 weeks of injury is ideal. However, repair remains a viable option as long as 4 to 6 months after injury.61 The most commonly performed surgical procedure in the acute setting is repair or reconstruction of the ligament with or without capsulodesis. It is thought that beyond 3 to 6 weeks after injury the scapholunate ligament may no longer be amenable to repair due to a decreased capacity for healing. When dealing with chronic tears, there are several important clinical parameters the surgeon typically considers. The first clinical parameter that the surgeon and radiologist should evaluate is the presence or degree of osteoarthritis. The degree of osteoarthritis profoundly affects surgical planning and treatment options. Two other important parameters that one must consider when planning treatment are the degree of scaphoid reducibility and the status of the scapholunate interosseous membrane.62 Two common surgical procedures considered in cases of chronic scapholunate tear with instability include ligament reconstruction and capsulodesis. In cases in which the scaphoid cannot be reduced or osteoarthritis is evident, then intercarpal arthrodesis may be the only option for treatment.63 In severe cases in which a SLAC wrist is already present, proximal row carpectomy is sometimes employed for treatment.64

Lunotriquetral Ligament There are three main surgical treatments for lunotriquetral ligament tears: ligament repair, ligament reconstruction, and joint arthrodesis. Isolated lunotriquetral ligament tears are uncommon but are associated with chronic wrist pain. The choice to move forward to surgery occurs typically after failed conservative therapy in chronic lunotriquetral ligament tears. Another indication for surgical management is lunotriquetral dissociation. The main goal of lunotriquetral ligament repair is concerned with not only the lunotriquetral joint but also the lunocapitate joint. The main goals of repair are maintaining or reestablishing the physiologic axis through the lunate and capitate. Additionally, repair preserves or reestablishes the intercalated segment, that is, the proximal row, as a functional unit rather than as disjointed segments.45 The three procedures are performed quite differently. Briefly, arthrodesis of the lunotriquetral joint involves using a corticocancellous bone graft from the distal dorsal radius or the iliac crest. The bone graft is then secured to the prepared surfaces of the dorsal lunate and triquetrum using a screw or wires. Ligament reconstruction is accomplished by using autologous tendon. The distal extensor carpi ulnaris tendon was used in the study per-

formed by Shin. A distal segment of this tendon is used as a lunotriquetral ligament graft that is placed in tunnels drilled into the lunate and triquetrum. Finally, ligament repair is accomplished by using nonabsorbable suture passed through drill holes in the triquetrum and then through the ligament to reapproximate the fibers against the bone. The joint is then reduced and pinned with percutaneous Kirschner wires. The choice of which surgery best suits each patient always remains in the hands of the surgeon. However, factors taken into consideration when making the choice include degree of wrist instability, time since injury occurred, and concurrent abnormalities such as scapholunate injury or underlying ulnar impaction syndrome. For those who wish to have a less invasive approach to treatment, débridement alone has been proposed as an option.50,51 In a series of 33 complete lunotriquetral tears and 43 partial-thickness tears of the lunotriquetral ligament, Weiss and coworkers had favorable short-term results. Treatment was purely arthroscopic and focused on débriding free and irregular margins after ligamentous injury in patients who were experiencing persistent wrist pain that did not improve after conservative therapy. Of those with partial-thickness lunotriquetral ligament tears, 100% of patients reported that their pain was improved to some degree. Some patients reported complete resolution of pain symptoms. In those with complete lunotriquetral ligament disruption, 78% reported decreased or resolved pain. None of the patients chosen for lunotriquetral ligament débridement as their sole treatment showed any radiographic evidence of VISI. The main limitation to the study was that follow-up was only 27 months and longterm outcomes have not been determined. Additionally, of those treated, only 23% demonstrated improvement in grip strength. A second smaller series had very similar results.51

What the Referring Physician Needs to Know ■ ■

■

■

■

Ulnar-sided wrist pain has many causes. MRI can frequently differentiate surgical from nonsurgical conditions. Triangular fibrocartilage (TFC) tears can be traumatic or degenerative. They can be described using the Palmer classification system. Ulnar impaction syndrome is a condition that results from abnormal mechanical forces at the ulnocarpal joint. Treatment of the TFC alone is not enough. In these cases, the underlying cause of the impaction must be addressed to alleviate the impaction from continuing. Treatment usually is in the form of ulnar shortening. Scapholunate ligament tears are a cause of wrist pain in the setting of trauma and negative wrist radiographs. The diagnosis is made with MRI. Lunotriquetral ligament tears are a cause of wrist pain in the setting of trauma and negative wrist radiographs. These tears can also be degenerative, related to ulnar impaction syndrome. There is no consistently reliable imaging method to diagnose lunotriquetral ligament tears. Nonetheless, MRI is the best noninvasive diagnostic technique utilizing small coils and high-resolution imaging. Wrist arthrography may aid in the diagnosis.

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SUGGESTED READINGS Berger RA. The anatomy of the ligaments of the wrist and distal radioulnar joints. Clin Orthop Relat Res 2001; 383:32–40. Cerezal L, del Pinal F, Abascal F. MR imaging in ulnar sided wrist impaction syndromes. Magn Reson Imaging Clin North Am 2004; 12:281–299. McAlinden PS, Teh J. Imaging of the wrist. Imaging 2003; 15:180–192. Oneson SR, Scales LM, Timmins ME, et al. MR imaging interpretation of the Palmer classification of triangular fibrocartilage complex lesions. Radiographics 1996; 16:97–106.

Palmer AK. Triangular fibrocartilage complex lesions: a classification. J Hand Surg 1989; 14:594–606. Yu JS, Habib PA. Normal MR imaging anatomy of the wrist and hand. Magn Reson Imaging Clin North Am 2004; 12:207–219. Zlatkin MB, Rosner J. MR imaging of ligaments and triangular fibrocartilage complex of the wrist. Magn Reson Imaging Clin North Am 2004; 12:301–331.

REFERENCES 1. Haims AH, Schweitzer ME, Morrison WB, et al. Limitations of MR imaging in the diagnosis of peripheral tears of the triangular fibrocartilage of the wrist. AJR Am J Roentgenol 2002; 178:419–422. 2. Palmer AK. Triangular fibrocartilage complex lesions: a classification. J Hand Surg [Am] 1989; 14:594–606. 3. Totterman SM, Miller RJ. Triangular fibrocartilage complex: normal appearance on coronal three-dimensional gradientrecalled-echo MR images. Radiology 1995; 195:521–527. 4. Smith DK. Volar carpal ligaments of the wrist: normal appearance on multiplanar reconstructions of three-dimensional Fourier transform MR imaging. AJR Am J Roentgenol 1993; 161:353–357. 5. Hogikyan JV, Louis DS. Embryological development and variations in the anatomy of the ulnocarpal ligamentous complex. J Hand Surg [Am] 1992; 17:719–723. 6. Berger RA. The anatomy of the ligaments of the wrist and distal radioulnar joints. Clin Orthop Relat Res 2001; 383:32–40. 7. Taleisnik J. The ligaments of the wrist. J Hand Surg [Am] 1976; 1:110–118. 8. Bednar MS, Arnoczky AP, Weiland AJ. The microvasculature of the triangular fibrocartilage complex: its clinical significance. J Hand Surg [Am] 1991; 16:1101–1105. 9. Chidgey LK, Dell PC, Bittar ES, Spanier SS. Histologic anatomy of the triangular fibrocartilage. J Hand Surg [Am] 1991; 16:1084–1100. 10. Totterman SM, Miller RJ, McCance SE. Lesions of the triangular fibrocartilage complex: MR findings with a three-dimensional gradient-recalled-echo sequence. Radiology 1996; 199:227–232. 11. Oneson SR, Scales LM, Timmins ME, et al. MR imaging interpretation of the Palmer classification of triangular fibrocartilage complex lesions. Radiographics 1996; 16:97–106. 12. Timmins ME, O’Conell SE, Erickson SJ, Oneson SR. MR imaging of the wrist: normal findings that may simulate disease. Radiographics 1996; 16:987–995. 13. Palmer AK, Glisson RR, Werner FW. Relationship between ulnar variance and triangular fibrocartilage complex thickness. J Hand Surg [Am] 1984; 9:681–682. 14. Shen J, Papadonikolakis A, Garrett JP, et al. Ulnar positive variance as a predictor of distal radioulnar joint ligament disruption. J Hand Surg [Am] 2005; 30:1172–1177. 15. Mikic ZD: Age changes in the triangular fibrocartilage of the wrist joint. J Anat 1978; 126:367–384. 16. Ishii S, Palmer AK, Werner FF, et al. An anatomic study of the ligamentous structure of the triangular fibrocartilage. J Hand Surg [Am] 1998; 23:977–985. 17. Theumann NH, Pfrrmann CW, Anonia GE, et al. Extrinsic carpal ligaments: normal MR arthrographic appearance in cadavers. Radiology 2003; 226:171–179. 18. Mayfield JK, Johnson RP, Kilcoyne RF. The ligaments of the human wrist and their functional significance. Anat Rec 1976; 186:417–428. 19. Nishikawa S, Toh S. Anatomical study of the carpal attachment of the triangular fibrocartilage complex. J Bone Joint Surg Br 2002; 84:1062–1065.

20. Nakamura T, Yabe Y, Horiuchi Y. Functional anatomy of the triangular fibrocartilage complex. J Hand Surg [Br] 1996; 21:581–586. 21. Sokolow C, Saffar P. Anatomy and histology of the scapholunate ligament. Hand Clin 2001; 17:77–81. 22. Berger RA. The gross and histologic anatomy of the scapholunate interosseous ligament. J Hand Surg [Am] 1996; 21:170–178. 23. Timins ME, Jahnke JP, Krah SE, et al. MR imaging of the major carpal stabilizing ligaments: normal anatomy and clinical examples. Radiographics 1995; 15:575–587. 24. Totterman SM, Miller R, Wasserman B, et al. Intrinsic and extrinsic ligaments: evaluation by three-dimensional Fourier transform MR imaging. AJR Am J Roentgenol 1993; 160:117–123. 25. Rominger MB, Bernreuter WK, Kenney PJ, Lee DH. MR imaging of anatomy and tears of wrist ligaments. Radiographics 1993; 13:1233–1246. 26. Brown RR, Fliszar E, Cotton A, et al. Extrinsic and intrinsic ligament of the wrist: normal and pathologic anatomy at MR arthrography with three-compartment enhancement. Radiographics 1998; 18:667–674. 27. Johnston RB, Seiler JG, Miller EJ, Drvaric DM. The intrinsic and extrinsic ligaments of the wrist: a correlation of collagen typing and histologic appearance. J Hand Surg [Br] 1995; 20:750–754. 28. Theumann NH, Etechami G, Duvoisin B, et al. Association between extrinsic and intrinsic carpal ligament injuries at MR arthrography and carpal instability at radiography: initial observations. Radiology 2006; 238:950–957. 29. Lindau T, Adlercreutz C, Aspenberg P. Peripheral tears of the triangular fibrocartilage complex cause distal radioulnar joint instability after distal radial fractures. J Hand Surg [Am] 2000; 25:464–468. 30. Palmer AK, Werner FW. Biomechanics of the distal radioulnar joint. Clin Orthop 1984; 187:26–35. 31. Berger RA, Imeada T, Berglund L, An K. Constrain and material properties of the subregions of the scapholunate interosseous ligament. J Hand Surg [Am] 1999; 24:953–962. 32. Watson HK, Ballet FL. The SLAC wrist: scapholunate advanced collapse pattern of degenerative arthritis. J Hand Surg [Am] 1984; 9:358–365. 33. Mayfield JK, Williams WJ, Erdman AG, et al. Biomechanical properties of human carpal ligaments. Orthop Trans 1979; 3:143–144. 34. Smith DK, Snearly WN. Lunotriquetral interosseous ligament of the wrist: MR appearances in asymptomatic volunteers and arthrographically normal wrists. Radiology 1994; 191:199–202. 35. Daily SW, Palmer AK. The role of arthroscopy in the evaluation and treatment of triangular fibrocartilage complex injuries in athletes. Hand Clin 2000; 16:461–476. 36. Sugimoto HS, Shinozaki T, Ohsawa T. Triangular fibrocartilage in asymptomatic subjects: investigation of abnormal MR signal intensity. Radiology 1994; 191:193–197. 37. Potter HG, Anis-Ernberg L, Weiland AJ, et al. The utility of highresolution magnetic resonance imaging in the evaluation of the wrist. J Bone Joint Surg [Am] 1997; 79:1675–1684.

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38. Hobby JL, et al. MR imaging of the wrist: effect on clinical diagnosis and patient care. Radiology 2001; 220:589–593. 39. O’Meeghan CJ, Stuart W, Mamo V, et al. The natural history of an untreated isolated scapholunate interosseous ligament injury. J Hand Surg [Br] 2003; 28:307–310. 40. Baek GH, Chung MS, Lee YH, et al. Ulnar shortening osteotomy in idiopathic ulnar impaction syndrome. J Bone Joint Surg [Am] 2005; 87:2649–2654. 41. Feldon P, Terrono AL, Belsky MR. The “wafer” procedure: partial distal ulnar resection. Clin Orthop Relat Res 1992; 275:124–129. 42. Epner RA, Bowers WH, Guilford WB. Ulnar variance—the effect of wrist positioning and roentgen filming technique. J Hand Surg [Am] 1982; 7:298–305. 43. Tomaino MM. The importance of the pronated grip x-ray view in evaluating ulnar variance. J Hand Surg [Am] 2000; 25:352–357. 44. Trentham DE, Hamm RH, Masi AT. Wrist arthrography: review and comparison of normals, rheumatoid arthritis and gout patients. Semin Arthritis Rheum 1975; 5:105–120. 45. Haims AH, Schweitzer ME, Morrison WB, et al. Internal derangement of the wrist: indirect MR arthrography versus unenhanced MR imaging. Radiology 2003; 227:701–707. 46. Zanetti M, Bram J, Hodler J. Triangular fibrocartilage and intercarpal ligaments of the wrist: does MR arthrography improve standard MRI? J Magn Reson Imaging 1997; 7:590–594. 47. Oneson SR, Timmins ME, Scales LM, et al. MR imaging of triangular fibrocartilage pathology with arthroscopic correlation. AJR Am J Roentgenol 1997; 168:1513–1518. 48. Yoshioka H, Teruko U, Tanaka T, et al. High resolution MR imaging of triangular fibrocartilage complex: comparison of microscopy coils and a conventional small surface coil. Skeletal Radiol 2003; 32:575–581. 49. Imaeda T, Nakamura R, Shionoya K, Makino N. Ulnar impaction syndrome: MR imaging findings. Radiology 1996; 201:495–500. 50. Haims AH, Moore AE, Schweitzer ME, et al. MRI in the diagnosis of cartilage injury in the wrist. AJR Am J Roentgenol 2004; 182:1267–1270. 51. Bordalo RM, Schweitzer ME, Bergin D, et al. Lunate chondromalacia: evaluation of routine MRI sequences. AJR Am J Roentgenol 2005; 184:1464–1469. 52. Smith DK. Scapholunate interosseous ligament of the wrist: MR appearances in asymptomatic volunteers and arthrographically normal wrists. Radiology 1994; 192:217–221.

53. Totterman SM, Miller RJ. Scapholunate ligament: normal MR appearance on three-dimensional gradient-recalled-echo images. Radiology 1996; 200:237–241. 54. Zlatkin MB, Chao PC, Osterman AL, et al. Chronic wrist pain: evaluation with high-resolution MR imaging. Radiology 1989; 173:723–729. 55. Scheck RJ, Kubitzek C, Hierner R, et al. The scapholunate interosseous ligament in MR arthrography of the wrist: correlation with non-enhanced MRI and wrist arthroscopy. Skeletal Radiol 1997; 26:263–271. 56. Schweitzer ME, Brahme SK, Hodler J, et al. Chronic wrist pain: spin echo and short tau inversion recovery MR imaging and conventional MR arthrography. Radiology 1992; 182:205–211. 57. Mikic Z. Arthrography of the wrist joint: an experimental study. J Bone Joint Surg Am 1984; 66:371–384. 58. Wright TW, Del Charco M, Wheeler D. Incidence of ligament lesion and associated degenerative changes in the elderly wrist. J Hand Surg [Am] 1994; 19:313–318. 59. Manton GL, Schweitzer ME, Weishaupt D, et al. Partial interosseous tears of the wrist: difficulty in utilizing either primary or secondary MRI signs. J Comput Assist Tomogr 2001; 25:671–676. 60. Darlis NA, Weiser RW, Sotereanos DG. Partial scapholunate ligament injuries treated with arthroscopic débridement and thermal shrinkage. J Hand Surg [Am] 2005; 30:908–914. 61. Taleisnik J. Scapholunate dissociation. In Strickland JW, Steichen JB (eds). Difficult Problems in Hand Surgery. St. Louis, Mosby, 1982, pp 341–348. 62. Taleisnik J, Linscheid RL. Scapholunate instability. In Cooney WP, Linscheid RL, Dobyns JH (eds). The Wrist, Diagnosis and Operative Treatment. Philadelphia, Mosby Electronic Publishing, 1998, pp 501–526. 63. Fortin PT, Louis DS. Long-term follow-up of scaphoidtrapezium-trapezoid arthrodesis. J Hand Surg [Am] 1993; 18:675–681. 64. Culp RW, McGuigan FX, Tutner MA, et al. Proximal row carpectomy, a multicenter study. J Hand Surg [Am] 1993; 1:19–25. 65. Kozin SH. The role of arthroscopy in scapholunate instability. Hand Clin 1999; 15:435–444. 66. Geissler WB, Freeland AE. Arthroscopic assisted reduction of intra-articular distal radius fractures. Clin Orthop Relat Res 1996; 327:125–134.

16

C H A P T E R

Acute Osseous Trauma to the Hand

Joshua Owen, Richard Oh, Peter Hrehorovich, and Manesh Mathew

PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS

PATHOLOGY Routine Imaging

Acute bony trauma to the hand represents some of the most commonly occurring fractures encountered in daily clinical practice. Whether the etiology is related to sports, occupation, or trauma, the consequences can be devastating and the potential for functional loss often underappreciated. Therefore, it is essential that an accurate diagnosis and treatment plan be implemented to restore full function and form. Injuries of the hand are some of the most frequently encountered orthopedic injuries. The true incidence of phalangeal and metacarpal fractures, however, is probably underreported, given the fact that a number of patients with hand injuries never seek treatment. In one survey, hand fractures represented 17.5% of all fractures seen in one emergency department during a 10-month period.1 In that series, phalangeal fractures comprised 46% and metacarpal fractures comprised another 36% of all hand and wrist fractures. Another survey of sporting injuries during a 4-month period in Scotland demonstrated injuries of the hand and wrist to be 47% of the total injuries diagnosed throughout the body.2 Although in most cases the diagnosis can be inferred by a good clinical history and physical examination, a confirmatory diagnosis is usually performed by radiographic means. Many bony injuries may be treated nonoperatively, but some injuries require operative treatment. Some common complications of hand injuries include limited range of movement, malunion, and instability. Pathologic fractures are occasionally encountered, most commonly secondary to an enchondroma, which are expansile and can weaken the cortex. Rarely, the lesion may be related to a chondromyxoid fibroma or metastasis.3

A standard three-view radiographic examination of the hand includes posteroanterior, lateral, and oblique views (Fig. 16-1). This series of films will usually reveal most fractures and dislocations of the metacarpals and phalanges. For phalangeal injuries, it is appropriate to obtain designated views of the injured finger. The posteroanterior view is taken with the palm down and the beam centered over the third metacarpal. This view is particularly helpful in the evaluation of the bases of the metacarpals and bases of the proximal phalanges. The posteroanterior view of the metacarpophalangeal joints of the second through fifth digits should form an M configuration, with loss of this configuration implying dislocations of these joints.4 The lateral view is obtained with the ulnar side of the hand adjacent to the cassette. Superimposition of the metacarpals and phalanges may be overcome by partially fanning

KEY POINTS Acute bony trauma to the hand represents some of the most commonly occurring fractures seen in daily clinical practice. ■ Although in most cases the diagnosis can be inferred by a good clinical history and physical examination, confirmatory diagnosis is usually performed by radiographic means. ■ Most bony injuries are treated by splinting or casting, but a few injuries require operative management. ■ Hand injuries are usually divided between the soft tissue type, bony type, or both. ■

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■ FIGURE 16-1

Posteroanterior, oblique, and lateral radiographic views of the hand.

the fingers. The lateral view is important in evaluating rotation and angulation of fractures, as well as dislocations. The oblique view is taken with the hand rotated approximately 45 degrees with the thumb up. This view more clearly evaluates the metacarpal heads and first and second carpometacarpal joints. Fractures of the thumb require a dedicated two-view radiographic examination of the thumb, although an oblique view can be obtained with a posteroanterior examination of the whole hand. A true anteroposterior view of the thumb, called a Roberts view, is preferable (Fig. 16-2); the posteroanterior view of the thumb is obtained more easily but has some ulnar-sided magnification compared with the anteroposterior view. Soft tissue swelling about the joint is easily detected radiographically. When it is identified, the underlying joint should be examined carefully. Cortical avulsions usually occur at the margins of the joint at the base of the phalanges. These may be nondisplaced and seen on only one projection.

Additional Imaging The Brewerton view can be used to evaluate abnormalities or fractures of the metacarpal heads, hook of the hamate, and the fourth and fifth carpometacarpal joints.5 This view is obtained by placing the palm up and the fingers flexed by about 65 degrees with the tube angled 15 degrees to the ulnar side of the wrist (Fig. 16-3). The Burman view provides improved visualization of the first carpometacarpal joint.6 To obtain this view, the hand is hyperextended and rotated radially so that the thumb is

laid against the cassette and the beam is angled 45 degrees cephalad (Fig. 16-4). Tears of the ulnar collateral ligament of the thumb metacarpophalangeal joint (i.e., skier’s thumb) present a special problem. In the absence of an associated bony avulsion of the distal metacarpal or proximal phalangeal base, the injury may be radiographically occult. In these cases, a stress examination of the joint with manually applied abduction stress (which can be gently applied by the patient or the examiner) may show subluxation compared with the contralateral, uninjured side. Although there is a theoretical risk of converting a nondisplaced ulnar collateral ligament tear into a displaced one by a stress examination, this is a rare occurrence.7 Rarely is another modality required in evaluating fractures and dislocations. CT may be helpful in providing better operative planning in comminuted articular fractures, as seen in complete articular fractures at the base of the middle phalanx. CT can also help in the evaluation of occult fractures. MRI can be used for detection of occult fractures or for the evaluation of infected joints. More frequently, MRI is utilized for its superior soft tissue contrast and is the study of choice for evaluation of tendon, ligamentous, and articular abnormalities. Nuclear medicine is occasionally used. The most common indications for a three-phase bone scintiscan include evaluation of reflex sympathetic dystrophy, bone ischemia, occult osseous injury, and early infection/inflammation. Ultrasonography has been reported to be used in the evaluation of osseous fractures but is more commonly

CHAPTER

■ FIGURE 16-2 Proper positioning for radiography (A) and anteroposterior Roberts view (B) of the thumb.

■ FIGURE 16-3 Proper positioning for radiography (A) and Brewerton view (B) to evaluate the hook of the hamate and fourth and fifth metacarpophalangeal joints.

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fracture-dislocations made up approximately 34% of all fractures involving the thumb.13 There is characteristically an oblique fracture line at the base that separates the distal larger metacarpal fragment from the smaller avulsion fragment (Fig. 16-5). While the proximal avulsion fragment is often stable in position in relation to the trapezium, the larger distal fragment is unstable secondary to the pull of the abductor pollicis longus and flexor pollicis longus tendons and aided by the adductor pollicis muscles.14 In rare cases, fracture may occur without subluxation or dislocation.3 Anatomic reduction can be accomplished by either open or closed means, but some type of operative fixation is recommended because cast immobilization alone is frequently unstable.

Rolando’s Fracture The second type of intra-articular fracture-dislocation of the first carpometacarpal joint was described by the Italian surgeon Silvio Rolando 4 decades later in 1910.12 Less common than Bennett’s fracture, Rolando’s fracture is seen in approximately 10% of all fractures of the first metacarpal.13 This is a comminuted Y- or T-shaped fracture-dislocation at the base of the thumb metacarpal (Fig. 16-6). Dorsal dislocation of the distal metacarpal fragment also accompa-

■ FIGURE 16-4 Proper positioning for radiography (A) and Burman view (B) for improved visualization of the first carpometacarpal joint space.

performed in the evaluation of soft tissue structures, including tendon pathology and synovial disorders.8 However, high false-negative rates have been reported in children.9

MANIFESTATIONS OF THE DISEASE Fractures of the Thumb Radiography The thumb is unique compared with the rest of the phalanges in terms of both anatomic and functional characteristics, requiring special views for radiographic evaluation. There is considerable mobility at the normal first carpometacarpal joint that should not be mistaken for subluxation on various projections. The thumb also has unique patterns of injury in the setting of trauma. An important distinction to recognize is whether the fracture is intra-articular or extra-articular. Intra-articular basilar fractures are more common than extra-articular fracture and are also considerably more demanding in terms of treatment.10,11

Bennett’s Fracture This intra-articular fracture-dislocation of the first carpometacarpal joint was originally described by the Irish surgeon Edward Bennett in 1881.12 In one series, these

■ FIGURE 16-5 Bennett’s fracture. Diagram (A) and posteroanterior radiograph (B) demonstrate a stable proximal volar fracture fragment with proximal and radial displacement of distal metacarpal secondary to pull of multiple tendons.

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nies the disruption of the articular surface of the proximal thumb metacarpal. Management of Rolando’s fracture is similar to that described for Bennett’s fracture when only a few fragments are present. However, in cases of severe comminution or multiple fragments, successful pin fixation by either percutaneous or open means may be challenging for the surgeon, requiring additional methods. Therefore, it is important to describe the degree of comminution in these cases.

Ulnar Collateral Ligament Avulsion (Skier’s Thumb)

■ FIGURE 16-6 Rolando’s fracture. Posteroanterior radiograph shows comminuted intra-articular fracture at the base of the first metacarpal.

The ulnar collateral ligament is a ligamentous band that originates from the metacarpal head and inserts onto the medial aspect and base of the proximal phalanx of the thumb. Occasionally, acute rupture of the ulnar collateral ligament avulses a small portion of the proximal phalanx at its insertion, leading to skier’s thumb (Fig. 16-7). This fracture may involve a substantial portion of the articular surface of the proximal phalanx. Gamekeeper’s thumb is chronic clinical instability of the first metacarpophalangeal joint caused by insufficiency/tearing of the ulnar collateral ligament of the thumb. If the bony avulsion is displaced significantly, operative treatment may be required. Significant initial subluxation of the joint may result in the Stener lesion. This occurs when the ruptured ulnar collateral ligament displaces superficial to the adductor aponeurosis and away from its site of insertion at the base of the proximal phalanx. This lesion is radiographically occult and may require MRI or ultrasonography for diagnosis.15 Stener lesions require open surgical intervention to reunite the torn ligament from its attachment.

■ FIGURE 16-7 Skier’s thumb. Avulsion of the ulnar collateral ligament. A, The diagram demonstrates a significantly displaced avulsion fragment that likely requires operative fixation. B, Posteroanterior radiograph of the thumb demonstrates a nondisplaced fracture more amenable to medical treatment.

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Extra-articular Fractures of Thumb Extra-articular fractures account for the remaining fractures of the proximal thumb, which comprise approximately 35% of all first metacarpal bone fractures.13 The majority of these fractures are transverse neck fractures with associated dorsal angulation and/or displacement of the distal fragment. A small number of extra-articular basilar fractures are of the oblique variety, which are more unstable and challenging both diagnostically and therapeutically. It is important to recognize these oblique extra-articular fractures as being separate from intraarticular fractures, specifically Bennett’s fracture. The oblique extra-articular fractures can usually be treated by closed means alone, whereas the intra-articular fractures usually necessitate operative treatment.9

Second through Fifth Metacarpal Fractures Radiography The second through fifth metacarpals can be divided into two groups by the way they relate with the carpal bones at the carpometacarpal joint.3 The second and third metacarpals (stable joints) normally have little motion at the carpometacarpal joints; therefore, fractures at these locations have less tolerance for angulation or rotation. These fractures often require operative care. In contrast, the fourth and fifth carpometacarpal joints have a greater degree of mobility. Therefore, a greater range of angulation can be accepted in neck fractures of the fourth and fifth metacarpal bones without functional impairment. However, operative reduction may be indicated in cases of malrotation, shortening, and excessive displacement or angulation.

■ FIGURE 16-8 Boxer’s fracture. Oblique view shows fractures of the fourth and fifth metacarpals.

Metacarpal Neck Fractures (Boxer’s Fracture) This type of fracture is the most common fracture of the metacarpal bones. It is most frequently a transverse fracture through the fifth and sometimes the fourth metacarpal neck associated with volar angulation of the distal fragment (Fig. 16-8). Boxer’s fracture describes the most common etiology of the fracture—hitting an object with a clenched fist, which in turn causes direct axial compression along the longitudinal axis. The injury is conspicuous on the posteroanterior view of the hand as a shortening of the metacarpal bone. Although seen on the oblique view, the lateral view best demonstrates the degree of volar angulation. This angulation of the distal fragment may be increased by comminution. A moderate degree of volar angulation is acceptable with minimal functional impairment, up to 40 degrees in the fifth metacarpal and up to 25 degrees in the fourth metacarpal.16 Complete displacement or malrotation requires appropriate reduction before immobilization. Neck fractures of the second and third metacarpals are less common than in the fifth metacarpal. As mentioned previously, displaced fractures involving the second and

third metacarpals are poorly tolerated and may require operative intervention.

Metacarpal Diaphyseal Fractures These fractures are less common in the second through fifth metacarpals but may exhibit adverse sequelae of deformity. Treatment of transverse diaphyseal fractures is generally the same as that for neck fractures. Shortening, instability, and malrotation are more common in spiral diaphyseal injuries, which often require internal fixation after closed or open reduction (Fig. 16-9).

Intra-articular Basilar Fractures of Metacarpals Intra-articular basilar fractures, although unusual in the second through fourth metacarpals, may occasionally be seen in the fifth metacarpal bone.17 Similar to Bennett’s fracture, instability is a frequent consequence of the musculotendinous pull on the distal fragment proximally, and operative fixation is advised in most cases. A nondisplaced or impacted fracture, occurring less commonly, can be treated with immobilization.

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■ FIGURE 16-9 Oblique fracture of the metacarpal. Posteroanterior radiograph demonstrates oblique fractures of the third and fourth metacarpals.

Traumatic Injuries to the Proximal Phalanx Radiography Fractures of the proximal phalanx of the hand are very common types of fractures. In one series, 50% of fractures involved the thumb, in 25% the index finger was affected, and the rest of the cases were evenly distributed among the middle, ring, and little fingers (Fig. 16-10).18 Fractures of the proximal phalanx can be categorized into essentially four different categories: 1. Articular fractures of the head. These fractures may be partial or complete, involving either one or both condyles and can be extremely small. Articular fractures of the phalangeal head may also be nondisplaced and appear innocuous but can be unstable secondary to traction displacement of the fracture fragment by the collateral ligament.14 If unstable, treatment may require open reduction and wire, screw, or pin fixation to maintain alignment.10

■ FIGURE 16-10 Posteroanterior radiograph demonstrates transverse fractures of the bases of the third and fourth proximal phalanges. There is also an intra-articular fracture involving the fifth proximal phalanx.

2. Transverse fractures of the shaft or base. These fractures typically exhibit volar angulation. This position results from the deforming forces of the intrinsic muscles, which flex the proximal fragment, and from the extrinsic extensor muscles, which extend the distal fragment. These fractures are common, particularly in the fifth digit in the pediatric population.12 Proximal diaphyseal fractures are more easily managed compared with their distal counterparts because they are usually minimally displaced and are often impacted and stable. Treatment can usually be maintained with closed reduction. 3. Oblique fractures of the shaft. These fractures are usually associated with shortening and rotation of the digit.Often the degree of rotation is not obvious on radiographs and needs to be evaluated clinically. One particular type of

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fracture, a very long spiral fracture extending into the epiphyseal region, may engage the volar plate recess at the proximal interphalangeal joint space and produce a bony block with resultant impairment of flexion.8 4. Articular fractures of the base. An avulsion fracture may occur at the lateral margin of the base of the proximal or middle phalanx. This is the site of the attachment of the collateral ligament and is usually the result of severe abduction or adduction of the digit. The clinical diagnosis is suggested when point tenderness is elicited at the lateral margins of the joint. Collateral ligament injuries may sometimes occur without an accompanying fracture.19 Stress films can help demonstrate rupture of these ligaments because the joint will open under stress. Comminuted articular fractures are uncommon. The injury may or may not be stable, depending largely on the amount of articular surface involved and displacement of the fracture fragments.16

Traumatic Injury to the Middle Phalanx Radiography Injuries to the middle phalanx occur just as often as proximal phalangeal injuries, with one series of 924 fractures quoting injuries of the middle phalanx constituting 30% of all hand fractures.20 Fracture patterns in the middle phalanx are similar to those in the proximal phalanx and can be grouped into anatomic regions of head, neck, shaft, and base. It is the complexity of fractures at the base that separate proximal from middle phalangeal fractures. Tendon insertions play an important role in the angulation and deformation of fractures of the middle phalanx. The flexor digitorum superficialis maintains a long insertion along the volar lateral aspect of the middle phalanx from the proximal fourth to the distal fourth of the shaft. Fractures at the neck of the shaft will usually angulate the apex volarly as the proximal fragment is flexed by the flexor digitorum superficialis and the distal fragment is extended by the extensor terminal tendon. Fractures at the base will usually angulate the apex dorsally as the distal fragment is flexed by the flexor digitorum superficialis and the proximal fragment is extended by the central slip of the extensor mechanism, which is attached to the dorsal base of the shaft.10 Avulsion fractures at the base of the middle phalanx can be divided into partial articular fractures (volar base, dorsal base, lateral base) and complete articular (or “pilon”) fractures. The “pilon” fractures are one of the most functionally devastating and most technically difficult injuries to treat.10

Volar Base Fractures Avulsion fractures of the volar plate from the base of the middle phalanx are common. The mechanism of volar plate injury includes hyperextension and direct axial jamming of the finger.11 The lateral and oblique views offer the best views for evaluation of this injury (Fig. 16-11). The avulsed fragment is often minuscule and nondisplaced, resulting in the injury being frequently overlooked radiographically. Fractures at the volar base can be particularly unstable, especially with increase in the size of the avulsed

fragment. When the fragment comprises more than 40% of the articular surface, the fragment carries the majority of the proper collateral ligament insertion in addition to the accessory ligament and volar plate insertions. This leads to dorsal subluxation of the distal fragment and shaft secondary to the pull of the central extensor slip and flexor digitorum superficialis.10 The joint then hinges directly on the dorsal fracture margin of the shaft, destroying articular cartilage at the head of the proximal phalanx.

Dorsal Base Fractures Dorsal base fractures tend to occur much less commonly than volar base fractures. This injury involves the insertion of the central extensor tendon and can result in a boutonnière deformity. This deformity is characterized by flexion at the proximal interphalangeal joint and hyperextension at the distal interphalangeal joint. Rarely, these injuries may be associated with volar subluxation of the middle phalanx. Dorsal base fractures can usually be treated effectively by extension splinting.

Comminuted or “Pilon” Fractures of the Base Pilon fractures involve the volar and dorsal bases as well as a majority of the articular surface of the base of the middle phalanx (Fig. 16-12). These are the most functionally devastating injuries to the proximal interphalangeal joint, being highly unstable and refractory to standard surgical techniques. This type of fracture is often so comminuted that late degenerative joint arthrosis is inevitable. Treatment should be tailored to the patient and may include splinting, skeletal traction, or open reduction and internal fixation. Most middle phalangeal disorders are somewhat easier to treat than proximal phalanx fractures because rotational or angular deformities have less of a functional impact than a more proximally located deformity.14 The more distal position also enables easier access for reduction and percutaneous hardware.

Traumatic Injury to the Distal Phalanx Radiography Injury to the distal phalanx is extremely common because of its distal location. The true incidence of distal phalangeal fractures, however, is unknown because they are likely underreported. Distal phalangeal fractures can be classified into tuft fractures, shaft fractures, and intra-articular fractures. Tuft fractures usually occur secondary to a direct crush. These may be simple or comminuted. Fractures of the tuft are typically stable because the bone fragments are held in place by a fibrous network of pulp volarly and are distal enough to be free from the internal deforming forces of tendons. Closed fractures can be associated with a painful subungual hematoma, and decompression can provide pain relief. Nonunion of the fracture may occur but is rarely symptomatic.14 When the fractures involve displacement of the nail root, the fracture becomes an open fracture and there is a risk of development of an infection in the bone.21

■ FIGURE 16-11 Volar base fracture of the proximal interphalangeal joint. A, The diagram demonstrates dorsal subluxation of the distal fragment when the avulsed fragment is large enough to retain the proper collateral ligament. B, The lateral radiograph demonstrates a smaller nondisplaced volar base fracture without subluxation.

■ FIGURE 16-12 Pilon fracture seen on this lateral radiograph demonstrates markedly comminuted fracture at the base of the proximal interphalangeal joint. Given the involvement of the volar and dorsal base and majority of the articular surface, end-stage degenerative joint disease is inevitable.

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Shaft fractures are less common and can be divided into transverse and longitudinal fractures. Transverse fractures may be associated with displacement and angulation of the distal fragment. They are also associated with nail bed lacerations. These fractures are important because they are usually open injuries and require appropriate antibiotic treatment. Articular fractures can be classified into dorsal (mallet fractures), volar (profundus avulsions), and epiphyseal fractures in children.

Dorsal Base Fracture (Baseball or Mallet Finger) This type of injury tends to occur from an avulsion of the extensor tendon at its insertion on the dorsal surface of the base at the distal phalanx (Fig. 16-13). This was named mallet finger owing to the resultant flexion of the distal interphalangeal joint that made the finger look like a hammer or mallet in the lateral profile.3 The mechanism of injury is hyperflexion of the distal phalanx while the extensor tendon is taut. The injury may avulse the extensor tendon with its bony attachment, or just the tendon itself. Clinically, the patient is unable to extend the distal phalanx completely. Management is partially determined by the presence of subluxation or dislocation of the distal fragment.22 A bony dorsal attachment containing a significant

portion of bone (usually >25% of articular surface) will tend to demonstrate volar subluxation of the distal phalanx and is usually treated by operative fixation.10

Volar Base Fractures Volar base fractures tend to occur when the flexor digitorum profundus tendon is avulsed from its insertion at the volar surface at the base of the distal phalanx.3 This usually involves the ring finger and most commonly occurs when a football player attempts to tackle a ball carrier by grabbing his jersey. As the ball carrier attempts to pull away, the tendon is avulsed from its insertion. The resultant inability to flex the distal interphalangeal joint is the key in appreciating this diagnosis. Leddy proposed a classification of subcutaneous flexor digitorum profundus tendon avulsion into three types according to the form of avulsion.23 In type 1, the avulsed tendon end without a bone fragment has retracted into the palm; in type 2, the avulsed tendon end with possible bone flakes lies at the level of the proximal interphalangeal joint; and in type 3, because a larger fragment of bone has been avulsed at the flexor digitorum profundus tendon insertion, the tendon is unable to pass the A4 pulley and lies at the midshaft of the middle phalanx. Injuries to the flexor digitorum

■ FIGURE 16-13 Mallet finger. Diagram (A) and lateral radiograph (B) demonstrate avulsion at the attachment of the extensor tendon. The radiograph shows volar subluxation of the distal fragment.

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profundus tendon, with or without bony avulsion, usually require operative fixation.22

Epiphyseal Fractures These fractures result from hyperflexion and can be a Salter-Harris type I, II, or III fracture. Originally described by Seymour, whose name describes these kinds of fractures, the patient usually presents with a mallet deformity.24 The nail plate and nail matrix are displaced superficial to the proximal nail fold (Fig. 16-14). If not relocated, sepsis frequently occurs. The extensor terminal tendon is attached to the proximal epiphyseal fragment and the flexor digitorum profundus tendon is attached to the distal fragment, causing it to flex. Reduction may not be possible secondary to interposition of a proximally based flap of nail fold. Improper treatment may result in a foreshortened digit that has a limited range of motion.25

Dislocations Involving the Metacarpals Radiography The most common metacarpal dislocations are those involving the thumb and are the result of fracture-dislocations, such as Bennett’s and Rolando’s fracture. Pure dislocations of the thumb carpometacarpal joint can occur and typically occur dorsally and radially (Fig. 16-15). Carpometacarpal dislocations of the second through fifth metacarpals, although relatively rare, require the highest degree of vigilance regarding associated neurologic injury.10 Dorsal displacement is more common than palmar dislocations.14 Like fracture-dislocations of the thumb, fracture-dislocations of the remaining carpometacarpal joints are frequently unstable requiring operative intervention.22 These most commonly occur from a high-energy fracture-dislocation injury involving multiple bones of the distal carpal or proximal metacarpal bones.25

Dislocations of the Interphalangeal Joints Radiography Proximal Interphalangeal Joint The proximal interphalangeal joint is the most commonly dislocated joint in the body.21 Most dislocations occur in

■ FIGURE 16-14

Seymour fracture. Diagram demonstrates this type of Salter-Harris fracture, which presents as a mallet deformity but involves displacement of the nail bed and is prone to sepsis.

■ FIGURE 16-15 Thumb dislocation without fracture. Posteroanterior radiograph of the hand demonstrates dislocation of the first carpometacarpal joint typically occurring dorsally and radially.

a dorsal direction and there may be an associated avulsion fracture of the middle phalanx. Almost all are associated with rupture of the cartilaginous volar plate.22 As stated earlier, dorsal dislocation is the most common type and is usually the result of a hyperextension injury (Fig. 16-16). It is also known as coach’s finger, named for the inappropriate treatment given to a player by the coach after a dislocation. Small avulsion fractures from the insertion of the volar plate at the base of the middle phalanx may or may not be seen on initial radiographs. Even in the absence of a displaced volar lip fracture, there is always disruption of the volar cartilaginous plate and varying degrees of collateral ligament damage.19 Congruence on the lateral radiograph is important in diagnosing residual subluxation. The most significant complications are subsequent stiffness and unrecognized dorsal joint subluxation with subsequent arthrosis.14 Volar proximal interphalangeal joint dislocations are much less common than posterior dislocations. In volar dislocations, the central slip of the extensor mechanism is torn from its insertion on the dorsal surface at the base of the middle phalanx.3 The mechanism of injury is hyperflexion and may be accompanied by an avulsion fracture. A boutonnière deformity may be present at the time of initial examination or develop subsequently.16 Rotatory dislocation occurs as the head of the proximal phalanx passes between the central slip of the extensor tendon and the lateral band of the extensor tendon (Fig. 16-17).10 This prevents reduction of this type of dislocation. A true

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bility after reduction is great enough to warrant operative treatment. Delayed presentation (>3 weeks) of a subluxed joint may require open treatment to resect scar tissue.

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment

■ FIGURE 16-16 Dorsal dislocation of the proximal interphalangeal joint without fracture as seen on this lateral radiograph. This is one of the most common dislocations and is usually the result of hyperextension. A volar lip fracture may or may not be seen with this injury.

lateral film will demonstrate the proximal phalanx in an oblique profile compared with the remaining phalanges.

Distal Interphalangeal Joint Dislocations at the distal interphalangeal joint also tend to occur in the dorsal direction. Volar dislocation is rare. With dorsal dislocation, the volar plate is usually disrupted from its proximal attachment. Radiographs are important to exclude a bony avulsion of the extensor or flexor tendons at their insertion. Reduction of dorsal dislocations can be complicated by a number of anatomic circumstances, including a trapped volar plate or flexor digitorum profundus tendon.10 Postreduction radiographs may reveal widening of the joint space. Reduced dislocations that are stable can be treated conservatively, but it is possible that the degree of insta-

Treatment of finger fractures is usually nonoperative, but a few fractures require operative treatment. Management depends on three factors: (1) involvement of a joint surface; (2) stability versus instability of fracture pattern; and (3) presence of deformities, such as displacement, shortening, and rotation. To determine stability of a fracture, the pattern of the break on the radiograph is examined to predict if the fracture will tend to slip out of place on reduction or over a period of time. Rotational deformities can be evaluated clinically with the fingers flexed in the palm. In this position, the fingers should normally point toward the scaphoid. In addition, while the hand is making a fist, the fingers should line up parallel to each other. Crossing of the fingers is an indication that there may be a rotational deformity caused by the fracture. If either of the joint surfaces do not line up well, if the fracture is unstable, or if there is a deformity present that needs correction, surgery may be necessary to prevent adverse sequelae to the injured finger. Fractures that are stable, reducible, or intra-articular without significant instability can usually be treated with splints. These constitute the majority of fractures in the hands and metacarpals. Closed stable fractures should be reassessed within 7 to 10 days after injury to ensure maintenance of alignment. After 5 to 6 weeks the patient can resume all finger activities as tolerated.10

Surgical Treatment A small number of fractures require operative fixation to hold them in place. Fixation is achieved by the use of pins, screws, and plates. The indications for surgical treatment have been discussed with each specific fracture type. Fractures that undergo operative management usually have a slightly longer healing time and increased risk of infection. Most patients with operative treatment of fractures can resume all finger activities as tolerated in 6 to 8 weeks.10

■ FIGURE 16-17 Rotatory dislocation. Diagram demonstrates how the lateral band of the extensor tendon slips over the head of the proximal phalanx. A true lateral film will show an oblique profile of the proximal phalanx compared with the remaining bones.

CHAPTER

When the joint is dislocated, the ligaments and joint capsule surrounding the injured joint are torn. Sometimes, these ligaments do not heal adequately and surgery is occasionally needed to repair the injured structures. Most finger dislocations, however, can be treated with a simple splint. Once the joint has been reset into position, the finger is splinted to allow the ligaments and joint capsule to heal.10 The prognosis for most phalangeal fractures that are appropriately treated is excellent. Almost all patients will regain full function and be pain free with minimal to no residual problems.

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What the Referring Physician Needs to Know ■ ■

■ ■

Most finger fractures are stable and can be treated with closed reduction. Stability of a fracture is determined by predicting if the fracture will tend to slip out of place upon reduction or over a period of time. A small number of fractures will require operative fixation to hold them in place. The prognosis for most phalangeal fractures that are appropriately treated is excellent.

SUGGESTED READINGS Henry MH. Fractures and dislocations of the hand. In Bucholz R, Heckman JD, Court-Brown CM (eds). Rockwood and Green’s Fractures in Adults. Philadelphia, Lippincott Williams & Wilkins, 2001, p 791. Leggit JC, Meko CJ. Acute finger injuries: II. Fractures, dislocations, and thumb injuries. Am Fam Physician 2006; 73:839.

Rogers LF. The hand. In Rogers LF. Radiology of Skeletal Trauma, 3rd ed. Philadelphia, Churchill Livingstone/Harcourt Health Sciences, 2001. Wood MB, Berquist TH. The hand and wrist. In Berquist TH (ed). Imaging of Orthopedic Trauma. New York, Raven Press, 1992.

REFERENCES 1. Hove LM. Fractures of the hand: distribution and relative incidence. Scand J Plast Reconstr Surg 1993; 27:317–319. 2. Simpson D, McQueen MM. Acute sporting injuries to the hand and wrist in the general population. Scott Med J 2006; 51:25–26. 3. Rogers LF. The hand. In Rogers LF. Radiology of Skeletal Trauma, 3rd ed. Philadelphia, Churchill Livingstone/Harcourt Health Sciences, 2001. 4. Fisher MR, Rogers LF, Hendrix RW. Systematic approach to identifying fourth and fifth carpometacarpal joint dislocations. AJR Am J Roentgenol 1983; 140:319–324. 5. Brewerton DA. A tangential radiographic projection for demonstrating involvement of the metacarpal head in rheumatoid arthritis. Br J Radiol 1967; 40:233–234. 6. Burman M. Anteroposterior projection of the carpometacarpal joint of the thumb by the radial shift of the carpal tunnel view. J Bone Joint Surg 1958; 40:1156–1157. 7. Curtis DJ, Downey EF. A simple first metacarpophalangeal stress test. Radiology 1983; 148:855–856. 8. Hodgkinson DW, Nicholson DA, Stewart G, et al. Scaphoid fracture: a new method of assessment. Clin Radiol 1993; 48:398–401. 9. Hubner U, et al. Ultrasound in the diagnosis of fractures in children. J Bone Joint Surg Br 2000; 82:1170–1173. 10. Henry MH. Fractures and dislocations of the hand. In Bucholz R, Heckman JD, Court-Brown CM (eds). Rockwood and Green’s Fractures in Adults. Philadelphia, Lippincott Williams & Wilkins, 2001, p 791. 11. Dobyns JH, Linscheid RL, Beckenbaugh RD, et al. Fractures of the hand and wrist. In Flynn JE (ed). Hand Surgery. Baltimore, Williams & Wilkins, 1982. 12. Hunter TB, Peltier LF, Lund PJ. Radiologic history exhibit: musculoskeletal eponyms: who are those guys? Radiographics 2000; 20:819–836.

13. Gedda KO. Studies on Bennett’s fracture: anatomy, roentgenology, and therapy. Acta Chir Scand Suppl 1954; 193:1–114. 14. Wood MB, Berquist TH. The hand and wrist. In Berquist TH (ed). Imaging of Orthopedic Trauma. New York, Raven Press, 1992. 15. Stener B. Displacement of the ruptured ulnar collateral ligament of the metacarpophalangeal joint. J Bone Joint Surg Am 1962; 44:869–879. 16. Ruby LK. Common hand injuries in the athlete. Orthop Clin North Am 1980; 11:819–839. 17. Green DP, Rowland SA. Fractures and dislocations in the hand. In Rockwood CA Jr, Green DP (eds). Fractures in Adults, 2nd ed. Philadelphia, JB Lippincott, 1975. 18. Butt WB. Fractures of the hand. Can Med Assoc J 1962; 86:731–735. 19. Bailie DS, Benson LS, Marymont JV. Proximal interphalangeal joint injuries of the hand: I. Anatomy and diagnosis. Am J Orthop 1996; 25:474–477. 20. Ip WY. A prospective study of 924 digital fractures of the hand. Injury 1996; 27:279–285. 21. Leggit JC, Meko CJ. Acute finger injuries: II. Fractures, dislocations, and thumb injuries. Am Fam Physician 2006; 73:839. 22. Weeks PM. Acute Bone and Joint Injuries of the Hands and Wrist: A Clinical Guide to Management. St. Louis, CV Mosby, 1981. 23. Leddy JP, Packer JW: Avulsion of the profundus tendon insertion in athletes. J Hand Surg 1977; 2:66–69. 24. Seymour N. Juxta-epiphyseal fracture of the terminal phalanx of the finger. J Bone Joint Surg Br 1966; 48:347–349. 25. Stern PJ. Fractures of the metacarpals and phalanges. In Green DP, Hotchkiss RN, Pederson WC (eds). Green’s Operative Hand Surgery, 5th ed. Philadelphia, Churchill Livingstone, 2005.

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C H A P T E R

Soft Tissue Injuries of the Hand and Wrist Luis Cerezal, Eva Llopis, Ana Canga, Faustino Abascal, and Alejandro Rolón

Hand and wrist pain and restricted movement are common disabling complaints that may be caused by a broad spectrum of soft tissue disorders. These injuries may be the result of a single incident, such as falling on an outstretched hand, or the result of repeated overuse, such as in ongoing athletic or occupational activities. Diagnosis and management of soft tissue disorders of the hand and wrist represent some of the most clinically challenging musculoskeletal disorders. Clinically, they are usually nonspecific, and similar findings can be found among the different pathologic conditions in the wrist and hand, so accurate diagnosis is a key element of a successful treatment plan in patients who present with hand and wrist pain or dysfunction. Outcome may be improved by timely implementation of various treatment options. Recent advances in diagnostic imaging have led to an improved ability to establish a noninvasive anatomic diagnosis with imaging. In this chapter we review the pathology, clinical and radiologic manifestations, differential diagnosis, and therapeutic strategies for the soft tissue injuries of the hand and wrist. Emphasis is placed on the current role of crosssectional imaging for precise diagnosis and therapeutic planning.

ULNAR-SIDED IMPACTION SYNDROMES Ulnar wrist pain has often been equated with low back pain because of its insidious onset, vague and chronic nature, intermittent symptoms, and the frustration that it induces in patients. Ulnar wrist pain may frequently be caused by a broad spectrum of osseous or soft tissue disorders, including triangular fibrocartilage complex (TFCC) tears, distal radioulnar joint (DRUJ) arthritis and instability, lunotriquetral ligament disruption, Kienböck’s disease, pisotriquetral arthritis, extensor carpi ulnaris lesions, and ulnar-sided wrist impaction syndromes.1–3 366

Ulnar-sided wrist impaction syndromes constitute a group of pathologic entities that result from repetitive or acute forced impaction between the distal ulna and ulnar carpus or distal radius and surrounding soft tissues resulting in bone or soft tissue lesions.1,2 In an adequate clinical setting, conventional radiographic findings of anatomic variants or pathologic conditions of the ulnar wrist can suggest the diagnosis of a given ulnar-sided impaction syndrome. However, significant disease and incapacitating pain may be present despite minimal evidence from conventional radiography. Conventional MRI and MR arthrography allow earlier detection of the bone and soft tissue lesions present in the various ulnar-sided wrist impaction syndromes and may offer different treatment alternatives.1–3

KEY POINT S: ULNAR-SIDED I M PA C T I O N S Y N D R O M E S Ulnar-sided wrist impaction syndromes constitute a group of pathologic entities that result from repetitive or acute forced impaction between the distal ulna and ulnar carpus or distal radius and surrounding soft tissues resulting in bone or soft tissue lesions. ■ The diagnosis of ulnar-sided wrist impaction syndromes is based primarily on the patient’s clinical history and physical examination and is supported by radiographic evidence of morphologic variations or pathologic conditions of the ulnar wrist. ■ MRI and MR arthrography allow earlier detection of the bone and soft tissue lesions, such as chondral or subchondral lesions or synovitis present in the various ulnar-sided wrist impaction syndromes, aiding in surgical planning. ■

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TABLE 17-1 Classification of Ulnar-Sided Wrist Impaction

Syndromes 1 2 3 4 5

Ulnar impaction syndrome Ulnar impingement syndrome Ulnar styloid impaction syndrome Hamatolunate impaction syndrome Combined ulnar and ulnar styloid impaction syndrome

Ulnar-sided wrist impaction syndromes can be divided into five main categories (Table 17-1). The most common type, ulnar impaction syndrome,4–6 is discussed in Chapter 15.

Ulnar Impingement Syndrome Prevalence, Epidemiology, and Definitions Ulnar impingement syndrome is a painful condition caused by a shortened distal ulna that impinges on the distal radius proximal to the sigmoid notch. The terms ulnar impingement and ulnar impaction are often used interchangeably, but these syndromes are not only distinct but also mutually exclusive.1,2

Pathology A markedly shortened distal ulna most frequently results from any of the surgical procedures that involve resection of the distal ulna secondary to prior wrist trauma, rheumatoid arthritis, or correction of Madelung’s deformity. Ulna head resection (Bowers), fusion or resection of the distal ulna (Sauvé-Kapandji), hemiresection interposition arthroplasty (Watson), and several modifications of these procedures are some of the surgical techniques that may be complicated by the development of ulnar impingement (Fig. 17-1A). Less commonly, ulnar impingement may be present in de novo cases of ulnar-negative variance or premature fusion of the distal ulna secondary to epiphysiolysis (see Fig. 17-1B).1

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Shortening of the distal ulna causes approximation of the distal radial and ulnar ends due to the contraction of the extensor pollicis brevis, abductor pollicis longus, and pronator quadratus muscles and the effect of the interosseous membrane, with loss of the buttress of the DRUJ. This is known as radioulnar convergence and is rarely symptomatic, in contrast to ulnar impingement syndrome, in which distal radioulnar contact is evident and causes pain.1

Manifestations of the Disease Clinical manifestations of ulnar impingement syndrome can be similar to those of ulnar impaction syndrome. Typically, the patients experience pain on pronation and supination of the forearm and weakness on lifting even relatively light objects. Compression of the DRUJ on forearm rotation increases the symptoms or produces grating in affected patients and is very useful in identifying incongruity of the DRUJ. The clinical diagnosis is commonly missed because it is not specifically sought.1

Radiography Ulnar impingement can produce erosive and proliferative cortical changes along the ulnar margin of the distal radius proximal to the sigmoid notch level that appear as scalloping and bone hypertrophy on conventional radiographs (Fig. 17-2A).1 By the time such changes are seen, the condition has been present for many years. The stress-loaded radiologic view described by Lees and Scheker will confirm the diagnosis before erosive changes are visible showing the radioulnar convergence. A stress-loaded projection is performed by asking the patient to grip a cylindrical object 2 cm in diameter as firmly as possible with the shoulder adducted, the elbow flexed to 90 degrees, and the forearm in the position of neutral rotation. The radiograph is then taken with the beam aligned in the coronal plane with respect to the anatomic position.1

■ FIGURE 17-1 Cardinal features of ulnar impingement. A, Ulnar impingement syndrome secondary to distal ulnar resection: shortened ulna proximal to the sigmoid notch, scalloping of the distal radius, and radioulnar convergence (arrow). B, Ulnar impingement secondary to significant ulnar-negative variance or premature fusion of the distal ulna. Note the scalloping of the distal radius proximal to the sigmoid notch (arrows).

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■ FIGURE 17-2

Ulnar impingement. Patient was referred for distal forearm pain after a Darrach procedure that was performed 6 years earlier. A, Posteroanterior radiograph shows extensive distal ulnar excision, focal remodeling, distal radius sclerosis (arrowheads), and proliferative changes in the distal ulnar stump (arrow). B, Coronal T1-weighted image reveals focal remodeling and sclerosis at the distal radius proximal to the sigmoid notch (arrowheads). Note soft tissue thickening interposed between distal radius and ulnar stump (arrow).

Computed Tomography Computed tomography is the most valuable method for defining the osseous anatomy of the DRUJ. CT allows the evaluation of scalloping or proliferative changes along the ulnar margin of the distal radius proximal to the sigmoid notch level. However, CT is less sensitive for detecting associated effusion, chondral lesions, and soft tissue and bone marrow changes.

Nuclear Medicine Isotope bone scintigraphy is rarely necessary for the evaluation of this disorder. Bone scintigraphy may show increased uptake about the ulnar side of the distal radius and ulnar head.

Magnetic Resonance Imaging Magnetic resonance imaging is helpful for confirming the diagnosis before erosive changes are visible in conventional radiographs, showing subtle sclerosis and bone edema at the corresponding level of the radius and on the distal ulna (Fig. 17-3; see Fig. 17-2B). In advanced stages, scalloping and sclerosis along the ulnar margin of the distal radius cephalad to the sigmoid notch, sclerosis in the ulnar seat, and bony spurs or osteophytes on both margins are clearly visualized on MR images.1,2

Differential Diagnosis Diagnosis of ulnar impingement remains difficult and often delayed because symptoms and clinical findings are usually nonspecific and similar among the different pathologic conditions in the ulnar-sided wrist.1,2

■ FIGURE 17-3

Ulnar impingement. Coronal, fat-suppressed, T2-weighted MR image demonstrates negative ulnar variance and subtle radial remodeling (arrows).

Synopsis of Treatment Options The current surgical options include the use of ulnar head prostheses that stabilize the ulnar head stump and correct convergence instability. There are several available (e.g., Shecker, Herbert, Avanta, Eclypse prosthesis). Early reported results are good, but follow-up loosening, stem breakage, and “sinking” of the prosthesis into the

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radius have been acknowledged. Prevention (i.e., avoidance of ulnar head resection) currently seems to be the best available option.1

Ulnar Styloid Impaction Syndrome Prevalence, Epidemiology, and Definitions Ulnar styloid impaction syndrome is an under-recognized etiology of ulnar wrist pain caused by impaction between the ulnar styloid and the triquetrum bone and the surrounding soft tissues.1,2,7 It appears more often in wrists with ulnar-negative variance and results from repetitive or acute forced ulnar deviation and dorsiflexion of the wrist.

Anatomy Anatomic variations are common in the ulnar wrist, including supernumerary ossicles and morphologic variations of the ulnar styloid. The ulnar styloid process is a continuation of the prominent subcutaneous ridge of the shaft of the ulna, which projects distally toward the triquetral bone for a variable distance (3–6 mm) and with medial angulation exceeding 15 degrees. GarciaElias has developed a method of assessing the relative size of the ulnar styloid called the ulnar styloid process index (USPI). An excessively long ulnar styloid has a USPI greater than 0.21 ± 0.07 or an overall length greater than 6 mm, predisposing to an impaction syndrome (Fig. 17-4).1,7 Ulnar styloid impaction syndromes can be classified into four subtypes based on different morphologic or pathologic conditions of the ulnar styloid implicated in the etiology of this clinical entity. Morphologic variations include an elongated, radially deviated, or enlarged ulnar styloid process, and pathologic conditions include nonunion, malunion, or hypertrophy of the ulnar styloid process (Fig. 17-5; Table 17-2).1

Pathology An elongated ulnar styloid is the most common variant implicated in the development of ulnar styloid impaction syndrome. Another anatomic variant is an ulnar styloid process curved in the volar and radial directions, giving a “parrot-beaked” appearance, which reduces significantly the styloid-carpal distance. A pathologic sequence of events has been postulated in patients with ulnar styloid impaction syndrome with a long or radially deviated ulnar styloid. Single-event or repetitive impaction between the tip of the ulnar styloid process and the triquetral bone results in contusion, which leads to chondromalacia of the opposing articular surfaces, synovitis, and pain. If a single-event trauma is forceful enough, fracture of the dorsal triquetral bone (chip fracture) may occur. Impaction over a long period of time can lead to lunotriquetral instability (see Fig. 17-4).1 An enlarged ulnar styloid can be an anatomic variant or secondary to malunion of avulsion fracture at the fovea of the ulna. This ulnar styloid morphologic variation reduces the ulnar joint space, resulting in repetitive impaction between the ulnar styloid and the ulnar aspect

■ FIGURE 17-4 Diagram (coronal view) illustrates ulnar styloid impaction syndrome findings and ulnar styloid process index (USPI). Note chondromalacia of the dorsal aspect of the triquetral bone (short arrow) and styloid process (long arrow) and tear of the lunotriquetral ligament. USPI is calculated by subtracting the degree of ulnar variance (B) from the length of the ulnar styloid process (C) and dividing the difference by the transverse diameter of the ulnar head (A). USPI normal range is 0.21 ± 0.07.

of the lunate bone and the radial aspect of the triquetral bone. TFCC wear or perforation is frequently present.1 Ulnar styloid fractures occur commonly in association with distal radius fractures. Symptomatic nonunions of the ulnar styloid are probably under-recognized and/or underreported in the literature.Two types of nonunion of the ulnar styloid have been classically described on an anatomic basis and have different treatments. Type 1 is defined as a nonunion associated with a stable DRUJ. It affects only the tip of the styloid and the TFCC remains intact, since its major attachments are at the base of the styloid.Type 2 is defined as a nonunion associated with subluxation of the DRUJ. It is the result of an avulsion of the ulnar attachment of the TFCC (Palmer class IB lesion). Recent evidence has shown that this is an oversimplified subdivision, because although severely displaced basilar fractures of the ulnar styloid are more commonly associated with DRUJ instability,“chip” fractures can also be associated with instability if there is a concomitant TFCC injury.1 Ulnar styloid nonunion may become symptomatic for different reasons. The nonunited fragment may act as an irritative loose body or abut the carpus. A malaligned fibrous nonunion may cause impingement of the extensor carpi ulnaris tendon sheath. The nonunion may also be symptomatic because of associated TFCC perforation or, as stated earlier, due to complete rupture of the ulnar attachments of the TFCC and hence an unstable DRUJ.1

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■ FIGURE 17-5 Anatomic variants and pathologic process related to the ulnar styloid impaction syndrome. Plain radiographs show elongated ulnar styloid (A); radially deviated ulnar styloid (parrot-beaked) (B); enlarged ulnar styloid (C); type 1 ulnar styloid nonunion (tip of the styloid process) (D); and type 2 ulnar styloid nonunion (base of the styloid process) (E).

TABLE 17-2 Classification of Ulnar Styloid Impaction

Syndromes 1 2 3 4 4A 4B

Ulnar styloid impaction syndrome secondary to elongated ulnar styloid Ulnar styloid impaction syndrome secondary to radially deviated ulnar styloid (parrot-beaked) Ulnar styloid impaction syndrome secondary to enlarged ulnar styloid Ulnar styloid impaction syndrome secondary to ulnar styloid nonunion With a stable distal radioulnar joint. Nonunion of the ulnar styloid with intact triangular fibrocartilage complex ulnar attachment With distal radioulnar joint instability. Nonunion of the ulnar styloid with avulsion of the ulnar attachment of the triangular fibrocartilage complex

Manifestations of the Disease Radiography The diagnosis of ulnar styloid impaction syndrome is based primarily on the patient’s clinical history and physical examination and is supported by radiographic evi-

dence of morphologic variations or pathologic conditions of the ulnar styloid (see Fig. 17-5).1 The ulnar styloid architecture measurements (ulnar styloid length, angle, and width) and ulnar variance should be recorded in the neutral posteroanterior view of the wrist. In advanced stages, plain radiographs may reveal degenerative changes in the ulnar styloid and the triquetrum bone.

Ultrasonography Ultrasonography can reveal focal synovitis in the dorsocubital aspect of the radiocarpal joint adjacent to the dorsal surface of the triquetral bone.

Multidetector Computed Tomography Computed tomographic scans with 3D reconstructions allow an exquisite assessment of the osseous anatomic variants in the ulnar wrist that can be related to development of this clinical entity. CT is inaccurate for revealing early soft tissue and osseous changes associated with ulnar styloid impaction syndromes, such as chondromalacia, synovitis, and subchondral bone edema. In advanced stages, CT may reveal degenerative osseous changes in

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the ulnar styloid and the triquetrum bone, including subchondral sclerosis and cortical irregularities.

Nuclear Medicine Isotope bone scintigraphy is not usually performed. Radioisotope bone scans may reveal pronounced activity at the ulnar-sided wrist in symptomatic cases. If clinical and conventional radiographic findings are inadequate, then scintigraphy could help to confirm the diagnosis prior to surgery.

Magnetic Resonance Imaging Magnetic resonance imaging is the most useful imaging method for detecting the osseous and soft tissue abnormalities present in this syndrome and to rule out other potential causes of chronic ulnar wrist pain (Fig. 17-6).1,2 In patients with an ulnar styloid that is elongated or radially deviated MRI may show chondromalacia on the tip of the ulnar styloid and dorsal aspect of the triquetrum bone (see Fig. 17-6B). Secondary subchondral changes, including bone marrow edema, sclerosis, and cysts, in characteristic locations can be detected by MRI in patients without significant abnormalities on routine plain radiographs.1 The presence of synovitis and joint effusion in the ulnocarpal joint is also a common indirect sign of ulnar styloid impaction syndrome. In patients with an enlarged ulnar styloid the same findings can be seen in the ulnar aspect of the lunate, triquetrum, and ulnar styloid. MRI is helpful in the detection of degenerative fraying or tears of the TFCC, which are frequent findings in these patients.1

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In patients with ulnar styloid impaction syndrome secondary to nonunion of the ulnar styloid, MRI is an excellent modality for visualizing the integrity of the TFCC and its ulnar attachments, the presence of nonunited bone fragments, and the associated chondromalacia and subchondral bone changes of the carpus. Tenosynovitis or tendinosis of the extensor carpi ulnaris secondary to an irritative loose body can also be detected by MRI.1 MR arthrography is a useful tool in the preoperative evaluation of ulnar styloid impaction syndromes, allowing diagnosis of chondromalacia in the dorsal aspect of the triquetrum and ulnar styloid tip, accurate diagnosis of associated tears of the dorsocubital aspect of the TFCC, and detection of synovial thickening and synovitis in the dorsal capsular recess.1,3

Arthroscopy Arthroscopic findings may be divided into three stages. The early stage shows only synovitis in the dorsal capsular recess and dorsal aspect of the triquetrum. In stage II, the synovitis is marked on the dorsal capsular recess; there is denudement of the dorsal aspect of the triquetrum, and synovitis is evident in the vicinity of the midcarpal joint. In more advanced cases the tip of the styloid can be seen perforating the TFCC and the dorsal part of the triquetrum can be totally devoid of cartilage.

Differential Diagnosis From clinical data, ulnar styloid impaction syndrome should be differentiated from other causes of ulnar-sided

■ FIGURE 17-6 Ulnar styloid impaction syndrome. A, Coronal, fat-suppressed, T1-weighted MR image reveals an excessive long ulnar styloid process (arrow). B, Sagittal, fat-suppressed, T1-weighted MR image shows chondromalacia on the dorsal aspect of triquetral bone and small subchondral cysts (arrowhead).

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pain, including fundamentally other ulnar impaction syndromes, TFCC lesions, lunotriquetral instability, and a pathologic process of the extensor carpi ulnaris.

Synopsis of Treatment Options There is little room for conservative treatment for this disorder. Only in acute cases, triggered by trauma, does it seem reasonable to try conservative treatment (rest, splinting, and nonsteroidal anti-inflammatory drugs). Otherwise, the best approach is to assess the joint under arthroscopy, to débride synovitis in the dorsal capsule/ dorsal triquetrum, and to remove the styloid. Although in some cases the styloid can be resected arthroscopically, in most cases it is better done through a 1.5-cm ulnar incision. The styloid is removed subperiosteally, taking care to preserve 2 to 3 mm of its more proximal base, so as not to interfere with the foveal attachment of the TFCC.1

Hamatolunate Impaction Syndrome Prevalence, Epidemiology, and Definitions Hamatolunate impaction is an uncommon cause of ulnarsided wrist pain secondary to chondromalacia of the proximal pole of the hamate bone in patients with lunate bones that have a medial articular facet on the distal surface for articulation with the hamate bone (Fig. 17-7).1,8

Anatomy

■ FIGURE 17-7

Illustration of hamatolunate impaction syndrome, Viegas type II lunate bone, chondromalacia of the proximal pole of the hamate bone, and secondary subchondral changes (arrow).

Viegas described two different anatomic variations of the lunate bone: type 1, in which the lunate does not have an articular facet with the proximal pole of the hamate and type 2, in which an articulation exists between the lunate and hamate. Type 2 lunate bone is present in 57% to 73% of wrists.1,8

bone should raise the question of arthrosis at the proximal pole of the hamate as the most likely source of the complaint.1,8

Pathology

Computed tomography allows a precise evaluation of anatomy of the mediocarpal joint and the anatomic lunate variants described by Viegas. CT is not sensitive to the early changes of hamatolunate impaction syndrome such as chondromalacia and subchondral edema in the proximal pole of the hamate bone. In more advanced stage disease, CT shows characteristic findings, sclerosis, and subchondral cyst in the proximal pole of the hamate.

The anatomic variation of type 2 lunate bone produces alteration of the normal uniform loading and focally altered mechanics that leads to a higher incidence of cartilage erosion with exposed subchondral bone on the proximal pole of the hamate bone than in those without this articulation (type 1 lunate bone). The repeated impingement and abrasion of these two bones when the wrist is used in full ulnar deviation has been suggested as the mechanism that causes the chondromalacia.1,8

Manifestations of the Disease Patients experience pain in full ulnar deviation of the wrist, and it is by repeating this maneuver, especially when combined with first holding the distal carpal row in forced supination, that their pain can be reproduced.

Radiography The hamatolunate articulation is seen relatively frequently during arthroscopy of the midcarpal joint, but only about 40% of those articulations are evident radiologically. This facet is variable in size (from 1.2 to 12 mm) and may occupy between 10% and 50% of the distal aspect of the lunate. In the clinical setting of ulnar-sided wrist pain, the radiographic evidence of a type 2 lunate

Multidetector Computed Tomography

Nuclear Medicine Isotope bone scintigraphy may show nonspecific increased radiotracer uptake at the ulnar aspect of the midcarpal joint.

Magnetic Resonance Imaging Magnetic resonance imaging has low sensitivity for early stages of chondromalacia but can detect bone edema (Fig. 17-8), sclerosis, and subchondral cysts in the proximal pole of the hamate bone as secondary signs of chondromalacia and focal osteoarthritis.1,8 Midcarpal synovitis is a common indirect MR sign of hamatolunate impaction.

Arthroscopy The loss of cartilage on the tip of the hamate body is common in the type 2 variant and in itself is a finding without

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any clinical implication. However, when it is accompanied by clinical symptoms and midcarpal synovitis, the arthroscopy is diagnostic.

Differential Diagnosis Clinically, the differential diagnosis is extensive and includes the full spectrum of ulnar wrist pain.

Synopsis of Treatment Options Arthroscopic burring of the apex of the hamate bone through a midcarpal portal represents the state-of-the-art treatment for this condition because it relieves symptoms but does not adversely affect carpal mechanics.

What the Referring Physician Needs to Know: Ulnar-Sided Impaction Syndromes ■ ■

■

Which anatomic lesions cause this specific ulnar-sided wrist pain An understanding of the spectrum of lesions that may be associated: bone changes, cartilage injuries, extensor carpi ulnaris lesion, synovitis, and other degenerative changes An ability to differentiate between ulnar impaction syndrome and other lesions such as TFCC lesions, lunotriquetral instability, or extensor carpi ulnaris pathology that can also cause ulnar-sided pain

WRIST INSTABILITY Prevalence, Epidemiology, and Definitions Injuries to the intrinsic ligaments are frequently associated with extrinsic volar and dorsal ligament lesions and may often be a cause of chronic wrist pain and dysfunction. Intrinsic and extrinsic ligaments play an important role in wrist stability.9–13 Carpal instability concept has evolved considerably during recent years. Although traditionally, instability was considered synonymous with malalignment, not every alteration of carpal alignment is pathologic, and instability can be present without malalignment. Congenital hyperlaxity can be present with marked malalignment, is frequently asymptomatic, and does not usually require treatment.9 Some patients refer only to pain and a sensation of “giving way” when performing some specific task. Therefore, stability must be maintained statically and dynamically. In dynamic instability malalignment occurs only under certain loads, whereas in static instability it is permanent irrespective of the load applied. A biomechanically normal wrist must be able to transfer loads and perform a whole range of movements. Instability, or “carpal dysfunction,” implies the loss of normal wrist ability to transfer loads without sudden changes of stress on the articular cartilage (normal kinetics) and the capacity to move throughout the normal range without sudden alterations of intercarpal alignment (normal kinematics).9 Classically, four major types of carpal instability were recognized, always to be diagnosed by plain radiography.

■ FIGURE 17-8 Hamatolunate impaction syndrome. Coronal, fatsuppressed, T2-weighted MR image shows type II lunate bone with advanced chondromalacia in the proximal pole of the hamate bone, secondary subchondral sclerosis, and bone marrow edema (asterisk). The symptoms resolved completely after arthroscopic resection of the proximal pole of the hamate bone.

Dorsiflexed intercalated segment instability (DISI) when the lunate is an intercalated segment between the distal row and the abnormally extended forearm; volar-flexed intercalated segment instability (VISI) when the lunate appears abnormally flexed; ulnar translocation when the proximal row has an ulnar deviation relative to the radius; and dorsal translocation when the carpus is subluxed in a dorsal direction secondary to a malunited radial fracture.9

Anatomy Anatomy of the carpal ligaments is complex, with anatomic variations in ligament size and shape and confusing descriptions (Fig. 17-9). Wrist ligaments can be divided into intracapsular or intra-articular except for the transverse carpal ligament and the two distal connections of the pisiform to the hamate and the base of the fifth metacarpal, which are extracapsular. Intracapsular carpal ligaments connect individual carpal bones (“intrinsic ligaments”) or link carpal bones to the radius or ulna (“extrinsic ligaments”). Variation in the description of the volar and dorsal extrinsic ligaments is due to anatomic variation and because they consist of focal capsular thickening and are not discrete structures. The volar complex is stronger than the dorsal one and plays a predominant role in carpal stability. However, dorsal ligaments are more important for carpal instability and kinematics than previously thought.9–13 Volar extrinsic radiocarpal ligaments include the radioscaphocapitate, radiolunotriquetral or long radiolunate, radioscapholunate, and short radiolunate ligaments. Volar ulnocarpal ligaments comprise ulnolunate and ulnotriquetral ligaments; they originate at the volar edge of the TFCC and insert into the lunate and the triquetrum, respectively. The arcuate, or deltoid ligament,

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■ FIGURE 17-9 Anatomy of the extrinsic ligaments. A and B, Diagrams illustrating the extrinsic radiocarpal and ulnocarpal ligaments. DRC, dorsal radiocarpal ligament; DIC, dorsal intercarpal ligament; RA, radial arm of the deltoid ligament; RLT, radiolunotriquetral; RSC, radioscaphocapitate; SRL, short radiolunate ligaments; UA, ulnar arm of the deltoid ligament; UL, ulnolunate ligament; UT, ulnotriquetral ligament.

is a V-shaped volar intrinsic ligament with a capitotriquetral (ulnar) and a capitoscaphoid (radial) arm. The dorsal extrinsic radiocarpal ligament includes the dorsal radiotriquetral and dorsal intercarpal ligaments.9–13 Intrinsic ligaments—scapholunate and lunotriquetral— join proximal carpal bones and separate them from the radiocarpal and midcarpal compartments.

Pathology Many different conditions such as trauma, inflammation, infection, tumor, or congenital disease may result in an unstable wrist. The traumatic mechanism of injury for most carpal dislocations is a fall on the outstretched hand, causing wrist extension, ulnar deviation, and intercarpal supination.9 Mayfield’s progressive perilunate instability describes a sequential pattern of four-stage ligamentous injury. It starts on the radial aspect of the wrist and extends though the perilunate ligaments to end at the ulnar side. Stage 1 consists of a tear of the volar extrinsic radioscaphocapitate ligament with elongation or partial tearing of the scapholunate ligament. Continuous loading leads to complete failure of the scapholunate joint, stage 2, followed by failure of the radioscaphocapitate ligament or an avulsion fracture of the radial styloid. Stage 3 consists of separation of the triquetrum from the lunate with associated injury to the radiolunotriquetral ligament and dorsal radiocarpal ligament disruption. Finally, in stage 4 the ultimate failure of the dorsal radiocarpal ligament with volar lunate dislocation occurs.9

Classification Carpal instability is classified into four major patterns (Table 17-3): dissociative carpal instability (CID), nondissociative carpal instability (CIND), complex carpal instability (CIC), and adaptive carpal instability (CIA).9 CID implies injury to one of the major intrinsic ligaments, such as scapholunate and lunotriquetral dissociation or capitate-hamate axial disruptions. CIND connotes an injury to a major extrinsic ligament, with intact intrin-

TABLE 17-3 Classification of Carpal Instabilities 1 2 3 4

Dissociative carpal instability (CID) Nondissociative carpal instability (CIND) Complex carpal instability (CIC) Adaptive carpal instability (CIA)

sic ligaments such as occurs in radiocarpal instability or midcarpal instability. Not unusually, both CID and CIND may be found together, which is classified as CIC. Carpal instability not located within the wrist but proximal or distal to it is classified as adaptive carpal instability. The most common types of carpal instability are scapholunate and lunotriquetral dissociation.

Manifestations of the Disease Radiography Routine radiographic examination when carpal instability is suspected should include six views: posteroanterior, lateral, radial and ulnar deviation, and flexion and extension. Important information can be missed with poor quality films. Posteroanterior radiographs should be made with the patient’s shoulder abducted 90 degrees, elbow flexed 90 degrees, and forearm in neutral rotation. To obtain a true lateral view the wrist must be adducted to the patient’s side and be in neutral rotation. Dorsal surfaces of the metacarpals, radius, and ulna should be straight to demonstrate any possible alteration of the alignment of the carpal bones. Palmar surface of the pisiform should lie between and equidistant to palmar surfaces of the distal scaphoid tuberosity and the capitate head. On a posteroanterior view three normal carpal radiographic arcs (Gilula’s lines) must be smoothly drawn and between the bones there must be a separation of 2 mm or less (Fig. 17-10). Any disruption of this arc indicates intercarpal derangement; and overlap between carpal bones or cortices asymmetric with the contralateral wrist suggests carpal joint abnormality.9 A normal lunate exhib-

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projection of the neutral-positioned wrist, are ulnar variance, carpal height ratio, capitate-radius index, and ulnar translocation ratio. One must be aware of normal wide ranges for these parameters, the low reproducibility, and that small rotational positioning of the hand at the time of radiation exposure may result in substantial variation in angle determinations.

Fluoroscopy Fluoroscopic imaging is used occasionally to assist in the diagnosis of dynamic instability. Instability is assessed during active wrist motion and with provocative testing. Asynchronous motion between the wrist bones and interval gapping are indicative of a destabilizing injury.

Stress Views

■ FIGURE 17-10 Gilula’s arcs. Posteroanterior view of a normal wrist. Three smooth arcs normally outline proximal and distal cortical margins of the proximal carpal row and proximal carpal surfaces of the hamate and capitate. Broken arc, loss of parallelism, and widening or overlapping of normally parallel joint spaces are strongly suggestive of ligamentous, bone, or joint injury and necessitate further evaluation.

its a trapezoidal configuration; a triangular lunate shape implies a tilted lunate, but not necessarily dislocated. Lunate shape helps to differentiate whether it is flexed or extended; for example, there is a triangular shape in DISI but a moon-like configuration in VISI.

Additional Views When the initial radiographic evaluation of a patient with a suspected carpal dysfunction does not confirm the diagnosis and clinical suspicion exists, additional views are recommended. Their purpose is to evaluate specific areas of tenderness and swelling and to clarify subtle changes seen in the routine views. In the literature, many projections have been suggested.9 The following are the most commonly used: an anteroposterior (palm up) view with clenched fist; a posteroanterior (palm down) view with 10 degrees of tube angulation from the ulna toward the radius; an oblique view at 20 degrees pronation off the lateral position; an oblique view at 30 degrees supination off the lateral position; and a lateral view with the wrist radially deviated and carpal tunnel view.

Measurement of Carpal Bone Alignment Carpal malalignment has traditionally been measured on posteroanterior or lateral radiographs, with specific distances and angles. More frequently used angles— capitolunate, scapholunate, and radiolunate—are based on axes traced on lateral radiographs. The more commonly used distances, measured on a posteroanterior

In some instances, dynamic instabilities cannot be diagnosed with a motion series but require stressing a specific joint in different directions to see the abnormality. A fairly common technique for investigating midcarpal instabilities involves a dorsopalmar translation of the distal carpal row relative to the radius (“drawer test”). Less commonly used, yet productive in terms of discovering abnormal behavior of the radial column, are views of the wrist in maximal passive ulnar deviation.

Cineradiography or Fluoroscopy with Videotape Cineradiography or videotaping a fluoroscopic examination of the wrist provides considerable information in the evaluation of a patient who has a painful snapping or “clunking” wrist in whom routine and special views do not demonstrate an underlying pathologic process. These are patients in whom abnormal gap, a step-off from joint subluxation, appears only under certain loading conditions, appearing normal on plain films (including fist compression views). In these cases, cineradiography is recommended. Routinely, cineradiography includes observation of active movement from radial to ulnar deviation in both anteroposterior and posteroanterior views, flexion and extension in the lateral view, and radial and ulnar deviation in the lateral view. If the patient has a painful clunk, it is important for that to be reproduced during the examination.

Arthrography Three-compartmental wrist arthrography with injection of contrast material into the radiocarpal, midcarpal, and distal radioulnar joints has long been considered the gold standard study for carpal ligament injuries. The assumption that any intra-articular contrast flow from the radiocarpal space to the midcarpal or vice versa is pathologic has been demonstrated as an overstatement and has poor arthroscopic correlation, especially in older patients who have asymptomatic degenerative, often bilateral, perforations. However, CT arthrography or MR arthrography has a potential role.

Multidetector Computed Tomography Computed tomography with 3D reconstruction is useful for evaluating the alignment of the carpal bones. However,

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■ FIGURE 17-11 Lunate dislocation associated with transscaphoid fracture. Sagittal (A), axial (B), and reformatted 3D (C) CT images show volar lunate dislocation associated with transscaphoid fracture (arrow, B).

CT’s more important role is for the evaluation of fractures or fracture-dislocations frequently associated with carpal instability (Fig. 17-11).

Nuclear Medicine The use of bone scintigraphy is limited. It can be used as a screening test to focalize lesions and especially to exclude osteochondral abnormality in a patient with nonspecific tenderness.

Magnetic Resonance Imaging The role of MRI for evaluating carpal ligament injuries is evolving. Recent developments in MR technology such as multichannel phased-array coils and 3-T scanners could dramatically improve the diagnostic performance of MRI of both intrinsic and extrinsic ligament lesions. For optimal visualization of the intrinsic and extrinsic ligaments, a high field strength magnet, dedicated wrist coil, and thin image slices are required. Partial tears and elongated, but intact, ligaments may be visualized with MRI. Partial tear is seen as focal thinning, irregularity, or high signal intensity within a portion of the ligament. Complete tears of a carpal ligament appear as distinct areas of discontinuity within the ligament or complete absence of the ligament (Fig. 17-12). Joint fluid and focal synovitis are sensitive but nonspecific findings of ligament tears. In advanced cases, widening of the joint spaces may be evident.3

Magnetic Resonance Arthrography Magnetic resonance arthrography can potentially evaluate the precise location and magnitude of any proximal carpal row intrinsic ligamentous defect and differentiate those lesions that may involve only the central membranous portion. Those central lesions that may have a degenerative origin can be painful but not indicate instability. MR arthrography increases sensitivity over MRI, especially in subtle injuries. Partial tears may show contrast leak or imbibition into a portion of an injured ligament, and MR arthrography outlines better morphologic alterations or stretching. MR arthrography may also depict dysfunctional healed ligaments and detect peripheral ligament avulsions more accurately when the ligament has not lost its normal morphology. The latter may be evident clinically but difficult to document with conventional MRI. In complete tears, MR arthrography shows contrast material communication between carpal compartments. Dorsal and volar extrinsic ligament tears can be evaluated with MR arthrography, but its exact relevancy still has to be defined (Fig. 17-13).3,10–13

Arthroscopy Diagnostic arthroscopy of the wrist is actually the definitive diagnostic study for wrists with suspected carpal instability, including radiocarpal and midcarpal joint evaluation. The arthroscopic findings in carpal instabilities depend

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■ FIGURE 17-12

Traumatic volar lunate dislocation. Coronal (A) and sagittal (B) T1-weighted MR images show complete volar lunate dislocation (stage 4 perilunate instability) secondary to tear of the volar extrinsic radiocarpal ligaments and tear of the intrinsic scapholunate and lunotriquetral ligaments.

on the ligament involved: excessive movement among the bones and synovitis in the area are clues for diagnosis. Arthroscopy is very helpful for ruling out associated osteochondral injuries.

■

Differential Diagnosis The principal differential diagnosis of wrist instability is congenital wrist hyperlaxity. In such patients, marked carpal malalignment can be present despite minimal or complete absence of symptoms. These patients do not require surgical treatment.

A ■ FIGURE 17-13

What the Referring Physician Needs to Know: Wrist Instability

B

■ ■ ■ ■

The number and degree of intrinsic and extrinsic ligament lesions The patterns of carpal malalignment The presence of secondary degenerative changes The presence of associated fractures The differentiation from congenital wrist hyperlaxity

C

Traumatic ulnar translocation of the carpus. A, Conventional radiograph shows ulnar translocation of the carpus (arrow) and scapholunate interosseous widening (arrowhead). B and C, Coronal T1-weighted MR arthrogram images reveal rupture of the scapholunate ligament (arrow), tear of the central portion of the TFC (arrowhead), and complete rupture of the radiolunotriquetral and the radioscapholunate ligaments (asterisk).

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K E Y P O I N T S : W R I S T I N S TA B I L I T Y Intrinsic and extrinsic ligaments play an important role in wrist stability. Injuries to the intrinsic ligaments are frequently associated with extrinsic volar and dorsal ligament lesions and may often be a cause of chronic wrist pain and dysfunction. ■ Routine radiographic examination is the first step in diagnosis of carpal instability (static forms). ■ Stress views are important to detect dynamic forms of carpal instability. ■ CT allows a precise evaluation of fractures and fracturedislocation associated with carpal instability. ■ MR arthrography allows accurate diagnosis of the intrinsic and extrinsic ligament tears, thus aiding in the diagnosis and surgical planning and reducing the number of diagnostic arthroscopic interventions. ■

Synopsis of Treatment Options There is no single treatment for carpal instability. The treatment is based on six basic criteria: chronicity (healing potential of the ligaments involved); constancy (dynamic or static); etiology (traumatic, congenital, inflammatory); location (site of the major dysfunction); direction of the abnormal rotation and/or translocation of the carpal bones; and pattern of instability (CID, CIND, CIC, or CIA).9 Acute ligament injuries with complete intrinsic ligament rupture and overt dissociation should be treated as soon as possible because the ability to heal decreases rapidly. Repairs can become impossible after 6 weeks. Ligament reinsertion and repair is performed with transosseous stitching or mini bone anchors. Nonstabilizing acute injuries respond to simple immobilization for 4 to 6 weeks, if minor, but require percutaneous Kirschner wiring if the injury is moderate to severe. Chronic injuries are best currently managed through a tendon graft reconstruction of the ligament instead of arthrodesis, for which prognosis is poorer and the nonunion rate is higher.9

Anatomy The MCP joint of the thumb is a condylar-type articulation that allows motion primarily in the flexionextension axis and also some degree of rotation. The MCP joint of the thumb is stabilized by the radial and ulnar collateral ligaments, the volar plate, the extensor tendons and their dorsal reinforcements, the flexor tendon and sheaths including pulley systems, as well as the thenar muscles including the adductor pollicis muscle and its aponeurosis.

Pathology Injury to the ulnar collateral ligament is caused by hyperabduction of the MCP joint accompanied by varying degrees of hyperextension.3,6,14,15 It is often produced after a fall when skiing with the thumb or the pole planted into the snow. Rupture of the ulnar collateral ligament may be total or partial and usually takes place at its phalangeal point of insertion, but the rupture can also appear at its metacarpal insertion or in its midsubstance. It may be accompanied by an avulsion fracture of the proximal phalanx. The rupture of the thumb ulnar collateral ligament can be an isolated lesion or occur in combination with other joint structures, such as the volar plate or dorsal capsule.6,14,15 When the ligament ruptures distally, retraction may be associated with the interposition of the adductor pollicis aponeurosis with the torn ulnar collateral ligament lying superficially at the proximal end of the aponeurosis (Fig. 17-14). This injury, called a Stener lesion, precludes successful primary healing, resulting in long-term morbidity.3,6,14,15 Associated compromise of neighboring structures may produce loss of pinch and grasp strength. Ultimately, the injury may culminate in chronic pain and osteoarthritis.

LESIONS OF THE LIGAMENTS OF THE FINGERS Metacarpophalangeal Joint of the Thumb Prevalence, Epidemiology, and Definitions Injuries to the ulnar collateral ligament of the thumb metacarpophalangeal (MCP) joint are common in contact sports and skiing.3,6,14,15 This lesion was originally noted in Scottish gamekeepers who developed a chronic ligamentous strain or “gamekeeper’s thumb” induced by repetitive stress from the method used to kill rabbits. This type of injury is now most commonly associated with skiing and known as “skier’s thumb.”6,14,15 The injuries of the radial collateral ligament of the thumb MCP joint are much less common than ulnar collateral ligament injuries. They account for no more than 30% of all collateral ligament injuries.14

■ FIGURE 17-14 Illustration of a Stener lesion. Distal tear of the ulnar collateral ligament of the metacarpophalangeal joint of the thumb retracted and superficial to the adductor aponeurosis (arrow).

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The mechanism of injury of the radial collateral ligament of the thumb is forceful adduction of the thumb in any position. Disruption of the radial collateral ligament is prone to producing a rapid pathologic sequence of joint instability, with progressive ulnar and volar subluxation and, ultimately, degenerative joint disease.3,6,14

Manifestations of the Disease At physical examination, a complete ulnar collateral ligament tear induces the appearance of a palpable mass in the ulnar aspect of the joint and instability to radial stress, reaching an angle of 30 degrees or higher when compared with the contralateral thumb. Nevertheless, it may be difficult to differentiate between a nondisplaced ulnar collateral ligament tear and a Stener lesion in the acute setting because of overlying soft tissue edema and hematoma.3,6,14,15

Radiography Patients with a suspected ulnar collateral ligament injury should undergo radiographic evaluation (posteroanterior and lateral views) before stressing the joint, to rule out an associated avulsion fracture from the base of the proximal phalanx. Displaced avulsion fractures or any fracture involving 25% or more of the MCP joint surface requires surgical treatment and should not be manipulated. However, avulsion fragments are rarely seen on radiographs (12% of injuries). In the absence of an avulsion fracture, findings on plain films are usually normal. Degenerative joint changes may be seen years later after the initial insult or with chronic injury. A volar mild subluxation of the MCP joint in the lateral radiograph of the first digit suggests a tear involving the dorsal capsule and the volar plate, indicating probable ulnar collateral ligament rupture and instability.14,15 If a fracture has been ruled out, abduction stress views of the thumb are frequently required. More than 30 degrees of stressed radial deviation and more than 20 degrees of difference compared with the uninjured side indicate complete ligamentous disruption. However, results of such

■ FIGURE 17-15

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radiographs are often difficult to interpret. Furthermore, there is concern that stress tests may potentially be detrimental to patient care by transforming nonsurgical injuries into surgical ones. Categorization of the tears into surgical and nonsurgical abnormalities is crucial and cannot always be accomplished with radiography.

Ultrasonography Ultrasonography allows direct visualization of the collateral ligaments and their surrounding structures. It may allow accurate diagnosis of the complete spectrum of ulnar collateral ligament injuries, including distention, partial tear, complete tear, and Stener lesion.15 Furthermore, other disorders such as tenosynovitis, tendon tears, and articular pathologic conditions can involve the thumb and thenar region and may also be diagnosed with ultrasonography. A dynamic stress study can be performed (Fig. 17-15), but valgus and varus stress tests are not recommended owing to concern over aggravating an injury. Ultrasonography has proven to be a valuable aid to therapeutic approach.15 The positive predictive value for tears of the ulnar collateral ligament is higher with ultrasonography (94%) than with clinical examination (80%). The radial collateral ligament can be elongated, ruptured, or associated with bone avulsion. The ultrasound characteristics of tears of this ligament are similar to those of ulnar collateral ligament tears with the exception of complications such as Stener lesion, which do not occur because of anatomic differences.15

Multidetector Computed Tomography Computed tomography is not useful in isolated injuries of the collateral ligaments. CT is indicated in the case of complex fracture-dislocations of the MCP joint of the thumb to define the degree of comminution within a fracture as well as suspected impaction of the articular surface.

Tear of the ulnar collateral ligament of the thumb. A, Ultrasound image reveals complete tear of the ulnar collateral ligament of the thumb metacarpophalangeal joint. B, Dynamic examination with slightly valgus stress of the joint shows radial deviation with joint space widening.

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Magnetic Resonance Imaging Magnetic resonance imaging must assess the degree of rupture (partial or complete), displacement, and associated injuries (Fig. 17-16). Discontinuity, detachment, or thickening are primary MRI signs of acute rupture of the collateral ligaments; extravasation of joint fluid, joint effusion, and bone bruises are secondary signs.3,6 The distinction between partial and complete tear is important because it affects treatment options. If the ligament ruptures distally from the base of the proximal phalanx, retraction may be associated with interposition of the adductor pollicis aponeurosis (Stener lesion) and can inhibit proper healing. MRI findings of a Stener lesion include disruption of the ulnar collateral ligament from the base of the proximal phalanx with retraction or folding of the ligament. The ligament usually appears as a rounded or stump-like area of low signal intensity lying superficially to the adductor aponeurosis (Fig. 17-17). This characteristic MRI appearance has been described as a “yo-yo on a string.”3,6 In chronic tears, secondary MRI signs disappear and the ligament can show thickening, elongation, and an irregular or wavy contour. Although MR arthrography is accurate for determining the presence of ulnar collateral ligament ruptures and Stener lesions, the real value of MR arthrography lies in the detection of chronic ligament lesions. In this latter case, patients present with chronic pain and often joint instability.3

Differential Diagnosis Other conditions may mimic injury to the ulnar collateral ligament. These include dorsal hood tear, tendon tear, joint effusion, bone injury, and vascular injury.

■ FIGURE 17-17 Stener lesion. Coronal gradient-echo, T2-weighted image shows a torn ulnar collateral ligament (arrow), retracted and superficial to the adductor aponeurosis.

Synopsis of Treatment Options Medical Treatment Partial and stable nondisplaced tears of the ulnar collateral ligament are usually treated conservatively. In most patients, conservative treatment with a short-arm cast with a thumb spica gives good results.14

Surgical Treatment Surgical collateral ligament repair procedures are indicated in Stener lesions and complete undisplaced tears with laterolateral instability because conservative treatment leads to chronic instability and arthrosis. The radial ligament is more forgiving because the aponeurosis cannot be interposed. Both ligaments can be a source of severe limitation in chronic cases and respond very well to tendinous plasties. Avulsion fractures involving more than 20% of the articular surface may require pinning.14

Basal Joint of the Thumb Prevalence, Epidemiology, and Definitions

■ FIGURE 17-16 Complete tear of the ulnar collateral ligament of the metacarpophalangeal joint of the thumb. Coronal gradient-echo, T2weighted MR image shows a tear at the phalangeal insertion point of the ligament (arrow).

Injuries to the carpometacarpal (CMC) joint of the thumb are usually associated with fractures, with Bennett’s fracture being the most common. A two-part intra-articular fracture results with the volar ulnar fragment attached to the volar beak ligament, and the remaining metacarpal may be displaced or dislocated.16 The mechanism of injury is usually axial loading on a partially flexed thumb metacarpal, leading to dorsal dislocation of the joint. Thumb pain secondary to arthritis at the basal joint of the thumb is a common condition, especially in women,

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and can be quite disabling. Instability of the thumb basal joint is a major factor in the etiology of degenerative disease.

Anatomy The basal joint of the thumb consists of four trapezial articulations: the trapeziometacarpal, trapeziotrapezoid, scaphotrapezial, and trapezium-index metacarpal articulations.16 Its unique anatomic configuration allows arcs of movement in three planes to position the thumb for axial loads. The shallow saddle-joint architecture has little intrinsic osseous stability and must rely on static ligamentous constraints to limit metacarpal base translation during these movements. Clinically relevant anatomy around the basal joint includes the following: the palmar (anterior) oblique ligament, the dorsoradial ligament, the intermetacarpal ligament between the two first metacarpals, the adductor pollicis longus tendon, and the flexor carpi radialis tendon.16 The two primary joint stabilizers of the basal joint are the anterior oblique ligament and the dorsoradial ligament complex.16

Pathology Rupture of the anterior oblique and dorsoradial ligaments may cause symptomatic mechanical instability of the basal joint of the thumb, which may lead to osteoarthritis and interfere with the normal function of the hand.16

Manifestations of the Disease Patients with basal joint instability can be diagnosed with a high degree of certainty with careful physical examination. Patients may complain of pain and will note weakness of pinch.16

Radiography Radiographs of the thumb in three planes and the special basal joint stress view are helpful in confirming diagnosis. The standard views will rule out other osseous abnormalities and areas of arthritis. The basal joint stress view, when performed correctly, provides an excellent view of the basal joint articulations and is useful in assessing the degree of trapeziometacarpal joint subluxation. This posteroanterior 30-degree oblique view is centered on both thumbs and should include the area from the carpus to the fingertips. As the film is exposed, the patient is instructed to press the opposing thumb tips firmly together.16

Magnetic Resonance Imaging Magnetic resonance imaging is useful in the detection of acute ruptures of the basal joint ligaments. However, the value of MRI in chronic cases, when secondary MRI signs such as edema and extravasation of joint fluid disappear, is limited. MR arthrography is useful in the awareness of acute or chronic ruptures of the basal joint ligaments, especially the most significant one, the anterior oblique ligament. In acute ruptures, MR arthrography reveals

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stretching or discontinuity of the ligament with contrast medium extravasation. The most frequent findings in chronic rupture are elongation, thickening, and an irregular and wavy contour.3

Synopsis of Treatment Options In an acute setting, closed reduction with immobilization is an acceptable method of treatment if the joint is stable after the reduction. Otherwise, early ligamentous reconstruction is recommended to reduce the likelihood of secondary arthritis. Treatment of chronic basal joint instability is with ligament reconstruction.

Proximal Interphalangeal Joint Prevalence, Epidemiology, and Definitions The proximal interphalangeal (PIP) joint is the most commonly injured joint in the hand. Injuries to the PIP joint are very common in athletes, particularly those who participate in contact sports that require catching or hitting a ball, such as basketball, football, and volleyball. PIP ligament injuries include collateral ligament injuries and volar plate injuries. The radial collateral ligament is most frequently injured, usually from its proximal attachment. Most injuries are incomplete ruptures with minimal instability. However, complete ruptures and collateral ligament avulsions can also be seen. Distal volar plate injuries occur due to dorsiflexion and axial load stress. Ulnar fingers of the nondominant hand are usually affected. It occurs most frequently at the distal insertion on the middle phalanx. Much more uncommonly the volar plate is torn proximally in the membranous portion. Occasionally, fractures of the middle phalanx at the attachment of the volar plate occur.

Anatomy The PIP joint is a hinged joint with a bicondylar anatomy that allows a wide range of flexion and extension movements. The main stabilizers of the joint are the surrounding soft tissues, especially the collateral ligaments and the volar plate (Fig. 17-18). The extensor mechanism, flexor tendons, and retinacular ligaments play a major role in dynamic stability. The collateral ligament complex consists of the collateral ligament proper and an accessory collateral ligament. The former begins at the dorsolateral aspect of the head of the proximal phalanx and inserts at the volar and lateral aspects of the base of the middle phalanx. The latter starts from the same area but inserts at the volar plate. The proper collateral ligament is taut in flexion, whereas the accessory collateral ligament is taut in extension. The volar plate is a thick fibrocartilaginous structure that constitutes the palmar aspect of the PIP joint capsule. Distally, it is firmly attached to the volar lip of the base of the middle phalanx. Proximally, the attachment of the volar plate to the proximal phalanx is more elastic and is U-shaped owing to two lateral bands, which are called the “checkrein” ligaments. The volar plate prevents hyperextension of the PIP joint.

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■ FIGURE 17-18 Anatomy of the proximal interphalangeal joint. Drawing (lateral view) shows the accessory collateral ligament (ACL), extensor central slip (ECS), flexor tendons (FT), middle phalanx (MP), proper collateral ligament (PCL), proximal phalanx (PP), and volar plate (VP).

Pathology Two main mechanisms of dislocation are described in the origin of PIP ligament injuries: dorsal and lateral luxation.17 Lesions caused by hyperextension are the most frequent. These lesions include different degrees of dorsal articular displacement, which are divided into three types according to the degree of articular instability. In type I lesions, hyperextension results in avulsion of the volar plate from the base of the middle phalanx or, less frequently, from the proximal insertion point of the checkrein ligaments on the proximal phalanx. The natural evolution of distal disruption of the volar plate from the middle phalanx is hyperextension of the PIP joint, which causes a swanneck deformity due to articular instability. Conversely, the natural evolution of proximal disruption of the volar plate from the proximal phalanx causes a flexion deformity of the PIP joint, the so-called pseudoboutonnière deformity, with an intact extensor mechanism.17 Lateral dislocation occurs when an abducting or adducting force is applied to the PIP joint while the finger is extended. Three main injuries may occur: a ligamentous sprain with no loss of articular stability, a partial ligamentous tear with laterolateral articular instability, and a complete ligamentous rupture with major instability and articular luxation. The latter is usually associated with total or partial avulsion of the volar plate from the base of the middle phalanx.17

in case of complex fracture-dislocations of the PIP joint to define the degree of comminution within a fracture as well as suspected impaction of the articular surface.

Magnetic Resonance Imaging On MR images, normal collateral ligaments appear as sharply defined low-signal-intensity bands extending from the proximal phalanx to the middle phalanx. They are best visualized in the coronal projection. The volar plate is a low-signal-intensity structure that is best seen in a sagittal plane. MRI criteria for diagnosis of acute collateral ligament tears include discontinuity, detachment, or thickening of the ligament together with increased intraligamentous signal intensity on T2-weighted images, which is indicative of edema or hemorrhage. Obliteration of the fat planes around the ligament and extravasation of joint fluid into the adjacent soft tissues may also be observed. Chronic tears often demonstrate thickening of the ligament, which is probably secondary to scar formation. Thinning, elongation, or a wavy contour of the ligament may also be seen. MRI findings of injury to the volar plate include nonhomogeneous signal intensity on T1and T2-weighted images, together with thickening and contour irregularities (Fig. 17-19). Disrupted attachment with a gap is observed when avulsion of the volar plate takes place. MRI can rule out associated injuries to the soft tissue or tendinous or osseous structures.

Manifestations of the Disease

Synopsis of Treatment Options

The finger is painful and swollen around the PIP joint. It is necessary to explore the active and passive flexionextension. The lateral stability must be explored in extension (accessory collateral ligament and volar plate) and in flexion (proper collateral ligament).

Rarely, surgery is required even in complete ligamentous rupture. At the PIP joint the most common problem after trauma is stiffness, not instability, and for this reason if at all possible a short course of immobilization followed by protected motion is the preferred treatment. In severe cases, surgery is necessary to repair extensive damage to the collateral ligaments or volar plate. Surgery is also necessary to remove the volar plate if it becomes trapped in the joint and prevents realigning the joint without surgery.

Radiography Anteroposterior and lateral conventional radiographs should be performed in patients with suggested PIP injuries. Careful analysis of subtle findings is required to avoid neglected fractures than may lead to prolonged disability, pain, and stiffness.

Multidetector Computed Tomography Computed tomographic scans do not have utility in isolated injuries of the collateral ligaments. CT is indicated

Metacarpophalangeal Joint Prevalence, Epidemiology, and Definitions Collateral ligament injuries in the MCP joints of the fingers are rare compared with those of the thumb. The MCP joints are most susceptible to ulnar extension injury forces. Therefore, almost all finger collateral liga-

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KEY POINTS: LIGAMENT LESIONS OF THE FINGERS Radiographic evaluation (posteroanterior and lateral views) is essential to rule out associated fractures. ■ Ultrasonography allows effective diagnosis of finger traumatic injuries in acute cases. ■ CT allows precise evaluation of articular fractures, aiding surgical planning. ■ MRI is a powerful method for evaluating acute and chronic lesions of the stabilizing articular elements (volar plate and collateral ligaments) of the fingers and thumb. ■ MRI allows precise assessment of the degree of rupture (partial or complete), displacement, and associated injuries. ■

Anatomy

■ FIGURE 17-19 Volar plate lesions of the proximal interphalangeal (PIP) joint. A, Chronic distal volar plate avulsion of the PIP joint secondary to hyperextension mechanism. Sagittal gradient-echo, T2-weighted MR image shows focal discontinuity of the volar plate (arrow). B, Proximal disruption of the volar plate from the insertion point of the checkrein ligaments on the proximal phalanx. Sagittal gradient-echo, T2-weighted MR image reveals proximal rupture of the volar plate (arrow). Note flexion deformity of the PIP joint, the so-called pseudoboutonnière deformity, with an intact extensor mechanism.

Although the supporting structures of the MCP joint and PIP joint are similar, the bony anatomy of the unicondylar MCP joint allows significant radial and ulnar deviation and some rotation.18 The collateral ligaments of the MCP joint are taut in flexion and lax in extension, allowing abduction and adduction. The volar plate is an important stabilizer of this joint and is interconnected with the adjacent MCP joints by the deep transverse metacarpal (interglenoid) ligament. The extensor hood (particularly its sagittal bands), which stabilizes the extensor tendon at this level, also contributes to the stability of the joint (Fig. 17-20).

Manifestations of the Disease ment tears occur on the radial side. The most commonly involved digit is the index finger, followed by the little finger. On the ulnar side of the little finger, displacement of the torn ligament over the intact sagittal band of the extensor hood may occur, similar to the Stener lesion of the first MCP joint. One collateral ligament may be ruptured after the dislocation and secondarily to the lateral deviation, with the MCP joint in a flexion position. Intraarticular interposition of the ligament is also possible. The ligament may rupture in its midsubstance or be avulsed from either attachment, with or without a fragment bone.

Patients report pain and swelling in the affected joint and pain on gripping.

Radiography Plain films should be performed to rule out small avulsion fractures.

Magnetic Resonance Imaging Magnetic resonance imaging allows an accurate evaluation of MCP joint collateral ligament tears. The MRI findings of the collateral ligament injuries of the MCP joint are similar to those described for thumb MCP injuries.18

■ FIGURE 17-20 Anatomy of the metacarpophalangeal (MCP) joint. Lateral drawing shows the accessory collateral ligament (ACL), extensor digitorum communis tendon (EDC), flexor tendons (FT), metacarpal (MC), proper collateral ligament (PCL), proximal phalanx (PP), A1 pulley (PS), sagittal bands (SB), and volar plate (VP).

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What the Referring Physician Needs to Know: Ligament Lesions of the Fingers ■ ■ ■ ■ ■

To differentiate between partial and complete rupture of collateral ligaments or volar plate To evaluate the degree of ligament retraction To identify Stener lesion in tears of the UCL of the thumb To rule out bone avulsion fragments To depict associated injuries such as articular fractures or tendon lesions

Synopsis of Treatment Options Most collateral ligament injuries can be treated nonoperatively with casting. Chronic ulnar ligament injuries requiring repair have not been reported at the MCP joint.

EXTENSOR TENDON INJURIES Injuries to the extensor tendons of the fingers are common because they are thin and superficially located structures. Traumatic injury predominates in the fingers, whereas overuse type syndromes secondary to chronic repetitive microtrauma are the most common tendon pathology in the more proximal zones of the extensor apparatus.19–21

Anatomy Extensor tendons are organized into six different compartments, numbered from 1 to 6 from the radial to the ulnar side (Fig. 17-21). The extensor retinaculum anchors restrict their motion. They are lined by a synovial sheath, allowing them to glide easily within their respective compartments. Each extensor compartment contains one single tendon sheath.19,20 At the level of the MCP joint the extensor tendon is stabilized over the dorsum of the metacarpal head by the extensor hood. Distal to the MCP joint, the extrinsic and intrinsic tendons blend into the dorsal apparatus and are circumferentially distributed over the dorsum of the fingers. In the region of the proximal phalanx the extensor tendon divides into central and lateral bands or slips. The central slip inserts on the base of the middle phalanx, whereas the lateral slips merge with the intrinsic tendons

of the lumbricals and interosseous muscles to form the conjoined tendons. The conjoined tendons are located at the radial and ulnar aspect of the middle phalanx and converge distally to form the terminal tendon, which inserts on the dorsum of the base of the distal phalanx. Between the conjoint tendons, the triangular ligament keeps these structures in a position that is dorsal to the rotational axis of the PIP joint. In the context of this complex anatomy the Verdan classification system is a useful tool to provide a common language with orthopedic surgeons (Fig. 17-22) and to facilitate the localization of extensor tendon lesions. This system provides a topographic classification of zones of the extensor anatomy and includes the extrinsic extensor muscles (zones VIII-X), the wrist extensor compartments (zone VII), the dorsum of the hand (zone VI), the MCP level (zone V), the proximal phalanx (zone IV), the PIP level (zone III), the middle phalanx (zone II), and the DIP level (zone I).

First Extensor Compartment (de Quervain’s Disease) Prevalence, Epidemiology, and Definitions First extensor compartment (de Quervain’s) disease is characterized by tendinopathy and stenosing tenosynovitis affecting the abductor pollicis longus and the extensor pollicis brevis tendons and its sheath.19–21 De Quervain’s disease occurs more commonly in middle-aged women and may be bilateral in up to 30% of patients. Chronic shear microtrauma from repetitive gliding of the first dorsal compartment tendons over the radial styloid (zone VII) has been considered a predisposing factor for this process. Activities requiring forceful grasping coupled with ulnar deviation or repetitive use of the thumb predispose to this condition, which affects manual workers and enthusiasts of certain sports, such as golf, rowing, fishing, and racquet sports. Underlying subclinical conditions such as myxedema, gout, and rheumatoid arthritis may also be present. Anatomic variations include the presence of a septum separating the first extensor tendon compartment tendons, which occurs in up to 70% of cases requiring surgical release, and multiple abductor pollicis longus tendons or congenital absence of the extensor pollicis brevis.20

■ FIGURE 17-21 Cross-sectional diagram of the six extensor tendon compartments of the wrist. 1. Abductor pollicis longus and extensor pollicis brevis tendons. 2. Extensor carpi radialis longus and brevis tendons. 3. Extensor pollicis longus tendon. 4. Extensor digitorum tendons and extensor indicis tendon. 5. Extensor digiti minimi tendon. 6. Extensor carpi ulnaris tendon. LT, Lister tubercle.

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Manifestations of the Disease De Quervain’s disease has classic clinical findings: swelling at the radial styloid, tenderness proximal to the tip of the radial styloid, and a positive Finkelstein test (pain in the radial styloid when the thumb is flexed and adducted with an ulnar deviated wrist).

Ultrasonography Ultrasound findings include tendon sheath fluid, nodularity, and hypoechoic sheath thickening (Fig. 17-23A and B). The tendon itself is usually normal in echotexture, but it can appear thickened and hypoechoic. Hypervascular changes might be observed in the tendon or thickened synovium with color Doppler ultrasonography. Dynamic ultrasound examination can reveal abnormal tendon gliding and focal thickening.22,23

Magnetic Resonance Imaging Tenosynovitis is seen as fluid signal on T2-weighted sequences within the tendon sheath as well as surrounding soft tissue edema with loss of adjacent fat planes (see Fig. 17-23C and D). Tendinosis represents a more advanced overuse injury manifested as an enlarged tendon with internal increased signal intensity. Increased signal intensity within the tendon substance as an isolated sign is an unreliable sign of de Quervain’s disease. Stenosing tenosynovitis appears as an intermediate-signal-intensity rind surrounding the tendons in both T1- and T2-weighted images.19,20

Differential Diagnosis The differential diagnosis includes infectious tenosynovitis of the first extensor compartment, first carpometacarpal joint osteoarthritis, scaphotrapezial joint osteoarthritis, flexor carpi radialis tenosynovitis, intersection syndrome, and isolated neuritis of the superficial radial nerve (Wartenberg’s syndrome).20

Synopsis of Treatment Options Medical Treatment Conservative treatment includes applying a thumb spica splint and injection of corticosteroids into the sheath.

Surgical Treatment The aim of surgery is to decompress the first extensor compartment by longitudinally opening the tendon sheath through the central aspect of the compartment roof and freeing the tendons concerned. The superficial radial nerve branches must be identified and rerouted away from the first compartment tendon sheath if necessary.

Second Extensor Compartment (Intersection Syndrome) Prevalence, Epidemiology, and Definitions ■ FIGURE 17-22

Extensor tendons of the wrist. Illustration of zones for extensor surgical repair (I-IX).

Intersection syndrome is a focal inflammatory process affecting the second extensor compartment tendons, at the point where they cross the first extensor compartment,

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■ FIGURE 17-23 De Quervain’s tenosynovitis. Longitudinal (A) and axial (B) ultrasound images and coronal (C) and axial (D) T1-weighted MR images demonstrate thickening and synovial enlarged sheath of the first extensor compartment tendons (arrows).

4 to 8 cm proximal to Lister’s tubercle (junction of zones VII and VIII).20,21,24 This is most commonly an overuse syndrome secondary to repetitive microtrauma from friction. It is therefore frequently seen in racquet sports, weight training, rowing, canoeing, and other activities requiring repetitive wrist extension.21 Entrapment of the extensor carpi radialis longus and extensor carpi radialis brevis tendons resulting from tendon sheath stenosis has also been identified as a causative factor.

chronic stenosing tenosynovitis or an adventitious bursa may develop.

Pathology

Ultrasonography and MRI can demonstrate peritendinous edema, tendon thickening, fluid within a tendon sheath, and an adventitial bursa surrounding the intersection of the first and second extensor compartments in the distal forearm (Fig. 17-24). After the administration of intrave-

Inflammatory peritendinitis occurs in the crossing point between the first and second extensor compartments. It can have associated acute tenosynovitis or be accompanied by

Manifestations of the Disease Pain, swelling, and crepitus described as a squeak may be appreciated with wrist motion or direct palpation (squeaker’s wrist).20,21,24

Ultrasonography and Magnetic Resonance Imaging

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■ FIGURE 17-24 Intersection syndrome. Axial ultrasound image (A) and axial fat-suppressed, T2-weighted MR image (B) show peritendinous edema and small amount of fluid within the tendon sheaths in the crossing intersection point between the first and second dorsal extensor tendon compartments (arrows).

nous gadolinium, peritendinous enhancement has been described.20,24

Differential Diagnosis The main differential diagnosis is de Quervain’s disease, but it is usually more distally located, thus helping to differentiate the two.

Synopsis of Treatment Options Medical Treatment Conservative treatment includes rest, nonsteroidal antiinflammatory medications, and splinting.

Surgical Treatment Surgical measures such as tenosynovectomy and fasciotomy of the abductor pollicis longus are reserved for patients who are unresponsive to therapy.

Third Extensor Compartment Prevalence, Epidemiology, and Definitions Extensor pollicis longus tenosynovitis and rupture are often a complication of nondisplaced fracture of the distal radius. Causes of extensor pollicis longus rupture include mechanical attrition at Lister’s tubercle and vascular impairment leading to delayed rupture, most often distal to the extensor retinaculum.20,25 Extensor pollicis longus ruptures develop more commonly between 3 weeks and 3 months after injury. Other etiologic conditions of rupture of this tendon include synovitis associated with rheumatoid arthritis, local or systemic use of corticosteroids, blunt trauma, stab wounds, and surgical iatrogenic cause. Inflammation may also arise as a result of anatomic variants such as an accessory extensor pollicis longus muscle within the third extensor compartment.

Manifestations of the Disease On physical examination, if the hand is placed flat on a table the patient is unable to raise the thumb in line with the second metacarpal.

Ultrasonography and Magnetic Resonance Imaging Fluid within the tendon sheath indicates tenosynovitis; associated intratendinous changes on Doppler imaging might be present. In chronic stenosing tenosynovitis, hypoechoic thickening or scar tissue of the extensor pollicis longus can be seen.20,22 In ruptured tendons it is important to identify the torn tendon ends and to measure the tendon gap, because this can minimize the length of surgical incision. Because of the obliquity of the tendon, axial or transverse sections are the most suitable for identifying the torn tendon edges. In acute cases, fluid will help to outline torn tendon edges. However, chronic tears often have scar tissue filling the tendon gap, which obscures the torn ends.20

Synopsis of Treatment Options Treatment options include direct repair, free palmaris longus tendon graft, and tendon transfer using extensor indicis tendon. In patients with underlying rheumatoid arthritis, tendon repair should be avoided if the articular surfaces are severely damaged and arthrodesis might be indicated.

Fourth and Fifth Extensor Compartments: Lacerations The extensor tendons are particularly prone to injury from laceration in open wounds due to their superficial location and predominate at the levels of the middle phalanx (zone II), the proximal phalanx (zone IV), the MCP (zone V), and the dorsum of the hand (zone VI).20 At the level of the middle phalanx (zone II), the conjoined tendons are located on radial and ulnar positions

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around the middle phalanx; therefore, a simple laceration rarely transects the entire extensor apparatus. Injuries at the level of the proximal phalanx (zone IV) are usually partial as the extensor apparatus is circumferentially distributed over the dorsum of the finger. Lesions at the MCP joint (zone V) are almost always open and are commonly secondary to a human bite. At the dorsum of the hand (zone VI), the extensor tendons are very superficial. An apparently trivial skin injury may result in the laceration of one or more tendons. Single or partial lacerations may not result in the loss of extension at the MCP on physical examination due to the duplication of tendons and the presence of intertendinous connections. For this very reason, imaging interpretation of tendon lesions can be challenging. Total laceration of extensor apparatus does not usually show significant retraction due to the extensive continuous soft tissue network in this region. The extensive vascularization of the extensor apparatus predisposes to formation of adhesions from the injured tendon to adjacent tissues, such as bone or the underlying joint. These adhesions may induce important functional impairment and deformities.20

Manifestations of the Disease Ultrasonography and Magnetic Resonance Imaging Combination of sagittal and axial images allows identification of focal areas of partial or complete discontinuity and, thus, tendon integrity. Characterization of the margins of the tendon lesion, which are sharp and linear in the case of laceration, the presence of an adjacent soft tissue, and the quality of the tendon should be described.20 Diagnosis of a partial-thickness tear with MRI is based on the presence of focal areas of increased signal intensity on T1-weighted (and sometimes T2-weighted) images within a portion of the tendon. Complete tendon laceration appears as an area of discontinuity with fraying and irregularities at both ends. Acute lacerations show intermediate signal intensity on T1-weighted images and high signal intensity on T2-weighted images within the gap due to edema and hemorrhage. MRI may show the presence of adhesions as an area of blurring at the margins of

the tendinous surface in association with abnormal signal intensity in the surrounding fat, together with distortion of the normal anatomy of the tendon.20 Open wounds secondary to metallic devices have artifacts with signal void areas.

Synopsis of Treatment Options The treatment of choice is tendinous surgical suturing. An injury involving less than 50% of tendon width is given conservative treatment but one greater than 50% requires primary repair.

Mallet Finger Prevalence, Epidemiology, and Definitions Injuries at zone I disrupt the terminal extensor attachment at the base of distal phalanx, so-called mallet finger, drop finger, or baseball finger.25,26 It may be the result of laceration, but it is most commonly a closed injury due to forced flexion of the distal interphalangeal (DIP) joint in an extended digit. It can also result from a direct blow to the dorsum of the distal DIP joint or secondary to a hyperextension force applied at the joint. With this mechanism of injury, structural failure may occur within the tendon, which is manifested by rupture at the osseous attachment with an avulsed bone fragment at the tendon insertion site.25,26 If left untreated, a mallet deformity will frequently progress to a swan-neck deformity. This is the result of a flexion deformity of the DIP joint together with hyperextension of the PIP joint, which is caused by retraction of the extensor mechanism.25,26

Manifestations of the Disease Diagnosis of a mallet finger is relatively uncomplicated. Patients experience pain and swelling at the dorsum of the DIP joint and cannot extend the joint.

Radiography Plain radiographs should be performed to rule out avulsion fractures of the distal phalanx (Fig. 17-25A).

■ FIGURE 17-25 Rupture of the conjoint tendon (mallet finger). A, Lateral plain radiograph shows avulsion of a bone fragment of the distal phalanx (arrow). B, Longitudinal ultrasound image shows a complete laceration of the conjoint tendon at its distal insertion on the base of the distal phalanx (arrow).

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Ultrasonography and Magnetic Resonance Imaging On MRI, the sagittal and axial planes are the most helpful for evaluating the course, quality, and integrity of the extensor tendon attachments. The diagnosis is made on the basis of discontinuity of the tendon proper or identification of the osseous avulsion injury (Figs. 17-25B and 17-26A).20

Synopsis of Treatment Options At present, the treatment most commonly used is closed splinting with the DIP joint in extension. Surgical treatment is reserved for displaced avulsion fractures of the distal phalanx.

Boutonnière Deformity Prevalence, Epidemiology, and Definitions The boutonnière injury refers to rupture of the central slip of the extensor mechanism at its insertion into the base of the middle phalanx.20,25 Injury results from direct trauma to the dorsum of the PIP joint, an acute flexion force at the DIP, or, more commonly, following lateral volar dislocation of the PIP joint that damages the central slip and collateral ligament. Less frequently, a boutonnière deformity is associated with a fracture of the central slip attachment. In the early acute phase, the clinical findings may be misleading because the lateral bands may still be in their

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proper anatomic position and still extend the PIP joint. Initial findings include pain and swelling of the PIP joint, a mild extension lag, and reduced extension strength against resistance. If the injury goes unrecognized (more than 7–14 days), the lateral bands move volarly to the axis of rotation of the PIP joint. This induces flexion of the PIP joint and an increase in the force on the intact terminal extensor insertion, with subsequent extension of the DIP joint. The head of the proximal phalanx can be displaced through the defect at the level of the extensor apparatus.20

Manifestations of the Disease In boutonnière deformity, the patient maintains the ability to passively extend the joint. This preservation of passive extension distinguishes boutonnière deformity from pseudoboutonnière deformity.20,25

Magnetic Resonance Imaging As in the case of mallet finger, MR images may detect lesions of the central slip and tears of the central extensor tendon (see Fig. 17-26B). MRI is helpful, especially during the acute phase, when the clinical diagnosis is not unequivocal. MRI can provide useful information about associated volar plate and capsular and ligamentous lesions of the PIP joint.20

■ FIGURE 17-26 Injuries to the extensor mechanism of the finger. A, Sagittal gradient-echo, T2-weighted MR image shows a complete laceration of the conjoint tendon at its distal insertion on the base of the distal phalanx (arrow) (mallet finger). B, Sagittal gradient-echo, T2-weighted MR image shows a laceration of the central slip at its insertion on the base of the middle phalanx (arrow). C, Sagittal gradient-echo, T2-weighted MR image shows an acute tear of the radial sagittal band (arrow) with ulnar subluxation of the extensor digitorum communis tendon.

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Synopsis of Treatment Options Medical Treatment

Sixth Extensor Compartment Prevalence, Epidemiology, and Definitions

Extension splinting of the PIP joint is the treatment of choice for acute boutonnière deformity.

Extensor carpi ulnaris tendinopathy is common, second only to de Quervain’s disease. The spectrum of injuries of this tendon includes tenosynovitis, subluxation, dislocation, and tendon tear (Fig. 17-27).27 Subluxation of the extensor carpi ulnaris results from rupture or attenuation of the subsheath, usually due to a sudden volar flexion ulnar deviation stress. It has been reported in sports such as tennis, golf, baseball, and weightlifting. Extensor carpi ulnaris tendon instability is frequently associated with tenosynovitis. Dislocation of the extensor carpi ulnaris tendon may develop as a result of recurrent instability, distal radial fractures with disruption of the extensor retinaculum, and post-traumatic or rheumatoid arthritis–related distal radioulnar subluxation. Closed, nonrheumatoid ruptures of the extensor carpi ulnaris tendon are rare. Partial tears are more frequent and result from chronic attrition of the tendon in patients with underlying instability or chronic stenosing tenosynovitis (Fig. 17-28).27

Surgical Treatment Surgical intervention is required when soft tissue interposition prevents congruent reduction after dislocation of the PIP joint or when a large displaced bone fragment is present. Surgical reconstruction is the treatment of choice for chronic symptomatic cases.25

Metacarpophalangeal (Zone V) Subluxation or Dislocation Prevalence, Epidemiology, and Definitions The extensor hood of the finger MCP joint is composed of a longitudinal central tendon, extensor digitorum communis, and transverse peripheral fibers (sagittal bands) that insert into the central tendon and arise from the transverse intermetacarpal ligaments and volar plate. Injury to this structure may occur due to repetitive direct trauma to the knuckle, such as with boxing, or from a laterally directed force that ruptures the sagittal band.25 Any of the fingers can be affected, although the most common is the long finger, since it is more prominent. Depending on the degree of initial trauma and its repetitiveness, the spectrum of injuries varies from tears of ulnar or radial side sagittal bands to longitudinal central tendon tears. If an excessive force causes extreme flexion and ulnar deviation of the joint, complete rupture of the radial sagittal band with ulnar dislocation of the central tendon occurs; radial subluxation is unusual.20,25

Manifestations of the Disease Clinically, the patient has pain and swelling over the MCP joint and is unable to extend the MCP joint completely. In chronic untreated cases, the patient reports multiple episodes of pain and swelling over the MCP joint with a snapping sensation in the finger.25

Magnetic Resonance Imaging Magnetic resonance imaging allows direct assessment of the position of the tendon relative to the metacarpal head. Subluxation and dislocation are best depicted on axial images with active flexion of the MCP joints. MRI is also useful in evaluation of extensor hood injuries. In acute cases, the findings include morphologic and signal intensity abnormalities within and around the extensor hood components (particularly the sagittal bands) on axial T1- and T2-weighted images, together with poor definition, focal discontinuity, and focal thickening (see Fig. 17-26C).20

Synopsis of Treatment Options If the injury is in its acute phase, conservative treatment with splinting of the MCP joint in extension is recommended. Surgical correction is necessary in chronic symptomatic cases.25

Pathology Isolated extensor carpi ulnaris lesions are rare, and associated triangular fibrocartilage complex tears and lunotriquetral ligament tears are frequently found, as are other pathologic processes, such as an anomalous tendon slip, an ulnar styloid nonunion, or a flat tendon groove.27

Manifestations of the Disease Extensor carpi ulnaris tendinopathy is manifested as pain and swelling just distal to the ulnar head, exacerbated by resisted wrist extension.27 When subluxation or dislocation is symptomatic, the patient usually complains of a painful snap over the dorsoulnar aspect of the wrist when the forearm supinates and wrist ulnarly deviates, and the subluxation can be visibly palpated and observed.27

Ultrasonography and Magnetic Resonance Imaging Characteristic features of tenosynovitis include thickening of the tendon sheath, tenosynovial effusion, and peritendinous inflammatory changes. Chronic stenosing tenosynovitis with adhesions are seen on MRI as peritendinous low signal intensity and an irregular margin from scarring (Fig. 17-29).20 Dislocation or subluxation of the extensor carpi ulnaris can be detected in dynamic MRI studies with forearm rotation.

Synopsis of Treatment Options If the injury is in its acute phase, conservative treatment with splinting is recommended. Surgical treatment is necessary in chronic symptomatic cases.27

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■ FIGURE 17-27

■ FIGURE 17-28

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Illustration of the spectrum of pathology of the extensor carpi ulnaris tendon.

Partial tear of the extensor carpi ulnaris tendon. A and B, Axial, fat-suppressed, T2-weighted MR images show partial tear with associated tendon sheath distention (arrows).

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■ FIGURE 17-29 Extensor carpi ulnaris subluxation. Axial, fatsuppressed, T2-weighted MR image reveals rupture of the subsheath and ulnar subluxation of the extensor carpi ulnaris tendon (arrow).

FLEXOR TENDON INJURIES Injuries to the flexor tendons (Fig. 17-30) are not as common as injuries to the extensor apparatus. As with extensor tendon injuries, we can divide the flexor tendon lesions with respect to lesion location or subdivide them into open or closed injuries.19,21 Flexor tendon ruptures are classified on the basis of location, according to the system of the International Committee on Tendon Injuries (Fig. 17-31). Zone I extends from the distal insertion of the flexor digitorum profundus tendon to the distal insertion of the flexor digitorum superficialis tendon. Zone II extends from the distal insertion of the flexor digitorum profundus tendon to the distal palmar fold. At this level, the flexor digitorum profundus and flexor digitorum superficialis course together in the narrow fibro-osseous digital canal. Zone III extends from the proximal part of the A1 pulley to the distal part of the flexor retinaculum. At this level, the lumbrical muscles insert on the flexor digitorum profundus tendons. Zone IV is the carpal tunnel. Zone V is the forearm proximal to the flexor retinaculum. The thumb has three separate zones: TI extends from the A2 pulley to the flexor pollicis longus tendon insertion, TII extends between the A1 and A2 pulleys, and TIII extends between the distal wrist crease and the A1 pulley.

Open Injuries Flexor tendon lacerations associated with skin wounds are more common than closed traumatic ruptures. In the major-

■ FIGURE 17-31

Illustration of the flexor tendon sheaths and zones of injury in the hand and wrist.

ity of cases, these types of lesions affect the midsubstance of the tendon rather than sites of osseous attachment.19,21 Zone I injuries are isolated lacerations of the flexor digitorum profundus and manifest clinically as loss of active flexion of the distal phalanx. Trauma to the four proximal zones implies lesions of both flexor digitorum superficialis and flexor digitorum profundus with resultant loss of active flexion of both the PIP and DIP joints. Lacerations in zone II (middle phalanx to proximal palmar fold) are the most frequent and carry the most severe prognosis (Fig. 17-32). The fixation system of flexor tendons to adjacent bone is not as strong as that of the extensor system; thus,

■ FIGURE 17-30

Illustration (lateral view) of the anatomy of the flexor tendons. FDS, flexor digitorum superficialis; FDP, flexor digitorum profundus.

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■ FIGURE 17-32 Open rupture of the superficialis and profundus flexor tendons at zone II. Sagittal (A) and axial (B) T2-weighted MR images demonstrate the complete rupture and permit identification of the level of tendon retraction (arrows).

a higher degree of retraction may be encountered. In addition, the gap between the torn ends of the tendon may be overestimated if the tendon is curled or overlaps itself (see Fig. 17-32A).

Manifestations of the Disease Clinical diagnosis of partial lacerations is difficult because the physical signs are nonspecific. Clinical diagnosis may be easy in complete lacerations, but assessment of the degree of proximal retraction of the tendon may be difficult, as the tendon can sometimes be displaced as far as the palmar fold.

Magnetic Resonance Imaging Magnetic resonance imaging has been successfully used to diagnose tendon disruption and to accurately visualize the locations of the ends of the lacerated tendon (see Fig. 17-32). This technique may also provide additional information about the degree of injury, thus allowing differentiation of partial and complete lacerations. Associated MRI findings include tenosynovitis, luxation of the injured tendon, and disruption of the pulley system.19

Synopsis of Treatment Options Surgical repair is the treatment of choice for complete lacerations. The treatment for partial tendon lacerations remains controversial, and conservative treatment is recommended in several cases.21

Closed Injuries Closed tendon injuries include avulsion of the flexor digitorum profundus and flexor digitorum superficialis tendons.19,21 Avulsion of the flexor digitorum profundus tendon is the most frequent type of closed rupture and is caused by a sudden hyperextension injury during active flexion, the “jersey finger” (Fig. 17-33). The flexor digitorum profundus tendon of the ring finger is most commonly injured. Imaging is important because it can be easily overlooked in the acute context. There is no classic deformity or alignment abnormality associated with it on physical examination, and the combination of pain and soft tissue swelling may mask the pathognomonic sign of loss of active flexion at the DIP joint. Four main variations of this lesion have been described based on the level of the lesion, the degree of retraction, and the presence or absence of an osseous fragment. Type I lesions are characterized by retraction of the tendon into the palm. Type II lesions show tendon retraction to the PIP joint with or without a small osseous avulsion at the joint. In the type III lesion there is an avulsion of a large osseous fragment that remains in situ. The type IV lesion demonstrates failure at the bone with a fracture fragment noted at the tendon attachment site, as well as failure of the tendon attachment to bone, with a concomitant detachment of tendon from fracture fragment. Isolated avulsion of the flexor digitorum superficialis is uncommon, with most reported cases occurring in conjunction with flexor digitorum profundus tendon

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■ FIGURE 17-33 Distal avulsion of the flexor digitorum profundus tendon of the ring finger. A, Lateral conventional radiograph shows avulsion of a large bone fragment displaced to the proximal interphalangeal joint level (arrow). B, Ultrasound image demonstrates a tendon retracted to the proximal interphalangeal joint level with bone fragment avulsion (arrow). C, Sagittal, fat-suppressed, T2-weighted MR image shows the flexor digitorum profundus tendon retracted to the proximal interphalangeal joint level (arrow).

injuries.19,21 Injury to the flexor digitorum superficialis occurs with forced extension in the actively flexed finger. This diagnosis is suggested on physical examination by the inability to independently flex the PIP joint. Closed ruptures of the digital flexors are uncommon compared with flexor tendon lacerations. Underlying chronic conditions that result in weakening of tendons are typically present, such as rheumatoid arthritis, osteoarthritis, scaphoid nonunion, Kienböck’s disease, hook-of-the-hamate fractures, nonhealed distal radial fractures, and carpal dislocations.

Manifestations of the Disease Ultrasonography and Magnetic Resonance Imaging Ultrasonography and MRI are useful for displaying the zone of rupture and the proximal and distal tendons and accurately measure the gap between the torn tendon ends. Gap size is considered an important factor for deciding treatment. If the gap is more than 30 mm, a tendon graft is preferred to primary tendon repair. Assessment of integrity of the adjacent tendons before performing a tendon graft can also be accomplished by using ultrasonography or MRI. Finally, both of these imaging techniques also help to locate the proximal end of the tendon, which in some cases may dislocate between the adjacent tendons or even curl up in the palm.

Synopsis of Treatment Options Transosseous reinsertion of the tendon could be performed, even with a large gap.

Digital Flexors Carpal tunnel syndrome may arise as a result of tenosynovitis of the flexor tendons contained by the flexor retinaculum. Causative factors include acute hyperextension injury, chronic repetitive trauma, tuberculous tenosynovitis, and systemic inflammatory disorders such as rheumatoid arthritis, psoriasis, collagen vascular diseases, and gout. The MRI diagnosis of digital flexor tenosynovitis includes thickening of the tendon sheath, tenosynovial effusion, and peritendinous edema. Associated bursitis within the carpal tunnel may be seen in patients with seropositive inflammatory disease. Intratunnel bursae are located along the radial aspect of the flexor pollicis longus and ulnar aspect of the flexor digitorum superficialis and profundus to the third and fourth digits.

Flexor Pollicis Longus Rupture of the flexor pollicis longus tendon may develop from chronic attrition against the scaphoid when this carpal bone has eroded through the palmar wrist capsule, as seen in patients with rheumatoid arthritis or as a result of volar carpal subluxation. Clinically, patients experience a loss of active thumb flexion at the interphalangeal joint. Carpal tunnel symptoms may result from the proximally displaced tendon edge, which may fold over itself at the entrance of the carpal tunnel. The volar aspect of the wrist should be explored to look for bony spicules that could have disrupted the flexor pollicis longus. The torn tendon end must be retrieved at the wrist because the

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flexor pollicis longus does not have a lumbrical and therefore is free to retract. Treatment options include flexor pollicis longus advancement and pull-through, bridge grafts, flexor digitorum superficialis tendon transfer, or arthrodesis of the PIP joint and synovectomy.

Flexor Carpi Radialis Tenosynovitis of the flexor carpi radialis can be the result of a direct injury or chronic repetitive trauma or may develop insidiously, unrelated to trauma. The condition is manifested by pain and crepitus over the flexor carpi radialis tendon in the region just proximal to the flexor creases of the wrist. Diagnosis can be confirmed by injection of anesthetic into the tendon sheath. MRI findings include tendon sheath thickening with associated hyperintensity on T2-weighted images. Associated inflammatory changes of the scaphotrapezial joint have been described as the flexor carpi radialis tendon being in partial contact with the trapezial crest and the scaphoid tubercle. Concomitant irritation of the median nerve secondary to flexor carpi radialis tenosynovitis may occur owing to their close relationship. Rupture of this tendon can occur as the result of falling onto an outstretched hand, causing avulsion at the insertion, with or without a bony fragment. Chronic partial tearing may develop from friction against bony spicules emanating from the scaphotrapezial joint. The differential diagnosis includes scaphotrapezial joint disease, soft tissue ganglion, distal scaphoid fracture, distal radial fracture, and the Linburg syndrome, which consists of pain in patients who exhibit simultaneous flexion of the DIP joint of the index finger with flexion of the interphalangeal joint of the thumb secondary to an anomalous connection between the flexor pollicis longus and the flexor digitorum profundus tendon of the index finger. This tendinous connection is a common anomaly found in 20% of people in all age groups.

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Flexor Carpi Ulnaris Tenosynovitis of the flexor carpi ulnaris may develop secondary to chronic repetitive trauma and may be bilateral. Clinical findings include pain on palpation of this tendon or the pisiform and painful ulnar flexion against resistance. Calcifications of the tendon sheath tend to occur most commonly close to the insertion of the flexor carpi ulnaris tendon into the pisiform.28 The differential diagnosis of flexor carpi ulnaris tenosynovitis/calcific tendinitis includes pisotriquetral arthritis and ulnar neuritis. Conservative treatment measures include splinting, anti-inflammatory medications, and injection of corticosteroids in the tendon sheath. Surgical resection of the pisiform and Z-plasty of the flexor carpi ulnaris tendon may be required for intractable cases.

Pulley System Injuries Prevalence, Epidemiology, and Definitions Finger flexion relies heavily on the delicate focal thickened areas of the flexor tendon sheath, referred to as the pulley system. Flexion requires proximal excursion of the flexor tendon and tight apposition of the tendon to adjacent osseous structures during this excursion, both of which are afforded by the pulley system.29–31 Frequency of lesions of the pulley system have increased due to the growing popularity of rock climbing activities. Powerful flexion of the fingers with MCP joint extension, PIP joint flexion, and DIP joint extension can lead to extensive stress forces on the A2 and A3 pulleys, with consequent ruptures. Injury of the pulley system follows a constant sequence, begins at the distal part of the A2 pulley (the most important component in flexor tendon function), progresses from partial to complete rupture, and is followed by involvement of the A3, A4 (Fig. 17-34), and, rarely, A1 pulleys.29–31

■ FIGURE 17-34 Illustration showing that the injury of the pulley system begins at the distal part of the A2 pulley, which is followed by involvement of the A3 and A4 pulleys.

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Manifestations of the Disease Disruption of the pulley system may be difficult to diagnose. The pain and swelling associated with acute injuries prevent complete evaluation of flexor tendon bowstringing. Factors that may affect the choice of treatment include the age of the patient, the degree of injury, and the number of pulleys involved. Early diagnosis and accurate assessment of the degree of digital annular pulley tear are essential for choosing between conservative treatment and surgery and can prevent both fibrous sequelae and flexion contracture of the PIP joint.

Ultrasonography and Magnetic Resonance Imaging Ultrasonography and MRI have proved successful in establishing the diagnosis of isolated disruption of the pulley system, both by means of direct visualization and by demonstrating useful indirect signs.29,30 In addition, they have been used to show the extent of the lesion and to determine adequate treatment. An indirect sign is a gap between the flexor tendon and the bone on sagittal images obtained during forced flexion, a finding referred to as the “bowstringing sign” (Fig. 17-35).29,30 This displacement is maximal at the proximal phalanx and middle phalanx when there are tears in the A2 and A4 pulleys, respectively. Owing to the anatomy, incomplete disruption of the A2 pulley is diagnosed on sagittal MR images when bowstringing does not extend proximally beyond the base of the proximal phalanx. Conversely, proximal extension of bowstringing beyond the base of the proximal

KEY POINTS: TENDON INJURIES Clinical examination is essential for the diagnosis of the full spectrum of pathology for tendon injuries. ■ Both high-resolution ultrasonography and MRI permit evaluation of superficially located tendons. Anatomic resolution and dynamic capabilities of ultrasonography allow an efficient, rapid, and inexpensive alternative to MRI for investigation of tendon diseases of the wrist and hand. ■ The radiologic role is the diagnosis of the structure affected and any associated soft tissue and bone lesions that can change treatment or prognosis. ■ Delay of surgery can impair good outcome due to fibrosis and tendon retraction. For good surgical planning, the surgeon needs to know if there is a partial or complete rupture. If a complete rupture is diagnosed, the exact location, quality of distal tendon ends, and distance of the gap should be known. ■ Avulsion bone fragments must be ruled out. ■

phalanx indicates a complete disruption. Other authors have reported that the size of the tendinous gap during forced flexion increases proportionally with the number of disrupted pulleys. This gap varies from 2 to 5 mm for isolated complete lesions to 5 to 8 mm for simultaneous complete lesions of multiple pulleys. Measurement of the tendinous gap has no significance in partial ruptures. With the development of more dedicated surface receiver coils, identification of normal A2 and A4 pulleys

C ■ FIGURE 17-35 Chronic complete rupture of A2, A3, and A4 pulleys of the fourth finger. A and B, Forced flexion sagittal, T1weighted and sagittal, gradient-echo, T2-weighted MR images reveal a gap between the flexor tendon and the bone (asterisks), the socalled bowstring sign. The extent from the proximal interphalangeal joint to the base up to the middle third of the intermediate phalanx indicates complete rupture of the A2, A3, and A4 pulleys. C, Axial T1-weighted MR image at the level of the middle proximal phalanx shows chronic rupture of the A2 pulley (arrows). Note the normal A2 pulley of the little finger (arrowheads).

A

B

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is possible, thus allowing detection of signs of rupture with direct visualization of disrupted pulleys in axial sections. This might be helpful in current practice because it would reduce motion artifacts associated with forced flexion, which currently represent one of the most important limitations of MRI in detection of pulley lesions.

Synopsis of Treatment Options Surgical repair is indicated in patients with complete, isolated A2, or combined pulley ruptures, whereas partial A2 pulley ruptures are treated primarily without surgery.31

What the Referring Physician Needs to Know: Tendon Injuries ■ ■ ■ ■ ■

To differentiate between partial and complete rupture of tendon To locate the tear and measure the exact gap distance of tendon ends To determine if there are bone avulsion fragments To assess the quality of distal tendon fragments to plan surgical repair To rule out associated diseases such as inflammatory tenosynovitis

GANGLION CYST Prevalence, Epidemiology, and Definitions Ganglion cysts are the most common soft tissue mass on the hand and wrist and account for 50% to 70% of masses in this anatomic region.32 Ganglion cysts may occur at any age but are most prevalent between 10 and 40 years of age. Ganglions are more common in women than men.

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Ganglions are usually located adjacent to joints and tendons. Common sites about the hand and wrist include the dorsal wrist (dorsal wrist ganglion), volar-radial wrist (volar carpal ganglion), dorsum of the DIP joint (mucous cyst), and the proximal digital flexion crease (volar retinacular ganglion cyst).32 The most common location for hand and wrist ganglions (60% to 70%) is at the dorsum of the wrist, at the level of the dorsal scapholunate interval (Fig. 17-36). At least 75% of dorsal wrist ganglions connect with the dorsal scapholunate interosseous ligament in the area of its capsular attachment through a tortuous duct-like system. Twenty percent of wrist ganglions are volar, nearly two thirds arise from the radioscaphoid, and one third occur from the scaphotrapezial joint. The mass is usually palpable between the radial artery and the flexor carpi radialis tendon (Fig. 17-37). Another common site for a ganglion is the flexor tendon sheath at the level of the A1 pulley (metacarpophalangeal joint) or the A2 pulley (proximal phalanx) (Fig. 17-38). Flexor tendon sheath ganglions, also called volar retinacular ganglion cysts, represent approximately 10% to 12% of wrist ganglions. This type of ganglion penetrates through the pulley and is tethered; thus, it does not move with flexor tendon motion. A less common location is the DIP joint (Fig. 17-39). This type of ganglion is referred to as a mucous cyst and is associated with osteoarthritis of the DIP joint. Mucous cysts usually occur in middle-aged women. Typically, they appear lateral to the midline, the stalk connects with the DIP joint, and it is displaced by the distal extensor tendon. Nail deformities are often associated with this type of cyst.32

Pathology A ganglion is a lesion of unknown origin that arises in the para-articular tissues. Synovial herniation, tissue

■ FIGURE 17-36

Coronal, gradient-echo, T2-weighted (A) and axial, fat-suppressed, T2-weighted (B) MR images show a dorsal wrist ganglion (arrows) that originated from the dorsal scapholunate ligament.

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■ FIGURE 17-37

Volar wrist ganglion that arose from the radioscaphoid joint. Axial ultrasound image shows a volar ganglion growing between the radial artery (arrow) and the flexor carpi radialis tendon.

degeneration, repetitive trauma, and internal derangement have been suggested as possible etiologic factors.32 Repeated trauma resulting in degeneration of the periarticular connective tissue has been hypothesized as a possible cause. Also, it has been reported that a subset of wrist ganglions represents the sequela of internal derangements of the wrist joint. They may be the result of a chronic irritation to the scapholunate or other intercar-

■ FIGURE 17-39 Sagittal, fat-suppressed, T2-weighted MR image shows a mucous cyst of the thumb distal interphalangeal joint.

pal ligaments. These wrist ganglions are more accurately termed synovial cysts and are similar to meniscal cysts in the knee and paralabral cysts in the shoulder. Most investigators agree that ganglion cysts arise from modified synovial or mesenchymal cells at the synovialcapsular interface, in response to repetitive minor injury. The cyst wall consists mainly of collagen fibers and has no synovial lining. Ganglions are mucin-filled cysts. Most cysts contain a highly viscous, clear jelly-like fluid. The viscosity of the fluid is attributed to a high concentration of hyaluronic acid and other mucopolysaccharides.32

Manifestations of the Disease The diagnosis is usually made on the basis of the history and physical examination.32 Many patients describe an asymptomatic mass present for months or years that changes its size, decreasing and increasing. They are usually asymptomatic, although they can be associated with aching wrist pain, tenderness, and interference with activity at the time of presentation. At physical examination, most wrist ganglions present as firm masses that may either be asymptomatic or may cause pain and tenderness due to compression of adjacent structures, such as tendons and nerves.32

Radiography Plain radiographs are usually negative. Occasionally, radiographs may reveal focal soft tissue prominence, underlying carpal instability, or bone erosion.

Ultrasonography ■ FIGURE 17-38

Volar retinacular ganglion cysts. Ultrasound image (A) and sagittal, fat-suppressed, T2-weighted MR image (B) show a ganglion of the flexor tendon sheath at the level of the A2 pulley (arrows).

Ultrasonography is the first imaging modality for evaluation of a soft tissue wrist mass.22,23,32 It is useful for imaging the hand in patients with persistent pain and suspected

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occult ganglion. Ganglions are identified as well-defined, homogeneously anechoic with acoustic enhancement masses (see Figs. 17-37 and 17-38). Occasionally, debris is present within the cyst, and they might be multiloculated as well. Ganglia complicated by hemorrhage, trauma, or infection may have an atypical appearance on ultrasound images.22,23,32

Magnetic Resonance Imaging The efficacy of MRI and ultrasonography in detecting a dorsal occult ganglion is similar; however, MRI offers an objective, reproducible display of anatomic relationships. MRI clearly aids the localization of ganglions and identification of their relationship to adjacent structures, which include vessels, tendons, and nerves (see Figs. 17-36, 17-38, and 17-39). The effect of the mass on the adjacent neurovascular structures is clearly demonstrated with MRI. Complicated (hemorrhage) ganglions or thick proteinaceous fluid may cause a variation in signal intensity.

Arthroscopy Only in one third of the patients can the surgeon see the ganglion stalk. In most cases the synovitis in relation to the dorsal aspect of the scapholunate ligaments is the only feature. In the volar ganglion, typically the long radiolunate ligament is ragged and has synovitis.

Differential Diagnosis The clinical diagnosis is usually straightforward. The differential diagnosis must be made with other soft tissue masses of the hand and wrist, such as giant cell tumor of the tendon sheath, nerve tumor, lipoma, pseudoaneurysm, anomalous muscle, and glomus tumor.

Synopsis of Treatment Options Treatment options include observation, aspiration, and surgical excision.32 Asymptomatic wrist ganglions are treated expectantly. Indications for more aggressive treatment include pain, interference with activity, nerve compression, and imminent ulceration (in the case of some mucous cysts). Symptomatic ganglions can be injected with corticosteroids and a local anesthetic, although there is a high rate of recurrence. Arthroscopic or open surgical resection are the treatment of choice for symptomatic wrist gan-

KEY POINTS: GANGLION CYST Most ganglions have a characteristic clinical examination and anatomic location. ■ Ultrasonography is the imaging modality of choice for the diagnosis of ganglions. ■ Ultrasonography is a valuable tool for the diagnosis of ganglions, especially in cases of small occult lesions, and shows their size, location, and relationships with adjacent vessels, nerves, and tendons. ■ MRI is not usually necessary for the evaluation of wrist ganglions, although it can be useful in deep ganglions for the identification of their relationship to adjacent structures. ■

17

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399

What the Referring Physician Needs to Know: Ganglion Cyst ■ ■ ■

To confirm clinical suspicion and rule out other wrist masses To locate the ganglion, and its relation with other adjacent structures, such as vascular or nerve structures To depict to which structure the ganglion neck is related

glions. Arthroscopy allows resection of the “root” of the ganglion in the vicinity of the scapholunate ligament for dorsal ganglions and the long radiolunate for volar ones. Surgical excision is effective, with a recurrence rate of only 5% if care is taken to completely excise the stalk of the cyst along with a small portion of joint capsule.

FOREIGN BODIES Prevalence, Epidemiology, and Definitions Penetrating injuries and suspected retained foreign bodies are a common reason for emergency department visits. Up to 38% of retained foreign bodies in the soft tissues are overlooked at the initial examination.33 The most common retained foreign bodies are wood, glass, or metal slivers. Despite advances in imaging techniques, the detection of retained wooden foreign bodies remains a difficult and challenging task.3,34

Pathology Retained foreign bodies produce a granulomatous inflammatory response.33,34 They may also lead to serious complications. Soft tissue infection is by far the most common complication of a penetrating foreign body, with nerve injury a distant second. The retained foreign bodies may result in cellulitis, abscess, or fistula formation. The foreign material may also result in synovitis if a joint is violated or in osteomyelitis if adjacent osseous structures become involved.

Manifestations of the Disease Patients often present for evaluation several months or even years after the initial injury, and, consequently, clinical evaluation may fail to elicit a history of antecedent skin puncture.33,34 Without a reported history of penetrating injury, clinical detection of retained foreign bodies can be exceedingly difficult because patients typically present with nonspecific symptoms. The initial physical examination may reveal a painful swollen soft tissue mass or pseudotumor that may simulate malignancy or infection, rather than suggesting a retained foreign body. When a history of penetrating trauma is suggested, its severity is difficult to estimate clinically. Even when there is a high suspicion of a retained foreign body, localization remains difficult. Foreign body fragments may remain in the wound even after apparent successful extraction by the patient at the time of injury.

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Radiography Foreign radiopaque bodies in the hand (glass, metal, stone) are readily diagnosed on plain radiographs.33,34 However, radiographs have been reported to reveal a wooden foreign body in only 15% of patients. Wooden foreign bodies are usually radiolucent, associated with gas in the matrix. When retained foreign bodies penetrate or lie adjacent to bone, osteolytic, osteoblastic, or a combination of changes can appear. Unfortunately, this can often confuse the situation further and suggest another underlying process rather than a retained foreign body.

Ultrasonography Ultrasonography is the study of choice for detection of foreign bodies. It is quite sensitive and specific in detecting all types of foreign bodies, including wood splinters, glass, metal, and plastic.33 Ultrasonography has been shown to accurately demonstrate the size, shape, and location of soft tissue foreign bodies. Radiolucent foreign bodies such as wood might not be visible on plain films but are easily detected with ultrasound (Fig. 17-40). For radiopaque foreign bodies that are easily detected on radiographs, ultrasonography can provide more precise localization. For all foreign bodies, ultrasonography can aid in the assessment of the surrounding soft tissues along with evaluation of their associated soft tissue complications. Foreign bodies are echogenic when imaged by ultrasound. If the foreign body has been present for a few days or weeks, a surrounding hypoechoic inflammatory reaction will often occur. Cadaveric and in vivo studies with suspected nonradiopaque foreign bodies demonstrated a sensitivity and specificity of more than 90% for detection by ultrasonography.33

Multidetector Computed Tomography Computed tomography easily detects all radiopaque foreign bodies. In cases of retained wooden foreign bodies,

KEY POINTS: FOREIGN BODIES Clinical evaluation may fail to elicit a history of skin puncture. ■ Radiopaque foreign bodies are readily diagnosed on plain radiographs. ■ Ultrasonography is the study of choice for detection of all types of foreign bodies. ■ The identification of foreign bodies may be exceedingly difficult on MRI. ■

CT typically shows a linear area of increased attenuation, which is best seen on wide window settings.34 The surrounding inflammatory response produces effacement of surrounding fat planes.

Magnetic Resonance Imaging The identification of foreign bodies may be exceedingly difficult on MRI, especially when foreign bodies are small and there is no associated abscess or fluid collection.34 On MRI the retained foreign bodies appear hypointense on all pulse sequences, surrounded by nonspecific granulation tissue. Retained wood, in contrast to metal, does not reveal susceptibility; artifact and linear signal voids may be mistaken for scar tissue, tendons, and calcifications. In the acute setting, surrounding hemorrhage and hematoma may be seen, being replaced in time with granulomatous tissue. This inflammatory reaction associated with retained foreign bodies shows prolonged T1 and T2 relaxation times and prominent contrast medium enhancement. Identification of the inflammatory response can help the radiologist identify the retained foreign body because the actual splinter may be difficult to visualize. The surrounding foreign body reaction may be mistaken for a soft tissue mass or a tumor if the central foreign body is not identified.

Differential Diagnosis In patients without a known history of penetrating injury, physical examination may be indicative of soft tissue mass or infection. MRI findings may reveal surrounding foreign body inflammatory reaction that can obscure the foreign body and mistake it for a soft tissue mass or tumor.

Synopsis of Treatment Options Most foreign bodies are easily surgically removed without complications after ultrasonographic localization.

What the Referring Physician Needs to Know: Foreign Bodies ■

■ FIGURE 17-40

Wood foreign body. Sagittal ultrasound image shows an echogenic linear foreign body (arrow) at the level of the metacarpophalangeal joint of the third finger.

■

Ultrasonography is the study of choice for detection of all types of foreign bodies. The identification of foreign bodies may be exceedingly difficult on MRI.

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401

SUGGESTED READINGS Bencardino JT. MR imaging of tendon lesions of the hand and wrist. Magn Reson Imaging Clin North Am 2004; 12:333–347. Bianchi S, Martinoli C, Abdelwahab IF. High-frequency ultrasound examination of the wrist and hand. Skeletal Radiol 1999; 28:121–129. Cerezal L, Del Pinal F, Abascal F. MR imaging findings in ulnar-sided wrist impaction syndromes. Magn Reson Imaging Clin North Am 2004; 12:281–299. Clavero JA, Alomar X, Monill JM, et al. MR imaging of ligament and tendon injuries of the fingers. Radiographics 2002; 22:237–256. Garcia-Elias M, Geissler WB. Carpal instability. In Green DP, Hotchkiss RN, Pederson WC, Wolfe SW (eds). Green’s Operative Hand

Surgery. Philadelphia, Elsevier Churchill Livingstone, 2005, pp 535–604. Gelberman RH, Cooney WP III, Szabo RM. Carpal instability. Instr Course Lect 2001; 50:123–134. Ragheb D, Stanley A, Gentili A, et al. MR imaging of the finger tendons: normal anatomy and commonly encountered pathology. Eur J Radiol 2005; 56:296–306. Rosner JL, Zlatkin MB, Clifford P, et al. Imaging of athletic wrist and hand injuries. Semin Musculoskelet Radiol 2004; 8:57–79. Timins ME, Jahnke JP, Krah SF, et al. MR imaging of the major carpal stabilizing ligaments: normal anatomy and clinical examples. Radiographics 1995; 15:575–587.

REFERENCES 1. Cerezal L, del Pinal F, Abascal F, et al. Imaging findings in ulnar-sided wrist impaction syndromes. Radiographics 2002; 22:105–121. 2. Coggins CA. Imaging of ulnar-sided wrist pain. Clin Sports Med 2006; 25:505–526. 3. Cerezal L, Abascal F, Garcia-Valtuille R, del Pinal F. Wrist MR arthrography: how, why, when. Radiol Clin North Am 2005; 43:709–731. 4. Dailey SW, Palmer AK. The role of arthroscopy in the evaluation and treatment of triangular fibrocartilage complex injuries in athletes. Hand Clin 2000; 16:461–476. 5. Palmer AK. Triangular fibrocartilage complex lesions: a classification. J Hand Surg [Am] 1989; 14:594–606. 6. Zlatkin MB, Rosner J. MR imaging of ligaments and triangular fibrocartilage complex of the wrist. Radiol Clin North Am 2006; 44:595–623. 7. Topper SM, Wood MB, Ruby LK. Ulnar styloid impaction syndrome. J Hand Surg [Am] 1997; 22:699–704. 8. Malik AM, Schweitzer ME, Culp RW, et al. MR imaging of the type II lunate bone: frequency, extent, and associated findings. AJR Am J Roentgenol 1999; 173:335–338. 9. Garcia-Elias M. The treatment of wrist instability. J Bone Joint Surg Br 1997; 79:684–690. 10. Theumann NH, Etechami G, Duvoisin B, et al. Association between extrinsic and intrinsic carpal ligament injuries at MR arthrography and carpal instability at radiography: initial observations. Radiology 2006; 238:950–957. 11. Scheck RJ, Romagnolo A, Hierner R, et al. The carpal ligaments in MR arthrography of the wrist: correlation with standard MRI and wrist arthroscopy. J Magn Reson Imaging 1999; 9:468–474. 12. Brown RR, Fliszar E, Cotten A, et al. Extrinsic and intrinsic ligaments of the wrist: normal and pathologic anatomy at MR arthrography with three-compartment enhancement. Radiographics 1998; 18:667–674. 13. Theumann NH, Pfirrmann CW, Antonio GE, et al. Extrinsic carpal ligaments: normal MR arthrographic appearance in cadavers. Radiology 2003; 226:171–179. 14. Melone CP Jr, Beldner S, Basuk RS. Thumb collateral ligament injuries: an anatomic basis for treatment. Hand Clin 2000; 16:345–357. 15. Ebrahim FS, De Maeseneer M, Jager T, et al. US diagnosis of UCL tears of the thumb and Stener lesions: technique, patternbased approach, and differential diagnosis. Radiographics 2006; 26:1007–1020. 16. Barron OA, Glickel SZ, Eaton RG. Basal joint arthritis of the thumb. J Am Acad Orthop Surg 2000; 8:314–323.

17. Rettig AC. Athletic injuries of the wrist and hand: I. Traumatic injuries of the wrist. Am J Sports Med 2003; 31:1038–1048. 18. Masson JA, Golimbu CN, Grossman JA. MR imaging of the metacarpophalangeal joints. Magn Reson Imaging Clin North Am 1995; 3:313–325. 19. Bencardino JT, Rosenberg ZS. Sports-related injuries of the wrist: an approach to MRI interpretation. Clin Sports Med 2006; 25:409–432. 20. Clavero JA, Golano P, Farinas O, et al. Extensor mechanism of the fingers: MR imaging–anatomic correlation. Radiographics 2003; 23:593–611. 21. Rettig AC. Athletic injuries of the wrist and hand: II. Overuse injuries of the wrist and traumatic injuries to the hand. Am J Sports Med 2004; 32:262–273. 22. Martinoli C, Bianchi S, Dahmane M, et al. Ultrasound of tendons and nerves. Eur Radiol 2002; 12:44–55. 23. Teefey SA, Middleton WD, Boyer MI. Sonography of the hand and wrist. Semin Ultrasound CT MR 2000; 21:192–204. 24. de Lima JE, Kim HJ, Albertotti F, Resnick D. Intersection syndrome: MR imaging with anatomic comparison of the distal forearm. Skeletal Radiol 2004; 33:627–631. 25. Scott SC. Closed injuries to the extension mechanism of the digits. Hand Clin 2000; 16:367–373. 26. Bendre AA, Hartigan BJ, Kalainov DM. Mallet finger. J Am Acad Orthop Surg 2005; 13:336–344. 27. Allende C, Le Viet D. Extensor carpi ulnaris problems at the wrist—classification, surgical treatment and results. J Hand Surg [Br] 2005; 30:265–272. 28. Blum AG, Zabel JP, Kohlmann R, et al. Pathologic conditions of the hypothenar eminence: evaluation with multidetector CT and MR imaging. Radiographics 2006; 26:1021–1044. 29. Klauser A, Frauscher F, Bodner G, et al. Finger pulley injuries in extreme rock climbers: depiction with dynamic US. Radiology 2002; 222:755–761. 30. Martinoli C, Bianchi S, Cotten A. Imaging of rock climbing injuries. Semin Musculoskelet Radiol 2005; 9:334–345. 31. Moutet F, Forli A, Voulliaume D. Pulley rupture and reconstruction in rock climbers. Tech Hand Up Extrem Surg 2004; 8:149–155. 32. Thornburg LE. Ganglions of the hand and wrist. J Am Acad Orthop Surg 1999; 7:231–238. 33. Boyse TD, Fessell DP, Jacobson JA, et al. US of soft-tissue foreign bodies and associated complications with surgical correlation. Radiographics 2001; 21:1251–1256. 34. Jacobson JA, Powell A, Craig JG, et al. Wooden foreign bodies in soft tissue: detection at US. Radiology 1998; 206:45–48.

18

C H A P T E R

Pelvis-Hip: Technical Aspects, Normal Anatomy, Common Variants, and Basic Biomechanics Eva Llopis, Pilar Ferrêr, and Francisco Aparisi

TECHNICAL ASPECTS Techniques and Relevant Aspects Conventional Radiography Rationale and Indications ● ●

●

For visualization of osseous anatomy and pathology, bone contours, and joint alignment Recommended for any primary evaluation of suspected hip pathology, including fractures, dislocations, bone tumors, and infection Gluteal, iliopsoas, and obturator fat pads

Advantages ● ●

Readily available Inexpensive

Limitations ● ●

● ●

Limited soft tissue evaluation Patient positioning difficult if there is limited motion for any reason (pain, fracture, ankylosis). Flexion and rotation can produce a false-positive result. Uses (minimal) ionizing radiation See Table 18-1 (Figs. 18-1 to 18-3).

Measurements from an Anteroposterior View1,2 Acetabular Measurements ●

The center-edge (CE) angle is the most important measurement on the anteroposterior view of the

●

●

pelvis, and if abnormal it is diagnostic of acetabular dysplasia. This angle is used to assess the superior and lateral coverage of the femoral head by the bony acetabulum. Coverage of the femoral head is considered adequate if the angle measures at least 25 degrees (Fig. 18-4). The horizontal toit externe (HTE) angle is used to evaluate the orientation of the acetabular roof in a coronal plane and the superior lateral coverage of the femoral head (Fig. 18-5). An acetabular index of depth to width establishes the depth of the acetabulum.

Femoral Head ●

Percentage of the femoral head covered by the acetabulum (Fig. 18-6). Coverage of less than 75% is pathologic.

Proximal Head ● ●

Neck-shaft angle (Fig. 18-7) Although femoral neck anteversion can be determined from plain films by direct or indirect methods, each method requires specific additional radiographic views and CT is usually performed when needed.

Multidetector Computed Tomography Rationale and Indications (Fig. 18-8) ● ●

MDCT defines or excludes suspected abnormality that is ambiguous using conventional radiography. Provides high-resolution true isotropic volume datasets 405

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

TABLE 18-1 Conventional Radiography of the Hip-Pelvis Projections

Main Visualized Anatomy and Pathology

Pelvis anteroposterior : Patient is placed supine with feet placed in approximately 15 degrees of internal rotation.The criteria for an acceptable pelvic radiograph include a symmetric appearance of obturator foramina and iliac crest and a true view of both femoral necks (Fig. 18-1) 1

Standing hip anteroposterior (Fig. 18-2) Oblique-45 degree anterior oblique* Oblique-45 degree posterior oblique Axial view—hip abducted* False profile (Le Quesne method)* Frog-leg view*

Sacrum, innominate bones (ilium, ischium and pubis, rami), and proximal femur Anterior column, iliopubic line Posterior column, ischiopubic line Anterior and posterior acetabular rims The medial acetabular wall normally projects lateral to the ilioischial line; if the acetabular wall projects medial to the ilioischial line, the patient has protrusio acetabuli.1 Normal trabecular pattern Osteoporosis Fat pads Acetabular dysplasia2 Anterior acetabular rim Posterior acetabular rim Femoral neck Articular joint View of the acetabulum in profile Used when a hip abnormality is suspected in newborn, toddler, or child Femoral physis Lateral projection of both hips and femoral neck

*Standard hip series (Fig. 18-3).

■ FIGURE 18-1 Normal anteroposterior pelvis radiograph. Patient is placed in supine position with feet in approximately 15 degrees of internal rotation. Normal acetabular trabecular pattern (black asterisk) forms as a triangular lucent region, and normal femoral metaphyseal trabeculae (white asterisk) form a distinctive arc that leaves a relative lucent area in the medial and lateral femoral head. Teardrop radiographic structure (arrow) represents the summation of shadows of the medial acetabular wall. 1, Iliac bone; 2, iliopubic rami; 3, ischiopubic rami; 4, pubis; 5, proximal femur.

●

●

●

Postprocessing orthogonal multiplanar, oblique multiplanar, and volume-rendered reconstructions of the osseous anatomy allow visualization of complex osseous anatomy and pathology. 3D reconstructions are performed in workstations; volume-rendered reconstructions are preferred over surface reconstructions (Fig. 18-9). Evaluation of trauma: complex fractures, intra-articular fragments, and dislocations. Contrast-enhanced CT

■ FIGURE 18-2

● ● ● ●

Normal standing hip anteroposterior radiograph.

and MDCT angiography may be necessary to rule out extravasation. Evaluation of acquired and congenital abnormalities Evaluation of bone tumor: matrix calcification (osteoid, cartilage) in some bone tumors Evaluation of soft tissue calcifications and infection Post-treatment evaluation, including degree of healing, adequate reduction, joint congruity, and fixation devices

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407

■ FIGURE 18-3 Standard hip series. A, Anterior oblique view. B, Axial view, hip abducted. C, False profile, Le Quesne projection. Patient standing with the unaffected hip moved forward so that the pelvis is rotated 65 degrees to the film and central ray centers on the affected hip. D, Frog-leg view, with patient supine with the knees flexed and thighs abducted to approximately 40 degrees so the soles of the feet are in contact.

Advantages ● ● ● ● ●

Excellent depiction of osseous structures and calcified tissues Multiplanar and volume-rendering capabilities Volume rendering compensates for metallic streak artifact. Nonclaustrophobic Availability

●

Limitations ● ● ● ●

Limited visualization of soft tissues, although better than conventional radiography Uses ionizing radiation Expensive Invasive when used with arthrography

Technical Aspects ●

See Table 18-2.3,4

Measurements

2,5

●

Femoral neck anteversion. The technique varies slightly from one author to another. It consists of two or three

slices, 5 to 10 mm thick, through the femoral neck to obtain a line through its axis and two or three slices through both femoral condyles to draw the posterior bicondylar tangential line. The angle between them represents the femoral-neck anteversion angle. Normal values for adults are 12 to 15 degrees (Fig. 18-10). Acetabular coverage: axial slice through the center of both femoral heads, anterior acetabular sector angle (AASA), posterior acetabular sector angle (PASA), and global acetabular coverage by the horizontal acetabular sector angle (HASA). A line is drawn through the center of both femoral heads; the angle between this center and the line to the most anterior point of the acetabulum is the AASA, whereas the angle between this center and the line to the most posterior point of the acetabulum is the PASA. Normal values of AASA are 63 degrees in men and 64 degrees in women, and values for the PASA are 105 degrees in both sexes. The HASA is obtained by adding the AASA to the PASA.

Computed Tomographic Arthrography6 ●

Intra-articular injection of iodine contrast material allows visualization of the internal capsular anatomy and pathology.

■ FIGURE 18-4

Center-edge (CE) angle. The vertical line is perpendicular to the horizontal line extending from the center of each femoral head (C1 and C2). The E (edge) point is the most lateral point of the acetabulum. The CE angle is measured between the vertical and the line passing through C1 or C2 and E. Normal values are greater than 25 degrees.

■ FIGURE 18-5 Horizontal toit externe (HTE angle). This is measured between the horizontal and a line extending from the most medial point of the weight-bearing acetabulum (T point) to E point. Its normal value should be 10 degrees or less.

■ FIGURE 18-6 Femoral head coverage. Percentage of the femoral head covered by acetabulum: (A/B) × 100. Coverage of less than 75% is pathologic.

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409

■ FIGURE 18-7 Neck-shaft angle. The angle between the axis of the femoral shaft and the axis of the femoral neck passing through the femoral head center.

■ FIGURE 18-8 Hip multidetector CT (MDCT). A, Axial plane. B, Postprocessing orthogonal multiplanar reformatted (MPR) coronal images. C, Postprocessing orthogonal multiplanar sagittal images. D, Coronal 7-mm thick MPR.

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

■ FIGURE 18-9 Volumerendering 3D reconstructions. A, Anteroposterior view. B and C, Oblique views. D, Posterior view.

TABLE 18-2 Imaging Protocol Used for a 16-Slice MDCT Slice thickness Collimation Table speed Kilovolt peak Milliampere seconds Intravenous contrast material (polytrauma patient) Kernel Pitch Reconstruction

3 mm × 3 mm 0.75 mm × 16 slices 3–6 120–140 240–280 120–150 mL 3–4 mL/s Soft tissue, bone 1–2 Multiplanar, surface rendering1,2

Note: Optimal scanning depends on the clinical question to be answered. Imaging parameters must be adjusted depending on the number of detectors and distribution of the detectors.3,4

■ FIGURE 18-10 Femoral neck anteversion. Anteversion is an angular measurement that relates the femoral neck’s position or posture to the frontal plane. Normal values for adults are 12 to 15 degrees.

CHAPTER ●

●

18

● Pelvis-Hip: Technical Aspects, Normal Anatomy, Common Variants

Indicated when MRI is contraindicated, in patients with claustrophobia, or in suspected associated injuries. Main indication: Assessment of suspected labral tears, associated bone lesions, and cartilage surface. The sensibility of CT arthrography is superior to that of MRI for detecting cartilage lesions, although there are no studies comparing CT arthrography with MR arthrography (Fig. 18-11).7,8

● ● ●

●

● ●

A conventional single- or double-contrast arthrogram is performed first (as described under MR arthrography) using diluted iodinated contrast material (3 to 5:1) with or without air for a total of 13 to 15 mL. The CT examination is performed without delay (to avoid extravasation and dilution of contrast agent and thus avoid loss of capsular expansion). Some authors recommend active exercise for approximately 20 minutes to facilitate extensive coating of the articular surface by the contrast material.7 Patient position: supine with feet in internal rotation. MDCT series 2 mm, table speed 0.75 mm/sec

Magnetic Resonance Imaging: Conventional Pelvis Imaging Rationale and Indication ●

Visualization and assessment of soft tissue anatomy and pathology

Advantages ● ●

Multiplanar Nonionizing

Limitations ● ●

Expensive Claustrophobic in closed magnets

Long examination time Patient motion and respiratory motion artifacts The optimal timing for dynamic technique has not yet been determined.

Technical Aspects ●

Technical Aspects ●

411

●

●

Suggested parameters using a 1.5-T magnet6 ● Pelvic or torso phased-array coil ● Slice thickness: 3 to 4 mm ● Matrix: 512 × 512 ● Field of view: 30 to 40 cm Axial sections from the top of the iliac crest to below the lesser trochanters (Fig. 18-12). Coronal sections from the sacroiliac joint to the pubic symphysis (Fig. 18-13). Sagittal sections from the anterior acetabulum to the posterior acetabulum (Fig. 18-14). Oblique sagittal sections following femoral neck orientation (Fig. 18-15). Gadolinium injection may be necessary to assess femoral head vascularization, suspected infection, or bone or soft tissue tumors. Always compare with the unaffected side. To depict Legg-Calvé-Perthes disease the use of dynamic technique is recommended.9 See Table 18-3.

Dedicated Hip Magnetic Resonance Imaging Rationale and Indications ● ●

Visualization and assessment of soft tissue anatomy and pathology Dedicated noncontrast MRI has been proposed by some authors as a valuable tool for the detection of labral tears with similar accuracy to MR arthrography.10,11

Advantages ● ●

Multiplanar, nonionizing, and noninvasive compared with MR arthrography High-resolution images

■ FIGURE 18-11 CT arthrography. A, Coronal multiplanar reformatted (MPR) image. B, Coronal thick MPR image; the iodine contrast nicely outlines labrum and cartilage.

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

■ FIGURE 18-12 Pelvis MRI, axial planning. Axial sections go from the top of the iliac crest to below the lesser trochanters.

■ FIGURE 18-13 Pelvis MRI, coronal planning. Coronal sections go from the sacroiliac joint to the pubic symphysis.

Limitations ● ●

Equal to conventional pelvis MRI May be difficult to discern subtle tears and chondral defects

Technical Aspects ●

Suggested parameters using a 1.5-T magnet12 ● Torso coil, surface phased-array coil (shoulder or pelvic specific coil), cardiac coil ● Slice thickness: 3 to 4 mm ● Matrix: 512 × 512, 512 × 318, 512 × 256 ● Field of view: 15 to 18 cm Axial (Fig. 18-16B) Coronal (see Fig. 18-16A) Sagittal (see Fig. 18-14)

●

Oblique sagittal sections following femoral neck orientation (see Fig. 18-15)13 See Table 18-4.

Measurements ●

●

●

Alpha angle. Reduced concavity of the anterior femoral neck junction has been related to early hip osteoarthritis and hip pain. An alpha angle quantifies the relationship between the contour of the femoral neck junction; an alpha angle less than 55 degrees is abnormal (Fig. 18-17).14,15 Head-neck offset: the difference between the maximal anterior radius of the adjacent femoral neck. This is also called the head-to-neck ratio.16 Epiphyseal extension

CHAPTER

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● Pelvis-Hip: Technical Aspects, Normal Anatomy, Common Variants

■ FIGURE 18-14 Pelvis-hip sagittal planning. Sagittal sections go from the anterior acetabulum to the posterior acetabulum.

■ FIGURE 18-15 Pelvis-hip oblique sagittal planning. Oblique sagittal sections follow femoral neck orientation.

TABLE 18-3 Features of Conventional Pelvis Magnetic Resonance Imaging of the Hip-Pelvis

Imaging Planes

Pulse Sequences

Axial

T1-weighted, fast spin-echo, proton density–weighted;T2-weighted fat saturated; STIR T1-weighted, fast spin-echo, proton density–weighted;T2-weighted fat saturated T1-weighted; fast spin-echo T2-weighted

Coronal Sagittal Additional Optional Oblique sagittal Axial

●

●

● ● ●

Indirect Magnetic Resonance Arthrography Rationale and Indications ●

Indirect MR arthrography takes advantage of bulk flow and diffusion of contrast material from the vascular supply into the synovial tissue lining the bursae, joint capsule, and tendon sheaths to ultimately pool into the joint space (Fig. 18-18). However, little distention is achieved without a preexisting joint effusion. Gadopentetate dimeglumine–based contrast agents shorten the T1 relaxation time of tissues and can be used to produce arthrographic T1-weighted

fat-suppressed images. This technique enables an anatomic and physiologic assessment of joint pathology to be made. It is indicated for postoperative patients and for patients who have suspected labral tears when a direct arthrogram is logistically impracticable. It is indicated in postsurgical patients and when it is not possible to perform MR arthrography.

Technical Aspects

T1-weighted, STIR Gradient-recalled echo

STIR, short tau inversion recovery.

413

●

Intravenous injection of a 15-mL solution of 0.1 mmol/ kg gadopentetate dimeglumine. Greater concentrations of gadopentetate dimeglumine, including 0.2 and 0.4 mmol/kg, have not been shown to result in greater arthrographic benefit. It requires 20 minutes of passive motion involving the affected joint. See Table 18-5. The entire pelvis must be evaluated with large fieldof-view, non–fat-suppressed coronal spin-echo T1-weighted sequence and axial T2-weighted fast spinecho with fat suppression–weighted sequence to rule out other causes of pelvis, hip, or groin pain. Fast spin-echo T2-weighted fat suppression sequence is included for the identification of preexisting extraarticular fluid collections (bursitis).

Advantages ●

It allows assessment of both intra- and extra-articular soft tissues. This concept is based on the fact that the synovial membrane is vascular and injected

414

P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

■ FIGURE 18-16 Dedicated hip MRI. A, Coronal planning. B, Axial planning.

TABLE 18-4 Features of Dedicated Hip Magnetic Resonance Imaging of the Hip-Pelvis Imaging Planes

Pulse Sequences

Axial Coronal Sagittal Oblique sagittal Additional Optional Axial Coronal Orthogonal view, oblique axial view Orthogonal view, oblique-coronal view, perpendicular to oblique axial view*

T1-weighted, fast spin-echo, proton density–weighted;T2-weighted fat saturated, STIR T1-weighted, fast spin-echo, proton density–weighted;T2-weighted fat saturated T1-weighted, fast spin-echo T2-weighted T1-weighted, STIR,T2-weighted fat saturated Gradient-recalled echo Volumetric sequences as fat-suppressed 3D spoiled gradient-echo (1–1.5 mm thickness) SET1, STIR

SET1, spin echo T1 weighted; STIR, short tau inversion recovery. *This technique permits images of femoral neck lesions to be obtained in two orthogonal planes.13

● ●

intravenous contrast will diffuse to the joint over time. This property is advantageous when diagnosing inflammatory arthropathies such as rheumatoid arthritis, which result in synovial hyperplasia. The contrast medium enhances this intermediate-signal synovial tissue, a finding that is conspicuous during indirect arthrographic imaging. Less costly than direct MR arthrography Does not require fluoroscopic guidance or joint injection and is superior to conventional MRI in delineating the labrum when there is minimal joint fluid

Limitations ● ●

■ FIGURE 18-17

Alpha angle. The anterior alpha angle is measured on the sagittal oblique section parallel to the femoral neck and passing through the narrowest portion of the femoral neck. A line is drawn perpendicular to the femoral neck at its narrowest point. A second line (A) is drawn perpendicular to this point bisecting the femoral neck. A best fit circle is drawn, outlining the femoral head. The alpha angle is calculated as the angle formed between line B and the point where the femoral head protrudes anterior to the circle. An angle of 55 degrees or more is considered abnormal.

Inability to control the volume of the contrast medium that diffuses into the joint Insignificant joint distention, even if there is preexisting effusion; therefore, intra-articular structures are difficult to depict.6

Direct Magnetic Resonance Arthrography Rationale and Indications ●

Distention of the joint capsule to demonstrate the intra-articular, central, and peripheral compartments separated by the labrum. Central compartment: lunate cartilage, acetabular fossa, ligamentum teres, and the

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■ FIGURE 18-18

Indirect MR arthrography. A, Axial fat-suppressed T1-weighted image. B, Coronal fat-suppressed T1-weighted image. C, Coronal proton density–weighted image. Although no significant joint distention has been achieved, the contrast medium diffused from the synovial tissue moderately outlines intra-articular structures (arrow).

TABLE 18-5 Features of Indirect Magnetic Resonance Arthrography of the Hip-Pelvis Imaging Planes

Pulse Sequences

Field of View

Coronal Axial Coronal Axial Oblique sagittal

T1-weighted spin-echo T2-weighted fast spin-echo, fat saturated T1-weighted fat saturated T1-weighted fat saturated T1-weighted fat saturated

Large (entire pelvis) Large (entire pelvis) Small (dedicated hip) Small (dedicated hip) Small (dedicated hip)

loaded articular surfaces of the femoral head. Peripheral compartment: unloaded cartilage of the femoral head, the femoral neck with the synovial folds, and the articular capsule17

Technical Aspects18–20 ●

●

MR arthrography of the hip is currently a two-step procedure. The patient is injected under fluoroscopic guidance and is then transferred to the MR scanner. The patient is placed supine on the fluoroscopic table. The lower extremity is held in neutral or slight internal rotation, taping the toes together. A bolster under the knees has been advocated by some authors. The skin is prepared in the usual sterile fashion, disinfected with iodine solution, and covered with sterile drapes. The landmarked skin is anesthetized with 1% lidocaine. The needle size may vary, but commonly a 22-gauge, 3-inch (7 to 9 cm) spinal needle is used. The needle is advanced under fluoroscopic control. Several techniques for the anterior approach have been described. Duc and colleagues compared neck and head injection techniques and concluded that both are well tolerated; neck injection produced less discomfort and was associated with greater extra-articular contrast medium leakage (Figs. 18-19 and 18-20).18 ● Femoral head: the target site for the femoral head injection is located at the lateral aspect of the superolateral quadrant of the femoral head. The needle is advanced until the tip reaches the cartilage of the femoral head.

■ FIGURE 18-19

MR arthrography techniques. Femoral head (black arrow): the target is located at the lateral aspect of the superolateral quadrant of the femoral head. Femoral neck (white arrow): the target is the midpoint between the superior and inferior outline of femoral neck.

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■ FIGURE 18-20 MR arthrography techniques. Different approaches to MR arthrography. A, Femoral neck. B, Femoral head. C, Oblique approach. D, CT-guided arthrography. White asterisk represents contrast medium encircling the femoral neck and orbicularis ligament.

Femoral neck: the target site of the femoral head injection is the midpoint between the superior and inferior outline of the femoral neck at the base of the femoral head and the intertrochanteric line.The needle is advanced until the bone of the femoral neck is reached. ● Oblique approach from lateral to medial. Infusion of a small quantity of iodinated contrast agent confirms either an intra-articular position or a misplaced position. When the iodinated contrast agent encircles the femoral neck or the orbicularis ligament is delineated, correct intra-articular placement is confirmed. When the contrast agent remains focal and globular extra-articular placement is suggested, the needle tip must be repositioned. A periosteal needle tip position can easily be adjusted to an intra-articular position by twisting the needle hub a half turn and rotating the bevel 180 degrees. Iliopsoas tendon and bursa locations generate a characteristic elongated pattern of contrast agent following the long axis of the tendon and can be adjusted by changing the needle position or with direct needle advancement to the periosteum (see Fig. 18-20). Subsequently, a dilute gadolinium solution is injected (approximately 15 mL of a 0.1-mmol/kg solution of gadopentetate dimeglumine) and the patient is taken ●

●

●

●

●

●

to the MR scanner for sequence acquisition. The volume of the injection ranges between 7 and 20 mL. MRI should begin within 30 minutes of joint injection to minimize absorption of the contrast agent. Additional maneuvers such as hip traction using 3- to 6-kg weights applied to the thigh to correct articular distention may improve the sensitivity and specificity for detection of cartilage lesions and labral tears owing to separation of the acetabulum and the femoral head.6,17 Alternatively, the intra-articular positioning of the needle can be performed using ultrasound guidance, CT, open MRI guidance, and even blindly, using anatomic landmarks, saving considerable time and scheduling coordination. See Table 18-6.

Advantages ●

●

Ability to detect capsulolabral pathology and partialthickness and vertical rotator cuff tendon tears (Figs. 18-21 to 18-23) Better distention of the joint capsule, particularly the labral-ligamentous complex, allows easier depiction of irregular tears versus more smoothly delineated anatomic variants such as sublabral sulci and foramina.

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TABLE 18-6 Features of Direct Magnetic Resonance Arthrography of the Hip-Pelvis

Imaging Planes

Pulse Sequences

Coronal

T1-weighted fat saturated, fast spin-echo T2-weighted fat saturated T1-weighted fat saturated, fast spin-echo T1-weighted fat saturated T1-weighted fat saturated T1-weighted fat saturated, spin-echo T1-weighted fat saturated

Axial Oblique sagittal Sagittal (optional) Radial imaging (optional) Traction (optional)

■ FIGURE 18-23 Oblique sagittal proton density–weighted MR image following the femoral neck axis. 1, Anterior labrum; 2, posterior labrum; asterisk, femoral cartilage.

Limitations ● ● ● ■ FIGURE 18-21

Coronal fat-suppressed T1-weighted MR arthrography. 1, labrum; 2, femoral head cartilage; 3, ligamentum teres; 4, transverse ligament; 5, acetabulum.

● ● ● ●

● ●

●

●

■ FIGURE 18-22 Sagittal T1-weighted MR arthrography delineates smoothly femoral (white arrow) and acetabulum (black arrow) cartilage.

Patient’s adversity to the procedure Safety Cost Extra time and labor hours per procedure Scheduling and coordinating use of both fluoroscopy and MRI Direct involvement of the radiologist Postprocedure assessment of pain and discomfort show that direct arthrography is better tolerated than the MRI itself. Use of ionizing radiation The potential for contrast reaction is considerably greater for the iodinated agents. Although the overall risk of complication with minimally invasive intraarticular needle arthrography is very low, the potential complications are considerable. An infection introduced into the joint can result in septic arthritis, osteomyelitis, or fasciitis. Arthrography may cause direct damage to the nerves, capsule, or ligaments. The cost of the fluoroscopy suite, nursing, and MRI scan time help to decrease efficiency when evaluating patient throughput. Cost of the radiologist’s time for direct arthrography is considerably greater than using a nurse or technician to obtain an intravenous line. Accidental injection of gas can lead to an incorrect diagnosis of loose bodies from the magnetic susceptibility artifact. However, attributing the exact cause of a susceptibility artifact should be based on its location; joint bodies are typically located in the more dependent portions, whereas gas bubbles rise to the nondependent portions of the joint.

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Ultrasonography Rationale and Indications (Fig. 18-24) ●

●

●

● ●

Developmental dysplasia of the hip. Real-time ultrasonography has been used for assessment of the hip in infants and has been accepted as a screening technique for the detection and treatment of developmental dysplasia of the hip. In the neonate, sonograms should be obtained before the infant is 6 weeks old (Fig. 18-25).21 Transient synovitis of the hip. Effusion within the anterior recess of the joint capsule is easily depicted (Fig. 18-26). Joint effusion. Difference in joint distention of greater than or equal to 2 mm between the symptomatic and asymptomatic hips has been reported as significant (see Fig. 18-26). Capsular thickening Synovial tissue vascularity can be graded with Doppler ultrasonography, especially in inflammatory disease, such as rheumatoid arthritis.22

●

● ●

Abnormalities of muscles and tendons, greater trochanter complex, iliopsoas, abductors, and hamstrings can be seen. Extra-articular fluid collections can be detected. The feasibility of ultrasound-guided aspiration of the hip effusion for diagnostic and therapeutic purposes has been demonstrated.23 Aspiration must be made at least 1 cm lateral to the neurovascular bundle.

Advantages ● ● ● ● ●

Easy to handle, safe, and inexpensive and noninvasive procedure Available in most radiology departments No radiation required and does not require sedation and therefore particularly useful in newborns and children Combines static and dynamic assessment of the newborn hip Synovial tissue perfusion can be assessed with color Doppler and power Doppler imaging without intravenous contrast medium enhancement.

■ FIGURE 18-24 Comparative plain hip radiograph (A) and coronal ultrasound images (B and C). 1, Greater trochanter; 2, lesser trochanter; 3, femoral head; 4, femoral neck; 5, acetabulum; 6, iliopubic rami; 7, ischiopubic rami; 8, triradiate cartilage.

■ FIGURE 18-25 Normal ultrasonographic anatomy, newborn (A) and 5-month-old infant (B). 1, Acetabulum; 2, femoral head; 3, pubis; 4, labrum; 5, gluteus minimus; 6, gluteus medius; 7, triradiate cartilage; 8, ossification center of the femoral head.

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419

■ FIGURE 18-26 Anterior joint capsule. A, Normal. B, Contralateral hip with joint effusion (white arrowheads) related to transient synovitis in synovial tissue (black arrowheads). 1, Femoral physis; 2, femoral shaft; white asterisks, anterior joint capsule.

●

Facilitates face-to-face communication between the patient and examiner

● ●

Limitations ●

● ● ●

●

It is operator dependent; it is essential that the persons who do hip sonography receive proper training. The current recommendation is that a person needs to perform approximately 100 studies to develop competence in this technique. The femoral head and acetabulum cannot be assessed once calcification has started. It cannot demonstrate bone marrow signal alterations. Underlying disorders in children with joint effusion can be difficult to diagnose, such as Legg-Calvé-Perthes disease, slipped capital femoral epiphysis (SCFE), and septic arthritis. Therefore, in children older than age 8 years, in whom Legg-Calvé-Perthes disease and SCFE are more likely, radiographs are generally advised. Limited use in obese adults

Technical Aspects ●

●

A high-frequency (5 to 12 MHz) transducer is used because the structures of interest are superficial, and the transducer needs to be linear because tendons are highly ordered, linear structures. Newborn: To perform the newborn ultrasonographic examination, the patient’s age should range from newborn to 6 months. The infant is placed in a supine or lateral position. Assessment should include views in orthogonal planes, and description of stability and morphology is essential.

●

●

●

See Table 18-7. To evaluate joint effusion the hip is examined with the patient in a supine position with the hip in neutral position (extension and slight external rotation). An anterior approach along the long axis of the femoral neck is used to visualize the anterior capsule of the hip. A contralateral asymptomatic hip study must be performed as the normal reference (Fig. 18-27).23 The anterior joint capsule is seen as a hyperechoic line of tissue between the anterior femoral neck and the fascia of the iliopsoas muscle. This line is simply the interface between joint and muscle and should not be interpreted as fibrous capsule (see Fig. 18-27). The contour of the capsule depends on rotation, being concave in exorotation and convex in endorotation. However, enlargement of the anterior joint capsule is the main indication of effusion. Normal lumps in the posterior layer should not be interpreted as debris or flocculation. Vessels can be shown with color Doppler imaging and do not migrate.

NORMAL ANATOMY Osseous Structures The hip is a ball-and-socket joint. The upper end of the femur is formed into a round ball (the head of the femur). A cavity in the pelvic bone forms the socket (acetabulum). The hip is an incongruent joint with the unloaded acetabular diameter slightly smaller than the femoral head. The acetabular labrum acts to deepen the hip joint and provide further stability.12,19 An examination of the pelvis should include surrounding structures, whereas

TABLE 18-7 Features of Ultrasonography of the Hip-Pelvis Imaging Planes

Definition

Measurements

Coronal neutral

The transducer is oriented in a coronal plane with respect to the acetabulum.The hip is in physiologic neutral. The hip is in 90 degrees of flexion. The transducer is oriented in a transverse (axial) plane with respect to the acetabulum (orthogonal to the coronal view).The hip is in 90 degrees of flexion. Dislocation may be demonstrated with a telescopic or piston maneuver of the adducted hip in a posterior direction. A reverse (stress) maneuver may be used to assess reduction.

Angle measurements (Fig. 18-27)

Coronal flexion Transverse flexion view Stress view

Angle measurements

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a dedicated hip examination is not likely to include this area (Fig. 18-28).

Femoral Head The femoral head forms two thirds of a sphere, and its articular surface is thicker along the mediocentral aspect and thinnest along the periphery. The greater trochanter is a quadrilateral bony eminence at the superior aspect of the junction of the femoral neck and proximal shaft. The surface of the greater trochanter has four distinct facets for the tendinous attachments and sites for bursae. The lesser trochanter is more of a triangular or conical eminence that arises at the lower part of the junction of the femoral neck and the proximal femur and projects backward. Again, there are three distinct facets along its bony margins that allow for tendinous insertions.24

Pelvis and Acetabulum

■ FIGURE 18-27 Hip angle measurement described by Graf for the evaluation of the maturity of infant’s hip. Alpha angle (1) is indicative of the slope of the bony acetabulum. Full maturity is indicated by an angle of 60 degrees or larger. The angle is formed by the intersection of two lines: A, baseline of the iliac, tangential to the iliac wing, and B, the acetabular line, from the lower edge of the acetabulum to the promontory. The beta angle (2) is indicative of the degree of cartilaginous roof coverage.

■ FIGURE 18-28

The acetabulum is formed by the confluence of the ilium, pubis, and ischium at the triradiate cartilage. Medially, the acetabulum is formed by the pubis; laterally and inferiorly, it is formed by the ischium; and superiorly, it is formed by the ilium. The osseous margin of the acetabulum is deficient along its anterior inferior portion. This deficiency is known as the acetabular notch. Opening anteriorly, laterally, and inferiorly the acetabulum provides a wide range of motion.

Normal osseous structures: volume-rendering 3D reconstructions. A, Anterior view of pelvis of 15-year-old boy. B, Same patient, posterior view. C, Newborn pelvis. D, Adult pelvis. 1, Greater trochanter; 2, lesser trochanter; 3, femoral head; 4, femoral neck; 5, iliac bone; 6, iliopubic rami; 7, ischiopubic rami; 8, triradiate cartilage; 9, anterior-superior iliac spine; 10, ischial tuberosity; 11, posterior iliac spine.

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In the iliac bone the anterior-superior and anteriorinferior iliac spines serve as important attachment sites for muscles of the anterior quadrant of the hip, and avulsion injuries from these sites are not uncommon. The anterior-superior iliac spine is an anterior protrusion at the junction of the iliac crest and the anterior border of the pelvis. The anterior-inferior iliac spine is the second anterior protrusion. The superior and inferior pubic rami should also be included in all examinations, as should the symphysis pubis. The most posterior and inferior border of the ischium is a roughened prominence, the ischial tuberosity, that allows the attachment of the hamstring tendons. There is some controversy in the literature concerning the orientation of the acetabulum. The average of adult male anteversion is 14 degrees (range, 5 to 19 degrees) and 19 degrees for women (range, 10 to 24 degrees). The degree of anteversion changes with position. When standing, the anterior-superior iliac spine and pubic symphysis are in the same coronal plane and the acetabulum is not as obviously anteverted, whereas when the pelvis is flexed, as it is when sitting, the forward facing of the acetabulum is accentuated.

■ FIGURE 18-29 A and B, Normal bone marrow conversion. Coronal T1-weighted (1) and coronal fat-suppressed T2-weighted (2) MR images of a 7-year-old. Yellow marrow is only seen in the epiphyses (femoral head) and apophyses (greater trochanter). Coronal T1-weighted (3) and coronal fat-suppressed T1-weighted (4) MR images of a 15-year-old. Conversion of bone marrow has extended to the femoral neck and acetabulum. Asterisk in A indicates triradiate cartilage; asterisk in B points to the greater trochanter cartilage.

(Continued)

421

Bone Marrow Marrow undergoes conversion from hematopoietically active red marrow to hematopoietically inactive yellow marrow in a very orderly and predictable fashion in a healthy person. At birth, all the marrow produces blood cells, but at age 1 year, marrow in the epiphyses and apophyses becomes inactive. As aging continues, the marrow continues to convert to yellow marrow but at a slower rate. This conversion is from distal to proximal, from the appendicular to the axial skeleton, and from the diaphyses of the long bones toward the metaphyses. Conversion of the marrow in the flat bones of the pelvis lags behind that in the lower extremity (Figs. 18-29 and 18-30).25 In the pelvis, hematopoietic marrow is diffusely distributed, with areas of focal fatty marrow found around the acetabula and symphysis pubis. This hematopoietic marrow may become more prominent or may be replaced by fatty marrow as the patient ages. These changes tend to be bilateral and symmetric. The trabecular and cortical bone yield very little signal and are hypointense on MR images obtained with all pulse sequences. The major tensile and compressive trabecular

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■ FIGURE 18-29—Cont'd

bands in the proximal femurs and all cortical bone have low signal intensity on both T1- and T2-weighted images.

zone of intermediate signal on spin-echo and gradientrecalled echo images.

Cartilage

Labrum

The acetabulum is lined with a nearly circumferential region of articular cartilage known as the lunate cartilage because of its moon-shaped appearance en face. The cartilage does not extend over the acetabular fossa. The fovea capitis is the only aspect of the femoral head that is not covered with articular cartilage. The thickest cartilage is located along the superior margin of the joint, which is the area that bears greatest weight, providing appropriate load bearing during the wide range of motion of the hip. The articular cartilage of the acetabulum is thickest anterosuperiorly (2 mm) and thinnest posteromedially (1 mm). Correspondingly, the femoral articular cartilage is thickest superiorly, medially, and slightly posteriorly (2.5 mm). The weight bearing of the femoral and acetabular cartilage area can be divided into three 30-degree ranges in a midsagittal plane: superoanterior, superior, and superoposterior (Fig. 18-31).7 On routine MRI of the hip the articular cartilage of the femoral head and the acetabulum are identified as a thin

The acetabular labrum is a fibrocartilaginous triangular ring that surrounds the bony acetabulum and blends inferiorly with the transverse acetabular ligament (Fig. 1832). It increases the joint surface area by adding depth to the acetabulum and thereby reduces mechanical stress on the articular cartilage. The labrum is widest in the anterior quadrant (mean 5.5 ± 2 mm), thickest in the posterosuperior segment (mean 5 ± 1.5 mm), and thinnest anteroinferiorly. The labrum can be divided under electron microscopy into three different layers: superficial layer, stratiform structure layer, and basal layer. The labrum joins the articular hyaline cartilage of the acetabulum through a transition zone. Small areas of intermediate signal intensity represent undifferentiated connective tissue and can produce a diagnostic pitfall with a labral tear. The parallel orientation of the articular cartilage to the labrum helps to differentiate it from a flap tear and has a more intermediate signal than the normal high-fluid signal intensity of a tear.10

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■ FIGURE 18-30 Normal adult bone marrow. Coronal T1-weighted (1) and coronal fat-suppressed T2-weighted (2) MR images of a 25-year-old woman. Hematopoietic marrow is diffusely distributed in the pelvis with focal patchy areas (white asterisk). Coronal T1-weighted (3) and coronal fatsuppressed T2-weighted (4) MR images of a 42-year-old woman.

The hip labrum is a relatively avascular structure, except for the outer 0.5 mm, the capsular area, where an increased vascularity can be found. The labrum is an innervated structure.26 At the inferior aspect of the acetabulum there is a focal deficiency of the bony acetabulum, termed the acetabular notch. This notch is bridged by the transverse ligament (Figs. 18-33 and 18-34). The remaining deep opening to the ligament is referred to as the acetabular foramen, which is filled with fat. Nutrient vessels and nerves perforate this structure to enter the joint. The periphery of the notch subsequently acts as an attachment site for the ligamentum teres.12

Joint Capsule

■ FIGURE 18-31 Articular cartilage. Axial fat-suppressed T1-weighted MR image shows femoral cartilage (arrow) and acetabular cartilage (arrowheads).

An inelastic fibrous capsule envelops the hip joint and attaches proximally to the acetabulum, labrum, and transverse ligament and extends distally to surround most of the femoral neck with attachment at the base of the trochanters. The transverse ligament is a part of the acetabular labrum, which bridges the acetabular notch at the inferolateral acetabulum to form a complete circle and blends with the labrum. It consists of strong flattened fibers that differ from the labrum in that they do not contain

■ FIGURE 18-32 The labrum is a fibrocartilaginous ring that deepens the acetabulum. A, Coronal proton density– weighted MR arthrogram. B, Axial fat-suppressed T1-weighted MR image. C, Sagittal fat-suppressed T1-weighted MR image. D, Oblique sagittal T1-weighted MR image. 1, Superior labrum; 2, anterior labrum; 3, posterior labrum.

■ FIGURE 18-33 Acetabular notch. Axial fat-suppressed T1-weighted MR image. Note focal deficiency of the bony acetabulum (arrow). This notch is bridged by the transverse ligament (asterisk).

■ FIGURE 18-34 Acetabular notch. Coronal T1-weighted MR image showing acetabular notch (arrow) and transverse ligament (asterisk).

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The fibrous capsule is reinforced by several ligaments, namely, the ischiofemoral, iliofemoral, and pubofemoral ligaments, which are discernible thickenings of the capsule. The iliofemoral ligament is the thickest and strongest ligament and extends from the anterior inferior iliac spine

to the intertrochanteric line of the femur with an inverted Y shape anteriorly, thus leading to its lesser used name, the Y ligament of Bigelow (Fig. 18-37). The pubofemoral ligament extends horizontally from the superior pubic ramus and obturator crest to the undersurface of the femoral neck and merges with the fibers of the capsule and deep surface of the iliofemoral ligament. There is an inherent weakening or hole between the vertical band of the iliofemoral ligament and the pubofemoral ligament anteriorly that can allow communication of the joint with the iliopsoas bursa. The ischiofemoral ligament extends superolaterally from the ischium along the posterior aspect of the femoral neck to combine with the fibers of the zona orbicularis and insert on the greater trochanter. The ligamentum teres is a weak intra-articular ligament with a pyramidal morphology. It is covered by synovial membrane and extends from its basal attachment as two bands on the acetabular notch and transverse ligament to its apex at the fovea capitis, a centrally located, roughened depression on the femoral head, which, incidentally, is the only region of the femoral head that is not covered by articular cartilage. In some individuals only the synovial sheath is present without a discernible ligament; and in a small percentage of the population, neither can be identified. The ligamentum teres transmits the foveal artery, which provides a minimal contribution of the blood supply to the femoral head. The ligamentum teres does not provide significant structural integrity to the hip joint; and, other than surrounding this small nutrient artery to the femoral head, its function is not known.12

■ FIGURE 18-35 Superior perilabral recess. Coronal fat-suppressed T1-weighted MR arthrogram shows proximal aspect of the superior capsule and inserts several millimeters above the labrum, creating a large perilabral recess (arrow).

■ FIGURE 18-36 Zona orbicularis. Coronal fat-suppressed T1-weighted MR arthrogram. 1, Zona orbicularis; 2, ligamentum teres.

cartilage and transform the acetabular notch into a foramen (see Figs. 18-33 and 18-34). The proximal attachment of the capsule joint is along the osseous rim of the acetabulum. The superior aspect of the joint capsule inserts several millimeters above the labrum, which creates a normal larger perilabral recess. In addition, the joint capsule inserts directly at the base of the labrum along the anterior and posterior margins of the joint, thus creating a small synovium-lined perilabral recess (Fig. 18-35). Distally the capsule extends farther along the anterior aspect of the femoral neck at the base of the trochanters laterally compared with the posterior aspect. Posteriorly its attachment is slightly more medial near the junction of the mid third and distal third of the femoral neck. Most fibers of the capsule are oriented longitudinally from the pelvis to the femur. There is a deep layer of circularly oriented fibers known as the zona orbicularis that encircles the capsule at the base of the femoral neck (Fig. 18-36). These fibers do not directly attach to bone and may be mistaken for the acetabulum labrum when arthroscopy is performed.

Ligaments

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Muscles and Tendons On MRI T1-weighted or proton density–weighted images, muscles demonstrate intermediate signal and are separated by high signal intensity fat along the fascial divisions. It is generally believed that muscular attachments to the bone demonstrate four consistent zones composed of tendon, undemineralized fibrocartilage, mineralized fibrocartilage, and Sharpey fibers.24 Hip musculature can be divided by anatomic location, quadrants (anterior, lateral, and posterior), or functional groups (flexors, abductors, external rotators, and adductors) (Figs. 18-38 and 18-39).

Anterior Quadrant

■ FIGURE 18-37 Coronal fat-suppressed T1-weighted MR arthrogram shows iliofemoral ligament (arrow).

The muscles in the anterior quadrant of the hip, including the iliopsoas, sartorius, rectus femoris, and the pectineus, act as the primary flexors of the hip. The iliopsoas muscle is seen anterior to the femoral head at the 12-o’clock position on axial images and traverses the pelvis and exits anteriorly over the superior pubic rami, beneath the inguinal ligament to insert on the lesser trochanter. As it exits from the pelvis it can often be seen beneath the femoral

■ FIGURE 18-38 Axial series of hip muscles and tendons: T1-weighted MR images from inferior plane (1) through superior plane (6). Muscle structures: 1, fascia lata tendon; 2, fascia lata muscle; 3, vastus intermedius; 4, iliopsoas; 5, rectus femoris; 6, sartorius; 7, adductor muscles; 8, obturator externus; 9, adductor magnus tendon; 10, semitendinosus tendon; 11, conjoined tendon of biceps femoris and semitendinosus tendon; 12, biceps femoris; 13, gluteus; 14, pectineus; 15, geminus; 16, vastus lateralis; 17, obturator internus; 18, quadratus femoris.

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■ FIGURE 18-39 Coronal series of hip muscles and tendons: T1-weighted MR images from anterior (A) through posterior (D). 1, pubis; 2, adductor; 3, pectineus; 4, femoral nerve, artery, and vein; 5, rectus femoris; 6, iliopsoas; 7, rectus femoralis tendon; 8, gluteus muscle; 8A, gluteus medius; 8B, gluteus minimus; 9, iliac bone; 10, obturator externus; 11, gracilis; 12, iliopsoas muscle; 13, iliofemoral ligament; 14, tensor fasciae latae; 15, obturator internus muscle; 16, ischium; 17, vastus lateralis; 18, vastus intermedius; 19, adductor magnus; 20, hamstring muscle complex; 21, gluteus.

vessels and medial to the iliacus muscle.27 The pectineus arises from the iliopubic ramus and inserts just distal to the lesser trochanter. The sartorius muscle arises from the anterior-superior iliac spine and runs inferiorly and medially along the thigh to insert on the proximal tibia as part of the pes anserinus tendon group. The rectus femoris muscle arises as two tendons, the anterior or straight and the posterior or reflected; the tendon is anterolateral to the iliofemoral ligament and follows the lateral brim of the acetabulum. The adductor muscles of the hip lie anterormedially and include the adductor longus, brevis, and magnus as well as the gracilis and pectineus and arise from the pubic bone. The obturator externus arises from the ramus of the surface of the pubis and ischium as well as from the external surface of the obturator membrane. Their tendon extends posterolaterally and inserts into the trochanteric fossa on the medial aspect of the greater trochanter.

Lateral Quadrant The lateral quadrant contains the abductor muscles, including the gluteus medius and minimus, and the tendon fasciae latae more superficially. The greater trochanter of the femur demonstrates a complex but consistent topographic anatomy; each of its four facets have specific tendinous attachments and specific nearby bursae. The gluteus medius muscle arises laterally from the wing of the ilium and inserts onto the lateral and superoposterior facet of the greater trochanter, which can be well visualized on sagittal images. The gluteus minimus muscle lies deep to the gluteus medius and inserts onto the anterior facet of the greater trochanter. There is a small amount of fat between these two tendinous insertions.24,28,29

Posterior Quadrant The muscles in the posterior quadrant include the extensors and external rotators, consisting of the gluteus maximus,

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piriformis, obturator internus, superior gemellus, inferior gemellus, and quadratus femoris. The gluteus maximus is the largest and strongest muscle of the body. Its origin is on the posterior third of the iliac crest and the dorsum of the sacrum and coccyx and inserts into the iliotibial band and in the posterior margin of the femur just below the level opposite the lesser trochanter. The piriformis muscle originates from the anterior sacrum and passes out of the pelvis through the greater sciatic notch to insert on the upper border of the greater trochanter between the iliofemoral ligaments anteriorly and the gluteus medius tendon posteriorly. The piriformis muscle is an abductor as well as an external rotator. Lying inferior to the piriformis, the obturator internus muscle also arises from the medial surface of the pubis, passes the lesser sciatic notch, and joins the superior and inferior gemelli muscles to insert onto the tip of the greater trochanter laterally, deep to the piriformis tendon. The tendinous insertions of these muscles can be well seen on sagittal images along the facets of the greater trochanter. The obturator externus covers the outer surface of the anterior wall of the pelvis, arising from the margin of the medial side of the obturator foramen; the tendon runs across the back of the neck of the femur and inserts into the trochanteric fossa. The last of the important short external rotators is the quadratus femoris, which arises from the upper part of the external border of the tuberosity of the ilium and inserts into the upper part of the posterior aspect of the greater trochanter and lies inferior to the gemelli muscles.30 The hamstring tendons originate at the ischial tuberosity and can be evaluated using all three imaging planes. The three muscles that constitute the hamstring muscle complex are the biceps femoris and semitendinosus and semimembranosus muscles; some anatomists consider the adductor magnus to be a hamstring muscle. The muscles of the hamstring muscle complex are important hip extensors and flexors of the knee. The semimembranosus tendon arises from the superolateral aspect of the ischial tuberosity, beneath the proximal half of the semitendinosus muscle. The semitendinosus tendon and the long head

of the biceps tendon form a conjoined tendon that arises from a medial impression on the superior aspect of the ischial tuberosity. It should be noted that the adductor magnus has a curvilinear attachment to the lateral surface of the ischiopubic ramus and the inferolateral aspect of the ischial tuberosity.31

Bursae There are about 20 bursae around the hip joint, with varying size and prevalence. Bursae are found where tendons move against each other or glide over bone surfaces. The iliopsoas or iliopectineal bursa is situated beneath the musculotendinous portion of the psoas muscle and is intimately related to the anterior aspect of the hip joint. A communication between the joint and this bursa exists in 10% to 15% of the normal population (Fig. 18-40). An enlarged bursa may extend into the pelvis.27 There are three bursae located around the greater trochanter: the trochanteric bursa, the subgluteus medius bursa, and the subgluteus minimus bursa. Some authors describe a separated subgluteus maximus bursa that lies distal to the trochanteric bursa. The trochanteric bursa is always seen in transverse T1-weighted spin-echo images as a thin hypointense line because it is surrounded by fat on both sides. The subgluteus medius bursa is depicted less frequently because of a separation of the bursa from the gluteus minimus tendon by a fat layer or a medial extension of the bursa. Its depiction is improved when it is distended with an effusion. The subgluteus medius bursa is found deep to the lateral part of the gluteus medius tendon and is not reliably identified on most nonenhanced MR images (Figs. 18-41 and 18-42).6,24,29 The obturator externus bursa is located between the tendon of the obturator externus and the posterior hip capsule. This bursa is formed by a protrusion of the posterior hip synovium between the posterior femoral capsule (ischiofemoral capsular thickening) and the zona orbicularis. The bursa lies between the ischiofemoral capsular ligaments and the tendon of the obturator externus

■ FIGURE 18-40 Coronal (A) and axial (B) T1-weighted MR arthrograms. Note normal communication between the joint and iliopsoas bursa.

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■ FIGURE 18-41

Normal bursae: subgluteus maximus bursa (green); subgluteus medius bursa (orange); subgluteus minimus bursa (light blue). 1, Gluteus medius muscle; 2, gluteus minimus muscle; 3, superior capsule; 4, greater trochanter; 5, tensor fascia lata; 6, vastus lateralis muscle.

■ FIGURE 18-42 Greater trochanter facets. 1, Gluteus minimus; 2, gluteus medius; white asterisks, anterior facet; arrowheads, lateral facet; black asterisks, posterior facet.

muscle as it spirals, posterior to the femoral neck, toward its insertion into the trochanteric fossa.30

foramen just anterior and inferior to the piriformis muscle, where it is generally seen as an isointense rounded structure or grouping of neural fascicles surrounded by fat.

Neurovascular Bundles The hip and thigh are vascularized by branches derived from the deep femoral artery, the obturator artery, and the gluteal artery. The primary source of blood supply comes from the most important branches of the deep femoral artery, the medial circumflex femoral artery, and the lateral circumflex femoral arteries, but it may also arise directly from the femoral artery. The medial circumflex femoral artery provides the majority of the blood supply to the iliopsoas muscle, pectineus muscle, and hip joint (femoral head and neck and greater trochanter) via ascending and descending branches. The lateral circumflex femoral artery supplies the lateral hip, thigh, and knee via ascending, transverse, and descending branches. There is also a small contribution from a small artery in the ligament of the head of the femur that is a branch of the posterior division of the obturator artery. Only a small and variable amount of the femoral head is nourished by the artery of the ligamentum teres. In addition to the vessels and muscles surrounding the hip and their tendinous attachments, the sciatic nerve is a structure that should be routinely identified on all imaging of the pelvis or hip. The sciatic nerve is the largest nerve in the body and measures approximately 2 cm in width. It begins as a continuation of the sacral plexus and travels laterally through the pelvis and out of the greater sciatic

COMMON VARIANTS Cystic Changes in the Femoral Neck, Herniation Pits Herniation pits have been considered to be an incidental finding in 5% of the population of healthy individuals. However, the presence of abnormalities at the femoral neck junction is a frequent alteration seen in hips with associated femoroacetabular impingement syndrome (Fig. 18-43).32,33

Labral Signal Signal alterations at the junction of the acetabular hyaline cartilage with labral fibrocartilage may be mistaken for a labral detachment.19

Sublabral Sulcus A posteroinferior sublabral groove is a relatively common normal anatomic hip variation. If not recognized as normal, the sulcus may serve as a diagnostic pitfall on MR arthrography (Fig. 18-44). Anterosuperior sublabral sulcus is a rare anatomic variant, but some authors have found an association with mild acetabular dysplasia.34

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■ FIGURE 18-43 Herniation pits. Although they have been considered as a normal variant, they are frequently associated with femoroacetabular impingement, especially those larger than 5 mm.

■ FIGURE 18-44 Posteroinferior sublabral groove. Sagittal fatsuppressed T1-weighted MR arthrogram shows anterior labrum (asterisk), acetabular notch (arrow), and posterior sulcus (arrowhead).

A cortical ridge and fat within the acetabular fossa should not be confused with cartilage defects (Fig. 18-45).

Anterior Capsule Variants

Variations of the Labrum The labrum is usually triangular, but rounded, blunted, and irregular labra have been described. The incidence of triangular labra decreases with increasing age, whereas the incidence of rounded, irregular margins increases with age. Absent labra have been noted in 10% to 14% of individuals.19 The inverted labrum is defined as a portion of the labrum that is interposed within the joint, overlying the articular surface of the acetabulum. Regardless of the etiology (congenital or acquired during postnatal development), it is recognized as a cause of primary osteoarthritis, labral tear, and acetabular dysplasia.

Trabecular Bars Normal thickened trabecular lines in the femoral metaphyseal region, adjacent to the lesser trochanter, can be misdiagnosed as a calcified chondroid matrix in an enchondroma. These trabecular bars are more apparent in the patient with osteoporosis.

Iliopsoas Bursa Communication A communication between the joint and this bursa exists in 10% to 15% of the normal population (see Fig. 18-40).

Normal variants include plicae and local thickness of the capsule.

Os Acetabuli Accessory ossification center may persist unfused. The ossicle most frequently described is the os acetabuli anterior (Fig. 18-46). Os acetabuli has been described in femoroacetabular impingement syndrome.

Otto Pelvis, Protrusio Acetabuli The pelvis has depressed acetabulum and protrusion of the femoral head, resulting in limitation of hip movement. The medial wall of the acetabulum projects medial to the ilioischial line; it can be primary, more frequently described in women, or secondary, associated with a number of disease processes (rheumatoid arthritis, Marfan syndrome, Paget’s disease, femoral head prosthesis, and, more recently, femoroacetabular impingement syndrome of the pincer type).

BASIC BIOMECHANICS As with any joint, the hip’s ability to provide mobility and stability depends on articular surface morphology, muscle forces, and soft tissue restraints. Forces across the hip joint are a combination of body weight, ground reaction forces, and abductor muscle force.35–37

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■ FIGURE 18-45 Normal cortical ridge (white arrow) and normal fat signal (black arrow) within the acetabular fossa should not be confused with cartilage or osseous defects.

The forces exerted on the hip have their biologic expression in the form of the femur and acetabulum, particularly in the location and orientation of the trabecular pattern. When the weight of the body is being borne on both legs, the center of gravity is centered between the two hips and its force is exerted equally on both hips. During daily activities and sports, forces across the hip are substantial. While standing, the body’s center of gravity lies just posterior to the axis of the hip in the sagittal plane, which causes the pelvis to tilt posteriorly on the femoral head. This tilt is opposed by the tensile forces from the stretching of the anterior capsule, implying that the energy required to stand stationary should be compensated by the ligaments without muscular contribution. Gait involves ranges of motion in all three planes. The force for motion is derived from the musculature of the lower limbs, although stability could not be maintained without the ligamentous capsule. The force from weight bearing in the acetabulum during gait is biphasic, with peaks in force occurring at heel strike and toe-off. Areas of contact form two columns of force on the anterior and posterior rims, joining together in the superior aspect of the fossa. As more force is applied to the hip, the areas enlarge as the femoral head settles deeper in the

acetabulum. The areas of most frequent weight bearing are also associated with the stiffest and thickest articular cartilage. Studies have been published that examine the specific forces encountered in walking, when climbing stairs, during skiing, and in routine daily activities. Variance of forces rises from incongruence of the femoral head to the acetabulum and the hip muscles that control these movements. It is estimated that the hip endures forces ranging from one third of the body weight with double leg support to five times the body weight during running. The asymmetry between the femoral head and the acetabulum distributes weight to multiple areas. This incongruence is inherent to the hip and necessary for sustaining normal function. When the hips are viewed in the sagittal plane and if the center of gravity is directly over the centers of the femoral heads, no muscular forces are required to maintain the equilibrium position, although minimal muscle forces will be necessary to maintain balance. If the upper body is made to lean slightly posteriorly so that the center of gravity comes to lie posterior to the centers of the femoral heads, the anterior hip capsule will become tight, so that stability will be produced by the Y ligament of Bigelow.

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■ FIGURE 18-46 Os acetabuli, with unfused ossification center. Axial CT volume-rendered 3D reconstructions.

Therefore, in symmetric standing on both lower extremities, the compressive forces acting on each femoral head represent approximately one third of body weight. Individual muscle contractions contribute significantly to the forces generated to counterbalance gravity and create movement. Many of the hip muscles involve very complex geometric architectures; thus, determining their exact mechanical influence on hip function is difficult. Computer modeling techniques enhanced by CT and MRI are some of the newer techniques for estimating complex hip muscular actions. These methods have allowed researchers to reconstruct the hip muscle

geometry. Dynamic biomechanical assessments will enable us to accurately and reliably detect mechanical dysfunction, functionally grade partial and combined soft tissue injuries, relate injury to the capability of performing activities of daily living and sports, and improve risk assessment of premature degenerative change. As arthroscopic treatments of the hip continue to evolve, there is an increasing need to understand the basic performance biomechanics of the hip joint. This information is important because it can provide the foundation by which joint function, pathology, and therapeutic modalities can be evaluated.

SUGGESTED READINGS Andrews CL. Evaluation of the marrow space in the adult hip. From the RSNA Refresher Courses. Radiographics 2000; 20(Spec No):S27–S42. Chatha DS, Arora R. MR imaging of the normal hip. Magn Reson Imaging Clin North Am 2005; 13:605–615. Delaunay S, Dussault RG, Kaplan PA, Alford BA, et al. Radiographic measurements of dysplastic adult hips. Skeletal Radiol 1997; 26:75–81. Ganz R, Parvizi J, et al. Femoroacetabular impingement: a cause for osteoarthritis of the hip. Clin Orthop Relat Res 2003; (417):112–120.

Koulouris G, Connell D. Hamstring muscle complex: an imaging review. Radiographics 2005; 25:571–586. Manaster BJ: Adult chronic hip pain: radiographic evaluation. From the RSNA Refresher Courses. Radiographics 2000; 20(Spec No): S3–S25. Petersilge C. Imaging of the acetabular labrum. Magn Reson Imaging Clin North Am 2005; 13:641–652. Van Dyke JA, Holley HC, et al. Review of iliopsoas anatomy and pathology. Radiographics 1987; 7:53–84.

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REFERENCES 1. Manaster BJ: Adult chronic hip pain: radiographic evaluation. From the RSNA Refresher Courses. Radiographics 2000; 20(Spec No): S3–S25. 2. Delaunay S, Dussault RG, Kaplan PA, Alford BA. Radiographic measurements of dysplastic adult hips. Skeletal Radiol 1997; 26:75–81. 3. Buckwalter KA, Farber JM. Application of multidetector CT in skeletal trauma. Semin Musculoskeletal Radiol 2004; 8:147–156. 4. Pretorius ES, Fishman EK. Volume-rendered three-dimensional spiral CT: Musculoskeletal applications. Radiographics 1999; 19:1143–1160. 5. Jacobsen S, Romer L, Soballe K. Degeneration in dysplastic hips: a computer tomography study. Skeletal Radiol 2005; 34:778–784. 6. Zoga AC, Morrison WB. Technical considerations in MR imaging of the hip. Magn Reson Imaging Clin North Am 2005; 13:617–634. 7. Nishii T, Tanaka H, Nakanishi K, et al. Fat-suppressed 3D spoiled gradient-echo MRI and MDCT arthrography of articular cartilage in patients with hip dysplasia. AJR Am J Roentgenol 2005; 185:379–385. 8. Nishii T, Sugano N, Sato Y, et al. Three-dimensional distribution of acetabular cartilage thickness in patients with hip dysplasia: a fully automated computational analysis of MR imaging. Osteoarthritis Cartilage 2004; 12:650–657. 9. Lamer S, Dorgeret S, Khairouni A, et al. Femoral head vascularisation in Legg-Calvé-Perthes disease: comparison of dynamic gadolinium-enhanced subtraction MRI with bone scintigraphy. Pediatr Radiol 2002; 32:580–585. 10. Mintz DN, Hooper T, Connell D, et al. Magnetic resonance imaging of the hip: detection of labral and chondral abnormalities using noncontrast imaging. Arthroscopy 2005; 21:385–393. 11. Rubin SJ, Totterman SM, Meyers SP, Hartley DF. Magnetic resonance imaging of the hip with a pelvic phased-array surface coil: a technical note. Skeletal Radiol 1998; 27:77–82. 12. Chatha DS, Arora R. MR imaging of the normal hip. Magn Reson Imaging Clin North Am 2005; 13:605–615. 13. Bui-Mansfield LT, Youngberg RA. MR orthogonal views of the femoral neck: oblique-axial view from the oblique-coronal plane. J Comput Assist Tomogr 1997; 21:299–301. 14. Notzli HP, Wyss TF, Stoecklin CH, et al. The contour of the femoral head-neck junction as a predictor for the risk of anterior impingement. J Bone Joint Surg Br 2002; 84:556–560. 15. Kassarjian A, Yoon LS, Belzile E, et al. Triad of MR arthrographic findings in patients with cam-type femoroacetabular impingement. Radiology 2005; 236:588–592. 16. Siebenrock KA, Wahab KH, Werlen S, et al. Abnormal extension of the femoral head epiphysis as a cause of cam impingement. Clin Orthop Relat Res 2004; (418):54–60. 17. Dienst M, Seil R, Godde S, et al. Effects of traction, distension, and joint position on distraction of the hip joint: an experimental study in cadavers. Arthroscopy 2002; 18:865–871. 18. Duc SR, Hodler J, Schmid MR, et al. Prospective evaluation of two different injection techniques for MR arthrography of the hip. Eur Radiol 2006; 16:473–478.

19. Petersilge C. Imaging of the acetabular labrum. Magn Reson Imaging Clin North Am 2005; 13:641–652. 20. Miller TT. MR arthrography of the shoulder and hip after fluoroscopic landmarking. Skeletal Radiol 2000; 29:81–84. 21. Harcke HT. The role of ultrasound in diagnosis and management of developmental dysplasia of the hip. Pediatr Radiol 1995; 25:225–227. 22. Walther M, Harms H, Krenn V, et al. Synovial tissue of the hip at power Doppler US: correlation between vascularity and power Doppler US signal. Radiology 2002; 225:225–231. 23. Zawin JK, Hoffer FA, Rand FF, Teele RL. Joint effusion in children with an irritable hip: US diagnosis and aspiration. Radiology 1993; 187:459–463. 24. Pfirrmann CW, Chung CB, Theumann NH, et al. Greater trochanter of the hip: attachment of the abductor mechanism and a complex of three bursae—MR imaging and MR bursography in cadavers and MR imaging in asymptomatic volunteers. Radiology 2001; 221:469–477. 25. Andrews CL. Evaluation of the marrow space in the adult hip. From the RSNA Refresher Courses. Radiographics 2000; 20(Spec No):S27–S42. 26. Kelly BT, Shapiro GS, Digiovanni CW, et al. Vascularity of the hip labrum: a cadaveric investigation. Arthroscopy 2005; 21:3–11. 27. Van Dyke JA, Holley HC, Anderson SD. Review of iliopsoas anatomy and pathology. Radiographics 1987; 7:53–84. 28. Kingzett-Taylor A, Tirman PF, Feller J, et al. Tendinosis and tears of gluteus medius and minimus muscles as a cause of hip pain: MR imaging findings. AJR Am J Roentgenol 1999; 173:1123–1126. 29. Cvitanic O, Henzie G, Skezas N, et al. MRI diagnosis of tears of the hip abductor tendons (gluteus medius and gluteus minimus). AJR Am J Roentgenol 2004; 182:137–143. 30. Robinson P, White LM, Agur A, et al. Obturator externus bursa: anatomic origin and MR imaging features of pathologic involvement. Radiology 2003; 228:230–234. 31. Koulouris G, Connell D. Hamstring muscle complex: an imaging review. Radiographics 2005; 25:571–586. 32. Daenen B, Preidler KW, Padmanabhan S, et al. Symptomatic herniation pits of the femoral neck: anatomic and clinical study. AJR Am J Roentgenol 1997; 168:149–153. 33. Leunig M, Beck M, Kalhor M, et al. Fibrocystic changes at anterosuperior femoral neck: Prevalence in hips with femoroacetabular impingement. Radiology 2005; 236:237–246. 34. Dinauer PA, Murphy KP, Carroll JF. Sublabral sulcus at the posteroinferior acetabulum: a potential pitfall in MR arthrography diagnosis of acetabular labral tears. AJR Am J Roentgenol 2004; 183:1745–1753. 35. Menschik F. The hip joint as a conchoid shape. J Biomech 1997; 30:971–973. 36. Siebenrock KA, Schoeniger R, Ganz R. Anterior femoro-acetabular impingement due to acetabular retroversion. Treatment with periacetabular osteotomy. J Bone Joint Surg Am 2003; 85:278–286. 37. Greenwald AS, O’Connor JJ. The transmission of load through the human hip joint. J Biomech 1971; 4:507–528.

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Acute Osseous Injury to the Pelvis and Acetabulum Eva Llopis, Victoria Higueras, Pilar Aparisi, José M. Mellado, and Francisco Aparisi

Fractures of the pelvic ring and acetabulum are a common consequence of high-speed collisions, usually related to motor vehicle accidents. They may also be caused by minor falls and occupational accidents.1 These injuries are associated with significant morbidity and mortality, derived from associated injuries (cardiovascular, gastrointestinal, respiratory, and genitourinary) and complications. In many cases the definitive treatment of pelvic ring and acetabulum fractures is surgical.2,3 Stress fractures, including fatigue and insufficiency fractures, are very prevalent in the pelvic skeleton. They may be clinically and radiologically overlooked. However, early recognition is important to avoid inappropriate studies and to start adequate treatment. Avulsion fractures of the pelvis are uncommon injuries, typically deriving from sports activities during childhood. Knowledge of the most common sites of pelvic avulsion fractures and a familiarity with their variable imaging appearances are required for a correct diagnosis, particularly in chronic injuries. Anteroposterior radiographs are included in the initial evaluation of patients suffering severe trauma, following the recommendations of the American College of Surgeons. However, the complex anatomy of the pelvic skeleton, with a number of overlapping structures, makes the radiographic assessment difficult. In addition, many pelvic radiographs are suboptimal because of poor positioning or severe pain, which decreases the sensitivity of the examination.3 Consequently, complementary multidetector CT (MDCT) is valuable. Pelvic CT allows multiplanar reformatted imaging, which is important in diagnosis, classification, and surgical planning. Diagnostic imaging strongly influences prognosis and treatment of pelvic fractures by providing precise assessment of injury patterns and complications. In this chapter we review acute fractures of the pelvis and acetabulum, their injury patterns, the most used classification systems, and the role of imaging for each type of fracture. The role of cross-sectional imaging, especially 434

MDCT, is emphasized. Pelvic stress fractures and avulsion fractures are also discussed as separate entities, owing to their specific biomechanics, radiologic appearance, and treatment.

PELVIC RING INJURIES Prevalence, Epidemiology, and Definitions The prognosis of a pelvic fracture depends on the severity of trauma, the stability of the injury, the adequacy of treatment, and the occurrence of complications, such as neural damage, urethral tear, or nonunion.4 Communication between the fracture site and the skin perineum or pelvic contents implies an open fracture, which connotes a significantly worse prognosis. The incidence of pelvic fractures is difficult to assess but has been reported as high as 20 to 37 per 100,000. During past decades the incidence of pelvic fractures has increased because of the high rates of high-speed motor vehicle accidents and falls from heights.5 Two thirds of pelvic fractures occur in patients with multiple trauma. Classification systems of pelvic fractures are based on analysis of force vectors and degree of instability. Proper categorization of pelvic fractures based on these classification systems is often done using MDCT. These classification systems provide a logical approach to the multidisciplinary management of pelvic ring disruption, allowing early and appropriate treatment. The mortality of major pelvic fracture, despite improvements in management, continues to be 10% to 20%. Open fractures have higher mortality, which may reach 50%. Morbidity and mortality mainly result from associated injuries, especially to the head, and/or from massive pelvic bleeding. Decreasing the mortality rates requires early diagnosis and aggressive treatment. Long-term complications such as nonunion, malunion, limb-length discrepancy, and

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low back pain result from up to 52% of fractures through the sacrum or sacroiliac joint.1

Anatomy The pelvis is composed of two innominate bones and the sacrum. The innominate bones are formed by joining of three ossification centers that form the ilium, the ischium, and the pubic bones. These are fused at the level of the acetabulum. The sacrum articulates posteriorly with the ilium through the sacroiliac joint and anteriorly with the pubis at the pubic symphysis. The pelvic ring has no inherent stability. Stability of the pelvic ring depends on soft tissues around the pelvis. Key structures are interosseous ligaments that run between the ilium and the sacrum posteriorly and between the pubic symphysis and anterior abdominal wall anteriorly. The extremely strong posterior sacroiliac ligaments maintain the normal position of the sacrum in the pelvic ring, and the entire complex has the appearance of a suspension bridge. They can be divided into transversal and vertically oriented. Transversal ligaments include short posterior and anterior sacroiliac ligaments, iliolumbar ligament, and sacrospinous ligament, which form a tension band. Vertically oriented ligaments include long posterior sacroiliac ligaments and sacrotuberous and lateral lumbosacral ligaments. These ligaments also contribute to the pelvic floor. Deep pelvic anatomy includes extraperitoneal organs such as rectum, bladder, urethra, uterus, vagina, and intraperitoneal intestinal structures. The two more important injuries related to pelvic trauma are direct vascular injury with hemorrhage and urologic injury (bladder or urethra). The pelvis is extremely well vascularized, with the majority of blood supply arising from the hypogastric artery. The superior gluteal artery is the most commonly injured vessel in posterior wall fractures, whereas injury to the obturator and internal pudendal arteries is related to pubic rami fractures. Nerve supply from the lumbar and sacral plexus is close to the posterior structures.

Biomechanics The pelvic skeleton is a weight-bearing structure that transmits forces from the lumbar spine to the lower extremity. In addition, the pelvic ring serves as a protector of internal pelvic organs. The osseous pelvis acts like a ring unit. Stability depends on the anatomic structures, bones and ligaments, resisting vertical and rotational forces, depending on their orientation. Transversely oriented ligaments resist rotational instability, whereas vertically oriented ligaments oppose vertical displacement. Pelvic muscles, rectus abdominis and its fascia, abdominal obliques, obturators, and adductors also contribute to ring stability. The anatomy of the pelvis is such that stresses placed on it by abnormal motion at any of three joints, sacroiliac or pubis, causes instability and leads to a second fracture in other structures of the pelvic ring. The loss of bone continuity or one of the joints of the pelvic arch changes the transmission of forces, increasing loads over other pelvic structures. Therefore, if the pelvic ring becomes

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broken in one area and the fragments become displaced, then there must be a fracture or dislocation in another portion of the ring. The orientation of the fractures and direction of displacement provides a clue to the mechanism of injury. The major forces acting on a hemipelvis are external, internal rotation (compression), and vertical shear (Fig. 19-1). In some complex high-energy injuries, the forces may defy detailed description. External rotation is caused by a direct blow on the posterior iliac spines or more commonly by forced external rotation of the legs and produces an open-book type of injury. This is characterized by disruption of the symphysis pubis and, as the force continues, by rupture of the anterior sacroiliac and sacrospinous ligaments. An end point is reached when the posterior ilium abuts against the sacrum; but if the force continues, the hemipelvis may be sheared off, resulting in gross instability. Internal rotation (lateral compression) may be caused by a direct blow on the lateral aspect of the iliac crest or an indirect force through the femoral head. This produces compression fractures of the posterior complex and fractures of the rami anteriorly (see Fig. 19-1). The posterior and anterior lesions may either be on the same side of the pelvis (ipsilateral type) or on the opposite side (bucket-handle type). This latter type is associated with major rotational deformities and may result in malunion. In some instances, a lateral compression force may stop short of rupture of the posterior structures, but in others, rupture will occur.

Imaging Techniques Conventional radiography is the first test, after clinical assessment, for the diagnosis of pelvic fractures. Although recently under debate, anteroposterior pelvic radiography is usually included in the protocol for all multiple trauma patients once the patient’s condition is stabilized. Pelvic radiography has a role in the initial trauma series in patients in whom there is a clinical suspicion of severe pelvic injury and who are hemodynamically unstable or unconscious. A portable pelvic film might help distinguish which patients need immediate external fixation, may be bleeding from a complex pelvic fracture, or might benefit from further radiographic evaluation. In hemodynamically stable patients screening with anteroposterior radiography is debated because of the availability of crosssectional imaging methods, especially MDCT, and the poor imaging quality of standard radiographs in a high percentage of these patients.3,6,7 Pelvic ring fractures are uncommon in children. In the pediatric trauma patient, routine screening radiography of the pelvis is unnecessary and not recommended, owing to the low yield in combination with high radiation exposure.7

Radiography Anteroposterior Radiographs of the Pelvis Analysis of the anteroposterior radiographs of the pelvis determines the mechanism of pelvic ring injury, and appropriate therapeutic approaches can be started. Additional radiographic views have allowed more precise

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■ FIGURE 19-1 Diagram showing the major patterns of injury (anteroposterior compression, lateral compression, and vertical shear patterns).

classification but currently have been mainly replaced by CT. Anteroposterior films should be done following a rational protocol: from inside to outside all pelvic lines must be smooth, continuous, and symmetric. Pubic rami fractures, symphysis diastasis, dislocation or fracturedislocation of sacroiliac joint, sacrum fractures, and iliac fractures must be ruled out. Pubic symphysis distance should not be more than 1 cm. Diastasis of the pubis is considered when the distance is greater than 2.5 cm. The pubic rami should be at the same level when they join the symphysis; overlapping of the pubic bones is related to injuries. The lower margins of the rami are a better guide because nonalignment of the upper margins may be a normal variation. The orientation of pubic rami fractures provides a clue to the mechanism of injury. Horizontal overlapping fractures of the superior and inferior pubic rami are associated with lateral compression. Vertical fractures of the rami without cranial displacement of the hemipelvis can be seen in anteroposterior compression injuries instead of pubic symphyseal diastasis (Fig. 19-2). Vertical rami fractures with cranial displacement are a hallmark of vertical shear injuries (Fig. 19-3).

The normal sacroiliac joint space is 2 to 4 mm wide. When the joint is analyzed for diastasis, the anterior and posterior aspects should be examined. Disruption of the sacroiliac joint with external rotation of the ipsilateral hemipelvis is characteristic of anteroposterior compression. If only the anterior sacroiliac joint is widened, the posterior ligaments are intact and preserving vertical stability. If the sacroiliac joint is anteriorly and posteriorly diastatic, the pelvis is completely unstable. Usually, the sacroiliac joint is completely disrupted in vertical shear injuries. Displaced vertical fractures through the sacrum or the iliac wing adjacent to the sacroiliac joint have the same implication as sacroiliac joint diastasis. Buckle (anterior crush) fractures of the sacrum are the hallmark of lateral compression injuries. The fractures are usually oriented vertically. They may be isolated to the sacral ala, pass through the neural foramina, or extend centrally into the sacral spinal canal. Radiographic findings of the fractures may be subtle (Fig. 19-4). The sacral promontory and arcuate foramina should be carefully examined for cortical disruption. Displaced vertical fractures through the sacrum can be seen in lieu of sacroiliac joint disruption in anteroposterior compression and

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vertical shear injuries. Horizontal fractures of the sacrum below the level of S2 do not affect the integrity of the pelvic ring. The iliolumbar ligament is inserted at the tip of the L5 transverse process. An avulsion fracture at this site is associated with disruption of the posterior sacroiliac ligament complex, as seen in severe anteroposterior compression and vertical shear injuries. Hence, an L5 transverse-process avulsion fracture may indicate complete pelvic instability (see Fig. 19-4).1

Inlet Radiographs of the Pelvis

■ FIGURE 19-2 Anteroposterior pelvic radiograph showing vertical sacral and pubic rami fractures indicating anteroposterior compression mechanism. (Courtesy of Dr. J. Martel, Fundación Alcorón, Madrid, Spain.)

■ FIGURE 19-3 Vertical shear pattern. A, Anteroposterior radiograph reveals inferior displacement of right sacrum, inferior displacement of iliopubic right rami, and superior displacement of left iliopubic rami. B, Oblique multiplanar reformatted CT image. C, 3D volume rendering. MDCT demonstrates the fracture lines and the marked anterior dislocation of the sacrum.

Inlet radiographs are obtained with the patient in the supine position, with the x-ray tube positioned at the patient’s head and angled 45 degrees toward the feet. The x-ray beam is perpendicular to the pelvic rim. The inlet view of the pelvis permits more accurate determination of the following: the degree of posterior displacement at the sacroiliac joint, the degree of internal or external rotation of the hemipelvis, the degree of pubic

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■ FIGURE 19-4 Young-Burgess type II lateral compression pattern. Lateral posterior force causes right iliac, pubic, and sacral fractures. A, Radiography shows iliac and pubic rami with overlapping of the fragments. Sacral fractures are difficult to depict on a radiograph. B, MDCT angiogram demonstrates right sacrum fracture through the foramen and arterial dissection of right proximal common iliac artery. C and D, Angiogram confirming arterial dissection and endovascular prosthesis treatment.

diastasis or overlap, and the presence of subtle sacral fractures.

Outlet Radiographs of the Pelvis Outlet radiographs are obtained with the patient in the supine position, with the x-ray tube positioned at the patient’s feet and angled 45 degrees toward the head. The x-ray beam is perpendicular to the sacrum. The primary purpose of the outlet view of the pelvis is to demonstrate the magnitude of vertical (cranial) displacement of the hemipelvis. Additionally, some sacral and pubic rami fractures are better visualized with the outlet view than with other views. The sacral neural foramina are especially well depicted by using the outlet view.

Lateral Projection Lateral cross-table radiographs should include the acetabulum, the ischial tuberosity, and the proximal femur. Transverse fractures of the sacrum and coccyx are best depicted. This projection also helps define dislocations of the hip posteriorly or anteriorly, which are frequently associated with acetabular fragments that are usually displaced in the same direction.

Ultrasonography If a patient’s hemodynamic state is unstable, treatment of hemorrhage is the priority. Bedside ultrasonographic abdominal screening must be performed to rule out

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intraperitoneal or retroperitoneal fluid. Moreover, internal visceral injuries, such as liver, spleen, or kidney lesions, can also be diagnosed.8

Computed Tomography Computed tomography is widely recognized as an important adjunct to plain films in the evaluation of patients with acute pelvic trauma. In one third of the patients it adds additional information and can change classification. MDCT has improved our ability to image patients with multiple trauma; therefore, in some hospitals it has replaced additional plain film projections (see Fig. 19-4). The advantages are higher speed, extended anatomic volume imaging, postprocessing, and enhancement from the intravenous use of a contrast agent. The use of a contrast agent and CT angiography allows evaluation of the aorta and the major pelvic vasculature at the same moment, providing a vascular map. Active hemorrhage can be diagnosed on MDCT on the basis of increased density compared with surrounding tissue, which results from the extravasation of intravascular contrast agent; surgery or angiographic therapy might be indicated (Fig. 19-5). Postprocessing imaging tools with multiplanar and volume-rendering reconstructions give important informa-

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tion in transversally oriented fractures and in complex injuries about the relationship between the fragments and adjacent structures. MDCT has also replaced cystography. If bladder rupture is suspected, CT cystography is indicated (Fig. 19-6).8–11

Angiography Significant pelvic arterial injuries occur in a minority of patients with multiple high-energy injuries regardless of the fracture type, ranging from 2.5% to 10% to 20% in hemodynamic compromise in unstable patients. Angiography is used to diagnose and treat potentially life-threatening hemorrhage secondary to pelvic ring injury. Angiography depicts better than CT angiography an injury to small vessels. Pelvic angiography with transcatheter embolization has been proved to be faster, less invasive, and more successful than open surgical procedures in controlling pelvic hemorrhage, but it still remains a controversial topic12 (Fig. 19-7; see Fig. 19-4).

Manifestations of the Disease Pelvic ring fractures occur as a result of high-energy trauma. Recognition of the pattern of injury helps to

■ FIGURE 19-5 Young-Burgess vertical shear injury. Force vector direction is inferior to superior. A, Radiograph shows superior displacement of the right hemipelvis, including sacrum, diastasis of the pubis symphysis, and right lumbar transverse fracture. Axial (B) and volume-rendering (C) MDCT angiography show active bleeding with contrast dye extravasation and obturator and pectineal muscle hematoma.

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■ FIGURE 19-6 A, Radiograph of complex fracture pattern after motor vehicle collision demonstrates features of both lateral compression and vertical shear patterns. Coronal multiplanar reformatted image (B) and see-through bone (C) reconstruction show fracture lines and external fixation. D, MDCT cystography reveals extraperitoneal bladder rupture with extravasation of intrabladder contrast agent. E, Posterior radiograph shows extravasation of bladder contrast agent.

■ FIGURE 19-7 Anteroposterior compression fracture, Young-Burgess type III. A, Radiograph demonstrates pubic diastasis, vertical pubic rami fractures, and sacral fractures. B, Axial CT depicts better right sacral joint diastasis and important pelvis hematoma. C, Diagnostic angiogram demonstrates active bleeding, posteriorly embolized with coils (D). E, Early control radiograph shows reduction of pubis diastasis. F, Later radiograph demonstrates evolution with healing of fractures and remodeling.

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TABLE 19-1 Frequency of Injuries Associated with Pelvic Ring Injuries

Closed-head injury Long-bone fracture Peripheral nerve injury Thoracic injury Urethra (male) Bladder Spleen

50% 48% 26% 15% 10% 10% 10%

diagnose associated injuries (Table 19-1). Open fractures have higher mortality rates, with an increased risk of complications, infection, and high frequency of visceral organ lesions. Clinical skin hemorrhages and vaginal, rectal, or genitourinary bleeding must be ruled out because of the high frequency of intrapelvic hemorrhage associated with this fracture. Anteroposterior compression and vertical shear injuries have a higher incidence of pelvic vascular injury and hemorrhage. Tenderness in the parasymphyseal area, pubic rami, ileus, or sacrum is a sign often reflecting the presence of fractures. Peripheral nerve and vascular injuries are directly attributable to pelvic ring fractures. Comparative arterial palpation of the lower limbs must be done from the femoral vessels down to the dorsal foot artery to exclude vascular lesions. A complete neurologic examination to rule out nerve root injuries, from L5 through the lower sacral roots, is indicated. Fractures of sacrum or sacroiliac joint can damage adjacent sacral plexus or sacral nerve roots. Fractures extending into the region of the greater sciatic notch may damage the sciatic nerve. Confusion in the pelvis ring classification system is due to a wide variety of classifications. Acronyms such as Malgaigne, open book, or straddle fractures are in disuse. Open book fractures consist of diastasis of the symphysis pubis and external rotation of one or both iliac bones hinging at the sacroiliac joint. A Malgaigne fracture is defined as a pelvic fracture of both pubic rami plus a posterior fracture of the sacroiliac complex. Straddle fractures consist of isolated fractures of the four pubic

rami. The most common systems of classification have regarded pelvic fracture predominantly as either stable or unstable, depending on the radiologic appearance and the physical findings. Stable fractures include single pelvic ring fractures and pure acetabular, pubic rami, and avulsion fractures. Unstable are those in which the pelvic ring is disrupted in more than one location, particularly if the posterior complex is disrupted. The advent of external fixation systems for pelvic fracture created the need to understand the force vectors causing the fracture so that the correct countering forces can be applied to the fixation. The Young-Burgess (Table 19-2) and the Tile (Table 19-3) systems are two major classification schemes that have been developed for describing pelvic ring fractures. Tile initiated a classification system based on the direction of the injuring force. This concept was redefined in the Young-Burgess classification, which provides a logical approach to pelvic ring fractures and the information needed by the surgeon to plan the type of treatment and which corrective forces must be applied. The major patterns of pelvic ring fractures are anteroposterior compression, lateral compression, vertical shear, or combined mechanical injury (see Fig. 19-1).13,14

Anteroposterior Compression Injury The disruptive force is in the sagittal plane and is usually associated with vehicular accidents in blows to the front of the pelvis. Thus, this is the hallmark injury to the pubic diastasis with or without fractures of the pubic rami (Fig. 19-8). Additional forces tend to open the pelvis and one or both hemipelves undergo external rotation, thus hinging and injuring the posterior sacroiliac complex (Fig. 19-9). The location and degree of diastasis is correlated with the magnitude of force imparted to the pelvis and with the amount of resulting instability. Division of the symphysis pubis allows 2.5 cm of diastasis. Further diastasis is achieved if the posterior ligamentous complex is disrupted, leading to instability. Anterior sacroiliac, sacrospinous, and sacrotuberous ligament disruption results in rotational instability (APC type II) (Fig. 19-10; see Fig. 19-9). The extension to the posterior sacroiliac ligaments

TABLE 19-2 Young-Burgess Classification Mechanism and Type

Characteristics

Hemipelvis Displacement

Stability

APC type I APC type II

Pubic diastasis < 2.5 cm Pubic diastasis > 2.5 cm, anterior sacroiliac joint disruption Type II plus posterior sacroiliac joint disruption Ipsilateral sacral buckle fracture, ipsilateral horizontal pubic rami fractures (or disruption of symphysis with overlapping pubic bones) Type I plus ipsilateral iliac wing fracture or posterior sacroiliac joint disruption Vertical pubic rami fractures, sacroiliac joint disruption ± adjacent fractures

External rotation External rotation

Stable Rotationally unstable, vertically stable

External rotation Internal rotation

Rotationally unstable, vertically unstable Stable

Internal rotation

Rotationally unstable, vertically stable

Vertical (cranial)

Rotationally unstable, vertically unstable

APC type III LC type I

LC type II Vertical shear

APC, anteroposterior compression fractures; LC, lateral compression fractures.

TABLE 19-3 Tile Classification System Type

Characteristics

Type A, posterior arch intact A1, pelvic ring fracture (avulsion) A1.1 Anterior iliac spine avulsion A1.2 Iliac crest avulsion A1.3 Ischial tuberosity avulsion A2, pelvic ring fracture (direct blow) A2.1 Iliac wing fracture A2.2 Unilateral pubic rami fracture A2.3 Bilateral pubic rami fracture A3, transverse sacral fracture A3.1 Sacrococcygeal dislocation A3.2 Nondisplaced sacral fracture A3.3 Displaced sacral fracture Type B, incomplete posterior arch disruption B1, anteroposterior compression B1.1 B1.2 B2, lateral compression

Anterior sacral buckle fracture Partial sacroiliac joint fracture-subluxation Incomplete posterior iliac fracture

B3.1

Bilateral pubic diastasis, bilateral posterior sacroiliac joint disruption

C1.3 C2, vertical shear and anteroposterior and lateral compression C3, bilateral vertical shear

None

Stable

None

Stable

None

Stable

External rotation

Rotationally unstable, vertically stable

Internal rotation

Rotationally unstable, vertically stable

External rotation

Rotationally unstable, vertically stable

Ipsilateral internal rotation, contralateral external rotation

Rotationally unstable, vertically stable

Bilateral internal rotation

Rotationally unstable, vertically stable

Vertical (cranial)

Rotationally unstable, vertically unstable

Ipsilateral vertical (cranial), contralateral internal or external rotation Bilateral vertical (cranial)

Rotationally unstable, vertically unstable

Ipsilateral B2 injury, contralateral B1 injury

B3.3, bilateral lateral compression B3.3 Bilateral B2 injury Type C, complete posterior arch disruption C1, vertical shear C1.1 C1.2

Stability

Pubic diastasis, anterior sacroiliac joint disruption Pubic diastasis, sacral fracture

B2.1 B2.2 B2.3 B3. anteroposterior compression

B3.2, anteroposterior and lateral compression B3.2

Hemipelvis Displacement

Displaced iliac fracture Sacroiliac joint dislocation or fracture-dislocation Displaced sacral fracture Ipsilateral C1 injury, contralateral B1 or B2 injury Bilateral C1 injury

Rotationally unstable, vertically unstable

■ FIGURE 19-8 Anteroposterior pelvic film (A) and MDCT volume rendering 3D reconstruction (B) of Young-Burgess anteroposterior compression type I. There is a vertical-oriented fracture of the left rami and a large vertical-oriented right fracture extending through the acetabulum and no widening of pubic symphysis. This is a stable lesion.

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■ FIGURE 19-9 Anteroposterior radiograph (A), MDCT sacral coronal multiplanar reformatted image (B), and 3D volume rendering (C) of Young-Burgess anteroposterior compression type II fracture with pubis diastasis and vertical sacral fracture.

leads to complete instability, both rotational and vertical (APC type III) (Fig. 19-11).

Lateral Compression Injury

■ FIGURE 19-10 Anteroposterior radiograph of Young-Burgess type II injury showing vertical rami fractures and right sacral wing fracture.

The force of the injury is from the side and is associated with horizontally oriented pubic fractures and impacted fractures of the sacrum (see Fig. 19-4). Lateral compression injury results in internal rotation of the affected hemipelvis. This internal rotation decreases rather than increases the pelvic volume. Consequently, pelvic vascular injuries and resulting hemorrhage are less common. The most common injury and the least destructive, LC type I results in a ipsilateral sacral buckle fracture and pubic rami fracture. Sacral bucket fractures are usually vertically oriented and can be isolated to the sacral ala or extend centrally into the sacral spinal canal (Fig. 19-12). If lateral force is increased and is more anterior, internal displacement of the anterior hemipelvis may result and, thus, potentially external rotation of posterior hemipelvis, with

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■ FIGURE 19-11 MDCT axial view (A) and volume-rendering reconstruction (B) of Young-Burgess anteroposterior type III fracture show bilateral pubic rami fracture and right sacroiliac joint diastasis.

the joint acting as a pivot (LC type II) (Fig. 19-13). When the force continues and affects the contralateral hemipelvis, the pelvis becomes severely unstable. The ipsilateral hemipelvis sustains either a type I or type II injury with associated internal rotation, whereas the contralateral pelvis undergoes external rotation (LC type III).

Vertical Shear Injury This injury results from a fall from height onto the lower limbs. At the anterior aspect, vertically oriented fractures of the pubic rami with cranial displacement are the hallmark of this injury (Fig. 19-14). Posteriorly, the sacroiliac joint is completely disrupted and therefore associated with complete instability (see Fig. 19-3).

Complex Injury Complex or mixed pattern pelvic fractures are due to a combination of fracture forces. The specific findings of

each pattern still are present. Pelvic stability can be determined by using the criteria outlined earlier (see Figs. 19-5 and 19-6). The Young-Burgess classification does not include ring-sparing injury, which is included in the Tile classification system, such as avulsion fractures, iliac wing (Fig. 19-15) or sacral fractures that do not involve the sacroiliac joint, or minimally displaced pubic rami fractures (Tile type A).

Synopsis of Treatment Options Hemodynamic stabilization in patients with unstable pelvic ring fractures must first be achieved. Immediate resuscitation protocols must kick into action in unstable fractures. The key to treatment success is an experienced balanced multidisciplinary team who rapidly makes decisions. Starting with mechanical measures such as a bandage around the pelvis and knees reduces the pelvis temporar-

K E Y P O I N T S : P E LV I C RING INJURIES Pelvic fractures are serious injuries with high mortality rates. ■ Considerable forces are necessary to fracture the pelvis; associated injuries are thus common and contribute significantly to clinical outcome. ■ Pelvic hemorrhage can originate from cancellous bone exposition, injured soft tissue, and vascular lesions. CT angiography allows one to rule out active bleeding and is useful in planning endovascular or surgical treatment. ■ Plain radiographs allow defining those patients who must be treated with external fixation to stabilize the pelvis. ■ MDCT is essential to classify fractures and to plan surgical treatment. ■

■ FIGURE 19-12 MDCT volume-rendering reconstruction of YoungBurgess lateral compression type I fracture with iliac and acetabular fracture. (Courtesy of Dr. J. Martel, Fundación Alcorcón, Madrid, Spain.)

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■ FIGURE 19-13

MDCT multiplanar coronal reconstruction (A) and volume rendering (B) of Young-Burgess lateral compression type II. Note iliac fracture extending to the right sacral wing.

ily and controls hemorrhage without major limitations to patient accessibility. Antishock therapy also includes intravenous fluid administration. After completing hemostasis, the choice of orthopedic management will rely on the associated visceral (neurologic, thoracic, or abdominopelvic) or osseous (femoral or acetabular) lesions. Treatment can be divided into provisional and definitive.8,15,16

Provisional Stabilization Provisional stabilization is used in unstable pelvic ring, such as Young-Burgess APC type II-III, or vertical shear injuries and in Tile type B1 and C injury (see Fig. 19-6). Stabilization with external fixation of the pelvis is an accepted emergency measure. Two centimeters of diastatic pubic symphysis can increase pelvic volume from 1.5 L to 5 L. If the patient does not respond to resuscitative methods and has no other bleeding sites, external fixation must be combined with laparotomy and packing of the pelvis.

■ FIGURE 19-14

Definitive Stabilization If the pelvic ring is stable and only minimally displaced (Young-Burgess APC type I or Tile type A2), only symptomatic treatment is necessary. These patients may be mobilized quickly and the pelvic fracture largely ignored. The definitive management of displaced fractures depends on their stability and requires clear definition of the risks and benefits of stabilization. If surgery is required, it must be completed the first 3 weeks after trauma to prevent lesions from becoming fixed or irreducible. If performed, internal fixation allows easier reduction and stabilization of fracture and facilitates patient mobilization.

Anteroposterior Compression Injuries In the Young-Burgess APC type II or Tile type B1 (open book) injury when the symphysis is open more than 2.5 cm, the pelvic ring may be closed by placing the patient in the lateral position. The reduction may be maintained either

Anteroposterior radiograph (A) of Young-Burgess vertical shear pattern showing vertical displacement and pubic diastasis. Sacral assessment is difficult and better seen on CT (B).

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■ FIGURE 19-15 Isolated iliac wing fracture, secondary to direct blow. A, Radiograph shows iliac fracture displacement. B, Axial CT shows fracture displacement and psoas muscle enlargement due to hematoma. C, Control film after surgical osteosynthesis.

by a simple external skeletal fixation or by a plate across the symphysis (see Fig. 19-14).

Lateral Compression Injuries In the Young-Burgess LC type II or Tile type B2 injury in most cases the elastic recoil of the pelvis restores the anatomy to near normal and no form of stabilization is required. In the Tile type B3 (bucket-handle injury) the posterior complex is commonly compressed, rendering the ring stable. It may be impossible to reduce the displacement by closed manipulation under general anesthesia and, in most cases, no stabilization is required. If the leg-length discrepancy is

greater than 1.5 cm, or if the pelvic deformity is excessive, more aggressive management may be indicated. Reduction may then be obtained by external rotation of the hemipelvis by pins in the iliac crest (Fig. 19-16). When reduction has been achieved, the anterior frame is completed to hold the necessary external rotation. In the rare case of a “tilt” fracture in which bone is protruding into the perineum, open reduction and internal fixation may be required. In complex instability fractures, with rotational and vertical instability (Young-Burgess APC type III) and vertical shear fractures (Tile type III) there is a need for definitive fixation with external frames with or without skeletal traction and open reduction with internal fixation.17,18

ACETABULAR FRACTURES Prevalence, Epidemiology, and Definitions

■ FIGURE 19-16 MDCT coronal multiplanar reformatted image after iliac wing reconstruction with internal fixation.

Acetabular fractures normally appear in the context of an important pelvic trauma, with severe damage. They can be classified into simple and complex patterns, which require an exhaustive understanding of the regional anatomy, and the associated radiologic correlates. The patterns of fracture determine the operative approach. The work of Judet and Letournel19–21 has provided the most accepted classification for acetabular fractures. In their classification, fractures are divided into elementary and associated patterns. The elementary pattern consists of a single main fracture line, whereas associated fractures involve combinations of elementary fractures. More recently, Brandser and Marsh22 proposed that rather than thinking in terms of elementary and associated fractures,

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another way of organizing the different fracture types was to divide them into those that are predominantly column type fractures, transverse type fractures, or wall type fractures. The three most common types of fractures are both column, transverse with posterior wall, and elementary posterior wall fractures.22,23

Anatomy The acetabulum is formed by the anterior and the posterior columns of bone, which join in the supra-acetabular region. Anterior and posterior columns have the appearance of a Greek lambda (λ). The anterior column represents the longer and larger portion, which extends superiorly from the superior pubic ramus into the iliac wing. The posterior column extends superiorly from the ischiopubic ramus as the ischium towards the ilium. The sciatic buttress extends posterior from the anterior and posterior columns to become the articular surface of the sacroiliac joint, which attaches these columns to the axial skeleton.22,24,25 The anterior and posterior walls extend from each respective column and form the cup of the acetabulum. These aid in stabilizing the hip joint. The anterior wall is smaller than the posterior, and it is rarely fractured. The posterior wall is larger, and it is commonly fractured.20,22,25 The iliac wing and the obturator ring are additional important structures in the setting of acetabular fractures.22,26

Imaging Techniques Radiography

TABLE 19-4 Radiographic Lines in Acetabular Fracture Classification Ilioischial Iliopectineal Anterior wall Posterior wall Acetabular roof Teardrop disruption

Posterior portion of the quadrilateral plate of the iliac bone Arcuate Anterior rim of the acetabulum Posterior rim of the acetabulum Acetabular roof Medial acetabular wall, acetabular notch, anterior portion of the quadrilateral plate

Data from Theumann NH.Traumatic injuries: imaging of pelvic fractures. Eur Radiol 2002; 12:1312–1330.

elementary fractures, which involve one structural component of the acetabulum or its supporting structures, and associated fractures, which are combinations of the elementary types.22,23,25

Manifestations of the Disease Elementary Fractures Posterior Wall Fracture The most common posterior wall fractures are the posterior lip or posterior rim fractures. These usually result from indirect forces transmitted through the length of

Evaluation of the acetabulum on conventional radiographs may be difficult because of the presence of overlying structures. If an acetabular fracture is suspected, MDCT with multiplanar reformatted imaging or a radiographic study in at least four projections (anteroposterior view of the pelvis, the hip, and the anterior and posterior oblique views) should be obtained to demonstrate the comminution and position of displaced fragments, also in relation to the hip joint.19,20,22,23,26,27 Judet and Letournel have identified six lines (Table 19-4) relating to the acetabulum and its surrounding structures, based on anatomy.27–29 Depending on which line is disrupted, classification of the fracture can be done (Fig. 19-17). 1. Fracture of the iliopectineal (anterior) column can be demonstrated in anteroposterior and internal oblique views. It is rare. 2. Fracture of the ilioischial (posterior) column can be demonstrated in anteroposterior and external oblique views. It is common. 3. Transverse fractures, through the acetabulum, involving both pelvic columns can be demonstrated in anteroposterior and both oblique views.They are common. 4. Complex fractures, including T-shaped and stellate fractures, in which the acetabulum is broken into three or more fragments are the most common type. CT and postprocessing reconstruction play a leading role in the evaluation of acetabular fractures.22,23,25,27,28 According to the Judet-Letournel classification (Table 19-5), fractures can be gathered into two broad categories:

■ FIGURE 19-17 Normal anteroposterior pelvic radiograph shows acetabular roof (red), posterior rim of the acetabulum (yellow), anterior rim of the acetabulum (blue), iliopectineal line (white), teardrop (black), and ilioischial line (green dots).

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TABLE 19-5 Judet-Letournel Classification Elementary Types Posterior wall fractures (27%) Transverse column fractures (9%) Anterior column fractures (5%) Posterior column fractures (4%) Anterior wall fractures (2%) Associated Fractures Transverse and posterior wall fractures (20%) Both columns (19%) T-shaped (6%) Anterior wall and posterior hemitransverse (5%) Posterior column and posterior wall (3%)

Data from Potok P, Hopper KD, Umlauf M. Fractures of the acetabulum: imaging, classification and understanding. Radiographics 1995; 15:7–23.

the femur, with a flexed hip joint, such as in car accident when the knee strikes the dashboard.23,30 The size and location of the posterior wall fragment are determined by the degree of hip abduction and flexion at the time of impact. Depending on the mechanism of injury, a posterior dislocation of the femur often occurs simultaneously (Figs. 19-18 and 19-19).26 The posterior wall can break in single or multiple fragments. The most severe type of posterior wall fracture can involve the sciatic notch, the quadrilateral plate, or both, resembling a posterior column fracture, but wall fractures do not disrupt the obturator ring and this feature differentiates posterior column from extended pos-

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terior wall fractures.22,25 The size and comminution of the posterior fracture determine the prognosis and risk of redislocation. The posterior wall fracture can be appreciated on anteroposterior radiographs, but the oblique view improves visualization, which gives information about the size and displacement of the wall fragment.25,27,31 CT assesses the amount of wall involved and the comminution and associated impaction, which strongly affect prognosis and treatment (Fig. 19-20).22,31

Transverse Fracture Transverse elementary fractures transect both the anterior and the posterior columns of the acetabulum. They usually have a relatively simple configuration, with an axial or oblique axial orientation, dividing the hemipelvis in two large fragments, an upper and a lower half. The upper half includes the roof of the acetabulum, which maintains its continuity with the acetabular strut and connects it to the axial skeleton.20,21,23,24 This distinguishes transverse and T-shaped fractures from bicolumn fractures, because these disrupt the roof and sciatic notch, breaking the connection with the axial skeleton. The obturator ring is intact, whereas in T-shaped fractures the ring is disrupted. Letournel describes three variants of transverse fractures, depending on their position as it is referred to the acetabular roof: juxtatectal, transtectal, and infratectal. MDCT, including multiplanar reformatted imaging, or multiple radiographic views are essential to study these fractures and because of the axial orientation of fracture lines multiplanar reconstructions play an important role (Fig. 19-21).

■ FIGURE 19-18 Anteroposterior (A) and oblique (B) radiographs show posterior wall fragments are detached from the acetabulum. Unless the fragment represents more than 40%, surgery will not be indicated. Notice the posterior rim line is disrupted. CT axial view (C) helps to rule out loose intra-articular fragments that would decrease prognosis and affect planning for surgery.

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■ FIGURE 19-19 A and B, MDCT 3D volume-rendering reconstructions of posterior hip dislocation. Posterior wall fractures, because of their traumatic mechanism, can be associated with posterior dislocation.

■ FIGURE 19-20

Anteroposterior hip film (A) and CT axial view (B) demonstrate the presence of loose intra-articular bodies, which can impair reduction maneuvers and are a surgical indication to improve prognosis.

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■ FIGURE 19-21

A, Anteroposterior radiograph shows both ilioischial and iliopectineal lines are disrupted. B, In axial CT slices, horizontal fractures are difficult to see unless they are oblique to the axial plane. MPR CT or 3D reconstructions help to recognize this type of fractures. C, 3D surface reconstruction shows the fracture pattern.

Anterior Column Isolated anterior column fractures are uncommon, and they are usually associated with a posterior column or transverse fracture. The anterior column is separated from the rest of the pelvis. The typical course begins at a point between the anterior iliac spines and, after traversing the acetabular fossa, ends at the ischiopubic ramus.22,23,30 Radiologically, the iliopectineal line and obturator ring disruption are characteristic features in this pattern and

■ FIGURE 19-22

may be better demonstrated on the oblique view (or CT) than in the anteroposterior radiograph. The orientation of this kind of fracture allows good visualization in axial CT images. CT demonstrates the coronal fracture line,32 distinguishing it from a transverse type, because a T-shaped fracture is the only other acetabular fracture to disrupt the obturator ring (Fig. 19-22). This kind of anterior fracture usually results from a strike to the great trochanter while the hip is externally rotated.23

Anterior column fracture, axial CT. The fracture line starts at the anterior portion of the iliac, goes across the acetabulum (A), and ends at the ischiopubic ramus (B).

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■ FIGURE 19-23 A, CT of anterior wall fractures shows separation of the anterior wall with detachment of the iliopubic ramus. This can be seen in axial slices but is better characterized in coronal reconstructions (B). C, 3D reconstructions give a spatial view of the size and position of fragments.

Posterior Column Posterior column fractures are usually associated with anterior column (bicolumn) and posterior wall fractures. Hip flexion with abduction detaches the whole posterior column. Posterior dislocation of the femoral head is usually associated. Injury to the sciatic nerve may result.23 The fracture runs from the area of the greater sciatic notch through the posterior aspect of the acetabular fossa and then through the ischiopubic ramus. Division of the ischiopubic ramus must be present for a fracture to be classified as a posterior column fracture.19,20,22,25,26

Anterior Wall Anterior wall fractures are the least common of acetabular fractures.22,23 They typically result from forces through the great trochanter. There is separation of the articular surface with detachment of the corresponding segment of the iliopubic column. The displacement in this elementary pattern is often minor because this region is not as heavily loaded as the roof and the posterior wall.24 The fracture originates on the anterior rim of the acetabulum and emerges on the lateral aspect of the superior pubic ramus (Fig. 19-23).

Associated Fractures Transverse and Posterior Wall Fractures The most common type of associated acetabular fracture is the transverse and posterior wall fracture.22,23,25,30 The obturator ring is preserved. Because the horizontal component

is difficult to evaluate in axial images, multiplanar and 3D reconstructions are of benefit (Fig. 19-24).26,32

Fractures of Both Columns These are the most complex of all fracture types. Frequently there is comminution, rotation, and displacement of the resultant fragments. The posterior component of this type of fracture is similar to an isolated posterior column fracture: from its superior extent near the greater sciatic notch, the fracture courses inferiorly through the acetabular fossa and then divides the ischiopubic ramus, separating the entire posterior fragment as a large fragment. The anterior component is more variable but usually extends from a point on the anterior iliac crest, descends vertically in a coronal orientation, and then joins the posterior fracture line in the acetabulum or near it. The only part that remains attached to the sacrum is the posterior iliac wing, so no part of the weight-bearing surface of the acetabulum remains stable. Radiologically, the spur sign distinguishes this fracture from a T-shaped fracture. The spur represents the sciatic strut’s detachment from the acetabulum and is demonstrated on the obturator oblique view as a fragment projecting into the gluteal musculature. CT evaluation reveals the lack of continuity between the acetabulum and the axial skeleton (Fig. 19-25).15,19,22,23,25,26,31,32

T-Shaped Fractures The T-shaped fracture is similar to a transverse fracture, with a vertical trace that disrupts the medial surface of the acetabulum and then divides the ischiopubic ramus. T-shaped fractures might be considered a posterior column

■ FIGURE 19-24 A, Oblique view of transverse and posterior column fracture. The obturator ring is not involved, which is what allows differential diagnosis from an anterior column fracture. B, In axial CT, the vertical component can be observed, affecting the posterior column at the acetabular fossa.

■ FIGURE 19-25

Both-column fractures are the most complex. A, The trace goes through the acetabular fossa dividing the ischiopubic ramus. B, The anterior trace descends from some point in the anterior iliac and joins the posterior at the acetabulum or near it. The only part that remains attached to the sacrum is the posterior iliac wing, and the weight-bearing surface of the acetabulum loses contact with the axial skeleton. C, The spur sign distinguishes this fracture from a T-shaped fracture. The spur represents the sciatic strut’s detachment from the acetabulum and is best seen on the obturator oblique view as a fragment projecting into the gluteal musculature.

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■ FIGURE 19-26

Axial CT scan showing the fracture trace at different heights. At the acetabular roof, the three different lines are confluent (A), and at the acetabular fossa they separate both columns (B). C, 3D surface reconstruction shows a lateral view of the acetabulum.

with a transverse fracture or a posterior column associated with an anterior transverse fracture (Fig. 19-26).23 Radiologically, they show disruption of the obturator ring and both the ilioischial and iliopectineal lines. These features also appear in bicolumn injuries, but in the T-shaped injury pattern the roof remains attached to the sciatic strut and thus to the axial skeleton.23

Anterior Wall or Anterior Column with Transverse Fracture

For posterior wall fractures affecting more than 40% of the posterior wall, operative reduction and internal fixation is indicated. Fractures with comminution and loose intraarticular fragments will undergo surgery to improve prognosis. Posterior column and posterior wall fractures also need a posterior approach and may be difficult to reduce if a loose fragment is not detected (Fig. 19-27).23,29 Anterior wall fractures with significant steps in the cortex or intra-articular fragments will require an open reduction, even though traditionally anterior wall

Association of an anterior wall or anterior column with a transverse fracture results in an anterior wall or column fracture associated with a posterior hemitransverse fracture. In these cases an anterior surgical approach is indicated.1

Posterior Column and Posterior Wall Fracture This is an uncommon association. It is difficult to differentiate from a single fracture.22,25 The surgical approach is likely to be the same for both of these fractures, but posterior wall fractures may result in multiple fragments that can become impacted into the reminder of the innominate bone, so suitable reduction may be impossible if the correct diagnosis is not made (Table 19-6).23,29,32

Synopsis of Treatment Options Acetabular fractures often compromise hip stability, and that is why most of them will have to be treated surgically. The patterns of fracture determine the operative approach, to reduce and internally fix fragments. In only few cases, when the fracture is isolated and does not affect hip stability, conservative treatment can be used, such as in some cases of posterior wall fractures.

K E Y P O I N T S : A C E TA B U L A R FRACTURES Acetabular fractures normally appear in the context of a major pelvic trauma. ■ Acetabular fractures can be classified into simple (anterior column, posterior column, or transverse) and complex patterns, which require an exhaustive understanding of the regional anatomy, and the associated radiologic correlates. ■ The three most common types of fractures are bothcolumn, transverse with posterior wall, and elementary posterior wall fractures. ■ Accurate radiographic diagnosis is the key to a successful treatment plan. Combination of the different imaging techniques provides understanding of the fracture pattern and location of the resulting fragments, which is decisive to plan surgery. Radiography will have to be supplemented by CT: it provides information about the extent of the fracture and is complementary to radiography to define the spatial distribution of the fracture fragments. ■

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TABLE 19-6 Summary of Findings in Judet-Letournel Fracture Types Obturator Ring Fracture

Ilioischial Line Disruption

Iliopectineal Line Disruption

Iliac Wing Fracture

Posterior Wall Fracture

Posterior wall Transverse

− −

Variable +

− +

− −

+ −

Anterior column

+

−

+

+

−

Posterior column

+

+

−

−

−

Anterior wall Transverse + posterior wall Both columns

− −

− +

+ +

− −

− +

+

+

+

+

−

T shaped

+

+

+

−

−

Anterior column + posterior hemi-transverse Posterior column + posterior wall

−

+

+

+

−

+

+

−

−

+

Pelvis into Halves

Spur Sign

− Upper and lower Anterior and posterior Anterior and posterior − Upper and lower Anterior and posterior Upper and lower *

− −

Oblique Vertical

−

Horizontal

−

Horizontal

− − +

Oblique Vertical and oblique Horizontal

−

Vertical

−

*

−

Horizontal and oblique

Anterior and posterior

CT Fracture Orientation

*In case of combination of column and transverse fracture types that do not fit anterior column plus hemitransverse, these radiographic features are not applicable.

■ FIGURE 19-27 A, Anteroposterior view of posterior wall fracture. Notice the presence of multiple fragments that involve more than 40% of posterior wall on MDCT 3D volume rendering (B) reconstructions. C, Postsurgical control film after posterior approach with internal fixation shows fragments have been reduced and fixed to restore stability.

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fractures do not compromise stability, because they involve a non–weight-bearing section of the acetabulum. Traditionally, an ilioinguinal approach has been used for anterior column and wall fractures, associated anterior column and posterior hemitransverse fractures, selected both-column fractures, and, more infrequently, T-shaped and transverse fractures.19,20,33 T-shaped fractures need a posterior approach.29,30 It is important not to miss T-shaped fractures when suspecting and studying a transverse elementary fracture, because the former sometimes needs a modified surgical approach to reduce and fix lower fragments.22

BONE STRESS FRACTURES OF THE PELVIS Prevalence, Epidemiology, and Definitions Bone stress fractures are classified either as insufficiency or fatigue fractures. Insufficiency fracture is a subgroup of stress fractures that is caused by the effect of normal or physiologic stress on weakened bone. Fractures develop when the elastic resistance of the bone is inadequate to withstand the stress of normal weight-bearing stress. Insufficiency fractures of the pelvic bones are prevalent in elderly women. The presence of osteoporosis, rheumatoid arthritis, or a history of pelvic irradiation often predisposes to such fractures. Such conditions also cause delayed healing of the fractures, giving an aggressive appearance. Pelvic insufficiency fractures have been documented in 34% of patients after pelvic irradiation for uterine cancer; 11% were asymptomatic, and 85% showed more than one fracture. Postmenopausal women who sustain pelvic irradiation are particularly at risk. Pretreatment measurement of bone density for these patients is recommended to evaluate a supplementary risk for and treatment of osteoporosis. Fatigue stress fractures occur when repetitive microtrauma overloads the capacity of the tissue to repair itself. This is related to overuse sports activities in athletes. Fatigue stress fractures of the pelvis are more common in women than in men.

Biomechanics and Pathology The distribution of stress injuries observed depends on the specifics of the population. The fracture may involve just one site; however, because of abnormal stress on other portions of the pelvis, multiple fractures or muscle edema are not infrequently associated.34–36 Loss of bone trabeculae decreases the bone’s elastic resistance. When stress occurs beyond the bone’s elastic range, it causes persistent plastic deformity as a result of microfractures. In this situation osteoclastic resorption exceeds osteoblastic activity and a fracture develops. There are multiple factors that weaken the bone elasticity; predisposing factors are therapy with corticosteroids, radiation therapy, inflammatory arthropathies, such as rheumatoid arthritis, and metabolic disorders. The most important and extended factor is postmenopausal osteoporosis.

Irradiation can kill osteoblasts, osteocytes, and osteoclasts and leave an acellular matrix that appears radiographically normal. Vascular damage can cause progressive ischemic changes that further weaken bone structure. These two processes result in bone atrophy, and risk of fracture, second malignancy, or infection is increased. Technical aspects of radiotherapy that increase the risk of radiation-associated damage include the number of fields treated per day, use of voltage energy, and delivery of a high daily dose per fraction. Other factors that increase the risk of fractures are tobacco use and radiographic evidence of osteoporosis.17 The mechanism of injury in athletes is the result of overuse repetitive strenuous conditioning of the rectus abdominis and adductor muscles. This has been described in many sports; long distance female runners have increased risk. Pubic rami stress fractures have been associated with soccer players owing to overuse of the adductor muscles. Limb-length discrepancy has been referred as an intrinsic factor that increases the risk for stress fractures. Patients with fatigue fractures often associate change of the rhythm of activity with an increase in training, change of footwear, or training surface. Women are thought to be at increased risk of stress fractures due to the relatively frequent occurrence of a hypoestrogenic status associated with intense activity, leading to reduced bone density. Fatigue sacral stress fractures have also been reported in the pediatric age group, even in those not involved in extensive physical training (Fig. 19-28).37–41

Manifestations of the Disease Clinical findings are nonspecific and patients are usually referred to rule out degenerative disease usually of the lumbar spine or hip. Since Lourie first described this disorder, many papers have been published on this often as undiagnosed, misdiagnosed, or unrecognized clinical syndrome.42–45 Sacral stress fractures present as low back or buttock pain without trauma or with low-impact trauma. Pain is insidious, is mechanical, and can be diffuse or radiate to the buttock or leg. The sudden onset of groin pain and tenderness over the parasymphyseal area suggests associated pubic rami fractures. Pain is relieved by rest and worse with physical activity. Tenderness on palpation and reduced range of motion are the features of the physical examination. The most important laboratory determination is the whether the serum level of alkaline phosphatase is elevated.41,43,45

Radiography The typical sites of pelvic stress fractures are the sacrum and pubic rami. Sacral fractures can be unilateral or bilateral. Pubic rami fracture can affect iliac and ischiopubic rami and are frequently bilateral and simultaneously involved. Parasymphyseal fractures are often bilateral. Supra-acetabular fractures are less frequent. The appearance of pelvic insufficiency fractures on plain radiographs can generally be classified into two categories: occult and aggressive (Figs. 19-29 and 19-30). Initially, undetectable or only minimal signs can be seen.

■ FIGURE 19-28

Early stage of sacral stress fracture in an 11-year-old boy. A, Axial CT shows a subtle linear sclerosis. B, MRI permits detection of a fracture line on coronal T1-weighted fast spin-echo image. C, Bone marrow edema is seen on an axial STIR sequence at early stages.

■ FIGURE 19-29 A, Sacral stress insufficiency fractures are difficult to depict on plain films owing to overlapping structures. B, Bilateral lineal fracture line or sclerosis parallel to the sacroiliac joint is a characteristic feature that can be seen on coronal CT or coronal multiplanar reconstruction. C, On MRI, a fracture line is best seen on T1-weighted fast spin-echo imaging.

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■ FIGURE 19-30 A, Pubic rami insufficiency fracture is easily visualized on plain radiography. Leg motion movement can lead to aggressive appearance and increase the fracture gap on iliac pubic rami (B) and ischial pubic rami (C). Note the presence of a contralateral old rami fracture with bone remodeling.

Then fracture develops and callus can form, resulting in an aggressive appearance. This is especially evident in the pubic rami, as thigh and leg motion act through the adductor muscles to move the medial fragment of the fracture at the pubic symphysis, acting as a hinge. As a result, lysis and callus formation produce a destructive malignant-appearing lesion. In irradiated patients, healing is impaired and increased osteolysis and bone fragmentation give an aggressive radiographic appearance.36,46 Radiographic assessment of the sacrum is difficult, owing to overlying bowel gas that obscures the body of the sacrum and the three-dimensional geometry of the sacral alae. The sensitivity of radiography is between 20% and 30%. A negative plain film does not exclude the possibility of stress fracture. The presence of multiple pelvic fractures is a valuable clue to the diagnosis. Primary findings of sacral fractures are vertical sclerosis owing to trabecular compression and callus formation or a vertical fracture line. Sacral fractures can be unilateral, bilateral, or H shaped. Osteoporosis can be detected in the pelvis in patients with insufficiency fractures.39,40 Pubic stress fractures can be more easily diagnosed with plain radiography, especially when displacement is seen, and can have an aggressive appearance.45

Computed Tomography The role of CT is to demonstrate fracture lines or sclerosis in the typical locations. Classically, for sacral stress fracture the “gold standard” diagnostic method has been CT.

The presence of a vertical fracture or lineal sclerosis parallel to the sacroiliac joint unilateral (Fig. 19-31) or bilateral is highly specific of stress sacral fracture (Fig. 19-32). CT without multiplanar reconstruction can be misleading if the fractures are oriented horizontally. Some authors have described vacuum phenomena within the fracture line, although the incidence varies depending on the series (Fig. 19-33). The diagnostic value is limited in early cases when the fracture line is not yet developed or in late stage cases when only sclerosis is shown (Fig. 19-34).36,47,48

Magnetic Resonance Imaging Magnetic resonance imaging is extremely sensitive in detecting the early signs of bone stress injury. Bone marrow edema is the earliest radiologic sign. It has been described as early as 18 days after the onset of the symptoms (see Fig. 19-34). A band that is hypointense on spinecho T1-weighted images and hyperintense on spin-echo T2-weighted images corresponds to the edema area and the fracture. Short tau inversion recovery (STIR) or fatsuppressed, T2-weighted images allow improved diagnostic accuracy for detection of the fracture line. Some series advocated the use of gadolinium sequences with fat suppression to improve the delineation of the fracture line, but its additional value to T2-weighted imaging with fat suppression has not been fully proved.35,36 Determination of the classic location of the edema pattern and the fracture line is essential for accurate diagnosis. Sacral fractures exhibit a vertical linear pattern that is unilaterally or bilaterally parallel to the sacroiliac joint

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■ FIGURE 19-31

459

Unilateral sacral fracture. A, MDCT coronal multiplanar reconstruction shows sclerosis and fracture line parallel to right sacroiliac joint. Coronal T1-weighted (B) and STIR (C) MR images demonstrate bone marrow edema.

■ FIGURE 19-32 Multiple pelvic stress fractures. A, See-through bone radiograph shows bilateral sacral fracture (arrow), parasymphyseal fracture (1), and iliopubic rami fracture (2). B, Axial CT of the same patient shows the classic H pattern with bilateral vertical fracture and horizontal fracture through a sacral body.

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■ FIGURE 19-33 Axial CT image shows vacuum phenomena within the fracture gap. This is highly specific for a benign lesion.

with a horizontal line through the sacral vertebral body. Some authors advocate the use of CT to confirm the fracture line in all cases (Fig. 19-35). If a patient has no known malignancy and has the classic pattern, MRI is probably not needed. Pubic rami fractures involve both iliac and ischial pubic rami and are frequently bilateral, especially when they affect the parasymphyseal pubic joint. Secondary to the hinge effect, abnormal movements in muscle insertions lead to muscle edema and hematoma (see Fig. 19-32). Muscular edema must not be mistaken as soft tissue mass. The swollen muscles are isointense to normal on T1-weighted imaging and hyperintense on T2weighted imaging and enhance after intravenous administration of gadolinium.49 Supra-acetabular fractures are an unusual location for a stress fracture. Characteristically, the fracture line is

■ FIGURE 19-34 A, On axial CT sclerosis parallel to the sacroiliac joint is difficult to see. B, Coronal STIR MR image nicely shows a bilateral fracture.

■ FIGURE 19-35

Right overuse stress fracture in a female marathon runner. Coronal T1-weighted (A) and T2-weighted (B) fast spin-echo MR images show an oblique fracture line. (Courtesy of Dr. M. Padron, Clinica Centro, Madrid, Spain.)

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■ FIGURE 19-36 A to C, Coronal STIR MR images of pubic rami stress fracture. Fluid cleft sign is seen within the right fracture on A, and abductor muscle edema is evident on B.

parallel to the acetabular roof with a curvilinear course or is obliquely oriented.50 Fluid signal intensity within the fracture gap has been highly specific for pubic and sacral stress fractures. This cleft-like elongated area of bright signal at the fracture line is highly specific for stress fractures and unrelated to tumors. The cause of this fluid collection has not been fully pathologically explained, but it is probably related to an unabsorbed hematoma (Figs. 19-36 and 19-37).45,49

Nuclear Medicine Scintigraphy is a very sensitive technique but lacks specificity. Scintigraphy shows weakly to strongly increased uptake, depending on the fracture stage. The advantage is that it simultaneously excludes associated fractures within the pelvis or in the proximal femur. The differential diagnosis from other causes of increased tracer uptake is limited owing to the absence of anatomic image definitions. Cross-sectional imaging is frequently needed to differentiate fractures from metastasis or other causes, such as inflammatory or infectious disease.

Sacral stress fractures have two different patterns: (1) linear vertical uptake parallel to the sacroiliac joint and (2) bilateral vertical uptake with a connecting horizontal line. The latest characteristic, the H, or Honda or butterfly, pattern is seen only in approximately 20% of patients.36

Differential Diagnosis Stress fractures of the pelvis in patients without previous malignancy are difficult to diagnose owing to the nonspecific low back or groin pain. Sacral stress fractures may be confused with mechanical impingement syndromes, such as disk disease, spinal stenosis, or cauda equina syndrome. Pubic rami fractures cannot be distinguished clinically from femoral neck fractures or other causes of hip pain. In athletes, the differential diagnosis includes muscle strain and, less frequently, infection. Clinically, the absence of pain with rest is a key feature that helps to distinguish fracture from other more serious diseases, such as neoplasms or infections.37

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■ FIGURE 19-37 A and B, Axial sacral T1 weighted STIR MR sequences of a sacral bilateral fracture showing cleft fluid sign on left sacral fracture (arrow).

In patients with previous malignant neoplasia, especially after pelvic radiation therapy, the differential diagnosis includes radiation bone changes, bone metastasis, or radiation-induced new tumor such as chondrosarcoma. Histologic changes with hemorrhage, fibrosis, and bone and cartilage formation (callus) might lead to misinterpretation by the pathologist, such as chronic osteomyelitis or chondro-osseous tissues. Therefore, the radiologic diagnosis is important.45 The absence of a soft tissue mass, the presence of a fracture line, a cleft fluid sign, multiple fractures, and no progression in serial scans provide the accurate diagnosis most of the time, thus avoiding unnecessary biopsy and radiotherapy.17 Pubic rami fracture due to muscular movement exhibits a more aggressive appearance. Sacral fractures characteristically have a vertical lineal fracture or sclerosis, whereas metastasis presents as a globular or rounded shape. Radiation changes are more diffuse, extending to the radiation portal; fractures lines can be seen within it.

KEY POINTS: BONE STRESS P E LV I C F R A C T U R E S Characteristic imaging findings and location of stress fractures permit an accurate diagnosis and avoid inappropriate studies. ■ CT better defines the fracture line, but early or late stages can be more difficult to depict with CT. ■ MRI allows early diagnosis of occult fractures based on the detection of bone marrow edema. ■ Careful analysis of spin-echo T1-weighted images and fat-suppressed T2-weighted images or STIR sequences shows the fracture line and specific features. ■ The aggressive aspect of pubic rami fractures is produced by distraction of the fragments and muscle edema; a cleft-like fluid collection aids in the accurate diagnosis. ■ Concomitant other pelvic stress fractures can contribute to a more confident diagnosis. ■

In patients without known malignancy the differential diagnosis must be made with sacroiliitis, infection, or tumor. If isotope scanning does not exhibit the classic H-shaped pattern, linear uptake close to the sacroiliac joint must be distinguished from sacroiliitis. Infection must be ruled out, especially when the fracture line is not clearly detected and muscle and soft tissue edema is associated.

Synopsis of Treatment Options Treatment usually consists of analgesics, physical therapy, and restriction of weight bearing. Calcitonin has been tried in some series with some initial good response. Treatment of osteoporosis is recommended in postmenopausal women. However, the long-term prognosis may be poor because of fracture progression and complications of prolonged immobility.44 In athletes, discontinuing training to allow healing is sufficient. Patients with stress pelvic fractures recover quickly with 4 to 6 weeks of rest. Athletes should rest and only gradually return to running when symptoms allow. Extrinsic factors such as training regimen, sports equipment, or nutritional habits must be reviewed to modify them and decrease the risk of refracture. In women athletes with multiple stress fractures, the female athlete triad syndrome must be ruled out: eating disorders, amenorrhea, and osteoporosis. Other therapies using ultrasound, electric, electromagnetic fields, or pharmacologic agents have also been used to reduce the healing time.39,41,51

AVULSION FRACTURES Prevalence, Epidemiology, and Definitions Physically active individuals who become involved in competitive or recreational sports activities are prone to suffer apophyseal injuries of the pelvis and hip. Sprinters, gymnasts, and cheerleaders as well as football, baseball, and

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■ FIGURE 19-38 Diagram of the most common avulsion fractures of the pelvic skeleton and proximal femur.

track athletes are especially predisposed to these injuries. Apophyseal injuries may be classified as apophysitis and apophyseal avulsion fractures. Apophysitis is an inflammation of the apophysis resulting from repetitive pull of muscles. Apophyseal avulsion fractures imply separation of the ossification center, in the adolescent, or fragmentation of the apophysis, in the skeletally mature patient. Pelvic avulsion fractures are uncommon. They traditionally predominate in male athletes, although up to 33% of the patients are girls. The patients’ ages typically range from 11 to 16. However, avulsion fractures may occur in all age groups. Chronic avulsion fractures or multiple avulsions at different healing stages may be found.52–57

Anatomy Apophyses are secondary ossification centers appearing during childhood. Apophyses are the point of insertion of muscles and tendons and are prone to avulsion injuries and fractures. The iliac crest, anterior-superior iliac spine, anterior-inferior iliac spine, and ischial tuberosity are the origin of the transverse abdominal and internal oblique abdominal muscles, sartorius muscle, rectus femoris muscle, and hamstring muscles, respectively. Knowledge of the most common sites of pelvic avulsion fractures, of the tendinous insertions at the pelvic ring, and of the biomechanical significance of each muscle group is instrumental for correctly diagnosing avulsion fractures (Fig. 19-38).56

Biomechanics Unbalanced eccentric contraction or passive lengthening may cause muscle strain, tendon rupture, or avulsion fracture. The apophyses are the weakest parts of the pelvic skeleton in children and adolescents. The relative weakness of the epiphyseal plate and the excessive functional demands provoked by hypertrophic muscles favor the occurrence of avulsion fractures in adolescents. Injuries that would cause

growth plate injuries in immature skeletons tend to cause muscle strains and tendon tears in adults. In addition, repeated pulling stresses imposed by intensive training may weaken the cohesion of the apophyseal plate. This weakening frequently leads to overuse injury, also termed apophysitis. Overuse injuries are often missed at the time of the initial presentation. Many patients do not consult a doctor because these lesions are often self-diagnosed as muscle injuries. If the training load is not properly reduced, apophysitis may complicate stress fractures.52–57

Imaging Techniques The diagnosis of avulsion fractures, suggested by clinical history, physical findings, patient’s age, and biomechanical analysis of the accident, is usually confirmed by radiographs. In acute avulsion fractures there is usually a clear history because the injury is abrupt, occurring during the activity. Conventional radiography is the technique of first choice. Plain radiographs, supplemented by oblique projections, are used for early diagnosis, treatment planning, and follow-up. Radiographic diagnosis is usually straightforward if there is a recent traumatic episode. Subtle or misleading findings may complicate radiographic recognition, particularly in skeletally immature patients. In this age group, comparison with the contralateral side is particularly important, to distinguish fracture from unfused apophysis. Ultrasonography, CT, MRI, and bone scintigraphy may help confirm the diagnosis and exclude other bone and soft tissue conditions.

Manifestations of the Disease The clinical and radiographic manifestations of pelvic avulsion fractures depend on the patient’s age, injury pattern, involved apophysis, and stage of the disease. The most commonly involved sites of the pelvic skeleton in decreasing order of prevalence are the ischium, the anterior-inferior iliac spine, the anterior-superior iliac spine,

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■ FIGURE 19-39

A, Anteroposterior radiograph shows a slightly displaced avulsion fracture of the left ischial tuberosity (arrow). B, Follow-up study reveals complete healing with hypertrophic callus formation. (Reprinted from Bencardino JT, Mellado JM. Hamstring injuries of the hip. Magn Reson Imaging Clin North Am 2005; 13:677–690.)

the pubic bones, and the iliac crest. Acute fractures present as sudden pain at the involved apophysis, which usually is associated with a popping or tearing sensation. Following this, an antalgic gait or inability to walk is usually found. Swelling, local tenderness, or hematoma may be observed. If there is muscle retraction, a contour defect may be palpated. Sciatic neuropathy or meralgia paresthetica may rarely occur.52–57

occasionally with a hypertrophic (Fig. 19-41) or aggressivelooking radiographic appearance. When there is no clear history of prior trauma, clinical diagnosis of chronic cases becomes particularly difficult and cross-sectional imaging or biopsy may be required. In cases of impingement on the sciatic nerve, cross-sectional imaging, particularly CT, may aid in surgical planning.52–57,64

Radiography Because avulsion fractures occur in skeletally immature patients and predictably involve a specific apophysis of the pelvic skeleton, the classic finding is a bony fragment immediately adjacent to, or slightly displaced from, the parent bone. In the acute setting, associated soft tissue findings (e.g., a soft tissue hematoma) are expected. In the chronic setting, exuberant callus formation may occur.

Avulsion Fractures of the Ischial Tuberosity Avulsion fractures of the ischium are among the most common avulsion fractures of the pelvic ring. However, these are relatively rare injuries and may be easily overlooked.52,58–62 In acute cases, avulsion fracture of the ischial tuberosity appears as a curved, sharply marginated piece of bone adjacent to the ischium (Fig. 19-39). On MRI, an acute avulsion fracture manifests as a local hematoma or periosteal stripping (Fig. 19-40). Waviness and retraction of the torn end of the tendon, with or without a bony fragment, may also be present. However, cortical fragments that do not contain bone marrow can be missed on MRI.63 Chronic avulsion injuries frequently lead to extensive periosteal reaction, callus formation, and fragment lysis,

■ FIGURE 19-40 Axial, fat-suppressed, T2-weighted MR image reveals an acute avulsion fracture of the right ischial tuberosity.

CHAPTER

■ FIGURE 19-41

19

● Acute Osseous Injury to the Pelvis and Acetabulum

465

Coronal T1-weighted (A) and STIR (B) MR images reveal a hypertrophic callus after prior avulsion fracture of the right ischial tuberosity.

Avulsion Fractures of the Anterior-Inferior Iliac Spine Acute avulsion fractures of the anterior-inferior iliac spine are usually found in soccer players, field hockey players, runners, and hurdlers. On plain films, avulsion of the rectus femoris muscle presents as a displaced bony fragment that arises from the anterior-inferior iliac spine or from the superior acetabular ridge (Fig. 19-42). Avulsion of the direct head of the rectus femoris at the anterior-

inferior iliac spine is more common than avulsion of the indirect head at the superior acetabular rim.65 Avulsion of the anterior-superior iliac spine can simulate fracture of the inferior spine if the fragment is caudally displaced. In chronic injuries, irregularity or proliferation of the underlying bone may be seen. Exuberant callus formation and myositis ossificans may occur.52–57,65

Avulsion Fractures of the Anterior-Superior Iliac Spine Avulsion fractures of the anterior-superior iliac spine are rare in comparison with other apophyseal injuries. They may involve the attachment site for the sartorius and tensor fasciae latae muscles. Avulsion of the sartorius muscle usually follows forceful extension of the hip, as occurs during sprinting, and presents as anterior displacement of a small avulsed bony fragment. Conversely, avulsion of the tensor fasciae latae muscle is caused by forceful rotation, typically during batting, and presents as lateral displacement of a larger fragment.66

Avulsion Fractures of the Pubic Bones

■ FIGURE 19-42 Anteroposterior radiograph shows a slightly displaced avulsion fracture of the left anteroinferior iliac spine.

Acute avulsion fractures of the anteroinferior aspect of the pubis may occur in soccer players who perform a forceful contraction against resistance, usually involving the origin of the adductor longus. Discrete bone fragments are rarely found in plain films, in contrast to injuries at other sites in the pelvis (Fig. 19-43). MRI may aid in identification of the specific muscle involved. Chronic avulsion injury leads to rarefaction or lysis of the pubic bones and may be confused with infection or tumor. Such avulsion injuries are usually unilateral and may be associated with a soft tissue mass in the upper medial thigh.52–57

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TABLE 19-7 Differential Diagnosis of Pelvic Avulsion Fractures

Acute Avulsion Fracture Nontraumatic avulsion fracture Soft tissue injury Aggressive-looking appearance Incidental normal variant Chronic Avulsion Fracture Apophyseal avulsion injury Soft tissue injury

Bone metastasis Prior graft harvesting Tendon tear Muscle strain Osteomyelitis Tumor Accessory bone Apophysitis Traction periostitis Bursitis Degenerative tendinopathy Calcific tendinitis

occur after graft harvesting in adult patients. Radiographs may show subtle asymmetry of the iliac crest apophyses, with mild separation that may remain undetected if comparison with the contralateral side is not performed.52–57 ■ FIGURE 19-43 Anteroposterior radiograph shows an avulsion fracture of the left pubic bone (arrowhead). (Reprinted from Rossi F, Dragoni S. Acute avulsion fractures of the pelvis in adolescent competitive athletes: prevalence, location and sports distribution of 203 cases collected. Skeletal Radiol 2001; 30:127–131. Reprinted with kind permission from Springer Science and Business Media.)

Avulsion Fractures of the Iliac Crest Avulsion fractures of the iliac crest involve the insertion of the external and internal oblique and transverse abdominal muscles. These injuries are very uncommon. The acute form of the avulsion fracture is associated with abrupt directional changes during motion or with repetitive microtrauma as seen in long-distance runners. This fracture has been reported in figure skaters and runners. More rarely, it may

■ FIGURE 19-44

Differential Diagnosis The clinical presentation of acute avulsion fractures of the pelvic skeleton may mimic injury to the muscle-tendon unit. In addition, a number of traumatic, degenerative, or inflammatory conditions of the pelvic soft tissues may also clinically resemble chronic avulsion injuries or fractures. Diagnostic imaging plays a crucial role in the differential diagnosis of avulsion fractures of the pelvic skeleton, particularly of injuries of the ischial tuberosity and hamstring muscle-tendon unit (Table 19-7). Nontraumatic avulsion fractures may reflect neoplastic infiltration, underlying osteopenia, or prior surgery. Metastatic tumor weakens the involved bone, which is then susceptible to avulsion fractures under normal stresses. Although pathologic fracture is more common at the

Anteroposterior radiograph (A) and axial fat-suppressed, T2-weighted MR image (B) reveal an avulsion fracture of the left anterosuperior iliac spine after graft harvesting. (Reprinted from Samartzis D, Shen FH. What’s your call? Postoperative iliac-crest avulsion fracture. Can Med Assoc J 2006; 175:475–476. © 2006 Canadian Medical Association. Reprinted by permission of the publisher.)

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proximal femur, it may also occur at the pelvic skeleton, usually involving the ischium, the anterior-inferior iliac spine, and the anterior-superior iliac spine. Radiographic depiction of a nontraumatic avulsion fracture of the pelvis must raise suspicion of an underlying malignancy, and a biopsy should be considered. Nontraumatic avulsion fractures may be found after graft harvesting of the iliac crest.67 The iliac crest, which is rich in cancellous and cortical bone stock, is a common donor site for bone grafts. Avulsion fracture of the anterior-superior iliac spine is an uncommon adverse event after graft harvesting (Fig. 19-44). There is increased risk of such fractures in patients in whom graft material was harvested less than 5 cm from the anterior-superior iliac spine and in whom an osteotome was used. Underlying osteopenia may also play a role. In the acute setting, a number of soft tissue injuries may mimic avulsion fractures, including tendon tears (Fig. 1945) and muscle strains (Fig. 19-46), which are more likely to occur in adult patients. For adequate depiction of these injuries, MRI has proved to be of great clinical value. Chronic avulsion fractures may occasionally present a bizarre or aggressive-looking radiographic appearance, which may simulate neoplasm or infection and prompt occasional biopsies.52–57 Familiarity with the regional anatomy and the mechanisms of injury is required for accurate interpretation of misleading chronic avulsion fractures. More rarely, hematogenous osteomyelitis may cause physeal widening, falsely suggesting avulsion fracture.68 Also, it should be remembered that some accessory bones such as the os acetabuli may be found in symptomatic patients, occasionally resembling chronic nonhealed avulsion fractures (Fig. 19-47).

■ FIGURE 19-45 Coronal STIR MR image reveals a degenerative tear of the right hamstring tendons.

467

■ FIGURE 19-46 Coronal STIR MR image reveals an acute strain of the right hamstring muscles.

Chronic avulsion fractures should also be distinguished from apophyseal avulsion injuries, also named apophysitis. Apophysitis usually presents as pain without any major trauma.69 Typically, there is sclerosis and enlargement of the involved apophysis at plain films and bone marrow edema at MRI (Fig. 19-48). Eventual traction periostitis may develop, and the whole process may lead to bone

■ FIGURE 19-47 Anteroposterior radiograph shows an accessory bone adjacent to the lateral rim of the left acetabulum (os acetabuli).

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and prescribe an analgesic. The patient will have to use crutches or a walker. Avulsion fractures of the ischial tuberosity are almost exclusively treated conservatively with an overall good prognosis for spontaneous healing. Patients with ischial avulsion tend to respond well to conservative treatment, and a return to normal activity over the next 6 to 12 weeks may be expected. Avulsions of both the anterior-superior and anteriorinferior iliac spines tend to be less symptomatic and disabling than avulsions of the ischial tuberosity, and recovery time is relatively short. Injuries of the iliac spine are first treated with bed rest with the hips and knees flexed, then with progressive ambulation. Full athletic potential is regained in 5 to 6 weeks. Avulsions of the pubic bones and iliac crest are also managed conservatively in most patients.

Surgical Treatment

■ FIGURE 19-48

Coronal STIR MR image reveals abnormal bone marrow edema at the right ischial tuberosity, which was interpreted as overuse apophysitis.

If the fragment is displaced more than 2 cm, however, fibrous union may occur, resulting in extended disability. Consequently, surgical repair may be indicated when there is displacement of the avulsed fragment greater than 2 cm.

weakening and stress fracture. Chronic avulsion fractures should also be distinguished from other soft tissue injuries, such as bursitis, tendinitis, and calcific tendinitis.

Synopsis of Treatment Options Medical Treatment Proper identification of nontraumatic avulsion fractures has important implications, because appropriate therapeutic schemes should be selected. However, most avulsion fractures are stable fractures and will usually heal without surgery. The physician may recommend bed rest

KEY POINT S: AVUL SION FRACTURES Apophyseal avulsion fractures are uncommon injuries. They predominate in young individuals who are involved in sport activities. ■ Avulsions of the ischial tuberosity and anterior-inferior iliac spine are the most common pelvic avulsion fractures. ■ An acute avulsion fracture should be distinguished from a muscle strain. ■ A chronic avulsion fracture may be seen on a radiograph. ■ ■

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9. Buckwalter KA, Rydberg J, Kopecky KK, et al. Musculoskeletal imaging with multislice CT. AJR Am J Roentgenol 2001; 176:979–986. 10. Pretorius ES, Fishman EK. Volume-rendered three-dimensional spiral CT: Musculoskeletal applications. Radiographics 1999; 19:1143–1160. 11. Willmann JK, Roos JE, Platz A, et al. Multidetector CT: Detection of active hemorrhage in patients with blunt abdominal trauma. AJR Am J Roentgenol 2002; 179:437–444. 12. Gansslen A, Giannoudis P, Pape HC. Hemorrhage in pelvis fracture: who needs angiography? Curr Opin Crit Care 2003; 9:515–523. 13. Young JW, Resnik CS. Fracture of the pelvis: current concepts of classification. AJR Am J Roentgenol 1990; 155:1169–1175. 14. Young JW, Burgess AR, Brumback RJ, Poka A. Pelvic fractures: value of plain radiography in early assessment and management. Radiology 1986; 160:445–451. 15. Hunter J, Brandser E, Tran K. Pelvic and acetabular trauma. Radiol Clin North Am 1997; 35:559–590. 16. Bircher M. Open pelvis fractures. Eur J Trauma 2005; 31:526–535.

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17. Mumber MP, Greven KM, Haygood TM. Pelvic insufficiency fractures associated with radiation atrophy: clinical recognition and diagnostic evaluation. Skeletal Radiol 1997; 26:94–99. 18. Grotz MRW. Open pelvic fractures: epidemiology. Injury 2005; 36:2–1. 19. Letournel E. Acetabulum fractures: classification and management. Clin Orthop Relat Res 1980; 151:81–106. 20. Letournel E, Judet R. Fractures of the Acetabulum, 2nd ed. Berlin, Springer Verlag, 1993. 21. Letournel E. Acetabulum fractures: classification and management. Clin Orthop Relat Res 1980; 151:81–106. 22. Brandser E, Marsh JL. Acetabular fractures: easier classification with a systematic approach. AJR Am J Roentgenol 1998; 171:1217–1228. 23. Potok P, Hopper K, Umlauf M. Fractures of the acetabulum: imaging, classification and understanding. Radiographics 1995; 15:7–23. 24. Govsa F, Ozer MA, Ozgur Z. Morphologic features of the acetabulum. Arch Orthop Trauma Surg 2005; 125:453–461. 25. Durkee N, Jacobson J, Jamadar D, et al. Classification of common acetabular fractures: radiographic and CT appearances. AJR Am J Roentgenol 2006; 187:915–925. 26. Judet R, Judet J, Letournel E. Fractures of the acetabulum: classification and surgical approaches of open reduction— preliminary report. J Bone Joint Surg Am 1964; 46:1615–1646. 27. Greenspan A. Orthopedic Imaging, 4th ed. Philadelphia, Lippincott Williams & Wilkins, 2004. 28. Beaulé PE, Lee JL, Le Duff MJ, et al. Orientation of the femoral component in surface arthroplasty of the hip. J Bone Joint Surg Am 2004; 86:2015–2021. 29. Patel V, Day A, Dinah F, et al. The value of specific radiological features in the classification of acetabular fractures. J Bone Joint Surg Br 2007; 89:72–76. 30. Davies AM, Johnson K, Whitehouse RW. Imaging of the Hip and Bony Pelvis: Techniques and Applications. Berlin, Springer, 2006. 31. Keith JE, Brashear H, Guilford WB. Stability of posterior fracture dislocations of the hip: quantitative assessment using computed tomography. J Bone Joint Surg Am 1988; 70:711–714. 32. Martinez C, Di Pasquele P, Helfet D, et al. Evaluation of acetabular fractures with two and three dimension CT. Radiographics 1992; 12:227–242. 33. Jakob M, Droeser R, Zobrist R, et al. A less invasive anterior intrapelvic approach for the treatment of acetabular fractures and pelvic ring injuries. J Trauma 2006; 60:1364–1370. 34. Ahovuo JA, Kiuru MJ, Visuri T. Fatigue stress fractures of the sacrum: diagnosis with MR imaging. Eur Radiol 2004; 14:500–505. 35. Kiuru MJ, Pihlajamaki HK, Ahovuo JA. Fatigue stress injuries of the pelvic bones and proximal femur: evaluation with MR imaging. Eur Radiol 2003; 13:605–611. 36. Grangier C, Garcia J, Howarth NR, et al. Role of MRI in the diagnosis of insufficiency fractures of the sacrum and acetabular roof. Skeletal Radiol 1997; 26:517–524. 37. Patterson SP, Daffner RH, Sciulli RL, Schneck-Jacob SL. Fatigue fracture of the sacrum in an adolescent. Pediatr Radiol 2004; 34:633–635. 38. Iwamoto J, Takeda T. Stress fractures in athletes: review of 196 cases. J Orthop Sci 2003; 8:273–278. 39. Major NM, Helms CA. Pelvic stress injuries: the relationship between osteitis pubis (symphysis pubis stress injury) and sacroiliac abnormalities in athletes. Skeletal Radiol 1997; 26:711–717. 40. Major NM, Helms CA. Sacral stress fractures in long-distance runners. AJR Am J Roentgenol 2000; 174:727–729. 41. Miller C, Major N, Toth A. Pelvic stress injuries in the athlete: management and prevention. Sports Med 2003; 33:1003–1012. 42. Lourie H. Spontaneous osteoporotic fracture of the sacrum: an unrecognized syndrome of the elderly. JAMA 1982; 248:715–717. 43. Aretxabala I, Fraiz E, Perez-Ruiz F, et al. Sacral insufficiency fractures: high association with pubic rami fractures. Clin Rheumatol 2000; 19:399–401.

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44. Dasgupta B, Shah N, Brown H, et al. Sacral insufficiency fractures: an unsuspected cause of low back pain. Br J Rheumatol 1998; 37:789–793. 45. Hosono M, Kobayashi H, Fujimoto R, et al. MR appearance of parasymphyseal insufficiency fractures of the os pubis. Skeletal Radiol 1997; 26:525–528. 46. Seo GS, Aoki J, Karakida O, et al. Ischiopubic insufficiency fractures: MRI appearances. Skeletal Radiol 1997; 26:705–710. 47. Stabler A, Beck R, Bartl R, et al. Vacuum phenomena in insufficiency fractures of the sacrum. Skeletal Radiol 1995; 24:31–35. 48. Peh WC, Ooi GC. Vacuum phenomena in the sacroiliac joints and in association with sacral insufficiency fractures: incidence and significance. Spine 1997; 22:2005–2008. 49. Peh WC. Intrafracture fluid: a new diagnostic sign of insufficiency fractures of the sacrum and ilium. Br J Radiol 2000; 73:895–898. 50. Otte MT, Helms CA, Fritz RC. MR imaging of supra-acetabular insufficiency fractures. Skeletal Radiol 1997; 26:279–283. 51. Raasch WG, Hergan DJ. Treatment of stress fractures: the fundamentals. Clin Sports Med 2006; 25:29–36, vii. 52. Tehranzadeh J. The spectrum of avulsion and avulsion-like injuries of the musculoskeletal system. Radiographics 1987; 7:945–974. 53. Sundar M, Carty H. Avulsion fractures of the pelvis in children: a report of 32 fractures and their outcome. Skeletal Radiol 1994; 23:85–90. 54. Stevens MA, El-Khoury GY, Kathol MH, et al. Imaging features of avulsion injuries. Radiographics 1999; 19:655–672. 55. Rossi F, Dragoni S. Acute avulsion fractures of the pelvis in adolescent competitive athletes: prevalence, location and sports distribution of 203 cases collected. Skeletal Radiol 2001; 30:127–131. 56. Metzmaker JN, Pappas AM. Avulsion fractures of the pelvis. Am J Sports Med 1985; 13:349–358. 57. Fernbach SK, Wilkinson RH. Avulsion injuries of the pelvis and proximal femur. AJR Am J Roentgenol 1981; 137:581–584. 58. Veselko M, Smrkolj V. Avulsion of the anterior-superior iliac spine in athletes: case reports. J Trauma 1994; 36:444–446. 59. Rossi F, Santilli G. Detachment of the apophyseal nucleus of the ischial tuberosity in adolescent athletes. Med Sport 1976; 29:447–472. 60. Rossi F, Conti F. Isolated tear fracture of the apophyseal nucleus of the anterior inferior iliac spine. Ital J Sports Traumatol 1979; 1:161–175. 61. Kujala UM, Orava S. Ischial apophysis injuries in athletes. Sports Med 1993;16:290–294. 62. El-Khoury GY, Brandser EA, Kathol MH, et al. Imaging of muscle injuries. Skeletal Radiol 1996; 25:3–11. 63. Bencardino JT, Mellado JM. Hamstring injuries of the hip. Magn Reson Imaging Clin North Am 2005; 13:677–690. 64. Barnes ST, Hinds RB. Pseudotumor of the ischium: a late manifestation of avulsion of the ischial epiphysis. J Bone Joint Surg Am 1972; 54:645–647. 65. Bordalo-Rodrigues M, Rosenberg ZS. MR imaging of the proximal rectus femoris musculotendinous unit. Magn Reson Imaging Clin North Am 2005; 13:717–725. 66. White PM, Boyd J, Beattie TF, et al. Magnetic resonance imaging as the primary imaging modality in children presenting with acute non-traumatic hip pain. Emerg Med J 2001; 18:25–29. 67. Samartzis D, Shen FH. What’s your call? Postoperative iliac crest avulsion fracture. Can Med Assoc J 2006; 175:475–476. 68. Studler U, Ledermann HP, Majeswski M, et al. Widening of the greater trochanteric physis in the immature skeleton: a radiographic sign of femoral osteomyelitis. Eur Radiol 2003; 13:2238–2240. 69. Yamamoto T, Akisue T, Nakatani T, et al. Apophysitis of the ischial tuberosity mimicking a neoplasm on magnetic resonance imaging. Skeletal Radiol 2004; 33:737–740.

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Acute Osseous Injury to the Hip and Proximal Femur José M. Mellado, Ana M. Hualde, Jorge Albareda, and Eva Llopis

Fractures of the proximal femur, loosely referred to as hip fractures, are particularly common in the elderly population and are associated with high mortality rates and great socioeconomic impact. In this age group, more than 90% of hip fractures result from low-energy trauma or minor falls. Osteoporosis remains the single most relevant predisposing factor, although other bone and systemic disorders also increase the risk of hip fracture.1–3 Hip fractures are less frequent in young or middle-aged patients. In this age group, hip fractures and dislocations are generally caused by high-energy trauma and frequently are associated with coexistent orthopedic, neurologic, or visceral complications. In these patients, true avulsion fractures of the greater and lesser trochanter may also occur as the result of forceful muscle contraction.1–5 Stress fractures, which are classified as fatigue and insufficiency fractures, can also involve the proximal femur. Fatigue fractures occur in young athletic individuals who undergo unaccustomed strenuous activities. Insufficiency fractures involve obese or overweight patients, frequently osteoporotic females. The term pathologic fracture is usually reserved for those fractures involving bone weakened by tumor.1–5 Conventional radiographs allow efficient detection of most hip fractures and dislocations. Occasionally, CT, MRI, and bone scintigraphy may be required for further characterization. Diagnostic imaging strongly influences prognosis and treatment of hip fractures and dislocations by providing precise assessment of injury patterns.4 In this chapter we review acute osseous injuries to the hip and proximal femur, including hip dislocations and fractures of the femoral head, femoral neck, greater and lesser trochanters, intertrochanteric region, and subtrochanteric area. Emphasis is put on the widely accepted role of conventional radiographs for routine workup of hip fractures and dislocations but also on the complementary aid provided by classic bone scintigraphy and modern cross-sectional imaging. 470

TRAUMATIC HIP DISLOCATIONS AND FEMORAL HEAD FRACTURES Prevalence, Epidemiology, and Definitions Traumatic hip dislocations are uncommon injuries, accounting for 2% to 5% of all joint dislocations. Failure to promptly recognize them may delay reduction, which increases the risk of osteonecrosis of the femoral head. Hip dislocations typically derive from high-energy trauma. However, in children and young adults, hip dislocations may occasionally arise from minor trauma, owing to ligamentous laxity. Traumatic hip dislocations are classified as posterior and anterior. Central hip dislocations may also occur but are usually considered a modality of acetabular fracture.1–5

Anatomy The hip joint is a large ball-and-socket synovial joint. The round head of the femur articulates with the cup-like acetabulum. The depth of the acetabulum is increased by the fibrocartilaginous labrum. The joint capsule is reinforced by strong ligaments, which extend from the acetabular rim to the anterior intertrochanteric line and posterior femoral neck. The sciatic nerve is in close relationship with the posterior capsule. The femoral head is irrigated by arterial branches originating at the anterior and posterior circumflex arteries but also by a branch of the obturator artery coursing through the ligamentum teres, the foveal artery.1,2 Most hip dislocations lead to disruption of the ligamentum teres and joint capsule, although labral tears, muscle injuries, fractures, and neural damage may also occur.

Biomechanics The degree of hip flexion, the direction of the applied forces, and the individual’s anatomy influence the injury

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■ FIGURE 20-1 Classification of hip dislocations according to the mechanism of injury: posterior (A), anterosuperior (B), and anteroinferior (C).

pattern, leading to posterior, anterosuperior, and anteroinferior dislocations (Fig. 20-1). Most hip dislocations occur in a posterior direction, which typically derive from hitting a dashboard. In this injury pattern, violent longitudinal forces act on a flexed knee and hip. With very slight degrees of hip flexion and adduction, there is increased probability of a posterior acetabular fracture. An iliofemoral ligament disruption may also occur. Anterior hip dislocations represent only 11% of all hip dislocations and may occur in a superior or inferior direction. In inferoanterior dislocation, which occurs with forced abduction, external rotation, and flexion of the hip, the femoral head extrudes beneath the pubofemoral ligament. In superoanterior hip dislocation, which occurs after forced abduction, external rotation, and extension of the femur, the femoral head extrudes between the iliofemoral and the pubofemoral ligaments. However, pubofemoral ligament disruption may also occur.1–3

(Fig. 20-2). If the femoral head lies immediately behind the acetabulum, hip dislocation may be more difficult to detect in anteroposterior views. However, the femoral head will appear smaller than usual and dislocation may be confirmed with a groin-lateral view.4,5 More rarely, purely inferior dislocations (luxatio erecta) of the hip may occur. An acetabular fracture is found in up to 60% of posterior hip dislocations. Posterior acetabular fractures are best evaluated with oblique or lateral views, may radiographically mask hip dislocation, and may interfere with closed reduction. When acetabular fracture is radiographically detected, a CT scan should be obtained before closed reduction.1–5 Osteochondral impaction fractures at the superolateral and anterior aspect of the femoral head occur in up to 63% of posterior hip dislocations. They appear as subtle areas of focal flattening at the lateral aspect of the femoral

Manifestations of the Disease Most patients with hip dislocation present in severe distress after a high-energy trauma. Associated neurologic and visceral injuries are common. Coexistent fractures of the spine, pelvis, and extremities are also possible and should always be ruled out. Direct vascular compromise or major sciatic nerve dysfunction may occur.1–3

Radiography In the acute setting, anteroposterior radiographs of the pelvis may show the hip dislocation and suggest the injury pattern in most patients. Occasionally, groin-lateral and oblique views of the hip may be required to confirm the diagnosis, suggest the direction, or depict associated injuries. Conventional radiographs may be occasionally supplemented by CT when reduction becomes difficult or associated injuries are not clearly shown. After reduction, conventional radiographs are used to confirm the adequacy of reduction. These should always be supplemented by CT for assessing loose body entrapment, acetabular fracture, joint instability, or surgical indications.5 In anteroposterior views of posterior hip dislocations the femoral head typically lies superior to the acetabulum (iliac), the femur is found in adduction and internal rotation, and the lesser trochanter is less visible than usual

■ FIGURE 20-2 Posterior hip dislocation. Anteroposterior view shows a cranially displaced femoral head, with a small impaction fracture (arrow) and a bony fragment overlying the acetabular fossa (arrowhead).

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TABLE 20-1 Pipkin Classification of Posterior Hip Dislocations Associated with Femoral Head Fracture Type I Type II Type III Type IV

Posterior hip dislocation with associated femoral head fracture below the fovea Posterior hip dislocation with associated femoral head fracture above the fovea Posterior hip dislocation with associated femoral head and neck fractures Types I, II, or III with associated posterior acetabular fracture

head, may be easily overlooked on plain films, and significantly increase the risk of post-traumatic osteoarthritis.6 Femoral head fractures may also occur in posterior hip dislocation, with a simple or comminuted appearance.1–3 Associated fractures of the femoral neck and shaft may also occur and should be systematically ruled out before closed reduction to avoid further displacement. Although several classifications have been suggested, the most commonly used is the scheme proposed by Pipkin (Table 20-1, Fig. 20-3). Other associated musculoskeletal injuries include vertebral fractures and posterior cruciate ligament injuries (Table 20-2).

TABLE 20-2 Associated Injuries in Posterior Hip Dislocation Vertebral fracture Pelvic fracture Posterior acetabular fracture Osteochondral impaction fracture of the femoral head Femoral head fracture Femoral neck fracture Femoral diaphysis fracture Cruciate ligament injury Sciatic nerve dysfunction

In inferoanterior dislocation the femoral head overlies the ischium and obturator foramen (Fig. 20-4) and an avulsion of the anterior inferior iliac spine may occur. In superoanterior hip dislocation, which hardly represents 1% of all hip dislocations, the femoral head overlies the medial or lateral aspect of the acetabulum, leading to pubic or iliac dislocations, respectively. Superoanterior dislocations may be occasionally misinterpreted as posterior dislocations. However, in superoanterior hip dislocation the lesser trochanter appears particularly prominent, owing to the external rotation of the femur and the femoral head may become slightly magnified on anteroposterior radiographs. In addition, anterior hip

■ FIGURE 20-3

Pipkin classification of posterior hip dislocations (see Table 20-1).

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■ FIGURE 20-4

Anterior hip dislocation. Anteroposterior views in two different patients show anteroinferior hip dislocations in slight external rotation (A) and complete abduction (B).

dislocations may present as chondral and osteochondral impaction fractures of the posterolateral aspect of the femoral head (Table 20-3).7 Classifications of anterior and posterior hip dislocations have been condensed in a more global scheme, such as that suggested by Levine (Table 20-4). After closed reduction, special attention should be paid to subtle widening of the joint space, caused by interposition of bony or soft tissue fragments. At this stage, plain films should always be supplemented by cross-sectional imaging. During the follow-up, conventional and cross-sectional imaging may also be used to detect potential complications, such as osteonecrosis of the femoral head, degenerative osteoarthritis, joint instability, or heterotopic ossification, which may cause up to 50% of unfavorable outcomes.1–3

Magnetic Resonance Imaging Although CT has traditionally been used to supplement conventional radiographs in the diagnostic workup of hip dislocations, MRI may also be valuable in various regards. MRI is very accurate in detecting osteochondral impaction

fractures of the femoral head (Fig. 20-5) and associated soft tissue injuries (Fig. 20-6). It is also valuable in detecting intra-articular labral entrapment. In children, MRI may help discriminate the real extent of posterior acetabular fracture, which is of prognostic significance. In addition, MRI is far superior to other imaging techniques in detecting secondary osteonecrosis of the femoral head.6,7

Computed Tomography After closed reduction, intra-articular entrapment of bony fragments is more easily identified on CT scans (Fig. 20-7). In addition, CT scans allow an accurate assessment of the extent and significance of posterior acetabular fractures (Fig. 20-8). CT scans are also accurate for detecting osteochondral impaction fractures of the femoral head, which increase the risk of post-traumatic osteoarthritis (Fig. 20-9). Complex, displaced fractures of the femoral head are also better evaluated with CT (Fig. 20-10). Consequently, either CT or MRI should be performed on a routine basis after closed reduction of hip dislocations for assessing congruence, stability, and related injuries (Table 20-5).8,9 TABLE 20-4 Levine Classification of Hip Dislocations

TABLE 20-3 Topographic Classification of Anterior Hip Dislocations Obturator Pubic Iliac Inferior

Inferoranterior dislocation with the femoral head overlying the obturator foramen Superoanterior dislocation with the femoral head overlying the medial acetabulum Superoanterior dislocation with the femoral head overlying the lateral acetabulum Luxatio erecta

Type I Type II Type III Type IV Type V

Hip dislocation without associated fracture or instability Nonreducible hip dislocation without associated fracture Hip dislocation with limited congruence, instability, or loose bodies after closed reduction Hip dislocation associated with acetabular fracture that requires surgical treatment Hip dislocation associated with femoral head or neck fracture

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■ FIGURE 20-5 Impaction fracture of the femoral head. Axial T1-weighted MR image after closed reduction of posterior hip dislocation shows a small impaction fracture of the femoral head (arrowhead) and a rim fracture of the posterior acetabulum (arrow).

■ FIGURE 20-6 Soft tissue injury. Axial, fat-suppressed, proton density–weighted MR image after closed reduction of posterior hip dislocation shows a small soft tissue hematoma (arrowhead) and signs of contusion of the femoral head (arrow).

■ FIGURE 20-7 Loose body entrapment. Scout view (A) reveals subtle widening of the joint space after closed reduction of posterior dislocation of the left hip (arrowheads). B, Axial CT scan reveals this asymmetric widening (arrowhead) to be caused by intra-articular entrapment of a small bony fragment (arrow).

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■ FIGURE 20-8

Acetabular fracture in a skeletally immature patient. Anteroposterior radiograph (A) and axial CT scan (B) after closed reduction of posterior hip dislocation reveal a small rim fracture of the posterior acetabulum (arrows). C and D, Reformatted CT scans in a different patient reveal in fine detail a comminuted fracture of the posterior acetabulum (arrows).

Classic Signs: Hip Dislocation POSTERIOR DISLOCATION ■ Femoral head small and superiorly displaced ■ Adduction and internal rotation ■ Decreased prominence of lesser trochanter ■ Anterolateral osteochondral impaction fracture of the femoral head ■ Common posterior acetabular fracture ■ Possible avascular necrosis

ANTERIOR DISLOCATION ■ Femoral head enlarged and superiorly or inferiorly displaced ■ Abduction and external rotation ■ Increased prominence of lesser trochanter ■ Posterolateral osteochondral impaction fracture of the femoral head ■ Common avulsion fracture of the anterior-inferior iliac spine ■ Rare avascular necrosis

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TABLE 20-5 Cross-Sectional Imaging in Hip Dislocation

Joint congruency Soft tissue injury Chondral loose bodies Bony loose bodies Acetabular fracture assessment Contusion of the femoral head Osteochondral impaction fracture of the femoral head Fracture of the femoral head Avascular necrosis of the femoral head

MRI

CT

+++ +++ +++ + ++ +++ +++

+++ + + +++ +++ + ++

++ +++

+++ +

■ FIGURE 20-9 Early osteoarthritis. Reformatted CT scan shows slightly decreased joint space and a small subchondral cyst-like lesion of the femoral head (arrowhead), probably related to prior hip dislocation.

■ FIGURE 20-10 A, Anteroposterior radiograph shows a Pipkin type II fracture-dislocation of the right hip. A large fragment of the femoral head is found within the acetabular fossa (arrows). B, After closed reduction, CT shows appropriate congruence of fragments (arrows). In a different patient, axial CT image (C) and corresponding 3D reconstruction (D) after closed reduction of a Pipkin type II fracture-dislocation show intra-articular displacement of the capital fragment (arrows).

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477

Nuclear Medicine

Surgical Treatment

Bone scintigraphy has traditionally been used to assess the vascularity of the femoral head after hip dislocations or proximal femoral fractures. However, previous investigations have shown the inability of isotopic bone scan for diagnosing or predicting osteonecrosis of the femoral head in the early stages. The emerging role of MRI has dramatically decreased the use of bone scintigraphy in this regard.

Blocking of concentric reduction after traumatic hip dislocation may be caused by associated acetabular fracture or by interposition of labrum, capsule, ligamentum teres, or intra-articular hematoma. In these patients, open reduction is required in the acute setting to avoid complications. After reduction, congruency and stability of the hip joint are important factors in determining the need for operative stabilization. In particular, fractures involving more than 40% of the posterior acetabulum may cause joint instability and thus require internal fixation to prevent osteoarthritis.1–3 Large femoral head fractures also require internal fixation.

Differential Diagnosis From a clinical standpoint, traumatic hip dislocations are hard to distinguish from fractures of the hip and proximal femur. In addition, it should be kept in mind that many of these fractures may coexist with hip dislocation and systematically should be ruled out. The radiographic detection of hip dislocation is usually straightforward, although posterior hip dislocations without cranial displacement of the femoral head may be occasionally overlooked. The true diagnostic dilemma in hip dislocations is distinguishing anterior from posterior dislocations and detecting associated injuries that may alter management and prognosis. In this regard, the complementary role of cross-sectional imaging may be crucial.

Synopsis of Treatment Options Medical Treatment Closed reduction of traumatic hip dislocations should be performed within 6 hours of injury, in order to decrease the risk of osteonecrosis and post-traumatic osteoarthritis. Nonsurgical management is preferred for those joints that demonstrate adequate congruence and stability after closed reduction.1–3

K E Y P O I N T S : T R A U M AT I C H I P D I S L O C AT I O N S A N D F E M O R A L HEAD FRACTURES Traumatic hip dislocations derive from high-energy trauma and are associated with multiple skeletal and visceral injuries. ■ Careful evaluation of anteroposterior and groin-lateral radiographs of the pelvis and hip is required for diagnosis and characterization of hip dislocations and for excluding associated fractures. ■ This should be followed by prompt closed reduction to decrease the risk of avascular necrosis of the femoral head. ■ Conventional radiographs and CT scans after closed reduction are used to confirm joint congruency, rule out labral or bony entrapment, and assess the posterior acetabulum. ■ MRI may help to diagnose secondary osteonecrosis of the femoral head and may complement CT in various other regards. ■

SUBCHONDRAL INSUFFICIENCY FRACTURES OF THE FEMORAL HEAD Prevalence, Epidemiology, and Definitions Traumatic femoral head fractures typically are associated with hip dislocations. Isolated femoral head fractures are rare and commonly occur in young patients. Those femoral head fractures that occur in the absence of major trauma have been termed subchondral insufficiency fractures. These injuries represent a rare type of stress fractures and are found in osteoporotic, overweight patients and in renal transplant recipients. They may also occur in competitive or recreational athletes and be termed fatigue fractures.10,11

Anatomy The subchondral bone of the weight-bearing portion of the femoral head is mainly supplied by the lateral epiphyseal arteries and is particularly prone to suffer avascular necrosis. A major compressive group of reinforcing trabeculae is found at the subchondral region of the femoral head, while the weakest point is located within the femoral neck, which is also termed Ward’s triangle. This explains why the femoral neck is much more prone to stress fractures than the subchondral region of the femoral head.1–3

Biomechanics Subchondral insufficiency fractures of the femoral head vary with different body constitutions and levels of physical activity. Progressive imbalance between bone resorption and bone repair after mechanical overload may lead to weakening of cortical bone, further propagation of cracks through cement lines, and eventual microfractures, which may subsequently lead to insufficiency fractures.10,11

Pathology Insufficiency fractures usually involve the weight-bearing portion of the femoral head and may or not extend through the articular cartilage. Microscopic examination

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of subchondral insufficiency fractures of the femoral head has revealed a small area of necrosis between the fracture and the articular surface, with a fracture callus along the fracture line. However, a well-defined area of wedgeshaped osteonecrosis is typically absent. Consequently, this band of subchondral osteonecrosis has been considered a secondary phenomenon, resulting from subchondral fracture.10

Manifestations of the Disease Symptoms of insufficiency fracture of the femoral head are characterized by sudden onset of pain, which progressively worsens. Some cases of femoral head fracture may resolve spontaneously. However, in some other patients the disease progresses, associated with increasing pain and restricted mobility of the hip joint.10,11

Classic Signs: Subchondral Insufficiency Fractures of the Femoral Head CONVENTIONAL RADIOGRAPHY ■ Normal during the first 3 months ■ Mixed altered radiodensity ■ Superolateral collapse of the femoral head ■ Occasional rapid destruction of the hip joint BONE SCINTIGRAPHY ■ Increased uptake of the femoral head MAGNETIC RESONANCE IMAGING ■ Subchondral low-intensity band of undulated contour on T1-weighted MRI ■ Bone marrow edema of the femoral head and neck on T2-weighted MRI ■ May simulate avascular necrosis of the femoral head

Radiography Osteoporosis may be apparent on plain films of patients suffering insufficiency fractures of the femoral head. However, the radiographic appearance of the involved femoral head may be unremarkable. Three to 4 months after the onset of pain, some collapse of the superolateral portion of the femoral head may occur. Narrowing of the joint space and areas of mixed increased and decreased bone density in the collapsed subchondral portion are present. Occasionally, an insufficiency fracture of the femoral head may be followed by rapid destruction of the hip joint, once the subchondral collapse has occurred.10–12

Magnetic Resonance Imaging On T1-weighted MR images, a subchondral band of low signal intensity is usually seen that may have a serpentine or undulated contour and lies parallel to the articular surface. This finding is believed to represent the fracture line and associated repair tissue. On T2-weighted or fat-suppressed sequences, a pattern of bone marrow edema is usually observed, with diffuse high signal intensity that extends from the superolateral part of the femoral head to the femoral neck or intertrochanteric region (Fig. 20-11). As the disease progresses, subchondral collapse of the femoral head may occur, but subsequent resolution of the low-intensity band with complete preservation of the femoral head may also be observed.10,11,13

Nuclear Medicine Bone scintigraphy may demonstrate global increased uptake of the affected femoral head, commonly extending into the femoral neck. This nonspecific appearance may be difficult to interpret and is also possible in other traumatic, inflammatory, or degenerative disorders of the hip region.10,11

Differential Diagnosis Insufficiency fractures of the femoral head should be differentiated from other conditions, including degenerative osteoarthritis, as the leading cause of hip pain and disability in the elderly population.14 From a clinical standpoint, insufficiency fractures of the femoral head cannot be distinguished from other more usual stress fractures of the pelvic region, including those involving the sacral wing, the pubic bones, and the femoral neck. Avascular necrosis of the femoral head may also cause hip pain and disability but usually occurs in a younger age group, often in patients with a history of corticosteroid intake or alcohol abuse. Transient osteoporosis of the hip may also present similar clinical manifestations but is more frequent in pregnant or puerperal young women.10–14 Imaging plays a major role in the differential diagnosis of subchondral insufficiency fractures of the femoral head (Table 20-6). The radiographic manifestations of degenerative osteoarthritis include asymmetric joint space narrowing, subchondral bone sclerosis, osteophytic proliferation, and subchondral geodes. Large geodes may undergo collapse, rarely simulating avascular necrosis or insufficiency fracture. Stress fractures of the sacrum, pubic bones, and femoral neck are much more common than insufficiency fractures of the femoral head and may be hard to detect on plain films. At present, MRI is the technique of choice when occult fractures of the pelvis and hip are suspected.14 In early stages, avascular necrosis and insufficiency fracture show no radiographic findings or minimal osteoarthritic changes. Both conditions also show similar MRI findings. However, in classic osteonecrosis the shape of the low-intensity band is usually concave to the articular surface, whereas it is typically band-like, or slightly undulated, in insufficiency fracture. In addition, the subchondral low-intensity band may resolve in insufficiency fracture, which rarely occurs in avascular necrosis.10–14

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■ FIGURE 20-11 Insufficiency fracture of the femoral head. A, Axial radiograph of the left hip shows no abnormalities. B, Bone scintigraphy reveals increased uptake of the left hip. Sagittal T1-weighted (C) and STIR (D) MR images reveal abnormal bone marrow edema of the femoral head and a subchondral low-intensity band of undulated contour (arrows).

TABLE 20-6 Differential Diagnosis of Subchondral Insufficiency Fractures of the Femoral Head Degenerative hip osteoarthritis Other regional stress fractures Avascular necrosis Rapidly destructive coxarthrosis Transient osteoporosis

Asymmetric joint space narrowing and subchondral bone sclerosis Osteophytic proliferation Subchondral geodes may collapse More common than femoral head fractures in osteoporotic patients Commonly occult on conventional radiographs Clear indication for bone scintigraphy or MRI No or minimal radiographic signs in early stages Subchondral hypointensity contour concave to the articular surface Spontaneous progression to femoral head collapse and osteoarthritis Rapid progression to femoral head collapse and osteoarthritis Simulates avascular necrosis stage IV Potential relationship with insufficiency fractures Osteoporosis selectively involving the proximal femur Bone marrow edema without subchondral hypointensity Spontaneous resolution without femoral head collapse

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In advanced stages, insufficiency fractures of the femoral head may lead to femoral head collapse and secondary osteoarthritis, which is also possible in avascular necrosis stages III to IV and also in rapidly destructive osteoarthritis of the hip joint. Occasional case reports have suggested there may be some causal or conceptual relationship between these conditions. In practical terms, an accurate distinction is crucial before femoral head collapse. After the onset of bone collapse, the etiologic diagnosis will fail to influence treatment.12 Transient osteoporosis of the hip may also simulate insufficiency fracture of the femoral head on MR images. However, in typical transient osteoporosis, a pattern of bone marrow edema of the proximal femur will rarely be associated with a subchondral low-intensity band. Radiographic follow-up of transient osteoporosis usually reveals recovery of bone density within months, but femoral head collapse is not expected to occur.10,11

Synopsis of Treatment Options Medical Treatment Insufficiency fractures of the femoral head are initially treated by conservative measures, including nonsteroidal anti-inflammatory drugs. A crutch or walker may be sometimes recommended and helps to decrease mechanical loads on the femoral head.11

Surgical Treatment Although conservative treatment is initially undertaken, subchondral insufficiency fracture of the femoral head may also be as devastating as avascular necrosis or rapidly progressive osteoarthritis of the hip joint, leading to femoral head collapse and severe loss of articular congruence. In theses severe cases, total hip replacement is usually required.11,12

KEY POINTS: SUBCHONDRAL INSUFFICIENCY FRACTURES OF THE FEMORAL HEAD Subchondral insufficiency fracture of the femoral head typically occurs in elderly, osteoporotic females. ■ These fractures are common in obese patients but also may occur in young active individuals. ■ Subchondral insufficiency fracture of the femoral head is uncommon. ■ Its radiographic detection may be impossible in the early stages. ■ MRI allows an early diagnosis and helps in the differential diagnosis. ■ The configuration of subchondral abnormalities and the age and condition of the patient are clues to differentiate insufficiency fractures of the femoral head from avascular necrosis. ■

TRAUMATIC FRACTURES OF THE FEMORAL NECK Prevalence, Epidemiology, and Definitions Femoral neck fractures are common injuries in the elderly population suffering minor falls, predominate in osteoporotic females, and are associated with high mortality rates. A few femoral neck fractures in young and middle-aged patients derive from high-energy trauma and are associated with great displacement and significant morbidity.1,2,5

Anatomy The femoral neck is mostly intracapsular. Consequently, severely displaced fractures that damage the lateral epiphyseal arteries increase the risk of retarded healing and avascular necrosis. The normal radiographic appearance of the femoral neck includes a smooth intact cortex and a concave outline joining the convex contour of the femoral head. This outline produces the image of a reversed S curve, which may be absent in neck fractures. In addition, the normal neck-shaft angle, which is about 120 degrees on the anteroposterior view, and the trabecular orientation, are useful anatomic landmarks that should be systematically explored when a fracture is suspected.2,3,15,16

Biomechanics Most femoral neck fractures derive from minor falls, which cause direct impact of the greater trochanter in elderly osteoporotic individuals who usually suffer muscle wasting and debilitated reflexes. A twisting injury or a high-energy trauma may also cause a neck fracture. Pathologic and stress fractures may also occur.10,11

Manifestations of the Disease Nondisplaced fractures will typically present as hip pain and limited passive mobilization. Patients may be ambulatory and show no significant limb shortening or rotation. In these patients, careful radiographic examination may reveal the fracture line but occult fractures require bone scintigraphy or MRI. With partially or completely displaced fractures the patient will present with pain and lie with the extremity in a slightly shortened, abducted, and externally rotated fashion. In high-energy trauma, femoral neck fractures may be overlooked when they are associated with visceral, neurologic, and musculoskeletal injuries, including femoral shaft fractures.1,2,3,15,16

Radiography Conventional radiographs are the first complementary test for diagnosis of femoral neck fractures. The anteroposterior radiograph of the pelvis, in the position the patient presents in the emergency department, will demonstrate most displaced fractures and will allow comparison of both hips. It will also be used for subjective evaluation of osteoporosis and for assessing other pathologic conditions,

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such as fracture of the pubic bones, Paget’s disease, or bone metastasis.1–3 Close-up anteroposterior views of the affected hip will improve depiction of subtle fracture lines, allowing more precise evaluation of the reversed S curve, of the neckshaft angle, and of the trabecular disposition of the femoral head and neck. Anteroposterior views of the hip with the limb in internal rotation may be required for detecting nondisplaced or minimally displaced femoral neck fractures. Groin-lateral views are also optimal for depicting subtle displacement and posterior comminution.5,15,16 According to topographic location, femoral neck fractures may be subcapital, transcervical, and basicervical. Basicervical fractures may be hard to distinguish from true intertrochanteric fractures. According to the orientation of the fracture line, femoral neck fractures may be horizontal, transverse, or vertical. Vertical fractures are more unstable and associated with a significantly higher risk of nonunion. According to the degree of trabecular angulation in the anteroposterior view, femoral neck fractures may be found in abduction (valgus displacement), in an intermediate position, or in adduction (varus displacement) (Fig. 20-12).

■ FIGURE 20-12 Diagram showing the topographic (A–C), Pauwell’s (D–F), and Linton’s (G–I) classifications of femoral neck fractures.

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Following the modified Garden classification, femoral neck fractures may be nondisplaced (types I and II) and displaced (types III and IV) (Figs. 20-13 to 20-17). The Garden classification is widely used but may be hard to apply and tends to underrate displacement. Also, the Garden classification ignores posterior comminution of the femoral neck, which has a high prevalence of nonunion, may influence internal fixation, and has prognostic significance. In spite of these shortcomings, the Garden classification is usually preferred to other classification schemes1,3,15,16 (Table 20-7).

Magnetic Resonance Imaging Magnetic resonance imaging or bone scintigraphy should be used when occult, nondisplaced fractures of the femoral neck are suspected. MRI is 100% sensitive in the assessment of occult hip fractures and has replaced bone scintigraphy in this regard. The rate of osteonecrosis of the femoral head after femoral neck fracture varies from 15% to 80% with conservative or surgical management (Fig. 20-18). MRI is the most sensitive technique for early detection of the femoral

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■ FIGURE 20-15 Complete slightly displaced femoral neck fracture, with mild varus angulation and retroversion, Garden type III.

■ FIGURE 20-13 Diagram showing Garden’s classification of femoral neck fractures (see Table 20-7).

■ FIGURE 20-14 Subcapital fracture, Garden type I. The anteroposterior (A) and axial (B) views of the left hip show a radiodense band traversing the subcapital region (arrowhead), which represents an impacted, incomplete fracture line. The anteroposterior view also shows a cortical stepoff at the lateral aspect of the head-neck junction (thin arrow), which is absent at the medial side (thick arrow) and at the axial view.

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TABLE 20-7 Garden’s Classification of Femoral

Neck Fractures Type I

Type II

Type III

Type IV

■ FIGURE 20-16

Nondisplaced, slightly impacted, incomplete fracture line The medial trabeculae of the femoral head and neck form an angle of 180 degrees. The femoral head is tilted into valgus. The distal fragment lies in external rotation. Nondisplaced, complete fracture line The medial trabeculae of the femoral head and neck form an angle of 160 degrees. Nondisplaced femoral head Normal distal alignment Complete fracture line, with displacement less than 50% The femoral head trabeculae are not in alignment with those of the pelvis. The femoral head is tilted into varus and medially rotated. The distal fragment lies in external rotation. Complete fracture line, with displacement greater than 50% and dissociation The femoral head trabeculae lie in alignment with those of the pelvis. The femoral head is detached and frequently realigns with the acetabulum. The distal fragment is proximally displaced and lies in external rotation.

Displaced femoral neck fracture, Garden type IV.

head. Enhanced MRI has shown adequate correlation with superselective digital subtraction angiography in this regard, and dynamic MRI has also allowed the identification of three distinct patterns of enhancement (normal, impaired, absent), which may be useful for selecting appropriate treatment.17 Finally, MRI may be valuable in assessing pathologic femoral neck fractures, by providing detailed depiction

of local bone and soft tissue involvement. More recently, whole-body MRI has shown enormous potential for detecting hematogenous spread in oncologic patients.

Computed Tomography Computed tomography has not been used for standard assessment of femoral neck fractures. However, preoperative CT scans of the femoral neck in high-risk patients such as those with associated fractures of the acetabulum, distal femoral shaft, or patella may prove valuable.18 In these patients, nondisplaced femoral neck fractures are frequent and should not be overlooked, in order to avoid significant morbidity.19 The advent of multidetector CT has dramatically improved the capabilities of musculoskeletal imaging. Rapid volumetric acquisition, unsurpassed spatial resolution, and exquisite multiplanar reconstructions are now possible even in severely injured patients with external fixations or metallic implants, which may prove valuable for assessing fracture healing and postoperative complications.

Nuclear Medicine

■ FIGURE 20-17 Basicervical fracture, with moderate varus angulation and preserved greater and lesser trochanters.

Bone scintigraphy has traditionally been used for detecting radiographically occult hip fractures in elderly patients with hip pain. In spite of its high accuracy, false-negative results may occur when scintigraphy is performed within 72 hours after trauma. Also, false-positive findings may be due to myositis ossificans, soft tissue calcifications, or degenerative osteoarthritis. Bone scintigraphy may also be used for assessing the viability of vascular supply at the femoral head. However, scintigraphic findings are difficult to interpret and are generally considered unreliable for predicting

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■ FIGURE 20-18 Osteonecrosis of the femoral head. After subcapital fracture of the right femur (A), internal fixation was performed (B, C). Months later, osteolysis of the femoral head was observed, consistent with evolved osteonecrosis of the femoral head.

early capital osteonecrosis after fracture of the femoral neck. Finally, bone scintigraphy is routinely used in the early screening of bone metastasis and may be useful when a pathologic fracture is suspected. However, bone scintigraphy tends to be progressively replaced by MRI in the just-mentioned clinical scenarios.15

Classic Signs: Traumatic Fractures of the Femoral Neck RADIOGRAPHY ■ Topographic classification (subcapital, transcervical, basicervical) ■ Pauwell’s classification (horizontal, transverse, vertical) ■ Linton’s classification (varus, neutral, valgus) ■ Garden’s classification (nondisplaced types I and II, displaced types III and IV) ■ Consider posterior comminution and capital avascular necrosis MAGNETIC RESONANCE IMAGING ■ Irregular fracture line, surrounded by bone marrow edema ■ Useful in avascular necrosis of the femoral head COMPUTED TOMOGRAPHY ■ Promising for assessing external fixations and metallic implants ■ Promising for assessing bone healing and postoperative complications BONE SCINTIGRAPHY ■ Increased uptake around the fracture site ■ Useful in avascular necrosis of the femoral head

Differential Diagnosis After minor falls or high-energy trauma, pain over the hip joint may be caused by other traumatic fractures of the pelvic ring and proximal femur. In addition, muscle injuries, soft tissue abscesses, and other inflammatory and degenerative diseases of the hip joint may simulate femoral neck stress fractures. Displaced subcapital fractures of the femoral neck may present as circular or oval radiolucencies that simulate pathologic fractures. Rotation and fragmentation about the fracture may account for this radiographic appearance. True pathologic subcapital fractures are rare, because most metastases usually arise on red marrow, which is typically absent at the femoral epiphysis and subcapital region of elderly people (Fig. 20-19).20 In rare cases, the fracture may be followed by a rapid process of bone destruction, leading to extensive osteolysis of the femoral neck. Radiographic examinations in such circumstances may reveal complete absence of femoral neck, multiple bony fragments surrounding the region of osteolysis, and a normal femoral head. In this particular setting, MRI may allow the exclusion of joint effusion and associated soft tissue mass. This presentation may resemble infection, tumor, and Gorham’s disease and will frequently require culture and analysis of tissue samples (Fig. 20-20).21 In bone scintigraphy, subcapital collar osteophytes may cause linear increased uptake around the femoral neck, thus simulating a femoral neck fracture. This false-positive finding may have potentially serious consequences, because it may precipitate urgent hip surgery. To avoid this serious pitfall, bone scintiscans should always be compared with radiographs. In patients with hip osteoarthritis and no significant osteoporosis, subcapital linear uptake may not represent a true femoral neck fracture but rather simple subcapital collar osteophytes (Fig. 20-21).22

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485

bone. Most metastatic lesions show a predominantly osteolytic appearance on plain films, although 30% to 50% of bone loss is required before bone metastasis becomes visible on plain films. However, metastatic disease of the proximal femur tends to involve the intertrochanteric region and proximal diaphysis, because in persons 50 to 70 years of age the remaining red marrow is found there. Consequently, femoral neck fractures after metastatic disease are considerably rare.

Synopsis of Treatment Options Medical Treatment Nonsurgical treatment may be attempted in Garden type I fractures, obtaining 80% of spontaneous healing.

K E Y P O I N T S : T R A U M AT I C FRACTURES OF THE FEMORAL NECK ■ FIGURE 20-19

Traumatic fracture of the femoral neck simulating pathologic fracture. Anteroposterior radiograph of a displaced subcapital fracture reveals an area of radiolucency (arrowheads) at the superolateral aspect of the femoral head, simulating a pathologic fracture.

A common cutaneous fold of the inguinal region should not be misinterpreted as a femoral neck fracture. This is typically avoided by noting the symmetric fashion of the finding and by observing how the cutaneous folding goes beyond the femoral neck (Fig. 20-22). Traumatic fractures of the femoral neck should also be distinguished from pathologic fractures on metastatic

Femoral neck fractures are common in the elderly population and are associated with osteoporosis and minor falls. ■ Femoral neck fractures in younger patients derive from high-energy trauma and are associated with severe injuries. ■ Femoral neck fractures are intracapsular and have an increased risk of retarded healing and avascular necrosis. ■ Nondisplaced fractures may be overlooked in anteroposterior views of the pelvis and hip. ■ Site and orientation of the fracture line, displacement, and posterior comminution are the key radiographic points. ■ Suspected occult fractures of the femoral neck require immediate MRI or bone scintigraphy after 3 days. ■

■ FIGURE 20-20 Rapid osteolysis of fractured femoral neck. A, Anteroposterior radiograph of the right hip reveals mild osteoporosis. B, The follow-up study 23 days after shows extensive osteolysis and some fragmentation of the femoral neck. C, Corresponding T1-weighted MR image shows femoral neck osteolysis with no associated findings. (Reprinted from Lambiase RE, Levine SM, Froehlich JA. Rapid osteolysis of the femoral neck after fracture. AJR Am J Roentgenol 1999; 172:489–491. Reprinted with permission of the American Journal of Roentgenology.)

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■ FIGURE 20-21

Collar osteophytes of the femoral head. A, Frontal radiograph of the left hip shows degenerative osteoarthritis of the hip joint. Large subcapital osteophytes are present (arrowheads). B, The corresponding bone scintiscan reveals linear increased uptake of the femoral neck, simulating fracture (arrows).

Surgical Treatment Garden types I and II femoral neck fractures are surgically stabilized with internal fixation. Garden types III and IV in young patients are treated with reduction and internal fixation. In less active, older patients, prosthetic replacement is usually applied.1–3

STRESS FRACTURES OF THE FEMORAL NECK Prevalence, Epidemiology, and Definitions A small proportion of femoral neck fractures are nondisplaced, frequently incomplete stress fractures. Stress fractures of the femoral neck are relatively uncommon injuries, which may involve military recruits, long-distance runners, and osteoporotic individuals. Stress fractures are more common in females, particularly in those suffering with amenorrhea and eating disorders.

Anatomy ■ FIGURE 20-22 Cutaneous folding of the inguinal region (arrows) coexists with a slightly impacted subcapital fracture line (arrowheads). (Reprinted from Garcia-Morales F, Seo GS, Chengazi V, Monu JU. Collar osteophytes: a cause of false-positive findings in bone scans for hip fractures. AJR Am J Roentgenol 2003; 181:191–194. Reprinted with permission of the American Journal of Roentgenology.)

Weight-bearing forces from the trunk rest on the inferior aspect of the femoral neck, where the strong cortex is reinforced by the calcar femorale. The calcar is a dense, vertically oriented bone plate that originates in the posteromedial portion of the femoral shaft under the lesser

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trochanter, extends into the intertrochanteric region, and progresses cranially to gather with the posterior side of the femoral neck. In addition, the superior aspect of the femoral neck is subject to tensile forces.

Biomechanics In stress fractures, progressive imbalance between bone resorption and bone repair after mechanical overload may lead to weakening of cortical bone, further propagation of cracks through cement lines, and eventual microfractures, which may subsequently lead to insufficiency fractures.10,11

Manifestations of the Disease Most patients with stress fracture of the femoral neck may experience anterior groin pain that is made worse with activity and that is relieved with rest. Limited range of motion and gait is usually found.

Radiography Stress fractures of the femoral neck may be compression or tension sided. Compression stress fractures occur at the inferior aspect of the femoral neck. Most compression fractures involve less than 50% of the femoral neck and are considered stable. Compression fractures involving more than 50% of the neck girdle are potentially unstable fractures, may be complicated with displacement, and consequently require immediate fixation. Tension stress fractures involve the superior aspect of the femoral neck and are also considered unstable fractures. Most stress fractures of the femoral neck are incomplete (Fig. 20-23A) and may be missed on plain films. At the early stages, the degree of trabecular microfracture may be insufficient to cause radiographic abnormalities.

■ FIGURE 20-23

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The progression of radiographic findings includes trabecular interruption, cortical radiolucency, endosteal callus, extracortical callus, partial or complete fracture line without displacement, and fracture with displacement. However, even late radiographs may fail to show reactive changes. Thus, patients with suspected stress fractures should have repeat radiographic examinations, bone scintigraphy, or MRI to avoid fragmental displacement, angular deformity, and further complications.1–4

Magnetic Resonance Imaging The detection of stress fractures is particularly suitable with MRI, which allows depiction of the incomplete fracture line, associated bone marrow edema, and early callus formation (Fig. 20-23B and C). MRI is also adequate for follow-up of stress fractures of the femoral neck. In a specific study, MRI showed that resolution of abnormal signal intensity on short tau inversion recovery (STIR) images may be expected within 6 months of the initial diagnosis of stress fractures of the femoral neck.23

Differential Diagnosis Other stress fractures of the pelvis and proximal femur may cause hip pain. In addition, various inflammatory and degenerative disorders of the joint may be considered, along with avascular necrosis of the femoral head, transient osteoporosis of the hip, and muscle/tendon injuries. From a purely imaging standpoint, osteomyelitis and osteoid osteoma may cause cortical abnormalities associated with bone marrow edema, although both are usually easy to detect and recognize on MRI. Avascular necrosis of the femoral head and transient osteoporosis of the hip

Stress fracture of the femoral neck. A, Anteroposterior radiograph shows an incomplete fracture line at the medial cortex of the femoral neck (arrow). Coronal T1-weighted (B) and STIR (C) MR images in a different patient show a focus of hypointensity at the medial cortex of the femoral neck (arrow) along with periosteal thickening (arrowheads) and regional bone marrow edema.

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Classic Signs: Stress Fractures of the Femoral Neck RADIOGRAPHY ■ No findings at early stages ■ Incomplete fracture line, with callus formation MAGNETIC RESONANCE IMAGING ■ Incomplete fracture line, surrounded by bone marrow edema COMPUTED TOMOGRAPHY ■ Incomplete fracture line, surrounded by bone sclerosis BONE SCINTIGRAPHY ■ Increased uptake around the fracture site

may cause extensive bone marrow edema of the proximal femur. Finally, completely displaced stress fractures of the femoral neck cannot be distinguished clinically or radiographically from traumatic subcapital femoral fractures.

Synopsis of Treatment Options Medical Treatment Compression fractures involving less than 50% of the medial femoral neck are managed conservatively with decreased level of activity and weight-bearing modification. If conser vative treatment is undertaken, serial radiography or MRI is mandatory.

Surgical Treatment Compression fractures involving more than 50% of the medial femoral neck, tension fractures, and displaced fractures are managed with internal fixation, in order to avoid further angulation and capital osteonecrosis.

KEY POINT S: S TRESS FRACTURES OF THE FEMORAL NECK Stress fractures of the femoral neck are possible in all age groups. ■ Suspected stress fractures of the femoral neck require MRI or bone scintigraphy. ■ Conservative treatment of incomplete compression fracture must be monitored with serial radiographs or MRI. ■ Compression fractures involving more than 50% of the femoral neck, and all tension fractures, require immediate internal fixation. ■

ISOLATED FRACTURES OF THE GREATER AND LESSER TROCHANTERS Prevalence, Epidemiology, and Definitions Most fractures of the greater trochanter present as components of intertrochanteric fractures. Isolated fractures of the greater trochanter are rare. They may occur in elderly patients who have sustained a direct lateral blow over the hip region after a minor fall. In young patients, avulsion fractures of the greater trochanter may occur after forceful contraction of the gluteus medius and gluteus minimus muscles, which causes great fragment displacement.1,24,25 True avulsion fractures of the lesser trochanter predominate in teenagers and young adults and are usually caused by forceful contraction of the iliopsoas muscle. Conversely, in the elderly population isolated fractures of the lesser trochanter are almost pathognomonic of pathologic fractures and may herald a neoplastic disease.

Manifestations of the Disease A patient with a greater trochanteric fracture will manifest pain at the hip region and buttock, which may increase with local pressure and passive mobilization, especially with abduction and extension. No deformity is apparent but local ecchymosis may be present. With a lesser trochanteric fracture, pain occurs during flexion and internal rotation.

Radiography Radiographic assessment of greater and lesser trochanteric fractures may be easily performed with an anteroposterior view of the pelvis, which enables comparison with the normal side. This may be supplemented by anteroposterior and groin-lateral views of the affected hip. Diagnosis of displaced fractures is usually straightforward (Figs. 20-24 and 20-25). Greater trochanter fractures may be classified as nondisplaced and displaced. Displacement greater than 1 cm for greater trochanteric fractures and greater than 2 cm for lesser trochanteric fractures is considered significant. Nondisplaced fractures of the greater trochanter may be easily overlooked or underestimated. In the anteroposterior view, the greater trochanter is frequently superexposed, which makes necessary evaluation under a bright spotlight.24,25

Magnetic Resonance Imaging Isolated fractures of the greater and lesser trochanter should not be confused with nondisplaced or incomplete intertrochanteric fractures, which have a very different significance, treatment, and prognosis. Seemingly isolated greater trochanteric fractures have been evaluated with MRI, which more accurately defines the true geographic extent of greater trochanteric fractures.24 With regard to lesser trochanter fractures, these are highly unstable fractures when associated with a subtrochanteric or intertrochanteric fracture. MRI may

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■ FIGURE 20-24

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● Acute Osseous Injury to the Hip and Proximal Femur

Avulsion fracture of the greater trochanter.

contribute to making this important distinction. MRI may also help to define a lesser trichanteric fracture as pathologic in elderly individuals with no history of trauma.25

Differential Diagnosis Various painful conditions of the trochanteric region should be considered in the differential diagnosis of nondisplaced greater trochanteric fractures in the elderly, including trochanteric bursitis, gluteus medius tendinitis and tear, and osteomyelitis.

K E Y P O I N T S : I S O L AT E D F R A C T U R E S O F T H E G R E AT E R AND LESSER TROCHANTERS Most fractures of the greater trochanter present as components of intertrochanteric fractures. ■ Isolated avulsion fractures of the greater and lesser trochanter occur in young patients. ■ Isolated greater trochanteric fractures in the elderly derive from minor falls. ■ Isolated lesser trochanteric fractures in the elderly may be pathologic. ■ MRI may demonstrate intertrochanteric extension of nondisplaced greater trochanteric fractures seen on plain films. ■

489

■ FIGURE 20-25 Seemingly isolated fracture of the greater trochanter. The coronal T1-weighted MR image reveals an irregular fracture line extending into the intertrochanteric region that was not seen on radiographs.

Synopsis of Treatment Options Medical Treatment Nondisplaced or minimally displaced (3 mm), likely owing to the more significant alteration of the hoop strain resistance, whereas oblique tears were associated with minor extrusion (3 mm). Meniscal root attachments are a primary factor in maintaining resistance to hoop strain during load bearing and prevent meniscal displacement in a radial direction (Fig. 24-17).60 Meniscal extrusion is important because it is thought to be related to the development of osteoarthritis.64,65

Complex Tears Meniscal tears can sometimes have multiple clefts that extend in several planes, often to both the superior and inferior articular surfaces (Fig. 24-18). These are considered unstable tears. The stability of a meniscal tear is important for determining whether surgical intervention is necessary.34,66 Vande Berg and coworkers assessed four MRI criteria for the recognition of instability of meniscal lesions; and in a retrospective study of 50 patients using arthroscopy as a gold standard, they found MRI to have a sensitivity and specificity of 82%, positive predictive value of 90%, and negative predictive value of 70% for the determination of meniscal tear stability.45 The four MRI criteria of instability of a meniscal tear included: 1. Tear cleft visualized on more than two 4-mm-thick sagittal and three 3-mm-thick coronal images—corresponding to a lesion greater than 10 mm 2. Tear complexity—if more than one cleavage plane or more than one lesion pattern (contour irregularity, peripheral meniscal separation and meniscal tear) was found in the same meniscal area, the lesion is more likely to be unstable. 3. Fluid-like signal intensity within the meniscus on T2weighted images suggests that the torn edges of the meniscus are moderately separated and therefore unstable with accumulation of intra-meniscal fluid in the cleavage plane. This sign is highly specific but has poor sensitivity for a meniscal lesion.45 4. Displaced meniscal fragment—direct evidence of an unstable lesion As previously mentioned, meniscal tears can lead to displacement of meniscal tissue. This tissue can displace centrally, which is known as a bucket handle tear; and if it is positioned below the posterior cruciate ligament it forms the appearance of a “double PCL sign.” Meniscal tissue can displace anteriorly and be located adjacent to the anterior horn of the meniscus, best visualized on sagittal images. Meniscal horns can displace and are often located centrally, posterior to the cruciate ligaments (Fig. 24-19). A flap tear represents a portion of meniscal tissue that displaces into the meniscal recesses or gutter, often located along the margin of the femoral condyles or tibial plateau (Fig. 24-20). These are very important to recognize

CHAPTER

■ FIGURE 24-14

24

● Internal Derangement of the Knee: Meniscal Injuries

577

Radial tear. Sagittal and coronal fast spin-echo, proton density–weighted (TR/TE 2200/15) (A and C) and sagittal and axial T2-weighted, fat-suppressed, fast spin-echo (2800/63) (B and D) MR images through the knee. A defect is seen in the normal bow tie configuration of the meniscus on the sagittal images, and there is a blunted appearance to the normal triangular configuration at the free apical margin of the meniscal body on the coronal image, consistent with a radial tear. This is confirmed on the axial image, which shows a radially oriented tear cleft through the body of the meniscus (arrows).

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

sents variations in signal at the junction of the anterior root of the lateral meniscus, centrally at its insertion, together with distal insertional fibers of the anterior cruciate ligament.69

Meniscal Flounce A meniscal flounce is an uncommon normal variant of the meniscus occurring with a prevalence of approximately 0.2%.70 It is characterized by a redundancy or fold that occurs along the free edge of the meniscus and can be mistaken for a meniscal tear (Fig. 24-22). This occurs in the absence of a tear and has generally been considered to not increase the risk of subsequent tearing.70

Meniscofemoral Ligament

■ FIGURE 24-15 Parrot beak tear. This schematic shows a radial tear configuration along the free apical margin of the meniscal body with a small contiguous portion that extends along the longitudinal orientation of the meniscus giving the appearance of a “parrot beak.”

because they can be missed at arthroscopy unless the surgeon is directed to look for these displaced fragments. When the meniscus has a smaller volume than expected and this finding cannot be explained (i.e., from previous meniscal surgery/resection), care should be taken to exclude a displaced meniscal fragment.

Symptomatic versus Asymptomatic Meniscal Tears Asymptomatic meniscal tears have been reported with a prevalence of up to 36%.67 Zanetti and associates studied a series of patients clinically suspected of having a meniscal lesion in one knee. The contralateral asymptomatic knee was also examined in 100 patients. In patients with a meniscal tear on the symptomatic side, the prevalence of asymptomatic tears on the contralateral side was 63% (36 of 57). This finding suggests a predisposition for bilateral meniscal changes.68 The study also found that horizontal or oblique meniscal tears are frequently encountered in both asymptomatic and symptomatic knees and may not always be related to symptoms. However, radial, vertical, or complex tears as well as displaced meniscal fragments are more commonly identified on the symptomatic side. As well, abnormalities of the collateral ligaments, pericapsular soft tissues, and bone marrow are seen more commonly on the symptomatic side.68

Errors and Pitfalls of Interpretation Anterior Horn of the Lateral Meniscus The anterior horn of the lateral meniscus can have a striated speckled or dotted appearance on sagittal short-TE MRI (Fig. 24-21). This has been shown to represent a normal variant and should not be mistaken for a meniscal tear. This heterogeneous appearance most likely repre-

The meniscofemoral ligaments of Wrisberg and Humphry both originate from the posterior horn of the lateral meniscus.71 The ligament of Humphry is located anterior to the posterior cruciate ligament and can be seen in approximately 33% of cases on sagittal MR images (Fig. 24-23).72 The Wrisberg ligament is located posterior to the posterior cruciate ligament and can also be seen on approximately 33% of sagittal images (Fig. 24-24).73 Fat or connective tissue can be present between the origin of these ligaments and the most medial part of the posterior horn of the lateral meniscus, and this interface can be incorrectly mistaken as a meniscal tear.71 This can be avoided by following the ligament over multiple adjacent images to confirm the presence of the origin of the meniscofemoral ligament(s) in this location and exclude a meniscal tear cleft.

Transverse Meniscal Ligament The transverse meniscal ligament connects the anterior horns of the medial and lateral menisci. This structure courses anterior to the menisci for a variable distance before it completely fuses with the meniscus. Loose connective tissue or fat can be located between the ligament and the meniscus that can be mistaken for a meniscal tear.71 This can be avoided by following the course of the ligament between the anterior horns of the menisci on multiple consecutive images (Fig. 24-25).

Popliteus Tendon The popliteus tendon courses obliquely across the posterolateral aspect of the knee, close to the posterior horn of the lateral meniscus (Fig. 24-26). The popliteus tendon and the popliteus hiatus separate the lateral meniscus from the joint capsule. Signal from the popliteus tendon sheath or fluid within the hiatus could be mistaken for a meniscal tear on both sagittal and coronal images.73-75 Alternatively, a torn meniscal fragment could be incorrectly assumed to be the tendon. The popliteus tendon is seen above the posterior aspect of the lateral meniscus only on the most lateral (superficial) sagittal image through the meniscus. On the subsequent image medially, the tendon is seen inferior to the meniscus. Any other structure above the lateral meniscus on any other section except the most lateral sagittal slice through the lateral meniscus should be considered as a tear, assuming it cannot be explained by a meniscofemoral ligament.72

CHAPTER

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● Internal Derangement of the Knee: Meniscal Injuries

579

■ FIGURE 24-16 Parrot beak tear. Coronal and sagittal fast spin-echo, proton density–weighted (TR/TE 2200/15) (A and B) and sagittal and axial T2-weighted, fat-suppressed fast spin-echo (2800/63) (C and D) MR images through the knee. The coronal and sagittal images demonstrate a radial type tear with blunting of the free apical margin of the meniscal body (long arrow, A to C). This can also be seen on the axial image, which has a small portion of the tear that begins to course along the longitudinal orientation of the meniscus forming a “parrot beak” configuration (short arrow, D).

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

■ FIGURE 24-17 Radial tear at the posterior root with meniscal extrusion. Coronal fast spin-echo, proton density–weighted (TR/TE 2200/15) (A) and axial T2-weighted fat-suppressed fast spin-echo (TR/TE 2800/63) (B) MR images through the knee. A radial tear is present at the posterior horn/posterior root junction of the medial meniscus (arrows) that extends through the entire thickness of the meniscus with a cleft of fluid tracking through the defect. There is associated medial extrusion of the meniscus beyond the margin of the medial tibial plateau (short arrow, A).

■ FIGURE 24-18 Complex meniscal tear. Sagittal fast spin-echo, proton density–weighted (TR/TE 2200/15) MR image through the medial meniscus. A complex tear is seen (arrow) in the posterior horn with extension of the tear to both the superior and inferior articular surfaces.

CHAPTER

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● Internal Derangement of the Knee: Meniscal Injuries

581

■ FIGURE 24-19 Centrally displaced meniscal fragment. Sagittal (A) and axial (B) T2-weighted, fat-suppressed, fast spin-echo (TR/TE 2800/63) and coronal (C) and sagittal (D) fast spin-echo proton density–weighted (TR/TE 2200/15) MR images through the knee. A centrally displaced meniscal fragment is seen in the posterior intercondylar region (long arrow, A to C). On the sagittal proton density–weighted sequence, the posterior horn is diminutive, confirming the origin of the meniscal fragment. An incidental leaking popliteal/Baker’s cyst is seen (short arrow, B).

582

P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

■ FIGURE 24-20 Flap tear displaced into the medial recess. Sagittal and coronal fast spin-echo, proton density–weighted (TR/TE 2200/15) (A and C) and sagittal and axial T2-weighted, fat-suppressed, fast spin-echo (TR/TE 2800/63) (B and D) MR images through the knee. A flap tear is seen with a displaced medial meniscal fragment located in the medial gutter/meniscal recess adjacent to the medial femoral condyle (arrows). This type of displaced flap tear is important to recognize because the arthroscopist may miss visualizing this fragment unless directed to look in this location.

CHAPTER

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583

Volume Averaging Because the outer margins of the menisci are concave, partial volume averaging on sagittal acquisitions can artificially cause the appearance of horizontal linear areas of signal abnormality, which could be mistaken for a tear. This can be avoided by examining the coronal images, which fail to show corresponding intrasubstance signal change or tearing of the meniscal body.72

Chondrocalcinosis Chondrocalcinosis is calcification in the cartilage. In the knee joint, chondrocalcinosis can be seen in hyaline articular cartilage or in the fibrocartilage of a meniscus and is most commonly due to calcium pyrophosphate dihydrate crystal deposition.76 On MRI, chondrocalcinosis can appear as high signal intensity on short-TE sequences and can be mistaken for a meniscal tear.77 Meniscal tears generally have a more linear appearance than the globular high signal seen in the setting of chondrocalcinosis.76 Correlation with plain films may be beneficial if there are intrameniscal signal changes on MRI that correspond to chondrocalcinosis of the meniscus on plain films. ■ FIGURE 24-21 Normal speckled appearance of the anterior horn of the lateral meniscus. Sagittal fast spin-echo, proton density–weighted (TR/TE 2200/15) image through the knee. There is a normal speckled appearance to the anterior horn of the lateral meniscus (arrow) that can be confused for a tear.

■ FIGURE 24-22

Magic-Angle Phenomenon The magic-angle phenomenon refers to the increase in signal intensity resulting when collagen fibers in tissues are oriented at 55 degrees relative to the static main magnetic

Meniscal flounce. Sagittal fast spin-echo, proton density–weighted (TR/TE 2200/15) (A) and sagittal T2-weighted fatsuppressed, fast spin-echo (TR/TE 2800/63) (B) MR images through the knee. There is redundancy in the posterior horn of the medial meniscus, consistent with a meniscal flounce.

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

field (B0) on short-TE MR images.78 The meniscal fibrocartilage, like many other collagen-containing tissues, may exhibit the magic-angle phenomenon on routine MR images and can potentially mimic or obscure meniscal abnormalities on short-TE MR images.78 The posterior horn of the lateral meniscus is susceptible to this artifact as it slopes upward while ascending from the lateral tibial plateau to its meniscal root insertion on the posterior portion of the tibial eminence. Along this portion of the meniscus collagen fibers may achieve an angle of 55 degrees relative to the long axis of the main magnetic field. The remainder of the lateral meniscus and entire medial meniscus are oriented at about 90 degrees to B0; therefore, abnormal signal within these structures on short-TE MR sequences cannot be accounted for by the magic-angle phenomenon.78

Computed Tomography Arthrography

■ FIGURE 24-23 Ligament of Humphry. Sagittal fast spin-echo, proton density–weighted (TR/TE 2200/15) MR image through the knee. A meniscal femoral ligament is present located anterior to the PCL (arrow), also known as the ligament of Humphry.

Dual-detector row, single-contrast, spiral CT arthrography has shown to be accurate in the assessment of the native meniscus.79,80 Sensitivities of 98% and specificities of 94% to 98% for overall assessment of meniscal tears and sensitivities of 94% to 97% and specificities of 81% to 90% have been reported for the diagnosis of unstable meniscal tears using arthroscopy as a gold standard.79 Spiral CT arthrography has also been assessed for evaluation of the postoperative meniscus. Mutschler and

■ FIGURE 24-24 Ligament of Wrisberg. Coronal (A) and sagittal (B) fast spin-echo proton density–weighted (TR/TE 2200/15) MR images through the knee. A meniscal femoral ligament is present located posterior to the posterior cruciate ligament (arrows) and also known as the ligament of Wrisberg.

CHAPTER

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● Internal Derangement of the Knee: Meniscal Injuries

585

■ FIGURE 24-25 Transverse meniscal ligament. Sagittal fast spin-echo, proton density–weighted (TR/TE 2200/15) (A to C) and axial fast spinecho T2-weighted, fat-suppressed (TR/TE 2800/63) (D) MR images of the knee. The transverse meniscal ligament courses horizontally across the anterior aspect of the knee (arrows) from the anterior horn of the medial meniscus to the anterior horn of the lateral meniscus. This can be mistaken for a meniscal tear because there is often loose connective tissue or fat between the meniscus and ligament that can appear as a tear cleft.

586

P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

■ FIGURE 24-26 Popliteus tendon. Coronal and sagittal fast spinecho proton density–weighted (TR/TE 2200/15) (A and B) and sagittal T2-weighted, fat-suppressed fast spin-echo (2800/63) (C) MR images through the knee. The popliteus tendon is seen running through the popliteus hiatus in close proximity to the posterior horn of the lateral meniscus as it courses obliquely across the posterolateral aspect of the knee (arrow). This can be mistaken for a meniscal tear, especially when there is a small amount of fluid or signal from the popliteus tendon sheath between the tendon and posterior meniscus.

colleagues found that by using standard criteria for diagnosis of a recurrent or residual meniscal tear (including intrameniscal contrast material, peripheral meniscal separation and displaced meniscal fragment) spiral CT arthrography demonstrated a sensitivity of 100% but a specificity of 78% for a tear and thus an overestimation of recurrent/residual tears of the postoperative meniscus using arthroscopy as a gold standard. However, a retrospective analysis of the data was performed with modification of the criteria for normal or almost nor-

mal postoperative menisci, including abnormal meniscal shape without intrameniscal extension of contrast material and abnormal meniscal shape with intrameniscal contrast material which involved less than one third of the meniscal length and height.81 The second criterion assumes a stable meniscus with a small partial tear/irregularity and may not be clinically important.34,82 Using modified criteria for the diagnosis of a “clinically relevant” postoperative meniscal tear including the presence of a full-thickness tear, displaced meniscal fragment,

CHAPTER

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● Internal Derangement of the Knee: Meniscal Injuries

meniscal separation, or a large partial-thickness tear involving at least one third of the meniscus length or height, spiral CT arthrography yielded a sensitivity of 97% and a specificity of 90% in the diagnosis of an arthroscopically proven recurrent or residual meniscal tear.81 The indications for CT arthrography have not been well studied, but the technique certainly would be an appropriate imaging investigation in the postoperative knee in a patient with contraindications to MRI. CT arthrography, however, is more invasive than conventional MR imaging,79 uses ionizing radiation, and has potential complications inherent to an intra-articular injection of iodinated contrast material.83

587

Miscellaneous Meniscal Conditions Meniscal Cysts

Ultrasonography can be useful in the diagnosis of masses related to the knee and is beneficial in determining if a lesion is solid or cystic. On ultrasonographic evaluation the normal meniscus appears as a triangular echogenic structure at the joint line (Fig. 24-27). Meniscal cysts are usually identified along the joint line adjacent to the meniscus (Fig. 24-28).84 An underlying meniscal tear can occasionally be identified as a hypoechoic defect within an echogenic meniscus that may communicate with the cyst (Fig. 24-29).85 The accuracy of ultrasonographic determination of meniscal tears has not been well studied.

Reports have shown that meniscal cysts occur in 4% to 6% of knees studied on MRI (Fig. 24-30).86,87 These cysts occur about twice as often in the medial meniscus and may or may not be confined to the meniscus.76 However, Campbell and coworkers found that medial meniscal cysts were nearly twice as common as lateral meniscal cysts but occur with nearly equal relative frequency when compared with the incidence of medial versus lateral meniscal tears (which occur approximately twice as commonly in the medial meniscus compared with the lateral meniscus).87 The most accepted cause of the development of a meniscal cyst is the extrusion of synovial fluid through an adjacent meniscal tear,88-92 although associated meniscal tears have been reported with variable frequency, from 90% 87 to less than 50%.86 Medial meniscal cysts are most commonly located adjacent to the posterior horn,88,89,93 and lateral meniscal cysts are most commonly located adjacent to the anterior horn or body.89,93 The finding of a meniscal cyst is important for the surgeon to know because this may alter the surgical approach.94 If no surfacing meniscal tear is present, the surgeon may approach the cyst percutaneously.76 The cysts can be a source of symptoms even if they are not associated with a discrete meniscal tear.76

■ FIGURE 24-27 Normal meniscus on ultrasound. Longitudinally oriented ultrasonographic image obtained at the medial margin of the knee joint. The normal ultrasound appearance demonstrates a triangular echogenic structure at the joint margin (black dashed line). (Courtesy of Dr. Karen Finlay, Hamilton Health Sciences Centre [Henderson General Hospital], McMaster University, Hamilton, Ontario.)

■ FIGURE 24-28 Meniscal cyst on ultrasound. Longitudinally oriented ultrasonographic image obtained at the medial margin of the knee joint. The meniscus is seen as an echogenic triangular structure at the joint margin (white arrow). There is an adjacent meniscal cyst (black arrow). (Courtesy of Dr. Karen Finlay, Hamilton Health Sciences Centre [Henderson General Hospital], McMaster University, Hamilton, Ontario.)

Ultrasonography

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

Diagnosis of an intrameniscal cyst is made on MRI when a focal region of high signal intensity on T2weighted sequences is identified within a swollen meniscus. The signal tends to not be as bright as fluid on T2-weighted sequences. The fluid can extend into the adjacent soft tissues as a parameniscal cyst, in which case the fluid tends to be as bright as joint fluid on T2weighted sequences.76 Occasionally the cyst can become quite large and dissect through the surrounding soft tissues (Fig. 24-31).

Meniscal Contusion A meniscal contusion occurs during a traumatic event when the meniscus is trapped between the femur and tibia, often during an anterior cruciate ligament tear.95 This is identified by seeing abnormal increased signal in the periphery of the meniscus that is indistinct and amorphous rather than sharp and discrete as seen with a tear or meniscocapsular separation. Meniscal contusions are often associated with the presence of an adjacent region of concomitant bone contusion.76

Discoid Meniscus ■ FIGURE 24-29 Meniscal tear on ultrasound. Longitudinally oriented sonogram obtained at the medial margin of the knee joint. There is a hypoechoic tear cleft in the meniscus (arrow). (Courtesy of Dr. Karen Finlay, Hamilton Health Sciences Centre [Henderson General Hospital], McMaster University, Hamilton, Ontario.)

A discoid meniscus is a meniscus that is abnormally tall and elongated and may be symmetrically or asymmetrically increased.96 The prevalence of a discoid lateral meniscus is 1.5% to 15.5%,97-99 whereas that of the medial

■ FIGURE 24-30 Horizontal tear with perimeniscal cyst. Sagittal fast spin-echo, proton density–weighted (TR/TE 2200/15) (A) and sagittal T2-weighted, fat-suppressed, fast spin-echo (TR/TE 2800/63) (B) MR images through the knee. A horizontal medial meniscal tear is present with extension to the undersurface of the posterior horn. Fluid is seen to track along the tear cleft, best seen on the T2-weighted sequence (B) with a small perimeniscal cyst at the posterior aspect of the posterior horn (arrows).

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589

■ FIGURE 24-31 Large meniscal cyst. Coronal fast spin-echo, proton-density–weighted (TR/TE 2200/15) (A), coronal T2-weighted, fat-suppressed, fast spin-echo (TR/TE 2800/63) (B), and axial T2weighted, fat-suppressed, fast spin-echo (TR/TE 2800/63) (C) images through the knee. A medial meniscal tear is present (long arrow, A) with a large perimeniscal cyst that dissects through the soft tissues at the medial aspect of the knee (short arrow, B and C).

meniscus is 0.1% to 0.3%.98-100 An uncommon variant of a discoid lateral meniscus is a Wrisberg variant, in which the posterior horn of a discoid meniscus is not attached to the capsule and is therefore mobile and can sublux into the joint, causing pain and occasionally locking.101 Criteria to diagnose a discoid meniscus on MRI have been established. The average transverse diameter of a meniscus is variable in the literature and ranges from 9.09 to 11.6 mm.102 A discoid meniscus is present if more than two 4- to 5-mm-thick contiguous sagittal images demonstrate continuity of the meniscus between the anterior and posterior horns (Fig. 24-32).9,96

Discoid menisci can be seen incidentally although are more likely to develop cystic degeneration and tears compared with a normal meniscus (Fig. 24-33).9

Meniscocapsular Separation Meniscocapsular separation refers to disruption of the meniscal attachment to the joint capsule.7 The most frequently involved region is the posterior horn of the medial meniscus. Disruption can lead to increased mobility of the meniscus and possibly increased predisposition to meniscal tears.7

590

P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

■ FIGURE 24-32 Discoid lateral meniscus. Coronal (A) and sagittal (B to G) fast spin-echo, proton density–weighted (TR/TE 2200/15) MR images through the knee. A discoid lateral meniscus is present (arrow, A).

(Continued)

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591

■ FIGURE 24-32—Cont’d Discoid lateral meniscus. On sagittal images, the lateral meniscus is seen on six consecutive images using 4-mm slice thickness with no interslice gap.

The diagnosis is made on MRI by identifying fluid between the peripheral portion of the meniscus and the joint capsule. On MR arthrography, contrast material can leak into this region. A pitfall is the presence of perimeniscal recesses, which can have a similar appearance.7 Visualization of fluid signal extending completely from the superior to inferior aspect of the meniscocapsular junction medially, however, is suggestive of a true meniscocapsular separation rather than prominent perimeniscal recesses.

Meniscal Ossicle A meniscal ossicle is a rare intrameniscal ossification. It occurs in the posterior horn of the medial meniscus103-105 with a prevalence of approximately 0.15%.106 It can be asymptomatic and discovered as an incidental finding or can cause diffuse knee pain and a sensation of locking similar to that of a torn meniscus or intra-articular body.106 The ossicle is well defined and has MRI characteristics of bone (peripheral low signal intensity rim on all

592

P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

of the meniscal tear cleft with meniscal fixation devices or more commonly, meniscal suturing.110

Postoperative Meniscus

■ FIGURE 24-33 Discoid lateral meniscus with perimeniscal cyst. Coronal fast spin-echo, proton density–weighted (TR/TE 2200/15) MR image through the knee. A discoid lateral meniscus is present with a horizontal/oblique tear cleft in the midbody extending to the inferior articular surface. There is an associated meniscal cyst seen extending along the lateral margin of the meniscus (arrow).

sequences with central marrow fat demonstrating high signal intensity on T1 and corresponding saturation on fat-suppressed acquisitions) (Fig. 24-34).106

SYNOPSIS OF TREATMENT OPTIONS Surgical Treatment Modern surgical management of meniscal pathology has been guided by a shift toward preservation of the meniscal tissue owing to a better understanding of the biomechanical properties and importance of the menisci to normal joint function.107-109 Loss of all or part of a meniscus alters the biomechanical forces across the knee joint and can result in premature articular cartilage wear.110 Tears in the peripheral (vascularized zone) are more likely to heal, whereas tears in the central (avascularized zone) are less likely to heal and often require surgical treatment.110 Treatment options include a conservative approach (if the tear is in a location of potential healing or not likely causing the patient symptoms), excision, or repair. Total meniscectomy was a commonly performed procedure in the past but has now fallen out of favor.111 Partial meniscectomy is advocated when repair is not feasible.111 However, long-term studies suggest increased incidence of osteoarthritis in these patients.112-114 With recent advances in surgical techniques most of these procedures are performed arthroscopically. Meniscal cysts may require an open decompression and repair.111 Many types of meniscal repair techniques are described and include a combination of open and arthroscopic techniques with fixation

Recurrent or residual symptoms after meniscal preservation surgery may be related to residual or new tears.115 Diagnostic criteria for a meniscal tear on conventional MRI were shown to have limited diagnostic utility in postoperative tears,116-119 and the classic criteria for diagnosing meniscal tears may represent normal findings postoperatively. The increased surfacing intrameniscal signal intensity on short-TE MR sequences may persist despite arthroscopic or clinical evidence of meniscal healing and is not an accurate indicator of a recurrent meniscal tear.117,120 It is not clinically relevant to distinguish a recurrent from a residual tear in the postoperative patient, and these tears are indistinguishable on MRI.115 Various imaging techniques have been studied for the diagnosis of recurrent or residual meniscal tears. Indirect MR arthrography has been proposed as a potential imaging technique.121,122 Although the joint is not distended, joint fluid enhancement is suggested as a means of increasing conspicuity of joint fluid at the site of a recurrent or residual meniscal tear. However, this also causes enhancement of vascular and cellular proliferation within the fibrovascular scar tissue at the margins of a torn or healing meniscus. Direct MR arthrography has been advocated as a means to assess the postoperative meniscus, with recurrent or residual tears manifested by the visualization of contrast material extending into the meniscus after iatrogenic distention of the joint (Fig. 24-35). However, studies have shown a small incremental increase in diagnostic accuracy for direct MR arthrography compared with conventional MRI and indirect MR arthrography in the diagnosis of recurrent or residual meniscal tears without a significant difference in diagnostic accuracy among the three techniques.115 Increased intrameniscal fluid signal intensity extending to the meniscal surface on T2-weighted images has been shown to be the most specific sign with the highest positive predictive value for diagnosing recurrent or residual meniscal tears. This signal intensity on T2-weighted MR images is presumed to represent an arthrographic effect of free joint fluid tracking through the tear site. Increased signal intensity extending to the meniscal surface on short-TE, intermediate, or T1weighted imaging is a sensitive sign although with low specificity in the diagnosis of recurrent tear.115 MRI has a high diagnostic accuracy in diagnosing recurrent meniscal tears with prior resection of less than 25% of the meniscus (accuracy 100%) and lower accuracy in the diagnosis of recurrent tears after prior resection of 25% to 75% of meniscal tissue (accuracy 78%). An accuracy of 100% has been reported by some investigators for the diagnosis of recurrent meniscal tears with prior meniscal repair regardless of the imaging technique used.115 Other investigators have advocated the use of direct MR arthrographic evaluation of the meniscus after prior meniscal repair.123

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● Internal Derangement of the Knee: Meniscal Injuries

■ FIGURE 24-34 Meniscal ossicle. Coronal fast spin-echo, proton density–weighted (TR/TE 2200/15) (A), sagittal fast spin-echo, proton density–weighted (TR/TE 2200/15) (B), and sagittal T2-weighted, fatsuppressed, fast spin-echo (TR/TE 2800/63) (C) MR images through the knee. A meniscal ossicle is present in the posterior horn of the medial meniscus (arrows). The signal characteristics follow the normal marrow, including demonstrating fat saturation on the fat-suppressed image (C).

593

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What the Referring Physician Needs to Know ■

■

■ ■ FIGURE 24-35

Meniscal recurrent/residual tear on MR arthrogram. Coronal T1-weighted, fat-suppressed spin-echo (TR/TE 500/15) MR image through the knee. An oblique tear is seen in the body of the medial meniscus that extends to the undersurface. The tear cleft fills with gadolinium and is consistent with a residual or recurrent tear in a patient who has previously undergone arthroscopy and partial meniscectomy for a meniscal tear.

■

MRI is the mainstay for meniscal imaging and in particular for diagnosis of meniscal pathology, especially meniscal tears. Many patterns of meniscal tearing exist, and the diagnostic criteria are important to understand for correct MR Imaging interpretation. In certain circumstances, CT arthrography or ultrasonography can be performed, although MR imaging is recommended when possible. In the postoperative meniscus, direct MR arthrography or CT arthrography may be of additional benefit in the evaluation of a recurrent or residual meniscal tear.

SUGGESTED READINGS Boyd KT, Myers PT. Meniscus preservation; rationale, repair techniques and results. Knee 2003; 10:1–11. Davis KW, Tuite MJ. MR imaging of the postoperative meniscus of the knee. Semin Musculoskelet Radiol 2002; 6:35–45. De Smet AA. MR imaging and MR arthrography for diagnosis of recurrent tears in the postoperative meniscus. Semin Musculoskelet Radiol 2005; 9:116–124. Helms CA. The meniscus: recent advances in MR imaging of the knee. AJR Am J Roentgenol 2002; 179:1115–1122. Kocher MS, Klingele K, Rassman SO. Meniscal disorders: normal, discoid, and cysts. Orthop Clin North Am 2003; 34:329–340.

McCauley TR. MR imaging evaluation of the postoperative knee. Radiology 2005; 234:53–61. Mesgarzadeh M, Moyer R, Leder DS, et al. MR imaging of the knee: expanded classification and pitfalls to interpretation of meniscal tears. Radiographics 1993; 13:489–500. Recht MP, Kramer J. MR imaging of the postoperative knee: a pictorial essay. Radiographics 2002; 22:765–774. Toms AP, White LM, Marshall TJ, Donnell ST. Imaging the postoperative meniscus. Eur J Radiol 2005; 54:189–198. Vande Berg BC, Lecouvet FE, Maldagne B, Malthem J. Spiral CT arthrography of the postoperative knee. Semin Musculoskelet Radiol 2002; 6:47–55.

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13. Arnoczky SP, Warren RF. Microvasculature of the human meniscus. Am J Sports Med 1982; 10:90–95. 14. Danzig L, Resnick D, Gonsalves M, Akeson WH. Blood supply to the normal and abnormal menisci of the human knee. Clin Orthop Relat Res 1983; 172:271–276. 15. Davies DU, Edwards DAW. The blood supply of the synovial membrane and intra-articular structures. Ann R Coll Surg Engl 1948; 2:142–156. 16. Day B, Mackenzie WG, Shim SS, Leung G. The vascular and nerve supply of the human meniscus. Arthroscopy 1985; 1:58–62. 17. Scapinelli R. Studies on the vasculature of the human knee joint. Acta Anat 1968; 70:305–382. 18. Mow VC, Fithian DC, Kelly MA. Fundamentals of articular cartilage and meniscus biomechanics. In Ewing JW (ed). Articular Cartilage and Knee Joint Function. New York, Raven, 1989, pp 1–18. 19. Myers ER, Zhu W, Mow VC. Viscoelastic properties of articular cartilage and meniscus. In Nimni ME (ed). Collagen: Chemistry, Biology and Biotechnology. Boca Raton, FL, CRC Press, 1988, pp 268–288. 20. Gatehouse PD, He T, Puri BK, et al. Contrast-enhanced MRI of the menisci of the knee using ultrashort echo time (UTE) pulse sequences: imaging of the red and white zones. Br J Radiol 2004; 77:641–647. 21. Fukabayashi T, Torzilli PA, Sherman MF, Warren RF. An in vitro biomechanical evaluation of anterior-posterior motion of the knee: tibial displacement, rotation and torque. J Bone Joint Surg Am 1982; 64:258–264. 22. King D. The function of semilunar cartilages. J Bone Joint Surg 1963; 18:1069–1076. 23. Kurosawa H, Fukubayashi T, Nakajima H. Load-bearing mode of the knee joint: physical behavior of the knee joint with or without menisci. Clin Orthop Relat Res 1980; 149:283–290. 24. MacConaill MA. The functions of intra-articular fibrocartilages with special reference to the knee and inferior radio-ulnar joints. J Anat 1932; 66:210–227. 25. Renstrom P, Johnson RJ. Anatomy and biomechanics of the menisci. Clin Sports Med 1990; 9:523. 26. Fu FH, Baratz M. Meniscal injuries. In DeLee JC, Drez D Jr (eds). Orthopaedic Sports Medicine: Principles and Practice. Philadelphia, WB Saunders, 1994, p 1146. 27. DeHaven EK. Meniscus repair. Am J Sports Med 1999; 27:242–250. 28. Newman AP, Daniels AU, Burks RT. Principles and decision making in meniscal surgery. Arthroscopy 1993; 9:33–51. 29. Stone RK. Current and future directions for meniscus repair and replacement. Clin Orthop Relat Res 1999; 367:273–280. 30. Summerlath K. The importance of the meniscus in unstable knees: a comparative study. Am J Sports Med 1989; 17:773–777. 31. Aglietti P, Zacherotti G, De Biase P, Taddei I. A comparison between medial meniscus repair, partial meniscectomy, and normal meniscus in anterior cruciate ligament reconstructed knees. Clin Orthop Relat Res 1994; 301:165–173. 32. Johnson MJ, Lucas GL, Desek JK, Henning CE. Isolated arthroscopic meniscal repair: a long-term outcome study (more than 10 years). Am J Sports Med 1999; 27:44–49. 33. Tuckman GA, Miller WJ, Remo JW, et al. Radial tears of the menisci: MR findings. AJR Am J Roentgenol 1994; 163:395–400. 34. DeHaven KE. Decision-making factors in the treatment of meniscus lesions. Clin Orthop Relat Res 1990; 252:49–54. 35. Newman AP, Daniles AU, Burks RT. Principles and decision making in meniscal surgery. Arthroscopy 1993; 9:33–51. 36. Lotysch M, Mink J, Crues JV, Schwartz SA. Magnetic resonance imaging in the detection of meniscal injuries. Magn Reson Imaging 1986; 4:185. 37. Aspden RM, Yarker YE, Hukins DWL. Collagen orientations in the meniscus of the knee joint. J Anat 1985; 140:371–380. 38. Bullough PG, Munuera L, Murphy J, Weinstein AM. The strength of the menisci of the knee as it relates to their fine structure. J Bone Joint Surg Br 1970; 52:564–570. 39. Peto S, Gillis P. Fiber-to-field angle dependence of proton nuclear magnetic relaxation in collagen. Magn Reson Imaging 1990; 8:705–712. 40. Stoller DW, Martin C, Crues JV III, et al. Meniscal tears: pathologic correlation with MR imaging. Radiology 1987; 163:731–735. 41. Hodler J, Haghighi P, Pathria M, et al. Meniscal changes in the elderly: correlation of MR imaging and histologic findings. Radiology 1992; 184:221–225.

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities abnormal findings in asymptomatic subjects. Clin Orthop Relat Res 1992; 282:177–185. Zanetti M, Pfirrmann CWA, Schmid MR, et al. Patients with suspected meniscal tears: prevalence of abnormalities seen on MRI of 100 symptomatic and 100 contralateral asymptomatic knees. AJR Am J Roentgenol 2003; 181:635–641. Shankman S, Beltran J, Melamed E, Rosenberg ZS. Anterior horn of the lateral meniscus: another potential pitfall in MR imaging of the knee. Radiology 1997; 204:181–184. Yu SJ, Cosgarea AJ, Kaeding CC, Wilson D. Meniscal flounce MR imaging. Radiology 1997; 203:513–515. Mesgarzadeh M, Moyer R, Leder DS, et al. MR imaging of the knee: expanded classification and pitfalls to interpretation of meniscal tears. Radiographics 1993; 13:489–500. Brantigan OC, Voshel AF. Ligaments of the knee joint: the relationship of the ligament of Humphry to the ligament of Wrisberg. J Bone Joint Surg 1946; 28:66–67. Watanabe AT, Carter BC, Teitelbaum GP, et al. Normal variations in MR imaging of the knee: appearance and frequency. AJR Am J Roentgenol 1989; 153:341–343. Herman LJ, Beltran J. Pitfalls in MR imaging of the knee. Radiology 1988; 167:775–781. Watanabe AT, Carter BC, Teitelbaum GP, Bradley WG Jr. Common pitfalls in magnetic resonance imaging of the knee. J Bone Joint Surg Am 1989; 71:857–862. Helms CA. The meniscus: recent advances in MR imaging of the knee. AJR Am J Roentgenol 2002; 179:1115–1122. Burke BJ, Escobedo EM, Wilson AJ, Hunter J. Chondrocalcinosis mimicking a meniscal tear on MR imaging. AJR Am J Roentgenol 1998; 177:905–909. Peterfy CG, Janzen DL, Tirman PFJ, et al. “Magic-angle” phenomenon: a cause of increased signal in the normal lateral meniscus on short-TE MR images of the knee. AJR Am J Roentgenol 1994; 163:149–154. Vande Berg BC, Lecouvet FE, Poilvache P, et al. Dual-detector spiral CT arthrography of the knee: accuracy for detection of meniscal abnormalities and unstable meniscal tears. Radiology 2000; 216:851–857. Vande Berg B, Lecouvet FE, Poilvache P, et al. Anterior cruciate ligament tears and associated meniscal lesions: assessment at dualdetector spiral CT arthrography. Radiology 2002; 223:403–409. Mutschler C, Vande Berg BC, Lecouvet FE, et al. Postoperative meniscus: assessment at dual-detector row spiral CT arthrography of the knee. Radiology 2003; 228:635–641. Warren RF. Meniscectomy and repair in the anterior cruciate ligament-deficient patient. Clin Orthop Relat Res 1990; 252:55–63. Newberg AH, Munn CS, Robbins AH. Complications of arthrography. Radiology 1985; 155:605–606. Lin J, Fessell DP, Jacobson JA, et al. An illustrated tutorial of musculoskeletal sonography: III. Lower extremity. AJR Am J Roentgenol 2000; 175:1313–1321. Jacobson JA, van Holsbeek MT. Musculoskeletal ultrasonography. Orthop Clin North Am 1998; 29:135–167. Lambert HS, Balen PF, Helms CA. Meniscal cysts on MR imaging. Radiology 2000; 217(P):218. Campbell SE, Sanders TG, Morrison WB. MR imaging of meniscal cysts: incidence, location, and clinical significance. AJR Am J Roentgenol 2001; 177:409–413. Ferrer-Roca O, Vilalta C. Lesions of the meniscus: II. Horizontal cleavages and lateral cysts. Clin Orthop Relat Res 1980;146:301–307. Tasker AD, Ostlere SJ. Relative incidence and morphology of lateral and medial meniscal cysts detected by magnetic resonance imaging. Clin Radiol 1995; 50:778–781. Barrie HJ. The pathogenesis and significance of meniscal cysts. J Bone Joint Surg Br 1979; 61:184–189. Burk DL Jr, Dalinka MK, Kanal E, et al. Meniscal and ganglion cysts of the knee: MR evaluation. AJR 1988; 150:331–336. Tyson LL, Daughters T II, Ryu RKN, Crues JV III. MRI appearance of meniscal cysts. Skeletal Radiol 1995; 24:421–424. Schuldt DR, Wolfe RD. Clinical and arthrographic findings in meniscal cysts. Radiology 1980; 134:49–52. Pedowitz R, Feagin J, Rajagopalan S. A surgical algorithm for treatment of cystic degeneration of the meniscus. Arthroscopy 1996; 12:209–216.

95. Cothran RL Jr, Major NM, Helms CA, Higgins LD. MR imaging of meniscal contusion in the knee. AJR Am J Roentgenol 2001; 177:1189–1192. 96. Silverman JM, Mink JH, Deutsch AL. Discoid menisci of the knee: MR imaging appearance. Radiology 1989; 173:351–354. 97. Jeannopoulos C. Observations on discoid menisci. J Bone Joint Surg 1950; 32:649–652. 98. Nathan PA, Cole SC. Discoid meniscus: a clinical and pathologic study. Clin Orthop Relat Res 1969; 64:107–113. 99. Smillie IS. The congenital discoid meniscus. J Bone Joint Surg 1948; 30:671–682. 100. Dickason JM, Del Pisso W, Blazina ME, et al. A series of ten discoid medial menisci. Clin Orthop Relat Res 1982; 168:75–78. 101. Dickhaut S, DeLee J. The discoid lateral-meniscus syndrome. J Bone Joint Surg Am 1982; 64:1068–1073. 102. Ferrer-Roca O, Vilalta C. Lesions of the meniscus: I. Macroscopic and histologic findings. Clin Orthop Relat Res 1980; 146:289–300. 103. Le Minor JM, Kemp JF. Intrameniscal ossicle of the knee. Rev Chir Orthop 1989; 75:501–505. 104. Glass RS, Barnes WM, Kells DU, et al. Ossicles of knee menisci: report of seven cases. Clin Orthop Relat Res 1975; 111:163–171. 105. Conforty B, Lotem M. Ossicles in human menisci: report of two cases. Clin Orthop Relat Res 1979; 144:272–275. 106. Schnarkowski P, Tirman PFJ, Fuhigami KD, et al. Meniscal ossicle: radiographic and MR imaging findings. Radiology 1995; 196:47–50. 107. Johnson RJ, Kettlekamp DB, Clark W, et al. Factors affecting late results after menisectomy. J Bone Joint Surg Am 1974; 56:719–729. 108. McGinty JM, Guess LF, Marvin RA. Partial or total menisectomy: a comparative analysis. J Bone Joint Surg Am 1977; 59:763–766. 109. Northmore-Ball MD, Dandy DJ, Jackson RW. Arthroscopic, open partial and total meniscectomy: a comparative study. J Bone Joint Surg Br 1983; 65:400–404. 110. Boyd KT, Myers PR. Meniscus preservation: rationale, repair techniques and results. Knee 2003; 10:1–11. 111. Greis PE, Holmstrom MC, Bardana DD, Burks RT. Meniscal injury: II. Management. J Am Acad Orthop Surg 2002; 10:177–187. 112. Fauno P, Neilsen AB: Arthroscopic partial meniscectomy: A longterm follow-up. Arthroscopy 1992; 8:345–349. 113. Rangger C, Klestil T, Gloetzer W, et al. Osteoarthritis after arthroscopic partial meniscectomy. Am J Sports Med 1955; 23:240–244. 114. Schimmer RC, Brulhart KB, Duff C, Glinz W. Arthroscopic partial meniscectomy: a 12-year follow-up and two-step evaluation of the long-term course. Arthroscopy 1988; 14:136–142. 115. White LM, Schweitzer ME, Weishaupt D, et al. Diagnosis of recurrent meniscal tears: Prospective evaluation of conventional MR imaging, indirect MR arthrography, and direct MR arthrography. Radiology 2002; 222:421–429. 116. Bornstein R, Kirk P, Hurely J. The usefulness of MRI in evaluating menisci after meniscus repair. Orthopedics 1992; 15:148–152. 117. Deutsch AL, Munk JH, Fox JM, et al. Peripheral meniscal tears: MR findings after conservative treatment or arthroscopic repair. Radiology 1990; 176:485–488. 118. Kent RH, Pope CF, Lynch K, Jokl P. Magnetic resonance imaging of the surgically repaired meniscus: six-month follow-up. Magn Reson Imaging 1991; 9:335–341. 119. Smith DK, Totty WG. The knee after partial meniscectomy: MR imaging features. Radiology 1990; 176:141–144. 120. Farley TE, Howell SM, Love KF, et al. Meniscal tears: MR and arthrographic findings after arthroscopic repair. Radiology 1991; 180:517–522. 121. Vahlensieck M, Peterfy CG, Wischer T, et al. Indirect MR arthrography: optimization and clinical applications. Radiology 1996; 200:249–254. 122. Yamato M. Intravenous MR arthrography of the knee. Nippon Igaku Hoshasen Gakkai Zasshi 1996; 55:466–469. (Japanese). 123. Magee T, Shapiro M, Williams D. Prevalence of meniscal radial tears of the knee revealed by MRI after surgery. AJR Am J Roentgenol 2004; 182:931–936.

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Internal Derangement of the Knee: Ligament Injuries Eugene G. McNally

THE ANTERIOR CRUCIATE LIGAMENT Prevalence, Epidemiology, and Definitions Injury to the anterior cruciate ligament (ACL) represents the most important ligament injury around the knee. It is relatively uncommon in the general population but is an important cause of injury in individuals involved in sports. Prevalence data are difficult to acquire, but more than 100,000 ACL reconstructions are performed per year in the United States. This suggests a prevalence of around 1 in 5000. A specific figure is difficult to calculate because many injuries will not undergo reconstruction. The injury is between two and 10 times more common in females, although more reconstructions are carried out in males. In a study in Finnish skiers the prevalence of injury was 1 in 6000.1

Anatomy The femoral origin of the ACL is semicircular and lies on the medial aspect of the lateral femoral condyle. The ligament passes in a spiral course forward and laterally to a fan-shaped insertion anterior to the tibial spines (Fig. 25-1). Its fibers blend with a condensation from the anterior horn of the lateral meniscus. Like the posterior cruciate ligament (PCL), the ACL comprises a number of collagen fiber bundles that are intertwined to form two dominant groups. The more anterior of these, the anteromedial bundle, is more densely packed and more easily depicted on MRI (Fig. 25-2). The posterolateral bundle is more loosely arranged and therefore appears larger and more disorganized and has a higher signal intensity on MRI. The ligament is enclosed in a fibrous connective tissue sheath, which also contains a little fluid. The size of the ACL varies both between different populations and between males and females. It averages 4 cm long and 1 cm thick,

although it is slightly smaller in women. The femoral notch is also correspondingly smaller in women, and this combination may account for the differences between the sexes in the incidence of ACL injury. The attachment site has, like other entheses, a transitional zone of fibrocartilage and mineralized cartilage. A number of variants in the normal appearance are recognized. Like other ligaments and tendons, separation of the fiber bundles may occur with interposition of fluid. Linear areas of high signal intensity on T2-weighted MR images should not therefore be regarded as abnormal. Because the ligament has a curved configuration, care should also be taken to disregard areas of signal alteration that can arise as a result of the magic angle phenomenon. This is particularly evident on gradient-echo and short echo time images. The lower third of the ligament can be rather poorly defined, probably as a consequence of splaying of the insertional fibers. This is especially the case in children. Indeed, in very young children the anteromedial bundle in its entirety may be so poorly demarcated that misdiagnosis of rupture may occur. As is outlined later, injuries of the ACL in children are relatively uncommon and tend to be associated with bony avulsion. The insertional fibers communicate with fibers attaching to the anterior horn of the lateral meniscus, giving a fibrillated appearance to the lateral meniscus that must not be interpreted as a tear (Fig. 25-3). The ACL receives its blood supply from branches of the lateral geniculate artery and a nerve supply from divisions of the tibial nerve. The ligamentum mucosum or infrapatellar plica runs anterior to the ACL, paralleling the anteromedial bundle. It then turns superiorly within Hoffa’s fat pad to attach close to the lower pole of the patella.

Biomechanics Although flexion and extension are the predominant movements at the knee joint, there is also rotation at 597

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■ FIGURE 25-1 Sagittal fat-saturated proton density–weighted MR image of the normal ACL. Note the fan-like expansion of the ligament at its tibial insertion (arrow). ■ FIGURE 25-3 Axial fat-saturated proton density–weighted MR image. The boxed area shows the normal fibers that run between the anterior horn of the lateral meniscus and the ACL insertion. On sagittal images this corrugated appearance of the anterior horn may mimic a meniscal tear.

■ FIGURE 25-2 Sagittal fat-saturated proton density–weighted MR image shows the normal hypointense band of the anteromedial bundle of the ACL (arrow).

full extension that allows the tibia to become more fully engaged with the femoral condyles. Because of this rotation there is a small component of anteroposterior femoral translation. To function, the cruciate ligaments must be capable of remaining taut throughout this more complex movement. The cruciate ligaments are made up of several bundles that are grouped together into two major groups, and it is this configuration that enables the

ligament to remain isotonic throughout the full range of knee motion. The anteromedial band becomes taut in flexion, whereas, in extension, the larger, posterolateral portion is under tension. ACL injury can occur by a variety of mechanisms but most frequently occurs with tibial internal rotation and abduction. It is an especially common skiing injury, in which, not uncommonly, valgus stress also results in distraction of the medial joint compartment and impaction of the lateral femoral condyle with the lateral tibia plateau. Skis may also act as a lever before release of bindings, which may augment the injury. Typically, patients will describe an instantaneous moment of injury, where an audible “pop” may be heard. Generally, the knee joint does not swell immediately but hemarthrosis develops slowly over the ensuing hours. The delay is due to a slow drip from the investing blood vessels, sometimes called the “leaking faucet.” The position of the knee at the time of injury determines whether the anteromedial bundle or the posterolateral bundle is taut and, consequently, which of these structures tears first. This information may be helpful in the evaluation of partial tears of the ACL, although usually the precise details of the position of the knee are either unknown or too complex for reliable evaluation. Occasionally, the pattern of microfracture can provide some additional information. Although the orthopedic literature often describes a high accuracy in clinical assessment, physical examination of the knee is rendered more difficult by the presence of acute injury. Clinical examination is associated with up

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to 20% false-negative findings. The classic clinical finding in ACL rupture is increased anterior motion of the tibia. This is tested clinically by the Lachman and the anterior drawer tests. The clinician places one hand on either side of the knee with the thumbs pressed against the femoral condyles. The examiner’s fingers lie in the popliteal fossa and press the tibia forward. These tests can be carried out in various degrees of knee flexion. The Lachman test is carried out at 30 degrees of flexion, and the anterior drawer test is done at 90 degrees of flexion. The Lachman test is thought to be more sensitive to posterolateral bundle tears, and the anterior drawer test is effective for tears of the anteromedial bundle. The quadriceps active test is similar: the knee is placed in 30 degrees of flexion and as the patient contracts the quadriceps muscle the ACLdeficient knee will pull the tibia slightly forward before the lower leg begins to extend. The pivot-shift test is carried out with the knee in full extension. Valgus and internal rotation stress is applied with anterior pressure on the fibula head. Flexion induces anterior tibial translation with a palpable clunk. These tests are more reliable in the chronic phase of injury. In the acute situation, examination of ligament stability is impeded by pain and tense hemarthrosis with a clinical false-negative rate that has been estimated between 12% and 60%. The presence of hemarthrosis itself is a sensitive indicator of ACL rupture but is nonspecific, with ACL rupture accounting for as few as 20% of all hemarthrosis, although the rate is much higher in the context of a sporting injury.

Pathology The most common pathologic process encountered by far in the ACL is injury. Tears can be complete or partial; if partial they may involve the anteromedial or posterolateral bundles. Complete rupture is divided into avulsion fracture and intrasubstance ligament tears. Avulsions may be proximal, but much more commonly involve the distal, tibial attachment. Recognition of an avulsed bony fragment is important. In children, the ACL is commonly disrupted at its insertion into the tibial plateau, where associated bony fragments may be avulsed. Avulsion fractures of the ACL are less common in adults. They are classified into three types. A type 1 fracture shows minimal avulsion from the underlying tibial plateau. A type 2 fracture is more significantly avulsed but the avulsion predominates on one side, resulting in a hinge-like appearance. Usually the anterior component is more significantly avulsed in ACL injury and the posterior component is more often affected when the PCL is involved. A type 3 fracture is one that is completely separated from the underlying tibial plateau. An avulsion fracture of the head of the fibula may be a sign of posterolateral corner injury associated with an ACL tear. In adults, different patterns of bony injuries are more typically associated with ACL rupture and these have been divided into three groups. Microfracture in the posterior and lateral aspect of the tibia is most commonly recognized. As the tibia internally rotates with respect to the femur, impaction of the posterior aspect of the lateral tibial plateau occurs against the lateral femoral condyle. The force of impaction is increased when there is associated

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valgus injury. The relationship between the abnormal biomechanics and the pattern of microfracture is characteristic for ACL rupture. The second type of microfracture that is associated with anterior ACL rupture is a consequence of femoral condylar impaction. This impaction occurs at or close to the anatomic location of the lateral condylar notch (Fig. 25-4). Impaction results in both the deepening of the notch, which is an alteration in the normally smooth curvature of its base, edema in the surrounding medulla, or a combination of these. Microfracture may also be present in the posteromedial tibia, although this is less common than the previously described posterolateral impaction. The injury occurs close to the location of the attachment of the central slip of the semimembranosus tendon, which may become avulsed from its insertion. Yao and Lee2 suggested that this was a true avulsion, although a similar injury has been described as a result of impaction of the medial tibia during varus and external rotation as it translates anteriorly. The latter scenario has been shown to occur experimentally, but the corresponding impaction injury that might be expected in the medial femoral condyle is not always present. Rupture of the ACL is commonly associated with injuries to other structures of the knee, including injuries to bone and cartilage and soft tissues including menisci and other ligaments. The associated bony contusions have been outlined earlier. The pattern and prevalence of other soft tissue injuries depend on whether the injury is due to direct trauma or related to sport and on the age and fitness of the patient. Meniscal tears are commonly associated with ACL rupture and may be found in up to 70% of cases. Once again,

■ FIGURE 25-4 Fracture of the lateral condylar notch (arrow) associated with a tear of the ACL. Note also the vertical tear of the superior strut of the lateral meniscus (arrowhead).

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the prevalence and pattern are dependent on the nature of the injury. Lateral meniscal injuries are reported as more common after skiing injuries, in which Duncan and associates3 found that the lateral meniscus was affected in 83% of cases. In children, meniscal tears occurred in 37% of cases of ACL rupture but two thirds involved the medial meniscus. Certain patterns of meniscal injury are particularly associated with ACL rupture. These patterns include a vertical tear of the meniscal periphery and a radial tear involving the posterior portion of the meniscus or its root. With this posterior predominance, particular attention should be paid to the posterior thirds of the menisci, especially the lateral meniscus when a torn ACL is encountered. From the nature of the injury, ACL ruptures also are frequently accompanied by injuries to the collateral ligaments. Because excessive valgus is a common component of the injury, tears of the medial collateral ligament (MCL) are frequent, although mostly minor. The combination of ACL rupture, medial meniscal tear, and MCL injury is sometimes referred to as the “O’Donoghue” or “Unhappy” triad. The full tetrad of injuries also includes osseous microfracture. However, this combination of injury is not particularly common. The grade of MCL injury may be helpful in predicting the likelihood of an associated meniscal lesion being present. Shelbourne and Nitz4 divided patients with ACL rupture and MCL tear according to the grade of MCL injury. Patients with grade 2 MCL injury had more medial meniscus tears than patients with minor sprains or complete MCL rupture. Lateral meniscal tears were more common in both groups. In the grade 2 MCL tear group, medial meniscal injuries were always associated with lateral meniscal injury.4 In children, MCL injuries are also common and will be present in up to a fourth of cases of ACL rupture. Injuries to the posterolateral corner are associated with ACL injury, although there is disagreement on both

their incidence and importance. Posterolateral instability has been listed as one of the most common causes of graft failure after ACL reconstruction, although not all authors agree and studies to support this hypothesis are lacking. The prevalence of posterolateral instability in patients with successful ACL reconstruction remains unknown. Despite this uncertainty, careful examination of the posterolateral corner in patients with ACL rupture is recommended. Tears of the ligamentum mucosum have been described, but variation in the normal appearances of this plica make reliable interpretation of the tear difficult. High signal changes may also be found in Hoffa’s fat pad in the presence of the tear of the ligamentum, and these need to be distinguished from normal clefts in the fat pad. Mucoid degeneration and ganglion formation may occur in relation to any ligament, and the cruciates are no exception. Congenital cruciate deficiency (Figs. 25-5 and 25-6) has been described in isolation but is more commonly associated with fibular dysplasia and proximal focal femoral deficiency.

Manifestations of the Disease Magnetic resonance imaging is the most important imaging technique for evaluating the ACL. Signs may be present on plain radiographs. CT and, more specifically, CT arthrography are useful adjuncts or when patients cannot undergo MRI.

Radiography Radiographs of the knee are generally not helpful in patients who have sustained twisting injuries, and they should be reserved for those who have undergone highimpact trauma. Occasionally, the radiograph may demonstrate positive findings in patients with ACL rupture. The absence of effusion in the acute, but not hyperacute, stage

■ FIGURE 25-5 Sagittal fat-saturated proton density–weighted MR image shows congenital cruciate deficiency. Note the dysplastic femoral notch and tibial plateau.

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suspicion of a compression fracture and ACL rupture. Deepening of the notch by more than 2 mm in particular has been shown to carry a high sensitivity for ligament disruption. The Segond fracture is an avulsion fracture of the anterolateral margin of the proximal tibial plateau, originally described by a French surgeon, Paul Ferdinand Segond. This is a tiny avulsion flake vertically orientated on the posterolateral aspect of the tibia at the site of attachment of the lateral capsular ligament. The Segond fracture results from internal rotation and varus stress on the ligament resulting in avulsion. Although uncommon, its presence carries a very high association with ACL rupture.

Magnetic Resonance Imaging

■ FIGURE 25-6 Coronal fat-saturated proton density–weighted MR image of the same patient in Figure 25-5. The femoral notch is grossly shallow, and the cruciates are absent.

makes cruciate injury unlikely, although its presence is a nonspecific finding. The principal findings that allow a more reliable diagnosis of ACL rupture are deepening of the lateral femoral notch and the presence of a Segond fracture. The lateral femoral notch is a normal depression on the anteroinferior aspect of the lateral femoral condyle. It should be sharply demarcated, be rounded rather than angulated, and have a depth of no more than 2 mm. Any alteration in the normal configuration should raise

The ACL can be detected on sagittal, axial, and coronal MR images. The sagittal image is the most useful, but corroboration on the coronal and axial sections is helpful in difficult cases or when partial tears are suspected. Slice thickness more than 4 mm may cause partial volume average artifact and give rise to the false-positive diagnosis of a tear. Sections should therefore be kept at least 4 mm in thickness and preferably less. The smaller the slice thickness, the less is the dependency on knee position. The ACL lies 20 to 25 degrees away from the true sagittal plane. A slight external rotation of the knee from the true sagittal position improves visualization of the ligament. The anterolateral margin of the lateral femoral condyle can be used as a guide for the degree of rotation necessary. In practice, with 3- to 4-mm slices on modern imaging equipment, angulation is rarely necessary, although it is useful to show the ACL in a single slice. Sagittal images can be supported by coronal (Fig. 25-7) and axial (Fig. 25-8) sections. These can be particularly helpful in providing alternative visualization of the femoral origin, which can sometimes be difficult to depict on sagittal images.

■ FIGURE 25-7 Comparative coronal fat-saturated proton density–weighted MR images. The boxed area on the left shows a tear of the femoral origin of the ACL. Compare this with the boxed area of the normal femoral attachment on the right.

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■ FIGURE 25-8

Comparative axial fat-saturated proton density–weighted MR images. The boxed area on the left shows a tear of the femoral origin of the ACL. Compare this with the boxed area of the normal femoral attachment on the right.

Primary Signs The anteromedial bundle is most easily identified on sagittal sections; when taut it shows as a hypointense line that can be traced from its origin to close to the insertion on the tibia. In the insertional area, the fibers of the anteromedial bundle spread out and may therefore become poorly defined as the space between them is filled with fluid, fat, or connective tissue. This apparent loss of conspicuity of the ligament should not be misinterpreted as an insertional tear. Although the anteromedial bundle becomes less well defined in this insertional area, the individual fibers can usually be traced, and this helps to exclude injury. The posterolateral bundle is more poorly defined but can be identified as a number of strands separated by fluid and connective tissue. The principal finding in acute ACL rupture on sagittal-orientated MR images is failure to identify the normal hypointense low signal line of the anteromedial bundle (Fig. 25-9). This carries a high positive predictive value for injury. Additional signs depend on whether the injury is acute or chronic. In the acute stage, the ligament fibers are grossly disrupted and separated by hemorrhage and edema. Individual fibers of the ligament are difficult to identify, and it is often unclear whether the injury involves the proximal, distal, or middle substance of the ligament.

■ FIGURE 25-9 Sagittal fat-saturated proton density–weighted MR image shows acute rupture of the ACL (arrow).

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Less commonly, the ACL may displace anteriorly within the notch. The presence of the ligamentous mass in the anterior compartment prevents full knee extension, and the patient will present with a locked knee. This lockedknee presentation may mimic a bucket-handle tear of the meniscus. Anterior displacement of the ACL can be difficult to recognize on MRI. Two patterns have been described by Huang and associates.5 The more common type 1 shows the ACL stump as a mass lying in the anterior recess of the joint. The second configuration, or type 2 stump, has the appearance of a tongue-like fold of ACL displacing out of the intercondylar notch into the anterior joint recess. An ACL stump should even be considered as a possible cause of knee locking in cases in which a displaced meniscal tear is not identified and the ACL has been shown to have been torn. The differential diagnosis on the locked knee in the absence of a displaced buckethandle tear also includes a tear of the MCL or other ligamentous injury leading to muscle spasm and pseudolocking. Reduced patellar dislocation in association with the tear of the medial retinaculum (Fig. 25-10) and possibly with an associated displaced osteochondral fragment should also be considered. Signs of reduced patellar dislocation include osseous microfracture on the anterolateral aspect of the lateral femoral condyle, microfracture on the medial retropatellar facet with or without an osteochondral defect and fluid-fluid level (Fig. 25-11), and edema medially as a consequence of the medial retinacular injury. Care should be taken not to confuse a prominent oblique intermeniscal ligament for a torn ACL.

■ FIGURE 25-10 Axial fat-saturated proton density–weighted image. There has been a bony avulsion of the medial retinaculum (arrow). Note the lateral condylar microfracture indicator of reduced patellar dislocation (arrowhead).

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The appearances in the chronic stage depend on the response of the ACL to injury, and this can be quite variable. In some cases it can undergo rapid atrophy such that within a number of weeks the ligament is completely absent. In other instances, as the edema and hemorrhage settle, the torn ligament may reappear, having fallen to the floor of the intercondylar groove (Fig. 25-12). It may also fall backward to lie against the PCL. In some cases it may reattach to this structure and derive a blood supply from it (Fig. 25-13). In these cases the structure of the ACL is relatively well maintained and it may even have a nearnormal configuration. Clinically, however, the ligament is functionally weak and lax to clinical examination. Although the sagittal plane remains the section of choice for evaluating the ACL, troublesome cases can be helped by reviewing the coronal and axial images. Attention should be directed at the femoral attachment, which provides the most useful information. The normal femoral attachment appears as a near round structure of low signal intensity in the coronal plane. On the axial images, the femoral attachment has an oval configuration with its anteroposterior diameter much larger than the medial to lateral diameter. In both cases, injury to the ligament shows edema and hemorrhage replacing the normal low signal ligamentous structure.

Secondary Signs Nonvisualization of the anteromedial bundle on sagittalorientated MR images of 4 mm thickness or less carries

■ FIGURE 25-11 Axial fat-saturated proton density–weighted MR image. There has been avulsion of the medial retinaculum at its insertion into the patella as a consequence of patellar dislocation. The patella has reduced. Note the intra-articular fluid-fluid level suggesting an associated osteochondral fracture. In this case there has been a tear of the vastus medialis obliquus, which is an uncommon finding.

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■ FIGURE 25-12 Sagittal fat-saturated proton density–weighted MR image. There is a chronic rupture of the ACL, with the tall ligament lying along the floor of the joint (arrow). Note the similarity to the appearance of an oblique intermeniscal ligament in Figure 25-30.

■ FIGURE 25-13 Sagittal fat-saturated proton density–weighted MR image. There is a femoral avulsion of the ACL. The ligament has fallen against the PCL to which it may reattach and derive a blood supply (arrow).

a high positive predictive value for ACL rupture. When correlated with the coronal and axial images, most patients can be correctly classified into those with intact and completely torn ACL. In some cases, the primary sign is less clear. The anteromedial bundle may be present but blurred, wavy, kinked, or less clearly visualized than normal. In these cases, it is important to determine whether the ligament is partially or completely torn. A variety of secondary signs of ACL disruption have been described, which may, however, be helpful in differentiating a partial- or low-grade tear from a complete or high-grade injury. Three groups of secondary signs are recognized. The first group includes signs of associated bony injury, some of which have been previously described. Certain characteristic patterns of bony injury have a strong association with ACL rupture. The second group of secondary signs includes changes within the soft tissues, most commonly an abnormal orientation of the ACL itself. The third group of secondary signs comprises those that reflect anterior tibial translation. These groups of secondary signs are each discussed in turn.

Bony Injuries Associated with Anterior Cruciate Ligament Rupture

■ FIGURE 25-14 Coronal fat-saturated proton density–weighted MR image in a patient with ACL rupture showing the characteristic posterolateral tibial distribution of microfracture (arrow).

There are three major bony injuries associated with ACL rupture. Microfracture in the posterior and lateral aspect of the tibia is most easily identified on coronal-orientated fat-saturated images (Figs. 25-14 and 25-15). This pattern arises as a consequence of internal tibial rotation with impaction against the lateral femoral condyle. Indeed,

this pattern of microfracture is so typical that, when identified, the patient should be regarded as having torn the ACL until proved otherwise. The presence of microfracture depends on the length of time since injury. Microfracture is most commonly identified in the acute

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■ FIGURE 25-15 Sagittal fat-saturated proton density–weighted MR image shows classic pattern of microfracture associated with ACL rupture. A high proportion of patients have microfracture in the posterolateral tibia in the acute stage (arrow). Half of these have associated lateral femoral condylar microfracture (arrowhead).

■ FIGURE 25-16 Sagittal fat-saturated proton density–weighted MR image shows extensive microfracture in the lateral femoral condyle and lateral tibial plateau as a consequence of valgus injury secondary to ACL rupture.

postinjury phase and can persist for up to 6 months. In general, microfracture resolves more quickly than this and therefore its absence should not be used as a useful sign in predicting an intact ligament. Occasionally, the injury can be seen on the plain radiograph. Posterolateral tibial microfracture may be associated with lateral femoral condylar microfracture in a proportion of patients. Kaplan and colleagues detected isolated occult fractures in 43% of patients with ACL rupture and combined tibial and femoral fracture in 46%.6 Less common patterns were fractures in the posterior aspect of the medial tibial plateau in 7% and fractures involving all three areas in 2%.6 In contrast, Murphy and associates detected posterolateral microfracture in 94% of 35 patients with a much higher association with microfracture in the femoral condyle, which was present in 91%.7 The pattern of microfracture seen in the lateral femoral condyle is somewhat variable. Most typically, impaction against the posterolateral tibial plateau occurs at or close to the anatomic location of the lateral condylar notch (Fig. 25-16). Impaction results in the deepening of the notch, in an alteration in the normally smooth curvature of its base, in edema in the surrounding medulla, or in a combination of these. The most useful finding is microfracture, with the increased signal intensity changes extending in a radiating pattern from the cortex of the lateral femoral notch. Deepening of the notch can be appreciated by measuring from the depth of the bony injury to its surface.

A measurement of more than 3 mm is definitely abnormal. Measurements of between 2 and 3 mm should also be regarded as suspicious. The contour of the floor of the notch should also be scrutinized. It is normally smooth so any angulation or cortical breach indicates fracture. Deepening of the notch and cortical interruption may sometimes be identified on plain radiographs. Microfracture has also been described in the posteromedial tibia where the central slip of semimembranosus may become avulsed from its insertion. Yao and Lee2 suggested that this was a true avulsion, although a similar injury has been described as a result of impaction of the medial tibia during varus and external rotation as it translates anteriorly. The latter has been shown to occur experimentally, but the corresponding impaction injury that might be expected in the medial femoral condyle is not always present.

Soft Tissue Secondary Signs Microfracture is most commonly seen during the acute phase after ACL rupture. In the more chronic phase microfracture will resolve and no longer serves as a useful secondary sign. The second group of secondary signs is related to changes within the ACL itself. As has been previously noted, after rupture the ACL may disappear entirely or may reattach either close to its normal bony insertion site or to an adjacent soft tissue structure, most

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commonly the PCL. If it fails to attach to an adjacent structure, the ligament may lie along the floor of the joint within the intercondylar notch. The abnormal orientation of the ligament can usually be readily appreciated, but in some cases, particularly those where it reattaches close to its original insertion, measurement may be required to detect subtle findings. The measurements used are the ACL angle and the Blumensaat angle. The ACL angle is the angle formed by the intersection of the anterior aspect of the distal portion of the ACL and the most anterior aspect of the intercondylar eminence on a midsagittal MR image. The normal angle is around 55 degrees. An angle of less than 45 degrees is regarded as abnormal and indicative of a torn ACL (Fig. 25-17). Sensitivity and specificity increase with decreasing angle, reaching 100% for both at angles less than 25 degrees.8 The Blumensaat angle is formed by the intersection of a line drawn through the distal portion of the ACL, along its anterior margin, and a line drawn through the intercondylar roof (see Fig. 25-17). Because the ACL parallels the intercondylar roof, the Blumensaat angle is normally close to 0 degrees. The angle may form with either the proximal or distal end of the roofline. By convention, angles that form proximally are considered negative and those that form distally are positive. An angle over 21 degrees positive is strongly associated with ACL rupture.

Secondary Signs due to Tibial Translation An intact ACL prevents forward displacement of the tibia with respect to the femur. Anterior tibial translation is free to occur when the ligament is ruptured, although it is not seen in all patients. It is less likely to occur in younger individuals with good muscle tone or where the posterior portions of the menisci remain intact. In these cases, the meniscus abuts the posterior aspect of the femoral condyle and prevents anterior translation. Anterior tibial translation can be measured directly or by noting the alteration in the configuration and normal alignment of other structures in and around the knee. The technique for direct measurement uses either the lateral condyle tangent distance or the posterior femoral line. The lateral condyle tangent distance is calculated by drawing a tangent at the most posterior point of the lateral femoral condyle to form the baseline from which the distance to the tibia will be measured.9 The section midway between the cortex adjacent to the PCL and the most lateral section containing the femoral condyle is used. Under normal circumstances the posterior margin of the tibial plateau passes within 5 mm of this line. A distance of greater than 5 mm separating the posterior margin of the tibial plateau from this line indicates anterior tibial translation (Fig. 25-18).

B

A

■ FIGURE 25-17 Sagittal fat-saturated proton density–weighted MR image shows complete rupture of the ACL. The abnormal orientation of the femoral attachment results in a decreased ACL angle (A) and an increase in the Blumensaat angle (B). ■ FIGURE 25-18 Sagittal fat-saturated proton density–weighted MR image through the lateral femoral condyle. A tear of the ACL has resulted in anterior tibial translation. There is an increased distance (arrows) between the posterior tibia margin and a tangent drawn to the lateral femoral condyle (white line).

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The more complex posterior femoral line is positive when a line drawn at 45 degrees from the posterosuperior corner of the Blumensaat line does not intersect the flat portion of the proximal tibial surface or within 5 mm of its posterior margin. Several indirect signs of anterior tibial translation have been described, most relying on changes in the configurations of other soft tissue structures. As the tibia translates anteriorly, an alteration in the normal configuration of the PCL occurs. On sagittal images, the PCL normally has an angulated appearance, with a slightly curved proximal third forming an angle between the straighter distal two thirds. With tibial translation, the angle between the proximal and distal portions becomes more exaggerated and a reverse curve may appear in the distal limb, giving the PCL a sigmoid shape. These changes are readily apparent on visual inspection, but several measures of this PCL laxity have been described. These include the PCL line sign, the PCL angle sign, and the PCL curvature ratio. The PCL line is drawn along the dorsal aspect of the PCL close to its insertion. The linear area is defined by two points, the more distal being within 3 to 4 mm of the PCL insertion. A line drawn connecting these two points when traced proximally should intersect the medullary cavity of the femur within 5 cm of its most distal point.10 The sign is positive when the proximally extended line does not intersect the medullary cavity of the femur. The reason for this becomes obvious when the line is drawn along the buckled PCL shown in Figure 25-19.

■ FIGURE 25-19 Sagittal fat-saturated proton density–weighted MR image through the PCL in a patient with complete rupture of the ACL and anterior tibial translation. Note the buckled or sigmoid appearance to the PCL.

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As the PCL buckles during anterior tibial translation, the angle formed between the proximal and distal parts becomes more acute. This angle is normally greater than 115 degrees and usually greater than 125 degrees. Angles less than 111 degrees, and in some cases less than 96 degrees, have been reported to be associated with ACL rupture. The variation in these findings probably reflects the variation in anterior tibial translation that will be present in the study populations. The normal configuration of the PCL has also been likened to a bow, with an imaginary line joining the attachments representing the string of the bow. The change in PCL angulation that occurs as the PCL buckles has also been quantified by measuring the amount of bowstringing that has occurred. A perpendicular is dropped from the apex of the PCL to the “string” of the bow. The ratio of the length of this perpendicular to the length of the “string” is calculated. The more the PCL is buckled, the larger this ratio becomes. Values over 0.39 have a high specificity for ACL rupture. Changes in the orientation of other soft tissue structures also occur with anterior tibial translation. The lateral collateral ligament runs in an oblique course posteriorly and inferiorly from its femoral attachment to its attachment into the fibular head. Normally, several sequential coronal sections must be viewed to see the ligament in its entirety. When anterior tibial translation occurs, the orientation of the lateral collateral ligament becomes more vertical and is oriented in a more parallel coronal plane. Depending on the degree of translation, the ligament may then be visualized on a single coronal slice. In extreme circumstances, a considerable proportion of the PCL may also appear on a single coronal slice. Other indirect signs of ACL rupture that have been described include the posterior synovial bulge sign, an irregular anterior margin of the ACL, rupture of the iliotibial band, severe buckling of the patellar tendon, a shearing injury of Hoffa’s fat pad, and posterior displacement of lateral meniscus. In the majority of cases the presence of an intact anteromedial bundle confirms an intact ACL and its absence is a reliable sign of complete rupture. The diagnosis of partial ACL rupture can be more difficult because the findings on MRI are not as clearly defined, the literature is less replete, and those signs that have been suggested are neither as sensitive nor as specific as those indicating complete rupture. A further contributor to the problem of defining reliable signs is the lack of a strict surgical definition. Despite this, the normally consistent appearance of the ACL means that any focal areas of loss of signal, other than at its insertion, kinks, buckles, or loss of parallelism between the ligament and the intercondylar roof should all be regarded as suspicious for a partial tear. Signs that are also moderately sensitive include bowing of the ACL and nonvisualization of the ACL on one MRI sequence with visualization of intact fibers on the other. Lawrence and associates,11 in a retrospective review, proposed four features that helped to differentiate partial ACL tears from either complete ACL tears or normal ligaments. These were the appearance of some intact fibers, thinning of the ligament, a wavy or curved ligament, and the presence of an inhomogeneous mass posterolateral to the ACL.

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These features have not been tested prospectively. Axial images have also been used to try to differentiate stable from unstable ligaments. Stable ACLs were described as elliptical, attenuated, or showing areas of increased intrasubstance signal intensity. Unstable ligaments were more likely to have an isolated ACL bundle, nonvisualization of the ligament, or the presence of a cloud-like mass in place of the ACL. In the presence of such findings, it is important to look carefully for secondary signs that, if present, are more likely to indicate a high-grade tear. This is especially true for signs of anterior tibial translation. In the absence of secondary signs the diagnosis is more circumspect. Many clinicians regard a partial ACL tear with less clinical concern if the knee is stable clinically. Clinical correlation, particularly the presence of an anterior drawer sign, can therefore be helpful in identifying a more significant ACL injury. A combination of clinical and MRI findings is usually sufficient to allow the correct choice of management. The ability of MRI to depict the internal anatomy of the knee with great detail has led to increased recognition of intra-articular ganglionic cysts. These are most commonly seen in association with Hoffa’s fat pad, where they may arise from the intermeniscal ligament, but they are also recognized as arising from the cruciate ligaments. Intraarticular ganglia are found in around 1 in 50 knees on MRI. The majority were not associated with any other internal derangement. Pain was described as the most common complaint, worse on activity and in sports participation, but medial joint line tenderness was also described. One fourth of patients gave a history of trauma. Only 5 (20%) of the patients in this group underwent arthroscopic débridement, and 4 of them had a decrease in symptoms. It is difficult on this basis to apply a pattern of symptoms to ACL ganglia or to comment on etiology, although a decrease in patient symptomatology has been described in other studies after arthroscopic or CT aspiration. ACL ganglia typically have two patterns. One is where the ganglion is interspaced between the fibers of the ACL, distending its sheath with posterior bulging. The fibers of the ACL are easily seen within the sheath, although their course may be deviated by the mucinous material (Fig. 25-20). The second pattern of ACL ganglia consists of a more cyst-like structure that extends from the ACL sheath, most commonly near its femoral attachment.

Computed Tomography Computed tomography has been used by a number of investigators to detect ACL injury, although in general it has played a subsidiary role to MRI, with its use most commonly reserved for those with either contraindication to MRI or when there is limited availability. Advanced multislice CT is capable of producing high-resolution images of the cruciate ligaments with a high diagnostic accuracy, and the role of CT in the assessment of internal derangement of the knee is likely to continue to develop. The ACL is best appreciated on reformatted sagittal sections as a soft tissue density structure contrasted to the surrounding fat. There are few studies that define the accuracy of reformatted plain CT in the assessment of ACL injury, but good sensitivities have been reported.

■ FIGURE 25-20 Sagittal gradient-echo T2*-weighted MR image. The fibers of the ACL are splayed by this cruciate ligament ganglion (arrow).

Detail in these studies is lacking, and confident sensitivity and specificity data are difficult to calculate. CT has more proven accuracy in the detection and assessment of ACL avulsion injuries. Two patterns of ACL avulsion fracture have been recognized. Most fractures involve the anteromedial bundle insertion, with one third extending beyond the insertional area. These latter injuries tend to be complete, involving the insertion of both the anteromedial and the posterolateral bundles. It should also be appreciated that many apparently incomplete avulsion fractures are associated with complete ligamentous avulsion, with the fracture line continued through the ligament itself. Care should therefore be taken in the diagnosis of an incomplete avulsion injury using CT. Although CT is superior to MRI in defining the configuration of ACL avulsion fractures, overall CT does not improve visualization of the degree of comminution, displacement, or extension of the fracture over the information provided by plain films. CT arthrography provides excellent depiction of ACL integrity with images and accuracy rivaling those of MRI. The normal ACL shows as a continuous tubular structure with a CT attenuation of soft tissue contrasting sharply to injected contrast material. Like MRI, a straight or slightly concave anterior margin is typical. Variants include linear streaks of contrast material parallel to its long axis. The signs of ACL rupture on CT arthrography have been derived from the MRI findings. Failure to visualize the ACL carries a high positive predictive value for ligament tears. Contrast medium extending into the ACL or loss of the normal contour, bowing, and loss of parallelism with the intercondylar roof have also been used to indicate a tear.12 Many of the indirect signs of ACL rupture that

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have been described in the MRI section also apply to CT arthrography. Using a combination of these signs, the sensitivity and specificity for the detection of ACL tears were 95% and 99%, respectively.12 The role of CT arthrography in detecting partial ACL tears has yet to be evaluated. CT arthrography can also be used to detect ganglion cysts of the ACL as a non–contrast-filled defect. CT can be used to guide aspiration and injection of these lesions.

in all.18 Increased activity is not always associated with symptoms, however, and may be found in the population actively involved in sports. Although SPECT may have some value in detecting more occult bone microfracture, comparative studies overall favor MRI for both cruciate injuries and meniscal tears.

Ultrasonography

There is considerable debate in the orthopedic literature regarding the indications for, timing of, and choice of procedure for ACL reconstruction. A consensus appears to suggest that more active patients will benefit particularly in the younger age groups. Early reconstruction has been associated with an increased risk of arthrofibrosis, although some authors attribute this to the rehabilitation program used rather than the surgery. A variety of grafts have been used. The four-strand hamstring (semitendinosus and gracilis) is the most popular at present because it has strength advantages over the patellar tendon graft and is not associated with the same level of postoperative extensor mechanism complications as the patellar tendon graft, which include patellar fracture, patellar tendon rupture, and anterior knee pain.

Ultrasonography has also been used to assess injuries to the ACL. Two approaches have been proposed. The earliest described technique is direct visualization of the ACL from an anterior approach with the knee in flexion. More recently, a posterior approach seeking to demonstrate an abnormal femoral attachment has been used. Both methods are technically demanding. The anterior approach requires more than 90 degrees of knee flexion. The described method requires a 30-degree rotation of the probe.13 Although some have found success with the anterior approach, others have favored the posterior approach, where failure to identify a normal femoral ACL attachment has been interpreted with high reliability as an ACL tear. Larsen and coworkers14 describe a sensitivity of 88%, specificity of 98%, and positive and negative predictive values of 93% and 96%, respectively, using hematoma at the femoral attachment site as a sign of ACL rupture. Similar results were previously reported by Ptasznik (91% sensitivity, 100% specificity, 100% positive predictive value), although in this study of patients with acute hemarthrosis the negative predictive value was lower at 63%.15 Indirect signs of ACL rupture may also translate to ultrasound. Hawe16 has used the S-shaped course and the thickening of the PCL to infer ACL rupture, and Fuchs17 describes posterior protrusion of the posterior fibrous capsule displacing the soft tissue structures. The latter sign was found to be less reliable, with a sensitivity of 68% and a specificity of 77%. Ultrasonography can also readily detect an associated Segond fracture. Despite these apparently favorable results, ultrasonography has yet to establish itself as a method of ACL evaluation in everyday practice. There may be several reasons for this. Many of the studies involve single reviewers so interobserver and intraobserver variation has not been firmly established. Variations in the described echogenicity of the cruciate ligaments coupled with some differences in anatomic labeling on published images have added to the uncertainties. Most likely, difficulties in the assessment of associated injuries, specifically meniscal and bony injury, mean that ultrasonography is unlikely to displace MRI in the near future. The dynamic nature of ultrasonography means that it is useful to guide aspiration of cruciate ganglion cysts. Because of the depth of these lesions, however, they can be difficult to visualize in some patients.

Nuclear Medicine There are several reports of the role of scintigraphy in the assessment of ACL rupture, with most centered on its ability to detect the associated bone injury. In a study of 28 patients with ACL injury, MRI detected microfracture in 64% but SPECT demonstrated increased uptake

Synopsis of Treatment Options

Classic Signs ■ ■ ■

Loss of the anterior hypointense line on thin-section sagittal MR images indicates ACL rupture. Posterolateral tibial plateau and deepening of the lateral femoral notch often indicate an underlying ACL tear. Anterior tibial translation can be measured directly or by noting changes in the configuration of the PCL and lateral collateral ligament.

THE POSTERIOR CRUCIATE LIGAMENT Prevalence, Epidemiology, and Definitions There is considerable variation in the incidence of PCL injury. It remains low in the general population and although it is recognized as occurring more often in athletes, an exact figure is difficult to calculate. PCL reconstructions are performed less frequently than ACL reconstructions, so surgical data do not provide a reliable estimate. Hemarthroses are common events, and in up to 40% of cases injury to the PCL may be associated. Contact sports and vehicle accidents account for the majority of PCL tears. The force required to disrupt the PCL is larger than that needed to tear the ACL; consequently, knee injuries resulting in PCL tears are most often a combination of other ligamentous injuries. The incidence of these combined injuries varies between 80% and 95%. The incidence of PCL injuries varies from 1% to 44% of all acute knee injuries. One third of all patients with knee hemarthrosis have an associated PCL injury. Injuries occur more frequently in persons involved in contact sports and in those involving high-contact forces. Not all injuries

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are symptomatic. Parolie and Bergfeld19 found a 2% incidence of PCL injury among asymptomatic college football players at the National Football League predraft examinations. The mechanism of PCL injury in the athlete is most commonly a fall on the flexed knee with a plantarflexed foot and hyperflexion of the knee. Dashboard injuries account for another high proportion of PCL injuries, where the flexed knee is impacted and the tibia is forced posteriorly. When this force is combined with a varus or rotational component, the lateral or posterolateral structures may also be injured. Hyperextension injuries also occur and are associated with a higher incidence of avulsion injuries. PCL injuries are isolated in about a fourth of cases,20 with associated meniscal tears in 25% to 50%. These tears are medial slightly more than lateral and ligamentous injuries in 40%, with most commonly ACL injury in a fourth and MCL injury in a fifth of patients. Posterolateral corner injuries are present in approximately half of PCL injuries, but two thirds of these will be minor with edema around the capsule, no discernable structural abnormality, and a stable knee at examination.21 Isolated PCL injuries carry a better prognosis. The incidence of bony injury has also been variously reported, with more recent studies identifying a higher incidence, possibly reflecting improved detection. Sonin and colleagues identified microfracture in 35%,20 whereas the incidence in Mair’s group was 83%.21 Of these 29 patients with microfractures, 16 lesions were in the lateral tibial plateau, 10 were in the lateral femoral condyle, 14 were in the medial tibial plateau, 5 were in the medial femoral condyle, and 4 were in the patella. Patients with medial bone bruises were more likely to have posterolateral ligamentous injuries, and patients with lateral bone bruises were more likely to have MCL injuries.

Biomechanics The primary function of the PCL is to restrict posterior tibial translation. It combines with the meniscofemoral ligaments (MFLs) to act as a secondary restraint to tibial varus, valgus, and external rotation. Division of the PCL complex (PCL and MFL) results in increased posterior translation, which is most pronounced at 90 degrees of flexion, with further translation when the posterolateral corner is injured.

Pathology The majority of PCL tears are intrasubstance and complete.20,21 The incidence of distal versus proximal injuries is more variably reported. In Sonin’s group of 71 patients, 27% of injuries were proximal and only 3% were distal. In contrast, Grover and coworkers found distal avulsions three times more common than proximal, although the number of patients was much smaller in this study group.22 In a more recent study of 35 high-grade PCL tears, Mair and associates also found tibial avulsions to be more common than femoral tears.21 The criteria for partial tear are less well defined. Sonin and colleagues20 suggest the criteria of abnormal signal intensity within the substance of the PCL or that some fibers appear intact and some appear discontinuous. Tears of the PCL may be associated with other internal derangement. Most common are meniscal tears and cruciate and collateral ligament disruptions. Tears of the posterolateral corner, popliteus, and posterior capsule may also occur (Fig. 25-21).

Anatomy The function of the ACL is balanced by its counterpart, the PCL. The PCL courses from the lateral aspect of the medial femoral condyle to its insertion in a depression in the posterior aspect of the intra-articular tibia, approximately 1 cm below the articular surface. The PCL is between 32 and 38 mm in length from origin to insertion and thicker (mean, 31 mm) and stronger than the ACL. Its main function is to prevent posterior translation of the tibia. Like the ACL, the PCL is made up of spirally arranged collagen fiber bundles. Functionally, there are two fiber bundles, an anterolateral and posteromedial bundle, named for the anatomic location of the femoral insertion to the tibial insertion. Like the ACL, the two main bundles are taut at different stages in the flexion-extension cycle. The anterolateral bundle tightens in knee flexion and loosens in knee extension. The posteromedial bundle tightens in knee extension and is lax in knee flexion. The PCL is also intracapsular but extrasynovial. It appears darker and more uniform than the ACL owing to the presence of a tighter and stronger investing sheath. The anterolateral and posteromedial bundles are less well separated and more difficult to make out on routine MR sequences. It takes considerably more force to rupture the PCL than it does the ACL, and the PCL has a more abundant blood supply than the ACL.

■ FIGURE 25-21 Sagittal fat-saturated proton density–weighted MR image shows a tear of the femoral attachment of the PCL (arrowhead) with associated rupture of the posterior capsule and fluid within the popliteal fossa (arrow).

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Partial tears of the PCL are less common owing to the high energy usually needed to disrupt this strong ligament. MR images demonstrate thinning of the ligament due to loss of one or another of the two main bundles (Figs. 25-22 and 25-23). Like the ACL, ganglion cysts of the PCL are also encountered, and their etiology is equally poorly understood (Figs. 25-24 and 25-25).

■ FIGURE 25-22

Sagittal fat-saturated proton density–weighted MR image shows a partial tear of the PCL that is markedly thinned close to its tibial insertion (arrow).

■ FIGURE 25-23

Axial fat-saturated proton density–weighted image of the same patient in Figure 25-22. The cross section of the PCL is reduced (arrow). Only the posteromedial bundle remains intact.

■ FIGURE 25-24 Sagittal fat-saturated proton density–weighted MR image. A multiloculated cystic structure lies behind the PCL (arrow). Medial meniscal cysts frequently mimic PCL ganglia. Look carefully for a tear of the medial meniscus (see Fig. 25-25).

■ FIGURE 25-25 Sagittal fat-saturated proton density–weighted MR image of the same patient in Figure 25-24. The posterior compartment cyst can be traced to the posteromedial aspect of the medial meniscus (arrowhead) where a meniscal tear was detected (arrow).

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Manifestations of the Disease Injuries to the PCL are usually acute, with pain and swelling as the presenting features. Like the ACL, a variety of clinical tests have been described to stress the PCL. These include the posterior Lachman and posterior drawer tests performed in 30 degrees and 90 degrees of flexion, respectively, and the posterior sag sign. The varus stress examination in full extension is also thought to include a component of the PCL, in that excessive lateral opening is said to only be possible if a lateral collateral ligament, posterolateral corner, and PCL injury are combined. MRI plays an important role in the assessment of PCL injuries, because not all are apparent on clinical examination, even with the patient under general anesthesia. The PCL can also be difficult to identify at arthroscopy in the presence of an intact ACL or MFL. Untreated lesions may predispose to early-onset osteoarthritis.

Magnetic Resonance Imaging

Radiographs are often normal in the presence of PCL injury. Reported findings include posterior tibial translation, and stress radiographs may improve the detection of this sign. More than 8 mm of posterior tibial translation with respect to the femur is indicative of a complete PCL rupture, with lower measurements associated with partial tear. Stress views may also improve visualization of lateral compartment laxity but are not recommended as a routine examination. The tibial insertional area of the PCL should be scrutinized for disruption of the cortex, which may be a sign of PCL avulsion. The insertional cortex is seen as a “7” superimposed on the posterior tibia. Disruption of the “7” is a sign of PCL avulsion. An avulsion fracture at the tibial insertion of the deep component of the MCL is a rare association with PCL.

Sagittal spin-echo MR images provide the most homogeneous depiction of the PCL. T2- or proton density– weighted images, preferably with fat saturation, are best. Internal signal changes on T1-weighted images may be due to magic angle phenomenon and unless supported by changes on T2 are considered nonspecific and may not indicate a tear.22 Some variation in signal can also be encountered in the proximal third, especially on gradient-echo sequences. A variety of explanations have been offered for this appearance; most likely it also represents a form of magic angle phenomenon. A number of apparent focal thickenings may be identified in the region of the middle third of the ligament. This is usually due to section through prominent MFLs (discussed later in the chapter). The appearance of the PCL on MRI has been classified according to the degree of internal derangement and surface disruption. A normal ligament with continuous, low-intensity signal was classified as grade 0. A grade 1 ligament tear (also referred to as an intrasubstance tear) is diagnosed when there are areas of increased signal within the ligament but with intact borders. A grade 2 tear (partial tear) is characterized by alterations in intrasubstance signal as for a grade 1 tear, but with interruption of the anterior or posterior border of the ligament. Disruption of both anterior and posterior borders indicates a complete, or a grade 3, tear. Signs of a complete PCL tear also include nonvisualization of the ligament (Fig. 25-26) with or without a hemorrhagic or edematous mass (Fig. 25-27). Discrete tears are identified more commonly than with ACL rupture. This is thought to be due to the tighter synovial sheath that invests the PCL. Secondary signs are rarely required in the assessment of PCL rupture, and there are few studies of either their

■ FIGURE 25-26 Sagittal gradient-echo T2*-weighted MR image shows a complete rupture of the PCL (arrow).

■ FIGURE 25-27 Sagittal gradient-echo T2*-weighted MR image shows a complete disruption of the PCL (arrow).

Radiography

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prevalence or usefulness. Posterior tibial translation is well recognized, and this may lead to a more vertical orientation of the ACL should it have remained intact. The sagittal images may be supported by coronal or axial images. Loss of the normal low signal intensity and replacement by hematoma (Fig. 25-28) are the usual findings in the acute postinjury state. Partial tears of the PCL may involve either the anterolateral bundle or the smaller posteromedial bundle. The anterolateral bundle is taut in flexion and is therefore more likely to be injured in this position. Because most injuries occur in flexion, the anterolateral bundle is more frequently involved than the posteromedial bundle. MRI has also been used to follow healing after PCL tears. Even ligaments that have disappeared almost entirely at the time of acute injury are seen to have a nearnormal configuration on follow-up. Continuity on MRI does not correlate with function, and stress radiography combined with MRI provides a better assessment of the healed ligament.

Computed Tomography There is very little in the radiologic literature regarding CT in the assessment of PCL injuries. The PCL is usually well seen on sagittal reconstructions because of the differences in contrast between its soft tissue intensity and the lower signal intensity of the surrounding femoral notch fat.

Ultrasonography The PCL is easier to visualize than the ACL. A posterior longitudinal approach shows the ligament as a poorly reflective structure. Much of the loss of reflectivity is due to anisotropy because it is difficult to get the probe parallel to the ligament. Because of the depth of the ligament,

■ FIGURE 25-28 Coronal fat-saturated proton density–weighted MR image shows a hematoma at the femoral attachment of the PCL indicative of a tear (arrow).

613

some authors have preferred using a curvilinear probe. The mean thickness of a normal PCL is approximately 0.5 cm, with an injured PCL measuring more than 0.7 cm due to edema, hemorrhage, and fluid collecting around the ligament. In some cases the torn end of the ligament can be appreciated.

Classic Sign ■

Tears of the PCL manifest as intrasubstance signal changes or disruption of the anterior, posterior, or both margins.

OTHER INTRA-ARTICULAR LIGAMENTS Prevalence, Epidemiology, and Definitions There are a large number of minor ligaments that lie within the joint. Although the function of these ligaments is incompletely understood, from a radiologic perspective disruption rarely imparts clinically significant instability. Their impact on imaging therefore is mainly that they mimic other pathology when enlarged or prominent and can thus lead to difficulties in interpretation. The principal ligaments are the intermeniscal ligaments and the MFLs. The prevalence of injury of these ligaments is not known.

Anatomy Intermeniscal Ligaments There are three intermeniscal ligaments: anterior, posterior, and oblique. The anterior ligament runs between the anterior aspect of the two menisci and is also called the transverse geniculate ligament or anterior transverse ligament. It is 33 mm long, and its average midsubstance width is 3.3 mm.23 Although the attachments are most commonly to the substance of the menisci themselves, some variation is seen and in some cases the ligament attaches to the capsule anterior to the meniscus. On MRI, a cord-like structure representing the anterior intermeniscal ligament can be identified on most studies. The ligament is generally round or oval on sagittal images and can be quite prominent. A small fluid cleft can be seen between the ligament and the meniscus that, when the ligament is prominent, can mimic a meniscal tear. The anterior intermeniscal ligament runs at the posterior tip of Hoffa’s fat pad, either through the fat or just below it. Hoffa’s ganglia, which are multiloculated fluid-filled structures, are most commonly found in this location; indeed, the ganglia may arise from degenerative or possibly post-traumatic changes to the anterior intermeniscal ligament (Fig. 25-29). There is also a posterior intermeniscal ligament, although this is less prominent than the anterior ligament and is much less commonly visualized. A number of small strands may be identified posterior to the PCL, but it is difficult to differentiate a substantial posterior intermeniscal ligament from other condensations of the posterior cap-

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■ FIGURE 25-29 Axial fat-saturated proton density–weighted MR image. There is a multiloculated cystic structure within Hoffa’s fat pad, probably arising from the anterior intermeniscal ligament. The signal intensity with septated or multiloculated appearance in this location is typical of Hoffa’s ganglia (arrow).

■ FIGURE 25-30 Sagittal fat-saturated proton density–weighted MR image shows a normal oblique intermeniscal ligament mimicking a chronic ACL tear (arrow).

sule. A further ligament runs in the transverse plane from the posterior horn of the lateral meniscus to the anterior horn of the medial meniscus. This is called the oblique intermeniscal ligament and it separates the PCL from the ACL (Fig. 25-30). When it is prominent it can give the impression of additional tissue lying within the notch. In such cases it can mimic a rupture of the ACL with the torn ligament lying along the floor of the notch, a displaced meniscal fragment, or an osteochondral loose body. Usually these can easily be differentiated. An intact ACL with lack of microfracture or fluid-blood levels is apparent to suggest an osteochondral fragment, and the location of the structure between the two cruciates provides the best evidence as to the true nature of the structure. Once the diagnosis is considered, the structure can be traced on the workstation or sequential images taken between the two meniscal horns.

The Meniscofemoral Ligaments Close to the attachment of the posterior intermeniscal ligament to the lateral meniscus are two further ligaments that run superiorly and obliquely to the lateral aspect of the medial femoral condyle. The MFLs have two components, either one of which may dominate. One component runs posterior to the PCL, where it is given the name ligament of Wrisberg (Fig. 25-31). A second component runs anterior to the PCL, and it is called the ligament of Humphry. Although sometimes reported as being divisions of the same ligament, Gupte24 postulated that the two MFLs are discrete

■ FIGURE 25-31 Coronal fat-saturated proton density–weighted MR image. The arrow indicates a normal meniscofemoral ligament.

and separate entities with separate attachments to the posterior horn of the lateral meniscus and to the femur. There is considerable variation in the size of the MFL. Care must be taken not to mistake the posteromedial PCL fibers, which can be distinct from the larger anterolateral bundle. This has been termed the oblique PCL

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or false MFL. One or the other of the MFLs will be visualized on over 80% of MRI examinations. Like the intermeniscal ligaments, the principal impact of the MFL is to mimic a tear of the posterior horn of the lateral meniscus. Fluid can gather between a prominent MFL and the meniscus, simulating a tear. This is more obvious when the MFL is enlarged. In these cases, it should be appreciated that the posterior horn of the lateral meniscus is approximately the same size as the anterior horn. If the ligament is torn, this normal morphologic rule would be broken. As for the intermeniscal ligaments, tracing the ligament medially to its insertion also confirms its true nature. Although the role of the MFLs is generally considered to be minor, they are believed to play a role in protecting the lateral menisci from femorotibial compression by moving it forward and medially when the knee is flexed. The movement of the MFLs opposes the posterior/distal pull of the popliteus muscle, with the balance between the two protecting the lateral meniscus. This has been offered as the reason why the medial meniscus is more prone to injury because it lacks this fine control. Others propose a mechanical role for the MFLs as a secondary restraint, supplementing the PCL. The MFLs have a greater strength than the posteromedial PCL bundle, represent 30% of the femoral attachment, and offer 30% to 60% of the resistance to the posterior stress with the knee at 90 degrees.

Miscellaneous Intra-articular Minor Ligaments A number of other rarer variants of MFLs have been described. The infrapatellar plica or ligamentum mucosum runs an arcuate course from its posterior femoral attachment just anterior to the ACL, anteriorly and inferiorly to the posteroinferior tip of Hoffa’s fat pad, before turning superiorly to approach the lower pole of the patella. When prominent, this ligament has been reported to be misinterpreted as the ACL, resulting in a false-negative diagnosis for ACL rupture. Anderson and associates25 identified the rare anterior MFL whose course matches the posterior portion of infrapatellar plica. A normal infrapatellar plica was found to coexist with the anterior MFL in all cases, and the attachment of the latter into the medial meniscus was clearly shown to be separate from the infrapatellar plica. An anterior MFL running from the lateral meniscus to the condylar notch has also been described.

615

LATERAL SUPPORTING STRUCTURES Prevalence, Epidemiology, and Definitions Iliotibial band syndrome is a common cause of lateral knee pain in runners. The syndrome results from repetitive compression of the periligamentous fat around the lateral femoral condyle. Friction of the iliotibial band itself has also been implicated, but this has not been confirmed by anatomic studies. The exact prevalence in the population is difficult to calculate. It is a commonly recognized injury, and not all affected individuals will come to medical attention. Injuries to the posterolateral supporting structures are usually encountered in combination with other ligament injuries, particularly cruciate disruption. Isolated injuries are uncommon, representing less than 2% of knee ligament injuries. In common with other ligament injuries of the knee, sports injuries, motor vehicle accidents, and falls are the most common causes.

Anatomy On the lateral side, ligamentous stability is due to two separate ligamentous components, one anterior and one posterior. Anteriorly, the principal ligament is the iliotibial band or tract. The iliotibial band is a condensation of fibrous tissue that extends from the tensor fascia lata at the hip along the entire length of the lateral aspect of the thigh to insert on Gerdy’s tubercle on the anterolateral aspect of the tibia (Fig. 25-32). Posterolateral stability is provided by the fibular collateral ligament, biceps, and popliteus complex as the principal ligaments, as well as a number of other smaller ligamentous structures, some of which are little more than condensations of the posterolateral capsule, the most important being the popliteofibular ligament. The biceps femoris arises from the ischial tuberosity and descends to insert on the fibular head. The insertion can be either

Classic Signs ■

■

Tears of the anterior limbs of the menisci must be differentiated from fluid lying between the normal attachment of the anterior intermeniscal ligament. Tracing the ligament across the joint on successive sagittal sections makes this differentiation easy. The oblique intermeniscal ligament may be prominent and look like tissue lying within the femoral notch. This normal finding must be differentiated from bucket-handle tears of the meniscus, a loose osteochondral fragment, and a torn ACL.

■ FIGURE 25-32 Coronal fat-saturated proton density–weighted MR image. Normal low signal iliotibial band is seen passing close to the lateral femoral condyle (arrow).

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on its own or in conjunction with the fibular collateral ligament as a conjoint tendon (Fig. 25-33). If they are separated, the insertion of the fibular collateral ligament is more anterior than the biceps femoris (Fig. 25-34). The fibular collateral ligament averages 67 mm in length and 3.4 mm in thickness. Its femoral attachment is 3 mm posterior to the ridge of the lateral femoral condyle above and a little anterior to the popliteus tendon.26 It inserts on a V-shaped bony depression on the distal one third of the lateral aspect of the fibula, with some fibers also inserting on the peroneus longus fascia.27 The posterolateral corner is reinforced by a number of ligamentous condensations that have specific names. These minor ligaments can be divided into the long and short ligaments. The long ligament is the fabellofibular ligament if the patient has a fabella and an arcuate ligament if the patient does not have a fabella. Coronal images have been advocated for visualizing these small ligaments, with sections oriented along the lower part of the PCL. Despite careful orientation, these ligaments are not always identified; consequently, nonvisualization cannot be interpreted as a sign of disruption. The short ligament is the fibulopopliteal ligament (Fig. 25-35). The fibulopopliteal ligament is a frequently but not invariably identified structure measuring 47 mm long and 9 mm2 in cross section that acts as a sling centered at the popliteal musculotendinous junction.27 Two divisions, anterior and posterior, are described. Its contribution to posterolateral stability is debated. The popliteus complex includes a muscular origin from the tibia, a fibular origin represented by the fibulopopliteal ligament, a tendinous element that inserts into the popliteus fossa, and the superior and inferior popliteomeniscal ligaments that form the popliteal hiatus and soft tissue attachments to the lateral meniscus

and posterior tibia. The complex is important in preventing external rotation.

Biomechanics Several factors have been implicated in the diagnosis of iliotibial band syndrome. These include recent-onset step aerobics, running in the same direction on a track,

■ FIGURE 25-34 Sagittal fat-saturated proton density–weighted MR image. The arrow indicates a normal fibular collateral ligament insertion.

■ FIGURE 25-33 Coronal fat-saturated proton density–weighted MR image shows a conjoined tendon insertion of the fibular collateral ligament and biceps tendon (arrow).

■ FIGURE 25-35 Sagittal fat-saturated proton density–weighted MR image. The arrow indicates a normal fibulopopliteal ligament.

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sudden increase in training distance, and downhill rather than uphill running. The most common cause of injury to the posterolateral corner is a posterolateral force when the fibular collateral ligament and popliteus tendon tears, usually at or near full extension. This pattern of hyperextension injury may also result in injury to the PCL. Hyperextension combined with external rotation and varus produce the most severe disruption.

Pathology Injuries to the anterolateral corner include iliotibial band rupture (Fig. 25-36), avulsion, and the more common injury called iliotibial band friction syndrome (Fig. 2537). Clinically, this condition presents as an area of tenderness overlying the tract 2 to 3 cm above the knee joint. The changes occur where the ligament passes close to the lateral femoral condyle separated from it by a little connective tissue and fat and two layers of synovial lining of the knee joint. In this position, it can impinge against the lateral femoral condyle, resulting in tendinosis. This condition is also referred to as “runner’s knee.” Although classically associated with runners, step aerobics and cycling are other reported associations. Ganglion cysts related to the iliotibial band are uncommon. Injuries to the posterolateral corner are most commonly caused by a combination of rotation and varus stress. They are less common than MCL injuries but are more disabling. They are associated with full-thickness ruptures of the ACL when, on occasion, the clinical signs of cruciate rupture can mask the presence of posterolateral instability. It has been said that an overlooked posterolateral corner injury is the most common cause of ACL graft failure, but not all authors agree. Tears of the fibular collateral liga-

■ FIGURE 25-36 Coronal STIR MR image. There has been an avulsion of the iliotibial band from Gerdy’s tubercle (arrow).

617

ment most commonly occur in the midsubstance; or fibular avulsions, though more proximal tears, can also occur. These tears are usually combined with other lateral injuries, although isolated injuries have been reported. Tears of the fibular collateral ligament are divided into sprains, partial tears, or complete tears. Biceps femoris injuries are less common. Most often they are seen as overuse tendinopathy with thickening of the tendon just proximal to its insertion. When the injury is more acute, a tendon tear can occur. This most commonly presents as an avulsion fracture. Like avulsion injuries elsewhere, the degree of microfracture associated with them is less than is normally expected for fracture. This presumably reflects the avulsive rather than the compressive nature of the injury. Occasionally biceps femoris injuries can occur in conjunction with injuries to the iliotibial tract from sharing of common fibers.28 Subluxation of the biceps has been reported.29 This occurs during knee extension from a flexed position when the long tendon may be displaced over the fibular head. Patients may complain of pain and a clicking sensation, but tendon subluxation can also occur without associated symptoms.29 A prominent fibular head or anomalous insertions of the tendon may predispose to biceps tendon subluxation. Injuries to the popliteus muscle tendon complex also occur during posterolateral corner strain, and once again this structure should be carefully scrutinized in patients with other ligamentous injuries, specifically disruption of the ACL. Clinical findings in popliteus injury include acute hemarthrosis, lateral or posterolateral tenderness, and pain on resisted internal tibial rotation. The most common site for injury to occur is at the musculotendinous junction (Fig. 25-38). Injuries to the popliteus complex may also occur to the tendon itself or at the tendon insertion in the popliteus fossa (Fig. 25-39). Chronic injuries have

■ FIGURE 25-37 Coronal STIR MR image. There are high signal changes in the soft tissues on the medial aspect of the iliotibial band (arrow) consistent with iliotibial band friction syndrome or runner’s knee.

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■ FIGURE 25-38 Coronal fat-saturated proton density–weighted MR image shows musculotendinous tear of the popliteus complex (arrow).

■ FIGURE 25-39 Coronal fat-saturated proton density–weighted MR image of the same patient as in Figure 25-38 shows an associated tear of the popliteus tendon (arrow).

been described with late-onset muscle atrophy. Snapping of the popliteus tendon may also occur and needs to be differentiated from iliotibial friction. Subluxation occurs proximal to the lateral meniscus and may be bilateral.30 This area cannot be appreciated at arthroscopy. The dynamic capabilities of ultrasonography offer a distinct advantage over MRI in depicting this entity. Chronic injuries to the small ligaments of the posterolateral corner are less easy to appreciate on both clinical and imaging criteria. Popliteomeniscal ligament tears in college wrestlers have been described.31 Increased lateral meniscal motion on flexion may be a clue, although the imaging appearances of this entity have yet to be described. Acute calcific tendinopathy may occur in relation to any ligament or tendon. The precise cause is unknown, but calcium in their position suggests a crystal disorder. Calcium hydroxyapatite and calcium pyrophosphate have both been implicated.

Magnetic Resonance Imaging

Manifestations of the Disease The clinical impact of injuries to the lateral collateral ligament complex differs depending on whether they are anterior or posterior. Injuries to the iliotibial band commonly present subacutely, with pain located to a point overlying the lateral femoral condyle. Injuries to the posterolateral structures usually have a much greater clinical impact where, in the case of high-grade injuries, even walking may be difficult. It must be appreciated, however, that in a small proportion of asymptomatic individuals abnormalities including thickening of the lateral collateral ligament may be detected.32 These are likely to be the consequence of previous unsuspected and healed injuries.

Injuries to the lateral stabilizing structures are best appreciated on MR images, although avulsion fractures can be detected on radiography. For both the iliotibial tract and posterolateral corner, the external anatomic relationship of the ligaments is fat. Consequently, the most subtle change of injury is fluid replacement of the periligamentous fat. Coronal fat-suppressed images, therefore, provide the best imaging plane and sequence. Signs of iliotibial band friction syndrome include changes within the ligament itself, which becomes thickened with altered signal intensity; however, increased signal intensity within the fat surrounding the iliotibial band at the level of the lateral femoral condyle should be regarded as a more reliable sign of this condition. In advanced cases, high signal intensity on fat-saturated images surrounds the ligament but this change may be confined to the deep portion only. In these cases, care should be taken to ensure that high signal is differentiated from normal joint fluid or knee effusion. Joint fluid is generally a more consistent and higher signal characteristic. Axial images can also help by providing a more precise definition of the margins of the joint. Treatment of this condition is by corticosteroid injection, which has been reported to be effective, although longer-term benefit is best achieved with modification of training or equipment adjustment to prevent overuse. Rupture of the iliotibial band can occur but is uncommon. Tears are most commonly seen at the level of the knee joint rather than where friction syndrome occurs. Injuries to the fibular collateral ligament are uncommon and occur less frequently than injuries to the MCL. The ligament runs in an oblique plane, and serial orthog-

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● Internal Derangement of the Knee: Ligament Injuries

onal coronal images are most commonly used to depict these injuries. As outlined earlier, fat-saturated images provide greater contrast between abnormal fluid and surrounding fat and have the highest sensitivity for ligament injury. The presence of edema surrounding the ligament with an otherwise normal ligament is termed a grade 1 injury or sprain. These are largely treated conservatively. A grade 2 injury is a partial tear of the ligament. Like a grade 1 injury, fluid surrounds the ligament; however, in addition, some disruption of the ligament fibers is present (Fig. 25-40). Complete interruption of the ligament constitutes a full-thickness rupture. Occasionally, avulsion fractures can occur, and these can be proximal or distal (Fig. 25-41). A further clue to the presence of a lateral ligament injury is microfracture in the medial femoral condyle. This occurs during varus strain with impaction of the tibial plateau against the medial femoral condyle. Biceps femoris injuries are less common and are most often the consequence of overuse injury with thickening of the tendon just proximal to its insertion. Changes in the ligament can be subtle, and intravenous administration of gadolinium will improve detection and visualization of these injuries. When the trauma is more acute, a tendon tear can occur, which is most commonly an avulsion fracture. Because bony clues to biceps injury may be subtle, this area needs to be examined specifically, particularly in patients with rupture of the ACL. Tracing the cortical margin of the fibula looking for cortical interruption with particular attention to the site of biceps insertion is a useful method of detecting this injury. Loss of cortical continuity indicative of tendon avulsion is termed the arcuate sign (Fig. 25-42).33 The oblique course of the popliteus muscle and tendon from its origin on the posterior aspect of the tibia to its

■ FIGURE 25-40 Coronal fat-saturated proton density–weighted MR image demonstrates a grade 2 injury of the fibular collateral ligament with the internal signal changes and some intact fibers (arrow).

619

■ FIGURE 25-41 Coronal STIR MR image. There is an avulsion of the fibular collateral ligament (arrow) with the small fragment of periosteum from the fibular head.

insertion in the popliteal fossa of the lateral femoral condyle makes imaging interpretation challenging. Both sagittal and coronal images should therefore be checked for signs of injury. The most common location of injury occurs within the musculotendinous junction. Acute findings

■ FIGURE 25-42 Coronal STIR MR image. There is an avulsion of the biceps tendon insertion into the fibular head. Note the cortical breach and relatively minor microfracture (arrow).

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are increased signal intensity, which is best appreciated on fat-saturated images. Characteristically the edema disseminates between the muscle fibers, producing a herringbone pattern. Injuries to the popliteus complex may also occur to the tendon itself or at the tendon insertion in the popliteus fossa. Chronic injuries have been described with late-onset muscle atrophy. In these cases there is often diffuse fatty replacement of the muscle that is best appreciated by increased signal on T1-weighted images. Snapping of the popliteus tendon is uncommon. Subluxation occurs proximal to the lateral meniscus and may be bilateral. Because this is an area that cannot be appreciated at arthroscopy, imaging plays an important role in diagnosis. The dynamic capabilities of ultrasonography offer a distinct advantage over MRI in depicting this entity. Tears of the individual small ligaments of the posterolateral corner are difficult to appreciate. In my view, it is more helpful to determine whether there is a significant capsular disruption by identifying abnormal fluid in the popliteal fossa. This indicates that there is a significant ligament disruption, although it is often difficult to determine precisely which ligament has been torn. The importance of precise delineation of the exact site of ligamentous disruption to a surgical planning has also been

■ FIGURE 25-43 Acute calcific tendinopathy adjacent to femoral attachment of the fibular collateral ligament. Note the increased reflectivity in the calcification (arrow), and the more normal distal portion of the ligament. Note also the periphery of the lateral meniscus (arrowhead).

debated. If fluid is detected in the popliteal fossa, it is important to transmit this information to the referring clinician, particularly if the patient is to undergo arthroscopy for associated internal derangement of the knee. In the presence of an unsealed capsular leak, fluid introduced during arthroscopy to distend the knee can leak into the posterior calf and cause a compartment syndrome. Acute calcific tendinopathy may have a rather aggressive appearance on MRI. An inflammatory mass with increased signal intensity after intravenous administration of a contrast agent may be misinterpreted as sarcoma. The acute onset should provide a clue. Ultrasonography is useful in demonstrating the calcification (Fig. 25-43).

Ultrasonography The size and superficial location of the iliotibial band make it easily accessible to ultrasound interrogation. The band has the typical appearance of the ligament or tendon. The characteristic feature that makes it easy to recognize is a fan-like expansion just before its insertion into Gerdy’s tubercle (Fig. 25-44). The ultrasound appearances of the lateral collateral ligaments are also typical of ligaments elsewhere, showing as a well-demarcated, brightly echogenic, fibrillar structure (Fig. 25-45). The ligament

■ FIGURE 25-44 Coronal ultrasound image of the normal iliotibial band (arrows). The typical structure of a ligament or tendon is shown with linear-oriented connective tissue bundles interspaced among the tendon fibrils.

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621

Ganglia can occur in relation to any ligament, and the collateral ligaments of the knee are no exception. Ganglia are readily detected by ultrasonography, where they have the usual appearance of cysts, with a well-demarcated border and, most commonly, poorly reflective homogeneous contents. Occasionally, they may appear complex or multiloculated, particularly if there has been hemorrhage or infection within them, although the latter is uncommon. Ganglia have been reported in association with the lateral ligament complex and involve both the iliotibial tract and fibular collateral ligament. A more common cause of an apparent ganglion on the lateral aspect of the knee is a synovial cyst arising from the proximal tibiofibular joint. Synovial cysts of the proximal tibiofibular joint are common and can be very large, extending, in rare cases, to the ankle. They may also extend along the articular branch of the common peroneal nerve to the main nerve trunk itself, where they can further extend proximally within the neural sheath, even as far as the sciatic nerve. Compression of the peroneal nerve may result in a peroneal compartment muscle atrophy. The ultrasonographic signs of muscle atrophy are a generalized increase in muscle reflectivity. ■ FIGURE 25-45 Coronal ultrasound image of the normal fibular collateral ligament (arrows).

is usually of uniform thickness throughout, although it increases in size at its attachments. Ligament injury manifests both as areas of focal thickening with loss of the normal reflective structure or, when injuries are more severe, as focal interruptions in the normal structure. The biceps tendon can easily be differentiated from the lateral collateral ligament because it is a larger structure and lies more posteriorly. The tendinous portion can be traced proximally to the musculotendinous junction and, if necessary, more proximally to its origin from the ischial tuberosity. The popliteus complex can similarly be followed from its origin to its insertion. Ultrasonography has an advantage over MRI in the detection of more chronic overuse injury and in the diagnosis of tendon subluxation. In the former, the changes on MRI are often subtle, frequently requiring intravenous gadolinium for detection. Changes within the tendon that occur from chronic overuse are often more readily apparent on ultrasonography, particularly if the area of abnormal tenderness is compared with the asymptomatic contralateral side. The increase in Doppler blood flow can sometimes be detected in these injuries. Calcification adjacent to a ligament or tendon is more easily detected on ultrasonography than on MRI, and an acute inflammatory mass with associated calcification on ultrasonography is most commonly due to acute calcific tendinopathy (see Fig. 25-43). The differential diagnosis is synovial sarcoma, which is not infrequently associated with calcification. The rapid onset of bold symptoms and the mass is a useful differentiating feature. In the case of tendon subluxation, the dynamic role of ultrasonography means that this anomaly can be readily depicted when static MRI is normal.

Classic Signs ■

■ ■

■

■

High signal intensity on fat-saturated proton density– weighted coronal MR images lateral to the fibular collateral ligament is a useful sentinel sign of posterolateral injury. Loss of fibular cortical continuity is a sign of biceps tendon avulsion. Popliteus complex injuries are most common at the musculotendinous junction, where a herringbone pattern of the edema is best appreciated on fat-saturated images. High signal intensity changes on coronal fat-saturated proton density–weighted images between the iliotibial band and the lateral femoral condyle are a good sign of runner’s knee or iliotibial band friction syndrome. The ultrasonographic appearance of ligament injury is loss of reflectivity, disorganization of the normal fibrillar structure, and ligament thickening. Calcification or ossification may also be apparent, particularly adjacent to the MCL.

MEDIAL SUPPORTING STRUCTURES Prevalence, Epidemiology, and Definitions The prevalence of injuries to the MCL is difficult to calculate. It is recognized that these injuries are common particularly in relation to sports, including soccer, American football, and skiing. The majority of injuries are relatively mild and many go untreated. Patients with untreated grade 1 and 2 MCL injuries have an average return to sports of approximately 3 weeks.34 Studies of sports cohorts suggest a prevalence similar to injury of the ACL of approximately 1:5000. In my experience, the true prevalence is likely to be much higher.

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Anatomy The medial knee is stabilized by the deep static components of the MCL and the dynamic pes anserine tendons. Anteriorly, the medial retinaculum and fibers of the vastus medialis obliquus are attached to the medial aspect of the patella. Posterior to the medial retinaculum, the MCL is made up of a number of layers. From the MRI perspective the strongest, outermost layer is the dominant structure and comprises two portions. The anterior is a strong low signal ligament that extends from approximately 5 cm above the knee joint from the medial femoral condyle to insert 7 cm below the knee joint in a broad elongated insertion. This is the most commonly identified and easily recognized portion of the MCL. The posterior, oblique portion of this ligament arises from the adductor tubercle, posterior to the medial epicondyle. Because of the separate origin, it is often referred to as a separate ligament termed the posterior oblique ligament (POL). Its insertion has three components: a tibial insertion close to the margin of the articular surface with a strong attachment to the medial meniscus, a capsular insertion, and an insertion reinforcing the semimembranosus tendon. Beneath the superficial component of the MCL are the deep fibers that comprise two separate components: the medial meniscofemoral and the meniscotibial ligaments (Fig. 25-46). These are separated from the outer or superficial fibers by a potential space, generally only filled with connective tissue but that may fill with a bursa called the tibial collateral ligament bursa. The medial supporting structures of the knee have also been described as comprising three distinct layers. Layer one is the most superficial and comprises the deep fascia, forming the medial retinaculum by combining with the second layer. The second layer includes the superficial MCL and POL, and the third layer is the capsule proper but also includes the deep MCL.

■ FIGURE 25-46 Coronal fat-saturated proton density–weighted MR image. The arrow indicates a normal meniscofemoral ligament (deep fibers of the MCL).

The dynamic stabilizers lateral to this area comprise the pes anserine tendons: sartorius, semitendinosus, gracilis, and the semimembranosus. The semimembranosus is the key structure and has a complex of five insertions. The direct insertion is augmented by two additional aponeuroses anteriorly and two posterior. The anterior two are the pars reflexa inferiorly and an expansion to the POL superiorly. The posterior expansions are the oblique popliteal ligament superiorly and the popliteus aponeurosis inferiorly. These are more fully covered in Chapter 26 on tendon injuries of the knee.

Biomechanics The relationships of these stabilizers and the medial meniscus are important in determining the combination of injuries and their pattern. Injuries can be divided into simple valgus injury with MCL tear and anteromedial rotatory instability, which is an abnormal opening of the medial joint space in abduction at 30 degrees of knee flexion with a simultaneous anteromedial rotatory subluxation of the medial tibial condyle on the PCL.

Pathology Injuries to the medial supporting structures of the knee occur as a result of trauma to the lateral aspect of the lower thigh or upper leg. They are commonly encountered in running sports that require sudden changes in direction and are most typical in soccer, American football, and skiing. Rotational injuries in these sports may be associated with contact, which introduces a component of valgus. Where there is minimal contact the injury may be confined to the POL and posterior fibers of the MCL. With contact injury there is usually more significant damage to the MCL, POL, and ACL. These injuries may also be associated with meniscal tears, which should be carefully sought. Tears of the MCL may involve the superficial or the deep fibers. Injury to the deep fibers is common and relatively trivial. The more significant components are the superficial fibers, where injuries may be partial or complete. They are divided into three grades: grade 1 or ligament sprain, grade 2 or partial tear, and grade 3 or complete ligament rupture. In the late stage after MCL injury, acute changes around the ligament resolve, leaving only a thickened ligament, which may persist for many years. Occasionally, ossification can occur in relation to the ligament, and this is termed the Pellegrini-Stieda lesion (Fig. 25-47) and needs to be distinguished from acute calcific tendinopathy. Acute pain and swelling provide reliable differentiating features. There is a moderately good correlation between clinical and MRI grading. A grade 1 injury clinically has medial sided pain, some laxity, but with a firm end point. A grade 2 injury has valgus laxity with a soft but definable end point. A grade 3 lesion has valgus laxity without a defined end point that is correlated with complete rupture on MRI. The relationship between the clinical and imaging findings is not linear, however. In some studies the degree of clinical instability has been greater with grade 1 injuries than with grade 3 injuries.35 This calls into question

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■ FIGURE 25-48 Coronal STIR MR image. There is complete rupture of the MCL. Note the discontinuity in the medial condylar cortex (arrow) indicative of an avulsion fracture.

■ FIGURE 25-47 Coronal ultrasound image showing ossification adjacent to the proximal attachment of the MCL (arrow).

the ability of MRI to correctly grade tears of the MCL. The clinical picture may be confused by pseudo-locking, however. This is well recognized in relation to tears of the MCL, and the presence of muscle spasm may impair the ability to clinically detect instability. Tears of the MCL may occur in any position along the ligament, but more commonly occur close to the femoral attachment. Midsubstance and distal tears also occur. Occasionally the ligament may avulse a small fragment of bone at its attachment (Fig. 25-48). When MCL injuries are detected, a careful study of medial structures is warranted, because, in a small proportion, tears of the semimembranosus and associated insertions may be found. As with ligaments elsewhere, ganglion cysts can occasionally be associated with the MCL. These need to be distinguished from the tibial collateral ligament bursa, the semimembranosus bursa, and the pes anserine bursa. The semimembranosus bursa (Fig. 25-49) and pes anserine bursa are distinguished by the presence of a central tendon, the semimembranosus and semitendinosus, respectively. The two bursae are distinguished by their position, with the semimembranosus bursa lying superior to the

■ FIGURE 25-49 Coronal fat-saturated proton density–weighted MR image. The arrow indicates a semimembranosus bursa. It lies at joint level with the semimembranosus passing through it.

pes anserine bursa. The tibial collateral ligament bursa lies between the superficial and the deep fibers of the MCL.

Manifestations of the Disease Patients with injuries to the MCL most commonly present with focal, medial-sided pain. The major clinical test for injury to the MCL is the valgus stress test. This is best carried out in 30 degrees of flexion, because the capsule is relaxed in this position and thus valgus stress examines the

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collateral ligament in isolation. Valgus stress at full extension includes a component of the posteromedial capsule. The posteromedial capsule can be examined in isolation using the Slocum test. This is an anterior drawer test carried out at 90 degrees of flexion with external rotation of the lower leg. When the tibia is rotated externally, the posteromedial capsule should tighten and allow less anterior excursion than with the anterior drawer in neutral rotation. When the posteromedial capsule is torn, the Slocum test demonstrates an increase in the anterior motion of the tibia compared with the same test carried out in the neutral position. Like the lateral collateral ligament, however, it must be remembered that imaging findings may also be detected in the asymptomatic population.32

Radiography Injuries to the medial supporting structures of the knee are generally not associated with changes on radiographs in the acute phase of the injury. Soft tissue swelling and opening of the medial compartment may be detected on stress radiography. Compression microfractures may also occur in the lateral compartment, but they are rarely of sufficient severity to manifest on the radiograph. In the later phases after injury, calcification or ossification in the region of the MCL may be seen. This is called the Pellegrini-Stieda lesion (see Fig. 25-47).

Magnetic Resonance Imaging As for the lateral collateral ligament complex, MRI is the most reliable means of detecting injury. Injuries to the deep fibers can be relatively subtle. Fluid will be noted

■ FIGURE 25-50 Coronal fat-saturated proton density–weighted MR image. There is a tear of the meniscofemoral ligament (deep fibers of the MCL) (arrow).

between the superficial fibers and the underlying bone, either the femur or tibia. Injuries of the proximal or meniscofemoral component are more common (Fig. 2550). Fluid secondary to injury of the deep fibers of the MCL needs to be distinguished from fluid within the MCL bursa. Usually, distention of the bursa provides a clear demarcation between the superficial and deep fibers and makes it easier to exclude deep fiber injury. Like the lateral collateral ligament, the immediate external relationship of the MCL is subcutaneous fat. Consequently, injuries to the collateral ligaments are best appreciated on coronal fat-suppressed images. A grade 1 injury clinically has medial-sided pain, some laxity but with a firm end point. The MRI findings under these circumstances are generally limited to edema around the ligament (Fig. 25-51). The low signal structure of the ligament itself should remain intact and easily traced from its femoral to its tibial attachments. A grade 2 injury has a valgus laxity with a soft but definable end point. Under these circumstances the ligament shows internal structural changes, and often it is multilayered, giving it an onionskin appearance (Fig. 25-52). It is also associated with edema that surrounds the ligament in the acute stages. A grade 3 lesion in which there is valgus laxity without a defined end point is correlated with complete rupture on MRI (Fig. 25-53). In these cases the ligament is clearly discontinuous and may be lax or wavy at the site of rupture. Occasionally, the ligament may avulse a small fragment of bone at either of its attachment sites, but this finding is most commonly seen at the proximal (femoral) attachment (Fig. 25-54). When MCL injuries are detected, a careful study of the posteromedial structures

■ FIGURE 25-51 Coronal fat-saturated proton density–weighted MR image. Grade 1 sprain of the MCL with an intact ligament surrounded by soft tissue edema (arrow). Valgus microfracture is also present in this case (arrowhead).

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■ FIGURE 25-52 Grade 2 tear of the MCL. Note the edema medial to the ligament within the subcutaneous fat and the loss of the normal low signal intensity within the ligament itself (arrow).

■ FIGURE 25-54 Coronal fat-saturated proton density–weighted MR image. Valgus injury with bony avulsion of the femoral attachment of the MCL (arrow) and lateral compartment microfracture (arrowhead).

is warranted, because in a small proportion of cases tears of the semimembranosus and associated insertions may be found. As yet, a detailed description of the MRI findings of injuries to these smaller structures has not been defined. Occasionally, MCL injuries are associated with popliteus tears when there is a significant rotational component to the injury (Fig. 25-55).

Ultrasonography

■ FIGURE 25-53 Grade 3 MCL sprain. Coronal fat-saturated proton density–weighted MR image shows valgus sprain injury with a tear of the MCL, extensive edema in the medial subcutaneous fat, and microfracture in the lateral tibial plateau.

■ FIGURE 25-55 Coronal fat-saturated proton density–weighted MR image. There is a tear of the MCL, which has a wavy appearance (arrow). This patient also has an extensive lateral injury that includes an avulsion of the popliteus tendon. Note the empty popliteus fossa (arrowhead).

The principal ultrasound findings in MCL injury are similar to those described in the section on lateral collateral ligament injury. Because MCL injuries are more commonly seen in isolation, there is a role for ultrasonography in their assessment. In contrast, lateral collateral ligament

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injuries usually result from higher force injuries and are therefore more commonly associated with the internal derangement. For this reason MRI is a better investigation. Like the lateral collateral ligament, MCL injury manifests both as areas of focal thickening with loss of the normal reflective structure and when injuries are more severe, as focal interruptions in the normal structure (Fig. 25-56). Ultrasonography is generally superior at detecting periligamentous calcification to both plain radiography and MRI.

Synopsis of Treatment Options Treatment of collateral ligament injuries is largely conservative, with a combination of splinting or bracing and protected weight bearing initially progressing through a rehabilitation program ultimately to full weight bearing. Individuals with grade 1 injuries are usually able to return to unrestricted participation in sports within 2 weeks, and those with grade 2 injuries can do so within 3 weeks.

Classic Signs ■ ■

■ ■ ■

■ FIGURE 25-56 Coronal composite ultrasound image of a sprain of the MCL. Note the loss of the normal fibular structure, decreased reflectivity, and swelling of the proximal two thirds (arrows) compared with the more normal area close to the tibial insertion (arrowheads).

■

MCL injuries are best appreciated on coronal fat-saturated MR images or with ultrasonography. On MRI, grade 1 injury or MCL sprain is characterized by fluid adjacent to the ligament within the subcutaneous fat and an intact ligament. Grade 2 injury demonstrates disorganization of the ligament structure, sometimes with an onionskin configuration. Grade 3 injury has a focal disruption and a lax or wavy ligament. The ultrasonographic findings in MCL tear include loss of the normal fibrillar echo texture, decreased reflectivity, and ligament thickening. Periligamentous calcification or ossification may be seen in the chronic stages.

ACKNOWLEDGMENT I am very grateful to Mary Morgan for her assistance in the preparation of this chapter.

REFERENCES 1. Asikainen P, Luthje P, Jarvinen M, et al. Downhill skiing injuries and their costs at a Finnish skiing area. Scand J Med Sci Sports 1991; 1:228–231. 2. Yao L, Lee JK. Avulsion of the posteromedial tibial plateau by the semimembranosus tendon: diagnosis with MR imaging. Radiology 1989; 172:513–514.

3. Duncan JB, Hunter R, Purnell M, Freeman J. Meniscal injuries associated with acute anterior cruciate ligament tears in alpine skiers. Am J Sports Med 1995; 23:170–172. 4. Shelbourne KD, Nitz PA. The O’Donoghue triad revisited: combined knee injuries involving anterior cruciate and medial collateral ligament tears. Am J Sports Med 1992; 19:474–477.

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5. Huang G-S, Lee C-H, Chan WP, et al. Acute anterior cruciate ligament stump entrapment in anterior cruciate ligament tears: MR imaging appearance. Radiology 2002; 225:537–540. 6. Kaplan PA, Walker CW, Kilcoyne RF, et al. Occult fracture patterns of the knee associated with anterior cruciate ligament tears: assessment with MR imaging. Radiology 1999; 183:835–838. 7. Murphy BJ, Smith RL, Uribe JW, et al. Bone signal abnormalities in the posterolateral tibia and lateral femoral condyle in complete tears of the anterior cruciate ligament: a specific sign? Radiology 1992; 182:221–224. 8. Mellado JM, Calmet J, Olona M, et al. Magnetic resonance imaging of anterior cruciate ligament tears: reevaluation of quantitative parameters and imaging findings including a simplified method for measuring the anterior cruciate ligament angle. Knee Surg Sports Traumatol Arthroscopy 2004; 12:217–224. 9. Chan WP, Peterfy C, Fritz RC, Genant HK. MR diagnosis of complete tears of the anterior cruciate ligament of the knee: importance of anterior subluxation of the tibia. AJR Am J Roentgenol 1994; 162:355–360. 10. Schweitzer ME, Cervilla V, Kursunoglu-Brahme S, Resnick D. The PCL line: an indirect sign of anterior cruciate ligament injury. Clin Imaging 1992; 16:43. 11. Lawrence JA, Ostlere SJ, Dodd CA. MRI diagnosis of partial tears of the anterior cruciate ligament. Injury 1996; 27:153–155. 12. Vande Berg BC, Lecouvet FE, Poilvache P, et al. Anterior cruciate ligament tears and associated meniscal lesions: assessment at dualdetector spiral CT arthrography. Radiology 2002; 223:403–409. 13. Suzuki S, Kasahara K, Futami T, et al. Ultrasound diagnosis of pathology of the anterior and posterior cruciate ligaments of the knee joint. Arch Orthop Trauma Surg 1991; 110:200. 14. Skovgaard Larsen LP, Rasmussen OS. Diagnosis of acute rupture of the anterior cruciate ligament of the knee by sonography. Eur J Ultrasound 2000; 12:163. 15. Ptasznik R, Feller J, Bartlett J, et al. The value of sonography in the diagnosis of traumatic rupture of the anterior cruciate ligament of the knee. AJR Am J Roentgenol 1995; 164:1461–1463. 16. Hawe W. The S-shape of the posterior cruciate ligament on the sonogram: an indirect sonographic sign of an anterior cruciate ligament rupture. Pract Sport Traumatol Sportmed 1999; 6:7. 17. Fuchs S, Chylarecki C. Sonographic evaluation of ACL rupture signs compared to arthroscopic findings in acutely injured knees. Ultrasound Med Biol 2002; 28:149. 18. Even-Sapir E, Arbel R, Lerman H, et al. Bone injury associated with anterior cruciate ligament and meniscal tears: assessment with bone single photon emission computed tomography. Invest Radiol 2002; 37:521. 19. Parolie JM, Bergfeld JA. Long-term results of nonoperative treatment of isolated posterior cruciate ligament injuries in the athlete. Am J Sports Med 1986; 14:35–38. 20. Sonin AH, Fitzgerald SW, Friedman H, et al. Posterior cruciate ligament injury: MR imaging diagnosis and patterns of injury. Radiology 1994; 190:455–458.

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21. Mair SD, Schlegel TF, Gill TJ, et al. Incidence and location of bone bruises after acute posterior cruciate ligament injury. Am J Sports Med 2004; 32:1681–1687. 22. Grover JS, Bassett LW, Gross ML, et al. Posterior cruciate ligament: MR imaging. Radiology 1990; 174:527–530. 23. Nelson EW, LaPrade RF. The anterior intermeniscal ligament of the knee: an anatomic study. Am J Sports Med 2000; 28:74–76. 24. Gupte CM, Smith A, McDermott ID, et al. Meniscofemoral ligaments revisited: Anatomical study, age correlation and clinical implications. J Bone Joint Surg Br 2002; 84:846–851. 25. Anderson AF, Awh MH, Anderson CN. The anterior meniscofemoral ligament of the medial meniscus: case series. Am J Sports Med 2004; 32:1035–1040. 26. Meister BR, Michael SP, Moyer RA, et al. Anatomy and kinematics of the lateral collateral ligament of the knee. Am J Sports Med 2000; 28:869–878. 27. LaPrade RF, Ly TV, Wentorf FA, Engebretsen L. The posterolateral attachments of the knee: a qualitative and quantitative morphologic analysis of the fibular collateral ligament, popliteus tendon, popliteofibular ligament, and lateral gastrocnemius tendon. Am J Sports Med 2003; 31:854–860. 28. Terry GC, LaPrade RF. The biceps femoris muscle complex at the knee: its anatomy and injury patterns associated with acute anterolateral-anteromedial rotatory instability. Am J Sports Med 1996; 24:2–8. 29. Bach BR Jr, Minihane K. Subluxating biceps femoris tendon: an unusual case of lateral knee pain in a soccer athlete: a case report. Am J Sports Med 2001; 29:93–95. 30. Cooper DE. Snapping popliteus tendon syndrome: a cause of mechanical knee popping in athletes. Am J Sports Med 1999; 27:671–674. 31. LaPrade RF, Konowalchuk BK. Popliteomeniscal fascicle tears causing symptomatic lateral compartment knee pain: Diagnosis by the figure-4 test and treatment by open repair. Am J Sports Med 2005; 33:1231–1236. 32. Zanetti M, Pfirrmann CWA, Schmid MR, et al. Patients with suspected meniscal tears: prevalence of abnormalities seen on MRI of 100 symptomatic and 100 contralateral asymptomatic knees. AJR Am J Roentgenol 2003; 181:635–641. 33. Huang G-S, Yu JS, Munshi M, et al. Avulsion fracture of the head of the fibula (the “arcuate” sign): MR imaging findings predictive of injuries to the posterolateral ligaments and posterior cruciate ligament. AJR Am J Roentgenol 2003; 180:381–387. 34. Holden DL, Eggert AW, Butler JE. The nonoperative treatment of grade I and II medial collateral ligament injuries to the knee. Am J Sports Med 1983; 11:340–344. 35. Schweitzer ME, Tran D, Deely DM, Hume EL. Medial collateral ligament injuries: evaluation of multiple signs, prevalence and location of associated bone bruises, and assessment with MR imaging. Radiology 1995; 194:825–829.

C H A P T E R C H A P T E R

26

Internal Derangement of the Knee: Tendon Injuries Theodore T. Miller

THE EXTENSOR APPARATUS The extensor apparatus consists of the quadriceps tendon, the patella, the patellar tendon, the infrapatellar fat pad, and the medial and lateral patellar retinacula.1,2

Quadriceps Tendon Rupture Anatomy The quadriceps tendon is the conglomeration of the distal tendons of the quadriceps muscle and usually has a striated appearance on sagittal MR images, with the anterior striation representing the contribution from the rectus femoris, the middle striations representing the vastus lateralis and medialis, and the deep striation representing the vastus intermedius muscles (Fig. 26-1). The quadriceps tendon inserts on the anterior aspect of the superior pole of the patella.

Prevalence The quadriceps tendon typically tears in the unconditioned “weekend” athlete and in patients with systemic diseases such as diabetes, chronic renal failure, rheumatoid arthritis, or on chronic corticosteroid therapy. It is more common in people older than 40 years of age than in teenagers or young adults.3

Manifestations of the Disease Radiography A lateral radiograph is the most useful projection and will show suprapatellar soft tissue swelling and effacement of the fat planes, loss of the normal shadow of the quadriceps tendon, and varying amounts of anterior tilt of the patella away from the femur (Fig. 26-2).

Magnetic Resonance Imaging Acute ruptures display high signal intensity edema in and around the tear on T2-weighted images, and the proximal tendon edge may be retracted and balled up. Sagittal and coronal planes are useful to assess tendon discontinuity and amount of tendon retraction (Fig. 26-3).

Ultrasonography Longitudinal scanning is useful to assess tendon discontinuity and amount of retraction. In cases where the torn edges are apposed to each other, longitudinal scanning with the knee flexed can distinguish a partial tear from a nonretracted rupture (Fig. 26-4).4,5

Synopsis of Treatment Options Partial tears and some nonretracted ruptures may be managed conservatively. Ruptures are usually surgically repaired.

Biomechanics The cause of tears is eccentric contraction of the extensor mechanism, usually due to stumbling, as the flexing knee tries to extend against the weight of the stumbling person. The ruptured tendon usually has some underlying abnormality such as tendinosis or generalized weakening due to a systemic chronic medical condition. 628

What the Referring Physician Needs to Know ■

The degree of tendon tear: mild partial, extensive partial, rupture. If ruptured, the physician needs to know if and how far apart the tendon edges are.

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KEY POINTS: THE EXTENSOR A P PA R AT U S Quadriceps Tendon Rupture: Sonographic scanning in the extended and flexed positions can distinguish a partial tear from a nonretracted rupture. ■ Patellar Tendinosis and Tear: The patellar tendon rupture usually occurs at the proximal aspect, through an area weakened by tendinosis or previous surgery. ■ Jumper’s Knee: Jumper’s knee is a spectrum of chronic degeneration and partial tearing. ■ Popliteus and Biceps Femoris Muscles and Tendons (the Posterolateral Corner): Injury of the posterolateral corner may be missed at physical examination if the patient has rupture of the ACL and/or PCL. ■ Patellar Sleeve Avulsion: The radiographic appearance of patellar sleeve avulsion often belies the true extent of the patellar fracture. ■ Patellar Position and Maltracking: Soft tissue restraints maintain proper patellar position between full extension and 20 degrees of flexion, and the patella engages the femoral trochlear groove at 20 to 30 degrees. ■ Patellofemoral Pain Syndrome: Patellar alignment may be normal in the patellofemoral pressure syndrome. ■ Excessive Lateral Pressure Syndrome: Axial radiographs and axial MR images show lateral patellar tilt and/or subluxation. ■ Patellar Dislocation: Offset bone bruises only occur if the medial retinaculum is competent enough to bring the patella back into the femoral groove. If the retinaculum is ruptured, bone bruises won’t occur. ■ Bipartite Patella and Dorsal Defect of the Patella: Both of these normal variants may become symptomatic. ■

■ FIGURE 26-1 Normal quadriceps and patellar tendons. Sagittal T1-weighted MR image shows the normal striated appearance of the quadriceps tendon (large black arrow). The patellar tendon (white arrow) is straight and thinner than the quadriceps tendon, and its superficial and deep surfaces are parallel to each other. It is uniformly of low signal intensity except for a small triangle of intermediate signal intensity (small black arrow) along its proximal deep surface.

Patellar Tendinosis and Tear Tendinosis refers to chronic degeneration of the tendon and is usually asymptomatic.

Anatomy The patellar tendon is the continuation of the quadriceps tendon and is composed mostly of the rectus femoris component, which passes over the anterior aspect of the patella and inserts on the tibial tubercle (see Fig. 26-1). The normal patellar tendon is less than 75% of the thickness of the quadriceps tendon and has parallel surfaces. It is histologically a tendon, not a ligament.

Prevalence and Epidemiology Patellar tendinosis is seen in adults, and it may occur anywhere along the course of the patellar tendon. The development of tendinosis is related to the age and weight of a person.6 Rupture of the patellar tendon most often occurs at the proximal aspect of the tendon, usually through an area weakened by tendinosis or previous surgery. Rupture of the tendon at its midportion is usually a result of a direct blow. Patellar tendon rupture is less common than quadriceps tendon rupture and tends to occur in younger adults, where

■ FIGURE 26-2 Quadriceps tendon rupture. Lateral radiograph shows marked suprapatellar soft tissue swelling (asterisk). The patella shows abnormal anterior tilt away from the femoral condyles. The unaffected patellar tendon (white arrow) is normal.

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Biomechanics Chronic overuse leads to areas of degeneration. A forceful tensile load during quadriceps contraction may cause the tendon to partially tear or rupture.

Pathology Histologically, tendon degeneration shows crimping and disorganization of collagen fibers and mucinous degeneration of collagen. Neovascularization due to angiofibroblastic proliferation may also be present.8

Clinical Presentation Patellar tendinosis is usually asymptomatic. A patient with an acutely ruptured patellar tendon will complain of infrapatellar pain and swelling and inability to actively extend the knee.

Manifestations of the Disease Radiography ■ FIGURE 26-3

Quadriceps tendon rupture. Sagittal, fat-suppressed, T2-weighted MR image shows complete discontinuity of the distal aspect of the quadriceps tendon with edema within the tendon gap (arrow). The proximal and distal torn ends of the tendon are heterogeneous and thickened, indicating underlying tendinosis. Edema evident by high signal intensity is present around the torn tendon edges. (Courtesy of Dr. Douglas Mintz, Hospital for Special Surgery, New York, NY.)

it is more common in males than females. In older adults, the same systemic diseases that are risk factors for quadriceps tendon tear, namely diabetes, chronic renal failure, rheumatoid arthritis, and chronic corticosteroid therapy, are also risk factors for patellar tendon rupture.7

■ FIGURE 26-4

The severely thickened patellar tendon may be seen on lateral radiographs of the knee as widening of the patellar tendon outline, but most foci of tendinosis are radiographically occult. In the case of tendon rupture, there is ill-defined soft tissue swelling with resultant loss of the outline of the tendon. The patella may be retracted proximally by the unopposed pull of the quadriceps muscle (Fig. 26-5).

Magnetic Resonance Imaging The appearance of tendinosis is variable. There may be focal areas of intermediate signal intensity on T1- and T2weighted images without focal tendon thickening. The degenerated tendon may also appear “wrinkled” or buckled

Quadriceps rupture. A, Longitudinal sonogram with knee extension shows torn tendon edges (T) closely apposed to each other. There is a heterogeneously hypoechoic gap involving the anterior aspect of the tendon (arrow). B, Longitudinal view of the same patient with the knee flexed shows complete rupture and distraction of the tendon edges (T) with only a thin strand of tissue remaining (arrow). The patella (P) is present on the right side of both images.

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■ FIGURE 26-5 Patellar tendon rupture. Lateral radiograph shows loss of the normal shadow of the proximal aspect of the patellar tendon with surrounding soft tissue edema (arrow). The patella is high riding owing to the unopposed pull of the quadriceps muscle.

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■ FIGURE 26-6 Patellar tendinosis. Sagittal, proton density–weighted MR image shows a wrinkled patellar tendon (arrow) with small foci of intermediate signal intensity representing mucinous degeneration.

(Fig. 26-6) or may be diffusely thickened (Fig. 26-7).6,9 A patellar tendon that is as thick as the quadriceps tendon is abnormal. Focal high signal intensity on T2-weighted images may result from marked mucinous degeneration and interstitial cyst formation (Fig. 26-8). Acute rupture appears as discontinuity of the tendon with high signal intensity edema and hemorrhage in the region of tear (Fig. 26-9). The patella may be retracted proximally.

Ultrasonography Tendinosis may appear as focal hypoechoic loss of the normal echogenic fibrillar appearance of the tendon and/ or tendon thickening (Fig. 26-10). Rupture appears as discontinuity of the tendon.

Jumper’s Knee (Patellar Tendinitis) Jumper’s knee refers to a symptomatic focus of tendinosis and partial tearing that occurs in the proximal aspect of the patellar tendon.

Prevalence “Jumper’s knee” gets its name because it is seen in basketball players, volleyball players, and any other athletes whose sport requires repetitive forceful extension of the knee.10 It usually occurs in teenagers and young adults.

■ FIGURE 26-7 Patellar tendinosis. Sagittal, proton density–weighted MR image shows a markedly thickened patellar tendon (arrow) with heterogeneous internal signal both proximally and distally.

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■ FIGURE 26-8 Mucinous degeneration of the patellar tendon. A, Sagittal, T1-weighted MR image shows thickening and intermediate signal intensity within the patellar tendon (arrow). B, Sagittal, fat-suppressed, T2-weighted MR image in the same patient shows the high signal intensity of mucinous degeneration (arrow).

Biomechanics Jumper’s knee is a chronic overuse injury of the proximal aspect of the patellar tendon, due to repetitive forceful extension of the knee.11 It occurs in the proximal aspect of the tendon because the stress in the tendon is greatest at the tendon’s insertion on the inferior pole of the patella.

Pathology There is mucoid degeneration of the collagen fibers and angiofibroblastic proliferation, with eventual partial tearing. The term tendinitis is a misnomer because there is no acute inflammation histologically.12

Manifestations of the Disease Magnetic Resonance Imaging

■ FIGURE 26-9 Patellar tendon rupture. Sagittal, proton density–weighted MR image shows rupture of the proximal aspect of the patellar tendon, which has balled up on itself (arrow) but with only minimal retraction. The tendon shows diffuse degeneration manifested by thickening and signal heterogeneity. There is similar tendinosis in the visualized portion of the distal quadriceps tendon. (Courtesy of Dr. Douglas Mintz, Hospital for Special Surgery, New York, NY.)

The normal patellar tendon exhibits uniformly low signal intensity on all pulse sequences, except at its proximal attachment, where there may be a V-shaped focus of high signal intensity on T1-weighted images along its deep surface (see Fig. 26-1).6,9 On sagittal and axial T2-weighted MRI of jumper’s knee there is focal swelling of the proximal aspect of the patellar tendon, most often affecting the central third of the tendon, with focal internal high signal intensity (Fig. 26-11). There may also be edema in the adjacent fat pad and in the inferior pole of the patella.13

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■ FIGURE 26-10

Patellar tendinosis. A, Longitudinal sonogram of the patellar tendon shows marked thickening. The superficial and deep surfaces (white arrows) are not parallel, and the tendon has a heterogeneous echotexture. The patella (P) is on the left of the image, and the proximal tibia (T) is on the right of the image. B, Longitudinal sonogram of a normal patellar tendon shows an echogenic fibrillar appearance with superficial and deep surfaces (white arrows) that are parallel to each other. P, patella; T, tibia.

■ FIGURE 26-11 Jumper’s knee. A, Sagittal, proton density–weighted MR image shows fusiform swelling of the proximal aspect of the patellar tendon and internal high signal intensity (arrow). B, Axial, fatsuppressed, T2-weighted MR image in the same patient shows the high signal intensity focus involving the deep aspect of the central third of the tendon.

Ultrasonography The normal patellar tendon exhibits an echogenic coarse fibrillar pattern. In jumper’s knee, the fibrillar appearance is effaced by hypoechogenicity and the tendon is thickened. Power or color Doppler imaging reveals hyperemia, reflecting the degenerative angiofibroblastic proliferation (Fig. 26-12).

refractory to conservative treatment may be treated with resection of the tendinotic focus or shift of the patellar tendon attachment.

Synopsis of Treatment Options

Osgood-Schlatter Disease, SindingLarsen-Johansson Syndrome, and Patellar Sleeve Avulsion Prevalence and Epidemiology

Initial treatment is conservative, consisting of rest, icing, and nonsteroidal anti-inflammatory medication. Percutaneous dry needling or sclerotherapy with sonographic guidance may also produce relief.14 Cases

These abnormalities affect adolescents, before the patella is completely ossified and before the tibial tubercle apophysis has fused. Girls may be affected at a slightly younger age than boys.

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■ FIGURE 26-12 Jumper’s knee. A, Longitudinal ultrasound image shows fusiform swelling of the proximal aspect of the patellar tendon (black arrows). The inferior pole of the patella is seen (white arrow). B, Longitudinal sonogram of a normal patellar tendon shows the normal fibrillar echogenic appearance of the tendon with parallel superficial and deep surfaces (black arrows). The inferior pole of the patella is seen (white arrow). C, Power Doppler image of the same patient as in A shows marked interstitial hyperemia representing angiofibroblastic proliferation.

Osgood-Schlatter disease (OSD) affects the distal aspect of the patellar tendon, whereas Sinding-Larsen Johansson syndrome (SLJS) and the patellar sleeve avulsion (PSA) affect the proximal aspect of the tendon.

Biomechanics Osgood-Schlatter disease and SLJS are chronic overuse injuries and PSA is an acute injury, all seen in sports that involve forceful contraction of the extensor mechanism, such as encountered in cutting maneuvers and jumping. There is controversy in the literature whether patella alta, patella infera, or tibial torsion predisposes to OSD by virtue of altered tensile stress on the patellar tendon/tibial tubercle apophyseal attachment.15

Pathology Patellar sleeve avulsion is a tear of the proximal aspect of the patellar tendon from the inferior pole of the incompletely ossified patella, taking with it an osteochondral fragment of the patella. SLJS proximally and OSD distally represent repetitive partial tearing of the tendon and small avulsions of the cartilaginous attachment of the patellar tendon to the lower pole of the patella and tibial tubercle apophysis, respectively. The small avulsed cartilage fragments may ossify, and the small tendon tears may eventually develop foci of heterotopic ossification.15–17

Manifestations of the Disease Radiography The lateral radiograph of PSA may belie the underlying injury, because most of the avulsed fragment is typically radiolucent cartilage, with only a small piece of bony patella (Fig. 26-13). Soft tissue swelling may be present and the patella may be high riding. Both OSD and SLJS demonstrate heterotopic ossification within the patellar tendon, but normal variations in development of the ossification centers of the tibial tubercle apophysis and lower pole of the patella may look similar. The distinguishing feature of these conditions from normal variation is the presence of tendon thickening and soft tissue swelling and the clinical presence of pain and tenderness in the affected region. A distended deep infrapatellar bursa may be visible as a soft tissue density deep to the tendon in OSD (Fig. 26-14).

Magnetic Resonance Imaging Sagittal T2-weighted images will display the fracture through the inferior pole of the patella in PSA and reveal the true extent of the fracture through the bone and cartilage anlage (Fig. 26-15). On sagittal MR images of OSD and SLJS, the distal and proximal aspects, respectively, of the patellar tendon are enlarged, with low signal intensity

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■ FIGURE 26-13 Patellar sleeve avulsion. Lateral radiograph shows a large fracture fragment (arrow) with smaller distal fracture fragments and blurring of the fat plane around the proximal aspect of the patella tendon.

■ FIGURE 26-14

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Osgood-Schlatter disease. Lateral radiograph shows heterotopic ossification (black arrow) in the distal aspect of the patellar tendon. The tendon is thickened. Ill-defined soft tissue density (white arrow) in Hoffa’s fat pad represents a distended infrapatellar bursa.

■ FIGURE 26-15 Patellar sleeve avulsion. A, Sagittal, proton density–weighted MR image. B, Sagittal gradient-echo, T2-weighted image. The black arrows outline the entire fracture fragment, and the white arrow identifies the small portion that is ossified and radiographically visible. Same patient as Figure 26-13. (Courtesy of Dr. Douglas Mintz, Hospital for Special Surgery, New York, NY.)

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foci of heterotopic ossification and possible enlargement or irregularity of the bony attachment site (Figs. 26-16 and 26-17). In OSD there may also be distention of the deep infrapatellar bursa, manifest as fluid located between the anterior cortex of the tibia and the deep surface of the patellar tendon (Fig. 26-18).

Ultrasonography Longitudinal scanning of PSA will demonstrate the echogenic fibrillar patellar tendon and attached piece of hypoechoic patellar cartilage separated from the rest of the patella. Longitudinal scanning in OSD and SLJS will demonstrate the thickened tendon. The foci of internal heterotopic ossification will have echogenic surfaces with varying amounts of posterior acoustic shadowing (Fig. 26-19). The distended deep infrapatellar bursa will be a hypoechoic collection deep to the distal aspect of the tendon.

Differential Diagnosis Patellar sleeve avulsion should be easily distinguished from other causes of acute knee pain in the adolescent because it is an acute event. The knee gives way, and the patient cannot stand or actively extend the knee. The area is painful and swollen, and there may be a palpable defect at the site of avulsion. Patients with OSD and SLJS have chronic pain and tenderness to palpation over the affected region. Other

■ FIGURE 26-16 Sinding-Larsens-Johansson syndrome. Sagittal, T1-weighted MR image shows thickening of the proximal aspect of the patellar tendon (white arrow), irregular ossification of the inferior pole of the patella (long black arrow), and focal heterotopic ossification within the patellar tendon (short black arrow).

■ FIGURE 26-17 Osgood-Schlatter disease. Sagittal, proton density– weighted MR image shows thickening of the patellar tendon and focal heterotopic ossification (arrow). (Courtesy of Dr. Douglas Mintz, Hospital for Special Surgery, New York, NY.)

■ FIGURE 26-18 Osgood-Schlatter disease. Sagittal, proton density– weighted MR image shows focal calcification (black arrow) in the distal patellar tendon and a distended infrapatellar bursa (white arrow). Same patient as Figure 26-14.

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■ FIGURE 26-19 Osgood-Schlatter disease. A, Longitudinal ultrasound image shows a normal-appearing midportion of the patellar tendon (small white arrows). The distal aspect of the patellar tendon is thickened and hypoechoic (black arrows) with interstitial focal heterotopic ossification (large white arrow). T, tibia. B, Longitudinal ultrasound image of the contralateral normal knee shows a normal-appearing patellar tendon (white arrows) inserting on the tibia (T).

causes of chronic anterior knee pain in the adolescent are jumper’s knee, chondromalacia patellae, patellar tracking abnormalities, irritation of a medial or infrapatellar plica, and abnormalities of Hoffa’s fat pad. Patellar tendon/lateral femoral condyle friction syndrome may affect adolescents but is more common in adults.18

Patellar Tendon/Lateral Femoral Condyle Friction Syndrome Prevalence This abnormality usually occurs in young adults but has a reported age range of 13 to 56 years.18 Most people affected do not participate in routine athletic activities.

Biomechanics The biomechanics are not well understood, but it may be an overuse injury in which the patellar tendon chronically rubs against the lateral femoral condyle or compresses the lateral aspect of Hoffa’s fat pad between itself and the lateral condyle.18 It is probably related to patellar maltracking or malalignment, because most patients with this abnormality have patella alta or lateral subluxation of the patella.18

Infrapatellar Fat Pad Impingement (Hoffa’s Disease) Anatomy The infrapatellar fad pad (also called Hoffa’s fat pad) is a roughly pyramidal fibrofatty structure located between the patella and femoral condyles superiorly and the tibia inferiorly. Its base is along the deep surface of the patellar tendon, and its apex points toward the intercondylar notch. The synovium of the anterior aspect of the knee joint is reflected over its deep surface, and thus the fat pad is intracapsular but extrasynovial. Synovial-lined vertical and horizontal clefts may be present within it. The fat pad is not freely mobile, being attached to the inferior pole of the patella and the roof of the intercondylar notch by the ligamentum mucosum (also called the infrapatellar plica) and having attachments to the anterior horns of the menisci and to the periosteum of the tibia.19,20 The deep infrapatellar bursa is located at the inferior edge of the fat pad. The blood supply comes from two vertically oriented and peripherally located vessels, which are branches of the superior and inferior genicular arteries, with horizontal anastomotic branches.19,20 It is well innervated by branches of the femoral, common peroneal, and saphenous nerves.20

Manifestations of the Disease Magnetic Resonance Imaging

Biomechanics

T2-weighted images demonstrate focal edema in the lateral aspect of Hoffa’s fat pad, with an occasional focal fluid collection in this region. Marrow edema may be present in the lateral aspect of the patella, the cartilage of the lateral patellar facet may be thinned, and there may be tears in the proximal aspect of the patellar tendon.

A single traumatic episode or repetitive overuse due to hyperextension and rotational forces leads to hemorrhage and inflammation of the fat pad, which in turn cause swelling of the fat pad; the enlarged fat pad then gets impinged between the tibia and femur, further exacerbating the inflammation and enlargement.20

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Pathology Acutely, there is inflammation and hemorrhage of the fat pad. This gives way to an influx of macrophages and the deposition of fibrin and hemosiderin. Chronically, there is fibroblast proliferation, leading to fibrosis of the fat pad which may undergo fibrocartilaginous metaplasia, and the fibrocartilaginous tissue may eventually ossify.19,20

Manifestations of the Disease Magnetic Resonance Imaging On sagittal T2-weighted images, the fat pad may have diffuse high signal intensity edema or a heterogeneous appearance due to hemorrhage. The patellar tendon may be bowed anteriorly by the swollen pat pad. Chronically, areas of low signal intensity within the fat pad may represent foci of hemosiderin, fibrosis, or ossified fibrocartilaginous tissue.19,20

Differential Diagnosis The causes of anterior knee pain, with or without locking or clicking, are myriad and may be due to abnormalities that can be broadly classified as extra-articular, such as those of the patella and the patellar tendon, and intraarticular, such as those of the menisci, synovium, or plicae. Hoffa’s fat pad, by virtue of its location, may be affected by both groups of processes. Thus, abnormalities of the fat pad can be grouped according to intrinsic processes, such as impingement (Hoffa’s disease and patellar tendon/ lateral femoral condyle friction syndrome), focal nodular synovitis, and postarthroscopy/postsurgical fibrosis, and extrinsic causes that can be due to both extra-articular and intra-articular abnormalities such as patellar tendon abnormalities, meniscal cysts, and synovitides.19,20 The patellar tendon/lateral femoral condyle friction syndrome and symptomatic infrapatellar plica may present with symptoms similar to Hoffa’s disease, and all three conditions may in fact be interrelated abnormalities. The edema of Hoffa’s disease should be diffuse, whereas the edema of the patellar tendon/lateral femoral condyle friction syndrome should just affect the lateral side of the fat pad and may also have edema in the lateral side of the patella and in the lateral femoral condyle. The edema of a symptomatic infrapatellar plica should be linear and follow the course of the plica. The linear fibrosis of the postoperative fat pad may mimic the thickened infrapatellar plica. An intracapsular chondroma can arise within the fat pad due to chondral metaplasia. It will have a heterogeneous appearance and may cause enlargement of the fat pad with associated bowing of the patellar tendon, all of which mimic the appearance of Hoffa’s disease,19 especially since chronic Hoffa’s disease is also characterized by fibrocartilaginous metaplasia. Similarly, synovial chondromatosis may affect the fat pad, either from direct invasion from the joint itself, or arising from the synovium that lines the clefts within the fat pad. Cysts may arise in the anterior aspect of the joint and insinuate into the fat pad. These cysts may be either ganglia arising adjacent to the anterior horn of the lateral meniscus or parameniscal cysts arising from a tear of the

adjacent meniscus. As expected, cysts are typically of low signal intensity on T1-weighted sequences and of high signal intensity on T2-weighted sequences, but focal nodular synovitis may look similar. Focal nodular synovitis is the focal form of pigmented villonodular synovitis and typically lacks the hemosiderin deposition of the pigmented, diffuse entity. Thus, it may appear only mildly heterogeneous and may be of high signal intensity on T2-weighted images instead of having low-signal dephasing artifact.19,20

Patellar Position and Maltracking Anatomy The patella is the largest sesamoid bone in the body, and its purpose is to protect the extensor tendon apparatus from friction against the femur during knee flexion and to give mechanical advantage to the apparatus by lifting it away from the joint itself. The patellar articular cartilage is the thickest articular cartilage in the body and engages the articular cartilage of the femoral trochlear groove as the knee flexes; in full knee extension the patella lies anterior to the supracondylar prefemoral fat pad and the patellar cartilage does not articulate with the femoral trochlear cartilage. The patella is normally composed of three facets: the lateral, which is the predominant articular surface in extension and early flexion; the medial, which is the predominant articular surface in flexion; and the odd facet, which is the smallest, the most medially located, and the predominant articular surface in extreme degrees of flexion (>135 degrees).1 There is a wide variation in the shape of the articular surface of the patella, based on the configuration of the medial and lateral facets. The Wiberg classification describes three types of patellar configuration, based on the axial (transverse) appearance of the facets: type 1—the lateral and medial facets are similar in length and orientation and are concave; type 2—the lateral facet is longer and more shallowly oriented than the medial facet, but both are concave; type 3—the lateral facet is longer and more shallowly oriented than the medial facet, and the medial facet is flat or convex.21 Medial and lateral stability of the patella is provided actively by the quadriceps muscles and the vastus medialis oblique and vastus lateralis oblique muscles. Passive stabilization is provided by the bony confines of the femoral trochlear groove and by the medial and lateral patellar retinacula. The retinacula are broad bands of fascial tissue that sweep forward from the medial and lateral sides of the knee to insert on the patella. They each have superficial and deep components, giving a bilaminar appearance on axial MR images (Fig. 26-20).22 On the lateral side, the superficial layer of the lateral retinaculum is formed by fascial tissue from the iliotibial band and vastus lateralis muscle and inserts on the patella and patellar tendon. The deep component is composed of the transverse band, which arises from the deep surface of the iliotibial band and inserts on the lateral side of the patella proximal to the inferior pole; the patellotibial band, which connects the tibia and lateral meniscus to the lateral margin of the patella inferior to the transverse band; and the epicondylopatellar band, which connects the lateral epicondyle to the patella, proximal to the transverse band.

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■ FIGURE 26-20 Patellar retinacula. Axial, proton density–weighted MR image shows the bilaminar appearance of the medial and lateral retinacula (white arrows). The nondistended suprapatellar recess is also seen (black arrows) and should not be mistaken for portions of the retinacula.

On the medial side, the superficial layer of the medial retinaculum is formed by a confluence of the anterior aspects of the first and second layers of the medial side of the knee, and is relatively unimportant to patellar stability.23 The deep portion is the most important for stability and is composed of three ligaments: the medial patellofemoral ligament, which is the largest, most superiorly located, and clinically most important, and which originates from the adductor tubercle of the medial condyle and blends with the superficial layer as it inserts on the patella; the patellomeniscal ligament, which is also clinically important to patellar stabilization and which courses obliquely from the medial meniscus and meniscotibial (coronary) ligament to the tibia; and the patellotibial ligament, which is the most inferiorly located and

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least important functionally, extending from the anteromedial tibia to the patella.22 Patellar position refers to the static location and orientation of the patella on lateral and axial tangential radiographs. On a lateral radiograph of the knee, obtained with 30 degrees of flexion, the patella is normally centered over the anterior aspects of the femoral condyles. Many methods exist for quantifying this normal patellar height on lateral radiographs. A common and easy to use method is the Insall-Salvati ratio, which compares the patellar tendon length to the patellar length; the ratio should normally be between 1:1 and 1.2:1.24 Axial views of the patella allow assessment of patellar location and orientation relative to the femoral trochlear groove and femoral condyles. Numerous techniques have been described for performing axial tangential radiographs; the method of Merchant and coworkers has the patient supine with the knees flexed 45 degrees over the edge of the x-ray table, with the radiographic beam angled caudally 30 degrees and the quadriceps muscles relaxed.25 Some investigators believe that 30 degrees of flexion is the optimal amount.26 Views obtained with more than 45 degrees of knee flexion may not detect patellar malalignment because the patella has been drawn back into the trochlear groove. Similarly, the quadriceps muscle should be relaxed because quadriceps contraction may correct a malalignment, although in two different series isometric quadriceps contraction had no statistically significant effect on the congruence angle at either 30 degrees of flexion27 or at 45 degrees of flexion.28 On the tangential view, the patellar apex normally is centered over the trochlear sulcus and the anterior cortex of the lateral femoral condyle, and the cortex of the lateral patellar facet is parallel. Commonly assessed parameters on tangential radiographs are the sulcus angle, congruence angle, lateral patellar displacement, and lateral patellofemoral angle. The sulcus angle is formed by the intersection of lines connecting the highest points on the femoral condyles to the lowest point of the trochlear sulcus (Fig. 26-21A); the angle is normally

■ FIGURE 26-21 Sulcus angle and congruence angle. A, Sulcus angle. Lines drawn from the lowest point of the trochlear sulcus to the highest point on the lateral and femoral condyles form the sulcus angle. B, The congruence angle is formed between a line from the patellar apex to the trochlear sulcus (dotted line) and a line (thin solid black line) bisecting the sulcus angle (thick solid black lines).

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by a line connecting the most anterior aspects of both condyles and a line along the lateral patellar facet; the angle normally opens laterally or the lines are parallel (Fig. 26-23).30

Prevalence

■ FIGURE 26-22

Lateral patellar displacement. The medial edge of the patella (white arrow) should normally lie medial or no more than 1 mm lateral to a line (dotted line) drawn at the most anterior aspect of the medial femoral condyle perpendicular to a line that connects the most anterior aspects of the medial and lateral femoral condyles (solid black line).

124 to 145 degrees.29 The congruence angle is the intersection between a line bisecting the sulcus angle and a line drawn from the patellar apex to the lowest point of the trochlear sulcus. The angle is negative if the patellar apex is medial to the line bisecting the sulcus angle and positive if lateral to the bisecting line; the normal angle is −17 to +5 degrees (see Fig. 26-21B).25 Lateral patellar displacement is assessed by drawing a line through the most anterior aspect of the medial femoral condyle perpendicular to a line connecting the most anterior aspects of both condyles; the medial tip of the patella should be medial to, or at most no more than 1 mm lateral to, the line through the medial femoral condyle (Fig. 26-22).30 The lateral patellofemoral angle is formed

On tangential radiographs of the patella with the knee flexed 30 degrees, 18% of 217 asymptomatic knees and 27% of 186 knees with patellofemoral pain showed malalignment.26 It is not uncommon to see the patella mildly laterally subluxed relative to the femoral trochlear sulcus or slightly laterally tilted on routine axial MR images in extension; 42% of asymptomatic knees in one series showed minimal to mild lateral subluxation and/or tilt,31 whereas 50% of asymptomatic knees in a different series showed slight lateral displacement.32 In some people this positioning is of no clinical importance because the patella will align correctly as the knee flexes and the patella engages the trochlear groove. However, in other people the patellar tilt or subluxation is painful or leads to recurrent dislocation. In a series of 474 patients with anterior knee pain, 40% had patellar subluxation or tilt on axial MR images and 68% of the patients with severe malalignment were female.33 Similarly, in a series of 50 patients with anterior knee pain studied with MRI, up to 86% of cases of severe malalignment were in females.31

Biomechanics Patellar maltracking and abnormal patellofemoral contact stress can occur if the patella is too high (“patella alta”) or too low (“patella infera” or “patella baja”) within the femoral trochlear groove or if the patella is too medially or laterally located within the groove. Causes of abnormal patellar tilt, patellar subluxation, and patellar maltracking include patella alta and infera, muscle imbalance, “tight” retinacula, a congenitally shallow femoral trochlear groove, or a congenitally flat patellar articular surface.

Manifestations of the Disease Radiography

■ FIGURE 26-23

Lateral patellofemoral angle. This angle is formed by a line connecting the most anterior aspects of the femoral condyles (solid black line) and a line drawn along the lateral patellar facet (dotted line). The angle should normally open laterally.

Using the Insall-Salvati method of measuring patellar height on lateral radiographs, patella alta is present when the ratio of patellar tendon length to patellar length is 1.3 or greater (Fig. 26-24).24 Patella infera is present when the patellar tendon length is less than 0.8 of the patellar length.34 On a lateral radiograph, patellar tilt can be assessed by the shape of the patellar articular cortex. In normal alignment, the cortex of the patellar apex (also called the median ridge) and the cortex of the lateral patellar facet have a mildly concave appearance and the cortex of the apex is closer to the femur. In mild tilt, the cortices of the apex and lateral facet are superimposed and in severe tilt the cortex of the lateral facet becomes convex and projects posterior to the cortex of the patellar apex.26 Patellar subluxation is not well assessed on the lateral view.26 Tangential radiographs of the patellofemoral joint can assess both patellar tilt and subluxation. Lateral patellar

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■ FIGURE 26-25 Lateral patellar tilt angle. The angle formed between a line drawn through the medial and lateral edges of the patella and a horizontal line is normally approximately 2 degrees. This case shows abnormal tilt.

■ FIGURE 26-24 Insall-Salvati ratio. On a lateral radiograph, the length of the patellar tendon (white line) should be approximately equal to the length of the patella (black line) and should not be longer than 1.3 times the length of the patella.

subluxation is present if the congruence angle is more than +16 degrees or if the medial edge of the patella is more than 1 mm from the perpendicular line through the medial femoral condyle. Severe lateral patellar tilt is present if the lateral patellofemoral angle opens medially, but a shortcoming of the lateral patellofemoral angle is that it fails to recognize less severe degrees of tilt in which the angle still opens laterally. To overcome the insensitivity of the lateral patellar angle method, Grelsamer and colleagues35 described a method of measurement of patellar tilt, using a 30-degree Merchant view, in which a line drawn connecting the medial and lateral edges of the patella is compared with a horizontal line (assuming the lower extremities are not internally or externally rotated); the mean tilt angle in their cohort of symptomatic patients was 12 degrees ± 6 degrees, whereas the tilt angle of the cohort of asymptomatic controls was 2 degrees ± 1 degree (Fig. 26-25). Those authors found that a patellar tilt angle of 5 degrees or more had 85% sensitivity and 92% specificity for detecting abnormal alignment. In their series of symptomatic patients, 20 degrees of tilt was necessary to make the lateral patellar angle open medially and only detected 7 of 100 symptomatic cases.

Magnetic Resonance Imaging The Insall-Salvati ratio can also be applied to sagittal MR images,36 using an image with the longest patellar length

and an image through the middle of the patellar tendon; the ratios for patella alta and patella infera are the same as for lateral radiographs (Fig. 26-26). Similarly, patellar tilt and subluxation can be assessed on axial MR or CT images using the same criteria as for the radiographic Merchant view. The use of quadriceps contraction at full extension is questionable, because results are contradictory; lateral patellar tilt was increased in one series,37 decreased in another,38 and mixed in another.39 Patellar tracking refers to the position of the patella dynamically in the axial plane as the knee ranges from extension to flexion with quadriceps contraction. The evaluation of patellar tracking can be performed with either CT or MRI. Static assessment at discrete degrees of flexion is performed by scanning the patient’s patellofemoral joint at 0 degrees of flexion (i.e., full extension), 15 degrees of flexion both at rest and isometric quadriceps contraction, and 30 degrees both at rest and isometric quadriceps contraction.40–43 This method allows assessment of both passive soft tissue restraints and active muscle balance. Thirty degrees is chosen as the maximum amount of flexion because soft tissue restraints provide stability between 0 degrees and approximately 20 degrees of flexion, and the patella engages the femoral trochlear groove at 20 to 30 degrees (Fig. 26-27). Flexion is achieved with either a bolster or rolled-up blanket, and isometric quadriceps contraction is achieved by placing a strap across the ankle joints and having the patient try to straighten the legs against the strap while being scanned. Inclusion of the contralateral (presumably normal) knee in the field of view is helpful for comparison. Dynamic assessment is performed by having the knees flexed over a bolster to 30 degrees, choosing a single slice location through the patellofemoral articulation and scanning continuously in that same location while the patient slowly and smoothly raises and lowers the legs. Such kinematic imaging can be performed with MRI using gradient-echo

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■ FIGURE 26-26 MRI of patella alta. A, The length of the central aspect of the patellar tendon on a sagittal MR image (dotted black line) should not be more than 30% longer than the longest dimension of the patella (white solid line). B, Sagittal, proton density– weighted MR image shows the patellar tendon length (dotted black line) more than 30% longer than the patellar length (solid white line).

sequences and with helical CT scanning by having the tube continually spin. The images are then placed in a cine loop for continuous viewing of patellar motion.

What the Referring Physician Needs to Know ■

The position of the patella on lateral and axial radiographs and whether the axial position changes with flexion or quadriceps contraction.

Excessive Lateral Pressure Syndrome and the Patellofemoral Pain Syndrome Prevalence Patellofemoral pain syndrome (PFPS) is a common entity, affecting 15% to 33% of adults and 21% to 45% of adolescents. It is more common in girls,44 but it may represent a conglomeration of painful patellofemoral disorders rather than being a specific entity. Excessive lateral pressure syndrome (ELPS) also affects both adolescents and adults,34 but its prevalence is unknown, and some patients

■ FIGURE 26-27 CT of patellar tracking. A, Axial CT image with the knee in full extension and without quadriceps contraction shows lateral subluxation and tilt of the patella. B, Axial CT in the same patient with 30 degrees of knee flexion and without quadriceps contraction shows that the patella has engaged the femoral trochlear groove and realigned itself. C, Axial CT scan in the same patient with 30 degrees of knee flexion and active contraction of the quadriceps muscles shows no change in alignment of the patella compared with B.

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with ELPS may be grouped into the more general group of those with PFPS.

Biomechanics The biomechanics of PFPS is unknown but may be related to increased contact stress across the patellofemoral joint. In ELPS, imbalance of the soft tissue restraints resulting from either a lax medial retinaculum or tight lateral retinaculum leads to lateral patellar tilt, without subluxation, causing increased contact stress at the lateral aspect of the patellofemoral joint.

Manifestations of the Disease Radiography Axial views of the patella in ELPS show a lateral tilt of the patella, usually without lateral subluxation (Fig. 26-28). The lateral patellofemoral joint space may be narrowed, and the tilt does not change with knee flexion.34 Patellofemoral alignment in the PFPS is typically normal on axial radiographs but may demonstrate patella alta on the lateral view in some cases.

■ FIGURE 26-29 Excessive lateral pressure syndrome. Axial, fatsuppressed, T2-weighted MR image shows lateral tilt of the patella with loss of articular cartilage overlying the lateral patellar facet (white arrow). Cartilage remains overlying the medial patellar facet (black arrow).

Magnetic Resonance Imaging Axial images in ELPS show a lateral tilt of the patella, and resultant degenerative changes manifest as loss of cartilage over the lateral patellar facet, subchondral fibrocystic change in the lateral patellar facet, and edema in the lateral side of the patella (Fig. 26-29). MRI of patients with PFPS is usually normal; one study45 showed a marginally significant trend toward lateral subluxation of the patella but there was enough overlap with control groups to make the finding clinically useless. Even after 7 years of follow-up, two thirds of patients with PFPS do not have abnormalities on MRI.46

Differential Diagnosis Causes of chronic anterior knee pain are myriad and include ELPS, PFPS, patellar malposition, jumper’s knee,

OSD, SLJS, chondromalacia patellae, bipartite patella, medial plica, and abnormalities of Hoffa’s fat pad.

Synopsis of Treatment Options Medical Treatment Conservative treatment of PFPS consists of physical therapy to strengthen the quadriceps muscles. Taping of the patella, to correct malalignment, has had mixed success, with some studies reporting improvement in symptoms47 and others not.48 The controversy may arise from the fact that the underlying abnormality may not have been the same in all patients with the diagnosis of PFPS. MRI of patients with patellar taping has shown a slight difference in position of the patella compared with the untaped patient.49

Surgical Treatment Surgical treatment of ELPS consists of release of the lateral retinaculum.

Patellar Dislocation Biomechanics

■ FIGURE 26-28 Excessive lateral pressure syndrome. Axial radiograph of the knee shows lateral tilt and subluxation of the patella. There is narrowing of the lateral aspect of the patellofemoral compartment (large white arrow) with secondary degenerative subchondral fibrocystic change (black arrow) and degenerative osteophytes (small white arrows).

Lateral dislocation of the patella is the result of a rotational force on the flexed knee in which the femur internally rotates on the fixed tibia. This may occur during a cutting maneuver or when landing badly after some type of jumping maneuver. The patella usually spontaneously reduces, and the patient does not know that it had dislocated but knows that he or she “twisted the knee” and that it now hurts. Certain anatomic conditions may predispose the patella to dislocation, such as a high-riding patellar position, a shallow femoral trochlear groove, lateral tilt of the patella, and an increased Q angle. The Q angle is formed by the intersection of a line drawn between the anterior superior

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iliac spine of the pelvis and the midpoint of the patella and a line drawn between the midpoint of the patella and the tibial tubercle. Normally, this angle is about 15 degrees; it is increased in knee valgus, lateralization of the tibial tubercle, and internal rotation of the femur.50–53

Pathology There is a spectrum of soft tissue, osseous, and chondral injury. The medial retinaculum may partially tear or rupture or avulse its patellar attachment. The vastus medialis oblique muscle may partially tear. As the patella dislocates over the lateral femoral condyle, a piece of cartilage may be sheared from the lateral patella facet and the lateral retinaculum may be stripped from its femoral and tibial attachments. As the patella spontaneously reduces, it may impact the lateral aspect of the lateral femoral condyle, producing bone bruises in the medial aspect of the patella and lateral side of the lateral femoral condyle or shearing off cartilage from the medial patellar facet.

Manifestations of the Disease Radiography An axial view of the knee (Merchant or sunrise) after spontaneous reduction may show medial soft tissue swelling. A small osseous fragment may be present adjacent to the medial side of the patella if the medial retinaculum avulsed from the patella rather than tore. The patella may be laterally tilted or subluxed, and the nonreduced patella will be lateral to the lateral femoral condyle.

■ FIGURE 26-30 Lateral patellar dislocation. Axial, fat-suppressed, T2-weighted MR image shows offset bone bruises in the medial aspect of the patella (long white arrow) and in the lateral aspect of the lateral femoral condyle (short white arrow), a pathognomonic sign of patellar dislocation. The medial retinaculum (black arrow) is mildly sprained and manifest as mild contour irregularity and mild surrounding high signal intensity edema.

Ultrasonography

Magnetic Resonance Imaging 54,55

Bone bruises cannot be seen on ultrasound evaluation, but ultrasonography can demonstrate the injury of the medial retinaculum as either discontinuous rupture or thickening or thinning and loss of the normal fibrillary appearance in partial tearing.

Axial, fat-suppressed, T2-weighted MR images may show pathognomonic offset bone bruises in the medial aspect of the patella and the lateral aspect of the lateral femoral condyle (Fig. 26-30); but in patients with such forceful dislocation that the medial retinaculum has ruptured completely, bone bruises are not present because there is no restraining medial tissue to bring the patella back into place (Fig. 26-31). In these patients, the patella remains dislocated or subluxed over the lateral femoral condyle. Partial tearing of the medial retinaculum is demonstrated as thickening, with internal and surrounding high signal intensity (see Fig. 26-30). Tear of the distal aspect of the vastus medialis oblique muscle is visualized as feathery high signal intensity within the muscle on T2-weighted sequences (see Fig. 26-31), and edema may be present around the medial femoral condyle at the site of stripping of the medial patellofemoral ligament.54,55 Soft tissue edema may be present laterally if the lateral retinaculum is stripped. The infrapatellar fat pad may also show signs of injury (Fig. 26-32). In one series, the fat pad was abnormal in all 18 cases of patellar dislocation, with 17 knees having diffuse edema in the fat pad, 16 knees having a shear injury of the fat pad from the inferior pole of the patella, and 12 knees having fluid-filled clefts within the fat pad. In nine cases the damage to the fad pad was so severe as to make the fat pad look like an intra-articular loose body.56

■ FIGURE 26-31 Lateral patellar dislocation. Axial, fat-suppressed, T2-weighted MR image shows rupture of the medial retinaculum (black arrow) from its attachment on the medial aspect of the patella and feathery high signal intensity edema in the vastus lateralis muscle (white arrow) representing muscle tear. The patella is laterally subluxed and bone bruises are absent.

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Biomechanics Bipartite patellae are usually asymptomatic but can become painful due to stress across the synchondrosis between the ossicle and the patella resulting from repetitive pull by the vastus lateralis muscle.59 The DDP is also usually asymptomatic but may occasionally be painful.

Clinical Presentation In the case of a symptomatic bipartite patella, the patient’s pain can be elicited by tapping over the symptomatic ossicle. The symptomatic DDP may have lateral patellar tenderness.

Manifestations of the Disease Radiography Anteroposterior and Merchant views of a bipartite patella show the separate ossicle, located at the superolateral aspect of the patella. The DDP appears as an oval or round lucency with a sclerotic rim on lateral, anteroposterior or Merchant radiographs, located at the subarticular surface of the upper outer aspect of the patella. ■ FIGURE 26-32 Fat pad injury. Sagittal, proton density–weighted MR sequence after lateral patellar dislocation shows disruption of the normal fat pad morphology (black arrows) due to shear injury. Note the bone bruise within the patella (white arrow).

What the Referring Physician Needs to Know ■ ■

Whether the medial retinaculum is ruptured Whether a piece of patellar or femoral articular cartilage has sheared off

Bipartite Patella and Dorsal Defect of the Patella Anatomy

Magnetic Resonance Imaging Axial images are the most useful for evaluating the bipartite patella. The asymptomatic bipartite patella has normal marrow signal intensity, thin high signal intensity between the accessory ossicle and the patella, and an underlying layer of normal-appearing articular cartilage that covers the posterior surfaces of both bones (Fig. 26-33). The symptomatic bipartite patella may demonstrate high signal intensity edema in the synchondrosis between the ossicle and patella, may show edema in the bones on either side of the synchondrosis,60 and may show an irregular contour of the articular cartilage with internal signal intensity changes. The signal intensity of the DDP is usually low to intermediate on both T1- and T2-weighted sequences. The overlying cartilage is usually intact but may be fissured (Fig. 26-34).61

A bipartite patella is a normal variant in which there is a separate ossification center of the upper, outer quadrant of the patella but the underlying articular cartilage surface is confluent over both the patella and the separate fragment. The dorsal defect of the patella (DDP) also occurs in the upper outer aspect of the patella and the overlying cartilage is also usually intact, but its origin as either a normal variation in ossification or a chronic traumatic lesion due to pull of the vastus lateralis muscle is unknown.57

Synopsis of Treatment Options

Prevalence

The iliotibial band (ITB) is a long fibrous tract that originates at the level of the hip and is composed of fusion of the aponeuroses of the gluteus maximus, gluteus medius, and tensor fascia lata muscles. It courses distally to insert at the lateral aspect of the knee; it has a deep layer that attaches to the lateral femoral condyle and a superficial layer that inserts on Gerdy’s tubercle of the tibia.64,65

The bipartite patella is present in approximately 2% of the population and is usually bilateral. The DDP is present in less than 1% of the population, most often in adolescents; it affects males and females equally and is bilateral in up to 30% of cases.58

Surgical options for the symptomatic bipartite patella that fails to respond to conservative measures such as rest include excision62 and release of the vastus lateralis attachment.63

ILIOTIBIAL BAND Anatomy

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■ FIGURE 26-33

Bipartite patella. A, Coronal, fat-suppressed, T2-weighted MR image shows the bipartite piece (B) in the upperouter aspect of the patella. Thin high signal intensity is present in the synchondrosis between the bipartite fragment and the patella (black arrow). Fibers of the vastus lateralis (white arrow) insert on the bipartite piece. B, Axial, fat-suppressed, T2-weighted MR image shows cartilage overlying the patella and bipartite piece (B). Mild signal heterogeneity is present in the overlying cartilage (white arrow).

■ FIGURE 26-34

Dorsal defect of the patella. A, Sagittal, proton density–weighted MR image shows the dorsal defect involving the subarticular aspect of the patella (white arrow). B, Axial, fat-suppressed T2-weighted MR image shows the defect (arrow) with intermediate signal intensity within it and mild heterogeneity in the cartilage overlying it.

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Prevalence

Ultrasonography

Iliotibial band friction syndrome may be seen in longdistance runners, bicyclists, and rowers.66,67

The ITB is well seen sonographically as a thin echogenic fibrillar structure. The ITB usually is normal in appearance in ITB friction syndrome, but there may be effacement of adjacent fat planes at the level of the femoral condyle due to edema or mild thickening and heterogeneity of the ITB itself.

Biomechanics This is an overuse phenomenon in which compression of the fat between the ITB and the lateral femoral condyle67 occurs during repetitive flexion and extension of the knee, leading to painful inflammation.68,69 Pain is maximal at 30 degrees of knee flexion70,71 because as the knee flexes to 30 degrees the tibia internally rotates and brings the ITB against the lateral femoral condyle, compressing the intervening fat that is well innervated and vascularized; as the knee extends the tibia rotates externally, moving the ITB away from the condyle and releasing the compressed fat.

Manifestations of the Disease Magnetic Resonance Imaging Coronal, fat-suppressed T2-weighted MR images are the most useful and demonstrate ill-defined high signal intensity edema between the ITB and lateral femoral condyle and occasionally superficial to the ITB (Fig. 26-35).70,71 A focal fluid collection may exist between the ITB and the lateral femoral condyle owing to adventitial bursa formation.71 The ITB itself may be thickened or normal.72 The accuracy of MRI for diagnosing ITB friction syndrome is 86% to 95%.65,73

POPLITEUS AND BICEPS FEMORIS MUSCLES AND TENDONS (THE POSTEROLATERAL CORNER) Anatomy The posterolateral corner of the knee is stabilized by a complex combination of ligaments and tendons. Static stabilization is provided by the fibular collateral ligament, the arcuate ligament, the popliteus tendon, the popliteofibular ligament, and the fabellofibular ligament. Dynamic stabilization is provided by the popliteus muscle, biceps femoris muscle, and lateral head of the gastrocnemius muscle. The distal tendon of the biceps femoris and the fibular collateral ligament blend together at their insertion on the fibular head to form the conjoined tendon.74–76 Of all these stabilizers, the fibular collateral ligament, popliteofibular ligament, and popliteus muscle and tendon are the most important.77 The popliteus muscle originates at the posteromedial aspect of the proximal tibia, in the deep layer of the posterior compartment of the leg, and its tendon courses superolaterally to insert on popliteus sulcus at the lateral aspect of the lateral femoral condyle. The action of the popliteus muscle is to externally rotate the femur at the initiation of knee flexion, thus unlocking the knee from full extension. The popliteus tendon has an attachment to the fibular head, called the popliteofibular ligament, which is one of the static stabilizers of the posterolateral corner, and has attachments to the posterior horn of the lateral meniscus, called the posterosuperior and anteroinferior popliteomeniscal fascicles, which form an oblique tunnel called the popliteal hiatus, through which the popliteus tendon courses on its way to its attachment on the lateral femoral condyle.78 The popliteomeniscal fascicles act in concert with the meniscofemoral ligaments of Humphry and Wrisberg, which attach to the root of the posterior horn of the lateral meniscus, to help to control motion of the posterior horn of the lateral meniscus during knee flexion.79

Prevalence

■ FIGURE 26-35 Iliotibial band friction syndrome. Coronal, fatsuppressed, T2-weighted MR image shows high signal intensity edema (black arrow) deep to the iliotibial band (white arrows).

The normal fibular collateral ligament, biceps femoris tendon, and popliteus muscle and tendon are consistently visualized with MRI. However, the normal popliteofibular ligament was only seen in 57% of cases in one series.80 The normal popliteomeniscal fascicles are almost always routinely seen on sagittal MR images: in a study of 66 knee MR examinations both the superior and inferior fascicles were identified in 64 cases (97%), either together on the same imaging slice or individually on adjacent images.81 The fascicles were better appreciated on T2-weighted images than proton density–weighted images, but the

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presence or absence of a joint effusion had no effect on the conspicuity of the fascicles. In a series of 2412 knee MRI examinations of patients with knee pain, injury of the popliteus muscle or tendon was present in 24 (1%).82 In a different series, popliteus muscle or tendon injuries were present in 53% and distal biceps tendon injuries were present in 10% of knees with posterolateral corner injuries, representing 3% and 0.6%, respectively, of 481 knees imaged for the evaluation of internal derangement and injury.75

Biomechanics Isolated injury of the posterolateral structures is due to pure hyperextension, but this is unusual. More often the mechanism of injury is a combination of hyperextension with either varus force or external rotation of the tibia, leading to injury of the posterolateral stabilizers and a variable combination of injury of other structures, such as the posterior cruciate ligament, anterior cruciate ligament, medial collateral ligament, menisci, and bone bruises.74,75,77,83 The peroneal nerve may also be injured by the offending mechanism of injury.74,77

Manifestations of the Disease Radiography Injury to the posterolateral stabilizers is suggested on radiographs by the “arcuate sign,” an avulsion fracture of the fibular head (Fig. 26-36),84 representing the avulsed attachment of the biceps femoris tendon and fibular collateral ligament. Associated injuries that have been noted in patients with this sign at subsequent MRI or surgery involve the cruciate ligaments, popliteofibular ligament, arcuate ligament, and menisci, as well as bone bruises in

■ FIGURE 26-37 Rupture of the biceps femoris tendon. Coronal, fatsuppressed, T2-weighted MR image shows the retracted and balled-up biceps femoris tendon (large arrow), with high signal intensity edema (small arrow) in the gap.

the anterior aspects of the medial femoral condyle and medial tibial plateau.85–87 Thus, this small avulsion fracture of the fibular head indicates major soft tissue injury and internal derangement.

Magnetic Resonance Imaging

■ FIGURE 26-36 Arcuate sign. Anteroposterior radiograph of the knee after dislocation shows a small displaced fragment of bone (white arrow) representing avulsion of the biceps femoris tendon and fibular collateral ligament from the fibular head. Note also the lateral subluxation of the tibia relative to the femoral condyles.

Injury is best assessed on fat-suppressed T2-weighted MR images in a search for the following: soft tissue edema surrounding these structures, which suggests mild sprain; thickening or thinning of these structures with internal high signal intensity and surrounding edema, suggesting moderate sprain; and frank discontinuity of these structures, indicating rupture (Fig. 26-37).75 In a prospective study of 20 patients with posterolateral injury and subsequent surgical confirmation, MRI had 94% sensitivity and 100% specificity for identifying the injured fibular collateral ligament and 69% sensitivity and 68% specificity for the injured popliteofibular ligament.65 Coronal images may be optimized by using an oblique plane oriented along the course of the fibular collateral ligament.65,88 Injury of the popliteus muscle almost always occurs at the musculotendinous junction or in the muscle belly75,82 and appears as feathery high signal intensity in the muscle on T2-weighted images, disruption of muscle fibers, and swelling of the muscle (Fig. 26-38). These injuries are usually part of a larger spectrum of injury to the other posterolateral stabilizers, the medial collateral ligament, cruciate ligaments, menisci, and osteochondral surfaces.75,82 Cases of isolated popliteus tendon rupture or avulsion have been reported and describe a discontinuous appearance of the tendon, with variable degrees of retraction

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■ FIGURE 26-40 Popliteus tendon rupture. Longitudinal ultrasound image of the posterolateral aspect of the knee shows the ruptured tendon edge (black arrow) with a small echogenic piece of avulsed bone (white arrow), in a different patient than Figure 26-39. The cortex of the popliteus sulcus is seen (small white arrow). (Courtesy of Dr. Ronald Adler, Hospital for Special Surgery, New York, NY.)

■ FIGURE 26-38 Popliteus muscle injury. Sagittal, fat-suppressed, T2weighted MR image shows feathery high signal intensity edema within the popliteus muscle (arrows).

a secondary sign of tear of the posterior horn of the lateral meniscus itself.94

Ultrasonography of the torn end.89–91 There is often a small osteochondral fragment with the avulsed tendon (Fig. 26-39).91 Tears of the popliteomeniscal fascicles are a form of meniscocapsular separation involving the posterior horn of the lateral meniscus. These tears are rare and often overlooked on MRI.92,93 The affected fascicles are disrupted on sagittal images.92 A disrupted, distorted, or thickened superior popliteomeniscal fascicle may also be

The distal biceps femoris tendon, fibular collateral ligament, and popliteus tendon all normally appear as echogenic fibrillar structures. Mild sprain or strain is manifested as effacement of surrounding fat planes by edema and alterations in echogenicity, with more extensive partial tears showing changes in the thickness of the structure. Rupture is focal discontinuity, with or without retraction (Fig. 26-40).

■ FIGURE 26-39 Popliteus tendon rupture. A, Coronal, proton density–weighted MR image shows the ruptured and discontinuous popliteus tendon (white arrow) with a possible small bony avulsion fragment (black arrow). B, Axial, fat-suppressed, T2-weighted MR image in the same patient shows high signal intensity edema and lack of a discernable tendon (arrow). C, Axial CT image in this same patient shows the small avulsed fragment of bone within the popliteus sulcus (arrow).

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Differential Diagnosis Injury to these stabilizers can be missed at physical examination, especially in the presence of injury of other ligaments such as the ACL and PCL. In one series of 30 patients with posterolateral corner injury, most of whom had accompanying variable injuries of the ACL, MCL, menisci, and PCL, only three instances of posterolateral injury were clinically suspected.75 Isolated rupture of the popliteus tendon usually presents as pain posterolaterally. Mild instability may be present89 but is usually absent.90,91 Patients with isolated injury of the popliteomeniscal fascicles may present with vague posterolateral pain and locking.92,93 The diagnosis may be suggested on physical examination by placing the patient’s knee in a “figure of 4” position in which the ankle of the affected side is placed on the knee of the contralateral side, thus putting the symptomatic knee in flexion and external rotation. A varus force is then applied by pushing on the affected knee, reproducing the symptoms.93

Synopsis of Treatment Options The stable knee with an isolated injury of the popliteus tendon may not need repair,91 whereas the unstable knee is usually treated surgically. Unrecognized posterolateral instability can lead to failure of subsequent anterior and posterior cruciate ligament reconstruction.75 Tears of the popliteomeniscal fascicles are treated surgically.92,93

What the Referring Physician Needs to Know ■

The status of the popliteus tendon and muscle, biceps femoris tendon, and ligaments of the posterolateral corner.

HAMSTRINGS Anatomy The hamstring group is composed of the biceps, semimembranosus, and semitendinosus muscles. The long head of the biceps muscle and the semimembranosus and semitendinosus muscles originate from the ischial tuberosity of the pelvis, and the short head of the biceps muscle originates from the femoral shaft. The distal biceps tendon inserts on the fibular head after joining with the fibular collateral ligament, the semimembranosus tendon inserts on the posterior aspect of the medial side of the proximal tibia, and the semitendinosus tendon inserts on the anterior aspect of the medial side of the proximal tibia as one of the pes anserinus tendons (see later).

Prevalence The biceps femoris is the most commonly injured hamstring muscle, accounting for 83% of injuries in one series in Australian Rules football players, using MRI to depict the injury, followed by the semimembranosus with 7% and the semitendinosus with 5%; 5% of injuries involved

K E Y P O I N T: H A M S T R I N G S ■

The extent of the tear, either in length or volume, is a good predictor of the person’s time to return to competition.

more than one muscle.95 In a different series using both MRI and ultrasonography, the biceps was affected in 80% of patients, the semimembranosus in 14%, and the semitendinosus in 6%.96 In a clinical study of professional soccer players in England, the biceps was also the most commonly injured hamstring, occurring in 53% of injuries, followed by the semitendinosus in 16% and the semimembranosus in 13%, with 18% of injury locations unspecified.97 Older players (>22 years old) were more often injured than younger (17- to 22-year-old) players, a finding also seen in other series.98

Biomechanics In one series 120 patients sustained hamstring injury during soccer, 32 with “athletics,” 17 with cricket, and 10 with water skiing; in soccer, the majority of hamstring injuries occur while running, with only 7% due to playerto-player contact.97 Muscle strain is related to the extreme tensile forces generated during sprinting. Susceptible muscles are those that are composed of a high proportion of type 2 muscle fibers because type 2 fibers produce a more powerful contraction than type 1 fibers and muscles that cross two joints and have more than one head of origin (such as the biceps femoris), because the forces generated by the muscle contraction are more complex.99 Muscle fatigue also contributes to injury, with 47% of injuries in professional soccer players occurring toward the end of each half of play.97 Lastly, previous hamstring injury is a risk factor for repeat injury.97

Pathology Tear of the hamstrings most often involves the musculotendinous junction, occurring in 52% to 76% of cases,95,96,100 followed by the myofascial junction of the epimysium in 35% of cases.95,96 Avulsion of the proximal or distal tendons themselves is rare, with 16 cases of proximal tendon avulsion, one case of distal biceps avulsion, and three cases of distal semitendinosus tendon avulsion in a series of 170 patients.96

Manifestations of the Disease Magnetic Resonance Imaging Mild strain is manifest as feathery high signal intensity edema or hemorrhage on T2-weighted images, usually along the central tendon (the musculotendinous junction) or at the surface of the muscle or along intramuscular fascial planes (the epimysium). Moderate strain demonstrates disruption of muscle fibers and may have a focal high signal intensity hematoma. Severe strain may demonstrate disruption of the central tendon (Fig. 26-41).

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Avulsion is manifest as a wavy discontinuous tendon. MRI shows no abnormality in 18% to 31% of patients with clinical hamstring injury.98,101

Ultrasonography The sonographic appearance of muscle injury is hypoechoic edema, typically adjacent to the linear echogenic tendon. Disruption of the muscle fibers is characterized by loss of the pennate architecture of the muscle. Intramuscular hemorrhage may appear hyperechoic.95,96 MRI is more sensitive than ultrasonography for detecting mild muscle strain because of its greater soft tissue contrast.96 Ultrasonography was also less accurate than MRI for diagnosing proximal hamstring avulsion because the presence of mixed echogenicity hematomas made detection of the avulsed tendon difficult.96 In a series of hamstring injuries imaged with both MRI and ultrasonography, the abnormalities always appeared larger on MRI because of the greater soft tissue contrast with consequent better conspicuity of muscle edema.95

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length of the tear on MRI was the best predictor of time to return to competition in one study.95 In a different study the percentage of abnormal muscle area and the volume of muscle injured correlated with the number of days lost from competition.100 The risk of recurrent hamstring injury increases with increased size of the initial injury; recurrence risk is over twofold if the transverse size of the injury is 55% or more of the muscle or if the volume of injury is more than 21.8 mL.103 The occurrence of hamstring injuries was reduced by a training program consisting of stretching of the muscle while it is fatigued, sport-specific training drills, and increasing the amount of high-intensity anaerobic training.104

What the Referring Physician Needs to Know ■

The muscle involved, the location of the injury within the muscle, and the size of the tear.

Synopsis of Treatment Options The treatment of hamstring strain is usually conservative, with the important question concerning professional or elite athletes being time until return to competition. Verrall and associates found that patients without MRI evidence of injury returned to competition sooner than those with positive MRI examinations.102 In patients with positive MRI or sonographic examinations, longitudinal

CALF Anatomy The plantaris muscle, gastrocnemius muscle, and soleus muscle are located in the superficial posterior compartment of the leg and comprise the triceps surae. The gastrocnemius muscle is the most superficial; it has medial

■ FIGURE 26-41 Biceps femoris tear. A, Coronal, proton density–weighted MR image shows focal disruption of the biceps femoris tendon (white arrow) with feathery high signal intensity edema within the muscle (black arrow). B, Axial, fat-suppressed, T2-weighted MR image shows the feathery high signal intensity edema (arrow) within the torn muscle. (Courtesy of Dr. Douglas Mintz, Hospital for Special Surgery, New York, NY.)

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and lateral heads arising from the posterior aspects of the respective femoral condyles and becomes tendinous about midway down the leg, merging with the fibers of the soleus muscle to become the Achilles tendon. The soleus muscle is deep to the gastrocnemius and arises from the posterior aspects of the proximal tibia and fibula. The plantaris muscle arises from the lateral femoral condyle, superior and medial to the origin of the lateral head of the gastrocnemius muscle; the plantaris muscle belly is short and small and tapers to a long tendon at the level of the proximal tibia. The plantaris tendon courses medially, running between the medial head of the gastrocnemius muscle and soleus muscle, and along

K E Y P O I N T: C A L F ■

Tears of the medial gastrocnemius muscle are most often responsible for the clinical syndrome of “tennis leg.”

the medial aspect of the Achilles tendon, to insert on the calcaneus. Thus, both the gastrocnemius and plantaris muscles span both the knee and ankle joints. The plantaris muscle is anatomically inconstant, being absent in 7% to 20% of people.105

Biomechanics “Tennis leg” refers to tear of the medial gastrocnemius muscle or plantaris muscle. Both muscles are composed of type 2 (fast) muscle fibers and cross two joints, all of which are risk factors for injury.105 The actions of dorsiflexion of the foot and extension of the knee can cause overstretching of either muscle.106 Patients report acute spontaneous pain in the calf, often associated with a popping sensation. In one series of 30 patients, symptoms occurred while playing soccer in 22 cases and during tennis in 8 cases.107 However, injury may also occur during routine activity.

common in the series of 65 patients reported by Bianchi and associates.108 Injury of the plantaris may affect the muscle, musculotendinous junction, or the tendon itself.109,110 In Helms and colleagues’ series of 15 patients, 3 had rupture at the musculotendinous junction and the rest had muscle strains; 10 of the patients with plantaris muscle strains also had tears of the anterior cruciate ligament.109

Manifestations of the Disease Magnetic Resonance Imaging T2-weighted sequences are most useful for imaging muscle injury. Partial tears demonstrate feathery high signal intensity in the muscle. Larger partial tears demonstrate focal disruption of the muscle, often with high signal intensity hematomas; and ruptures are manifested as muscle discontinuity, usually at the musculotendinous junction and usually with surrounding high signal intensity edema or hemorrhage (Fig. 26-42).

Ultrasonography Partial tear of the medial head of the gastrocnemius muscle appears as focal disruption of the pennate appearance of the musculotendinous junction of the muscle or as anechoic edema/hemorrhage tracking along the central tendon (Fig. 26-43), whereas rupture appears as complete discontinuity.105–108 The transverse plane is best for distinguishing the two. Often, an initially hypoechoic hematoma is present between the gastrocnemius and soleus muscles, which becomes echogenic over the course of 1 to 2 weeks.106,108 Kwak and colleagues106,107 also report the development of echogenic fibrous tissue between the torn muscle and tendon at 2 to 4 weeks after injury, as part of the healing process, with eventual bridging of the

Prevalence Tennis leg most often affects middle-age people, usually men, with an average age in one series of 39 years106 and of 45 years in another series,105 but its prevalence is unknown. Although injury of either the gastrocnemius or plantaris muscles may give rise to symptoms that are clinically regarded as “tennis leg,” it is the gastrocnemius muscle that is usually affected. In a series of 141 patients with clinical tennis leg examined with ultrasonography, 94 had injury of the medial head of the gastrocnemius muscle, 2 had plantaris tendon ruptures, and 1 had tear of the soleus muscle.105

Pathology Injury of the medial head of the gastrocnemius muscle may take the form of partial tear or complete rupture and occurs at the musculotendinous junction. Complete rupture was more common in the two series reported by Kwak and coworkers,106,107 whereas partial tear was more

■ FIGURE 26-42 Gastrocnemius tear. Axial, fat-suppressed, T2weighted MR image shows feathery high signal intensity edema (white arrow) within the medial aspect of the medial gastrocnemius muscle, with a heterogeneous hematoma (black arrow) located between the gastrocnemius muscle and deep fascia.

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■ FIGURE 26-43

Gastrocnemius tear. Longitudinal ultrasound of the calf shows a heterogeneous hematoma (arrows) within the gastrocnemius muscle (G). (Courtesy of Dr. Ronald Adler, Hospital for Special Surgery, New York, NY.)

tear. Similar hyperechoic scar was noted in the patients in Bianchi and associates’ series who were rescanned ultrasonographically 1 year or more after the initial injury.108 Plantaris rupture appears as tendinous discontinuity, with retraction of the echogenic tendon.105,110 A large hypoechoic hematoma is often present between the medial head of the gastrocnemius muscle and the soleus muscle.

Differential Diagnosis The differential diagnosis for acute pain in the calf is tennis leg, rupture of a Baker cyst, and deep venous thrombosis. In the series of 141 patients with clinical tennis leg, 30 had a fluid collection between the medial gastrocnemius muscle and soleus muscle (without visible injury of the muscles themselves), which the investigators considered as being either a hematoma or a ruptured Baker cyst, and 14 had deep venous thrombosis.105

Synopsis of Treatment Options Treatment is usually conservative and consists of rest, ice, elevation of the leg, and stretching exercises.106 Fasciotomy is performed only for those patients who develop compartment syndrome as a result of a large hematoma or muscle swelling.

What the Referring Physician Needs to Know ■

The muscle involved and the extent of injury.

SEMIMEMBRANOSUS AND PES ANSERINUS TENDONS (THE POSTEROMEDIAL CORNER) Anatomy The semimembranosus tendon has five distal slips; three of these slips (the anterior arm, the direct arm, the inferior arm) are attachments of the tendon to the tibia. The fourth slip, the capsular arm, blends with the posteromedial joint capsule, to form the posterior oblique

Injury of the semimembranosus tendon may accompany injury to the posteromedial joint capsule and result in anteromedial rotatory instability of the knee.

ligament,111–113 and the fifth slip forms the oblique popliteal ligament (of Winslow) of the posterior capsule, which is also reinforced by the medial limb of the arcuate ligament.112,113 The pes anserinus group consists of the confluence of the distal aspects of the three tendons: the sartorius, which originates on the anterior superior iliac spine of the pelvis; the gracilis, which originates from the inferior pubic ramus of the pelvis; and the semitendinosus, which originates on the ischial tuberosity. These three tendons pass superficial to the medial collateral ligament of the knee and insert on the medial side of the proximal tibia anterior to the medial collateral ligament. They also have aponeurotic extensions that blend with the adjacent superficial fascial layer of the knee (layer 1) to provide medial stability to the knee.114

Biomechanics The semimembranosus and pes anserinus tendons are flexors of the knee joint and assist in medial rotation of the tibia. They help to stabilize the knee, particularly during flexion, by acting in concert with the biceps femoris tendon laterally to balance rotational forces on the flexed knee.112 In addition, the capsular slips of the semimembranosus reinforce the posterior joint capsule and help to pull the posterior horn of the medial meniscus posteriorly during knee flexion, thus preventing it from being trapped between the medial femoral condyle and tibial plateau.112 The semimembranosus tendon may be injured by valgus stress, usually with external rotation of the femur, such as occurs during cutting maneuvers,115 similar to the mechanism of injury that produces injury of the anterior cruciate ligament. Such a mechanism may cause the semimembranosus tendon to avulse from the tibia with a small fragment of avulsed bone, almost always accompanied by tear of the periphery or meniscocapsular junction of the posterior horn of the medial meniscus.116 Less commonly, the semimembranosus tendon is ruptured in isolation.112,115 Injury to the posteromedial capsule, potentially leading to anteromedial rotatory instability of the knee, always involves the posterior oblique ligament and may also involve the semimembranosus tendon.113 Three patterns of injury have been described: (1) injury of the posterior oblique ligament and the contributing slip of the semimembranosus tendon, occurring in 70% of cases; (2) injury of the posterior oblique ligament with peripheral meniscal detachment, occurring in 30% of cases; and (3) injury of the posterior oblique ligament, tear of the semimembranosus tendon, and peripheral meniscal detachment.113 The

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most common sports causing posteromedial injury in the series were football, basketball, and skiing.113

Manifestations of the Disease Radiography A small fragment of bone may be seen occasionally on lateral radiographs, although there is some controversy regarding its cause. Both Yao and Lee and Chan and associates believe the fragment is due to an avulsed semimembranosus tendon.117,118 However, Vanek, in a series of cadaveric experiments, found that the fracture occurred proximal to the attachment site of the semimembranosus tendon and was more likely to be caused by varus force, external rotation, and anterior subluxation of the tibia after the anterior collateral ligament had ruptured than from an avulsion fracture.119

Magnetic Resonance Imaging Injury to the semimembranosus tendon is manifested as high signal intensity edema in the soft tissue of the posteromedial aspect of the knee on T2-weighted images.112,115 The ruptured tendon is wavy and may be discontinuous and retracted (Fig. 26-44). Edema may be present in the posteromedial aspect of the tibia either due to avulsion or due to impaction. The partially torn tendon may also demonstrate surrounding and internal edema. Tendinosis may appear as tendon thickening and mild signal heterogeneity (Fig. 26-45), and degenerative osseous changes such as bone irregularity and fibrocystic change may occur at the tibial insertion.112 Lastly, the bursa around the semimembranosus (the tibial collateral-semimembranosus bursa) may become inflamed, appearing as a distended saddleshaped collection around the tendon (see later). Injury of the pes anserinus tendons is rare,64 but the pes anserinus bursa, which is located between the pes anserinus and the medial collateral ligament, may become inflamed by overuse or a single traumatic event.

BURSAE Anatomy Bursae are synovial-lined sacs typically located between a tendon and bone or between two tendons to reduce friction. Anteriorly, the prepatellar bursa is located anterior to the patella, and the superficial and deep infrapatellar bursae are located anterior and posterior, respectively, to the distal aspect of the patellar tendon. Medially, the tibial collateral bursa is located within the medial collateral ligament between the superficial and deep fibers, and the pes anserinus bursa is located between the pes anserinus tendons superficially and the medial collateral ligament deeply. Posteriorly, the medial gastrocnemius-semimembranosus bursa (also called a Baker cyst) is located on the medial side of the posterior aspect of the knee, between the tendons of the semimembranosus and the medial gastrocnemius, forming a comma-shaped collection around the medial gastrocnemius muscle; the semimembranosus-tibial collateral ligament bursa forms an inverted U or

■ FIGURE 26-44 Semimembranosus rupture. Sagittal, proton density–weighted MR image shows rupture of the semimembranosus tendon without retraction (black arrow). There is marked thickening and abnormal signal within the distal aspect of the tendon (white arrow) and feathery high signal intensity indicating edema and hemorrhage within the distal aspect of the muscle (small black arrow). (Courtesy of Dr. Douglas Mintz, Hospital for Special Surgery, New York, NY.)

a saddle shape around the distal aspect of the semimembranosus tendon. Laterally, the iliotibial bursa is located between the distal aspect of the iliotibial band and the tibia, and the fibular collateral ligament/biceps femoris bursa is located superficial and anterior to the distal aspect of the fibular collateral ligament. None of the bursae around the knee connect to each other, and only the Baker cyst connects to the knee joint.

Prevalence The prevalence of Baker cysts in the general adult population, based on MRI, is 19%, with increased probability of having the cyst if there is also a joint effusion, meniscal tear, or degenerative joint disease.120 In patients with rheumatoid arthritis, the prevalence is higher, approaching 60%. In the general pediatric population, the prevalence is 6% and is unrelated to the presence of joint effusion or internal derangement of the knee.121 In children, these cysts do not communicate with the knee joint and are

K E Y P O I N T: B U R SA E ■

A distended or ruptured Baker cyst may mimic or cause deep venous thrombosis.

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■ FIGURE 26-45 Semimembranosus tendinosis. A, Axial, fatsuppressed, T2-weighted MR image shows thickening and intermediate signal intensity within the tendinotic semimembranosus tendon (arrow). B, Sagittal, proton density–weighted MR image in the same patient shows the thickened and high signal intensity mucinous degeneration (arrow). C, Coronal, proton density–weighted MR image shows the enlarged degenerated semimembranosus tendon (arrow). Incidentally noted is a parameniscal cyst (asterisk).

more properly referred to as popliteal cysts rather than Baker cysts. The prevalence of a distended pes anserinus bursa is 0.5%, and that of the semimembranosus-tibial collateral ligament bursa is 2%.122 The deep infrapatellar bursa is seen in 68% of routine knee MRI examinations.123

Biomechanics Because the bursae act to cushion the tendons about the knee, they are subject both to acute traumatic injury and to chronic repetitive stress and overuse. In addition, as synovial structures, they are subject to the same synovial disorders that affect the joint itself. Prepatellar bursitis is also called “housemaid’s knee,” because in the days when housemaids used to scrub floors on their hands and knees the irritation of the

patella rubbing against the hard surface of the floor would cause inflammation and distention of this bursa (Fig. 26-46). The symptomatic superficial infrapatellar bursa is called “preacher’s knee” because this bursa is compressed between the tibial tubercle and the wooden bench on which a preacher kneels (Fig. 26-47). The deep infrapatellar bursa may be distended due to abnormalities of the adjacent patellar tendon, such as Osgood-Schlatter disease (see Fig. 26-18).

Manifestations of the Disease Radiography When large, a bursa may appear as a soft tissue density mass (Fig. 26-48). Bursae located anteriorly or posteriorly will be best appreciated on a lateral view, whereas

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■ FIGURE 26-46 Housemaid’s knee. Sagittal, fat-suppressed, T2weighted MR image shows a distended prepatellar bursa (arrow) with internal debris and surrounding soft tissue edema. (Courtesy of Dr. Douglas Mintz, Hospital for Special Surgery, New York, NY.)

■ FIGURE 26-48 Housemaid’s knee. Lateral radiograph shows marked soft tissue fullness in the expected region of the prepatellar bursa (arrow) consistent with housemaid’s knee.

the medial and lateral bursae may be seen on a frontal view.

Magnetic Resonance Imaging

■ FIGURE 26-47 Preacher’s knee. Sagittal, proton density–weighted sequence shows a distended superficial infrapatellar bursa (arrow). Note also the degenerative change in the femoral condyle. (Courtesy of Dr. Douglas Mintz, Hospital for Special Surgery, New York, NY.)

A fluid-filled bursa appears as a well-defined mass with low signal intensity on T1-weighted images and with high signal intensity on T2-weighted images. Sometimes the bursa may be septated or loculated and it may contain debris or a frank cell-fluid level. The synovial wall is usually thin and imperceptible and does not enhance with intravenous gadolinium contrast, but it can be thickened and may enhance if there is an underlying synovial disorder such as rheumatoid arthritis or chronic irritation. A Baker cyst is best appreciated on axial MR images, appearing comma shaped, with its neck extending between the tendon of the medial gastrocnemius and the semimembranosus tendon (Fig. 26-49). When large, the cyst may track superiorly into the posterior aspect of the thigh or inferiorly into the calf, especially in patients with rheumatoid arthritis. The cyst may leak or rupture, which is best appreciated on axial fat-suppressed T2 weighted images as ill-defined soft tissue edema adjacent to the distal aspect of the cyst, thus exposing the surrounding tissue to irritative synovial fluid, which can cause severe pain and swelling. The pes anserinus bursa is located between the tendons of the pes anserinus and the distal aspect of the medial collateral ligament (Fig. 26-50).124 The semi-

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■ FIGURE 26-49 Baker cyst. A, Axial, fat-suppressed, T2-weighted MR image shows the comma-shaped cyst (asterisk) lying between the semimembranosus tendon (black arrow) and the tendon of the medial gastrocnemius muscle (white arrow). B, Sagittal, proton density– weighted MR image shows the Baker cyst (asterisks) around the gastrocnemius tendon (G) and the semimembranosus tendon (S).

■ FIGURE 26-50 Pes anserinus bursitis. A, Axial, fat-suppressed, T2-weighted MR image shows a multiloculated pes anserinus bursa (asterisks). It is deep to the sartorious (SA), gracilis (GR), and semitendinosus (ST) tendons and superficial to the medial collateral ligament (M) and the semimembranosus tendon (SM). Note that it is not related to the gastrocnemius tendon (G). B, Coronal, proton density–weighted MR image of the same patient shows the multiloculated cyst (asterisk) lying superficial to the medial collateral ligament (arrows).

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■ FIGURE 26-51

Semimembranosus-tibial collateral ligament (STCL) bursa. A, Axial, fat-suppressed, T2-weighted MR image shows the STCL bursa (asterisk) lying superficial to the semimembranosus tendon (black arrow), unrelated to the medial gastrocnemius tendon (white arrow). B, Sagittal, proton density–weighted MR image shows the STCL bursa (asterisks) surrounding the distal aspect of the semimembranosus tendon, whose insertion is tendinotic (arrow).

■ FIGURE 26-52 Tibial collateral ligament bursa. Coronal, fatsuppressed, T2-weighted MR image shows a heterogeneous, distended tibial collateral ligament bursa (white arrow) between the medial collateral ligament and the medial joint capsule. Joint fluid is present in the normal meniscosynovial recesses of the lateral aspect of the joint and should not be mistaken for bursae.

■ FIGURE 26-53 Baker cyst. Transverse sonographic image shows the comma-shaped cyst (asterisks) surrounding the tendon of the medial gastrocnemius (arrow).

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membranosus-tibial collateral ligament bursa is located along the medial side of the distal aspect of the semimembranosus tendon (Fig. 26-51) and can be distinguished from the Baker cyst by the fact that it is medial to the semimembranosus tendon, whereas the Baker cyst is lateral to the semimembranosus tendon and it should be distinguished from the pes anserinus bursa by the fact that the semimembranosus-tibial collateral ligament bursa is adjacent to the semimembranosus tendon and follows the tendon’s course.124,125 The tibial collateral ligament bursa, located within the medial collateral ligament, may mimic a meniscocapsular separation on coronal T2-weighted images if it is distended (Fig. 26-52).

Ultrasonography Sonographically, bursae are typically anechoic structures with thin imperceptible walls and posterior acoustic enhancement, but the appearance can be complicated by internal echogenic debris and a thick wall if there is chronic irritation or an underlying synovial disorder (Figs. 26-53 to 26-55).

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Differential Diagnosis When a Baker cyst is large, the patient may complain of pain or tightness in the back of the knee. If the cyst leaks or ruptures, the synovial fluid may irritate the surrounding tissue, which can cause severe pain and swelling, clinically mimicking a deep venous thrombosis. These cysts can also actually cause deep venous thrombosis either due to frank compression of the popliteal vein or to the irritative synovial fluid, causing a reactive thrombophlebitis. Pain and swelling on the medial side of the knee can be due to a distended pes anserinus bursa but may also be due to a large ganglion cyst or a large dissecting parameniscal cyst.

Synopsis of Treatment Options Treatment usually consists of rest and nonsteroidal antiinflammatory medications. Painful bursae can be aspirated and injected with cortisone using sonographic guidance.

PLICAE Anatomy Plicae are intra-articular folds of synovial tissue that persist as the fetal knee forms by cavitation. They occur in three typical locations: infrapatellar (the so-called ligamentum mucosum), which courses from the inferior pole of the patella through the infrapatellar fat pad in an oblique coronal plane, inserting either on the transverse meniscal ligament or on the roof of the intercondylar notch anterior to the anterior cruciate ligament (Fig. 26-56)126,127;

■ FIGURE 26-54

Housemaid’s knee. Extended field of view ultrasound image shows the distended prepatellar bursa (asterisk) containing mild internal debris, anterior to the patella (P). (Courtesy of Dr. Ronald Adler, Hospital for Special Surgery, New York, NY.)

■ FIGURE 26-55 Deep infrapatellar bursa. Longitudinal ultrasound image shows the anechoic distended deep infrapatellar bursa (asterisk) lying between the distal aspect of the patella tendon (arrows) and the anterior aspect of the tibia (T).

■ FIGURE 26-56 Infrapatellar plica. Sagittal, proton density–weighted MR image shows the infrapatellar plica (black arrow) extending from the inferior pole of the patella to the transverse meniscal ligament (white arrow).

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suprapatellar, which occurs in the suprapatellar recess in the horizontal plane (Fig. 26-57)128,129; and medial parapatellar, which arises from the medial side of the joint and courses toward the infrapatellar fad pad in the coronal plane (Fig. 26-58).130 They may be complete sheets of tissue extending entirely across the compartment in which they reside or may be incomplete.

Prevalence The prevalence of these synovial bands is variable, in part depending on the method of detection. In a study of 200 cadaveric knees, the most common plica was the infrapatellar plica, present in 65.5%, followed by the suprapatellar in 55.5% and the medial parapatellar in 24.5%.131 However, a series of 400 knee arthroscopies revealed the suprapatellar plica in 87%, the infrapatellar in 86%, and the medial plica in 72% of knees,132 whereas a series of MRI examinations of 66 knees demonstrated the medial plica in 70% of cases.130 The ligamentum mucosum was present in 90% of 50 knee MRI examinations.133

Biomechanics ■ FIGURE 26-57 Suprapatellar plica. Sagittal, fat-suppressed, T2weighted MR image shows a suprapatellar plica (arrow) outlined by fluid within the suprapatellar recess.

■ FIGURE 26-58

All three types can become symptomatic, causing anterior knee pain with or without snapping, but it is the medial type that is most often symptomatic. The medial plica can become symptomatic if it is complete, forming

Medial plica. A, Axial, fat-suppressed, T2-weighted MR image shows a thick medial plica (arrow) extending from the medial joint capsule to the infrapatellar fat pad, crossing over the medial femoral condyle. B, Sagittal, fat-suppressed, T2-weighted MR image of the same patient shows the longitudinal extent of the medial plica (arrow). Incidentally the patient has a tear of the posterior horn of the medial meniscus and degenerative change of the medial femoral condyle.

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KEY POINTS: PLICAE Medial and infrapatellar plicae may become symptomatic due to irritation. ■ A superior plica may become symptomatic if imperforate. ■

a shelf from the medial side of the joint capsule to the infrapatellar fat pad; it can then rub against the anterior aspect of the medial femoral condyle, becoming thickened, inflamed, and painful. This is typically an overuse injury, associated with such sports as running and bicycling. The infrapatellar plica may also be irritated by athletic activities,127 whereas the suprapatellar plica becomes symptomatic only if it is imperforate, becoming distended because of trapped synovial fluid.

Manifestations of the Disease Magnetic Resonance Imaging Because of their orientations, a medial plica is best seen on axial and sagittal images, the suprapatellar plica is best seen on sagittal and coronal images, and the infrapatellar plica is best seen on sagittal images. The medial and suprapatellar plicae are best appreciated on T2-weighted sequences, particularly if there is a joint effusion to outline the low signal intensity plica; if an effusion is absent, visualization of the plica is decreased.134 Although a symp-

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tomatic complete medial plica tends to be thickened due to the chronic irritation against the medial condyle, Boles and coworkers found no features of medial plicae on MRI that could predict which ones would get resected at arthroscopy.130 The symptomatic infrapatellar plica may also be thick and will display linear edema-like signal intensity in Hoffa’s fat pad.127 The suprapatellar plica may also become thickened; and if it is imperforate it may cause fluid in the suprapatellar recess to become trapped, clinically mimicking a mass.128,129

Differential Diagnosis The symptomatic plicae cause anterior knee pain, occasionally with clicking or snapping. Other causes of anterior knee pain are tears of the anterior horn of either meniscus, jumper’s knee, SLJS, OSD, excessive lateral pressure syndrome, and patellofemoral pressure syndrome.

Synopsis of Treatment Options If symptoms do not resolve with rest, the management is arthroscopic resection of the symptomatic plica.

What the Referring Physician Needs to Know ■

If a medial plica forms a complete shelf across the medial aspect of the knee.

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12. Khan KM, Bonar F, Desmond PM. Patellar tendinosis (jumper’s knee): findings at histopathologic examination, US, and MR imaging. Victorian Institute of Sports Tendon Study Group. Radiology 1996; 200:821–827. 13. Peace KA, Lee JC, Healy J. Imaging the infrapatellar tendon in the elite athlete. Clin Radiol 2006; 61:570–578. 14. Hoksrud A, Ohberg L, Alfredson H, Bahr R. Ultrasound-guided sclerosis of neovessels in painful chronic patellar tendinopathy: a randomized controlled trial. Am J Sports Med 2006; 34: 1738–1746. 15. Demirag B, Ozturk C, Yazici Z, Sarisozen B. The pathophysiology of Osgood-Schlatter disease: a magnetic resonance investigation. J Pediatr Orthop B 2004; 13:379–382. 16. Medlar RC, Lyne ED. Sinding-Larsen-Johansson disease: its etiology and natural history. J Bone Joint Surg Am 1978; 60:1113–1116. 17. Rosenberg ZS, Kawelblum M, Cheung YY. Osgood-Schlatter lesion: fracture or tendinitis? Scintigraphic, CT, and MR imaging features. Radiology 1992; 185:853–858. 18. Chung CB, Skaf A, Roger B, et al. Patellar tendon-lateral femoral condyle friction syndrome: MR imaging in 42 patients. Skeletal Radiol 2001; 30:694–697. 19. Jacobson JA, Lenchik L, Ruhoy MK. MR imaging of the infrapatellar fat pad of Hoffa. Radiographics 1997; 17:675–691. 20. Saddik D, McNally EG, Richardson M. MRI of Hoffa’s fat pad. Skeletal Radiol 2004; 33:433–444. 21. Wiberg G. Roentgenographic and anatomic studies on the femoropatellar joint. Acta Orthop Scand 1941; 12:319–410. 22. Starok M, Lenchik L, Trudell D, et al. Normal patellar retinaculum: MR and sonographic imaging with cadaveric correlation. AJR Am J Roentgenol 1997; 168:1493–1499.

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23. Hautamaa PV, Fithian DC, Kaufman KR, et al. Medial soft tissue restraints in lateral patellar instability and repair. Clin Orthop Relat Res 1998; (349):174–182. 24. Insall J, Salvati E. Patella position in the normal knee joint. Radiology 1971; 101:101–104. 25. Merchant AC, Mercer RL, Jacobsen RH, Cool CR. Roentgenographic analysis of patellofemoral congruence. J Bone Joint Surg Am 1974; 56:1391–1396. 26. Murray TF, Dupont JY, Fulkerson JP. Axial and lateral radiographs in evaluating patellofemoral malalignment. Am J Sports Med 1999; 27:580–584. 27. Masri BA, McCormack RG. The effect of knee flexion and quadriceps contraction on the axial view of the patella. Clin J Sport Med 1995; 5:9–17. 28. Al-Habbal GA, Lintner DM, Kohl HW 3rd. Effect of quadriceps contraction on tangential patellar radiography. Am J Knee Surg 2000; 13:132–136. 29. Beaconsfield T, Pintore E, Maffulli N, Petri GJ. Radiological measurements in patellofemoral disorders: a review. Clin Orthop Relat Res 1994; (308):18–28. 30. Laurin CA, Dussault R, Levesque HP. The tangential x-ray investigation of the patellofemoral joint: x-ray technique, diagnostic criteria and their interpretation. Clin Orthop Relat Res 1979; (144):16–26. 31. O’Donnell P, Johnstone C, Watson M, et al. Evaluation of patellar tracking in symptomatic and asymptomatic individuals by magnetic resonance imaging. Skeletal Radiol 2005; 34:130–135. 32. Tennant S, Williams A, Vedi V, et al. Patello-femoral tracking in the weight-bearing knee: a study of asymptomatic volunteers utilising dynamic magnetic resonance imaging: a preliminary report. Knee Surg Sports Traumatol Arthrosc 2001; 9:155–162. 33. McNally EG, Ostlere SJ, Pal C, et al. Assessment of patellar maltracking using combined static and dynamic MRI. Eur Radiol 2000; 10:1051–1055. 34. Elias DA, White LM. Imaging of patellofemoral disorders. Clin Radiol 2004; 59:543–557. 35. Grelsamer RP, Bazos AN, Proctor CS. Radiographic analysis of patellar tilt. J Bone Joint Surg Br 1993; 75:822–824. 36. Miller TT, Staron RB, Feldman F. Patellar height on sagittal MR imaging of the knee. AJR Am J Roentgenol 1996; 167:339–341. 37. Biedert RM, Gruhl C. Axial computed tomography of the patellofemoral joint with and without quadriceps contraction. Arch Orthop Trauma Surg 1997; 116:77–82. 38. Kujala UM, Osterman K, Kormano M, et al. Patellar motion analyzed by magnetic resonance imaging. Acta Orthop Scand 1989; 60:13–16. 39. Pinar H, Akseki D, Karaoglan O, Genc I. Kinematic and dynamic axial computed tomography of the patellofemoral joint in patients with anterior knee pain. Knee Surg Sports Traumatol Arthrosc 1994; 2:170–173. 40. Shellock FG, Mink JH, Deutsch AL, et al. Kinematic MR imaging of the patellofemoral joint: comparison of passive positioning and active movement techniques. Radiology 1992; 184:574–577. 41. Muhle C, Brinkmann G, Skaf A, et al. Effect of a patellar realignment brace on patients with patellar subluxation and dislocation: evaluation with kinematic magnetic resonance imaging. Am J Sports Med 1999; 27:350–353. 42. Dupuy DE, Hangen DH, Zachazewski JE, et al. Kinematic CT of the patellofemoral joint. AJR Am J Roentgenol 1997; 169:211–215. 43. Niitsu M. Kinematic MR imaging of the knee. Semin Musculoskelet Radiol 2001; 5:153–157. 44. Naslund J, Naslund UB, Odenbring S, Lundeberg T. Comparison of symptoms and clinical findings in subgroups of individuals with patellofemoral pain. Physiother Theory Pract 2006; 22:105–118. 45. MacIntyre NJ, Hill NA, Fellows RA, et al. Patellofemoral joint kinematics in individuals with and without patellofemoral pain syndrome. J Bone Joint Surg Am 2006; 88:2596–2605. 46. Kannus P, Natri A, Paakkala T, Jarvinen M. An outcome study of chronic patellofemoral pain syndrome: seven-year follow-up of patients in a randomized, controlled trial. J Bone Joint Surg Am 1999; 81:355–363. 47. Whittingham M, Palmer S, Macmillan F. Effects of taping on pain and function in patellofemoral pain syndrome: a randomized controlled trial. J Orthop Sports Phys Ther 2004; 34:504–510.

48. Kowall MG, Kolk G, Nuber GW, et al. Patellar taping in the treatment of patellofemoral pain: a prospective randomized study. Am J Sports Med 1996; 24:61–66. 49. Herrington L. The effect of corrective taping of the patella on patella position as defined by MRI. Res Sports Med 2006; 14:215–223. 50. Katchburian MV, Bull AM, Shih YF, et al. Measurement of patellar tracking: assessment and analysis of the literature. Clin Orthop Relat Res 2003; (412):241–259. 51. Insall J, Goldberg V, Salvati E. Recurrent dislocation and the highriding patella. Clin Orthop Relat Res 1972; 88:67–69. 52. Aglietti P, Insall JN, Cerulli G. Patellar pain and incongruence: I. Measurements of incongruence. Clin Orthop Relat Res 1983; (176):217–224. 53. Neyret P, Robinson AH, Le Coultre B, et al. Patellar tendon length—the factor in patellar instability? Knee 2002; 9:3–6. 54. Elias DA, White LM, Fithian DC. Acute lateral patellar dislocation at MR imaging: injury patterns of medial patellar soft-tissue restraints and osteochondral injuries of the inferomedial patella. Radiology 2002; 225:736–743. 55. Pope TL. MR imaging of patellar dislocation and relocation. Semin Ultrasound CT MR 2001; 22:371–382. 56. Apostolaki E, Cassar-Pullicino VN, Tyrrell PN, McCall IW. MRI appearances of the infrapatellar fat pad in occult traumatic patellar dislocation. Clin Radiol 1999; 54:743–747. 57. van Holsbeeck M, Vandamme B, Marchal G, et al. Dorsal defect of the patella: concept of its origin and relationship with bipartite and multipartite patella. Skeletal Radiol 1987; 16:304–311. 58. Safran MR, McDonough P, Seeger L, et al. Dorsal defect of the patella. J Pediatr Orthop 1994; 14:603–607. 59. Vanhoenacker FM, Bernaerts A, Van de Perre S, et al. MRI of painful bipartite patella. JBR-BTR 2002; 85:219. 60. Kavanagh EC, Zoga A, Omar I, et al. MRI findings in bipartite patella. Skeletal Radiol 2006; Dec 6 [Epub ahead of print]. 61. Sueyoshi Y, Shimozaki E, Matsumoto T, Tomita K. Two cases of dorsal defect of the patella with arthroscopically visible cartilage surface perforations. Arthroscopy 1993; 9:164–169. 62. Azarbod P, Agar G, Patel V. Arthroscopic excision of a painful bipartite patella fragment. Arthroscopy 2005; 21:1006. 63. Adachi N, Ochi M, Yamaguchi H, et al. Vastus lateralis release for painful bipartite patella. Arthroscopy 2002; 18:404–411. 64. Bencardino JT, Rosenberg ZS, Brown RR, et al. Traumatic musculotendinous injuries of the knee: diagnosis with MR imaging. Radiographics 2000; 20:S103–S120. 65. LaPrade RF, Gilbert TJ, Bollom TS, et al. The magnetic resonance imaging appearance of individual structures of the posterolateral knee: a prospective study of normal knees and knees with surgically verified grade III injuries. Am J Sports Med 2000; 28:191–199. 66. Rumball JS, Lebrun CM, Di Ciacca SR, et al. Rowing injuries. Sports Med 2005; 3:537–555. 67. Fairclough J, Hayashi K, Toumi H, et al. The functional anatomy of the iliotibial band during flexion and extension of the knee: implications for understanding iliotibial band syndrome. J Anat 2006; 208:309–316. 68. Farrell KC, Reisinger KD, Tillman MD. Force and repetition in cycling: possible implications for iliotibial band friction syndrome. Knee 2003; 10:103–109. 69. Orchard JW, Fricker PA, Abud AT, et al. Biomechanics of iliotibial band friction syndrome in runners. Am J Sports Med 1996; 24:375–379. 70. Murphy BJ, Hechtman KS, Uribe JW. Iliotibial band friction syndrome: MR imaging findings. Radiology 1992; 185:569–571. 71. Muhle C, Ahn JM, Yeh L. Iliotibial band friction syndrome: MR imaging findings in 16 patients and MR arthrographic study of six cadaveric knees. Radiology 1999; 212:103–110. 72. Ekman EF, Pope T, Martin DF, Curl WW. Magnetic resonance imaging of iliotibial band syndrome. Am J Sports Med 1994; 22:851–854. 73. Theodorou DJ, Theodorou SJ, Fithian DC, et al. Posterolateral complex knee injuries: magnetic resonance imaging with surgical correlation. Acta Radiol 2005; 46:297–305.

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74. Malone AA, Dowd GS, Saifuddin A. Injuries of the posterior cruciate ligament and posterolateral corner of the knee. Injury 2006; 37:485–501. 75. Miller TT, Gladden P, Staron RB. Posterolateral stabilizers of the knee: anatomy and injuries with MR imaging. AJR Am J Roentgenol 1997; 169:1641–1647. 76. Harish S, O’Donnell P, Connell D, et al. Imaging of the posterolateral corner of the knee. Clin Radiol 2006; 61:457–466. 77. Stannard JP, Brown SL, Robinson JT, et al. Reconstruction of the posterolateral corner of the knee. Arthroscopy 2005; 21:1051–1059. 78. Cohn AK, Mains DB. Popliteal hiatus of the lateral meniscus: anatomy and measurement at dissection of 10 specimens. Am J Sports Med 1979; 7:221–226. 79. Miller TT, Stein BE, Staron RB, et al. Relationship of the meniscofemoral ligaments of the knee to lateral meniscus tears: magnetic resonance imaging evaluation. Am J Orthop 1998; 27:729–732. 80. Munshi M, Pretterklieber ML, Kwak S, et al. MR imaging, MR arthrography, and specimen correlation of the posterolateral corner of the knee: an anatomic study. AJR Am J Roentgenol 2003; 180:1095–1101. 81. Johnson RL, De Smet AA. MR visualization of the popliteomeniscal fascicles. Skeletal Radiol 1999; 28:561–566. 82. Brown TR, Quinn SF, Wensel JP, et al. Diagnosis of popliteus injuries with MR imaging. Skeletal Radiol 1995; 24:511–514. 83. Yoon KH, Bae DK, Ha JH, et al. Anatomic reconstructive surgery for posterolateral instability of the knee. Arthroscopy 2006; 22:159–165. 84. Shindell R, Walsh WM, Connolly JF. Avulsion fracture of the fibula: the ‘arcuate sign’ of posterolateral knee instability. Nebr Med J 1984; 69:369–371. 85. Juhng SK, Lee JK, Choi SS, et al. MR evaluation of the “arcuate” sign of posterolateral knee instability. AJR Am J Roentgenol 2002; 178:583–588. 86. Lee J, Papakonstantinou O, Brookenthal KR, et al. Arcuate sign of posterolateral knee injuries: anatomic, radiographic, and MR imaging data related to patterns of injury. Skeletal Radiol 2003; 32:619–627. 87. Huang GS, Yu JS, Munshi M, et al. Avulsion fracture of the head of the fibula (the “arcuate” sign): MR imaging findings predictive of injuries to the posterolateral ligaments and posterior cruciate ligament. AJR Am J Roentgenol 2003; 180:381–387. 88. Yu JS, Salonen DC, Hodler J. Posterolateral aspect of the knee: improved MR imaging with a coronal oblique technique. Radiology 1996; 198:199–204. 89. Westrich GH, Hannafin JA, Potter HG. Isolated rupture and repair of the popliteus tendon. Arthroscopy 1995; 11:628–632. 90. Conroy J, King D, Gibbon A. Isolated rupture of the popliteus tendon in a professional soccer player. Knee 2004; 11:67–69. 91. Guha AR, Gorgees KA, Walker DI. Popliteus tendon rupture: a case report and review of the literature. Br J Sports Med 2003; 37:358–360. 92. Simonian PT, Sussmann PS, Wickiewicz TL, et al. Popliteomeniscal fasciculi and the unstable lateral meniscus: clinical correlation and magnetic resonance diagnosis. Arthroscopy 1997; 13:590–596. 93. LaPrade RF, Konowalchuk BK. Popliteomeniscal fascicle tears causing symptomatic lateral compartment knee pain: diagnosis by the figure-4 test and treatment by open repair. Am J Sports Med 2005; 33:1231–1236. 94. De Smet AA, Asinger DA, Johnson RL. Abnormal superior popliteomeniscal fascicle and posterior pericapsular edema: indirect MR imaging signs of a lateral meniscal tear. AJR Am J Roentgenol 2001; 176:63–66. 95. Connell DA, Schneider-Kolsky ME, Hoving JL, et al. Longitudinal study comparing sonographic and MRI assessments of acute and healing hamstring injuries. AJR Am J Roentgenol 2004; 183:975–984. 96. Koulouris G, Connell D. Evaluation of the hamstring muscle complex following acute injury. Skeletal Radiol 2003; 32: 582–589. 97. Woods C, Hawkins RD, Maltby S, et al. The Football Association Medical Research Programme: an audit of injuries in professional

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football—analysis of hamstring injuries. Br J Sports Med 2004; 38:36–41. Verrall GM, Slavotinek JP, Barnes PG, et al. Clinical risk factors for hamstring muscle strain injury: a prospective study with correlation of injury by magnetic resonance imaging. Br J Sports Med 2001; 35:435–439. Robinson P, White LM. The biomechanics and imaging of soccer injuries. Semin Musculoskelet Radiol 2005; 9:397–420. Slavotinek JP, Verrall GM, Fon GT. Hamstring injury in athletes: using MR imaging measurements to compare extent of muscle injury with amount of time lost from competition. AJR Am J Roentgenol 2002; 179:1621–1628. Schneider-Kolsky ME, Hoving JL, Warren P, Connell DA. A comparison between clinical assessment and magnetic resonance imaging of acute hamstring injuries. Am J Sports Med 2006; 34:1008–1015. Verrall GM, Slavotinek JP, Barnes PG, Fon GT. Diagnostic and prognostic value of clinical findings in 83 athletes with posterior thigh injury: comparison of clinical findings with magnetic resonance imaging documentation of hamstring muscle strain. Am J Sports Med 2003; 31:969–973. Verrall GM, Slavotinek JP, Barnes PG, et al. Assessment of physical examination and magnetic resonance imaging findings of hamstring injury as predictors for recurrent injury. J Orthop Sports Phys Ther 2006; 36:215–224. Verrall GM, Slavotinek JP, Barnes PG. The effect of sports specific training on reducing the incidence of hamstring injuries in professional Australian Rules football players. Br J Sports Med 2005; 39:363–368. Delgado GJ, Chung CB, Lektrakul N, et al. Tennis leg: clinical use study of 141 patients and anatomic investigation of four cadavers with MR imaging and US. Radiology 2002; 224:112–119. Kwak HS, Han YM, Lee SY, et al. Diagnosis and follow-up US evaluation of ruptures of the medial head of the gastrocnemius (“tennis leg”). Korean J Radiol 2006; 7:193–198. Kwak HS, Lee KB, Han YM. Ruptures of the medial head of the gastrocnemius (“tennis leg”): clinical outcome and compression effect. Clin Imaging 2006; 30:48–53. Bianchi S, Martinoli C, Abdelwahab IF, et al. Sonographic evaluation of tears of the gastrocnemius medial head (“tennis leg”). J Ultrasound Med 1998; 17:157–162. Helms CA, Fritz RC, Garvin GJ. Plantaris muscle injury: evaluation with MR imaging. Radiology 1995; 195:201–203. Leekam RN, Agur AM, McKee NH. Using sonography to diagnose injury of plantaris muscles and tendons. AJR Am J Roentgenol 1999; 172:185–189. Robinson JR, Bull AM, Thomas RR, et al. The role of the medial collateral ligament and posteromedial capsule in controlling knee laxity. Am J Sports Med 2006; Jun 30 [Epub ahead of print]. Beltran J, Matityahu A, Hwang K, et al. The distal semimembranosus complex: normal MR anatomy, variants, biomechanics and pathology. Skeletal Radiol 2003; 32:435–445. Sims WF, Jacobson KE. The posteromedial corner of the knee: medial-sided injury patterns revisited. Am J Sports Med 2004; 32:337–345. Mochizuki T, Akita K, Muneta T, et al. Pes anserinus: layered supportive structure on the medial side of the knee. Clin Anat 2004; 17:50–54. Alioto RJ, Browne JE, Barnthouse CD, Scott AR. Complete rupture of the distal semimembranosus complex in a professional athlete. Clin Orthop Relat Res 1997; 336:162–165. Kaplan PA, Gehl RH, Dussault RG. Bone contusions of the posterior lip of the medial tibial plateau (countercoup injury) and associated internal derangements of the knee at MR imaging. Radiology 1999; 211:747–753. Yao L, Lee JK. Avulsion of the posteromedial tibial plateau by the semimembranosus tendon: diagnosis with MR imaging. Radiology 1989; 172:513–514. Chan KK, Resnick D, Goodwin D, Seeger LL. Posteromedial tibial plateau injury including avulsion fracture of the semimembranous tendon insertion site: ancillary sign of anterior cruciate ligament tear at MR imaging. Radiology 1999; 211:754–758.

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119. Vanek J. Posteromedial fracture of the tibial plateau is not an avulsion injury: a case report and experimental study. J Bone Joint Surg Br 1994; 76:290–292. 120. Miller TT, Staron RB, Koenigsberg T. MR imaging of Baker cysts: association with internal derangement, effusion, and degenerative arthropathy. Radiology 1996; 201:247–250. 121. De Maeseneer M, Debaere C, Desprechins B. Popliteal cysts in children: prevalence, appearance, and associated findings at MR imaging. Pediatr Radiol 1999; 29:605–609. 122. Miller TT, Brandoff J, Fealy S. Incidence of semimembranosustibial collateral bursitis: MR imaging evaluation. Radiology 2002; 225(Suppl):656. 123. Aydingoz U, Oguz B, Aydingoz O, et al. The deep infrapatellar bursa: prevalence and morphology on routine magnetic resonance imaging of the knee. J Comput Assist Tomogr 2004; 28:557–561. 124. Forbes JR, Helms CA, Janzen DL. Acute pes anserine bursitis: MR imaging. Radiology 1995; 194:525–527. 125. Rothstein CP, Laorr A, Helms CA. Semimembranosus-tibial collateral ligament bursitis: MR imaging findings. AJR Am J Roentgenol 1996; 166:875–877. 126. Boyd CR, Eakin C, Matheson GO. Infrapatellar plica as a cause of anterior knee pain. Clin J Sport Med 2005; 15:98–103.

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Internal Derangement of the Knee: Cartilage and Osteochondral Injuries Koenraad L. Verstraete and Wouter C. J. Huysse

PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS The term osteochondral lesion is used to describe a defect of the articular surface involving separation of the cartilage and the underlying bone, without making any pretense to etiology. Possible causes of osteochondral lesions are traumatic osteochondral lesions, osteochondritis dissecans, and insufficiency fractures of the subchondral bone. The underlying mechanism in all cases is believed to be repetitive and prolonged overloading or sudden compressive stress of the hyaline cartilage and the subchondral bone.1 These lesions are most often seen on the talus, the femoral condyles, and the elbow joint. Other, less frequently affected sites include other tarsal and metatarsal bones, the distal tibia, the acetabulum, the metacarpal bones, and the glenoid cavity.2 Distinguishing between the different etiologic entities of an osteochondral lesion is made through a combination of clinical symptoms, patient history, and demographics, on the one hand, and imaging findings such as location of the lesion and associated structural abnormalities on the other hand. In early stages of the disease, symptoms are often obscure and functionality of the joint is rarely impaired, making imaging findings and demographics all the more important.1 Injury to the articular cartilage in the knee is reported in 63% of arthroscopies, and the vast majority of these lesions is associated with other problems, such as anterior cruciate ligament injury (23%) and meniscal lesions.3 MRI of the knee shows a prevalence of hyaline cartilage defects similar to arthroscopy but reports solitary lesions in almost one fourth of patients. In immature knees, cartilage lesions are more common than meniscal or anterior cruciate ligament tears. All types of

osteochondral lesions occur two to three times more often in men than in women, although the incidence in females is increasing as higher numbers of young women are participating in intensive sports. Tenderness and joint effusion are variably present early on but become more apparent as the disease progresses. Quadriceps atrophy will be present if the injury becomes

KEY POINTS Osteochondral lesions can be caused by osteochondritis dissecans, insufficiency fractures, and post-traumatic osteochondral fractures. ■ It is sometimes impossible to differentiate between the three entities, as discussed in text. ■ MRI, possibly with intravenous contrast agent administration, can unambiguously differentiate between stable and unstable osteochondritis dissecans based on the presence or absence of a high signal intensity line beneath the lesion on fluid-sensitive images, a cystic lesion larger than 5 mm, a cartilage defect larger than 5 mm, or a split through the bony end plate and the covering cartilage. ■ In a patient presenting with acute knee pain without a history of trauma, the presence of a nonenhancing, hypointense subchondral region abutting the bony end plate is pathognomonic for osteonecrosis and differentiates the lesion from a self-resolving pathologic process such as transient osteoporosis or an uncomplicated subchondral insufficiency fracture. ■ Although small traumatic chondral and osteochondral fractures do not necessarily need treatment, their presence should be noted because it can explain the patient’s symptoms. ■

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chronic. Intermittent knee swelling with activity is common. Catching, locking, grinding, and giving way may be intermittent at first but become more constant with the appearance of loose bodies.

Traumatic Chondral or Osteochondral Lesions When shearing or rotational forces are transmitted from one congruent articular surface to another, fracture lines paralleling the surface can arise in the cartilage proper or in the subchondral bone. Depending on the depth of the fracture, chondral (cartilage alone) or osteochondral fragments (consisting of cartilage and underlying bone) can break away (Fig. 27-1). In many cases the fracture line does not re-enter the joint space but is deflected by the most superficial cartilage layer (lamina splendens, see later), which has strong collagen fibers paralleling the surface, and forms an intracartilaginous tear (Fig. 27-2). After a variable amount of time subchondral cystic lesions can develop beneath these lesions. Their appearance can be explained by two mechanisms (Fig. 27-3). When compressive forces are transmitted over a joint, fracture lines are more perpendicular to the articular surface and impaction of cartilage and subchondral bone occurs. These chondral or osteochondral fractures can occur on one or on both apposing joint surfaces and are surrounded by areas of bone marrow edema. The whole of fractures and edema is often referred to as a bone bruise. Full-thickness clefts or fissures allow synovial fluid to reach the subchondral bone. In situations of elevated intra-articular pressure, it is thought that joint fluid is forced down these fissures and penetrates the subchondral bone, with subsequent resorption of trabecular bone and formation of cystic lesions. Another theory explaining the origin of these cystic lesions is focal post-traumatic osteonecrosis, with cyst formation occurring as necrotic trabeculae are removed by osteoclasts. Most likely, both mechanisms play a role in the formation of subchondral cysts.

■ FIGURE 27-1 Diagram explaining the difference between a chondral (A) and an osteochondral (B) fracture. A chondral fracture can provoke a cartilaginous loose body, as depicted, but can also remain intracartilaginous as a tear paralleling the articular surface, as a defect, or as a fissure, perpendicular to the surface.

■ FIGURE 27-2 Sagittal CT arthrography image of intracartilaginous tear. A residual layer of cartilage can be seen as a hypodense layer (arrow) between the tear and the subchondral end plate.

In most cases the traumatic event is easily recalled by the patient. Tenderness, impaired function, joint effusion, and even hemarthrosis are seen in patients with acute (osteo)chondral fractures and allow some degree of distinction between trauma and other causes of osteochondral lesions.

Osteochondritis Dissecans Osteochondritis dissecans most commonly involves patients between the ages of 10 and 20 years and is more prevalent in children, especially in active boys. This form of osteochondritis dissecans, called juvenile osteochondritis dissecans, includes patients with open metaphysis and has a higher rate of spontaneous healing. The causes of osteochondritis dissecans are still not fully understood, although there is an undeniable association with trauma, both repetitive and solitary. In 40% to 60% of cases, a significant history of trauma can be found. This trauma is believed to disrupt the blood supply to the subchondral bone, which can be tenuous in a rapidly growing person. Apparently, the medial femoral condyle is most susceptible because 80% to 85% of osteochondritis lesions in the knee are found there. The lateral aspect of the medial condyle is especially affected. This is probably due to microinjuries caused by repetitive impingement of the intercondyloid eminence against the medial condyle during internal rotation of the tibia. This abutment of the eminence against the osteochondral lesion explains the pain patients complain about when they rotate the tibia internally with extended knee. This sign was first described by Wilson and is sometimes seen in patients with osteochondritis. It does, however, not exclude other forms of osteochondral lesions. The appearance of osteochondral lesions in other locations in the knee and the observation that both knees are affected in 20% to 30% of patients demonstrate, however, that trauma, repetitive or acute, is not the only possible

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■ FIGURE 27-3 Illustration of the possible mechanisms explaining the development of a subchondral cystic lesion after trauma.

cause. Increased intraosseous pressure, similar to that seen in osteonecrosis, has been described in osteochondritis dissecans. Abnormal centers of ossification, endocrine imbalances, and genetic factors have also been proposed as causes, but these have not been definitely shown to play a role in osteochondritis dissecans. Another location of osteochondritis dissecans in the knee is the patella. In comparison to osteochondritis dissecans of the femoral condyle, this is a much rarer diagnosis and is possibly related to ligamentous laxity and patellar (sub)luxation. Lesions are generally found on the bottom half of the medial facet with involvement of the lateral facet in approximately 30% of patients.

Subchondral Insufficiency Fractures Besides traumatic chondral and osteochondral lesions and osteochondritis dissecans, subchondral insufficiency fractures can also cause cartilage and osteochondral lesions. These subchondral insufficiency fractures can be associated with focal, subchondral areas of osteonecrosis or bone marrow edema. According to recent theory, based on the work of Yamamoto and colleagues,4 the underlying cause of the fracture is thought to be osteoporosis and osseous insufficiency. Although it is still often referred to as spontaneous osteonecrosis of the knee, the osteonecrosis seen between the fracture line paralleling the articular surface and the bony end plate is probably secondary to vascular disruption caused by the fracture.

Other authors see subchondral insufficiency fractures and spontaneous osteonecrosis as two separate entities that need to be differentiated because of the therapeutic consequences. A subchondral insufficiency fracture is considered to be self-resolving, whereas spontaneous osteonecrosis can lead to collapse of the joint surface and has to be treated surgically. Subchondral insufficiency fractures are classified by these authors in the same group as other self-resolving lesions presenting as bone marrow edema, such as transient bone marrow edema, transient osteoporosis, and reflex sympathetic dystrophy. From a clinical point of view, however, an insufficiency fracture associated with osteonecrosis is still a distinct entity and unchanged since it was first described in 1968 by Ahlbäck and colleagues. It differs from classic osteonecrosis, which is associated with corticosteroid therapy, alcohol use, and hematologic diseases, and is associated with obesity and age, with most patients being older than age 60 years. Although it is predominantly seen in elderly women with osteoporotic bone, men can be affected, too. A subchondral insufficiency fracture is typically situated on the weight-bearing part of the medial femoral condyle. Clinically, it is characterized by an abrupt onset of pain without obvious trauma, allowing distinction of this entity from an acute traumatic (osteo)chondral lesion and osteochondritis dissecans of the knee.4 Typically, pain is worse at night in osteonecrosis. Other clinical symptoms, such as joint effusion, stiffness, and tenderness are generally more pronounced than in osteochondritis dissecans but can also be absent.2

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ANATOMY The hyaline cartilage covering the articular surface of joints is composed of chondrocytes embedded in an extracellular matrix. This matrix contains dissolved gases, electrolytes, and small proteins, on the one hand, and macromolecules such as collagen and proteoglycans on the other hand. A functional way of dividing cartilage is the four-layer model first proposed by Benninghoff in 1925 (Fig. 27-4).5 The most superficial layer can be subdivided into two compartments: the lamina splendens, composed of tightly packed bundles of collagen arranged parallel to each other, and a second layer, made of collagen fibers that are oriented more perpendicularly to the surface. The transitional zone or middle layer is located underneath the superficial layer. It contains fewer chondrocytes that have a more rounded appearance. The collagen fibrils in this layer have a random orientation and larger diameters than those in the superficial zone. The deep or radial zone is located between the transitional zone and the thin, calcified layer of cartilage overlying the subchondral bone. This layer has the highest proteoglycan concentration and lowest cellularity and collagen content. The diameter of the collagen fibrils, however, is maximal. The collagen fibers are oriented toward the surface and are arranged in large fibrils. The calcified zone anchors the large collagen fibrils to the subchondral bone and has mechanical properties intermediate between those of uncalcified cartilage and subchondral bone. It is separated from the uncalcified cartilage by the tide mark, a wavy line representing the mineralized front of the calcified cartilage. The calcified cartilage is intimately connected to the subchondral

bone plate, also called the cortical end plate or the articular bone plate. The interface between both structures is highly irregular with deep recesses and large protuberances, somewhat like the pieces of a jigsaw puzzle. Underneath the end plate is situated the subcortical space, containing fatty bone marrow, vascular structures, and trabecular bone. The density of this subchondral trabecular network and of the blood vessels is correlated with the compressive forces acting on the cartilage and subchondral bone.6 It also varies with age, from person to person, and from joint to joint. Directly underneath the subchondral end plate, the vascular structures have merged together to form a transverse sinus. It is fed by terminal arterial branches ending in irregular sinusoids.6 Originating from this transverse sinus are multiple small vascular branches that penetrate the cortical end plate and can reach through the calcified cartilage up to the tide mark. An estimated 50% of the oxygen and glucose required by cartilage is supplied by these vessels. The other 50% directly diffuses into the cartilage from the synovial fluid. Macroscopically, the articular surface of the knee joint can be divided into several different regions. A grid-like mapping system was proposed by the members of the International Cartilage Repair Society of the femoral condyles (Fig. 27-5), the tibial plateaus, and the patellar facets.7 The central and posterior areas of the femoral, the central areas of the tibial condyles, and the lateral patellar facet are subjected to the greatest forces in upright position and during flexion of the knee. As such, they are most often affected by osteochondral pathology. Other ways of localizing osteochondral lesions have been devised (Fig. 27-6).

■ FIGURE 27-4 Schematic representation of the different layers within the cartilage. Hyaline cartilage is a fibrous tissue that consists of chondrocytes lying within an extracellular matrix. This is composed of tissue fluid containing dissolved electrolytes and macromolecules such as proteoglycans and collagen II. Water content decreases toward the deeper regions, whereas proteoglycan (PG) content increases, with the exception of the calcified cartilage, where no PG is found. The matrix is secured to the bony end plate in a jigsaw-like fashion. The collagen II fibers form fibrils that are anchored in the calcified cartilage and have a largely vertical orientation in the radial zone and a more random orientation in the transitional zone. The superficial layer consists of densely packed collagen bundles paralleling the articular surface.

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■ FIGURE 27-5 This grid-like mapping system allows accurate localization of articular lesions. (Image courtesy of ICRS—International Cartilage Repair Society.)

femorotibial compartment into two equal parts, 3 encompassed the notch, and 4 and 5 divided the lateral compartment into two equal parts.

BIOMECHANICS Hyaline cartilage is a viscoelastic material that is resistant to compressive and shearing forces. Although elastic, cartilage attenuates only 1% to 3% of the load forces. The majority of the load forces (30%) are taken up by the subchondral bone. The main function of cartilage in weight bearing is dissipating the loading forces to a larger area.6

Reaction of Cartilage to Loading ■ FIGURE 27-6 Divisions of the lateral and anteroposterior views of the knee according to Cahill and Berg.

Based on the lines along the posterior femoral cortex and the Blumensaat line, Cahill and Berg divided the lateral projection of the knee into three segments: A: anterior to the Blumensaat line B: between the Blumensaat line and the line along the posterior cortex of the femur C: posterior to the line along the posterior cortex of the femur They also divided the anteroposterior projection of the knee into five segments where 1 and 2 divided the medial

The collagen framework and the negatively charged hyaluron-aggrecan complexes confined within this framework provide a hydroelastic suspension mechanism. Loading of articular surfaces causes movement of fluid within the cartilage matrix that dampens and distributes the load within the cartilage and to the subchondral bone. When load is applied slowly, proteoglycan-bound water is squeezed out of the cartilage or into uncompressed regions of the matrix distributing the forces. After removing the load, osmotic swelling pressure exerted by proteoglycans and dissolved electrolytes pulls water molecules back into the matrix and reestablishes equilibrium.

Reaction of Cartilage to Injury In a traumatic event, the applied forces are too high or applied too rapidly for redistribution of fluid to occur.

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This results in rupture of the framework and, in more extreme cases, in fracturing of the subchondral bone. When the articular surface is injured, there is damage not only to the cartilage matrix but also to the chondrocytes. This results in an area of cell death, both trough necrosis and apoptosis, that extends further than the actual cartilaginous lesion. Because chondrocytes are responsible for the maintenance of the extracellular matrix, the framework in this acellular rim becomes prone to rapid degeneration, allowing the lesion to progress. In a cartilaginous lesion caused by sharp trauma (e.g., a surgical tool) this rim of cell death is not seen.8 This is important in cartilage repair because an acellular region interferes with adhesion of the repair tissue to the surrounding cartilage. Although the forces encountered by the articular surface during every day use are easily redistributed, repetitive minor trauma can result in damage to the subchondral bone and the deeper regions of the cartilage without visual disruption of the surface. This damage results in subchondral bone marrow edema and possibly in associated microfractures of subchondral trabeculae. Healing of these fractures leads to microcallus formation and focal subchondral sclerosis. Owing to the rigidity of calcified cartilage, the cortical end plate, and, to a lesser extent, the subchondral bone, the probability of these regions sustaining microinjuries is higher than that of the softer cartilage. Especially at the periphery of these areas, small cracks can be found.6 Eventually these changes lead to deterioration of both deep and superficial cartilage. On the surface the cartilage starts to display fibrillation and fissuring. As explained earlier, these fissures are thought to play a role in the formation of subchondral cystic lesions, which are frequently seen in degenerative joint disease but can also appear after a traumatic event. In the deeper regions of the cartilage these changes lead to production of abnormal matrix proteins, which initiates swelling of the cartilage and can result in delamination of the articular surface if (repetitive) overloading persists.

cartilage or softening of cartilage); I, slight swelling and signal heterogeneity; II, fissuring or ulcerations less than 50% of cartilage thickness (Fig. 27-7); III, fissuring or ulcerations more than 50% of cartilage thickness (Fig. 27-8); and IV, ulcerations and erosion with exposure of subchondral bone (Fig. 27-9). A final grade could be added to allow for differentiation between full-thickness lesions with intact subchondral bone or with penetration of the bony end plate (grade V). Lesions of grade V are often associated with focal areas of bone marrow edema. A limitation of this classification is the inability of routinely used MR sequences to reliably demonstrate grade I changes.11 Signal changes associated with early degeneration of the cartilage cannot be differentiated from imaging shortcomings, such as truncation artifact, magic angle artifact, or partial volume artifact. Size of a lesion is not taken into account in this classification. It should be reported as a separate parameter.

■ FIGURE 27-7 Coronal DESS-3D MR image of a grade II chondromalacia with superficial fraying (arrow) and fissuring of the cartilage on the medial condyle. Note the bone marrow edema in the subchondral bone (arrowheads) underneath the defect.

MANIFESTATIONS OF THE DISEASE Traumatic Chondral or Osteochondral Lesions and Intra-Articular Fractures Grading of Cartilage Lesions The most well-known arthroscopic staging method for articular cartilage lesions is that proposed by Outerbridge in 1961. In 1985, Shahriaree modified this classification, describing four grades of chondromalacia where grade 1 involved softening of the cartilage; grade 2, shallow fibrillation, ulceration, or blister-like swelling; grade 3, surface irregularities and areas of thinning; and grade 4, ulceration and exposure of subchondral bone.9 Based on the Shahriaree classification and in analogy with the Outerbridge classification, Yulish proposed three stages of chondromalacia patellae for use in MRI. In later studies,10 this classification was modified to 5 grades: 0, normal cartilage (corresponds arthroscopically to normal

■ FIGURE 27-8 Sagittal CT arthrography image of a recent grade III cartilage defect. The contrast medium does not reach the subchondral end plate.

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■ FIGURE 27-9 Transverse proton density–weighted FSE MR image with fat suppression of a chronic grade IV cartilage defect (arrow) with bone marrow edema (arrowheads) and exposure of the subchondral bone over a large area. There is no defect in the bony end plate.

One of the latest classification systems was proposed by Bohndorf in 1998 based on a combination of arthroscopic and magnetic resonance findings.12 It differentiates between lesions with intact (A) or disrupted (B) cartilage and further subdivides these classifications based on the extent of cartilage damage, the involvement of subchondral bone, and the state of the bony end plate. An overview is given in Figure 27-10 and Table 27-1. The major advantage of this classification is it can be applied to acute chondral or osteochondral lesions in the knee and ankle as well as less frequently involved locations.

Radiography A radiographic examination of patients with a suspected traumatic osteochondral lesion or an intra-articular fracture should include not only the standard anteroposterior and lateral views but also a posteroanterior view with the knee flexed 20 degrees (Schuss or MTP view). This view allows a better evaluation of the posterior articular surface, which is often affected in trauma to the flexed knee. The axial view of the patella with 15 to 20 degrees of flexion is essential for evaluating the articular surface of the patella and the trochlear groove. Although it is important in evaluating the patellofemoral joint after patellar luxation, it will only detect 32% of osteochondral injuries caused by this trauma. Long-leg views can help determine abnormal varus or valgus alignment after compression fractures of the medial or lateral tibial plateau but should not be taken routinely. Even with these different views, osteochondral fractures can easily go undetected on plain radiographs because the bone fragments tend to be small, even if a large osteochondral defect is present. The main radiographic features of an osteochondral fracture include a linear radiodense area paralleling the subchondral bone plate (Fig. 27-11). This is due to either impacted trabecular bone or callus around the fracture line. The double contour is typically seen in a depression

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fracture of a tibial condyle. An irregular bony contour, bony defect, or bony fragments are sometimes seen in osteochondral fractures (Fig. 27-12). It is not always possible to detect the origin of this fragment because the natural healing processes tend to remodel the fracture site. All osteochondral lesions can give rise to loose, intraarticular bodies, although they are more frequent in osteochondral fractures and osteochondritis dissecans. Most fragments become embedded in the synovial lining, especially in the posterior recesses of the knee, where the majority are broken down and reabsorbed. If these embedded fragments revascularize, growth and formation of trabecular bone can be seen on consecutive radiographs. The fragments that remain free can also disappear due to osteoclastic properties of the synovial fluid. Others develop degenerative calcifications, becoming denser on follow-up radiography, or acquire a laminated aspect as they add consecutive layers of new cartilage and even bone, nourished by the synovial fluid. The radiologic appearance of intra-articular fractures is similar to that of any other fracture in the osteoarticular system: a discontinuity of cortical or subchondral bone, a more or less sharply demarcated radiolucent line extending into the articular surface, one or more bony fragments that may or may not be displaced, soft tissue damage, and excessive joint fluid.

Magnetic Resonance Imaging The main advantage of MRI is the direct visualization of the articular cartilage. The ideal MR pulse sequence for the evaluation of articular cartilage in general and, more to the point, of acute cartilage injury should have a number of properties. Most importantly, it must display cartilage with an optimal contrast and spatial resolution. It has to be able to show changes in the subchondral bone plate and display its exact thickness. It should detect bone marrow edema, subchondral cysts, and granulation tissue, on the one hand, and changes in the internal structure of cartilage on the other hand. These changes should be clearly visible, both in the superficial and the deep layers of cartilage. It should also allow segmentation, volume calculation, and three-dimensional (3D) reconstruction. Currently, two sequences broadly used in clinical practice allow good morphologic evaluation of cartilage and chondral abnormalities.10 These are the two-dimensional fast spin-echo (FSE) and the 3D spoiled gradient-recalledecho (SPGR) sequences. Proton-density– and T2-weighted FSE images, especially with fat suppression, accurately detect chondral abnormalities owing to a higher signal in the joint fluid compared with the articular cartilage. The advantage of these sequences over SPGR sequences is their short acquisition time, high signal-to-noise ratio, and resistance to artifacts. Unfortunately, they do not display the deepest cartilage layers well, which may lead to an overestimation of the depth of a cartilage lesion. 3D-SPGR images, either using water-selective excitation (SPGRwe) or fat-suppression techniques, are best suited for the evaluation of the deeper regions of cartilage. The sensitivity and specificity of these sequences in demonstrating cartilage lesions was reported to be

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■ FIGURE 27-10 Drawing representing the different types of traumatic chondral and osteochondral lesions according to the classification proposed by Bohndorf.

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TABLE 27-1 Classification of Acute Chondral and Osteochondral Lesions (According to Bohndorf)

A: Acute injury of the articular surface with intact cartilage B: Acute injury of the articular surface with disrupted cartilage

Subchondral microfracture and bone marrow edema Subchondral impaction (linear or geographic) and bone marrow edema Softening of cartilage with or without fissuring Intracartilaginous tear or loose cartilage fragment Compression of cartilage and immediate subchondral bone Osteochondral compression with fracture of the bony end plate Partially or completely detached osteochondral fragment

From Bohndorf K. Osteochondritis (osteochondrosis) dissecans: A review and new MRI classification. Eur Radiol 1998; 8:103–112.

higher than that of FSE sequences, but recent studies report a similar accuracy. This sequence allows easy multiplanar reconstructions and cartilage volume measurements. It is, however, still hampered by image artifacts. New sequences, especially 3D FSE imaging, may provide a solution to these problems.13 The diagnosis of cartilage lesions on MRI is based on several criteria. First there has to be visualization of a contour defect. This is only possible on MR sequences that allow good differentiation between cartilage and intraarticular fluid. In general, if the edges of the contour defect are sharp and the cartilaginous lesion is accompanied by bone marrow edema in the subjacent bone, an acute lesion must be suspected. A shallow lesion with wide margins and a more gradual slope to its edges suggests a chronic, degenerative lesion (Fig. 27-13). Acute cartilage damage can

■ FIGURE 27-12 Lateral radiograph of an osteochondral fracture with mildly displaced loose fragments (arrow). (Courtesy of Dr. F. Plasschaert, Ghent University Hospital, Ghent, Belgium.)

■ FIGURE 27-11 Anteroposterior (A) and lateral (B) radiographs of an intra-articular fracture (black arrowhead, A) runs perpendicular to the surface of the lateral tibial plateau. Underneath the articular surface a subchondral sclerotic line (white arrows) can be seen indicating a subchondral compression fracture.

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■ FIGURE 27-13 Sagittal proton density–weighted FSE MR image with fat suppression (A) and T2-weighted FSE MR image (B). A, A cartilage defect is seen on the weight-bearing part of the condyle. The sharp edges and the presence of bone marrow edema (arrowheads) indicate that this is a recent defect. B, A chronic grade II to III lesion with a gradual slope to its edges. Note the blunted posterior horn of the lateral meniscus.

also manifest itself as a tear in the cartilage, as discussed earlier (Fig. 27-14). A second criterion is focal thinning compared with the width of the surrounding cartilage. A third and more debated argument allowing the diagnosis of cartilage injury is the presence of circumscribed signal alterations. Although it is not always possible to differentiate these changes from imaging artifacts, focal areas of signal change are still considered suspect for cartilage injury. Post-traumatic abnormalities in the subchondral bone are also well visualized on MRI. Minor trauma to the subchondral bone gives rise to a bone bruise, which is a combination of trabecular microfractures and bone marrow edema. On MRI, this is seen as a poorly demarcated area of high signal in the subchondral bone on fat-suppressed proton-density– and T2-weighted images. It may be the only abnormality found on MRI because trabecular microfractures are not discernable. The patterns are indicative

■ FIGURE 27-14

of the mechanism of the injury and provide clues to associated soft tissue injuries. After more extensive trauma, curvilinear hypointense fracture lines on T1-weighted images can be seen. On T2weighted images, the signal intensity can be either high or low, depending on the presence or absence of fluid or blood in the fracture line. As mentioned earlier, these fracture lines can re-enter the articular surface, creating completely or partially detached osteochondral fragments that may become displaced (Fig. 27-15).

Multidetector Computed Tomography Articular cartilage is visible as a band of low density tissue adjacent to the subchondral bone. No variations in cartilage density are seen, but its thickness varies considerably from one area of the knee to another and among individuals.14 Hyaline cartilage has a density similar to that of joint

Sagittal 3D-SPGR (A) and coronal DESS-3D (B) MR images. A, The pattern of bone marrow edema in femoral condyle (arrowheads) and tibial plateau (asterisk) suggests forceful posterior displacement of the tibia, which provoked an intracartilaginous tear (arrow). B, Underneath the cartilage defect a hypointense line (arrowheads) marks the compression of the subchondral bone (grade B3 according to Bohndorf).

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■ FIGURE 27-15 Coronal (A) and transverse (B) DESS-3D MR images. A loose osteocartilaginous fragment is seen consisting mainly of cartilage with a small fragment of cortical bone at the inferior end (arrow, A).

fluid, which makes it difficult to reliably assess the cartilage surface without prior intra-articular contrast administration. CT arthrography provides an excellent view of the cartilage surface.14 Because of its higher spatial resolution, it is more accurate in demonstrating narrow cartilage fissures than MRI. Similar to MRI, it has very poor accuracy for the detection of superficial cartilage fibrillations,14 with the added disadvantage that it is insensitive to bone marrow edema, which sometimes accompanies such lesions on MRI. In the detection of all cartilaginous defects, specificity and sensitivity of CT arthrography do not differ significantly from those of MRI14 (Fig. 27-16). MDCT is the imaging modality of choice for demonstrating minor cortical defects, small fracture lines, and the possible extension of fracture lines into the articular surface, although it is as yet unable to detect trabecular microfractures.

Ultrasonography Ultrasonography is not valuable for the assessment of the articular surface of the knee. Only indirect signs of

■ FIGURE 27-16

articular trauma such as soft tissue swelling or hemarthrosis are visible after acute (osteo)chondral trauma. It is, however, a very good tool for the evaluation of concomitant injury to the ligaments and tendons around the knee joint.

Nuclear Medicine Bone scintigraphy is highly sensitive and can show increased uptake of technetium 99m as early as 12 hours after the injury, but it has low specificity. It is used as a means to demonstrate clinically suspected minor articular trauma in patients with normal radiographs. However, its place in the workup of traumatic osteochondral injury about the knee has been largely taken over by MRI since this technique became more readily available. It is also unable to provide direct information about the articular cartilage.

Positron Emission Tomography/Computed Tomography Positron emission tomography has no place in the evaluation of traumatic chondral and osteochondral lesions and intra-articular fractures.

Sagittal (A) and transverse (B) CT arthrography images. A, Intracartilaginous tear (curved arrow) in the weight-bearing part of the lateral femoral condyle. B, A small grade III defect can be seen in the cartilage on the lateral articular facet of the patella.

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Arthroscopy

Osteochondritis Dissecans of the Knee

The normal appearance of healthy hyaline cartilage of the deep surface of the patella is bluish-white, smooth, glistening, and resilient. The appearance of cartilage overlying a subchondral fracture can be either normal or similar to that of the early stages of chondromalacia. After more serious trauma, findings during arthroscopic examination range from cracks and fissures in the cartilage to genuine osteochondral fractures (Fig. 27-17). Much debate has been held about arthroscopy as the gold standard in identifying cartilage lesions. It is also inherently inaccurate in evaluating the depth of a lesion as long as the subchondral bone is not exposed. Additionally, blind spots in the joint are difficult to assess. Especially, the posterior aspect of the femoral condyles cannot always be evaluated during a routine arthroscopic investigation.

Grading of Osteochondritis Dissecans

Classic Signs ■ ■ ■ ■

■

Acute onset of the complaints occurs after a clearly remembered trauma. These injuries can easily remain undetected on plain radiographs. Contour defect in the cartilage surface on MRI or CT arthrography and/or focal thinning of cartilage is seen. Areas of high signal intensity on T2-weighted images are compatible with bone bruise and associated bone marrow edema. Curved lines, hypointense on T1-weighted images and with variable signal on T2-weighted images, correspond with subchondral fractures.

The different radiologic stages of osteochondritis dissecans are based on the classification of osteochondral lesions of the talus that was first described by Berndt and Harty. They proposed four stages. Stage I lesions are stable, show no discontinuity between the lesion and the surrounding bone, and are covered by intact cartilage. Stage II lesions are partially detached but stable. Stage III lesions are completely detached but not dislocated. These lesions are considered unstable. In stage IV lesions, the fragment is displaced and located away from the lesion site. In 1982, Clanton and colleagues adapted this classification to lesions found in the knee. The most notable change was made to stage I, which now includes a depressed osteochondral fracture. The classification of Berndt and Harty was modified first by Ferkel and later by Hepple, adding a stage for subchondral cyst formation and taking into account the changes seen on MRI. An earlier and more widely used MRI classification of talar lesions, the Anderson classification,1 can be found in Table 27-2 and Figure 27-18, where it is compared with the arthroscopic classification after Guhl. This classification does not put much emphasis on the presence of bone marrow edema.

Radiography Routine radiography remains the standard initial study in osteochondritis dissecans and is capable of detecting the osseous component. Radiographs must be carefully assessed for the presence of small ossified fragments. Although single- or double-contrast arthrography is more accurate in diagnosing osteochondral fragments than

■ FIGURE 27-17 Arthroscopic image of a recent osteochondral lesion shows the absence of cartilage and subchondral bone plate. At the bottom of the osteochondral defect only bleeding trabecular bone is found. (Courtesy of Dr. D. De Clercq, City Hospital, Lokeren, Belgium.)

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TABLE 27-2 Classifications for Osteochondritis Dissecans of the Knee

MR Classification* Stage I

Bone marrow edema

Arthroscopic Classification† Stage I

Cartilage intact but soft and ballotable

Stage IIa Subchondral cyst formation Stage IIb Incomplete separation Stage II of the osteochondral fragment Stage III Fluid around an undisplaced osteochondral fragment Stage IV Displaced osteochondral fragment

Lesion showing early separation with interruption of the cartilage Stage III Partially detached lesion

Stage IV Crater with loose bodies

*The Anderson classification was developed for osteochondral lesions of the talus but can be used for osteochondritis dissecans of the knee. † According to Guhl.

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plain radiography, CT and CT arthrography are the imaging modalities of choice for detecting loose bodies. A Schuss or tunnel view allows a better visualization of lesions in the intercondylar notch that are easily overlooked on standard radiographs.12 The typical appearance of osteochondritis dissecans on standard radiography is a well-circumscribed area of sclerotic subchondral bone, usually on the lateral side of the medial femoral condyle, separated from the surrounding bone by a radiolucent line. This area may be fragmented (Fig. 27-19). Early stages of the disease are seen as a radiolucent fracture line in the subchondral bone. This presentation is only seen in acute cases and is very rare, but it is becoming more and more frequent as patients tend to seek medical advice more quickly. A sclerotic rim develops around this small radiolucent area, progressively turning it into a relatively sharply delineated sclerotic area still attached to the surrounding bone (Fig. 27-20). With proper, conservative treatment (see later), a lesion in this stage can still heal without surgical intervention, especially if the patient has not reached skeletal maturity yet. In this case,

■ FIGURE 27-18 The different stages of osteochondritis dissecans according to Anderson.

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■ FIGURE 27-19

Anteroposterior (A) and lateral (B) radiographs of a large osteochondritis dissecans lesion with undisplaced loose fragments. (Courtesy of Dr. M. Obradov, Sint-Maartenskliniek, Nijmegen, The Netherlands.)

■ FIGURE 27-20 (arrowheads).

Anteroposterior (A) and lateral (B) radiographs of early osteochondritis dissecans, which is visible as a radiolucent area

follow-up radiographs will show gradual resolution of the lesion. If it does not heal, it will become detached, fragmented, and eventually displaced. Lesions tend to contain a loose fragment if they are larger than 0.8 cm2 or have a sclerotic margin wider than 3 mm. In some cases, a healing process can be seen at the base of the lesion. This healing can be recognized as a small island of new bone formation between the lesion and the normal subchondral bone. In time, the healing process can remodel the defect, making it more difficult to detect (Fig. 27-21). A secondary finding on standard radiographs is degenerative calcifications in the cartilage, either around the fragment or in the remaining articular cartilage. These calcifications are often hazy and ill defined.

Magnetic Resonance Imaging The aim of an MR investigation in suspected osteochondritis dissecans is to (1) diagnose the lesion, (2) determine the stability of a lesion and differentiate those that need surgery from those that can be treated conservatively, and (3) describe complications associated with the lesion.

To achieve this, the imaging protocol in case of a suspected osteochondritis should include a 3D-SPGR sequence, preferably with fat suppression or water excitation, to assess the cartilage and the subchondral trabecular bone. Because of field inhomogeneities caused by the many fat-bone interfaces between fatty bone marrow and trabeculae, signal intensity in normal trabecular bone is low on 3D SPGR images. In case of focal trabecular loss, such as bone resorption around osteochondritis dissecans, less trabecular bone results in a reduction of field inhomogeneities. This, in turn, results in focal higher signal intensity (Fig. 27-22). T2-weighted FSE images with fat suppression or short tau inversion recovery (STIR) sequences are also needed because these are most sensitive for detecting bone marrow edema. Intra-articular contrast medium administration followed by T1-weighted fat-suppressed images can be performed because it has been shown that these are more accurate in assessing the overlying cartilage. The diagnosis of an osteochondral lesion on MRI is made by identifying signal changes or morphologic abnormalities at the articular surface. One of the most obvious

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■ FIGURE 27-21 Posteroanterior (A) and lateral (B) radiographs of healing osteochondritis dissecans of left medial condyle. The lesion is hardly visible on the lateral view.

■ FIGURE 27-22

Sagittal 3D SPGR (A) and T2-weighted FSE (B) MR images. A, Trabecular loss between the area of osteochondritis dissecans and the surrounding condyle results in a high signal on this sequence. The curved white arrows indicate focal persistent connection between the osteochondritis lesion and the surrounding epiphysis. B, Low signal intensity in the interface is suggestive of a stable lesion, even taking into account the partial absence of trabecular bone between the lesion and the surrounding bone.

features of osteochondritis dissecans on MRI is the high signal intensity in the subchondral bone on fluid-sensitive sequences such as T2-weighted sequences with fat suppression and STIR. This high signal in and around the lesion is probably due to bone marrow edema, hypervascularity, or scar tissue. Although prominent in most cases, it does not allow differentiation between stable and unstable lesions. The main focus in evaluating osteochondritis dissecans on MRI should, however, go to the interface between the lesion and the surrounding epiphysis. This transitional zone is always of low signal intensity on T1-weighted images. On T2-weighted sequences, the signal intensity of the junction can be both high and low and is often inhomogeneous. A linear area of high signal can represent either fluid or granulation tissue1 and was reported by several authors to be a suggestive but not an absolute indicator of an unstable lesion (Fig. 27-23). Because this line may represent vascular granulation tissue, it can also be seen as a healing response. Bohndorf suggested the intravenous administration of contrast agent to differentiate between synovial fluid and

vascular tissue because only the latter will show enhancement. The absence of such a line is a reliable sign of healed osteochondritis dissecans (see Fig. 27-22). Other criteria for instability defined by De Smet and coworkers are (1) a discrete, round area of homogeneous high signal intensity 5 mm or more in diameter beneath the lesion (Fig. 27-24), (2) a focal defect with a width of 5 mm or more in the articular surface of the lesion, and (3) a line of high signal intensity running through the articular cartilage and the subchondral bone plate into the lesion.

Multidetector Computed Tomography The appearance of osteochondritis dissecans on CT is comparable with that on MRI; typically, a sclerotic region is seen that may or may not be surrounded by a radiolucent line. Although partial attachment of the fragment by an osseous bridge is more reliably detected on CT, the most important feature, the state of the articular cartilage, cannot be assessed on CT without intra-articular contrast agent administration.

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■ FIGURE 27-23 Sagittal fat-suppressed T2-weighted FSE MR image. The high signal intensity rim (arrowheads) is indicative of, but not pathognomonic for, an unstable lesion.

■ FIGURE 27-25 Sagittal CT arthrography image. A large cartilaginous loose fragment is completely surrounded by contrast medium indicative of an unstable lesion. Note the presence of large defects in the covering cartilage (arrows). (Courtesy of Prof. B. Vande Berg , Université Catholique de Louvain, Brussels, Belgium.)

Nowadays, a bone scan is sometimes used as a screening method in the workup of chronic knee pain but has lost its place in the therapeutic evaluation of osteochondritis dissecans to MRI.

Arthroscopy

■ FIGURE 27-24 Sagittal fat-suppressed T2-weighted FSE MR image of a completely detached and partially displaced fragment with a large cystic lesion, a broad hyperintense, fluid-filled rim, and extensive bone marrow edema. All these findings indicate unstable osteochondritis dissecans.

During arthroscopy the surgeon attempts to assess the stability of an osteochondritic lesion. When the overlying cartilage is intact, the lesion can be identified as an area of slight discoloration, cartilage softening, or focal depression. Lesions are considered stable if the cartilage does not show softening (Fig. 27-26) or fracturing and the lesion is not ballotable with probing. When a lesion underneath an abnormal area shows mobility during probing, it is considered to be partially detached. If the overlying cartilage is fissured or fractured, a partially

CT arthrography has roughly the same sensitivity and specificity as MRI for evaluating the overlying cartilage, but it does not permit an adequate assessment of the healing potential of an osteochondritis lesion (Fig. 27-25).12

Nuclear Medicine Before the advent of MRI, findings on technetium bone scintigraphy were used to plan a course of treatment. Lesions visible on plain radiography but with normal findings on bone scan were considered to be fully healed or unhealed but without osteoblastic activity. Lesions with high uptake of technetium in the femoral condyle were believed to have potential for repair as a result of the apparent osteoblastic activity. Cahill and Berg concluded that the chance of spontaneous healing correlated with the extent of the local activity and consequently advocated a conservative treatment in these cases, regardless of the radiographic findings. Mesgarzadeh and associates concluded that high accumulation of tracer during the flow, blood pool, and late phases of the radionuclide examination tended to indicate the presence of loose fragments.

■ FIGURE 27-26 Arthroscopic image showing softening of cartilage overlying an unstable osteochondritis dissecans lesion. (Courtesy of Dr. D. De Clercq, City Hospital, Lokeren, Belgium.)

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detached lesion is ballotable or can be elevated. In these cases loose fibrous granulation tissue is often found at the bottom of the partially attached fragments. In more advanced stages, arthroscopy shows a fragment that is loose within the bed or an empty bed. In this case, the surgeon needs to search the knee joint thoroughly for the presence of loose bodies, although these are not always present (Fig. 27-27).

Classic Signs

TABLE 27-3 Radiographic Classification According to Aglietti and Koshina

Stage I Stage II

Stage III

Stage IV Stage V

■ ■ ■ ■

Onset is insidious. Chronic disease can be hard to identify due to remodeling of the lesion site. Typically the lesion is seen as a sclerotic area on a plain radiograph, although early stages are more radiolucent. Cyst formation, cartilage defect, and a high signal intensity line running through the articular surface or beneath the lesion are MR criteria for an unstable lesion.

Subchondral Insufficiency Fracture Associated with Spontaneous Osteonecrosis of the Knee Grading of Subchondral Insufficiency Fractures The radiographic findings of a subchondral insufficiency fracture allow a classification of this entity into five stages4 (Table 27-3). A conclusive classification based on MR findings has to date not been proposed, although MRI is essential for both diagnosis and choice of therapy.

Radiography Because a subchondral insufficiency fracture associated with osteonecrosis is most often situated immediately subarticular to the weight-bearing area of the medial femoral condyle, most abnormalities can be picked up on the

681

Symptomatic patient with normal radiographs Oval radiolucent subtle flattening or focal depression of the bony end plate without narrowing of the joint space Subchondral radiolucent crescent or obvious depression of the end plate, sometimes surrounded by a discrete sclerotic area Focal epiphyseal collapse as described in stage III but with a marked sclerotic halo Deformation of the condyle resulting in secondary osteoarthritis

standard lateral and anteroposterior radiographs. If these are not conclusive, radiographs of the knee in 45 degrees of internal and external rotation may be helpful. The typical presentation of this disease is a radiolucent subchondral crescent, sometimes surrounded by a sclerotic margin (Fig. 27-28). If located in the medial femoral condyle, this makes it hard to differentiate radiologically from the early stages of osteochondritis dissecans. Later stages of both diseases also have a similar presentation on plain radiographs, each displaying more obvious subchondral sclerosis, particularly if osteonecrosis develops between the articular surface and the fracture line.4 The same radiologic abnormalities are found in a subchondral insufficiency fracture of the medial tibial plateau (Fig. 27-29), the second most common location of this disease, and in the lateral femoral condyle. The lateral tibial plateau is rarely affected. Regardless of the location, lesions with a width larger than 45% of the joint surface or a surface area larger than 5 cm2 have a poor prognosis with early progression to collapse and rapidly progressive osteoarthritis.

Magnetic Resonance Imaging Because a subchondral insufficiency fracture and spontaneous osteonecrosis of the knee are accompanied by bone marrow edema, a fluid-sensitive sequence, such as a

■ FIGURE 27-27 Arthroscopic image after removal of the loose fragment. Sclerotic bone becomes visible in the bed. This sclerotic layer inhibits the healing process and has to be removed or pierced. (Courtesy of Dr. D. De Clercq, City Hospital, Lokeren, Belgium.)

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■ FIGURE 27-29 Standard anteroposterior radiograph. A radiolucent line in the medial tibial plateau indicates an intra-articular insufficiency fracture (arrow). (Courtesy of Dr. M. Obradov, Sint-Maartenskliniek, Nijmegen, The Netherlands.)

■ FIGURE 27-28 Anteroposterior (A), posteroanterior (B), and lateral (C) radiographs. The subcortical radiolucent crescent (arrow) seen in the early stage of this subchondral insufficiency fracture is almost invisible on the normal anteroposterior view.

STIR or a T2-weighted FSE sequence with fat saturation, is required for the diagnosis and adequate evaluation of this entity. A T1-weighted or a gradient-echo sequence with good anatomic resolution, such as a dual-echo steadystate (DESS) sequence, is also important to demonstrate fracture lines. Intravenous gadolinium administration can be used to assess the presence of an avascular region.

As stated earlier, the most prominent feature of a subchondral insufficiency fracture with associated osteonecrosis on MRI are poorly demarcated areas of bone marrow edema. However, this pattern of bone marrow edema is not specific and is also seen in transient bone marrow edema and bone bruise. A more specific characteristic of spontaneous osteonecrosis on MR imaging is an area of low signal both on T1- and T2-weighted images adjacent to the bony end plate. This area can be thin and elongated, resulting in an apparent thickening of the bone plate. After intravenous contrast administration, this region shows no enhancement on fat-suppressed T1-weighted images, thus proving it is avascular. The subchondral insufficiency fracture itself is seen as a squiggly line of low signal intensity on T1-weighted images roughly paralleling the articular surface. On T2weighted images Zanetti and associates16 and Yamamoto and colleagues4 described this line as being always hypointense, partially differentiating them from traumatic fracture lines, which can display both high and low signal intensity on T2-weighted images. Lecouvet, however, also reported subchondral fracture clefts with a fluid-like signal. The high signal intensity area corresponds to bone marrow edema and an acute fracture, whereas a hypointense line is caused by compressed trabeculae or focal osteonecrosis (Fig. 27-30). If no conservative treatment is started in the early stages of the disease, an insufficiency fracture associated with osteonecrosis will provoke collapse of the articular surface (Fig. 27-31). In the later stages of the disease the fracture line is often no longer visible owing to progressive collapse of the articular surface and subsequent repair processes. The area of bone marrow edema diminishes, and alterations associated with osteoarthritis become more and more apparent.

Multidetector Computed Tomography As long as there are no abnormalities visible on plain radiographs, CT remains normal, too. Because it is not capable of showing bone marrow edema, it has no added

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value in the diagnosis of subchondral insufficiency fractures or osteonecrosis. Although not diagnostic, multidetector CT is a helpful tool in predicting the outcome of a subchondral insufficiency fracture associated with osteonecrosis. Multiplanar or 3D reconstructions allow a more precise measurement of the lesion size and a better correlation between its area and that of the articular surface.

Nuclear Medicine In a patient complaining of acute and spontaneous knee pain in later life, a subchondral insufficiency fracture has to be ruled out. Because the early stages of this disease are not visible on conventional radiography, a scintigram can be obtained. Typically, technetium bone scintigraphy shows localized increased activity in the medial side of the tibial metaphysis or in the medial femoral condyle4 on blood flow, blood pool, and delayed images. The region of maximum activity invariably corresponds to the articular and subarticular region.15 This pattern of uptake remains virtually unchanged in the first year, after which blood flow becomes gradually less intense. Normalization of

683

Classic Signs ■ ■ ■ ■ ■

Acute onset of the complaints occurs without a clearly remembered trauma. A subchondral radiolucent crescent is present on plain radiographs. Extensive bone marrow edema is a prominent but not a specific finding. Nonenhancing hypointense region of osteonecrosis abuts the subchondral bone plate. A hypointense subchondral insufficiency fracture is often seen in the first stages.

tracer uptake is most likely to occur if no articular collapse takes place, indicating a complete remission. If deformation of the articular surface does occur, uptake remains slightly elevated and gradually assumes a pattern compatible with osteoarthritis. Combined with the clinical signs and symptoms, the pattern of uptake in the acute phase can be enough to establish the diagnosis of spontaneous osteonecrosis.

■ FIGURE 27-30 Sagittal T2-weighted FSE (A), coronal proton density–weighted fat-suppressed (B), sagittal T1-weighted spin-echo (C), and coronal T1-weighted spin-echo (D) MR images. A, A small osteonecrotic area abuts the subchondral bone plate (curved arrow). Beneath it, a subchondral insufficiency fracture is visible as an area of discretely increased signal intensity (straight arrow). B, This line (arrow) is more clearly visible on this fluid-sensitive image. Note the extensive bone marrow edema in the medial femoral condyle. C and D, The fracture line can be seen as an irregular hypointense line (arrows) on the T1-weighted images paralleling the articular surface.

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■ FIGURE 27-31 Sagittal T2-weighted FSE (A) and 3D SPGR (B) MR images. A, The subchondral insufficiency fracture is visible as a hypointense line on the T2-weighted image (arrowheads). B, The gradient-echo image nicely displays trabecular loss around the fracture line and focal collapse of the bony end plate and the overlying cartilage (arrow).

Although a radionuclide scan is still very sensitive for spontaneous osteonecrosis or insufficiency fractures, it has low specificity and is more and more replaced by MRI.

Arthroscopy In the acute stage, insufficiency fractures are not arthroscopically visible. It is only from stage II onward, when subtle flattening of the articular surface occurs, that changes become apparent.

DIFFERENTIAL DIAGNOSIS Although clinical data and imaging findings may suggest a possible cause of an osteochondral lesion, it is sometimes impossible to differentiate between the three entities discussed in this chapter. Minor lesions and the early stages of major lesions are very similar.

From Clinical Data Both osteochondritis dissecans and a subchondral insufficiency fracture associated with osteonecrosis are preferentially found on the medial femoral condyle, but osteochondritis dissecans is typically located on the lateral rim of the medial condyle, whereas an insufficiency fracture has a predilection for the weight-bearing part of the condyle. Spontaneous osteonecrosis of the knee typically occurs in older individuals, whereas patients with osteochondritis dissecans are generally between 12 and 20 years old. Post-traumatic osteochondral fractures can occur at any age but are more often seen in young people, because these individuals tend to be more physically active. As older people become more active, it becomes harder to differentiate between traumatic osteochondral and subchondral insufficiency fractures if they consult their physician with acute knee pain. However, patients with (osteo)chondral fractures tend to be able to recall a traumatic event, whereas patients with insufficiency fractures typically recall a sudden onset of the pain but no trauma.

In younger patients, the acute onset and history of trauma also help in differentiating between osteochondritis dissecans and traumatic (osteo)chondral lesions. Distinguishing between spontaneous and secondary osteonecrosis should first of all be attempted by thoroughly exploring the patient’s history. Sudden onset of the pain is more common in primary osteonecrosis, as is a meniscal lesion in the patient’s history. Causes of secondary osteonecrosis are well known and include, among others, alcoholism, connective tissue diseases, organ or bone marrow transplantation, chemotherapy, and administration of high doses of systemic corticosteroids. Another important difference is the age at onset. Patients with secondary osteonecrosis tend to be younger. They also have more extensive lesions and are often affected bilaterally. This does not mean that patients with a predisposition for secondary osteonecrosis cannot develop primary osteonecrosis. In that case, differentiation should be made on the basis of MR findings.

From Supportive Diagnostic Techniques In elderly patients focal areas of subchondral bone marrow edema associated with osteoarthritis have been described.16 They are seen in the same population as subchondral insufficiency fractures and therefore they need to be differentiated. The areas of bone marrow edema in osteoarthritis are generally much smaller and often located subjacent to areas of chondromalacia. The absence of a hypointense linear structure representing a fracture line is also suggestive of osteoarthritis. Focal osteonecrotic regions can be seen both in osteoarthritis and in association with subchondral insufficiency fractures.16 On MRI both idiopathic and secondary osteonecrosis show abnormal marrow signal. However, bone marrow edema in primary or idiopathic osteonecrosis is ill defined, whereas signal changes in the secondary form display a clear demarcation rim in three fourths of patients (Fig. 27-32). A small sclerotic zone adjacent to the cortical bone, on the other hand, is almost exclusively seen in spontaneous osteonecrosis. Focal deformity of the articu-

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685

■ FIGURE 27-32 Sagittal T2-weighted FSE (A), 3D SPGR (B), and coronal DESS-3D (C) MR images. A and B, Extensive and delineated osteonecrosis in a patient with systemic lupus erythematosus. Both sagittal images show focal subcortical bone resorption with minimal collapse (arrows) of the bony end plate. C, The coronal image clearly illustrates the sharp delineation of the lesion.

lar surface and ipsilateral meniscus lesions also suggest primary osteonecrosis. Transient bone marrow edema or transient osteoporosis, on the one hand, and insufficiency fractures associated with spontaneous osteonecrosis, on the other hand, have nearly identical clinical presentation and patterns

of bone marrow edema but very different outcomes. Transient bone marrow edema or transient osteoporosis can be considered as a diffuse trabecular microfracture surrounded by bone marrow edema (Fig. 27-33). A subchondral insufficiency fracture with associated osteonecrosis is a genuine fracture with disruption of the local

■ FIGURE 27-33 Consecutive coronal DESS-3D images at 1 month (A) and 6 months (B) after sudden knee pain without trauma. In this patient with transient bone marrow edema the absence of an osteonecrotic area warranted conservative therapy, which led to spontaneous resolution of the area of bone marrow edema.

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vascular system. The former is self-resolving, whereas the latter may evolve to irreparable articular damage. The most important prognostic information is the presence of a nonenhancing area of low signal intensity on both T1and T2-weighted images abutting the articular bone plate. Areas thicker than 4 mm, longer than 14 mm, or with a surface area of more than 3 cm2 are pathognomonic for spontaneous osteonecrosis. If not associated with osteonecrosis, a subchondral insufficiency fracture can be either self-resolving or evolve to osteonecrosis. The presence of a hypointense fracture line is therefore not valuable in the differential diagnosis. On CT and especially on MRI, osteochondritis dissecans in children should be differentiated from irregularities seen during the normal maturation of the epiphyseal cartilage.

SYNOPSIS OF TREATMENT OPTIONS The objective of treatment of osteochondral lesions is to obtain normal subchondral bone, preserve or restore the articular cartilage, and ultimately prevent or delay osteoarthritis. If left untreated, adult osteochondritis dissecans, acute osteochondral fractures, and insufficiency fractures associated with osteonecrosis progress to severe osteoarthritis.

Medical Treatment Because there are an unknown number of people who sustain chondral lesions without seeking treatment, it is extremely difficult to uncover the natural progression of an untreated cartilage lesion. According to a number of investigators, many of these lesions, and especially the partial-thickness injuries, are nonprogressive, so no rest, reduced loading, or surgical intervention is needed.17 According to some authors,12 conservative therapy is indicated in osteochondral lesions with intact covering of cartilage (osteochondritis dissecans stage I and IIa, with the exception of cysts larger than 5 mm and insufficiency fractures with absent or small osteonecrotic area). Other authors believe that the adult form of osteochondritis dissecans rarely heals with conservative treatment. Only the juvenile form can be treated conservatively, even to the extent where osteochondral lesions with cartilage damage can demonstrate spontaneous healing. However, if incorporation of the fragment has not occurred by the time of skeletal maturation, the clinical history is similar to that of the adult form. Conservative treatment consists of non–weight bearing, restriction of sports activity, and sometimes the application of a plaster cast during a variable amount of time.

the stem cells first differentiate into osteoblasts and chondroblasts, depending on the tissue surrounding the clot, and later into fibroblasts and fibrocartilaginous cells. Although these cells form an extracellular matrix and take the appearance of chondrocytes, the repair tissue shows rapid degeneration because it does not have the same viscoelastic properties as normal adult hyaline cartilage. Some of the underlying reasons for this are the low amounts of type II collagen in the matrix and the accelerated loss of chondroitin and keratan sulfate. The different mechanical properties also give rise to microscopic movement between the repair tissue and the surrounding cartilage, resulting in lack of integration at the interface between both tissues.18,19 Migration of stem cells can occur from bone marrow, synovium, and periosteal or perichondrial grafts. The migration of adult chondrocytes should be possible but has not been described in vivo. Another way of bringing stem cells into a chondral lesion is by deliberately perforating the subchondral lamina.20 The most well-known procedure in this context is microfracturing, which was first reported by Steadman and colleagues in 1997. Pridie drilling and abrasion arthroplasty are other reparative procedures in which the subchondral bone is pierced or partially removed (Fig. 27-34). Palliative procedures for treatment of cartilage lesions include débridement, lavage, and shaving. Lavage is reported to alleviate pain, whereas débridement and shaving reduce mechanical and inflammatory symptoms. None of these techniques, however, induces the formation of repair tissue, and the relief they bring is usually temporary.20 If the procedure includes the implantation or transplantation of autogenic or allogenic tissues, it is considered restorative. These tissues can be purely soft tissue, such as periosteum or perichondrium, include chondrocytes, or consist of both cartilage and bone.

Surgical Treatment Because of the lack of stem cells in adult hyaline cartilage, there is no intrinsic repair capability. Spontaneous repair is initiated when the subchondral bone plate is damaged and stem cells can migrate from the subchondral space.18 In the blood clot that forms in an osteochondral lesion,

■ FIGURE 27-34 Coronal DESS-3D MR image. A cartilage defect in this knee was treated with microfracturing. This explains the indentations in the bony end plate at regular intervals (arrow). The covering fibrocartilage has a slightly higher signal intensity than the surrounding cartilage in this patient.

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687

■ FIGURE 27-35 Sagittal T2-weighted FSE (A) and coronal DESS-3D (B) MR images. A large osteochondral plug is still clearly demarcated by a sclerotic rim around the osseous part. There is a small resorption cyst at the proximal end of the plug (arrow, A).

The implanted soft tissues are a source of progenitor cells and fill the cartilaginous defects in a similar way and with a similar kind of repair tissue as do the reparative procedures. Osteochondral transfer can be done with either autologous or allogenic osteochondral plugs or even with entire femoral condyles (Fig. 27-35).21 These techniques can cope with both large and small osteochondral defects and are reported to have a similar clinical outcome as repair based on cultured chondrocyte implantation, the third major type of restorative procedure. This group includes all cell transplantation based repair, such as autologous chondrocyte implantation (ACI), allogenic chondrocyte transplantation (ACT), and autogenic or allogenic stem cell transplantation (Fig. 27-36). Before they are implanted, these cells are cultured in monolayer or on a scaffold, often hyaluronan or collagen based. The just-mentioned techniques can be used for all osteochondral lesions. In the case of osteochondritis dissecans in an adult patient, the lesion can be treated by drilling or fixation of the fragment. Unstable lesions in which the fragment is still in the bed have to be

■ FIGURE 27-36

Sagittal 3D SPGR image. The site of chondrocyte implantation is demarcated by microscopic metallic artifacts in the covering periosteum and at the interface between the repair tissue and the native cartilage, producing a band of low signal intensity around the repair tissue.

What the Referring Physician Needs to Know 1. The best techniques for detection of suspected osteochondritis dissecans are plain radiography and MRI. 2. The best techniques for evaluation of osteochondritis dissecans are a. MRI to detect bone marrow edema and evaluate the overlying cartilage. b. MRI to evaluate the stability of the lesion. c. CT arthrography to detect dissecting fissures in the overlying cartilage. d. CT and MRI to assess the extent of the lesion. 3. The best techniques for detection of suspected osteochondral or chondral trauma are MRI and CT arthrography, because they allow assessment of the cartilage surface. 4. The best techniques for evaluation of osteochondral or chondral trauma are a. MRI to detect bone marrow edema, evaluate the morphologic changes in the damaged cartilage, and detect a detached osteochondral fragment. b. CT to detect damage to the cartilage surface and to detect a detached osteochondral fragment. c. CT and MRI to assess the extent of the lesion. 5. The best techniques for evaluation of subchondral insufficiency fracture or spontaneous osteonecrosis are a. Plain radiography to detect a subchondral lucency and/ or focal depression of the subchondral bone plate. b. MRI to detect bone marrow edema and demonstrate a subchondral hypointense fracture line or associated osteonecrosis. c. CT and MRI to assess the extent of the lesion. 6. In all cases, MRI is the best technique to evaluate concomitant articular derangement.

stabilized. This, too, can be done with drilling or fixation (Fig. 27-37). The short-term results of excision are good, but the long-term results are extremely poor. Consequently, most authors recommend bone grafting and replacement of the fragment when it is technically possible because the long-term results are better than those after excision.

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■ FIGURE 27-37 Posteroanterior (A) and lateral (B) radiographs and coronal CT arthrographic image (C). A loose osteochondral fragment has reattached itself to the surrounding bone after fixation with three compression screws.

SUGGESTED READINGS Bohndorf K. Imaging of acute injuries of the articular surfaces (chondral, osteochondral and subchondral fractures). Skeletal Radiol 1999; 28:545–560. Brittberg M, Winalski CS. Evaluation of cartilage injuries and repair. J Bone Joint Surg Am 2003; 85(Suppl 2):58–69. Buckwalter JA. Articular cartilage injuries. Clin Orthop Relat Res 2002; 402:21–37. Cahill BR. Current concepts review: osteochondritis dissecans. J Bone Joint Surg Am 1997; 79:471–472. Huber M, Trattning S, Lintner F. Anatomy, biochemistry and physiology of articular cartilage. Invest Radiol 2000; 35:573–580.

Imhof H, Nobauer-Huhmann IM, Krestan C, et al. MRI of the cartilage. Eur Radiol 2002; 12:2781–2793. Lecouvet FE, Malghem J, Maldague BE, Vande Berg BC. MR imaging of epiphyseal lesions of the knee: current concepts, challenges, and controversies. Radiol Clin North Am 2005; 43:655–672. Recht M, White LM, Winalski CS, et al. MR imaging of cartilage repair procedures. Skeletal Radiol 2003; 32:185–200. Verstraete KL, Almqvist F, Verdonk P, et al. Magnetic resonance imaging of cartilage and cartilage repair. Clin Radiol 2004; 59:674–689. Yoshida S, Recht MP. Postoperative evaluation of the knee. Radiol Clin North Am 2002; 40:1133–1146.

REFERENCES 1. Chung CB, Isaza IL, Angulo M, et al. MR arthrography of the knee: how, why, when. Radiol Clin North Am 2005; 43:733–746. 2. Resnick D, Goergen TG. Physical injury: concepts and terminology. In Resnick D (ed). Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, 2002, pp 2627–2782. 3. Curl WW, Krome J, Gordon ES, et al. Cartilage injuries: a review of 31,516 knee arthroscopies. Arthroscopy 1997; 13:456–460. 4. Yamamoto T, Bullough PG. Spontaneous osteonecrosis of the knee: the result of subchondral insufficiency fracture. J Bone Joint Surg Am 2000; 82:858–866.

5. Benninghoff A. Form und Bau der Gelenkknorpel in ihren Beziehungen zur Funktion. Z Zellforsch 1925; 2:783–862. 6. Imhof H, Sulzbacher I, Grampp S, et al. Subchondral bone and cartilage disease—a rediscovered functional unit. Invest Radiol 2000; 35:581–588. 7. Brittberg M, Aglietti P, Gambardella R, et al. ICRS Cartilage Injury Evaluation Package. ICRS—International Cartilage Repair Society 2005; available at: http://www.cartilage.org. 8. Redman SN, Dowthwaite GP, Thomson BM, Archer CW. The cellular responses of articular cartilage to sharp and blunt trauma. Osteoarthritis Cartilage 2004; 12:106–116.

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9. Shahriaree H. Chondromalacia. Contemp Orthop 1985; 11:27–39. 10. Verstraete KL, Almqvist F, Verdonk P, et al. Magnetic resonance imaging of cartilage and cartilage repair. Clin Radiol 2004; 59:674–689. 11. Peterfy CG. Scratching the surface: articular cartilage disorders in the knee. Magn Reson Imaging Clin North Am 2000; 8:409–430. 12. Bohndorf K. Osteochondritis (osteochondrosis) dissecans: a review and new MRI classification. Eur Radiol 1998; 8:103–112. 13. Lang P, Farima N, Hiroshi Y. MR imaging of articular cartilage: current state and recent developments [abstract]. Radiol Clin North Am 2005; 43:629–639. 14. Vande Berg BC, Lecouvet FE, Poilvache P, et al. Assessment of knee cartilage in cadavers with dual-detector spiral CT arthrography and MR imaging. Radiology 2002; 222:430–436. 15. Greyson ND, Lotem MM, Gross AE, Houpt JB. Radionuclide evaluation of spontaneous femoral osteonecrosis. Radiology 1982; 142:729–735.

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16. Zanetti M, Bruder E, Romero J, Hodler J. Bone marrow edema pattern in osteoarthritic knees: correlation between MR imaging and histologic findings. Radiology 2000; 215:835–840. 17. Shelbourne KD, Jari S, Gray T. Outcome of untreated traumatic articular cartilage defects of the knee: a natural history study. J Bone Joint Surg Am 2003; 85(Suppl 2):8–16. 18. Shapiro F, Koide S, Glimcher MJ. Cell origin and differentiation in the repair of full-thickness defects of articular-cartilage. J Bone Joint Surg Am 1993; 75:532–553. 19. O’Driscoll SW, Marx RG, Beaton DE, et al. Validation of a simple histological-histochemical cartilage scoring system. Tissue Eng 2001; 7:313–320. 20. Smith GD, Knutsen G, Richardson JB. A clinical review of cartilage repair techniques. J Bone Joint Surg Br 2005; 87:445–449. 21. Alford JW, Cole BJ. Cartilage restoration: I. Basic science, historical perspective, patient evaluation, and treatment options. Am J Sports Med 2005; 33:295–306.

C H A P T E R

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Ankle/Foot: Technical Aspects, Normal Anatomy, Common Variants, and Basic Biomechanics Lisa O. Ballehr

TECHNICAL ASPECTS

Computed Tomography (Table 28-2)

Conventional Radiography (Table 28-1)

Indications

Indication

●

●

Primary initial evaluation of a majority of foot and ankle pathologic processes, including trauma, infection, tumor, arthritis, congenital or biomechanical dysfunction, hardware placement, and foreign bodies

Advantages ●

● ●

Detailed evaluation of bone integrity, contour, and joint alignment and efficient initial evaluation of soft tissue and fat interfaces Readily available, fast, efficient, and inexpensive Readily distinguishes calcification, ossification, bone proliferation, spurring, periosteal and cortical pathologic processes, and otherwise inconspicuous cortical avulsion fractures

●

● ●

Advantages ●

●

Disadvantages ● ●

Exposure to ionizing radiation (minimal) Limited sensitivity and specificity of soft tissue pathology

Technical Aspects ● ●

High-definition film/screen combination for foot and toes Medium-speed film/double-screen combination for ankle

690

Details fracture pattern, alignment, apposition, and healing response Details transarticular osseous pathology, including arthritis, coalitions, and acute or chronic traumatic arthrosis Primary osseous lesions in patients with contraindication for MRI Distinguishes osteoid versus chondroid tumor matrix

●

CT provides excellent osseous detail, and multiplanar and surface reconstructed images provide 3D anatomic and osseous transarticular detail. Thirty-two- to 64-slice volume acquisition, 3D multiplanar imaging provides reduced beam-hardening artifact seen with conventional CT and allows improved evaluation of hardware placement and alignment. Reconstructed multiplanar imaging details complex fractures and is utilized for surgical planning.

Disadvantages ● ● ●

Exposure to ionizing radiation Expensive Limited sensitivity and specificity of soft tissue pathologic processes. Sensitivity has shown to be improved by intravenous use of a contrast agent.

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foot, myopathies, entrapment syndromes, osteomyelitis, synovitis, ligament and tendon pathologic processes, sesamoid disorders, plantar plate pathology, Morton’s neuroma, turf toe, plantar fascial disorders, nonradiopaque retained foreign bodies

TABLE 28-1 Radiographic Projections Projection

Anatomy/Indication

Routine Toe (coned) Anteroposterior toes only Anteroposterior foot

Tufts, subungual, interphalangeal space

Oblique toes only Lateral toes only Sesamoid (coned tangential view) Calcaneus Axial (plantardorsal) Lateral Foot Anteroposterior (10–15° toward heel) Medial oblique Lateral (mediolateral) Lateral oblique Anteroposterior (weight bearing) Lateral (weight bearing)

Intertarsal space, metatarsophalangeal joints Bone contours, phalanges Dislocation Sesamoids Transverse (mediolateral) calcaneus Anteroposterior calcaneus Metatarsals, tarsometatarsal joints, 1st and 2nd intermetarsal alignment of 3rd, 4th, 5th tarsometatarsal joints, talonavicular joint, calcaneocuboid joint, sinus tarsi, lateral cuneiforms Tibiotalar joint, subtalar joint, navicular, metatarsal alignment of 1st, 2nd tarsometatarsal joints, medial cuneiforms Tibiotalar articular alignment, coalition Coalition, subtalar joint, functional measurements

Ankle Anteroposterior (no Tibiotalar joint, medial mortise rotation) Anteroposterior mortise Talar dome, medial and lateral mortise, (15–20° internal oblique) distal talofibular joint distal fibular tip Medial oblique (45° internal) Lateral (mediolateral) Anteroposterior tibiotalar joint, base of 5th metatarsal, posterior malleolus, distal tibia and fibula, posterior subtalar joint, joint recess fat plane, pre-Achilles fat plane Varus and valgus stress: Primarily used for ligament insufficiency. 45° internal oblique, Has largely been replaced by MRI 45° external oblique

691

Advantages ●

●

●

●

Provides excellent spatial resolution and tissue contrast of soft tissue pathology and delineates intratrabecular, marrow, cortical, and periosteal bone pathologic processes Allows localization of pathologic processes of osseous, articular, chondral, neurovascular, ligament, tendon, capsular, retinacular, and supporting structures High sensitivity and specificity for evaluating intraarticular pathology, including nonossified debris and bodies No ionizing radiation

Disadvantages ● ●

● ●

●

●

Expensive Claustrophobic in closed magnets (high-field open magnet provides high-resolution imaging as an alternative for claustrophobic patients) Long examination times, leading to patient motion Contraindicated in patients with many types of implanted mechanical devices such as pacemakers. Manufacturer guidelines should be referred to before the examination. Contraindicated for patients with metal in orbits, intracranial aneurysm clips, and surgery within a 6- to 8-week period Risk of MRI to fetus is unknown in first trimester of pregnancy and considered a relative contraindication.

Technical Aspects ●

TABLE 28-2 Multidetector Computed Tomography: Protocol Slice thickness Matrix kVP mAs Collimation Pitch Kernel Reformatting

1.25–2.00 mm 512 × 512 120–130 kVP 75–130 mAs 0.75–1.00 mm (16 slices) 0.5-s gantry rotation B31 soft tissue, B70 bone Multiplanar reformatting/surface rendering using 2-mm slice thickness at every 0.5-mm interval using 136- to 200-mm reconstruction field of view. Generally reconstructed from axial plane.

Magnetic Resonance Imaging (Table 28-3) Indications ●

Osteonecrosis, avascular necrosis, soft tissue and osseous tumors, occult fractures, osteochondral pathology, sinus tarsi syndrome, arthropathies, neuropathy, diabetic

●

●

There are several variations in imaging protocols: proton density–weighted and proton density–weighted, fat-saturated sequences are obtained in three planes; alternatively, T1- and T2-weighted fast spin-echo, fatsaturated sequences in three planes are also commonly used. T1-weighted sequences are preferred for demonstrating trabecular detail and osseous pathology and should be used for suspected bone lesions and marrow pathology such as osteomyelitis. Short echo time sequences produce intermediate signal artifact within normal tendons when tendons are at an orientation of greater than 55 degrees to the main magnetic field. This creates false-positive findings. For this reason, higher echo time proton density/T2weighted sequences are preferred over T1-weighted sequences for routine imaging of the foot and ankle and in particular when a pathologic process of a tendon pathology is clinically questioned. This occurs particularly in the sagittal plane at the retromalleolar course of the peroneal tendons, posterior tibial tendon, and flexor digitorum longus and flexor hallucis longus tendons.

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TABLE 28-3 Magnetic Resonance Imaging: Protocol 1.5T MRI Ankle Protocol ■ Routine MRI of the ankle includes tibiotalar joint, subtalar joint, and chopart (transverse tarsal) joints and should include the Achilles tendon and plantar fascia. ■ An open FOV sagittal image should be included for suspected myotendinous junction pathology of the Achilles tendon. This is generally seen in young athletes. ■ FOV should include the base of the 5th MT or navicular for suspected distal insertion PBT or PTT pathology. Alternatively, if this is the primary area of interest a dedicated midfoot MRI is preferred.

Axial

Parallel to distal tibial plafond. Scan 3 slices above tibial plafond and 1 slice below plantar fascia.

Sagittal

90 Degrees perpendicular to axial plane. Parallel to talar axis. Include 1 slice within subcutaneous tissues adjacent to the malleoli.

Coronal

Perpendicular to sagittal plane and include navicular cuneiform joint anteriorly and Achilles tendon posteriorly.

1.5T MRI Midfoot Protocol Preferred evaluation of the inframalleolar course of PTT and peroneal tendons and distal insertions of the ATT, PTT, and peroneal tendons. Preferred evaluation of the transverse tarsal, intertarsal, and Lisfranc ligament and joints. ■ 45 Degree oblique plane allows imaging perpendicular to the inframalleolar course of the PTT and details tendon and medial ankle ligaments. ■

Axial

Axial plane is parallel to the long axis of the 2nd metatarsal. 90 Degrees perpendicular to coronal plane. Include dorsal and plantar skin from talus to sole.

Sagittal

90 Degrees perpendicular to axial plane and include the width of the foot and 2 slices within subcutaneous tissues adjacent to the medial cuneiform and 5th metatarsal base.

ATT, anterior tibial tendon; DIP, distal interphalangeal; FOV, field of view; MTP, metatarsophalangeal; MT, metatarsal; PBT, peroneus brevis tendon; PIP, proximal interphalangeal; PTT, posterior tibial tendon.

(Continued)

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693

TABLE 28-3 Magnetic Resonance Imaging: Protocol—Cont’d

Coronal

Perpendicular to long axis of the shaft of the 2nd metatarsal. Cover from mid talocalcaneal joint to the metatarsal necks or heads.

45-Degree oblique axial

Alternative 45-degree oblique axial plane, obtained in prone position. Plane is parallel to line that bisects the peroneal tendons at the apex of the arc of the malleolus or parallel to line that bisects angle between long axis of the tibia and long axis of the calcaneus.

1.5T MRI Forefoot Protocol ■ Preferred evaluation of the MTP, PIP and DIP joints, hallux sesamoid complex, plantar plates, intermetatarsal space and distal digits. ■ Foot is plantar flexed and patient is imaged in prone position.

●

Axial

Axial plane is parallel to the long axis of the 2nd metatarsal. 90 Degrees perpendicular to coronal plane. Include dorsal and plantar skin.

Sagittal

90 Degrees perpendicular to axial plane. Include the entire width of the foot.

Coronal

Perpendicular to long axis of the shaft of the 2nd metatarsal. Cover from the metatarsal shafts or necks to the tip of the toes.

Short tau inversion recovery (STIR) sequences alternatively may be used in place of fat-saturated sequences and provide greater sensitivity for fluid signal, but proton density–weighted and T2-weighted, fat-saturated sequences provide higher spatial resolution, allowing localization of fluid signal denoting a pathologic process.

● ●

STIR sequences may be more sensitive for evaluating subtle diffuse pathologic processes of muscle. To decrease metal hardware susceptibility artifact: maximize the bandwidth, decrease the echo time, increase the interecho train length, and use STIR sequences in place of fat-saturated sequences. Phase and frequency encoding direction should be parallel

694

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●

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to the shaft of the hardware or parallel to the area of interest. Multiple sequences have been used for chondral pathologic processes. Research continues with specialized sequences, but, to date, proton density– weighted, fast spin-echo, fat-saturated and STIR fast spin-echo sequences are preferred and widely utilized. Postcontrast fat-suppressed T1-weighted images are useful in imaging inflammatory processes and vascular lesions. Indirect MR arthrography when images are obtained after 30 minutes has been found to be useful in increasing contrast and spatial resolution of ligament and tendon tears and in visualization of joint debris and chondral defects and pathologic processes. Direct MR arthrography allows visualization of distention of the joint space and intravasation of contrast medium through the suspected ligament, diagnosis of capsular or retinacular tears, as well as evaluation of stability of osteochondral lesions and detection of intra-articular bodies. Parameters using a 1.5-T magnet: ● Phased-array four- or eight-channel send-receive coil (standard knee coil with foot chute for ankle and midfoot; wrist coil for forefoot and toes); surface coil for isolated toe pathologic process can be used, but newer phased-array coils provide higher resolution. ● Slice thickness in three planes is generally 3 to 5 mm with field of view 12 to 16 cm for ankle and midfoot; 2 to 4 mm with field of view 12 to 14 cm for forefoot; and matrix 256 × 192 to 256. If signal-to-noise ratio allows, smaller slice thickness can be used for fine anatomic detail of plantar plates, intermetatarsal space, and hallux sesamoid complex.

Ultrasonography Indications ●

Tendon tears and pathologic processes, ligament tears, muscle lesions or tears, muscle perfusion, bursal inflammation or fluid collection, soft tissue foreign bodies, nerve inflammation or focal lesions, dynamic imaging of tendon dysfunction, joint effusions, ganglion cysts, and plantar fascial fibromas or tears

Advantages ● ● ●

Used as a tool to complement MRI and CT Quick, efficient, dynamic, and noninvasive Relatively inexpensive

Disadvantage ●

Highly dependent on skill of the technologist and experience of the interpreting radiologist

Technical Aspects ●

● ● ●

●

●

Dependent on high-resolution and high-frequency transducer and advanced hardware and software ultrasonographic capabilities Needs 5- to 10-MHz transducer for deep soft tissues and broader field of view Needs 10- to 15-MHz transducer for superficial ligaments, tendons, and soft tissue structures Needs 17-MHz transducer or higher for detailed resolution of small field of view and superficial structures Tissue harmonic imaging and compound imaging provide finer resolution of deep structures and improve real-time spatial resolution. Power Doppler imaging and use of contrast agents improve detection of blood flow and muscle and soft tissue perfusion.

NORMAL ANATOMY Talocrural Joint Medial Ankle Mortise (Figs. 28-1 to 28-4) The talocrural joint is composed of the tibia, fibula, and talus. The distal tibia has two hyaline cartilage–covered synovial-lined articular surfaces. The lateral surface of the medial malleolus articulates intimately with a broad medial articular facet of the talus. It is formed by the anterior and posterior colliculus and intercollicular groove to which the deltoid ligament attaches and forms a strong, fairly rigid medial ankle mortise.

Medial Collateral Ligament Complex (see Figs. 28-3 to 28-5)

Nomenclature referring to the components that comprise the deltoid ligament is variable in the literature. Radiologists generally refer to a superficial and deep ligament based on MRI resolution of individual fibers being limited. The deep deltoid ligament (anterior and posterior tibiotalar fibers) is a broad fan-shaped fasciculated ligament that originates from the intercollicular groove and adjacent surfaces of the anterior and posterior colliculus. It is a synovial-lined intra-articular ligament. The superficial deltoid ligament (anterior and posterior tibiotalar, tibionavicular, and tibiocalcaneal fibers) is a broad, flat, triangular fibrous band that originates from the anteromedial surface of the anterior colliculus and medial subcutaneous surface of the malleolus. Distal fibers interdigitate with the superomedial fibers of the calcaneonavicular ligament. This is referred to as the tibiospring ligament.

Central Ankle Mortise and Joint Capsule (see Figs. 28-1 to 28-6)

The distal tibia is covered by hyaline cartilage and articulates with the dorsal surface of the talus called the trochlea. The dorsal surface of the talus from anterior to posterior is concave, and the tibia is convex. From medial to lateral the talus is mildly convex and the tibia is mildly concave.

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■ FIGURE 28-1 The articulating bones in different joints of the right foot. Anterior view with the talocrural joint in plantarflexion. (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

A fibrous joint capsule attaches to the anterior and inferior ridge of the distal tibia and medial and lateral malleoli and is intimate with the trochlear articular margins of the talus except anteriorly where it attaches to the talar neck. The anterior and posterior capsule is weak and lined by synovium.

Lateral Ankle Mortise (see Figs. 28-1 to 28-6) The lateral ankle mortise tends to be flexible as opposed to the rigid medial mortise. The lateral talus and medial facet of the lateral malleolus form a small triangular articulation. The lateral surface of the distal tibia is in the shape of a convex triangular notch in which the distal fibular shaft rests. It is attached to the tibia by the syndesmotic ligament complex, the interosseous ligament, and the interosseous membrane.

695

■ FIGURE 28-2 Overview of the joints in the foot: talocrural joint (ankle joint), subtalar joint (talocalcaneal joint and talocalcaneonavicular joint),* calcaneocuboid joint (between the calcaneus and cuboid bone), talonavicular joint (between the talus and navicular bone), transverse tarsal joint (calcaneocuboid joint and talonavicular joint), cuneonavicular joint (between the cuneiform and navicular bones), intercuneiform joints (between the cuneiform bones), cuneocuboid joint (between the lateral cuneiform and cuboid bones), tarsometatarsal joints, intermetatarsal joints (between the bases of the metatarsal bones), metatarsophalangeal joints (between the bases of the metatarsal bones), proximal interphalangeal joints, distal interphalangeal joints. *In the subtalar joint the talus articulates with the calcaneus and the navicular bone to form two separate articulations, the talocalcaneal joint posteriorly and the talocalcaneonavicular joint anteriorly. Both are often referred to collectively as the “subtalar joint.” (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

Syndesmotic Ligament Complex (see Figs. 28-3 to 28-6) The anteroinferior tibiofibular syndesmotic ligament is a multifasciculated, flat, fibrous laminar band that originates from the anteromedial tubercle of the distal fibula and inserts on the anterolateral tubercle of the distal tibia. The caudal fibers at the fibular origin interdigitate with origin of the anterior talofibular ligament. The posteroinferior tibiofibular syndesmotic ligament is made up of a deep transverse and superficial component. The deep transverse fibers twist about each other to

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

■ FIGURE 28-4 The ligaments of the right foot. Posterior view (plantigrade foot position). (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

■ FIGURE 28-3

The ligaments of the right foot. Anterior view (talocrural joint in plantarflexion). (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

Below the syndesmotic ligament complex is the posterosuperior tibiofibular recess, which can contain a synovial fold that extends cranially from the talocrural joint.

Lateral Collateral Ligament Complex form a very strong thick fibrous band. It originates from the posterior fibular tubercle and attaches across the entire posterior tibial plafond to the medial border of the malleolus. It courses inferior to the tibial plafond, deepening the articular surface of the tibia, and forms a true functional labrum. The triangular fibular origin forms an articular surface for the talar facet. The superficial syndesmotic ligament is broad and fan shaped. It originates from the posterior crest of the fibula. It extends above and below the posterior fibular tubercle and has two attachments. The first attachment is to the posterolateral tibial tubercle, and the second is a broad attachment across the tibial plafond to the border of the posterior tibial tendon groove. The interosseous ligament is a short dense band extending from the medial surface of the fibula to the lateral surface of the tibia.

(see Figs. 28-3, 28-4, and 28-6) The anterior talofibular ligament, posterior talofibular ligament, and calcaneofibular ligament comprise the lateral collateral ligament complex. The anterior talofibular ligament is composed of two flat, thick, fibrous bands. The cranial band is thicker and stronger and originates from the anteromedial distal fibula and attaches to the lateral neck of the talus. The posterior talofibular ligament is a broad, flat, triangular ligament interspersed with fatty fibers. The widest portion of the ligament originates from the deep posterior lateral malleolar fossa and attaches to the lateral tubercle of the talus. The calcaneofibular ligament is a fibrous band that originates from the deep posterior lateral malleolar fossa and courses inferiorly and posteriorly to the lateral surface of the calcaneus. The medial peroneal tendon sheath

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● Ankle/Foot: Technical Aspects, Normal Anatomy, Common Variants

697

■ FIGURE 28-5 The ligaments of the right foot, medial view. The medial and lateral collateral ligaments, along with the syndesmotic ligaments, are of major importance in stabilizing and guiding the subtalar joint, because portions of these ligaments are taut in every joint position and thus in every movement. The ligaments of the foot are classified by their location as belonging to the talocrural or subtalar joint, the metatarsus, the forefoot, or the sole of the foot. (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

■ FIGURE 28-6 The ligaments of the right foot, lateral view. Sprains of the ankle joint and especially of its lateral ligaments (usually supination trauma—buckling of the ankle in a supinated position) are extremely common injuries. They often occur during plantarflexion of the foot, a position that provides less bone stability to the talocrural joint. Most of these injuries occur during sports and other leisure activities when the ankle gives way on uneven ground. Typically the trauma will cause stretching or tearing of the anterior talofibular ligament, the calcaneofibular ligament, or both. If the leg is twisted violently while the foot is fixed, there may also be separation of the ankle mortise with disruption of the tibiofibular syndesmosis. (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

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is intimately attached to the calcaneofibular ligament in the inframalleolar course.

Talocalcaneal Joint (Figs. 28-7 to 28-11) The talocalcaneal joint is made up of two independent synovial-lined articulations: the anterior (talocalcaneonavicular) and posterior (talocalcaneal) subtalar joints.

Anterior Subtalar Joint The anterior subtalar joint is formed by the head of the talus, which is oval, convex, and medially rotated, and the proximal concave body of the navicular. The plantar surface of the head of the talus articulates anterolaterally with the superior surface of the calcaneus and posteriorly with the sustentaculum tali of the calcaneus. The plantar and medial articulation is supported by the deltoid ligament and calcaneonavicular ligament (spring ligament complex).

Posterior Subtalar Joint ■ FIGURE 28-7

The right talus and calcaneus. Dorsal view. The two tarsal bones have been separated at the subtalar joint to demonstrate their articular surfaces. (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

The posterior calcaneal facet of the talus articulates with the posterior talar facet of the calcaneus. The posterior subtalar joint may communicate with the talocrural joint in up to 20% of persons.

■ FIGURE 28-8 The right talus and calcaneus. Medial view. The two tarsal bones have been separated at the subtalar joint to demonstrate their articular surfaces. (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

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● Ankle/Foot: Technical Aspects, Normal Anatomy, Common Variants

699

■ FIGURE 28-9 The right talus and calcaneus. Lateral view. The two tarsal bones have been separated at the subtalar joint to demonstrate their articular surfaces. (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

Spring Ligament Complex

Talocalcaneonavicular Ligament Complex

(see Figs. 28-10 and 28-11)

There are three major supporting ligaments of the subtalar joint: the cervical ligament, inferior extensor retinaculum, and interosseous talocalcaneal ligament. The anterior, medial, posterior, and lateral talocalcaneal ligaments and portion of the interosseous talocalcaneal ligament in part comprise the cervical ligament. Minor supporting ligaments exist but are not always resolved on MRI. Numerous variations of the sinus tarsi ligamentous anatomy exist in literature. The cervical ligament originates from the anteromedial floor of the sinus tarsi (cervical tubercle) and courses anteromedially and upward to attach to the neck of the talus. The cervical ligament is the strongest ligament of the sinus tarsi. Posterior and medial reflections of the inferior extensor retinaculum course parallel and lateral to the cervical ligament and form a strong support for the lateral sinus tarsi. The interosseous talocalcaneal ligament (ligament of the tarsal canal) is a broad, flat, oblique and medially oriented band originating from the sulcus of the calcaneus at the anterior border of the posterior talocalcaneal joint and attaches to the medial undersurface of the sustentaculum tali.

The spring ligament complex is a major support structure for the longitudinal arch of the foot. It primarily supports the head of the talus at the anterior and middle facets of the calcaneus. It is composed of the inferoplantar band, medioplantar oblique band, and inferoplantar band. The inferoplantar ligament originates from the coronoid fossa of the calcaneus and inserts on the navicular beak. The medioplantar oblique ligament originates from the medial margin of the coronoid fossa and attaches to the caudal surface of the navicular tuberosity. The superomedial ligament originates from the medial surface of the sustentaculum tali, interdigitates with fibers of the tibiospring ligament, and attaches to the superior and peripheral border of the navicular tuberosity.

Sinus Tarsi (see Figs. 28-8 and 28-9) The sinus tarsi is a cone-shaped soft tissue canal with a medial apex called the tarsal canal and a lateral outlet. The posterior talar facet is separated from the middle and anterior talar facet by the sinus tarsi. It contains fat and branches from the posterior tibial artery and nerve, peroneal artery and nerve, and supporting ligaments.

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

■ FIGURE 28-11 Course of the plantar calcaneonavicular ligament. Plantar view. The plantar calcaneal navicular (spring) ligament stretches between the sustentaculum tali and the navicular. It completes the bony socket of the talocalcaneal joint from the plantar side. (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

■ FIGURE 28-10 The articular surfaces of an opened subtalar joint. Right foot, dorsal view (after separation of the talus). In the subtalar joint the talus articulates with the calcaneus and the navicular. It consists of two completely separate articulations: a posterior compartment (the talocalcaneal joint) and anterior compartment (the talocalcaneal navicular joint). The boundary between the two compartments is formed by the interosseous talocalcaneal ligament located in the tarsal canal (bony canal formed by the sulcus tali and sulcus calcanei; its entrance is the sinus tarsi). The plantar calcaneonavicular ligament, which has cartilage cells in its medial surface, loops like a tendon around the plantar head of the talus, which acts as a fulcrum. It stabilizes the position of the talus on the calcaneus and helps to support the apex of the longitudinal pedal arch. Overstretching of the plantar calcaneonavicular (spring) ligament due to flattening of the plantar vault promotes the development of flatfoot. (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

The lateral talocalcaneal ligament courses parallel with the calcaneofibular ligament, and it is often difficult to differentiate the two on MRI. It originates from the inferior surface of the lateral talar process and attaches to the lateral and posterior surface of the calcaneus and is generally just anterior and slightly medial to the insertion of the calcaneofibular ligament. The posterior talocalcaneal ligament is a short, flat ligament that originates from the lateral surface of the talar tubercle and inserts on the superior and medial aspect of the calcaneus. Fibers may variably interdigitate with the posterior talofibular ligament.The ligament may originate from an os trigonum and form a trigonocalcaneal ligament. The medial talocalcaneal ligament originates from the posteromedial border of the talar tubercle and attaches to the posterior border of the sustentaculum tali of the calcaneus.

The talonavicular ligament has both a superficial and a deep component and crosses both dorsal and plantar to the superomedial calcaneonavicular ligament. The dorsal fibers interdigitate with the ligament. They originate from the dorsal surface of the talar neck and insert on the dorsum of the navicular.

Calcaneocuboid Joint (see Figs. 28-6, 28-10, and 28-11) Both the calcaneal and cuboid articular surface is rectangular. The joint is supported by a capsule, the long plantar ligament, and the bifurcate, dorsolateral, and plantar calcaneocuboid ligament. The bifurcate ligament is composed of fibers of the lateral inferoplantar calcaneonavicular ligament and medial calcaneocuboid ligament.

Chopart Joint (see Figs. 28-1, 28-5, and 28-6) The Chopart joint (transverse tarsal joint) is a biomechanically intricate unit made up of the anterior subtalar joint (talocalcaneonavicular joint) and the calcaneocuboid joint and cubonavicular joint. The joints act in unison to coordinate transmission of forces from hindfoot to forefoot and provide transverse arch support. There is a dorsal, plantar, and interosseous cubonavicular ligament.

Intertarsal Joints (see Figs. 28-1, 28-10, and 28-11) Intertarsal joints are composed of the distal navicular and proximal medial, intermediate and lateral cuneiform articulations, and all are reinforced by one joint capsule.

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■ FIGURE 28-12 The dorsal muscles of the foot (extensor digitorum brevis and extensor hallucis brevis). Right foot, dorsal view. (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

The cuboid and lateral cuneiform and the cuboid and navicular articulations comprise two additional intertarsal joints. Gliding and rotation of the joints occurs simultaneously as a functional unit. Each joint has a dorsal, plantar, and interosseous ligament named for the bone origin and bone insertion.

Tarsometatarsal Joints (see Figs. 28-1, 28-5, 28-6, 28-10, and 28-11) The medial tarsometatarsal joint is formed by the medial cuneiform and the first metatarsal. The intermediate tarsometatarsal joint is formed by the intermediate and lateral cuneiform and articulation with the base of the second and third metatarsals. The lateral tarsometatarsal joint is formed by the cuboid and fourth and fifth metatarsal bases. The joint spaces extend to include the articulation between the metatarsal bases. The three

701

■ FIGURE 28-13 The plantar muscles of the medial and lateral compartments (abductor hallucis, adductor hallucis, flexor hallucis brevis, abductor digiti minimi, flexor digiti minimi, and opponens digiti minimi). Right foot, plantar view. (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

tarsometatarsal joints are supported by individual capsules. Ligaments support both the plantar and dorsal surface of each tarsometatarsal joint. There are seven dorsal ligaments, with the first being the strongest, and variably between five and seven plantar ligaments. Medial plantar ligaments are generally present; lateral ligaments are variably present. The intermetatarsal bases of the second through fifth digits are supported by dorsal, plantar, and interosseous transverse metatarsal base ligaments.

Lisfranc Ligament (see Fig. 28-10) The strongest interosseous cuneometatarsal ligament is the first ligament (Lisfranc ligament), which in 22% of the populace there are two bands that originate from the lateral distal surface of the medial cuneiform and attach to the medial base of the second metatarsal. A second ligament bridges the medial and intermediate cuneiforms in direct transverse orientation.

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

■ FIGURE 28-14 The intrinsic muscles of the right foot from the plantar view. All of the short foot muscles except for the dorsal and plantar interossei have been removed, leaving behind their origins and insertions. Note the course of the tibialis posterior and fibularis longus tendon insertion, both of which help to support the transverse arch of the foot. (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

The second and third interosseous cuneometatarsal ligaments have variable morphology but in general form attachments between the second and third metatarsal bases and the intermediate and lateral cuneiforms.

Lesser Digit Metatarsophalangeal Joints, Plantar Plates (Phalangeal Apparatus) (Figs. 28-12 to 28-15) The metatarsophalangeal joint is formed by the convex ball of the head of the metatarsal and the concave cup of the phalanx base. The main articular unit for the “ball of the foot” is formed by the plantar plates and their phalangeal apparatus. It is formed by a 20-mm-long and 2mm-thick rectangular fibrocartilaginous ridge that arises from the plantar aspect of the metatarsal head fascial band and inserts on the plantar base of the phalanx. It is supported by the suspensory glenoid ligaments (plantar plate ligaments) to either side, the medial and lateral collateral ligaments, and the deep transverse intermetatarsal ligaments.

The lateral collateral ligament tends to be thicker and stronger than the medial collateral ligament. Both originate from the metatarsal head lateral tubercle and are directed distally and anteriorly to the lateral tubercle of the phalanx base. The suspensory glenoid ligament (plantar plate ligament) originates posterior and inferior to the lateral tubercle of the metatarsal head and is fan shaped and broad distally where it inserts on the posterolateral and anterolateral surfaces of the plantar plate. The fibers are in continuity with the dependent border of the collateral ligaments. The deep transverse metatarsal ligament attaches to the dorsal surface of the sides of the plantar plates at the junction of the interosseous muscle insertion.

Muscles, Tendons, and Retinacula about the Ankle Tendons about the ankle are divided into four groups. The origins, insertions, and innervations are detailed in Table 28-4.

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TABLE 28-4 Muscle Compartments, Innervation, Origin, and Insertions of the Ankle and Foot Muscle Compartment

Innervation

Origin

Insertion

Anterior Compartment Anterior tibial tendon

DPN

Extensor digitorum longus

DPN

Extensor hallucis longus

DPN

Upper two thirds of lateral surface of tibia and interosseous membrane Anterior border of distal fibula and interosseous membrane Middle third of medial surface of fibula

Peroneus tertius Lateral Compartment Peroneus brevis Peroneus longus

DPN

Anterior border of distal fibula

Medial and plantar surface of medial cuneiform and 1st metatarsal base 2nd-5th toes of dorsal aponeurosis and base of distal phalanx 1st toe of dorsal aponeurosis and base of distal phalanx 5th metatarsal base

SPN SPN

Distal half of lateral surface of fibula Proximal two thirds of lateral surface of fibula

5th metatarsal base Plantarmedial surface of medial cuneiform and 1st metatarsal base

Medial Compartment Posterior tibial tendon

PTN

Interosseous membrane and adjacent surface of tibia and fibula Middle third of posterior surface of tibia Distal two thirds of posterior surface of fibula

Navicular tuberosity, cuneiforms, 2nd-4th metatarsal base Base of 2nd-5th distal phalanx Base of 1st distal phalanx Posterior calcaneal tuberosity

Medial sesamoid, base of proximal phalanx of 1st toe Medial and lateral sides of 2nd-5th middle phalanx base 5th proximal phalanx and metatarsal base

Flexor digitorum longus Flexor hallucis longus Posterior Compartment Achilles tendon

PTN PTN

Plantaris tendon First Layer (Superficial Layer) Abductor hallucis

PTN

Formed by soleus and medial and lateral heads of gastrocnemius Posterolateral epicondyle of the femur

MPN

Medial process of calcaneal tuberosity

Flexor digitorum brevis

MPN

Medial tubercle of calcaneal tuberosity

Abductor digiti minimi Second Layer 1st-2nd lumbricals

LPN

Lateral process of calcaneal tuberosity

MPN

Dorsal aponeurosis of respective toes

3rd-4th lumbricals

LPN

Quadratus plantae

LPN

Medial border of flexor digitorum longus tendon Medial border of flexor digitorum longus tendon Medial and plantar calcaneal tuberosity

Third Layer Adductor hallucis transverse, and oblique heads

LPN

Transverse: 3rd-5th metatarsophalangeal joints and deep transverse ligaments Oblique: 2nd-5th metatarsal bases, cuboid, lateral cuneiform Medial and intermediate cuneiforms and plantar calcaneocuboid ligament Medial and intermediate cuneiforms and plantar calcaneocuboid ligament Base of 5th metatarsal and long plantar ligament Long plantar ligament, plantar tendon sheath peroneus longus

Conjoined tendon to lateral sesamoid, base of proximal phalanx of 1st toe

PTN

Flexor hallucis brevis, medial head Flexor hallucis brevis, lateral head Flexor digiti minimi brevis

MPN

LPN

Opponens digiti minimi

LPN

Fourth Layer Extensor digitorum brevis

DPN

Dorsal surface of the calcaneus

1st-3rd plantar interossei 1st-4th dorsal interossei

LPN LPN

Medial border of 3rd-5th metatarsals Two heads of opposing borders of 1st-5th metatarsals

LPN

Posterior calcaneal tuberosity

Dorsal aponeurosis of respective toes Lateral border of flexor digitorum longus tendon

Medial sesamoid, base of proximal phalanx of 1st toe Lateral sesamoid, base of proximal phalanx of 1st toe 5th proximal phalanx base 5th metatarsal neck Dorsal base of middle phalanx of 2nd-4th toes Medial base of 3rd-5th proximal phalanges 1st: medial base and dorsal aponeurosis of 2nd proximal phalanx 2nd-4th: lateral base and dorsal aponeurosis of proximal phalanx

DPN, deep peroneal nerve; SPN, superficial peroneal nerve; PTN, posterior tibial nerve; MPN, medial plantar nerve; LPN, lateral plantar nerve.

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■ FIGURE 28-15 A, The articular surfaces of the sesamoids. Dorsal view with the first metatarsal removed. B, The capsule and ligaments of the sesamoids and muscular attachments. First metatarsophalangeal joint of the right foot, plantar view. Both sesamoids are attached to the joint capsule and to the collateral ligaments of the metatarsophalangeal joint. They are embedded in the tendons of insertion of the medial sesamoid (abductor hallucis, medial head of flexor hallucis brevis) and lateral sesamoid (lateral head of flexor hallucis brevis, transverse head of adductor hallucis, oblique head of adductor hallucis). The lateral and medial sesamoids are hemispherical bones, each presenting a slightly convex dorsal articular surface that articulates with the grooved plantar articular surfaces on the head of the first metatarsal. Sesamoids protect the tendons from excessive friction. They are important functionally for their ability to lengthen the effective lever arm of the muscle, so that muscular forces can be applied more efficiently. The development of sesamoids can be interpreted as a functional adaptation to the presence of pressure tendons. (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

Medial Tendons (Figs. 28-14, 28-16, and 28-17)

Anterior Tendons (see Figs. 28-16, 28-18, and 28-19)

The medial tendon group contains the posterior tibial tendon, flexor digitorum longus tendon, and flexor hallucis longus tendon and is supported by the medial flexor retinacula, which is septated and encases and supports each tendon unit and the tarsal tunnel. The tarsal tunnel contains the posterior tibial artery, vein, and nerve and is situated between the tendons of the flexor digitorum longus and flexor hallucis longus at the ankle. The retinaculum extends between the medial malleolus and the calcaneus. The posterior tibia has two grooves medially for the posterior tibial tendon and flexor digitorum longus tendon and laterally for the flexor hallucis longus tendon. The distal 2-cm segment of the posterior tibial tendon is not encased by tenosynovium.

The anterior tendon group contains the anterior tibial tendon, extensor hallicis longus, extensor digitorum longus, and peroneus tertius. It contains the anterior tibial artery and vein and deep peroneal nerve and is supported by the superior and inferior extensor retinacula. The superior extensor retinaculum attaches just medial to the anterior tibial tendon at the medial margin of the distal tibia, extends across the extensor tendons and the anterior compartment, and attaches to the medial margin of the distal fibula. The inferior extensor retinaculum is a Y-shaped fascial band that originates from the medial malleolus and the plantar fascia and attaches to the anterior and lateral surface of the calcaneus.

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■ FIGURE 28-16 The tendon sheaths and retinacula of the right foot. Medial view. (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

■ FIGURE 28-17 The intrinsic muscles of the right foot from the plantar view. The plantar aponeurosis and flexor digitorum brevis have been removed. (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

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■ FIGURE 28-18 The tendon sheaths and retinacula of the right foot from the anterior view. The foot is plantarflexed, with superficial fascia removed, to display the deep fascial bands (retinacula) that hold in place the tendon sheaths of the long foot extensors and flexors. The superior and inferior extensor retinacula retain the long extensor tendons, allowing efficient redirecting of the forces generated by their muscles (tibialis anterior, extensor digitorum longus, extensor hallucis longus, and fibularis tertius) while preventing the tendons from rising away from the bones of the ankle when the foot is dorsiflexed. Similarly, the fibular muscle tendons in place posterior to the lateral malleolus and the flexor retinaculum retain the long flexor tendons behind the medial malleolus, preventing displacement of these tendons while enabling them to operate smoothly regardless of the orientation of the ankle joint. (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

Lateral Tendons (see Figs. 28-13, 28-14, and 28-17 to 28-19)

distally, it is more cord-like and rounded; and anteriorly, it is concave at its distal insertion on the os calcis.

The lateral tendon group contains the peroneus longus and brevis tendons. The posterior lateral malleolus has a groove for the peroneal tendons. It is supported by the superior and inferior peroneal retinacula. A triangular component of the retinacula called the fibrocartilaginous ridge attaches to the posterolateral tip of the fibula and acts to support the peroneal tendons in the lateral retromalleolar groove.

Plantar Aponeurosis (see Figs. 28-14 and 28-17)

Posterior Tendons (see Figs. 28-16, 28-18, and 28-19) The posterior tendon compartment contains the Achilles tendon and plantaris tendon. The Achilles tendon is formed by the medial and lateral heads of the gastrocnemius tendons and the soleus muscles. The distal 2 cm of the Achilles tendon is not encased by tenosynovium. It is separated from the posterior ankle joint by the pre-Achilles fat or Kagers fat pad. Proximally, the tendon is flattened and concave;

The plantar aponeurosis is a longitudinal strong fibrous band that extends and supports the plantar aspect of the heel, arch, and foot. There are three discernible components: the central band, which is the thickest at the calcaneal tuberosity attachment, and the medial and lateral bands. Distally, the aponeurosis becomes thin and then divides into five separate bundles that extend to attach to the distal toes. The aponeurosis forms two vertical septa that divide the plantar musculature into three compartments.

Muscles, Tendons, and Retinacula about the Foot The muscles of the foot are described by layer. There are four layers of the foot. The origins, insertions, and innervation are detailed in Table 28-4.

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707

■ FIGURE 28-19

The tendon sheaths and retinacula of the right foot. Lateral view. (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

First Plantar Muscle Layer (see Figs. 28-13, 28-14, and 28-17) The first plantar muscle layer, from medial to lateral, includes the abductor hallucis, flexor digitorum brevis, and abductor digiti minimi, which originate at the calcaneal tuberosity and support the plantar aspect of the arch to their insertions on the toes. The medial and lateral plantar nerve and vessels course deep to the proximal abductor hallucis muscle. There is a groove plantar aspect of the fifth metatarsal base where the abductor digiti minimi courses.

Second Plantar Muscle Layer (see Figs. 28-13,

strong sesamoid phalangeal ligaments and an intersesamoid ligament. The third plantar layer is made up of the flexor hallucis brevis muscle proximally. Distally it splits into a medial and lateral head that attaches to their respective sesamoids. The adductor hallucis muscle originates proximally as two separate muscles (the oblique and transverse head) that join distally and attach to the lateral sesamoid. The flexor hallucis longus tendon is not a component of the third layer, but it courses within the intersesamoid groove. The third layer is also made up of the flexor digiti minimi brevis.

28-14, and 28-17)

Fourth Plantar Muscle Layer (see Figs. 28-12

The second muscle layer is made up of the quadratus plantae and the lumbrical muscles that arise from the flexor digitorum longus tendon.

and 28-14)

Hallux Sesamoid Complex and Third Plantar Muscle Layer (see Figs. 28-13 and 28-17) Hallux sesamoid complex is made up of the muscles of the third layer, tibial and fibular sesamoids, and their articulation with the base of the first metatarsal. The sesamoid complex is contained within the first metatarsophalangeal joint capsule that forms an attachment at the plantar metatarsal neck. The sesamoids are supported by

The fourth layer is made up of the dorsal and plantar interosseous muscles and the extensor digitorum brevis muscle.

COMMON VARIANT ANATOMY Accessory Ossicles (Fig. 28-20) There are numerous accessory ossicles of the foot and ankle, but the three that are important to document because of their association with pain, tendon pathology,

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■ FIGURE 28-20 Illustration of ossicles in the foot. (Redrawn from Netter FH. Atlas of Human Anatomy, 4th ed. Philadelphia, Saunders, 2006, plates 505–528.)

and arthrosis are the os naviculare, os peroneum, and os trigonum.

Posterior Intermalleolar Ligament The tibial slip or posterior intermalleolar ligament is a rare anatomic ligament that originates from fibers of the posterior talofibular ligament and inserts on the posterior medial malleolus. It can cause crowding of the posterior joint and contribute to soft tissue impingement.

Low-Lying Peroneus Brevis Muscle (Fig. 28-21) The low-lying peroneus brevis muscle is an uncommon normal variant that may cause soft tissue mass effect in its retromalleolar course and may contribute to tearing and tendinopathy of the peroneal tendons or instability of the peroneal retinacular mechanism.

Peroneus Quartus Muscle (Fig. 28-22) The peroneus quartus is reported to be present in 10% to 13% of persons. There are several variant origins and insertions, including the retrotrochlear eminence (most common), cuboid bone, and peroneus longus tendon. This anomalous muscle is important to recognize and report because of its association with chronic lateral ankle pain, longitudinal tears of the peroneus brevis tendon, and laxity of the superior peroneal retinaculum. It can also be used for tendon and ligament reconstruction.

Peroneus Calcaneus Internus (Fig. 28-23) The peroneus calcaneus internus is a rare variant of the peroneus quartus anomalous muscle and may cause crowding of the posterior compartment and impingement of the tarsal tunnel. The muscle and tendon course lateral to the flexor hallucis longus muscle and tendon in the posterior compartment. It inserts on the deep medial surface of the calcaneus plantar to the sustentaculum tali.

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■ FIGURE 28-21 Axial (A) and sagittal (B) drawings of the ankle demonstrate the position of a low-lying peroneus brevis muscle belly in the retromalleolar location extending below the tip of the fibula causing crowding of the retromalleolar tunnel.

■ FIGURE 28-22 Axial at the ankle (A), axial at the calcaneus (B), and coronal of the posterior ankle (C) drawings demonstrate an accessory peroneus quartus muscle and tendon coursing in the lateral retromalleolar tunnel causing crowding and encroachment of the peroneus longus and brevis tendons.

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Accessory Soleus (Fig. 28-24) The accessory soleus is a rare anatomic variant that may present as a soft tissue mass in the posterior ankle, deep to the Achilles tendon. It usually inserts anteromedial to the Achilles insertion on the os calcis. It is important to recognize because of its association with pain on exercise. It has a typical diagnostic appearance on plain film, CT, and MRI and should not be confused with a pathologic mass.

Accessory Flexor Digitorum Longus Muscle (Fig. 28-25) The accessory flexor digitorum longus muscle can be seen coursing superficial in the posterior flexor compartment of the ankle. It may, on rare occasion, cause crowding in the flexor compartment.

BASIC BIOMECHANICS Function of walking involves intricate coordination of not only the ankle joint, subtalar joint, intertarsal joints, metatarsal tarsal joints, and metatarsal phalangeal joints but also transmission of forces, strength, and support provided by the static stabilizers (articular alignment, ligaments, and retinacula) and active stabilizers (tendons

A ■ FIGURE 28-23

B

and muscles). All joints of the ankle, hindfoot, midfoot, and forefoot and the static and dynamic stabilizers must function as a coordinated unit to provide adequate support and maintain proper biomechanical function to perform proper gait, whether when walking, running, or jumping. If one component fails (e.g., post-traumatic bone remodeling distorting dynamics of the articular unit, ligament failure, retinacular or tendon dysfunction), working units must compensate for the pathologic component; and, eventually, overcompensation and additive stress will lead to additional areas of dysfunction about the ankle and foot as a whole. The ankle, midfoot, and forefoot absorb a considerable amount of force during routine daily activities of walking. There are two main phases of foot and ankle movement during one cycle of gait. The first phase is the stance phase and begins with heel strike and ends with toe off. The second phase begins with toe off and ends with heel strike. Foot and ankle movement and function during phases of gait will be broken down into the talocrural joint, subtalar joint, and transverse tarsal and metatarsal joints and the motion of the forefoot. The talocrural joint functions predominantly in the sagittal plane and dorsiflexes to a range of 20 to 30 degrees and plantarflexes to a range of 40 to 50 degrees. Coronal range of motion is restricted by the collateral ligaments.

C

Axial at the ankle (A), axial at the calcaneus (B), and coronal of the mid ankle (C) drawings demonstrate an accessory peroneus calcaneus internus muscle and tendon coursing in the posterior compartment lateral to the flexor hallucis longus muscle and tendon.

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■ FIGURE 28-24

Coronal of the posterior ankle (A) and sagittal of the ankle (B) drawings demonstrate an accessory soleus muscle in the posterior compartment anterior to the Achilles tendon and filling the pre-Achilles space. It courses medial to the flexor hallucis longus muscle.

■ FIGURE 28-25 Axial at the ankle (A) and sagittal (B) drawings demonstrate an accessory flexor digitorum longus tendon coursing within the posterior flexor compartment as the most superficial posterior structure and causing crowding of the flexor compartment.

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The subtalar joint moves about an oblique axis extending from anteromedial to posterolateral and forms a 30-degree angle with the horizontal plane and a 20-degree angle with the sagittal plane. It provides rotational motion about the longitudinal axis of the foot in a range of 20 degrees of inversion (supination, adduction, flexion) and 10 degrees of eversion (pronation, abduction, extension). The interosseous talocalcaneal ligament provides the strongest static support structure of the subtalar joint.

The transverse tarsal and tarsometatarsal joints act as the supinator and pronator of the ankle and hindfoot and provide 20 degrees of pronation and 40 degrees of supination. When the joints function as a unit, mechanically a plantar longitudinal arch (talus, navicular, cuneiforms and three medial rays, plantar aponeurosis, long plantar ligament, and plantar calcaneonavicular ligament) and plantar transverse arch (calcaneus, cuboid and lateral rays) absorb and transmit forces evenly throughout the ankle and foot.

SUGGESTED READINGS Berquist T. Anatomy, normal variants, and basic biomechanics. In Berquist T (ed). Radiology of the Foot and Ankle, 2nd ed. Philadelphia, Lippincott Williams & Wilkins, 2000, pp 1–40. Bianchi S, Martinoli C, Gaignot C. Ultrasound of the ankle: anatomy of the tendons, bursae, and ligaments. Semin Musculoskelet Radiol 2005; 9:17. Erickson SJ, Rosengarten JL. MR imaging of the forefoot: normal anatomic findings. AJR Am J Roentgenol 1993; 160:565–571. Jacobson J. Musculoskeletal ultrasound and MRI: which do I choose? Semin Musculoskelet Radiol 2005; 9:135–149. Jacobson JA. Musculoskeletal sonography and MR imaging: a role for both imaging methods. Radiol Clin North Am 1999; 37:713–735. Kaplan PA, Helms CA, Anderson MW, et al. Musculoskeletal MRI, 2nd ed. Philadelphia, WB Saunders, 2001. Kirsch MD, Erickson SJ. Normal magnetic resonance imaging anatomy of the ankle and foot. Magn Reson Imaging Clin North Am 1994; 2:1–21. Lieber GA, Lemont H. The posterior triangle of the ankle: determination of its true anatomical boundary. J Am Podiatr Assoc 1982; 72:363. Lin J, Fessell DP, Jacobson JA, et al. An illustrated tutorial of musculoskeletal sonography: I. Introduction and general principles. AJR Am J Roentgenol 2000; 175:637–645. Lin J, Fessell DP, Jacobson JA, et al. An illustrated tutorial of musculoskeletal sonography: III. Lower extremity. AJR Am J Roentgenol 2000; 175:1313–1321. Mengiardi B, Pfirrmann C, Zanetti M. MR imaging of tendons and ligaments of the midfoot. Semin Musculoskelet Radiol 2005; 9:11. Netter FH. Atlas of Human Anatomy, 3rd ed. ICON Learning Systems, 2003, plates 505–528. Newman J. MR Imaging of the foot and hindfoot: anatomy and injuries. Presented before the American Roentgen Ray Society, April 28-May 4, 2001.

Patel S, Fessell DP, Jacobson JA, et al. Artifacts, anatomic variants, and pitfalls in sonography of the foot and ankle. AJR Am J Roentgenol 2002; 178:1247–1254. Potter HG, Deland JT, Gusmer PB, et al. Magnetic resonance imaging of the Lisfranc’s ligament of the foot. Foot Ankle Int 1998; 19:438–446. Preidler KW, Wang YC, Brossman J, et al. Tarsometatarsal joint: anatomic detail on MR images. Radiology 1996; 199:733–736. Resnick D. Internal derangement of joints. In Resnick D (ed). Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, 2002, vol 4, pp 3285–3296. Resnick D, Kang HS. Ankle and foot. In Resnick D, Kang HS (eds). Internal Derangements of Joints: Emphasis on MR Imaging. Philadelphia, WB Saunders, 1997, pp 787–925. Rubin DA, Towers JD, Britton CA. MR imaging of the foot: utility of complex imaging planes. AJR Am J Roentgenol 1996; 166:1079–1084. Rule J, Yao L, Seeger LL. Spring ligament of the ankle: normal MR anatomy. AJR Am J Roentgenol 1993; 161:1241–1244. Sarrafian S. Anatomy of the Foot and Ankle. Philadelphia, JB Lippincott, 1983, pp 107–332. Schreibman K. MRI of the ankle tendons: normal anatomy and key abnormalities. Presented before the American Roentgen Ray Society, April 28-May 4, 2001. Schuenke M, Sculte E, Schumacher U. General Anatomy and Musculoskeletal System: Atlas of Anatomy. New York, Thieme, 2006, pp 402–509. Stoller D, Tirman P, Bredella M, Diagnostic Imaging. Salt Lake City, UT, Amirsys, 2004. Stoller DW, Ferkel RD. The ankle and foot. In Stoller D (ed). Magnetic Resonance Imaging in Orthopaedics Sports Medicine, 2nd ed. Philadelphia, Lippincott Williams & Wilkins, 1997, pp 443–595.

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Acute Osseous Injury to the Ankle A. Bassem Elaini and William E. Palmer

PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS Of all of the major weight-bearing joints in the body, the ankle is the most frequently injured.1 In athletes, foot and ankle injuries account for up to one fourth of sport-related injuries, with the ankle ranking first as the most common cause of time lost in sports competition.1 In otherwise healthy patients, ankle injuries may be complicated by chronic joint instability and pain. Female gender, obesity (elevated body mass index), and diabetes with associated comorbidities have been reported to be significant risk factors for ankle fractures,2 with the latter associated with an increased risk of post-treatment complications, including infection, nonunion, malunion, and Charcot-type neuroarthropathy.3 Unlike with other sites commonly involved by fracture such as the hip, wrist, and spine, osteoporosis is not considered a risk factor in ankle fracture.4 Ankle injuries are often complex, encompassing injuries to tendons, ligaments, and bones. In this chapter we focus on acute osseous injuries to the ankle whose mechanism of injury may sometimes be determined from radiographic images.

ANATOMY For practical purposes, the ankle may be regarded as a ring-like bony structure supported by numerous ligaments; disruption and instability result when the ring is broken in two places, as a result of bony and/or ligamentous injury.5 The bony structures that comprise the ankle include the distal tibia, distal fibula, and talus. The ankle mortise is formed by the medial malleolus, distal tibial articular surface, and lateral malleolus, within which the talus should be symmetrically centered. The ankle joint proper is composed of the tibiotalar articulation and the distal tibiofibular articulation. The ankle joint is a synovial hinge joint with a single axis (transverse between the malleoli

through the body of the talus) about which the only naturally occurring motions are flexion (plantarflexion) and extension (dorsiflexion). The important landmarks of the distal tibia include the medial malleolus, the laterally located fibular groove, the anterior and posterior processes, and the plafond, which comprises the inferior tibial articular surface.6 The medial malleolus is defined as the medial process of the distal tibia, which is composed of two colliculi: anterior and posterior. The anterior process of the tibia forms its caudal anterior edge and may be referred to by some as the anterior malleolus. Anterolaterally, the anterior process

KEY POINTS Of all the major weight-bearing joints in the body, the ankle is the most frequently injured. ■ Mechanisms of acute osseous ankle injury may sometimes be ascertained by radiographic findings. ■ Associated ligamentous injury patterns may subsequently be predicted. ■ The orthopedist’s goal in treating ankle injuries is restoration of near-anatomic alignment and articular congruity ultimately to impart normal weight-bearing capability. ■ Closed manipulation and cast immobilization is most successful with lower-stage injuries, nondisplaced fractures, and injuries complicated by infection in which ORIF would not be indicated. ■ Open methods of treatment are most often used for higher-stage injuries, displaced fractures, and talar subluxation. ■ Radiographic complications to be aware of after treatment include osteomyelitis or infection about hardware, hardware loosening or failure, malunion or nonunion, osteoarthritis, delayed syndesmotic instability, tibiofibular synostosis, and reflex sympathetic dystrophy. ■

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gives rise to the anterior tibial tubercle, also known as the tubercle of Chaput. The posterior tibial process of the tibia refers to its caudal posterior edge and may be referred to by some as the posterior malleolus. Posterolaterally, this terminates as the posterior tibial tubercle. The space outlined by this and the tubercle of Chaput is referred to as the fibular groove. The distal fibula is the lateral malleolus and demonstrates a convex articular surface. The talus articulates with the medial and lateral malleoli and tibial plafond to comprise the ankle joint. The posterior tibial process or posterior malleolus does not limit movement of the talus as the medial and lateral malleoli do but does contribute significantly to the overall weight-bearing surface at the ankle joint. Three sets of ligamentous structures facilitate osseous support about the ankle. These include the medial collateral ligamentous complex (deltoid), lateral collateral ligamentous complex (consisting of the anterior talofibular, posterior talofibular, and calcaneofibular ligaments), and the syndesmotic ligamentous complex of the distal tibiofibular articulation. The latter consists of the anterior tibiofibular ligament, posterior tibiofibular ligament, and interosseous membrane. The deltoid ligament has superficial and deep components. Superficially, three bands take origin from the anterior tibial colliculus. These attach to the navicular/ spring ligamentous complex (plantar calcaneonavicular ligament), the sustentaculum tali of the calcaneus, and the medial tubercle of the talus. The superficial fibers provide little overall stability to the ankle joint. The deep component is composed of anterior and posterior tibiotalar ligaments, the latter being the principal stabilizer of the mortise. The syndesmotic ligamentous complex is composed of the anterior and posterior tibiofibular ligaments, which attach, respectively, to anterior tibiofibular tubercles and posterior tibiofibular tubercles, the inferior transverse ligament, and the interosseous ligament, which is a cranial thickening of the tibiofibular interosseous membrane. The latter comprises the roof of the syndesmosis.6 The lateral collateral ligamentous complex has three components. The anterior talofibular ligament attaches the lateral neck of the talus to the fibula just distal to its anterior tubercle. The calcaneofibular ligament extends posteriorly and caudally from the distal aspect of the posterior fibula to the lateral calcaneus. The posterior talofibular ligament extends axially from the fibula to the posterior process of the talus; its orientation readily facilitates visualization on axial cross-sectional imaging of the ankle.

BIOMECHANICS Motion about the ankle joint and foot is an often confusing topic. Over the years, certain specific terms have been used by various authors to refer to different movements about the ankle joint. For purposes of simplicity, the following definitions will hold for describing motions about the ankle joint in this chapter. The term adduction refers to a linear medial translation of the forefoot. The term abduction refers to a linear lateral translation of the forefoot. The term eversion refers to an angular upward

rotation of the lateral aspect of a structure relative to its medial aspect. The term inversion refers to an angular upward rotation of the medial aspect of a structure relative to its lateral aspect. Given these definitions, the terms supination and pronation refer to compound motions combining the previous movements. Supination is a combination of adduction and inversion of the forefoot as well as inversion of the heel. Plantarflexion of the foot follows naturally from supination. The term pronation refers to a compound motion of abduction and eversion of the forefoot in combination with eversion of the heel. Dorsiflexion of the foot follows naturally from pronation. Additional terms often used in describing ankle injuries include internal rotation and external rotation. In certain classification systems involving acute osseous injury to the ankle, these latter terms refer to the applied force on the ankle imparting injury. The term internal rotation is often erroneously confused with inversion with which it is not synonymous. Internal rotation refers to a medial rotational movement of the talus around the vertical axis of the tibia.6 The term external rotation is often erroneously confused with eversion with which it is not synonymous. External rotation refers to a lateral rotational movement of the talus around the vertical axis of the tibia.6 The articular surface contour of the talar dome is ordinarily very closely matched to the configuration of the tibial plafond. The tibiotalar joint is, in fact, the most congruent of the weight-bearing joints in the body.7 Any talar displacement results in a marked reduction of surface contact between the two bones. Ramsey and Hamilton have estimated that 1 mm of lateral shift produces an approximately 42% decrease in joint contact area8 ; continued weight-bearing forces are dispersed on a smaller surface area, resulting in premature degenerative changes. The integrity of the ankle mortise is thus a critical factor to assess on radiographs. The syndesmotic ligamentous complex is the most important about the ankle joint. Loss of its structural integrity inevitably leads to displacement of the lateral malleolus and, consequently, an abnormal tibiotalar relationship with lateral talar shift, even with an intact deltoid complex.9

MANIFESTATIONS OF THE DISEASE Radiography The foot and ankle comprise the most commonly imaged portions of the musculoskeletal system.1 The standard radiographic examination of the ankle includes anteroposterior, lateral, and oblique projections; a variant of the former in which the ankle is internally rotated 10 to 20 degrees has been termed the mortise view (Fig. 29-1). The ankle mortise is seen to best advantage on the mortise view and is formed by the medial malleolus, distal tibial articular surface, and lateral malleolus. The talus should be centered symmetrically within the mortise view; any distance greater than 5 mm between the talar dome and the structures comprising the mortise is considered abnormal.1 The oblique view is best performed with the foot internally rotated by 30 to 40 degrees.

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■ FIGURE 29-1 Anteroposterior (A), lateral (B), and mortise (C) views of the ankle constitute a standard radiographic examination of the ankle. The latter is performed with somewhere between 10 and 20 degrees of internal rotation and provides a view of the ankle mortise formed by the medial and lateral malleoli and the distal tibial articular surface.

Stress views may also be obtained in the evaluation of ligamentous injuries when suggested in the setting of radiographically obvious osseous injury. With the advent of MRI, these views are less frequently obtained but knowledge of these views is nonetheless important. An inversion stress examination of ankle is performed while there is varus stress on the ankle, inverting the heel (Fig. 29-2). The degree of talar tilt as identified on the anteroposterior

view helps to determine the degree of the lateral ligamentous injury. The contralateral ankle is usually subjected to the same procedure for comparison because up to 25 degrees of talar tilt has been reported as within normal limits.6 Another type of stress view that may be obtained is the anterior drawer stress view obtained in the lateral projection with a pressure plate positioned anteriorly. This helps

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■ FIGURE 29-2 Inversion stress radiographs of the ankle are performed with a varus stress. Neutral (A) and inversion stress (B) radiographs of the left ankle are performed followed by neutral (C) and inversion stress (D) radiographs of the right ankle for comparison in a single patient. The degree of talar tilt as determined by the angle between lines drawn parallel to the distal tibial and talar articulating surfaces is compared from side to side. As is demonstrated in this example, talar tilt on the left exceeds that on the right, confirming clinically suspected left lateral complex ligamentous injury.

to determine injury to the anterior talofibular ligament when anterior subluxation of the talus is demonstrated. External rotation stress radiography may show more than 3 mm of widening of the superomedial corner of the mortise if the deep fibers of the deltoid are injured. Eversion stress examination with valgus stress on the ankle is less reliable for detection of medial collateral ligamentous complex injuries.6 A stress mortise view may be obtained

in which a mortise view is obtained as described earlier but the talus is pulled laterally and held in such position while the radiograph is obtained. Even 1 mm of lateral shift is considered significant. Other regional structures that might be injured with, or in lieu of, the ankle joint proper, including the anterior process of the calcaneus (Fig. 29-3), the navicular bone (Fig. 29-4), the bones and ligaments of the midfoot, and

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■ FIGURE 29-3 Anteroposterior (A) and lateral (B) radiographs of the ankle with axial (C) and sagittal reformatted (D) CT scan of a patient who presented to the emergency department with persistent ankle pain and swelling 3 days after a “twisting” injury to her ankle demonstrate a nondisplaced fracture of the anterior process of the calcaneus (arrows).

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B ■ FIGURE 29-4

Axial proton density–weighted (A) and axial fat-saturated T2-weighted (B) images demonstrate a hypointense linear signal abnormality on both sequences extending through the navicular (long arrows) with evidence of surrounding hyperintense signal on the T2-weighted images (short arrow in B) consistent with a nondisplaced navicular fracture with surrounding bone marrow edema.

the base of the fifth metatarsal, may not be optimally visualized on standard views of the ankle and should prompt the acquisition of dedicated radiographs of the foot.

Magnetic Resonance Imaging Magnetic resonance imaging is most commonly used in evaluating patients with subacute or chronic symptoms in the setting of unrevealing radiographs or when ligamentous or tendinous injury needs to be fully characterized. In addition, in the setting of unrevealing radiographs in the patient with diffuse demineralization (in whom evaluation for nondisplaced fracture is made difficult), MRI may reveal the presence of bony contusion or a nondisplaced fracture line. MRI has demonstrated increased sensitivity relative to radiography and increased specificity relative to technetium-99m MDP (methylene diphosphonate) bone scan in detecting occult fractures in osteopenic patients.10 Bony contusion or trabecular injury usually manifests as decreased signal intensity on T1-weighted images and increased signal intensity on T2-weighted or inversion recovery images without a discrete fracture line (Fig. 29-5). Bone contusions usually resolve in 8 to 12 weeks, and, in

most cases, correlative radiographic findings are lacking.10 Continued abnormal stress forces may lead to progression to a frank fracture. A fracture line usually manifests as a discrete linear area of decreased signal intensity on all pulse sequences with surrounding edema or hemorrhage, usually of increased T2-weighted signal intensity (see Fig. 29-4). At our institution, following a three plane localizer, MR images of the ankle are obtained in neutral position in the following planes and sequences: axial proton density–weighted, axial inversion recovery, sagittal inversion recovery, sagittal T1-weighted, and coronal proton density–weighted with fat saturation. Inversion recovery imaging is preferred over frequency selective fat saturation because the former is less susceptible to field inhomogeneity–related artifacts. MR arthrography of the ankle is becoming a more frequently performed procedure because it expands the diagnostic capability of the standard MRI examination, allowing more detailed examination of the tibiotalar joint. The modality is more sensitive and accurate than standard MRI in the detection of ligament tears; characterization of their chronicity is also improved.11 MR arthrography

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■ FIGURE 29-5 Sagittal T2-weighted images with fat saturation in two different patients (A and B) demonstrate areas of increased T2-weighted signal intensity (arrows) without an associated hypointense fracture line consistent with bone marrow edema, likely in the setting of microtrabecular injury.

is also useful in the detection of soft tissue scarring and synovitis in the presence of various impingement syndromes of the ankle. Cartilage injury and talar osteochondral lesions are also evaluated to better advantage with MR arthrography.11 MR arthrography has been shown to be the best currently available imaging modality to detect intra-articular bodies, with a sensitivity just over 85%.11 Synovial disorders and arthrofibrosis may also be further evaluated with arthrography. Direct MR arthrography is performed after the (usually fluoroscopically guided) intra-articular injection of approximately 7 mL of a mixture that, at our institution, is composed of 10 mL of a mixture of 0.1 mL of gadolinium diluted in 50 mL of normal saline, 5 mL of iodinated contrast, and 5 mL of 1% lidocaine. Imaging should be performed shortly after the intra-articular injection, to maintain capsular distention. Fat-suppressed T1-weighted imaging dominates the imaging protocol (Fig. 29-6); however, at least one T2-weighted fat-suppressed sequence should be performed for detection of subtle bone marrow edema, detection of extra-articular fluid collections, and characterization of soft tissue masses. Indirect MR arthrography is performed after the intravenous administration of gadolinium, followed by 5 to 10 minutes of light activity. The main disadvantage of the indirect technique is lack of capsular distention; however, it avoids the pitfalls of direct MR arthrography, which include the possibility of extra-articular injection, leak of contrast material through the capsular puncture site mimicking disruption of the capsule, and instillation of air bubbles with consequent susceptibility artifact

■ FIGURE 29-6 Sagittal T1-weighted image of the ankle with fat saturation after the intra-articular administration of contrast agent demonstrates a loose body (long arrow) in the anterior aspect of the ankle joint. There is also evidence of cranial extension of intra-articularly administered contrast agent suggestive of an anterior capsular avulsion (short arrow).

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degrading evaluation.11 Additionally, enhancing periarticular structures such as bursae, tendon sheaths, and normal vasculature may impart diagnostic uncertainty. The main advantage over direct MR arthrography is the ability to obtain physiologic information related to enhancement of extra-articular structures in addition to improved evaluation of the joint proper. High cost, long duration of a given examination, and limited availability of high-field-strength systems in the acute setting have limited the role of MRI in the evaluation of acute ankle trauma. A recently published study attempted to assess the predictive value of a short MRI examination, in addition to or instead of radiography, to identify those who may require additional treatment and those who do not. A low-field-strength, 0.2-T, dedicated-extremity MRI system was used with an examination time of 30 to 45 minutes on average. The study determined that although a short MRI examination may demonstrate a number of clinically important lesions and can aid in the identification of patients who may need additional treatment, it does not assist in determining which patients can be safely discharged without further follow-up and cannot be used as a substitute for radiographic imaging.12 Another study evaluating acute pediatric ankle injuries demonstrated no significant added value for MRI as a supplement to conventional radiography.13 In a study specifically designed to assess for fracture with MRI in the setting of unrevealing radiographs of the distal extremities (including the ankle), accuracy of MRI was 81.4% compared with 79.5% for conventional radiography.14 Common critical points raised by authors of the former two studies for MRI in the acute setting included relative insensitivity for detection of small avulsed cortical fracture fragments and a limited field of view, resulting in missed fractures outside the evaluated region. Although contusions were more readily diagnosed on MRI, the clinical relevance and impact of this imaging diagnosis in the overall management scheme of patients in the acute setting is questionable.

Multidetector Computed Tomography Computed tomography is used to best advantage in evaluating degree of displacement, intra-articular extension, presence of loose intra-articular fragments, and degree of healing for treatment planning purposes. Direct acquisition in a true axial plane with sagittal and coronal reformatted images is the standard protocol for CT of the ankle. If multidetector CT is not available, direct coronal images can be acquired by flexing the knee within the gantry with the foot flat on the table.

DIFFERENTIAL DIAGNOSIS From Clinical Data An adequate history regarding acute osseous injuries to the ankle is often difficult to fully obtain. Knowing the position of the foot and ankle at the time of injury is important in predicting the pattern of osseous and/or ligamentous injury. Limitation to weight bearing and a history of chronic ankle injury, instability, or pain as well as

chronic medical conditions that may either predispose to injury or impaired healing (peripheral neuropathy, vascular disease, or chronic infection) are also critical factors to ascertain from the patient. Examination should focus on the presence of open wounds, swelling, bruising, or obvious deformity using the contralateral normal ankle as a standard for comparison. Palpation for point or focal tenderness may help direct attention to a specific area on subsequent imaging evaluation.15 The integrity of the anterior talofibular ligament, the most commonly injured ankle ligament, can be performed with the anterior drawer test. In mild plantarflexion, the ankle is subjected to attempts at anterior translation of the foot with an anteriorly directed force placed on the heel, all while the distal tibia and fibula are held stationary by the examiner’s contralateral hand.15 A difference of more than 3 to 5 mm in laxity between the injured and uninjured sides signifies probable injury to the anterior talofibular ligament.16 The analogous radiographic stress examination is described in a subsequent section. The talar tilt test is performed with the foot in neutral position and is helpful in determining the integrity of the calcaneofibular ligament. With the patient seated or supine the affected foot is placed in anatomic position. The distal aspect of the leg is stabilized cranial to the tibiotalar joint while the examiner’s other hand holds the bottom of the foot on the affected side and places a varus stress on the tibiotalar joint, assessing the degree of talar tilt and comparing it with that of the contralateral side.15 A difference in tilt of more than 10 degrees between sides is considered abnormal.16 The analogous radiographic stress examination is described in a subsequent section. Instability of the ankle mortise may be suspected when mediolateral motion of the talus within the mortise is elicited. Such movement may produce pain and possibly notation by the patient of lateral talar motion or a clicking sensation as the talar dome repositions itself against the medial malleolus after lateral displacement by physical examination.17 A stress view mortise radiograph as described in a subsequent section may be helpful for further evaluation. When should one obtain ankle radiographs? It has been estimated that up to 6 million ankle radiographs are obtained yearly in North America, costing approximately 300 million U.S. dollars.18 The Ottawa Ankle Rules (Table 29-1) have been in use for some time, in an attempt to

TABLE 29-1 Ottawa Ankle Rules Accepted Indications: Ankle Radiographs

Accepted Indications: Midfoot Radiographs

Point tenderness about the inferior or posterior aspect of either malleolus (to include the distal 6 cm of the lateral malleolus) Inability to bear weight at the time of injury and/or clinical evaluation (four independent steps)

Point tenderness about the navicular or the base of the fifth metatarsal

Inability to bear weight at the time of injury and/or clinical evaluation (four independent steps)

CHAPTER

decrease the number of unnecessary imaging studies, and have met with high sensitivity and negative predictive value but relatively low specificity.18 They have been shown to be helpful in deciding when to obtain ankle radiographs in adults who are older than 18 years of age, not intoxicated, without other multiple painful injuries, not pregnant, without evidence for head injury, and without altered sensation as a result of neurologic deficit (as, for example, in patients with neuroarthropathy).15 In pediatric patients, point tenderness, bruising, and inability to bear weight constitute indications for radiography, often with comparison views of the uninjured side.15

From Supportive Diagnostic Techniques Several classification systems have been developed to categorize ankle fractures. Most of these classification systems are based on radiographic findings because fracture patterns are often able to determine the mechanism of injury. Simply put, transverse fracture patterns of a bone (the malleoli in the ankle) usually result from a distractive force and oblique fracture patterns of a bone usually result from a compressive force. In addition, it is important to note that in injuries sustained with the ankle pronated, the deltoid ligament is always under tension, with its rupture always predating any associated fibular fracture. In injuries sustained with the ankle supinated, the deltoid ligament is lax and the fibular fracture always predates injury to the deltoid ligament, if the latter occurs at all.6

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721

The Lauge-Hansen classification of ankle injuries is based on determining the position of the ankle at the time of injury (either supinated or pronated) and the direction of the deforming force (external rotation, adduction, or abduction). The findings described in this system are based on cadaver experiments. Greater degrees of supination or pronation at the time of injury were found to result in lower fibular fracture sites in the following descriptions.6 Classification in the Lauge-Hansen system implies progression of an injury complex through stages, although injuries to the ankle are often dynamic and patterns may subsequently demonstrate significant overlap. Because of its historical significance, this classification system is briefly discussed. Pronation-abduction injuries (Fig. 29-7) comprise the first group of ankle injuries in this classification. The ankle is in a pronated position at the time of injury. An abduction force is applied. Stage 1 injuries involve rupture of the deltoid ligament or transverse fracture through the medial malleolus. Progressing to stage 2, there is disruption of the syndesmotic complex to include the distal anterior and posterior tibiofibular ligaments. And, lastly, stage 3 injuries involve a fracture of the fibula, which is usually at or above the level of the ankle joint. The fracture is often oblique extending cranially and laterally from the medial cortical margin and is characterized to best advantage on frontal views of the ankle (Figs. 29-8 and 29-9). The fibular fracture may also be predominantly transverse in orientation with mild comminution, rendering open reduction and internal fixation (ORIF) more

■ FIGURE 29-7 Pronationabduction injuries progress through three stages (1 to 3) of failure, each leading to greater overall instability. The ankle is in a pronated position at the time of injury; an abduction force is applied (arrow). Stage 1 injuries involve injury and failure of either the deltoid ligament complex or, alternatively, a transverse fracture through the medial malleolus. Stage 2 injuries involve disruption of the anterior and/or posterior tibiofibular ligamentous components of the syndesmosis. Stage 3 injuries involve a distal fibular fracture at or above the level of the ankle joint that may be comminuted or predominantly oblique, extending cranially and laterally from the medial cortical margin.

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■ FIGURE 29-8 Anteroposterior view of the ankle (A) demonstrates widening of the medial ankle mortise consistent with deltoid ligament injury in addition to an obliquely oriented fracture of the fibula above the level of the mortise extending cranially and laterally from the medial cortical margin. Findings are consistent with a stage 3 pronation-abduction type injury. After surgical fixation (B), a lateral fibular plate and multiple screws, including a syndesmotic screw terminating in the tibia, have been used to facilitate stabilization.

■ FIGURE 29-9 Anteroposterior (A) and mortise (B) views of the left ankle demonstrate disruption of the ankle mortise, a transverse fracture through the medial malleolus, and an obliquely oriented fracture of the fibula above the level of the mortise extending cranially and laterally from the medial cortical margin.

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■ FIGURE 29-10 Pronation–external rotation injuries progress through four stages of failure (1 to 4), each leading to greater overall instability. The ankle is in a pronated position at the time of injury; an external rotational force is applied (curved black arrow). Stage 1 injuries involve injury and failure of either the deltoid ligament complex or, alternatively, a transverse fracture through the medial malleolus. Stage 2 injuries involve disruption of the anterior tibiofibular ligament and interosseous membrane, components of the syndesmotic ligamentous complex. Stage 3 injuries involve a fracture of the distal fibula proximal to the joint line extending posteriorly and caudally from the anterior cortex. Stage 4 injuries involve disruption of the posterior tibiofibular ligament or, more commonly, a chip fracture of the posterior tibia or posterior malleolar fracture (dotted line).

tedious. Impaction injury to the lateral tibial plafond may occur with pronation-abduction injuries. Pronation–external rotation injuries (Fig. 29-10) comprise the second broad category. The ankle is in a pronated position at the time of injury. An external rotational force is applied. Stage 1 in this classification also involves rupture of the deltoid ligament or transverse fracture of the medial malleolus. Stage 2 in this category involves disruption of the anterior tibiofibular ligament and interosseous membrane, components of the syndesmotic ligamentous complex. Progressing to stage 3, there is a fracture of the fibula, which is usually proximal to the joint line. The typical fracture extends from the anterior edge in a posterior and caudal direction (as seen to best advantage on the lateral view). The Maisonneuve fracture (see later) may result from a pronation–external rotation mechanism. Stage 4 pronation–external rotation injuries involve a chip fracture of the posterior tibia or, more rarely, rupture of the posterior tibiofibular ligament (Figs. 29-11 and 29-12).

A key radiographic point is that an apparently isolated medial or posterior malleolar fracture should prompt a search for a proximal fibular fracture. Supination-adduction injuries (Fig. 29-13) involve the third complex in this classification. The ankle is in a supinated position at the time of injury. An adduction force is applied. This usually occurs from unanticipated weight bearing on the lateral border and comprises the most common mechanism of injury to the ankle joint. Stage 1 usually involves either injury to the lateral collateral ligamentous complex or transverse fracture of the lateral malleolus below the level of the joint (Fig. 29-14). This is essentially a “mirror image” of stage 1 of the pronationabduction stage 1 injury pattern. Progressing to stage 2, one may find an oblique or vertically oriented fracture of the medial malleolus that is often medially displaced by the talus. A vertical fracture through the medial malleolus is a signature for the supination-adduction mechanism of injury, even if stage 1 is purely ligamentous (Fig. 29-15).

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

■ FIGURE 29-11 Anteroposterior (A) and lateral (B) views of the left ankle show mild widening of the medial ankle mortise and a questionable chip fracture involving the posterior tibia. Additional anteroposterior (C) and lateral (D) views of the left leg demonstrate an obliquely oriented fracture extending caudally and posteriorly from the anterior cortical margin of the proximal fibula consistent with a Maisonneuve fracture.

CHAPTER

■ FIGURE 29-12 Anteroposterior (A), oblique (B), and lateral (C) views of the left ankle demonstrate widening of the medial ankle mortise without a discrete fracture. Additional anteroposterior (D) and lateral (E) views of the left leg demonstrate an obliquely oriented fracture extending caudally and posteriorly from the anterior cortical margin of the mid fibula.

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

■ FIGURE 29-13 Supination-adduction injuries progress through two stages of failure (1 to 2), each leading to greater overall instability. The ankle is in a supinated position at the time of injury; an adduction force is applied (black arrow). Stage 1 injuries involve injury and failure of either the lateral collateral ligamentous complex or, alternatively, a transverse fracture through the lateral malleolus below the level of the ankle joint. Stage 2 injuries involve an oblique or vertical fracture through the medial malleolus that may be displaced medially, all with or without associated impaction injury to the medial tibial plafond.

■ FIGURE 29-14 Anteroposterior view of the left ankle demonstrates a transversely oriented linear lucency consistent with a transverse fracture of the lateral malleolus below the level of the ankle joint with overlying soft tissue swelling in a pattern consistent with a supination-adduction type injury mechanism.

■ FIGURE 29-15 Oblique (left) and anteroposterior (right) views of the left ankle demonstrate a vertical fracture through the medial malleolus without evidence for a transverse lateral malleolar fracture in a pattern that is diagnostic of a stage 2 supination-adduction type injury mechanism.

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■ FIGURE 29-16 Supination–external rotation injuries progress through four stages of failure (1 to 4), each leading to greater overall instability. The ankle is in a supinated position at the time of injury; an external rotational force is applied (curved black arrow). Stage 1 injuries involve disruption of the syndesmotic ligamentous complex, usually the anterior tibiofibular ligament. Note that disruption of this complex may be intrasubstance as illustrated or manifest as either an avulsion of Chaput’s tubercle on the tibia or an avulsion of its fibular attachment. Stage 2 injuries involve a spiral or oblique fracture of the distal fibula usually at or above the level of the joint. The fracture often extends from the anterior cortical margin, posteriorly and cranially. Stage 3 injuries involve rupture of the posterior tibiofibular ligament with or without a chip fracture of the posterior tibia, often as a small posterior malleolar fragment (dotted line). Stage 4 injuries involve deltoid ligament injury without fracture (upper diagram) or, alternatively, a transverse fracture of the medial malleolus (lower diagram).

In patients who have preexisting lateral ligamentous laxity related to prior injury, a nondisplaced or minimally displaced medial malleolar fracture may represent the only evidence of injury.17 Impaction injury to the medial tibial plafond may occur with supination-adduction injuries, which is a mirror image to pronation-abduction injuries. Supination–external rotation injuries (Fig. 29-16) comprise the last broad category of injuries in the LaugeHansen classification. The ankle is in a supinated position at the time of injury. An external rotational force is applied. Stage 1 injuries in this group involve disruption of the syndesmotic ligamentous complex, usually the anterior tibiofibular ligament. This disruption may be intrasubstance or manifest as either an avulsion of Chaput’s tubercle on the tibia (Fig. 29-17) or an avulsion of its fibular attachment (the Wagstaffe–Le Fort type of fracture discussed later).17 Stage 2 injuries involve a spiral or oblique fracture of the distal fibula usually at or above the level of the joint. Uncommonly, these fractures may extend below the level of the ankle joint. The fracture often extends from the anterior cortical margin, posteriorly and cranially, as best characterized on the lateral view) (Figs. 29-17, 29-18, and 29-19), similar in plane but opposite in orientation to the pronation–external rotation fracture. Stage 3 injuries usually involve rupture of the posterior tibiofibular ligament. There may also be a chip fracture of the posterior tibia,

often as a small posterior malleolar fragment that is usually extra-articular (see Fig. 29-18); avulsion fractures in this location are sometimes referred to as “Volkmann fragments” (Fig. 29-20).17 Stage 4 injuries may involve a transverse fracture of the medial malleolus (Fig. 29-21) or deltoid ligament injury without fracture (see Fig. 29-18). Radiologically, a fibular fracture indicative of supination–external rotation mechanism may be noted; however, stage 2, 3, and 4 injuries may all masquerade identically on radiographs because the latter two stages may manifest with only ligamentous injuries. Lateral talar shift, Volkmann fragments, and fibular fracture displacement are subtle radiographic findings, which thus must be assessed for in addition to clinical correlation to assess for higher stage, unstable injuries of the supination–external rotation type. Rarely, a combination-type supination-adduction/ supination–external rotation injury may result in a vertical or oblique fracture of the medial malleolus instead of the classic transverse type associated with the supination– external rotation mechanism. This is said to occur as the external rotation force changes to an adduction force as the injury takes place.6 Another important variation of the supination–external rotation injury complex is a fracturedislocation of the fibula posterior to the tibia, which may occur with a supination–external rotation mechanism.6 This represents the so-called Bosworth fracture-dislocation. Additionally, a Maisonneuve fracture (see later) may

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■ FIGURE 29-17 Anteroposterior (A) and lateral (B) views of the right ankle demonstrate a stage 4 supination–external rotation type ankle injury with a transverse medial malleolar fracture and an oblique fracture of the distal fibula that extends cranially and posteriorly from the anterior cortical margin. In addition, there is a minimally displaced fracture involving Chaput’s tubercle identified on the lateral view (arrow).

■ FIGURE 29-18 Anteroposterior (A) and lateral (B) views of the right ankle demonstrate widening of the medial ankle mortise consistent with deltoid ligament injury in addition to an obliquely oriented distal fibular fracture extending posteriorly and cranially from the anterior cortical margin. There is a posterior malleolar fracture. Findings are consistent with a stage 4 supination–external rotation type ankle injury.

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■ FIGURE 29-19 Mortise (A) and lateral (B) views of the left ankle demonstrate widening of the medial ankle mortise consistent with deltoid ligament injury in addition to an obliquely oriented distal fibular fracture extending posteriorly and cranially from the anterior cortical margin. Findings are consistent with a stage 4 supination–external rotation type ankle injury.

■ FIGURE 29-20

Mortise (A) and lateral (B) views of the right ankle demonstrate widening of the medial ankle mortise consistent with deltoid ligament injury in addition to an obliquely oriented distal fibular fracture extending posteriorly and cranially from the anterior cortical margin. Findings are consistent with a stage 4 supination–external rotation type ankle injury. In addition, there is a small avulsion fracture involving the posterior malleolus with a resultant small Volkmann fragment (arrow).

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

■ FIGURE 29-21 Anteroposterior (A), mortise (B) and lateral (C) views of the left ankle demonstrate a stage 4 supination–external rotation type ankle injury with a transverse medial malleolar fracture and an oblique fracture of the distal fibula that extends cranially and posteriorly from the anterior cortical margin. There is also a posterior malleolar fracture seen on the lateral view.

result from a supination–external rotation mechanism. Therefore, as with pronation–external rotation injuries, it is critical to note that an apparently isolated medial or posterior malleolar fracture should prompt a search for a proximal fibular fracture. Syndesmotic stability is key in clinical assessment of supination–external rotation, pronation–external rotation, and pronation-abduction injury types consequent to their tendency to involve the syndesmotic ligamentous complex, the primary ligamentous stabilizer of the ankle joint. Syndesmotic injuries are fortunately rare, with the most common type of ankle injury mechanism being supination-adduction. Consequent to the complexity of the Lauge-Hansen mechanistic classification, many clinicians favor the Weber classification. This anatomic classification system is based primarily on the level of the fibular fracture. Weber type A injuries involve a transverse distal fibular fracture or lateral collateral ligamentous disruption, the former being distal to the tibiotalar joint. There may be an associated fracture of the medial malleolus. The syndesmotic and medial collateral ligamentous complexes are intact. For correlative purposes, supination-adduction would be a typical mechanism. Infrequent involvement of the syndesmosis renders type A fractures relatively stable from a clinical standpoint. Weber type B injuries involve a spiral fracture of the distal fibula usually at the level of the tibiotalar joint. There is either an avulsion injury to the medial malleolus

or deltoid ligament disruption. For correlative purposes, pronation-abduction and supination–external rotation mechanisms are most commonly responsible for type B injuries. Weber type C injuries involve a fracture of the fibula above the level of the ankle joint. The syndesmotic ligamentous complex is usually torn to the level of the fibular fracture. Medial malleolar or deltoid ligamentous injury is also usually present. Pronation–external rotation is the typical mechanism involved. These fracture types are usually clinically unstable, warranting surgical intervention. However, stage 2 supination–external rotation fractures may be responsible for type C injuries, and lack of displacement and significant syndesmotic injury may indicate clinical stability, obviating the need for surgical intervention. Hence, categorization of a fracture as type C, in and of itself, does not necessarily indicate the need for aggressive intervention. Specific named fractures involving the ankle include the following: Maisonneuve fracture (see Fig. 29-11). This fracture involves the proximal fibula, often the neck, with occasional association to peroneal nerve injury. External rotational force applied to an otherwise neutrally (or close to neutrally) positioned foot and ankle is said to result in this injury pattern. The fracture is a supination–external rotation or pronation–external rotation fracture (extending

CHAPTER

posterocranially or posterocaudally from the anterior cortical margin, respectively). Stage 1 injuries involve the anterior tibiofibular and interosseous complex. Stage 2 injuries progress to involve the posterior tibiofibular portion of the syndesmotic ligamentous complex. Stage 3 injuries comprise rupture of the anteromedial joint capsule. Stage 4 injuries progress to the aforementioned proximal fibular fracture types. Stage 5 injuries involve injury to the deltoid or fracture of the medial malleolus; these injuries are unstable, often necessitating ORIF.6 Direct fibular fracture. This obliquely oriented fibular fracture extends from the lateral surface in a cranial

29

● Acute Osseous Injury to the Ankle

731

and medial direction and is best characterized on frontal views with usual medial displacement of the distal fragment resulting from a force arising laterally.6 Bosworth fracture-dislocation. As previously described, a supination–external rotation mechanism of injury may result in a proximal fibular fracture fragment that is displaced posterior to the tibia and often requires open reduction. Pilon fracture (Fig. 29-22). A pilon fracture refers to a fracture of the distal tibia whose fracture line extends into the tibiotalar joint. There is usually evidence of comminution of the distal tibia, usual association with a talar fracture (Fig. 29-23), and usual preservation

■ FIGURE 29-22 Anteroposterior (A), oblique (B), and lateral (C) radiographic views of the left ankle as well as axial CT (D) with sagittal (E) and coronal (F) reformatted images demonstrate a comminuted fracture of the distal tibia with intra-articular extension into the tibiotalar joint consistent with a pilon fracture.

(Continued)

732

P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

■ FIGURE 29-22—Cont’d Additionally, there is a comminuted fracture of the distal fibula with apex posterior angulation. CT shows to better advantage the degree of comminution and separation of fracture fragments. According to Mueller’s classification, this would qualify as a type III fracture. Axial CT (G) with sagittal (H) and coronal (I) reformatted images demonstrate a comminuted fracture of the distal tibia with intra-articular extension into the tibiotalar joint consistent with a pilon fracture. There is mild articular surface incongruity. According to Mueller’s classification, this would qualify as a type II fracture.

■ FIGURE 29-23 Axial CT (A) with sagittal (B) and coronal (C) reformatted images demonstrate a comminuted fracture of the distal tibia with intra-articular extension into the tibiotalar joint consistent with a pilon fracture. In addition, there is an associated fracture involving the left talar dome (arrow in C). CT demonstrates to best advantage the degree of comminution and separation of fracture fragments. According to Mueller’s classification, this would qualify as a type III fracture.

of the syndesmotic complex.19 Given its propensity for intra-articular extension, this type of fracture has great potential for inducing changes of secondary osteoarthritis. The classification of Mueller divides pilon fractures into three categories. Type I fractures are those without significant displacement of the major components of the tibial plafond. Type II fractures demonstrate mild articular incongruity. Type III fractures demonstrate compression and displacement of the weight-bearing segments of the tibial plafond. Abrupt and forceful craniocaudal loading comprises

the mechanism of injury; spinal and pelvic fractures are not uncommonly associated. Tillaux fracture. This type of fracture usually results from abduction and external rotation. The fracture line usually extends from the tibial articular surface proximally in vertical fashion with an additional horizontal component that extends laterally through the lateral tibial cortex. In children, a similar fracture known as the juvenile variant occurs because the growth plate fuses from the medial to lateral (Fig. 29-24). Displacement of the tibial fracture fragment by more than 2 mm or

CHAPTER

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● Acute Osseous Injury to the Ankle

733

■ FIGURE 29-24 Mortise (A) view of the ankle demonstrates a fracture involving the distal tibial epiphysis with extension into and consequent widening of the lateral aspect of the growth plate in a pattern consistent with a juvenile Tillaux fracture. Lateral (B) view of the ankle demonstrates no additional oblique metaphyseal component to suggest the presence of a triplane fracture.

articular surface incongruity mandates surgical treatment. A fracture with a similar mechanism but with avulsion of the medial portion of the fibula in lieu of avulsion of the lateral margin of the distal tibia as the end result (with an intact anterior tibiofibular ligament) is named a Wagstaffe–Le Fort fracture.19 Triplane fracture. This is usually caused by a combination of plantarflexion and external rotation and is an

■ FIGURE 29-25 Coronal (A) and sagittal (B) reformatted images from an axial CT scan of the left ankle in a patient with open growth plates demonstrate a vertical fracture through the distal tibial epiphysis, a horizontal fracture through the distal lateral tibial growth plate, and an oblique fracture through the distal tibial metaphysis, all in a pattern consistent with a triplane fracture.

aptly named fracture because the planes of involvement include the sagittal, axial, and coronal planes. There is a vertical fracture through the epiphysis, a horizontal fracture through the lateral aspect of the growth plate, and a coronal component with an oblique fracture through the metaphysis extending cranially into the diaphysis (Fig. 29-25). This fracture type is best seen to full advantage on both antero-

734

P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

■ FIGURE 29-26 Sagittal reformatted image from an axial CT scan of the left ankle in a patient with a forced dorsiflexion injury demonstrates an acute fracture through the talar neck with extension into the sinus tarsi.

posterior and lateral views. It can be thought of as a combination of a juvenile Tillaux fracture and a SalterHarris type II fracture.19 Additionally, fractures of the talus should be considered. These comprise the second most common tarsal bone fractures following those of the calcaneus. Talar neck fractures (Fig. 29-26) are most common, with ver-

tical types comprising the majority. Forced dorsiflexion of the foot is the most common inciting mechanism, and associated dislocations involving subtalar or talonavicular joints are commonly seen.19 The lateral process of the talus presents two articular surfaces, one for the lateral malleolus and the other for the posterior aspect of the posterior talocalcaneal (subtalar) joint. It can easily become pinched between the two bones during a traumatic malposition as when the ankle is pronated with placement of an abduction force. In addition, the talocalcaneal and talofibular ligaments of the lateral complex of ankle ligaments insert onto the lateral process of the talus, and injuries to these ligaments may translate into bony avulsion injury at this site. Fractures of the lateral process of the talus are uncommon but have become more frequent as certain predisposing activities have gained in popularity, particularly snowboarding.20 These patients usually present with lateral ankle pain and swelling, and, because of bony overlap, these fractures are frequently overlooked radiographically (with a reported “miss” rate of up to 50% in certain series) 20 ; the mortise view is the most sensitive for evaluation of this fracture type. Fractures of the lateral process of the talus are often intra-articular (Fig. 29-27) and are thus critical to diagnose, especially given their propensity to occur in younger populations. Failure to treat can result in nonunion and long-term morbidity (Fig. 29-28). Osteochondral fractures can occur as a result of repetitive axial loading to the talar dome or as a result of acute transchondral injury in conjunction with an inversion injury. Clinically, patients usually present with exerciserelated discomfort or abnormal sensations of clicking and instability. Lesions are most often noted in the pos-

■ FIGURE 29-27 Axial (A) CT image through the right ankle demonstrates a comminuted fracture of the lateral process of the talus with intraarticular extension into the posterior subtalar joint (arrow). Sagittal reformatted CT image from the same patient (B) shows to additional advantage the degree of comminution and intra-articular involvement (arrow). Coronal reformatted CT image (C) shows to best advantage the vulnerable position of the lateral process of the talus as it articulates with the lateral malleolus and the posterior aspect of the posterior subtalar joint. The process can become “pinched” during a pronation-abduction type injury, leading to fracture.

CHAPTER

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735

■ FIGURE 29-28

Axial (A), coronal reformatted (B), and sagittal reformatted (C) images through the right ankle demonstrate a well-corticated bony fragment consistent with an ununited fracture of the lateral process of the talus (arrows). There is evidence of intra-articular extension into the posterior subtalar joint, most easily visualized on the sagittal image.

teromedial aspect of the talar dome but are also seen in the middle third of the lateral border of the talar dome.10 Most medial osteochondral lesions have a deep, craterlike appearance (Fig. 29-29), whereas most lateral osteochondral lesions are usually thin and shallow (Fig. 29-30), with width usually exceeding depth.11 A classification system engendered by Berndt and Harty for osteochondral lesions of the talar dome divides lesions into four types or stages based on the intactness of the articular cartilage and the status of the subchondral fragment. Stage I lesions demonstrate intact articular cartilage overlying lesions involving subchondral bone. Stage II lesions are partially detached fragments containing subchondral bone and its overlying articular cartilage. Stage III lesions are completely detached fragments that are still located within the talar dome donor site. Stage IV lesions are similar to stage III lesions with the exception that the bony fragment is located in a position distant to the donor site.10 Standard radiographs may demonstrate a lucency abutting the articular surface with or without subarticular fragmentation. MRI is useful in assessing extent and any displacement for purposes of clinical management. A rim of hyperintense (fluid) signal on T2-weighted images suggests instability of the osteochondral fragment (see Fig. 29-29); however, this has been disputed in the literature with one author reporting reduced accuracy of MRI in distinguishing between fluid and granulation tissue on fluid-sensitive sequences.10 In general, an interface that is hyperintense but with signal intensity less than fluid suggests the presence of fibrovascular granulation tissue and a lesion that is likely unstable but with the capacity to attain stability with healing after a period of non–weight bearing or operative fixation.11 An interface isointense

to fluid or with associated cystic-appearing areas usually indicates the need for operative intervention. The signal intensity of the fragment also factors into clinical management (see later); necrosis is indicated by low signal intensity on all pulse sequences whereas hyperintense marrow signal intensity on T1-weighted images and/or enhancement on fat-saturated post-gadolinium T1-weighted images indicate viability. MR arthrography may be helpful in full characterization of lesions that are indeterminate by standard imaging techniques. Differentiation of stage II from stage III lesions is made easier with intra-articular injection of a contrast agent by documenting the presence of the agent around the lesion (see Fig. 29-30). Stress fractures of the ankle occur in athletes in sports that involve running and jumping. Medial malleolar stress injuries are the most common and are thought to occur due to lack of muscular attachments and subsequent disproportionate transmission of body weight through the medial malleolus. Standard radiography may be unrevealing or demonstrate subtle periosteal reaction; MRI may show focal marrow edema at the junction of the medial malleolus and tibial plafond on inversion recovery imaging (Fig. 29-31).1 An unusual type of acute ankle injury described by Edwards and DeLee21 is ankle diastasis without fracture where widening of the mortise with syndesmosis disruption occurs in the absence of fracture (Fig. 29-32). Lower grades demonstrate lateral displacement of the fibula with or without plastic fibular deformation. Higher grades demonstrate increasing degrees of malalignment with interposition of a superiorly dislocated talus comprising the most advanced described degree of injury. Lower grades are usually managed with closed reduction, whereas ORIF is required for higher-grade injuries.

F ■ FIGURE 29-29

Anteroposterior and mortise views (A) of the right ankle demonstrate an abnormal lucency involving the medial aspect of the talar dome (arrow) without definite evidence of articular surface incongruity. Additional MR images (sagittal T1-weighted [B], axial proton density–weighted [C], and axial [D], sagittal [E], and coronal [F] fatsaturated T2-weighted images) demonstrate a bony lesion with a deep, crater-like appearance that is mildly hypointense on T1-weighted images, is mildly hyperintense on T2-weighted images, and has a near complete rim of hyperintense T2weighted signal consistent with an unstable osteochondral lesion of the posteromedial talar dome (arrows).

CHAPTER

■ FIGURE 29-30

29

● Acute Osseous Injury to the Ankle

Fat-saturated T1-weighted images in the sagittal (A, B) and coronal (C, D) planes after the intra-articular administration of contrast agent (MR arthrography) demonstrate a thin, shallow bony lesion involving the lateral talar dome that is completely undercut by contrast agent (arrows) consistent with a stage III osteochondral lesion of the lateral talar dome.

737

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

■ FIGURE 29-31

Sagittal T1-weighted (A), sagittal short tau inversion recovery (B), axial T2-weighted with fat saturation (C), and coronal proton density–weighted with fat saturation (D) images of the left ankle in a runner with medial ankle pain show marrow signal abnormality with decreased T1-weighted signal intensity and increased T2-weighted signal intensity involving the medial malleolus. Plain radiography had been unrevealing. Axial fat-saturated T2-weighted image from a second patient (E) demonstrates similar, less extensive findings of bone marrow edema involving the medial malleolus at its articulation with the medial talar dome.

CHAPTER

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● Acute Osseous Injury to the Ankle

739

■ FIGURE 29-32

Anteroposterior and mortise views in one patient (A) and a mortise view in another patient (B) demonstrate widening of the medial ankle mortise and distal tibiofibular syndesmosis in each patient without radiographic evidence of a fracture in a pattern consistent with ankle diastasis without fracture.

Post-traumatic osteonecrosis of the talus may occur, with findings most reliably noted on MRI, including the “double line sign” as frequently cited to occur in the femoral heads with serpiginous lines of low signal intensity indicative of reparative bone and high signal intensity indicative of granulation tissue. Subchondral fracture and

collapse may also be assessed with radiography or MRI and indicate advanced osteonecrosis. Tibiotalar joint dislocations may occur, usually in conjunction with a fracture (Fig. 29-33). Isolated dislocations are uncommon. About 30% are open, and many are associated with neurovascular injury.22

■ FIGURE 29-33 Anteroposterior (A) and lateral (B) views of the left ankle demonstrate an abnormal configuration of the tibiotalar joint on the anteroposterior view and evidence of frank posterior dislocation of the talar dome relative to the tibial plafond on the lateral view. On the lateral view, bony fragments project over the expected location of the posterior malleolus. An additional anteroposterior view of the left knee (C) demonstrates an associated displaced oblique proximal fibular fracture confirming associated syndesmotic injury.

740

P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment An understanding of a few basic tenets of treatment protocols for the injured ankle goes a long way in assisting the radiologist in the interpretation of postoperative and post-treatment changes. There are numerous treatment options available for ankle fractures, with low scientific uniformity and great controversy in the current literature regarding appropriate surgical indications. A recent study23 showed large geographic variations in the proportion of ankle fractures treated operatively throughout the United States. Possible explanations provided included higher-energy injuries with more articular displacement or open configuration in certain geographic regions. In addition, different surgeons possess varying thresholds to recommend and initiate surgical intervention—the “local aggressiveness phenomenon.” This is unlike low-variability procedures such as treatment of hip fractures in which operative stabilization is generally uniformly accepted throughout the country as the standard of care. The study found that factors associated with a decreased chance of surgical intervention after ankle fracture were older age, female gender, large number of comorbidities, the presence of diabetes or peripheral vascular disease, and treatment in a hospital service area containing a designated teaching hospital.23 The orthopedist’s goal in treating ankle injuries is restoration of near anatomic alignment and articular congruity to ultimately impart normal weight-bearing capability. This can be accomplished with closed manipulation and cast immobilization. This is most successful with lower-stage injuries, nondisplaced fractures, and injuries complicated by infection in which ORIF would not be indicated. Open methods of treatment are most often used for higher-stage injuries, displaced fractures, and talar subluxation.6 With Weber type A injuries, truly nondisplaced fractures of either medial or lateral malleolus may be managed well with a short-leg cast. Mildly displaced fractures in the setting of a supination-adduction mechanism may sometimes undergo successful closed reduction with maneuvers that essentially reverse the mechanism of injury. Articular surface impaction and plafond incongruity in the setting of type A injuries may warrant open reduction.17 With Weber type B injuries, usually supination–external rotation or pronation-abduction, nondisplaced fractures may be suited to nonoperative management. In cases in which it is difficult to differentiate stage 2 from higher-stage supination–external rotation injuries, as described previously, a short-leg walking cast for 6 weeks may be attempted with radiographs in the cast taken at 2 weeks’ time to assess for talar shift and, hence, instability and need for more aggressive treatment. With anatomic reduction of the lateral malleolus and demonstration of syndesmotic stability, repair of a torn deltoid ligament has not been shown to render any long-term benefit.17,24

Surgical Treatment With Weber type C injuries, usually pronation–external rotation, displacement and syndesmotic instability render operative management necessary. Anatomic fixation of the fibular fracture is key, followed by syndesmotic stabilization. ORIF of the medial malleolus and/or plafond fragment completes the repair (Fig. 29-34). ORIF usually begins with fibular fixation, progressing to medial malleolar repair, because clinical instability is usually directed laterally. The exception to this occurs when the medial malleolar fracture is vertical or oblique, as seen in high-stage variants of the supination-adduction and some supination–external rotation injuries and in cases in which the lateral fracture is comminuted. Clinical instability in these cases is usually directed medially.6 In repairing lateral malleolar fractures, length, rotation, and obliquity are important characteristics to note, and successful reduction is dependent on reseating of

■ FIGURE 29-34 A mortise view of the left ankle demonstrates prior ORIF. Two screws have been used to secure a medial malleolar fracture. A lateral plate and multiple associated screws as well as two interfragmentary screws (separate from the plate and screw complex situated in a different spatial plane) secure a long oblique fracture of the distal fibula. The screw transfixing medial and lateral tibial and fibular cortices represents a syndesmotic screw.

CHAPTER

the fibula in its incisural notch. Any residual proximal displacement translates into lateral displacement due to the increasing diameter of the distal fibula, with resultant widening of the mortise. Because anatomic healing of the lateral malleolus is critical, failure to reduce the distal fibula in anatomic position constitutes a widely accepted indication for conversion to or revision of ORIF to prevent premature secondary degenerative change, especially in younger, active, otherwise healthy persons. Adequate tibiofibular overlap on the anteroposterior view as well as maintenance of the mortise are key findings to evaluate for on follow-up radiographs. The fibular fixation method of choice is usually based on the fracture type. Transverse and short oblique types are usually treated with a small plate and two or three screws cranial and caudal to the fracture line. Long oblique or spiral fractures are treated with interfragmentary screws along with plate fixation (see Fig. 29-34). Comminuted fracture fragments may be held together with interfragmentary screws or cerclage wires as well as plate fixation.6 Fixation of the medial malleolus is usually facilitated with one or two small cancellous screws in combination with one or two Kirschner wires or, alternatively, with a malleolar screw.6 Fixation of large anterior or posterior fragments originating from the distal tibia follows the same principles. Repair of the deltoid ligament is only necessitated with rupture of deep fibers because this is thought to represent a medial malleolar fracture equivalent and is performed with heavy absorbable suture material. Six weeks of cast immobilization almost always follows. Syndesmotic complex injuries may necessitate fibular stabilization with a tibiofibular syndesmotic screw (see Fig. 29-34). Syndesmotic disruption can be stabilized equally well with three- or four-cortex fixation.25 A fracture involving the tubercle of Chaput or a Wagstaffe–Le Fort fracture is fixed with cancellous screws when possible. The former is usually fixed last because this fixation tends to be the most tenuous in the grand scheme of repair.6 Treatment of fractures in diabetics is of special concern in that complications such as skin ulceration, infection, nonunion, and malunion occur more frequently than in the general population.26,27 It is critical to ensure that any injury being treated is acute and not subacute, related to a Charcottype neuroarthropathy. The latter often requires a “cool down” period of casting, elevation, and limited weight bearing to allow inflammation to subside and render the surgical field, if necessary, a favorable one. Rigid fixation is often utilized with tendency to err on the side of syndesmotic fixation. Cast immobilization for 6 weeks to allow unimpeded healing is necessary. Extra vigilance is warranted in the clinical and imaging follow-up of these patients.17 Treatment of osteochondral lesions is aimed at early recognition, revascularization, and prevention of detachment and hence progression to stage 3 and 4 status. Stage 1 and most stage 2 lesions are treated conservatively. Surgical curettage and drilling to promote revascularization may be undertaken when the lesion appears unstable, with surface incongruity, or when ischemic changes of the fragment are identified.10

29

● Acute Osseous Injury to the Ankle

741

Rehabilitation of ankle injuries focuses on maintenance of a normal functional position, protection of the ankle joint from excessive force, restoration of anatomic motion, and progressive weight bearing as soon as is clinically determined to be safe. Radiographic complications to be aware of after treatment include osteomyelitis or infection about hardware, hardware loosening or failure, malunion or nonunion, osteoarthritis, delayed syndesmotic instability, tibiofibular synostosis, and reflex sympathetic dystrophy. Infection is most commonly noted in open ankle fractures and often involves the ankle joint proper (Fig. 29-35); aspiration of the tibiotalar joint is thus standard in the exclusion of postoperative infection. Removal of hardware in the setting of infection and ununited fracture fragments is a controversial topic, with some advocating that removal before healing with subsequent fracture instability leads to a poorer outcome (Fig. 29-36), whereas others state that the nidus provided by infected hardware prevents successful resolution of infection. Therefore, adequate débridement of infected tissues, adequate reduction and stability, antibiotic coverage, and aggressive rehabilitation are all necessary elements in the care of the infected joint. Radiographic criteria for hardware loosening are similar to those utilized in other anatomic locations. Specific to the ankle, syndesmotic screws tend to develop evidence of motion and loosening fairly frequently (Fig. 29-37). Malunion may occur with unsuccessful closed reduction or loss of previously near-anatomic alignment (Fig. 29-38); if caught early, successful revision with ORIF may ensue. Shortening and malrotation of the fibula constitutes the most common malunion.17 Distraction, rotation, and fixation with bone grafting may help to restore anatomic congruity. Nonunions are rare (Fig. 29-39); bone grafts (especially with comminution or osteolysis) and rigid fixation are important factors in salvaging stability. Post-traumatic, secondary degenerative changes are common and may occur in up to one fourth of patients, even after adequate fixation and restoration of nearanatomic alignment. Predisposing factors are thought to include posterior malleolar involvement and healing with residual displacement. Secondary osteoarthritis related to prior trauma is much more frequently encountered than primary osteoarthritis. Manifestations include osteophytosis, narrowing of the ankle mortise, subchondral sclerosis, and subchondral cyst formation (Fig. 29-40). If conservative measures fail, ankle arthrodesis (Fig. 29-41) remains a treatment consideration. Although one author found a success rate at 5 years of 93% after the placement of ankle arthroplasties in 200 patients, the procedure has not met with widespread acceptance.28 If there happens to be prominent anterior osteophytosis, resection may prove beneficial (Fig. 29-42).17 Delayed syndesmotic instability may occur with widening of the medial mortise and clinical symptoms of pain and swelling, all as a result of insufficiency of the deltoid ligament and/or the syndesmotic complex, even in the setting of normal osseous anatomy. Reconstruction of the anterior tibiofibular ligament and syndesmotic reduction constitute preferred operative treatment.

742

P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

■ FIGURE 29-35 Mortise view of the right ankle (A) demonstrates evidence of prior ORIF with screw tracks in the tibial diaphysis; all hardware has been removed with the exception of suture anchors about the medial malleolus. There is an ununited, impacted fracture of the distal fibula with extensive surrounding periosteal reaction. Axial fat-saturated T2-weighted (B), coronal (C), and axial (D) postgadolinium fat-saturated T1-weighted images demonstrate extensive abnormal fluid signal intensity and enhancement about the soft tissues surrounding the right distal tibia and fibula in addition to abnormal marrow signal intensity and enhancement of the distal fibula in this patient with postoperative infection.

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29

● Acute Osseous Injury to the Ankle

■ FIGURE 29-36 Three serial radiographs of the right ankle in the same patient demonstrate (A) changes status post ORIF of a medial malleolar fracture with Kirschner wires as well as a distal fibular fracture and the syndesmosis with a lateral plate and multiple, including interfragmentary and syndesmotic, screws. This radiograph was taken approximately 8 weeks after surgery; there is extensive soft tissue swelling with an ulcer in the medial soft tissues. Because of suspicion of infection involving the tibiotalar joint, hardware was subsequently removed, as confirmed on a follow-up postoperative radiograph (B), where there is also evidence of progressive demineralization about the medial malleolus and incomplete healing of previously noted distal fibular fracture. One month after hardware removal (C), a radiograph demonstrates progressive narrowing of the tibiotalar joint space and collapse at the distal fibular fracture site.

■ FIGURE 29-37 Two serial mortise radiographs of the left ankle separated in time by 4 months demonstrate (A) ORIF of the tibiofibular syndesmosis with two syndesmotic screws (three-cortex fixation) that, on follow-up examination (B), demonstrates interval development of surrounding lucency consistent with loosening of hardware.

743

744

P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

D ■ FIGURE 29-38

Sagittal (A, B) and coronal (C, D) reformatted images of the right ankle in a patient with a history of prior “ankle injury” demonstrate malunion of a stage 4 supination–external rotation type ankle injury. There is partial bony bridging with malalignment involving a distal fibular fracture with an oblique orientation extending cranially and posteriorly from the anterior cortical margin (A and C), a fracture of the posterior malleolus (B), and a transverse fracture through the medial malleolus (D). Abnormal increased density within the talar dome suggests osteonecrosis without collapse.

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29

● Acute Osseous Injury to the Ankle

745

Tibiofibular synostosis results from heterotopic bone formation, which may form post-traumatically, bridging the tibia and fibula (Fig. 29-43). This finding may or may not be associated with symptoms29; excision may prompt relief of symptoms. Reflex sympathetic dystrophy is an uncommon clinical syndrome that may occur after trauma and whose manifestations include pain, swelling, and demineralization of the affected extremity. Radiographic findings are not pathognomonic, as disuse osteopenia may render a similar appearance (Fig. 29-44). Persistent, disabling pain may occur after apparently successful surgical fixation. Injury to the lateral ligaments of the ankle occur in about one third of patients with Weber type B or C ankle fractures and may account for ankle instability after fracture healing in some patients.30 Sometimes, associated traumatic injuries may occur that

What the Referring Physician Needs to Know ■ ■

■ FIGURE 29-39

Single mortise view in a patient 6 months after initial injury demonstrates evidence of nonunion involving a transverse medial malleolar fracture of the right ankle. A fracture of the distal fibula in the late stages of healing is also present.

■

Misdiagnosed and untreated ankle injuries can lead to long-term morbidity. Understanding mechanisms of ankle injury allows for proper interpretation of radiographs. Understanding treatment protocols for the injured ankle allows for appropriate assessment of post-treatment complications.

■ FIGURE 29-40 Oblique view (A) of the right ankle demonstrates changes status post ORIF with subsequent removal of hardware and screw tracks in the distal fibula and across the tibiofibular syndesmosis. There is evidence of joint space narrowing involving the lateral mortise and subchondral sclerosis and cyst formation involving the lateral tibial plafond. A coronal proton density–weighted image with fat saturation in another patient (B) with prior ankle trauma demonstrates evidence of articular cartilage loss and subchondral cyst formation involving the medial tibial plafond and medial talar dome.

746

P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

A

B

C

■ FIGURE 29-41

Anteroposterior (A) and lateral (B) views of the right ankle in a patient with prior ankle injury and persistent ankle pain who has undergone arthrodesis of the tibiotalar joint with two screws in addition to placement of surrounding bone graft material to facilitate fusion. A coronal (C) reformatted CT image from another patient demonstrates advanced bony bridging across the tibiotalar joint status post arthrodesis with a single screw.

■ FIGURE 29-42

Sagittal T1-weighted image with fat saturation after the intra-articular administration of contrast agent demonstrates a prominent anterior osteophyte involving the distal tibia.

■ FIGURE 29-43 Mortise view of the left ankle in a patient with posttraumatic deformities of the distal tibia and fibula demonstrates evidence of heterotopic bone formation about the distal tibiofibular syndesmosis consistent with post-traumatic tibiofibular synostosis.

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● Acute Osseous Injury to the Ankle

747

■ FIGURE 29-44 In a patient with history of prior right ankle injury there is diffuse patchy demineralization and evidence of mild soft tissue swelling. These radiographic findings were concordant with the clinical diagnosis of reflex sympathetic dystrophy syndrome but are indistinguishable from those of disuse osteopenia.

are not detectable by plain radiographs but that may represent the cause of pain. One prospective study evaluated arthroscopic findings in acute fractures of the ankle. Findings of acute injury to the articular cartilage of the ankle joint were noted in almost 80% of cases, most often in the talus, followed by the distal tibia, the fibula, and

the medial malleolus.31 Cartilaginous injuries were more frequent in men and at the extremes of age. These findings may help to explain why final clinical results do not always correlate with the success of reduction and degree of stability achieved postoperatively. Ankle arthrodesis may be required in severe cases.

SUGGESTED READINGS Cerezal L, Abascal F, Garcia-Valtuille R, Canga A. Ankle MR arthrography: How, why, when. Radiol Clin North Am 2005; 43:693–707, viii. Dunfee WR, Dalinka MK, Kneeland JB. Imaging of athletic injuries to the ankle and foot. Radiol Clin North Am 2002; 40:289–312, vii. Lassiter TE Jr, Malone TR, Garrett WE Jr. Injury to the lateral ligaments of the ankle. Orthop Clin North Am. 1989; 20:629–640.

Pankovich AM. Acute indirect ankle injuries in the adult. J Orthop Trauma 2002; 16:58–68. Rosenberg ZS, Beltran J, Bencardino JT. From the RSNA refresher courses. Radiological Society of North America. MR imaging of the ankle and foot. Radiographics 2000; 20(Spec No): S153–S179.

REFERENCES 1. Dunfee WR, Dalinka MK, Kneeland JB. Imaging of athletic injuries to the ankle and foot. Radiol Clin North Am. 2002; 40:289–312, vii. 2. Hasselman CT, Vogt MT, Stone KL, et al. Foot and ankle fractures in elderly white women: incidence and risk factors. J Bone Joint Surg Am 2003; 85:820–824.

3. Jones KB, Maiers-Yelden KA, Marsh JL, et al. Ankle fractures in patients with diabetes mellitus. J Bone Joint Surg Br. 2005; 87:489–495. 4. Greenfield DM, Eastell R. Risk factors for ankle fracture. Osteoporos Int. 2001; 12:97–103.

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5. Paton DF. Notes on Fractures. Edinburgh, Churchill Livingstone, 1984. 6. Pankovich AM. Acute indirect ankle injuries in the adult. J Orthop Trauma 2002; 16:58–68. 7. Inman VT. The Joints of the Ankle. Baltimore, Williams & Wilkins, 1976. 8. Ramsey PL, Hamilton W. Changes in tibiotalar area of contact caused by lateral talar shift. J Bone Joint Surg Am 1976; 58:356–357. 9. Lassiter TE Jr, Malone TR, Garrett WE Jr. Injury to the lateral ligaments of the ankle. Orthop Clin North Am. 1989; 20:629–640. 10. Rosenberg ZS, Beltran J, Bencardino JT. From the RSNA refresher courses. Radiological Society of North America. MR imaging of the ankle and foot. RadioGraphics. 2000; 20(Spec No):S153–S179. 11. Cerezal L, Abascal F, Garcia-Valtuille R, Canga A. Ankle MR arthrography: how, why, when. Radiol Clin North Am 2005; 43:693–707, viii. 12. Nikken JJ, Oei EH, Ginai AZ, et al. Acute ankle trauma: value of a short dedicated extremity MR imaging examination in prediction of need for treatment. Radiology 2005; 234:134–142. 13. Lohman M, Kivisaari A, Kallio P, et al. Acute paediatric ankle trauma: MRI versus plain radiography. Skeletal Radiol 2001; 30:504–511. 14. Remplik P, Stabler A, Merl T, et al. Diagnosis of acute fractures of the extremities: comparison of low-field MRI and conventional radiography. Eur Radiol 2004; 14:625–630. 15. Pommering TL, Kluchurosky L, Hall SL. Ankle and foot injuries in pediatric and adult athletes. Prim Care 2005; 32:133–161. 16. Young CC, Niedfeldt MW, Morris GA, Eerkes KJ. Clinical examination of the foot and ankle. Prim Care 2005; 32:105–132. 17. Carr JB. Malleolar fractures and soft tissue injuries of the ankle. In Browner BD, et al (eds). Skeletal Trauma—Basic Science, Management, and Reconstruction, 3rd ed. Philadelphia, WB Saunders, 2003, vol 3, pp 2307–2374. 18. Nugent PJ. Ottawa Ankle Rules accurately assess injuries and reduce reliance on radiographs. J Fam Pract 2004; 53:785–788. 19. Greenspan A. Orthopedic Radiology: A Practical Approach, 3rd ed. Philadelphia, Lippincott Williams & Wilkins, 2000.

20. Bonvin F, Montet X, Copercini M, et al. Imaging of fractures of the lateral process of the talus, a frequently missed diagnosis. Eur J Radiol 2003; 47:64–70. 21. Edwards GS Jr, DeLee JC. Ankle diastasis without fracture. Foot Ankle 1984; 4:305–312. 22. Toohey JS, Worsing RA Jr. A long-term follow-up study of tibiotalar dislocations without associated fractures. Clin Orthop Relat Res 1989; (239):207–210. 23. Koval KJ, Lurie J, Zhou W, et al. Ankle fractures in the elderly: what you get depends on where you live and who you see. J Orthop Trauma 2005; 19:635–639. 24. Baird RA, Jackson ST. Fractures of the distal part of the fibula with associated disruption of the deltoid ligament: treatment without repair of the deltoid ligament. J Bone Joint Surg Am 1987; 69:1346–1352. 25. Miller RA, Decoster TA, Mizel MS. What’s new in foot and ankle surgery? J Bone Joint Surg Am 2005; 87:909–917. 26. Blotter RH, Connolly E, Wasan A, Chapman MW. Acute complications in the operative treatment of isolated ankle fractures in patients with diabetes mellitus. Foot Ankle Int 1999; 20:687–694. 27. Flynn JM, Rodriguez-del Rio F, Piza PA. Closed ankle fractures in the diabetic patient. Foot Ankle Int 2000; 21:311–319. 28. Wood PL, Deakin S. Total ankle replacement: the results in 200 ankles. J Bone Joint Surg Br 2003; 85:334–341. 29. McMaster JH, Scranton PE Jr. Tibiofibular synostosis: a cause of ankle disability. Clin Orthop Relat Res 1975; (111):172–174. 30. Bombaci H, Katioz HF, Gorgec M. Assessment of the lateral ligaments of the ankle after healed fractures. Foot Ankle Int 2004; 25:857–860. 31. Hintermann B, Regazzoni P, Lampert C, et al. Arthroscopic findings in acute fractures of the ankle. J Bone Joint Surg Br 2000; 82:345–351.

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Soft Tissue Injury to the Ankle: Ligaments Yvonne Y. Cheung and Zehava S. Rosenberg

GENERAL CONSIDERATIONS Prevalence, Epidemiology, and Definitions Ankle injuries are common and account for 10% of visits to an emergency department.1,2 A vast majority of the injuries are ligamentous sprains; an estimated 23,000 sprains occur daily, with an incidence of 1 in 10,000 individuals affected per day in the United States.3 In young individuals the number of ankle injuries is staggering, with ankle injuries accounting for approximately 40% of all athletic injuries.4 One of every 17 high school students who participates in sports sustains an ankle injury per season; 85% of these are ankle sprains. Thirty-three percent of West Point Cadets reported one or more ankle inversion injuries during their 4-year enrollment.4 The incidences of ankle sprains in basketball and soccer players are 53% and 29%, respectively.1 Although men sustain more ankle sprains than women, there is no gender difference in the incidence of ankle sprains among participants in similar sport activities.5 Common risk factors for ligamentous ankle injury include generalized ligamentous laxity, wearing of inappropriate shoes, irregular playing surface, sports involving a cutting activity, and previous history of inversion injury.

subject of much debate. For most patients, the clinical history rarely provides diagnostic clues because sprains occur so quickly.6 Furthermore, the physical examination and stress radiography are limited by pain and swelling during the acute stage of the disease. In most patients with ankle sprains, aside from radiographs, additional imaging evaluation is not necessary because the outcomes of ankle sprains are similar regardless of the pattern of injury.7,8 In selected cases, however, when the diagnosis is less apparent, such as in the highdemand athletes whose treatment of choice is primary surgical repair or in those patients who fail conservative management,7,8 advanced imaging techniques, such as MRI, are useful to document the extent of ligamentous tear.9 The group who seek further medical attention for residual pain and instability, however, is not insignificant and constitutes 20% to 40% of those who failed conservative treatment.10

Pathology Ankle ligamentous injuries are commonly divided into lateral ankle sprain, medial ankle sprain, syndesmotic sprain, and spring ligament injuries. This division, based on anatomic regions, is convenient but arbitrary because many ankle sprains involve multiple groups of ligaments.11

Anatomy Most of the ankle ligaments and their components are named based on their origins and attachment sites. The ligaments covered in this chapter are listed in Table 30-1.

Biomechanics Despite the extensive research on the mechanism of injury, the sequence of ligamentous damage, treatment and outcome, the diagnosis of ankle sprains remains a

KEY POINTS: GENERAL C O N S I D E R AT I O N S The treatment outcome of ankle sprains is similar regardless of the therapy, and specialized imaging may not be practical during the acute stage of injury. ■ Multiple groups of ligaments may be involved in ankle sprain. ■

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TABLE 30-1 Ligament Groups Lateral Collateral Ligaments Anterior talofibular ligament (ATAF or ATFL) Calcaneofibular ligament (CF) Posterior talofibular ligament (PTAF or PTFL) Intermalleolar ligament (IML) Deltoid (Medial Collateral Ligaments) Superficial Tibionavicular ligament Tibiospring ligament Tibiocalcaneal ligament Superficial posterior tibiotalar ligament Deep Deep anterior tibiotalar ligament Deep posterior tibiotalar ligament Ankle Syndesmosis Anterior inferior tibiofibular ligament (AITB) Posterior inferior tibiofibular ligament (PITB) Inferior transverse ligament Distal interosseous ligament Spring Ligament Complex (CNL) Superomedial calcaneonavicular ligament (smCNL) Medioplantar oblique calcaneonavicular ligament (mpoCNL) Inferoplantar longitudinal calcaneonavicular ligament (iplCNL) Sinus Tarsi Ligaments Inferior extensor retinaculum Interosseous talocalcaneal ligament (ITC) Cervical ligament (CL) Lisfranc ( Tarsometatarsal) [ TMT] Complex Lisfranc ligament Intermetatarsal (IMT) Intertarsal

For example, inversion sprain often involves both lateral and syndesmotic ligaments,6 whereas eversion sprain may involve both deltoid and syndesmotic ligaments.11

Classification of Ligamentous Sprain Many grading systems for acute ligamentous sprains are available, but no single system is routinely used. A simple but general classification is provided by the American Medical Association and is based on the extent of ligament injury (Table 30-2).12 Specific to the lateral collateral ligaments of the ankle, supplementary classification schemes

based on anatomy (the number of involved ligaments) and functional assessment (the clinical presentation and physical exam) are also commonly employed. These are reviewed in the section on lateral ankle ligaments.

Manifestations of the Disease Radiography In the emergency department, the clinical guidelines for ordering ankle radiographs are known as the Ottawa Ankle Rules (Table 30-3).13,14 Use of these guidelines reduces the cost and number of unnecessary radiographs ordered for ankle sprains while maintaining the sensitivity of detecting fractures. After acute ankle injury, radiographs of the ankle and occasionally the foot are typically acquired in three projections: anteroposterior, mortise, and lateral (Fig. 30-1). Radiographic assessment includes detection of fractures, osteochondral injuries, and malalignment. An ankle effusion with a combined anterior and posterior joint distention of more than 13 mm is associated with an 82% sensitivity and a 91% specificity for the presence of a fracture that may be radiographically occult (Fig. 30-2).15 A variety of measurements have been devised to evaluate the integrity of the distal tibiofibular joint and to guide treatment.16 The reliability of these values, however, is subjected to much debate because of precision errors and variability related to positioning and rotation.17–19 The commonly used measurements (see Fig. 30-1) are listed in Table 30-4.17, 20, 21 Weight-bearing views of the ankle allow assessment of the thickness of the articular cartilage as well as joint congruity during loading. Although weight-bearing examinations are a valuable part of follow-up evaluation after ankle fractures, they can be limited in acute trauma because of pain. Stress views are utilized to identify ligamentous instability (Fig. 30-3). Comparison with the opposite ankle has been proposed, but symmetric findings may not be consistently present even in normal individuals.

Magnetic Resonance Imaging Magnetic resonance imaging has been shown to be highly sensitive and accurate in identifying ligament injuries in

TABLE 30-2 AMA Classification of Ligamentous Sprain

TABLE 30-3 Ottawa Ankle Rules

Grades

Ligament Injury

1 2 3

Stretched ligament Partial tear Complete rupture

1. Obtain radiographs in the presence of ankle pain and one of the following: a. Bone tenderness at the base of the fifth metatarsal b. Inability to bear weight immediately after injury and to walk four steps in the emergency department c. Bone tenderness at the tip or posterior edge of either malleoli 2. Above rule does not apply to: Patient > 55 years old Injury > 10 days Return visit for recurrent pain

Adapted from Rachun A. Standard Nomenclature of Athletic Injuries. Chicago, American Medical Association, 1968.

Adapted from Verma S, Hamilton K, Hawkins HH, et al. Clinical application of the Ottawa Ankle Rules for the use of radiography in acute ankle injuries: an independent site assessment. AJR Am J Roentgenol 1997; 169:825–827.

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■ FIGURE 30-1 Ankle radiographic measurements. Measurements are taken from anterior-posterior (A) and mortise (B) views. The anterior-posterior (AP) tibiofibular clear space (TFCS), or syndesmosis A, is the horizontal distance between the lateral border of the posterior tibial malleolus (P) and the medial border (M) of the fibula (M-P distance) on the AP view. Anterior-posterior tibiofibular overlap (TFO), or syndesmosis B, is the horizontal distance between the anterior tibial eminence (A) and the medial border of the fibula (A-M distance). Both the TFO and the TFCS are obtained at 10 mm proximal to the talar dome. The mortise medial tibiotalar clear space (MCS) is obtained at 0.5 cm beneath the talar dome (small black arrows). The MCS is less than or equal to the superior clear space (T-S distance, white vertical line).

■ FIGURE 30-2 Ankle effusion. A, Lateral radiograph of the ankle after trauma reveals a large ankle effusion (arrows). B, A combined anterior and posterior joint distention (a + b) of more than 13 mm is associated with an 82% sensitivity and 91% specificity for the presence of a fracture, which may be radiographically occult.

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TABLE 30-4 Radiographic Measurements

Tibiofibular clear space (TFCS) or syndesmosis A Tibiofibular clear space Tibiofibular overlap (TFO) or syndesmosis B Tibiofibular overlap or syndesmosis C Medial clear space (MCS)

View

Normal Values (mm)

Anteroposterior

≤6* (TFCS: fibular width < 44%19)

Mortise

≤6*

Anteroposterior

≥6* (TFO: fibular width > 24%19)

Mortise

>1

Anteroposterior and mortise

≤420 or ≤ superior clear space16

* The absolute value varied in the literature and did not apply to children.

TABLE 30-5 Magnetic Resonance Imaging Features in Ligamentous Injuries Ligament Abnormalities Morphology: Wavy, indistinct borders, discontinuity or nonvisualization Signal: Increased signal on either T1- or T2-weighted images Size: Thick, thin, or normal Edema around the injured ligament Associated Findings Joint effusion or hemarthrosis Periarticular soft tissue edema Ruptured joint capsule, retinacular tears, tendon injuries Osteochondral lesions Fractures Intra-articular bodies Sinus tarsi abnormalities Bone marrow edema Data from references 23, 29, and 30.

the ankle (Table 30-5).22–27 MR arthrography, not commonly performed in acute trauma, was noted to improve visualization of the ligaments.28,29 Except in professional athletes, MRI is rarely performed in the acute setting except for identifying associated injuries such as an occult fracture or an osteochondral talar lesion. In chronic ligamentous injuries, when surgery is contemplated, MRI can play a vital role in identifying the number and extent of ligamentous tears and in the detection of other associated conditions such as high syndesmotic injuries, impingement syndromes, sinus tarsi syndrome, superior peroneal retinacular tears, tears and dislocations of the peroneal tendons, and occult bony injuries.

■ FIGURE 30-3 Widened medial clear space (MCS) on stress radiographs of both ankles. The widened right MCS (arrowheads) reflects a torn deep deltoid ligament requiring operative treatment. The left is normal. Small arrows indicate a nondisplaced fracture of the right lateral malleolus.

MRI is generally performed with the patient supine in an extremity coil and the ankle in neutral position (approximately 20% of plantarflexion).25,28–30 Axial T1-weighted and fat-suppressed, T2-weighted images are optimal for detecting abnormalities of the lateral collateral, deltoid (or medial collateral), and syndesmotic ligaments. Coronal, T2-weighted, fat-suppressed images are also useful for assessing the posterior talofibular, the syndesmotic, and the deltoid ligaments. An additional transverse oblique image (a plane that bisects the coronal and axial sections) provides better visualization of the spring ligament complex.31 After injury, the MR appearance of the affected ligament evolved over time.27 Within 2 weeks of injury, discontinuity and/or attenuation and poorly defined margins of the ligament were common findings. Periarticular edema and fluid in the common peroneal tendon sheath were also reported. The indistinct margins of the injured ligament improved over time. Periarticular edema was consistently seen throughout the first 6 months after the initial injury. In chronic injury, the ligament was either attenuated or stretched while its borders had become better defined. Over time, the ligamentous defect is replaced by a thickened band inseparable from the joint capsule.26,27 Radiographic evidence of talar tilt and shift was also present. MR arthrography of the ankle improves visualization of the ankle ligaments28,29 and is especially useful in analyzing soft tissue impingement syndromes. The lateral and syndesmotic ligaments, in particular, are more clearly demonstrated with joint distention during MR arthrography than during standard MRI. In light of its invasiveness, additional time requirements, and increased cost, the added benefit of MR arthrography in the routine evaluation of ligaments, however, remains to be determined. The 3D MRI technique allows reconstruction of selected anatomic structures in all desired planes and shows promise in the assessment of ankle ligaments.32 The long imaging time is one of the limitations of the 3D MRI technique. Furthermore, MR images are more difficult to render than CT images because the pixel values of MR images are of unpredictable ranges.33

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With its high intrinsic contrast, MRI is superior in the evaluation of the ligamentous injuries around the ankle. Routine MRI of the ankle, however, is not typically indicated unless associated injuries are suspected because imaging findings do not generally predict outcome or alter initial management.34

made.39,40 When healing, the ligament always appears thicker than normal on sonograms. Because clinical evaluation is often sufficient to determine the management of ankle sprains, sonographic evaluation is commonly reserved for difficult cases and for those with persistent pain after initial conservative treatment.

Multidetector Computed Tomography

Nuclear Medicine

Normal ligaments, if surrounded by fat, can be visualized on CT. When the injured ligament is inseparable from surrounding soft tissue swelling, CT is less useful.35 CT is superior to MRI in depicting post-traumatic ossifications in the ligaments or small avulsed bone fragments associated with the ligamentous tear. Although 3D CT with volume rendering technique has proved useful in demonstrating the relationships of the ankle tendons with underlying osseous structures,33 the role of CT imaging of ankle ligaments, however, has not been investigated.

Bone scintigraphy is a sensitive yet nonspecific method in the evaluation of osseous lesions. Its use in the imaging of ankle ligaments is limited. During the acute and subacute phases increased bone uptake may be seen at sites of ligamentous avulsions. Increased uptake is also noted at sites of contralateral bony contusions, such as the medial talar dome and medial malleolus. Bone scintigraphy has been employed in assisting the diagnosis of early stages of Lisfranc ligament injuries41 (see later section on Lisfranc ligament).

Ultrasonography The superficial ligaments of the ankle can be effectively depicted by ultrasonography. Detailed assessment of the ligaments requires high-frequency, up to 14- to 15-MHz probes, state of the art scanning systems, and a high level of operator skill. Because ankle ligaments are seldom oriented parallel to the probe, and their bony insertions are used as reference structures, detailed knowledge of the anatomy of the ligaments is mandatory to produce an accurate evaluation.36–38 The ultrasonographic image of an intact ligament, obtained along the long axis, reveals a parallel-layered echogenic structure with well-defined sharp margins. Putting the ligaments under stress by changing the ankle position often improves visualization. The ankle ligaments are subject to anisotrophy and may become hypoechoic if the ultrasound beam is not perpendicular to their fibers. Pathologic ligaments are also generally hypoechoic, but their sonographic features vary depending on the age of the injury (Table 30-6). A complete ligament tear is diagnosed when the parallel fibers are completely interrupted and a hypoechoic zone occupies the ligamentous defect. If residual parallel fibers can be seen, a diagnosis of incomplete tear is

TABLE 30-6 Ultrasonographic Features of Ligament Injury Acute Thickened ligament Anechoic zone (hematoma or edema) across ligament Anechoic band surrounding ligament representing edema Avulsion at bony insertions Chronic Thickened and hypoechoic ligament Osseous formation within enlarged ligament Bony irregularities at the tip of the malleoli Resolution of the superficial edema Abnormal lengthening of the ligament Adapted from Peetrons P, Creteur V, Bacq C. Sonography of ankle ligaments. J Clin Ultrasound 2004; 32:491–499.

Differential Diagnosis Although lateral collateral ligament sprain is the most common occurrence after an acute ankle inversion injury, other conditions that may masquerade as an ankle sprain are listed in Table 30-7.42

LATERAL LIGAMENT INJURY Prevalence, Epidemiology, and Definitions Lateral ankle sprains are the most common ankle injuries in the athletes.1,4,5,43 Within specific sports activities, the incidence of sprain among males and females is similar.1,5

TABLE 30-7 Ligamentous Lesions and Other Injuries Presenting as Ankle Sprain Ligamentous Injuries Ankle: Lateral collateral*, deltoid, syndesmosis Midfoot: tarsal-metatarsal or Lisfranc complex Hindfoot: Sinus tarsi, calcaneocuboid, bifurcate ligament Fractures Malleolar Lateral process of the talus Anterior process of the calcaneus Base of fifth metatarsal Tarsal Osteochondral Lesion Anterolateral talus Posteromedial talus Distal tibia Tendon Injury Peroneus brevis (most common) Peroneus longus Peroneal retinaculum avulsion (dislocation and subluxation of peroneal tendons) Nerve Damage Superficial peroneal nerve Others Tarsal coalition *Most common. Adapted from DiGiovanni BF, Partal G, Baumhauer JF. Acute ankle injury and chronic lateral instability in the athlete. Clin Sports Med 2004; 23:1–19, v.

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K E Y P O I N T S : L AT E R A L LIG AMENT INJURY The lateral collateral ligaments are the most commonly injured ligaments in ankle sprain. ■ Lateral collateral ligament injuries frequently occur in conjunction with injuries of other groups of ligaments, including the syndesmotic, sinus tarsi, and deltoid ligaments. ■ Additional osseous and soft tissue injuries should be searched for when lateral ankle sprain is suspected. ■

Among the lateral collateral ligaments, the anterior talofibular ligament (ATAF) is the most commonly injured. The calcaneofibular ligament (CF) is seldom ruptured in isolation. Commonly sited risk factors for lateral ankle sprain are a history of a previous ankle sprain44 and preexisting laxity of the lateral collateral ligaments, manifested as increased talar tilt on stress radiographs.45 Other factors predisposing to ankle sprain include varus heel, peroneal muscle weakness, and repetitive axial and inversion loads on the ankle and foot. In sports such as basketball, the rates of recurrent sprains have been reported to exceed 70%. The validity of these commonly held risk factors, however, has been questioned by a prospective study46 that found no difference between the injured and uninjured groups of college athletes with regard to these risk factors.

■ FIGURE 30-5 Diagram of ankle ligaments, anterior view. AITF, anterior inferior tibiofibular ligament; ATAF, anterior talofibular ligament; ITC, interosseous talocalcaneal ligament. Arrow indicates Bassett’s ligament or the inferior fascicle of the AITF.

Anatomy The lateral collateral ligamentous complex consists of three discrete focal thickenings of the capsule: the ATAF, CF, and posterior talofibular (PTAF) ligaments (Figs. 30-4 to 30-6). The ATAF, the weakest of the three ligaments, originates approximately 1 cm proximal to the tip of the

■ FIGURE 30-4 Diagram of the lateral collateral ligaments, lateral view. ATAF, anterior talofibular ligament; CF, calcaneofibular ligament; PTAF, posterior talofibular ligament.

■ FIGURE 30-6 Diagram of ankle ligaments, posterior view. PITF, posterior inferior tibiofibular ligament; PTAF, posterior talofibular ligament; CF, calcaneofibular ligament; T, inferior transverse ligament.

CHAPTER

lateral malleolus and inserts on the talar neck. It stabilizes the talus against anterior displacement, internal rotation, and inversion. The CF runs deep to the peroneal tendons, connecting the tip of the lateral malleolus to the trochlear eminence (Fig. 30-7). It crosses both the tibiotalar and subtalar joints and acts as the floor of the peroneal tendon sheath. It acts as a lateral restraint to the subtalar joint and is stressed in extreme inversion. The PTAF connects the malleolar fossa of the fibula to the lateral tubercle of the posterior talar process. It is the strongest of the three lateral collateral ligaments.

Biomechanics The most common mechanism of ankle injury is plantarflexion, inversion, and internal rotation of the foot, resulting in tearing or sprain of the lateral collateral ligamentous complex. The ligaments are usually sequentially injured. Aside from being the weakest ligament, the ATAF is also taut in plantarflexion and is, therefore, most susceptible to injury. It is the first component to be injured, with concomitant injury to the CF ligament occurring next. The PTAF is injured only under extreme inversion forces that commonly produce an avulsion fracture of the posterior malleolus rather than a rupture of the PTAF. Lateral collateral ligament injuries often occur in conjunction with injuries to other groups of ligaments, including the syndesmotic ligaments, the deltoid ligament, and

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the sinus tarsi ligaments. These combined injuries have been well illustrated on MRI studies.11 In 24 patients with acute inversion injury, MRI detected 23 ATAF, 15 CF, 11 PTAF, 13 interosseous talocalcaneal ligament (ITC), 12 cervical ligament, and 8 deltoid ligament tears.11 The ITC, a component of the sinus tarsi ligaments, was injured in 43% to 56% of cases of ankle sprains in another MRI study.47

Pathology Surgical studies reveal that two thirds of ankle sprains are isolated injuries to the ATAF. ATAF injury can be a midsubstance rupture or an avulsion at the ligament’s attachment site.48,49 The CF is the second most frequently injured ligament but is usually torn in conjunction with the ATAF. The most common combination of lateral ligamentous tears is a complete tear of the ATAF and a partial or complete tear of the CF.50,51A tear of the CF may be associated with a tear of the common peroneal tendon sheath, an observation that is the basis for diagnosing ligamentous tears with ankle arthrography.52 Many different classifications of lateral collateral ligament sprain exist with lack of uniformity of grading. The American Medical Association’s guidelines (see Table 30-2), a general classification scheme for any ligaments, is simple to use. For the lateral collateral ligaments, a commonly cited alternative grading system is based on the location of pain and the presence of instability on physical examination (Table 30-8).18

■ FIGURE 30-7 Normal lateral collateral ligaments. Axial T2-weighted, fat-suppressed MR images at talar body (A) and at distal tip of lateral malleolus (B). The anterior talofibular ligament (ATAF) is a thin band of low signal (arrow), extending from the talus (T) to the fibula. At this level of the ATAF origin, the talus has an oblong configuration. The posterior talofibular ligament (curved arrow) has a broad-based, fan-shaped attachment to the fibular malleolar fossa (open arrow). The calcaneofibular ligament (arrowhead) lies deep to the peroneal tendons (P) along the lateral wall of the calcaneus (c).

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TABLE 30-8 The West Point Ankle Grading System Criteria

Grade 1

Grade 2

Grade 3

Instability on examination Pain on examination

None

None or slight

Definite

Mild

Moderate

Location of pain

Over ATAF

Over ATAF and CF

None to intense Over ATAF, CF, PTAF

Adapted from Brage ME, Bennett CR, Whitehurst JB, et al. Observer reliability in ankle radiographic measurements. Foot Ankle Int 1997; 18:324–329.

Manifestations of the Disease The most common clinical presentation of acute lateral collateral ligamentous sprain is swelling, ecchymosis, and tenderness along the lateral ankle. Tenderness to palpation over the ATAF is common. Patients with grade 3 (or complete) tears may describe a popping sensation followed by swelling. Depending on the extent of injury, symptoms can also be present at the syndesmosis and along the medial aspect of the ankle. Residual symptoms after an ankle sprain have been described in over 40% of patients,10,53 with complaints of pain during activity, recurrent swelling, repetitive reinjury, and feeling of “giving way,” usually on uneven surfaces.10 Subtalar instability, post-traumatic arthritis, syndesmotic injuries, osteochondral talar lesions, sinus tarsi syndrome, and peroneal tendon weakness are just a few of the additional potential long-term sequelae of lateral ankle sprain.54 Chronic ankle dysfunction or instability may be subdivided into functional and mechanical. Functional instability, more prevalent, is defined as the patient’s subjective sense of instability. Mechanical instability,10 defined by the objective findings of ligamentous incompetence, can be documented on clinical examination or stress radiography as hypermobility of the tibiotalar or subtalar joints.

Radiography The Ottawa Ankle Rules provide guidelines for ordering ankle radiographs in the emergency department (see Table 30-3). When these rules are implemented, 19% to 30%55 reduction in the number of foot and ankle radiographs are noted without missing significant fractures. When radiographs are indicated in cases of ankle sprains, three projections are acquired: anteroposterior, mortise (or oblique view with 15 to 20 degrees of internal rotation of the ankle), and lateral. Radiographic findings include fractures, osteochondral injuries, and alignment deformities. Talar osteochondral lesions are reported in 17%56 to 23%57 of patients undergoing arthroscopy and surgery, respectively, for chronic ankle instability after lateral ankle sprain. Stress radiographs generally are not necessary because they do not change the treatment protocol. Typically, cutoff values for the tilt angles are arbitrarily chosen at less than 5 degrees, 5 to 15 degrees, and over 15 degrees to

designate normal, mild, and severe injury, respectively.58 In addition, the accuracy of radiography to detect ligamentous tear is compromised by pain response, variable stress technique, and lack of consensus in the literature regarding normal and pathologic values. Arthrography59 and peroneal tenography60 have been used in the past to diagnose acute ligament injury but have been replaced by noninvasive modalities such as MRI and ultrasonography.

Magnetic Resonance Imaging Ankle MR studies are not indicated in the setting of acute lateral collateral ligament injuries because these injuries are initially treated conservatively. MRI should be limited to those instances in which the clinical diagnosis is unclear or associated injuries such as occult fracture, peroneal tendon dislocation, and avascular necrosis are suggested.61 In the setting of either clinical or MRI evidence of acute or chronic lateral collateral ligament sprains a number of osseous and soft tissue abnormalities must be meticulously searched for (see Table 30-7). Osseous conditions include malleolar fractures, osteochondral talar or, less commonly, tibial lesions, bone contusions, fractures of the anterior process of the calcaneus or the base of the fifth metatarsal, and post-traumatic arthritis. Soft tissue conditions that may be seen on MRI in conjunction with lateral ankle sprains include syndesmotic (high) ankle sprains, deltoid injuries, anterior or posterior soft tissue impingement, sinus tarsi syndrome, superior peroneal retinacular injuries, and peroneal tendon tears and dislocations. Axial and coronal MR images are usually adequate for assessing the lateral collateral ligaments, although oblique axial images and 3D gradient-echo images have also been recommended.24,25,29,30 The sagittal images are less useful for assessing the ligaments and are usually better for assessing associated bony or other soft tissue injuries. The normal ATAF is a thin band of low signal extending from the talus to the fibula (see Fig. 30-7A). Representing a capsular thickening, this ligament is often best seen on fluid-sensitive images because it is highlighted by joint fluid. The ligament can be distinguished from the more superiorly located anterior inferior tibiofibular ligament (AITF) by two major criteria. On axial images, the talus appears oblong at the ATAF ligament origin (see Fig. 307A) while the talus is square at the talar dome where the anterior tibiofibular ligament is visualized. The shape of the fibula also helps differentiate the ATAF from the AITF. The ATAF inserts at the level of the fibular malleolar fossa where the fibula demonstrates a normal medial notch (see Fig. 30-7A), whereas the fibula is round at the insertion of the AITF. The normal CF is frequently seen on axial images of the ankle obtained in about 20 degrees of plantarflexion (see Fig. 30-7B). The ligament is found deep to the peroneal tendons along the lateral wall of the calcaneus. Sequential coronal images of the ankle may better depict the ligament’s origin and insertion sites (Fig. 30-8A). The PTAF can be consistently visualized on routine axial MR images (see Fig. 30-7B). The ligament is fan shaped with a broad insertion into the fibular malleolar

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■ FIGURE 30-8 Normal posterior ligaments of the ankle. Coronal, fat-suppressed, T2-weighted MR images through the posterior malleolus are obtained at the origin of the calcaneofibular ligament (CF) (A) and slightly more posteriorly (B). The posterior talofibular ligament (PTAF) connects the malleolar fossa (f) of the fibula to the lateral tubercle of the posterior talar process. The intermalleolar ligament (arrowheads), a common variant, is located between the posterior tibiofibular ligament (arrows) and the PTAF. The CF lies deep to the peroneal tendons (P).

fossa. Its fascicles are separated by fibrofatty tissue, similar to the anterior cruciate ligament of the knee,29 resulting in a normally striated appearance of the ligament. This striation should not be confused with a tear. MRI features of injury to the lateral collateral ligaments include disruption, thickening, attenuation, heterogeneity, and wavy appearance of the ligaments (see Table 30-5, Figs. 30-9 to 30-13). Acute ligamentous tears are associated with adjacent soft tissue edema, and fluid extravasation outside the joint capsule (see Fig. 30-9A). Obliteration of the fat normally highlighting the ligaments is a reliable sign for ligament injury. Ligaments commonly heal through filling of the defect with a fibrous scar that may occur as early as 7 days after the injury. Scar formation is typically ligament specific. The location of the sprain also influences healing: the closer the site of ligamentous injury to the bony attachment, the greater the likelihood of delayed healing.62 A study using MRI to track the changes in the injured ligaments over time showed progression from an obvious defect to a hypoplastic or hyperplastic appearance of the ligament. For example, 50% of the imaged ATAF ligaments had a defect at 2 weeks. By the seventh week, only 11% of the ATAF ligaments displayed a defect. During healing, the margins of the ATAF also became better defined.27

Concomitant ATAF and CF injury is frequent (see Fig. 30-9); syndesmotic and deltoid tears or contusions are often seen in conjunction with lateral collateral ligament tears (see Fig. 30-10). Complete tear of the CF allows communication between the common peroneal tendon sheath and the ankle joint (see Fig. 30-12B). Fluid within the common peroneal tendon sheath was noted in 52% of patients within 2 weeks of acute sprain but was more common in cases of CF tears.27 In contrast, at 7 weeks, 75% of patients with fluid in the peroneal tendon sheath had an intact CF. This increased incidence of fluid in the peroneal tendon sheath is thought to represent tenosynovitis resulting from the added stress to the peroneal tendons as they attempt to stabilize the lateral laxity of the ankle joint.27 Thirty-five percent of cases of lateral ligament injuries had bone bruises,63 predominantly in the talar dome. Contralateral bone contusions in the medial tibia, talus, and calcaneus and more subtle ipsilateral bone contusions of the distal fibula are other common findings associated with acute tears (see Fig. 30-10). Talar and navicular bone contusions are related to talar head rotational instability. Using surgery as the gold standard, MRI was demonstrated to be 74% sensitive and 100% specific for detecting complete lateral ligament tears.64 In another study,

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■ FIGURE 30-9

Concomitant anterior talofibular ligament and calcaneofibular ligament tears and osteochondral lesion in a 16-year-old with a history of multiple ankle sprains. A, T2-weighted, fat-suppressed axial MR image shows a midsubstance tear of the ATAF (white arrow) with extravasation of fluid outside the capsule. B, An associated calcaneofibular ligament tear (black arrow) is best seen on the coronal image. Concomitant tears of these two ligaments are common. Edema of the deltoid ligament (DD) is also noted. The posterior talofibular ligament (A, open arrow) is intact. Multiple foci of bone bruises and a lateral talar dome osteochondral lesion (B, arrowhead) are also seen. F, fibula.

MRI correctly detected 92% of surgically proven cases of lateral ligament tears.26 Despite the ability of MRI to document the extent of ligamentous injury in acute sprain, one study found that the severity of MRI findings cannot consistently predict clinical outcome in patients who are conservatively treated for their lateral collateral ligament injuries.34

Ultrasonography

■ FIGURE 30-10

Acute lateral ankle sprain with multiple ligamentous injuries. Axial fat-suppressed, T2-weighted MR image shows a tear of the anterior talofibular (ATAF) ligament (arrow). Other ligamentous injuries include sprain to both the posterior talofibular (PTAF) and the deltoid (D) ligaments, characterized by loss of normal striation and increased signal on T2-weighted images in these ligaments. Bone bruise of the medial talar dome (arrowhead) is present.

The ATAF is about 2 mm wide. Its fibers are hyperechoic when perpendicular to the ultrasound beam. Lying deep to the peroneal tendons, the CF can only be visualized when the ankle is in dorsiflexion. The normal CF is 2 mm wide and its distal two thirds are hyperechoic. Because of the close proximity between the CF and the peroneal tendons, fluid is commonly found in the common peroneal tendon sheath after CF tears. An indirect sign of CF tear is lack of motion of the peroneal tendons toward the probe during dorsiflexion. Also, the attenuated or torn CF allows the peroneal tendons to fall deeper toward the calcaneus. The PTAF is difficult to visualize40 on ultrasonography, owing to its deep location. A sonographic study on 105 patients who underwent surgery for lateral ankle sprain showed accuracies of 100% and 92% for diagnosing ATAF and CF lesions, respectively.37

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■ FIGURE 30-11

Anterior talofibular ligament (ATAF) tear near its fibular attachment in two patients. A, Axial, proton density–weighted MR image through the anterolateral gutter shows an irregular, bowed ATAF (small arrows) with a small bone fragment (arrowhead) avulsed from its fibular attachment. B, Fat-suppressed, axial MR image in another patient demonstrates a thickened and partially torn ATAF at its fibular attachment (curved arrow).

■ FIGURE 30-12 Calcaneofibular ligament tear. Coronal, T2-weighted, fat-suppressed (A) and axial, proton density–weighted (B) MR images show discontinuity of the ligament (arrow), which is located deep to the peroneal tendons (P).

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stabilize the lateral ankle have been described. These can be categorized into four general groups: (1) direct lateral ligament repair; (2) peroneus brevis tendon rerouting, (3) peroneus brevis tendon loop, and (4) peroneus brevis tendon loop and rerouting. The postsurgical appearance after ligamentous reconstruction may be assessed by radiography, ultrasonography, and MRI.67 The presence of suture anchors in the region of the ATAF indicates direct ligamentous repair, whereas detection of a fibular tunnel suggests a peroneus brevis loop or rerouting. T1-weighted MR images, in particular, can clearly depict the rerouted peroneus brevis tendon within the fibular tunnel. The integrity of the rerouted tendon is best assessed by backward tracing of the peroneus brevis from its distal attachment at the base of the fifth metatarsal. The distal attachment of the peroneus brevis is typically not disturbed during surgical intervention.

SYNDESMOTIC SPRAIN Prevalence, Epidemiology, and Definitions

■ FIGURE 30-13 Posterior talofibular ligament (PTAF) injury in a ballet dancer. Axial, T2-weighted, fat-suppressed MR image shows a thick and irregular PTAF (arrowhead).

Synopsis of Treatment Options Medical Treatment Randomized studies comparing surgical and nonsurgical treatments of acute lateral ankle sprain found that a functional nonsurgical approach was preferable and provided the earliest recovery of ankle range of motion and return to work or activity. The incidence of late mechanical instability was similar among the varying treatment protocols. Functional nonsurgical regimens include elastic wrap, frequent applications of ice, short period of weight-bearing immobilization, and initiation of range of motion exercise during the acute phase of injury. Once swelling has receded, neuromuscular training stressing peroneal muscle strengthening and proprioceptive exercise should begin. A functional brace that controls inversion and eversion is commonly used during the strengthening period and prophylactically for high-risk activities thereafter. Grade 3 sprain requires an extended initial immobilization period in a weight-bearing cast or removable boot for up to 3 weeks.65

Surgical Treatment Surgical repair of acute lateral ligament ruptures is rarely indicated. The exception may be in cases of sprains in the competitive athlete.66 A few studies suggested a decreased incidence of late recurrent instability after surgical intervention.66 Operative indications in chronic ligamentous injuries include instability and arthrosis, which can typically be detected clinically or on routine weightbearing radiographs. Over 50 procedures designed to

Syndesmotic ligamentous injury, also called high ankle sprain, occurs as an isolated injury or in association with lateral and medial collateral ligament injuries. The injury is common in young athletic individuals, especially those involved in high contact sports. Syndesmotic disruption is commonly associated with Weber C (Lauge-Hansen pronation–external rotation fracture pattern) or with Weber B (Lauge-Hansen supination–external rotation ankle fractures) fractures.68,69 An arthroscopic study reported syndesmotic injuries occurring in 53% to 67% of all external rotation ankle fractures.70 Syndesmotic sprains are estimated to involve over 10% of ankle injuries.71,72 Among high-performance athletes with ankle injuries the incidence may be as high as 40%.10,73 Syndesmotic disruptions are more frequent in high-impact activities when greater stress is placed on the ankle.73 Isolated syndesmotic injuries often do not present as gross diastasis and can be difficult to diagnose, leading to underestimation of injury, incomplete rehabilitation, and prolonged pain and disability.10,74,75

KEY POINTS: SYNDESMOTIC SPRAIN Unlike lateral ankle sprains, syndesmotic injury requires a longer recovery time. ■ Although radiographic measurements of the distal tibiofibular syndesmosis have limited use, decreased or absent tibiofibular overlap on the anteroposterior and mortise views and a tibiofibular clear space of 6 mm or more on the anteroposterior view are indicative of syndesmotic injury. ■ MRI is highly sensitive and specific in diagnosing syndesmotic tears. ■ Tibiofibular recess height of 1.2 cm or more on MRI is suggestive of a syndesmotic sprain. ■ Surgical management is indicated in the presence of diastasis. ■

CHAPTER

Anatomy The syndesmosis ligament complex is made up of the interossesous membrane and four ligaments, the anterior inferior tibiofibular ligament (AITF), the posterior inferior tibiofibular ligament (PITF), the inferior interosseous ligament, and the inferior transverse tibiofibular ligament. The anatomy for the syndesmosis is constant for the AITF

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and PITF with variation seen in the interosseous ligament (Fig. 30-14; see also Figs. 30-5 and 30-6).76,77 The AITF ligament attaches to the anterior tibial (Chaput) and fibular (Le Fort) tubercles and has been studied in detail.76 A distinct distal fascicle of the AITF, described by Bassett and Bartonicek, is also called Bassett’s ligament (see Figs. 30-5 and 30-14C).78 Occasionally, with ankle laxity associated with an ATAF ligament tear,

■ FIGURE 30-14 Normal syndesmosis. Axial, proton density– weighted MR images at the ankle joint (A) and at the talar dome (B) and an oblique axial image (C). The anterior tibiofibular ligament (AITF) and posterior inferior tibiofibular ligament (PITF) are identified when the talus is square at the talar dome and the fibula (F) is round (above malleolar fossa). The inferior transverse ligament (B, arrowhead) is the distal fascicle of the posterior inferior tibiofibular ligament. A distinct distal fascicle of the AITF is also known as Bassett’s ligament (small arrow). The posterior talofibular ligament (PTAF) and peroneal tendons (P) are also noted.

B

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Bassett’s ligament may come into contact with the talar dome and may lead to anterolateral impingement.79 The PITF attaches to the posterior tibial and fibular tubercles. The inferior transverse ligament is the distal fascicle of the posterior inferior tibiofibular ligament (see Figs. 30-5 and 30-14). The inferior interosseous ligament is a stout ligament, commonly thought of as the distal condensation of the interosseous membrane (IOM). The interosseous ligament has a variable attachment that ranges from 2 to 6 cm above the joint line. A synovial-lined interosseous recess or a diverticulum extends from the ankle joint, in between the distal tibia and fibula, and ends proximally at the base of the interosseous ligament. The recess is formed by a posteriorly located V-shaped synovial plica that blends laterally with the fibula.76 The medial aspect of the plica lies loosely on the tibia, thus creating the diverticulum. The normal tibiofibular recess measures approximately 1 cm in height80 in anatomic studies and averages 0.5 cm on MRI.81

The stability of the syndesmosis after ankle fractures has a significant positive correlation with the clinical outcomes.86 Rupture of the AITF and PITF ligaments is a crucial part of the Lauge-Hansen classification scheme.87 In the Danis-Weber classification of distal fibular fractures, Weber C fractures typically involve the syndesmosis and up to 40% of Weber B fractures are associated with ankle diastasis.88,89 Although attempts were made to correlate Weber B and C fractures with the level of IOM injury, a recent study showed that the integrity and extent of IOM tears could not be predicted accurately in 33% of patients with these fibular fractures.90 The Wagstaffe fracture is a vertical fibular fracture produced by AITF ligament avulsion. Eighty-five percent of the Wagstaffe fragments are associated with ankle diastasis88 and syndesmosis injury. Thus, the presence of a Wagstaffe fragment necessitates careful examination of the syndesmotic ligaments and, if necessary, a surgical repair of the torn ligaments.

Biomechanics

Patients with acute syndesmotic injury present with pain in the anterolateral ankle. Pain with external rotation, swelling, and palpable tenderness over the syndesmosis are typical findings. Isolated syndesmotic ligament injury may be distinguished from lateral ligament sprains based on injury mechanism, history, and physical examination. Lateral ankle sprains produce tenderness over the ATAF and CF, along with pain with a talar tilt test. In contrast, syndesmosis sprains generate pain more proximally on palpation over the AITF, PITF, and IOM. A calf compression test is positive in syndesmosis sprain but not in lateral collateral ligament injury.71

The syndesmotic ligaments stabilize the distal tibiofibular articulation and prevent diastasis of the tibia and fibula at the ankle. Although the mechanism of syndesmotic sprain has not been firmly established, external rotation has been commonly recognized as a major mechanism for syndesmotic disruption.71 Twisting maneuvers, commonly seen in sports such as soccer and football, in which there is simultaneous external rotation of the ankle and internal rotation of the leg, have also been implicated as a cause of syndesmotic sprains. Of the syndesmotic ligaments the AITF is the most vulnerable to injury. The contributions of the IOM and interosseous ligament to the stability of the tibiofibular joint are controversial. Whereas Nunley considered the interosseous ligament and membrane to be the strongest portion of the syndesmosis,82 one biomechanical study estimated that the AITF, PITF, and the interosseous ligament contributed, respectively, 35%, 40%, and 22% to lateral displacement restraint.83 Tibiofibular diastasis has to be differentiated from lateral talar shift and talar tilt. The former requires concomitant injuries to the deltoid, and the latter entails lateral ligamentous disruption.11

Pathology Syndesmotic injuries are more debilitating than lateral collateral ligamentous sprains and require a longer recovery time.71,74 One major cause for the poor outcome is the failure to recognize and stabilize the injury. Interrupted syndesmotic ligaments may lead to ankle instability and distal tibiofibular diastasis, a decrease in the tibiotalar articular contact area, and an increase in the tibiotalar contact pressure. All these factors can result in early tibiotalar arthrosis.84 Calcification or ossifications of the syndesmosis may be seen after syndesmotic injury and are generally thought to be asymptomatic. Painful ossifications, however, have been reported in cases of syndesmotic sprain without diastasis.85

Manifestations of the Disease

Radiography There has been an ongoing controversy, further fueled in recent years by the advent of CT and MRI, regarding the sensitivity and specificity of radiographs in detecting syndesmotic ligamentous injuries. Standard radiographic assessment includes anteroposterior, lateral, and mortise views. Measurements obtained from the anteroposterior (AP) view are reported to be between 44% and 48% sensitive, and those from the mortise view are reported to be between 64% and 65% sensitive for syndesmotic disruption.91,92 Commonly used measurements, made on either the anteroposterior or mortise views, include the tibiofibular clear space (TFCS) on the AP view (or syndesmosis A), the tibiofibular overlap (TFO) on the AP view (or syndesmosis B), tibiofibular overlap on the mortise view (or syndesmosis C), and the medial tibiotalar clear space on the mortise view (MCS) (see Fig. 30-1). Whereas Harper and Keller16 obtained the TFO and the TFCS at 1 cm above the tibial plafond (see Fig. 30-1), Pettrone93 and Brage19 and their associates made these measurements at the widest level of the lateral malleolus. The absolute normal value for the TFCS on AP view, the distance between the medial border of the fibula and the lateral border of the posterior tibia (also known as the incisura fibularis), varies in the literature, ranging from

CHAPTER

4 to 6 mm. Accounting for gender difference, one study proposed using a TFCS value of less than 5.16 mm in women and 6.47 mm in men.20 The TFO on AP view is the overlap between the medial fibula and the most lateral projection of the distal tibia. The absolute normal value of the TFO on the AP view also varies in the literature, and measurements ranging from 6 to 10 mm have been proposed. A CT study, which allowed direct measurement of the syndesmosis, an anterior-posterior TFO over 6 mm or 42% of fibular width, and a mortise TFO of over 1 mm, were proposed as a reasonable number for a normal syndesmosis (see Fig. 30-1 and Table 30-4).20,94 Instead of relying on absolute radiographic values, ratios of the TFCS and TFO to the fibular width (FW) have been proposed as reliable, gender-independent measurements.20 The proposed values of TFO:FW and TFCS:FW are more than 24% and less than 44%, respectively.20 The superior tibiotalar clear space is the distance between the tibial plafond and the highest point of the talar dome. The medial tibiotalar clear space (MCS) is measured at 0.5 cm beneath the plafond, on a line parallel to the superior talar joint surface (see Fig. 30-1B). Although the MCS and the superior tibiotalar clear space change considerably in different positions of rotation and in plantarflexion versus dorsiflexion, the MCS was smaller than or equal to the superior tibiotalar clear space on two separate studies.17,95

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The just-described radiographic criteria for evaluating the integrity of the distal tibiofibular syndesmosis do not apply to young children because the posterior border of the distal tibia or the incisura fibularis is not apparent in young children. The incisura is detectable at a mean age of 8.2 years and 11.2 years for girls and boys, respectively.96 Radiographic measurements are unreliable and are dependent on gender, body habitus, and filming technique.18,95 In addition, radiographic diagnosis depends on widening of the tibiofibular spaces and may not detect cases of syndesmotic injury in which there is no diastasis between the distal tibia and fibula. Recent MRI studies were able to directly visualize the injured syndesmosis. These studies similarly concluded that both the TFO and TFCS measurements correlated poorly with MRI evidence of syndesmotic injury.97 In addition, the level of the fibular fracture alone cannot predict the extent of IOM disruption and syndesmotic instability.90

Magnetic Resonance Imaging Magnetic resonance imaging is highly sensitive and specific in identifying tibiofibular syndesmotic injuries. MR findings indicative of a syndesmotic interruption include ligamentous discontinuity, contour alterations (wavy or curved ligaments), or nonvisualization of the ligament.98 Using these criteria, seen on either T1- or T2-weighted images (Figs. 30-15 and 30-16), the reported sensitivity

A ■ FIGURE 30-15

Ten-day-old syndesmosis injury in a college lineman. Axial, proton density–weighted (A) and fat-suppressed, T2-weighted (B) MR images show avulsion of the anteroinferior tibiofibular ligament (arrowhead) from its tibial attachment. The posteroinferior tibiofibular ligament is heterogeneous with linear fluid signal within the ligament indicating partial tear (arrow). Extravasated fluid anteriorly highlights the debris or synovitis (curved arrow). F, fibula.

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■ FIGURE 30-16

Syndesmotic injury manifested as abnormal tibiofibular recess in a 33-year-old man with functional instability. T2-weighted, fat-suppressed axial (A) and coronal (B) MR images show a chronic anteroinferior tibiofibular ligament injury (arrowhead). The mean height of the tibiofibular recess measures 13 mm, which is significantly increased when compared with an ankle without a syndesmotic injury (0.5 ± 0.68 mm). An osteochondral lesion of the talus (curved arrow) is also found. F, fibula.

A

and specificity of MRI, compared with arthroscopy, were 100% and 83% to 92%, respectively.98 The normal, oblique superior to inferior course of the syndesmotic ligaments should be kept in mind when assessing for syndesmotic tears, because this may simulate disruption on routine axial images. Similarly, the normal fascicular pattern, especially of the anterior tibiofibular ligament, should not be misinterpreted as a tear. By using a tear of the AITF ligament as a marker of injury to the syndesmosis, the following associated findings have been identified: increase in the height of the tibiofibular recess (average of 1.2 cm in acute tears and 1.4 cm in chronic tears), osteochondral lesions of the talus (28%), and tibiofibular joint incongruity (33%) (see Fig. 30-16). Based on these results, syndesmotic injury should be considered when a tibiofibular recess height of 1.2 cm is encountered.81

(Fig. 30-17). In a cadaveric study, all cases with a 2-mm diastasis and 50% of cases with a 3-mm diastasis were demonstrated on CT but not on radiography.94 In normal subjects, the anterior syndesmotic width on an axial CT image is 1.9 mm (range: 1 to 3 mm); the posterior syndesmotic width is 4.4 mm (range: 3 to 6 mm).

Multidetector Computed Tomography

Arthroscopy

Computed tomography is more accurate than radiography in detecting subtle widening of the syndesmosis

Arthroscopic findings in patients with persistent symptoms long after ankle injury revealed a triad of findings

Ultrasonography Because of the depth of the syndesmotic ligaments, only the AITF can be imaged by ultrasonography. This ligament is less than 2 mm wide40 and is best visualized with the ligament under slight tension, produced during dorsiflexion of the ankle. The sprained ligament is hypoechoic and thick. Using MRI as a standard, one study of 20 AITFs showed a sensitivity of 66%, a specificity of 91%, a positive predictive value of 86%, and a negative predictive value of 77% for ultrasonographic assessment of syndesmotic injury.39

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■ FIGURE 30-17 CT evidence of diastasis of syndesmosis not appreciated on radiographs. Axial CT image through the plafond shows persistent widening of the right syndesmosis after screw fixation. An asymptomatic left syndesmosis is shown for comparison. The normal measurement for the anterior syndesmotic width (black arrow) ranges from 1 to 3 mm, and the posterior syndesmotic width (white arrow) ranges from 3 to 6 mm. A small bone fragment or ossification along the right posteroinferior tibiofibular ligament suggests concomitant injuries to both the anteroinferior and posteroinferior tibiofibular ligaments.

consisting of scarring of the PITF, disruption of the interosseous ligament, and chondral injury to the posterolateral tibial plafond. Resection of the injured segment of the interosseous ligament and the chondral pathology during arthroscopy was noted to relieve symptoms.75 Because syndesmotic disruption occurs commonly with ankle sprains, there is no consensus as to whether arthroscopy leads to excessive diagnosis and subsequent overtreatment of syndesmotic injury.

The few studies on treatment of purely syndesmotic ligamentous injury without diastasis in athletes suggest a nonoperative treatment, including activity modification with or without a short-leg cast for up to 6 weeks. This is followed by an aggressive physical therapy program involving strengthening, range of motion, and proprioceptive training, allowing return to sports and regular activities as tolerated within 4 to 8 weeks.100–102

Surgical Treatment Classic Signs DIAGNOSIS OF SYNDESMOTIC DIASTASIS ■ Radiography: tibiofibular overlap (TFO) on AP view > 6 mm overlap; TFO on mortise view > 1 mm; anterior tibiofibular clear space (TFCS) on AP view 6 cm) segment of tendon is involved, resection and, if feasible, primary repair or augmentation using a flexor hallucis longus tendon transfer is considered.21 Surgical treatment of refractory insertional tendinopathy with Haglund’s deformity is treated by resection of the prominent tuberosity and retrocalcaneal bursa and tendon débridement. Surgical débridement of the paratenon may be required.22

Tibialis Posterior Tendon Distal tears of the tendon can be reattached with suture anchors. If there is a symptomatic ossicle this may be resected, with the tendon inserted onto the underlying navicular bone. For stage 2 dysfunction (flexible or reducible deformity, consisting of pes planus/arch collapse, overpronation and hindfoot valgus), treatment generally consists of tendon transfer, typically using a graft from the flexor digitorum longus. For stage 3 (fixed deformity) and stage 4 (advanced arthritis) disease, joint fusion is often performed.

Peroneal Tendon Primary repair or débridement of longitudinal split tears is reserved for refractory cases. Bone spurs or sharp edges on the peroneal process can be smoothed down or shaved if it is believed that they contribute to the injury. Refractory tenosynovitis often responds to surgical tenosynovectomy. A subtalar fusion may be required as a last resort to stabilize the hindfoot.6 Surgery is usually required for peroneal tendon dislocation. The peroneal retinaculum is reattached and plicated. The fibular groove may be remodeled and peroneal tendons rerouted.7

What the Referring Physician Needs to Know ■ ■ ■

■

■

Determine the location and extent of tendon tear and measurement from insertion and gap if present. For partial Achilles tear, estimate the percentage of crosssectional area torn. Realize that associated findings may have an impact on surgical management, including presence of an ossicle (i.e., accessory navicular os). In the case of tibialis posterior pathology, identify associated deformity and arthritis resulting in classification as a more advanced stage. In the case of fracture (especially calcaneal fracture), identify associated tendon displacement or intraosseous entrapment.

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SUGGESTED READINGS Bencardino J, Rosenberg ZS. Normal variants and pitfalls in MR imaging of the ankle and foot. MRI Clin North Am 2001; 9:447–463. Bencardino J, Rosenberg ZS, Serrano LF. MR imaging of tendon abnormalities of the foot and ankle. MRI Clin North Am 2001; 9:475–492.

Bencardino J, Rosenberg ZS, Serrano LF. MR imaging features of diseases of the peroneal tendons. MRI Clin North Am 2001; 9:493–504.

REFERENCES 1. http://www.tendinosis.org 2. Soila K, Karjalainen PT, Aronen HJ, et al: High-resolution MR imaging of the asymptomatic Achilles tendon: new observations. AJR Am J Roentgenol 1999; 173:323–328. 3. Lawson JP. Not-so-normal variants. Orthop Clin North Am 1990; 21:483–495. 4. Bencardino J, Rosenberg ZS, Serrano LF. MR imaging features of diseases of the peroneal tendons. MRI Clin North Am 2001; 9:493–504. 5. Wang ZT, Rosenberg ZS, Mechlin MB, Schweitzer ME. Normal variants and disease of the peroneal tendons and superior peroneal retinaculum: MR imaging features. Radiographics 2005; 25:587–602. 6. Pfeffer GB. Peroneal tendon injury. In: Advanced Reconstruction of the Foot and Ankle. Rosemount, IL, American Academy of Orthopaedic Surgeons, 2004, pp 147–152. 7. Fortin PT. Acute peroneal tendon dislocation. In: Advanced Reconstruction of the Foot and Ankle. Rosemount, IL, American Academy of Orthopaedic Surgeons, 2004, pp 141–145. 8. Mengiardi B, Pfirrmann CW, Vienne P, et al. Anterior tibial tendon abnormalities: MR imaging findings. Radiology 2005; 235:977–984. 9. Crimm JR, Gold RH, Cracchiolo A. Arthritis. In Crimm JR (ed). Imaging of the Foot and Ankle. Philadelphia, Lippincott-Raven, 1996, pp 95–135. 10. Pavlov H, Heneghan MA, Hersh A, et al: The Haglund syndrome: initial and differential diagnosis. Radiology 1982; 144:83–88. 11. Major NM, Helms CA. Tendons and Ligaments: Practical MR Imaging of the Foot and Ankle. Boca Raton, FL, CRC Press, 2000, pp 97–117. 12. Mantel D, Falutre B, Bastian D, et al. Structural MRI study of the Achilles tendon: correlation with microanatomy and histology. Radiology 1996; 77:261–265.

13. Crimm JR. Tumors and tumor-like conditions. In Crimm JR (ed). Imaging of the Foot and Ankle. Philadelphia, Lippincott-Raven, 1996, pp 210–229. 14. Karjalainen PT, Soila K, Aronen HJ, et al: MR imaging of overuse injuries of the Achilles tendon. AJR Am J Roentgenol 2000; 175:251–260. 15. Rosenberg ZS, Cheung YY, Jahss MH, et al: Rupture of the posterior tibial tendon: CT and MR imaging with surgical correlation. Radiology 1988; 169:229–235. 16. Rosenberg ZS. Chronic rupture of the posterior tibial tendon. MRI Clin North Am 1994; 2:79–87. 17. Hartgerink P, Fessell DP, Jacobson JA, Holsbeeck MT. Full- versus partial-thickness Achilles tendon tears: sonographic accuracy and characterization in 26 cases with surgical correlation. Radiology 2001; 220:406–412. 18. Grant TH, Kelikian AS, Jereb SE, McCarthy RJ. Ultrasound diagnosis of peroneal tendon tears: a surgical correlation. J Bone Joint Surg Am 2005; 87:1788–1794. 19. Patel S, Fessell DP, Jacobson JA, et al. Artifacts, anatomic variants and pitfalls in sonography of the foot and ankle. AJR Am J Roentgenol 2002; 178:1247–1254. 20. Calhoun JH. Acute repair of the Achilles tendon. In: The Foot and Ankle, 2nd ed. Philadelphia, Lippincott Williams & Wilkins, 2002, pp 311–322. 21. Marks RM. Achilles tendinopathy. In: Advanced Reconstruction of the Foot and Ankle. Rosemount, IL, American Academy of Orthopaedic Surgeons, 2004, pp 155–160. 22. Wapner KL. Chronic Achilles tendon rupture. In: Advanced Reconstruction of the Foot and Ankle. Rosemount, IL, American Academy of Orthopaedic Surgeons, 2004, pp 163–167.

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Soft Tissue Injury to the Ankle: Osteochondral Injury and Impingement Luis Cerezal

Ankle impingement syndromes are painful conditions caused by the friction of joint tissues, which is both cause and effect of altered joint biomechanics. The leading causes of impingement lesions are post-traumatic ankle injuries, usually ankle sprains. These syndromes are classified from the anatomic and clinical viewpoints as anterolateral, anterior, anteromedial, posteromedial, and posterior.

ANTEROLATERAL IMPINGEMENT SYNDROME Prevalence, Epidemiology, and Definitions Anterolateral impingement is a relatively uncommon cause of chronic ankle pain produced by entrapment of abnormal soft tissue in the anterolateral gutter of the ankle after single or multiple ankle inversion injuries. Approximately 3% of ankle sprains may lead to anterolateral impingement. This type of ankle impingement is most common in athletic young males.1–4

Anatomy The anterolateral gutter of the ankle is a space bounded anteriorly by the capsule of the tibiotalar joint, the anteroinferior tibiofibular ligament, the anterior talofibular ligament, and the calcaneofibular ligament. Its lateral border is the fibula, and its medial border is the talus and tibia. The space extends inferiorly to the calcaneofibular ligament and superiorly to the tibial plafond and distal tibiofibular syndesmosis.1,3,4

Pathology Anterolateral impingement is thought to occur subsequent to relatively minor trauma involving forced ankle plantarflexion and supination. Such trauma may result in tearing of the anterolateral soft tissues and ligaments without substantial associated mechanical instability. Repeated microtrauma and soft tissue hemorrhage produce synovial scarring, inflammation, and hypertrophy in the anterolateral gutter of the ankle, with subsequent soft tissue impingement (Fig. 32-1). With chronicity, the reactive soft tissue changes and scarring may organize into a “meniscoid” mass that causes pain and mechanical impingement. Wolin coined the term meniscoid owing to its resemblance at surgery to meniscal tissue.1–4

KEY POINTS Chronic anterolateral ankle pain occurs in young patients after ankle sprain. ■ Tenderness on palpation and anterolateral pain with forced ankle dorsiflexion and eversion are noted. ■ Radiography, bone scintigraphy, and CT are often negative. ■ Ultrasonography shows a soft tissue fibrous mass and synovitis with increased vascularity on power Doppler imaging. ■ Conventional MRI has low-accuracy diagnosis in the absence of ankle joint effusion. ■ MR arthrography is key to confirm anterolateral impingement diagnosis and to rule out other common causes of anterolateral chronic ankle pain; it can show soft tissue thickening in the anterolateral gutter of the ankle. ■

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■ FIGURE 32-1

Diagram shows the site and extent of anterolateral impingement lesion (arrow).

■ FIGURE 32-2

Other contributing factors are hypertrophy of the inferior portion of the anteroinferior talofibular ligament and osseous spurs. First described by Bassett, a separate distal fascicle of the anteroinferior tibiofibular ligament is a common variant (Fig. 32-2). It becomes pathologic when a tear of the anterior talofibular ligament results in anterolateral joint laxity.5 With increasing joint laxity, the talus extrudes anteriorly in dorsiflexion and comes into contact with the fascicle. Constant rubbing of the fascicle against the talus thickens the fascicle, developing an impinging lesion in the anterolateral gutter. Several authors refer to this condition as syndesmotic impingement. Histologic examination of the impinging lesion shows synovial hyperplasia, subsynovial capillary proliferation, hyalinized scar, and fibrous stroma consistent with a chronic inflammatory process.1–4

cases, CT arthrography, MRI, and MR arthrography have been employed to aid the diagnosis.

Manifestations of the Disease When the clinical diagnosis is straightforward, no supplementary imaging examination is necessary. In doubtful

Diagram shows Bassett’s ligament (accessory fascicle of the anterior tibiofibular ligament) (arrow).

Radiography Routine radiographic examination of the ankle consists of anteroposterior, lateral, and mortise views. Radiographs are used to screen for osteochondral lesions, osteoarthritis, or intra-articular ossicles, which may contribute to chronic ankle pain after an ankle sprain or inversion injury. Radiographs can detect neither soft tissue pathology nor chondromalacia associated with anterolateral impingement.

Ultrasonography In the setting of chronic ankle pain after an ankle sprain, ultrasonography can detect amorphous scar tissue and synovitis into the lateral gutter. There may be associated increased vascularity on Doppler imaging (Fig. 32-3). Sideto-side comparison is helpful in confirming the abnormality. Post-traumatic ossicles are also well demonstrated by ultrasonography.

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■ FIGURE 32-3

Ultrasound images reveal irregular soft tissue mass in the anterolateral gutter of the ankle (arrow) with increased vascularity on power Doppler imaging (arrowhead) related to active synovitis.

Multidetector Computed Tomography The role of noncontrast high-resolution CT in patients with chronically painful ankle sprains is to exclude radiographic occult fracture, osteochondral talar dome lesion, and avulsed intra-articular or juxta-articular fragments of traumatic origin that were not readily apparent on standard radiographs. CT is unable to differentiate ankle effusion from the synovial hypertrophy within the joint space. CT arthrography of the ankle can provide high spatial resolution assessment of the anterolateral gutter. Four CT arthrography patterns have been described in the anterolateral recess.4 Nodular thickening (type II) and frayed appearance without an individually recognizable nodular image (type III) clearly appear pathologic and correspond to anterolateral impingement. The other two patterns correspond either to normal appearance (type 0) or to an anatomic variant related to the accessory anteroinferior tibiofibular ligament (type I).

filled recess between the anterolateral soft tissues and the anterior surface of the fibula is another MR arthrographic finding that suggests the diagnosis of anterolateral impingement. This may be due to the presence of adhesions and scar tissue that impairs the entrance of fluid into the normal recess between the fibula and joint capsule. Nevertheless, the identification of abnormal soft tissue itself does not imply the presence of clinical anterolateral impingement because anterolateral scarring and/or synovitis at MR arthrography can be noted in patients without clinical features consistent with those of anterolateral impingement. Therefore, MR arthrography features of anterolateral soft tissue abnormalities must be correlated with clinical findings. The normal distal fascicle of the anteroinferior tibiofibular ligament can be readily visualized on MRI and MR arthrography. A distal fascicle causing impingement can be seen as a thickened anteroinferior talofibular ligament (Fig. 32-5).

Nuclear Medicine

Arthroscopy

Isotope bone scintigraphy is rarely necessary. It may show mildly increased uptake about the distal tibia and fibula but is usually negative.3

Arthroscopic examination of the anterolateral gutter recess demonstrates focal or irregular nodular soft tissue thickening, hyalinized tissue, meniscoid lesions, and synovitis (see Fig. 32-4B).1,2,4 Chondromalacia, thickened fascicles or septa, and osteophytes are also frequently seen. Occasionally, a thickened distal fascicle of the anteroinferior tibiofibular ligament may be present.

Magnetic Resonance Imaging The MRI findings of abnormal soft tissue mass or fibrous band in the anterolateral ankle gutter, distinct from the anterior talofibular ligament, suggest the diagnosis of anterolateral impingement.1–3 The mass has low signal intensity on T1-weighted images and low or intermediate signal intensity on T2-weighted images. Care should be taken not to confuse the frayed margins of the torn anterior talofibular ligament with the meniscoid lesion. Controversies exist about the accuracy of the MRI in the diagnosis of anterolateral impingement. Most authors believe that the assessment of the anterolateral recess with conventional MRI is accurate only when a substantial joint effusion is present.1 Intravenous gadolinium administration can be useful in demonstrating focal synovial enhancement. MR arthrography has been proved as an accurate technique for assessing the presence of soft tissue scarring in the anterolateral recess of the ankle and elucidating its extent in patients with anterolateral impingement before arthroscopy (Fig. 32-4).6 The absence of a normal fluid-

Classic Signs ■ ■ ■ ■ ■

Chronic ankle pain after an ankle sprain in the anterolateral ankle joint. Tenderness on palpation and anterolateral pain with forced ankle dorsiflexion and eversion. Ultrasonography: soft tissue fibrous mass and synovitis with increased vascularity on Doppler imaging. MRI: focal soft-tissue mass with irregular gadolinium enhancement. CT arthrography and MR arthrography: abnormal soft tissue mass or fibrous band in the anterolateral ankle gutter; obliteration of a recess between the anterolateral soft tissues and the anterior surface of the fibula.

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■ FIGURE 32-4

Anterolateral impingement syndrome. A, Sagittal T1-weighted spin-echo MR arthrogram of left ankle shows irregular soft tissue thickening in the anterolateral gutter (arrow). B, Arthroscopic image showing scarring and synovitis in the anterolateral gutter (asterisk). L, lateral malleolus; T, talus.

■ FIGURE 32-5 Anterolateral impingement syndrome. A, Axial T1-weighted spin-echo MR image of right ankle demonstrates nodular lesion surrounding Bassett’s ligament in the superior aspect of the anterolateral gutter (arrow). B, Arthroscopic images depict nodular fibrous thickening in the superior aspect of the anterolateral gutter (asterisk) and an intact anterior tibiofibular ligament (arrow) after arthroscopic removal of the lesion. L, lateral malleolus; T, talus.

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Differential Diagnosis The clinical diagnosis of anterolateral impingement can be established based on the combined presence of the following signs and symptoms: chronic ankle pain after an ankle sprain, anterolateral ankle joint tenderness, recurrent joint swelling, anterolateral pain with forced ankle dorsiflexion and eversion, pain during the singleleg squat, and lack of lateral ankle stability.1,3 However, anterolateral impingement is a diagnosis of exclusion. Lesions producing similar symptoms including peroneal tendon tears or subluxations, sinus tarsi syndrome, stress fractures, loose bodies, osteochondral lesions, bony impingement, and degenerative joint disease have to be excluded before invasive treatment. MRI finding of an abnormal soft tissue mass in the anterolateral ankle gutter makes it necessary to exclude conditions such as pigmented villonodular synovitis and idiopathic synovial osteochondromatosis.

Synopsis of Treatment Options Medical Treatment Most patients with anterolateral impingement respond to conservative therapy, including nonsteroidal antiinflammatory drugs, rehabilitative physiotherapy, or local injection of corticosteroids.1,7

■ FIGURE 32-6

Diagram shows characteristics of anterior ankle impingement including chondral fraying, anterior tibial and talar osteophytes (arrows), synovitis in anterior capsular recess (asterisk), reduction of joint space, and osteochondral loose bodies (arrowhead).

Surgical Treatment

Anatomy

After 6 months of conservative treatment failure, ankle arthroscopy may be performed for débridement of hypertrophic synovial tissue (synovitis and/or scarring) in the anterolateral gutter. If a separate fascicle of the anteroinferior tibiofibular ligament is seen, it should be removed. Arthroscopic treatment has good-to-excellent results.1,2,7

The articular capsule surrounds the joint. It is attached to the borders of the articular surfaces of the tibia and the malleoli proximally and to the distal articular surface of the talus distally. A natural sulcus is present on the superior aspect of talar neck and accommodates the anterior tibial ridge in most ordinary circumstances of dorsiflexion. The anterior aspect of the capsule is broad, thin, and membranous.

What the Referring Physician Needs to Know ■ ■

Radiography, bone scintigraphy, and CT are often negative. MR arthrography is the best imaging method in the diagnosis of anterolateral impingement and to rule out other causes of anterolateral chronic ankle pain.

Pathology The origin of anterior impingement is uncertain, and many factors are likely involved.Three different hypotheses have

KEY POINTS Chronic anterior ankle pain in young athletic patients is related to repeated stress in ankle dorsiflexion. ■ There is painful limitation of end range of ankle dorsiflexion. ■ Impingement is due to soft tissues being trapped between a beak-like prominence at the anterior rim of the tibial plafond and a corresponding area over the apposing margin of the talus proximal to the talar neck. ■ Conventional radiography is the only imaging technique required in most cases. ■ CT is the most efficient means of evaluating the osseous anatomy of these lesions before arthroscopic or open surgical treatment. ■ MRI and MR arthrography are useful in detecting the extent of the lesions and other associated pathologic conditions, allowing for a better therapeutic plan. ■

ANTERIOR IMPINGEMENT SYNDROME Prevalence, Epidemiology, and Definitions Anterior impingement is a relatively common cause of chronic anterior ankle pain. It is frequent in young athletes subjected to repeated stress in dorsiflexion of the ankle, such as soccer players and dancers. It is usually the result of impingement with trapping of soft tissues between a beak-like prominence typically formed at the anterior rim of the tibial plafond and the corresponding area over the apposing margin of the talus proximal to the talar neck, well within the anterior ankle joint capsule (Fig. 32-6).8

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been proposed to explain the formation of talotibial osteophytes in the anterior ankle impingement syndrome.8 Forced dorsiflexion results in repeated microtrauma on the tibia and talus, leading to microfractures of trabecular bone or periosteal hemorrhage, healing with new bone formation. Another mechanism suggested is forced plantarflexion trauma, with capsular avulsion injury. However, the majority of the talotibial osteophytes are not located at the capsular attachment and this hypothesis to the formation of traction spurs is therefore plausible only in the minority of cases. A recent hypothesis suggested that formation of osteophytes in the ankle is related to direct damage to the rim of the anterior ankle cartilage combined with recurrent microtrauma, such as by direct impact of a soccer ball on the anterior ankle region. At this anatomic point, there is only subcutaneous fat covering the anterior articular cartilage rim. Therefore, direct recurrent microtrauma by repetitive kicking actions will induce inflammation, the development of scar tissue, calcification, and, subsequently, spur formation.8 Given that all three of the mechanisms just described are common occurrences in soccer, it is not surprising that this condition is extremely prevalent among professional soccer players.8 Once formed, forced dorsiflexion of the ankle causes impingement between reciprocating talotibial “kissing” lesions. The primary symptom is anterior pain on dorsiflexion with limited end range of motion. However, these changes are very common in asymptomatic athletic populations and require no treatment. Histologic examination of the impingement lesions reveals bony spurs, synovial hyperplasia, and fibrous ingrowth.

Manifestations of the Disease Radiography Conventional radiography is the only imaging study required in most cases, allowing evaluation of osseous spurs and the tibiotalar joint space. Another less frequent radiologic pattern is localized divot in the anterior talar neck secondary to tibial spur abutment. A lateral stress radiograph taken in maximum dorsiflexion may demonstrate physical impingement of the osteophytes (Fig. 32-7A).

Ultrasonography Ultrasound examination allows assessment of the size and location of the talotibial osteophytes and detection of synovitis and capsular thickening in the anterior capsular recess. Doppler imaging may show synovitis with increased vascularity in symptomatic patients.

However, CT is less sensitive for detecting associated effusion, chondral lesions, and bone marrow changes.

Nuclear Medicine Isotope bone scanning is not usually performed. Latephase bone scan may reveal pronounced activity in symptomatic cases.

Magnetic Resonance Imaging Magnetic resonance imaging is useful to confirm the diagnosis and to rule out other causes of chronic ankle pain. MRI shows low signal intensity bony spurs, hypointense subchondral sclerosis, subchondral bone marrow edema, anterior recess joint effusion, capsular thickening, fibrosis, and synovitis in the anterior recess of the tibiotalar joint. The presence of anterior tibiotalar joint effusion and bone marrow edema in the anterior talar neck or distal anterior tibia are the more consistent findings associated with symptomatic anterior impingement. Variable enhancement of the inflamed synovium and focal enhancement in the opposing subchondral areas of impingement can be seen after intravenous gadoliniumenhanced MRI. MR arthrography is useful in assessing the degree of cartilage damage, in delineating loose bodies, and in the detection of capsular thickening and synovitis in the anterior capsular recess (see Fig. 32-7B).

Arthroscopy Arthroscopic examination confirms the findings from imaging studies showing anterior talar and distal anterior tibial spurs, chondral lesions, capsular thickening, fibrosis, and synovitis in the anterior recess of the tibiotalar joint. The so-called tram track lesion in the articular cartilage of the talar dome is a characteristic finding in anterior impingement syndrome of the ankle.9 This lesion is a longitudinal trough with variable width and a fullthickness cartilage defect typically found in the anterior half of the talar dome caused by repeated carving of the prominent osteophytes of the anterior lip of the tibia (see Fig. 32-7C). However, currently the principal role of arthroscopy is in the treatment of these lesions.

Classic Signs ■

■

Multidetector Computed Tomography Sagittal reformatted and 3D CT images are the most efficient and reproducible means of evaluating the osseous anatomy of this condition (Fig. 32-8). The spurs on the medial aspect of the talar neck and the lateral aspect of the distal anterior tibia typically do not overlap each other. The tibial spur is triangular and wider than the talar spur.

■

Radiographic and CT examinations reveal talar spurs on the medial aspect of the talar neck and the lateral aspect of the distal anterior tibia. Anterior tibiotalar joint effusion and bone marrow edema in the anterior talar neck or distal anterior tibia are the MRI findings more consistently associated with symptomatic anterior impingement. MR arthrography is useful in assessing the degree of cartilage damage, in delineating loose bodies, and in the detection of capsular thickening and synovitis in the anterior capsular recess.

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■ FIGURE 32-7

Anterior impingement syndrome. A, Dorsiflexion radiograph demonstrates impingement of tibial and talar osteophytes (arrow). B, Sagittal T1-weighted spin-echo MR arthrogram shows anterior tibial and talar osteophytes (arrows), capsular thickening, and synovitis in anterior capsular recess (asterisk). C, Arthroscopic images show dorsal talar neck osteophyte (asterisk), anterior capsular recess synovitis, characteristic linear cartilage defects of the talar dome (“tram track” lesion) (arrowheads), anterior tibial osteophyte, and articular cartilage fraying (arrows).

Differential Diagnosis Most osteophytes are asymptomatic. However, patients may present with limited ankle range of motion, pain, catching, and swelling. Pain is elicited by pressure on the anterior ridge of the tibia and forced dorsiflexion of the foot. Lesions producing similar symptoms have to be excluded before invasive treatment including generalized tibiotalar arthritis, talar fracture, synovitis of the tibiotalar joint, and loose bodies. Radiographic, ultrasonographic, CT, and MRI findings should be differentiated from those of generalized tibiotalar osteoarthritis. In anterior impingement, the findings are confined to the anterior tibiotalar joint; in tibiotalar osteoarthritis, the changes affect the entire articulation.

Synopsis of Treatment Options Medical Treatment Treatment should initially consist of conservative measures. This includes heel lifts, rest, modification of activities, and physical therapy.

Surgical Treatment In patients with persistent pain despite conservative treatment, arthroscopic or open resection of both soft tissue overgrowths and osteophytes is an effective way of treating anterior impingement. Concomitant abrasion arthroplasty or drilling of any associated cartilage lesions can be performed if necessary. Arthroscopic intervention is successful in most cases.

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based on anatomic location in anteromedial or posteromedial impingement (Fig. 32-9). Medial impingement is rarely an isolated condition; it is most commonly associated with an inversion mechanism of injury with lateral as well as medial ligamentous injury. It can occur after a severe ankle inversion injury with the deep anterior or posterior fibers of the deltoid ligament becoming crushed between the talus and the medial malleolus. Initially, medial symptoms do not predominate, compared with the symptoms of the lateral ligament disruption, and they usually resolve without specific treatment. However, inadequate healing of the contused deep deltoid ligament fibers may lead to chronic inflammation, hypertrophic fibrosis, and metaplasia. In these cases, the anomalous soft tissue may impinge between the medial wall of the talus and the medial malleolus.10,11 ■ FIGURE 32-8

Sagittal reformatted CT image shows spurs (arrows) on the medial aspect of the talar neck and the distal anterior tibia.

What the Referring Physician Needs to Know ■ ■

■

Conventional radiographs in an appropriate clinical context are usually the only imaging study required. CT is the most efficient means to evaluate the osseous anatomy of these lesions before arthroscopic or open surgical treatment. The principal role of MRI in the diagnosis of anterior impingement is to rule out other causes of chronic ankle pain.

MEDIAL IMPINGEMENT SYNDROME Prevalence, Epidemiology, and Definitions Medial impingement is an uncommon cause of chronic ankle pain after an ankle trauma. It can be subdivided

KEY POINTS Chronic medial ankle pain occurs in young patients after ankle sprain. ■ Tenderness on palpation and medial pain with forced ankle plantarflexion and inversion are noted. ■ Ultrasonography shows soft tissue fibrous mass and synovitis with increased vascularity on Doppler imaging. ■ Conventional MRI has a low accuracy for diagnosis in the absence of ankle joint effusion. ■ MR arthrography is key to confirm medial impingement diagnosis and to rule out other common causes of medial chronic ankle pain; it can show soft tissue thickening in the anteromedial or posteromedial aspect of the ankle. ■

Anatomy The deltoid ligament is a complex structure with superficial and deep components that arise from the tip of the medial malleolus. From posterior to anterior, the superficial layer is composed of the tibiocalcaneal, tibiospring, and tibionavicular ligaments. The deep component is composed of the anterior and posterior tibiotalar ligaments. Medial impingement lesions may be related to tearing of the deep component of the deltoid ligament or injury of the overlying medial joint capsule.

Biomechanics and Pathology Slight variation in biomechanics of the injury determines which structures are affected. Medial contusion injury results in damage to the anterior tibiotalar ligament between the tip of the medial malleolus and the anterior part of talus medial wall, whether or not the more posterior contusion of the deep posterior fibers of the deltoid ligament between the posterior margin of the medial malleolus and the posterior part of the medial wall of the talus occurs. The former lesion occurs with inversion of the ankle in a near-neutral position, whereas the latter lesion occurs with a severe inversion injury with the talus more plantarflexed. Both lesions may coexist in some injured ankles. Anteromedial impingement can be caused by a meniscoid lesion, represented by a mass of hyalinized connective tissue arising from a partially torn deep deltoid ligament or by a thickened anterior tibiotalar ligament. This thickened ligament or meniscoid lesion, along with hypertrophic synovium, impinges on the medial corner of the talus during dorsiflexion of the ankle. Frequent findings at the site of impingement where the tibiotalar ligaments made contact with the talus are osteophytes and denuded cartilage.10 In posteromedial impingement the deep posterior fibers of the deltoid ligament remain disorganized and impinge between the medial wall of the talus and the medial malleolus.11 The histologic examination reveals subsynovial connective tissue thickened by fibrosis, fibrocartilaginous metaplasia, and myxoid collagen degeneration rather than just synovial inflammation.

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■ FIGURE 32-9

Diagrams illustrating findings of anteromedial (A) and posteromedial (B) ankle impingement including meniscoid lesion (arrows), thickened anterior tibiotalar ligament (arrowhead), and chondral damage or anterior medial corner articular surface osteophytes.

Manifestations of the Disease

Magnetic Resonance Imaging

Patients complain of persistent medial to posteromedial activity-related ankle pain after a severe inversion injury, localized tenderness on palpation, and reproduction of symptomatic pain on provocative testing by palpating this site while moving the ankle into plantarflexion and inversion. Anteromedial impingement symptoms may be exacerbated in dorsiflexion.

Conventional MRI has not yet proved useful in detecting the medial impingement syndromes. MRI can depict a partially torn deep deltoid ligament but is insensitive for other findings.10 MR arthrography is the imaging method of choice, clearly defining medial meniscoid lesion, thickened tibiotalar ligaments, and chondral or osteochondral associated lesions (Figs. 32-10 and 32-11).

Radiography and Multidetector Computed Tomography

Nuclear Medicine

Radiographs and CT are usually normal. Occasionally, they can reveal anteromedial talar osteophytes in anteromedial impingement and periosteal new bone formation or a separate ossicle in association with the posteromedial lesion.11

Radioisotope bone scans aid to confirm the diagnosis, showing focal increased uptake at the anteromedial recess of the ankle or behind the medial malleolus.11

Ultrasonography

Arthroscopy

Ultrasound examination has not generally been used, but high-resolution ultrasound can reveal fibrosis, partial tears or thickening of the deltoid ligament, synovitis, and capsular thickening in the anteromedial or posteromedial ankle joint, respectively. Increased vascularity on Doppler imaging can be seen.

The anteromedial impingement lesion can be detected via conventional anterior portals, revealing soft tissue in the anteromedial recess of the tibiotalar joint related to fibrosis and synovitis, partial tears or abnormal thickenings of the deep deltoid ligament, and chondral defects and osteophytes in the anteromedial talus.10

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■ FIGURE 32-10

Anteromedial impingement syndrome. Axial T1-weighted spin-echo MR arthrographic images from two different patients: (left) normal striated profound component of the deltoid ligament and (right) irregular soft tissue thickening in the anteromedial capsular recess (arrow) and in the deep component of the deltoid ligament.

■ FIGURE 32-11

Posteromedial impingement syndrome. A, Axial T1-weighted spin-echo MR image of the ankle shows hypertrophic fibrotic tissue in the posteromedial aspect of the ankle (arrow). B, Arthroscopic image depicting the posteromedial impingement lesion (arrow). T, talus.

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The posteromedial lesion cannot generally be fully appreciated arthroscopically via anterior portals in a stable ankle and requires a high index of suspicion and careful examination for the diagnosis to be made clinically. Arthroscopic appearances of excessive soft tissue fronds posteromedially or soft tissue bulging forward between the talus and the medial malleolus are highly suggestive of the presence of the lesion. Posterior portals can be used to detect this posteromedial lesion and associated conditions (see Fig. 32-11B).11

Classic Signs ■ ■ ■ ■ ■

Chronic ankle pain occurs after an ankle sprain in the medial ankle joint. Tenderness on palpation and medial pain with forced ankle plantarflexion and inversion are noted. Soft tissue fibrous mass and synovitis with increased vascularity are seen on Doppler imaging. MRI is usually inaccurate for the diagnosis of medial impingement syndromes. MR arthrography reveals abnormal soft tissue mass in the anteromedial or posteromedial ankle joint, the thickened tibiotalar ligaments, and the chondral or osteochondral associated lesions.

Differential Diagnosis In the clinical context of chronic medial ankle pain after an inversion ankle trauma the main differential diagnoses are chronic deltoid ligament tears and osteochondral lesions. Posteromedial impingement can be confused clinically with posterior tibial tendon pathology.

Synopsis of Treatment Options Medical Treatment

POSTERIOR IMPINGEMENT SYNDROME Prevalence, Epidemiology, and Definitions Posterior ankle impingement syndrome is a clinical disorder characterized by posterior ankle pain, including a group of pathologic conditions secondary to repetitive or acute forced plantarflexion of the foot, which produce compression of the talus and surrounding soft tissue between the tibia and the calcaneus.12 Different names have been given to this syndrome, including os trigonum syndrome, talar compression syndrome, and posterior block of the ankle. Although the most common causes are an enlarged os trigonum or prominent posterior tubercle of the talus, other osseous and soft tissue causes justify using posterior ankle impingement as a more general term.12

Anatomy The anatomy of the posterior aspect of the ankle is a key factor in the occurrence of posterior ankle impingement syndrome.12 The posterior process of the talus extends both posteriorly and medially from the talus and has two projections designated as the posteromedial and posterolateral processes. These processes are divided by a groove containing the flexor hallucis longus tendon. The posterolateral process, whose injuries are the most common cause of posterior ankle impingement syndrome, is also named the trigonal process. When the posterolateral process remains unfused into adulthood, it is called os trigonum. Os trigonum is seen in 7% to 14% of individuals, occurring bilaterally in 1.4% of the population. It is completely corticalized and has an anterior synchondrosis with the talus. The posterior intermalleolar ligament is a normal variant of the posterior ligaments of the ankle, reported as a cause for posterior impingement. This ligament is identified in 56% of dissected cadaveric specimens and 19% of subjects imaged with MRI. The intermalleolar ligament spans the posterior ankle, between the posterior talofib-

Medial impingement lesion usually resolves with nonoperative treatment, such as rest, physical therapy, and antiinflammatory medication.

Surgical Treatment If conservative treatment fails, débridement of the impinging lesion by open arthroscopic methods yields good clinical results.10,11

What the Referring Physician Needs to Know ■ ■

Radiographs and CT are often negative. MR arthrography is the best imaging method in the diagnosis of medial impingement, of associated conditions, and to rule out other causes of medial chronic ankle pain.

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KEY POINTS Posterior ankle impingement syndrome refers to a group of pathologic conditions characterized by posterior ankle pain that result from repetitive or acute forced plantarflexion of the foot. ■ Posterior ankle impingement syndrome of the ankle results from the compression of the talus and surrounding soft tissue between the tibia and the calcaneus and has been likened to a “nut in a nutcracker.” ■ Lateral radiographs reveal anatomic variants frequently associated with posterior ankle impingement, but the presence of these variants does not necessarily imply clinical relevance. ■ MRI is the most useful diagnostic method to confirm the diagnosis and to rule out other causes of chronic ankle pain. ■

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ular ligament and the transverse inferior posterior tibiofibular ligament, and connects the malleolar fossa of the fibula to the medial posterior tibial cortex.13,14 In the posterior aspect of the ankle, five different accessory muscles have been recently related as uncommon etiology of posterior ankle impingement. These muscles are the peroneus quartus, located posterolaterally; the peroneocalcaneus internus; the long accessory to the long flexors or quadratus plantae; the tibiocalcaneus internus; and the accessory soleus, located posteromedially.15

Biomechanics and Pathology Injury mechanisms have been likened to a “nut in a nutcracker,” because the posterior talus and surrounding soft tissues are compressed between the tibia and the calcaneus during plantarflexion of the foot (Fig. 32-12). This syndrome has been extensively described in classical ballet dancers, due to repetitive movements required in the choreography that impose chronic stress on the posterior ankle.12 The more common causes are osseous, such as the os trigonum, an elongated lateral tubercle termed a Stieda process, a downward sloping posterior lip of the tibia, the prominent posterior process of the calcaneus, and loose

bodies (Fig. 32-13). Soft tissue causes of impingement encompass synovitis of the flexor hallucis longus tendon sheath, the posterior synovial recess of the subtalar and tibiotalar joints, ganglia, low-lying flexor hallucis longus muscle belly, anomalous muscles, and the intermalleolar ligament (Fig. 32-14).12 Posterior ankle impingement syndrome may manifest as an inflammation of the posterior ankle soft tissues, as an osseous injury, or as a combination of both. The osseous injuries include fracture, fragmentation, and pseudarthrosis of the os trigonum or lateral talar tubercle. The soft tissue changes associated are posterior ankle and subtalar synovitis as well as flexor hallucis longus tenosynovitis. Intra-articular displacement of the intermalleolar ligament during plantarflexion can entrap the ligament. Repeated entrapment can tear or thicken the ligament, leading to locking and worsening of pain.13,14 The symptoms of posterior impingement related to anomalous muscles appear to be the result of direct soft tissue impingement from the space-occupying anomalous muscle bellies, especially in individuals with high activity levels.15

Manifestations of the Disease The diagnosis of posterior ankle impingement syndrome is based primarily on the patient’s clinical history and physical examination results, and it is supported by radiographic findings, scintigraphy, CT, and MRI.

Radiography Ankle radiographs should be obtained routinely. Lateral radiographs clearly define posterior osseous ankle anatomy, including the presence of an os trigonum, an elongated lateral tubercle termed a Stieda process, a downward sloping posterior lip of the tibia, or prominent posterior process of the calcaneus. The sole presence of these anatomic variants in conventional radiographs is not necessarily indicative of clinical relevance. Radiographs can demonstrate an acute or chronic fracture of the trigonal process. The bony fragment in an acute fracture of the trigonal process is more likely to be triangular and jagged. However, in old fractures, the fragment of bone may well be corticated.12

Magnetic Resonance Imaging

■ FIGURE 32-12

Diagram showing “nut in a nutcracker” phenomenon of posterior ankle impingement (arrow).

Magnetic resonance imaging in the sagittal plane using T1-weighted and fat-suppressed or inversion recovery sequences can afford optimal visualization of an os trigonum, a Stieda process, a downward sloping posterior malleolus, or a prominent calcaneal tubercle.12 MRI is useful in establishing the diagnosis of posterior ankle impingement syndrome, showing abnormal signal intensity in the lateral talar tubercle and/or os trigonum, consistent with bone marrow edema, which is believed to be the result of bone impaction and thus represents bone contusions or occult fractures (Figs. 32-15 and 32-16). MRI also depicts inflammatory changes in the posterior ankle soft tissues, namely, the posterior synovial recess of the subtalar and tibiotalar joints and the flexor hallucis longus tendon sheath. Diagnosis of an abnormal intermalleolar ligament on MRI requires a thickened intermalleolar ligament, which can readily be separated from the

CHAPTER

■ FIGURE 32-13

32

● Soft Tissue Injury to the Ankle: Osteochondral Injury and Impingement

Diagram showing osseous anatomic structures involved in posterior impingement. A, Stieda process. B, Os trigonum. C, Fractured lateral tubercle of the talus. D, Prominent downslope in the posterior tibial articular surface. E, Calcified inflammatory tissue. F, Prominent superior surface of the calcaneal tuberosity.

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■ FIGURE 32-16

Posterior impingement syndrome. Sagittal fatsuppressed, proton density–weighted MR image. Abnormal high signal intensity is seen in the os trigonum and posterior aspect of the talus (arrow) with associated flexor hallucis longus tenosynovitis (asterisks).

■ FIGURE 32-14

Diagram shows anatomy of the posterior intermalleolar ligament (arrowheads).

■ FIGURE 32-15

Posterior impingement syndrome. A, Sagittal fat-suppressed, proton density–weighted MR image demonstrates abnormal high signal intensity in the posterior aspect of the talus and in the os trigonum (arrows). Joint effusion in the posterior synovial recess of the tibiotalar and subtalar joints is noted. B, Arthroscopic images confirm os trigonum (OT) and show posterior ankle after os trigonum removal (arrow).

CHAPTER

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● Soft Tissue Injury to the Ankle: Osteochondral Injury and Impingement

825

■ FIGURE 32-17

Posterior ankle impingement syndrome. A, Coronal fat-suppressed, proton density–weighted MR image shows poorly defined intermalleolar ligament (arrow). B, Arthroscopic view of the ankle reveals frayed intermalleolar ligament (IML, asterisk). Débridement of the ligament relieved the patient’s symptoms. PITF, posteroinferior tibiofibular ligament.

surrounding posterior talofibular ligament and the transverse inferior tibiofibular ligament (Fig. 32-17).12,13 MRI is also useful in detecting accessory muscles related to posterior ankle impingement.15 It is equally important that MRI can specifically identify the wide range of pathology that may contribute to posterior ankle pain that might be clinically confused with posterior ankle impingement. MR arthrography is rarely necessary in the assessment of posterior ankle impingement syndrome. The intermalleolar ligament is often not visualized on conventional MRI. MR arthrography improves the visualization of this ligament, which can readily be separated from the surrounding posterior tibiofibular ligament and the transverse inferior tibiofibular ligament.

Multidetector Computed Tomography Computed tomography is the most valuable method to define the osseous anatomy of the posterior aspect of the ankle. CT allows the evaluation of irregularities or degenerative changes at the os trigonum synchondrosis, can differentiate between an old fracture and an os trigonum, and can evaluate 3D anatomy of a Stieda process, a downward sloping posterior lip of the tibia, the prominent posterior process of the calcaneus, and loose bodies.

However, CT usually fails to evaluate lesions of soft tissue that accompany posterior ankle impingement.

Ultrasonography Ultrasound can be used to detect soft tissue injuries in the posterolateral ankle. The os trigonum is also easily identified by ultrasonography. Sonographically guided corticosteroid and anesthetic injection into the posterolateral impinging lesion can be a useful treatment procedure of posterior ankle impingement.16

Nuclear Medicine Bone scintigraphy is a helpful diagnostic tool. A normal bone scintiscan virtually rules out trigonal process pathology. Increased activity on bone scintiscans is present in patients with an acute fracture of the trigonal process, as well as in those with disruption of the os trigonum synchondrosis.

Arthroscopy Arthroscopy has a limited role in the diagnosis of posterior ankle impingement. The standard posteromedial arthroscopic portal has recognized risks owing to the

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proximity of the posterior neurovascular structures. Arthroscopic posterior portals have been developed for a posterior approach of the ankle with the treatment purpose of posterolateral impingement syndrome without any complications.

Classic Signs ■ ■ ■ ■

Posterior ankle pain is a result of acute trauma or repetitive stress in acute plantarflexion. Radiographs clearly define posterior ankle anatomic variants that may be related to posterior impingement. Bone scintiscans are positive in most patients with posterior ankle impingement. MRI is most useful in the assessment of posterior ankle impingement, clearly depicting both the osseous and the soft tissue abnormalities associated with posterior ankle impingement syndrome.

Differential Diagnosis Clinical differential diagnosis of posterior ankle impingement should include other causes of chronic posterior ankle pain such as Achilles tendinopathy, retrocalcaneal bursitis, flexor hallucis longus tenosynovitis, Haglund’s deformity, ankle or subtalar arthritis, osteochondral lesion, tarsal tunnel syndrome, post-traumatic instability, or peroneal tendon subluxation.

Synopsis of Treatment Options Medical Treatment Treatment of posterior ankle impingement syndrome is initially conservative with rest, anti-inflammatory medication, avoidance of forced plantarflexion, and, occasionally, placement in a cast for 4 to 6 weeks.

Surgical Treatment Surgery may be required in refractory cases. Excision, either in an open or an arthroscopic technique of the osseous impingement structures such as os trigonum, with potential release of the flexor hallucis longus tendon, is an effective and safe method of treatment.

What the Referring Physician Needs to Know ■ ■

The presence of anatomic variants of the posterior ankle on radiographs is not necessarily clinically relevant. MRI is the best imaging method for the diagnosis of posterior impingement and to rule out other causes of posterior ankle pain before treatment.

OSTEOCHONDRAL LESION OF THE TALUS Prevalence, Epidemiology, and Definitions Osteochondral lesion of the talus is the accepted term for a variety of disorders including osteochondritis dissecans, osteochondral fracture, transchondral fracture, and talar dome fracture. It is more common in men than in women. The talus is the third most common location of this disorder, following the knee and elbow joints. Osteochondral lesion of the talus represents 4% of all osteochondral lesions in the body. Medial and lateral aspects of the talar dome are involved in approximately 55% and 45% of the cases, respectively. Lateral osteochondral lesions are typically located over the anterolateral portion of the talar dome. Medial lesions are most commonly located over the posteromedial portion (Fig. 32-18). Lateral lesions are almost always associated with an acute traumatic episode and most likely represent true osteochondral or transchondral fractures. Patients are more likely to have a medial osteochondral lesion when a clearcut history of trauma is absent. Trauma is the most common cause, but ischemic necrosis, endocrine disorders, and genetic factors may have etiologic significance. Furthermore, 10% to 25% of patients have lesions in both ankles.

Anatomy The talar dome is trapezoidal, and its anterior surface is wider than the posterior surface, with an average of 2.5 mm. The talus has medial and lateral articular facets that articulate with the medial and lateral malleoli. The articular surface of these facets is contiguous with the superior articular surface of the talar dome. The talus has no muscular or tendinous attachments, and 60% of the surface is covered by articular cartilage.

Biomechanics and Pathology The primary lesional mechanism is a talar dome impaction due to inversion injuries. Lateral lesions on the anterolateral aspect of the talar dome occur after inversion and

KEY POINTS Osteochondral lesions of the talus manifest as persistent pain, swelling, and catching of the ankle in a patient with a prior history of ankle inversion injury. ■ Radiographs should be the initial imaging method used, but radiographs are insensitive in the detection of the first stages of this lesion. ■ CT is the most efficient means of evaluating the osseous anatomy of these lesions. ■ MRI is useful in the identification of radiographically occult lesions and determining stability and viability. ■ MR arthrography provides better analysis of articular cartilage, assessment of stability, and detection of intra-articular bodies. ■

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■ FIGURE 32-18 Diagram shows the main locations of osteochondral lesions of the talus and the Berndt and Harty classification system.

dorsiflexion force that causes an impact of the anterolateral aspect of the talar dome against the fibula. Posttraumatic medial lesions are created by a combination of inversion, plantarflexion, and external rotation forces (i.e., impact between the posteromedial tibia and medial talar margin). Morphologically, lateral lesions tend to be shallower and more wafer shaped than medial lesions, which appear as deeper, cup-shaped defects.

Osteochondral lesions of the talus usually manifest as persistent ankle pain frequently localized to the side of the lesion, accompanied by intermittent episodes of swelling, catching, and reduced motion of the joint in patients with prior history of ankle inversion injury.

two stages of the Berndt and Harty classification and are also relatively insensitive in evaluating the stability of these lesions. Radiographs cannot identify cartilaginous defects or grade I (nondisplaced) lesions. Varying degrees of plantarflexion and dorsiflexion radiographs may help diagnose posteromedial and anterolateral lesions, respectively (see Fig. 32-19B). If there is suspicion of a posteromedial lesion, a mortise view in plantarflexion may better delineate the abnormality. An anterolateral lesion may be better visualized in ankle dorsiflexion, which brings the lesion parallel to the x-ray beam. Radiographs of the asymptomatic opposite ankle should be obtained to investigate the possibility of a contralateral lesion, which is noted in 10% to 25% of patients. If an osteochondral lesion is seen on plain radiographs, the size, location, and intactness of the lesion should be assessed.

Radiography

Magnetic Resonance Imaging

The classification introduced by Berndt and Harty is the most widely accepted staging system of osteochondral talar lesions. This classification describes four progressive stages. Stage I represents subchondral compression fracture. Stage II consists of a partially detached osteochondral fragment. In stage III, the osteochondral fragment is completely detached from the talus but is not displaced from crater. In stage IV, the osteochondral fragment is detached and displaced away from the fracture site (see Fig. 32-18).17,18 Radiographs, including anteroposterior, lateral, and mortise views (Fig. 32-19A), should be the initial imaging method used when this lesion is suspected. However, radiographs are less sensitive in the detection of the first

Magnetic resonance imaging is effective in characterizing all stages of osteochondral lesions of the talus but is most useful in the identification of a radiographically occult lesion (Fig. 32-20) and stratification of in situ lesions into stable and unstable subsets (Fig. 32-21). MRI diagnosis of instability of osteochondral lesions of the talus has relied on the interface between the osteochondral fragment and the parent bone on T2-weighted images. A stable or healed osteochondral fragment is characterized by lack of high signal intensity at the interface between the lesion and the parent bone. The presence of a high signal line on T2-weighted images at the talar interface with the osteochondral fragment is the most reliable sign of instability (see Fig. 32-21). It may represent granulation

Manifestations of the Disease

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■ FIGURE 32-19

A and B, Mortise and plantarflexion ankle lateral radiographs reveal stage III medial osteochondral lesions of the talus (arrows).

tissue or fluid. A moderate hyperintense interface, not as hyperintense as fluid, indicates the presence of fibrovascular granulation tissue or developing fibrocartilage. At this stage, the lesion is unstable but has the ability to heal after a period of non–weight bearing or internal fixation. If the interface is isointense with fluid or associated with cystic-appearing areas at the base of a nondisplaced lesion, surgery is indicated. There is some controversy concerning the accuracy of MRI in assessing the stability

of the osteochondral fragment. Although arthroscopy remains the gold standard, MRI is an excellent predictor of fragment stability. In surgical series, correlation between preoperative MRI and arthroscopic assessment of fragment stability ranges between 72% and 100%. Moreover, MRI can precisely identify and localize talar osteochondral lesions with the advantage of assessing the integrity of the overlying cartilage (Fig. 32-22). MRI can also assess viability of the osteochondral fragment.

■ FIGURE 32-20

■ FIGURE 32-21

Stage I medial osteochondral lesion of the talus. Coronal T1-weighted image shows hypointensity focal subchondral bone (arrow) with extensive perilesional edema.

Stage III osteochondral lesion of the talus. Coronal 3D fat-suppressed, T1-weighted MR image demonstrates completely detached osteochondral fragment from the talus that remains located within the crater (arrow).

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■ FIGURE 32-22

Cystic osteochondral lesion of the talus. Sagittal fatsuppressed T2-weighted MR image shows cystic medial osteochondral lesion of the talus (arrow) with surrounding edema. Note existence of cartilage detached flap (arrowhead).

■ FIGURE 32-23

Necrotic fragments present low signal intensity on both T1- and T2-weighted images and do not enhance after gadolinium injection. Fat-suppressed T1-weighted sequences are helpful in assessing osteochondral fragment with gadolinium enhancement (Fig. 32-23). MR arthrography provides a better analysis of articular cartilage, the assessment of stability (Fig. 32-24), and the detection of intra-articular bodies (Fig. 32-25). MR arthrography is useful for differentiating between a stage II versus a stage III lesion by documenting intra-articu-

lar communication of fluid around the lesion, which aids planning therapeutic arthroscopy.

■ FIGURE 32-24

■ FIGURE 32-25

Stage III osteochondral lesion of the talus. Indirect MR arthrography. Sagittal, fat-suppressed, T1-weighted MR arthrography shows contrast medium–enhanced fluid in the ankle joint around the osteochondral lesion of the talus (arrow). This indicates complete loosening of the osteochondral fragment.

Necrotic unstable osteochondral lesion of the talus. Gadolinium-enhanced, sagittal, fat-suppressed, T1-weighted image shows a completely detached osteochondral fragment without enhancement consistent with necrotic bone (arrow).

Multidetector Computed Tomography Computed tomography is superior to radiographs for the diagnosis of osteochondral lesions of the talus. CT is the most efficient and reproducible means of evaluating the osseous anatomy of these lesions (Figs. 32-26 and 32-27). However, CT has limited ability to visualize certain osteo-

Intra-articular loose bodies. Sagittal T1-weighted MR arthrography shows osteochondral lesion of the talar dome and small loose body in the anterior tibiotalar capsular recess (arrow).

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■ FIGURE 32-26

Coronal CT image demonstrates medial unstable stage III osteochondral lesion of the talus (arrow).

■ FIGURE 32-27

chondral lesions, especially cartilaginous or nondisplaced (grade I) lesions.18–20

Grade I lesions have an intact appearance; grade II overlying cartilage is soft; and grade III have frayed appearance of the cartilage. They found that radiographic and arthroscopic findings correlated poorly. Fifty percent of lesions classified as stage IV according to the Berndt and Harty system were found to be intact when viewed through the arthroscope.18,20 However, direct visualization of an intact articular surface does not permit the underlying bone to be examined; thus, the extent of a bony lesion may be underestimated. This concept underscores that MRI and ankle arthroscopy play complementary roles in the evaluation of these injuries.

Nuclear Medicine Bone scintigraphy is useful in evaluating ankle injuries when radiographs appear to be normal. It may show increased radionuclide uptake within the talar dome (Fig. 32-28).

Arthroscopy Pritsch and colleagues graded lesions according to articular injury visualized during ankle arthroscopy.

Coronal CT image shows cystic lateral osteochondral lesion of the talus (arrow) in patient previously treated for medial malleolus fracture.

Classic Signs ■

■

■ ■

■

■ FIGURE 32-28

(arrow).

Scintiscan shows marked reaction in the talar dome

Osteochondral lesions of the talus manifest as persistent pain, swelling, and catching of the ankle in patients with a prior history of ankle inversion injury. Radiographs should be the initial imaging method used when this lesion is suspected, but radiographs are insensitive in the detection of the first stages of osteochondral lesions of the talus. CT is the most efficient means of evaluating the osseous anatomy of these lesions. MRI is useful for the identification of occult radiographically osteochondral lesions of the talus and in determining stability and viability. MR arthrography provides better analysis of articular cartilage, assessment of stability, and detection of intra-articular bodies.

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831

■ FIGURE 32-29

A, Arthroscopic photographs illustrating débridement and microfracture treatment of osteochondral lesion of the talus. 1, Completely detached lesion. 2, Removal of the loose body and débridement of the bony bed. 3, Penetration of the subchondral bone with specialized arthroscopic instrument to stimulate formation of a fibrin clot and fibrocartilaginous repair tissue. 4, Punctate bleeding should be visualized when inflow pressure is decreased. B, Postoperative MR imaging. Sagittal, fat-suppressed, T2-weighted MR image reveals fibrocartilaginous repair tissue partially filling the bed of the removed lesion (arrowheads).

Differential Diagnosis Lesions producing similar symptoms to osteochondral lesions of the talus should be excluded before treatment, including soft tissue and bony impingement, osteochondral lesions of the tibia, sinus tarsi syndrome, stress fractures, loose bodies, and degenerative joint disease. Based on the imaging findings the top differential diagnoses are osteonecrosis, subchondral focal alterations in arthritis or degenerative disease, and transient osteoporosis.

Synopsis of Treatment Options For treatment decisions, it is important to distinguish between stable and unstable lesions. In stable osteochon-

dral lesions of the talus, including stage I and most stage II lesions, conservative treatment is recommended. Surgical treatment is advocated for unstable lesions, including stage IV and the majority of stage III lesions. A subset of stage II lesions, especially those laterally located, may be treated surgically. Conversely, a subset of stage III lesions, in particular those located in the medial talar border, may be managed conservatively.

Medical Treatment Nonoperative management of osteochondral lesions, including restricted weight bearing and/or immobilization, is recommended unless a loose fragment is clearly present. The success rate for nonoperative treatment ranges from 25% to 56%. Nevertheless, osteoarthrosis is a rare sequela of osteochondral lesions of the talus.

Surgical Treatment Failure of nonsurgical management or the presence of advanced grade III or IV lesions often necessitates surgical intervention. Current principles of surgical treatment fall into one of three categories:

■ FIGURE 32-30

Intraoperative view of the medial talar dome articular surface exposed through a medial malleolar osteotomy after reconstruction of medial defect using autologous osteochondral graft.

1. Loose body removal with or without stimulation of fibrocartilage growth (microfracture, curettage, abrasion, or transarticular drilling) (Fig. 32-29). 2. Securing the osteochondral lesion of the talus to the talar dome through retrograde drilling, bone grafting, or internal fixation. 3. Stimulating development of hyaline cartilage through osteochondral autografts, allografts, or cell culture (Fig. 32-30).

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What the Referring Physician Needs to Know ■

MRI is the best imaging method to detect radiographically occult osteochondral lesions of the talus and determine stability and viability.

■

MRI reveals the full spectrum of associated injuries in a patient with chronic ankle pain such as lateral ligament lesions, peroneal tendon pathology, or sinus tarsi syndrome before treatment.

SUGGESTED READINGS Cerezal L, Abascal F, Canga A, et al. MR imaging of ankle impingement syndromes. AJR Am J Roentgenol 2003; 181:551–559. Cerezal L, Abascal F, Garcia-Valtuille R, Canga A. Ankle MR arthrography: how, why, when. Radiol Clin North Am 2005; 43:693–707. Linklater J. Ligamentous, chondral, and osteochondral ankle injuries in athletes. Semin Musculoskelet Radiol 2004; 8:81–98. Maquirriain J. Posterior ankle impingement syndrome. J Am Acad Orthop Surg 2005; 13:365–371. Narvaez JA, Cerezal L, Narvaez J. MRI of sports-related injuries of the foot and ankle: I. Curr Probl Diagn Radiol 2003; 32:139–155.

Robinson P, White LM. Soft-tissue and osseous impingement syndromes of the ankle: role of imaging in diagnosis and management. RadioGraphics 2002; 22:1457–1469. Santrock RD, Buchanan MM, Lee TH, Berlet GC. Osteochondral lesions of the talus. Foot Ankle Clin 2003; 8:73–90. Schachter AK, Chen AL, Reddy PD, Tejwani NC. Osteochondral lesions of the talus. J Am Acad Orthop Surg 2005; 13:152–158. Stone JW. Osteochondral lesions of the talar dome. J Am Acad Orthop Surg 1996; 4:63–73. Umans H. Ankle impingement syndromes. Semin Musculoskelet Radiol 2002; 6:133–139.

REFERENCES 1. Rubin DA, Tishkoff NW, Britton CA, et al. Anterolateral soft-tissue impingement in the ankle: diagnosis using MR imaging. AJR Am J Roentgenol 1997; 169:829–835. 2. Farooki S, Yao L, Seeger LL. Anterolateral impingement of the ankle: effectiveness of MR imaging. Radiology 1998; 207:357–360. 3. Jordan LK III, Helms CA, Cooperman AE, Speer KP. Magnetic resonance imaging findings in anterolateral impingement of the ankle. Skeletal Radiol 2000; 29:34–39. 4. Hauger O, Moinard M, Lasalarie JC, et al. Anterolateral compartment of the ankle in the lateral impingement syndrome: appearance on CT arthrography. AJR Am J Roentgenol 1999; 173:685–690. 5. Bassett FH III, Gates HS III, Billys JB, et al. Talar impingement by the anteroinferior tibiofibular ligament: a cause of chronic pain in the ankle after inversion sprain. J Bone Joint Surg Am 1990; 72:55–59. 6. Robinson P, White LM, Salonen DC, et al. Anterolateral ankle impingement: MR arthrographic assessment of the anterolateral recess. Radiology 2001; 221:186–190. 7. Kim SH, Ha KI. Arthroscopic treatment for impingement of the anterolateral soft tissues of the ankle. J Bone Joint Surg Br 2000; 82:1019–1021. 8. Tol JL, Slim E, van Soest AJ, van Dijk CN. The relationship of the kicking action in soccer and anterior ankle impingement syndrome: a biomechanical analysis. Am J Sports Med 2002; 30:45–50. 9. Kim SH, Ha KI, Ahn JH. Tram track lesion of the talar dome. Arthroscopy 1999; 15:203–206. 10. Robinson P, White LM, Salonen D, Ogilvie-Harris D. Anteromedial impingement of the ankle: using MR arthrography to assess the anteromedial recess. AJR Am J Roentgenol 2002; 178:601–604.

11. Paterson RS, Brown JN. The posteromedial impingement lesion of the ankle: a series of six cases. Am J Sports Med 2001; 29:550–557. 12. Bureau NJ, Cardinal E, Hobden R, Aubin B. Posterior ankle impingement syndrome: MR imaging findings in seven patients. Radiology 2000; 215:497–503. 13. Fiorella D, Helms CA, Nunley JA. The MR imaging features of the posterior intermalleolar ligament in patients with posterior impingement syndrome of the ankle. Skeletal Radiol 1999; 28:573–576. 14. Rosenberg ZS, Cheung YY, Beltran J, et al. Posterior intermalleolar ligament of the ankle: normal anatomy and MR imaging features. AJR Am J Roentgenol 1995; 165:387–390. 15. Best A, Giza E, Linklater J, Sullivan M. Posterior impingement of the ankle caused by anomalous muscles: a report of four cases. J Bone Joint Surg Am 2005; 87:2075–2079. 16. Robinson P, Bollen SR. Posterior ankle impingement in professional soccer players: effectiveness of sonographically guided therapy. AJR Am J Roentgenol 2006; 187:53–58. 17. Mintz DN, Tashjian GS, Connell DA, et al. Osteochondral lesions of the talus: a new magnetic resonance grading system with arthroscopic correlation. Arthroscopy 2003; 19:353–359. 18. Schuman L, Struijs PA, van Dijk CN. Arthroscopic treatment for osteochondral defects of the talus: results at follow-up at 2 to 11 years. J Bone Joint Surg Br 2002; 84:364–368. 19. Verhagen RA, Maas M, Dijkgraaf MG, et al. Prospective study on diagnostic strategies in osteochondral lesions of the talus. Is MRI superior to helical CT? J Bone Joint Surg Br 2005; 87:41–46. 20. Robinson DE, Winson IG, Harries WJ, Kelly AJ. Arthroscopic treatment of osteochondral lesions of the talus. J Bone Joint Surg Br 2003; 85:989–993.

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Acute Osseous Injury to the Foot Thomas H. Berquist

PREVALENCE, EPIDEMIOLOGY, DEFINITIONS, AND ANATOMY Acute fracture-dislocations of the foot can be overlooked because changes may be subtle or patients may present with clinical features suggesting an ankle sprain. Anterior calcaneal process fractures, talar dome fractures, lateral and posterior talar process fractures, cuboid fractures, and fractures of the fifth metatarsal base are among the injuries that may present as ankle sprains.1,2 There has been renewed interest in foot fractures in the orthopedic literature as treatment options have improved. It has become clear that most long-term disabilities after lower extremity trauma are related to fractures of the foot.3,4 For purposes of discussion, we will consider fractures and fracture-dislocations of the foot based on the anatomic location. Thus, the hindfoot (talus and calcaneus), the midfoot (navicular, cuboid, cuneiforms), and the forefoot (metatarsals and phalanges) are discussed separately.

Hindfoot The calcaneus is the most frequently fractured tarsal bone. Treatment of fractures and dislocations about the calcaneus frequently result in significant long-term disability. The talus is the second most commonly fractured tarsal bone. Certain talar fractures (talar dome and talar process) may be difficult to detect, resulting in delay in diagnosis and management.1,3,4

Talus The talus is the second most commonly fractured tarsal bone.1,4 The talar articulations account for the majority (>90%) of the motion in the foot and ankle. Therefore, it is critical to stabilize this structure after injury.3,4

The blood supply of the talus is tenuous because 60% of the surface is covered by articular cartilage and there are no muscle or tendon insertions on its surface.1,4,5–7 The superior articular surface, the trochlea, articulates with the tibia superiorly. Articular cartilage extends medially and laterally in a plantar direction to articulate with the medial and lateral malleoli forming the ankle mortise.1,4,7,8 The inferior articular surface is complex, forming three articulations with the calcaneus. The anterior and posterior facets articulate with similarly named calcaneal facets.7,8 The middle facet is just posterior to the anterior facet and articulates with the sustentaculum tali. The talar sulcus lies between the anterior and middle facets, forming the roof of the tarsal sinus. The interosseous talocalcaneal ligament lies within the tarsal sinus (Fig. 33-1).1,7,8 The talar neck is angled 15 to 20 degrees and has a coarse surface due to ligament attachments and vascular supply.4 The distal aspect of the talus (head of the talus) articulates with the tarsal navicular and is contiguous with the spring ligament and sustentaculum tali inferiorly and the deltoid ligament medially (see Fig. 33-1).1,4,8 The talus has lateral and posterior processes. The posterior process is divided by a groove for the flexor hallucis longus tendon into medial and lateral tubercles. The os trigonum is a common variant that arises from a separate ossification center posterior to the lateral tubercle. When fusion of this ossification center occurs, it forms Stieda’s process. The ossicle remains unfused in up to 50% of patients.9,10 The lateral talar process is a wedge-shaped structure that articulates with the distal fibula superiorly and a portion of the posterior calcaneal articulation inferiorly (Fig. 33-2).1,4,8,11,12 Talar fractures and fracture-dislocations are discussed separately. However, Table 33-1 summarizes fracture types, incidence, and mechanism of injury. 833

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Middle facet Middle facet

A

Sustentaculum tali

D

Posterior facet

Anterior facet

E

B

■ FIGURE 33-1 MR and CT anatomy of the talus and subtalar articulations. Coronal (A) and sagittal (B and C) fat-suppressed T2-weighted MR images, coronal (D) and sagittal (E) CT images. Arrow in A, flexor digitorum longus; arrow in C, sustentaculum; open arrow in C, flexor digitorum longus.

Middle facet

C

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A

B ■ FIGURE 33-2 Lateral radiograph (A) and axial T1- (B) and fat-suppressed fast spin-echo T2-weighted (C) MR images demonstrating the os trigonum or posterior process. Note the relationship of the os trigonum (open arrowhead) to the flexor hallucis longus tendon (arrow) in B.

C

KEY POINTS The talus is the second most commonly fractured tarsal bone after the calcaneus. ■ Talar articulations account for over 90% of motion in the foot and ankle. ■ Talar neck fractures account for 30% to 50% of talar fractures. ■ Subtle talar fractures (lateral process, talar dome, posterior process) are initially overlooked on radiographs in 40% to 50% of cases. ■ Seventy-five percent of calcaneal fractures are intraarticular and 25% are extra-articular. CT is critical to classify and manage calcaneal fractures. ■ Isolated cuboid, navicular, and cuneiform fractures are uncommon. ■ Tarsometatarsal fracture-dislocations may be difficult to detect and clearly define on radiographs. CT is essential for management. ■ Fractures of the second through fifth metatarsals are common. ■ Fractures of the proximal fifth metatarsal are divided into three zones: zone 1, avulsion; zone 2, Jones fractures; and zone 3, stress fractures. ■ Dislocations of the metatarsophalangeal joint most commonly involve the great toe. ■ Phalangeal dislocations most commonly occur at the proximal interphalangeal joint. ■

Talar Neck Fractures Talar neck fractures are uncommon compared with all skeletal injuries but account for 30% to 50% of talar fractures.4,13,14 Depending on the type of fracture, complication rates may be high.13–16 Talar neck fractures most commonly occur with hyperdorsiflexion of the foot on the tibia (see Table 33-1). TABLE 33-1 Talar Fracture and Fracture-Dislocations Type

Incidence (% Talar Injuries)

Mechanism of Injury

Talar neck

30%–50%

Hyperdorsiflexion of the foot on the tibia

Talar body Talar dome

40% 1%–6%

Lateral process

Rare

Posterior process

Rare

Crush fractures Talar head Subtalar dislocation

28%–33% Rare 15%

Total dislocation

Rare

Data from references 1, 3–5, 7, 11, and 12.

Inversion, eversion, twisting injuries Dorsiflexion and inversion of the foot Avulsion, direct compression Axial compression Extreme plantarflexion Inversion (medial) eversion (lateral) Extreme inversion or eversion

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

A

B

■ FIGURE 33-3

Hawkins type II. Mortise (A) and lateral (B) radiographs of a displaced talar neck fracture (arrow) with subluxation of the subtalar joint (B, open arrowhead).

Although originally described in pilots, most are due to motor vehicle accidents or falls from a significant height.1,4,15 The injury is most common in young males.4,15,16 Open fractures are common (16% to 25%) when there is significant displacement of the talar body. Open fractures have poor results and a high incidence of infection.4,16,17 Hawkins16 classified talar neck fractures and associated subluxation-dislocations (Fig. 33-3). This classification (Table 33-2) is useful for long-term prognosis and management (Fig. 33-4).1,4,16 Complications are common despite adequate reduction, increase in severity as the classification level increases, and include skin necrosis, infection, delayed and nonunion, malunion, avascular necrosis, and post-traumatic arthrosis.1,4,6,7,15–17

Delayed union (no evidence of healing in 6 months) is more common with Hawkins types II to IV injuries, which is likely related to the higher incidence of avascular necrosis. The incidence of delayed union approaches

TABLE 33-2 Talar Neck Fractures: Hawkins Classification Type

Definitions

Incidence

I II

Undisplaced neck fracture Displaced neck fracture with subluxation or dislocation of the subtalar joint Displaced neck fracture with subluxation/dislocation of the ankle and subtalar joint Type III plus dislocation of the talonavicular joint

11%–21% 10%–24%

III

IV

Data from references 15 and 16.

23%–47%

5%

■ FIGURE 33-4

Hawkins type IV. Single view of the hindfoot with subtalar dislocation and talonavicular dislocation. The talar neck fracture is obscured.

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837

■ FIGURE 33-5 Illustration of the mechanism of injury and types of lateral talar dome fractures. Inversion injury causes the lateral dome to impact the fibula. Stage I, compression injury; stage II, incomplete fracture with partial elevation; stage III, complete fracture without displacement; stage IV, complete fracture with displacement.

13%.4 Nonunion is uncommon, but malunion may be evident in 45% to 77% of displaced neck fractures.15 Avascular necrosis is uncommon (0% to 13%) with Hawkins type I fractures (see Table 33-2). Osteonecrosis develops in 20% to 50% of type II and 83% to 100% of type III fractures (see Figs. 33-3 and 33-4).15,16

Talar Body Fractures There are a wide range of talar body fractures ranging from osteochondral fractures to comminuted crush or shear fractures (see Table 33-1).1–4,7,11,18,19 Table 33-1 summarizes talar body fractures, their incidence, and the mechanism of injuries.

Talar dome fractures result from inversion, eversion, and twisting injuries of the ankle. Both the medial and lateral aspects of the talar dome may be involved. Lateral talar dome fractures are more often acute. These injuries are associated with inversion or inversion-dorsiflexion trauma. These lesions usually are shallow or flake-like. Medial lesions are more often deeper, and when acute they are associated with lateral rotation on a plantarflexed ankle.1,11,20,21 The most commonly used classification of these injuries was devised by Berndt and Harty (Figs. 33-5 and 33-6).11 Stage I lesions are compressions of the talar dome without associated ligament injury, and the overlying

■ FIGURE 33-6

Illustration of the mechanism of injury and stages of medial talar dome fractures. A, Stage I, compression, and stage II, fracture with partial elevation. B, Stage III, complete fracture, and stage IV, displaced fragment.

838

P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

cartilage is intact. Stage II lesions are incomplete osteochondral fractures with partial elevation of the fragment. Stage III lesions are complete fractures without displacement, and stage IV lesions are complete fractures with displacement.

Lateral Process Fractures Fractures of the lateral talar process are easily overlooked on radiographs. These fractures result from inversion and dorsiflexion of the foot.3,4 In recent years, this fracture has been commonly seen in snowboarders, hence the name “snowboarder’s fracture.”22–24 Hawkins25 classified these fractures into three groups: (1) chip fractures, (2) a single large fragment involving the talofibular and subtalar joints, and (3) comminuted fractures involving both articular surfaces. Persistent symptoms, nonunion, and eventual resection or subtalar fusion are more common when the subtalar joint is involved.4,22,23

A

Posterior Process Fractures The posterior process consists of medial and lateral tubercles separated by the groove for the flexor hallucis longus tendon.4,10 Both tubercles have articular cartilage on the plantar surface forming the posterior margin of the posterior subtalar facet. The lateral tubercle remains unfused in 50% of patients (os trigonum) (see Fig. 33-2).1,7 The lateral tubercle is fractured by forced plantarflexion or avulsion (posterior talofibular ligament avulsion) (Fig. 33-7). Pronation and dorsiflexion may cause avulsion of the deltoid ligament attachment.

Comminuted Talar Body Fractures Complex fractures of the talar body (Fig. 33-8) may be related to crush or shearing injuries. These fractures are B

C ■ FIGURE 33-8 Complex talar body fracture. A to C, Coronal CT images demonstrate two inferior subtalar fracture lines (A, arrows), comminution of the body (B), and a fracture with displacement of the lateral process (C, arrow).

■ FIGURE 33-7

Illustration of a posterior talar process fracture.

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839

much more uncommon than talar neck fractures. There is a high incidence of avascular necrosis, malunion, and post-traumatic arthrosis with these injuries.1,3,4,7

Talar Head Fractures Fractures of the talar head (Fig. 33-9) are rare (see Table 33-1). The fracture line extends into the talonavicular joint. Compression forces with plantarflexion of the foot cause this injury. Associated talar dislocations have also been reported with talar head fractures.1,7

Talar Dislocations Subtalar dislocations may be medial or lateral. Medial dislocations occur with inversion and lateral dislocations with eversion injuries.1,4 Subtalar dislocations account for 15% of talar injuries but only 1% of all dislocations (see Fig. 33-4).26-28 It is not surprising that associated osteochondral fractures of the talus, calcaneus, and navicular occur in 45% of patients.29 Total talar dislocation is rare (Fig. 33-10). This injury is caused by extreme supination (total medial dislocation) and extreme pronation (total lateral dislocation). Most injuries are open with a high incidence of infection and avascular necrosis. Detenbeck and Kelly30 reported an 89% incidence of infection requiring eventual talectomy.

■ FIGURE 33-9

Fracture-dislocation of the talonavicular joint. On this radiograph the talus is rotated laterally with a displaced fracture (arrow) of the head.

■ FIGURE 33-10 Anteroposterior radiograph demonstrating total dislocation of the talus (arrow).

Calcaneus Calcaneal Fracture-Dislocations Fractures and dislocations of the calcaneus present significant short- and long-term treatment challenges.1,3,31–34 The calcaneus is the largest tarsal bone, with three facets on the anterosuperior surface for articulation with the talus (see Fig. 33-1). The cortex is thickened posteriorly at the Achilles attachment.1,7,31 Medially, the sustentaculum tali projects from the body of the calcaneus. This structure contains the middle facet. The flexor hallucis longus tendon passes inferior to the sustentaculum tali (see Fig. 33-1). The medial position of the flexor tendons and neurovascular structures places them at risk after fracture or during reduction.1,3,31 Laterally, the peroneal tubercle and retinaculum contain the peroneal tendons. The lateral ankle ligament complex (anterior talofibular, calcaneofibular, and posterior talofibular) provide important support laterally. The deltoid ligament complex provides medial support to the ankle.1,3,4 There are two critical angle measurements that are routinely evaluated on lateral radiographs. Bohler’s angle (normal, 25 to 40 degrees) is a useful measurement for evaluating calcaneal height. This angle is formed by a line from the posterior calcaneal margin to the margin of the posterior facet and a second line from the margin of the posterior facet to the superior margin of the anterior calcaneal process (Fig. 33-11).1,31,35 The crucial angle of Gissane (normal about 100 degrees) is formed by a line along the posterior facet and a second line along the anterior calcaneal process (Fig. 33-12).36

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

into the angle of Gissane.4,33 Fractures result in loss of calcaneal height, widening of the calcaneus, and articular deformity in the posterior facet (see Figs. 33-11 and 33-12).1,7,31,34

Intra-articular Fractures

■ FIGURE 33-11 Complex intra-articular fracture of the calcaneus (arrow) with reduction of Bohler’s angle to 4 degrees.

The calcaneus is the most commonly fractured tarsal bone but accounts for only 2% of all fractures. Calcaneal fractures may be extra-articular or intra-articular or may result in fracture-dislocations. Seventy-five percent of fractures are intra-articular and 25% are extra-articular.34 Extra-articular fractures occur from a multitude of mechanisms, including falls and twisting injuries. Intraarticular fractures result from compression injuries due to significant falls (>8 feet) or motor vehicle accidents.1,7,31 Two fracture patterns occur with intra-articular fractures due to shearing or compression forces. A shear fracture line occurs in the sagittal plane involving the posterior facet with extension that may reach the calcaneocuboid articulation. This fracture separates the calcaneus into sustentacular (anteromedial) and tuberosity (posterolateral) fragments.31,34 Compression fracture lines cause displacement of the anterolateral calcaneus

Numerous fracture classifications have been used over the years based on radiographic features and the extent of articular involvement.1,3,4,7,33 However, CT is the accepted technique for determining the extent of injury and most appropriate surgical approach. Therefore, CT classifications are most commonly used by orthopedic surgeons. CT systems include the Crosby-Fitzgibbons classification based on coronal CT images of the posterior facet, the Sanders classification, which is similar to the Crosby-Fitzgibbons but more complex, and the Hannover classification.33,36,37 The Sanders classification, based on reformatted CT images, is most commonly used (Fig. 33-13).34,38 Type I fractures are undisplaced. Type II fractures (a single fracture line) involve the posterior facet and are further subdivided (IIA to IIC) depending on the location of the fracture (A, lateral; B, mid posterior facet; C, medial posterior facet). Medial fractures (type IIC) are more difficult to detect and reduce surgically.38 Type III fractures (two fracture lines in the posterior facet) result in three fragments with a central depressed fragment. Type IV fractures are comminuted with four or more articular fragments.34,38

Extra-articular Fractures Extra-articular fractures include all fractures that do not involve the posterior facet. Injuries may be caused by twisting or compression forces or avulsion forces. The posterior, medial, or anterior calcaneus may be involved.1,31,34 Fractures of the anterior calcaneal process can be easily overlooked because inversion injuries such as these usually present as ankle sprains (Fig. 33-14).1–3,33 Fractures of the calcaneal body spare the facets but may result in articular deformity or incongruency. The mechanism of injury is similar to intra-articular fractures. Although prognosis is better for nonarticular fractures, there may still be considerable deformity of the calcaneus.4 Fractures of the peroneal tubercle or lateral calcaneal process are uncommon. This injury usually is secondary to inversion plantarflexion forces or direct trauma.1,7,31 Again, the injury may present as an ankle sprain.1,2 Calcaneal tuberosity fractures result from Achilles avulsion and occur more commonly in elderly individuals or osteopenic patients (Fig. 33-15).31,34 Fractures of the medial process of the calcaneus are more likely to result from vertical shearing force than avulsion of the plantar fascia, adductor hallucis, or flexor digitorum muscles.31,33

Calcaneal Dislocations

■ FIGURE 33-12 Calcaneal fracture with crucial angle of Gissane increased to 130 degrees (normal, 100 degrees).

Calcaneal dislocations are rare and result from very high velocity trauma, greater than that required to cause a fracture. Only eight cases have been reported in the medical literature.39

■ FIGURE 33-13 A, Illustration of the Sanders classification for intraarticular calcaneal fractures. Type I fractures are undisplaced and not demonstrated. Type II fractures have a single fracture line (two parts) with fracture located laterally (IIA), mid (IIB), or medially (IIC) in the posterior facet. Type III fractures have three fragments with fractures lateral and mid posterior facet (IIIAB), lateral and medial (IIIAC), or mid to medial (IIIBC). Type IV fractures are severely comminuted. B, Coronal CT image with two fracture lines in the lateral and mid (type IIAB) facet. (A from Sanders R, Fortin P, DiPasquale T, et al. Operative treatment of 120 displaced intra-articular calcaneal fractures: results using a prognostic computed tomography classification. Clin Orthop Relat Res 1993; 290:87-95.)

A

B

B

■ FIGURE 33-14

Lateral radiograph in a patient presenting with ankle sprain. There is an anterior calcaneal process fracture (arrows).

■ FIGURE 33-15 avulsion.

Lateral radiograph demonstrating a tuberosity

842

P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

Midfoot Midfoot Fracture-Dislocations The midfoot is the anatomic region distal to Chopart’s joint and proximal to Lisfranc’s joint line. The bones of the midfoot include the navicular, cuboid, and medial, middle (intermediate), and lateral cuneiforms.1,7,40,41 There is no weight-bearing contact in the midfoot. These structures are supported by strong plantar ligaments.40,42 The lateral column is composed of the calcaneocuboid articulation, cuboid, and fifth metatarsal joint. The medial column is composed of the talonavicular, navicular cuneiform, and first and second metatarsal articulations. The medial column is more rigidly fixed than the lateral column (Fig. 33-16).40–43

Navicular Fractures The navicular is the key structure in the medial longitudinal arch of the foot.40–42 The concave proximal facet articulates with the talus. There are three distal facets that articulate with the cuneiforms. Laterally the navicular rests on the cuboid with an inconsistent articular

facet.42 There is a tuberosity medially for attachment of the posterior tibial tendon. Accessory ossicles (os tibiale externum) lie within the distal posterior tibial tendon in up to 25% of patients. Ninety percent of these ossicles are bilateral.1,39–41 Multiple navicular fracture patterns have been described. Fractures include the tuberosity, cortical avulsions, body fractures, and stress fractures. Dorsal avulsion fractures occur with twisting injuries and with inversion plantarflexion or eversion of the foot. This fracture is the most common navicular fracture (47%). Navicular tuberosity fractures are avulsion injuries at the attachment of the deltoid ligament and posterior tibial tendon. Injuries to the tuberosity may also result from twisting or eversion forces.41 Navicular body fractures are uncommon (Fig. 33-17), resulting from axial loading or direct trauma.3,40,41,43 Multiple classification systems have been applied to body fractures including the Pinney and Sangeorzan44 and the more complex Orthopedic Trauma Association classifications.45 The former is easier to use and simply categorizes navicular body fractures into three groups. Type 1 fractures are transverse in the coronal plane with a dorsal fragment involving less than 50% of the

■ FIGURE 33-16 Illustration of the arches of the foot at three levels. Lateral column: calcaneus, cuboid, and fifth metatarsal articulations. Medial column: navicular cuneiform and cuneiform and first and second metatarsal articulations.

CHAPTER

A ■ FIGURE 33-17

fracture (arrow).

33

● Acute Osseous Injury to the Foot

843

B Navicular fractures. A, Lateral radiograph of a dorsal avulsion fracture (arrow). B, Posteroanterior radiograph of a sagittal plane

body. With type 2 fractures (most common) the fracture line passes dorsolateral to plantarmedial with the larger fragment dorsomedial.44 Type 3 fractures have central or lateral comminution. There may be associated subluxation or dislocation of the calcaneocuboid articulation.41,44

Cuboid Fractures The cuboid maintains the lateral column. Therefore, fractures may have significant functional consequences. Isolated cuboid fractures are rare. There usually are associated injuries involving the talonavicular articulation, midfoot fractures, or a Lisfranc injury (Fig. 33-18). Medial or dorsal avulsions of the navicular should lead one to search carefully for an associated cuboid fracture. Cuboid fractures are the result of direct trauma to the lateral foot or a fall with associated twisting injury.40,41 They are typically classified as avulsion, coronal plane fractures, or comminuted crush injuries.45

Cuneiform Fractures Cuneiform injuries are related to direct trauma or indirect axial loading and associated with more complex tarsometatarsal fracture-dislocations. Isolated cuneiform fractures are rare.40,41,46 Again, fractures may be extra-articular (avulsion), coronal plane, or intra-articular. Intra-articular fractures typically involve more than one articulation.39

Tarsometatarsal Fracture-Dislocations The anatomy of the Lisfranc articulation is important to review. This includes the articulations and ligamentous supporting structures of the cuboid, cuneiforms, and five

■ FIGURE 33-18 Complex midfoot injury with a cuboid avulsion (arrow) and a second metatarsal fracture (open arrowhead). CT should be obtained for complete evaluation.

844

P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

falling on the stationary foot can result in fracture and soft tissue injury. Indirect forces applied to a plantarflexed foot are more common and may be associated with fractures of the cuneiforms, cuboid, and metatarsal bases.47 The second metatarsal is most commonly involved due to the above anatomy (see Fig. 33-19).47,48 Several Lisfranc injury patterns have been described (Fig. 33-20), but none is very useful for treatment planning owing to their complexity.1,3,7,40,49,50 The homolateral pattern (total incongruity) occurs when all five metatarsals are displaced. Displacement is almost always in the lateral direction, but medial displacement can occur.1,3,49,50 Alignment of both the first and second metatarsal bases is abnormal. Fractures of the second metatarsal base are common with this pattern due to its position between the cuneiforms.1,48–50 Partial incongruity occurs when the first metatarsal fractures at the base and the shaft displaces medially accompanied by lateral displacement of the second through fifth metatarsals. Associated cuneiform and navicular fractures are common with this displacement pattern.1,48–50

Forefoot Fractures of the metatarsals and phalanges are common. Dislocations of the metatarsophalangeal and interphalangeal joints also occur, with or without associated fractures. Sesamoid injuries are also common, especially in long distance runners.1,7

Metatarsal Fractures ■ FIGURE 33-19

Illustration of the tarsometatarsal ligaments and articulations. There is no transverse ligament between the first and second metatarsal bases. The oblique ligament extends from the medial cuneiform to the second metatarsal base. The second metatarsal base is situated in a mortise between the medial and lateral cuneiforms. (From Berquist TH. Radiology of the Foot and Ankle. Philadelphia, Lippincott Williams & Wilkins, 2000.)

metatarsal bases (Fig. 33-19).1,7,42,47 The lateral metatarsals (second through fifth) are connected proximally by the transverse metatarsal ligaments. This is not the case at the bases of the first and second metatarsals. The second metatarsal base is situated in a mortise formed by the medial and lateral cuneiforms. Ligament support is provided by the transverse ligament laterally and the oblique ligament medially (see Fig. 33-19). The oblique ligament extends from the medial cuneiform to the second metatarsal base. This can result in avulsion of the metatarsal base. The plantar ligaments are stronger than the dorsal ligaments.42,47 Therefore, most dislocations occur dorsally.1,41,46 The dorsalis pedis artery is susceptible to injury as it passes between the first and second metatarsal bases to form the plantar arch.1 Injuries to the Lisfranc complex may be mild to extremely complex. Findings on radiographs may be subtle, with up to 20% of injuries initially overlooked.1,40 Mild ligament sprains may occur with athletic injuries. More significant injuries are related to high-velocity motor vehicle accidents and direct or indirect loading injuries.39,46 Direct loading dorsally from a heavy object

The first metatarsal is shorter and wider than the second through fifth metatarsals. As noted earlier, there is no transverse metatarsal ligament between the first and second metatarsal bases. There is a thick capsule about the first tarsometatarsal joint with the anterior tibial tendon inserting on the base medially and the peroneus longus inserting on the lateral plantar base. There are plantar grooves distally for the medial and lateral sesamoids.51 The second through fifth metatarsals are fixed by dorsal, plantar, and central ligaments. The unique anatomy and position of the second metatarsal was reviewed in the prior section.42 Metatarsal fractures may be extra- or intra-articular. Fractures may occur in isolation or as part of more complex injuries. Fractures of the second through fourth metatarsals are more common than the first metatarsal. Fractures of the fifth metatarsal deserve more in-depth discussion.52–54 Fractures of the fifth metatarsal are categorized as proximal or distal. Proximal fractures are divided into three zones (Fig. 33-21).54 Zone 1 is the avulsion zone where fractures result from the attachment of the lateral band of the plantar aponeurosis and, to a lesser degree, the peroneus brevis insertion.54,55 Zone 2 fractures are Jones fractures caused by adduction of the forefoot.40,52,53,55 Fractures in zone 3 are usually athletic stress fractures. Distal fractures (dancer’s fractures) are usually due to a direct blow resulting in an oblique or spiral fracture.40,55

CHAPTER

A

E ■ FIGURE 33-20

B

33

● Acute Osseous Injury to the Foot

C

F

D

G

Illustrations of Lisfranc injury patterns. A and B, Total incongruity. C to E, Partial incongruity. Divergent type with total (F) and partial (G) displacement. (From Berquist TH. Radiology of the Foot and Ankle. Philadelphia, Lippincott Williams & Wilkins, 2000.)

845

846

P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

Phalangeal Fractures Phalangeal fractures are the most common forefoot injury. The proximal phalanx of the fifth toe is most often involved.40,51 A direct blow from a heavy object or jamming the toe results in fracture. Fractures may be intraarticular, involve the shaft, or be comminuted.1,40

Metatarsophalangeal and Interphalangeal Dislocations

■ FIGURE 33-21 Zone I avulsion fracture (arrow). The proximal fifth metatarsal is divided into three zones: zone I, avulsion fractures; zone II, metaphyseal diaphyseal junction; zone III, proximal shaft.

Sesamoid Fractures The sesamoids function in weight bearing and as functional fulcrums for the great toe. The sesamoids are located in the tendon of the flexor hallucis brevis. The flexor hallucis longus runs between the sesamoids.1,42 The medial sesamoid is frequently bipartite.1,42,51 Injuries to the sesamoid may result in stress fracture, acute fracture, or sesamoiditis.1,7,39 Acute fractures are a result of falls on the ball of the foot, hyperpronation, or association with metatarsophalangeal joint dislocations (Fig. 33-22).39,50 Improper foot wear has been implicated with sesamoid stress fractures. The medial sesamoid is most commonly injured.1,39,50

A ■ FIGURE 33-22

Dislocations of the metatarsophalangeal or interphalangeal joints may occur as isolated injuries or be associated with more complex injuries. Metatarsophalangeal dislocations usually are hyperextension injuries with the proximal phalanx forced dorsal to the metatarsal tearing the plantar capsule.1,40,56 The first metatarsophalangeal joint is most commonly involved (Fig. 33-23). Interposition of the plantar plate or sesamoid may result in inability to reduce the dislocation. This results in persistent widening of the joint space on radiographs. Phalangeal dislocations are most common at the proximal interphalangeal joint. The mechanism of injury is similar to metatarsophalangeal dislocations (Fig. 33-24).56,57

MANIFESTATIONS OF THE DISEASE Radiography Multiple imaging modalities may be required to detect, classify, and plan appropriate treatment approaches. Techniques include radiographs or computed radiography (CR) images, radionuclide scans, CT, ultrasonography, MRI, angiography, and diagnostic/therapeutic injections. Acute osseous injuries should initially be evaluated with radiographs or CR images. CT is frequently required to detect subtle injuries and completely assess complex injuries. The other modalities are more frequently used to assess soft tissue injuries (ultrasonography and MRI) or localize the site of pain (diagnostic

B

Sesamoids. A, Sesamoid view demonstrating the normal position of the lateral (L) and bipartite medial (m and M) sesamoids. B, Lateral radiograph of a fracture of the proximal portion of the bipartite sesamoid (arrow).

CHAPTER

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● Acute Osseous Injury to the Foot

847

A ■ FIGURE 33-23 Dislocation of the first metatarsophalangeal joint. A, Posteroanterior radiograph shows overlap of the metatarsal and proximal phalanx with lateral and proximal displacement of the sesamoids (arrows). B, Lateral radiograph shows dorsal displacement of the phalanx. C, Postreduction view demonstrates small osteochondral fractures (arrows) with reduction of the dislocation.

C

848

P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

A

B

■ FIGURE 33-24

Dislocation of the left second proximal interphalangeal joint. A, Posteroanterior radiograph shows dislocation of the joint (arrow). B, Postreduction radiograph shows widening of the joint with an osteochondral fragment (arrow).

injections) and vascular injury (angiography or MR angiography).1,7 Routine radiographs using appropriate views for the anatomy to be examined remain the primary screening technique for patients with suspected acute osseous injuries.1,7,8,56 The hindfoot can be evaluated with standard ankle views (anteroposterior, lateral, and mortise views). These views demonstrate the tibia, fibula, talus, and calcaneus. Unfortunately, other fractures that may mimic ankle sprains (anterior calcaneal process, base of the fifth metatarsal, peripheral talar fractures, and cuboid fractures) may not be consistently included on routine ankle views. Communication with the referring physician or examiner is essential to know when radiographs of the foot may also be required. The presence of an ankle effusion should lead one to search for subtle osteochondral fractures that may require additional studies such as CT or MRI.1,7,18 Subtle peripheral talar fractures are also easily overlooked on radiographs.10,23,24,26 Midfoot injuries can usually be detected with routine ankle and foot (anteroposterior, lateral, and oblique) radiographs. Undisplaced fractures, osteochondral fractures, and avulsion fractures may be overlooked on radiographs. The only finding on a subtle Lisfranc injury may be widening of the first and second metatarsal bases. This finding may go undetected if both feet are not available for comparison (Fig. 33-25). Up to 20% of Lisfranc injuries are overlooked on initial radiographs.1,40 If the findings on radiographs are equivocal, CT should be obtained to exclude subtle midfoot fractures.1,48

Fractures and dislocations of the forefoot are usually easily detected on routine views of the foot (see Figs. 33-23 and 33-24).57 Subtle avulsion injuries, stress fractures, and metatarsal base fractures may be overlooked if additional studies are not performed.

■ FIGURE 33-25

Radiograph demonstrates subtle widening of the cuneiform and one to two metatarsal bases (arrow). There is a subtle avulsion fracture (open arrowhead).

CHAPTER

Magnetic Resonance Imaging Magnetic resonance imaging is most commonly reserved for subtle fractures and soft tissue injuries. Stress fractures, stress reaction, bone bruises, osteochondral fractures, and ligament, tendon, and neurovascular structures can be clearly demonstrated (Fig. 33-26).1,7,48,54,58–61 New coil technology, pulse sequences, and image plane flexibility have improved peripheral extremity MRI examinations.59 Multiple imaging units are also available, including open bore, low- and high-field systems and extremity units. Because of image quality and flexibility we prefer highfield (1.5T to 3T) units with more conventional gantries to low-field or extremity magnets. For osseous injury, placing the patient supine with the foot in neutral position is most easily tolerated by the patient. At least two image planes at 90 degrees to the structure being examined should be obtained. Other image parameters include a field of view of 9 to 12 cm, matrix of 256 × 256, and image sections of 3 mm. Conventional T1-weighted spin-echo sequences demonstrate marrow clearly. Edema is of low signal intensity compared with the high signal intensity of yellow marrow. Fast spin-echo, T2-weighted MR sequences with fat suppression demonstrate edema as high signal intensity, and cortical fractures are also of high signal intensity. Dual-echo steady-state (DESS) sequences are preferred for articular cartilage and osteochondral injuries. Contrastenhanced, fat-suppressed T1-weighted images are useful in selected cases.59 Limitations of MRI include metal artifact from orthopedic appliances and certain small avulsion fractures without adequate marrow to confirm the osseous nature of the fragment. These small fragments may be more easily

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849

appreciated with CT. Patients with significant pain may have difficulty maintaining foot position, resulting in image degradation due to motion artifact.1,59

Multidetector Computed Tomography Computed tomography has become an essential tool for detection and classification of fracture-dislocations of the foot. The technique is particularly useful in the midfoot and hindfoot.1,7,31,34,37,38 Forty to 50 percent of osteochondral or talar process fractures are missed radiographically.24,58 CT and MRI are superior for detection and staging of these injuries. CT is also the technique of choice for classification and surgical treatment planning for calcaneal fractures.32,34,37 CT is less frequently required for fracture-dislocations of the forefoot.1,7,54 Multichannel helical CT scanners allow rapid evaluation of the foot with very thin sections. Image quality is as good or better with reformatted reconstruction than directly acquired data produced by older CT units.34 We typically position the patient supine with the foot in neutral position (toes up) and use 1-mm sections reconstructed at 0.5-mm intervals with a bone algorithm. The field of view varies with the region of interest (9 cm or more). The gantry angle is parallel to the foot. Appropriate coronal, sagittal, or oblique reformatted images are obtained based on the region of interest. Although 3D reconstruction is often preferred by orthopedic surgeons, most radiologists prefer multiplanar reformatted images. CT can be limited in the presence of orthopedic hardware owing to streak artifact; however, this problem has been reduced significantly with MDCT. Also, soft tissue pathology is not as clearly depicted compared with MRI.1,7

B ■ FIGURE 33-26

Type III talar dome fracture. Coronal CT arthrogram (A) and coronal, fat-suppressed T2-weighted MR image (B) demonstrate a complete fracture without displacement.

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

Ultrasonography Ultrasonography is not commonly used to evaluate acute osseous injuries. The technique may be of value to evaluate associated tendon and soft tissue injuries. Also, complications such as soft tissue infection or fluid collections can be evaluated with ultrasonography.1,7

Nuclear Medicine Radionuclide scans in the setting of osseous trauma are useful for detection of subtle fractures or stress fractures.1,62,63 Initial radiographs may be normal in the acute setting. Radionuclide scans using technetium-99m methylene diphosphonate with delayed or three-phase plus delayed images may be positive in 80% of patients at 24 hours after injury, and 95% are positive 72 hours after injury. Fractures are demonstrated as focal regions of increased radiotracer uptake (Fig. 33-27).62,63 In the appropriate setting, increased tracer accumulation can confirm the clinical diagnosis or allow focused CT or MRI to confirm the abnormal tracer uptake is related to a fracture. Today, because of lack of specificity and time delay (24 to 72 hours), CT or MRI is more often performed in the acute setting without first obtaining a radionuclide scan.1,7,60

Imaging of Specific Structures Radiographs (CR images) remain the primary screening technique for patients with suspected osseous injury. If negative or equivocal, additional studies may be necessary. When radiographs are positive, CT is not uncommonly necessary to classify the injury for treatment planning purposes.1,7,24,34 Earlier sections discussed anatomy, mechanisms of injury, and the types of fracture-dislocations in

the hindfoot, midfoot, and forefoot. In this section the focus is on imaging findings and the appropriate use of the different modalities.

Talar Fracture-Dislocations Talar neck, comminuted talar body, and fracture-dislocations are usually obvious on radiographs. Radiographs are capable of identifying the fracture, degree of displacement, and the direction of dislocations in many cases. However, complex injuries often require additional studies with CT for complete evaluation.1,7,24 Osteochondral fractures (see Fig. 33-26) and fractures of the lateral and posterior talar processes are often more subtle and may be easily overlooked on radiographs. The presence of a joint effusion (best seen on the lateral radiograph) should result in a careful search for a talar dome fracture. These fractures are usually most easily appreciated on the mortise view (Fig. 33-28).1,7 Classification (Berndt and Harty)11 may also be possible radiographically. In difficult cases or when more detail is required, CT or MRI should be obtained to appropriately classify the injury and measure the size and location of the fragment.18,58 Fractures of the lateral or posterior talar processes may be easily overlooked on radiographs.10,23,24 Radiographs are negative in 40% of lateral process fractures.23 Understanding the mechanism of injury with these fractures should result in selection of CT when talar process fractures are suspected.10,23,24 Dislocations about the talus are usually easily detected on radiographs. Subtalar dislocations may be medial or lateral. Talonavicular dislocations also occur. Total dislocations are rare.30 Osteochondral fractures commonly occur with dislocations. Therefore, CT studies should be obtained after reduction to ensure joint congruity and exclude associated osteochondral fractures.27–29

B ■ FIGURE 33-27 Frontal (A) and lateral (B) scintigrams of the foot demonstrate increased tracer (arrow) in the midfoot due to a Lisfranc injury.

A

CHAPTER

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■ FIGURE 33-28

Talar dome fracture. A, Lateral radiograph demonstrates a joint effusion (arrows) with no fracture. B, Mortise view shows fragmentation of the medial talar dome (arrow).

Calcaneal Fracture-Dislocations Anteroposterior, lateral, and axial radiographs of the calcaneus can identify the majority of fractures and provide measurement of Bohler’s angle and the critical angle of Gissane (Fig. 33-29, see also Figs. 33-11 and 33-12).1,7,31 Certain calcaneal fractures are obviously extra-

articular (Fig. 33-30; see also Fig. 33-15). However, if there is a question of articular involvement or if articular involvement is evident (see Fig. 33-29), then thin-section CT with reformatting in the coronal and sagittal planes is essential for classification and management of the injury (Fig. 33-31).1,7,31,32,34,37,38

A ■ FIGURE 33-29

Lateral (A) and axial (B) radiographs demonstrate a calcaneal fracture (white arrow) that appears to extend into the posterior facet. There is an associated fracture of the fifth metatarsal base (A, black arrow).

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

■ FIGURE 33-30 Lateral radiograph of the hindfoot demonstrates an avulsion fracture of the plantar fascia attachment (arrow). Is there a cuboid fracture as well?

■ FIGURE 33-31

Complex calcaneal fracture. A, Lateral radiograph shows a calcaneal fracture with loss of height. Axial (B), reformatted sagittal (C and D) images demonstrate a comminuted intra-articular fracture.

(Continued)

A

C

B

D

CHAPTER

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■ FIGURE 33-31—Cont’d Coronal (E and F) images demonstrate a comminuted intra-articular fracture. There is severe comminution involving the posterior facet. This is a Sanders type IV fracture.

E

Subtle anterior calcaneal process or peroneal tubercle fractures may also require CT for detection.1,33,34 Additional imaging techniques are usually not indicated during the initial stages of diagnosis and treatment.

Midfoot Fracture-Dislocations Imaging of midfoot injuries can be difficult owing to the complex anatomy and bony overlap. Lesions are

F

often subtle (osteochondral, avulsion, or compression) and easily overlooked on radiographs (Fig. 33-32).7,41,46 Previously, bone scans were commonly performed.62,63 However, today CT, and in some cases MRI, is preferred (Fig. 33-33). MRI is superior for subtle compression injuries or bone bruises that demonstrate marrow edema with or without obvious fracture lines.59,61 However, subtle osteochondral fragments and articular deformities are more easily appreciated on thin-section multiplanar

A ■ FIGURE 33-32 Subtle cuboid fractures. A, Lateral radiograph demonstrating condensation (arrows) due to a cuboid compression fracture. B, Anteroposterior radiograph of the ankle with a cuboid avulsion (arrow).

B

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

CT images.48–50 Tarsometatarsal or Lisfranc injuries may be subtle or complex (see Figs. 33-20 and 33-25). Radiographs may demonstrate subluxation or dislocation and fractures (Fig. 33-34). However, once again, reformatted CT images are optimal to fully evaluate the extent of injury (Fig. 33-35).1,7,47–50

Forefoot Fracture-Dislocations

■ FIGURE 33-33 CT image demonstrates a cuboid fracture (arrows) not evident on radiographs.

Fractures of the metatarsals and phalanges are typically obvious on radiographs. Fractures of the fifth metatarsal base are easily identified (see Fig. 33-21).52–54 Fractures of the first metatarsal base are uncommon as isolated injuries but easily identified on radiographs. However, fractures of the second through fourth metatarsal bases may be difficult to visualize owing to bony overlap (Fig. 33-36).40,47,48 As a rule, suspected fractures of the tarsometatarsal joints or second through fourth metatarsal bases should be evaluated with CT to ensure complete evaluation (see Fig. 33-35).1,7 Fractures of the distal metatarsals and phalanges can be identified and followed with radiographs (Figs. 33-37 and 33-38). Additional imaging studies are not required in the majority of cases. Similarly, dislocations of the metatarsophalangeal and interphalangeal joints can be identified and followed with radiographs (see Figs. 33-23 and 33-24). In the case of failure of reduction or possible osteochondral fracture, CT or MRI may be indicated.56,59

A ■ FIGURE 33-34

Lisfranc injuries. A, Radiograph shows widening of the first tarsometatarsal joint (black arrow) and the 1-2 metatarsal bases (white arrow) with no obvious fracture. B, Posteroanterior radiograph demonstrates an obvious fracture-dislocation.

■ FIGURE 33-35 Lisfranc injury. Coronal (A to C) and axial (D to F) CT images show multiple fracture fragments and articular position of the tarsometatarsal articulations.

■ FIGURE 33-36 Fractures of the third and fourth metatarsal bases. A, Anteroposterior radiograph demonstrates a fracture of the fourth metatarsal shaft (arrow). B, Three weeks later the fracture of the third metatarsal is evident (arrowhead) as well.

A

B

■ FIGURE 33-37

Localized view of a displaced fracture of the fifth proximal phalanx.

■ FIGURE 33-38 Comminuted fracture of the distal fifth metatarsal. A, Lateral radiograph demonstrates the fracture (arrow). B, Initial reduction view in traction to restore length. Follow-up radiographs (C and D) after healing demonstrate residual angular deformity and shortening (lines).

856

CHAPTER

Sesamoid fractures may be obvious on routine and sesamoid views.1,7,51 Stress injuries may be more easily detected with radionuclide scans, CT, or MRI.1,7,51,59

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vative (closed) and open treatment options are reviewed by location.

Talar Fracture-Dislocations

DIFFERENTIAL DIAGNOSIS Patients with acute osseous injury or dislocation of the foot present with a history of acute injury in most cases. Clinical findings and imaging features are usually specific for the diagnosis, with several notable exceptions. First, patients presenting with a history of ankle sprain may have a variety of fractures and soft tissue injuries.1,2,7 Subtle peripheral talar process, talar dome, anterior calcaneal process, and fifth metatarsal base fractures must be excluded along with ligament tears and peroneal tendon subluxation or dislocation.1,2,59 Lisfranc injury patterns may be seen in patients with chronic neuropathy, with diabetes mellitus being most common. Focused imaging with CT or MRI may be required to confirm the etiology is trauma related.1,56,63 Pathologic fractures are uncommon except in patients with osteopenia. Underlying bone lesions such as enchondroma or primary osseous malignancy are less common in the foot than other anatomic regions.1,7,59

SYNOPSIS OF TREATMENT OPTIONS Treatment options for acute osseous injuries vary with location, associated injuries, patient condition, and surgical preference.4,5,31,52,64–69 For discussion purposes, conser-

Treatment of talar fracture-dislocations varies with the type and category of injury. Talar neck fractures (see Table 33-2) can be treated with cast immobilization for 6 weeks in patients with Hawkins type I or minimally displaced type II fractures. Open reduction and internal fixation to achieve anatomic reduction is used when conservative treatment fails for type II and for initial treatment of type III and IV fracture-dislocations (Fig. 33-39).4,13,14 Twenty-five to 50 percent of type III fractures are open, increasing the risk of infection. In this case, internal fixation with delayed wound closure (3 to 5 days) is preferred.4,13 Complications after talar neck fractures are common.1,4,13–16 Infection is common with both closed and open fractures. Delayed union is common, although nonunion occurs in only 4% of patients.70 Avascular necrosis is very common with complex injuries. The incidence of avascular necrosis is 0% to 13% with Hawkins type I fractures, 20% to 58% with type II, and 83% to 100% with types III and IV injuries.14–16 Detection of avascular necrosis can be predicted on radiographs 6 to 8 weeks after injury (Fig. 33-40).1,15 Definitive diagnosis may require CT or MRI depending on the type of orthopedic hardware in place. Osteoarthritis in the tibiotalar and subtalar joints occurs in 54% of patients.14

■ FIGURE 33-39 A, Hawkins type III fracture after reduction. There is still separation and fragmentation of the neck fracture. B, Lateral radiograph after Kirschner wire and screw fixation shows normal anatomic reduction.

B

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

■ FIGURE 33-40 Hawkins sign. Hyperemia after injury causes subchondral lucency in viable bone. Anteroposterior radiograph after reduction of talar and medial malleolar fractures shows subchondral lucency medially (viable) and sclerosis of the talus laterally indicating avascular necrosis.

A ■ FIGURE 33-41

Crush fractures of the talar body have a high complication rate when treated with closed reduction.4,19,71 Therefore, open reduction and internal fixation is preferred. Avascular necrosis occurs in 40% of cases, and subtalar and tibiotalar arthrosis occurs in 48% to 90% of patients.19 Osteochondral and talar process fractures may be difficult to detect. Lateral process fractures are initially overlooked in 40% to 50% of cases.24 Talar process fractures can be treated with closed reduction if the fragment is not displaced more than 2 mm and the fracture is not comminuted. In the latter setting, open reduction with removal of small fragments is more optimal. Nonunion occurs in up to 60% of patients treated with closed reduction compared with only 5% of patients treated with open reduction.4,10,23,24 Talar dome fractures that are not displaced (types I to III) may be treated with cast immobilization unless open reduction of other injuries is required. In this case the fragment should be removed. If closed reduction fails, arthroscopic evaluation with drilling of type II and débridement of type III lesions should be considered. Displaced fragments (type IV, Fig. 33-41) usually result in chronic symptoms and should be removed.4,18,58 Preoperative imaging with CT or MRI is important to evaluate the integrity of the cartilage and the size and position of the fragment.1,59

B Axial CT images of a type IV talar dome fracture (A, open arrowhead) with fragments (A and B, white arrows) in the joint space.

CHAPTER

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B ■ FIGURE 33-42

Axial (A) and lateral (B) radiographs after reconstruction plate and screw fixation of an intra-articular fracture (arrow). Bohler’s angle (lines) has been restored to 30 degrees and the width restored.

Dislocations can be reduced with closed techniques. Open wounds are managed with delayed closure in 3 to 5 days.4 Postreduction CT images in the axial, coronal, and sagittal planes are important to assess the joint space and unrecognized osteochondral fractures.1,4,69 Total talar dislocations are rare, and prognosis is poor owing to the extensive soft tissue injury. Therefore, talectomy with tibiocalcaneal fusion is recommended.30

Calcaneal Fracture-Dislocations Treatment of calcaneal fractures has varied considerably over the years in an attempt to reduce the high incidence

■ FIGURE 33-43 Subfibular impingement, peroneal tendinopathy, and arthrosis. Coronal CT image demonstrates widening of the calcaneus extending beyond the peroneal line with swelling (arrows) of the peroneal tendons and subtalar arthrosis.

of long-term disability.1,3,31 The goals of treatment are to restore calcaneal height, length, and calcaneal axis; reduce articular deformities; and restore function.3,31,72 Treatment approaches vary with the type of fracture (intra-articular vs. extra-articular), degree of displacement, and patient factors.31 Extra-articular fractures do not involve the posterior facet. Although frequently obvious on radiographs, CT is still preferred for treatment planning and to improve certainty regarding the extent of injury.1,7,31,32 Anterior calcaneal process fractures (see Fig. 33-14) can be treated with closed reduction if less than 25% of the articular surface is involved and there is less than 3 mm of displacement.3,4 If closed treatment fails, internal fixation or resection of the fragment should be considered.31 Other fractures including the sustentaculum tali, peroneal tubercle, and tuberosity can also be managed with cast immobilization if there is not displacement.1,3,31 Intra-articular fractures most often require semiopen or open procedures with internal fixation (Fig. 33-42).3,31,67,68,72 Again, CT is essential to classify, manage, and follow these injuries (see Fig. 33-31).1,31,32,37,72 Early complications may be related to the fracture (skin necrosis, compartment syndrome, neural injury) or the surgical procedure (infection, wound healing, sural nerve injury, medial neurovascular injury).31 Late complications may also be related to the injury or surgical procedure. Long-term complications include nonunion, malunion, subfibular impingement, peroneal and flexor tendon injuries, neurovascular injury, and reflex sympathetic dystrophy.1,7,37,72 Soft tissue injuries may be most easily detected with MRI unless there is metallic fixation immediately adjacent to the area of interest. CT is useful for evaluating articular deformity, calcaneal shape, and subfibular impingement (Fig. 33-43).1,7,59

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

Midfoot Fracture-Dislocations Isolated fractures of the navicular, cuboid, and cuneiforms are not common. Undisplaced fractures of the navicular or cuboid can be treated with cast immobilization (see Fig. 33-33). Open reduction with screw fixation is reserved for displaced fractures or when conservative measures fail.40,43,44 Injuries to the cuneiforms are more significant because of the important role they play in structural stability. Therefore, internal fixation is usually required.40,46

Lisfranc injuries (see Fig. 33-20) may be subtle and easily overlooked or more complex. In either setting, CT is important to completely evaluate the injury before treatment planning (see Fig. 33-35).1,7,47,49,50 Injuries with no evidence of instability on weight bearing can be managed with closed reduction and cast immobilization.3,40 In other settings, open reduction and internal fixation is required (Fig. 33-44). Fusion of the fourth and fifth metatarsal bases should be avoided when possible.40

B

■ FIGURE 33-44

Anteroposterior (A) and lateral (B) radiographs of a Lisfranc injury with fracture of the second metatarsal base and lateral displacement of the metatarsals. Anteroposterior (C) and lateral (D) radiographs after screw and Kirschner wire fixation.

CHAPTER

Forefoot Fracture-Dislocations Fractures of the first metatarsal can be difficult to manage. Isolated fractures, although uncommon, can be treated with cast immobilization unless there is evidence of instability or displacement on stress radiographs. In the latter case, internal fixation is required to preserve function.40 Fractures of the second through fourth metatarsals can be treated conservatively unless there is displacement or angular deformity. In this setting, Kirschner wire or screw fixation may be required.3,40 Management of fractures of

■ FIGURE 33-45

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the fifth metatarsal is more controversial. Fractures in zone 1 and distal fractures can be treated with cast immobilization.3,40,52–55 Fractures in zone 2 and fractures with symptoms prior to fracture in zone 3 (stress fractures) are approached more aggressively. Although cast immobilization may be successful, screw fixation is often required to avoid nonunion (Fig. 33-45).40 Sesamoid fractures can be treated conservatively, but they may remain symptomatic for up to 6 months. When conservative measures fail, resection of the sesamoid may be required.40,51

Fractures of the proximal fifth metatarsal. A, Fracture in zone I (arrow) treated with cast immobilization. B, Stress fracture in zone III is un-united and underwent screw fixation. Anteroposterior (C) and lateral (D) radiographs after screw fixation.

B

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P A R T O N E ● Injury: Appendicular Skeleton, Lower Extremities

What the Referring Physician Needs to Know ■ ■

■

■

The talus is the second most commonly fractured tarsal bone after the calcaneus. Subtle talar fractures (lateral process, posterior process, talar dome) are initially missed on radiographs in 40% to 50% of cases. Complications of talar neck fracture include delayed union (13%), malunion (45% to 77%), and avascular necrosis in 83% to 100% of Hawkins type III and IV fractures. Intra-articular calcaneal fractures typically require open reduction. CT is critical to classify and manage calcaneal fractures.

■

■

■

Early complications of calcaneal fractures include infection and skin necrosis. Long-term complications include malunion, subfibular impingement, tendon injuries, neurovascular injury, and reflex sympathetic dystrophy. Tarsometatarsal fracture-dislocations may be difficult to detect on radiographs. CT is essential to fully evaluate and treat these injuries. Fractures of the fifth metatarsal base are divided into three zones. Fractures in zones II and III may require internal fixation.

SUGGESTED READINGS Boack DH, Manegold S. Peripheral talar fractures. Injury 2004; 35:B23–B25. Canale ST, Belding RA. Osteochondral lesions of the talus. J Bone Joint Surg Am 1980; 62:97–102. Crosby LA, Fitzgibbon TC. Computed tomography scanning of acute intraarticular fractures of the calcaneus: a new classification system. J Bone Joint Surg Am 1990; 72:852–859. Hawkins LG. Fractures of the neck of the talus. J Bone Joint Surg Am 1970; 52:991–1002. Judd DB, Kim DH. Foot fractures frequently misdiagnosed as ankle sprains. Am Fam Physician 2002; 66:785–794. Linsenmaier U, Brunner U, Schoning A, et al. Classification of calcaneal fractures by spiral CT: implications for surgical treatment. Eur Radiol 2003; 13:2315–2322.

Markwana NK, Van Liefland MR. Injuries of the mid foot. Curr Orthop Relat Res 2005; 19:231–242. Schachter AK, Chen AL, Reddy PD, et al. Osteochondral lesions of the talus. J Am Acad Orthop Surg 2005; 13:152–158. Theodorou DJ, Theodorou SJ, Kakitubata Y, et al. Fractures of the fifth metatarsal bone: anatomic and imaging evidence of the pathogenesis of avulsion of the plantar aponeurosis and short peroneal muscle tendon. Radiology 2003; 226:857–865. Vuori J, Aro H. Lisfranc joint injuries: trauma mechanisms and associated injuries. J Trauma 1993; 35:40–45.

REFERENCES 1. Berquist TH. Fractures and dislocations. In Berquist TH (ed). Radiology of the Foot and Ankle, 2nd ed. Philadelphia, Lippincott Williams & Wilkins, 2000, pp 171–280. 2. Judd DB, Kim DH. Foot fractures frequently diagnosed as ankle sprains. Am Fam Physician 2002; 66:785–794. 3. Hansen ST. Foot injuries. In Browner BD, Levine AM, Jupiter JB, et al (eds). Skeletal Trauma: Fractures, Dislocations and Ligament Injuries, 2nd ed. Philadelphia, WB Saunders, 1998, vol III, pp 2405–2438. 4. Heckman JD. Fractures of the talus. In Bucholz RW, Heckman JD (eds). Rockwood and Green’s Fractures in Adults, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2001, pp 2091–2132. 5. Raffo CS. Fractures and fracture/dislocations of the talus. Trauma 2004; 46:7–32. 6. Mulfinger GL, Tueta JC. The blood supply of the talus. J Bone Joint Surg Br 1970; 52:160–167. 7. Berquist TH, Morrey BF, Cass JR, et al. The foot and ankle. In Berquist TH (ed). Imaging of Orthopedic Trauma, 2nd ed. New York, Raven Press, 1992, pp 453–570. 8. Resnick D. Radiology of the talocalcaneal articulations. Radiology 1974; 111:581–586. 9. Karasick D, Schweitzer ME. The os trigonum syndrome: imaging features. AJR Am J Roentgenol 1996; 166:125–129. 10. Giuffrida AY, Lin SS, Abidi N, et al. Pseudo os trigonum syndrome: missed posterior talar facet fracture. Foot Ankle 2003; 24:642–649. 11. Berndt AL, Harty M. Transchondral fractures (osteochondritis dissecans) of the talus. J Bone Joint Surg Am 1959; 41:188–1020. 12. Valderrabono V, Perren T, Ryf C, et al. “Snow-boarders” talus fracture—treatment outcome of 20 cases after 3.5 years. Am J Sports Med 2005; 33:871–880.

13. Archdeacon M, Wilber R. Fractures of the talar neck. Orthop Clin North Am 2002; 33:247–262. 14. Vallier HA, Nork SE, Barei DP, et al. Talar neck fractures: results and outcomes. J Bone Joint Surg Am 2004; 86:1616–1624. 15. Canale ST, Kelly FB. Fractures of the neck of the talus. J Bone Joint Surg Am 1978; 60:143–156. 16. Hawkins LG. Fractures of the neck of the talus. J Bone Joint Surg Am 1970; 52:991–1002. 17. Szyeszkowitz R, Rechauer R, Seggl W. Eighty-five talar fractures treated with ORIF with five to eight years of follow-up study on 69 patients. Clin Orthop Relat Res 1985; 199:97–107. 18. Schachter AK, Chen AL, Reddy PD, et al. Osteochondral lesions of the talus. J Am Acad Orthop Surg 2005; 13:152–158. 19. Vallier HA, Nork SE, Benirschke SK, et al. Surgical treatment of talar body fractures. J Bone Joint Surg Am 2003; 86:1711–1724. 20. Canale ST, Belding RA. Osteochondral lesions of the talus. J Bone Joint Surg Am 1980; 62:97–102. 21. Pettine KA, Morrey BF. Osteochondral lesions of the talus: a longterm follow-up. J Bone Joint Surg Br 1987; 69:89–92. 22. Vlahovich A, Mehin R, O’Brien PJ. An unusual fracture of the talus in a snow boarder. J Orthop Trauma 2005; 19:498–500. 23. Chang GM, Yoshida D. Fracture of the lateral process of the talus associated with snowboarding. Ann Emerg Med 2003; 41:854–858. 24. Boack DH, Manegold S. Peripheral talar fractures. Injury 2004; 35: B23–B25. 25. Hawkins LG. Fractures of the lateral process of the talus. J Bone Joint Surg Am 1965; 47:1170–1175. 26. Cedell CA. Rupture of the posterior tibiotalar ligament with avulsion of a bone fragment from the talus. Acta Orthop Scand 1974; 4:454–461.

CHAPTER 27. Leitner B. Obstacles to reduction of subtalar dislocations. J Bone Joint Surg Am 1954; 36:299–306. 28. Pennal GF. Fractures of the talus. Clin Orthop Relat Res 1963; 30:53–63. 29. DeLee JD, Curtis R. Subtalar dislocation of the foot. J Bone Joint Surg Am 1982; 64:433–437. 30. Detenbeck LC, Kelly PJ. Total dislocation of the talus. J Bone Joint Surg Am 1965; 51:283–288. 31. Fitzgibbons TC, McMullen ST, Mormino MA. Fractures and dislocations of the calcaneus. In Bucholtz RW, Hechman JD (eds). Rockwood and Green’s Fractures in Adults, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2001, pp 2133–2179. 32. Linsenmaier U, Brunner U, Schoning A, et al. Classification of calcaneal fractures by spiral CT: implications for surgical treatment. Eur Radiol 2003; 13:2315–2322. 33. Gilheany MF. Injuries to the anterior process of the calcaneus. Foot 2002; 12:142–149. 34. Daftary A, Haims AH, Baugaertner MR. Fractures of the calcaneus: a review with emphasis on CT. RadioGraphics 2005; 25:1215–1226. 35. Bohler L. Diagnosis, pathology and treatment of fractures of the os calcis. J Bone Joint Surg 1931; 13:75–89. 36. Gissane W. Proceedings of the British Orthopedic Association. J Bone Joint Surg 1947; 29:254–255. 37. Crosby LA, Fitzgibbons TC. Computed tomography scanning of acute intraarticular fractures of the calcaneus: a new classification system. J Bone Joint Surg Am 1990; 72:852–859. 38. Sanders R, Fortin P, DiPasquale T, et al. Operative treatment of 120 displaced intra-articular calcaneal fractures: results using a prognostic computed tomography scan classification. Clin Orthop Relat Res 1993; 290:87–95. 39. Viswonath SS, Shepard E. Dislocation of the calcaneum. Injury 1977; 9:50–52. 40. Early JS. Fractures and dislocations of the midfoot and forefoot. In Bucholtz RW, Heckman JD (eds). Rockwood and Green’s Fractures in Adults, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2001, pp 2181–2245. 41. Makwana NK, Van Liefland MR. Injuries of the mid foot. Clin Orthop Relat Res 2005; 19:231–242. 42. Sarrafian S. Anatomy of the Foot and Ankle, 2nd ed. Philadelphia, JB Lippincott, 1993. 43. Eichenholtz SN, Levine DB. Fractures of the tarsal navicular bone. Clin Orthop Relat Res 1964; 34:142–157. 44. Pinney SJ, Sangeorzan BJ, Benirsckke SK, et al. Displaced intraarticular fractures of the tarsal navicular. J Bone Joint Surg Am 1989; 71:1504–1510. 45. Classifications of the Orthopedic Trauma Association Committee for Coding and Classifications. OTAC (Ca.) Fracture and dislocation compendium. J Orthop Trauma 1996; 10(Suppl 1):100–152. 46. Patterson RH, Petersen D, Cunningham R. Isolated fracture of the medial cuneiform. J Orthop Trauma 1993; 7:94–95. 47. Vuori J, Aro H. Lisfranc joint injuries: trauma mechanisms and associated injuries. J Trauma 1993; 35:40–45. 48. Norris G, Nix K, Goldman FD. Fracture of the second metatarsal base—an overlooked cause of midfoot pain. J Am Podiatr Assoc 2003; 93:6–10. 49. Aiken AP, Paulsen D. Dislocation of the tarsometatarsal joints. J Bone Joint Surg Am 1963; 45:246–260. 50. Hardcastle PH, Seschauer R, Kutcha-Lissberg E, et al. Injuries of the tarsometatarsal joint: incidence, classification and treatment. J Bone Joint Surg Br 1982; 64:349–356.

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51. Mittimeier T, Haar P. Sesamoid and toe fractures. Injury 2004; 35(Suppl B):B87–B97. 52. Reese KA, Litsky A, Kaeding C, et al. Cannulated screw fixation of Jones’s fractures—a clinical and biomechanical study. Am J Sports Med 2004; 32:1736–1742. 53. Ekrol I, Court-Brown CM. Fractures of the base of the 5th metatarsal. Foot 2004; 14:96–98. 54. Theodorou DJ, Theodorou SJ, Kakitubata Y, et al. Fractures of the fifth metatarsal base: anatomic and imaging evidence of a pathogenesis of avulsion of the plantar aponeurosis and short peroneal muscle tendon. Radiology 2003; 226:857–865. 55. Dameron T. Fractures of the proximal 5th metatarsal: selecting the best treatment option. J Am Acad Orthop Surg 1995; 3:110–114. 56. Karasick D. Fractures and dislocations of the foot. Semin Roentgenol 1994; 29:152–175. 57. Brunet J, Tubin S. Traumatic dislocation of the lesser toes. Foot Ankle 1997; 18:406–411. 58. Verhagen RAW, Mass M, Dijkgraaf MGW, et al. Prospective study on diagnostic strategies in osteochondral lesions of the talus. J Bone Joint Surg Br 2005; 87:41–46. 59. Berquist TH. Foot, ankle and calf. In Berquist TH (ed). MRI of the Musculoskeletal System, 5th ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp 430–556. 60. Rossi F, Dragoni S. Talar body stress fractures: three observations in elite female gymnasts. Skeletal Radiol 2005; 34:389–394. 61. O’Donnell P, Safualdin A. Cuboid edema due to peroneus longus tendinopathy: a report of four cases. Skeletal Radiol 2005; 34:381–388. 62. Wilcox JR, Miniot AL, Green JP. Bone scanning and the evaluation of exercise related injuries. Radiology 1977; 123:699–703. 63. Rupani HD, Holder LE, Espinosa DA, et al. Three phase radionuclide bone imaging in sports medicine. Radiology 1995; 156:187–196. 64. Berquist TH. Diagnostic and therapeutic injections as an aid to musculoskeletal diagnosis. Semin Intervent Radiol 1993; 10:326–343. 65. Lee LM, Wang Y, Schwartz LH, et al. Distal lower extremity arteries: evaluation with 2-dimensional MR digital subtraction angiography. Radiology 1998; 207:505–512. 66. Wang Y, Leitt M, Khilnani NM, et al. Bolus-chase digital subtraction angiography of the lower extremity. Radiology 1998; 207:263–269. 67. Lawerence SJ, Grau GF. Evaluation of treatment of open calcaneal fractures: a retrospective analysis. Orthopedics 2003; 26:621–626. 68. Zwipp H, Rammelt S, Barthel S. Calcaneal fractures: open reduction and internal fixation. (ORIF). Injury 2004; 35: SB46–SB54. 69. Samoludas E, Fotiades H, Christoforides J, et al. Talonavicular dislocation and non-displaced fractures of the navicular. Arch Orthop Trauma Surg 2005; 125:59–61. 70. Lorentzen JE, Christensen SB, Krogsoe O, et al. Fractures of the neck of the talus. Acta Orthop Scand 1977; 48:115–120. 71. Sneppen O, Christensen SB, Krogsoe O, et al. Fractures of the body of the talus. Acta Orthop Scand 1977; 48:317–324. 72. Kuvozumi T, Jinno Y, Sato T, et al. Open reduction for intraarticular calcaneal fractures: evaluation using computed tomography. Foot Ankle 2003; 24:942–948.

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C H A P T E R

Imaging of the Forefoot Hilary Umans

IMAGING TECHNIQUES Radiographs are an essential tool in the initial assessment of most conditions affecting the foot, be they acute or chronic traumatic lesions or infectious, inflammatory, or neoplastic conditions. Standard views include anteroposterior, lateral, and external oblique projections. Assessment of developmental or acquired osseous malalignment and evaluation of the arch requires radiographs taken with the patient bearing weight on the affected extremity. A sesamoid view may supplement standard radiographs when evaluating the first metatarsophalangeal (MTP) joint. CT offers more precise cortical, trabecular, and articular bone detail in the assessment of fracture, postfracture deformity, fracture healing, arthritis, osteonecrosis, or neoplasm. Multidetector CT permits acquisition of 1-mm-thick slices in a single plane, with high-resolution reformatted images typically generated in three orthogonal planes. Ultrasonography offers a high-resolution, targeted examination, ideal for evaluating tendinopathy, capsulitis, bursitis, Morton’s neuroma, or retained foreign body and is ideal for guiding therapeutic injection. The dynamic, real-time nature of ultrasonography enhances the evaluation of myotendinous or ligamentous injury and adds important information, differentiating clinically silent from symptomatic abnormalities. MRI of the forefoot permits small field-of-view, highresolution imaging to answer specific clinical questions that may have eluded diagnosis by radiographs, CT, and ultrasonography. This is particularly useful in assessment of occult osseous and soft tissue pathology about the MTP joints and within the intermetatarsal and submetatarsal soft tissues. Dedicated forefoot imaging is best accomplished utilizing small-diameter quadrature or surface coils. Short-axis (coronal plane) imaging through the forefoot is ideal for evaluation of the MTP capsuloligamentous structures as well as the hallucal sesamoids and for assessment of Morton’s neuroma and intermetatarsal bursitis. Long-axis (axial plane) imaging demonstrates

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the tarsometatarsal joints, metatarsal shafts, and MTP joints and is particularly useful for evaluation of metatarsal stress fracture. Sagittal imaging complements the coronal and axial planes and may be optimized by selecting an obliquity off of the axial localizer to correspond to the metatarsal or ray of clinical interest.

MANIFESTATIONS OF THE DISEASE Disorders of the First Metatarsophalangeal Joint The head of the first metatarsal articulates with the base of the first proximal phalanx as well as with the tibial (medial) and fibular (lateral) sesamoids. The first MTP joint differs from the “lesser” MTP joints by the presence of the sesamoids, which function to transfer pressure from the skin surface to the metatarsal head, unloading and increasing the mechanical advantage of the flexor tendons of the great toe. The sesamoids also act as shock absorbers at the first metatarsal head and limit abduction at the first MTP joint. Although invariably present, the sesamoids may be

KEY POINTS Sesamoid bones are susceptible to stress injury, the end stage of which can be avascular necrosis. ■ Turf toe is a dorsiflexion injury of the plantar capsule of the first MTP joint. Lesser MTP joint injuries are common in women wearing high-heeled shoes; second and third MTP involvement is most common. MRI findings can mimic those of Morton’s neuroma. ■ Morton’s neuroma is actually perineural fibrosis occurring most commonly at the second or third intermetatarsal spaces. ■ Intermetatarsal bursitis can cause symptoms and is often associated with Morton’s neuroma. ■

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bipartite or, less commonly, multipartite.1,2 They straddle a longitudinal bony ridge called the “crista” and articulate with a double trochlear surface to either side at the plantar surface of the first metatarsal head. The crista limits mediolateral displacement of the sesamoids and encourages sagittal plane motion at the first MTP joint (Fig. 34-1).

■ FIGURE 34-1

Coronal CT image through the first metatarsal head and hallucal sesamoid. The medial (tibial) and lateral (fibular) sesamoid straddle the crista (arrow), a longitudinal bony ridge at the plantar surface of the first metatarsal head.

■ FIGURE 34-2

A, Coronal, gradient-recalled-echo 2D MR image through the level of the first metatarsal-sesamoid articulation shows the intersesamoid ligament portion of the plantar plate (straight arrow). The flexor hallucis longus tendon (arrowhead) is cradled between the hallucal sesamoids, plantar to the intersesamoid ligament. The medial aspect of the fibrous joint capsule is indicated by the curved arrow. B, T1-weighted MR image permits evaluation of osseous contours and marrow signal alteration. C, Fat-suppressed, T2-weighted MR image permits detection of marrow edema, synovitis, tenosynovitis, capsuloligamentous, or myotendinous signal abnormalities.

● Imaging of the Forefoot

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Apposed articular surfaces at the plantar head of the first metatarsal and the dorsal aspect of the sesamoids are covered with hyaline cartilage and comprise a synovial joint.3 The first MTP articulation is a shallow ball-and-socket joint. Four sets of paired ligaments run between the metatarsal head, the sesamoids, and the proximal phalanx; together with the plantar metatarsophalangeal, the intersesamoid, and the deep transverse ligaments, these stabilize the first MTP joint. Medial and lateral slips of the flexor hallucis brevis tendon attach to the sesamoids before inserting on the medial and lateral margins of the proximal phalanx. All but the articular surfaces of the hallucal sesamoids are embedded within the fibrocartilaginous plantar plate.2 They are bound to each other by the intersesamoid ligament portion of the plantar plate (Fig. 34-2). The tibial sesamoid is further stabilized by attachments of the abductor hallucis tendon, whereas the fibular sesamoid is stabilized by attachments from the adductor hallucis tendon. The tendon of the flexor hallucis longus is cradled between the hallucal sesamoids, plantar to the intersesamoid ligament. The fibrous joint capsule surrounds the entire first MTP joint and attaches to the sesamoids at its plantar aspect. The first MTP joint may be damaged by degenerative or inflammatory arthritis, infection, or trauma. Acute

B A

34

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traumatic hyperextension at the first MTP joint may result in sesamoid fracture or diastasis at the synchondrosis of a bipartite sesamoid. The two may be difficult to differentiate radiographically. Typically, a fracture is characterized by sharp margins that fit together, whereas bipartite sesamoids have corticated margins that do not fit together.4 Serial radiographs show increasing callus and can reliably differentiate the two.1 Alternatively, bone scintigraphy and MRI can be used to direct radiotracer uptake or marrow signal alteration, respectively. Hallux valgus is typically an acquired forefoot deformity, four times more common in women than men.5 There is associated fibular deviation and pronation of the hallux with prominence of the dorsomedial eminence of the first metatarsal. With deviation of the great toe, the exposed articular cartilage at the medial aspect of the first metatarsal head undergoes disuse atrophy, laying the bone bare to external forces of footwear.6 Bony erosion and proliferation ensue, enlarging the prominence or “bony bunion” at the dorsomedial eminence of the first metatarsal head. An adventitial bursa or “soft tissue bunion” may develop overlying the dorsomedial eminence, formed by the body to cushion the acquired bony prominence. Associated metatarsus primus varus, defined as abnormal widening of the first intermetatarsal angle, can exacerbate the severity of hallux valgus and bunion formation. Surgical treatment is dictated by the degree of hallux valgus, metatarsus primus varus, the size of the bunion, and the presence of associated incongruency or arthrosis of the first MTP joint. Hallux valgus is invariably associated with fibular subluxation of the hallucal sesamoids (Fig. 34-3). Lateral subluxation renders the sesamoids useless in preventing abduction of the great toe. Over time, chondromalacia of the sesamoids and pressure erosion of the crista ensue.7 Ultimately, there is accommodative stretching of the medial and tightening of the lateral ligamentous structures. This causes soft tissue imbalance at the first MTP joint, resulting in a mechanical advantage of the muscles on the lateral side. The result is increasingly severe hallux valgus. Hallux valgus must be evaluated using weight-bearing anteroposterior and lateral radiographs. The normal angle between the long axis of the first metatarsal and the first proximal phalanx measures less than 15 degrees. The first intermetatarsal angle, between the long axis of the first and second metatarsals, should measure between 8 and 12 degrees.8 Incongruency of the joint often accompanies hallux valgus and is defined as medial or lateral subluxation of the apposed articular surfaces of the MTP joint. A bunionette deformity has also been referred to as a “tailor’s bunion.” It is an acquired painful condition characterized by chronic swelling over the fifth metatarsal head. Most often due to pressure (i.e., the cross-legged tailor’s foot on a bench), congenital splaying of the forefoot, lateral bowing of the fifth metatarsal, or developmental prominence of the fifth metatarsal head may be intrinsic predisposing factors. The normal fourth and fifth intermetatarsal angle is 6.2 degrees and the normal fifth MTP angle is 10 degrees9; either or both may be exceeded in the bunionette deformity. Bunionette deformity may be exacerbated by medial deviation and rotation of the phalanx at the MTP joint.

■ FIGURE 34-3

Anteroposterior weight-bearing radiograph shows severe hallux valgus. There is fibular deviation and subluxation of the great toe (curved arrow) and fibular subluxation of the sesamoids (straight arrow). The articular surface of the medial head of the first metatarsal (arrowhead) is laid bare and is prone to external forces of footwear and bunion formation.

Sesamoiditis Sesamoiditis is a clinical term used generically to refer to painful conditions in and around the region of the hallucal sesamoids. Some expand the term to refer to all painful conditions at the first MTP joint. Yet other authors have more specifically reserved the term to indicate chondromalacia of the sesamoids. Depending on its definition, this may account for up to 4% of overuse injuries of the foot.10 There is a consensus that the condition results from overload at the plantar aspect of the first MTP joint. This may be related to acute injury or chronic repetitive trauma. Predisposing risk factors include wearing highheeled shoes, dancing, sports, and a cavus foot deformity with a rigidly plantarflexed first ray.11 Patients may present with symptoms of sesamoiditis in the context of inflammatory arthritis, osteoarthritis, osteochondritis, or chondromalacia at the metatarsosesamoid articulation. Alternatively, there may be stress fracture or osteonecrosis of the sesamoid.12 Imaging must include standard anteroposterior and lateral radiographs obtained with the patient bearing

CHAPTER

34

● Imaging of the Forefoot

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weight to assess congenital forefoot deformities and possibly identify arthritic changes. A sesamoid view is essentially an oblique, coronally oriented radiograph, obtained tangential to the metatarsosesamoid joint, which permits direct visualization of the joint space and articular surfaces and eliminates osseous superimposition. Over time, radiographs may reveal fragmentation and sclerosis of the sesamoids. Bone scintigraphy is sensitive for demonstration of pathologic radiotracer uptake in the sesamoid region but does not effectively narrow the differential diagnosis. When compared with conventional radiography, CT affords more sensitive and specific detection of fracture and may permit visualization of periostitis, callus formation, articular irregularity, pseudocyst formation, as well as subarticular or articular collapse of osteonecrosis. MRI may be reserved for use when CT is unrevealing, as in stress-related marrow edema (Fig. 34-4), occult fracture, early osteonecrosis (Fig. 34-5), or chondromalacia.13 In addition to elucidating radiographically occult osseous changes, MRI delineates reactive soft tissue changes, including synovitis, tendinitis, and bursitis.

Turf Toe The introduction of artificial sports surfaces in the late 1960s heralded a marked increase in injuries to the capsuloligamentous structures of the first MTP joint, presumably due to the higher friction coefficient of Astroturf as compared with grass. The term turf toe was coined to describe this sports-related injury.14 Turf toe is broadly defined by the Orthopedic Foot and Ankle Society as a “plantar capsular ligament sprain” of

B ■ FIGURE 34-4

A, Coronal T1-weighted MR image demonstrates sesamoiditis, manifest as low T1-signal marrow edema within the tibial hallucal sesamoid (white arrow). There is no linear marrow signal alteration to suggest either fracture or osteonecrosis. B, Coronal fast spin-echo inversion recovery MR image at the same level reveals bright signal marrow edema. (Courtesy of Timothy Sanders, MD.)

B ■ FIGURE 34-5

A, Sagittal T1-weighted MR image through the tibial hallucal sesamoid demonstrates dark signal marrow replacement without cortical irregularity or fragmentation (arrowhead). B, This corresponding coronal fat-suppressed T2-weighted MR image demonstrates persistent dark signal in the tibial sesamoid (arrowhead), indicative of osteonecrosis. Note the mild submetatarsal soft tissue edema. (Courtesy of Timothy Sanders, MD.)

the first MTP joint. The mechanism of injury in the majority of cases is forced hyperextension. The injury occurs when the forefoot becomes fixed due to high friction and is positioned plantigrade with slight dorsiflexion and elevation of the heel off of the ground. Subsequently an external force (another player) forces the first MTP joint into an even greater degree of dorsiflexion with a resultant tear of the capsular attachment at the level of the first metatarsal, which is its weakest point (Fig. 34-6). The soft tissue injury may be complicated by cartilaginous or subchondral injury, as well as sesamoid fracture (Fig. 34-7). American football cleats have evolved to include an increased number of cleats, with greater flexibility of the forefoot. Both of these adaptations have been associated with an increased incidence of turf toe.15 Although it has not been proved, hardening of the artificial turf over time may have a small contributory role to the increased incidence of turf toe.16 The diagnosis is often evident from the history. Clinically, the patient presents with acute inflammation of the first MTP joint that worsens over the first day. Painful guarding limits active range of motion. Nevertheless, passive ranging reveals a pathologically increased range of motion, often 100 degrees (as compared with a normal of 65 degrees of dorsiflexion from a neutral position), reflecting plantar capsuloligamentous insufficiency. Pain is typically worst at the plantar surface of the first MTP

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A

B

C

■ FIGURE 34-6

A, Coronal fat-suppressed, T2-weighted MR image through the level of the first metatarsal head demonstrates turf toe. There is a defect in the plantar plate (straight arrow) with nonvisualization of the intersesamoid ligament. Note the edema within the adductor hallucis muscle (curved arrow). B, Sagittal fat-suppressed, T2-weighted MR image through the first metatarsal phalangeal joint demonstrates a capsuloligamentous tear at the insertion site onto the base of the hallux (curved arrow). C, Axial fat-suppressed, T2-weighted MR image through the plantar soft tissues of the forefoot demonstrates edema within the abductor hallucis muscle (asterisk). (Courtesy of Timothy Sanders, MD.)

B ■ FIGURE 34-7

C

A, Sagittal T1-weighted MR image through the first metatarsophalangeal joint demonstrates low signal marrow edema within the tibial hallucal sesamoid. B, Sagittal fat-suppressed, fluid-sensitive MR sequence permits better visualization of the low signal fracture line (curved arrow) amid the bright signal marrow edema. C, In the axial plane, the fractured tibial hallucal sesamoid (arrow) appears bright on fat-suppressed, T2-weighted MRI, as compared with the uninjured dark signal of the fibular sesamoid. (Courtesy of Timothy Sanders, MD.)

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joint and is potentiated with passive dorsiflexion. Turf toe may be complicated by associated dorsal dislocation of the great toe.17 Conventional radiographs may be used in the differential diagnosis of possible fracture or dislocation about the first MTP joint. Alternatively, sesamoiditis, tendinitis, and bursitis may be considered; however, sesamoiditis may be differentiated clinically from turf toe by its more indolent onset and association with repetitive trauma rather than acute, traumatic hyperextension of the first MTP joint. The gold standard for diagnosis of turf toe is MRI, which permits direct visualization of a tear through the plantar capsule (see Fig. 34-6).18 MRI also allows direct visualization of concomitant soft tissue injury, including synovitis, plantar soft tissue swelling, and tendinitis of the flexor hallucis longus and adductor hallucis (Fig. 34-8), as well as possible associated osseous or cartilaginous injury to the sesamoids or first metatarsal.

Plantar Plate Anatomy The plantar plate of the lesser MTP joints primarily differs from that of the first MTP joint by the absence of the hallucal sesamoids. That means that the plantar plate articulates directly with the plantar surface of the lesser metatarsal head and functions without the benefit of the sesamoids to provide critical articular stability and shock absorption. Whereas turf toe represents a sports-related, acute traumatic rupture of the plantar plate of the first MTP joint, rupture of the plantar plate of the lesser MTP joints is typically an acquired chronic degenerative condition, developed over time due to increased loading.19 The plantar plate is a firm, flexible fibrocartilaginous structure that has a mean length of 20 mm and average thickness of 2 mm at the second MTP joint.20 Similar to the hallux, the plantar plate serves as the central attachment for ligamentous, capsular, and tendinous structures at the lesser MTP joint. It represents the distal insertion of the plantar fascia. The plantar third of the fibrocartilaginous plate blends with the deep transverse intermetatarsal

A ■ FIGURE 34-8

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ligament, whereas the dorsal surface has a smooth, articular-like surface, gliding deep to the metatarsal head during ambulation (Fig. 34-9). Paired accessory collateral ligaments course proximal to distal and dorsal to plantar originating at the dorsal tubercle of the lesser metatarsals to broadly insert on the medial and lateral margins of the plantar plate. Smaller, more obliquely oriented paired phalangeal collateral ligaments also arise from the dorsal tubercle but share a conjoint insertion along with the plantar plate at the medial and lateral base of the proximal phalanx20 (Fig. 34-10). The flexor tendon sheath is cradled within a central concavity at the deep surface of the plantar plate, anchored by a fibrous pulley (Fig. 34-11).21 The tendon sheath contains the flexor digitorum brevis and the flexor digitorum longus tendons. It is easy to remember that the brevis tendon lies below (deep to) the longus tendon within the common tendon sheath. The flexor digitorum brevis splits to straddle the flexor digitorum longus at the level of the proximal interphalangeal joint to insert bilaterally onto the base of the middle phalanx, whereas the flexor digitorum longus inserts onto the plantar base of the distal phalanx. Dorsally, the extensor hood and sling represent a fibroaponeurotic expansion extending bilaterally from the borders of the extensor digitorum longus tendon sheath, with direct insertions onto the plantar plate, the deep transverse intermetatarsal ligament, and the base of the proximal phalanx.20

Metatarsalgia Metatarsalgia is a generic term applied to a spectrum of painful conditions in the region of the metatarsal heads resulting from chronic repetitive stress at the forefoot, most commonly affecting the second MTP joint. Differential diagnosis of metatarsalgia includes plantar plate injury, MTP joint synovitis, stress fracture, Freiberg’s infraction (see Fig. 34-11; osteonecrosis of the metatarsal head), arthritis, interdigital (Morton’s) neuroma, and synovial cyst formation. Morton’s neuroma is more common in

B

A, Sagittal fat-suppressed, T2-weighted MR image demonstrates edema within the adductor hallucis muscle (curved arrow) without capsuloligamentous disruption, indicative of mild turf toe. B, Corresponding coronal, fat-suppressed, T2-weighted MR image similarly demonstrates edema within the adductor hallucis muscle (arrow). (Courtesy of Timothy Sanders, MD.)

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■ FIGURE 34-9

A, Coronal illustration of plantar plate anatomy. The curved arrow indicates the fibrocartilaginous plantar plate. Note that the tendon sheath of the flexor digitorum tendons (brevis lies below the longus tendon) is nestled in a concave groove at the midline plantar plate. The deep transverse intermetatarsal ligament (arrowhead) blends with the plantar plate from ray to ray. Intermetatarsal bursae (thin arrow) are situated above the intermetatarsal ligament, between the metatarsal heads. Collateral ligaments attach bilaterally to the plantar plate below. Dorsally, note the extensor hood and sling extending bilaterally from the extensor digitorum longus tendon sheath. B, Sagittal illustration of plantar plate anatomy. The accessory collateral ligaments (thin straight arrow) broadly insert onto the lateral margins of the plantar plate (thick straight arrow). The phalangeal collateral ligaments (curved arrow) course more obliquely from the dorsal tubercle of the lesser metatarsals to insert along with the plantar plate onto the medial and lateral base of the proximal phalanx.

A ■ FIGURE 34-10

B

A, Sagittal, 2D gradient-recalled-echo MR image demonstrates the insertion of the accessory collateral ligament (arrows) onto the plantar plate. B, More distally the sagittal image demonstrates the phalangeal collateral ligament (curved arrow) and its conjoint insertion along with the plantar plate onto the base of the proximal phalanx.

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A

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B

■ FIGURE 34-11

A, Sagittal T1-weighted MR image through the metatarsal phalangeal joint demonstrates articular collapse and subarticular marrow edema (curved arrow) related to Freiberg’s infraction. B, Sagittal fat-suppressed, T2-weighted MR image in the same individual better demonstrates the curvilinear subarticular low signal (curved arrow) indicative of osteonecrosis. (Courtesy of Timothy Sanders, MD.)

women; this may be due in part to the relatively more pliable female foot or, more likely, the popularity of shoes with high heels. MTP joint synovitis may result from inflammatory arthritis or, more commonly, from chronic excessive loading of the MTP joint.22 At the lesser MTP joints, compressive and tensile forces of weight bearing and ambulation are greatest at the second ray and are increased in the context of hallux valgus or developmental elongation of the second metatarsal (second metatarsal protrusion, “Morton’s foot”). High-heeled shoes with a narrow toe box increase axial loading and compressive forces to the greatest degree at the second MTP joint. Chronic synovitis often stretches the joint capsule and contributes to MTP joint instability.23 Degeneration and attritional change of the plantar plate and collateral ligaments may ensue. Synovitis without capsuloligamentous rupture manifests as clinical limitation, with pain exacerbated by passive dorsiflexion. MTP joint instability often accompanies plantar plate degeneration and rupture. Symptoms include pain and capsular and submetatarsal swelling. Pain is typically worst in the toe-off phase of ambulation, at which time the tensile forces across the degenerated plantar plate are maximal. Instability is detected and quantified by the vertical stress test, which is simply performed by stabilizing the metatarsal head and forcibly displacing the proximal phalanx dorsally.23 A positive test not only reveals instability but also elicits pain at the dorsal base of the proximal phalanx.

Plantar Plate Rupture Plantar plate rupture typically occurs in the context of chronic synovitis and capsular distention. The rupture most commonly occurs at the distal insertion of the plantar plate at its insertion onto the base of the proximal phalanx. There is a relative predilection toward tearing of the lateral insertion of the plantar plate.

Historically, conventional arthrography has been utilized to diagnose plantar plate rupture.24 An intact MTP joint capsule does not communicate with the flexor tendon sheath. Rupture of the plantar plate permits pathologic leakage of contrast agent injected into the MTP joint capsule into the flexor tendon sheath. Extension of contrast agent into the intermetatarsal bursa may imply rupture of the collateral ligaments. High-resolution MRI of the forefoot is the gold standard for imaging of plantar plate rupture and differentiating it from other possible causes of metatarsalgia. Coronal (short-axis) MR images (Fig. 34-12A) through the forefoot demonstrate the plantar plate as a thick, low signal band deep to the metatarsal head, thinnest centrally and thickest distally. A shallow groove at the central plantar surface accommodates the flexor tendon sheath. Collateral ligaments are seen as vertically oriented bands medially and laterally, inserting bilaterally onto the margins of the plantar plate and the base of the proximal phalanx. Oblique sagittal images are plotted off of an axial localizer along the axis of the second metatarsal shaft. In the normal plantar plate, oblique sagittal imaging permits visualization of a distinct, narrow zone of high signal intensity representing hyaline cartilage undercutting25 the low signal fibrocartilage near the distal insertion of the plantar plate (see Fig. 34-12B), which should not measure more than 2.5 mm.19 Visualization of the accessory collateral ligaments and phalangeal collateral ligaments is inconstant and fortuitous with imaging in the oblique sagittal plane. Whereas axial (long-axis) imaging is not useful in detection of plantar plate or collateral ligament rupture, it permits qualitative evaluation of hallux valgus, second metatarsal protrusion, and identification of possible marrow signal abnormalities attendant to stress injury, osteonecrosis, and arthritis. In the context of plantar plate degeneration or rupture there is pathologic elongation and marginal indistinctness of the high signal intensity zone at the distal insertion of the plantar plate (Fig. 34-13). With capsular insufficiency

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A ■ FIGURE 34-12

A, Coronal 2D, gradient-recalled-echo MR image demonstrates the normal plantar plate (short straight arrows), the accessory collateral ligament (arrowheads) and the flexor digitorum tendons (curved arrow). B, In the sagittal plane note the low signal plantar plate (straight arrow) and the distinct, narrow high signal intensity zone (curved arrow) of hyaline cartilage undercutting the dark signal fibrocartilage near the distal insertion of the plantar plate. Arrowheads indicate the flexor tendons.

B

A ■ FIGURE 34-13

A, Sagittal 2D, gradient-recalled-echo MR image demonstrates degenerative widening of the high signal intensity zone at the distal insertion of the plantar plate (curved arrow). B, The degenerative high signal intensity zone is more elongated in this case (curved arrow). Note progressive passive dorsiflexion of the toe with worsening plantar plate degeneration.

B

CHAPTER

and its attendant plantar plate and ligamentous degeneration, there is progressive hyperextension of the toe at the MTP joint. Degenerative thickening or thinning and signal distortion of the plantar plate and/or collateral ligaments is best demonstrated in the coronal plane. A rupture, seen as a high signal defect on fluid-sensitive sequences, most commonly at the distal lateral conjoint insertion of the plantar plate and PCL at the base of the proximal phalanx, is often accompanied by medial displacement of the plantar plate with respect to the metatarsal head.19 Partial tear may be associated with adjacent ganglion formation (Fig. 34-14). Complete rupture may be associated with dorsal dislocation of the toe (Fig. 3415). Coronal fluid-sensitive sequences best demonstrate

■ FIGURE 34-14

Coronal 2D gradient-recalled-echo MR image demonstrates a partial tear of the plantar plate with a ganglion (arrowhead) subjacent to the defect.

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synovitis, submetatarsal soft tissue edema, and intermetatarsal bursitis, all of which are common in the setting of plantar plate degeneration.

Morton’s Neuroma Morton’s neuroma (interdigital neuroma) is not a nerve sheath tumor but rather perineural fibrosis that causes entrapment of the interdigital nerve at the level of the metatarsal heads, most commonly in the third intermetatarsal space. The etiology is controversial but may include reactive fibrosis due to neural entrapment by the intermetatarsal ligament, ischemia, or compression by an inflamed intermetatarsal bursa.26,27 Histologic findings include neural degeneration with epineural and endoneural vascular hyalinization and perineural fibrosis surrounding the interdigital nerve.28 Symptoms, first described by Thomas Morton in 1876,29 include pain in the region of the metatarsal head that is exacerbated by walking in narrow shoes and relieved by rest. Palpation of the intermetatarsal space may elicit pain that radiates to the toes. A palpable mass is detected in a third of affected individuals. In these persons, Mulder’s sign may be elicited on examination; this is a palpable click when pressure is applied to the sole of the foot as the metatarsals are squeezed together.30 The clinical differential diagnosis includes causes of metatarsalgia, in addition to intermetatarsal bursitis, true neuroma, pigmented villonodular synovitis (giant cell tumor of the tendon sheath), and foreign body granuloma. Although clinicians often treat symptomatic Morton’s neuroma conservatively with modified foot gear, forefoot

■ FIGURE 34-15

A, Sagittal 2D gradient-recalled-echo MR image demonstrates complete plantar plate rupture (curved arrow) with dorsal dislocation of the toe. B, Coronal 2D gradient-recalled-echo MR image demonstrates complete rupture of the plantar plate. The collateral ligaments (arrowheads) are lax; the flexor tendons (arrow) are laterally subluxed. Note the marked fluid signal distention of the metatarsophalangeal joint capsule and the fluid signal distention (curved arrow) of the intermetatarsal bursa.

A

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taping, padding, orthoses, or corticosteroid injection, refractory cases may require imaging. Surgical neurectomy has reported failure rates of 14% to 27%, which may in part be related to clinical underdiagnosis of multiple neuromas and variable communicating branches of the intermetatarsal nerves.31,32 Zanetti and associates found that MRI changed the presumptive diagnosis in 28% of feet and altered the number and location of Morton’s neuromas in another one third, resulting in a change of treatment plan in 57% of forefeet imaged.33 Morton’s neuroma appears as a soft tissue mass in the intermetatarsal space that is of low to intermediate signal intensity on T1-weighted MR imaging and of variable but relatively low signal on T2-weighted MR imaging (Fig. 34-16). Contrast medium enhancement is variable and unnecessary for MRI detection of Morton’s neuroma. Often there is associated intermetatarsal bursitis, which is visible as high signal intensity on fluid-sensitive sequences dorsal to the deep transverse intermetatarsal ligament in the coronal plane. Although MRI permits sensitive and specific detection of Morton’s neuroma, Bencardino and colleagues reported the presence of Morton’s neuroma in 33% of asymptomatic forefeet.34 Ultrasonography has a reported sensitivity of 95% to 98% for detection of Morton’s neuroma,35–37 which most commonly appears as a hypoechoic intermetatarsal mass (Fig. 34-17). Quinn and coworkers reported ultrasonographic variability, with approximately 20% of masses appearing either mixed in echogenicity or anechoic. They found it difficult to distinguish Morton’s neuroma from the adjacent intermetatarsal bursa and had an 11% falsepositive rate, including a complex synovial cyst, ganglion, and giant cell tumor of the tendon sheath.38 The dynamic nature of targeted ultrasonography is advantageous. Real-

A ■ FIGURE 34-17

A

B ■ FIGURE 34-16

A, Coronal T1-weighted MR image demonstrates a large Morton neuroma appearing as an intermediate soft tissue mass in the second intermetatarsal space. B, Contrast-enhanced coronal, fat-suppressed, T1-weighted MR image shows avid enhancement in this case. Note that enhancement may be variable and is not necessary for the diagnosis of Morton’s neuroma. (Courtesy of William Morrison, MD.)

time examination negates the problem of detecting clinically silent lesions. In addition, Torriani and Kattapuram reported use of Mulder’s clinical test in conjunction with ultrasonography, which may permit detection of smaller, otherwise occult Morton’s neuromas.39

B

A, Short-axis sonographic image of Morton’s neuroma. Imaging through the forefoot demonstrates the hypoechoic interdigital neuroma (curved arrow) situated between the shadowing metatarsals (short arrows). B, In the longitudinal axis, sonographic imaging again demonstrates the ovoid hypoechoic mass (curved arrow) indicative of Morton’s neuroma. Note the hypoechoic linear nerve (arrowheads) entering and exiting the interdigitial neuroma. (Courtesy of Mihra Taljanovic, MD.)

CHAPTER

SUMMARY Evaluation of painful conditions of the forefoot is primarily accomplished by clinical examination complemented by standard radiographs. CT affords finer cortical, trabecular, and articular detail while eliminating osseous overlap that limits radiographic assessment. Ultrasonography is unparalleled in targeted, real-time dynamic assessment of capsuloligamentous, myotendinous, and soft tissue structures, integrating elements of clinical examination

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such as assessment of pain and range of motion while also serving as guidance for therapeutic injection when applicable. MRI permits high-resolution imaging for sensitive detection of osseous, articular, and soft tissue pathology that remains occult by other imaging modalities. The MRI assessment of the forefoot should be tailored to address the clinical question. Large field-of-view imaging of the hindfoot through the toes is often not feasible and does not afford adequate detail to detect often subtle pathology in the forefoot.

REFERENCES 1. Feldman F, Pochaczevsky R, Hecht H. The case of the wandering sesamoid and other sesamoid afflictions. Radiology 1970; 96:275–283. 2. Frankel JP, Harrington J. Symptomatic bipartite sesamoids. J Foot Surg 1990; 29:318–323. 3. Potter HG, Pavlov H, Abrahams TG. The hallux sesamoids revisited. Skeletal Radiol 1992; 21:437–444. 4. Rodeo SA, Warren RF, O’Brien SJ, et al. Diastasis of bipartite sesamoids of the first metatarsophalangeal joint. Foot Ankle 1993; 14:425–434. 5. Bryant AR. Satisfaction following modified Austin bunionectomy. Aust Podiatrist 1996; 30:9–12. 6. Birrer RB. In Birrer RB, Dellacorte MP, Grisalfi PJ (eds). Common Foot Problems in Primary Care, 2nd ed. Philadelphia, Hanley Belfus, 1998, pp 59–62. 7. Stainsby GD. Pathological anatomy and dynamic effect of the displaced plantar plate and the importance of the integrity of the plantar plate–deep transverse metatarsal ligament tie-bar. Ann R Coll Surg Engl 1997; 79:58–68. 8. Palladino SJ. Preoperative evaluation of the bunion patient: etiology, biomechanics, clinical and radiographic assessment. In Gerber J (ed). Textbook of Bunion Surgery, 2nd ed. Mount Kisco, NY, Futura Publishing, 1991, pp 1–87. 9. Cooper PS. Disorders and deformities of the lesser toes. In Myerson MS (ed). Foot and Ankle Disorders. Philadelphia, WB Saunders, 2000, vol 1, pp 335–340. 10. McBryde AM, Anderson RB. Sesamoid foot problems in the athlete. Clin Sports Med 1988; 7:41–60. 11. Velkes S, Pritsch M, Horoszowski H. Osteochondritis of the first metatarsal sesamoids. Arch Orthop Trauma Surg 1988; 107:369–371. 12. Chelevitte E, Fleischli J. Avascular necrosis of the hallucal sesamoids. J Foot Ankle Surg 1995; 34:358–365. 13. Karasick D, Schweitzer ME. Disorders of the hallux sesamoid complex: MR features. Skeletal Radiol 1998; 27:411–418. 14. Bowers KD, Martin RB. Turf-toe: a shoe related football injury. Med Sci Sports Exercise 1976; 8:81–83. 15. Clanton TO, Ford JJ. Turf toe. Clin Sports Med 1994; 13:731–741. 16. Nigg BM, Segesser B. The influence of playing surfaces on the load on the locomotor system and on football and tennis injuries. Sports Med 1988; 5:375–385. 17. Rodeo SA, O’Brien SJ, Warren RF, et al. Turf-toe: an analysis of metatarsophalangeal joint sprains in professional football players. Am J Sports Med 1990; 18:280–285. 18. Tewes DP, Fischer DA, Fritts HM, Guanche CA. MRI findings of acute turf toe. Clin Orthop Rel Res 1994; 304:200–203. 19. Umans H, Elsinger E. The plantar plate of the lesser metatarsophalangeal joints. MRI Clin North Am 2001; 9:659–669.

20. Deland JT, Lee KT, Sobel M, DiCarlo EF. Anatomy of the plantar plate and its attachments in the lesser metatarsal phalangeal joint. Foot Ankle Int 1995; 16:480–485. 21. Johnston RB, Smith J, Daniels T. The plantar plate of the lesser toes: anatomical study in human cadavers. Foot Ankle Int 1994; 15:276–282. 22. Cooper PS. Disorders and deformities of the lesser toes. In Myerson MS (ed). Foot and Ankle Disorders. Philadelphia, WB Saunders, 2000, vol 1, p 308. 23. Thompson FM, Hamilton WG. Problems of the second metatarsophalangeal joint. Orthopedics 1987; 10:83–89. 24. Yao L, Do HM, Cracchiolo A, Farahani K. Plantar plate of the foot: findings on conventional arthrography and MR imaging. AJR Am J Roentgenol 1994; 163:641–644. 25. Yao L, Cracchiolo A, Farahani K, Seeger LL. Magnetic resonance imaging of plantar plate rupture. Foot Ankle Int 1996; 17:33–36. 26. Alexander IJ, Johnson KA, Parr JW. Morton’s neuroma: a review of recent concepts. Orthopedics 1987; 10:103–106. 27. Nissen KI. Plantar digital neuritis: Morton’s metatarsalgia. J Bone Joint Surg Br 1948; 30:84–94. 28. Read JW, Noakes JB, Kerr D, et al. Morton’s metatarsalgia; sonographic findings and correlated histopathology. Foot Ankle Int 1999; 20:153–161. 29. Morton TG. A peculiar and painful affection of the fourth metatarsophalangeal articulation. Am J Med Sci 1876; 71:37–45. 30. Mulder JD. The causative mechanisms in Morton’s metatarsalgia. J Bone Joint Surg Br 1951;33:94–95. 31. Mann RA, Reynolds JC. Interdigital neuroma: a critical clinical analysis. Foot Ankle Int 1983; 3:228–234. 32. Younger AS, Claridge RJ. The role of diagnostic block in the management of Morton’s neuroma. Can J Surg 1998; 41:127–130. 33. Zanetti M, Strehle JK, Kundert H-P, et al. Morton neuroma: effect of MR imaging findings on diagnostic thinking and therapeutic decisions. Radiology 1999; 213:583–588. 34. Bencardino J, Rosenberg ZS, Beltran J, et al. Morton’s neuroma: is it always symptomatic? AJR Am J Roentgenol 2000; 175:649–653. 35. Shapiro PP, Shapiro SL. Sonographic evaluation of interdigital neuroma. Foot Ankle 1995; 16:604–606. 36. Redd RA. Morton’s neuroma: sonographic evaluation. Radiology 1989; 171:415–417. 37. Pollack R, Bellacosa R, Dornbluth NC, et al. Sonographic analysis of Morton’s neuroma. J Foot Surg 1992; 31:534–537. 38. Quinn TJ, Jacobson JA, Craig JG, van Holsbeeck MT. Sonography of Morton’s neuroma. AJR Am J Roentgenol 2000; 174:1723–1728. 39. Torriani M, Kattapuram SV. Dynamic sonography of the forefoot: sonographic Mulder sign. AJR Am J Roentgenol 2003; 180:1121–1123.

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Upper Extremity Injuries in Children (Including Sports Injuries) Ann M. Johnson and Matthew A. Marcus

PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS Patterns of injury in children are different from those of adults, partly owing to the unique structure of the pediatric skeleton. Injuries of the upper extremity account for 65% of all fractures and dislocations in children and often are the result of a fall on an outstretched hand. The distal radius, the supracondylar elbow, and the clavicle are among the most common sites of upper extremity injury. In this chapter, the most common patterns of injury in the upper extremity are discussed.

and undergo apoptosis in the hypertrophic zone.The zone of provisional calcification is the portion of the hypertrophic zone that is adjacent to the metaphysis and is the site of transition between cartilage and bone.The shape of the physis changes during development so that fracture patterns differ with age. For example, the initial discoid shape of the physis of the proximal femur and humerus becomes highly contoured. Fractures that propagate directly through the physis without a metaphyseal component become less common as children mature.

KEY POINTS

ANATOMY During development, the skeleton changes in length, width, shape, alignment, and rotation. Enchondral ossification is the process of continuous replacement of cartilaginous tissue by osseous tissue and represents the primary mechanism of longitudinal growth. This process is centered at the growth plates interposed between the metaphysis and epiphysis. There is a separate spherical growth plate in the epiphysis surrounding the secondary ossification center. With maturation, the secondary ossification center assumes a more hemispheric shape and in time directly apposes the physis. Radial growth of the diaphysis and portions of the metaphysis occurs by intramembranous ossification. This process involves direct formation of cortical bone by osteoblasts. The physis is divided into zones based on cell histology and function.The germinal zone is the area adjacent to the epiphysis and consists of poorly organized chondrocytes that serve as the stem cells for the growing physis. The proliferative zone contains flattened chondrocytes that are rapidly dividing. The chondrocytes enlarge, vacuolate,

Physeal cartilage is the weakest site of the growing skeleton—weaker than cortical bone and ligaments. ■ Elbow effusions in children should prompt a careful search for fracture. If a fracture is not immediately identified, consider a nondisplaced supracondylar fracture or subtle radial neck fracture. ■ Radius and ulna are usually injured together. The elbow and wrist joints should be carefully examined in an isolated fracture of either bone. ■ Glenohumeral instability is relatively common in adolescents and teenagers. MR arthrography is the study of choice. ■ Elbow dislocations are most frequently accompanied by fractures of the medial epicondyle. The fracture fragment may become entrapped in the joint space. ■ An apparent elbow dislocation in a very young patient should raise the suspicion for fracture separation of the distal humerus. ■ Buckle fractures of the distal forearm may be seen only on the lateral view because they primarily involve the dorsal cortex. ■

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The physis has a dual blood supply. The epiphysis, germinal matrix, and upper proliferative zones are supplied by the epiphyseal artery. The metaphysis receives blood supply from the nutrient artery centrally and the metaphyseal arteries peripherally. The metaphyseal blood supply extends into the lowermost portions of the hypertrophic chondrocytes, which are responsible for synthesizing bone matrix. The perichondrium and peripheral physis also receive contributions from the perichondrial artery. The central portion of the physis remains relatively avascular and is particularly prone to ischemic injury.There are connections between the epiphyseal and metaphyseal vessels that involute within the first year of life. After this stage, transphyseal vascular communication occurs physiologically only at the time of physeal closure. The periosteum plays a unique role in osseous injury. It is thicker than in adults and is less often disrupted in trauma, contributing to more stable fractures in children.1 Subperiosteal collections are common in children because the periosteum is loosely adherent to the bone throughout most of its length. However, at the physis, the periosteum is continuous with the perichondrium, which is a firm point of attachment. The perichondrium attachment is a barrier to the spread of subperiosteal disease. The periosteum also plays an important role in new bone formation, contributing to the rapid healing of children’s fractures. Joint development in the upper limb involves a predictable pattern of appearance and fusion of the secondary ossification centers. Ossification centers usually appear and fuse with the metaphysis earlier in girls than in boys. The clavicle is the first bone in the body to ossify, with intramembranous ossification occurring at two sites in the central portion of the bone at around 5 weeks’ gestation. Most of the longitudinal growth of the clavicle during childhood and adolescence occurs at the medial physis. Ossification of the medial epiphysis usually occurs between 12 and 19 years of age, and fusion usually takes place by the mid 20s or later. The lateral ossification center is often not observed as it ossifies and subsequently fuses in a relatively short period at the end of the second decade of life. At the medial end of the clavicle, the diarthrodial articulation with the sternum allows a wide range of motion, including elevation, anterior and posterior translation, and rotation.There is osseous incongruity with limited contact between the medial clavicle and superior sternum while there is strong ligamentous support from the costoclavicular, interclavicular, and capsular ligaments. The anterior and posterior capsular ligaments attach primarily to the medial epiphysis, in part explaining why medial physeal injuries are more common than true sternoclavicular separations in children.2 The acromioclavicular joint is also a diarthrodial joint. It allows several degrees of movement in anteroposterior and superoinferior planes and allows synchronous clavicular-scapular rotation. As in adults, the strong acromioclavicular and coracoclavicular ligaments provide joint stability. The coracoclavicular ligamentous attachment at the distal clavicle is stronger than the periosteum, predisposing children and adolescents to distal clavicular physeal injuries as opposed to true acromioclavicular separation.3

The scapula begins as a cartilaginous anlage during the fifth week of gestation, originating at the midcervical level. It descends to the upper thoracic levels during subsequent development of the shoulder joint, with failure of appropriate descent resulting in a Sprengel deformity. The scapula begins to ossify by the eighth week of gestation. The primary ossific nucleus is completely ossified at birth. Additional ossification centers are later evident at the coracoid, glenoid, acromion, and inferior margin of the scapula and should not be mistaken for avulsion injuries. Acromial ossification centers appear at puberty and usually fuse by age 22 to 25 years. Failure of fusion results in an os acromiale. Development of the glenohumeral joint is complete at approximately 40 weeks’ gestation. Mahasen and associates demonstrated that the 40-week fetus and adult share comparable glenohumeral joint structure and morphology.4 The primary ossification for the humerus appears at approximately the sixth week of fetal life. The ossified humeral diaphysis and proximal and distal metaphyses are present at birth. An ossified proximal humeral epiphysis is seen in approximately 20% of full-term newborns and is normally present in the remainder by 6 months. A greater tuberosity ossification is usually evident between 7 months and 3 years of age. The lesser tuberosity ossification is usually evident approximately 2 years after appearance of the greater tuberosity. Between 5 and 7 years of age, the humeral head, lesser tuberosity, and greater tuberosity merge. The proximal humeral physis accounts for nearly 80% of the growth of the humerus. The proximal humeral physis remains open until age 14 to 17 years in girls and age 16 to 18 years in boys. The normal proximal humeral physis should not be mistaken for a fracture. The elbow is a hinge joint. Surrounding soft tissues provide primary stability. The ligamentous structures about the elbow in children have sufficient laxity such that dislocation, spontaneous reduction, and reduction by manipulation are relatively easy. The annular ligament is primarily responsible for stability of the proximal radioulnar joint. None of the secondary ossification centers of the elbow is present at birth.The age at appearance of the ossification centers is highly variable; however, the chronologic order is relatively constant. The capitellum is the first to appear, at between 6 months and 2 years of age. The radial head appears at between age 2 and 4 years. The medial epicondyle appears at between 4 and 6 years of age, the trochlea between 9 and 10 years of age, the olecranon between 9 and 11 years of age, and the lateral epicondyle between 9.5 and 11.5 years of age (Fig. 35-1).The trochlea usually develops from multiple sites of ossification. The distal humeral ossification centers, except the medial epicondyle, fuse with one another and then the distal humeral metaphysis between age 14 and 16 years. The medial epicondyle may not fuse until age 18 or 19 years. The wrist joint is surrounded by dense ligamentous and capsular attachments. The triangular fibrocartilage complex (TFCC) consists of the triangular fibrocartilage and the ulnocarpal ligaments. The TFCC firmly attaches to the distal radius, distal ulna, and the volar carpus.This provides a flexible mechanism for stable rotational movements of

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distal phalanges. Fusion of the phalangeal physes begins distally, between ages 13 and 14 years in girls and ages 15 and 16 years in boys.The proximal phalanges are next.The growth plates of the middle phalanges and the metacarpals fuse last, at approximately age 15 years in girls and age 17 years in boys.5 The collateral ligaments and dorsal and volar capsules provide significant stability to the metacarpophalangeal and interphalangeal joints. In the interphalangeal joints and the first metacarpophalangeal joint, the collateral ligaments originate from the head of the more proximal phalanx or metacarpal and insert on the metaphysis of the phalanx. This provides protection for the physis and may account for the low incidence of Salter-Harris type III injuries in these joints. In the second through fifth metacarpophalangeal joints, the collateral ligaments arise from the metacarpal epiphysis and insert on the epiphyses of the proximal phalanges. Salter-Harris type III injuries are relatively more common in these joints.

Remodeling

■ FIGURE 35-1

Order of appearance of ossification centers about the elbow. Though the actual age of appearance is variable, the order of ossification should follow the mnemonic “CRITOE” (Capitellum, Radial head, Internal (medial) epicondyle, Trochlea, Olecranon, External (lateral) epicondyle).

the distal radius and ulna and maintains congruity of the radioulnar joint. It also provides a cushion for forces transmitted through the ulnar-carpal axis. The secondary ossification center of the distal radius appears between 6 and 12 months of age. The center in the distal ulna appears at approximately age 6 years.There may be a separate ossification center at the tip of the ulnar styloid. The distal radial physis fuses at approximately age 17 years in girls and between ages 18 and 19 years in boys. The distal ulna fuses between ages 16 and 17 years in girls and between ages 17 and 18 years in boys. The physes of the distal radius and ulna contribute 75% to 80% of the total growth of the forearm. Development of the carpus and hand occurs in an orderly fashion and is commonly used as a means of assessing overall skeletal maturation.5 The capitate is the only carpal bone that may be ossified at birth.The hamate is the next carpal bone to ossify, beginning by 3 months of age. The other carpal bones are not radiographically apparent until around 30 months.The pisiform is the last to ossify at around 10 years. The scaphoid bone ossifies in a distal to proximal direction. The epiphyses of the metacarpals, except for the first, are distal. The phalangeal epiphyses are proximal. The epiphyses of the metacarpals and proximal phalanges begin to ossify around 1 year of age, followed by the middle and

The ability of children’s bones to undergo a large degree of remodeling aids fracture healing and makes perfect fracture reduction less critical. The age of the child, the distance from the end of the bone, and the degree of angulation are the principal considerations in remodeling. In general, the younger the child, the greater the potential for remodeling.1 Fractures near the end of a long bone in a child with 2 or more years of expected bone growth have good remodeling potential. Remodeling occurs most readily in the plane of the joint and near the end of a bone. Remodeling is poor or nonexistent in intra-articular fractures, fractures with a rotational component, or angular deformities outside the plane of the joint.1,6

BIOMECHANICS Skeletal development is influenced by growth and activity in childhood. Under normal conditions, three types of stress occur: tension, compression, and shear. If these exceed the strength of cartilage or bone, a fracture may result. The bones in children are more porous than in adults. This prevents the propagation of fracture lines and is probably why children’s bones tend to fail in compression. Children’s bones can also fail in tension, which is the mechanism that almost always occurs in adults. With bending, bones almost always fail first on the tension side. If the fracture line does not propagate, an incomplete greenstick type of fracture results. Pediatric bone, compared with adult bone, is also less likely to return to its original shape after a force has been removed; it is less elastic. Therefore, bowing deformity may occur in the absence of an overt fracture. The tensile strength of children’s bones is less than that of ligaments; therefore, mechanisms that might cause ligament injury in an adult are more likely to cause bone injury in children.The physeal cartilage is the weakest site of the growing skeleton. It is weaker than cortical bone, which is, in turn, weaker than ligaments.

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PATHOLOGY Pediatric fractures can be classified into five types: plastic deformation, buckle fracture, greenstick fracture, complete fracture, and physeal injury. Plastic deformation is a manifestation of the ability of children’s bone to absorb more energy prior to fracture than adult bone. This injury is most common in children younger than the age of 5 years. Radiographs reveal a smoothly bowed appearance of the bone without a discrete cortical break (Fig. 35-2). Although this is a common injury of the forearm, it can often be overlooked. Buckle fractures represent compression failure of bone that usually occurs at the junction of the metaphysis and diaphysis (Fig. 35-3). The porous bone of the metaphysis is buckled by the denser bone of the diaphysis. The distal radius is the most common site of buckle fracture in the upper extremity. Greenstick fractures are incomplete fractures typically in the diaphysis of a long bone.These injuries result from a failure of the convex side of a bending bone. The fracture line does not propagate through the concave side (Fig. 35-4). Complete fractures propagate entirely through the bone and may be transverse, oblique, or spiral. Spiral fractures usually result from a rotational force and may be associated with child abuse.Spiral and transverse fractures are relatively

stable and easier to reduce because of the remaining intact periosteum. Oblique fractures are unstable because of their tendency to cause more periosteal disruption. Approximately 15% of all children’s fractures involve the physis. The distal radius is the most frequent site of injury. Physeal fractures are usually classified according to the Salter-Harris system7 (Fig. 35-5). A type I injury is a fracture through the physis that causes widening of the physeal space. Type II fractures extend through the physis and metaphysis. Growth disturbance is an infrequent result of type I and type II injuries. Type III fractures involve the physis and epiphysis, interrupting the articular surface. Type IV injuries involve the metaphysis, physis, and epiphysis. Type V injuries are compression or crushing injuries to the physis. Ogden and Rang have made additions to the original classification.8,9 A type VI lesion involves an injury to the perichondrium at the periphery of the physis. A type VII fracture is an injury to the epiphysis that does not involve the physis. A type VIII lesion involves an injury to the metaphyseal vasculature and impairs enchondral ossification. A type IX injury involves the periosteum and interferes with membranous bone formation. In the original article by Drs. Robert Salter and William Harris, the principal line of fracture was stated to be confined to the hypertrophic zone of the growth plate.7

■ FIGURE 35-2

Plastic deformation (“bowing”) of the radius (short arrow) accompanied by a complete fracture of the ulna (long arrow). Unless there is a direct blow to the forearm, the radius and ulna are usually both injured.

■ FIGURE 35-3 Buckle fractures of the distal radius and ulna. As in this case, this type of fracture most commonly occurs at the junction of the metaphysis and diaphysis.

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883

Experimental studies have since shown that the line of fracture may involve any portion of the growth plate.10 Although most of these injuries heal without complication, damage to the growing physis can cause limb shortening, deformity, and growth arrest. Shapiro has provided a pathophysiologic classification for physeal fractures.11 In type A fractures, the avascular physeal cartilage remains as a barrier between the metaphyseal and epiphyseal vessels. Normal growth continues after cartilage repair. In type B fractures, transphyseal vascular communication occurs secondary to either gross displacement of a type IV SalterHarris fracture or in the setting of physeal crushing or fissuring (which can occur in Salter-Harris type I to V fractures). Type C fractures disrupt the epiphyseal vascularity, causing loss of the physeal chondrocytes. MRI may provide important information regarding the potential for growth disturbance in physeal injuries. Fracture lines that traverse the juxtaepiphyseal region are more likely to result in growth disturbance. Studies have demonstrated that the course of a physeal fracture line can be traced with MRI.12 MRI can also show the early changes of ischemia in the setting of physeal injuries.13 The role of MRI in diagnosis of physeal injuries has not been fully defined; however, it may be important in identifying a subset of patients for whom early intervention may be indicated.

MANIFESTATIONS OF THE DISEASE Injuries of the Clavicle

■ FIGURE 35-4

Both radius and ulna demonstrate plastic deformation. There is also an incomplete, greenstick-type fracture of the radius (arrow).

■ FIGURE 35-5

Salter-Harris classification of physeal fractures. Types I to IV are most common. Type V injuries are the result of compressive forces at the physis. A type VI injury involves the perichondrium. Type VII injuries are isolated epiphyseal lesions. Type VIII injuries involve the juxtaphyseal portion of the metaphysis. A type IX injury involves the periosteum.

The clavicle is the most commonly fractured bone at birth, with a reported incidence of less than 2% after vaginal delivery.14,15 Many (>30%) of these fractures are first identified at follow-up appointments. Risk factors include prolonged labor, high birth weight, shoulder dystocia, and instrumented deliveries.14,15 The mechanism of injury is believed to be axial compression in the birth canal. Affected infants will often demonstrate decreased

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P A R T O N E ● Injury: Pediatric Injuries

■ FIGURE 35-6

A, Female newborn with birth-related clavicle fracture. B, Follow-up study obtained 10 days later demonstrates early healing with prominent callus formation.

movement of the ipsilateral arm (pseudoparalysis). There is an association between birth-related clavicle fractures and Erb’s palsy, which is not surprising in light of the shared risk factors. On examination, there is often a palpable abnormality. Birth-related clavicle fractures are typically undisplaced or minimally displaced, usually occurring at the junction of the middle and lateral thirds of the clavicle (Fig. 35-6). Incomplete fractures require no treatment. Complete fractures are often immobilized by pinning the arm sleeve to the shirt. Uneventful, complete recovery is the norm. Identification of callus formation around a clavicle fracture is useful in determining the age and probable nature of the injury. Birth injuries typically demonstrate dense callus by 6 weeks with complete remodeling by 6 months (Figs. 35-6 and 35-7). Fractures demonstrating absence or a lesser degree of healing are not likely to be the result of birth trauma. After the newborn period, the clavicle is one of the most frequently fractured bones in children, and the most commonly fractured bone around the shoulder, usually involving the midshaft (Fig. 35-8). In a large review of clavicle fractures in children 2 to 16 years of age, approximately half were related to a fall and approximately a fourth were related to other sports injury.16 Typically, fractures result either from a fall onto the point of the shoulder, a fall on an

outstretched hand, a direct blow to the clavicle, or a lateral compression injury. Aside from acute trauma, the distal clavicle can be a site of repetitive microtrauma in young athletes who are involved in cross training and weightlifting.17 Patients usually complain of worsening discomfort around the acromioclavicular joint after workouts.The symptoms relate to stress fracture of the subchondral bone at the distal clavicle, often associated with bench pressing. As with most overuse injuries, treatment involves rest with avoidance of weightlifting. With continued training, symptoms may worsen, leading to interference with activities of daily living.17 Radiographs will often demonstrate osteolysis or cystic changes in the distal clavicle, often most conspicuous with slight cephalic angulation. MRI will demonstrate edema in the distal clavicle.18

■ FIGURE 35-7

A 17-day-old male newborn was referred for palpable abnormality in left clavicular region. Given the patient’s age and extent of callus formation, this healing left clavicular fracture is most consistent with birth-related injury.

■ FIGURE 35-8

3-year-old girl.

Undisplaced clavicular shaft fracture (arrow) in a

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Lateral Clavicular Physis and Acromioclavicular Joint Whereas true acromioclavicular (AC) separations can be seen in older adolescents, AC separations in children are rare.19,20 A direct blow to the AC joint in a younger child will more often result in a lateral physeal injury with tearing of the periosteal sleeve away from the medial fracture fragment.21 The periosteal sleeve is firmly attached to the intact acromioclavicular and coracoclavicular ligaments. The retained periosteal sleeve usually allows for adequate healing and remodeling (Fig. 35-9). True AC separations in older adolescents are clinically and radiologically equivalent to adult AC joint injuries.

Medial Clavicular Physis and Sternoclavicular Joint As with the lateral clavicle, medial clavicular physeal injuries (Salter-Harris I and II) in children and adolescents can mimic true sternoclavicular dislocations.21 These injuries usually occur as a result of a lateral compressive force. If the shoulder is rolled posteriorly during the compressive force, the adjacent first rib will act as a fulcrum and the medial clavicle will be anteriorly displaced. If the shoulder is rolled anteriorly during the compressive force, the result will be posterior displacement of the medial clavicle.2 Posteriorly displaced fractures and dislocations, particularly those with pronounced posterior displacement, are often associated with significant neurovascular and upper mediastinal abnormalities. Consequently, contrast medium–enhanced CT is extremely useful for the diagnosis of regional osseous and extraosseous abnormalities.

Radiography Standard radiographic views of the clavicle typically include straight and cephalad angled anteroposterior projections. The cephalad angled view minimizes superimposition of ribs and scapula. The sternoclavicular joint can be examined with frontal, oblique, and lateral

■ FIGURE 35-9

885

views. Numerous special views such as the “serendipity” view (40-degree cephalad tube angulation centered at the manubrium) (Fig. 35-10) may improve conspicuity of abnormality but can be difficult to perform and interpret. The acromioclavicular joint is commonly examined with anteroposterior views performed with 15 degrees of cephalad angulation to minimize acromial superimposition.

Magnetic Resonance Imaging Magnetic resonance imaging and MR angiography may be useful in the diagnosis of soft tissue and vascular injuries associated with medial clavicle/sternoclavicular injuries (Fig. 35-11).

Multidetector Computed Tomography Computed tomography is the study of choice for sternoclavicular injuries. CT can be useful in discerning medial clavicle physeal injuries from true sternoclavicular separations (Fig. 35-12). Contrast-enhanced CT with multiplanar and 3D reconstruction is extremely useful in the setting of fracture-dislocations involving the medial clavicle and sternoclavicular joints, particularly when there is posterior displacement (see Fig. 35-10). Aside from osseous and joint abnormality, CT permits examination of subjacent vascular and upper mediastinal structures. There is usually little need for CT in the setting of clavicle shaft fractures, although thoracic CT may be indicated in the setting of significant chest trauma with clinical concern for mediastinal injury. Additionally, CT may be helpful in preoperative assessment of severely displaced acromioclavicular or lateral clavicle injuries.

Ultrasonography Blab and associates demonstrated slightly greater accuracy of ultrasonography in diagnosing clavicle fractures in infants as compared with radiography, noting better visualization of greenstick-type fractures. These authors also demonstrated earlier identification of callus when using ultrasonography.22

A, A 9-year-old boy presented with shoulder pain after a sports injury. There is a distal clavicle fracture. The medial fragment is superiorly displaced relative to the coracoid, raising concern for concomitant coracoclavicular ligamentous injury. B, Follow-up radiograph obtained approximately 5 weeks later demonstrates periosteal reaction along the distal clavicle. Note the normal relationship of the coracoid to the periosteal new bone in keeping with intact coracoclavicular ligaments.

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■ FIGURE 35-10

Anteroposterior (A) and serendipity (40-degree cephalad angulation) (B) radiographs demonstrate asymmetry of sternoclavicular joints and dorsally angulated medial clavicle fracture. Axial CT image (C) and 3D reconstruction (D) demonstrate dorsally angulated fragment with surrounding hematoma. There is mild associated narrowing of the subjacent left subclavian vein.

■ FIGURE 35-11

A, Radiograph of a 12-year-old girl after a motor vehicle accident. Mild deformity of the distal right clavicle (arrow) was overlooked on the initial chest radiograph. B and C, MR images obtained 9 days later for persistent right shoulder pain demonstrate bone marrow edema and mild deformity of the distal clavicle in keeping with an undisplaced fracture (arrows).

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■ FIGURE 35-12

A to C, Salter-Harris type IV injury of the medial clavicle in a 16-year-old boy. Note fracture involving both the medial clavicular epiphysis and metaphysis (arrows) with posterior displacement. The medial clavicular epiphysis articulates with the sternum.

Scapular Fractures Scapular fractures in infants should be viewed as highly specific for nonaccidental trauma23,24 (Fig. 35-13). As in adults, scapular body fractures are typically the result of high-energy trauma to the thorax, usually with significant concomitant thoracic injuries, including chest wall and

neurovascular injuries. Scapular fractures are associated with longer hospital stays, higher injury severity scores, and greater mortality.25 These fractures may be easily missed on preliminary radiography, particularly when there are significant associated injuries. Coracoid process fractures can result from significant direct trauma, including humeral head impaction with anterior glenohumeral dislocation, or indirect trauma related to myotendinous or coracoclavicular ligament avulsive forces. There is a strong association between coracoid fractures and acromioclavicular injuries.26

Radiography Scapular body fractures may be evident on initial chest radiographs obtained in trauma patients. Dedicated radiographic views including anteroposterior and particularly scapular Y-views will aid in detection of fractures and fragment separation (Fig. 35-14). The axillary view is useful for identification of extra-articular glenoid fractures. Coracoid fractures are often not evident on anteroposterior views. Anteroposterior views with cephalic angulation of at least 30 degrees and Stryker views have been reported to improve detection of coracoid fractures.26

Computed Tomography

■ FIGURE 35-13

Right acromion fracture (arrow) in 6-week-old female newborn related to nonaccidental trauma.

Multidetector CT with multiplanar and 3D reconstructions may be helpful in defining fracture morphology (see Fig. 35-14). Usually the scapula is included in CT examinations performed on patients with significant thoracic trauma.

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P A R T O N E ● Injury: Pediatric Injuries

■ FIGURE 35-14

A 14-year-old boy with scapular body fracture as seen on axillary (A) and Y views (B). CT without contrast enhancement in the same patient (axial [C] and oblique [D] coronal reformatted images) similarly demonstrates fracture alignment.

Injuries of the Glenohumeral Joint, Rotator Cuff, and Proximal Humerus Glenohumeral Dislocation Glenohumeral dislocation within the first decade of life is rare. It is most common in adolescents and young adults. In a series of 500 glenohumeral dislocations, less than 2% were observed in children up to 10 years of age, whereas approximately 20% were diagnosed in patients in the second decade of life.27 Another large series found approxi-

mately 40% of dislocations occurred in patients younger than 22 years old.28 More than 90% of glenohumeral dislocations are anterior dislocations.20,29 The precipitating trauma is often related to contact sports. External rotation of an abducted shoulder is a common mechanism of injury. Alternatively, an anteriorly directed force to the posterior aspect of the shoulder can also result in anterior dislocation. Acute anterior dislocation results in impaction of the posterolateral humeral head against the anterior inferior glenoid with resultant Hill-Sachs deformity of the humeral head in many if not most cases.30 Less frequently

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observed fractures include avulsions of the anterior inferior glenoid rim (Bankart lesion) and greater tuberosity humeral fractures.30 Based on arthroscopy in a series of 45 patients with recent anterior dislocations, Baker and colleagues demonstrated capsular tears in all patients and labral detachments in approximately 87% of patients.31 Pediatric and adolescent patients with anterior dislocation have very high rates of recurrent instability with reported recurrent dislocation rates of 75% to 100%.32 Factors increasing the risk for recurrent dislocation include short or inadequate rehabilitation, younger age at time of initial injury, and evidence of Hill-Sachs deformity.30,32 There is controversy regarding the relative benefit of surgical stabilization versus rehabilitation for recurrent instability. Several more recent reports demonstrated better outcomes in patients treated operatively.33,34 Posterior dislocation of the shoulder is rare, accounting for less than 3% of glenohumeral dislocations.20 These tend to result from an axial load applied to an adducted internally rotated arm and are encountered as sports injuries. Glenoid hypoplasia and retroversion can contribute to posterior instability. Posterior dislocations are believed to be frequently overlooked, probably related to inadequate lateral imaging. There are

■ FIGURE 35-15

A, Radiograph of a birthrelated humeral shaft fracture. B, Ultrasound image of both proximal humeri of a different newborn demonstrates right proximal humeral Salter-Harris type II fracture (arrow) with mild epiphyseal angulation. C, Follow-up radiograph of the humerus nearly 3 weeks later demonstrates pronounced callus formation around the healing fracture.

889

often associated posterior capsulolabral or bony avulsions of the posterior glenoid (reverse Bankart lesion) and impaction injuries of the anterior humeral head (“trough line sign”).35 As compared with anterior dislocations, recurrence rates are believed to be lower with better response to conservative therapy.

Rotator Cuff Injuries Rotator cuff tendinitis and muscle strain are frequently encountered in skeletally immature athletes in overhead and throwing sports, although rotator cuff tears are extremely rare. Most rotator cuff tendinitis in young athletes probably relates to laxity and muscle imbalance as opposed to impingement at the coracoacromial arch.30 Treatment of rotator cuff tendinitis is usually conservative with nonsteroidal anti-inflammatory medications and physical therapy.17

Proximal Humeral Fractures Humeral shaft fractures are the second most common birth-related fracture and share the same risk factors and clinical presentation of the more common birthrelated clavicle fracture. These are typically transverse fractures of the proximal-to-mid shaft36 (Fig. 35-15).

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P A R T O N E ● Injury: Pediatric Injuries

■ FIGURE 35-16

Healing proximal humeral metaphyseal fracture in 1-month-old male newborn.

Beyond the newborn period, acute and healing humeral fractures other than supracondylar fracture in children younger than 3 years of age should raise significant concern for nonaccidental trauma.37 In particular, spiral or oblique fractures indicate a forceful twisting mechanism. Metaphyseal corner fractures, as in other locations, are highly specific for nonaccidental trauma (Fig. 35-16). Transverse fractures typically result from direct trauma36 (Fig. 35-17).

■ FIGURE 35-17

A 6-month-old infant presented with an early healing proximal humeral fracture (vertical arrow). There is also an ipsilateral distal radial fracture (angled arrow).

In children older than 3 years, most humeral fractures are the result of direct trauma and often sports related. These are typically transverse or short oblique fractures.36 Surgical neck fractures are the second most common injury around the shoulder in children and adolescents and often involve the proximal humeral physis.19 Alignment of proximal humeral fracture fragments depends on relation of the fracture line to the rotator cuff and deltoid insertions and pectoralis major origin as well as thinner periosteum along the anterior aspect of the proximal humerus. Fractures involving the proximal humeral epiphyseal plate are graded according to the Neer-Horowitz classification depending on the degree of displacement.38 Because of the close anatomic relations, fractures of the mid-distal portions of the humeral shaft can be associated with radial nerve injury. Fortunately, there is almost always complete recovery with rare need for surgical exploration. Proximal humeral fractures in neonates and children younger than 5 years are usually Salter-Harris type I injuries. In children ages 5 through 11 years, metaphyseal fractures are most common (Fig. 35-18), whereas Salter-Harris type II fractures predominate in older children and adolescents (Fig. 35-19).

■ FIGURE 35-18

a 6-year-old boy.

Proximal humeral metaphyseal fracture after a fall in

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891

■ FIGURE 35-19

Adolescent male with sports-related Salter-Harris type II proximal humeral fracture as demonstrated on anteroposterior (A) and axillary (B) radiographs.

The proximal humeral physis can be a site of sportsrelated stress and overuse.30 Little Leaguer’s shoulder refers to a condition in which there is gradual onset of shoulder pain in an overhead throwing athlete. On physical examination there is often pain to palpation over the lateral aspect of the proximal humerus. Complex distraction and twisting forces during throwing appear to cause damage to the physeal plate. Widening of the physis is evident on internal and external rotation anteroposterior radiographs. Often, findings are subtle and comparison views of the unaffected contralateral shoulder are useful.39 Pathologic fractures of the proximal humerus related to tumors and tumor-like conditions of bone can occur with minor trauma (Fig. 35-20). The proximal humerus is the most common site of unicameral bone cysts.40

Radiography Radiography is almost always the initial means of examination for injuries of the shoulder and proximal humerus. Anteroposterior projections can be obtained with neutral, internal rotation, and external rotation positioning. Views defining the anatomic relationship between the glenoid and humeral head including Y, axillary, transthoracic, and Grashey (true anteroposterior) views are critical in the setting of trauma30 (Fig. 35-21). A Hill-Sachs fracture will often be most conspicuous on axillary and internally rotated anteroposterior projections. Like other long bones, the humeral shaft is typically examined with anteroposterior and lateral views.

Magnetic Resonance Imaging Magnetic resonance imaging is extremely useful for examination of the labrum and glenohumeral ligaments in the setting of acute dislocation or recurrent instability.

■ FIGURE 35-20

Unicameral bone cyst. There is a mildly expanded lucent lesion in the proximal humerus. A pathologic fracture is present in the lateral cortex.

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P A R T O N E ● Injury: Pediatric Injuries

■ FIGURE 35-21

A and B, Anterior shoulder dislocation in a 16-year-old boy. C, Note Hill-Sachs deformity on postreduction radiograph (arrow).

MR arthrography is the study of choice in imaging glenohumeral instability in young, athletic patients30,41 (Fig. 35-22). In addition to imaging in neutral position, images obtained with the arm in an abducted, externally rotated position increase sensitivity for anterior labral abnormality. MRI is also useful for examination of the rotator cuff muscles and tendons. Tendinopathy and partial-thickness tendon tears will demonstrate abnormalities in T2 signal characteristics, as discussed elsewhere in this volume. As with other chronic growth plate injuries, MRI of Little Leaguer’s shoulder will demonstrate physeal widening and irregularity with vertical and horizontal fractures and extension of physeal cartilage signal into the metaphysis.30,42,43

Computed Tomography Computed tomography is rarely used for the examination of childhood shoulder and proximal humeral injuries, although multidetector CT with multiplanar and 3D reformatted images provides excellent detail of complex bony injuries that may be incompletely assessed with radiography. This information may be useful for determining need for internal fixation of complex injuries and SalterHarris fractures.

Ultrasonography As with infant hips, ultrasonography can be useful for determining the location of the nonossifed humeral head in term and premature infants. Additionally, proximal humeral physeal injuries in newborns may be better visualized with ultrasound as compared with radiography.44 Good correlation has been demonstrated between sonography and both arthroscopy and MRI evaluation of rotator cuff pathology.45 Ultrasonography offers a fast, inexpensive and easily tolerated examination when done by an experienced sonographer.

Injuries of the Elbow Supracondylar Fractures

■ FIGURE 35-22 Glenolabral articular disruption. An axial T1weighted image from a shoulder MR arthrogram demonstrates disruption of the glenoid articular cartilage in this patient with a history of shoulder dislocation. (Courtesy of John Mackenzie, MD.)

The most common fractures about the elbow occur in the supracondylar region with highest incidence between ages 3 and 8 years. Supracondylar fractures account for 60% of injuries to children’s elbows. This area is particularly susceptible to injury owing to the very thin central area of bone interposed between the coronoid and olecranon fossae. Extension-type fractures account for 95% of supracondylar fractures, usually resulting from a fall on an outstretched hand with the elbow hyperextended. These fractures have been classified by Gartland as type I, undisplaced (Fig. 35-23); type II, angulated but hinged on an intact posterior cortex; and type III, complete and posteriorly displaced.46 Much less common is a hyperflexion injury that occurs secondary to a fall on the olecranon with the elbow flexed (Fig. 35-24). On a lateral radiograph of the elbow, displacement of fat pads provides an

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893

■ FIGURE 35-23

Undisplaced supracondylar fracture. A, A lateral view of the elbow demonstrates a posterior fat pad sign indicating a joint effusion (arrow). Notice that a line drawn along the anterior humeral cortex still passes through the middle third of the capitellar ossification center. B, A frontal view reveals a subtle supracondylar fracture line (arrow).

important clue to localize the elbow as a site of pathology. There is commonly posterior displacement of the capitellum relative to the humeral shaft (Fig. 35-25). Plain radiographs are usually adequate for diagnosis. Type I fractures are managed by immobilization. Type III fractures require closed reduction with pin placement or open reduction if irreducible (Fig. 35-26). Management of type II fractures is based on the achievable reduction as well as rotation and angulation of the distal fragment. Reduction is considered satisfactory if the anterior humeral line passes through the capitellum ossification center on a lateral radiograph.47 Cubitus varus (Fig. 35-27) is the most

common long-term complication of these fractures, occasionally requiring osteotomy. Nerve and vessel injuries can also occur with supracondylar fractures; therefore, neurovascular assessment, both before and after reduction, is extremely important. T- or Y-condylar fractures are less common variants of supracondylar injury, occurring in an older age group. There is a transverse supracondylar fracture with an additional longitudinal intra-articular component.The mechanisms of injury are similar to those producing supracondylar fractures but are of higher energy. It has been postulated that the olecranon acts as a wedge in these injuries, splitting the trochlea.

Lateral Condyle Fractures

■ FIGURE 35-24

Flexion-type supracondylar fracture. The anterior humeral line passes posterior to the capitellar ossification center. Only a small percentage of supracondylar fractures result from a flexion injury.

Lateral condyle fractures account for 10% to 15% of elbow fractures in children. These injuries are most common in children between 3 and 8 years of age. This is usually a Salter-Harris type IV injury. The fracture line involves a small portion of the metaphysis and extends into the mostly unossified epiphysis. The mechanism of injury is most commonly a varus stress to an extended elbow. The stability of these fractures is determined by the epiphyseal extent of the fracture line (Fig. 35-28) and the degree of displacement. Type A fractures have minimal or no displacement and do not extend to the articular surface. Type B fractures are identical to type A but they extend to the articular surface. Type C fractures are complete and involve a fracture gap that is as wide medially as it is laterally48 (Fig. 35-29). The size of the metaphyseal fragment is variable and, particularly in younger patients, can be very small (Fig. 35-30). Oblique radiographs may help to identify the metaphyseal component and may be more accurate in assessing fracture gap and stability. The condylar fragment may also be severely displaced and rotated.

894

P A R T O N E ● Injury: Pediatric Injuries

■ FIGURE 35-25

Type II supracondylar fracture in a 5-yearold. A, A joint effusion is present. The distal humerus, including the capitellar ossification center, is posteriorly displaced relative to the humeral shaft. A line drawn along the anterior humeral cortex passes anterior to the capitellum. B, A normal anterior humeral line, drawn along the anterior cortex, should pass through the middle of the capitellar ossification center.

■ FIGURE 35-27

■ FIGURE 35-26

Type III supracondylar fracture in a 5-year old. There is complete displacement of the distal humeral fragment (arrow).

Cubitus varus after supracondylar fracture. Two months after sustaining a supracondylar fracture, periosteal new bone formation and bony remodeling are noted with increased varus angulation. This is the most common complication of supracondylar fracture.

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895

■ FIGURE 35-28 Lateral condyle fracture classification. A, A type I lateral condyle fracture line involves the distal humeral cartilage but does not extend to the articular surface. B, A type II fracture extends to the articular surface but is not displaced. C, A type III fracture is complete with a displaced fragment.

Fractures displaced less than 2 mm may be treated conservatively with splinting and close follow-up. However, many surgeons elect treatment with percutaneous pinning because late displacement has been reported in up to 10% of these patients.47 Type B and C fractures are potentially unstable and require internal fixation.47,49 A nonunion may result if there is inadequate fixation or a late presentation (Fig. 35-31). This may cause pain, particularly in the dominant arm. Treatment is controversial. Some advocate no treatment or delayed treatment until close to physeal closure. Others suggest internal fixation with bone grafting.49

Medial Epicondyle Fractures

■ FIGURE 35-29

Displaced lateral condyle fracture. A type C lateral condyle fracture extends to the articular surface with a displaced fragment.

■ FIGURE 35-30

Subtle lateral condyle fracture. A, Initial radiograph reveals a nondisplaced lateral condyle fracture with a tiny metaphyseal component (arrow). B, A follow-up radiograph 1 month later shows periosteal reaction of fracture healing (arrow).

Ten percent of pediatric elbow fractures involve the medial epicondyle. Up to 50% of these fractures are associated with elbow dislocation (Fig. 35-32). These injuries typically occur in older children with a peak age of incidence between 9 and 14 years. The injury involves an avulsion fracture of the epicondyle in the setting of a valgus stress. On plain radiographs, these

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P A R T O N E ● Injury: Pediatric Injuries

■ FIGURE 35-31

Nonunion of lateral condyle fracture. A radiograph reveals an irregular ossific fragment at the lateral aspect of the distal humerus consistent with a fracture nonunion (arrow).

■ FIGURE 35-33

injuries have the appearance of Salter-Harris type I fractures (Fig. 35-33); however, because the medial epicondyle is an integral component of the distal humeral epiphysis, they are actually Salter-Harris type III or IV injuries. The epicondyle is variably displaced (Fig. 35-34)

and may dislocate into the joint space that is widened by the valgus stress. When the stress is removed, the epicondyle can become entrapped in the joint (Fig. 35-35). It is important to not mistake the entrapped epicondyle for the trochlear ossification center. There should not

■ FIGURE 35-32

Minimally displaced medial epicondyle fracture. The medial epicondyle is avulsed with a small metaphyseal component. Also note the associated soft tissue swelling at the medial aspect of the elbow (arrow).

Medial epicondyle fracture with elbow dislocation. A, A frontal view shows the proximal radius and ulna are laterally dislocated. The avulsed medial epicondyle ossification center is displaced and entrapped in the joint space (arrow). B, The avulsed ossification center is also seen on the lateral view (arrow).

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897

■ FIGURE 35-34

Medial epicondyle fracture with displaced fragment. A, Radiograph shows medial soft tissue swelling. A portion of the medial epicondyle remains normally positioned (short arrow). An avulsed fragment is displaced inferiorly (long arrow). B, Axial CT image shows the normally located portion in a relatively posterior location (arrow). C, The avulsed fragment is inferiorly displaced and rotated but not entrapped in the joint space (arrow).

be a visible trochlear ossification center prior to the center of the medial epicondyle. Clinically, there is swelling and tenderness localized to the medial aspect of the joint. Children who engage in activities that place significant valgus stress on the elbow, such as gymnastics and pitching, are at particular risk for medial epicondyle fractures. Undisplaced and minimally dis-

■ FIGURE 35-35

Mechanisms of medial epicondyle injury. A, Normal medial epicondyle. B, Avulsed and displaced medial epicondyle. C, Avulsed medial epicondyle entrapped in the joint space.

placed medial epicondyle fractures are typically treated with splinting. If there is more than 5 mm displacement, treatment is variable. The only absolute indication for surgery is irreducible entrapment of the fracture fragment in the joint or an open fracture.47 Athletes, particularly gymnasts and pitchers, are often treated with internal fixation.47

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P A R T O N E ● Injury: Pediatric Injuries

epicondyle ossification center may be confused with a fracture (Fig. 35-36).

Distal Humerus Fracture Separation Fracture separation of the distal humerus is rare in children. It occurs most commonly between 2 and 3 years of age. Although the fracture line may be limited to the physis, it is most commonly a Salter-Harris type II fracture of the distal humerus. These injuries are often mistaken for fractures of the lateral condyle, supracondylar fracture, or elbow dislocation. In contrast to a true dislocation of the elbow, the radiocapitellar articulation is maintained (Fig. 35-37). Also, the distal fracture fragment is usually displaced posteromedially; elbow dislocations are usually lateral (see Fig. 35-32). If a diagnosis of elbow dislocation is entertained in a very young patient, there should be a high level of suspicion of a fracture separation. Birth trauma, fall onto an extended arm, and nonaccidental injury are potential mechanisms. If the diagnosis is uncertain, multidetector CT, ultrasonography, MRI, or arthrography may be necessary. Reduction with pin fixation is the usual treatment. ■ FIGURE 35-36

Normal lateral epicondylar ossification center. This early lateral epicondyle ossification center (arrow) may be confused for an avulsion fracture. This irregular appearance is common. True fractures in this location are infrequent.

Lateral Epicondyle Fractures Fractures of the lateral epicondyle are infrequent. These injuries are most common in children approaching skeletal maturity and often accompany elbow dislocation. The normal irregular appearance of the lateral

Fractures of the Proximal Radius Fractures of the proximal radius account for 4% to 5% of elbow injuries in children. These injuries vary from those of adults in that they usually involve the radial neck and physis rather than the head (Fig. 35-38). The mechanism of injury is a fall on an outstretched hand with additional valgus stress that causes compression of the radial head against the capitellum. This mechanism may also cause associated injuries, such as fractures of the medial epicondyle, olecranon, proximal ulna, or lateral condyle or tears of the medial collateral ligament20 (Fig. 35-39). These inju-

■ FIGURE 35-37

Fracture separation of the distal humeral epiphysis. Lateral (A) and frontal (B) views. The tiny metaphyseal component of the fracture can be seen on the lateral view (arrow). Although the radiocapitellar alignment is maintained on both views, there is medial displacement of the radius, ulna, and humeral epiphysis. (With permission from Karasick D, Burk DL, Gross GW. Trauma to the elbow and forearm. Semin Roentgenol 1991; 26:318–330.)

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899

■ FIGURE 35-38

A frontal image of the elbow demonstrates buckling of the cortex in the lateral radial neck, a common pediatric fracture pattern (arrow). The radial head remains in normal alignment relative to the capitellum.

■ FIGURE 35-40

ries often result in angulation of the radial head relative to the shaft. The proximal radius may also be fractured in the setting of a posterior elbow dislocation (Fig. 35-40). These fractures usually occur through the physis and may occur at the time of dislocation or during spontaneous reduction.

The radial head epiphysis may be displaced anteriorly or posteriorly. There is controversy in the orthopedic literature regarding acceptable reduction. Fifteen to 30 degrees of angulation is widely accepted if there is significant

■ FIGURE 35-39

Radial neck fracture with associated injury. Frontal (A) and lateral (B) views of the elbow demonstrate a fracture of the radial neck (short arrows). An associated undisplaced fracture of the proximal ulna is also noted (long arrow). Associated injuries are usually the result of distraction in the medial joint.

Radial head dislocation. A sagittal T2-weighted MR image reveals posterior radial head dislocation as well as a fracture involving the cartilaginous radial head (arrow).

900

P A R T O N E ● Injury: Pediatric Injuries

■ FIGURE 35-41

Greenstick fracture of olecranon in a 6-year-old (arrow). Because of the thick periosteum surrounding the olecranon, fractures in this location are frequently minimally displaced or incomplete.

remaining growth potential. Open reduction is generally recommended if there is greater than 45 to 60 degrees of residual angulation after attempted closed or percutaneous reduction.50

■ FIGURE 35-43

Olecranon stress injury. A sagittal fluid-sensitive sequence reveals bone marrow edema in the olecranon (arrow) in this 15-year-old baseball pitcher.

Olecranon Fractures Olecranon fractures account for 4% to 6% of elbow fractures in children. The mechanisms are various, including hyperextension, hyperflexion, direct blow to a flexed elbow, or a shear force. There is a very thick periosteum surrounding the proximal ulna, and these injuries are often minimally displaced greenstick fractures (Fig. 35-41). There may be associated elbow injuries, such as radial neck fractures, medial epicondyle fractures, coronoid fractures, and osteochondral injuries. The fracture line may extend transversely through the olecranon process (Fig. 35-42). However, longitudinal fractures can also

■ FIGURE 35-42

Displaced fracture of the olecranon in a 16-year old. The olecranon fracture fragment is displaced secondary to traction from the triceps tendon.

occur. A wide separation of the metaphysis and apophysis should not be mistaken for a fracture. If there is less than 3 mm of displacement, treatment is conservative. Intraarticular fractures require open reduction and internal fixation. The olecranon is also a potential site of stress injury, predominantly related to repetitive overuse, for example, as a result of baseball pitching (Fig. 35-43).

Radial Head Subluxation Subluxation of the radial head is a common injury in toddlers and preschool children with a peak incidence between 1 and 3 years of age. It is variously referred to as a “pulled elbow” or “nursemaid’s elbow.” This injury occurs when there is sudden traction on the hand or forearm with the elbow extended and pronated. The oval radial head slips under the annular ligament. As the traction is released, the ligament becomes entrapped between the radial head and the capitellum.51 Children typically present with refusal to move the arm, which is often held in a partially flexed and pronated position. The diagnosis is often established clinically; however, radiographs may be obtained to exclude another injury (Fig. 35-44). The subluxation is reduced by forceful supination of the forearm. This injury rarely occurs after 5 years of age because of progressive thickening of the annular ligament.51

Elbow Dislocation Although uncommon, the elbow joint is the most frequent site of dislocation in children. The peak incidence is

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901

■ FIGURE 35-44

Radial head subluxation. Frontal (A) and lateral (B) radiographs of the elbow. This infant’s mother heard a “popping” sound in the left elbow that was reproducible on physical examination. Although the capitellar ossification center is not yet visible in this 2-month old, the radial head is displaced from its expected location.

during the second decade. Pure dislocations, without an accompanying fracture, are unusual. Posterior dislocations are most common and may be accompanied by fractures of the medial epicondyle or coronoid process. The proximal radius and ulna are bound by the annular ligament and interosseous membrane and usually dislocate together. Recurrent dislocation and chronic instability after elbow dislocation is rare. The high incidence of accompanying fractures allows chondro-osseous failure, rather than true ligament failure. Dislocation of the radial head is very rare as an isolated injury in children. It is usually related to Monteggia fracturedislocations. Congenital dislocations may be distinguished from traumatic injuries by dysplastic changes in the radiohumeral joint. In the setting of congenital dislocation, the radial head is often dome shaped without a central depression.

Sports Injuries about the Elbow Sports injuries about the elbow are commonly associated with throwing sports and gymnastics. The forces involved are typically distraction of the medial elbow joint and compression laterally. In children with open growth plates, the patterns of injury that result are distinct from those of older athletes because the physis is the weakest point and a common site of injury. An avulsion fracture of the medial epicondyle may result from an acute valgus stress to the elbow. More chronic abnormalities of the growth plate of the medial epicondyle, including overgrowth, separation, and fragmentation, are often observed in young athletes prior to physeal closure. These injuries are treated conservatively and may be observed on radiographs even in the absence of clinical symptoms.52 After physeal closure, medial epicondylitis and injuries of the ulnar collateral ligament are more common. They can be distinguished on MRI; however, they

may coexist. Medial epicondylitis is an avulsion injury of the common flexor tendon at its medial epicondylar insertion. The common flexor tendon is just superficial to the ulnar collateral ligament and may demonstrate thickening, increased T1 and T2 signal, and surrounding edema on MRI. Injuries of the ulnar collateral ligament usually involve the anterior bundle. On MRI, the ligament may be poorly defined or thickened with abnormal increased T1 and T2 signal. The ulnar collateral ligament may have higher T1 and T2 signal before physeal closure that should not be misinterpreted as abnormal.30 Radiographs occasionally show calcification at the medial aspect of the joint. Osteochondral injuries of the capitellum can cause lateral elbow pain. Progressive cases are often referred to as osteochondritis dissecans. This entity should be distinguished from Panner’s disease, which is a self-limited osteochondrosis of the capitellum. Panner’s disease typically occurs between 4 and 8 years of age and usually involves no specific traumatic event. Almost all cases resolve spontaneously without residual radiographic or functional abnormality. Osteochondritis dissecans of the capitellum is believed to be the result of repetitive valgus compression, resulting in an osteochondral fracture (Fig. 35-45).This injury is most common in boys 10 to 15 years of age, usually in the dominant arm. Lateral epicondylitis is more common than medial epicondylitis but is more frequently seen in adults.This is related to repetitive trauma to the extensor tendon and lateral epicondyle apophysis, frequently occurring in racquet sport athletes.

Radiography True anteroposterior and lateral views of the elbow should be obtained at a minimum. A true lateral view can be confirmed by identifying the “teardrop” shape of the distal humerus, formed by the olecranon and coronoid fossae.

902

P A R T O N E ● Injury: Pediatric Injuries

■ FIGURE 35-45

Osteochondritis dissecans in a 13-year old boy. Lucency and irregularity are noted in the subchondral capitellum consistent with osteochondritis dissecans.

■ FIGURE 35-46

Additional oblique views may help to further determine the character and extent of injury. Comparison views of the contralateral extremity may be obtained if there is difficulty in distinguishing true abnormalities from a growth variant; however, these are not usually necessary and a more experienced observer’s opinion is likely to resolve most questions. Routine examination of the contralateral limb is prohibited by many national guidelines for imaging. A number of lines have been described to help assess the radiographic anatomy of the elbow. The anterior humeral line is drawn along the anterior cortex of the humerus. On a true lateral elbow radiograph, it should normally pass through the middle third of the capitellar ossification center (see Fig. 35-25). If this line is anterior to the middle third of the capitellum, it suggests posterior angulation of the distal humerus, usually in the setting of a supracondylar fracture. The radiocapitellar line, drawn along the long axis of the radius, should pass through the capitellum on all views (Fig. 35-46). If it does not, the radial head is likely dislocated. The Baumann angle is formed by the intersection of a line drawn along the physis of the capitellum and a line perpendicular to the long axis of the humerus on a true anteroposterior view of the elbow49 (Fig. 35-47). It describes the degree of varus angulation and is used to evaluate the adequacy of reduction of supracondylar fractures. A normal Baumann angle is 70 to 75 degrees. The Baumann angle in a fractured elbow should be within 10

Radiocapitellar line. Frontal (A) and lateral (B) radiographs of the elbow. A line through the long axis of the radius should pass through the capitellar ossification center on all views, as in this case. If it does not, the radial head is subluxed or dislocated.

CHAPTER

■ FIGURE 35-47

35

● Upper Extremity Injuries in Children (Including Sports Injuries)

The Baumann angle describes the degree of angulation between a line perpendicular to the long axis of the humerus and a line along the capitellar physis. It is normally 70 to 75 degrees.

■ FIGURE 35-48

Elbow effusion. A, Lateral elbow. Displacement of anterior (short arrow) and posterior (long arrow) fat pads indicates a joint effusion. B, Frontal view. No obvious fracture line is identified in this case. However, in the setting of trauma, the presence of an elbow effusion should prompt a careful search for fracture.

903

degrees of the opposite side to keep the change in carrying angle to less than 5 degrees. Examination of the fat pads about the elbow helps to determine the presence or absence of a joint effusion. Both anterior and posterior fat pads are extrasynovial, intracapsular structures. On a normal lateral view of the elbow, the anterior fat pad can be identified as a thin, dark line that parallels the anterior humerus.The posterior fat pad lies deep in the olecranon fossa and is not normally seen on a lateral radiograph. In the presence of an elbow effusion, the posterior fat pad is displaced and becomes visible (Fig. 35-48). Although an elbow effusion is not specific for a fracture, it should prompt a careful search. Recent studies using MRI to study patients with elbow effusion suggest a high incidence of undisplaced fractures. Some of these fractures may not show periosteal reaction on plain radiographic follow-up,53 which has commonly been used as a gold standard for the presence of fracture. In young children, subtle supracondylar fractures and nondisplaced fractures of the lateral condyle should be considered. Subtle fractures of the radial neck may be present in older children. Fractures of the proximal olecranon and radial neck may occasionally not cause a joint effusion. Ultrasound examination is a simple and effective means of detecting joint effusions. Anatomic variations in the appearance of the elbow can be misinterpreted as disease. A fragmented or irregular appearance of the ossification center is particularly common in the capitellum and trochlea.The ossification center of the lateral epicondyle frequently has a linear or flake-like appearance that should not be mistaken for an avulsion fracture. The posterior location of the medial epicondyle should also not be mistaken for a displaced fracture on a rotated lateral view (Fig. 35-49).

904

P A R T O N E ● Injury: Pediatric Injuries

■ FIGURE 35-49

Improper positioning for lateral elbow radiograph. The medial epicondyle should project through the distal humerus on a normally positioned lateral view. Slightly oblique positioning will cause the medial epicondyle to appear posterior to the humerus (arrow).

■ FIGURE 35-50

Magnetic Resonance Imaging Magnetic resonance imaging can be an especially powerful tool in examination of children’s elbows because of its ability to provide high-resolution images of numerous radiolucent structures. T1-weighted sequences are useful for anatomic evaluation, and proton density–weighted, T2weighted fast spin-echo, and 3D gradient-echo sequences demonstrate disease and cartilaginous structures. MRI has helped to elucidate a broad spectrum of abnormalities that cannot be appreciated on plain radiographs. Not all of these findings will affect patient management, but MRI can provide additional information that may affect treatment in select cases. MRI can distinguish stable lateral condyle fractures that terminate in the humeral epiphysis from unstable fractures that extend to the articular surface (Fig. 35-50).This can be difficult to determine with plain radiographs because the distal humeral epiphysis remains largely unossified in most cases. In patients with persistent elbow pain, MRI can be used to identify osteochondral lesions that are not seen radiographically (Fig. 35-51). If there is established osteochondral disease, MRI can provide important information regarding (1) the size of the lesion, (2) the integrity of the overlying cartilage, (3) stability, and (4) the presence of associated loose bodies. The normal MRI appearance of the preossification center has been described by Chapman and coworkers.54 Histologically, this represents the stage of chondrocyte hypertrophy before mineralization. They described the appearance as lobular in configuration with increased signal on T2-weighted sequences (Fig. 35-52). This should not be confused with a traumatic, infectious, or ischemic lesion.

Unstable lateral condyle fracture. A lateral condyle fracture was noted on plain radiographs; however, this coronal, fatsuppressed T2-weighted sequence clearly demonstrates extension of the fracture line to the articular surface (arrow), which could not be determined with plain radiographs. Fracture lines that extend to the articular surface, rather than terminating in the epiphysis, are unstable and require internal fixation.

Multidetector Computed Tomography Multidetector CT (MDCT) provides rapid scanning time and 3D postprocessing capabilities. Attention must be paid to dose optimization. Chapman and coworkers have described a multidetector CT protocol for the examination of elbow injuries in children using automatic tube-current modulation.55 They found that optimal dose reduction was achieved by placing the patient’s flexed arm above the head such that the elbow joint is above the vertex of the skull and the long axis of the forearm is angled into the x-y plane (Fig. 35-53). MDCT has advantages relative to MRI in increased speed and decreased need for patient sedation. It is also less user-dependent than ultrasonography and less painful than arthrography. MDCT is particularly useful in imaging fractures and determining relationships of fracture fragments.The use of MDCT for injuries of children’s elbows has been described in the setting of supracondylar fractures, fracture separation of the distal humeral epiphysis, fractures of the lateral condyle, fractures of the proximal radius, and post-traumatic elbow effusions (Fig. 35-54). CT is also useful for the diagnosis of loose bodies or fragmented osteochondral lesions. Displaced medial epicondyle fractures can also be identified with CT (see Fig. 35-34).

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905

■ FIGURE 35-51

Subtle capitellum osteochondritis dissecans. A, There is subtle irregularity of the capitellum (arrow) in this patient with lateral elbow pain. B, Sagittal T1-weighted MR image shows the defect to better advantage. Note low signal intensity in the subchondral area (arrow). C, Coronal inversion recovery MR image. Associated increased signal is present. The overlying cartilage is intact.

■ FIGURE 35-52

Preossification center of trochlea in a 6-year-old boy. A, Coronal T2-weighted MR sequence. The trochlea is homogeneously increased in signal intensity (arrow). B, Coronal T1-weighted MR sequence. The trochlea ossification center is homogeneously low in signal intensity (arrow). This is the normal MR appearance of the ossification center before ossification, during the stage of chondrocyte hypertrophy, and should not be mistaken for a pathologic process.

906

P A R T O N E ● Injury: Pediatric Injuries

Classic Signs: Elbow Injuries ■

■

■

■

■ FIGURE 35-53

Recommended multidetector CT positioning for elbow imaging. The flexed elbow is above the patient’s head and angled in the x-y plane. This position provides optimal dose reduction.

Ultrasonography Ultrasonography of the child’s elbow with a linear transducer allows imaging of unossified soft tissues as well as provides dynamic information. This may be useful in diagnosis of fractures and joint effusions. Markowitz and colleagues described two cases of transphyseal fracture of the elbow in which ultrasonography clarified the diagnosis and provided additional information regarding fracture stability.56 Intraoperative ultrasonography may also provide a less invasive means of assessing the adequacy of fracture reduction. Ultrasonography is less useful for the diagnosis of intraosseous lesions when there is no cortical breach, but it is useful for the diagnosis of soft tissue injuries about

Posterior fat pad sign: Identification of the posterior fat pad on a lateral radiograph signifies a joint effusion and should alert the radiologist to search for an associated fracture. Anterior humeral line: A line drawn along the anterior humeral cortex on a lateral view should pass through the middle third of the capitellum ossification center. If it passes anterior to the middle third, there is posterior displacement of the distal humerus, usually related to a supracondylar fracture. Radiocapitellar line: A line drawn through the long axis of the radius should pass through the capitellum on all radiographic views. If it does not, the radial head is dislocated. Apparent dislocation of the elbow in a child younger than 2 years of age should raise suspicion for a fracture separation of the distal humeral epiphysis.

the elbow, particularly in the setting of sports injury. The ulnar collateral ligament and flexor/extensor tendons are relatively superficial structures that can be well visualized with ultrasound. Potential findings include thickening and relative hypoechogenicity.

Injuries of the Forearm, Wrist, and Carpus Forearm fractures are common injuries of childhood, most occurring after 5 years of age. The peak age of incidence is 12 to 14 years in boys and 10 to 12 years in girls. Seventy-five to 84 percent of these fractures occur in the distal forearm, 15% to 18% are in the middle third, and 1% to 7% occur in the proximal forearm.57 Forearm fracture types include plastic deformation, buckle fracture, greenstick fracture, complete fracture, and physeal fractures.

■ FIGURE 35-54

CT in the setting of post-traumatic elbow effusion. A, Lateral elbow radiograph reveals an elbow effusion in this 14-year-old patient (long arrow). A subtle fracture of the coronoid process (short arrow) was not identified prospectively. B, The coronoid process fracture was much more conspicuous on a sagittal CT reformatted image (arrow).

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● Upper Extremity Injuries in Children (Including Sports Injuries)

907

Fractures of the forearm may accompany fractures of the ipsilateral elbow—the so-called floating elbow.57 Most forearm fractures in children are successfully treated by closed reduction because of the substantial remodeling potential of pediatric bone.

ment, open reduction may be required. Potential complications of this injury include radial or median nerve palsy and compartment syndrome.

Diaphyseal Injuries of Radius and Ulna

Fractures of the distal forearm are very common injuries in childhood. Displacement of the distal fracture fragment is dependent on the position of the wrist at the time of injury but is usually dorsal (Fig. 35-56). Buckle fractures occur at the junction of the diaphysis and metaphysis. They are usually the result of low-energy trauma and heal well even without specific treatment (Fig. 35-57). Complete fractures involve higher energy and are most frequently Salter-Harris type II fractures, although type I injuries are also seen (Fig. 35-58). Fractures of the distal radius are often accompanied by fractures of the distal ulna, most frequently involving the ulnar styloid. They require no specific treatment and often result in an asymptomatic nonunion. The distal ulnar physis is rarely involved. A Galeazzi fracture-dislocation is a fracture of the radius, most commonly at the junction of the middle and distal thirds, with associated distal radioulnar joint dislocation. This is a rare injury in children with a peak incidence between 9 and 12 years of age. One must be alert to the possibility of this type of injury with an isolated fracture of the distal radius. These lesions are unstable due to disruption of the triangular fibrocartilage complex. A fracture of the distal radius accompanied by a separation of the distal ulnar physis has been described as a Galeazzi equivalent lesion in children59 (Fig. 35-59).

Injuries of the mid forearm in younger children are frequently the greenstick type. In older children, fractures are usually complete. Unless there is a direct blow to the forearm, both radius and ulna are usually injured. Acute bowing deformity of one bone may be accompanied by a greenstick or complete fracture of the other bone (see Figs. 35-2 and 35-4). Complete fractures of the forearm have the potential to be significantly displaced and angulated, with overriding fracture fragments. In general, if there is less than 15 to 20 degrees of angular deformity in the forearm midshaft in a patient younger than 8 years of age there will be adequate remodeling before closure of the growth plates to preserve forearm function. In older patients, correction of angular and rotational deformity is required to preserve forearm rotation. Intramedullary fixation is suitable for unstable transverse fractures of the forearm shaft.47

Monteggia Fracture-Dislocations The Monteggia fracture-dislocation was originally described as a fracture of the proximal third of the ulna with an associated dislocation of the proximal radial epiphysis (Fig. 35-55). Bado redefined this injury to include a group of traumatic lesions having in common a dislocation of the radiohumeroulnar joint and an ulnar fracture at various locations.58 In children, the ulnar injury may be an incomplete fracture or even plastic deformation. Radiographs of the elbow should be obtained in any isolated fracture of the ulna to exclude a Monteggia injury. These injuries can usually be treated with closed reduction. However, when adequate reduction cannot be achieved or when there is a delay in diagnosis or treat-

■ FIGURE 35-55

Monteggia fracture-dislocation. A fracture of the proximal ulna is accompanied by dislocation of the radial head.

Fractures of the Distal Forearm and Wrist

■ FIGURE 35-56

Fractures of the distal forearm are usually the result of a fall on an outstretched hand. The distal fragments are most frequently displaced or angulated in the dorsal direction.

908

P A R T O N E ● Injury: Pediatric Injuries

■ FIGURE 35-57

Buckle fractures of the distal radius (short arrow) and ulna (long arrow). These injuries most frequently involve the dorsal cortex.

■ FIGURE 35-58

Salter-Harris type II fracture of distal radius. Frontal (A) and lateral (B) wrist radiographs. Higher-energy mechanisms are usually involved.

■ FIGURE 35-59

Pediatric Galleazzi equivalent. This patient has a fracture of the distal radius (arrow in B) and separation of the distal ulnar physis (arrow in A). A similar mechanism in an adult would likely cause a tear of the triangular fibrocartilage complex.

CHAPTER

A

35

● Upper Extremity Injuries in Children (Including Sports Injuries)

B

C

909

D

■ FIGURE 35-60

Wrist physeal injury. Frontal (A) and lateral (B) views of the wrist in a 12-year-old gymnast show widening and irregularity of the distal radial physis, particularly in the ventral aspect. C and D, There is significant improvement in radiographic findings after 6 months of conservative treatment.

Sports-related injuries of the wrist are commonly seen in gymnasts who engage in activities of repeated axial loading and dorsiflexion. Plain radiographs may be normal or demonstrate widening of the distal radial physis, osseous fragmentation, metaphyseal sclerosis, or metaphyseal flaring60 (Fig. 35-60). The distal radius is involved

much more commonly than the ulna. A high incidence of positive ulnar variance in this population is presumably related to growth abnormality in the radius. Shih and associates described corresponding MRI patterns of abnormality.43 They noted bands of physeal cartilage signal extending into the metaphysis either parallel or perpendicular to the growth plate (Fig. 35-61).These patients usually respond to conservative treatment.

Carpal Fractures

■ FIGURE 35-61

Chronic wrist physeal injury. A coronal fluid-sensitive MR sequence demonstrates widening and irregularity of the distal radial physis in an 11-year-old gymnast. Note perpendicular lines extending from the physeal cartilage. (From Jaramillo D. Pediatric upper extremity trauma. Radiol Soc North Am 2005.)

Because the carpus in young children is mostly cartilaginous, carpal bone fractures are rare. During growth, the carpal ossification centers are surrounded by a thick protective layer of cartilage. With progressive ossification, the carpus becomes more susceptible to traumatic injury and, by adolescence, fracture patterns in the carpus are similar to those of adults. The scaphoid bone is the most commonly fractured carpal bone. In younger children, the distal pole of the scaphoid is most commonly injured. This is likely related to the distal to proximal pattern of ossification. The clinical presentation is similar to that of adults; however, possibly because of decreased frequency of these injuries in childhood, there is a higher rate of misdiagnosis.61 Initial radiographs may not reveal the scaphoid fracture. The diagnosis may also be difficult to establish radiographically in young children before carpal ossification. The current standard of care is immobilization in all cases of suspected scaphoid fracture. If follow-up radiographs 2 weeks later show evidence of fracture, immobilization is continued for a longer course. Alternatively, MRI or CT may reveal occult fractures (Fig. 35-62). Scaphoid nonunion may result from

910

P A R T O N E ● Injury: Pediatric Injuries

described in children as well as adults.62 The injury consists of a fracture through the waist of the scaphoid and the neck of the capitate with 90 to 180 degrees rotation of the head of the capitate, usually as a result of a fall from a height. Because of incomplete ossification of a child’s carpus, this injury can be very difficult to detect radiographically. If displacement is present, a delay in reduction may lead to avascular necrosis of both scaphoid and capitate secondary to the single route of retrograde blood supply in these bones. Fractures of other carpal bones have been reported in children but are rare. A fall on or direct trauma to the ulnar border of the hand or an attempt to catch a hard ball may result in a fracture of the hamate bone. Carpal tunnel views of the hand or CT may confirm the diagnosis. Fractures of the triquetrum should be considered in cases of post-traumatic wrist pain.They are often subtle avulsion or impingement fractures that require appropriate oblique radiographs for diagnosis. Ligamentous injuries are uncommon but can occur in children, particularly adolescents.

Radiography

■ FIGURE 35-62

Subtle scaphoid fracture (arrow). CT may identify fractures that are not clearly seen with plain radiographs.

delayed/failed diagnosis or occur in spite of appropriate treatment (Fig. 35-63). The capitate is the second most commonly fractured carpal bone in children, rarely occurring as an isolated injury. It often accompanies fractures of other carpal bones, particularly the scaphoid. The scaphocapitate syndrome has been

At least two orthogonal views of the forearm should be obtained for fracture diagnosis. The elbow and wrist joints should also be imaged, particularly when only one bone is fractured. Greenstick fractures may be apparent in only one projection. A buckle fracture of the distal forearm may be seen only on a true lateral view because it involves primarily the dorsal cortex. A true lateral view is also important in displaced fractures of the distal radius, which can be subtle and difficult to recognize on a frontal view. The soft tissues about the distal forearm may provide clues to diagnose a nondisplaced fracture of the distal radius. The pronator quadratus muscle is attached to the distal radius and ulna. On a normal lateral radiograph of the wrist, the fat pad between the pronator quadratus and the flexor digitorum profundus muscle can be identified as a thin lucent line with a mild ventral convexity in the soft tissues anterior to the distal radius and ulna (Fig. 35-64). This fat pad should not be displaced from the distal radius more than 7 mm in females and 10 mm in males. In the setting of underlying bony injury, this fat plane may appear bowed or obscured. The diagnosis of scapholunate dissociation can be difficult to make on plain radiographs because of the normal developmental pattern of the carpal bones. The scapholunate distance is age and gender dependent, and one should not mistake this development for a true ligamentous injury.63

Magnetic Resonance Imaging

■ FIGURE 35-63

Scaphoid nonunion. Displacement and sclerosis of the edges of the fracture fragments suggest nonunion.

Fractures of the wrist are usually apparent and adequately assessed with plain radiographs. Fractures of the distal radius may be associated with injuries to the triangular fibrocartilage or scapholunate ligament; however, these are rare in children. MRI, and direct MR arthrography in particular, provides soft tissue information that is not delineated on plain radiographs (Fig. 35-65). MRI is more sensitive than plain radiographs for detection of chronic physeal stress injury in the wrist.43 However, plain radiographs are usually adequate for clinical assess-

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911

■ FIGURE 35-66

A, A coronal reconstruction of axially acquired CT images demonstrates a complex fracture of the distal radius with an intra-articular component. The CT information helps facilitate surgical planning. B, Postoperative radiograph.

■ FIGURE 35-64

Pronator fat pad. In a normal lateral wrist, the pronator fat pad appears as a linear lucency with mild ventral convexity (arrow).

ment. MRI may be indicated if there is persistent pain to look for an abnormality in the triangular fibrocartilage or a ligament.30

Multidetector Computed Tomography Multidetector CT is not routinely performed in the setting of wrist or forearm trauma. However, complex fracture relationships are well demonstrated (Fig. 35-66). This may aid in surgical planning.

Classic Signs ■

■ ■

■ FIGURE 35-65

Triangular fibrocartilage and scapholunate ligament tears on an MR arthrogram of the wrist. A small tear is noted in the body of the triangular fibrocartilage (short arrow). There is also a second tear near the radial attachment (long arrow). There is increased signal in the scapholunate interspace with loss of the normal dark signal of the scapholunate ligament (curved arrow). Contrast material has extended to the middle carpal row. This skeletally mature 17-year-old girl demonstrates a pattern of injury that is not commonly seen in younger children.

Pronator fat pad sign: A nondisplaced fracture of the distal radius may cause bowing or obscuration of the pronator quadratus fat pad in the soft tissues anterior to the distal forearm. Be sure to carefully examine the elbow and wrist joints, particularly when only one bone of the forearm is fractured. Scapholunate distance is age and gender specific. Apparent widening of the scapholunate distance may represent normal development.

Metacarpal and Phalangeal Fractures Metacarpal and Phalangeal Injuries Fractures of the metacarpal neck are common childhood injuries. Fractures of the fifth digit metacarpal neck account for 41% to 80% of all metacarpal fractures in children. These injuries are usually the result of an axial

912

P A R T O N E ● Injury: Pediatric Injuries

■ FIGURE 35-67

Metacarpal neck fractures. This is a common pattern of injury in children, usually with palmar angulation of the distal fragments. The fifth metacarpal is most frequently involved.

■ FIGURE 35-68

load. In younger children these fractures may be nondisplaced, resulting from a buckle of the palmar cortex. However, often there is significant palmar angulation that can be assessed with plain radiographs (Fig. 35-67). More angulation is acceptable in younger patients and in the

ulnar two metacarpals. Most can be treated with closed reduction. Metacarpal shaft fractures are not common in children, but when they occur they often have a spiral pattern. These fractures are slower to heal than fractures of the metacarpal neck or base (Fig. 35-68). Fractures of

■ FIGURE 35-69

Metacarpal shaft fracture. There is a fracture through the mid fifth metacarpal shaft with associated angulation.

Metacarpal base fractures. A, Fracture lines are noted at the bases of the fourth and fifth metacarpals. B, CT clearly demonstrates relationship of the fracture fragments. C, An intra-articular component (arrow) is evident.

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■ FIGURE 35-71 Salter Harris type III fracture at the base of the thumb (arrow). Such injuries have been described as pediatric Stener lesions. ■ FIGURE 35-70

Oblique phalangeal fracture. Slight angulation at the fracture site results in finger overlap in the closed fist position.

the metacarpal base are usually transverse and most commonly at the base of the fifth digit. Adequate oblique and lateral radiographs are important. CT may be important to fully characterize these injuries and to assess for an intra-articular component (Fig. 35-69). Fractures of the phalanges are common in the early teenage years. A second peak in these injuries occurs during the toddler years, mostly related to crush injuries. The proximal phalanx is the most common site of fracture.The small finger is the most common digit involved. As long as there is not a significant rotational component, most of these injuries can be treated with closed reduction. The presence of a significant rotational component may require open reduction because of the potential for entrapment. Finger overlap in the flexed position is a complication of inadequate reduction of a fracture with rotational deformity (Fig. 35-70). Fractures of the proximal phalanx are usually SalterHarris type II fractures at the base. In the proximal phalanx of the thumb, a strong adduction force may cause a Salter-Harris type III avulsion fracture of the ulnar base, attached to the ulnar collateral ligament (Fig. 35-71). These lesions often require surgical reduction because of the risk of interposition of the adductor tendon between the fracture fragments. This has been described as a pediatric Stener lesion.64 Fractures of the distal phalanges are commonly the result of crush injuries (Fig. 35-72).

■ FIGURE 35-72

(arrow).

Crush injury resulting in fracture of the distal tuft

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These injuries may be complicated by damage to the nail bed or infection.

Magnetic Resonance Imaging Plain radiographs are usually adequate for radiologic assessment of traumatic injuries of the metacarpus and phalanges. In certain cases, MRI may provide useful additional information to assess the presence of a tendon or ligament tear, the extent of injury, and appropriate surgical planning. Injuries of the ulnar collateral ligament of the thumb and injuries to the pulley system are particularly suited to MRI evaluation.

Multidetector Computed Tomography As in other areas, MDCT aids in demonstration of complex fracture fragment relationships but is not typically required for evaluation of trauma to the metacarpals and phalanges.

Ultrasonography Ultrasonography of the hand and fingers may provide valuable information in the setting of trauma if there is suspected injury of the ulnar collateral ligament or digital flexor pulley injury.

SUGGESTED READINGS Carson S, Woolridge DP, Colletti J, Kilgore K. Pediatric upper extremity injuries. Pediatr Clin North Am 2006; 53:41–67. Connolly SA, Connolly LP, Jaramillo D. Imaging of sports injuries in children and adolescents. Radiol Clin North Am 2001; 39:773–790. Ecklund K. Magnetic resonance imaging of pediatric musculoskeletal trauma. Topics Magn Reson Imaging 2002; 13:203–218. Ecklund K, Jaramillo D. Imaging of growth disturbance in children. Radiol Clin North Am 2001; 39:823–841.

Emery KH. Imaging of sports injuries of the upper extremity in children. Clin Sports Med 2006; 25:543–568. Jaramillo D, Shapiro F. Musculoskeletal trauma in children. Magn Reson Imaging Clin North Am 1998; 6:521–536. John SD, Wherry K, Swischuk LE, Phillips WA. Improving detection of pediatric elbow fractures by understanding their mechanics. RadioGraphics 1996; 16:1443–1460.

REFERENCES 1. Jones E. Skeletal growth and development as related to trauma. In Green NE, Swiontkowski MF (eds). Skeletal Trauma in Children, 2nd ed. Philadelphia, WB Saunders, 1998, vol 3, pp 1–16. 2. Wirth MA, Rockwood CA. Injuries to the sternoclavicular joint in the adult and child. In DeLee JC, Drez D Jr, Miller MD (eds). DeLee and Drez’s Orthopaedic Sports Medicine, 2nd ed. Philadelphia, Elsevier Science, 2003. 3. Rudzki JR, Matava MJ, Paletta GA Jr. Complications of treatment of acromioclavicular and sternoclavicular joint injuries. Clin Sports Med 2003; 22:387–405. 4. Mahasen LM, Sadek SA. Developmental, morphological, and histological studies on structures of the human fetal elbow joint. Cells Tissues Organs 2000; 166:359–372. 5. Gruelich WW. Radiographic Atlas of Skeletal Development of the Hand and Wrist, 2nd ed. Stanford, CA, Stanford University Press, 1964. 6. Ogden JA. General principles. In Ogden JA (ed). Skeletal Injury in the Child, 2nd ed. Philadelphia, WB Saunders, 1990, pp 1–22. 7. Salter RB, Harris WR. Injuries involving the epiphyseal plate. J Bone Joint Surg Am 1963; 45:587. 8. Ogden JA. Injury to the growth mechanisms of the immature skeleton. Skeletal Radiol 1981; 6:237–253. 9. Rang M. Children’s Fractures, 2nd ed. Toronto, JB Lippincott, 1983. 10. Bright RW, Burstein AH, Elmore SM. Epiphyseal-plate cartilage: a biomechanical and histological analysis of failure modes. J Bone Joint Surg Am 1974; 56:688–703. 11. Shapiro F. Epiphyseal growth plate fracture-separations: a pathophysiologic approach. Orthopedics 1982; 5:720–736. 12. Jaramillo D, Kammen BF, Shapiro F. Cartilaginous path of physeal fracture-separations: evaluation with MR imaging—an experimental study with histologic correlation in rabbits. Radiology 2000; 215:504–511. 13. Jaramillo D, Laor T, Zaleske DJ. Indirect trauma to the growth plate: results of MR imaging after epiphyseal and metaphyseal injury in rabbits. Radiology 1993; 187:171–178. 14. Hsu T-Y, Hung F-C, Lu Y-J, et al. Neonatal clavicular fracture: clinical analysis of incidence, predisposing factors, diagnosis, and outcome. Am J Perinatol 2002; 19:17–21. 15. Many A, Brenner SH, Yaron Y, et al. Prospective study of incidence and predisposing factors for clavicular fracture in the newborn. Acta Obstet Gynecol Scand 1996; 75:378–381.

16. Calder JDF, Solan M, Gidwani S, et al. Management of paediatric clavicle fractures—is follow-up necessary? An audit of 346 cases. Ann R Coll Surg Engl 2002; 84:331–333. 17. Kocher MS, Waters PM, Micheli LJ. Upper extremity injuries in the paediatric athlete. Sports Med 2000; 30:117–135. 18. de la Puente R, Boutin RD, Theodorou DJ, et al. Post-traumatic and stress-induced osteolysis of the distal clavicle: MR imaging findings in 17 patients [see comment]. Skeletal Radiol 1999; 28:202–208. 19. Bishop JY, Flatow EL. Pediatric shoulder trauma. Clin Orthop Relat Res 2005; (432):41–48. 20. Carson S, Woolridge DP, Colletti J, Kilgore K. Pediatric upper extremity injuries. Pediatr Clin North Am 2006; 53:41–67. 21. Webb LX. Fractures and dislocations about the shoulder. In Green NE, Swiontkowski MF (eds). Skeletal Trauma in Children. Philadelphia, WB Saunders, 2002, vol 3. 22. Blab E, Geissler W, Rokitansky A. Sonographic management of infantile clavicular fractures. Pediatr Surg Int 1999; 15:251–254. 23. Kleinman PK. Diagnostic imaging in infant abuse. AJR Am J Roentgenol 1990; 155:703–712. 24. Kogutt MS, Swischuk LE, Fagan CJ. Patterns of injury and significance of uncommon fractures in the battered child syndrome. Am J Roentgenol Radium Ther Nucl Med 1974; 121:143–149. 25. Buckley SL, Gotschall C, Robertson W Jr, et al. The relationships of skeletal injuries with trauma score, injury severity score, length of hospital stay, hospital charges, and mortality in children admitted to a regional pediatric trauma center. J Pediatr Orthop 1994; 14:449–453. 26. Deutsch A, Williams GR. Fractures of the coracoid in adults and children. In DeLee JC, Drez D Jr, Miller MD (eds). DeLee and Drez’s Orthopaedic Sports Medicine, 2nd ed. Philadelphia, Elsevier Science, 2003. 27. Rowe CR. Prognosis in dislocations of the shoulder. J Bone Joint Surg Am 1956; 38:957–977. 28. Hovelius L, Augustini BG, Fredin H, et al. Primary anterior dislocation of the shoulder in young patients: a ten-year prospective study [see comment]. J Bone Joint Surg Am 1996; 78:1677–1684. 29. Burra G, Andrews JR. Acute shoulder and elbow dislocations in the athlete. Orthop Clin North Am 2002; 33:479–495.

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30. Emery KH. Imaging of sports injuries of the upper extremity in children. Clin Sports Med 2006; 25:543–568. 31. Baker CL, Uribe JW, Whitman C. Arthroscopic evaluation of acute initial anterior shoulder dislocations. Am J Sports Med 1990; 18:25–28. 32. Deitch J, Mehlman CT, Foad SL, et al. Traumatic anterior shoulder dislocation in adolescents. Am J Sports Med 2003; 31:758–763. 33. Bottoni CR, Wilckens JH, DeBerardino TM, et al. A prospective, randomized evaluation of arthroscopic stabilization versus nonoperative treatment in patients with acute, traumatic, firsttime shoulder dislocations [see comment]. Am J Sports Med 2002; 30:576–580. 34. Kim S-H, Ha K-I, Cho Y-B, et al. Arthroscopic anterior stabilization of the shoulder: two to six-year follow-up. J Bone Joint Surg Am 2003; 85:1511–1518. 35. Gor DM. The trough line sign. Radiology 2002; 224:485–486. 36. Caviglia H, Garrido CP, Palazzi FF, Meana NV. Pediatric fractures of the humerus. Clin Orthop Relat Res 2005; (432):49–56. 37. Thomas SA, Rosenfield NS, Leventhal JM, Markowitz RI. Longbone fractures in young children: distinguishing accidental injuries from child abuse. Pediatrics 1991; 88:471–476. 38. Neer CS 2nd, Horowitz BS. Fractures of the proximal humeral epiphysial plate. Clin Orthop Relat Res 1965; 41:24–31. 39. Fleming JL, Hollingsworth CL, Squire DL, Bisset GS. Little Leaguer’s shoulder. Skeletal Radiol 2004; 33:352–354. 40. Ortiz EJ, Isler MH, Navia JE, Canosa R. Pathologic fractures in children. Clin Orthop Relat Res 2005; (432):116–126. 41. Hall FM. Shoulder MR arthrography: which patient group benefits most? [comment]. AJR Am J Roentgenol 2005; 184:1708–1709. 42. Connolly SA, Connolly LP, Jaramillo D. Imaging of sports injuries in children and adolescents. Radiol Clin North Am 2001; 39:773–790. 43. Shih C, Chang CY, Penn IW, et al. Chronically stressed wrists in adolescent gymnasts: MR imaging appearance [erratum appears in Radiology 1995 Oct;197(1):319]. Radiology 1995; 195:855–859. 44. Keller MS. Musculoskeletal sonography in the neonate and infant. Pediatr Radiol 2005; 35(12):1167–1173; quiz 1293. 45. Teefey SA, Middleton WD, Payne WT, Yamaguchi K. Detection and measurement of rotator cuff tears with sonography: analysis of diagnostic errors. AJR Am J Roentgenol 2005; 184:1768–1773. 46. Gartland JJ. Management of supracondylar fractures of the humerus in children. Surg Gynecol Obstet 1959; 109:145. 47. Flynn JM, Sarwark JF, Waters PM, et al. The surgical management of pediatric fractures of the upper extremity. Instruct Course Lect 2003; 52:635–645. 48. Finnbogason T, Karlsson G, Lindberg L, Mortensson W. Nondisplaced and minimally displaced fractures of the lateral

49. 50. 51. 52. 53. 54. 55.

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humeral condyle in children: a prospective radiographic investigation of fracture stability. J Pediatr Orthop 1995; 15:422–425. Green NE. Fractures and dislocations about the elbow. In Green NE, Swiontkowski MF (eds). Skeletal Trauma in Children. Philadelphia, WB Saunders, 1998, vol 3, pp 259–316. Lins RE, Simovitch RW, Waters PM. Pediatric elbow trauma. Orthop Clin North Am 1999; 30:119–132. Salter RB, Zaltz C. Anatomic investigations of the mechanism of injury and pathologic anatomy of “pulled elbow” in young children. Clin Orthop Relat Res 1971; 77:134–143. Hang DW, Chao CM, Hang Y-S. A clinical and roentgenographic study of Little League elbow. Am J Sports Med 2004; 32:79–84. Griffith JF, Roebuck DJ, Cheng JC, et al. Acute elbow trauma in children: spectrum of injury revealed by MR imaging not apparent on radiographs [see comment]. AJR Am J Roentgenol 2001; 176:53–60. Chapman VM, Nimkin K, Jaramillo D. The pre-ossification center: normal CT and MRI findings in the trochlea. Skeletal Radiol 2004; 33:725–727. Chapman VM, Kalra M, Halpern E, et al. 16-MDCT of the posttraumatic pediatric elbow: optimum parameters and associated radiation dose. AJR Am J Roentgenol 2005; 185:516–521. Markowitz RI, Davidson RS, Harty MP, et al. Sonography of the elbow in infants and children. AJR Am J Roentgenol 1992; 159:829–833. Armstrong PF, Joughin VE, Clarke HM. Pediatric fractures of the forearm, wrist, and hand. In Green NE (ed). Skeletal Trauma in Children, 2nd ed. Philadelphia, WB Saunders, 1998, vol 3, pp 161–258. Bado JL, Bado JL. The Monteggia lesion. Clin Orthop Relat Res 1967; 50:71–86. Landfried MJ, Stenclik M, Susi JG. Variant of Galeazzi fracturedislocation in children. J Pediatr Orthop 1991; 11:332–335. Chang CY, Shih C, Penn IW, et al. Wrist injuries in adolescent gymnasts of a Chinese opera school: radiographic survey [erratum appears in Radiology 1995; 197:319]. Radiology 1995; 195:861–864. Nafie SA. Fractures of the carpal bones in children. Injury 1987; 18:117–119. Anderson WJ. Simultaneous fracture of the scaphoid and capitate in a child. J Hand Surg [Am] 1987; 12:271–273. Kaawach W, Ecklund K, Di Canzio J, et al. Normal ranges of scapholunate distance in children 6 to 14 years old. J Pediatr Orthop 2001; 21:464–467. White GM. Ligamentous avulsion of the ulnar collateral ligament of the thumb of a child. J Hand Surg [Am] 1986; 11:669–672.

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Lower Extremity Injuries in Children (Including Sports Injuries) D. Barron, J. Farrant, and Philip O’Connor

PREVALENCE AND EPIDEMIOLOGY Recently there has been a reported rise in the incidence of both acute and chronic musculoskeletal injury among children and adolescents.1 Sports-related injury is a significant factor in this change and is the result of both increased and earlier participation in competitive sports. This is compounded by the widespread belief that to achieve international success at senior level it is necessary to start intensive training well before puberty. Indeed, academy training schemes for young aspiring athletes have been set up in a number of sporting arenas with these principles in mind. Increasing numbers of chronic overuse injuries in young athletes may be related to limited recovery time from longer competitive seasons and year-round training.1 In children, unlike adults, the vast majority of acute athletic injuries represent bone trauma. However, children who train intensively for a specific sport at an early age are at particular risk of developing overuse injuries. This may be secondary to improper technique, poorly fitting protective equipment, training errors, and muscle weakness and imbalance. The Centers for Disease Control and Prevention estimates that one half of all sports injuries in children are preventable with proper education and use of protective equipment.1 These concerns have led to the issuing of guidelines for sports participation by children and warnings of increasing risk of acute and overuse injuries as children undergo the repetitive demands dictated by the specialized pattern of movement imposed by a single sport at high level. Early diagnosis is vital and requires the reporting radiologist or clinician to have a clear understanding of the 916

way force affects the immature skeleton. Most pediatric sports injuries can be managed conservatively with proper and timely diagnosis.

DEFINITIONS AND ANATOMY There are fundamental differences in the young skeleton from that of the mature adult, which lead to disparate patterns of injury from the same force. The skeletally immature patient differs in that cartilaginous growth centers are present around joints (epiphyses) and at attachments of tendon and ligament to bone (apophyses). These junctions between mature and growing bone are the weakest point in the kinetic chain. Distraction force from the attached musculotendinous unit will thus cause failure at the growth plate within the apophysis rather than damage the muscle and tendon. Compressive and rotational forces will preferentially damage the epiphyseal growth plate.

BIOMECHANICS The primary function of the lower limb is to support the weight of the body and provide a stable foundation in standing, walking, and running. The muscles, tendons, ligaments, bones, and joints of the lower extremity act together to form a kinetic chain that allows movement. Acute injury is the response of tissue to kinetic energy applied to the body that, if large enough, will produce tissue failure in a reasonably predictable way. Damage can occur locally or distant from the site of trauma due to transmitted forces and may be acute or chronic depending on the nature and size of the force. The site of failure will usually be at the weakest point within the kinetic chain.

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KEY POINTS Injuries to the lower limb are becoming more common in children with increasing involvement in sports. ■ The growing epiphysis changes the biomechanical properties of bone when compared with the mature skeleton. ■ More pliable bone leads to greenstick and bowing fractures. ■ The apophyseal insertion is weaker than the tendon or ligament in children, and avulsion is more likely than tendon or ligament rupture. ■ MRI and bone scintigraphy may be useful in detecting occult fractures. ■ The Salter-Harris classification is widely used to describe physeal injuries. ■ Injuries of the upper femoral epiphysis may be difficult to detect and often require a frog-leg lateral radiograph for diagnosis. ■ Traction apophysitis may be diagnosed clinically, but MRI and ultrasonography may have roles in selected cases. ■ Osteochondral lesions including osteochondritis dissecans may be detected on radiographs but commonly require MRI, CT, or ultrasonography for accurate diagnosis. ■ Tendon and muscle injuries are best diagnosed with MRI or ultrasonography. ■

Skeletally immature patients usually experience either injuries to the epiphyseal growth plate, which are classified using the Salter-Harris system,2 or apophyseal avulsion. Sport-related injury more frequently occurs after repetitive strain, when the force applied is sufficiently large to damage tissues but does not cause complete structural failure. Training for many sports focuses on general fitness and technique. The aim is to improve technique, producing more reproducible, higher performance levels. This uniformity of action tends to focus the stresses through the same area of the musculoskeletal system during training, increasing the likelihood of overuse injury. This is best appreciated in golf in which players with low handicaps and professional players have very different injury patterns compared with players with higher handicaps. This results because less experienced players have fewer reproducible actions and get more acute injuries and professionals and low handicappers repeat the same action and develop repetitive strain, over-training–type injuries. Repetitive strain occurs when the athlete is given insufficient recovery time from a partial injury. The initial tissue damage causes weakening with a reduction in tissue tolerance; if the force is then reapplied to this weakened tissue, the same magnitude of force now produces a greater degree of damage. Repeating this will cause progressive weakening until the point where the cyclical force is sufficiently large to cause complete structural failure. The forces applied will have either a predominantly passive compressive or active distractive nature. Passive compressive injuries result more in damage to osseous structures and are particularly seen in association with higher impact cyclical injury (e.g., long distance running on hard surfaces). In the skeletally immature patient

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this usually occurs at the physes, which is the site of growing bone. Failure can occur elsewhere in the kinetic chain in the very young and in those patients approaching skeletal maturity. In the very young the diaphysis of long bones can be the site of injury because the bone itself has different mechanical properties, making this area more prone to injury; this is seen in toddler’s and bowing fractures. In patients approaching skeletal maturity, fusing epiphyses no longer represent the weakest point in the chain and compressive forces can again result in stress injury to the diaphysis. Within children’s joints, osteochondral injury occurs much more commonly than internal derangement or ligamentous disruption, except where there are preexisting congenital variants such as discoid menisci in the knee. Active forces are related to the contraction of the muscle tendon unit. Injury most commonly occurs in muscles crossing two joints because these are inherently subject to greater forces, for example, the hamstring, rectus femoris, quadriceps, and gastrocnemius muscles. In the musculoskeletally immature patient the apophysis represents the weakest point in this chain and is most commonly injured in cyclical injuries. As the patient approaches skeletal maturity, an increase in incidence of musculotendinous junction injuries will become apparent as the apophyses begin to fuse. As a rule, the individual’s biomechanics will determine the pattern of injury within the site of failure, with point of failure in the kinetic chain determined by the nature of the applied force and the skeletal maturity of the patient.

DIAPHYSEAL AND METAPHYSEAL INJURIES Manifestations of the Disease Radiography Immature bone is more porous and less dense than adult bone, owing to increased vascular channels and a lower mineral content. The biomechanical properties of this bone may lead to incomplete fractures that are peculiar to children. Increased plasticity and elasticity of young bone means that it is more likely to buckle than to snap. The periosteum is thicker, more elastic, and less firmly bound to bone so it will usually remain intact over an underlying fracture. Healing and remodeling is therefore more predictable than in adults, and nonunion is rare. Rogers3 classifies these injuries broadly as classic greenstick, torus, and bowing fracture. These classically occur in the upper limb but are also seen in the fibula, often in association with a spiral or oblique tibial fracture. The classic greenstick fracture arises from bending forces that produce a complex break of the cortex on the tension side and plastic deformation of the opposite cortical border. An incomplete transverse fracture is produced in the convex cortex and usually extends to the middle of the shaft involving half the circumference of the bone. The resulting fracture line may then extend at right angles to its medial extent, causing a longitudinal split in the shaft. The concave cortex remains bowed but is intact. These fractures are much more common in the upper limb4 but are also seen in the lower limb (Fig. 36-1).5

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Bowing fractures result principally from compressive forces with an element of angulation producing a gradual curve across the length of the whole bone with no visible cortical break (Figs. 36-3 and 36-4).8 In the lower limb the fibula is the most commonly involved and is associated with a concomitant tibial fracture. Bowing is also seen in patients with reduced bone strength and who have conditions such as metabolic bone disease, osteogenesis imperfecta, and osteopetrosis (Fig. 36-5). Bony rings are an important principle in radiology. The bones of the calf represent such a bone ring. They are nearly always disrupted at two sites, with a single-site injury an unusual diagnosis (Fig. 36-6). Single-point injuries normally relate to an exceptional force such as a sharp blow. Exclusion of an injury elsewhere in the bone ring of the tibia and fibula either to the interosseous articulations or within the bones themselves may require recourse to scintigraphy or cross-sectional imaging with MRI or CT.

Toddler’s Fracture

■ FIGURE 36-1 Lateral (A) and anteroposterior (B) radiographs demonstrating buckle fracture of distal tibia (arrows). Young patients often localize the site of pain poorly so radiography or scanning with a large field of view is required.

A torus or buckle fracture is produced by compressive forces that cause the cortex to buckle to a varying degree. They are mostly seen in the metaphyses of the long bones of the upper limb (Fig. 36-2).6,7

Children between the ages of 1 and 3 years commonly present with a limp of acute onset without a clear history of specific injury. The classic lesion is a nondisplaced oblique fracture of the distal tibia termed a toddler fracture. The classic toddler’s fracture is frequently difficult to diagnose radiographically and is often only demonstrated on one view (Fig. 36-7). Ultrasonography can be of value in diagnosing these “radiographically difficult” fractures.9 However, it should be recognized that limp may arise from occult fractures at many other sites, including the femur, metatarsals, tarsal bones, pubic rami, or patella. Radiography of the whole leg is often warranted.3,9–11

Fracture of the Tibial Metaphysis Fractures involving the tibial metaphysis in children younger than age 6 years may result in valgus angulation at the fracture site and overgrowth of the tibia.

■ FIGURE 36-2 Lateral (A) and anteroposterior (B) radiographs showing subtle greenstick type fracture of tibia (arrows).

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■ FIGURE 36-3 A and B, Bowing fracture of tibia and fibula at presentation.

■ FIGURE 36-4

Same patient depicted in Figure 36-3 at 2-year followup. There has been improvement in the degree of deformity related to the bowing fracture without complete resolution.

■ FIGURE 36-5 Anteroposterior (A) and lateral (B) radiographs of tibia and fibula showing bowing associated with diffuse sclerosis and metaphyseal remodeling in a patient with osteopetrosis.

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■ FIGURE 36-6 Anteroposterior (A) and lateral (B) radiographs of calf showing typical fractures at two points (arrows) in the bony ring of the tibia and fibula.

■ FIGURE 36-7 Lateral (A) and anteroposterior (B) radiographs of a toddler’s fracture of the distal tibia (arrows). These fractures are typically spiral in orientation and as such can be difficult to visualize radiographically.

Fractures with Nonossifying Fibromas

of transition without any matrix calcification. Fracture through these lesions is the most common symptomatic presentation and is associated with the classic “fallen fragment sign”13,14 in which a fracture fragment drops down under the influence of gravity to lie within the cyst itself. This can only occur in purely cystic lesions and as such is pathognomonic of unicameral bone cysts.

Pathologic fractures do occur in children in association with a variety of lesions. Nonossifying fibromas are relatively common benign lesions associated with fracture during childhood and adolescence.12 The radiographs are characteristic, and biopsy or further investigation should not be necessary. The lesion is a cortically based expanded lucency with a narrow sclerotic zone of transition. It may cause thinning and slight bulging of the overlying cortex, and there may be multiple lesions. Fractures associated with these lesions tend to heal spontaneously, but fractures in long bones may require fixation (Fig. 36-8).

Unicameral Bone Cyst Another lesion seen more in adolescence is the unicameral bone cyst. This lesion is purely cystic with no solid components and is typically centrally located within the metaphysis of long bones. The calcaneus is also a common lower limb site for these lesions. An expanded welldefined lytic lesion is seen with a narrow sclerotic zone

Fractures of the Femoral Neck Fractures of the neck of the femur are rare in childhood and result from a considerable force. The majority are caused by vehicular accidents or falls from a great height. Radiographic diagnosis is usually sufficient, although occasionally there may be nothing more than linear lucencies traversing the femoral neck.

Hip Fractures and Dislocations Subcapital fractures account for 50% of pediatric hip fractures. Most of these are displaced (80%), with 40% to 50% complicated by avascular necrosis.15 Basicervical fractures

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■ FIGURE 36-8 Anteroposterior (A) and lateral (B) radiographs of knee in patient with multiple nonossifying fibromas. There has been a pathologic fracture through the femur that has intramedullary nails (arrows).

account for a third of hip fractures, and approximately half are displaced at the time of diagnosis. Intertrochanteric fractures are rare and uncomplicated. Union usually occurs within 6 weeks. Dislocations of the hip can occur in children often without associated fracture of the acetabular rim and are usually posterior. They may result from trivial injuries, which is in contradistinction to causes of these injuries in adults. Subsequent growth disturbances occur in up to 30% of cases, with enlargement of the femoral head; other complications include avascular necrosis and premature osteoarthritic changes.

This is because it does not provide sufficient information about a fracture for diagnosis, prognosis, and management decisions.

Bone Scintigraphy

Fracture of the shaft of the femur tends to result from higher-energy mechanisms, and associated further injuries should be actively excluded. The most frequent site of femoral shaft fracture is in its middle third, where normal anterolateral bowing of the diaphysis is at a maximum. Oblique fractures tend to result more from indirect forces, with transverse fractures due to high-energy direct trauma such as from vehicular accidents. These fractures often significantly displace and overlap, owing to muscular action on the fracture fragments. Greenstick fractures are more frequently seen in the distal third of the bone (Fig. 36-9).

When the cause of a child’s limp cannot be localized by history or clinical examination, bone scintigraphy can help to localize a pathologic process. Fractures, sepsis, and tumors will show as regions of increased uptake on bone scintigraphy. The area of increased uptake on bone scintigraphy can then be further diagnosed with plain radiographs, CT, or MRI. In toddler’s fractures, a bone scintigram usually demonstrates a diffuse increase in activity over the entire length of the bone even when a radiograph demonstrates a fracture of the metaphysis. Occasionally with highresolution techniques the increased activity can be seen confined to an oblique band involving the diaphysis and metaphysis. Bowing fractures may be difficult to diagnose on radiographs, and bone scintigraphy may be necessary to demonstrate increased activity in a large portion of the diaphysis over the length of the bone. If nonaccidental injury is suspected, other fractures will show as regions of increased uptake on bone scintigraphy.

Ultrasonography

Magnetic Resonance Imaging

Although ultrasound examination has been shown to be reliable in detection of simple femoral diaphyseal fractures,16 it is seldom used as a primary diagnostic tool.

Magnetic resonance imaging may be required to confirm the presence of a fracture when radiographs have proved equivocal. The disadvantage is that a general anesthetic is

Fractures of the Femoral Shaft

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muscular, or developmental causes. Referred pain must also be considered, such as pain in the back radiating to the leg or pain in the knee originating in the hip and vice versa.

Synopsis of Treatment Options Medical Treatment The type of injury must be taken into consideration because it will influence the management of the patient. These factors include: ● ● ● ● ● ●

■ FIGURE 36-9 Anteroposterior (A) and lateral (B) radiographs of right femur. There is a spiral fracture of the mid femoral shaft (arrows) associated with varus angulation with considerable fragment overlap.

necessary in the very young and sedation can be required in older children.

Computed Tomography Computed tomography is rarely used as the initial imaging modality for these injuries. However, when there is a complex injury pattern requiring extensive surgery or there is concern for a subtle cortical injury, then the detailed three-dimensional overview that CT provides can be invaluable. CT is also of value in surgical planning for internal fixation, demonstrating in detail fracture fragment size and relations.

Differential Diagnosis There are multiple causes that need to be considered when one sees a child with an acute limp. Very young children can rarely verbalize the location of the discomfort and clinical examination can be difficult. The differential diagnosis is wide and includes traumatic, infectious, neoplastic, inflammatory, congenital, neuro-

Site of fracture Closed or open fracture Degree of comminution Neurovascular injury Degree of displacement and stability Age of the child

Management changes with the age of the child because there is a different potential for remodeling and healing with age. In early infancy the potential for spontaneous correction of displacement is very high but this decreases as the child matures. In addition, healing time increases with age and, therefore, the required period of immobilization differs. In general, children of all ages with stable lower-limb metaphyseal or diaphyseal fractures are usually treated conservatively with a cast for 3 to 5 weeks, and satisfactory healing usually occurs. Traction may be used and is applied with pins placed across the distal tibial shaft or within the calcaneum. Fractures involving the tibial metaphysis in children younger than 6 years old can lead to obvious angulation and overgrowth. However, most cases resolve within 2 to 3 years and surgical intervention is rarely required.

Surgical Treatment Unstable fractures can be defined as a fracture that demonstrates progressive displacement or failure to heal despite conservative (noninvasive) immobilization. These fractures should be considered for surgery. Surgical techniques vary widely. External fixation devices are used for comminuted fractures without sizeable fragments to allow screw fixation. Open fractures with skin loss also carry a high risk of infection and are best treated with external fixation. Pins are placed proximal and distal to the fracture site to control the angulation and rotation of the fracture and the length of the bone. The type of fracture is important. For example, bowing fractures must be recognized because they may show progressive angulation and possess little potential for remodeling. Bowing fractures of the fibula can interfere with healing of the tibial fracture and may require osteotomy or fracture of the fibula to allow reduction of the tibial fracture.

Hip and Femoral Shaft Surgical treatment of transcervical fractures is recommended in all cases because most are unstable. Internal

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fixation is performed using screws, but there is controversy as to whether these should cross the physis. Without internal fixation both displaced and nondisplaced fractures tend to drift into coxa vara. Treatment of nondisplaced cervicotrochanteric fractures involves several weeks of traction followed by abduction spica cast. A displaced fracture requires internal fixation with screws. The results of both conservative and surgical management are poor because of the tenuous blood supply to the femoral head in children. Avascular necrosis, coxa vara, malunion, leg-length inequality, and premature growth plate closure are relatively frequent complications.

Hip Dislocation In children, widening of the hip joint after reduction is most frequently due to interposed soft tissue, infolding of either the labrum or the joint capsule, and, less frequently, an entrapped osteochondral fragment. Widening of the joint should never be attributed to a simple hemarthrosis. CT confirms widening of the joint space, but because of the absence of bone in the labrum and joint capsule,

What the Referring Physician Needs to Know ■

■

■

■

■

Nonaccidental injury: With knowledge of the most common types of injury for a child’s developmental level, a physician may predict the type of injury sustained. Nonaccidental injury should be considered when fractures in the newborn and infant are encountered. Femoral shaft fractures are the result of high-energy trauma. In children younger than 3 years old with limited mobility, approximately 70% (especially before the age of 1), the majority of femoral shaft fractures are nonaccidental. It is essential that the entire length of the femur from the knee to the hip be imaged by radiography at the time of the initial injury to search for occult fractures. Bowing fractures may be easily overlooked unless the observer is aware of the possibility or has comparison views of the contralateral side. Toddler’s fractures are classically undisplaced and may be visualized in only one projection. Oblique views may therefore be necessary for diagnosis. Fractures of the tibial shaft may be associated with compartment syndrome of either the anterior, lateral, or posterior compartments of the leg. Hemorrhage may occur in one or more of the compartments from a tibial fracture that forms one of the boundaries of these closed spaces. The hemorrhage leads to an increase in tissue pressure, and the vascular perfusion by the microcirculation is reduced. This causes tissue anoxia and tissue edema. Fasciotomies are required to release the elevated tissue pressure. In the acute phase MRI may demonstrate edema in the muscles affected. Later, atrophy and persistent edema can be seen. Gonad shields should not be used in the evaluation of suspected injuries of the pelvis or hip because they may easily obscure underlying fractures of the pubic rami.

923

the precise reason for the widening may not be evident. The enfolded and entrapped joint capsule or cartilage may be seen on MRI or CT arthrography. Surgery is required to remove any entrapped capsule or infolded labrum and restore normal anatomic relations in the joint.

Femoral Shaft Fracture The problem in pediatric femoral fractures is the potential for subsequent growth disturbance, particularly overgrowth. The degree of overgrowth is principally determined by the reduction of the fracture. On average the overgrowth is approximately 1 cm, but it may be increased by distraction of the fracture. Therefore, femoral shaft fractures in children are usually not completely reduced but are allowed to overlap by approximately 1 cm to counter any subsequent overgrowth and to lessen the opportunity for the development of a discrepancy in leg length. To the contrary, femoral shaft fractures may shorten and angulate due to longitudinal muscle pull and spasm. The physical development of the child and knowledge of the fracture site and type are important in decision making. Management depends on the age of the child. Children younger than 2 years of age are treated conservatively with a spica cast or overhead traction. Children between 2 and 5 years of age may be treated conservatively using a hip spica or traction or surgically with elastic stable intramedullary nailing (ESIN) or external fixation. In children between 5 and 15 years of age ESIN or external fixation, or a combination of both, is used.

PHYSEAL INJURIES Manifestations of the Disease Radiography The peak incidence of physeal, or growth plate, injury occurs during adolescence, perhaps due to increased exposure to high-energy trauma combined with weakening of the growth plate that occurs with puberty.17 Physeal injuries are more common in males, probably owing to greater exposure to trauma and sports and to the relative delay in physeal closure.3 Damage to the physis can cause premature physeal closure, which may lead to temporary or permanent disturbance of growth. Growth plate injuries are usually classified according to the Salter-Harris system (Box 36-1). The classification relates to the fracture’s potential for growth disturbance. Type I injuries have little or no effect on growth with type V fractures causing most growth disturbance.2,18 In general, it has been found that the prognosis is worse in the lower extremities compared with upper limb injuries.19 Most of these fractures are apparent on plain radiographs, which may demonstrate epiphyseal displacement, widening of the physis, and loss of definition of the opposing surfaces of the epiphysis and metaphysis.20 Diagnosis of undisplaced fractures can be very difficult, and radiography of the opposite side for comparison may

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BOX 36-1 ■ ■ ■ ■ ■

Salter-Harris Classification

Type I: Fracture through the physis without involvement of the metaphysis or epiphysis. The only radiographic evidence is epiphyseal displacement (Fig. 36-10). Type II: A fracture through the physis and metaphysis, with a fragment of the metaphysis remaining attached to the physis. (Fig. 36-11). Type III: A fracture involving the epiphysis and the physis (Fig. 36-12). Type IV: A fracture involving the epiphysis, physis, and metaphysis (Fig. 36-13). Type V: The physis is crushed (compressed) without fracture of the epiphysis or metaphysis. The distal femoral and both tibial epiphyseal centers are most commonly affected, usually in association with fractures of the shaft of the femur or the tibia and fibula (Fig. 36-14).

■ FIGURE 36-10 A, Diagram of Salter-Harris type I fracture with the fracture line (red line) passing purely through the growth plate without bone osseous fracture. B, Salter-Harris type I fracture of distal fibula associated with opening up of the lateral growth plate (arrow) and marked overlying soft tissue swelling(s).

■ FIGURE 36-11 A, Diagram of Salter-Harris type II fracture with the fracture line (red line) passing through the growth plate and extending into the adjacent metaphysis. B, Salter-Harris type II fracture of the proximal phalanx of the foot. The metaphyseal fragment can vary in size substantially. In this case the metaphyseal fragment is large (arrow). C, Sagittal CT reformatted image of the ankle showing a Salter-Harris type II fracture of the distal tibia with posterior metaphyseal extension (arrow).

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925

■ FIGURE 36-12 A, Diagram of Salter-Harris type III fracture with the fracture line (red line) passing through the growth plate and extending into the adjacent epiphysis. B, Anteroposterior radiograph of ankle showing a medial malleolar Salter-Harris type III fracture (arrow).

■ FIGURE 36-13 A, Diagram of Salter-Harris type IV fracture with the fracture line (red line) passing through the growth plate and extending into both the adjacent metaphysis and epiphysis. B to D, Anteroposterior and lateral ankle radiographs with sagittal CT reformatted image. These demonstrate a medial malleolar epiphyseal fracture and a posterior metaphyseal fracture (arrows) with fracture of the anterolateral growth plate. This is a triplane fracture, which is a form of Salter-Harris type IV injury.

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P A R T O N E ● Injury: Pediatric Injuries

■ FIGURE 36-14 Diagram of Salter-Harris type V fracture with the fracture line (red line) passing through the growth plate without extending into the adjacent bone. This differs from Salter-Harris type I injury in that it is a compressive injury rather than a shearing one. This axial loading causes substantial damage to the growth plate and results in much greater growth disturbance than type I injury.

help in diagnosis. However, routine examination of the normal side should not be considered a substitute for a more experienced opinion. In type V injuries there is usually no immediate radiographic evidence and the effects are manifested only later as bone shortening and joint deformities. There are two distinctive forms of physeal fracture encountered in the distal tibia. These occur because of a predictable pattern of closure of the distal tibial growth plate that fuses from medial to lateral and posterior to anterior. While the physis is in the process of closing, the result is a medial fused and an unfused anterolateral growth plate. The medial and lateral parts of the bone now respond differently to applied stress, with the medial bone fracturing and failure of the growth plate anterolaterally. This produces complex fracture patterns, and three radiographic views are recommended (anteroposterior, lateral, and oblique) for the assessment of these ankle fractures. The Tillaux fracture describes a fracture of the anterolateral tibial epiphyseal plate that extends across the epiphysis and distally into the joint, creating a SalterHarris type III injury. The fragment is avulsed owing to the strong anterior tibiofibular ligament. It is commonly seen in adolescents and is caused by external rotation injury of the ankle (Fig. 36-15).21 The triplane fracture consists of three planes: a vertical fracture of the epiphysis, a horizontal cleavage plane within the physis, and an oblique fracture of the adjacent metaphysis. The last fracture differentiates it from a Tillaux fracture (Fig. 36-16).

■ FIGURE 36-15 Axial CT scan showing a Tillaux fracture with avulsion of the anterolateral tibia by the anterior distal tibiofibular syndesmotic ligament.

Hip Acute physeal injuries of the proximal femur are rare. Those that do occur are almost always Salter-Harris type I injuries, with the fracture line limited to the physis without extension into the metaphysis.22 These injuries occur as a result of falls, usually from a considerable height, or vehicle-pedestrian accidents, and they are frequently associated with other injuries, particularly fractures of the pelvis. Separation of the proximal femoral epiphysis has also been described in association with fractures of the femoral shaft and posterior dislocations of the hip. On the anteroposterior projection the epiphysis may appear to be centered normally in relation to the femoral neck, even in comparison with the other side, and diagnosis of epiphyseal separation may not be obvious. There is usually slight widening of the growth plate on the injured side. An oblique or frog-leg view is often required to demonstrate the epiphyseal displacement. The femoral epiphysis remains in its normal position within the acetabulum, and the femoral neck is displaced superiorly with the leg in the abducted position. Traumatic physeal fractures are the result of severe violence and can occur in children of any age. Epiphysiolysis, or slipped upper femoral epiphysis, is the result of chronic repetitive trauma to the proximal femoral growth plate. It characteristically occurs in adolescents (boys more frequently than girls) aged from 11 to 16 years and is associated with either no injury or minor force. Childhood obesity is also believed to be an etiologic factor. The onset of symptoms in epiphysiolysis is gradual, and, on occasion, displacement is completed by a minor traumatic event. Bilateral hip involvement is common.

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927

■ FIGURE 36-16 A, Coronal CT reformatted image of the ankle. There is a sagittal fracture of the distal tibial epiphysis with disruption of the lateral portion of the growth plate. B, Sagittal CT reformatted image of the ankle. There is also a coronally oriented fracture of the epiphysis with anterior growth plate fracture and posterior metaphyseal fracture (arrows). C, Axial CT section shows coronal (arrowheads) and sagittal (arrows) elements of the fracture. D, In the posterior metaphysis there is a coronally orientated fracture (arrowheads). The combination of horizontal growth plate, sagittal epiphysis, and coronal epiphysis/metaphyseal fractures is the classic triplane fracture.

The radiographic changes in epiphysiolysis may be subtle because of minor displacement of the capital femoral epiphysis. Frog-leg lateral views of the hip better demonstrate displacement compared with standard anteroposterior views (Fig. 36-17). Most commonly the epiphysis is displaced posteriorly and medially. The growth plate appears widened on the affected side, although in early cases irregularity or poor definition of the growth plate compared with the other side is the only radiographic clue. Normally, a line drawn along the

superior cortex of the femoral neck cuts through a small portion of the femoral epiphysis. In slipped epiphysis, the femoral epiphysis on the affected side lies more medial to this line than its counterpart on the opposite side. In severe cases this results in a characteristic hump deformity of the lateral femoral neck called “Hernden’s hump” (Fig. 36-18). The displacement may be so severe that no portion of the epiphysis is crossed by the line. Initial radiographs can be negative, and follow-up radiography can be used in patients who have persisting

928

P A R T O N E ● Injury: Pediatric Injuries

symptoms. An alternative in these patients is to investigate the integrity of the growth plate with MRI. Rarely, separation of the proximal femoral epiphysis occurs as the result of a birth injury. However, this may not be identified immediately because the proximal femoral epiphysis is not ossified. The superolateral displacement of the femur gives the appearance of congenital dislocation of the hip. The two are distinguished by the fact that the acetabulum is normally formed in epiphyseal separation but it is dysplastic in congenital dislocation. The combination of dislocation or subluxation and a shallow acetabulum is more accurately described as developmental dysplasia of the hip.

Ultrasonography Ultrasonography is frequently used as a primary diagnostic tool in young patients with hip pain. It is not used as a diagnostic tool for growth plate injury, but this must always be borne in mind when performing this procedure. This is especially the case in older children and adolescents in whom radiography should be a mandatory part of the investigation (Fig. 36-19).

Magnetic Resonance Imaging ■ FIGURE 36-17

A, Anteroposterior radiograph of pelvis in an adolescent. There is clear slipped capital upper femoral epiphysis on the left (arrow) with malalignment of the femoral neck and epiphysis. The right side looks comparatively normal. B, Turned (frog-leg) lateral view of right hip in same patient. The turned lateral view demonstrates clear slip of the proximal epiphysis on the right (arrow) with a line drawn through the superior cortex of the femoral neck not intersecting the epiphysis. The patient has bilateral slipped capital upper femoral epiphysis.

Magnetic resonance imaging can be of value in patients when there is clinical suspicion of epiphysiolysis without diagnostic growth plate change or displacement on radiography (Fig. 36-20).23,24 The typical features are widening of the growth plate associated with high signal on T2-weighted scans in the growth plate and surrounding bone marrow. Both hips should be examined when performing MRI because treatment of the contralateral side will be considered.25

Pelvis

■ FIGURE 36-18 Anteroposterior radiograph of right hip. The patient has a severe slipped capital upper femoral epiphysis with the classic convex configuration to the superior femoral neck called Hernden’s hump (arrow).

The degree of displacement of pelvic fractures is often less in children than in adults. Fractures through the triradiate cartilage are often difficult to identify, and displacement may be minimal. Usually the ischiopubic segment is displaced medially. Before making the diagnosis of minimally displaced disruption of the triradiate cartilage it is important to obtain a true anteroposterior pelvic radiograph. Faulty positioning with rotation of the pelvis may give the impression of displacement. An inlet view of the pelvis is useful. Bucholz and associates described three different types of triradiate cartilage fracture: Salter-Harris types I, II, and V. The diagnosis of type I is based on the identification of displacement or widening of the cartilage without fracture of the bony margins. Type II is identified by a fracture through bone adjacent to the triradiate cartilage, the equivalent of a metaphyseal corner sign. These fractures are better visualized on CT and should not be mistaken for free bone fragments within the joint. Secondary centers of ossification do not occur about the margins of the acetabulum or about the margins of the triradiate cartilage until adolescence. Therefore, separate fragments of bone at the margins of the triradiate cartilage in younger patients are due to fractures and do not represent normal

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929

■ FIGURE 36-19 A, Ultrasound image of left hip in a patient presenting with left hip pain. The proximal femoral epiphysis is not visualized with the metaphysis (MET) seen surrounded by effusion fluid (EFF). B, Frog-leg lateral views of both hips in the same patient demonstrate slipped capital upper femoral epiphysis in the left hip (arrows).

■ FIGURE 36-20 Earliest stage of slipped capital upper femoral epiphysis with chronic Salter-Harris type I injury to the proximal growth plates without slip. Metabolic causes such as vitamin D deficiency and renal osteodystrophy need to be excluded in these cases. A, Anteroposterior view of pelvis with irregularity of both proximal femoral growth plates (arrows). STIR (B) and T1-weighted coronal (C) MR images of pelvis with irregularity and edema around the proximal growth plate (arrows) in keeping with Salter-Harris type I injury without slip. D, Axial T1-weighted MR image of pelvis with irregularity of growth plate without evidence of slip (arrows).

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P A R T O N E ● Injury: Pediatric Injuries

developmental variants. Premature closure of the triradiate cartilage or acetabular epiphyses may result in a subsequent deformity of the acetabulum and subluxation of the hip.

What the Referring Physician Needs to Know ■

Computed Tomography Thin-section, volume-acquisition CT with multiplanar reformatting is used to more fully diagnose complex injuries identified on a plain radiograph to aid in management decisions and surgical planning. It is most commonly used in the ankle and knee. CT is particularly helpful in SalterHarris type IV fractures to determine whether the articular surface is aligned along the entire length of the fracture.20 CT is also valuable in the analysis of growth arrest and in the surgical planning of removal of bone bars that have bridged across the physis.26 The remainder of the epiphyseal complex continues to grow, creating an angular deformity.

■ ■ ■

Magnetic Resonance Imaging Magnetic resonance imaging has distinct advantages in the analysis of complex physeal injuries and in the evaluation of subsequent growth arrest. MRI can detect: ● ● ● ● ● ● ●

Occult physeal injury Cartilage, ligament, and soft tissue injuries Injury to unossified epiphyses Osteochondral injury Bone marrow edema and stress fractures Bone bridges causing premature physeal arrest Intact growth plate when physeal injury is suspected on the plain radiograph, thereby excluding injury

■

■ ■

■

Differential Diagnosis ●

Nonaccidental injury

Synopsis of Treatment Options The effective management of physeal injuries is crucial for two reasons. First, the growth plate is involved with the possibility of growth impairment. Second, the joint surface may be involved and current recommendations suggest that the interfragmentary gap should be no more than 2 mm.27 Shortening or deformities are less well tolerated in the lower extremity because of weight bearing. Salter-Harris type I and II fractures can be treated with cast or splint immobilization. It is the periosteum that provides stability to the reduced fracture. They do not require perfect alignment and have an excellent prognosis. An exception to this rule is type II fractures of the distal femur, which carry a poor prognosis unless anatomic alignment is attained by closed or open techniques. It has been shown that neglected type I and II fractures are best left untreated, especially in children younger than age 12 years. Subsequent bone growth corrects the angulation and restores length. Salter-Harris type III and type IV injuries require precise anatomic reduction to minimize future joint or

■

Radiographs of the contralateral asymptomatic side for comparison may be useful in distinguishing growth plates from fracture lines. Three view radiographs (anteroposterior, oblique, and lateral) are useful for distal tibial ankle fractures in children. Radiographs should include the joints proximal and distal to the injury. The possibility of an associated Salter-Harris type V injury of the proximal tibial or distal femoral physis must be considered with a fracture of the tibial shaft or femoral shaft or neck as a result of impaction forces. The possibility of growth arrest must be considered and this possibility discussed with the patient and parents. The physeal arrest characteristically involves either the posterolateral part of the distal femoral physis or the anterior part of the proximal tibial physis. The follow-up radiographs of shaft fractures of the lower extremity should include the proximal and distal epiphyseal centers. The proximal tibial physis is the most common site of the Salter-Harris type V injury. At the time of the initial evaluation of the fracture the proximal tibial physis may appear normal, but on follow-up examinations a recurvatum deformity of the knee becomes increasingly apparent. Radiographs reveal closure of the anterior portion of the growth plate. The presence of a joint effusion can help in diagnosis of fractures at the ankle and knee. There is a greater risk of avascular necrosis and growth arrest or deformity in children’s hip fractures owing to the vascularity and presence of a physis. Whenever a pelvic fracture is identified in a child the possibility of separation of the proximal femoral epiphysis should be considered. A child with multiple injuries should have anteroposterior and frog-leg views of the pelvis due to the potential difficulty in visualizing epiphyseal separations of the proximal femur. A single anteroposterior projection is insufficient to exclude injuries of the proximal femoral epiphysis in a child.

growth abnormalities. Most require open reduction and fixation to prevent growth arrest and joint surface deformity. Bone bridging is a result of fracture displacement, which may result in angular deformity of the joint surface or impaired growth. Salter-Harris type V fractures are usually recognized in retrospect as a consequence of premature physeal closure and subsequent premature growth cessation. Growth arrest is usually partial and may be treated surgically by resection of the bone bridge and interposition of a free fat graft or inert material. It is important to recognize bone bridging as early as possible to maximize the potential benefit of surgery. Treatment of proximal femoral epiphyseal separation consists of closed reduction when possible and placement of the patient in a plaster spica cast. When the displacement is more severe, open reduction with threaded pin fixation is required. Complications of separation of

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● Lower Extremity Injuries in Children (Including Sports Injuries)

the proximal femoral epiphysis include premature fusion, avascular necrosis, and nonunion. These complications occur in more than 50% of patients.

ACUTE APOPHYSEAL INJURY Manifestations of the Disease Radiography Apophyseal injuries are unique to skeletally immature patients and are prominent in young athletes. A sudden forceful muscular contraction can cause acute apophyseal separation, particularly in sports requiring sudden powerful acceleration or change of direction such as football, dance, or gymnastics. Clinically, it may be difficult to distinguish between a simple muscle strain and an apophyseal avulsion. Acute avulsion injuries are seen on plain radiographs as crescentic osseous fragments; but if the ossification center of the apophysis has not yet formed, then radiographs may not be helpful. Follow-up radiography, however, will demonstrate healing with abundant callus (Fig. 36-21). Apophyseal injuries occur most commonly around the pelvis, including the ischial tuberosity (hamstrings), anterior inferior iliac spine (rectus femoris), anterior superior iliac spine (sartorius and tensor fascia lata), iliac crest (abdominal obliques, latissimus dorsi), the lesser trochanter (iliopsoas), the greater trochanter (external hip rotators), and the symphysis pubis (adductor muscles).28 At these sites the fracture edge may extend directly through the physeal cartilage, into the ossifying apophysis or the underlying bone. Around the knee, the tibial eminences may be avulsed.29 The anterior tibial eminence is most commonly avulsed at the site of insertion of the anterior cruciate ligament. Unlike in adults this injury is usually isolated and is not associated with internal derangement. Diagnosis with

931

radiography can be difficult and often requires additional tunnel view and oblique imaging. Undisplaced fractures consist of a horizontal fracture line at the base of the anterior portion of the tibial spine. These are difficult to visualize and are best seen on the lateral view. The fragment can also be partially or completely detached. Avulsions of the tibial tuberosity are uncommon and are associated with sports activities that require jumping. Although an acute injury, tibial tuberosity avulsion is most frequently seen in young adolescents with ongoing Osgood-Schlatter disease. Three types of fracture are described in the WatsonJones classification scheme on the basis of extent of involvement of the proximal tibial epiphysis and degree of displacement of the fracture fragment. Type 1: Avulsion of the apophysis without injury to the tibial epiphysis Type 2: An epiphysis that is lifted cephalad and incompletely fractured Type 3: Displacement of the proximal base of the epiphysis with the fracture line extending into the joint

Computed Tomography Computed tomography can help to demonstrate the avulsed apophysis.

Ultrasonography Ultrasound examination is useful in cases in which it is clinically difficult to differentiate between a simple muscle strain and an apophyseal avulsion, especially if the plain radiographs are not helpful, usually when the ossification center of the apophysis has not yet formed. An irregular bony surface, a thickened physeal surface with fissures, small hyperechoic structures with posterior acoustic enhancement from avulsed fragments, and local hematoma may be demonstrated on ultrasound examination. The size and displacement of the avulsed fragments is variable (Fig. 36-22).30 Lazovic and coworkers31 described the use of ultrasound examination in 243 cases of suspected apophyseal avulsion. They found it to be more sensitive than plain radiography, with the advantage that it allows dynamic examination to elicit an unstable apophyseal avulsion. Ultrasonography is also of value in distinguishing acute from chronic change by demonstrating hematoma in or around the apophyseal growth plate in acute injury.

Magnetic Resonance Imaging

■ FIGURE 36-21 Anteroposterior radiograph of pelvis in a patient with sudden onset of right hip pain. There is bony protuberance seen related to the ischial tuberosity (arrows) in keeping with hamstring origin avulsion of the ischial tuberosity.

Magnetic resonance imaging of avulsion injuries is increasingly being undertaken in difficult cases.32–36 The main advantage is better imaging of deep tendons or areas difficult to reach with ultrasound examination. T1- and T2-weighted and fat-suppression images with planes appropriate for the joint being examined should be obtained. The bone fragment may be seen in continuity with the tendon. Bone marrow edema at the site of detachment can be seen as high signal intensity on T2-weighted images. More chronic injuries have a low-to-

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P A R T O N E ● Injury: Pediatric Injuries

■ FIGURE 36-22 A, There is avulsion of the anterior superior iliac spine in keeping with a sartorius avulsion (arrow). B, Ultrasound image shows the avulsed fragment and attached sartorius muscle (arrows).

intermediate signal on both T1- and T2-weighted images (Fig. 36-23).

Differential Diagnosis Sometimes there is no history or only a remote history of a minor traumatic event. Healing avulsions can have an

aggressive appearance at radiography, including lysis and destruction. Such findings can mimic those seen with osteomyelitis or Ewing’s sarcoma37 and lead to excessive imaging, biopsy, and incorrect diagnosis. The location of the lesion, the age of the patient, the absence of symptomatology, normal hematology, and an awareness of the problem should prevent diagnostic difficulty.

■ FIGURE 36-23 A, T2-weighted sagittal MR image of patient in Figure 36-21. There is a large avulsion of the ischial tuberosity apophysis by the common hamstring origin tendons (arrows). This is associated with a large amount of soft tissue edema in keeping with acute avulsion. B, T1-weighted sagittal MR image in same patient. This better demonstrates the avulsed bone fragment (arrow) and the donor site from the ischium and posterior acetabular wall.

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● Lower Extremity Injuries in Children (Including Sports Injuries)

Synopsis of Treatment Options Ischial Tuberosity Avulsion Patients tend to respond well to conservative treatment such as several days of bed rest, restricted activity, and return to normal activity over 6 to 12 weeks. If the fragment is displaced by more than 2 cm, however, fibrous union may occur, resulting in extended disability. Avulsions of the anterior superior iliac spine and the anterior inferior iliac spine tend to be less symptomatic and disabling than avulsions of the ischial tuberosity, and recovery time is relatively short. Bed rest is the first line of treatment, followed by progressive ambulation. Isolated avulsion of the anterior tibial spine is treated conservatively when undisplaced or minimally displaced. Surgical reattachment is required for those avulsions that are widely displaced or completely detached. Anterior cruciate ligament avulsion of the medial tibial spine can be treated surgically or conservatively. If there is no clinical evidence of anterior cruciate ligament laxity with minimal displacement of the fracture fragment, conservative management and follow-up can be undertaken. This is, however, an unusual clinical scenario, with the majority of these avulsions reattached surgically (Fig. 36-24).

What the Referring Physician Needs to Know ■

In young athletes the correct diagnosis is essential to establish the appropriate treatment and rehabilitation program.

933

CHRONIC APOPHYSEAL INJURY: OSGOOD-SCHLATTER DISEASE Manifestations of the Disease Radiography Osgood-Schlatter disease is a chronic or acute-on-chronic avulsion injury thought to result from repetitive microtrauma and traction on the tibial tubercle at the site of distal patellar tendon insertion. Osgood and Schlatter first recorded this entity as a manifestation of trauma in 1903. It is typically seen in young adolescents, especially those who participate in sports that require jumping, squatting, and kicking, and can be bilateral in up to 50% of patients. Boys tend to be affected more than girls. Osgood pointed out the importance of radiographs as an adjunct to clinical examination. Radiographs show fragmentation of the tibial tubercle, although this can represent a normal ossification center and is nonspecific. Additional features on radiographs have been described that include irregularity of the infrapatellar fat pad outline, obliteration of the inferior angle of the infrapatellar fat pad, and thickening of surrounding soft tissues. Patients with Osgood-Schlatter disease are at increased risk of avulsions of the tibial tuberosity.

Magnetic Resonance Imaging The most consistent finding in Osgood-Schlatter disease is thickening and edema of the inferior patellar tendon. Other features include soft tissue swelling anterior to the tibial tuberosity, loss of the sharp inferior angle of the infrapatellar fat pad and surrounding soft tissues, and infrapatellar bursitis. Edema of the tibial tuberosity and

■ FIGURE 36-24 A, Horizontal-beam lateral view of left knee. There is a large, somewhat dense effusion (*) in keeping with hemarthrosis. There is also an elongated bone fragment seen projected over the joint space (arrows). B, Anteroposterior view shows the bone fragment lies in the intercondylar region (arrow) close to the anteromedial tibial spine. This is the typical site for an anterior cruciate ligament avulsion.

(Continued)

934

P A R T O N E ● Injury: Pediatric Injuries

■ FIGURE 36-24—Cont’d C, Sagittal proton density–weighted, fat-suppressed MR image shows an avulsion fracture of the anterior cruciate ligament (arrow) with the ligament remaining intact (*). D, T1-weighted coronal MR image shows the fragment is the avulsed medial tibial spine (arrow). E, Proton density–weighted, fat-suppressed coronal MR image shows fluid around and edema within the avulsed medial tibial spine (arrow).

tibial epiphysis and thickening of the cartilage anterior to the ossification center of the tibial tubercle are further MRI features. Edema may be noted extending to involve the physis and the area between the tibial tuberosity and the proximal tibia. During the later phase of the disease the peritendinous edema becomes less evident and eventually the ossification centers of the tibial tuberosity coalesce and fuse with the tibial epiphysis.

■ FIGURE 36-25

Ultrasonography The distal patellar tendon appears thickened and of increased echogenicity. A hypoechoic zone of soft tissue swelling may be present around the apophysis of the anterior tibial tuberosity. If a fragment of tuberosity is avulsed, a curvilinear echogenic line may be seen anterior to the tibial tuberosity (Fig. 36-25).38

A, Longitudinal sonogram showing normal patellar tendon (PT) inserting on the tibial tuberosity. B to D, Longitudinal sonograms from contralateral symptomatic knee in same patient as in A. There are typical features of Osgood-Schlatter disease. There is fragmentation of the tibial tuberosity apophysis (arrows) associated with thickening and hypervascularity in the distal patellar tendon (PT).

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Differential Diagnosis The diagnosis is usually made from clinical findings, but radiography and MRI may be used to exclude other causes of knee pain. This includes patellar tendinosis, osteochondritis dissecans, and proximal tibial stress fracture.

Synopsis of Treatment Options Medical Treatment Most patients respond to conservative measures such as rest and analgesia and can return to activity within a few weeks. Osgood-Schlatter disease usually resolves completely once the patient reaches skeletal maturity.

Surgical Treatment Complications that can occur include residual deformity and painful ossicles in the distal patellar tendon, and in these cases surgical removal of the ossicle may be considered.

What the Referring Physician Needs to Know ■

Although imaging may show what appears to be severe injury, these patients do well with appropriate rest and rehabilitation. Intervention is seldom required.

CHRONIC APOPHYSEAL DISEASE: SINDING-LARSEN-JOHANSSON DISEASE Manifestations of the Disease Radiography Sinding-Larsen-Johansson disease is an avulsive fragmentation of the inferior pole of the patella caused by repetitive microtrauma at the patellar tendon insertion at the inferior patellar pole. It is similar to jumper’s knee. Like Osgood-Schlatter disease it is a self-limiting and benign condition. On lateral radiographs the inferior patellar pole apophysis may be fragmented.

Ultrasonography The proximal patellar tendon appears thickened and hypoechoic due to tendinosis, and there may be a fluid collection from infrapatellar bursitis. Ultrasound examination can reveal small calcified fragments and irregularity in the bony outline resulting from the osteochondrosis. The physeal cartilage and overlying soft tissue is edematous and appears hypoechoic. During the acute phase localized hyperemia may be demonstrated on proton density–weighted imaging (Fig. 36-26).

Magnetic Resonance Imaging Fragments of bone or cartilage may demonstrate perifocal high-signal-intensity edema on T2-weighted images.

■ FIGURE 36-26 A, Longitudinal sonogram of the lower pole of the patella and proximal patellar tendon (PT). There is irregularity of the bone cortex of the lower pole of the patella with hyporeflective thickening of the adjacent patellar tendon (arrows) in keeping with Sinding-Larsen-Johansson disease. B, Power Doppler sonogram of the same area shows marked neovascularization in the tendinopathic tendon (arrows).

During the chronic phase, fibrotic tissue of intermediate signal replaces the edema with eventual incorporation of the fragment to the patella.

Differential Diagnosis ● ●

Jumper’s knee Patellar sleeve fracture

Synopsis of Treatment Options Initial treatment of Sinding-Larsen-Johansson disease consists of ice to relieve pain, stretching and strengthening exercises, and modification of activities. Specifically, kneeling, jumping, squatting, stair climbing, and running on the affected knee should be avoided.

THE PATELLAR SLEEVE FRACTURE Manifestations of the Disease Radiography A patellar sleeve fracture is an osteochondral avulsion fracture from the patella and more commonly occurs at the lower pole at the insertion of the patellar tendon.

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They are rare but are the most common type of patellar injury in children younger than 16. These injuries are due to failure of the physis after excessive traction stresses. Patients present acutely with lipohemarthrosis and an inability to raise a straightened leg.39 The radiographic findings are those of patellar tendon disruption (high-lying patella or patella alta) and osteochondral fragment (Fig. 36-27A). The fracture becomes intra-articular if it extends into the articular cartilage of the inferior pole of the patella, and in these cases a lipohemarthrosis may be evident. However, the avulsed fragment from the inferior pole of the patella may be occult radiographically if there is a small avulsed bony fragment.40 The cartilaginous injury is often large and extends far beyond the avulsion fracture seen radiographically.

The superior pole of the patella can also be the site of a superior sleeve avulsion by the quadriceps tendon. Partial patellar sleeve injuries are also seen with lesser degrees of avulsion (see Fig. 36-27B). This fracture differs from straightforward avulsion because of the “sleeve” of periosteum that is pulled off the patella and will continue to form bone if not treated, thus enlarging or even duplicating the patella. Also, simple excision of the bony fragment when present should be avoided, at least in the acute stage because it leaves an irregular lower pole of the patella. In a sleeve fracture, when it is missed at the time of the injury, the new bone formed will be too large to reduce and fix and will have to be removed, emphasizing the importance of an awareness of this injury and prompt diagnosis and treatment.

■ FIGURE 36-27 A, Patellar sleeve fracture with high-lying patella (P) with the avulsed osteochondral fragment (arrow) lying just anterior to Hoffa’s fat pad. B, More subtle patellar sleeve avulsion with the avulsed fragment (arrow) remaining close to the patella. C, Ultrasound image from patient in A with the large osteochondral fragment (arrows) clearly demonstrated still attached to the patellar tendon (PT), helping distinguish this injury from other causes of osteochondral fragments. Effusion (E) is seen within the joint deep to Hoffa’s fat pad.

(Continued)

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■ FIGURE 36-27—Cont’d D, T1weighted sagittal MR image from patient in B. The sleeve avulsion fragment is clearly visualized on the MR image (arrow), still closely related to the patella (P). E, T2-weighted, fat-suppressed sagittal MR image from patient in B. The avulsion fragment has quite marked surrounding bone marrow and soft tissue edema in keeping with an acute sleeve avulsion.

Ultrasonography

Medical Treatment

The osteochondral fragment is identified on ultrasound examination as a broad sleeve of cartilage that is often associated with an osseous fragment pulled away with the tendon (see Fig. 36-27C). Ultrasound examination allows measurement of separation of the fragments. In more subtle cases, high-resolution ultrasound examination may demonstrate a “double cortical sign” as a result of elevation of the most superficial layer of the bony cortex or a wavy and thickened periosteal line, separated from the bone by an effusion.41 This injury is differentiated from an osteochondral body by the fact that the patellar tendon remains attached to the fragment.

The degree of fragment displacement is crucial in therapeutic planning. If a bony fragment is visible on radiographs and the displacement is less than 2 mm, closed treatment in a cast in extension is justified. However, the results of conservative treatment are often unsatisfactory. Conservative therapy may be used for minimally displaced fractures and involves placing the knee in an extension splint.40

Magnetic Resonance Imaging Definition of the extent of cartilaginous injury, joint involvement, and displacement of the fragments with MRI is useful for determining treatment options and assessing the need for surgery.40 Fractures are best seen in the sagittal plane along the axis of the patella. The cartilaginous fracture is usually extensive and is seen as a hyperintense fracture line that contrasts to the hypointense cartilage.40 Distraction of the fragments may be mild (see Fig. 36-27D).

Differential Diagnosis ● ●

Jumper’s knee Sinding-Larsen-Johansson disease

Synopsis of Treatment Options The problem in treatment is the reduction of the injured tissue, to restore the length of the patella tendon and reduce the extent of patella alta.

Surgical Treatment Most cases require surgery, with the exception of those with minimal displacement. The treatment recommended for displaced patellar avulsion fractures involves open surgical reduction and realignment of the articular surfaces, with or without internal fixation, and reconstruction of the extensor apparatus. This prevents further deformity of the patella and loss of motion.

ACUTE OSTEOCHONDRAL INJURIES Manifestations of the Disease Radiography Abnormal joint motion leading to shearing, rotatory, or impaction forces may fracture one or both of the opposing joint surfaces. Resultant fracture fragments may consist purely of cartilage (chondral fracture) or cartilage attached to a bone fragment (osteochondral fracture). These injuries may be difficult to diagnose from the plain radiograph in the acute phase because a chondral portion of the fragment is not radiopaque. The radiodensity related to osteochondral fragments depends on the thickness of subchondral bone that separates away with the

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P A R T O N E ● Injury: Pediatric Injuries

cartilage. Fracture fragments may become more apparent as loose bodies when their cartilage undergoes degenerative calcification (Fig. 36-28).

Ultrasonography Osteochondral fragments have characteristic appearances at ultrasound examination with hypoechoic cartilage attached to a variable amount of subchondral bone (Fig. 36-29).

Magnetic Resonance Imaging Magnetic resonance imaging can provide a definitive diagnosis when distinguishing osteochondral lesions from the normal irregularity of the epiphysis that is found in some children on plain radiographs. It can help to establish whether the fracture fragment is stable, which is essential in management decisions. High-signal edema on T2-weighted imaging between the fragment and the underlying bone is the best indicator of articular cartilage disruption and fragment instability. It represents joint fluid tracking into the cleft between the fragment and underlying bone. The presence or absence of a joint effusion is thus important when interpreting this sign. If no effusion is present, the absence of a rim of high T2 signal is less reliable and recourse to MR arthrographic assessment may be required. MRI can also help exclude any further internal joint disruption and is useful for assessment of the donor site and mechanism of injury. The knee is a common site for acute osteochondral lesions, with occult patella dislocation a frequent causative mechanism. The classic features are lipohemarthrosis, bone bruising in the medial patella and lateral femoral condyle, medial retinacular disruption, and osteochondral injury (Fig. 36-30). Patella alta may also

■ FIGURE 36-29 Transverse sonogram of anterior femoral condyle (FC) with osteochondral fragment (*) lying within its donor site.

be better appreciated by the MRI than on radiographic examination.42–44

Arthroscopy Arthroscopy can be used to diagnose and grade osteochondral lesions in the hip, knee, and ankle and to detect loose bodies. Therapeutic arthroscopy is increasingly being utilized for less invasive management of these lesions.

■ FIGURE 36-28 A, Horizontal-beam lateral radiograph demonstrates a lipohemarthrosis (arrows). B, Anteroposterior radiograph in same patient shows two densities (arrows) on the lateral aspect of the distal femur with typical appearances of osteochondral fragments.

CHAPTER

■ FIGURE 36-30

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939

MR images from patient in Figure 36-28 who has acute osteochondral injury from patellar dislocation. A, Proton density– weighted, fat-suppressed sagittal MR image shows effusion containing fat lobules (arrowhead) in keeping with lipohemarthrosis. There is bone edema (E) in the lower pole of the patella associated with a large area of cartilage damage (arrows). B, Axial proton density–weighted, fatsuppressed sagittal MR image. There is bone edema (E) in the lower pole of the patella associated with a large area of cartilage damage (arrows). Edema is noted in the medial retinaculum of the patella in keeping with damage during dislocation (arrowhead). C, Axial proton density–weighted, fat-suppressed sagittal MR image from slightly lower section than shown in B. The osteochondral fragment is clearly visualized with intermediate cartilage signal (arrows) and a thin sliver of low signal subchondral bone (*). There is bone edema in the lateral femoral condyle (E) at the site of impaction injury during patellar dislocation. D, T2-weighted, fat-suppressed MR image of same section as shown in C. The edema (E) is slightly more clearly visualized, and it is easier to appreciate the fluid-fluid level within the effusion, indicating this is a hemarthrosis (arrowheads).

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P A R T O N E ● Injury: Pediatric Injuries

Synopsis of Treatment Options Most nondisplaced lesions in patients with open physes will heal with conservative management.45 However, displaced fragments or skeletally mature patients often require surgical intervention45 to relieve symptoms and prevent osteoarthritis. If adequate cortical bone is attached to the fragment, drilling of stable lesions or drilling with fixation of unstable or loose fragments is indicated. Autologous bone graft can be necessary to stimulate healing and properly reconstruct the subchondral bony contour. For failed fixation attempts, or lesions not amenable to fixation, an articular surface reconstruction technique may be used. The goal for the reconstructive procedure, to produce a smooth gliding articular surface of hyaline or hyaline-like cartilage, is possible using current techniques, including autologous osteochondral mosaicplasty and autologous chondrocyte implantation. Débridement, drilling, microfracture, and abrasion chondroplasty have been shown to result in fibrocartilage with inferior mechanical properties when compared with hyaline cartilage. No long-term studies have been published, however, to confirm the benefits of replacing osteochondral defects with hyaline cartilage rather than fibrocartilage. Autologous chondrocyte implantation involves harvesting autologous chondrocytes from an area of healthy cartilage and culturing them with the use of growth factors to promote chondrocyte growth and differentiation. They are then reimplanted to the chondral defect and held in place beneath either a periosteal patch or a type I/III collagen matrix to synthesize and maintain normal chondral

matrix.46 The advantage is the higher degree of hyalinelike rather than fibrous cartilage. Disadvantages include high cost, the open procedure involved (with higher morbidity), technically difficult surgery, and availability. Although the results of many reconstructive procedures are quite encouraging with early follow up, the ultimate goal is to prevent long-term osteoarthritis.45 A recent follow-up study over 4 years has shown that favorable factors for collagen covered autologous chondrocyte implantation include younger patients, a less than 2-year history, a single defect, and a defect on the trochlea or lateral femoral condyle.47

OSTEOCHONDRITIS DISSECANS Manifestations of the Disease Radiography Osteochondritis dissecans is a lesion of unknown cause that results in an island of abnormal subchondral bone separating from the normal bone. It may also break away entirely, leading to an osteochondral loose body that can interfere with joint function. The exact etiology is unknown, but it is thought to be due to overuse and is mainly seen in adolescent athletes. Osteochondritis dissecans is usually evident on a plain radiograph and is seen as a lucency in the articular epiphysis or loss of the sharp cortical line. The separated fragment will not be seen if it contains only a small amount of subchondral bone (Fig. 36-31A and B).

■ FIGURE 36-31 A, Anteroposterior radiograph of knee showing normal appearances. B, Lateral view shows evidence of a defect and fragment within the anterior femoral condyle (arrows).

(Continued)

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941

■ FIGURE 36-31—Cont’d C, Transverse sonogram demonstrates the osteochondritic fragment (*), which lies in the usual orientation with the cartilage on the fragment facing away from the donor site (arrows) and underlying femoral condyle (FC). D, Transverse sonogram from a different patient with osteochondritis dissecans. Note fragment lying within the donor site; there is no cartilage cover, suggesting either the fragment has no cartilage cover or is inverted. E, Sagittal proton density–weighted, fat-suppressed MR image from patient in D. The osteochondritic fragment (arrows) is seen inverted within the donor site.

The most common site in the knee is the lateral aspect of the medial femoral condyle (75%). The weight-bearing surfaces of the medial and lateral femoral condyles, the patella, and the medial tibial plateau may also be involved. In the ankle joint, osteochondritis dissecans occurs most frequently in the talar dome, affecting either the posteromedial or anterolateral aspect. The tibial plafond is less frequently involved. Occasionally, mirror-image osteochondritis dissecans of the talar dome and tibial plafond occurs, suggesting trauma as the cause for both lesions, or osteochondritis dissecans of the tarsal navicular occurs that is limited to the proximal articular surface and may require further imaging to differentiate it from stress fracture. Osteochondritis dissecans of the hip occurs predominantly in the femoral capital epiphysis in patients with a prior history of Legg-Calvé-Perthes disease.

Ultrasonography Ultrasonography has been used to diagnose osteochondritis dissecans of the knee and may show cartilage irregularity or even a bone defect. The advantage of ultrasonography is dynamic scanning with motion of the examined joint (see Fig. 36-31C and D).

Magnetic Resonance Imaging Magnetic resonance imaging will show bone edema at an early stage.48 It can provide a definitive diagnosis when

distinguishing the lesions of osteochondritis dissecans from the normal irregularity of the epiphysis that is found in some children on plain radiographs. As with acute osteochondral lesions, MRI showing high signal fluid on T2-weighted or short tau inversion recovery (STIR) sequences between the fragment and the underlying bone indicates fragment instability and is important in management decisions. MRI can also show change in lesion orientation and determine cartilage integrity over the osteochondral lesion (see Fig. 36-31E). With improved MR technology, this can now normally be successfully performed in the knee without MR arthrographic contrast enhancement being required. This is particularly the case when a joint effusion is present (Fig. 36-32). The hip cartilage is more difficult to assess, with MR arthrography more often required; fortunately, this is a relatively rare site for osteochondritis dissecans. MRI is an ideal modality for follow up of the lesions of osteochondritis dissecans to determine healing or progression.

Computed Tomography A cystic lesion of the talar dome, cortical depression, or a loose bony fragment within the osteochondral defect may be demonstrated. CT arthrography is rarely required in the pediatric age group.

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P A R T O N E ● Injury: Pediatric Injuries

■ FIGURE 36-32 A, Coronal T1-weighted MR image of knee showing osteochondritis dissecans of the weight-bearing portion of the medial femoral condyle (arrows). The cartilage overlying the osteochondritis dissecans is intact. Coronal (B) and sagittal (C) proton density–weighted, fat-suppressed MR images show the osteochondritis dissecans is less clearly delineated on the fatsuppressed proton density–weighted MR sequences (arrows); the continuity of the overlying cartilage is, however, more clearly seen. This is stable osteochondritis dissecans.

Bone Scintigraphy

Differential Diagnosis

Scintigraphic findings are nonspecific, demonstrating a mild to marked increase in focal uptake in the involved bone, depending on the age of the osteochondritis dissecans. Dynamic bone scintigraphy is more sensitive than static scintigraphy in the detection of osteochondritis dissecans of the femoral condyles. The scintigraphic appearance is probably a result of the slow repair process around a lesion of osteochondritis dissecans, involving only the bone tissue surrounding the lesion and not the result of the osteochondritis dissecans itself.

● ● ●

Stress fracture Primary osteoarthritis and avascular necrosis Meniscal injury

Synopsis of Treatment Options Treatment consists of discontinuation of the injurious activity, protected immobilization of the joint, and administration of nonsteroidal anti-inflammatory agents. Surgery may be required to remove the intra-articular loose body

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943

■ FIGURE 36-33 Kohler’s disease. A, Oblique radiograph of the foot shows initial normal appearances of the tarsal navicular (TN). B, Lateral radiograph 2 years later shows typical changes of Kohler’s disease with flattening and sclerosis of the tarsal navicular (arrows).

and/or correct the resulting degenerative changes. See the previous section on treatment options under Acute Osteochondral Injuries.

OTHER OSTECHONDROSES Manifestations of the Disease Radiography There are several osteochondroses reported in the literature, many with eponymous names. The common factor appears to be repetitive trauma, and the diagnosis can usually be made from the plain radiograph. Kohler’s disease results in osteonecrosis of the tarsal navicular while the surrounding cartilage is preserved (Fig. 36-33). There is also Kohler’s disease of the patella, which represents osteochondrosis of the primary ossification center of the patella. Freiberg’s disease is osteonecrosis of the metatarsal head after osteochondral fracture. This presents as flattening and collapse of the second metatarsal head and is associated with joint synovitis. Freiberg’s disease tends to occur in adolescence to young adult life and is more common in females (Fig. 36-34). Sever’s disease is described as an apophysitis of the posterior calcaneal apophysis. This condition results, however, from a chronic Salter-Harris type I injury to the calcaneal apophysis under loading from the Achilles

■ FIGURE 36-34 A, Anteroposterior radiograph of the forefoot showing evidence of Freiberg’s disease with squaring off and flattening of the subchondral plate of the second metatarsal head (arrows).

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P A R T O N E ● Injury: Pediatric Injuries

■ FIGURE 36-35 A, Lateral radiograph of the heel showing features suggestive of Sever’s disease. There is fragmentation and sclerosis in the calcaneal apophysis (arrows). These changes can, however, be seen in asymptomatic individuals. B, STIR sagittal MR image shows MR appearance of Sever’s disease with edema within the apophysis and growth plate (arrows).

and plantar fascia.49 Radiographic diagnosis is difficult because sclerosis and fragmentation of the calcaneal apophysis is seen as a normal variant. The MR findings are more reliable, with edema and high signal centered on the apophyseal growth plate associated with fragmentation of the apophysis (Fig. 36-35).49

■ FIGURE 36-36 Axial T2-weighted, fat-suppressed MR image through the calf. There is evidence of shin splints with periosteal edema present around the medial side of the tibia (arrows). The cortical bone and medullary cavity are normal.

STRESS FRACTURES Manifestations of the Disease Radiography Stress injuries result from repetitive, cyclical loading of bone that overwhelms the reparative ability of the skeletal system. In children, these are commonly due to early participation in competitive sports. The majority occur in the lower limb, particularly the proximal tibia, metatarsals, and calcaneum. The most common cause is running, although gymnastics has also been heavily implicated.50 These injuries encompass shin splints, stress reactions, and stress fractures, which comprise a continuum of increasing severity of injury. At the lowest level (shin splints), periostitis develops, either anteriorly or posteriorly due to the increased muscle demands at their origins. Importantly, there is no evidence of marrow involvement. This is well demonstrated by either MRI or bone scintigraphy but is radiographically occult (Fig. 36-36). If the patient persists in the activity, then this can progress onto a stress reaction. The differentiating feature is that bone marrow edema is now visible on MRI, although there should be no evidence of cortical sclerosis. Once again this is radiographically occult (Fig. 36-37). The final stage, if the patient persists with an unabated exercise regimen, is the development of a stress fracture. This is characterized by a developing sclerotic line across the bone that if left untreated can go on to frank fracture (Fig. 36-38). At the knee, stress fractures may involve the metaphysis of either the distal femur or, more commonly, the

CHAPTER

■ FIGURE 36-37

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● Lower Extremity Injuries in Children (Including Sports Injuries)

Stress fracture. A, Lateral radiograph of the tibia and fibula showing subtle cortical irregularity on the posterior aspect of the lower tibial shaft. B, Sagittal STIR MR image in the same patient shows cortical thickening with periosteal and endosteal edema in keeping with a developing stress fracture (arrows). C, Axial STIR MR image in the same patient shows cortical thickening with periosteal edema (arrows) and endosteal edema (E).

945

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P A R T O N E ● Injury: Pediatric Injuries

■ FIGURE 36-38

Anteroposterior (A) and lateral (B) views of tibia and fibula show stress fracture of the proximal tibia (arrows). Anteroposterior (C) and lateral (D) views of tibia and fibula at 6-month follow-up. There has been healing of the stress fracture with now only subtle cortical irregularity (arrows). Axial (E) and sagittal (F) T2-weighted fat-suppressed MR image with advanced stress injury. Note periosteal edema (arrows), cortical thickening (*), and medullary edema (E).

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proximal tibia. The neck and proximal shaft of the fibula are less commonly involved. Radiography is the first investigation for a stress injury. Diagnosis requires a high index of suspicion because the initial radiographs are usually normal. In this scenario where there remains ongoing clinical concern, then further imaging either by MRI or bone scintigraphy should be undertaken to look for either shin splints or stress reactions. Sequential radiographs can be helpful, and films taken 3 to 4 weeks after the onset of symptoms may show localized periosteal and endosteal thickening, callus formation, or a cortical radiolucent line.50 Stress fracture of the proximal tibia manifests as a transverse band of increased density on the anteroposterior projection. On the lateral view, callus formation may be seen along the posterior cortical surface. There may be widening of the physis with sclerosis at both epiphyseal and metaphyseal margins. Fractures of the navicular and tarsal bones are frequently missed or are invisible on radiographs.

Nuclear Medicine Bone scintigraphy is a very sensitive method for the diagnosis of stress fractures, although it is not specific. Increased uptake of the radionuclide is seen 24 to 36 hours after the onset of symptoms that remains altered during several months. The characteristics of radionuclide uptake differ depending on the extension and on the time evolution of the fracture. Bone uptake can be focal and localized, linear, or very extensive, as is the case with longitudinal diaphyseal fractures, owing to the increase in bone remodeling. Three-phase bone scintigraphy usually demonstrates increased uptake in the perfusion, blood pool, and delayed phases. This usually allows differentiation from shin splints, medial tibial stress syndrome, and compartment syndrome, which have similar presenting features and do not demonstrate increased uptake during the perfusion and blood pool phases.51 There is no underlying cortical break in these conditions. Most stress fractures, such as metatarsal and tibial fractures, can be diagnosed using a combination of radiography and scintigraphy. Occasionally, some fractures, such as those of the femur and tarsus, are difficult to identify and need additional tests for diagnosis.

Magnetic Resonance Imaging The lack of specificity of scintigraphy means that, in general, MRI is of greater diagnostic value because it differentiates between periosteal, cortical, and medullary disruption. It is particularly useful in the small bones of the feet in which the relatively poor spatial resolution of the radionuclide bone scintigraphy can be a disadvantage. MR findings can be positive within 24 hours of onset of symptoms. Shin splints show as edema centered on the periosteum and adjacent muscles with no evidence of extension into the marrow. Stress reactions show as

947

periosteal, muscle, and bone marrow edema, which is clearly demonstrated with MRI using a STIR or fat-suppressed T2-weighted sequence.50 This can represent bone contusion without a linear component rather than a stress fracture, which can be difficult to distinguish on early MRI (37 ms).54 On MRI, readers often focus on internal derangement. It is important to make the proximal patellar tendon a regular review area. Patellar tendon rupture is usually the end stage of patellar tendinitis resulting from the cumulative effects of repetitive microtrauma of the patellar tendon55 and secondary to corticosteroid injection therapy. It therefore tends to occur most often at the proximal tendon insertion site. Complete tears appear as total discontinuity of fibers, with edema, hematoma, and patella alta. Partial tears demonstrate some intact fibers, edema, hematoma, indistinct tendon margins, and tendon thickening.

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949

■ FIGURE 36-41 A, Longitudinal power Doppler sonogram of the proximal patellar tendon (PT) obtained in a knee-flexed position. There is evidence of proximal patellar tendinopathy with hyporeflective thickening of the tendon associated with loss of normal tendon internal architecture. No power Doppler signal is demonstrated in the tendon in the flexed position. B, Longitudinal power Doppler sonogram of the proximal patellar tendon (PT) obtained in a knee-extended position. There was no change in the tendon appearances except now there is substantial power Doppler signal in the tendinopathic tendon (arrows), showing the effect of positioning on vessel demonstration. P, patella.

Ultrasonography High-resolution demonstration of internal fibrillar architecture of the tendon and dynamic assessment make ultrasonography the investigation of choice. Hypoechoic areas and tendon thickening represent tendon inflammation, and hyperechoic areas represent calcification. Neovascularization is frequently seen in areas with structural tendon changes56 and correlates well with symptoms.57 It is important to examine the knee when extended so that the tendon is relaxed to best demonstrate neovascularization (Fig. 36-41). Paratendinitis is seen as a hypoechoic halo around the tendon that can appear patchy due to lack of tendon sheath. Subtle bone avulsions may be identified. It is important to be aware of anisotropy of the proximal tendon. This occurs when the linearly arranged tendon fibers are not orientated at 90 degrees to the probe. This causes reduced echogenicity of the tendon and can be mistaken for tendinopathy. It should be remembered that a tendon demonstrating anisotropy will not be thickened. Beam edge artifact gives rise to circumferential low echogenicity surrounding the tendon that can mimic paratendinitis. The complication of patellar tendon rupture is best assessed on dynamic ultrasound interrogation. This helps to differentiate partial-thickness from full-thickness tears.

Differential Diagnosis ● ●

Sinding-Larsen-Johansson disease Patellar sleeve fracture

Synopsis of Treatment Options Medical Treatment Most patients with overuse tendinopathy fully recover within 3 to 6 months after conservative treatment.58 However, athletes refractory to conservative measures may benefit from ultrasound-guided autologous blood injection into the tendon or “dry needling” of the ten-

don, which both use the same principle to promote healing.59,60 Certain growth factors and cytokines have been shown to be upregulated during tendon wound repair, which are most likely to be involved in revascularization of the tendon. Blood is a rich source of growth factors that can stimulate fibrocyte migration and help induce neovascular ingrowth, which may be able to stimulate a healing response in chronic degeneration. A study of ultrasound-guided autologous blood injection and dry needling in patients with lateral epicondylitis showed decreased pain, tendinopathic changes, and neovascularization at 6 months after injection.

Surgical Treatment Excellent function usually follows repair of patellar tendon ruptures with early surgical repair.55

MYOTENDINOUS INJURY Manifestations of the Disease Magnetic Resonance Imaging Muscle and tendon injuries are uncommon in the immature skeleton because the weakest link in the muscle-tendonbone chain is the growth plate. However, young athletes may incur sprains and tears, especially at myotendinous junctions, although complete rupture is rare. These injuries arise from indirect trauma due to excessive stretching during rapid acceleration or deceleration that occurs particularly in football, basketball, rugby, and track events. The rectus femoris, semitendinosus, semimembranosus, soleus, and medial head of gastrocnemius are susceptible to strain. Contributing factors include: ● ● ● ● ●

Extension across two joints Type 2 fibers Eccentric origin Fusiform shape Recent previous muscle injury

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P A R T O N E ● Injury: Pediatric Injuries

Muscle contusions are secondary to direct trauma, usually by a blunt object. They usually occur in the muscle belly; the damage crosses anatomic boundaries with the lesion not centered on the myotendinous junction. MRI identifies associated ligament tears and bone marrow injury at muscle origins and insertions. However, it has difficulty separating muscle edema, hematoma, and structural disruption and, as a result, tends to overestimate the severity of injury. Hematomas are common after myotendinous injury. MRI findings may vary depending on the time elapsed since the injury but usually show characteristics of methemoglobin with increased signal on both T1- and T2-weighted sequences. Hematomas tend to resorb over a period of 6 to 8 weeks but may occasionally leave serous fluid within a connective tissue sheath. These pseudotumors are seen mainly in the rectus femoris but also in semimembranosus and semitendinosus muscles.

Classification of Myotendinous Strains Grade 1: Microscopic damage to the myotendinous junction where the normal architecture is maintained. Hemorrhage and edema may track along muscle fascicles. Grade 2: Partial thickness tears with discontinuity of some of the muscle fibers Grade 3: Complete musculotendinous disruption that may result in a palpable defect or a soft tissue mass

MRI Appearances Grade 1: In the acute phase, high signal intensity on T2-weighted imaging is seen (edema and hemorrhage) (Fig. 36-42). Grade 2: General increased signal intensity is seen on T2/STIR imaging with discontinuity of some fibers.

■ FIGURE 36-42 A, Axial STIR MR image of both thighs demonstrates a grade 1 tear of the rectus femoris. There is muscle edema centered around the central septum of the muscle (arrows). B, Coronal STIR MR image of both thighs shows a grade 1 tear of the rectus femoris with feather-like appearance of the edema around the central septum (arrows).

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951

■ FIGURE 36-43 A, Axial T2-weighted, fat-suppressed MR image of the thigh demonstrates an area of peripheral high signal within the semitendinosus muscle belly (arrows) in keeping with a grade 2 muscle tear. B, Axial T1-weighted post–gadolinium enhanced, fat-suppressed MR image shows peripheral enhancement of the grade 2 tear around the hematoma (arrows).

The area enhances after injection of gadolinium (Fig. 36-43). Grade 3: Same as for grade 2 but with complete discontinuity of muscle fibers and possible muscle retraction with hematoma in the defect (Fig. 36-44).

■ FIGURE 36-44 Sagittal STIR MR image of thigh shows a grade 3 tear of the hamstrings (arrows). Hematoma is seen tracking distally from the tear site (H).

Ultrasonography Ultrasonography has many advantages, including excellent spatial resolution, and the dual-screen facility allows realtime comparison of two different areas. Dynamic evaluation helps differentiate full- from partial-thickness tendon and myotendinous injury with active contraction, giving an excellent assessment of the degree of disruption present. Ultrasonography demonstrates any structural disruption of the myotendinous junction well but does not demonstrate edema well. This, in part, results from muscle anisotropy, making the assessment of muscle echotexture difficult. Therefore, ultrasonography has a low sensitivity for grade 1 tears and really only demonstrates the size of the hematoma and the degree of structural disruption. Hematoma is echogenic in the acute phase (Fig. 36-45A) and difficult to discriminate from normal muscle. Later, ultrasonography may show a complex ovoid mass, with internal septations due to clot retraction eventually becoming anechoic. There is usually lack of inflammatory change in the surrounding subcutaneous soft tissues. Grade 1: Appearances may be normal or increased echogenicity (hematoma) and perifascial fluid may be seen (see Fig. 36-45B). Grade 2: Discontinuity of some fibers with acute hematoma that is echogenic but soon becomes hypoechoic. Perifascial fluid may track along muscle boundaries. Dynamic assessment identifies disrupted portions of muscle as separation of frayed ends on contraction. Later hypervascularity on Doppler imaging and echogenic granulation tissue may be identified (see Fig. 36-45C).

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■ FIGURE 36-45 A, Transverse sonogram demonstrates acute hyperreflective hematoma (arrows) in between the biceps femoris and semitendinosus muscle bellies. B, Longitudinal sonogram of grade 1 rectus femoris tear with hyporeflective change around the distal portion of the central septum of rectus femoris (arrows). C, Longitudinal sonogram of grade 2 calf muscle tear. The hematoma is shown by mixed low and intermediate reflectivity (arrows) interposed between the medial head of gastrocnemius and the Achilles aponeurosis. D, Longitudinal sonogram demonstrating grade 3 muscle tear with “bell clapper” sign of the tendon ends surrounded by hematoma (H).

Grade 3: Same as for grade 2 but there is complete discontinuity of tendon fibers with absence of movement as a unit. The typical “bell clapper” appearance of retracted echogenic muscle surrounded by hypoechoic hematoma may be seen (see Fig. 36-45D).

Differential Diagnosis Differential diagnosis between muscle contusion and myotendinous strain is based on the nature of the imaging findings. Both show edema and hematoma on ultrasonography and MRI. Contusion, however, is not centered on the myotendinous junction and the imaging abnormalities cross anatomic boundaries (i.e., two-muscle involvement

with edema of the soft tissues adjacent to the affected muscle) (Fig. 36-46).

Synopsis of Treatment Options Treatment of hamstring injuries includes rest and immobilization immediately after injury and then a gradually increasing program of mobilization, strengthening, and activity.61 When complete return of muscle strength, endurance, and flexibility has been achieved the athlete can return to competition. Failure to achieve full rehabilitation will only predispose the athlete to recurrent injury. The best treatment for hamstring injuries is prevention, which should include training to maintain and/or improve strength, flexibility, endurance, coordination, and agility.61

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● Lower Extremity Injuries in Children (Including Sports Injuries)

953

■ FIGURE 36-46 Transverse (A) and longitudinal (B) sonograms of a mild muscle contusion. The muscle damage is hyperreflective and is not centered on the myotendinous junction (arrows). C, Longitudinal scan shows severe vastus medialis contusion with full-thickness defect in the muscle (arrowheads) filled with hematoma (H).

ACCESSORY OSSICLES Manifestations of the Disease Radiography Accessory ossicles are normal variants that can become symptomatic. They are joined to normal bone by fibrous tissue, which can lead to the development of a painful pseudarthrosis if disturbed by frequent, vigorous exercise. The os trigonum posterior to the talus is a commonly reported source of pain, particularly in young gymnasts and dancers. This is thought to be due to repetitive impaction of the os trigonum between the calcaneus and posterior malleolus during plantarflexion.62 The os trigonum may even develop as a result of impingement, with the posterior of the talus more prone to damage and fragmentation because it is the last portion of the talus to ossify. Other common symptomatic accessory ossicles seen in adolescent patients are the os tibiale externum at the site of the tibialis posterior insertion on the navicular and the bipartite patella. These syndesmoses can become disrupted and symptomatic. Radiographs will show the presence of an accessory ossicle if it is ossified but give no indication to its symptomatology.

Magnetic Resonance Imaging Magnetic resonance imaging will show bone edema in the accessory ossicle and on either side of the synchondrosis (Fig. 36-47).

Ultrasonography Ultrasonography can locate the synchondrosis and show whether the patient’s symptoms correlate with the lesion.

Scintigraphy Bone scintigraphy shows increased uptake within the accessory ossicle compared with the asymptomatic side.

Differential Diagnosis ●

Fracture

Synopsis of Treatment Options Medical Treatment If physiotherapy and rest fail to improve symptoms, then ultrasonography can be used to perform guided injections with corticosteroid and local anesthetic either for diagnostic or therapeutic purposes. These can be aimed locally around the accessory ossicle or into the synchondrosis.

Surgical Treatment Excision of the os trigonum and/or offending osteophyte will allow the foot to be plantarflexed with no bony impingement. In the case of a bipartite patella, treatment may include excision of the painful fragment, lateral retinacular release, or detachment of the vastus lateralis insertion, generally performed as open surgical procedures. Recently, a case of arthroscopic removal of painful bipartite patella has been described.63

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■ FIGURE 36-47 Coronal (A) and sagittal (B) T1-weighted MR images through the patella. There is a bipartite patella with an irregular somewhat ill-defined synchondrosis with the patella (arrows). Axial (C) and sagittal (D) T2-weighted, fat-suppressed sequences through patella. There is marked bone marrow edema both with the accessory ossicle and the synchondrosis (arrows) in keeping with a symptomatic bipartite patella.

REFERENCES 1. Emery CA. Risk factors for injury in child and adolescent sport: a systematic review of the literature. Clin J Sport Med 2003; 13:256–268. 2. Vahvanen V, Aalto K. Classification of ankle fractures in children. Arch Orthop Trauma Surg 1980; 97:1–5. 3. Rogers LF. Radiology of Skeletal Trauma. New York, Churchill Livingstone, 1992.

4. Schlickewei W, Oberle M. [Forearm fractures in children]. Unfallchirurg 2005; 108:223–232; quiz 233–234. 5. Skak SV, Jensen TT, Poulsen TD. Fracture of the proximal metaphysis of the tibia in children. Injury 1987; 18:149–156. 6. Rogers LF, Malave S Jr, White H, Tachdjian MO. Plastic bowing, torus and greenstick supracondylar fractures of the humerus: radiographic clues to obscure fractures of the elbow in children. Radiology 1978; 128:145–150.

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7. Peh WC. Torus fracture of the radius. Am J Orthop 2004; 33:625. 8. Aponte JE Jr, Ghiatas A. Acute plastic bowing deformity: a review of the literature. J Emerg Med 1989; 7:181–184. 9. Lewis D, Logan P. Sonographic diagnosis of toddler’s fracture in the emergency department. J Clin Ultrasound 2006; 34:190–194. 10. Shravat BP, Harrop SN, Kane TP. Toddler’s fracture. J Accid Emerg Med 1996; 13:59–61. 11. Clancy J, Pieterse J, Robertson P, et al. Toddler’s fracture. J Accid Emerg Med 1996; 13:366–367. 12. Drennan DB, Maylahn DJ, Fahey JJ. Fractures through large nonossifying fibromas. Clin Orthop Relat Res 1974; (103):82–88. 13. McGlynn FJ, Mickelson MR, El-Khoury GY. The fallen fragment sign in unicameral bone cyst. Clin Orthop Relat Res 1981; (156):157–159. 14. Reynolds J. The “fallen fragment sign” in the diagnosis of unicameral bone cysts. Radiology 1969; 92:949–953. 15. Kurz W, Grumbt H. [The femoral neck fracture in childhood]. Zentralbl Chir 1988; 113:881–892. 16. Hubner U, Schlicht W, Outzen S, et al. Ultrasound in the diagnosis of fractures in children. In J Bone Joint Surg Br 2000; 82:1170–1173. 17. Martin TJ, Martin JS. Special issues and concerns for the high school- and college-aged athletes. Pediatr Clin North Am 2002; 49:533–552. 18. Bylander B, Aronson S, Egund N, et al. Growth disturbance after physial injury of distal femur and proximal tibia studied by roentgen stereophotogrammetry. Arch Orthop Trauma Surg 1981; 98:225–235. 19. Chadwick CJ, Bentley G. The classification and prognosis of epiphyseal injuries. Injury 1987; 18:157–168. 20. Rogers LF, Poznanski AK. Imaging of epiphyseal injuries. Radiology 1994; 191:297–308. 21. Pannier S, Odent T, Milet A, et al. [Tillaux fractures in teenagers: a review of nineteen cases]. Rev Chir Orthop Reparatrice Appar Mot 2006; 92:158–164. 22. Thompson GH, Bachner EJ, Ballock RT. Salter-Harris type II fractures of the capital femoral epiphysis. J Orthop Trauma 2000; 14:510–514. 23. Kocher MS, Tucker R. Pediatric athlete hip disorders. Clin Sports Med 2006; 25:241–253, viii. 24. Magnano GM, Lucigrai G, De Filippi C, et al. Diagnostic imaging of the early slipped capital femoral epiphysis. Radiol Med (Torino) 1998; 95:16–20. 25. Loder RT. Controversies in slipped capital femoral epiphysis. Orthop Clin North Am 2006; 37:211–221, vii. 26. Young JW, Bright RW, Whitley NO. Computed tomography in the evaluation of partial growth plate arrest in children. Skeletal Radiol 1986; 15:530–535. 27. Slongo TF. The choice of treatment according to the type and location of the fracture and the age of the child. Injury 2005; 36 (Suppl 1):A12–A19. 28. Rossi F, Dragoni S. Acute avulsion fractures of the pelvis in adolescent competitive athletes: prevalence, location and sports distribution of 203 cases collected. Skeletal Radiol 2001; 30:127–131. 29. Hirano A, Fukubayashi T, Ishii T, Ochiai N. Magnetic resonance imaging of Osgood-Schlatter disease: the course of the disease. Skeletal Radiol 2002; 31:334–342. 30. Pisacano RM, Miller TT. Comparing sonography with MR imaging of apophyseal injuries of the pelvis in four boys. AJR Am J Roentgenol 2003; 181:223–230. 31. Lazovic D, Wegner U, Peters G, Gosse F. Ultrasound for diagnosis of apophyseal injuries. Knee Surg Sports Traumatol Arthrosc 1996; 3:234–237. 32. Carty H. Children’s sports injuries. Eur J Radiol 1998; 26:163–176. 33. Jaramillo D, Shapiro F. Musculoskeletal trauma in children. Magn Reson Imaging Clin North Am 1998; 6:521–536. 34. Bencardino JT, Palmer WE. Imaging of hip disorders in athletes. Radiol Clin North Am 2002; 40:267–287, vi–vii. 35. Stevens MA, El-Khoury GY, Kathol MH, et al. Imaging features of avulsion injuries. RadioGraphics 1999; 19:655–672. 36. Prince JS, Laor T, Bean JA. MRI of anterior cruciate ligament injuries and associated findings in the pediatric knee: changes with skeletal maturation. AJR Am J Roentgenol 2005; 185:756–762.

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37. Brandser EA, el-Khoury GY, Kathol MH, et al. Hamstring injuries: radiographic, conventional tomographic, CT, and MR imaging characteristics. Radiology 1995; 197:257–262. 38. Blankstein A, Cohen I, Heim M, et al. Ultrasonography as a diagnostic modality in Osgood-Schlatter disease: a clinical study and review of the literature. Arch Orthop Trauma Surg 2001; 121:536–539. 39. Duri ZA, Patel DV, Aichroth PM. The immature athlete. Clin Sports Med 2002; 21:461–482, ix. 40. Bates DG, Hresko MT, Jaramillo D. Patellar sleeve fracture: demonstration with MR imaging. Radiology 1994; 193:825–827. 41. Peace KA, Lee JC, Healy J. Imaging the infrapatellar tendon in the elite athlete. Clin Radiol 2006; 61:570–578. 42. King SJ. Magnetic resonance imaging of knee injuries in children. Eur Radiol 1997; 7:1245–1251. 43. Rubin DA. Magnetic resonance imaging of chondral and osteochondral injuries. Top Magn Reson Imaging 1998; 9:348–359. 44. Pope TL Jr. MR imaging of patellar dislocation and relocation. Semin Ultrasound CT MR 2001; 22:371–382. 45. Cain EL, Clancy WG. Treatment algorithm for osteochondral injuries of the knee. Clin Sports Med 2001; 20:321–342. 46. Gooding CR, Bartlett W, Bentley G, et al. A prospective, randomised study comparing two techniques of autologous chondrocyte implantation for osteochondral defects in the knee: periosteum covered versus type I/III collagen covered. Knee 2006; 13:203–210. 47. Krishnan SP, Skinner JA, Bartlett W, et al. Who is the ideal candidate for autologous chondrocyte implantation? J Bone Joint Surg Br 2006; 88:61–64. 48. Long G, Cooper JR, Gibbon WW. Magnetic resonance imaging of injuries in the child athlete. Clin Radiol 1999; 54:781–791. 49. Ogden JA, Ganey TM, Hill JD, Jaakkola JI. Sever’s injury: a stress fracture of the immature calcaneal metaphysis. J Pediatr Orthop 2004; 24:488–492. 50. Spitz DJ, Newberg AH. Imaging of stress fractures in the athlete. Radiol Clin North Am 2002; 40:313–331. 51. Allen MJ, O’Dwyer FG, Barnes MR, et al. The value of 99mTc-MDP bone scans in young patients with exercise-induced lower leg pain. Nucl Med Commun 1995; 16:88–91. 52. Banal F, Etchepare F, Rouhier B, et al. Ultrasound ability in early diagnosis of stress fracture of metatarsal bone. Ann Rheum Dis 2006; 65:977–978. 53. McLoughlin RF, Raber EL, Vellet AD, et al. Patellar tendinitis: MR imaging features, with suggested pathogenesis and proposed classification. Radiology 1995; 197:843–848. 54. Peh WC, Chan JH. The magic angle phenomenon in tendons: effect of varying the MR echo time. Br J Radiol 1998; 71:31–36. 55. Kelly DW, Carter VS, Jobe FW, Kerlan RK. Patellar and quadriceps tendon ruptures—jumper’s knee. Am J Sports Med 1984; 12:375–380. 56. Gisslen K, Alfredson H. Neovascularisation and pain in jumper’s knee: a prospective clinical and sonographic study in elite junior volleyball players. Br J Sports Med 2005; 39:423–428; discussion 423–428. 57. Zanetti M, Metzdorf A, Kundert HP, et al. Achilles tendons: clinical relevance of neovascularization diagnosed with power Doppler US. Radiology 2003; 227:556–560. 58. Wilson JJ, Best TM. Common overuse tendon problems: a review and recommendations for treatment. Am Fam Physician 2005; 72:811–818. 59. Suresh SP, Ali KE, Jones H, Connell DA. Medial epicondylitis: is ultrasound guided autologous blood injection an effective treatment? Br J Sports Med 2006; 40:935–939; discussion 939. 60. Connell DA, Ali KE, Ahmad M, et al. Ultrasound-guided autologous blood injection for tennis elbow. Skeletal Radiol 2006; 35:371–377. 61. Agre JC. Hamstring injuries: proposed aetiological factors, prevention, and treatment. In Sports Med 1985; 2:21–33. 62. Connolly SA, Connolly LP, Jaramillo D. Imaging of sports injuries in children and adolescents. Radiol Clin North Am 2001; 39:773–790. 63. Azarbod P, Agar G, Patel V. Arthroscopic excision of a painful bipartite patella fragment. Arthroscopy 2005; 21:1006.

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C H A P T E R

Skeletal Manifestations of Child Abuse Susanne Lardenoye-Broker and Alan Sprigg

PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS Child abuse is a widespread social problem of special concern to all physicians and medical personnel. It is present throughout the world but may take different forms in differing cultures. The apparent greater prevalence in Western societies may be a reflection of increased awareness and recognition and decreased tolerance of the problem in the developed world. The symptoms and signs of abuse range from neglect and/ or deprivation, through sexual misuse, to the physically “battered child” now referred to as “nonaccidentally injured.” The true incidence of morbidity and mortality due to inflicted injury is hard to obtain due to various factors. First, neglect and abuse frequently occur behind closed doors—it is unobserved, and confessions are rare. Second, when abuse is recognized, legal issues of parental rights and family preservation may interfere with diagnosis. In 2003, state and local child protective services received an estimated 2.9 million referrals alleging child abuse or neglect for investigation or assessment and approximately 906,000 children were determined to be victims of child abuse or neglect by these agencies. In the United States an estimated 1500 children die each year as a result of child abuse.1 Boys and girls are affected equally, and almost all cases of physical child abuse occur before the age of 6 years. Over half of all children are affected in their first year of life,2 whereas accidental injuries are rare in children younger than 1 year of age. Risk factors for child abuse include prematurity, low socioeconomic level, low birth weight, and physical disability.3 The predominant relationship between perpetrator and abused victim is a parental relationship in any form (father, mother, step-parent, parent’s significant other). 956

Over 55 years ago Caffey4 first described the association of unexplained subdural hematomas and long-bone fractures in infants. In 1953, Silverman5 concluded that the skeletal injuries were the result of repetitive nonaccidental trauma; and by 1962, Kempe6 presented radiographic skeletal manifestations of child abuse and introduced the term battered child syndrome. Radiologic imaging has evolved to play a major role in the diagnosis of physical abuse, and investigative protocols have been established that commonly include routine skeletal survey in the evaluation of suspected child abuse.

ANATOMY Radiologic imaging has become progressively more important in the diagnosis of physical child abuse over time. The goals of radiologic imaging in child abuse are threefold: ● ● ●

To identify and diagnose (unsuspected) child abuse To provide evidence for prosecution or defense of alleged abuse To assist in excluding child abuse in true accidental trauma or variants of normal that may mimic child abuse

With the introduction of ultrasonography, nuclear medicine, CT, and MRI, the diagnosis of child abuse is no longer limited to the identification of skeletal injury. However, radiologic imaging of the skeleton still plays a crucial role in documenting child abuse. The fractures encountered in abuse are among the most common injuries seen in these children and are often highly specific for diagnosing abused infants. This chapter concentrates on the radiology of the bony injuries, but neurocranial and abdominal injury may be presenting or accompanying features. The most important skeletal findings in child abuse are discussed, as well as differential diagnostic considerations and imaging strategies.

CHAPTER

KEY POINTS In 2003 there were over 900,000 cases determined to be child abuse in the United States. ■ Imaging is an important tool in detecting these cases. ■ Normal variants may mimic child abuse. ■ The clinical history provided is often inaccurate and possibly misleading. ■ Specific patterns of injury lead to suspicion of child abuse. ■ Multiple fractures at different stages of healing is moderately suspicious. ■ A radiographic skeletal survey is an important tool. ■ Scintigraphy has a supportive rather than primary role. ■ The differential diagnosis includes accidental trauma, obstetric trauma, normal variants, rickets, other metabolic disorders, osteogenesis imperfecta, osteomyelitis, Caffey’s disease, and certain bone dysplasias. ■

BIOMECHANICS Victims of child abuse are usually presented to the pediatrician with an inaccurate history of the injury. Suspicion of abuse may be raised when an explanation offered by the caregiver is not consistent with the injury observed. The radiologist may be the first to suspect child abuse when characteristic lesions on imaging studies are recognized. This underlines the essential role of radiologic imaging in the final goal: protecting the abused child from ongoing abuse and escalating force that may ultimately be fatal or disabling. An incorrect diagnosis of child abuse based on misinterpretation of radiologic imaging has tremendous consequences for individual children and caregivers. In each individual case, the presented history must be correlated with other possible preexisting factors such as prematurity, skeletal dysplasia, and metabolic disease to differentiate between child abuse and other diagnoses. In the literature, several reports describe the distribution of fractures in child abuse.7–11 Certain patterns of skeletal injury are reported in these studies. In infancy, skull fractures, rib fractures, and metaphyseal injuries predominate. In the older infant, the diaphyseal fractures of long bones are often diagnosed. Specific skeletal injuries can be classified according to index of suspicion of child abuse and the age of the child.12 There is a high level of suspicion for child abuse in children with classic metaphyseal lesions and posterior fractures to the rib cage. Moderate suspicion arises when multiple fractures, especially bilateral, at different stages of healing are recognized. Clavicular fractures in older children and subperiosteal new bone formation in infants are common findings with low specificity. In general, multiple fractures of different ages associated with an inconsistent history are highly suggestive of abuse (Table 37-1).

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TABLE 37-1 Specificity of Radiologic Findings High Specificity Classic metaphyseal lesions Fractures of different ages Multiple fractures, especially bilateral Rib fractures, especially posterior Scapular fractures Spinous process fractures Moderate Specificity Epiphyseal separations Vertebral body fractures and subluxations Digital fractures in infants Skull fractures in infants Common But Low Specificity Subperiosteal new bone formation Clavicular fractures in older children Long bone shaft fractures in older children

From Kleinman PK. Diagnostic Imaging of Infant Abuse, 2nd ed. St. Louis, Mosby, 1998, p 9.

PATHOLOGY Radiographic Evaluation In all cases of suspected abuse in children younger than 2 years of age a skeletal survey is mandatory. A “babygram” (a single radiograph or several films of the entire infant) is unsatisfactory. The initial survey (Table 37-2) should TABLE 37-2 Suggested Protocol for Skeletal Survey Babygram A single radiograph gives an unsatisfactory exposure and combined views of chest, abdomen, pelvis and limbs. Limb detail is poor, with oblique projections of most joints. Skull Anteroposterior and lateral views plus Towne’s view for occipital injury Skull radiographs should be taken with a skeletal survey even if a CT has been performed. Body Frontal chest (including clavicles) Oblique views of the ribs (left and right) Anteroposterior view of abdomen with pelvis and hips Spine Lateral spine—cervical and thoracolumbar Limbs Anteroposterior views of humeri and forearms Anteroposterior views of femurs, tibia, and fibulas Anteroposterior views of hands Anteroposterior views of feet Supplemental Views Lateral views of any suspected shaft fracture Lateral coned views of the elbows/wrists/knees/ankles may demonstrate metaphyseal injuries in greater detail than anteroposterior views of the limbs alone.

Created by Dr. Susan King of Bristol for the British Society of Paediatric Radiology.

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consist of anteroposterior and lateral views of the skull and spine with anteroposterior and lateral views of the extremities, including hands and feet. Additional views of any suspected abnormality must be obtained. Oblique views of the thorax increase the screening sensitivity for rib fractures. A follow-up skeletal survey performed 2 weeks after the initial examination frequently provides additional information. Follow-up survey may detect additional fractures, differentiate fractures from normal developmental variants, and assist in dating fractures. There has to be a balance between the forensic process and the radiation dose. A follow-up chest radiograph plus localized views of suspicious areas is a minimal evaluation and should be directed by the radiologist. Pediatric health care facilities are rapidly migrating from film-based to digital imaging technology. Although skeletal survey imaging protocols are comparable for the two systems, the practice of high-detail imaging is significantly greater at screen-film facilities. Kleinman13 recently concluded that as pediatric health care facilities transition from screen-film technology, there are importing imaging practices that are directly applicable to the digital environment. It appears that less attention is being paid to technical elements specific to digital imaging that may affect image quality. Laboratory and clinical studies should be encouraged to compare the diagnostic performance of current digital imaging technologies with traditional high-detail screen-film imaging systems to establish minimum requirements for high-detail digital pediatric skeletal survey examinations in cases of suspected infant abuse. Routine use of skeletal scintigraphy for the investigation of child abuse is infrequently practiced, which may be due to the lack of readily available facilities and the need for sedation. It must be performed with high-resolution collimation and meticulous symmetric positioning of the limbs with imaging in comparable posture. The lower limbs should be imaged separately from the torso, especially if the bladder is full of radionuclide. Scintigraphy is highly sensitive in detecting rib, spinal, and diaphyseal fractures but has a low sensitivity for skull fractures and is variable for metaphyseal fractures.14 Metaphyseal fractures that are entirely intracapsular generate a diagnostic problem owing to the high uptake normally seen at the growth plates. Scintigraphy should be considered as a complementary imaging technique: ● ● ● ●

To resolve a doubtful fracture on a radiograph To detect additional rib fractures before they are visible radiographically When radiographs are negative with a high clinical suspicion of abuse To demonstrate possible further injury in a child with a single fracture on a conventional skeletal survey to diagnose abuse

Dating of Fractures The radiologist has an important role in the management of child abuse by dating fractures. Precise dating is impossible, and fracture maturation depends on the age of the child; a truthful clinical history may narrow the range.

TABLE 37-3 Dating of Fractures

Soft tissue resolution Early periosteal new bone Loss of fracture line definition Soft callus Hard callus Remodeling

Band

Peak (days)

2–10 days 4–21 days 10–21 days 10–21 days 14–90 days 3 months-2 years

4–10 10–14 14–21 14–21 21–42

Adapted from: O’Connor JF and Cohen J. Dating Fractures. In Kleinman PK (Ed): Diagnostic Imaging in Child Abuse. 1998. St Louis MO. CV Mosby.

We may only define a likely time range in which the injury took place. The longer from the time of injury, the more imprecise is the estimate. The duration of the repair process generally depends on the severity of the injury but may be altered by repeated trauma in abused children. In Table 38-3 the details of accepted appearances are shown for dating fractures of the long bones, but this is not applicable to skull, rib, finger, or metaphyseal injuries.

MANIFESTATIONS OF THE DISEASE Fractures of the Extremities Classic Metaphyseal Lesion/Metaphyseal Fracture (Fig. 37-1) The incidence of metaphyseal fractures in child abuse in small children is variously reported from 11%11 to 28%.9 These fractures are often multiple and found in various stages of healing. Metaphyseal fractures are more common in the lower limbs than in the upper limbs; sites of predilection are the distal femur, proximal and distal tibia and fibula, and proximal humerus.8 They are often bilateral and symmetric but may be isolated. The classic metaphyseal lesion was first described radiologically by Caffey in 1974. It is referred to as a “corner” or “bucket-handle” fracture and is a distinctive feature of child abuse. Kleinman re-examined this type of fracture in 198615 using detailed histopathologic and radiographic studies and determined that it represents a transmetaphyseal disruption, through the most immature portion of the primary spongiosa, rather than an avulsion injury at the sites of periosteal attachment as stated by Caffey. The repair pattern of metaphyseal fractures is variable and depends on the degree of subperiosteal bleeding. The radiologic appearance varies with the orientation of the x-ray beam, and what may be seen as a bucket-handle fracture on one view may be evident as a corner fracture on another (Fig. 37-2), or the fragment may only be identified on one of several views. Localized views of a joint give a better profile than a single view of a whole limb. When extensive, the fracture line may result in an entire disc of metaphyseal bone. In some cases only a subtle lucency in the subphyseal region of the metaphysis is seen without an obvious fracture fragment that may resemble similar lesions seen in stressed infants or those with metabolic disturbances. The metaphyseal lesions in infant

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37 ● Skeletal Manifestations of Child Abuse

■ FIGURE 37-1 Metaphyseal fractures in nonaccidental injury. A, Lateral complete fracture of proximal tibia through the metaphysis. B, Corner fractures of distal tibia healing with periosteal reaction. C, Nondisplaced partial metaphyseal fracture of distal femur and buckethandle fracture of proximal tibia. D, Displaced proximal humeral epiphysis and healing metaphyseal corner fracture (periosteal reaction). Also note healing acromial fracture.

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■ FIGURE 37-2 Corner fracture versus bucket-handle fracture. The classic metaphyseal lesion is seen tangentially as a corner fracture pattern (A) and obliquely as a bucket-handle fracture pattern (B). Arrows indicate fracture line. (From Kleinman PK. Diagnostic Imaging of Child Abuse, 2nd ed. St. Louis, Mosby, 1998.)

abuse must be distinguished from normal variants such as metaphyseal beaks and spurs. When present, they are in continuity with normal bone and are not separated as most true metaphyseal fractures. Similarly, the normal proximal tibial cortical irregularity may cause confusion.12

Diaphyseal Fractures (Fig. 37-3) In the older abused child, long-bone shaft fractures are four times more common than metaphyseal fractures.10 The most frequently injured long bones are the femur,

■ FIGURE 37-3 Diaphyseal fractures in nonaccidental injury. A, Acute angulated spiral fracture of femur due to forceful twisting. B, Acute spiral fracture of humerus and healing rib fractures. The patient presented with arm swelling without a history of trauma.

humerus, and tibia. Diaphyseal fractures raise more suspicion when found in a state of healing, implying failure to seek appropriate medical attention. Other factors that increase the likelihood of an abuse injury include association with another fracture, other clinical features with a high suspicion for abuse, and an inappropriate clinical history. No specific conclusion can be drawn from the type of fracture, because transverse, oblique, and spiral diaphyseal fractures all occur with true accidental trauma as well as abuse. Particular attention has to be given or attributed to the spiral fracture, which has been considered as synonymous with abuse in the preambulatory infant. A spiral fracture indicates a torque component of stress applied to the bone. It may be the result of grabbing or shaking an infant using the extremity as a handle. However, spiral fractures may occur as accidental trauma in an ambulatory or young child. “Toddler’s fracture” may cause confusion. This occurs when a child falls while learning to walk. If the foot is wedged under a sofa, the body weight twists against the fixed foot, resulting in a torque force and hairline fracture to the tibia. There is usually immediate pain and refusal to bear weight for several days. The initial radiograph may appear normal, with periosteal reaction appearing 10 days later. Caregivers may not present the infant to the hospital immediately because they may not have witnessed the incident directly. It is important to consider each longbone fracture in the context of the clinical history and to

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assess whether the history, mode of clinical presentation, and the fracture type are compatible. Several authors have reviewed fracture patterns. With the exception of supracondylar fractures in the ambulatory child, all fractures of the humerus in infants and young children are strongly suggestive of abuse.10 Femoral fractures in infants younger than the age of 1 year usually are secondary to abuse.16-17 Spiral fractures of the tibia in nonambulatory children should raise suspicion.10,11,16 Long-bone fractures in children older than 2 years are more likely the result of accidental trauma, provided the history is consistent. Subperiosteal new bone formation may be due to traumatic separation of the periosteum secondary to excessive torsional stress due to shaking or rough gripping and subperiosteal bleeding. Subperiosteal new bone formation may be found along the diaphysis of abused children. In the acute stage, scintigraphy is the most sensitive diagnostic modality, showing increased radionuclide uptake at sites of subperiosteal hemorrhage even when radiographs are normal. However “physiologic” subperiosteal new bone formation is sometimes seen as a normal variation in children aged 6 weeks to 6 months due to circumferential diaphyseal bone growth (Fig. 37-4). In the physiologic form the new bone is always smooth, confined to the diaphysis, and usually most obvious on the medial aspect of the shaft. Periosteal reaction is often irregular and extends to the metaphysis in cases of child

■ FIGURE 37-4 Physiologic periostitis versus healing fracture. A, Physiologic “periostitis” in the femurs and tibias. This 6-week-old patient had a thin periosteal reaction parallel to the shaft that was confined to the diaphyses and symmetrical. B, A 6-month-old patient has a healing periosteal reaction in a hairline spiral fracture that appears thick, heaped up, and irregular.

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abuse. Subperiosteal new bone formation may also reflect infection or systemic disease.

Epiphyseal Injuries (Fig. 37-5) Salter-Harris type fractures are relatively rare in child abuse but are common in accidental trauma in the older child. However, epiphyseal separations in the proximal or distal humerus are strongly associated with abuse. These fractures extend through the epiphyseal plate with posteromedial displacement of the distal humeral epiphysis. Radiographic findings may be quite subtle; ultrasonography and MRI aid in diagnosis of epiphyseal separations. Proximal humeral and femoral epiphyseal fracture separations can be the result of both abuse and birth trauma.

Fractures of the Hands and Feet (Fig. 37-6) Fractures of the hands and feet are uncommon but have a strong association with abuse. In infants, phalangeal, metacarpal, or metatarsal fractures are due to squeezing the extremity, trampling on the hand or foot, or forced hyperextension of the digits. Careful attention should be paid to these areas that are now included on skeletal surveys. Torus fractures of the metacarpals or metatarsals are best viewed on oblique films or on follow-up skeletal examinations showing callus formation or periosteal reaction.

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■ FIGURE 37-5 Epiphyseal fracture separation in nonaccidental injury. This can be difficult to diagnose on plain radiographs in the acute situation. A, The patient presented with a swollen elbow; a history of trauma was denied. Note healing fracture of the distal humerus with medial displacement. These injuries are commonly missed in the trauma room only to become evident when healing. B, Knee swelling in a child with no history of trauma. Plain radiograph shows subtle displacement of the tibial ossific center. C, MR image shows edema in the soft tissues and physeal plate and confirms displacement of the unossified physis.

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Acute rib fractures are difficult to detect radiographically because of overlapping structures and obliquity of the fracture relative to the x-ray beam. Nuclear imaging may play an important role in early detection of posterior rib fractures. Acute rib fractures may not be detectable on the initial films and only become detectable on a follow-up chest film 2 weeks after the initial study, owing to abundant callus or subperiosteal new bone formation. Many units perform this delayed film routinely. Sometimes there may only be slight widening of the rib, leading to increased visibility of the fractures.

Fractures of the Shoulder Girdle and Sternum

■ FIGURE 37-6 Fracture of a metacarpal caused by a stamping or squeezing injury.

Fractures about the shoulder girdle in abuse typically are multiple and include injury to the scapula, clavicle, proximal humerus, and upper ribs. Mid to distal clavicular fractures are nonspecific and seen in birth trauma and accidental injury, as well as abuse. However, fractures of the proximal clavicle are strongly associated with abuse. Although uncommon, fracture of the scapula, in particular the acromion, is specific for abuse. It occurs secondary to violent shaking or manual traction on the arm. A normal anatomic variant in the ossification of the acromion process may mimic a fracture. Follow-up films to assess healing are needed to differentiate between these two entities. Sternal fractures, although rare, are suggestive of abuse in small children and imply massive forces were applied to the thorax. Special attention to this area is needed on lateral chest radiographs.

Spinal Fractures (Fig. 37-9)

Thoracic Trauma Rib Fractures (Fig. 37-7) The incidence of rib fractures in child abuse has been variously reported from 5% to 27%.8 They are virtually diagnostic of abuse, being seldom seen as an accidental injury even in severe road traffic accidents. Feldman18 stated that even the forces used in cardiopulmonary resuscitation rarely result in rib fractures in children. Consequently, the discovery of rib fractures on a chest radiograph should always raise the suspicion of abuse. The fractures occur at all rib sites, but most commonly in the axillary portion, the posterior shafts, and the rib necks. Similar points along the arcs of adjacent ribs are often involved, often at multiple levels and bilaterally. They result from a squeezing injury to the chest when the infant is squeezed around the thorax. Shaking injury may occur during the same action, and some authors suggest routine neurocranial imaging is performed. Kleinman12 stated that the anteroposterior compression applied during gripping levers the rib over the fulcrum of the transverse processes in such a manner that the rib fails mechanically at the head or neck (Fig. 37-8). Depending on the direction and magnitude of the forces applied, fractures of the lateral and anterior parts of the ribs may also occur. A predilection for first rib involvement has been described by Strouse and Owings.19 Like metaphyseal fractures, rib fractures are most commonly encountered in children younger than 1 year old.

Spinal fractures do occur but are rare in child abuse compared with limb and rib fractures. The mechanism is thought to be hyperextension or hyperflexion often associated with axial loading and rotation. Radiographically, the injuries are displayed as compression deformities of the vertebral body, often with end plate defects and avulsive fractures of the spinal processes, the latter being highly specific for abuse. Vertebral crush injury is typically located near the thoracolumbar junction and can be easily missed on plain radiographs unless lateral spine films are included. More severe fracture-dislocation spinal injuries have been described in addition to the classic hangman’s fracture of the C2 vertebral body. Disc herniation and isolated spinal cord injuries can be seen in abused children. MRI aids in assessment of the spinal canal when neurologic symptoms are present. There may be associated abdominal injury.

Craniofacial Fractures (Fig. 37-10) Facial fractures are uncommon in child abuse. Among these fractures, mandibular injury is most frequently seen in abuse and is typically associated with other skeletal fractures. Skull fractures are infrequent in accidental trauma in small children. The immature skull tends to bend and deform rather than fracture. If an accidental skull injury does occur, it typically results in a linear, nondiastatic fracture. Several authors have tried to characterize

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■ FIGURE 37-7 Rib fractures in nonaccidental injury caused by squeezing. A, Localized view of posterior ribs. An acute rib fracture is just visible due to fracture displacement. B, Localized view of posterior ribs 2 weeks later. Multiple fractures are identifiable. C, Multiple healing anterior rib fractures on a chest radiograph taken in a child with tachypnea.

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■ FIGURE 37-8

With anteroposterior compression of the chest, there is excessive leverage of the posterior ribs over the fulcrum of the transverse processes. This position places tension along the inner aspects of the rib head and neck regions, resulting in fractures at these sites (arrows). This mechanism would also account for fractures at other sites along the rib arcs and at the costochondral junctions (arrows). (From Kleinman PK. Diagnostic Imaging of Child Abuse, 2nd ed. St. Louis, Mosby, 1998.)

■ FIGURE 37-9 Spinal fracture in nonaccidental injury. A and B, Spinal fractures are more difficult to detect on the anteroposterior view. A lateral spine radiograph should be performed as part of a skeletal survey. Vertebral wedge fractures may occur. These images show facet dislocation due to inflicted spinal trauma at the thoracolumbar junction.

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■ FIGURE 37-10

Skull fracture: simple versus complex. A, Hairline simple linear parietal fracture. This could be accidental or nonaccidental, depending on clinical history. B, Bilateral complex fractures. Note widened branching skull fractures with sutural diastasis due to nonaccidental injury.

unique features of skull fractures in abuse. It seems that no pattern of skull injury is diagnostic of child abuse. There is some agreement that multiple fractures, bilateral fractures, diastasis of fractures, and fractures that cross suture lines are significantly associated with nonaccidental trauma. The linear parietal fracture is the more common skull fracture, whether accidental or not. The appropriateness of the history should be compared with the type of injury when trying to discriminate between abuse and accidental trauma. Neuroradiologists have discarded skull radiographs in favor of CT in the acute management of head injury, but CT may miss hairline linear fractures in the plane of the scan and may not detect wormian bones in skeletal dysplasia; two views of the skull should be included in a skeletal survey requested for forensic purposes. A skull fracture shown on a radiograph may be the only convincing evidence of prior impact injury.

DIFFERENTIAL DIAGNOSIS The radiologist must be familiar with the various conditions that may simulate nonaccidental trauma. Failure to recognize these diseases, normal variants, or true accidental injury will result in unnecessary investigation by child protection agencies and unnecessary imaging studies. Intense involvement with the legal system may follow with considerable social issues. On the other hand, a missed diagnosis of abuse may have serious consequences, subjecting the child to repeated assaults and escalating violence. Caregivers may present a child with a “herald injury” as a cry for help, which if ignored may result in later permanent injury (Table 37-4).

TABLE 37-4 Differential Diagnostic Considerations Trauma True accidental trauma Birth trauma Dysplasia Osteogenesis imperfecta Metaphyseal and spondylometaphyseal dysplasias Variants of Ossification and Maturation Acromion Metaphyseal Accessory skull sutures Physiologic periosteal new bone Neurogenic Spina bifida Congenital insensitivity to pain Metabolic Bone disease or prematurity Copper deficiency Menkes’ syndrome Rickets Scurvy Miscellaneous Caffey’s disease Congenital syphilis Leukemia Neoplastic-metastatic round cell tumors (e.g., neuroblastoma) Osteomyelitis

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Diseases Simulating Abuse A substantial number of diseases display imaging findings that may be confused with inflicted injury. Most of these entities can readily be excluded by clinical findings and an appropriate radiologic evaluation supplemented by appropriate laboratory tests. However, uncertainty may persist despite all efforts to determine the nature of the findings.

Rickets and Metabolic Disease of Prematurity (Fig. 37-11) Metaphyseal irregularity and subperiosteal new bone formation occur both in rickets and abuse. In untreated cases, bony mineralization is diminished and physeal widening with an indistinct zone of provisional calcification is noted. With healing, the osseous architecture may begin to return to normal but metaphyseal fractures may still occur with forces less than those required to fracture normally mineralized bone. In older children this may be due to metabolic, liver, or renal disease or poor nutrition.

■ FIGURE 37-11 Rickets. This child presented with swollen wrists. The radiograph shows splaying of the metaphyses, poor definition of the end plate, widened physis due to nonmineralized matrix, reduced bone density, and delayed bone age. A periosteal reaction may be seen when healing. Fractures (ribs or long bone) may be seen in neonates when there is metabolic bone disease due to liver disease, problems of nutrition, or malabsorption.

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Premature infants, particularly those with a birth weight less than 1500 g, who have prolonged parenteral nutrition for a gastrointestinal disorder, have a chronic lung disease, or are on diuretic or corticosteroid therapy may be at increased risk for fracture due to metabolic bone disease.20 Fractures typically involve the ribs and long bones, and they can be identical to those seen with nonaccidental trauma. Prematurity is an independent risk factor for abuse owing to social issues of poor bonding.21,22 The challenge is to differentiate inflicted injury in a high-risk infant from fracture caused by metabolic bone disease associated with prematurity. A multidisciplinary approach and biochemical assessment are needed.

Osteogenesis Imperfecta (Fig. 37-12) Osteogenesis imperfecta (OI) is a relatively rare disorder with an incidence of 1 in 20,000 births. A child who has OI and presents with his or her first fracture with minimal force may be suspected of being abused. Fractures in OI may result from a significant traumatic event or may be spontaneous, particularly in the weight-bearing child. The diagnosis of OI is established on a combination of clinical features and accurate family history and radiology. This approach is usually sufficient for diagnosis, and only rarely is collagen analysis or genetic studies necessary.23 OI is classified into at least four different types. Most cases are of type 1. Types 2 and 3 are usually severe enough not to cause diagnostic difficulties in infancy. Type 4 constitutes less than 5% of all cases of OI but generates a particularly problematic differential diagnosis given the absence of blue sclerae. Clinical findings, family history, and radiographic features should aid the differentiation in most cases. Dental abnormalities may occur in some types of OI, but most infants are not old enough to have teeth at the time when this issue arises. Most fractures in OI are situated in the diaphyses and demonstrate gross bony demineralization and bowing. Metaphyseal fractures are rare but are usually associated with other evidence of OI and typically conform to nonspecific metaphyseal injuries seen in accidental trauma. They rarely show the corner fracture pattern noted with abuse. OI needs to be considered in the differential diagnosis of every case of suspected nonaccidental injury; its exclusion depends on careful clinical examination, adequate history, and high-quality radiology (including a skull radiograph for wormian bones). Controversy exists around the diagnosis of “temporary brittle bone disease” proposed by several authors24,25 as a self-limiting variant of OI. They suggested that a temporary deficiency of a metalloenzyme (e.g., copper) was thought to cause diminished bone strength. Other researchers have been highly critical of the methodology used in these studies and as yet there is no scientific proof of its existence.

Osteomyelitis (Fig. 37-13) Osteomyelitis tends to involve the metaphyses in children and occasionally the fragmentation associated with metaphyseal destruction may resemble a metaphyseal corner fracture. In the healing phase, both processes show healing new

■ FIGURE 37-13 Osteomyelitis. The child had a painful leg for several weeks. There is extensive bone destruction throughout the tibia and fibula and across the knee joint into the distal femur. A periosteal reaction is seen in the healing phase and also a tibial sequestrum. The diagnosis of osteomyelitis is confirmed by pyrexia, raised inflammatory markers, and positive blood cultures. Pus was found at surgery with positive cultures. The early changes are much more subtle with minimal lucency confined to the metaphysis. Fractures are unusual, because sepsis is usually treated clinically before chronic osteomyelitis develops to a stage where bone strength is compromised and fracture occurs.

■ FIGURE 37-12 Osteogenesis imperfecta. A, The infant presented with leg pain during changing of the diaper. Both femurs show healing midshaft fractures. B, Radiograph of chest and arms shows multiple healing fractures of differing ages, overtubulated bones, and reduced bone density. C, Multiple wormian bones. This shows the benefit of obtaining a routine skull film in a skeletal survey.

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bone formation. In most cases an accurate diagnosis can be made by high-detail images in multiple projections and correlation with the clinical findings (e.g., pyrexia, raised white blood cell count, and inflammatory markers).

Other Diseases Syphilis may mimic child abuse (Fig. 37-14). When widespread metaphyseal destructive lesions caused by congenital syphilis are seen in association with fractures, it may be impossible to differentiate spontaneous pathologic fractures from inflicted injuries. Caffey’s disease (infantile cortical hyperostosis) (Fig. 37-15) is a rare condition characterized by extensive subperiosteal new bone formation. Because bone density is normal and a history of trauma is absent, child abuse may be suspected initially.

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Scurvy is incredibly rare in clinical practice (Fig. 37-16). Radiologically, it presents as significant osteoporosis, metaphyseal changes, subperiosteal hemorrhage with periosteal reaction, and fractures—findings that are similar to those seen in nonaccidental injury. In sickle cell disease, subperiosteal new bone formation can be seen along the long bones related to infarction that may simulate nonaccidental trauma, particularly in the hands and feet. Certain bone dysplasias including spondylometaphyseal dysplasia and metaphyseal chondrodysplasia may demonstrate metaphyseal fragmentation that is indistinguishable from the classic metaphyseal lesion of child abuse, but these usually affect all the bones not just occasional limbs (Fig. 37-17). Malignancy may present as pain, bruising, bone infiltrate on radiography, or occasionally periosteal reaction

■ FIGURE 37-14 Syphilis. A and B, Views of both legs show involvement of multiple metaphyses. Destructive “bites” are seen in the metaphyses with diaphyseal periosteal reaction. Fractures are rare.

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■ FIGURE 37-15

Caffey’s disease. A, Mandible shows diffuse symmetric periosteal reaction—a cherub. B, Left clavicle shows diffuse periosteal reaction similar to that of a healing fracture.

■ FIGURE 37-16 Scurvy. A, Radiograph of both legs shows faint periosteal reaction in the distal left femur due to periosteal hemorrhage, widened metaphyses with spurs, and reduced bone density. The ossific centers had a typical “white pencil” outline. Fractures are rare. B, Localized view of knee shows metaphyseal changes and periosteal reaction. Note that the end plate is still well defined and the physis is not widened (compare with rickets).

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■ FIGURE 37-17 Skeletal dysplasia. Metaphyseal changes affect all limbs and there is platyspondyly and spondylometaphyseal dysplasia, not metaphyseal fractures due to child abuse.

or pathologic fracture. Neuroblastoma and leukemia can present as multifocal bone involvement (Fig. 37-18). Primary bone tumors are rare in infants.

Accidental Trauma The spectrum of accidental injuries simulating abuse is constantly expanding; and when a solitary fracture of the long bones is identified, it is crucial to assess the findings in the context of the child’s age and the recorded mechanism of injury. Femoral shaft fractures can occur during running in older toddlers and young infants. Excluding supracondylar fractures of the elbow in children, all humeral fractures in infants are strongly suggestive of abuse. Once again, it must be emphasized that knowledge of the pattern of accidental trauma is essential to discriminate between true accidental and inflicted injury.

■ FIGURE 37-18 Leukemia. Metaphyseal infiltrates on both sides of the knee with periosteal reaction. The child presented with painful legs and bruising.

Obstetric Injury Obstetric trauma is a recognized cause of bone injury. Breech extractions or difficult cesarean deliveries are especially at risk for skeletal injuries. Clavicle fractures are the most common fractures encountered with birth trauma (shoulder dystocia) (Fig. 37-19), but humeral and femoral fractures do occur (breech and cesarean section extraction). Birth fractures are frequently characterized by good callus formation within the first few weeks of life. The absence of callus at 11 days of age should raise a high suspicion of child abuse.26

■ FIGURE 37-19

Occult obstetric injury. A 6-week-old infant presented with painless swelling of the clavicle only noticed that day. Radiograph shows healing clavicular fracture. There was a history of shoulder dystocia. The infant weighed 4.6 kg at birth.

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What the Referring Physician Needs to Know ■

■

■

Diagnostic imaging plays a fundamental role in the evaluation of suspected child abuse. The radiologist needs to carefully analyze the imaging findings in the context of the clinical history. Familiarity with the typical osseous lesions in abuse and awareness of normal variants and pitfalls are crucial. High-detail radiographs of the entire skeleton, at times supplemented with nuclear imaging, Ultrasonography, CT, and MRI are indispensable in reaching an early and accurate diagnosis on the basis of which appropriate measures can be taken to protect the infant against possible further injury. Clinicoradiologic correlation is important to recognize the expected and deviant patterns of injury with age. If nonaccidental injury is suspected, then the radiologist must discuss this with the pediatrician directly.

Normal Variants A variety of normal anatomic variants have imaging features that can be confused with abuse. Normal metaphyseal variants including spurs, beaks, and step-off configurations have been described.27 Subperiosteal new bone formation involving the diaphysis of long bones, particularly in the lower extremity, can be a physiologic finding between 1 and 6 months of age but is rarely thicker than 2 mm.28 Unusual contour deformities or trabecular irregularities may be seen in the shafts of long bones, particularly in the lower arm. Developmental variants of the acromial process are an important differential diagnostic consideration in case of an acromial fracture, a distinctive high-specificity injury of child abuse.29 Finally, irregularity of the distal ulna is common in the infant, and this is an uncommon site for an isolated metaphyseal fracture.

REFERENCES 1. National Child Abuse and Neglect Data System, report 2003. 2. Carty HM. Fractures caused by child abuse. J Bone Joint Surg Br 1993; 75:849–857. 3. Reece RM. Child Abuse: Medical Diagnosis and Management. Philadelphia, Lea & Febiger, 1994. 4. Caffey J. Multiple fractures in the long bones of infants suffering from chronic subdural haematoma. AJR Am J Roentgenol 1946; 56:163–173. 5. Silverman FN. The roentgen manifestations of unrecognized skeletal trauma in infants. AJR Am J Roentgenol 1953; 69:413–427. 6. Kempe CH, Silverman F, Steele BF. The battered-child syndrome. JAMA 1962; 181:105–112. 7. King J, Diefendorf D, Apthorp J. Analysis of 429 fractures in 189 battered children. J Pediatr Orthop 1988; 8:585–589. 8. Kleinman PK. Diagnostic imaging in infant abuse. AJR Am J Roentgenol 1990; 155:703–712. 9. Loder RT, Bookout C. Fracture patterns in battered children. J Orthop Trauma 1991; 5:428–433. 10. Merten DF, Radkowski MA, Leonidas JC. The abused child: a radiological reappraisal. Radiology 1983; 146: 377–381. 11. Worlock P, Stower M, Barbor P. Patterns of fractures in accidental and non-accidental injury in children: a comparative study. BMJ (Clin Res Ed) 1986; 293:100–102. 12. Kleinman PK. Diagnostic Imaging of Infant Abuse, 2nd ed. St. Louis, Mosby, 1998. 13. Kleinman PL, Kleinman PK, Savageau JA. Suspected infant abuse: radiographic skeletal survey practices in pediatric health care facilities. Radiology 2004; 233:477–485. Epub 2004 Sep 16. 14. Conway JJ, Collins M, Tanz RR, et al. The role of bone scintigraphy in detecting child abuse. Semin Nucl Med 1993; 23:321–333. 15. Kleinman PK, Marks SC Jr, Blackbourne BD. The metaphyseal lesion in abused infants: a radiologic-histopathologic study. AJR Am J Roentgenol 1986; 146:895–905.

16. Thomas SA, Rosenfield SN, Leventhal JM, Markowitz RI, et al. Long-bone fractures in young children: distinguishing accidental injuries from child abuse. Pediatrics 1991; 88:471–476. 17. Beals RK, Tufts E. Fractured femur in infancy: the role of child abuse. J Pediatr Orthop 1983; 3:583–586. 18. Feldman KW, Brewer DK. Child abuse, cardiopulmonary resuscitation, and rib fractures. Pediatrics 1984; 73:339–342. 19. Strouse PJ, Owings CL. Fractures of the first rib in child abuse. Radiology 1995; 197:763–765. 20. Amir J, Katz K, Grunebaum M, et al. Fractures in premature infants. J Pediatr Orthop 1988; 8:41–44. 21. Elmer E, Gregg G. Developmental characteristics of abused children. Pediatrics 1967; 40:596–602. 22. Klein M, Stern L. Low birth weight and the battered child syndrome. Am J Dis Child 1971; 122:15–18. 23. Steiner RD, Pepin M, Byers PH. Studies of collagen synthesis and structure in the differentiation of child abuse from osteogenesis imperfecta. J Pediatr 1996; 128:542–547. 24. Miller ME. Temporary brittle bone disease: a true entity? Semin Perinatol 1999; 23:174–182. 25. Paterson CR, Burns J, McAllion SJ. Osteogenesis imperfecta: the distinction from child abuse and the recognition of a variant form. Am J Med Genet 1993; 45:187–192. 26. Cumming WA. Neonatal skeletal fractures. Birth trauma or child abuse? J Can Assoc Radiol 1979; 30:30–33. 27. Kleinman PK, Belanger PL, Karellas A, et al. Normal metaphyseal radiologic variants not to be confused with findings of infant abuse. AJR Am J Roentgenol 1991; 156:781–783. 28. Shopfner CE. Periosteal bone growth in normal infants: a preliminary report. Am J Roentgenol Radium Ther Nucl Med 1966; 97:154–163. 29. Currarino G, Prescott P. Fractures of the acromion in young children and a description of a variant in acromial ossification which may mimic a fracture. Pediatr Radiol 1994; 24:251–255.

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C H A P T E R

Stress Injury Joong Mo Ahn and Georges Y. El-Khoury

PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS Stress injuries are a common cause of pain and morbidity and have become commonplace among the members of our increasingly active society.1 There is some confusion regarding the numerous terms used to describe these injuries, and the clinical diagnosis of stress fractures can be difficult because symptoms are often vague and soft tissue injuries may mimic bony abnormalities. Stress injuries represent a wide spectrum of osseous and soft tissue injuries that occur in response to changes in the mechanical environment. They account for at least 10% of the cases encountered in a typical sports medicine practice.2 Although the reported incidence of stress fractures in the general athletic populations is less than 1%, the incidence in runners may be as high as 20%.3 Stress fractures occur at all ages, and there is no sex predilection. Athletics, or track and field sports, account for 50% of stress fractures in men and 64% in women.4 People today are more concerned about physical fitness and, with the increasing popularity of running, stress fractures of the lower extremity, especially the tibia, ankle, and foot, have been common.5 Stress fractures can involve multiple bones, can occur bilaterally (Fig. 38-1), and can be considered as a multifocal entity. In both men and women, stress fractures tend to recur.6 Approximately 60% of individuals with a stress fracture have had a clinical history of a previous stress fracture.6 Stress fractures develop when bone is subjected to repeated cyclic loading in specific areas with the load being less than that capable of causing acute fractures.7 Even though the terminology is debated, many investigators consider isolated periostitis and/or edema to represent a stress reaction or a stress response, whereas the presence of a fracture line indicates a true stress fracture. In other words, a stress reaction occurs when microfractures are healing and a complete fracture has not yet developed.5 In reality, these two conditions represent a continuum. The term pathologic fracture should be restricted to any fracture due to any type of stress occurring in bone weakened by preexisting neoplastic or infectious processes. The term

occult fracture may be used for a fracture initially not seen by radiography.8 These fractures are still termed occult even when confirmed by other imaging tests or if the fracture is seen in retrospect.8 From an etiologic standpoint, two general types of stress fractures have been identified: fatigue fracture and insufficiency fracture.1,2,9 A fatigue fracture is caused by the prolonged cyclical application of abnormal mechanical stresses to a bone that has normal elastic resistance, whereas an insufficiency fracture occurs with normal or physiologic stresses on a weakened skeleton that is deficient in mineral or elastic resistance.1,2 Stress injuries are therefore divided into three types: stress reaction, fatigue fracture, and insufficiency fracture. Within physiologic limits, mechanical overload stimulates bone growth; but once these limits are exceeded, fatigue fractures may develop. Sudden vigorous exercise without prior training seems to be a particular precipitating factor. Classically, the pain is relieved by rest

KEY POINTS For the diagnosis of stress fracture, the most important thing is to be aware of and suspect the condition. ■ The radiologic appearance depends on the amount of time between the onset of symptoms and the imaging examination and on whether the patients continued to participate in the offending activity. ■ In cases that are atypical in location or clinical presentation the radiologists rely more on MRI and CT. MRI detects early changes of osseous stress injury and allows precise definition of anatomy and extent of injury and is the preferred modality for evaluating the continuum of osseous manifestations of stress injury. ■ MRI is useful in evaluating shin splints, early osseous stress injuries, and overt stress fracture. In the elite athletes, prompt diagnosis and early rehabilitation are the goals. ■ Knowledge of imaging findings of stress injuries as well as their related clinical conditions can improve the chances of early diagnosis. ■

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■ FIGURE 38-1

A, Standing anteroposterior radiograph of the right ankle obtained in a 56-year-old woman shows horizontal sclerosis in right tibia (arrow). Note the underlying diffuse osteopenia. B, Standing anteroposterior radiograph of the left ankle obtained from the same patient shows another horizontal stress fracture (arrow) in the left distal tibia.

and then recurs when activity is restarted. A period of rest can allow the process to halt and the bone to heal. The further the fracture process develops the longer the rest period is required for healing. As the injury becomes more severe, the patient may develop rest pain and this can be a source of clinical confusion for the referring physician. Fatigue fractures are generally seen in young adults and are particularly common in certain populations, especially in athletes and military recruits, but they are also observed in elderly persons and children. The following triad is typically observed in most fatigue fractures: the activity is new or different for the individual, the activity is strenuous, and the activity is repeated with a frequency that ultimately produces signs and symptoms.10 Usually, patients present with pain and localized tenderness and a history of either an increase in activity or an alteration in the pattern of exercise. Symptoms are typically relieved by rest. Rarely, fatigue fractures are asymptomatic. Fatigue fractures may be classified as low-risk injuries, which have a favorable

prognosis when treated with restriction of physical activity, or as high-risk injuries, which are prone to delayed union or nonunion, especially if the diagnosis is delayed.3 Examples of low-risk stress fractures include those in the upper extremity, ribs, pelvis, femoral and tibial shafts, fibula, calcaneus, and metatarsal shaft; examples of high-risk stress fractures include those in the femoral neck, patella, anterior tibial cortex, medial malleolus, talus, tarsal navicular, sesamoid, and fifth metatarsal.3 Insufficiency fractures generally occur in a variety of conditions where the mineral content or the elasticity of bone is abnormal and are more common after the age of 50.9 Although insufficiency fractures occur most often in elderly women who have postmenopausal osteoporosis, they also occur in patients with osteoporosis of any cause, including corticosteroid use, rheumatoid arthritis, and diabetes mellitus.11,12 The causes of these injuries are diverse and also include Paget’s disease, osteomalacia, rickets, hyperparathyroidism, renal osteodystrophy, osteogenesis

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imperfecta, osteopetrosis, fibrous dysplasia, and irradiation.7,9,13 In addition, some drugs including sodium fluoride, methotrexate, and etidronate have been associated with the development of stress fractures.9,14 Additional factors may include skeletal deformities and leg-length discrepancies.7,9 In patients with osteoporosis, such fractures occur in the sacrum, pubic rami, and lower extremities. In patients with rheumatoid arthritis, predisposing factors include osteopenia, angular deformities of the extremities, and arthroplasties. In Paget’s disease, the convex aspects of the tubular bones, especially the femur and tibia, are affected.9 Stress fractures are not infrequent after certain surgical procedures that result in altered stress or an imbalance of muscular force on bones associated with injury, casting, or surgery. Common examples are noted in the metatarsals after bunion surgery, the lower extremities after arthrodesis or arthroplasty, the pubic rami after hip or knee surgery, the calcaneus of the patients who have undergone immobilization, and the clavicles after radical mastectomy or neck dissection.9 The occurrence of subchondral bone abnormalities in the femur or tibia after meniscal surgery likewise may be indicative of a stress fracture. Stress fractures are also observed in the distal portion of the tibia or in the bones of the foot in patients with healing or healed gross traumatic fractures of a more proximal portion of the tibia, fibula, or femur. They are also more likely to occur in normal bones at the sites of previous surgical screw holes. Both fatigue and insufficiency fractures can occur in the same person if abnormal stress is placed on bones. Multiple insufficiency fractures usually are seen in patients with predisposing conditions, such as osteoporosis, osteomalacia, hyperparathyroidism, and osteogenesis imperfecta.

ANATOMY An understanding of basic skeletal anatomy helps in evaluating the stress fractures. Human bone is a highly specialized form of connective tissue and is made up of two components; cortical (dense or compact) bone and cancellous (spongy or trabecular) bone.15 Although both types of bone tissue have the same histologic structure, differences exist in their detailed structures. Cortical bone has a solid, compact architecture interrupted only by the narrow canals of the haversian systems, which contain neurovascular bundles. Cancellous bone consists of a meshwork of primary longitudinal and secondary transverse trabeculae separated by fatty or hematopoietic marrow. Cortical bone is typically present along the outer margin of a long bone. It is made up of individual components called osteons. Cortical bone has two types of surfaces: endosteum on the inner side facing the bone marrow and trabeculae and periosteum on the outer side facing the surrounding soft tissue. Cancellous bone is a structure of internal struts, usually found in the central portions or ends of long bones.1,15 Regarding the anatomic locations of involvement, stress fractures most commonly occur in the bones of the lower limb. Lower extremity stress fractures can also occur anywhere and include the femur, tibia, fibula, calcaneus, tarsal

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navicular, metatarsal, and sesamoid. The anatomic sites of involvement can often be predicted by analysis of the specific sporting activity that has led to the fatigue fractures.7 Typical examples are the fatigue fractures of the metatarsal of military recruits7 and ballet dancers, the tibial diaphysis of runners, the tarsal navicular of the soldiers and runners, the calcaneus of the jumpers and parachute jumpers, the patella of hurdlers, and the obturator ring of bowlers and gymnasts. Sacral fatigue fractures have also been recognized in runners and adolescents without athletic participation. According to the specific activities, runners are prone to fatigue fractures of the proximal posteromedial surface of the tibia, the distal shaft of the fibula, the tarsal navicular, and femoral neck. Dancing is associated with stress fractures of the metatarsal, the anterior shaft of the tibia, and the neck and shaft of the femur. Leaping activities in basketball can cause cortical fatigue fractures of the anterior surface of the tibia and the calcaneus. Although most common in the lower extremity, stress injury to bone and stress fractures have been reported in nearly every bone in the body, including the upper extremity. The ulna, humerus, and carpal bones are the sites of involvement in the upper extremity.

BIOMECHANICS Bone is a dynamic and adaptable tissue that continually reacts to stress16 and requires stress for normal development. It undergoes constant remodeling, repair, and regeneration in response to changing forces and stress from the environment. Remodeling refers to the lifelong renewal process of the bone in which the osteoclasts and the osteoblasts remove and replace bone without significantly affecting bone shape or density. Under normal circumstances, the bone is able to keep up with necessary repairs and avoid clinically manifesting injury as it remodels appropriately. However, when a reparative capacity of the bone is overwhelmed by overload, damages begin to accumulate. The progression of damage accumulation eventually results in a stress fracture. A stress fracture should be viewed as the end point of a spectrum along which a bone responds to a changing mechanical environment, a spectrum ranging from early remodeling to frank fracture. Material properties can be described according to their response to the application of loads. Stress refers to the force or load applied to a bone that may arise from weight bearing or muscular action. The force may be applied as an axial, bending, or torsional load.2 Tensile forces are produced along the convex side of a bone, whereas compressive forces occur along its concave margin.1 When a bone is stressed, osteon remodeling takes place, as identified by resorption of circumferential lamellar bone and its subsequent replacement by dense bone. Unlike an acute fracture, which usually occurs from a single supraphysiologic stress, a stress fracture is a result of a dynamic process over time.16 The precise pathogenesis of a stress fracture is still poorly understood, and the etiology of stress fractures appears to be multifactorial. There are several theories to explain the mechanism of these injuries in a biomechanical standpoint.3 One explanation of

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the pathogenesis relates to the role of a muscle. Because bone is more resistant to force in compression than tension, the supporting muscles help prevent fatigue fractures. When the muscles fatigue, the tensile forces increase, rendering bone failure more likely. Accordingly, fatigue of muscles in the poorly conditioned athlete creates increased tensile stress on bone, resulting in stress fracture. Initially, osseous remodeling manifests as osteoclastic activity and resorption of lamellar bone. This is subsequently replaced by denser bone. In repetitive stress overload, however, the accelerated remodeling results in an imbalance between bone resorption and bone replacement, leading to weakness of the bone. Continued stress results in further imbalance, leading to bone fatigue and fracture. Osseous stress is not an all-or-nothing phenomenon but a physiologic continuum ranging from normal osseous remodeling, to accelerated remodeling with fatigue and early injury, to frank stress fracture.10 Another explanation of the pathogenesis relates to increased muscle strength. Increased activity results in an increase in the strength of both bones and muscles.17 Conversely, a decrease in activity results in muscle and bone atrophy.17 Under normal conditions, when a new stress is applied, muscle tone is achieved more quickly than bone is strengthened. This results in a mechanical imbalance,10 with muscle exerting excess force on bone, resulting in bone fatigue. As the amount of stress on a bone is increased, progressive deformity occurs throughout the elastic range of a bone. As long as the deformity remains within the elastic range, when the deforming force stops, the bone returns to normal original configuration. Beyond the elastic range, further stress results in plastic deformity and microfractures.7 As the number of microfractures increase, small cortical cracks occur. The cracks progress as the stress continues or become more exaggerated, and such progression is characterized by the appearance of subcortical infraction in front of the advancing main crack in the bone.9 Thus, continued stress results in progression of microfractures, leading to further structural failure.

PATHOLOGY Pathologically, a stress fracture reflects microfractures of trabeculae, cortical fractures, or bone repair with periosteal and/or endosteal callus and thickening of trabeculae. If any possibility exists that a bone lesion may represent a healing stress fracture, biopsy should be avoided unless there is evidence that the appearance of the lesion on radiographs has not changed over several weeks. A biopsy specimen of a stress fracture may contain immature bone cells, which are part of the healing fracture process but that may be misinterpreted as representing bone sarcoma.7

MANIFESTATIONS OF THE DISEASE Radiography Radiographs play an important role in the workup of a suspected stress fracture and should be the first imaging studies obtained. They can be used to confirm the

■ FIGURE 38-2

Anteroposterior radiograph of the right foot obtained in a 61-year-old woman reveals abundant callus formation (arrow) at the junction of the distal and middle thirds of the second metatarsal of the right foot.

diagnosis at a relatively low cost. The diagnosis of a stress fracture on the basis of radiography is usually made by recognition of callus (Fig. 38-2). However, callus is not seen radiographically until substantial calcium has been deposited, which does not occur until the second week. Therefore, stress fractures are commonly occult. This poor radiographic sensitivity compared with a technique such as bone scintigraphy has long been recognized. In early osseous stress reaction and stress fracture, radiographs may initially be entirely normal, but, with time, a fracture line can be identified and only one cortex may be involved; a hint of periosteal reaction with some endosteal new bone may develop. It may take 3 to 4 weeks for changes to occur in the metaphyseal area of bone and 4 to 6 weeks for them to occur in the diaphysis. During the healing phase, both periosteal and endosteal new bone are incorporated in the cortex, resulting in a fusiform expansion of the cortex. The sensitivity of early fracture detection by radiography can be as low as 15% to 28%, and follow-up radiography may demonstrate diagnostic findings in only 50% of cases. The lag time between manifestations of initial symptoms and detection of radiographic findings ranges from 1 week to several months. In most instances, periosteal reaction is not evident within the first several weeks of symptoms. When the initial radiographs are negative, the best next test would be MRI.

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An early stress fracture in the shaft of a long bone may appear typically as a lucency through the cortex without any periosteal reaction or callus. The gray cortex sign refers to a cortical area of decreased density. This sign could be seen in the initial stage of the stress injury and is easily overlooked. Focal hyperemia could be responsible for this initial graying cortex. As the bone heals, solid or thick lamellar periosteal reaction occurs. Often, this occurs on the endosteal surface as well as on the periosteal surface. Reactive bone is generally confined to a small area of cortex and usually involves only one of the cortical surfaces. Ultimately, the area of periosteal reaction thickens and the fracture line disappears. The radiographic findings depend on when the images are obtained relative to the spectrum of osseous remodeling. In bones that are predominantly cancellous, such as the calcaneus or femoral neck, radiographs initially demonstrate subtle blurring of trabecular margins and focal faint linear sclerosis perpendicular to the trabeculae representing the fracture and peritrabecular callus.

Magnetic Resonance Imaging Magnetic resonance imaging is an effective diagnostic technique for the evaluation of patients in whom there is clinical suspicion for stress fracture and radiographs are negative. Several studies have demonstrated the efficacy of MRI in the evaluation of stress injuries to bone.18,19 When radiographs fail to reveal a fracture, the search for a cortical infraction can be accomplished with MRI because it is sensitive in detecting a small fracture line. Thin-section MRI should be employed. MRI allows depiction of abnormalities weeks before the development of radiographic abnormalities and has comparable sensitivity and superior specificity compared with bone scintigraphy. It has the additional advantage of demonstrating concomitant soft tissue injury. Both resorption and replacement of bone characterize the early changes of stress injury to bone. This is manifested by local hyperemia and edema. Because of its high sensitivity for the detection of edema, MRI is an excellent modality for the detection of early osseous stress injury. Subsequently, MRI clearly depicts the more advanced findings of cortical bone breakdown and frank stress fracture. It is this differentiation between the changes of early stress injury to bone, and later stress fracture, that has predictive value in estimating the duration of disability, helping to guide therapy. When evaluating for stress injury, MRI parameters should include both a T1-weighted sequence and a fluid-sensitive T2-weighted sequence with fat suppression or short tau inversion recovery (STIR) sequence. Fat-suppressed T2-weighted or STIR images are important for detection of the edema of the periosteum, muscle, or bone marrow. These findings are the earliest changes of stress reaction (Fig. 38-3). Edema results in high signal intensity against the dark background of the suppressed fat. As the injury becomes more severe, findings include marrow edema identified on both T1- and T2-weighted MR images and signal abnormalities in the cortical bone. Frank stress fractures are diagnosed by identifying band-like areas of low signal intensity in the intramedullary space that may be continuous with the cortex. The most common pat-

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tern of a fatigue-type fracture is low signal intensity line on all pulse sequences, surrounded by a larger, ill-defined zone of edema. The fracture line is continuous with the cortex and extends into the intramedullary space oriented perpendicular to the cortex and the major weightbearing trabeculae (see Fig. 38-3). MRI is more accurate than bone scintigraphy in correlating the degree of bone involvement with clinical symptoms, allowing for more accurate recommendations for rehabilitation and return to activity. Muscle edema on MRI may be predictive of a shorter clinical course, whereas a finding of a fracture line or a cortical signal abnormality could be predictive of a longer symptomatic period. An MRI finding of either a medullary line or a cortical abnormality seems to indicate a more severe stress injury to bone (see Fig. 38-3).18 MRI findings parallel those found on bone scintigraphy. If the patient is imaged within days after the patient becomes symptomatic, MR images will show low signal intensity in the marrow areas on T1-weighted images. The signal is increased on T2-weighted or STIR images, and contrast medium enhancement is seen after intravenous injection of MR contrast agents. The findings can be confused with those seen in transient osteoporosis, neoplasm, or infection. If the patient is imaged much later, linear areas of low signal intensity may be seen on T1-weighted images. These linear abnormalities have low signal intensity on T2-weighted or STIR images and represent callus and new bone formation at the fracture site and are suggestive of a stress fracture. In addition, MRI has been found to be more sensitive than radiography and more specific than bone scintigraphy in the detection of occult fractures in the elderly and in osteoporotic patients. Advanced MRI techniques may be more accurate in distinguishing stress fractures from pathologic fractures. These include chemical shift imaging, diffusion-weighted imaging, dynamic contrast-enhanced imaging, and MR spectroscopy. Chemical shift imaging is based on the principle that a voxel that contains both water and fatty marrow elements, as present in a stress fracture, should demonstrate a decreased signal intensity on an opposedphase gradient-echo sequence compared with an inphase gradient-echo sequence. However, in a voxel in which normal marrow elements are completely replaced by tumor in patients with pathologic fractures there is no decrease of the signal intensity expected on the opposedphase sequence compared with the in-phase sequence. Diffusion-weighted imaging has been successfully used in the assessment of vertebral fractures and is the only noninvasive technique that maps the motion of water protons. In the case of a pathologic fracture there is restriction of water motion at the site of tumor, whereas in a stress fracture, mobility of the water protons is preserved.

Multidetector Computed Tomography Computed tomography has been a useful imaging tool to diagnose a stress fracture, and it has inherent advantages when examining high-attenuation tissue such as bone. CT is also helpful in defining the extent of the suspected stress fracture. The typical appearance of a stress fracture on CT is that of focal callus formation and endosteal thickening around a fracture site. Occasionally, increased density

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■ FIGURE 38-3

A, Anteroposterior radiograph of the left tibia from a 41-year-old woman demonstrates thickening of the left tibial cortex (arrow) extending approximately 4 cm in length over the distal shaft of the left tibia. B, Lateral radiograph of the left tibia from the same patient again shows cortical thickening (arrow) of the left tibia. C, T1-weighted coronal MR image of the left lower leg shows cortical thickening (arrowhead) and intramedullary low signal intensity reflecting marrow edema (arrow). D, T2-weighted STIR coronal MR image of the left lower leg demonstrates hyperintense marrow edema (black arrow), hyperintense periosteal edema or periosteal reaction (white arrowhead), cortical thickening (white arrow), and hypointense linear band reflecting fracture line (black arrowhead). E, T1-weighted axial MR image of her left lower leg shows decreased signal intensity of the bone marrow (arrowhead) with cortical thickening (arrow) of the left tibia. F, T2-weighted axial MR image obtained at the same level as in E reveals thickened tibial cortex (arrow), hyperintense periosteal edema (arrowhead), and a low signal intensity area within the bone marrow space suggesting intramedullary callus formation (thin arrow).

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of the medullary cavity and adjacent soft tissue swelling are identified. However, it has been suggested that CT has only a limited role in stress fracture detection, because its inferior sensitivity compared with that of bone scintigraphy and MRI. Therefore, the use of CT should be reserved for specific indications such as more advanced injuries and injuries in specific anatomic locations where the role of radiography is limited. These indications include suspected fractures of the tarsal navicular, longitudinal fractures of the tibia, stress fractures in the sacrum, or the differentiation of stress fracture from osteoid osteoma. CT may also help problem solve when there are equivocal findings on radiographs, MR images, or bone scintiscans. The value of CT in this regard lies in the detection of a discrete fracture line or periosteal reaction. A fracture line in the axial plane may be overlooked on axial CT images but be well demonstrated by coronal or sagittal multiplanar or volume-rendered 3D images. Additionally, the advent of multidetector CT scanners allows the production of thin axial sections, resulting in high-resolution multiplanar reconstructions.20 These advances allow the demonstration of bone cortex and trabecular pattern with fine detail, which is helpful in the diagnosis of stress fractures when the findings on other modalities are equivocal or inconclusive. CT has proven to be valuable in the diagnosis of pediatric stress fractures, which can be difficult to detect and characterize by other modalities. The appearance of such fractures may mimic that of tumors on other modalities. Furthermore, CT can be used as an ancillary examination, particularly in the sacrum, to confirm a diagnosis suggested by other imaging studies.

Ultrasonography The superficial margins of cortical bone can be evaluated with ultrasonography, in which the cortex appears linear and echogenic. Ultrasonography can be used to evaluate superficial bone cortices such as the feet and distal tibia, where it can depict periosteal and muscle edema, cortical fracture lines, and callus. In addition, power Doppler imaging may provide a semi-quantitative evaluation of bone turnover activity by showing increased perfusion at the injury site. However, given the acoustic impedance properties of cortical bone, the deeper margins of bone are not able to be visualized because of the posterior acoustic shadowing from the more superficial layers of bone.

Nuclear Medicine Bone scintigraphy with a bone-seeking radiopharmaceutical is very sensitive to metabolic changes in bone and has become an effective modality in the evaluation of patients with clinically suspected osseous stress injuries.21 Although routine radiography plays an essential role in the diagnosis of stress fractures, it is the bone scintigraphy that provides not only one means of early detection but also a visual account of the biomechanical properties of bone that are fundamental to the pathogenesis of stress fracture. Before the advent of MRI, bone scintigraphy was the gold standard for evaluating stress fractures, and its high sensitivity in detecting stress fracture

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has been described in many studies. Bone scintigraphy demonstrates abnormal findings early in the continuum of the stress response in bone by detecting the increased bone metabolism and osteoblastic activity associated with osseous remodeling. Bone scintigraphy shows abnormalities early in the course of the stress fracture, which become abnormal days to 2 weeks before the radiographic changes become obvious.21 In the early stages of osseous stress injury, bone scintigraphy will show ill-defined areas of a slightly increased uptake of radionuclide,22 which may represent stress reaction. As injury becomes more severe, bone scintigraphy exhibits more intense and focal radionuclide localization. This eventually progresses to well-marginated areas of increased uptake, which represents a stress fracture. Early recognition of mild scintigraphic patterns representing the beginning of bone response to stress can enable prompt treatment to prevent progression of the lesions. Bone scintigraphy should optimally be performed using the three-phase technique, because it can help differentiate between soft tissue injury and osseous injury. In the blood flow phase, imaging is performed by acquiring dynamic 2- to 5-second images over the area of clinical concern for 60 seconds after the bolus intravenous injection. In the blood pool or soft tissue phase, imaging is acquired within 5 minutes after injection. In the final or the delayed skeletal phase, images should be acquired 2 to 4 hours after the bolus injection to maximize clearance of the radiopharmaceutical agent from the overlying soft tissues. Acute stress fractures typically demonstrate abnormal radionuclide activity on all three phases of the scintigraphy. Soft tissue injuries are characterized by increased uptake in the first two phases only. Shin splints, a clinical entity of activity-related lower leg pain, are typically positive on only the delayed images, demonstrating long, linear foci of increased radionuclide uptake along the posterior cortex of the tibia. Despite its very high sensitivity, bone scintigraphy lacks specificity; and conditions such as tumors, infection, and infarction may mimic stress injury. Additionally, although bone scintigraphy may be useful in the initial staging of bone stress injury, it is less useful for follow-up because abnormal uptake may persist for several months.

SPECIFIC ANATOMIC SITES FOR STRESS INJURIES Femur Stress fractures in the femur are rare, representing only about 5% of all stress fractures, and they are difficult to diagnose because the pain pattern can be atypical and the pain may be referred to the knee. However, the diagnosis of the stress fracture in the femur is important because of the high incidence of fracture nonunion, complete fractures, or avascular necrosis, which may result in an unrecoverable injury. Stress fractures in the femur can be observed at various levels: neck, femoral head, diaphysis, and distal femur. Two types of femoral neck stress fracture have been described: compression type and tensile type.3 A compression type may occur on the inferomedial side of the

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femoral neck and is more common in younger patients. It appears as a haze of callus in the inferior aspect of the neck and tends to be stable in most cases.3 Most athletic-induced stress fractures occur medially, where, fortunately, there is less risk of the fracture displacing. A tensile type involves the superolateral side of the femoral neck and is more frequent in older patients. It appears as a small radiolucent area in the superior aspect of the femoral neck and becomes displaced in some situations.3 Whereas radiographs are usually normal at the time of presentation, bone scintigraphy is often positive.22 After several weeks, the radiographs may show a linear area of ill-defined sclerosis perpendicular to the primary trabeculae of the femoral neck (Fig. 38-4). This faint sclerosis can be difficult to visualize, and careful inspection of the radiographs and comparison with the contralateral hip could be helpful. MRI is the diagnostic test of choice in detecting and following stress fractures of the femoral neck. Compression type of stress fractures in the femoral neck are diagnosed on MRI as a rounded area of decreased signal intensity on a T1-weighted image with corresponding bright signal intensity on T2-weighted or STIR images, extending a variable distance across the femoral neck. If a fracture line is present on MRI it appears as a line of decreased signal intensity perpendicular to the cortical margin and is visualized on all the coronal imaging sequences. Femoral neck stress fractures may show return of the normal bone marrow signal intensity on STIR images at 3 to 6 months after the fracture diagnosis. Full clinical healing may not be synonymous with MRI edema signal resolution. Spontaneous insufficiency femoral neck fractures are frequently associated with osteoporosis.

In recent years, emphasis has been placed on the occurrence of insufficiency fractures of the femoral head that may occur in patients with renal osteodystrophy or osteoporosis.13 Subtle flattening of the femoral head or a subchondral fracture line or both are the observed radiographic findings in some cases, but CT or MRI is often required for accurate diagnosis. The findings simulate those of osteonecrosis or even osteoarthritis. Insufficiency fractures of the femoral head may also be encountered during the course of transient osteoporosis, or transient marrow edema, of the femoral head.13 Fatigue fractures of the femoral head have also been described in athletes and military recruits. Stress fractures of femoral diaphysis may be observed in soldiers and frequently are asymptomatic. They are also found in patients with Paget’s disease, typically appearing on the convex surface. Longitudinal diaphyseal insufficiency fractures have also been reported, some of them associated with osteoporosis.14 Supracondylar insufficiency fractures in the distal region of the femur can be seen in osteoporotic patients (Fig. 38-5) or after knee arthroplasty simulating local knee processes. Bone scintigraphy shows a local increased uptake, and radiography shows local sclerosis in the femoral condyle.14 Because spontaneous osteonecrosis of the knee had been recognized as a distinct form of osteonecrosis, subsequent reports have suggested that the etiology of this condition would be a subchondral insufficiency fracture associated with localized osteonecrosis resulting from underlying osteoporosis. The classic location is the subchondral bone of the medial femoral condyle. Radiography shows radiolucent oval area in the subchondral bone, flattening of the convexity of the condyle, sclerotic halo, and osteoarthritis with joint space narrowing, sclerosis, and osteophyte formation (Fig. 38-6). MRI reveals focal or diffuse hypointensity on T1-weighted images and variable signal intensity on T2-weighted images (see Fig. 38-6).

Tibia

■ FIGURE 38-4

Anteroposterior radiograph of right femur in an 80-year-old woman shows insufficiency fracture of the right femoral neck. It appears as linear sclerosis (arrow).

Tibial stress fractures may account for up to 73% of all stress fractures18 and are the most common lower extremity stress fractures. Most tibial stress fractures are identified by the development of a fracture line in the cortex of the tibia, usually affecting the proximal part and midshaft (Fig. 38-7).14 Often, a variable amount of cortical thickening or periosteal reaction is present. Alternatively, jumping athletes, such as basketball players and ballet dancers, may develop single or multiple horizontal anterior tibial striations that are well visualized on lateral radiographs (Fig. 38-8). Most cases of the classic, horizontally oriented stress fracture (Fig. 38-9) and the longitudinal stress fracture cannot be seen on radiographs until weeks after the onset of symptoms, which results in a delay in diagnosis. Over time, radiographs may demonstrate a subtle increase in bone reaction along the outer cortex of the involved bone, with subsequent development of linear sclerosis and new bone formation. The investigation of choice is bone scintigraphy, which shows a linear area of increased radionuclide uptake at the fracture site. When insufficiency fractures occur in the tibia, they often involve the distal metaphysis

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■ FIGURE 38-5

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A, Anteroposterior radiograph of a 99-year-old woman shows step-off of the supracondylar cortex (arrow) with intramedullary linear sclerosis (arrowhead) reflecting incomplete fracture line. Note also advanced osteopenia of the left lower extremity. B, Lateral radiograph of the same patient reveals linear sclerosis secondary to insufficiency fracture (arrow) of the left distal femur. C, T1-weighted coronal MR image of the left knee reveals linear hypointense band (arrows) that begins at medial supracondylar area and extends to the medullary space of the left distal femur. D, T2-weighted coronal MR image of the left knee depicts linear low signal intensity (arrow) reflecting fracture line and area of bright signal intensity suggesting bone marrow edema (arrowhead).

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■ FIGURE 38-6

A, Anteroposterior radiograph from a 75-year-old woman shows flattening and subchondral collapse of the left medial femoral condyle (arrow). B, T1-weighted coronal MR image of the left knee shows decreased signal intensity of the subchondral region of the left femoral condyle (arrow). C, T2-weighted coronal MR image of the left knee reveals a curvilinear bright signal intensity in the corresponding area (arrow). Note also medial extrusion of the medial meniscus (arrowhead). D, Anteroposterior radiograph of the left knee, obtained 6 months later, demonstrates a progression of the subchondral collapse (arrow) in the medial femoral condyle of the left distal femur.

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■ FIGURE 38-7

A, Anteroposterior radiograph of the left lower leg in a 38-year-old woman shows a questionable periosteal reaction in the midshaft of the left tibia (arrow). B, The lateral radiograph of the same patient shows a horizontal and transverse lucency through the anterior cortex with cortical thickening (arrow).

and are transverse. The dreaded black line sign, which refers to a transverse fracture line across the entire anterior shaft of the tibia, is considered a poor prognostic sign with increased likelihood of nonunion.16 Although a horizontal orientation (see Fig. 38-9) is typically demonstrated, longitudinally oriented stress fractures (Fig. 38-10) are becoming more common.18 These longitudinal stress fractures usually occur in slightly older patients and almost exclusively involve the tibial shaft. This fracture may involve the anterior or posterior tibial cortex. Periosteal new bone formation can be detected, and there may be some focal endosteal sclerosis adjacent to the fracture. MRI has the advantage of demonstrating the presence of marrow edema or soft tissue edema if present. In most cases, the fracture line extends through a single cortex, with abnormal signal intensity in the marrow cavity and in the adjacent soft tissues.18 The term shin splints (Fig. 38-11) has been used to describe the clinical entity of activity-related lower leg pain, typically associated with diffuse tenderness along the posteromedial tibia. The symptoms typically are localized along the posteromedial aspect of the tibia in the region of the soleus muscle origin. Radionuclide scintigraphic studies have concluded that shin splints represent a distinct clinical entity from early osseous stress injuries. Recent MRI studies have, however, suggested that shin splints are a part of the continuum of fatigue damage in bone. Studies have described that increased cortical signal intensity on T2-weighted MR images may reflect overt stress fractures in athletes (see Fig. 38-11). Periosteal edema is present at the origins of the tibialis posterior, flexor digitorum longus, and

soleus muscles of runners with tibial stress injuries. The clinical significance of bone marrow edema depends on the severity of the findings and the clinical context. The finding of bone marrow edema on STIR imaging is a relatively sensitive finding and may be seen very early in the stress response. Fracture of the tibial plateau may present in older patients with preexisting osteoarthritis and varum or valgum knee deformities, making the diagnosis of this process difficult. Because this fracture may evolve toward collapse of the tibial plateau, it is important to be aware of this condition.

Calcaneus Calcaneal stress fractures were first described in military recruits, but they have been noted in runners, walkers, and aerobics participants.16 The presence of osteoporosis and muscle spasm favor the development of this injury.9 Radiography demonstrates a characteristic sclerosis, parallel to the posterior border of the calcaneus (Fig. 38-12).14 A band of increased density is seen between the tuberosity and posterior facet (see Fig. 38-12).16 Bone scintigraphy typically shows focal increase in bone uptake. Calcaneal insufficiency avulsion fractures appear to be a distinct entity seen in diabetic patients. They are extraarticular and confined to the posterior calcaneus.11 The primary fracture line of the calcaneal insufficiency avulsion fracture is parallel to the apophyseal growth plate and generally involves the superior calcaneal cortex but does not always extend to the inferior cortex.

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■ FIGURE 38-8

A, Lateral radiograph of a 36-year-old man with bilateral shin pain shows multiple perpendicular striations of lucency in the anterior cortex of the left tibia (arrowheads). B, CT scan of the left tibia reveals radiolucent fracture line (arrowhead) and cortical thickening (arrow) of the anterior tibial cortex. C, Sagittal multiplanar reformatted CT image demonstrates multiple perpendicular lucencies (arrowheads) in the anterior tibial cortex. D, CT scan of the right tibia obtained from the same patient reveals radiolucent fracture lines (arrowheads) of the anterior cortex of the right tibia. E, 99mTc MDP bone scan shows increased focal radiotracer uptakes in the bilateral anterior tibiae, right greater than left.

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■ FIGURE 38-9

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A, CT scan of the right lower leg in a 14-year-old boy shows curvilinear lucencies (arrowhead) and cortical thickening (arrow) secondary to callus formation in the posterior cortex of the right tibia. B, Sagittal multiplanar reformatted CT image demonstrates linear fracture lucency (arrowhead) and cortical thickening secondary to callus formation (arrow) in the posterior tibial cortex. C, Coronal multiplanar reformatted CT image reveals linear fracture lucency (arrow) in the posterior tibial cortex. D, T1-weighted coronal MR image shows decreased marrow signal intensity (arrow) and focal low signal intensity (arrowhead) in the right proximal tibia. E, T2-weighted coronal MR image reveals increased marrow signal intensity representing marrow edema (arrow) and focal low signal intensity reflecting fracture (arrowhead) in the right proximal tibia.

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■ FIGURE 38-10

A, Anteroposterior radiograph of the right lower leg in a 71-year-old woman shows a linear longitudinal sclerotic band (arrow) in the distal shaft of the right tibia. B, Lateral radiograph demonstrates a linear longitudinal sclerotic band (arrow) posteriorly. C, CT scan demonstrates a linear fracture lucency (arrow), endosteal callus (arrowhead), and periosteal callus (thin arrow) in the posterolateral tibia. D, Coronal multiplanar reformatted CT image reveals a linear sclerotic band (arrow), representing longitudinal stress fracture of the distal tibia. E, Sagittal multiplanar reformatted CT image demonstrates a linear sclerotic band (arrow), indicating a longitudinal stress fracture.

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989

■ FIGURE 38-11

A, T1-weighted axial MR image of the right lower leg in an 18-year-old female runner with right shin pain shows decreased marrow signal intensity (arrow) at the level of the mid diaphysis of the right tibia. B, T2-weighted axial MR image from the same patient reveals bright signal intensity caused by marrow edema (arrow) and high signal intensity of the periosteum (arrowhead), suggesting a shin splint.

Talus In the talus, stress fractures can occur in different regions: talar neck, medial tubercle and posterolateral tubercle (lateral tubercle of the posterior process), and lateral process.14 Stress fractures at the neck are the most frequent, and stress fractures of the lateral process are extremely rare. The fractures of the medial tubercle are related to repetitive movement of foot dorsiflexion, whereas fractures of the posterolateral tubercle can be seen in dancers. The latter should be differentiated from the os trigonum. Radiographs often fail to reveal the stress fracture, and CT is helpful in identifying the lesions. The stress fracture often extends into the subtalar joint, which explains the symptoms in the region of the tarsal sinus.3

Tarsal Navicular

■ FIGURE 38-12

Lateral radiograph of the right ankle obtained from an 18-year-old man shows a band of sclerosis (arrow) parallel to the posterior border of the right calcaneus between the tuberosity and posterior facet, which is a characteristic appearance for a calcaneal stress fracture.

Tarsal navicular stress fractures occur primarily in physically active sprinting and jumping athletes, such as runners, gymnasts, basketball players, and football players, typically linebackers.3 In addition, this injury has been seen in athletes who practice and play extensively on an artificial turf surface, including that used in football and women’s field hockey. The correct diagnosis of a tarsal navicular stress fracture is often delayed for several months, partly because the clinical onset is insidious with nonspecific signs and symptoms and also because these stress injuries are not evident on radiographs in most cases (Fig. 38-13). The interval between the onset of symptoms and the diagnosis may be from 7 weeks to 4 months but may be much longer in some patients. Stress fracture of the tarsal navicular must be considered as one of the causes of long-standing foot pain.

990

P A R T O N E ● Injury: Other Musculoskeletal Injuries

■ FIGURE 38-13 A, Anteroposterior radiograph of the right foot obtained from a 15-year-old female cross country runner shows a normal appearance of the right tarsal navicular (arrow). B, Coronal multiplanar reformatted CT image shows subtle lucencies in the tarsal navicular (arrow). C, T1-weighted sagittal MR image shows decreased bone marrow signal intensity (arrow) in the tarsal navicular. D, T2-weighted sagittal MR image demonstrates increased bone marrow signal intensity (arrow), representing marrow edema of the tarsal navicular.

(Continued)

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■ FIGURE 38-13—Cont’d E, T1weighted sagittal MR image shows decreased bone marrow signal intensity (arrow) in the tarsal navicular. F, T2-weighted coronal MR image demonstrates increased bone marrow signal intensity (arrow) of the tarsal navicular, representing early finding of stress reaction.

Most tarsal navicular stress fractures occur in the central one third of the tarsal navicular or at the junction of the central and lateral thirds of the bone (Fig. 38-14). These sites correspond to the zone of maximum shear stress on the tarsal navicular from the surrounding bones.3 Microvascular studies show that there is relative avascularity of the central one third of the tarsal navicular. These findings suggest that repetitive cyclic loading may result in fatigue fracture through the relatively avascular central portion of the tarsal navicular. The consistent site of the fracture seems to correspond with the plane of maximum shear stress especially during plantarflexion combined with pronation. Tarsal navicular stress fractures may be incomplete or complete. Incomplete fractures usually involve the dorsal 5 mm of the navicular adjacent to the talonavicular joint, an area that is difficult to evaluate on radiographs.23 There may be associated foot anomalies in patients with tarsal navicular stress fractures. These include a short first metatarsal, a relatively long second ray, metatarsal hyperostosis, or an associated stress fracture of the second through the fourth digits.23 A short first metatarsal or long second metatarsal may tend to accentuate shear stress because of the greater force being transmitted through the second metatarsal and intermediate cuneiform. Because radiographs are often not sensitive enough to detect the original fracture, it is clear that radiography is not a reliable indicator of fracture healing. Once a fracture is identified, CT should be used to assess fracture healing. The CT appearance of a healing fracture does not necessarily mirror clinical union. In general, the imaging evidence of tarsal navicular fracture healing lags behind the clinical features. Because most of the tarsal navicular fractures

are oriented in the sagittal plane, and are located in the central or lateral one third of the tarsal navicular, CT performed parallel and perpendicular to the midfoot clearly demonstrates the fracture. MRI detects the bone marrow edema associated with osseous stress reaction that may be present before a fracture line is visualized and MRI is a choice if there is suspicion of early injury. Coronal, sagittal, and axial MR imaging sequences are recommended, and at least one fat-suppressed sequence should be performed. With MRI of tarsal navicular stress fracture, the fracture line is best visualized on coronal images.

Stress Fractures in the Metatarsal and Sesamoid Bones The metatarsals are frequent sites of stress fracture, which may be caused by marching, ballet dancing, prolonged standing, foot deformities, and surgical resection of adjacent metatarsals. The middle and distal portions of the shafts of the second and third metatarsal bones are affected most often (Figs. 38-15 and 38-16), but any metatarsal bone may be involved, including the first. This fracture may be bilateral, and when the stress persists it can be recurrent. In patients with rheumatoid arthritis these fractures can be misdiagnosed as an inflammatory arthritis. Stress fractures of the lateral metatarsal bones accompany metatarsus adductus foot deformity. At the beginning of symptoms radiographs are usually normal, whereas after 3 to 4 weeks, periostitis, increased bone density, or fracture callus may be seen. Bone scintigraphy shows increased uptake at the site of the fracture. MRI has a role in identifying stress changes in the metatarsals, and early diagnosis can alter treatment and outcome.

992

P A R T O N E ● Injury: Other Musculoskeletal Injuries

■ FIGURE 38-14

A, Anteroposterior radiograph of the left foot obtained from a 20-year-old university football player shows no definite fracture line or sclerosis in the left tarsal navicular (arrow). B, T1-weighted axial MR image demonstrates diffuse low signal intensity (arrow) in the left tarsal navicular. C, T2-weighted axial MR image reveals markedly increased bone marrow signal intensity (arrow) in the left tarsal navicular. D, T1-weighted coronal MR image shows area of low signal intensity (arrow) in the left tarsal navicular. E, Corresponding CT image reveals definite incomplete linear fracture lucency (arrowhead) with bone sclerosis (arrow) in the central portion of the tarsal navicular. F, After the application of a non–weight-bearing short-leg cast, the pain did not improve and a percutaneous screw fixation was performed. CT scan shows a persistent fracture lucency (arrowhead) and placement of a cannulated screw set (arrow).

Stress fractures of the sesamoids of the big toe have been described after repetitive jumping and long walks, more often at the medial sesamoids. Radiography can be misdiagnosed for bipartite sesamoid. Bone scintigraphy and CT are more reliable in confirming the diagnosis.

Other Sites of Lower Extremity Stress fractures of the patella are either transverse or longitudinal, occur in both children and adults, and may become displaced. Patellar stress fractures are associated

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■ FIGURE 38-15

A, Anteroposterior radiograph of the right foot obtained from a 60-year-old woman shows transverse lucency in the distal shaft of the right second metatarsal (arrow). B, Follow-up anteroposterior radiograph obtained 4 months later reveals fusiform callus formation (arrow) at the fracture site.

with physical activities that include hurdling, running, walking, soccer, playing basketball, weight lifting, and fencing. Cuboid, cuneiform, and os peroneum can also be affected. Stress fractures of these tarsal bones are difficult to see by radiography and require more sensitive diagnostic tests.

Sacrum Although stress fractures of the sacrum are a common cause of lower back and buttock pain, they are commonly unrecognized. Sacral fatigue fractures in younger patients are unusual but may be encountered as the result of serious athletic training for long distance running. Pelvic and low back pain in children can be difficult to evaluate clinically. Unfortunately, when the patient does not present with a classic history, an alternative diagnosis such as a muscle strain, infection, or malignancy is often considered before a stress fracture. The pain is typically of insidious onset, which initially is relieved by rest and made worse with physical activity. Sacral stress fracture should be considered a potential cause of buttock and low back pain in children, even in those not involved in athletic training. Sacral insufficiency fractures typically occur in postmenopausal, osteoporotic women or in patients taking long-term corticosteroid treatment, those with rheumatoid

arthritis or those who have undergone radiation therapy. Radiographs often appear normal in these cases. Irregularity of the contour or an actual break in the sacral arcuate lines and/or patchy sclerosis (Fig. 38-17) in an H-shaped configuration may be seen. This type of fracture is better demonstrated by bone scintigraphy, which reveals the characteristic “H” or “Honda” sign24 that appears as a result of intense radiopharmaceutical uptake, or by CT scan. MRI may be used to make the correct diagnosis of a sacral stress fracture. T1- and T2-weighted MR images often demonstrate an area of linear signal void usually in a vertical orientation (Fig. 38-18). Surrounding this is usually diffuse low marrow signal intensity on T1-weighted images and increased signal intensity on T2-weighted images. CT may be of help in these situations. Linear vertical or oblique medullary sclerosis is usually seen at this site on CT scan. Sacral insufficiency fractures also may occur in conjunction with insufficiency fractures at other sites. Occasionally, the bone scintigraphy will appear normal early in the course of a stress injury.

Pelvis The pelvis can present fractures in the pubic ramus, the parasymphyseal, and the supra-acetabular regions and, infrequently, the acetabulum (Fig. 38-19).25 All of these fractures may present as isolated25 or associated. These

994

P A R T O N E ● Injury: Other Musculoskeletal Injuries

■ FIGURE 38-16

A, Anteroposterior radiograph of the left foot obtained from a 23-year-old man with foot pain shows no obvious osseous abnormality. B, T1-weighted coronal MR image taken 2 weeks later shows decreased bone marrow signal intensity (arrowhead) and hypointense periosteal thickening (arrow) of the left second metatarsal shaft. C, T2-weighted coronal MR image demonstrates marked periosteal callus formation (arrow) and surrounding soft tissue edema (arrowhead). D, T1-weighted sagittal MR image of the left second metatarsal shows decreased marrow signal intensity (arrow). E, Corresponding sagittal T2-weighted image reveals linear low signal intensity band (arrow) representing fracture line. Also note abundant periosteal callus formation (arrowheads).

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● Stress Injury

■ FIGURE 38-17

A, Anteroposterior radiograph of the pelvis of a 78-year-old woman shows vertically oriented sclerosis in the left sacral ala, representing sacral insufficiency fracture (arrow). Also note widely displaced fracture with exuberant callus formation in the left superior pubic ramus (arrowhead). B, Follow-up anteroposterior pelvic radiograph obtained 6 months later shows markedly increased sclerosis of the left sacral insufficiency fracture (arrow) and progression of bone healing in the left superior pubic ramus (arrowhead).

■ FIGURE 38-18

A, T1-weighted axial MR image of a 70-year-old woman with right sacral pain shows area of decreased signal intensity (arrow) of the right sacral ala. B, Corresponding T2-weighted axial MR image obtained from the same level as in A reveals bright signal intensity (arrow) in the right sacral ala. C, T1-weighted oblique coronal MR image shows a vertically oriented band-like area of low signal intensity (arrow) representing insufficiency fracture of the right sacrum. D, Corresponding T2-weighted oblique coronal MR image shows a hyperintense vertical band (arrow) suggesting insufficiency fracture of the right sacrum.

995

996

P A R T O N E ● Injury: Other Musculoskeletal Injuries

■ FIGURE 38-19 A, Anteroposterior radiograph of the left hip from a 90-year-old man shows no osseous abnormality. B, 99mTc-MDP scintiscan shows markedly increased uptake in the region of the left acetabulum. C, T1-weighted coronal MR image shows decreased signal intensity in the left supra-acetabular region. D, T2-weighted coronal MR image obtained at the same level as in C reveals increased signal intensity in the left acetabular and supra-acetabular region. In addition, there is a curvilinear linear low signal intensity, parallel to the left acetabular roof (arrowheads), reflecting insufficiency fracture line with surrounding edema. (From Berst MJ, El-Khoury GY. Acetabular insufficiency fracture. Emerg Radiol 2000; 7:98–102.)

stress fractures may be seen in patients with osteoporosis, osteomalacia, rheumatoid arthritis, and after radiotherapy or hip arthroplasty.14 Stress fracture that involves the pubic rami may have a particularly aggressive appearance that is due to patchy areas of sclerosis, osteolysis, and fragmentation, simulating a bone tumor. The anterior arch of the pelvis is significantly weaker than the posterior arch, so fractures of the pubic rami and symphysis are not uncommon and may be extremely difficult to identify on anteroposterior

pelvic radiographs. These fractures tend not to be widely displaced. They may be impacted and thus seen only as a subtle, minor irregularity of the cortical margin or a region of sclerosis. If widely displaced, a thorough search for a second fracture is mandatory and must include evaluation of the sacroiliac joints and symphysis pubis. Parasymphyseal stress fracture may occasionally show delayed healing with osteolysis at the pubis, making it difficult to differentiate from neoplastic or infectious processes. Stress fractures of the base of the pubis may also

CHAPTER

involve the acetabulum. Supra-acetabular stress fractures show bone sclerosis over the acetabulum parallel to the acetabular roof. If the acetabulum is involved along with other fractures in the sacrum or pubis, there are usually enough clues to help in making the diagnosis. However, when the fracture is limited to the acetabulum, making the correct diagnosis can be challenging. And, diagnosing acetabular insufficiency fractures with radiographs is difficult because the fracture may not be visible. Osteopenia may be the only radiographic finding. When visible, the insufficiency fractures are seen as a break in the acetabular cortex or as asymmetric linear arc of sclerosis parallel to the acetabular roof on the affected side (see Fig. 38-19).25 MRI has high sensitivity in detecting acetabular insufficiency fractures. Visualization of a linear lesion of low signal intensity on T1- and/or T2-weighted images is characteristic of insufficiency fractures. Acetabular insufficiency fractures are well demonstrated on coronal or sagittal MR images. MRI also has the ability to detect early medullary bone edema, which may be the first sign in insufficiency fractures. Diagnosis of acetabular insufficiency fracture must be considered in the differential diagnosis of osteoporotic, elderly patients with complaints of abrupt groin or hip pain on weight bearing and whose initial radiographs do not reveal any fractures.

Pars Interarticularis Stress Fracture (Spondylolysis) Spondylolysis is also considered a fatigue fracture of the pars interarticularis and common in athletes who

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participate in sports activities demanding repetitive movement of the lumbar spine.14 The most common level of involvement is L5, followed by L4.14 On radiographs, spondylolysis appears as a linear lucency in the pars interarticularis (Fig. 38-20). Spondylolysis on CT of the lumbar spine is seen as a linear lucency or defect extending through the pars interarticularis (Fig. 38-21). In some patients, fragmentation of the pars interarticularis may be seen.

Upper Extremity Although upper extremity stress fractures are far less common than lower extremity stress fractures, they also have been described and are not uncommon in certain types of sports activities. Stress fractures of the upper extremity may occur in sports involving repetitive use of the arms, such as baseball, tennis, weight lifting, javelin, and racket sports. It is important to recognize stress fractures of the upper extremity because of the difficulties in their diagnosis, especially those of the clavicle and sternum. Radiography in patients with stress fracture of the clavicle is usually normal at the beginning of symptoms. Later, a pseudotumor appears in the medial third of the clavicle that corresponds to the fracture callus and can be misdiagnosed as a tumor or infection. Other fractures of the upper extremity are related to specific activities, such as ulnar fractures associated with certain sports including tennis, baseball, volleyball, and weight lifting, and with individuals in wheel chairs; fractures of the olecranon are related to baseball and javelin-throwing.

■ FIGURE 38-20

A, Flexion lateral radiograph in a 34-year-old woman demonstrates a linear lucency (arrow) through the pars interarticularis of L4. Note also the anterior translation of L4 on L5. B, Extension lateral radiograph from the same patient also shows a linear lucency (arrow) through the pars interarticularis of L4. Note backward reduction of L4 on L5, which is suggestive of a segmental instability.

998

P A R T O N E ● Injury: Other Musculoskeletal Injuries

■ FIGURE 38-21

A, CT scan of lumbar spine in a 13-year-old boy demonstrates an incomplete lucency (arrowhead) through the left pars interarticularis of L5. Radiographs of the lumbosacral spine were negative. B, Follow-up CT image, obtained 2 months later, reveals less conspicuous lucency (arrowhead) than that on previous image, representing healing process.

Stress Injuries of the Physis Stress-induced sports-related physeal injuries are not uncommon. The weakest portion of the growing skeleton is the physeal region. Widening and irregularity of the physis without accompanying displacement of the epiphysis have been recognized as stress-induced changes in adolescent athletes. This lesion is common in the distal radius and ulna of gymnasts, and similar changes have been reported to involve the physes of distal femur, proximal tibia, and distal fibula in adolescent runners and the lateral margin of the physis of the proximal humerus in baseball pitchers. Proximal humeral epiphyseal overuse syndrome, or Little Leaguer’s shoulder, is a clinical entity in a youth or adolescent baseball player with throwing-related pain localized to the proximal humerus. Although most commonly described in youth and adolescent baseball players, similar proximal humeral injuries have been described in other overhand athletes including a cricket bowler, a volleyball player, and a badminton player. Little Leaguer’s shoulder might most likely be a fracture similar to the classic SalterHarris type I fracture, where the epiphysis separates completely from the metaphysis. The classic radiographic finding in Little Leaguer’s shoulder is widening of the physis of the proximal humerus (Fig. 38-22). The lateral portion of the physis appears to be more commonly involved than the medial aspect, most likely because of the thicker periosteum posteromedially over the proximal humerus. Associated radiographic findings include demineralization, cystic changes, sclerosis of the proximal humeral metaphysis, and fragmentation of the lateral aspect of the proximal humeral metaphysis. In subtle cases, radiographs of the contralateral shoulder have been advised. Radiographic

remodeling of the widened proximal humeral physis can take several months and a decision on when to return to throwing is based on clinical rather than radiologic grounds because many of the patients can become asymptomatic even though radiographs demonstrate continued widening of the proximal humeral physis.

DIFFERENTIAL DIAGNOSIS The differential diagnosis of stress fractures includes acute fracture, osteoid osteoma, chronic sclerosing osteomyelitis, Langerhans cell histiocytosis, osteomalacia, metastasis, osteogenic sarcoma, and Ewing’s tumor. Usually a careful clinical history and sequential radiographs help differentiate a stress fracture from a more aggressive lesion. A stress fracture, especially the fatigue fracture, is differentiated from an acute fracture by the absence of a history of specific injury. Usually, the onset of symptoms is gradual and void of any constitutional change. After the precipitating activity, a nagging discomfort that is localized to the area of affected bone is noted. The pattern of the discomfort coincides with the underlying activity and progressively increases to pain that may be constant. If the activity is continued, the incomplete fatigue fracture can progress to a complete fracture. Rest typically relieves the discomfort or pain. Patients with osteoid osteoma often have pain that is worse at night and relieved by aspirin or other analgesics. This is in contradiction to stress fractures, which are characteristically made worse by activity and relieved by rest. On radiographs, the typical osteoid osteoma has a dense sclerotic area surrounding a lucent nidus. Both osteoid osteomas and stress fractures may be eccentric, with stress fractures occasionally involving both sides of the shaft of

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■ FIGURE 38-22

A, Anteroposterior radiograph of the left shoulder obtained from a 9-year-old gymnast shows lateral widening of the left proximal humeral physis (arrow). B, Anteroposterior radiograph of the right shoulder from the same patient shows lateral widening of the right proximal humeral physis (arrow).

the affected bone. As a rule, however, stress fractures affect only one of the cortical surfaces. Periosteal reaction is often absent in osteoid osteoma and is quite common in a stress fracture. The sclerosis associated with an osteoid osteoma is much greater than the reactive change seen in a stress fracture. CT is very helpful in differentiating between stress fracture and osteoid osteoma, because both entities may be hot on bone scintigraphy, show edema on MRI, and demonstrate sclerosis on radiographs. CT, however, detects the radiolucent nidus of osteoid osteoma. CT is useful in demonstrating the fracture lines and for characterizing the nature of a periosteal reaction or cortical destruction. Chronic sclerosing osteomyelitis of Garré has a dense sclerotic appearance and often no associated lucency on radiographs. The lesion usually involves the entire circumference of the bone and is much more widespread than a stress fracture. The thinner linear sclerotic appearance of a stress fracture should be characteristic enough to distinguish the two lesions. Serial radiographs generally show little or no change within a short time in sclerosing osteomyelitis. A typical stress fracture, however, has a rapidly evolving course over several weeks. Looser’s zone or osteoid seams are insufficiency types of stress fractures often seen in patients with osteomalacia.

They are more common in adults than in children. Patients with Looser’s zones may have the characteristic findings of osteomalacia or renal osteodystrophy such as decreased mineralization, coarsened texture of the bones, ruggerjersey appearance of the spine, and, occasionally, bowed long bones. Insufficiency fractures of the sacrum and pelvis may be confused with metastatic lesions, especially if bony resorption occurs at the fracture ends. Quite often, these injuries occur in patients with known malignant disease who have a sudden onset of pain in the lower back, hip, or groin. Insufficiency fractures of the sacrum can occur with normal activities such as walking. MRI can depict abnormalities in the bone marrow and is suited to distinguish stress fractures from pathologic fractures. In stress fractures, T2 signal intensity changes suggest edema; in pathologic fractures, T2 signal intensity changes may represent a mixture of tumor and edema. The assessment of T1 signal intensity changes is fundamental to the detection of a pathologic fracture. In long bones, the most sensitive discriminating feature between stress and pathologic fractures is that of a well-defined low signal T1-weighted abnormality around a fracture indicating an underlying tumor. The signal intensity changes on T2-weighted MR images are usually nonspecific.

1000 P A R T O N E

● Injury: Other Musculoskeletal Injuries

Some of the clinical and radiologic features of stress fractures may mimic surface malignant bone tumor. Stress fracture can be seen in patients who suddenly adopt a strenuous physical program. Radiologically, stress fracture presents as a thin lucent fracture line with periosteal reaction and cortical thickening. Osteogenic sarcoma and occasionally Ewing’s tumor are often included in the differential diagnosis of stress fractures, particularly in children or adolescents. The appearance of these neoplasms is usually sufficiently characteristic, but they should not be confused with a stress fracture. Osteosarcomas are generally located within the metaphysis of the involved bone. In osteosarcoma, the lesion has a more aggressive appearance with bone destruction and aggressive periosteal reaction. The osteolytic pattern is generally of the moth-eaten variety, and osteosarcomas do not change in a short time. If a stress fracture is suspected, but imaging studies do not show an abnormality, radiographs should be obtained again in 1 to 2 weeks. CT may be necessary to establish the diagnosis of a stress fracture. Once the patient ceases the activity that produces the injury, evidence of healing within 1 to 2 weeks is sufficient to establish the proper diagnosis. In most instances, a delay of that short a time will not be detrimental. Biopsy samples should be avoided until radiographs clearly show that no healing has occurred, suggesting that a lesion other than stress fracture may be present.

SYNOPSIS OF TREATMENT OPTIONS Medical Therapy Early diagnosis and specific treatment are crucial for optimal outcomes. The fundamental principle in the initial management of a stress fracture is modified rest to allow the bone remodeling process to equilibrate. Conservative therapy for stress fractures involves the use of ice, nonsteroidal anti-inflammatory drugs, and rest of the affected bone for several weeks or until the patient is free from pain. Additionally, pre-exercise warm-up, stretching, and a gradual return to the offending exercise intensity are indicated. In the symptomatic athletes, an early stress injury may be treated with a short period of rest, in contrast to the several months required for healing of an overt stress fracture. For the fatigue fractures, treatment depends primarily on the location of the fatigue fracture and establishment of the responsible activity. Certainly, the responsible activity should be discontinued and the affected part rested until the symptoms clear and healing has occurred. Not bearing weight on the affected area may be all of the treatment that is necessary; however, if complete fracture threatens, or if the patient is irresponsible, plaster cast immobilization is recommended. In adolescent athletes with stress fracture, treatment should generally be conservative, including interruption of sports activity and reduction in weight bearing. In regard to frequently observed persistence of symptoms in cases of early return to sports activity, it is recommended to wait a period of at least 2 weeks after symptoms have disappeared.

For the insufficiency fractures, treatment may be directed toward the underlying disease to stabilize or improve the elastic resistance of bone. When the infraction remains static, local treatment is unnecessary, as exemplified by the infractions occurring in Paget’s disease of bone. Not bearing weight on the affected area may be sufficient therapy; however, if there is progression of the infraction to a complete fracture, other appropriate measures should be taken.22 For the talus stress fractures, a 6-week trial of non– weight-bearing cast immobilization is recommended, followed by rehabilitation and use of an orthosis.3 Tarsal navicular or metatarsal fractures may require short-leg casting for 6 to 8 weeks unless they are displaced. Modified rest and training technique corrections or alterations usually result in early healing and return to activity in patients with upper extremity stress fractures.

Surgical Therapy Although nonoperative management is the standard treatment for the stress fractures, surgical intervention may be necessary (see Fig. 38-14). Different stress fracture sites mandate certain specific management approaches. For the femoral neck, nondisplaced complete fractures are stabilized with multiple screws. In young people with displaced fractures, emergent open reduction with internal fixation is mandatory. In older patients, consideration can be given to hip arthroplasty depending on the individual situation. In cases of displaced tarsal navicular fractures, compression screw fixation is undertaken.3 For tarsal navicular or metatarsal fractures in elite athletes, it is common to perform intramedullary nailing if a joint is not involved. When olecranon fracture is displaced or shows delayed union, tension band fixation is usually effective.

What the Referring Physician Needs to Know ■ ■

■ ■

■

■

A careful history is important in establishing the clinical diagnosis of stress injury. An accurate and thorough clinical history and sequential radiographs often suffice to make the diagnosis especially when the fractures occurs in one of the common locations, such as the tibia, metatarsals, or calcaneus. The diagnosis of a fatigue fracture should be considered in patients with pain after a change in their activity. Clinically, the diagnosis of stress injuries may be difficult because they may mimic other musculoskeletal complaints such as tendon or muscle injuries; therefore, imaging of these injuries is essential for arriving at a prompt diagnosis. The imaging evaluation of a patient in whom a stress reaction or stress fracture is clinically suspected should begin with radiographs of the area in question. The lack of awareness and the subtle findings on radiographs are probably the most important causes for missing the diagnosis.

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SUGGESTED READINGS Anderson MW, Greenspan A. Stress fractures. Radiology 1996; 199:1–12. Brittenden J, Robinson P. Imaging of pelvic injuries in athletes. Br J Radiol 2005; 78:457–468. Daffner RH, Pavlov H. Stress fractures: current concepts. AJR Am J Roentgenol 1992; 159:245–252. Deutsch AL, Coel MN, Mink JH. Imaging of stress injuries to bone: radiography, scintigraphy, and MR imaging. Clin Sports Med 1997; 16:275–290. Kiuru MJ, Pihlajamaki HK, Ahovuo JA. Bone stress injuries. Acta Radiol 2004; 45:317–326.

Lassus J, Tulikoura I, Konttinen YT, et al. Bone stress injuries of the lower extremity: a review. Acta Orthop Scand 2002; 73:359–368. Peris P. Stress fractures. Best Pract Res Clin Rheumatol 2003; 17:1043–1061. Sanderlin BW, Raspa RF. Common stress fractures. Am Fam Physician 2003; 68:1527–1532. Sofka CM. Imaging of stress fractures. Clin Sports Med 2006; 25:53–62. Spitz DJ, Newberg AH. Imaging of stress fractures in the athlete. Radiol Clin North Am 2002; 40:313–331.

REFERENCES 1. Anderson MW, Greenspan A. Stress fractures. Radiology 1996; 199:1–12. 2. Jones BH, Harris JM, Vinh TN, Rubin C. Exercise-induced stress fractures and stress reactions of bone: epidemiology, etiology, and classification. Exerc Sport Sci Rev 1989; 17:379–422. 3. Boden BP, Osbahr DC. High-risk stress fractures: evaluation and treatment. J Am Acad Orthop Surg 2000; 8:344–353. 4. Bennell KL, Brukner PD. Epidemiology and site specificity of stress fractures. Clin Sports Med 1997; 16:179–196. 5. Eisele SA, Sammarco GJ. Fatigue fractures of the foot and ankle in the athlete. J Bone Joint Surg Am 1993; 75:290–298. 6. Korpelainen R, Orava S, Karpakka J, et al. Risk factors for recurrent stress fractures in athletes. Am J Sports Med 2001; 29:304–310. 7. Daffner RH, Pavlov H. Stress fractures: current concepts. AJR Am J Roentgenol 1992; 159:245–252. 8. Weishaupt D, Schweitzer ME. MR imaging of the foot and ankle: patterns of bone marrow signal abnormalities. Eur Radiol 2002; 12:416–426. 9. Resnick D, Goergen TG. Physical injury: concept and terminology. In Resnick D (ed). Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, 2002, pp 2649–2671. 10. Daffner RH, Martinez S, Gehweiler JA Jr, Harrelson JM. Stress fractures of the proximal tibia in runners. Radiology 1982; 142:63–65. 11. Kathol MH, El-Khoury GY, Moore TE, Marsh JL. Calcaneal insufficiency avulsion fractures in patients with diabetes mellitus. Radiology 1991; 180:725–729. 12. El-Khoury GY, Kathol MH. Neuropathic fractures in patients with diabetes mellitus. Radiology 1980; 134:313–316.

13. Ikemura S, Yamamoto T, Nakashima Y, et al. Bilateral subchondral insufficiency fracture of the femoral head after renal transplantation: a case report. Arthritis Rheum 2005; 52:1293–1296. 14. Peris P. Stress fractures. Best Pract Res Clin Rheumatol 2003; 17:1043–1061. 15. Soames RW. Skeletal system. In Williams PL (ed). Gray’s Anatomy, 38th ed. New York, Churchill Livingstone, 1995, pp 464–468. 16. Maitra RS, Johnson DL. Stress fractures: clinical history and physical examination. Clin Sports Med 1997; 16:259–274. 17. Jones HH, Priest JD, Hayes WC, et al. Humeral hypertrophy in response to exercise. J Bone Joint Surg Am 1977; 59:204–208. 18. Umans HR, Kaye JJ. Longitudinal stress fractures of the tibia: diagnosis by magnetic resonance imaging. Skeletal Radiol 1996; 25:319–324. 19. Lee JK, Yao L. Stress fractures: MR imaging. Radiology 1988; 169:217–220. 20. El-Khoury GY, Bennett DL, Ondr GJ. Multidetector-row computed tomography. J Am Acad Orthop Surg 2004; 12:1–5. 21. Geslien GE, Thrall JH, Espinosa JL, Older RA. Early detection of stress fractures using 99mTc-polyphosphate. Radiology 1976; 121(3 pt 1):683–687. 22. El-Khoury GY, Wehbe MA, Bonfiglio M, Chow KC. Stress fractures of the femoral neck: a scintigraphic sign for early diagnosis. Skeletal Radiol 1981; 6:271–273. 23. Pavlov H, Torg JS, Freiberger RH. Tarsal navicular stress fractures: radiographic evaluation. Radiology 1983; 148:641–645. 24. Schneider R, Yacovone J, Ghelman B. Unsuspected sacral fractures: detection by radionuclide bone scanning. AJR Am J Roentgenol 1985; 144:337–341. 25. Berst MJ, El-Khoury GY. Acetabular insufficiency fractures. Emerg Radiol 2000; 7:98–102.

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Radiation Effects in the Musculoskeletal System Tamara Miner Haygood and William A. Murphy, Jr.

HISTORY AND RADIATION SOURCES Radium found its way into human bodies in varied ways during the first 3 decades of the 20th century. Watchmakers licked radioactive paintbrushes while painting radium onto dials. Patients took radium for numerous medical indications. Manufacturers used radium in food, drink, and toothpaste because of its amusing glow-in-the dark properties. Both medical and recreational use of radium fell by the wayside as its deleterious effects, including bone damage and tumor induction, became apparent. Thorotrast, another historically important source of radiation exposure, caused lesser amounts of bone damage. It was used as a radiographic contrast agent between 1928 and the early 1950s. Now, in the early years of the 21st century, by far the most common source of radiation exposure seen in medical practice is therapeutic radiation, which is almost exclusively used for malignant tumors. All subsequent discussion of radiation effects will assume this source, but many of the effects of radiation are the same independent of the source.

Osteochondroma is the most common benign bone tumor arising with radiation exposure. It occurs only in patients irradiated in childhood and is both radiographically and histologically identical to osteochondromas occurring spontaneously. Patients receiving total-body irradiation may develop several osteochondromas.1 Other benign tumors occur rarely as a result of radiation. Radiation-induced sarcomas occur in both bone and soft tissue. W. G. Cahan and colleagues in 1948 published a series of cases of radiation-induced sarcoma and suggested criteria for distinguishing radiation-induced sarcomas from their spontaneously occurring counterparts. These criteria included a benign primary disease; a history of therapeutic radiation with the sarcoma arising within the radiated field; a long asymptomatic latent period, with 5 years being used for their cases; and histologic proof of the sarcoma.2 These criteria were later altered by other writers to allow for the prior existence of a primary malignancy that histologically differed significantly from the subsequent sarcoma.3 Some writers

ANATOMY Any site that has been irradiated may exhibit either the beneficial effects or the deleterious side effects of radiation therapy. Some of the most commonly affected areas are: ● ● ● ●

Jaw: radiation osteonecrosis Spine: fatty marrow replacement Pelvis: insufficiency fracture Femoral heads: radiation osteonecrosis

PATHOLOGY Radiation osteonecrosis, also called radiation osteitis, develops in irradiated bone as a result of destruction of osteoblasts, damage to blood vessels, and ensuing ischemia. 1002

KEY POINTS Common types of radiation-induced change include osteoradionecrosis in the mandible and insufficiency fracture in the pelvis. ■ Radiation in childhood may produce growth retardation and formation of osteochondromas. ■ Radiation-induced neoplasms may be either benign or malignant and are histologically and radiologically indistinguishable from spontaneously occurring neoplasms. ■ Diagnostic criteria for radiation-induced malignancies include location within a radiation field and at least a 4-year time interval between radiation therapy and the development of the new tumor. ■

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have suggested 4 years as a minimal latency,4 and Kohn and Fry, in a literature review published in 1984, found a median latency period of 10 to 12 years.5 Various histologic types of sarcoma occur after radiation therapy, with different series of studied cases producing different occurrence rates. Osteosarcoma and malignant fibrous histiocytoma are the two most common varieties. Kim and colleagues, in 1978, found spindle cell sarcoma to be the most common radiation-induced soft tissue sarcoma, with osteosarcoma the most common in bone.4 Sarcoma induction may also be linked to chemotherapy with cyclophosphamide and other alkylating agents. The likelihood of tumor induction increases with radiation dose up to 60 Gy.6 Pathology of radiation-induced neoplasms is identical to that of spontaneously occurring neoplasms.

MANIFESTATIONS OF THE DISEASE Beneficial Effects Radiation may be used either for cure or for palliation and is used in the treatment both of primary musculoskeletal lesions such as soft tissue sarcomas and of primary tumors arising in other organ systems such as breast cancer and lung cancer. In systemic disease such as lymphoma, disseminated metastatic tumor, or multiple myeloma, radiation therapy may be used palliatively against especially troublesome sites of disease. Desired goals may include shrinkage of the tumor, elimination of micrometastases, and, in the case of skeletal lesions, reconstitution of functional bone. When radiation successfully addresses a bone tumor, there may be radiographically evident healing (Fig. 39-1).

■ FIGURE 39-1 A 50-year-old woman presented with breast cancer. A, Anteroposterior radiograph of left femur in March 1999 shows a lytic metastasis in the diaphysis. B, Ten months later, after radiation therapy, the lytic lesion is smaller and is remineralizing.

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Chemotherapy is often used in conjunction with radiation, and both may contribute to the healing effect.

Side Effects in Soft Tissue Radiography With time, dystrophic calcifications may form in soft tissues. As radiation therapy techniques have changed over the decades, these dystrophic calcifications are becoming less common, but they are still encountered in clinical practice, particularly in patients who completed radiation therapy in the 1980s or earlier (Fig. 39-2).

Magnetic Resonance Imaging Soft tissue changes compatible with edema occur in skeletal muscles and in adjacent fat subjected to therapeutic doses of radiation. Edema manifests as increased signal intensity on T2-weighted MR images in the irradiated muscle. Bright-signal strands appear in the fat on T2-weighted or inversion recovery images, whereas dark strands are

■ FIGURE 39-2 Anteroposterior radiograph of the right hip in a 54-year-old woman who had received lower extremity radiation therapy in 1988 for melanoma. Florid, widespread dystrophic soft tissue calcification attests to previous radiation therapy. Lateral air collection at the level of the hip joint indicates a decubitus sore. Oval lucencies in the cortex of the remaining portion of the femur represent radiation osteitis. The amputation was due to insufficiency fracture. (Case courtesy of John Madewell, MD.)

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■ FIGURE 39-3 A 28-year-old man presented with myxoid liposarcoma of the medial left thigh. After induction chemotherapy, he was irradiated to a dose of 50 Gy in 25 fractions. Coronal T2-weighted (TR/TE 5067/84) fast spin-echo (A) axial gadolinium-enhanced T1-weighted (TR/TE 450/9) fast spin-echo (B) and axial T2-weighted (TR/TE 4500/82) fast spin-echo (C) MR images obtained 5 months after completion of radiation therapy and 3 months after surgical resection of the mass. Both at the cephalad margin (on the coronal image) and at the lateral margin (on the axial images) of the radiation field there is a nonanatomic interface between normal tissue and tissue with increased T2 signal and contrast enhancement, typical of radiation therapy. Note, for example, abnormal signal in the medial third of the thigh (vastus medialis muscle) (arrow at demarcation line) but not in the lateral two thirds (vastus intermedius and lateralis muscles).

evident in fat on T1-weighted images (Fig. 39-3). The changes occur by 6 weeks after conclusion of radiation therapy and may persist for over a year. They have been reported to conform to the geometric shape of the radia-

tion field.7 In our experience, geometric cutoff between normal and irradiated soft tissue in patients irradiated for extremity soft tissue sarcomas is commonly but not always visible on MRI. Muscle atrophy also occurs.

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1005

Non-neoplastic Side Effects in Bone Radiography Irradiation of growing bone causes a decrease in growth, which may result in evenly distributed growth retardation or may cause bowing deformity or scoliosis, particularly if one side is affected more than the other (Fig. 39-4). Metaphyseal growth abnormalities have been reported in children who received as little as 10 Gy of total-body irradiation before bone marrow transplantation for leukemia.1 Bone affected by radiation osteonecrosis becomes demineralized, and the osteopenia is detectable on conventional radiographs. With time, new bone is laid down on extant trabeculae, resulting in sclerosis that is often patchy in distribution (Fig. 39-5). Cortices of long bones will often develop fusiform lucencies, usually (in our experience) oriented parallel to the long axis of the bone. The foci of intracortical resorption usually increase gradually in size and number for months to years before becoming

■ FIGURE 39-5 Anteroposterior view of the pelvis of an 83-year-old woman irradiated 18 years previously for endometrial cancer, including a pathologically proven metastasis to the right ischium. Note the healed, expansile right ischial metastasis that was stable at least for the previous 4 years. There is generalized osteopenia, which may relate both to age and to radiation therapy. Note also patchy sclerosis in the sacrum (arrows) and lower lumbar vertebrae consistent with radiation osteonecrosis.

stable. The linear lucencies lack associated periosteal new bone formation or a soft tissue mass (see Fig 39-2).8 Any irradiated bone is weakened and subject to insufficiency fracture (Fig. 39-6). A common site of such

■ FIGURE 39-4 Lateral view of the thoracolumbar spine in a 33-yearold woman treated by abdominal radiation therapy for a neuroblastoma diagnosed at 3 months of age. Compare the normal size and shape of the two upper included thoracic vertebrae with the lower thoracic vertebrae. Instead of becoming gradually larger, the lower vertebrae are shorter and dysplastic, with irregular, wavy end plates.

■ FIGURE 39-6 Same patient as in Figure 39-1, nearly 2 years later, now 52 years old. Anteroposterior radiograph of left femur shows an incomplete transverse fracture (arrow) across the lateral cortex of the femoral diaphysis in the same location where she had previously been successfully irradiated for a breast cancer metastasis.

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Radiation-Induced Neoplasms OSTEOCHONDROMA ■ Benign ■ Exclusively with childhood irradiation ■ Histologically identical to spontaneous osteochondroma SARCOMA ■ Malignant ■ Latent period of 4 years or more ■ Histologically identical to spontaneous sarcoma ■ Commonly malignant fibrous histiocytoma or osteosarcoma ■ Occurs in either bone or soft tissue ■ FIGURE 39-7 A 66-year-old woman was treated 4 years previously with external-beam radiation therapy to 55 Gy for a squamous cell cancer of the anus. Anteroposterior view of pelvis shows severe destructive changes at both femoral heads from radiation-associated avascular necrosis but resembling neuropathic joints.

TUMORS IN OTHER ORGAN SYSTEMS ■ Squamous cell cancer of the skin ■ Breast cancer ■ Leukemia, with shorter latent period than sarcoma

fractures is the pelvic ring, particularly in women who have undergone radiation for gynecologic malignancies. Blomlie and associates found that 89% of women irradiated for cervical cancer developed fracture of the sacrum and/or the ilium between 3 and 24 months after conclusion of radiation therapy.9 These fractures may be subtle by conventional radiography. Rapidly progressive fragmentation of the irradiated femoral head may resemble a neuropathic arthropathy (Fig. 39-7). Children who have undergone radiation therapy may develop slipped capital femoral epiphysis or rarely the equivalent injury at the humeral head.

Magnetic Resonance Imaging

■ FIGURE 39-8 A 51-year-old man was treated with both anterior and posterior radiation therapy for a renal cell cancer metastasis at L4. Fourteen months later the bone marrow in L3, L5, and the sacrum has been almost completely replaced by fat, producing homogeneous high signal intensity on this T1-weighted (TR/TE 416/11.6) fast spin-echo sagittal MR image. Local control of the metastasis has not been achieved. L4 marrow has been replaced by a low-signal tumor, and the tumor bulges posteriorly from the vertebral body into the epidural space. The L1 and L2 marrow contains normal hematopoietic tissue.

Loss of myeloid marrow elements with fatty replacement evident on MRI is the mildest manifestation of the pathologic changes that, if unchecked, will culminate in radiation osteonecrosis. Increased marrow fat content may be visible as early as 2 weeks after the beginning of radiation therapy, and conversion to fatty marrow may be complete by 3 to 7 weeks after beginning of therapy (Fig. 39-8).10 Development of radiation osteonecrosis is related to dose, with a threshold at about 30 Gy for changes visible on conventional radiography. Children’s bones are more sensitive to radiation and exhibit damage at lower levels of exposure. On MRI the fusiform lucencies in the cortex of irradiated bone manifest as intracortical foci of variably increased signal in the background signal void of cortex (Fig. 39-9). MRI is more sensitive than conventional radiography to minimally displaced fractures through mainly cancellous bone. A radiation-induced insufficiency fracture will have the same appearance (edema and a fracture line) as fractures elsewhere but may coexist with a background of excessively fatty marrow or other signs of radiation osteonecrosis.

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Computed Tomography Computed tomography will demonstrate the same manifestations of radiation change that are evident on conventional radiographs. In addition, it may show to advantage subtle cortical offsets that will reveal a radiographically occult insufficiency fracture.

Tumor Induction Radiography The radiographic appearance of radiation-induced neoplasms is identical to that of their spontaneously occurring counterparts (Fig. 39-10). They may arise in areas of preexisting radiation osteonecrosis (Fig. 39-11).

Magnetic Resonance Imaging Radiation-induced sarcoma of bone often occurs in areas of radiation osteonecrosis and may also occur in bone that previously hosted a different tumor (see Fig. 39-11). Because radiation treatment of benign bone conditions is now rare and usually confined to bone in sites poorly accessible to surgical intervention, the latter situation is becoming more unusual. Both situations, however, complicate diagnosis of the new tumor because it must be differentiated from preexisting conditions and from insufficiency fracture. Cross-sectional imaging can be helpful in this regard. A sarcoma will often produce an

■ FIGURE 39-9

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Benign Side-Effects in Bone GROWTH IMPAIRMENT ■ Symmetric atrophy, bending deformity, or scoliosis OSTEONECROSIS ■ Conversion of myeloid to fatty marrow on MRI ■ Osteopenia SECONDARY TRABECULAR COARSENING AND SCLEROSIS ■ Sometimes resembles Paget’s disease ■ Permeative intracortical resorption DESTRUCTIVE FOCAL NECROSIS ■ Mandible ■ Femoral head ■ Humeral head PATHOLOGIC FRACTURE ■ Incomplete insufficiency fracture ■ Complete stress fracture

adjacent soft tissue mass, bone destruction, or a change in the appearance of irradiated bone that had previously been stable.11

A 62-year-old man was treated 6 years previously with external-beam radiation for malignant fibrous histiocytoma of the left thigh. A, T2-weighted coronal fast spin-echo (TR/TE 4150/92) MR image of the thigh reveals edematous marrow signal that had been stable for more than a year. B, T1-weighted axial fast spin-echo (TR/TE 550/14) MR image of the thigh in the same area shows tiny foci of increased signal in the signal void of the femoral cortex (arrow).

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■ FIGURE 39-10 A 42-year-old man had irradiation of the mediastinum and axillae at age 6 for Hodgkin’s disease. A, Anteroposterior view of the chest coned to the left shoulder. B, CT of the chest. An osteochondroma arises from the proximal metadiaphysis of the left humerus. As best seen on the CT in B (arrow), its cortex is continuous with the cortex of the remainder of the humerus and the osteochondroma contains marrow.

■ FIGURE 39-11 A 51-year-old woman was treated 7 years previously with radiation therapy to 60 Gy for malignant fibrous histiocytoma. A, Anteroposterior radiograph of right femur shows medullary sclerosis and cortical thickening in the mid diaphysis. These changes are consistent with radiation osteitis and had been stable for years. B and C, Anteroposterior views of the proximal and distal portions of the right femur. One and a half years later, after intramedullary nailing at an outside hospital for a femoral diaphyseal fracture, the patient now has a radiation-induced osteosarcoma involving the entire femur. In this case, extension of the tumor into the adjacent soft tissues is obvious by conventional radiography.

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SUGGESTED READINGS Bluemke DA, Fishman EK, Scott WW. Skeletal complications of radiation therapy. RadioGraphics 1994; 14:111–121. Boivin JF. Second cancers and other late side effects of cancer treatment. Cancer 1990; 65:770–775. Dalinka MK, Haygood TM. Radiation changes. In Resnick D (ed). Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, 2002. Fletcher BD. Effects of pediatric cancer therapy on the musculoskeletal system. Pediatr Radiol 1997; 27:623–636.

Goldwein JW. Effects of radiation therapy on skeletal growth in childhood. Clin Orthop Relat Res 1991; 262:101–107. Libshitz HI. Radiation changes in bone. Semin Roentgenol 1994; 29:15–37. Mitchell MJ, Logan PM. Radiation-induced changes in bone. RadioGraphics 1998; 18:1125–1136. Travis LB. Therapy-associated solid tumors. Acta Oncol 2002; 41:323–333.

REFERENCES 1. Fletcher BD, Crom DB, Krance RA, Kun LE. Radiation-induced bone abnormalities after bone marrow transplantation for childhood leukemia. Radiology 1994; 191:231–235. 2. Cahan WG, Woodard HQ, Higinbotham NL, et al. Sarcoma arising in irradiated bone: report of eleven cases. Cancer 1948; 1:3–29; reprinted in Cancer 1998; 82:8–34. 3. de Santos LA, Libshitz HI. Growing bone and radiation-induced neoplasia. In Libshitz HI (ed). Diagnostic Roentgenology of Radiotherapy Change. Baltimore, Williams & Wilkins, 1979. 4. Kim JH, Chu FC, Woodard HQ, et al. Radiation-induced soft-tissue and bone sarcoma. Radiology 1978; 129:501–508. 5. Kohn HI, Fry RJM. Radiation carcinogenesis. N Engl J Med 1984; 310:504–511. 6. Tucker MA, D’Angio GJ, Boice JD Jr, et al. Bone sarcomas linked to radiotherapy and chemotherapy in children. N Engl J Med 1987; 317:588–593.

7. Fletcher BD, Hanna SH. Muscle edema associated with musculoskeletal neoplasms and radiation therapy. In Fleckenstein JL, Crues JV III, Reimers CD (eds). Muscle Imaging in Health and Disease. New York, Springer, 1996. 8. Paling MR, Herdt JR. Radiation osteitis: a problem of recognition. Radiology 1980; 137:339–342. 9. Blomlie V, Rofstad EK, Talle K, et al. Incidence of radiationinduced insufficiency fractures of the female pelvis: evaluation with MR imaging. AJR Am J Roentgenol 1996; 167:1205–1210. 10. Blomlie V, Rofstad EK, Skjønsberg A, et al. Female pelvic bone marrow: serial MR imaging before, during, and after radiation therapy. Radiology 1995; 194:537–543. 11. Lorigan JG, Libshitz HI, Peuchot M. Radiation-induced sarcoma of bone: CT findings in 19 cases. AJR Am J Roentgenol 1989; 153:791–794.

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Complications of Osseous Trauma Dechen Tshering and Suzanne Anderson

There are many complications of skeletal trauma, although fortunately in most cases fracture healing is uncomplicated. The complications can result from the direct trauma to bone and soft tissue structures or from the treatment of the fractures. Complications of fractures may have systemic effects or may be local and involve the bones or the adjacent soft tissues and joints. In this chapter an overview is presented of the various complications in which radiology plays a role in evaluation, the various imaging modalities that are available, as well as the imaging appearances of the various complications. Complications discussed include delayed union and nonunion with pseudarthrosis formation, malunion, cartilage damage, and early degenerative changes; growth disturbance due to physeal injury; post-traumatic osteomyelitis; avascular necrosis; post-traumatic osteoporosis and osteolysis; Sudeck’s atrophy; and post-traumatic cyst and pseudotumor formation. Other complications related to vascular and nerve injuries and soft tissue aspects are discussed elsewhere.

PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS Complications of trauma can be divided into acute, subacute, or chronic. Acute is defined as having occurred immediately and usually refers to the injuries to the adjacent soft tissues, nerves, and vessels caused by the fracture fragments. Subacute is defined as having occurred after days to a week and is typified by delayed union or infection. Chronic is defined as having developed weeks to several months after an injury and is typified by a nonunion, pseudarthrosis formation, malunion, osteoarthritis, or growth abnormalities. Further definitions are found within each relevant subsection. 1010

Complications of osseous trauma include delayed fracture healing or failure of healing with formation of pseudarthrosis, or the bone fracture components may unite poorly with malalignment, called malunion. Development of osteomyelitis at the fracture site, after direct penetrating injury, or after interventional treatment may occur. Osteomyelitis complicating trauma can be divided into acute, subacute, and chronic. This may be associated with abscess and draining sinus formation if chronic. Malunion with deformities can lead to abnormal stresses in the adjacent joints and early onset of degenerative changes. Trauma can also lead to cartilage loss and early degenerative changes. There can be compromise of the blood supply to bone, leading to avascular necrosis and bone collapse. The development of this complication makes treatment more complex. Osteoporosis after immobilization or in the setting of Sudeck’s atrophy can predispose the bone to fractures. In children, epiphyseal injury can lead to early bone fusion and discrepancy in limb lengths. Malalignment in adults or complications of therapy may also be associated with leg-length discrepancy or advanced joint degeneration and may be treated by osteotomy. The incidence of fractures has been reported as 7.4 to 10 per 1000 persons per year.1,2 The incidence of nonunion in tibial fractures has been reported as 2.5% and that of delayed union as 4.4% in 22 series that included 5517 fractures.3 The incidence of osteomyelitis after open fractures is reported to be 2% to 16%,4 and in cases with operative management for closed fractures it is between 0.5% and 2%.5 The tibia is the most common site for open fractures and the most common site for post-traumatic osteomyelitis.6,7

CHAPTER

KEY POINTS Bone healing, and therefore also delayed union and nonunion, is determined clinically and supported by radiography. Different bones heal at different rates. ■ Malunion, cartilage damage, as well as epiphyseal injury and avascular necrosis with involvement of the joint surface can lead to abnormal stresses and early degenerative changes. In children, limb-length discrepancies can occur. ■ Osteomyelitis is one of the worst complications of osseous injury. The diagnosis is based on a combination of clinical, laboratory, and imaging findings. ■ Sudeck’s atrophy, post-traumatic osteoporosis, and osteolysis predispose to fractures, along with inappropriate load bearing. ■ Post-traumatic cysts and pseudotumors can present as tumors. ■ There are many imaging modalities available, each having its plus and minus points and, depending on the availability and the clinical indication, the appropriate modality should be chosen. ■

MANIFESTATIONS OF THE DISEASE Delayed Union, Pseudarthroses, or Nonunion of Fractures Immediately after a fracture of a bone there is bleeding and formation of a hematoma. There is invasion of the hematoma by granulation tissue. This is followed by callus formation, differentiation of precursor cells by local mediators, and osseous bridging. Remodeling is the last stage of fracture healing. Evaluation in the healing of fractures is made clinically and confirmed by imaging. Delayed union and nonunion are judged commonly clinically. Delayed union is failure of union at the expected date, but the expected date often may not be objectively determined. This is because different bones heal at different rates. The rate of healing depends on the age of the patient, the health status of the patent, and the type of fracture. The normal duration of fracture healing varies according to the bone involved and ranges from 4 to 20 weeks. In the presence of delayed union, motion at the fracture is evident clinically and a radiologically persistent fracture line with deficient or scarce callus is noted.8 Nonunion is the complete cessation of the healing process, and this term is usually reserved until after the fracture is at least 6 months old. The terms delayed union and nonunion are often used interchangeably because there are no well-defined criteria to separate the two. In both circumstances, the area between the fracture fragments is filled with dense fibrous tissue. Nonunion can be “hypertrophic,” with marked callus formation, or “atrophic,” without significant callus formation. Delayed union or nonunion is most common in the tibia, fibula, and scaphoid.8 Pseudarthrosis, a term referring to formation of a false joint at the site of injury, is sometimes used interchangeably with nonunion. In this situation, fluid or a mixture of

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1011

fluid and fibrous-like material develops between the fracture fragments and may result in continued motion at the fracture site that retards healing. Radiologically, it may be difficult to differentiate pseudarthrosis from nonunion. However, with pseudarthrosis formation there is often hypertrophic excessive sclerotic bone with rounded smooth edges. Causes of nonunion and delayed union include interruption of blood supply, anatomic distortion with multiple comminuted fractures, loss of bone fragments, severely displaced fractures, open fractures, and extensive soft tissue damage. The general condition of the patient, nourishment status, and other concurrent diseases also play a role in the healing of fractures. The use of corticosteroids can also delay fracture healing.8 The presence of infection can lead to nonunion and is discussed under osteomyelitis.

Radiography In the early stages no distinct features are present. Serial radiographs will either show an abundance of callus without bridging in the case of hypertrophic nonunion or failure of adequate callus to form in atrophic nonunion. In hypertrophic nonunion, the margins of the fracture fragments are well defined, sclerotic, and smooth and the medullary cavity is occluded with eburnation (sclerosis). In atrophic nonunion there is a paucity of callus formation and the gap of the fracture is widened and filled with fibrous tissue. When the fracture fragments remain widely separated, soft tissue interposition should be suspected and excluded by other imaging tests, such as ultrasonography, CT, and MRI. Pseudarthrosis formation is diagnosed clinically. The radiographic manifestations include persistence of the fracture line with sclerosis of the margins and rounded smooth edges (Fig. 40-1A).

Magnetic Resonance Imaging Magnetic resonance imaging is not generally utilized in the evaluation of callus when healing is progressing as expected. It may be rarely used only when a delayed union, nonunion, or pseudarthrosis is clinically suspected or if there are any other unusual features. Discontinuity of bone on T1-weighted sequences and the presence of fluid between the fracture fragment edges are helpful imaging features for evidence of inadequate healing.

Multidetector Computed Tomography Conventional radiography can often be difficult to interpret because overlying hardware obscures bone and callus is not always seen. CT offers a potentially more accurate method to discriminate fracture union from nonunion. Use of high-resolution CT has allowed for quick and easy reconstruction in multiple planes (sagittal and coronal) and may correct for patient positioning. Bhattarcharyya and associates9 assessed the diagnostic accuracy of multidetector CT in this setting and concluded that this technique was highly accurate with a high sensitivity for callus differentiation. However, in some instances there were clefts, which if misinterpreted could potentially

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Radiography Radiography is the gold standard and is used in the follow up of all patients with fractures. Linear and angular deformity can be well demonstrated. Radiographs, however, are not able to demonstrate rotational deformity, and CT is suggested for that circumstance. More advanced degenerative changes of the adjacent joints as well as those joints that have been dislocated can be well seen on radiographs by the presence of osteophytes, decrease in the joint space, subchondral sclerosis, and formation of geodes (Fig. 40-2).

Magnetic Resonance Imaging

■ FIGURE 40-1

A, Pseudarthrosis. Lateral radiograph of the distal tibia shows persistent fracture line with surrounding sclerosis. B, Sagittal reconstructed CT image shows the nonbridging callus and persistence of the fracture line.

lead to a false diagnosis of nonunion in the presence of fracture union. The exact clinical importance of this was not totally assessed. When there is suspicion of fracture nonunion clinically or at radiography, CT is the next imaging study to perform. CT is optimal for reviewing complex fracture cases and also when joint surfaces are involved. The technique also allows more accurate presurgical review and surgical planning (see Fig. 40-1B).

Malunion, Cartilage Damage, and Early Degenerative Changes Malunion is fracture healing in an abnormal position or alignment. Rotational malalignment is never corrected spontaneously, so it should be evaluated carefully on radiography or CT, although it is often difficult to detect. In children, angulations up to 30% may correct spontaneously, but in adults, spontaneous healing rarely occurs even with angulations much less than 30%.8 Trauma to the skeleton may be associated with premature degenerative joint disease. If the fracture involves the joint surface, this will increase the likelihood of more advanced osteoarthritis, particularly when there is a gap or offset of the cortical joint surfaces. If fracture fragments remain within the joint, this may also be associated with more advanced joint degeneration.

Magnetic resonance imaging is the gold standard for evaluating traumatized joints because it allows for the depiction of all anatomic structures, including bone, joint, and soft tissues. It is also the gold standard for the assessment of cartilage lesions after trauma. The location, size, and depth of the lesions and the presence of any underlying bony abnormalities should be described. The presence of cartilage flaps or fissures may be more amenable to therapy with early surgery.10,11 MRI is useful in the demonstration of post-traumatic cartilage damage, which can lead to early degenerative changes. This technique also shows the other features of degeneration and the presence of joint fluid, bone marrow contusion, and free joint bodies.

Multidetector Computed Tomography Computed tomography may be used to assess for rotational deformity, which is not easily detected on radiography. Degenerative changes such as osteophyte formation, joint space narrowing, sclerosis, and geode formation are also well demonstrated with CT, especially since sagittal and coronal reconstructions may be easily obtained.

Arthroscopy Cartilage damage is seen on arthroscopy and is commonly graded using the Outerbridge classification system: Grade 0: normal cartilage Grade I: cartilage with softening and swelling Grade II: a partial-thickness defect with fissures on the surface that do not reach subchondral bone or exceed 1.5 cm in diameter Grade III: fissuring to the level of subchondral bone in an area with a diameter more than 1.5 cm Grade IV: exposed subchondral bone

Growth Disturbances due to Physeal Injuries Trauma to the immature physeal plate may be associated with growth disturbances. Growth acceleration may occur 6 months to 1 year after injury, but it is not progressive. Metallic fixation devices may be a cause of continued stimulation for growth.8 Early fusion of the epiphysis leads to growth arrest. Physeal injuries are most common in adolescents and more frequent in the upper limbs. The incidence

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1013

■ FIGURE 40-2

A and B, Conventional radiographs of the knee showing post-traumatic structure and contour alteration of the femur with early degenerative changes in the knee joint.

of growth arrest is just over 1%. The prognosis depends more on the location of the injury than the Salter-Harris classification, with the proximal tibia being a common site for growth disturbances.12

Radiography Orthoradiographs show limb-length discrepancies well. Radiographs can show early epiphyseal union when compared with the joint on the other side. Post-traumatic deformity such as pseudo-Madelung’s deformity is also demonstrated well, with the early fusion of epiphysis and resulting bowing deformity of the radius.

Magnetic Resonance Imaging Magnetic resonance imaging is critical, particularly in young patients with immature physeal plates, for accurate fracture typing and classification. The use of fat-suppressed, 3D, spoiled gradient-recalled echo MR imaging in chronic physeal injuries enables an accurate reconstruction of a 3D model of the growth plate and can determine the site of the physeal fusion or bony bridges and allow for more accurate surgical therapy.13–15 It may also help in predicting the chances of early degenerative joint disease in older patients.

Multidetector Computed Tomography Computed tomography with sagittal and coronal reconstructions is also very helpful in the patient with chronic

physeal injury where there has been premature physeal plate closure, allowing for more accurate surgery. However, CT results in radiation exposure to the patient whereas MRI uses no ionizing radiation, one of the major advantages of the technique, especially in the pediatric population.

Post-traumatic Osteomyelitis Osteomyelitis is one of the most severe complications of open fractures or operative treatment of bone injuries. Despite important advances in surgical and medical treatment, it often remains refractory to therapy and leads to chronic disease. Even after years of quiescence, it may recur. Post-traumatic osteomyelitis remains a lifelong disease and is nearly exclusively induced by direct inoculation of microorganism into bone.16 It can also be induced by adjacent soft tissue infection.5 Multiple organisms are usually isolated from bone infected as a result of direct inoculation or contiguous focus infection, but Staphylococcus aureus remains the most commonly isolated pathogen.17 Osteomyelitis can be classified into acute or chronic types depending on the duration of the disease or according to the causative microorganism. The Cierny-Mader classification of osteomyelitis classifies the infection morphologically and is based on anatomic osseous involvement and on the physiologic status of the patient. The anatomic disease types, which are prognostic for dead space and osseous management, are grouped into four

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types. Type I is defined as medullary osteomyelitis and includes hematogenous osteomyelitis and infections of intramedullary rods. Type II is defined as superficial osteomyelitis, which is limited to the surface of the bone. This does not require either dead space management or osseous stabilization but often requires soft tissue coverage of the exposed bone. Type III is localized osteomyelitis, involving the full thickness of the cortex. This often requires complex dead space management and simple osseous stabilization. Type IV osteomyelitis is defined as diffuse osteomyelitis, involving the circumference of the cortex. This requires complex dead space management and complex osseous stabilization. The physiologic class of the patient is determined by the local and systemic factors that affect the response to infection and treatment. Patients in class A have normal systemic defenses, metabolic capabilities, and vascular supply to the affected area. Patients considered to be in class B have local or systemic wound healing deficiency (e.g., from suppressed immune systems, corticosteroid therapy, and peripheral vascular disease). Patients in class C are those whose anticipated treatment morbidity is worse than the presenting condition and who have a poor prognosis for cure. The Cierny-Mader classification system correlates with the treatment and prognosis of patients.6 The diagnosis is made on the basis of clinical findings, with supportive radiographic features, such as the presence of periarticular osteopenia and joint effusion. However, clinical signs and symptoms may be absent or make it difficult to diagnose chronic infection. Also in the setting of immune suppression or compromise it may be very difficult to diagnose either acute or chronic infection, particularly since there is commonly less adjacent soft tissue inflammatory reaction compared with the noncompromised patient. The clinical symptoms of acute osteomyelitis are those of acute inflammation. However, these signs are also seen in the physiologic phase of healing after tissue damage and normally disappear after 5 to 7 days. In the case of bacterial contamination, however, they persist or become more severe.16 The diagnosis of chronic osteomyelitis, however, requires a detailed history with sufficient information about the original injury, treatment, and actual disability. There may be signs of inflammation and limitation of movement and weight bearing. In chronic osteomyelitis, the symptoms may be subtle. A good physical examination of the scar with special emphasis on the presence of ulcers and draining sinus tracts is needed. Diagnosis of osteomyelitis requires both bacteriologic and histologic examinations. Swabs from bone or fistulas have a poor sensitivity. Therefore, biopsy should be performed instead of using swabs. If sinus or the open wound is cultured, the material should be obtained from the deepest portion of the wound because superficial cultures may give false information about infecting organisms. Culture specimens should be obtained before antibiotic therapy or after stopping the antibiotics at least 1 to 2 days before.16 Atypical infections are particularly difficult to diagnose

and require a high degree of clinical suspicion as well as special staining and growth media for diagnosis. The radiologist’s paramount task is to confirm or exclude the presence of active infection and, if infection is present, to delineate the extent of the bone, joint, and soft tissue involvement to enable appropriate therapy.18 There are many imaging modalities available, each with their different capabilities and limitations. Depending on the needs of the treating physician, and local availability, the appropriate modality should be used.

Radiography Radiography represents the basic examination that may support the clinical suspicion of bone infection, delineates anatomic distortion and the presence of metallic implants, and helps in the selection and interpretation of the second-line imaging modality.16 It is also the basic modality for the follow-up of patients with fractures and also in the evaluation of the progress of post-traumatic osteomyelitis. Detection of infection, however, can be difficult in bone that has been altered by trauma and surgery. Comparison with previous images may be extremely helpful to determine active infection by the presence of new bone destruction or evidence of focal lytic regions near or around screws suggestive of infection. The presence of multiple fracture fragments and bone defects along with the presence of orthopedic hardware and the presence of disuse osteopenia can mask the appearance of osteolysis caused by infection. Delayed union or nonunion of fractures and loosening of orthopedic devices may be caused by infection but cannot be reliably discriminated from aseptic complications. The physiologic signs of bone remodeling and healing include periosteal and endosteal reaction, cortical thickening and sclerosis, and even cortical irregularity that may resemble the involucrum of infected bone. Tumeh and associates19 reported that sequestration was the only reliable radiographic finding of active bone infection when there had been prior surgery or fracture. The sensitivity and specificity reported was only 14% and 70%, respectively, for radiography, even when changes on serial plain films were considered. Brodie’s abscess is a low-grade osteomyelitis, usually of staphylococcal origin, that can be post-traumatic in origin.20 Radiographs may show a medullary-based osteolytic lesion surrounded by sclerosis typically in the diaphysis or metaphysis of tubular bone, or less commonly it may have a periosteal epicenter.21

Magnetic Resonance Imaging Because of its capability to demonstrate anatomic details as well as pathologic changes of bone marrow, joint, and surrounding soft tissues with high sensitivity and excellent spatial resolution, MRI has been recognized as a very useful modality for detecting acute and chronic bone infection. Its multiplanar capability also makes it an attractive choice. Typical MRI findings of osteomyelitis include illdefined low signal intensity on T1-weighted images that replaces the normal marrow fat signal intensity and high

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signal intensity on T2-weighted and STIR images and contrast enhancement. However, these primary criteria used to identify inflammatory changes such as edema pattern on T2-weighted sequences and contrast enhancement after intravenous gadolinium application are nonspecific because of hyperemia and increased endothelial permeability and can lead to diagnostic inaccuracy in posttraumatic and postoperative situations.5,16 Reparative fibrovascular scar tissue in bone marrow and soft tissue exhibit similar signal intensities and contrast enhancement characteristics, and these findings may persist for up to 12 months after surgical intervention. Ledermann and associates18 have shown that granulation tissue in surgical bone defects is first characterized by a homogeneous enhancement that decreases over time in a centrifugal pattern toward the borders of the bone cavity, thus leaving a less vascularized scar in the center. This time-dependent process progresses faster in small bony defects, but equivocal findings, particularly in large defects, may persist up to 1 year. This phenomenon would be easier to detect if serial MRI were obtained. However, this finding cannot be differentiated from a medullary phlegmon or from an abscess in the later stages. The time interval for followup MRI examination should be at least 2 months to see a definite progression in scarring. Gross and coworkers16 strongly recommended the use of gadolinium in chronic post-traumatic osteomyelitis, because the pattern of contrast enhancement could allow discrimination of fibrovascular scar from infectious foci. Contrast enhancement also helped to differentiate abscess formation from diffuse inflammatory changes and noninfectious fluid collections.21 The penumbra sign, referring to the slightly hyperintense signal on unenhanced T1-weighted images between an abscess cavity and the surrounding edematous or sclerotic bone, is a helpful sign in the diagnosis of subacute osteomyelitis. This finding corresponds to a layer of granulation tissue that lines the abscess cavity and contains less fluid and more protein. This characteristic but not pathognomonic finding supports the diagnosis of bone infection and helps to exclude the presence of tumor. This sign is most useful in subacute, chronic, or acute on chronic cases.22–24 Secondary signs of osteomyelitis, such as cutaneous ulceration, cortical discontinuity, and abscess formation can be supportive evidence of osteomyelitis, but they are not infallible. The presence of a fistula is the only sign that could favor osteomyelitis over soft tissue infection. Orthopedic implants lead to susceptibility artifacts on MRI, which can degrade image quality. Even after removal of the implants, some small fragment of metal remains in the bone and these can cause susceptibility artifacts that appear as a local signal distortion with a central signal void surrounded by a halo of increased signal intensity. For the differentiation of artifacts and infectious foci, meticulous comparison of the precontrast and postcontrast T1-weighted images is mandatory. The presence of an extramedullary fat-fluid level has been described as an indicator of cortical breach and therefore the presence of osteomyelitis in the setting of soft tissue infection.25

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Another technical limitation of MRI is its inability to diagnose infection around a metallic foreign body due to field inhomogeneities. The use of fast spin-echo sequences with shortened echo spacing is recommended to decrease the size of susceptibility artifacts. The closely spaced 180-degree pulse leaves little time for spins to dephase as they diffuse through regions of magnetic nonuniformity. T1-weighted subtraction images without and with contrast medium enhancement can be used to minimize this shortcoming.18 Scarring and postoperative changes can cause falsepositive MR images up to 13 months after surgery, and these studies should be correlated with scintigraphy and positron emission tomography if available.18 If MRI discloses a possible cortical fistula in severely thickened bone after intramedullary reaming, CT should be performed to confirm or exclude its presence.18 The appearance of a Brodie abscess on MRI is described as high signal intensity on proton density– and T2-weighted imaging, with low intensity on T1 weighting with homogeneous and strong enhancement of the lesion after gadolinium injection.20.26 Another appearance described is that of a target with four layers in long-bone abscesses: (1) low signal intensity on T1 weighting and high signal intensity on T2 weighting and STIR images, (2) an inner ring isointense to muscle on T1-weighted and high signal intensity on T2-weighted and STIR images, (3) an outer ring hypointense on all sequences, and (4) a peripheral halo hypointense on T1-weighted images.20 In immunocompromised or suppressed patients after trauma, infection may not have classic clinical or radiologic features. Therefore, care should be taken to include infection in the differential diagnostic list of focal MRI findings in this setting.

Multidetector Computed Tomography Computed tomography is a useful adjunct to conventional radiographs. With the advent of multidetector CT it is possible to get excellent multiplanar reconstructions with high spatial resolution of the bony structures. CT correctly depicts osseous changes such as cortical destruction, periosteal proliferation, and soft tissue changes such as sinus tracts and abscesses along with sequestration, intraosseous fistula, foreign bodies, and intramedullary gas.27,28 Sequestra may be exceedingly small and difficult to see on conventional radiographs. CT is the method of choice in the demonstration of sequestrate and for bony fistula and allows for ready identification of the bony fragments. Their position along with cortical defects that lead to subcutaneous sinus tracts is important in planning surgery. CT also shows the presence of abscesses and foreign bodies.27 Because resection of necrotic bone and thorough débridement of intraosseous and soft tissue fistula are two major aims of surgical treatment, CT is very useful in preoperative planning. The disadvantage of CT is the need for ionizing radiation and the fact that there is significant degradation of image quality in the presence of orthopedic hardware because of the beam-hardening effect.

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Ultrasonography Ultrasonography cannot assess the bone marrow changes associated with osteomyelitis, but it can evaluate the soft tissue changes that are associated with osteomyelitis and thus support the diagnosis.29 It is useful in the demonstration of joint effusions and soft tissue abscesses. In children, the presence of subperiosteal abscesses is easily demonstrated. Although ultrasonography cannot penetrate the bone, the presence of fluid near the cortex is suggestive of osteomyelitis. The finding of extension of a fluid collection into the bone through a break in the cortex is almost pathognomonic of reactivated chronic osteomyelitis.29 With the high-resolution transducers, the sinus tract can also be well demonstrated. In the presence of orthopedic hardware, ultrasonography is useful in the evaluation of the surrounding soft tissues because it is not limited by the artifacts that are present in CT or MRI.

Nuclear Medicine The current best nuclear medicine study for the detection of bone infection is three-phase bone scintigraphy followed by leukocyte scintigraphy because this is more specific for inflammation. This combined study provides information about bone metabolism and the presence, grade, and extent of inflammation. Also, it is especially useful in patients with orthopedic devices. The choice of the radiopharmaceutical depends on the grade of inflammation, age of infection, availability, and cost as well as radiation exposure.16 The three-phase bone scintiscan with technetium-99m (99mTc) methylene diphosphonate is the basis of nuclear medicine imaging of bone because it is independent of orthopedic implants and can differentiate between soft tissue and bone infection.4 Acute osteomyelitis shows tracer enhancement in all three phases of examination. In chronic infection the arterial phase accentuation is often missing. It has a high sensitivity but low specificity.4,5,17 Findings are difficult to differentiate from postoperative or degenerative changes, and infection-specific scintigraphy is required. The mechanism of uptake in infection is the detection of increased vascular permeability with an interstitial extracellular distribution of the nanomolecules. This has been described as more sensitive than when radiolabeled leukocytes are used.5 Leukocytes may be labeled with indium-111 or with 99mTc-hexamethylpropylene amine oxime (99mTc-HMPAO). Because the leukocytes migrate to the infectious sites, this method permits the detection of local leukocyte accumulation in peripheral infection. In chronic osteomyelitis, 111In-leukocyte scintigraphy still represents the gold standard of detection of infection because the stable radiolabeling of the granulocytes without elution of the tracer out from the cells and the long physical half-life of indium-111 allow the observation of cell migration over 48 hours.16 This represents an advantage in the detection of low-grade infection that is characterized by a reduced migration of white blood cells. The disadvantages of this method are its time-consuming labeling process, substantial technical expertise requirements, and handling of the patient’s blood, along with a high radiation exposure (0.5–0.6 mSv) and reduced image quality in comparison with 99mTc-HMPAO–labeled leukocytes (0.017 mSv).

Labeling with 99mTc-HMPAO permits the acquisition of images with a better signal-to-noise ratio, which proves to be advantageous in acute and subacute infection. The disadvantages of labeling of leukocytes with 99mTc-HMPAO is that the radioisotope is less stable and has a short half-life so that late scanning is not possible. Fracture healing without complication shows mild uptake with labeled leukocytes, whereas the three-phase bone scintiscan shows high osteoblastic activity in the area of fracture. False-positive results of leukocyte scintigraphy may arise from heterotopic ossification, hematoma, and post-traumatic synovitis. Mechanical insertion of orthopedic devices, for instance, may dislocate and compress bone marrow to an area distal to the metal.4 Granulocytes labeled with 99mTc-monoclonal antigranulocyte antibody (99mTc-MAB) show an in-vivo distribution quite similar to that of radiolabeled granulocytes, thus allowing detection of granulocyte accumulation. The antibodies are directed against the myeloid-specific antigen NCA-95 expressed by granulocytes. Problems in the detection of infection occur in areas with active hematopoietic bone marrow such as the spine, pelvis, and the proximal femur because the more mature precursor cells of the granulopoietic system as well as the vast granulocyte pool residing in this marrow are also labeled. Another disadvantage of 99mTc-MAB is the induction of human anti-mouse antibodies (HAMA) in 3% to 10% of patients. Notable problems were similar to those experienced with 99m Tc-HMPAO–radiolabeled leukocytes.5 Low-grade osteomyelitis, which is characterized by decreased granulocyte infiltration as compared with acute osteomyelitis, may be missed and cannot be reliably distinguished from nonpurulent inflammation. Particularly, postoperative granulation tissue and inflammatory reactions due to fracture nonunion may lead to false-positive scans. Another pitfall is that unexpected ectopic, hematopoietic active bone marrow at the former fracture site may cause false-positive studies.5 Gallium-67 citrate is an unspecific tracer that accumulates in inflammatory changes due to in-vivo labeling of serum proteins, leukocytic lysosomes, and endoplasmic reticulum along with direct bacterial uptake. Because of high radiation exposure, long examination time, reduced availability, and high-energy gamma rays with subsequent low spatial resolution, it has been widely replaced by other radiopharmaceuticals.16

Positron Emission Tomography Positron emission tomography (PET) is very sensitive in imaging of infection because uptake and metabolism of fluorodeoxyglucose (FDG) is elevated in activated inflammatory cells such as leukocytes, granulocytes, and macrophages owing to an increase of glucose metabolism and an expression of glucose transporter in these cells.16,30 The advantages of FDG-PET for imaging of infection include a higher spatial resolution in comparison with conventional nuclear medicine modalities, cross-sectional imaging, high sensitivity in detecting disease-involved areas, fast examination time (results available within 2 hours), and differentiation between hematopoietic bone marrow and activated white blood cells. PET is an inherently quantitative

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imaging method, which therefore not only permits disease localization but also potentially treatment monitoring. Normal bone marrow has only a low glucose metabolism under physiologic conditions, and this allows the distinction of inflammatory cellular infiltrates from ectopic hematopoietic marrow and the use of PET in suspected infection of the central skeleton. Reactive changes in aseptic fracture nonunion also show only a faint uptake that can be clearly distinguished from osteomyelitis. The major drawback of FDG-PET is the lack of anatomic landmarks, which makes it sometimes very difficult to assign the lesion to a particular structure. The other disadvantage is the accumulation in different inflammatory processes such as sarcoidosis, pulmonary granuloma, and joint inflammation.30 The integration of FDG-PET and CT combines the advantages of both scintigraphy and CT. High-quality anatomic CT maps and FDG-PET scans are acquired in one study and allow functional-morphologic correlation by immediate digital imaging fusion.

Avascular Necrosis Loss of blood supply and resulting avascular necrosis are known to occur after fractures or dislocation and can be due to disruption of the arterial blood supply either through vessel transection, dissection, or compression.8 Bone necrosis may involve the long ends of bone with injury to the endarterial supply or occur within medullary bone. The latter is unusual in normal fracture circumstances, owing to the very prolific collateral vascular supply. Features that may be associated with avascular necrosis of medullary bone after trauma include stripping of cortical vessels to butterfly fragments or extensive arterial injury. The most common site of avascular necrosis is the femoral head.31 Other sites include the humeral head, the scaphoid, lunate, capitellum, femoral condyle, and talus.32 Trauma is the most common cause of avascular necrosis of the femoral head.

Radiography Radiologic changes in the femoral heads include subtle relative sclerosis of the head secondary to resorption of surrounding vascularized bone. The radiolucent crescent sign is parallel to the articular surface in the weight-bearing portion secondary to subchondral structural collapse of the necrotic segment. There is preservation of joint space with flattening of the articular surface and increased density of the femoral head. Avascular necrosis at other sites also presents in the early phases as an increased density due to reactive osteopenia of the viable surrounding bone (Fig. 40-3). This can be followed by fragmentation and collapse.

Magnetic Resonance Imaging In the early stages, MRI with its ability to detect marrow edema is useful for detection of avascular necrosis. The Mitchell classification of avascular necrosis on MRI is as follows: Class A lesions have a center with MRI characteristics of fat on all sequences. Class B lesions have signal higher than fat on T2-weighted images, suggesting blood products.

■ FIGURE 40-3 Anteroposterior radiograph shows sclerosis of the proximal pole of the scaphoid compatible with avascular necrosis.

Class C lesions have MRI characteristics of fluid with relatively slow signal on T1-weighted images and high signal on T2-weighted images. Class D lesions have low signal centrally on all sequences suggesting fibrosis or sclerosis. A low-signal line defining the margin of the abnormality completely or partially is commonly seen in avascular necrosis. A second high-signal line may be seen on proton density–weighted images. The “double line” sign is seen on T2-weighted images and refers to the low signal margin that is often accompanied by a second inner band of high signal intensity within the low signal intensity margin. After gadolinium administration there can be enhancing areas of viable tissue and nonenhancing areas that correspond to areas of necrosis. Secondary signs that may also be seen include adjacent joint effusions and fatty conversion of the bone marrow in the intertrochanteric region of the femur.32 Once avascular necrosis has occurred and an articulating joint is involved, secondary osteoarthritis will develop. MRI is useful in the initial diagnosis of avascular necrosis and in monitoring the efficacy of surgical treatment. The study can also be utilized to determine whether vascularized bone graft incorporation and revascularization of the proximal pole of the scaphoid has occurred in the setting of avascular scaphoid nonunion. It can potentially influence decision making by allowing early prognosis of graft healing.33 The MRI appearance of avascular necrosis at other sites is similar to that at the hip (Fig. 40-4).

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■ FIGURE 40-4 A to C, MR images in a patient with posttraumatic necrosis of the talus.

Multidetector Computed Tomography Computed tomography can be used for the staging of known disease and for preoperative planning, and it is more sensitive than radiography but less sensitive than MRI. In the hips, there is smudging of the weight-bearing trabeculae with clumping and fusion of the peripheral radiation. There is usually a margin of peripheral sclerosis correlating to the band of low signal seen on MRI. In advanced cases there is frank collapse of the femoral head.32

The multiplanar reconstructions allow for good depiction of the complex anatomy, especially of the wrist and ankle. And, in particular, coronal CT image resolution is required for viewing the articular surface of the talar dome.

Nuclear Medicine Bone marrow imaging with radiocolloid is more sensitive than imaging with diphosphonates. Scintigraphy is more sensitive than radiography in the early stages, but the technique

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is less sensitive than MRI. In the early phase there is a photopenic defect due to interrupted blood supply. In the late phase there is the appearance of the doughnut sign, which is a cold spot surrounded by increased uptake secondary to degenerative osteoarthritis and capillary revascularization.3

Post-traumatic Osteoporosis and Osteolysis Disuse osteoporosis occurs characteristically in patients with immobilized limbs secondary to fracture or paralysis. It usually becomes apparent during the first 7 months to 2 years after trauma. The radiographic findings include patchy osteoporosis, most commonly in a periarticular distribution. In addition, there may be a more diffuse osteoporosis in the region of immobilization. The pathogenesis of diffuse osteopenia is not entirely clear but may represent a reduction in new bone formation versus increased bone resorption. Therefore, disuse osteoporosis is generally considered a high turnover osteoporosis that is self limited and generally reversible. Osteoporosis may be generalized and diffuse or spotty or may appear as linear translucent bands, cortical lamellation, and scalloping. The diaphyses can show cortical tunneling and endosteal scalloping. Disuse osteoporosis can be confused with an aggressive permeative process such as infection or metastatic disease or tumor. Post-traumatic osteolysis is recognized to occur commonly at certain anatomic sites such as the distal clavicle, ulna, and pubic rami. Involvement of the clavicle generally occurs some 6 weeks after trauma and is limited to the lateral aspect of the clavicle. Findings include soft tissue swelling over the acromioclavicular joint that is followed by demineralization of the lateral clavicle. Other findings include cortical bone irregularity or erosion, bone fragmentation, and synovitis. The signal intensity of the osteolysis is low on T1-weighted images and heterogeneous on T2-weighted images. The osteolysis progresses up to 18 months, and this is followed by reconstitution. The self-limiting nature differentiates this process from the osteolysis of Gorham.8 This condition is frequently associated with subchondral fractures.34

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On ultrasonography or MRI, soft tissue swelling as well as synovial changes including edema and hyperemia are seen in the early stage. In the late stage there is atrophy and fibrosis. MRI may also play a role in excluding tumors. On three-phase bone scintigraphy there is increased blood flow, blood pool, and periarticular increased uptake in the affected areas. This diffuse delayed uptake in the juxta-articular region is reported to be characteristic.36

Re-fracture The fracture site is relatively weak, even after healing, and is at risk of re-fracture. Re-fracture can occur through the same fracture or through the screw holes of surgical plates and below or above the screws due to post-traumatic osteopenia. In the presence of early load bearing there can be re-fracture and fracture of the compression plate (Fig. 40-5). Deluca and associates37 stated that removal of compression plates could be complicated by re-fracture that could occur through the original fracture line or may go through the screw hole. Patients at risk of re-fracture include those with high-energy trauma or a crush injury, an open injury, other fractures in the extremity, failure of adequate initial compression or reduction in a comminuted fracture, and persistence of the radiolucent line on radiographs.

Post-traumatic Cysts and Pseudotumors Moore and colleagues38 described the asymptomatic transient cortical lesions in children after fracture that are

Sudeck’s Atrophy Sudeck’s atrophy or reflex sympathetic dystrophy is a difficult entity both to diagnose and to treat. Patients may present a week to several months after trauma with pain, hyperesthesia, and tenderness. The causative trauma can be very trivial. Commonly, they will have increased warmth and temperature of the limb or region involved and the skin is thickened.8 The incidence has been reported as 0.01% in patients with fractures.35 The diagnostic criteria of Genant include pain and tenderness in the extremity, soft tissue swelling, diminished motor function, trophic skin changes, vasomotor instability, and patchy osteoporosis. On radiography, diffuse osteopenia is present and is often severe or may be patchy or spotty. Endosteal resorption and cortical tunneling may be dominant, but mild subperiosteal resorption may be observed. Osteopenia is usually marked, mostly around nearby joints.

■ FIGURE 40-5 A and B, Radiographs show re-fracture of the femur with fracture of the fixation plate.

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believed to be subperiosteal defects only seen during the course of fracture healing. Expanding lesions located more centrally after trauma may be due to aneurysmal bone cysts and also possibly simple bone cysts. These occur in children and young adults and cause pain and swelling and pathologic fractures. According to Papadimitriou and associates,39 post-traumatic cystic lesions are uncommon complications of fractures in children. They are benign, asymptomatic, and nonexpansile and usually resolve spontaneously. These investigators believed that the lesions resulted most likely from inclusion of medullary fat within subperiosteal hematomas.

DIFFERENTIAL DIAGNOSIS The clinical history and treatment history of the patient are critical for making the most accurate diagnosis. The trauma history needs to be reviewed to ensure that the imaging findings, whether acute or more chronic, fit with the clinical history. If the imaging findings do not fit with the given history, then the images should be reviewed to exclude a pathologic fracture associated with a potentially primary or metastatic tumor. These two tumor types may have very different treatment options, so it is imperative that junior staff enlist help from senior or more experi-

enced colleagues if they are in doubt about a case. Missed diagnoses and inappropriate treatment may have a negative impact on limb salvage procedures if a real sarcoma is involved. Equally, infection complicating trauma may have extensive impact on a patient’s health and function if it is missed or the diagnosis is delayed.

What the Referring Physician Needs to Know ■ ■ ■

■ ■ ■ ■ ■ ■ ■ ■

Where is the injury? Site and extent? Is the joint involved? What is the fracture type? Describe the fracture: alignment, displacement, any butterfly fracture fragments, any complications to vessels or nerves Which is the most expedient imaging test for this trauma? Which is the most cost-effective imaging modality for this trauma? Is the fracture healing? Is it healing correctly without malalignment? Is there infection? Is there avascular necrosis? Is there any other pathologic process that has to be treated? Is the treatment adequate? Should reoperation be done?

SUGGESTED READINGS Gross T, Kaim AH, Regazzuoni P, Widmer AF. Current concepts in posttraumatic osteomyelitis: a diagnostic challenge with new imaging options. J Trauma Injury 2002; 52:1210–1219.

Parikh J, Hyare H, Saifuddin A. The imaging features of posttraumatic myositis ossificans, with emphasis on MRI. Clin Radiol 2002; 57:1058–1066.

REFERENCES 1. Donaldson LJ, Cook A, Thomas RG. Incidence of fractures in a geographically defined population. J Epidemiol Community Health 1990; 44:241–245. Accessed online March 19, 2007. 2. Brinker MR, O’Connor DP. The incidence of fractures and dislocations referred for orthopaedic services in a capitated population. J Bone Joint Surg Am 2004; 86:290–297. Accessed online March 19, 2007. 3. Phieffer LA, Goulet JA. Delayed unions of the tibia. J Bone Joint Surg Am 2006; 88:205–216. Accessed online January 17, 2007. 4. Bühne K-H, Bohndorf K. Imaging of posttraumatic osteomyelitis. Semin Musculoskelet Radiol 2004; 8:199–204. 5. Kaim AH, Gross T, von Schulthess GK. Imaging of chronic posttraumatic osteomyelitis. Eur Radiol 2000; 12:1193–1202 6. Holtom P, Smith AM. Introduction to adult posttraumatic osteomyelitis of the tibia. Clin Orthop 1999; 360:6–13. 7. Mader JT, Cripps MW, Calhoun JH. Adult posttraumatic osteomyelitis of the tibia. Clin Orthop 1999; 360:14–21. 8. Ehara S. Complications of skeletal trauma. Radiol Clin North Am 1997; 35:767–781. 9. Bhattarcharyya T, Bouchard KA, Phadke A, et al. The accuracy of computed tomography for the diagnosis of tibial non-union. J Bone Joint Surg Am 2006; 88:692–697. Accessed online January 17, 2007. 10. Schindle MK, Foo LF, Kelly BT, et al. Magnetic resonance imaging of cartilage in the athlete: current techniques and spectrum of disease. J Bone Joint Surg Am 2006; 88:27–46.

11. Kendell SD, Helms CA, Rampton JW, et al. MRI appearance of chondral delamination injuries of the knee. AJR Am J Roentgenol 2005; 184:1486–1489. 12. Mizuta T, Benson WM, Foster BK, et al. Statistical analysis of the incidence of physeal injuries. J Pediatr Orthop 1987; 7:518–523. 13. Craig JG, Cramer KE, Cody DD, et al. Premature partial closure and other deformities of the growth plate: MR imaging and threedimensional modeling. Radiology 1999; 210:835–843. 14. Ecklund K, Jaramillo D. Patterns of premature physeal arrest: MR imaging of 111 children. AJR Am J Roentgenol 2002; 178:967–972. 15. Sailhan F, Chotel F, Guibal AL, et al. Three-dimensional MR imaging in the assessment of physeal growth arrest. Eur Radiol 2004; 14:1600–1608. 16. Gross T, Kaim AH, Regazzuoni P, Widmer AF. Current concepts in posttraumatic osteomyelitis: a diagnostic challenge with new imaging options. J Trauma Injury 2002; 52:1210–1219. 17. Lazzarini L, Mader JT, Calhoun JH. Current concepts review: osteomyelitis in long bone. J Bone Joint Surg Am 2004; 86:2305–2318. 18. Ledermann HP, Bongartz G, Steinbrich W. Pitfalls and limitations of magnetic resonance imaging in chronic posttraumatic osteomyelitis. Eur Radiol 2000; 10:1815–1823. 19. Tumeh S, Aliabadi P, McNeil B. Disease activity in osteomyelitis: role of radiography. Radiology 1987; 165:781–784.

CHAPTER 20. Guermazi A, Mohr A, Genant HK. Brodie abscess: another type of chronic posttraumatic osteomyelitis. Eur Radiol 2003; 13:1750–1752. 21. Hopkins KL, Li KCP, Bergman G. Gadolinium-DTPA–enhanced magnetic resonance imaging of musculoskeletal infectious processes. Skeletal Radiol 1994; 24:325–330. 22. Grey AC, Davies AM, Mangam DC, et al. The “penumbra sign” on T1-weighted MR imaging in subacute osteomyelitis: frequency, cause and significance. Clin Radiol 1998; 53:587–592. 23. Davies AM, Grimer R. The penumbra sign in subacute osteomyelitis. Eur Radiol 2005; 15:1268–1270. 24. McGuinness B, Wilson N, Doyle AJ. The penumbra sign on T1-weighted MRI for differentiating musculoskeletal infection from tumour. Skeletal Radiol 2007; Mar 6 [Epub ahead of print]. 25. Hui CL, Naido P. Extramedullary fat fluid levels on MRI as a specific sign for osteomyelitis. Australas Radiol 2003; 47:443–446. 26. Marti-Bonmati L, Aparisi F, Poyatos C, Vilar J. Brodie abscess: MR imaging appearance in 10 patients. J Magn Reson Imaging 1993; 3:543–546. 27. Wing VW, Jeffrey RB, Federle MP, et al. Chronic osteomyelitis examined by CT. Radiology 1985; 154:171–174. 28. Mäurer J, Lehmann-Beckow, Vosshenrich R, et al. Wertigkeit von Computertomographie und Kernspintomographie in der Diagnostik von Knochensequestern. Akt Radiol 1992; 2:345–349. 29. Cardinal C, Bureau NJ, Aubin B, Chhem RK. Role of ultrasound in musculoskeletal infections. Radiol Clin North Am 2001; 39:191–201.

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30. Robiller FC, Stumpe KDM, Kossmann T, et al. Chronic osteomyelitis of the femur: value of PET imaging. Eur Radiol 2000; 10:855–858. 31. Levine M, Fajadhyaksha A, Mont M. Osteonecrosis hip. E Med, October 2006. Accessed March 21, 2007. 32. Stark DD, Bradley WG. Magnetic Resonance Imaging, 3rd ed. St. Louis, Mosby, 1999. 33. Anderson SE, Steinbach LS, Tshering DW, et al. MR imaging of avascular nonunion before and after vascularized bone grafting. Skeletal Radiol 2005; 34:314–320. 34. Kassarajian A, Llopis E, Palmer WE. Distal clavicular osteolysis: MR evidence for subchondral fracture. Skeletal Radiol 2007; 36:17–22. 35. McDougali IR, Keeling CA. Complications of fractures and their healing. Semin Nucl Med 1988; 18:113–125. 36. Greenspan A. Orthopedic Imaging: A Practical Approach, 4th ed. Philadelphia, Lippincott Williams and Wilkins, 2004. 37. Deluca PA, Lindsey RW, Ruwe P. Refracture of bones of the forearm after the removal of compression plates. J Bone Joint Surg Am 1988; 70:1372–1376. 38. Moore TE, King AR, Travis AC, et al. Posttraumatic cysts and cystlike lesions of bone. Skeletal Radiol 1989; 18:93. 39. Papadimitriou NG, Christophorides J, Beslikas TA, et al. Posttraumatic cystic lesion following fracture of the radius. Skeletal Radiol 2004; 34:411–414.

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Muscle Injury and Sequelae Donald J. Flemming and Robert D. Boutin

PREVALENCE, EPIDEMIOLOGY, AND DEFINITIONS Injury of muscle, whether contusion, laceration, or strain, is one of the most frequently encountered injuries in athletes. Strain injury accounts for 90% of sports injuries of muscle and may result in significant disability.1 Muscle injuries are not limited to athletes, however, and the interpreting radiologist must be comfortable with recognizing their radiologic presentation. Normal muscle activity relies on innervation and perfusion; thus, injuries that result in denervation or decreased circulation will impair function.

ANATOMY Normal skeletal muscle function is dependent on intact muscle fibers, normal innervation, and intact blood flow. Skeletal muscle is composed of myofibers supported by organized connective tissue. Individual myofibers are surrounded by a delicate sheath called the endomysium. Tens to hundreds of myofibers are then surrounded by the perimysium. The epimysium is the connective tissue that surrounds the entire muscle belly. This ordered connective tissue network mechanically supports the contraction of individual cells into an organized force that is converted into motion. Individual muscles are composed of multiple motor units. Each motor unit contains either slow fibers (slow contraction but resistant to fatigue) or fast-twitch fibers (fast but less resistant to fatigue). The composition of fast and slow fibers in a given muscle is dependent on the muscle group and genetics. Muscle is attached to bone by a tendon. The tendon is formed at each end of a muscle from a condensation of connective tissue fibers. The tendon is then attached to bone via Sharpey’s fibers. Injury to the muscle-tendon-bone unit can occur at any level.

BIOMECHANICS Skeletal muscle biomechanics can be separated into various actions. Concentric contraction is defined as shortening of a muscle, such as biceps tightening with elbow 1022

flexion. Eccentric contraction (also known as lengthening) occurs when a muscle is lengthened during its contraction, such as in the triceps while lowering weights. Isometric exercise represents contraction of muscle without action shortening or lengthening of the total length of muscle. Eccentric exercise tends to result in less recruitment of motor units and is associated with less metabolic demand than concentric exercise. Strain injury is one of the most common sport injuries and represents a tear of fibers from excess force or tension placed on the muscle. Any muscle can sustain a strain injury, but muscles that contain a higher percentage of fasttwitch fibers or that cross two joints such as the hamstrings and rectus femoris are at higher risk.2 An important additional risk factor is prior injury. Finally, muscles subjected to eccentric forces are more likely to sustain tears than those used in concentric exercise.2 Tears tend to occur at the mechanically weakest point of the bone-tendon-muscle unit, and this can vary by age.3 For instance, muscle injuries are more common in the young and tendon tears are more common in the elderly. Strain injuries occur at the structurally weakest portion of the muscle, where muscle fibers join the tendon, also known as the myotendinous junction.4 The myotendinous junction is not a single point in a muscle but represents a continuum that stretches nearly the entire length of some muscles, such as a hamstring.5

PATHOLOGY Muscle injury can occur with ischemia, denervation, inflammation, infection, or physical force. In physical trauma, the healing process represents repair rather than regeneration; thus, a scar will be the end result of healing depending on the magnitude of the original injury.1 Healing of muscle is separated into three phases: destruction, repair, and remodeling.6 The destruction phase of healing is initiated with rupture of the muscle, which is followed by necrosis, hematoma, and inflammation. Once the destruction phase subsides, the gap created in the injured muscle is bridged by two processes: the regeneration of muscle fibers and the formation of scar tissue.6,7 The ability to regenerate muscle fibers decreases with

CHAPTER

KEY POINTS Increased muscle signal on T2-weighted MR images can be a nonspecific finding and requires correlation with the patient’s history. ■ Acute injury presents as increased signal intensity on T2-weighted or STIR MR images centered on the myotendinous junction. ■ Increased signal intensity can be seen normally in muscle for up to 1 hour after exercise. ■ Both lower extremities are imaged and the injured side is compared with the asymptomatic side to increase detection of subtle chronic injuries. ■ Ultrasonography is an excellent modality for detection of muscle herniation and acute muscle tear. ■ Correlate MR images with plain radiographs or CT if myositis ossificans is a diagnostic possibility. ■ Concern for tumor as a cause of intramuscular hematoma is increased if the bleeding is spontaneous in an elderly patient. Enhancing nodules in the periphery of a mass and a mass that does not become smaller with time should also alert the radiologist to the possibility of neoplasm. ■ A painful mass in the thigh musculature of a diabetic patient that shows streaky internal and peripheral enhancement should raise suspicion for diabetic muscle infarction. ■

age and is dependent on mechanical stress. The muscle regenerative process, however, directly competes with the formation of connective tissue scar. Connective tissue scarring is initially the mechanical weak link in the repair process, and reinjury from early mobilization or extensive scar formation can result in a true mechanical barrier that prevents regeneration of myofibers across a gap.8 Most muscle injuries do not result in excessive scar formation. The repair process must also be accompanied by revascularization and reinnervation of the injured muscle. It can take weeks for an injured muscle to return to preinjury level, which is why professional athletes are subjected to conditioning regimens to reduce the likelihood of injury.9

MANIFESTATIONS OF THE DISEASE Muscle Strain or Tear Magnetic Resonance Imaging Magnetic resonance imaging is considered the best modality to diagnose and characterize strain injuries of muscle. The imaging of a strain injury will be dependent on the severity and acuity of the injury. Evaluation of muscle injury should be performed in the axial plane and a plane longitudinal to the muscle using both T1-weighted imaging and a fluid-sensitive sequence such as short tau inversion recovery (STIR).3,10 Because muscle tears can occur in multiple synchronous locations, the entire length of the muscle should generally be imaged, so coil selection will be predicated on the size of the muscle in question. In the lower extremity, imaging of both legs is recommended. Some injuries, particularly those that are chronic, may be more readily detected if compared with the unaffected extremity.

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In the acute setting, fluid-sensitive sequences such as STIR or fat-suppressed T2-weighted sequences are the most important images for the detection of injury, with increased signal centered on the tear representing the pathology.11–15 Once the injury is visualized, the radiologist should attempt to characterize the extent of damage. The severity of the injury will dictate the extent of findings. In a grade 1 injury, increased signal is centered on the myotendinous junction, with fluid signal tracking into the adjacent muscle producing a feathered appearance (Fig. 41-1). Grade 2 injury represents a partial tear of the myotendinous junction and is distinguished from grade 1 injury by a wavy appearance of the myotendinous junction and the presence of a hematoma (Fig. 41-2).15 In grade 3 injury, the myotendinous junction is completed disrupted (Fig. 41-3). In grade 2 and grade 3 lesions, a hematoma may be confused for neoplasm.16 The presence of feathery edema extending away from the mass should favor a hematoma rather than tumor. Additional findings may include perifascial edema, which can be seen in up to 87% of acutely injured athletes.17 Although grading these lesions is important from a research perspective, in clinical practice it can be difficult to differentiate between grades of injury. MRI has been used to predict the time to recovery from injury, which is particularly important in elite athletes.18–22 The literature on this topic is somewhat contradictory, but, in general, the more extensive the injury, the more time it takes to recover. The imaging features of the injury that have an effect on prognosis include the length of injured muscle, the percentage of cross-sectional area of injury compared with normal muscle, and the presence of a gap and/or hematoma in the involved muscle. On follow-up imaging, increased signal intensity in the damaged muscle may be seen on T2-weighted MRI even without clinical symptoms or pain at the time of resumption of athletic activity. It is not clear if this finding indicates an increased risk of reinjury.22 Whereas most injuries occur in the central portion of a muscle, some tears may be centered at the epimysium between two muscles, such as the short head and long head of the biceps femoris.19,22 In the acute setting, increased signal intensity will still be seen but will be appreciated at the periphery of the involved muscle belly in cross section rather than in the center. In the chronic setting, a subtle area of focal low signal intensity will be visible in the periphery of the injured muscle (Fig. 41-4). Chronic injuries may be very hard to detect if the interpreting radiologist is not searching for their MRI manifestations. As stated previously, the affected extremity should be compared with the asymptomatic side. This comparison is most practical in the lower extremity. Chronic injuries present as subtle thickening of the myotendinous junction that is low in signal intensity on both T1- and T2-weighted images. The subtle thickening of the myotendinous junction may be accompanied by focal fatty atrophy in the injured muscle (Fig. 41-5).

Ultrasonography The ultrasound manifestations of acute muscle injury have been well described in the literature.19,23–25

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● Injury: Other Musculoskeletal Injuries

■ FIGURE 41-1

A, Grade 1 myotendinous injury. Axial, fat-suppressed, fast spin-echo, T2-weighted MR image demonstrating faint increased signal (arrowhead) in muscle adjacent to thickened myotendinous junction. B, Grade 1 myotendinous tear. Coronal, fat-suppressed, fast spin-echo T2-weighted MR image showing faint increased signal in muscle (arrowheads) adjacent to thickened myotendinous junction.

■ FIGURE 41-2

Coronal, fat-suppressed, fast spin-echo, T2-weighted MR image of hematoma (arrowhead) in grade 2 injury of rectus femoris.

■ FIGURE 41-3

Coronal, fat-suppressed, fast spin-echo MR image of anterior thigh. Complete disruption of the myotendinous injection is seen (arrowhead), indicating a grade 3 injury.

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■ FIGURE 41-4

A, Axial T1-weighted MR image of the thigh with low-signal-intensity thickening of the lateral aspect of the biceps femoris (arrowhead) representing chronic injury of the epimysium. B, Axial fat-suppressed, fast spin-echo, T2-weighted MR image of thigh. Lowsignal-intensity thickening of the fascia (arrowhead) at the lateral aspect of the biceps femoris representing chronic injury of the epimysium.

■ FIGURE 41-5

Axial T1-weighted MR image through the thighs. Chronic injuries are shown in the left rectus femoris (arrow) and vastus intermedius (arrowhead). Note the thickened myotendinous junction and focal increased signal because of focal fat atrophy.

Ultrasonography is an outstanding way to detect severe acute injuries on the playing field because of the availability of portable units utilizing linear high-frequency transducers. Despite being an excellent method for detecting acute muscle pathology, ultrasonography is not superior to MRI for global evaluation of muscle pathology, particularly nonacute and deep injuries.19,25 Normal muscle is heterogeneous in echotexture, with linear foci of bright echotexture representing fat and fascia interdispersed among relatively hypoechoic tissue of muscle fibers.23 Tendons and the myotendinous junction are hyperechoic structures with fine linear architecture visible at the ends of the muscle. The ultrasound appearance of a muscle injury is dependent on the acuity and extent of the injury. The ideal time to evaluate a muscle tear is between 2 and 48 hours from the time of injury.23 Prior to 2 hours, a hematoma may not be visible; and after 48 hours, a hematoma may no longer be contained at the site of injury. If the perimysium is disrupted, a localized hematoma may not be detectable, thus potentially decreasing the diagnostic yield of the examination. At the time of examination, the operator will be able to focus the evaluation on the point of maximal tenderness. Injuries typically present as a hypoechoic focus in the injured muscle (Fig. 41-6), although hyperacute injuries may be hyperechoic or not visible. With gentle pressure, free edges and disrupted fibers may be appreciated floating in a fluid collection (bell clapper sign).23,24 The

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● Injury: Other Musculoskeletal Injuries

■ FIGURE 41-7

Chronic muscle injury. Longitudinal ultrasound image shows hyperechoic scar (arrowheads) in muscle surrounding a small, resolving, linear hypoechoic hematoma (arrow). (Courtesy of Gina Allen, MD, University of Birmingham Hospitals, UK.)

■ FIGURE 41-6 Grade 2 injury. Longitudinal ultrasound image through vastus medialis showing hypoechoic hematoma (arrowheads) displacing normal fibrillar appearance of muscle. (Courtesy of Gina Allen, MD, University of Birmingham Hospitals, UK.)

identification of a hematoma and interrupted muscle fibers is critically important. Recovery is expected to take 1 to 2 weeks if the manifestations are limited to hematoma, but healing takes at least 4 to 6 weeks if a gap in muscle fibers is visible on examination. Scar presents as hyperechoic zones in muscle (Fig. 41-7).23

Hematoma Hematoma is a common consequence of muscle injury but may be confused with a neoplasm both clinically and by imaging, particularly if there is an equivocal or remote history of trauma. Most hematomas resorb spontaneously over the course of 6 to 8 weeks after trauma.

Radiography The findings are nonspecific and are limited to soft tissue swelling.

Magnetic Resonance Imaging The MRI appearance of a hematoma is dependent on the time between injury and imaging.26 Acute hematomas (hours to days old) are similar to muscle in signal intensity on T1-weighted images and lower in signal intensity than normal muscle on T2-weighted images.27 Prominent increased signal intensity can be seen on T2-weighted images adjacent to an acute hematoma (Fig. 41-8).

For subacute hematomas (1 week to 3 months old) the MRI presentation is variable but typically homogeneous increased signal intensity is seen on T1- and T2-weighted images.27 A high signal ring may surround an intermediate signal center in subacute hematomas (Fig. 41-9). Chronic hematomas (older than 3 months) show central increased signal intensity on all sequences surrounded by low signal intensity because of hemosiderin in the periphery of the hematoma.27 Differentiating a traumatic hematoma from hemorrhage in a neoplasm can be challenging. Extensive increased signal intensity in the soft tissues surrounding a mass on T2-weighted images suggests a hematoma but should not be relied on as the sole discriminating feature between hematoma and neoplasm. The presence of an enhancing nodule in the periphery of a hemorrhagic mass suggests a neoplasm as an underlying cause (Fig. 41-10). However, this finding may be seen in the setting of organizing hematoma as well, contributing to the confusion that can occur when trying to establish a definitive diagnosis based on imaging alone. On follow-up examination, hematomas typically become smaller with time, although enlargement of a chronic hematoma can rarely occur. The presence of enhancing nodules or enlargement of an intramuscular mass on follow-up imaging should alert the radiologist to the possibility of neoplasm, and biopsy should be recommended in this setting.

Ultrasonography The ultrasound appearance of an intramuscular hematoma depends on the age of the lesion and its location and size. In the immediate postinjury setting, the hematoma may appear hyperechoic relative to muscle and then become hypoechoic within hours.23 Fluid-fluid

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■ FIGURE 41-8

A, Axial, fat-suppressed, fast spin-echo, T2-weighted MR image through the thigh. An acute hematoma with intermediate signal intensity (arrowheads) is seen anterior to an injured rectus femoris. B, Sagittal, T1-weighted MR image through the thigh. An acute hematoma (arrowheads) showing intermediate signal intensity is seen anterior to the rectus femoris.

■ FIGURE 41-9

A, Axial, noncontrast, T1-weighted MR image through the thigh. A subacute hematoma is shown in the vastus intermedius that has high signal intensity in the periphery. B, Coronal, fat-suppressed, fast spin-echo, T2-weighted MR image of thigh. Hematoma is intermediate in signal intensity (arrowheads) with slightly more hyperintense signal in periphery. Note the extensive edema in the muscle adjacent to the hematoma.

1027

1028 P A R T O N E

● Injury: Other Musculoskeletal Injuries

■ FIGURE 41-10

A, Inflammatory malignant fibrous histiocytoma in a 48-year-old man. Sagittal, nonenhanced, T1-weighted MR image through the thigh. Mass with internal high signal intensity (arrow) from hemorrhagic necrosis of tumor in adductor magnus. Note the low signal intensity of the nodule at the superior portion of the mass (arrowhead). B, Sagittal STIR MR image through tumor (arrow). The mass shows heterogeneous increased signal intensity with edema in the adjacent muscle (red asterisks). C, Sagittal, fat-suppressed, T1-weighted MR image through the tumor after the intravenous administration of gadolinium. The nodule at the superior aspect of the lesion enhanced.

levels may be visible in the collection, and with time the hematoma will become anechoic. Blood may dissect outside the muscle, and intermuscular fluid collections may be seen.

Myositis Ossificans Myositis ossificans, also known as heterotopic ossification, is bone formation that occurs in the soft tissue usually as a result of trauma, although genetic, neurogenic, and idiopathic causes have also been described.28 Patients are typically in their first and second decades of life, and

the thigh and buttock musculature are the most common locations for presentation. After trauma, the injured soft tissue presumably releases cytokines that signal nearby undifferentiated mesenchymal cells to differentiate into osteoblasts or chondroblasts. A painful mass is clinically evident. Pathologically, fibrovascular granulation tissue is seen that is followed by the formation of bone and occasionally cartilage. This formation of soft tissue ossification histologically duplicates that of intramembranous bone. The mature mass may eventually contain fatty or red marrow surrounded by neocortex. The radiologist plays a critical

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role in the diagnosis of this condition because the histology may simulate a sarcoma early in the process. Heterotopic ossification may also be seen in patients who sustain neurologic injury either from closed-head or spinal cord injury.29,30 Twenty to 25 percent of spinal cord–injured patients, particularly if the injury is at the low cervical or high thoracic levels, develop ossification in the soft tissues. Only 10% to 20% of patients with closedhead injury develop the same complication. Ossification is most commonly seen about the hips, followed by the knees and elbows. Limited range of motion may be seen in up to 35% of neurologically impaired patients secondary to periarticular ossification. The etiology is not known, but possible causes include venous stasis, edema, and trauma from physical therapy.31

Radiography Initially, a soft tissue mass may be apparent. The first radiographic indication of heterotopic bone formation is flocculent densities in the mass, which may be seen 11 days to 6 weeks after the injury. In the ensuing weeks, the flocculent densities enlarge and become more confluent, resulting in peripheral density in the mass. If the mass directly abuts bone, periosteal reaction may be visible. Eventually, peripheral ossification will result in an eggshell appearance of the mass with full maturation into bone occurring over 5 to 6 months after the initial insult. Recognition of this pattern of peripheral ossification is critical because this pattern is rarely seen in soft tissue sarcomas. Recognition of a lucent band between the ossification and underlying bone will guide the radiologist away from a diagnosis of surface osteosarcoma (Fig. 41-11). The mass may then shrink and even completely resorb, particularly in young patients.

Magnetic Resonance Imaging The MRI findings depend on the histologic stage of the lesion.32,33 In the acute setting, the mass is typically difficult to appreciate on T1-weighted images and has high signal intensity on fluid-sensitive sequences. The mass may present as dramatic increased signal intensity on T2-weighted images, raising the concern for sarcoma. However, extensive perilesional high signal intensity in the muscle and soft tissues on fluid-sensitive sequences should alert the radiologist to the diagnostic possibility of myositis ossificans rather than sarcoma because this is an unusual occurrence in the setting of neoplasm. Peripheral enhancement may be seen in the mass after the intravenous administration of gadolinium (Fig. 41-12). On occasion, fluid-fluid levels may be seen in the central portion of the lesion. The imaging features change as the lesion matures. A curvilinear band of low signal intensity on both T1- and T2-weighted images in the periphery of the mass reflects ossification. Perilesional edema gradually resolves. Increased signal on T1-weighted images may eventually be seen in the central portion of the mass, reflecting the development of fatty marrow. The importance of correlating the MR images with radiography cannot be overemphasized. Mineralization and ossification that are clearly evident on radiographs may be very difficult to appreci-

■ FIGURE 41-11

Lateral view of the femur shows heterotopic ossification projecting over the anterior surface of the femoral diaphysis.

ate on MRI, leading to false concern for a neoplastic cause for the findings on cross-sectional imaging.

Multidetector Computed Tomography Heterotopic ossification is ideally assessed by CT.28 This modality is particularly helpful in the early stages of the disorder when ossification may be subtle or not apparent on radiography. CT readily shows the peripheral nature of mineralization in this condition (Fig. 41-13). As the mass matures, it may demonstrate fat attenuation centrally secondary to marrow. Additionally, focal atrophy of the muscle adjacent to the mass may be seen. CT may also be helpful in visualizing a separation between soft tissue ossification and underlying bone when radiography cannot demonstrate this important feature that distinguishes myositis ossificans from surface osteosarcoma.

Nuclear Medicine Bone scintigraphic agents will show nonspecific uptake in the soft tissues at the site of injury in all three phases.

Delayed-Onset Muscle Soreness Delayed-onset muscle soreness is a clinical syndrome that many readers will have experienced that consists of pain on palpation or motion of muscles after activity.34 Although the syndrome is commonly encountered, the etiology remains unclear. Patients who experience this syndrome are usually unaccustomed to exercise and develop pain

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● Injury: Other Musculoskeletal Injuries

■ FIGURE 41-12

A, Myositis ossificans in a 16-year-old boy who presented for evaluation of a painful mass in his anterior thigh. Coronal, T1-weighted MR image through the thigh shows a subtle mass in the vastus lateralis (arrowheads). B, Coronal, STIR MR image through the thigh shows a high-signal-intensity mass (arrowheads) with extensive perilesional edema. The mass is bounded by a band of low signal intensity. C, Coronal, fatsuppressed, T1-weighted MR image after the intravenous administration of gadolinium shows heterogeneous but predominantly peripheral enhancement of the mass (arrowheads). D, Anteroposterior radiograph of the femur shows peripheral ossification in the mass, confirming the diagnosis of myositis ossificans (arrows).

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■ FIGURE 41-13

A, Anteroposterior radiograph of the humerus shows ossifying mass (arrows) in the soft tissues adjacent to the humerus. B, Axial CT image through the upper arm shows mass in the triceps (arrows). The mass demonstrates the typical zonal ossification pattern.

that can be severe and disabling approximately 12 hours after intense activity. The pain peaks at 48 to 72 hours after exercise, and muscles that are exposed to lengthening forces such as the quadriceps in runners and the triceps when lowering weights (also known as eccentric contractions) are at more risk than muscles exposed to concentric exercise.35 The onset of pain is usually accompanied by a rise in the serum creatine kinase concentration.36 Eccentric or lengthening muscle action is associated with lower metabolic demands than shortening muscle action of concentric exercise, and it appears that, histologically, this painful syndrome is a strain injury induced by mechanical forces rather than caused by an ischemic or metabolic etiology.37 However, the role of free radicals in delayed-onset muscle soreness is being explored.38 The clinical presentation and history are usually sufficient to establish the diagnosis. It is not uncommon, however, for imaging to be performed in the setting of delayed-onset muscle soreness because the clinical presentation can be dramatic and the radiologist must therefore be familiar with its radiologic manifestations. The research in this field has been somewhat hampered by nonstandard exercise routines, varied imaging parameters, and the normal physiologic increase in T2-weighted signal intensity in exercised muscle. Regardless, the basic imaging manifestations of this syndrome are well accepted at this time. The MRI findings of diffuse edema in a muscle group are not specific for delayed-onset muscle soreness. If a

patient is imaged within 1 hour of exercise, the muscles involved in that activity may demonstrate increased signal secondary to shifts in extracellular water content that normally occur with exercise.

Magnetic Resonance Imaging Magnetic resonance imaging is superior to other modalities for demonstrating the extent of muscle involvement. Muscle groups affected by delayed-onset muscle soreness are diffusely high in signal on fluid-sensitive sequences such as STIR or fat-suppressed T2-weighted images (Fig. 41-14).11,39 Peripheral increased signal and perifascial edema may also be seen, but diffuse increased muscle signal is a better predictor of muscle injury. The best correlations with pain on imaging include the volume of muscle involved and volume of muscle edema.39 Muscle that demonstrated increased signal on STIR images in one study showed ultrastructural damage of sarcomeres on electron microscopy after biopsy in otherwise normal volunteers.37 Interestingly, there was no correlation between areas of delayed-onset muscle soreness clinically and increased signal intensity on T2-weighted images in this same report.

Ultrasonography Ultrasonography has no role in the evaluation of delayedonset muscle soreness. It has neither sufficient sensitivity nor specificity for clinical usefulness.

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■ FIGURE 41-14

A, A 43-year-old woman presented with severe pain in her posterior upper arm after an intense weightlifting workout. Axial, STIR MR image shows diffuse edema in the triceps muscle belly typical of delayed-onset muscle soreness. B, Sagittal, fat-suppressed, fast spin-echo, T2weighted MR image through the upper arm shows diffuse increased signal in triceps and perifascial edema (arrowheads).

Muscle Herniation Muscle herniation occurs when muscle protrudes in a defect in the surrounding epimysium. It often is imaged because of a clinical concern for neoplasm. A fascial defect can be seen after penetrating trauma, but more commonly muscle herniation occurs from increased intracompartmental pressures, leading to protrusion of muscle through a relative area of weakness. Fascial weakness and resulting herniation can be a congenital condition.40 A mass that is only present or increases in size with active muscle contraction is the typical presenting history. On occasion, the mass may actually become smaller, with active contraction of the extremity. The mass may be painless or be associated with pain, cramping, and tenderness.41,42 Muscle herniation usually occurs in the lower extremity and rarely is seen in the thigh or upper extremity.43,44 The most common muscle associated with herniation is the tibialis anterior,45 but herniation has also been described in the extensor digitorum longus,46 peroneus brevis,47 peroneus longus,48 and gastrocnemius.49

Magnetic Resonance Imaging The MRI findings of uncomplicated muscle herniation can be subtle. A marker placed by the technologist over the palpable mass at the time of examination can dramatically aid in the detection and characterization of this abnormality. The findings are typically limited to an abnormal peripheral contour and outward bulging of the muscle (Fig. 41-15).50 The protruding muscle usually has the same signal characteristics as surrounding muscle unless the herni-

ated segment is incarcerated or ischemic in which case it shows increased T2-weighted signal. Imaging of the hernia with and without contraction of the affected muscle may help increase the conspicuity of the hernia, but images may be degraded by motion artifact with this technique. Motion artifact can be minimized by using fast scanning gradient-echo techniques.50 Prescanning exercise to induce increased intracompartmental pressure has been used by some investigators to increase the likelihood of hernia detection. Plantarflexion or dorsiflexion of the ankle may also lead to increased detection of fascial defects and hernias. The fascial defect can be directly visualized and characterized in many cases.

Multidetector Computed Tomography Muscle hernia can be detected by CT examination. The diagnosis is established when muscle is visualized protruding through a fascial defect (Fig. 41-16). Multiplanar reconstruction may assist in characterizing the extent of fascial defect. As in MRI, the examination may be obtained during active contraction of the muscle group in question or after pre-examination exercise if this is clinically known to result in accentuation of a hernia.

Ultrasonography Ultrasonography is an outstanding modality to allow detection and characterization of muscle hernias.41,43,51 High-frequency linear transducers should be utilized after the mass is palpated and the overlying skin is marked. The near-field focus should be optimized, and care must

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■ FIGURE 41-15

A, A 28-year-old man presented with a palpable mass and a muscle hernia in his lateral lower leg. Coronal, T1weighted MR image through the lower leg shows subtle contour abnormality under the marker in the lateral aspect of the peroneus brevis muscle. B, Axial T1-weighted MR image at level of hernia. The protrusion is difficult to detect.

mushroom-shaped hypoechoic mass if it extends over the free edge of the fascial defect responsible for the hernia. One of the distinct advantages of ultrasonography is the opportunity to examine the development or accentuation of the hernia in real time while the patient contracts and relaxes the affected muscle. The ability to show this finding to the patient during the examination contributes to reassurance in the setting of concern for neoplasm. Small hernias may be very difficult to appreciate on ultrasound interrogation. Employing 3D sonographic techniques can aid in the detection of subtle muscle hernias.52

Compartment Syndrome

■ FIGURE 41-16

Axial CT scan through the lower leg showing contour abnormality (arrowhead) at the anterolateral aspect of the extensor digitorum longus muscle representing a muscle hernia.

be employed to use light pressure to avoid reducing the hernia during the examination. Muscle hernias present as a contour abnormality through the overlying fascia (Fig. 41-17). Fascia is visualized as a thin echogenic structure, and the herniated muscle may be appreciated as a

Compartment syndrome is the clinical presentation that occurs when pressures in a muscle-fascial compartment are excessive, leading to impaired vascular and lymphatic flow.53–55 Ischemia in the compartment may then lead to capillary leaking and increased interstitial edema that results in a further rise in intracompartmental pressure. If the compartment is not decompressed, the ensuing vicious ischemic cycle may lead to permanent fibrosis and disability known as Volkmann’s ischemic contracture. While the symptoms predominate in the affected extremity, ischemia in muscle may lead to systemic disease, including rhabdomyolysis, renal failure, and death. The majority of cases of compartment syndrome occur in the setting of trauma with factors such as hypotension, compromised venous return, and compartment fibrosis contributing to onset and severity of findings.

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● Injury: Other Musculoskeletal Injuries

of neurovascular structures, and inaccurate or imprecise measurements. An effective nonradiologic, noninvasive technique for assessing chronic exertional compartment syndrome is near-infrared spectroscopy. In a recent study, this technique was shown to be superior to MRI and comparable to invasively obtained intracompartmental pressures.60

Magnetic Resonance Imaging

■ FIGURE 41-17

Transverse ultrasound image through muscle herniation in the distal lower leg. A bulge is seen in the anterior contour (arrowheads) of the tibialis anterior when the patient is standing. (Courtesy of Gina Allen, MD, University of Birmingham Hospitals, UK.)

Compartment syndrome is clinically subdivided into acute and chronic forms of the disorder. Acute compartment syndrome is usually seen in the setting of trauma. Fracture is the most common injury associated with compartment syndrome. Any form of trauma leading to hematoma can produce compartment syndrome, including muscle rupture.56 Compartment syndrome can be induced by extravasation of contrast agent during power injection in an extremity. Therefore, radiologists must be attuned to the clinical manifestations of compartment syndrome after inadvertent misadministration of contrast agents. The main symptom of acute compartment syndrome is pain, particularly pain that is unexpectedly severe for the injury sustained.57 Pain may manifest as throbbing, aching, and tightness that worsens with palpation or passive motion of the affected muscle group. The arterial pulses usually remain palpable, but venous and lymphatic drainage are impaired. Impairment of motor or sensory nerve function is a late finding. Chronic compartment syndrome can be separated clinically into exertional and nonexertional causes. Exertion may lead to up to 20% enlargement of the exercised muscle volume.58 If this enlargement occurs in a noncompliant compartment, pain may ensue. The most common sites of exertional compartment syndrome are in the anterior lower leg in runners, followed by the thigh, forearm, and foot in other athletes. The clinical diagnosis of compartment syndrome is typically confirmed by direct measurement of pressures after placement of a catheter into the affected compartment. Normal compartment pressures should not exceed 15 to 20 mm Hg or 30 mm Hg immediately after the completion of exercise when trying to establish the diagnosis of chronic compartment syndrome.59 Direct measurement of pressures is the gold standard for diagnosing compartment syndrome but is not without problems, including erroneous placement of the catheter, damage

Noninvasive confirmation of compartment syndrome may be established by near-infrared spectroscopy or suggested by MRI.60 MRI offers the opportunity to directly evaluate the compartment in question to determine if a hematoma or mass is present to account for elevated pressures in the acute setting and may also be useful for follow-up evaluations. The MR manifestations of compartment syndrome are nonspecific and depend on the chronicity of symptoms.61 In the acute setting, hyperintense T2-weighted signal may be present in the muscle of affected compartment; the affected muscles may be enlarged, and muscle herniation from increased compartment pressures may be seen; and, finally, a hematoma may be seen in the affected compartment. Findings indicating more chronic changes may include (1) fatty atrophy of the muscle with concomitant increased signal intensity on T1-weighted images; (2) low signal intensity in the involved muscle on both T1- and T2-weighted images secondary to fibrosis or calcification; (3) decreased size of the involved muscle; and (4) thickening of the surrounding fascia secondary to fibrosis. Intravenous contrast-enhanced imaging of a patient with suspected compartment syndrome may show either increased or decreased enhancement of muscle in the affected compartment. Decreased or absent enhancement is an indication of severe ischemia and may indicate devitalized tissue. MRI of a symptomatic extremity before and after exercise may help establish the diagnosis of chronic compartment syndrome. In this setting, the muscle in the abnormal compartment will show higher signal on T2weighted images than surrounding normal muscle.62,63

Diabetic Muscle Infarction Diabetic muscle infarction is an important entity to recognize because it is often confused with sarcoma or lymphoma.64,65 This diagnosis should be considered when a diabetic patient presents with the history of the sudden onset of severe pain, with or without palpable mass, in a lower extremity involving either the thigh or calf musculature. The patients typically are poorly controlled insulin-dependent diabetics with other sequelae of diabetic microangiopathy, including nephropathy, retinopathy, and neuropathy. The differential diagnosis includes abscess, pyomyositis, deep vein thrombosis, necrotizing fasciitis, hematoma, and neoplasm.64 Most of the differential diagnoses can be excluded by clinical and laboratory evaluation. The patients with diabetic muscle infarction do not have an elevated white blood cell count or fever. The erythrocyte sedimentation rate is usually normal, and creatine kinase levels may either be normal or elevated. One important differentiating feature is the recurrent nature of diabetic muscle infarction that can be appreciated in

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some patients. Up to one half of patients may experience a recurrence in the same or opposite extremity.64

are the lack of anechoic foci in the lesion and the lack of motion or swirling of fluid or debris with compression.66

Magnetic Resonance Imaging

Denervation

Magnetic resonance imaging remains the most commonly employed imaging modality to investigate the painful extremity in these patients.64–66 The affected muscle is usually enlarged. The ischemic portion of the muscle is isointense to normal tissue on T1-weighted images and shows hyperintense signal on fluid-sensitive sequences. In one case report, the involved muscle showed a hyperintense signal on T1-weighted images because of hemorrhage in the affected tissue. Additional findings that may be seen on T2-weighted images include perifascial and subcutaneous edema. The appearance on postcontrast images is variable, ranging from diffuse enhancement to rim enhancement. Peripheral enhancement with or without streaky serpentine central enhancement is the most common appearance on fat-suppressed, T1-weighted images after the intravenous administration of a contrast agent (Fig. 41-18). Serpentine foci of enhancing and nonenhancing tissue are highly suggestive of muscle infarction and help differentiate this process from other diagnostic considerations, such as neoplasm and abscess.65,67

Muscle function is dependent on normal innervation. Denervation can have numerous causes, including blunt and penetrating trauma, neuropathy, and entrapment syndromes; but regardless of the etiology, the radiologic manifestations are the same.

Ultrasonography The literature describing the appearance of diabetic muscle infarction on ultrasonography is very limited and somewhat inconsistent.66 The most common appearance is that of a well-marginated focus of hypoechogenicity in muscle that contains linear foci consistent with muscle fibers extending through the lesion. Important features that help differentiate diabetic muscle infarction from abscess

■ FIGURE 41-18

Magnetic Resonance Imaging The effect of denervation on the MRI appearance of muscle is dependent on the time from injury. Injuries can be classified as acute (1 year).68 MRI findings correlate well with electromyography, which is the gold standard for the evaluation of denervation states.69–71 MRI is not as sensitive for denervation when compared with electromyography but offers the ability to assess deep muscles not accessible to electromyographic needles and can assess for masses that might be responsible for nerve compression. Additionally, MRI can be used when electromyography is either contraindicated or more difficult to perform, such as in coagulopathic patients or children. After acute denervation, a muscle will demonstrate prolonged T1- and T2-weighted characteristics, resulting in increased signal intensity on fat-suppressed, fluid-sensitive sequences.68,70,72 The exact cause for the T2 prolongation in human muscle is unknown, but in animal models there is an increase in the ratio of extracellular to intracellular water.70 The resulting “edema”-like pattern is best appreciated on STIR sequences. The timing of the appearance of edema after acute denervation is variable

A, A 51-year-old diabetic man had a painful mass in the anteromedial distal thigh and muscle infarct. Axial, fast spin-echo, T2-weighted MR image through the distal thigh shows a mass (arrowheads) in the vastus medialis that mimics a sarcoma. However, note the extensive perilesional intramuscular edema. B, Axial, postcontrast, fat-suppressed, T1-weighted MR image of the distal thigh shows peripheral enhancement (arrowheads) of the ischemic muscle in the vastus medialis. C, Sagittal, postcontrast, fat-suppressed, T1-weighted MR image through the ischemic muscle (arrowheads) shows streaky internal enhancement typical of diabetic muscle infarction.

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■ FIGURE 41-19 A, Axial, fat-suppressed, proton density–weighted MR image of the shoulder shows a paralabral cyst (arrowhead) extending into the spinoglenoid notch. Mass effect on the nerve has resulted in subacute atrophy of the infraspinatus muscle that demonstrates diffuse increased signal (arrows) as a result of denervation. B, Coronal, T1-weighted MR image of the shoulder shows the paralabral cyst (arrowhead) at the level of the spinoglenoid notch. Increased signal indicating fatty atrophy from denervation is seen in the infraspinatus muscle (arrows).

and dependent on the muscle group. Edema may be visible as early as in 4 days but typically is appreciable within 3 weeks of an injury. In the subacute setting, muscle will demonstrate increased signal intensity on both T1- and T2-weighted images (Fig. 41-19).68,70,72 This increased signal intensity in muscle on T1-weighted images directly correlates with fatty atrophy and is generally an indication of irreversible damage. However, fatty atrophy in the subacute setting may be reversible if the muscle can be successfully reinnervated.68 In fact, resolution of atrophy is a useful imaging marker of successful intervention on follow-up imaging after surgery. In the setting of chronic nerve injury, muscle will typically demonstrate marked increased signal intensity on T1-weighted images from diffuse extensive fatty atrophy.68,70,72 On occasion, the denervated muscle may paradoxically hypertrophy and present clinically as a mass.71 This can be seen because of excessive accumulation of fat in the muscle (pseudohypertrophy) or because part of the muscle may remain innervated (intact functional motor unit from crossed innervation) and these fibers may hypertrophy.

Multidetector Computed Tomography The utility of MDCT lies primarily in the assessment of subacute to chronic denervation because this modality relies on the detection of fat atrophy. The finding of fatty atrophy on CT is not sensitive or specific for denervation and may be seen in a variety of neuromuscular disorders.

What the Referring Physician Needs to Know ■ ■

■

Whether an injury is present and if so, its severity In the acute trauma setting, determination of the presence of a hematoma, interruption of muscle fibers, and injury extending through greater than 50% of a muscle in cross section, which are indicators of delayed recovery Whether a mass lesion is present in the setting of compartment syndrome or entrapment neuropathy

SUGGESTED READINGS Armfield DR, Kim DH, Towers JD, et al. Sports-related muscle injury in the lower extremity. Clin Sports Med 2006; 25: 803–842.

Boutin RD, Fritz RC, Steinbach LS. Imaging of sports-related muscle injuries. Magn Reson Imaging Clin North Am 2003; 11:341–347. Peetrons P. Ultrasound of muscles. Eur Radiol 2002; 12:35–43.

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REFERENCES 1. Jarvinen TA, Jarvinen TL, Kaariainen M, et al. Muscle injuries: biology and treatment. Am J Sports Med 2005; 33:745–764. 2. Anderson K, Strickland SM, Warren R. Hip and groin injuries in athletes. Am J Sports Med 2001; 29:521–533. 3. Boutin RD, Fritz RC, Steinbach LS. Imaging of sports-related muscle injuries. Magn Reson Imaging Clin North Am 2003; 11:341–371. 4. Garrett WE Jr, Nikolaou PK, Ribbeck BM, et al. The effect of muscle architecture on the biomechanical failure properties of skeletal muscle under passive extension. Am J Sports Med 1987; 15:448–454. 5. Hughes CT, Hasselman CT, Best TM, et al. Incomplete, intrasubstance strain injuries of the rectus femoris muscle. Am J Sports Med 2004; 32:710–719. 6. Kalimo H, Rananen J, Jarvinen M. Muscle injuries in sports. Baillieres Clin Orthop 1997; 2:1–24. 7. Hurme T, Kalimo H, Lehto M, Jarvinen M. Healing of skeletal muscle injury: an ultrastructural and immunohistochemical study. Med Sci Sports Exerc 1992; 23:801–810. 8. Jarvinen M. Healing of a crush injury in rat striated muscle: 2. A histologic study of the effect of early immobilization on the repair processes. Acta Pathol Microbiol Scand [A] 1975; 83:269–282. 9. Verrall GM, Slavotinek JP, Barnes PG. The effect of sports specific training on reducing the incidence of hamstring injuries in professional Australian Rules football players. Br J Sports Med 2005; 39:363–368. 10. Armfield DR, Kim DH, Towers JD, et al. Sports related muscle injury in the lower extremity. Clin Sports Med 2006; 25:803–842. 11. Fleckenstein JL, Weatherall PT, Parkey RW, et al. Sportsrelated muscle injuries: evaluation with MR imaging. AJR Am J Roentgenol 1989; 172:793–798. 12. Greco A, McNamara MT, Escher RM, et al. Spin-echo and STIR MR imaging of sports-related muscle injuries at 1.5T. J Comput Assist Tomogr 1991; 15:994–999. 13. DeSmet AA. Magnetic resonance findings in skeletal muscle tears. Skeletal Radiol 1993; 22:479–484. 14. Steinbach LS, Fleckenstein JL, Mink JH. Magnetic resonance imaging of muscle injuries. Orthopedics 1994; 17:991–999. 15. Palmer WE, Kuong SJ, Elmadbouh HM. MR imaging of myotendinous strain. AJR Am J Roentgenol 1999; 173:703–709. 16. Temple HT, Kuklo TR, Sweet DE, et al. Rectus femoris muscle tear appearing as a pseudotumor. Am J Sports Med 1998; 24:544–548. 17. De Smet AA, Best TM. MR imaging of the distribution and location of acute hamstring injuries in athletes. AJR Am J Roentgenol 2000; 174:393–399. 18. Pomeranz SJ, Heidt RS Jr. MR imaging in the prognostication of hamstring injury: work in progress. Radiology 1993; 189:897–900. 19. Connell DA, Schneider-Kolsky ME, Having JL. Longitudinal study comparing sonographic and MRI assessments of acute and healing hamstring injuries. AJR Am J Roentgenol 2004; 183:975–984. 20. Slavotinek JP, Verrall GM, Fon GT. Hamstring injury in athletes: using MR imaging measurements to compare extent of muscle injury with amount of time lost from competition. AJR Am J Roentgenol 2002; 179:1621–1628. 21. Verrall GM, Slavotinek JP, Barnes PG, Fon GT. Diagnostic and prognostic value of clinical findings in 83 athletes with posterior thigh injury. Am J Sports Med 2003; 31:969–973. 22. Cross TM, Gibbs N, Huoang MT, et al. Acute quadriceps muscle strains: magnetic resonance imaging features and prognosis. Am J Sports Med 2004; 32:710–719. 23. Peetrons P. Ultrasound of muscles. Eur Radiol 2002; 12:35–43. 24. Lee JC, Healy J. Sonography of lower limb muscle injury. AJR Am J Roentgenol 2004; 182:341–351. 25. Megliola A, Eutropi F, Scorzelli A, et al. Ultrasound and magnetic resonance imaging in sports-related muscle injuries. Radiol Med 2006; 111:836–845. 26. Sundaram M, McLeod RA. MR imaging of tumor and tumorlike lesions of bone and soft tissue. AJR Am J Roentgenol 1990; 155:817–824. 27. Rubin JI, Gomori JM, Grossman RI, et al. High-field MR imaging of extracranial hematomas. AJR Am J Roentgenol 1987; 148:813–817.

28. McCarthy EF, Sundaram M. Heterotopic ossification: a review. Skeletal Radiol 2005; 34:609–619. 29. Damanski M. Heterotopic ossification in paraplegia. J Bone Joint Surg Br 1961; 43:286–299. 30. Botte MJ, Keenan MAE, Abrams RA, et al. Heterotopic ossification in neuromuscular disorders. Orthopedics 1997; 20:335–341. 31. Myositis ossificans and heterotopic bone. In Milgram JW. Radiologic and Histologic Pathology of Nontumorous Diseases of Bones and Joints. Northbrook Publishing, 1990, p 454. 32. DeSmet AA, Norris MA, Fisher DR. Magnetic resonance imaging of myositis ossificans: analysis of seven cases. Skeletal Radiol 1992; 21:503–507. 33. Shirkhoda A, Armin AR, Bis KG, et al. MR imaging of myositis ossificans: variable patterns at different stages. J Magn Reson Imaging 1995; 5:287–292. 34. Armstrong RB. Mechanisms of exercise-induced delayed-onset muscle soreness: a brief review. Med Sci Sports Exerc 1984; 16:529–538. 35. Shellock FG, Fukunaga T, Mink JH, Edgerton VR. Acute effects of exercise on MR imaging of skeletal muscle: concentric vs eccentric actions. AJR Am J Roentgenol 1991; 156:765–768. 36. Friden J, Sfakianos PN, Hargens AR. Blood indices of muscle injury associated with eccentric muscle contractions. J Orthop Res 1989; 7:142–145. 37. Nurenberg P, Giddings CJ, Stray-Gundersen J, et al. MR imagingguided muscle biopsy for correlation of increased signal intensity with ultrastructural change and delayed-onset muscle soreness after exercise. Radiology 1992; 184:865–869. 38. Close GL, Ashton T, McArdle A, MacLaren DPM. The emerging role of free radicals in delayed onset muscle soreness and contraction induced muscle injury. Comp Biochem Physiol A Mol Integr Physiol 2005; 142:257–266. 39. Evans GFF, Haller RG, Wyrick PS, et al. Submaximal delayed-onset muscle soreness: correlations between MR imaging findings and clinical measures. Radiology 1998; 208:815–820. 40. Braunstein JT, Crues JV 3rd. Magnetic resonance imaging of hereditary hernias of the peroneus longus muscle. Skeletal Radiol 1995; 24:601–604. 41. Bianchi S, Abdelwahab IF, Mazzola CG. Sonographic evaluation of muscle herniation. J Ultrasound Med 1995; 14:357–360. 42. Burg D, Schnyder H, Buchmann R, Meyer VE. Effective treatment of a large muscle hernia by local botulinum toxin. Handchir Mikrochir Plast Chir 1999; 31:75–78. 43. Kendi TK, Altinok D, Erdal HH, Kara S. Imaging in the diagnosis of symptomatic forearm muscle herniation. Skeletal Radiol 2003; 32:364–366. 44. Roberts JO, Regan PJ, Dickinson JC, Bailey BN. Forearm muscle herniae and their treatment. J Hand Surg [Br] 1989; 14:319–321. 45. Siliprandi L, Martini G, Chiarelli A, et al. Surgical repair of an anterior tibialis muscle hernia with Mersilene mesh. Plast Reconstr Surg 1993; 91:154–157. 46. Goldberg HC, Comstock GW. Herniation of muscles of the leg. War Med 1944; 5:365–367. 47. Sherry RH. Herniation of peroneus brevis muscle: report of a case. Bull Hosp Jt Dis 1942; 3:69–72. 48. Berglund HT, Stocks GW. Muscle hernia in a recreational athlete. Orthop Rev 1993; 22:1246–1248. 49. Alhadeff J, Lee CK. Gastrocnemius muscle herniation at the knee causing peroneal nerve compression. Spine 1995; 20:612–614. 50. Mellado JM, Perez del Palomar L. Muscle hernias of the lower leg: MRI findings. Skeletal Radiol 1999; 28:465–469. 51. Beggs I. Sonography of muscle hernias. AJR Am J Roentgenol 2003; 180:395–399. 52. Gokhale S. Three-dimensional sonography of muscle hernias. J Ultrasound Med 2007; 26:239–242. 53. Jobe MT. Compartment syndromes and Volkmann contracture. In Canale ST (ed). Campbell’s Operative Orthopedics. St. Louis, Mosby, 1998, pp 3661–3674. 54. Mubarak SJ, Pedowitz RA, Hargens AR. Compartment syndromes. Clin Orthop Relat Res 1989; 3:36–40.

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55. Bong MR, Polatsch DB, Jazrawi LM, Rokito AS. Chronic exertional compartment syndrome: diagnosis and management. Bull Hosp Jt Dis 2005; 62:77–84. 56. Mendelson S, Mendelson A, Holmes J. Compartment syndrome after acute rupture of the peroneus longus in a high school athlete. Am J Orthop 2003; 32:510–512. 57. Whitesides TE, Heckman MM. Acute compartment syndrome: update on diagnosis and treatment. J Am Acad Orthop Surg 1996; 4:209–218. 58. Eisele SA, Sammarco GJ. Chronic exertional compartment syndrome. Instr Course Lect 1993; 42:213–217. 59. Pedowitz RA, Hargens AR, Mubarak SJ, Gershuni DH. Modified criteria for the objective diagnosis of chronic compartment syndrome. Am J Sports Med 1990; 18:35–40. 60. van den Brand JG, Nelson T, Verleisdonk EJ, van der Werken C. The diagnostic value of intracompartmental pressure measurement, magnetic. Am J Sports Med 2005; 33:699–704. 61. Rominger MB, Lukosch CJ, Bachmann GF. MR imaging of compartment syndrome of the lower leg: a case control study. Eur Radiol 2004; 14:1432–1439. 62. Verleisdonk EJ, van Gils A, van der Werken C. The diagnostic value of MRI scans for the diagnosis of chronic exertional compartment syndrome of the lower leg. Skeletal Radiol 2001; 30:321–325. 63. Eskelin MK, Lötjönen JM, Mantysaari MJ. Chronic exertional compartment syndrome: MR imaging at 0.1 T compared with tissue pressure measurement. Radiology 1998; 206:305–307. 64. Aboulafia AJ, Monson DK, Kennon RE. Clinical and radiological aspects of idiopathic diabetic muscle infarction. J Bone Joint Surg Br 1999; 81:323–326.

65. Jelinek JS, Murphey MD, Aboulafia AJ, et al. Muscle infarction in patients with diabetes mellitus: MR imaging findings. Radiology 1999; 211:241–247. 66. Delaney-Sathy LO, Fessell DP, Jacobson JA, Hayes CW. Sonography of diabetic muscle infarction with MR imaging, CT, and pathologic correlation. AJR Am J Roentgenol 2000; 174:165–169. 67. Kattapuram TM, Suri R, Rosol MS, et al. Idiopathic and diabetic skeletal muscle necrosis: evaluation by magnetic resonance imaging. Skeletal Radiol 2005; 34:203–209. 68. Fleckenstein JL, Watumull D, Conner KE, et al. Denervated human skeletal muscle: MR imaging evaluation. Radiology 1993; 187:213–218. 69. McDonald CM, Carter GT, Fritz RC, et al. Magnetic resonance imaging of denervated muscle: comparison to electromyography. Muscle Nerve 2000; 23:1431–1434. 70. Kullmer K, Sievers KW, Reimers CD, et al. Changes of sonographic, magnetic resonance tomographic, electromyographic, and histopathologic findings within a 2-month period of examinations after experimental muscle denervation. Arch Orthop Trauma Surg 1998; 117:228–234. 71. Petersilge CA, Pathria MN, Gentili A, et al. Denervation hypertrophy of muscle: MR features. J Comput Assist Tomogr 1995; 19:596–600. 72. Bendzus M, Koltzenburg M, Wessig C, Solymosi L. Sequential MR imaging of denervated muscle; experimental study. AJNR Am J Neuroradiol 2002; 23:1427–1431.

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Complex Regional Pain Syndrome Conrado F. Cavalcanti and Mark E. Schweitzer

Complex regional pain syndrome (CRPS), formerly referred to as reflex sympathetic dystrophy (RSD) or causalgia, is a neuropathic pain disorder. CRPS most often affects one or more limbs, often developing as a disproportionate consequence of trauma, nerve lesion, fracture, or another remote process (myocardial infarction, stroke, spinal cord injury, among many others).1–4 This syndrome was first described in the 1860s by Mitchell as causalgia (derived from the Greek words kausis, “burning,” and algos, “pain”)5,6 in the distal extremities of soldiers in the American Civil War after traumatic nerve injury.1,2,5,7 Since then, the nosology and terminology of this limb pain syndrome have undergone a series of changes that have led to considerable confusion and controversy regarding diagnosis and treatment. Historical terms that have been used to describe this pain syndrome include RSD, post-traumatic dystrophy, algodystrophy, Sudeck’s atrophy, shoulder-hand syndrome, and minor or major causalgia.1,2,5,7 Of these, the most popular label used was RSD, introduced by Evans in 1946, to accommodate the suggested pathophysiologic role of the sympathetic nervous system in the generation and perpetuation of the pain. This theory was strengthened by many reports of pain relief after pharmacologic or anesthetic sympathetic ganglion blockade.2 However, although still an important feature, recent studies showed that this syndrome is not mediated by a true reflex and the sympathetic nervous system is not necessarily involved and is not obligatorily necessary for the diagnosis of such disorders. Moreover, dystrophic changes are not always present.5 To bring some order and uniformity to this terminology problem, the International Association for the Study of Pain (IASP) organized a consensus meeting in 1994 and established a standard classification based on elements of history, symptoms, and clinical findings.8 They introduced the term complex regional pain syndrome (CRPS), which is now being widely used (Table 42-1).1–3,5,7,9

CRPS was further subdivided into type I (similar to what was formerly known as RSD) and type II (similar to what was termed causalgia). Both types have the same clinical features, with the difference between them being the absence (CRPS type I) or presence (CRPS type II) of a traumatic peripheral nerve injury.1–3,5,7–9

PREVALENCE AND EPIDEMIOLOGY The incidence of CRPS is difficult to estimate, because the literature is replete with studies in which the clinical criteria for the diagnosis of CRPS vary dramatically. CRPS can occur in 1% to 15% of peripheral nerve injury cases, and the incidence after fractures and contusions ranges from 8% to 10%, but many clinicians report the incidence as much lower.

KEY POINTS Soft tissue swelling and patchy and periarticular osteoporosis can be seen on plain radiographs. However, these findings can be subtle and are usually nonspecific and indicative of the chronicity of disease. ■ Increased periarticular activity in the affected limb is the usual finding on triple-phase bone scintigraphy in CRPS. This pattern is more commonly found in the delayed images. ■ Bone scintigraphy can support and confirm the diagnosis of CRPS early in the course of the disease, owing to its high sensitivity. ■ MRI can detect skin thickening and contrast agent enhancement, soft tissue edema, and joint effusions in the first (hyperemic) stage of CRPS. ■ Muscle atrophy is the main MR feature of the third (atrophic) stage of CRPS. ■ It is controversial if bone marrow edema is encountered in the limbs affected by CRPS. ■

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TABLE 42-1 Diagnostic Criteria for Complex Regional Pain

Syndrome I (IASP/CRPS)

1. The presence of an initiating noxious event, or a cause of immobilization 2. Continuing pain, allodynia, or hyperalgesia with which the pain is disproportionate to any inciting event 3. Evidence at some time of edema, changes in skin blood flow, or abnormal sudomotor activity in the region of pain 4. This diagnosis is excluded by the existence of conditions that would otherwise account for the degree of pain and dysfunction

Most patients with CRPS have an identifiable inciting or initiating injury, ranging from minor trauma (sprains, soft tissue trauma, bruises, frostbite) to severe trauma (bone fractures, surgery, nerve lesions). Occasionally, other medical events such as myocardial infarction, central nervous system lesions/infarcts, cast/splint immobilization, and prolonged bed rest can also determine the onset of CRPS.1,2,10 CRPS is more prevalent in women (60% to 80% of cases). There is no age predilection, and persons of all ages can be affected. The upper extremities are more likely to be involved than the lower extremities.

CLINICAL PRESENTATION The clinical presentation of CRPS is variable and difficult to characterize. Classic findings and presentations have been described, but these are not necessarily the most common clinical findings.5,11 Delayed or failed diagnosis is common because of the syndrome’s wide variability and nonspecific set of signs and symptoms. Because there is no strong gender predilection and all ages may be affected, epidemiologic factors are not helpful in the diagnosis. The clinical picture of CRPS is characterized by sensory, autonomic, trophic, motor, and inflammatory symptoms. Sensory symptoms include burning pain in the distal affected extremity that is classically disproportionate in intensity to the inciting injury. Allodynia (disproportionate increased pain response to a non-noxious stimulus) and hyperalgesia (disproportionate increased pain response to a mild noxious stimulus) are also key features. The pain usually appears early in the course of the disease and is not confined to individual nerve territories.1,2,10 Autonomic symptoms secondary to sympathetic dysfunction may be present and may manifest as vasomotor and sudomotor instability of the affected limb. Swelling, excessive sweating, color, blood flow, and temperature changes may be present. The diagnosis of CRPS is excluded by the existence of painful conditions with a known pathologic process that could account for the degree of pain and dysfunction.12

CLINICAL STAGING The natural history of sympathetic dysfunction has classically been divided into three sequential but overlapping stages.5 The first (acute or hyperemic) stage lasts less than 6 months, is characterized by sympathetic hyperfunction, and manifests as extra-articular swelling with red, warm, and dry skin. The second (dystrophic) stage starts

when the sympathetic activity is reduced, classically 3 to 9 months after the onset of symptoms, and is characterized by cyanotic cold and moist skin, muscle wasting, thick nails, and coarse hair. The third (atrophic) stage begins after a chronic period of sympathetic dysfunction and is characterized by thin, tight, glossy skin, osteoporosis, and joint contractures.5 This last stage may be clinically similar to progressive systemic sclerosis. However, those stages are not always present, and a common scenario is the frequent toggling back and forth between stages in almost random order.5 Furthermore, 10% to 20% of CRPS starts with a primarily cold extremity. Also, in other patients, the extremities are still warm after several years. Therefore, the concept of three consecutive stages has been abandoned by some, although it may be conceptually helpful for the consideration of a therapeutic approach.12 Because pain can accompany the sympathetic dysfunction, the pain that is sustained by sympathetic innervation/ circulating catecholamines and relieved after sympathetic blockage is termed sympathetically maintained pain.1,5,13 Pain that is not relieved by true sympathetic blockage is known as sympathetically independent pain.1,5,13 Motor symptoms have more recently been associated with CRPS, including muscle weakness, muscle spasms, tremor, and dystonia. Trophic changes usually occur in the later stages of the disease and may be present in up to 30% of patients.12,14 These trophic changes include abnormal nail and hair growth, fibrosis, thin glossy skin, hyperkeratosis, and osteoporosis. The severity of the pain and associated symptoms may impair the patient’s ability to perform necessary rehabilitation and normal daily activities. Therefore, it is no surprise that psychological disturbances such as anxiety and depression are frequently observed.1,5 This psychogenic overlap may lead to frequent clinical misdiagnosis or cause physicians to withdraw from these patients. Early diagnosis and treatment are essential in preventing permanent damage to the affected limb. The earlier the diagnosis and treatment, the better the prognosis. If untreated, the illness will progress to increasing pain, dystrophy and limb atrophy, and often severe depression.10

PATHOPHYSIOLOGY The pathophysiology of CRPS is incompletely understood, especially the role of the sympathetic nervous system. In the past it was presumed to be sympathetically mediated because pain relief in some cases was achieved after sympathetic blockade.2,10 However, this theory fell out of favor when a significant number of patients did not respond to sympathetic blockade.15,16 At present, the most accepted theory on the pathogenesis of CRPS suggests that a critical excitation of the sensory afferent nerve fibers at the axonal level releases certain neuropeptides (substance P, neuropeptide Y, and calcitonin gene–related peptide) at the nerve fiber endings, which, in turn, induce vasodilatation, increased vascular permeability, and erythema, leading to further stimulation of more sensory nerve fibers. This inflammatory response lowers the pain threshold13,17,18 and is termed neurogenic inflammation.10

CHAPTER

IMAGING TECHNIQUES At present, the diagnosis of CRPS is based on the clinical and physical examination findings just described. The major role of the imaging studies and diagnostic testing is to exclude pathologic processes that can produce a clinical scenario similar to that of CRPS. From the techniques available, radiographs, triplephase radionuclide bone scanning (TPBS), Doppler ultrasonography, and MRI may aid in the diagnosis of CRPS. However, these techniques have a low specificity for diagnosis but do have a role in staging the disease, monitoring the treatment, and excluding other pain states with known pathology.

MANIFESTATIONS OF THE DISEASE Up to now no specific diagnostic test has been available for CRPS, and the diagnosis remains based on the patient’s history and the findings of clinical and physical examination.1 Hematologic studies such as white blood cell count, erythrocyte sedimentation rate, and C-reactive peptide are neither sensitive nor specific in the diagnosis of CRPS. However, they may be useful in excluding other inflammatory conditions.12 Other diagnostic examinations can estimate and quantify the extent of autonomic, sensory, and motor disturbances. Infrared thermography, the most common of these methods, utilizes infrared cameras that sense heat that are connected to a computer to produce colorized images of the limbs. This method can detect and quantify differences in temperature between the left and right extremities in patients with CRPS with a sensitivity ranging from 70% to 90%.12 Some authors have also reported that thermography may provide earlier detection of CRPS.19,20 Currently, the cutoff value temperature difference between limbs is 1.0° C.5,20 Quantitative sensory testing (QST) is a method to assess the function of small nerve fibers. QST systems measure and quantify the amount of physical stimuli (touch, pressure, pain, thermal, or vibratory) required for sensory perception to occur in the patient. QST may show a typical pattern of hyperalgesia and hypothermesthesia to warm stimulus with reduced heat pain thresholds.12,14,21,22 Sudomotor tests include quantitative sudomotor axon reflex test (QSART), resting sweat output (RSO), and sympathetic skin response (SSR). QSART is the most commonly used method for measuring the sweat output. In this test, the sweat response to a topical sweat-inducing agent (acetylcholine) is measured and compared with resting sweat output levels.23 Sweating abnormalities may appear in about 50% of the patients with CRPS, although subclinical involvement may be more prevalent.12 Response to sympathetic blockade is no longer used in the diagnosis of CRPS because a positive response can be seen with other forms of sympathetically mediated pain.10

Radiography The evaluation of most patients with pain in an extremity usually starts with routine radiography. Radiographs of

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the affected areas in CRPS can reveal soft tissue swelling and osteoporosis, which are the most important findings (Fig. 42-1).7 The osteoporosis is best described as patchy and periarticular. Five types of bone resorption are described by finedetail radiography24: (1) band-like, patchy, or periarticular osteoporosis in the metaphyseal region, especially prominent in children; (2) subperiosteal bone resorption similar to that in hyperparathyroidism; (3) intracortical bone resorption leading to striation or tunneling of the cortices; (4) endosteal bone resorption leading to scalloping of the endosteal surface and widening of the medullary canal; and (5) subchondral and juxta-articular erosions leading to periarticular erosions and intra-articular gaps in the subchondral bone. However, these radiographic findings can be subtle and are usually nonspecific and indicative of chronicity of disease.25

Scintigraphy The use of TPBS in CRPS is somewhat controversial,5,26 and there is no consensus about the scintigraphic patterns, because many abnormalities have been described.26–30 However, because it has been used for more than 20 years, TPBS has become widely accepted as an adjunct to the physical findings for the diagnosis of CRPS.26,29,31 The scan consists of images obtained seconds (blood flow), minutes (blood pool), and hours (delayed images) after the intravenous administration of the radionuclide tracer (99mTc- pertechnetate). The usual finding on bone scintigraphy in CRPS is increased periarticular activity in the affected limb (Figs. 42-2 and 42-3). This pattern is more commonly

■ FIGURE 42-1

Post-traumatic and surgical CRPS. Radiograph of the wrist demonstrates diffuse patchy osteoporosis. This finding is usually nonspecific and positive only in chronic stages. Note associated radioulnar dislocation and vascular calcification in the radial artery.

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■ FIGURE 42-2

Three-phase radionuclide bone scanning (TPBS) in CRPS patient. Dynamic flow study (A) depicts asymmetric perfusion of the wrists, being markedly increased on the right. Delayed imaging (B) demonstrates diffuse increased uptake in the wrists, especially on the right.

■ FIGURE 42-3

Radiograph of the elbow in a posttraumatic CRPS patient depicts focal osteopenia in the olecranon (A). Delayed image of a TPBS (B) demonstrates increased focal uptake in the elbow and wrist joints.

CHAPTER

found in the delayed images, although it can, often but less frequently, be found in the blood flow and pool images.5,10,26 The presumed mechanism of this increased tracer uptake is a combination of increased blood flow (from neurogenic mediated vasodilatation) as well as increased bone metabolism and turnover that occurs in the early stages of the disease. This increased activity eventually gives way to normal or reduced uptake that is characteristic of the dystrophic and atrophic stages. Three separate scintigraphic patterns, related to the duration of symptoms, were described by Demangeat and colleagues32:

■ FIGURE 42-4

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1. In the first (acute or hyperemic) clinical stage, 0 to 20 weeks from onset of symptoms, scintigraphy may show abnormal asymmetric perfusion, increased vascularity on blood pool imaging, as well as increased activity on delayed images (Fig. 42-4). 2. In the second (dystrophic) clinical stage, 20 to 60 weeks from the onset of symptoms, the TPBS may show overall normal-appearing perfusion and blood pool images but persistent increased activity in the delayed images. 3. In the third (atrophic) clinical stage, 60 to 100 weeks after onset of symptoms, decreased vascularity in blood pool images and normalization of the previous increased activity in the delayed images may be seen.

Post-traumatic CRPS of the right foot. Lateral radiograph (A) demonstrates diffuse patchy osteoporosis. The TPBS demonstrates increased uptake in the right foot in the blood flow study (B), as well as in the delayed images (anterior [C] and lateral [D] views).

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However, most of the attempts to stratify the CRPS patients showed considerable overlap in each of these separate scintigraphic patterns.32 There is considerable debate about the sensitivity, specificity, positive predictive value, and negative predictive value of TPBS,33 with variable results throughout the literature, ranging from sensitivity from 54% to 100%; specificity from 80% to 98%; positive predictive value from 67% to 95%; and negative predictive value from 61% to 100%.5,28,33–35 Some of the factors that are probably affecting those reported values are33: ●

●

●

Diagnostic criteria of RSD used in each study: the stricter the clinical and scan interpretation criteria, the greater the reported sensitivity and specificity. Duration of symptoms: because the TPBS is more accurate within 20 weeks of onset,32 the sensitivity is inversely affected by duration of symptoms. Age of patient population: patients 50 years of age or older have greater TPBS sensitivity in the detection of CRPS.36

Because of the natural tendency for the scintiscan to return to normal, it is important to stress that a normal scintiscan does not exclude CRPS. Cases of clinically diagnosed CRPS with normal TPBS have been described.26,28,37 In addition, after successful sympatholysis procedures, a paradoxical intensification of tracer uptake may occur; therefore, a hyperintense scan may represent a successful procedure and not disease progression. Because of these reasons, the TPBS should not be used to monitor treatment. The real role of bone scintigraphy is to support and confirm the diagnosis of CRPS early in the course of the disease, because the earlier the diagnosis and treatment, the better the prognosis. Bone scintigraphy is also useful in localizing the patient’s symptoms. Moreover, it is also helpful in excluding other diagnoses such as arthritis, bone tumors, fractures, and metabolic diseases such as Paget’s disease of bone.5,10,26 Currently, new nuclear medicine techniques are being studied for the assessment of CRPS patients: technetium99m sestamibi scintigraphy is being used to assess soft tissue perfusion and metabolism of the affected limb38 ; the tomographic scan mode of 99mTc-HDP pinhole SPECT is being used to generate images of small bones and joints with improved spatial resolution when compared with other nuclear medicine studies39; and scintigraphy using radiolabeled human polyclonal nonspecific immunoglobulin (99mTc HIG) is being used to determine the associated inflammatory component of the CRPS and to help clinicians to predict the response to anti-inflammatory therapies.40 However, the validation of these new methods needs to be assessed in future studies.

Single Photon Emission Computed Tomography of the Brain The role of brain SPECT in CRPS has not been well established. Changes in regional cerebral blood flow (rCBF) have been described, with abnormal contralateral thalamic rCBF being the most common brain SPECT finding.10,41,42

Doppler Ultrasonography Vascular abnormalities including transient vascular hyperpermeability, capillary and venous dilatation, arteriolar wall thickening, vasospasm, and changes in blood flow may be encountered in patients with CRPS.43–49 Doppler ultrasonography may in some patients with stage I CRPS detect flow abnormalities, such as transformation of a normal triphasic waveform to monophasic or low-pulsatility triphasic waveforms and decrease in the pulsatility (PI) and resistive (RI) indexes.47 Power Doppler ultrasonography may similarly show increased flow in the affected limb’s soft tissues.48 Doppler ultrasonography cannot be used for the diagnosis of CRPS because of low sensitivity and specificity. It can, however, help in staging the disease and monitoring treatment, because the hemodynamic changes tend to disappear in patients who were treated or in whom symptoms resolved. In addition, it may also be used for objective follow-up of CRPS patients after surgical sympathectomy (in this situation, a low pulsatility index and biphasic waveform, indicating vasodilatation, is seen due to successful sympathetic denervation).47,49

Magnetic Resonance Imaging The major role of MRI is to exclude conditions that can produce a clinical scenario similar to CRPS, such as diabetic neuropathy and peripheral and cartilage injuries. MRI has also been used with variable success in diagnosing CRPS. The first (hyperemic) stage is when it appears to be more useful50 because it can demonstrate skin thickening and contrast enhancement, soft tissue edema, and joint effusions, with high sensitivity (87% to 91%) but low specificity (17% to 24%) (Fig. 42-5).50,51 Skin thickness should be accessed in the dorsal aspect of the extremity, because this area is relatively unaffected by stress-related trophic changes. Also, because the skin is difficult to see in MRI, optimal fat suppression, usually via turbo gradient-echo MR images, is necessary. Joint effusions, being a nonspecific finding, should only be used as a diagnostic criterion when present in atypical joints, especially the Lisfranc joint (Fig. 42-6). In the second (dystrophic) stage, MRI does not accurately diagnose CRPS abnormalities but, occasionally, skin thinning can be seen.50,51 Muscle atrophy is the main MR feature of the third (atrophic) stage. Despite being a nonspecific finding, it is important to report because it has prognostic implications (treatment is less effective in this stage).50 In the foot, it is important to assess for atrophy of the intrinsic muscles in terms of differential diagnosis, because other muscles may atrophy from other debilitating disorders. In the past, CRPS was linked to other entities such as transient osteoporosis of the hip, regional migratory osteoporosis, and transient bone marrow edema. Because these disorders characteristically cause bone marrow abnormalities, detected by MRI,25,52–55 it was hypothesized that with CRPS similar bone marrow findings would be encountered in the limbs. Results regarding this issue

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■ FIGURE 42-5

Stage 1 CRPS. Oblique coronal gradient-echo fat-suppressed MR image demonstrates skin thickening (arrowheads) in the dorsal aspect of the left foot.

■ FIGURE 42-6

Stage 1 CRPS. Oblique coronal gradient-echo fat-suppressed post-gadolinium MR image depicts synovial enhancement in the Lisfranc joints (arrows), as well as mild skin thickening in the dorsal aspect of the left foot (arrowheads).

have been conflicting: two studies found no bone marrow abnormalities,50,56 and three studies consistently showed bone marrow edema at stage 1 with sensitivity of up to 50% (Fig. 42-7).57–59

can cause significant cartilaginous and osseous destruction, which are absent in CRPS. In addition, MRI will easily diagnose the presence of conditions such as osteonecrosis, bone contusions, stress fractures, and internal derangements.

DIFFERENTIAL DIAGNOSIS

SYNOPSIS OF TREATMENT OPTIONS

The many diseases that may have clinical findings similar to those of CRPS include regional osteoporosis associated with disuse, septic arthritis, osteomyelitis, rheumatoid arthritis, pigmented villonodular synovitis (PVNS), synovial osteochondromatosis, bone tumors, metabolic diseases, avascular osteonecrosis, diabetic neuropathy, peripheral neuropathies, nerve entrapment syndromes, myofascial pain, bone fractures/contusions, and internal derangements of the affected joint. However, imaging studies can exclude many of these conditions. For example, septic arthritis will lead to articular space narrowing and osseous erosions, which are not present in CRPS. Similarly, in synovial osteochondromatosis, rheumatoid arthritis, and PVNS, synovial inflammation

The successful treatment of CRPS depends on both an aggressive and a multidisciplinary approach. Because pain and eventual limb dysfunction are the major clinical problems, the primary treatment objectives are physical rehabilitation and pain control.1,60,61 The goal of physical therapy is to improve function of the patient’s affected limb in an orderly sequence, starting with combinations of heat, cold, and massage, passing through strengthening exercises (from isometric to isotonic), and finally resulting in vocational/functional rehabilitation. Pain control can be achieved through drug therapy, which includes nonsteroidal anti-inflammatory agents, membrane stabilizers (anticonvulsants, local anesthetics), corticosteroids, opioids, and others.62

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■ FIGURE 42-7

Transient osteoporosis of the hip. Coronal T1- (A) and T2- (B) weighted images demonstrate bone marrow edema in the left femoral head. Coronal T2-weighted image (C) obtained 10 months later depicts complete resolution of the bone marrow edema.

Psychotherapy is important in patients with depression. Currently, however, the first therapeutic route in these patients is antidepressant medication. The psychogenic consequences of this not uncommon disorder cannot be overemphasized. These symptoms may be what brings the patient to medical attention, and musculoskeletal pain is a major treatable cause of depression. Sympatholysis, previously used for diagnosis, is, at the present, used for treatment in some patients with CRPS in whom conservative measures have failed. Sympatholysis can be achieved through topical patches (clonidine), oral medications (clonidine, α-adrenergic blockers), interventional techniques (paravertebral sympathetic chain ganglion blockage), and surgical sympathectomy.1–3,5,7,9,12,13,63

What the Referring Physician Needs to Know ■ ■ ■

■

The diagnosis of CRPS remains primarily based on history and the findings of clinical and physical examinations. The sympathetic nervous system is not necessarily involved in CRPS. The major role of the imaging studies is to exclude pathologic processes that can produce a clinical scenario similar to that of CRPS. The earlier the diagnosis and treatment of CRPS, the better the prognosis.

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SUGGESTED READINGS Fournier RS, Holder LE. Reflex sympathetic dystrophy: diagnostic controversies. Semin Nucl Med 1998; 28:116–123. Intenzo CM, Kim SM, Capuzzi DM. The role of nuclear medicine in the evaluation of complex regional pain syndrome type I. Clin Nucl Med 2005; 30:400–407. Schott GD. Reflex sympathetic dystrophy. J Neurol Neurosurg Psychiatry 2001; 71:291–295. Sintzoff S, Sintzoff S Jr, Stallenberg B, Matos C. Imaging in reflex sympathetic dystrophy. Hand Clin 1997; 13:431–442.

Teasdall RD, Smith BP, Koman LA. Complex regional pain syndrome (reflex sympathetic dystrophy). Clin Sports Med 2004; 23:145–155. Vacariu G. Complex regional pain syndrome. Disabil Rehabil 2002; 24:435–442. Wasner G, Schattschneider J, Binder A, Baron R. Complex regional pain syndrome—diagnostic, mechanisms, CNS involvement and therapy. Spinal Cord 2003; 41:61–75.

REFERENCES 1. Rho RH, et al. Complex regional pain syndrome. Mayo Clin Proc 2002; 77:174–180. 2. Wasner G, et al. Complex regional pain syndrome—diagnostic, mechanisms, CNS involvement and therapy. Spinal Cord 2003; 41:61–75. 3. Schott GD. Reflex sympathetic dystrophy. J Neurol Neurosurg Psychiatry 2001; 71:291–295. 4. Sandroni P, et al. Complex regional pain syndrome type I: incidence and prevalence in Olmsted county, a population-based study. Pain 2003; 103:199–207. 5. Mehta S. Complex regional pain syndromes including reflex sympathetic dystrophy and causalgia. In DeLee J, Drez D (eds). DeLee and Drez’s Orthopaedic Sports Medicine—Principles and Practice, 2nd ed. Philadelphia, WB Saunders, 2003, vol 1, pp 441–460. 6. Mitchell S. On the diseases of nerves, resulting from injuries. In Flint A (ed). Sanitary Memoirs of the War of the Rebellion. New York, Hurd & Houghton, 1867, pp 412–468. 7. Resnick D. Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, 2002, vol 3, pp 1783–1859. 8. Merskey H. Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Pain Terms, 2nd ed. Seattle, IASP Press, 1994, pp 40–43. 9. van de Beek WJ, et al. Diagnostic criteria used in studies of reflex sympathetic dystrophy. Neurology 2002; 58:522–526. 10. Intenzo CM, Kim SM, Capuzzi DM. The role of nuclear medicine in the evaluation of complex regional pain syndrome type I. Clin Nucl Med 2005; 30:400–407. 11. Zyluk A. Scoring system in the assessment of the clinical severity of reflex sympathetic dystrophy of the hand. Hand Clin 2003; 19:517–521, xi. 12. Vacariu G. Complex regional pain syndrome. Disabil Rehabil 2002; 24:435–442. 13. Teasdall RD, Smith BP, Koman LA. Complex regional pain syndrome (reflex sympathetic dystrophy). Clin Sports Med 2004; 23:145–155. 14. Veldman PH, et al. Signs and symptoms of reflex sympathetic dystrophy: prospective study of 829 patients. Lancet 1993; 342:1012–1016. 15. Goldstein DS, Tack C, Li ST. Sympathetic innervation and function in reflex sympathetic dystrophy. Ann Neurol 2000; 48:49–59. 16. Drummond PD, Finch PM, Smythe GA. Reflex sympathetic dystrophy: the significance of differing plasma catecholamine concentrations in affected and unaffected limbs. Brain 1991; 114:2025–2036. 17. Pham T, Lafforgue P. Reflex sympathetic dystrophy syndrome and neuromediators. Joint Bone Spine 2003; 70:12–17. 18. Kurvers HA. Reflex sympathetic dystrophy: facts and hypotheses. Vasc Med 1998; 3:207–214. 19. Karstetter KW, Sherman RA. Use of thermography for initial detection of early reflex sympathetic dystrophy. J Am Podiatr Med Assoc 1991; 81:198–205. 20. Bruehl S, et al. Validation of thermography in the diagnosis of reflex sympathetic dystrophy. Clin J Pain 1996; 12:316–325.

21. Wahren LK, Torebjork E, Nystrom B. Quantitative sensory testing before and after regional guanethidine block in patients with neuralgia in the hand. Pain 1991; 46:23–30. 22. Verdugo R, Ochoa JL. Quantitative somatosensory thermotest: a key method for functional evaluation of small calibre afferent channels. Brain 1992; 115:893–913. 23. Sandroni P, et al. Complex regional pain syndrome I (CRPS I): prospective study and laboratory evaluation. Clin J Pain 1998; 14:282–289. 24. Genant HK, et al. The reflex sympathetic dystrophy syndrome: a comprehensive analysis using fine-detail radiography, photon absorptiometry, and bone and joint scintigraphy. Radiology 1975; 117:21–32. 25. Sintzoff S, et al. Imaging in reflex sympathetic dystrophy. Hand Clin 1997; 13:431–442. 26. Tondeur M, Sand A, Ham H. Interobserver reproducibility in the interpretation of captopril renograms from patients suspected of having renovascular hypertension. Clin Nucl Med 2004; 29:479–484. 27. Fano N, Holm C. Bone scintigraphy in post-traumatic reflex dystrophy. Scand J Rheumatol 1988; 17:455–458. 28. Holder LE, Cole LA, Myerson MS. Reflex sympathetic dystrophy in the foot: clinical and scintigraphic criteria. Radiology 1992; 184:531–535. 29. Constantinesco A, et al. Three phase bone scanning as an aid to early diagnosis in reflex sympathetic dystrophy of the hand: a study of eighty-nine cases. Ann Chir Main 1986; 5:93–104. 30. Vande Streek P, et al. Upper extremity radionuclide bone imaging: the wrist and hand. Semin Nucl Med 1998; 28:14–24. 31. Simon H, Carlson DH. The use of bone scanning in the diagnosis of reflex sympathetic dystrophy. Clin Nucl Med 1980; 5:116–121. 32. Demangeat JL, et al. Three-phase bone scanning in reflex sympathetic dystrophy of the hand. J Nucl Med 1988; 29:26–32. 33. Fournier RS, Holder LE. Reflex sympathetic dystrophy: diagnostic controversies. Semin Nucl Med 1998; 28:116–123. 34. Kline SC, Holder LE. Segmental reflex sympathetic dystrophy: clinical and scintigraphic criteria. J Hand Surg Am 1993; 18:853–859. 35. Hoffman J, et al. Effect of sympathetic block demonstrated by triple-phase bone scan. J Hand Surg Am 1993; 18:860–864. 36. Werner R, et al. Factors affecting the sensitivity and specificity of the three-phase technetium bone scan in the diagnosis of reflex sympathetic dystrophy syndrome in the upper extremity. J Hand Surg Am 1989; 14:520–523. 37. Doury P. Algodystrophy: reflex sympathetic dystrophy syndrome. Clin Rheumatol 1988; 7:173–180. 38. Sarikaya A, et al. Technetium-99m sestamibi limb scintigraphy in post-traumatic reflex sympathetic dystrophy: preliminary results. Eur J Nucl Med 2001 28:1517–1522. 39. Kim SH, et al. 99mTc-HDP pinhole SPECT findings of foot reflex sympathetic dystrophy: radiographic and MRI correlation and a speculation about subperiosteal bone resorption. J Korean Med Sci 2003; 18:707–714. 40. Okudan B, Celik C. Determination of inflammation of reflex sympathetic dystrophy at early stages with Tc-99m HIG scintigraphy: preliminary results. Rheumatol Int 2006; 26:404–408.

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41. Fukumoto M, et al. Contralateral thalamic perfusion in patients with reflex sympathetic dystrophy syndrome. Lancet 1999; 354:1790–1791. 42. Fukui S, Shigemori S, Nosaka S. Changes in regional cerebral blood flow in the thalamus after electroconvulsive therapy for patients with complex regional pain syndrome type 1 (preliminary case series). Reg Anesth Pain Med 2002; 27:529–532. 43. Oyen WJ, et al. Reflex sympathetic dystrophy of the hand: an excessive inflammatory response? Pain 1993; 55:151–157. 44. Masson C, et al. Further vascular, bone and autonomic investigations in algodystrophy. Acta Orthop Belg 1998; 64:77–87. 45. Pollock FE Jr, et al. Patterns of microvascular response associated with reflex sympathetic dystrophy of the hand and wrist. J Hand Surg Am 1993; 18:847–852. 46. Goris RJ. Reflex sympathetic dystrophy: model of a severe regional inflammatory response syndrome. World J Surg 1998; 22:197–202. 47. Pekindil G, Pekindil Y, Sarikaya A. Doppler sonographic assessment of posttraumatic reflex sympathetic dystrophy. J Ultrasound Med 2003; 22:395–402. 48. Nazarian LN, et al. Increased soft-tissue blood flow in patients with reflex sympathetic dystrophy of the lower extremity revealed by power Doppler sonography. AJR Am J Roentgenol 1998; 171:1245–1250. 49. Tu ES, Mailis A, Simons ME. Effect of surgical sympathectomy on arterial blood flow in reflex sympathetic dystrophy: Doppler US assessment. Radiology 1994; 191:833–834. 50. Schweitzer ME, et al. Reflex sympathetic dystrophy revisited: MR imaging findings before and after infusion of contrast material. Radiology 1995; 195:211–214. 51. Graif M, et al. Synovial effusion in reflex sympathetic dystrophy: an additional sign for diagnosis and staging. Skeletal Radiol 1998; 27:262–265.

52. Massara A, et al. [Transient regional osteoporosis]. Reumatismo 2005; 57:5–15. 53. Yamasaki S, et al. Three cases of regional migratory osteoporosis. Arch Orthop Trauma Surg 2003; 123:439–441. 54. Toms AP, et al. Regional migratory osteoporosis: a review illustrated by five cases. Clin Radiol 2005; 60:425–438. 55. Yamamoto T, et al. A clinicopathologic study of transient osteoporosis of the hip. Skeletal Radiol 1999; 28:621–627. 56. Koch E, et al. Failure of MR imaging to detect reflex sympathetic dystrophy of the extremities. AJR Am J Roentgenol 1991; 156:113–115. 57. Lechevalier D, et al. [Magnetic resonance imaging in the warm and cold forms of algodystrophy of the foot]. J Radiol 1996; 77:411–417. 58. Darbois H, et al. [MRI symptomatology in reflex sympathetic dystrophy of the foot]. J Radiol 1999; 80:849–854. 59. Crozier F, et al. Magnetic resonance imaging in reflex sympathetic dystrophy syndrome of the foot. Joint Bone Spine 2003; 70: 503–508. 60. Oerlemans HM, et al. Pain and reduced mobility in complex regional pain syndrome I: outcome of a prospective randomised controlled clinical trial of adjuvant physical therapy versus occupational therapy. Pain 1999; 83:77–83. 61. Stanton-Hicks M, et al. Complex regional pain syndromes: guidelines for therapy. Clin J Pain 1998; 14:155–166. 62. Wasner G, Backonja MM, Baron R. Traumatic neuralgias: complex regional pain syndromes (reflex sympathetic dystrophy and causalgia): clinical characteristics, pathophysiological mechanisms and therapy. Neurol Clin 1998; 16:851–868. 63. Schwartzman RJ, Popescu A. Reflex sympathetic dystrophy. Curr Rheumatol Rep 2002; 4:165–169.

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Degenerative Disorders of the Spine Iain McCall

ETIOLOGY Degeneration of the spine is universal and involves structural changes in the disc, bone, ligaments, and articular cartilage of the facet joints. Despite the high prevalence of degeneration, the underlying etiology is still only partially understood. There is, however, an interrelationship of the different components of the spine in that changes in one component, such as the disc, will have an effect on another, such as altered biomechanics of the facets. Similarly, alterations in the structure of the vertebral end plate may affect the nutrition of the disc and the viability of the chondrocytes. Degeneration of the spine is a natural aging process and increases in extent and severity with age. Miller and associates1 reported an increase in disc degeneration from 16% at age 20 to 98% at age 70 based on microscopic disc degeneration grades of 600 autopsy specimens. Reduction in disc signal intensity on MRI is one of the degenerative findings most highly associated with age.2 Environmental factors such as heavy physical loading related to occupation have been suggested as a factor, but the evidence is not conclusive and may be influenced by confounding factors including socioeconomic status and lifestyle. Series of studies with monozygotic twins found that heavy physical loading demands at work and leisure explained only a minor portion of the overall variance in lumbar disc degeneration.3 Driving has also been proposed as a possible etiologic factor, but the current weight of evidence suggests no notable effect of driving on disc degeneration. The only chemical exposure associated with disc degeneration is smoking. Finally, there is likely to be a genetic influence on degeneration, and initial results suggested a substantial family influence on degenerative findings. A study of both cervical and lumbar spine using MRI showed heritable estimates were very high for both lumbar and cervical spine after adjusting for age, weight, smoking, occupation, and physical activity; and disc bulging and height

were the primary contributors to the disc degeneration summary score that relate to the genetic determination.4 Disc bulging and disc height are the individual features that are the most highly heritable in both cervical and lumbar spine.4

PREVALENCE AND EPIDEMIOLOGY Low back and neck pain are common ailments in developed countries, with an estimated 40% to 70% of adults having suffered low back pain. Low back and neck pain are a major source of disability and loss of working time.

KEY POINTS Forty to 70 percent of adults have experienced low back pain, but the prevalence of symptomatic herniated nucleus pulposus is only 1%. ■ The prevalence of asymptomatic herniated nucleus pulposus reaches 76% in the adult population. ■ There is no correlation between symptoms and imaging features of disc degeneration. ■ Incidence of posterior annular tears increases with age; they are common in the asymptomatic population, but it is uncertain whether high signal intensity zones on MRI are more commonly painful. ■ The importance of imaging is to demonstrate anatomic features and extent of herniation and its effect on nerve roots. ■ Potential disc herniations are, based on morphologic criteria, classified as normal, bulging, protrusion, extrusion, and sequestration. ■ Cysts and osteoarthritis of facet joints, including degenerative spondylolisthesis, are diagnosed and classified using well-defined criteria and may be an important cause of low back pain. ■ Spinal stenosis is accurately diagnosed using conventional radiographs and especially CT and MRI. ■

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In most cases the pain resolves, but recurrent episodes may occur, ranging from 20% to 44% within 1 year after an episode of acute low back pain, with 80% suffering a recurrence within 10 years. For approximately 5% of the adult population low back pain becomes persistently disabling and chronic. The incidence and prevalence of symptomatic herniated nucleus pulposus are much lower, with 1% of those between 17 and 64 years reporting discomfort from lumbar intervertebral disc herniation and between 0.1% and 0.5% of the population per year within the age range of 20 to 64 having a new clinically manifest herniated nucleus pulposus,5 with a peak incidence between 38 and 44 years of age.

CLINICAL PRESENTATION There is no correlation between the presence of symptoms and the imaging features of disc degeneration. Pain may arise from the structures of the spine—sclerotomal pain—or be due to compression of the nerve roots passing through the spinal canal—dermatomal pain. The sclerotomal pain may be localized to the spinal region or may be referred to adjacent areas or to the limbs. Cervical sclerotomal pain is often referred to the shoulder, and lumbar pain is often referred to the buttocks and thighs, although more distal limb referral may occur. Dermatomal pain may also be present in the region of the spine but will often be present in the limbs in the distribution of the compressed nerve. The discogenic pain is exacerbated by activity such as bending or lifting and relieved by rest, especially in recumbency. The individual begins the day relatively free of pain.6 Patients may occasionally find themselves immobilized by pain and spasm. On examination, the erector spinae muscles are tense and movement is limited and there may be a variable degree of tenderness on palpation. Neurologic examination does not identify any objective loss, although straight-leg raising may be limited. Facet pain may be aggravated by rest, resulting also in sleep disturbances, whereas movement decreases pain.7,8 Pain and stiffness are present on rising but improve during the day. Symptoms may be exacerbated by extended periods of sitting or standing with the spine in a lordotic position. Examination is unremarkable except that the patient may flex the cervical spine or touch the toes but may be significantly restricted in extension. Deep palpation may reveal tenderness in the region of the affected facet joints and no neurologic deficit. Discogenic and facet pain may occur together, resulting in a combination or mixture of clinical features sometimes resulting in constant pain6 and marked restriction of spinal movement in all directions and considerable tenderness. The pain in nerve root compression by degeneration in the spine is usually in the distribution of the nerve root but may not affect the whole extent of the distribution, and there is overlap between dermatomes. In the cervical spine, compression of the cord may also affect the distribution of the pain; and in the thoracic spine, disc herniations commonly present as back pain that is nonspecific or a myelopathy that includes progressive paraparesis,

hyperreflexia, altered sensation and pinprick levels, and, occasionally, urinary problems. Nerve root compression will also lead to motor and sensory changes, and examination includes assessment of motor strength, sensory loss, and deep tendon reflexes in the extremities. Central nuclear herniations may produce severe back pain and bilateral leg pain. Lesions of the peripheral nerve roots must always be distinguished from root irritation by the degenerate spine. Pain from root compression in the upper cervical spine may extend into the occiput.

PATHOPHYSIOLOGY Anatomy The spine consists of a column of vertebrae with a vertebral body linked by two pedicles to the lamina, which has two superior and two inferior articular processes and a spinous process. Each vertebra, with the exception of the sacrum and coccyx, is linked as a three-joint complex. The intervertebral disc with associated vertebral cartilage end plates forms the anterior component, whereas the facet joints form the posterior component. The intervertebral disc is made up of two components, the outer being the annulus that surrounds the inner nucleus pulposus. The annulus is divided into outer and inner concentric rings with dense fibrous lamellae containing fibroblasts in the outer ring and less densely packed collagen with chondrocytes and some ground substance in the inner ring. The central nucleus pulposus has an infrastructure of collagen with chondrocytes and a high content of hydrophilic proteoglycans and thus water content. The intervertebral disc and adjacent vertebral end plates form a continuum with the collagen fibers of the disc passing directly into the cartilage of the central part of the vertebral end plate and directly into the bone at the anterior and posterior rims of the vertebra called the enthesis. The collagen from the cartilage is in continuity with the subchondral bone of the vertebra. Because the intervertebral disc is avascular, it obtains most of its nutrients by diffusion through the cartilage end plate from the vascular arcade along the subchondral trabecular bone, with a small component in the outer annulus from vessels around the outer rim of the disc. The transport of water, nutrients, and metabolic waste products to and from the disc is enhanced by pressure, and the nucleus pulposus loses water and metabolic waste products during the day in the upright posture, resulting in reduction in height; while a person is in the recumbent position, water and metabolites reenter the disc, increasing its height. The facet joints have appositional articular cartilage surfaces and are lined by synovium. The inner capsule is continuous with the ligamentum flavum, and the outer capsule is covered by the ligaments. The alignment of the facets is site dependent, with more horizontal alignment in the cervical spine that facilitates flexion and extension, with some limited potential for rotation and lateral flexion. In the thoracic spine the facets have coronal and more vertical alignment and there is only a limited range of movement. In the lumbar spine the upper facets are aligned vertically in the sagittal plane but become more coronal in the lower lumbar spine.

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The motion segments are connected throughout the spine by the anterior and posterior longitudinal ligaments, the ligamentum flavum, and the interspinous ligments posteriorly. The anterior longitudinal ligament is attached to the anterior vertebral wall and end-plate rim but is not attached to the intervertebral disc. The posterior longitudinal ligament is inserted at the enthesis of each vertebral end plate and is firmly attached to the intervertebral disc by lateral expansions but is not attached to the posterior wall of the vertebral body. In the lumbar spine the anterior elements of the vertebral column are surrounded by a plexus of nerves derived anteriorly from the sympathetic trunks, laterally from the gray rami communicantes, and posteriorly from the sinuvertebral nerve. The plexuses supply the anterior longitudinal ligaments, the periosteum of the vertebral body, penetrating branches into the vertebral body, the posterior longitudinal ligament, the ventral aspect of the dural sac, and the outer third of the annulus. The facet joints are innervated by the medial branches of the dorsal rami and have multisegmental innervation.9 The epidural space mainly contains fat and blood vessels, which make up the epidural venous plexus. The anterior epidural veins pass over the discs on either side of the midline. The vertebral bodies are supplied by a central artery that arborizes out to the vertebral end plates, and the veins drain back into a central vein in a similar fashion. The vertebral/intervertebral disc combination, pedicles, facet joints, and foramina at each level also provide a conduit for the spinal cord and nerve roots. The cord terminates at T12-L1 and becomes the cauda equina. Nerve roots emerge from the dural sac passing under the lamina and out through the foramina.

Pathology Degeneration is a natural process in the spine, with autopsy studies showing changes of spondylosis in 60% of women and 80% of men by the age of 49 years and in 95% of both by the age of 70.10 Disc degeneration begins with a gradual loss of hydration of the nucleus with a drop from 90% at birth to about 75% in the third decade. There is a gradual centripetal encroachment of collagen into the nucleus from the annulus, a reduction of chondrocytes, and changes in the proteoglycans of the nucleus. Subsequently, the nucleus becomes solid, nonturgescent, and dry, with a marked increase in collagen content and no discernable differentiation from annulus. In middle age, splits and clefts form parallel with the end plate toward the upper and lower parts of the nucleus; and as aging progresses, they extend to the outer parts of the annulus, where vascular ingrowth may occur.11 In the annulus, initially fragmentation of fibers, mucinous degeneration, and cracks and cavities occur that may result in tears at the annular rim of the vertebral body, which are commonly present by age 50 years.12 Concentric circumferential cracks or tears develop between the layers of the collagen in the annulus, and radiating ruptures may also occur radially from the nucleus to the periphery. These radial tears may or may not extend through the outer annular fibers and are also the conduit for nuclear material to pass through the annulus and produce a herniation of

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the nucleus pulposus. Such prolapses have been shown to often contain fibrocartilage in both the cervical and lumbar spine. Early degenerative changes of the cartilage end plate include fibrillation, longitudinal fissures, and cleft formation. This may also be enhanced by calcification of the end plates and occlusion of the marrow contact channels that is observed with advancing age.13 As degeneration progresses, there is extensive loss of cartilage with vascular ingrowth and ossification with islands of residual cartilage. The irregular ossification may be extensive with dense bony sclerosis in the adjoining vertebral bodies and irregularity of the residual vertebral bony end plate. Osteophyte formation at the peripheral margins of the vertebral bodies is present where there are degenerative changes in the disc. They form initially at the vertebral rim by advancing endochondral ossification of the annulus and increase in size by the formation of subperiosteal new bone. The osteophytic bone is initially coarsely trabeculated or compact but becomes cancellous with marrow cavities continuous with the vertebral body11 and may vary in size but only rarely becomes united across the disc. Degeneration may affect a number of motion segments but most commonly involves the mid cervical and lower lumbar spine. In some cases it may begin at a relatively early age and be associated with trauma or overuse. Degeneration may also result in compression of the cord or nerve roots due to herniation of the nucleus pulposus through the annulus, bulging of the annulus, osteoarthritis of the facet joints, or instability of the motion segment secondary to the degenerative changes.

MANIFESTATIONS OF THE DISEASE Intervertebral Disc Degeneration Radiography Radiographs of the spine delineate the vertebra satisfactorily but have significant limitations in demonstrating spinal soft tissue. The demonstration of disc changes is limited to the evaluation of disc height; although the later stages of disc height loss are clearly demonstrated (Fig. 43-1), early disc space loss may be subject to interobserver variation and difficulties of lateral angulation and rotation of the radiographs.14 Comparison is made to adjacent discs to see early reduction, but it should be noted that disc height normally gradually increases in the lumbar spine between L1 and L4-L5, whereas L5-S1 height is again less. Disc space narrowing may be asymmetric and should be assessed on both anteroposterior and lateral views of the spine. Bony vertebral end-plate irregularity is usually accurately assessed, but sclerosis is a relative feature and varies normally between subjects and may be limited to part of the end plate if there is asymmetric narrowing and particularly if it is related to vertebral osteoporosis. In the thoracic spine, disc space narrowing associated with endplate irregularity may be seen in conjunction with loss of anterior vertebral height. Although individual disc levels may be affected, if three or more consecutive disc levels are involved, it is referred to as Scheuermann’s disease and the presence of these changes in adolescence may result in a degree of kyphosis in severe cases.15

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■ FIGURE 43-1

Radiographs of the lumbar spine. Lateral (A) and coned lateral (B) views demonstrate narrowing of the L4-L5 disc space associated with a forward displacement of L4 on L5 as a degenerative spondylolisthesis due to osteoarthritis of the facet joints. C, Anteroposterior radiograph shows sclerosis at the L4-L5 facet joints and a mild lateral curve.

A vacuum phenomenon appearing as low attenuation areas within the disc may be seen that is enhanced by extending the spine. These areas may be limited to the vertebral rim at the insertion of the annulus and may be associated with osteophyte formation. A vacuum phenomenon within the disc substance reflects the cleft formation and is also helpful in excluding infective pathology, which is rare as a cause of disc gas. The presence of total disc resorption with severe sclerosis of the end plate at only one level in an otherwise normal-looking spine is seen in some younger patients and has been reported as a separate entity.16 Multiple disc space narrowing, sclerosis, and osteophyte formation may be present in older subjects in the

cervical (Fig. 43-2) and lumbar spine and may be associated with a degenerative scoliosis in the latter, with asymmetric disc space narrowing. Osteophytes appear as bony projections from the rim of the vertebral body usually slightly below the end plate, less commonly from the end-plate rim. Osteophytes must be differentiated from the flowing ossification of the anterior longitudinal ligament of diffuse idiopathic skeletal hyperostosis (Forestier’s disease), which may bridge the whole disc space and involves the anterior surface of the vertebral body. Lateral radiographs in flexion and extension have also been used to evaluate relative linear and rotational interbody displacement. The normal range of movement has

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■ FIGURE 43-2

A, Lateral radiograph of the cervical spine demonstrates multiple narrowed disc spaces with anterior osteophyte formation and a retrolisthesis of C4 on C5. Facet joint space narrowing with some sclerosis is present. B, Anteroposterior view demonstrates osteoarthritic osteophyte proliferation along the lateral margins of the facet joints and narrowing and sclerosis of the neurocentral joints.

been a subject of dispute. In both the cervical and lumbar spine, translation in the lumbar spine of 4 mm or more was seen in 20% of normal subjects and 10% had 3 mm or more at all levels except L5-S1.17

Magnetic Resonance Imaging The process of intervertebral disc degeneration is best visualized on MRI. The normal nucleus is high signal on the spin-echo, T2-weighted MR sequence, and the surrounding annulus is of low signal. The appearance of the disc on a T2-weighted, spin-echo MR sequence has been graded by Pfirrmann and coworkers (Table 43-1; Fig. 43-3).18 Grade 1 is described as a “cotton ball” with a uniform high signal throughout the disc and is the appearance in young people. Grade 2 differs only by the presence of a central horizontal low signal cleft and is also considered to be normal. In grade 3 there is a reduction of high signal in the nucleus without loss or with minor loss of disc height representing the early stages of degeneration, and there may be loss of distinction between the

nucleus and the annulus. Grade 4 shows some loss of disc height, which can also be appreciated on the plain radiographs, with a generalized loss of signal. Grade 5 represents the end stage with almost complete loss of the disc space. This grading system has good intraobserver and interobserver correlation and is useful as a descriptive method, although there is no relationship with symptoms. Disc height may be measured on the monitor directly and special techniques may be used, but comparison with an adjacent disc is most commonly utilized. The degenerative process also results in the annulus losing its strength and bulging outward beyond the outline of the vertebral rim. This is a circumferential process, although it may be greater in one area than another, depending on the compressive forces on the disc. In the axial plane, the annulus is seen extending beyond the vertebral body outline uniformly around the whole vertebra; and on sagittal MR images the annulus will be seen to be bulging beyond the vertebra on each section (Fig. 43-4). Cervical discs begin the process of degeneration at a relatively early age with

TABLE 43-1 Classification of Disc Degeneration Based on Sagittal T2-Weighted Magnetic Resonance Imaging Grade

Differentiation*

Signal Intensity†

Disc Height

I II III IV V

Yes Yes Blurred Lost Lost

Homogeneously hyperintense Hyperintense with horizontal dark band Slightly decreased, minor irregularities Moderately decreased, hypointense zones Hypointense, with or without horizontal hyperintense band

Normal Normal Slightly decreased Moderately decreased Collapsed

*Of nucleus pulposus from annulus. † Of nucleus pulposus. Data from Pfirrmann CW, Metzdorf A, Zanetti M, et al. Magnetic resonance classification of lumbar intervertebral disc degeneration. Spine 2001; 26:1873-1878.

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■ FIGURE 43-3

Sagittal, T2-weighted, turbo spin-echo MR images of the intervertebral disc showing the five grades of disc degeneration. A, Grades 1 and 2. B, Grade 3. C, Grades 4 and 5 (see also Table 43-1).

■ FIGURE 43-4

Disc bulge. Axial T1-weighted (A) and T2-weighted (B) turbo spin-echo MR images demonstrate the disc extending circumferentially beyond the outline of the vertebral body.

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the development of clefts in the posterolateral aspects of the disc from the nucleus into the neurocentral joints. Focal linear areas of high signal within the degenerated disc occasionally occur that are thought to be due to free water within degenerate clefts, and the presence of gas in the disc may result in low signal on T1- and T2weighted images. Calcification within the degenerated disc will produce low signal on T1, but occasionally fine calcification may lead to T1 shortening and increased signal intensity.

Discography Although MRI demonstrates the features of degeneration well, attempts to predict the source of back pain have proven unreliable, especially when more than one disc has degenerated. If accurate delineation of a painful level is required before surgery, an injection of water-soluble contrast agent into the nucleus will confirm the degenerate changes and may provide confirmation of the disc as a source of pain (Fig. 43-5). CT may be performed in conjunction with the injection because this enables internal annular changes to be demonstrated as concentric rings of contrast medium and thus the degree of degeneration to be graded.19 A good correlation between discographic and MR morphology has been shown, but discograms have identified abnormalities on apparently normal MR images.20 Pain production is assessed during and after injection of the contrast agent and is rare if the disc is normal. Symptom provocation from degenerated or injured discs is variable, but in a study of discography in asymptomatic control subjects pain was not produced from abnormal discs,21 although others have found a higher false-positive rate.22 The diagnostic accuracy of discography is still unclear because double-blind controlled trials have not been performed.

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However, using successful surgical fusion as an end point, an 82% accuracy with an 89% sensitivity has been recorded. The specificity was low at 43%, but abnormal discs with no pain reproduction that were left at surgery did not result in poor results.23 However, if discography is used only for cases in which all other clinical and diagnostic criteria for the diagnosis of discogenic pain are fulfilled in sequence, the false-positive rate is decreased. Discography is most accurate and useful when the diagnosis of discogenic pain is highly probable.24 In the cervical spine there is a greater degree of discordance between MRI and discography owing to posterolateral cleft formation. The accuracy of cervical discography is less clear, and there is an increased potential for infection in the disc after the investigation.

Posterior Annular Tears Clefts may develop in the annular fibers between the concentric fibers or in a radial pattern, or a combination of the two may occur. This process may be associated with a traumatic episode, particularly in younger patients, but it has been demonstrated with increased frequency with age, as shown in cadaver studies. These clefts are only demonstrated by MRI or discography.

Magnetic Resonance Imaging and Computed Tomographic Discography The posterior tears can be seen on MR sagittal studies. The disc height is usually maintained on the T1-weighted image and is associated with a small central bulge of the posterior annulus on the midline image and on the axial scan through the disc. On T2-weighted, fast spinecho MR sequences there is a high signal intensity linear

■ FIGURE 43-5

Disc degeneration. A, Three-level discogram shows a normal delineation of the nucleus at L3-L4, degeneration with circumferential posterior annular disruption at L4-L5, and marked degeneration at L5-S1. B, CT discography demonstrates that the contrast medium injected into the nucleus has extended through the posterior annular fibers and circumferentially between the fibers.

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track through the low-signal annulus and a small central bulge. In some cases they may be seen as a bright focus within the outer annulus, which is separated from the remainder of the nucleus as a high intensity zone (Fig. 43-6). Posterior annular tears may not be visible on MRI; compared with cadaver anatomic sections, MRI only had a 67% sensitivity.25 If gadolinium diethylenetriamine pentaacetic acid (Gd-DTPA) is injected, enhancement of the posterior annular cleft may be visualized, and enhancement of the posterior annular tear almost always occurs in the presence of a high intensity zone. Posterior annular tears are best demonstrated by discography with the injection of contrast medium directly into the nucleus, followed by CT, which will define the pattern of flow in the annulus. The tears with high intensity zones on MRI have been shown on CT discography to represent a combination of radial and concentric tears (see Fig. 43-6), and the significance in relation to symptoms has been the subject of considerable debate. Aprill and Bogduk 26 found that the presence of high intensity zones had a positive predictive value of 86% for a severely disrupted and symptomatic disc. They concluded that a high intensity zone was a sign of painful internal disc disruption. Subsequent investigators looking for correlation between high intensity zones and pain on discography have come to conflicting conclusions. The sign has also been reported to have a high specificity and positive predictive value (95.2% and 88.9%, respectively) for discography-induced pain but was limited by poor sensitivity (26.7%).27 A high rate of concordance between high intensity zones and painful discography was also reported by other authors.28 However, other studies have also found no statistical correlation between the presence of high intensity zones and pain response on discography.29 To further

■ FIGURE 43-6

complicate this issue, discographic injection in subjects with high intensity zones provoked significant pain in approximately 70% of subjects whether symptomatic with low back pain or not.30 In studies of MRI of the lumbar spine, high intensity zones have been reported to be a common finding (prevalence, 45.5%) in patients with low back and leg pain but a group of patients with particular clinical features was not defined.31 A high incidence of high intensity zones in asymptomatic volunteers between ages 20 and 50 years (32% and 33% between two observers) has also been reported.32 A recent study of the natural history of high intensity zones has shown that many stay unchanged, whereas others regress or increase in intensity and that no correlation existed between improvement or exacerbation of high intensity zones and changes in symptoms.33 On the basis of all available evidence, posterior annular tears increase in incidence with age and are common in the asymptomatic population. They may be a source of pain, but it is uncertain whether high intensity zones are more commonly painful than other posterior annular tears.

Herniation of the Nucleus Pulposus Radial tears in the posterior annulus enable the nucleus pulposus to pass through the annulus and result in a herniation extending beyond the normal margin of the disc and delineated by the margins of the vertebral body end plate. Such herniations may include annular and endplate material, especially in the cervical spine. The importance of imaging is to demonstrate the precise anatomic features and extent of the herniation and its effect on the nerve roots. Classification of disc herniations is most commonly based on the morphologic model, with categories of normal disc, bulging disc, protrusion, extru-

Posterior annular tear. A, Sagittal, T2-weighted, turbo spin-echo MR image demonstrates a high signal zone in the outer fibers of the annulus with no evidence of nuclear material herniating through the posterior annulus. B, CT discography demonstrates a radial posterolateral tear through the annulus with a concentric component.

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sion, and sequestration. A bulging disc refers to a circumferential symmetric disc extension beyond the disc space. A protrusion indicates focal or asymmetric disc extension beyond the interspace with preservation of the outer annular/posterior longitudinal ligament complex with the base against the parent disc broader than any other diameter of the protrusion and with continuity of nuclear material to the nucleus pulposus. An extrusion is focal with disruption of the outer annular fibers; the base against the parent disc is narrower than any diameter of the extruding material, but continuity with the parent nucleus is maintained. Finally, sequestration indicates complete loss of continuity of the disc material with the parent disc with migration away from the disc in some cases (Table 43-2).34

Radiography Plain radiographs are of little value in the diagnosis of disc herniation and cannot visualize neurologic structures either directly or indirectly. They only provide information on disc height, instability, bony canal size in the cervical spine, and more severe causes of neck pain, such as infection or neoplasm. In the cervical spine, if the herniation is chronic it may be associated with a visible osteophyte, which may be important in surgical planning but does not provide any information about the soft tissue mass. Similarly, in the thoracic and lumbar spine, an old calcified disc herniation may be visible on lateral plain radiographs in chronic cases. Anteroposterior radiographs are useful in the lumbar spine in the presence of transitional vertebra to confirm the level before surgery.

Computed Tomography Computed tomography can demonstrate a disc herniation in the spinal canal and is an alternative method of investigation in patients in whom MRI is contraindicated. In the cervical spine there may be streak artifacts from the shoulders, but this is unusual with multislice scanners and can be partially negated by reconstructions. Unenhanced CT does not differentiate the cord from the theca in the cervical and thoracic spine. On CT, the herniated disc material will appear as a focal mass contiguous with the disc, having an attenuation value of 50 to 100 Hounsfield units and encroaching on the spinal canal either centrally or posterolaterally. The low-attenuation epidural fat will be obliterated and the dural sac deformed. The nerve root will be displaced posteriorly and may be compressed against the bony margin of the canal. Fragments that have migrated should be carefully evaluated and not confused with epidural veins, conjoint TABLE 43-2 Classification of Disc Herniations Bulging disc Protrusion Extrusion Sequestration

Circumferential symmetric disc extension Focal/asymmetric disc extension, preserved annulus/PLLC Focal extension with disruption of annulus/PLLC Loss of continuity fragment—parent disc

PLLC, posterior longitudinal ligamental complex.

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nerve roots, and dorsal root ganglia. Large herniations that occupy most of the canal may be misdiagnosed owing to loss of clarity between the disc and dural sac. CT is ideal for demonstrating calcification in the disc material, which has been reported to occur in up to 75% of thoracic disc herniations, and any associated osteophyte formation or end-plate fragments, particularly in the cervical spine. It is difficult to differentiate between protrusions and extrusions on CT, but disc herniation and nerve root compression in the foramen is visualized and is further improved on multislice CT systems by volume acquisition and reconstructions in the sagittal plane. The reported accuracy of CT in the cervical spine ranges from 72% to 91%, but these studies were performed before multislice CT.35,36 The accuracy in the lumbar spine has been reported to be between 73% and 83%.37,38 In the cervical and thoracic spine the CT examination should be combined with an intrathecal injection of contrast agents, which will increase visualization of the nerve roots and cord, with accuracy reported up to 96%.35

Magnetic Resonance Imaging Magnetic resonance imaging is the imaging modality of choice for evaluating a patient with a suspected disc herniation. Most centers will perform T1- and turbo spin-echo (TSE) T2-weighted sequences in the sagittal and axial planes, although some advocate more limited initial sequences. In the cervical spine a gradient-echo, T2-weighted, axial MR sequence may be preferred. On the T1-weighted, sagittal image the disc is of uniformly intermediate signal with the prolapse extending posteriorly behind the line of the posterior rim of the vertebral body on one or two images. The degree of indentation of the lowsignal dural sac is dependent on the position of the herniation and on the thickness of the high-signal epidural fat. On the sagittal T2-weighted, turbo spin-echo sequence the herniated nuclear material will show as increased signal through the low-signal posterior annulus that projects beyond the posterior vertebral line. The relationship of the protrusion to the nerve root is clearly defined, and root deformity and displacement can be identified. The evaluation of this relationship is of major importance and has been graded depending on whether the disc is touching, displacing, or compressing the nerve root.39 A protrusion will show a low-signal intact line of outer annular fibers and the posterior longitudinal ligament. On the axial T1-weighted studies the localized protrusion can be identified outlined against the low-signal dural sac and high-signal epidural fat (Fig. 43-7). The T2-weighted sequence will demonstrate the nerve roots in and emerging from the dural sac. Extruded herniations that have penetrated the outer annular fibers appear as a globular mass of intermediate signal on T1-weighted images with incomplete outer low-signal fibers but with continuity of the herniated material maintained with the nucleus pulposus. The height of the disc of origin is narrower at the base of the herniation than the diameter of the extruding material on the sagittal view, and/or the diameter of the base of the herniated material on the axial view is similar or narrower than the anteroposterior measurement of the herniated material (Fig. 43-8). The extruded disc

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■ FIGURE 43-7

Disc protrusion. A, Sagittal, T2-weighted, turbo spin-echo MR image shows the herniation continuous with the nucleus pulposus, similar width to the disc space, and an intact low signal annular margin. B, Axial, T1-weighted MR image shows the base of the herniation is much wider than the height. The right nerve root is compressed, and the surrounding epidural fat is obliterated.

■ FIGURE 43-8

Disc extrusion. A, Sagittal, T1-weighted, turbo spin-echo MR image demonstrates a large L5-S1 herniated nucleus pulposus that has no low signal outline of outer annular fibers. B, Sagittal, T2-weighted, turbo spin-echo MR image shows the herniated material remains with increased signal and has not migrated away from the remainder of the disc. C, Axial, T2-weighted, turbo spin-echo MR image shows the herniation with a narrow base that is similar to the height of the prolapse. There is grade 3 compression of the right S1 nerve root.

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may remain deep to the posterior longitudinal ligament or may penetrate it, but differentiation on MRI has been reported to have a low accuracy.40 If the nuclear material becomes sequestrated, the continuity with the parent nucleus pulposus is lost and fragments may migrate behind the adjacent vertebra (Fig. 43-9). Careful evaluation of the MRI is required to identify free fragments that have migrated particularly into the nerve root canals. If the disc herniation is acute, the herniated material is of high signal on T2-weighted images, but persistent herniations become dehydrated and lose signal. Herniations

■ FIGURE 43-9

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may occur into the foramen in a far-out posterolateral position and may displace the nerve root outside the foramen or compress the root in the foramen (Fig. 43-10). Paramagnetic contrast agents have not been found to be of great value in the evaluation of uncomplicated disc herniations,41 although the perception of size and location of the herniation may be significantly changed by the contrast medium enhancement and improved delineation between disc material and nerve root. Contrast medium enhancement may be useful in recurrent herniations and in the postoperative evaluation for differentiating between

Disc sequestration. Sagittal T1-weighted (A) and T2-weighted (B) turbo spin-echo MR images demonstrate a large mass of herniated nucleus pulposus that has migrated away from the disc behind the body. C and D, Axial T2-weighted turbo spin-echo MR images show the mass of nuclear material behind the vertebral body and migration into the right nerve root canal compressing the nerve root.

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■ FIGURE 43-10

Lateral disc herniation. A, Axial, T1-weighted turbo spin-echo MR image shows an intermediate signal mass extending out from the outer foramen with a base against the disc and displacing dorsally the exiting nerve root. B, Axial, T2-weighted, turbo spin-echo MR image demonstrated that the mass is of increased signal with some surrounding edema. C, Sagittal, T1-weighted, turbo spin-echo MR image through the foramen shows the mass compressing the nerve root in the foramen.

fibrosis and recurrent herniation and between a lateral disc herniation and a nerve sleeve tumor. Enhancement of compressed nerve roots has been demonstrated in a number of series, although the percentage of cases with enhancement has varied between 21% and 68%.42,43 Tyrrell and colleagues,44 in a large series of patients, found a statistically significant relationship between nerve root enhancement and the presence of a sequestrated disc, but the sensitivity of nerve root enhancement overall was 23.5%. Finally, an epidural hematoma associated with a posterior annular tear may result in symptoms indistinguishable from a disc herniation. On MRI the hematoma appears as an extradural mass that is often largest at the level of the

midvertebral body, with a tapered indistinct margin at the level of the disc (Fig. 43-11). It may have a high intensity on T1-weighted images and an intermediate signal on T2-weighted images, although the timing of the imaging will affect the signal characteristics and resorption is usually rapid.45-48

Vertebral End Plate Vertebral end-plate changes occurring in conjunction with disc degeneration vary considerably in severity, depending on the degree of disruption of the cartilage end plates and the response of the adjacent subchondral bone.

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■ FIGURE 43-11

Cervical epidural hematoma. Sagittal T1-weighted (A) and T2-weighted (B) turbo spin-echo MR images show a tapered mass behind the body that is of intermediate signal on the T1-weighted image and of increased signal on the T2-weighted image. Six weeks later there was complete resolution of the hematoma.

Radiography The most common lesion seen on the lateral radiograph of the thoracic and lumbar spine is the Schmorl node, which appears as a well-defined indentation of the bony end plate just posterior to the midline. More extensive interosseous end-plate herniations may occur, especially anteriorly, and these may result in increased anteroposterior growth of the vertebral bodies with slight wedging. The end plate may be irregular and sclerotic if there is moderate to severe disc degeneration, and in some cases hemispheric sclerosis of the anterior part of the vertebral body may be present. End-plate irregularity and Schmorl’s nodes are also a feature of Scheuermann’s disease.

Magnetic Resonance Imaging Schmorl’s nodes appear on MRI as indentations of the end plate containing small extensions of high signal intensity in the nucleus within them on T2-weighted sequences. MRI may show a rim of low signal in the vertebral marrow on T1 weighting around the interosseous herniation, with high signal on T2 weighting, suggesting some marrow reaction to the herniation. Signal intensity changes are also seen in the end plates and adjacent vertebral bodies of both cervical and lumbar vertebrae in association with disc degeneration. These changes tend to fall into three main categories, as described by Modic and coworkers,49 but mixed features may also be present: type 1 changes have areas of low T1 and high T2 signal and have high signal on the short tau inversion recovery (STIR) sequence (Fig. 43-12) and enhancement after paramagnetic contrast injection and have been shown on histology to relate to an increase in marrow vascularity, with some inflammatory cell infiltration. Type 2 changes are more common and have a high

T1-weighted signal and isointense or slightly hyperintense T2 signal, with a low signal on STIR (Fig. 43-13) and no evidence of enhancement. Histologic studies have shown thickened trabeculae and replacement of normal marrow by fat. Type 3 is characterized by low T1- and T2-weighted signals and is associated with sclerosis on radiographs due to marked trabecular thickening. This classification has been shown to be reliable and reproducible. In some patients, type 1 and type 2 changes may occur at different levels in the same patient and a mixture of types 1 and 2 may occur at the same level. Type 1 changes are considered to be the earliest and the most active stage in the process with evolution to type 2,49 although recent longitudinal studies have demonstrated some type 2 changes converting to type 1.50 The symptomatic significance of these changes is still being evaluated with varying result. Type 1 lesions were not reported in a series of asymptomatic subjects, but a recent study has identified all types of end-plate changes in a series of subjects without significant recent back pain. Comparative studies with pain provocation at discography have suggested a close relationship between type 1 changes and back pain reproduction,51 as well as a high specificity and positive predictive value for the various types of endplate changes as an indicator of a painful disc at discography.52,53 In a small longitudinal study, which included six patients with type 1 changes, Modic and colleagues49 suggested a temporal evolutionary trend of type 1 to type 2. A recent longitudinal study has shown that type 1 end-plate changes are dynamic lesions that either increase in size or convert to type 2; if the type 1 lesion does convert to type 2, it starts to do so within 2 years in most cases. There is also evidence, although not at a statistically significant level, that conversion from type 1 to type 2 is related to an improvement in a patient’s symptoms.54

■ FIGURE 43-12

Modic type 1 end-plate changes. A, Sagittal, T1-weighted, turbo spin-echo MR image shows decreased signal in the vertebra adjacent to L4-L5. B, Sagittal, T2-weighted, turbo spin-echo MR image shows increased signal in the same region. C, STIR MR sequence shows high signal of edema. Modic type 2 changes are present at L5-S1.

■ FIGURE 43-13

Modic type 2 end-plate changes. T2-weighted (A) and T1-weighted (B) turbo spin-echo MR images show focal irregularity of the cartilage end plate and subchondral bone with increased signal in the adjacent vertebral bodies on both sequences.

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Osteoarthritis of the Facet Joints Facet joint pain has been described as an ache in the neck or low back and may refer to the shoulder and buttock, respectively. The pain may also refer to both upper and lower limbs, respectively, and in the lower limbs may refer along the back of the leg, sometimes to the ankle. It may be increased in extension and in the case of the lumbar spine may be eased by exercise. In the neck, muscle spasm secondary to facet joint pain may produce a torticollis. Osteoarthritis of the facet joints is seen as early as 30 years of age and is almost constant after 60 years of age.

Radiography Radiographic features are present on the lateral and anteroposterior views of the cervical and lumbar spine but are more difficult to appreciate in the thoracic spine owing to the overlying ribs and the alignment of the joints. The initial loss of cartilage thickness is not visualized, but once articular cartilage loss is well established, resultant joint space narrowing will be seen where the joint spaces are parallel to the beam, in particular the lateral cervical projection or the anteroposterior view of the upper lumbar spine. Sclerosis of the subchondral bone and marginal osteophyte formation with hyperostosis

■ FIGURE 43-14

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results in increased density in the region of the facet and hypertrophy of the apophyseal process, which may be seen projecting laterally on an anteroposterior radiograph, particularly in the cervical spine (see Fig. 43-2) and lower lumbar spine. On the lateral view, remodeling may be seen but subchondral cysts are difficult to appreciate on plain radiographs. Oblique views may show the facet joint spaces more clearly when they are more coronally aligned, as in the lower lumbar spine. The articular process of the facet joints may impinge on the upper surface of the lamina above and below, causing further sclerosis.

Computed Tomography Computed tomography is considerably superior to radiographs in demonstrating the facet joints in the thoracic and lumbar spine. The horizontal orientation of the joints in the cervical spine requires volume acquisition and multiplanar reconstruction. Although the cartilage is not visualized, the joint space can be accurately evaluated and bony articular surface irregularities, subchondral sclerosis, and subchondral cysts all clearly seen. Osteophyte formation occurs on both dorsal and ventral margins of the joint, resulting in displacement of the capsule and ligaments, and ventral osteophytes may cause compression of adjacent nerve roots. CT appearances of degeneration have been graded in the lumbar spine (Fig. 43-14).55 Grade 0

Facet osteoarthritis. CT of facet joints. A, Grade 0: normal joint space and subchondral bone. B, Grade 1: both facet joint spaces are narrowed and slightly hypertrophied. C, Grade 2: The joint space is narrowed with subchondral sclerosis and small cysts and mild osteophyte formation. D, Grade 3: severe degeneration with joint space irregularity, marked osteophyte formation, and bone sclerosis.

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is normal with a joint space of 2 to 4 mm. In grade 1, the joint space is reduced to less than 2 mm and/or minor osteophytes and/or hypertrophy of the articular process are present. Grade 2 has narrowing of the joint space with or without any combination of moderate osteophyte formation and articular process hypertrophy, but mild subchondral irregularity is present. Finally, grade 3 has joint space narrowing, severe subarticular bone irregularity, and/or severe osteophytes and/or articular process hypertrophy. When this system of grading was used, interobserver correlation was 0.6 with one grade agreement in 95% to 97%.55 The severity of CT changes in the lumbar spine does not, however, correlate with the presence of back pain.56

Magnetic Resonance Imaging Magnetic resonance imaging particularly in the axial plane can similarly demonstrate the features of osteoarthritis of the facet satisfactorily but, unlike CT, the articular cartilage is seen as intermediate signal on T1- and proton density–weighted sequences, although the separation of the two surfaces is rarely possible unless an effusion is

■ FIGURE 43-15

present. Subchondral line irregularity is not as clearly seen on MRI, but T2-weighted sequences demonstrate effusions and cysts as fluid collections with high signal intensity within the joint or in the subchondral bone, respectively (Fig. 43-15). Osteophytes may also be demonstrated on both T1- and T2-weighted sequences, but bone sclerosis is less easily appreciated. The same grading system can be used for MRI as CT, but the interobserver correlation is lower at 0.41; however, one grade agreement was again 95% to 97%.55 Both CT and MRI will also demonstrate the ligamentum flavum, which may appear thickened or buckled, and the capsular ligamentum flavum combination is better seen with MRI. Calcification in the ligamentum flavum is difficult to define on MRI, and CT is the imaging method of choice if this feature is of diagnostic importance.

Pain Testing To precisely relate the symptoms of neck or back capsular pain to the facet joints, image-guided injections of local anesthetic are required. The rationale is to identify whether the patient’s neck, back, and/or limb pain

Facet osteoarthritis. MRI of facet joints. A, Grade 0 normal cartilage thickness is seen with a smooth, low signal, subchondral bone line. B, Grade 1: the joint spaces are reduced with slight bony hypertrophy. C, Grade 2: joint space loss and mild to moderate osteophyte formation. D, Grade 3: there is marked irregularity of the articular surfaces, joint space loss, and marked osteophyte formation.

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Computed Tomography The typical appearance is of a rounded juxtafacet mass with relatively low attenuation contents. Calcification may occur within the cyst or in the wall and is well demonstrated by CT (Fig. 43-17). Gas may also be present in the cyst, appearing as low attenuation and sometimes associated with gas in the facet joint. The associated osteoarthritis of the facet joint is well demonstrated on CT, which can also be utilized to guide injections of local anesthetic or corticosteroid into the cyst either directly or via the facet.58

Magnetic Resonance Imaging

■ FIGURE 43-16

Facet injection. CT-guided needle is inserted into the posterior capsule of the facet and a very small quantity of contrast agent is injected to check the position, followed by local anesthetic. Corticosteroid may also be injected for therapeutic purposes.

is significantly reduced or removed by the injection of local anesthetic into the facet joint. The needle may be placed in the cervical or lumbar facets using either fluoroscopic or CT guidance (Fig. 43-16). A small quantity of contrast medium may be injected to confirm the intraarticular position, and this is followed by up to 1 mL to avoid rupture or epidural extravasation of a longer-acting local anesthetic. The response to the injection is provided by the patient over the following 2 or 3 hours. A corticosteroid may be added after the local anesthetic as a therapeutic element, but it is not part of the diagnostic test. Studies of the effectiveness of this examination as a diagnostic test have been conflicting, which is compounded by the absence of a clear gold standard. The injections, however, may provide short- or longer-term relief, enabling mobilization and exercise programs to be instituted.

Cysts of the Intervertebral Facet Joints Juxta-articular cysts of the facet joints of the lumbar spine have been recognized to be more common with the advent of CT and MRI. They may be synovial, arising from the facet joints containing xanthochromic fluid, or ganglion cysts containing gelatinous material and may or may not communicate with the joint. They have an incidence of 0.65% in the lumbar spine and are much less commonly documented in the cervical spine.57 They more commonly occur in women, with an age range of 16 to 81 years and a mean of 57 years. These patients have low back pain and are often diagnosed only after imaging, but they also present with, or exhibit, radicular symptoms. The majority occur at L4-L5, but other lumbar levels may be affected, and bilateral cysts may occur. Facet osteoarthritis is an almost universal finding, and the incidence of degenerative spondylolisthesis varies between 42% and 65%.

Facet cysts are usually situated posterolaterally in the spinal canal and proportionally vary in size relative to the surface area of the spinal canal from 20% to 90%, resulting in varying degrees of nerve root and thecal compression. The cysts are best seen on T2-weighted sequences, where they have a discrete low-signal wall less than 3 mm thick. On T1-weighted images the wall may be mildly hyperintense or isointense, with the thecal contents making the cyst difficult to visualize, although the rim does enhance in the majority of cases in which contrast agent was administered. The cyst exhibits a variable pattern, depending on its contents; in the majority, the contents are hyperintense on T2-weighted images and isointense on T1-weighted images (see Fig. 43-17). However, nearly 25% of cysts have been reported to be hyperintense on T1-weighted images and hypointense on T2-weighted images. The mild T1 hyperintensity has been ascribed to a number of factors, including a high protein content or breakdown products of hemorrhage. Uncommonly, cysts may be hypointense or hyperintense on both sequences. Facet cysts must be distinguished from conjoint nerve roots, a sequestrated disc herniation, an intraspinal cyst, or a cystic neurofibroma. The natural history of cysts is variable, with spontaneous regression being seen in some cases. If symptomatic radicular compression is present, injections of corticosteroid may result in regression, but surgery remains the definitive treatment.

Degenerative Spondylolisthesis The displacement of one vertebra on another is dependent on a biomechanical failure of the support of the posterior elements and may be anterolisthesis or retrolisthesis depending on the direction of stress of the vertebral bodies. Thus, retrolisthesis is more common in the upper lumbar spine, whereas degenerative anterolisthesis is more frequent at L4-L5. The prevalence of anterolisthesis in the lumbar spine increases sharply with age, with approximately 25% of those persons older than age 75 years showing subluxation of 5 mm or more; women may be affected more often than men.59 Degeneration of the facet joints is the most common cause of spondylolisthesis. In the cervical spine, the facet joints are horizontally aligned and osteoarthritic changes in the facet joints may lead to a loss of support of the vertebral body by the posterior elements, with forward displacement of the vertebral body. The pathology is that of severe osteoarthritis of the facet joints, with destruction of the articular surfaces, and loss of support of the ligamentum flavum and facet capsule.

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■ FIGURE 43-17

Facet cyst. A, Axial, T2-weighted, turbo spin-echo MR image demonstrates the cyst with the base on the inner aspect of the facet joint. The outer wall of the cyst is of low signal, whereas the contents are of increased signal. The nerve root and dural sac are compressed by the cyst. B, Sagittal, T2-weighted, turbo spin-echo MR image shows the cyst occupying the spinal canal. C, CT shows extensive calcification with the wall of the cyst and air within the fluid content.

In most cases of degeneration of lumbar spondylolisthesis, the facets are aligned in the sagittal plane. The presence of a marked coronal alignment of the facets tends to reduce the likelihood of a degenerative spondylolisthesis. Disc degeneration may also lead to forward displacement of one vertebral body on another. The presence of a degenerative spondylolisthesis may be associated with pain, and this may be due to osteoarthritis of the facets, the presence of disc degeneration, or a combination of these causing nerve root ischemia. There is a good correlation between the presence of low back and leg pain and the presence of degenerative spondylolisthesis.60

Radiography The recorded normal range of forward displacement of one lumbar vertebra on another has been wide, with up to 5 mm being quoted as normal, but 3 mm should be used as the upper limit of normal. Recent studies indicate overall incidence of anterolisthesis in women older than the age of 65 as 28.9% and those with retrolisthesis as 14.2%, whereas if 5-mm slip is used as a guide, then the prevalence drops to 14.2% and 3.2%, respectively.61 Most degenerative spondylolisthesis is at a single level, with 10% at two levels, and rarely exceeds 25% of the adjacent

CHAPTER

vertebral body. The lateral radiograph will demonstrate the forward displacement of the superior vertebral body with the lamina and spinous process, and the extent of the slip is measured from the posterior rim of the adjacent vertebral end plates (see Fig. 43-1). Disc degeneration is usually present with narrowing of the disc space, and some sclerosis of the vertebral end plate may also be seen. Sclerosis and bone proliferation are often present in the facet joints. On the anteroposterior radiographs the facet joints are usually sagittally aligned, and this can be confirmed on CT, which will also demonstrate the severe facet osteoarthritis that may produce considerable osteophyte formation and ossification of the ligamentum flavum. Dynamic demonstration of the effect on the dural sac by the degenerative spondylolisthesis can be achieved with flexion and extension views in combination with myelography, which shows increased dural sac compression on extension and widening of the dural sac on flexion.

Magnetic Resonance Imaging The sagittal studies demonstrate the disc degeneration and the distortion of the posterior annulus due to the vertebral displacement, which results in the posterior disc margin being stretched and sometimes bulging into the canal. The axial scans will demonstrate the pseudodisc appearance of spondylolisthesis, because the slice through the disc will demonstrate the position of the disc in relation to the inferior vertebral body, with an apparent absence of a superior vertebral body, giving the appearance of a disc prolapse. The smooth nature of the disc and its uniform curvature will differentiate this

■ FIGURE 43-18

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pseudo-disc appearance of spondylolisthesis from a disc prolapse (Fig. 43-18). The facet joint degeneration is shown by the irregularity of the articular surface, cartilage loss, and proliferation of osteophyte formation. The combination of forward displacement and disc degeneration and bulging, associated with the reparative changes around the osteoarthritic facets, and thickening or buckling of the ligamentum flavum is a common cause of spinal stenosis. This may be severe, with central canal stenosis causing compression of the nerve roots within the dural sac and narrowing of the subarticular space by the ventral slip of the inferior articular process reducing the entry zone of the nerve root canal. The intervertebral foramen at the involved level assumes a more horizontal configuration, resulting in reduced foraminal height; and in combination with the bulging annulus into the foramen, this results in foraminal stenosis. The degree of stenosis is well demonstrated on MRI, which will also clearly demonstrate, in the sagittal plane, the degree of dural sac compression and the relationship of the disc, the facets, and the ligamentum flavum as to their relative contribution to the degree of stenosis. Dynamic sagittal views in flexion and extension may be helpful in assessing the degree of stenosis.

Spinal Stenosis Spinal stenosis has been defined as any type of narrowing of the spinal canal causing compression of the content of the canal due to conflict between the available space and its content. The stenosis may involve the central canal, the entry zones of the nerve root canals, or the intervertebral

Degenerative spondylolisthesis. A, Sagittal, T2-weighted, turbo spin-echo MR image demonstrates the forward displacement of L4 on L5 with stretching of the posterior annulus and degeneration of the disc. B, Axial, T2-weighted, turbo spin-echo MR image shows grade 4 osteoarthritis of the facet joints with the posterior overlap of the annulus producing a mild pseudo-disc appearance.

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foramina and, in many cases of degenerative stenosis, a combination of narrowing. Degenerative stenosis particularly involves the cervical and lumbar spine, and underlying developmentally short pedicles and a small spinal canal will increase the likelihood of degenerative stenosis. Degenerative spinal stenosis is due to osteoarthritis of the facet joints with or without hypertrophy, osteophyte formation on the posterior vertebral rim, degenerative bulging of the intervertebral discs, and degenerative changes in the ligamentum flavum. It occurs increasingly with increasing age and presents as long tract or root signs in the cervical spine and root compression in the lumbar spine. In cervical stenosis with spinal cord myelopathy, the symptoms may be long tract or segmental. Long tract involvement is shown by exaggerated tendon reflexes, the presence of pathologic reflexes, spastic quadriplegia, a spastic type of myelopathy of the hand, glove and stocking sensory loss, and bladder and bowel disturbance, whereas segmental signs are motor deficits affecting that segment.62 Stenotic impingement of the cervical nerve root usually manifests as occipital, posterior neck, shoulder, or upper extremity radicular symptoms. Pain radiation to the legs may be unilateral or bilateral and may involve single or multiple nerve root distributions. Claudication is commonly related to the position of the lumbar spine, and the walking distance may vary, with greatest limitation being related to the more severe level of pain. Symptoms fluctuate in severity and increase gradually in most patients over a period of years. Motor and sensory disturbances vary in incidence, with sensory disturbances in the legs being common, weakness being less common, and bowel and bladder disturbances being unusual.

Radiography In the cervical spine, central canal stenosis is caused by osteophytosis and ligamentous thickening. Quantitative measurements of the width of the cervical spinal canal are frequently performed on radiographs because these measurements are predictive for the presence of spinal canal stenosis. The spinal canal width is calculated as the ratio between the anteroposterior diameter of the spinal canal and the anteroposterior diameter of the vertebral body. In normal volunteers, this ratio is about 1. If the ratio is below 0.8, a developmental spinal canal stenosis may be present.63 On conventional lateral radiographs the distance between the posterior surface of the vertebral body and the spinolaminar line can be measured. A spinal cord compression may occur if this distance is 10 mm or less. On the other hand, if this distance is 13 mm or more, spinal canal stenosis is unlikely. In the lumbar spine the anteroposterior diameter of the canal is measured from the posterior aspect of the vertebral body to the line joining the upper and lower tips of the articular process, and at L4 the normal mean is 13 mm (range, 10 to 16 mm).63 On the anteroposterior lumbar films, interpedicular distance has a mean at L4 of 23 mm (range, 19 to 27 mm) but sagittal alignment of the facet joints lying inside the pedicles with a short lamina is particularly prone to spinal stenosis. Plain radiographs are unable to demonstrate the shape of the canal or the size of the dural sac.64,65

Computed Tomography Computed tomography enables the cross-sectional shape and area of the spinal canal to be measured. The combination of the internal canal soft tissue and bony dimensions is of major relevance with regard to the space for the dural sac. In the majority of cases the minimal crosssectional area in both the cervical and lumbar spine is at the level of the discs and facet joints. In the cervical spine, a cross-sectional area of 60 mm2 is reported to be predictive of cervical spinal stenosis. CT of the cervical spine will also demonstrate the presence of ossification of the posterior longitudinal ligament (OPLL), which is a major cause of spinal stenosis, particularly in Japan. OPLL is more frequently present in men than in women and typically manifests in the fifth to seventh decades. The diagnosis of OPLL is established by its characteristic appearance on CT as a dense ossified strip of variable thickness that is evident along the posterior margins of the vertebral bodies and the intervertebral disc. OPLL may extend over multiple levels but also can be segmental. In the lumbar spine, the cross-sectional area of the lumbar spinal canal, including the ligamentum flavum, is normally 2.5 cm2; and less than 1.45 cm2 would be considered small, but below 0.75 cm2 impairment of circulatory and nerve function will occur. In the cervical spine, accurate evaluation of the cross-sectional size of the dural sac usually requires intradural administration of a contrast agent; and on CT myelography a measurement below 60 mm2 would confirm significant stenosis. CT myelography will also enable dynamic evaluation of flexion and extension on the spinal canal to assess the effect on the degree of stenosis of buckling of the ligamentum flavum and disc bulging in extension. It will also assist in the cervical spine in the differentiation of nerve and cord compression between osteophytes and disc bulge or herniation if this is of therapeutic importance or in patients in whom the results of MRI were ambiguous or technically suboptimal. Comparison with MRI has shown only moderately good concordance, with CT myelography tending to upgrade the degree of spinal compromise, neural foraminal encroachment, and cord diameter reduction.66

Magnetic Resonance Imaging Magnetic resonance imaging is the preferred method for evaluating spinal stenosis in both the cervical and lumbar spine, particularly utilizing the T2-weighted sequence as it enables both the bony and soft tissue effect on the dural sac dimensions and cord and nerve roots to be assessed without the use of intrathecal contrast agents. However, in most cases osteophytes and disc bulge or herniation cannot be differentiated, particularly in the cervical spine on MRI and thus are referred to as disc-osteophyte complex by some authorities. The T2-weighted sequences show loss of cerebrospinal fluid in front and behind the cord in the sagittal and axial planes with flattening of the cord. The normal differential of gray and white matter may be lost on the T2-weighted, gradient-echo, axial MR studies. In severe cases of cervical cord compression the cord may have high signal intensity within its substance on the T2-weighted images (Fig. 43-19).

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■ FIGURE 43-19

Cervical spondylitic myelopathy. A, Sagittal, T2-weighted, turbo spin-echo MR image shows compression of the canal and cord by degenerative retrolisthesis of C3-C4 combined with extruded disc material and indentation posteriorly by the buckled ligamentum flavum. A line of high signal intensity is present in the cord at the site of compression. B, Axial, T1-weighted, turbo spin-echo MR image demonstrates the flattened and distorted cord. C, Axial, T2weighted, gradient-echo MR image shows the flattened cord with high signal intensity in the gray and white matter due to myelopathy.

In the lumbar spine, loss of the high signal intensity of the cerebrospinal fluid around the nerve roots on T2-weighted axial images is also valuable for assessing clinically relevant spinal stenosis. In central stenosis, the dural sac is compressed at the disc level anteriorly by the bulging disc and posterolaterally by the osteophytes of the osteoarthritic facets and the buckled ligamentum flavum. Individual nerve roots are not seen on either the axial or sagittal images because they are compressed together (Fig. 43-20). On the axial sequences the nerve roots in the lateral recess can be identified. The lateral recess is bordered posteriorly by the superior articular facet, laterally by the pedicle, and anteriorly by the vertebral body and disc. Lumbar lateral recess stenosis occurs when a hypertrophic superior facet encroaches on the

recess, often in combination with a narrowing due to a bulging disc and osteophyte. Foraminal stenosis occurs when a hypertrophic facet, vertebral body osteophyte, or bulging disc narrows the neural foramen and encroaches on the nerve roots. The foramina are assessed on both the sagittal and axial studies because stenosis may be in the anteroposterior direction, craniocaudal, or a combination of both and visualization of the nerve root is the clinically relevant feature. When the epidural fat surrounding the nerve root within the foramen is obliterated on sagittal T1-weighted scans, marked encroachment is present. The nerve root may also be compressed in one plane only. A systematic review of the accuracy of diagnostic tests for lumbar spinal stenosis concluded that the quality of

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■ FIGURE 43-20

Lumbar spinal stenosis. A, Sagittal, T1-weighted, turbo spin-echo MR image demonstrates marked narrowing of the spinal canal at each disc level. B, Sagittal T2-weighted, turbo spin-echo MR image shows the compression of the dural sac at the disc levels due to bulging and facet indentation. C, Axial, T2-weighted, turbo spin-echo MR image shows grade 3 degeneration of the facets, shortened pedicles, and severe compression of the dural sac. There is no cerebrospinal fluid remaining around the nerve roots in the dural sac.

the studies’ design was insufficient to draw a conclusion on which imaging modality is most accurate.67 Foraminal stenosis may occur at more than one level, there may be a discrepancy between the clinical evaluation and the imaging, or the symptoms and signs may be equivocal for chronic nerve root compression. In these circumstances a CT-guided selective nerve root block (Fig. 43-21) with local anesthetic may be helpful in isolating the symptomatic level or confirming the origin of the symptoms. Localized injections of corticosteroids around the nerve root have also been performed.

DIFFERENTIAL DIAGNOSIS Correlation between Clinical and Imaging Findings Imaging has been extensively used to demonstrate degenerative changes in the spine in subjects with neck and low back pain, and MRI in particular has become the gold

standard in evaluation of spinal pathology. However, there is a lack of correlation between the presence or absence of symptoms and the imaging findings. The advent of MRI, which is noninvasive and enables the different components of the spine and the cord and nerve roots to be imaged, has enabled the detailed evaluation of asymptomatic subjects. A number of studies have now documented a high rate of abnormal imaging findings in the lumbar spine of an asymptomatic subject (Table 43-3).32,68-72 Only the presence of a disc extrusion and sequestration may represent a clinically significant finding if the symptoms of the patient correspond to the imaging findings. The role of Modic changes is still a subject of debate. Neural compromise, however, is important in the correlation between symptoms and MRI findings. The only substantial morphologic difference between symptomatic patients and asymptomatic volunteers was with the presence of neural compromise (83% vs. 22%), differentiating between asymptomatic subjects and symptomatic disc herniation patients matched according to age, sex, and occupational risk factors.69

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■ FIGURE 43-21

Nerve root injection. A, Sagittal, T2-weighted, turbo spin-echo MR image shows degeneration at the C5-C6 disc with osteophytes and degenerative end-plate changes. B, CT demonstrates narrowing of the foramen by osteophyte formation in the neurocentral joints. C, CTguided needle placement posterior to the root and the vertebral artery.

The pathophysiologic mechanisms that cause nerve root symptoms are still not completely understood. Currently, two concepts are discussed: mechanical nerve root compression and nerve root inflammation caused by inflammatory cytokines present in the herniated nucleus pulposus.

SYNOPSIS OF TREATMENT OPTIONS Disc herniations vary in their natural history, and the majority are treated conservatively. Follow-up studies have indicated that protrusions remained little changed, but larger extrusions and particularly sequestrations may be completely resorbed.45 These findings are supported by a study of asymptomatic subjects that showed little change in protrusions over an average 5-year period.46 A recent report also indicated that the MR appearances of the disc herniation are not of value in planning

conservative care.47 However, if nerve root pain is severe and motor sensory disturbances are present, microdiscectomy may be required. Evidence indicates that surgery provides more rapid relief of symptoms in these cases, but the long-term results between conservative and surgical therapy are similar. If the herniation is large and cauda equina symptoms are present, surgical intervention on an emergency basis is required. The rates of surgical intervention for nerve root compression due to disc herniation vary considerably in different health care systems. Spinal stenosis is usually initially treated conservatively, but surgical decompression of the cervical or lumbar canal may be required in severe cases. The results of decompression are unpredictable because permanent structural and vascular changes in the nerve roots or cord may have occurred, resulting in a relatively poor outcome. The treatment of nonradicular neck and low back pain is considerably more controversial, with many different

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TABLE 43-3 Prevalence of Disc Abnormalities on Magnetic Resonance Imaging in Asymptomatic Subjects Study, Year

Age Group No. Subjects

HNP

Bulging Disc

Degenerated Disc

HIZ

Other

Weishaupt, 199832

20-50 yr (mean, 35) n = 60

60%

20%

72%

33%

Nerve root contact or deviation, 26% Nerve root compression, 2%

Stadnik, 199868

17-71 yr (mean, 42) n = 36 20-50 yr (mean, 36) n = 46 20-80 yr (mean, 42) n = 98 < 60 yr, n = 53 > 60 yr, n = 14 females, 19-24 yr (mean, 28) n = 86

33%

81%

72%

56%

76%

51% of discs

85%

14%

28%

52%

22% 36% 9%

54% 79% 44%

Boos, 199569 Jensen, 199470 Boden, 199071 Weinreb, 198972

46% 93%

No sequestered disc; nerve root contact or deviation, 22%; 64% had disc bulge, protrusion, or extension

HNP, herniated nucleus pulposus; HIZ, high intensity zone.

therapies available, including drugs for pain relief and to treat inflammation, manipulation, physiotherapy, cognitive therapy, and many others. Image-guided local anesthetic injections may provide temporary or longer-term relief and may be repeated. Surgery in the form of spinal fusion is usually reserved for intractable cases and may be performed with or without supplementary metal fixation. The role of disc replacement is still being clinically evaluated, and cellular regeneration of the nucleus pulposus remains at the experimental stage.

What the Referring Physician Needs to Know ■ ■ ■ ■

Are the findings related to normal aging or abnormal? What is the specific nature of the abnormality? What is the location of abnormalities in relation to the nervous system? Can the abnormal findings explain the clinical findings?

SUGGESTED READINGS Boutin RD, Steinbach LS, Finnessey K. MR imaging of degenerate disease in the cervical spine. Magn Reson Imaging Clin North Am 2000; 8:471-490. Loredo JD (ed). Imaging of low back pain. Radiol Clin North Am 2000; 36(6).

Loredo JD (ed). Imaging of low back pain. Radiol Clin North Am 2001; 37(1). Saal JS. General principles of diagnostic testing as related to painful lumbar spine disorders. Spine 2002; 27:2538-2545.

REFERENCES 1. Miller JA, Schmatz C, Schultz AB. Lumbar disc degeneration: correlation with age, sex, and spine level in 600 autopsy specimens. Spine 1988; 13:173-178. 2. Videman T, Nummi P, Battie MC, et al. Digital assessment of MRI for lumbar disc desiccation: a comparison of digital versus subjective assessments and digital intensity profiles versus discogram and macroanatomic findings. Spine 1994; 19:192-198. 3. Batttie MC, Videman T, Gibbons IE, et al. Determinants of lumbar disc degeneration: a study relating life-time exposures and magnetic resonance imaging findings in identical twins. Spine 1995; 20:2901-2612.

4. Sambrook PN, MacGregor AJ, Spector TD. Genetic influences on cervical and lumbar disc degeneration: a magnetic resonance imaging study in twins. Arthritis Rheum 1999; 42:366-372. 5. Kelsey JL, White AA III. Epidemiology and impact of low back pain. Spine 1980; 5:133-142. 6. Coste J, Paolaggi JB, Spira A. Classification of non-specific low back pain: II. Clinical diversity of organic forms. Spine 1992; 17:1038-1042. 7. Mooney V, Robertson J. The facet syndrome. Clin Orthop Relat Res 1976; 115:149-156.

CHAPTER 8. Eisenstein SM, Parry CR. The lumbar facet arthrosis syndrome: clinical presentation and articular surface changes. J Bone Joint Surg Br 1987; 69:3-7. 9. Bogduk N. The sources of low back pain. In Jayson M (ed). The Lumbar Spine and Back Pain, 4th ed. Edinburgh, Churchill Livingstone, 1992, p 64. 10. Schmorl G, Junghanns H. The Human Spine in Health and Disease (E. F. Besemann, trans.). New York, Grune & Stratton, 1971. 11. Vernon RB. Aged related and degenerative pathology of intervertebral discs and apophyseal joints. In Jayson M (ed). The Lumbar Spine and Back Pain, 4th ed. Edinburgh, Churchill Livingstone, 1992, pp 21-22. 12. Hilton RC, Ball J. Vertebral rim lesions in the dorsolumbar spine. Ann Rheum Dis 1984; 43:302-307. 13. Roberts S, Urban JP, Evans H, et al. Transport properties of the human cartilage endplate in relation to its composition and calcification. Spine 1996; 21:415-420. 14. Andersson GBJ, Schultz A, Nathan A, et al. Roentgenographic measurement of lumbar intervertebral disc height. Spine 1981; 6:154-158. 15. Sorensen HK. Scheuermann’s Kyphosis: Clinical Appearances, Radiography, Aetiology and Prognosis. Copenhagen, Munksgaard, 1964. 16. Venner RM, Crock HV. Clinical studies of isolated disc resorption in the lumbar spine. J Bone Joint Surg Br 1981; 63:491-494. 17. Hayes A, Howard TC, Gruel CR, et al. Roentgenographic evaluation of lumbar spine flexion-extension in asymptomatic individuals. Spine 1989; 14:327-331. 18. Pfirrmann CW, Metzdorf A, Zanetti M, et al. Magnetic resonance classification of lumbar intervertebral disc degeneration. Spine 2001; 26:1873-1878. 19. Sachs B, Vanharanta H, Spivey MA, et al. Dallas discogram description: a new classification of CT discography in low back disorders. Spine 1987; 12:287-294. 20. Osti OL, Fraser RD. MRI and discography of annular tears and intervertebral disc derangement. J Bone Joint Surg Br 1992; 74:431. 21. Walsh TR, Weinstein JN, Spratt KF, et al. Lumbar discography in normal subjects. J Bone Joint Surg Am 1990; 77:1081-1088. 22. Carragee EJ, Tanner CM, Khurana S, et al. The rates of falsepositive lumbar discography in selected patients without low back symptoms. Spine 2000; 25:1373-1381. 23. Colhoun E, McCall IW, Williams W, et al. Provocative discography as a guide to planning operations on the spine. J Bone Joint Surg Br 1988; 70:267-271. 24. Saal JS. General principles of diagnostic testing as related to painful lumbar spine disorders. Spine 2002; 27:2538-2545. 25. Yu S, Sether LA, Ho PSP, et al. Tears in the annulus fibrosus: correlation between MR and pathologic findings in cadavers. Am J Neuroradiol 1988; 9:367-370. 26. Aprill C, Bogduk N. High intensity zone: a diagnostic sign of painful lumbar disc on magnetic resonance imaging. Br J Radiol 1992; 65:361-369. 27. Saifuddin A, Braithwaite I, White J, et al. The value of lumbar spine magnetic resonance imaging in the demonstration of annular tears. Spine 1998; 23:453-457. 28. Schellhas K, Pollei S, Gundry C, Heithoff K. Lumbar disc highintensity zone. Spine 1996; 21:79-86. 29. Ricketson R, Simmons J, Hauser B. The prolapsed intervertebral disc: the high-intensity zone with discography correlation. Spine 1996; 21:2758-2762. 30. Carragee E, Paragioudakis S, Khurana S. Lumbar high-intensity zone and discography in subjects without low back problems. Spine 2000; 25: 2987-2992. 31. Rankine J, Gill K, Hutchinson C, et al. The clinical significance of high-intensity zone on lumbar spine magnetic resonance imaging. Spine 1999; 24:1913-1920. 32. Weishaupt D, Zanetti M, Hodler J, Boos N. MR imaging of the lumbar spine: prevalence of intervertebral disc extrusion and sequestration, nerve root compression, end plate abnormalities and osteoarthritis of the facet joints in asymptomatic volunteers. Radiology 1998; 209:661-666. 33. Mitra D, Cassar-Pullicino VN, McCall IW. Longitudinal study of high intensity zones on MR of lumbar intervertebral discs. Clin Radiol 2004: 59:1002-1008.

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34. Milette PC. Classification, diagnostic imaging, and imaging characterization of a lumbar herniated disc. Radiol Clin North Am 2000; 38:1267-1292. 35. Landman JA, Hoffman JC, Braun IF, et al. Value of computed tomographic myelography in the recognition of cervical herniated disc. Am J Neuroradiol 1988; 5:391-394. 36. Jahnke RW, Hart BL. Cervical stenosis, spondylosis and herniated disc disease. Radiol Clin North Am 1991;29:777-793. 37. Modic MT, Masaryk TJ, Boumphrey F, et al. Lumbar herniated disc disease and canal stenosis: prospective evaluation by surface coil MR, CT, and myelography. Am J Neuroradiol 1986; 7:709-717. 38. Jackson RP, Cain JE, Jacobs RR, et al. The neuroradiographic diagnosis of lumbar herniated nucleus pulposus: a comparison of computed tomography (CT), myelography, CT myelography, and magnetic resonance imaging. Spine 1989; 14:1362-1367. 39. Pfirrmann CW, Dora C, Schmid MR, et al. MR image-based grading of lumbar nerve root compromise due to disk herniation: reliability study with surgical correlation. Radiology 2004; 230:583-588. 40. Silverman CS, Lenchik L, Shimkin PM, et al. The value of MR in differentiating subligamentous from supraligamentous lumbar disc herniations. Am J Neuroradiol 1995; 16:571-579. 41. Modic MT, Ross JS, Obuchowski NA, et al. Contrast enhanced MR imaging in acute radiculopathy: a pilot study of the natural history. Radiology 1995; 195:429-435. 42. Toyone T, Takahashi K, Kitahara H, et al. Visualisation of symptomatic nerve roots. J Bone Joint Surg Br 1993; 75:529-533. 43. Jinkins JR. MR of enhancing nerve roots in unoperated lumbar spine. Am J Neuroradiol 1993; 14:193-202. 44. Tyrrell PNMT, Cassar-Pullicino VN, McCall IW. Gadolinium DTPA enhancement of symptomatic nerve roots in MRI of the lumbar spine. Eur Radiol 1998; 8:116-122. 45. Komori H, Shinomiya K, Nakai O, et al. The natural history of herniated nucleus pulposus with radiculopathy. Spine 1996; 21:225-229. 46. Boos N, Semmer N, Elfring A, et al. Natural history of individuals with asymptomatic disc abnormalities in magnetic resonance imaging. Spine 2000; 25:1484-1492. 47. Modic MT, Obuchowski NA, Ross JS, et al. Acute low back pain and radiculopathy: MR imaging findings and their prognostic role and effect on outcome. Radiology 2005; 237:597-604. 48. Gundry CR, Heitoff KB. Epidural haematoma of the lumbar spine: 18 surgically confirmed cases. Radiology 1993; 187:427-431. 49. Modic M, Steinberg P, Ross J, et al. Degenerative disk disease: assessment of changes in vertebral body marrow with MR imaging. Radiology 1988; 166:193-199. 50. Kuisma M, Karppinen J, Niinimaki J, et al. A three year followup of lumbar spine endplate (Modic) changes. Spine 2006; 31:1714-1718. 51. McCall IW, Cassar-Pullicino VN, Tyrrell PN. MR vertebral changes and back pain. Abstracts presented at the 25th annual meeting of the International Society for the Study of the Lumbar Spine, Singapore, 1998. 52. Braithwaite I, White J, Saifuddin A, et al. Vertebral end-plate (Modic) changes on lumbar spine MRI: correlation with pain reproduction at lumbar discography. Eur Spine J 1998; 7: 363-368. 53. Weishaupt D, Zanetti M, Hodler J, et al. Painful lumbar disk derangement: relevance of endplate abnormalities at MR imaging. Radiology 2001; 218:420-427. 54. Mitra D, Casssar-Pullicino VN, McCall IW. Longitudinal study of vertebral type-1 endplate changes on MR of the lumbar spine. Eur Radiol 2004; 14:1574-1581. 55. Weishaupt D, Zanetti M, Boos N, Hodler J. MR imaging and CT in osteoarthritis of the lumbar facet joints. Skeletal Radiol 1999; 28:215-219. 56. Schwartzer AC, Wang SC, O’Driscoll D, et al. The ability of computed tomography to identify a painful zygapophyseal joint in patients with chronic low back pain. Spine 1995; 20:907-912. 57. Apostolaki K, Davies AM, Evans NM, Cassar-Pullicino VN. MR imaging of lumbar facet joint synovial cysts. Eur Radiol 2000; 10:615-623. 58. Lim AKP, Higgins SJ, Saifuddin A, Lehovsky J. Symptomatic lumbar synovial cyst: management with direct CT-guided puncture and steroid injection. Clin Radiol 2001; 56:990-993.

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59. Rosenberg NJ. Degenerative spondylolisthesis, predisposing factor. J Bone Joint Surg Am 1975; 57:467-474. 60. Magora A, Schwartz A. Relationship between low back pain syndrome and x-ray findings: lysis and olisthesis. Scand J Rehabil Med 1980; 12:47-52. 61. Vogt MT, Rubin D, San Valentin R, et al. Lumbar olisthesis and lower back symptoms in elderly white women. Spine 1998; 23:2640-2647. 62. Yonenobu K: Cervical radiculopathy and myelopathy: when and what can surgery contribute to treatment? Eur Spine J 2000; 9:1-7. 63. Pavlov H, Torg JS, Robie B, Jahre C. Cervical spinal stenosis: deter mination with vertebral body ratio method. Radiology 1987; 164:771-775. 64. Eisenstein SM. The morphometry and pathological anatomy of the lumbar spine in South African Negros and Caucasoids with specific reference to spinal stenosis. J Bone Joint Surg 1977; 54:173-180. 65. Schonstrom NSR, Bolender NF, Spengler DM. The pathomorphology of spinal stenosis as seen on CT scans of the lumbar spine. Spine 1985; 10:806-812. 66. Shafaie FF, Wippold FJ, Gado M, et al. Comparison of computed tomography myelography and magnetic resonance imaging in the

67. 68.

69.

70. 71. 72.

evaluation of cervical spondylotic myelopathy and radiculopathy. Spine 1999; 24:1781-1785. de Graaf I, Prak A, Bierma-Zeinstra S, et al. Diagnosis of spinal stenosis. Spine 2006; 31:1168-1176. Stadnik TW, Lee RR, Coen HL, et al. Annular tears and disk herniation: prevalence and contrast enhancement on MR images in the absence of low back pain or sciatica. Radiology 1998; 206:49-55. Boos N, Rieder R, Schade V, et al. 1995 Volvo Award in clinical sciences. The diagnostic accuracy of magnetic resonance imaging, work perception, and psychosocial factors in identifying symptomatic disc herniations. Spine 1995; 20:2613-2625. Jensen MC, Brant-Zawadzki MN, Obuchowski N, et al. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med 1994; 331:69-73. Boden SD, Davis DO, Dina TS, et al. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects: a prospective investigation. J Bone Joint Surg Am 1990; 72:403-408. Weinreb JC, Wolbarsht LB, Cohen JM, et al. Prevalence of lumbosacral intervertebral disk abnormalities on MR images in pregnant and asymptomatic nonpregnant women. Radiology 1989; 170:125-128.

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Aging Iain Watt

WHAT IS AGING? The processes and inevitability of aging are as certain as death and paying taxes! In the past 5 years the population of the world has grown by approximately 1.7% per year. On the other hand, the number of elderly people has increased by 2.7% per year. In the developing world, the number of people older than age 65 years will increase by 200% to 400% in the next 30 years. By 2030 70 million people will be older than the age of 65 in the United States and by 2050 22% of the United States population will be considered elderly.1 It is generally agreed that with increasing longevity and health, especially in the developed world, the enlarging graying population will create a significant imbalance in health and welfare provision while, at the same time, the younger, wealth-creating proportion of the population will carry an unsustainable burden to support them. Traditional views about retirement age, the naïve view that older people have reduced expectations about the duration and quality of their lives, and the need for older people to contribute to the gross domestic product are being realized slowly. Already, retirement ages are being moved upward in those countries where they still apply. Age-related chronic diseases may be expected to increase, especially those with major health care provision needs such as cerebrovascular and cardiovascular diseases, dementia, malignancy, osteoarthritis, and degenerative disc disease. Perhaps more importantly, the healthy but aging population will demand as full and a rewarding standard of health as can be achieved. The understanding, arrest, or even reversal of the processes of aging will become a major research issue in the expectation that a healthy, long-living older population can not only expect a fulfilled life but also, in exchange, contribute to the wealth of society as a whole. It may be time also to revise an important benchmark in medicine. When studying the effect of age on the musculoskeletal system, an important consideration arises. That is, what is normal? For example, currently, bone density and the diagnosis of osteoporosis is made in comparison

to peak bone mass in the young, mature skeleton. Is this reasonable? Can what is seen as normal for a 25-year-old really apply to an 80-year-old? That we grow old and our skeletons continue to remold and adapt is obvious. That the processes involved alter with time is irrefutable. Archaeologists and anthropologists have long used these molding changes to assess the probable age of their clients in funerary and other collections. Hence, thickening of the skull vault, progressive closure of the cranial sutures, deepening of dural venous indentations, and roughening of the articular surfaces of the symphysis pubis are but a few of the signs that are relied upon. Perhaps, rather than consider the majority of older people to be abnormal by young adult standards, it would be more rewarding to ask why some older people have been able to maintain the standards of youth in their old age?

KEY POINTS Genotype largely determines the onset and progression of osteoarthritis. ■ Age-related hyaline cartilage degeneration starts in the unloaded parts of the joint before migrating to weightbearing zones. ■ Bone remodeling decreases from childhood up to skeletal maturity, but accelerates again over the age of 60 years. ■ Decrease of hyaline cartilage thickness and function with advancing age is related to increased joint surface area. The distinction between this normal aging process and similar changes that occur in osteoarthritis is not always clear. ■ The decrease of bone marrow perfusion and increase in intraosseous blood volume (venous engorgement) with advancing age may be factors in developing osteoarthritis. ■ Because function, morphology, and consistency of all joint components (cartilage, bone, marrow, ligaments, capsule) change with advancing age, intervention aimed at only one joint structure seems conceptually flawed. ■

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MECHANISMS OF AGING The means by which the human animal grows old are unclear. Obviously environmental issues are important. A life spent in a coal mine or a childhood without adequate nutrition will inevitably prejudice against a long and healthy life span. A number of complex cellular processes are working also toward entropy. One such may be telomere length. Telomeres are repeated sequences of five bases that preserve the integrity of genes during DNA replication. Their function has been likened to preventing the DNA strands from unraveling. The telomere chain length varies in individuals at birth, but every time a cell replicates daughter cells have shorter chains until they are spent. Older people with shorter telomeres are eight times more likely to die from an infectious disease and three times more likely to have a heart attack. On the other hand, it has been suggested that deficient telomere chains may be beneficial by inhibiting further cell replication and thereby be a means of inhibiting malignant transformation. It also has been suggested that an inverse relationship may exist between life span and the number of children borne to an individual. Widespread endocrine changes occur also in the older human. These include the menopause in women, androgen deficiency in men, subsequent loss of skeletal mass of about 1% per year when older than the age of 50 years, decreased concentration of serum growth hormone, and increased incidence of type 2 diabetes. For example, growth hormone loss is associated with reduced gonadal steroids in serum, increasing body fat, reduced muscle mass, and decreasing bone mass. The inherent substantial physiologic organ reserve of youth becomes lost, together with the impact of increasing other pathologic processes.2 These include the problems of frailty, vascular disease, and loss of cognitive function. A third area of recent interest is the understanding of age-related changes in mitochondrial function. The essential function of mitochondria is to burn sugars to produce intracellular energy. However, errors or interruptions in this process can result in the production of excess quantities of highly reactive free radicals that damage both mitochondrial and nuclear DNA. Mitochondrial DNA has 13 genes but lacks the crucial ability of nuclear DNA to repair genome damage, such as that associated with cell replication. Furthermore, as mitochondrial DNA is replaced more frequently than nuclear DNA, uncorrected mutations may contribute to the aging process. Research in a mouse model has shown that animals whose ability has been impaired to proofread accurately copies of mitochondrial DNA show reduced life span and premature onset of aging-related phenotypes such as weight loss, reduced subcutaneous fat, alopecia (hair loss), kyphosis, osteoporosis, anemia, reduced fertility, and heart enlargement.3 Whatever processes are involved, it is clear that a familial or genetic tendency occurs with some disorders that are age related. For example, osteoarthritis is known to have strong linkages in first-degree female relatives and data from population studies have suggested that progression of osteoarthritis in probands is

strongly associated with progression in their siblings.4 Similarly, hyaline cartilage defects in the knee have a genetic component related to symptomatic knee pain and bone size.5

THE AGING MUSCULOSKELETAL SYSTEM The individual components of the skeleton are each associated with specific age-related changes, some of which overlap. For convenience, each component will be considered separately. However, the concept that a joint is a whole organ within a whole patient must never be forgotten. Thus, a stumbling old man who fractures his hip is more than just an osteoporotic individual. His variable, weak gait may correlate with depression scores rather than his age, gender, muscle strength, or neurologic features, except in terms of frontal lobe and extrapyramidal function. His cautious gait equates to loss of higher cerebral function. In other words, gait changes in older adults, who may walk in fear of falling, may be an appropriate response to unsteadiness and are likely to be a marker of an underlying cerebral pathologic process and not simply a physiologic or psychological consequence of normal aging.6

Within the Joint Organ as a Whole Age-related hyaline cartilage degenerative changes appear to occur first in unloaded parts of a joint but spread to the more central, weight-bearing zones with increasing age. The argument is that a normal, young joint resembles a ball within a Gothic arch. Initial loading contact is made at the periphery of the joint. With increasing load, both bone and cartilage, being viscoelastic structures, deform and the contact between the joint surfaces increases, distributing the load more evenly. This type of designed incongruent geometry provides for stability, ease of motion, and physiologic loading (Fig. 44-1). Furthermore, and perhaps the most important role, is the normal nutrition of hyaline cartilage. Chondrocytes, that without a blood supply produce all of the crucial components of hyaline cartilage, are dependent solely on circulating synovial fluid for their energy requirements. Thus, the circulation of synovial fluid with oxygen and sugars is facilitated by the pump action of a deformable joint congruence.7 Aging is associated with a progressive alteration in this crucial joint morphology. Joints become more congruent and deeper and fit more precisely with age (Fig. 44-2). 8 Congruence is achieved by progressive remolding of the articular surfaces as a result of vascular invasion and endochondral ossification of calcified cartilage. In the case of the femoral head, vascular invasion is predominantly superior and gradually declines until the age of about 60 years when a dramatic and persistent increase occurs that continues into old age. Why this should happen is not known, nor why the threshold age should be 60. Other work has shown that a high hip contact stress relates to cartilage degeneration and osteoarthritis. Hip joints that remain

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■ FIGURE 44-1

Diagram of the effect of geometry on the distribution of stress in the loaded joint. Too narrow a contact point causes high focal loading and inherent instability (A). Too broad a cup evens out load initially but becomes more focal as it increases. Congruity is total, and synovial fluid circulation is inhibited (B). Only in C, when the ball fits into the Gothic arch with a narrower diameter of contact, can load become more evenly distributed, stability increase, and synovial fluid be pumped around the joint. (Reprinted by permission from Teitelbaum SL, Bullough PG: The pathophysiology of bone and joint disease. Am J Pathol 1979; 96:282-354.)

anatomically normal in older age have a lower estimated peak contact stress (body weight corrected) than those that do not.9 Changes are occurring also in hyaline cartilage. Data from both femoral and humeral heads show that the thickness of the calcified zone decreases with age while, at the same time, the number of tidemarks increases, especially in those older than the age of 60. The changes in thickness of calcified cartilage depend on progressive endochondral ossification, resulting in additional subchondral bone and secondary thinning of calcified cartilage. Endochondral ossification occurs continuously throughout life in the calcified zone, but the rate of remodeling is variable, falling progressively from skeletal maturity until the sixth decade when a sudden increase in the number of tidemarks occurs.10 It is unclear why bone remodeling accelerates with increasing older age. Thus, an intimate interrelationship exists between bone and cartilage remodeling. Not surprisingly, correlations are reported in the knee between increasing patient age, the severity of hyaline cartilage defects and their prevalence, cartilage thinning, and increased bone surface area.11 How much of this represents age-related, “normal” findings and how distinct it is from what we call osteoarthritis remain unanswered.

Age-Related Changes within Bone Bone mineral density and total bone mass increase until about the age of 20 years. Both remain stable until about the age of 35 years. The peak bone mass determines the subsequent chance of osteoporosis and is a factor in predicting fracture risk. The determinants of peak bone mass include genetic and environmental factors. Bone mass declines after the age of 35 years at a relatively steady rate throughout the remainder of life. Ovarian failure in women starts around the age of 40 years, and reproductive ovarian function ceases about 15 years later. At the menopause, rapid bone loss occurs with an associated increase in cardiovascular risk. The loss is secondary to reduced estrogen added to the underlying age-related bone loss. Thus, women may lose 5% to 15% of their bone mass in the perimenopausal period, with 80% coming from trabecular bone because it is metabolically more active than cortical bone. At the same time, although serum parathyroid hormone and vitamin D levels remain normal, a rapid increase in bone resorption occurs. The result is a secondary increase in bone formation. However, the net outcome is bone loss, suggesting that the osteoblastic response of aging bone may be hindered. It seems likely that the increased rate of bone loss is attributable, at least

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■ FIGURE 44-2 Radiographs of the ankle in a young child (A), a mature male (B), and an old adult (C) show the obvious deepening of the ankle mortise and increasing congruity with age.

partly, to the increased number of resorption cycles, in each of which bone resorption is unmatched by bone formation.2 As the result, one third of women older than the age of 50 have osteoporosis with increased fracture risk. Peak bone mass, and the rate of postmenopausal bone loss, may be related also to ethnicity. A study of Native American women suggested that peak bone mineral density may be higher but the rate of postmenopausal bone loss greater than in white women.12 Age is associated with

a third factor that enhances bone loss, beyond the effects of normal age-related loss and gonadal failure, and that is pure atrophy. Many older people are incapacitated, even chair- or bed-bound. In these circumstances unloading of the skeleton occurs also, akin to the bone loss of astronauts. In aging men levels of free and bioavailable testosterone decline. Levels of sex hormone–binding globulin also increase, further reducing available hormone.

CHAPTER

An andropause does not seem to exist, but the gradually reducing serum testosterone is associated with reducing blood hemoglobin, lean body mass, and bone mass and perhaps with memory changes. Testosterone replacement may partially reverse these changes but is not a widespread therapy. Some data suggest that the reduction in bone mineralization is not uniform. Change in distribution of bone density within cancellous bone has been shown to vary with age in the femoral neck. Bone loss is greater, and more variable, in the inferior aspect of the femoral neck and trochanteric region.13 Does this explain the varus impaction nature of elderly femoral neck fractures? Similarly, tibial plateau fractures are age related and may be a common cause of knee pain in the elderly.14 Certainly, subchondral insufficiency fractures of the tibial plateaus and many cases of so-called spontaneous osteonecrosis of femur are due to subchondral insufficiency fractures, leading to rapidly progressive osteoarthritis.15 Cardiovascular disease is clearly a major age-related factor. However, very little is known about the normal rate of bone blood flow in the aging skeleton and the possible contribution of vascular disease to bone and joint pathology. The rate of vertebral bone marrow perfusion is significantly decreased in subjects older than 50 years. Women demonstrate a higher marrow perfusion rate than men younger than 50 years and a more marked decrease than men older than 50 years.16 Furthermore, a correlation may exist between perfusion, bone marrow fat content and osteoporosis. It has been shown that the greater the degree of bone loss, the greater the reduction in perfusion, as assessed by MR spectroscopy, and marrow fat content.17 Another study using positron emission tomography in the femoral head has shown that bone blood flow becomes reduced with age while, at the same time, intraosseous blood volume increases.18 These data serve to confirm the nearly 40-year-old concept that venous engorgement and slow bone blood flow with a high intraosseous blood volume may be underlying factors in hip osteoarthritis19 and underpin older decompression strategies for relieving joint pain in the hip and knee.

Age-Related Changes in Hyaline Cartilage In addition to the hyaline cartilage and subchondral bone changes, articular cartilage undergoes significant intrinsic structural, matrix composition, and mechanical changes with increasing age. These changes are distinct from those of osteoarthritis. Although osteoarthritis is age related, it is not an inevitable consequence of age. In aging, articular surface fibrillation is almost universal and more common in some joints than others. It is asymptomatic and does not necessarily lead to the degeneration and structural failure associated with osteoarthritis. Within the cartilage matrix the size of proteoglycan aggregates decreases significantly with age as aggrecan molecules become shorter and the mean number of aggrecans in each aggregate decreases.20 It is not known if this is due to deficient synthesis or degradation in the matrix or both. It may be due to reduced func-

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tion of aging chondrocytes as shown in culture experiments. Age is also associated with reducing collagen cross-linkages and reduced water concentration secondary to the less hydrophilic negative charge of these older aggrecans. The overall effect is to reduce tensile stiffness and strength, making cartilage more susceptible to injury. Chondrocyte mitotic and synthetic abilities also reduce with age; in particular, chondrocytes exhibit an age-related decline in anabolic response to insulin-like growth factor (IGF-1). IGF-1 appears to have a critical role in stimulating chondrocyte synthetic activity that, in turn, stimulates maintenance and repair of the articular cartilage matrix.20 How do these changes relate to osteoarthritis, which has a marked age-related incidence? Older cartilage is less able to repair and restore itself, compared with younger individuals. Hence, the risk of developing post-traumatic osteoarthritis after an intra-articular fracture increases threefold to fourfold after the age of 50. However, although older cartilage is less able to repair itself, it does not explain the quite different pathologic process of osteoarthritis per se. In MRI T2 relaxation times are sensitive to the organization of collagen fibers in hyaline cartilage. Hence, if aging is associated with collagen degeneration, T2 values could be used as a surrogate marker. T2 values are indeed longer in the superficial 40% of cartilage in the 46- to 65year age group as opposed to 18- to 30-year-old subjects. This suggests that age-related changes in collagen occur near the articular surface,21 perhaps alongside the fibrillation changes described earlier. As hyaline cartilage becomes thinner as the result of aging, it also displays a different degree of deformation under load compared with younger subjects. A study of knee cartilage confirmed that patellar cartilage thins significantly in older women (−12%) but not in men (−6%). Femoral cartilage was thinner in both sexes (women, −21%; men, −13%), whereas tibial cartilage showed nonsignificant trends. The striking feature is the reduced ability of cartilage to deform under load at the patella when compared with a younger knee. In other words, older cartilage is less efficient at load shedding.22 The relationship between load shedding in cartilage and subchondral bone dictates the relative size of the articular surfaces of joints compared with the midshaft cross-sectional area. In the normal long bone, the articular surface area is approximately five times greater than that of the midshaft. Hence, in older subjects with less effective cartilage, it is to be expected that the area of the subarticular bone will increase in compensation. Thus, medial and lateral tibial bone surface area and patellar bone volume increase with age.11 From these data we must learn that the normal aging joint shows thinner hyaline cartilage and minor marginal spurs that reflect the effects of age and should not be confused with the more progressive and devastating pathology we call osteoarthritis (Fig. 44-3).

Age-Related Changes in Skeletal Muscle Men have significantly more skeletal muscle than women, both in absolute terms and also in relation to total body mass. These gender differences are greater in the upper than the lower body.23 Skeletal muscle mass decreases

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■ FIGURE 44-3 Two examples of normal, age-related changes in joint architecture. Both the hip (A) and the knee (B) show modest hyaline cartilage thinning and minor marginal spurs. These features should not be confused with the more destructive process of osteoarthritis.

from the third decade but becomes more noticeable from the fifth decade. Lean body mass decreases steadily with age from the fifth or sixth decades onward. This is due mainly to a loss of lower body muscle mass. At the same time body fat increases until about the age of 65 when it begins to decrease again. To what extent such changes actually cause decreased strength or function or vice versa are unclear. Naturally, the reducing muscle mass has an effect on the activities of normal daily living. For example, it correlates with reduced ability to climb stairs (quadriceps and psoas muscle cross-sectional areas).24 Furthermore, in the elderly, maximal voluntary contraction torque is reduced owing to incomplete muscle activation. However, prolonged exercise programs (12 months or more) show that muscle bulk and activation can be increased significantly compared with controls.25 On MRI, features of muscle atrophy and fatty infiltration can be seen in the older patient. More subtle changes include an increase in T2 relaxation time of fast-twitch muscle with age (e.g., the gastrocnemius muscle) due mainly to increased extracellular space reflecting age-related type II fiber atrophy. However, slow-twitch muscle does not show such a change (e.g., the soleus muscle).26

Age-Related Changes in Ligaments and Tendons Age-related changes in tendons have been studied in the rotator cuff and lateral epicondyles at post mortem. They are similar at each site and comprise minor blood vessel wall changes, loss of tenocytes, and patchy calcification. The most frequent finding was glycosaminoglycan

infiltration and fibrocartilaginous transformation. These changes occurred in less than 17% of younger specimens but rise to 40% to 50% in later life.27 Cystic changes in bone are common around the shoulder in older patients and are held to be evidence of rotator cuff disease. A study of 140 painful shoulders in 136 older patients has clarified this. Of these patients 35% had cystic lesions. The most common site was the bare area around the humeral neck. Lesions here were equally common in patients with or without cuff pathology, whereas cystic lesions at the insertion of either supraspinatus or subscapularis tendons were specific to cuff tears.28 Other histologic changes are occurring concurrently in aging ligaments and tendons. In the young anterior cruciate ligament, the diameter of the collagen fibrils that comprise it are highly variable. In adults and older subjects the maximal diameter decreases remarkably and fibril concentration increases considerably. The reduction in diameter and the relative changes in fibril concentration may relate to changes in elastic stiffness in the older ligament. Similar findings are recorded in the Achilles tendon.29 However, whereas elastic quality may be altered by age, the question arises as to whether the older tendon heals less well after trauma. This is the commonly held wisdom, yet a recent study suggests that, at least in the experimental situation, no reduction occurs in the biomechanics of an older healing tendon.1 Enthesis ossification in the form of “osteophytes” occurring at the margins of the intervertebral discs and more florid ossification in the anterior longitudinal ligament, especially in the form usually described as diffuse idiopathic skeletal hyperostosis, are also age related.

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However, risk factors for diffuse idiopathic skeletal hyperostosis extend beyond age and include a greater body mass index, as compared with patients with disc degeneration alone. These patients also have higher serum levels of uric acid and a greater likelihood of diabetes mellitus.30 The biomechanics of the anterior longitudinal ligament have been studied with regard to bone density, disc degeneration, and tensile stress-strain characteristics. In the young anterior longitudinal ligament, the elastic modulus of the insertion and substance of the ligament was similar. During aging, the elastic modulus of the substance increased twofold, whereas that of the insertion decreased threefold. Thus a fivefold change occurs. At the same time, the strength of the bone-ligament complex decreased by half during aging. The outer portions of the anterior longitudinal ligament consistently had the highest peak tensile strains. Whether this is related to the etiology of diffuse idiopathic skeletal hyperostosis is unknown. Equally of interest is the interrelationship between these findings, disc disease, and bone density. Experiments on preparations with normal discs and high bone density were significantly stronger than in the converse. Older patients with degenerative discs and lower bone density fail mechanically at the ligament insertion regions.31 Other data support these findings insofar as the mechanical strength of the lumbar posterior spinal ligaments decreases with age owing to a negative correlation between age and tensile strength and is even worse in the presence of facet joint osteoarthritis.32

also. However, unlike findings in hyaline cartilage, the distinction between aging and degeneration in the spine is not clear.36 As a person ages the water content of the nucleus pulposus decreases, the turgidity reduces, and gaps and a system of fissures develop, radiating out into the annulus fibrosus. The fissures may fill with vapor to create the vacuum phenomenon typical of degenerative discs as seen on radiographs. The fissures may become filled with liquid also on T2-weighted images. The progressive reduction in water content is associated with signal intensity loss on T2-weighted sequences and reduced disc space height. Careful measurement of signal intensity change has confirmed a significant correlation with age, although signal intensity changes less than 8% by 80 years of age!37 Calcification also may be part of the aging process, occurring most frequently in thoracic discs. Normal discs exhibit a diurnal variation in T2 values, reflecting water loss associated with weight bearing. This variation disappears after the age of 35 years, which is also thought to be a specific feature of aging.38 Aging changes occur also in the annulus fibrosus. Typically, this results in a loss of distinction between the annulus and the nucleus, with also the development of annular fissures. The end plates as they degenerate may exhibit fractures, cleft formation, increased vascular permeability, and calcification.

Other Age-Related Changes in the Spine

It must never be forgotten that a tissue does not exist in isolation in life. A joint is an organ comprising hyaline cartilage, bone, marrow constituents, and ligaments that is surrounded by a capsule and controlled by muscles. From the foregoing it is clear that a number of parallel processes are in operation as we grow old. At present, aging is an inevitable “normal” process. To arrest it requires more than simple protection of chondrocytes, for example. The combination of reducing cognitive function, falling bone density, increasing cartilage deformability, and poor muscle strength will predicate toward falls and injury, perhaps often forgotten or undocumented. For example, they may promote tibial and femoral subchondral fractures, previously thought to be idiopathic necrosis or suddenonset necrosis of the condyle, and promote sudden and catastrophic joint failure. The combination of disc dehydration, reducing bone mass, and postural control lead to a thoracic kyphosis, increased skeletal loading, and wedge compression fractures. Indeed, bone density does not correlate with the degree of thoracic kyphosis; the severity of disc degeneration does.39 At the outset, the question was posed—what is normal for an older person? At what stage do these age-related processes become abnormal? Is it from the moment of conception, or birth, or peak skeletal maturity? Or, would it be more appropriate to dissect out the age-related from the other changes to which we are susceptible so that therapy can be directly more specifically? Our aging populations will demand it!

Apart from morphologic changes directly associated with osteoporosis, changes in the bony shape of vertebrae also occur. The bony neural canal becomes narrower with age in the cervical spine,33 as it does in the lumbar canal. Although slow bone accretion and narrowing occur per se, they are enhanced by associated degenerative changes.34 The reduction in area can be demonstrated and quantified using cross-sectional imaging. In addition to axial age-related changes, an MRI study demonstrated a linear age-related decline in anteroposterior height ratio occurs in the thoracic spine (anterior wedging) with increasing vertebral biconcavity. These changes were not corrected for possible osteoporosis, however. At the same time an age-related increase occurs in annular, nuclear, and disc margin abnormalities on MRI data, particularly in the middle and lower thoracic spine. The degree and extent of disc degenerative changes are greater in males.35 The intervertebral discs comprise about one third of the total height of the vertebral column. That we shrink with age is self-evident, just as we are shorter in the evening than when we first arise from bed in the morning. These changes are held to be due to hydration loss within the turgid proteoglycan of the nucleus pulposus, reflecting degenerative disease. As in hyaline cartilage, age-related degradation of proteoglycan reduces the hydrophilic ability of the nucleus to maintain turgidity. The elastic, constraining quality of the annulus fibrosus is reduced

Age-Related Changes in the Whole Joint Organ

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REFERENCES 1. Dressler MR, Butler DL, Boivin GP. Age-related changes in the biomechanics of healing patellar tendon. J Biomech 2006; 39:2205–2212. 2. Perry MH III. The endocrinology of aging. Clin Biochem 1999; 45:1369–1376. 3. Trifunovic A, Wredenberg A, Falkenberg M, et al. Premature ageing in mice expressing defective mitochondrial DNA polymerase. Nature 2004; 429:417–423. 4. Botha-Scheppers SA, Watt I, Slagboom E, et al. Radiological disease progression over two years is influenced by familial factors in siblings with generalized osteoarthritis. The GARP study. Arthritis Rheum (in press). 5. Ding C, Cicuttini F, Scott F, et al. The genetic contribution and relevance of knee cartilage defects: case-control and sib-pair studies. J Rheumatol 2005; 32:1937–1942. 6. Herman T, Giladi N, Gurevich T, Hausdorff JM. Gait instability and fractal dynamics of older adults with a “cautious” gait: why do certain older adults walk fearfully? Gait Posture 2005; 21:178–185. 7. Bullough PG. The role of joint architecture in the etiology of arthritis. Osteoarthritis Cartilage 2004; 12:S2–S9. 8. Bullough PG. The geometry of diarthrodial joints, its physiologic maintenance, and the possible significance of age-related changes in geometry-to-load distribution and the development of osteoarthritis. Clin Orthop Relat Res 1981; 156:61–66. 9. Mavcic B, Slivnik T, Antolic V, et al. High contact hip stress is related to the development of hip pathology with increasing age. Clin Biomech 2004; 19:939–943. 10. Lane LB, Bullough PG. Age-related changes in the thickness of the calcified zone and the number of tidemarks in adult human articular cartilage. J Bone Joint Surg 1980; 62:372–375. 11. Ding C, Cicuttini F, Scott F, et al. Association between age and knee structural change: a cross sectional MRI based study. Ann Rheum Dis 2005; 64:549–555. 12. Perry HM III, Bernard M, Horowitz M, et al. The effect of aging on bone mineral metabolism and bone mass in Native American women. J Am Geriatr Soc 1998; 46:1418–1422. 13. Lundeen GA, Vajda EG, Bloebaum RD. Age-related cancellous bone loss in the proximal femur of Caucasian females. Osteoporosis Int 2000; 11:505–511. 14. Luria S, Liebergall M, Elishoov O, et al. Osteoporotic tibial plateau fractures: an underestimated cause of knee pain in the elderly. Am J Orthop 2005; 34:186–188. 15. Yamamoto T, Bullough PG. Spontaneous osteonecrosis of the knee: the result of subchondral insufficiency fracture. J Bone Joint Surg 2006; 82:858–866. 16. Chen WT, Shih TT, Chen RC, et al. Vertebral bone marrow perfusion evaluated with dynamic contrast-enhanced MR imaging: significance of aging and sex. Radiology 2001; 220:213–218. 17. Griffith JF, Yeung DKW, Antonio GE, et al. Vertebral bone mineral density, marrow perfusion, and fat content in healthy men and men with osteoporosis: dynamic contrast-enhanced MR imaging and MR spectroscopy. Radiology 2005; 236:945–951. 18. Kubo T, Kimori K, Nakamura F, et al. Blood flow and blood volume in the femoral heads of healthy adults according to age: measurement with positron emission tomography (PET). Ann Nucl Med 2001; 15:231–235. 19. Brookes M, Helal B. Primary osteoarthritis, venous engorgement and osteogenesis. J Bone Joint Surg Br 1968; 50:493–504.

20. Martin JA, Buckwalter JA. Aging, articular cartilage chondrocyte senescence and osteoarthritis. Biogerontology 2002; 3:257–264. 21. Mosher TJ, Liu Yi, Yang QX, et al. Age dependency of cartilage magnetic resonance imaging T2 relaxation times in asymptomatic women. Arthritis Rheum 2004; 50:2820–2828. 22. Hudelmaier M, Glaser C, Hohe J, et al. Age-related changes in the morphology and deformational behavior of knee joint cartilage. Arthritis Rheum 2001; 44:2556–2561. 23. Janssen I, Heymsfield SB, Wang Z, Ross R. Skeletal muscle mass and distribution in 468 men and women aged 18–88 yr. J Appl Physiol 2000; 89:81–88. 24. Masuda K, Kinugasa R, Tanabe K, Kuno SY. Determinants for stair climbing by elderly from muscle morphology. Percept Motor Skills 2002; 94:814–816. 25. Morse CI, Thom JM, Mian OS, et al. Muscle strength, volume and activation following 12-month resistance training in 70-year-old males. Eur J Appl Physiol 2005; 95:197–204. 26. Hatakenaka M, Ueda M, Ishigami K, et al. Effects of aging on muscle T2 relaxation time: difference between fast- and slowtwitch muscles. Invest Radiol 2001; 36:692–698. 27. Chard MD, Cawston TE, Riley GP, et al. Rotator cuff degeneration and lateral epicondylitis: a comparative histological study. Ann Rheum Dis 1994; 53:30–34. 28. Sano A, Itoi E, Konno N, et al. Cystic changes of the humeral head on MR imaging: relation to age and cuff tears. Acta Orthop Scand 1998; 69:397–400. 29. Strocchi R, De Pasquale V, Facchini A, et al. Age-related changes in human anterior cruciate ligament (ACL) collagen fibrils. Ital J Anat Embryol 1996; 101:213–220. 30. Kiss C, Szilagyi M, Paksy A, Poor G. Risk factors for diffuse idiopathic skeletal hyperostosis: a case-controlled study. Rheumatology (Oxford) 2002; 41:27–30. 31. Neumann P, Ekstrom LA, Keller TS, et al. Aging, vertebral density, and disc degeneration alter the tensile stress-strain characteristics of the human anterior longitudinal ligament. J Orthop Res 1994; 12:103–112. 32. Iida T, Abumi K, Kotani Y, Kaneda K. Effects of aging and spinal degeneration on the mechanical properties of lumbar supraspinous and interspinous ligaments. Spine 2002; 2:95–100. 33. Ishikawa M, Matsumoto M, Fujimura Y, et al. Changes of cervical spinal cord and cervical spinal canal with age in asymptomatic subjects. Spinal Cord 2003; 41:159–163. 34. Szpalski M, Gunzburg R. Lumbar spinal stenosis in the elderly: an overview. Eur Spine J 2003; 12(Suppl 2):S170–S175. 35. Goh S, Tan C, Price RI, et al. Influence of age and gender on thoracic vertebral body shape and disc degeneration: an MR investigation of 169 cases. J Anat 2000; 197:647–657. 36. Cassar-Pullicino VN. MRI of the ageing and herniating intervertebral disc. Eur J Radiol 1998; 27:214–228. 37. Sether LA, Yu S, Haughton VM, Fischer ME. Intervertebral disk: normal age-related changes in MR signal intensity. Radiology 1990; 177:385–388. 38. Karakida O, Ueda H, Ueda M, Miyasaka T. Diurnal T2 value changes in the lumbar intervertebral discs. Clin Radiol 2003; 58:389–392. 39. Manns RA, Haddaway MJ, McCall IW, et al. The relative contribution of disc and vertebral morphometry to the angle of kyphosis in asymptomatic subjects. Clin Radiol 1996; 51:258–262.

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Degenerative Disease: Cartilage Anatomy, Physiology, and Advanced Imaging Timothy J. Mosher

ETIOLOGY Degeneration and loss of joint function is a common end point for many arthropathies, the most prevalent of which is osteoarthritis (OA). The American College of Rheumatology defines OA as a heterogeneous group of conditions that leads to joint signs and symptoms that are associated with defective integrity of articular cartilage and associated changes in the underlying bone and at the joint margins.1 Although OA is a multifactorial disease process, the degeneration and ultimate loss of articular cartilage is a central feature and a significant contributor to clinical symptoms. Despite a high prevalence of this disease, the etiology and pathogenesis of this condition are poorly understood. It is generally accepted that damage to articular cartilage occurs when local biomechanical forces exceed the material properties of cartilage, leading to structural and biochemical changes in the cartilage matrix and alteration in gene expression of the chondrocyte. These biomechanical forces are determined by many variables, including body habitus, intensity and type of physical activity, stiffness of the subchondral bone, joint trauma, as well as alignment of the joint and laxity in the stabilizing tissues. The material properties of cartilage are also influenced by many factors, including senescent changes as a result of normal aging, genetics, diet, exercise, and coexisting systemic diseases or conditions. The complex interplay of these many variables produces an imbalance in cartilage homeostasis in which degradation of the cartilage matrix exceeds synthesis, ultimately progressing to structural loss of tissue.

Although OA involves the entire joint, the primary focus of this chapter is articular cartilage, with particular emphasis on MRI for identification of early cartilage injury.

PREVALENCE AND EPIDEMIOLOGY Current estimates are that symptoms and disability related to OA afflict more than 20 million Americans. With a rising mean age of the American population and growing incidence of secondary OA in younger individuals it is projected that by the year 2020 OA will afflict more than 60 million Americans. Age is the primary risk factor for development of both radiographic and clinical OA. In individuals younger than age 45 the prevalence of OA increases slowly in a linear fashion with age. After age 45 the rate of disease prevalence of OA increases exponentially with age, afflicting approximately 50% of people at age 65, increasing to 85% in those individuals 75 years or older.2 Obesity has been shown to be a risk factor for knee OA; however, the relative risk for hip OA is less conclusive. Studies have shown weight loss can reduce the risk of OA. Of note, obesity has been shown to increase the risk of OA in non–weight-bearing joints such as the interphalangeal joints of the hand, suggesting that systemic as well as local biomechanical factors may be responsible. Physical activity, particularly that related to long-term repetitive activities associated with particular occupations, can increase the risk of OA. Hip arthritis is more common in farmers. Hip and spine OA is more prevalent 1085

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KEY POINTS The primary constituents of articular cartilage are water, type II collagen, and large molecules of aggregating proteoglycans (aggrecan). ■ The composition and structure of the cartilage matrix vary with depth of the articular surface as well as with location in the joint. ■ Normal cartilage biomechanics relies on a high interstitial tissue pressure that is generated by swelling of hydrated proteoglycans and constraint by the surrounding type II collagen matrix. ■ MR T2-weighted images are sensitive to variation in the cartilage matrix as a result of differences in collagen fibril orientation and water content. ■ Loss of normal spatial variation in MRI T2-weighted signal intensity is an early finding in cartilage degradation. ■ More severe grades of cartilage damage are associated with loss of tissue and surface irregularity. ■ Cartilage delamination occurs when cartilage fibrils are cleaved, thereby separating cartilage from subchondral bone. It is characterized by linear high MRI T2-weighted signal at the bone-cartilage interface. ■ Underlying bone marrow MRI T2-weighted hyperintensity (bone marrow edema) is an important secondary sign of cartilage injury. ■

in miners. Unusual repetitive activities may lead to OA in atypical joints. For example, there is an increased frequency of upper extremity OA in pneumatic drill operators. Although a slightly higher incidence of OA is observed in high-performance competitive athletes, this is frequently associated with prior joint trauma, which is strongly associated with secondary OA. Moderate recreational exercise such as running has not been associated with an increased risk of OA.

CLINICAL PRESENTATION Pain along with loss of joint mobility is a common symptom of OA. Typically, the pain is poorly localized around the joint, increases with activity, and is relieved with rest. The source of pain in OA is not entirely clear but may be associated with the presence of joint effusion, mild synovitis, and changes in subchondral bone marrow. Radiographic features of OA such as joint space narrowing and osteophyte formation correlate poorly with clinimetric measures of pain. OA may be associated with transient episodes of morning stiffness. With further progression of the disease, loss of joint congruity and development of osteophytes and intra-articular osteochondral bodies can lead to loss of joint function and disability with difficulties in activities of daily living. Complaints of joint instability are common, particularly in knee OA. Focal chondral or osteochondral lesions may have a clinical presentation that mimics meniscal pathology in the knee or labral pathology in the hip or shoulder. Symptoms consist of nonspecific pain or episodes of locking. With MRI, focal chondral abnormalities are frequently

observed in subjects without joint symptoms and in otherwise healthy volunteers. Because cartilage lacks nociceptive receptors, cartilage injury alone is not responsible for pain but may contribute secondarily to pain through associated changes in subchondral bone marrow or synovium.

PATHOPHYSIOLOGY Anatomy Under physiologic conditions articular cartilage is exposed to high compressive and shear forces. For example, it is estimated that during a squatting maneuver, patellar cartilage undergoes compressive loads that are greater than six times body weight, with transient pressures that may be substantially higher.3 These forces are applied repetitively many times a day throughout the course of a lifetime. What is remarkable is not that cartilage degrades but that it is capable of functioning normally under these conditions throughout a human life span. The biomaterial properties of articular cartilage are a result of the composition and organization of the extracellular matrix. Cartilage is 65% to 85% water, with water content decreasing slightly with depth from the articular surface. The major solid components of the extracellular matrix are type II collagen, which comprises 10% to 20% of the wet weight of cartilage, and large molecules of aggregating proteoglycans, termed aggrecan, that contribute 5% to 10% wet weight. The content and structure of collagen and proteoglycans in the matrix differ substantially from bone to the articular surface and strongly influence the biomaterial properties of cartilage. The components of type II collagen, tropocollagen molecules, are polymerized into larger collagen fibrils, which in turn are organized into a leaf-like architecture.4 As illustrated in Figure 45-1, the orientation and alignment of the collagen matrix vary with depth from the articular surface as well as regionally within the joint. Collagen fibrils cross the bone-cartilage interface at the tidemark zone and secure cartilage to the subchondral bone. In the deep layer of cartilage near bone, collagen fibrils have a preferential orientation perpendicular to the bone surface. This is frequently termed the radial zone, referring to the radial orientation of the collagen matrix as well as the columnar alignment of chondrocytes observed in this layer. Near the surface the orientation of the collagen matrix curves tangentially in the transitional zone, becoming parallel to the articular surface in the superficial zone. The superficial layer is covered with a distinct layer of dense collagen fibers termed the lamina splendens. The tangential and superficial layers of cartilage are relatively thin in regions of the joint habitually exposed to high compressive loads, such as the central portion of the femoral condyle and tibial plateau uncovered by the meniscus. These layers are thicker in regions exposed to less load, such as articular surfaces covered by the meniscus. Interposed in the meshwork of type II collagen fibrils are large molecules of aggregating proteoglycans consisting of aggrecan (Fig. 45-2). Concentration of proteoglycans also varies within cartilage, with the highest levels found below the articular surface and decreasing in

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■ FIGURE 45-1 Schematic illustration of type II collagen matrix in cartilage. The primary constituents of the cartilage matrix are water, type II collagen, and aggregating proteoglycans (aggrecan). The structural organization of the collagen matrix varies with depth from the articular surface and influences the T2 relaxation time of cartilage. In the radial zone the collagen matrix is aligned perpendicular to bone. This high degree of orientation or anisotropy provides an efficient mechanism for spin-spin relaxation, leading to short T2 values. Toward the articular surface, the oblique orientation and lower anisotropy in the transitional zone leads to a lengthening of T2, resulting in high signal intensity on T2-weighted images. At the surface, fibrils are aligned parallel to the articular surface. At the articular surface, a distinct surface layer, or lamina splendens, is adherent to the horizontally oriented fibers of the superficial collagen leaves. This layer is generally too thin to resolve with clinical MR images.

■ FIGURE 45-2 Cartilage swelling pressure. Large molecules of aggregating proteoglycans (aggrecan) are imbedded within the fibrils of the type II collagen matrix. When aggrecan is hydrated, the high density of negative charges draws in sodium and water, causing the aggrecan molecule to swell. Aggrecan swelling is restrained by the surrounding collagen fibrils, resulting in a large interstitial swelling pressure responsible for the compressive stiffness of cartilage. In early cartilage damage, fragmentation of the collagen matrix allows unrestrained swelling of aggrecan and lowers the internal pressure of cartilage. This makes the cartilage more compressible and susceptible to further degeneration.

concentration near bone. The aggrecan molecules consist of a central core fiber of hyaluronic acid. Bound to this fiber are numerous, large, negatively charged glycosaminoglycan molecules consisting of chondroitin sulfate and keratin sulfate. When these molecules are hydrated, the

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high density of negative charges on the proteoglycans bind sodium and draw water into cartilage, causing the proteoglycans to swell. Swelling of the proteoglycans is constrained by the surrounding collagen meshwork, producing an interstitial fluid pressure of approximately 9 MPa. This large pressure contributes to the compressive stiffness of cartilage. As such, the balance of aggrecan swelling and an intact collagen matrix is an essential feature for normal cartilage function. The MRI relaxation properties of articular cartilage and the appearance of cartilage with standard clinical MRI techniques are strongly influenced by the composition and structure of the extracellular matrix. As a result of this sensitivity, MRI has the potential to function as a noninvasive image marker of changes in the extracellular matrix that occur during early cartilage injury that precedes fibrillation and loss of tissue. Because these observations can be made noninvasively in human joints, MRI is a valuable clinical research technique, providing unique information regarding the natural history of OA, human cartilage physiology, and in situ biomechanics. The influence of cartilage structure and composition on MRI signal intensity is most evident on T2-weighted images. As illustrated in Figure 45-3, the signal intensity of cartilage varies with location in the joint as well as with depth from the articular surface. This is primarily a function of regional and zonal differences of the type II collagen matrix, which influences T2 relaxation of cartilage as well as variation in water content. Within the radial zone the high content and anisotropic orientation of collagen fibrils provide efficient T2 relaxation, leading to low signal intensity on proton-density (PD)– or T2-weighted images. With very high resolution images, the darker radial zone has a striated appearance with alternating fine bands of high and low signal intensity radiating from the bone cartilage interface. In lower-resolution images, individual striations are not resolved and, instead, this layer is characterized by low signal intensity. Closer to the articular surface less fibril anisotropy and oblique orientation of the collagen matrix lead to a gradual increase in T2 relaxation time and thus a relative increase in signal intensity on T2-weighted images. At the articular surface collagen fibers are oriented parallel to the articular surface. The superficial tangential layer and the lamina splendens are approximately 20 µm thick and can be identified on MR microscopy images of excised cartilage specimens as a thin hypointense layer; however, it is too thin to resolve on routine clinical MR images. The organization and orientation of collagen within the cartilage matrix have a strong influence on the MRI appearance of cartilage. In connective tissues such as tendons, ligaments, and articular cartilage, the highly ordered arrangement of collagen fibers produces residual quadripolar coupling with mobile protons, an efficient mechanism for T2 relaxation. For these tissues with a highly preferred or anisotropic organization of collagen fibrils, T2 relaxation is dependent on the relative orientation of the collagen fibers with the static magnetic field (B0).5 Tissues containing fibers oriented parallel or perpendicular to B0 have efficient T2 relaxation and low signal intensity on T2-weighted images. However, when fibers are oriented 54 degrees relative to B0, there

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■ FIGURE 45-3 A, Coronal, 3T, fat-suppressed, PD-weighted, TSE MR image of the knee illustrating normal spatial variation in cartilage signal intensity. Areas chronically exposed to high compressive loads such as the uncovered cartilage of the medial compartment (arrows) demonstrate a striated hypointense signal intensity of the radial zone, with a thin hyperintense superficial zone. This is a result of the high type II collagen content of the radial zone that has an anisotropic orientation perpendicular to the bonecartilage interface. The hyperintense superficial zone is thicker in regions of the joint with less compressive load. B, Sagittal, 3T, fatsuppressed, PD-weighted, TSE MR image of the knee illustrating uniformly high cartilage signal intensity in the trochlea and posterior femoral condyle. Note the striated appearance of the central load-bearing regions of the femoral condyle and tibial plateau.

is averaging of the residual quadripolar coupling, which minimizes this contribution to T2 relaxation and leads to an increase in signal intensity. Because of this effect, 54 degrees is termed the “magic angle,”6 derived from the technique of magic angle spinning used to increase the T2 relaxation of crystalline samples in solid-state nuclear magnetic resonance spectroscopy. The high concentration of collagen in the radial zone also decreases signal intensity through magnetization transfer. As suggested by the name, magnetization transfer is a process in which magnetization from a proton located on collagen is transferred to the mobile proton pool that gives rise to the MR signal.7 Magnetization transfer effects are most pronounced for techniques that use a large number of radiofrequency pulses such as multislice fast spinecho (FSE) or turbo spin-echo (TSE) techniques. The rapid application of off-resonance radiofrequency energy quickly saturates protons bound to the collagen molecules but does not saturate the mobile pool in the surrounding water. This saturated magnetization is then transferred either through chemical exchange or exchange of magnetization to nearby water protons in the mobile pool. Type I and II collagen demonstrate substantial magnetization transfer with FSE techniques.8,9 The effect of magnetization transfer is to decrease signal intensity of tissues rich in collagen on the MR image.10 For tissues such as cartilage, incidental magnetization transfer reduces signal intensity by 15% to 20% as the number of slices and thus the amount of offresonance irradiation increases.11 Because gradient-echo techniques use significantly less radiofrequency energy, there is less incidental magnetization transfer with gradient-echo techniques compared with spin-echo (SE) and FSE techniques. As a result of less magnetization transfer and T2 weighting, cartilage has relatively uniform high signal intensity on T1-weighted fat-suppressed gradientecho images.

Recognizing the normal heterogeneity of cartilage is important to avoid erroneously interpreting nonuniform signal as disease on T2-weighted images. As discussed previously, the signal intensity of cartilage normally increases toward the surface. In addition to variation in signal intensity with respect to depth from the articular surface, there are differences with respect to location in the joint and relative orientation of cartilage to the applied magnetic field. This variation in signal intensity closely follows variation in histologic and biomechanical properties of cartilage. For example, cartilage consistently exposed to high compressive load such as tibial cartilage not covered by meniscus has a thin superficial layer of high signal intensity, whereas the covered portion of tibial cartilage has a thicker layer of superficial hyperintensity. Goodwin and associates have correlated this regional variation in signal intensity with obliquity of the collagen matrix cleavage planes on freeze-fracture specimens, indicating that the relative orientation of the cartilage matrix to the applied magnetic field is a major factor.12 Regional differences in cartilage T2 relaxation are most pronounced in the femoral condyle. This is a result of two processes. First, there are substantial differences in the organization of extracellular matrix and chondrocytes between the central femoral surface and posterior femoral condyles, which are not habitually exposed to high compressive load but experience shear forces during knee flexion. Whereas type II collagen in the central femoral condyle has a high degree of anisotropy, results from electron microscopy and x-ray diffraction studies indicate the collagen matrix in the posterior femoral condyle has less anisotropy and has a fine fibrillar organization. This region of cartilage lacks the regular bands of condensed collagen seen in the central femoral condyle. Second, the oblique orientation of the collagen matrix in this region with respect to the direction of B0 is close to

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the magic angle of 54 degrees. As a result of differences in organization and orientation of the type II collagen matrix, cartilage in the posterior femoral condyle demonstrates uniformly high signal intensity compared with the layered pattern of signal intensity observed in the central femoral condyle. Although regional variation in the MRI appearance of cartilage has been extensively studied for the knee, similar variation is observed in other joints with MR images of sufficient resolution.13

Pathology Normal cartilage function depends on a balance of aggrecan swelling and constraining forces provided by the collagen meshwork. Investigators in the early 1970s proposed that one of the earliest processes of cartilage degeneration was fragmentation of the collagen matrix. Because damaged collagen no longer constrains the proteoglycans, they swell and draw in more water. The increased water content and loss of interstitial fluid pressure allow water to move more freely through the tissue. As a result, more compressive load is carried by the solid components, leading to structural fatigue. This results in a cascade of events in which damage to the solid matrix increases mobility of water, thereby transferring more of the compressive load onto the matrix and producing further damage. Eventually, this leads to gross loss of cartilage. Although chondrocytes are capable of producing new proteoglycan, there is limited capacity to repair collagen damage. Most investigators believe damage to the collagen meshwork is irreversible. Several factors can increase susceptibility of cartilage collagen to damage. First, genetic

■ FIGURE 45-4

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mutations of the type II collagen gene have been implicated in several syndromes associated with premature onset of OA (Fig. 45-4). These are collectively known as type II collagenopathies and include Stickler’s syndrome, Kniest’s dysplasia, and spondyloepiphyseal dysplasia, along with other conditions. With the relatively large degree of genetic diversity in the type II collagen gene it is likely that inherited factors contribute to the relative risk of OA in the general population. Additional mutations have been identified in genes encoding for other cartilage macromolecules. Second, senescent accumulation of advanced glycation end products in cartilage and cross-linking of collagen fibrils make the collagen matrix more brittle and prone to fracture. Because of the slow turnover of collagen in cartilage, these byproducts accumulate with age. Age also influences chondrocyte metabolism; in particular there appears to be a diminished capacity of older chondrocytes to synthesize proteoglycan. As a result, older cartilage may be more susceptible to damage from fatigue fractures and may have less capacity to replenish aggrecan, thereby predisposing older individuals to development of OA. Third, two families of enzymes are observed to be unregulated in early OA and may contribute to progression of cartilage damage. Matrix metalloproteinases break down collagen, whereas aggrecanases degrade aggrecan. In the healthy state the activity of these degradative enzymes is balanced by that of synthetic enzymes, as well as production of specific enzyme inhibitors. Inflammatory mediators such as interleukin-1 and tumor necrosis factor are increased in OA and tip the balance of enzymatic pathway toward the side of matrix degradation.

A, Coronal, fat-suppressed, PD-weighted, FSE MR image of a 27-year-old man with Stickler’s syndrome, an inherited point mutation of the type II collagen gene. Extensive cartilage loss is present in the medial compartment with associated degenerative changes in the subchondral bone. Although there is normal thickness of cartilage in the lateral compartment, note the loss of spatial variation in signal intensity observed in normal cartilage. B, Sagittal, fat-suppressed, T2-weighted MR image of same patient as in A. Note the linear hyperintensity at the bone-cartilage interface compatible with cartilage delamination (arrow).

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BIOMECHANICS

IMAGING TECHNIQUES

Normal cartilage biomechanics relies on a balance of aggrecan swelling pressure and constraint by the surrounding collagen meshwork. This balance is similar to an automobile tire in which the swelling pressure from the proteoglycans is analogous to the tire pressure from the air and the constraint of the collagen meshwork is like the walls of the tires. Just as driving on tires with low air pressure leads to rapid deterioration of the tire, low interstitial pressure in cartilage leads to deterioration of the matrix. High fluid pressure, along with the high osmolarity, viscosity, and electrostatic forces of the extracellular cartilage matrix restrict the movement of interstitial water and provides compressive stiffness to cartilage. When cartilage is compressed, the energy imparted into the tissue is dissipated by frictional drag forces as water moves through the extracellular matrix. For cartilage to resist compression the movement of water through the extracellular cartilage matrix must be restricted. Under normal conditions, approximately 90% of the load is carried by water, which is the primary reason cartilage is so resilient to repetitive compression. In addition to compression, cartilage is also exposed to shear stress as one articular surface moves against another. The normal articular surface of cartilage has an extremely low coefficient of friction, allowing the surfaces to move smoothly. Damage to the surface such as fibrillation or focal cartilage defects increases friction at the surface and tensile strain in the extracellular matrix. Shear stiffness in cartilage is a function of tensile strain that develops in the type II collagen matrix. Aggrecan also contributes to shear stiffness by buttressing the collagen fibers and inflating the collagen meshwork. Mechanical factors influence the susceptibility of cartilage to damage. It is acknowledged that high mechanical load such as impact injuries may exceed the material properties of even healthy tissue, producing fracture fissures through the matrix. However, a certain amount of mechanical loading is necessary for normal cartilage health. Moderate cyclical loading has been shown to increase proteoglycan production in cultured chondrocytes; however, high compressive forces, particularly static forces, have a deleterious effect on cartilage physiology. Increased levels of exercise have been shown to increase proteoglycan levels in cartilage, indicating the tissue has the potential to adapt to changes in demands.14 In contrast, joint immobilization leads to rapid depletion of proteoglycan and increased susceptibility to cartilage injury. An emerging theory for the etiology of OA and cartilage degradation is based on a growing body of evidence that indicates cartilage adapts to local biomechanical forces in the joint. In this theory cartilage is conditioned to withstand the local forces applied to it. When local forces are substantially altered, such as after meniscal resection, with abnormal joint alignment, or with increased joint laxity, biomechanical forces are transferred to unconditioned cartilage that exceeds the stress threshold of the tissue, leading to progressive deterioration of tissue.

Techniques and Relevant Aspects Historically, clinical evaluation of articular cartilage has primarily relied on two acquisition techniques: 3D fat-suppressed T1-weighted spoiled-gradient-echo (SGE) and 2D PD-weighted FSE techniques. Each has relative advantages and disadvantages with respect to evaluation of articular cartilage and diagnosis of osteochondral injuries. Initial MRI investigations of focal cartilage lesions used 3D T1-weighted gradient-echo acquisitions to identify focal defects. This technique provides high-resolution images with excellent differentiation of cartilage and underlying subchondral bone. As demonstrated in Figure 45-5, the major advantage of this technique is high spatial resolution, which is particularly important in evaluation of small joints or curved articular cartilage surfaces such as the talar dome or femoral head, in which thin sections are needed to clearly delineate cartilage interfaces and minimize volume averaging. Using this technique at 1.5 tesla (T), it is possible to obtain images with a 1 to 2 mm section thickness and in-plane resolution of 200 to 350 µm per pixel. For comparison, 2D FSE techniques are generally limited to 3- to 4-mm section thickness and 300- to 500 µm in-plane resolution. Because of high spatial resolution, 3D T1weighted gradient-echo acquisitions are becoming valuable tools in clinical research applications to quantitatively determine cartilage volume, thickness, and surface area. These tissue measures are being explored as possible end points in assessment of new chondroprotective therapies.15 Several disadvantages limit routine clinical application of gradient-echo techniques in larger joints where spatial resolution is less of a premium. A practical limitation of the 3D acquisition is the relatively long imaging times, ranging from 6 to 10 minutes, needed for coverage of large joints such as the knee. Imaging times can be shortened by approximately 30% by using more efficient water excitation techniques rather than chemical shift fat suppression. This is particularly effective at 3 T where greater separation of the fat and water resonances places less stringent demands on frequency-selective excitation pulses. A second limitation of the gradient-echo technique is relatively poor image contrast, particularly at the articular surface. Although the technique produces reliable high-contrast images of cartilage and subchondral bone, contrast at the articular surface can vary depending on protein content or blood degradation products in the synovial fluid. This can lower sensitivity for detection of superficial fibrillation or fissures occurring with cartilage injury. In addition, the T1-weighted technique is relatively insensitive to signal alterations within the cartilage or subchondral bone marrow that can be important indicators of osteochondral injury. In the knee the T1-weighted, fat-suppressed, gradientecho technique has a diagnostic accuracy of 65% to 95% for detection of focal cartilage defects. Diagnostic sensitivity has generally been shown to be substantially lower for superficial cartilage lesions confined to the outer 50% of cartilage. The ability to characterize the size of the lesion can be helpful for preoperative planning. In validation studies of focal cartilage defects, MRI has been shown to

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■ FIGURE 45-5 A, A 3T, 3D, coronal, water-excited, T1-weighted, SGE MR image of a 22-year-old professional hockey player with a nondisplaced fracture of the capitate. This provides high-resolution evaluation of the thin articular cartilage of the wrist but is insensitive to the marrow edema observed in the capitate and lunate on the fat-suppressed T2-weighted TSE image shown in B. The 3D, SGE sequence is particularly useful in evaluating thin articular cartilage of small joints such as the wrist and elbow and curved articular surfaces such as the hip and ankle and for providing quantitative assessment of cartilage morphology for research applications.

underestimate the depth of the articular defect. Size of the lesion has been shown to be important in accuracy of MRI. Although MRI is relatively accurate for measuring knee cartilage lesions 5 mm or larger, it has been shown to overestimate size of smaller lesions. Routine clinical evaluation of articular cartilage, particularly in the knee, relies heavily on PD-weighted FSE images either with or without fat suppression. The primary advantage of this technique is excellent soft tissue contrast with relatively modest image acquisition times of 3 to 4 minutes. As discussed previously, the fat-suppressed, PD-weighted FSE technique demonstrates heterogeneity of the cartilage signal resulting from regional and zonal differences in composition and structure of the extracellular cartilage matrix. This sensitivity to internal cartilage damage is particularly important for identifying injuries of the bone-cartilage tidemark zone that may not be associated with a visible cartilage surface defect but can have long-term consequences for tissue integrity. Also with the addition of chemical shift fat suppression, the technique is sensitive to elevated T2-weighted signal in the subchondral bone marrow that is frequently associated with overlying cartilage injury. The technique also provides clinically useful information regarding other articular tissues, such as menisci and ligaments. The primary disadvantage of the technique is lower spatial resolution compared with 3D acquisitions. Initial studies by Potter and coworkers report an accuracy of 92% for diagnosis of focal cartilage lesions in the

knee using the PD-weighted FSE technique.16 Similar accuracy has been identified in subsequent studies for full-thickness defects and for partial-thickness defects involving greater than 50% cartilage thickness. As with gradient-echo techniques, sensitivity is generally less than 50% for diagnosis of superficial fibrillation and erosion. New techniques based on the steady-state free precession gradient-echo sequences and multi-echo T2*-weighted sequences have been proposed for cartilage imaging. These techniques provide high resolution images of cartilage with image contrast similar to that obtained with FSE techniques. Although preliminary results are promising, these techniques are not widely available and have undergone limited validation for routine clinical use.

Controversies Evaluation of cartilage injury requires high contrast resolution and places a premium on a high signal-to-noise ratio (SNR) of the image. With other acquisition parameters remaining constant, the SNR of the MR image increases with magnetic field strength. Whereas low-field open configuration or dedicated extremity magnets have demonstrated accuracy comparable with 1.5T scanners in diagnosis of meniscal or anterior cruciate ligament tears, accuracy in diagnosis of cartilage injury is substantially lower on low-field scanners. This is particularly true for partial-thickness cartilage lesions. Although clinical

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experience with 3 T in cartilage is limited, preliminary results suggest the higher field strength provides improved contrast resolution and greater diagnostic accuracy in detection of focal defects. For quantitative determination of cartilage morphology, preliminary findings indicate higher spatial resolution images available at 3 T improve reproducibility but have not been shown to improve accuracy in defining the size of focal defects.

MANIFESTATIONS OF THE DISEASE Grade I Lesions Current MRI grading systems of articular cartilage damage are based on modifications of the Outerbridge classification originally described for surgical grading of patellar lesions.17 The original Outerbridge surgical classification is based on size of surface fragmentation and fissuring. As shown in Table 45-1, the MRI modification of the Outerbridge classification incorporates the depth of the lesion from the articular surface. Arthroscopic grading of cartilage frequently uses the Noyes classification.18

Magnetic Resonance Imaging In the surgical Outerbridge classification, grade I lesions are identified by a subjective assessment of cartilage softening with an intact articular surface. Because there is no direct MRI finding that corresponds to cartilage softening, this has been modified to reflect MRI signal changes without morphologic changes of the cartilage surface. Early studies found poor correlation between grade I MRI lesions and arthroscopy, as well as low sensitivity in MRI detection of patellar cartilage softening found at arthroscopy. A lack of correlation should not be interpreted as a deficiency in either MRI or arthroscopy. Studies in isolated osteochondral samples indicate the two techniques are evaluating different properties of cartilage damage. In studies on enzymatically treated cartilage specimens, degradation of the type II collagen matrix is correlated with elevation in cartilage T2, whereas removal of proteoglycans has minimal effect. In correlation studies between biomechanical testing and MRI of cartilage specimens it has been shown that while

removal of proteoglycan significantly decreases cartilage stiffness, elevation of T2 with degradation of the collagen matrix does not substantially change cartilage compressibility. In light of these results it is likely that elevation in T2-weighted signal intensity reflects structural changes of the collagen matrix that do not substantially alter the biomechanical qualities of cartilage evaluated at surgery that are primarily related to alterations in cartilage proteoglycans. Remote areas of T2 hyperintensity are frequently found in patients with more advanced areas of focal cartilage loss. Although the clinical significance of this finding is unknown, small longitudinal studies suggest grade I lesions are common and progress to sites of morphologic damage. The pattern of T2 elevation can reflect the underlying mechanism of cartilage injury. A more diffuse heterogeneous pattern of high T2-weighted signal can be observed after acute trauma, frequently in association with hyperintensity in the adjacent subchondral bone marrow. Isolated areas of T2 hyperintensity can be identified in cartilage of patients with no reported history of trauma. In our experience, focal elevation of T2 at the articular surface is frequently associated with visible cartilage damage at arthroscopy. Less frequently, T2 elevation may be limited to the deeper layers of cartilage. In this setting the cartilage surface frequently appears normal at surgery. This is most often seen in thicker patellar cartilage where the cartilage is sufficiently thick to resolve the deep layer of cartilage. As illustrated in Figure 45-6, focal elevation in cartilage T2 can be associated with a focal blister or smooth contour abnormality of the overlying articular surface. Similar findings of focal swelling and alterations in the fibril density in the superficial zone of patellar cartilage have been reported in the electron microscopy literature, supporting the hypothesis that these lesions represent structural reorganization/degeneration of the collagen matrix. In contrast to focal elevation in T2 seen with grade I lesions, a diffuse increase in the T2 of cartilage occurs with aging.19 This begins near the articular surface in the mid 40s, extending to the deeper layers of cartilage with increasing age. In addition to T2 hyperintensity, which is frequently present in the acute setting, focal areas of decreased T2-weighted cartilage signal may be observed adjacent to sites of cartilage injury (Fig. 45-7). Decreased T2-weighted

TABLE 45-1 Classification Systems for Evaluation of Chondropathy Description

Modified Outerbridge (MRI Evaluation)

Original Outerbridge (Surgical Evaluation)

Noyes Classification

Normal Cartilage softening and swelling with an intact surface

Grade 0 Grade I:T2-weighted signal alteration with an intact articular surface

Grade 0 Grade I: Softening and swelling

Superficial fragmentation and fissuring

Grade II: Extending less than 50% of depth

Deep fragmentation and fissuring

Grade III: Surface irregularity extending to the deep 50% of the cartilage thickness Grade IV

Fragmentation and fissuring equal to or less than 0.5 inch in diameter Fragmentation and fissuring greater than 0.5 inch in diameter Grade IV

Grade 0 Grade 1A: Moderate softening Grade 1B: Extensive softening with swelling of the articular surface Grade 2A: Surface irregularity less than one half of the cartilage thickness Grade 2B: Surface irregularity greater than one half of the cartilage thickness Grade 3A: Exposed bone Grade 3B: Cavitation or erosion of exposed bone

Exposed bone

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■ FIGURE 45-6 Grade I lesion: 3T, coronal, fat-suppressed, PDweighted MR image in a 54-year-old man with chronic knee pain demonstrates focal elevated signal intensity in the radial zone of the lateral femoral condyle (arrow) with an intact articular surface.

signal is generally not observed immediately after trauma but can develop several weeks after cartilage injury. The etiology of the decreased T2 signal intensity has not been determined but may reflect a hypertrophic healing

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response or fragmentation of the collagen fibrils exposing additional water binding sites on collagen. Areas of low T2-weighted signal intensity are also observed with sites of chondrocalcinosis, particularly with gradient-echo techniques or with high magnetic field strengths. A variation of the grade I cartilage lesion is cartilage delamination or debonding. This occurs when shear forces applied to the cartilage-bone interface injure the tidemark zone and disrupt collagen fibers that hold cartilage to the subchondral bone. In addition to shear force applied directly to the articular surface, high shear strain at the bone-cartilage interface develops with axial compression.20 Cartilage delamination may not be readily apparent at arthroscopy because the articular surface is often intact.21 In addition to biomechanical factors, recent evidence demonstrates that genetic factors influence the risk of cartilage delamination.22 MRI findings of cartilage delamination consist of linear T2 elevation at the bone-cartilage interface (Fig. 45-8). This is likely due to focal elevation in water content as well as to reduced collagen fibril anisotropy in the radial zone that occurs when cartilage is cleaved from bone.23 These injuries are best seen on T2- or PD-weighted images with fat saturation. Direct MR arthrography has been used to assess acetabular cartilage delamination in the hip, which is a frequent finding in the presence of femoral acetabular impingement. With this technique, cartilage delamination is inferred by the presence of high signal on T1-weighted fat-suppressed images between bone and cartilage. In the knee, delamination injuries may be seen in the femoral condyle, frequently in cartilage adjacent to the posterior horn of the meniscus. In the

■ FIGURE 45-7 A, A 3T, coronal, fat-suppressed, PD-weighted, TSE MR image of a 55-year-old man with medial and anterior knee pain demonstrates a subchondral insufficiency fracture (arrow) with collapse of the articular surface and an overlying full-thickness cartilage defect of the medial femoral condyle. Extensive marrow edema is present throughout the medial femoral condyle. B, Axial, fat-suppressed MR image demonstrates advanced cartilage loss of the medial patella facet. Focal areas of hypointense T2-weighted signal are present in the adjacent segments of cartilage on the median ridge (arrow).

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■ FIGURE 45-8 A 3T, axial, fat-suppressed, PD-weighted, TSE MR image of 39-year-old woman with right knee pain. A full-thickness linear fissure extends to the bone interface near the median ridge. Linear T2weighted hyperintensity is present at the bone-cartilage interface of the medial patella facet (arrow) with subtle marrow edema in the adjacent patella consistent with cartilage delamination.

setting of patellar dislocation, shearing injury can lead to delamination injuries of the median patellar ridge and may be associated with full-thickness cartilage fissures or flap tears. Delamination injuries are also frequently observed in the femoral trochlea after blunt anterior knee trauma, frequently in association with patellar cartilage injury.

■ FIGURE 45-9 Patella dislocation with chondral fissure (modified Outerbridge grade II) in a 33-year-old woman (black arrow). Note the characteristic pattern of marrow edema in the inferomedial patella and anterolateral femoral condyle seen after transient patellar dislocation (white arrows). Superficial fibrillation and fraying (Noyes 2A) were identified on the median ridge and medial patellar facet during surgery for patellar instability.

Grade II Lesions Magnetic Resonance Imaging Grade II lesions represent fissures, erosion, ulceration, or fibrillation involving the superficial 50% of cartilage thickness. There is no consensus in the MRI literature regarding terminology used to report cartilage lesions. Fissures represent linear clefts of the articular surface. They are most frequently observed after joint trauma, particularly in patellar cartilage. As seen in Figure 45-9, obliquely oriented fissures or flap tears can be seen after patellar dislocation, most frequently near the median ridge. The rate and magnitude of loading of the shear force influence the location of cartilage injury. When shear force is applied at high speed but with low energy, cracks are produced along the articular cartilage surface. At low speed and low energy, splits initially occur in the deeper layers. Ulceration of superficial cartilage blisters results in a small focal irregular crater (Fig. 45-10). Erosion refers to a smoothly marginated area of thinned cartilage and is frequently seen in older patients. Cartilage erosion is often identified in the posterior tibial plateau and femoral condyle, particularly in patients with chronic tears of the anterior cruciate ligament. Fibrillation or fraying of the articular surface appears

■ FIGURE 45-10 Axial, PD-weighted, FSE MR image of a 31-year-old man with persistent anterior knee pain 4 months after a fall onto the patellofemoral joint. Partial-thickness ulceration is present in the median ridge of the patella extending to the deep 50% of cartilage (modified Outerbridge grade III).

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visually as a fine velvety surface and is a common finding in subjects with OA. MRI has insufficient spatial resolution to resolve the individual fibrillations and they generally appear as an indistinct articular margin. MRI has relatively poor sensitivity and accuracy in identifying grade II lesions when using arthroscopy as the gold standard. This is partly due to limited spatial resolution of MRI and partly due to the subjective nature in estimating lesion depth with arthroscopy. Because of greater contrast between the bright signal intensity of synovial fluid and intermediate signal intensity of cartilage, T2-weighted images have greater sensitivity in identifying superficial fibrillation. Magnetization transfer enhances the surface contrast resolution and can improve conspicuity of these lesions. Despite higher spatial resolution, on T1-weighted gradient-echo images the low signal intensity of fluid and resulting poor contrast decreases the conspicuity of superficial fibrillation.

Grade III Lesions Magnetic Resonance Imaging As illustrated in Figure 45-10, lesions that extend more than 50% of the depth of the articular cartilage but do not result in exposure of the underlying bone are classified as grade III lesions. In correlation with arthroscopy or surgical grading, both T1-weighted fat-suppressed SGE and PD-weighted TSE MRI have high diagnostic accuracy in identification of grade III lesions.

Grade IV Lesions Magnetic Resonance Imaging Full-thickness lesions with exposure of the underlying subchondral bone are classified as grade IV lesions. The margin of the lesion can suggest the mechanism of cartilage injury. Sharply marginated borders are characteristic of traumatic cartilage injuries, whereas shallow or irregular margins are features more characteristic of chronic degeneration. Abnormal signal intensity from the underlying bone marrow and central osteophytes are frequently associated with grade IV lesions. MRI has demonstrated high specificity and sensitivity for detection of grade IV defects.

Bone Marrow Lesions Associated with Cartilage Injury Magnetic Resonance Imaging Increased T2-weighted signal intensity from the subchondral bone marrow is a frequent finding in acute traumatic osteochondral injury (see Fig. 45-9), as well as the setting of chronic osteochondral injury (see Fig. 45-7) or OA (Fig. 45-11). Similar alterations in bone marrow signal intensity are observed after high-intensity exercise or with altered joint biomechanics. It is a nonspecific MRI finding but can be associated with pain and with internal derangement in the knee. The characteristics of the MRI signal abnormality in the marrow are similar to those of water, which is dark on

■ FIGURE 45-11 A 3T, coronal, fat-suppressed, PD-weighted FSE image of a 29-year-old woman with anterior cruciate ligament reconstruction and partial lateral meniscectomy 3 years before the examination. Extensive cartilage loss is present in the lateral compartment associated with a horizontal cleavage tear of the lateral meniscus, tibial osteophyte formation, femoral subluxation, and degenerative T2-weighted hyperintensity and cyst formation in the subchondral marrow.

short echo time sequences and bright on fluid-sensitive sequences such as fat-suppressed PD- or T2-weighted SE or FSE sequences or short tau inversion recovery (STIR) images. Because the abnormal signal closely follows water, this finding has been erroneously termed bone marrow edema. Correlation studies with histology indicate a mixture of tissue types contribute to the abnormal marrow signal. In the setting of acute trauma, areas of fluid-like signal are associated with regions of trabecular microfracture, hemorrhage, necrosis, and edema.24 In this clinical setting the marrow findings represent a bone marrow contusion. Follow-up studies have shown that the abnormal marrow signal intensity can persist for several months after resolution of symptoms and is infrequently associated with long-term sequelae.25 In contrast to lesions with an ill-defined reticular border, bone marrow contusions that have a well-demarcated margin that extends to the subchondral plate have a 50% likelihood of progressing to localized cartilage loss.26 In the presence of OA or chronic focal osteochondral injury, the region of abnormal marrow signal has a heterogeneous histology consisting of necrosis, fibrosis, subchondral cysts, edema, hemorrhage, and granulation tissue.27 In the setting of OA, the presence of subchondral marrow T2 hyperintensity is correlated with pain28 and malalignment and has been shown to be prognostic of disease progression.29 The presence of elevated T2-weighted signal in bone marrow may be a secondary indication of an overlying fullthickness articular cartilage defect. In correlation with

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arthroscopic grading of focal cartilage defects, the prevalence of subchondral marrow hyperintense T2-weighted signal is 1% for athroscopically normal cartilage, 10% for partial-thickness defects, and 53% for full-thickness articular cartilage defects.30

DIFFERENTIAL DIAGNOSIS Laboratory tests are primarily used to exclude other causes of joint pain such as inflammatory or crystalinduced arthropathies as well as infection. Several serum and urinary biologic markers (biomarkers) are being explored as possible measures of disease severity and progression in clinical trials on OA. These may be used to either select or exclude subjects with preclinical stages of OA or may be used as an end point to monitor response to therapy. To be effective a biomarker must be valid (a true measure of the disease), reliable (provides a reproducible measure of disease severity), and responsive (capable of detecting significant differences in disease severity). In OA, biomarkers are being evaluated as indicators of cartilage matrix degradation or synthesis. Combinations of biomarkers are frequently employed to indicate loss of cartilage homeostasis in which there is an imbalance of matrix synthesis and breakdown products. Because of their high abundance in the cartilage matrix, type II collagen and aggrecan are major targets for biomarker development. Other matrix proteins such as cartilage oligomeric matrix protein (COMP) have been studied because of their proposed specificity for cartilage or serum markers of matrix metalloproteinases (MMPs) because of their critical role in matrix degradation. Markers from other joint tissues such as serum osteoclastin, a marker of new bone formation, and urinary type I collagen cross-links, a measure of bone turnover, may also have a role in OA. Currently, routine application of biomarkers has been limited by low sensitivity and specificity. This is partly due to the substantial dilutional effect that occurs when OA is confined to a single joint with relatively small cartilage volume. Greater specificity may be gathered by combining biologic markers with MR image markers of matrix degradation.31

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment Current management of patients with OA and cartilage degeneration is focused on reducing disability by reducing pain and improving joint function. Although disease modification therapies for inflammatory arthropathies have been successful in reducing disease progression, disease-modifying OA drugs (DMOADs) are in preliminary stages of development and evaluation. Mild to moderate pain in patients is generally treated with over-the-counter analgesics such as acetaminophen, ibuprofen, or nonsteroidal anti-inflammatory drugs (NSAIDs); however, longterm use of these agents is limited by side effects. Opioid analgesics are reserved for more severe pain when NSAIDs are not tolerated or efficacious. Supplemental nutraceuticals such as glucosamine and chondroitin sulfate are

commonly used in patients with OA. Although a recent multicenter trial suggested the combination of these supplements may have benefit in a subset of patients with moderate to severe knee pain, they were not found to be efficacious compared with placebo in controlling pain in OA in the general OA cohort.32 Intra-articular injections of hyaluronic acid have had limited efficacy in large clinical trials. For short-term relief of pain, intra-articular injections of corticosteroids have been found to be moderately efficacious; however, the comparative efficacy decreases after 3 weeks.

Surgical Treatment Surgical management of patients with OA or focal chondral defects consists of techniques to reduce symptoms, alter joint biomechanics, joint reconstruction, and a variety of new techniques targeted toward repair of focal cartilage lesions. Arthroscopic lavage has been shown to alleviate pain. This may occur through removal of inflammatory mediators in the synovial fluid; however, the mechanism for pain relief is unknown. For patients with unicompartmental arthritis and malalignment, osteotomies may be used to improve joint biomechanics. For patients with more severe forms of OA, joint reconstruction remains the mainstay of surgical therapy. Given the growing evidence that focal cartilage defects represent a substantial risk factor for developing OA, more patients are undergoing surgical repair procedures to either restore cartilage function or decrease the rate of cartilage degradation. The techniques are limited to focal cartilage defects and are aimed at filling the articular void with tissue, preferably with biomechanical properties similar to native cartilage, which is integrated into adjacent native tissue. There are two general surgical approaches for cartilage repair: local stimulation techniques and transplantation techniques. Local stimulation techniques such as Pridie drilling, microfracture, or abrasion arthroplasty are aimed at disrupting the subchondral cortical surface to induce bleeding. This process induces fibrocartilage production in the chondral defect and is considered palliative rather than reparative. The long-term clinical response of these techniques varies with the quality of the repair tissue, body habitus, age, and activity level. As demonstrated in Figure 45-12, the MRI initial postoperative examinations typically demonstrate subchondral hyperintensity on fluid-sensitive sequences. The initial tissue fill is usually less than that of the adjacent native tissue. Over time, the edema generally resolves and there is an increase in thickness of the reparative tissue. Failure is generally defined by a paucity of reparative tissue, chondral fissures, or gaps in the articular surface. A variety of chondral transplantation techniques are available. Large defects may be treated with allografts, whereas autologous osteochondral grafts are reserved for smaller defects. With autologous osteochondral transplantation, small osteochondral cylinders or plugs are harvested from non–weight-bearing surfaces of the joint and then transferred into the prepared site of the cartilage defect. The intervening gaps between the osteochondral

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■ FIGURE 45-12

Microfracture repair. Coronal, fat-suppressed, PD-weighted FSE (A) and sagittal, fat-suppressed T2-weighted FSE (B) MR images from a 55-year-old man 5 months after microfracture repair for a focal osteochondral defect of the medial femoral condyle. The repair tissue is heterogeneously bright compared with native cartilage. A linear zone of marrow hyperintensity persists at the repair site.

grafts fill with fibrocartilage repair tissue. The goal is to produce a smooth surface that is congruent with the adjacent native cartilage. MRI can be used postoperatively to evaluate surface congruity and integration of the fibrocartilage repair tissue surrounding the osteochondral plugs. Cartilage in the osteochondral plugs retains the signal characteristics of the donor site. The fibrocartilage tissue has heterogeneously elevated signal intensity compared with the osteochondral plugs. Autologous chondrocyte implantation (ACI) is an alternative transplantation technique. In contrast to autologous osteochondral transplantation this is a twostage procedure. First, cartilage tissue is harvested from a non–weight-bearing articular surface. In the laboratory, chondrocytes are isolated and grown in culture to increase their numbers. In the second procedure the osteochondral defect is débrided and covered with a periosteal patch that is sealed with fibrin glue. The cultured chondrocytes are injected beneath the periosteal patch. A more recent variation is matrix-induced autologous chondrocyte implantations (MACI) in which chondrocytes are placed into a collagen scaffold, thereby providing stabilization to the repair tissue. In ACI, the repair tissue passes through three phases as it matures from implanted cells to tissue. During the initial 6 weeks the cells proliferate and expand to fill the defect. This is followed by the transitional phase, lasting approximately 6 months, in which cells produce an extracellular matrix and the repair tissue stiffens. In the final phase the tissue undergoes remodeling

and develops tissue properties resembling that of hyaline cartilage. The MRI appearance of the repair site changes during the maturation process. During the proliferative phase the tissue is of intermediate signal intensity on T1weighted images and of high signal intensity on fluid-sensitive images. As the extracellular matrix develops and matures, the MRI appearance begins to resemble hyaline cartilage. Complications of ACI include failure to incorporate with the adjacent tissue, characterized by fluid-like signal intensity at the demarcation zones, and periosteal hypertrophy (Fig. 45-13) or delamination. Cartilage repair techniques are an active area of research. There is ongoing research on cartilage tissue engineering using mesenchymal stem cells, tissue scaffolds, and growth factors to generate repair tissue that more closely resembles the biomechanical properties of native hyaline cartilage.

What the Referring Physician Needs to Know ■ ■ ■ ■ ■

Location of cartilage injury Size and extent of cartilage lesion Presence or absence of subchondral marrow abnormalities Associated derangement of the joint (e.g., meniscal pathology, ligament tear) Presence or absence of joint effusion

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■ FIGURE 45-13 Autologous chondrocyte implantation (ACI) repair. Sagittal 3T PD-weighted TSE (A) and coronal 3D water-excited T1-weighted gradient-echo (B) MR images of a 14-year-old girl 5 months after ACI repair. The sagittal image demonstrates heterogeneous signal of the reparative tissue, which is isointense to cartilage on the coronal image. There is thickening of the repair tissue compatible with hyperplasia of the periosteal flap.

SUGGESTED READINGS Eckstein F, Glaser C. Measuring cartilage morphology with quantitative magnetic resonance imaging. Semin Musculoskelet Radiol 2004; 8:329–353. Felson DT. An update on the pathogenesis and epidemiology of osteoarthritis. Radiol Clin North Am 2004; 42:1–9, v. Felson DT, Lawrence RC, Dieppe PA, et al. Osteoarthritis: new insights: I. The disease and its risk factors. Ann Intern Med 2000; 133:635–646. Gold GE, McCauley TR, Gray ML, Disler DG. What’s new in cartilage? Radiographics 2003; 23:1227–1242.

Goodwin DW, Dunn JF. High-resolution magnetic resonance imaging of articular cartilage: correlation with histology and pathology. Top Magn Reson Imaging 1998; 9:337–347. Mosher TJ, Dardzinski BJ. Cartilage MRI T2 relaxation time mapping: overview and applications. Semin Musculoskelet Radiol 2004; 8:355–368. Recht MP, Goodwin DW, Winalski CS, White LM. MRI of articular cartilage: revisiting current status and future directions. AJR Am J Roentgenol 2005; 185:899–914. Xia Y. Magic-angle effect in magnetic resonance imaging of articular cartilage: a review. Invest Radiol 2000; 35:602–621.

REFERENCES 1. Altman R, Asch E, Bloch D, et al. Development of criteria for the classification and reporting of osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association. Arthritis Rheum 1986; 29:1039–1049. 2. Felson DT. An update on the pathogenesis and epidemiology of osteoarthritis. Radiol Clin North Am 2004; 42:1–9. 3. Huberti HH, Hayes WC. Patellofemoral contact pressures: the influence of q-angle and tendofemoral contact. J Bone Joint Surg Am 1984; 66:715–724. 4. Jeffery AK, Blunn GW, Archer CW, Bentley G. Three-dimensional collagen architecture in bovine articular cartilage. J Bone Joint Surg Br 1991; 73:795–801. 5. Fullerton GD, Cameron IL, Ord VA. Orientation of tendons in the magnetic field and its effect on T2 relaxation times. Radiology 1985; 155:433–435. 6. Erickson SJ, Prost RW, Timins ME. The “magic angle” effect: background physics and clinical relevance. Radiology 1993; 188:23–25. 7. Morris GA, Freemont AJ. Direct observation of the magnetization exchange dynamics responsible for magnetization transfer contrast in human cartilage in vitro. Magn Reson Med 1992; 28:97–104.

8. Kim DK, Ceckler TL, Hascall VC, et al. Analysis of watermacromolecule proton magnetization transfer in articular cartilage. Magn Reson Med 1993; 29:211–215. 9. Henkelman RM, Stanisz GJ, Kim JK, Bronskill MJ. Anisotropy of NMR properties of tissues. Magn Reson Med 1994; 32:592–601. 10. Wolff SD, Chesnick S, Frank JA, et al. Magnetization transfer contrast: MR imaging of the knee. Radiology 1991; 179:623–628. 11. Yao L, Gentili A, Thomas A. Incidental magnetization transfer contrast in fast spin-echo imaging of cartilage. J Magn Reson Imaging 1996; 6:180–184. 12. Goodwin DW, Wadghiri YZ, Zhu H, et al. Macroscopic structure of articular cartilage of the tibial plateau: influence of a characteristic matrix architecture on MRI appearance. AJR Am J Roentgenol 2004; 182:311–318. 13. Lazovic-Stojkovic J, Mosher TJ, Smith HE, et al. Interphalangeal joint cartilage: high-spatial-resolution in vivo MR T2 mapping—a feasibility study. Radiology 2004; 233:292–296. 14. Roos EM, Dahlberg L. Positive effects of moderate exercise on glycosaminoglycan content in knee cartilage: a four-month, randomized, controlled trial in patients at risk of osteoarthritis. Arthritis Rheum 2005; 52:3507–3514.

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15. Eckstein F, Glaser C. Measuring cartilage morphology with quantitative magnetic resonance imaging. Semin Musculoskelet Radiol 2004; 8:329–353. 16. Potter HG, Linklater JM, Allen AA, et al. Magnetic resonance imaging of articular cartilage in the knee: an evaluation with use of fast-spin-echo imaging. J Bone Joint Surg Am 1998; 80:1276–1284. 17. Outerbridge RE. The etiology of chondromalacia patellae. J Bone Joint Surg Br 1961; 43:752–757. 18. Noyes FR, Stabler CL. A system for grading articular cartilage lesions at arthroscopy. Am J Sports Med 1989; 17:505–513. 19. Mosher TJ, Liu Y, Yang QX, et al. Age dependency of cartilage magnetic resonance imaging T2 relaxation times in asymptomatic women. Arthritis Rheum 2004; 50:2820. 20. Wong M, Carter DR. Articular cartilage functional histomorphology and mechanobiology: a research perspective. Bone 2003; 33:1–13. 21. Levy AS, Lohnes J, Sculley S, et al. Chondral delamination of the knee in soccer players. Am J Sports Med 1996; 24:634–639. 22. Holderbaum D, Malvitz T, Ciesielski CJ, et al. A newly described hereditary cartilage debonding syndrome. Arthritis Rheum 2005; 52:3300–3304. 23. Keinan-Adamsky K, Shinar H, Navon G. The effect of detachment of the articular cartilage from its calcified zone on the cartilage microstructure, assessed by 2H-spectroscopic double quantum filtered MRI. J Orthop Res 2005; 23:109–117. 24. Rangger C, Kathrein A, Freund MC, et al. Bone bruise of the knee: histology and cryosections in 5 cases. Acta Orthop Scand 1998; 69:291–294.

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25. Boks SS, Vroegindeweij D, Koes BW, et al. Follow-up of occult bone lesions detected at MR imaging: systematic review. Radiology 2006; 238:863–871. 26. Vellet AD, Marks PH, Fowler PJ, Munro TG. Occult posttraumatic osteochondral lesions of the knee: prevalence, classification, and short-term sequelae evaluated with MR imaging. Radiology 1991; 178:271–276. 27. Bergman AG, Willen HK, Lindstrand AL, Pettersson HT. Osteoarthritis of the knee: correlation of subchondral MR signal abnormalities with histopathologic and radiographic features. Skeletal Radiol 1994; 23:445–448. 28. Felson DT, Chaisson CE, Hill CL, et al. The association of bone marrow lesions with pain in knee osteoarthritis. Ann Intern Med 2001; 134:541–549. 29. Felson DT, McLaughlin S, Goggins J, et al. Bone marrow edema and its relation to progression of knee osteoarthritis. Ann Intern Med 2003; 139:330–336. 30. Kijowski R, Stanton P, Fine J, De Smet A. Subchondral bone marrow edema in patients with degeneration of the articular cartilage of the knee joint. Radiology 2006; 238:943–949. 31. King KB, Lindsey CT, Dunn TC, et al. A study of the relationship between molecular biomarkers of joint degeneration and the magnetic resonance–measured characteristics of cartilage in 16 symptomatic knees. Magn Reson Imaging 2004; 22:1117–1123. 32. Clegg DO, Reda DJ, Harris CL, et al. Glucosamine, chondroitin sulfate, and the two in combination for painful knee osteoarthritis. N Engl J Med 2006; 354:795–808.

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Rheumatoid Arthritis Marcy B. Bolster and Johnny U. V. Monu

Rheumatoid arthritis (RA) is a chronic and progressive inflammatory systemic disease that primarily affects the synovium and is characterized by destruction of bone and cartilage. The small joints of the hands and feet are typically affected, although the larger joints are also affected by the disease. Radiographic changes, characterized by joint space narrowing and marginal erosions, typically occur within the first 2 years of disease onset. The natural history of the disease involves progressive joint damage and disability. Newer therapies, however, appear to be having an impact on the radiographic disease progression.

ETIOLOGY The etiology of RA is not well understood. Certain human leukocyte antigen (HLA) class II alleles or haplotypes have been associated with the development of RA. HLADR4 is the most frequently associated haplotype with the development of RA and is associated with its more severe form.

PREVALENCE AND EPIDEMIOLOGY Rheumatoid arthritis occurs in approximately 1% of the U.S. population. Its incidence is 0.75 per 1000 adults per year.1 RA occurs more frequently in women and has a 3:1 predilection for women as compared with men. The disease may present at any age, but the peak onset is in the fourth to sixth decades. Patients with RA are at an increased risk for the development of cardiovascular disease and have a high mortality rate related to its presence.2 Additionally, patients with RA are at an increased risk for the development of certain malignancies, including lymphoma and leukemia.

CLINICAL PRESENTATION Rheumatoid arthritis is an inflammatory, symmetric polyarthritis that typically involves the hands and feet, although all synovial joints are susceptible to disease. It may have a sudden, explosive onset, or it may have a more indolent course. Typical of the inflammatory arthritides, 1100

the patient will experience joint swelling, erythema, warmth, and/or pain. The diagnosis of rheumatoid arthritis requires that the inflammatory polyarthritis be present for at least 6 weeks. As with other forms of inflammatory arthritis, the patient usually experiences prolonged stiffness on awakening, or morning stiffness, as well as stiffness after prolonged periods of immobility, termed gelling. The criteria for the diagnosis of RA include the following: ● ● ● ● ●

Osteopenia Osteolysis Erosions Lax ligaments Subluxations

The laboratory abnormalities associated with rheumatoid arthritis include a serum rheumatoid factor (RF) that is positive in 85% of patients; however, at the time of presentation, the RF is positive in only 40% of patients. Frequently, the antinuclear antibody (ANA) is also positive. There is a newer autoantibody test termed the anticitrullinated cyclic peptide (anti-CCP) that has a sensitivity of 65% but is highly specific for RA and, in combination with a positive RF, has a specificity of 95% for the diagnosis of RA.3–5 The anti-CCP antibody may also be positive in patients many years before the development of RA. The

KEY POINTS Periarticular osteopenia may initially occur. There is a bilateral, symmetric disease pattern. Involvement of the small joints of the hands and feet is characteristic of RA. ■ Anti-CCP antibody is associated with a worse prognosis and a higher likelihood of erosive disease. ■ Marginal erosions progress centrally. ■ RA is a disease of small joints; therefore, large joint effusions (i.e., of large joints or large volumes) are not characteristic. ■ Ligamental laxity and rupture manifest as subluxations and dislocations. ■ ■ ■

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inflammatory markers—erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)—are also typically elevated in patients with active disease. A normochromic, normocytic anemia may also be seen in patients with RA. Subcutaneous nodules, also termed rheumatoid nodules, occur in approximately 25% of patients 6,7 but may not be present at the time of presentation. The nodules most commonly involve the extensor surfaces of the upper extremities, the joints of the hands, and the Achilles tendon. Pathologically, these nodules comprise a central area of fibrinoid necrosis surrounded by palisading histiocytes that do not have an inflammatory appearance.

IMAGING TECHNIQUES Radiographs have remained the basis of imaging diagnosis.8 Initial diagnostic studies should include radiographs of both joints or appendages, such as hands, wrists, feet, and ankles because the disease is typically bilaterally symmetric (Fig. 46-1). Radionuclide scans using technetium-99 m–labeled methylene diphosphonate (99 mTc-MDP) may show increased radioisotope uptake in the affected joints. The uptake reflects both increased synovial activity and increased bone turnover. The findings are nonspecific and do not necessarily reflect active inflammation. Gallium scanning may also be positive and reflects chronic inflammatory response. The scans also lack specificity. Unusual or new symptoms, a change in the symptomatology, or failed response to treatment should trigger an additional evaluation with other modalities.

■ FIGURE 46-1 Radiographs of both hands in oblique projection (the ball catcher’s view) show juxtaarticular osteopenia and narrowing of radiocarpal and midcarpal joint spaces. There are erosions at the head of the first metacarpal of the left hand and medial subluxation at the first metacarpophalangeal joint.

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Ultrasonography and MRI should be used to evaluate and follow the course of established disease.8–13 High field MRI is more sensitive than radiographs and CT scans in detecting erosions.14,15 MRI also depicts other changes such as synovial proliferation, bursal enlargement, and bone inflammation or edema (Figs. 46-2 and 46-3). Bursal inflammation similarly may show enhancing synovium. The fluid distending the bursal space will not enhance immediately after intravenous contrast administration (see Fig. 46-3). Osteitis will be seen as abnormal high signal on T2-weighted images and will enhance after intravenous administration of a contrast agent.16,17 There is a positive correlation between the number of enhancing bones and the severity of disease activity.18 Some areas of bone marrow edema and enhancement will progress to cavitation and cyst formation.18 Joint swelling often due to the presence of effusion is more easily detectable in early disease using ultrasonography when compared with clinical examination.19–23 Ultrasonography is more sensitive than radiographs and CT in detecting erosion. It is believed to be equally as sensitive as or more sensitive than MRI in detecting erosion.14,16,17,24 On ultrasonography, erosion appears as a cortical defect usually greater than 2 mm in depth, with variable width and irregular floor. The subjacent marrow usually shows acoustic enhancement.17,18 Some studies suggest that ultrasonography is more sensitive than MRI in detecting and evaluating synovitis.12,25 Identification of various intra-articular structures and assessment of inflammatory activity in the disease process can be achieved with color Doppler imaging.13,26,27

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■ FIGURE 46-2 Coronal proton density–weighted (A), fast spin-echo, fat-saturated, T2-weighted (B), and contrast-enhanced, fat-saturated, T1-weighted (C) MR images of the wrist show erosive change at the ulnar styloid (large arrow), radial styloid (small arrows), triquetrum (arrowheads), and hamate. On the T2-weighted and contrast-enhanced T1-weighted MR images, synovial expansion is seen as areas of abnormal mixed high and intermediate signal pattern in the radiocarpal, midcarpal, and distal radioulnar joints.

General Radiographic Observations Joint Swelling One of the earlier radiographic observations in RA is para-articular soft tissue swelling (Fig. 46-4). This is mostly from the presence of joint effusions and synovitis. Synovitis with attendant wrist swelling is commonly located around the flexor carpi ulnaris and extensor carpi radialis longus tendons. Soft tissue swelling is also frequently observed at the metacarpophalangeal, metatarsophalangeal, and proximal interphalangeal joints.

The soft tissue swelling may be subtle and inapparent on initial radiographs. Later in the course of the disease the soft tissue swelling may be due to the presence of rheumatoid nodules.6 The presence of large joint effusions and bursal fluid collections is a frequent observation in RA and another reason for joint swelling (see Fig. 46-4).28–32 In fact, an unexplained large bursal fluid collection should prompt evaluation for RA or other inflammatory arthropathies. The source of the fluid collection is the synovitis related to RA.30,32

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■ FIGURE 46-3

Axial, fat-suppressed, contrast-enhanced, T1weighted (A), fast spin-echo, T2-weighted (B), and fat-suppressed, contrast-enhanced, T1-weighted (C) MR images of the hand show abnormal signal surrounding the flexor tendons of the second and third digits in a patient with rheumatoid arthritis. This is consistent with tenosynovitis. The contrast medium–enhanced T1-weighted image shows extensive synovial enhancements seen as high signal around the ulna (arrowheads) at the distal radioulnar joint. The abnormal signal in the distal radius is due to inflammation (osteitis) and subarticular cyst formation.

■ FIGURE 46-4 Radiographs of both hands show focal soft tissue swelling over the ulnar styloid likely due to tenosynovitis in this region. There is subtle diffuse osteopenia and loss of joint space at the radiocarpal, midcarpal, and metacarpophalangeal joints. Erosions are present at the heads of the third and fifth left metacarpals. There is mild medial subluxation at the right first metacarpophalangeal joint.

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Subluxations

Erosions

Rheumatoid arthritis due to active synovitis and pannus formation weakens ligaments and tendons, making them susceptible to rupture. Ligament or tendon ruptures result in subluxations and dislocations (see Figs. 46-1 and 46-4). Spontaneous rupture of the extensor tendons and ligaments is frequent in RA.33 Boutonnière deformities (Fig. 46-5), swan-neck deformities, and ulnar drift of the carpus, although not pathognomonic, are frequently seen in RA. These deformities result from selective involvement of the tendons and ligaments in the hands and feet. Nontraumatic massive rotator cuff tears with large shoulder joint effusions are often seen in RA. Subluxations and dislocations are late observations.

Erosions develop early and occur within the first 2 years of the disease. The erosion of RA may be marginal or central but typically starts from the margins and extends centrally (Figs. 46-7 and 46-8; see also Fig. 46-4). Erosions frequently involve the ulnar styloid such that in some cases the ulnar styloid is virtually absent due to osteolysis (see Figs. 46-5 and 46-8). Excessive central erosions may produce the “pencil-in-cup” deformity that is seen in more advanced cases at the metacarpophalangeal and metatarsophalangeal joints. Generally, erosions are seen proximally at these joints and at the proximal interphalangeal joints and less at the distal interphalangeal joints. Sites of tendon or ligament attachments (enthesis) may also show erosive activity (enthesopathy and enthesitis) (Figs. 46-9 and 46-10).

Osteopenia A common observation is osteopenia.34,35 The osteopenia is initially periarticular, is observed around the joints, and may be partly due to periarticular hyperemia. Ultimately, the osteopenia my become diffuse in long-standing RA (Fig. 46-6), particularly if the patient has taken long-term corticosteroid therapy.

Loss of Joint Space Usually, concentric loss of joint space is seen as RA progressively affects a joint. The loss of joint space is due to progressive destruction of cartilage by the inflammatory exudates in the rheumatoid joint (see Figs. 46-1, 46-4 to 46-6).

Osteolysis Rheumatoid arthritis is essentially an atrophic process in which the body’s ability to form bone is impaired. Thus, there is continued unimpaired bone resorption (osteopenia, osteolysis, and erosions) with little repair. In the wrist the loss of volume in the carpal bones results in various forms of carpal crowding and collapse (see Figs. 46-5, 46-7, and 46-8).

Osteitis Osteitis or active bone inflammation will show as abnormal signal on T1- and T2-weighted images. The abnormal areas will enhance after intravenous administration of a contrast agent (see Fig. 46-3).

Subchondral Cysts Subchondral cysts are common in RA. In the larger joints, such as the knee, the hip, the shoulder, the ankle, and the wrist, the subchondral cysts may be quite large and may be referred to as geodes (Figs. 46-7 and 46-11). It is believed that increased pressure in the joint due to synovitis forces synovial fluid through microfissures into the bones and by hydraulic pressure these small accumulations gradually enlarge into large subchondral cystic collections.

Osteonecrosis Avascular necrosis and infarcts are not a usual manifestation of uncomplicated RA. Corticosteroids and cytotoxic drugs are often used in the management of RA, and these may predispose patients to bone infarction and avascular necrosis.

Selected Joints Hands and Feet ■ FIGURE 46-5

Severe chronic changes of rheumatoid arthritis in the hand. There is marked diffuse osteopenia. Note the complete collapse of the carpus. Osteolysis of the distal ulna is present. Flexion deformity at the metacarpophalangeal joint and dorsal subluxation at the interphalangeal joint of the thumb are present, and these create the appearance of the so-called hitchhiker’s thumb.

Rheumatoid arthritis particularly affects the small joints of the hands and feet. In the hands there may be narrowing of the radiocarpal, midcarpal, and carpometacarpal joints. The metacarpophalangeal joints are narrowed, and the proximal interphalangeal joints are also narrowed. Disease changes in the distal interphalangeal joints,

■ FIGURE 46-6 Radiographs of both hands show changes of established rheumatoid arthritis. There is diffuse osteopenia. In the wrist there is carpal crowding, and collapse is worse on the left. Erosions are seen at the carpal bones, ulnar styloid, the bases of the metacarpals, and the first metacarpophalangeal joint. There is also medial subluxation at the first metacarpophalangeal joints of both hands.

■ FIGURE 46-7

Radiograph of the wrist in a patient with established rheumatoid arthritis. There is a large subchondral cyst (geode) in the distal radius and loss of joint space at the radiocarpal and midcarpal joints. Erosive change is seen at the head of the second metacarpal.

■ FIGURE 46-8 Frontal radiograph of a wrist with severe changes of rheumatoid arthritis. There is resorption of, and a large subchondral cyst at, the ulnar styloid. There are erosions at the base of the ulnar styloid, lunate, triquetrum, hamate, and first metacarpal. Cysts are also seen at the bases of the second and third metacarpals.

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■ FIGURE 46-9 Foot of a patient with rheumatoid arthritis shows early erosive changes in the posterior aspect of the calcaneus (short arrows). There is diffuse osteopenia.

although unusual, may occur later in the disease. Other changes that may be seen late in the disease include boutonnière deformity (flexion at the proximal interphalangeal joint and hyperextension at the distal interphalangeal joint), swan-neck deformity (hyperextension at the proximal interphalangeal joint and flexion at the distal interphalangeal joint), ulnar drift (occurs at the metacarpophalangeal joints), palmar subluxations at metacarpophalangeal joints, hitchhiker’s thumb (flexion at the metacarpophalangeal joint and hyperextension at the interphalangeal joint) (see Fig. 46-5), and radial deviation at the wrist. A combination of radial subluxation at the wrist and ulnar drift at the metacarpophalangeal joints results in the zigzag hand seen in severe RA. Erosion at the head of the fifth metatarsal is characteristic for RA. Other metatarsophalangeal joints are also commonly involved. Changes that may be found in the posterior aspect of the calcaneus include retrocalcaneal erosion (see Figs. 46-10 and 46-11) and bursitis.

Rheumatoid arthritis commonly affects only the cervical spine. In the spine as elsewhere there is remarkable paucity of osteophytes in untreated RA. The disc spaces are not usually directly affected by RA. The zygapophyseal joints are narrowed and may show erosive changes. The atlantoaxial joints may be widened or narrowed secondary to erosive and/or osteolytic changes in the odontoid (Figs. 46-12 to 46-14). Erosion of support ing structures leads to atlantoaxial instability as well as basilar invagination. Central canal narrowing is a prominent feature (see Figs. 46-13 and 46-14) and can lead to cervical cord injury. In the cervical spine, multilevel spondylolisthesis may create a stepladder appearance in the vertebral bodies (see Fig. 46-12). The presence of subaxial subluxations and absence of osteophytes is seen almost exclusively in RA. Often in such cases the disc spaces may be normal or minimally reduced in height.

MANIFESTATIONS OF THE DISEASE Extra-articular Manifestations Extra-articular disease manifestations occur in patients with RA. The extra-articular manifestations typically occur in conjunction with active joint disease and occur in patients with a positive RF titer. Other organ involvement that occurs in patients with RA include ocular, skin, peripheral nerve (mononeuritis multiplex), hematologic, pulmonary, and cardiac manifestations. The ocular manifestations associated with RA include scleritis and episcleritis. The scleritis is characterized by an inflammatory infiltration of the sclera and may have associated nodular changes, which are pathologically identical

■ FIGURE 46-10 Lateral radiograph of the foot in a patient with rheumatoid arthritis. There is diffuse osteopenia and erosion at the posterior aspect of the calcaneus (arrow).

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■ FIGURE 46-11 Frontal (A) and lateral (B) radiographs of the knees of a 19-year-old woman with early-onset rheumatoid arthritis. In addition to diffuse osteopenia, there is circumferential joint space narrowing at the knee joint, an unusual finding in early-onset RA. There is also a large joint effusion seen as soft tissue density filling the suprapatellar recess.

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■ FIGURE 46-12

Radiographs of the lateral cervical spine in flexion (A) and extension (B) show a widened pre-dens space and diffuse osteopenia. There is a stepwise subluxation at multiple levels from C3 to C6. The absence of osteophytes and facet joint change suggests inflammatory arthritis, not degenerative arthritis.

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* ■ FIGURE 46-13

Sagittal T2-weighted (A) MR image and axial CT (B) image in soft tissue and bone windows at the level of the foramen magnum show basilar invagination. The odontoid (asterisk) is seen protruding into the foramen magnum thus narrowing the foramen. Irregularity of the margins of the odontoid (in B) is due to erosive change.

■ FIGURE 46-14

Sagittal CT image (A) and fast spin-echo T2-weighted MR image (B) of the cervical spine in a patient with rheumatoid arthritis showing cysts and erosions at the odontoid. Note the increased space between the posterior margin of the odontoid and the anterior margin of the contrast column in the cerebrospinal fluid space (subarachnoid space). The MR image shows abnormal signal in the odontoid area, consistent with the pathologic finding of pannus. Note indentation of the cerebrospinal fluid column at the same level as on the CT image due to the pannus. Also note narrowing of the spinal canal at C4.

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to the rheumatoid nodules occurring on the skin and can result in a condition termed corneal melt. This process can ultimately cause disruption of the globe; thus, a “red eye” in a patient with RA warrants urgent medical attention. Rheumatoid (necrobiotic) nodules may occur in subcutaneous tissues around stress-prone periarticular locations, such as around the Achilles tendon, knees, extensor surfaces of the arms, and buttock.36 Skin involvement includes rheumatoid nodules, and a less common occurrence is the development of palpable purpura. A skin biopsy of a patient with palpable purpura will typically reveal a leukocytoclastic vasculitis. The presence of palpable purpura and a leukocytoclastic vasculitis can signify the risk or presence of peripheral nerve involvement that may result in a peripheral neuropathy or a mononeuritis multiplex. A mononeuritis multiplex can cause wristdrop or footdrop and portends a poor prognosis for the patient.

Radiography The earliest changes noted on radiographs are osteopenia and soft tissue swelling (see Figs. 46-1, 46-4 to 46-6). The osteopenia is initially periarticular and subsequently becomes diffuse, particularly in long-standing disease. The soft tissue swelling may be subtle or inapparent on radiographs (see Fig. 46-6).

Magnetic Resonance Imaging Magnetic resonance imaging is very sensitive in detecting erosions.14,15 Synovial proliferation in joints, tendon sleeves, and bursa may appear as “dirty” high signal intensity on T2-weighted images and will enhance on postcontrast scans. Ordinarily, joint effusions will not enhance on postcontrast images. Bursal inflammation similarly may show enhancing synovium. The fluid distending the bursal space may not enhance immediately. Tendinopathy or ruptures may be seen. Osteitis will be seen as osseous abnormal signal that is low on T1-weighted images and high on T2-weighted images and will enhance after intravenous administration of contrast medium.

Multidetector Computed Tomography Multidetector CT will show erosive changes and may be as good as MR images for their detection. Effusions may also be visualized as joint distention with hypodensity.

Ultrasonography Ultrasonography has been shown to be useful and versatile. Erosions are easily demonstrated. Synovial proliferation has been seen using ultrasound. Effusions similarly are well demonstrated. Superficial ligaments are also optimally evaluated using ultrasound. Ultrasonography is dependent, however, on operator experience.

Nuclear Medicine Radionuclide scans using technetium-99 m–labeled methylene diphosphonate (99 mTc-MDP) show increased radioisotope uptake in the affected joints. The uptake reflects both increased synovial activity and increased

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bone turnover. The findings are nonspecific and do not necessarily reflect active inflammation. Gallium scan may also be positive and reflects chronic inflammatory response. These scans also lack specificity.

Positron Emission Tomography/ Computed Tomography There is no clearly defined role for PET/CT at this time for the diagnosis and management of RA.

DIFFERENTIAL DIAGNOSIS The differential diagnosis of a patient with a symmetric, inflammatory polyarthritis includes RA, a seronegative spondyloarthropathy, systemic lupus erythematosus, viral etiology, hepatitis C, and crystalline arthritis. The seronegative spondyloarthropathies, including ankylosing spondylitis, psoriatic arthritis, reactive arthritis, and arthritis associated with inflammatory bowel disease, are discussed elsewhere in this book. They may be associated with a peripheral joint arthritis; however, the associated spondylitis helps in the differentiation from RA. Also of interest is the fact that patients with the arthritis associated with psoriasis or inflammatory bowel disease may have the onset of the joint disease many years before the onset of the skin or bowel disease. Systemic lupus erythematosus (SLE) may present with inflammatory arthritis. SLE occurs most frequently in young women, thus making it difficult, at times, to differentiate from RA. The polyarthritis of SLE is typically nonerosive but may have a similar joint distribution as that seen in RA. Alternatively, patients with SLE may have an overlap syndrome with RA and develop true RA. Approximately 5% of patients with SLE will develop an erosive arthritis. Some distinguishing features between RA and SLE include the presence of other disease manifestations characteristic of SLE, including malar erythema, discoid rash, photosensitivity, oral ulcers, central nervous system disease such as seizures, renal involvement with glomerulonephritis, and hematologic abnormalities including low platelets, hematocrit, or white blood cell counts, in addition to the laboratory features of SLE. Infection by many viral agents such as Epstein-Barr virus, parvovirus B19, and hepatitis C virus may present with polyarthralgias and acute symmetric nonerosive polyarthritis similar in appearance to RA.38 The arthropathy tends to run a self-limited course over approximately 6 weeks. In the typical postviral course the onset of arthritis is within 1 to 2 weeks of the viral infection, characterized by a noninflammatory synovial fluid production with resolution of the symptoms within approximately 6 weeks. Hepatitis C infection is frequently associated with a positive RF; thus, the serologic test for hepatitis C antibody and a negative anti-CCP antibody can be helpful in the differentiation of hepatitis C arthritis from RA. Nonsteroidal anti-inflammatory agents are efficacious and rarely are glucocorticoids required to treat the symptoms of viral arthritis. Chronic forms of the crystalline arthropathies, such as gout or pseudogout, may present as inflammatory polyarthritis similar in appearance to RA and may be difficult

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to differentiate from RA. The presence of synovial fluid crystals using polarized microscopy (monosodium urate or calcium pyrophosphate) is useful for differentiating crystalline arthritis from other inflammatory arthritides, such as RA. Patients with chronic polyarticular tophaceous gout typically have arthritis involving the proximal interphalangeal joints, metacarpophalangeal joints, wrists, and metatarsophalangeal joints. Patients with gout or RA may have associated subcutaneous nodules, tophi, or rheumatoid nodules, making it difficult to differentiate chronic tophaceous gout from RA. An RA variant called rheumatoid nodulosis may be confused with gouty arthritis. The patients present with acute intermittent arthritis in the hands and feet and have numerous nodules in the hand.22,25 The radiographs show punched-out lesions without the typical overhanging edges in the bones. The nodules can be sampled or excised for pathologic confirmation of the underlying etiology. However, RA nodules almost never calcify, whereas gouty tophi may (though uncommonly) calcify so the presence of calcification within the nodules will facilitate diagnosis.

Laboratory evaluation is not as definitive as crystal identification in differentiating between crystalline arthropathy and RA. An elevated serum uric acid level does not confirm the diagnosis of gouty arthritis, and a positive RF titer may be present in up to 25% of patients with gout. Anti-CCP antibody is highly specific and, in combination with a positive RF, has a specificity of 95% for the diagnosis of RA.3–5 The antiCCP and other inflammatory markers such as ESR and CRP are also typically elevated in patients with active disease.

SYNOPSIS OF TREATMENT OPTIONS The goal of treatment in RA is to reduce the pain and inflammation of the joint involvement as well as to halt or slow progressive deformity, radiographic erosive disease, and associated disability (Table 46-1). Surgery can be performed to ameliorate deformities and to control pain.

TABLE 46-1 Medical Treatment of Rheumatoid Arthritis Drug or Treatment Agent Anti-inflammatory Agents Nonsteroidal anti-inflammatory drugs (NSAIDs) Glucocorticoids

Disease-Modifying Antirheumatic Drugs (DMARDs) Marrow suppressants Methotrexate Sulfasalazine Azathioprine Leflunomide Gold salts Penicillamine Non–marrow suppressants Hydroxychloroquine

Biologics Tumor necrosis factor (TNF)-α inhibitors: the five agents available for use are etanercept (Enbrel), infliximab (Remicade), adalimumab (Humira), abatacept, and rituximab.

Actions

Complications

NSAIDS are useful in alleviating pain associated with inflammatory arthritis but are not disease modifying in any way. Glucocorticoids are potent anti-inflammatory medicines that provide rapid and effective reduction in pain, inflammation, and swelling associated with inflammatory arthritis.There is some evidence that early intervention with prednisone can reduce the development of erosive disease.

Gastric irritation, hepatotoxicity, and renal toxicity Osteoporosis, avascular necrosis

DMARDs are medications that are added to control disease activity in patients with rheumatoid arthritis, and many may impact the development of erosive joint disease. Methotrexate is often the first choice of medications to treat a patient with rheumatoid arthritis.There is some evidence that methotrexate can slow the radiographic disease progression. A mild anti-inflammatory DMARD used in combination with other DMARDs appears to slow progression of erosive disease.

Depresses bone marrow and is an immunosuppressant with an increased risk of infection, e.g., hepatic, mucosal (ulcerations), and pulmonary (pneumonitis) Teratogenic: must be avoided in pregnancy and discontinued 3 months prior to conception in a man or woman

The TNF-α inhibitors demonstrate strong evidence for reducing the progression of erosive joint disease.These agents act very quickly in improving a patient’s signs and symptoms, are approved for use in early rheumatoid arthritis, and have the greatest impact on validated clinical measures of disease activity.

The most significant adverse events in patients taking TNF-α inhibitors relate to the risk of infection.TNF-α is an important cytokine in the host’s defense against infection, and it is a growth factor that is overproduced in patients with rheumatoid arthritis. The increased incidence of tuberculosis reported with TNF-α inhibitors is most frequently of extrapulmonary disease. Anti-TNF-α agents are associated with the development of increased usual and unusual infections; thus, a high index of suspicion is recommended in evaluating a patient with rheumatoid arthritis taking one of these agents when there are signs or symptoms of infection.

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What the Referring Physician Needs to Know ■

■ ■ ■

Rheumatoid arthritis is a symmetric inflammatory erosive polyarthritis typically involving the small joints of the hands and feet. The larger joints such as the hips and knees may rarely be affected. Early identification and treatment of the patient with rheumatoid arthritis helps slow disease progression. There are many extra-articular manifestations of rheumatoid arthritis.

■

■

Newer therapies, including biologic agents, have had a large impact on slowing the progression of disease (clinically and radiographically) and have reduced resultant disability. A significant cause of patient morbidity relates to infectious complications of therapy and an increased risk of cardiovascular disease in patients with rheumatoid arthritis.

SUGGESTED READINGS Bohndorf K, Schalm J. Diagnostic radiography in rheumatoid arthritis: benefits and limitations. Baillieres Clin Rheumatol 1996; 10:399–407. Tehranzadeh J, Ashikyan O, Dascalos J. Advanced imaging of early rheumatoid arthritis. Radiol Clin North Am 2004; 42:89–107.

Tehranzadeh J, Ashikyan O, Dascalos J. Magnetic resonance imaging in early detection of rheumatoid arthritis. Semin Musculoskelet Radiol 2003; 7:79–94.

REFERENCES 1. Doran MF, Pond GR, Crowson CS, et al. Trends in incidence and mortality in rheumatoid arthritis in Rochester, Minnesota, over a forty-year period. Arthritis Rheum 2002; 46:625–631. 2. Pincus T, Callahan LF. Taking mortality in rheumatoid arthritis seriously—predictive markers, socioeconomic status and comorbidity. J Rheumatol 1986; 13:841–845. 3. Tamai K, Yamato M, Yamaguchi T, Ohno W. Dynamic magnetic resonance imaging for the evaluation of synovitis in patients with rheumatoid arthritis. Arthritis Rheum 1994; 37:1151–1157. 4. Vallbracht I, Helmke K. Additional diagnostic and clinical value of anti-cyclic citrullinated peptide antibodies compared with rheumatoid factor isotypes in rheumatoid arthritis. Autoimmun Rev 2005; 4:389–394. 5. van Venrooij WJ, van de Putte LB. Early diagnosis of rheumatoid arthritis with a test based upon a specific antigen: cyclic citrullinated peptide. Ned Tijdschr Geneeskd 2003; 147:191–194. 6. Batalov AZ, Kuzmanova SI, Sapoundjiev LI. Intraarticular rheumatoid nodule detection in the knee joint using ultrasonography. Fol Med (Plovdiv) 2000; 42:27–29. 7. Kaye BR, Kaye RL, Bobrove A. Rheumatoid nodules: review of the spectrum of associated conditions and proposal of a new classification, with a report of four seronegative cases. Am J Med 1984; 76:279–292. 8. Bohndorf K, Schalm J. Diagnostic radiography in rheumatoid arthritis: benefits and limitations. Baillieres Clin Rheumatol 1996; 10:399–407. 9. Keen HI, Brown AK, Wakefield RJ, Conaghan PG. MRI and musculoskeletal ultrasonography as diagnostic tools in early arthritis. Rheum Dis Clin North Am 2005; 31:699–714. 10. Ostergaard M, Ejbjerg B, Szkudlarek M. Imaging in early rheumatoid arthritis: roles of magnetic resonance imaging, ultrasonography, conventional radiography and computed tomography. Best Pract Res Clin Rheumatol 2005; 19:91–116. 11. Ostergaard M, Gideon P, Sorensen K, et al. Scoring of synovial membrane hypertrophy and bone erosions by MR imaging in clinically active and inactive rheumatoid arthritis of the wrist. Scand J Rheumatol 1995; 24:212–218.

12. Stone M, Bergin D, Whelan B, et al. Doppler ultrasound assessment of rheumatoid hand synovitis. J Rheumatol 2001; 28:1979–1982. 13. Weidekamm C, Koller M, Weber M, Kainberger F. Diagnostic value of high-resolution B-mode and Doppler sonography for imaging of hand and finger joints in rheumatoid arthritis. Arthritis Rheum 2003; 48:325–333. 14. Alasaarela E, Suramo I, Tervonen O, et al. Evaluation of humeral head erosions in rheumatoid arthritis: a comparison of ultrasonography, magnetic resonance imaging, computed tomography and plain radiography. Br J Rheumatol 1998; 37:1152–1156. 15. Corvetta A, Giovagnoni A, Baldelli S, et al. Imaging of rheumatoid hand lesions: comparison with conventional radiology in 31 patients. Clin Exp Rheumatol 1992; 10:217–222, 1992. 16. Tehranzadeh J, Ashikyan O, Dascalos J: Advanced imaging of early rheumatoid arthritis. Radiol Clin North Am 2004; 42:89–107. 17. Tehranzadeh J, Ashikyan O, Dascalos J. Magnetic resonance imaging in early detection of rheumatoid arthritis. Semin Musculoskelet Radiol 2003; 7:79–94. 18. Conaghan PG, O’Connor P, McGonagle D, et al. Elucidation of the relationship between synovitis and bone damage: a randomized magnetic resonance imaging study of individual joints in patients with early rheumatoid arthritis. Arthritis Rheum 2003; 48:64–71. 19. Gibbon WW. Applications of ultrasound in arthritis. Semin Musculoskelet Radiol 2004; 8:313–328. 20. Grassi W, Filippucci E, Farina A, Cervini C. Sonographic imaging of the distal phalanx. Semin Arthritis Rheum 2000; 29:379–384. 21. Naredo E, Bonilla G, Gamero F, et al. Assessment of inflammatory activity in rheumatoid arthritis: a comparative study of clinical evaluation with grey scale and power Doppler ultrasonography. Ann Rheum Dis 2005; 64:375–381. 22. Szkudlarek M, Court-Payen M, Strandberg C, et al. Contrast-enhanced power Doppler ultrasonography of the metacarpophalangeal joints in rheumatoid arthritis. Eur Radiol 2003; 13:163–168.

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23. Szkudlarek M, Court-Payen M, Jacobsen S, et al. Interobserver agreement in ultrasonography of the finger and toe joints in rheumatoid arthritis. Arthritis Rheum 2003; 48:955–962. 24. Hau M, Schultz H, Tony HP, et al. Evaluation of pannus and vascularization of the metacarpophalangeal and proximal interphalangeal joints in rheumatoid arthritis by high-resolution ultrasound (multidimensional linear array). Arthritis Rheum 1999; 42:2303–2308. 25. Guermazi A, Taouli B, Lynch JA, Peterfy CG. Imaging of bone erosion in rheumatoid arthritis. Semin Musculoskelet Radiol 2004; 8:269–285. 26. Taylor PC. Serum vascular markers and vascular imaging in assessment of rheumatoid arthritis disease activity and response to therapy. Rheumatology 2005; 44:721–728. 27. Teh J, Stevens K, Williamson L, et al. Power Doppler ultrasound of rheumatoid synovitis: quantification of therapeutic response. Br J Radiol 2003; 76:875–879. 28. Barbaric ZL, Young LW. Synovial cysts in juvenile rheumatoid arthritis. Am J Roentgenol Radium Ther Nucl Med 1972; 116:655–660. 29. Grassi W, De Angelis R, Lamanna G, Cervini C: The clinical features of rheumatoid arthritis. Eur J Radiol 1998; 27:S18–S24.

30. Watson JD, Ochsner SF. Compression of bladder due to “rheumatoid” cysts of hip joint. AJR Am J Roentgenol 1967; 99:695–696. 31. Weissman BN, Sledge CB. Orthopedic Radiology. Philadelphia, WB Saunders, 1986. 32. Grassi W, Tittarelli E, Blasetti P, et al. Finger tendon involvement in rheumatoid arthritis: evaluation with high-frequency sonography. Arthritis Rheum 1995; 38:786–794. 33. Birkett V, Ring EF, Elvins DM, et al. A comparison of bone loss in early and late rheumatoid arthritis using quantitative phalangeal ultrasound. Clin Rheumatol 2003; 22:203–207. 34. Madsen OR, Suetta C, Egsmose C, et al. Bone status in rheumatoid arthritis assessed at peripheral sites by three different quantitative ultrasound devices. Clin Rheumatol 2004; 23:324–329. 35. Jacobs CV, Fultz PJ, Totterman SMS, Condemi JJ. Extra-articular manifestations of rheumatoid arthritis. Postgrad Radiol 1995; 15:153–163. 36. Buskila D, Shnaider A, Neumann L, et al. Musculoskeletal manifestations and autoantibody profile in 90 hepatitis C virus–infected Israeli patients. Semin Arthritis Rheum 1998; 28:107–113.

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Psoriatic Arthritis and Psoriatic Spondylarthropathy Karsten Jablonka and Jürgen Freyschmidt

Psoriatic arthritis (also known as psoriatic osteoarthropathy) is an autoimmune response disorder that belongs to the seronegative spondyloarthropathies. It is strongly associated with dermatologic psoriasis. Psoriatic spondylarthropathy refers to the involvement of the axial skeleton in patients who suffer from psoriatic arthritis.

ETIOLOGY The etiology of all clinical manifestations of psoriasis, psoriatic arthritis, and psoriatic spondylarthropathy seems to be a T cell–dependent tumor necrosis factor–mediated multifactorial autoimmune disorder.

PREVALENCE AND EPIDEMIOLOGY Psoriasis has no known sex predilection. Its peak incidence is between 30 and 50 years of age. It has been estimated that between 1% and 6% of the population in Western countries have some clinical degree of psoriasis vulgaris. Up to 15% of these patients develop clinically and radiographically variable degrees of psoriatic arthritis. Other sites of involvement besides the skin and bones are the tendons at bony insertions, referred to as the entheses. Psoriatic spondylarthropathy accounts for almost 20% of the seronegative spondyloarthropathies. A genetic association via the HLA-B27 antigen has been identified. Among HIV-infected patients, psoriasis arthropathy is 40 times more common than in the general population.1–5

CLINICAL PRESENTATION Dermatologic changes include erythematous macules with a silvery-white scale; nail changes (oil spots, pitting,

crumbling), and sterile pustules. The changes can be very subtle, for instance, on the scalp. Psoriatic arthritis and psoriatic spondylarthropathy are disorders resulting in inflammation of entheses (enthesitis) and erosion or destruction of joints; affected sites often exhibit bone proliferation. Patients may present with diffuse swelling of one or more digits (dactylitis).6 In 20% to 30% of cases there are no psoriatic skin changes when arthritis sets in. After a sudden onset (pseudogout arthritis) the course of the disease usually waxes and wanes. Only rarely is the course of the disease primarily chronic.

IMAGING TECHNIQUES Techniques and Relevant Aspects Early changes in psoriatic arthritis are nonspecific. They are detectable using MRI and, to a certain extent, ultrasound. In early stages of the disease osseous changes

KEY POINTS Primary features are the combination of erosive and proliferative bone changes. ■ If there is radiologic suspicion of psoriasis, a careful history (including family history) and a close dermatologic examination are necessary. ■ Radiographic signs: erosive, mutilating, and ankylosing joint changes, mainly involving the hands and feet, with a typical axial, transverse, or mixed pattern of involvement; proliferative changes (periosteal ossification, protuberances); spondylarthritis with sacroiliitis, parasyndesmophytes, and enthesopathy. ■

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(especially periostitis) are very subtle and require highresolution radiographs. Findings in late stages of the disease are typical and diagnostic in most cases. They are sufficiently visualized on routine radiographs.7–9

Pros and Cons In combination with observation of skin changes, radiographic examinations are sufficient in most cases. It can be argued that inflammatory changes naturally are better examined with MRI than on radiographs or CT. Once bony changes have occurred then radiographs are sufficient for detection of the typical changes of psoriatic arthritis. MRI is thought to help in the differentiation of psoriatic arthritis and rheumatoid arthritis; this statement is based on differing sites of edema (see later).

MANIFESTATIONS OF THE DISEASE Peripheral Skeleton Initial joint complaints are usually monarticular or oligoarticular. Typical sites of the skeletal disease are the entheses and articulations. There is a slight predilection for the great toe. Large joints are involved in fewer than 10% of cases. In later stages, the distribution changes to being oligoarticular or polyarticular. Polyarticular disease is characterized by the distribution among the small joints of the fingers and toes. One manifestation of this condition is “sausage digit” (see later under Enthesitis).

Radiography The basis of imaging psoriatic arthritis is conventional radiography. According to Freyschmidt, examinations should include views of both hands and feet, the lower thoracic spine, the lumbar spine, and other symptomatic regions or joints, in two projections.3 Examinations of the hands and feet are preferably performed using highresolution techniques. Very useful and convenient in this respect is the use of mammography systems. Relatively early changes (Fig. 47-1) that can be visualized radiographically include the following: ●

● ●

Spiculated or woolly sites of epiphyseal ossification on the distal phalanges, sometimes only visible by using a magnifying tool Acro-osteolysis Layered or periosteal ossifications on the shafts of tubular bones

Later signs in the appendicular skeleton (Fig. 47-2) include: ● ● ● ● ● ● ● ●

Nondelineation of the subchondral plate Erosions Destructive changes Joint space narrowing Ankylosis Mutilations Protuberances (spicular ossifications at joint margins, especially at the bases of the distal phalanges) Insufficiency and stress fractures

■ FIGURE 47-1 Early manifestations of psoriatic arthritis of the peripheral skeleton. A, Anteroposterior radiograph of the hand. Note soft tissue swelling of the thumb and second digit, with fluffy bone proliferation of the terminal tuft of the thumb. B, Bone scintiscan of the same patient shows increased uptake in regions of involvement.

Most often the distal interphalangeal joints of the hands and feet are involved. The distribution of the visible changes is of key importance in the radiographic assessment and classification of the disease. The lesions tend to be asymmetric with an oligoarticular or polyarticular distribution. If all the joints of one finger or toe are involved, the pattern of involvement is called “axial” or “vertical.” If all the distal interphalangeal joints of a hand or foot are affected, a “transverse” or “horizontal” pattern is present. There are also asymmetric mixed patterns.

Magnetic Resonance Imaging Magnetic resonance imaging can detect erosions and early articular and entheseal inflammation significantly better than conventional radiography and CT.

Multidetector Computed Tomography Computed tomography can be very useful as an adjunct to radiographs to verify the presence of osseous manifestations of psoriatic spondyloarthropathy, including erosions at the sacroiliac joints. When combined with intravenous contrast media administration, CT can characterize inflammatory tissue; however, this is inferior to MRI.

Ultrasonography Ultrasonography is an effective tool to visualize joint effusions associated with psoriatic arthritis.

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■ FIGURE 47-2 Psoriatic arthritis with arthritis mutilans. A, Anteroposterior radiograph of the hand showing gross destruction of the proximal interphalangeal joints with rounded, whittled margins and, to a lesser degree, involvement of the metacarpophalangeal joints. Note also fusion of the carpus and distal interphalangeal joints. B, Radiograph of the foot showing similar changes.

Nuclear Medicine

Radiography

Bone scintigraphy is a very convenient tool especially for claustrophobic patients for whom MRI is difficult. Because of its lack of specificity, findings should be compared with radiographs and clinical history. Nuclear bone scintiscans can be helpful in establishing the diagnosis, because they clearly define affected joints and make the pattern of involvement more obvious.

Early signs of an evolving psoriatic spondylarthropathy are not detectable radiographically. Later, one half of the patients show signs of a (usually unilateral) sacroiliac joint involvement with erosions and sclerosis. Conventional radiographs of the spine show typical changes of the vertebra. The predilection site is the upper lumbar spine. Just as in rheumatoid arthritis, involvement of the cervical spine can lead to atlantoaxial instability. Typical features seen in seronegative spondarthritis include:

Classic Signs

● ●

On radiographs of the hands and feet: ■ Erosive and coexistent osteoproliferative changes ■ Joint space narrowing ■ Arthritis mutilans with “pencil-in-cup” appearance ■ Ankylosis

● ● ● ●

Marginal syndesmophytes Nonmarginal syndesmophytes Paravertebral ossification Destructive discovertebral lesion Romanus lesion (“shiny corners” or sclerosis of the anterosuperior end plate) Sacroiliitis

Magnetic Resonance Imaging

Axial Skeleton Psoriatic spondylarthropathy is present if one or both sacroiliac joints and the spine are involved.

Magnetic resonance imaging is the best modality for visualizing ongoing inflammation (Fig. 47-3). With the possible exception of periosteal changes, all imaging features of psoriatic arthritis are visualized to a better advantage by

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● Arthropathies and Neurologic/Muscular Disorders and Connective Tissue Disease

Psoriatic spondylarthritis. A, Lateral radiograph of the cervical spine. B, Bone scintiscan of cervical spine showing abnormal uptake in the lower cervical region. C, STIR MR image of the cervical spine showing edema of C5 and C6 vertebral bodies and multiple spinous processes. Findings can simulate infection. D, Radiograph of the same patient showing sacroiliitis. E, Corresponding bone scintiscan showing abnormal radiotracer uptake at the sacroiliac joints.

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using MRI than by using any other modality. If instability of the craniocervical junction is suspected, MRI of the cervical spine is mandatory.

Multidetector Computed Tomography If radiographs are insufficient to visualize psoriatic spondylarthropathy, CT can be very helpful.

Ultrasonography Ultrasonography is a useful tool for observing inflammatory changes in patients with proven psoriatic arthritis.

Nuclear Medicine Bone scintigraphy can be useful for documenting spinal or sacroiliac involvement (see Fig. 47-3) and for acquiring an overview of all sites involved around the body.

Classic Signs Typical signs of seronegative spondylarthropathy include: ■ Marginal syndesmophytes ■ Nonmarginal syndesmophytes ■ Paravertebral ossification ■ Destructive discovertebral lesion ■ Romanus lesion (“shiny corners” or sclerosis of the anterosuperior end plate) ■ Sacroiliitis

Entheses Entheses are the regions of direct contact between bone and tendons, ligaments, or fascia.

Radiography The findings in enthesitis vary. Enthesitis is typical of an extra-articular manifestation of a psoriatic arthropathy and spondylarthropathy (Fig. 47-4). An enthesopathy can cause polymorphic ossifications of insertions of tendons, ligaments, fascia, and articular capsules. Massive swelling of the extra-articular soft tissues of a digit is termed psoriatic dactylitis.6 The affected fingers or toes have a sausage-shaped appearance (“sausage digits”).

Magnetic Resonance Imaging Even in early stages of the disease, intense bone marrow edema closely related to entheses is typical. MRI is the best modality for examination of active inflammation of entheses, for instance, at the gluteal region.

Multidetector Computed Tomography Computed tomography is not commonly indicated for psoriatic arthritis manifestations other than spinal and sacroiliac involvement. However, CT can show enthesial bone production with high detail, allowing for narrowing of the differential diagnosis especially when the disease is manifest in atypical locations (see Fig. 47-4).

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Ultrasonography Ultrasonography can give useful information on the extent of abnormality of the entheses. It is also capable of visualizing tenosynovitis that contributes to the diffuse, sausage-like swelling of involved fingers (dactylitis).

Nuclear Medicine Bone scintigraphy can provide a useful overview regarding sites of entheseal, articular, and spinal involvement (see Fig. 47-4).

DIFFERENTIAL DIAGNOSIS Psoriatic arthritis is probable if three or more of the following criteria are met, including at least one of criteria 5, 6, or 8. If rheumatoid factor is positive, two additional criteria must be fulfilled. 1. Involvement of the distal interphalangeal joints 2. Involvement of the metacarpophalangeal and interphalangeal joints of the same finger 3. Early involvement of the joints of the toes 4. Heel pain 5. Dermatologically confirmed psoriatic lesions of the skin or nails 6. Close relative with confirmed psoriasis 7. Negative rheumatoid factor 8. Radiographs of the hands and/or feet showing typical osteolytic changes along with bony proliferation and no periarticular osteoporosis 9. Clinical and/or radiographic involvement of the sacroiliac joints 10. Typical paravertebral ossifications on spinal radiographs Evidence of Reiter’s disease, ankylosing spondylitis, or polyarthritis of the fingers makes the diagnosis of psoriatic arthropathy unlikely. Reiter’s disease appears radiographically identical but is more common in the lower extremity. Quite often, the patient’s history makes one diagnosis more likely than the other; Reiter’s disease is seen in males, whereas psoriatic arthritis shows similar incidence in males and females; Reiter’s disease also involves conjunctivitis and urethritis. Psoriatic arthritis also commonly involves the skin and nails with characteristic lesions. Ankylosing spondylitis is characterized clinically by a stiff, painful back and radiographically by symmetric sacroiliitis and spinal syndesmophytes (bamboo spine). Paravertebral ossification can be a characteristic of latestage psoriatic spondylarthropathy but is usually large, nonuniform, and asymmetric. Laboratory tests usually are not diagnostic of psoriatic arthritis. The erythrocyte sedimentation rate is slightly elevated. The rheumatoid factor usually is negative; a positive test may signify a concomitant rheumatoid arthritis.

SYNOPSIS OF TREATMENT OPTIONS Anti-inflammatory drugs are the basis of treatment. Immune modulators are being introduced. Surgical interventions can become necessary, including joint replacement and arthrodesis.

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B

C

D ■ FIGURE 47-4

Psoriatic spondylarthropathy: enthesopathy. A, Radiograph of the lumbar spine taken on initial presentation showing no parasyndesmophytes. B, Radiograph of the same patient taken 4 years later, now showing parasyndesmophytes. Note also sclerosis at the sacroiliac joints. C, Anteroposterior radiograph of the same patient showing enthesopathy of the tibia. D, Lateral radiograph with enthesopathy of the tibia particularly at the soleus origin; note reactive sclerosis of adjacent bone with proliferative bone formation. E, Bone scintiscan with uptake representing enthesopathy of the proximal tibia. F, CT image of the same patient showing reactive sclerosis.

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Patients with psoriatic arthritis must be treated by specialists in this field. Radiographs are the baseline imaging modality. MRI, CT, ultrasonography, and bone scintigraphy are useful additional tools.

SUGGESTED READINGS Evangelisto A, et al. Imaging in early arthritis. Best Pract Res Clin Rheumatol 2004; 18:927–943. Kainberger F. Imaging of systemic rheumatoid diseases involving the musculoskeletal system. Radiologie 2004; 4:395–416. Kassimos D, et al. The hand x-ray in rheumatology. Hosp Med 2004; 65(1). Klecker RJ, et al. Imaging features of psoriatic arthritis and Reiter’s syndrome: advanced imaging of arthritis. Semin Musculoskelet Radiol 2003; 7:115–126. Myers W, et al. Common clinical features and disease mechanisms of psoriasis and psoriatic arthritis. Curr Rheumatol Rep 2004; 6:306–313.

Taylor WJ, et al. Operational definitions and observer reliability of the plain radiographic features of psoriatic arthritis. J Rheumatol 2003; 30:2645–2658. Taylor WJ, et al. Development of diagnostic criteria for psoriatic arthritis: methods and process. Curr Rheumatol Rep 2004; 6:299–305. Veale DJ, et al. Immunopathology of psoriasis and psoriatic arthritis. Ann Rheum Dis 2005; 64(Suppl II):ii26–ii29.

REFERENCES 1. Anandarajah AP, et al. Pathogenesis of psoriatic arthritis. Curr Opin Rheumatol 2004; 16:338–343. 2. Freyschmidt J. SKIBO-Diseases: Disorders affecting the skin and bones: A clinical, dermatologic, and radiologic synopsis. Heidelberg, Springer-Verlag Telos, 1998. 3. Freyschmidt J. Skeletterkrankungen. Heidelberg, Springer, 2003, pp 433–457. 4. Gladman DD, et al. Psoriatic arthritis: epidemiology, clinical features, course, and outcome. Ann Rheum Dis 2005; 64(Suppl II): ii14– ii17. 5. Moll JM, Haslock I, Macrae IF, Wright V. Associations between ankylosing spondylitis, psoriatic arthritis, Reiter’s disease, the intestinal arthropathies, and Behçet’s syndrome. Medicine 1974; 53:343–364.

6. Olivieri I, Barozzi L, Favaro L, et al. Dactylitis in patients with seronegative spondylarthropathy. Arthritis Rheum 1996; 39: 1524–1528. 7. Lingg G, et al. Insufficiency and stress fractures of the long bones occurring in patients with rheumatoid arthritis and other inflammatory diseases, with a contribution on the possibilities of computed tomography. Eur J Radiol 1997; 26:54–63. 8. Lingg G, et al. Bildgebende Verfahren bei der Arthritis psoriatica. Akt Rheumatol 2000; 25:123–131. 9. Totterman SMS. Magnetic resonance imaging of psoriatic arthritis: Insight from traditional and three-dimensional analysis. Curr Rheumatol Rep 2004; 6:317–321.

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Reactive Arthritis Daniel Nissman and Thomas L. Pope

Reactive arthritis is a postinfectious seronegative spondyloarthropathy (SNSA) syndrome characterized by a spectrum of specific musculoskeletal and extra-articular manifestations. The syndrome occurs after infection with specific organisms in two major settings: diarrheal illness and urogenital infection. The majority of patients have an underlying predisposing factor, either the presence of the human leukocyte antigen (HLA)-B27 or infection with the human immunodeficiency virus (HIV). Onset of symptoms is usually within 4 weeks of the triggering infection and usually after the triggering infection has resolved. Like the other SNSA syndromes such as ankylosing spondylitis and psoriatic arthritis, reactive arthritis shares an association with HLA-B27 and a particular symptomcomplex. Musculoskeletal complaints include joint pain from enthesitis and peripheral arthritis and back pain from sacroiliitis. Extra-articular complaints include conjunctivitis, urethritis, and a variety of mucocutaneous lesions. The symptom triad of arthritis, conjunctivitis, and urethritis after a triggering infection is classically known as Reiter’s syndrome even though Reiter was not the first to describe this triad. This triad was described previously in 1776 after a diarrheal illness and again in 1818 after a urogenital infection.1 Reports of cases with similar features predate even these descriptions. Hans Reiter published a similar case in 1916, and the term Reiter’s syndrome was coined in 1942 by Bauer and Engelman. The term reactive arthritis was suggested by Ahvonen in 1969 and is now the favored term.2 Reasons for abandoning the reference to Reiter include the facts that he was not the first to describe the syndrome, he attributed the syndrome incorrectly to infection by a spirochete, and he was a very high ranking Nazi physician who personally authorized medical experiments on prisoners that led to many deaths in concentration camps, including 250 people from experimental typhus infection.3,4

ETIOLOGY Reactive arthritis is unique among the SNSA syndromes in that it occurs after a clearly associated trigger—an enteric or urogenital infection. Enteric organisms that have a well1120

documented association with reactive arthritis include Campylobacter, Salmonella, Shigella, and Yersinia species. Chlamydia trachomatis is responsible for the vast majority of cases of reactive arthritis after a urogenital infection. Many other organisms, including parasites, and situations that trigger this syndrome have been reported. Chlamydia pneumoniae, Ureaplasma urealyticum, and Giardia intestinalis are examples. Reactive arthritis after intravesical instillation of bacille Calmette-Guérin (BCG) for bladder cancer has been reported.5 As a member of the SNSA syndromes there is a strong association with HLA-B27, although its presence is not necessary for the diagnosis. However, symptomatic disease is more likely in individuals with HLA-B27. An estimated 1% to 4% of individuals who are HLA-B27 negative will develop reactive arthritis, whereas 20% to 30% of individuals who are HLA-B27 positive will develop reactive arthritis. An important subgroup of HLA-B27–negative individuals are those infected with HIV. Individuals who are positive for both HIV infection and HLA-B27 can experience particularly severe manifestations of reactive arthritis. The exact pathogenesis of reactive arthritis is unknown. Factors that are important in its development include a triggering infection with specific types of bacteria and

KEY POINTS Reactive arthritis is an asymmetric, lower limbpredominant spondyloarthropathy that follows a triggering infection, usually within 4 weeks. ■ Conjunctivitis, urethritis, and skin lesions may be associated. ■ There is a strong association with HLA-B27 and HIV infection. ■ Heel pain and back pain are the most common complaints. ■ Radiographs of the spine, sacroiliac joints, and other affected joints are used to evaluate disease progression. ■ MRI and CT can detect early sacroiliitis. ■ Septic arthritis should be excluded first. ■

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an altered immune response, manifested by either HLAB27 positivity or HIV infection. Recent data suggest a central role for macrophages in the development of erosive disease. Subclinical intestinal inflammation has been associated with the entire spectrum of SNSA syndromes, including reactive arthritis. Mechanical factors may also be important but have not been sufficiently studied. Many other potential genetic factors beyond HLA-B27 positivity likely play a role. All bacterial organisms definitively linked to reactive arthritis are gram-negative and are either obligate intracellular organisms or are capable of intracellular survival. Antigenic material from these organisms disseminates from the site of primary infection to other parts of the body where this material has been recovered from the joint fluid and synovium of affected joints. In the case of Chlamydia, entire living organisms have been recovered, but with an altered gene expression profile from those involved with active infection.6 The antigenic material produced by these organisms persists in the tissues for long periods, especially material associated with chlamydial infection. These organisms all have a variety of means for evading the host immune response in addition to the capacity to live intracellularly, including the production of lipopolysaccharide (LPS), a proinflammatory molecule, and the ability to manipulate various cell membrane signaling molecules. The end result is a prolonged proinflammatory environment created by the presence and poor clearance of this antigenic material. These factors alone do not explain the manifestations of reactive arthritis because most people with primary infections with these organisms do not develop the disease. The majority of individuals with symptomatic disease are either HLA-B27 positive or are infected with HIV, and the common thread between these is an altered T-cell response. HLA-B27 is part of the major histocompatibility complex machinery responsible for antigen presentation to CD8-positive T cells. The specific role that HLA-B27 plays in the pathogenesis of reactive arthritis is not known, although there are a number of hypotheses.7,8 The HLA-B27 molecule folds more slowly than other HLA molecules and may become trapped in the endoplasmic reticulum. On the cell surface, the HLA-B27 molecule has the capacity to dimerize. Aberrant folding on the cell surface can cause part of the HLA-B27 molecule to occupy the antigen binding site. Through a variety of mechanisms, all these properties may lead to an elevated and prolonged inflammatory response. Antigenic mimicry may play a role as well. Peptides from HLA-B27 share sequence homology with antigens from Chlamydia and the reactive arthritis–associated enteric bacteria. HIV infection significantly alters the T-cell response to infection in patients with reactive arthritis in an unknown manner. Early in HIV infection, the CD8-positive T cells are relatively spared. In end-stage disease, the symptoms of reactive arthritis disappear and are likely due to further alteration in the proportions of the various T-cell subtypes. Tumor necrosis factor-α (TNF-α) is a proinflammatory cytokine that plays a key role in the inflammatory arthritis in the spondyloarthropathies. Anti-TNF-α therapeutics have shown benefit in arresting the progression of these diseases, although no specific studies have been

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performed in patients with reactive arthritis. Histologic analysis of samples obtained from sites of enthesitis has revealed a macrophage-predominant cellular infiltrate and not a T-cell–predominant infiltrate as previously expected.9 Macrophages are the primary producers of TNF-α. The role of TNF-α and its potential modulation by HLA-B27 positivity and HIV infection is not understood. Chronic intestinal inflammation has been observed in many patients with an SNSA syndrome, including individuals with reactive arthritis, particularly those with enteric-associated reactive arthritis. The degree of gut inflammation appears to follow the activity of the articular symptoms.10 The exact nature of the association, however, is not clear. Does the gut inflammation predispose to reactive arthritis, or is it simply another extra-articular manifestation of the syndrome? Finally, the musculoskeletal manifestations of reactive arthritis are most common in the lower extremity and particularly in the heel. These sites represent areas of increased stress when compared with the upper extremity. A single study demonstrated microfractures in the vicinity of the entheses that were not seen in the comparison population of patients with rheumatoid arthritis.11 This trauma is also proinflammatory and may explain the lower limb predominance.

PREVALENCE AND EPIDEMIOLOGY The incidence of reactive arthritis follows the prevalence of HLA-B27 in the geographic region of study. The Scandinavian countries have a particularly high prevalence of HLA-B27 in the general population (10% to 16%) and a correspondingly high incidence of reactive arthritis (10 to 28 per 100,000).12,13 In Africa, where the SNSA syndromes are relatively unheard of, the prevalence of HLAB27 is also very low. The prevalence of HLA-B27 in general Western populations is approximately 8%. A study examining the prevalence in Rochester, Minnesota, between 1950 and 1980 found a prevalence of 3.5 per 100,000 in men younger than age 50.14 In individuals with reactive arthritis, the prevalence of HLA-B27 is nearly 50%. Numbers regarding the incidence and prevalence of reactive arthritis should be regarded as very loose approximations of their real values. Many of the studies reporting these data use different criteria for making the diagnosis of reactive arthritis. Strict criteria requiring the presence of an extra-articular manifestation will be very specific but not very sensitive. Those using more lax criteria, such as monoarthritis after any infection, will have improved sensitivity but low specificity. A factor that could result in a substantial underestimation of the true incidence of reactive arthritis is that mild self-limited cases may never be recognized or may never come to the attention of health care personnel. Overall, the disease is most common in those between 20 and 40 years old, with an overall slight male predominance that is attributed specifically to Chlamydia-associated reactive arthritis. Enteric infection–associated reactive arthritis, on the other hand, affects men and women with equal frequency. Reactive arthritis is rare in children, but when it occurs it is almost always due to a gastrointestinal infection.15,16

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Unlike adults in whom extra-articular manifestations often precede articular complaints, children usually express the articular complaints first. As in adults, the prevalence of HLA-B27 in children with reactive arthritis is likely near 50%, with reported prevalences ranging from near 0% to near 100%. The incidence of reactive arthritis in elderly individuals hospitalized for arthritis is reported to be between 3% and 16%.17 Reactive arthritis is thought to be rare in the elderly, but many of these patients have joint complaints related to osteoarthritis and other conditions, such as polymyalgia rheumatica, that may obscure the musculoskeletal findings in reactive arthritis. Among HIV-infected individuals, the incidence of reactive arthritis is at least 10 times greater than for an individual of the general population. In sub-Saharan Africa, the incidence of reactive arthritis among HIV-infected individuals is extremely high but quite low among individuals not infected. The prevalence of SNSA in Zambia is 180 per 100,000 in HIV-infected individuals but only 15 per 100,000 in HIV-negative individuals.18 At least one third of cases of SNSA are attributable to reactive arthritis. In one series, 94% of patients with reactive arthritis were HIV positive.19 A longitudinal cohort study examining rheumatic complications associated with HIV infection spanning the years 1989 to 2000 conducted at the Cleveland Clinic showed a dramatic drop in the incidence of reactive arthritis in HIV-infected individuals after the widespread use of highly active anti-retroviral therapy (HAART) (late 1995).20 Studies following patients prior to 1995 failed to show significant changes in HIV-associated rheumatic complications even after the introduction of one- and two-drug therapies.10 Among individuals presenting with acute anterior uveitis, approximately 10% have reactive arthritis. Among individuals with a spondyloarthropathy in the same sample, acute anterior uveitis was twice as common in individuals with ankylosing spondylitis.21

CLINICAL PRESENTATION Reactive arthritis represents a spectrum of disease after a gastrointestinal or urinary tract infection usually within 4 weeks. The predominant feature is an asymmetric lower limb–predominant oligoarthritis (four or fewer affected joints). The addition of extra-articular symptoms, including urethritis and conjunctivitis, represents more severe disease. The classic triad of symptoms of urethritis, conjunctivitis, and arthritis is only observed in up to 30% of patients. When extra-articular symptoms are present, they typically precede the arthritis. A number of diagnostic criteria exist for reactive arthritis, ranging from very specific to more general in nature. Specific criteria include the American College of Rheumatology criteria that require the presence of at least one extra-articular manifestation. More general criteria, such as the Third International Working Group on Reactive Arthritis criteria, require only onset of an asymmetric oligoarthritis within 4 weeks of a documented infection. Practically, confidence in a diagnosis of reactive arthritis hinges on identification of an associated pathogen or a typical constellation of symptoms.

The vast majority of enteric infections that precede reactive arthritis are caused by certain subspecies of Shigella, Salmonella, Yersinia, and Campylobacter. Chlamydia trachomatis causes almost all cases of urogenital tract infections preceding reactive arthritis. However, a triggering infection is only identified in up to 60% of cases. Evaluation of joint fluid or the synovium of an affected joint reveals no living organisms, but polymerase chain reaction assays often identify genetic material from the triggering organism. Because reactive arthritis is a member of the SNSA syndromes, serum rheumatoid factor and other antibodies found in association with the other rheumatic diseases are absent. Erythrocyte sedimentation rate, C-reactive protein, and levels of other acute-phase reactants are frequently elevated. Analysis of joint fluid reveals a predominant neutrophilia and no organisms on Gram stain.

Musculoskeletal Manifestations The musculoskeletal manifestations of reactive arthritis include enthesitis, peripheral arthritis, and sacroiliitis in an asymmetric lower limb–predominant pattern of distribution. Enthesitis is the most common manifestation, with the Achilles tendon and plantar aponeurosis insertions on the calcaneus most frequently involved. Heel pain is very common in patients with reactive arthritis. Dactylitis results from inflammation of the entheses, and the synovial linings of the tendons and joints of an entire digit. When associated with significant swelling, the result is the “sausage digit,” a characteristic but nonspecific feature of both reactive arthritis and psoriatic arthritis. Other sites associated with enthesitis in reactive arthritis include the iliac crests, ischial tuberosities, and the tibial tuberosities. Bursitis and enthesitis often occur simultaneously, particularly at the Achilles tendon insertion on the calcaneus. The peripheral arthritis of reactive arthritis is asymmetric and nonmigratory and preferentially affects the large joints of the lower extremity. The most frequently involved joints are the knee, ankle, and metatarsophalangeal joints. Manifestations include erythema, swelling, and joint effusion. Often, only a single joint is affected, but it is not unusual for several to be affected simultaneously. Polyarthritis is rare. When the upper extremity is affected, the most common affected joints are the elbow, wrist, and the finger joints. Several studies have reported different distributions of arthritic symptoms for nonChlamydia reactive arthritis and Chlamydia-associated reactive arthritis. The enteric form appears to affect the upper extremities more frequently than in the reactive arthritis triggered by Chlamydia.22 Chlamydia-associated reactive arthritis is also more likely to be monoarticular than non-Chlamydia reactive arthritis. Low back pain is a frequent symptom and due to spondylitis or sacroiliitis. Asymmetric sacroiliitis may present as low back and buttock pain. Owing to its asymmetric nature, this pain pattern may be confused for sciatica. Late in the disease process, the sacroiliitis may become symmetric. Rarely, erosive disease of the temporomandibular and manubriosternal joints can occur.

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Extra-articular Manifestations Extra-articular symptoms are signs of a systemic disease process and most commonly involves the eyes, urogenital system, and skin. Rarely, cardiac involvement is present. Extra-articular symptoms are more common in Chlamydia-associated reactive arthritis. Systemic complaints of fatigue, fever, and weight loss are not uncommon. Conjunctivitis is the most common ocular manifestation (30% to 60% of patients), followed by acute anterior uveitis (5%). When present, these ocular symptoms generally follow urethritis. The conjunctivitis is usually bilateral, whereas the uveitis is usually unilateral and if not treated may result in visual loss or blindness. The primary urogenital tract manifestation is urethritis. In men, prostatitis is common; and in women, localized inflammation of the reproductive tract, such as cervicitis, can be present. Cutaneous manifestations include keratoderma blennorrhagicum, circinate balanitis, and painless oral ulcers. Psoriatic skin and nail changes may be present in up to 15% of patients. Cardiac involvement is uncommon and can manifest as aortitis, valve abnormalities, myocarditis, or cardiac conduction abnormalities.

Natural History and Prognosis The disease is generally self-limited and lasts from 3 to 5 months. Information regarding long-term sequelae of reactive arthritis is predominantly due to study of patients with enteric-associated reactive arthritis. Approximately 50% of individuals will have persistent mild musculoskeletal complaints for years after the acute syndrome and up to 15% progress to ankylosing spondylitis. Radiologic evidence of sacroiliitis is seen in up to 30%. Reactive arthritis after urogenital infection is prone to recurrence, perhaps due to repeated infections.

PATHOLOGY Evaluation of the synovial fluid reveals macrophages containing entire phagocytized cells within their cytoplasm. The function of these cells appears to be to ingest apoptotic polymorphonuclear leukocytes to prevent them from spilling their proinflammatory contents into the synovial fluid. These cells are called Reiter cells but are not specific to reactive arthritis. Although more common in the SNSA syndromes, these cells have also been seen in the synovial fluid of patients with rheumatoid arthritis and crystal-induced arthritis.23 Histologic examination of synovial biopsy specimens in reactive arthritis reveals inflammatory changes that are nonspecific. Thickening of the synovial cell lining, inflammatory cell infiltration, and increased cellularity of the stroma are common findings. A macrophage-predominant infiltrate is present at the sites of enthesitis.9

IMAGING TECHNIQUES The diagnosis of reactive arthritis is primarily clinical. Imaging is used to evaluate for progression of disease, evaluate difficult cases, and guide therapeutic interventions.

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Radiography is the technique of choice in evaluating progression of disease. CT and MRI are used to evaluate patients early in the disease course when radiographs are normal. MRI and ultrasonography are used to evaluate the entheses. In the United States MRI is the preferred modality, whereas elsewhere in the world ultrasonography is the preferred modality, because it is less expensive. Image-guided intervention is predominantly performed using CT and ultrasonography, although MRI is gaining popularity as an image-guidance modality. Bone scintigraphy is sensitive but not as useful as MRI for evaluating extent of inflammatory changes. Standard techniques are used in the performance of all imaging studies with few exceptions. The imaging appearances of all manifestations of reactive arthritis are indistinguishable from those of psoriatic arthritis. The only difference is that reactive arthritis preferentially affects the lower limbs and psoriatic arthritis preferentially affects the upper limbs. As a significant proportion of patients, up to 15%, with reactive arthritis progress to ankylosing spondylitis, features of ankylosing spondylitis may also be seen.

MANIFESTATIONS OF THE DISEASE Spondylitis In the spine, reactive arthritis causes asymmetric, coarse and thick paravertebral ossifications called parasyndesmophytes or nonmarginal syndesmophytes. In contrast to ankylosing spondylitis, these paravertebral ossifications are nonmarginal and originate away from the vertebral body end plate. The syndesmophytes of ankylosing spondylitis are thin, are symmetric, and involve the fibers of the annulus fibrosus. The lower thoracic and upper lumbar spine are preferred sites of involvement. According to one study, uroarthritis is more likely to have spine manifestations than enteroarthritis.24 The primary differential diagnosis is diffuse idiopathic skeletal hyperostosis, which can result in asymmetric, thick nonmarginal flowing osteophytes. The parasyndesmophytes of reactive arthritis are indistinguishable from those seen in psoriatic arthritis. The finding of erosion at the peripheral attachment of the annulus fibrosus that subsequently heals resulting in bony sclerosis and, ultimately, remodeling that results in loss of the normal convexity of the anterior vertebral bodies is less likely to be seen in reactive arthritis than in ankylosing spondylitis.25 Diffuse idiopathic skeletal hyperostosis is not associated with erosive disease.

Radiography Radiographic evaluation of the spine in reactive arthritis consists of the standard anteroposterior and lateral views covering the region of interest. When radiographic changes are present, the asymmetric parasyndesmophytes are most common. Rarely, Romanus lesions (erosion at attachment site of the annulus fibrosus) and “shiny corners” (the resultant bony reaction to the erosion) may be seen. The Romanus lesion and the “shiny corner” are typical features of ankylosing spondylitis, however, and are rarely seen in reactive arthritis (Figs. 48-1 and 48-2).

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Magnetic Resonance Imaging Magnetic resonance imaging findings are nonspecific and illustrate end-plate changes, edema, and signal dropout in the ossified syndesmophytes. Before the appearance of radiographic changes, however, MRI may help to identify early enthesitis and erosive disease.

Multidetector Computed Tomography Computed tomography demonstrates similar findings as radiography but has greater sensitivity for early changes.

Nuclear Medicine Bone scintigraphy shows increased radiotracer accumulation at sites of bone deposition, but the appearance is nonspecific.

Classic Signs ■ ■

Asymmetric parasyndesmophytes: nonmarginal thick syndesmophytes Romanus lesion and “shiny corner”: more common in ankylosing spondylitis

■ FIGURE 48-1 Anteroposterior radiograph of the lumbar spine demonstrates isolated large nonmarginal syndesmophytes, one on either side of the spine.

Sacroiliitis

■ FIGURE 48-2 A close-up anteroposterior view of the lumbar spine reveals bilateral asymmetric parasyndesmophytes with bridging on the right at L1-L2.

■ FIGURE 48-3 Frontal view of the sacrum reveals sclerosis and joint space widening involving the left inferior sacroiliac joint compatible with sacroiliitis. (Courtesy of Dr. Johnny Monu, University of Rochester, Rochester, NY.)

The sacroiliac joint is a curved joint composed of an upper ligamentous portion and a lower synovial portion. The inflammatory changes of interest occur in the lower aspect of the joint. Like psoriatic arthritis, the sacroiliitis of reac-

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tive arthritis is asymmetric but usually bilateral. Very early in the disease process, the sacroiliitis may be unilateral. Over time, however, involvement of both sacroiliac joints may become symmetric. Ankylosis is a late finding.

Radiography The standard anteroposterior view of the sacrum is supplemented by a 15- to 25-degree cephalad view, the Ferguson view, which allows better visualization of the inferior sacroiliac joint. The progression of changes at the joint due to chronic inflammation begins with tiny erosions and periarticular sclerosis without joint space narrowing. Increased sclerosis on both sides of the joint follows and is associated with some widening of the joint. This process continues with increased production of bone that eventually crosses the joint, resulting in ankylosis (Figs. 48-3 to 48-5).

■ FIGURE 48-5 Asymmetric sacroiliitis, left greater than right. A, Anteroposterior view. B, A 45-degree right postero-oblique image. C, A 45-degree left postero-oblique image.

■ FIGURE 48-4 Close-up view of the sacroiliac joints reveals marked asymmetric sacroiliitis on the right characterized by irregular joint space widening and subchondral sclerosis. See Figure 48-7 for CT of the sacroiliac joints in the same patient.

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■ FIGURE 48-6 T2-weighted, fat-saturated axial (A) and coronal (B) MR images demonstrate increased signal intensity in the anterior aspect of the left sacroiliac joint, predominantly on the sacral side, compatible with sacroiliitis. (Courtesy of Dr. Johnny Monu, University of Rochester, Rochester, NY.)

Magnetic Resonance Imaging Magnetic resonance imaging is the most sensitive method for the detection of sacroiliitis due to its ability to identify cartilage abnormalities and associated bone marrow edema.26 The use of intravenous gadolinium contrast material can be helpful in identifying inflammation and after response to therapy (Fig. 48-6).

Multidetector Computed Tomography The ability to image the sacroiliac joint in thin axial sections using CT is useful for eliminating the extensive overlap of the anterior and posterior sides of the joint that limits plain radiographic analysis. In very early cases or cases in which there is a question of osteitis condensans ilii versus sacroiliitis, CT may show small erosions and sclerosis when plain radiographs are normal or indeterminate (Fig. 48-7).

Nuclear Medicine Bone scintigraphy is a sensitive technique for detecting sacroiliitis but is nonspecific and does not provide as much information as MRI.

Erosive Arthritis and Proliferative New Bone Formation The arthritis of reactive arthritis is characterized by marginal erosions, proliferative new bone formation, joint space narrowing, and joint effusions. In the acute phase, periarticular osteopenia is usually present. Ankylosis is a finding in advanced disease. The joints of the foot are particularly affected, and the specific aspects of the disease

at those locations are mentioned separately. In the digits, significant soft tissue swelling can be present.

Radiography Radiographic evaluation of the joints uses standard radiographic projections. Marginal erosions with fluffy periosteal reaction are classic, particularly in the digits. The erosions progress from the periphery of the joint toward the central subchondral bone. Proliferative periosteal reaction is particularly common in the small bones of the foot. Any joint of the lower extremity can be involved, usually in an asymmetric pattern. The bones and joints of the forefoot are frequently involved in reactive arthritis (Fig. 48-8). Among the joints in the forefoot, the first metatarsophalangeal joint is most commonly affected. Ankylosis may occur between bones in the foot but less frequently than seen in the hand in patients with psoriatic arthritis. The calcaneus is one of the most common sites of involvement with indistinct periosteal reaction on the inferior posterior surface leading to the formation of a plantar calcaneal spur with indistinct margins. A posterior superior calcaneal spur can also develop with similar characteristics. The most common manifestation of reactive arthritis in the knee is a joint effusion. When the upper extremities are affected, the pattern of involvement is identical to that seen in psoriatic arthritis (Fig. 48-9).

Magnetic Resonance Imaging The MRI findings are nonspecific and are related to generic signs of inflammation. These include bone mar-

■ FIGURE 48-7 A to C, Axial CT images at three levels of the lower sacroiliac joint demonstrate bilateral asymmetric (right greater than left) subchondral sclerosis, irregular joint space widening, and erosions.

■ FIGURE 48-8 Oblique radiographs of the feet reveal fluffy periosteal new bone with underlying erosions at the first metatarsophalangeal joint of the right foot. The left foot is unaffected. Incidental note is also made of medial dislocation of the left fifth metatarsophalangeal joint. (Courtesy of Dr. Don Flemming, Penn State University, Hershey, PA.)

■ FIGURE 48-9 Posteroanterior radiograph of the left hand reveals fluffy periosteal new bone and erosive disease involving the entire carpus and the first carpometacarpal joint.

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■ FIGURE 48-10 A and B, Lateral radiographs of the calcaneus and midfoot in two patients reveal plantar and superior calcaneal spurs with an indistinct quality typical of the enthesopathic changes seen in reactive arthritis. Note the large enthesophyte involving the attachment site of the peroneus brevis tendon on the base of the fifth metacarpal.

row edema, joint fluid, and thickened soft tissue structures. Irregularities in marginal bone can be appreciated but are poorly resolved on MRI.

Multidetector Computed Tomography Computed tomography is more sensitive than radiography for subtle erosions and periosteal reaction, primarily owing to its ability to eliminate overlapping structures. MRI, however, is more sensitive for inflammatory changes.

Ultrasonography Ultrasonography does not have a role in the imaging of erosions and the proliferative new bone. However, it can detect the surrounding tissue edema and the presence of a joint effusion.

Nuclear Medicine Bone scintigraphy with a bone-seeking agent can identify areas of bone turnover and therefore can be used to identify extent of disease, particularly in new cases.

Enthesitis Enthesitis is one of the most frequent manifestations of reactive arthritis and is a feature of the SNSA syndromes as a whole. In reactive arthritis, any of the entheseal insertions on the foot may be involved. The most commonly affected sites are the Achilles tendon and plantar aponeurosis insertions on the posterior calcaneus. Retrocalcaneal bursitis is also frequently present. MRI and ultrasonography are the imaging modalities of choice for evaluating the entheses. Enthesitis is associated with proliferative new bone formation. Therefore, radiography can detect long-term changes via calcium deposition and soft tissue swelling, but these are nonspecific.

Radiography Radiographic findings in enthesitis are nonspecific. Tiny erosions and new bone formation may be seen. The inflammatory context, however, is not visualized. The presence of erosions can help to distinguish the enthesopathic changes of the SNSA syndromes from diffuse idiopathic skeletal hyperostosis (Fig. 48-10).

Magnetic Resonance Imaging Evaluation of the enthesis is performed using T1-weighted, T2-weighted, and short tau inversion recovery (STIR) sequences. Findings include increased signal intensity on T2-weighted imaging, increased tendon thickness, and neighboring bone edema. In long-standing enthesitis, fatty infiltration is represented by intermediate-level signal on T1-weighted images. For retrocalcaneal bursitis, MRI shows increased Achilles tendon thickness and fluid within the bursa. MRI is twice as sensitive for bursitis as ultrasonography.

Ultrasonography Findings on ultrasound examination of enthesitis include thickening and loss of the uniform, linear echo pattern of the involved tendon. The tendon margins may become indistinct. Hyperechoic intratendinous foci may represent fatty infiltration. Microcalcifications can also be seen. One recent study suggests that ultrasonography is better able to detect early enthesitis than MRI.27 Ultrasonography is also useful for the detection of subclinical enthesitis.28 For retrocalcaneal bursitis, ultrasonography shows increased Achilles tendon thickness and fluid within the bursa. However, ultrasonography is much less sensitive than MRI for bursitis at this location.

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Dactylitis Inflammation of an entire digit is termed dactylitis and can be due to any number of causes. When associated with significant soft tissue swelling, the result is a “sausage digit.” Recent investigations into dactylitis secondary to the spondyloarthropathies reveal that this form of dactylitis is due to flexor tendon synovitis with marked adjacent soft tissue swelling.29 Synovitis of the finger joints, however, is present in only up to 62% of cases. Depending on the digit involved, inflammation can extend to associated palmar bursae. Imaging of dactylitis is primarily with MRI but it is seen on plain radiographs of the hands and feet when evidence of erosive arthritis is sought.

Radiography Radiographic evaluation in dactylitis reveals only soft tissue swelling.

Magnetic Resonance Imaging MRI demonstrates fluid in the flexor tendon sheaths of the affected digits. Surrounding soft tissue edema may also be seen. MRI is better than ultrasonography in detecting fluid in potentially involved joint capsules.

Ultrasonography Ultrasonography demonstrates fluid within the flexor tendon sheaths as well as thickening of the surrounding tissues. It can show fluid within the joints but not as well as MRI.

DIFFERENTIAL DIAGNOSIS The primary differential diagnostic considerations include other postinfectious arthropathies and the other SNSA syndromes. Exclusion of a septic joint is the essential first step. Several particular postinfectious entities deserve special mention. These are poststreptococcal reactive arthritis, Poncet’s disease, and the HIV-related arthropathies. Poststreptococcal reactive arthritis is an acute sterile arthritis at a remote site associated with a positive throat culture or positive antistreptococcal antibody titers. The patient cannot satisfy the Jones criteria for acute rheumatic fever. Like reactive arthritis, the condition primarily affects the lower limbs and can be associated with an enthesitis. With the exception of uveitis, extra-articular symptoms typical for reactive arthritis have not yet been reported in association with this syndrome. Rash, vasculitis, and glomerulonephritis can occur in this and other poststreptococcal syndromes.

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Poncet’s disease is an aseptic arthritis that is associated with an active pulmonary tuberculosis. The knees, ankles, and elbows are preferred sites of involvement. Symptoms resolve after adequate treatment for tuberculosis. HIV infection is associated with many conditions that lead to arthritic pain. HIV-associated arthropathy and painful articular syndrome are examples. Hypertrophic osteoarthropathy preferentially affects the lower limbs and can present as arthralgias. The prevalence of other rheumatic diseases is higher in those infected with HIV, which also need to be considered in the differential diagnosis. Additional entities to be considered include Lyme disease, Whipple’s disease, and syphilis. The primary differential diagnosis for the imaging findings is the other SNSA syndromes, owing to the considerable overlap in manifestations.

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment Treatment of reactive arthritis is supportive using nonsteroidal anti-inflammatory drugs and corticosteroids as needed for pain control. Intra-articular injections of corticosteroids can be used to control particularly severe localized pain. If the patient demonstrates progressive radiographic changes, treatment is similar to that of psoriatic arthritis, including the use of TNF-α inhibitors such as infliximab and etanercept. Antibiotics play no role in the control or prevention of reactive arthritis with the possible exception of Chlamydia-associated reactive arthritis. In a single study, a course of lymecycline was shown to shorten the symptomatic period in patients with Chlamydia-associated reactive arthritis but not enteric-associated reactive arthritis.30

What the Referring Physician Needs to Know ■

■ ■ ■

Aside from the asymmetric lower limb–predominant distribution, the imaging findings in reactive arthritis are common to the other spondyloarthropathies and particularly overlap with psoriatic arthritis. If it is important to document early sacroiliitis, MRI and CT may be useful. Radiographs of the spine, sacroiliac joints, and other affected joints are used to evaluate disease progression. Other inflammatory arthritides, including septic arthritis, should be excluded before considering a diagnosis of reactive arthritis.

SUGGESTED READINGS Carter JD. Reactive arthritis: defined etiologies, emerging pathophysiology, and unresolved treatment. Infect Dis Clin North Am 2006; 20:827–847.

Petersel DL, Sigal LH. Reactive arthritis. Infect Dis Clin North Am 2005; 19:863–883.

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REFERENCES 1. Leirisalo-Repo M. Reactive arthritis. Scand J Rheumatol 2005; 34:251–259. 2. Ahvonen P, Sievers K, Aho K. Arthritis associated with Yersinia enterocolitica infection. Scand J Infect Dis 1971; 3:37–40. 3. Panush RS, Wallace DJ, Dorff EN, Englemann EP. Retraction of the suggestion to use the term “Reiter’s syndrome” sixty-five years later: the legacy of Reiter, a war criminal, should not be eponymic honor but rather condemnation. Arthritis Rheum 2007; 56:693–694. 4. Lu DW, Katz KA. Declining use of the eponym “Reiter’s syndrome” in the medical literature, 1998–2003. J Am Acad Dermatol 2005; 53:720–723. 5. Tinazzi E, Ficarra V, Simeoni S, et al. Reactive arthritis following BCG immunotherapy for bladder carcinoma. Clin Rheumatol 2005; 24:425–427. 6. Zeidler H, Kuipers J, Kohler L. Chlamydia-induced arthritis. Curr Opin Rheumatol 2004; 16:380–392. 7. Kim T, Uhm W, Inman RD. Pathogenesis of ankylosing spondylitis and reactive arthritis. Curr Opin Rheumatol 2005; 17:400–405. 8. Vahamiko S, Penttinen MA, Granfors K. Aetiology and pathogenesis of reactive arthritis: role of non-antigen-presenting effects of HLA-B27. Arthritis Res Ther 2005; 7:136–141. 9. McGonagle D, Marzo-Ortega H, O’Connor P, et al. Histological assessment of the early enthesitis lesion in spondyloarthropathy. Ann Rheum Dis 2002; 61:534–537. 10. Mielants H, De Vos M, Cuvelier C, Veys EM. The role of gut inflammation in the pathogenesis of the spondyloarthropathies. Acta Clin Belg 1996; 51:340–349. 11. McGonagle D, Reade S, Marzo-Ortega H, et al. Human immunodeficiency virus associated spondyloarthropathy: pathogenic insights based on imaging findings and response to highly active antiretroviral treatment. Ann Rheum Dis 2001; 60:696–698. 12. Soderlin MK, Borjesson O, Kautiainen J, et al. Annual incidence of inflammatory joint diseases in a population based study in southern Sweden. Ann Rheum Dis 2002; 61:911–915. 13. Sieper J, Rudwaleit M, Khan MA, Braun J. Concepts and epidemiology of spondyloarthritis. Best Pract Res Clin Rheumatol 2006; 20:401–417. 14. Michet CJ, Machado EB, Ballard DJ, McKenna CH. Epidemiology of Reiter’s syndrome in Rochester, Minnesota: 1950–1980. Arthritis Rheum 1988; 31:428–431. 15. Zivony D, Nocton J, Wortmann D, Esterly N. Juvenile Reiter’s syndrome: a report of four cases. J Am Acad Dermatol 1998; 38:32–37. 16. Liao C, Huang J, Yeh K. Juvenile Reiter’s syndrome: a case report. J Microbiol Immunol Infect 2004; 37:379–381.

17. Toussirot E, Wendling D. Late-onset ankylosing spondylitis and related spondyloarthropathies: clinical and radiological characteristics and pharmacological treatment options. Drugs Aging 2005; 22:451–469. 18. Njobvu P, McGill P, Kerr H, et al. Spondyloarthropathy and human immunodeficiency virus infection in Zambia. J Rheumatol 1998; 25:1553–1559. 19. Mijiyawa M, Oniankitan O, Khan MA. Spondyloarthropathies in sub-Saharan Africa. Curr Opin Rheumatol 2000; 12:281–286. 20. Calabrese LH, Kirchner E, Shrestha R. Rheumatic complications of human immunodeficiency virus infection in the era of highly active antiretroviral therapy: emergence of a new syndrome of immune reconstitution and changing patterns of disease. Semin Arthritis Rheum 2005; 35:166–174. 21. Linder R, Hoffman A, Brunner R. Prevalence of the spondyloarthropathies in patients with uveitis. J Rheumatol 2004; 31:2226–2229. 22. Ozgul A, Dede I, Taskaynatan MA, et al. Clinical presentations of chlamydial and non-chlamydial reactive arthritis. Rheumatol Int 2006; 26:879–885. 23. Selvi E, Manganelli S, De Stefano R, et al. CD36 and CD14 immunoreactivity of Reiter cells in inflammatory synovial fluids. Ann Rheum Dis 2000; 59:399–400. 24. Mannoja A, Pekkola J, Hamalainen M, et al. Lumbosacral radiographic signs in patients with previous enteroarthritis or uroarthritis. Ann Rheum Dis 2005; 64:936–939. 25. Helliwell PS, Hickling P, Wright V. Do the radiological changes of classic ankylosing spondylitis differ from the changes found in the spondylitis associated with inflammatory bowel disease, psoriasis, and reactive arthritis? Ann Rheum Dis 1998; 57:135–140. 26. Inanc N, Atagunduz P, Sen F, et al. The investigation of sacroiliitis with different imaging techniques in spondyloarthropathies. Rheumatol Int 2005; 25:591–594. 27. Kamel M, Eid H, Mansour R. Ultrasound detection of heel enthesitis: a comparison with magnetic resonance imaging. J Rheumatol 2003; 30:774–778. 28. Borman P, Koparal S, Babaoglu S, et al. Ultrasound detection of entheseal insertions in the foot of patients with spondyloarthropathy. Clin Rheumatol 2006; 25:373–377. 29. Olivieri I, Scarano E, Padula A, et al. Dactylitis, a term for different digit disease. Scand J Rheumatol 2006; 35:333–340. 30. Laasila K, Laasonen L, Leirisalo-Repo M. Antibiotic treatment and long term prognosis of reactive arthritis. Ann Rheum Dis 2003; 62:655–658.

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Ankylosing Spondylitis Corinna Schorn and Gerwin Lingg

ETIOLOGY Ankylosing spondylitis (AS) is the prototype of the seronegative spondyloarthropathies, a moderately heterogeneous group of distinct entities composed of AS, psoriatic spondyloarthropathy, reactive spondyloarthropathy (Reiter’s disease), enteropathic spondyloarthropathy in Crohn’s disease and ulcerative colitis, and so-called undifferentiated spondyloarthropathy.1 As such, it shares several characteristics with the latter diseases: the genetic background (HLA-B27), the promotion by genitourinary or gastrointestinal bacterial infection and its subsequent or persistent immunologic response, the typical sites of inflammatory involvement, and the peri-inflammatory and postinflammatory osseous proliferation.2,3 However, there are some manifestations virtually unique to this disease.4 The exact etiology remains unclear, even though the role of some autoimmunologic effector mechanisms has been illuminated in recent years. Animal model studies as well as human studies address the humoral and cellular immunity to certain proteoglycans found in cartilage, fibrocartilaginous entheses, and intervertebral discs (aggrecan and versican). This immunity promotes the typical lesions found in AS.5–7 The pathophysiologic role of HLA B27 remains to be defined. This molecule is involved in the antigen-presenting process of T cell–mediated defense. It is currently hypothesized that cytotoxic T-cell autoreactivity is induced as a cross reactivity to bacteria-derived peptides or by mispresentation of arthritogenic self-peptides derived from cartilage. Several other less studied hypotheses exist.

PREVALENCE AND EPIDEMIOLOGY The annual incidence of AS in the white population in the United States is approximately 6.6/100,000, with a prevalence of 0.1 (2%).8 The male predominance is not as pronounced as classically suggested and is now accepted to be 2 to 5:1.9 In some cases, the racial and ethnic variance is

considerable. Specifically, AS rarely affects blacks and has a higher-than-average prevalence in Native Americans. Unlike epidemiologic data about the prevalence of AS, data concerning HLA-B27 positivity are widely available for multiple ethnic groups. For example, 4% to 13% of Eurocaucasians are HLA-B27 positive, as are 20% to 40% of Native Americans and less than 1% of Japanese. For African blacks, HLA-B27 positivity is extremely rare.10 The prevalence of HLA-B27 in a population has a significant impact on the occurrence of AS. Nevertheless, HLA-B27–negative individuals may develop typical AS. The proportion of cases that are HLA-B27 negative is higher in populations with low HLA-B27 positivity. For Eurocaucasians, 90% to 95% of AS patients are HLA-B27 positive. Thus, HLA-B27 positivity can be considered as a risk factor for development of sacroiliitis and progression to AS.11 However, HLA-B27 positivity is not the only genetic basis of disease predisposition, contributing 20% to 30% of the risk, and it is not a self-sufficient diagnostic criterion.12 Certain subtypes of HLA-B27 may be only weakly disease associated, and additional HLA loci and non-HLA loci contribute, as do environmental factors. The peak incidence of AS is in early adulthood or adolescence (mean 25 years). Disease onset after the age of 45 is rare. In 15% of AS patients, arthritis and enthesitis are present from childhood, with some delay of the vertebral symptoms.

KEY POINTS Diagnose sacroiliitis early and accurately with MRI or CT. Basic documentation should include radiographic images of the lumbar spine. ■ Radiologic follow-up should be used sparingly. ■ Consider osteoporosis and perform DEXA or QCT. ■ Consider Andersson lesion type B in patients with considerable pain after minor trauma. ■ ■

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CLINICAL PRESENTATION The key symptom of ankylosing spondylitis is inflammatory back pain. This pain is characterized mainly by late night or early morning attacks of low back pain; it is associated with morning stiffness, which improves with exercise, in a patient younger than the age of 40.13 Onset of the relapsing attacks is insidious; periods of pain last for more than 3 months. Approximately 30% to 65% of patients with inflammatory back pain have sacroiliitis.14,15 Buttock pain may alternate sides. All these categories of pain respond to NSAIDs. Further in its course, the inflammatory process migrates up the vertebral column with some predilection for the thoracolumbar and cervical segments, leaving behind new bone formation and ankylosis and causing deteriorated posture. In late stages, thoracic and thoracolumbar deformity with severe kyphosis may severely handicap patients. The stiffness of the cervical spine hampers head turning, so that activities of daily living such as driving become difficult. Apart from the vertebral complaints of pain and stiffness, symmetric or asymmetric synovitis/arthritis, mainly of the lower extremity or the proximal joints, may be present. Hips, shoulders, and knees are the most common locations affected by arthralgia and arthritis in AS. Pain, swelling, and tenderness in the ankles and feet may occur at the plantar aspect, or more often at the distal Achilles tendon insertion, as a result of retrocalcaneal bursitis or enthesitis. A characteristic extraskeletal symptom of AS is anterior uveitis.16–18 In fact, the most frequent diagnosis in patients with anterior uveitis is AS.19 In addition, patients often complain of fatigue. Physical examination reveals tenderness at the sacroiliac joints (Mennell’s sign).20 Motion restriction of the vertebral column, as well as restricted chest expansion, occurs mainly as a result of the ankylosing condition but sometimes precedes actual bony ankylosis.21–23 Flexion deformity of the hip joints occurs frequently, and in its early stage it is only appreciated with special tests, such as patientsupine, maximal flexion of the contralateral hip, in order to balance the compensatory hyperlordosis. In fixed-flexion deformity, the knee and hip of the affected side will involuntarily remain flexed as well.

LABORATORY FINDINGS Elevated levels of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are seen but are nonspecific signs of inflammation. As stated, HLA-B27 is usually positive. However, a positive result does not indicate the presence of sacroiliitis and a negative result is not an exclusion criterion (see Prevalence earlier).

DIAGNOSIS The modified New York Classification criteria for AS demand, in addition to radiographically proven sacroiliitis, at least one clinical manifestation of inflammatory back pain, vertebral motion restriction, and/or respiratory motion restriction. Average diagnostic delay is 5 to 9 years

and is, in part, a result of the low sensitivity of radiographic imaging for early arthritis. There have been proposals for early clinical diagnosis, and the diagnosis of “undifferentiated spondyloarthropathy” has been introduced as a new subgroup in 1991, covering, in part, patients with subsequent development of AS.1,24–26 New diagnostic approaches employ MRI, which provides high enough sensitivity to detect inflammatory changes.

PATHOPHYSIOLOGY Anatomy The junction of the sacrum with the iliac bone can be divided into two compartments. At the ventral portion there is a synovial joint with asymmetric cartilage lining. The diagnostic clues for sacroiliitis are located in this synovial portion. Posteriorly, there is a tight ligamentous junction containing the ligamenta sacroiliaca interossea dorsalia. This is referred to as the retroarticular space. The ligamentous attachments of the retroarticular space may be affected by degeneration or inflammatory disease. The joint space of the synovial portion of the sacroiliac joint is oriented in varying angles. Consequently, on an anteroposterior view, the joint space is only partially visible, such that the laterally projected contours of the joint margins correspond to the ventral aspect and the medially visible parts correspond to the dorsal aspect of the joint space, respectively. The joint facets are C shaped and in opposition to the C shape of the os sacrum. On cross-sectional images (CT as well as MRI), in paracoronal angulation, this may result in a display of joint space ventrally and dorsally and of retroarticular space in between for one or two dorsally located images. A considerable amount of variation exists: 1. Segmental variants can occur with unilateral or bilateral accessory articulation of large transverse processes of the lowest lumbar vertebra with the sacral ala (hemilumbarization, hemisacralization, incomplete sacralization of L5, or incomplete lumbarization of S1). These accessory articulations are prone to premature degenerative disease and may be a reason for onset of low back pain in early and middle adulthood. 2. Some patients show a sulcus or even a canal at the dorsal surface of the posterior process of the iliac bone in close vicinity to the joint margin. On CT or MRI, this sulcus or canal will appear as a small groove and should not be confused with an erosion. To confirm diagnosis, this irregularity can be followed on multiple images. 3. The form of the joint facet itself is highly variable, with flat, curved, and wavy surfaces.

Pathology Early features of sacroiliitis are synovitis and subchondral bone marrow inflammation. Synovitis in MRI is characterized by thickening and contrast enhancement in the synovial and capsular structures, reflecting these structures’ hyperemia and vascular permeability. This feature is, however, not very conspicuous, because in the

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sacroiliac joint the capsule is tight and marginally attached, and therefore in tomographic techniques the capsule appears as merely a tiny dot-like structure at the joint margin. Subchondral bone marrow inflammation—osteitis—in AS is highlighted in short tau inversion recovery (STIR) or spectral presaturation inversion recovery (SPIR) MR images and is described as “bone marrow edema”; rather, it is granulation tissue, or infiltration by inflammatory cells, and/or hyperemia. Contrast material uptake in the corresponding area is typical. On CT, neither synovitis nor early osteitis is visible. Later osteitis leads to sclerosis and is then visible on both CT and radiography. The sclerosis is cloudy and ill defined. With further disease progression, the subchondral granulation tissue erodes through the joint cartilage into the joint space, penetrating the calcified zone of the cartilage and producing central erosions. On MRI, erosions appear as contrast-enhancing defects in the subchondral bone. Intra-articular granulation tissue is the reason for contrast enhancement in the joint space itself. The erosion process progresses to widespread destruction of the subchondral bone and cartilage. Bony erosions are easily visible in CT. On radiography, early erosions are inconspicuous due to superimposition. Blurring of the joint margins may be the only sign of early erosions. Later, discrete erosions become visible with loss of the subchondral white line and an appearance of a widened joint space. Irregular endochondral ossification and subsequent replacement of subchondral bone and calcified cartilage by new bone leads to intra-articular ankylosis. CT is the best imaging tool for visualization of osseous bridging and intra-articular ankylosis. In late stages of complete or partial ankylosis, the inflammatory signs completely fade away, leaving behind normal lamellar bone that will eventually replace parts of the joint space. Therefore, in late stages, no contrast enhancement or bone marrow edema is found on MRI. On radiographs the sclerosis, which is a sign of periarticular osteitis, disappears. In contrast to the intra-articular erosive and ankylosing arthritis of AS, osseous bridging of capsuloligamentous structures at the margin of the synovial sacroiliac joint (capsular ankylosis) is very common in elderly individuals. These ossifications are best visualized on CT, which clearly demonstrates the osseous encapsulation of an otherwise normal joint. On radiographs, superimposition effects lead to a faint sclerosis at the upper sacroiliac joint. This capsular ankylosis should not be mistaken for inflammatory disease. In addition to affecting the synovial part of the sacroiliac junction, AS may cause enthesitis of the ligamenta sacroiliaca interossea in the retroarticular space. Pathology of ligamentous attachments may occur in degenerative disease as well; this is referred to as fibro-ostosis. In radiographic imaging, both degenerative and inflammatory enthesitis in the retroarticular space are occult, due to superimposition. In the synovial sacroiliac joints as well as in the hip joints, enthesitis does not appear to be prominent at any stage.27 The hallmark of AS, as well as its pathologic feature in many other locations is enthesitis.28 It begins with an erosive phase, followed by a defective healing, with new

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bone formation resulting in a bony irregular prominence. The inflammatory hyperemia leads to hyperintensity on STIR images and contrast enhancement. The described bony irregular prominence forms a new enthesis, which corresponds to a radiographically visible spur.29 As the inflammatory process relapses, the bony outgrowth can finally bridge, resulting in a capsular bony ankylosis, for example, at an apophyseal joint. At the intervertebral discs, the annulus fibrosus is affected by this type of bone-producing inflammation. The bony prominence corresponds to the well-known syndesmophyte. The final stage is a circularly ossified annulus fibrosus providing an osseous casing for the disc. When it is present at multiple levels it is referred to as a “bamboo spine.” Additional or isolated central transdiscal ossification occurs as a result of either lack of motion or subsequent to the inflammatory process. Typical enthesitis may take place in various locations: in joint capsules and intracapsular ligaments of large synovial joints, in the ligamentous structures of a synchondrosis (cartilaginous joints like symphysis, manubriosternal joint, intervertebral discs), and in overall ligamentous attachments.

BIOMECHANICS The vertebral column provides both firm support for the body and considerable mobility for bending and torsion. These diametrically opposed tasks are achieved through the vertebral column’s construction as a chain of small, joined elements. The junctions of the vertebrae regulate movement. The apophyseal joints are positioned symmetrically dorsal to the vertebral bodies. Because their facets are obliquely oriented, the apophyseal joints of both sides work together to provide hinge-like movements for ventral or lateral flexion/extension and sliding movement for axial torsion. The extent, limitation, and direction of movements are determined mostly by the angle between the joint spaces of the bilateral joints. Ventrally, the annulus fibrosus attaches the adjacent vertebrae tightly, limiting the movement of the vertebrae, and encasing the nucleus pulposus. The latter functions like an elastic ball that distributes compressive forces (e.g., of weight bearing and bending) equally over the entire vertebral end plate. The microarchitecture of a vertebral body, with its dense three-dimensional trabeculation of cancellous bone, adapts perfectly to weight bearing in different postures, such as inclining, reclining, axial torsion, and lateral flexion. In an immobile ankylosed spine, the weight bearing takes place in static segments. The nucleus pulposus no longer distributes the forces to the end plate nor from there to the cancellous bone. Instead, the cortical shell of the vertebrae, the syndesmophytic bridges, and the ossified columns of the apophyseal joints transmit the weight along the axial skeleton. Bone is a living tissue, and its structure is remodeled due to mechanical requirements. Vertical load application in an immobile body segment is best adapted with cortical long bones. Thus, the structural remodeling of the primarily inflammatory ankylosed spine bears some resemblance to a long bone: the cancellous bone is eliminated

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and replaced by a fat-containing marrow canal. The cortical shell is reinforced and broadened. The end plates are partially reabsorbed, completing the bamboo-like appearance. Because the typical vertebral microstructure is completely rearranged in the bamboo spine, the aspect of vertebral fractures, either due to trauma or in osteoporosis, differs from those in normal individuals. Specifically, the “bamboo spine” is infrequently affected by compression/ wedge-shaped fractures but is relatively prone to slice and Chance fractures. A marked thoracolumbar kyphosis is a point of decreased mechanic stability and, together with osteoporosis, it is a risk factor for transvertebral or transdiscal fractures. In an ankylosed spine, posture deterioration and stiffness attract the physician’s attention and cause a great deal of discomfort to the patient. The thoracolumbar kyphosis in long-standing disease forces the patient to compensate by hyperextending the cervical spine (with consequent muscular pain) to provide forward vision. In addition, the shock-absorbing quality that is provided by the physiologic double S-form of the mobile vertebral column is lost; therefore, running, jumping, or skipping may produce discomfort.

IMAGING TECHNIQUES Techniques and Relevant Aspects The first-line method remains radiographic imaging despite its known low sensitivity for early arthritis.30,31 There is no radiographic projection that provides a purely tangential view of the joint space, because of the curved shape of the joint facets. On anteroposterior views, only relatively short and individually different segments of the joint contours are outlined. In clinical practice, in back pain patients with suspected AS, anteroposterior and lateral views of the lumbar spine should be taken. The anteroposterior view must include the sacroiliac joints and their surroundings. Only in severe lumbosacral hyperlordosis may an additional Barsony (Ferguson) view be necessary. Tomographic techniques such as MRI and CT show the complicated anatomy of the sacroiliac joint and are able to close the diagnostic gap between symptom onset and objective changes. CT images should be acquired primarily in paracoronal orientation, which is facilitated with the patient prone, and requires breath-hold technique. Three-millimeter slices using a helical scan with a pitch of approximately 1.5, 140 kVp, and 250 mAs are recommended. Obese patients may require a higher dose (mAs) to prevent a low signal-to-noise ratio. Multidetector CT provides a more comfortable examination in supine position, with slice thicknesses of 1 to 2.5 mm and multiplanar reformatted imaging in a paracoronal angulation. Sacroiliac STIR or T2*- and T1-weighted MR images should be acquired in paracoronal (paratransversal) orientation tilted in plane with the sacrum and with long repetition time/echo time images in an oblique transverse plane perpendicular to the paracoronal images. For optimal visualization of the pathology, contrast-enhanced images are recommended, either with high-resolution technique

and fat saturation or as a dynamic examination with a time resolution of 1 to 2 minutes to assess the activity of the inflammatory process.32

Pros and Cons Radiography is known to be insensitive in early sacroiliitis. However, it is inexpensive, reliable, and quick; it provides the diagnosis in typical cases and gives additional information about lumbar inflammatory manifestations. Thus, radiographic imaging provides an advantageous overview of the disease spread and is useful to confirm or exclude other causes of back pain. Bone scintigraphy is very sensitive to any osteoblastic process, but it lacks the specificity to fulfill the requirements for a powerful diagnostic tool in the diagnosis of sacroiliitis. MRI uniquely combines a high degree of anatomic information and visualization of inflammatory activity. It is the best imaging tool for early diagnosis especially in young patients. CT shows equally high anatomic resolution and provides even better information about bony erosions and osseous bridges. It seems to be advantageous in middle-aged patients with marked sclerosis and for the differential diagnosis of diffuse idiopathic skeletal hyperostosis (DISH). Because arthritis is only detected when bony erosions or bridges are present, the sensitivity of CT for early diagnosis is inferior to that of MRI.

Controversies Computed tomography of the sacroiliac joints is not an established procedure in all rheumatologic centers. Because of its superior sensitivity, MRI is most commonly preferred. Whether CT can serve as a powerful tool depends on the patient population; for example, it can be helpful in examining patients of middle or higher age with long-standing back pain. In these patients, the arthritis is usually advanced, producing unmistakable bony changes. Studies of contrast uptake over time have been proposed to differentiate simple reactive bone marrow edema from osteitis. Reactive edema, due to causes such as degenerative disease or asymmetric weight bearing, is characterized by lower peak enhancement and slower uptake. Dynamic sequences are often optimized for speed rather than resolution; subsequent imaging of the joint with high resolution and fat saturation allows for better morphologic evaluation of the inflammatory features of the entire joint.

MANIFESTATIONS OF THE DISEASE Sacroiliitis The imperative diagnostic clue for AS is the radiographic proof of sacroiliitis (i.e., grade II bilaterally or grade III unilaterally). Radiologic grading is as follows33,34: 0: Without abnormality 1: With suspicious findings 2: With minor abnormalities 3: With definite abnormalities 4: With ankylosis

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Radiography

Sclerosis

Sacroiliitis is characterized by a triad of erosion, sclerosis, and the bony bridges that mark the beginning of ankylosis.35 These three findings should be visible at the same time.

Rheumatic sacroiliitis is associated with various degrees of sclerosis. Typically it involves not only the caudad but also the middle portion of the joint. It is broad and woolly and more pronounced in the iliac bone (see Fig. 49-1A and B). Differential diagnosis of sacroiliac sclerosis comprises:

Erosions The first aspect of sacroiliitis is a certain obscuration of the joint outlines, which is actually only in part due to erosion and in part due to bony bridging. Radiographically definite erosions mainly become visible as dentate illdefined contours in the caudad portion of the joint. If the erosive component is prominent, a “string of pearls” appearance with pseudo-widening of the joint space may result (Fig. 49-1A and B). Differential diagnosis of sacroiliac joint erosions comprises: ● ● ●

Hyperparathyroidism in which sclerosis is not present Bacterial infection that is mostly unilateral and does not fulfill the triad (In cases of indistinct contours) the normal unfused physis in adolescence

■ FIGURE 49-1 Sacroiliitis is the hallmark of ankylosing spondylitis. The triad of sclerosis, erosion, and bony bridges is diagnostic. Early arthritis is often not very conspicuous on radiography. A, Asymmetric sclerosis and indistinct joint margins. B, Pseudodilatation and “string of pearls” erosions are typical. C, Late-stage sacroiliitis is characterized by complete ankylosis. The sclerosis fades away and normal bone replaces the entire joint. The ventral capsular insertion may be seen as a sclerotic triangle, which is known as the star sign.

●

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Osteitis condensans ilii, associated with childbirth, which is typically triangular in configuration, relatively well delineated, and often bilateral36 Anterior capsular ossification in DISH, which produces a sclerosis in the cranial third of the joint

Bony Bridges and Ankylosis Radiographs do not show individual bony bridges. Early bony bridging leads to blurring of the joint outlines and may be relatively difficult to detect, because only various parts of the joint space are visible even in normal individuals. Progressive partial ankylosis is detected easily in follow-up studies. Even if no previous examinations are available for comparison, partial ankylosis can be suspected when only minor parts of the joint contours

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are detected. Ankylosis is present when no joint space is visible (see Fig. 49-1C). In long-standing ankylosis, the sclerotic bone reaction fades away and normally structured bone replaces the joint.

Magnetic Resonance Imaging The occurrence of STIR/T2-weighted hyperintense and T1-weighted hypointense zones in the marrow surrounding the sacroiliac joint, the so-called bone marrow edema, is a nonspecific sign in that it is associated with fracture, traumatic joint disruption, asymmetric weight bearing, degenerative disease, tumor, or inflammation. MRI is so sensitive to this process in AS, and the finding persists for so long after the inciting event, that it is not suitable for the estimation of disease activity. Nevertheless, it is one feature of sacroiliitis and adjacent osteitis and appears often as an indistinct rim around a center of para-articular sclerosis (Fig. 49-2). On MRI, sclerosis appears as hypointensity on T2weighted and T1-weighted images. It begins at the iliac side and may later affect the sacrum. The joint margins grow indistinct with increasing sclerosis. Bone marrow edema may be masked by extensive sclerosis. Sclerosis is a marker of chronicity and can be detected in degenerative disease as well.32

■ FIGURE 49-2 MRI findings in sacroiliitis. Para-articular bone marrow edema in the left posterior iliac process (A, paracoronal STIR image), intra-articular fluid signal, erosions (C, small arrowhead, paracoronal contrast-enhanced T1-weighted, spin-echo, fat-saturated image), bony bridges, and capsular enhancement (C, large arrowhead) are typical for sacroiliitis. Fat accumulation (■) and sclerosis are signs of chronic disease and best visualized in short repetition time/echo time pulse sequences (B, T1-weighted turbo spin-echo image).

In chronic joint affliction, patchy areas of para-articular fat accumulation can be detected para-articularly in the sacrum and ilium (see Fig. 49-2). In sacroiliitis, paraarticular fat accumulation is not as pronounced as after irradiation and it is more focal than in long-term corticosteroid medication. Para-articular fat accumulation may occur also in degenerative disease and with asymmetric weight bearing. The features of para-articular fat accumulation may be similar to the features of Modic type II disc degeneration.37 Bone marrow edema, sclerosis, and para-articular fat accumulation are typical but not specific for sacroiliitis. In sacroiliitis, all three signs often occur together and in middle and late stages are arranged in a certain pattern: the sclerosis is directly para-articularly located (with preference for the ilium) and is surrounded by an indistinct rim of bone marrow edema. Areas of fat accumulation are found in para-articular segments that are not affected by sclerosis or bone marrow edema, and there is some predilection for the sacrum. Joint effusion (intra-articular fluid signal) may be present in sacroiliitis, in traumatic joint disruption, in fracture with joint affection, and in degenerative disease. The diagnostic clue for sacroiliitis is the erosion that is a contrast material–enhancing defect of the subchondral bone. The diagnosis is certain when multiple erosions are

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visible. Early arthritis is probable when two separate erosions are visible (see Fig. 49-2). A typical pitfall is to mistake vessels in the retroarticular space (especially in the dorsally located paracoronal images) for intra-articular lesions, but correct identification occurs on examining the next and prior images. Typically, contrast enhancement is seen in the joint space itself, in the joint capsule, in erosions, and in the para-articular bone; the latter is considered to be juxtaarticular osteitis. Retroarticular enhancement or pathologic T2 hyperintensity and contrast medium uptake in the posterior process of the iliac bone are not necessarily associated with sacroiliitis but are frequent in AS patients due to enthesitis. In patients with degenerative disease, these indicate ligamentous attachment disease. Signs of bacterial infection that should not be mistaken for rheumatic sacroiliitis include enhancement of the periarticular soft tissue, especially ventrally; skip lesions of osseous enhancement; soft tissue fluid accumulations; and abscesses or sinus tracts.

Multidetector Computed Tomography Computed tomography makes visible the complex anatomy of the sacroiliac joint. Careful consideration should be given to the discrimination of the retroarticular from the articular space. The articular space is identified by the two parallel lines of the subchondral bone with typical distance. In the more dorsally located images, the C shape of the joint leads to a projection phenomenon, with articular space (cranial and caudal) and retroarticular space in between (Fig. 49-3A). Contour irregularities of the os ilium and sacrum in the retroarticular space are normal but, if extensive, are called fibro-ostosis. Fibro-ostosis may be part of DISH. As in radiographs, the triad erosions, bony bridges/ ankylosis and sclerosis are the diagnostic clues for sacroiliitis. With tomography, the joint space is freely visible, and iliac erosions and bony bridges, as well as sclerosis,

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are easily detected (see Fig. 49-3).38,39 Sacral lesions tend to appear later in the disease course. Demineralization of the os sacrum is frequent in patients with long-standing AS.

Ultrasonography Ultrasonography is not well established in the diagnostic pathway of sacroiliitis. In children, bulging ligamentous and capsular contours and hypoechoic articular structures may be found.

Nuclear Medicine In the 1970s there were attempts to close the diagnostic gap between symptom onset and diagnosis of AS by means of scintigraphy.40,41 To distinguish the normal registration of the sacroiliac joints from inflammatory disease, it had been necessary to develop a quantification technique. With this technique, the specificity for early arthritis of the sacroiliac joint in selected patients with HLA-B 27 and inflammatory back pain seemed to be acceptable. However, the subsequent development of CT offered complete display of the joint space without superposition effects, outstripping the scintigraphic efforts by far. The only advantage of scintigraphy over CT is the superior detection of the osteoblastic activity that may indicate sacroiliitis. At present, MRI equals scintigraphy in sensitivity and display of inflammatory features and exceeds it in revealing anatomic changes and specificity. The scintigraphic technique has developed over time as well, and single positron emission CT (SPECT) has been found to be useful in revealing inflammatory foci of the complete spine in AS patients.42,43 Even special techniques like immunoglobulin G scintigraphy have been tried for diagnosis of AS, but in clinical practice nuclear medicine is of limited use for the primary diagnosis of sacroiliitis, especially because MRI is widely available. Nevertheless, bone scintigraphy can show inflammatory foci of the complete skeleton and therefore can direct the following workup to these foci.

■ FIGURE 49-3 CT findings in sacroiliitis. Differential diagnosis of para-articular sclerosis is the so-called hyperostosis triangularis ossis ilii (HTI), which is typically sharply delineated and triangular (A). Diagnostic pitfall is a section phenomenon of the retroarticular space that is due to the C shape of the articular surface. Thus, in paracoronal angulation there are often images with articular space ventrally and dorsally and retroarticular space in between that may simulate intra-articular erosion (A). Some patients show a sulcus in the proximity of the joint space, which should not be mistaken for an erosion (A). In arthritis, erosions are intra-articularly located and produce a dentate joint contour. Bony bridges develop intraarticularly, too. Para-articular woolly sclerosis may be of variable amount (B, same patient as Figure 49-1B).

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Positron Emission Tomography/Computed Tomography

●

The combination of PET/CT is not universally available and is exceptionally expensive. Therefore, it is not in the routine diagnostic pathway for sacroiliitis.

Arthroscopy is not performed for the diagnosis of sacroiliitis.

Classic Signs

■

Radiography: Triad of sclerosis, erosions, and bony bridging/ankylosis MRI: Joint effusion, adjacent bone marrow edema, paraarticular sclerosis, periarticular fat accumulation, contrast material uptake in the joint space, erosions, para-articular bone (osteitis), capsular structures

VERTEBRAL MANIFESTATIONS Vertebral manifestations in AS include: ● ●

A

●

Radiography

Arthroscopy

■

●

Discovertebral inflammation (spondylitis marginalis, Romanus lesion, Andersson lesion A = discitis, rheumatic spondylodiscitis) Square vertebra, barrel-shaped vertebra Enthesitis and ligament ossification.

Syndesmophytes Apophyseal joint ankylosis

B

C

The characteristic feature of spine involvement in AS is the syndesmophyte, which grows from the vertebral body corner in the exact position of the anulus fibrosus (Figs. 49-4A and 49–5). This is in contrast to its degenerative counterpart, the spondylophyte, which originates from the lateral or ventral aspect of the vertebral body near the corner. The syndesmophyte progressively bridges the intervertebral space circularly. Multisegmental involvement of complete circular annulus fibrosus ossification is called “bamboo spine” and is typical of the late stages of AS. The affected discs often show dystrophic calcification. Ankylosis of the spine mostly develops in a kyphotic posture of the thoracolumbar region. If the inflammatory process takes place in primarily degenerated discs, the form of the syndesmophyte may be modified, with a more bulging contour corresponding to a mixture of spondylophyte and syndesmophyte. Sometimes, syndesmophytic growth begins consecutively in a Romanus lesion. Syndesmophytes are best visualized by radiography. Discovertebral inflammation (discitis, rheumatic spondylodiscitis) is another typical manifestation in AS. According to Cawley, three types are possible:

D

■ FIGURE 49-4 Radiographic findings in ankylosing spondylitis. The syndesmophyte is the characteristic intervertebral osteophyte in ankylosing spondylitis. A, In contrast to the spondylophyte in degenerative disease, it grows vertically, as shown in this lateral view of the lumbar spine in a 32-yearold man with a 10-year history of ankylosing spondylitis (arrowhead). B, Especially in adolescent-onset ankylosing spondylitis the apophyseal joint ankylosis is pronounced with broad bands of ossification in this lateral view in a 45-year-old man with approximately 30 years of symptoms who was diagnosed at the age of 28. C, This ossification produces the so-called trolley track sign in the anteroposterior view. C, Dagger sign refers to multisegmental ossification of the interspinous ligaments. D, Square vertebra (!) and barrel-shaped anterior vertebral aspect (") are additional characteristic features of ankylosing spondylitis. Multisegmental vertebral corner sclerosis is often detected in the thoracolumbar junction segments. Without erosion it is called “shiny corner” (#). A Romanus lesion consists of a vertebral corner sclerosis with an erosion of the vertebral end plate also corresponding to a Cawley lesion type II.

CHAPTER

A

B

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C

■ FIGURE 49-5

Radiography of the spine in ankylosing spondylitis. Cervical involvement is very frequent and leads to significant movement restriction. Syndesmophytes as well as apophyseal joint ankylosis may develop over years. A, The lateral view of the cervical spine in a 25-year-old woman with onset of ankylosing spondylitis shows square vertebrae and apophyseal joint space narrowing as a sign of minor cervical inflammatory affection. B, Example of complete multisegmental ankylosis by means of syndesmophytes and apophyseal joint arthritis. C, Barrel-shaped vertebrae are characteristic and may develop not exclusively in the lumbar spine.

Type I: localized central lesions (cartilaginous nodules) Type II: localized peripheral lesions (Romanus lesions) Type III: extensive central and peripheral lesions (fracture with pseudarthrosis, Andersson lesion B) The Romanus lesion is confined to the anterior upper or inferior corner of the vertebra and occurs mainly in the lumbar region. It is characterized by a triangular sclerosis and an erosion of the anterior vertebral end plate and corresponds to Cawley type II (see Fig. 49-4D). Similar lesions at the posterior vertebral corners are referred to as spondylitis marginalis. A faint sclerosis at the anterior vertebral corner (a minimal variant of the Romanus lesion) has been termed “shining corner.” Romanus lesions tend to resolve over years and “heal” with syndesmophyte formation. They are found mainly in younger patients. Erosions or destructions of the subdiscal bone resemble spondylodiscitis and are called Andersson lesion type A or inflammatory type. Unlike the destruction caused by bacterial spondylitis, the destruction in rheumatic disease remains mild, focal, and unchanged for months or even years. In clinical practice, the diagnosis is based on plain films. The predilection site of rheumatic spondylodiscitis in AS is the thoracolumbar region. Typically it is found in the first decade of the disease. Approximately in 10% of AS patients radiographs show end-plate erosions, depending on the age of the patient. However, MRI is much more

sensitive for rheumatic discitis; in fact, mild manifestations are often radiographically occult.44,45 The lesions are in most cases asymptomatic; therefore, MRI is not necessarily indicated. In the past, the Andersson lesion type B was described in connection with the rheumatic spondylodiscitis (Andersson lesion type A) due to a certain radiographic similarity.46 Today it is considered to correspond to a malunion or nonunion of a transdiscal insufficiency fracture in a multisegmental vertebral column ankylosis. Consequently it is found in late-stage disease. It is a rare but grave diagnosis. Risk factors for the development of an Andersson lesion type B are osteoporosis, marked thoracolumbar kyphosis, and (minimal or repeating) trauma. The predilection site is the thoracolumbar region. The lesions are painful, and patients report a newly arisen mobility after a minor trauma. The prognosis for local control is moderate. Primarily the lesion can be very difficult to detect, especially if no previous films are available (e.g., in case of a formerly complete, now incomplete syndesmo phytic bridging). The dorsal vertebral elements are usually involved. A transverse lamina fracture is most conspicuous in an anteroposterior projection. The lateral projection may show unisegmental dehiscence of the spinous processes. In Andersson lesion type B, vertebral end-plate destruction is a result of fragment resorption and appears as subchondral bone defects or erosions in radiographic

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images. In long-standing nonunion, the destruction of the subdiscal bone is much more pronounced than in Andersson lesion type A. The surrounding sclerosis is a reactive feature and its extent depends on the mobility in the fracture/pseudarthrosis. Square vertebra and barrel-shaped vertebra are the result of inflammatory and osteoproliferative affection of the ventral vertebral aspect (see Fig. 49-5C). Apophyseal joint ankylosis is the result of either a capsular ossification due to enthesitis or of an erosive arthritis. On radiographs this feature is not very conspicuous, especially in early involvement. Then it is responsible forthose cases with considerable vertebral column movement restriction and relatively unremarkable radiographic results. In late stages, broad ossification bands over the dorsolateral aspect of the vertebral column are seen. In the anteroposterior view they correspond to two parallel bands of sclerosis, a phenomenon called the tramlines sign (see Figs. 49-4B and C and 49-5). Subaxial cervical spine involvement is very frequent and may precede thoracic involvement. In contrast to rheumatoid arthritis, involvement of the craniocervical junction in AS is relatively uncommon. In patients with complete syndesmophytic and apophyseal joint ankylosis of the cervical spine, the rest of cervical mobility is provided in C0-C2. Nevertheless, there are patients with atlantoaxial ligament destruction typically followed by ventral subluxation of the atlas. Subluxation is defined as a distance between the anterior arch of the atlas and the anterior contour of the odontoid process exceeding 3 mm. In AS patients with this deformity, the risk for subsequent myelopathy seems to be higher than in rheumatoid arthritis and the risk increases with the degree of subluxation. Ligament ossifications such as of the ligamentum interspinale and ligamentum iliolumbale occur in late stages of ankylosing spondylitis. Predilection sites is the ligamenta interspinalia, in which polysegmental ossification is called the “dagger sign.”

Magnetic Resonance Imaging Magnetic resonance imaging is the most sensitive and accurate diagnostic tool for discovertebral inflammation, but because it lacks therapeutic relevance, it is not routinely indicated. Individually MRI may be employed for differential diagnosis of localized pain when radiographic imaging results are equivocal or for detection of inflammation before TNFa-blockage. Romanus lesions are characterized by triangular bone marrow edema of the anterior upper vertebral corner and by an erosion. The erosion consists of a small defect of the ventral vertebral end plate. After administration of a contrast agent the defect and the adjacent subdiscal bone show considerable enhancement. In chronic lesions, T2 hyperintensity and contrast agent uptake completely fade away. T1-weighted images display fat accumulation of the bone marrow in a typically triangular configuration at the anterior upper or lower vertebral corner. In long-standing disease, multilevel triangular fat accumulation at the vertebral corners is common (Fig. 49-6). Andersson lesions type A resemble Schmorl’s nodes of Scheuermann’s disease with central end-plate defects and a rim of adjacent bone marrow edema. There is usually

moderate contrast material enhancement in the subdiscal bone, in the erosion, and in the disc itself (see Fig. 49-6). Andersson lesions type B typically cause massive edema of the bone marrow and perivertebral soft tissue. The fracture line is hyperintense in STIR images. Bone fragments of the end plates appear as dotted hypointense structures in all pulse sequences. The posterior elements are involved, and fractures of the apophyseal joint processes, or of the lamina and spinous process, are highlighted. Intensive contrast material enhancement is displayed in the surroundings of the fracture. Costotransversal and costovertebral joint arthritis give rise to persistent thoracolumbar pain and cause respiratory movement restriction. In radiographic images, this feature is mostly occult; therefore, MRI is the best method for assessing these joints. One drawback, however, is that standard MR images of the thoracic spine may result in false-negative readings. In sagittal angulation, the far lateral images show the adjacent bone marrow edema and effusion of the costovertebral joints as a faint, rounded, ill-defined hyperintensity at the upper third of the vertebral body. Transversal images show bone marrow edema/ osteitis in the vertebral body and the caput costae, joint effusion, synovial hypertrophy, and contrast medium enhancement (see Fig. 49-6). Syndesmophytes are not conspicuous in MRI. The new bone formation appears just as hypointense as the normal annulus fibrosus. Rarely, active inflammatory foci are seen as tiny dots of contrast material enhancement. Enthesitis of the ligamenta interspinalia are highlighted in STIR images and in contrast enhanced studies as hyperintensities in the ligamentous attachments and in the adjacent bone (see Fig. 49-6).

Multidetector Computed Tomography Computed tomography shows spinal manifestations as well as other modalities do, but because it lacks therapeutic impact, it is rarely necessary when radiography is available. In some cases of Andersson lesions type B, helical scans with sagittal multiplanar reformatted images may be employed. The fracture line, bony defects, reactive sclerosis, and dorsal element involvement can be easily assessed.

Ultrasonography For vertebral manifestations, ultrasonography is not beneficial.

Nuclear Medicine In bone scintigraphy and SPECT, abnormalities of the thoracic and lumbar vertebral spine are frequently identified in patients with AS. Most often, facetal joint uptake is found at multiple sites. The other common site of uptake is in the vertebral bodies. These hot spots usually correspond to inflammatory foci such as capsular ossifying enthesitis or arthritis of the apophyseal joints and Romanus/Andersson lesions type A, respectively.43 Scintigraphy may be helpful in the early detection of pseudarthrosis (Andersson lesion B) when MRI is not available or is contraindicated.47

CHAPTER

■ FIGURE 49-6

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1141

MRI of vertebral involvement in ankylosing spondylitis. A, Transverse T1-weighted fat-saturated, contrast-enhanced MR image of the costovertebral joints shows intraosseous contrast enhancement (osteitis), erosions and synovitis in costovertebral arthritis. B, Multisegmental apophyseal joint arthritis in the chronic stage is characterized by hypointensity due to sclerosis and absence of uptake of contrast material. In active arthritis (L3/4), enhancement is present (sagittal T1-weighted, fat-saturated, contrast-enhanced). C, Romanus’ lesions (discovertebral inflammatory affection type Cawley II) show triangular enhancement of the upper or lower vertebral body corner (T1-weighted, fat-saturated, contrast enhanced). Note enhancement in and between the spinous processes represents enthesitis. In the chronic stage of Romanus lesions the enhancement fades away and is replaced by fat signal, a phenomenon that is frequently multisegmental (precontrast [D] and postcontrast [E] T1-weighted images).

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Classic Signs SYNDESMOPHYTES ■ Radiography: marginal intervertebral osteophyte ■ MRI: inconspicuous ROMANUS LESIONS ■ Radiography: triangular sclerosis of the anterior upper vertebral corner (Cawley II) and end-plate erosion ■ MRI: ❑ Active: STIR hyperintense/contrast-enhancing erosion at the anterior upper vertebral corner ❑ Chronic: triangular fat accumulation in the vertebral corner ANDERSSON LESION A ■ Radiography: central vertebral end-plate defect, minor involvement occult ■ (Cawley I) MRI: ❑ Enhancing central end-plate defects (often multilevel) ❑ Discal enhancement ❑ Subdiscal bone marrow edema and enhancement ANDERSSON LESION B ■ Radiography: transdiscal insufficiency fracture/malunion (Cawley III), transverse lamina fracture ❑ In early stages, inconspicuous ❑ In late stages, considerable destruction and sclerosis ■ MRI: hyperintense fracture line (STIR/T2) adjacent edema, and contrast enhancement APOPHYSEAL JOINT ANKYLOSIS ■ Radiography: at early stages, inconspicuous; at late stages, broad ossification, trolley track sign COSTOTRANSVERSAL AND COSTOVERTEBRAL ARTHRITIS ■ Radiography: occult ■ MRI: edema in bone marrow and in capsular structures; contrast enhancement in capsule, osteitis, erosions ENTHESITIS OF LIGAMENTA INTERSPINALIA ■ Radiography: polysegmental ossification: “dagger sign” ■ MRI: hyperintensity/enhancement at the ligamentous attachments

Radiography In AS, the predilection sites of arthritis are the hips, knees, and shoulders. Periarticular demineralization, joint effusion, and diffuse joint space narrowing are the radiologic signs of arthritis. In contrast to rheumatoid arthritis, erosions are seldom seen. In a considerable number of patients, the radiographic signs of arthritis are not very conspicuous and premature degenerative disease (osteophyte formation) is the most prominent finding. In fact, concentric joint space diminution combined with osteophytosis is characteristic of hip disease in AS (Fig. 49-7).48 Sometimes the inflammatory process is aggressive, and marked destruction develops in a few years. Postarthritic ankylosis at end stage is well known but not very frequent. The small joints of the hands and feet as well as of the wrists are affected less frequently than large joints. The distribution tends to be asymmetric. In comparison, rheumatoid arthritis predominantly affects the lower extremity and the distal interphalangeal joints. Periarticular osteoporosis, soft tissue swelling, joint space narrowing, erosion, and destruction occur (see Fig. 49-7C). Sometimes postarthritic ankylosis can appear very soon after arthritic onset. Enthesitis (fibro-ostitis, inflammatory affection of the ligamentous, tendinous, and capsular insertions) is the most characteristic sign of seronegative rheumatic disease. The predilection sites are the tubera ischiadica, trochanter, plantar calcaneal surface, triceps insertion, and patella, but enthesitis may affect virtually any attachment. Radiographically, the cortical lining disappears and an ill-defined erosion develops, forming a small groove. Subsequently, osteoproliferation with new bone formation in the groove and the surroundings takes place. The process relapses, and erosive and proliferative features are seen at the same time. Symphysitis with erosion and prominent sclerosis is common. Further evaluation by other techniques is not necessary. Inflammatory involvement of the manubriosternal synchondrosis is characterized by soft tissue swelling, bony sclerosis, fuzzy contours, and erosions. Bursitis compromising the underlying bone is most often seen at the Achilles tendon insertion (bursa subachillea), bursa trochanterica, and iliopsoas bursa. Soft tissue swelling is found in the typical places (see Fig. 49-7D). Pressure erosions of the bone and inflammatory destructions, as well as new bone formation, are possible. In fact, they are very common at the os calcis.

Magnetic Resonance Imaging

Extravertebral Skeletal Manifestations The inflammatory involvement of proximal joints is very frequent in AS. The most frequent site of involvement is the hip joint, followed by the shoulder and knee. Nevertheless, peripheral synovitis/erosive arthritis is well known. The overall characteristic of AS is the presence of enthesitis, which may be found near virtually any joint. Bursitis with involvement of the adjacent bone is also typical (e.g., at the Achilles tendon insertion). Synchondritis (inflammatory involvement of cartilaginous joints) is a frequent symptom at the manubriosternal junction or clinically silent at the symphysis pubis.

Magnetic resonance imaging is very sensitive and accurate for the detection of enthesitis, arthritis, and bursitis. Nevertheless, in clinical practice it is not really necessary for the diagnosis. The characteristic feature of enthesitis is the edema (T2/STIR hyperintensity) and contrast medium enhancement in the surroundings of a capsular, ligamentous, or tendinous attachment. The ligament or tendon is often thickened and attenuated. The adjacent bone often shows signs of osteitis. Typical sites of affection seen in musculoskeletal MRI are the plantar calcaneal surface, the Achilles tendon insertion (often with associated bursitis), the tibial apophysis, the tubera ischiadica, the scapular triceps insertion, and similar structures.

CHAPTER

49

● Ankylosing Spondylitis

■ FIGURE 49-7 Arthritis and enthesitis in ankylosing spondylitis. Proximal joint arthritis with involvement of hips and shoulders is typical. A, Arthritis often results only in mild premature degenerative disease with concentric joint space narrowing as a sign of cartilage destruction. Note the typical posture of the pelvis in a patient with ankylosing spondylitis and considerable fibro-ostosis of the ischial tuberosities. B, The shoulder is the second most frequent location of proximal joint involvement. Joint space narrowing and premature degenerative osteoarthritis are common. Erosions are found primarily marginal at the humeral head and at the glenoid, later in the central part of the joint. Peripheral arthritis is less frequent. In contrast to rheumatoid arthritis, it is more often asymmetric in distribution and also affects the distal small joints. C, In a number of patients, however, imaging features of peripheral arthritis do not differ from those of rheumatoid arthritis as shown in this 38-year-old man with metatarsophalangeal arthritis and long-standing ankylosing spondylitis. D, In retrocalcaneal bursitis, soft tissue swelling at the Achilles tendon insertion and a typical pressure erosion of the dorsal aspect of the calcaneus are present as shown in this 49-year-old man with an approximate 30-year history of ankylosing spondylitis.

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In active arthritis, thickening and contrast medium enhancement in the synovial membrane and capsule as well as joint effusion are typical. The synovial membrane may show focal or diffuse thickening, nodules, or massive proliferations with intermediate signal in T1-weighted images. In rheumatoid arthritis, pannus is found with moderate frequency and extent. Various degrees of pannus activity are recognized according to their signal intensity: STIR/T2 hyperintensity and contrast medium uptake characterize active pannus; T2 hypointensity and lack of enhancement correspond to fibrous pannus. Erosions are contrast-enhancing focal defects of the subchondral bone. They can be recognized earlier than in radiographic imaging in the same predilection sites (bare areas, joint margins). In long-standing disease, secondary degenerative disease with smoothing of the eroded contours and spur formation occurs. Bursitis, at the Achilles tendon insertion or the iliopsoas, for example, is characterized by an effusion that appears as a localized fluid collection surrounded by contrastenhancing synovial lining in typical location. Synchondritis manubriosternalis may be imaged by means of MRI. Respiratory motion and flow artifacts from the large vessels and heart may obscure the images if not carefully omitted. Coronal and sagittal angulations are recommended. STIR/T2 hyperintensity and contrast medium enhancement of the bone marrow of the manubrium and of the corpus sterni corresponding to osteitis, and of the intrathoracic and extrathoracic soft tissue, are typical, as are erosions of the cartilaginous joint itself.

Computed Tomography Synchondritis manubriosternalis and arthritis of the sternoclavicular joints are easily imaged by means of CT with additional sagittal and coronal, curved multiplanar reformatted imaging. Bony erosions, sclerosis, and adjacent soft tissue swelling are typical. If the sclerosis and new bone formation are tremendous, the differential diagnosis of SAPHO syndrome arises. For SAPHO syndrome, the findings of ossification of the costoclavicular ligaments, cartilaginous ribs, and surrounding soft tissue and sclerosis and broadening of the affected bones are typical.

Ultrasonography Especially in enthesitis and bursitis, ultrasonography is advantageous. Bursitis is characterized by fluid accumulation in typical locations. The echogenicity is mostly equivalent to fluid. However, fibrinous contents floating, or constant isoechogenic structures, are frequent. Isoechogenicity (with consequent difficulties for detection and evaluation) is possible. Enthesitis is characterized by thickening of the tendon or ligament and by hypoechogenicity and structure inhomogenity at the attachment and its surroundings.

Nuclear Medicine Bone scintigraphy shows inflammatory foci as hot spots. It demonstrates the extent, activity, and sites of involvement. It may direct the diagnostic workup of certain foci. The therapeutic impact, however, remains limited.

Positron Emissions Tomography/Computed Tomography The combination of PET/CT is not established in the routine diagnostic workup of AS.

Arthroscopy Arthroscopy is not performed for diagnostic workup but as a therapeutic tool to perform a synovectomy (see later).

Classic Signs ENTHESIS ■ Radiography: fuzzy contoured grooves and osseous proliferations at muscular, ligamentous, capsular or tendon attachment sites ■ MRI: Thickening and structure inhomogeneity of ligament or tendon; STIR/T2 hyperintensity, T1 intermediate signal/ contrast enhancement in the preinsertional ligament or tendon, the surroundings, and the adjacent bone ■ Ultrasonography: thickening and structure inhomogeneity/hypoechogeneity of the preinsertional ligament or tendon and in the surroundings ARTHRITIS ■ Radiography: joint effusion, periarticular demineralization, joint space narrowing, erosions, destruction. Secondary premature degenerative osteoarthritis ■ MRI: joint effusion, thickening, T1-weighted intermediate signal and contrast enhancement of the synovial membrane, nodules, intra-articular pannus, erosions of the joint surface ■ Ultrasonography: joint effusion, synovial thickening, pannus, erosions BURSITIS ■ Ultrasonography: fluid accumulation, echogenic structures SYNCHONDRITIS MANUBRIOSTERNALIS ■ Radiography: sclerosis, erosions ■ CT: sclerosis, erosions, soft tissue swelling ■ MRI: erosions, osteitis, soft tissue swelling

Osteoporosis Despite the relatively young age of the patients and the male predominance, the incidence of osteoporosis in AS patients is high (18%-62%).49,50 It increases in prevalence with patient age, disease duration, severity of vertebral involvement, and peripheral arthritis.51 Unlike osteoporosis in rheumatoid arthritis patients, osteoporosis in AS patients is confined mostly to the axial skeleton. Osteoporosis significantly increases the risk of vertebral compression fractures as well as transdiscal and transvertebral insufficiency fractures (Andersson lesion B).52 Therefore, AS patients should be considered as a highrisk group who will eventually need regular spinal bone

CHAPTER

mineral density (BMD) scans and therapy. However, measuring bone density is challenging. Dual-energy x-ray absorptiometry (DEXA) of the lumbar spine is affected by superposition due to syndesmophyte formation, sclerotic Romanus lesions, and apophyseal joint ankylosis with excessive bone formation especially in patients at risk (Fig. 49-8).53,54 There have been different approaches to overcome this disadvantage, such as DEXA measurement of the hip, lateral projection DEXA of the third lumbar vertebra, quantitative CT (QCT), peripheral quantitative CT (pQCT), and calcaneal quantitative ultrasonography (QUS).55–57 For DEXA measurement of the hip, the possibility of periarticular osteoporosis due to coxitis should be kept in mind. Lateral projection DEXA of only one vertebra has its limits for estimation of fracture risk of the whole axial

49

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1145

skeleton and is of minor reliability. Peripheral QCT allows no estimation of axial skeleton fracture risk in patients with AS.50 QCT is unique in its ability to detect selectively cancellous bone loss without superimposition. It is much more sensitive, and therefore can be of use in detecting demineralization earlier than with other methods. In patients with AS, the loss of cancellous bone is often tremendous when lumbar affection is present (see Fig. 49-8). The fracture risk, however, is not increased to the same extent. Estimations of fracture risk by means of BMD measurements are based on normal microarchitecture and macroarchitecture of the spine. In longstanding AS, ankylosis of the dorsal elements (often with extensive bone formation and syndesmophytic growth, with bridging of the disc space as well as broadening

■ FIGURE 49-8 Bone mineral density in AS. BMD measurement in a patient with long-standing disease and complete syndesmophytic ankylosis of the lumbar spine. A, The DEXA measurement of the lumbar spine displays high values. This result is probably not valid because of overlying syndesmophytes. B and C, Quantitative CT reveals a marked osteoporosis of the cancellous bone with 14 mg/mL hydroxyapatite equivalent. Such a very low BMD in the quantitative CT measurement is not uncommon in patients with ankylosing spondylitis. Sometimes the values are even negative owing to nearly complete transformation into fat. The cortical shell is in contrast broad and dense, reflecting new bone formation. Thus, the low BMD value does not represent the same fracture risk as in postmenopausal osteoporosis. For the fracture risk estimation in patients with ankylosing spondylitis apart from the BMD measurement factors that must be taken into consideration include the thoracolumbar kyphosis, the extent or absence of coarse new bone formation, the presence of spinal inflammatory activity, the peripheral joint affection, and a corticosteroid medication. D and E, Transvertebral fractures after minor trauma in a 46-year-old patient with a 30-year history of ankylosing spondylitis.

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of the cortical shell of the vertebra) is present. The microarchitecture and macroarchitecture are completely altered, so that the formation of the vertebral bodies mimics that of the long bones. Hence, the weight and power transmission in the ankylosed vertebral column is different from that of normal individuals. Abnormal ossification contributes to load-bearing capacity.58 This leads to different fracture mechanisms in trauma and to the unusual transdiscal or transvertebral form of AS-typical insufficiency fractures (Fig. 49-8D and E). In spite of these limitations for clinical practice, BMD assessment by means of lumbar DEXA in patients with only minor radiographic abnormalities, by means of hip DEXA in patients without coxitis, and by means of QCT in patients with severe vertebral and hip affection will give sufficient information for estimation of fracture risk and decisions about therapy.

DIFFERENTIAL DIAGNOSIS Low back pain in early adulthood may arise from degenerative disease (e.g., spondylolysis with spondylolisthesis), disc degeneration with protrusion, or asymmetric segmental variants. In some patients nighttime attacks of low back pain and sacroiliac tenderness result from degenerative disease with enthesopathy of the dorsal sacral and iliac surface. Because radiographic imaging has a low negative predictive value for early diagnosis, tomographic techniques should be employed. Retroarticular fibro-ostosis is a relatively common finding in these patients. Stiffness of the lumbar and thoracic spine in elderly patients is commonly seen in DISH. On radiography, the differential diagnosis of sacroiliitis comprises degenerative disease in DISH or triangular sclerosis, asymmetric weight bearing, the normal joints, and, in cases of pseudodilatation, hyperparathyroidism. Infectious arthritis of the sacroiliac joint is mainly unilateral and causes considerable destruction with minor sclerosis. Syndesmophytes can be distinguished from degenerative intervertebral osteophytes by their marginal growth. Andersson lesions should not be mistaken for bacterial spondylitis. With sacroiliac CT, retroarticular fibro-ostosis and marginal sacroiliac irregularities may be a pitfall and should be carefully localized to distinguish them from erosions. On sacroiliac MRI, bone marrow edema, joint effusion, para-articular fat accumulations, and sclerosis are unspecific features and may occur in degenerative osteoarthritis, asymmetric weight bearing, or post-traumatically. For the diagnosis of arthritis, central erosions of the joint surface should be visible. Bacterial sacroiliitis is characterized by soft tissue abnormalities, abscesses, sinus tracts, and skip lesions. Abnormalities in sacral insufficiency fractures are found medial to the joint space. The fracture line is usually visible in T1-weighted images. On lumbar MRI, Andersson lesions B may resemble spondylitis. One should note the fracture line in the dorsal elements and the absence of epidural collections or paravertebral abscesses. Schmorl’s nodes and Andersson lesions A have a striking resemblance to each other; some authors suggest that their pathogenesis is identical. Scheuermann’s disease may be included in the differential diagnosis.

For the diagnosis of AS, the sacroiliitis is absolutely necessary. Patients with AS may show additional features of Scheuermann’s disease. There is no therapeutic impact from additional diagnosis of Scheuermann’s disease in a patient with AS. On a scintiscan, tracer uptake in the sacroiliac region is not easy to interpret. In addition to normal conditions, it may indicate premature degeneration in the obese and in multipara or indicate asymmetric weight bearing due to scoliosis and sacroiliitis. Hot spots in the facetal joints or vertebrae are equivocal. Facetal hypertrophy, degenerative spurs, and other bone remodeling conditions may be the cause.

SYNOPSIS OF TREATMENT OPTIONS Physiotherapy Physiotherapy is the most important element in the therapeutic management of AS.59 Symptom relief is achievable with exercise.60 Because lifelong regular exercise is mandatory, major educational effort and constant reinforcement is crucial. Thus, from the moment of accurate diagnosis, the patient should undergo both an intensive educational program and a physiotherapeutic program. A thorough understanding of the disease and its management is the basis for building and maintaining the impetus for maximal self-care and appropriate lifestyle. In the beginning, the patient should be referred for physiotherapy. The objective of the initial phase is to restore as much movement as possible. Hydrotherapy is particularly valuable.61 A dedicated exercise regimen must be taught to the patient. It must include not only exercises for mobilization of the vertebral column and joints but also breathing exercises for better chest expansion. Passive stretching may help even in patients with long-standing disease. Because regaining lost movement causes discomfort in this early phase, pain relief should be attempted to allow full mobilization. Pulsed short wave, local heat or cold, interferential therapy, local ultrasonography, or transcutaneous nerve stimulation may be employed and adapted to the individual. Drug therapy will support these efforts. Psychologic training can lead to the development of pain-control strategies.62 The initial phase of therapy yields especially striking improvements in mobility and pain relief. This initial phase should be used to persuade the patients to establish long-term management habits. Lifelong maintenance of appropriate lifestyle and daily exercise is crucial for disease management. In the chronic phase, maximal self-care should be attempted and drugs should be cautiously prescribed. The objectives are to reduce pain and stiffness by selfmanagement; to maintain symptom relief, posture, and movement; and to enable full work capacity. Educational efforts have an extraordinary impact on the success of disease management in the chronic phase. Understanding, help, and support of the family members is important. For that reason, the family should also receive educational advice. Joining self-help groups may support these efforts. Repeated supervision of the exercises by a physiotherapist has been proven to improve the persistence of a home exercise program.62

CHAPTER

Medical Treatment Pain relief is the primary goal of most patients. Pain is difficult to estimate, and many patients add analgesics without prescription, without knowledge of the treating physician. Analgesic medication is needed especially in the initial phase to allow maximal mobilization. Nonsteroidal anti-inflammatory drugs (NSAIDs) such as indomethacin, diclofenac, or naproxen are the first choice. Local problems of enthesitis may be addressed with local corticosteroid injections if needed. In the chronic phase, drug therapy should be minimal and exercise should be used as the first choice to reduce pain. If no relief is achieved despite appropriate exercise, NSAIDs can support the regimen. Systemic therapy with corticosteroids for short-term control of severe symptoms is effective. Long-term corticosteroid medication is not recommended for AS patients. Local corticosteroid injections for peripheral joints and enthesitis can be helpful. The risk for tendon rupture as a complication is increased by local corticosteroid application. Despite their use in cases of RA, disease-modifying anti-rheumatic drugs (DMARDs) are not entirely proven to be valuable for AS. With sulfasalazine there is evidence of short-term efficacy in peripheral synovitis. The use of sulfasalazine should be considered in patients with poor response to physical treatment and NSAIDs and persistent inflammatory activity as evident by laboratory results. Low dose therapy with methotrexate appears to have an effect on peripheral joints and spinal disease but should be used only in cases of severely active and unremittingly progressive disease. Tumor necrosis factor-α blockade studies are promising in a hope for genuine disease retardation. Its efficacy seems to be very encouraging. Currently, it is indicated only in severe active cases and progressive cases and otherwise uninfluenced early cases. Its exact role in the medical management of AS remains to be defined.

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such as inflammation in the knee or the ankle joint. The objective is to avoid destruction of the cartilage, bone, capsule, ligaments, and tendons. The procedure is usually performed arthroscopically in early stages or as open synovectomy in advanced cases. Endoprosthetic reconstruction is the predominant procedure in advanced joint destruction and severe postinflammatory degenerative osteoarthritis. It is performed very frequently at the hip or knee. For the hip, cementless replacement offers good long-term results in the young patient population in which necessity of frequent revision surgery must be anticipated. For the knee, bicondylar resurfacing prostheses in cases of stable ligaments or constrained prostheses for instable ligaments or varus/ valgus malalignment are available. Spinal surgery for posture improvement may be indicated in select patients with severe kyphosis and consequent alteration of their forward vision. The procedure is associated with considerable risk of neurologic damage and should therefore only be performed in highly specialized centers. The upper cervical segments remain mostly unaffected in AS and provide a rest of movement. In some cases, however, atlantoaxial subluxation occurs. The risk for subsequent myelopathy is higher in AS than in rheumatoid arthritis, in which this deformity is much more common. Severe headache and occipital numbness are two of the symptoms of impending neurologic damage. In these patients, cervical fusion is required.

What the Referring Physician Needs to Know ■ ■

Surgical Treatment

■

Synovectomy is performed for local control of lingering inflammatory activity unresponsive to drug therapy,

■

Early accurate, confident diagnosis of sacroiliitis Vertebral manifestation and extent of ankylosis Presence of Andersson lesion type B (transdiscal insufficiency fracture) Enthesitis/arthritis of proximal or peripheral joints

SUGGESTED READINGS Resnick D, Niwayama G. Ankylosing spondylitis. In Resnick D, Niwayama G eds). Diagnosis of Joint and Bone Disorders, 2nd ed. Philadelphia, WB Saunders, 1988, pp 1103–1170.

Russell AS, van der Linden S, van der Heijde D, et al. Ankylosing spondylitis. In Hochberg MC, Silman AJ, Smolen JS, et al (eds). Rheumatology. Amsterdam, Elsevier, 2003, pp 1145–1224.

REFERENCES 1. Dougados M, van der Linden S, Juhlin R, et al. The European spondyloarthropathy study group preliminary criteria for the classification of spondyloarthropathy. Arthritis Rheum 1991; 34:1218–1227. 2. Moll JM, Wright V. New York clinical criteria for ankylosing spondylitis. Ann Rheum Dis 1973; 32:354–363. 3. Moll JM, Haslock I, McRae IF, Wright V. Associations between ankylosing spondylitis, psoriatic arthritis, Reiter’s disease, the intestinal arthropathies, and Behçet’s syndrome. Medizine 1974; 53:343–364. 4. Helliwell PS, Hickling P, Wright V. Do the radiological changes of classic ankylosing spondylitis differ from the changes found in the

spondylitis associated with inflammatory bowel disease, psoriasis and reactive arthritis? Ann Rheum Dis 1998; 57:135–140. 5. Zhang Y, Guerassimov A, Leroux JY, et al. Arthritis induced by proteoglycan aggrecan G1 domain in BALB/c mice: evidence for T-cell involvement and the immunosuppressive influence of keratan sulfate on recognition of G and B cell epitopes. J Clin Invest 1998; 101:1678–1686. 6. Mikecz K, Glant TT, Baron M, Poole AR. Isolation of proteoglycanspecific T Lymphocytes from patients with ankylosing spondylitis. Cell Immunol 1988; 112:55–63.

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7. Glant T, Mikecz K, Arzoumanian A, Poole AR. Proteoglycan-induced arthritis in Balb/c mice. Arthritis Rheum 1987; 30:201–212. 8. Carter ET, McKenna CH, Brian DD, Kurland LT. Epidemiology of ankylosing spondylitis in Rochester, Minnesota 1935–1973. Arthritis Rheum 1979; 22:365–370. 9. van der Linden SJ, van der Heijde S. Ankylosing spondylitis: clinical features. In Yu D (ed). Spondyloarthropathies. Rheum Dis Clin North Am 1998; 24:663–676. 10. Khan MA. HLA and ankylosing spondylitis. In Calabro JJ, Carson Dick W (eds). Ankylosing Spondylitis: New Clinical Applications. Lancaster, MTP, 1987, pp 23–44. 11. Mielants H, Veys EM, Goemaere S, et al. A prospective study of patients with spondyloarthropathy with special reference to HLAB27 and to gut histology. J Rheumatol 1993; 20:1353–1358. 12. van der Linden SM, Valkenburg HA, De Jong BM, Cats A. The risk of developing ankylosing spondylitis in HLA-B27 positive individuals: a comparison of relatives of spondylitis patients with the general population. Arthritis Rheum 1984; 27:241–249. 13. Calin A, Kaye B, Sternberg M, et al. The prevalence and nature of back pain in an industrial complex: a questionnaire and radiographic and HLA analysis. Spine 1980; 5:201–205. 14. Underwood MR, Dawes P. Inflammatory back pain in primary care. Br J Rheumatol 1995; 34:1074–1077. 15. Brandt J, Bollow M, Haberle J, et al. Studying patients with inflammatory back pain and arthritis of the lower limbs clinically and by magnetic resonance imaging: most but not all patients with sacroiliitis have spondyloarthropathy. Rheumatology 1999; 38:831–836. 16. Linssen A, Feltkamp TE. B27 positive diseases versus B27 negative diseases. Ann Rheum Dis 1988; 47:431–439. 17. Derhaag DJ, De Waal LP, Linssen A, Feltkamp TE. Acute anterior uveitis and HLA-B27 subtypes. Invest Ophthalmol Vis Sci 1988; 29:1137–1140. 18. van der Linden SM, Rentsch HU, Gerber N, et al. The association between ankylosing spondylitis, acute anterior uveitis and HLAB27: the results of a Swiss family study. Br J Rheumatol 1988; 27(Suppl 2):39–41. 19. Paivonsalo-Hietanen T, Vaahtoranta-Lehtonen H, Tuominen J, Saari KM. Uveitis survey at the University Eye Clinic in Turku. Acta Ophthalmol Copenh 1994; 72:505–512. 20. Mennell JB. Physical Treatment by Movement, Manipulation and Massage. London, Churchill Livingstone, 1977, p 328. 21. Schober P. Lendenwirbelsäule und Kreuzschmerzen. Münch Med Wochenschr 1937; 84:336–428. 22. Moll JMH, Wright V. An objective study of chest expansion. Ann Rheum Dis 1972; 31:1–8. 23. Archer IA, Moll JM, Wright V. Chest and spinal movement in ankylosing spondylitis. Rheumatol Rehabil 1974; 13:30–31. 24. Cats A, van der Linden SJ, Goei The HS, Khan MA. Proposals for diagnostic criteria of ankylosing spondylitis and allied disorders. Clin Exp Rheumatol 1987; 5:167–171. 25. Mau W, Zeidler H, Mau R, et al. Outcome of possible ankylosing spondylitis. Clin Rheumatol 1987; 6(Suppl 2):60–66. 26. Mau W, Zeidler H, Mau R, et al. Clinical features and prognosis of patients with possible ankylosing spondylitis: results of a 10-year follow up. J Rheumatol 1988; 15:1109–1114. 27. Francois FJ, Gardner DL, Degrave EJ, Bywaters EGL. Histopathologic evidence that sacroiliitis in ankylosing spondylitis is not merely enthesitis. Arthritis Rheum 2000; 4:2011–2024. 28. Ball J. Enthesopathy of rheumatoid and ankylosing spondylitis. Ann Rheum Dis 1971; 30:213–223. 29. Benjamin M, Rufai A, Ralphs JR. The mechanism of formation of bony spurs (enthesophytes) in the Achilles tendon. Arthritis Rheum 2000; 43:576–583. 30. Forrester DM. Imaging of the sacroiliac joints. Radiol Clin North Am 1990; 28:1055–1072. 31. Dale K, Vinje O. Radiography of the spine and sacroiliac joints in ankylosing spondylitis and psoriasis. Acta Radiol Diagn 1985; 26:145–159. 32. Bollow M, Braun J, Hamm B, et al. Early sacroiliitis in patients with spondyloarthropathy: evaluation with dynamic gadoliniumenhanced MR imaging. Radiology 1995; 194:529–536. 33. Bennett PH, Burch TA. New York symposium on population studies in the rheumatic diseases: new diagnostic criteria. Bull Rheum Dis 1968; 17:453–458. 34. van der Linden SJ, Valkenburg HA, Cats A. Evaluation of diagnostic criteria for ankylosing spondylitis: a proposal for modification of the New York criteria. Arthritis Rheum 1984; 27:361–368. 35. Dihlmann W. Radiologic Atlas of Rheumatic Diseases. Stuttgart, Thieme, 1986.

36. Resnick D, Niwayama G, Goergen TG. Comparison of radiographic abnormalities of the sacroiliac joint in degenerative disease and ankylosing spondylitis. AJR Am J Roentgenol 1977; 128:189–196. 37. Modic MT, Masaryk TJ, Ross JS, Carter JR. Imaging of the degenerative disk disease. Radiology 1988; 168:177–186. 38. Carrera WF, Foley WD, Kozin F, et al. CT of sacroiliitis. AJR Am J Roentgenol 1981; 136:41–46. 39. Fam AG, Rubenstein JD, Chin-Sang H, Leung FY. Computed tomography in the diagnosis of early ankylosing spondylitis. Arthritis Rheum 1985; 28:930–937. 40. Lentle BC, Russell AS, Percy JS, Jackson FI. Scintigraphic findings in ankylosing spondylitis. J Nucl Med 1977; 18:524–528. 41. Lentle BC, Russell AS, Percy JS, Jackson FI. The scintigraphic investigation of sacroiliac disease. J Nucl Med 1977; 18:529–533. 42. Jacobsson H, Larsson SA, Vesternkold L, Lindvall N. The application of single photon emission computed tomography to the diagnosis of ankylosing spondylitis of the spine. Br J Radiol 1984; 57:133–140. 43. Ryan PJ, Gibson T, Fogelman I. Spinal bone SPECT in chronic symptomatic ankylosing spondylitis. Clin Nucl Med 1997; 22:821–824. 44. Kenny JB, Hughes PL, Whitehouse GH. Discovertebral destruction in ankylosing spondylitis: the role of computed tomography and magnetic resonance imaging. Br J Radiol 1990; 63:448–455. 45. Wienands K, Lukas P, Albrecht HJ. Clinical value of MR tomography of spondylodiscitis. Z Rheumatol 1990; 49:356–360. 46. Dihlmann W, Delling C. Disco-vertebral destructive lesions (so-called Andersson lesions) associated with ankylosing spondylitis. Skeletal Radiol 1978; 3:10–15. 47. Peh WC, Hoh WY, Luk KD. Application of bone scintigraphy in ankylosing spondylitis. Clin Imaging 1997; 21:54–62. 48. Resnick D, Niwayama G: Ankylosing spondylitis. In Resnick D, Niwayama G (eds). Diagnosis of Joint and Bone Disorders, 2nd ed. Philadelphia, WB Saunders, 1988, pp 1103–1170. 49. Mitra D, Elvins DM, Speden DJ, Collin AJ.The prevalence of vertebral fractures in mild ankylosing spondylitis and their relationship to bone mineral density. Rheumatology 2000; 39:85–89. 50. Bessant R, Keat A. How should clinicians manage osteoporosis in ankylosing spondylitis? J Rheumatol 2002; 29:1511–1519. 51. Ralston SH, Urquhart GD, Brzeski M, Sturrock RD. Prevalence of vertebral compression fractures due to osteoporosis in ankylosing spondylitis. BMJ 1990; 3:563–565. 52. Devogelaer JP, Maldague B, Malghem J, et al. Appendicular and vertebral bone mass in ankylosing spondylitis: a comparison of plain radiographs with single- and dual-photon absorptiometry and with quantitative computed tomography. Arthritis Rheum 1992; 35:1062–1067. 53. Donnelly S, Doyle DV, Denton A, et al. Bone mineral density and vertebral compression fracture rates in ankylosing spondylitis. Ann Rheum Dis 1994; 53:117–121. 54. Sivri A, Kilinc S, Gokce-Kutsal Y, Ariyre KM. Bone mineral density in ankylosing spondylitis. Clin Rheumatol 1996; 15:51–54. 55. Karberg Z, Zochling J, Sieper J, et al. Bone loss is detected more frequently in patients with ankylosing spondylitis with syndesmophytes. J Rheumatol 2005; 32:1290–1298. 56. Gilgil E, Kacar C, Tuncer T, Butun B. The association of syndesmophytes with vertebral bone mineral density in patients with ankylosing spondylitis. J Rheumatol 2005; 32:292–294. 57. Jansen TL, Aarts MH, Zanen S, Bruyn GA. Risk assessment for osteoporosis by quantitative ultrasound of the heel in ankylosing spondylitis. Clin Exp Rheumatol 2003; 21:599–604. 58. Andresen R, Werner HJ, Schober HC. Contribution of the cortical shell of the vertebrae to mechanical behaviour of the lumbar vertebrae with implications for predicting fracture risk. Br J Radiol 1998; 71:759–765. 59. Kraag G, Stokes B, Groh J, et al. The effects of comprehensive home physiotherapy and supervision on patients with ankylosing spondylitis—a randomised controlled trial. J Rheumatol 1990; 17:228–233. 60. Wynn Parry CB. Physical measures of rehabilitation. In Moll JMH (ed). Ankylosing Spondylitis. Edinburgh, Churchill Livingstone, 1980, pp 214–226. 61. Tishler M, Brostovski Y, Yaron M. Effect of spa therapy on patients in Tiberias with ankylosing spondylitis. Clin Rheumatol 1995; 1:21–25. 62. Haslock I. Ankylosing spondylitis: management. In Hochberg MC, Silman AJ, Smolen JS, et al (eds). Rheumatology. Amsterdam, Elsevier, 2003, pp 1211–1224.

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Progressive Scleroderma Karsten Jablonka and Jürgen Freyschmidt

ETIOLOGY Progressive scleroderma (progressive systemic sclerosis) is one of the collagen vascular diseases, which makes it one of the systemic autoimmune disorders. Collagen vascular diseases include: ● ● ● ● ● ● ● ●

Progressive systemic sclerosis (progressive scleroderma) Systemic lupus erythematosus Polymyositis and dermatomyositis Sjögren’s syndrome Jo-1 syndrome Mixed connective tissue disease (Sharp’s syndrome) Undifferentiated inflammatory systemic connective tissue disease Relapsing polychondritis

These diseases have in common a fibrinoid degeneration of the connective tissues. Typical features are clinical overlap phenomena and non–organ-specific autoantibodies.

PREVALENCE AND EPIDEMIOLOGY Scleroderma is a rare disease with an estimated prevalence of about 1 new case per 100,000 persons per year. The peak incidence is between 30 and 50 years of age. About 90% of patients are female.

CLINICAL PRESENTATION Clinical features include an insidious onset with Raynaud’s phenomenon, shrinking of skin, especially of the fingertips (Madonna fingers) and the face (microstomia), and swallowing difficulties as a result of an immobilization of the esophagus or the small bowel. A claw-like deformity of the hands and “rat-bite” mutilations of the fingertips may occur. Soft tissue calcifications are common. These deposits can ulcerate through the skin. The sclerosis leads to a restricted mobility of the affected skin, including the tongue (Fig. 50-1). Other clinical features are poikiloderma, telangiectases, and alopecia; pulmonary arterial hypertension; pleurisy; and a pulmonary fibrosis.

The myocardial abnormalities that are associated with systemic sclerosis usually are subclinical. Pericarditis may develop. Vasculitis in the kidneys can lead to infarctions, hypertension, and loss of function. A distinct group of mostly female patients suffers from typical features of organ involvement of systemic sclerosis but show only limited or no skin involvement. Diffuse involvement of the skin is more typical for male patients.1,2

PATHOPHYSIOLOGY Pathology Activation of T cells, monocytes, and macrophages leads to a production of cytokines, stimulating fibroblast proliferation and leading to increased collagen synthesis. Additionally endothelial cell damage leads to intimal proliferation, which accounts for an occlusive vasculopathy. Ultimately, infarcts and necrosis occur in the skin, bone (typically osteolytic lesions), kidneys, and other organs.3,4 Variants of classic progressive systemic sclerosis are: ● ●

●

Localized scleroderma (morphea): localized cutaneous sclerosis without involvement of internal organs CRESTA syndrome stands for calcinosis, Raynaud’s phenomenon, esophageal dysfunction, sclerodactyly, telangiectasia, and arthritis (this supposedly has a better prognosis) Secondary progressive systemic sclerosis as a result of exposure to chemicals or certain drugs such as solvents, polyvinyl chloride, bleomycin, and many others.

KEY POINTS ■ ■ ■ ■

Hardening and retraction of skin Soft tissue calcifications Organ infarctions Soft tissue and bone necrosis

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■ FIGURE 50-1

● Arthropathies and Neurologic/Muscular Disorders and Connective Tissue Disease

Sclerosis of the frenulum of the tongue.

■ FIGURE 50-2

Raynaud phenomenon of the first through third distal phalanges of the left hand and the second and third distal phalanges on the right, with fingertip necrosis and ulcerating calcification of the third distal phalanx on the left.

IMAGING TECHNIQUES In typical cases of scleroderma the clinical diagnosis is straightforward. Radiography is the modality of choice to depict soft tissue calcifications and locate possible future ulcerations. Shrinking of soft tissues, especially the fingertips, is also detectable on radiographs. MRI has been utilized for its ability to show sites of active inflammation that eventually will form necrosis and calcification. Organ involvement is visualized using an upper gastrointestinal series or abdominal CT or MRI.

MANIFESTATIONS OF THE DISEASE Radiography Flexion contracture is present in more than 90% of patients. The most prominent feature is a typical interstitial calcinosis (Thibierge-Weissenbach syndrome). Another feature is a diffuse osteoporosis of the hands with resorption of the distal phalanges and terminal tufts. Additionally, the bones of the wrist sometimes show fine osteolytic or cystic lesions. Definition of atrophy of the soft tissues of the fingertips5 has been described as when the distance from the edge of soft tissue of the fingertip to the end of the distal phalanx is less than 20% of the width of the base of the distal phalanx. In healthy individuals this ratio is at least 25% (Figs. 50-2 to 50-4). Osteolytic foci and erosions may be seen in other skeletal regions (Figs. 50-5 and 50-6).

Computed Tomography

■ FIGURE 50-3

Fingertip necrosis, with retraction of the fingertips.

Computed tomography is advantageous to localize soft tissue calcifications and to characterize possible erosions and osteolytic foci.

Magnetic Resonance Imaging Contrast-enhanced MRI is capable of showing sites of “active disease” with signs of edema that in the later stages of the disease will evolve into the chronic phase (“sclerosing disease”).6

Classic Signs ■ ■ ■

Interstitial calcinosis (Thibierge-Weissenbach syndrome) Resorption of distal phalanges and terminal tufts May occur in other sites (e.g., ribs and spine)

CHAPTER

■ FIGURE 50-4 deviation).

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● Progressive Scleroderma

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Soft tissue calcifications of the fingers (with ulnar

■ FIGURE 50-6

Soft tissue calcifications at the elbow.

DIFFERENTIAL DIAGNOSIS Scleroderma is generally a clinical diagnosis. The Raynaud phenomenon, which is painful blanching of the skin of the face (especially the nose and ears), hands (especially the fingers), and feet (especially the toes), alternating with blueness and redness that is often induced by temperature variations, especially in combination with swallowing difficulties and organ infarction, makes the diagnosis straightforward. It is much more difficult to establish the diagnosis in patients with limited cutaneous (musculoskeletal) involvement.7 In less well-defined cases the primary differential diagnosis is composed of the other collagen vascular diseases. Laboratory tests are not very sensitive for detection of progressive scleroderma. On the other hand, anti-centromeric antibodies and antibodies against the chromosomal antigen Scl-70 are highly specific. Of all the known antibodies that are related to scleroderma, anti-topoisomerase I antibodies seem to have the greatest association with digital joint deformity and distal osteolysis.8,9

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment ■ FIGURE 50-5

Soft tissue calcifications at the shoulder.

The search for an effective therapy for patients with progressive systemic sclerosis has been frustrating. Until now

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the most widely used drug has been nifedipine. Iloprost seems to have potential. Methotrexate, cyclophosphamide, and other anti-inflammatory drugs are also being evaluated.3

What the Referring Physician Needs to Know ■

Surgical Treatment The goals of surgery for advanced progressive systemic sclerosis affecting the hand are pain relief through sympathectomy and increased perfusion, improving mobility through resection arthroplasty, and repositioning the digit to provide a functional position for fusion.

■

■

Like other collagen vascular diseases, progressive systemic sclerosis involves specialists of different medical fields, especially dermatology, vascular surgery, immunology, rheumatology, gastroenterology, and orthopedic surgery. The disease is characterized by inflammatory and fibrotic changes of the skin, synovial membranes, and internal organs (gastrointestinal tract, lungs, kidneys, heart) that result from excessive production of collagens and from obliterative changes in small blood vessels. Late in the course of the disease radiologically visible changes occur.10

SUGGESTED READINGS Bassett LW, Blocka KL, Furst De, et al. Skeletal findings in progressive systemic sclerosis (scleroderma). AJR Am J Roentgenol 1981; 136:1121–1126. Bogoch ER, Gross DK. Surgery of the hand in patients with systemic sclerosis: outcome and considerations. J Rheumatol 2005; 32:642–648.

Hanlon R, King S. Overview of the radiology of connective tissue disorders in children. Eur J Radiol 2000; 33:74–84. Leighton C. Drug treatment of scleroderma. Drugs 2001; 61:419–427. LeRoy EC, Black C, Fleischmajer R, et al. Scleroderma (systemic sclerosis): classification, subsets and pathogenesis. J Rheumatol 1989; 15:202–205.

REFERENCES 1. Coghlan JG, Mukerjee D. The heart and pulmonary vasculature in scleroderma: clinical features and pathobiology. Curr Opin Rheumatol 2001; 13:495–499. 2. Pinstein ML, Sebes JI, Leventhal M, Robertson JT. Case report 579: Progressive systemic sclerosis (PSS) with cervical cord compression syndrome: osteolysis and bilateral facet arthropathy. Skeletal Radiol 1989; 18:603–605. 3. Faggioli P, Giani L, Mazzone A. Possible role of iloprost (stable analog of PG12) in promoting neoangiogenesis in systemic sclerosis. Clin Exp Rheumatol 2006; 24:220–221. 4. Vlachoyiannopoulos PG, Drosos AA, Wiik A, Moutsopoulos HM. Patients with anticentromere antibodies, clinical features, diagnoses and evolution. Br J Rheumatol 1993; 32:297–301. 5. Yune HY, Vix VA, Klatte EC. Early fingertip changes in scleroderma. JAMA 1971; 215:1113–1116. 6. Bonél H, Messer G, Seemann M, et al. [MRI of the fingers in patients with systemic scleroderma: early results of contrast-

7.

8. 9. 10.

enhanced examinations on a dedicated MRI system.] Radiologe 1997; 37:794–801. German. Poormoghim H, Lucas M, Fertig N, Medsger TA Jr. Systemic sclerosis sine scleroderma: demographic, clinical, and serologic features and survival in forty-eight patients. Arthritis Rheum 200; 43:444–451. Ferri C, Bernini L, Cecchetti R, et al. Cutaneous and serologic subsets of systemic sclerosis. J Rheumatol 1991; 18:1826–1832. Jacobsen S, Halberg P, Ullman S, et al. Clinical features and serum antinuclear antibodies in 230 Danish patients with systemic sclerosis. Br J Rheumatol 1998; 37:39–45. Pope JE, Ouimet JM, Krizova A. Scleroderma treatment differs between experts and general rheumatologists. Arthritis Rheum 2006; 55:138–145.

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Systemic Lupus Erythematosus Corinna Schorn and Gerwin Lingg

ETIOLOGY Despite the explosion of the molecular genetic research in the past decades the etiology of this prototype autoimmune disease is still elusive. A confusing complexity of serologic, immunopathologic, and genetic phenomena have been described, most of which are likely to be secondary effects. The current main hypotheses for the initiation of autoimmune response propose a defect in the clearance of apoptotic cells (cells undergoing programmed cell death).1 Apoptotic cells release nucleosomes and histones, the typical autoantigens in systemic lupus erythematosus (SLE), from the nucleus into the cytoplasm. Ultraviolet irradiation leads to cell surface expression of lupus autoantigens of dying keratocytes.2 Because apoptosis is a normal physiologic event, this means it is controlled by immunotolerance: SLE is only manifested when apoptosis is combined with certain autoimmune characteristics. The precise susceptible condition is unknown and probably varies from one affected individual to another. Consequently, a considerable genetic heterogeneity with variable relationships and occasional multiple associations in differing populations and clinical phenotypes exist. A number of genes are important for characterization of the disease risk: class II HLA genes, complement component genes/tumor necrosis factor, and immunoglobulin receptor genes.3–9 However, there is a high frequency of associated alleles in the normal population suggesting complex factor composition, incomplete penetrance, and environmental influences. HLA genes have an important role in the immune response. The products of class II genes (DR, DQ, DP) present peptides from the extracellular milieu to CD4+ helper cells. Excessive or poorly controlled T-helper cells are involved in the activation and differentiation of autoantibody-forming B cells.10 The cellular dysfunction is influenced by genetic and hormonal factors and probably triggered by viruses, particularly retroviral products, ultraviolet radiation, and certain drugs. The result is an excessive autoantibody formation with characteristics of a secondary immune response (polyclonal IgG) resembling

properties of antibodies to foreign antigens. Complement deficiency decreases the ability to eliminate immune complexes both from circulation and from tissues.The immune complex deposition causes tissue damage, vasculitis, and glomerulonephritis.

PREVALENCE AND EPIDEMIOLOGY The characterization of serologic phenomena in the past century with better recognition of mild cases transformed SLE from a rare fulminant disease to a relatively common entity with a wide range of manifestations and a chronic course. The racial/ethnic and gender differences in incidence and prevalence are considerable. For the U.S. white population incidence rates are reported to be approximately 0.5 and 3.5 per 100,000 for men and women, respectively, which is similar to the European rates.11,12 The incidence is increased in African Americans, reaching 1.5 and 10 per 100,000 for men and women, respectively.

KEY POINTS Musculoskeletal complaints are common in SLE, but imaging often remains unremarkable. ■ Typical lupus-associated findings include ■ Symmetric nonerosive polyarthritis of the small joints ■ Jaccoud-like arthropathy (joint deformities in absence of joint destruction) ■ Myositis, which is (in contrast to myalgia) not frequent but which indicates a dismal outcome ■ Disease complications and treatment associated findings include: ■ Osteonecrosis, mostly of the hip but also in unusual or multiple sites ■ Bone infarctions ■ Tendon rupture ■ Septic arthritis ■ Rarely, in more or less typical SLE, destructive arthritis or tuftal resorption and soft tissue calcifications may occur. ■

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Prevalence is 15 and 50 per 100,000. Interestingly in Africa the disease is rare. Asian populations seem to exhibit increased prevalence rates compared with Caucasians. The peak onset of the disease is in early and middle adulthood, in the child-bearing years of women, although it may begin at any age.13 Mortality rates for SLE patients are increased by a factor of 3 to 5 compared with the general population. Risk factors for SLE-related mortality include older age at disease onset; male sex; African American ethnicity, which is eventually linked with low socioeconomic status; disease severity at the time of diagnosis; and especially renal and central nervous system involvement.14 Early diagnosis and modern treatment options have contributed to improvement in the survival rate over the past 50 years, which is now approaching 70% over 20 years.15,16

CLINICAL PRESENTATION Various symptoms and symptom combinations are seen depending on organ systems involved.17 Nonspecific complaints include weakness, fever, malaise, fatigue, loss of appetite, and weight loss. Major abnormalities affect the skin, musculoskeletal system, central and peripheral neural systems, kidneys, lungs, and cardiovascular system. Skin manifestations with photosensitivity are very common. Patients present typically with a malar rash with butterfly appearance or a discoid rash with keratotic scaling. Musculoskeletal involvement constitutes the most common presenting manifestation. The spectrum ranges from weakness, myalgia, and arthralgia to myositis and joint deformities. Morning stiffness, pain, tenderness, soft tissue swelling, and moderate joint effusion are associated with symmetric polyarthritis. Arthritis affects commonly the small joints of the hand, the wrists, and the knees with a migratory, relapsing or chronic deforming course. Tenosynovitis and spontaneous tendon ruptures occur. In late stages, especially with prolonged corticosteroid medication, localized arthralgia may be the result of osteonecrosis. This most commonly affects the hips but may involve any joint. Multiple or unusual sites of involvement are characteristic for SLE. Myalgia and weakness are equivocal complaints that may be from joint disease, fibromyalgia, medications, or sometimes true myositis. Neuropsychiatric disorders with cerebral thrombotic vasculopathy as well as peripheral neuropathy may occur. Cognitive dysfunction, personality changes, seizures, ataxia, hemiplegia, and chorea are possible symptoms.18 Frequently, patients complain about headache. However, it is difficult to determine in which cases headaches are part of the disease spectrum.19 Renal involvement can lead to proteinuria and hematuria, hypertension,nephrotic or nephritic syndrome,progressive glomerulonephritis, and chronic renal failure.20 Pulmonary symptoms include pleurisy with effusion, pneumonia, vasculitis, fibrosis, and atelectasis. Cardiovascular disease comprises cardiomyopathy, pericarditis, endocarditis, and vasculitis. Peripheral thrombophlebitis or vasculitis may occur. Gastrointestinal manifestations include peritonitis, pancreatitis, perihepatitis, and intestinal involvement. Splenomegaly and lymphadenopathy are less frequent.

Patients are prone to infections, probably due to secondary effects of the immune related disease and immunosuppressive medication. Serologic findings include anemia, leukopenia, abnormalities of the plasma proteins (hyperglobulinemia, hypalbuminemia), positive rheumatoid factor, cryoglobulinemia, and low serum complement activity. More specific signs are LE cells and antinuclear factors. Recent development of advanced immunologic tests have significantly improved the diagnostic evaluation.21 Genetic studies reveal an association to major histocompatibility complex HLA-DR2, HLA-DR3, and HLA-B8. Patients with SLE have multiple risk factors for osteoporosis. Lupus disease–associated damage, renal involvement, corticosteroid medication, low body mass index, and especially older age are associated with reduced bone mineral density. In addition, vitamin D deficiency is common. Osteoporosis with vertebral fractures develops in 4% to 20% of SLE patients, and osteopenia occurs in 40% to 50%.22,23 This is a significant comorbidity and mandates routine bone mineral density evaluation in SLE patients with multiple risk factors.

PATHOLOGY Systemic lupus erythematosus manifests in multiple organs. Prominent pathologic features are the generalized immunocomplex deposition that forms, for example, the lupus band (a feature of immunofluorescence), vasculitis, and a thrombotic microangiopathy. Hematoxylin (LE) bodies are a characteristic but not very frequent finding in various tissues. They correspond to basophilic lumpy structures consisting of chromatin and immunoglobulin. The LE cell is a phagocyte with ingested LE-body material, an in-vitro phenomenon. The histo/immunopathology reflects the basic mechanisms of tissue injury. For example, in the skin the immunoglobulins are deposited at the dermal-epidermal junction and may be found in normal or affected skin. Ultraviolet irradiation leads to increased apoptosis of keratinocytes with subsequent nuclear debris and immune complex precipitation. In acute lesions in the upper regions of the dermis a vascular, perivascular, and periappendageal inflammation and mononuclear cell infiltration is prominent. Liquefactive degeneration of the basal cell layer of the dermis and fibrinoid necrosis is present. The universal immune complex deposition in the walls of small arteries and arterioles with or without inflammatory response and facultatively necrotizing vasculitis is very characteristic for SLE. Similar aspects may be found in multiple organs. Renal involvement with mesangial deposits and hypercellularity or proliferative, sclerosing, or membranous features has major impact on the disease course, and the World Health Organization classification of glomerulonephritis allows prognostic conclusions. Interestingly, most cerebral involvement constitutes thrombotic lesions associated with anticardiolipin or antiphospholipid antibodies, and only a minority correspond to vascular inflammation. Compared with these major findings in multiple organs the musculoskeletal disease appears relatively unremarkable. Histologic examination of the synovium

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in acute lupus arthritis reveals perivascular inflammatory cell infiltrates, mild synovial cell proliferation, and mild fibrinous deposition. In the chronic stage the synovial cell proliferation may increase, but usually it remains moderate compared with rheumatoid arthritis. Features of tenosynovitis are similar to those in arthritis. Tendon ruptures, however, do not exhibit inflammatory changes but indicate degenerative disease. In myositis, histopathology reveals atrophy, microtubular inclusions, and mononuclear cell infiltrates.

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MANIFESTATIONS OF THE DISEASE Musculoskeletal Manifestations Musculoskeletal involvement is only one part of the disease spectrum. Features directly associated with lupus include the following: ● ●

Symmetric polyarthritis Jaccoud-like arthropathy (deformity of the hand in the absence of destructive arthritis).

Disease complications and treatment sequelae comprise:

BIOMECHANICS The typical deforming arthropathy in lupus is characterized by ulnar drift of the digits, swan-neck (hyperextension of the proximal interphalangeal joint and flexion of the distal interphalangeal joint) and boutonnière deformities (flexion of the proximal interphalangeal joint and hyperextension of the distal interphalangeal joint), and hyperextension of the interphalangeal joint of the thumb and is known as Jaccoud’s hand. Destruction and laxity of the metacarpophalangeal joint connective tissues with ulnar slippage of the extensor tendon is the main reason for the ulnar drift.24 The initiation of the swan-neck deformity takes place in the metacarpophalangeal joint. Primarily, the deformities are nonfixed and reversible at the patient’s own efforts with normal active flexion. In later stages, adhesions between the extensor tendons on the dorsum of the proximal interphalangeal joint fix the later band to the middle slip insertion, leading to fixed swan-neck deformity.25 The boutonnière deformity, in contrast to the swan-neck deformity, begins at the proximal interphalangeal joint itself with swelling followed by elongation of the central slip, subluxation of the later bands, and contracture of the retinacular ligament.26 Patients with Jaccoud hands suffer from instability of the metacarpophalangeal joints, pain, weakness, and loss of dexterity. The grip function is severely hampered when the thumb/index finger opposition for the pinch grip is lost. Daily activities such as buttoning and writing become obstacles for affected patients.

IMAGING TECHNIQUES Radiography is the method of choice for evaluation of symptomatic joints. Anteroposterior views of the hands and feet should be taken using high-resolution technique. These images must guarantee display of soft tissues and bony structures at the same time to assess for fusiform articulosynovitis. In cases of osteonecrosis, radiographic images do not provide early diagnosis. Additional methods such as MRI or nuclear bone scan may be necessary. For tendon disease, ultrasonography is advantageous. MRI for myositis is performed with short tau inversion recovery (STIR), spectral presaturation inversion recovery (SPIR), or T2-weighted turbo spin-echo, fat saturated and T1-weighted spin-echo pulse sequences in coronal and axial planes mostly of the thigh or calf. Usually, contrast medium–enhanced sequences do not provide additional information.

● ● ●

Osteonecrosis Spontaneous tendon weakening and rupture Septic arthritis due to immunologic impairment and/or immunosuppressive therapy

Soft tissue calcifications and tuftal resorption or destructive arthritis are features sometimes associated with SLE and, if pronounced, may be signs of an overlap syndrome with scleroderma or rheumatoid arthritis, respectively.

Radiography Symmetric polyarthritis is very common (90% of patients). The predilection sites are the small joints of the hand and feet, the wrists, knees, and shoulders. Synovial soft tissue swelling especially at the proximal interphalangeal and metacarpophalangeal joints is frequent. Periarticular demineralization may progress to diffuse osteoporosis. In contrast to findings in rheumatoid arthritis, no joint space narrowing, marginal erosion, or destruction occurs. Sometimes small subchondral cysts are visible and are thought to correspond to micronecrotic foci. In long-standing disease 4% to 50% of patients develop a Jaccoud-like arthropathy also known as deforming nonerosive arthropathy that is characterized by reducible joint deformities (Fig. 51-1). Because deformities are reduced by the radiographer the radiographic image is to some degree insensitive. Swan-neck deformities, boutonnière deformities, and hyperextension of the interphalangeal joint as well as ulnar deviation of the metacarpophalangeal joint is typical. Unless associated with rheumatoid arthritis usually no joint destruction occurs. If present, joint space narrowing is not a result of cartilage destruction but a sign of atrophy and erosions are not caused by pannus invasion but by pressure in subluxation. SLE patients are prone to epiphyseal osteonecrosis and metaphyseal/diaphyseal bone infarction with a frequency of 5% to 40%.27,28 Avascular necrosis is not strongly associated with corticosteroid therapy or disease-related vasculitis, but it is more frequent in such cases.29 Often atypical (metacarpal and metatarsal heads, carpals), multiple, or symmetric sites are affected—a feature relatively suggestive for SLE.30 Nevertheless, the femoral head is the most frequent site of manifestation. The radiologic appearance of avascular necrosis does not differ in patients with and without SLE. Subchondral fracture, depression, fragmentation of the osseous surface, sclerosis, and cyst formation are signs of avascular necrosis. Secondarily, degenerative osteoarthritis leads to osteophyte formation, cartilage loss, sclerosis, and cyst formation of the opposing joint surface.

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■ FIGURE 51-2

Osteonecrosis of the humeral head. There is a large defect of the humeral head resulting from necrosis and resorption of the necrotic fragments. In this late stage, the contours are smooth and well defined and secondary degenerative disease takes place.

Magnetic Resonance Imaging ■ FIGURE 51-1

Radiographic imaging of the hand in systemic lupus erythematosus. Because deformities of the finger joints are corrected by the radiographer, they may become apparent only when they are fixed. Therefore, the swan-neck deformities and increased flexion of the metacarpophalangeal joints displayed in this patient are not an early sign of Jaccoud’s hand. There are no erosions despite the advanced deformity, a feature very suggestive of SLE, but the clinical diagnosis usually precedes this finding. In general the radiographic appearance of the hands remains unremarkable in SLE despite considerable clinical symptoms.

Radiographic imaging is not positive in early cases; in fact, a normal radiograph in patients with hip pain and corticosteroid therapy should raise the suspicion for osteonecrosis (Fig. 51-2) and additional imaging (MRI or bone scan) should be performed. Bone infarctions present as serpiginous lines of calcification centrally in the metaphysis and/or diaphysis of long bones surrounding and surrounded by apparently normal bone. If the calcified rim of the osteonecrosis is not entirely visible, especially in smaller bones, wavy lines of sclerotic shadows are seen. Soft tissue calcification and tuftal resorption have been described in SLE patients, but these features may be a sign of an overlap syndrome with scleroderma. Diffuse linear, streaky, plaque-like, or nodular calcifications are found subcutaneously or periarticularly, sometimes associated with skin lesions.31 Septic arthritis and osteomyelitis as complications of SLE show similar features as in standard cases.

Spontaneous tendon weakening and rupture is much more frequent in SLE patients than in degenerative disease. Its features do not differ from those in normal individuals, and likewise it is mostly associated with local or systemic corticosteroid therapy. The best imaging techniques are ultrasound and MRI. An acute and subacute rupture is characterized by surrounding fluid, edema, and tendon sheath effusion. The tendon is attenuated, and in complete rupture the retracted end is curled and wavy (Fig. 51-3). Incomplete rupture is characterized by intermediate signal intensity on T1-weighted images, intratendinous dots or stripes of fluid signal, decreased or increased diameter, or deformity. MRI is much more sensitive for a vascular necrosis than radiographic imaging. In SLE, epiphyseal osteonecrosis often occurs in unusual sites. The features, however, do not differ from osteonecrosis in otherwise normal individuals. Geographically shaped or triangular bone marrow edema is seen in ARCO (Association Recherche Circulation Osseous) stage I, followed by demarcation by the so-called doubleline sign in ARCO stage II (serpiginous line of hypointensity on T1-weighted images and hyper/hypointense double line on T2-weighted images at the margin of the necrotic area). An insufficiency fracture of the affected epiphyseal area is called a crescent sign, representing ARCO stage III. In stage IV, deformity and secondary degenerative osteoarthritis have taken place. The necrotic area itself may exhibit various signal characteristics from fat to sclerosis or fluid components. Myalgia is reported in up to 40% of patients, but only 4% develop myositis with pain, diffuse tenderness, weakness, atrophy, and elevated muscle enzymes. Myositis is a risk factor for dismal outcome.32 In some patients it may

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C

A

■ FIGURE 51-3

B

be part of an overlap syndrome. MRI is sensitive to muscle edema and fatty atrophy. Contrast medium enhancement may be seen in affected muscles.

Multidetector Computed Tomography Computed tomography is not in the routine diagnostic algorithm for SLE musculoskeletal manifestations.

Spontaneous tendon rupture. Pain and swelling at the ulnar styloid process primarily raised suspicion of tenosynovitis. Coronal (A), transverse (B), and sagittal (C) planes show the retracted extensor carpi ulnaris tendon end curling inside the synovial sheath (arrow).

Ultrasonography For spontaneous tendon rupture in most cases ultrasonography is an excellent diagnostic method. An acute and subacute rupture is characterized by surrounding fluid, edema, and tendon sheath effusion. The tendon pattern is inhomogeneous, and in complete rupture the retracted end is curled and wavy.

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Nuclear Medicine Hip pain despite normal radiography in SLE patients with or without corticosteroid therapy is typical for osteonecrosis of the femoral head. MRI and nuclear medicine are powerful tools for definitive diagnosis. 99 mTc-methylene diphosphonate triphasic bone scintigraphy reveals arterial hypoperfusion and a cold area in the femoral head. SPECT is considered to be positive when a cold defect is detected with or without presence of adjacent increased uptake (cold spot within a hot spot).33 Later stages may show a hot spot within a hot spot.

Classic Signs ■ ■ ■

■ ■

■

Nonerosive polyarthritis: synovial soft tissue swelling, demineralization Deforming arthropathy (Jaccoud’s hand): ulnar drift of the digits, swan-neck and boutonnière deformities Avascular necrosis: commonly affecting the hips, characteristically multiple or unusual sites ■ Radiographic: early—occult; late—subchondral fracture, fragmentation ■ MRI: well-defined epiphyseal region of signal alteration sharply demarcated by the double-line sign (ARCO classification) ■ Bone scan: triangular area of hypoperfusion Bone infarctions: radiographs/MRI—metaphyseal and/or diaphyseal serpiginous lines Spontaneous tendon ruptures: ultrasound/MRI—edema, retracted tendon end in complete ruptures, thickened attenuated tendon in incomplete ruptures Septic arthritis: radiographic—patchy demineralization, rapid destruction

DIFFERENTIAL DIAGNOSIS Some of the most common symptoms of SLE are completely nonspecific. The changeable nature and the intermittently relapsing multiplicity of features make the diagnosis challenging. Primarily established for research purposes, the classification criteria serve as helpful for the diagnosis, although by no means describing the complete disease spectrum (Table 51-1).34 Positivity for at least 4 of the 11 criteria allows classification of a patient as having SLE. Serologic features are widely used to confirm a clinical diagnosis, but antibodies cannot be used alone to diagnose autoimmune disease. The LE cell phenomenon was primarily considered to be lupus specific. Now it is clear that it can be present in some other autoimmune conditions, for example, in 16% of patients with rheumatoid arthritis. Nevertheless, it is positive in 50% to 70% of lupus patients. Antinuclear antibodies (ANA) are highly important in the diagnosis of SLE. A negative ANA test makes the diagnosis of SLE unlikely. Some of the antibodies seen in SLE are specific for certain subgroups: anti-dsDNA antibodies and anti-Sm are highly specific for SLE, anti-histone is common in drug-induced lupus, and anti-Ro and anti-La occur in SLE and Sjögren’s disease. Almost all sera containing

TABLE 51-1 1997 Revised Criteria for Diagnosis of Systemic Lupus Erythematosus Malar rash Discoid rash Photosensitivity Oral ulcers Arthritis (two or more peripheral joints) Serositis Renal disorders (proteinuria, cellular casts) Neurologic disorders (seizures, psychosis) Hematologic disorders (hemolytic anemia, leukopenia, lymphopenia, thrombopenia) Immunologic disorders (antibodies to native DNA, anti-Sm, antiphospholipid) Antinuclear antibodies

Data from Hochberg MC. Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum 1997; 40:1725.

anti-Sm also contain anti-RNP. The converse, however, anti-RNP without anti-Sm, is typical for mixed connective tissue disease. Anti-ssDNA antibodies are produced in infections and other autoimmune disorders. Antibody levels are not appropriate for monitoring disease activity. Most imaging features of SLE, especially the musculoskeletal afflictions (e.g., nonerosive polyarthritis or osteonecrosis), are highly nonspecific. Nonerosive deforming arthropathy was primarily described in poststreptococcal disease, which is nowadays very rare. Therefore, the Jaccoud hand is considered to be a sign of SLE; but it is no early manifestation, and radiographic imaging is insensitive to reducible deformities. Usually the diagnosis is known or suspected from clinical and serologic criteria and imaging is performed to exclude destructive arthritis or complications. Musculoskeletal complaints such as arthralgia and myalgia are frequent constitutional symptoms, along with fever, malaise, and fatigue, and can occur alone or may accompany organ flares. In this setting it is important to bear in mind the differential diagnosis of an infectious disease.

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment Nonsteroidal Anti-inflammatory Drugs For lupus-associated constitutional symptoms such as musculoskeletal complaints in the acute phase, NSAIDs are often effective and if not may be combined with lowdose corticosteroid therapy. Adverse effects of NSAIDs may mimic features of SLE, such as nephritis, liver enzyme abnormalities, or neuropsychiatric symptoms. If there is doubt, NSAIDs should be discontinued before assuming a flare.

Corticosteroids Corticosteroids are promptly efficacious for resolving the inflammatory activity of a lupus flare. For control of arthralgia and myalgia, low-dose therapy in addition

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to NSAIDs is frequently necessary. High-dose therapy is reserved for life- or organ-threatening active disease. After disease control, dose tapering and finally total discontinuation should be attempted. However, many patients require maintenance therapy to prevent flares. In this case antimalarial agents or, in more severe cases, immunosuppression should be considered.

Antimalarial Agents Antimalarial agents are commonly used for chronic therapy for repeatedly recurrent or persistent constitutional symptoms especially when corticosteroids cannot be discontinued. These agents have complex immunomodulatory effects, and the response is to be expected with a delay of several weeks. The combination of different antimalarial agents (hydroxychloroquine, chloroquine, quinacrine) is synergistic. Smoking significantly decreases the efficacy of these drugs. A special adverse effect, the hemolytic anemia in glucose-6-phosphate dehydrogenase deficiency, mandates screening before administration, especially in people of African descent. The toxic effect on the retina is of major concern and is dose and duration dependent. Because early lesions are reversible, careful follow-up with ophthalmologic examinations is mandatory.

Immunosuppressive Agents

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Methotrexate Methotrexate is useful in lupus arthritis and also in corticosteroid-sparing and antimalarial- resistant constitutional disease. However, lupus patients seem to be more prone to adverse effects, such as hepatopathy compared with patients with rheumatoid arthritis. Teratogenic effects must be considered.

Surgical Treatment Numerous procedures are available for the operative correction of the Jaccoud hand, such as realignment of the ulnarly drifted digits by soft tissue rebalancing and extensor centralization or, in later stages with fixed deformity and articular surface damage, arthroplasty. The choice of the surgical procedure is dependent on the ability for passive correction, state of the articular cartilage, and/or the presence of additional deformities. Boutonnière deformities do not limit the hand function to the same degree as swan-neck deformities and ulnar drift of the digits.35 The goal of surgical deformity correction is the induction of pain relief and re-creation of balance of forces with improvement of the grip function.36 However, late recurrence remains a problem.37,38

What the Referring Physician Needs to Know ■

Azathioprine If corticosteroid discontinuation is not possible, azathioprine may be used as a corticosteroid-sparing drug. Additionally, it is used for patients with repeated flares. Women of child-bearing age need effective contraception because of its teratogenic effects. Nevertheless, for the fetus the risk of a lupus flare is considerable, and for this reason azathioprine is not necessarily discontinued during pregnancy.

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■ ■ ■

Typical deformities of the hands may be inconspicuous on radiographic images because they are routinely reduced by radiographers. Destructive arthritis, tuftal resorption, and calcifications may be signs of an overlap syndrome. Patchy demineralization and rapid joint destruction are suggestive of infectious arthritis. Discrepancy between considerable joint pain, especially at the hip joints, and unremarkable radiography may be a sign of osteonecrosis and calls for MRI or bone scan.

SUGGESTED READINGS Gladman DD, Urowitz MB. Connective tissue disorders: Systemic lupus erythematosus. In Hochberg MC, Silman AJ, Smolen JS, et al (eds). Rheumatology, 3rd ed. St. Louis, Mosby, 2003, pp 1285–1430.

Resnick D. Systemic lupus erythematosus. In Resnick D, Niwayama G (eds). Diagnosis of Joint and Bone Disorders, 2nd ed. Philadelphia, WB Saunders, vol 2, 1988.

REFERENCES 1. Gaipl US, Voll RE, Sheriff A, et al. Impaired clearance of dying cells in systemic lupus erythematosus. Autoimmun Rev 2005; 4:189–194. 2. LeFeber WP, Norris DA, Ryan SR, et al. Ultraviolet light induces binding of antibodies to selected nuclear antigens on cultured human keratinocytes. J Clin Invest 1984; 74:1545–1551. 3. Merrill JT, Buyon JP. The role of biomarkers in the assessment of lupus. Best Pract Res Clin Rheumatol 2005; 19:709–726. 4. Takeuchi T, Tsuzaka K, Abe T, et al. T cell abnormalities in systemic lupus erythematosus. Autoimmunity 2005; 38:339–346. 5. Arnett FC, Reveille JD, Moutsopoulos HM, et al. Ribosomal P autoantibodies in systemic lupus erythematosus: Frequencies in different ethnic groups and clinical immunogenetic associations. Arthritis Rheum 1996, 39:1833–1839.

6. Steinsson K, Jonsdottir S, Arason GJ, et al. Ann Rheum Dis 1998; 57:503–505. 7. Hong GH, Kim HY, Takeuchi F, et al. Association of complement C4 and HLA-DR alleles with systemic lupus erythematosus in Koreans. J Rheumatol 1994; 21:442–447. 8. Howard PF, Hochberg MC, Bias WB, et al. Relationship between C4 null genes, HLA-D region antigens and genetic susceptibility to systemic lupus erythematosus in Caucasian and black Americans. Am J Med 1986; 81:187–193. 9. Reveille JD, Moulds JM, Ahn C, et al. Systemic lupus erythematosus in three ethnic groups: I. The effects of HLA class II, C4, and CR1 alleles, socioeconomic factors, and ethnicity at disease onset. LUMINA Study Group. Lupus in minority populations, nature versus nurture. Arthritis Rheum 1998; 41:1161–1172.

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10. Crow MK. Cellular immunology. In Hochberg MC, Silman AJ, Smolen JS, et al. Rheumatology, 3rd ed. St. Louis, Mosby, 2003, pp 1347–1358. 11. Hochberg MC. The incidence of systemic lupus erythematosus in Baltimore, Maryland, 1970–77. Arthritis Rheum 1985; 28:80–86. 12. McCarty DJ, Manzi S, Medsger TA, et al. Incidence of systemic lupus erythematosus: race and gender differences. Arthritis Rheum 1995; 38:1260–1270. 13. Petri M. Epidemiology of systemic lupus erythematosus. Best Pract Res Clin Rheumatol 2002, 16:847–858. 14. Waard MM, Pyun E, Studenski S. Long-term survival in systemic lupus erythematosus: patient characteristics associated with poorer outcomes. Arthritis Rheum 1995; 38:274–283. 15. Abu-Shakra M, Urowitz MB, Gladman DD, Gough J. Mortality studies in systemic lupus erythematosus: results from a single centre: II. Predictor variables for mortality. J Rheumatol 1995; 22:1265–1270. 16. Petri M, Genovese M. Incidence of and risk factors for hospitalisations in systemic lupus erythematosus: a prospective study of the Hopkins Lupus Cohort. J Rheumatol 1992; 19:1559–1565. 17. Haq I, Isenberg DA. How does one assess and monitor patients with systemic lupus erythematosus in daily clinical practice? Best Pract Res Clin Rheumatol 2002; 16:181–194. 18. Hermosillo-Romo D, Brey RL. Neuropsychiatric involvement in systemic lupus erythematosus. Curr Rheumatol Rep 2002; 4:337–344. 19. Cuadrado MJ, Sanna G. Headache and systemic lupus erythematosus. Lupus 2003; 12:943–946. 20. Balow JE. Clinical presentation and monitoring of lupus nephritis. Lupus 2005; 14:25–30. 21. Esdaile JM, Joseph L, Abrahamowicz M, et al. Routine immunologic tests in systemic lupus erythematosus: is there a need for more studies. Comment in: J Rheumatol 1996; 23:1891–1896. 22. Leventhal GH, Dorfman HD. Aseptic necrosis of bone in systemic lupus erythematosus. Semin Arthritis Rheum 1974; 4:73–93. 23. Siemsen JK, Brook J, Meister L. Lupus erythematosus and vascular bone necrosis: a clinical study of three cases and review of the literature. Arthritis Rheum 1962; 5:492–501. 24. Bielefeld T, Neumann DA. The unstable metacarpophalangeal joint in rheumatoid arthritis: anatomy, pathomechanics and physical rehabilitation considerations. J Orthop Sports Phys Ther 2005; 35:502–520.

25. Heywood AW. The pathogenesis of the rheumatoid swan neck deformity. Hand 1979; 11:176–183. 26. Ferlic DC. Boutonnière deformities in rheumatoid arthritis. Hand Clin 1989; 5:215–222. 27. Abeles M, Urman JD, Rothfield NF. Aseptic necrosis of bone in systemic lupus erythematosus: relationship to corticosteroid therapy. Arch Intern Med 1978; 138:750–754. 28. Urman JD, Abeles M, Houghton AN, Rothfield NF. Aseptic necrosis presenting as wrist pain in SLE. Arthritis Rheum 1977; 20:825–828. 29. Budin JA, Feldmann F. Soft tissue calcifications in systemic lupus erythematosus. Am J Roentgenol 1975; 124:358. 30. Dayal NA, Isenberg DA. SLE/myositis overlap: are the manifestations of SLE different in overlap disease. Lupus 2002; 11:293–298. 31. Bultink IE, Lems WF, Kostense PJ, et al. Prevalence of and risk factors for low bone mineral density and vertebral fractures in patients with systemic lupus erythematosus. Arthritis Rheum 2005; 52:2044–2050. 32. Pineau CA, Urowitz MB, Fortin PJ, et al. Osteoporosis in systemic lupus erythematosus: Factors associated with referral for bone mineral density studies, prevalence of osteoporosis and factors associated with reduced bone density. Lupus 2004; 13:436–441. 33. Ryu JS, Kim JS, Moon DH, et al. Bone SPECT is more sensitive than MRI in the detection of early osteonecrosis of the femoral head after renal transplantation. J Nucl Med 2002; 43:1006–1011. 34. Hochberg MC. Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum 1997; 40:1725. 35. Boyer MI, Gelberman RH. Operative correction of swan-neck and boutonniere deformities in the rheumatoid hand. J Am Acad Orthop Surg 1999; 7:92–100. 36. Wood VE, Ichtertz DR, Yahiku H. Soft tissue metacarpophalangeal reconstruction for treatment of rheumatoid hand deformity. J Hand Surg 1989: 14:163–174. 37. Burezq H, Polyhronopoulos GN, Beaulieu S, et al. The value of radial collateral ligament reconstruction and abductor digiti minimi release in metacarpophalangeal joint arthroplasty. Ann Plast Surg 2005; 54:397–401. 38. Dell PC, Renfree KJ, Below Dell R. Surgical correction of extensor tendon subluxation and ulnar drift in the rheumatoid hand: longterm results. J Hand Surg 2001; 26:560–564.

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Mixed Connective Tissue Disease Corinna Schorn and Gerwin Lingg

ETIOLOGY, EPIDEMIOLOGY, AND PREVALENCE The distinctiveness of the connective tissue diseases is less pronounced than the classification system implies. In practice there is a continuous spectrum of symptom combinations, merging features of various entities. Mixed connective tissue disease (MCTD) is the prototype of an overlap syndrome, combining features of systemic lupus erythematosus (SLE), systemic scleroderma (SSc), polymyositis (PM), and rheumatoid arthritis (RA). As described by Sharp and colleagues, MCTD constitutes a likewise separate entity and is now, despite previous debate, a commonly used label for the anti-U1-RNP–associated disease spectrum.1–6 The etiology underlying this special symptom combination is unknown. There are several hypotheses, such as the induction of autoantibodies due to molecular mimicry after retrovirus infection (or Epstein-Barr virus infection) or defects in the clearance of apoptotic cells similar to SLE concepts. The exact prevalence and incidence rates are unknown but estimated to be approximately one of every four SLE patients. The female predominance is nearly 10-fold. Genetic studies show mostly HLA-DR4 and HLA-Dw4 association, a genetic background that is different from that of SLE patients.7

CLINICAL PRESENTATION Due to the overlapping nature, MCTD does not present a constant clinical picture. Especially in the early disease course the diagnosis often remains limited to undifferentiated connective tissue disease (UCTD). This term, however, has received its own definition and can self-sufficiently serve as a basis for patient care.8,9 In patients with Raynaud’s phenomenon, factors have been defined that have prognostic significance for the future development of a specific connective tissue disease.10 Most patients with UCTD and anti-U1 RNP develop MCTD.11

Nonspecific signs such as fatigue, weight loss, and fever are often associated with more specific manifestations, the latter including: ● ● ● ● ● ● ● ● ● ● ●

Puffy hands Raynaud’s phenomenon Keratoconjunctivitis sicca Arthralgia, unexplained polyarthritis Myalgia, myositis Skin symptoms: rash, sclerodactyly Serositis Central nervous system symptoms, peripheral neuropathy Fibrosing alveolitis and pulmonary hypertension Esophageal dysfunction Adenopathy, hematologic disorders

Presentation with symptoms of two or more welldefined connective tissue diseases (SLE, SSc, RA, PM) is typical. Even the characteristic of swollen hands may incorporate features of more specific diseases: erythema of the dorsum of the proximal interphalangeal joint and metacarpophalangeal joint like in PM or sclerodactyly and fixed finger flexion like in SSc. The disease course may be stable over many years or progress to one of the

KEY POINTS In early disease the most prominent finding on radiographs of the hands may be the soft tissue swelling. If present, more specific radiographic signs may appear slightly atypical, owing in part to the combination of features of two different connective tissue diseases and in part to an unusual involvement or an irregular distribution of the polyarthritis compared with RA. ■ Prognosis is not always favorable. One should especially search for pulmonary hypertension with or without fibrosing alveolitis at regular follow-up evaluations and treat myositis efficiently. ■

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well-defined connective tissue diseases in later stages (i.e., evolving into more or less typical SLE, SSc, PM, or RA). Serologic findings include raised erythrocyte sedimentation rate (ESR) and elevated C-reactive protein (CRP), which are nonspecific signs of inflammation. The presence of antibodies against U1 ribonucleoprotein (antiU1-RNP) is fundamental for the diagnosis and has been initially stressed to be specific.4,12–15 Nowadays it is known that high titers can also be found in 40% of patients with SLE, as well as some cases of SSc, RA, PM and other overlapping syndromes.16–19 IgG and complement levels are usually high. In addition to clinical overlap, serologic overlap has also been recognized. Antinuclear antibodies (ANA) and rheumatoid factor (Waaler-Rose as well as enzymelinked immunosorbent assay) may be found in patients with MCTD, and anti-ds-DNA and anti-Sm suggest SLE. Sharp and colleagues initially described a favorable prognosis. However, this notion has been disproven; myositis as well as fibrosing alveolitis and pulmonary hypertension are potentially fatal, and therefore the overall prognosis is worse than that for SLE.7,20–22

MANIFESTATIONS OF THE DISEASE Multiple classification criteria sets have been proposed owing to the variability of the disease presentation and course. Alarcón-Segovia’s criteria have been accepted for the definition of MCTD and include only five clinical criteria.23 Prerequisite is a high titer of anti-U1 RNP; however, the exact levels for assays commonly used have not been described. Clinical criteria are swollen hands, Raynaud’s phenomenon, acrosclerosis, synovitis, and myositis. According to Alarcón-Segovia, MCTD can be diagnosed with reasonable specificity and sensitivity when in addition to the serologic marker, three clinical criteria are present. If the criteria of swollen hands, Raynaud’s phenomenon, and acrosclerosis are positive, one of the other two criteria is additionally necessary. Fulfillment of the criteria of another connective tissue disease (RA, SLE, SSc, PM) in a patient with positive diagnosis of MCTD should not be considered an association but refers to the nature of MCTD being an overlap syndrome itself.

RADIOGRAPHY Radiographically the overlapping nature of the disease is once more confirmed.24,25 Bone and soft tissue abnormality often resemble SSc. Joint involvement is more variable and shows features of RA or SLE, sometimes with a slightly atypical pattern ranging from mild effusion to mutilating arthritis. Diffuse soft tissue swelling of the hand and periarticular or diffuse osteoporosis are nonspecific signs. RA features such as synovitis, joint space narrowing, marginal erosions that progress to destruction, and deformities with predilection for the metacarpophalangeal and proximal interphalangeal joints, wrist, and metatarsophalangeal and interphalangeal joints can be seen. Slightly atypical RA manifestations have been stressed to be typical for MCTD, that is, asymmetric involvement, distal interphalangeal joint involvement, and postarthritic capitate-trapezoid ankylosis.26,27 Deformity without joint destruction is some

■ FIGURE 52-1 Mixed connective tissue disease. Anteroposterior view of the hand shows periarticular demineralization (arrows). Soft tissue loss of the tip of the index finger, soft tissue calcification, and bandlike destruction of the distal interphalangeal joints resemble the features of scleroderma. Carpal involvement and soft tissue swelling due to tenosynovitis of the extensor carpi ulnaris are similar to the findings in rheumatoid arthritis. (Courtesy of Dr. Kapp, Schlangenbad, Germany.)

hint of the SLE component. Osteonecrosis of the femoral head, condyles, diaphysis, carpal bones, and metacarpal heads may occur with or without corticosteroid therapy. SSc-like involvement includes soft tissue atrophy and calcification, tuft resorption, and band-like distal interphalangeal joint destruction (Fig. 52-1). Punctate, linear, or extensive soft tissue calcification with predilection for the fingertips and periarticular as well as subcutaneous location is not uncommon (Fig. 52-2).

SYNOPSIS OF TREATMENT OPTIONS Treatment depends entirely on the pattern of clinical involvement. For arthralgia and arthritis as well as constitutional symptoms nonsteroidal anti-inflammatory agents are used and, if needed, combination with low-dose corticosteroid therapy has been shown to be effective. It is very important to monitor and treat the serious manifestations of myositis as well as fibrosing alveolitis and pulmonary hypertension. For more severe disease, immunosuppressive drugs such as cyclophosphamide are used, followed by maintenance therapy with drugs such as azathioprine.

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A

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C

B

■ FIGURE 52-2

Mixed connective tissue disease. A to C, Late stage with subcutaneous calcifications (B, arrow) and atypical erosive arthritis. The arthritis affects the carpals with joint space narrowing and postarthritic instability (bent arrow indicates the tilted scaphoid) and secondary degenerative osteoarthritis with subchondral sclerosis. The metacarpophalangeal joints show small erosions similar to rheumatoid arthritis; the proximal and distal interphalangeal joints are already severely deformed (A, arrowhead). Atypical distal interphalangeal joint arthritis is present with erosions in the third and fourth fingers and ankylosis in the fifth finger. Note the sclerosis of the unguicular processes, which is unspecific but relatively frequent in systemic lupus erythematosus.

Classic Signs ■ ■

Nonspecific signs are the most common finding. Polyarthritis ranges from nonerosive to a mutilating course, but only sometimes with unusual involvement or distribution compared with RA.

■

Mixture of radiologic symptoms belonging to two or more “classic” connective tissue diseases is very typical but not regularly seen.

SUGGESTED READINGS Mixed connective tissue disease and collagen vascular overlap syndromes. In Resnick D: Diagnosis of Joint and Bone Disorders, 4th ed. Philadelphia, WB Saunders, 2002, vol 2, pp 1249–1259.

Venables PJW. Overlap syndromes. In Hochberg MC, Silman AJ, Smolen JS, et al (eds): Rheumatology, 3rd ed. St. Louis, Mosby, 2003, pp 1573–1580.

REFERENCES 1. Sharp GC, Irwin WS, Tan EM, et al. Mixed connective tissue disease: an apparently distinct rheumatic disease syndrome associated with a specific extractable nuclear antigen. Am J Med 1972; 52:148–159. 2. Maddison PJ. Mixed connective tissue disease: overlap syndromes. Baillieres Best Pract Res Clin Rheumatol 2000; 14:111–124. 3. Hoffman RW, Greidinger EL. Mixed connective tissue disease. Curr Opin Rheumatol 2000; 12:386–390. 4. Nimelstein SH, Brady S, McShane D, Holman HR. MCTD: a subsequent evaluation of the original 25 patients. Medicine 1980; 59:239–248. 5. Reichlin M: Problems in differentiating SLE and MCTD. N Engl J Med 1976; 295:1194–1195.

6. Gendi NST, Welsh KI, Van Venrooij WJ, et al. HLA type as a predictor of mixed connective tissue disease differentiation. Arthritis Rheum 1995; 38:259–266. 7. Ruuska P, Hämeenkorpi R, Forsberg S, et al. Differences in HLA antigens between patients with mixed connective tissue disease and systemic lupus erythematosus. Ann Rheum Dis 1992; 51:52–55. 8. Alarcón GS, Williams GV, Singer JZ, et al. Early undifferentiated connective tissue disease: I. Early clinical manifestation in a large cohort of patients with undifferentiated connective tissue disease compared with cohorts of well established connective tissue disease. J Rheumatol 1991; 18:1332–1339.

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9. Clegg DO, Williams HJ, Singer JZ, et al. Early undifferentiated connective tissue disease: II. The frequency of circulating antinuclear antibodies in patients with early rheumatic diseases. J Rheumatol 1991; 18:1340–1343. 10. Kallenberg CGM: Connective tissue disease in patients presenting with Raynaud’s phenomenon alone. Ann Rheum Dis 1991; 50:666–667. 11. Lundberg I, Hedfors E. Clinical course of patients with anti-RNP antibodies: a prospective study of 32 patients. J Rheumatol 1991; 18:1511–1519. 12. Alarcón-Segovia D, Villareal M. Classification and diagnostic criteria for mixed connective tissue disease. In Kasukawa R, Sharp GC (eds). Mixed Connective Tissue Disease and Antinuclear Antibodies. Amsterdam, Elsevier, 1987, pp 33–40. 13. Kasukawa R, Tojo T, Miyawaki S: Preliminary diagnostic criteria for classification of mixed connective tissue disease. In Kasukawa R, Sharp GC (eds). Mixed Connective Tissue Disease and Antinuclear Antibodies. Amsterdam, Elsevier, 1987, pp 41–47. 14. Sharp GC. Diagnostic criteria for classification of MCTD. In Kasukawa R, Sharp GC (eds). Mixed Connective Tissue Disease and Antinuclear Antibodies. Amsterdam, Elsevier, 1987, pp 23–32. 15. Alarcón-Segovia D, Cardiel MA. Comparison between 3 diagnostic criteria for connective tissue disease: Study of 593 patients. J Rheumatol 1989; 16:328–334. 16. Sharp GC, Irwin WS, May CM. Association of antibodies to ribonucleoprotein and Sm with mixed connective tissue disease, systemic lupus erythematosus and other rheumatic diseases. N Engl J Med 1976; 29:1149–1154. 17. Leibfarth JH, Perselin RH. Characteristics of patients with serum antibodies to serum extractable nuclear antigens. Arthritis Rheum 1976; 9:851–856.

18. Farber SJ, Bole GG. Antibodies to components of extractable nuclear antigens. Arch Intern Med 1976; 136:425–431. 19. Lemmer JP, Curry NH, Mallory JH. Clinical characteristics and course in patients with high titer anti-RNP antibodies. J Rheumatol 1982; 9:536–542. 20. Cooke CL, Lurie HI: Case report: Fatal gastrointestinal hemorrhage in mixed connective tissue disease. Arthritis Rheum 1977; 20:1421–1426. 21. Weiss TD, Nelson JS, Woosley RM, et al. Transverse myelitis in mixed connective tissue disease. Arthritis Rheum 1978; 21:982–986. 22. Jones MB, Osterholm RK, Wilson RB, et al. Fatal pulmonary hypertension and resolving immune-complex glomerulonephritis in mixed connective tissue disease. Am J Med 1978; 65: 855–862. 23. Amigues JM, Cantagrel A, Abbal M, Mazieres B. Comparative study of 4 diagnosis criteria sets for mixed connective tissue disease in patients with anti-RNP antibodies. J Rheumatol 1996; 23:2055–2062. 24. Resnick D. Mixed connective tissue disease and collagen vascular overlap syndromes. In: Resnick D, Niwayama G (eds): Diagnosis of Joint and Bone Disorders, 2nd ed. Philadelphia, WB Saunders. 2002, vol 2, pp 1342–1352. 25. Udoff EJ, Genant HK, Kozin F, Ginsberg M. Mixed connective tissue disease: The spectrum of radiographic manifestations. Radiology 1977; 124:613–618. 26. Bennett RM, O’Connel DJ: The arthritis of mixed connective tissue disease. Ann Rheum Dis 1978; 37:397–403. 27. Halla JT, Hardin JG. Clinical features of the arthritis of mixed connective tissue disease. Arthritis Rheum 1978; 21:497–503.

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C H A P T E R

Juvenile Idiopathic Arthritis Karl Johnson

ETIOLOGY

Pathology

Juvenile idiopathic arthritis (JIA) represents a heterogeneous group of autoimmune disorders that begin in childhood and involve persistent inflammation of one or more joints. It is a disorder of unknown etiology, but in a minority of cases there is an association with rheumatoid factor and human leukocyte antigen (HLA)-B27. The JIA classification of childhood arthropathies unifies and replaces the criteria of juvenile rheumatoid arthritis (JRA), used by the American College of Rheumatology, and juvenile chronic arthritis (JCA), used by the European League Against Rheumatism. The purpose of this new classification is to be able to identify disease entities of true etiologic and pathologic homogeneity. The different subclassifications of JIA and the corresponding JRA and JCA equivalents are shown in Table 53-1.1–5

Within the joint the primary pathologic process is autoimmune-related synovial proliferation. There is associated soft tissue swelling and effusion. This is a hypervascular process that can result in periarticular osteopenia, localized bone overgrowth, and remodeling. If left untreated, the synovial proliferation will cause cartilage thinning and bone erosions. Involvement of adjacent soft tissues and ligaments can cause joint deformity and loss of function. Initially, the hypervascularity can cause accelerated localized growth, but in the patient with more chronic disease there is reduction in growth.7–10

PREVALENCE AND EPIDEMIOLOGY The incidence of JIA is 6 to 12 per 100,000, with a prevalence of approximately 1 in 1,000. Overall, females are more affected than males.1

CLINICAL PRESENTATION The diagnosis of JIA is a clinical one, in which there is persisting arthritis for at least 6 weeks in a child younger than the age of 16 years in whom there is no known underlying cause. Other symptoms include general fatigue, weight loss, fevers, and generalized systemic ill health. There may be associated lymphadenopathy, pericarditis, hepatosplenomegaly, dermatologic features, pleuritis, interstitial lung disease, and uveitis.1,5

PATHOPHYSIOLOGY Anatomy The disease can affect any joint. Extra-articular sites include the eye (uvea), chest, heart, and skin. Systemic symptoms may be widespread and generalized.5–8

IMAGING TECHNIQUES Techniques and Relevant Aspects Radiographs of an involved joint are useful as a primary imaging investigation to exclude other causes of joint disease such as dysplasias, tumors, and other localized pathologic processes such as Legg-Calvé-Perthes disease. The radiographic features are osteopenia, periarticular swelling, epiphyseal overgrowth, loss of joint space, and erosions. There may be subluxation of the joint and periosteal new bone formation in bone adjacent to the joint.5,6,9,10 Ultrasonography will demonstrate hypoechoic joint effusions with thickened mixed echogenic synovial lining of the joint. Synovial cysts and inflammatory changes

KEY POINTS Sepsis needs to be excluded in all children with an inflamed joint. ■ MRI with gadolinium enhancement is most sensitive in detecting synovial hypertrophy. ■

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TABLE 53-1 Classification of Different Subtypes of Juvenile Idiopathic Arthritis and Comparison with Previous Classification Systems Characteristic

JIA (ILAR)

JCA (EULAR)

JRA (ACR)

Age at onset Minimum duration of symptoms Subtypes

upper extremity) and the spine. Syphilitic and alcoholic neuropathies affect the weight-bearing joints of the lower extremity, most commonly the knee. Alcoholic pedal neuroarthropathy manifests in the forefoot.5 The inherited nerve disorder of Charcot-Marie-Tooth disease (type 1 demyelization, type 2 axonal) is manifested by progressive motor and sensory neuropathy due to damage to the peroneal nerve. Fatty replacement and atrophy of calf and pedal flexor and extensor muscles results in high arch and claw-toe deformities.6 Diabetic neuroarthropathy usually affects the ankle and tarsus and, less commonly, the metatarsophalangeal joints. Large-joint Charcot involvement does occur in diabetes, although uncommonly.7 The neuroarthropathy of Hansen’s disease commonly involves the feet or hands, resembling other conditions with sensory deficit, such as frostbite and scleroderma. Vertebral involvement is seen with cord pathologic processes such as meningomyelocele, congenital insensitivity to pain,8 syphilis, and, rarely, diabetes. If the spine is fused, Charcot changes usually are seen just caudal to the lowest fused level (Fig. 60-2).3 With congenital insensitivity to pain, trivial trauma may result in fracture or epiphyseal detachment. Beginning at birth, manifestations include fractures, dislocations, Charcot joints, osteonecrosis, and osteomyelitis, most commonly of femur, tibia, metatarsals, and spine (Fig. 60-3).9,10 In the chronic setting, the extremities may be shortened due to premature epiphyseal fusion.

■ FIGURE 60-2 Vertebral Charcot joint with fracture and frank vertebral dislocation, just caudal to the level of stabilization hardware.

Diabetic Pedal Neuropathy Pedal neuropathy is often asymmetric in diabetics, with the acutely affected foot edematous, with or without pain. Chronic motor neuropathy produces muscle atrophy resulting in alignment deformities.11,12 If neuropathy is unchecked, Charcot changes may ensue. The acute Charcot foot will be hot and edematous with

■ FIGURE 60-3 Congenital insensitivity to pain. Anteroposterior radiograph shows comminuted fracture of the distal humerus with fragmentation and exuberant callus formation. The known context of congenital insensitivity to pain militates against a diagnosis of tumor. (Courtesy of Gary Gold, MD, Stanford University, Palo Alto, CA.)

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palpable pulses and is clinically worrisome for cellulitis or even osteomyelitis. The mean skin temperature increases from 2° to 5° C in the Charcot joint as compared with the contralateral foot.13 Rearfoot valgus, forefoot adductus, and hypermobile joints are common. Diabetic ischemic ulcers usually occur at the toes or the plantar aspect of the first and fifth metatarsal heads14 and are shallow, erythematous, and painful and do not bleed. In contradistinction, diabetic neuropathic ulcers are fungating and callused, may bleed, can be painless, and typically occur over midfoot and hindfoot bony protuberances.

PATHOPHYSIOLOGY Jean Martin Charcot posited that neuropathic arthropathy (usually luetic in the 1860s) resulted from damage to the central nervous system and “trophic” peripheral centers controlling the nutrition of bones and joints. His concepts are no longer in currency, but Charcot’s name continues as the descriptor for neuropathic osteoarthopathy. Two theories—the neurovascular and the neurotraumatic—elucidate the pathophysiology of neuroarthropathy. According to the neurovascular theory, in the absence of neural stimulus to the extremities, sympathetic tone is compromised. This results in vasodilatation and hyperemia in the soft tissues and marrow, predisposing to osteopenic subchondral bone liable to pathologic fractures.15 The fractures can heal with exuberant and bizarre callus formation. Diabetic Charcot changes require intact vascularity. Therefore, diabetic persons with vasculopathy and neuroarthropathy are nearly mutually exclusive cohorts, although there are case examples of persons with vasculopathy developing neuropathy after a revascularization procedure.16 The neurotraumatic theory explains neuroarthropathy as the result of diminished proprioception and loss of normal sensory feedback, with progressive joint destruction from repeated trauma. The patient may be unaware of the problem and add insult to injury by continuing to use the joint. Most likely, both neurotraumatic and neurovascular causes are collusive in the diabetic neuropathic foot. Furthermore, hyperglycemia causes adverse effects on nerve metabolism, perineural vasoconstriction, and hypoxia. It is not understood why Charcot foot is often unilateral and occurs only in a small subset of diabetics.

Anatomy Regarding pedal neuroarthropathy, the foot can be divided longitudinally into medial and lateral columns, with the medial column involved earlier and more frequently by neuroarthropathy. In diabetics, the forefoot is more often involved with ischemia and the midfoot and hindfoot are more often involved with neuroarthropathy. The weightbearing line is drawn from the calcaneal tuberosity to the sesamoids on lateral radiographs taken with the patient bearing weight. If the pedal arch collapses and a bony structure extends below this line (i.e., rocker-bottom deformity), the overlying soft tissues may ulcerate (Fig. 60-4).

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■ FIGURE 60-4 The weight-bearing line is drawn on a standing lateral view of the foot between the plantar aspect of the calcaneus and the sesamoid bones. Any bone extending below this line in the setting of arch collapse comprises a “rocker” exostosis.

■ FIGURE 60-5 Gross specimen of a Charcot joint (knee) shows bone and cartilage fragments embedded in the synovium. (Courtesy of German Steiner, MD, Hospital for Joint Diseases, New York, NY.)

Pathology The gross Charcot foot specimen has bone fragments embedded in synovium (Fig. 60-5). On histologic study the specimen may demonstrate calcium, cartilage, and shards of bone lining the deep layers of the synovium. This is termed detritic synovitis and may also be seen with osteonecrosis, calcium pyrophosphate deposition disease, psoriatic arthritis, and osteoarthritis. Biopsy may be performed to confirm infected Charcot foot or differentiate Charcot foot from tumor (e.g., chondrosarcoma is occasionally initially considered in Charcot shoulder), but biopsy and histologic analysis are infrequently performed now to diagnose an uninfected Charcot joint.

BIOMECHANICS Regarding pedal neuroarthropathy, in advanced Charcot joint disease, the plantar arch (medial > lateral) may collapse, resulting in a rocker-bottom deformity. There are several orthopedic classification systems for evaluation of patterns of pedal collapse. The classification system developed by Schön and colleagues17 delineates four midfoot and hindfoot patterns that are readily discernable on radiographs and cross-sectional studies:

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may be misleading, if there is clinical concern for infection either an MR scan or a nuclear medicine study may be requested.

Controversies Marrow edema in the setting of neuropathy or Charcot joint may enhance after the intravenous administration of gadolinium. If osteomyelitis is considered, the demonstration of marrow enhancement on routine MRI does not increase specificity. Gadolinium enhancement does improve sensitivity for secondary signs of osteomyelitis, including ulcer, adjacent sinus tracts and abscesses; and enhancement may help differentiate necrosis and abscess from vascularized tissue.18

MANIFESTATIONS OF THE DISEASE Radiography

■ FIGURE 60-6

A, Lateral radiograph of the foot demonstrates the Lisfranc pattern of arch collapse (Schön pattern I) with fracturedislocation at the tarsometatarsal joints. The cuboid bone protrudes below the weight-bearing line. B, Lateral view of the foot demonstrates the transtarsal pattern of arch collapse (Schön pattern IV) with downturned talar head, dislocated from the navicular. There is reversal of the normal calcaneal pitch, with anterior calcaneus and cuboid fragment “rocker” exostoses.

Class I: Lisfranc pattern at the tarsometatarsal joints (Fig. 60-6A) Class II: Naviculocuneiform pattern Class III: Chopart/perinavicular pattern Class IV:Transverse tarsal pattern (see Fig. 60-6B) with plantargrade talar head, subluxed or dislocated from the navicular bone. As the pedal arches collapse, weight bearing transfers to bone protruding below the weight-bearing line, the plantar-prominent “rocker.” The pathogenesis of ulcer formation is not fully understood but may be related to ischemia and subcutaneous tissue breakdown over these plantar exostoses, allowing the ingress of pathogens. Awareness of the collapse patterns helps the radiologist localize the site of infection.

IMAGING TECHNIQUES Techniques and Relevant Aspects Imaging of a suspected neuropathic joint should always begin with routine standard radiographs and comparison with results of examinations if available. Because radiographs

In the setting of a warm erythematous neuropathic joint, the radiologist may be asked to exclude superimposed infection. Radiographs may be negative or show soft tissue swelling and osteopenia. If Charcot derangement ensues, radiographs reveal classic findings of joint disorganization, dislocation, debris, and destruction. Charcot changes may occur gradually or catastrophically with derangement within days of minor trauma, such as a twisted ankle. Charcot osteoarthropathy evolves from the acute osteopenic phase (which mimics infection) to the bone-forming phase, characterized by exuberant repair, osteosclerosis, and bony fragmentation. A chronic neuroarthropathic joint shows derangement, bony hypertrophy, eburnation, and subchondral cysts. With offloading and casting, the hyperemia abates and the joint may be stabilized, but ulcers can develop over bony protuberances (see Chapter 65, Diabetic Pedal Infection). Radiographs can be misleading in all phases of Charcot joint deformity, because the “bag of bones” may be so fragmented and indistinctly marginated that infection can be overcalled.

Magnetic Resonance Imaging Magnetic resonance imaging is the anatomic gold standard for evaluating the neuropathic joint. It reveals edema due to neuropathic vasodilatation in the subcutaneous soft tissues, the muscles, and the bone marrow. Before the development of frank Charcot joint disease, marrow edema seen on MRI is presumed to be due to medullary hyperemia. This is called the “ghost sign” and in the absence of ulcer or other signs of soft tissue infection does not imply osteomyelitis (Fig. 60-7). If the neuropathic joint collapses, interpretation of MRI is challenging. There are significant overlapping MRI findings between acute Charcot foot and infection, including effusions, adventitial bursae, and extensive soft tissue and bone marrow edema. The marrow edema in noninfected neuroarthropathy has an articular epicenter (Fig, 60-8), whereas osteomyelitis has a marrow epicenter, involving fewer bones (Fig. 60-9).18 It should be stressed that, in adults, pedal infection is introduced transcutaneously in more than 90% of cases. If there is no ulcer, osteomyelitis is unlikely, despite the

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■ FIGURE 60-7 Short-axis, T2-weighted, fat-saturated MR image of the midfoot shows marrow edema of the cuneiforms. In the absence of secondary soft tissue findings of infection, this comprises the MRI “ghost sign” and reflects medullary hyperemia, not osteomyelitis. ■ FIGURE 60-9 T1-weighted, fat-saturated, postcontrast, short-axis image of the midfoot shows an ulcer and tract directly underlying an edematous and enhancing first cuneiform. This bone protrudes below the weight-bearing line. Regardless of the presence of marrow edema in the adjacent bones due to Charcot foot collapse, the association of the tract and ulcer to the first cuneiform raises suspicion of osteomyelitis in this bone. (Courtesy of Mark Schweitzer, NYU Medical Center, New York City.)

frankly disconcerting marrow edema that is seen in acute Charcot foot. A close assessment of the marrow edema and arch collapse patterns, in concert with a search for “rocker” exostoses and associated secondary soft tissue findings, allows for a more confident and accurate differentiation. This directs a more conservative débridement.

Multidetector Computed Tomography Computed tomography can be useful for evaluating subtle flake fractures, such as an early Lisfranc fracturedislocation. It is of limited utility in differentiating the uninfected from the infected Charcot joint, but contrast enhancement helps with abscess localization. CT is useful to diagnose the extensive perivertebral bone fragments characteristic of spinal Charcot deformity but not expected in infection or neoplasm.

Nuclear Medicine ■ FIGURE 60-8 Acute Charcot foot. Inversion recovery MR image parallel to the plantar surface shows small subchondral fracture lines and marrow edema pattern with an articular epicenter.

The nuclear medicine test of choice to differentiate between Charcot joint and superinfected Charcot deformity is combined indium-111-labeled leukocyte/technetium-99m sulfur colloid scan.

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Classic Signs ■ ■

■

■

Neuropathy (before the development of a Charcot joint)— soft tissue edema Acute Charcot joint: Hyperemic, osteopenic bone is predisposed to fracture, leading to deformity, joint derangement, and bony fragmentation, with an articular epicenter. Chronic Charcot joint: Soft tissue swelling and marrow edema may subside. A stabilized osteoarthritic Charcot joint eventually shows bony ankylosis, subchondral cysts, alignment deformities, and exostoses that predispose to ulcer formation (Fig. 60-10). Infected Charcot joint (acute or chronic): Cutaneous ulcer over a bony exostosis or “rocker” prominence may track to bone or joint, leading to septic arthritis and/or osteomyelitis. This results in characteristic MRI findings of synovial and osseous infection. In the acute setting, this is difficult to tease from the “backdrop” of neuropathic edema and joint disorganization, but knowledge of collapse patterns and likely “rocker” location can direct the search for the likeliest site(s) of infection.

A Charcot joint will show either no focal white cell accumulation or white cell activity correlating to the distribution of marrow as imaged by 99mTc sulfur colloid. Osteomyelitis will show focal white cell accumulation without corresponding marrow activity.19

DIFFERENTIAL DIAGNOSIS Neuroarthropathy may mimic, and be misdiagnosed as, cellulitis, osteomyelitis, gout, severe osteoarthritis, and, rarely, matrix-producing tumor. Spinal Charcot deformity may resemble discitis or even neoplasm. Delay in diagnosis is common. Peripheral nerve function is tested with SemmesWeinstein monofilaments, which test perception of sensation with different thickness filaments and distances between filaments applied to the skin. Electrodiagnostic testing (velocity and electromyography) may be required to establish the etiology and level of a neural insult. Dermal thermography of Charcot foot is assessed with a handheld, infrared thermometer.

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment Since the mid 1990s the trend for treating the acute Charcot joint has been immobilization and non–weight bearing with casting or bracing to halt the cascading joint destruction. If an ulcer is present, infection should be excluded. Débridement is kept as minimal as feasible. A surgical shoe, brace, or total contact cast is used to offload an ulcer. Nonoperative treatment is preferred, but up to 50% of patients with Charcot deformities eventually undergo surgery for ulcer recurrence or painful arthropathy.

Surgical Treatment Salvage arthrodesis is becoming the procedure of choice over amputation.20,21 Arthrodesis provides for corrective reshaping of deformities and elimination of instability. Internal fixation is performed if there is no ulcer, and external fixation (with pins at a distance from the infection site) is done if there is ulceration. The goal is stability and remodeling of the deformity not joint function, that is, an ambulating flat foot.

What the Referring Physician Needs to Know ■ FIGURE 60-10 Chronic Charcot foot. T1-weighted, fat-saturated MR image parallel to the plantar surface after intravenous administration of gadolinium. Hyperemia has subsided, but hindfoot derangement, subchondral cysts, and synovial enhancement are present. Rockerbottom deformity may predispose to ulcers and infection.

■

The critical question posed to the radiologist in the setting of neuroarthropathy and ulcer is: Are the deep soft tissues and/or bones infected?

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SUGGESTED READINGS Brower AC, Allman RM. The neuropathic joint: a neurovascular bone disorder. Radiol Clin North Am 1981; 19:571–580. Gupta RA. A short history of neuropathic arthropathy. Clin Orthop Relat Res 1993; 296, 43–49. Hartemann Huertier A, The Charcot foot. Lancet 2002; 360:1776–1779. Jones EA, Manaster BK, May DA, Disler MD. Neuropathic osteoarthropathy: diagnostic dilemmas and differential diagnosis. RadioGraphics 2000; 20:S279–S293.

Ledermann HP, Morrison WB, Schweitzer M. MR image analysis of pedal osteomyelitis. Radiology 2002; 223:747–755. Ledermann HP, Morrison WB. Differential diagnosis of pedal osteomyelitis and diabetic neuroarthropathy: MR imaging. Semin Musculoskel Radiol 2005; 9:272–328.

REFERENCES 1. National Institute of Neurological Disorders and Stroke. CharcotMarie-Tooth Fact Sheet. NIH 07-4897, 2007. 2. www.cdc.gov/diabetes/statistics 3. Jones EA, Manaster BK, May DA, Disler MD. Neuropathic osteoarthropathy: diagnostic dilemmas and differential diagnosis. RadioGraphics 2000; 20:S279–S293. 4. Tristano AG, Willson ML, Montes De Oca I. Axillary vein thrombosis as a manifestation of rapidly progressive neuropathic arthropathy of the shoulder associated with syringomyelia. Mayo Clin Proc 2005; 80:416–418. 5. Thornhill HL, Richter RW, Shelton ML, Johnson CA. Neuropathic arthropathy (Charcot forefeet) in alcoholics. Orthop Clin North Am 1973; 1:7–20. 6. Stilwell G, Kilcoyne RF, Sherman JL. Patterns of muscle atrophy in the lower limbs in patients with Charcot-Marie-Tooth disease as measured by magnetic resonance imaging. J Foot Ankle Surg 1995; 34:593–596. 7. Lambert AP, Close CF. Charcot neuroarthopathy of the knee in type 1 diabetes: treatment with TKA. Diabet Med 2002; 19:338–341. 8. Ingram CM, Harris MB, Dehne R. Charcot spinal arthropathy in congenital insensitivity to pain. Orthopedics 1996; 19:251–255. 9. Gherlinzoni F, Gherlinzoni G. Neurogenic joint disease secondary to congenital insensitivity to pain. Ital J Orthop Traumatol 1982; 8:487–492. 10. Greider TD. Orthopedic aspects of congenital insensitivity to pain. Clin Orthop Relat Res 1983; (172):177–185.

11. Bus SA, Yang QX, Wang JH, et al. Intrinsic muscle atrophy and toe deformity in the diabetic neuropathic foot: a magnetic resonance imaging study. Diabetes Care 2002; 25:1444–1450. 12. Greenman RL, Khaodhiar L, Lima C, et al. Foot small muscle atrophy is present before the detection of clinical neuropathy. Diabetes Care 2005; 28:1425–1430. 13. Archer AG, Roberts VC, Watkins PJ. Blood flow patterns in diabetic neuropathy. Diabetologia 1984; 27:563–567. 14. Ledermann HP, Morrison WB, Schweitzer M. MR image analysis of pedal osteomyelitis. Radiology 2002; 223:747–755. 15. Brower AC, Allman RM. The neuropathic joint: a neurovascular bone disorder. Radiol Clin North Am 1981; 19:571–580. 16. Edelman SV, Kosofsky EM, Paul RA, Kozak GP. Neuroarthropathy (Charcot’s joint) in diabetes mellitus following revascularization surgery. Arch Intern Med 1987; 147:1504–1508. 17. Schön LC, Easley ME, Weinfeld SB. Charcot neuroarthropathy of the foot and ankle. Clin Orthop 1998; (349):116–131. 18. Ledermann HP, Morrison WB. Differential diagnosis of pedal osteomyelitis and diabetic neuroarthropathy: MR imaging. Semin Musculoskelet Radiol 2005; 9:272–283. 19. Palestro CJ, Megta HH, Patel M, et al. Marrow vs. infection in the Charcot joint: indium-111 leukocyte and technetium-99m sulfur colloid scintigraphy. 20. Cooper PS. Application of external fixators for management of Charcot deformities of the foot and ankle. Foot Ankle Clin 2002; 7:207–254. 21. Herbst SA. External fixation of Charcot arthropathy. Foot Ankle Clin 2004; 9:596–609.

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Soft Tissue Disease: Cellulitis, Pyomyositis, Abscess, Septic Arthritis David Wilson and Bridget Atkins

Infections of the soft tissues range clinically from indolent low-grade conditions to fulminant disease that may be life threatening within a matter of hours. A wide range of organisms can produce an infection, although there are common culprits. Clinical confusion may occur because the presentation may mimic tumor or degenerative disease and vice versa. Infection should always be in the mind of those involved in diagnosis of musculoskeletal disorders. Antibiotics provide an important part of the treatment, but in many cases drugs alone are inadequate to deal with the disease. It may be necessary to perform surgery to remove dead and necrotic tissue and allow drainage of deep cavities. Resistance to antibiotic regimens is an increasing problem, and the recognition of failure of response to antibiotic therapy is an important part of the diagnostic process.

Systemic disorders and immune suppression not only change the individual’s susceptibility but also affect the way in which infection manifests and which organisms are the likely cause. Imaging plays a fundamental role in the diagnosis, assessment, treatment, management, and follow-up of patients with soft tissue and bone infection.

PREVALENCE AND EPIDEMIOLOGY Staphylococcus aureus infection is the most common cause of soft tissue infection throughout the world. However, there are regional variations in the incidence and causative organism. For example, abscesses due to melioidosis are typically seen in rice field workers and Mycobacterium marinum is a hazard to those who keep tropical fish.

ETIOLOGY Organisms may be introduced into the body by a variety of means, depending on environmental, organism, and host factors. These routes include inhalation, direct inoculation (often by trauma or surgery), and ingestion. These can be followed by further local invasion, hematogenous or lymphatic spread, and thereby invasion of organisms into regions of the body where their presence is damaging. Once the organism has reached the location where infection might develop, the chance of establishing infection depends on organism factors and the host’s local and systemic immunity. Poor vascular supply, dead or damaged tissue, collections of blood or lymph, and foreign implanted material including endoprostheses all increase the risk of infection. Tumors are also destructive and produce necrotic areas within them that may be the center of secondary sepsis.

KEY POINTS There are a variety of manifestations of soft tissue infection that overlap and merge in some cases. ■ Imaging is useful to define the extent of disease, and this is most accurately achieved by MRI. ■ Ultrasonography is particularly effective at distinguishing abscess cavities from edematous tissue. ■ MRI has supplanted sinography in the definition of sinus tracts and cavities. ■ Image-guided biopsy is useful to confirm the diagnosis and determine the causative organisms. ■ Repeat MRI examination is a useful way to follow progress of therapy. ■

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CLINICAL PRESENTATION

Soft Tissue Swelling with Erythema

Given the wide variety of organisms and means of infections, there are many ways in which soft tissue infection may present. The clinical entities described here are not really separate diseases but more an emphasis of one part of the spectrum. One may lead to the next, and two or more may be present in the same case.

In acute cellulitis and in abscess formation radiographs may show no abnormality. Later in the disease there may be subtle periosteal reaction and large abscesses may cause bone damage. The only circumstance in which early radiography is contributory is when gas-forming organisms are present (e.g., in clostridial myonecrosis) because the gas may be identified. However, these patients are critically ill and clinical features will be more important in the initial assessment. Tissue crepitus is occasionally palpable. The radiologist is unlikely to add to the clinician’s view of the severity of the case by finding gas in the immune-competent patient. Ultrasound examination is useful to discriminate cavitating abscess formation from diffuse cellulitis. Areas of fluid collection may be aspirated both to obtain a microbiologic diagnosis and to alleviate pressure from an abscess cavity. The ultrasound appearances will be of a hypoechoic area that may appear as clear fluid or alternatively could contain particulate matter. The adjacent soft tissues will have increased blood flow on Doppler imaging. MRI is useful for assessing the extent of edema and the size of any abscess cavity. It is the definitive way of determining whether an abscess communicates with a joint. MRI is particularly useful in determining the extent of sinus tracks and the involvement of adjacent bones and has virtually replaced sinography. Although ultrasonography can be used as described earlier, the majority of patients suspected of having an infection should have MRI as the initial examination after radiography.

PATHOLOGY In the early stages of infection when the organism is establishing itself there will be an acute associated inflammatory response leading to soft tissue edema and opening of normal vascular channels with increased blood flow to the affected area. The patient will complain of swelling, pain, and heat if the site is superficial. There is likely to be a systemic response with a febrile illness. Subsequent progress depends on the location and nature of the organisms involved. Some infections lead to rapid tissue destruction and necrosis. This, in turn, leads to systemic toxicity and severe ill health. Septicemic shock, hypotension, and tachycardia may result. In other infections in which the growth rate is slower there may be local destruction of tissue with abscess formation. At first microcavities containing pus will occur, but these may coalesce into larger collections. These abscesses, in turn, may spread and penetrate adjacent structures. They may perforate the skin and discharge through a sinus track. They may enter joint spaces or abdominal viscera. When soft tissue infections are located adjacent to bone they may excite a periosteal reaction and cause underlying bone edema. Those that are particularly destructive may cause erosion of the bone cortex. Infections that begin within or enter joints can cause early damage to the articular cartilage, which intrinsically has a poor blood supply. This destruction is likely to be irreversible. Joint effusion will occur early, either due to pus within the joint or, more commonly, a reactive effusion. Joint space narrowing occurs late because the early manifestation of cartilage involvement will be edema. Secondary osteomyelitis may be due to direct spread of the organism into the adjacent bone. This implies penetration of the articular cartilage and joint capsule if the infection arose primarily within the joint. Osteomyelitis is infection arising principally in bone. However, sometimes it will present as a soft tissue infection due to cortical penetration and spread into the adjacent structures. Chronic infection is when the disease process reaches a stable state or one that is changing very slowly. Here the combination of reactive changes to the infection will be seen with the acute structure or residual necrosis. Chronic abscess cavities may be associated with fibrous reaction in the adjacent soft tissue. Cloacae and sinus tracks may become lined by epithelium. In the very long term, areas of chronic infection may be complicated by amyloid formation and rarely by malignant change.

IMAGING TECHNIQUES Imaging is pivotal in the diagnosis and management of soft tissue and bone infections. The appropriate investigation depends on the clinical presentation.

Unexplained Pain with or without Fever In the assessment of acute osteomyelitis, radiographs may be normal or may show some patchy and localized osteopenia in the region of the infection. The finding of periosteal reaction is a specific one but is not often present in the early stages. Ultrasonography is of less value unless periosteal edema is detected with increased blood flow on power Doppler imaging. This constellation of ultrasound findings is useful in this setting. Unfortunately, patients with acute osteomyelitis may not exhibit this finding. Therefore, the combination of ultrasonography and MRI is the best way to discriminate soft tissue infection from bone infection (Fig. 61-1). The combination of rapid and slow growth in the same patient are features that suggest a lesion is infectious rather than tumorous in origin. Nuclear medicine studies have a minor role to play in the assessment of infection and would probably only be of value when MRI is not available. This technique is less specific than MRI and no more likely to show up areas of edema. The patients normally present with pain in a specific location, and so a limited examination of that area by MRI is appropriate. Furthermore, the epiphyseal regions of the younger child with active growth will show increased radionuclide accumulation on the nuclear medicine study, and this finding may be misleading or confusing. Bone scintigraphy may show areas of uptake in soft tissue infection due to the increased vascular supply and areas of necrosis. A central area of activity void suggests an

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■ FIGURE 61-1 Septic arthritis of the metacarpophalangeal joint of the index finger is seen as rarefaction of bone on either side of the joint. A, Note narrowing of the joint space and marginal erosion. Unlike an inflammatory joint disease this is a monarthropathy isolated to one articulation. B, The infected joint imaged by ultrasound shows thickened and ill-defined joint margins and echogenic (bright) synovial proliferation. C, Note markedly increased blood supply as shown by Doppler ultrasound examination.

abscess. More specific techniques to show infected areas including gallium citrate– and indium chloride–labeled white blood cell scintigraphy. These studies are more specific and have an occasional role in complex cases.

MANIFESTATIONS OF THE DISEASE Cellulitis This is an acute inflammatory response due to a soft tissue infection and is most commonly caused by S. aureus or Streptococcus pyogenes (group A streptococcus). Other organisms are possible offenders depending on the environmental exposure. The infection is usually acquired by inoculation (e.g., via athlete’s foot), although in about half of cases the actual route is unclear. Edema, redness, and swelling may spread throughout the affected limb, producing pain and dysfunction. The patient is likely to have a fever and will feel systemically unwell. Cellulitis may spread in a progressive “wild fire” fashion and sometimes

by a lymphatic spread producing red lines or marks in the distribution of the inflamed lymph tracks. Reactive nodes will be seen in drainage areas. The infection may also spread along tendon sheaths and be relatively confined to these cavities (Fig. 61-2). Today cellulitis is most commonly treated actively and acutely with antibiotics and the more advanced stages of the disease are rare. Prior to antibiotic therapy, soft tissue infection of this type was often lethal. Indeed, the introduction of penicillin to treat patients with acute streptococcal cellulitis produced miraculous results for the times.

Abscess Abscesses may occur as the result of a variety of soft tissue infections. They are probably more commonly associated with infection due to inoculation (Fig. 61-3). S. aureus is the most common cause of an abscess, particularly if it is acquired by a hematogenous route. This includes methicillin-resistant S. aureus (MRSA), particularly if the patient

■ FIGURE 61-2 Soft tissue infection may involve the tendon sheaths. In this case of Staphylococcus aureus tenosynovitis the patient was unable to tolerate the high field magnet. A, This open MR image shows swelling around the carpal tunnel. B, Ultrasound examination shows extensive tenosynovitis and distortion of the tendon sheath, which is filled with thickened echogenic synovial tissue. C, Axial ultrasound image shows marked Doppler signal from the intense vascular reaction.

■ FIGURE 61-3 A, Axial T2-weighted MR image shows a mass in the right psoas muscle that extends through the posterolateral abdominal wall. B, T1-weighted MR image shows that the abscess contains gas. This could be the result of gas-forming organisms, perforation of a viscus, a sinus tract to the skin, or severe central necrosis. In this case, necrosis resulted from a methicillin-resistant Staphylococcus aureus infection.

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has frequent contact with the health care environment. Organisms including bowel flora may also be the source of infection. When abscesses are established, particularly within the sinus tracks, multiple secondary infections may occur, producing a mixed growth on culture.

Impetigo Impetigo is the cutaneous and subcutaneous reaction to S. aureus or Streptococcus pyogenes infection and is more common in children than in adults. It can be bullous or nonbullous and results in crusting lesions often around the mouth and nose.

Acute Septic Arthritis Joint infections may occur at any age. Irritable hip is a clinical condition in children in the 4- to 12-year age range and is most often due to a benign transient synovitis with no apparent cause and no serious sequelae. Unfortunately, imaging (ultrasonography and MRI), although sensitive to the detection of joint effusion, cannot determine its nature because pus looks like transudate on MRI and ultrasonography (Figs. 61-4 and 61-5). Therefore, the small but important minority of cases with septic arthritis may be overlooked. Some patients with sepsis have normal body temperature, normal hematologic investigations, and small joint effusions. The only safe course is to aspirate all effusions found in acutely painful joints and to send the aspirate for urgent microscopy and culture. Fortunately, in many instances, this will also alleviate the symptoms. In the adult patient, debility from other conditions such as systemic arthropathy may mask the signs and symptoms of septic arthritis and a similarly cautious approach must be taken. S. aureus, Streptococcus pneumoniae, and β-hemolytic streptococci are common

■ FIGURE 61-5 Septic arthritis of the knee caused by infection with Pseudomonas. Note the large effusion and the bone marrow edema in the proximal tibia. If these cases are not treated aggressively and rapidly, severe joint destruction is inevitable.

causes of acute septic arthritis in the adult, but Neisseria gonorrhoeae is also a possible factor if there is a relevant sexual history. Effusions should be aspirated and samples sent for microscopy and culture. When gout or pyrophosphate arthropathy is suspected, microscopy for crystals should be requested. Microorganisms in a joint are highly destructive, and permanent damage to the articular surfaces occurs quickly so early therapy is mandatory. Simple aspiration is rarely sufficient, and formal surgical drainage should be combined with antibiotic therapy. In acute prosthetic joint septic arthritis, diagnostic aspiration is also the initial investigation of choice.

Chronic Septic Arthritis

■ FIGURE 61-4 Ultrasound examination of the hip in a child shows an echo-free joint effusion. The appearance of a benign transient synovitis can be identical to that of an aggressive septic arthritis. There are no secure clinical or laboratory indicators of infection to help differentiate the two. Therefore, ultrasound-guided aspiration is the best way to exclude infection and at the same time immediately relieve the patient’s pain.

It is imperative to obtain the microbiologic organism before starting therapy in the case of chronic septic arthritis. In this situation, obtaining a prior environmental and travel history may help. A synovial biopsy for histology (including fungal and acid-fast bacillus stains) should be considered along with microscopy and culture requesting the inclusion of mycobacteria and fungi. It may also be important to consult a microbiologist in unusual cases. In chronic prosthetic joint infection, the infection is often caused by native skin organisms such as coagulasenegative staphylococci. These microbacteria can also be a contaminant in the aspiration, so aseptic technique when sampling is imperative. Infection eventually results in loosening of the prosthesis, which can be detected on radiographs as a lucency developing at the bone/prosthesis or bone/cement interface.

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Radiologically, it is difficult to distinguish aseptic from septic loosening. Around 15% of loosening is due to infection, and the presence of rapidly progressive lysis or periosteal reaction is highly suggestive of this diagnosis. In cases of suspected infection, synovial biopsy under ultrasound or periprosthetic biopsy of lucent areas may be helpful adjunct procedures in addition to synovial fluid aspiration. Ideally, several samples using separate instruments should be sent. However, this is usually only possible when open biopsies are performed in the operating room; and, in such cases, samples should be sent for both histology and microbiology. It is crucial to mention the presence of a prosthetic device to the microbiology laboratory so that the correct tests can be requested and to avoid skin contaminants as being interpreted as the infecting organism (Fig. 61-6).

ing organism. Clostridial myonecrosis (gas gangrene) is a very acute, life-threatening infection accompanied by systemic signs of severe toxicity. It can follow surgery or trauma, and early surgical débridement is often the only chance for survival (Figs. 61-7 and 61-8).

Pyomyositis Although once thought to be a disease of tropical countries, pyomyositis is being increasingly observed throughout the world. Patients usually present with a short history of fever and have localized pain and tenderness on passive movement of the muscle. Inflammatory markers are usually raised. In the typical example, there is diffuse infection of a muscle or muscle group, leading to edema and enlargement of the muscle. Soft tissue fluid collections may follow. S. aureus is the most common infect-

■ FIGURE 61-7 Muscle infection is rare but dramatic on MRI. Pyomyositis is seen as edema and swelling within a muscle group. Later necrosis and abscess formation may change the imaging appearances.

■ FIGURE 61-6 When an implant becomes infected it is necessary to remove the metal, débride dead tissue, and begin antibiotic treatment. After removal of the implant and treatment for infection it may be possible to revise the implant or, as in this case, attempt a fusion.

■ FIGURE 61-8 Pyomyositis of the thigh with perhaps less dramatic muscle involvement than was seen in the case of necrotizing fasciitis. The distinction between these conditions is dependent on clinical presentation and speed of progression.

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Necrotizing Fasciitis

Fungal Infections

This is a rapidly destructive disease that is associated with group A streptococcal infections but may often be the consequence of polymicrobial infection with a variety of gram-positive, gram-negative, aerobic and anaerobic bacteria. It results in rapid tissue destruction and has been called “flesh-eating disease” in the lay press. A form of necrotizing fasciitis involving the scrotal fascia in males is termed Fournier’s gangrene. Necrotizing fasciitis usually requires radical surgery and is often life threatening (Fig. 61-9).

Fungi most often affect those who are immune compromised. In these circumstances they may produce a variety of signs and symptoms. A travel and exposure history in a competent host may raise the possibility of a dimorphic fungal infection, usually acquired by inhalation followed by dissemination to other sites. Fungal infection should be considered whenever the bacteriologic findings do not fit the clinical picture. Most cases should be discussed with a local microbiologist because a tissue diagnosis is usually crucial.

Tuberculosis

MANIFESTATIONS OF THE DISEASE

Although most infections are due to S. aureus or Streptococcus pyogenes, Mycobacterium tuberculosis is probably the third most common infecting organism worldwide. Tuberculosis typically produces a low-grade infection that leads to abscess formation without a pyrexial illness, the so-called cold abscess. It may be slowly destructive and produce lytic lesions as part of the tissue reaction of caseation. These lesions may mimic a malignant processes in bone. Typically, tuberculosis may cross joint spaces and, in the spine, spread across disc spaces. However, it may present in a myriad of fashions and is known for its ability to mimic other disorders. Several mycobacteria other then tuberculosis (“atypical mycobacteria”) can cause soft tissue infections and/or ulceration. For example, Mycobacterium marinum has been reported to cause a nodular lymphadenitis as a consequence of inoculation of the skin in individuals cleaning tropical fish tanks.

The imaging of soft tissue infections is similar for each of the previously mentioned clinical manifestations.

Ultrasonography Ultrasonography is useful for assessing the progress of cavitating abscesses because reasonably accurate measurements can be taken, particularly with extended field of views. Ultrasonography is also useful for discriminating fluid from edematous soft tissues, which may be a more difficult distinction on MRI.

Magnetic Resonance Imaging For staging the extent and following the progress of infection of both soft tissue and bone, MRI is the definitive technique. Axial, coronal, and sagittal planes should be obtained with a combination of T1-weighted and fluid

■ FIGURE 61-9 Extensive muscle and soft tissue necrosis in a case of severe necrotizing fasciitis. A, Coronal FSTIR MR image shows the extent of tissue damage. B, Axial MR image.

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sensitive sequences such as T2-weighted images with fat suppression or, alternatively, a short tau inversion recovery (STIR) sequence (see Fig. 61-3B). Intravenous gadolinium is rarely of diagnostic discriminatory use, because all infective processes lead to increased blood flow.

Image-Guided Biopsy Aspiration or fine-needle biopsy is a simply performed technique, but the results are often unrewarding. The most accurate culture specimens are obtained from the margins of a lesion where tissue is not necrotic using a cutting needle or open biopsy. Imaging is important in selecting the location for biopsy in all cases and in guiding the needle when a percutaneous route is attempted. The best imaging for the purpose will be one that shows the abnormal area clearly and allows real-time guidance of the needle. Ultrasonography is likely the easiest and best method of guidance, although CT and even MRI

guidance can be utilized by individuals without experience or access to the appropriate ultrasound techniques to perform the procedure.

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment Antibiotic therapy is best targeted to the specific organism. However, treatment should optimally be delayed until the exact organism and its antibiotic sensitivities have been identified by the methods described earlier, except in the most life-threatening situations.

Surgical Treatment Excision, drainage, and removal of dead and necrotic tissue is essential. The timing and extent of surgical intervention will depend on a team approach with advice from clinical microbiologists, imagers, and surgeons.

SUGGESTED READINGS Atkins BL, Bowler IC. The diagnosis of large joint sepsis. J Hosp Infect 1998; 40:263–274. Atkins BL, Gottlieb T, Shaw D. Soft tissue, bone and joint infections. Med J Aust 2002; 176:609–615. Atkins BL, Berendt AR. Prosthetic joint infection. In Bulstrode C, Buckwalter J, Carr A, et al (eds). Oxford Textbook of

Orthopaedics and Trauma. Oxford, Oxford University Press, 2002, pp 1443–1454. Mandell GL, Bennett JE, Dolin R (eds). Mandell’s Principles and Practice of Infectious Diseases. Edinburgh, Elsevier Churchill Livingstone, 2005.

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Infection in the Appendicular Skeleton (Including Chronic Osteomyelitis) Shah H. M. Khan and Hans L. Bloem

Infection of bone or bone marrow can be characterized using various definitions that reflect the interaction between the causative organism and the host’s response (Box 62-1). The clinical diagnosis is relatively straightforward in the late stages of osteomyelitis. However, despite the tremendous advancement in the imaging of bone infection, the challenge remains to detect and diagnose osteomyelitis at an early stage. The implication of early diagnosis is that early treatment can be instituted that significantly increases the cure rate and reduces the complications and associated morbidity. A clear understanding of the clinical, radiologic, and biochemical background is paramount in early diagnosis, thus enabling rapid and effective treatment as well as diagnosing activity of chronic osteomyelitis. The focus of this chapter is on effective use of imaging in dealing with these aspects of osteomyelitis based on an understanding of information displayed using conventional and advanced imaging techniques.

ETIOLOGY Bacteria are the most common cause of osteomyelitis, but viruses, fungi, and protozoa are reported to be causative agents, particularly in the immunocompromised patient. The bacterial pathogens vary with age and also with certain groups of patients (Table 62-1). However, the predominant cause of osteomyelitis is Staphylococcus aureus. Haemophilus influenzae and group B streptococcus are common causes of osteomyelitis in children, whereas gram-negative bacteria such as Escherichia coli and anaerobes are found in adult and diabetic cases. Staphylococcus epidermidis osteomyelitis is common in intravenous drug abusers and those with joint implants. Salmonella osteomyelitis is frequently seen in patients

with sickle cell disease, although S. aureus is still the most common cause in this group.1 S. aureus adheres to bone by expressing receptors (adhesins) for components of bone matrix (fibronectin, laminin, collagen, and bone sialoglycoprotein) and cartilage. It also elaborates fibronectin-binding adhesins, which enables it to attach to surgically implanted devices in bone.2

PREVALENCE AND EPIDEMIOLOGY Acute hematogenous osteomyelitis is predominantly a disease of children (85% of cases occur in children), whereas the post-traumatic or contiguous-focus type of osteomyelitis is more common in adults and adolescents. Contiguous-focus osteomyelitis forms about half of all cases of osteomyelitis. According to the literature, the incidence of acute osteomyelitis in the developed world is 1 case per 5000 children. Data on the incidence or prevalence of acute and chronic osteomyelitis in adults are not available. The incidence is thought to be much lower with widespread use of antibiotics. The risk of chronic osteomyelitis after an episode of acute osteomyelitis is 5% to 25%. Appendicular osteomyelitis is predominantly a disease of the lower limbs, accounting for about 90% of cases, and the remaining 10% occur in the upper limbs. The most common bones affected are the tibia (50%) and the femur (30%).

CLINICAL PRESENTATION The main factors that determine clinical presentation are virulence of the infective pathogen, the dose of the inoculum, and the immune status of the host. Traditionally, 1255

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KEY POINTS Osteomyelitis can occur by four main routes: hematogenous (common in children,) contiguous focus spread (most frequently seen), implantation, and post traumatic. ■ Staphylococcus aureus is the most common etiologic pathogen. ■ The metaphysis is the most common site affected in hematogenous osteomyelitis. ■ Bone scintigraphy has high sensitivity but low specificity for detecting osteomyelitis. ■ MRI has high sensitivity and specificity in diagnosing osteomyelitis and is thus particularly useful in the diagnosis of chronic osteomyelitis. ■ Abscess can only be excluded or diagnosed using gadolinium chelate–enhanced MRI. ■ The differential diagnosis of acute osteomyelitis includes Ewing’s sarcoma, osteosarcoma, and histiocytosis. An extensive soft tissue mass with spiculated periosteal reaction is suggestive of tumor. ■ PET-FDG has high sensitivity and specificity, particularly in the difficult cases of chronic osteomyelitis. ■ Return of yellow bone marrow seen on T1-weighted MR images is a late but specific sign of cure. ■

BOX 62-1

Definitions

Acute osteomyelitis: abrupt-onset infection Subacute osteomyelitis: subacute presentation Brodie’s abscess: abscess cavity (type of subacute osteomyelitis) Chronic osteomyelitis: late-stage infection with marked host reaction Sequestrum: dead or necrotic bone Involucrum: new bone formation following onset of healing process Cloaca: opening in involucrum Garré’s osteomyelitis: sclerosing osteomyelitis

osteomyelitis has been subdivided into acute, subacute, and chronic on the basis of speed of onset and course of the infection. Acute osteomyelitis commonly occurs in children. It is rapid in onset and may present as systemic toxicity. This is especially seen in children in the bacteremic phase of the infection. Nonetheless, almost 50% of cases may not manifest any of the acute systemic features. The bones most commonly affected are the tibia, the femur, and the humerus. The patient presents with pain and unwillingness to use the affected limb and as an unwell and irritable child. Redness, swelling, and warmth due to acute inflammatory response may be seen in the affected part. However, this is also seen in bone tumors. The laboratory results may indicate an elevated white blood cell count and increased levels of inflammatory markers such as erythrocyte sedimentation rate (ESR) and C-reactive protein, but the absence of such changes does not exclude the diagnosis. The blood cultures are positive in only 50% of cases. The presentation of subacute osteomyelitis or Brodie’s abscess is more insidious. This may be secondary to inadequate treatment or low virulence of the organism. The disease may have been present for several months. Indolent pain is the predominant presentation, which may be worse after activity. Swelling may be present, but redness is normally not seen. Effusion in the adjacent joint and some atrophy of the muscles may be noted. Systemic toxicity is conspicuously absent. Subacute osteomyelitis is more common in adolescent boys, with the knee and ankle being the sites of predilection. Subacute osteomyelitis may progress to chronic osteomyelitis, which generally presents as recurrent attacks of acute inflammation over a period of more than 6 weeks to many years. Pain is the predominant presenting symptom. Occasionally, a discharging sinus may be the presenting complaint in an otherwise asymptomatic patient. On examination, the bone may feel thickened and a number of skin scars from old healed sinuses may be seen. Anemia and generalized malnourishment may be noticed in long-standing cases. A previous history of acute osteomyelitis, trauma, or orthopedic implants that was complicated by infection is often present.

PATHOPHYSIOLOGY TABLE 62-1 Common Organisms Seen in Different Age Groups and Some Special Conditions Age/Subtype

Organisms

Infants

Staphylococcus aureus, group B streptococcus, Escherichia coli, Enterobacter S. aureus, group A streptococcus, Haemophilus influenzae S. aureus, coagulase-negative Staphylococcus, Pseudomonas, E. coli, Serratia Polymicrobials: S. aureus, Streptococcus, enterococcus, Proteus, anaerobes Coagulase-positive S. aureus, Streptococcus, Pseudomonas, Kingella S. aureus, Salmonella

Children Adults Diabetic foot Brodie’s abscess Sickle cell disease

The infection of bone can occur by one of four main routes: hematogenous, spread from contiguous source, direct implantation, and postoperative infections. The infection has a predilection for growing ends of appendicular bones. The infective pathogen tends to lodge at the metaphyseal vessels in acute hematogenous infection. These metaphyseal vessels have slow but turbulent flow of blood, reduced leukocytes, as well as impaired phagocytic ability, which are conducive to proliferation of infective organisms.

Anatomy The anatomy of the vasculature of the appendicular long bones varies with age. The metaphyseal and epiphyseal vessels are distinct and separated by the growth plate in children, but communication is present in infants and

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adults after the fusion of the growth plate. Therefore, infection can easily extend into the epiphyseal region in the infants and adults. Infection in the epiphyseal region can potentially spread to the joint, causing septic arthritis. In some joints, such as the hip or shoulder, where the metaphysis lies within the capsule, septic arthritis can occur from a breach of the metaphyseal cortex.

Pathology Acute hematogenous osteomyelitis commonly affects children and is relatively uncommon in healthy adults, but it can occur in immunocompromised individuals or intravenous drug abusers. The metaphyses, especially around the knee, are sites of predilection. These are sites of rapid growth and are also more prone to trauma in children. The onset of infection triggers the inflammatory response with influx of leukocytes and exudate formation. The intraosseous pressure is raised due to edema within the rigid medullary cavity, producing thrombosis of vessels. This further exacerbates and spreads the infective process. Ultimately, the exudates track through the haversian canals of the cortex, which is particularly thin at the metaphysis. The spread of inflammatory exudates to the subperiosteal region elevates the periosteum. This causes periosteal vessel thrombosis, leading to cortical necrosis. The enzymes released by the bacteria, polymorphonuclear cells, and dying tissues further contribute to the local bone marrow and cortical necrosis.

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The elevation of the periosteum also triggers the osteoblasts to produce new bone, which manifests as periosteal reaction. This response is earlier and more florid in children but is delayed and somewhat patchy in adults. In children, the periosteum is loosely attached and thus can be easily peeled off, manifesting as an early periosteal reaction, whereas in adults it is more firmly attached. This periosteal new bone formation is also well seen radiographically when using MRI and ultrasonography. Necrotic bone fragment bereft of vascularization is dense relative to vascularized bone. The vascularized bone undergoes demineralization due to the inflammatory response. Areas of infected bone also undergo destruction due to osteoclastic action. These are seen as patchy osteopenic areas on plain radiographs, whereas the devascularized bone fragment, which is referred to as a sequestrum, stands out as a dense bony fragment within patchy osteopenia on radiographs and CT. The sequestrum is of low signal intensity on all pulse sequences on MRI (Fig. 62-1). The dead sequestrum can harbor infective organisms. These may be difficult to eradicate unless the sequestrum is removed and the infective area is thoroughly cleaned and débrided. Therefore, the presence of sequestrum has the potential to make the infection chronic with risk of future acute exacerbations. The periosteal new bone formation that takes place is referred to as involucrum and attempts to contain the infection. This tends to surround the infected area and

■ FIGURE 62-1 Osteomyelitis mimicking osteoid osteoma. This patient had nonspecific symptoms of pain in the thigh. A, The initial radiograph showed a lucent lesion in the proximal femur with marked surrounding sclerosis. Subtle density is seen within the lucent lesion. This was suspected to be an osteoid osteoma, but osteomyelitis was considered in the differential diagnosis. Sagittal (B) and axial (C) T1-weighted, fat-suppressed, gadolinium-enhanced MR images demonstrate high signal intensity in the marrow with a small nonenhancing lesion of low signal intensity noted within. The nonenhancing lesion is a sequestrum within infected marrow, a classic feature of osteomyelitis. Note the breach of the cortex in the axial image (C) with periosteal reaction.

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has pathologically a soft spongy texture. If the infection is controlled, then the involucrum undergoes remodeling and bridges the gap in the cortex. If the infection is not adequately controlled, then the infective exudates may breach through the involucrum, producing an opening called a cloaca. The pus may then accumulate in the soft tissues to form abscesses before tracking through the soft tissues to break through the skin as a sinus. The cloaca may be seen on plain radiographs but is difficult to detect unless a sinogram is performed before the examination. The sinogram can delineate the soft tissue track of the sinus and abscesses as well as indicate the sites of the cloacae (Fig. 62-2). Sinography is now less frequently undertaken because the cloaca and soft tissue abscesses and fistulous track may be exquisitely seen on MRI (Fig. 62-3). CT can delineate the cloacae and abscesses in the soft tissues as rim-enhancing collections. When the infection is adequately controlled and healing has taken place, the infected marrow undergoes cystic changes with fatty infiltration and the bony cortex undergoes remodeling.

BIOMECHANICS The biomechanical significance of osteomyelitis is that the infected bone is not strong and is prone to pathologic fractures. This is a particular problem of long-standing chronic osteomyelitis.

■ FIGURE 62-2 Sinogram. A 73-year-old woman presented with discharging sinus about 3 years after internal fixation of a femoral shaft fracture. Sinogram demonstrates the catheter extending into the femur with contrast medium seen at multiple sites along the bone. This demonstrates communication between the bone and a soft tissue abscess as well as multiple cloacae.

IMAGING TECHNIQUES Osteomyelitis is a potentially treatable disease, but early diagnosis is critical to avoid extensive damage and morbidity. Although clinical findings combined with laboratory results and imaging findings are unambiguous in most cases, there are a significant number of cases in which the diagnosis may not be clear, especially in children. In addition, the differentiation from other conditions such as tumors and fractures that have completely different management pathways means that the imaging has to be tailored with close cooperation between various disciplines.

Techniques and Relevant Aspects In suspected cases of osteomyelitis, a baseline radiograph is essential. Although the radiographic changes of acute osteomyelitis may lag behind by 10 to 14 days, the radiograph can exclude other causes and, more pertinently, serve as a means of assessing progress after treatment. Both bone scintigraphy and MRI are equally sensitive in detection of infection in the bone. However, MRI is able to detect infection earlier and also affords precise anatomic localization and soft tissue contrast in three dimensions, which makes it more specific than nuclear imaging. MRI using a short tau inversion recovery (STIR) sequence is a very cost-effective method of screening for osteomyelitis. CT is useful in the assessment of osteomyelitis, particularly in detecting early bone destruction or the presence of small sequestrum, which may not be evident on other imaging methods. It is very helpful in the assessment of atypical bones, such as clavicle, sternum, and pelvis, and may provide useful information especially when coupled with 3D reconstruction. CT is commonly used in the assessment of the spinal disease when overlapping bones may elude detection of small infective foci. CT also enables precise localization for biopsy and aspirations of infected bone or abscesses. Ultrasonography has a complementary role in the investigation of osteomyelitis. It is extremely useful in detecting soft tissue abscesses but in children can also detect the elevation of periosteum and subperiosteal collections. It is the first line of investigation in joint effusions, particularly in the hips of children. It also affords guided aspiration but avoids the risk of radiation, as is the case with CT. Note that if a periosteal reaction is not detected using ultrasonography then the diagnosis of osteomyelitis is not excluded. Newer imaging techniques of positron emission tomography (PET) are proving to be useful, with current literature suggesting improved detection, particularly in cases of chronic osteomyelitis. However, they remain less specific than MRI. Other techniques occasionally used are sinography, which can delineate the track in the soft tissue extending to the infected bone (see Fig. 62-2).

Pro and Cons (Table 62-2) After a baseline radiograph, MRI is preferred for imaging of osteomyelitis owing to its superior soft tissue contrast

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■ FIGURE 62-3 Chronic osteomyelitis. A, Plain radiograph shows erosion in the metatarsal head of the third toe. Bony remodeling with thickening of the cortex of the metatarsal shaft is noted. B, Axial T1-weighted fat-suppressed MR sequence with gadolinium chelate demonstrates erosion of the metatarsal head of the third toe with marrow edema and soft tissue enhancement that is likely to represent extension of infection into the soft tissue. C, T2-weighted MR sequence with fat suppression clearly demonstrates the soft tissue abscess adjacent to the infected third metatarsal.

and ability to demonstrate 3D anatomy. It also enables preoperative planning. Although both the sensitivity and specificity is over 90%, it can be nonspecific and the clinical context along with laboratory results are important in reaching an exact diagnosis. Nuclear medicine is sensitive in detecting infection but has a relatively low specificity and the anatomic localization can be difficult. However, negative bone scintigraphy virtually excludes an infection. Because scintigraphy easily images the whole body it is extremely useful in assessing multiple sites of infection, as can occur in chronic recurrent multifocal osteomyelitis. Early studies using PET have demonstrated higher sensitivity and specificity than nuclear medicine and MRI, being particularly useful in chronic osteomyelitis. In chronic osteomyelitis, white blood cell–labeled scans are useful in detecting recurrence and have reasonable specificity.

CT is useful in delineating small sequestrum especially in chronic osteomyelitis, and it can also detect early bone destruction.

Controversies In cases of chronic osteomyelitis the diagnosis can be difficult. MRI is very sensitive and can show abnormal areas due to tissue edema and increased perfusion, but this may persist for up to 12 months after treatment of infection or after surgery, making it less specific. In the absence of abscess or sequestrum and other morphologic signs of osteomyelitis the detection of recurrent infection can be difficult. This may be further compounded by the presence of metal implants and the associated degradation of image quality on MRI. Recent meta-analysis reviewing the accuracy of diagnosis in chronic osteomyelitis showed fluorodeoxy-

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TABLE 62-2 Pros and Cons of the Various Imaging Modalities Imaging Modality

Pros

Cons

Radiography

Useful baseline

Ultrasonography

Can detect soft tissue abscess and subperiosteal collection, particularly in pediatric cases Image guided aspiration Assessment of atypical bones such as sternum, pelvis and spine Accurately detects subtle changes of bony destruction, sequestrum, and periosteal reaction Enables guided aspirations and biopsies Excellent soft tissue contrast and exquisite anatomic detail High sensitivity and specificity of over 90% in detection of osteomyelitis Can assess the whole body, which is useful in multiple site involvement High negative predictive value High accuracy in chronic osteomyelitis

Low sensitivity Lags behind the pathology by 7–14 days Cannot assess sequestrum and intraosseous pathology

Computed tomography

Magnetic resonance imaging

Nuclear medicine Positron emission tomography

glucose-labeled PET (FDG-PET) to be the most accurate, with a sensitivity of 96% and specificity of 91%. On the other hand, the sensitivity was 84% and specificity 60% for MRI. The accuracy of leukocyte scintigraphy was reasonably high for the peripheral skeleton, with sensitivity of 84% and specificity of 80%. However, these figures reduced significantly when accuracy for both axial and peripheral skeleton was combined.3 It is likely that both MRI and PET have complementary roles. MRI provides morphologic and anatomic assessment and PET assesses the functional aspect, thus enabling the distinction of infected areas in chronic osteomyelitis.

MANIFESTATIONS OF THE DISEASE Understanding of the previously described pathophysiology makes it easy to understand and predict the imaging findings irrespective of the technique used.

Radiography Radiographic signs of osteomyelitis are delayed by 7 to 14 days behind the disease process. Radiographs are often negative at the initial stage because the destruction of more than 60% of trabecular bone is necessary before osteomyelitis can be detected reliably. However, the earliest sign observed may be effacement of fat planes with diffuse soft tissue swelling. Epiphyseal, metaphyseal, or diaphyseal ill-defined radiolucencies corresponding to the osseous destruction are seen on radiographs of the mature skeleton. Endosteal scalloping, intracortical lucencies or tunneling, and poorly defined subperiosteal bony defects are also seen. Mild periosteitis is usually associated, but periosteal reaction is more prominently observed in the immature skeleton on radiographs (see Fig. 62-4A). In virulent infection the perios-

Soft tissue contrast is not as good as MRI Degree of marrow involvement cannot be adequately assessed

Can still be nonspecific, particularly in the setting of chronic complex osteomyelitis and neuroarthropathy Low specificity in children and elderly Low resolution Limited availability Expensive

teal reaction may be irregular and similar to periosteal reaction seen in bone sarcoma. Periosteal reaction implies increased intramedullary pressure. When intramedullary pressure does not increase because cortical bone is not intact as a result of fracture or surgery, then periosteal reaction may be absent. In subacute osteomyelitis a lucent lesion is seen that is normally located in the epiphysis or the metaphysis, and it may be associated with a linear track. Periosteal reactions may be subtle or even absent (Fig. 62-5A). In the chronic stages of osteomyelitis there is extensive bony remodeling with considerable radiodensity and contour irregularity. Cystic changes may occur within the sclerotic area and sequestra are common (see Fig. 62-1A). Patchy osteopenic areas may herald acute exacerbations and may be associated with periosteal reaction. Dense sequestrum may be seen standing among the altered bone, but this is generally difficult to detect. Cloacae, which are defects in the involucrum, are also difficult to detect on plain radiographs. A sequestrum was visible in only 9% of cases in one series. The sensitivity increases with serial review of radiographs to 14% and specificity of 70%.4 Differentiating active from inactive chronic osteomyelitis can be extremely difficult. The extensive bony remodeling and osteosclerosis of the chronic osteomyelitis may obscure changes of reactivation. Radiographically, signs of reactivation are new areas of destruction, thin linear periostitis, and sequestration (Figs. 62-6A and 62-7B; see also Fig. 62-3A). In cases with prostheses, lucency at the cement-prosthesis or cement-bone interface in cemented prostheses or at the prosthesis-bone interface in uncemented prostheses is suggestive, but not specific, for infection. This may be associated with evidence of movement of the prosthesis and extensive destruction or even fracture of the bone.

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■ FIGURE 62-4 Acute osteomyelitis. A, Plain radiograph of a child showing ill-defined lucency adjacent to the growth plate of the distal fibula with surrounding sclerosis. B, Coronal CT reconstruction demonstrating the lucent areas adjacent to the growth plate with prominent surrounding sclerosis. Axial T1-weighted (C) and T1-weighted, fat-suppressed, gadoliniumenhanced (D) MR images. The abnormal infected marrow is of low signal intensity on the T1-weighted pulse sequence. After administration of the gadolinium chelate, osteomyelitis is demonstrated by the high signal-enhancing area adjacent to the growth plate in the distal fibula associated with periosteal new bone formation.

Magnetic Resonance Imaging Magnetic resonance imaging is the most sensitive (approaching 100%) of all methods for diagnosing osteomyelitis and has a high specificity (greater than 81%) in most series. Fat-suppressed, contrast medium–enhanced imaging significantly increases the specificity (93%) in the diagnosis of osteomyelitis when compared with three-phase bone scintigraphy and has higher specificity than nonenhanced MR, particularly in complicated cases (e.g., chronic osteomyelitis, postoperative state, and neuroarthropathy).5 The infected bone produces prolongation of both the T1- and T2-weighted relaxation times owing to tissue

edema. On T1-weighted pulse sequences, the abnormal area has intermediate to low signal intensity with replacement of the high signal intensity fatty marrow. There is high signal intensity on T2-weighted pulse sequences (see Figs. 62-1 and 62-3). The abnormal marrow demonstrates enhancement after gadolinium administration. Pus within an abscess does not enhance after administration of gadolinium chelates. Areas with abscess formation demonstrate central low signal intensity with peripheral rim enhancement on T1-weighted pulse sequences with gadolinium. An abscess can thus be diagnosed or excluded using gadolinium chelate–enhanced MRI and not on nonenhanced T1- and T2-weighted MRI.

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■ FIGURE 62-5 Brodie’s abscess. A, Plain radiograph of the ankle shows a lucent lesion in the calcaneus with sclerotic margins. B, Multislice CT with 3D reconstruction in the sagittal plane demonstrates the abscess cavity within the calcaneus. C, On a T1-weighted, gadolinium-enhanced MR sequence, the calcaneal abscess appears to have four rings. The low signal central abscess cavity, the enhancing inner ring, and the low signal outer ring are seen, but the peripheral ring is not evident because of relative lack of surrounding marrow edema.

Despite the relatively high sensitivity and specificity of MRI, it may still be nonspecific. The abnormal marrow signal may be seen in trauma and tumor. However, the STIR sequence has the highest sensitivity (96%) and negative predictive value (94%) and can thus be used to screen patients suspected of having osteomyelitis. In subacute osteomyelitis, the lesion has a characteristic four-ring appearance. This consists, on T1-weighted images, of a central low signal area, which is the abscess, surrounded by a rim of slightly higher signal intensity that is the granulation tissue (Fig. 62-8; see also Fig. 62-5). This line of granulation tissue is sometimes referred to as the penumbra sign. On T2-weighted sequences, the high signal intensity of the central abscess is indistinguishable from the granulation tissue second ring, which is also of high signal intensity. These two central rings are surrounded by a rim of low signal intensity in all pulse

sequences representing fibrosis and sclerosis. External to this third layer lies an ill-defined low signal area on T1-weighted sequences that represents surrounding marrow edema and inflammatory response. The marrow edema is of high signal intensity on T2-weighted pulse sequences. After administration of a gadolinium chelate, the granulation tissue layer (second ring) demonstrates intense enhancement while the central abscess remains of low signal intensity on T1-weighted pulse sequences. The surrounding marrow edema also demonstrates enhancement.6 In chronic osteomyelitis, abnormal areas demonstrate low signal intensity on T1-weighted sequences and high signal intensity on T2-weighted sequences. The sequestrum remains of low signal intensity, similar to cortex, on all pulse sequences. After administration of a contrast medium, enhancement of infected marrow is seen but

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■ FIGURE 62-6 Osteomyelitis in a diabetic. A, Lateral plain radiograph of the ankle shows cortical erosion on inferior aspect of calcaneus. A deep heel ulcer is delineated by the air extending up to the calcaneus. T1-weighted (B) and T1weighted, fat suppressed, gadolinium-enhanced (C) MR images of the calcaneus demonstrate low signal intensity in the calcaneal marrow with marked enhancement after gadolinium administration. Erosion of the inferior cortex of calcaneus is seen in the base of the deep ulcer of the heel. Note the enhancement of the lining of the ulcer.

the sequestrum never demonstrates enhancement (see Fig. 62-6). Marrow abscesses may show rim enhancement. Enhancement is also seen along the sinus tract as well as granulation lining of soft tissue abscesses. The marrow may remain abnormal in treated osteomyelitis, trauma, tumor, and neuroarthropathy. Distinguishing osteomyelitis from neuroarthropathy becomes particularly important in the setting of diabetic foot, which is discussed in detail elsewhere in this text. However, there are secondary MRI findings that augment confidence in diagnosing infection. These are presence of a deep ulcer adjacent to abnormal bone, associated cortical discontinuity, and soft tissue abscess or sinus tract demonstrating enhancement.7 MRI is effective in monitoring treatment, especially in subacute and chronic osteomyelitis. When the patient responds well to treatment, clinical improvement precedes changes on MR images. These changes consist of decreased high signal intensity areas on T2-weighted

images, decrease of enhancement, disappearance of abscess cavities, and return of yellow bone marrow seen on T1-weighted images. Return of yellow bone marrow is a late, but very specific sign of healing.

Computed Tomography Computed tomography is quite useful in demonstrating early cortical destruction that may not be evident on other imaging methods. It is possible to unravel a sequestrum that may be enveloped by grossly remodeled bone in chronic osteomyelitis. Soft tissue or marrow abscesses may demonstrate rim enhancement after contrast agent administration. Subtle periosteal new bone formation may be evident. Gas within the infected bone is considered to be the earliest sign seen on CT. With the advent of multislice CT with multiplanar reconstruction, CT plays a very useful role in the imaging of infections involving the irregular bones and joints such

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■ FIGURE 62-7 A, Sonogram of the foot of patient with a discharging sinus who had bone grafting after resection of the first metatarsal for tumor. Erosion of the cortical outline of the bone graft is noted. A small amount of pericortical collection is seen in keeping with a small abscess. B, Subsequent radiograph confirmed osteomyelitis. Extensive erosive changes are seen in the bone graft, also in keeping with osteomyelitis.

as the sternoclavicular joint, pelvis, and spine (see Figs. 62-4B and 62-5B). It is particularly useful as image guidance enabling aspiration or biopsy.8 However, CT is limited by inability to accurately distinguish between suppuration, reactive granulation tissue, edema, and fibrosis.9

Ultrasonography Ultrasonography is useful in the assessment of the soft tissue component of the infection. Being noninvasive and easily accessible, it enables rapid assessment of joints for effusion, which may be seen in septic arthritis. Soft tissue abscess can be confidently diagnosed on ultrasonography (see Fig. 62-7A). In children, it is possible to visualize elevation of the periosteum and the underlying collection before mineralization of the periosteum. This is useful in the early stages of acute osteomyelitis when plain radiographs may be normal, although the absence of this sign does not exclude the disease. Ultrasonography plays a particularly valuable role in assessment of the possible soft tissue causes of pain or swelling, which are factors in the differential diagnosis of osteomyelitis, which includes cellulitis, thrombophlebitis, bursitis, hematoma, tenosynovitis, or subcutaneous abscess. Ultrasonography is very useful in enabling guided aspiration and biopsy of collections or joint effusion.10

Nuclear Medicine Nuclear medicine is a functional imaging modality that assesses bone turnover, which increases in the presence of infection. Conventional bone scintigraphy uses technetium-99m–labeled methylene diphosphonate (99mTc-MDP) and 99mTc-labeled hydromethylene diphosphonate (99mTcHMDP), which are sensitive in detecting osteomyelitis. The uptake of the 99mTc-phosphonate complex depends on the perfusion and vascular permeability of the infected bone. The images are acquired at 4 hours because optimal target to background ratio is achieved at about 3 hours after injection of the radionuclide. Triple-phase bone scintigraphy is commonly used in investigation of osteomyelitis. The vascular and blood pool phases are useful in assessing the hyperemia and inflammation. There is generally increased uptake in all three phases of the bone scintigraphy in osteomyelitis. However, this is not very specific and may be abnormal in fracture, tumor, treated osteomyelitis, and neuroarthropathy (see Fig. 62-8B). Occasionally, photopenia may be seen in osteomyelitis. This may be due to aggressive infection, subperiosteal pus, or joint effusion.11 Bone scintigraphy has been found to have a mean sensitivity of 85% to 93% and specificity of 43% to 54%.12 The sensitivity is lower in children and the elderly. In children, the epiphyses are active on bone scintigraphy

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■ FIGURE 62-8 Brodie’s abscess mimicking a tumor. This patient was suspected to have an osteosarcoma but results of the MRI cast doubt on the diagnosis. The diagnosis was confirmed to be Brodie’s abscess after a second biopsy because the first was not conclusive. A, Lucent expanded lesion seen in the distal tibia with sclerotic margin. B, Anterior and posterior bone scans demonstrate intense uptake in the distal tibia. This is nonspecific because increased uptake is seen in both tumor and osteomyelitis. Note the intense uptake seen normally at the epiphyses. Coronal (C) and axial (D) T1-weighted, fat-suppressed, gadolinium-enhanced MR images show typical penumbra sign with intense enhancement of the inner granulation ring. Marked surrounding bone marrow edema also demonstrates enhancement.

and may obscure sites of infection in the metaphysis, which limits its usefulness. However, scintigraphy enables examination of the whole skeleton, which is particularly useful for multiple sites involvement as can occur in chronic recurrent multifocal osteomyelitis. Radionuclide imaging is also limited by poor resolution, which restricts the ability to accurately pinpoint the lesion. This may be overcome to a certain extent by employing single photon emission computed tomography (SPECT). Nevertheless, bone scintigraphy may be important in the workup of patients suspected of having osteo-

myelitis. A negative scan can exclude osteomyelitis with a sensitivity that is greater than 90%. In chronic osteomyelitis, bone scintigraphy may be abnormal despite adequate treatment making distinction of active infection from inactive disease difficult. However, white blood cell scans are considered superior to bone scintigraphy and gallium-67 scans in the assessment of chronic osteomyelitis. Accuracy figures for white blood cell scans in literature indicate a higher specificity of 78% to 91%, particularly in difficult cases of chronic osteomyelitis. White blood cell scintigraphy entails labeling separated

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autologous granulocytes with indium-111 or 99mTc-labeled hexamethylpropylene amine oxime (99mTc-HMPAO). Granulocytes are preferentially tagged and infiltrate areas of chronic infections as part of the inflammatory response. Therefore, it is possible to detect a focus of infection by increased uptake of the radionuclides. The images are acquired 24 hours after injection. Significant radiation dose remains a concern with indium-111, particularly in children. White blood cell scans have a higher specificity in infections of appendicular bones than in the axial skeleton, owing to false-positive uptake in the normal red marrow of spine. In-vivo agents are also available that consist of technetium-99m labeled with monoclonal murine antigranulocyte antibodies against the surface antigen NCA-95. This has the same accuracy as in-vitro white blood cell agents but is easier to use.8 Gallium scans are useful in chronic infections that are very difficult to diagnose. However, this examination is associated with significant radiation dose to the patient and is falling out of favor.

Positron Emission Tomography Positron emission tomography uses 18F-fluorodeoxyglucose as an agent that mimics glucose. This can be used to study the metabolic function depending on the degree of glycolysis. Infection is associated with increased glycolysis, and hence there is increased uptake. It is particularly useful in the assessment of infection in the spine and in complex cases of osteomyelitis. Extensive research is being carried out to assess the usefulness of PET in osteomyelitis. Preliminary studies indicate that in metal implant infection, FDG-PET is not hampered by metal artifact as is the case with CT and

Classic Signs ■ ■ ■ ■ ■ ■ ■ ■ ■ ■ ■ ■ ■

Osteolysis is most prominent in acute osteomyelitis. Reactive sclerosis is most prominent in chronic osteomyelitis. Irregular periosteal reaction is most prominent in acute osteomyelitis. Regular periostitis and thickened cortex are most prominent in chronic osteomyelitis. Periosteal reaction may be absent when the medullary canal is not intact (after surgery). Brodie’s abscess Sequestrum Involucrum Cloaca Four-ring appearance on MRI, with high signal intensity on T1-weighted images of the ring surrounding the central area Unminerilized periosteal reaction is seen on MRI and ultrasonography. Inflammatory changes outside periosteum are seen on MRI or ultrasonography. Presence of low signal sequestrum within an abscess or abnormal marrow is highly suggestive of acute osteomyelitis or acute exacerbation of chronic osteomyelitis.

MRI, but its usefulness in the diagnosis of a failed joint prosthesis is debatable. The accuracy of PET in diagnosis of musculoskeletal infections was 94% compared with 81% for combined bone and leukocyte scan. It demonstrated the ability to distinguish areas of hematopoiesis in the axial skeleton from foci of infection, which are difficult to tell apart using imaging.13 Recent meta-analysis assessing the diagnostic accuracy of all available imaging found PET to be the most accurate, with a sensitivity of 96% and a specificity of 91%. However, the anatomic localization can be a problem with PET. This can be easily remedied with combined PET/CT. Nevertheless, there is currently limited availability of PET scanners.

DIFFERENTIAL DIAGNOSIS (Table 62-3) The main differential diagnoses are trauma and tumors. It is essential that these be distinguished, because the management is very different. Acute osteomyelitis can occasionally pose a problem in distinguishing it from osteosarcoma or Ewing’s tumor and fracture. Chronic osteomyelitis may be difficult to distinguish from osteoid osteoma (in particular intracortical abscess), fracture, and osteosarcoma (see Figs. 62-1 and 62-8). The clinical symptoms and signs of warm, red, and painful swelling seen in acute osteomyelitis are also seen in tumors such as osteosarcoma and Ewing’s sarcoma. This is further complicated by the preponderance of all three conditions in children. Tumors may manifest as systemic toxicity, such as pyrexia. Toddlers may present with unwillingness to use the affected limb. A history of trauma may not always be available in children. In children, acute osteomyelitis is common and generally has an acute onset with systemic features. Tumors tend to be more indolent in presentation. A recent history of sinus or other infections needs to be elicited because this may be the cause of osteomyelitis. Radiographic findings may be normal in osteomyelitis, early greenstick fracture, and tumors. Although both osteomyelitis and osteosarcoma may demonstrate destruction at the metaphysis with periosteal reactions there are important differences. The tumor is associated with soft tissue mass that may show variable degree of ossification and/or calcification. The periosteal reaction

TABLE 62-3 Differential Diagnosis of Osteomyelitis Cellulitis Septic arthritis Fracture Benign bone tumors Eosinophilic granuloma Osteoid osteoma Malignant bone tumors Osteosarcoma Ewing’s sarcoma Crystal arthropathy

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in tumors tends, as in acute osteomyelitis, to be spiculated and associated with Codman’s triangle, whereas in chronic osteomyelitis it is typically linear, multilamellar, or solid. The presence of a soft tissue mass is readily seen on MRI, enabling distinction from osteomyelitis. Occasionally, greenstick or spiral fractures may not be detectable on initial radiographs but may become evident in subsequent films. However, these fractures can be detected on MRI as a break in the cortex with a low signal fracture line surrounded by edema on T2-weighted images even when radiographs are normal. Similarly, insufficiency fractures can mimic osteomyelitis. Distinguishing chronic osteomyelitis from osteoid osteoma is usually possible on radiographs, CT, and MRI. The nidus of the osteoid osteoma, depending on the degree of mineralization, is intermediate to high signal intensity on MRI, whereas the sequestrum is always of low signal intensity on all pulse sequences. The nidus demonstrates marked enhancement, unlike the sequestrum (see Fig. 62-1). CT may play a complementary role in delineating the nidus, which will be surrounded by an extensive sclerotic reaction.

SYNOPSIS OF TREATMENT OPTIONS The aim of treatment is eliminating the organism, stopping the spread of infection, and avoiding destruction, deformity, and associated morbidity. Complications such as growth disturbance and fractures should be kept to a minimum. Reconstructive surgery in case of deformities will require complete eradication of the infective organism. Good preoperative preparation, operating theaters with laminar flow, and use of prophylactic antibiotics have greatly reduced infection rates. In any bone surgery, prophylactic antibiotics should be administered intravenously 30 minutes before skin incision and for no longer than 24 hours after the operation. Patients with open bone injuries should receive a firstor second-generation cephalosporin intravenously, which should be given for 24 to 48 hours. If postoperative infection develops, then appropriate antibiotics guided by culture growth should be administered. In complex open fractures, therapy with broad-spectrum antibiotics for longer periods of 4 to 6 weeks is recommended.14

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be changed to more appropriate antibiotics depending on the result of the culture.15 Hyberbaric oxygen therapy has been shown to augment healing of infected bone by improving leukocyte activity, particularly in osteomyelitis associated with reduced vascularity.16

Surgical Treatment Surgical treatment is indicated for cases not responding to medical therapy or when there is clear evidence of bone necrosis and abscess formation. The main principles of surgical management of osteomyelitis include the following17: Débridement is done to resect necrotic bone and soft tissues, ensuring adequate drainage. External fixation is performed for stabilization. This is useful in difficult cases of chronic osteomyelitis complicated by nonunion or malunion. Reconstruction is done by filling of bony and soft tissue defects with bone grafts and free muscle or fasciocutaneous flaps transfer to provide vascularity. Amputation is reserved for cases with poor vascularity, as occurs in diabetic foot. The level of amputation is determined by the vascularity of the viable tissues proximal to the site of infection.

● ●

●

●

Recent advances using microvascular techniques involving fibular grafts and a composite osteocutaneous iliac flap reduce the duration of bone union and period of immobilization.18 In infection involving joint prosthesis, it is best to remove the prosthesis. There are two common approaches. In the two-stage exchange arthroplasty, surgical débridement of infected bone and soft tissues is carried out after removal of the infected prosthesis. This is followed by a period of 4 to 6 weeks of antibiotics therapy, and antibiotic-impregnated beads may be left in situ. Revision surgery is subsequently carried out. In the one-stage procedure a new prosthesis is placed after removal of the infected prosthesis at one sitting. However, antibiotics containing cement are used to reduce recurrence of infection. Nonetheless, the twostage procedure has less risk of recurrent infection than the one-stage procedure.

Medical Treatment Antibiotics may be adequate treatment in early hematogenous osteomyelitis. Antibiotic treatment should be started promptly whenever there is a suspicion of osteomyelitis, but prior blood culture and/or bone biopsy must be obtained. Antibiotics effective against the common pathogens may be administered initially. S. aureus is the most common etiologic agent, and the antibiotics that are effective against this organism include flucloxacillin, nafcillin, cefuroxime, and cefazolin. Ciprofloxacin, gentamicin, and vancomycin are used in methicillin-resistant infections. Courses of antibiotics are generally given intravenously in the acute phase, lasting up to a week, and then replaced by oral antibiotics for the next 6 weeks. This can

What the Referring Physician Needs to Know ■ ■ ■ ■ ■ ■

Can osteomyelitis be excluded based on normal radiograph or is the radiograph taken too early to exclude osteomyelitis? Is sarcoma excluded as an alternative diagnosis? What is the best advanced imaging method in case of a nonspecific finding? Is there an abscess? Is there a sequestrum? What is the best advanced imaging method to produce answers to planning treatment in chronic osteomyelitis?

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ACKNOWLEDGMENT We are grateful to Mr. J. L. Barrie, Consultant Orthopaedic Surgeon, Royal Blackburn Hospital, United Kingdom, for valuable help with this manuscript.

SUGGESTED READINGS Bureau NJ, Chhem RK, Cardinal E. Musculoskeletal infections: US manifestations. RadioGraphics 1999; 19:1585–1592. Crim JR, Seeger LL. Imaging evaluation of osteomyelitis. Crit Rev Diagn Imaging 1994; 35:201–256. Lew DP, Waldvogel FA. Osteomyelitis. N Engl J Med 1997; 336:999–1007. Marti-Bonmati L, Aparisi F, Poyatos C, Vilar J. Brodie abscess: MR imaging appearance in 10 patients. J Magn Reson Imaging 1993; 3:543–546. Morrison WB, Schweitzer ME, Batte WG, et al. Osteomyelitis of the foot: relative importance of primary and secondary MR imaging signs. Radiology 1998; 207:625–632.

Sammak B, Abd EB, Al Shahed M, et al. Osteomyelitis: a review of currently used imaging techniques. Eur Radiol 1999; 9:894–900. Schauwecker DS. The scintigraphic diagnosis of osteomyelitis. AJR Am J Roentgenol 1992; 158:9–18. Tehranzadeh J, Wong E, Wang F, Sadighpour M. Imaging of osteomyelitis in the mature skeleton. Radiol Clin North Am 2001; 39:223–250. Termaat MF, Raijmakers PG, Scholten HJ, et al. The accuracy of diagnostic imaging for the assessment of chronic osteomyelitis: a systematic review and meta-analysis. J Bone Joint Surg Am 2005; 87:2464–2471. Unger E, Moldofsky P, Gatenby R, et al. Diagnosis of osteomyelitis by MR imaging. AJR Am J Roentgenol 1988; 150:605–610.

REFERENCES 1. Resnick D, Niwayama G. Osteomyelitis, septic arthritis, and soft tissue infection: mechanisms and situations. In Resnick D (ed). Diagnosis of Bone and Joint Disorders. Philadelphia, WB Saunders, 2004, pp 2354–2418. 2. Lew DP, Waldvogel FA. Osteomyelitis. Lancet 2004; 364:369–379. 3. Termaat MF, Raijmakers PG, Scholten HJ, et al. The accuracy of diagnostic imaging for the assessment of chronic osteomyelitis: a systematic review and meta-analysis. J Bone Joint Surg Am 2005; 87:2464–2471. 4. Tumeh SS, Aliabadi P, Weissman BN, McNeil BJ. Disease activity in osteomyelitis: role of radiography. Radiology 1987; 165:781–784. 5. Morrison WB, Schweitzer ME, Bock GW, et al. Diagnosis of osteomyelitis: utility of fat-suppressed contrast-enhanced MR imaging. Radiology 1993; 189:251–257. 6. Grey AC, Davies AM, Mangham DC, et al. The “penumbra sign” on T1-weighted MR imaging in subacute osteomyelitis: frequency, cause and significance. Clin Radiol 1998; 53:587–592. 7. Morrison WB, Schweitzer ME, Batte WG, et al. Osteomyelitis of the foot: relative importance of primary and secondary MR imaging signs. Radiology 1998; 207:625–632. 8. Sammak B, Abd EB, Al Shahed M, et al. Osteomyelitis: a review of currently used imaging techniques. Eur Radiol 1999; 9:894–900.

9. Gold RH, Tong DJF, Crim JR, Seeger LL. Imaging the diabetic foot. Skeletal Radiol 1995; 24:563–571. 10. Bureau NJ, Chhem RK, Cardinal E. Musculoskeletal infections: US manifestations. RadioGraphics 1999; 19:1585–1592. 11. Schauwecker DS. The scintigraphic diagnosis of osteomyelitis. AJR Am J Roentgenol 1992; 158:9–18. 12. Larcos G, Brown ML, Sutton RT. Diagnosis of osteomyelitis of the foot in diabetic patients: value of 111In-leukocyte scintigraphy. AJR Am J Roentgenol 1991; 157:527–531. 13. de Winter F, Vogelaers D, Gemmel F, Dierckx RA. Promising role of 18-F-fluoro- D -deoxyglucose positron emission tomography in clinical infectious diseases. Eur J Clin Microbiol Infect Dis 2002; 21:247–257. 14. Bamberger DM. Diagnosis and treatment of osteomyelitis. Compr Ther 2000; 26:89–95. 15. Healy B, Freedman A. Infections. BMJ 2006; 332:838–841. 16. Kindwall EP. Uses of hyperbaric oxygen therapy in the 1990s. Cleve Clin J Med 1992; 59:517–528. 17. Tetsworth K, Cierny G III. Osteomyelitis débridement techniques. Clin Orthop Relat Res 1999; (360):87–96. 18. Zweifel-Schlatter M, Haug M, Schaefer DJ, et al. Free fasciocutaneous flaps in the treatment of chronic osteomyelitis of the tibia: a retrospective study. J Reconstr Microsurg 2006; 22:41–47.

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Spinal Infection Bernhard Tins and Victor Cassar-Pullicino

ETIOLOGY Spinal infection is still a potentially lethal disease with several causes. The three most commonly encountered routes of infection are hematogenous spread, direct spread, and direct inoculation, which is usually iatrogenic. Arterial hematogenous spread can be due to an infectious focus anywhere in the body. This can be responsible for pyogenic as well as nonpyogenic infections and is the most common source of infection. Venous spread is unusual. The second main cause of spinal infection is direct spread from an infectious focus adjacent to the spine. Spread from infection in the pelvic, perirenal, pleural, and pharyngeal areas is particularly common. The third main group of spinal infections results from direct inoculation. These are usually due to iatrogenic infections, that is, infection of the spine after a medical intervention. This can be after spinal surgery but is also seen after discography, myelography, facet joint injection, and epidural anesthesia and also after minor interventions such as paraspinal injections of trigger points or acupuncture. It may be seen as a consequence of vertebroplasty. The most common infectious agent is Staphylococcus aureus, which is encountered in about 60% of cases. Apart from S. aureus, virtually any infectious agent may cause spinal infection. Bacterial infections are much more common than fungal or parasitic infections. After Staphylococcus and Mycobacterium tuberculosis, commonly found infectious agents are Escherichia coli and, in immunocompromised patients, gram-negative bacteria; intravenous drug users often suffer Pseudomonas infections.1–5

PREVALENCE AND EPIDEMIOLOGY Spontaneous spinal infection most commonly occurs in the elderly and the immunocompromised individual. Recognized risk factors are advanced age, male gender, immunosuppression, intravenous drug abuse, human immunodeficiency virus infection/AIDS, diabetes mellitus, sickle cell disease, use of corticosteroids, chemotherapy,

rheumatologic or immunologic disease, hepatic or renal failure, malnutrition, myelodysplastic disease, and other severe systemic diseases. The increased frequency of tuberculosis in developed as well as underdeveloped countries and the increased number of chronically debilitated patients all contribute to a greater incidence of spinal infection.6–9 The peak age for spinal infection is in the sixth and seventh decades of life, and more than 50% of patients with spinal infection are older than 50 years of age. Spinal infection represents 2% to 8% of all cases of osteomyelitis. Spinal involvement in tuberculosis occurs in about 50% of all tuberculosis cases when there is musculoskeletal involvement, although musculoskeletal involvement in tuberculosis overall is not common and occurs in only 1.5% to 3% of patients infected with M. tuberculosis. However, about a third of the world’s population harbors tuberculosis and this results in a significant prevalence of infections. Spinal infections due to nonpyogenic and nontuberculous agents such as brucellosis or fungal infections are comparatively rare in the Western world. Iatrogenic spinal infections occur in up to 4% of all spinal surgery patients and represent up to 30% of all cases of spinal infection. The use of preoperative antibiotic prophylaxis dramatically decreases the risk of postoperative infection by about a factor 10.

KEY POINTS MRI is the imaging method of choice. Bone marrow edema is evident. Bone destruction occurs. The infection is often centered around the intervertebral disc, but any part of the spine can be affected. ■ Phlegmon and abscess formation are best imaged with contrast agent enhancement. ■ Epidural involvement is a surgical emergency; the whole spine needs to be imaged. ■ ■ ■ ■

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The incidence and pathway of spinal infection differs according to age as the blood supply changes (see later). Infants have a direct vascular supply to the intervertebral disc up to the age of about 6 months. The area most commonly affected by infection is the lumbar spine, followed by the thoracic spine, and then the cervical spine. Polymicrobial spondylodiscitis (concurrent infection with more than one infectious agent) is typically seen after surgery. Its incidence is as high as 50% of all cases. Otherwise, polymicrobial spondylodiscitis is unusual and seen overall in less than 2.5% of cases.

CLINICAL PRESENTATION The clinical presentation of spinal infection is highly varied and ranges from asymptomatic to critically ill patients. The severity and type of signs and symptoms depend on the part of the spine infected, the type of organism, and the host’s immune response. The clinical symptoms are usually nonspecific. Back pain, which is often localized, coupled with local tenderness, increased body temperature with raised C-reactive protein, and erythrocyte sedimentation rate is common. Leukocytosis can be present but is an unreliable sign. The back pain caused by spinal infection often worsens with standing and activity and is improved by not bearing weight. Pain can occur at night with varying severity. The varied and often vague symptoms make it difficult to differentiate spinal infection from simple mechanical back pain.10–12 Involvement of the epidural space results in clinical deterioration and the onset of neurologic symptoms and signs. The clinical diagnosis of spinal infection poses a particular challenge in patients with underlying preexisting disease. In patients with prior chronic back pain a change in the type or quality of pain can be a sign of spinal infection. However, this finding is nonspecific and more often is due to deterioration of mechanical back pain. In patients who have had back surgery, recurrence of pain may be the only indicator of clinical infection. Biopsies and blood cultures aid the diagnosis and help to identify the infective pathogen but do not exclude spinal infection if they are negative! The yield of positive cultures varies greatly and is reported in the literature to be between 50% and 90% for biopsies and 25% and 60% for blood cultures. However, the combination of both tests can result in diagnostic yields of up to 96%! If a spinal biopsy sample is taken, the infected end plate (not the disc) usually results in the highest yield. More samples result in a higher diagnostic yield. Antibiotic therapy before biopsy or blood culture results in poorer diagnostic yields. The diagnosis of spinal infection is often delayed by 2 to 3 months. This potential delay is important because good clinical outcome depends on early diagnosis!

PATHOPHYSIOLOGY Anatomy The understanding of the disease process in spinal infection requires a good knowledge of spinal anatomy.

In infants younger than 6 months old there is a direct vascular supply to the intervertebral disc so that direct hematogenous infection can occur. As infants age the direct vascular supply disappears but there are still focal areas of vascular channels in the cartilaginous end plate of the vertebral bodies that are seen to an age of 5 to 7 years. These enable hematogenous deposition of pathogens into the immediate vicinity of the intervertebral disc. Finally, in the normal adult the vertebral body end plate poses a considerable barrier to bloodborne infection. However, in severe degenerative disc disease, blood vessels can secondarily invade the intervertebral disc and direct hematogenous infection can occur. In the adult, the spinal column is surrounded by a dense anastomotic network of arteries formed by segmental vessels and their branches. These segmental arteries enter the spinal canal through the intervertebral foramina. Nutrient arteries enter the vertebral body from inside as well as outside the vertebral canal. The terminal branches of the nutrient arteries are end arterioles. This predisposes to embolic infarctions in the richly vascularized paradiscal area of the vertebrae. The metaphyseal anterolateral part of the vertebral body, adjacent to the cartilaginous end plates, has a particularly dense vascular supply. This area is often the starting point of infection by oxygen-loving M. tuberculosis, but it is also the site of most change in inflammatory spondyloarthropathies and the origin of degenerative osteophytes. The paravertebral venous plexus is valveless, but whether the venous plexus contributes significantly to the spread of infection remains unclear.

Pathology In the most commonly encountered cases of hematogenous spinal infection the primary infected area is often the anterolateral paradiscal area of the vertebral body as a consequence of the increased vascular supply to this area. Initially, an inflammatory, edematous bone marrow reaction occurs. Bone destruction, paravertebral spread, and involvement of the adjacent intervertebral disc follow. The pattern of spread of a spinal infection is partly dictated by the location of the initial infection and the aggressiveness and type of the infectious agent (Fig. 63-1). Pathogens producing proteolytic enzymes (e.g., S. aureus) quickly spread into adjacent structures. The vertebral body end plate and the intervertebral disc are not effective barriers. Disc involvement in infection with pyogenic pathogens is most often seen after 1 to 3 weeks and usually leads to involvement of an intervertebral disc and the two adjacent vertebrae. Disc destruction leads to loss of disc height. The concurrent end-plate destruction becomes clearer with time. At 8 to 12 weeks after the onset of spinal infection reactive bony sclerosis is observed. When spread to adjacent tissues takes place there will be edema, phlegmon (diffuse inflammatory mass), and abscess formation. Pathogens that do not produce proteolytic enzymes (such as M. tuberculosis) typically spread slowly and

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■ FIGURE 63-1 A 75-year-old woman presented with worsening severe back pain. Radiographs (A and B) demonstrate L4-L5 disc and vertebral end-plate destruction with focal kyphosis. STIR (C), T2-weighted (D), and T1-weighted precontrast (E) and postcontrast (F) MR images show vertebral high signal intensity in STIR, less marked signal increase with T2 weighting, and signal decrease with T1 weighting. Note the increased signal intensity after contrast medium administration in the remnants of L4 and L5 vertebral bodies and a rim-enhancing abscess centered onto the L4–5 disc space bulging posteriorly into the spinal canal. Note also the improved depiction of edema on STIR as compared with T2-weighted images. These are typical findings of spondylodiscitis.

insidiously (Fig. 63-2). Complications of the infection such as fistulating abscesses (either along fascial spaces or even into peritoneum or pleura) or gibbus formation can be the presenting features. The intervertebral disc can be spared completely or may be involved very late in the disease process. Apparent loss of disc height can be due to disc herniation into vertebral bodies through

weakened end plates rather than disc involvement by the infection. Involvement of paravertebral tissue can be in the form of a phlegmon or abscess formation. Abscess can spread underneath the paraspinous ligaments, elevating them and even leading to compromise of the vertebral vascular supply, ultimately causing avascular necrosis of the vertebrae.

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In spinal infection by direct inoculation there is usually a relevant clinical history either of penetrating trauma or an iatrogenic intervention. The localization of the infection is obviously dependent on the history. The most serious complications of spinal infection are epidural or meningeal and spinal cord involvement. Epidural phlegmon or abscess formation can lead to rapid deterioration with permanent disability or death if not treated early (Fig. 63-3; see also Fig. 63-1). Epidural abscesses frequently demonstrate discontinuous spread within the spinal canal; and if epidural infection is noted, the whole of the spine should be imaged. Epidural involvement constitutes a surgical emergency! Involvement of the subdural space with meningitis or direct involvement of the spinal cord is relatively rare.

A diagnostic approach solely based on radiographs is inaccurate because of the poor sensitivity particularly for early infection and spinal infection other than spondylodiscitis and because of its poor specificity. Destruction of the vertebral end plate is the most specific sign of spinal infection but is seen at the earliest several weeks (4 to 6 weeks) into a pyogenic infection. Loss of disc height is nonspecific, and its most common cause is degenerative disc disease. Paraspinal masses are not often identified on radiographs and, if observed, are not specific for infection. If children are affected, the radiographic changes develop significantly faster. Loss of disc height may be seen after a few days to 2 weeks, end-plate erosion/ destruction may be noted after a few weeks, and reactive bone sclerosis may be observed after 1 month.

IMAGING TECHNIQUES Techniques and Relevant Aspects

Magnetic Resonance Imaging

Radiography Radiography is often the first examination performed in a patient with back pain. The first radiographic signs of spondylodiscitis are loss of disc height, vertebral end-plate destruction, and possibly paraspinal soft tissue masses (see Figs. 63-1 and 63-3). New bone formation or paraspinal calcification may also be observed. With advanced destruction, spinal deformity may occur.13–15

Magnetic resonance imaging is the examination of choice in cases of suspected or established spinal infection. Its sensitivity, specificity, and accuracy have been reported as 96%, 92%, and 94%, and these are the best values for any imaging.16–29 In addition, MRI is the ideal method for evaluation of epidural and paraspinal spread, facilitating medical and surgical management. Other imaging methods are superior only in postoperative imaging (nuclear medicine) or in the assessment of an early bony response (CT).

■ FIGURE 63-2 A 31-year-old man presented with complaints of persistent neck pain. An initial MRI of the cervical spine was reported as normal. The T1-weighted (A) and T2-weighted (B) midline slices demonstrate subtle abnormal signal in relation to the anterior aspect of the atlantodental articulation. Parasagittal slices (C) demonstrated a soft tissue mass between the lateral masses of C1 and C2. This was not appreciated at the time. Axial images were acquired from the C2-3 interforaminal level caudally and did not include the area of abnormality.

(Continued)

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■ FIGURE 63-2—Cont’d A repeat examination due to persistent severe pain 5 months later with T1-weighted precontrast (D) and postcontrast (E) and STIR (F and G) MR images demonstrate abscess formation in relation to the anterior aspect of the atlantodental articulation; the laterally extending inflammatory soft tissue mass is much better demonstrated after contrast medium enhancement and in STIR weighting. CT (H) shows a soft tissue mass with calcific debris and bone destruction. Mycobacterium tuberculosis was isolated in culture. Spinal infection can be missed even on MRI, especially when not presenting in a typical fashion. M. tuberculosis infection is more likely not to present as typical spondylodiscitis.

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■ FIGURE 63-3 A 69-year-old woman presented with pyogenic infection at T5–6 with epidural abscess formation. A, Lateral radiograph demonstrates disc and end-plate destruction. MRI shows bone marrow edema and epidural abscess formation causing cord compression on STIR (B), T2-weighted (C), T1-weighted (D), and contrast-enhanced T1-weighted (E) images. The epidural abscess is best appreciated on the T2-weighted image in C. Note also the involvement of the anterior inferior edge of T4 vertebral body. Antibiotic drug therapy was begun. One month later, T2-weighted (F), T1-weighted (G), and T1-weighted contrast-enhanced (H) images show that the epidural abscess has decreased in size but the spinal cord shows abnormally high signal intensity on T2 weighting. The patient now was paraplegic.

(Continued) Bone marrow edema (shown by high short tau inversion recovery [STIR], high T2-weighted, fat saturated, low T1-weighted signal) is the hallmark of spinal infection (see Figs. 63-1 and 63-3). Via the disc the adjacent vertebral body is often also involved early in spondylodiscitis. The infected intervertebral disc loses the low T2-weighted signal intranuclear cleft and displays

a very high T2-weighted signal intensity in its entire body. The disc height is usually reduced early but can sometimes appear widened due to erosion of the adjacent vertebral end plate. Contrast agent enhancement helps differentiate nonenhancing disc fragments from inflammatory tissue because normal disc does not enhance.

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■ FIGURE 63-3—Cont’d Further follow-up imaging 3 months later (I, T2 weighted image; J, T1-weighted image; K, contrast-enhanced T1-weighted image) shows regression of the epidural abscess but progression of bone destruction. Contrast medium enhancement is reduced, indicating reduction of inflammation. At 2 years later (L, T2 weighted image; M, T1-weighted image) there is complete healing with fusion of the T5 and T6 vertebral bodies. Both are reduced in height, and there is also anterior fusion to the T4 vertebral body.

Infection of the spinal canal and the posterior elements is imaged most accurately by MRI. Epidural involvement in spinal infection is indicated by a decrease in T1-weighted signal intensity of epidural fat; increase in T2weighted signal can be difficult to appreciate without fat suppression. STIR or fluid-attenuated inversion recovery (FLAIR) imaging is more sensitive. Abnormal fluid collections usually demonstrate higher T1-weighted and lower T2-weighted signal intensity than cerebrospinal fluid, but phlegmon as well as abscess collections can show mixed signal on T1- and T2-weighted images. The use of contrast agents permits reliable differentiation of phlegmon

and abscesses. Collections show rim enhancement only whereas phlegmon shows uniform contrast enhancement. Diffusion-weighted imaging also has been shown to help in the diagnosis of collections because they exhibit markedly hyperintense signal against adjacent tissue and appear dark on apparent diffusion coefficient (ADC) maps. Meningitis can be diagnosed by observing abnormal contrast enhancement. If enhancement is nodular or “shaggy,” it suggests granulomatous disease (including tuberculosis). Involvement of the spinal cord is indicated by an increase in T2-weighted signal intensity, abnormal contrast enhancement, and, if severe, vacuolization.

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In cases of proven epidural involvement the whole spine has to be imaged because there is often very extensive involvement of the spinal canal with areas of relative sparing. Paravertebral involvement can occur as phlegmon, diffuse infection of tissue, or abscess. Care must be taken to image paravertebral infection in its entirety because otherwise fistulas and tracking abscesses can be overlooked. Once a spinal infection has been diagnosed and treatment begun there is no clear body of opinion as to the role of imaging in clinically uncomplicated cases. MRI findings of healing are the decrease in contrast enhancement, reduction of edema and abscess size, and beginning normalization of the signal pattern, which is seen a few weeks to months after the start of treatment. The absence of contrast medium enhancement and return of the spine to a normal signal pattern are both sure signs of complete healing of a spinal infection. However, the reverse is not true. Persistence of contrast medium enhancement in the intervertebral disc as opposed to the vertebral body is more common. The signal pattern of the bone marrow can revert to normal, but sclerosis and fibrosis can lead to low T1- and T2-weighted signal patterns. If fatty marrow replacement occurs, high T1-weighted signal will be seen (see Fig. 63-3). Surgical implants can cause artifact and make image interpretation more difficult or impossible. The imaging protocols for MRI of spinal infection are straightforward. Sagittal imaging should include edema-sensitive sequences such as STIR or T2-weighted, fat-saturated images. If a reliable fat-saturation technique is not available T2-weighted spin-echo imaging (TR > 2000 ms; TE 100–200 ms) is advised. Fast spin-echo imaging should not be used in these cases because edema may not be reliably diagnosed. Contrast medium enhancement is more clearly seen on T1-weighted, fat-saturated images. Abnormal areas should be assessed in sagittal and axial planes and particularly for axial imaging an enlarged field of view may be necessary to demonstrate paraspinal involvement. If epidural infection is seen, whole-spine imaging with contrast medium enhancement is mandatory.

Diffusion-Weighted Imaging Diffusion-weighted imaging of spinal abnormalities can be used as an adjunct in select cases. Sometimes the imaging features of spinal infection and malignancy are very similar and confident diagnosis is not possible. Paraspinal abscesses are hyperintense compared with adjacent tissue in diffusion-weighted imaging and low signal on the ADC map. Usually the ADC of neoplastic lesions is significantly lower than that of infection.

Computed Tomography Computed tomography of the spine is not normally the examination of choice for diagnosis of spinal infection. CT has relatively poor soft tissue contrast and cannot demonstrate the earliest sign of spondylitis, which is bone marrow edema. It usually can demonstrate paraspinal masses and abscesses but not as well as MRI.30 CT can show loss of disc height, although the differentiation of degeneration and infection can be difficult. Epidural

phlegmon and even epidural abscess formation are not well imaged or differentiated using CT. CT is well suited to demonstrate bone destruction and bony reaction in the form of sclerosis. It also is the best imaging method to show calcification and gas in soft tissue. CT best allows the assessment of an early healing response (new bone formation) after successful treatment of spondylodiscitis. It can demonstrate sclerosis of the remaining bone cortex and marrow at about 6 weeks after the onset of infection whereas these changes are only clearly appreciated on MRI at around 12 weeks after the onset. CT is valuable for the imaging of postoperative infections.

Ultrasonography Ultrasonography plays little role in the diagnosis of spinal infection, although its use in children has been suggested. It is sometimes used intraoperatively especially for localizing epidural abscess collections, and it is sometimes of value in differentiating paravertebral abscesses from diffusely solid phlegmon. It has been used to guide percutaneous drainage of abscesses.

Nuclear Medicine Nuclear medicine techniques include technetium-99m– labeled bone scintigraphy and infection-specific techniques, such as labeled white cells, labeled antibody fragments, ciprofloxacin, gallium, and also positron emission tomography.31–33 All these methods offer good sensitivity but poor specificity and anatomic resolution even when combined with single photon emission computed tomography. For the initial diagnosis these techniques have been superseded by MRI, but they are still sometimes useful in the imaging of postoperative infection.

Pros and Cons MRI is the imaging method of choice for spinal infection. Cost considerations may play a role, and MRI may not be possible in all patients with back pain. The only feature in favor of radiography is its almost universal availability. The problem with radiographs is poor or absent sensitivity for any spinal infection other than destructive spondylodiscitis. Radiographs can play a role in monitoring complications. CT is well suited to assess bone response to spinal infection and can be performed under virtually any circumstances. Disadvantages are the poor depiction of soft tissues when compared with MRI and that it uses ionizing radiation. Nuclear medicine techniques (including positron emission tomography) offer reasonable sensitivity but poor specificity and poor anatomic detail. Ultrasonography does not play any significant role in the initial diagnosis of spinal infection.

Controversies There are no real controversies in the imaging of spinal infection. The main caveat in imaging of spinal infection is to image the whole spine when spinal infection has been diagnosed so as to not miss epidural or other multilevel involvement.

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MANIFESTATIONS OF THE DISEASE Infection with Mycobacterium tuberculosis

After treatment, progression of destructive change is regularly seen and can last up to 14 months. This is significantly longer than for pyogenic infection.

Infection with M. tuberculosis is the most common granulomatous disease of the spine, and spinal tuberculosis accounts for half of all cases of musculoskeletal tuberculosis. In developed countries, musculoskeletal tuberculosis affects mainly the elderly and is thought to be due to reactivation of an old focus of tuberculosis; however, it may be seen in immigrants of any age who are in otherwise good health when they come from countries with a high prevalence of tuberculosis. In underdeveloped countries, children and young adults are primarily affected and the disease tends to be more aggressive. Tuberculous spinal infection usually presents as relatively mild symptoms and progresses slowly, often leading to a long delay before diagnosis (see Fig. 63-2). Spinal tuberculosis is usually due to hematogenous spread from a focus in the lung or the genitourinary tract. The thoracolumbar junction or lumbar spine is most commonly affected. The more cranial parts of the spine are more often infected with tuberculous infection than pyogenic infection. Spinal tuberculosis typically starts in the well-vascularized anterolateral edge of a vertebral body. It can spread underneath the longitudinal ligaments to adjacent vertebral bodies and can cause vascular compromise with avascular necrosis and subsequent vertebral body collapse. Central abscess formation within the vertebral body is relatively common whereas bone sclerosis is less common and florid than for pyogenic infection, although in chronic cases reactive new bone formation can be considerable. Arachnoiditis, meningitis, and infection of the spinal cord occur more frequently in tuberculosis of the spine than other spinal infections. Often there is no associated spondylitis. Erosion of the vertebral body end plate can cause disc herniation into the vertebral body and loss of disc height without actual infection of the disc. Large paravertebral abscesses are commonly seen in tuberculosis of the spine. They are often symmetric and tend to be larger than in pyogenic infections. Abscesses can track long distances, and sinuses are frequently seen in the groin, buttock, and chest. If an abscess is calcified, this is very suggestive of tuberculosis; if an air-fluid level is seen, then tuberculosis is virtually excluded (provided that there is no sinus connecting to the skin surface or gas-containing structures). Vertebral body destruction is common in spinal tuberculosis (up to 73%), and this makes spinal deformity with gibbus or vertebra plana and neurologic compromise more common than in other infections. Kyphotic deformities tend to be more severe in the thoracic spine. Neurologic compromise rarely occurs due to bony collapse alone. It is either due to associated subluxation/dislocation or occurs in the acute disease as the result of epidural involvement. Involvement of the posterior elements is common in spinal tuberculosis and seen in more than 40% of cases. This leads to an increased incidence of neurologic complications and a more difficult differential diagnosis, especially against neoplasia. Isolated infection of the posterior elements is rare (1 month’s duration) Cytomegalovirus disease (other than liver, spleen, or nodes) Cytomegalovirus retinitis (with loss of vision) Encephalopathy, HIV-related Herpes simplex: chronic ulcer(s) (>1 month’s duration); or bronchitis, pneumonitis, or esophagitis Histoplasmosis, disseminated or extrapulmonary Isosporiasis, chronic intestinal (>1 month’s duration) Kaposi sarcoma Lymphoma, Burkitt’s (or equivalent term) Lymphoma, immunoblastic (or equivalent term) Lymphoma, primary, of brain Mycobacterium avium complex or M. kansasii, disseminated or extrapulmonary Mycobacterium tuberculosis, any site (pulmonary or extrapulmonary) Mycobacterium, other species or unidentified species, disseminated or extrapulmonary Pneumocystis jiroveci (carinii) pneumonia Pneumonia, recurrent Progressive multifocal leukoencephalopathy Salmonella septicemia, recurrent Toxoplasmosis of brain Wasting syndrome due to HIV

*Categories A3, B3, C1, C2, and C3 meet the case definition for AIDS. Musculoskeletal entities associated with HIV/AIDS are in boldface type.

without treatment. Opportunistic infections as listed in the case definition (Table 67-1) are the hallmarks of progression to AIDS and usually happen with a CD4-positive count 50% of cases) is S. aureus, including methicillin-resistant S. aureus (MRSA) strains, which have increased in incidence over the past 4 years in people living with HIV/AIDS.17 MRSA strains cause a rapidly progressive and exquisitely painful suppurative infection; patients often complain of a “spider bite.” Other pathogens include Pseudomonas species, Escherichia

Necrotizing Fasciitis Necrotizing fasciitis is commonly preceded by trauma or intravenous drug use in people living with HIV/AIDS. It is a rapidly progressive infection accompanied by severe

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systemic toxicity, caused by mixed aerobic and anaerobic infection, including Clostridium species with gas formation along fascial planes, and can be fatal if not promptly diagnosed and treated. Clinically, the patient’s pain is out of proportion to the objective findings of fever and brawny edema. When employed, imaging should be expedient but should not delay surgical exploration if the diagnosis is suspected (Fig. 67-5). Cross-sectional imaging demonstrates fascial thickening with or without enhancement, fluid along fascial septa, muscle edema, occasional soft tissue gas, and associated collections. Necrotic muscle is low in attenuation on CT. Lack of enhancement is seen on MRI in nonviable foci. Antibiotics are not effective unless the necrotic tissue is extensively débrided; hyperbaric oxygen therapy may provide some benefit.

Pyomyositis ■ FIGURE 67-3

Pyomyositis. Axial CT image (with contrast) of the left thigh demonstrates intramuscular abscesses with enhancing margins in the vastus lateralis and medialis muscles and intermuscular fluid collections between the vastus intermedius and rectus muscles.

■ FIGURE 67-4

A middle-aged woman with AIDS presented with clinical suspicion of tibiotalar joint septic arthritis. A, Axial, T2-weighted MR image of tenosynovitis of the anterior compartment extensors. B, Axial, T1-weighted MR image shows an abscess in the anterior compartment of the calf associated with extensor tenosynovitis. C, Axial, T1-weighted, fat-saturated MR image shows an abscess in the plantar compartment of the forefoot associated with the tracking tenosynovitis of the extensors. A small communicating tract insinuating between the first and second metatarsals was present (not shown).

Although bacterial myositis was formerly considered rare outside the tropics the incidence has been rising recently in the West because this is a fairly common entity in people living with HIV/AIDS. Pyogenic myositis is most com-

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common. Intravenous antibiotics are effective if instituted early. Blood cultures are positive in 20% to 50% of patients; by far the most common pathogen isolated is S. aureus, followed by Streptococcus and Salmonella species. M. tuberculosis and numerous opportunistic organisms have been described.19–21 CT of pyogenic myositis shows muscle enlargement and decreased attenuation of edematous muscle; contrast enhancement may reveal intramuscular collections/abscesses. MRI better depicts the muscle edema, and contrast reveals the microabscesses (Fig. 67-6). MRI or CT is helpful in defining the extent of infection and guiding the drainage of the infected areas, and ultrasonography is useful for followup. Treatment is surgical drainage and long-term therapy with appropriate antibiotics. ■ FIGURE 67-5

Septic Arthritis

monly seen in the thigh or buttocks, most commonly in the quadriceps muscles. In people living with HIV/AIDS, pyomyositis is mostly seen in males (95% of cases) with CD4 count less than 100 cells/mm3; pyomyositis is also seen in the context of diabetes or other systemic illnesses. Pyomyositis is characterized as a multifocal suppurative abscess-forming infection of the muscles presenting as local tenderness and stiffness (“woody induration”), associated with fever, leukocytosis, and systemic symptoms. The skin and subcutis are relatively unaffected. Initially, there is a stage of inflammatory myositis followed by myonecrosis and abscess formation. A history of preceding intravenous drug abuse, local trauma, or exercise is

The most common predisposing factor in the Western world is intravenous drug use, followed by hemophilia. It presents as monarthritis in more than two thirds of the cases, involving a peripheral joint (knee, wrist, hip, shoulder, sternoclavicular joint, ankle and metacarpophalangeal joints), but the spine is also affected in a third of cases. The most commonly implicated organisms are S. aureus in 30%, atypical mycobacteria (M. haemophilum, M. kansasii, M. avium complex, M. terrae), Salmonella species, Streptococcus species (including S. pneumoniae), fungi, and M. tuberculosis (Fig. 67-7). In cases of prosthetic joint infections, an indolent organism such as coagulase-negative Staphylococcus is most commonly implicated. Fever, leukocytosis-localizing signs of inflammation, and extreme pain are common, especially with native joint infections. Septic arthritis is usually hematogenous in people living with HIV/AIDS owing to intravenous drug abuse; blood cultures are posi-

A middle-aged woman with profound sepsis presented with clinical suspicion of appendicitis. Axial CT image of the pelvis with enhancement shows necrotizing fasciitis, with gas tracking within the soft tissues of the buttocks, ischiorectal fossae, and paraspinal muscles and fascia.

■ FIGURE 67-6

A young patient with AIDS presented with fever and swelling of the left thigh. A, Coronal inversion recovery MR image shows extensive edema in the adductor compartment. B, Axial, T1-weighted MR image with fat saturation, after intravenous administration of gadopentetate dimeglumine, shows enhancement of the adductor brevis muscle and a small abscess collection with enhancing margins.

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■ FIGURE 67-7

Musculoskeletal tubercular septic joint. Axial, T2-weighted MR image of the wrist demonstrates wrist effusion, synovitis, small bone erosions, and tenosynovitis.

tive in about 40% of cases. It is not clear whether people living with HIV/AIDS have a higher incidence of septic arthritis or if the septic arthritis is related to concomitant risk factors (e.g., intravenous drug abuse); however, the spectrum of pathogens is more diverse in HIV infection and the prognosis can be worse. Imaging is important to assess the extent of infection and the number of associated abscess cavities that need to be drained and to assist in aspiration of difficult-to-access spaces; occasionally, joints can be irrigated via a catheter placed by interventional radiology. Ultrasonography is useful for the assessment of associated bursitis and tenosynovitis. The diagnosis of septic arthritis is confirmed by analysis of the synovial fluid, which is critical for Gram stain and cultures (60% are positive) to guide intravenous antibiotic therapy. Since in most cases rapid destruction of the joint space can ensue, prompt arthrotomy and irrigation of the affected joint is essential. In prosthetic joint infections, removal of the prosthesis and interval placement of antibiotic-laced spacers is usually warranted to manage the infection.22,23

Osteomyelitis (Nontuberculous) Acute osteomyelitis often involves the axial skeleton in people living with HIV/AIDS, usually presenting in patients with lower CD4 counts than those with septic arthritis. Infecting organisms can reach the bone by hematogenous dissemination, contiguous spread, and trauma/wound/direct inoculation. Atypical mycobacteria are commonly isolated, followed by S. aureus (most often associated with intravenous drug use), Streptococcus species, Candida, other fungi including endemic ones (Coccidioides immitis) and gram-negative organisms. Because blood cultures are positive only in 20%, bone biopsy, open débridement, and cultures may be needed to guide therapy. Acute bacterial osteomyelitis of the spine usually presents as discitis extending subsequently to adjacent

vertebral bodies, in contradistinction to tuberculous spondylitis, which involves the disc late. MRI is helpful in identifying the extent of infection of marrow and in the surrounding tissues and to follow response to treatment. Bone scintigraphy can be sensitive but is not specific for infection, and gallium scanning may be employed. Depending on the infecting organisms and extent of involvement, osteomyelitis can be difficult to treat and carries a mortality rate of about 20%.24 Cases of bacillary angiomatosis have been described in patients with AIDS since the early 1980s. The causative organisms are Bartonella henselae and B. quintana, which also cause cat scratch disease and trench fever. Cats are the main host, and fleas are the vector. The patient presents with fever, anemia, hepatosplenomegaly, characteristic reddish skin papules, and hemangioendothelial lesions of varying size and number. The lymph nodes, central nervous system, eyes, gastrointestinal tract, and gingiva may be involved. About 25% of cases also demonstrate underlying painful nonsclerotic osteolysis, usually without sclerosis. The skin and subcutaneous lesions resemble Kaposi sarcoma. Diagnosis is made by serology for Bartonella and verified by biopsy; Warthin-Starry silver stain is required for histologic confirmation. Treatment is with antibiotics.25

Tuberculous Osteomyelitis, Spondylitis, Spondylodiscitis Mycobacterium tuberculosis and M. bovis (the two most common causes of tuberculosis) infect approximately one third of the global human population, with 2 million deaths annually as a result of tuberculosis complications.26 The HIV epidemic and its impact on tuberculosis epidemiology, the emergence of multidrugresistant strains, malnutrition, poverty, and increasing urban population concentration are all factors that make the control of tuberculosis difficult to achieve. The World Health Organization declared tuberculosis a global public health emergency in 1993, focusing on implementation of directly observed therapy. Humans are the only reservoir for M. tuberculosis; transmission of musculoskeletal tuberculosis occurs by inhalation of infectious respiratory droplet nuclei, causing primary infection, which can later reactivate. In non–HIV-infected individuals, the risk of reactivation is 5% to 15% overall, versus 7% to 10% per year for people living with HIV/AIDS. Musculoskeletal tuberculosis is the most common opportunistic infection in HIV-seropositive individuals in many countries. People living with HIV/AIDS co-infected with musculoskeletal tuberculosis have a higher rate of conversion to active disease than non–HIV-infected individuals, a shorter period of incubation, and more atypical and extrapulmonary manifestations of musculoskeletal tuberculosis, including musculoskeletal involvement, which is found in 3% to 5% of patients with tuberculosis. The majority (30%–50%) of musculoskeletal tuberculosis cases involve the spine (tuberculous spondylitis/Pott’s disease), with the lower thoracic area involved more than the lumbar region and the least involvement of the cervical and sacral areas. Transmission is usually hematogenous but can also be due to contiguous disease or lymphatic spread from tuberculous pleuritis. In contradistinction to pyogenic

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Classic Signs ■

■

About one fourth of cases of bacillary angiomatosis demonstrate underlying osteolytic bone involvement, usually without sclerosis. Osteoarticular musculoskeletal tuberculosis infection has a nonspecific radiographic appearance, but periarticular osteopenia, calcifications, abscesses and tenosynovitis with clinical history of indolence support this diagnostic consideration.

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people living with HIV/AIDS than in the noninfected population, with a reported prevalence of 1% to 32%,33 but severity is often greater and progresses with the disease. The cause of psoriatic arthritis in this population is not well understood. Radiographic evidence of spinal or sacroiliac joint involvement is rare. Nail changes and radiographic findings of digital “pencil in cup” deformities, single-ray involvement, erosions, and proliferative periosteal reaction may be seen. HIV-related psoriatic arthritis presents most commonly in the foot and ankle with enthesopathy and dactylitis but minimal synovitis and effusions.

Reactive Arthritis spinal infection, which initially presents as discitis with adjacent vertebral body involvement, tuberculous spondylitis characteristically insinuates along the anterior longitudinal ligament and then infiltrates the vertebral body. With time, spread to the adjacent disc and vertebrae occurs. Paraspinal “cold” abscesses develop in 50%, which can track along tissue planes and present as masses in remote areas (supraclavicular, inguinal, popliteal, posterior iliac). Aspiration of abscesses yield a paucity of bacilli, but biopsy can reveal bone marrow granulomas in about 75% of cases. In uncomplicated cases of Pott’s disease, response rates to systemic chemotherapy and bed rest until pain resolves exceeds 90%. Surgical intervention including laminectomy is helpful for neurologic complications and for advancing defects and/or significant spinal instability. Extravertebral tuberculous infection can occur in any bone or joint (most commonly in the large weight-bearing joints) and should be considered in people living with HIV/AIDS, particularly with low CD4 count, indolent history of bone or joint involvement, and atypical soft tissue or skeletal lesions. The findings of periarticular osteopenia, soft tissues abscess, and calcifications support this diagnosis. Diagnostic delay with osteoarticular tuberculosis is the unfortunate norm. Radiologists need to bear in mind that tuberculosis is 200 times more likely to occur in people living with HIV/AIDS and to have atypical, extrapulmonary and disseminated manifestations of tuberculosis than in noninfected individuals.

Related Inflammatory Conditions: Arthritides, Polymyopathies A number of arthritides and arthralgias including entities that may be unfamiliar to radiologists are seen in people living with HIV/AIDS.27–32 These include HIVassociated arthritis, painful articular syndrome (severe pain, short duration, self-limited, usually of the knees), and acute symmetric polyarthropathy. These show minimal changes at radiography and may not be imaged. Classification of arthritis in people living with HIV/AIDS can be difficult because these patients often present with incomplete or atypical manifestations of rheumatologic disease.

Psoriatic Arthritis The incidence of psoriatic arthritis (with or without psoriatic skin changes) is 10 to 40 times more common in

Reactive arthritis, formerly known as Reiter’s disease, was the first rheumatologic manifestation associated with AIDS and is the most common aseptic arthritis seen in people living with HIV/AIDS, with an estimated prevalence of 5% to 10%. It is commonly associated with enteric pathogen infections. In people living with HIV/ AIDS the classic triad of arthritis, urethritis, and conjunctivitis is the exception. There is no consensus of the role of HIV in the development of reactive arthritis. An asymmetric oligoarthritis of the lower extremity more so than upper extremity joints is seen, with involvement of ankle and foot most common. Plantar fasciitis, dactylitis, and enthesopathies (e.g., calcaneus, epicondyles) are demonstrated on radiographs. As for psoriatic arthritis, synovitis is uncommon. Differentiation between HIV-related psoriatic and reactive arthritis cannot be performed on the basis of radiographic appearance.34 Treatment is with nonsteroidal anti-inflammatory agents.

Acute Symmetric Polyarthritis Acute symmetric polyarthritis is characterized by acute onset, negative rheumatoid factor, and proliferative periosteal new bone formation. Radiographic manifestations are similar to those of rheumatoid arthritis and include alignment abnormalities of the digits, erosions, joint space narrowing, and periarticular osteopenia. Periosteal proliferation is highly suggestive of this HIVassociated arthritis and is the differentiating feature from rheumatoid arthritis.

Nonspecific Arthralgias Nonspecific arthralgias are the most common noninfectious musculoskeletal complaint in people living with HIV/AIDS, occurring in up to 45% of patients; they often accompany primary HIV but are also seen in latency. They usually respond to mild analgesics and anecdotally improve after virologic suppression with HAART. A more severe painful syndrome of oligoarticular intermittent pain requiring narcotics for relief has also been described, occasionally associated with syphilitic infection in people living with HIV/AIDS.

Inflammatory Conditions of Muscle Idiopathic inflammatory polymyositis, which is often seen early in the course of HIV infection (prevalence < 1%), is of unknown pathogenesis but is hypothesized to

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be due to viral invasion of muscle versus an autoimmune response. Patients present with heliotrope rash, bilateral proximal muscle weakness and soreness, and elevated levels of creatine phosphokinase (CPK). The diagnosis is suggested by electromyography and muscle edema without discrete/rim-enhancing collections on MRI and is verified by muscle fiber biopsy.35 Rhabdomyolysis is manifested as abnormal release of creatine kinase and myoglobin from insulted muscle cells into the circulation. In people living with HIV/AIDS, rhabdomyolysis may be due to the HIV itself or may be secondary to bacteremia and sepsis or to alcohol and substance abuse. Common findings include the detection of pigments in urine in association with diffuse myalgia, muscle swelling, weakness, pain, and elevated CPK levels, along with some degree of hematuria. MRI may be used to exclude infectious causes of muscle pain such as abscess and pyomyositis. Treatment is supportive and aimed at protection of the kidneys. Inclusion-body myositis and nemaline myopathy are rare conditions, presenting as muscle weakness and wasting in people living with HIV/AIDS; the biopsy shows characteristic findings. Diffuse infiltrative lymphocytosis syndrome, a rare condition in people living with HIV/AIDS, usually presents as painless parotid enlargement (with sicca syndrome in 60% of cases), associated with polymyositis, lymphocytic infiltration of muscles, and inflammatory myopathy. Treatment is based on HAART and corticosteroids.

Related Musculoskeletal Neoplasms Kaposi sarcoma is the most common AIDS-associated neoplasm, previously seen in up to 20% of people living with HIV/AIDS, with recent decreasing incidence considered a direct result of HAART.36–39 Kaposi sarcoma is usually seen in people living with HIV/AIDS with CD4 counts less than 200 cells/mm3 and in endemic form in HIV-negative individuals in the Mediterranean area. Kaposi sarcoma is a vascular-endothelial tumor related to infection with human herpesvirus type 8 (HHV8), which usually presents as multifocal hyperpigmented skin lesions. These can progress to involve the lymph nodes, mucosa of the gastrointestinal and respiratory tract, lungs, liver, and spleen and may involve contiguous muscle and bone. Bone involvement is not as common as with bacillary angiomatosis or nonHodgkin’s lymphoma. Kaposi sarcoma involving bone must be differentiated from bacillary angiomatosis and tuberculous osteitis, which they resemble radiographically with nonspecific findings of erosion and osteolysis. On MRI, lobulated subcutaneous lesions are seen that rarely extend to involve muscle and bone; Kaposi sarcoma lesions do not enhance as intensely as those of bacillary angiomatosis (Fig. 67-8). Kaposi sarcoma will uptake thallium but not gallium, which suggests the diagnosis.40 Biopsy is necessary for definitive diagnosis. Non-Hodgkin’s lymphoma is considered one of the criteria for the diagnosis of AIDS and is the second most common neoplasm in people living with HIV/AIDS, occurring late in the disease course and associated with a low CD4 count. In this patient population, non-Hodgkin’s lym-

phoma is more advanced and aggressive at presentation and associated with greater extranodal involvement than in non–HIV-infected individuals. Bone is affected in 20% to 30% of cases, usually lytic lesions of the long bones of the lower extremities and axial skeleton.41 On radiographs and CT, extensive osteolysis, sclerosis, periosteal reaction, and pathologic fractures may be seen. MRI reveals any medullary infiltration and associated soft tissue masses. Biopsy is necessary for definitive diagnosis. Treatment is with chemotherapy and radiotherapy; the disease usually follows an aggressive course, with median survival at 12 months. Occasionally, adjacent or isolated muscle infiltration occurs; systemic symptoms (fever, weight loss, night sweats) are common. Other tumors that are seen in people living with HIV/AIDS that may infiltrate and/or metastasize to bone include multiple myeloma, lung, anal and cervical carcinomas, and Burkitt’s lymphoma. Kaposi sarcoma rarely invades bone, potentially a differentiating point from bacillary angiomatosis.

Musculoskeletal Complications of Antiretroviral Therapy Zidovudine myopathy and toxic mitochondrial myopathies related to other nucleoside-analogue reverse-transcriptase inhibitors (NRTIs) present as proximal muscle weakness after several months of NRTI treatment; the myopathy is most likely related to mitochondrial toxicity of this class of agents. Biopsy shows multifocal necrotizing myopathy without inflammatory infiltrate, and the mitochondria reveal structural abnormalities at electron microscopy. Imaging is nonspecific. Treatment is withdrawal of the offending agent. Immune reconstitution inflammatory syndrome presents as an adverse effect of HAART usually within 8 to 12 weeks of treatment initiation. It is believed to be due to immune restoration due to HAART and intensification of the inflammatory reaction to a preexisting opportunistic infection. Associated opportunistic infections can be musculoskeletal tuberculosis, Mycobacterium avium disease, cytomegalovirus end-organ disease, hepatitis B or C flares, and so on. Patients may present with fever, diffuse lymphadenopathy, and worsening of opportunistic infection symptoms. Although radiographic imaging can assist with diagnosis of lymphadenopathy (because intense contrast enhancement suggests increased nodal vascularity such as in acute infection, Kaposi sarcoma, and lymphomas), a muscle biopsy is required for diagnosis. Treatment is with corticosteroids, and, if needed, cessation of HAART. Rarely described as a side effect of long-term protease inhibitor treatment in the shoulder joints, adhesive capsulitis presents as soreness and progressive restriction in range of motion of the shoulders; it subsides gradually with discontinuation of the offending agent.

Miscellaneous Musculoskeletal Manifestations Avascular Necrosis The cause of avascular necrosis (AVN) among people living with HIV/AIDS is not well understood; the incidence

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■ FIGURE 67-8

A young man presented with AIDS and skin lesions of Kaposi sarcoma. A, Axial, T2 weighted MR image with fat saturation shows a lobulated mass with fluid signal intensity in the posterior medial subcutaneous soft tissues of the distal calf. B, Axial, T2-weighted MR image with fat saturation demonstrates subcutaneous Kaposi sarcoma lesions with infiltration into the distal tibia. Osseous involvement is uncommon with Kaposi sarcoma.

has increased in the past few years in people living with HIV/AIDS but not in the general population.42 Children with HIV/AIDS also demonstrate increased incidence of Legg-Calvé-Perthes disease.43 Large, weight-bearing joints are involved, the lower extremity more than the upper extremity. AVN is often multiarticular and usually presents as pain with ambulation and eventually at rest. Causes advanced include corticosteroid use, hyperlipidemia, alcoholism, “hypercoagulable” state, hypergammaglobulinemia, protein S deficiency, and antiphospholipid antibodies.44 There is poor correlation with CD4 count and suggestive but conflicting evidence of implication of HAART in the pathogenesis of AVN.45 Advanced AVN can be detected on radiographs. MRI is the most sensitive method for detecting early changes. The management of AVN depends on stage and the clinical treatment philosophy, ranging from observation and avoidance of weight bearing in early cases to decompression and, in advanced cases, femoral capping or joint replacement (Fig. 67-9).

Osteopenia and Osteoporosis A high prevalence (45%–70%) of decreased bone mineral density has been reported in HIV-infected individuals.46 The cause has not been established; hypothesized causes implicate the HIV virus, protease inhibitors, nucleosiderelated mitochondrial toxicity or lactic acidosis, development of lipodystrophy, immune reconstitution, nutritional and hormonal factors, prior AIDS-related wasting, and immobility. Dual-energy x-ray absorptiometry (DEXA) scans have been utilized for diagnosis and follow-up but

■ FIGURE 67-9

Coronal, T1-weighted MR image of the knee in a patient infected with HIV and experiencing knee pain shows extensive osteonecrosis/avascular necrosis of the distal femur, evidenced by a large lesion with geographic borders extending from the diaphysis to the articular surface. There is a minimal lateral condyle articular contour irregularity. A small infarct is present in the proximal tibial metaphysis.

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are not well standardized in people living with HIV/AIDS. The management and follow-up of people living with HIV/AIDS with low bone density remains controversial, but calcium and vitamin D supplementation along with bisphosphonates is used.

Hypertrophic Osteoarthropathy People living with HIV/AIDS with pulmonary infections such as Pneumocystis jiroveci or other pneumonitides may develop hypertrophic osteoarthropathy. Wavy periosteal reaction along the lower extremity tubular bones first involves the diaphysis but eventually can become more irregular and extend to the metaphysis and epiphysis.

Myositis Ossificans Circumscripta Myositis ossificans circumscripta is focal, nonmalignant heterotopic bone and/or cartilage formation in soft tissues and muscles, which may be seen in people living with HIV/AIDS, usually with antecedent trauma/insult. The appearance on radiographs, cross-sectional images, and scintiscans of hypertrophic osteoarthropathy and myositis ossificans is identical with findings in patients without HIV/AIDS.

SYNOPSIS OF TREATMENT OPTIONS Further curbing of the rates of the HIV epidemic will be difficult because prevention strategies are usually underused or partially effective, a vaccine is not available, and treatment cannot so far eradicate the virus. Therefore, managing the mortality and suffering associated with the pandemic needs to be addressed primarily through provision of effective treatment. Since 1996, potent antiretrovi-

ral agents became available in the privileged parts of the world, allowing for effective and durable virologic suppression and immunologic benefits in HIV infection. As of the end of 2006, 22 agents have been approved by the U.S. Food and Drug Administration (FDA) for treatment of HIV infection, in four major therapeutic classes: (1) nucleoside and nucleotide reverse transcriptase inhibitors, (2) nonnucleotide reverse transcriptase inhibitors, (3) protease inhibitors, and (4) fusion inhibitors. Presently, there are novel agents undergoing advanced-phase clinical trials that are expected to enter the therapeutic armamentarium soon in all the above and in newer classes. Access to treatment and care has greatly increased in recent years, and the number of people living with HIV/AIDS who have access to care and treatment in nonprivileged countries in 2006 is finally surpassing those in privileged ones. The benefits of HAART are dramatically significant and well documented in both settings.47 However, access to HAART in the areas that need it most is still significantly limited because of cost, lack of infrastructure and knowledge base for its use, local conflicts, and stigma, hence the underachievement of most of the global efforts for antiretroviral rollout so far.

What the Referring Physician Needs to Know ■

■

In the setting of infection, the clinician needs to assess the presence and extent of deep soft tissue and/or bone involvement. Imaging is sought to detect the presence of a gas-forming infection, abscess, myositis, necrosis, or underlying osteomyelitis.

ACKNOWLEDGMENT The authors would like to thank Kent Friedman, MD, Doohi Lee, MD, and Jamshid Tehranzadeh, MD, for their assistance in assembling this chapter.

SUGGESTED READINGS Belzunegui J, Gonzalez C, Lopez L, et al. Osteoarticular and muscle infectious lesions in patients with the human immunodeficiency virus. Clin Rheumatol 1997; 16:450–453. Bureau NJ, Cardinal E. Imaging of musculoskeletal and spinal infections in AIDS. Radiol Clin North Am 2001; 39:343–355. Lane N. Rheumatologic and Musculoskeletal Manifestations of HIV. HIV InSite Knowledge Base (web publication), October 1998, pp 1–14. Major NM, Tehranzadeh J. Musculoskeletal manifestations of AIDS. Radiol Clin North Am 1997; 35:1167–1189. Marquez J, Candia L, Restrepo CS, Espinoza LR. HIV-associated musculoskeletal involvement: the AIDS reader. 2004; 14:175–179, 183–184. Restrepo CS, Martinez S, Lemos JA, Carillo JA. Imaging manifestations of Kaposi sarcoma. RadioGraphics 2006; 26:1169–1185. Restrepo CS, Lemos DF, Gordillo H, et al. Imaging findings in musculoskeletal complications of AIDS. RadioGraphics 2004; 24:1029–1049.

Tehranzadeh J, Raymon RT, Steinbach L. Musculoskeletal disorders associated with HIV infection and AIDS: I. Infectious musculoskeletal conditions. Skeletal Radiol 2004; 33:249–259. Tehranzadeh J, Raymon RT, Steinbach, L. Musculoskeletal disorders associated with HIV infection and AIDS: II. Non-infectious musculoskeletal conditions. Skeletal Radiol 2004; 33:331–320. Tehranzadeh J, O’Malley P, Rafii M. The spectrum of osteoarticular and soft tissue changes in patients with human immunodeficiency virus (HIV) infection: Crit Rev Diagn Imaging 1996; 37:305–347. Tehranzadeh J, O’Malley P, Rafii M. The spectrum of osteoarticular and soft tissue changes in patients with human immunodeficiency virus (HIV) Infection. Crit Rev Diagn Imaging 1996; 37:305–347. Vassilopoulos D, Chalasani P, Jurado RL, et al. Musculoskeletal infections in patients with human immunodeficiency virus infection. Medicine 1997; 76:284–294.

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25. Pape M, Kollaras P, Mandraveli K, et al. Occurrence of Bartonella henselae and Bartonella quintana among human immunodeficiency virus infected patients. Ann NY Acad Sci 2005; 1063:299–301. 26. World Health Organization: Global Tuberculosis Control: Surveillance, Planning, Financing. WHO Report 2005 (WHO/ HTM/TB/2005.349). Geneva, WHO, 2005. 27. Havlir DV, Barnes PF. Tuberculosis in patients with human immunodeficiency virus infection. N Engl J Med 1999; 340:367. 28. Berman A, Cahn P, Perez H, et al. HIV infection associated arthritis: clinical characteristics. J Rheumatol 1999; 26:1158–1162. 29. Marquez J, Restrepo CS, Candia L, et al. Human immunodeficiency virus-associated rheumatic disorders in the HAART era. J Rheumatol 2004; 31:741–746. 30. Mody GM, Parke FA, Reveille JD. Articular manifestations of human immunodeficiency virus infection: best practice & research. Clin Rheumatol 2003; 17:265–287. 31. Solinger AM. Rheumatic manifestations of human immunodeficiency virus. Curr Rheumatol 2003; 5:205–209. 32. Cuellar ML. HIV infection-associated inflammatory musculoskeletal disorders. Rheum Dis Clin North Am 1998; 24:403–421. 33. Plate AM, Boyle BA. Musculoskeletal manifestations of HIV infection. AIDS Read 2003; 13:62–72. 34. Teranzadeh J, Tran M. Musculoskeletal imaging in AIDS. In: Medical Radiology—Diagnostic Imaging and Radiation Oncology: Radiology of AIDS. A Practical Approach. Berlin, Springer, 2001, pp 169–197. 35. Authier FJ, Gherardi RK. [Muscular complications of human immunodeficiency virus (HIV) infection in the era of antiretroviral therapy.] Rev Neurol (Paris) 2006; 162:71–81. French. 36. Cattelan AM, Calabro ML, De Rossi A, et al. Long-term clinical outcome of AIDS-related Kaposi’s sarcoma during highly active antiretroviral therapy. Int J Oncol 2005; 27:779–785. 37. Cattelan AM, Calabro ML, De Rossi A, et al. Acquired immunodeficiency syndrome related Kaposi’s sarcoma regression after highly active antiretroviral therapy: biologic correlates of clinical outcome. J Natl Cancer Inst Monogr 2001; (28):44–49. 38. Restrepo CS, Martinez S, Lemos JA, Carillo JA. Imaging manifestations of Kaposi’s sarcoma. RadioGraphics 2006; 26:1169–1185. 39. Schwartz RA. Kaposi’s sarcoma: an update. J Surg Oncol 2004; 87:146–151. 40. Turoglu HT, Akisik MF, Naddaf SY, et al. Tumor and infection localization in AIDS patients: Ga- 67 and Tl-201 findings. Clin Nucl Med 1998; 23:446–459. 41. Little RF, Gutierrez M, Jaffe ES, et al. HIV-associated non-Hodgkin lymphoma: incidence, presentation, and prognosis. JAMA 2001; 285:1880–1885. 42. Tehranzadeh J, Raymon RT, Steinbach L. Musculoskeletal disorders associated with HIV infection and AIDS: II. Non-infectious musculoskeletal conditions. Skeletal Radiol 2004; 33:331–320. 43. Gaughan DM, Mofenson LM, Hughes MD, et al. Pediatric AIDS Clinical Trials Group Protocol 219 Team. Osteonecrosis of the hip (Legg-Calvé-Perthes disease) in human immunodeficiency virusinfected children. Pediatrics 2002; 109:E74-E4. 44. Allison GT, Bostrom MP, Glesby MJ. Osteonecrosis in HIV disease: epidemiology, etiologies, and clinical management. AIDS 2003; 17:1–9. 45. Mary-Krause M, Billaud E, Poizot-Martin I, et al. Risk factors for osteonecrosis in HIV-infected patients: impact of treatment with combination antiretroviral therapy. AIDS 2006; 20:1627–1635. 46. Delaunay C, Loiseau-Peres S, Benhamou CL. Osteopenia and human immunodeficiency virus. Joint Bone Spine 2002; 69:105–108. 47. Sow PS, Otieno LF, Bissagnene E, et al. Implementation of an antiretroviral access program for HIV-1-infected individuals in resource-limited settings: clinical results from 4 African countries. J Acquir Immune Defic Syndr 2006; 69:105–108.

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Atypical Mycobacterial Infection Mihra S. Taljanovic

PREVALENCE AND EPIDEMIOLOGY

Mycobacterial Infection In the 1950s the atypical mycobacteria were recognized as human pathogens. They are morphologically similar to Mycobacterium tuberculosis but have different colonial characteristics. Because there is no evidence of humanto-human transmission, the atypical mycobacteria do not pose public health hazards.1,2

ETIOLOGY The mycobacterial organisms known to cause musculoskeletal system infections in humans are: M. aviumintracellulare (found in soil, water, swine, cattle, birds, and fowl), M. xenopi (found in water), M. malmoense (reservoir unknown), M. haemophilium (reservoir unknown), M. ulcerans (reservoir unknown), M. terrae (found in soil and water), M. triviale (found in soil and water), M. gastri (found in soil and water), M. kansasii (found in water, cattle, and swine), M. marinum (found in fish and water), M. simiae (found in primates and possibly water), M. asiaticum (found in primates), M. scrofulaceum (found in soil, water, and moist or liquid foodstuffs), M. szulgai (reservoir unknown), M. fortuitum (found in soil, water, animals, and marine life), M. chelonae (found in soil, water, animals, and marine life), M. abscessus (found in soil, water, animals, and marine life), M. smegmatis (found in soil, water, animals, and marine life), M. phlei (found in grass and hay), and M. nonchromogenicum (found in grass and hay). Most osseous infections, however, are caused by M. kansasii and M. scrofulaceum, followed in frequency by M. avium-intracellulare and M. fortuitum.1 1342

Atypical mycobacteria account for 0.5% to 30% of all mycobacterial infections. The rate of clinical infection by atypical mycobacteria is low, because they colonize rather than invade the host. The infection of skin and lungs is most common. The involvement of the musculoskeletal system occurs in 5% to 10% of patients with atypical mycobacterial infections. Although the atypical mycobacterial infections are more commonly seen in elderly and immunocompromised patients, they can occur in a normal host.1–18 In patients with AIDS, the atypical mycobacteria usually produce musculoskeletal infections in advanced stages of disease.10,11

CLINICAL PRESENTATION Musculoskeletal infections caused by atypical mycobacteria resemble those caused by M. tuberculosis, although they tend to have a milder course. However, in children, atypical mycobacterial infections can be more aggressive and can result in gross disturbance. Presenting symptoms are nonspecific and include local pain and swelling, joint stiffness, low-grade fever, sweats, chills, anorexia, malaise, and weight loss. The diagnosis is frequently delayed, with average diagnosis from the onset of symptoms up to 10 months. With the disseminated infection, osseous manifestations are common.1,2

KEY POINTS The infection is indolent. Imaging characteristics are similar to those for infection with M. tuberculosis. ■ Antimycobacterial chemotherapy and surgical removal of the lesion are recommended. ■ ■

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In patients with mycobacterial spondylitis, local tenderness, pain, and limitation of spinal mobility are the presenting symptoms, whereas constitutional symptoms such as fever, malaise, and weight loss may also occur. On neurologic examination, evidence of compressive neuropathy with or without paralysis may be revealed.1 Dermal inoculation of atypical mycobacteria can result in soft tissue infection including skin ulcers, cellulitis, cutaneous granulomas, deep necrotizing infection, and abscesses. Septic myositis, polymyositis, septic bursitis, septic tenosynovitis, and carpal tunnel syndrome can also occur. The presenting symptoms are nonspecific and include pain, swelling, erythema, warmth, stiffness, and functional compromise.1,7,12,18

PATHOPHYSIOLOGY Mechanisms of musculoskeletal infection include hematogenous spread and contamination after injury or surgery. In particular, atypical mycobacterial strains usually acquired by trauma are M. fortuitum, M. chelonae, and M. marinum. The gastrointestinal tract is also suggested as a portal of entry because some of the atypical mycobacteria are found in the mouth of normal persons.1,2 Granulomatous lesions with or without caseation are typical, but a spectrum of abnormalities can occur. The diagnosis is made by aspiration, tissue sampling, and culturing. In case the cultures are negative, DNA amplification and subsequent determination of the nucleic acid sequence have reportedly been helpful in identifying the pathogen (Figs. 68-1 and 68-2).1,2,6

IMAGING TECHNIQUES Radiologic imaging techniques used in the diagnosis of atypical mycobacterial infections are radiography, CT, MRI, nuclear medicine scans, and ultrasonography.

■ FIGURE 68-2 Mycobacterium avium-intracellulare. Note the huge number of bright rose-pink bacilli that have been engulfed by macrophages (black arrow). This finding of enormous numbers of bacilli being phagocytosed by macrophages is a common finding in immunodeficient patients. (Acid-fast bacillus stain.) (Courtesy of Anna Graham, MD, Tucson, AZ.)

MANIFESTATIONS OF THE DISEASE Osteomyelitis and septic arthritis caused by atypical mycobacteria resemble acute pyogenic infections but have a more indolent course. Muscles, bursae, and tendon sheaths can also be affected. Atypical mycobacteria can also cause carpal tunnel syndrome.1–18 Penetrating trauma results in cutaneous and/or deep soft tissue infection and can also result in septic arthritis.12,18 Most cases of atypical mycobacterial infections in the musculoskeletal system are recognized in a subacute stage of osteomyelitis.1–2

Radiography

■ FIGURE 68-1 Mycobacterium avium-intracellulare. Note the epithelioid cells (black arrow), the lack of good circumscription of the granuloma at its margin, and the small number of lymphocytes (pink arrow), which have failed to form a well-defined peripheral cuff. These are the hallmarks of a poorly formed granuloma characteristic of the immunocompromised patient. (Hematoxylin and eosin stain.) (Courtesy of Anna Graham, MD, Tucson, AZ.)

Radiography should be the initial imaging modality in evaluation of any musculoskeletal infection. The differentiation of tuberculous and atypical mycobacterial musculoskeletal infection is not possible in the majority of cases.1–2,10 Early radiographic findings include soft tissue swelling related to inflammatory changes, followed by bone involvement. Radiographic characteristics of atypical mycobacterial musculoskeletal infections have not been well delineated for each group. Multiple lesions predominate over solitary lesions, the metaphyses and diaphyses of long bones are commonly involved, and discrete lytic lesions may have sclerotic margins. Osteoporosis may not be as prominent as in tuberculous infection, there may be a tendency for development of abscesses and sinus tracts, and articular disease can simulate tuberculosis or rheumatoid arthritis.1,2 Atypical mycobacterial osteomyelitis shares similar morphologic abnormalities with tuberculous spondylitis (Pott’s disease).1,2 The findings in mycobacterial osteomyelitis of the spine may include involvement of one or several contiguous vertebral bodies that may result in kyphosis, destruction of the intervening discs, absence of reactive sclerosis,

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and formation of soft tissue abscesses, usually containing calcifications. Soft tissue abscesses may extend into the epidural space or may spread into adjacent soft tissue structures. The infection may include a single end plate or noncontiguous levels.1,2,9 The triad of Phemister, consisting of osteoporosis, peripheral marginal erosions, and slowly progressing destruction of articular cartilage, characterizes mycobacterial arthritis. If untreated, mycobacterial arthritis can result in severe osseous destruction and fibrous ankylosis. Less frequently, a linear periostitis and bone proliferative changes may be seen.1–2

of a three-phase scintiscan, whereas in patients with osteomyelitis a focal increase in the accumulation of the radionuclide is evident in all three phases of the scintiscan. 111 In-labeled leukocytes may be helpful in differentiating cellulitis from osteomyelitis.1,20,21

Magnetic Resonance Imaging

DIFFERENTIAL DIAGNOSIS

Magnetic resonance imaging is regarded as the most sensitive imaging method for the early detection of osteomyelitis and may show the absolute extent of the inflammatory process, thus contributing to preoperative planning. Infected areas demonstrate decreased signal intensity on T1-weighted sequences and increased signal intensity on T2-weighted and short tau inversion recovery (STIR) sequences. T1-weighted imaging with fat saturation after the intravenous administration of a gadolinium-based contrast medium may allow detection and delineation of the extent of epidural involvement in spinal infection, may indicate whether the infection is limited to soft tissues or to bones and joints, and may show the absolute extent of the inflammatory process and delineate abscesses, thus contributing to preoperative planning (Figs. 68-3 to 68-6).1–2,20

Musculoskeletal infections by atypical mycobacteria are clinically indistinguishable from those of tuberculosis, and diagnosis is usually delayed. Information regarding specific occupational history, recreational activities, and geographic region is important.1–18 Early radiographic findings of atypical mycobacterial osteomyelitis may be inconspicuous. Differential diagnosis includes acute pyogenic or fungal osteomyelitides, malignant bone tumors, neuropathic osteoarthropathy, reflex sympathetic dystrophy, transient regional osteoporosis, stress fractures, and healing fractures.1 Imaging findings of atypical mycobacterial arthritis are nonspecific. The differential diagnosis generally includes different types of synovial arthropathy, including tuberculous, pyogenic and fungal arthritides, inflammatory and metabolic arthritides, as well as pigmented villonodular synovitis, idiopathic synovial osteochondromatosis, and idiopathic chondrolysis.1 The differential diagnosis for mycobacterial spondylitis includes pyogenic or fungal infections, primary and metastatic tumors of the spine, and sarcoidosis.1 Imaging findings of atypical mycobacterial soft tissue infections are nonspecific with a broad differential diagnosis that includes tuberculous, pyogenic, and fungal infections and rheumatologic diseases. In atypical mycobacterial tenosynovitis the differential diagnosis also includes giant cell tumor of the tendon sheath.1

Multidetector Computed Tomography Computed tomography is superior to radiography in depicting early cortical erosions, bone fragmentation, small fluid collections, cloacae, bone sequestra, and increased intraosseous density that corresponds to the accumulation of pus replacing bone marrow fat. Contrastenhanced CT may also facilitate visualization of abscesses and necrotic tissue, may provide supplemental diagnostic information regarding paraspinal and intraspinal extension of infection, and may characterize the extent of bone and disc involvement, which may be not be visible on radiography. In addition, CT can be used to facilitate percutaneous biopsy of infected areas (Figs. 68-5 and 68-6).1–2,19

Ultrasonography Ultrasonography may be used in diagnosis of atypical mycobacterial soft tissue infection and septic joint. It can be used to guide percutaneous aspiration, biopsy, or drainage of the infected soft tissue structures or joints. Ultrasonography has a limited value in diagnosis of osteomyelitis.1

Nuclear Medicine Technetium-99m methylene diphosphonate (99mTc-MDP) scintigraphy may be useful in differentiating cellulitis from subjacent osteomyelitis. It is also useful in evaluation of multifocal infection. In patients with cellulitis, accumulation of the radionuclide in the infected area is increased during the angiographic and blood pool images

Positron Emission Tomography/ Computed Tomography The value of positron emission tomography (PET) in evaluation for atypical skeletal mycobacterial infection has not been determined.

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment Patients with tuberculosis caused by atypical mycobacteria are treated by regimens containing amikacin, a fluoroquinolone, rifabutin, clarithromycin, or clofazimine, to which they are more susceptible, along with other standard chemotherapeutic drugs. The outcome of treatment in patients with mycobacterial infections is more favorable in previously healthy individuals than in patients with underlying disease.22

Surgical Treatment Antimycobacterial chemotherapy alone usually is not sufficient. Whenever possible, surgical débridement of infected tissue followed by chemotherapy is recommended.22,23

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■ FIGURE 68-3 Mycobacterium marinum infection in a fish-tank worker. A, Coronal T2-weighted image with fat saturation shows a well-circumscribed soft tissue lesion of high signal intensity adjacent to the ulnar aspect of the proximal fourth phalanx compatible with and proven to be a soft tissue abscess. The lesion demonstrates intermediate signal intensity on coronal (B) and axial (C) T1-weighted images. Note extension of the lesion to the skin at both dorsal and palmar aspects on the axial image. (Courtesy of T. Berquist, MD, Jacksonville, FL.)

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■ FIGURE 68-4 Mycobacterium kansasii infection after animal bite. A, Coronal T2-weighted image with fat saturation shows soft tissue swelling and increased signal intensity involving the flexor tendon sheath of the index finger consistent with tenosynovitis. B and C, Axial T1-weighted images show intermediate signal intensity within and about the distended flexor tendon sheath. D, Sagittal T1-weighted image with fat saturation after the intravenous administration of gadolinium-based contrast agent shows significant enhancement of the affected soft tissues with areas of nonenhancement compatible with fluid/pus. (Courtesy of Ruth Ceulemans, MD, Chicago, IL.)

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■ FIGURE 68-5 Mycobacterium avium-intracellulare infection. A, Axial CT image of the chest shows destructive changes involving the T7 vertebral body compatible with osteomyelitis. Note perispinal soft tissue thickening consistent with an abscess. T1-weighted (B), T2-weighted (C), and proton density–weighted (D) sagittal images of the thoracic spine in the same patient show signal abnormality involving the T7 and T8 vertebral bodies and T7–T8 disc space consistent with discitis and osteomyelitis. Note epidural extension of infection. (Courtesy of J. Alcala, MD, Tucson, AZ.)

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■ FIGURE 68-6 Mycobacterium avium-intracellulare infection. A, Axial CT image of the upper thorax shows destructive changes involving the right sternoclavicular joint consistent with infection. Axial T1weighted (B) and axial T2-weighted (C) with fat saturation images of the upper thorax show abnormal signal intensity involving the right sternoclavicular joint consistent with infection. Axial (D) and coronal (E) T1-weighted images with fat saturation after the intravenous administration of gadolinium based contrast agent show abnormal enhancement consistent with infection in the region of the abnormality, with an area of nonenhancement about the joint seen on the coronal image consistent with a soft tissue abscess.

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What the Referring Physician Needs to Know ■ ■ ■ ■ ■

There is no evidence of human-to-human transmission. The course of infection is usually indolent. Imaging characteristics are similar to those seen with M. tuberculosis. Tissue diagnosis is necessary. Antimycobacterial chemotherapy alone usually is not sufficient, and surgical removal of the lesion is recommended.

SUGGESTED READING

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17. Butorac R, Littlejohn GO, Hooper J. Mycobacterial disease in the musculoskeletal system. Med J Aust 1987; 147:388–391. 18. Barton A, Bernstein RM, Struthers JK, O’Neill TW. Mycobacterium marinum infection causing septic arthritis and osteomyelitis. Br J Rheumatol 1997; 36:1207–1209. 19. Sharif H, Morgan J, Shahed M, Al Thagafi M. Role of CT and MR imaging in the management of tuberculous spondylitis. Radiol Clin North Am 1995; 33:787–804. 20. Gilday D, Paul D, Paterson J. Diagnosis of osteomyelitis in children by combined blood pool and bone imaging. Radiology 1975; 117:331–335. 21. Schauwecker D. Osteomyelitis: diagnosis with In-111–labeled leukocytes. Radiology 1989; 171:141–146. 22. Shembekar A, Babhulkar S. Chemotherapy for osteoarticular tuberculosis. Clin Orthop Relat Res 2002; (398):20–26. 23. Noonburg GE. Management of extremity trauma and related infections occurring in the aquatic environment. J Am Acad Orthop Surg 2005; 13:243–253.

Theodorou DJ, Theodorou SJ, Kakitsubata Y, et al. Imaging characteristics and epidemiologic features of atypical mycobacterial infections involving the musculoskeletal system. AJR Am J Roentgenol 2001; 176:341–349.

REFERENCES 1. Theodorou DJ, Theodorou SJ, Kakitsubata Y, et al. Imaging characteristics and epidemiologic features of atypical mycobacterial infections involving the musculoskeletal system. AJR Am J Roentgenol 2001; 176:341–349. 2. Resnick D. Osteomyelitis, septic arthritis, and soft tissue infection: organisms. In Resnick D (ed). Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, 2002, pp 2510–2624. 3. Wolinsky E. Mycobacterial diseases other than tuberculosis. Clin Infect Dis 1992; 15:1–12. 4. Wolinsky E. Nontuberculous mycobacteria and associated diseases. Am Rev Respir Dis 1979; 119:107–159. 5. Hofer M, Hirschel B, Kirshner P, et al. Brief report: disseminated osteomyelitis from Mycobacterium ulcerans after a snakebite. N Engl J Med 1993; 328:1007–1009. 6. Marchevsky A, Damsker B, Green S, Tepper S. The clinicopathological spectrum of nontuberculous mycobacterial osteoarticular infections. J Bone Joint Surg Am 1985; 67:925–29. 7. Kelly P, Weed L, Lipscomb P. Infections of tendon sheaths, bursae, joints and soft tissues by acid-fast bacilli other than tubercle bacilli. J Bone Joint Surg Am 1963; 45:327–336. 8. Rougraff B, Reeck C, Slama T. Mycobacterium terrae osteomyelitis and septic arthritis in a normal host. Clin Orthop 1989; 238:308–310. 9. Miller W, Perkins M, Richardson W, Sexton D. Pott’s disease caused by Mycobacterium xenopi: case report and review. Clin Infect Dis 1994; 19:1024–1028. 10. Tehranzadeh J, Ter-Oganesyan RR, Steinbach LS. Musculoskeletal disorders associated with HIV infection and AIDS: I. Infectious musculoskeletal conditions. Skeletal Radiol 2004; 33:249–259. Epub 2004 Mar 18. 11. Nalaboff KM, Rozenshtein A, Kaplan MH. Imaging of Mycobacterium avium-intracellulare infection in AIDS patients on highly active antiretroviral therapy: reversal syndrome. AJR Am J Roentgenol 2000; 175:387–390. 12. Mateo L, Rufi G, Nolla JM, Alcaide F. Mycobacterium chelonae tenosynovitis of the hand. Semin Arthritis Rheum 2004; 34:617–622. 13. Corrales-Medina V, Symes S, Valdivia-Arenas M, Boulanger C. Localized Mycobacterium avium complex infection of vertebral and paravertebral structures in an HIV patient on highly active antiretroviral therapy. South Med J 2006; 99:174–177. 14. Girard DE, Bagby GC Jr, Walsh JR. Destructive polyarthritis secondary to Mycobacterium kansasii. Arthritis Rheum 1973; 16:665–669. 15. Loddenkemper K, Enzweiler C, Loddenkemper C, et al. Granulomatous synovialitis with erosions in the shoulder joint: a rare case of polyarthritis caused by Mycobacterium kansasii. Ann Rheum Dis 2005; 64:1088–1090. 16. van der Werf TS, Stienstra Y, Johnson RC, et al. Mycobacterium ulcerans disease. Bull World Health Org 2005; 83:785–791. Epub 2005 Nov 10.

Brucellosis Human brucellosis (also known as undulant fever, Mediterranean fever, Malta fever, Cyprus fever, Gibraltar fever, or typhomalarial fever) is a systemic zoonotic infection caused by gram-negative coccobacilli of the Brucella genus. This infection is typically transmitted by ingestion of unpasteurized milk or milk products. Brucellosis can also be transmitted through skin contact with infected tissues or secretions. Human-to-human transmission is unusual but has been reported. Brucellosis can affect any organ system.1–3

ETIOLOGY The causative organisms include more virulent B. melitensis and B. suis, less virulent B. abortus and B. canis,1 and sometimes B. ovis.3 Various polymerase chain reaction/restriction fragment length polymorphisms are used for identification of Brucella species and biotypes.4

PREVALENCE AND EPIDEMIOLOGY Brucellosis is a worldwide disease with 500,000 new cases annually. It is more prevalent in the Mediterranean basin, Arabian peninsula, Indian subcontinent, and parts of Mexico and Central and South America. This reportable disease most often affects young or middle-aged predominantly male adults and has a low incidence rate in children and the elderly. Brucellosis is an occupational risk among farmers, laboratory personnel, and veterinarians and can occur in several family members, especially with the common source of infected food.1,5

CLINICAL PRESENTATION The causative organisms localize in tissues of the reticuloendothelial system, such as the liver, spleen, lymph nodes, and bone marrow. The first symptoms of brucellosis usually appear 1 to 4 weeks after inoculation. Any organ system can be affected. The presenting symptoms

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of brucellosis are nonspecific and include fatigue, fever, loss of appetite, nausea, and diarrhea and are more common in the acute stage of disease. Weight loss, palpitations, and osteoarticular symptoms are more common in the chronic stage of brucellosis, whereas sweating, headache, abdominal pain, psychiatric disorders, cutaneous lesions, and pulmonary symptoms are equally common in acute, subacute, and chronic stages.1,2 An elevated erythrocyte sedimentation rate, anemia, elevated level of serum C-reactive protein, and elevated transaminase levels are observed. The diagnosis is made by serologic testing with rising serum agglutination titer or by clinical symptoms combined with a positive blood culture. Culture of the organisms from the tissues, joint, or bursal aspirate confirms the diagnosis.1,2 Osteoarticular involvement is the most common complication of chronic brucellosis, and its incidence varies significantly in the literature, ranging from 5% to greater than 85%.3 Bones, joints, and bursae can be involved. The most common form of musculoskeletal brucellosis is brucellar spondylodiscitis, with the most frequent involvement that of the lumbar spine. Other regions of the spine and multiple sites of spinal involvement may be encountered. Subligamentous spread of disease is not a characteristic of spinal brucellosis. With spinal disease an acute clinical onset and rapid progression of radiologic findings are observed.1–3

Brucellar arthritis is usually monoarticular or pauciarticular, with the hip and knee joints the most frequently involved peripheral joints. Unilateral or bilateral involvement of sacroiliac joints is common. Sternoclavicular joints can also be involved. Osteomyelitis can affect the long, short, and flat bones. It is frequently chronic, and the bony structures may be secondarily infected by staphylococci.2 Avascular necrosis secondary to brucellosis is extremely rare and has been reported in the femoral head.1 The most commonly affected bursa is the prepatellar bursa.2

PATHOPHYSIOLOGY Histologic examination of the synovial membrane reveals granulomatous tissue, cellular infiltration with large or small mononuclear cells, and granulomatous formation. Bone biopsy specimens may show granulomatous osteomyelitis.2 Noncaseating granulomatous tissue and chronic inflammation are characteristic histologic features of spinal brucellosis.3

IMAGING TECHNIQUES Radiography Radiographic findings of brucellar spondylodiscitis resemble those of pyogenic or tuberculous infection and include destructive changes of the affected vertebrae

■ FIGURE 68-7

Brucellar spondylodiscitis. A, Frontal radiograph of the lumbar spine shows destructive changes at the inferior end plates of L1 and L2 on the left, destructive changes at the superior end plate of L5, and less extensive destruction at the adjacent inferior end plate of L4 on the left. Note mild intervertebral disc space narrowing at the L1–L2 and L4–L5 levels and parrot beak–like end plate osteophytes at multiple levels on the left. Note also a large left paraspinal mass consistent with soft tissue abscess. B, Axial CT image through the upper lumbar spine in the same patient shows destructive changes of a vertebral body, more pronounced on the left, with an associated large paraspinal abscess larger on the left. (Courtesy of Raymond Carmody, MD, Tucson, AZ.)

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and intervertebral discs, sclerosis, paravertebral abscess formation, and healing with bony fusion and osteophytosis. Large parrot beak–like osteophytes can be seen with spinal brucellosis (Fig. 68-7A). In early disease initial radiographs may be normal and the diagnosis can be delayed. The earliest radiographic finding is epiphysitis of the anterosuperior angle of the vertebra. Osteoporosis, large soft tissue abscesses, and paraspinal calcifications are more common in tuberculosis than in brucellosis. Brucellar spondylodiscitis shows less disc space loss and more common bony ankylosis of the affected vertebrae than is seen in tuberculous infection. A peripherally located gas within the intervertebral disc can be seen in brucellar infection.1–3 Radiologic findings of sacroiliitis include poor definition of the cortex, narrowing or widening of the joint space, erosive changes, sclerosis, and ankylosis.6 With involvement of peripheral joints, joint effusion, periarticular soft tissue swelling, and joint space narrowing can be observed that may be associated with osteomyelitis. Initial radiographs are frequently unremarkable. In patients with periarticular brucellosis soft tissue swelling is seen on radiographs.6

Magnetic Resonance Imaging Magnetic resonance imaging is the study of choice in the diagnosis and evaluation of the extent of disease in brucellar spondylodiscitis and osteomyelitis. Vertebral destruction, epidural abscesses, spinal cord, and nerve root compression are nicely demonstrated by MRI. Involvement of the apophyseal joints is common. Abnormal signal in vertebral bodies without morphologic changes and enhancement of the facet joints after intravenous gadolinium-based contrast agent injection have been identified as specific MRI features of brucellar spondylitis. The lesions display low signal intensity on the T1-weighted images, high signal intensity on the fluid-sensitive sequences, and enhancement on the postcontrast images. Postcontrast images are useful in delineation of paraspinal and intraosseous abscesses.1–3,6 MRI is the study of choice in the evaluation of brucellar arthritis, osteomyelitis, and periarticular soft tissue infection.6

Multidetector Computed Tomography Computed tomography is useful in evaluation of brucellar spondylodiscitis (see Fig. 68-7B). However, it has been reported that some cases were initially misdiagnosed as lumbar disc herniation or tuberculosis.3 CT is also useful in evaluation of brucellar arthritis and osteomyelitis.6

Ultrasonography Ultrasonography may be utilized in evaluation of joint effusions, synovitis, and bursitis caused by brucellar infection and may provide guidance for fluid aspiration.2

Nuclear Medicine Radionuclide bone scintigraphy with 99mTc-MDP is useful in the evaluation of osteoarticular brucellosis and shows increased radiotracer uptake in the affected regions. Bone scintigraphy is particularly useful in searching for multifocal

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disease.1,6,7 However, scintigraphy is not very useful in determining the outcome of brucellar musculoskeletal infection, because the abnormal radiotracer uptake persists for a long time.6

Positron Emission Tomography/ Computed Tomography Utility of PET/CT in evaluation of brucellar musculoskeletal infection is to be determined. There is a case report suggesting the usefulness of PET scanning in detection of skeletal brucellar infection in a patient with human immunodeficiency virus infection.8

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment Osteoarticular brucellosis is treated with a combination of two or three antibiotics, including ciprofloxacin, doxycycline, tetracycline, rifampicin, and streptomycin, with median duration of therapy of 6 to 8 weeks. If the patient does not respond to the usual treatment regimen or the disease relapses, longer treatment of 3 to 6 months or different regimens are sometimes needed.1,3,6

Surgical Treatment In the patients with spinal involvement and spinal instability or radiculopathy, surgery is performed.1,3,9

SUGGESTED READING Pourbagher A, Pourbagher MA, Savas L, et al. Epidemiologic, clinical, and imaging findings in brucellosis patients with osteoarticular involvement. AJR Am J Roentgenol 2006; 187:873–880.

REFERENCES 1. Pourbagher A, Pourbagher MA, Savas L, et al. Epidemiologic, clinical, and imaging findings in brucellosis patients with osteoarticular involvement. AJR Am J Roentgenol 2006; 187:873–880. 2. Resnick D. Osteomyelitis, septic arthritis, and soft tissue infection: organisms. In Resnick D (ed). Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, 2002, pp 2510–2624. 3. Turgut M, Turgut AT, Kosar U. Spinal brucellosis: Turkish experience based on 452 cases published during the last century. Acta Neurochir (Wien) 2006; 148:1033–1044. Epub 2006 Sep 8. 4. Al Dahouk S, Tomaso H, Prenger-Berninghoff E, et al. Identification of Brucella species and biotypes using polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP). Crit Rev Microbiol 2005; 31:191–196. 5. Pappas G, Papadimitriou P, Akritidis N, et al. The new global map of human brucellosis. Lancet Infect Dis 2006; 6:91–99. 6. Geyik MF, Gur A, Nas K, et al. Musculoskeletal involvement of brucellosis in different age groups: a study of 195 cases. Swiss Med Wkly 2002; 132:98–105. 7. Aydin M, Fuat Yapar A, Savas L, et al. Scintigraphic findings in osteoarticular brucellosis. Nucl Med Commun 2005; 26:639–647. 8. Zaknun JJ, Zangerle R, Gabriel M, Virgolini I. 18FDG-PET for monitoring disease activity in an HIV-1 positive patient with disseminated chronic osteomyelitic brucellosis due to Brucella melitensis. Eur J Nucl Med Mol Imaging 2005; 32:630. 9. Tezer M, Ozturk C, Aydogan M, et al. Noncontiguous dual segment thoracic brucellosis with neurological deficit. Spine J 2006; 6:321–324.

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Cat-Scratch Disease Cat-scratch disease was first described by Debré and colleagues in 1931 in Paris, and it was first recognized by physicians in the United States in 1932. The first published American case of cat-scratch disease was reported by Greer and Keefer in 1951, and the first large series of 160 patients was reported by Daniels and MacMurray in 1954.1 Cat-scratch disease most often presents as a selflimited benign, localized lymphadenopathy near the site of organism inoculation. A skin papule at the sight of inoculation often occurs before the development of adenopathy. Typically, the incubation period is 3 to 10 days. Cat-scratch disease generally occurs in young immunocompetent individuals and infrequently causes serious illness. However, 5% to 10% of patients, especially immunocompromised individuals, develop disseminated disease. In addition to the lymphatics, infection can affect the central nervous system, eyes, liver, spleen, bone, and lungs. Erythema nodosum and thrombocytopenia purpura also have been reported. Current data suggest that cat-scratch disease can result from a cat scratch or bite as well as possibly from a flea bite. Rare cases have been reported after exposure to a dog.1–4

ETIOLOGY Bartonella henselae, a soil-borne protobacterium (also known as Rochalimaea henselae) that is a gram-negative coccobacillus, is currently believed to be the most common cause of cat-scratch disease. The disease is rarely linked to another soil-borne protobacterium, Afipia felis. B. henselae can cause bacillary angiomatosis in the immunocompromised patients, especially in those with human immunodeficiency virus infection.1

PREVALENCE AND EPIDEMIOLOGY The overall incidence of cat-scratch disease in the United States is unknown. This is not a reportable disease, and few cases require hospitalization. However, in an analysis of three national databases, it was concluded that there are more than 2,000 patients hospitalized annually with the diagnosis of cat-scratch disease or 0.77 to 0.86/100,000 hospital discharges. Also based on these data it was estimated that in the United States there are 22,000 ambulatory patients with cat-scratch disease annually or 9.3/100,000 population. It occurs slightly more often in males than in females.1,5

KEY POINTS Although cat-scratch disease is usually self-limited, localized regional lymphadenopathy can occur near the inoculation site. ■ Dissemination and skeletal lesions can occur. ■

Although cat-scratch disease may be associated with significant morbidity, no deaths have been reported to have been caused by this disease in immunocompetent patients. This infection appears to confer lifelong immunity because reports of recurrences of clinical cat-scratch disease are rare.1 Clinically, well flea-infested, B. henselae–bacteremic cats, primarily kittens, are a major reservoir for this organism and humans become naturally infected through direct and indirect contact with infected cats. Direct human-to-human transmission of B. henselae infection has not been reported.1

CLINICAL PRESENTATION A history of contact with a cat, usually a kitten, in the previous 1 to 2 weeks is common in individuals with catscratch disease. The classic history of an individual with cat-scratch disease is a local rash followed by lymphadenopathy. The rash, which is present in more than 90% of infected patients, consists of one or more red papules that are 0.5 cm or less in diameter and appear at the site of inoculation, which often is a cat scratch or bite. Single lymph node involvement occurs in more than one half of patients. Frequently painful lymphadenitis usually persists for 4 to 6 weeks but can last 1 year or more. The lymphadenopathy in the decreasing order of frequency is observed in the axillary and epitrochlear, the cervical and submandibular, the inguinal and femoral, and the preauricular, postauricular, and supraclavicular chains. Adenopathy that involves more than one anatomic site may be accompanied by constitutional symptoms. Occasionally, the affected lymph nodes can suppurate. Fever of unknown origin and fatigue are observed in one third of patients. Parinaud oculoglandular syndrome occurs in 2% to 3% of patients. Central nervous system findings occur in 5% of patients. Disseminated illness is more common in immunocompromised patients. It is manifested by persistent spiking fever, hepatosplenomegaly, and abdominal pain associated with diffuse granulomatous disease of liver and spleen.1

PATHOPHYSIOLOGY The pathologic response to infection with B. henselae varies significantly with the status of the host immune system. In immunocompetent patients the response is granulomatous and suppurative. In immunocompromised hosts the response is vasculoproliferative.1 Organisms are not seen in routinely stained tissue preparations. Diagnostic tests include a B. henselae antibody test, a silver impregnation Warthin-Starry stain, polymerase chain reaction, and DNA sequence analysis. In silver-stained lymph nodes, argyrophilic, non–acid-fast, pleomorphic bacilli may be seen. The primary inoculation site and involved lymph nodes show a central area of avascular necrosis surrounded by lymphocytes. Histiocytes and giant cells often are present. Histologic findings in individuals with cat-scratch disease progress over time. Lymphoid hyperplasia, reticular cell hyperplasia, and arteriolar proliferation are followed by granulomas with central necrosis. Later, microabscesses appear.1

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IMAGING TECHNIQUES

Nuclear Medicine

Magnetic resonance imaging is the most sensitive imaging modality in evaluation of musculoskeletal cat-scratch disease. The other imaging modalities include radiography, CT, PET/CT, ultrasonography, and nuclear medicine imaging.2–4,6–13

On bone scintigrams, the lesions demonstrate increased radionuclide uptake.2–4,13

MANIFESTATIONS OF THE DISEASE

A PET/CT scan shows increased radiotracer uptake in the affected lymph nodes.11

Bartonella henselae infection usually occurs early in children and young adults, is generally asymptomatic, and in most cases revolves spontaneously in 2 to 4 months. It may, however, produce a wide spectrum of clinical symptoms, the most frequent feature being cat-scratch disease. Disseminated atypical B. henselae infection may follow catscratch disease after a symptom-free period or may present de novo, mimicking a wide range of clinical disorders.1–16

Radiography Radiography in patients with lymph node enlargement shows soft tissue swelling, mass, or both. Bone lesions may develop remote from the inoculation site, involving the axial and appendicular skeleton. The radiographic appearance of bone lesions is nonspecific and resembles other lytic lesions, such as eosinophilic granuloma or malignancies. The lesions are generally lytic, although associated sclerosis and periosteal reaction have been described.1,2,6,7

Magnetic Resonance Imaging Magnetic resonance imaging is a useful modality for evaluation of both lymphadenopathy and rare skeletal lesions. An enlarged lymph node, which is typically seen in the axillary and epitrochlear regions, demonstrates heterogeneous low signal intensity on the T1-weighted images and high signal intensity on the fluid-sensitive sequences. On the T1-weighted images after intravenous administration of gadolinium-based contrast medium, peripheral enhancement of the lesion may be seen with nonenhancement of a central necrotic region. Diffuse heterogeneous enhancement of the infected lymph nodes can also be observed. Surrounding soft tissue edema is common (Fig. 68-8).6–8 Bone lesions demonstrate intermediate-to-low signal intensity on the T1-weighted images and high signal intensity on the fluid-sensitive sequences (Fig. 68-9).9–10

Multidetector Computed Tomography On the CT images enlarged lymph nodes appear often ill defined and may display a central low attenuation consistent with necrosis. Extensive soft tissue edema in an efferent lymphatic distribution is observed. Skeletal lesions demonstrate the same characteristics as on radiographs.2,6,7

Ultrasonography Ultrasonography can be used in evaluation of lymphadenopathy and soft tissue edema as well as liver and splenic lesions.2,6,8

Positron Emission Tomography/ Computed Tomography

Classic Signs ■ ■ ■ ■

■

Rash at the inoculation site Regional lymphadenopathy Nonspecific lytic lesions on radiography and CT that can be accompanied by sclerosis and periosteal reaction Nonspecific low signal intensity on the T1-weighted, increased signal intensity on the fluid-sensitive, and variable enhancement on the T1-weighted post-contrast MR images Increased radiotracer uptake on bone scintiscans and PET scan.

DIFFERENTIAL DIAGNOSIS Cat-scratch disease may produce a wide spectrum of clinical symptoms that can mimic multiple other diseases.1 Adenopathy observed with cat-scratch disease may mimic a variety of bacterial or fungal infections as well as malignancies. Lytic lesions observed on radiography and CT have a broad differential diagnosis, including eosinophilic granuloma, malignancies, and bacterial and fungal infections.1–4,6–16

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment In most patients who are immunocompetent, cat-scratch disease is self-limited and symptoms resolve in 2 to 4 months. Effective antibiotics used in treating cat-scratch disease include rifampin, ciprofloxacin, trimethoprimsulfamethoxazole, and gentamicin. Clarithromycin, azithromycin, and tetracycline are likely to be effective. Although data are lacking, patients with cat-scratch disease who are treated should receive treatment for 10 to 14 days. Immunocompromised patients may require much longer courses of therapy.1

Surgical Treatment In a patient with lymphadenopathy and skeletal lesions caused by cat-scratch disease, surgical treatment is typically not indicated. If needed, biopsy is performed. In a few cases in which the diagnosis was not initially recognized and simulated soft tissue sarcoma and osteomyelitis, surgical drainage and evacuation of the suppurated lymph node was performed. In one case, irrigation and débridement of spinal infection was performed. The patients recovered without sequelae.15,16

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■ FIGURE 68-8

A 39-year-old otherwise healthy man presented with cat-scratch disease. Coronal STIR (A) and T2-weighted axial (B) with fat saturation MR images of the elbow show enlarged epitrochlear lymph node of heterogeneous increased and centrally higher signal intensity within the medial subcutaneous soft tissues of the elbow. Note streaky areas of increased signal intensity in the adjacent subcutaneous soft tissues consistent with edema. Axial T1-weighted (C) image shows intermediate-to-low signal intensity in the regions of abnormalities.

(Continued)

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■ FIGURE 68-8—Cont’d

(D) T1-weighted axial image with fat saturation and axial T1-weighted (E) image with fat saturation after intravenous administration of gadolinium-based contrast agent show heterogeneous enhancement in the regions of abnormalities, with prominent enhancement of the central part of the lymph node on the postcontrast image.

■ FIGURE 68-9 Cat-scratch disease with multiple osseous lesions in a child. A, Coronal T1-weighted image of the pelvis shows a lesion of intermediate-to-low signal intensity in the region of the left femoral neck. B, The lesion demonstrates high signal intensity on the coronal STIR image.

(Continued)

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■ FIGURE 68-9—Cont’d C, Note multiple additional lesions of similar signal intensity in the left acetabulum on the coronal STIR image and on the axial T1-weighted images (D and E) in the right iliac bone. (Courtesy of Hilary Umans, MD, Bronx, NY.)

What the Referring Physician Needs to Know ■ ■

■

Commonly there is a history of recent contact with a cat. Most often a self-limited rash appears at the site of organism inoculation and benign and localized lymphadenopathy is evident near the inoculation site. Lytic skeletal lesions and dissemination are uncommon.

SUGGESTED READINGS Bass JW, Vincent JM, Person DA. The expanding spectrum of Bartonella infections: II. Cat-scratch disease. Pediatr Infect Dis J 1997; 16:163–79. Dong PR, Seeger LL, Yao L, et al. Uncomplicated cat-scratch disease: findings at CT, MR imaging, and radiography. Radiology 1995; 195:837–839.

REFERENCES 1. Bass JW, Vincent JM, Person DA. The expanding spectrum of Bartonella infections: II. Cat-scratch disease. Pediatr Infect Dis J 1997; 16:163–179. 2. Hopkins KL, Simoneaux SF, Patrick LE, et al. Imaging manifestations of cat-scratch disease. AJR Am J Roentgenol 1996; 166:435–438. 3. Fretzayas A, Papadopoulos NG, Moustaki M, et al. Unsuspected extralymphocutaneous dissemination in febrile cat scratch disease. Scand J Infect Dis 2001; 33:599–603. 4. Keret D, Giladi M, Kletter Y, Wientroub S. Cat-scratch disease osteomyelitis from a dog scratch. J Bone Joint Surg Br 1998; 80:766–767. 5. Jackson LA, Perkins BA, Wenger JD. Cat scratch disease in the United States: an analysis of three national databases. Am J Public Health 1993; 83:1707–1711. 6. Resnick D. Osteomyelitis, septic arthritis, and soft tissue infection: organisms. In Resnick D (ed). Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, 2002, pp 2510–2624. 7. Dong PR, Seeger LL, Yao L, et al. Uncomplicated cat-scratch disease: findings at CT, MR imaging, and radiography. Radiology 1995; 195:837–839.

CHAPTER 8. Gielen J, Wang XL, Vanhoenacker F, et al. Lymphadenopathy at the medial epitrochlear region in cat-scratch disease. Eur Radiol 2003; 13:1363–1369. 9. LaRow JM, Wehbe P, Pascual AG. Cat-scratch disease in a child with unique magnetic resonance imaging findings. Arch Pediatr Adolesc Med 1998; 152:394–396. 10. Hipp SJ, O’Shields A, Fordham LA, et al. Multifocal bone marrow involvement in cat-scratch disease. Pediatr Infect Dis J 2005; 24:472–474. 11. Jeong W, Seiter K, Strauchen J, et al. PET scan-positive cat scratch disease in a patient with T cell lymphoblastic lymphoma. Leuk Res 2005; 29:591–594. 12. Rolain JM, Chanet V, Laurichesse H, et al. Cat scratch disease with lymphadenitis, vertebral osteomyelitis, and spleen abscesses. Ann N Y Acad Sci 2003; 990:397–403. 13. Bruckert F, de Kerviler E, Zagdanski AM, et al. Sternal abscess due to Bartonella (Rochalimaea) henselae in a renal transplant patient. Skeletal Radiol 1997; 26:431–433. 14. Massei F, Gori L, Macchia P, Maggiore G. The expanded spectrum of bartonellosis in children. Infect Dis Clin North Am 2005; 19:691–711. 15. Bernini PM, Gorczyca JT, Modlin JF. Cat-scratch disease presenting as a paravertebral abscess: a case report. J Bone Joint Surg Am 1994; 76:1858–1863. 16. Nimityongskul P, Anderson LD, Sri P. Cat-scratch disease: orthopaedic presentation. Orthop Rev 1992; 21:55–59.

Fungal and Higher Bacterial Infections There are approximately 100,000 species of fungi and as many species not yet discovered as estimated by mycologists. Many have a worldwide distribution, but some are seen in predominantly endemic areas. All are dimorphic with a free mycelial form that produces infectious spores that when inhaled are converted to yeast-like pathogens. Signs of infection are usually mild with chronic evolution and delay in diagnosis common; however, all fungi are more virulent in an immunocompromised host.

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Interpretation of these cases requires knowledge of predisposing factors, imaging findings, and appropriate index of clinical suspicion. The final diagnosis often requires tissue sampling. Here the emphasis is on the musculoskeletal findings caused by fungal infections including coccidioidomycosis, North American blastomycosis, South American blastomycosis, cryptococcosis, sporotrichosis, histoplasmosis, aspergillosis, candidiasis, mucormycosis, maduromycosis and higher bacterial infections including actinomycosis and nocardiosis.1,2

ETIOLOGY, PATHOPHYSIOLOGY, PREVALENCE AND EPIDEMIOLOGY, CLINICAL PRESENTATION, PATHOLOGY, AND DIFFERENTIAL DIAGNOSIS Coccidioidomycosis Coccidioidomycosis (valley fever) is a systemic infection caused by the soil fungus Coccidioides immitis and Posadasii, and is endemic in northern Mexico and the southwest part of the United States, including Texas, New Mexico, Arizona, California, and parts of South America.1,2 It is saprophytic but highly infective. It exists in the mycelial form within the soil and becomes infective when the airborne arthrospores are inhaled. In the infected host, the arthrospore develops into spherule, which may contain a few to several hundred endospores. Each endospore may then enlarge to spherule form (Fig. 68-10). The endosporespherule cycle in the host continues indefinitely unless altered by an immune reaction or the endospore is extruded from the tissue. The extruded endospore may germinate in the soil within a week to produce hyphae and the mycelialarthrospore cycle. There is no known human-to-human or animal-to-human transmission. The lungs are the primary focus of infection, but less than 40% of patients have a symptomatic disease. Of these, less than 1% of patients develop disseminated disease, which is often fatal and may involve any organ, including skin, lymphatics, lungs, osseous structures, liver, kidneys, and central nervous system.3

■ FIGURE 68-10 A and B, Coccidioides immitis spherules with light microscopy (40×). Inflammatory reaction is present, which includes segmented neutrophils, epithelioid cells, and rare eosinophils. (Courtesy of Anna Graham, MD, Tucson, AZ.)

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Skeletal coccidioidomycosis is seen in 10% to 50% of patients with disseminated disease.1 It is frequently multicentric and may involve almost any bone, although the axial skeleton is more frequently involved.4 At least three risk factors have been described that may lead to disseminated coccidioidomycosis: ethnicity (Filipino, AfricanAmerican, Native American, Hispanic), gender (male > female), and immunosuppression.1 All age groups can be affected, but patients younger than age 5 years or older than age 50 years are more likely to develop disseminated disease. Symptoms and signs can be prominent and include pain, swelling, and draining abscess.2 Skeletal involvement can be seen as osteomyelitis or septic arthritis. A self-limited migratory sterile polyarthritis (“desert rheumatism”) occurs as a hypersensitivity syndrome in 33% of cases. Septic arthritis usually occurs due to direct extension from an adjacent bone and rarely due to hematogenous spread. The most commonly involved joints are ankles and knees.1 Coccidioidal bursitis, tenosynovitis, and soft tissue abscesses can occur.2 A positive serology test is diagnostic.5 Biopsy reveals granulomatous lesions similar to tuberculosis with monocytes, giant cell epithelial cells, necrosis, and caseation. Differentiation requires isolation of the causative organism.2 The differential diagnosis includes lytic metastatic disease, multiple myeloma, Kaposi’s sarcoma, and other fungal or mycobacterial infections.2,4 During 2003–2004, the number of reported cases of coccidioidomycosis increased 32%. In 2004, 6,449 cases of coccidioidomycosis were reported, yielding a national average of 4.1 cases for every 100,000 persons. The majority of these cases occurred in California and Arizona. Increases are probably attributable to recent changes in land use, demographics, and climate in endemic areas, although there may be increased physician awareness and testing.6

North American Blastomycosis Blastomycosis is caused by the fungus Blastomyces dermatitidis and is most common in the southeastern United States, the Ohio-Mississippi Valley area, and the MidAtlantic states. It is also endemic to part of Africa. The primary infection is often pulmonary,1 but the skin may be a portal entry for infection in some cases after cutaneous injuries.2 Hematogenous dissemination may occur to lungs and other organs. The most common sites for dissemination include skin, skeletal structures, and the genitourinary tract.1 An abscess can develop in the subcutaneous soft tissue and spread to the other viscera, lymph nodes, and skeletal structures. The peak age is between 20 and 50 years, but both males and females may be affected at any age.2 Osteomyelitis is seen in 14% to 60% of patients with disseminated blastomycosis, which can be the result of hematogenous seeding or direct extension from the adjacent soft tissues. The most common sites of skeletal involvement are the vertebrae, skull, ribs, and distal half of the extremities, but any bone can be affected. In the long bones the infection typically begins in the epiphysis or subarticular region.1 Metaphyses of

the long bones and small bones are also frequently involved. Blastomycotic septic arthritis is common after dissemination, with most frequent involvement of the elbows, knees, and ankles.1 The presentation of blastomycosis clinically and radiographically is nonspecific and often mistaken for a neoplasm. Delay in diagnosis is common. Patients with osseous blastomycosis may present as pain, swelling, abscesses, septic joints, and draining sinuses.7 The osseous lesions may also be asymptomatic.8 The definite diagnosis is made through identification of B. dermatitidis in body fluids, tissue, or cultured material. Serologic testing is available but not reliable.7 Histologic examination reveals round and broad-based budding yeast with an associated pyogranulomatous reaction. Another important finding is thermal dysmorphism on cultures.7

South American Blastomycosis South American blastomycosis is caused by the fungus Blastomyces (Paracoccidioides) brasiliensis. The disease is endemic to South America and parts of Mexico and Central America. The causative fungi invade the pharynx and then spread locally or hematogenously to the other body sites. The musculoskeletal involvement is similar to that of North American blastomycosis.2

Cryptococcosis Cryptococcosis (torulosis, European blastomycosis, Busse-Buschke disease) is a worldwide fungal infection caused by the encapsulated fungus Cryptococcus neoformans, a fungus that has an unusual predilection for the central nervous system.2 The causative fungus can be found in the respiratory tract, intestinal tract, or skin in healthy individuals or can be recovered from the soil, pigeon droppings, or fruit. The disease starts after inhalation of C. neoformans aerosolized spores to the lungs with possible hematogenous spread to the brain, meninges, visceral organs, bones, and joints. Cryptococcosis is the fourth most life-threatening infection in patients with AIDS. It can also be seen in the other immunocompromised patients and patients with chronic diseases, including leukemia, lymphoma, Hodgkin’s disease, sarcoidosis, tuberculosis, diabetes mellitus, and transplant patients. Less often this disease occurs in otherwise healthy individuals.1,2 Neurologic manifestations include dizziness, ataxia, diplopia, headache, and convulsions; and the disease is frequently lethal.2 In the patients with disseminated disease, skeletal involvement occurs in 5% to 10% of cases. The most common site of skeletal involvement is the spine. The other common locations are pelvis, ribs, skull, tibia, and bones about the knees.1,2 Bony prominences can be involved. A single site of infection can be present, but the disease can also be multifocal. Occasionally, the infection can be implanted into bone during soft tissue injury.2 Cryptococcal septic arthritis is rare and usually is a result of extension from the adjacent bone. This can later result in destructive changes of the involved joint. Bursal infections or tenosynovitis are rare.2

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The adults are affected more frequently than children. The patients present with swelling and pain.2 For definitive diagnosis a tissue sample is needed.9–11 The diagnosis can also be made by positive serology.11 The granulomatous infection caused by C. neoformans is similar to that of sarcoidosis, and differentiation between the two disorders may be difficult. There is striking paucity of cellular reaction. The absence of suppuration and necrosis is typical.2

Sporotrichosis Sporotrichosis is a chronic fungal infection caused by Sporothrix schenckii. This fungus resides as a saprophyte on vegetation and in soil. It can invade the human body through a skin wound or a thorn puncture. Sporotrichosis is a recognized occupational hazard of florists and farmers in whom the dominant upper limb is commonly affected. Human disease can also result from animal bites from rats, mice, gophers, and parrots.2,12 Most of the time this infection is limited to the skin and subcutaneous soft tissues, but hematogenous dissemination that includes bones and joints can occur. The disease starts with an erythematous, ulcerated or varicose nodule on the skin with common subsequent nodular lymphangitic spread. Extracutaneous sporotrichosis results from the hematogenous spread from the primary inoculation site or from inhalation of conidia. Disseminated disease is more common and can be fatal in immunocompromised patients.2,13 Sporotrichosis is seen worldwide but mainly in warm and tropical areas.1 The skeletal involvement includes osteomyelitis or septic arthritis. The osteomyelitis progresses slowly and can affect a single location or be multifocal. The most commonly involved bones are tibia, fibula, femur, humerus, and short tubular bones of hands and feet. Both large and small extremity joints can be involved. Involvement of the synovial bursae can be present. Indolent tenosynovitis usually about the wrist and ankle can be observed.1 Skeletal findings of sporotrichosis are similar to those seen in tuberculosis and other fungal disorders, but involvement of small joints of hands and feet is more common.1 The definite diagnosis is made by fungal culture. The organisms are rarely seen in the biopsy specimens owing to their small number.13,14

Histoplasmosis Histoplasmosis is an infection caused by a dimorphic fungus Histoplasma capsulatum, which is present in the United States predominantly in the Ohio and Mississippi river valleys as well as in certain areas of Central or South America, or H. capsulatum var. dubosii, present in Africa. Both species cause the same disease. H. capsulatum is a soil fungus.1,15 The disease usually starts in lungs after inhalation of fungal spores, but the gastrointestinal tract can be portal entry in some patients. The fungi proliferate in the reticuloendothelial system.2 The vast majority of human infections are self limited and asymptomatic.15 The disease can spread hematogenously to other organs, including bones.

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Skeletal involvement is more common with H. capsulatum var. dubosii infection with predilection to flat and small tubular bones.1 The radiologic findings are similar to those in tuberculosis and sarcoidosis.1,2 With H. capsulatum infection children are infected more commonly than adults. Joints as well as bones can also be affected. Sometimes, joint involvement is a result of hypersensitivity reaction to H. capsulatum. Tenosynovitis caused by this fungus can occur.2,15 Fasciitis and myositis caused by this organism have also been reported.16 With histoplasmosis caused by H. capsulatum var. dubosii, granulomatous ulcerating and papular skin lesions can be associated with bone and joint involvement in as many as 80% of patients. The disease is frequently multifocal, predominantly involving the flat bones, but the spine and tubular bones can be involved.2 The diagnosis can be made with antigen testing from urine or blood. Fungal cultures from the affected tissues are also useful.17 With the involvement of bone marrow, noncaseating granulomas are seen in histologic specimens. Histologic findings of histoplasmosis are similar to those in sarcoidosis and tuberculosis.2

Aspergillosis Aspergillosis is a fungal disease defined as any other illness other than mycotoxicosis caused by various Aspergillus species. These fungi are ubiquitous and include the human upper respiratory tract, but disease is uncommon. The severe and invasive form of aspergillosis is typically seen in immunocompromised patients, in whom it represents an opportunistic infection with a high mortality rate.1,18 The most common causative organism is A. fumigatus.1 Skeletal involvement is rare and usually occurs due to hematogenous dissemination, which is more common in adults or due to direct invasion of pulmonary disease into the chest wall, which is more common in children.2 Vertebral, rib, or sternal involvement follows after respiratory infection, but the other skeletal sites can be involved.1,2,19 Aspergillous spondylitis can occur in both immunocompetent and immunocompromised patients of any age. This is generally related to a contiguous spread of pulmonary disease, with the thoracic spine most commonly involved. Spinal involvement resembles tuberculous spondylitis. Contiguous spread of this infection is also observed in the orbital bones. Involvement of the appendicular skeleton is rare. Aspergillous arthritis is rare and usually associated with osteomyelitis.2 The diagnosis can be made with serology, but the result can be false negative.18 The definite diagnosis is made by fungal culture.19

Candidiasis Candidiasis (moniliasis) is a fungal infection caused by several species of Candida. The major causative organism is C. albicans. Other pathogenic Candida species include C. tropicalis, C. guilliermondii, C. krusei, C. lusitanie, C. rugosa, C. pseudotropicalis, C. parapsilosis, C. glabrata, and C. lambica.2 This fungus is common in the normal human flora and presumably resides on the mucous

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membranes. Candidiasis represents an opportunistic infection that is mainly seen in patients with indwelling catheters, in intravenous drug abusers, and in immunocompromised patients.1–2 In disseminated disease, involvement of bones and joints is uncommon and occurs in 1% to 2% of patients. Candidal osteomyelitis can affect any age group. The most commonly involved bones are the pelvis, sternum, and scapula. The ribs, spine, and tubular bones of the extremities can also be involved. Spine infection can occur from the direct extension of a contiguous infection or secondary to hematogenous seeding, with involvement of the lumbar spine most common. Candidal osteomyelitis cannot be differentiated from other bacterial or fungal infections by imaging.1,2 Septic arthritis caused by C. albicans can occur by hematogenous spread, owing to direct invasion from infected adjacent osseous or soft tissue structures, or from joint replacement surgery. The most commonly affected joint is the knee.1 Monarticular involvement is more common than polyarticular involvement. Candidal pyomyositis is rare.20,21 Septic bursitis can also occur. Osteoarticular candidiasis is seen in approximately one third of heroin addicts with most typical osteochondral involvement.2 Systemic candidiasis is an iatrogenic disease of modern neonatal intensive care that deserves urgent attention for its prevention as well as effective treatment to minimize neonatal morbidity and mortality. The sources of candidiasis in neonatal intensive care units are often endogenous following colonization of the newborns with fungi. About 10% of these newborns are colonized in the first week of life, and up to 64% are colonized by 4 weeks of hospital stay. Disseminated candidiasis presents very much like bacterial sepsis and can involve multiple organs such as the kidneys, brain, eyes, liver, spleen, bones, joints, meninges, and heart.22 Confirming the diagnosis by laboratory tests is difficult, and a high index of suspicion is required. The definitive diagnosis of fungemia can be made only by recovering the organism from blood or other sterile body fluids.22 With the bone or joint involvement the diagnosis is made by isolation of the organism from joint aspirate or sampled material.2

Mucormycosis Mucormycosis is the most acute, fulminant, and fatal of all fungal infections in humans. It is also known as zygomycosis and phycomycosis. This infection is caused by fungi of the class Zygomycetes and order Mucorales, usually including the genera Rhizopus, Absidia, Mortierella, and Mucor. The organisms exist in soil and air.23 The frequency of mucormycosis has been increasing over the past 10 years; infections have been identified in up to 6.8% of patients at autopsy. The most common route of transmission for Zygomycetes fungi is inhalation of spores from the environment. Patients at highest risk for infections caused by Mucorales fungi include those with profound immunosuppression or diabetes, intravenous drug abusers, premature infants, those receiving deferoxamine, and recipients of bone marrow transplants. Mucormycosis

commonly presents as rhinocerebral or pulmonary disease; gastrointestinal presentations also occur.24 The preexisting disease influences the port of entry, but usually the lesions start from the paranasal sinuses.1 Hematogenous dissemination of the disease can also occur.2 Clinical manifestations of invasive mucormycosis are tissue necrosis and subsequent thrombosis. Common features of pulmonary disease include fever, dyspnea, hemoptysis, and cavitation upon radiologic examination.24 From the paranasal sinuses, the infection extends to the adjacent structures: to the lateral wall of the middle turbinate, the hard palate, the ethmoidal sinus, maxillary sinuses, orbit, retrobulbar region, and sphenoidal sinus. Intracranial extension and maxillary sinus thrombosis can occur.1 Imaging shows destructive osteolytic lesions in the involved osseous structures, but in chronic cases osteosclerosis is also evident.2 The differential diagnosis of mucormycosis includes other types of osteomyelitis and neoplasm.2 Involvement of other osseous structures is rare and reported in spine,23 femur, and cuboid bones.2 The Zygomycetes are easily identified in a tissue sample by the presence of predominantly aseptate (pauciseptate) wide, ribbon-like hyphae and of tissue necrosis and angioinvasion. The diagnosis can be made by fungal culture, but the result is frequently false negative.25 Overall, disease with the Mucorales tends to be fulminant and is uniformly fatal if not aggressively treated. Even with appropriate surgical and medical management, the vast majority of patients are expected to die of this disease process.25

Maduromycosis Maduromycosis (mycetoma) is a chronic, granulomatous, subcutaneous, inflammatory disease caused by the true fungi of the Eumycetes class or the filamentous bacteria of the Actinomycetes. These infections are most prevalent in India, sub-Saharan Africa, the southern part of the Arabian Peninsula, and central and South America.1,26 The disease was named after the Madura District of India, where it was described for the first time by Gill in 1842.27 The causative organisms are present in the soil and may enter the subcutaneous tissue by traumatic inoculation. Mycetoma commonly affects the feet in adults aged 20 to 40 years who are usually male. Both forms of mycetoma present as a progressive, subcutaneous swelling, but actinomycetoma has a more rapid course. After soft tissue contamination, the causative organism may penetrate the underlying muscles, tendons, bones, and joints. Multiple nodules develop that may suppurate and drain through sinuses, discharging grains during the active phase of the disease with subsequent contiguous involvement of the bones. Sinus tracts arising from the affected bones are common.1,2,26 Infections of the hands, arms, legs, or scalp are less common. In the United States the most frequent cause of Madura foot is Petriellidium boydii (Monosporium apiosermum), although Aspergillus, Penicillium, Madurella, Cephalosporium, Streptomyces, and Phialophora can be causative organisms. Outside the United States, Nocardia species (N. brasiliensis, N. madurae) may cause this disease.2

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The diagnosis may involve radiology, cytology, culture, histology, immunodiagnosis, and serology. Mycetoma lesions can be diagnosed by fine-needle aspiration biopsy and cytology. They are characterized by the presence of polymorphous inflammatory cells consisting of neutrophils, lymphocytes, plasma cells, histiocytes, macrophages, and foreign-body giant cells and grains. There is no known human-to-human or animal-to-human transmission.26

Actinomycosis Actinomycosis is an uncommon noncontagious suppurative infection caused by gram-positive filamentous obligate or facultative anaerobic bacteria of the Actinomyces species, which belong to the normal flora of the intestinal tract and oral cavity. The most common causative organism is A. israelii.2,28 These organisms represent higher bacteria and are frequently misclassified as fungi. Some of the other human Actinomyces pathogens are A. bovis, A. naeslundii, A. viscous, and A. odontolyticus.2 In tissues, Actinomyces aggregate into microcolonies and grow in a radial configuration, with the peripheral layer of organisms having club-shaped ends. These microcolonies form the characteristic sulfur granules. Actinomycosis is frequently associated with other organisms.28 Actinomycosis is usually seen in debilitated patients or in devitalized tissue. Trauma is important in the inoculation of the organism into the soft tissue.2 Foreign body aspiration or ingestion, such as teeth or fish bone, is another predisposing factor.2,29 The usual localizations of this disease are cevicofacial, pulmonary, or gastrointestinal.2 The cevicofacial location is the most common and is seen 40% to 55% of patients.30 Contiguous spread of this disease is more common than hematogenous.28 There is a tendency for fistulization, and soft tissue abscesses also can occur.31,32 Musculoskeletal actinomycosis is more commonly the result of the direct spread of disease rather than hematogenous seeding.2,28 Bone infection ranges between 1% and 15% in all patients with actinomycosis.31 The most commonly involved bones are the mandible, the axial skeleton, as well as the major joints of the appendicular skeleton, but other bones can be involved.2,33,34 The lesions can occur after extraction of a tooth or after a human bite.2 Diagnosis of skeletal actinomycosis is difficult and is often delayed until an advanced stage of the disease. The diagnosis is made by the isolation of the causative organism from the sampled biopsy material as well as the isolation of the sulfur granules, which are characteristic histologic findings. Successful isolation requires culturing multiple samples in enriched media under anaerobic conditions in the presence of carbon dioxide.28

Nocardiosis Nocardia are gram-positive organisms that belong to the aerobic Actinomycetes. Human Nocardia pathogens include N. asteroides, N. brasiliensis, N. farcinica, and N. caviae.2

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Humans are infected via the respiratory tract or gastrointestinal tract or through skin trauma. Immunocompromised patients and patients with chronic diseases are more susceptible to this disease. Pulmonary infection may extend into the chest wall. Skin infection may extend into the adjacent soft tissue and lead to cellulitis and soft tissue abscesses. Primary infection of the bursae is rare.2 The most common sites of nocardiosis are the lungs, followed by the central nervous system and soft tissues. The other extrapulmonary sites are rare.35,36 Bones and joints are more commonly affected by contiguous extension from the adjacent tissues or rarely by hematogenous seeding.2,35 The tubular and flat bones and the spine can be affected.2 The clinical and radiologic manifestations of musculoskeletal nocardiosis are nonspecific and resemble those of Mycobacterium tuberculosis and fungal infections.35 The diagnosis is made by identification of branching filaments in tissue specimens, Gram staining, and culture.37

MANIFESTATIONS OF THE DISEASE Radiography Coccidioidomycosis Radiographs frequently show multiple lytic osseous lesions with permeative borders or well-defined punchedout lytic lesions with or without sclerotic borders. There is predilection to the metaphyses of long tubular bones and bone protuberances. In the tubular bones of hands and feet diaphyseal lesions are common. Soft tissue swelling and periosteal reaction and periostitis can be present, but sequestration is uncommon. Sclerosis is an attempt to heal or contain the lesion. The intervertebral discs are relatively spared, and vertebral body collapse is an uncommon and late manifestation.2 In patients with septic arthritis osteoporosis, joint space narrowing and bone destructive changes are similar to those seen in other granulomatous infections (Figs. 68-11 to 68-15).1

North American Blastomycosis Early in the disease process there may be no visible osseous radiographic abnormalities or there could be faint osteopenia in the involved location. Later an area of lucency is seen with either ill-defined or well-defined borders.8 The radiographic appearance can be variable, but an eccentric lytic lesion without sequestrum or periosteal reaction is common. However, a periosteal reaction also can be present. The lesions are often mistaken for benign or malignant bone tumors.7 Skeletal lesions can appear moth-eaten and can be associated with osteoporosis. Sclerotic margins can also be seen as well as an area of cortical erosion beneath the soft tissue abscesses.2 The metaphyseal lesions tend to be eccentric, well circumscribed, and lytic.8 In the spine the blastomycotic infection resembles tuberculosis (Figs. 68-16 and 68-17).2

Cryptococcosis The skeletal lesions may be lytic with well-defined margins and mild surrounding sclerosis. Aggressive periosteal

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■ FIGURE 68-11 Frontal (A) and lateral (B) radiographs of the hand in a child with disseminated coccidioidomycosis show an expansile lytic lesion involving the proximal phalanx of the fourth digit with associated cortical breakthrough at the ulnar aspect. (Courtesy of George Barnes, MD, Tucson, AZ.)

reaction is infrequent. Spinal cryptococcosis resembles pyogenic infection with more frequent paravertebral abscesses and extradural cryptococcal granulomas.1 Extradural granulomas can cause myelopathy and cauda equina syndrome.2 There can be extension of the vertebral body infection into the pedicle or adjacent rib.1 Lytic lesions without a sclerotic margin and with associated soft tissue swelling can also be seen (Fig. 68-18).11

osseous and intervertebral disc destruction and paraspinal masses. If there is involvement of other skeletal sites or joints, destructive changes of typical osteomyelitis with or without associated periostitis can be seen. With septic joints, periarticular osteopenia, joint space loss, and erosive changes are observed (Fig. 68-20).2

Sporotrichosis Skeletal lesions are lytic or patchy or have a motheaten appearance, usually without periosteal reaction.1,2 The findings with joint involvement include joint effusion, periarticular soft tissue swelling, joint space loss, and destructive changes (Fig. 68-19).1–2,14

In vertebral osteomyelitis caused by Candida there are erosive and destructive changes and possible intervertebral disc involvement. Extension into the paravertebral soft tissues or spinal canal can occur.1,40 With candidal arthritis, radiography shows massive soft tissue swelling, joint effusion, joint space narrowing, erosions, bone collapse, and fragmentation (Fig. 68-21).1

Histoplasmosis

Mucormycosis

The radiographic findings of skeletal histoplasmosis are similar to those of sarcoidosis and tuberculosis.1 With skeletal involvement destructive lesions are seen.38 With H. capsulatum var. dubosii infection cystic lytic areas in the affected osseous structures are most typical.2 In the spine, H. capsulatum var. dubosii shows radiographic changes consistent with spondylodiscitis, with or without paravertebral abscesses.39

Radiography may show destructive osteolytic and later osteosclerotic changes.2 In the early phase of mucormycosis the radiographic changes of spondylodiscitis can be subtle and show only mild focal osteopenia2 if compared with other unaffected vertebrae.23

Aspergillosis The radiographic features of skeletal aspergillosis resemble those of tuberculosis. Spinal involvement includes

Candidiasis

Maduromycosis The many findings in maduromycosis of the foot include soft tissue swelling, bone scalloping and cortical erosions, aggressive periostitis, coarse trabeculation, sclerosis and mottling, cavitary lesions, and, in advanced disease, intraarticular osseous fusion leading to an appearance of

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■ FIGURE 68-12 Frontal (A) and lateral (B) radiographs of the left ankle in a 54-year-old male patient with disseminated coccidioidomycosis infection show lytic lesions in the talar trochlea and medial and lateral malleoli. Note a large synovial-fluid complex in the ankle joint seen in the lateral projection. Sagittal STIR MR image (C) shows a lobulated lesion of abnormal, predominantly increased signal intensity involving the talar trochlea with associated bone marrow edema extending into the talar body and a large synovial fluid complex in the ankle joint. The region of abnormality shows intermediate-to-low signal intensity on the sagittal T1-weighted MR image (D).

(Continued)

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■ FIGURE 68-12—Cont’d

E, Axial T1-weighted MR image with fat saturation shows abnormal enhancement in the region of abnormalities with rim-enhancing abscesses in the talar trochlea and medial and lateral malleoli. Note thick synovial enhancement in the ankle joint. F, Postoperative frontal radiograph of the ankle after surgical débridement in the same patient shows amphotericin B–impregnated cement in the talar trochlea and medial and lateral malleoli.

melting snow.1,2,26,41 Bone cavities are larger, fewer, and better defined in eumycetoma when compared with actinomycetoma. These cavities are filled with solid masses of grains and fibrous tissues, providing a bone support. Because of this phenomenon pathologic fractures in mycetoma are rare. Radiographic findings in the skull are purely sclerotic, with dense bone formation and loss of trabeculation. In advanced maduromycosis, osteoporosis is seen that occurs secondary to disuse and compression of the bone and its blood supply by a mycetoma (see Fig. 68-22 and 68-23A).26

Actinomycosis Skeletal actinomycosis is characterized by a combination of osteolysis and osteosclerosis.2,28 With rib involvement, bony proliferation may be extensive, with the combination of severe osteosclerosis, cutaneous sinus tracts, and pleuritis suggestive of actinomycosis.2 Infection of the spine may be a result of invasion from the adjacent mediastinal or retroperitoneal foci. Multiple vertebrae are usually involved that demonstrate lytic lesions with surrounding sclerosis. The intervertebral discs are usually spared. Posterior elements are frequently affected, and with involvement of the thoracic spine there is frequent involvement of the adjacent ribs. Paravertebral abscesses may be present but are usually smaller and without calcifications when compared with tuberculous abscesses. Vertebral body collapse and gib-

bus deformities are less common than in tuberculosis. Neurologic complications associated with spinal cord involvement can occur.2

Nocardiosis Radiographic finding of nocardiosis are nonspecific and resemble those that are seen in tuberculosis and fungal infections.35

Magnetic Resonance Imaging Coccidioidomycosis Magnetic resonance imaging reveals lesions of intermediate-to-low signal intensity on the T1-weighted images and increased signal intensity on the T2-weighted and STIR sequences.4 The MR signal characteristics are nonspecific. Intraosseous and soft tissue abscesses show rim enhancement. MRI is particularly useful in finding the local osseous and soft tissue extent of disease and spinal involvement.2 In septic arthritis, enhancement of the synovial proliferation usually indicates active disease (see Figs. 68-12C to E, 68-13C to E, and 68-15A to C).42

North American Blastomycosis Magnetic resonance imaging is helpful in evaluation of local osseous and soft tissue extension of the lesion. MRI

■ FIGURE 68-13

Frontal (A) and lateral (B) radiographs of the thoracic spine in a 50-year-old male patient with disseminated coccidioidomycosis infection and paraplegia show destructive lytic lesions involving the left side of the two lower thoracic vertebrae including the vertebral bodies and posterior elements. Note preservation of the disc space. C, Sagittal STIR MR image in the same patient shows destructive lesions of intermediate-increased signal intensity involving the posterior aspect of the two lower thoracic vertebral bodies and their posterior elements with extension into the spinal canal and the posterior soft tissues. Note associated bone marrow edema in the lower vertebral body. Only the posterior aspect of the disc space is affected.

(Continued)

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■ FIGURE 68-13—Cont’d

D, Sagittal T1-weighted image demonstrates intermediate-to-low signal intensity in the regions of abnormality. E, Sagittal T1-weighted fat-saturated image after the intravenous administration of gadolinium-based contrast agent shows prominent enhancement in the region of abnormality with small intrinsic areas of nonenhancement consistent with osteomyelitis associated with intraosseous and soft tissue abscesses. F, Axial CT image of the lower thoracic spine after intravenous contrast agent administration in the same patient shows a destructive lytic lesion involving the posterior left aspect of the lower thoracic vertebral body and the posterior elements with associated rim-enhancing epidural abscess that extends into the posterior paravertebral soft tissues. (Courtesy of Ray Carmody, MD, Tucson, AZ.)

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■ FIGURE 68-14 A 65-year-old white woman presented with coccidioidomycosis in the left greater trochanter and left ischial tuberosity. A, Frontal radiograph of the left hip shows ill-defined lytic lesions involving the left greater trochanter and ischial tuberosity. B, CT image of the lower pelvis with the patient in prone position shows a destructive lesion with associated soft tissue mass in the left ischial tuberosity. C, Axial CT image of the lower pelvis with the patient in prone position shows a destructive lesion at the periphery of the left greater trochanter. Note biopsy needle within the lesion. Anteroposterior (D) and posteroanterior (E) technetium-99m methylene diphosphonate bone scintiscans of the pelvis show increased radiotracer uptake in the left ischial tuberosity and greater trochanter.

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■ FIGURE 68-15 A, Axial T2-weighted MR image with fat saturation of the pelvis in a 45-year-old male patient with disseminated coccidioidomycosis shows a destructive lesion of intermediateincreased signal intensity involving the anterior and central and left aspect of the sacrum with associated soft tissue mass. B, The lesion is of intermediate signal intensity on the T1-weighted axial MR image. C, Moderate enhancement is seen on the T1-weighted axial MR image with fat saturation after intravenous administration of gadoliniumbased contrast agent.

findings are nonspecific and include increased signal intensity on the T2-weighted images and decreased signal intensity on the T1-weighted images.7

Cryptococcosis Magnetic resonance imaging is useful in detection and evaluation of local extent of cryptococcal osteomyelitis and soft tissue abscesses.10 The lesions can demonstrate enhancement on the postcontrast images (Fig. 68-24).9

Sporotrichosis Magnetic resonance imaging can be utilized in evaluation of soft tissue or skeletal lesions. The findings are nonspecific.12,43

Histoplasmosis Magnetic resonance imaging may be utilized in evaluation of musculoskeletal histoplasmosis, for both osseous and soft tissue infection. However, there is no relevant literature on MRI of osseous lesions. The findings of soft tissue infections are nonspecific.15,16

Aspergillosis Magnetic resonance imaging is the study of choice for evaluation of the local extent of skeletal aspergillosis, especially with cranial and facial involvement.44 The findings seen with involvement of peripheral skeletal structures and joints are nonspecific2 (see Fig. 68-20B-D). The MRI appearance of aspergillous spondylitis is also nonspecific and resembles that of tuberculous infection.45

Candidiasis Magnetic resonance imaging is very useful in delineation of the extent of candidal osteomyelitis. The signal characteristics are nonspecific with enhancement on the postcontrast images, as in other fungal or bacterial infections.1,40,46

Mucormycosis Magnetic resonance imaging is the modality of choice in evaluation of the local extent of this devastating disease, especially with common rhinocerebral involvement1,47 or rare spinal involvement.23 With the involvement of

■ FIGURE 68-18

■ FIGURE 68-16 Frontal radiograph of the right hemithorax in a patient with blastomycosis shows a destructive lesion involving the lateral chest wall with associated soft tissue mass. (Courtesy of Richard Daffner, MD, Pittsburgh, PA.)

An 85-year-old patient presented with cryptococcal osteomyelitis and septic arthritis of the proximal third interphalangeal joint. Frontal radiograph of the hand shows destructive lytic lesions involving the proximal and, to a lesser extent, middle phalanges of the third digit with associated septic arthritis and soft tissue swelling. Note a large soft tissue ulcer at the ulnar aspect of the proximal phalanx. (Courtesy of Ruth Ceulemans, MD, Chicago, IL.)

■ FIGURE 68-17 Blastomycosis osteomyelitis. Axial (A) and lateral (B) radiographs of the calcaneus show a destructive lesion in the calcaneal tuber. (Courtesy of Richard Daffner, MD, Pittsburgh, PA.)

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■ FIGURE 68-19 Sporotrichosis osteomyelitis in a florist. A, Gross photograph of the hands shows bilateral soft tissue nodules and ulcers. B, Frontal radiograph of the hands shows a destructive lesion involving the entire left fifth metacarpal bone with associated pathologic fracture through the metacarpal neck. An additional destructive lesion is seen involving the ulnar aspect of the base of the left third proximal phalanx. (Courtesy of George Barnes, MD, Tucson, AZ.)

CHAPTER

■ FIGURE 68-20 Osteomyelitis resulting from aspergillosis with extension into the soft tissues. A, Frontal radiograph of the left hip shows an ill-defined lytic lesion involving the left acetabulum and superior pubic ramus. Note the associated soft tissue mass. B, Coronal STIR MR image of the pelvis shows an extensive lesion of predominantly increased signal intensity involving the left acetabulum and the superior pubic ramus with associated large soft tissue component about the medial pelvic wall and the periphery of the left acetabulum. Note the edema in the adjacent gluteal, pelvic floor, and adductor musculature. Some mass effect to the urinary bladder is present. C, Coronal T1-weighted MR image of the pelvis shows intermediate signal intensity in the regions of abnormality.

(Continued)

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■ FIGURE 68-20—Cont’d

D, Axial T1-weighted MR image with fat saturation after intravenous administration of gadoliniumbased contrast agent shows enhancement in the affected areas and a rim-enhancing abscess posterior to the left hip in the left gluteal musculature. E and F, Axial CT images of the hips with the patient in prone position show a destructive lytic lesion involving the posterior aspect of the left acetabulum with areas of cortical breakthrough and associated soft tissue component. In F, note a biopsy needle within the soft tissue mass at the posterior aspect of the left hip. (Courtesy of Hilary Umans, MD, Bronx, NY.)

paranasal sinuses the MRI findings are similar to those of bacterial sinusitis. Necrosis of the turbinates, palate, or face and invasion of ophthalmic and carotid arteries are known complications of advanced mucormycosis.1 In mucormycotic spondylodiscitis MRI shows local osseous and soft tissue extent of disease. The signal characteristics are nonspecific.23

Maduromycosis Magnetic resonance imaging investigation is superior to the other imaging techniques in the evaluation of mycetoma and the assessment of therapy.41 MRI allows good visualization of soft tissue involvement and bone destruction. T1-weighted images demonstrate decreased signal intensity of the affected bones and the adjacent soft tissues, findings suggestive of chronic osteomyelitis. Some enhancement is observed on the postcontrast images. T2-weighted and STIR sequences reveal increased signals in the affected regions27,41 (see Fig. 68-23B-D). In 80% of patients small low signal intensity lesions can be seen on both T1-weighted and T2-weighted images consistent with grains, which seem to differentiate mycetoma from other infections and tumorous lesions. MRI is useful in evaluation of healing.41

Actinomycosis The MRI findings and signal characteristics are nonspecific and resemble those of pyogenic, tuberculous, and other atypical infections. Decreased signal intensity on T1-weighted images and increased signal intensity on fluid-sensitive sequences are observed. Postcontrast images show enhancement in the affected regions.28–30,48

Nocardiosis Magnetic resonance imaging findings of nocardiosis are nonspecific and resemble those that are seen in tuberculosis and fungal infections.35

Multidetector Computed Tomography Coccidioidomycosis Computed tomographic findings parallel those found on radiography. This imaging modality is effective in further assessment of the local extent of coccidioidomycosis in those with skeletal and soft tissue involvement (see Figs. 68-13F and 68-14B and C).4

■ FIGURE 68-21 Disseminated candidiasis with multifocal osteomyelitis and septic knee. A, Frontal radiograph of the knee in a 4-week-old male newborn shows bone destruction and sclerosis with associated periostitis involving the distal femur, proximalto-mid tibia, and proximal fibula. B, Frontal radiograph of the wrist shows ill-defined lytic lesions involving the distal radial and ulnar metaphyses. (Courtesy of George Barnes, MD, Tucson, AZ.)

■ FIGURE 68-22 Madura foot in a veteran patient. Oblique (A) and lateral (B) radiographs of the right foot show extensive destructive changes involving multiple bones at the lateral aspect of the foot with soft tissue ulcers and swelling. (Courtesy of Richard Daffner, MD, Pittsburgh, PA.)

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■ FIGURE 68-23

● Infection

Madura foot. A, Lateral radiograph of the foot shows soft tissue swelling most pronounced at the dorsal aspect of the metatarsals. B, Sagittal STIR MR image of the foot shows extensive increased signal intensity at both dorsal and plantar aspects in the soft tissues centered in the metatarsal region. Note a skin ulcer in the dorsal metatarsal region. No osseous abnormalities are seen. C, Coronal T1-weighted image shows intermediate signal intensity in the regions of abnormalities. D, Coronal T1-weighted image after intravenous administration of gadolinium-based contrast agent shows heterogeneous enhancement in the involved soft tissues. E, Sonographic axial image obtained in the dorsal metatarsal region shows a heterogeneous irregular soft tissue lesion with multiple hypoechoic foci. (Courtesy of Hilary Umans, MD, Bronx, NY.)

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■ FIGURE 68-24

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Cryptococcal osteomyelitis with cortical abscess. A, Sagittal T1-weighted MR image of the leg shows a small lesion of intermediate signal intensity in the anterior tibial cortex with a larger area of associated periostitis and medullary edema also of intermediate signal intensity. B, Axial T2-weighted image with fat saturation shows increased signal intensity in the region of abnormality. Sagittal (C) and axial (D) T1-weighted images with fat saturation after intravenous administration of gadolinium-based contrast agent show enhancement of the region of abnormality with rim enhancement of the intracortical abscess. (Courtesy of Ruth Ceulemans, MD, Chicago, IL.)

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North American Blastomycosis

Histoplasmosis

Computed tomography is helpful in further characterization of radiographic findings and assessment of local skeletal and soft tissue extension of the lesion.7

Radiographic findings of skeletal histoplasmosis are similar to those of sarcoidosis and tuberculosis.1 CT parallels and further characterizes the radiographic findings.39

Cryptococcosis

Aspergillosis

Computed tomography is useful in further characterization of radiographic findings and assessment of bone and soft tissue extension of the cryptococcal musculoskeletal lesions (Fig. 68-25).9,11

Computed tomography of skeletal aspergillosis parallels those seen on radiographs19 with better characterization of local extension (Fig. 68-26).44–45

Sporotrichosis

Candidiasis

Computed tomography can be utilized to characterize destructive skeletal and soft tissue lesions as well as other organ involvement.13,49

Computed tomographic findings of candidal osteomyelitis parallel those seen on radiographs and better delineate osseous destruction and extension into the soft tissues and spinal canal.1,40,46

Mucormycosis Computed tomography is a useful imaging modality in evaluation of local osseous and soft tissue extent of mucormycosis.23,47

Maduromycosis Computed tomography is helpful in visualization of bone destruction, periosteal reaction, and soft tissue involvement in maduromycosis.41

Actinomycosis Computed tomography is a helpful imaging modality in evaluation of local extent of skeletal and soft tissue actinomycosis (Fig. 68-27).2,31,48

Nocardiosis ■ FIGURE 68-25

A 25-year-old man presented with cryptococcal osteomyelitis involving the sacrum. Axial CT image of the pelvis shows a destructive lytic lesion involving the anterior aspect of the right sacrum with associated osteomyelitis. (Courtesy of Richard Daffner, MD, Pittsburgh, PA.)

The CT findings of nocardiosis are nonspecific and resemble those that are seen in tuberculosis and fungal infections.35

■ FIGURE 68-26 A and B, Axial CT images of the chest in a child with invasive aspergillosis show pulmonary lesions in the right lung base with extension into the pleura and chest wall. Note destructive lesions involving multiple ribs.

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Histoplasmosis There is no relevant English literature on the use of bone scintigraphy in musculoskeletal histoplasmosis.

Aspergillosis Technetium bone scintigraphy shows increased radiotracer uptake in the skeletal lesions of invasive aspergillosis.19

Candidiasis Technetium bone scintigraphy shows increased radiotracer uptake in candidal osteomyelitis.46 A gallium scan was reported as useful in the detection of early candidal septic arthritis and soft tissue abscess.21,53 ■ FIGURE 68-27 Actinomycosis involving the iliopsoas muscle. Axial CT image of the pelvis shows a large abscess involving the right iliopsoas muscle. (Courtesy of Jennifer Weaver, MD, Ann Arbor, MI.)

Ultrasonography The literature on sonographic evaluation of musculoskeletal fungal infections is limited. In a case report of soft tissue blastomycosis of the forearm in a child, ultrasound could not distinguish an inflammatory mass from a soft tissue tumor, including malignancy, and the diagnosis was made by biopsy.50 Ultrasonography is a useful imaging modality in diagnosis of mycetoma. Eumycetoma is characterized by the numerous sharp bright hyperechoic echoes produced by the black grains. Multiple thick-walled cavities are seen without acoustic enhancement. In actinomycetoma, the findings are similar but the grains are less distinct (see Fig. 68-23E).26

Nuclear Medicine Coccidioidomycosis

Mucormycosis There is no recent English literature on the use of bone scintigraphy in the evaluation of mucormycosis. Scinticans typically show increased radiotracer uptake in any inflammatory involvement of the skeleton.54,55

Maduromycosis Three-phase technetium scintigraphy reveals increased radiotracer uptake in the mycetoma lesions. It is very helpful in assessment of the healing process characterized by normalization of radiotracer uptake on follow-up studies.41

Actinomycosis The technetium bone scan is a sensitive examination that may show abnormal radionuclide uptake in an affected area in an early stage of the skeletal actinomycosis, before obvious radiographic findings.28

Nocardiosis

Radionuclide bone scanning either with 99mTc-MDP or gallium-67 radiopharmaceutical agents is a sensitive method for detection of disseminated musculoskeletal coccidioidomycosis. Gallium scan delineates well the soft tissue involvement (see Fig. 68-14D and E).2,4

Nuclear medicine scans may show nonspecific increased uptake in the regions of nocardial osteomyelitis.37

North American Blastomycosis

The utility of PET and PET/CT imaging in musculoskeletal fungal and higher bacterial infections has yet to be determined.

Scanning with Tc-MDP is useful in evaluation of skeletal blastomycosis and shows increased radiotracer uptake in the affected osseous structures.7 99m

Cryptococcosis Bone scintigraphy shows increased radiotracer uptake in the cryptococcal skeletal lesions and is helpful in evaluation of multifocal involvement.9,11

Sporotrichosis Three-phase 99mTc-MDP and gallium-67 bone scintigraphy is useful in evaluation of the extent of sporotrichosis. Increased radiotracer uptake in the affected regions can be seen.14,51,52

Positron Emission Tomography/ Computed Tomography

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment Coccidioidomycosis Osteomyelitis secondary to coccidioidomycosis remains a rare but difficult disease to treat, with a lifelong risk of recurrence. A combined medical and surgical approach has been shown to be effective, and medical therapy alone with intravenous amphotericin B followed by suppressive azole therapy may be effective in selected patients (see Fig. 68-12F).56

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Blastomycosis

Maduromycosis

Treatment with amphotericin B and ketoconazole, in conjunction with operative treatment, is very effective.8 Current medications also include itraconazole and fluconazole. Osteomyelitis caused by B. dermatitidis requires at least 1 year of medical therapy.7

Itraconazole is now considered the therapy of choice for chronic histoplasmosis.15,58 Combined medical and surgical treatments are utilized if needed.39

Actinomycetoma is amenable to treatment by antibiotics, preferably by combined drug therapy for long periods. Eumycetoma is usually treated by aggressive surgical excision combined with medical treatment.26 Therapy for actinomycetoma is given over a long period and in higher doses because the microorganisms are locked in fibrous tissue. The mean duration of treatment is 1 year. The cure rate varies from 60% to 90%. The commonly used drugs include a combination of streptomycin sulfate and dapsone. If there is no response in a few months or if there are persistent side effects, then dapsone is replaced by co-trimoxazole. An excellent therapeutic response to amikacin sulfate alone or in combination with co-trimoxazole has been reported. In resistant cases other drugs such as rifampicin, sulfadoxine-pyrimethamine (Fansidar), and sulfonamides have been tried. Because the actinomycetoma has an ill-defined border a margin of healthy tissue should be excised with the lesion.26 In many centers, surgery is still the most acceptable line of treatment for eumycetoma. Aggressive surgical excision, debulking, or amputation in advanced cases has been carried out. Medical treatment of the patients with eumycetoma may continue for periods ranging from a few months to many years. Ketoconazole or itraconazole is utilized. When the lesion becomes well localized and encapsulated, it can be easily removed surgically. There is no justification for mutilating surgery or amputation before trying medical treatment.26

Aspergillosis

Actinomycosis

Optimum treatment of aspergillous osteomyelitis involves débridement and antifungal treatment with amphotericin B, although this drug has relatively poor bone penetration and a high incidence of side effects. Oral itraconazole has been used as a single agent in patients with invasive and osseous aspergillosis. It has been limited to improvement and not cure in many cases. It is usually very well tolerated and is therefore a good alternative to intravenous treatment.19

Penicillin is considered the best therapeutic agent in the treatment of the musculoskeletal actinomycosis and is generally given for 6 to 12 months. Others drugs, including cephalosporins, erythromycin, and cyclines, are also effective.28 With the treatment of complicated cases with spinal infection, the use of an external fixator may be of benefit in conjunction with medical therapy.48

Candidiasis

Sulfamethoxazole-trimethoprim is an effective antibiotic agent for the treatment of nocardiosis.35 Different subspecies show variable susceptibility to amikacin, the third generation of cephalosporins, imipenem/meropenem, and sulfur-based antimicrobial agents.37

Cryptococcosis The therapeutic protocol for treatment of cryptococcal osteomyelitis has not yet been defined. Most authors advocate a combined medical and surgical treatment. Medical treatment includes amphotericin B, fluconazole, and itraconazole.9–11

Sporotrichosis Amphotericin B is recommended for the treatment of systemic infection caused by S. schenckii. However, because of toxicity, frequent relapses, and the resistance of some strains, newer drugs may be more effective. Itraconazole is effective in cutaneous and lymphocutaneous sporotrichosis, but data on their efficacy in systemic infections are scarce.13,57

Histoplasmosis

Amphotericin B continues to be the mainstay of therapy for systemic fungal infections including candidiasis, but its use is limited because of the risks of nephrotoxicity and hypokalemia. Newer formulations of amphotericin B, namely, the liposomal and the lipid complex forms, have become available and have been reported to have less toxicity. Fluconazole, a triazole that has far less toxicity, has been used with some success. It has the additional advantage of being available as an oral formulation.22,59 With candidal osteomyelitis surgical débridement and or resection combined with medical therapy may be needed.60

Mucormycosis The standard treatment is a combination of amphotericin B therapy, surgical débridement, and reversal of the underlying disease or immunosuppression. Posaconazole, a new triazole antifungal, has been used successfully in a number of cases that did not respond to amphotericin B.24

Nocardiosis

SUGGESTED READING Arkun R. Parasitic and fungal disease of bones and joints. Semin Musculoskelet Radiol 2004; 8:231–242.

REFERENCES 1. Arkun R. Parasitic and fungal disease of bones and joints. Semin Musculoskelet Radiol 2004; 8:231–242. 2. Resnick D. Osteomyelitis, septic arthritis, and soft tissue infection: organisms. In Resnick D (ed). Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, 2002, pp 2510–2624.

CHAPTER 3. McGahan JP, Graves DS, Palmer PE, et al. Classic and contemporary imaging of coccidioidomycosis. AJR Am J Roentgenol 1981; 136:393–404. 4. Zeppa MA, Laorr A, Greenspan A, et al. Skeletal coccidioidomycosis: imaging findings in 19 patients. Skeletal Radiol 1996; 25:337–343. 5. Bronnimann DA, Galgiani JN. Coccidioidomycosis. Eur J Clin Microbiol Infect Dis 1989; 8:466–473. 6. Centers for Disease Control and Prevention (CDC) and Jajosky RA, Hall PA, Adams DA, et al. Summary of notifiable diseases—United States, 2004. MMWR Morb Mortal Wkly Rep 2006; 53:1–79. 7. Saiz P, Gitelis S, Virkus W, et al. Blastomycosis of long bones. Clin Orthop Relat Res 2004; (421):255–259. 8. MacDonald PB, Black GB, MacKenzie R. Orthopaedic manifestations of blastomycosis. J Bone Joint Surg Am 1990; 72:860–864. 9. Armonda RA, Fleckenstein JM, Brandvold B, Ondra SL. Cryptococcal skull infection: a case report with review of the literature. Neurosurgery 1993; 32:1034–1036; discussion 1036. 10. Zanelli G, Sansoni A, Ricciardi B, et al. Muscular-skeletal cryptococcosis in a patient with idiopathic CD4+ lymphopenia. Mycopathologia 2001; 149:137–139. 11. Raftopoulos I, Meller JL, Harris V, Reyes HM. Cryptococcal rib osteomyelitis in a pediatric patient. J Pediatr Surg 1998; 33:771–773. 12. Patramanis GM, Rosengarten JL. MR imaging appearance of cutaneous sporotrichosis. AJR Am J Roentgenol 1999; 172:1697. 13. Yang DJ, Krishnan RS, Guillen DR, et al. Disseminated sporotrichosis mimicking sarcoidosis. Int J Dermatol 2006; 45:450–453. 14. Kumar R, van der Smissen E, Jorizzo J. Systemic sporotrichosis with osteomyelitis. J Can Assoc Radiol 1984; 35:83–84. 15. Cucurull E, Sarwar H, Williams CS 4th, Espinoza LR. Localized tenosynovitis caused by Histoplasma capsulatum: case report and review of the literature. Arthritis Rheum 2005; 53:129–132. 16. Voloshin DK, Lacomis D, McMahon D. Disseminated histoplasmosis presenting as myositis and fasciitis in a patient with dermatomyositis. Muscle Nerve 1995; 18:531–535. 17. Stevens DA. Diagnosis of fungal infections: current status. J Antimicrob Chemother 2002; 49(Suppl 1):11–9. 18. Trullas JC, Cervera C, Benito N, et al. Invasive pulmonary aspergillosis in solid organ and bone marrow transplant recipients. Transplant Proc 2005; 37:4091–4093. 19. Allen D, Ng S, Beaton K, Taussig D. Sternal osteomyelitis caused by Aspergillus fumigatus in a patient with previously treated Hodgkin’s disease. J Clin Pathol 2002; 55:616–618. 20. Tsai SH, Peng YJ, Wang NC. Pyomyositis with hepatic and perinephric abscesses caused by Candida albicans in a diabetic nephropathy patient. Am J Med Sci 2006; 331:292–294. 21. Oster MW, Gelrud LG, Lotz MJ, et al. Psoas abscess localization by gallium scan in aplastic anemia. JAMA 1975; 232:377–379. 22. Rao S, Ali U. Systemic fungal infections in neonates. J Postgrad Med 2005; 51(Suppl 1):S27–S29. 23. Chen F, Lu G, Kang Y, et al. Mucormycosis spondylodiscitis after lumbar disc puncture. Eur Spine J 2006; 15:370–376. Epub 2005 Nov 18. 24. Brown J. Zygomycosis: an emerging fungal infection. Am J Health Syst Pharm 2005; 62:2593–2596. 25. Greenberg RN, Scott LJ, Vaughn HH, Ribes JA. Zygomycosis (mucormycosis): emerging clinical importance and new treatments. Curr Opin Infect Dis 2004; 17:517–525. 26. Fahal AH. Mycetoma: a thorn in the flesh. Trans R Soc Trop Med Hyg 2004; 98:3–11. 27. Ispoglou SS, Zormpala A, Androulaki A, Sipsas NV. Madura foot due to Actinomadura madurae: imaging appearance. Clin Imaging 2003; 27:233–235. 28. Voisin L, Vittecoq O, Mejjad O, et al. Spinal abscess and spondylitis due to actinomycosis. Spine 1998; 23:487–490. 29. Yamada H, Kondo S, Kamiya J, et al. Computed tomographic demonstration of a fish bone in abdominal actinomycosis: report of a case. Surg Today 2006; 36:187–189. 30. Stewart AE, Palma JR, Amsberry JK. Cervicofacial actinomycosis. Otolaryngol Head Neck Surg 2005; 132:957–959. 31. Aldamiz-Echebarria San Sebastian M, Vesga Carasa JC, Aspiazu Alonso-Urquijo A, et al. [An ischiorectal abscess due to Actinomyces]. Rev Clin Esp 1992; 190:258–260. Spanish.

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32. Langloh JT, Lauerman WC. Primary actinomycosis of the quadriceps. J Pediatr Orthop 1987; 7:222–223. 33. Pinilla I, Martin-Hervas C, Gil-Garay E. Primary sternal osteomyelitis caused by Actinomyces israelii. South Med J 2006; 99:96–97. 34. Mah E, Stanley P, McCombe DB. Actinomycosis infection of the finger. Hand Surg 2005; 10:285–288. 35. Moore SL, Jones S, Lee JL. Nocardia osteomyelitis in the setting of previously unknown HIV infection. Skeletal Radiol 2005; 34:58–60. Epub 2004 Nov 13. 36. Malani AK, Gupta C, Weigand RT, et al. Thigh abscess due to Nocardia farcinica. J Natl Med Assoc 2006; 98:977–979. 37. Larobina M, McLean C, Davis BB. Clinical-pathologic conference in general thoracic surgery: disseminated nocardiosis presenting as Pancoast syndrome. J Thorac Cardiovasc Surg 2004; 127:568–571. 38. Berdeaux DH, Grogan TM, Pond GD. Disseminated histoplasmosis diagnosed by computed tomography directed needle biopsy of an adrenal mass. Comput Radiol 1985; 9:101–104. 39. N’dri Oka D, Varlet G, Kakou M, et al. [Spondylodiscitis due to Histoplasma dubosii. Report of two cases and review of the literature]. Neurochirurgie 2001; 47:431–434. French. 40. Miller DJ, Mejicano GC. Vertebral osteomyelitis due to Candida species: case report and literature review. Clin Infect Dis 2001; 33:523–530. Epub 2001 Jul 20. 41. Czechowski J, Nork M, Haas D, et al. MR and other imaging methods in the investigation of mycetomas. Acta Radiol 2001; 42:24–26. 42. Lund PJ, Nisbet JK, Valencia FG, Ruth JT. Magnetic resonance imaging in coccidioidal arthritis. Skeletal Radiol 1996; 25:661–665. Skeletal Radiol 1996; 25:661–665. 43. Zacharias J, Crosby LA. Sporotrichal arthritis of the knee. Am J Knee Surg 1997; 10:171–174. 44. Gotze G, Bloching M, Hainz M, Knipping S. [Invasive aspergillosis of the skull base with orbit infiltration]. HNO 2006; (Epub ahead of print) German. 45. Alkhunaizi AM, Amir AA, Al-Tawfiq JA. Invasive fungal infections in living unrelated renal transplantation. Transplant Proc 2005; 37:3034–3037. 46. Gursel T, Kaya Z, Kocak U, et al. Candida vertebra osteomyelitis in a girl with factor X deficiency. Haemophilia 2005; 11:629–632. 47. Mnif N, Hmaied E, Oueslati S, et al. [Imaging of rhinocerebral mucormycosis]. J Radiol 2005; 86(9 pt 1):1017–1020. French. 48. Fenichel I, Caspi I. The use of external fixation for the treatment of spine infection with Actinomyces bacillus. J Spinal Disord Tech 2006; 19:61–64. 49. Kumar R, Kaushal V, Chopra H, et al. Pansinusitis due to Sporothrix schenckii. Mycoses 2005; 48:85–88. 50. Albert MC, Zachary SV, Alter S. Blastomycosis of the forearm synovium in a child. Clin Orthop Relat Res 1995; (317):223–226. 51. Anees A, Ali A, Fordham EW. Abnormal bone and gallium scans in a case of multifocal systemic sporotrichosis. Clin Nucl Med 1986; 11:663–664. 52. Patange V, Cesani F, Phillpott J, Villanueva-Meyer J. Three-phase bone and Ga-67 scintigraphy in disseminated sporotrichosis. Clin Nucl Med 1995; 20:909–912. 53. Bittini A, Dominguez PL, Martinez Pueyo ML, et al. Comparison of bone and gallium-67 imaging in heroin users’ arthritis. J Nucl Med 1985; 26:1377–1381. 54. Zwas ST, Czerniak P. Head and brain scan findings in rhinocerebral mucormycosis: case report. J Nucl Med 1975; 16:925–927. 55. Meyer RD. Scan findings in rhinocerebral mucormycosis. J Nucl Med 1977; 18:96. 56. Holley K, Muldoon M, Tasker S. Coccidioides immitis osteomyelitis: a case series review. Orthopedics 2002; 25:827–831; discussion 831–832. 57. Winn RE, Anderson J, Piper J, et al. Systemic sporotrichosis treated with itraconazole. Clin Infect Dis 1993; 17:210–217. 58. Meier JL. Mycobacterial and fungal infections of bone and joints. Curr Opin Rheumatol 1994; 6:408–414. 59. Masood A, Sallah S. Chronic disseminated candidiasis in patients with acute leukemia: emphasis on diagnostic definition and treatment. Leuk Res 2005; 29:493–501. Epub 2004 Dec 30. 60. Armstrong N, Schurr M, Helgerson R, Harms B. Fungal sacral osteomyelitis as the initial presentation of Crohn’s disease of the small bowel: report of a case. Dis Colon Rectum 1998; 41:1581–1584.

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Hydatid Disease (Echinococcosis) ETIOLOGY Hydatid disease (echinococcosis, hydatidosis) is a parasitic infection caused by the larval stage of two species of the tapeworm Echinococcus: E. granulosus (cystic hydatid disease) and E. multilocularis (alveolar hydatid disease). E. granulosus is endemic in sheep-raising areas worldwide, whereas E. multilocularis is limited to certain areas of Central Europe, Canada, and Alaska. Few cases of infections due to E. oligarthrus (polycystic hydatid disease) have also been reported in South America. Rare cases of E. vogelii are also reported.1,2 The intermediate hosts of the larval stage of E. granulosus are usually sheep, but they can also be found in cattle, hogs, and other domestic livestock and, occasionally, humans. The definitive hosts are dogs, foxes, and other carnivores that harbor the adult tapeworm in the small intestine. The carnivore becomes infected by ingesting the larval form of the intermediate host. The intermediate host becomes infected by ingesting eggs passed in the carnivore feces. The larval stages are referred to as hydatid cysts.2 Current data, based on genome patterns, generally support previous characterizations based on morphologic and biologic criteria, although at least 10 genetically distinct populations exist within the complex until recently denoted E. granulosus. It is important to recognize that important biologic differences exist between populations presently identified in many texts as E. granulosus, the causative agent of cystic echinococcosis, and that these may account for local differences in patterns of transmission and clinical and public health significance of the disease.3

PREVALENCE AND EPIDEMIOLOGY In many endemic regions, incidence rates of cystic echinococcosis range from 5 to 20 per 100,000 population. Most urban populations are at low risk, but in rural endemic areas diagnostic incidence is significantly higher. The rates based on clinically diagnosed cases underestimate the burden of infection, but surveys of populations in endemic areas using ultrasonographic diagnostic techniques often measure cystic echinococcosis prevalences of 2% to 6%, which are manyfold higher than evident from clinically diagnosed cases. Consistently highest prevalence is found among populations involved with sheep raising, thus emphasizing the predominant public health importance of E. granulosus.3 E. multilocularis is largely confined to life cycles involving foxes and arvicolid rodents in ecosystems generally separate from humans; therefore, exposure of humans to E. multilocularis is relatively less common than exposure of humans to E. granulosus, the cause of cystic echinococcosis. However, domestic dogs or cats may become infected when they eat infected wild rodents, and infected pets are an important source of infection for humans.

The incidence of diagnosed disease in humans remains low, between 0.02 and 1.4 per 100,000 worldwide or larger in endemic regions. The known distribution and prevalence of infection in foxes and coyotes has increased in the United States and now extends from Montana to western Ohio. Exposure of humans appears rare.3 A network of collaborating groups working on echinococcosis was created through the auspices of the World Health Organization (Informal Working Group on Echinococcosis) and has facilitated the production of guidelines on disease treatment and control.3

CLINICAL PRESENTATION The most commonly affected organ by E. granulosus is the liver. The skeletal structures are rarely involved. The presenting symptoms of skeletal echinococcosis are nonspecific and variable and include pain, swelling, functional impairment, muscle wasting, nerve root pain, and fracture. General health is usually unaffected. The men and women seem equally affected. This disease is rare in children.1,4

KEY POINTS Hydatid disease (echinococcosis, hydatidosis) is a parasitic infection caused by the larval stage of two species of the tapeworm: Echinococcus granulosus (cystic hydatid disease) and Echinococcus multilocularis (alveolar hydatid disease). ■ E. granulosus is endemic in several areas (mostly sheepraising) worldwide, whereas E. multilocularis is limited to certain areas of Central Europe, Canada, and Alaska. ■ The intermediate hosts of the larval stage of E. granulosus are usually sheep, but they can also be cattle, hogs, and other domestic livestock and, occasionally, humans. ■ The definitive hosts of E. granulosus are dogs, foxes, and other carnivores that harbor the adult tapeworm in the small intestine. The carnivore becomes infected by ingesting the larval form of the intermediate host. ■ The intermediate host becomes infected by ingesting eggs passed in the carnivore feces. The larval stages are referred to as hydatid cysts. ■ Human infection by E. granulosus occurs when eggs passed in dog feces are accidentally swallowed through consumption of contaminated food or water. Embryos liberated from the eggs penetrate the intestinal mucosa and enter the portal venous system and the liver where they are trapped and become hydatid cysts, with less common involvement of other organs including the musculoskeletal system. ■ Imaging should start with radiographs. CT and MRI are very valuable imaging modalities in evaluation of local extent of disease. ■ Serologic tests are useful for confirming the presumptive imaging diagnosis of E. granulosus. ■ The treatment of skeletal echinococcosis is surgical and similar to oncologic therapy. ■ For the skeletal lesions, the World Health Organization suggests adjuvant chemotherapy with mebendazole or albendazole for at least 2 years after surgery. The efficiency of the medical treatment remains debated. ■

CHAPTER

Skeletal lesions caused by E. granulosus occur by hematogenous seeding. The parasite spreads along cancellous trabeculae and through the medullary canal. Because no adventitia is formed in bone, the cysts enlarge and give rise to daughter cysts that may spread to adjacent bones. Skeletal hydatid lesions are usually polycystic. The disease can remain asymptomatic for a protracted period of time. Because of the rigid structure of cortical bone, hydatid cysts tend to grow slowly and rarely exceed 2 cm in diameter but can be significantly larger. The growing cysts lead to bone destruction and deformity, and in some cases, to cortical erosion, pathologic fracture, or compressive myelopathy with vertebral lesions. Secondary infection may also occur.2 The most frequently involved skeletal structure is the spine in 35% of cases, followed by the pelvis in 21% of cases, the femur in 16% of cases, and the tibia in 10% of cases. The ribs, skull, scapula, humerus, fibula, and tarsal bones are less frequently involved.5 Spinal lesions typically appear multiloculated, usually with epidural and paraspinal extension.6 Muscles are rarely involved.7 Hydatid synovitis can occur usually due to secondary extension from the adjacent bone or infrequently after hematogenous spread.8 Concomitant hepatic involvement can be seen with the skeletal echinococcosis.9 Complications associated with skeletal echinococcosis include pathologic fracture, secondary infection especially with staphylococci, and rupture into the spinal canal with neurologic impairment including paraplegia.1,10 Eosinophilia is seen in 25% to 45% of patients.1 Serologic tests are useful for confirming presumptive imaging diagnosis of E. granulosus. However, the limitations of serodiagnosis in cystic echinococcosis must be understood to correctly interpret the findings. Specific confirmation of reactivity can be obtained by demonstrating echinococcal antigens by immunodiffusion (arc 5) procedures or immunoblot assays (8-, 16-, 21-kDa bands). These latter serodiagnostic markers are the most E. granulosus-specific criteria described, but even they may be detected in serum of patients with other forms of echinococcosis and 5% to 10% of patients with T. solium cysticercosis.3 Alveolar echinococcosis closely mimics hepatic carcinoma and is a challenge to diagnose. Serologic tests are usually positive at high titers and highly specific antigens and have been identified and synthesized that, when used in serologic assays, are highly sensitive and specific for diagnosis of alveolar echinococcosis and can distinguish this infection from other forms of echinococcosis. Antibodies of the IgG1 and IgG4 isotypes are the most sensitive IgG responses in alveolar echinococcosis, and monitoring of these isotypes tended to correlate with active versus inactive disease and successful treatment. In seronegative patients polymerase chain reactions for detection of echinococcal-specific RNA or DNA, in closed- or open-biopsy specimens, have been developed and may confirm the diagnosis.3 Fewer cases of alveolar echinococcosis of the bone were reported. Most common involvement was of the spine, soft tissues, and sternum from contiguous spread of disease from the liver. Distant metastases to the bone and soft tissue structures can also occur. Endovesicular daughter cysts are never observed.11

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PATHOPHYSIOLOGY Human infection by E. granulosus occurs when eggs passed in dog feces are accidentally swallowed through consumption of contaminated food or water. Embryos liberated from the eggs penetrate the intestinal mucosa and enter the portal venous system and the liver where they are trapped and become hydatid cysts (70%–75% of all cases). Some larvae reach the lungs (15%–25%) and develop into pulmonary hydatid cyst disease. Infrequently (10%), cysts form in the brain, skeletal muscles, bones, kidneys, spleen, or other tissues. In 20% of patients the disease is multifocal. Bone involvement varies between 0.5% and 4%.2 The histologic and gross pathologic features of skeletal echinococcosis differ from those seen in the other organs. The wall of the cyst has three layers: the inner germinal layer that gives rise within the cyst to scoleces (the infectious embryonic tapeworms), brood cysts, and daughter cysts; the intermediate layer that consists of an acellular laminated membrane; and the outer granulomatous adventitial layer that is produced by the host, in contrast to the other two layers that come from the parasite. Cysts developed in bones lack the adventitial layer that is typically seen with the visceral organ involvement. As the lesion grows, secondary/daughter cysts are seen. This gives a multifocal appearance, which is related to apposing walls of the daughter cysts. In pathologic specimens the cystic spaces tend to be larger with E. granulosus than with E. multilocularis.1,2

IMAGING TECHNIQUES Imaging should start with radiographs. CT and MRI are very valuable imaging modalities in evaluation of local extent of disease. Ultrasonography and bone scintigraphy may also be used.

MANIFESTATIONS OF THE DISEASE Radiography The most common radiologic manifestation of skeletal hydatid disease is a lucent expansile lesion with cortical thinning. Single or multiple expansile lytic lesions containing trabeculae can be seen. With associated cortical interruption an adjacent soft tissue mass with calcifications can be noted. Calcifications represent dystrophic changes in dead parasites. In early stages there is no sclerosis or periosteal reaction. Osteosclerosis may be seen in the later stages of disease. A periosteal reaction is not seen unless there is a pathologic fracture (Fig. 68-28).1,10,12

Magnetic Resonance Imaging Magnetic resonance imaging is helpful in verifying the extent of the disease, texture of the cyst, degree of medullary involvement, and viability of the cyst. On T1-weighted images there is a mixed morphologic appearance. High signal intensity content of the cyst may correlate with high cell or protein content, which is suggestive of extensive parasite-host reaction. Daughter cysts are more hypointense than the parent cyst on T1-weighted images. The

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abscesses, with peripheral enhancement on the postcontrast T1-weighted fat-saturated images and variable signal intensities on T1-weighted MR images. The absence of calcifications or endovesicular daughter cysts does not exclude the diagnosis of cystic echinococcosis (Fig. 68-29A-G).9

Multidetector Computed Tomography Computed tomography is a useful imaging modality in evaluation of skeletal hydatid disease. Single or multiple cystic lesions can be of variable size and typically are well defined, with no contrast enhancement, no daughter cysts, and no germinal membrane detachment. They may display a honeycomb appearance, cortical thinning or cortical destruction, pathologic fracture, and soft tissue mass.5 CT may show endovesicular daughter cysts, which are frequently observed in hepatic disease but are rare in musculoskeletal manifestations of this disease (Figs. 68-29H-I and 68-30).9

Ultrasonography Ultrasonography has a limited value in evaluation of musculoskeletal hydatid disease and may be utilized to show the extraosseous extension of the lesions into the adjacent soft tissues or to evaluate rare soft tissue lesions.4,7

Nuclear Medicine

■ FIGURE 68-28 Frontal radiograph of the humerus shows an eccentrically located mildly expansile bubbly lytic lesion with internal trabeculae involving the mid diaphysis in a Bosnian patient with hydatid disease. Note cortical thinning and sclerotic rim at the inner margin of the lesion. (Courtesy of Department of Radiology, UMC Sarajevo, Bosnia & Herzegovina.)

cyst wall or capsule is seen as a low intensity rim, which shows enhancement after intravenous administration of gadolinium. On T2-weighted imaging the daughter cysts are of slightly higher signal intensity than the parent cyst. Signal intensities may change with coexisting infection, calcification, or hemorrhage. With spinal involvement extradural spread of the hydatid cysts through a widened neural foramen into the muscle planes may result in the appearance of a “bunch of grapes.” The T2- weighted sequence indicates whether a cyst is viable. A decrease in hyperintensity and an increase is hypointensity from a collapsed cyst wall is suggestive of a succumbed cyst. MRI may show endovesicular daughter cysts, which are frequently observed in hepatic disease but are rare in musculoskeletal manifestations of this disease.1,9,10,12 Patients with musculoskeletal lesions of cystic echinococcosis typically have cystic structures in adjacent soft tissues. These cysts morphologically resemble

The literature related to utility of nuclear medicine bone scans in evaluation of musculoskeletal echinococcosis is limited. Scanning with 99mTc-MDP scan may demonstrate increased uptake particularly at the peripheral borders.13

Positron Emission Tomography/ Computed Tomography Positron emission tomography using (18F) fluorodeoxyglucose (FDG) has been developed for the follow-up of the patient with inoperable E. multilocularis liver disease who has undergone long-term therapy with a benzimidazole. This approach seems very promising to assess inflammatory activity and thereby to indirectly depict parasitic activity. PET/CT can evaluate the morphologic and functional aspects of the disease and assess the efficacy of treatment.14 The utility of PET and PET/CT imaging in musculoskeletal hydatid disease is to be determined.

DIFFERENTIAL DIAGNOSIS The differential diagnosis of skeletal echinococcosis is broad and includes plasmacytoma, brown tumor of hyperparathyroidism, cartilaginous neoplasms, fibrous dysplasia, metastatic disease, hemophiliac pseudotumor, giant cell tumor, aneurysmal bone cyst, and lymphoma. The differential diagnosis for spinal lesion includes chronic pyogenic and tuberculous osteomyelitis.1,12

CHAPTER

■ FIGURE 68-29

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Coronal (A and B) and axial (C) fluid-sensitive images with fat saturation, coronal (D) and axial

(Continued)

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■ FIGURE 68-29—Cont’d

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(E) T1-weighted images, and axial (F) and coronal (G) T1-weighted MR images with fat saturation after intravenous administration of gadolinium-based contrast agent in a patient with hydatid disease involving multiple right pelvic and thigh muscles. Note the multiloculated multifocal cystic lesion involving several muscles, of predominantly high signal intensity, on the fluidsensitive sequences, intermediate-increased signal in respect to the skeletal muscle on the T1-weighted images, and low signal and rim enhancement on the T1-weighted, fat-saturated postcontrast images, consistent with hydatid cyst disease. H and I, Contrast enhanced axial CT images of the pelvis and proximal thighs in the same patient show multiloculated multifocal intramuscular cystic lesions of internal fluid signal intensity with rim and septal enhancement. (Courtesy of Ruth Ceulemans, MD, Chicago, IL.)

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of anaphylaxis and implantation during surgery. A local recurrence rate of 70% to 80% has been reported. Radical resection of the involved segment and bone grafting is now recommended.2,15

SUGGESTED READINGS Schantz PM. Progress in diagnosis, treatment and elimination of echinococcosis and cysticercosis. Parasitol Int 2006; 55(Suppl):S7–S13. Epub 2006 Jan 4. Merkle EM, Schulte M, Vogel J, et al. Musculoskeletal involvement in cystic echinococcosis: report of eight cases and review of the literature. AJR Am J Roentgenol 1997; 168:1531–1534.

REFERENCES

■ FIGURE 68-30

Coronal reformatted CT image of the femur shows an intraosseous cystic/lytic lesion involving the midproximal femoral diametaphysis with associated cortical thinning and pathologic fracture through the femoral neck, intertrochanteric, and subtrochanteric region in a Bosnian patient. (Courtesy of Department of Radiology, UMC Sarajevo, Bosnia & Herzegovina.)

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment Since the 1970s, with introduction of the derivates of the benzimidazoles, medical treatment has been attempted. For the skeletal lesions, the World Health Organization suggests adjuvant chemotherapy with mebendazole or albendazole for at least 2 years after surgery. In cases in which only a palliative treatment is possible, the anthelminthic drug administration can be continuous. However, its efficiency remains debated.2,15,16 Progress in developing effective vaccination against infection with oncospheres and immunotherapy of the metacestode has been reviewed by Lightowlers and others. Vaccination may provide an additional tool for control and prevention of this infection.17

Surgical Treatment Skeletal echinococcosis is treated surgically. The treatment is similar to oncologic therapy. The surgical approach requires preoperative cross-sectional imaging for the evaluation of local extent of the lesion and its relationship to adjacent structures. Curettage carries the risk

1. Resnick D. Osteomyelitis, septic arthritis, and soft tissue infection: organisms. In Resnick D (ed). Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, 2002, pp 2510–2624. 2. Papanikolaou A, Antoniou N, Pavlakis D, Garas G. Hydatid disease of the tarsal bones: a case report. J Foot Ankle Surg 2005; 44:396–400. 3. Schantz PM. Progress in diagnosis, treatment and elimination of echinococcosis and cysticercosis. Parasitol Int 2006; 55(Suppl): S7–S13. Epub 2006 Jan 4. 4. Loudiye H, Aktaou S, Hassikou H, et al. Hydatid disease of bone: review of 11 cases. Joint Bone Spine 2003; 70:352–355. 5. Tuzun M, Hekimoglu B. CT findings in skeletal cystic echinococcosis: CT findings in skeletal cystic echinococcosis. Acta Radiol 2002; 43:533–538. 6. Mellado JM, Perez del Palomar L, Camins A, et al. MR imaging of spinal infection: atypical features, interpretive pitfalls and potential mimickers. Eur Radiol 2004; 14:1980–1989. 7. Mseddi M, Mtaoumi M, Dahmene J, et al. [Hydatid cysts in muscles: eleven cases]. Rev Chir Orthop Reparatrice Appar Mot 2005; 91:267–271. French. 8. Vallianatos PG, Tilentzoglou AC, Seitaridis SV, Mahera HJ. Echinococcal synovitis of the knee joint. Arthroscopy 2002; 18: E48. 9. Merkle EM, Schulte M, Vogel J, et al. Musculoskeletal involvement in cystic echinococcosis: report of eight cases and review of the literature. AJR Am J Roentgenol 1997; 168:1531–1534. 10. Raut AA, Nagar AM, Narlawar RS, et al. Echinococcosis of the rib with epidural extension: a rare cause of paraplegia. Br J Radiol 2004; 77:338–341. 11. Merkle EM, Kramme E, Vogel J, et al. Bone and soft tissue manifestations of alveolar echinococcosis. Skeletal Radiol 1997; 26:289–292. 12. Morris BS, Madiwale CV, Garg A, Chavhan GB. Hydatid disease of bone: a mimic of other skeletal pathologies. Australas Radiol 2002; 46:431–434. 13. Yildirim M, Varoglu E, Gursan N, et al. Unusual localization of hydatid cyst: bone scintigraphy, brain SPECT, and magnetic resonance imaging findings. Clin Nucl Med 2002; 27:449–450. 14. Bresson-Hadni S, Delabrousse E, Blagosklonov O, et al. Imaging aspects and non-surgical interventional treatment in human alveolar echinococcosis. Parasitol Int 2006; 55(Suppl):S267–272. Epub 2006 Jan 5. 15. Zlitni M, Ezzaouia K, Lebib H, et al. Hydatid cyst of bone: diagnosis and treatment. World J Surg 2001; 25:75–82. 16. Diedrich O, Perlick L, Kraft CN, Sommer T. [Orthopedic aspects of osseous echinococcosis—radiologic diagnosis, current surgery and drug therapy aspects]. Z Orthop Ihre Grenzgeb 2001; 139:261–266. German. 17. Lightowlers MW, Lawrence SB, Gauci CG, et al.Vaccination against hydatidosis using a defined recombinant antigen. Parasit Immunol 1996; 18:457–462.

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Leprosy Leprosy (Hansen’s disease) is an infectious disease characterized by a long incubation period. It takes a chronic course with involvement of the skin, mucous membranes, and peripheral nervous system. Leprosy has been eliminated at the national level in 113 of the 122 countries in which it was a public health problem in 1985. It is still encountered in India, Brazil, Myanmar, Madagascar, Mozambique, Nepal, and Tanzania, where the prevalence rates still exceeded 1 per 10,000 at the beginning of 2004.1,2

ETIOLOGY The causative agent, Mycobacterium leprae, is a nonmotile, non–spore-forming, microaerophilic bacterium that usually forms slightly curved or straight rods. It has a predilection for Schwann cells, where the organism multiplies unimpeded by organism-specific host immunity, resulting in destruction of myelin, secondary inflammatory changes, and destruction of the nerve architecture.3,4

PREVALENCE AND EPIDEMIOLOGY The number of reported cases of leprosy in the United States peaked at 361 in 1985 and has declined since 1988. In 2004, 105 cases of leprosy were reported in the United States. Eighty-five percent of detected cases are in immigrants, in whom this disease may mimic many common dermatologic and neurologic entities, leading to delay of diagnosis.4–6 Despite being infrequent in the United States, leprosy is not uncommon in areas of Africa, South America, and Asia. In 1991, the World Health Organization adopted a resolution establishing a goal of eliminating leprosy as a public health problem by the year 2000, which meant reducing the prevalence to 1 case or fewer per 10,000 population. In some countries where the leprosy is endemic, such as India and Brazil, this goal could not be reached by the year 2000 and a new goal for elimination of this disease was pushed to the year 2005 but was not reached.5

CLINICAL PRESENTATION Leprosy is best understood as two conjoined diseases. The first is a chronic mycobacterial infection that elicits an extraordinary range of cellular immune responses in humans. The second is a peripheral neuropathy that is initiated by the infection and the accompanying immunologic events. M. leprae remains nonculturable, and for over a century leprosy has presented major challenges in the fields of microbiology, pathology, immunology, and genetics; it continues to do so today.3 This disease is more common in men than women and can affect any age group, although more commonly individuals younger than 20 years of age are affected. Prodromal symptoms include malaise, fever, drowsiness, rhinitis, and profuse sweating.

According to the microscopic appearance leprosy is divided into four principal types: lepromatous, tuberculoid, dimorphous, and intermediate, with variable clinical manifestations. Typically the tuberculoid type of disease is less progressive than the lepromatous type.1 Currently, the WHO recommends counting external lepromatous lesions to distinguish paucibacillary from multibacillary disease, with fewer than five lesions being classified as paucibacillary and five or more lesions as multibacillary.3 The clinical manifestations vary among these types of leprosy. The tuberculoid type is typically less progressive than the lepromatous type. In tuberculoid leprosy, the skin and nerves are principally affected, whereas in lepromatous leprosy a more acute and generalized process may be evident. In lepromatous (multibacillary) leprosy, skin nodules, papules, macules, and diffuse infiltrations are bilaterally symmetric and usually numerous and extensive. Involvement of the nasal mucosa may lead to crusting and obstructed breathing and epistaxis; ocular involvement leads to iritis and keratitis. In tuberculoid (paucibacillary) leprosy, skin lesions are single or few, sharply demarcated, anesthesic or hypoesthesic, and bilaterally asymmetric; involvement of peripheral nerves tends to be severe. Borderline leprosy has features of both polar forms and is more labile. Indeterminate leprosy is characterized by hypopigmented maculae with ill-defined borders; if untreated, it may progress to tuberculoid, borderline, or lepromatous disease. Lymphadenopathy is seen in all types of leprosy, although it is more prominent in the lepromatous type. In patients with prominent neurologic findings (neuritic variety), lepromatous granulation tissue forms about the nerves, leading to their thickening, tenderness, and paresthesias. Muscular atrophy and contractures may occur, as well as subsequent mutilations and secondary infections.1,7 Mycobacterium leprae has a predilection for the cooler appendages of the body with characteristic involvement of the small bones of the hands and feet. Bone lesions in patients with leprosy are usually due to trauma and secondary bacterial infection superimposed on denervated tissues.8 The cardinal diagnostic features of leprosy

KEY POINTS This infectious disease is caused by Mycobacterium leprae and characterized by a long incubation period. ■ It has been eliminated at the national level in 113 of the 122 countries but is still encountered in India, Brazil, Myanmar, Madagascar, Mozambique, Nepal, and Tanzania. ■ The infection probably enters the body through the skin and mucous membranes, especially nasal mucosa. The causative organisms are disseminated via the bloodstream and the lymphatics and localize in the skin, the nerves, and, in advanced cases, in the viscera. ■ It has a predilection for the cooler appendages of the body with characteristic involvement of the small bones of the hands and feet. ■ It is curable but requires long-term multidrug therapy. ■

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are anesthetic skin lesions, neuropathy, and positive skin smears for the bacilli. However, patients may rarely present without skin lesions in pure neuritic leprosy.4 Articular inflammatory manifestations involving small joints, large joints, or both and sacroiliitis may exist in patients with different forms of leprosy and can follow a chronic course.9 Erythema nodosum is seen in leprosy and is associated with arthritis. Soft tissue swelling of the hands (swollen hand syndrome) with intra- and extraarticular inflammation in response to organisms and granulomatous reaction and subcutaneous nodules has been described.1 The frequency, nature, and importance of vascular lesions in leprosy are debated. Occasionally, soft tissue calcifications involving the nerves can be seen. As in chronic osteomyelitis with soft tissue sinuses, leprosy with cutaneous ulcerations may be associated with development of secondary malignancy, specifically squamous cell carcinoma of the skin.1 Leprosy is diagnosed by finding lepromatous bacilli in typical histologic lesions.1 The lepromin skin test is not approved by the U.S. Food and Drug Administration and is not recommended or provided for diagnostic use in the United States. This test provides a measure of the individual’s ability to mount a granulomatous response against a mixture of lepromatous antigens. Responses to lepromin are not specific, and many individuals who have never been exposed to M. leprae will develop a positive lepromin reaction. Rapid molecular type assays (polymerase chain reaction analysis) of tissues for M. leprae now provide a valuable means for identifying this organism.3

PATHOPHYSIOLOGY Patients affected with leprosy typically have a history of prolonged contact with the bacilli, but the exact mode of the transmission is not clear. The infection probably enters the body through the skin and mucous membranes, especially nasal mucosa. The M. leprae organisms are disseminated via the bloodstream and the lymphatics and localize in the skin, the nerves, and in advanced cases in the viscera. The incubation period is estimated to vary from 3 to 6 years.1 In the lepromatous type of disease the bacilli are numerous with paucity of cellular reaction. Skin lesions have a widespread symmetric distribution. Macrophages, containing fat droplets, leprae cells, and numerous bacilli, are distinctive. In the tuberculoid type of disease the bacilli are less numerous but they initiate a severe granulomatous reaction similar to tuberculosis and sarcoidosis. Asymmetrically distributed skin macules are seen. The dimorphous type is uncommon with microscopic features of both lepromatous and tuberculoid types. In the intermediate type a few bacilli stimulate a slight cellular reaction in the perivascular and perineural areas, with the pathologic features not prominent enough to allow classification into tuberculoid or lepromatous types.1 The histologic characteristics of involved joints in leprosy are similar to those in other neuropathic osteoarthropathies including serous joint effusion, villous

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proliferation of the synovial membrane, erosive and proliferative changes of cartilage, sclerosis and eburnation of bone, fragmentation, and osseous excrescences.1

IMAGING TECHNIQUES Imaging should start with radiography. MRI, nuclear medicine bone scintiscans, ultrasonography, and CT may be useful in detection of occult musculoskeletal abnormalities associated with leprosy or in further characterization of known lesions.

MANIFESTATIONS OF THE DISEASE Radiography The skeleton is directly involved by leprosy in 3% to 5% of cases, typically involving the small bones of hands and feet. The radiographic findings comprise periostitis, osteitis, and osteomyelitis. Metaphyses of the phalanges are commonly involved, and metacarpal and metatarsal involvement is less frequent. Radiographs show soft tissue swelling, osteoporosis, endosteal thinning, enlargement of nutrient foramina, and destructive osseous lesions with a cystic or honeycombing appearance. With healing, the definition of the involved bones increases with remaining residual deformity. Destruction of the alveolar process and anterior nasal spine of the maxilla results in direct lepromatous involvement of the bone, and secondary infection is sometimes referred to as the rhinomaxillary or Bergen syndrome. In the long tubular bones symmetric periostitis of the tibia, fibula, and distal portion of the ulna may be noted. The constellation of erythematous skin lesions, pain, and periostitis in the lower extremity has been called “red leg.”1 With less common hematogenous dissemination to bone, intramedullary foci of infection are seen including the tubular bones of the extremities and the ribs. The lesions are usually epiphyseal or metaphyseal in the long tubular bones, but medullary involvement can occur. The disease progresses slowly, but the cortex and periosteum can be violated. Periostitis and sclerosis are not prominent.1 Lepromatous arthritis is not common and may result from direct intra-articular extension or, less commonly, from hematogenous dissemination. Radiographs demonstrate joint effusion with associated soft tissue swelling. Small joints, large joints, or both can be affected, including the sacroiliac joints. The ankles, knees, wrists, finger joints, and the elbows are affected in decreasing frequency.1,9 The skeletal abnormalities occurring on a neurologic basis are much more frequent and severe than those produced by direct leprous infiltration of the bone. Motor denervation due to leprous infection of peripheral nerves results in neuropathic osteoarthropathy in 20% to 70% of hospitalized patients and contributes to deformities such as clawhand and clawtoes. This is sometimes associated with the development of concentric bone atrophy. Absorption of bone in leprosy manifests as a decrease in bone length and width and results in a tapered appearance

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at the end of the bone, which has been likened to a licked candystick. When complicated by repeated microtrauma, secondary bacterial infection, or both, digits may be resorbed (Figs. 68-31 and 68-32).1,8

Magnetic Resonance Imaging Magnetic resonance imaging is able to detect abnormalities of the nerves in leprosy. Active reversal reaction of peripheral nerves is indicated by an increased T2 signal and gadolinium enhancement. These signs are suggestive of rapid progression of nerve damage and poor prognosis unless antireactional treatment is started.10

One study revealed significant MRI changes in clinically asymptomatic neuropathic feet in patients with leprosy. The most striking were the changes located in the region of the first metatarsophalangeal (MTP) joint. These changes ranged from degradation and interruption of the subcutaneous fat to effusion/synovitis in the first MTP joint, indicating that MRI may play an important role in detecting feet at risk and may influence clinical decision-making. Another study showed that MRI could play an important role in detecting osteomyelitis in leprosy patients with long-standing neuropathic feet.11,12 MRI findings of symmetric flexor and extensor tendons synovitis with pitting edema of the hands and feet

■ FIGURE 68-31 Frontal radiograph of the hands (A) and frontal radiograph of the feet (B) show neuropathic lesions in a patient with leprosy. Note concentric bone atrophy in the hands and feet with tapered osseous structures and osteolysis involving multiple digits. (Courtesy of Michael Pitt, MD, Birmingham, AL.)

■ FIGURE 69-32 Lateral radiograph of the foot and ankle in a patient with leprosy shows tapered appearance of the digits with associated soft tissue swelling, lack of the soft tissues about the digits, and an ulcer at the plantar aspect of the forefoot. (Courtesy of Department of Radiology, UMC Sarajevo, Bosnia & Herzegovina.)

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■ FIGURE 68-33

Axial T2-weighted MR images with fat saturation of the hands (A) and of the feet (B) in a patient with leprosy show soft tissue edema predominantly involving the dorsal subcutaneous tissues. (Courtesy of Claudia Helling, MD, Buenos Aires, Argentina.)

were described in a patient with skin lesions and borderline tuberculoid leprosy (Fig. 68-33).13

Multidetector Computed Tomography In the past, CT was reported as a useful imaging modality for evaluation of peripheral nerve lesions in patients with leprosy.14 CT findings of the paranasal sinuses in patients with leprosy comprise nonspecific mucosal thickening that may mimic chronic sinusitis. The diagnosis of leprosy requires biopsy.15

In the reactive phase of leprosy, on the bone scan, erythema nodosum can cause a symmetric double stripe sign bilaterally involving the distal tibiae similar to those seen in hypertrophic osteoarthropathy.21

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment

Ultrasonography can be utilized to demonstrate normal peripheral nerves as well as their pathology, including leprosy. The lesions of tuberculoid leprosy appear hypoechoic on ultrasound examination.16 Active reversal reactions of peripheral nerves are indicated by endoneural color flow signals, suggesting rapid progression of nerve damage and a poor prognosis unless antireactional treatment is started.10

Several effective antimicrobial agents are now available to treat leprosy, and this infection is curable. Long-term multidrug therapy with dapsone, clofazimine, and rifampin has been very practical and successful for treatment of leprosy. However, even with this powerful drug combination the overall number of newly registered cases has not fallen consistently, and drug resistance still occurs.3 Bacillus Calmette-Guérin vaccine provides a low but measurable degree of protection against M. leprae, but a highly effective, specific vaccine has not yet been developed.3

Nuclear Medicine

Surgical Treatment

Bone scintigraphy may be useful to determine disease activity in cases of mutilation caused by leprosy. It seems to be superior to conventional radiography and may enable bone biopsies to be avoided.17 Radionuclide bone scans in patients with leprosy show scan patterns simulating hypertrophic osteoarthropathy and diffuse arthritis consistent with a primary disease process.18 Gallium-67 imaging shows diffuse moderate radiotracer uptake over the entire skin surface except in the face, where it shows homogeneous, diffuse, and marked uptake in a series of 12 untreated patients with multibacillary disease. Internal organ involvement was variable. The pattern of body skin (“skin outlining”) and facial skin (“beard distribution”) may be distinct for untreated patients with multibacillary leprosy.17 In one patient with borderline leprosy, gallium-67 showed increased radiotracer uptake in the subcutaneous tissues of the face and thighs.19 In patients with lepromatous leprosy with an erythema nodosum leprosum, gallium-67 may reveal multiple patchy areas of radiotracer uptake in the skin of the face, trunk, arms, and thighs.20

Deformities in leprosy are the consequence of impairments of nerve function. The aim of reconstructive surgery on the hand in patients with leprosy is to augment its capabilities for the activities of daily living and for safe vocations and to restore form and structure adequately to accelerate the patient’s integration into society.2

Ultrasonography

SUGGESTED READING Scollard DM, Adams LB, Gillis TP, et al. The continuing challenges of leprosy. Clin Microbiol Rev 2006; 19:338–381.

REFERENCES 1. Resnick D. Osteomyelitis, septic arthritis, and soft tissue infection: organisms. In Resnick D (ed). Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, 2002, pp 2510–2624. 2. Anderson GA. The surgical management of deformities of the hand in leprosy. J Bone Joint Surg Br 2006; 88:290–294. 3. Scollard DM, Adams LB, Gillis TP, et al. The continuing challenges of leprosy. Clin Microbiol Rev 2006; 19:338–381.

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4. Ooi WW, Srinivasan J. Leprosy and the peripheral nervous system: basic and clinical aspects. Muscle Nerve 2004; 30:393–409. 5. Centers for Disease Control and Prevention (CDC) and Jajosky RA, Hall PA, Adams DA, et al. Summary of notifiable diseases—United States, 2004. MMWR Morb Mortal Wkly Rep 2006; 53:1–79. 6. Ooi WW, Moschella SL. Update on leprosy in immigrants in the United States: status in the year 2000. Clin Infect Dis 2001; 32:930–937. 7. Case Definition Leprosy. Epidemiol Bull 2002; 23(No. 2). 8. Jones EA, Manaster BJ, May DA, Disler DG. Neuropathic osteoarthropathy: diagnostic dilemmas and differential diagnosis. RadioGraphics 2000; 20(Spec No):S279–S293. 9. Cossermelli-Messina W, Festa Neto C, Cossermelli W. Articular inflammatory manifestations in patients with different forms of leprosy. J Rheumatol 1998; 25:111–119. 10. Martinoli C, Derchi LE, Bertolotto M, et al. US and MR imaging of peripheral nerves in leprosy. Skeletal Radiol 2000; 29:142–150. 11. Maas M, Slim EJ, Akkerman EM, Faber WR. MRI in clinically asymptomatic neuropathic leprosy feet: a baseline study. Int J Lepr Other Mycobact Dis 2001; 69:219–224. 12. Maas M, Slim EJ, Heoksma AF, et al. MR imaging of neuropathic feet in leprosy patients with suspected osteomyelitis. Int J Lepr Other Mycobact Dis 2002; 70:97–103. 13. Helling CA, Locursio A, Manzur ME, et al. Remitting seronegative symmetrical synovitis with pitting edema in leprosy. Clin Rheumatol 2006; 25:95–97. 14. Barbancon O, Rath S, Alqubati Y. Hansen’s disease: computed tomography findings in peripheral nerve lesions. Ann Radiol (Paris) 1989; 32:579–581. 15. Srinivasan S, Nehru VI, Bapuraj JR, et al. CT findings in involvement of the paranasal sinuses by lepromatous leprosy. Br J Radiol 1999; 72:271–273. 16. Fornage BD. Peripheral nerves of the extremities: imaging with US. Radiology 1988; 167:179–182. 17. Braga FJ, Araujo EB, Camargo EE, et al. Gallium scintigraphy in Hansen’s disease. Eur J Nucl Med 1991; 18:866–869. 18. Goergen TG, Resnick D, Lomonaco A, O’Dell CW Jr. Radionuclide bone-scan abnormalities in leprosy: case reports. J Nucl Med 1976; 17:788–790. 19. Mouratidis B, Lomas FE. Gallium-67 scintigraphy in borderline lepromatous leprosy. Australas Radiol 1993; 37:270–271. 20. Peng NJ, Wang JH, Hsieh SP, et al. Ga-67 and Tc-99m HMPAO labeled WBC imaging in erythema nodosum leprosum reaction of leprosy. Clin Nucl Med 1998; 23:248–250. 21. Datz FL. Erythema nodosum leprosum reaction of leprosy causing the double stripe sign on bone scan: case report. Clin Nucl Med 1987; 12:212–214.

Lyme Disease Lyme disease caused by the spirochete Borrelia burgdorferi is the most common vector-born illness in the United States and is transmitted to humans by the bite of infected blacklegged ticks.1

ETIOLOGY The causative organism Borrelia burgdorferi normally lives in small animals. Certain species of ticks, Ixodes dammini (scapularis) or related ticks, transmit disease among the animals and to humans. In the northeastern and north-central United States the deer tick Ixodes scapularis transmits Lyme disease. In the Pacific coastal United States the disease is spread by the tick Ixodes pacificus.

Deer are an important host in transmitting ticks, but they do not become infected with Lyme disease. There is no known human-to-human transmission.1,3–5

PREVALENCE AND EPIDEMIOLOGY Lyme disease was first identified as a distinct entity in the United States in 1975. It was named after the town in Connecticut in which it was first encountered. In 2004, 19,804 cases of Lyme disease were reported, yielding a national average of 6.8 cases for every 100,000 persons. In the 12 states where Lyme disease is most common, the average was 27.4 cases for every 100,000 persons. Nearly 80% of cases are reported between May and August. Lyme disease has a global distribution and has been detected on all continents except Antarctica. This disease occurs in both adults and children, with a slight male predominance.1–4

CLINICAL PRESENTATION Clinical manifestations usually appear 1 week after a tick bite, although they may be delayed for several weeks. The disease begins with a distinctive skin lesion: erythema chronicum migrans. This lesion appears as a macule or papule in the area of a previous tick bite, most often on the trunk or proximal portion of the extremities, and expands to an annular lesion with an intensely red border, which may be pruritic or burning. The skin lesion resolves in a period of weeks. The cutaneous manifestations are not constant and are not always remembered by the patient. Other signs and symptoms commonly associated with the early stage of this disease include fever, chills, myalgias, arthralgias, headache, stiff neck, and exhaustion.3,4 Articular involvement may develop from 2 weeks to 2 years after infection or onset of systemic symptoms, making attribution to Lyme disease difficult. After several months, approximately 60% of patients with untreated infection will begin to have intermittent bouts of arthritis, with severe joint pain and swelling. Large joints are most often affected, particularly the knees in 80% of patients. Other areas involved include shoulders, elbows, ankles, hips, wrists, small joints of the extremities, and the temporomandibular joints. Recurrent, brief attacks (weeks or months) of objective joint swelling in one or more joints are sometimes followed by chronic arthritis in one or

KEY POINTS Lyme disease is the most common vector-borne illness in the United States and is transmitted to humans by the bite of infected blacklegged ticks. ■ The causative organism is Borrelia burgdorferi. ■ Erythema chronicum migrans is a characteristic skin lesion and usually the first manifestation of disease. ■ Articular involvement may develop from 2 weeks to 2 years after infection or onset of systemic symptoms, making diagnosis of Lyme disease difficult. ■ Most patients can be cured with a few weeks of oral antibiotics. ■

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more joints. Approximately 10% of patients develop Lyme carditis typically 4 weeks after onset of disease. In addition, up to 5% of untreated patients may develop chronic neurologic complaints months to years after infection. These include shooting pains, numbness or tingling in the hands or feet, and problems with concentration and short-term memory.1,3,4 Nonspecific laboratory findings include mild leukocytosis, increased sedimentation rate, and minimally increased serum levels of transaminases. Increased total serum IgM occurs in 33% of patients, which if persistent in untreated patients is a predictor for later manifestations of Lyme disease.3 A two-test approach for active disease and for previous infection using a sensitive enzyme immunoassay (EIA) or immunofluorescent assay (IFA) followed by a Western immunoblot is the algorithm of choice. All specimens positive or equivocal by a sensitive EIA or IFA should be tested by a standardized Western immunoblot. Specimens negative by a sensitive EIA or IFA need not be tested further. When Western immunoblot is used during the first 4 weeks of disease onset (early Lyme disease), both immunoglobulin M (IgM) and immunoglobulin G (IgG) procedures should be performed. A positive IgM test result alone is not recommended for use in determining active disease in patients with illness greater than 1 month’s duration because the likelihood of a false-positive test result for a current infection is high for these patients. If a patient with suspected early Lyme disease has a negative serology, serologic evidence of infection is best obtained by testing of paired acute- and convalescent-phase serum samples. Serum samples from patients with disseminated or late-stage Lyme disease almost always have a strong IgG response to B. burgdorferi antigens.5

PATHOPHYSIOLOGY Blacklegged ticks live for 2 years and have three feeding stages: larvae, nymph, and adult. When a young tick feeds on an infected animal, the tick takes the bacterium into its body along with the blood meal. The bacterium then lives in the gut of the tick. The infected tick transmits disease to its new host. Sometimes the new host is a human.3,4 Although adult ticks often feed on deer, these animals do not become infected. Deer are nevertheless important in transporting ticks and maintaining tick populations.3 Lyme disease acquired during pregnancy may lead to infection of the placenta and possible stillbirth, but no negative effects on the fetus have been found when the mother receives appropriate antibiotic treatment. There are no reports of Lyme disease transmission from breast milk.4,6 The Lyme disease bacteria can live in blood that is stored for donation. As a precaution, the American Red Cross and the U.S. Food and Drug Administration ask that individuals with chronic illness due to Lyme disease do not donate blood. Lyme disease patients who have been treated with antibiotics and have recovered can donate blood beginning 12 months after the last dose of antibiotics was taken. There is no credible evidence that Lyme disease can be transmitted through air, food, water, or from the bites of mosquitoes, flies, fleas, or lice.

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Aspiration of the affected joints reveals inflammatory synovial fluid with or without eosinophilia. The causative organism is occasionally isolated from the blood, skin, cerebrospinal fluid, and synovial membrane of affected patients, which suggests hematogenous spread of disease. Biopsy of the synovial membrane reveals hypertrophy, vascular proliferation, and cellular infiltration with mononuclear cells and scattered lymphoid follicles. In chronic arthritis the histology of the synovial membrane reveals pannus formation similar to rheumatoid arthritis. It is possible that Lyme arthritis that is initially infectious later evolves to an antigen-induced arthritis. HLA-DR2 and DR4 antigens are found more often with chronic Lyme arthritis.4

IMAGING TECHNIQUES Radiography should be the initial imaging modality in evaluation of any type of arthritis including Lyme arthritis. The local extent of disease including the joint effusion and articular and periarticular inflammation is best further characterized by MRI. Bone scintiscans are most helpful for detection of polyarticular involvement. CT and ultrasonography may also have a role in the diagnosis of Lyme arthritis. The role of positron emission tomography in the diagnosis and evaluation of Lyme arthritis is to be determined.

MANIFESTATIONS OF THE DISEASE Radiography Radiographic findings of Lyme arthritis are nonspecific. The most common finding is joint effusion, typically involving the large joints, most commonly the knee (Fig. 68-34A-B). A large joint effusion may lead to a rupture of the joint capsule with dissection of the joint fluid into the periarticular soft tissue planes, which about the knee can resemble thrombophlebitis. Periarticular soft tissue swelling is frequently present. This finding is frequently associated with edema of the infrapatellar fat pad. Erosive changes are not common but can occur in advanced disease. Subchondral cystic changes with typical thin sclerotic margins may be detected. Juxta-articular osteoporosis may occur and vary from mild to severe. Proliferative enthesopathic changes with associated calcifications or ossifications at the sites of capsular or ligamentous attachments may be seen. Symmetric joint space loss with associated loss of articular cartilage can be seen in the advanced disease. Chondrocalcinosis may occasionally occur.3,4,7

Magnetic Resonance Imaging Magnetic resonance imaging is a useful imaging modality for detection of Lyme arthritis. The findings are nonspecific. Joint effusion, synovitis, myositis, adenopathy, and occasionally subcutaneous edema, popliteal cysts and hemarthrosis are observed. T1-weighted fat-suppressed images after intravenous administration of a contrast agent are most helpful in determining the severity of synovitis (see Fig. 68-34C to E). In advanced disease erosive

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■ FIGURE 68-34

Frontal (A) and lateral (B) radiographs of a knee in a 10-year-old girl with Lyme arthritis show a large joint effusion seen on the lateral projection and no evidence of erosions. Sagittal STIR (TR 4616, TE 75, TI 110) (C),

(Continued)

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■ FIGURE 68-34—Cont’d Sagittal T1-weighted (TR 316, TE 16) (D), and axial T1-weighted with fat-saturation postcontrast (E) images of the same knee show a large joint effusion and moderate synovial enhancement (on E).

changes can also be observed (Fig. 68-35). One study on Lyme versus septic arthritis evaluated by MRI in children showed that the presence of subcutaneous edema significantly favors septic over Lyme arthritis.1 Multifocal bone marrow abnormalities were reported in a middle-aged woman suffering from Lyme disease and presenting as acrodermatitis chronica atrophicans.8

Multidetector Computed Tomography Joint effusions, periarticular soft tissue edema, and all other abnormalities that are seen in Lyme arthritis on radiographs can be better characterized by CT.3

Ultrasonography Ultrasonography is reported to be utilized in the evaluation of joint effusion and articular and periarticular inflammation in patients with Lyme arthritis.9,10

Nuclear Medicine Bone scintigraphy is nonspecific but can help in detecting multiple sites of inflammatory joint involvement by Lyme disease.9–11 Gallium-67 shows increased radiotracer uptake in the affected muscle groups.3

Positron Emission Tomography/ Computed Tomography Although MRI is the primary imaging modality for most suspected central nervous system pathology, the practical

■ FIGURE 68-35 Sagittal T2-weighted image with fat saturation in a patient with advanced Lyme arthritis shows a joint effusion and erosive changes in the proximal tibia. (Courtesy of Sandra Moore, MD, NYU Medical Center, NY.)

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applications of PET continue to expand.12 The role of PET in the diagnosis and evaluation of Lyme arthritis is to be determined.

DIFFERENTIAL DIAGNOSIS With its numerous manifestations Lyme disease has become the latest great imitator in the spirochete family like syphilis.6 Early differentiation of Lyme arthritis from septic arthritis is difficult and is particularly important because of the disparate therapeutic implications of each diagnosis. The differential diagnosis also includes inflammatory and degenerative arthritides as well as granulomatous infection such as tuberculosis.1,3,4

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment Most patients can be cured with a few weeks of oral antibiotics. Antibiotics commonly used for oral treatment are doxycycline, amoxicillin, or cefuroxime axetil. Patients with certain neurologic or cardiac forms of disease may require intravenous treatment with drugs such as ceftriaxone or penicillin. A few patients, particularly those diagnosed with later stages of disease, may have persistent or recurrent symptoms. These patients may benefit from a second 4-week course of therapy.1,13,14 Ten to 20 percent of untreated patients with Lyme arthritis achieve spontaneous long-term remission yearly.3 Prior vaccination with the second-generation polyvalent outer-surface protein (OspC) vaccine preparation may reduce the risk of developing Lyme disease associated with tick bites. The development of the next generation of Lyme disease vaccine is in its infancy.15

Surgical Treatment Surgery is generally not utilized in the treatment of Lyme disease. There was a case report of Lyme arthritis with advanced degenerative changes localized to the midcarpal joint treated with a limited wrist arthrodesis with relief of pain and improved function.16 Malawista found that in persistent Lyme arthritis, arthroscopic synovectomy was often curative, although this statement is not accepted for all age groups.17

SUGGESTED READINGS Ecklund K, Vargas S, Zurakowski D, Sundel RP. MRI features of Lyme arthritis in children. AJR Am J Roentgenol 2005; 184:1904–1909. Lawson JP, Rahn DW. Lyme disease and radiologic findings in Lyme arthritis. AJR Am J Roentgenol 1992; 158:1065–1069.

REFERENCES 1. Ecklund K, Vargas S, Zurakowski D, Sundel RP. MRI features of Lyme arthritis in children. AJR Am J Roentgenol 2005; 184:1904–1909. 2. Centers for Disease Control and Prevention (CDC) and Jajosky RA, Hall PA, Adams DA, et al. Summary of notifiable diseases—United States, 2004. MMWR Morb Mortal Wkly Rep 2006; 53:1–79.

3. Lawson JP, Rahn DW. Lyme disease and radiologic findings in Lyme arthritis. AJR Am J Roentgenol 1992; 158:1065–1069. 4. Resnick D. Osteomyelitis, septic arthritis, and soft tissue infection: organisms. In Resnick D (ed). Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, 2002, pp 2510–2624. 5. Aguero-Rosenfeld ME, Wang G, Schwartz I, Wormser GP. Diagnosis of Lyme borreliosis. Clin Microbiol Rev 2005; 18:484–509. 6. Stechenberg BW. Lyme disease: the latest great imitator. Pediatr Infect Dis J 1988; 7:402–409. 7. Buchmann RF, Jaramillo D. Imaging of articular disorders in children. Radiol Clin North Am 2004; 42:151–68, vii. 8. Schmitz G, Vanhoenacker FM, Gielen J, et al. Unusual musculoskeletal manifestations of Lyme disease. JBR-BTR 2004; 87:224–228. 9. Ushakova MA, Anan’eva LP, Mach ES, et al. [The clinical instrumental characteristics of the locomotor involvement in patients who have had Lyme disease]. Ter Arkh 1995; 67:45–49. Russian. 10. Ushakova MA, Mach ES, Anan’eva LP, et al. [Methods for the instrumental diagnosis and verification of Lyme arthritis]. Ter Arkh 1997; 69:15–19. Russian. 11. Brown SJ, Dadparvar S, Slizofski WJ, et al. Triple-phase bone image abnormalities in Lyme arthritis. Clin Nucl Med 1989; 14:730–733. 12. Kalina P, Decker A, Kornel E, Halperin JJ. Lyme disease of the brainstem. Neuroradiology 2005; 47:903–907. Epub 2005 Sep 13. 13. Wormser GP, Nadelman RB, Dattwyler RJ, et al. Practice guidelines for the treatment of Lyme disease. The Infectious Diseases Society of America. Clin Infect Dis 2000; 31(Suppl 1):1–14. 14. Wormser GP, Ramanathan R, Nowakowski J, et al. Duration of antibiotic therapy for early Lyme disease: a randomized, double-blind, placebo-controlled trial. Ann Intern Med 2003; 138:697–704. 15. Hanson MS, Edelman R. Progress and controversy surrounding vaccines against Lyme disease. Expert Rev Vaccines 2003; 2:683–703. 16. Scerpella TA, Engber WD. Chronic Lyme disease arthritis: review of the literature and report of a case of wrist arthritis. J Hand Surg [Am] 1992; 17:571–575. 17. Malawista SE. Resolution of Lyme arthritis, acute or prolonged: a new look. Proceedings of the International Conference on Lyme Borreliosis, Brussels, November 16, 2001.

Syphilis ETIOLOGY Syphilis originates from ancient myth and was highlighted in 1530 in a poem “Syphilis, sive morbus Gallicus” by Girolamo Fracastoro.1 It is caused by a spirochete Treponema pallidum that is transmitted by sexual and intimate contact (acquired syphilis). A fetus can be infected by transmission of the organism through the placenta (congenital syphilis).2,3

PREVALENCE AND EPIDEMIOLOGY In some parts of the world, syphilis remains a common heterosexually transmitted disease. The World Health Organization estimated in 1999 that of a global total of 12 million adults with syphilis, 11 million were living in sub-Saharan Africa, Latin America, and south and southeast

CHAPTER

Asia. In recent years there has been a striking increase in the number of cases of syphilis in Eastern Europe, especially in the former Soviet Union. In Western Europe and North America, although there are some cases reflecting international contacts, there has also been an increase in cases among homosexual men, which seems to reflect changing patterns of sexual behavior. In 2000, the rate of primary and secondary syphilis in the United States was 2.1 cases per 100,000 population, the lowest since reporting began in 1941. From 2001 to 2004, the rate increased to 2.7, primarily as a result of increases in cases among homosexual men. The disparity between syphilis rates among blacks and whites in 2004 increased for the first time since 1993 and is associated with a substantial increase of syphilis among black men. After declining for 13 years, the rate of primary and secondary syphilis in 2004, compared with 2003, increased in the South and remained the same among women. The rate of infection among Hispanics also increased. A higher rate of syphilis might increase the transmissibility of human immunodeficiency virus (HIV) infection.4

PATHOPHYSIOLOGY Congenital Syphilis Congenital syphilis results from the transplacental migration of T. pallidum, which invades multiple organs, including perichondrium, cartilage, and bones, with active osteochondral ossification, such as metaphysis of the tubular bones. Depending on the severity of infection the fetus may be aborted or the infant can be stillborn, can die shortly after birth, or survive with early or late characteristics of congenital syphilis. Clinical manifestations of early congenital syphilis include rhinorrhea, rash, anemia, hepatosplenomegaly, ascites, and the nephrotic syndrome (Figs. 68-36 and 68-37). The characteristic stigmata of late congenital syphilis are interstitial keratitis, saber-shin

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KEY POINTS Osteoarticular manifestations of syphilis can be seen with congenital, secondary, and tertiary syphilis. ■ Manifestations of congenital syphilis include osteochondritis, diaphyseal osteomyelitis (osteitis), periostitis, and miscellaneous changes. ■ The characteristic stigmata of late congenital syphilis are interstitial keratitis, saber-shin deformity of the tibia, and Hutchinson’s teeth (peg-shaped, notched, and hypoplastic dental structures). ■ Clutton’s joints represent a late manifestation of congenital syphilis. ■ Musculoskeletal manifestations of secondary syphilis are rare and include arthralgias, arthritis, back pain, sacroiliitis, spondylitis, osteitis, and periostitis. ■ Neuropathic arthropathy (Charcot joint), gummatous and nongummatous syphilitic periostitis, osteitis, and osteomyelitis represent musculoskeletal manifestations of tertiary syphilis. ■

deformity of the tibia, and Hutchinson’s teeth (peg-shaped, notched, and hypoplastic dental structures).2,3,5

Acquired Syphilis In acquired syphilis, T. pallidum penetrates mucous membranes and enters the lymphatics. The organism reaches the regional lymph nodes in a few hours. It may enter the bloodstream and cause spirochetemia. Three to 6 weeks after the initial infection a primary lesion, which represents a skin ulceration known as a chancre, develops at the inoculation site. This lesion heals spontaneously.2,3,5 Approximately 6 weeks later the patient develops secondary syphilis with various systemic manifestations, including skin eruption, arthritis, tenosynovitis, and a variety of visceral involvement. Secondary syphilis

■ FIGURE 68-36

A 1-day-old newborn with congenital syphilis with characteristic skin lesions. (Courtesy of G. Barnes, MD, Tucson, AZ.)

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■ FIGURE 68-37 Neonate with congenital syphilis with skin lesions. (Courtesy of G. Barnes, MD, Tucson, AZ.)

is observed in up to 20% of patients. Patients with HIV infection may have unusual clinical manifestation of syphilis, including prominent constitutional symptoms (lues maligna).2,3,5,6 Latent syphilis follows the primary and secondary disease. During this phase of the disease the patient may be without symptoms, although the disease may be progressing slowly in various organ systems.2,3,5 Syphilitic meningitis and meningovascular syphilis occur early, within the first few years of infection. General paresis and tabes dorsalis occur later, typically 5 to 30 years after infection. Tertiary syphilis, including cardiovascular and neurosyphilis, may occur in approximately 50% of infected patients. Late manifestations include large destructive lesions in any organ of the body, termed gummas, and neuropathic arthropathy.2,3,5,7 In patients with coexisting HIV infection the course of disease may be modified.2,3,8,9 The diagnosis can be made by darkfield microscopic visualization of T. pallidum sampled from chancre. Under the microscope this organism has a distinctive spiral appearance. Two types of serologic testing are normally used to diagnose syphilis. Both tests detect antibodies, but neither is fully reliable in diagnosing the disease. The first type of test detects antibodies to lipids, called “reagin” antibodies. The Venereal Disease Research Laboratory (VDRL) test is used on serum or sometimes on cerebrospinal fluid taken from the spinal column by lumbar puncture. The rapid plasma reagin (RPR) test is used only on serum. These tests may be positive in patients with a range of other infections, including malaria and rheumatologic illnesses such as systemic lupus erythematosus or during pregnancy. Reagin antibody levels due to syphilis go down when syphilis is treated, so these tests can be used to monitor treatment. The treponemal-specific tests that are used to detect the antibodies to proteins made by T. pallidum are very specific but usually remain positive even after a patient has been cured of syphilis. These “treponemal” tests include T. pallidum hemagglutination assay (TPHA), T. pallidum

particle agglutination test (TPPA), and fluorescent treponemal antibody absorption test (FTA-ABS), along with a number of enzyme immunoassay (EIA) tests that are similar to antibody tests for HIV. It can take up to 90 days for the body to develop antibodies to the bacterium that causes syphilis, so a blood test immediately after exposure to syphilis may not detect infection. In HIV-infected patients the test result can be false negative.2,3,10

MANIFESTATIONS OF THE DISEASE Osteoarticular manifestations of syphilis were recognized since the beginning of the 20th century and can be seen with congenital, secondary, and tertiary syphilis.1,3,5 Musculoskeletal manifestations of congenital syphilis in fetuses, neonates, and very young children include osteochondritis, diaphyseal osteomyelitis (osteitis), periostitis, and miscellaneous changes.2,3,5 Musculoskeletal manifestations of secondary syphilis are nonspecific. The diagnosis is usually suspected because of association with mucocutaneous findings, including an erythematous maculopapular rash involving the palms and soles, mucosal patches, condylomata lata, and generalized lymphadenopathy.2,3,6 Musculoskeletal manifestations of tertiary syphilis are rare, and the neuropathic or Charcot joint is the most characteristic finding. Gummatous involvement of the joints is an unusual manifestation.2,3,5,7

Radiography Early Congenital Syphilis Osteochondritis Radiographic findings of syphilitic osteochondritis, which usually results in symmetric involvement of sites of enchondral ossification, are seen in approximately 60% of infants with congenital syphilis. This is seen during the first 3 to 6 weeks of life and rarely after 3 months.

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The upper extremity is more commonly involved than the lower. The epiphyseal-metaphyseal junction of the long bones, the costochondral regions, and, in severe cases, the flat and the other bones are affected. Radiography demonstrates irregular epiphyseal lines, subchondral metaphyseal radiolucent bands, diaphyseal cupping, metaphyseal erosion at the growth plate junction, and periosteal thickening. Metaphyseal destruction may result in epiphyseal separation. Bone erosion at the surface of the proximal tibial shaft, usually sparing the most recently formed few millimeters of metaphysis (Laval-Jeantet collar), is considered characteristic and termed Wimberger’s sign. Complete healing is usually achieved after penicillin therapy within 2 months. Residual osseous deformities and scars are not common but include saddle-nose, nasal septal perforation, Deformity of frontal bones, and saber shins (anterior bowing of the tibia) (Figs. 68-38 to 68-40).2,3,5

Osteitis (Diaphyseal Osteomyelitis) Osteitis may occur in untreated infants or after inadequate antibiotic treatment. It affects the metaphysis and extends to the diaphysis of large tubular bones (Fig. 68-41). Osteolytic areas surrounded by dense bone, and periosteal new bone formation may be observed. Bone lesions are usually polyostotic. Nontubular bone is occasionally involved (Fig. 68-42).2,3,5

Periostitis Periostitis may be seen as an isolating diffuse and symmetric finding or in combination with the other findings and usually affects the long tubular bones. It is less frequent than osteochondritis. Periostitis is associated with pain and decreased motion, which is termed pseudoparalysis of Parrot2,3,5 (see Figs. 68-38, 68-41 and 68-42C).

■ FIGURE 68-38 A 9-month-old newborn was born with congenital syphilis. Radiograph of the right femur demonstrates an erosion at the medial aspect of the proximal metaphysis consistent with osteochondritis. There is associated periostitis along the femoral shaft. (Courtesy of G. Barnes, MD, Tucson, AZ.)

Miscellaneous Findings

Late Congenital Syphilis

Gummas are rarely seen in congenital syphilis, usually in flat bones. Joint effusions may complicate epiphyseal destruction or separation.2,3,5

The late lesions of congenital syphilis correspond to the tertiary lesions of acquired syphilis. They occur after the age of 2 years and rarely after the third decade of life.2,3,5

■ FIGURE 68-39 Neonate with congenital syphilis. Frontal radiograph of both knees shows lucent metaphyseal lines. (Courtesy G. Barnes M.D. Tucson, AZ.)

■ FIGURE 68-40 Neonate with congenital syphilis. Radiograph of the wrist shows metaphyseal irregularities with associated pathologic fractures. (Courtesy of G. Barnes, MD, Tucson, AZ.)

■ FIGURE 68-41 A to C, Radiographs in neonates with congenital syphilis show osteomyelitis (osteitis), periostitis, and lucent metaphyseal lines involving the long tubular bones.

(Continued) 1398

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■ FIGURE 68-41—Cont’d D and E, Radiographs in neonates with congenital syphilis show osteomyelitis (osteitis), periostitis, and lucent metaphyseal lines involving the long tubular bones. (Courtesy of G. Barnes, MD, Tucson, AZ.)

Both gummatous and nongummatous osteomyelitis result in diffuse hyperostosis of the involved bone. Endosteal proliferation narrows the medullary cavity, whereas the periosteal proliferation creates undulating, enlarged, and dense bone contour. Anterior bowing of the tibia can result, termed saber shin. The flat bones, including cranium, can be involved. Dactylitis can also occur (Fig. 68-43).3,5

Clutton’s Joints Clutton’s joints represent late manifestation of congenital syphilis and manifests usually as symmetric oligoarthritis that involves predominantly the large joints. Joint effusion, periarticular soft tissue swelling, and synovitis are

observed. The synovitis generally occurs between the ages of 8 and 15 years.2,3,5

Secondary Syphilis Musculoskeletal manifestations of secondary syphilis are rare and were first described by Wile in 1914.6 They include arthralgias, arthritis, back pain, sacroiliitis, spondylitis, osteitis, and periostitis.2,3,5,6

Tertiary Syphilis Neuropathic arthropathy (Charcot joint) is observed in 5% to 10% of patients with tabes dorsalis. Lost of deep sensation and chronic trauma lead to extensive destructive changes

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■ FIGURE 68-42 A and B, Multiple lytic lesions in calvarial bones in an infant with congenital syphilis. C, In the same infant note the presence of osteomyelitis and periostitis involving the long bones. (Courtesy of W. Martel, MD, Ann Arbor, MI.)

in the affected bones. The most commonly affected joints are knees, hips, and those of the spine. Upper extremity joints and sacroiliac joints are affected less commonly. Radiography demonstrates extensive destructive changes, cupping of the articular surfaces, new bone formation, bone fragmentation, increased density, intra-articular loose bodies, and intra-articular and periarticular calcifications, with associated soft tissue swelling and joint effusion. Association between the Charcot joints due to tertiary syphilis and

calcium pyrophosphate deposition disease arthropathy has been reported (Figs. 68-44 and 68-45).2,7,11,12 Gummatous involvement of joints and bones became rare after initiation of penicillin therapy. Radiographs show erosive changes of subchondral bone, areas of bone resorption, and reactive changes mimicking those in other chronic infections. A gumma is a discrete lesion of variable size that contains necrotic material. On microscopic examination it contains granulation tissue, and the

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organisms are usually not seen. Resorption of bone about the gumma is termed caries sicca, and detachment of necrotic bone caries necrotica. Radiography shows lytic and sclerotic lesions in bone of variable size. The lesions are frequently associated with periostitis. Pathologic fractures may be observed (Fig. 68-46).2,3,5 Nongummatous syphilitic periostitis, osteitis, or osteomyelitis can occur independently or in conjunction with gummas. Radiography reveals destructive and productive bone changes associated with periostitis.2,3,5 In gummatous and nongummatous acquired syphilis skeletal lesions can be seen in both the axial and the appendicular skeleton.2,3

Nuclear Medicine Bone scintigraphy typically demonstrates increased radiotracer uptake in the regions of skeletal abnormality caused by syphilis.13–15

DIFFERENTIAL DIAGNOSIS

■ FIGURE 68-43 Late congenital syphilis. Osteomyelitis is evident in the long bones of the leg. (Courtesy of D. Resnick, MD, San Diego, CA.)

Musculoskeletal manifestations can be associated with congenital, secondary, and tertiary syphilis and can mimic a wide variety of rheumatic and systemic diseases. The differential diagnosis of skeletal syphilis includes yaws, an infection caused by T. pertenue, an organism morphologically indistinguishable from T. pallidum. Yaws occurs in tropical climates and has radiologic manifestations similar to those of syphilis. The correct diagnosis is made by the isolation of T. pertenue from a skin lesion. Other types of infections caused by bacteria, fungi, and mycobacteria are also included in the differential

■ FIGURE 68-44 Acquired tertiary syphilis. Frontal (A) and lateral (B) radiographs of the knee show marked destructive changes consistent with a neuropathic/Charcot joint. (Courtesy of D. Resnick, MD, San Diego, CA.)

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diagnosis. Sometimes the lesion can resemble a tumor such as osteosarcoma.3

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment Treponema pallidum remains exquisitely sensitive to penicillin. Patients allergic to penicillin should be treated with tetracycline or erythromycin. In HIV-positive patients, syphilis is usually treated with high doses of antibiotics such as penicillin, benzylpenicillin (Crystapen), or doxycycline (Vibramycin/Vibramycin D).2,8,9,16

Surgical Treatment Surgery may be offered to those most impaired by forms of tabes arthropathy. Joint arthrodesis may be performed. Joint arthroplasty often resulted in loosening, although fair results have been reported in some cases.2,11,17,18

What the Referring Physician Needs to Know ■ ■ ■ FIGURE 68-45 Tertiary syphilis. Lateral radiograph of the lumbar spine shows changes compatible with a neuropathic/Charcot joint. (Courtesy of D. Resnick, MD, San Diego, CA.) ■

■

Syphilis is transmitted by sexual and intimate contact. Syphilis again has become a significant clinical problem, and clinicians must be familiar with the classic as well as the changing clinical manifestations, new diagnostic methods, interaction with HIV infections, and outcomes of therapy. Musculoskeletal manifestations can be associated with congenital, secondary, and tertiary syphilis and can mimic a wide variety of rheumatic and systemic diseases. Musculoskeletal manifestations due to congenital and secondary syphilis usually subside completely after accurate diagnosis and antibiotic therapy.

SUGGESTED READING Reginato AJ. Syphilitic arthritis and osteitis. Rheum Dis Clin North Am 1993; 19:379–398.

REFERENCES

■ FIGURE 68-46 Tertiary syphilis. Images of the long bones show findings of osteomyelitis with destructive lesions consistent with gummas. (Courtesy of D. Resnick, MD, San Diego, CA.)

1. Lipozencic J, Marinovic B. 2005 centennial year marking the discovery of the spirochete treponema pallidum. Acta Dermatovenerol Croat 2006; 14:61. 2. Reginato AJ. Syphilitic arthritis and osteitis. Rheum Dis Clin North Am 1993; 19:379–398. 3. Resnick D. Osteomyelitis, septic arthritis, and soft tissue infection: organisms. In Resnick D (ed). Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, 2002, pp 2510–2624. 4. Centers for Disease Control and Prevention (CDC). Primary and secondary syphilis—United States, 2003–2004. MMWR Morb Mortal Wkly Rep 2006; 55:269–273. 5. Jeffe HL. Metabolic, Degenerative, and Inflammatory Diseases of Bones and Joints. Philadelphia, Lee & Febiger, 1972. 6. Wile UJ. Arthopathy in secondary syphilis. J Cutan Incl Syph 1914; 32:20–23; J Clin Microbiol 2006; 44:1335–1341. 7. Resnick D. Neuropathic osteoarthropathy. In Resnick D (ed). Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, 2002, pp 3564–3595. 8. From the MMWR. Recommendations for diagnosing and treating syphilis in HIV-infected patients. Arch Dermatol 1989; 125:15–16.

CHAPTER 9. Recommendations for diagnosing and treating syphilis in HIVinfected patients. MMWR Morb Mortal Wkly Rep 1988; 37:600–602, 607–608. 10. Muller I, Brade V, Hagedorn HJ, et al. Is serological testing a reliable tool in laboratory diagnosis of syphilis? Meta-analysis of eight external quality control surveys performed by the German infection serology proficiency testing program. 11. Allali F, Rahmouni R, Hajjaj-Hassouni N. Tabetic arthropathy: a report of 43 cases. Clin Rheumatol 2006; 25:858–860. 12. Jones EA, Manaster BJ, May DA, Disler DG. Neuropathic osteoarthropathy: diagnostic dilemmas and differential diagnosis. RadioGraphics 2000; 20(Spec No):S279–S293. 13. Gomez Martinez MV, Gallardo FG, Cobo Soler J, et al. [Osteitis in secondary syphilis]. Rev Esp Med Nucl 2003; 22:424–426. Spanish. 14. Cronin EB, Williams WH, Tow DE. Radionuclide imaging in a case of tertiary syphilis involving the liver and bones. J Nucl Med 1987; 28:1047–1051. 15. Moreno AJ, Yedinak MA, Rahnema A, Fredericks P. Bone scintigraphy in latent congenital syphilis. Clin Nucl Med 1985; 10:824–825. 16. Lafond RE, Lukehart SA. Biological basis for syphilis. Clin Microbiol Rev 2006; 19:29–49. 17. Gualtieri G, Sudanese A, Toni A, Giunti A. Loosening of a hip prosthesis in a patient affected with tabetic disease. Chir Organi Mov 1991; 76:83–85. 18. Yoshino S, Fujimori J, Kajino A, et al. Total knee arthroplasty in Charcot’s joint. J Arthroplasty 1993; 8:335–340.

Tuberculosis Tuberculosis is still a common disease in underdeveloped parts of the world. The prevalence of this disease has significantly decreased after development of chemotherapy. In the 1940s and 1950s, skeletal tuberculosis occurred in 3% to 5% of patients with pulmonary tuberculosis and in approximately 30% of patients with extrapulmonary tuberculosis. In the 1960s and 1970s the prevalence of tuberculosis had decreased, but it started to rise again in the mid 1980s in the United States. The factors that have contributed to an increased rate of tuberculosis include an increased number of immunocompromised patients, the development of drug- resistant strains of mycobacteria, changing patterns of travel and immigration, and an increased number of health care workers exposed to the disease. Additionally, in rare occasions modern therapeutic techniques, including bacille Calmette-Guérin vaccination, can cause an iatrogenic infection.1–3

ETIOLOGY Mycobacterium tuberculosis is the main causative organism of musculoskeletal tuberculosis. A few cases are attributable to M. bovis. Atypical mycobacteria such as M. kansasii, M. marinum, M. sacrofulaceum, and M. avium complex account for 1% to 4% of tuberculosis cases. These produce chronic infection, are of low virulence, and usually are more resistant to the standard drugs.4

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PREVALENCE AND EPIDEMIOLOGY The majority of cases are found in south and east Asia, sub-Saharan Africa, and Eastern Europe. In 1997, 1.9 billion people were infected with tuberculosis.8 During 2004, a total of 14,511 confirmed tuberculosis cases (4.9 cases per 100,000 population) were reported in the United States, representing a 3.3% decline in the rate from 2003. Slightly more than half (53.7%) of U.S. cases were in foreign-born persons. Findings indicate that although the 2004 tuberculosis rate was the lowest recorded in the United States since national reporting began in 1953, the declines in rates for 2003 (2.3%) and 2004 (3.3%) were the smallest since 1993. In addition, tuberculosis rates greater than the U.S. average continue to be reported in certain racial/ethnic populations; in 2004, Hispanics, blacks, and Asians had tuberculosis rates 7.5, 8.3, and 20.0 times higher than whites, respectively. Essential elements for controlling tuberculosis in the United States include sufficient local resources, interventions targeted to populations with the highest tuberculosis rates, and continued collaborative efforts with other nations to reduce tuberculosis globally.9,10 Bone and joint tuberculosis may account for up to 30% to 35% of cases of extrapulmonary tuberculosis. Skeletal tuberculosis most often involves the spine, followed by tuberculous arthritis in weight-bearing joints and extraspinal tuberculous osteomyelitis.1,10 Skeletal tuberculosis equally affects males and females. Lesions in hands and feet are not uncommonly seen in children, immunocompromised patients, and the elderly. Extra-axial tuberculous arthritis is usually monarticular, and involvement of multiple joints is rare.1,11

CLINICAL PRESENTATION Skeletal tuberculosis can be seen in any age group; it is rare in the first year of life. In the non-Hispanic white population the median age is about 60 years, and among the minority groups it is about 40 years. In the communities with a high prevalence the majority of patients are infected by the age of 20 years. Extrapulmonary tuberculosis is more common in children than in adults, with common involvement of lymph nodes (scrofulosis). The delay in diagnosis is common and is reported to be 16 to 19 months.13 The spine is most commonly affected, followed by the pelvis, hip, and knee joints. The joints of the lower extremity are more commonly involved than the joints of the upper extremity. Tuberculosis of the spine was first described by Sir Percival Pott in 1779. The initial symptoms vary. The patients with tuberculous spondylitis present with an insidious onset of back pain, stiffness, local tenderness, neurologic abnormalities,

KEY POINTS ■ ■ ■

The disease has an indolent course. There is commonly a delay in diagnosis. Prompt diagnosis and treatment are important.

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and possibly fever. Paralysis can occur as a result of spinal cord compression from abscesses, granulation tissue, bone fragments, arachnoiditis, ischemia of the cord from endarteritis, or intramedullary granulomas. This form of skeletal tuberculosis is most commonly associated with pulmonary disease. Tuberculous arthritis can lead to pain, swelling, weakness, muscle wasting, and a draining sinus. A history of trauma may be obtained in 30% to 50% of cases. Tuberculous dactylitis usually manifests as a painless swelling of the hand and foot. Tuberculous tenosynovitis and bursitis can produce soft tissue swelling and tenderness. Very infrequently carpal tunnel syndrome results from tuberculous involvement of tendon sheaths and bursae in the wrist. A positive tuberculin skin test is not reliable for the diagnosis of tuberculosis. Elderly patients who have never had any clinical manifestation of tuberculosis as well as those who have received the bacillus Calmette-Guérin vaccine have a high frequency of a positive skin test. However, a negative tuberculin skin test generally excludes the disease, except in immunocompromised and malnourished patients in whom the test can be false negative.

■ FIGURE 68-47 Mycobacterium tuberculosis. Note a small number of slightly beaded, bright rose-pink bacilli. This paucity of organisms is the usual finding in an immunocompetent patient. (Acid-fast bacillus stain.) (Courtesy of Anna Graham, MD, Tucson, AZ.)

PATHOPHYSIOLOGY Musculoskeletal tuberculosis mainly results from hematogenous dissemination or lymphangitic spread from a primary or reactivated infected focus. Rarely, this disease may be the result of direct inoculation. Injuries may result in reactivation of preexisting tuberculous infection. The contributing factors for the reactivation of disease include poor socioeconomic conditions, and immunodeficiency, mainly in the patients with HIV infection and AIDS.4 Mycobacteria reach the skeletal system through the vascular system, mainly arterial as a result of bacteremia, but may also reach the axial skeleton through the venous plexus of Batson.4 Localization to the metaphyseal segments of the long bones is noted in this disease, like in pyogenic osteomyelitis, perhaps related to tuberculous infarcts from emboli within the nutrient vessels.1 Tuberculous involvement of the joints may result from hematogenous dissemination through the subsynovial vessels, or indirectly form epiphyseal or metaphyseal lesions, which erode into the joint space. A tuberculous granuloma develops within the bone at the site of mycobacterial deposition. This lesion undergoes caseous necrosis and expands, causing trabecular destruction. Further expansion can cause cortical destruction, with subsequent development of a soft tissue mass.4 The margins of the bony lytic lesions are usually distinct.1,5 In children, the periosteal reaction can occur. Bone sclerosis and ankylosis occur only when the disease has chronically faded out.5–7 Tuberculosis is one among multiple many other diseases associated with formation of bone marrow granulomas. The typical response of tissue is the formation of sharply demarcated tubercles. In the central part of the tubercle are multinucleated giant cells and at the periphery is a mantle of lymphocytes. Around a central zone are clusters of epithelioid cells with elongated vascular nuclei. The tuberculin produced by the acid-fast bacilli causes the characteristic caseating necrosis. As necrosis

■ FIGURE 68-48

Mycobacterium tuberculosis. Note the giant cell (black arrow), the epithelioid histiocyte cells (pink arrow), lymphocytes (blue arrow), and caseation necrosis (green arrow). These features characterize a well-formed granuloma, formed as a response to M. tuberculosis in an immunocompetent patient. (Hematoxylin and eosin stain.) (Courtesy of Anna Graham, MD, Tucson, AZ.)

progresses the epithelioid cells degenerate and become grouped into an amorphous mass. Peripheral growth of the tubercle relates to the influx of new mononuclear cells that mature into the epithelioid cells, as long as viable bacilli are present. Healing lesions are associated with the production of hyaline fibrous nodules and encapsulation, which leads to formation of a connective tissue scar. Calcifications and ossifications of caseating lesions may also occur (Figs. 68-47 and 68-48).1,13

IMAGING TECHNIQUES Radiography should be always the initial imaging modality obtained in evaluation of skeletal tuberculosis.13,38 Regardless of results of the radiographic study MRI

CHAPTER

should be performed for evaluation of local extent of disease. MRI has a superb contrast resolution and multiplanar imaging capability and is superb in evaluation of soft tissue and bone involvement.1,13 CT with the better spatial resolution than MRI is superior in evaluation of cortical destruction especially in the posterior elements, and for depiction of soft tissue calcifications (within an intraspinal abscess).13 Nuclear medicine studies including 99mTcmethylene diphosphonate (MDP) and 67gallium citrate scans are of limited value but should be performed to evaluate for multicentricity of disease.13 Ultrasonography is of limited value but can demonstrate abdominal paraspinal abscesses and soft tissue infection.1

MANIFESTATIONS OF THE DISEASE The spine is involved in the majority of cases of musculoskeletal tuberculosis, followed by hips and knees. Other joints and soft tissues can also be involved. Tuberculosis can also affect any bone in the body as well as soft tissues including bursae, tendon sheaths, muscles, and other soft tissue structures. Tuberculous spondylitis frequently affects the lower thoracic and upper lumbar spine in adults. Other sites in the spine are less frequently involved. Most frequently, tuberculous spondylitis begins in the anterior aspect of the vertebral body adjacent to the subchondral end plate. The lesion can be detected by radiography usually in 2 to 5 months. Infection can spread beneath the anterior or posterior longitudinal ligaments, allowing the osseous invasion at distant sites. The infection can violate

■ FIGURE 68-49

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the peripheral aspect of the intervertebral disc. The disease can penetrate the subchondral bone and involve the disc and cause decrease of disc height. The involvement of posterior elements is rare. Discovertebral destruction is similar as in pyogenic infection but usually more indolent. Long segments of the spine can be involved. Extension of tuberculous infection into the paraspinal, usually anterolateral and rarely posterior, soft tissues is common. Paraspinal abscesses can cause periosteal stripping and avascular necrosis. The infection can also penetrate the adjacent organs. Tuberculous psoas abscesses are prone to calcify. Destruction of vertebral bodies leads to kyphotic deformities that are more severe in thoracic than in cervical or lumbar region. Scoliosis and ankylosis of multiple vertebral bodies can be observed (Figs. 68-49 to 68-54). Tuberculous osteomyelitis can involve any bone but is most common in femur and tibia and small bones of the hands and feet. Typically the metaphyses are involved. Transphyseal extension is more common in tuberculous than in pyogenic osteomyelitis. The cystic type of tuberculous osteomyelitis is more common in children than in adults. In children these lesions involve the metaphysis of long bones, whereas in adults the skull, shoulder, and axial skeleton are more commonly involved. Solitary involvement is predominant. Tuberculous dactylitis is more common in children than in adults. Hands are affected more often than feet, with the proximal phalanges of the index and middle fingers and the metacarpals of the middle and ring fingers being the most frequent locations. Soft tissue swelling is

Tuberculous spondylitis. Frontal (A) and lateral (B) radiographs of the lumbar spine show tuberculous involvement of L1 vertebral body with loss of height, wedging, and kyphosis, and with associated calcified paraspinal abscess (cold abscess). (Courtesy of G. Barnes, MD, Tucson, AZ.)

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■ FIGURE 68-50

Tuberculous spondylitis. Frontal (A) and lateral (B) radiographs of the lumbar spine show disc space loss and end plate erosions at the L3-L4 level. (Courtesy of G. Barnes, MD, Tucson, AZ.)

■ FIGURE 68-51 Tuberculous spondylitis. Frontal (A) and lateral (B) radiographs of the chest/thoracic spine show gibbus deformity in the lower thoracic spine secondary to tuberculous infection. (Courtesy of G. Barnes, MD, Tucson, AZ.)

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■ FIGURE 68-52

Tuberculous spondylitis. Frontal (A) and lateral (B) radiographs of the thoracolumbar spine show marked loss of height of L1 and, to a lesser extent, of T12 vertebral bodies with erosive changes at the T12–L2 levels and associated kyphosis and calcified soft tissue abscess. (Courtesy of G. Barnes, MD, Tucson, AZ.)

the initial symptom in virtually all cases, whereas stiffness, pain, and finger numbness may be present in some (Fig. 68-55).1,13 Tuberculous arthritis most commonly involves hip and knee joints, but any joint can be involved. It is most commonly monarticular disease. The presenting symptoms are usually the insidious onset of joint pain and swelling. Other presenting symptoms include weakness, muscle wasting, and draining sinuses. Trauma, drug addiction, intra-articular corticosteroid injection, and systemic illness predispose to tuberculous arthritis (Figs. 68-56 and 68-57). In tuberculous bursitis and tenosynovitis synovial membrane of bursae and tendon sheaths and tendons themselves are infected. Typical sites of infection include the radial and ulnar bursae of the hand, flexor tendon sheaths of the fingers, bursae about the ischial tuberosity, subacromial-subdeltoid bursa and subgluteal bursae. The other locations are affected less often. Tuberculous myositis and soft tissue infection are frequently associated with underlying disease such as collagen vascular disease, immunosuppression therapy, or local trauma. Soft tissue abscesses are more frequent in patients with AIDS. Tuberculous myositis is rare.

Radiography Early radiographic findings in tuberculous spondylitis are loss of end plate definition and only slight disc space narrowing. Later radiography shows vertebral end plate destruction with paucity of sclerosis or periosteal reaction, associated with paraspinal abscesses. Paraspinal abscesses may be detected as areas of fusiform soft tissue swelling around the spine. They frequently contain calcifications. Bone loss results in vertebral deformity. Multiple vertebral levels may be involved in noncontiguous fashion. In most severe cases, nearly an entire vertebral body is destroyed with progression to vertebra plana. Severe kyphosis (gibbus deformity) develops as the disease progresses (see Figs. 68-49 to 68-54).1,14,28 Radiographic findings of tuberculous osteomyelitis include osteopenia, osteolytic foci with poorly defined edges, and minimal surrounded sclerosis. Transphyseal extension of disease is common. In tuberculous dactylitis, prominent fusiform soft tissue swelling and periostitis are the most common findings. Periostitis is the earliest sign of bone involvement, followed by gradual bone destruction and sequestrum formation. Destruction of underlying bone leads to cyst-like

1408 P A R T T H R E E

■ FIGURE 68-53

● Infection

Tuberculous spondylitis. Frontal (A) and lateral (B) radiographs of the lumbosacral spine show a lytic lesion involving the anterior aspect of the L5 vertebral body with associated cortical erosions of the anterior aspect of the L5 and S1 vertebrae and prevertebral soft tissue thickening/paraspinal abscess. C, T2-weighted sagittal MR image shows increased signal intensity in the regions of abnormality and associated paraspinal abscess. D and E, Sagittal T1-weighted images after intravenous administration of gadolinium-based contrast agent show heterogeneous enhancement in the regions of abnormality consistent with osteomyelitis and paraspinal abscess. Note sparing of the L5–S1 disc space. (Courtesy of Hilary Umans, MD, Bronx, NY.)

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■ FIGURE 68-54 Sacral tuberculous osteomyelitis. A, Axial CT image of the sacrum shows destructive lytic lesion involving the right sacral site with associated cortical discontinuity and parasacral mass/abscess anteriorly. B, Axial T1-weighted image after intravenous administration of gadoliniumbased contrast agent heterogeneous enhancement in the region of abnormality consistent with osteomyelitis and abscess. (Courtesy of Hilary Umans, MD, Bronx, NY.)

■ FIGURE 68-55 Tuberculous dactylitis is evident as spina ventosa in this child. Radiograph shows expansion and destructive changes involving the proximal phalanges of the right index finger and left third finger. (Courtesy of George Barnes, MD, Tucson, AZ.)

cavity formation with the remaining bone ballooned out. This is most marked in the diaphyses of metacarpal and metatarsal bones in children and is termed spina ventosa (“wind-filled sail”). Other radiographic features include diffuse bone infiltration with a coarse trabecular pattern and localized destruction of the end of the phalanx with reactive sclerosis and bone involvement (see Fig. 68-55).1,13

In early stages, joint effusion and soft tissue edema may be the only signs of tuberculous arthritis. Classic radiographic signs of tuberculous arthritis include juxta-articular osteoporosis, peripheral osseous erosions, and gradual reduction of the joint space and are termed Phemister’s triad (see Fig. 68-56). If the disease is left untreated, complete joint obliteration and fibrous ankylosis of the joint may result. Periostitis and bone proliferation are less

1410 P A R T T H R E E

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common and less extensive than in pyogenic arthritis. When present, tuberculous periostitis is linear, paralleling the contour of the bone. In skeletally immature patients synovitis and chronic hyperemia can lead to epiphyseal overgrowth and premature physeal fusion.13 In tuberculous bursitis and tenosynovitis, soft tissue swelling and osteoporosis may be observed. Osseous involvement may develop in the region of the greater trochanter. In any bursal location dystrophic calcifications may appear.

Magnetic Resonance Imaging In tuberculous spondylitis MRI is best for assessing signal change within the disc space and adjacent vertebral bodies, intraosseous abscess, skip lesions, subligamentous spread of infection and epidural extension. Characteristic changes in affected vertebral bodies are decreased signal intensity on the T1-weighted, increased signal on the T2weighted and inversion recovery images, and enhancement after intravenous administration of gadolinium-based contrast. A thick enhancing rim is observed about the paraspinal abscesses.1,13,14,28,29 Intraosseous abscesses also

demonstrate rim enhancement. MRI is very sensitive in detection of early changes of tuberculous arthritis, but the appearances are nonspecific. MRI is useful in diagnosis of tuberculous tenosynovitis, bursitis, and myositis with similar signal abnormalities as with osseous infection (see Figs. 68-53C-E, 68-54-B, and 68-56C-E).

Multidetector Computed Tomography In tuberculous spondylitis CT is sensitive in detecting early bone changes, paraspinal abscesses, and involvement of posterior elements. It provides superb visualization of bone fragmentation and calcifications within paraspinal abscesses. Multislice CT provides thin-cut imaging that enables superb coronal, sagittal, and 3D reformatted images (see Figs. 68-54-A and 68-57).1,14,28 MRI is superior to CT in evaluation of soft tissue infection, including tenosynovitis, bursitis, and myositis.

Ultrasonography Ultrasonography allows diagnosis of abdominal tubercular abscesses and can confirm clinical suspicion. It is

■ FIGURE 68-56

Tuberculous arthritis in a 66-year-old man. Frontal (A) and lateral (B) radiographs of the ankle show osteopenia, small ankle effusion, narrowing of the subtalar joint, and probable erosive changes about the subtalar joint.

(Continued)

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■ FIGURE 68-56—Cont’d

Sagittal (C) and coronal (D) T1-weighted images show abnormal low signal intensity of the talus and portion of calcaneus and distal tibia consistent with osteomyelitis and tuberculous arthritis. In C, note the abnormal intermediate signal intensity in the region of Kager’s fat pad and erosion of the Achilles tendon compatible with soft tissue infection. Ankle joint effusion is present. E, The regions of abnormality show intermediate increased signal intensity on the fluid-sensitive sequence. (Courtesy of E. Outwater, MD, Tucson, AZ.)

also useful to guide percutaneous drainage and to follow the patients after drainage. However, MRI and CT remain methods of choice to depict vertebral involvement. Ultrasonography can be used in evaluation of tuberculous tenosynovitis, bursitis, and myositis.

Nuclear Medicine Evaluation of spinal tuberculosis with scintigraphy early in the course of infection is limited by the indolent nature of skeletal tuberculosis. 99mTc-methylene diphosphonate and 67gallium citrate scans may be negative initially despite the presence of active disease clinically and radiographically.13 The complementary use of these two radionuclide agents is recommended by some investigators to improve accuracy (86%). As the infection progresses,

extensive osseous changes and attempts at healing result in increased bone metabolism, manifested as areas of increased radionuclide uptake on bone scans. Bone scintigraphy is helpful in evaluation of multifocal involvement and in monitoring the response to therapy.1,14 111In-labeled white blood cells may show either increased or decreased radiotracer accumulation in the affected region, with reported accuracy for vertebral osteomyelitis of 63% to 66%.1,14,30

Positron Emission Tomography/ Computed Tomography The value of PET in evaluation of skeletal tuberculosis is not determined. A preliminary study showed moderate uptake of fluorodeoxyglucose (FDG) in the capsule

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■ FIGURE 68-57 Tuberculous arthritis in a 1-year-old child with pulmonary tuberculosis. A and B, Axial CT images of the upper thorax show destructive changes involving the left sternoclavicular joint with associated periarticular abscess and soft tissue calcifications. (Courtesy of George Barnes, MD, Tucson, AZ.)

and low uptake in the center of two tuberculous cold abscesses. These features are unique compared with nontuberculous abscess and typical tuberculosis lesions, which are characterized by high FDG uptake. Pathologically, a tuberculous cold abscess is not accompanied by active inflammatory reaction. These findings suggest that the FDG uptake by tuberculous lesions varies according to the grade of the inflammatory activity. This new diagnostic feature of a tuberculous cold abscess may be useful in the evaluation of such lesions by FDG PET.41,42

Classic Signs ■ ■ ■ ■ ■ ■ ■

Late disc involvement Cold paraspinal abscess with calcifications Multiple vertebral levels may be involved in noncontiguous fashion Thick enhancing rim about paraspinal abscess Phemister’s triad Transphyseal extension of metaphyseal infection Spina ventosa

CHAPTER

DIFFERENTIAL DIAGNOSIS Differential diagnosis for tuberculous spondylitis includes low-grade pyogenic infection such as brucellosis, fungal infections, tumors, and sarcoidosis. Clinical data favoring tuberculosis are an insidious onset of symptoms, presence of pulmonary tuberculosis, late onset of paraplegia, and a normal erythrocyte sedimentation rate.1,13 Tuberculous osteomyelitis and arthritis have a more indolent course similar to fungal infection when compared with pyogenic infections. None of the radiographic findings is pathognomonic for tuberculous spondylitis. However, delay in destruction of intervertebral disc, large calcified paravertebral abscesses with thick enhancing rim, subligamentous spread, and absence of sclerosis favor tuberculous infection.1,13,28 Differentiation of tuberculous and pyogenic osteomyelitis is difficult. Acute pyogenic osteomyelitis has a more rapid course and less frequent extent across the physis into the adjacent joint than tuberculous osteomyelitis. Tuberculous infection has a similar course as fungal skeletal infection. Differential diagnosis for tuberculous dactylitis includes syphilitic dactylitis with bilateral and symmetric involvement, more prominent periostitis, and less prominent soft tissue swelling. Phalangeal, metacarpal, and metatarsal changes can be observed in various other diseases, including fibrous dysplasia, hyperparathyroidism, leukemia, sarcoidosis, and sickle cell anemia but radiographic abnormalities at other sites allow accurate diagnosis of these conditions. Dactylitis in coccidioidomycosis can have a similar appearance. The differential diagnosis of tuberculous arthritis includes pyogenic and fungal arthritis, rheumatoid arthritis, gout, idiopathic chondrolysis, pigmented villonodular synovitis, and synovial osteochondromatosis. Slow progression of disease, significant osteoporosis, and mild sclerosis are typically seen in tuberculous and fungal disease.

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment Chemotherapy for tuberculosis in general and osteoarticular tuberculosis in particular poses certain peculiar problems that include chronicity of infection, infection by resistant mycobacteria, persistent mycobacteria, possibility of concomitant human immunodeficiency virus infection, and drug toxicity during prolonged treatment. Although the success rate of chemotherapy is greater than 90% with optimum drug combination regimens currently used, there is a need for additional improvement.4,36,37 Of the commonly used first-line drugs against the large population of mycobacteria actively multiplying in the walls of a cavity, isoniazid, rifampicin, and streptomycin are bactericidal, pyrazinamide is inactive, whereas ethambutol is bacteriostatic. Against a small bacterial population multiplying slowly inside the microphage at acidic pH, pyrazinamide is the most effective drug, followed by isoniazid and rifampicin, with streptomycin being inactive. Against intermittently multiplying

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bacilli in solid caseous lesions, only rifampicin is active. Therefore, rifampicin is effective in preventing relapse of disease.4 Second-line (reserve) drugs include capreomycin, kanamycin, fluoroquinolones (ciprofloxacin, ofloxacin, sparfloxacin), ethionamide, cycloserine, and paraaminosalicylic acid. In general, these drugs are less effective and more toxic than the standard drugs. The newer drugs include amikacin, fluoroqinolones, rifabutin, clarithromycin, and clofazimine. Glucocorticoids may be required during chemotherapy to counter a hypersensitivity reaction to standard antimycobacterial agents. Bacillus Calmette-Guérin vaccination has some role in prophylaxis of tuberculosis.4 On diagnosis, treatment is started immediately without waiting for the results of susceptibility test, which may take a long time. If required, the regimen can be modified after the results of susceptibility tests are available. From a bacteriostatic viewpoint, isoniazid and rifampicin is the most effective combination. To prevent primary and secondary drug resistance a combination of three rather than two bactericidal drugs should be used initially in an optimum regimen. Isoniazid usually always is present. The duration of treatment never must be less than 6 months.4,36 Treatment of multidrug-resistant latent tuberculosis infection can represent a challenge.37

Surgical Treatment Spinal tuberculosis is usually seen at an advanced anatomic and clinical stage with major destruction of several vertebrae. Significant instability and deformity of the spine can result, mandating prompt diagnosis and treatment to prevent permanent neurologic damage. Surgery allows assessment of the diagnosis, opportunity to treat a vertebral compression, evacuation of pus, and treatment or stabilization of spinal deformation.13,39 Anti-tuberculous therapy is beset by important factors that limit its efficacy, such as the emergence of drug toxicity and multiresistant mycobacterial strains. Surgical treatment may be indicated in selected cases where medical therapy alone is not sufficient to eradicate the problem. Chemotherapy should be commenced preferably before surgery to prevent miliary disease.36,39

What the Referring Physician Needs to Know ■

■

■

■

The diagnosis of musculoskeletal tuberculous infection remains a challenge to clinicians and requires a high index of suspicion. The combination of indolent onset of symptoms, positive tuberculin skin test, and compatible radiographic findings strongly suggest the diagnosis. Tuberculosis, however, must be confirmed by positive culture or histologic proof from the aspiration of synovial fluid or biopsy of the bone or synovium. Prompt diagnosis and treatment of skeletal TB are important to prevent serious bone and joint destruction and severe neurologic sequelae in the case of spinal involvement.

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SUGGESTED READINGS Extrapulmonary tuberculosis: an overview. Am Fam Physician 2005; 72:1761–1768. Moore SL, Rafii M. Advanced imaging of tuberculosis arthritis. Semin Musculoskelet Radiol 2003; 7:143–153.

Moore SL, Rafii M. Imaging of musculoskeletal and spinal tuberculosis. Radiol Clin North Am 2001; 39:329–342. Shembekar A, Babhulkar S. Chemotherapy for osteoarticular tuberculosis. Clin Orthop Relat Res 2002; (398):20–26.

REFERENCES 1. Resnick D. Osteomyelitis, septic arthritis, and soft tissue infection: organisms. In Resnick D (ed). Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, 2002, pp 2510–2624. 2. De Backer AI, Mortele KJ, Vanhoenacker FM, Parizel PM. Imaging of extraspinal musculoskeletal tuberculosis. Eur J Radiol 2006; 57:119–130. 3. Moore SL, Rafii M. Imaging of musculoskeletal and spinal tuberculosis. Radiol Clin North Am 2001; 39:329–342. 4. Shembekar A, Babhulkar S. Chemotherapy for osteoarticular tuberculosis. Clin Orthop Relat Res 2002; (398):20–26. 5. De Vuyst D, Vanhoenacker F, Gielen J, et al. Imaging features of musculoskeletal tuberculosis. Eur Radiol 2003; 13:1809–1819. 6. Morris BS, Varma R, Garg A, et al. Multifocal musculoskeletal tuberculosis in children: appearances on computed tomography. Skeletal Radiol 2002; 31:1–8. 7. Teo HE, Peh WC. Skeletal tuberculosis in children. Pediatr Radiol 2004; 34:853–860. 8. Moore SL, Rafii M. Advanced imaging of tuberculosis arthritis. Semin Musculoskelet Radiol 2003; 7:143–153. 9. Centers for Disease Control. Trends in tuberculosis morbidity— United States, 2004. MMWR Morb Mortal Wkly Rep 2005; 54:245–249. 10. Jensen PA, Lambert LA, Iademarco MF, Ridzon R and Centers for Disease Control. Guidelines for preventing the transmission of Mycobacterium tuberculosis in health-care settings, 2005. MMWR Recomm Rep 2005; 54:1–141. 11. Extrapulmonary tuberculosis: an overview. Am Fam Physician 2005; 72:1761–1768. 12. Koh DM, Bell JR, Burkill GJ, et al. Mycobacterial infections: still a millennium bug—the imaging features of mycobacterial infections. Clin Radiol 2001; 56:535–544. 13. Yao DC, Sartoris DJ. Musculoskeletal tuberculosis. Radiol Clin North Am 1995; 33:679–689. 14. Shanley DJ. Tuberculosis of the spine: imaging features. AJR Am J Roentgenol 1995; 164:659–664. 15. Schultz E, Richterman I, Dorfman HD. Case report 739: Tuberculous arthritis of knee. Skeletal Radiol 1992; 21:330–334. 16. Araki Y, Tsukaguchi I, Shino K, Nakamura H. Tuberculous arthritis of the knee: MR findings. AJR Am J Roentgenol 1993; 160:664. 17. Merdina EV, Mitusova GM, Sovetova NA. [Ultrasound diagnosis of retroperitoneal abscesses in spinal tuberculosis]. Probl Tuberk 2001; (4):19–21. Russian. 18. Gandolfo N, Serrato O, Sandrone C, Serafini G. [The role of echography in osteolytic tubercular abscesses]. Radiol Med (Torino) 1993; 85:574–578. Italian. 19. Babic M, Mihelic R. [Ultrasonic diagnosis of abscesses in tubercular spondylitis of the vertebrae]. Reumatizam 1991; 38:39–43. Croatian. 20. Soler R, Rodriguez E, Remuinan C, Santos M. MRI of musculoskeletal extraspinal tuberculosis. J Comput Assist Tomogr 2001; 25:177–183. 21. Cormican L, Hammal R, Messenger J, Milburn HJ. Current difficulties in the diagnosis and management of spinal tuberculosis. Postgrad Med J 2006; 82:46–51. 22. Li H, You C, Yang Y, et al. Intramedullary spinal tuberculoma: report of three cases. Surg Neurol 2006; 65:185–188; discussion 188–189.

23. Almeida A. Tuberculosis of the spine and spinal cord. Eur J Radiol 2005; 55:193–201. 24. Narlawar RS, Shah JR, Pimple MK, et al. Isolated tuberculosis of posterior elements of spine: magnetic resonance imaging findings in 33 patients. Spine 2002; 27:275–281. 25. Yago Y, Yukihiro M, Kuroki H, et al. Cold tuberculous abscess identified by FDG PET. Ann Nucl Med 2005; 19:515–518. 26. De Backer AI, Mortele KJ, Vanschoubroeck IJ, et al. Tuberculosis of the spine: CT and MR imaging features. JBR-BTR 2005; 88:92–97. 27. Kalita J, Misra UK, Mandal SK, Srivastava M. Prognosis of conservatively treated patients with Pott’s paraplegia: logistic regression analysis. J Neurol Neurosurg Psychiatry 2005; 76:866–868. 28. Joseffer SS, Cooper PR. Modern imaging of spinal tuberculosis. J Neurosurg Spine 2005; 2:145–150. 29. Smith AS, Weinstein MA, Mizushima A, et al. MR imaging characteristics of tuberculous spondylitis vs vertebral osteomyelitis. AJR Am J Roentgenol 1989; 153:399–405. 30. Lisbona R, Derbekyan V, Novales-Diaz J, Veksler A. Gallium67 scintigraphy in tuberculous and nontuberculous infectious spondylitis. J Nucl Med 1993; 34:853–859. 31. Chang DS, Rafii M, McGuinness G, Jagirdar JS. Primary multifocal tuberculous osteomyelitis with involvement of the ribs. Skeletal Radiol 1998; 27:641–645. 32. Evangelista E, Itti E, Malek Z, et al. Diagnostic value of 99mTcHMDP bone scan in atypical osseous tuberculosis mimicking multiple secondary metastases. Spine 2004; 29:E85–E87. 33. Bakshi G, Satish R, Shetty SV, Anjana J. Primary skeletal muscle tuberculosis. Orthopedics 2003; 26:327–328. 34. Ahmed J, Homans J. Tuberculosis pyomyositis of the soleus muscle in a fifteen-year-old boy. Pediatr Infect Dis J 2002; 21:1169–1171. 35. Kapukaya A, Subasi M, Bukte Y, et al. Tuberculosis of the shoulder joint. Joint Bone Spine 2006; 73:177–181. 36. Butorac R, Littlejohn GO, Hooper J. Mycobacterial disease in the musculoskeletal system. Med J Aust 1987; 147:388–391. 37. Papastavros T, Dolovich LR, Holbrook A, et al. Adverse events associated with pyrazinamide and levofloxacin in the treatment of latent multidrug-resistant tuberculosis. Can Med Assoc J 2002; 167:131–136. 38. Taljanovic MS, Hunter TB, Fitzpatrick KA, et al. Musculoskeletal magnetic resonance imaging: importance of radiography. Skeletal Radiol 2003; 32:403–411. 39. Ghadouane M, Elmansari O, Bousalmame N, et al. [Role of surgery in the treatment of Pott’s disease in adults. Apropos of 29 cases]. Rev Chir Orthop Reparatrice Appar Mot 1996; 82:620–628. French. 40. Paradisi F, Corti G. Skeletal tuberculosis and other granulomatous infections. Baillieres Best Pract Res Clin Rheumatol 1999; 13:163–177. 41. Yago Y, Yukihiro M, Kuroki H, et al. Cold tuberculous abscess identified by FDG PET. Ann Nucl Med 2005; 19:515–518. 42. Ichiya Y, Kuwabara Y, Sasaki M, et al. FDG-PET in infectious lesions: The detection and assessment of lesion activity. Ann Nucl Med 1996; 10:185–191.

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C H A P T E R

General Principles of Magnetic Resonance Imaging of the Bone Marrow Bruno Vande Berg

The current chapter addresses general concepts on MRI of the bone marrow with emphasis on common normal and abnormal marrow patterns. MRI plays a key role in marrow imaging because of its high sensitivity for detecting focal or diffuse alterations in marrow content. MRI of the bone marrow is also performed for other purposes, including medullary lesion characterization, disease staging, prognosis, and monitoring of treatment response. MRI of the skeleton yields information on the medullary content of the bones (Fig. 69-1). The calcified components of the skeleton—either cortical or cancellous—are best depicted by using ionizing imaging modalities (radiographs, CT, and bone scintigraphy). Therefore, it is not surprising that MR and CT images of the same lesion occasionally yield different information (Fig. 69-2).

Yellow marrow almost exclusively contains fat cells and few capillaries. It is mainly found in the appendicular skeleton of the human adults. All long bones epiphyses, except the proximal humeral and femoral epiphyses, contain yellow marrow. The possibility of red marrow to convert to yellow marrow and, conversely, of yellow marrow to transform into red marrow, is a unique feature of the marrow.3 It occurs as a physiologic process during growth and until adulthood: at birth, red marrow occupies almost the entire skeleton. It progressively converts to yellow marrow, starting distally in the limbs and centrally in the long bones. In case of demand for more hematopoietic cells, expansion of red marrow occurs in a centripetal direction.

ANATOMY AND PHYSIOLOGY OF NORMAL BONE MARROW

MAGNETIC RESONANCE IMAGING TECHNIQUES T1-Weighted Spin-Echo Sequence

The medullary cavity of the adult human skeleton contains red and yellow marrow. In adults, red marrow occupies the cranial vault, the spine, the ribs, the sternum, the pelvic region, and the proximal aspects of the femur and humerus.1,2 Red marrow contains about 50% of fat cells and 50% of hematopoietic cells embedded in a network of highly permeable sinusoids (Table 69-1). The relative proportion of fat and non-fat cells varies among individuals according to poorly understood parameters but also according to age and sex; it also depends on the bone considered and on the anatomic region of each individual bone (Fig. 69-3).

The T1-weighted spin-echo (SE) sequence is the most important sequence for bone marrow MRI. It is able to depict the wide changes in normal red marrow distribution and composition that occur with aging because the marrow signal intensity is directly proportional to the amount of fat-laden adipocytes of the marrow cavity. The rationale for its use as the main sequence for marrow imaging is that it is able to demonstrate the changes in the amount of fat cells that occur in almost any abnormal marrow condition (Fig. 69-4). Consequently, this sequence lacks specificity because it depicts the disappearance of fat and not the concomitant appearance of

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■ FIGURE 69-1

Bone and marrow imaging. A, Radiograph of a spine specimen depicts the cortical and trabecular bone. B, The corresponding T1-weighted SE MR image depicts red and yellow marrow, as demonstrated on the specimen photograph (C). The bone pattern seen on the radiograph differs from that of the marrow seen on the T1-weighted SE MR image.

A ■ FIGURE 69-2

B

A, Sagittal CT reformatted image of the lumbar spine shows multiple sclerotic bone lesions in L2 (arrow), L3, and L4. B, On the corresponding T1-weighted SE MR image, the signal pattern of these sclerotic lesions is variable: the L2 lesion shows low signal intensity (disappearance of fat?) (arrow); the L3 and L4 lesions show high signal intensity (presence of fat?). Similar bone patterns on the CT image can have variable MR appearance that depends on each marrow alteration.

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● General Principles of Magnetic Resonance Imaging of the Bone Marrow

TABLE 69-1 Anatomy of Red and Yellow Marrow

Chemical Composition Main Cellular Composition Vasculature Main Distribution

Yellow Marrow

Red Marrow

80% lipids, 15% water Fat cells

40% lipids, 40% water Hematopoietic and fat cells Permeable sinusoids Axial skeleton

Few capillaries Appendicular skeleton

abnormal cells. In addition, the T1-weighted SE sequence is widely available and it is reproducible over time and among imaging centers.

Intermediate-Weighted Spin-Echo Sequence The intermediate-weighted SE sequence without fat saturation has no role to play in marrow imaging because many marrow constituents show a similar intermediate signal intensity.

T2-Weighted Fast Spin-Echo Sequence The T2-weighted fast SE sequence has a limited value for lesion detection but can contribute to lesion characterization. However, it is generally obtained mainly for the assessment of adjacent structures (see Fig. 69-4). Many

■ FIGURE 69-3

1419

marrow lesions do not significantly alter the amount of marrow water, and the lesion’s signal intensity widely varies according to poorly understood parameters (Fig. 69-5).

Fat-Saturated Spin-Echo Sequences Fat saturation plays an important role in bone marrow imaging.4 Actually, fat protons so heavily contribute to the medullary signal on T1- and T2-weighted SE images that they occasionally decrease the MR sensitivity for the detection of abnormal marrow components. Therefore, the application of techniques that decreases the influence of fat protons on signal intensity is likely to facilitate lesion detection (Fig. 69-6). The STIR sequence, in which the inversion time is selected to suppress fat contribution, provides valuable information because the signal of fat is suppressed and T1 and T2 contrast are additive. Fat saturation can also be achieved by selective presaturation of hydrogen protons from fat molecules and can be followed by T1-, intermediate-, or T2-weighted sequences.5 STIR sequence and fat-saturated intermediate-weighted sequences give similar results in the detection of subtle marrow alterations.6 As a significant drawback, the specificity of fat-saturated sequences is lower than that of T1- and T2-weighted SE sequences, partly because several tissue components that can be recognized on T1- or T2-weighted SE images will present a less specific signal intensity after fat saturation.

Variation in MR appearance of the bone marrow with age. Coronal T1-weighted SE MR images of the proximal humeri of different patients age 4 years (A), 10 years (B), and 64 years (C). The metaphyseal cavity of the child contains red marrow, whereas that of the adult contains fatty marrow. Fatty marrow is consistently seen in the epiphyses.

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Gradient-Echo Sequences Gradient-echo sequences play a limited role in marrow imaging. The network of cancellous bone is responsible for local field inhomogeneities that account for a marked decrease in signal intensity of cancellous bone containing areas on T2*-weighted gradient-echo sequences. These sequences are occasionally used for the detection of purely lytic lesions and also for the selective evaluation of the cancellous bone network such as in osteoporosis.

Gadolinium-Enhanced Sequences

A ■ FIGURE 69-4

A, Sagittal T1-weighted SE MR image of the spine shows multiple marrow areas (arrows) of low signal intensity, indicating marrow replacement by metastases. B, On the corresponding T2weighted SE image, marrow lesions are barely visible. Note spinal cord compression due to a posterior mass at C4 level and high signal in C5-C6 vertebral bodies due to fatty marrow as demonstrated in A.

Gadolinium-enhanced sequences may contribute to bone marrow imaging in many ways. It may be used to demonstrate normal signal enhancement in questionable red marrow areas or abnormal enhancement for lesion characterization. Gadolinium-enhanced T1-weighted SE sequence is recommended for intradural lesion detection, but it is generally not necessary for bone marrow lesion detection, at least without fat saturation, because many lesions become invisible on this sequence. If fat saturation is applied, marrow lesions become more conspicuous. There is general agreement that fat-saturated gadolinium-enhanced T1-weighted SE images and fat-saturated intermediate-weighted SE images are equivalent for the detection of subtle marrow changes that are not obvious on T1- and T2-weighted SE images.6

Other Sequences Several techniques including diffusion-weighted sequences, perfusion imaging, spectroscopy, and relaxation

Low High

Intermediate

B ■ FIGURE 69-5

Marrow replacement due to bone metastases on sagittal T1-weighted (A) and fat-saturated T2-weighted (B) SE MR images. The signal intensity is consistently low on the T1-weighted image, whereas it is variable on the T2-weighted SE MR image.

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■ FIGURE 69-6

A, Coronal T1-weighted image of the knee shows normal fatty marrow in the femoral condyles. Note the presence of normal red marrow in the femur metaphysis. B, The corresponding fat-saturated intermediate-weighted SE MR image shows abnormal increase in signal intensity in both femoral condyles. Subtle marrow alterations seen on fat-saturated images are occasionally occult on T1-weighted SE MR images, most likely due to the presence of fat.

times measurements are under evaluation for the detection of components of specific lesions. There is a need for better detection of specific cell components in two situations: (1) the amount of specific cells is limited (low tumor burden cancers, assessment of response to chemotherapy) and (2) the specific cells are hidden in a background of abnormal marrow (in edema-like changes around tumors or in spontaneous vertebral fractures, in hypercellular but normal red marrow). There is no general agreement on the added value of these sequences to resolve these two challenges. One should always keep in mind that even a normal looking T1-weighted SE image of the marrow does not enable one to exclude marrow infiltration by abnormal cells because a certain level of infiltration must be reached before the water/fat balance becomes sufficiently altered.

NORMAL ANATOMY Magnetic Resonance Appearance of the Normal Marrow Normal red marrow of the adult human shows intermediate signal intensity on both T1- and T2-weighted SE images (Table 69-2; Fig. 69-7). On T1-weighted SE images, signal intensity of normal lumbar vertebral bodies must be higher than that of adja-

cent intervertebral disc in an adult patient.7 In the thoracic spine, marrow signal intensity can be lower than that of disc because of the relatively high signal of thoracic discs. In the pelvis, normal marrow signal intensity should be higher than that of adjacent normal muscles on T1-weighted SE images.8 It is unreliable to assess the marrow status on T2-weighted SE images because there is no internal standard with which marrow signal intensity can be compared. On fat-saturated T2- or intermediateweighted fast SE images, vertebral marrow signal intensity normally ranges from intermediate to moderately elevated. Magnetic Resonance Imaging Characteristics of Red and Yellow Marrow

TABLE 69-2

MR Sequence

Red Marrow

Yellow Marrow

T1-weighted SE T2-weighted fast SE STIR, fat-saturated intermediate SE Gradient-echo Contrast medium enhancement

Intermediate Intermediate Moderately high

High Intermediate/high Low

Low Moderate

Intermediate None

SE, spin-echo; STIR, short tau inversion recovery.

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■ FIGURE 69-7

Sagittal T1- (A), T2- (B), and enhanced T1- (C) weighted SE MR images of the lumbar spine show normal marrow pattern with low signal intensity red marrow and moderate signal intensity enhancement after injection of contrast material. Intramedullary and perivertebral veins normally enhance, which indicates that contrast material has been successfully injected.

After intravenous injection of gadolinium-containing contrast material, enhancement of marrow signal intensity is barely visible at visual inspection on T1-weighted SE images (see Fig. 69- 7) despite the important marrow vascularization. This observation can be partly explained as follows: on T1-weighted images, signal intensity enhancement of a given tissue parallels the gadoliniuminduced shortening of the T1 relaxation time in that tissue. Because of the short T1 relaxation time of red marrow due to the presence of fat, the gadolinium-induced shortening in T1 relaxation time is small and, therefore, barely visible. Signal enhancement is more obvious on fatsaturated T1-weighted SE images or can be quantitatively assessed by performing dynamic MR studies. Usually, normal marrow signal intensity should not increase by more than 35% in adults older than 35 years of age.9 In normal fatty marrow, contrast-induced alteration of signal intensity is not visible. There are important interindividual variations in marrow MR appearance among normal subjects of the same age range, partly because of variations in red marrow cellularity. However, there is limited variation in marrow MR appearance in the same subject, in the spine (between

different vertebral bodies), and in the axial skeleton (between paired bones) (see Fig. 69-7). Several distribution patterns of red marrow can be recognized in each bone, which are systematically observed in the paired bones of the same subject.8,10

MAGNETIC RESONANCE IMAGING PATTERNS OF MARROW LESIONS Bone marrow lesions can be classified into a small number of lesion categories based on their signal intensity on T1-weighted SE images (Table 69-3; Fig. 69-8).2,11 These patterns are generally nonspecific and can be observed within the same lesion.

Marrow Depletion Marrow depletion is a pattern characterized on T1weighted images by an increase in signal intensity in comparison to adjacent red marrow (Figs. 69-9 and 69-10). This signal pattern reflects an increase in fat content and a concomitant decrease in the non-fat marrow content. Focal red marrow depletion occurs in the spine of normal

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Elementary Lesion Patterns on Magnetic Resonance Imaging

TABLE 69-3

Lesion Patterns

Signal Intensity on T1 Weighting

Fat Amount

Depletion Infiltration Replacement

High Moderately low Low

Increased Moderately reduced Markedly reduced

subjects, with an increased frequency according to age12; it also occurs in bone lesions, including quiescent lesions, Paget’s disease, and vertebral hemangioma. Regional red marrow depletion occurs after radiation therapy. Diffuse red marrow depletion can be induced by drugs, including corticosteroids and chemotherapeutic agents, and in aplastic anemia.

Marrow Infiltration Marrow infiltration is a pattern characterized by a subtle to moderate decrease in marrow signal intensity on T1-weighted spin-echo images (see Fig. 69-10). Margins are generally indistinct with a gradual zone of transition

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toward normal bone marrow. The term infiltration suggests that the abnormal marrow component infiltrates or permeates the normal marrow constituents with some possible residual adipocytes in the lesion. The term bone marrow edema is frequently used to characterize marrow infiltration with high signal intensity on T2-weighted SE images and a return to normal signal intensity on gadolinium-enhanced T1-weighted images. The term edema-like changes could be more appropriate because numerous marrow changes can alter signal intensity in a similar manner, including interstitial hemorrhage, edema, necrosis, or fibrosis. Focal marrow infiltration involves the periphery of many abnormal processes including fracture, tumor, infection, osteoarthritis, and so on. Diffuse marrow infiltration occurs in systemic disorders including anemia, chronic infection, the acquired immunodeficiency syndrome (AIDS), and bone marrow cancers. Marrow infiltration by neoplastic cells, interstitial fibrosis, or storage disorders can result in a similar MR abnormality.

Marrow Replacement Marrow replacement is a pattern characterized by a marked decrease in signal intensity on T1-weighted SE

■ FIGURE 69-8

Schematic drawings of three marrow lesion patterns on T1-weighted SE image including (A) marrow depletion (increased signal intensity), (B) marrow infiltration (slight decrease in signal intensity) and (C) marrow replacement (marked decrease in signal intensity).

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WHAT THE RADIOLOGIST NEEDS TO KNOW How Does One Increase Sensitivity of Bone Marrow Magnetic Resonance Imaging?

B ■ FIGURE 69-9

A, Marrow depletion. B, Several vertebral bodies show increased signal intensity with respect to adjacent vertebral bodies on a T1-weighted SE MR image. These lesions correspond to healed vertebral fractures in a young male patient with severe osteoporosis.

images (Fig. 69-11). The term replacement suggests that normal marrow components are completely replaced by abnormal marrow components without residual adipocytes. Margins can be either sharp or indistinct depending on the absence or presence of surrounding marrow infiltration. Signal intensity on other sequences and enhancement patterns vary greatly, probably reflecting the histopathologic changes of the abnormal marrow component. Marrow replacement can be diffuse or focal (Fig. 69-12). Differentiating focal marrow “replacement” from “infiltration” is important: marrow infiltration is frequently reactional to adjacent lesions and its biopsy is unlikely to be diagnostic. Marrow replacement is nonspecific but can be a valuable target for a biopsy if necessary. In red marrow, the distinction between marrow replacement and infiltration can be difficult because, in red marrow, a slight increase in non-fat cells can rapidly induce complete marrow replacement.

Three fundamental options can be proposed to increase sensitivity for marrow lesion detection, including optimal sequence selection, utilization of gadolinium, and wholebody imaging. The T1-weighted SE sequence generally enables accurate marrow lesion detection. Its value decreases in many situations in which the difference in amount of fat between the lesion and the adjacent marrow—or fat gradient—is reduced (Fig. 69-13). The fat gradient is decreased if the lesion still contains fat cells or if the adjacent marrow contains little fat. In those situations, fat-saturated intermediate or T2-weighted fast SE sequences or STIR sequences are superior to the T1-weighted SE image for lesion detection, probably because of the low signal intensity of the background marrow and the intermediate to high signal intensity of the abnormal marrow. Fatsaturated gadolinium enhanced T1-weighted SE images seem to provide similar results. Examples of situations in which the signal of normal marrow is low (and cause decreased fat gradient) include children (Fig. 69-14) and young adults, patients treated with drugs that induce marrow hypercellularity, and patients with chronic infection. In these situations, fat-saturated intermediate- or T2weighted images or gadolinium-enhanced fat-saturated T1-weighted SE images are superior to the standard T1weighted SE sequence for lesion detection. Several studies demonstrated the value of T2*-weighted gradient-echo images in patients with purely lytic bone lesions such as in multiple myeloma. MRI of the spine generally enables accurate lesion detection in cancer patients. Adding coronal T1-weighted SE images of the pelvis enables assessment of a larger amount of the red marrow–containing space and increases the likelihood of lesion detection. Whole-body MRI enables to analyze the largest amount of body and should become more popular with the development of new technologies.13

How Does One Increase Specificity of Bone Marrow Magnetic Resonance Imaging? As a rule, characterization of bone marrow lesions with MRI remains limited, mainly in the setting of multiple focal or diffuse marrow replacement for which biopsy may still be the most accurate diagnostic modality. In the setting of an isolated bone lesion, analysis of several MR sequences, including gadolinium-enhanced images, may contribute to narrow the differential diagnosis list. Plain films and CT images also greatly contribute to lesion characterization by depicting several lesional components that are not easily recognized at MRI: cartilaginous, bony or fibrous matrices, calcium, sequestrum, and gas are all more specifically recognized on CT than on MR images. In addition, the patterns of adjacent

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C ■ FIGURE 69-10

A, Marrow infiltration and depletion. Sagittal T1- (B) and T2- (C) weighted SE MR images of the lumbar spine with focal marrow infiltration in L3 (C, arrows) and focal marrow depletion in L4 and L5 (C, arrowheads) adjacent to intervertebral disc disease. Marrow infiltration shows moderate decrease in signal intensity on the T1-weighted SE image and moderate increase in signal intensity on the T2-weighted image, consistent with marrow edema. The T2-weighted image cannot be used to discriminate between both lesions’ patterns because they have similar signal intensities.

trabecular bone and periosteum changes can help in lesion characterization by indicating growth patterns. In a nutshell, combining bone and marrow analysis by looking at CT and MR images, respectively, often contribute to a specific diagnosis of an isolated lesion.

Is This a Normal Variant?

With or Without Fat Suppression?

During adulthood, foci of yellow marrow appear in the vertebral bodies.12 Their signal intensity is high on T1weighted SE images and low on fat-saturated images (see Fig. 69-11). On intermediate- or T2-weighted fast SE images, they also show high signal intensity and they should not be confused with clinically significant marrow lesions (see Fig. 69-4).

The use of fat suppression with either T2- or enhanced T1-weighted images has gained general agreement mainly because it displays marrow lesions in a favorable way, that is, with high signal intensity on a low signal intensity background. The dynamic range of signal intensity is smaller on fat-saturated images than on T1- and T2-weighted SE images. Therefore, the use of fat saturation can induce loss in signal intensity information. At this stage of understanding of MRI, we consider that, in general, fat saturation should be used for optimal lesion detection but not for lesion characterization. This hypothesis remains to be validated.

Several marrow alterations are fortuitously discovered and should not be confused with significant marrow changes.

Islands of Fatty Marrow

Vertebral Hemangioma Vertebral hemangioma, a common asymptomatic vertebral lesion, contains dilated, blood-filled vascular spaces set in a stroma containing large amounts of adipose tissue without hematopoietic cells. On T1-weighted images, its

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B ■ FIGURE 69-11

A, Marrow replacement. B, A sagittal T1-weighted SE MR image shows marrow areas of decreased signal intensity consistent with marrow replacement (arrows). Areas of high signal intensity in L2 and L3 vertebral bodies are not clinically significant (fatty marrow). C, On the fat-saturated intermediate-weighted SE MR image, lesions are barely visible.

signal is generally higher than that of adjacent marrow, although it can also be equivalent and therefore not visible on T1-weighted images.14 On T2-weighted SE images, their signal is consistently high (see Fig. 69-4). The presence of fat cells and dilated vessels with interstitial edema most likely accounts for its high signal intensity on T1-and T2-weighted images, respectively.15 Punctuated or linear areas of low signal intensity are also seen on T1- and T2weighted images, probably due to the presence of thickened trabeculae. Signal enhancement of hemangioma after gadolinium injection is variable, depending on its appearance on T1-weighted images and the type of sequence that is obtained after contrast medium injection.

Enostosis Enostosis or a compact bone island consists of lamellar cortical bone embedded within cancellous bone. Its

signal intensity is very low on all sequences, its contours are spiculated, and adjacent marrow generally has a normal appearance.

Islands of Red Marrow Random variations in red marrow cellularity occur and cause the presence of areas of more pronounced decrease in signal intensity than adjacent marrow on T1-weighted SE MR images (Fig. 69-15). The margins of these nodules are sharp if the marrow conversion process is advanced and fuzzier if the marrow conversion process is limited.16 Occasionally, central areas of high signal intensity on T1weighted images due to the persistence of fat cells are present, which are an additional argument in favor of a normal variant. Presence of low to intermediate signal intensity on T2-weighted, lack of evident signal enhancement on T1-weighted images after gadolinium injection,

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■ FIGURE 69-12

Diffuse marrow replacement shows a homogeneous low signal intensity. Marrow replacement can be either diffuse (A) or focal (B). C, The variegated or pepper-and-salt pattern is defined by the presence of multiple tiny areas of decreased signal intensity on T1-weighted images.

■ FIGURE 69-13

Schematic drawings of situations in which the T1-weighted SE MR sequence shows limited value for lesion detection. A, In the normal situation, the intensity gradient is important between normal marrow and focal lesion. Decreased lesion conspicuity can occur if the lesion shows a relatively high signal intensity (B) or if the normal marrow shows decreased signal intensity on the T1-weighted SE MR image (C) (lower intensity gradient).

● General Principles of Magnetic Resonance Imaging of the Bone Marrow

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and lack of trabecular bone changes on CT images and of changes at follow-up MR studies generally help to differentiate these benign heterogeneities from clinically relevant abnormalities. Experience with glucose-6phosphate dehydrogenase (G6PD)- fluorodeoxyglucose (FDG)–labeled positron emission tomography is limited, but these areas may show slight increased hypermetabolic uptake in comparison with adjacent red marrow.17

Hematopoietic Marrow Hyperplasia

■ FIGURE 69-14

A 15-year-old boy presented with Ewing’s tumor of the iliac wing. A, The lumbar bone marrow shows diffuse low signal intensity on the T1-weighted SE MR image and focal lesions are barely visible. B, On the corresponding fat-saturated T2-weighted fast SE MR image, multiple focal lesions with intermediate to high signal intensity become visible.

Diffuse hematopoietic marrow hyperplasia is defined by the presence of hypercellular hematopoietic marrow in the axial skeleton and by expansion of hematopoietic marrow in the appendicular skeleton (marrow reconversion).18 It can be idiopathic, mainly in middle-aged obese woman (Fig. 69-16). It also occurs in heavy smokers and in subjects with intensive sports activities, mainly long distance runners.19 It is similar to what occurs in patients in response to stimuli that trigger the production of red marrow cells, including administration of hematopoietic growth factors during chemotherapy, chronic infection, and any other cause of chronic anemia, such as hereditary hemoglobinopathies. On T1-weighted SE images, hematopoietic marrow hyperplasia is associated with a marked decrease in signal intensity of vertebral marrow that becomes lower than that of adjacent disc (or gluteus muscles in the pelvis). Marrow signal intensity is low on T2-weighted SE images and intermediate on fat-saturated intermediate-weighted

■ FIGURE 69-15

Presumed island of red marrow. A, On the sagittal T1-weighted MR image, a small area of slight decrease in signal intensity is present in the center of the vertebral body (arrow). B, The lesion shows low signal intensity on the T2weighted SE MR image. Note that the central vein of the body and its surrounding fat (arrow) is preserved, although they are within the lesion.

A

B

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■ FIGURE 69-16

On the coronal T1- (A) and T2- (B) weighted SE MR images of the right knee of a 64-year-old obese woman, the distal femur metaphysis shows low signal intensity, indicating the presence of red marrow, which is uncommon by that age and indicates red marrow hyperplasia. The signal intensity of red marrow is higher than that of muscles and there is no red marrow in the epiphyses.

images. After intravenous gadolinium injection, signal intensity enhancement is moderate but can increase up to 80% on dynamic T1-weighted SE images. In the appendicular skeleton, expansion of red marrow in distal limbs can be observed along with nodules of regenerating red marrow that can simulate bone metastasis. Differentiation of hematopoietic marrow hyperplasia from diffuse marrow infiltration remains extremely difficult, and blind iliac crest biopsy could be the most accurate technique to definitely address this occasionally difficult

problem. As a rule, normal marrow hyperplasia should have a signal intensity similar to that of red marrow on all sequences. In- and out-phase gradient-echo images, T1 relaxation time determination, hydrogen proton spectroscopy, dynamic contrast MR studies, and diffusion-weighted images have all been shown to be of some help, but none has demonstrated definite conclusive results. Preliminary observations with FDG-PET imaging also shown confusing overlapping findings because diffuse hypermetabolic marrow can be observed in both conditions.20

SUGGESTED READINGS Steiner RM, Mitchell DG, Rao VM, et al. Magnetic resonance imaging of bone marrow: diagnostic value in diffuse hematologic disorders. Magn Reson Q 1990; 6:17–34. Steiner RM, Mitchell DG, Rao VM, Schweitzer ME. Magnetic resonance imaging of diffuse bone marrow disease. Radiol Clin North Am 1993; 31:383–409. Vande Berg BC, Galant C, Lecouvet FE, et al. The lumbar vertebral body and diskovertebral junction. Radiol Clin North Am 2000; 38:1153–1175.

Vande Berg BC, Malghem J, Lecouvet FE, Maldague BE. Magnetic resonance imaging of the normal bone marrow. Skeletal Radiol 1998; 27:471–483. Vande Berg BC, Malghem J, Lecouvet FE, Maldague BE. Classification and detection of bone marrow lesions with magnetic resonance imaging. Skeletal Radiol 1998; 27:529–545. Vogler JBI, Murphy WA. Bone marrow imaging. Radiology 1988; 168:679–693.

REFERENCES 1. Kricun ME. Red-yellow marrow conversion: its effect on the location of some solitary bone lesions. Skeletal Radiol 1985; 14:10–19. 2. Vogler JBI, Murphy WA. Bone marrow imaging. Radiology 1988; 168:679–693. 3. Cristy M. Active bone marrow distribution as a function of age in humans. Phys Med Biol 1981; 26:389–400. 4. Mirowitz SA. Fast scanning and fat-suppression MR imaging of musculoskeletal disorders. AJR Am J Roentgenol 1993; 161:1147–1157.

5. Delfaut EM, Beltran J, Johnson G, et al. Fat suppression in MR imaging: techniques and pitfalls. Radiographics 1999; 19:373–382. 6. Zanetti M, Bruder E, Romero J, Hodler J. Bone marrow edema pattern in osteoarthritic knees: correlation between MR imaging and histologic findings. Radiology 2000; 215:835–840. 7. Carroll KW, Feller JF, Tirman PF. Useful internal standards for distinguishing infiltrative marrow pathology from hematopoietic marrow at MRI. J Magn Reson Imaging 1997; 7:394–398.

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8. Dawson KL, Moore SG, Rowland JM. Age-related marrow changes in the pelvis: MR and anatomic findings. Radiology 1992; 183:47–51. 9. Baur A, Stabler A, Bartl R, et al. MRI gadolinium enhancement of bone marrow: age-related changes in normals and in diffuse neoplastic infiltration. Skeletal Radiol 1997; 26:414–418. 10. Ricci C, Cova M, Kang YS, et al. Normal age-related patterns of cellular and fatty bone marrow distribution in the axial skeleton: MR imaging study [see comments]. Radiology 1990; 177:83–88. 11. Vande Berg BC, Malghem J, Lecouvet FE, Maldague BE. Classification and detection of bone marrow lesions with magnetic resonance imaging. Skeletal Radiol 1998; 27:529–545. 12. Hajek PC, Baker LL, Goobar JE, et al. Focal fat deposition in axial bone marrow: MR characteristics. Radiology 1987; 162(1 pt 1):245–249. 13. Eustace S, Tello R, DeCarvalho V, et al. A comparison of whole-body TurboSTIR MR imaging and planar 99mTc-methylene diphosphonate scintigraphy in the examination of patients with suspected skeletal metastases. AJR Am J Roentgenol 1997; 169:1655–1661. 14. Laredo JD, Assouline E, Gelbert F, et al. Vertebral hemangiomas: fat content as a sign of aggressiveness. Radiology 1990; 177:467–472.

15. Baudrez V, Galant C, Vande Berg BC. Benign vertebral hemangioma: MR-histological correlation. Skeletal Radiol 2001; 30:442–446. 16. Levine CD, Schweitzer ME, Ehrlich SM. Pelvic marrow in adults. Skeletal Radiol 1994; 23:343–347. 17. Bordalo-Rodrigues M, Galant C, Lonneux M, et al. Focal nodular hyperplasia of the hematopoietic marrow simulating vertebral metastasis on FDG positron emission tomography. AJR Am J Roentgenol 2003; 180:669–671. 18. Deutsch A, Resnick D, Niwayama G. Case report 145: bilateral, almost symmetrical skeletal metastases (both femora) from bronchogenic carcinoma. Skeletal Radiol 1981; 6:144–148. 19. Shellock FG, Morris E, Deutsch AL, et al. Hematopoietic bone marrow hyperplasia: high prevalence on MR images of the knee in asymptomatic marathon runners. AJR Am J Roentgenol 1992; 158:335–338. 20. Elmstrom RL, Tsai DE, Vergilio JA, et al. Enhanced marrow [18F]fluorodeoxyglucose uptake related to myeloid hyperplasia in Hodgkin’s lymphoma can simulate lymphoma involvement in marrow. Clin Lymphoma 2004; 5:62–64.

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C H A P T E R

Ischemic Bone Lesions Bruno Vande Berg

Ischemic bone lesions cover a wide spectrum of conditions with variable clinical, imaging, and pathologic findings. In general, oxygen delivery to the bone and marrow cells is impaired at least in some areas of any ischemic bone lesion. Epiphyseal ischemic lesions have been more extensively investigated because of their clinical importance.1 MRI has definitely contributed to their detection and staging.

ETIOLOGY Ischemic bone lesions occur in several conditions, although they are frequently idiopathic. The etiologic factors that have been identified include joint fracture and dislocation, systemic corticosteroid use, Cushing’s disease, alcohol abuse, sickle cell disease, other hemoglobinopathies, vasculitis, trauma, renal transplantation and osteodystrophy, radiation therapy, pancreatitis, gout, Gaucher’s disease, connective tissue diseases (e.g., systemic lupus erythematosus), caisson disease, and cytotoxic agents (e.g., vinblastine, vincristine, cisplatin, cyclophosphamide, methotrexate, bleomycin, 5-fluorouracil).1 Several diseases including the acquired immunodeficiency syndrome (AIDS) and severe acute respiratory syndrome (SARS) seem to be associated with an increased prevalence of ischemic bone lesions, although lesions could be related either to the diseases or to their treatments. A Japanese survey of femoral head osteonecrosis estimated that 34.7% were due to corticosteroid use, 21.8% to alcohol abuse, and 37.1% to idiopathic mechanisms.2

PREVALENCE AND EPIDEMIOLOGY The prevalence of ischemic bone lesions is unknown, mainly because many lesions are clinically silent. The rate of symptomatic epiphyseal osteonecrosis of the hip is 2 to 4.5 cases per patient-year with approximately 15,000 new cases reported each year in the United States. Femoral head osteonecrosis accounts for more than 10% of total hip replacement surgeries performed in the United States. A Japanese survey estimated that 2500 to 3300 cases of epiphyseal osteonecrosis of the hip occur each year.2

Age at onset of epiphyseal osteonecrosis depends on the underlying cause. Idiopathic femoral head osteonecrosis most often develops in male subjects aged between 35 and 55 years and is bilateral in 40% to 80% of cases. On average, women present almost 10 years later than men. The male-to-female ratio also depends on the underlying cause, although idiopathic epiphyseal osteonecrosis is more common in men, with an overall male-to-female ratio ranging from 4 to 8:1. There is no racial predilection, except for osteonecrosis associated with sickle cell disease and hemoglobin S and SC disease, which predominantly occurs in people of African and Mediterranean descent.

CLINICAL PRESENTATION Clinical presentation ranges from fortuitous discovery at MRI in asymptomatic patients to deep excruciating bone pain in patients with sickle cell crisis. In post-traumatic and in corticosteroid-induced osteonecrosis, symptoms occur generally several months after the trauma or the onset of treatment, respectively. Joint pain develops spontaneously, and in the lower limbs pain is generally worsened by weight bearing.

PATHOPHYSIOLOGY The pathophysiology of osteonecrosis remains poorly understood, and four different conditions are recognized (Table 70-1). In systemic osteonecrosis (e.g., corticosteroid-induced osteonecrosis) impaired perfusion with subsequent necrosis of bone and marrow can be caused by several mechanisms, including thrombotic or embolic occlusion of blood vessel (e.g., fat embolism, sickle cell crisis, caisson disease), injury to vessel wall (e.g., vasculitis, connective tissue diseases such as systemic lupus erythematosus, radiation, infection), and increased pressure on the vessel wall (e.g., extravasated blood in marrow, inflammation caused by lipid accumulation in osteocytes, intraosseous hypertension from proliferating Gaucher cells in Gaucher’s disease). Systemic osteonecrosis can involve any bone segment and yellow or red marrow. 1431

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TABLE 70-1 Post-traumatic, Systemic, and Overuse Osteonecrosis in Adults Post-traumatic Osteonecrosis

Likely Pathophysiology Lesion Number Age Topography Background MR Pattern Lesion Model

Interrupted blood supply Unique Any Epiphysis Yellow Segmental Subcapital femoral neck fracture

Systemic

Overuse Osteonecrosis

Yellow Marrow*

Red Marrow

Various causes of ischemia Multiple Any Epi-metaphysis Yellow Segmental Corticosteroid-induced osteonecrosis

Various causes Multiple Any Any Red Edema Vaso-occlusive crisis in sickle cell disease

Trabecular bone fracture Unique Elderly Epiphysis Yellow Edema Spontaneous osteonecrosis of the knee

*The segmental pattern can also be idiopathic and unique in case of no risk factor.

In post-traumatic osteonecrosis anatomic disruption of the blood supply after bone fracture or joint dislocation can cause bone osteonecrosis, given the terminal blood supply of the involved area (an epiphysis or a cortical bone fragment). In overuse osteonecrosis (e.g., “spontaneous osteonecrosis of the knee”) subchondral trabecular bone fracture could impair perfusion with subsequent bone and marrow necrosis. Overuse osteonecrosis is confined to the epiphyses, mainly of the lower limbs.

Histopathology At the microscopic level cell necrosis may take several patterns. but coagulation necrosis is the most common pattern of necrosis in bones. It results in complete absence of osteocytes within the bone trabeculae, loss of adipocyte nuclei with lipid cysts formation, and death of hematopoietic cells (Fig. 70-1).3 An infarct is a localized area of necrosis in tissue resulting from reduction from either its arterial supply or venous drainage.4 The term bone infarct is generally

used to describe a metaphyseal or diaphyseal ischemic lesion but not an epiphyseal lesion rather for cultural than for medical reasons (Fig. 70-2). The histopathologic changes that occur in infarcts merely depend on the type of marrow vasculature. In yellow marrow, arterial occlusion produces a bloodless or white infarct because of the poor vasculature of yellow marrow. Marrow remains fatty and demonstrates normal signal intensity on MR images. The reactive interface of fibrovascular tissue that progressively appears and surrounds the ischemic lesion is the hallmark of yellow marrow infarct. In red marrow, hemorrhagic or red infarcts may develop because of the rich vascular network of red marrow.4 Collapsed epiphyseal osteonecrosis is characterized by the presence of an irreversible fracture of the subchondral bone plate and adjacent trabeculae that frequently runs parallel underneath the subchondral bone plate itself (Fig. 70-3). Collapsed epiphyseal osteonecrosis is a radioclinical condition characterized by pain and functional disability of the joint considered as an organ, related to an irreversible spontaneous fracture of the epiphysis, generally associated with an epiphyseal infarct.

IMAGING TECHNIQUES

■ FIGURE 70-1 Necrosis. Microscopic features of bone necrosis: bone trabeculae with empty lacunae (arrow) and marrow with preserved fatty content.

Radiographs are relatively insensitive for the detection of the early stages of ischemic bone lesions. However, they play a key role in the assessment of symptomatic joints because they may demonstrate the subchondral bone fracture and the epiphyseal collapse in case of epiphyseal osteonecrosis or they may indicate another condition. Multiple high-resolution radiographs including distraction views (frog-leg view of the hips) are often required to demonstrate the epiphyseal fracture. MRI is the imaging modality of choice in the assessment of both symptomatic and asymptomatic joints because it is sensitive in the detection of marrow content alteration. Technical characteristics of the MR unit such as magnetic field strength do not influence its accuracy in the detection of bone lesions. Investigation of both sides of the body is advisable in patients with unilateral symptoms (mainly in the hips) because of the high frequency

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■ FIGURE 70-2 Diaphyseal infarct. A, Coronal T1-weighted image of the femur shows a fat-containing lesion (arrow) with serpiginous contours located a few millimeters at a distance from the endosteal bone. B, Corresponding T2-weighted image shows the double-line sign (arrow).

generally do not contribute significantly to the assessment of ischemic bone lesions in the adult except in posttraumatic lesions in which the interface may be lacking at the early stage or when complications such as infection or tumor are suspected.

MANIFESTATIONS OF THE DISEASE Radiography

■ FIGURE 70-3 Femoral head osteonecrosis. Photograph of a resected femoral head with osteonecrosis shows the subchondral fracture (black arrow), the infarct (thin arrows), and surrounding marrow changes.

of bilateral involvement in systemic epiphyseal osteonecrosis (Fig. 70-4). T1-weighted spin-echo images should first be obtained because of their sensitivity to the presence of any marrow changes. Normal T1-weighted images may be sufficient to rule out ischemic marrow lesions in the vast majority of the cases. T2-weighted spin-echo or fat-saturated intermediate-weighted images are also necessary to accurately assess the articular cartilage and the subchondral bone plate. Contrast-enhanced MR images

Radiographs are insensitive to the detection of early infarcts because dead bone remains normal on radiographs and because the reactive interface that surrounds the infarct cannot be detected before it calcifies (see Fig. 70-4). With some nuances, post-traumatic, systemic, and overuse osteonecrosis show similar radiographic changes because they depict late reactive changes and subchondral bone plate fractures. Bone sclerosis that delineates the ischemic lesion is an early radiographic sign, although it occurs late in the disease course. Bone resorption is generally limited, and cystic changes generally indicate collapsed epiphyseal osteonecrosis. Periosteal bone reactions adjacent to diaphyseal or metaphyseal lesions are rarely present. The fracture of the subchondral bone plate is the hallmark of epiphyseal osteonecrosis. It can appear as frank and abrupt depression of the subchondral bone plate or as a crescentic radiolucent line parallel to the subchondral bone plate (Fig. 70-5; also see Fig. 70-4). These two features may coexist in the same epiphysis, although in different areas, probably owing to the joint biomechanics.

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■ FIGURE 70-4 Patient with right hip pain. A, Coronal T1-weighted image of the pelvis shows right hip joint effusion and ischemic lesions in both femoral heads (arrows) with right femoral neck marrow infiltration. The rim of low signal intensity is specific for ischemic lesions. B, Oblique radiograph of the right hip demonstrates fracture of the subchondral bone plate (arrow). C, Sagittal CT reformatted image shows the sclerotic interface. Subtle deformity of the anterior aspect of the femoral head with a small gas bubble is depicted (arrow). D, Sagittal fat-saturated intermediateweighted MR image better displays the subchondral trabecular bone fracture (arrow). The interface is no longer visible (well seen on the T1-weighted image). E, Sagittal CT reformatted image of the left hip shows the sclerotic interface but neither subchondral bone fracture nor femoral head deformity.

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■ FIGURE 70-5 A, Specific radiographic signs of osteonecrosis include epiphyseal collapse (arrow) and subchondral fracture (arrowheads). Note sclerosis of the trabecular bone within the humeral head. B, On a coronal T1-weighted spin-echo MR image, the entire lesion shows a homogeneous low signal intensity that lacks specificity. C, On the corresponding T2-weighted spin-echo MR image, the lesion shows low signal and the subchondral fracture (arrow) has high signal intensity. D, On the fat-saturated intermediate-weighted MR image, the lesion’s signal is intermediate and nonspecific. Abnormal epiphyseal contour is better depicted on the fat-saturated intermediate-weighted image than on the T1- and T2-weighted images. MR images of advanced epiphyseal osteonecrosis are generally more complex and less specific than the corresponding radiographs.

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Later on, radiographs accurately depict the abnormal epiphyseal shape and the altered bone structure (mixed bone sclerosis and resorption) of the involved epiphysis (see Fig. 70-5). Generally, the rate of development of secondary osteoarthritis parallels the degree of epiphyseal deformity: the more important the deformity, the more rapid the development of osteoarthritis.

Magnetic Resonance Imaging The MR pattern of ischemic necrosis merely depends on the marrow in which it develops and therefore on its origin, its topography, and its stage. The MR appearance of a yellow marrow infarct is that of an area of normal fatty signal intensity delineated by a rim of low signal intensity on T1-weighted images (see Fig. 70-4).5 At the early stage, the signal of an ischemic yellow marrow lesion remains normal on T1- and T2-weighted spin-echo images because of the persistence of mummified lipid-containing cells.5 Later, a rim of reactive tissue develops at the periphery of the lesions. On T2-weighted spinecho images, the peripheral rim shows the double-line sign with an outer low and inner high signal intensity line, in 65% to 85% of ischemic lesions.5 This double-line pattern probably results from chemical-shift misregistration artifact6 related to the fact that there is fat on both sides of a water-like equivalent component (the interface). In more advanced lesions, MRI depicts the fracture of the subchondral bone plate as a frank and abrupt depression of the subchondral bone plate or as a high signal intensity line on T2-weighted images extending under the subchondral bone plate (see Fig. 70-5). Occasionally, the fracture shows low signal intensity on T2-weighted images (Fig. 70-6). Contour depression usually occurs in the weight-bearing areas of the epiphysis (e.g., lateral aspect of femoral head) and subchondral cleft fracture usually appears in the non–weight-bearing areas (e.g., anterior aspect of the femoral head). In late stages of the disease, with marked epiphyseal deformity (which can be more conspicuous on radiographs than on MR images), signal intensity changes within the lesion are prominent and complex (without residual fat) whereas surrounding marrow may appear normal (see Figs. 70-5 and 70-6). Ischemic bone lesions developing in patients with marrow diseases including chronic anemia (sickle cell disease) or marrow infiltration (Gaucher’s disease) frequently show a nonspecific pattern of low signal intensity on T1-weighted images and high signal intensity on T2-weighted images, in other words, the bone marrow edema pattern (Fig. 70-7). Because yellow marrow has been replaced by abnormal cells, all infarcts develop in red marrow equivalent areas and demonstrate bone marrow edema, whatever the topography.7,8 After contrast injection, nonenhanced areas are visible within the lesion, the extent of which could depend on the chronicity of the lesion. The differential diagnosis between infected and noninfected marrow infarcts remains delicate, and the presence of soft tissue abscess could be the most important finding indicative of infection. At a later stage, several other MR patterns will develop that differ from those observed in yellow marrow infarcts.

Post-traumatic Osteonecrosis Post-traumatic epiphyseal osteonecrosis also shows the segmental pattern because it involves a fat-containing epiphysis (Fig. 70-8). Early changes after the fracture or joint dislocation are absent or include marrow and soft tissue changes directly related with the trauma. Several weeks after the trauma, a reactive interface surrounding an ischemic area appears at some distance from the fracture level. Fatsuppressed enhanced T1-weighted sequences could enable early depiction of the infarcted area before the development of the interface, although it remains difficult to differentiate normal fatty marrow from avascular fatty marrow.

Overuse Epiphyseal Osteonecrosis Overuse osteonecrosis generally involves a unique and subchondral area of a lower limb epiphysis. It is consistently symptomatic and is not associated with classic risk factors of systemic osteonecrosis. Additional infarcts at a distance from the involved joint are generally lacking. This pattern typically involves the medial femoral condyle of an elderly patient, but it can be observed in other lower limb epiphyses, including the femoral head, the medial tibial plateau, the talus, the metatarsal heads, as well as the lunate. In the femoral head, this pattern represents about 10% of symptomatic femoral head osteonecrosis. On T1-weighted spin-echo images, overuse osteonecrosis shows decreased signal intensity in a subchondral area, with normal overlying cartilage (Fig. 70-9). The lesion lacks well-delimited margins, and there is no residual fat within the lesions (Fig. 70-10; also see Fig. 70-9). On T2-weighted spin-echo images, the lesion has low signal intensity in the subchondral area corresponding to necrotic, avascular tissue with adjacent edema-like marrow changes (see Figs. 70-9 and 70-10).9 Subchondral bone plate fracture is usually present, but it usually appears as contour deformity without fluid-containing subchondral cleft, probably because the lesion involves a weight-bearing region of the joint. Spontaneous osteonecrosis of the knee is frequently associated with a medial meniscal lesion (frequently a radial tear or a root tear) and with subchondral impaction fractures.10 The demonstration with MRI of two different patterns of epiphyseal osteonecrosis—the systemic or segmental pattern and the edema-like pattern—suggests that epiphyseal osteonecrosis could represent a common end point of at least two different pathways.11,12 In the segmental pattern of systemic or post-traumatic origin, vascular failure of the bone marrow is the triggering event and leads to marrow infarct with possible subsequent epiphyseal fracture. In the diffuse pattern of overuse origin, mechanical failure of bone (trabecular bone fracture) or cartilage abrasion could lead to fracture of the subchondral bone plate with subsequent development of necrosis at the interface between the broken osteocartilaginous plate and the epiphysis.10,13

Multidetector Computed Tomography Multidetector computed tomography has not been widely used for the assessment of ischemic bone lesions.

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■ FIGURE 70-6 A, Coronal T1-weighted MR image of the pelvis of a woman with treated non-Hodgkin’s lymphoma and acute left hip pain demonstrates an ischemic lesion of the left femur (arrow). B, On a high-resolution coronal T1-weighted spin-echo MR image the subchondral lesion has both high and low signal intensity with subtle depression of the lateral aspect of the femoral head (arrow). The femoral neck marrow is infiltrated. C, On the corresponding T2-weighted spin-echo MR image, the ischemic lesion also shows variable signal intensity patterns. The interface is barely visible. Joint effusion is present. D, Coronal FDG-PET image shows mild hypermetabolic activity in the left capsule (arrow). E, Coronal T1-weighted MR image obtained several months later shows epiphyseal collapse. The lesion shows low signal intensity, and femoral neck marrow is normal.

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■ FIGURE 70-7 Systemic osteonecrosis in red marrow. On the sagittal (A) T1- and (B) T2-weighted MR images of the knee of a patient with sickle cell disease the whole marrow shows an abnormal low signal intensity. High signal intensity areas involve the center of the medullary cavity. These focal marrow alterations are not specific but are compatible with marrow infarcts. C, On the enhanced T1-weighted image the focal lesions show peripheral enhancement. Note associated joint effusion.

■ FIGURE 70-8 Post-traumatic osteonecrosis. A, Coronal T1-weighted spin-echo MR image of the right shoulder shows a neck fracture (arrow) and a humeral head infarct. B, On the corresponding T2-weighted spin-echo MR image, the fracture converts to high signal intensity and a double-line sign is visible at the periphery of the subchondral infarct (arrow).

A preliminary study suggested that MDCT could be valuable in the detection of the subchondral bone plate fracture.14 In our experience, MDCT could also contribute to the assessment of post-traumatic osteonecrosis treated with metallic hardware.

Nuclear Medicine Bone scintigraphy using technetium diphosphonate has been used for decades in the assessment of articular pain, mainly because of the relatively high negative predictive

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■ FIGURE 70-9 Spontaneous osteonecrosis of the knee. A, Sagittal T1-weighted MR image demonstrates ill-delimited infiltration of the subchondral marrow of the femoral condyle and deformity of the subchondral bone plate. B, Sagittal T2-weighted MR image shows a low signal intensity subchondral area (arrow). C, On the fat-saturated intermediate-weighted MR image, the lesion more clearly consists of a low signal subchondral area (arrow) and edema-like changes in the adjacent marrow. D, Sagittal reformatted image after CT arthrography also shows condyle deformity, subchondral sclerosis, and a normal overlying cartilage.

value in the setting of symptomatic epiphyseal osteonecrosis. Its use has progressively decreased because of the availability of MRI and the well-known limitations in the analysis of abnormal bone scans owing to its poor specificity and poor spatial resolution.

Positron Emission Tomography/ Computed Tomography There are limited literature data on the value of PET in ischemic bone lesions. Ischemic bone lesions could

remain occult on PET images except for slight marker accumulation in the joint capsule (see Fig. 70-6).

Classification Systems Over the years, numerous different classification systems have been developed to stage the disease, mainly for femoral head osteonecrosis. Although there is no standard unified classification system used by all investigators, there is general agreement on the fact that the presence of subchondral bone fracture represents a pivotal

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■ FIGURE 70-10

Overuse osteonecrosis of the ankle. A, Sagittal T1-weighted MR image of the ankle shows talar dome collapse and low signal in the talus. B, On the corresponding T2-weighted MR image, the subchondral area shows low signal intensity (arrow), suggestive of necrotic tissue. C, On the fat-saturated intermediate-weighted MR image the subchondral area (arrow) also shows low signal intensity. Adjacent marrow infiltration is better depicted. D, The enhanced T1-weighted MR image demonstrates marked enhancement in abnormal marrow except in the necrotic subchondral area (arrow).

position (generally at stage III, whatever the classification system). Ficat and Arlet originally developed a four-stage classification system based on radiographic changes and the functional exploration of bone (intraosseous phlebography and measurement of bone marrow pressure) (Table 70-2).15 Steinberg’s and Arco’s classification systems included MRI evaluation, allowing for quantification and topography of the epiphyseal lesion (Table 70-3).16 Mitchell’s classification system5 included signal pattern of

necrotic lesion (A: fat; B: blood; C: edema; D: fibrosis), but it showed limited utility because of the variability of signal intensity of the lesion within the same lesion.

Natural History of Ischemic Bone Lesions Metaphyseal marrow infarcts remain stable for life and do not lead to bone fracture. Infection and malignant transformation are two rare complications.

CHAPTER

TABLE 70-2 Ficat Staging System of Avascular Necrosis

of the Hip Stage

Clinical and Radiologic Findings

Stage I

Normal radiographs Decreased or increased uptake on bone scan No pain Increased medullary pressure Variable change in trabecular bone appearance (sclerosis, delimited area of sclerosis, cyst changes) but preserved femoral head shape Variable pain Specific changes on radiographs include collapse of subchondral bone and/or crescent sign due to subchondral bone fracture Pain Marked collapse of subchondral bone with preserved joint space Secondary osteoarthritis

Stage II

Stage III

Stage IV Stage V

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The natural history of epiphyseal infarcts is more controversial. Natural outcome of symptomatic femoral head osteonecrosis conservatively treated is usually poor, with a high frequency of irreversible collapse. Conversely, the natural history of asymptomatic femoral head lesions discovered fortuitously at systematic MRI performed in a patient with a high risk of necrosis showed a 15% to 20% risk of appearance of symptoms at 1-year follow-up, with the majority of lesions remaining silent at follow-up (see Fig. 70-11). Quantitative determination of the extent and location of uncollapsed femoral head infarcts on MR images enables one to estimate the fracture risk.17–19 Femoral heads in which the infarct is either small or involves a limited proportion of the weight-bearing area are less likely to collapse than those with large lesions. Signal changes in lesions could also indicate impending fractures because infarcts with fat-like signal intensity show a collapse-free survival much longer than those with heterogeneous signal.17

DIFFERENTIAL DIAGNOSIS

TABLE 70-3 Staging System Based on the Consensus of the Subcommittee of Nomenclature of the International Association on Bone Circulation and Bone Necrosis (ARCO) Stage

Clinical and Laboratory Findings

Stage 0

No symptoms Normal radiographs and MR images Osteonecrosis at histology Presence or absence of symptoms Normal radiographs Abnormal MR images Osteonecrosis at histology Symptoms Trabecular bone changes on radiographs without subchondral bone changes Preserved joint space Diagnostic MR findings Symptoms Variable trabecular bone changes with subchondral bone fracture (crescent sign and/or subchondral bone collapse) Preserved shape of femoral head and preserved joint space Subclassification based on extent of crescent, as follows: Stage IIIa: Crescent is less than 15% of the articular surface. Stage IIIb: Crescent is 15%-30% of the articular surface. Stage IIIc: Crescent is more than 30% of the articular surface. Symptoms Altered shape of femoral head with variable joint space Subclassification depends on the extent of collapsed surface, as follows: Stage IVa: Less than 15% of surface is collapsed. Stage IVb: Approximately 15%-30% of surface is collapsed. Stage IVc: More than 30% of surface is collapsed.

Stage I

Stage II

Stage III

Stage IV

The diagnosis of ischemic bone lesions heavily relies on medical imaging. The alert clinician may suspect the diagnosis when facing a patient with acute and spontaneous articular pain and risk factors for ischemic lesions. Clinical examination has little diagnostic value except for accurate localization of the involved area (knee pain due to femoral head osteonecrosis). Blood tests generally do not contribute to the diagnosis of the ischemic lesions, but it is of importance in the recognition of eventual underlying disease (e.g., anemia, hyperuricemia, intoxication).

Magnetic Resonance Imaging Metaphyseal infarcts should not be confused with enchondromas. On T1-weighted images, the signal of enchondromas is low with small fatty-like signal intensity septa trapped between cartilaginous nodules. Contours are lobulated and not serpiginous-like in infarcts. A noncollapsed epiphyseal infarct has a typical MR appearance. Rarely, a chronic subchondral fracture can show a transient similar pattern with a subchondral low signal intensity line and adjacent fatty marrow. Generally, this line that represents the healed trabecular bone fracture does not completely circumscribe a subchondral marrow area and is located very near to the subchondral bone plate. Collapsed epiphyseal osteonecrosis shows a more complex MR appearance and must be differentiated from other lesions, including subchondral cysts in osteoarthritis, sequelae of osteochondritis dissecans, fractures, and tumors. Analysis of the overlying cartilage is critical: cartilage adjacent to subchondral cysts is generally abnormal, whereas cartilage adjacent to recently collapsed osteonecrosis remains relatively preserved. In clinical practice, radiographs of advanced lesions are easier to understand than MR images. Overuse epiphyseal osteonecrosis must be differentiated from numerous conditions showing the bone marrow edema pattern because of their considerable differences

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■ FIGURE 70-11 A and B, Coronal T1-weighted spin-echo MR images of the right hip obtained in a patient 1 and 2 years after the onset of corticosteroid treatment show a femoral head infarct that does not collapse at follow-up.

in treatment and prognosis.20 Transient osteoporosis, transient bone marrow edema, and epiphyseal stress fracture are generally self-limited.6,10,21,22 On the contrary, osteoarthritis (Fig. 70-12) 23–25 and epiphyseal osteonecrosis17–19,26-28 are not reversible. Insufficiency stress fracture can be either reversible or irreversible. Careful analysis of the articular cartilage, the subchondral bone plate, and the subchondral marrow on high-resolution coronal and sagittal T2-weighted fast spin-echo images or fat-saturated intermediate-weighted fast spin-echo images is mandatory for this differential diagnosis. Several prognostic rules must be used: (1) abnormal cartilage indicates a clinically irreversible lesion, even if marrow edema resolves at follow-up MRI; (2) epiphyseal collapse indicates an irreversible lesion, whatever the marrow pattern at MRI; and (3) a fluid-like signal intensity line underneath the epiphyseal contour also suggests irreversibility. If the hyaline cartilage and the epiphyseal shape are preserved, and if there is no subchondral bone cleft, detection and determination of the size of low signal intensity subchondral areas help to differentiate osteonecrosis from transient lesions. In the hip and knee joints, a crescent-shaped low signal intensity area in the subchondral region with a thickness equal or superior to 4 mm on T2-weighted images suggests an irreversible lesion. In other situations, the outcome is uncertain, unless there are no other changes than edema, in which case the lesion is reversible.

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment Treatment efficacy of ischemic epiphyseal lesions remains controversial for many reasons: the lack of generally accepted diagnostic gold standard (intraosseous pressure determination, histology, MRI), the difficulty in classifying

the patients and in detecting subchondral bone plate fracture, the coexistence of different lesion patterns in the same studies, and the limited knowledge on the natural history of ischemic bone lesions. Despite the use of a large spectrum of drugs or conservative methods, medical management of symptomatic ischemic bone lesions has not proved to be effective in preventing or arresting the disease process.29 Pain control is usually achieved by nonsteroidal analgesics, and patients should be advised to use crutches or other supports to avoid weight bearing. Several drugs or other therapeutic methods can be applied, including diphosphonates, hyperbaric oxygen therapy, and magnetic field strength appliance.

Surgical Treatment Several surgical procedures have been tried with variable success, mainly in the femoral head. Core decompression of the hip with or without bone graft is the most common procedure currently used to treat the early stages of femoral head osteonecrosis, and it is effective in pain control. This procedure has been used for approximately three decades, but there are numerous publications analyzing its efficacy, and there is no consensus among investigators regarding either the indication for this procedure or its effect on the fate of the femoral head.30 In late stages, characterized by collapse, femoral head deformity, and secondary osteoarthritis, total hip arthroplasty is the most appropriate treatment, although several osteotomy procedures have been tried with variable success.1

SUMMARY OF MAGNETIC RESONANCE IMAGING FINDINGS Epiphyseal osteonecrosis may show two different patterns of involvement based on a T1-weighted spin-echo image, namely, the segmental and the diffuse patterns. The

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■ FIGURE 70-12 A, Coronal T1-weighted spin-echo MR image shows a low signal lesion in the left femoral head and neck. B, On the sagittal T1-weighted MR image, the subchondral marrow demonstrates low signal intensity, without clear margin. The sphericity of the femoral head is preserved. C, On the corresponding fat-saturated intermediate-weighted MR image, extensive cartilage abrasion (arrow) indicative of osteoarthritis is clearly demonstrated. In osteonecrosis, cartilage abrasion is secondary to epiphyseal deformity, which is lacking in the current case.

segmental pattern is observed in yellow marrow areas in patients with systemic osteonecrosis (with known risk factors for marrow infarcts) (see Fig. 70-5). On T1-weighted spin-echo images, the segmental pattern is defined by the presence of a well-demarcated lesion with necrotic tissue of variable signal intensity, generally including some high signal intensity areas in the subchondral lesion. Specific MRI features include the reactive interface and the subchondral bone fracture. The reactive interface shows the same MR appearance as in marrow infarcts, but it is frequently blurred by adjacent reactive changes.31 The signal intensity of the necrotic tissue is either equivalent to that of fat or is low on T1-, T2-, and enhanced T1-weighted images, reflecting the presence of mummified fat or

eosinophilic necrosis, respectively.32–34 Reactive changes that surround the lesion show low signal intensity on T1weighted images and intermediate to high signal intensity on T2-weighted images, depending on the balance among fibrous, sclerotic, edematous hemorrhagic and cellular components.32,33,35–37 These surrounding changes that are more frequent in symptomatic than in asymptomatic lesions35 probably indicate incipient epiphyseal fracture14,35,36,38,39 rather than extension of ischemia. Actually, in rapidly progressive and destructive osteoarthritis (see Fig. 70-11), in which cartilage destruction is the primary event, subchondral bone plate fracture and bone contusion could also lead to irreversible collapse of the epiphysis.23,40

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What the Referring Physician Needs to Know ■ ■ ■

Is there a bone lesion? Is it likely to be the cause of the pain? Is it an ischemic lesion or not?

■

If thought to be an ischemic lesion: Is there a fracture of the subchondral bone plate (staging)? ■ If there is no fracture, what is the risk for fracture (prognosis)? ■

REFERENCES 1. Mankin HJ. Nontraumatic necrosis of bone (osteonecrosis). N Engl J Med 1992; 326:1473–1479. 2. Ito H, Kaneda K, Matsuno T. Osteonecrosis of the femoral head. J Bone Joint Surg Br 1999; 81:969–974. 3. Glimcher MJ, Kenzora JE. Nicolas Andry award. The biology of osteonecrosis of the human femoral head and its clinical implications: 1. Tissue biology. Clin Orthop Relat Res 1979; (138):284–309. 4. Robbins SL, Cotran RS, Kumar V. Fluid and hemodynamic derangements. In Robbins SL, Cotran RS, Kumar V (eds). Pathologic Basis of Disease. Philadelphia, WB Saunders, 1984, pp 85–117. 5. Mitchell DG, Rao VM, Dalinka MK, et al. Femoral head avascular necrosis: correlation of MR imaging, radiographic staging, radionuclide imaging, and clinical findings. Radiology 1987; 162:709–715. 6. Vande Berg BC, Malghem J, Labaisse MA, et al. MR imaging of avascular necrosis and transient marrow edema of the femoral head. RadioGraphics 1993; 13:501–520. 7. Rao VM, Fishman M, Mitchell DG, et al. Painful sickle cell crisis: bone marrow patterns observed with MR imaging [published erratum appears in Radiology 1987;162(1 pt 1):289]. Radiology 1986; 161:211–215. 8. Vande Berg BC, Malghem J, Labaisse MA, et al. Apparent focal bone marrow ischemia in patients with marrow disorders: MR studies. J Comput Assist Tomogr 1993; 17:792–797. 9. Lecouvet FE, Vande Berg BC, Maldague BE, et al. Early irreversible osteonecrosis versus transient lesions of the femoral condyles: prognostic value of subchondral bone and marrow changes on MR imaging. AJR Am J Roentgenol 1998; 170:71–77. 10. Yamamoto T, Schneider R, Bullough PG. Subchondral insufficiency fracture of the femoral head: histopathologic correlation with MRI. Skeletal Radiol 2001; 30:247–254. 11. Mitchell DG. Using MR imaging to probe the pathophysiology of osteonecrosis. Radiology 1989; 171:25–26. 12. Vande Berg BC, Malghem J, Lecouvet FE, Maldague B. Magnetic resonance imaging and differential diagnosis of epiphyseal osteonecrosis. Semin Musculoskelet Radiol 2001; 5:57–67. 13. Glimcher MJ, Kenzora JE. The biology of osteonecrosis of the human femoral head and its clinical implications: III. Discussion of the etiology and genesis of the pathological sequelae; comments on treatment. Clin Orthop Relat Res 1979; (140):273–312. 14. Stevens K, Tao C, Lee SU, et al. Subchondral fractures in osteonecrosis of the femoral head: comparison of radiography, CT, and MR imaging. AJR Am J Roentgenol 2003; 180:363–368. 15. Ficat RP. Idiopathic bone necrosis of the femoral head. Early diagnosis and treatment. J Bone Joint Surg Br 1985; 67:3–9. 16. Steinberg ME, Hayken GD, Steinberg DR. A quantitative system for staging avascular necrosis. J Bone Joint Surg Br 1995; 77:34–41. 17. Shimizu K, Moriya H, Akita T, et al. Prediction of collapse with magnetic resonance imaging of avascular necrosis of the femoral head. J Bone Joint Surg Am 1994; 76:215–223. 18. Lafforgue P, Dahan E, Chagnaud C, et al. Early-stage avascular necrosis of the femoral head: MR imaging for prognosis in 31 cases with at least 2 years of follow-up. Radiology 1993; 187:199–204. 19. Takatori Y, Kokubo T, Ninomiya S, et al. Avascular necrosis of the femoral head: natural history and magnetic resonance imaging. J Bone Joint Surg Br 1993; 75:217–221. 20. Conway WF, Totty WG, McEnery KW. CT and MR imaging of the hip. Radiology 1996; 198:297–307.

21. Bloem JL. Transient osteoporosis of the hip: MR imaging. Radiology 1988; 167:753–755. 22. Wilson AJ, Murphy WA, Hardy DC, Totty WG. Transient osteoporosis: transient bone marrow edema? Radiology 1988; 167:757–760. 23. Boutry N, Paul C, Leroy X, et al. Rapidly destructive osteoarthritis of the hip: MR imaging findings. AJR Am J Roentgenol 2002; 179:657–663. 24. Sugano N, Ohzono K, Nishii T, et al. Early MRI findings of rapidly destructive coxopathy. Magn Reson Imaging 2001; 19:47–50. 25. Watanabe W, Itoi E, Yamada S. Early MRI findings of rapidly destructive coxarthrosis. Skeletal Radiol 2002; 31:35–38. 26. Turner DA, Templeton AC, Selzer PM, et al. Femoral capital osteonecrosis: MR finding of diffuse marrow abnormalities without focal lesions [see comments]. Radiology 1989; 171:135–140. 27. Mitchell DG, Kressel HY. MR imaging of early avascular necrosis [letter]. Radiology 1988; 169:281–282. 28. Thickman D, Axel L, Kressel HY, et al. Magnetic resonance imaging of avascular necrosis of the femoral head. Skeletal Radiol 1986; 15:133–140. 29. Lieberman JR, Berry DJ, Mont MA, et al. Osteonecrosis of the hip: management in the twenty-first century. J Bone Joint Surg Am 2002; 84:834–853. 30. Lieberman JR. Core decompression for osteonecrosis of the hip. Clin Orthop Relat Res 2004; (418):29–33. 31. Coleman BG, Kressel HY, Dalinka MK, et al. Radiographically negative avascular necrosis: detection with MR imaging. Radiology 1988; 168:525–528. 32. Lang P, Jergesen HE, Moseley ME, et al. Avascular necrosis of the femoral head: high-field-strength MR imaging with histologic correlation. Radiology 1988; 169:517–524. 33. Jergesen HE, Lang P, Moseley M, Genant HK. Histologic correlation in magnetic resonance imaging of femoral head osteonecrosis. Clin Orthop Relat Res 1990; (253):150–163. 34. Vande Berg BC, Malghem J, Labaisse MA, et al. Avascular necrosis of the hip: comparison of contrast-enhanced and nonenhanced MR imaging with histologic correlation. Work in progress. Radiology 1992; 182:445–450. 35. Koo KH, Ahn IO, Song HR, et al. Bone marrow edema and associated pain in early stage osteonecrosis of the femoral head: prospective study with serial MR images. Radiology 1999; 213:715–722. 36. Sakai T, Sugano N, Nishii T, et al. MR findings of necrotic lesions and the extralesional area of osteonecrosis of the femoral head. Skeletal Radiol 2000; 29:133–141. 37. Kubo T, Yamamoto T, Inoue S, et al. Histological findings of bone marrow edema pattern on MRI in osteonecrosis of the femoral head. J Orthop Sci 2000; 5:520–523. 38. Iida S, Harada Y, Shimizu K, et al. Correlation between bone marrow edema and collapse of the femoral head in steroidinduced osteonecrosis. AJR Am J Roentgenol 2000; 174:735–743. 39. Huang GS, Chan WP, Chang YC, et al. MR imaging of bone marrow edema and joint effusion in patients with osteonecrosis of the femoral head: relationship to pain. AJR Am J Roentgenol 2003; 181:545–549. 40. Ryu KN, Kim EJ, Yoo MC, et al. Ischemic necrosis of the entire femoral head and rapidly destructive hip disease: potential causative relationship. Skeletal Radiol 1997; 26:143–149. 41. Kopecky KK, Braunstein EM, Brandt KD, et al. Apparent avascular necrosis of the hip: appearance and spontaneous resolution of MR findings in renal allograft recipients. Radiology 1991; 179:523–527.

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Hemophilia and Related Disorders G. M. Allen, C. J. Fang, and D. J. Wilson

The term hemophilia is used to refer to a group of blood coagulation disorders that result from deficiencies in specific plasma clotting factors. The earliest descriptions of what appears to be hemophilia date to the 11th and 12th centuries. Jewish writings describe rabbinical rulings exempting male boys from circumcision if two previous brothers had died of bleeding after the procedure, suggesting an appreciation of the hereditary nature of the condition. The first modern description of hemophilia is attributed to Dr. John Conrad Otto, a physician in Philadelphia, who clearly appreciated the cardinal feature of hemophilia: an inherited tendency of males to bleed. In 1803 he published a treatise entitled “An Account of a Hemorrhagic Disposition Existing in Certain Families.” It is not until 1828 that the first use of the word “hemophilia” appears in an account of the condition written by Hopff (“Uber die Haemophilie oder die erbliche Anlage zu todlichen Blutungen”). Despite these historical descriptions of hemophilia dating back to ancient times and the early 19th and 20th century understanding of the symptoms and inheritance, the biochemical basis was only elucidated in the early 1950s. In the 19th century, the majority of physicians believed that bleeding in hemophilia was due to a structural abnormality in the blood vessels. The major breakthrough took place in 1937, when Patek and Taylor, at Harvard University, identified a fraction precipitated from normal plasma by dilution with mild acid. They showed this fraction would correct the clotting of hemophilic blood. In 1944, Pavlovsky, from Buenos Aires, described a case in which mutual correction of in-vitro clotting tests occurred when plasma from two different hemophiliacs was mixed. This finding was only explained in 1952 when Macfarlane and Biggs, at Oxford University, described the first case of hemophilia B, which they named Christmas disease after the surname of the 10-year-old boy they studied. They determined that the disease was due to deficiency of factor IX. It was subsequently appreciated

that many proteins were involved in the coagulation pathway. Names were assigned to the various coagulation factors by an International Committee in 1962: the factor missing in hemophilia A was subsequently termed factor VIII. A scheme for the interaction of the various factors in a coagulation pathway was independently devised by two groups shortly thereafter. Macfarlane called his scheme a “cascade” in an article in Nature in 1964, and Ratnoff used the term “waterfall” in a publication in the same year. In the musculoskeletal system, these disorders manifest in a spectrum of abnormalities affecting joints and soft tissues. Imaging plays an important part in detecting, staging, and monitoring disease. The severe damage that may occur in joints is apparent on plain films, whereas cross-sectional techniques are ideal for judging the extent and progress of soft tissue hemorrhage. Imaging may assist in locating the source of chronic pain. This patient group is also afflicted by conventional diseases unrelated to their hemophilia, and imaging is useful in excluding other causes of symptoms.

ETIOLOGY Of all causes of hemophilia, types A and B are most associated with intraosseous and intra-articular bleeding. Hemophilia A (classic hemophilia) results from a deficiency

KEY POINTS Hemophilia is a rare, sex-linked recessive but devastating disease. ■ It can be treated by replacing the relevant blood-clotting factors VIII and IX. ■ Radiologists can detect hemorrhage in joints and soft tissue. ■ Radiologists can detect the chronic diseases associated with the condition: arthropathy and pseudotumors. ■

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of factor VIII. Hemophilia B (Christmas disease) is due to a functional deficiency of plasma thromboplastin component (factor IX). These disorders are both X linked and therefore manifest clinically in men but are carried by women.

PREVALENCE AND EPIDEMIOLOGY Classic hemophilia occurs in 1 in 10,000 males in the United States. Christmas disease is rarer, affecting approximately 1 in 100,000 males. Although both forms are almost exclusive to males, reports exist of disease occurring in females. Twenty-five percent of hemophilia is due to spontaneous mutation. Acquired hemophilia due to antibodies to factor VIII is rare but severe and can affect women.

CLINICAL PRESENTATION Acute Hemarthrosis Between 75% to 90% of hemophilia patients will suffer from hemarthrosis. Adults are better able to protect their joints from trauma and, consequently, hemarthrosis is more common in young children and adolescents. Acute intra-articular bleeding will present as pain and dysfunction. Swelling and effusion will be apparent in the more superficial joints. When it is already known that the patient has a coagulation disorder and the clinical findings are clearcut, imaging is of limited immediate value. Because these patients are often in severe pain and are prone to worsening of the hemorrhage it is unwise to perform even the least invasive examination. In the acute phase the priority is resuscitation and coagulation control with blood factor replacement not radiologic investigation. Once the patient is stabilized, radiographs and other imaging may be useful to exclude fracture and evaluate preexisting arthropathy. Deep and impalpable joints such as the hip are difficult to examine, and ultrasonography is the best means of demonstrating or excluding intra-articular bleeding or effusion. This will also be the case in peripheral joints with small effusions or in obese patients. Joints related to the spine may require CT or MRI to detect involvement, although this would be an unusual occurrence. Hemarthrosis may be first detected by imaging when patients present with less specific complaints, including pain, anemia, and limitation of movement. Therefore, the imaging criterion for the diagnosis of blood in a joint should be known for all the standard techniques.

Recurrent Hemarthrosis Synovial thickening occurs as a result of repeated hemarthrosis. There seems to be a trigger that can turn reactive synovial thickening into an aggressive and progressively destructive synovitis leading to subsequent destruction of the articular surface. Repeated bleeding is the most potent cause, although the exact reason for its onset is not clear. Clinically the patient will suffer from progressive joint dysfunction, manifest by increased stiffness. In this stage of disease, imaging may be misleading in distinguishing free fluid from synovial thickening, especially if too much reliance is placed on MRI. Synovial thick-

ening and fluid are indistinguishable on plain films. The synovial tissue will have a rich blood supply, and although bone scintigraphy may reflect this on blood pool images it cannot reliably differentiate between the low-grade synovial irritation seen in virtually all joint effusions and significant synovial proliferation. Ultrasonography is arguably the most useful test. Fluid has minimal echoes whereas synovial thickening is echogenic with blood flow seen on spectral Doppler imaging. CT with intravenous contrast medium enhancement can be used, whereas plain CT may confuse the two intra-articular substances. Regrettably, the MRI appearances of fluid and synovial thickening are the same on T1- and T2-weighted images. The blood supply to synovium will become apparent after intravenous administration of gadolinium-diethylenetetramine-pentaacetic acid (Gd-DTPA), especially if fat suppression is employed on postcontrast T1-weighted images. It is tempting but inaccurate to rely on conventional MR signal changes to “exclude” synovitis. Intra-articular contrast would work with either CT or MRI, but fortunately there is a better alternative. If ultrasonography is available this is a less expensive and faster means to diagnose synovial fluid and thickening than either CT or MRI contrast studies.

Chronic Joint Pain and Dysfunction Whereas radiographs will give an overview of joint degeneration, showing a widened intercondylar notch, MRI is usually the investigation of choice when surgery is being contemplated. MRI will show hemorrhage at varying ages with hemosiderin deposition, which appears as a signal void (i.e., “black”) on all sequences. The differential diagnosis of such a patient’s arthropathy would be pigmented villonodular synovitis. Operating on a hemophilic patient is so hazardous and expensive that it would be wise to obtain as much data as possible by noninvasive techniques even when clinical circumstances may not warrant complex imaging in a similar patient with normal coagulation.

Acute Soft Tissue Hemorrhage Patients present with acute pain, swelling, and dysfunction. There may be secondary complications resulting from the enlargement of a hematoma. For example, there may be compression of adjacent nerves or vascular structures. In this phase of disease, acute hematomas or soft tissue collections can cause severe compression of a nerve or vessel such that urgent surgery will be considered. It may be argued that MRI should be the first and only investigation for the investigation of soft tissue hemorrhage and its complications. CT with ultrasonography should only be employed when MRI is not available (Fig. 71-1).

Recurrent Soft Tissue Hemorrhage For the reasons listed earlier, ultrasonography or MRI is the best means of showing a recurrent soft tissue hemorrhage.

Chronic Mass Lesion/Pseudotumor Pseudotumors are a rare complication of hemophilia, occurring in 1% to 2% of patients with severe hemophilia

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Exceptions to this rule would be in a penetrating injury or fracture when the same protocols that would be considered for those with normal coagulation should be applied.

Fracture When the nature of the injury might have caused a fracture, then radiographs are always indicated. CT may be used to support the diagnosis and further characterize complex fractures if surgery is necessary.

PATHOPHYSIOLOGY

■ FIGURE 71-1

Soft tissue hemorrhage. A, Clinical photograph depicting soft tissue swelling due to a hematoma compressing the radial nerve resulting in paresthesia (as demarcated by the ink markings). B, Axial T1-weighted MR image through the forearm shows an acute hematoma.

(clotting factor level 23 mm in women Spine Increased anteroposterior and transverse diameter without corresponding increase in height Increased height of intervertebral disc space in lumbar spine Extensive anterior and lateral osteophytes Thoracic kyphosis Scalloping of posterior vertebral bodies in lumbar spine Peripheral Joints Early changes include widening of joint spaces Advanced stage manifested by joint space narrowing, subchondral cyst formation, sclerosis, and osteophytosis resembling degenerative disease Distinguished from degenerative disease by involvement of sites not commonly affected by degenerative disease and presence of prominent bony excrescences Bony Excrescences At sites of tendon and ligament attachments

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DIFFERENTIAL DIAGNOSIS Acromegaly A combination of radiographic findings would be sufficient to suggest a diagnosis of acromegaly. Some of these radiographic findings when viewed individually are not specific to acromegaly and may be seen in other disorders. For example, widened phalangeal tufts are seen in patients working in heavy manual labor.14 Scalloped vertebral bodies can result from increased intraspinal pressure from intraspinal neoplasm, cyst, or syringomyelia or from dural weakness predisposing vertebral bodies to deformity, as may be seen in Marfan syndrome, neurofibromatosis, and Ehlers-Danlos syndrome.15 The joint space narrowing, osteophytosis, cyst formation, and sclerosis seen in late stages of acromegalic arthropathy resemble those in degenerative disease. Soft tissue enlargement and peripheral neuropathy such as carpal tunnel syndrome may be seen in hypothyroidism secondary to myxedematous tissue. A prognathic jaw can also be seen in hypopituitarism. One disorder that has been reported to have similar clinical and radiographic findings to acromegaly is familial pachydermoperiostosis, characterized by abundant periosteal new bone formation, enlargement of the distal extremities with spade-like hands, squaring of the phalanges, thickening of the skin, coarsening of facial features, and prominent paranasal sinuses.16 However, unlike acromegaly, there are no signs of endochondral bone formation. The sella turcica is normal, the phalangeal tufts are not widened, the mandibular size and angle are normal, and the articular joint spaces are preserved. In pachydermoperiostosis, the growth hormone level is normal. Another condition that can mimic acromegaly is longterm therapy with phenytoin (Dilantin), which can lead to development of thickened calvaria, thickened heel pad, and coarse facies.13,17

Pituitary Gigantism Most children who present with gigantism do not have pituitary gigantism. There are many causes of tall stature that should be excluded, including chromosomal causes of tall structure (Sotos, Weaver, Marshall-Smith, and XYY syndromes), precocious puberty, hyperthyroidism, Marfan syndrome, and Beckwith-Wiedemann syndrome. Other associated disorders should be considered as well, such as McCune-Albright syndrome, multiple endocrine neoplasia type 1, neurofibromatosis, tuberous sclerosis, and Carney complex.

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treatment can also be considered as a primary therapy in patients who are not surgical candidates due to unacceptable risks, patients who refuse surgery, and patients with adenomas that are surgically inaccessible. The medical treatments available include pharmacologic agents such as somatostatin analogues, dopamine agonists, and GH receptor antagonists. The somatostatin analogues commonly used are octreotide and lanreotide.18 The somatostatin analogues are effective in lowering the serum GH level, reducing the tumor size, and improving the clinical manifestations of acromegaly. The dopamine agonists have limited effectiveness in the treatment of acromegaly. They are generally less effective than the somatostatin analogues. An exception is with tumors that co-secrete prolactin, which have a better response rate to dopamine agonists than to the somatostatin analogues. The dopamine agonists include bromocriptine and cabergoline, with the latter being somewhat more effective. These dopamine agonist agents have the advantage over other treatments in that they are taken orally. A novel pharmacologic option when there is no response to the just-listed medical treatments is a GH receptor antagonist such as pegvisomant. This mutated GH molecule blocks the native hormone from binding and is reported to be very effective in lowering the IGF-1 level. Long-term studies are still needed, and this antagonist has not been tested in children.

Surgical Treatment Surgery is the first-line therapy for acromegaly in most patients. The treatment of choice is transsphenoidal surgical resection if the pituitary adenoma is small or large but still resectable. If the adenoma is very large and not completely resectable or if it is not entirely accessible surgically, as much tissue should be surgically removed as possible to facilitate other treatment options. A remission rate of 80% to 85% can be expected for microadenomas, with a rate of 50% to 65% for macroadenomas. Surgery is

What the Referring Physician Needs to Know ■

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SYNOPSIS OF TREATMENT OPTIONS Medical Treatment Surgery is usually the first-line therapy for most patients because pituitary adenoma is the most common cause of GH hypersecretion and often can be resected. If surgery fails to sufficiently reduce the GH and IGF-1 levels to normal, medical treatment is usually the first choice for secondary treatment for residual disease. Medical

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Combination of radiographic findings would be sufficient to suggest diagnosis of acromegaly; however, some findings when viewed individually are not specific to acromegaly and may be seen in other disorders. Most gigantism is not pituitary gigantism. One must exclude other causes of tall stature. After laboratory confirmation, MRI of the sella turcica should be performed to evaluate for pituitary tumor. If MRI is negative, CT of the chest, abdomen, and pelvis is done to look for ectopic GH/GHRH secretion by tumors in the lung, adrenal, pancreas, and ovaries. Transsphenoidal surgical resection of pituitary adenoma is the first choice of treatment. Medical treatments are available if surgery fails to induce complete remission or if surgery is contraindicated. Radiation treatment is generally reserved for refractory cases.

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as safe in children as it is for adults. The major morbidity of surgery is permanent diabetes insipidus. Radiation treatment is generally reserved for refractory cases or used as an adjuvant when surgery is contraindicated. Adenoma growth is arrested, but the decline in GH secretion and the clinical improvement is very slow. More than half of the patients eventually develop panhypopituitarism. And cranial irradiation in children may cause learning disabilities and emotional changes.

SUGGESTED READINGS Colao A, Marzullo P, Vallone G, et al. Reversibility of joint thickening in acromegalic patients: An ultrasonography study. J Clin Endocrinol Metab 1998; 83:2121–2125. Melmed S. Acromegaly. N Engl J Med 1990; 322:966–977. Molitch ME. Clinical manifestations of acromegaly. Endocrinol Metab Clin North Am 1992; 21:597–614.

REFERENCES 1. Melmed S. Acromegaly. N Engl J Med 1990; 322:966–977. 2. Colao A, Marzullo P, Vallone G, et al. Reversibility of joint thickening in acromegalic patients: An ultrasonography study. J Clin Endocrinol Metab 1998; 83:2121–2125. 3. Gonticas SK, Ikkos DG, Stergiou LH. Evaluation of the diagnostic value of heel-pad thickness in acromegaly. Radiology 1969; 92:304–307. 4. Steinbach HL, Russell W. Measurement of the heel pad as an aid to diagnosis of acromegaly. Radiology 1964; 82:418–423. 5. Kho KM, Wright AD, Doyle FH. Heel pad thickness in acromegaly. Br J Radiol 1970; 43:119–125. 6. Anton HC. Hand measurements in acromegaly. Clin Radiol 1972; 23:445–450. 7. Lin SR, Lee KF. Relative value of some radiographic measurements of the hand in the diagnosis of acromegaly. Invest Radiol 1971; 6:426–431. 8. Littlejohn GO, Urowitz MB, Smythe HA, Keystone EC. Radiographic features of the hand in diffuse idiopathic skeletal hyperostosis (DISH): comparison with normal subjects and acromegalic patients. Radiology 1981; 140:623–629. 9. Kleinberg DL, Young IS, Kuperman HS. The sesamoid index: an aid in the diagnosis of acromegaly. Ann Intern Med 1966; 64:1075–1078. 10. Epstein N, Whelan M, Benjamin V. Acromegaly and spinal stenosis. J Neurosurg 1982; 56:145–147. 11. Kumar R. The vertebral body: radiographic configurations in various congenital and acquired disorders. RadioGraphics 1988; 8:469–484. 12. Detenbeck LC, Tressler HA, O’Duffy JD, Randall RV. Peripheral joint manifestations of acromegaly. Clin Orthop Relat Res 1973; 91:119–127. 13. Kattan KR. Thickening of the heel-pad associated with long-term Dilantin therapy. AJR Am J Roentgenol 1975; 124:52–56. 14. Poznanski AK. The Hand in Radiologic Diagnosis. Philadelphia, WB Saunders, 1974, pp 510–513. 15. Mitchell GE, Lourie H, Berne AS. The various causes of scalloped vertebrae with notes on their pathogenesis. Radiology 1967; 89:67–74. 16. Harbison JB, Nice CM Jr. Familial pachydermoperiostosis presenting as an acromegaly-like syndrome. AJR Am J Roentgenol 1971; 112:532–536. 17. Lefebvre EB, Haining RG, Labbe RF. Coarse facies, calvarial thickening and hyperphosphatasia associated with long-term anticonvulsant therapy. N Engl J Med 1972; 286:1301–1302. 18. Drange M, Melmed S. Long-acting lanreotide induces clinical and biochemical remission of acromegaly caused by disseminated growth hormone-releasing hormone-secreting carcinoid. J Clin Endocrinol Metab 1998; 83:3104–3109.

Hypopituitarism ETIOLOGY Hypopituitarism refers to a condition in which there is partial or complete insufficiency of pituitary hormone secretion. The most common pituitary hormone deficiency, growth hormone deficiency (GHD), is the main focus of this section. The cause of hypopituitarism in pediatric patients can be divided into two categories: congenital and acquired. Congenital causes include central nervous system tumors (e.g., craniopharyngioma, metastatic carcinoma, pituitary adenoma, pituitary carcinoma, meningioma), central nervous system malformations, septo-optic dysplasia, pituitary hypoplasia or aplasia, and empty sella syndrome. Acquired causes include cranial irradiation, infection (e.g., tuberculosis, fungal, abscess), infiltrative diseases (e.g., sarcoidosis, histiocytosis X, hemochromatosis, lymphocytic hypophysitis, and leukemia), trauma, and hypoxic insult.1 In adults, most patients have pituitary disease caused by a pituitary tumor, surgery, or radiation therapy for the tumor. Other causes include trauma and infiltrative diseases (e.g., sarcoidosis, tuberculosis, histiocytosis X, hemochromatosis, and lymphocytic hypophysitis).

PREVALENCE AND EPIDEMIOLOGY In the United States, the incidence of hypopituitarism with multiple pituitary hormone deficiency is very rare in childhood, with possibly less than 3 cases per million people per year. However, GHD is more frequent and has a prevalence of approximately 1 in 4000 children.2 The prevalence of adult-onset GHD in the United States is not known.

CLINICAL PRESENTATION Clinical manifestations of GHD in children are summarized in Table 78-3.1–4

PATHOPHYSIOLOGY Anatomy The pituitary gland (hypophysis) lies in the sella turcica, where it is suspended from the hypothalamus by the

KEY POINTS The radiographic manifestation for hypopituitarism is nonspecific. ■ The skeletal findings in children include delayed skeletal growth and maturation, delayed appearance and growth of ossification centers as well as delayed fusion and disappearance of the ossification center, delayed dental eruptions, and osteopenia. ■ The skeletal findings in adults are nonspecific and mainly consist of osteoporosis with increased incidence of fracture. ■

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TABLE 78-3 Clinical Presentation of Growth Hormone Deficiency GHD in Children

Adult-Onset GHD

Short stature Low growth velocity Characteristic facies with frontal bossing, flattened nasal bridge, and prominent forehead Delayed dental eruption Delayed skeletal maturation and bone age Increased weight-to-height ratio Abnormal distribution of fat with excess subcutaneous fat and central obesity Poor hair and nail growth Delayed puberty and sexual maturity

Reduced bone mineral density Increased risk of osteoporotic bone fractures Reduced muscle strength Altered body composition with increased fat and central obesity and decreased muscle volume Impaired cardiac function High-risk cardiovascular profile (elevated low density lipoprotein cholesterol levels, high body fat, insulin resistance) Impaired renal functions Decreased exercise capacity Emotional and psychosocial disturbances

infundibular stalk. It is regulated by neuropeptide-releasing and release-inhibiting hormones produced in the hypothalamus and delivered via the infundibular stalk. The pituitary gland comprises two regions. The posterior gland is the neurohypophysis, which is an extension of the hypothalamus and releases vasopressin and oxytocin into the blood. The anterior gland is the adenohypophysis, which is a pharyngeal derivative that secretes six trophic hormones, including GH, prolactin, adrenocorticotropic hormone, thyroid-stimulating hormone, follicle-stimulating hormone, and luteinizing hormone.

Pathology Any disease process affecting the pituitary gland or infundibular stalk can affect the pituitary’s secretion of growth hormones along with other pituitary hormones. Trauma causing transection of the infundibular stalk will prevent GH-releasing hormone and other neuropeptide-releasing hormones produced in the hypothalamus from reaching the pituitary gland. Cranial irradiation can lead to panhypopituitarism. Infiltrative diseases, brain tumors affecting the pituitary gland, and pituitary aplasia or hypoplasia can all lead to hypopituitarism.

IMAGING TECHNIQUES Techniques and Relevant Aspects Radiography is helpful in determining bone age. Skeletal maturation is a useful diagnostic tool to determine the status of GH secretion because it more accurately reflects an individual’s growth and development. Weight and height are less reliable because they vary with familial characteristics, nutritional state, and fluctuations in health. Anteroposterior radiographs of the left hand and wrist, or knee or ankle in children younger than 1 year old, are used to evaluate the progress of epiphyseal ossification by comparing the results with age- and sex-matched reference ranges. A lateral skull radiograph is occasionally obtained to evaluate the sella turcica. However, with the high falsenegative rate of plain skull radiographic findings, MRI is the procedure of choice to exclude an intracranial mass or developmental abnormalities arising from the pituitary gland. In cases in which MRI of the pituitary gland cannot be done, CT should be performed.

Pros and Cons Magnetic resonance imaging has several advantages over CT in the evaluation of the pituitary gland, including the ability to display pathologic lesions in multiple planes and the ability to provide more detailed information on the structures surrounding the pituitary gland, such as the optic chiasm and cavernous sinuses. On the other hand, CT has the advantage of providing better visualization of the bony septa in the sphenoidal sinus, which may be important if a transsphenoidal surgical approach is being considered for treatment of a tumor.

MANIFESTATIONS OF THE DISEASE Radiography The skeletal manifestation of GHD is delayed skeletal growth and maturation. Hypopituitarism has been reported to affect the linear growth and stature of the bones more than the skeletal maturation.5 There is a delay in the appearance and growth of ossification centers. Their fusion and disappearance are also delayed. Absence of growth lines in tubular bones may be observed. The bones may be osteoporotic if GHD is not treated. There is also an increased incidence of slipped capital femoral epiphysis.6 The findings on the skull radiograph may include a small pituitary fossa or empty sella turcica. Alternatively, an enlarged or eroded sella turcica may be seen, suggesting the possible presence of a tumor. Suprasellar calcifications may suggest a craniopharyngioma. Other findings on the skull radiograph that may be noted include delayed closure of sutures and delayed dental eruptions. The skeletal finding in adult-onset GHD is nonspecific and mainly characterized by osteoporosis due to reduced bone mineral density with an increased rate of fracture.3 Spine radiographs may demonstrate reduced vertebral body height due to vertebral compression fracture and osteoporosis (Table 78-4).

DIFFERENTIAL DIAGNOSIS Pituitary dwarfism accounts for less than 10% of short stature. Other conditions to consider in the differential diagnosis are listed in Table 78-5.

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TABLE 78-4 Radiographic Findings of Growth

Hormone Deficiency GHD in Children

Adult-Onset GHD

Delayed skeletal growth and maturation

Nonspecific, mainly characterized by osteopenia with increased incidence of fracture Reduced vertebral body height due to vertebral compression fractures and osteopenia

Delay in appearance and growth of ossification centers Delay in fusion and disappearance of ossification centers Delayed closure of sutures and dental eruptions Osteopenia

well. Response to GH therapy should be monitored every 3 to 6 months by height measurements and occasionally by bone age determination.

Surgical Treatment Surgery may be needed if a brain tumor or congenital abnormality is detected.

SUGGESTED READINGS Carroll PV, Christ ER, Bengtsson BA, et al. Growth hormone deficiency in adulthood and the effects of growth hormone replacement: a review. Growth Hormone Research Society Scientific Committee. J Clin Endocrinol Metab 1998; 83:382–395. Preece MA. Diagnosis and treatment of children with growth hormone deficiency. Clin Endocrinol Metab 1982; 11:1–24.

TABLE 78-5 Differential Diagnosis of Short Stature Familial short stature Hypothyroidism Turner syndrome Noonan syndrome Laron syndrome Prader-Willi syndrome Osteochondrodysplasia Intrauterine infection causing growth retardation Child abuse and neglect with failure to thrive or psychosocial dwarfism Malabsorption Inflammatory bowel disease Hypercortisolism Diabetes Renal tubular acidosis Short stature accompanying systemic disease

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment Growth hormone deficiency can be effectively treated with GH replacement therapy. GH replacement therapy can reverse many of the clinical manifestations of GHD, such as stimulating linear growth and skeletal maturation in children if treated promptly, increasing the bone mineral density, improving muscle strength, improving exercise capacity, and improving the psychological wellbeing in adults. For GH replacement to be effective, other pituitary deficiencies should be detected and treated as

What the Referring Physician Needs to Know ■

■ ■

There is a broad differential diagnosis for short stature. Pituitary etiology accounts for less than 10% of short stature. Other causes must be excluded. Many of the clinical manifestations of GHD can be reversed with GH replacement therapy if treated promptly. In order for GH replacement to be effective, other pituitary deficiencies should be detected and treated.

REFERENCES 1. Edeiken J, Murray D, Karasick D (eds). Edeiken’s Roentgen Diagnosis of Diseases of Bone, 4th ed. Baltimore, Williams & Wilkins, 1990, vol 1, pp 1431–1460. 2. Preece MA. Diagnosis and treatment of children with growth hormone deficiency. Clin Endocrinol Metab 1982; 11:1–24. 3. Carroll PV, Christ ER, Bengtsson BA, et al. Growth hormone deficiency in adulthood and the effects of growth hormone replacement: a review. Growth Hormone Research Society Scientific Committee. J Clin Endocrinol Metab 1998; 83:382–395. 4. Shalet SM, Toogood A, Rahim A. The diagnosis of growth hormone deficiency in children and adults. Endocr Rev 1998; 19:202–223. 5. Hernandez RJ, Poznanski AW, Hopwood NJ. Size and skeletal maturation of the hand in children with hypothyroidism and hypopituitarism. AJR Am J Roentgenol 1979; 133:405–408. 6. Rappaport EB, Fife D. Slipped capital femoral epiphysis in growth hormone-deficient patients. Am J Dis Child 1985; 139:396–399.

Hyperthyroidism ETIOLOGY Hyperthyroidism refers to a condition in which the thyroid hormones, specifically free thyroxine (T4) and triiodothyronine (T3), are elevated and lead to a clinical state of thyrotoxicosis. The most common causes of hyperthyroidism are toxic diffuse goiter (Graves disease), toxic multinodular goiter (Plummer disease), and solitary toxic adenoma. Less common causes include thyroiditis, pituitary neoplasm with hypersecretion of thyroid-stimulating hormone, and thyroid carcinoma.1,2

PREVALENCE AND EPIDEMIOLOGY Because Graves disease is the most common cause of hyperthyroidism in the United States, the prevalence of hyperthyroidism can be approximated to the prevalence of Graves disease. In adults, Graves disease contributes to

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KEY POINTS Musculoskeletal abnormalities of hyperthyroidism: ● Accelerated skeletal maturation ● Osteopenia from increased bone turnover ● Myopathy ● Thyroid acropachy ■ Clinical and radiographic features of thyroid acropachy: ● Exophthalmos ● Soft tissue swelling ● Pretibial myxedema ● Clubbing ● Periostitis—usually seen involving the metacarpal or metatarsal bones and proximal phalanges bilaterally, predominantly on the radial sides ■

60% to 80% of hyperthyroidism and occurs in up to 2% of women but it is about one tenth as frequent in men.3,4 In children, Graves disease accounts for more than 95% of hyperthyroidism. The prevalence of hyperthyroidism in children is 0.02%, which is less than 5% of all cases of hyperthyroidism. Hyperthyroidism is quite rare in infancy and is usually seen when the mother is hyperthyroid at the time of delivery. If the mother has had medical treatment or surgical thyroidectomy during gestation, the infant may be born hyperthyroid, even if the mother reverts back to a euthyroid state during the remainder of the pregnancy.

CLINICAL PRESENTATION The clinical symptoms of hyperthyroidism include weight loss, heat intolerance, tachycardia with episodes of palpitations, diarrhea, arthralgias, muscle weakness, muscle cramps, anxiety, insomnia, and inability to concentrate.1,5 Physical examination may demonstrate an enlarged thyroid; moist, warm, and smooth skin; onycholysis; fine hair; stare and lid lag, tachycardia or atrial fibrillation; fine resting finger tremors; hyperreflexia; and proximal greater than distal muscle weakness (Table 78-6). Hyperthyroidism is also associated with syndromes such as polyostotic fibrous dysplasia (McCune-Albright syndrome) and ovarian dermoids.

PATHOPHYSIOLOGY Anatomy The thyroid gland is located in the neck anterior to the trachea and between the cricoid cartilage and suprasternal notch. It usually consists of two lobes, with the left and right lobes extending around the trachea and esophagus to as far as the carotid sheath on each side in the neck. The isthmus connects the left and right thyroid lobes and lies just anterior to the trachea. A pyramidal lobe is occasionally seen extending superiorly from the middle of the isthmus. This important endocrine gland contains follicular cells that produce thyroxine, which regulates metabolism, and parafollicular cells, that produce calcitonin, which regulates calcium balance. The thyroid gland is part of the hypo-

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TABLE 78-6 Clinical Presentation of Hyperthyroidism Heat intolerance Tachycardia, palpitations, atrial fibrillation Weight loss Muscle weakness (proximal > distal) and cramps Insomnia Inability to concentrate Fine resting finger tremors Fine hair, warm and smooth skin Stare and lid lag Hyperreflexia Arthralgia Palpable enlarged thyroid

thalamus-pituitary-thyroid axis and is closely regulated by thyrotropin-releasing hormone from the hypothalamus and thyroid-stimulating hormone from the pituitary gland.

Pathology In hyperthyroid patients, the laboratory findings of hyperphosphatemia, hypercalcemia, elevated alkaline phosphatase, and hypercalciuria suggest increased bone turnover with a negative calcium balance. The increased bone turnover and bone loss can be seen radiographically as osteoporosis with increased spontaneous fracture rates in the spine, pelvis, femoral neck, long bones, hands, and feet. In the spine, osteoporosis causes rarefaction of the midportion of the vertebral body with exaggerated biconcave deformity of the anterior and posterior margins, giving a “fish” vertebrae appearance. The spine can also be characterized by vertebral compression fractures and kyphosis. In the hands and feet, cortical striations have been observed in the phalanges due to hyperosteoclastosis in the cortical bone that results in longitudinal splitting of the cortex, giving it a striated appearance.6 Interestingly, the cancellous bone is relatively spared. Osteoblastic foci are also seen more prominent in the cortical bone than the trabecular bone, suggesting the presence of both increased bone resorption and bone formation in the cortex. However, in the setting of osteoporosis and reduced bone mass, osteoclastic activity is more dominant. Hyperthyroidism is rare in children, and its course is usually rapid without any bone abnormality. In long-standing hyperthyroidism, the most notable effect on the bones is acceleration of skeletal maturation, premature craniosynostosis, and decreased bone mass.7 In the hand, the second metacarpal bone is the most sensitive to bone loss. In addition to osseous changes in hyperthyroid patients, the muscles are commonly affected in hyperthyroidism. Muscle weakness, cramps, tenderness, and wasting have been observed, more commonly involving the proximal muscles of the extremities than the distal muscles.8

IMAGING TECHNIQUES Whereas ultrasonography and nuclear medicine thyroid scan can be used to evaluate the thyroid gland, skeletal manifestations of hyperthyroidism are often adequately evaluated with radiography.

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MANIFESTATIONS OF THE DISEASE Radiography The main radiographic findings of hyperthyroidism include accelerated skeletal maturation, osteoporosis from increased bone turnover, and thyroid acropachy. The degree of acceleration of skeletal maturation depends on the timing and degree of the hormonal imbalance. Long exposures lead to faster linear growth and maturation. Neonatal and infantile forms manifest as premature craniosynostosis and brachydactyly. Older children can develop myopathy with cardiomegaly seen on chest radiography from cardiomyopathy. Because of marked acceleration of maturation, there is early epiphyseal fusion and premature calcification of costochondral cartilage in adolescents. Mothers with severe thyrotoxicosis, particularly in the third trimester, can also affect their children with these changes. Acceleration of bone turnover from stimulation of osteoblastic and osteoclastic activity can result in net osteoporosis, which is radiographically more detectable if the patient is hyperthyroid for more than 5 years. Skeletal changes are less apparent in patients younger than age 50 and more common in older men and postmenopausal women. The accelerated osteoporosis transcends that which is expected after menopause. Hyperthyroidism can demonstrate intracortical striations of tubular bones, showing evidence of rapid bone turnover, most pronounced in the metacarpals. Cortical striations can also be seen in acromegaly and hyperparathyroidism. Hyperthyroid osteoporosis is best observed at the distal femurs and shows a more diffuse distribution, including the extremities, cranium, and pelvis. Like other forms of osteoporosis, spinous changes include loss of vertebral body height due to vertebral compression fractures and biconcave “fish mouth” vertebrae, which are more pronounced in the thoracic and lumbar vertebrae. Focal rarefaction of bone may be seen throughout the skeleton and may be confused with multiple myeloma, especially when it is seen in the skull (Fig. 78-4). Thyroid acropachy (hyperthyroid osteoarthropathy) is detected in approximately 1% of patients with Graves disease, although the incidence is likely higher because it is asymptomatic and therefore underdiagnosed.9 Although the etiology is unknown, it is usually seen in patients after treatment for hyperthyroidism who had radioactive iodine ablation or thyroidectomy. The patient may be euthyroid, hypothyroid, or hyperthyroid at the time of radiographic presentation. Although thyroid acropachy can occur at any age, it is more common in adults and is relatively rare in children. The clinical symptoms include soft tissue swelling of the extremities, clubbing of the fingers (Fig. 78-5) and toes, pretibial myxedema, and exophthalmos.10 Erythema of fingers and toes may also accompany the soft tissue swelling. There is no associated pain. Radiographically, thyroid acropachy is characterized by diaphyseal periosteal reaction that is most pronounced in the metacarpal, metatarsal, proximal, and middle phalanges and less common in other long tubular bones. Periostitis is noted beginning as early as 18 months after treatment

■ FIGURE 78-4 Hyperthyroid osteoporosis in the spine. There are biconcave “fish mouth” deformities of the lumbar vertebral bodies in this osteoporotic patient. (From Kumar R. The vertebral body: radiographic configurations in various congenital and acquired disorders. RadioGraphics 1988; 8:472.)

and does not depend on the current thyroid state of the patient. Periostitis of the bone initially results in a solid and dense appearance with lacy and feathery margins. In later stages, a thick, smooth, periosteal cloaking is formed. The periostitis in thyroid acropachy is usually asymmetric and more prominent in the radial sides of the bones.Acropachy is seen only with patients with a history of Graves disease treated with thyroidectomy and radioactive iodine and is not noted in patients treated with antithyroid drugs (e.g., propylthiouracil) alone.11

DIFFERENTIAL DIAGNOSIS The differential diagnosis for periostitis involving multiple bones is long (Table 78-7). The periostitis seen in hypertrophic pulmonary osteoarthropathy (HPO) is most commonly seen symmetrically in the tibia, fibula, radius, and ulna. Periostitis involving the hands and feet as in thyroid acropachy is very unusual for HPO. In addition, the feathery pattern of periostitis seen in thyroid acropachy is not seen in HPO. Pachydermoperiostitis, also known as primary hypertrophic osteoarthropathy, also has periosteal bone formation that is generally seen symmetrically in the tibia, fibula, radius, and ulna. Fluorosis affects the axial skeleton and long bones to a greater extent than thyroid acropachy. Phalangeal

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■ FIGURE 78-5 Thyroid acropachy in the hand. Fluffy diaphyseal periosteal reaction is most pronounced in the metacarpal bones in the hand and more prominent on the radial sides of the bones. Soft tissue swelling and clubbing of the fingers are also present (arrows). (From Resnick D. Thyroid disorders. In Resnick D. Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, 2002, vol 3, p 2031.)

A

TABLE 78-7 Differential Diagnosis of Hyperthyroidism Differential Diagnosis of Periosteal Reaction of Multiple Bones Thyroid acropachy Hypertrophic pulmonary osteoarthropathy Venous stasis/varicose veins Vascular insufficiency Pachydermoperiostosis Hypervitaminosis A Fluorosis Leukemia Infection Trauma Differential Diagnosis of Accelerated Skeletal Age Hyperthyroidism (maternal or acquired) Polyostotic fibrous dysplasia (McCune-Albright syndrome) Idiopathic isosexual precocious puberty Premature thelarche Premature adrenarche Hypothalamic tumors Pinealoma Liver tumors (choriocarcinoma, hepatoma) Adrenocortical tumor or hyperplasia Gonadal tumors (androgen or estrogen secreting) Exogenous steroids Acrodysostosis Cerebral gigantism (Soto syndrome) Pseudohypoparathyroidism Lipodystrophy Weaver syndrome

B

involvement of leukemic acropachy is different from that of thyroid acropachy in that it is most pronounced in the terminal phalanges.12 Clinical correlation can often distinguish periostitis found in venous stasis, hypervitaminosis A, infection, and trauma.

SYNOPSIS OF TREATMENT OPTIONS Medical Treatment The medical therapies available for hyperthyroidism include pharmacologic agents and radioactive iodine ablation of the thyroid gland. The pharmacologic agents available include thiourea drugs such as propylthiouracil and methimazole, iodinated contrast agents, and propranolol for symptomatic relief. Use of radioactive iodine (131I) is an excellent way of destroying overactive thyroid tissue. It causes damage to the thyroid cells that concentrate it without increasing the risk of subsequent thyroid cancers, leukemia, or other malignancies. It is contraindicated in pregnant or breastfeeding patients.

Surgical Treatment Thyroid surgery is performed less frequently as radioactive iodine ablation has become more widely accepted.

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It is usually performed in pregnant patients who cannot undergo radioactive iodine ablation, in patients with very large goiters, or in patients who have a high chance of malignancy. In children with total craniosynostosis, surgery may be needed to relieve the increased intracranial pressure. The methods used to treat hyperthyroidism will depend on the etiology, severity, patient’s age, clinical situation, and patient’s preference.

What the Referring Physician Needs to Know ■ ■

■

The presence of thyroid acropachy on radiograph is virtually diagnostic of thyrotoxicosis. Treating hyperthyroidism can reverse some of the clinical manifestations of the condition, such as myopathy and osteoporosis. Radioactive iodine (131I) is contraindicated in pregnant or breast-feeding women.

SUGGESTED READINGS Chew FS. Radiologic manifestations in the musculoskeletal system of miscellaneous endocrine disorders. Radiol Clin North Am 1991; 29:135–147. Kinsella RA Jr, Back DK. Thyroid acropachy. Med Clin North Am 1968; 52:393–398. McKeown NJ, Tews MC, Gossain VV, Shah SM. Hyperthyroidism. Emerg Med Clin N Am 2005; 23:669-685.

REFERENCES 1. McKeown NJ, Tews MC, Gossain VV, Shah SM. Hyperthyroidism. Emerg Med Clin N Am 2005; 23:669-685. 2. Reid JR, Wheeler SF. Hyperthyroidism: diagnosis and treatment. Am Fam Physician 2005; 72:623-630. 3. Turnbridge WM, Evered DC, Hall R, et al. The spectrum of thyroid disease in a community: the Whickham survey. Clin Endrocrin (Oxf) 1977; 7:481-493. 4. Weetman AP. Graves disease. N Engl J Med 2000; 343:1236-1248. 5. American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for Evaluation and Treatment of Hyperthyroidism and Hypothyroidism (AACE Thyroid Guidelines). Endocr Pract 2002; 8:457-467. 6. Meunier PJ, Bianchi CS, Edouard CM, et al. Bony manifestation of thyrotoxicosis. Orthop Clin North Am 1972; 3:745–774. 7. Riggs W Jr, Wilroy RS Jr, Etteldorf JN. Neonatal hyperthyroidism with accelerated skeletal maturation, craniosynostosis, and brachydactyly. Radiology 1972; 105:621–625. 8. Segal AM, Sheeler LR, Wilke WS. Myalgia as the primary manifestation of spontaneously resolving hyperthyroidism. J Rheumatol 1982; 9:459–461. 9. Gimlette TMD. Thyroid acropachy. Lancet 1960; 1:22–24. 10. Vanhoenacker FM, Pelckmans MC, De Beuckeleer LH, et al. Thyroid acropachy: correlation of imaging and pathology. Eur Radiol 2001; 11:1058–1062. 11. Kinsella RA Jr, Back DK. Thyroid acropachy. Med Clin North Am 1968; 52:393–398. 12. Glatt W, Weinstein A. Acropachy in lymphatic leukemia. Radiology 1969; 92:125–126. 13. Fisher DA. Thyroid disease in the neonate and in childhood. In DeGroot LJ, editor. Endocrinology. 2nd ed. Philadelphia, WB Saunders, 1989, pp 733–745.

Hypothyroidism ETIOLOGY Hypothyroidism refers to a clinical condition in which there is inadequate production of thyroid hormone. Primary hypothyroidism is the most common cause of hypothyroidism, and it is characterized by an abnormality in the thyroid gland that results in deficient production of thyroid hormone. Causes include treatment of Graves disease (thyroidectomy or radioiodine ablation), autoimmune thyroiditis such as Hashimoto thyroiditis, iodine deficiency, poor iodine metabolism, medications (e.g., lithium), and infiltrative processes such as metastatic disease, lymphoma, and amyloidosis.1 Congenital hypothyroidism, which is characterized by hypothyroidism present since birth and previously known as cretinism, may result from in utero iodine deficiency, inborn error of thyroid hormone metabolism, or anatomic defect in the thyroid gland (e.g., thyroid agenesis, dysgenesis, or ectopia). Secondary hypothyroidism is less common and results from an abnormality in the pituitary gland, resulting in deficient thyroid-stimulating hormone (TSH), or from an abnormality in the hypothalamus, resulting in inadequate thyrotropin-releasing hormone.

PREVALENCE AND EPIDEMIOLOGY The incidence of thyroid disorders in North America is approximately 2% in women and 0.2% in men. The prevalence of overt hypothyroidism is around 0.1% to 2% and subclinical hypothyroidism is around 4%1. There are no known racial differences. For congenital hypothyroidism, the incidence is 1 in 4000 newborns.2 It is observed in all racial and ethnic groups. Any observed racial difference is most likely related to geographic and socioeconomic status rather than to any specific racial predilection. Congenital hypothyroidism caused by iodine deficiency has all but been eliminated in the developed world. The populations of areas of the world with underiodinated or noniodinated salt, and with less seafood consumption such as Africa and land-locked regions of Asia and Indonesia, still suffer.

KEY POINTS The key radiographic finding for congenital hypothyroidism is retarded skeletal maturation and epiphyseal dysplasia with secondary articular degeneration. ■ There is no diagnostic radiographic finding for adultonset hypothyroidism, although dystrophic calcification and arthropathy may be seen. ■ Many clinical manifestations are reversible with thyroid hormone replacement. ■

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CLINICAL PRESENTATION The extent of clinical findings generally depends on the etiology, severity, and duration of hypothyroidism. Infants with in utero thyroid hormone deficiency during the critical period of development of the central nervous system often develop cerebral diplegia, severe mental retardation, and deaf-mutism. If thyroid hormone deficiency is perpetrated after birth, diffuse edema, severe growth retardation, and delayed skeletal maturation ensue. There is reported interaction between thyroid hormone levels affecting the amount of growth and sex hormones excreted. At birth, congenital hypothyroid neonates may demonstrate prolonged jaundice, large fontanelles, umbilical hernia, hypotonia, or hoarse cry or may subtly present as a “good baby” who sleeps most of the time and rarely cries. Newborns can initially appear normal in size. The child will progressively fall off the growth chart over several months, as slow skeletal growth and delayed ossification centers manifest. Closure of the fontanelles is also delayed and accompanies delayed ossification. Thyroid deficiency occurring in children results in juvenile myxedema with mental retardation and developmental delays. The symptoms and signs of infantile and childhood hypothyroidism, depending on the age of onset, are presented in Table 78-8.2,3

PATHOPHYSIOLOGY Anatomy The thyroid gland develops from the buccopharyngeal cavity between the 4th and 10th weeks of gestation. It arises from the fourth brachial pouches and develops into a bilobed gland that is located in the neck just anterior to the trachea between the cricoid cartilage and suprasternal notch. Both thyroid lobes normally extend from the side

TABLE 78-8 Clinical Presentation of Hypothyroidism Infantile and Childhood Hypothyroidism Prolonged jaundice Large fontanelles Umbilical hernia Hypotonia Mottled, cool, and dry skin Hoarse cry Hypersomnia and minimal crying Decreased activity Constipation Poor feeding and weight gain Small stature or poor growth Developmental delay, mental retardation Coarse facial features Macroglossia Pallor Myxedema Prolonged deep tendon reflex relaxation phase Goiter Myalgia, arthralgia, paresthesias

Adult-Onset Hypothyroidism Fatigue, lethargy, weakness Mental or physical slowness Dry waxy skin Coarse brittle hair, alopecia Diffuse nonpitting edema, periorbital edema Pallor Cold intolerance, hypothermia Hoarseness Constipation Weight gain Macroglossia Bradycardia Menstrual disturbance Depression Prolonged deep tendon reflex relaxation phase Myalgia, arthralgia, paresthesias

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to the level of the carotid sheath. The two lobes are connected by the isthmus, which lies anterior to the trachea. Occasionally, a pyramidal lobe can be seen arising superiorly from the middle of the isthmus. Errors in the formation or migration of thyroid tissue can result in thyroid aplasia, dysplasia, or ectopy (lingual or sublingual location). The thyroid gland is regulated by TSH from the pituitary gland, which in turn is regulated by thyrotropin-releasing hormone from the hypothalamus.

Pathology Thyroid hormones are vital to skeletal growth because they stimulate differentiation and maturation of the chondrocytes at the growth plate cartilage. They also stimulate osteoblast and osteoclast activities for bone remodeling. They are required for the expression of many of the skeletal actions of growth hormone.4 The consequences of hypothyroidism include delayed skeletal maturation and growth in infants and children, delayed closure of growth plates, and delayed appearance of secondary ossification centers. Whereas skeletal retardation can be seen in other conditions, it is usually more severe in hypothyroidism. Although children with hypothyroidism commonly have low levels of growth hormone as well, treatment with growth hormone alone does not restore normal development. The degree and progress of skeletal maturation strongly correlate with thyroid function. Lack of thyroid hormone stimulation prevents normal growth and maturation at the cartilaginous growth plate. It also prevents expression of the growth hormones. Delayed closure of the growth plates can be seen into adulthood secondary to delayed appearance of secondary ossification centers. Histologic examination of the persisting growth plate does not show any evidence of cellular proliferation in the cartilage.5 The bony tissue of the metaphysis apposed to the cartilage growth zone eventually closes off the growth plate and subsequently impedes longitudinal growth of the bone even though there is persistence of the growth plate. Delayed, fragmented, and irregular ossification centers are commonly seen, most often described in the femoral heads and knees. Unlike normal focal growth and enlargement, hypothyroid children can have numerous ossification centers that grow and coalesce to form an irregular epiphysis with uneven density called hypothyroid epiphyseal dysgenesis. Epiphyseal dysgenesis classically occurs in the hips and less commonly in the hands and feet. The irregular ossifications are less pronounced than those from Down syndrome or osteochondrodystophy. Chronic irregular epiphysis in the femoral head can lead to flattened femoral heads, widening of the femoral neck, and coxa vara deformity. Abnormal epiphyseal development may also be a risk factor for slipped capital femoral epiphysis reported in a few hypothyroid children, but such association is rare.6 Epiphyseal dysgenesis may be explained by an imbalance in thyroid function between the stimulatory mitogenic effect of elevated TSH and the lack of differentiation by thyroid hormones, which are deficient.7 In addition to epiphyseal dysgenesis, hypothyroidism may manifest as destructive joint arthropathies. Joint pain,

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effusion, and stiffness are common complaints in patients with hypothyroidism. Arthropathic changes commonly involve the hands and knees in adults, whereas the hips and epiphysis of the femoral heads are more often involved in children. The joints may be enlarged and painful secondary to thickening of the synovium, joint effusion, or both. The joint effusion is cloudy and viscous but noninflammatory.8 It has a high hyaluronic acid content and may be explained by the presence of a TSH-responsive adenylate cyclase in the synovial membrane and the stimulation of hyaluronic acid production as well as synovial thickening by elevated TSH in hypothyroidism.8 Destructive arthropathy of the proximal interphalangeal and metacarpal joints presenting similarly to rheumatoid arthritis has been described.9,10 A destructive lesion in the tibial plateau suggesting compression has also been reported in literature.6 Avascular necrosis has been described in the femoral head and carpal lunate.11 The association of hypothyroidism with calcium pyrophosphate dihydrate crystal deposition, although suggested, remains uncertain because results to date have been conflicting. Hypothyroid myopathy may also manifest as diffuse muscular hypertrophy and muscle weakness that is predominantly proximal. Diffuse muscle hypertrophy, stiffness, weakness, and cramps are known as Hoffman’s syndrome.12 Symmetric proximal muscle weakness with marked serum muscle enzyme elevations clinically resemble polymyositis and has been misdiagnosed as such.13 Generalized myalgias when accompanied by trigger point tenderness may suggest fibromyalgia and may be the initial presentation of hypothyroidism.14 Myxedema can cause entrapment neuropathy such as carpal tunnel syndrome, which is seen in 7% of hypothyroid patients.

IMAGING TECHNIQUES Although ultrasonography and nuclear medicine thyroid scan are the most commonly used modalities to evaluate the thyroid gland, plain radiographs are sufficient to evaluate most of the musculoskeletal changes of hypothyroidism. The radiographs can be supplemented with CT or MRI in evaluating joint complaints for signs of joint destruction, effusion, or avascular necrosis. MRI is also helpful in evaluating extremities for suspicion of neuropathy caused by nerve compression by myxedema (e.g., carpal tunnel syndrome).

clinical findings suggest the diagnosis. The distal femoral epiphysis is usually ossified at 36 weeks’ gestation, and the proximal tibial epiphysis is ossified at 38 weeks’ gestation. Epiphyseal plates may stay open well into adulthood if untreated. Delayed areas of synchondrosis in the sacrum or sternum parallel areas of delayed ossification (Figs. 78-6 to 78-8 and Table 78-9. In the epiphyses, irregular epiphyseal appearance may result from ossification occurring from multiple centers rather than from a single site. The fragmented appearance of the epiphysis can simulate other conditions and can be mistaken for Legg-Calvé-Perthes disease. Chronic epiphyseal dysgenesis and delayed or inadequate treatment can lead to irregular epiphysis with eventual articular degeneration and intra-articular loose osseous and cartilaginous bodies. In the hips this can lead to the trifecta of coxa plana, coxa magna, and coxa vara. In the skull, plain radiographs or CT may show delayed closure of fontanelles, prominent sutures with accessory (wormian) bones developing within the sutures, hypoplastic paranasal sinuses and mastoid air cells, delayed dentition, protruding mandible, and brachycephaly resulting from decreased growth of the spheno-occipital synchondrosis. The sella turcica may be enlarged secondary to hyperplasia of the pituitary gland as a result of feedback from low thyroid hormone level on the hypothalamus and pituitary gland (Figs. 78-9 and 78-10).16 In the spine, one to three of the vertebral bodies at the thoracolumbar junction may demonstrate a short, bullet-shaped appearance with beak-like anterior margin or anterosuperior vertebral body notching.17 Exaggerated kyphosis at the thoracolumbar junction may be observed, resulting in a gibbus deformity that may improve with thyroid hormone replacement. These findings are nonspecific and may be seen in a number of other conditions, such as Hurler disease, Morquio disease, and achondroplasia. In the hands, delayed skeletal maturation can be seen as it can be seen elsewhere. Hypothyroidism affects the linear

MANIFESTATIONS OF THE DISEASE Radiography Retardation of skeletal maturation is a key radiographic finding in hypothyroidism. Delayed skeletal maturation is radiographically detected by observing a delay in appearance and growth of epiphyseal ossification centers, which is best seen in the infant by examining the knees or feet.15 Prompt appearance of the ossifications (best evaluated at the knees) followed by normal osseous development after thyroid hormone replacement can confirm the diagnosis of juvenile hypothyroidism if laboratory and

■ FIGURE 78-6

Bilateral femoral epiphyseal dysgenesis. (Courtesy of Javier Beltran, MD.)

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■ FIGURE 78-8 The epiphyses in the hand are still open in this 23-yearold patient. (Courtesy of Javier Beltran, MD.)

TABLE 78-9 Reported Musculoskeletal Abnormalities in Hypothyroidism ■ FIGURE 78-7 The epiphyseal end plates of the vertebral bodies remain open in this 23-year-old patient. (Courtesy of Javier Beltran, MD.)

growth less than it affects skeletal maturation, whereas in hypopituitarism, linear growth is affected more than skeletal maturation.18 In addition to delayed skeletal maturation, a radiographic finding of the hand specific to untreated primary hypothyroidism is osseous projections from the midportion of the metaphyses of the distal phalanges into the epiphyseal plate, which is noted in 80% of the cases.19 Its presence along with delayed skeletal maturation suggests the diagnosis of hypothyroidism. In adult-onset hypothyroidism, the skeletal changes are mild and may include slightly increased bone density and joint arthropathies. Destructive changes in the proximal interphalangeal joints and metacarpal joints simulating rheumatoid arthritis should include hypothyroid arthropathy on the differential diagnosis. Sclerosis in the femoral heads and neck should also raise the suspicion for avascular necrosis. In the knees, destructive lesions in the tibial plateau suggest compression. Abnormal soft tissue calcification and increased bone sclerosis may be seen on imaging studies. Increased bony eburnation of the periorbital region results in the “lunette” sign of hypothyroidism.20 Parotid calcification, premature atherosclerosis, nephrocalcinosis, and dystrophic calcifications in various soft tissues may all be evident.

Retarded skeletal maturation Accessory sutural bones Epiphyseal dysplasia Epiphyseal deformity with secondary degenerative joint disease Gibbus deformity Dystrophic calcification Carpal tunnel syndrome Synovial effusion, tenosynovitis Myopathy Neuropathy Soft tissue edema Osteoporosis Slipped capital femoral epiphysis Ligamentous laxity Calcium pyrophosphate dihydrate crystal deposition Erosive arthritis

Reprinted from Resnick D.Thyroid disorders. In Resnick D. Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, vol 3, p 2034.

Magnetic Resonance Imaging A hyperplastic pituitary with a relatively enlarged pituitary fossa can be seen with a chronically hypofunctioning thyroid and should not be mistaken for a pituitary tumor.

DIFFERENTIAL DIAGNOSIS The differential diagnosis of hypothyroidism is presented in Table 78-10.21

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■ FIGURE 78-9

A, Note the prominent sutures and accessory (wormian) bones. The paranasal sinuses are hypoplastic. B, Wormian bones (arrow). (B from Resnick D. Thyroid disorders. In Resnick D. Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, 2002, vol 3, p 2036.)

TABLE 78-10 Differential Diagnosis of Hypothyroidism Generalized Delayed Skeletal Age

Stippling of Epiphyseal Ossification Centers

Wormian Bones

Hypothyroidism Chronic severe anemia (e.g., sickle cell anemia, thalassemia) Constitutional Addison disease Cushing syndrome Corticosteroid therapy Hypogonadism (e.g.,Turner syndrome) Panhypopituitarism Growth hormone deficiency Chromosomal disorders (e.g., trisomy 21, trisomy 18) Skeletal dysplasia Congenital malformation syndrome Congenital heart disease (especially cyanotic) Juvenile diabetes mellitus Chronic illness Inflammatory bowel disease Intrauterine growth retardation Legg-Calvé-Perthes disease Malnutrition Malabsorption (e.g., celiac disease) Neurogenic disorders Chronic renal disease Rickets Idiopathic

Congenital hypothyroidism Spondyloepiphyseal dysplasia Multiple epiphyseal dysplasia (Fairbank disease) Legg-Calvé-Perthes disease Aseptic necrosis Normal variant Endemic cretinism Down syndrome Mucopolysaccharidosis (Morquio syndrome) Stickler syndrome (hereditary arthroophthalmopathy) Osteopoikilosis Osteopathia striata Dysplasia epiphysialis hemimelica (Trevor disease)

Pyknodysostosis Pachydermoperiostosis Osteogenesis imperfecta Rickets—hypophosphatasia Kinky hair syndrome Cleidocranial dysostosis Hypothyroidism, cretinism Primary acro-osteolysis (Hadju-Cheney) Down syndrome Normal variant Congenital hypophosphatasia Chromosomal abnormalities Major central nervous system abnormalities

Reprinted from Kottamasu SR. Bone changes in endocrinopathies. In Kuhn JP, Slovis TL, Haller JO (eds). Caffey’s Pediatric Diagnostic Imaging, 10th ed. St. Louis, Mosby, 2004, vol 2, p 2436–2437.

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SYNOPSIS OF TREATMENT OPTIONS Levothyroxine (thyroxine, T4), also known as Synthroid, is the treatment of choice. It is taken daily orally, and the dose is adjusted every 3 weeks until the patient is euthyroid.

What the Referring Physician Needs to Know ■

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■

■

■ ■

■ ■ ■ FIGURE 78-10 Enlarged sella turcica suggesting pituitary hyperplasia secondary to chronic hypothyroidism. (Courtesy of Javier Beltran, MD.)

Although the key radiographic manifestation of hypothyroidism is delayed skeletal maturation, the diagnosis of hypothyroidism is based on clinical findings. In infants, absence of the distal femoral and proximal tibial epiphyses is an important radiographic clue for hypothyroidism. Unexplained delay in closure of the fontanelles or sutures in children should raise the suspicion of hypothyroidism and prompt investigation. Hypothyroidism can initially present in children or adults with unexplained joint pain or effusion, local or generalized muscle pain, or paresthesias. Hypothyroid myopathy may simulate polymyositis clinically. Hypothyroidism in adults can present like rheumatoid arthritis of the hand as pain and swelling in the metacarpophalangeal and proximal interphalangeal joints. Hypothyroidism can lead to life-threatening myxedema coma with a mortality rate of up to 100% if it is not treated. Many of the clinical manifestations of hypothyroidism can be at least partially reversed if it is treated promptly with thyroid hormone replacement.

SUGGESTED READINGS Chew FS. Radiologic manifestations in the musculoskeletal system of miscellaneous endocrine disorders. Radiol Clin North Am 1991; 29:135–147.

McLean RM, Podell DN. Bone and joint manifestations of hypothyroidism. Semin Arthritis Rheum 1995; 24:282–290.

REFERENCES 1. Devdhar M, Ousman YH, Burman KD. Hypothyroidism. Endocrinol Clin N Am 2007; 36:595-615. 2. Delange F. Neonatal screening for congenital hypothyroidism: results and perspectives. Horm Res 1997; 48:51-61. 3. American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for Evaluation and Treatment of Hyperthyroidism and Hypothyroidism. Endocr Pract 2002; 8:457467 (AACE Thyroid Guidelines). 4. Lewinson D, Harel Z, Shenzer P, et al. Effect of thyroid hormone and growth hormone on recovery from hypogonadism of epiphyseal growth plate cartilage and its adjacent bone. Endocrinology 1989; 124:937–945. 5. Jaffe HL. Metabolic, Degenerative and Inflammatory Diseases of Bones and Joints. Philadelphia, Lea & Febiger, 1972, p 346. 6. Crawford AH, MacEwen GD, Fonte D. Slipped capital femoral epiphysis co-existent with hypothyroidism. Clin Orthop Relat Res 1977; 122:135–140. 7. McLean RM, Podell DN. Bone and joint manifestations of hypothyroidism. Semin Arthritis Rheum 1995; 24:282–290. 8. Dorwart BB, Schumacher HR. Joint effusions, chondrocalcinosis and other rheumatic manifestations in hypothyroidism: a clinicopathologic study. Am J Med 1975; 59:780–790. 9. Neeck G, Riedel W, Schmidt KL. Neuropathy, myopathy and destructive arthropathy in primary hypothyroidism. J Rheumatol 1990; 17:1697–1700. 10. Gerster JC, Valceschini P. Destructive arthropathy of fingers in primary hypothyroidism without chondrocalcinosis. J Rheumatol 1992; 19:637–641. 11. Rubinstein HM, Brooks MH. Aseptic necrosis of bone in myxedema. Ann Intern Med 1977; 87:580–581.

12. Klein I, Parker M, Sherbert R, et al. Hypothyroidism presenting as muscle stiffness and pseudohypertrophy: Hoffmann’s syndrome. Am J Med 1981; 70:891–894. 13. Madariaga MG. Polymyositis-like syndrome in hypothyroidism: review of cases reported over the past twenty-five years. Thyroid 2002; 12:331–336. 14. Wilke WS, Sheeler LR, Makarowski WS. Hypothyroidism with presenting symptoms of fibrositis. J Rheumatol 1981; 8:626–631. 15. Resnick D. Thyroid disorders. In Resnick D (ed). Diagnosis of Bone and Joint Disorders, 4th ed. Philadelphia, WB Saunders, 2002, vol 3, pp 2026–2042. 16. Swischuk LE, Sarwar M. The sella in childhood hypothyroidism. Pediatr Radiol 1977; 6:1–3. 17. Swischuk LE. The beaked, notched, or hooked vertebra: its significance in infants and young children. Radiology 1970; 95:661–664. 18. Hernandez RJ, Poznanski AW, Hopwood NJ. Size and skeletal maturation of the hand in children with primary hypothyroidism. AJR Am J Roentgenol 1979; 133:405–408. 19. Hernandez RJ, Poznanski AK. Distinctive appearance of the distal phalanges in children with hypothyroidism and hypopituitarism. Radiology 1979; 132:83–84. 20. Borg SA, Fitzer PM, Young LW. Roentgenologic aspects of adult cretinism: two case reports and review of the literature. Am J Roentgenol Radium Ther Nucl Med 1975; 123:820–828. 21. Kottamasu SR. Bone changes in endocrinopathies. In Kuhn JP, Slovis TL, Haller JO (eds). Caffey’s Pediatric Diagnostic Imaging, 10th ed. Philadelphia, Elsevier, 2004, pp 2436–2439.

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C H A P T E R

Gaucher Disease Daniel Rosenthal

ETIOLOGY Gaucher disease bears the name of Philippe Gaucher, a French dermatologist who first described the clinical syndrome. Understanding of the condition was greatly enhanced in 1965 when it was recognized that the disease was due to a functional deficiency of the enzyme β-glucosidase. This deficiency results in accumulation of glucosylceramide, a cell membrane metabolite, in lysosomes of cells of the monocyte/macrophage lineage.1

PREVALENCE AND EPIDEMIOLOGY There are several thousand individuals in the United States with Gaucher disease. It is particularly prevalent among the Ashkenazi Jewish population, among whom as many as 1 in 14 may be carriers. More than 300 mutations that may result in clinical disease have been identified; 7 of these account for the majority of nucleotide substitutions. Four alleles account for approximately 90% of cases: N370S, 84GG, L444P, and IVS2+1. Inheritance is autosomal recessive.

tem. Although this has been referred to as the “adult type,” 66% of individuals with type 1 Gaucher disease develop some manifestations of the disease in childhood. Onset early in childhood is usually predictive of a severe, rapidly progressive phenotype, and young children with type 1 Gaucher disease are at high risk for morbid complications. Type 2 Gaucher disease is characterized by onset in infancy with severe central nervous system involvement and death in early childhood. Severely affected individuals have been identified as early as the second trimester of pregnancy, exhibiting polyhydramnios, hydrops fetalis with bilateral hydrothorax, hepatosplenomegaly, arthrogryposis, absent fetal movements, and thickened skin. Patients with type 3 Gaucher disease demonstrate milder central nervous system involvement with onset in adolescence or early adulthood and a more indolent course. Diagnosis of Gaucher disease is typically confirmed by enzyme assay, DNA analysis, bone marrow biopsy, spleen or liver biopsy, or some combination of these four methods. Of these, assay for glucocerebrosidase activity of peripheral blood leukocytes is considered to be the most efficient and reliable means of diagnosis.

CLINICAL PRESENTATION The clinical features result from the accumulation of glucosylceramide in cells of the reticuloendothelial system. Apoptosis is inhibited in these cells. Their relative immortality leads to progressive accumulation of characteristic Gaucher cells, which replace normal marrow elements and cause hepatosplenomegaly. Although the severity of disease is variable, the most prevalent forms of Gaucher disease are associated with a normal or near-normal life expectancy. The presence and degree of central nervous system involvement has been used to delineate three more-or-less distinct forms of the disease.2 The most prevalent form of Gaucher disease is known as the type 1 variant. It does not affect the central nervous sysPortions of this chapter appear in the author’s own discussion on this topic in the textbook Weissman B: Imaging of Arthritis and Metabolic Bone Disease. Philadelphia: Mosby, 2009.

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KEY POINTS MRI is the best modality to identify the major sites of organ involvement and areas of infarction in Gaucher disease. ■ CT is an alternative modality that is useful but exposes the patient to radiation. ■ Gaucher disease is due to functional deficiency of β-glucosidase, leading to accumulation of abnormal metabolites in the reticuloendothelial system. ■ The most severe types produce visceral and hematologic disorders in infancy. Skeletal disorders predominate in less severely affected individuals. ■ Skeletal imaging is dominated by marrow replacement, osteopenia, focal lytic lesions, osteonecrosis, fracture, and osteomyelitis. ■ Erlenmeyer flask deformity is a highly characteristic, but inconstant and not pathognomonic, feature of the disease. ■

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PATHOPHYSIOLOGY Anatomy Nonskeletal The accumulation of glucocerebroside in the lysosomes of visceral macrophages gives rise to multiple manifestations, including hepatosplenomegaly, anemia, thrombocytopenia, growth retardation, and skeletal disease. The most severe variants of Gaucher disease may cause death at an early age from visceral and hematologic manifestations. Pulmonary infiltrates and thoracic lymph node enlargement can be the predominant imaging findings of some of the severe forms.1 Even patients with type 1 disease may occasionally develop pulmonary involvement. Interlobular septal and intralobular interstitial thickening may result in a reticulated pattern, irregular interfaces at the pleural surfaces, and ground-glass appearance as seen on radiographs and high-resolution CT. Cardiac involvement in Gaucher disease has been reported in only a few patients, mostly adults with pericardial changes. However, thickened, relatively immobile mitral and aortic valves have been seen, resulting in significant mitral regurgitation. Therefore, echocardiographic investigation of patients with suspected cardiac involvement with Gaucher disease is recommended. Brain involvement occurs in the severe, neuronopathic forms. The severity of neurologic abnormalities has been shown to correlate with multifocal areas of cerebral hypoperfusion. Extensive hypoperfusion foretells clinical deterioration, and progressive cerebral atrophy has been demonstrated in the frontal and temporal lobes. Enlargement of the liver and spleen is almost universal in patients with Gaucher disease (Fig. 79-1A). In addition, about 5% of patients have focal splenic or hepatic lesions. These presumably represent areas of infarction

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or fibrosis related to previous infarction, but focal defects can also be caused by other conditions such as metastatic carcinoma. Hypersplenism leading to thrombocytopenia and moderate immunocompromise is a frequent complication of Gaucher disease, often requiring splenectomy. Partial splenic embolization may be performed to avoid the increased risk of serious infectious complications.4 Complete removal of the spleen is thought to cause deterioration of the disease in other organs (especially the bones) possibly by removal of an important reservoir for the Gaucher cells. After institution of enzyme replacement therapy, there is usually an initial dramatic decline and then sustained decreases in organ size, especially in pediatric patients (see Fig. 79-1B).

Skeletal Features In general, skeletal complications require time to develop; therefore, skeletal manifestations are less characteristic of the more fulminant forms of the disease. However, when present, the fundamental features of skeletal involvement are the same in all clinical forms of the disease.3 In some affected individuals there may be no clinical, radiographic, scintigraphic, or histologic evidence of bone involvement, but in others the skeleton can be completely devastated. Findings from the International Collaborative Gaucher Group Registry, an international database of more than 2600 patients, show that nearly all patients with Gaucher disease have radiologic evidence of skeletal involvement and the majority have a history of serious skeletal complications. For most patients with type 1 disease, the skeletal manifestations are probably its most disabling aspect. The skeleton is not affected uniformly. With the exception of generalized osteopenia and marrow replacement, most manifestations are multiple and localized.

■ FIGURE 79-1

A, Abdominal CT scan reveals massive hepatosplenomegaly in this untreated child with Gaucher disease. B, After 3 years of enzyme replacement therapy there is no longer organ enlargement.

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Sometimes much of the skeleton is preserved. These observations suggest that bone is affected by scattered, focal collections of Gaucher cells. It is possible that local effects may be the result of a toxic process around these foci. Alternatively, the storage of glucocerebroside in tissue macrophages may disturb the generation of competent osteoclasts and thus result in a failure to maintain a healthy skeleton.5 Patients commonly experience nonspecific bone pain, and some suffer from intermittent episodes of severe pain (bone crises) similar to those seen in sickle cell disease. Up to 20% have impaired mobility. Radiographically demonstrable involvement results from five basic processes:

ity of the disease itself, whereas others find their use in evaluation of the complications of the disease. In many instances, the evaluation of specific complications is not different when they occur in patients with Gaucher disease than when they occur in the general public. Thus, for example, fractures and osteomyelitis are evaluated no differently, although they are treated somewhat differently because of the bleeding tendencies and immune deficiencies often present in this population. For purposes of this discussion, we will focus on imaging aspects that are specific to Gaucher disease.

1. Marrow replacement 2. Generalized osteopenia 3. Skeletal resorption due to adjacent heavily involved marrow leading to focal lytic lesions 4. Acute focal bone disease including a. Osteonecrosis, especially collapse of the femoral head b. Osteomyelitis and “pseudo-osteomyelitis” c. Fractures 5. The Erlenmeyer flask deformity, a characteristic (but not universally present) modeling abnormality of the distal femur

A number of quantitative and semiquantitative techniques have been applied to the investigation of Gaucher disease. These have been used to evaluate the severity of marrow replacement and the extent of organomegaly. Although these have been important in understanding the natural history of the disease, and in evaluating the effectiveness of therapy, they are probably too laborious and imprecise to be applied to individual patients. Furthermore, the effects of therapy are now largely known (see later) and therefore in most instances investigational techniques are not required.

Pathology

MANIFESTATIONS OF THE DISEASE Radiography

The histologic hallmark of Gaucher disease is the presence of lipid-laden histiocytes. These are widely distributed among the organs of the reticuloendothelial system and are particularly prominent in the liver, spleen, bone marrow, and lymph nodes but may also be found in other connective tissues. Accumulation of glucocerebroside within the macrophages imparts a characteristic foamy or “wrinkled cigarette paper” appearance to the cytoplasm (Fig. 79-2).

IMAGING TECHNIQUES Techniques and Relevant Aspects Because it affects multiple organ systems, virtually every imaging modality has a role to play in evaluation of patients with Gaucher disease. Some are used to evaluate the sever-

■ FIGURE 79-2 Toluidine blue stain shows a Gaucher cell with the so-called wrinkled cigarette paper appearance of the cytoplasm.

Pros and Cons

Radiography is the standard approach to detection and evaluation of fractures. Fractures are relatively common in patients with Gaucher disease. They may occur due to generalized osteopenia or to focal bone replacement, resulting in weakened skeletal areas at sites of osteolysis (Fig. 79-3A). Radiography is also the best means to detect the presence of an Erlenmeyer flask deformity. This is a wellknown and characteristic feature of Gaucher disease. It represents undertubulation of the distal femur due to failure of bone resorption in the “cut-back” zone of the metaphysis (Fig. 79-4). The Erlenmeyer flask deformity is not unique for Gaucher disease. It may also be seen in disorders associated with osteoclast failure (e.g., osteopetrosis) and may be associated with certain other rare marrow-packing diseases such as mannosidosis, a glycoprotein storage disease of lysosomes due to specific absence of α- D -mannosidase.6 The Erlenmeyer flask deformity can be strikingly obvious or extremely subtle in patients with Gaucher disease. In our experience, its presence does not invariably reflect either the severity of disease or the local marrow involvement. Notching of the medial aspect of the proximal humeral metaphysis, in some cases contributing to pathologic fracture, has also been reported as a manifestation of Gaucher disease and certain other infiltrative marrow processes such as leukemia, Niemann-Pick disease, Hurler syndrome, and metastatic neuroblastoma, but controversy remains as to whether this represents a normal variant.7 Focal accumulation of Gaucher cells may result in lytic lesions. These are typically not symptomatic unless

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■ FIGURE 79-3 A, Plain radiograph of the pelvis demonstrates severe osteopenia and bilateral large focal lytic lesions of the proximal femora. This is a common location for these lesions, which are typically bilaterally symmetric. B, Radiograph of the pelvis obtained on the same patient 7 months later shows a fracture through the lytic lesion of the left femur. Note that the trabecular bone of the femoral head appears somewhat dense, indicating osteonecrosis. C, Slightly less than a year later, a radiograph demonstrates nonunion of the femoral fracture and a subchondral “crescent sign” indicating subarticular fracture and impending collapse of the femoral head.

infarction or fracture supervenes (see Fig. 79-3B). When focal marrow deposits become so large that the cortex is violated, then extraosseous extension of Gaucher disease may occur (Fig. 79-5). Commonly referred to as a “gaucheroma,” such focal deposits might simulate malignancy. This differential diagnosis may occasionally become problematic in view of the increased risk of multiple myeloma in patients with Gaucher disease. In one rare instance, an extraosseous Gaucher cell accumulation even produced a monoclonal IgG kappa gammopathy, further simulating a myeloma.8 Gaucheromas tend to be very slowly progressive.9 In some instances the connection to the bone (although always present) may be subtle, giving the incorrect impression of a soft tissue mass.10

Radiographs may also demonstrate the effects of bone infarction, although they are not useful for early diagnosis of this condition. Macroscopic infarction takes the form of a medullary zone demarcated from adjacent bone by a serpiginous sclerotic boundary. Occasionally, this may result in a “bone-within-bone” appearance (Fig. 79-6A). If the end of a bone is affected, osteoarticular necrosis may be followed by collapse of the surface and the need for total joint arthroplasty (see Fig. 79-3B and C). In the spine, collapse of the vertebral end plates with vertical or square sides may be seen, similar to sickle cell anemia. As in the latter condition, microscopic bone infarction may result in diffuse medullary sclerosis (see Fig. 79-6B). Complete replacement of the vertebral marrow with collapse may result in the findings of vertebra plana (see Fig. 79-6C).

■ FIGURE 79-4 A, Anteroposterior radiograph of both distal femora demonstrates striking widening of the distal metaphyses. In normal individuals, the distal metaphyses abruptly widen into the femoral condyles. In patients with an Erlenmeyer flask deformity, the femur takes on a conical shape due to dysfunction of the “cut-back” zone. B, After 3 years of treatment with enzyme replacement, the femur has taken on a more normal shape. This type of improvement may be observed in children who undergo therapy but is rare in adults.

■ FIGURE 79-5 Lateral radiograph of the distal femur demonstrates osteopenia, multiple lytic lesions, and a “hair-on-end” pattern of periosteal new bone formation due to extraosseous spread of Gaucher disease.

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■ FIGURE 79-6 A, Anteroposterior spine radiograph (different patient from Fig. 79-3A) shows a “bone-within-bone” appearance due to multiple vertebral body infarctions. This is a relatively rare manifestation. B, Lateral radiograph of the spine demonstrates diffuse medullary sclerosis, a pattern that may also be observed in sickle cell disease. Presumably this represents the skeletal response to small vessel occlusion, without a discrete infarcted territory. C, Vertebra plana. As in other diseases that cause marrow replacement, vertebral fractures may result in vertebra plana.

Bone Densitometry Low levels of bone density in Gaucher disease are associated with serum markers of accelerated bone turnover and breakdown, suggesting that the osteopenia associated with type 1 Gaucher disease is due to increased bone resorption.11 Patients with Gaucher disease are usually found to have osteopenia at all sites. The severity of osteopenia is related to overall disease severity and is correlated with genotype; the more severely affected individuals with the N370S/84GG mutation have lower density than those with the milder N370S/N370S mutation. As in individuals without Gaucher disease, density declines as a function of age. Bone densitometry (dual-energy x-ray absorptiometry [DEXA]) has been advocated for following the response to therapy for children with Gaucher disease, although absolute measurements do not correlate with severity of disease.12 It is interesting that DEXA measurements are more consistently abnormal in patients than quantitative CT scans, an order of sensitivity that is opposite from that seen with osteoporosis. Because quantitative CT scans measure trabecular bone only, perhaps this indicates that in Gaucher disease the osteopenia has an important component of cortical bone loss.

Magnetic Resonance Imaging Magnetic resonance imaging can also be used to evaluate the visceral and soft tissue manifestations of Gaucher

disease. Like CT and ultrasonography, it can be used to accurately measure the volume of the liver and spleen. It is more expensive than ultrasonography, but more reproducible, and it does not involve radiation exposure like CT, something that is probably important in affected children who may require serial measurements. MRI of the brain may demonstrate progressive cerebral atrophy in the frontal and temporal lobes. MRI is the most useful method for evaluation of bone marrow replacement, which is the most universally present skeletal manifestation of Gaucher disease. Normal bone marrow becomes infiltrated by cellular elements containing foam cells (macrophages packed with glucocerebroside). This feature is impossible to recognize on radiographs and is extremely subtle on CT scans but is quite obvious on MRI. Marrow affected by Gaucher disease characteristically demonstrates either homogeneous or patchy low signal intensity on both T1- and T2-weighted imaging sequences (Fig. 79-7). These signal alterations presumably reflect the combined effects of replacement of marrow fat and the highly structured microtubular arrays in which the glucocerebroside accumulates. Gaucher disease extends into the marrow in a moreor-less predictable pattern. This pattern reverses the sequence of marrow conversion that normally occurs during childhood. During normal development, the maximal extent of red marrow occurs at the ninth month in utero. Subsequently, the red marrow is replaced by much less cellular yellow or fatty marrow, beginning in the distal parts of the appendicular skeleton and proceeding

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■ FIGURE 79-7 T1-weighted coronal MR image of the knees. The bright marrow signal that is normally due to the presence of fat is absent because of infiltration of the marrow.

proximally. These changes cause progressive increase in the marrow signal on T1-weighted images. By age 10, adult degrees of signal intensity are achieved in most pelvic sites, although fatty replacement remains ongoing throughout life. Even by age 6, adult levels of fat content (40% to 45%) are reached in the posterior ilium; therefore, marrow with homogeneous low signal on T1-weighted images in these areas is abnormal. Most epiphyseal centers have fatty marrow throughout life. We believe that this is because the secondary centers are cartilaginous during early childhood and ossification occurs when physiologic requirement for red marrow is declining. Therefore, the normal pattern of marrow conversion is centripetal, except for the fact that the secondary centers do not participate. In Gaucher disease the process is reversed, with accumulation of Gaucher-affected tissue beginning in the axial skeleton and proceeding into the proximal and then the distal long bones. The epiphyses are relatively spared, although with advanced disease they, too, are affected.13 This pattern is thought to reflect the availability of the macrophages that serve as reservoirs for the glucocerebroside accumulation. Such macrophages are primarily found in red marrow, and therefore areas of residual red marrow tend to be affected first. Replacement of the proximal marrow causes areas of red marrow to develop further peripherally, and Gaucher cell accumulation follows. This reverse process is known as “reconversion” and may also be seen in other marrow-replacing disorders.14 A number of different approaches have been devised to quantify the extent of marrow replacement. Simple scales based on the known pattern of disease progression and visual determination of the presence of disease have been developed by Rosenthal and Hermann.15,16

Since the vertebral marrow appears darker than expected on T1 images due to absence of fat, a “semiquantitative” approach has been devised to compare vertebral body signal intensity to disk brightness. If the normalized vertebra to disk ratio (NVDR) is taken to be 1.0 (95% confidence limits, 0.70 to 1.30), for untreated patients with Gaucher disease the ratio is below 0.7.17 It is also possible to calculate a numerical value for the volume percent of fat (fat fraction). This is generally done using the technique of quantitative chemical shift imaging. The fat fraction is decreased severalfold in patients with Gaucher disease compared with normal individuals.18 These approaches are valuable because the extent of marrow replacement indicates the probability of skeletal symptoms. There is a significant positive correlation between liver size, the risk of avascular necrosis, and the marrow scale used by Hermann. The spleen size does not seem to be related to these factors.19 A correlation has been demonstrated between fat fraction of axial bone marrow as calculated by Dixon quantitative chemical shift imaging (Dixon QCSI) and bone complications, with an 85% increase in risk of bone complication for every decrease of 0.1 in the fat fraction. Fat fractions are significantly lower in patients with Gaucher disease than in normal patients, and lower in Gaucher disease patients who have undergone splenectomy than in those who have not. The latter observation supports the clinical impression that removal of the splenic “reservoir” may worsen the skeletal disease.20 Other studies have also demonstrated a relationship between fat fraction and clinical disease severity, although not always with bone complications.15

Computed Tomography Like ultrasonography and MRI, CT can be used to demonstrate changes in the size of the liver and spleen. CT is faster to perform than MRI and can for that reason usually be done in children without the need for sedation. As with the other imaging techniques, focal changes due to infarction and infiltration can also be demonstrated by CT scans. As mentioned earlier, CT can be used to measure bone density (quantitative CT [QCT]). In patients with osteoporosis this is advantageous because of its specific sensitivity to loss of trabecular bone, which makes it highly sensitive to early bone loss in the spine. However, in Gaucher disease, the reduction in trabecular bone mass as demonstrated by QCT has been only moderate. DEXA demonstrates greater degrees of loss. Presumably this is a reflection of the fact that cortical bone loss predominates. In addition, when performed using conventional singleenergy QCT methods, replacement of normal marrow fat with Gaucher cells tends to artifactually elevate the apparent bone mass. Although rarely performed because of technical complexity, dual-energy measurements more accurately reflect the degree of bone loss.

Ultrasonography Ultrasonography may be used to assess volume changes in the liver and spleen. As is the case for MRI, this is of particular interest in children because of the lack of

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exposure to ionizing radiation. Focal splenic or hepatic lesions can be hypoechoic, hyperechoic, or mixed. These lesions presumably represent areas of infarction or fibrosis related to previous infarction. After institution of enzyme replacement therapy, ultrasound has been used to demonstrate an initial dramatic decline and then sustained decrease in organ size. Ultrasonography can also be used to demonstrate suspected cardiac involvement.

Nuclear Medicine Liver scintigraphy has been used to demonstrate both enlargement and inhomogeneous uptake. Focal defects may represent liver involvement with Gaucher disease; but as is the case in individuals without Gaucher disease, focal defects can also be caused by other conditions such as metastatic carcinoma. Like ultrasonography, scintigraphy can be useful in detecting splenic infarction and in following enlargement of the spleen after partial splenectomy. Brain scans with technetium-99m hexamethylpropylene-amine-oxime and SPECT imaging have been used to demonstrate brain involvement in the severe, neuronopathic forms. Multifocal hypoperfusion of the brain has been shown to correlate with neurologic abnormalities, and extensive hypoperfusion foretells clinical deterioration. Radioisotope scans have also been used to evaluate the marrow changes of Gaucher disease. As determined by 99m Tc sulfur colloid, the extent of marrow involvement correlated well with the clinical and radiologic changes of the skeleton, but a normal pattern was found in the early stages of the disease. Bone scanning after inhalation of xenon gas has also been shown to correlate with disease activity.15 Initially attempted in the belief that the Gaucher deposits would have xenon uptake characteristics similar to those of fat, it is now believed that the observed uptake is more likely due to increased blood flow in the affected marrow. 99mTc sestamibi (MIBI) has also been utilized to demonstrate glycolipid deposits in the bone marrow. Although MIBI scanning is a sensitive technique for detecting bone marrow deposits, it is unclear whether the observed uptake correlates well with clinical disease. Some studies suggest that MIBI scans are inadequate for early identification of patients at high risk for skeletal complications or for the follow-up of patients treated with enzyme replacement. Others, however, have found that a semiquantitative scintigraphic score was highly correlated with an overall clinical severity score index (SSI) and with various parameters contributing to the SSI, either positively or negatively. Scintigraphic score is most highly correlated with measurements of serum chitotriosidase, an overall biochemical marker of disease severity. Enzyme replacement therapy–naive patients showed high correlation of the scintigraphic score with the clinical SSI, with a radiographically based score, and with serum chitotriosidase. In patients receiving enzymereplacement therapy the scintigraphic score was correlated with the clinical SSI, with hepatomegaly, and with hemoglobin.21

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SYNOPSIS OF TREATMENT OPTIONS Medical Treatment Enzyme Replacement Before the development of enzyme replacement therapy, treatment of Gaucher disease was mainly focused on symptomatic relief. However, enzyme replacement therapy makes it possible to reverse the manifestations of the disease itself. Alglucerase (Ceredase, Genzyme Corporation, Cambridge, MA) is a mannose-terminated form of glucocerebrosidase derived from human placentae and developed to treat patients with Gaucher disease. The first objective evidence (1992) that enzyme replacement therapy with alglucerase might be effective for treatment of bone disease was the report of one child treated for 2 years. Bone biopsies showed a progressive return to normal marrow and cortical thickness.22 Since then, in vitro methods of protein production have led to creation of imiglucerase (Cerezyme, Genzyme Corporation, Cambridge MA), a synthetic enzyme with a more predictable composition.2 Enzyme replacement allows removal of the lipid metabolite whose accumulation causes the pathology. After implementation of therapy, improvements became evident within 6 months. Patients have increased hemoglobin levels and platelet counts and decreased incidence of epistaxis and bruising. Spleen and liver size are reduced, and skeletal symptoms improve. Children gain height, and most patients are able to resume work and daily activities. Enzyme replacement therapy is well tolerated, with few mild adverse reactions reported.23

Enzyme Replacement Therapy in Children It appears clear that symptomatic children treated with enzyme replacement therapy will experience significant increases in skeletal growth and bone mineral density (BMD). Enzyme replacement therapy therefore has the potential to prevent serious and irreversible skeletal complications such as fractures and vertebral compression later in life.24 Because early disease onset frequently heralds a poor prognosis, and because optimal doses of enzyme therapy can ensure adequate, potentially normal, development through childhood and adolescence, very few children diagnosed by signs and symptoms should go untreated.

Monitoring the Effects of Treatment Imaging can be used to track the progress of improvement with enzyme replacement therapy. MRI demonstrates return of marrow fat in treated individuals.18 Subsequently, response to enzyme replacement therapy has been repeatedly observed as a quantitative increase in signal intensity on T1-weighted images, even when it is not perceptible as a change in the pattern of marrow involvement.25 In our own work, the lipid composition of bone marrow, determined by direct chemical analysis, began to improve after 6 months of treatment at a time when noninvasive imaging studies showed no significant changes.

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By 42 months, improvement in marrow composition was demonstrable on all noninvasive, quantitative imaging modalities (magnetic resonance score, quantitative xenon scintigraphy, and quantitative chemical shift imaging). Quantitative chemical shift imaging, the most sensitive technique, demonstrated a dramatic normalization of the marrow fat content in all patients. Net increases in either cortical or trabecular bone mass, as assessed by combined cortical thickness measurements and dualenergy quantitative CT, respectively, also occurred.26 Other studies have also demonstrated modest improvement in patients treated for 2 years or more, and there have been a number of anecdotal reports of improvement. Changes in the skeleton in response to enzyme replacement therapy have been most striking in children. In adults, the marrow response (increase in fat fraction) is similar. However, whether enzyme replacement produces demonstrable changes in the bone mass of adult skeletons has been controversial. In some reports there was little benefit, possibly because of the splenectomized state.27

Costs Enzyme replacement therapy for Gaucher disease is among the most expensive of all drug regimens. Alternative approaches to lowering the cost of treatment include the use of lower dosages28 and alternatives to this type of therapy. It is unclear when in the course of the disease that enzyme replacement therapy should be implemented. In the opinion of some experts, it is important that patients be monitored closely and that enzyme replacement should be initiated before development of irreversible skeletal complications such as infarction and fibrosis.29 Some evidence indicates that the vulnerable period is during childhood, adolescence, or early adulthood when there is the greatest risk of progression. There is a marked tendency for stabilization thereafter. This observation suggests that Gaucher disease is not necessarily a relentlessly progressive disorder but may become stable during adulthood. There has been an effort to reach consensus recommendations for a comprehensive schedule of monitoring of all relevant aspects to confirm the achievement, maintenance, and continuity of the therapeutic response.30 The current recommendations for enzyme replacement therapy suggest that adults at increased risk of complications and all affected children should begin therapy with an intravenous infusion of 60 units/kg every 2 weeks. Adults at lower risk may begin at a dose of 30 to 45 units/kg every 2 weeks. After clinical improvement, dose decreases may be considered in 15% to 25% increments every 3 to 6 months in higher-risk adults and children, with a minimum recommended maintenance dose of 30 units/kg

every 2 weeks; adults at lower risk can be maintained at a minimum of 20 units/kg every 2 weeks.31

Surgical Treatment Surgical interventions continue to be required in the era of enzyme replacement therapy. Osteonecrosis of the joints—particularly the hips but also the knees and shoulders—and pathologic fractures of the long bones including the ribs, as well as episodic “crises” of bone pain in children and young adults, are common manifestations. Surgical interventions such as joint arthroplasties are important adjuvant treatments in this population. Surgical treatment may be complicated because of problems related to marrow insufficiency and increased risk of infection. Therefore, presurgical hematologic profiling plus antibiotic coverage are important.32 Because many patients are young, aseptic loosening of total hip arthroplasty may occur soon after operation. Osteotomy may be an alternative to arthroplasty for such individuals.33 Hypersplenism leading to thrombocytopenia and moderate immune compromise is a frequent complication of Gaucher disease, often requiring splenectomy. Partial splenic embolization may be performed to avoid the increased risk of serious infectious complications and deterioration of the disease associated with operative splenectomy.4 Efforts continue to be made to find a more “biologic” cure. Bone marrow transplantation has been successful in a small number of patients (although attended with the usual problems), suggesting that in advanced Gaucher disease bone marrow transplant may be an option if a human leukocyte antigen–identical related or unrelated donor is available.34

What the Referring Physician Needs to Know ■ ■ ■

■

Sites and degrees of organ involvement Monitoring of changes in organ involvement to plan and monitor therapy Quantitative imaging techniques (other than dual-energy x-ray absorptiometry) have produced advances in understanding the disease but are probably not necessary for the management of the individual patient. Enzyme replacement therapy has been highly effective in suppressing the manifestations of Gaucher disease. For visceral disease, treatment can be withheld until symptoms warrant it. However, skeletal disease is difficult to reverse; therefore, prevention should be the goal.

SUGGESTED READINGS Mankin HJ, Rosenthal DI, Xavier R. Gaucher disease. Curr Concepts Rev 2001; 83A:748–762.

Pastores GM, Weinreb NJ, Aerts H, et al. Therapeutic goals in the treatment of Gaucher disease. Semin Hematol 2004; 41(4 Suppl 5):4–14.

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REFERENCES 1. Brady RO, Kanfer JN, Shapiro D. Metabolism of glucocerebrosides: II. Evidence of an enzymatic deficiency: Gaucher disease. Biochem Biophys Res Commun 1965; 18:221–225. 2. Mankin HJ, Rosenthal DI, Xavier R. Gaucher disease. Curr Concepts Rev 2001; 83A:748–762. 3. Hill SC, Damaska BM, Tsokos M, et al. Radiographic findings in type 3b Gaucher disease. Pediatr Radiol 1996; 26:852–860. 4. Thanopoulos BD, Frimas CA, Mantagos SP, Beratis NG. Gaucher disease: treatment of hypersplenism with splenic embolization. Acta Paediatr Scand 1987; 76:1003–1007. 5. Stowens DW, Teitelbaum SL, Kahn AJ, Barranger JA. Skeletal complications of Gaucher disease. Medicine (Baltimore) 1985; 64:310–322. 6. DeFriend DE, Brown AEM, Hutton CW, Hughes PM. Mannosidosis: an unusual cause of a deforming arthropathy. Skeletal Radiol 2000; 29:358–361. 7. Li JK, Birch PD, Davies AM. Proximal humeral defects in Gaucher disease. Br J Radiol 1988; 61:579–583. 8. Kaloterakis A, Cholongitas E, Pantelis E, et al. Type I Gaucher disease with severe skeletal destruction, extraosseous extension, and monoclonal gammopathy. Am J Hematol 2004; 77:377–380. 9. Hermann G, Shapiro R, Abdelwahab IF, et al. Extraosseous extension of Gaucher cell deposits mimicking malignancy. Skeletal Radiol 1994; 23:253–256. 10. Poll LW, Koch J-A, et al. Type I Gaucher disease: extraosseous extension of skeletal disease. Skeletal Radiol 2000; 29:15–21. 11. Fiore CE, Barone R, Pennisi P, et al. Bone ultrasonometry, bone density, and turnover markers in type 1 Gaucher disease. J Bone Miner Metab 2002; 20:34–38. 12. Charrow J, Andersson HC, Kaplan P, et al. Enzyme replacement therapy and monitoring for children with type 1 Gaucher disease: consensus recommendations. J Pediatr 2004; 144:112–120. 13. Rosenthal DI, Scott JA, Barranger J, et al. Evaluation of Gaucher disease using magnetic resonance imaging. J Bone Joint Surg Am 1986; 68:802–808. 14. Baur A, Stabler A, Lamerz R, et al. Light chain deposition disease in multiple myeloma: MR imaging features correlated with histopathological findings. Skeletal Radiol 1998; 27:173–176. 15. Rosenthal DI, Barton NW, McKusick KA, et al. Quantitative imaging of Gaucher disease. Radiology 1992; 185:841–845. 16. Hermann G, Shapiro RS, Abdelwahab IF, Grabowski G. MR imaging in adults with Gaucher disease type I: evaluation of marrow involvement and disease activity. Skeletal Radiol 1993; 22:247–251. 17. Vlieger EJP, Maas M, Akkerman EM, et al. The application of the vertebra-disc ratio in a population of patients with Gaucher disease [Abstract]. Proc Intl Soc Magn Reson Med 2000; 8:2131. 18. Johnson L, Hoppel B, Gerard E, et al. Quantitative chemical shift imaging of vertebral bone marrow in patients with Gaucher disease. Radiology 1992; 182:451–455.

19. Terk MR, Esplin J, Lee K, et al. MR imaging of patients with type I Gaucher disease: relationship between bone and visceral changes. AJR Am J Roentgenol 1995; 165:599–604. 20. Maas M, Hollak CEM, Akkerman EM, et al. Quantification of skeletal involvement in adults with type I Gaucher disease: fat fraction measured by Dixon quantitative chemical shift imaging as a valid parameter. AJR Am J Roentgenol 2002; 179:961–965. 21. Mariani G, Filocamo M, Giona F, et al. Severity of bone marrow involvement in patients with Gaucher disease evaluated by scintigraphy with 99mTc-sestamibi. J Nucl Med 2003; 44:1253–1262. 22. Barton NW, Brady RO, Dambrosia JM, et al. Dose-dependent responses to macrophage-targeted glucocerebrosidase in a child with Gaucher disease. J Pediatr 1992; 120(2 pt 1):277–280. 23. Whittington R, Goa KL. Alglucerase: a review of its therapeutic use in Gaucher disease. Drugs 1992; 44:72–93. 24. Bembi B, Ciana G, Mengel E, et al. Bone complications in children with Gaucher disease. Br J Radiol 2002; 75(Suppl 1): A37–A44. 25. Poll LW, Koch J-A, vom Dahl S, et al. Magnetic resonance imaging of bone marrow changers in Gaucher disease during enzyme replacement therapy: first German long-term results. Skeletal Radiol 2001; 30:496–503. 26. Rosenthal DI, Doppelt SH, Mankin HJ, et al. Enzyme replacement therapy for Gaucher disease: skeletal responses to macrophagetargeted glucocerebrosidase. Pediatrics 1995; 96(4 pt 1):629–637. 27. Schiffmann R, Mankin H, Dambrosia JM, et al. Decreased bone density in splenectomized Gaucher patients receiving enzyme replacement therapy. Blood Cells Mol Dis 2002; 28:288–296. 28. Figueroa ML, Rosenbloom BE, Kay AC, et al. A less costly regimen of alglucerase to treat Gaucher disease. N Engl J Med 1992; 327:1632–1636. 29. Pastores GM, Patel MJ, Firooznia H. Bone and joint complications related to Gaucher disease. Curr Rheumatol Rep 2000; 2:175–180. 30. Pastores GM, Weinreb NJ, Aerts H, et al. Therapeutic goals in the treatment of Gaucher disease. Semin Hematol 2004; 41(4 Suppl 5):4–14. 31. Andersson HC, Charrow J, Kaplan P, et al. Individualization of long-term enzyme replacement therapy for Gaucher disease.[erratum appears in Genet Med 2005 Jul-Aug;7(6):460]. Genet Med 2005; 7:105–110. 32. Itzchaki M, Lebel E, Dweck A, et al. Orthopedic considerations in Gaucher disease since the advent of enzyme replacement therapy. Acta Orthop Scand 2004; 75:641–653. 33. Iwase T, Hasegawa Y, Iwata H. Transtrochanteric anterior rotational osteotomy for Gaucher disease: a case report. Clin Orthop Relat Res 1995; (317):122–125. 34. Ringden O, Groth CG, Erikson A, et al. Ten years’ experience of bone marrow transplantation for Gaucher disease. Transplantation 1995; 59:864–870.

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C H A P T E R

Storage Diseases (Mucopolysaccharidoses/ Glycogenoses) Calvin Ma and Rodrigo Dominguez

Lysosomal storage diseases are a group of inborn errors of metabolic disorders characterized by accumulation of incompletely metabolized substrates inside lysosomes due to deficiency in one of the numerous enzymes required for substrate degradation. They comprise more than 30 different syndromes and are generally divided into lipidoses, glycogenoses, and mucopolysaccharidoses. Most of these disorders are severely debilitating and lead to premature death. The focus of this chapter is on mucopolysaccharidoses and glycogenoses. Only the clinical and radiographic findings are discussed. Detailed biochemical and pathophysiologic aspects of each disorder are extensively covered in many articles and textbooks, some of which are listed in the suggested readings and references at the end of this chapter.

Glycogenoses

ETIOLOGY Mucopolysaccharidoses

PREVALENCE AND EPIDEMIOLOGY

Mucopolysaccharidoses (MPS) result from the absence or defect of enzymes required for the breakdown of glycosaminoglycan (GAG), also formerly known as mucopolysaccharide. GAGs are long-chain carbohydrates that contribute to the formation of bones, cartilage, tendons, corneas, skin, and connective tissues. A deficiency in one of the enzymes that break down GAG will result in intracellular substrate accumulation, leading to structural and functional abnormalities at the cellular and tissue level. The specific enzyme deficiencies that lead to a specific substrate accumulation and their corresponding syndromes are listed in Table 80-1.1 The mucopolysaccharidoses are inherited in an autosomal recessive pattern, with the exception of MPS II (Hunter syndrome), which is inherited in an X-linked recessive mode. 1558

The glycogenoses (glycogen storage diseases, GSD) are another group of lysosomal storage disorders that result from deficiency in enzymes required for the breakdown of glycogen. Failure to completely metabolize glycogen results in accumulation and storage of glycogen substrates in lysosomes of hepatic and muscle tissues where glycogen is most abundant. These tissues are therefore most commonly and severely affected by the glycogen storage disorders. The specific enzyme deficiency and its associated syndromes are summarized in Table 80-2.2–4 The glycogenoses are inherited in an autosomal recessive pattern, with the exception of type IX in which several subtypes are inherited as an X-linked pattern.

The incidence for all types of mucopolysaccharidoses is estimated to be 1 in 25,000 births.5 There is no known racial or gender predilection for any of these disorders

KEY POINTS Mucopolysaccharidoses are progressive disorders involving multiple organs, including the brain, liver, spleen, heart, and blood vessels; and many are associated with coarse facial features, clouding of the cornea, and mental retardation. ■ Glycogenoses are also progressive disorders involving multiple organs, but the liver and skeletal muscles are most commonly and severely affected. Most types of glycogenoses are associated with some degree of hepatomegaly or muscle weakness. ■

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TABLE 80-1 Mucopolysaccharidoses Type

Enzyme Deficiency

Substrate Accumulated

MPS I H-Hurler MPS I H/S-Hurler-Scheie MPS I S-Scheie MPS II-Hunter

α-L-Iduronidase

Heparan sulfate Dermatan sulfate

Iduronidate sulfatase

MPS IIIA-Sanfilippo A MPS IIIB-Sanfilippo B MPS IIIC-Sanfilippo C MPS IIID-Sanfilippo D MPS IV-Morquio MPS VI-Maroteaux-Lamy MPS VII-Sly

Heparan-N-sulfatase N-Acetyl-α-glucosaminidase α-Glucosaminidase N-Acetylglucosamine-6-sulfate N-Acetylgalactosamine-6-sulfatase Arylsulfatase B β-Glucuronidase

Heparan sulfate Dermatan sulfate Heparan sulfate

MPS IX-Natowicz

Hyaluronidase

Keratan sulfate, chondroitin sulfate Dermatan sulfate Heparan sulfate Dermatan sulfate Chondroitin sulfate

Data from Neufeld EF, Muenzer J.The mucopolysaccharidoses. In Scriver C, Beaudet AL, Valle D, Sly W (eds).The Metabolic and Molecular Bases of Inherited Disease, 8th ed. New York, McGraw-Hill, 2001, vol 3, pp 3421–3452.

TABLE 80-2 Glycogen Storage Diseases Type

Enzyme Deficiency

Target Organ

Key Clinical Findings

I: von Gierke, hepatorenal glycogenosis

Ia: Glucose-6-phosphatase Ib: Glucose-6-phosphate translocase

Liver, spleen, kidney, intestines, leukocytes

II: Pompe, acid maltase deficiency III: Forbes-Cori, limit dextrinosis IV: Andersen, amylopectinosis

α-1,4-Glucosidase (acid maltase)

Heart, skeletal muscles

Hypoglycemia, hyperuricemia, hyperlipidemia, lactic acidosis, hepatosplenomegaly, nephromegaly Hypotonia, cardiomyopathy

Amylo-1,6-glucosidase (debrancher)

Liver, heart, muscle, leukocytes Liver

V: McArdle

Amylo-1,4-1,6-transglucosidase (debrancher) Muscle phosphorylase

Skeletal muscles

VI: Hers VII:Tarui

Liver phosphorylase Phosphofructokinase

Liver, leukocytes Skeletal muscles, erythrocytes

IX

Liver phosphorylase kinase

Liver, skeletal muscles, heart, erythrocytes

Hypotonia, hepatomegaly, cirrhosis, fasting ketosis Hepatomegaly, cirrhosis Exercise intolerance, rhabdomyolysis, renal failure Hepatomegaly, mild hypoglycemia Exercise intolerance, rhabdomyolysis, renal failure Hepatomegaly, hyperlipidemia, fasting ketosis

Data from references 2 to 4.

except for Hunter syndrome (MPS II), which is inherited as X-linked recessive and thus predominantly affects males. The cumulative incidence of glycogen storage diseases is estimated to be around 1:20,000 to 1:25,000 births.4 There are no racial differences for most of the glycogen storage diseases. However, the highest incidence for GSD III has been recorded in non-Ashkenazi Jews in northern Africa, and GSD VI has been most commonly reported in Japanese and Ashkenazi Jews. There is no gender preference except for subtypes of GSD IX that are inherited in an X-linked pattern in which mostly male patients are affected.

CLINICAL PRESENTATION Mucopolysaccharidoses6–11 Hurler Syndrome (MPS I H) Hurler syndrome is the most severe form and one of the most commonly encountered mucopolysaccharidoses. Infants with Hurler syndrome usually appear normal at birth and are not diagnosed until early in their second year of life. Clinical features begin to develop after 6 to 12 months with coarsening of facial features. The head is enlarged with widely spaced eyes, corneal clouding, frontal bossing, flattened nasal bridge, everted lips, protruded tongue, and

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widely separated and hypoplastic teeth. Umbilical or inguinal hernias may be present. Hepatosplenomegaly results in a protuberant abdomen. Lumbar gibbus leads to a stooped posture accentuated by flexion contractures of the hip and knee joints. Flexion contracture of the hand leads to claw hand deformity, stiff joints, and carpal tunnel syndrome. Mucopolysaccharide deposition in the trachea, nasopharynx, and esophagus leads to aerodigestive tract obstruction with persistent rhinitis, adenotonsillar hypertrophy, sleep apnea, recurrent upper respiratory tract infection, and feeding difficulties.12 Deposition in cardiac valves and coronary arteries eventually results in valvular dysfunction, coronary artery disease, and ischemic cardiomyopathy.13 Deposition in the leptomeninges leads to communicating hydrocephalus and an enlarged cranium with sutural diastasis. Growth disturbance results in severe dwarfism. There is progressive mental deterioration. These children eventually die between 10 and 15 years of age from pneumonia or cardiac failure. Many of the other mucopolysaccharidoses, with the exception of MPS IV or Morquio syndrome, have clinical and radiographic findings similar to Hurler syndrome, although with different degrees of severity (Fig. 80-1).

Scheie Syndrome (MPS I S) Scheie syndrome is the least severe form of the MPS I group. There is nearly normal height, intellect, and life span, although the life span may be somewhat shortened by the presence of aortic valve disease, which is seen in almost all cases. Somatic presentations include corneal clouding, joint stiffness, and carpal tunnel syndrome. Psychosis is common.

Hurler-Scheie Syndrome (MPS I H/S) Hurler-Scheie syndrome is intermediate in severity between Hurler syndrome and Scheie syndrome. The clinical and skeletal features more closely resemble those of Hurler syndrome, but the patients survive slightly longer into their 20s and the psychomotor retardation and dwarfism are less severe.

Hunter Syndrome (MPS II) Hunter syndrome is the only mucopolysaccharidosis that is X-linked recessive. The clinical features are similar to those of Hurler syndrome but less severe. Coarse facies, hepatosplenomegaly, growth failure, and joint stiffness occur later than in Hurler syndrome. Psychomotor retardation is less severe. Seizures are common. Corneal clouding is not apparent but can be detected on slit-lamp examination. Half of the children become deaf. Cutaneous nodules over the scapula and upper back are uniquely seen with Hunter syndrome. The patients are typically diagnosed around 2½ to 5 years old. Patients with the severe form of Hunter syndrome usually die in 10 to 15 years secondary to cardiac causes, and those with the mild form may survive to the fourth decade or later.

Sanfilippo Syndrome (MPS III) The Sanfilippo syndrome can result from four different enzyme deficiencies (see Table 80-1) that lead to accumulation of the same substrate—heparan sulfate— and result in clinically indistinguishable features. The patients appear normal until 3 to 5 years old when there is progressive and profound mental deterioration, which is the most striking feature in this mucopolysaccharide group. There are learning difficulties and behavioral disturbances characterized by severe hyperactivity and aggression. Seizures are common. The patients do not have dwarfism and do not have cardiac disease. Corneal clouding is minimal and detected on slit-lamp examination. Joint stiffness is mild. Other clinical and skeletal changes are similar to those of Hurler syndrome and Hunter syndrome but milder. Most patients die between 10 and 30 years of age.

Morquio Syndrome (MPS IV) Previously, Morquio syndrome was divided into types A and B, with both types thought to occur from defects in separate enzymes. However, MPS IVB is now considered a variant of GM1-gangliosidosis. Morquio syndrome does not closely resemble other mucopolysaccharide disorders; it has distinctive skeletal manifestations that are usually diagnostic. Morquio syndrome is usually not apparent at birth but can be diagnosed by 1 year old. There is striking dwarfism, with height rarely exceeding 4 feet in adult life. Intelligence is normal; mental retardation is rare. The cornea is slightly clouded and only detectable on slitlamp examination. The head is of normal size. Morquio syndrome is one of the most commonly encountered mucopolysaccharidoses, along with Hurler syndrome.

Maroteaux-Lamy Syndrome (MPS VI)

■ FIGURE 80-1 Corneal clouding in Hurler syndrome. (From Ashworth JL, Biswas S, Wraith E, Lloyd IC. Mucopolysaccharidoses and the eye. Surv Ophthalmol 2006; 51:7. Copyright 2006 by Elsevier, with permission.)

The striking clinical features of this syndrome are dwarfism and corneal clouding without mental impairment. The somatic and skeletal changes are very similar to those of Hurler syndrome. Patients have coarse facial features, hepatosplenomegaly, inguinal hernias, severe cardiac abnormalities, hydrocephalus, and hearing defects. Growth slows down at 4 years old and stops completely by 8 years of age, resulting in severe dwarfism.

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Sly Syndrome (MPS VII) The clinical and radiographic findings of Sly syndrome are similar to those of Hurler syndrome, but there is great variation in severity. In general, there is restricted growth and mental development. Sly syndrome often presents as nonimmune hydrops fetalis, and the patients rarely survive more than a few months.

Natowicz Syndrome (MPS IX) There has only been one patient reported to date with this syndrome. Mild short stature and periarticular soft tissue masses were noted, but there were no neurologic or ocular findings.14

Glycogenoses Glycogen is most abundantly found in the liver and skeletal muscles. Consequently, these organs are most commonly and seriously affected by the glycogen storage diseases.2,3,4,9,15,16 A disorder in hepatic glycogen metabolism results in fasting hypoglycemia, seizures, hepatomegaly, and, in some types, cirrhosis of the liver. A disorder in muscle glycogen metabolism results in muscle weakness, cramps, and exercise intolerance. A summary of the enzyme deficiency of each specific glycogen storage disease and the target organs with key clinical findings is provided in Table 80-2.

von Gierke Disease (GSD I) Type I glycogenosis, also called von Gierke disease, presents early in infancy with hypoglycemia, lactic acidosis, and marked hepatomegaly. Severe hypoglycemia results in seizures. Hepatomegaly results in a protuberant abdomen and may be the first sign noted by the mother. Splenomegaly and nephromegaly may be seen. Hyperuricemia also develops and predisposes to gouty arthritis, which is found later in life around puberty along with uric acid renal stones. Hyperlipidemia is also present and manifests as skin xanthomas in the extremities and predisposes to pancreatitis. Easy bruising and epistaxis are common as a result of impaired platelet aggregation and adhesion. Hepatic adenomas develop in most patients by their second or third decades of life. Growth retardation results in short stature, and puberty is delayed. Osteoporosis is present, with frequent fractures reported. Other late complications include renal disease, renal stones, and hypertension. A variant of GSD I known as type Ib is caused by a deficiency in glucose-6-phosphate translocase. In addition to these clinical findings, von Gierke disease is further characterized by neutropenia and presents as recurrent bacterial infections and chronic inflammatory diseases such as inflammatory bowel disease with oral lesions and intestinal ulcers.

Pompe Disease (GSD II) Type II glycogenosis, or Pompe disease, has three different clinical phenotypes: classic or infantile form (type IIa), juvenile form (type IIb), and adult form (type IIc). The classic or infantile form presents early in infancy as profound hypotonia and muscle weakness manifesting as respiratory and feeding difficulties. Cardiomegaly, cardio-

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myopathy, and heart failure are prominent. Macroglossia and hepatomegaly may be noted. These patients typically die in the first year of life. Despite the hypotonia and flaccidity, the muscles in these patients are actually firm and even hypertrophic. The juvenile form presents later in infancy after age 6 to 12 months and may have both cardiac enlargement and muscle weakness or muscle involvement only without cardiomegaly. Muscle weakness is predominantly proximal. Patients may have recurrent pneumonia due to respiratory muscle weakness. Death is usually in the first decade of life. In the adult form, the disease course is milder and more slowly progressive, with symptoms beginning from the second to sixth decades. There is progressive myopathy in striated muscles that may eventually lead to paralysis of diaphragmatic muscles and death. The heart is not affected in the adult form.

Forbes-Cori Disease (GSD III) Type III glycogenosis, also known as Forbes-Cori disease or limit dextrinosis, results from a deficiency of glycogen debranching enzyme activity, resulting in impaired release of glucose from glycogen. GSD III shares many similar clinical features with GSD I, but the symptoms are milder and most patients with type III disease survive longer. During infancy and childhood, GSD III may be clinically indistinguishable from GSD I, with hypoglycemia, hepatomegaly, hyperlipidemia, and growth retardation as the predominant clinical findings. Splenomegaly may be seen, but the kidneys are not enlarged in type III disease. Unlike type I disease, lactic acid and uric acid levels are normal in GSD III. On the other hand, elevated levels of liver transaminases are prominent and progressive liver cirrhosis and failure may occur. In adults, progressive muscle weakness and distal muscle wasting can become severe after the third or fourth decade. Fasting ketosis is a common finding in this type of glycogenosis.

Andersen Disease (GSD IV) Type IV glycogenosis, also called Andersen disease or amylopectinosis, is another disease resulting from deficiency of a debranching enzyme. It is very rare and typically presents in the first few months of life as hepatomegaly, splenomegaly, and failure to thrive. The infant develops progressive hepatic cirrhosis and subsequently portal hypertension, ascites, and esophageal varices. Most patients die before 5 years of age.

McArdle Disease (GSD V) Type V glycogenosis, known as McArdle disease, exclusively involves skeletal muscles and restricts physical activity. Clinical symptoms typically present in young adulthood with complaints of muscle cramps and exercise intolerance. These patients may report lack of endurance and weakness since childhood. They are unable to sustain brief intense activities such as sprinting or carrying heavy loads and less intense but sustained activities such as climbing stairs or walking up a hill. However, they are able to sustain exercises that are moderate in intensity at their own pace. Rhabdomyolysis with myoglobinuria and even acute renal failure may develop after vigorous exercise.

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Hers Disease (GSD VI) Type VI glycogenosis, or Hers disease, shares many features with type I but is milder and has a benign course. The patients present with hepatomegaly and growth retardation early in childhood. They may have mild hypoglycemia, hyperlipidemia, and hyperketosis. Unlike GSD I, lactic acid and uric acid are normal. The heart and skeletal muscles are not affected in Hers disease. The hepatomegaly usually regresses by puberty.

to communicating hydrocephalus or arachnoid cysts. Diastasis of the coronal sutures may be observed. There is usually a scaphocephalic configuration due to premature fusion of the sagittal and lambdoid sutures. There is frontal bossing and calvarial thickening. Deepening of the optic chiasm recess results in a J-shaped sella turcica. The mandible is thickened and short, the mandibular angle is widened, the rami are short, and the condyles are flat or concave secondary to hypoplasia. The teeth are hypoplastic and widely spaced (Fig. 80-2).

Tarui Disease (GSD VII)

Chest

Type VII glycogenosis, also known as Tarui disease, is clinically similar to GSD V but results from a deficiency in a different enzyme. The patients present with fatigue and pain with exercise. Vigorous activities will result in muscle cramps and rhabdomyolysis. However, compared with McArdle disease, the exercise intolerance is seen at a younger age in childhood and is more severe. A compensated hemolytic anemia also occurs in this disease. Hyperuricemia is often seen and exaggerated by exercise.

GSD IX Type IX glycogenosis has many subtypes, but the most common form of type IX is liver phosphorylase kinase deficiency, which accounts for 75% of all cases and is X-linked, unlike the rest of the GSD types. Patients present with growth retardation, hepatomegaly, mild hyperlipidemia, and fasting ketosis. These clinical findings disappear with time, and most adults are asymptomatic. Although initially presenting with growth retardation, most patients reach a final normal adult height.

PATHOPHYSIOLOGY

The ribs are oar-shaped and wider than the intercostal spaces but become narrower in the paravertebral region. The clavicles are short and thick medially and hookshaped laterally. The scapulas are small and irregular. The glenoid fossa may be hypoplastic. Tracheal narrowing may be observed on the chest radiograph (Fig. 80-3).

Spine A thoracolumbar gibbus deformity usually develops by age 18 months due to hypoplasia of the anterosuperior aspect of the vertebral body at the thoracolumbar junction, which gives an anteroinferior beaking appearance. The other vertebral bodies have short anteroposterior diameter with concave anterior and posterior surfaces. The vertebral bodies are ovoid with convex superior and inferior end plates. The spinous process is dysplastic (Fig. 80-4). Odontoid hypoplasia, a characteristic feature of Morquio syndrome, has been described in Hurler syndrome and a few other mucopolysaccharidoses.23 Under fluoroscopy, dynamic craniovertebral junction instability may be observed secondary to odontoid hypoplasia and ligamentous laxity (see Fig. 80-8).

Briefly, the lysosomal storage diseases result from a deficiency in one of the many enzymes required for substrate degradation. Absence of any one of the enzymes in the sequence of substrate metabolism results in an incompletely digested product that accumulates within lysosomes, cells, and tissues, altering the structural and biomechanical properties of the affected tissue.

MANIFESTATIONS OF THE DISEASE: MUCOPOLYSACCHARIDOSES With the exception of Morquio syndrome, the skeletal abnormalities of the mucopolysaccharidoses are qualitatively similar and referred to as dysostosis multiplex.6–10,17–22 They have varying degrees of dysostosis multiplex. Radiographic abnormalities are not present at birth but generally can be seen by 2 years of age. The mucopolysaccharidoses that have significant skeletal manifestations include MPS I, II, IV, VI, and VII.

Radiography Hurler Syndrome (MPS I H) Skull The skull is normal at birth with the earliest changes noted after 6 months. The skull will usually enlarge due

■ FIGURE 80-2

Hurler syndrome. The cranium is enlarged with premature fusion of the sagittal and lambdoid sutures, resulting in a scaphocephalic configuration. The sella turcica is J shaped. The mandibular rami are short, and the mandibular angle is widened. The teeth are hypoplastic and widely spaced.

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■ FIGURE 80-3

Hurler syndrome. The ribs are oar-shaped and wider than the intercostal spaces but become narrower in the paravertebral region. The iliac wings of the pelvis are flared, and the iliac body is constricted inferiorly.

Pelvis The iliac wings are flared, and the iliac body is constricted inferiorly. The acetabula are oblique (Figs. 80-3, 80-5). Coxa valga is frequently seen, but dislocation of the hip is uncommon (see Fig. 80-5).

Hand The carpal bones are small and irregular. The metacarpals and proximal and middle phalanges are short and wide without normal diaphyseal constrictions. The second to fifth metacarpal bones are tapered and pointed proximally. The distal phalanges are hypoplastic (Fig. 80-6). There is coarse bony trabeculation. Flexion contracture of the hand results in a claw hand deformity.

Long Bones There is defective modeling in the long bones with diaphyseal widening. The upper extremities are generally affected more than the lower extremities. Proximal

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■ FIGURE 80-4 Hurler syndrome. There is hypoplasia of the anterosuperior aspect of the vertebral body at the thoracolumbar junction resulting in an anteroinferior beaking appearance. The other vertebral bodies have a short anteroposterior dimension and are ovoid with concave anterior and posterior margins and convex superior and inferior end plates. Thoracolumbar gibbus deformity is typically present in Hurler syndrome.

humeral constriction leads to varus configuration of humeral heads. The long tubular bones are short and poorly modeled. The diaphyses are wide, whereas the metaphyses are concomitantly constricted. The humeral neck is in varus configuration. The distal radius and ulna are tilted toward each other (see Fig. 80-6).

The Other Mucopolysaccharidoses (Except Morquio Syndrome) In Scheie syndrome, the radiographic findings are minimal. The skeleton and stature are almost normal. There are mild hypoplastic and cystic deformities of the carpal bones and base of the metacarpophalangeal bones. There is a claw hand deformity. In Hurler-Scheie syndrome the dysostosis multiplex is moderate. In Hunter syndrome there is moderate dysostosis multiplex in the classic form and mild dys-

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■ FIGURE 80-6 Hurler syndrome. The metacarpal bones are tapered and pointed proximally. The distal phalanges and carpal bones are hypoplastic. There is defective modeling of the long bones with diaphyseal widening, with the upper extremities generally affected more than the lower extremities. The distal radius and ulna are tilted toward each other. ■ FIGURE 80-5 Hurler syndrome. The iliac wings are flared with constriction of the iliac body inferiorly. The acetabula are oblique. Coxa valga is observed.

ostosis in the mild form of the disease. However, unlike in Hurler syndrome, gibbus deformity and coxa valga are not usually seen. The calvaria is normal, and the sella turcica is also normal. In Sanfilippo syndrome, the dysostosis multiplex may be mild. However, marked hyperostosis of the parietal and occipital bones, normal sella turcica, and sclerotic nonpneumatized mastoids are commonly observed. Morquio syndrome has distinctive skeletal findings (see later). Maroteaux-Lamy syndrome has skeletal changes that are very similar to those of Hurler syndrome but with varying severity. There is characteristic deficient ossification of the superior portion of femoral capital epiphyses in most children, and this may be misdiagnosed as LeggCalvé-Perthes disease or cretinism. In later stages of the disorder, the femoral heads are flat and wide (coxa plana, coxa magna). Coxa valga is observed. Joint restriction at the hips, knees, and elbows is common. Pectus carinatum is also observed. In Sly syndrome there is great variability in the radiographic findings.

Morquio Syndrome (MPS IV) Unlike the other mucopolysaccharidoses, Morquio syndrome has distinctive skeletal findings. In the spine there is universal vertebra plana or platyspondyly, which can be distinguished from the oval vertebral bodies of Hurler and other mucopolysaccharidoses. In addition, the anterior beaking in Morquio is central, compared with the inferior beaking in Hurler syndrome (Fig. 80-7). Odontoid hypoplasia is characteristic of Morquio syndrome, with associated ligamentous laxity potentially resulting in atlantoaxial subluxation and spinal cord compression (Fig. 80-8). Cervical cord compression from atlantoaxial instability was a major cause of death in Morquio syndrome, but nowadays patients often undergo elective cervical fusion so they can survive to their third or fourth decades, where they often die of respiratory complication. Another characteristic finding is a fixed pectus carinatum deformity with restriction of chest wall motion. In the upper extremities, ulnar deviation may

be seen secondary to shortening of the ulna. The articular surfaces of the distal radius and ulna are angled toward each other. The carpal bones are small and irregular, the scaphoid does not ossify, and the metacarpal bones are short. The metaphyseal ends of the bones are widened and the epiphyseal ends are irregular. There is brachydactyly. In the pelvis, there is flaring of the iliac wings with sloping acetabular roofs beginning at 1 year old. The body of the iliac bones becomes very constricted inferiorly. The developing femoral capital epiphyses show early compression. The epiphyses initially appear fragmented and eventually disappear. The femoral necks become progressively wider and are eroded. Coxa valga increases. The lower limbs also include prominent features such as pes planus and genu valgum, with the latter resulting from hypoplasia of the lateral portions of the proximal tibial epiphyses. There are flexion deformities of both knees and hips, resulting in a semicrouching stance. The long bones are characterized by diaphyseal constriction with abrupt metaphyseal widening (Figs. 80-7 and 80-8). Although certain types of mucopolysaccharidoses may have prominent features that suggest one type over another, urinary testing for excretion of mucopolysaccharides should be performed when the disorder is suspected. Confirmation is made by demonstration of specific enzyme deficiency in peripheral blood leukocytes or fibroblast cells.

Magnetic Resonance Imaging Magnetic resonance imaging is usually obtained of the brain and cervical spine, with particular attention made to the craniocervical junction. The odontoid may be hypoplastic, predisposing the patient to atlantoaxial instability. In addition, thickening of the dura mater can result in cord compression. On T1-weighted images, there is hypointense to isointense periodontoid soft tissue mass and hypointense thickened dura. On T2-weighted images, the hypoplastic dens, periodontoid soft tissue mass, and thickened dura are hypointense. If cord compression is present, there is hyperintense signal within the cord.

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■ FIGURE 80-7 Morquio syndrome. A, There is universal vertebra plana, or flattened vertebral bodies. This can be distinguished from the ovoid vertebral bodies of Hurler syndrome and other mucopolysaccharidoses. The central anterior beaking of Morquio syndrome also differs from the anteroinferior beaking of Hurler syndrome and other mucopolysaccharidoses. B, Note again the platyspondyly of the vertebral bodies and the severe changes in the hip. (From Resnick D. Osteochondrodysplasias, dysostoses, chromosomal aberrations, mucopolysaccharidoses, and mucolipidoses. In Resnick D, Kransdorf MJ [eds]. Bone and Joint Imaging, 3rd ed. Philadelphia, Elsevier, 2005, pp 1321, 1323.)

On contrast-enhanced T1-weighted images, no abnormal enhancement is seen (Fig. 80-9).

Multidetector Computed Tomography On CT images of the cervical spine, central and foraminal narrowing may be observed at the craniovertebral junction. In severe cases, compression on the cord may be observed. On contrast-enhanced CT, there is marked dural thickening without or with only mild enhancement.24 Abnormal dens ossification may also be noted (Fig. 80-10).

MANIFESTATONS OF THE DISEASE: GLYCOGENOSES Unlike mucopolysaccharidoses, glycogenoses do not involve many skeletal changes. The bone changes are nonspecific.2,9,25

Radiography The radiograph may demonstrate osteopenia, as evidenced by thinned cortices, expansion of medullary cavities, and loss of trabeculation. Fractures are frequently seen as a result of osteopenia and hypoglycemic seizures. Bone maturation is retarded. Multiple growth arrest lines may be seen. Scalloping of the anterior surface of the thoracolumbar vertebral bodies (T11-L2) has been reported in several types of glycogenoses. Exaggerated lumbosacral lordosis or scoliosis may be seen. Nutrient foramina may be prominent in the middle phalanx of the third finger. Failure of constriction of the metaphysis of tubular bones has been described in some cases. In other cases there is overconstriction of the long bones. Spiculation of the physeal plate was seen in all types except GSD II. Patients with type I disease may develop gouty arthritis secondary to long-standing hyperuricemia.

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■ FIGURE 80-8 Flexion (A) and extension (B) views of the cervical spine from a patient with Morquio syndrome. There is hypoplasia of the odontoid that predisposes to atlantoaxial subluxation and spinal cord compression. Also observed is platyspondyly of the vertebral bodies. (Courtesy of Martin Williams, MD.)

■ FIGURE 80-9 MR images of the cervical spine in a patient with Hunter syndrome. A, Sagittal T1-weighted image demonstrates marked cord compression at the level of C2 and C3 by hypointense thickened dura. B, Axial T2-weighted gradient-echo MR image demonstrates thinned spinal cord surrounded by a hypointense thickened dura (arrow). (From Vinchon M, Cotten A, Clarisse J, et al. Cervical myelopathy secondary to Hunter syndrome in an adult. AJNR Am J Neuroradiol 1995; 16:1403. Copyright 1995 by American Society of Neuroradiology, with permission.)

Magnetic Resonance Imaging Magnetic resonance imaging may demonstrate pseudohypertrophy of skeletal muscles. In GSD type 1b, MRI of the extremities may demonstrate hematopoietic marrow in regions in which normal fatty conversion is expected, reflecting bone marrow hypercellularity accompanying the neutropenia.26

Multidetector Computed Tomography Computed tomography may demonstrate atrophy of the posterior paraspinal and psoas muscles.27 The psoas muscles were observed to be spared in McArdle disease.

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Medical Treatment

■ FIGURE 80-10 Axial nonenhanced CT image of the cervical spine in a patient with Hunter syndrome demonstrates markedly thickened dura mater with cord compression (arrow). (From Vinchon M, Cotten A, Clarisse J, et al. Cervical myelopathy secondary to Hunter syndrome in an adult. AJNR Am J Neuroradiol 1995; 16:1403. Copyright 1995 by American Society of Neuroradiology, with permission.)

DIFFERENTIAL DIAGNOSIS The differential diagnosis of the mucopolysaccharidoses and glycogen storage diseases is presented in Table 80-3.

SYNOPSIS OF TREATMENT OPTIONS Managing the systemic involvement of lysosomal storage disorder patients requires a multidisciplinary team effort coordinated by the patient’s pediatrician or internist.

In mucopolysaccharidoses, the main therapeutic options include bone marrow transplantation and enzyme replacement therapy.1,7 Bone marrow transplantation may result in improvement of airway disease, cardiomyopathy, and abdominal organ enlargement. Neurologic conditions may stabilize. Skeletal changes unfortunately do not respond to treatment, and patients continue to need orthopedic intervention. Laronidase treatment in MPS I patients has been reported to decrease storage of GAG and improve respiratory function, sleep apnea, and overall functional capacity. In glycogenoses, the current treatment includes nocturnal nasogastric infusion of glucose or oral administration of uncooked cornstarch for GSD I, high-protein diet and supportive therapies in GSD II, symptomatic treatment in GSD III, oral administration of glucose or fructose during exercise for GSD V and GSD VII, and high-carbohydrate diet and frequent feedings in GSD VI.4,15 Enzyme replacement therapy has been reported to improve cardiac function and structure, increase overall muscle strength, and improve survival in patients with Pompe disease.28

Surgical Treatment Surgical management of mucopolysaccharidoses may include elective occipital-cervical fusion to avoid compromising the cord from atlantoaxial instability and surgery to relieve compression on the cord from thickened dura mater, surgery for hip dislocation, bracing for thoracolumbar kyphosis, epiphyseal stapling, and tibial osteotomy for knee deformity. Other possible procedures include valve replacements, angioplasty, hernia repair, carpal tunnel release, and ventriculoperitoneal shunting for hydrocephalus. In the glycogenoses, surgical treatment may include liver transplantation and renal transplantation.

What the Referring Physician Needs to Know ■

TABLE 80-3 Differential Diagnosis of Mucopolysaccharidoses

and Glycogen Storage Diseases

■

Mucopolysaccharidoses

Glycogen Storage Diseases

Achondroplasia Spondyloepiphyseal dysplasia Other skeletal dysplasias Down syndrome Klinefelter syndrome

Duchenne muscular dystrophy Limb girdle dystrophy Polymyositis Danon disease Other myopathies or neuromuscular disorders Other storage disorders

Mucolipidoses such as Gaucher disease, Fabry disease Other storage disorders

■

■

■

Diagnosis of mucopolysaccharidosis can often be made by examination of urine for excretion of GAG fragments. Prenatal screening for mucopolysaccharidosis is possible with sampling of amniotic fluid or chorionic villus. Patients with odontoid hypoplasia should undergo elective cervical spine fusion to avoid cord compression from atlantoaxial subluxation. In glycogenosis, abdominal ultrasonography should be performed to detect for hepatic adenomas in the liver and rare but possible malignant degeneration. Echocardiography should be performed to detect for cardiac involvement in glycogenosis.

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SUGGESTED READINGS Ashworth JL, Biswas S, Wraith E, Lloyd IC. Mucopolysaccharidoses and the eye. Surv Ophthalmol 2006; 51:1–17. Eggli KD, Dorst JP. The mucopolysaccharidoses and related conditions. Semin Roentgenol 1986; 21:275–294. Kachur E, Del Maestro R. Mucopolysaccharidoses and spinal cord compression: case report and review of the literature with implications of bone marrow transplantation. Neurosurgery 2000; 47:223–228.

Mikles M, Stanton RP. A review of Morquio syndrome. Am J Orthop 1997; 26:533–540. Muenzer J. Mucopolysaccharidoses. Adv Pediatr 1986; 33:269–302. Northover H, Cowie RA, Wraith JE. Mucopolysaccharidosis type IVA (Morquio syndrome): a clinical review. J Inherit Metab Dis 1996; 19:357–365.

REFERENCES 1. Neufeld EF, Muenzer J. The mucopolysaccharidoses. In Scriver C, Beaudet AL, Valle D, Sly W (eds). The Metabolic and Molecular Bases of Inherited Disease, 8th ed. New York, McGraw-Hill, 2001, vol 3, pp 3421–3452. 2. Miller JH, Stanley P, Gates GF. Radiography of glycogen storage diseases. AJR Am J Roentgenol 1979; 132:379–387. 3. Kishnani PS, Howell RR. Pompe disease in infants and children. J Pediatr 2004; 144:S35-S43. 4. Chen YT. Glycogen storage diseases. In Scriver CR, Beaudet AL, Sly WS, Valle D (eds). The Metabolic and Molecular Bases of Inherited Diseases, 8th ed. New York, McGraw-Hill, 2001, vol 1, pp 1521–1551. 5. Mucopolysaccharidoses Fact Sheet. National Institute of Neurological Disorders and Strokes. Available at: http://www. ninds.nih.gov/disorders/mucopolysaccharidoses/detail_ mucopolysaccharidoses.htm. Accessed 3/20/06. 6. Edeiken J, Dalinka M, Karasick D (eds). Edeiken Roentgen Diagnosis of Diseases of Bone, 4th ed. Baltimore, Williams & Wilkins, 1990, vol 2, pp 1745–1764. 7. Eggli KD, Dorst JP. The mucopolysaccharidoses and related conditions. Semin Roentgenol 1986; 21:275–294. 8. Murray RO, Jacobson HG, Stoker DJ. The Radiology of Skeletal Disorders, Exercises in Diagnosis, 3rd ed. Edinburgh, Churchill Livingstone, 1990, vol 2, pp 930–945. 9. Taybi H, Lachman RS. Radiology of Syndromes, Metabolic Disorders, and Skeletal Dysplasias, 4th ed. St. Louis, Mosby, 1996, pp 593–598, 669–681. 10. Resnick D, Kransdorf MJ. Bone and Joint Imaging, 3rd ed. Philadelphia, Elsevier Saunders, 2005, pp 1318–1325. 11. Ashworth JL, Biswas S, Wraith E, Lloyd IC. Mucopolysaccharidoses and the eye. Surv Ophthalmol 2006; 51:1–17. 12. Sharpiro J, Strome M, Crocker AC. Airway obstruction and sleep apnea in Hurler and Hunter syndromes. Ann Otol Rhinol Laryngol 1985; 94:458–461. 13. Schieken RM, Kerber RE, Ionasescu VV, et al. Cardiac manifestations of the mucopolysaccharidoses. Circulation 1975; 52:700–705. 14. Natowicz MR, Short MP, Wang Y, et al. Clinical and biochemical manifestations of hyaluronidase deficiency. N Engl J Med 1996; 335:1029–1033. 15. Hirschhorn R, Reuser AJ. Glycogen storage disease type II: Acid α1,4-glucosidase (acid maltase) deficiency. In Scriver CR, Beaudet

16. 17. 18. 19. 20. 21.

22. 23. 24. 25. 26. 27.

28.

AL, Sly WS, Valle D (eds). The Metabolic and Molecular Bases of Inherited Diseases, 8th ed. New York, McGraw-Hill, 2001, vol 3, pp 3389–3420. Kannourakis G. Glycogen storage disease. Semin Hematol 2002; 39:103–106. Ross JS, Brant-Zawadzki M, Moore KR, et al (eds). Diagnostic Imaging, Spine. Amirsys, 2004, pp 156–159. Steinbach HL, Gold RH, Preger L (eds). Roentgen Appearance of the Hand in Diffuse Disease. Chicago, Year Book Medical Publishers, 1975, pp 158–165. Kulkarni MV, Williams JC, Yeakley JW, et al. Magnetic resonance imaging in the diagnosis of the cranio-cervical manifestations of mucopolysaccharidoses. Magn Reson Imaging 1987; 5:317–323. Vinchon M, Cotten A, Clarisse J, et al. Cervical myelopathy secondary to Hunter syndrome in an adult. AJNR Am J Neuroradiol 1995; 16:1402–1403. Kachur E, Del Maestro R. Mucopolysaccharidoses and spinal cord compression: case report and review of the literature with implications of bone marrow transplantation. Neurosurgery 2000; 47:223–229. Schmidt H, Ullrich K, von Lengerke HJ. Radiological findings in patients with mucopolysaccharidosis I H/S (Hurler-Scheie syndrome). Pediatr Radiol 1987; 17:409–414. Thomas SL, Childress MH, Quinton B. Hypoplasia of the odontoid with atlanto-axial subluxation in Hurler syndrome. Pediatr Radiol 1985; 15:353–354. Taccone A, Tortori Donati P, Marzoli A, et al. Mucopolysaccharidosis: thickening of dura mater at the craniocervical junction and other CT/MRI findings. Pediatr Radiol 1993; 23:349–352. Preger L, Sanders GW, Gold RH, et al. Roentgenographic skeletal changes in the glycogen storage diseases. Am J Roentgenol Radium Ther Nucl Med 1969; 107:840–847. Schrerer A, Engelbrecht V, Neises G, et al. MR imaging of bone marrow in glycogen storage disease type 1b in children and young adults. AJR Am J Roentgenol 2001; 177:421–425. Cinnamon J, Slonim AE, Black KS, et al. Evaluation of the lumbar spine in patients with glycogen storage disease: CT demonstration of patterns of paraspinal muscle atrophy. Am J Neuroradiol 1991; 12:1099–1103. Schiffmann R, Brady RO. New prospects for the treatment of lysosomal storage diseases. Drugs 2002; 62:733–742.

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Osteogenesis Imperfecta James Teh and Roger Smith

Osteogenesis imperfecta (OI), also known as brittle bone syndrome, is an uncommon heritable disorder of collagen synthesis that results in defective, weak bony matrix, leading to bone fragility with fractures and deformity. A wide range of clinical manifestations may be seen, ranging from perinatal death to premature osteoporosis presenting in middle-aged adults. Important secondary clinical features are growth impairment, resulting in a rhizomelic dwarfism, hearing loss, blue sclerae, dentinogenesis imperfecta, cardiopulmonary complications, and neurologic compromise due to basilar invagination. The radiologic findings play a key role in diagnosing the condition. The multiple fractures encountered in OI often raise suspicion of nonaccidental injury, and radiologists must therefore have an understanding of the clinical manifestations of OI, the range of its genetic variability, and its imaging findings.

ETIOLOGY Osteogenesis imperfecta may be inherited (autosomal dominant) or result from a sporadic mutation. Autosomal recessive cases are possible but rare. The main pathologic process in OI is a disturbance in the synthesis of type I collagen, which is the predominant protein of the extracellular matrix of most tissues. Type I collagen fibers are found in bones, ligaments, sclera, dentin, tendons, meninges, and skin. In bone, the defective extracellular matrix causes osteoporosis, which leads to bone fragility. The collagen molecule is synthesized from procollagen, which is secreted into the extracellular compartment. These molecules then assemble into an ordered fibril. Gene mutations that interfere with the expression of the collagen gene, formation of the triple helix, or procollagen secretion affect the structure and function of collagen fibrils, resulting in OI.1 Most forms of OI arise from mutations in one of two genes that encode the synthesis and/or structure of type I collagen: the COL1A1 gene on chromosome 17 and the COL1A2 gene on chromosome 7. Mutations in these genes may result in abnormal collagen or decreased production of normal collagen, or a combination, resulting in the

different phenotypic expressions of OI.2 Milder forms of OI are caused primarily by the decreased production of normal collagen, whereas more severe forms are caused primarily by the production of abnormal collagen. A wide variation in clinical severity may occur between family members with the same genetic mutation.3

PREVALENCE AND EPIDEMIOLOGY The frequency of OI is based primarily on data from Sillence and associates in Australia.4 OI is reported to occur in around 1 in 20,000 births, but this is likely to be an underestimate because milder forms may remain undiagnosed.1 Males and females are equally affected. Over the 30-year period between 1950 and 1979 it was estimated that there were 10,000 individuals with skeletal dysplasia in the United Kingdom (excluding stillbirths, perinatal deaths, and patients with chromosome anomalies and metabolic bone disease).5 About 6000 required substantial orthopedic care, and half of these were severely physically handicapped throughout life. In this group OI was the most common diagnosis.

CLINICAL PRESENTATION AND PATHOPHYSIOLOGY The Sillence classification is the most widely recognized.4 This classification is based on both clinical and radiographic features. Four main types of OI were initially

KEY POINTS Osteogenesis imperfecta is an uncommon heritable disorder caused by abnormal collagen synthesis. ■ There is a very wide range of clinical presentation. ■ Four main types are described in the original Sillence classification, and several additional types have been described subsequently. ■ Diagnosis relies on clinical and radiologic features. ■ Treatment requires a multidisciplinary approach. ■

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described, but over the years several subsequent types have been added. Previously, OI was divided into two forms: “congenita” and “tarda,” depending on the severity of disease, but this classification has been superceded because it fails to encompass the wide range of clinical presentation. In OI congenita the fractures occur in utero, whereas in OI tarda the fractures occur at birth or later. OI tarda can be further subdivided into “gravis,” with fractures first occurring at the time of birth or during the first year of life, and “levis,” with fractures first occurring after the first year.

patients. Postnatal growth failure is often severe, and fractures are frequent in the first 2 years of life. Children with type III OI tend to have severe dwarfism due to vertebral compression fractures, limb deformities, and disruption of growth plates. Individuals are frequently wheelchair bound, although some are able to walk with aids. The sclerae are normal. The midface is flat with frontal bossing. Patients with type III OI can have a full life span, but many succumb to cardiorespiratory or neurologic complications, either during childhood or in early adulthood.9

Type I

Type IV OI is rare.4 Although type IV OI may be considered as intermediate in severity between types I and III, this is a heterogeneous group, with a wide spectrum of disease. The mode of inheritance is autosomal dominant. Type IV OI is classified into two groups according to the absence (type IVA) or presence (type IVB) of dentinogenesis imperfecta. Type IV OI is clinically distinguished from type I OI by the increased severity of bone fragility and by the presence of white sclerae. Furthermore, in type IV OI the first fracture occurs more commonly at birth, dentinogenesis imperfecta is more frequent, and bruising is less common. Differentiation between these two types may be difficult, however.10

Type I OI is the most common form of disease, comprising up to 60% of people with OI.4 It is generally associated with the best prognosis. This condition is transmitted as an autosomal dominant trait, although new mutations may occur. The most frequent genetic mutation causing type I OI results in a decreased production of normal collagen. Type I OI is divided into A and B subtypes based on the absence or presence of dentinogenesis imperfecta, respectively. Individuals with type IB have more severe disease, with a greater fracture rate and a greater likelihood of growth impairment.6 Life expectancy of patients with type IA OI is normal. In type 1B OI, mortality is slightly increased compared with that of the general population. Type I OI is usually not detected at birth. Clinically, its distinguishing features are blue sclerae and presenile conductive hearing loss.4 Patients may have their first fracture when learning to walk. In the prepubertal years mild trauma may lead to a series of fractures. The incidence of fractures tends to decrease significantly after puberty. In some cases exuberant callus formation may occur with healing. Patients may be of small or normal stature. Ligamentous laxity, resulting in joint hypermobility or subluxation, is common. Cardiovascular problems, particularly aortic valve disease, can occur. In some patients postmenopausal vertebral compression fractures may be the first presentation.7

Type II In type II OI collagen is improperly formed. Type II OI is the most severe form, characterized by extreme bone fragility, leading to intrauterine or early infant death.8 Clinically, distinguishing features include intrauterine growth retardation, thin and beaded ribs, crumpled long bones, and poor craniofacial bone ossification. The affected infants tend to have flat triangular facies with a small beaked nose. The sclerae are blue and occasionally almost black. Unexplained widespread arterial calcification occurs in some infants.1

Type III Type III OI, also known as the progressive deforming type, is the most severe form of OI compatible with survival beyond infancy. In this form, collagen is improperly formed. Its hallmark feature is severe bone fragility. Abnormalities are present at birth in more than 50% of

Type IV

Other Forms of Osteogenesis Imperfecta Some cases of OI do not fit neatly into the four main types described by Sillence. Types V and VI OI fall within the phenotypic range of type IV OI but are primarily distinguished from patients with type IV OI by iliac crest histology and histomorphometry. Type V OI includes individuals with osteoporosis, dense metaphyseal bands, interosseous membrane ossification of the forearms and legs, and a high frequency of hypertrophic callus formation.11 Inheritance is autosomal dominant. Qualitative histology of iliac biopsy shows that lamellae are arranged in an irregular fashion or have a mesh-like appearance. Quantitative histomorphometry reveals decreased amounts of cortical and cancellous bone. The type I collagen of these patients has normal electrophoretic mobility, and no mutations have been detected at the gene level. The proposed type VI OI is phenotypically similar to type IV but is distinguished on histologic criteria. Inheritance is autosomal dominant. Patients with this type of OI are moderately to severely affected. Qualitative histology of iliac crest bone biopsy specimens shows an absence of the birefringent pattern of normal lamellar bone under polarized light, often with a “fish-scale” pattern. Quantitative histomorphometry reveals thin cortices and hyperosteoidosis. The proposed type VII phenotype is characterized by fractures at birth, bluish sclerae, early deformity of the lower extremities, coxa vara, and osteopenia.12 Rhizomelia is a prominent feature. Inheritance is autosomal recessive. Histomorphometric analyses of iliac crest bone reveals findings similar to OI type I, with decreased cortical width and trabecular number, increased bone

CHAPTER

turnover, and preservation of the birefringent pattern of lamellar bone. There are also unusual forms of OI that are not classified into the numerical system described by Sillence. Bruck syndrome is a recessively inherited phenotypic disorder featuring the combination of skeletal changes resembling OI with congenital arthrogryposis multiplex (contractures of the large joints).13 In the Cole-Carpenter syndrome there are bone deformities and multiple fractures reminiscent of osteogenesis imperfecta but also ocular proptosis with craniosynostosis and hydrocephalus.14

IMAGING FINDINGS Type I Many imaging features are shared with other types of OI, particularly type IV. The radiographic hallmark is osteopenia, which is manifest by decreased bone density and cortical thinning, particularly of the metaphyses. “Feathering” and coarsening of trabeculae may also be seen.15 Harris growth arrest lines are often present, corresponding to transient periods of epiphyseal disturbance and growth arrest (Fig. 81-1). Apart from osteopenia, bowing and healing fractures may be evident. The long bones may appear overtubulated and gracile. In mild forms of OI, radiographs of the skull may be normal. With more severe forms of OI the skull demon-

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strates poor mineralization and multiple wormian, or intrasutural, bones.16 Wormian bones are considered significant when there are more than 10 and they measure more than 6 by 4 mm and are arranged in a general mosaic pattern (Fig. 81-2; Table 81-1).16 Basilar invagination may be demonstrated on radiographs of the cervical spine or skull (see Fig. 81-2).17 Although seen in all types of OI, it is more commonly associated with type IV, in which it may eventually lead to brain-stem compression.18 Although numerous radiographic criteria have been described for assessing basilar invagination (e.g., Clark, Chamberlain, McGregor), no single criterion is completely accurate and a combination of criteria may be required for a definitive diagnosis.17 Basilar invagination combined with a large, thin skull vault may lead to the “tam-o’-shanter” skull on the anteroposterior view, with flattening in the vertical axis and widening in the transverse axis (Fig. 81-3). On the lateral view the skull shape has also been described as resembling Darth Vader’s helmet (Fig. 81-4). If basilar invagination is suspected, the patient should be further assessed for brain-stem compression or syringohydromyelia by MRI (Fig. 81-5).

■ FIGURE 81-2 Lateral radiograph of the skull demonstrating decreased enchondral ossification of the skull (arrowheads) leading to the appearance of very large intrasutural bones. Multiple small wormian bones are also seen (long arrow). There is basilar invagination.

TABLE 81-1 Differential Diagnosis of Wormian Bones

■ FIGURE 81-1 Lateral radiograph of the ankle demonstrating osteopenia with prominent Harris growth arrest lines.

Osteogenesis imperfecta Pyknodysostosis Rickets in healing phase Menkes kinky hair syndrome Cleidocranial dysostosis Hypothyroidism Hypophosphatasia Otopalatodigital syndrome Primary acro-osteolysis (Hajdu-Cheney syndrome) Pachydermoperiostosis Progeria Down syndrome

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■ FIGURE 81-3 Anteroposterior radiograph of the skull showing widened biparietal diameter with superior flattening giving the “tam-o’shanter” appearance.

■ FIGURE 81-5 Sagittal T2-weighted MRI demonstrating basilar invagination with brain stem compression (arrowhead) and a small syringohydromyelia (arrow). Projection of the tip of the dens above McGregor line (which is defined as a straight line between the upper surface of the posterior edge of the hard palate to the most caudal point of the occiput) suggests basilar invagination.

■ FIGURE 81-4 Lateral radiograph of the skull demonstrating basilar invagination and wormian bones. The skull shape resembles Darth Vader’s helmet.

OI is sometimes associated with either relative or absolute macrocephaly.19 Between the ages of 2 to 3 years, the child’s head circumference may rapidly increase. Communicating hydrocephalus may occur, with prominence of sulci and ventricular enlargement seen on CT or MRI.19

The association of OI with hearing impairment is known as Van der Hoeve-de Kleyn syndrome.20 The CT findings of temporal bone involvement in OI include proliferation of undermineralized bone involving the otic capsule, proliferation of the bony labyrinthine capsule just anterior to the oval window, and envelopment of the stapes footplate. The osteosclerotic foci may be single or multiple. The bone changes may extend to the upper margin of the superior semicircular canal.21 Eventually, the cochlea may become completely surrounded by a ring of hypodense bone. The changes seen in OI are identical to those seen in patients with otosclerosis. (Fig. 81-6). The differential diagnosis includes Paget disease, syphilis, and CamuratiEngelmann disease. The incidence of scoliosis in OI has been documented as between 39% and 80% with a greater incidence in the more severe forms.22 There is often severe platyspondyly with vertebral compression fractures giving the appearance of codfish vertebrae (Fig. 81-7). Vertebral compression fractures after menopause may be the first presentation of OI.7

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■ FIGURE 81-6 DEXA scan demonstrating the dramatic improvement in bone mineral density (BMD) after bisphosphonate treatment at the age of 8. Scan Information: Scan Type: xLeft hip; Analysis: 13:44 version 12.4 left hip; Operator: MW; Model: Discovery A (s/N 80379); Comment: NOC 4303E.

Type II Radiographic examination reveals multiple in utero fractures at various stages of healing.23 The long bones are extremely osteoporotic with very thin cortices. The morphology of the long bones in the upper extremities is better maintained than in the lower extremities. There is severe rhizomelic dwarfism with short, curved, and angulated long bones (Fig. 81-8). The legs are often abducted into a frog-leg position. Relative macrocephaly with enlargement of the anterior and posterior fontanelles invariably occurs. Only the lateral plates of the skull may be ossified due to the enlarged fontanelles. Type II OI can be further subdivided into types IIA, IIB, and IIC on the basis of the radiographic features of the long bones and ribs.8 Individuals with type IIA demonstrate short, broad, “crumpled” long bones, angulation of tibiae, and continuously beaded ribs. With type IIB there are short, broad, crumpled femora, angulation of tibiae, but normal ribs (or ribs with incomplete beading). With type IIC there are long, thin, inadequately modeled, undertubulated long bones with multiple fractures and thin beaded ribs.

Type III

■ FIGURE 81-7 Lateral radiograph of the lumbar spine demonstrating multiple osteoporotic collapses with the appearance of “codfish” vertebrae.

The imaging findings in type III OI overlap with other types. The bones are soft as well as fragile. Bowing deformities of up to 90 degrees may be present, caused either by the tension of normal muscle deforming the bone or by previous fractures.24 In the upper limb bowing deformity most commonly affects the humerus, followed by the ulna and radius. With bowing deformity the bone may become buttressed, usually on the concavity of the curve (Fig. 81-9).15 In the lower limb the femur

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■ FIGURE 81-8 Type IIB osteogenesis imperfecta. Postmortem radiograph. There is relative macrocephaly with severe shortening of the long bones and multiple fractures. The ribs are thin but not crumpled.

■ FIGURE 81-10

Radiograph of the pelvis showing marked osteopenia with severe bilateral protrusio acetabuli and modeling deformity of the pelvis with marked bowing of the femora. A nonexpandable rod has been inserted into the left femoral shaft.

■ FIGURE 81-9 Lateral radiograph of the tibia demonstrating marked bowing deformity with buttressing of the cortex in the concavity (arrows). There is an old malunited fracture (arrowhead).

is most commonly involved. In the pelvis, protrusio acetabuli is a common finding in association with coxa vara (Fig. 81-10).25 As the child develops, there may be undertubulation of the long bones with development of an Erlenmeyer flask deformity. Alternatively, there may be overtubulation with exaggerated metaphyseal flaring accompanied by a slender diaphysis resulting in a trumpetshaped deformity (Fig. 81-11). The extreme slenderness of the diaphysis combined with bone fragility may result in pseudarthrosis of the fibula (Fig. 81-12; Table 81-2). The cyclical treatment of OI with bisphosphonates can result in distinctive imaging findings, with bands of sclerotic growth arrest lines (also known as “Harris lines”) seen at the metaphyses of the long bones. There is no evidence that these iatrogenic changes have any clinical implications, but their appearance should be recognized to prevent unnecessary further investigation (Fig. 81-13). A characteristic but inconstant finding is the presence of “popcorn” calcifications in the metaphyses or epiphyses of the long bones, usually at the knee or ankle. This is thought to result from repeated microfractures at the growth plate, leading to spread of cartilaginous islands into the adjacent metaphysis or epiphysis (Fig. 81-14).1,15

CHAPTER

■ FIGURE 81-11 Radiograph of the left lower limb demonstrating severe osteopenia with “trumpet-shaped” long bones with metaphyseal flaring and slender diaphyses.

■ FIGURE 81-12 Radiograph of the fibula demonstrating an extreme thinning of the fibula diaphysis leading to a fibular pseudoarthrosis. There is an expandable rod across the tibia.

Virtually all individuals with OI type III develop significant kyphoscoliosis (Fig. 81-15).26 Patients with type III osteogenesis imperfecta demonstrate elongation of the pedicles, which may be very thin, a deformity that is not seen in other types of OI (Fig. 81-16).27 Pars defects are common, which may result in spondylolisthesis (Fig. 81-17). Spinal deformity combined with rib fractures and remodeling result in a very high incidence of chest wall abnormalities.28 Pectus carinatum occurs more frequently than pectus excavatum (Fig. 81-18). Restrictive lung dis-

TABLE 81-2 Differential Diagnosis of Pseudarthrosis of

the Fibula

Osteogenesis imperfecta Neurofibromatosis Fibrous dysplasia Osteofibrous dysplasia

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■ FIGURE 81-13 Radiograph of the knee demonstrating alternating dense metaphyseal bands in a patient who had undergone cyclical bisphosphonate therapy. There is an expandable rod across the tibia.

ease due to chest wall deformity, as well as decreased mobility, predisposes the patients to recurrent pneumonias, which are a major cause of morbidity and mortality. As with other forms, in the skull there is relative macrocephaly, often with basilar invagination; and wormian bones are usually present.29

Type IV There is a wide overlap between the imaging findings in type IV and type I, and, to a lesser degree, type III OI (see earlier). Hyperplastic callus formation can occur after fractures or surgical intervention in all types of OI but is particularly associated with types IV and V.11 Patients present with a painful vascular mass. The femur is most often affected, with the callus appearing as a dense, irregular mass arising from the cortex of bone. The appearances may mimic osteosarcoma, myositis ossificans, chronic osteomyelitis, or osteochondroma. CT may demonstrate a well-defined

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■ FIGURE 81-14 Radiograph of the knee showing “popcorn” calcifications of the diametaphyseal regions (arrows), thought to result from spread of cartilaginous islands from the growth plate.

■ FIGURE 81-15 Sagittal T1-weighted MR image demonstrating a severe thoracic kyphoscoliosis.

calcified rim, allowing differentiation of hyperplastic callus from more aggressive lesions such as osteosarcoma. The plasma alkaline phosphatase level may be elevated.

MANIFESTATIONS OF THE DISEASE Radiography

■ FIGURE 81-16 Axial CT scan through the lumbar region demonstrating severe osteopenia with prominence of the trabeculae (asterisk). The pedicles are thin and elongated (arrows).

In cases of suspected OI, a selective skeletal survey should be performed. Views of the long bones, skull, chest, pelvis, and thoracolumbar spine should be obtained. The radiographic features are dependent on the type of OI and on the severity of disease. The radiographic findings may be nonspecific because some findings may be seen across

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all subtypes. In the more severe forms of OI (i.e., type II) the radiographic findings are considered diagnostic.

Magnetic Resonance Imaging Magnetic resonance imaging is particularly useful for assessment of neurologic impairment in OI. In patients with basilar invagination, MRI has the advantage over radiographs and CT of detecting associated cord compression or syringohydromyelia.

Classic Signs TYPE I ■ Most frequent and mildest type of OI ■ Most fractures occur before puberty ■ Normal or near-normal stature ■ Joint laxity ■ Sclerae usually blue ■ Bone deformity absent or minimal ■ Dentinogenesis imperfecta may occur ■ Hearing loss possible ■ Collagen structure normal, but amount of collagen less than normal

■ FIGURE 81-17 Sagittal CT reformatted image of the lumbar spine demonstrating severe osteopenia with a 40% spondylolisthesis.

TYPE II ■ Most severe form ■ Frequently lethal at or shortly after birth, often due to respiratory compromise ■ Multiple fractures and severe bone deformity ■ Triangular facies ■ Small stature with hypoplastic lungs ■ Collagen structure abnormal TYPE III ■ Bones fracture easily ■ Fractures often present at birth ■ Short stature ■ Sclerae usually blue ■ Joint laxity and poor muscle development ■ Chest deformity ■ Triangular face ■ Kyphoscoliosis ■ Bone deformity often severe ■ Dentinogenesis imperfecta may occur ■ Hearing loss possible ■ Collagen improperly formed

■ FIGURE 81-18 Chest radiograph demonstrating chest wall deformity due to a combination of kyphoscoliosis and rib remodeling.

TYPE IV ■ Between type I and type III in severity ■ Bones fracture easily, mostly before puberty ■ Short stature ■ Normal sclerae ■ Mild to moderate bone deformity ■ Scoliosis common ■ Barrel-shaped rib cage and chest wall deformities ■ Dentinogenesis imperfecta may occur ■ Hearing loss possible ■ Collagen structure abnormal

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In patients who develop scoliosis, MRI is the modality of choice for evaluating neurologic symptoms or for excluding congenital anomalies such as a tethered cord or Arnold-Chiari malformation before surgery.30 MRI is the investigation of choice for back pain and should be used in lieu of radiographs. Both sagittal T1-weighted and short tau inversion recovery images should be obtained to allow the differentiation of acute from chronic vertebral fractures.

Multidetector Computed Tomography Computed tomography has an important role in evaluating neurologic symptoms and hearing impairment. CT with 2D and 3D reformatted images can also be used to assess the vertebral column anatomy in cases of scoliosis or spondylolisthesis before surgery. CT also has a role in the detection of occult fractures.

■ FIGURE 81-19 CT scan of the temporal bone demonstrating low density mineralization around the cochlea (arrows).

Ultrasonography Ultrasonography plays a key role in the prenatal diagnosis of OI, which is one of the more commonly encountered skeletal dysplasias in utero. In the more severe types of OI (types II and III), ultrasonography during the second trimester may reveal hypoechogenicity of the calvaria owing to decreased mineralization, with supervisualization of the intracranial structures.31 Compression of the skull vault by the ultrasound probe should raise the suspicion of skeletal dysplasia but is not diagnostic for OI. Bowing and fractures of the long bones may be present, along with shortening of the long bones. Multiple rib fractures may also be seen. Increased nuchal translucency has also been described. The diagnosis of OI may be confirmed by DNA analysis of chorionic villus cells obtained by ultrasound-guided chorionic villus sampling.

Bone Mineral Densitometry Measurements of bone mineral density can be used to help establish the diagnosis, assess prognosis, and monitor the response to treatment in patients with OI.32 In recent years, dual-energy x-ray absorptiometry (DEXA) has become the most widely accepted technique for bone mineral density measurements in children, superceding single-photon absorptiometry and quantitative CT of the lumbar spine (Fig. 81-19). A clear relationship between bone mineral density and clinical severity in patients with OI is not always present, but bone mineral density may predict long-term functional outcome.33 Serial DEXA scanning is now routinely used as an objective assessment of response to bisphosphonate therapy, but there are considerable difficulties in interpretation, particularly if there are bone deformities in the spine and/or hip (see Fig. 81-6).

DIFFERENTIAL DIAGNOSIS The differential diagnosis of OI varies according to the age of the patient. On prenatal ultrasonography, severe OI may be confused with thanatophoric dysplasia,

achondrogenesis type I, or campomelic dysplasia, all of which demonstrate relative macrocephaly and limb shortening. Type III OI may appear similar to infantile hypophosphatasia, which presents as severe osteoporosis and micromelia. Serum biochemistry in hypophosphatasia demonstrates low serum alkaline phosphatase and increased inorganic pyrophosphate, whereas in OI the serum alkaline phosphatase level is normal or increased. After infancy, OI may be confused with primary juvenile osteoporosis or other secondary causes of osteoporosis in childhood, such as hypogonadism or chronic steroid use. An important consideration in early childhood is nonaccidental injury (NAI). In middle-aged women, OI may be mistaken for postmenopausal osteoporosis.7

Differentiation from Nonaccidental Injury Osteogenesis imperfecta type IVA is the form most likely to be confused with NAI.34 The diagnosis of NAI can be reached in the majority of cases by assessment of the social circumstances combined with careful clinical and imaging evaluation by experienced clinicians. When diagnostic uncertainty persists in cases of suspected NAI, such as when the supposed force of the injury seems insufficient to have caused the fracture, when fractures occur in a protected environment, or when there are no external signs of abuse, collagen analysis may be useful.35 However, routine biopsy for children suspected to have been abused is unwarranted. Some authors have suggested that there is a self-limiting variant of OI, referred to as temporary brittle bone disease.36 It is postulated that a transient defect in collagen formation results in multiple fractures in children younger than the age of 6 months. The condition is highly controversial because the main radiologic and clinical features described for this variant are very similar to those seen in NAI.35 Unless further research establishes the exis-

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■ FIGURE 81-21 Chest radiograph showing multiple posterior rib fractures (arrows) in a child suffering from nonaccidental injury. The endotracheal tube lies in the right main bronchus with collapse of the left lung.

Collagen Analysis ■ FIGURE 81-20

Radiograph of the knee in a child showing small corner metaphyseal fractures (arrowheads) typical for nonaccidental injury.

tence of temporary brittle bone disease, it should only be considered a hypothetical entity. It should always be remembered that OI and NAI can coexist; however, there are specific features that help differentiate these two conditions. Metaphyseal corner fractures, which are common in child abuse, are very rare in OI (Fig. 81-20).35 If metaphyseal corner fractures are present in OI, they are usually associated with thin cortices and osteopenia.37 In addition, bucket-handle fractures and fractures of the sternum, scapula, and skull vault are rare in OI. Certain fractures in infants, such as hand fractures in the nonambulatory child, fractures of the outer end of the clavicle, and spinal and posterior rib fractures are strongly suggestive of NAI (Fig. 81-21).35 In children subject to NAI, serial radiographs should show normal healing and remineralization. In children with OI, fractures continue to occur even with the child in protective custody. NAI can also be differentiated from OI on the basis of nonskeletal manifestations, such as intracranial hemorrhages and visceral trauma.35

DNA Testing DNA testing can be performed on blood samples to determine the presence of a genetic mutation causing OI. There is a false-negative rate of around 5%.

Collagen synthesis analysis can be performed to determine the quantity or quality of type I collagen by culturing dermal fibroblasts obtained from skin biopsy. This may be useful for prenatal screening, genetic counseling, and differentiating OI from child abuse, but the process takes around 3 months or longer.38 Furthermore, there is a consensus that the routine use of collagen analysis is unnecessary because in most cases comprehensive clinical evaluation by an experienced clinician is adequate for diagnosis. There is a false-negative rate of approximately 15%.

SYNOPSIS OF TREATMENT OPTIONS The prevention and management of fractures in individuals with OI require a multidisciplinary approach. Treatment should be tailored to the individual needs of the patient, taking into account the age and severity of disease. The long-term goal for children with OI is independence in the daily functions of life, including self-care, mobility, and recreation. Regular exercise and a good diet should be encouraged in all patients. Individuals with OI should avoid smoking, excessive alcohol or caffeine consumption, and corticosteroids, which may affect bone density. In patients with severe disease, bisphosphonates are being routinely used for improving bone density.

Medical Treatment Cyclical intravenous bisphosphonates have been shown to reduce bone pain and fracture incidence and to increase bone density and mobility, with minimal side effects.39 Most clinical trials have involved treatment of

1580 P A R T F I V E

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Metabolic/Hormonal/Systemic Disease

children with severe forms of OI. At present, there is insufficient evidence to recommend bisphosphonates for all children with mild OI. A number of issues regarding the use of bisphosphonate therapy in children and adolescents remain to be resolved, including the optimal dose, frequency, and duration of administration. Bisphosphonate therapy should, therefore, only be administered by specialist physicians. Other drugs, such as the parathyroid hormone–like protein teriparatide are also being studied as treatments for patients with OI.

Future therapeutic options for OI may include allogeneic bone marrow transplantation to engraft functional mesenchymal progenitor cells and thus help increase the production of normal bone.

Surgical Treatment Surgical intervention is indicated for recurrent fractures or deformity that impairs function. In many circumstances it may be preferable to treat fractures with short-term immobilization in lightweight casts, splints, or braces to allow mobilization as soon as possible. Surgery is often undertaken in children with OI in which metal rods are inserted into the long bones to control fractures and improve bowing deformities.40 Fractures may still occur after rodding, but the rod provides an internal splint that can maintain bony alignment. There are two basic types of rods. Nonexpandable rods are more versatile but may need replacement as the child grows (see Fig. 81-9). Expandable rods have a telescopic design and can change in length as the bone grows. Due to their thickness they can only be used in larger bones, such as the femur and tibia. These rods need to be firmly anchored at both ends (Fig. 81-22; see also Figs. 81-12 and 81-13). Percutaneous vertebroplasty is an effective technique for relieving painful vertebral compression fractures in osteoporosis, but its routine use in OI has not been established.

What the Referring Physician Needs to Know ■ ■ ■ ■ ■ ■

■ FIGURE 81-22

Radiograph of both lower limbs demonstrating extendable rods in situ within both femoral shafts in a child with OI type III. Note that the rods are anchored at both ends.

■

The diagnosis of OI is based on clinical and radiologic features. Many radiologic findings are nonspecific and may be seen across all subtypes. The differential diagnosis of OI is based on the age at presentation. The cornerstone of imaging is radiography. CT is useful for evaluating neurologic complications and for investigating hearing loss. MRI is useful for evaluating neurologic complications and for differentiating acute from chronic vertebral fractures. DEXA can sometimes help to establish the diagnosis, assess prognosis, and monitor response to treatment.

SUGGESTED READINGS Chapman S, Hall CM. Non-accidental injury or brittle bones. Pediatr Radiol 1997; 27:106–110. Smith R. Osteogenesis imperfecta, non-accidental injury, and temporary brittle bone disease. Arch Dis Child 1995; 72:169–171; discussion 171–176.

Smith R, Wordsworth P. Osteogenesis Imperfecta: Clinical and Biochemical Disorders of the Skeleton. Oxford, Oxford University Press, 2005.

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REFERENCES 1. Smith R, Wordsworth P. Osteogenesis Imperfecta: Clinical and Biochemical Disorders of the Skeleton. Oxford, Oxford University Press, 2005. 2. Byers PH. Inherited disorders of collagen gene structure and expression. Am J Med Genet 1989; 34:72–80. 3. Smith R. Osteogenesis imperfecta: from phenotype to genotype and back again. Int J Exp Pathol 1994;75:233–241. 4. Sillence DO, Senn A, Danks DM. Genetic heterogeneity in osteogenesis imperfecta. J Med Genet 1979; 16:101–116. 5. Wynne-Davies R, Gormley J. The prevalence of skeletal dysplasias: an estimate of their minimum frequency and the number of patients requiring orthopaedic care. J Bone Joint Surg Br 1985; 67:133–137. 6. Paterson CR, McAllion S, Miller R. Heterogeneity of osteogenesis imperfecta type I. J Med Genet 1983; 20:203–205. 7. Paterson CR, McAllion S, Stellman JL. Osteogenesis imperfecta after the menopause. N Engl J Med 1984; 310:1694–1696. 8. Bauze RJ, Smith R, Francis MJ. A new look at osteogenesis imperfecta: a clinical, radiological and biochemical study of forty-two patients. J Bone Joint Surg Br 1975; 57:2–12. 9. Cremin B, et al. Wormian bones in osteogenesis imperfecta and other disorders. Skeletal Radiol 1982; 8:35–38. 10. Riew KD, et al. Diagnosing basilar invagination in the rheumatoid patient: the reliability of radiographic criteria. J Bone Joint Surg Am 2001; 83:194–200. 11. Hayes M, et al. Basilar impression complicating osteogenesis imperfecta type IV: the clinical and neuroradiological findings in four cases. J Neurol Neurosurg Psychiatry 1999; 66:357–364. 12. Charnas LR, Marini JC. Communicating hydrocephalus, basilar invagination, and other neurologic features in osteogenesis imperfecta. Neurology 1993; 43:2603–2608. 13. Ross UH, et al. Osteogenesis imperfecta: clinical symptoms and update findings in computed tomography and tympanocochlear scintigraphy. Acta Otolaryngol 1993; 113:620–624. 14. Mafee MF, et al. Use of CT in the evaluation of cochlear otosclerosis. Radiology 1985; 156:703–708. 15. Benson DR, Donaldson DH, Millar EA. The spine in osteogenesis imperfecta. J Bone Joint Surg Am 1978; 60:925–929. 16. Sillence DO, et al. Osteogenesis imperfecta type II: delineation of the phenotype with reference to genetic heterogeneity. Am J Med Genet 1984; 17:407–423. 17. Spranger J, Cremin B, Beighton P. Osteogenesis imperfecta congenita: features and prognosis of a heterogenous condition. Pediatr Radiol 1982; 12:21–27. 18. McAllion SJ, Paterson CR. Causes of death in osteogenesis imperfecta. J Clin Pathol 1996; 49:627–630. 19. Amako M, et al. Functional analysis of upper limb deformities in osteogenesis imperfecta. J Pediatr Orthop 2004; 24:689–694. 20. Aarabi M, et al. High prevalence of coxa vara in patients with severe osteogenesis imperfecta. J Pediatr Orthop 2006; 26:24–28. 21. Engelbert RH, et al. Spinal complications in osteogenesis imperfecta: 47 patients 1–16 years of age. Acta Orthop Scand 1998; 69:283–286.

22. Versfeld GA, et al. Costovertebral anomalies in osteogenesis imperfecta. J Bone Joint Surg Br 1985; 67:602–604. 23. Widmann RF, et al. Spinal deformity, pulmonary compromise, and quality of life in osteogenesis imperfecta. Spine 1999; 24:1673–1678. 24. Sillence DO, et al. Osteogenesis imperfecta type III: delineation of the phenotype with reference to genetic heterogeneity. Am J Med Genet 1986; 23:821–832. 25. Paterson CR, McAllion S, Miller R. Osteogenesis imperfecta with dominant inheritance and normal sclerae. J Bone Joint Surg Br 1983; 65:35–39. 26. Glorieux FH, et al. Type V osteogenesis imperfecta: a new form of brittle bone disease. J Bone Miner Res 2000; 15:1650–1658. 27. Ward LM, et al. Osteogenesis imperfecta type VII: an autosomal recessive form of brittle bone disease. Bone 2002; 31:12–18. 28. Viljoen D, Versfeld G, Beighton P. Osteogenesis imperfecta with congenital joint contractures (Bruck syndrome). Clin Genet 1989; 36:122–126. 29. Cole DE, Carpenter TO. Bone fragility, craniosynostosis, ocular proptosis, hydrocephalus, and distinctive facial features: a newly recognized type of osteogenesis imperfecta. J Pediatr 1987; 110:76–80. 30. Alam A, Teh J. MRI assessment of scoliosis. Imaging 2005; 17:226–235. 31. Constantine G, et al. Prenatal diagnosis of severe osteogenesis imperfecta. Prenat Diagn 1991; 11:103–110. 32. Astrom E, Soderhall S. Beneficial effect of bisphosphonate during five years of treatment of severe osteogenesis imperfecta. Acta Paediatr 1998; 87:64–68. 33. Huang RP, et al. Functional significance of bone density measurements in children with osteogenesis imperfecta. J Bone Joint Surg Am 2006; 88:1324–1330. 34. Smith R. Osteogenesis imperfecta, non-accidental injury, and temporary brittle bone disease. Arch Dis Child 1995; 72:169–171; discussion 171–176. 35. Chapman S, Hall CM. Non-accidental injury or brittle bones. Pediatr Radiol 1997; 27:106–110. 36. Paterson CR, Burns J, McAllion SJ. Osteogenesis imperfecta: the distinction from child abuse and the recognition of a variant form. Am J Med Genet 1993; 45:187–192. 37. Astley R. Metaphyseal fractures in osteogenesis imperfecta. Br J Radiol 1979; 52:441–443. 38. Gahagan S, Rimsza ME. Child abuse or osteogenesis imperfecta: how can we tell? Pediatrics 1991; 88:987–992. 39. Glorieux FH, et al. Cyclic administration of pamidronate in children with severe osteogenesis imperfecta. N Engl J Med 1998; 339:947–952. 40. Cole WG. Orthopaedic treatment of osteogenesis imperfecta. Ann N Y Acad Sci 1988; 543:157–166.

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C H A P T E R

Marfan Syndrome Filip M. Vanhoenacker, A. Snoeckx, and M. Biervliet

ETIOLOGY Marfan syndrome is an autosomal dominant disorder.

PREVALENCE AND EPIDEMIOLOGY The incidence in the general population is estimated as 1 in 5,000 to 10,000.1 The majority of patients will have familial incidence, although approximately 15% of cases occur sporadically, representing new mutations.

CLINICAL PRESENTATION Marfan syndrome is a disorder of connective tissue, involving the cardiovascular, ocular, and skeletal systems, as well as the lungs, dura, and skin.1,2

PATHOPHYSIOLOGY Abnormalities in synthesis, secretion, or matrix incorporation of the glycoprotein fibrillin-1 are responsible for the clinical manifestations. The genetic defect has been linked to the FBN1 gene on chromosome 15q21.1. More than 135 mutations have been described so far.2,3 At present, it is possible to identify mutations in 70% of affected people.4 Prenatal and preimplantation diagnosis is currently possible for families with known mutations.5,6

flatness, and lens subluxation. Cardiovascular manifestations (Fig. 82-1A) include mitral valve prolapse, aortic root dilatation, mitral and/or aortic valve regurgitation, and aortic dissection and rupture. Cardiovascular complications, which begin in the first or second decade of life, are responsible for a reduction of the life expectancy.7,8 Clinical musculoskeletal findings include increased height and arm span, chest and vertebral column deformity, joint hypermobility, arachnodactyly, pes planus, and a narrow, highly arched palate and a narrow jaw, resulting in crowded and poor dentition.2 Skeletal symptoms are predominant in childhood.9 Other clinical features include spontaneous pneumothorax, recurrent inguinal hernia, and striae atrophicae.2 The diagnostic criteria (including major and minor criteria for various organ systems) for Marfan syndrome have been described in detail by De Paepe and colleagues.10 These clinical criteria, regarding the musculoskeletal system, are summarized in Table 82-1. Further discussion of diagnostic criteria of other organ systems is, however, beyond the scope of this chapter. In the absence of family history, an affected person should display major criteria in at least two organ systems and involvement of a third organ system. In the presence of a positive family history, only one major criterion of an

IMAGING TECHNIQUES Plain radiography still plays a pivotal role in the initial imaging evaluation of Marfan syndrome. For evaluation of spinal manifestations (dural ectasia), CT and/or MRI are more appropriate techniques.

MANIFESTATIONS OF THE DISEASE The phenotypic features of Marfan syndrome are highly variable, but most patients can be diagnosed clinically. The major clinical findings involve three major organ systems: ocular, cardiovascular, and skeletal.2 Ocular signs are myopia, increased axial globe length, corneal 1582

KEY POINTS Chest deformity including pectus excavatum or pectus carinatum is encountered in 66% of patients. ■ Severe scoliosis with a curve of more than 20 degrees or midthoracic lordosis and thoracolumbar kyphosis occurs in about two thirds of patients. ■ Dural ectasia occurs in up to 63% of patients and is best assessed by MRI. ■ Acetabular protrusion is seen in nearly 50% of patients. ■ The value of the metacarpal index for assessment of arachnodactyly has been questioned. ■

CHAPTER

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■ FIGURE 82-1

Posteroanterior (A) and lateral (B) chest radiographs of a patient with Marfan syndrome. There is dilatation of the descending aorta. Note also a localized bulla in the right upper lung.

TABLE 82-1 Major and Minor Diagnostic Skeletal Criteria for Marfan Syndrome Major Criteria Presence of at least four of the following manifestations: Pectus carinatum Pectus excavatum requiring surgery Reduced upper to lower segment ratio or arm span to height ratio greater than 1.05 Wrist and thumb signs Scoliosis of more than 20 degrees or spondylolisthesis Reduced extension at the elbows (5 cm), deep (intramuscular), or of low echogenicity with no septa, MRI is needed. ■ Hematoma can be followed with ultrasonography until the lesion is completely liquefied. If solid elements remain or if it is getting larger, then MRI is needed. ■ A foreign body is a highly echogenic lesion surrounded by low echogenicity. It will not be seen on MRI unless it is large. ■ Muscle hernias and tears have characteristic appearances. Hernias may be missed on MRI. ■ Complex, large, solid, and solid/cystic lesions on ultrasonography need MR staging and biopsy. ■

Ultrasonography is particularly useful in children; ionizing radiation is avoided and there is no need for the prolonged immobility needed for MRI. In many children, MRI may be possible only with the use of sedation or anesthesia. With ultrasonography the trust of both the child and the parent can be gained, and the experience of an ultrasound examination is usually far less psychologically traumatic than other forms of imaging. The greatest strength of ultrasonography is its ability to distinguish a cystic from a solid lesion (Table 89-1). An anechoic lesion with acoustic enhancement seen behind the lesion is a cystic lesion (Fig. 89-1). Sometimes the use of ultrasound allows the examiner to fully reassure the patient that the lump is a benign lesion that needs no further investigation, for example, a small subcutaneous lipoma or a ganglion cyst in the popliteal fossa.

TABLE 89-1 Ultrasound Appearance of Cystic versus

Solid Lesion

Echogenicity Acoustic enhancement behind lesion Movement of contents on bouncing the probe on the skin Vascularity

Solid

Cystic

Either hypoechoic, isoechoic, or hyperechoic Not usually; some nerve tumors may have Never

Anechoic

May be within the lesion or absent

Present unless a very small lesion Commonly present Never seen centrally unless artifact from movement of contents

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● The Patient with a Soft Tissue Lump

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Other benign lesions that can be excluded are muscle hernias (Fig. 89-2),3 which are rarely visible using other imaging techniques, small foreign bodies (Fig. 89-3),4 which have a characteristic appearance on ultrasonography, the presence of asymmetry of fatty tissue, or the presence of a normal variant. Ultrasound examination is an especially useful imaging technique because the patient can be shown the images during the study, thus enabling much more effective reassurance. Ultrasonography is particularly useful for lumps less than 5 cm in diameter in the first 10 cm below the skin because high-resolution linear array probes can be used. Larger and deeper lumps can be seen by ultrasound using curvilinear array probes or on more modern apparatuses by using extended field-of-view technology, which builds up a composite picture along the length of a lesion (Fig. 89-4). The presence of early calcification can be identified owing to the presence of acoustic shadowing behind the lesion. Ultrasonography is probably much more sensitive than radiography in the detection of calcium. The presence of vascularity within a lesion will not determine whether the lump is benign or malignant. A vascular malformation can be identified on ultrasonography by the presence of serpiginous low signal intensity surrounded by high echogenicity, which is due to the presence of fat around the vessels. Some vascular malformations may have a predominance of slow flowing blood within them because they are mainly venous. In these lesions the use of compression of the lesion with the ultrasound probe while using color Doppler imaging can confirm the diagnosis because flow will be seen to fill all the serpiginous areas on releasing the pressure. These areas will not show flow within them using static color flow Doppler imaging or with conventional angiography or MR angiography. It may be possible to occlude the vessels in small lesions by the use of compression, a sign that will also be visible when using color Doppler imaging. This is a technique that sonographers also use for the detection of deep vein thrombosis.

Magnetic Resonance Imaging Magnetic resonance imaging is the next best imaging technique for the screening of soft tissue abnormality and the best for staging its spread (see Chapter 98). It will show the extent of the lesion in detail and will also show bone marrow involvement. The lesion can be marked by the technician/radiographer who is performing the examination by a water/oil capsule to aid localization of the abnormality. Some lesions can be diagnosed confidently with MRI, for example, uniform areas of fat, which show absence of signal intensity using spectral fat suppression (see Chapters 93 and 94). One of the potential pitfalls when using MRI is the recognition of fluid versus a solid lesion. Sometimes a solid lesion with high water content can be misinterpreted as cystic. The use of intravenous contrast agents may confirm that the lesion is solid when enhancement is seen.5 Alternatively, ultrasound can be used to further characterize a lesion found on non–contrast-enhanced MRI. The main advantage of MRI over ultrasonography is its ability to display

1672 P A R T S I X

A

●

Musculoskeletal Tumors and Tumor-like Lesions

B

■ FIGURE 89-1

A, Seroma with all the characteristic features of a cystic lesion. B, Popliteal cyst with classic “soap-bubble” appearance. C, Anaplastic lymphoma, which is a solid lesion with homogeneous low echogenicity.

■ FIGURE 89-2 site.

C

A, Muscle hernia through a fascial plane of the peroneal muscles. B, Color Doppler image shows perforating vessels at the same

■ FIGURE 89-3 Foreign body is seen next to flexor tendon. An oval surrounds the foreign body.

■ FIGURE 89-4

Extended field-of-view sonogram of lipoma within the left erector spinae muscle; the right side is normal.

CHAPTER

the lesion in relation to its surroundings, including bone (staging), but disadvantages include a patient’s claustrophobia and the inability to safely examine patients who have intracranial aneurysm clips and pacemakers. With the growing obesity of the world’s population a number of patients will not be able to have an MRI in a conventional MR scanner because they are too big to fit into the bore of the magnet!

Computed Tomography Computed tomography is at best a modest means of imaging soft tissue. It has the same positive and negative attributes of radiographs, although reconstruction will allow a three- dimensional appearance. It may identify calcification in the presence of a lesion such as myositis ossificans, and it will demonstrate the pattern of calcium distribution. It will also show destruction of bone.6 Unfortunately, CT cannot reliably show the true extent of the soft tissue lesion and, indeed, occasionally soft tissue lesions may be missed using CT. If circumstances mean that CT is the only way of imaging in cross section, then the use of an intravenous contrast agent can help improve the conspicuity of the lesion. CT will, as with radiographs, show fat as a low-attenuation lesion, which sometimes can be diagnostic (Fig. 89-5).

MANIFESTATIONS OF THE DISEASE Defining the Shape and Structure of a Lesion Ultrasonography can be confidently used to determine whether a lesion is cystic or solid (see Table 89-1). Ultrasonography gives a specific appearance of a low echogenic lesion with acoustic enhancement behind it. The use of compression in the assessment of a fluid filled lesion can also be helpful where swirling of the contents can be observed.

■ FIGURE 89-5 CT scan of a lipomatous tumor in the right axillary region. In this case no reliable differentiation between benign and malignant can be made on CT only.

89

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The only pitfall is that some nerve-related tumors and homogeneous lymphatic tissue can give a similar appearance; for example, schwannomas can show hypoechogenicity and acoustic enhancement in approximately 50% of cases. This problem is overcome simply by careful attention to technique. If the gain (amplification) of the machine is set appropriately, then the solid but hypoechoic lesion will not be completely dark; there will be some echoes within it. If there is any doubt about the gain setting on an ultrasound machine, then an adjacent vessel should be examined and the gain setting adjusted so that the echoes within the vessel just disappear.7 Some common lesions can be very easily excluded or diagnosed using ultrasound, for example, ganglion cysts around the wrist and fingers and popliteal cysts in the knee. Fat-containing lesions are well seen by CT and MRI, but ultrasonography is also a useful technique. Fat- containing masses will be hyperechoic. If they are less than 5 cm, have no features of neovascularity, and are superficial with no extension through the deep fascia, they are likely to be benign (Fig. 89-6). However, well-differentiated liposarcomas may look very similar, and after a review of practice in one hospital, there has been some concern that low-grade liposarcomas may be overlooked. The tumor shown in Figure 89-6B is not very likely to be benign because of its size and homogeneous texture. Absence of flow does not exclude malignancy. Experienced examiners remain confident that ultrasonography may be used to determine which fatty masses should be referred for further investigation. Depending on the clinical circumstances, the certainty of diagnosis, and the experience or confidence of the operator, ultrasonography may be used as a test that predicts the safe postponement of other imaging. However, if there are any concerns that this may not be truly a fat containing lesion, then the performance of more sophisticated imaging such as MRI is indicated.

Vascularity The vascularity of a lesion can be assessed by ultrasonography using either color or power Doppler imaging (Fig. 89-7). Conventional angiography and MR angiography can also be useful when assessing vascularity, especially in arteriovenous malformations when the possibility of treatment can also be included. Note that some low-flow arteriovenous lesions may be difficult to detect using contrast studies via an arterial route and retrograde examination by venography may show a much more extensive lesion. Ultrasonography and MRI will not miss slow-flowing regions. Ultrasonography is effective as a first-line study in vascular lesions (Fig. 89-8). This can give an idea as to where the vascular supply originates and also whether there is a predominance of arterial and venous flow. The use of compression can also be invaluable. Some slow-flowing arteriovenous malformations are best seen by using color or pulsed Doppler imaging and applying pressure via the probe on the tissue and then gently releasing the pressure. If this is done, then a slow-flowing arteriovenous malformation will show flow.

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A ■ FIGURE 89-6

A, Sonogram of a lipoma (arrow). B, Sonogram of a liposarcoma. Color Doppler image shows homogeneous image of the large lesion with no flow.

■ FIGURE 89-7

■ FIGURE 89-8

Sonogram of a Merkel cell tumor in the left buttock with (right) and without (left) color Doppler imaging.

A, Color Doppler ultrasound image of a vascular malformation without compression. B, Compression has been applied, and on release of the probe pressure, more vessels can be seen.

CHAPTER

Calcification Calcification is best seen on plain films and CT. Early calcification can also be clearly identified using ultrasound where it causes acoustic shadowing behind the calcified region (Fig. 89-9). This is a specific finding in larger lesions, but in small lesions it can be absent. When large areas of calcification are present, the sonographer may not be able to see behind the initial calcification and therefore may underestimate its extent. MRI is a poor means of assessing small areas of calcification. These areas have low signal intensity and are often overlooked, because the presence of low signal intensity can also be encountered in flow from a vessel or, indeed, fibrosis. If the amount of calcification present within a lesion needs to be analyzed, then CT is the best imaging method to use. Mature fibrosis is of low signal intensity on all MR sequences and is of high echogenicity on ultrasonography (immature fibrosis may be rather cellular and may have fairly high signal intensity on T2-weighted MR images). The region behind the fibrosis will not have acoustic enhancement or shadowing. It is often easily detected in areas of previous injury to muscles and tendons, where it is often seen in association with the loss of the normal fibrillary structure. Some patients admit no history of injury, but on imaging a lump there is the presence of a partial muscle tear or a myofascial hernia that determines that it is from a previous but forgotten injury.

Muscle Injury Scarring is common in muscles, and this can be seen with ultrasonography. The site of some lumps increases the chance that they are secondary to trauma. The rectus femoris muscle is a frequently injured muscle. The location of the lesion along the aponeurosis of the two muscle bellies is the most common area of injury. At this site, hematoma, loss of the normal fibrillary pattern, calcification due to myositis ossificans, and scarring may all be seen.

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Muscle hernias can be invisible because they may only be present when the patient is standing or straining. This means that when a supine MRI is performed it may appear completely normal. The use of dynamic ultrasound scanning can be invaluable in these patients. The patient can be imaged standing and after running. It is on stressing these muscles that muscle hernias can become obvious.

Ultrasonography of Muscle Trauma Hematomas When there has been an injury and hematoma forms it is initially of high echogenicity. After approximately 6 hours the hematoma starts to liquefy and becomes gradually anechoic (Fig. 89-10). This liquefaction can take up to 6 months to complete. A completely liquefied hematoma can therefore look like a cyst. These lesions will present as lumps either with a clear history of trauma or no history (see also Chapter 94). The problem then is whether there is an underlying tumor that has bled. If the lesion is clearly anechoic with no echoes, then a liquefied hematoma can be confidently diagnosed. If there are echoes within the lesion, then the hematoma must be followed to resolution and liquefaction (Fig. 89-11). Alternatively, MRI and even biopsy may be indicated when suspicion for tumor is high.

Nerve-Related Lesions The presence of a tail within a lesion, if it arises in the region of a neurovascular bundle, can suggest that it is a nerve-related lesion (see also Chapter 93). On MRI, nerve lesions can show a central low signal intensity. On ultrasonography there is usually a central high signal intensity with a ring shadow, called a target lesion, within a neuroma. Schwannomas, if they become large, can become necrotic and cavitating. Nerve lesions can also show acoustic enhancement behind, which might suggest a more fluid-containing lesion. The importance of setting the machine appropriately cannot be overstated. Modern ultrasonography can effectively identify small nerves clearly down to the level of the digital nerves. The nerve fibers can be seen, and therefore small neuromas can be detected. The extent of disease within the nerve can also be assessed; for example, a portion of the nerve may be spared by the tumor, or it may only affect a branch of the nerve (Fig. 89-12). Ultrasonography can be used to answer these questions with its superior line pair resolution in the superficial regions when compared with MRI. A pitfall of MRI is interpreting a neuroma as a ganglion when it does not have a tail because it often appears as a “fluid”-containing lesion with high signal intensity. Again, contrast-enhanced MRI is useful in differentiating these two conditions.

Lesions According to Site

■ FIGURE 89-9 Sonogram of myositis ossificans. Calcifications are marked by arrows. Posterior to the calcifications a liquefying hematoma can be seen (arrowhead).

Some lesions can be identified according to their site. In the hand, for example, the ganglion is the most common soft tissue swelling to be identified, followed by other rarer lesions, such as nerve tumors, giant cell tumors of tendon sheath, and lipomas. In the foot and ankle,

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■ FIGURE 89-10 A, Sonogram of liquefying hematoma in rectus femoris muscle. B, Liquefying hematoma with a mixture of cystic and solid components. C, Liquefied hematoma. D, Liquefied hematoma, injury seen behind the muscle belly (fascial plane injury).

ganglions are the most common lesions, followed by plantar fibromas and osteophytes. Tendinopathy around the ankle and wrist can also cause swelling. Around the knee the most common soft tissue swelling is the popliteal cyst. When this ruptures it is a great mimicker of a deep vein

thrombosis. Here, ultrasonography is very useful because the assessment of the deep veins can be followed by an assessment of the presence of a popliteal cyst. Note that popliteal cyst rupture may lead to deep vein thrombosis, and both diagnoses may be made using ultrasonography.

CHAPTER

■ FIGURE 89-11

Sonogram of telangiectatic osteosarcoma. Patient was originally thought to have a liquefying hematoma because he had a clear history of trauma. Note the fluid layers of acute (highly echogenic) hemorrhage and liquefied hemorrhage (low echogenicity).

A V

■ FIGURE 89-12 Schwannoma (long arrow) arising from the medial calcaneal branch of the tibialis posterior nerve, with the main nerve trunk seen separately (short arrow). A, artery, V, vein.

Locating Spread The presence and significance of spread will depend on the histology of the lesion. Local spread can be assessed by ultrasound initially, but MRI will be needed to assess extent in detail. MRI will then ascertain whether the lesion is arising from bone or whether indeed the soft tissue lesion is affecting bone by erosion or indentation. Local staging and diagnosis or exclusion of distant spread is addressed in Chapter 98.

The Decision to Biopsy As indicated earlier, some lesions are very easily assessed and dismissed by the use of an ultrasound examination. The most common lesions that are imaged that are benign are ganglions and popliteal cysts (Fig. 89-13), followed by muscle

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■ FIGURE 89-13 Sonogram of a biopsy specimen of a complex popliteal cyst with synovitis.

hernia, fibrosis, and myositis ossificans after trauma and also foreign bodies, especially within the fingers and feet. There may be no history of foreign body inclusion even though one is clearly seen on imaging. The presence of a foreign body within the hand is very common and may be related to an injury after gardening or as a result of the patient’s occupation, for example, metal working. Sometimes there has been a history of foreign body inclusion many years previously. It is not uncommon to see foreign bodies that relate to an injury over 20 years prior to the examination. The rate of growth of a lesion is very important. The size of a lesion is a major risk factor; for example, if a lipoma is greater than 5 cm and is deep, the likelihood of malignancy is much greater and these lesions should always be sampled after local staging with MRI.8 Small lesions may be excised, or they could be followed up by ultrasound imaging to assess for an increase in growth. Lesions of less than 1 cm are difficult to biopsy. It can be attempted under ultrasound guidance, but if a diagnosis is vital, then sometimes an excision biopsy will need to be performed anyway (Table 89-2 and Figure 89-14).

SUMMARY Imaging of soft tissue masses is of considerable value in showing which lesions are real and require investigation. Initial screening with ultrasound allows the examiner to take a specific history and to exclude patients with no mass, a cyst, a ganglion, and some of the sequelae of injury from further investigation. MRI is the best method of local staging and surgical planning and is mandatory in unexplained solid mass lesions. CT is an aid to diagnosis in some selected cases.

What the Referring Physician Needs to Know ■ ■ ■

Is the lesion a “leave me alone” lesion such as a ganglion or cyst? Is malignancy excluded? Is additional imaging needed?

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TABLE 89-2 Comparison of Imaging Methods for Soft Tissue Lesions Radiography

CT

MRI

Ultrasound

Uses radiation Show calcification Show bone involvement Show soft tissue Patient tolerance

Yes Excellent Yes Poorly Excellent

Yes Excellent Excellent Sometimes Good

No Good Sometimes if accessible cortex eroded Excellent, especially in extremities Excellent

Cross-sectional view Contraindications Assessment of vascularity

No No No

Good No With intravenous contrast

No Low signal may be calcium Excellent Excellent May need sedation or general anesthesia in children Excellent Pacemakers, aneurysm clips With intravenous contrast

Limited (extended field-of-view imaging) No Excellent

Lump Ultrasound

Foreign body No diagnosis MRI

Solid Lipoma

Cystic Ganglion, cyst

Muscle hernia or tear

Hematoma Unsure

Benign lesion

Repeat US

Unsure diagnosis

Hematoma

Complex CD US

AVM, Hemangioma

MRI

Benign lesion Reassure Biopsy

Unsure diagnosis

■ FIGURE 89-14 Algorithm for imaging soft tissue lesions. CT and radiographs have not been included here because they add little in the initial diagnosis and should be reserved for those lesions in which the assessment of calcification is needed or when the patient cannot undergo MRI. Advantages and disadvantages of the various imaging techniques are listed in Table 89-2.

REFERENCES 1. Siegel MJ. Magnetic resonance imaging of musculoskeletal soft tissue masses. Radiol Clin North Am 2001; 39:701–720. 2. Hwang S, Adler RS. Sonographic evaluation of the musculoskeletal soft tissue masses. Ultrasound Q 2005; 21:259–270. 3. Beggs I. Sonography of muscle hernias. AJR Am J Roentgenol 2003; 180:395–399. 4. Soudack M, Nachtigal A, Gaitini D. Clinically unsuspected foreign bodies: the importance of sonography. J Ultrasound Med 2003; 22:1381–1385.

5. Kransdorf MJ, Murphey MD. The use of gadolinium in the MR evaluation of soft tissue tumors. Semin Ultrasound CT MR 1997; 18:251–268. 6. Knapp EL, Kransdorf MJ, Letson GD. Diagnostic imaging update: soft tissue sarcomas. Cancer Control 2005; 12:22–26. 7. Hughes DG, Wilson DJ. Ultrasound appearances of peripheral nerve tumours. Br J Radiol 1986; 59:1041–1043. 8. Liu JC, et al. Sonographically guided core needle biopsy of soft tissue neoplasms. J Clin Ultrasound 2004; 32:294–298.

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Primary Bone Tumors A. Mark Davies

Primary bone tumors are rare and, unlike osseous metastases and myeloma, tend to occur in otherwise fit children, adolescents, and young adults. Patients typically present with either pain or swelling that may be initially mild or intermittent but in time becomes more severe and nonmechanical, particularly if the tumor is malignant. A pathologic fracture may be the initial presenting feature in a minority of cases, and small benign bone tumors can be incidental findings on radiographs obtained for other purposes. The vast majority of bone tumors will be first detected on radiographs, with only a minority of occult lesions being identified on other imaging, such as bone scintigraphy and MRI. This situation is unlikely to change significantly in the near future, because the radiograph remains relatively inexpensive and readily available. There is, however, an increasing tendency, particularly in younger patients, to go straight to noninvasive imaging such as MRI. Should a bone tumor be suspected on MRI then it is important to correlate the findings with contemporary radiographs as, arguably, of all the imaging techniques, the radiographs reveal the most diagnostic information in terms of pattern of bone destruction, periosteal new bone formation, and matrix mineralization. It can be a daunting task for the physician unfamiliar with bone tumors to understand the bewildering spectrum of bone tumors. The easiest way to comprehend primary bone tumors is to apply a pathologic classification according to their predominant tissue production and then the benign and malignant subtypes (Table 90-1). We, therefore, have both benign and malignant osteoid-producing/ osteogenic tumors, cartilage-producing/chondrogenic, round cell tumors, and so on. Both benign and malignant bone tumors may recur locally after surgical treatment, but only malignant tumors have the propensity to metastasize to distant organs. The likelihood of developing metastases depends on the histologic grade of the malignant tumor as well as the efficacy of the treatment. Some benign bone tumors have the ability to undergo malignant change, and some malignant tumors can dedifferentiate into a higher-grade sarcoma. The purpose of this chapter is to review the different types of primary bone tumors and provide a description of the principal

imaging features. A number of non-neoplastic conditions are frequently included with bone tumors because of their tumor-like clinical and imaging features. These include simple bone cyst, aneurysmal bone cyst, and fibrous dysplasia and are covered in Chapter 92.

MANIFESTATIONS OF DISEASE Osteoid-Producing Tumors Osteoid-producing/osteogenic tumors are defined as neoplasms that produce an osteoid or bony matrix. According to their biologic behavior they are divided into benign and malignant lesions (see Table 90-1).

Osteoma Osteoma is a slow-growing benign lesion surface lesion comprising well-differentiated mature bone. It classically occurs in the frontal and ethmoidal sinuses, the so-called ivory osteoma, and less commonly on the outer skull vault and the mandible (Fig. 90-1). In Gardner’s syndrome, an autosomal-dominant disorder, osteomas particularly of the mandible are associated with cutaneous/subcutaneous lesions and colonic polyposis with a propensity for malignant change. Radiographs show an ivory dense mass with sharply defined margins firmly attached to the outer surface of bone. Osteomas rarely arise on the long bones, but if large they can mimic a parosteal osteosarcoma or melorheostosis. With the exception of Gardner’s syndrome the identification of an osteoma is usually of little clinical significance. Large paranasal osteomas, however, may cause compressive and obstructive symptoms and erode into the anterior cranial fossa. Excision of large vault or mandibular lesions may be required for cosmetic reasons. A lesion histologically identical to an osteoma but arising within trabecular bone is the bone island or enostosis. These are a common incidental finding on radiographic examinations and are typically small, oval or rounded, with a streaky or brush border that blends with the host trabeculae. Multiple bone islands crowded in the epimetaphyseal regions are a feature of the sclerosing bone 1679

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KEY POINTS The histologic grade of a bone tumor is a measure of its biologic aggressiveness and therefore indicates the risk of local recurrence after treatment and development of metastases. ■ Peritumoral edema on MRI is more florid in benign conditions such as osteoid osteoma and chondroblastoma than sarcomas. ■ A painful scoliosis in an adolescent may be the presenting feature of an osteoid osteoma or osteoblastoma. ■ A tumor arising in the epiphysis before skeletal fusion is most commonly a chondroblastoma with sarcoma extremely unlikely. ■ Malignant transformation of enchondroma and osteochondroma to central and peripheral chondrosarcoma is rare. The incidence is greater in Ollier’s disease (20%) and hereditary multiple exostoses ( 5 g/dL Bence Jones proteinuria: excretion > 12 g/24 hr

II III

Subclassifications for I and III: (A) normal renal function (serum creatinine < 2.0 mg/dL, no extramedullary disease); (B) abnormal renal function (serum creatinine > 2 mg/dL, extramedullary disease). Data from Durie BGM, Salmon SE.A clinical staging system for multiple myeloma: correlation of measured myeloma cell mass with presenting clinical features, response to treatment and survival. Cancer 1975; 36:842–854.

TABLE 91-2 Durie and Salmon PLUS Staging System Classification

Whole-Body MRI and/or FDG PET

Monoclonal gammopathy of unknown significance (MGUS) Stage IA (smoldering myeloma) Multiple myeloma Stage IB

All negative

Stage IIA/B Stage IIIA/B

Normal skeletal survey or single lesion (limited disease) < 5 focal lesions or mild diffuse disease* 5–20 focal lesions or moderate diffuse disease† > 20 focal lesions or severe diffuse disease‡

Subclassifications in stages II and III: (A) normal renal function, (B) abnormal renal function (serum creatinine > 2 mg/dL, extramedullary disease); stage was predictive of survival. *Mild diffuse disease is a normal signal intensity or a slight homogeneous reduction of signal on T1-weighted spin-echo images and is often hard to detect. † Moderate diffuse infiltration is a more apparent reduction in signal on T1weighted spin-echo MR images. ‡ Severe diffuse infiltration is a strong reduction in signal in which the signal intensity of bone marrow is almost equal to the intervertebral disc or the muscle on T1-weighted spin-echo images. Signal intensity on fatsuppressed images (e.g., STIR) is markedly increased. Data from Durie BGM, Salmon SE. Myeloma management guidelines: a consensus report from the Scientific Advisors of the International Myeloma Foundation. Hematol J 2003; 4:379–398.

can be increased, especially in the axial skeleton, and hematopoiesis (red marrow conversion) may increase in the peripheral skeleton as a reaction to decreased hematopoiesis in the axial skeleton. In more advanced disease, both yellow and red bone marrow are replaced by myeloma. Reduction of bone mass, seen on radiographs and CT as focal osteolysis, or general osteopenia is mainly caused by tumor-induced resorption of bone and not by mechanical destruction of bone by solid tumor. A crucial interaction between tumor and host, using complicated signaling pathways, develops, resulting in activation of osteoclasts and inhibition of osteoblasts. This interaction

■ FIGURE 91-1 Histology (Giemsa staining) of a patient with multiple myeloma of asynchronous type. The atypical plasma cells have a large, irregular, centrally located nucleus.

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has a major impact on usefulness of imaging techniques. The impact of amyloid deposition in tumor on imaging is not well known. Amyloid deposition may also occur away from tumor, and this may be detected with MRI.

IMAGING TECHNIQUES Techniques and Relevant Aspects In patients with multiple myeloma the basic diagnostic workup in many institutions still consists of radiographs of the skull (two projections), the rib cage, the upper arms, the spine (two projections), the pelvis, and the upper legs. More and more cross-sectional imaging methods, such as multidetector CT (MDCT) and MRI, are used owing to the low sensitivity of radiography to demonstrate involvement by myeloma.4,5

Pros and Cons Radiography versus Magnetic Resonance Imaging Several studies demonstrated that radiographs often yield false-negative results, especially in the spine and pelvis secondary to superposition of complex osseous structures and soft tissues such as bowel. When radiographs are compared with MR images, high false-negative rates between 29% and 90% have been reported for radiographs in patients with multiple myeloma.4,5 Even in asymptomatic patients (stage I according to the staging criteria of Durie and Salmon) with normal radiographs, MRI depicted diffuse or focal tumor infiltration in 29% to 50% of patients.6,7 In approximately one third of patients the disease is understaged if MRI is not used.8 However, disease stage would be underestimated in 10% of patients if conventional radiographs would have been replaced with limited MRI of the spine and pelvis because of lesions in the peripheral long bones, ribs, or skull.9 Current MR techniques allow a time-effective comprehensive skeletal survey using T1-weighted fast spin-echo and short tau inversion recovery (STIR) sequences in combination with dedicated receiver-coil elements, such as the total imaging matrix function in combination with parallel imaging (Siemens Medical Systems, Malvern, PA, USA) or the rolling table platform (AngioSURF Innovations, Essen, Germany). Thus, the entire bone marrow can be displayed, without patient repositioning, within approximately 35 minutes.

■ FIGURE 91-2 A, Sagittal STIR MR image of a female patient with multiple myeloma displaying many small foci and a fracture of the T9 vertebra. B, Sagittal reconstruction of the spine from a whole-body MDCT examination gave a false-negative finding.

in detecting myeloma infiltration (Fig. 91-2).11 MRI displays tumor directly, whereas CT depends, like radiographs, on visualization of osseous destruction, resulting in a relatively high rate of false-negative results. Another consequence of this difference between MRI and CT is that after therapy, tumor load visualized on MR changes or even disappears while the secondary osseous changes seen on CT usually do not change. False-positive results in MDCT may be due to inhomogeneous osteoporosis. In a prospective study in 41 patients with multiple myeloma, MRT detected significantly more lesions than did MDCT. This resulted in significant understaging with MDCT alone.11

Computed Tomography versus Radiography

Controversies

Computed tomography is more sensitive than radiography in detecting myeloma. Usually, radiographs show lesions and CT shows additional lesions but patients with combinations of negative radiographic surveys and positive CT scans have been reported.10

A current issue is the choice of imaging modality in patients with multiple myeloma on a routine basis. Radiographs proved to be false negative in many studies; therefore, in many institutions whole-body MRI or wholebody MDCT is performed for primary diagnosis and for follow-up (Fig. 91-3). Up to now there is no consensus whether whole-body MRI or whole-body MDCT should be used. MDCT is more widely available, is a quick examination technique, and is especially useful for demonstration of osseous destructions and fractures. On the other hand, MRI is much more sensitive for evaluating early bone marrow involvement.

Multidetector Computed Tomography versus Magnetic Resonance Imaging Magnetic resonance imaging (whole-body protocol at 1.5 T using T1-weighted and STIR sequences) is more sensitive than CT (16 or 64 detector rows using 0.75-mm collimation)

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Radiography Predilection sites are the axial skeleton (spine and pelvis) but also the ribs, the shoulder region, the skull, and the proximal femur (Figs. 91-4 and 91-5). The appearance of multiple myeloma in radiographs is either focal circumscribed “punched out” osteolyses or diffuse inhomogeneous osteopenia, especially in the spine (Fig. 91-6). In the skull, multiple osteolytic lesions of similar size are found. In the long bones the osteolytic lesions are often, but not exclusively, centrally located (Figs. 91-7 and 91-8). With increasing size they lead to endosteal scalloping of the cortex. Large lesions may penetrate the cortex and demonstrate a soft tissue component. Enlargement may lead to apparent expansion of bone with a soap bubble appearance. Involvement of the ribs is usually seen as osteolyses or an inhomogeneous appearance of the spongiosa in combination with a circumscribed expansion of the bone. Differentiation of multiple myeloma from metastatic skeletal disease can be very challenging without the knowledge of laboratory parameters. The most important discriminating features of myeloma versus metastases are osteolytic rather than the combination of osteolytic and sclerotic lesions, diffuse osteopenia, lesions that are well defined and uniform in size, and cortical scalloping rather than cortical destruction. Sclerotic lesions or osteolytic lesions with a sclerotic rim are rarely seen in myeloma.13 Primary diffuse sclerosis of the skeleton is also rare (50 volume % in bone marrow biopsy) the signal intensity on T1-weighted spin-echo MR images is nearly equal to that of the intervertebral disc or muscle (Figs. 91-13 and 91-14). In cases of intermediate grade of involvement (20 to 50 volume %) the signal reduction is only moderate and often hard to diagnose.15 In those cases intravenous injection of gadolinium chelates is recommended to verify diffuse involvement. Enhancement of normal bone marrow varies between 3% and 40% (Fig. 91-15), with a mean of 17%, in patients older than 40 years of age. An increase of signal intensity after

Magnetic Resonance Imaging In patients with multiple myeloma, five patterns of infiltration patterns can be described by MRI.4 First, in 28% of the patients a normal-looking bone marrow signal is found in all sequences with high signal intensity on T1weighted images and an intermediate signal intensity on T2-weighted spin-echo images, as well as low signal intensity in fat-saturated sequences such as STIR. In histology, this corresponds to a slight interstitial plasma cell infiltration (5 cm high specificity) Located deep to fascia Extracompartmental extension Ill-defined margins Broad contact with fascia Inhomogeneity on all pulse sequences High signal intensity on T2-weighted images Invasion of bone and/or neurovascular bundle Intralesional hemorrhage Intralesional necrosis Marked and merely peripheral enhancement (static contrast examination) Fast enhancement, steep slope, long-standing plateau phase (dynamic contrast examination)

combination of multiple imaging parameters. In this regard, diagnostic accuracy, as reported in literature, is estimated between 30% and 80%. In a prospective study of 548 histologically verified soft tissue tumors, Gielen and colleagues obtained a sensitivity of 93%, a specificity of 82%, a negative predictive factor of 98%, and a positive predictive factor of 60% in differentiating between benign and malignant soft tissue tumors.7 Even better results are obtained by van Rijswijk and associates, who used a multivariate logistic regression to identify the best combination of MRI parameters that might be predictive of malignancy and concluded that combined nonenhanced, static and dynamic contrast-enhanced MRI parameters were significantly superior to nonenhanced MRI parameters alone and to nonenhanced MRI parameters combined with static contrast-enhanced MRI parameters in prediction of malignancy. The most discriminating parameters were presence of liquefaction, start of dynamic enhancement (time interval between start of arterial and tumor enhancement), and the size of the lesion (diameter).8 In addition to differentiating benign from malignant soft tissue tumors, a specific diagnosis is also possible in specific circumstances. Kransdorf and colleagues stated in 1993 that “a correct histologic diagnosis reached on the basis of imaging studies is possible in only approximately one quarter of cases.”9 Gielen and coworkers, however, recently reported on a series of 548 histologically proven soft tissue tumors in which a correct tissue-specific diagnosis on MRI was made in 294 of 425 benign tumors (69%) and in 47 of 123 malignant tumors (38%).7 It is important to realize that a specific diagnosis is more often possible in benign conditions than in malignant ones. Thus,

making a confident tissue-specific benign diagnosis may help in differentiating benign from malignant soft tissue tumors. The best results in tissue-specific diagnosis are obtained by using a combination of different parameters. The usefulness of prevalence, age at presentation, and zonal distribution (preferential location) has already been stressed. Morphology (i.e., the shape of the lesion) may be useful in making a specific diagnosis (Table 93-7). Typically, soft tissue tumors have low signal intensity on T1-weighted images and high signal intensity on T2weighted images. These common patterns are not helpful in making a specific diagnosis. Unusual signal intensities, that is, high signal intensity on T1 weighting and low signal intensity on T2 weighting, can frequently be used in making a specific diagnosis. Intermediate to high signal intensity on T1 weighting, when compared with signal intensity of normal muscle, may indicate presence of fat (fatty components), methemoglobin in subacute hematomas, slow-flowing blood in cavernous hemangiomas and alveolar soft part sarcomas, high protein content in lymphangiomas, and melanin in metastases of malignant melanoma and clear cell sarcomas or deep-seated malignant melanomas. A combination of low signal intensity on T1-weighted images and high signal intensity on T2-weighted images is seen in cystic lesions (ganglia) and all myxoid-containing tumors such as myxoma, fibromyxoid sarcoma, and the more frequent myxoid liposarcoma.10 Low signal intensity on T2-weighted images can be caused by fibrous tissue in desmoids and other fibromatoses, desoxyhemoglobin in acute hematomas, and hemosiderin in old hematomas, pigmented villonodular synovitis, and giant cell tumors of tendon sheath. Also, xanthomas and amyloidomas may present as low signal intensity on T2-weighted images. Low signal intensity can also be due to hypercellularity in high-grade malignancies and lymphomas. Calcifications (see also Table 94-4) or ossifications are seen in extraskeletal osteosarcomas, chondrosarcomas, and chondromatosis articularis and phleboliths occur in hemangiomas. Blooming effect on gradient-echo sequences is a consequence of susceptibility artifacts due to the presence of calcifications or ossifications or hemosiderin. Also, behavior after fat suppression can help in the identification of some tumors

TABLE 93-7 Morphology Related to Specific Diagnoses Shape

Commonly Seen in

Fusiform, ovoid Multinodular, stellar, dumbbell Moniliform Rounded Serpiginous Branching, finger-like Broccoli-like, frond-like Target sign* Inverted target sign†

Neurofibromas, lipomas Desmoids Neurofibromas, ganglion cysts Schwannomas, ganglion cysts Hemangiomas Plexiform neurofibromas Lipoma arborescens Neurofibromas Nodular fasciitis, soft tissue metastases

*High signal intensity peripheral zone on T2-weighted images. † Low signal intensity peripheral zone on T2-weighted images.

CHAPTER

or tumor components. In this regard, myxoid-containing lesions show a relative decrease in signal intensity after fat suppression when compared with non–fat-suppressed T1-weighted imaging. Slow-flow hemangiomas, on the contrary, show a relative increase in signal intensity after fat suppression.11 Although a specific benign diagnosis can occasionally be made with high confidence, a biopsy is needed in the vast majority of patients. In general, a sample is taken using image guidance to allow a histologic diagnosis to be made. A biopsy is necessary when the orthopedic surgeon and the radiologist believe they are dealing with an unspecified, or even potentially malignant, soft tissue mass. Biopsy is not without risk because manipulation of the lesion may trigger different biologic behavior, such as dedifferentiation or progressive disease (e.g., in myositis ossificans) and complications related to all interventions (hemorrhage, infection). Moreover, biopsy of soft tissue tumors with large needles involves a risk of seeding malignant cells along the needle track. Because biopsy is considered part of the surgical therapy, en bloc resection of tumor and needle track is required. As a general rule, the shortest path between skin and the lesion should be chosen and the anticipated needle path should be discussed with the surgeon who will perform the definitive surgical treatment. The needle should not traverse uninvolved compartments. Percutaneous musculoskeletal biopsy can be performed by fine-needle aspiration, core-needle biopsy, or open (incisional) biopsy. Excisional biopsy should be used only for small lesions (30%) and is more frequently superficially located. High-grade myxofibrosarcoma is defined by hypercellularity, high mitotic activity, pleomorphism, and intralesional necrosis and is usually located deep to the fascia. MRI of low grade lesions reflects the high myxoid content and presents as low signal intensity on T1-weighted imaging and high signal intensity on T2-weighted imaging. High-grade lesions are indistinguishable from other pleomorphic soft tissue sarcomas (Figs. 93-10 and 93-11).20

Fibrohistiocytic Tumors

■ FIGURE 93-7 Desmoid tumor of the popliteal fossa infiltrating toward the muscles, the subcutaneous compartment, and the paraperiosteal tissue. Although histologically benign, the lesion has an aggressive behavior (aggressive fibromatosis).

The neoplastic and non-neoplastic fibrohistiocytic tumors are subdivided into three categories (Table 93-9), but only types that are relevant to radiology because of frequency or typical radiologic features are briefly discussed in this chapter. Giant cell tumor of tendon sheath and pigmented villonodular synovitis are the most frequent in the group of benign lesions, whereas dermatofibrosarcoma protuberans is the most frequently one seen in the group of intermediate malignancy.

A

B

■ FIGURE 93-8

A, Desmoid tumor of the flexor compartment of the thigh, with characteristic low signal intensity areas on a T2-weighted MR image. At a higher level there is a second desmoid tumor, superficially at the hamstrings. B, At the same level there is an exostosis at the posterior aspect of the femoral diaphysis. The association of multiple desmoids and an exostosis is seen in Gardner’s syndrome.

A ■ FIGURE 93-9

B

C

A to C, Desmoid tumor at the flexor compartment of the thigh with a characteristic evolution from highly cellular to collagenous and also with a characteristic centripetal migration pattern. All three images are obtained after intravenous administration of contrast material. There is enhancement of the proximal, noncollagenous components and no enhancement of the distal, collagenous components.

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■ FIGURE 93-10 Myxofibrosarcoma at the extensor compartment of the right thigh. The lesion is characterized by a large volume, a nonhomogeneous appearance on T1-weighted imaging (A), a high signal intensity on T2-weighted imaging (B), and a nonhomogeneous, merely peripheral and septal enhancement after contrast agent administration (C). D, On a macrophotograph of the resected specimen there is a remarkable correlation with the MRI findings.

D

Giant Cell Tumor of Tendon Sheath This tumor consists of a circumscribed proliferation of synovial-like mononuclear cells, accompanied by a variable number of multinucleate osteoclast-like cells, foam cells, siderophages (hemosiderin deposition), and inflammatory cells, histologically similar to pigmented villonodular synovitis. The lesion is hypervascular with numerous proliferative capillaries in the collagenous stroma and is covered by a fibrous capsule. It is a small (0.5 to 4 cm), nodular, or polylobular, painless, slowly growing mass, mostly located at the flexor tendons of the fingers (67%-85%), adjacent or circumferential to the synovium of the tendon sheath. It mostly occurs in the third to fourth decade, with a 2:1 female predominance. Findings on radiography and CT are soft tissue mass, pressure erosion/atrophy (15%) on adjacent osseous

structures, true bone invasion, cortical defect, extension into the medullary cavity, cystic changes, periosteal reaction, and, rarely, intralesional calcification. Findings on MRI are a round, oval, or polylobolar solid mass, eccentric to, or enveloping, the tendon sheath, with intermediate signal intensity on T1-weighted images, low signal intensity on T2-weighted images (reflecting the presence of collagen and hemosiderin), and marked enhancement on contrast enhanced T1-weighted images (Figs. 93-12 and 93-13).21

Pigmented Villonodular Synovitis There is a diffuse, intra-articular form of pigmented villonodular synovitis that is monarticular and involves the knee in 80% of cases; a localized, more nodular and extraarticular form has a predilection for the infrapatellar fat

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A

B

■ FIGURE 93-11

Myxofibrosarcoma at the subcutaneous compartment of the forearm. The lesion is of low signal intensity on T1 weighting (A) and high signal intensity on T2 weighting (B) and is heterogeneous on both sequences.

TABLE 93-9 Fibrohistiocytic Tumors Benign Giant cell tumor of tendon sheath* Pigmented villonodular synovitis* Xanthoma* Juvenile xanthogranuloma Reticulohistiocytoma Benign fibrous histiocytoma Intermediate Malignancy Dermatofibrosarcoma protuberans* Bednar tumor Plexiform fibrohistiocytic tumor Giant cell fibroblastoma Angiomatoid fibrous histiocytoma Giant cell tumor of soft tissues Malignant Atypical fibroxanthoma Malignant fibrous histiocytoma*

*Described in this chapter.

pad. Pigmented villonodular synovitis, which is histologically similar to giant cell tumors of the tendon sheath, presents as finger-like hyperplasia of the synovium (diffuse form) or with a more nodular appearance (localized form). Both kinds of lesions contain intracellular and extracellular hemosiderin (yellow to yellow-brown).

A ■ FIGURE 93-12

B

A and B, Two examples of giant cell tumor of tendon sheath, adjacent to or wrapped around the flexor tendons of the fingers. All lesions are of low to intermediate signal intensity on T2 weighting.

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■ FIGURE 93-13

Giant cell tumor of tendon sheath. Dumbbell-shaped lesion in between bone and flexor tendon of the finger. The lesion is of intermediate signal intensity on T1 weighting (A), enhances markedly after contrast agent administration (B), and has a low signal intensity on T2 weighting (C).

On radiography, concomitant bone erosions with sclerotic margins may be present and are more obvious in joints with a tight capsule, such as the hip (Fig. 93-14). There are characteristic MRI features due to the abundance of hemosiderin, causing low signal intensity on all pulse sequences, especially on T2-weighted images, and a “blooming” effect on gradient-echo sequences. This is more pronounced at high field strengths and a consequence of signal loss due to local changes in susceptibility. After contrast agent administration lesions enhance to a moderate or marked degree (Fig 93-15; also see Fig 93-14).22

Xanthoma Tendinous xanthomas especially of the Achilles tendons are the hallmark of familial hypercholesterolemia. On histology, the picture is dominated by collagenous fibers, separated by broad sheets of foamy histiocytes that contain cholesterol, cholesterol esters, triglycerides, and phospholipids. Ultrasonography will depict the number and extent of focal intratendinous lesions. MRI findings consist of a mass of low signal intensity in which a reticulated or speckled network of high signal intensity can be appreciated on T2-weighted images. Normal tendon and cholesterol are of low signal intensity, whereas the high signal intensity lines are secondary to presence of triglycerides. On fat-suppressed, T1-weighted MRI the signal of xanthomas is only partly suppressed because 80% of the lesion is made up of liquid cholesterol and cholesterol esters.

Dermatofibrosarcoma Protuberans Dermatofibrosarcoma protuberans accounts for 6% of all soft tissue sarcomas. Preferential locations are the trunk, head, and neck. The lesions are originally located in the dermis and subcutis. The “protuberant” character is seen at the end stage. Patients are mostly in the first to fifth decade, and there is a definite male preponderance. On histology, lesions present with myxoid components and hemorrhagic and cystic changes. The lesion has a tendency to recur in 50% of patients after surgery.

The MRI presentation is, apart from location and morphology of the exophytic components, nonspecific, showing low signal intensity on T1-weighted images and high signal intensity on T2-weighted images.

Malignant Fibrous Histiocytoma As a result of recent cytogenetic studies, the term malignant fibrous histiocytoma has been partly abandoned in the new WHO classification of soft tissue neoplasms and the formerly named malignant fibrous histiocytomas are now renamed as undifferentiated pleomorphic sarcomas (formerly giant cell malignant fibrous histiocytoma) and myxofibrosarcoma (formerly myxoid malignant fibrous histiocytoma). The MRI appearance is not specific.

Lipomatous Tumors Lipoma Lipoma is the most common mesenchymal tumor. It is a painless, slow growing, well-circumscribed, encapsulated mass composed of mature fat. It affects patients in the fifth to seventh decades. It may be superficially or deeply located and intermuscular or intramuscular. Parosteal lipoma (Fig. 93-16), also called periosteal lipoma, is located adjacent to cortical bone with or without concomitant bony excrescence. On ultrasonography the lesion is compressible and mostly hyperechogenic (75%). It has a low attenuation value (−100 HU) on CT. On MRI, the lesion is of homogeneous high signal intensity on T1 weighting and intermediate signal intensity on T2 weighting, and does not enhance after contrast agent administration. Thin septa between the fatty lobules may be seen on CT as well on MRI and may enhance slowly (>6 seconds after arterial enhancement) (Fig. 93-17).23

Chondroid Lipoma Chondroid lipoma is a rare lipomatous tumor, containing fatty, myxoid, and cartilaginous components and, more

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■ FIGURE 93-14 Pigmented villonodular synovitis. A, On T1 weighting there are synovial masses eroding the adjacent femoral bone, responsible for the so-called apple core image. B, On T2 weighting the villous components are of low signal intensity and the fluid entrapped between the villi is of high signal intensity. C, Extrinsic osseous lesions are well seen on radiography. D, A gradient-echo MR sequence demonstrates the characteristic “blooming” effect due to susceptibility artifacts caused by the presence of hemosiderin within the lesion.

■ FIGURE 93-15

Localized form of pigmented villonodular synovitis of the anterior recess of the ankle joint. The lesion is of low signal intensity on axial T2 weighting (A) and has low signal intensity areas on the sagittal, fatsuppressed, T2-weighted image (B).

A

B

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■ FIGURE 93-16

Parosteal, low-grade liposarcoma. Axial (A) and sagittal spin-echo (B) T1-weighted MR images show polylobular mass lesion enveloping the femoral diaphysis without osseous or surrounding soft tissue involvement. Interlobular septa are of lower signal intensity. C, Axial, fat-suppressed, spin-echo T1-weighted MR image after administration of gadolinium shows area of high signal intensity components suppressed; intervening septa enhance moderately and remain of intermediate signal intensity.

on T2-weighted imaging. There is little and slow (>6 seconds after arterial enhancement) enhancement after contrast agent administration (Fig. 93-19).25

Lipoma of Tendon Sheath and Joint

■ FIGURE 93-17 Two cases of usual lipoma. Both lesions are superficially located, homogeneous, well delineated and of high signal intensity comparable with signal intensity of normal fat on T1-weighted MRI.

specifically, irregular and curvilinear calcifications. It may mimic myxoid liposarcoma. It is mostly of low signal intensity with a few high signal intensity components (fat) on T1-weighted images. Signal intensity is inhomogeneous and high on T2-weighted images. Enhancement is nonhomogeneous and slow (>6 seconds after arterial enhancement) (Fig. 93-18).24

Lipoblastoma Lipoblastoma is a well-encapsulated lesion, confined to the subcutis and containing lipoblasts in different stages of development. When it is more infiltrative it is called lipoblastomatosis. Eighty-eight percent occur in patients younger than 3 years of age, and boys are more affected than girls. It is a painless lesion, mostly seen in the extremities. Presentation on MRI varies according to the amount of lipomatous versus nonlipomatous components. It is mostly hyperintense on both T1- and T2-weighted imaging. Myxoid components present with rather low signal intensity on T1-weighted imaging and high signal intensity

The first form is a lipomatous mass spreading along the tendon sheaths; the second form is an intra-articular lipomatous lesion consisting of hypertrophic synovial villi distended by fat that replaces the subsynovial tissue. This lesion, called “lipoma arborescens,” is more common than the tendon sheath variety. The first form is preferentially located at the wrist, the second form at the knee (Fig. 93-20). On MRI the first form presents as a peritendinous fatty mass, with signal intensity characteristics of a usual lipoma; the second form is a frond-like fatty mass arising from the synovium and associated with joint effusion.26

Lipomatosis of Nerve (Fibrolipomatous Hamartoma) This lesion consists of a proliferation of fatty and fibrous components surrounding the thickened nerve bundles that infiltrate both the epineurium and the perineurium. It occurs mainly at the volar aspect of the hand and wrist and usually involves the median nerve. It may be associated with macrodactyly. On MRI, the contrast between the low signal intensity of the nerve fascicles and surrounding high-signal fat results in a so-called fascicular appearance on axial images and a spaghetti-like appearance on longitudinal planes (Fig. 93-21).27

Diffuse Lipomatosis This is a group of rare diseases in which multiple symmetric lipomatosis or Madelung’s disease is the most frequent. It is characterized by massive symmetric deposition of mature fat in the neck.

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D ■ FIGURE 93-18 Chondroid lipoma. A, Axial T1-weighted MR image through the cranial part of the lesion shows merely fatty tissue. B, Axial T1-weighted MR image through the distal part of the lesion shows the presence of fatty and nonfatty components. C, Axial T2-weighted MR image with fat suppression shows signal suppression of fatty components and moniliform components of higher signal intensity located at the periphery of the lesion. D, T1-weighted MR image with fat saturation after contrast agent administration shows the peripheral and septal enhancement. E and F, Findings on radiography show extensive calcification/ossification at the distal part in a fatty tumor, thus differentiating the diagnosis from liposarcoma.

E

F

Hibernoma This rare benign tumor contains brown fat, which on MRI presents as a heterogeneous or septated mass, with high signal intensity on T1-weighted images. The signal intensity, however, is lower than that of normal fat. The signal intensity is variable on T2-weighted images. Enhancement is nonhomogeneous and moderate. The clue to the diagnosis is that fat-suppression techniques fail to suppress the signal of fat because of the nature and the amount of lipids (Fig. 93-22).28

Malignant Lipomatous Tumors

■ FIGURE 93-19 Lipoblastoma at the gluteus muscle protruding into the ischiorectal fossa. On this T1-weighted MR image the lesion is nonhomogeneous with interspersed areas of high signal intensity that are similar to that of fat.

Liposarcoma is the second most common soft tissue sarcoma. There are four subtypes, but in up to 10% of cases at least two histologic types are combined into the fifth subtype: mixed type liposarcoma. Liposarcomas are mostly located deep to the fascia and enhance fast (within 6 seconds after arterial enhancement on dynamic MRI), and the amount of fat that can be identified on MRI decreases from almost exclusively fatty tissue to no fat exhibited on MRI when moving from low- to high-grade liposarcoma. The well-differentiated subtypes are more common than the high-grade subtypes (atypical lipoma, 48%; myxoid liposarcoma, 21%).

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■ FIGURE 93-20

Lipoma arborescens. A, On a coronal T1weighted MR image there is a frond-like synovial mass that has the same signal intensity as subcutaneous fat. B, A macrophotograph shows the villous synovial proliferations.

■ FIGURE 93-21 Lipomatosis of the median nerve (fibrolipohamartoma). Fibrous and fatty components are responsible for the mixed signal intensity of the lesion on T1- (A) and T2-weighted (B) MR images. Longitudinally coursing nerve bundles are responsible for the fascicular sign on axial images (A, B) and for the spaghetti-like appearance on the longitudinal image (C). D, Perioperative photograph shows the enlarged median nerve.

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■ FIGURE 93-22

Hibernoma of the trunk. A, On T1 weighting the lesion is slightly hypointense when compared with signal intensity of normal subcutaneous fat. B, Degree and pattern of enhancement are difficult to judge on contrast-enhanced T1 weighting without fat saturation. C, Enhancement is well appreciated on T1 weighting with fat suppression. D, Enhancement is confirmed on a subtraction image. Signal intensities and behavior after contrast agent administration allow the differentiation of the lesion from a usual lipoma.

Atypical Lipomatous Tumor, Well-Differentiated Liposarcoma, or Lipoma-like Liposarcoma This tumor grossly resembles lipoma, but besides variably sized fat cells (>75%) it consists of scattered lipoblasts, broad fibrous septa, and thick-walled blood vessels. On MRI the bulk of the tumor has signal intensities comparable with signal intensities of normal fat. Thick, or even nodular fibrous septa of low signal intensity on T1-weighted imaging and of high signal intensity on T2weighted imaging are appreciated. These thick septations enhance fast (within 6 seconds after arterial enhancement) after contrast agent administration.

is currently classified as a subgroup of myxoid liposarcoma (high-grade myxoid liposarcoma with round cell component). MR signal intensities reflect their mixed composition. They are heterogeneous on all pulse sequences and show a marked, also nonhomogeneous enhancement (Fig. 93-24).

Dedifferentiated Liposarcoma Dedifferentiation occurs as a late complication of a preexisting, well-differentiated liposarcoma, most commonly of the retroperitoneum, mediastinum, or groin. Dedifferentiation mostly occurs into myxofibrosarcoma and should be suspected when areas within a preexisting tumor exhibit signal intensities other than those commonly seen in fatty tissue.29

Myxoid Liposarcoma This tumor is characterized by a basophilic myxoid matrix or ground substance that accounts for more than 90% of the tumoral mass. The thigh and buttocks are preferential locations. Frequently, there is no radiologic evidence of fat because of the small amount of mature fat in this subtype. This makes a tissue-specific diagnosis difficult. On MRI, minute fatty components present as signal intensities of normal fat; myxoid components are of low signal intensity on T1-weighted images and very high signal intensity on T2-weighted images. After contrast agent injection, there is a variable degree of enhancement allowing differentiation with cystic (nonenhancing) lesions (Fig. 93-23).

Pleomorphic and Round Cell Liposarcoma These high-grade subtypes contain variable amounts of fatty, myxoid, and cellular tissue. Round cell liposarcoma

Tumors of Vascular Origin The majority of vascular tumors are benign and are located in the skin or subcutis. They represent a dysplasia rather than a neoplasm. Classification of vascular tumors is compromised by confusion secondary to the various classification systems that are being used. The oldest classification system is that of Mulliken, which was updated in 1992 by the International Society for the Study of Vascular Anomalies (ISSVA). It is based on endothelial growth characteristics and correlates well with clinical and imaging findings. It distinguishes between hemangioma (cellular proliferation, small or absent at birth, rapid growth during infancy, spontaneous involution during childhood) and vascular malformations (dysplastic vessels, present at birth, grows with the child, no spontaneous regression). Vascular malformations can be subdivided into subtypes depending on composition: capillary, venous, arterial,

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■ FIGURE 93-23

Myxoid liposarcoma. A, There are no obvious fatty components within the lesion and as a consequence, no tissue signal suppression on T1 weighting with fat suppression. B, The lesion is of high signal intensity on T2 weighting owing to the abundance of myxoid substance.

and lymphatic. Usually, combinations occur. Vascular malformations can also be subdivided into high- or lowflow lesions. In the second classification system, the clinical perspective is replaced by a histologic perspective. All lesions, including the vascular malformations of Mulliken, are called hemangiomas. Hemangioma is defined as a benign, but nonreactive process in which there is an increase in the number of normal- or abnormal-appearing vessels. The two classification systems using this approach are those of Enzinger and the WHO. Both are very similar and distinguish between benign, intermediate, and malignant subgroups. The WHO classification is used in this chapter.30

Benign Vascular Tumors

■ FIGURE 93-24 Pleomorphic liposarcoma of the thigh region with components of high (arrow), intermediate, and low signal intensity on T1 weighting.

Hemangiomas of the subcutis/deep soft tissue and capillary, cavernous, arteriovenous, venous, intramuscular, and synovial types of hemangioma (Figs. 93-25 to 93-28), as well as angiomatosis and lymphangioma (vascular and lymphatic endothelium are indistinguishable), belong to this group. Hemangiomas may present as intralesional phleboliths on radiographs and CT and osseous changes such as periosteal reaction or erosion. Color Doppler ultrasonography may differentiate between low flow (no Doppler signal) and high flow (low resistance flow pattern) vascular malformations. On MRI, hemangiomas are characterized by their high signal intensity on T2-weighted images and intermediate (between that of muscle and fat) signal intensity on T1-weighted images. They are frequently multilobular, resembling a “bunch of grapes.” Fluid-fluid levels are merely seen in cavernous hemangiomas. Areas of high signal

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■ FIGURE 93-25

Cavernous hemangioma of the thenar eminence. A, There is a phlebolith on the CT scan. The lesion is nonhomogeneous on T1 weighting (B) and shows multiple small fluid-fluid levels with high signal intensity of the supernatans on T2 weighting (C).

C

■ FIGURE 93-26 Hemangioma showing intermediate signal intensity on T1 weighting (A) and high signal intensity on T2 weighting with fat suppression (B) with perilesional fat induction.

intensity corresponding to fat are seen at the periphery of the lesions (“fat induction” phenomenon). High-flow lesions may show signal voids on all pulse sequences. After contrast agent administration they exhibit a serpiginous, marked enhancement, seen within 6 seconds after enhancement of feeding arteries. The identification of low-flow venous hemangiomas, characterized by

the presence of large venous convolutes in combination with late enhancement, is especially important, because these patients can be treated with percutaneous techniques without using diagnostic arterial angiography.31 Synovial hemangioma presents as the same MRI features and also as pressure erosions at adjacent osseous structures.

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■ FIGURE 93-27

Arteriovenous malformation (hemangioma) within the soleus muscle, showing a serpiginous morphology on all pulse sequences and draining veins toward the superficial vena saphena parva. The lesion is of high signal intensity when compared with the signal intensity of normal muscle on T1 weighting (A), is of very high signal intensity on T2 weighting with fat suppression (B), and enhances markedly after contrast agent administration (C).

A

B

■ FIGURE 93-28

Diffuse hemangioma with foci within the retroperitoneum (A, B), the subcutaneous compartment (B), and even the right scrotum (C), best appreciated on T2-weighted imaging with fat suppression.

C Angiomatosis only differs from this solitary component by its multiplicity. Glomus tumors are lesions consisting of cells resembling cells of the normal glomus body. They are subungually located and cause radiating pain, elicited by changes in temperature. An associated bone erosion with sclerotic borders is frequently noted. On MRI, glomus tumors are seen as homogeneous lesions with high signal intensity on T2-weighted images (Fig. 93-29).

Vascular Tumors of Intermediate Malignancy Grade Hemangioendothelioma and angiosarcomas are very rare and have no specific imaging characteristics. Angiosarcoma

is most common in the lower extremity and pelvis region and may be multifocal, surrounding the hip.

Tumors of Lymphatic Origin Tumors of lymphatic origin are rare and are usually detected early in childhood. They have been reported in every type of tissue except in neural tissue. MRI is the imaging method of choice to demonstrate the full extent of the lesion, especially on fat-suppressed images. Signal intensities of lymphangioma are nonspecific and are similar to those of hemangioma. On T1-weighted images with fat suppression, lymphangioma is of low signal intensity

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B

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D

■ FIGURE 93-29

Glomus tumor at the subungual region. Oval lesion of high signal intensity on T2-weighted imaging (A, B), intermediate signal intensity on T1-weighted imaging (C), and marked enhancement after contrast agent administration (D).

whereas hemangioma is of high signal intensity. On T2weighted images, both lesions are of high signal intensity. Differentiation can be facilitated by the presence of phleboliths, by flow voids arising from feeding arteries or draining veins in hemangioma, and by a less pronounced and less homogeneous enhancement in lymphangioma. A special entity and by far the most frequent is the cystic lymphangioma or cystic hygroma. It consists of a lobulated, fluctuating mass in the supraclavicular fossa, the posterior triangle, or the axillary region that is not attached to the skin but fixed to the deep tissues of the neck. About 60% of these lesions are found at birth, and as many as 90% are noticed within the first 2 years of life. Intralesional hemorrhage may be responsible for the presence of fluid-fluid levels.32

Tumors of Muscular Origin Smooth muscle tumors have no specific imaging features except for vascular leiomyosarcoma, which mostly occurs within the inferior vena cava. Leiomyosarcoma mostly presents as large, spindle-shaped masses with variable signal intensities, central necrosis, and marked peripheral and septal enhancement. Benign striated muscle tumors

are extremely rare. Rhabdomyosarcoma is the most common soft tissue tumor in children, the embryonal subtype being by far the most frequent (Fig. 93-30).

Synovial Tumors Cystic soft tissue lesions can be divided into four groups based on the combination of their anatomic location and histologic composition: synovial cyst, ganglion cyst, bursa de novo, and permanent bursa. The diagnosis of a cystic lesion is usually straightforward on ultrasonography and/or MRI. If there is any doubt, however, of the true cystic nature of the lesion, contrast-enhanced MRI should be performed to exclude a pseudocystic benign or malignant tumor (Table 93-10). Baker’s cyst is the prototype of the synovial cyst. Ganglion cysts may occur anywhere but are frequently seen in fatty tissue. Meniscal and labral cyst also belong to the group of ganglion cysts. The most common example of a bursitis de novo is the bursa developing at the medial side of the first metatarsal head secondary to mechanical friction. A bursa is a normal structure that is only seen when it enlarges secondary to friction, inflammation, or

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■ FIGURE 93-30 Alveolar rhabdomyosarcoma of the hypothenar eminence. On T1-weighted imaging there is a large mass within the hypothenar muscles (abductor digiti minimi) that is inhomogeneous and slightly hyperintense to adjacent normal muscle. A, Infiltration is seen toward the muscle belly. B, On T2-weighted imaging with fat suppression the lesion is ill defined and of very high signal intensity, with a scar-like central component of lower signal intensity. C, On T1-weighted imaging after contrast agent administration there is a septal and peripheral enhancement. Although features are in favor of a malignant soft tissue tumor, MRI does not allow a more tissue-specific oriented diagnosis in this case.

TABLE 93-10 Classification of Para-articular Cystic Lesions Lesion

Communication with Joint

Wall Composition

Cell Lining

Content

Synovial cyst Ganglion cyst Bursitis de novo Permanent bursa

Yes May be present Absent Absent

Continuous mesothelial lining Discontinuous mesothelial lining Fibrous wall lining Continuous mesothelial lining

True cells Flattened pseudo-synovial cells No mesothelial lining True synovial cells

Mucinous fluid Mucinous fluid Fibrinoid necrosis Mucoid fluid

new communication with a joint (subdeltoid bursa filling secondary to rotator cuff tear). According to the most recent WHO classification, giant cell tumors of tendon sheath and pigmented villonodular synovitis are categorized in the group of fibrohistiocytic tumors. Lipoma arborescens belongs to the group of lipomatous tumors, whereas synovial cell sarcoma is included in the group of tumoral lesions of uncertain differentiation.5,33

Tumors of Peripheral Nerves This group comprises schwannomas, neurofibromas, and malignant peripheral nerve sheath tumors. Benign neurogenic tumors (schwannomas, neurofibromas) are well demarcated, round or fusiform lesions located on the course of a peripheral nerve. Other imaging features suggestive of a neurogenic tumor are findings of an entering/ exiting nerve, the so-called target sign (high signal intensity peripheral area and low signal intensity center on

T2-weighted images), the fascicular sign (transverse image of enlarged longitudinally coursing nerve bundles), the split fat sign, and associated muscle atrophy (Figs. 93-31 and 93-32). Although neurofibromas occur centrally in the nerve and schwannomas have a more peripheral (nerve sheath) location, differential diagnosis between a schwannoma and a neurofibroma cannot be reliably made on imaging studies. This is relevant because schwannomas allow, because of their peripheral location relative to the nerve, resection without damaging the nerve. MRI features suggestive of a schwannoma include a fascicular appearance on T2-weighted images, a thin, hyperintense rim on T2-weighted images, and diffuse enhancement after contrast agent administration. Imaging findings suggestive of neurofibroma include a target sign on T2-weighted imaging, central enhancement, or a combination of both findings (Figs. 93-33 to 93-35). Criteria that can help in establishing the diagnosis of malignant peripheral nerve sheath tumors include a large mass (>5 cm) with mass

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A C ■ FIGURE 93-31 Schwannoma of the flexor compartment of the lower leg. The well-delineated lesion is of intermediate signal intensity on T1weighted imaging (A), is of very high signal intensity on T2-weighted imaging (B), and enhances markedly after administration of contrast material (C).

B

effect, inhomogeneous tumor architecture (due to areas of necrosis and hemorrhagic foci), ill-defined margins, perilesional edema, fast (within 6 seconds after arterial enhancement) heterogeneous enhancement, destruction of adjacent bony structures, and involvement of regional lymph nodes (Figs. 93-36 and 93-37). Schwannomas, neurofibromas, and malignant peripheral nerve sheath tumors can all occur in patients with neurofibromatosis (Fig. 93-38). Schwannomatosis is a rare tumor syndrome characterized by the presence of multiple schwannomas arising on cranial, spinal, and peripheral nerves, without clinical or radiologic evidence of neurofibromatosis. These patients do not develop vestibular tumors. The hallmark of this condition is chronic pain.5,34

Extraskeletal Cartilaginous and Osseous Tumors Extraskeletal chondroma consists of mostly small, welldefined nodules composed of focal areas of cartilage,

without any connection to bone, periosteum, or articular synovium. Some of them may have undergone focal fibrosis or ossification. Hands and feet are preferential locations. They present as a specific intermediate signal intensity on T1-weighted images and high signal intensity on T2-weighted images. “Ring and arc” enhancement may be seen on contrast-enhanced MRI. Para-articular chondroma is a very rare tumor, composed of hyaline cartilage with variable endochondral ossification in the central area and preferentially located at Hoffa’s fat pad of the knee.

Synovial Osteochondromatosis The primary form is characterized by the formation of numerous, metaplastic cartilaginous or osteocartilaginous nodules of small size, originating in the outer lining of the synovial membrane of joint or tendon sheath. Knees and hips are most affected. When the entire synovial membrane becomes involved, communication with the joint cavity is established and nodules will detach and form loose bodies in the joint space.

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■ FIGURE 93-32 Schwannoma at the left medial gastrocnemius muscle. A, The lesion is isointense with muscle and as a consequence hardly visible on T1-weighted imaging. It becomes better visible after fat suppression (B) and enhances moderately after contrast agent administration, merely at the center of the lesion (C).

C

■ FIGURE 93-33 Neurofibroma of the sciatic nerve. The lesion is located on the course of a major nerve and has a central position within the nerve. A, On T1-weighted imaging the lesion is isointense to muscle. B, It enhances markedly after contrast agent administration.

A

B

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A

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Musculoskeletal Tumors and Tumor-like Lesions

B

C

■ FIGURE 93-34

Neurofibroma of the tibial nerve. The lesion presents as a characteristic “target” sign consisting of a low signal intensity peripheral rim on T1 weighting before (A) and after (B) contrast agent administration. C, On T2 weighting the peripheral rim is of high signal intensity.

■ FIGURE 93-35 Plexiform neurofibroma of the ulnar nerve (A) and presacral plexus (B). Both lesions present with the characteristic moniliform aspect.

A

B

A

B

C

■ FIGURE 93-36

Malignant peripheral nerve sheath tumor on the course of the sciatic nerve. Axial MR images of the thigh. The lesion is highly inhomogeneous on T1-weighted sequence (A), T2-weighted sequence with fat saturation (B), and T1-weighted sequence after gadolinium contrast administration (C).

ROI LAESIE (Dynamic Scan) Sc 6, T1-TFE/M, SI 5

Intensity

750

500

250

0 0

C

85

170 Time (second)

255

B ■ FIGURE 93-37 A, Dynamic sagittal, contrast-enhanced, T1-weighted MR image of a malignant peripheral nerve sheath tumor (arrows) in the lower extremity. B, Subtracted images of the dynamic series. Every 3 seconds one section is imaged. Arrival of contrast agent in the artery (2, arrowhead). Six seconds later distinct tumor enhancement (4, arrow) is seen. C, The graph depicts the early enhancement of the lesion and the rapid progression of enhancement in time.

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A ■ FIGURE 93-38

B Neurofibromatosis with plexiform neurofibromas of the cervical spinal nerves (A) and of the presacral nerve plexus (B).

Secondary osteochondromatosis is much more common and develops inside the joint when cartilage is released in the joint cavity. The diagnosis is preferentially made on radiography or CT.

Primitive Neuroectodermal Tumors

A distinction is made between myxoid, mesenchymal, and well-differentiated types. A common feature is that all, except the well-differentiated type, show only minimal cartilage formation. Appearance on MRI depends on the type of and any related tumoral components, such as high signal intensity of myxoid types on T2-weighted images (Fig. 93-39).35 Benign extraskeletal osseous tumors comprise myositis ossificans (see Chapter 94); fibrodysplasia ossificans progressiva, which is a rare inheritable disorder characterized by progressive ossification of connective tissue and muscles and by osseous anomalies (abnormalities best seen on radiography and CT); and extraskeletal osteoma, which may be the end stage of myositis ossificans.

These tumors form part of the heterogeneous group of small, round (blue) cell tumors of childhood and adolescence, which also includes conventional neuroblastoma, rhabdomyosarcoma, lymphoma, and Ewing’s sarcoma. They occur preferentially in the thoracopulmonary region, abdomen, pelvis, and lower extremities. A special entity of primitive neuroectodermal tumors is the Askin tumor, which is mostly located at the chest wall. Both are highly aggressive soft tissue tumors. Extraskeletal Ewing’s sarcoma is histologically indistinguishable from the osseous form. In contrast to the osseous form, these tumors are deeply seated and occur in an older age group. Imaging features of both primitive neuroectodermal tumors and Ewing’s sarcoma are similar to those of other malignant soft tissue tumors. They frequently exhibit areas of cystic degeneration, necrosis, and hemorrhage. They mostly present with intermediate, nonhomogeneous signal intensity on spin-echo sequences and with heterogeneous, fast enhancement after contrast agent administration.37

Extraskeletal Osteosarcoma

Tumors of Uncertain Differentiation

This is a mesenchymal neoplasm that forms osteoid or bone. It is located in soft tissues and is not attached to underlying bone or periosteum. This tumor is mostly located in the lower extremities and retroperitoneum. Calcifications within the tumor are observed on plain radiography and CT in about half of all cases. Signal intensity is low and nonhomogeneous on T1-weighted images and high and also nonhomogeneous on T2-weighted images.36

Myxoma and synovial cell sarcoma are by far the most frequent representatives of this group. Myxoma is benign and histologically characterized by the presence of abundant, avascular myxoid stroma in which a small number of cells are embedded. It is a tumor of adults. Areas most frequently involved are the large muscles of the thigh, shoulder, buttocks, and upper arm (Fig. 93-40). There is an association with polyostotic

Extraskeletal Chondrosarcoma

CHAPTER

A

B

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C

■ FIGURE 93-39

Recurrence of a soft tissue chondrosarcoma. A, No recurrent tumor on a control MRI, 6 months after surgery for a soft tissue chondrosarcoma. B, Small recurrent lesion anterior to the Achilles tendon on a control examination after 1 year. C, Second control examination 6 months later. Recurrent tumors are best detected on T2-weighted imaging with fat suppression.

fibrous dysplasia (bones involved are usually in the vicinity of the myxoma) in so-called Mazabraud’s syndrome. On MRI, myxomas present as very low signal intensity on T1-weighted images (lower than signal intensity of normal muscle) and as high signal intensity on T2-weighted images (higher than signal intensity of fat). There may be moderate, central enhancement after contrast agent administration, having a “smoke”-like appearance.38 In the group of malignant lesions of uncertain differentiation, synovial cell sarcoma is by far the most frequent. Synovial cell sarcoma occurs primarily in the para-articular region, usually in close relationship with tendon sheaths, bursae, and joint capsules, with the knee region being most often affected. It is most prevalent in adolescents and young adults between 15 and 40 years of age. The term synovial cell sarcoma is a misnomer because it is not related to normal synovial structures. Intra-articular synovial sarcoma does occur but is extremely rare. The name is derived from the microscopic resemblance to normal synovium, the real origin being undifferentiated mesenchymal tissue. Chromosomal rearrangements have been reported in association with synovial cell sarcoma. On radiography, focal calcifications/ossifications are seen in 20% to 30%, and osseous invasion in 5% to 30%. On MRI lesions are isointense to muscle on T1-weighted images but areas of increased signal intensity are frequently seen and due to intralesional hemorrhage. On T2-weighted images large lesions are nonhomogeneous and have a socalled “triple signal” sign, consisting of a mixture of low, intermediate, and high signal intensity. Here also fluidfluid levels are seen and are a consequence of intratumoral bleeding. After contrast agent administration there is an early, marked enhancement that is homogeneous in small lesions and nonhomogeneous in large lesions.

Because of location and cyst-like signal intensities on nonenhanced MRI, synovial cell sarcomas are frequently mistaken for para-articular cysts.39,40 Alveolar soft part sarcoma constitutes less than 1% of all soft tissue sarcomas. Its histology mimics the alveolar pattern of the respiratory alveoli. It is a highly vascular lesion surrounded by tortuous blood vessels and minute amounts of fat. It occurs between 11 and 40 years of age and has a female predominance. The lesion is highly aggressive with a metastatic potential of more than 50% at the moment of detection. Preferential location is the anterior portion of the thigh. On MRI the lesion is nodular with internal septations and high signal intensity on both T1- and T2weighted images, due to abundant slow flowing blood. The lesion is nonhomogeneous on all pulse sequences and also on postcontrast images (Fig. 93-41).41 Epithelioid sarcoma, which is the most common malignant neoplasm of the hand, presents as noncharacteristic malignant features on MRI. Clear cell sarcoma or malignant melanoma of soft parts is a slow-growing malignant tumor, the cells of which are capable of producing melanin. It arises deeply in the soft tissues of the limbs in the vicinity of tendons, aponeuroses, and fasciae. Young adults between the ages of 20 and 40 years are most frequently affected. All lesions present on T1-weighted MR images with hyperintensity relative to normal muscle; this results from the shortening of the T1-relaxation time, which is due to the paramagnetic effect of intralesional melanin. Although melanin also shortens T2-relaxation time, most lesions are of high signal intensity on T2-weighted images, which is due to the high water and myxoid content of the lesions. Marked enhancement after contrast agent administration is the rule (Fig. 93-42).42

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A

B ■ FIGURE 93-40 Myxoma of the lower leg (soleus muscle). Signal intensity on T1-weighted imaging (A) is lower than the signal intensity of normal muscle. B, Note very high signal intensity on T2-weighted imaging. C, Subtle, smoke-like, central enhancement after contrast agent administration.

C

Soft Tissue Metastases Although skeletal muscle metastases are relatively rare, they are not uncommon, especially in end-stage cancer. Primary tumors responsible for soft tissue metastases are adenocarcinomas and squamous cell carcinomas, mostly originating from lung, kidney, and gastrointestinal tract. Soft tissue metastases are frequently painful lesions, in contradistinction to primary soft tissue tumors, which are mostly painless. Most metastases have nonspecific features on imaging, except for metastases of osteosarcoma (intralesional ossification), and melanosarcoma (increased signal intensity on T1-weighted MR images). MR findings of low to intermediate signal intensity on T2-weighted images, owing

to hypercellularity and increased nuclear- cytoplasmic index, and especially the “inverted target sign” (high central signal on T2-weighted images with low signal intensity of the peripheral rim, and inversion of signal intensities after contrast administration, i.e., peripheral enhancement and lack of central enhancement, due to central necrosis) are more specific features seen in soft tissue metastases (Fig. 93-43).43,44

Pediatric Soft Tissue Tumors Soft tissue tumors are rare in childhood and adolescence. They are mostly benign. Hemangiomas are the most common benign tumors of childhood, and rhabdomyosarcomas are the most common malignant soft tissue tumors.

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A

C ■ FIGURE 93-41 Alveolar soft part sarcoma. Characteristic MRI features of this rare tumor are its preferential location in the extensor compartment of the thigh, its high signal intensity on T1-weighted imaging, due to abundant slow flowing blood within the lesion (A), and the presence of prominent vessels at both poles of the lesion (B). C, There is marked enhancement as seen on T1-weighted imaging after contrast agent administration and with fat suppression.

B

In rhabdomyosarcomas a specific staging system is used in which the TNM classification, anatomic site, and clinical status at presentation are major parameters. Tissue-specific diagnosis by imaging is possible in many benign tumors but difficult in the malignant group. Children with a soft tissue tumor should be treated in specialized centers during diagnosis and for treatment and follow-up.45

DIFFERENTIAL DIAGNOSIS Cytogenetics and Molecular Genetics of Soft Tissue Tumors

■ FIGURE 93-42 Clear cell sarcoma or deeply seated melanoma characterized by an intermediate to high signal intensity on this T1-weighted MR image.

Because long-term survival of children with malignant soft tissue tumors is strongly related to disease stage at the time of diagnosis, early detection is mandatory. Notwithstanding the limitations of ultrasonography, it remains the first diagnostic modality to use in children suspected of having a soft tissue tumors. Plain radiography and CT are best suited for demonstration of calcified lesions or intralesional calcifications. MRI is also used in children as the main modality for grading, staging, and characterizing soft tissue tumors.

Human tumors are primarily caused by anomalies affecting two types of genes: (1) dominantly acting oncogenes, whose protein products serve to accelerate cell growth and whose functions are altered by increased gene dosage (amplification) or by activating mutations or participation in fusion genes, resulting from chromosomal translocations, inversions, or insertions; and (2) tumor suppressor genes, whose products normally serve as brakes on cell growth and runaway cell proliferation and whose inactivation leads to uncontrolled cell proliferation and downregulation of apoptosis (programmed cell death). Specific translocations are diagnostic of the tumors in which they are found; they have not been observed in other tumor types and can be of crucial value in establishing the correct diagnosis in confusing cases. Tumors for which the cytogenetic and/or molecular changes are diagnostic are listed in Table 93-11. The radiologist is in an unique position for determining which soft tissue tumor may require cytogenetic

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B

A

C

■ FIGURE 93-43

Metastasis of a squamous cell carcinoma showing the “inverted target sign.” Note the hyperintense, peripheral rim on a T1-weighted MR image (A), the hypointense peripheral rim and hyperintense center on a T2-weighted MR image (B), and peripheral enhancement after contrast agent administration on a T1-weighted MR image (C).

A ■ FIGURE 93-44

Metastasis of a papillary renal carcinoma showing the “inverted target sign.” Note the hyperintense peripheral rim on a T1-weighted MR image (A), hypointense peripheral rim and hyperintense center on a T2-weighted MR image (B), and peripheral enhancement after contrast agent administration on a T1-weighted MR image (C).

and/or molecular diagnostic studies. When the radiologic findings are confusing and raise uncertainty regarding the exact diagnosis, the radiologist is in a position to alert the responsible surgeons and physicians before surgical or therapeutic procedures are initiated to the possibility

that genetic studies may be indicated. This is particularly true if cytogenetic analysis is contemplated, because fresh (not fixed) tissue is required for such an analysis and may be obtained at the time of surgery or biopsy. Emphasis must be placed on the combined use of cytogenetic and

CHAPTER

TABLE 93-11 Tumors with Specific Cytogenetic

and/or Molecular Changes

Synovial sarcoma Liposarcoma Extraskeletal Ewing’s sarcoma Rhabdomyosarcoma Clear cell sarcoma (malignant melanoma of soft parts) Desmoplastic round-cell tumor Dermatofibrosarcoma protuberans Congenital (infantile) fibrosarcoma Inflammatory myofibroblastic tumor Extraskeletal chondrosarcoma Alveolar soft part sarcoma Malignant peripheral nerve sheath tumor Desmoid tumor Leiomyosarcoma Chondroma

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regard are fluorescence in-situ hybridization (cytogenetic changes) and reverse transcriptase polymerase chain reaction (molecular changes).12

SYNOPSIS OF TREATMENT OPTIONS Treatment strategies are discussed in Chapter 88. The importance of multidisciplinary approach and treatment planning is addressed in Chapter 89. The role of MRI in local staging is discussed in Chapter 98.

What the Referring Physicians Needs to Know ■

molecular techniques in obtaining an optimal and full picture of diagnostic value of the genetic changes in tumors, because tumors may have molecular changes exceeding in number that of the cytogenetic anomalies and at the same time present cytogenetic changes not reflected in the molecular abnormalities. Particularly useful in that

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■ ■ ■ ■ ■

Is there a soft tissue tumor or pseudotumor? Is the lesion benign or (potentially) malignant? Is there a tissue-specific diagnosis? Is additional imaging needed? Is biopsy needed? In which compartments does the lesion extend? (see Chapter 98)

REFERENCES 1. Fletcher CD, Unni KK, Mertens F. World Health Organization Classification of Tumours. Pathology and Genetics. Tumours of Soft Tissue and Bone. Lyon, IARC Press, 2002. 2. Enzinger F, Weiss S, Goldblum J. Enzinger and Weiss’s Soft Tissue Tumors, 4th ed. St. Louis, CV Mosby, 2001. 3. Kransdorf M. Malignant soft tissue tumors in a large referral population: distribution of specific diagnoses by age, sex and location. AJR Am J Roentgenol 1995; 164:129–134. 4. Kransdorf M. Benign soft tissue tumors in a large referral population: distribution of specific diagnoses by age, sex and location. AJR Am J Roentgenol 1995; 164:395–402. 5. De Schepper AM, Vanhoenacker F, Gielen J, Parizel P (eds). Imaging of Soft Tissue Tumors, 3rd ed. Berlin, Springer Verlag, 2005. 6. Oliveira AM, Nascimento AG. Grading in soft tissue tumors: principles and problems. Skeletal Radiol 2001; 30:543–559. 7. Gielen JL, De Schepper AM, Vanhoenacker F, et al. Accuracy of MRI in characterization of soft tissue tumors and tumor-like lesions: a prospective study in 548 patients. Eur Radiol 2004; 14:2320–2330. 8. van Rijswijk CS, Geirnaerdt MJ, Hogendoorn PCW, et al. Soft tissue tumors: value of static and dynamic gadopentate dimeglumine-enhanced MR imaging in prediction of malignancy. Radiology 2004; 233:493–502. 9. Kransdorf M, Jelinek J, Moser R. Imaging of soft tissue tumors. Radiol Clin North Am 1993; 31:359–372. 10. Sundaram M. MR imaging of soft tissue tumors: an overview. Semin Musculoskelet Radiol 1999; 3:15–20. 11. Gielen J, De Schepper AM, Parizel PM, et al. Additional value of magnetic resonance with spin echo T1-weighted imaging with fat suppression in characterization of soft tissue tumors. J Comput Assist Tomogr 2003; 27:434–441. 12. Sandberg AA. Cytogenetics and molecular genetics in soft tissue tumors. In De Schepper AM, Vanhoenacker F, Gielen J, Parizel P (eds). Imaging of Soft Tissue Tumors, 3rd ed. Berlin, Springer Verlag, 2005.

13. Anderson MW, Temple HT, Dussault RG, Kaplan PA. Compartmental anatomy: relevance to staging and biopsy of musculoskeletal tumors. AJR Am J Roentgenol 1999; 173:1663–1671. 14. Kransdorf MJ, Murphey MD, Smith SE. Imaging of soft tissue neoplasms in the adult: benign tumors. Semin Musculoskeletal Radiol 1999; 3:21–37. 15. Kransdorf MJ, Murphey MD, Smith SE. Imaging of soft tissue neoplasms in the adult: malignant tumors. Semin Musculoskeletal Radiol 1999; 3:39–58. 16. Wang XL, De Schepper AM, Vanhoenacker F, et al. Nodular fasciitis: correlation of MRI findings and histopathology. Skeletal Radiol 2002; 31:155–161. 17. Lang P, Suh KJ, Grampp S, et al. CT and MRI in elastofibroma: a rare benign soft tissue tumor. Radiologe 1995; 35:611–615. 18. Morrison W, Schweitzer M, Wapner K, Lackman R. Plantar fibromatosis: a benign aggressive neoplasm with a characteristic appearance on MR images. Radiology 1994; 193:841–845. 19. Vandevenne J, De Schepper AM, De Beuckeleer L, et al. New concepts in understanding evolution of desmoid tumors: MR imaging of 30 lesions. Eur Radiol 1997; 7:1013–1019. 20. Rosenberg AE. Malignant fibrous histiocytoma: past, present, and future. Skeletal Radiol 2003; 32:613–618. 21. De Beuckeleer L, De Schepper A, De Belder F. Magnetic resonance imaging of localized giant cell tumor of tendon sheath. Eur Radiol 1997; 7:198–201. 22. Llauger J, Palmer J, Roson N, et al. Pigmented villonodular synovitis and giant cell tumors of the tendon sheath: radiological and pathological features. AJR Am J Roentgenol 1999; 172:1087–1091. 23. Kransdorf MJ, Bancroft LW, Peterson JJ, et al. Imaging of fatty tumors: distinction of lipoma and well-differentiated liposarcoma. Radiology 2002; 224:99–104. 24. Green RA, Cannon SR, Flanagan AM. Chondroid lipoma: correlation of imaging findings and histopathology of an unusual benign lesion. Skeletal Radiol 2004; 33:67–73.

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25. Reiseter T, Nordshus T, Borthne A, et al. Lipoblastoma: MRI appearances of a rare paediatric soft tissue tumor. Pediatr Radiol 1999; 29:542–545. 26. Soler T, Rodriguez E, Bargiela A, Da Riba M. Lipoma arborescens of the knee: MR characteristics in 13 joints. J Comput Assist Tomogr 1998; 22:605–609. 27. Maron EM, Helms CA. Fibrolipomatous hamartoma: pathognomonic on MR imaging. Skeletal Radiol 1999; 22:260–264. 28. Seynaeve P, Mortelmans L, Kockx M, et al. Hibernoma of the left thigh. Skeletal Radiol 1994; 23:137–138. 29. Peterson JJ, Kransdorf MJ, Bancroft LW, O’Connor MI. Malignant fatty tumors: classification, clinical course, imaging appearance and treatment. Skeletal Radiol 2003; 32:493–503. 30. Teo EHJ, Strause PJ, Hernandez RJ. MR imaging differentiation of soft tissue hemangiomas from malignant soft tissue masses. AJR Am J Roentgenol 2000; 174:1623–1628. 31. van Rijswijk CS, van der Linden E, van der Woude HJ, et al. Value of dynamic contrast-enhanced MR imaging in diagnosing and classifying peripheral vascular malformations. AJR Am J Roentgenol 2002; 178:1181–1187. 32. Schuster T, Grantzow R, Nicolai T. Lymphangioma colli: a new classification contributing to prognosis. Eur J Pediatr Surg 2003; 13:97–102. 33. Vanhoenacker FM, Van de Perre S, De Vuyst D, De Schepper AM. Cystic lesions around the knee. JBR-BTR 2003; 86:302–304. 34. Simoens WA, Wuyts FL, De Beuckeleer LH, et al. MR features of peripheral nerve sheath tumors: can a calculated index compete with radiologist’s experience? Eur Radiol 2001; 11:250–257. 35. Okamoto S, Hara K, Sumita S, et al. Extraskeletal myxoid chondrosarcoma arising in the finger. Skeletal Radiol 2002; 31:296–300. 36. Vanhoenacker FM, Van de Perre S, Van Marck E, et al. Extraskeletal osteosarcoma: a report of a case with unusual

37. 38. 39. 40. 41. 42.

43. 44. 45.

features and histopathological correlation. Eur J Radiol Extra 2004; 49:97–102. Ibarburen C, Haberman JJ, Zerhouni EA. Peripheral neuroectodermal tumors: CT and MRI evaluation. Eur J Radiol 1996; 21:225–232. Peterson KK, Renfrew DL, Feddersen RM, et al. Magnetic resonance imaging of myxoid containing tumors. Skeletal Radiol 1991; 20:245–250. Jones BC, Sundaram M, Kransdorf MJ. Synovial sarcoma: MR imaging findings in 34 patients. AJR Am J Roentgenol 1993; 161:827–830. van Rijswijk CS, Hoogendoorn PC, Taminiau AH, Bloem JL. Synovial sarcoma: dynamic contrast-enhanced MR imaging features. Skeletal Radiol 2001; 30:25–30. Lorigan JG, O’Keefe FN, Evans HL, Wallace S. The radiologic manifestations of alveolar soft part sarcoma. AJR Am J Roentgenol 1989; 153:335–339. De Beuckeleer LH, De Schepper AM, Vandevenne JE, et al. MR imaging of clear cell sarcoma (malignant melanoma of the soft parts): a multicenter correlative MRI-pathology study of 21 cases and literature review. Skeletal Radiol 2000; 29:187–195. Glockner JF, White LM, Sundaram M, McDonald DJ. Unsuspected metastases presenting as solitary soft tissue lesions: a fourteenyear review. Skeletal Radiol 2000; 29:270–274. Damron TA, Heiner J. Distant soft tissue metastases: a series of 30 new patients and 91 cases from the literature. Ann Surg Oncol 2000; 7:526–534. Harms D. Soft tissue malignancies in childhood and adolescence: pathological and clinical relevance based on data from the Kiel pediatric tumor registry. Handchir Mikrochir Plast Chir 2004; 36:268–274.

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94

Tumor-like Soft Tissue Lesions Rodrigo Salgado and Arthur de Schepper

Every radiologist occasionally will be confronted with a mass of undetermined imaging characteristics. Eventually, many of these lesions turn out to be non-neoplastic. These non-neoplastic masses belong to a large and heterogeneous group usually named “pseudotumors.” Soft tissue pseudotumors are a frequent clinical problem and can present at any age, occur in any location, and affect both men and woman. Many of these lesions share a common feature, being essentially reactive in nature and therefore mostly self-limiting without the need for further investigation and significant intervention. Nevertheless, other lesions (e.g., necrotizing fasciitis) are acute life-threatening conditions in which prompt recognition and subsequent intervention are essential for the survival of the patient. It is the aim of this chapter to provide an overview of the most commonly encountered soft tissue pseudotumors, ranging from pure anatomic variants to posttraumatic lesions to metabolic conditions and other origins. Knowledge of the existence and common presentation of these entities, in combination with relevant clinical findings, can direct the radiologist and physician to the correct diagnosis, thereby limiting the need for invasive procedures in these often reactive benign lesions.

soleal line of the tibia and fibula, clinically appearing as an asymptomatic soft tissue mass medial to the calcaneus (Fig. 94-2). Symptoms, when present, have been attributed to closed compartment ischemia and are accentuated by exercise. The accessory breast or nipple presents along the primitive milk line above or below the normal breast location (Fig. 94-3). Because the primitive milk line extends from the axilla to the groin, these masses may occasionally also be found in the axilla, scapula, thigh, and labia majora. It is the most frequently encountered congenital anomaly of the breast. These accessory breasts are subject to the same physiologic and pathologic changes as proper breast tissue. Although they are often dismissed as cosmetic curiosities, they have nevertheless potential for pathologic degeneration and may be associated with significant congenital abnormalities.

INFLAMMATORY AND INFECTIOUS LESIONS In general, differentiation between infection and sarcoma may be easy in typical cases, but it may be impossible to differentiate the two in atypical cases. Epidemiologic data

NORMAL ANATOMIC VARIATIONS AND MUSCULAR ANOMALIES Normal anatomic variants presenting as soft tissue tumors are occasionally seen in clinical practice. Many of these occur in specific locations, facilitating their diagnosis (Table 94-1; Fig. 94-1). In this chapter, normal variants that may mimic soft tissue tumors are briefly discussed. In the lower extremities, anatomic variants occur almost exclusively in the soleus muscle. Although present from birth, an accessory soleus muscle (or low lying muscle belly of the normal soleus muscle) usually becomes clinically apparent in the late adolescent age secondary to increased physical activity. This occurs especially in athletes and other professions requiring increased physical activity. It presents as a soft tissue mass, arising either from the anterior surface of the soleus muscle or from the

KEY POINTS Soft tissue pseudotumors encompass a vast range of pathologic processes, varying from normal anatomic variants, inflammatory and infectious lesions, posttraumatic masses, and other lesions. ■ Knowledge of the common presentation of these entities in combination with relevant clinical findings can direct the clinician to the correct diagnosis, thereby limiting the need for invasive procedures in these often reactive benign lesions. ■ The radiologic approach of soft tissue pseudotumors is no different than for their “true” tumoral counterparts. When there is doubt, a biopsy should be performed. ■ Finally, always consider an infectious or reactive origin for a mass with undetermined imaging characteristics. ■

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TABLE 94-1 Common Anatomic Variants Presenting as Soft

Tissue Masses Structure

Location

Accessory palmaris longus muscle Duplication of hypothenar muscle Anomalous extensor indicis Langer’s axillary arch* Soleus muscle; low position muscle belly Accessory breast, nipple

Upper extremity Upper extremity Upper extremity Upper extremity Lower extremity Primitive milk line

*Langer’s arch is a musculotendinous structure that usually extends from the latissimus dorsi to the pectoralis major muscle.

■ FIGURE 94-2

Accessory soleus muscle in an adult man. On this sagittal, spin-echo, T1-weighted MR image there is a muscle belly (arrow) within Kagher’s fat triangle, anterior to the Achilles tendon. Signal intensity and location of this abnormality are in favor of an accessory soleus muscle. (Courtesy of Dr. Filip Vanhoenacker.)

■ FIGURE 94-1

Accessory palmaris longus muscle in a 15-year-old boy. Axial T1-weighted MR image after intravenous contrast medium administration. The additional mass located superficially to the flexor digitorum tendons (arrow) can be identified as accessory muscle because of its signal intensity and texture that are identical to that of skeletal muscle. (From Salgado R, Alexiou J, Engelholm JL. Pseudotumoral lesions. In De Schepper AM [ed]. Imaging of Soft Tissue Tumors, 3rd ed. Berlin, SpingerVerlag, 2006, pp 415–446.)

■ FIGURE 94-3

such as location, morphology, and sometimes MRI characteristics may be helpful in differentiating infection from sarcoma. Dynamic contrast-enhanced MRI is not very helpful in differentiating infection from sarcoma because both will display rapid, aggressive enhancement.

Necrotizing Fasciitis Necrotizing fasciitis is a rare, rapidly evolving and lifethreatening soft tissue infection that, unlike cellulitis, typically extends into deep fascial planes. The causative

Accessory breast in a 17-year-old girl. Axial, spin-echo, T1-weighted (A) and axial, turbo spin-echo, T2-weighted (B) MR images demonstrate a small soft tissue mass lateral to the left pectoralis muscle with signal intensities similar to the signal intensity of normal adjacent breast. (From Salgado R, Alexiou J, Engelholm JL. Pseudotumoral lesions. In De Schepper AM [ed]. Imaging of Soft Tissue Tumors, 3rd ed. Berlin, Spinger-Verlag, 2006, pp 415–446.)

CHAPTER

organisms are mostly group A hemolytic streptococci and Staphylococcus aureus, on occasion acting in synergy. Other both aerobic and anaerobic pathogens may also be involved. Known predisposing factors include older patients, especially in combination with malignancy, poor nutrition, and alcohol or drug abuse. It can also be found after trauma or around foreign bodies in surgical wounds. However, it can also appear in otherwise healthy subjects with no known risk factors (Fig. 94-4). The clinical course can be fulminant, with reported mortality rates as high as 73%. Early recognition is mandatory, because survival depends on prompt surgical intervention. On MRI, this condition shows as hyperintense signal intensity on T2-weighted images extending into the deep fasciae with fluid collections. After intravenous administration of a contrast agent, peripheral enhancement is clearly seen. However, this presentation can be seen in other nonnecrotizing conditions. When no deep fascial involvement is revealed, necrotizing fasciitis can be excluded.

Abscess A soft tissue abscess is a well-delineated fluid collection surrounded by a well-vascularized fibrous pseudocapsule. Although in many cases there will be a suggestive preceding event (e.g., puncture) or underlying illness, it can also occur without a suggestive history or symptoms. Therefore, when confronted with a mass with undetermined imaging characteristics one must always consider a possible infectious origin. Abscesses can be multiple and can distort normal muscle anatomy and fascial planes due to their inflammatory nature. Their margins can be well defined or infiltrating, depending on the organism involved. Conventional radiography has no or little value in the imaging workup. It may occasionally show gas within

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● Tumor-Like Soft Tissue Lesions

the lesion. Ultrasonography reveals an elongated or lobulated fluid collection and can assist in guiding an aspiration biopsy or percutaneous catheter drainage. On MRI, an abscess is hypointense to isointense compared with muscle tissue on T1-weighted images. On T2-weighted images, the central portion of the abscess is usually hyperintense but the capsule may display an isointense or hypointense signal intensity relative to subcutaneous fat. On T1-weighted images the pseudocapsule can have a variable signal intensity compared with skeletal muscle. After intravenous contrast medium injection, a peripheral rim of enhancement is seen, corresponding to the inflammatory and cellular component of the abscess (Fig. 94-5). When occurring near bone, an association with osteomyelitis or a periosteal reaction can be seen. Inflammatory edematous changes in the surrounding tissues (muscle, subcutaneous tissue) are seen as a hyperintense signal intensity on T2-weighted images. Inhomogeneity on T2-weighted sequences may be a consequence of intralesional gas bubbles and/or necrotic material. However, imaging characteristics may be different in an immunocompromised host. The peripheral edema usually seen on T2-weighted images is sometimes absent. Similarly, T1-weighted images will not always show the pseudocapsule. The infected fluid in the center of the abscess can have an inhomogeneous signal intensity. If the content is sufficiently viscous, it can even show mild increased signal intensity on T1-weighted images. Enhancement after intravenous contrast medium injection can also be absent.

Pyomyositis Pyomyositis, also known as bacterial myositis, is a rare cause of single or multiple abscesses of skeletal muscle of unknown etiology. In general, normal skeletal muscle has a

A ■ FIGURE 94-4

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A 36-year-old previously healthy man presented with a rapidly spreading skin infection and swelling of the right upper leg. Axial, turbo spin-echo, T2-weighted MR image with fat suppression (A) and coronal, turbo spin-echo, T2-weighted MR image with fat suppression (B) are shown. In contrast to cellulitis, this case shows extensive subcutaneous thickening and reticular infiltration, extending to the superficial adductor fascia. No signal changes in the muscles are seen, which is an important finding in the preoperative planning. The combination of both clinical and imaging findings were consistent with this surgically proven necrotizing fasciitis. (From Salgado R, Alexiou J, Engelholm JL. Pseudotumoral lesions. In De Schepper AM [ed]. Imaging of Soft Tissue Tumors, 3rd ed. Berlin, Spinger-Verlag, 2006, pp 415–446.)

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■ FIGURE 94-5

A 40-year-old woman presented with a swelling at the left knee. A, Axial, spin-echo, T1-weighted MR image shows an ill-defined mass at the vastus lateris muscle of the left knee. B, On axial, spin-echo, T1-weighted MR image after gadolinium contrast medium administration a clear peripheral enhancement of an irregular mass is seen, with concomitant diffuse perilesional enhancement. The center of the lesion remains unchanged. The imaging characteristics are consistent with those of an intramuscular abscess.

high intrinsic resistance to bacterial infection and abscess formation. Therefore, some authors suggest that underlying muscle damage may facilitate the onset of pyomyositis. Whereas pyomyositis was initially mainly found in tropical regions (e.g., after minor trauma or insect bite), in recent years there has been an increased incidence of this disease in industrialized regions with a more temperate climate. This is due to the presence of predisposing immune-compromising conditions including diabetes, human immunodeficiency virus infection, and malignancy. Pyomyositis is considered one of the most common musculoskeletal complications of the acquired immunodeficiency syndrome (AIDS). The causative organism is mostly S. aureus, although a number of other pathogens such as Streptococcus pyogenes and Mycobacterium tuberculosis have also been reported. The clinical course can be divided into three stages. Initially, there is localized pain in one muscle group with induration of the overlying skin. This is accompanied by signs of systemic inflammation such as low-grade fever and mild elevation of the white blood cell count. Subsequently, in the second stage there is development of pus in the lesion, with increasing pain, fever, and edema of the affected muscle. Finally, a clear abscess develops with necrosis of the affected muscle. Blood cultures are positive in only 5% of cases, and in 1.8% the outcome is fatal due to sepsis and shock. Nevertheless, many of these symptoms may be absent when the lesion is deep seated. The muscles of the thigh and gluteus region are most often affected (Fig. 94-6), although the infection can appear in many other locations. In AIDS patients, pyomyositis may present as multiple lesions. However, multiplicity in this setting is not very specific for pyomyositis, because it may be found in other pathologic conditions, such as polymyositis, Kaposi sarcoma, and lymphoma.

On T1-weighted images the abscess collection has a low signal intensity compared with surrounding muscle tissue. On occasion, a high intensity peripheral rim is noted, probably representing blood breakdown products or granulation tissue. This has been described as very specific for infection.1,2 Pus in the abscess can have an intermediate to high signal on T1-weighed images depending on the protein content. T2-weighed images reveal a hyperintense collection in the affected muscle, with increased signal in the surrounding muscle tissue representing edema, organized phlegmonous collections, or hyperemia. Intravenous administration of contrast material can further discriminate between viable and necrotic muscle tissue, with the latter lacking enhancement. On occasion, the imaging presentation of pyomyositis can be confused with a sarcomatous lesion, especially when further clinical and biochemical information is inconclusive. Key elements in the differential diagnosis favoring an infectious origin are the extent of the perilesional inflammatory reaction and the possible association of cellulitis (in the absence of previous surgery or local radiotherapy). Gallium scintigraphy is very sensitive for detection, on occasion also revealing additional distant abscesses. Because no anatomic detail is obtained, it must be reserved for those cases in which in spite of very suggestive clinical findings CT or MRI gives no additional relevant information.

Hydatid Cystic Disease Hydatid cystic disease is a parasitic disease usually caused by the tapeworm parasite Echinococcus granulosus. Infection by E. multilocularis is more rare but has a more invasive nature sometimes mimicking a malignant

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■ FIGURE 94-6

Pyomyositis in a 48-year-old man (A) and a 72-year-old man (B, C), both after minor trauma during travel in tropical regions. A, CT scan in the first patient shows a distinctive increase in size of the vastus medialis, intermedius, and lateralis muscles of the right leg, with multiple ill-defined low-density areas. B, Similar findings can be seen in the second patient, with an ill-defined collection located between the L4-L5 intervertebral disc and the right psoas muscle. C, This is better illustrated on the coronal T2-weighted MR image, which shows bilateral, descending, soft tissue abscesses between the spine and the psoas muscles. These two cases demonstrate the typical history, location, and imaging characteristics of pyomyositis. (From Salgado R, Alexiou J, Engelholm JL. Pseudotumoral lesions. In De Schepper AM [ed]. Imaging of Soft Tissue Tumors, 3rd ed. Berlin, SpingerVerlag, 2006, pp 415–446.)

lesion.3 Hydatid cystic disease is a rare finding in Western countries. It is more common in parts of South America, the Middle East, Africa, Australia, and Mediterranean areas with sheep rearing, where the parasite is endemic. Although it may affect any organ, soft tissue involvement is unusual (1.75%-2.42%) because intramuscular growth of a cyst is countered by muscle contractility and lactic acid. Soft tissue hydatid cysts are nevertheless usually intramuscular and most frequently found in the head, neck, trunk, and the root of the extremities. A subcutaneous localization is also possible. The imaging characteristics of soft tissue involvement resemble those of hydatid cysts found in the liver, showing a multiseptated or multicystic mass surrounded by a rim. Typically, the lesion consists of a mother cyst, containing multiple daughter cysts. On T1-weighted images these daughter cysts are seen as hypointense cysts within the intermediate signal of the mother cyst. The signal intensity of the daughter cysts on T2-weighted images can be high or low, with some authors suggesting a relation with the presence and absence, respectively, of viable scolices.4 Still, the value of MRI in determining the viability of the cysts remains controversial. A rim of low and/or high signal intensity on T2weighted images surrounds the lesion. This rim is composed of three layers: an endocyst, ectocyst, and pericyst. The pericyst develops as a reaction after compression and inflammation of surrounding tissue. It is well vascularized, enhancing after intravenous contrast injection, and has thus an appearance like a pseudocapsule of sarcoma.4 MRI has proven superior over ultrasonography in detecting this multivesicular structure. More solid appearances are also possible, making it sometimes difficult to differentiate it from other soft tissue tumors.5 Even in these cases, MRI can often reveal the vesicular nature of the lesion.

Focal Myositis Focal myositis is a relative rare, usually self-limiting soft tissue pseudotumor. Although it can occur in many locations, it is usually found in the lower extremities, with 50% of the cases being located in the thigh and 25% in the lower leg. There is no sex or age preference. Approximately one third of the patients with focal myositis evolve to polymyositis or a polymyositis-like syndrome,6 suggesting that focal myositis may be a localized form of polymyositis. Focal myositis usually presents as a sometimes painful local intramuscular soft tissue mass, which can rapidly grow in a few weeks (Fig. 94-7). While the process is normally limited to a single muscle, involvement of multiple muscles has been reported. MRI reveals a heterogeneous signal pattern, with increased signal intensity on T2-weighted images, in one or more affected muscle groups. It can also clearly depict the extensive surrounding edema. A focal mass, when visualized, may enhance less than the surrounding edema.

Diabetic Muscle Infarction Diabetic muscle infarction is a rare complication of diabetes mellitus. Patients with poorly controlled type 1 insulindependent diabetes mellitus and severe end-organ damage are most frequently affected, although it may occur in a well-controlled patient without known diabetic complications. Although the pathogenesis is still to be completely clarified, the most likely hypothesis is that muscle infarction is secondary to vascular disease such as arteriosclerosis and diabetic microangiopathy. MRI can detect subclinical muscle infarction months before the onset of clinical symptoms. Whether MRI in conjunction with additional clinical and biochemical

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■ FIGURE 94-7

A 45-year-old man presented with a recently detected, nonpainful lesion at the anterior aspect of the left thigh. There was no history of trauma. Axial, spin-echo, T1-weighted (A), axial, turbo spin-echo, T2-weighted (B), and axial spin-echo, T1-weighted, contrast enhanced (C) MR images are shown. The T1-weighted MR images reveal a hardly visible lesion at the rectus femoris muscle. The lesion is clearer on the T2-weighted image, which shows the inhomogeneous and ill-defined aspect of this lesion. After intravenous contrast administration there is marked inhomogeneous and mainly peripheral enhancement with a nonenhancing central core. This case illustrates a biopsy-proven case of focal myositis.

information can reliably establish the diagnosis remains nevertheless unclear. As a consequence, the place of a biopsy in the diagnosis remains controversial. MR images display enlargement of the involved muscles, with uniform increased signal intensity on T2weighted and short tau inversion recovery (STIR) images, demonstrating the edematous and inflammatory changes (Fig. 94-8). T1-weighted images show normal or decreased signal intensity in the involved muscles, with the swelling being sometimes less appreciated on this sequence. The role of intravenous contrast medium injection in the differentiation with other entities such as pyomyositis, muscle abscess, or a necrotic tumor is not yet clearly established.

Bursitis Bursae are defined as spaces near joints containing small amounts of fluid, thereby reducing friction between different structures. Whereas more than 140 different bursae have been described, the most frequently affected ones are the trochanteric, subdeltoideal, ischiogluteal, pes anserina, iliopsoas, and retrocalcaneal and olecranon bursae. The amount of fluid may increase due to inflammation, which can have a infectious or noninfectious origin (overuse, direct trauma). In noninfectious bursitis repeated movements cause microtrauma in the tendon, tendon sheaths, and/or bursae. It may also be a first presentation of rheumatoid arthritis. Infectious bursitis is a rarer pathologic process, usually associated with S. aureus infection or, on rare occasions, with β-hemolytic streptococci. It frequently affects the olecranon and prepatellar and infrapatellar bursa, probably because of their superficial location, which makes them susceptible to trauma and subsequent infection. Nevertheless, a clear history of trauma is not always found. On MRI the increased fluid is hypointense on T1weighted images and hyperintense on T2-weighted images. After intravenous administration of contrast

medium, enhancement of hypertrophied synovium and surrounding soft tissue edema can be seen in both infectious and noninfectious bursitis. Although no single imaging feature is able to reliably distinguish infectious from noninfectious bursitis, the combination of bone erosions with marrow edema is more suggestive for septic bursitis. Other features favoring an infectious origin are marked synovial thickening, synovial edema, soft tissue edema, and a complex appearance of the lesion. On occasion, the differentiation with a soft tissue sarcoma may be difficult, especially when the lesion has a complex appearance. However, the anatomic location of bursitis is often characteristic (e.g., iliopsoas bursitis) (Fig. 94-9), further adding to the correct diagnosis.

Sarcoidosis Muscle involvement in sarcoidosis is rare, reported in only 1.4% to 6% of patients with known sarcoidosis.7 Three main clinical presentations of muscular sarcoidosis can be distinguished: an acute myositic form, a diffuse atrophic form, and a nodular form. However, a diagnosis of sarcoid is typically not yet made and specific symptoms are often absent when a patient presents with a mass secondary to sarcoid infection. The acute myositis type occurs exclusively in the early stage of sarcoidosis, presenting as myalgia secondary to inflammation. MRI is usually negative, presumably because of the sparse distribution and small size of epithelioid cell granulomas. In the diffuse atrophic myopathic form, patients can present with myalgia, muscle weakness, and atrophy. The muscles of the proximal portions of the extremities are frequently involved. MRI findings are nonspecific, revealing proximal muscle atrophy with fatty replacement. Differentiation from a corticoid myopathy is mainly based on clinical and laboratory findings. The least common form is the nodular presentation, presenting as single or multiple, often bilateral, sarcoid nodules (Fig. 94-10). They may, or may not be, clinically

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■ FIGURE 94-8

Desmoid tumor at the flexor compartment of the thigh with a characteristic evolution from highly cellular to collagenous and also with a characteristic centripetal migration pattern. A to C, All three images are performed after intravenous administration of contrast material. There is enhancement of the proximal, noncollagenous components and no enhancement of the distal, collagenous components.

palpable. These nodules appear elongated and extend along muscle fibers. On ultrasound examination, sarcoid nodules present as a hyperechoic center and a hypoechoic peripheral zone. They may also present with well-defined borders and an overall hypoechogenic aspect. On MRI, the nodules may have a star-shaped hypointense center on all axial pulse sequences (“dark star” sign) that is believed to correspond with fibrous tissue, which does not enhance after intravenous administration of a contrast agent.8,9 However, this central structure is not present in the acute stage of the disease. It can also be absent in small nodules ( 6 Seconds after Artery

X X No enhancement X, margin may enhance fast X, or no enhancement X, diffusion takes minutes Enhancement < 10 seconds X X X

in the start of enhancement are best appreciated on subtraction images. The subtraction images can also be used to place regions of interest for more quantitative analysis of enhancement curves (see Chapter 99). Because of this time frame it is important to have a temporal resolution of at least 3 seconds. Spatial resolution and number of sections sampled in this time frame should be as high as possible but should not be increased at the cost of the temporal resolution. The temporal resolution and the cutoff value of 6 seconds are based on empirical evidence as well as on theoretical pharmacokinetic modeling.8 Gd-chelate– enhanced MR angiography may be used as an additional sequence to evaluate involvement of the neurovascular bundle.

Computed Tomography Multidetector row CT is the optimal modality in identifying, or excluding, pulmonary metastases. The 3D dataset is obtained with small collimation (e.g., 1 mm), and axial reconstructions of 3 to 5 mm are analyzed in cine mode and multiplanar reconstructions on a viewing station (Figs. 98-2 and 98-3). The thicker reconstructions facilitate differentiation between vessels and nodules. Multiplanar reconstructions may increase accuracy because they allow a second look and because the periphery of the lung, the area where metastases preferentially occur, can be analyzed in planes that are orthogonal on bordering structures such as the diaphragm. Unless conventional chest radiographs show metastatic disease, CT should be obtained before treatment to diagnose, or exclude, metastatic disease. Because of the high sensitivity of CT, many small benign nodules are also detected; therefore, histologic proof of pulmonary metastases is needed when a few small nodules are found.9 The use and timing of CT relative to radiographs in follow-up is discussed in Chapter 99.

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A ■ FIGURE 98-2

Axial (A) and coronal (B) images show, respectively, two metastases and one metastasis in a patient with osteosarcoma.

B

metastases because of its capability to image the entire skeleton. However, whole-body MRI using T1-weighted and STIR sequences and a floating table has become available and has the advantage of superior sensitivity and specificity compared with planar bone scintigraphy (see Chapter 97).8

Positron Emission Tomography/ Computed Tomography Because of limited spatial resolution, PET with or without CT has no role in local staging of musculoskeletal tumors. Its role in detecting sarcoma metastases is not yet determined (see also Chapter 97).

Controversies ■ FIGURE 98-3

Axial image of patient with pleuritis carcinomatosis. Note the pleural effusion and the multiple ossified nodules in the pleura.

The role of CT in local staging is limited to a small number of specific situations. The anatomic detail that CT offers is useful when anatomic information is needed preoperatively in osseous benign tumors and tumor-like conditions. CT is routinely used in planning and executing percutaneous therapy and biopsy procedures.

Bone Scintigraphy Technetium-99 m methylene diphosphonate (99 mTc-MDP) has been the method of choice for screening for osseous

The use of the extracellular, interstitial contrast agent Gdchelate in imaging musculoskeletal tumors is somewhat controversial. There is ample evidence that it adds clinically relevant information in specific situations, such as in monitoring therapy (see Chapter 99), in differentiation between benign and malignant soft tissue tumors (see Chapter 93), in diagnosing some bone tumors, such as low-grade chondrosarcoma and giant cell tumor, and in specific problems related to local staging. Usually, staging can be accurately done without the use of contrast agents. In some situations, for instance, tumor extending toward structures that are critical for surgical planning, the highresolution Gd-chelate–enhanced images provide essential information. For this reason we routinely use Gd-chelates in the workup of musculoskeletal tumors. It can be argued that contrast agents should only be administered when problems arise on the native MR studies. This approach

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has two disadvantages. First, some patients need to be rescheduled, or the needed second-look examination is not obtained because of practical reasons. Second, there is no dynamic Gd-chelate–enhanced dataset allowing follow-up of chemotherapy (see Chapter 99).

malignancies, and knowledge of biologic behavior of tumors, as described later, will be useful in differentiating between invasion and displacement without invasion.

MANIFESTATIONS OF THE DISEASE

Magnetic resonance imaging is superior to other imaging techniques in displaying bone marrow involvement.14,15 MRI has an almost perfect correlation with pathologic/ morphologic examination of the resected specimen (Fig. 98-4). The osseous tumor margin may be obscured by the presence of accompanying intraosseous edema (Fig. 98-5). Often, a double margin can be visualized. The margin nearest to the center of the tumor represents the true tumor margin, whereas the outer margin represents the margin of the edematous reactive zone toward normal bone marrow.4 Differentiation between tumor and reactive zone can be facilitated by using intravenous Gd-DTPA or similar Gdchelates. Tumor and edematous reactive zone display different enhancement patterns: a well-vascularized tumor will enhance more rapidly than the reactive zone on dynamic sequences.4,5 The intraosseous reactive zone is usually not a clinical problem, because it disappears after one or two cycles of chemotherapy. The true tumor margin is then easily identified. The extent of bone marrow involvement should thus be evaluated on the post-chemotherapy MR images obtained before surgery. Because cartilage is a relatively difficult barrier to cross for most tumors, an open growth plate is not easily crossed. The main exception

Magnetic resonance imaging has had a dramatic impact on the accuracy of local staging and has contributed to replacement of ablative by limb-salvage surgery. Only after meticulous preoperative staging is it possible to execute limb-saving surgery, resulting in control of the primary tumor and satisfactory residual function. Anatomic compartments are used in analyzing local tumor extent on MRI. As discussed in Chapter 97, the surgeon uses surgical compartments that often encompass multiple anatomic compartments such as individual muscles.10 Knowledge of these surgical compartments and communication between surgeon and radiologist is important in focusing on clinically relevant problem areas when planning surgical intervention.11–13 Although risks cannot be taken, it is important to realize that MRI is so sensitive in visualizing tumor extent that equivocal findings are more often than not negative for tumor invasion. Also because most sarcomas grow in an expansile fashion, contact of an anatomic structure with the tumor does not necessarily mean that the structure is invaded. Invasion is more likely in high-grade

Bone Marrow Involvement

■ FIGURE 98-4 Osteosarcoma in a 14year-old girl. A, Anteroposterior radiograph shows classic signs of osteosarcoma: osteoid formation in tumor, irregular cortical destruction, and interrupted periosteal reaction including Codman’s triangle. Note that tumor ossification extends into the epiphysis. B, T1-weighted coronal MR image shows precise tumor margin in bone. These proximal and distal tumor margins are used to plan osteotomy planes close to the tumor. (Courtesy of Netherlands Committee of Bone Tumors.)

A

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A

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C

■ FIGURE 98-5

Osteosarcoma in the proximal femur. A, Coronal T1-weighted image shows marrow extension and cortical breakthrough on the lateral site. Note ill-defined reactive changes in the bone marrow distally and proximally. B and C, Soft tissue extension (lateral in fascia lata and anterior in gluteus minimus, medius, vastus lateralis) and ill-defined reactive changes in gluteal muscle compartment, short rotator muscles (arrow) (gemelli superior, inferior, and quadratus femoris muscle) are well demonstrated on the fat-suppressed, Gd-DTPA–enhanced coronal (B) and axial fat-suppressed, T2-weighted (C) MR images.

is osteosarcoma. When a tumor located in the metaphysis crosses the physis and extends into the epiphysis, an osteosarcoma is very likely. Ewing’s sarcoma, on the other hand, usually bypasses the physis by extending into the soft tissues, invading the epiphysis via the soft tissues. Caution is needed in the diagnosis of skip metastases in osteosarcoma and Ewing’s sarcoma because they should also be resected together with the primary tumor (Fig. 98-6). Presence of skip metastases adversely affects prognosis. The prevalence of skip metastases in osteosarcoma has been reported to be up to 10% in osteosarcoma and 6% in Ewing’s sarcoma.16,17 Because Ewing’s sarcoma is considered to be a systemic disease, bone marrow biopsies are taken from the iliac crest. Skip metastases can be detected with bone scintigraphy unless the size is below the detection threshold. Skip lesions of less than 5 mm may thus pose a diagnostic problem and are usually detected by MRI proximal to the tumor. Imaging the entire bone on T1-weighted images using a large field of view may be of help.

Cortex Destruction of cortical bone can be evaluated with plain radiographs, CT scans, or MR images. Invasion of cortex by tumor is best shown on fat-suppressed T2-weighted or fat-suppressed Gd-chelate–enhanced T1-weighted images as a disruption of the cortical line and replacement of cortex by high signal intensity of tumor (see Figs. 98-1 and 98-5). Ewing’s sarcoma and lymphoma may permeate cortical bone without displaying gross destruction (Fig. 98-7). MRI is usually as accurate as CT in displaying involvement of cortical bone. It only has an advantage over CT in densely ossified osteosarcoma or when permeation of cortex by lymphoma or Ewing’s sarcoma is subtle.2 Invasion by sarcoma is the rule when sarcoma originates in bone. Soft tissue sarcoma rarely invades bone, with the exception of synovial sarcoma. Also rare is osseous sarcoma extending into soft tissue and invading a second bone. This occurs occasionally when joints are immobile, such as in sacroiliac or tibiofibular joints (Fig. 98-8)

■ FIGURE 98-6 Sagittal T1-weighted image of osteosarcoma in the femur. The distal physis is the distal margin; the proximal margin is well demarcated and seen in the proximal diaphysis. Note the three rounded low-signal-intensity skip lesions: in the distal epiphysis, proximal to the proximal margin, and in the trochanter apophysis.

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A

B

■ FIGURE 98-7 Permeative, rather than gross, cortical destruction is demonstrated in this patient with osseous lymphoma showing the osseous component, areas of abnormal signal intensity within cortex that is mainly preserved, and the large soft tissue component in the vastus intermedius muscle on T1-weighted (A), T2-weighted (B), and Gd-chelate–enhanced (C) axial images. Note the continuity between the vastus intermedius (containing tumor), vastus lateralis, and vastus medialis, due to absence of fascia between these three muscles. In contrast, the rectus femoris muscle is separated from the vastus muscles by its own fascia. D, The corresponding lateral radiograph depicts thickened abnormal cortex with lucent areas but no massive destruction.

C

D

■ FIGURE 98-8 Osteosarcoma originating in the fibula of a 22-year-old man before chemotherapy. Axial fatsuppressed, T2-weighted (middle bottom) and fat-suppressed, Gd-DTPA–enhanced (middle top) images show circumferential soft tissue extension (extensor digitorum longus, peroneus longus, posterior tibial, and soleus muscles) of osteosarcoma of the fibula. The tumor extends toward the neurovascular bundle but does not encase it. Superior extension is seen invading the tibia on coronal T1-weighted (left) and fat-suppressed Gd-DTPA–enhanced (right) images.

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and in severe osteoarthritis. Osseous tumor types most frequently exhibiting this behavior are osteosarcoma, giant cell tumor, chondrosarcoma, and chordoma (leaving one vertebral body and invading another one at a different level).

Periosteum When an osseous tumor breaches the periosteum, it extends beyond its original compartment and becomes thus an extracompartmental tumor. Ossified periosteum, especially when periosteal reaction is present as a result of tumor activity within the medullary canal and/ or cortex, is well seen on radiographs, and especially

■ FIGURE 98-9 T-cell lymphoma in a 4-year-old boy. The intraosseous tumor and soft tissue extension are easily appreciated. Cortical bone and ossified periosteum is black (signal void). Note the continuous cellular periosteal reaction (arrows), which has an intermediate signal on T1-weighted (A) and high signal intensity on STIR (B) and fat-suppressed T2-weighted (C) MR images. (Courtesy of Netherlands Committee of Bone Tumors.)

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on CT. When not yet mineralized, the cellular layer or cambium of the periosteum is very well seen on MRI, especially when it is lifted off the bone by the tumor (Fig. 98-9).

Muscular Compartments Magnetic resonance imaging is highly accurate and significantly superior to other imaging techniques in identifying muscle compartments containing tumor (see Figs. 98-1, 98-5, 98-7, 98-8, 98-10, and 98-11).2 For tumors, muscular fascia is a relatively difficult border to cross. Macroscopically, tumors tend to grow in an expansile, rather than an invasive, fashion. Therefore, muscle is initially

B

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B

■ FIGURE 98-10

Same patient as in Figure 98-8 with images obtained after chemotherapy. A and B, Axial fat-suppressed T2-weighted images at two levels. Tumor is well defined and is seen to extend in the peroneus longus and extensor digitorum longus muscles. Reactive changes are seen in the anterior and posterior tibialis muscles and in the soleus muscle. Neurovascular bundle is free of tumor.

A

B

■ FIGURE 98-11

Large Ewing’s sarcoma in the pelvis. Axial fat-suppressed, T2-weighted (A) and fat-suppressed, Gd-chelate–enhanced (B) MR images at the different levels. The tumor originates from the acetabulum and extends into the pelvis (internal obturator muscle), displaces and compresses the urinary bladder, extends into the pectineus and iliopsoas muscles anteriorly, and compresses the femoral vein, which is flattened (arrow). The femoral artery (lateral to the vein) is not compressed, but tumor is seen anterior to the artery and vein (on A).

displaced and invasion is a late event. The presence or absence of fascia is the reason that tumor located in one of the vastus muscles extends easily in the other vastus muscles but does not easily invade the rectus femoris muscle. The reason for this is that no fascia is present between the three vastus muscles, whereas the rectus femoris muscle has its own fascia (see Fig. 98-7). The expansile mode of growth results in the presence of a well-defined pseudocapsule, which is often surrounded by a reactive zone that may contain microscopic tumor, especially in high-grade sarcoma.18 When the lesion has an infiltrative growth pattern (e.g., in aggressive fibromatosis) rather

than the usual expansile pattern, strings of tumor, not visible on MRI, extend beyond the macroscopically detectable tumor margins. The reactive zone, when present, is well seen on MRI outside the well-defined pseudocapsule of the tumor. It is as a rule easily identified because of slightly different signal intensity as compared with that of the tumor and because of the fading outward margins (see Fig. 99-5). When needed, using multiple echos can highlight differences between tumor and reactive zone or Gd-chelate–enhanced MRI. Especially dynamic Gdchelate–enhanced imaging may provide additional information. The soft tissue component of osseous or soft tissue

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sarcoma typically enhances within 6 seconds of arterial enhancement in the area of the tumor, whereas the reactive zone enhances later.

Neurovascular Bundle The neurovascular bundle is invaded by tumor in approximately 10% of patients. It is reported to be higher in soft tissue sarcoma than in bone sarcoma.19 Neurovascular bundles are more often displaced than encased by tumor. When a fat plane is seen between tumor and neurovascular bundle, the neurovascular bundle is free of tumor. Evaluation is challenging when the fat plane has disappeared and the tumor is in contact with the neurovascular bundle but does not yet encase the bundle (see Figs. 98-8 and 98-10). When contact between tumor and vessels or nerves is less than 180 degrees of the circumference, invasion usually is not present and the nerve, or even vessels, are not fixed to the tumor. In these cases MR angiography may be of help. When no stenosis is seen, invasion of the neurovascular bundle is unusual. The neurovascular bundle may be lifted from the pseudocapsule during surgery, but, especially in high-grade sarcoma, the resection is usually not radical (see Chapter 97). Encasement of vessels or nerves is rare; but when it occurs, no surgical cleavage plane between these structures and tumor is present (see Figs. 98-11 and 98-12).

A ■ FIGURE 98-12

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The neurovascular bundle is seen to be surrounded by tumor, and on MR angiography a stenosis is typically seen. The major vessels are easily identified on MRI. The nerves are not always well depicted. It is important to realize that around the knee, where most tumors occur, the sciatic nerve and its branches are located posterior to the popliteal artery and vein. This means that a soft tissue tumor that is located posterior to the popliteal vessels and that is in contact with, or even displaces, these vessels may very well encase the sciatic nerve and its branches. When, however, the tumor lies anterior to the popliteal vessels, the tumor typically does not invade the nerve, because the vessels are between tumor and nerve. Also, the perineurium is a border that is difficult to breach. Invasion of small veins surrounding the tumor are not consistently well visualized with MRI. This is not a clinical problem because these do not extend beyond the reactive zone.

Joints Joints are invaded in approximately 30% of patients. CT and especially MRI are able to demonstrate joint involvement with high accuracy (Fig. 98-13).2 False-positive findings can be avoided if pitfalls related to biologic behavior of the tumor are recognized. Anterior to the distal femur,

B

The wall of the brachial artery (A, arrow) is part of this vascular soft tissue tumor (myopericytoma). The tumor surrounds the artery for more than 50%, and there is no cleavage plane visible on T2-weighted, fat-suppressed (A) or T1-weighted, fat-suppressed, Gd-chelate–enhanced (B) MR images.

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A ■ FIGURE 98-13

Leiomyosarcoma in a 69-year-old woman. The enhancing soft tissue tumor invades the enhancing synovium as demonstrated on these axial (A) and sagittal (B) fat-suppressed, GdDTPA–enhanced images. Note the low signal intensity of the synovial fluid. This intra-articular space is distorted.

B

sarcoma easily extends into the prefemoral fat. This is an extra-articular compartment posterior to the patellar recess. Extension of tumor in the prefemoral fat is frequently mistaken for intra-articular involvement (Fig. 98-14). Insertion of tendons and ligaments are vulnerable areas, because these structures function as scaffolds for soft tissue extension. Cartilage is an effective barrier that is not easily crossed by most tumors. However, osteosarcoma and giant cell tumor have, in contrast to Ewing’s sarcoma, the capability to cross cartilage. When joints are immobile, because of either anatomy (sacroiliac joints) or pathology (severe osteoarthritis), tumor crossing such a joint and invading the opposite bone may occur (see Fig. 98-8). Joint effusion with or without hemorrhage can be reactive and is not always a secondary sign of a contaminated joint.

What the Referring Physician Needs to Know ■ ■ FIGURE 98-14

Juxtacortical chondroma of the distal femur in 53year-old woman extends into prefemoral fat but does not reach into the articular space, as demonstrated on this axial fat-suppressed, T2-weighted MR image. (Courtesy of Netherlands Committee on Bone Tumors, Leiden.)

■ ■

In what compartments does the tumor extend? What is the level of confidence? Are there pulmonary metastases?

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SUGGESTED READINGS Berquist TH, Dalinka MK, Alazraki N, et al. Bone tumors. American College of Radiology. ACR Appropriateness Criteria. Radiology 2000; 215(Suppl):261–264.

Bloem JL, van der Woude HJ, Geirnaerdt M, et al. Does magnetic resonance imaging make a difference for patients with musculoskeletal sarcoma? Br J Radiol 1997; 70:327–337.

REFERENCES 1. Enneking WF, Spanier SS, Goodman MA. The surgical staging of musculoskeletal sarcoma. J Bone and Joint Surg Am 1980; 62:1027–1030. 2. Enneking WF, Spanier SS, Goodman MA. A system for the surgical staging of musculoskeletal sarcoma. Clin Orthop Relat Res 2003; 415:4–18. 3. Holscher HC, Bloem JL, Vanel D, et al. Osteosarcoma: chemotherapyinduced changes at MR imaging. Radiology 1992; 182: 839–844. 4. MacVicar AD, Olliff JFC, Pringle J, et al. Ewing’s sarcoma: MR imaging of chemotherapy-induced changes with histologic correlation. Radiology 1992; 184:859–864. 5. Van der Woude HJ, Bloem JL, Verstraete KL, et al. Osteosarcoma and Ewing’s sarcoma after neoadjuvant chemotherapy: value of dynamic MR imaging in detecting viable tumour before surgery. AJR Am J Roentgenol 1995; 165:593–598. 6. Bloem JL, Taminiau AHM, Eulderink F, et al. Radiologic staging of primary bone sarcoma: MR imaging, scintigraphy, angiography, and CT correlated with pathologic examination. Radiology 1988; 169:805–810. 7. Verstraete KL, van der Woude HJ, Hogendoorn PCW, et al. Dynamic contrast-enhanced MR imaging of musculoskeletal tumours: basic principles and clinical applications. JMRI 1996; 6:311–321. 8. Tofts PS, Brix G, Buckley DL, et al. Estimating kinetic parameters from dynamic contrast-enhanced T1-weighted MRI of a diffusable tracer: standardized quantities and symbols. JMRI 1999; 10:223–232. 9. Grampp S, Bankier AA, Zoubek A, et al. Spiral CT in the lung in children with malignant extra-thoracic tumors: distribution of benign vs malignant pulmonary nodules. Eur Radiol 2000; 10:1318–1322.

10. Anderson MW, Temple HT, Dussault RG, Kaplan PA. Compartmental anatomy relevance to staging and biopsy of musculoskeletal tumors. AJR Am J Roentgenol 1999; 173:1663–1671. 11. van Trommel MF, Kroon HM, Bloem JL, Taminiau AH. MR imaging based strategies in limb salvage surgery for osteosarcoma in the distal femur. Skeletal Radiol 1997; 26(11): 636–641 12. Toomayan GA, Robertson F, Major NM. Lower extremity compartmental anatomy: clinical relevance to radiologists. Skeletal Radiol 2005; 34:307–313. 13. Toomayan GA, Robertson F, Major NM, Brigman BE. Upper extremity compartmental anatomy: clinical relevance to radiologists. Skeletal Radiol 2006; 35:195–201. 14. Onikul E, Fletcher BD, Parham DM, Chen G. Accuracy of MR imaging for estimating intraosseous extent of osteosarcoma. AJR Am J Roentgenol 1996; 167:1211–1215. 15. Gillespy T, Manfrini M, Rugierri P, et al. Staging of intraosseous extent of osteosarcoma: Correlation of preoperative CT and MR imaging with pathologic macroslides. Radiology 1988; 167:765–767. 16. Sajadi KR, Heck RK, Neel MD, et al. The incidence and prognosis of osteosarcoma skip metastases. Clin Orthop Relat Res 2004; 426:92–96. 17. Jiya TU, Wuisman PL. Long-term follow-up of 15 patients with nonmetastatic Ewing’s sarcoma and a skip lesion. Acta Orthop 2005; 76:899–903. 18. Beltran J, Simon DC, Katz W, Weis LD: Increased MR signal intensity in skeletal muscle adjacent to malignant tumours: pathologic correlation and clinical relevance. Radiology 1987; 162:251–255. 19. Panicek DM, Go SD, Healey JH, et al. Soft tissue sarcoma involving bone or neurovascular structures: MR imaging prognostic factors. Radiology 1997; 205:871–875.

99

C H A PP T T EE RR

Monitoring Therapy in Bone and Sof t Tissue Tumors Catharina S. P. van Rijswijk and Hans L. Bloem

The objectives of treatment of bone and soft tissue sarcomas are described in Chapter 97. Information on effectiveness of treatment plays an important role in the quest for these objectives. Monitoring the response to local or systemic chemotherapy comprises accurate identification and quantification of the proportion of therapy-induced necrosis and residual viable tumor. This may have an impact on prognosis, modification of neoadjuvant (presurgical) treatment protocols, timing and planning of surgery, planning of radiation therapy, and selection of postoperative radiation therapy and/or chemotherapy regimens. Secondly, imaging modalities strongly influence the therapeutic strategies by revealing absence or presence and location of recurrent local, regional, or distant tumor after initial treatment. In this chapter we address histopathologic changes occurring after chemotherapy and radiotherapy as they pertain to imaging response to treatment and identification of recurrent tumor, as well as the corresponding imaging findings and required imaging strategies.

PATHOPHYSIOLOGY The histologic response to neoadjuvant chemotherapy is one of the most important prognostic factors for patients with bone or soft tissue sarcoma who are scheduled for surgical treatment. Patients whose tumors show little necrosis relative to the fraction of viable tumor after neoadjuvant chemotherapy have poorer survival than patients with tumors that have more chemotherapy-induced necrosis. The amount of spontaneous, or non–chemotherapyinduced necrosis as a result of the tumor outgrowing its blood supply can be quite substantial. Therefore, both histologic and radiologic techniques focus on determination of the fraction of the entire tumor that is still viable 1860

instead of the fraction that is necrotic. Historically, only one or two macrosections of the resected tumor have been used in the pathologic laboratory to determine the fraction of viable tumor. To avoid sample errors that are secondary to this limited analysis, MRI can presently be used by the pathologist to target components of the tumor that are viable, thereby avoiding these errors. Although the principle of classifying response of musculoskeletal sarcoma to therapy, based on fraction of viable tumor, is the same for all sarcomas, some differences do exist. The basis for the classification system has initially been described for osteosarcoma (Table 99-1).1 Residual viable tumor in osteosarcoma preferentially persists within the soft tissues, cortical bone and endosteal surface, zones adjacent to cartilage, ligaments, and areas around zones of liquefaction.

KEY POINTS DCE MRI allows differentiation between good and poor response. ■ Clinical evaluation is key in detecting recurrent tumor. ■ MRI is superior to clinical evaluation when physical examination is difficult (retroperitoneum, head and neck) and in aggressive fibromatosis. ■ DCE MRI and ultrasonography are pivotal tools in diagnosing recurrent sarcoma. ■ Always sample a suspicious mass that was found with MRI. ■ Chest CT for lung metastases is required when local recurrence of a sarcoma is proven. ■ Timing of follow-up imaging should depend on the patient’s risk factors at presentation. ■

CHAPTER

99

● Monitoring Therapy in Bone and Soft Tissue Tumors

TABLE 99-1 Histologic Classification of Response to

Chemotherapy in Osteosarcoma Grade

Necrosis (%)

Histologic Appearance

I II

0–49 50–89

III

90–99

IV

100

Little or no necrosis Areas of acellular tumor osteoid and/or fibrotic material attributable to the effect of chemotherapy, with other areas of viable tumor Predominant areas of acellular tumor osteoid and/or fibrotic material attributable to the effect of chemotherapy, with only scattered foci of viable tumor cells No pathologic evidence of viable tumor within the specimen

Data from Huvos AG, Rosen G, Marcove RC. Primary osteogenic sarcoma: pathologic aspects in 20 patients after treatment with chemotherapy en bloc resection, and prosthetic bone replacement. Arch Pathol Lab Med 1977; 101:14–18.

TABLE 99-2 Histologic Classification of Response to Chemotherapy in Ewing’s Sarcoma of Bone Poor Response Class I Class II Good Response Class IIIa

Class IIIb

Class IV

Minimal or no effect of chemotherapy: ≥90% of viable tumor, 3 mm) may also predispose to impingement of the anterior rotator cuff. Although there are no absolute contraindications to subacromial decompression, some factors such as age, activity level, general medical condition, patient expectations, and the severity of disease will determine the likelihood of proceeding to surgery. The partial-thickness tear in a young throwing athlete must be approached cautiously and examined for occult instability leading to

■ FIGURE 106-3

Comparison with preoperative imaging studies is of particular importance in accurately assessing the postsurgical changes as they relate to impingement. Understanding of the patient’s presurgical anatomy enables the radiologist to give a more accurate description of the changes to the osseous outlet. After acromioplasty, MRI may demonstrate a change from a curved or hooked acromial configuration to a flat undersurface (see Fig. 106-3).7 Low signal artifact from small metal fragments is often present as a result of burring of the acromion, and typically the anterior third of the acromion is not visualized due to resection (Fig. 106-4). Residual microscopic metal shavings resulting from burring of the acromion often result in extensive susceptibility artifact on MRI. If AC joint pathology was considered the source of impingement, postoperative changes may include absence of the distal 1.5 to 2.0 cm of the clavicle (Mumford procedure) or widening of the AC joint (Fig. 106-5). Fibrosis often develops at the site of acromioplasty, resulting in low T1- and T2-weighted signal within the remaining acromion (Fig. 106-6). If inflamed, the subacromial/subdeltoid bursa is often resected at the time of acromioplasty, resulting in scar tissue and residual fluid in the region of the bursa. As a result, fluid in the location of the bursa is not a useful secondary sign of cuff injury or bursal inflammation after acromioplasty (Fig. 106-7).8 The coracoacromial ligament may also be lysed or débrided at the time of the surgery, typically near its attachment to the acromion (Fig. 106-8).

A, Preoperative sagittal oblique T1-weighted MR image demonstrates a type 3 acromial configuration. B, After acromioplasty, an oblique sagittal T1-weighted MR image demonstrates conversion to a type 1 acromial configuration (flat undersurface).

1982 P A R T E I G H T

● Postsurgical Imaging and Complications

■ FIGURE 106-4

A, After acromioplasty, an axial proton density–weighted image shows postsurgical artifact along the anterior aspect of the acromion. B, After acromioplasty, a coronal oblique proton density–weighted image shows absence of the anterior portion of the acromion.

■ FIGURE 106-6 ■ FIGURE 106-5

Oblique sagittal proton density–weighted image reveals widening of the acromioclavicular joint after joint excision.

Acromion fibrosis. Coronal T1-weighted MR image reveals decreased signal in the acromion as a result of fibrosis after acromioplasty. The patient also has a full-thickness tear of the supraspinatus with tendon retraction and fatty atrophy.

CHAPTER

106

● Postoperative Imaging of the Shoulder

1983

After subacromial decompression without rotator cuff repair there may be slight improvement in the altered MR signal intensity seen within the rotator cuff tendon and peritendinous tissues; however, most changes of tendinosis and additional alterations in the tendon such as bursal or articular surface fraying or partial tear usually persist.9

Potential Complications and Radiologic Appearance There are many potential sources of continued or recurrent pain after subacromial decompression. One source of pain is inadequate acromioplasty. Sagittal and coronal MR images are typically most helpful in assessing for the presence of persistent anatomic changes of the osseous outlet that may be associated with continued impingement, such as residual spur formation along the undersurface of the acromion that indents the supraspinatus muscle or tendon (Fig. 106-9). After acromioplasty, the patient may continue to have pain because of osteoarthritis of the AC joint that was not addressed at the time of surgery or progression of disease in the region of the AC joint (Fig. 106-10).10 An additional cause for persistent impingement would be the formation of extensive postoperative scarring interposed between the cuff tendon and the remaining acromion. The persistence or progression of rotator cuff disease is also a common source of pain after acromioplasty (Fig. 106-11).8 This may occur because of inadequate decompression or the natural progression of cuff disease not treated at the time of acromioplasty. Because many of these patients have coexisting disease of the rotator cuff disease to some degree, MRI is indicated in the setting

■ FIGURE 106-7

Subacromial fluid is noted after acromioplasty on this oblique coronal fat-saturated T2-weighted MR image. This does not suggest a cuff tear or bursitis.

■ FIGURE 106-8

Postoperative appearance of the coracoacromial ligament. Oblique sagittal fat-saturated proton density–weighted MR image shows resection of the coracoacromial ligament at its distal attachment to the acromion after acromioplasty.

of persistent postoperative symptoms. Clinical findings such as night pain, loss of motion, and weakness are not considered to be specific. Rotator cuff tendinosis may progress to a tear, or unrecognized partial or small complete tears may extend (see Fig. 106-11).

■ FIGURE 106-9

Post-acromioplasty pain. Oblique coronal T1weighted image shows persistent mass effect on the supraspinatus muscle from an osteophyte arising along the undersurface of the clavicle after acromioplasty.

1984 P A R T E I G H T

■ FIGURE 106-10

● Postsurgical Imaging and Complications

Post-acromioplasty pain. Oblique coronal T2-weighted fast spin-echo MR sequence with fat saturation after acromioplasty shows persistent acromioclavicular joint arthritis with marginal edema and joint space fluid. There has also been interval development of a small partial-thickness undersurface tear.

■ FIGURE 106-11

The assessment of cuff integrity after surgery is complicated by the fact that there may be persistent signal in the cuff tendons after acromioplasty. However, MRI remains sensitive but not as specific in this setting for the assessment of cuff tear. It is fairly sensitive (84%) and specific (87%) for residual impingement according to a study by Magee and associates.11 The typical criteria for a cuff tear in which there is tendon discontinuity and a fluid signal defect on long repetition time/echo time (TR/ TE) sequences still applies. MR arthography may also be helpful in further evaluating for more subtle cuff tears because contrast agent extravasation though a cuff defect may be more readily apparent.12 Another potential cause of unsuccessful acromioplasty is failure to recognize and treat an unstable os acromiale. A persistent unstable os acromiale can lead to continued impingement on the rotator cuff during deltoid contraction and continued symptoms of impingement (Fig. 106-12). Finally, in some patients, symptoms of impingement result from unrecognized glenohumeral instability rather than from extrinsic impingement, and acromioplasty can, in fact, worsen the situation in these patients.6 Open surgical procedures for subacromial decompression and rotator cuff repair carry the risk of deltoid detachment or atrophy because this procedure involves a deltoid takedown in an open approach or a deltoid-splitting procedure in a mini-open approach (Fig. 106-13). The miniopen procedure may carry a lower risk of this complication (Table 106-7).

A, Progression of rotator cuff disease after acromioplasty. Oblique coronal T2-weighted fast spin-echo image with fat saturation shows the interval development of a articular surface partial tear after acromioplasty. B, Progression of rotator cuff disease. Coronal oblique, turbo inversion recovery sequence in another patient. Status post acromioplasty there had been interval development of a full-thickness tear of the supraspinatus tendon anterodistally.

CHAPTER

106

● Postoperative Imaging of the Shoulder

1985

■ FIGURE 106-12

A, Persistent os acromiale after acromioplasty. Axial proton density–weighted MR sequence with fat saturation reveals the presence of marginal edema within a previously unrecognized os acromiale after acromioplasty. B, Persistent os acromiale after acromioplasty. Oblique coronal proton density–weighted MR image shows a flat undersurface of the acromion after acromioplasty, but a persistent os acromiale is noted that may contribute to continued impingement.

TABLE 106-7 Complications of Subacromial Decompression • • • • • • •

■ FIGURE 106-13

Detachment and atrophy of the deltoid muscle after acromioplasty. Oblique coronal proton density–weighted image reveals retraction and fatty atrophy of the deltoid muscle. Deltoid detachment in combination with a large rotator cuff tear and acromioplasty has led to superior migration of the humeral head.

Rotator Cuff Repair or Débridement Description Several surgical techniques are available for repair of the rotator cuff, and a general knowledge of the most commonly used methods can be helpful when attempting to understand the postoperative anatomy of the shoulder.

Inadequate acromioplasty Failure to recognize acromioclavicular joint degenerative change Postoperative scarring interposed between the cuff and acromion Failure to address an os acromiale Unrecognized instability as the cause of symptoms Deltoid detachment General postoperative complications: adhesive capsulitis, synovitis, abscess formation, osteomyelitis, chondrolysis, and hematoma formation

The general principle of rotator cuff repair is subacromial decompression, rotator cuff mobilization, and repair of the tendon if possible back to the tuberosity (Fig. 106-14). Most open repairs are performed via an anterosuperior approach through a takedown of the proximal deltoid whereas mini-open repairs involve a split of the deltoid without a takedown. Arthroscopic procedures involve the use of three bursal portals: anterior, lateral, and posterior. Small full-thickness tears are typically repaired using a side-to-side suturing technique. Distal small tears may be repaired with a tendon-to-bone repair. Larger tears with retraction also require the reattachment of tendon to bone. In the past, a trough was created in the greater tuberosity for tendon-to-bone reattachment; however, most surgeons now typically freshen the articulartuberosity junction for tendon to bone reattachment.13 Cuff repairs can be performed with suture material or suture anchors that can be made of ferromagnetic metal,

1986 P A R T E I G H T

● Postsurgical Imaging and Complications

■ FIGURE 106-14

Tendon-to-bone rotator cuff repair using a trough. The edge of the torn tendon is sutured into the trough using a combination of drill holes and nonabsorbable sutures. (From Zlatkin MB. MRI of the Shoulder, 2nd ed. Philadelphia, Lippincott Williams & Wilkins, 2003. Diagram by Salvador Beltran, MD.)

nonferromagnetic material such as titanium, plastic, or bioabsorbable polymers. Massive tears may require mobilization of the remainder of the rotator cuff or incorporation of the long head of the biceps and subscapularis tendons to achieve an effective repair, and for these reasons open surgery is usually indicated. Recently, some surgeons have even advocated an all arthroscopic approach for repair of these lesions.14 In massive tears where coverage of the humeral head cannot be achieved even with these techniques, synthetic meshes have been placed by some. Subacromial decompression is often performed in conjunction with rotator cuff repair and may be performed using either an open or arthroscopic approach.15 Finally, a bursal release may also be performed at the time of rotator cuff repair to relieve the cuff of adhesions from chronic inflammation.

Indications, Contraindications, Purpose, and Underlying Mechanics The decision to treat a rotator cuff tear depends on the size and character of the tendon tear in combination with the severity of impingement. The surgeon will typically evaluate whether the patient’s pain is secondary to rotator cuff pathology related to impingement, by assessing for impingement signs and a positive impingement test (described earlier). Shoulder pain worsened by overhead activity, crepitus, weakness, and decreased range of motion can all be seen as a result of rotator cuff pathology. Atrophy in the supraspinatus and infraspinatus fossa may further suggest a large chronic tear.5 Simple débridement may be utilized for younger patients without significant bony changes about the coracoacromial arch or with cuff injuries related to instability or internal impingement. Débridement tends to be less effective in older patients or in those with high-grade

tears. Partial tears either along the bursal or articular surface are typically treated based on the grade of the tear. High-grade tears may be completed with excision of the damaged tissue and then treated as a full-thickness tear. This more aggressive repair is often used for more active patients younger than 40 years of age. Intermediategrade tears can be débrided, and the bridge formed by the débridement may be sutured with treatment of the underlying cause of the partial tear. Low-grade tears may simply be débrided and the underlying cause treated. Subacromial decompression may also be undertaken if there is a bursal surface tear or if there are changes in the coracoacromial arch (e.g., osteophytes, type 3 acromion) that predispose to impingement.1,4,14 The basic principle of cuff repair is complete closure of the defect without tension at the repair site. Often, smaller tears may be managed with arthroscopic decompression and cuff repair while larger tears may be managed by open decompression and cuff repair. Large chronic tears may be managed by tendon transfer (e.g., a latissimus dorsi transfer), although at times an aggressive subacromial decompression alone may also result in an improvement in symptoms.16 The patient with a full-thickness tear who has good strength and a normal range of motion will typically first have nonoperative treatment. If the pain does not resolve after conservative treatment for 3 to 6 months, surgery may then be suggested. Pain is the primary indication for treatment of a full-thickness tear in an older patient. As was mentioned earlier, younger functional patients will have early repair of a full-thickness tear.5 Although there are no absolute contraindications to rotator cuff repair, patients with movement disorders, poor surgical candidates, and those with severe underlying osteoarthritis or underlying muscle atrophy limiting motion may be considered as having relative contraindications (Tables 106-8 and 106-9).

Expected Appearance on Relevant Modalities Comparison with preoperative examinations and correlation with surgical notes (if available) is suggested to render a reliable evaluation of postoperative findings. After repair of a high-grade partial- or full-thickness tear, the tendon may be medialized. A surgical trough may be seen on the greater tuberosity in many older repairs (Fig. 106-15). In the event of an end-to-end repair, there may only be some distortion of the tendon and peritendinous structures due to suture placement (Fig. 106-16). Artifacts due to soft tissue metal and suture artifacts can occur due to nonabsorbable sutures and anchors.7 Large balloon artifact may occur, particularly if ferromagnetic sutures are employed. These suture anchor artifacts will often be in close proximity to the site of reattachment created in the greater tuberosity and can impair evaluation of the tendon integrity (Fig. 106-17).17 Extensive granulation tissue often surrounds the sutures and may result in intermediate-to- high T2-weighted signal intensity in the peritendinous tissues. Within the cuff tendon, granulation tissue may mimic a tear, especially in the early postoperative period. Granulation tissue will demonstrate intermediate signal intensity on both T1and proton density–weighted images and may enhance

CHAPTER

106

● Postoperative Imaging of the Shoulder

1987

TABLE 106-8 Indications for Cuff Repair • Positive physical signs and symptoms of cuff disease or impingement • Degree of tear and patient activity level typically dictate surgical approach with high-grade tears usually excised and treated as fullthickness tears, intermediate-grade tears débrided with suturing of the defect created by débridement, and low-grade tears treated with simple débridement. • Full-thickness tears are usually managed aggressively unless the patient has normal strength and/or range of motion as well as minimal cuff-related symptoms. • Subacromial decompression is often added especially in the presence of bursal tears.

TABLE 106-9 Relative Contraindications for Cuff Repair • • • •

Severe cuff muscle atrophy or severe tendon retraction Poor surgical candidates Minimal activity level Patients with movement disorders or advanced age

■ FIGURE 106-16

Tendon distortion after an end-to-end tendon repair. Coronal oblique T1-weighted MR image with fat suppression and intra-articular administration of gadolinium shows suture artifact at the level of tendon repair. The repair is watertight and contrast agent remains within the joint.

■ FIGURE 106-15

Medialization of the repaired tendon end. Coronal oblique proton density–weighted MR image shows a tendon-to-bone rotator cuff repair with medialization of the supraspinatus tendon. A surgical trough is also seen laterally.

■ FIGURE 106-17

after the administration of gadolinium (Fig. 106-18).18 However, on T2-weighted images, granulation tissue within the tendon should be only intermediate in signal intensity whereas a tear will usually demonstrate water signal intensity within the defect. The cuff tendons may also be further distorted if an allograft is utilized or if there is transfer of other tendons. Superior migration of the humeral head (often thought of as a secondary sign of cuff tear) may also occur in the

postoperative setting as a result of scarring, bursectomy, cuff atrophy, or capsular tightening.12 Decreased acromiohumeral distance may not predict a tear of the rotator cuff but may increase the stress on the cuff by humerus. After bursectomy, there may be nonvisualization of subdeltoid fat or fluid (Fig. 106-19). As with subacromial decompression, the presence of fluid in the subacromial space does not imply a cuff tear or bursitis but may simply be the sequela of recent bursal resection or leakage of fluid from

Metallic artifact resulting from suture material within a surgical trough. Coronal oblique proton density–weighted sequence reveals extensive metallic artifact at the site of the surgical trough and cuff repair.

1988 P A R T E I G H T

● Postsurgical Imaging and Complications

■ FIGURE 106-18

A, Granulation tissue. Coronal oblique fat-saturated T2-weighted MR image shows intermediate T2-weighted signal intensity (not fluid signal) within the distal supraspinatus tendon representing granulation tissue at the site of repair. B, Granulation tissue. Oblique coronal T1-weighted image with fat saturation shows enhancement of granulation tissue after the intravenous administration of gadolinium.

the joint in a cuff repair that is not watertight (see Fig. 106-7).19 Bone marrow edema in the humeral head is also another common finding that may persist for years after surgery.

Recurrent rotator cuff tear is a common complication after rotator cuff repair and can occur as a result of untreated

impingement, premature resumption of activity, poor tendon tissue quality, suture fixation failure, or excessive tension at the anastomotic site.8 The presence of fluid signal on T2-weighted images within a tendon defect is the most reliable indicator of tendon tears in the postoperative setting (Fig. 106-20).7 The most specific finding is absence or retraction of the tendon. Magee and associates found the sensitivity and specificity for rotator cuff tears (partial and complete) after repair were 100% and 87%,

■ FIGURE 106-19

■ FIGURE 106-20

Potential Complications and Radiologic Appearance

Nonvisualization of the subdeltoid bursa or fat after bursectomy. Coronal T2-weighted MR image in a patient status post bursectomy shows nonvisualization of the subacromial bursa and fat with some mild superior migration of the humeral head.

Full-thickness tear after cuff repair. Coronal oblique T2-weighted MR image with fat suppression demonstrates a fullthickness tear of the supraspinatus tendon with retraction to the level of the glenohumeral joint and extensive fraying of the tendon edges.

CHAPTER

respectively. For partial-thickness tears alone, the sensitivity and specificity dropped to 83% and 83%.11 In some cases the incidence of low signal tear may increase owing to the presence of chronic granulation tissue. In this setting, secondary signs such as muscle atrophy and tendon retraction (see Fig. 106-6) along with comparison with a baseline postoperative study may be of benefit. Given the alterations in the tendon appearance after surgery, direct MR arthrography may be of particular value in demonstrating leakage of contrast agent through either a partial- or full-thickness tendon defect. It may better characterize the extent of a tendon tear that can be obscured by postoperative artifact (Fig. 106-21). Characterization of the rotator cuff recurrent tear in terms of muscle atrophy, tendon retraction, and fragmentation is necessary to determine the feasibility of revision of the postoperative cuff. It should be noted that the location of the musculotendinous junction may not be a reliable secondary finding of rotator cuff tear because its position can change if the cuff has been mobilized during repair. Additional potential causes of failure of rotator cuff repair include deltoid detachment (see Fig. 106-13), axillary or suprascapular nerve injury, inadequate acromioplasty, and unidentified symptomatic AC joint arthritis (see Fig. 106-10). Interestingly, defects of the articular cartilage along the humeral head or glenoid are also a common mimicker of subacromial impingement syndrome and cuff pathologic processes that may also be missed (Fig. 106-22). Occasionally, cuff tears may be produced iatrogenically, especially during arthroscopy, in some cases due to aggressive débridement (Table 106-10).20

■ FIGURE 106-21

106

● Postoperative Imaging of the Shoulder

1989

Repairs for Glenohumeral Instability Description Glenohumeral instability may be unidirectional, bidirectional, or multidirectional and can occur in the anterior, posterior, inferior, or, rarely, superior directions. Unidirectional instability is usually traumatic and can result from a single traumatic event or after repetitive microtrauma, as occurs in activities such as throwing or weight lifting. Approximately 95% of all cases of glenohumeral instability are anterior in direction, with most occurring after a dislocation. Associated injuries include avulsion or tear of the anterior labrum, capsule, or glenohumeral ligaments (anteroinferior labroligamentous complex), and these lesions are referred to as the Bankart lesion and its variants.21 Surgical repair techniques are classified as either direct or indirect. A direct repair is one in which the labral or capsular injury is directly repaired in an attempt to prevent recurrent instability, whereas an indirect repair alters the anatomy in ways such as capsular tightening to prevent recurrent instability without specifically addressing the underlying lesion of the labroligamentous complex. Because of frequent patient dissatisfaction and a high rate of recurrence, indirect repairs are rarely performed today. Direct repairs can be accomplished via either an open or arthroscopic22 approach, with the latter resulting in less damage to the surrounding tissues and less scarring. Regardless of the approach, repair is typically performed by placing suture anchors at the 3-, 4-, and 5-o’clock positions with subsequent reattachment of the labrum (Fig. 106-23). The suture anchors can be ferromagnetic or instead made of plastic or bioabsorbable materials. A second type of direct

A, Recurrent rotator cuff tear. Coronal oblique T2-weighted MR image reveals a probable recurrent tear of supraspinatus tendon that is obscured due to artifact from prior repair. B, Recurrent rotator cuff tear. MR arthrography on the same patient better shows the extent of this full-thickness tear as well contrast agent imbibition into the degenerated tendon edges.

1990 P A R T E I G H T

● Postsurgical Imaging and Complications

■ FIGURE 106-22

Focal chondral defects of the glenoid. Coronal oblique T2-weighted sequence with fat suppression reveals multiple chondral defects along the superior aspect of the glenoid.

TABLE 106-10 Complications of Rotator Cuff Repair • Recurrent rotator cuff tear • Axillary or suprascapular nerve injury • Inadequate acromioplasty or failure to recognize acromioclavicular joint arthritis • Chondral defects of the glenoid mimicking impingement and cuff disease • Iatrogenic tears of the cuff during aggressive débridement • Deltoid detachment • General postoperative complications: adhesive capsulitis, synovitis, abscess formation, osteomyelitis, chondrolysis, and hematoma formation

repair is the capsulorrhaphy, which can also be performed as an open or arthroscopic procedure. Capsulorrhaphy may be performed in conjunction with labral repair; or if no labral lesion is identified, capsulorrhaphy may be performed as an isolated procedure. Sutures are used to tighten or plicate the capsule. In the past, staple or thermal capsulorrhaphy has been performed, but these techniques have largely fallen out of favor because of either a high rate of failure or as a result of other associated complications. Techniques for indirect repair include the Putti-Platt procedure, in which the subscapularis tendon is divided 2.5 cm proximal to its insertion. The lateral stump is then attached to the glenoid while the medial stump is imbricated over the lateral stump, in effect shortening the subscapularis and capsule (Fig. 106-24). The Magnuson-Stack procedure involves transfer of the subscapularis from the lesser tuberosity to the greater tuberosity. Finally, the Bristow procedure involves transfer of the coracoid process with the conjoined tendon to the anteroinferior

■ FIGURE 106-23

Bankart repair. Suture anchors are placed at the 3, 4, and 5-o’clock positions. (From Zlatkin MB. MRI of the Shoulder, 2nd ed. Philadelphia, Lippincott Williams & Wilkins, 2003. Diagram by Salvador Beltran, MD.)

glenoid to create a bony block, thus preventing anterior instability (Fig. 106-25). Posterior instability is treated similar to anterior instability with direct repair of the labral lesion and posterior capsular plication or shift. Bone deficiency of either the anterior or posterior glenoid is treated with a bone graft (Laterjet procedure) or an opening wedge osteotomy. Multidirectional instability often results from ligamentous laxity, and it is frequently bilateral. These patients are first treated with rehabilitation to strengthen the dynamic stabilizers (rotator cuff) of the glenohumeral joint. Surgical repair with an inferior capsular shift is reserved for individuals not responsive to conservative therapy. A T-shaped incision of the anterior capsule is performed via the deltopectoral interval, and the inferior capsule is advanced in a superior direction with resultant capsular tightening (Fig. 106-26).23 Isolated labral tears such as SLAP lesions may be independent of instability and can be treated with débridement of loose tissue and staple/suture repair of the labrum back down to the bony glenoid. Labral fraying may also occur posterosuperiorly in patients with internal impingement. Paralabral cyst formation may be an additional complication of a labral tear and can extend into the spinoglenoid or suprascapular notch. These cysts may be removed arthroscopically, but if they become too large, they may

CHAPTER

106

● Postoperative Imaging of the Shoulder

1991

■ FIGURE 106-24

Putti-Platt procedure. A, The subscapularis muscle is divided into a medial and lateral stump. B, The lateral stump is then attached to the glenoid. C, The medial stump is imbricated over the lateral stump, effectively shortening the subscapularis and indirectly tightening the capsule. (Diagrams by Salvador Beltran, MD.)

be unroofed and decompressed. Large cysts may also be excised in an open procedure.

Indications, Contraindications, Purpose, and Underlying Mechanics Nonoperative management depends on the type and direction of instability as well as the age and level of activity of the patient. Initially, the patient may be treated with 2 to 3 weeks of immobilization after closed reduction with a specific rehabilitation program to strengthen the dynamic

stabilizers of the cuff and scapula. However, young active patients who have sustained a Bankart lesion have a high rate of recurrence even with conservative treatment and will often require surgical intervention either direct or indirect. The goal of surgical repair is anatomic repair of the capsular ligaments to the glenoid rim in Bankart repair. Early Bankart repair may also be performed in those young patients aiming to return to their previous level of activity. Open procedures may be performed for those in contact sports, whereas in first-time dislocators arthroscopic repair may be best.5 The presence of a

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In contrast to anterior instability, nonoperative treatment is favored as the initial treatment for posterior, multidirectional, and atraumatic unidirectional instability. Strengthening of the cuff, deltoid, and scapular stabilizing muscles along with activity modification are successful in 80% to 90% of cases. These measures are typically exhausted before surgery is considered. Surgery for traumatic posterior instability typically focuses on repair of the posterior labrum. Posterior capsulorrhaphy may also be performed. If there is coexisting anterior and posterior instability, both may be addressed at the time of surgery. Multidirectional instability in those who have failed conservative treatment is usually approached from the side of greatest instability. The inferior capsular shift procedure aims to decrease the capsular volume, thicken the capsule on the side of the approach, and, as a result, provide tension to the capsule on the opposite side. Volitional dislocators are considered a contraindication to surgical repair (Tables 106-11 and 106-12).5

Expected Appearance on Relevant Modalities ■ FIGURE 106-25 Bristow procedure. The coracoid process with the conjoined tendon is transferred to the anterior inferior glenoid through a split in the subscapularis. (Diagram by Salvador Beltran, MD.)

bony glenoid deficiency involving more than 25% of the articular surface (inverted pear–shaped glenoid) with associated instability is considered an indication for open surgery, with reduction of a bone fragment if present or bone grafting to fill the defect. If there is redundancy of the anterior capsule and inferior capsular recess, a capsular shift will also be performed.

■ FIGURE 106-26

At the time of Bankart repair, suture anchors are placed along the anteroinferior margin of the glenoid rim and these anchors result in varying degrees of artifact, depending on their composition (Fig. 106-27).8 Scar or granulation tissue is often present in the region of incision and may result in the loss of fat planes and decreased tissue contrast. After direct repair, the labrum and capsule should demonstrate a normal anatomic position but subtle changes are often noted in their morphology. The labrum may appear thickened or blunted but should remain firmly attached to the glenoid with no evidence of detachment. MR arthrography is particularly useful in demonstrating the altered capsular and labral anatomy and in identifying subtle areas of recurrent detachment. Abduction and external rotation (ABER) imaging is useful

A, Inferior capsular shift. A horizontal T-shaped incision is made and the capsule is opened. B, Inferior capsular shift. The inferior capsule is advanced in a superior direction and oversewn, with resultant tightening of the anterior capsule.

CHAPTER

TABLE 106-11 Indications for Repair of Glenohumeral

Instability

• Anterior instability generally requires surgical intervention in a young active patient due to a high rate of recurrence. • Capsular redundancy may require concomitant capsular shift at the time of surgery. • Bony defect of the glenoid involving more than 25% of the articular surface is an indication for open surgery. • Repair of posterior and multidirectional instability is performed only after failure of an exhaustive rehabilitation program.

TABLE 106-12 Contraindications to Glenohumeral

Instability Repair

• Volitional dislocators • Posterior, multidirectional and atraumatic instability repair not indicated unless conservative therapy has failed • Advanced age and minimal activity level of the patient • Poor surgical candidates

in better visualizing the anterior band of the inferior glenohumeral ligament and its glenoid attachment.24 Although rarely performed today, indirect repairs will show alteration in shoulder anatomy depending on the specific procedure performed, but the labral pathology will remain clearly evident because it is not addressed or repaired in these procedures. Following the Putti-Platt

■ FIGURE 106-27

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1993

procedure, the subscapularis tendon or anterior capsule will appear thickened (Fig. 106-28).25 A transfer of the subscapularis tendon from the lesser to the greater tuberosity will be seen after a Magnuson-Stack procedure (Fig. 106-29). Repairs of multidirectional instability typically demonstrate thickening of the anteroinferior capsule on MRI. Coronal images will demonstrate a decrease in the size of the axillary pouch (Fig. 106-30), and suture material is often seen as low signal foci located in the region of the anterior capsule and subscapularis tendon. Distention of the joint using MR arthrography is ideal for evaluation of residual capsular redundancy after capsular plication. Some have postulated that an anterior-to-posterior capsular width ratio of less than 1 after arthrography predicts a good outcome, particularly after capsulorhaphy.8

Potential Complications and Radiologic Appearance The recurrence rate for instability procedures performed as an open procedure varies between 1% and 10%. Arthroscopic procedures have recurrence rates on the order of 15% to 20%. Because of potential artifact, scarring, and the possibility of residual untreated lesions, MR arthrography (either direct or indirect) provides better visualization of recurrent lesions (Fig. 106-31). Signs indicative of a recurrent labral tear include detachment or displacement of the labrum seen on MRI as fluid signal intensity or contrast agent extension into or beneath the labrum. Wagner and colleagues studied 24 patients who had MRI after instability repair and retrospectively

A, Post Bankart repair. Axial turbo spin-echo MR image. Artifact is seen from the suture anchor in the anterior inferior glenoid. Note the scar tissue at the site of capsular reattachment to the glenoid. B, Suture anchor artifact. Sagittal oblique proton density–weighted MR image shows artifact along the site of fixation of the labrum to the anterior glenoid rim, from the 3 to 5 o’clock positions.

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■ FIGURE 106-29 ■ FIGURE 106-28

Post Putti-Platt repair. Axial T2-weighted MR image demonstrates thickening and deformity of the subscapularis tendon. The anterior labrum is absent in this nonanatomic indirect repair.

Magnuson-Stack procedure. Axial proton density– weighted MR sequence. The subscapularis tendon has been transferred from the lesser to the greater tuberosity as part of an indirect repair.

■ FIGURE 106-30

A, Capsular plication. Axial gradient-echo MR sequence reveals thickening of the capsule and a decrease in the volume of the glenohumeral joint anteriorly and posteriorly after capsular plication in a patient with multidirectional instability. B, Capsular plication. Coronal oblique proton density–weighted MR sequence reveals a decrease in the size of the axillary pouch in a patient who is status post inferior capsular shift.

reviewed these studies for the presence of recurrent labral tear. The accuracy was on the order of 79% in demonstrating recurrent labral tear.26 It should be noted that after repair the capsule may become stretched out and redundant. A capsular detachment may be suggested if the capsular attachment is more medial than would be expected for a type 3 capsular attachment. Paralabral cyst may arise as a result of a recurrent labral tear or may be a cause of persistent symptoms if not ade-

quately excised (Fig. 106-32).27 Damage to the suprascapular nerve or artery is another potential complication of paralabral cyst excision and may manifest as atrophy of the supraspinatus and infraspinatus muscle bellies, depending on the site of injury. MRI or MR arthrography may also visualize recurrent SLAP lesions after débridement or repair. MR arthrography may best accomplish this by revealing contrast agent extending between the labrum and the subjacent site of repair to the bony glenoid (Fig. 106-33).

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1995

■ FIGURE 106-31

Post Bankart repair, recurrent labral tear and degenerative change. MR arthrogram, axial T1-weighted image with fat saturation shows the anterior inferior labrum to be detached and blunted. There is also early articular cartilage loss of the glenohumeral joint with minimal osteophyte formation along the posterior margin of the humeral head. A Hill-Sachs lesion is noted posteriorly.

■ FIGURE 106-33

Recurrent SLAP tear. MR arthrogram reveals the presence of a recurrent SLAP tear in the superior and posterior labrum after repair.

■ FIGURE 106-34 Overtight repair of the anterior capsule. Axial T2weighted image demonstrates mild posterior subluxation and degenerative change of the glenohumeral joint. ■ FIGURE 106-32

Paralabral cyst. Axial T2-weighted image. There is paralabral cyst formation arising from the posterior labrum with some extension to the spinoglenoid notch.

In addition to a recurrent tear of the labrum, an additional cause of recurrent/persistent instability may include an inadequate or incorrect surgical procedure to address the specific type of instability. It is also possible that anterior and posterior instability may coexist, with one masking the other. Treatment addressing only one form of instability may unmask the other, resulting in instability in the opposite direction.

Overtightening of the capsule can lead to degenerative change of the glenohumeral joint or to instability in the opposite direction (Fig. 106-34). This complication is more common after indirect repairs. Inferior capsular shift may also be overtightened, resulting in either loss of the axillary pouch or posterior subluxation of the humeral head. At times, misplaced or detached staples, tacks, or suture anchors can result in recurrent pain and (if left untreated) can eventually lead to degenerative change (Fig. 106-35). Adhesive capsulitis is an uncommon complication after instability repair. The normal

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■ FIGURE 106-35

Displaced tack. Coronal oblique image, fast spinecho T1-weighted MR arthrogram without fat suppression shows a displaced tack in the axillary recess after a Bankart repair. A Hill-Sachs lesion is present.

postoperative capsule is usually 2 to 4 mm in thickness. A measurement of the capsule in the region of the axillary exceeding 4 mm in thickness suggests adhesive capsulitis when seen in the appropriate clinical setting.28 Reactive synovitis and postoperative infection can occur as a complication of any of the procedures described earlier. They have some overlap in terms of their imaging appearance. Synovitis is associated with joint effusions and nodular thickening of the joint capsule (Fig. 106-36). Intravenous gadolinium injection will often better demonstrate the thickening of the synovium. If synovitis is the result of infection, joint destruction may become evident with resultant cartilage loss, cysts, and erosions. The patient with synovitis may be difficult to differentiate from the inflammation that may be seen in the immediate postoperative period. In this case, often an interval follow-up may be necessary. Osteomyelitis may be suggested by the presence of marrow edema or abscess formation on short tau inversion recovery (STIR) and fat-saturated T2-weighted sequences as well as a loss of normal marrow signal intensity on the T1-weighted sequences (Fig. 106-37). Additional complications that may occur with any of these procedures include hematoma formation, abscess formation, or avascular necrosis. The appearance of a hematoma will typically depend on its stage but in the early stages will typically be bright on T1- and T2weighted sequences with fluid-fluid levels occasionally seen. Abscess formation will appear as a localized cavity similar in signal intensity to fluid but with a rim of tissue that demonstrates avid enhancement and may be bright on the T2-weighted or STIR images. Rapid-onset chondrolysis of the glenohumeral joint is a devastating complication that has recently been reported with increasing frequency in young patients after shoulder

■ FIGURE 106-36

Postoperative synovitis. Axial T1-weighted MR image with fat suppression demonstrates extensive enhancement and nodular thickening of the synovium as well as a large joint effusion.

reconstruction for glenohumeral instability.29 The exact etiology is not certain, but one theory suggests that an immune response to some unknown inciting factor leads to the onset rapid of cellular death of all of the chondrocytes on both sides of the glenohumeral joint. Some have proposed that the use of thermal energy in the performance of capsulorrhaphy is a potential etiology; however, not all

■ FIGURE 106-37

Postoperative osteomyelitis. Coronal oblique T2-weighted image with fat saturation shows osteomyelitis and abscess formation surrounding a suture anchor in the humeral head.

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TABLE 106-13 Complications of Repair for Glenohumeral Instability • • • • • • •

■ FIGURE 106-38

Acute onset of chondrolysis after Bankart repair. Coronal T2-weighted image shows complete loss of the articular cartilage on both sides of the glenohumeral joint with subtle subchondral marrow edema involving the glenoid and humeral head. Note the lack of joint effusion and the lack of synovial thickening.

Recurrent labral tear Inadequate paralabral cyst resection Suprascapular nerve injury during paralabral cyst resection Failure to address occult instability in another direction Overtight repair resulting in subluxation or degenerative change Detached staples, tacks, sutures General postoperative complications: adhesive capsulitis, synovitis, abscess formation, osteomyelitis, chondrolysis, and hematoma formation

patients have been exposed to thermal energy. Additional research is going to be required to determine the exact etiology. Patients developing rapid-onset chondrolysis typical develop shoulder pain and loss of normal range of motion at some time during the first 3 to 12 months after shoulder reconstruction. MRI demonstrates complete loss of the articular cartilage on both sides of the joint with subchondral sclerosis and marrow edema (Fig. 106-38). There is a conspicuous absence of osteophyte formation and usually a paucity of joint fluid and no synovial thickening, which helps in differentiating this entity from synovitis or acute infection (Table 106-13).

SUGGESTED READINGS Feller JF, Howey TD, Plaga BR. MR imaging of the postoperative shoulder. In Steinbach LS,Tirman PFJ, Petrfy CG, Feller JF (eds). Philadelphia, Lippincott-Raven, 1998, pp 187–221. Haygood TM, Oxner KG, Kneeland JB, Dalinka MK. Magnetic resonance imaging of the postoperative shoulder. MRI Clin North Am 1993; 1:143–155. Longobardi RSF, Rafii M, Minkoff JM. MR imaging of the postoperative shoulder. MRI Clin North Am 1997; 5:841–859.

Mohana-Borges A, Chung C, Resnick D. MR imaging and MR arthrography of the postoperative shoulder: spectrum of normal and abnormal findings. RadioGraphics 2004; 24:69–85. Owen RS, Iannotti JP, Kneeland JB, et al. Shoulder after surgery: MR imaging with surgical validation. Radiology 1993; 186:443–447. Rand T,Trattnig S, Breitensher M, et al.The postoperative shoulder.Topics Magn Reson Imaging 1999; 10:203–213. Zlatkin MB. MRI of the postoperative shoulder. Skelet Radiol 2002; 31:63–80.

REFERENCES 1. Matsen FA, Arntz CT, Lippitt SB. Rotator cuff. In Rockwood CE, Matsen FA (eds). The Shoulder. Philadelphia, WB Saunders, 1998, pp 755–795. 2. Yamaguchi K. Mini-open rotator cuff repair: an updated perspective. Instr Course Lect 2001; 50:53–61. 3. Rockwood CA, Lyons FR. Shoulder Impingement syndrome: diagnosis, radiographic evaluation, and treatment with a modified Neer acromioplasty. J Bone Joint Surg Am 1993; 75:409–424. 4. Beach WR, Caspari RB: Arthroscopic management of rotator cuff disease. Orthopedics 1993; 16:1007–1015. 5. Cameron BD, Iannotti JP. Clinical evaluation of the painful shoulder. In Zhatkin MB (ed). MRI of the Shoulder. Philadelphia, Lippincott Williams & Wilkins, 2003, pp 47–84. 6. Kvitne RS, Jobe FW. The diagnosis and treatment of anterior instability in the throwing athlete. Clin Orthop Relat Res 1993; (291):107–123. 7. Owen RS, Ianotti JP, Kneeland JB, et al. Shoulder after surgery: MR imaging with surgical validation. Radiology 1993; 186:443–447.

8. Longobardi RSF, Rafii M, Minkoff JM. MR imaging of the postoperative shoulder. MRI Clin North Am 1997; 5:841–859. 9. Gusmer PB, Potter HG, Donovan WD, O’ Brien SJ: MR imaging of the shoulder after rotator cuff repair. AJR Am J Roentgenol 1997; 168:559–563. 10. Ogilvie-Harris D, Wiley A, Sattarian J: Failed acromioplasty for impingement syndrome. J Bone Joint Surg Br 1990; 72:1070–1072. 11. Magee TH, Gaenslen ES, Seitz R, et al. MR imaging of the shoulder after surgery. Am J Roentgenol AJR 1997; 168:925–928. 12. Rand T, Trattnig S, Breitensher M, et al. The postoperative shoulder. Topics Magn Reson Imaging 1999; 10:203–213. 13. Arroyo JS, Flatow EL. Management of rotator cuff disease: intact and repairable cuff. In Iannotti JP, Williams GR Jr (eds). Disorders of the Shoulder: Diagnosis and Management. Philadelphia, Lippincott Williams & Wilkins, 1999, pp 31–56. 14. Burkhart SS. Shoulder arthroscopy: new concepts. Clin Sports Med 1996; 15:635.

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15. Budoff JE, Nirschl RP, Guidi EJ. Débridement of partial thickness tears of the rotator cuff without acromioplasty. J Bone Joint Surg Am 1988; 80:733–748. 16. Melilo AS, Savoie FH, Field LD. Massive rotator cuff tears: débridement versus repair. Orthop Clin North Am 1997; 28:117–124. 17. Haygood TM, Oxner KG, Kneeland JB, Dalinka MK: Magnetic resonance imaging of the postoperative shoulder. MRI Clin North Am 1993; 1:143–155. 18. Gaenslen ES, Stterlee CC, Hinson GA, Wetzel LH. Magnetic resonance imaging for evaluation of failed repairs of the rotator cuff: relationship to operative findings. J Bone Joint Surg Am 1996; 78:1391–1396. 19. Zanetti MD, Jost B, Hodler J. MR findings in asymptomatic patients after supraspinatus reconstruction. Radiology 1999; 213:157. 20. Norwood L, Fowler FH: Rotator cuff tears: a shoulder arthroscopy complication. Am J Sports Med 1989; 17:837–841. 21. Feller JF, Howey TD, Plaga BR. MR imaging of the postoperative shoulder. In Steinbach LS, Tirman PFJ, Peterfy CG, Feller JF (eds). Shoulder Magnetic Resonance Imaging. Philadelphia, LippincottRaven, 1998, pp 187–192. 22. Matthews LS, Pavlovich LJ Jr. Anterior and anteroinferior instability: diagnosis and management. In Iannotti JP, Williams GR

23. 24. 25. 26. 27. 28. 29.

Jr (eds). Disorders of the Shoulder: Diagnosis and Management. Philadelphia, Lippincott Williams & Wilkins, 1999, pp 251–294. Neer CS, Foster CR. Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder: a preliminary report. J Bone Joint Surg Am 1980; 62:897–908. Sugimoto H, Suzuki K, Mihara K, et al. MR arthrography of shoulders after suture-anchor Bankart repair. Radiology 2002; 224:105–111. Hashiuchi T, Ozaki J, Sakurai G, Imada K. The changes occurring after the Putti-Platt procedure using magnetic resonance imaging. Arch Orthop Trauma Surg 2000; 120:286–289. Wagner SC, Schweitzer ME, Morrison WB, et al. Shoulder instability: accuracy of MR imaging performed after surgery in depicting recurrent injury. Radiology 2002; 222:196–203. Tirman PF, Feller JF, Janzen DL, et al. Association of glenoid labral cysts and tears and glenohumeral instability: radiological findings and clinical significance. Radiology 1994; 190:653–658. Emig W, Scweitzer ME, Karasick D, Lubowtiz J. Adhesive capsulitis of the shoulder: MR diagnosis. Am J Roentgenol AJR 1994; 164:1457–1459. Levine WN, Clark AM Jr, D’Alessandro DF, Yamaguchi K. Chondrolysis following arthroscopic thermal capsulorrhaphy to treat shoulder instability. J Bone Joint Surg Am 2005; 87:616–621.

C H A P T E R

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The Postoperative Elbow, Wrist, and Hand Lynne S. Steinbach and Christine B. Chung

Elbow, wrist, and hand surgery are frequently done to repair bone and soft tissues such as fractures and disruptions of ligaments and tendons. Nerves also traverse the area and are released from various tunnels. In this chapter we discuss common indications for surgery on various bone and soft tissue structures in and around these joints and describe some of the procedures with their postoperative imaging appearances.

Ulnar Collateral Ligament of the Elbow Reconstruction DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS The ulnar collateral ligament (UCL) complex is composed of an anterior, a posterior, and a transverse bundle. Although the entire complex is charged with providing valgus stability to the elbow, it is the anterior bundle that has been shown to be the most important stabilizer against valgus stress at the joint from 30 to 120 degrees of flexion. Interestingly, a single acute traumatic episode to this ligament rarely leads to symptomatic instability in the majority of those injured.1,2 Rather it is chronic repetitive microtrauma with recurrent valgus stress at the medial elbow, such as that encountered in the overhead throwing athlete, that has been implicated in symptomatic valgus instability.3–9 It is the near-failure tensile stress encountered in the overhead throwing motion that results in the injury to the UCL and the need to expose an injured ligament to this stress that forms the basis for two of the indications for

surgical management. These include (1) throwing athletes with a complete UCL tear; (2) partial tears that have failed rehabilitation; and (3) symptomatic nonthrowing athletes after a minimum of 3 months of rehabilitation.3,6,10 There are six phases of throwing: wind up, early cocking, late cocking, acceleration, deceleration, and follow through. It is the combination of large valgus loads initiated in the late cocking phase with the rapid elbow extension generated in acceleration that produces compression overload laterally, sheer stress in the posterior compartment, and tensile overload medially. This phenomenon, termed valgus extension overload syndrome forms the basic pathophysiologic model behind most common elbow injuries in the overhead throwing athlete, including UCL injury.11 This concept, although incompletely developed, was introduced in the literature in the late 1960s and was termed medial elbow-stress syndrome.12 This marked the advent of a heightened awareness and new understanding of the pathophysiology of a major cause of elbow pain in the

KEY POINTS The anterior band of the ulnar collateral ligament is usually reconstructed rather than repaired. ■ There are a variety of techniques used to reconstruct the ulnar collateral ligament, and it is important to understand which one was used. ■ The ulnar nerve may be transposed during surgery and is occasionally injured. ■ The reconstructed ligament should be evaluated for fullthickness and partial-thickness tears that may occur at any location. ■ Metal hardware may dislodge after surgery. ■ Metal suppression techniques and MR arthrography are useful for evaluating postoperative complications. ■

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overhead throwing athlete, one that would clearly require operative treatment for a successful outcome. In 1974, the first UCL reconstruction was performed by Dr. Frank Jobe, who gave his patient, Tommy John (a Los Angeles Dodgers pitcher), a 1% chance of avoiding retirement with the intervention. Tommy John returned to baseball 2 years later, and the successful procedure revolutioned the treatment of UCL reconstruction. Although early studies advocated primary repair of UCL injuries, the applicability of these studies to current patient populations is limited because they did not include high performance athletes or document the type or level of sports involvement.13,14 Numerous recent studies have concluded that UCL reconstruction is more effective than primary repair in correcting medial elbow instability and returning overhead throwing athletes to a preinjury level of play in less than 1 year, the measure of a successful procedure.5,15,16

Figure-of-Eight Repair The original UCL reconstruction was performed by Jobe and associates.6 The ligament was exposed by detaching and elevating the flexor-pronator muscle mass from the medial epicondyle of the humerus. A submuscular ulnar nerve transposition was performed. The anterior bundle of the UCL was reconstructed with a harvested autograft (palmaris longus) in a figure-of-eight fashion through two drill holes in the ulna and three in the medial epicondyle (Fig. 107-1). The posterior cortex of the humerus was penetrated, and the graft was sutured to itself. At 2-year follow-up, 63% of elite throwing athletes returned to a preinjury level of throwing for at least 1 year.5,6 Despite the ground-breaking success of this procedure, the rate of complication was 31%. Postoperative dysfunction of the ulnar nerve was the most commonly cited complication, often requiring decompression. Similar results were seen in a subsequent larger study group with 68% of elite throwing athletes returning to a preinjury level

of throwing for at least 1 year.1 In this group, postoperative ulnar nerve dysfunction occurred in 21% of patients, several of whom required revision decompression of the ulnar nerve. These results prompted the development of surgical modifications to simplify the technique, evade dissection and detachment of the flexor-pronator mass, and limit handling of the ulnar nerve.

Muscle-Splitting Modification In 1996, Smith and associates described the “safe zone” of the medial elbow.17 This zone refers to an internervous plane of exposure to the medial ulnohumeral articulation that extends from the medial epicondyle to 1 cm distal to the insertion of the UCL on the sublime tubercle of the ulna. It is between the median and ulnar nerve sites of innervation of surrounding muscles. Rather than completely detach the flexor-pronator mass from the medial epicondyle, the muscle group was split along its “safe zone,” through the posterior third of the common flexor bundle (the most anterior fibers of the flexor carpi ulnaris), to access the joint and perform the ligament reconstruction using Jobe’s original technique. This modified technique also obviated the need to transpose the ulnar nerve. At 2-year follow-up, 82% of elite overhead throwing athletes returned to play.18 In athletes without prior surgery, this number increased to 93%. In the immediate postoperative period, only 5% of the patients had transient ulnar nerve problems. All resolved without surgery.

American Sports Medicine Institute (ASMI) Modification Andrews and colleagues modified Jobe’s original technique by retracting the flexor carpi ulnaris anteriorly and by performing a subcutaneous rather than submuscular nerve transposition.15,16 In a large retrospective review comparing primary ligament repair with this modified technique, 79% of patients undergoing reconstruction returned to a preinjury level of play an average of 9.8 months after surgery.16 In comparison, only 63% of patients treated with direct repair returned to the same level of sport. Only one of the patients with ligament reconstruction developed transient postoperative ulnar nerve changes. Moreover, 9 of 10 patients who had preoperative ulnar neuritis experienced resolution of symptoms.

Suture Anchor Method

■ FIGURE 107-1 Figure-of-eight repair, known as the Tommy John procedure, was the first ulnar collateral ligament reconstruction method. The ligament was exposed by detaching and elevating the flexor-pronator muscle mass from the medial epicondyle of the humerus. A submuscular ulnar nerve transposition was performed. The anterior bundle of the ligament was reconstructed with a harvested autograft (palmaris longus) in a figure-of-eight fashion through two drill holes in the ulna and three in the medial epicondyle.

In the mid 1990s, suture anchors were introduced into the UCL reconstruction techniques in an attempt at further simplifying the procedure.A cadaveric study by Hechtman and associates compared the suture anchor and bone tunnel techniques in 31 cadaveric specimens (15 underwent reconstruction with bone tunnels, 16 with suture anchors).19 The strength of each reconstruction was compared with the original strength of the ligament. Results of this study showed that there was no significant difference in reconstruction strength between the suture anchor (76.3%) and the bone tunnel (63.9%) techniques. Both methods produced reconstructions that were significantly

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2001

weaker than a native UCL. It was apparent, however, that the suture anchor technique reproduced normal UCL anatomy and mechanical function more closely than bone tunnels. Despite the apparent success of this cadaveric work, the technique fell out of use when clinical applications yielded a failure rate of 30%.9

Docking Technique In 1996, Altchek and coworkers implemented a musclesplitting approach to modify the UCL reconstruction in a technique called the “docking procedure.”20 Unlike Jobe’s technique, in which the graft is placed in a figure-of-eight position, in this technique the graft is placed in a triangular configuration through a single humeral tunnel and the limbs are brought out through separate bone tunnels and tied over a bone bridge. It has been suggested that the docking technique allows for better tensioning of the ligament graft. In an uncontrolled retrospective review by Rohrbough and associates, 92% of patients returned to a preinjury level of play for at least 1 year. No complications were reported.

Interference Technique Ahmad and coworkers described an interference technique for fixation of the UCL graft. The goal was to reconstruct the central isometric fibers of the native UCL, which lie between the anterior one third and the posterior two thirds of the anterior bundle of the UCL.21 Through a muscle-splitting approach, grafts are fixed with interference screws placed in single bony tunnels in the humerus and ulna. Unlike Jobe’s original technique, only two bone tunnels are needed. The ulnar nerve is less at risk. Likewise, without an intervening bony bridge on the ulna, the risk of tunnel fractures between the two tunnels, is theoretically eliminated. The biomechanical results of this technique have been mixed. In a cadaveric study comparing intact with reconstructed elbows using the interference technique, the normal elbow kinematics were restored with the interference fixation.The failure strength of the UCL reconstruction with interference fixation was reported to be similar to that of the native intact UCL.22 In this study, the ligament was loaded once to failure. However, in a study in which a cyclic loading protocol is used to better replicate the clinical mechanism of injury, this technique as well as other reconstruction techniques showed reconstruction failure at significantly lower loads than the normal intact ligament.23

■ FIGURE 107-2

This coronal T1-weighted MR arthrographic image of a pitcher’s elbow demonstrates an intact ulnar collateral ligament 5 years after surgical reconstruction (arrow). (Courtesy of William Morrison, MD, Philadelphia, PA.)

substance related to suture material and granulation tissue. With time (approximately 6 months) the normal ligament decreases in signal intensity on all imaging sequences. It may be thickened (Fig. 107-3).There are often tunneling defects in the distal humerus and proximal ulna. Metal anchors and screws may be present.These metallic devices could interfere with assessment of the ligament on MRI (Fig. 107-4). Metal reduction techniques such as increasing bandwidth, avoiding fat-suppression and gradient-echo

EXPECTED APPEARANCE ON IMAGING Little has been written on imaging evaluation of ulnar collateral ligament reconstruction. Stress radiographs are limited for examination of the ulnar collateral ligament. Sometimes they are normal in the presence of a rupture. CT arthrography is also limited. In our experience, the reconstructed ligament is continuous and water tight, as demonstrated on MR arthrography (Fig. 107-2).The integrity of the ligament can be assessed with MRI, MR arthrography, or ultrasound. On MRI performed in the early stages, the ligament may demonstrate high signal intensity within its

■ FIGURE 107-3 Intact ulnar collateral ligament repair on a coronal T2-weighted MR image. Notice the normally thickened tendon graft (arrowhead) as well as the scarring above the graft (arrow). (Courtesy of William Morrison, MD, Philadelphia, PA.)

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■ FIGURE 107-4 Sagittal T2-weighted MR image of the elbow demonstrates artifact from screws at both ends of an ulnar collateral ligament reconstruction. The ligament was intact. (Courtesy of William Morrison, MD, Philadelphia, PA.)

For the 20 intact specimens in the study, complete disruption of the ligament occurred at the humeral attachment in 9 specimens, the ulnar attachment in 4, and the midsubstance of the anterior bundle of the medial collateral ligament in 2.23 In the remaining five specimens the joint gapped 5 mm without complete visual disruption of the ligament. In the reconstruction, no complete disruption occurred for any technique. For the docking, EndoButton, and figure-of-eight procedures, the mode of failure was the suture pulling out of the suture/ligament interface. For the interference screw reconstruction, the tendon pulled out at the tendon/screw interface. Regarding visualization of complications on imaging, one should evaluate the elbow for abnormal valgus angulation and dislodgement of hardware on radiographs, ultrasonography, and MRI. The tendon or graft should be assessed for discontinuity, laxity, thinning, and irregularity. MR arthrography is helpful for evaluating continuity of the ligament and for outlining the undersurface of the ligament for irregularity or laxity related to partial tears. Median, radial, and ulnar nerve injury is a complication of elbow surgery due to laceration or compression. One should look for other postoperative changes such as excessive scar tissue, infection, synovial fistula formation, and instruments or other hardware left in the joint.

SUGGESTED READINGS techniques, and using lower magnetic field strength aid in evaluation of the ligament reconstruction. MR arthrography is useful for evaluation of the intact ligament. The ulnar nerve may have been transposed from the cubital tunnel and placed in a submuscular or subcutaneous location. One should assess the nerve signal and size related to itself in other locations or to other nerves around the elbow to determine if it is abnormal.

POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE The success rates of reconstruction vary between 63% and 97%, depending on the technique. Reported complication rates are less than 10%. Despite the variability in techniques, the unifying features are that decreased dissection of the flexor-pronator mass and decreased handling of the ulnar nerve leads to improved outcomes.7 As noted previously, four UCL reconstruction techniques have been compared biomechanically (docking, interference screw fixation, figure-of-eight, single-stranded UCL reconstruction using an EndoButton [Smith & Nephew, London, England] for ulnar fixation).23 Cadaveric specimens were subjected to pneumatic cyclic valgus loading. All techniques showed significantly lower peak load to failure than the intact native ligament. No difference in strength was found between the docking and single-stranded UCL reconstruction using EndoButton fixation. Both of these techniques were stronger than the interference screw or figure-ofeight techniques.

Cain EL, Dugas JR, Wolf RS, Andrews JR. Elbow injuries in throwing athletes: a current concepts review. Am J Sports Med 2003; 31:621–635. Jobe FW, Start H, Lombardo SF. Reconstruction of the ulnar collateral ligament in athletes. J Bone Joint Surg Am 1986; 68:1158. Kaplan LJ, Potter HG. MR imaging of ligament injuries to the elbow. Magn Reson Imaging Clin North Am 2004; 12:221–232. O’Holleran JD, Altchek DW.The throwers elbow: arthroscopic treatment of valgus extension overload syndrome. HSS J 2006; 2:83–93.

REFERENCES 1. Morrey BF, An KN. Articular and ligamentous contributions to the stability of the elbow joint. Am J Sports Med 1983; 11:315–319. 2. Schwab GH, Bennett JB, Woods GW, Tullos HS. Biomechanics of elbow instability: the role of the medial collateral ligament. Clin Orthop Relat Res 1980; (146):42–52. 3. Chen FS, Rokito AS, Jobe FW. Medial elbow problems in the overhead-throwing athlete. J Am Acad Orthop Surg 2001; 9:99–113. 4. Ciccotti MG, Jobe FW. Medial collateral ligament instability and ulnar neuritis in the athlete’s elbow. Instr Course Lect 1999; 48:383–391. 5. Conway JE, Jobe FW, Glousman RE, Pink M. Medial instability of the elbow in throwing athletes: treatment by repair or reconstruction of the ulnar collateral ligament. J Bone Joint Surg Am 1992; 74:67–83. 6. Jobe FW, Stark H, Lombardo SJ. Reconstruction of the ulnar collateral ligament in athletes. J Bone Joint Surg Am 1986; 68:1158–1163. 7. Langer P, Fadale P, Hulstyn M. Evolution of the treatment options of ulnar collateral ligament injuries of the elbow. Br J Sports Med 2006; 40:499–506. 8. Pappas AM, Zawacki RM, Sullivan TJ. Biomechanics of baseball pitching: a preliminary report. Am J Sports Med 1985; 13:216–222. 9. Williams RJ 3rd, Urquhart ER, Altchek DW. Medial collateral ligament tears in the throwing athlete. Instr Course Lect 2004; 53:579–586. 10. David TS. Medial elbow pain in the throwing athlete. Orthopedics 2003; 26:94–103; quiz 104–105. 11. Wilson FD, Andrews JR, Blackburn TA, McCluskey G. Valgus extension overload in the pitching elbow. Am J Sports Med 1983; 11:83–88.

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12. King J, Brelsford HJ, Tullos HS. Analysis of the pitching arm of the professional baseball pitcher. Clin Orthop Relat Res 1969; 67:116–123. 13. Kuroda S, Sakamaki K. Ulnar collateral ligament tears of the elbow joint. Clin Orthop Relat Res 1986; (208):266–271. 14. Norwood LA, Shook JA, Andrews JR. Acute medial elbow ruptures. Am J Sports Med 1981; 9:16–19. 15. Andrews JR, Timmerman LA. Outcome of elbow surgery in professional baseball players. Am J Sports Med 1995; 23:407–413. 16. Azar FM, Andrews JR, Wilk KE, Groh D. Operative treatment of ulnar collateral ligament injuries of the elbow in athletes. Am J Sports Med 2000; 28:16–23. 17. Smith GR, Altchek DW, Pagnani MJ, Keeley JR. A musclesplitting approach to the ulnar collateral ligament of the elbow: neuroanatomy and operative technique. Am J Sports Med 1996; 24:575–580. 18. Thompson WH, Jobe FW, Yocum LA, Pink MM. Ulnar collateral ligament reconstruction in athletes: muscle-splitting approach without transposition of the ulnar nerve. J Shoulder Elbow Surg 2001; 10:152–157. 19. Hechtman KS, Tjin A, Zvijac JE, et al. Biomechanics of a less invasive procedure for reconstruction of the ulnar collateral ligament of the elbow. Am J Sports Med 1998; 26:620–624. 20. Rohrbough JT, Altchek DW, Hyman J, et al. Medial collateral ligament reconstruction of the elbow using the docking technique. Am J Sports Med 2002; 30:541–548. 21. Ochi N, Ogura T, Hashizume H, et al. Anatomic relation between the medial collateral ligament of the elbow and the humero-ulnar joint axis. J Shoulder Elbow Surg 1999; 8:6–10. 22. Ahmad CS, Lee TQ, El Attrache NS. Biomechanical evaluation of a new ulnar collateral ligament reconstruction technique with interference screw fixation. Am J Sports Med 2003; 31:332–337. 23. Armstrong AD, Dunning CE, Ferreira LM, et al. A biomechanical comparison of four reconstruction techniques for the medial collateral ligament-deficient elbow. J Shoulder Elbow Surg 2005; 14:207–215.

Lateral Collateral Ligament of the Elbow Reconstruction DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS The lateral collateral ligament (LCL) complex consists of four components: the annular ligament, the radial collateral ligament, the lateral ulnar collateral ligament, and the accessory annular ligament.1 The ligament complex originates from the undersurface of the lateral epicondyle at a point through which the center of rotation passes. Therefore, it is isometric throughout the normal range of flexion and extension. The radial collateral ligament has a distal point of attachment on the annular ligament, stabilizing the proximal radioulnar joint.The lateral ulnar collateral ligament also attaches to the annular ligament but has a point of attachment distally at the supinator crest of the ulna.2 Because this ligament crosses the articulation and has both a proximal and distal osseous attachment, it is considered to be a major stabilizer of the lateral elbow. In 1991, O’Driscoll and associates first described posterolateral rotatory instability of the

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elbow.3 The cause for this condition was thought to be a laxity of the lateral ulnar collateral ligament allowing a transient rotatory subluxation of the ulnohumeral joint and a secondary dislocation of the radiocapitellar joint. Ordinarily, the LCL complex maintains these joints in a reduced position. A mechanism for elbow subluxation and dislocation was then described in which there was increasing ligamentous and capsular damage progressing from lateral to medial across the joint.4 Dislocation was the final of three sequential stages of elbow instability resulting from posterolateral rotation.

Presentation and Indications for Operative Treatment Most patients with lateral elbow instability present with symptoms after an elbow dislocation. Less commonly, there is a history of surgery to the lateral side of the elbow. Although most studies indicate that both medial and lateral collateral ligament complexes are disrupted after dislocation, residual instability more commonly involves the lateral side.5 The clinical presentation is quite variable, although patients often present with a history of recurrent painful clicking, catching, or snapping of the elbow. Symptoms typically occur in the extension portion of the motion arc with the forearm in supination. The classic activity that reproduces a patient’s symptoms is pushing down on the armrest when rising from a chair. The physical examination may be unremarkable.The classic physical examination finding is that of a positive pivot shift maneuver.The elbow is supinated by applying torque at the wrist, and a valgus moment is applied to the elbow during flexion. This action results in a typical apprehension response with reproduction of the patient’s symptoms and a sense that the elbow is about to dislocate.3 Reproducing the actual subluxation and the clunk that occurs with reduction can usually be accomplished only with the patient under general anesthesia.6 Indications for surgical treatment of the LCL complex include patients with symptomatic instability. Reconstruction of the LCL complex has been recommended to restore stability of the elbow in patients with posterolateral rotatory instability.3,7–9 Although there are no absolute contraindications to surgical treatment

KEY POINTS The lateral collateral ligament complex can be repaired or reconstructed. ■ There are a variety of techniques used to reconstruct the lateral collateral ligament, and it is important to understand which one was used. ■ The reconstructed ligament should be evaluated for fullthickness and partial-thickness tears that may occur at any location. ■ Metal hardware may dislodge after surgery. ■ Metal suppression techniques and MR arthrography are useful for evaluating postoperative complications. ■

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there are relative ones. Children with open epiphyseal plates should not have their ligaments reconstructed with tendon grafts across the physis.9 Instead, the existing lateral collateral ligament tissues are imbricated and reattached to bone iosmetrically. The absence of a radial head adversely affects the prognosis of surgical therapy but is not a contraindication.

Primary Ligament Repair As on the medial side, the LCL complex can be treated with a primary repair or reconstruction. Sanchez-Sotelo and coworkers reported that reconstruction using a tendon graft seemed to provide better results than ligament repair for the treatment of posterolateral rotatory instability of the elbow.10 Osborne and Cotterill first described repair of the lateral capsuloligamentous structures of the elbow for recurrent dislocation.9 Currently, acute ligament repair is recommended only for gross instability after reduction of the elbow or in conjunction with open reduction of fracture-dislocations. This is particularly indicated when there has been internal fixation of the radial head and or coronoid process.11 In such cases, the ligamentous and muscular origins have usually been avulsed from the lateral epicondyle and can be repaired directly back down to bone, thereby reestablishing lateral elbow stability. Most authors believe that acute ligament repairs should be augmented with a heavy suture along the course of the lateral ulnar collateral ligament.12 This serves to stress-shield the repair during the early postoperative period.The LCL complex can also be augmented using three fan-shaped arcades of suture secured through holes drilled in the lateral epicondyle.13 The first arcade follows the path of the lateral ulnar collateral ligament, the second follows the path of the lateral collateral ligament and engages the annular ligament, and the third engages the posterior capsule and anconeus muscle.

and those who had an augmented reconstruction using a tendon graft.10 Most LCL complex reconstructions use the technique introduced by O’Driscoll, or some modification of it.3 This technique begins with a 10-cm incision between the epicondyle and olecranon. The deep fascia is incised along the supracondylar ridge and distally between the anconeus and extensor carpi ulnaris muscles.The triceps and anconeus are reflected in continuity off the posterior humerus and capsule, exposing the lateral side of the ulna. The common extensor origin is partially reflected to expose the capsule. Capsuloligamentous attenuation is assessed and laxity confirmed. The capsule is opened along the capitellum in an arc to permit inspection of the joint and later imbrication of the capsule. The insertion site for the tendon graft is then prepared by creating two drill holes in the ulna, one near the tubercle on the supinator crest and the other 1.25 cm proximally at the base of the annular ligament. The underlying bone is channeled. Suture is passed through the holes, and the isometric ligament insertion is determined by flexing and extending the elbow to see if the suture moves. No movement occurs when suture and hemostat are on the isometric point. A hole for the graft entry site on the humerus is then created. If the hole is placed distal or posterior, the graft will be lax in extension and tight in flexion. An exit for the graft is created just posterior to the supracondylar ridge about 1.5 cm proximally with a tunnel extending between the entry and exit sites. A third and final hole is placed in the distal humerus and is referred to as the reentry site. It is located just posterior to the initial entry site hole, and a tunnel will extend between it and the entry site. The graft will pass through this tunnel and will be sutured to itself at the entry site.3,10,14

EXPECTED APPEARANCE ON IMAGING Lateral Collateral Ligament Complex Reconstruction While there is little in the way of long-term results of this treatment, the procedure appears successful. O’Driscoll and associates briefly mention results in five patients in their initial description of the posterolateral rotatory instability of the elbow.3 In 1992, Nestor and colleagues reported results of LCL complex reconstruction in 11 patients with an average of 42 months’ follow-up.14 Stability was obtained in 10 patients, 7 of whom had an excellent functional result. The 4 patients with less than excellent results had had previous surgery. If the radial head has been excised or there is degenerative change in the joint, the satisfactory result decreases, although stability is usually achieved.11 More recently, Sanchez-Sotelo and associates described the intermediate results of lateral ligamentous reconstruction for posterolateral rotatory instability of the elbow. Surgery restored stability in all except 5 patients. In 2 of the 5, the elbow became stable after a second procedure. Better results were obtained in patients with a post-traumatic etiology, subjective symptoms of instability at presentation,

On MRI, the ligament should be continuous after primary repair or graft reconstruction. It will be heterogenous in signal intensity at first but should decrease in signal intensity with time. It may be helpful to see this ligament using the 20-degree posterior oblique axis with regard to the elbow joint from a sagittal scout image.16

POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE Delayed laxity, recurrent dislocation, and reinjury have been observed after lateral collateral ligament complex reconstruction (Fig. 107-5). Complications associated with graft harvesting are possible. Iatrogenic fracture of the osseous tunnels can occur but are generally not problematic with careful surgical technique. Mild flexion contracture can be accepted as the most vulnerable position of instability in full extension. As always, infection is also a possible complication of surgery (Fig. 107-6).

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■ FIGURE 107-5 Lateral ulnar collateral ligament tear with repair. A, There is a high-grade partial tear of the origin of the lateral ulnar collateral ligament at the lateral epicondyle (arrow) on this coronal proton density–weighted MR image of the elbow. Also note the torn common extensor tendon (arrowhead). B, The lateral ulnar collateral ligament tore again after repair, this time in the mid- distal aspect (arrow). Notice the metallic hardware (arrowhead) and the joint debris. (Courtesy of the Department of Radiology and Imaging, Hospital for Special Surgery, New York, NY.)

■ FIGURE 107-6 A, Coronal, fat-suppressed, T2-weighted MR image of the elbow demonstrates a high signal intensity abscess (arrow) communicating with the elbow joint after surgery on the lateral ulnar collateral ligament. B, The abscess rim enhances on the fat-suppressed, coronal, T1-weighted MR image after intravenous administration of gadolinium (arrow). Notice the postoperative metallic artifact (arrowhead). (Courtesy of William Morrison, MD, Philadelphia, PA.)

SUGGESTED READINGS Kaplan LJ, Potter HG. MR imaging of ligament injuries to the elbow. Magn Reson Imaging Clin North Am 2004; 12:221–232. O’Driscoll S, Morrey BF. Surgical reconstruction of the lateral collateral ligament. In Morrey BF (ed). The Elbow, 2nd ed. Philadelphia, Lippincott Williams & Wilkins, 2002, pp 249–263.

REFERENCES 1. Morrey BF, An KN. Functional anatomy of the ligaments of the elbow. Clin Orthop Relat Res 1985; (201):84–90. 2. O’Driscoll SW, Morrey BF, Carmichael SW. Anatomy of the ulnar part of the lateral collateral ligament of the elbow. Clin Anat 1992; (5):296–303.

3. O’Driscoll SW, Bell DF, Morrey BF. Posterolateral rotatory instability of the elbow. J Bone Joint Surg Am 1991; 73:440–446. 4. O’Driscoll SW, Morrey BF, Korinek S, An KN. Elbow subluxation and dislocation: a spectrum of instability. Clin Orthop Relat Res 1992; (280):186–197. 5. Josefsson PO, Johnell O, Wendeberg B. Ligamentous injuries in dislocations of the elbow joint. Clin Orthop Relat Res 1987; (221):221–225. 6. Ball CM, Galatz LM, Yamaguchi K. Elbow instability: treatment strategies and emerging concepts. Instr Course Lect 2002; 51:53–61. 7. Olsen BS, Sojbjerg JO. The treatment of recurrent posterolateral instability of the elbow. J Bone Joint Surg Br 2003; 85:342–346. 8. Olsen BS, Sojbjerg JO, Nielsen KK, et al. Posterolateral elbow joint instability: the basic kinematics. J Shoulder Elbow Surg 1998; 7:19–29. 9. Osborne G, Cotterill P. Recurrent dislocation of the elbow. J Bone Joint Surg Br 1966; 48:340–346.

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10. Sanchez-Sotelo J, Morrey BF, O’Driscoll SW. Ligamentous repair and reconstruction for posterolateral rotatory instability of the elbow. J Bone Joint Surg Br 2005; 87:54–61. 11. O’Driscoll SW, Jupiter JB, King GW, et al. The unstable elbow. Instr Course Lect 2001; 50:89–102. 12. O’Driscoll SW. Elbow instability. Hand Clin 1994; 10:405–415. 13. King JC, et al. Lateral ligamentous instability: techniques of repair and reconstruction. Tech Orthop 2000; (15):93–104. 14. Nestor BJ, O’Driscoll SW, Morrey BF. Ligamentous reconstruction for posterolateral rotatory instability of the elbow. J Bone Joint Surg Am 1992; 74:1235–1241. 15. Rijke AM, Goitz HT, McCue FC, et al. Stress radiography of the medial elbow ligaments. Radiology 1994; 191:213–216. 16. Cotton A, Jacobson J, Brossmann J, et al. Collateral ligaments of the elbow: conventional MR imaging and arthrography with coronal oblique plane and elbow flexion. Radiology 1997; 204:806–812.

Ulnar Nerve Decompression DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS Ulnar nerve entrapment at the elbow is the second most common peripheral nerve compression neuropathy.At the level of the elbow, the ulnar nerve is housed in the cubital tunnel. The cubital tunnel is a fibro-osseous conduit along the posterior aspect of the medial epicondyle. This fibroosseous space is formed by the medial epicondyle anteriorly and the medial margin of the trochlea and olecranon laterally. The posterior bundle of the ulnar collateral ligament forms the floor of the cubital tunnel and the arcuate ligament the roof. The arcuate ligament may be absent in up to 23% of subjects.1 Fatty tissue usually surrounds the ulnar nerve and posterior recurrent ulnar artery as they pass through the cubital tunnel. The ulnar nerve innervates the skin and muscles of the ulnar side of the forearm and hand. This includes the flexor carpi ulnaris and half of the flexor digitorum profundus muscles. Several provocative tests can be used to identify the presence of ulnar nerve compression. Percussion over the ulnar nerve can elicit paresthesias or numbness, resulting in a positive “Tinel” sign. The elbow flexion test is analogous to the Phalen test in diagnosing carpal tunnel syndrome. With the elbow maximally flexed, forearm in supination, and wrist in full extension, patients with cubital tunnel syndrome can experience paresthesias and numbness along the distribution of the nerve.2 Unfortunately, false-positive results can occur in approximately 10% of normal individuals.3 Numbness along the small and ulnar half of the ring finger commonly can be due to ulnar nerve compression at the level of the elbow or as the nerve passes Guyon’s canal. Sensory deficits over the dorsal ulnar aspect of the hand and the dorsum of the small finger can help in determining the level of compression. This area is innervated by the dorsal sensory branch of the ulnar nerve arising proximal to Guyon’s canal, implying compression at the elbow.

Indications for Operative Ulnar Nerve Treatment The clinical evaluation of ulnar nerve entrapment is crucial to guiding treatment, predicting success rates for treatment, as well as assessing post-therapy success. Although it appears that there is no uniformly accepted grading system to evaluate ulnar nerve entrapment, most assessments are based on subjective symptoms, muscle strength, and sensory disturbance. Some very detailed classification systems, such as the Yokohama City University scoring system, also consider the presence of finger deformity.4 In general, surgical indications include patients with fixed sensory loss, pain, weakness, or significant denervation on electromyography.5 Patients presenting with transient paresthesias and normal clinical findings are generally managed conservatively with behavioral modification that includes minimizing elbow flexion and prolonged pressure on the elbow.6 Not only does the initial clinical assessment of ulnar nerve dysfunction serve as the basis for conservative versus operative treatment, it may indicate prognosis. Reports have suggested that prognosis may be more closely related to the level of preoperative damage of nerves and the period between the occurrence and surgery than to surgical methods.4,7

Surgical Therapy for Ulnar Nerve Decompression Operative procedures for ulnar nerve entrapment at the elbow can be divided into two groups: decompression with transposition of the ulnar nerve and decompression without transposition of the ulnar nerve. The latter is also referred to as decompression in situ or a simple decompression.

Simple Decompression of the Ulnar Nerve The operative procedure for simple decompression was described by Osborne.6 An 8-cm long curved skin incision is made posterior to the medial epicondyle of the humerus.

KEY POINTS Ulnar neuropathy at the elbow can be treated with simple decompression of the arcuate ligament, medial epicondylectomy, or decompression with transposition. ■ With transposition, the ulnar nerve is repositioned in an anterior subcutaneous, submuscular, or intramuscular location. ■ The ulnar nerve should be evaluated for abnormal enlargement with MRI and ultrasonography. ■ Abnormal high signal intensity in the nerve on MRI or hypoechogenicity on ultrasonography are postoperative signs of ulnar neuropathy. ■ Scar tissue may cause complications for ulnar nerve surgery. ■ Muscles should be evaluated for denervation. ■

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The subcutaneous tissues are dissected, and the nerve is identified. The cubital tunnel retinaculum or arcuate ligament of Osborne is released.This is followed by widening of the entrance to the cubital tunnel between the two heads of the flexor carpi ulnaris muscle. Those who argue for simple decompression point out the potential for ischemia when the nerve is separated from its primary blood supply.The vascular stripping incurred during transposition may cause a significant decrease in regional blood flow.8 Animal studies have shown that a devascularized nerve is more susceptible to pressure than a normal nerve.9 One major aim of the simple decompression is to preserve the vascularity of the nerve.10 Several studies have compared the simple decompression to both anterior submuscular transposition as well as anterior subcutaneous transposition.6,11–14 In general, no statistically significant differences existed between outcomes of the simple decompression versus either transposition method. Because the simple decompression carries less risk of complication, many authors favor it. Another method to decompress the ulnar nerve includes medial epicondylectomy. This procedure, the modified King’s method, consists of a medial epicondylectomy of the humerus with resection of the fibrous band bridging the two heads of the flexor carpi ulnaris (arcuate ligament). Some advocate the use of a subtotal medial epicondylectomy with resection of 50% of the epicondyle.2 The advantages of this procedure include removing or releasing all the compressing structures, creating minimal additional trauma to the nerve with preservation of the native blood supply, and allowing the nerve to follow a course of least resistance. The disadvantages can include bone tenderness at the site of osteotomy, nerve subluxation, flexor-pronator weakness, flexion contracture, and valgus instability. Numerous studies reporting the effectiveness of medial epicondylectomy for cubital tunnel syndrome have been published.2,15,16 Geutjens and coworkers conducted the only randomized prospective study of 52 patients comparing medial epicondylectomy and anterior transposition. In this study, better results were found with medial epicondylectomy. This study found no evidence of ligamentous instability after removal of the medial epicondyle.

Ulnar Nerve Transposition The issue of nerve transposition is a controversial one. It has two main advantages. The first, depending on the cause of the nerve entrapment, is that the nerve may be removed from an unfavorable environment.17,18 This may occur when the etiology is scar tissue, fibrosis, or other lesions within the epicondylar groove.19,20 The second advantage is that by transposing the nerve into a new pathway volar to the axis of elbow flexion, the nerve is effectively lengthened, thereby decreasing tension on it. Most authors intuitively agree that the presence of a structural abnormality of the elbow, as noted earlier, or hypermobiity of the nerve constitute good indications for a transposition.13 There are three types of anterior transposition: subcutaneous, submuscular, and intramuscular. All are widely used. Subcutaneous transposition is the most commonly used

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method of ulnar nerve transposition because of its technical ease, high success rate, and low complication rate.17 With this procedure, the anterior subcutaneous soft tissues are dissected to form a “bed” for the nerve. The nerve is transposed and retained in the bed with a fascial sling raised from the underlying muscle fascia that is sutured to the dermis.6 This is an effective procedure, particularly in the elderly and patients who have a thick layer of adipose tissue. The disadvantages are risk of failure to decompress the nerve at the most distal site of the cubital tunnel.21 In addition, the nerve is most vulnerable to direct trauma after subcutaneous transposition. In one series, unsatisfactory results were reported in up to 15% of cases after this procedure.22 Submuscular anterior transposition has become established in the management of chronic ulnar neuropathy, but its success rate in published series has varied considerably.23,24 This procedure is generally achieved through a modified Learmonth technique (similar to that described by Kline and colleagues).25 A curved incision extends from the distal arm to the volar aspect of the medial elbow and into the forearm. The ulnar nerve is identified and a 360degree neurolysis is performed at the level of the elbow and distal to the cubital tunnel.A plane of dissection is created on the lateral edge of the pronator teres, taking care to avoid injury to the median nerve. A submuscular plane is created with the median nerve serving as the lateral boundary. The ulnar nerve is transposed into the submuscular bed, and the muscle is subsequently repaired. The advantages of this procedure are that potential sites for nerve compression are definitely explored and released and the nerve lies in an unscarred anatomic plane not subject to traction forces.5,21,26,27 This procedure can cause more scarring than others and is usually contraindicated if there is scarring of the joint capsule or distortion of the joint due to arthritis or a malunited fracture.5 One study comparing submuscular transposition with subcutaneous transposition found that submuscular transposition achieved better results.6 Intramuscular transposition is the most controversial of the three methods of ulnar transposition.28–30 One study evaluating intramuscular transpositions reported 15% of patients with no improvement.31

EXPECTED APPEARANCE ON IMAGING With simple decompression, the ulnar nerve should be located in the cubital tunnel. If there has been transposition, the ulnar nerve will be repositioned anteriorly between muscles (Fig. 107-7) or in the subcutaneous tissues (Fig. 107-8). In all cases, the size of the ulnar nerve should be normal on MRI and ultrasonography and should not deviate from that above or below the region of surgery. The signal intensity should be intermediate on MRI. With medial epicondylectomy, there will be absence of a portion of the medial epicondyle.

POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE The ulnar nerve may sublux or dislocate out of the cubital tunnel in cases of simple decompression (Fig. 107-9) or medial epicondylectomy. Adjacent vascular structures

■ FIGURE 107-7 Axial, fat-suppressed, T2-weighted MR image shows the ulnar nerve transposed anteriorly underneath the pronator muscle (arrow). (Courtesy of Javier Beltran, MD, Brooklyn, NY.)

A

B

■ FIGURE 107-8

Coronal, T1-weighted (A) and gradient-echo (B) MR images of the elbow after ulnar nerve transposition. The nerve lies superficial in the subcutaneous fat (arrows). (Courtesy of Javier Beltran, MD, Brooklyn, NY.)

■ FIGURE 107-9

Ulnar nerve decompression with retinacular release. Axial T1-weighted (A) and fat-suppressed, T2weighted (B) MR images of the elbow show the enlarged ulnar nerve subluxed out of the cubital tunnel (arrow) that has undergone a retinacular release. The nerve is abnormally high in signal intensity on the T2-weighted image.

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should also be assessed for patency and absence of damage. Excessive scar tissue can interfere with nerve function. The muscles innervated by the ulnar nerve should be evaluated for denervation changes. Infection or inflammatory changes may present with increased signal intensity on MRI in the area of surgery. Abscesses or seromas will be identified as rim-enhancing collections of fluid in the region on post-contrast MRI and as hypoechoic areas of fluid on ultrasonography.

SUGGESTED READINGS Bordalo-Rodrigues M, Rosenberg ZS. MR imaging of entrapment neuropathies at the elbow. Magn Reson Imaging Clin North Am 2004; 12:247–263. Izzi J, Dennison D, Noerdlinger M, et al. Nerve injuries of the elbow, wrist, and hand in athletes. Clin Sports Med 2001; 20:203–217. Keefe DT, Lintner DM. Nerve injuries in the throwing elbow. Clin Sports Med 2004; 23:723–742.

REFERENCES 1. Dellon AL. Musculotendinous variations about the medial humeral epicondyle. J Hand Surg [Br] 1986; 11:175–181. 2. Dinh PT, Gupta R. Subtotal medial epicondylectomy as a surgical option for treatment of cubital tunnel syndrome. Tech Hand Up Extrem Surg 2005; 9:52–59. 3. Rayan GM, Jensen C, Duke J. Elbow flexion test in the normal population. J Hand Surg [Am] 1992; 17:86–89. 4. Yamamoto K, Shishido T, Masaoka T, et al. Postoperative clinical results in cubital tunnel syndrome. Orthopedics 2006; 29:347–353. 5. Asamoto S, Boker DK, Jodicke A. Surgical treatment for ulnar nerve entrapment at the elbow. Neurol Med Chir (Tokyo) 2005; 45:240–244; discussion 244–245. 6. Nabhan A, Ahlhelm F, Kelm J, et al. Simple decompression or subcutaneous anterior transposition of the ulnar nerve for cubital tunnel syndrome. J Hand Surg [Br] 2005; 30:521–524. 7. Muermans S, De Smet L. Partial medial epicondylectomy for cubital tunnel syndrome: outcome and complications. J Shoulder Elbow Surg 2002; 11:248–252. 8. Ogata K, Manske PR, Lesker PA. The effect of surgical dissection on regional blood flow to the ulnar nerve in the cubital tunnel. Clin Orthop Relat Res 1985; (193):195–198. 9. Ogata K, Shimon S, Owen J, Manske PR. Effects of compression and devascularisation on ulnar nerve function: a quantitative study of regional blood flow and nerve conduction in monkeys. J Hand Surg [Br] 1991; 16:104–108. 10. Messina A, Messina JC. Transposition of the ulnar nerve and its vascular bundle for the entrapment syndrome at the elbow. J Hand Surg [Br] 1995; 20:638–648. 11. Adelaar RS, Foster WC, McDowell C. The treatment of the cubital tunnel syndrome. J Hand Surg [Am] 1984; 9A:90–95. 12. Bartels RH, Verhagen WI, van der Wilt GJ, et al. Prospective randomized controlled study comparing simple decompression versus anterior subcutaneous transposition for idiopathic neuropathy of the ulnar nerve at the elbow: I. Neurosurgery 2005; 56:522–530; discussion 522–530. 13. Biggs M, Curtis JA. Randomized, prospective study comparing ulnar neurolysis in situ with submuscular transposition. Neurosurgery 2006; 58:296–304; discussion 296–304. 14. Gervasio O, Gambardella G, Zaccone C, Branca D. Simple decompression versus anterior submuscular transposition of the ulnar nerve in severe cubital tunnel syndrome: a prospective randomized study. Neurosurgery 2005; 56:108–117; discussion 117. 15. Froimson AI, Anouchi YS, Seitz WH Jr, Winsberg DD. Ulnar nerve decompression with medial epicondylectomy for neuropathy at the elbow. Clin Orthop Relat Res 1991; (265):200–206.

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16. Froimson AI, Zahrawi F. Treatment of compression neuropathy of the ulnar nerve at the elbow by epicondylectomy and neurolysis. J Hand Surg [Am] 1980; 5:391–395. 17. Artico M, Pastore FS, Nucci F, Giuffre R. 290 surgical procedures for ulnar nerve entrapment at the elbow: physiopathology, clinical experience and results. Acta Neurochir (Wien) 2000; 142:303–308. 18. Bartels RH. History of the surgical treatment of ulnar nerve compression at the elbow. Neurosurgery 2001; 49:391–399; discussion 399–400. 19. Amako M, Nemoto K, Kawaguchi M, et al. Comparison between partial and minimal medial epicondylectomy combined with decompression for the treatment of cubital tunnel syndrome. J Hand Surg [Am] 2000; 25:1043–1050. 20. Grewal R, Varitimidis SE, Vardakas DG, et al. Ulnar nerve elongation and excursion in the cubital tunnel after decompression and anterior transposition. J Hand Surg [Br] 2000; 25:457–460. 21. Black BT, Barron OA, Townsend PF, et al. Stabilized subcutaneous ulnar nerve transposition with immediate range of motion: longterm follow-up. J Bone Joint Surg Am 2000; 82:1544–1551. 22. Osterman AL, Davis CA. Subcutaneous transposition of the ulnar nerve for treatment of cubital tunnel syndrome. Hand Clin 1996; 12:421–433. 23. Amadio PC, Beckenbaugh RD. Entrapment of the ulnar nerve by the deep flexor-pronator aponeurosis. J Hand Surg [Am] 1986; 11:83–87. 24. Broudy AS, Leffert RD, Smith RJ. Technical problems with ulnar nerve transposition at the elbow: findings and results of reoperation. J Hand Surg [Am] 1978; 3:85–89. 25. Davis GA, Bulluss KJ. Submuscular transposition of the ulnar nerve: review of safety, efficacy and correlation with neurophysiological outcome. J Clin Neurosci 2005; 12:524–528. 26. Lundborg G. Surgical treatment for ulnar nerve entrapment at the elbow. J Hand Surg [Br] 1992; 17:245–247. 27. Nathan PA. Surgical treatment of ulnar nerve entrapment at the elbow. J Hand Surg [Br] 1993; 18:133. 28. Posner MA. Compressive ulnar neuropathies at the elbow: II. Treatment. J Am Acad Orthop Surg 1998; 6:289–297. 29. Posner MA. Compressive ulnar neuropathies at the elbow: I. Etiology and diagnosis. J Am Acad Orthop Surg 1998; 6:282–288. 30. Posner MA. Compressive neuropathies of the ulnar nerve at the elbow and wrist. Instr Course Lect 2000; 49:305–317. 31. Hollerhage HG, Stolke D. [Results of volar transposition of the ulnar nerve in cubital tunnel syndrome]. Neurochirurgia 1985; 28:64–67.

Epicondylitis DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS Lateral and medial pain and localized tenderness that occurs at the distal humeral epicondyles with repetitive eccentric or concentric loading of the flexor or extensor muscles is termed epicondylitis. This word is a misnomer because the pain is related to microtraumatic events that lead to tendinosis and tears of the tendons and muscles rather than inflammation. Epicondylitis is more common laterally than medially by a ratio ranging from 4-7:1,1,2 affecting the dominant elbow twice as often as the nondominant one. Men and women have epicondylitis with equal incidence with an average peak age of 42 years. Young patients tend to have acute pain after tennis or throwing activities. Lateral epicondylitis,

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also called “tennis elbow,” is almost exclusively related to tennis and is felt with the backhand stroke when extensor tendons are tensed up to absorb the impact from the tennis ball. Medial epicondylitis, also referred to as golfer’s elbow, can affect golfers or throwing athletes. Baseball pitchers and javelin throwers are especially affected due to valgus overload of the elbow.The chronic pain that presents in the older individual is usually related to occupational exposure or activity overload. The most common sites for pathology are the tendons of the extensor carpi radialis brevis laterally and the flexor carpi radialis and pronator teres medially. An ulnar neuropathy can coexist with medial epicondylitis in up to 50% of cases.3 Except for acute injuries that are commonly seen in elite or upper-level athletes, most cases of epicondylitis are treated nonoperatively with a 90% success rate. Conservative therapy includes physical therapy, antiinflammatory medication, icing, bracing, and splinting with reduction in activities that provoke the problem. If pain remains after 3 months, corticosteroid is usually injected into the area of pain. If pain persists and limits activity and function after 6 months, operative treatment is considered. Surgical options for epicondylitis include débridement or excision of tendinosis or partial tears, production of neovascularization, repair, or release. This can be done by open or arthroscopic procedures. Percutaneous extensor tenotomy has been recently described.4 Laterally, a synovial fringe or a radiohumeral bursa can be resected. Excellent results are seen after resection and repair for lateral epicondylitis with a success rate of more than 90%.5 The outcomes are not as good for medial epicondylitis with a 50% success rate. This depends on the presence of concomitant ulnar nerve abnormalities. Release of the tendon may lead to weakness of the muscle.

KEY POINTS Most epicondylitis is not treated surgically. Surgical procedures for medial and lateral epicondylitis include débridement, excision, repair, and release. ■ Lateral epicondylitis has a much better surgical success rate than medial epicondylitis. ■ Ulnar neuropathy frequently accompanies medial epicondylitis and can also be a complication of surgery for medial epicondylitis. ■ Check for underlying ligament pathology on postsurgical epicondylitis imaging studies. ■ ■

Contraindications to surgery include a noncompliant patient or one who has not completed the nonoperative regimen stated earlier. If a patient with medial epicondylitis has symptoms associated with the ulnar nerve, the nerve is released at surgery.

EXPECTED APPEARANCE ON IMAGING Stress radiographs can be obtained to evaluate for valgus or varus instability. If damage is suspected to the tendons, MRI or ultrasonography may be obtained before surgery. These tests will quantitate the degree or tendon damage, allowing for accurate preoperative assessment, determination of the best procedure for therapy, as well as postoperative recovery time course. Little has been written about the MRI appearance of the postoperative tendon. In our experience, it may take some time for the signal intensity to return to normal after surgery. The tendon should demonstrate continuity and will become low

■ FIGURE 107-10 This patient had a repair of the flexor tendons with medial epicondylar suture anchors and ulnar nerve transposition. A and B, The tendon repair appears intact with normal continuity, signal intensity, and thickening on these coronal, fat-suppressed, T2-weighted MR images of the elbow (arrows). Suture anchors are attached to bone in proper position in B (arrowheads). (Courtesy of William Morrison, MD, Philadelphia, PA.)

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in signal intensity, often with thickening (Fig. 107-10). Metallic artifact may lie in the area, obscuring evaluation by MRI, especially on gradient-echo images (Fig. 107-11). Re-tear manifests as architectural disruption of the tendon (Fig. 107-12). It has been shown that epicondylitis can be accompanied by underlying ligament pathology,6 and such abnormalities should be included in the search pattern on a postoperative MRI.This is particularly important in patients who have continuing pain, and it may further destabilize the elbow in those who have had surgical tendon release.

POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE Incomplete resection of abnormal tissue can be a problem, presenting with an appearance similar to tendinosis or tendon tear. Ligament abnormalities and adventitial bursa

■ FIGURE 107-11

Normal postoperative lateral epicondylitis repair. Coronal, gradient-echo (A) and axial T1-weighted (B) MR images show an intact extensor tendon repair after lateral epicondylitis (arrows). The micrometallic artifact is obscuring the tendon on the gradient-echo image (arrowhead). (Courtesy of William Morrison, MD, Philadelphia, PA.)

■ FIGURE 107-12 Lateral epicondylar débridement with re-tear. Coronal, T1-weighted (A) and coronal (B) and axial (C) fat-suppressed, T2-weighted MR images demonstrate fiber disruption consistent with a partial tear (white arrows). Note the adjacent bone marrow edema in the lateral epicondyle on the fluid-sensitive sequences (arrowheads). There is poor fat suppression on the other side, mimicking edema in the axial plane (black arrow). The underlying radial collateral ligament is intact. (Courtesy of William Morrison, MD, Philadelphia, PA.)

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formation may be seen postoperatively. Percutaneous techniques occasionally result in synovial fistula formation. Excessive scar tissue may be a problem in the surgical bed. Medial procedures could affect the ulnar nerve as stated earlier. Care should be taken when interpreting an MRI when a failed surgical tendon has been injected with corticosteroid or anesthetic. The injectate will elevate signal intensity on T2-weighted sequences. A failed postoperative tendon can undergo another excision and repair.7

SUGGESTED READINGS Cain EL, Dugas JR, Wolf RS, et al. Elbow injuries in throwing athletes: A current concepts review. Am J Sports Med 2003; 621–635. Kraushaar B, Nirschl RP.Tendinosis of the elbow (tennis elbow). J Bone Joint Surg Am 1999; 81:259–278.

REFERENCES 1. Gabel GT, Morrey BF. Tennis elbow. Instr Course Lect 1998; 47:165–172. 2. Leach RE, Miller JK. Lateral and medial epicondylitis of the elbow. Clin Sports Med 1987; 6:259–272. 3. Gabel GT, Morrey BF. Operative treatment of medical epicondylitis: influence of concomitant ulnar neuropathy at the elbow. J Bone Joint Surg Am 1995; 77:1065–1069. 4. Yerger B,Turner T. Percutaneous extensor tenotomy for chronic tennis elbow: an office procedure. Orthopedics 1985; 8:1261–1263. 5. Nirschl RP, Pettrone FA. Tennis elbow: the surgical treatment of lateral epicondylitis. J Bone Joint Surg Am 1979; 61:832–839. 6. Bredella MA, Tirman PF, Fritz RC, et al. MR imaging findings of lateral ulnar collateral ligament abnormalities in patients with lateral epicondylitis. AJR Am J Roentgenol 1999; 173:1379–1382. 7. Organ SW, Nirschl RP, Kraushaar BS, Guidi EJ. Salvage surgery for lateral tennis elbow. Am J Sports Med 1997; 25:746–750.

Biceps Tendon DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS Biceps tendon tears usually result from eccentric loading of the muscle.They may result from athletic activities such as weightlifting but are also seen after routine activities such as carrying a heavy unbalanced load. In these cases in which there is minimal trauma, weakening of a tendon that has undergone degeneration is suspect.1 Mechanical impingement during pronation and a radial tuberosity enthesophyte can also cause tears of the tendon.2 Most tears occur 1 to 2 cm above the radial tuberosity where the tendon is less vascular and there is a histologic transition.3 Disruption of the biceps tendon is more common in men between 40 and 60 years of age. Surgery is preferred over nonoperative treatment in cases of ruptured biceps tendon. Surgery restores supination and improves cosmetic appearance when there is biceps tendon retraction.When possible, the torn tendon is reattached to the radial tuberosity with suture anchors via an anterior approach.4 In instances of delayed diagnosis, scarring of the muscle makes reattachment of the tendon more difficult.2 An Achilles tendon allograft may be required or the biceps tendon can be attached to the brachialis tendon.5

EXPECTED APPEARANCE ON IMAGING On MRI and ultrasonography, the biceps tendon may appear thickened postoperatively. It should be continuous from the muscle to the radial tuberosity if it has been reattached or if a graft has been placed (Fig. 107-13). It may be reattached to the brachialis muscle in some cases (Fig. 107-14).

■ FIGURE 107-13 Normal postoperative biceps tendon. Axial T1-weighted (A) and sagittal T2-weighted (B) MR images of the elbow show an intact biceps tendon repair (arrows). The tendon is of normal caliber and in continuity to its distal attachment on the bicipital tuberosity. (Courtesy of William Morrison, MD, Philadelphia, PA.)

A

B

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KEY POINTS Rupture of the distal biceps tendon is rare and usually occurs 1 to 2 cm from the radial attachment. ■ The biceps is usually reattached to the radial tuberosity with sutures via drill holes or anchors; grafts are used for delayed reconstruction. ■ The postoperative biceps tendon is thickened and continuous with heterogenous signal intensity. ■ Complications include nerve palsies, tendon re-rupture, and heterotopic bone formation. ■

for visualization of the tendon from the musculotendinous junction to the insertion on a single image.6 ■ FIGURE 107-14

Normal biceps tendon repair inserted on brachialis (arrow) on this sagittal, fat-suppressed T2-weighted MR image. (Courtesy of Tim Sanders, MD, Charlottesville, VA.)

The normal tendon occasionally displays intermediate signal intensity on MRI.6 Suture anchors or an osseous defect may be present at the radial tuberosity. The tendon can be imaged with the elbow in flexion, abduction, and supination that places slight tension on the tendon and allows

POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE Complications of distal biceps tendon repair are uncommon. They include re-rupture (Figs. 107-15 to 107-17) and nerve injuries involving the median and radial nerves and the branch of the radial nerve, the posterior interosseous nerve. Proximal radioulnar synostosis7 and heterotopic ossification around the elbow are also complications that can best be seen on radiographs or CT.6,8 The latter may be related to the degree of soft tissue dissection during surgery as well as exposure of the periosteal surface of the ulna.

■ FIGURE 107-15 Re-rupture of biceps tendon after surgery. The biceps tendon is proximally retracted on sagittal, proton density– weighted (A) and axial, fat-suppressed (B) T2-weighted MR images (arrows). Metallic artifact is seen in the proximal biceps (arrowhead). (Courtesy of William Morrison, MD, Philadelphia, PA.)

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■ FIGURE 107-16 Re-rupture of a biceps repair as shown on axial T2-weighted (A) and sagittal (B) MR images (arrows). (Courtesy of Tim Sanders, MD, Charlottesville, VA.)

■ FIGURE 107-17 Re-ruptured distal biceps repair on a sagittal ultrasound image (arrow). (Courtesy of Gina Allen, MD, Birmingham, England.)

SUGGESTED READINGS Chung CB, Chew FS, Steinbach L. MR imaging of tendon abnormalities of the elbow. Magn Reson Imaging Clin North Am 2004; 12:233–245. Falchook FS, Zlatkin MB, Erbacher GE, et al. Rupture of the distal biceps tendon: evaluation with MR imaging. Radiology 1994; 190:659–663. Morrey BF.The Elbow. Philadelphia, Lippincott Williams & Wilkins, 2002. Safran MR, Graham SM. Distal biceps tendon ruptures. Clin Orthop 2002; 404:275–283.

REFERENCES 1. Morrey BF, Askew LJ, An KN, Dobyns JH. Rupture of the distal tendon of the biceps brachii: a biomechanical study. J Bone Joint Surg Am 1985; 67:418–421.

2. Seiler JG 3rd, Parker LM, Chamberland PD, et al. The distal biceps tendon: two potential mechanisms involved in its rupture: arterial supply and mechanical impingement. J Shoulder Elbow Surg 1995; 4:149–156. 3. Koch S, Tillmann B. The distal tendon of the biceps brachii: structure and clinical correlations. Ann Anat 1995; 177:467–474. 4. Lintner S, Fischer T. Repair of the distal biceps tendon using suture anchors and an anterior approach. Clin Orthop Relat Res 1996; (322):116–119. 5. Hovelius L, Josefsson G. Rupture of the distal biceps tendon: report of five cases. Acta Orthop Scand 1977; 48:280–282. 6. Giuffre BM, Moss MJ. Optimal positioning for MRI of the distal biceps brachii tendon: flexed abducted supinated view. AJR Am J Roentgenol 2004; 182:944–946. 7. Failla JM, Amadio PC, Morrey BF, Beckenbaugh RD. Proximal radioulnar synostosis after repair of distal biceps brachii rupture by the two-incision technique: report of four cases. Clin Orthop Relat Res 1990; (253):133–136. 8. Davison BL, Engber WD, Tigert LJ. Long term evaluation of repaired distal biceps brachii tendon ruptures. Clin Orthop Relat Res 1996; (333):186–191.

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Triceps Tendon DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS The triceps tendon is composed of three components: the long, lateral, and medial muscles. It inserts as a common tendon on the posterosuperior surface of the olecranon process. Triceps tendon ruptures are rare.1 They usually occur as a result of eccentric contraction against resistance, deceleration stress on a contracted muscle, or direct insult to the posterior arm. Radial head fractures may also be seen with triceps tendon tears. Involvement at the musculotendinous junction or avulsion of the tendon from the olecranon with a small osseous fragment are more common presentations of injury to this muscle, but the insult can occur anywhere.2,3 Underlying systemic diseases such as chronic renal failure and hyperparathyroidism are also causes for this problem. Chronic olecranon bursitis or bursectomy can also lead to triceps tears. Rupture is usually accompanied by ecchymosis. Elbow extension is either weak or absent. Partial ruptures of the triceps are treated nonoperatively. Because nonoperative treatment of a full-thickness tear results in weakness and incomplete extension, those tears are repaired surgically with a good prognosis and almost full range of motion. The tendon is reattached to the ulna with drill holes. Periosteum may be closed over the tendon or a proximal flap of forearm fascia or distal triceps can be used to reinforce the repair. Tendon grafts can also be used. If a large avulsion fragment is present, then it is fixed with a screw and washer.

■ FIGURE 107-18

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KEY POINTS ■ ■ ■ ■

Triceps tendon tears are rare. Surgery is reserved for full-thickness triceps tendon tears. The triceps tendon is reattached to the olecranon. Excluding re-tear, there are few complications of repair.

EXPECTED APPEARANCE ON IMAGING On radiographs, one may see soft tissue swelling and hardware after surgery. Drill holes are sometimes present in the olecranon. An avulsion fragment should be attached to the olecranon. On MRI and ultrasonography, the tendon should be continuous without architectural disruption to suggest a partial- or full-thickness tear. It can be slightly elevated in signal intensity on MRI in the early repair stage but should decrease to a normal tendinous signal intensity within a year. A re-tear of a surgical repair could demonstrate an avulsion fragment of the olecranon.

POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE The triceps tendon can re-rupture after surgical repair. This is manifest as discontinuity of the tendon with high signal intensity on fluid-sensitive sequences (Fig. 107-18). Except for re-tear, there are few complications of triceps tendon repair. One should look for excessive scar tissue, olecranon bursitis, heterotopic bone formation, evidence of infection, or nerve damage including ulnar neuropathy (Fig. 107-19), which may result in anconeus denervation.

Disrupted triceps tendon repair. A, Sagittal, fat-suppressed, T2-weighted image of the elbow preoperatively shows a fullthickness tear of the distal triceps at the olecranon attachment. B, The follow-up sagittal, fat-suppressed, T2-weighted image shows a partial re-tear of the triceps (arrow).

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■ FIGURE 107-19

Ulnar neuritis after triceps repair seen on axial, T1-weighted (A) and fat-suppressed T2-weighted (B) MR images (under marker). (Courtesy of Tim Sanders, MD, Charlottesville, VA.)

SUGGESTED READINGS Chung CB, Chew FS, Steinbach L. MR imaging of tendon abnormalities of the elbow. Magn Reson Imaging Clin North Am 2004; 12:233–245. Morrey BF. The Elbow. Philadelphia, Lippincott Williams & Wilkins, 2002. Tarnsey FF. Rupture and avulsion of the triceps. Clin Orthop 1972; 83:177–183.

REFERENCES 1. Anzel SH, Covey KW, Weiner AD, Lipscomb PR. Disruption of muscles and tendons; an analysis of 1,014 cases. Surgery 1959; 45:406–414. 2. Farrar EL 3rd, Lippert FG 3rd. Avulsion of the triceps tendon. Clin Orthop Relat Res 1981; (161):242–246. 3. Pina A, Garcia I, Sabater M. Traumatic avulsion of the triceps brachii. J Orthop Trauma 2002; 16:273–276.

Olecranon Bursitis DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS The olecranon bursa is located in the subcutaneous tissues posterior to the olecranon process. It serves to reduce friction in the region. Distention of the bursa can occur after trauma, infection, or arthropathy, such as gout or rheumatoid

KEY POINTS Olecranon bursitis is usually treated conservatively. Operative treatment of olecranon bursitis is reserved for chronic pain and discomfort. ■ The surgery can be performed open or arthroscopically. ■ Complications include poor wound healing, scar tissue that envelops the adjacent tendon and bone, and fistula formation. ■ ■

arthritis. In addition, infection is a cause of olecranon bursits.1 Calcium pyrophosphate dihydrate deposition has also been implicated.2 Most patients with noninfectious olecranon bursitis are treated with aspiration and corticosteroid injections. If this fails and pain and discomfort persist, surgical excision of the olecranon bursa is performed.3 This can be performed along with open surgical drainage or endoscopically using an arthroscope. The latter procedure is thought to have fewer complications such as poor wound healing, infection, and loss of joint mobility, although it does not fare well in rheumatoid patients who have bursae that communicate with the elbow joint.4 A prominent adjacent olecranon process or spur can be resected.

EXPECTED APPEARANCE ON IMAGING A postoperative MRI or ultrasonography should show lack of fluid in the region of the olecranon bursa. A small amount of scar tissue may be present (Fig. 107-20).

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■ FIGURE 107-20 Olecranon bursectomy. Sagittal fast spin-echo, T2-weighted (A) and axial, gradient-echo (B) MR images show low signal scarring in the location of prior olecranon bursectomy (arrows). (Courtesy of Javier Beltran, MD, Brooklyn, NY.)

POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE The most common complication of open olecranon bursectomy is poor wound healing.4 Scar can adhere to tendon or bone.3 A synovial-cutaneous fistula may form.5 Fluid should not be present within the olecranon bursa. A triceps tendon tear may result after olecranon bursectomy.

SUGGESTED READINGS Degreef I, De Smet L. Complications following resection of the olecranon bursa. Acta Orthop Belg 2006; 72:400–403. Ogilvie-Harris DJ, Gilbart M. Endoscopic bursal resection: the olecranon bursa and prepatellar bursa. Arthroscopy 2000; 16:249–253.

REFERENCES 1. Ho G Jr, Tice AD, Kaplan SR. Septic bursitis in the prepatellar and olecranon bursae: an analysis of 25 cases. Ann Intern Med 1978; 89:21–27. 2. Gerster JC, Lagier R, Boivin G. Olecranon bursitis related to calcium pyrophosphate dihydrate crystal deposition disease. Arthritis Rheum 1982; 25:989–996. 3. Kerr DR. Prepatellar and olecranon arthroscopic bursectomy. Clin Sports Med 1993; 12:137–142. 4. Quayle JB, Robinson MP. A useful procedure in the treatment of chronic olecranon bursitis. Injury 1978; 9:299–302. 5. Thompson GR, Manshady BM, Weiss JJ. Septic bursitis. JAMA 1978; 240:2280–2281.

Common Elbow Fractures DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS Fractures commonly affect the elbow in the supracondylar region of the distal humerus, radial head, coronoid process, and ulna. Insults to the capitellum result in osteochondral lesions. Supracondylar fractures are the second most common type of fracture in children.1 In 95% of cases these are caused by a fall on an outstretched hand with an extended elbow. The distal fragment is posteriorly displaced. Five percent of supracondylar fractures occur with the elbow flexed and result in anterior displacement of the distal fragment. These types of fractures are associated with ulnar nerve injury.2,3 A severely displaced fracture can buttonhole the triceps muscle.3 Supracondylar fractures may be treated conservatively with closed reduction and splinting or casting. Percutaneous pinning is often an option that provides superior results to closed reduction.4 The elbow is less flexed, decreasing the chance of Volkmann’s ischemic contracture. Displaced, comminuted, or open fractures or any that are associated with nerve entrapment or vascular injury are treated with open reduction and internal fixation.

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KEY POINTS Fractures of the elbow should be reduced to near anatomic alignment. ■ Postoperative complications include malunion, malalignment, nonunion, infection, loosening of hardware, particle disease around hardware, and neurovascular injury. ■ Radiographs are the main imaging modality for evaluation of the postoperative elbow. Careful comparison with prior postoperative images is important. CT can be used to evaluate healing and alignment. MRI and ultrasonography are useful for neurovascular injury. ■

Radial head fractures are seen mainly in adults between the ages of 30 and 60 years. They result from a fall on the outstretched arm or less commonly from a direct impact from the lateral side of the elbow. They can be nondisplaced, displaced with marginal fractures, or comminuted. The elbow may be dislocated in between 10% to 30% of injuries.5 Most radial head fractures are treated conservatively. Comminuted or cleavage fractures of the radial head often require open reduction and internal fixation, especially if they block motion of the elbow.6,7 Complete or partial excision of the radial head is also performed as an open or arthroscopic procedure.8 Radial head prostheses are used for complex injuries about the elbow. Coronoid process fractures are usually associated with posterior elbow dislocation.9,10 Type I fracture is an avulsion of the tip of the coronoid process.A type II fracture is called when the fragment that is less than 50% of the coronoid process. Type II fractures are those where the fragment is more than 50% of the coronoid process. Nondisplaced type I and II fractures are treated conservatively whereas type III fractures

and displaced fractures are highly unstable and are treated with open reduction and internal fixation using a compression screw or similar hardware. Olecranon fractures usually result from a sudden contraction of the triceps hyperextension injury with high force trauma or a direct force from a fall on the flexed elbow. Displaced olecranon fractures are treated with internal fixation with tension-band wiring using parallel Kirschner wires or an intramedullary cancellous screw.11 Small avulsion fractures at the triceps are excised with reattachment of the triceps. Osteochondral injury to the capitellum is often the result of valgus stress. This produces compression on the capitellum. It is more common in adolescents who perform throwing sports in the dominant elbow. Nondisplaced, stable fragments are treated conservatively or with arthroscopic drilling. Loose fragments can be arthroscopically removed or reattached to the parent bone. Newer techniques to reduce complications such as arthritis such as osteochondral plug transfer (mosaicplasty), chondrocyte transplant, or allograft reconstruction have not been thoroughly evaluated.12,13

EXPECTED APPEARANCE ON IMAGING In general, normal postoperative radiographs show fractures reduced to near anatomic alignment. Nonunion and malunion is commented on. Hardware remains in the same position as shown on the postoperative radiograph, and there is no evidence of lucency or periosteal reaction around the hardware to suggest loosening or infection.The elbow is not subluxed or dislocated on a normal postoperative radiograph. A line drawn through the radius should intersect with the capitellum on anteroposterior and lateral radiographs. Intra-articular bodies may be present and are noted in the report. The supracondylar fracture should be reduced to near anatomic alignment (Fig. 107-21). Occasionally the line drawn down the front of the humerus does not intersect

■ FIGURE 107-21 Supracondylar fracture fixation. Anteroposterior (A) and lateral (B) radiographs of the left elbow demonstrate two crossed Kirschner wires traversing a supracondylar fracture of the distal humerus near the elbow. The fracture is in anatomic alignment.

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the capitellum at the junction of the anterior and middle third even with satisfactory reduction. The elbow should be in mild valgus. Pins may have four configurations, including medial and lateral crossed pins, three lateral pins, two lateral parallel pins, or two lateral crossed pins. Pins are removed at 3 weeks if the fracture appears healed. The radial head should line up with the capitellum on anteroposterior and lateral views. It can be evaluated on a radial head view obtained with the elbow in lateral position, flexed to 90 degrees with the beam projected over the capitellum, and angled at 45 degrees to the forearm. Fracture fragments are noted.The radial head may be absent or replaced with a metallic or plastic prosthesis on the postoperative radiograph (Fig. 107-22). Olecranon fractures are usually seen with tension-band wiring using parallel Kirschner wires or an intramedullary cancellous screw (Fig. 107-23). Radiographs should show anatomic alignment of the fragments with progressive fracture healing. It may be difficult to see coronoid process fractures well on radiographs due to the overlap of the radius. Reformatted CT images are useful in such cases. Small fractures are usually treated conservatively, whereas large fractures are pinned back to the parent bone. Osteochondral lesions are treated in a variety of ways. If the fragment is pinned back to the parent bone, it should be in anatomic alignment. Bone plugs and chondrocyte transplant can be assessed with MRI. Radiographically, the graft is incorporated with a normal contour of the subchondral cortex. MRI shows normalization of the signal intensity of cartilage overlying the lesion.13

POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE Complications of elbow fractures include malunion and nonunion. Alignment, callus formation, and healing of the

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fracture line should be assessed on radiographs taken at 90 degrees to each other. If there is any question of malunion or nonunion, multiplanar reformatted CT images can be performed. Plates and screws should not pull out of the fracture. New periosteal reaction or increasing lucency around hardware can suggest loosening or infection (Fig. 107-24). The elbow may be subluxed or dislocated. Heterotopic bone frequently forms around the elbow and restricts motion. Specific complications are seen for the various fractures.These are discussed in the following paragraphs. Treatment of supracondylar fracture may cause the elbow to go into varus.This is related to poor reduction or loss of reduction and can be seen in up to 58% of supracondylar fractures.14,15 Cubitus varus can interfere with throwing sports, swimming, and push-ups and may lead to lateral condylar fracture.15 Cubitus varus can be treated with osteotomy.16 Pin tract infections and nerve injuries, particularly of the ulnar nerve, related to the pins or reduction may occur.17,18 Posterolateral displacement is associated with median nerve and brachial artery injury.2 Posteromedial displacement is more often associated with radial nerve injury.2,19 The brachial artery may also be compromised. Volkmann’s ischemic contracture can result. This may be evaluated with arteriography, MR angiography or Doppler ultrasonography before exploration.20 Radial head fracture reductions may displace postoperatively. The hardware can loosen. Radial head excision can result in injury to the radial nerve or its branches as well as the ulnar nerve. These nerves can be studied with MRI or ultrasonography as well as electromyography. Radial head excision also results in occasional proximal radial migration and asymptomatic subluxation at the distal radioulnar joint that can lead to degenerative arthropathy in that region.4 Radial head prostheses may loosen, sublux (Fig. 107-25), dislocate, or break.21 Silicone synovitis is another complication that results in a destructive arthropathy that requires removal of the prosthesis.22

■ FIGURE 107-22 Radial head replacement in anatomic alignment. Anteroposterior (A) and lateral (B) views show the radial head replacement in anatomic alignment (arrows).

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■ FIGURE 107-23 Olecranon fracture with distraction of the fragments. A and B, Postoperative radiographs demonstrate figure-of-eight tension band and two Kirschner wires with the elbow in a plaster splint. The fracture is reduced to anatomic alignment.

■ FIGURE 107-24 Infected postsurgical reduction of an olecranon fracture. There is a Brodie abscess in the proximal fragment (arrowhead) with a nonunion of the fracture (arrow).

Olecranon fractures may displace. Olecranon bursitis is a complication of open reduction and internal fixation of the olecranon fracture. It will be seen as a soft tissue swelling on radiographs and a fluid-filled mass on CT, MRI, and ultrasonography. Fragments associated with osteochondral lesions should be removed from the joint and not visible on imaging. Arthrography can be useful to look for these bodies and to determine if they are intra-articular. CT arthrography and MR arthrography also demonstrate cartilaginous bodies not seen on radiographs. Loosening of osteochondral fragments are recognized by the development of increasing lucency at the interface of the fragment with the parent bone. This can be evaluated with MRI or MR arthrography. Radiographic degenerative changes are frequently seen in the radiocapitellar joint and may be associated with radial head enlargement.23

■ FIGURE 107-25 Posteriorly subluxed radial head replacement (arrow) on lateral radiograph. Note the suture anchors for extensor and flexor tendon repairs (arrowheads).

SUGGESTED READINGS Anderson SE, Otsuka NY, Steinbach LS. MR imaging of pediatric elbow trauma. Semin Musculoskelet Radiol 1998; 2:185–198. Green NE. Fractures and dislocations about the elbow. In Green NE (ed). Skeletal Trauma in Children. Philadelphia, WB Saunders, 1994, pp 213–256.

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REFERENCES 1. Farnsworth CL, Silva PD, Mubarak SJ. Etiology of supracondylar humerus fractures. J Pediatr Orthop 1998; 18:38–42. 2. Campbell CC, Waters PM, Emans JB, et al. Neurovascular injury and displacement in type III supracondylar humerus fractures. J Pediatr Orthop 1995; 15:47–52. 3. Williamson DM, Cole WG. Flexion supracondylar fractures of the humerus in children: treatment by manipulation and extension cast. Injury 1991; 22:451–455. 4. Pirone AM, Graham HK, Krajbich JI. Management of displaced extension-type supracondylar fractures of the humerus in children. J Bone Joint Surg Am 1988; 70:641–650. 5. Gaston SR, Smith FM, Baab OD. Adult injuries of the radial head and neck; importance of time element in treatment. Am J Surg 1949; 78:631–635; discussion, 647–651. 6. Sanders RA, French HG. Open reduction and internal fixation of comminuted radial head fractures. Am J Sports Med 1986; 14:130–135. 7. Esser RD, Davis S, Taavao T. Fractures of the radial head treated by internal fixation: late results in 26 cases. J Orthop Trauma 1995; 9:318–323. 8. Coleman DA, Blair WF, Shurr D. Resection of the radial head for fracture of the radial head: long-term follow-up of seventeen cases. J Bone Joint Surg Am 1987; 69:385–392. 9. Regan W, Morrey B. Fractures of the coronoid process of the ulna. J Bone Joint Surg Am 1989; 71:1348–1354. 10. Regan W, Morrey BF. Classification and treatment of coronoid process fractures. Orthopedics 1992; 15:845–848. 11. Gartsman GM, Sculco TP, Otis JC. Operative treatment of olecranon fractures: excision or open reduction with internal fixation. J Bone Joint Surg Am 1981; 63:718–721. 12. Oka Y, Ohta K, Fukuda H. Bone-peg grafting for osteochondritis dissecans of the elbow. Int Orthop 1999; 23:53–57. 13. Iwasaki N, Kato H, Ishikawa J, et al. Autologous osteochondral mosaicplasty for capitellar osteochondritis dissecans in teenaged patients. Am J Sports Med 2006; 34:1233–1239. 14. Levine MJ, Horn BD, Pizzutillo PD. Treatment of posttraumatic cubitus varus in the pediatric population with humeral osteotomy and external fixation. J Pediatr Orthop 1996; 16:597–601. 15. Davids JR, Maguire MF, Mubarak SJ, Wenger DR. Lateral condylar fracture of the humerus following posttraumatic cubitus varus. J Pediatr Orthop 1994; 14:466–470. 16. Barrett IR, Bellemore MC, Kwon YM. Cosmetic results of supracondylar osteotomy for correction of cubitus varus. J Pediatr Orthop 1998; 18:445–447. 17. Brown IC, Zinar DM. Traumatic and iatrogenic neurological complications after supracondylar humerus fractures in children. J Pediatr Orthop 1995; 15:440–443. 18. Rasool MN. Ulnar nerve injury after K-wire fixation of supracondylar humerus fractures in children. J Pediatr Orthop 1998; 18:686–690. 19. Sairyo K, Henmi T, Kanematsu Y, et al. Radial nerve palsy associated with slightly angulated pediatric supracondylar humerus fracture. J Orthop Trauma 1997; 11:227–229. 20. Copley LA, Dormans JP, Davidson RS. Vascular injuries and their sequelae in pediatric supracondylar humeral fractures: toward a goal of prevention. J Pediatr Orthop 1996; 16:99–103. 21. Knight DJ, Rymaszewski LA, Amis AA, Miller JH. Primary replacement of the fractured radial head with a metal prosthesis. J Bone Joint Surg Br 1993; 75:572–576. 22. Vanderwilde RS, Morrey BF, Melberg MW, Vinh TN. Inflammatory arthritis after failure of silicone rubber replacement of the radial head. J Bone Joint Surg Br 1994; 76:78–81. 23. Jackson DW, Silvino N, Reiman P. Osteochondritis in the female gymnast’s elbow. Arthroscopy 1989; 5:129–136.

Distal Forearm Fractures at the Wrist DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS Fractures of the distal forearm at the wrist are common after a fall on an outstretched hand. Distal radial fractures may be accompanied by a fracture of the ulnar styloid. Isolated distal ulnar fractures are much less common. There are many types of distal radial fractures. The distal radius may have a fracture that extends to the articular surface or the fracture may be extra-articular. Colles’ fracture typically occurs 2 to 3 cm from the articular surface in the distal radial metaphysis and may extend to the articular surface. It is characterized by a dorsal tilt of the radius. The Barton’s fracture also has a dorsal tilt and occurs on the dorsal or volar (reverse Barton’s) lip of the radius with associated subluxation of the carpus. Smith’s fractures are characterized by an extra- or intra-articular fracture with a volar tilt of the radial articular surface. The chauffer’s fracture (also called Hutchinson’s or bumper fracture) occurs in the radial styloid. A die-punch fracture refers to fractures that involve the lunate fossa of the distal radius. The Galeazzi fracture-dislocation consists of a fracture of the distal third of the radius that may extend to the articular surface, is often dorsally displaced, and is associated with dorsal ulnar dislocation of the distal radioulnar joint. A fracture can be treated conservatively with closed reduction in a cast if it appears stable, being minimally displaced or impacted. Distal fractures that have significant displacement or comminution require surgery. Articular fractures that unite with more than 2 mm of surface incongruity result in arthrosis and are treated surgically. The unstable lesions can be semi-constrained with closed reduction and external fixation, percutaneous pins, or pins and plaster. Those fractures that cannot be reduced with this method or are severely comminuted with soft tissue

KEY POINTS Distal forearm fractures at the wrist may require closed reduction with or without fixation. ■ Unstable fractures are treated with open reduction and internal fixation. ■ Distal radial articular surface should be in neutral or volar tilt after treatment. ■ The ulnar inclination of the distal radius should be more than 15 degrees. ■ The radius and ulna should be at approximately the same length at the distal radioulnar joint. ■ Arthrography, CT, ultrasonography, and MRI can be helpful in assessing for complications such as malunion, nonunion, and soft tissue injury after treatment. ■

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injury require fixation of the distal radius. The fractures that require open reduction and internal fixation include Barton’s, reverse Barton’s, and radial styloid fractures. Buttress plate fixation is often performed on these types of fractures.1,2 Compression fractures of the radial articular surface or fractures with displaced and rotated fragments also require open reduction and internal fixation.

EXPECTED APPEARANCE ON IMAGING After treatment, the fracture fragments should be reduced to anatomic alignment without significant displacement. The distal radius is expected to have a neutral or volar tilt on lateral radiographs (Fig. 107-26). On the posteroanterior view, the radius may have an ulnar inclination of greater than 15 degrees. The radial articular surface may be compromised if it contains more than a 2-mm stepoff. The ulna should be equal to the length of the radius at the distal radioulnar joint on a neutral wrist view obtained with the wrist on the radiographic table, in neutral forearm rotation, and with 90 degrees of elbow flexion and shoulder abduction. Bone graft may be used to fill in the fracture site3 and should not be misinterpreted for fracture fragments. An ulnar styloid fracture is usually left alone and variably unites with the shaft.

POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE Malunion of the distal radius is more common in the wrist than in any other site in the body, occurring in 5% of patients.4 Complications of radial fractures include malunion, nonunion, neurologic complications due to nerve retraction, unstable internal fixation, extension of fixation screws into the articulation (Fig. 107-27), loss of reduction or fixation, infection, and peritendinous adhesions. If the radius has not been adequately reduced from impaction, continued radial shortening is associated with positive ulnar variance, which can lead to ulnocarpal impaction syndrome. The distal radial cartilage can be damaged, leading to radiocarpal arthropathy. The triangular fibrocartilage, proximal row intrinsic carpal ligaments, and extrinsic carpal ligaments may also be torn in the presence of a fracture of the distal forearm. Osseous displacement, malunion, and nonunion can be identified on CT. The soft tissue abnormalities are best seen on MRI if there is not too much hardware in place to obscure them. Arthrography can be used to evaluate for ligament or triangular fibrocartilage damage in those situations in which the hardware would produce significant artifact on MRI.

■ FIGURE 107-26 Colles’ fracture reduced to anatomic alignment and treated with plate and screws. Posteroanterior (A) and lateral (B) radiographs.

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■ FIGURE 107-27 Colles’ fracture with internal fixation plate. The distal screws extend into the radiocarpal joint (arrows). Posteroanterior (A) and lateral (B) radiographs.

SUGGESTED READINGS Fernandez DL. Correction of post-traumatic wrist deformity in adults by osteotomy, bone-grafting, and internal fixation. J Bone Joint Surg Am 1982; 64:1164–1178. Goldfarb CA,Yin Y, Gilula LA, et al. Wrist fractures: what the clinician wants to know. Radiology 2001; 219:11–28.

REFERENCES 1. Axelrod TS, McMurtry RY. Open reduction and internal fixation of comminuted, intraarticular fractures of the distal radius. J Hand Surg [Am] 1990; 15:1–11. 2. Bradway JK, Amadio PC, Cooney WP. Open reduction and internal fixation of displaced, comminuted intra-articular fractures of the distal end of the radius. J Bone Joint Surg Am 1989; 71:839–847. 3. Herrera M, Chapman CB, Roh M, et al.Treatment of unstable distal radius fractures with cancellous allograft and external fixation. J Hand Surg [Am] 1999; 24:1269–1278. 4. Cooney WP 3rd, Dobyns JH, Linscheid RL. Complications of Colles’ fractures. J Bone Joint Surg Am 1980; 62:613–619.

Carpal Tunnel Syndrome DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS Carpal tunnel syndrome is the most common nerve entrapment syndrome in the upper extremity. It can be caused by repetitive motion, acute trauma, infection, mass lesions, variant anatomy, infiltrative disorders, and intrinsic

nerve abnormalities or a combination of these factors. The syndrome may disappear with splinting, medication, injections, and a decrease in or avoidance of certain activities. In patients with excisable masses such as ganglia or neurogenic tumors, excision of the mass is performed. Most other patients require surgical decompression of the transverse carpal ligament. The flexor retinaculum is usually divided at its ulnar aspect with complete release. Additional epineurotomy for thickened and scarred epineurium is also occasionally performed. This may be done with an open procedure or with endoscopic release.

EXPECTED APPEARANCE ON IMAGING The postoperative appearance of the carpal tunnel presents several challenges to the radiologist. Normal postoperative findings must be differentiated from persistent pathologic changes. The carpal tunnel volume is usually increased in the anteroposterior dimension with volar displacement of the contents. The transverse carpal ligament

KEY POINTS The content of the carpal tunnel displaces volarly after transverse carpal ligament release. ■ The median nerve may decrease in size and signal intensity on T2 weighting after surgery. ■ The transverse carpal ligament should be discontinuous from the level of the pisiform to the hook of the hamate. ■ The median nerve and ulnar nerve may be lacerated, and a neuroma could result. ■ A mass in or around the carpal tunnel may be responsible for symptoms if not diagnosed preoperatively. ■

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■ FIGURE 107-28 Normal postoperative carpal tunnel release. There is discontinuity of the central flexor retinaculum where it has been surgically released on axial T1-weighted and gradient-echo sequences (arrows). The contents of the carpal tunnel are shifted volarly. (Courtesy of Javier Beltran, MD, Brooklyn, NY.)

is discontinuous at the site of surgical release (Fig. 107-28). Widening of the fat stripe in Perona’s space at the floor of the carpal tunnel dorsal to the flexor digitorum profundus tendons is another common finding. If preoperative imaging is available, comparison will generally demonstrate some improvement in the signal intensity and size of the median nerve without complete resolution. Both MRI and ultrasound imaging have been advocated for the assessment of the asymptomatic, postoperative patient. Several normal postoperative changes are routinely demonstrated with ultrasonography. In a study comparing the appearance of the median nerve before and after successful carpal tunnel release in 20 hands, significant increase in median nerve volume was documented at the level of the pisiform and hamate.1 Also, the carpal volume increased in volume at the level of the hamate, largely owing to increased volar displacement of the transverse carpal ligament. After successful carpal tunnel surgery, the MR appearance of the median nerve normalizes.The nerve decreases in size at the level of the pisiform, flattening at the level of the hook of the hamate, and signal intensity usually returns to normal.2,3 Wu and colleagues4 found that the best MR predictor of recurrent carpal tunnel syndrome was enlargement of

the median nerve at the level of the pisiform. Enlargement was seen in 40% of patients with recurrent carpal tunnel syndrome and only 8% with clinically successful surgery (P =.007). Another good predictor of persistent carpal tunnel syndrome in this study was persistent tenosynovitis seen in 60% compared with 35% of controls (P =.02).

POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE A small number of patients continue to experience symptoms after surgical release of the retinaculum.This clinical scenario is a difficult clinical problem. Nerve conduction studies are generally positive for weeks to months after successful carpal tunnel release and are not helpful in this clinical setting. Several complications should be sought on MRI and ultrasonography. Incomplete release of the transverse carpal ligament results in continued symptoms. This occurs more frequently with the endoscopic procedure. The imaging characteristics include a continuous transverse carpal ligament spanning the carpal tunnel anywhere between the pisiform and hook of the hamate levels (Fig. 107-29).5 It is hard to differentiate an incom-

■ FIGURE 107-29 Recurrent carpal tunnel syndrome after retinacular release presents with continuity of the flexor retinaculum at the level of the pisiform (A) and hook of the hamate (B) (arrows). (Courtesy of Javier Beltran, MD, Brooklyn, NY.)

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plete release from a transverse carpal ligament that has reconstituted due to inflammation and scarring. In some of those cases, the carpal tunnel pressure decreases after surgery but increases the second month due to the filling in of the defect.6 Occasionally, this reconstitution of the transverse carpal ligament is associated with increased volume in the carpal tunnel and there are no symptoms of carpal tunnel.4 Other complications include laceration of the median nerve, which can result in nerve deficits and a neuroma, ulnar artery laceration, and fracture of the hook of the hamate.7 When imaging is not performed preoperatively, failure to diagnose a mass in or around the carpal tunnel will result in the mass being visualized on postoperative studies.

SUGGESTED READINGS Berquist TH. Nerve compression syndromes. In Berquist TH (ed). MRI of the Hand and Wrist. Philadelphia, Lippincott Williams & Wilkins, 2003. Bordalo-Rodriques M, Amin P, Rosenberg AS. MR imaging of common entrapment neuropathies at the wrist. Magn Reson Imaging Clin North Am 2004; 12:265–279.

REFERENCES 1. Lee CH, Kim TK,Yoon ES, Dhong ES. Postoperative morphologic analysis of carpal tunnel syndrome using high resolution ultrasonography. Ann Plast Surg 2005; 54:143–146. 2. Cudlip SA, Howe FA, Clifton A, et al. Magnetic resonance neurography studies of the median nerve before and after carpal tunnel decompression. J Neurosurg 2002; 96:1046–1051. 3. Allmann KH, Horch R, Gabelmann A, et al. Morphology of the carpal tunnel. Movement studies in patients with constriction symptoms and healthy probands using MR tomography. Unhallchinurgie 1996; 22:5–11. 4. Wu HT, Schweitzer ME, Culp RW. Potential MR signs of recurrent carpal tunnel syndrome: initial experience. J Comput Assist Tomogr 2004; 28:860–864. 5. Bonel HM, Heuck A, Frei KA, et al. Carpal tunnel syndrome: assessment by turbo spin echo, spin echo and magnetization transfer imaging applied in a low-field MR system. J Comput Assist Tomogr 2001; 25:137–145. 6. Sanz J, Lizaur A, Sanchez Del Campo F. Post-operative changes of carpal canal pressure in carpal tunnel syndrome: a prospective study with follow-up of 1 year. J Hand Surg [Br] 2005; 30:611–614. 7. Rowland EB, Kleinert JM. Endoscopic carpal tunnel release in cadavera: an investigation of the results of 12 surgeons with this training model. J Bone Joint Surg Am 1994; 76:266–268.

Scaphoid Fractures DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS Scaphoid fractures are the most common carpal bone fractures and usually result from a fall on an outstretched hand. The waist of the scaphoid is the most frequent site

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KEY POINTS Scaphoid fractures are treated operatively when there is displacement, comminution, malunion, or nonunion. ■ Kirschner wires and compression screws are used. ■ Complications of surgically treated scaphoid fractures include nonunion, avascular necrosis, SNAC wrist, and neuroma. ■ Sagittal cross sectional imaging is useful to detect the humpback deformity. ■ Avascular necrosis is difficult to diagnose and can be overlooked if the proximal fragment is sclerotic. MRI with intravenous contrast is more sensitive than routine MRI for diagnosis. ■

of fracture, followed by the proximal and the distal pole. The more proximal the fracture, the higher the risk of osteonecrosis in the proximal fragment, because the vascular supply to the scaphoid runs from distal to proximal. Instability of the fracture is characterized by greater than 1 mm of fragment displacement, a scapholunate angle of more than 60 degrees (normal, 30–60 degrees), and/or a radiolunate or capitolunate angle greater than 15 degrees (normal, 0 ± 15 degrees). Displaced fractures can lead to malunion or nonunion, which results in carpal collapse and degenerative arthritis. After casting, the scaphoid fracture should show healing within 20 weeks. If no healing occurs, surgical fixation is indicated. Fractures of the waist displaying more than 1 mm of displacement, comminution, angulation, or malrotation are treated with open reduction and internal fixation. Surgery can be performed via open procedure or arthroscopy. Options include closed reduction with percutaneous pinning or compression screw insertion,1 and open reduction with Kirschner wires or a compression screw. Comminuted fractures may require bone grafting. Most scaphoid fractures detected more than 4 weeks after injury are best treated surgically.

EXPECTED APPEARANCE ON IMAGING Posteroanterior and lateral radiographs (Fig. 107-30) along with an ulnarly deviated posteroanterior (scaphoid) view (Fig. 107-31) allow for assessment of alignment, nonunion, and avascular necrosis.The fracture may be located in the proximal, middle, or distal third. Hardware such as a pin or compression screw normally traverses the fracture site (see Figs. 107-30 and 107-31). The fragments should be reduced, and the fracture should heal over a few months. CT can be used to evaluate the fracture for nonunion and malunion when deciding if surgery is needed (Fig. 107-32) and after surgical intervention (Fig. 107-33). Use of metal reduction techniques such as higher kVp and mAs as well as narrower x-ray beam collimation and lower pitch setting improves evaluation of the postoperative scaphoid by CT.2 MRI is helpful for identifying avascular necrosis in the postoperative setting, although hardware artifact may make it difficult to evaluate (Fig. 107-34). Special techniques to reduce artifact on MRI have been described.3

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■ FIGURE 107-30

Scaphoid fracture after surgery with good result. A screw traverses the healed fracture on posteroanterior (A) and lateral (B) views without evidence of nonunion or avascular necrosis.

POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE Scaphoid nonunion, characterized by a lack of fusion at the surgical site, can be a complication of conservative treatment or surgical repair (see Fig. 107-32). There is often sclerosis and/or cyst formation at the margins of the fracture. Fractures of the waist of the scaphoid may collapse and dorsally angulate, resulting in a flexion (humpback) deformity (see Fig. 107-32). This is best

■ FIGURE 107-31 This scaphoid view shows postoperative pinning for the scaphoid fracture shown in Figure 107-34. The patient did well postoperatively with fracture healing and no avascular necrosis.

seen on sagittal CT and MRI studies. Osteotomies are performed when a humpback deformity is discovered. Dorsal intercalated segment instability (DISI) may also be seen. This should be diagnosed on a neutral lateral wrist radiograph. Nonunion leads to a pattern of instability and articular degeneration known as SNAC (scaphoid nonunion advanced collapse) wrist. Four progressive stages of SNAC wrist have been identified, including arthritis of the radial styloid, extension of the arthritic

■ FIGURE 107-32 There is a scaphoid fracture nonunion (arrow) with possible avascular necrosis in the proximal pole presenting as sclerosis on this sagittal CT reformatted image. There is also excessive dorsal angulation at the apex of the fracture consistent with a humpback deformity. These three criteria are indications for surgery.

■ FIGURE 107-33 Treated scaphoid fracture with traversing screw shows healed fracture with proximal scaphoid sclerosis that may represent avascular necrosis (arrow). The bone posteriorly is the adjacent displaced carpal bone.

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■ FIGURE 107-34 Scaphoid fracture. A, There is a subtle fracture of the scaphoid on this posteroanterior radiograph manifest as sclerosis and stepoff in the waist portion (arrow). B, Coronal, T1weighted MR image shows the fracture with low signal intensity in the proximal pole (arrow). C, The entire scaphoid enhances after intravenous administration of gadolinium (arrow) on this T1-weighted, fat-suppressed image. The patient had a scaphoid pinning and did well postoperatively with fracture healing and no avascular necrosis as shown in Figure 107-31.

change to the scaphoid fossa of the radius, capitolunate arthritis, and diffuse carpal arthritis. Avascular necrosis can result with or without nonunion. It is usually seen in the proximal portion of the scaphoid. Sclerosis of the proximal fragment on radiographs or CT suggests the presence of avascular necrosis, but this is not always a specific finding.4 MRI with intravenous contrast can be useful in this setting.5 If the proximal fragment shows low signal intensity on T1 and T2 weighting without contrast medium enhancement, it is likely affected by avascular necrosis. However, contrast enhancement and high signal intensity on T2 weighting are not always specific

for viability (see Fig. 107-34). Avascular necrosis is more accurately diagnosed by intraoperative assessment, and, when diagnosed, it is treated with bone grafting. MRI can also be used to detect avascular necrosis in cases of nonunion treated with a vascular pedicle graft.6 Nonviable or fragmented proximal poles are treated with salvage procedures that include fragment excision, intercarpal arthrodesis, and proximal row carpectomy. Adhesions cause stiffness, nerve damage, and development of a neuroma at the surgical site. Silastic implants are no longer used because they cause synovitis that produces bone and cartilage destruction (Fig. 107-35).

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Postsurgical Imaging and Complications computed tomography imaging of the wrist. J Comput Assist Tomogr 2006; 30:850–857. 5. Cerezal L, Abascal F, Canga A, et al. Usefulness of gadoliniumenhanced MR imaging in the evaluation of the vascularity of scaphoid nonunions. AJR Am J Roentgenol 2000; 174:141–149. 6. Anderson SE, Steinbach LS, Tschering-Vogel D, et al. MR imaging of avascular scaphoid nonunion before and after vascularized bone grafting. Skeletal Radiol 2005; 34:314–320.

Postoperative Evaluation of Carpometacarpal, Metacarpal, and Phalangeal Trauma including the Surrounding Soft Tissue Structures DESCRIPTION, INDICATIONS, CONTRAINDICATIONS, PURPOSE, UNDERLYING MECHANICS

■ FIGURE 107-35

Silastic implant for scaphoid fracture caused Silastic synovitis. Coronal T1-weighted (A) and gradient-echo (B) MR images demonstrate the low signal intensity Silastic implant (arrows). There was a reaction to the Silastic material that produced bone destruction, including the cyst in the lunate (arrowhead). (Courtesy of Javier Beltran, MD, Brooklyn, NY.)

SUGGESTED READINGS Amadio PC,Taleisnik J. Fractures of the carpal bones. In Green DP, Hotchkiss RN, Pederson WC (eds). Green’s Operative Hand Surgery, 4th ed. New York, Churchill Livingstone, 1999. Gelberman RH, Wollock BS, Siegel DB. Current concepts review: fractures and nonunions of the carpal scaphoid. J Bone Joint Surg Am 1989; 71:1560–1565.

REFERENCES 1. Herbert TJ, Fisher WE. Management of the fractured scaphoid using a new bone screw. J Bone Joint Surg Br 1984; 66:114–123. 2. Buckwalter KA, Parr JA, Choplin RH, Capello WN. Multichannel CT imaging of orthopedic hardware and implants. Semin Musculoskelet Radiol 2006; 10:86–97. 3. Olsen RV, Munk PL, Lee MJ, et al. Metal artifact reduction sequence: early clinical applications. RadioGraphics 2000; 20:699–712. 4. Cheung YY, Naspinsky SR, Goodwin DW, et al. Increased radiodensity of the proximal pole of the scaphoid: a common finding in

Nondisplaced fractures of metacarpals and phalanges that do not extend to the articular surface are often treated conservatively with immobilization. Surgery is usually indicated for unstable fractures of the metacarpals and phalanges. Fractures with articular stepoff, open fractures, displaced or angulated fractures, those with bone loss or shortening, as well as multiple fractures or joint displacement usually require open reduction and internal fixation. Most fractures can be treated with initial traction and then percutaneous fixation techniques. Hardware used include Kirschner wires, plates, and screws that are placed so that they avoid the tendons, blood vessels and nerves. Kirschner wires are eventually removed and therefore are either cut off under the skin or protrude above the skin surface. Some intra-articular fractures may also be stabilized with hardware placed arthroscopically. Arthritis of the thumb carpometacarpal joint can be treated with resection arthroplasty, ligament reconstruction, and tendon interposition with the entire flexor carpi radialis tendon (Fig. 107-36). The flexor carpi radialis

KEY POINTS Surgery is indicated for unstable fractures of the metacarpals and phalanges. ■ Kirschner wires, plates, screws, and external fixators are used for fractures of the hand. ■ Three views of the affected bone are recommended for evaluation. ■ There should not be a stepoff at the joint surface. ■ MRI and ultrasonography are useful for evaluation of ligament and tendon repairs in the hand. ■

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■ FIGURE 107-36 Postoperative appearance of trapeziometacarpal arthroplasty using the flexor carpi radialis tendon. The trapezoid has been resected (arrow). There is a hole drilled at the base of the second metacarpal through which the reinforcing tendon traverses (arrowhead).

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■ FIGURE 107-37 Rolando fracture at the base of the first metacarpal treated with Kirschner wires. The fracture line is still visualized, and there is some callus formation around the site (arrow).

tendon is used for reconstruction and interposition. A partial trapezoidectomy is provides excellent pain relief and restoration of function. No morbidity is usually observed with use of the entire flexor carpi radialis tendon.1 Fractures at the carpometacarpal joints are often unstable and require surgery. Frank or subtle dislocations may be present in this region. Fractures at the base of the first metacarpal include the Bennett’s fracture, which is a small intra-articular avulsion fracture at the attachment of the first metacarpocarpal ligament that produces a single fragment with volar lip fracture. Bennett’s fractures are often treated with closed reduction, but if the volar lip fragment involves more than 25% to 30% of the articular surface, it is considered unstable and screw fixation can be performed. The comminuted fracture at the base of the first metacarpal that extends to the carpometacarpal joint is called the Rolando fracture. Rolando’s fractures are considered unstable and are treated with open reduction and internal fixation (Fig. 107-37). Unstable fractures of the metacarpal shafts usually angulate with the apex dorsal. This is due to pull by wrist extensors proximally and interosseous muscles and long finger flexors distally. Many of these fractures are treated with immobilization. Open reduction and internal fixation is indicated if there is severe dorsal angulation. Fractures of the metacarpal head are intra-articular, and precise reduction is indicated. Large fragments are treated with open reduction and internal fixation using Kirschner wires. Metacarpophalangeal joints that have comminuted fractures or arthritis can be treated with fusion using pins, wires, and bone graft (Fig. 107-38).

2029

■ FIGURE 107-38 Postoperative appearance in psoriatic involvement of the hand. Trapeziometacarpal arthroplasty (arrowhead) with first metacarpophalangeal and fourth proximal interphalangeal joint fusions with Kirschner and cerclage wires for arthritis (arrows). Note the distal interphalangeal joint erosions characteristic of psoriatic arthropathy.

Fractures that involve the base of a proximal phalanx that extend to the articular surface are unstable and treated surgically. Phalangeal shaft fractures may be treated surgically if they are comminuted or displaced (Fig. 107-39). Fractures of the mid proximal phalanges often angulate with the apex volar owing to forces from the extensor tendons and intrinsic muscles. Proximal interphalangeal joint injuries are usually treated conservatively unless they are severely comminuted with large fracture fragments.2 The gamekeeper’s thumb represents a tear of the ulnar collateral ligament.This is caused by a valgus stress.The ligament may avulse off of the base of the first metacarpal or may be disrupted distally without bony avulsion (Fig. 107-40).

■ FIGURE 107-39 Posteroanterior, oblique, and lateral radiographic views of a healed comminuted fracture of the diaphysis of the fourth proximal phalanx after open reduction and internal fixation with side plate and screws.

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Nondisplaced bony avulsions are immobilized in a cast or splint while displaced fragments are pinned back to the parent bone.3,4 Partial ligament tears are treated with immobilization for 2 to 3 weeks. A complete ligament tear may remain near the proximal phalanx under the adductor aponeurosis or can displace superficial to the adductor aponeurosis. The latter arrangement is called a Stener lesion.5 Ligament healing is prevented when there is interposition of the adductor aponeurosis between the ligament and the bone (see Fig. 107-40). This type of lesion requires reattachment of the ligament to the proximal phalanx under the adductor aponeurosis with surgical reduction and internal fixation. It is ideal to perform this surgery within 10 days of injury. Fractures that are treated surgically in the distal phalanx include a type II hyperflexion fracture of the base of the distal phalanx that involves more than a third of the articular surface or the type III fracture called a mallet finger, which is a hyperextension injury of the articular surface that usually involves more than half of the articular surface.

EXPECTED APPEARANCE ON IMAGING ■ FIGURE 107-40 Stener lesion that was surgically repaired. Coronal, T1-weighted (A) and T2-weighted (B) MR images of the thumb demonstrated a disrupted retracted ulnar collateral ligament of the thumb consistent with a Stener lesion. The ligament lies over the adductor hood, indicating a surgical lesion (arrows).

■ FIGURE 107-41 Flexor carpi radialis tendon repair re-tear. Coronal T1-weighted (A), axial T1-weighted (B), and axial T2-weighted (C) MR images demonstrate the retracted flexor carpi radialis tendon after repair (arrows). Note the micrometallic artifact at the tendon end (arrowhead). (Courtesy of Mark Skirgaudas, MD, Hartford, CT.)

After surgery, the metacarpals and phalanges as well as the neighboring articulations should be restored to near anatomic alignment without articular subluxation or dislocation. It is best to do posteroanterior, lateral, and oblique radiographic views of the region (see Fig.107-39). Joint surfaces should be reduced without stepoff. Radiographic

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evaluation requires serial comparison of fracture alignment and hardware location. MRI or ultrasonography are useful for evaluation of ligament and tendon healing after surgical repair.These structures may thicken but should appear continuous. On MRI, the signal intensity will decrease with time. Surrounding hardware and micrometallic artifacts related to surgical instrument placement during repair may make MRI less reliable for evaluation.

POTENTIAL COMPLICATIONS AND RADIOLOGIC APPEARANCE Each follow-up examination should be scrutinized for hardware fractures, displacement, or pullout. Fracture alignment changes should be noted. Ligament and tendon re-tears present as partial- or full-thickness loss in continuity of the structure after breakdown of a suture repair on MRI and ultrasonography (Fig. 107-41). The tendon or ligament may retract from its attachment site. Scarring around ligament and tendon tears along with involvement of adjacent structures by scar, seen with MRI or ultrasonography, should be noted (Figs. 107-42 and 107-43). In one study of flexor tendon repair of the hand by MRI,6 MRI showed isolated low signal intensity peritendinous adhesions as a frequent finding around intact tendons. Tendon ruptures were of two types: frank rupture or elongated scar tissue that the authors called callus. Tendon gaps were significantly larger in frank rupture. With elongated fibrous scarring, there was a thin fibrous continuity to the tendon. Tenolysis was used for short and mature callus. MRI is useful for evaluating partial or complete tears of the collateral ligaments around the metacarpophalangeal joints of the fingers and their surgical

■ FIGURE 107-42 Previously repaired scarred flexor tendon of the left thumb. The flexor tendon is dynamically not working smoothly because of the repair. Postoperative ultrasound image shows scarring/sutures and loss of clarity between the superficialis and profundus tendons (arrow). (Courtesy of Gina Allen, MD, Birmingham, England.)

complications.7 Infection is rare but should be considered when there is bone destruction, cortical loss or periosteal reaction, lucency surrounding pins, or soft tissue swelling. Abscesses present with fluid collections that can be identified by ultrasonography, CT, or MRI.

■ FIGURE 107-43

Excess scar tissue after flexor digitorum profundus tendon repair with contracture of the finger. Sagittal T1-weighted (A) and axial T2-weighted (B) MR images of the finger demonstrate intermediate signal intensity scar tissue in the surgical region (arrows).

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SUGGESTED READINGS Ebrahim FS, De Maeseneer M, Jager T, et al. US diagnosis of UCL tears of the thumb and Stener lesions:Technique, pattern-based approach, and differential diagnosis. RadioGraphics 2006; 26:1007–1020. Gutow AP, Slade JF, Mahoney JD. Phalangeal injuries. In Trumble T (ed). Hand Surgery Update 3: Hand, Elbow and Shoulder. Rosemont, IL, American Society for Surgery of the Hand, 2003, pp 1–27.

Markiewitz AD. Metacarpal fractures. In Trumble T (ed). Hand Surgery Update 3: Hand, Elbow and Shoulder. Rosemont, IL, American Society for Surgery of the Hand, 2003, pp 29–35.

REFERENCES 1. Varitimidis SE, Fox RJ, King JA, et al.Trapeziometacarpal arthroplasty using the entire flexor carpi radialis tendon. Clin Orthop Relat Res 2000; 370:164–170. 2. Blazar PE, Steinberg DR. Fractures of the proximal interphalangeal joint. J Am Acad Orthop Surg 2000; 8:383–390. 3. Kozin SH, Bishop AT. Gamekeeper’s thumb: Early diagnosis and treatment. Orthop Rev 1994; 23:797–804. 4. Weiland AJ, Berner SH, Hotchkiss RN, et al. Repair of acute ulnar collateral ligament injuries of the thumb metacarpophalangeal joint with an intraosseous suture anchor. J Hand Surg [Am] 1997; 22:585–591.

5. Stener B. Skeletal injuries associated with rupture of the ulnar collateral ligament of the metacarpophalangeal joint of the thumb: a clinical and anatomical study. Acta Chir Scand 1963; 125: 583–586. 6. Drape JL, Silbermann-Hoffman O, Houvet P, et al. Complications of flexor tendon repair in the hand: MR imaging assessment. Radiology 1996; 198:219–224. 7. Theumann NH, Pessis E, Lecompte M, et al. MR imaging of the metacarpophalangeal joints of the fingers: evaluation of 38 patients with chronic joint disability. Skeletal Radiol 2005; 34:210–216.

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The Postoperative Hip

Derek R. Armfield, Jon K. Sekiya, Marc J. Philippon, Eoin C. Kavanagh, and George Koulouris

Postoperative Imaging in Arthroscopic Hip Surgery Derek R. Armfield, Jon K. Sekiya, and Marc J. Phillipon Although first described in 1931, hip arthroscopy has only recently gained acceptance as a major tool for diagnosing and treating hip disorders, especially for the athlete. Consequently, the diagnosis of intra-articular pathology, particularly labral tears, has increased. MR arthrography is the accepted modality for the definitive evaluation of labral injury.1–3 Patients with labral injuries often undergo labral débridement for symptomatic treatment.4 It is known that injury to fibrocartilaginous structures in other joints can cause increased contact forces across the joint (i.e., glenoid labrum, knee meniscus) and can predispose to arthritis.5,6 The exact etiology of acetabular labral tears and the relation to the development of osteoarthritis is unclear and unique for each patient, but several theories have been postulated, including trauma, degeneration, femoroacetabular impingement, and rotational capsular laxity. Therefore, the concept of labral repair is increasing in an effort to preserve joint mechanics and avoid the longterm possibility of the development of osteoarthritis.7 Currently, treatment is primarily directed toward pain relief and long-term studies of the efficacy of labral repairs and prevention of osteoarthritis do not exist. One of the authors (M.J.P.) has significant experience with repair of labral tears with initial good results.7–9 A recent 2-year study compared patients who underwent labral debridement with those who underwent labral repair and found that the repair group had better outcome at 2 years (80% vs. 28% excellent results and less radiographic findings of osteoarthritis), prompting the authors to recommend labral repair over resection.10 Repair techniques of the labrum are based on experience and analogous arthroscopic techniques in the

shoulder and knee. For example, suture banding of intrasubstance labral tears is similar to meniscal repairs and using suture anchors to reattach detached labral tears is similar to a glenoid labral repair in the shoulder (Fig. 108-1). The labrum, however, is not the only intra-articular structure that can be injured or cause pain. Chondral injuries are another obvious source of pain and injury. Recently, tears of the ligamentum teres have been found to be a significant source of intra-articular hip pain.11 Capsular injuries of the hip have been associated with hip injury and subject to repair as well. Techniques to treat these nonlabral injuries include microfracture and cartilage transfer techniques, bony arthroscopic osteochondroplasty for femoroacetabular impingement (i.e., similar to subacromial decompression), and capsular shrinkage or plication of the hip for rotational instability (i.e., similar to shoulder capsule surgery).

KEY POINTS Arthroscopic treatment of hip pathology is increasing and addresses the labrum and other structures, including ligamentum teres, joint capsule, cartilage, and femoroacetabular impingement. ■ MRI evaluation of the hip should include description of tears as either intrasubstance or detached, along with the length and extent of intact tissue to guide preoperative planning. ■ Femoroacetabular impingement is a more recently recognized structural abnormality associated with labral tears and chondral injury that can be treated arthroscopically and with open procedures. ■ Each hip should be carefully assessed for femoroacetabular impingement because radiographic findings may be subtle. ■ Ligamentum teres pathology can be a significant source of hip pain and should be evaluated. ■ Capsular laxity is often a clinical diagnosis, although some MR findings may exist. ■ Cartilage injuries can be difficult to detect with MRI. ■

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B ■ FIGURE 108-1 A, Oblique axial, T2-weighted, fatsaturated MR image shows a complex labral tear with intrasubstance tearing (white arrow) and detachment that underwent intrasubstance suture banding and reattachment. B, Arthroscopic image shows a probe in a labral tear (black arrows) that was surgically treated with intrasubstance suture banding (C, black arrows).

C

Although the common end point and manifestation of clinical symptoms may be related to labral injury, one should evaluate all structures of the hip, including surrounding soft tissues, because treatment may involve several anatomic problems. This chapter reviews the current leading edge arthroscopic techniques and imaging findings associated with intra-articular hip pathology to form a basis for understanding this new and rapidly changing field.

LABRAL INJURY Labral injuries are a common source of hip pain and intraarticular pathology, often presenting with mechanical symptoms. The diagnosis is largely clinical and similar to patients with meniscal injury. Patients may have distinct mechanical symptoms or subtle positional symptoms or dull pain. MR arthrography is currently the preferred imaging modality for preoperative assessment with improved sensitivity and specificity over nonarthrogram MRI.

Indications, Contraindications, Purpose, and Underlying Mechanics Patients with intra-articular pathology are often treated for several months before the diagnosis of labral abnormalities is made. One study of athletes showed that nearly 60% required 7 months before the source of pain was recognized.12 Patients commonly experience deep hip pain that can emanate toward the groin. The log-rolling test for labral pathology is the most specific maneuver because it prevents confounding stressing of surrounding structures. Arthroscopy is typically performed under general anesthesia with the patient in supine or lateral position. Multiple ports are available, with the two most common being the anterior and the anterolateral portals. Mild distraction is used to access the intra-articular portion of the joint.13 Contraindications to arthroscopy include, are but not limited to, advanced arthritis, superficial infection, obesity, and joint ankylosis. Biomechanical studies suggest that the labrum has an important role in hip mechanics.14 It provides negative

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intra-articular pressure by maintaining seal, enhancing joint stability and containment of the femoral head. Removal of labral tissue can have deleterious biomechanical effects on cartilage. Based on techniques from the shoulder and knee, labral repair techniques have been applied to the hip. New techniques comprise primarily intrasubstance suture banding for intrasubstance tears and suture anchor reattachment for detached labral tears. Some tears are complex and may undergo several repair techniques, including débridement (Figs. 108-2 to 108-4). Our preoperative MRI evaluation includes evaluation of the type of tear (intrasubstance vs. detached), length, location, and assessment of amount of residual tissue, which helps the surgeon determine which type of procedures may be used.

Expected Appearance on Relevant Modalities Postoperative imaging of the labrum requires understanding of the techniques utilized. Postoperative MR arthrography in patients who have undergone traditional labral débridement portray the normal triangular labrum as a blunted structure with volume loss proportional to the degree of surgical resection. It is not uncommon for two thirds of the preoperative volume of the labrum to be resected. The residual tissue should still have decreased signal intensity on T1- and T2-weighted images, but the normal triangular morphology no longer exists. It is important to ensure that the residual labral tissue remains firmly adhered to the acetabular margin. The postoperative appearance of the labrum that has undergone surgical intervention with suture banding or acetabular reattachment can have a different appearance. In these cases the volume of labral tissue should

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be similar to that shown on preoperative imaging. The labral morphology, however, may be altered with loss of the normal triangular structure. The residual labral tissue should be closely approximated to the acetabular rim. Intrasubstance suture material may have mildly increased signal on long and short echo time sequences compatible with suture and granulation tissue, which can last months or longer; but unless fluid and contrast equivalent signal intensity is present, caution should be exercised before diagnosing a recurrent tear (Fig. 108-5).

Potential Complications and Radiologic Appearances Complications from prior surgery include primarily recurrent tears. Interposition of contrast/fluid between the labrum and the acetabular margin or within the labral tissue itself suggests recurrent detachment or tearing (Fig. 108-6). Suture material and granulation tissue may have increased signal on long and short echo time images but generally not that of fluid or intensity on long echo time sequences, as in the case of recurrent tears. Postoperative adhesions may also occur between the labrum and capsule, which appear as thin, fibrous strands and may be symptomatic (Fig. 108-7). Complications associated with hip arthroscopy include postoperative bleeding, infection, soft tissue injury, and nerve injury (traction or direct) as well as traumatic injury to the joint from scope placement. Postprocedural imaging is rarely performed except for refractory cases and persistent pain. Sometimes in cases of nerve injury, MRI may be obtained to exclude a macroscopic abnormality. Postoperative myositis ossificans has been seen owing to localized trauma and bleeding. In these rare instances, matured ossification can be resected (Fig. 108-8).

■ FIGURE 108-2 A, Oblique axial, T2-weighted, fat-saturated MR image depicts capsular-side-only tear of the labrum treated with débridement (arrowhead). B, Postoperative images in same patient show healing of previous tear (arrowhead).

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■ FIGURE 108-3 Detached anterosuperior labral tear seen in oblique axial (white arrow) (A) and coronal (black arrow) (B) planes before surgery that was treated with suture anchor reattachment. C, Fluoroscopic spot film demonstrates placement of suture anchor in the acetabular rim (black arrow). D, Oblique axial, T2-weighted, fat-saturated MR image shows minimal artifact from suture anchor within the acetabulum (black arrows).

CARTILAGE INJURY Chondral injuries of the hip may be difficult to see owing to the relative thinness and curvilinear articular surfaces of the hip with cross-sectional imaging. Chondral injuries are often associated with labral tears and involve the anterosuperior aspect of the hip. This area is not evaluated with weight-bearing anteroposterior views of the hip; therefore, cross-sectional imaging and/or arthroscopic visualization is needed when a chondral injury is clinically suspected and radiographs are negative. MR arthrography can help identify chondral injury, and the sensitivity is decreased as compared with the gold standard of arthroscopy.16,17 Delamination cartilage injuries have also been described using MR arthrography. Multidetector or multichannel CT allows for higher spatial resolution to evalu-

ate cartilage with initial promising results when applied to dysplastic hips with CT arthrography.18

Indications, Contraindications, Purpose, and Underlying Mechanics Arthroscopic techniques for repair are limited and consist primarily of chondroplasty for low-grade, partial-thickness defects and microfracture for full-thickness defects or an unstable flap lesion on a weight-bearing surface.19 Occasional arthritis may be an indication for intervention. Chondroplasty is performed with either a bur or a radiofrequency device to stabilize cartilage defects. The technique of microfracture has been used successfully in the knee and other joints. This technique utilizes a surgical

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cases. Cartilage injuries are often associated with labral problems. Postoperative appearance of microfracture technique in the first few months includes subchondral marrow edema (Fig. 108-9).

Potential Complications and Radiologic Appearances Postoperative imaging is usually limited. Radiographs can be used to assess for osteoarthritis progression.

CAPSULAR INJURY

■ FIGURE 108-4 Macerated tear (white arrows) of anterosuperior labrum treated with combination of débridement, intrasubstance sutures, and suture anchor reattachment.

awl to puncture the subchondral bone, which allows marrow blood (and associated undifferentiated stem cells) to form a clot and ultimately develop into fibrocartilage (not articular cartilage). Anecdotally, defects have been repaired using chondral plugs. Contraindications include inabililty to follow the extensive postprocedural rehabilitation, partial-thickness lesion, and lesion with an underlying bone defect.

Expected Appearance on Relevant Modalities Again due to the nature of spherocity and thinning, cartilage defects can be difficult to image. In our experience, MR arthrography often underestimates the degree of chondrosis when compared with arthroscopy. Rarely is postprocedural imaging performed and only in refractory

Although considered a stable joint due to large bony contact areas and coverage, the hip can be subject to soft tissue instability. The diagnosis of instability is often clinical and difficult to diagnose.8 Instability may be due to chronic overuse from microinstability in athletes or culminate in hip pain from generalized ligamentous laxity in the average patient (advanced cases related to connective tissue disorders would be included in this category). Soft tissue restraints of the hip include the iliofemoral ligament, labrum, and ligamentum teres as well as surrounding musculature. The iliofemoral ligament form the joint capsule anteriorly and are usually the injured structures that undergo repair.

Indications, Contraindications, Purpose, and Underlying Mechanics The role of arthroscopic treatment is unclear at this time but consists of either thermal capsulorrhaphy or suture plication. Thermal treatment uses a radiofrequency probe that heats the collagen of capsule causing collagen damage, which the body subsequently heals over time with decreased laxity. This technique has been used in the shoulder with marginal success, but in the hip (potentially due to the much thicker capsule than seen in the shoulder) the technique seems to work well. Suture plication may be used in conjunction or separately from thermal treatment. The medial and lateral limbs of the iliofemoral ligament are sutured together until the appropriate tension of the capsule is achieved as assessed during arthroscopy.8

■ FIGURE 108-5 Oblique axial image from an MR arthrogram in a 30-year-old professional football player shows postoperative granulation tissue seen on T1(left) and T2- (right) weighted images within the labral substance (white arrowheads) 2 months after intrasubstance banding.

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■ FIGURE 108-6 A, Oblique axial, T2-weighted image from an MR arthrogram in a 21-year-old college running back shows diminutive appearance of labrum (white arrow) from prior surgery with detachment of the acetabular rim (white arrowhead). B, Intraoperative image of anterosuperior detached labral tear (white arrows) with diminutive scarred morphology (white arrowheads) from prior débridement and residual separation from acetabular rim (black arrows). C, Residual labral tissue (black arrows) was reattached with suture anchors. This case shows the importance of trying to restore biomechanical integrity.

Expected Appearance on Relevant Modalities Hip instability is usually a clinical diagnosis confirmed with arthroscopy. Some have found that gentle traction of the hip under fluoroscopy may show asymmetric joint space widening, which can be associated with instability. Our preliminary investigations have found that the morphology of the anterior capsule can be altered in cases of capsular laxity. In our experience, the anterior capsule without laxity is of uniform thickness and does not demonstrate undersurface fraying or perforation. In cases of laxity, the lateral aspect of the joint capsule is hypertrophic with an irregular undersurface (Fig. 108-10). Postoperatively, the capsule appears thicker as compared with preoperative imaging using either thermal treatment or plication (Fig. 108-11). Depending on the type of suture there is minimal magnetic field inhomogeneity artifact (Fig. 108-12).

■ FIGURE 108-7 Oblique axial, T2-weighted image from a postoperative MR arthrogram shows arthroscopically proven adhesions (black arrowhead) between the capsule and previously repaired anterosuperior labrum (white arrow).

Potential Complications and Radiologic Appearances Occasionally, patients may experience an inflammatory reaction, possibly to the suture material, and develop synovitis, resulting in hip pain. In our experience this is

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■ FIGURE 108-8

A, Oblique axial, T2-weighted, fat-saturated MR image shows hyperintensity involving the proximal anterior capsule at a portal site consistent with postsurgical hematoma (black arrows). B, Anteroposterior radiograph shows mature ossification of myositis ossificans (black arrows) due to soft tissue hemorrhage at a portal site. Treatment with resection was successful.

FEMOROACETABULAR IMPINGEMENT

■ FIGURE 108-9

Coronal T2-weighted, fat-saturated image from an MR arthrogram shows advanced chondrosis of the femoral head (black arrow) with postoperative marrow edema in the femoral head (white arrow) from microfracture technique.

not seen on conventional MR arthrography. Postcontrast imaging with an intravenous contrast agent may have a role. Occasionally, additional surgery may be needed to remove excessive granulation tissue. Unlike the shoulder, thermal capsulorrhaphy of the hip capsule has been used successfully without complications.

Femoroacetabular impingement is a recently recognized source of hip pain that is related to labral tears. The exact etiology is controversial and could be congenital, acquired during trauma in skeletal development, or even secondary to underlying soft tissue injury with subsequent bone remodeling. There are two basic types: type 1 (cam) and type 2 (pincer), with cam impingement being more common.20,21 The radiographic findings can be very subtle and best seen as aspherocity on anteroposterior radiographs or loss of offset of the normal femoral head-neck junction on a cross-table lateral radiograph.22 Cross-sectional imaging on CT and MRI can be used to generate an alpha angle to evaluate the degree of offset. Pincer impingement is often associated with acetabular retroversion best seen on a wellcentered anteroposterior radiograph of the hip showing a crossover sign where the anterior bone of the acetabular rim projects beyond the margin of the posterior rim.23 This can be seen with cross-sectional imaging as well but often must be measured at the superior aspect of the acetabular, not the midpoint; otherwise, it looks normal. Two basic procedures are available for treatment.20,21,24,25 Open osteoplasty requires an extensive approach including a trochanteric osteotomy and, more recently, an allarthroscopic version called osteochondroplasty. The second technique essentially removes the bone bump or excessive acetabular coverage. Recent studies have shown the accuracy of bone removal is similar to that in an open procedure. In general, one can remove 30% of the diameter of the femur without risk of postintervention fracture.26 Postoperative radiographs can assess the degree of residual bony impingement (Fig. 108-13).

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■ FIGURE 108-10 A, Oblique axial, T2-weighted, fat-saturated MR image with irregular anterior capsule undersurface (white arrows) with nonuniform thickness compatible with anterior capsular laxity on this surgically proven case. B, Normal-appearing capsule in a different patient for comparison. Note smooth undersurface and uniform thickness of the anterior capsule (white arrows) in this surgically proven case without laxity.

■ FIGURE 108-11 A, Coronal T2-weighted, fat-saturated image from MR arthrogram shows markedly attenuated iliofemoral ligament (white arrows) and capsule that was treated with thermal capsulorrhaphy. B, Note the postoperative hypertrophic change and enlarged morphology of the ligament (white arrows) as compared with the preoperative state 6 months earlier.

Indications, Contraindications, Purpose, and Underlying Mechanics Before surgical intervention patients often have failed conservative management, which is not surprising owing to the underlying mechanical process. The choice between open and arthroscopic treatments is primarily dependent on the surgeon’s preference. Similar to situations that occur in many other fields, arthroscopic treatment appears to offer similar treatment with decreased recovery time and iatrogenic trauma. Contraindications

are similar to those of hip arthroscopic procedures in general, as described earlier. Whatever method is utilized, it is important that all relevant pathology is addressed, including labral and chondral injuries. The goal of the surgery is to remove the mechanical source of impingement, which in the case of cam type impingement occurs at the femoral head/neck junction. It is essential to restore the appropriate contour and remove the bony bump. This is performed using an arthroscopic motorized bur. Once the procedure is

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■ FIGURE 108-12

A, Coronal T2-weighted, fat-saturated MR image shows attenuated iliofemoral ligament (white arrows) that was treated with suture plication. B, Postoperative image shows minimal artifact from suture material with enlarged appearance of the iliofemoral ligament (white arrows), implying improved structural integrity.

■ FIGURE 108-13

A, Anteroposterior radiograph of a patient with degenerative change and femoroacetabular impingement (white arrowhead) of the hip who underwent arthroscopic osteochondroplasty. B, Postoperative appearance demonstrated removal of impinging bony excrescence (white arrowhead).

performed, the hip joint is evaluated during arthroscopy with passive range of motion to ensure clearance at the femoral head/neck junction. Open procedures often require transient dislocation of the hip for exposure of the femoral head/neck junction and removal with a chisel to accomplish the same means. Unfortunately, the open procedure requires a greater trochanteric osteotomy, which violates the hip abductor attachments. Although these are rigidly fixed after comple-

tion of the procedure, nonunions have been described. In addition, with either open or arthroscopic surgery, care should be exercised to protect as many perforating vessels as possible so that the blood supply to the femoral head is preserved. Pincer-type impingement can be treated arthroscopically in a similar fashion using an osteotome and motorized bur (Fig. 108-14).24 The open surgical approach counterpart is an acetabular osteotomy.

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be visualized with MRI. Intra-articular bleeding is a possible complication as well but rarely imaged. If the original symptoms persist, an MR arthrogram may demonstrate recurrent labral injuries or progression of chondrosis.

LIGAMENTUM TERES INJURY Tears of the ligamentum teres are a recently recognized source of hip pain. In one large series, this was the third most common cause of hip pain among athletes.11 Other studies have shown that tears of the ligamentum teres can affect at least 8% of patients.27 These tears have been arthroscopically classified previously as complete, partial, and degenerative.

■ FIGURE 108-14 Intraoperative image shows arthroscopic burring of prominent acetabular rim (white arrows) before labral reattachment.

Expected Appearance on Relevant Modalities A recent study found no increased fracture risk when less than 30% of the femoral head/neck junction is removed. Postoperative appearances for arthroscopic repair demonstrate focal notched defects at the site of surgical intervention. Radiographs are obtained for documentation and assessment of the amount of bone removed.

Potential Complications and Radiologic Appearances If symptoms persist, recurrent labral injuries can be a source of this pain. Postoperative fractures would be a potential complication but are very uncommon. Excessive bone removal can be detected with radiographs. Postprocedural avascular necrosis during long open procedures is also a theoretical concern that could

■ FIGURE 108-15

Indications, Contraindications, Purpose, and Underlying Mechanics The role of the ligamentum teres is unclear. It does contain nerve fibers, and biomechanically it tightens with external rotation and, therefore, may play a role in joint stability, particularly if there is underlying rotational instability. Partial tears of the ligamentum teres are often treated by débridement with an arthroscopic shaver to remove excessive or irregular tissue, which may be a source of impingement or pain.8 Complete tears of ligamentum teres may also be resected and rarely reconstructed in patients in whom their hips undergo extremes of motion and are exposed to high axial forces, such as enthusiasts of the martial arts. In the past, partial tears have been difficult to diagnose with MR arthrography because there is little if any published literature. We recently found MR arthrography demonstrated good correlation with arthroscopy for detecting partial tears. Criteria for partial tears included abnormal increased signal on T2-weighted images and/or abnormal irregular morphology, depending on the presence of foveal hypertrophy, which is defined as greater than 2-mm medial extension of ligamentum teres tissue around a best fit circle of the femoral head on oblique axial images parallel to the femoral neck (Fig. 108-15).

A, Hypertrophic appearance of the ligamentum teres (black arrow) with abnormal signal and enlarged morphology extending several millimeters beyond a best fit circle of the femoral head, a useful measuring technique in our practice. B, Arthroscopic image of partially torn ligamentum teres (black arrow) in a different patient.

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■ FIGURE 108-16

A, Oblique axial, T2-weighted, fat-saturated MR image from MR arthrogram with hypertrophic and irregular appearance of partial torn ligamentum teres (white arrows) that was confirmed arthroscopically and débrided. B, Postoperative image 6 months later in same patient demonstrates smooth well-marginated appearance of the ligamentum teres (white arrows).

Expected Appearance on Relevant Modalities Postoperative imaging is often unremarkable using MR arthrography. The ligament often has a smooth surface with decreased volume due to partial resection. Signal characteristics on MR arthrography demonstrate uniform decreased T2 signal intensity (Fig. 108-16). Recurrent tears are a possibility.

Potential Complications and Radiologic Appearances No known complications of ligamentum teres débridement have been identified as of yet with MRI. Complications associated with arthroscopy in general, however, remain.

SUGGESTED READINGS Armfield DR, Towers JD, Robertson DD. Radiographic and MR imaging of the athletic hip. Clin Sports Med 2006; 25:211–239, viii. Kelly BT, et al. Arthroscopic labral repair in the hip: surgical technique and review of the literature. Arthroscopy 2005; 21:1496–1504. Kelly BT, Williams RJ 3rd, Philippon MJ. Hip arthroscopy: current indications, treatment options, and management issues. Am J Sports Med 2003; 31:1020–1037. Philippon MJ. New frontiers in hip arthroscopy: the role of arthroscopic hip labral repair and capsulorrhaphy in the treatment of hip disorders. Instr Course Lect 2006; 55:309–316.

REFERENCES 1. Petersilge CA. From the RSNA Refresher Courses. Radiological Society of North America. Chronic adult hip pain: MR arthrography of the hip. RadioGraphics 2000; 20(Spec No):S43–S52.

2. Czerny C, et al. Lesions of the acetabular labrum: accuracy of MR imaging and MR arthrography in detection and staging. Radiology 1996; 200:225–230. 3. Toomayan GA, et al. Sensitivity of MR arthrography in the evaluation of acetabular labral tears. AJR Am J Roentgenol 2006; 186:449–453. 4. McCarthy JC. The diagnosis and treatment of labral and chondral injuries. Instr Course Lect 2004; 53:573–577. 5. Baratz ME, Fu FH, Mengato R. Meniscal tears: the effect of meniscectomy and of repair on intraarticular contact areas and stress in the human knee: a preliminary report. Am J Sports Med 1986; 14:270–275. 6. Greis PE, et al. Glenohumeral articular contact areas and pressures following labral and osseous injury to the anteroinferior quadrant of the glenoid. J Shoulder Elbow Surg 2002; 11:442–451. 7. Kelly BT, et al. Arthroscopic labral repair in the hip: surgical technique and review of the literature. Arthroscopy 2005; 21:1496–1504. 8. Kelly BT, Williams RJ 3rd, Philippon MJ. Hip arthroscopy: current indications, treatment options, and management issues. Am J Sports Med 2003; 31:1020–1037. 9. Philippon MJ. New frontiers in hip arthroscopy: the role of arthroscopic hip labral repair and capsulorrhaphy in the treatment of hip disorders. Instr Course Lect 2006; 55:309–316. 10. Espinosa N, et al. Treatment of femoro-acetabular impingement: preliminary results of labral refixation. J Bone Joint Surg Am 2006; 88:925–935. 11. Byrd JW, Jones KS. Traumatic rupture of the ligamentum teres as a source of hip pain. Arthroscopy 2004; 20:385–391. 12. Byrd JW, Jones KS. Hip arthroscopy in athletes. Clin Sports Med 2001; 20:749–761. 13. Byrd JW. The role of hip arthroscopy in the athletic hip. Clin Sports Med 2006; 25:255–278, viii. 14. Ferguson SJ, et al. The influence of the acetabular labrum on hip joint cartilage consolidation: a poroelastic finite element model. J Biomech 2000; 33:953–960. 15. Lieberman JR, Altchek DW, Salvati EA. Recurrent dislocation of a hip with a labral lesion: treatment with a modified Bankart-type repair. Case report. J Bone Joint Surg Am 1993; 75:1524–1527. 16. Schmid MR, et al. Cartilage lesions in the hip: diagnostic effectiveness of MR arthrography. Radiology 2003; 226:382–386. 17. Beaule PE, Zaragoza E, Copelan N. Magnetic resonance imaging with gadolinium arthrography to assess acetabular cartilage delamination: a report of four cases. J Bone Joint Surg Am 2004; 86:2294–2298.

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18. Nishii T, et al. Fat-suppressed 3D spoiled gradient-echo MRI and MDCT arthrography of articular cartilage in patients with hip dysplasia. AJR Am J Roentgenol 2005; 185:379–385. 19. Crawford K, et al. Microfracture of the hip in athletes. Clin Sports Med 2006; 25:327–335, x. 20. Ganz R, et al. Femoroacetabular impingement: a cause for osteoarthritis of the hip. Clin Orthop Relat Res 2003; (417):112–120. 21. Lavigne M, et al. Anterior femoroacetabular impingement: part I. Techniques of joint preserving surgery. Clin Orthop Relat Res 2004; (418):61–66. 22. Meyer DC, et al. Comparison of six radiographic projections to assess femoral head/neck asphericity. Clin Orthop Relat Res 2006; 445:181–185. 23. Li, PL, Ganz R. Morphologic features of congenital acetabular dysplasia: one in six is retroverted. Clin Orthop Relat Res 2003; (416):245–253. 24. Philippon MJ, Schenker ML. A new method for acetabular rim trimming and labral repair. Clin Sports Med 2006; 25:293–297, ix. 25. Philippon MJ, Schenker ML. Arthroscopy for the treatment of femoroacetabular impingement in the athlete. Clin Sports Med 2006; 25:299–308, ix. 26. Mardones RM, et al. Surgical treatment of femoroacetabular impingement: evaluation of the effect of the size of the resection. J Bone Joint Surg Am 2005; 87:273–279. 27. Gray AJ, Villar RN. The ligamentum teres of the hip: an arthroscopic classification of its pathology. Arthroscopy 1997; 13:575–578.

Postoperative Imaging in Arthroplastic Hip Surgery Eoin C. Kavanagh and George Koulouris Radiographic evaluation of the hip, both before and after any operative procedure, is the cornerstone of radiologic assessment. Radiographic evaluation serves as the first line of investigation in the postoperative hip, providing an overall view of the hip joint, where the diagnosis is often made, before the introduction of cross-sectional imaging, which may be used for disease confirmation and determination of severity and extent. The relative ease of radiographic comparison allows for accurate monitoring of disease progression. Importantly, in the postarthroplasty patient, subtle changes are often indicators of loosening and thus hardware failure. More sophisticated imaging and image-guided interventions may then be used to determine the cause of hardware failure, primarily to exclude sepsis. The high prevalence of hip pathology and the general success of hip replacement surgery have resulted in hip arthroplasty becoming a routine procedure, with an estimated 170,000 such procedures performed on an annual basis in the United States as a primary procedure and approximately 35,000 as revision surgery.1 Although the types of prostheses continuously evolve, hip prostheses may be divided simply into unipolar, bipolar, and total arthroplasty, with the latter further divided into metal on polyethylene, metal on metal, and ceramic on ceramic systems. Hip fractures requiring orthopedic fixation are also very common, with many types of internal fixation devices currently available. Given sufficient time, all prostheses and fixation devices eventually fail. Because component

failure may have a protracted subclinical course, detecting any findings of malfunction relies heavily on routine radiographic assessment. Although these findings may be subtle, a high index of suspicion of hardware failure is critical. Close monitoring is paramount to prevent complications, which may limit the success of possible future revision surgery, such as the loss of adequate bone stock.

Indications, Contraindications, Purpose, and Underlying Biomechanics There are myriad indications for hip arthroplasty, including osteoarthritis, rheumatoid arthritis, gout, seronegative arthropathies, hemophilia, developmental dysplasia, and femoroacetabular impingement. Most fractures of the femoral neck and head will require operative internal fixation, with either dynamic hip screw placement or arthroplasty. Many operative procedures are also performed for avascular necrosis of the hip, depending on its severity, including core decompression, placement of vascularized fibular grafts, and arthroplasty. There are not many contraindications for arthroplasty and fracture fixation, but they include active sepsis at the operative site, bleeding diathesis, and concomitant medical illness rendering the patient unfit for anesthesia. The goal of these procedures is to restore the affected hip with normal biomechanics, thereby allowing the patient to ambulate more affectively.

Expected Appearance on Relevant Modalities The radiographic appearance of the postoperative hip should show the entire fixation device or prosthesis in at least two planes. These images should demonstrate the components in their entirety, extending above and beyond the hardware by several centimeters, such that adjacent soft tissues, bones, and cement restrictors may be analyzed. Typically, anteroposterior and lateral radiographs are obtained to evaluate the anatomic alignment of the prosthetic device and to check for any potential complications, such as periprosthetic fracture or malalignment. The strength of the radiograph includes the general overview

KEY POINTS The imaging assessment of the postoperative hip begins with the presurgical radiologic examination, which is often accompanied by sophisticated cross-sectional imaging studies. ■ After hip surgery, the radiograph is the most important imaging modality in routine and symptomatic assessment, with comparison with any prior radiographs with the prosthesis in situ critical. ■ Although the differential diagnostic possibilities of postarthroplasty pain are broad, mechanical, or aseptic, loosening is the most common condition confronting the clinician and radiologist. Because loosening is a diagnosis of exclusion, ensuring infection is not the cause of loosening is paramount and, as such, cross-sectional imaging, scintigraphy, and arthrocentesis may be required. ■

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that may be obtained, as well as the ability to directly compare for any changes, often subtle, with the most recent prior examination. Postoperative CT can be performed to evaluate hardware alignment, but usually postoperative radiographs will suffice. MRI with metal reduction techniques can be employed to evaluate the postoperative hip, but this modality is typically reserved for more complicated cases, as discussed later.

Potential Complications and Radiologic Appearance Detecting complications after hip fracture fixation and hip arthroplasty is the result of thorough clinical history taking and examination and with the judicious use of supportive radiologic and laboratory parameters. Again, as for the preoperative hip, radiologic examination begins with the basic radiographic examination, with an anteroposterior and lateral radiograph as a minimum. Routine radiographic surveillance after arthroplasty and fracture fixation commences in the acute postoperative period. This is repeated at regular intervals, with many prosthetic hips often observed clinically and radiographically on an annual basis for the life of the patient. Although the specific causes and modes of failure for an individual prosthesis vary, prosthetic failure most commonly manifests as loosening and, as such, radiographic assessment is aimed at the detection of this finding. The diagnosis and detection of sepsis has the critical therapeutic implication of requiring a two-stage revision arthroplasty, which is first performed with hardware removal and insertion of antibiotic-impregnated cement, followed by insertion of the new prosthesis 6 weeks later. This contrasts to the typical single-stage revision for all other causes of component failure. Imaging modalities thus available include arthrography, with the ability to also perform simultaneous arthrocentesis, ultrasonography, CT, MRI, and nuclear scintigraphy. Soft tissue pathologic processes should also be evaluated as possible sources of pain.

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in femoral component version of greater than 2 degrees is diagnostic when comparing views obtained with maximal external and internal rotation.5 Irrespective of the cause, loosening of a cemented prosthesis manifests as an increase in periprosthetic lucency at the bone-cement interface of 2 mm or more. Progression of lucency (even if less than 2 mm) or fracture of cement is also consistent with loosening.6 In the setting of revision arthroplasty, lucency greater than 2 mm is allowed, but reference in this instance should be made with the early postrevision radiographs. Ideally, the flange of the femoral stem should sit flush with the cut surface of the femoral shaft. Movement occurring inferior to this level, or subsidence, is consistent with femoral prosthesis loosening. Lucency adjacent to the femoral stem should be described with reference made to the standardized Gruen zones (Fig. 108-17).7 Insertion of a femoral component results in the well-known localized form of disuse osteopenia known as stress shielding, a phenomenon occurring secondary to the bypassing of mechanical forces. In most instances, only proximal loss occurs8; however, in a proportion of cases, loss of periprosthetic bone density along the entire femoral stem may result in loosening (Fig. 108-18). In these circumstances, the osteopenia is typically more prominent laterally along the femoral stem (Fig. 10819) and in the retroacetabular region, with the latter best appreciated with CT.9 Stress shielding may predispose to periprosthetic fracture, usually at the tip of the femoral component (Fig. 108-20). Note should be made that a distal femoral cement restrictor plug may be utilized, which acts to form a seal, preventing distal cement migration such that adequate contact with the prosthesis may be optimized. Often, a small focus of entrapped gas may be visualized and should not be confused as the consequence of infection. Although loosening of the femoral component may be simply evaluated on the standard anteroposterior and lateral

LOOSENING Aseptic, or mechanical, loosening is the most common cause for revision arthroplasty,2 followed by osteolysis (“particle disease”) and infection (septic loosening). Aseptic loosening is often a diagnosis of exclusion, when investigations for the cause of loosening are importantly negative for infection and the radiologic findings are not typical for osteolysis. Unfortunately, with respect to loosening, it is unrealistic to rely on radiographic observation to have the desired precision of detecting submillimeter motion, particularly within the first 2 years after replacement where early motion is equated with a universally poor outcome. This precise measurement is now possible with the use of template matching algorithms,3 further improved with the use of bone marking and stereometry.4 Despite these advanced methods, knowledge of the more familiar radiographic manifestations of loosening as assessed on observation is critical. An alteration in component position as when compared with prior radiographs is unequivocally diagnostic of loosening. In addition to this, motion on stress views is also diagnostic. On stress views obtained with CT, a difference

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■ FIGURE 108-17 Anteroposterior radiograph delineating the standard seven Gruen zones for the referencing of abnormality.

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■ FIGURE 108-18 Anteroposterior radiograph of the left hip demonstrating stress shielding at both trochanters, with periprosthetic lucency extending distally, ultimately resulting in loosening of the femoral stem (arrowheads). ■ FIGURE 108-20 Oblique anteroposterior radiograph of the right hip demonstrating a displaced periprosthetic fracture as a consequence of loosening.

■ FIGURE 108-19 Anteroposterior radiograph of the right hip demonstrating breach of the cortex of the proximal femur at the flange of the femoral stem, diagnostic of loosening.

■ FIGURE 108-21 Anteroposterior radiograph of the pelvis after bilateral arthroplasty demonstrates lucency at bone-cement interface of all three Gruen zones of the acetabulum involving the left hip.

views of a hip radiographic series, radiographic assessment of the acetabulum is relatively more difficult owing to its shape. Apart from measuring the lucent interval at the bone-cement interface, additional criteria for loosening of the acetabular component have been described and include lucent zones developing or progressing after 2 years in uncemented systems, radiolucent lines in all three zones (Figs. 108-21 and 108-22), radiolucent lines greater than 2 mm in any area, and migration.10 The sensitivity and specificity of these findings is 94% and 100%, respectively. Often, the

subtle findings of lucency are not detected early, such that the diagnosis of loosening may only be made radiographically finally when component malalignment or migration has occurred, typically medially and/or superiorly.11,12 The inclination of the acetabulum is an important and simple measurement, which is the angle of tilt that the acetabular component makes with the horizontal. Despite patient positioning, a horizontal line forms a standard reference and is drawn either connecting the inferiormost aspect of both ischial tuberosities (the bi-ischial line) or both teardrops

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■ FIGURE 108-22 Anteroposterior radiograph of the pelvis after bilateral arthroplasty demonstrates lucency at bone-cement interface (arrowhead) of all three Gruen zones of the acetabulum involving the right hip.

(the bi-teardrop line). Ideally, this angle should approximate 45 degrees (range: 35-55 degrees), with an alteration of angle of greater than 4 degrees or movement greater than 4 mm compatible with loosening.13 A line drawn from Kohler’s line to either the acetabular margin or femoral head is utilized to exclude medial migration on subsequent evaluation. Any form of protrusion or intrapelvic migration is also consistent with acetabular component loosening.14 Multidetector CT (MDCT), with its ability to reduce beam-hardening artifact, has a higher sensitivity for the detection of periacetabular lucency (Fig. 108-23) and thus a higher pick-up rate for diagnosing early component loosening.15 This modality may be utilized in the setting in which radiographic assessment is equivocal or clinical suspicion for loosening is high but radiographic findings are negative.15 CT allows for highly accurate measurement of cup orientation despite the degree of patient pelvic tilt and rotation.16,17 Although acetabular anteversion may be roughly estimated on a lateral radiograph, this technique suffers from poor reliability and lacks the high degree of precision required in accurately assessing component migration. Lateral radiographs in particular suffers from variation in patient positioning and are too imprecise when an exact measurement is required.18 Anteversion, however, may be measured with great accuracy on CT, first by drawing a line tangential to the opening of the acetabulum, which is then measured in comparison to the anteroposterior plane. Anatomic derivation of the anteroposterior plane is made by first accurately drawing a true horizontal line, which may vary depending on patient positioning. As such, a line drawn along the posterior aspect of the posterior columns serves as the basis from which a line in the anteroposterior plane is drawn perpendicular to it. The intersection made with the line drawn tangential to the acetabulum therefore defines the degree of acetabular version.19 CT has the additional advantage of accurately assessing further parameters of acetabular geometry, specifically,

■ FIGURE 108-23 CT scan of the right hip clearly delineates a region of extensive periacetabular lucency compatible with loosening, as well as the general poor quality of the bone stock.

the acetabular depth and degree of anterior and posterior wall cover.20,21 These measurements are of particular use in preoperative planning for revision arthroplasty.22 The quality of screw fixation23 and the assessment of the degree and quality of osseointegration of bone substitutes24 can also be made. Furthermore, the quality and degree of bone stock25 may be assessed on CT, with dualenergy x-ray absorptiometry (DEXA) scanning26 being an alternative imaging modality. Finally, CT-guided obturator nerve block may also be used for control of chronic, recalcitrant hip pain, including that in patients for whom surgery is not suitable.27,28 Several arthrographic techniques have been described in the diagnosis of prosthetic loosening. After successful needle placement into the prosthetic hip, these techniques rely on the principle of demonstrating the presence of contrast material below the level of the intertrochanteric line interposed between the bone-cement interface. In its simplest form, standard fluoroscopic demonstration of contrast agent may be utilized, but digital subtraction techniques are superior.29,30 Contrast medium insinuating between the bone-cement interface is diagnostic of loosening and may be more apparent after ambulation.31 Highpressure techniques have decreased the false-positive rate of this technique, but a false-negative result may occur in the setting of adhesions and fibrous tissue formation, limiting the spread of contrast. In addition, a negative result may still be obtained despite the presence of loosening owing to the inability to achieve adequate high pressures and distention in the patient with a lax pseudocapsule or communicating bursae. The sensitivity and specificity of the test may reach up to 100%, with the addition of the less viscous radiotracer technetium-99 m (99 mTc) sulfur colloid.32–34 Overall, arthrography tends to have a lower accuracy for acetabular component loosening.35

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Bone scintigraphy with 99 mTc-labeled methylene diphosphonate (99 mTc-MDP) is a sensitive, although nonspecific, modality for determining aseptic loosening of the prosthetic hip. Increased tracer uptake, consistent with increased marginal osteoblastic activity, is considered

physiologic for up to 12 months after surgery. After this time, uptake is reflective of microinstability and thus diagnostic of loosening, typically occurring medial to the inferior aspect of the femoral stem and at the greater trochanter (Figs. 108-24 and 108-25). This appearance, however, also

■ FIGURE 108-24 Anterior and posterior images of a 99 mTc MDP bone scan in two separate patients demonstrating abnormal scintigraphic periprosthetic uptake (arrowheads) compatible with loosening.

■ FIGURE 108-25 Anterior and posterior images (upper images) of a 99 mTc MDP bone scan in two separate patients demonstrating abnormal scintigraphic periprosthetic uptake compatible with loosening. Gallium scintigraphy in both cases was negative (lower images), thereby excluding infection as a cause of loosening.

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may be seen in infection, which may be excluded in the setting when other tests are negative for infection, including a negative 99 mTc sulfur colloid or labeled white blood cell scan. In the setting in which a standard 99 mTc-MDP study is negative, any cause of hardware loosening, including infection, may be confidently excluded. With the aim of improving stability, uncemented prostheses have recently gained popularity. These systems are also indicated in the young patient in whom preserving bone stock is critical, given that future revisions are likely. Simplistically, uncemented systems achieve fixation by using components causing either bone ingrowth or chemical bonding between the metal-bone interface. Bone ingrowth systems achieve fixation via fibrous and osseous ingrowth between metallic beads coating the prosthesis. On the other hand, chemical bonding occurs as the result of coating a prosthesis with hydroxyapatite. Stability is further enhanced by limited reaming of the femoral medullary canal so that a very close fit between the prosthesis and the femoral canal and endosteum occurs. Unfortunately, the lack of a cement-bone interface makes the diagnosis of prosthetic loosening difficult radiographically. A lucent line may be produced at the bone-prosthesis interface consistent with a fibrous union but should not be confused with loosening. After 2 years, progression of lucency and an increase in the number of free metal beads, or “bead shedding,” is consistent with loosening. Loosening due to stress shielding is more common in uncemented prostheses. Serial nuclear medicine bone scans are required to determine loosening, and, unfortunately, arthrography may lead to false-positive results.

DISLOCATION Dislocation is the second most common reason for revision surgery.36 It was previously more common utilizing the traditional posterior approach but has been minimized with the standard lateral (Hardinger) approach. Dislocation occurring soon after surgery is usually due to a lax pseudocapsule (Fig. 108-26). This has been correlated arthrographically, where leakage of contrast agent may be seen in the patient with early dislocation, consistent with the lack of adequate pseudocapsule formation.37 After the first 3 months, dislocation is usually due to acetabular malposition, such as excessive anteversion (>20 degrees) or inclination (>60 degrees). After 5 years, dislocation is usually due to progressive pseudocapsule laxity, the latter more common in elderly females. In this subgroup of patients, no leakage is seen, consistent with progressive, chronic stretching.37 Postoperative abductor muscle avulsion results in the loss of the vital dynamic hip stability that these muscles provide and, thus, is also a risk factor for dislocation. MRI, ultrasonography,38 and CT39 may be utilized to visualize the integrity of the abductor muscles, as well as the sequelae of avulsion, particularly muscle denervation and atrophy, with success.

INFECTION Improved sterility, operative technique, and patient care has resulted in a decrease in the frequency of infection, such that it is now the third most common reason for revision

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■ FIGURE 108-26 Anteroposterior radiograph of the pelvis demonstrating acute postoperative dislocation of a revised right hip prosthesis, initially indicated after complex traumatic pelvic fractures.

arthroplasty, occurring in 1% to 5% of hip replacements.36 The radiographic signs of infection may be identical to that of mechanical aseptic loosening, particularly in low-grade chronic sepsis. With increasing severity, however, several additional signs may be present that may alert the clinician to the diagnosis of infection. Radiographic abnormality developing rapidly and with an aggressive appearance favors the diagnosis of infection, whereas aseptic loosening typically has a gradual and progressive course of clinical symptoms, similarly matched radiographically. Overt, well-established radiographic findings of septic arthritis and osteomyelitis, such as rapidly developing osseous erosions and periosteal reaction, are diagnostic. The diagnosis may be also be suggested by the presence of irregular joint capsules, loculation, complex effusions, pseudobursae, sinus tracts, fistulas, and abscesses on arthrography, ultrasonography, CT, and contrast-enhanced MRI. The imaging modality of choice in the diagnosis of infection, however, has been with the use of scintigraphy. Identifying the presence of loosening, as evidenced by increased scintigraphic uptake using standard 99 mTc scintigraphy is nonspecific, because this does not reliably distinguish septic loosening from mechanical loosening or particle disease. In addition to this, standard bone scintigraphy may remain positive for years after arthroplasty when using an uncemented prosthesis in which bone ingrowth is designed to occur. As such, additional radioisotopes must be employed to increase specificity. Gallium-67 (67Ga)labeled white blood cells are highly sensitive for infection, given the recruitment of neutrophils in the inflammatory cascade. When negative, 67Ga-labeled white blood cell scintigraphy effectively excludes infection. Infection may also be excluded when the degree of uptake is less than that demonstrated on technetium scanning or when radiotracer uptake is concordant. Gallium uptake specifically within the joint is consistent with septic arthritis. Diagnostic accuracy of greater than 90% is now possible combining a marrow sensitive study (typically

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Tc-labeled sulfur colloid) with a white blood cell–labeled study (99 mTc or indium-110). 110In-labeled white blood cell scintigraphy is the test of choice, but it is time consuming, labor intensive, and expensive.40 Because the labeled white blood cells accumulate in areas of infection, however, not as avidly in areas of normal marrow, the characteristic finding of radiotracer discordance is diagnostic of infection (Fig. 108-27). Conversely, 99 mTc sulfur colloid accumulation may occur in normal marrow but not to the same extent as in areas of infection. Other criteria for infection using scintigraphy include areas of indium uptake exceeding that of technetium.41 As seen in standard 99 mTc scintigraphy, uptake on white blood cell–labeled imaging may be part of the normal postoperative response for up to 2 years, although the degree of uptake is less than that seen with technetium. More recently, positron emission tomography is finding wider applications in musculoskeletal imaging and may be combined with CT to diagnose infection. Although the presence of increased glucose metabolism adjacent to a prosthesis is consistent with an inflammatory reaction,42,43 the site of infection is critical for specificity as opposed to the degree of intensity of fluorodeoxyglucose uptake.44 Abnormal increased glucose metabolism consistent with infection occurs in the prosthesis-bone interface along the 99 m

femoral component. Increased glucose metabolism around the head and neck of the prosthesis is nonspecific, because it may be normal or even seen in aseptic loosening. Preoperative joint aspiration and culture may be the most useful single test in the workup of the patient with painful joint arthroplasty.45,46 The sensitivity of arthrocentesis, however, varies from 50% to greater than 90%,47,48 with a negative predictive value approaching 100%. In some series, arthrocentesis may have a low sensitivity in detecting chronic, low-grade, occult sepsis,47 when operative culture is used as a gold standard. Furthermore, false-positive findings may be due to skin contaminants. Careful attention to technique is vital, with avoidance of a dry tap by passing the needle past the lateral aspect so that the needle goes into the most dependent portion of the pseudojoint.49 More recently, using techniques designed to reduce magnetic susceptibility artifact, MRI may also be used to evaluate the postoperative hip and has particular use in defining surrounding soft tissue complications of infection, such as abscess, sinuses tracts, and fistulas. By replacing standard fat-saturation techniques with short tau inversion recovery (STIR) sequences, “blooming” secondary to metallic artifact is minimized, although STIR sequences are of slightly poorer resolution when com-

■ FIGURE 108-27

Combined Tc MDP (top: anterior and posterior) and gallium-67–labeled white blood cell (bottom: anterior and posterior) scintigraphy status after right total hip arthroplasty demonstrating discordant areas of uptake, compatible with infection.

99 m

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pared with routine T2-weighted fat-saturation imaging. One advantage, however, of STIR imaging is the robustness of this sequence because T2-weighted fat saturation suffers from inhomogeneous suppression of fat signal, which may potentially be confused with hyperintense signal and thus incorrectly attributed to a pathologic process. Other options also include using thin sections, increasing the receiver and slice select bandwidth (with the subsequent decrease in resolution partially offset by increasing the number of excitations), minimizing echo time (by using fast spin-echo imaging), using increased frequency encoding gradient strengths, and orienting the frequency encoding direction along the longitudinal axis of the prosthesis.50 Also, lower magnetic field strength (less than 1.0 T) systems may decrease metallic susceptibility artifact. As such, MRI may reliably diagnose cellulitis, abscesses, sinus tracts, fistulas, periprosthetic collections, osteomyelitis, and septic arthritis. It may also be utilized for anatomic delineation and further characterization of equivocal scintigraphic findings. CT is also sensitive for similar pathology involving the soft tissues,51 including intrapelvic extension and psoas muscle involvement.52 Ultrasonography also is particularly sensitive for evaluating soft tissue collections and joint effusions. Again, it may be utilized for guidance in performing arthrocentesis, as well as evaluating postoperative collections, reliably distinguishing a hematoma or abscess from a seroma. Power and color flow Doppler imaging is an added feature, enabling the detection of hyperemia indicative of inflammation, which would favor an effusion or collection being infected. Ultrasonographic demonstration of an effusion resulting in less than 3.2 mm in distention of the anterior pseudocapsule from the anterior femoral cortex indicates that infection is unlikely. Conversely, an infected prosthesis typically demonstrates an effusion with an average anterior displacement of the pseudocapsule of 10.2 mm.53

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2051

■ FIGURE 108-28 Anteroposterior pelvic radiograph demonstrating an area of cortical thickening of the medial aspect of the right femoral stem tip in keeping with a “stress riser.”

decrease in distance between the femoral head and superior margin of the acetabulum, with a concomitant increase in distance between the femoral head and inferior acetabular margin. Serial comparison with radiographs is paramount, with wear up to 1.5 mm per year within the normal range. Rarely the acetabular liner may fracture or completely dislocate, in which case the femoral head typically articulates directly with the acetabular cup superiorly and the liner may be visualized as a distinct radiolucent focus (Fig. 108-29). Positron emission tomography may show polyethylene wear, owing to the inflammatory reaction elicited, which is a potential pitfall for infection.56

PERIPROSTHETIC FRACTURE Periprosthetic fracture is an uncommon, although increasingly noted complication after arthroplasty,54 attributed to in part by the increasing frequency of revision arthroplasty (poorer bone stock) as well as the popularity of uncemented prostheses (tight press fit required for ingrowth). Periprosthetic fractures typically occur at the tip of the femoral stem, often preceded by an area of increased cortical thickening or “stress riser” (Fig. 108-28). Cerclage wires may be utilized for reinforcement. Should a fracture occur, a long-stem femoral prosthesis is usually indicated, bypassing the fracture. Periprosthetic fracture involvement of the acetabulum is extremely uncommon.55

ACETABULAR LINER WEAR The polyethylene cup lining the acetabulum commonly progressively wears in a steady manner over the years after arthroplasty, preferentially involving its superior, weightbearing aspect. Ideally, the femoral head should be demonstrated radiographically to be equidistant between the superior and inferior margins of the acetabular cup on the anteroposterior radiograph. Wear therefore manifests as eccentric positioning of the femoral head, resulting in a

■ FIGURE 108-29 Anteroposterior radiograph of the right hip demonstrating dislocation of the polyethylene liner, as indicated by the metallic marker and adjacent lucency encircling the femoral head.

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PARTICLE DISEASE Particle disease, also known as particle inclusion disease or giant cell granulomatous response, is most commonly secondary to microabrasive wear and shedding of any portion of the prosthesis, with the polyethylene used in the acetabular liner and/or polymethyl methacrylate (PMMA) cement having a higher inflammatory profile than metal and ceramic particles. The foreign materials are engulfed by macrophages, resulting in the release of cytokines and therefore attracting inflammatory cells. With time, chronic inflammation ensues, with a granulomatous response and giant cells (histiocytes). This cascade causes an increase in osteoclastic activity, ultimately radiographically manifesting as osteolysis. Early detection of osteolysis is critical, because the condition is asymptomatic until substantial bone loss has occurred, which may limit or complicate future surgical options. Particle diseases typically occur 1 to 5 years after arthroplasty, with the presence of lucency during this time interval at the prosthesis/bone (or bone/cement) interface, in the setting of acetabular liner wear, consistent with the diagnosis. Such lesions are lytic, are characteristically expansile, and demonstrate smooth endosteal scalloping (Fig. 108-30).57 This scalloped morphology is in contrast to the linear areas of osseous resorption characteristic of aseptic mechanical loosening. CT and MRI are sensitive modalities in detecting and estimating the size of osteolytic foci due to particle disease, as well as the often associated soft tissue fluid collections. Although these collections have an underlying inflammatory cause, extension to the pelvis or skin implies the diagnosis of infection and thus is an important differentiating feature. In an effort to reduce the incidence of particle disease, the polyethylene liner has been eliminated from the design of modern systems, resulting in either ceramic-on-ceramic or metal-on-metal designs. These designs. however, are not without their disadvantages, with ceramic-on-ceramic systems having been associated with catastrophic breakage in 2% of

■ FIGURE 108-30 Anteroposterior radiograph of a prosthetic right hip demonstrating a scalloped lucency at Gruen zone 6 typical of particle disease.

patients. The concern of a carcinogenic effect of metalon-metal systems has limited its universal application until further long-term data become available.

HETEROTOPIC BONE FORMATION Heterotopic ossification is a common, although rarely clinically significant, finding after arthroplasty. Risk factors for extensive heterotopic ossification limiting joint range of motion include ankylosing spondylitis, diffuse idiopathic skeletal hyperostosis, and a past history of heterotopic ossification. If extensive enough, heterotopic ossification may result in complete ankylosis (Fig. 10831). In such instances, confirmation of stability or maturation of the ossification is vital, because early surgery may worsen the extent of ossification. This may be evaluated radiographically, where lesion stability of 3 months is consistent with quiescence. 99 mTc scintigraphic uptake of similar intensity to the native bone, or less, also implies that osteoblastic activity is minimal, as is the absence of edema within the heterotopic foci on MRI. MDCT is useful in staging the extent of bone formation and helping guide therapeutic radiotherapy and surgery.58 CT is also useful in guiding needle placement in cases in which ossification makes aspiration with routine fluoroscopy difficult.59

PSEUDOBURSAE After arthroplasty, pseudobursae commonly form typically adjacent to both trochanters60 and may limit the maximal achievable joint pressure and thus provide a false-negative result on arthrography. Pseudobursae may be assessed with MRI, CT, and ultrasonography, with the

■ FIGURE 108-31 Anteroposterior radiograph of the left hip status after revision arthroplasty demonstrating complete ankylosis secondary to postoperative heterotopic ossification.

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latter modality providing the capability for simultaneous treatment with image-guided corticosteroid administration, as well as the ability to aspirate where infection within these structures is considered a possibility.

ILIOPSOAS IMPINGEMENT Impingement of the iliopsoas tendon occurs secondary to an oversized acetabular cup. In conjunction with positive clinical findings, overhang of greater than 12 mm,61 as assessed on CT, is consistent with the diagnosis. An effusion of the hip joint, as may occur in loosening,62 may result in

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iliopsoas bursitis63 and thus result in the clinical findings of iliopsoas impingement. Rarely, this may be mimicked by iliopectineal bursitis.64 Iliopsoas impingement may also be diagnosed sonographically,65 as evidenced by the loss of normal tendon fibrillar echogenicity (compatible with tendinosis), as well as the normal smooth movement and glide that the tendon makes during dynamic assessment. Ultrasonography may again be utilized to percutaneously administer corticosteroid into the iliopsoas bursa for symptomatic relief. Depending on the exact cause of iliopsoas impingement, surgical release66 may be occasionally required.

REFERENCES 1. American Academy of Orthopaedic Surgeons. Osteoarthritis of the Hip: A Compendium of Evidence-based Information and Resources; Joint Replacement. http://www.aaos.org/Research/ documents/oainfo_hip.asp. Accessed November 13, 2006. 2. Clohisy JC, Calvert G, Tull F, et al. Reasons for revision hip surgery: a retrospective review. Clin Orthop Relat Res 2004; 429:188–192. 3. Burkhardt K, Szekely G, Notzli H, et al. Submillimeter measurement of cup migration in clinical standard radiographs. IEEE Trans Med Imaging 2005; 24:676–688. 4. Karrholm J, Hultmark P, Carlsson L, et al. Subsidence of a nonpolished stem in revisions of the hip using impaction allograft: evaluation with radiostereometry and dual-energy X-ray absorptiometry. J Bone Joint Surg Br 1999; 81:135–142. 5. Berger R, Fletcher F, Donaldson T, et al. Dynamic test to diagnose loose uncemented femoral total hip components. Clin Orthop Relat Res 1996; 330:115–123. 6. Weissman BN. Current topics in the radiology of joint replacement surgery. Radiol Clin North Am 1990; 28:1111–1134. 7. Gruen TA, McNiece GM, Amstutz HC. “Modes of failure” of cemented stem-type femoral components: a radiographic analysis of loosening. Clin Orthop Relat Res 1979; 141:17–27. 8. Boden H, Adolphson P, Oberg M. Unstable versus stable uncemented femoral stems: a radiological study of periprosthetic bone changes in two types of uncemented stems with different concepts of fixation. Arch Orthop Trauma Surg 2004; 124:382–392. 9. Schmidt R, Muller L, Kress A, et al. A computed tomography assessment of femoral and acetabular bone changes after total hip arthroplasty. Int Orthop 2002; 26:299–302. 10. Udomkiat P, Wan Z, Dorr LD. Comparison of preoperative radiographs and intra operative findings of fixation of hemispheric porous-coated sockets. J Bone Joint Surg Am 2001; 83:1865–1871. 11. Bassett LW, Gold RH, Hedley AK. Radiology of failed surfacereplacement total-hip arthroplasty. AJR Am J Roentgenol 1982; 139:1083–1088. 12. Puri L, Wixson RL, Stern SH, et al. Use of helical computed tomography for the assessment of acetabular osteolysis after total hip arthroplasty. J Bone Joint Surg Am 2002; 84:609–614. 13. Yoder SA, Brand RA, Pederson DR, et al. Total hip acetabular component position affects component loosening rates. Clin Orthop 1988; 220:79–87. 14. Sudanese A, Giardina F, Garagnani L. Intrapelvic migration of prosthetic acetabular component. Chir Organi Mov 2004; 89:223–232. 15. Claus AM, Engh CA Jr, Sychterz CJ, et al. Computed tomography to assess pelvis lysis after total hip replacement. Clin Orthop Relat Res 2004; 422:167–174. 16. Tannast M, Langlotz U, Siebenrock KA, et al. Anatomic referencing of cup orientation in total hip arthroplasty. Clin Orthop Relat Res 2005; 436:144–150. 17. Olivecrona H, Weidenheim L, Olivecrona L, et al. A new CT method for measuring cup orientation after total hip arthroplasty: a study of 10 patients. Acta Orthop Scand 2004; 75:252–260. 18. Marx A, von Knoch M, Pfortner J, et al. Misinterpretation of cup anteversion in total hip arthroplasty using planar radiography. Arch Orthop Trauma Surg 2006; 126:487–492.

19. Goodman SB, Adler SJ, Fyhrie DP, et al. The acetabular teardrop and its relevance to acetabular migration. Clin Orthop 1988; 236:199–204. 20. Dias JJ, Johnson GV, Finlay DB, et al. Pre-operative evaluation for uncemented hip arthroplasty: the role of computerized tomography. J Bone Joint Surg Br 1989; 71:43–46. 21. Chiang PP, Burke DW, Freiberg AA, et al. Osteolysis of the pelvis: evaluation and treatment. Clin Orthop Relat Res 2003; 417:164–174. 22. Berman AT, McGovern KM, Paret RS, et al. The use of preoperative computed tomography scanning in total hip arthroplasty. Clin Orthop Relat Res 1987; 222:190–196. 23. Seel MJ, Hafez MA, Eckman K, et al. Three-dimensional planning and virtual radiographs in revision total arthroplasty for instability. Clin Orthop Relat Res 2006; 442:35–38. 24. Nishii T, Sugano N, Miki H, et al. Multidetector-CT evaluation of bone substitutes remodeling after revision hip surgery. Clin Orthop Relat Res 2006; 442:158–164. 25. Howard JL, Hui AJ, Bourne RB, et al. Computed tomographic analysis of bone support for three acetabular cup designs. Clin Orthop Relat Res 2005; 434:163–169. 26. Laursen MB, Nielsen PT, Soballe K. J Clin Densitom 2005; 8:476–483. 27. Heywang-Kobrunner SH, Amaya B, Okoniewski M, et al. CTguided obturator nerve block for diagnosis and treatment of painful conditions of the hip. Eur Radiol 2001; 11:1047–1053. 28. House CV, Ali KE, Bradshaw C, et al. CT-guided obturator nerve block via the posterior approach. Skeletal Radiol 2006; 35:227–232. 29. Walker CW, FitzRandolph RL, Collins DN, et al. Arthrography of painful hips following arthroplasty: digital versus plain film subtraction. Skeletal Radiol 1991; 20:403–407. 30. Ginai AZ, van Biezen FC, Kint PA. Digital subtraction arthrography in preoperative evaluation of painful total hip arthroplasty. Skeletal Radiol 1996; 25:357–363. 31. Hardy DC, Reinus WR, Totty WG, et al. Arthrography after total hip arthroplasty: utility of postambulation radiographs. Skeletal Radiol 1988; 17:20–23. 32. Resnik CS, Fratkin MJ, Cardea A. Arthroscintigraphic evaluation of the painful total hip prosthesis. Clin Nucl Med 1986; 11:242–244. 33. Swan JS, Braunstein EM, Wellman HN, et al. Contrast and nuclear arthrography in loosening of the uncemented hip prosthesis. Skeletal Radiol 1991; 20:15–19. 34. Koster G, Munz DL, Kohler HP. Clinical value of combined contrast and radionuclide arthrography in suspected loosening of hip prostheses. Arch Orthop Trauma Surg 1993; 112:247–254. 35. Tehranzadeh J, Gubernick I, Blaha D. Prospective study of sequential technetium-99 m phosphate and gallium scanning in painful hip prostheses (comparison of diagnostic modalities). Clin Nucl Med 1988; 13:229–236. 36. Bauer TW, Schils J. The pathology of total joint arthroplasty: II: Mechanisms of implant failure. Skeletal Radiol 1999; 28:483–497. 37. Miki H, Masuhara K. Arthrographic examination of the pseudocapsule of the hip after posterior dislocation of total hip arthroplasty. Int Orthop 2000; 24:256–259. 38. Connell DA, Bass C, Sykes CA, et al. Sonographic evaluation of gluteus medius and minimus tendinopathy. Eur Radiol 2003; 13:1339–1347.

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39. Roy BR, Binns MS, Horsfall H. Radiological diagnosis of abductor denervation after hip surgery. Skeletal Radiol 2001; 30:117–118. 40. Palestro CJ, Roumanas P, Swyer AJ, et al. Diagnosis of musculoskeletal infection using combined In-111 labeled leukocyte and Tc-99 m SC marrow imaging. Clin Nucl Med 1992; 17:269–273. 41. Love C, Tomas MB, Marwin SE, et al. Role of nuclear medicine in diagnosis of the infected joint replacement. RadioGraphics 2001; 21:1229–1238. 42. Zhuang H, Duarte DS, Pourdehnad M, et al. Exclusion of chronic osteomyelitis with F-18 fluorodeoxyglucose positron emission tomographic imaging. Clin Nucl Med 2000; 25:281–284. 43. Zhuang H, Chacko TK, Hickeson M, et al. Persistent non-specific FDG uptake on PET imaging following hip arthroplasty. Eur J Nucl Med 2002; 29:1328–1333. 44. Chacko TK, Zhuang H, Stevenson K, et al. The importance of the location of fluorodeoxyglucose uptake in periprosthetic infection in painful hip prostheses. Nucl Med Commun 2002; 23:851–855. 45. Levitsky KA, Hozack WJ, Balderston RA, et al. Evaluation of the painful prosthetic joint. Relative value of bone scan, sedimentation rate and joint aspiration. J Arthroplasty 1991; 6:237–244. 46. Ali FD, Wilkinson JM, Copper JR, et al. Accuracy of joint aspiration for the preoperative diagnosis of infection in total hip arthroplasty. J Arthroplasty 2006; 21:221–2226. 47. Fehring Tk, Cohen B. Aspiration as a guide to sepsis in revision total hip arthroplasty. J Arthroplasty 1996; 11:543–547. 48. Tigges S, Stiles RG, Meli RJ, et al. Hip aspiration: a cost effective and accurate method of evaluating the potentially infected hip prosthesis. Radiology 1993; 189:485–488. 49. Brandser EA, El-Khoury GY, FitzRandolph RL. Modified technique for fluid aspiration from the hip in patients with prosthetic hips. Radiology 1997; 204:580–582. 50. White LM, Kim JK, Mehta M, et al. Complication of total hip arthroplasty: MR imaging—initial experience. Radiology 2000; 215:254–262. 51. Jacquier A, Champsaur P, Vidal V, et al. CT evaluation of total hip infection. J Radiol 2004; 85:2005–2012. 52. Buttaro M, Della Valle AG, Piccaluga F. Psoas abscess associated with infected total hip arthroplasty. J Arthroplasty 2002; 17:230–234.

53. Van Holsbeeck MT, Eyler WR, Sherman LS, et al. Detection of infection in loosened hip prostheses: efficacy of sonography. AJR Am J Roentgenol 1992; 163:318–384. 54. Younger ASE, Dunwoody J, Duncan CP. Periprosthetic hip and knee fractures: the scope of the problem. Instr Course Lect 1998; 47:251–256. 55. Peterson CA, Lewallen DG. Periprosthetic fracture of the acetabulum after total hip arthroplasty. J Bone Joint Surg Am 1996; 78:426–431. 56. Kisielinski K, Cremerius U, Reinartz P, et al. Fluorodeoxyglucose positron emission tomography detection of reactions due to polyethylene wear in total hip arthroplasty. J Arthroplasty 2003; 18:528–532. 57. Reinus WR, Gilula LA, Kyriakos M, et al. Histiocytic reaction to hip arthroplasty. Radiology 1985; 155:315–318. 58. Magid D. Preoperative interactive 2D-3D computed tomography assessment of heterotopic bone. Semin Arthroplast 1992; 3:191–199. 59. Chew FS, Bwon JH, Palner WE, et al. CT-guided aspiration in potentially infected total hip replacements complicated by heterotopic bone. Eur J Radiol 1995; 20:72–74. 60. Berquist TH, Bender CE, Maus TP, et al. Pseudobursae: a useful finding in patients with painful hip arthroplasty. AJR Am J Roentgenol 1987; 148:103–106. 61. Cyteval C, Sarrabere MP, Cottin A, et al. Iliopsoas impingement on the acetabular component: radiologic and computed tomography findings of a rare hip prosthesis complication in eight cases. J Comput Assist Tomogr 2003; 27:183–188. 62. Morrison KM, Apelgren KN, Mahany BD. Back pain, femoral vein thrombosis, and an iliopsoas cyst: unusual presentation of a loose total hip arthroplasty. Orthopedics 1997; 20:347–348. 63. Matsumoto K, Hukuda S, Nishioka J, et al. Iliopsoas bursal distension caused by acetabular loosening after total hip arthroplasty: a rare complication of total hip arthroplasty. Clin Orthop Relat Res 1992; 279:144–148. 64. Lin YM, Ho TF, Lee TS. Iliopectineal bursitis complicating hemiarthroplasty: a case report. Clin Orthop Relat Res 2001; 392:366–371. 65. Cheung YM, Gupte CM, Beverly MJ. Iliopsoas bursitis following total hip replacement. Arch Orthop Trauma Surg 2004; 124:720–723. 66. Della Valle CJ, Rafii M, Jaffe WL. Iliopsoas tendonitis after total hip arthroplasty. J Arthroplasty 2001; 16:923–926.

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The Postoperative Knee Douglas Mintz

Imaging the postoperative knee can be challenging. The postoperative knee can have all of the pathologic processes of the preoperative knee in addition to specific issues related to the surgery performed, general problems with surgery, and specific postoperative complications. The imaging is often confounded by artifact produced from instrumentation or surgical scar, so that often special imaging technique is required, especially for CT and MRI. Because imaging is used to answer clinical questions, knowledge of the procedures performed and the reason for the postoperative imaging can be very helpful and important in interpreting studies. If not provided on the ordering physician’s request, this information usually can be obtained with a telephone call. Because surgical procedures have evolved and continue to evolve, it helps to have a working knowledge of these procedures and interaction with the referring physicians fosters that knowledge. The discussion in this chapter is on some of the postoperative findings one may encounter. The emphasis is on MRI because that is the modality most commonly used. Radiography, fluoroscopy, CT, ultrasonography, and nuclear imaging also have roles for some postoperative issues.

ARTHROSCOPY Description Arthroscopy is the technique of percutaneous visualization of a joint. By adapting a cystoscope, Takagi, a Japanese surgeon, first used arthroscopy in the early 1900s to diagnose tuberculosis of the knee. His student, Wantanabe, worked on the technique, producing the first modern arthroscope in the late 1950s. With the advent of fiberoptics and improvement of cameras, arthroscopy became much better in the 1970s and widely used in the 1980s.1

Indications, Contraindications, Purpose, and Underlying Mechanics Before good noninvasive diagnostic procedures became available, arthroscopy was used as a diagnostic tool. Now

it is commonly used to perform therapeutic interventions and has largely replaced arthrotomy for many operative procedures in the knee. It has the advantages of reduced morbidity and shorter recovery times. Some of the procedures that are commonly performed through an arthroscope include cruciate ligament reconstructions, meniscectomies and meniscal repairs, chondroplasty, removal of intra-articular bodies, and removal of other masses. The importance of knowing if arthroscopy has been performed lies in the need to know if a finding on the study is postsurgical. For example, if a meniscus is small, and no surgery was performed, a more thorough search for a displaced flap will ensue.

Expected Appearance on Relevant Modalities On radiography, it is impossible to tell that arthroscopy has been performed unless there has been some kind of instrumentation. On MRI, arthroscopic portals cause scar that appears as low signal on all pulse sequences (Fig. 109-1). They are characteristic in location in the medial and lateral aspects of the infrapatellar fat. Evidence of whatever procedure was performed through the arthroscope may also be seen.

Potential Complications and Radiologic Appearance Whenever a foreign body is placed in a joint the potential for infection exists. The appearance of septic arthritis is described elsewhere and has the same appearance in the postoperative as well as the native state—effusion with rapidly progressive joint space narrowing on the radiograph with eventual resorption/destruction of subchondral bone. The MRI features of infection are effusion with synovitis and reactive abnormal signal in the surrounding tissues. Noninfectious inflammatory arthropathy does not generally cause the degree of soft tissue signal abnormality on MRI. 2055

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KEY POINTS The postoperative ACL should be evaluated for integrity, position, and scar formation. ■ The postoperative meniscus should be evaluated for re-tear, degeneration, and associated arthrosis. ■ The postoperative meniscal transplant should be evaluated for bone plug incorporation, meniscal integrity, capsular healing, degree of extrusion, and associated arthrosis. ■ Treated cartilage should be evaluated for incorporation/ viability of plugs (if present), integrity of the articular surface, smoothness of surface, quality and extent of repaired cartilage, postoperative scar, and adjacent chondral loss. ■ Arthroplasties can exhibit osteolysis, extending to loosening, periprosthetic fractures, wear, and infection. Comparison with early postoperative radiographs and sequential radiographs is very helpful. ■ Tumor recurrence often looks like the original lesion. Preoperative and early postoperative studies should be reviewed whenever possible. ■ Fractures, infection, and re-tears can complicate most procedures, so one should be alert to these possible situations. ■ Attention to technique is important, especially when trying to reduce metal artifact on CT and MRI. ■

Occasionally, an arthroscopic portal is placed through a portion of the patellar tendon. This often causes an extensive reaction in the tendon, with focal thickening on MRI (Fig. 109-2). It used to be thought that patients who undergo arthroscopy can develop avascular necrosis. The theory was that the increase in pressure from the joint distention

during arthroscopy could decrease blood flow and cause necrosis. More likely, the sudden new pain that patients get after arthroscopy has to do with subtle subchondral insufficiency fractures (Fig. 109-3).2 Rarely, the arthroscope can directly hit and injure the articular surface. Another complication is complex regional pain syndrome, formerly known as reflex sympathetic dystrophy.Although it can occur after trauma without surgery, it may also be related to surgery (Fig. 109-4).

ARTHROTOMY Description Before arthroscopy was common, orthopedic surgeons performed knee surgeries through long incisions made lateral or medial to the patella.These incisions give excellent exposure to the joint.

Indications, Contraindications, Purpose, and Underlying Mechanics An arthrotomy is currently used when a procedure cannot be performed arthroscopically. Before arthroscopy became available and popular, arthrotomies were more common. Meniscectomies and reconstructions of the anterior cruciate ligament (ACL), now done arthroscopically, used to require arthrotomy. The most common indication for arthrotomy is joint arthroplasty. Tumor resections and chondral repair and replacement procedures require arthrotomy, as does meniscal transplantation. Pigmented villonodular synovitis may require arthrotomy for complete resection, depending on the extent of disease and ability of the arthroscopist.

■ FIGURE 109-1 Arthroscopy scars. Axial (A) and sagittal (B) intermediate echo time MR images show the typical scars (arrows) from arthroscopic portal placement. There are usually medial and lateral scars. (©Hospital for Special Surgery, New York, New York.)

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■ FIGURE 109-2 Patellar tendon scar. Axial (A) and sagittal (B) MR images show patellar tendon abnormality (arrows) from an arthroscopic portal being placed through it. (©Hospital for Special Surgery, New York, New York.)

■ FIGURE 109-3

Subchondral fracture. Some weeks after partial medial meniscectomy, this patient’s sudden onset of pain was due to a subchondral fracture. Sagittal, fat-suppressed MR image (A) better shows the high signal intensity of the bone marrow edema (e) associated with the fracture, which is shown by the low signal intensity line (arrow, A, B). (©Hospital for Special Surgery, New York, New York.)

■ FIGURE 109-4 Complex regional pain syndrome (reflex sympathetic dystrophy). Blood pool images from a bone scintiscan (A) show diffuse uptake around the knee. Sagittal, intermediate echo time MR image (B) shows patchy, rounded periarticular foci of relative increased signal (arrows) that appear to be associated with complex regional pain syndrome. (©Hospital for Special Surgery, New York, New York.)

A

B

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Expected Appearance on Relevant Modalities As with arthroscopy, an arthrotomy itself leaves no radiographic findings. It is other findings on a radiograph that indicate that arthrotomy was performed, such as the implant placed for knee replacement. On MRI, a long vertical low signal line represents the scar left from arthrotomy (Fig. 109-5). It lies either lateral or medial to the patella, depending on the approach used. The incision is long enough to be able to peel back the patella to expose the joint. With time, these scars become less conspicuous so that after many years it may be difficult to tell if an arthrotomy was performed.

Potential Complications and Radiologic Appearance The arthrotomy itself has few associated complications. As in arthroscopy, the potential for infection exists and has the same appearance, regardless of etiology.

ANTERIOR CRUCIATE LIGAMENT RECONSTRUCTION Description Tears of the ACL of the knee can lead to joint instability and subsequent arthrosis. First repaired in 1895 and reconstructed in 1903, many materials and techniques have been used to fix ACL tears. The first patellar autograft was used in 1935. A hamstring graft followed shortly thereafter in 1939. Despite these early descriptions, people tried to primarily repair the ACL for many years afterward. Most of the primary repairs failed: only the proximal tears repaired early had success. Other than in proximal tears and bony

avulsions (a minority of ACL injuries) we see reconstructions. During the 1970s extra-articular stabilizations were used (Fig. 109-6). During the 1980s different graft materials such as carbon fiber and Dacron were used.Reconstructions as they are currently performed became popular in the late 1980s because of the introduction of interference screws and advances in arthroscopic surgery.1,3 Because the ACL is the most commonly reconstructed knee ligament, we are most often called upon to evaluate it.There are about 100,000 ACL reconstructions performed in the United States annually. There is an about 10% failure rate (often due to reinjury). Radiologists in a busy MRI practice will see many knees with ACL reconstruction for problems with the graft or a different problem in the same knee. Because they are so common, one should know how they look and what can go wrong with them.

Indications, Contraindications, Purpose, and Underlying Mechanics Tears of the ACL are reconstructed in active patients whose tears cause instability that impedes normal activities for that individual. An ACL-deficient, unstable knee will, over time, progress to premature arthrosis. In patients whose knees are not unstable (because of arthritis, for example) or who are not very active, the ligament may remain torn. The purpose of the reconstruction is to restore the stabilizer of the tibia to anterior translation.

Expected Appearance on Relevant Modalities Over the years, different techniques and materials have been used for reconstructions. Artificial grafts have been used but failed because the grafts would fall apart or the

■ FIGURE 109-5 Arthrotomy scar. Axial (A) and sagittal (B) MR images show scar from medial arthrotomy (white arrow and black arrows) for cartilage repair. The scar is similar to that for arthroscopy but more extensive. (©Hospital for Special Surgery, New York, New York.)

A

B

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■ FIGURE 109-6 Extra-articular stabilization. Sagittal MR image through the lateral side of the knee showing an extra-articular graft (arrows) that was used to stabilize the knee after ACL tear, before constructions were commonly performed. (©Hospital for Special Surgery, New York, New York.)

■ FIGURE 109-7 Iliotibial band autograft for ACL reconstruction. Coronal, intermediate echo time MR image shows ACL autograft with iliotibial band (arrows). This technique was popular in the 1970s. The only way to know that the reconstruction was done with an iliotibial band is to follow the structure over sequential images. (©Hospital for Special Surgery, New York, New York.)

body would react to them. A variety of autograft reconstructions have been used from the extra-articular ACL reconstruction (essentially a stabilization procedure that was not with an in-situ graft) to the autologous patellar tendon remaining fixated on the tibial tubercle (Marshall Mackintosh) to a variety of other autografts—iliotibial band (Fig. 109-7), patellar tendon with bone plugs, or hamstring autograft. Allografts are also used (usually Achilles tendon but also patellar tendon). Rarely, contralateral patellar tendon is used. The commonly used current material is either bonepatella-bone or hamstring autograft or allograft. A variety of fixation devices are also in use: fixation screws that grab bone plug and native bone (interference screws), endobuttons (plastic buttons that the graft that holds the graft outside the bone preventing it from sliding back), and a few other devices including horizontal femoral fixation devices and staples (Figs. 109-8 to 109-10). The interference screws can be made from metal or bioabsorbable radiolucent materials (polymers such as polylactic acid [PLA] or polyglycolic acid [PGA]). They have a similar appearance on MRI, although the nonmetallic ones have less artifact. When hamstring is used, it is often folded on itself and one can see up to four strands of tendon used for ligament reconstruction. Any of the grafts can be augmented with suture.This augmentation gives rise to a dephasing artifact that runs along the graft (Fig. 109-11). The proximal and distal ends of a graft arthroscopically placed through tunnels in the tibia and femur line up in the maximally flexed knee. The outline of the tunnels are

discernible on radiography (see Fig. 109-8). More important than knowing what graft was used or what fixation was used is knowing its integrity and appropriateness of placement (position). Recently, some surgeons have reconstructed the two discrete bands of native ligament, yielding two separate proximal points of fixation.

Position Appropriate placement of the graft is important to prevent some of the complications of inappropriate placement—graft impingement, knee instability, and laxity. Whereas some surgeons are starting to use two bands of graft to better simulate the native ACL, most use only one. To mimic function of the native ligament, the tibial tunnel should be at the back of the native ACL footprint (it used to be placed more anterior than that). The femoral tunnel hugs the posterior cortex of the femur such that the graft parallels Blumensaat’s line in the sagittal plane (Fig. 109-12). In the coronal plane, the graft should be angled about 15 degrees to prevent the knee from turning on itself (see Fig. 109-8).4 Some surgeons place the graft a bit looser than others.This is a matter of technique and preference so that just because a tibia appears a bit more anterior than a native ACL it does not imply inappropriate laxity, re-tear, or misplacement. The position thought to be optimal for the tibial tunnel has moved over the years. It is now believed that the tibial graft should enter the tibia at the posterior portion of the native ligament. This practice will likely be modified with the increasing use of two bundle grafts and with further research into biomechanics.

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B

C

■ FIGURE 109-8

ACL reconstruction. Radiographs show the different types of fixation: staples (thin black arrows, A, B), buttons (short white arrow, A), and screws (black arrowhead, C). Some devices, such as bioabsorbable screws (small white arrows, C) are not easily visible on radiography. Sometimes the bone plug of a bone-patella-bone construct can be seen. On the frontal view the graft should be angulated about 15 degrees. On the lateral view the tibial tunnel should be at the posterior aspect of the anterior tibial spine. (©Hospital for Special Surgery, New York, New York.)

■ FIGURE 109-9 Transverse fixation. Some surgeons prefer a transverse fixation. Frontal radiograph in a patient with ACL reconstruction shows tibial tunnel and lateral wall of the femoral tunnel. A transverse lucency represents a bioabsorbable fixation device of the proximal graft (small black arrows). (©Hospital for Special Surgery, New York, New York.)

■ FIGURE 109-10 Endobutton. Axial MR image at the level of the distal femur (F) shows the radiolucent endobutton (arrows), which can be used for fixation of cruciate ligament reconstructions. The graft is tied through the button with a suture, but the button is too large to pull back through the graft’s tunnel. The top of the patella is visible (P). (©Hospital for Special Surgery, New York, New York.)

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vascularized, resorbed to some extent, and then replaced. The MRI appearance reflects those changes. Initially a graft is of homogeneously low signal intensity. Over a couple of months the graft becomes higher in signal intensity during the vascularization phase. Over 6 months to 2 years it again becomes of homogeneously high signal intensity. During the revascularization stage the graft is weak and susceptible to re-injury. Normally, a graft should be a continuous low signal structure (Fig. 109-12).

Harvest Site

■ FIGURE 109-11 Hamstring reconstruction augmentation. Sagittal, intermediate echo time MR image shows ACL reconstruction. Multiple low signal foci with dephasing artifact are related to graft augmentation, often done with suture (arrows). (©Hospital for Special Surgery, New York, New York.)

The site of allograft harvest shows postoperative abnormalities. For patellar harvest, the defect in the central third may or may not be apposed by suture and the patellar bone plug harvest side may or may not have bone graft placed into it. Both bone plug harvest sites are usually visible on the axial images forever. The patellar tendon is initially thick and high signal on MR and, with time, becomes more normal. There are more subtle findings in hamstring harvest: there is loss of the semitendinosus and often the gracilis tendon with a thin, and eventually thicker, fibrous sheath over the length of the harvest (Fig. 109-13). Regeneration of the tendon that results in a fibrous scar in the region from where the tendon was harvested has been described.

Signal

Potential Complications and Radiologic Appearance

Ligament reconstructions go through a well-documented pattern of incorporation in which the graft initially serves as a stabilizer and then as a scaffold for a new fibrous support to form. For this to happen, the graft must become

Complications of ACL grafts include problems related to placement (e.g., persistent instability or graft impingement); reactions to the graft (scar, inflammation, infection); and trauma (re-tears, degeneration, ganglion formation).

■ FIGURE 109-12 Normal ACL reconstruction. Sagittal, fast spin-echo, intermediate echo time MR image shows a low signal graft parallel to Blumensaat’s line (arrowheads). The tibial tunnel (black arrow) enters the tibia at the posterior portion of the native ligament, and the femoral attachment is posterior, at the posterior cortex of the distal femur. (©Hospital for Special Surgery, New York, New York.)

■ FIGURE 109-13 Hamstring harvest. Axial, intermediate echo time MR image at the level of the femorotibial joint demonstrates poor definition of the hamstring tendons, indicating that they have been harvested for the patient’s ACL reconstruction. (©Hospital for Special Surgery, New York, New York.)

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When a graft is malpositioned, impingement can occur either against the bone of the tibia or at the intercondylar notch. The graft curves around or rubs against bone. This can wear down the graft or impede its function (Fig. 109-14). During the graft placement some surgeons will remove some of the bone around the intercondylar notch (notchplasty) to prevent this from happening (Fig. 109-15). If the graft is too vertical, the knee will be unstable to rotation and the femur and tibial can twist on each other (Figs. 109-16 and 109-17). Focal scar formation in the intercondylar notch can block terminal extension and cause pain.This phenomenon is the so-called Cyclops lesion because of its similar appearance to the single eye of the Cyclops. This lesion may be

related to inadequate removal of the native ACL or simply exuberant inflammatory response (Fig. 109-18). More extensive inflammatory response can lead to arthrofibrosis, which is characterized on MRI as low signal intensity tissue replacing the infrapatellar fat and extending from the femoral trochlea to the patella and patellar tendon (Fig. 109-19). Clinically, these involved knees will be painful and have limited flexibility. Some patients develop an inflammatory reaction to the graft. This traditionally was a greater problem with synthetic grafts because there would be bone resorption and the tunnels would widen. This same phenomenon occasionally happens with allografts. In this circumstance, it can be difficult to differentiate this inflammatory

■ FIGURE 109-14

Graft impingement. A, Coronal MR image of the knee shows that the ACL graft is displaced by the lateral femoral condyle in the intercondylar notch (white arrow). This is related to poor placement of the graft. B, Lateral radiograph shows by the position of the interference screws that the femoral tunnel is too far anterior and the tibial tunnel is too anterior and shallow (black arrows). (©Hospital for Special Surgery, New York, New York.)

A

B

■ FIGURE 109-15

Over-the-top ACL reconstruction. Notchplasty. A, Coronal intermediate echo time MR image shows an ACL reconstruction (white arrows) that courses over the lateral femoral condyle, rather than going through an osseous femoral tunnel. B, Both the coronal and the axial (B) MR image show notchplasty (black arrows) in which bone is removed from the condyle to prevent graft impingement. (©Hospital for Special Surgery, New York, New York.)

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■ FIGURE 109-16 Poor ACL graft placement. Proper graft placement is important to the proper function of the graft. Sagittal (A), and coronal (B), intermediate echo time MR images show posterior placement of the ACL graft (A, arrow), causing a relative vertical orientation in the sagittal plane. The graft is also vertical in the coronal plane. Early arthrosis is evident, with chondral loss in all compartments, a lateral tibial plateau small subchondral cyst, prior partial medial meniscectomy, and lateral meniscal surgery with persistent signal. (©Hospital for Special Surgery, New York, New York.)

■ FIGURE 109-17

Poor ACL graft placement. Oblique sagittal T2weighted MR sequence shows anterior placement on the femoral side (arrow), causing vertical orientation of the graft. This contributes to rotational instability. (©Hospital for Special Surgery, New York, New York.)

■ FIGURE 109-18

reaction from infection. The graft and tunnels show high signal intensity, and the knee has a generalized inflammatory response, with joint effusion and synovitis being the most prominent features. The diagnosis of infection can best be confirmed with joint aspiration (Figs. 109-20 and 109-21).

Like the native ligament, one can perceive tears—both partial and complete. They are evaluated in the same way as for the native ligament, looking for contiguous low signal fibers (Fig. 109-22). As with the native ligament, ganglia can form in the reconstructed ligament. These ganglia (fluid

Cyclops lesion. Sagittal, midline, intermediate echo time MR image shows intermediate signal scar in the intercondylar notch anterior to the ACL, called a Cyclops lesion (arrow). (©Hospital for Special Surgery, New York, New York.)

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POSTERIOR CRUCIATE LIGAMENT RECONSTRUCTION Description Posterior cruciate ligament (PCL) tears are less common than ACL tears.The PCL stops posterior translation of the tibia, and tears most commonly occur from direct impaction of the tibia with the knee flexed (the so-called dashboard injury). Hyperextension and knee dislocation are the other major mechanisms of injury to the PCL. PCL reconstruction can be performed using a one- or two-bundle technique (Fig. 109-25). Two bundles are more commonly used for the PCL than for the ACL reconstruction.

Indications, Contraindications, Purpose, and Underlying Mechanics As with ACL tears, instability can lead to arthrosis. To prevent this, reconstruction of the ligament is performed. Isolated PCL tears may not be fixed, especially in an older or inactive individual. ■ FIGURE 109-19 Arthrofibrosis. Some patients have an inflammatory reaction that results in dense scar of the joint and limited motion. This sagittal MR image shows complete filling of the infrapatellar fat with abnormal low signal (arrow)—the hallmark of arthrofibrosis. (©Hospital for Special Surgery, New York, New York.)

signal regions) can extend into the bone tunnels and cause widening of the tunnel (Fig. 109-23). Other pathologic processes that occur in the unoperated knee, such as stress fractures, are also “fair game” for the postoperative knee (Fig. 109-24).

Expected Appearance on Relevant Modalities Posterior cruciate ligament reconstruction is less common but has a similar appearance to ACL reconstruction. More often with the PCL reconstruction two bands are used with slightly different insertion points on the femur. The ligaments themselves should maintain the same signal as the ACL and be of homogeneously low signal intensity and continuous.5

■ FIGURE 109-20

Infected ACL reconstruction. Sagittal short tau inversion recovery (A) and fatsuppressed, contrast-enhanced, T1-weighted (B) MR images show high signal with enhancement in the tibia, around the graft, in the joint, and in the surrounding soft tissues anterior and posterior to the tibia, indicating graft infection with associated septic arthritis. (©Hospital for Special Surgery, New York, New York.)

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Potential Complications and Radiologic Appearance The complications of PCL reconstruction are the same as those associated with ACL reconstruction: infection, graft re-tear, and malposition. Arthrofibrosis and intercondylar notch scarring are not as common.

MEDIAL COLLATERAL LIGAMENT RECONSTRUCTION Description Tears of the medial collateral ligament (MCL) are common sports injuries. The ligament usually heals without help, but repair/reconstruction is sometimes necessary. Autograft reconstruction of the MCL was first reported in 1914. The common technique currently used was published by Bosworth in 1952 and is referred to as a Bosworth procedure.1

■ FIGURE 109-21 Infected ACL reconstruction. Same patient as in Figure 109-20. On this axial, intermediate echo time MR image, the layered synovial thickening suggests the presence of infection (arrows). (©Hospital for Special Surgery, New York, New York.)

Indications, Contraindications, Purpose, and Underlying Mechanics Because most tears heal on their own, we see relatively few repairs and reconstructions. As with the ACL, primary

■ FIGURE 109-22 Re-tear of ACL reconstruction. A, Sagittal MR image shows a defect (long arrow) in the middle third of this ACL reconstruction, reflecting acute complete tear. Anterior tibial translation is a secondary sign. B, Sagittal fat-suppressed image of a different patient with acute ACL reconstruction re-tear shows the characteristic translational impaction injuries (short arrows). (©Hospital for Special Surgery, New York, New York.)

A

B

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■ FIGURE 109-23 Postoperative tibial tunnel widening/ACL ganglion. Frontal radiograph (A) and coronal MR image using an intermediate echo time sequence (B) show evidence of ACL reconstruction with widening of the tibial tunnel (between the arrows) related to ganglion (G) within the reconstructed ligament. Normally the tunnel width is less than 1.5 cm. (©Hospital for Special Surgery, New York, New York.)

A

B

■ FIGURE 109-24 Stress fracture. Sagittal short tau inversion recovery (A) and coronal intermediate echo time (B) MR images in a patient who has undergone ACL reconstruction and has a stress fracture of the proximal tibia. On A there is extensive reactive high signal (s) and the hint of the fracture line (arrow). The higher-resolution, fast spin-echo sequence in B shows the medullary fracture (small arrows). The interference screw is visible (arrowhead). The appearance is the same as it would be if there had been no surgery. (©Hospital for Special Surgery, New York, New York.)

A

B

repairs are less common than reconstructions. The setting for reconstruction is usually that of an unstable knee, such as in multiple ligament injuries. Occasionally, patients who have ACL and MCL tears will have the MCL reconstructed if the surgeon thinks the knee is too unstable to valgus load after the ACL reconstruction. Sometimes high-performance athletes with repeated MCL injury will undergo ACL reconstruction.

Expected Appearance on Relevant Modalities The healing MCL can be quite thick and exhibit high signal intensity on MRI.A reconstructed ligament will have either interference screws or staples in the medial femoral condyle related to the surgery. The fixation devices (or holes associated with them), but not the ligament, are visible

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■ FIGURE 109-25 Posterior cruciate ligament reconstruction. Sagittal midline (A) and medial (B) MR sections through the knee demonstrate an intact reconstruction (white arrows) (the proximal aspect is just not visible on these slices). There is one distal and two proximal interference screws (black arrows) to better approximate the native ligament. Previous chondroplasty was performed (B, long arrow), and the overlying reparative cartilage is minimally thin and mildly of high signal. (©Hospital for Special Surgery, New York, New York.)

A

B

on radiography. On MRI the reconstructed ligament can be thick but should be low in signal and continuous. On ultrasonography, it should also be continuous and show homogeneous echogenicity.

Potential Complications and Radiologic Appearance As with other ligaments, re-tear and failure of fixation are the most common complications. Failure is rare, and the MRI findings of a re-tear or a discontinuous or thick ligament are the same as in a torn native MCL.

POSTEROLATERAL CORNER RECONSTRUCTION Description The important implication of posterolateral corner injuries of the knee is relatively recent, as is their repair or reconstruction. The anatomy is complex, and it is only with improvements in MRI technique and therapeutic arthroscopy that the details of these injuries have been elucidated.

Indications, Contraindications, Purpose, and Underlying Mechanics The need for repair or reconstruction of the posterolateral corner of the knee (posterior capsule, popliteofibular ligament, popliteus tendon, lateral collateral ligament, biceps femoris, and lateral meniscus) derives from preventing instability and preserving other ligament repairs.

Posterolateral corner injury and instability can result in ACL reconstruction failure. To prevent this, for high-grade injuries, the posterolateral corner is augmented, repaired, or reconstructed. The need for repair or reconstruction can be made after the ACL is treated. The surgeon examines the knee for stability in the operating room to determine whether the posterolateral corner needs attention. Isolated posterolateral injuries are rarely severe enough to require ligament or tendon repair or reconstruction.

Expected Appearance on Relevant Modalities There are various techniques for providing more stability to the posterolateral corner. An anatomic reconstruction requires an allograft tendon to be placed and fixed along the lines of the native structures. As many as three grafts can be placed for reconstruction (Fig. 109-26). As with the grafts described previously, they should be of low signal intensity and continuous. Because they do not always perfectly follow the native structures, simple description of the course and assessment of integrity suffices because there is often significant associated scar tissue. Reconstruction of the lateral structures is often combined with reconstruction of the ACL (Fig. 109-27).

Potential Complications and Radiologic Appearance Whereas hardware failure and re-injury would be the most common complications, other typical problems such as infection may also occur. As with all surgeries, there may be an inflammatory or granulomatous reaction to the graft or suture.

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■ FIGURE 109-26

Posterolateral corner reconstruction. Coronal image of an intermediate echo time MR study (A) shows bioabsorbable interference screws (long white arrows) fixating the lateral collateral ligament (white arrow) and popliteus tendon (black arrow) reconstructions in a patient with additional ACL reconstruction. Tibial staple fixation is also present and better seen on radiograph (B) where the tunnels for the reconstructions are visible (long black arrows) but not the interference screws. (©Hospital for Special Surgery, New York, New York.)

Indications, Contraindications, Purpose, and Underlying Mechanics To restore stability in a joint where many structures have been injured, many structures need to be repaired. Multiple ligament reconstructions can be difficult. From an imaging standpoint, one need merely to evaluate each structure and its integrity, as described earlier.

Expected Appearance on Relevant Modalities The expected appearance of a multiligament reconstruction is a composite of the individual ligaments.They should all be anatomic in position and continuous. On MRI, they are of low signal intensity. On radiography, the fixation devices should not extend into the joint or excessively into the soft tissues.

■ FIGURE 109-27

Posterolateral corner and ACL reconstruction. Coronal, intermediate echo time MR image shows ACL and fibular collateral ligament reconstructions (short white arrows). After meniscectomy, change is noted in the medial meniscus (long white arrow). (©Hospital for Special Surgery, New York, New York.)

MULTIPLE LIGAMENT RECONSTRUCTION Description Severe trauma, such as knee dislocations, can injure many structures and render the knee unstable. For any hinged joint, if both collateral ligaments are torn the cause is likely to be dislocation.

Potential Complications and Radiologic Appearance Complications have also been discussed previously and include poor graft placement, re-injury, infection, and reactive scar formation, none of which is specific to multiligament reconstruction.

MENISCECTOMY Description Meniscectomy is the process of removing a portion or all of a meniscus. Partial removal, the process of shaving an irregular edge, may simply be referred to as débridement. Meniscal resections are commonly performed arthroscopically, but in the past they required an open procedure through an arthrotomy.

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Indications, Contraindications, Purpose, and Underlying Mechanics

MENISCAL REPAIR Description

Meniscal tears are common and can be caused by both degenerative and traumatic processes.The tears can cause pain, catching, and clicking. Displacement of potions of the torn meniscus can cause locking of the knee or the inability to flex or extend the knee. Because the meniscus is important for the normal function of the joint—to dissipated load and add stability— surgeons try to preserve meniscal tissue. This can be done by repairing or sometimes replacing or transplanting meniscal tissue. If the meniscal tissue is abnormal, is thought to be the source of the patient’s symptoms, and cannot be salvaged, it is resected. Formerly, before the importance of preserving meniscal tissue was realized, surgeons resected the entire meniscus. Now they resect only as much as they have to for relief of symptoms and restoration of function.

Because the meniscus is important for the normal function of the joint—to dissipate load and add stability—surgeons try to preserve meniscal tissue.This can be done by repairing or sometimes replacing/transplanting meniscal tissue. Different methods of meniscal repair (tack fixation and inside-out and outside-in techniques) are at the discretion of the surgeon.

Indications, Contraindications, Purpose, and Underlying Mechanics

The appearance of the postoperative meniscus depends on the surgery performed. In partial meniscectomy, in which a portion of the meniscus is shaved to restore a smooth edge, the meniscus may simply appear smaller on MRI (Fig. 109-27). If there was a large tear, such as a long oblique tear, the appearance may be that of a smaller meniscus with persistent oblique increased signal intensity in the meniscal remnant that can persist for years after surgery.6 If the meniscus is severely degenerated or so extensively torn that it cannot be salvaged, all or most of the meniscus will be removed (resected).

The peripheral aspect of the meniscus (toward the capsule) is more vascular than the central aspect. This vascularity may allow healing and repair so that peripheral tears may be repaired, whereas central tears cannot be repaired, because they will not heal. The peripheral part of the meniscus is called the red zone, the midportion is called the red-white zone, and the central portion is the white zone. The red zone corresponds to zones 0 and 1; the red-white zone is zone 2; and the white zone is zone 3. Meniscocapsular separations fall into zone 0 tears and can be repaired. Complete radial tears are difficult because they extend to the nonvascular zone and, if approximated, have a lot of stress put on a repair during weight bearing. In young people, attempts may be made to repair these with suture and blot clot to promote healing, because the resection would remove a large portion of meniscus and accelerate arthrosis. In oblique tears the central portion may be resected, with the peripheral portion being repaired.

Potential Complications and Radiologic Appearance

Expected Appearance on Relevant Modalities

The primary complication of partial meniscectomy for meniscal tear is re-tear or degeneration of that meniscus. If the meniscus is re-torn, it can appear very similar to a torn native meniscus: on arthrography or MR arthrography, contrast medium would get into the tear. Without contrast medium enhancement we have to rely on signal intensity, and it can be difficult to distinguish on MRI between the residual healing or healed scar after partial meniscectomy from a re-tear. The re-tear is supposed to have higher abnormal signal intensity than fluid, whereas the repaired, healed, or healing meniscus is supposed to have slightly lower signal intensity. Often we do not have the preoperative study to see where a meniscus was torn originally. Of course if the new signal abnormality is in a different place from the original tear, the abnormality is evaluated as if there was no surgery and careful examination for tears and flaps should be undertaken as usual. An almost expected result of meniscal resection is joint arthrosis. It is not so much a complication as a consequence. Evaluation of articular cartilage is at least as important in the postoperative knee as in an unoperated knee.

On conventional MR or CT arthrography, a meniscal repair would look like a normal meniscus, unless partially resected, in which case it would look like a partial meniscectomy. There may be some irregularity at the repair site, but there will be no contrast imbibition.6 On MRI, we usually see scar from the repair, with small foci of dephasing near the capsule that indicate that there has been surgery. Often scar extends to the subcutaneous fat in the region of the repair. Artifact may also be present in the meniscus, depending on the method of repair used, with tack fixation having slightly more artifact. The site of a normal meniscal repair can have abnormal signal in the orientation of the original tear that represents fibrous tissue (Fig. 109-28). There may also be high signal that is more extensive than in the original tear, related to the repair (Fig. 109-29). Persistent increased signal intensity is part of the normal healing process and can remain for up to 2 years after surgery. This intermediate signal, however, will not be as high as the signal intensity of joint fluid. Unless the signal intensity is as high as that as fluid, or fluid is definitely in the prior defect, one cannot say

Expected Appearance on Relevant Modalities

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■ FIGURE 109-28

Meniscal healing versus re-tear. Sagittal intermediate echo time MR images of the medial compartment. Abnormal signal in these postoperative medial menisci meets the tibial articular surface. The higher (fluid) signal in B reflects retear, whereas the intermediate signal in A represents healing (fibrous tissue). These subtle criteria apply whether evaluating the meniscus after débridement in that location or repair. (©Hospital for Special Surgery, New York, New York.)

A

B

A promising technique to evaluate healing, forwarded by Dr. Lawrence White of Mt. Sinai Hospital in Toronto, is to perform an MR meniscal perfusion study to look for contrast medium flowing across the meniscus in the region of prior tear/repair. If the contrast medium passes, then blood is crossing the gap and the meniscus is healed. It is also true that menisci can tear in places different from where the repair was performed. In that case they are treated as an unoperated meniscus.

Potential Complications and Radiologic Appearance

■ FIGURE 109-29 Meniscal repair. Sagittal, short echo time MR image shows the multiple areas of high signal (arrows) that can be present after meniscal repair, without re-tear. (©Hospital for Special Surgery, New York, New York.)

that the meniscus has re-torn. This is also true on MR arthrography where it would be easier to see re-tears. Parameniscal cysts are usually, but not always, drained at the time of meniscal surgery, so their presence does not indicate there is a re-tear. Fluid can also dissect into the meniscus from the capsular side. Whereas this suggests that the meniscal repair is not healing well and that there is breakdown of the repair, this fluid, if it does not extend to an articular surface, is not considered a re-tear (Fig. 109-30).

The most common complication of meniscal repair is lack of healing and re-tear.As described earlier, re-tear is characterized by fluid imbibition into the repair site (Fig. 109-31). Fluid at the capsule extending into the meniscus suggests that the meniscus is not healing well (see Fig. 109-30). In repairing menisci, sutures are fed percutaneously into the joint.Although an attempt is made to avoid important structures while doing this, occasionally a suture will tether the peroneal nerve, causing early postoperative neuralgia and requiring surgery to remove the offending suture (Fig. 109-32). Subcutaneous scar is less likely to do this postoperatively.

MENISCAL TRANSPLANT Description Because the meniscus is important for the normal function of the joint—to dissipate load and add stability—surgeons try to preserve meniscal tissue.This can be done by repairing or sometimes replacing or transplanting meniscal tissue. It would be ideal for patients to be able to regenerate meniscal tissue, and scaffolds are being developed to help promote this.7 Until those or other techniques for tissue regeneration or replacement are available and successful,

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■ FIGURE 109-30

Postoperative meniscal repair. Sagittal, intermediate echo time MR images through the medial compartment without (A) and with (B) fat suppression demonstrate high signal with fluid intensity at the capsule and extending into the meniscus (arrows), indicating capsular-sided breakdown of the repair. When the fluid clearly extends to the articular surface, it defines a re-tear. (©Hospital for Special Surgery, New York, New York.)

A

B

■ FIGURE 109-31 Re-tear meniscal repair. This sagittal intermediate echo time MR image of an orthopedic surgery resident shows fluid signal coursing through the posterior horn of the medial meniscus (black arrows), indicating complex (more than one plane) tear. There is a small apical flap (long white arrow). (©Hospital for Special Surgery, New York, New York.)

■ FIGURE 109-32

the only option that patients have is to have their menisci replaced with cadaveric meniscal transplants.8 Meniscal allografts were first performed almost 100 years ago as partial knee transplantation to avoid amputation.The first isolated meniscal allografts were placed in the mid 1980s.9 Artificial menisci that would allow native fibrocartilage to grow into an artificial scaffold are being developed but are not yet available in the United States.

Indications, Contraindications, Purpose, and Underlying Mechanics

Peroneal nerve injury. Coronal, intermediate echo time MR image shows a deviation in the course of the peroneal nerve (arrows) after lateral meniscus repair. There are specks of dark signal with dephasing in this area. The finding is related to suture tethering of the peroneal nerve, requiring surgery to release the nerve. It is important to extend the coronal images far enough posterior to include the peroneal nerve if that is a clinical concern. (©Hospital for Special Surgery, New York, New York.)

Because meniscal transplantation is a potential way to prevent arthrosis in patients who have required meniscectomy, the indication is just that—for patients without menisci who have not yet developed arthrosis. Once the knee is arthritic, the transplant has a high likelihood of

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failure,Therefore, arthrosis is a relative contraindication to meniscal transplantation.10 For the allograft to work, alignment and, therefore, mechanics of the joint have to be normal. For this reason, in some individuals, standing hip to ankle radiographs are performed to see if a concomitant osteotomy is necessary to correct any abnormal mechanical axis of the knee before transplantation. The clinical and radiographic outcome measures for meniscal allografts do not always agree. Patients can be asymptomatic but still have a torn, extruded, or degenerated graft. Likewise, a patient can have a normal graft from an imaging standpoint but have continued symptoms. Imaging becomes an important way to objectively judge success and evaluate new techniques, such as meniscal allografts.

Expected Appearance on Relevant Modalities Recognizing that a patient has had a meniscal allograft placed is half the battle. Once that is realized, there are five things to evaluate on postoperative meniscal transplants: the meniscus integrity itself, attachment to the joint capsule, attachment to bone, degree of extrusion, and underlying joint (Fig. 109-33).10 Whereas there are different ways to treat the allograft,the radiographic appearances of these methods are the same. The meniscus should maintain normal signal and morphology: it should be of low signal intensity without tear (using the criteria for a native meniscus) (Fig. 109-34).

A

B

C

D

The allograft is sutured to the native capsule circumferentially. This attachment can have high signal, but there should be no separation or fluid interposition.They usually heal to the capsule very well (see Figs. 109-33 and 109-34). Two methods of meniscal attachment to bone are commonly used: the plug method and the slot method. In the plug method the tibial attachments of the anterior and posterior horns are harvested with a small plug of bone that is inserted into holes made in the native knee (much like the mosaicplasty technique described for osteochondral autograft discussed later). These plugs are incorporated into the native bone. In the slot method, a cylindrical slot of bone is harvested. This slot incorporates the bony attachments of the anterior and posterior horns of the allograft. A similar cylinder of bone removed from the native tibia allows the allograft cylinder to be slotted in to fill the gap.The slotted bone becomes incorporated into the native bone. Initially, the allograft bone is of high signal intensity on fat-suppressed sequences and the interface between it and native bone is clearly visible. Over time, the allograft develops normal bony signal intensity and this interface disappears. Because the lateral tibial plateau is smaller and there is less room to place separate plugs, slots are almost always used on the lateral side. The degree of meniscal extrusion (the amount that the meniscus extends beyond the tibial margin on the coronal view) is one of the measurements associated with graft failure. The more it is extruded (and this can be measured in millimeters or percent), the more likely the meniscus is to have lost its integrity and the worse it will function to

■ FIGURE 109-33 Medial meniscal allograft. One of the hardest parts about evaluating meniscal allografts is knowing that one has been placed. Evaluation for bone plug incorporation, capsular healing, meniscal integrity, and meniscal extrusion follow. A, Midline sagittal MR image shows the two plugs with suture lines (small black arrows) extending from them in this patient with a medial meniscal allograft. The plugs are not normal bony signal and may have necrosed (white arrows). B, Coronal MR image shows meniscal extrusion (arrow) beyond the medial joint line (line). C, Sagittal MR image shows persistent high signal at the capsule, indicating that it has not entirely incorporated (small arrows). D, Sagittal MR image shows peripheral high signal extending to the tibial articular surface reflecting subtle tear of the allograft meniscus (arrow). (©Hospital for Special Surgery, New York, New York.)

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■ FIGURE 109-34 Meniscal transplant. Sagittal (A) and coronal (B), intermediate echo time MR images 6 years after successful medial meniscal transplant using plugs. The meniscus is not torn or extruded. The anterior capsule and infrapatellar fat are scarred. The posterior capsule is healed (A, arrow). (©Hospital for Special Surgery, New York, New York.)

A

B

dissipate force. Some surgeons like to evaluate the knee with weight-bearing views to get an idea of extrusion in a more functional situation.8 Lastly, as with all joints, whether or not surgery has been performed, the rest of the joint must be evaluated for chondral loss, status of the other meniscus, and any other pathologic process.

Potential Complications and Radiologic Appearance The specific complications of meniscal allograft involve each of the things that are listed as needing to be evaluated and have to do with failure of the allograft, either by poorly incorporating or intrinsically failing, such as

from tearing or losing its characteristics. There is also the possibility that the meniscus was poorly sized or poorly placed.The size that is requested for the meniscal allograft is determined by measurements made from preoperative radiographs. Re-tears of the meniscal allograft have the same appearance as that of the native meniscus and are evaluated and described similarly (Figs. 109-35 and 109-36). The capsular attachment may show dephasing related to suture. Otherwise the signal of the capsule varies from high to low on intermediate echo time, T2-weighted sequences. Fluid signal indicates capsular detachment. Bone plugs or slots can fail to incorporate, yielding a persistent line of demarcation. This may occur when the bone becomes ischemic (persistent increased intermediate

■ FIGURE 109-35 Medial meniscal transplant, plug technique. Posterior coronal (A) and axial (B) MR images in a patient with meniscal transplant show a radial tear of the posterior horn (arrows). (©Hospital for Special Surgery, New York, New York.)

A

B

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■ FIGURE 109-36 Lateral meniscal transplant, slot technique. Bucket handle tear. Coronal (A) and axial (B) MR images in a patient with meniscal transplant show displacement of the entire meniscus into the intercondylar notch (arrows). The slot appears low in signal, indicating fibrosis (black arrow). An interface surrounding it indicates that it has not incorporated (small arrows). (©Hospital for Special Surgery, New York, New York.)

A

B

echo time T2-weighted signal) or necrotic (low signal on all sequences) (see Figs. 109-33 and 109-36). The plugs should be placed near to the native tibial attachments so the meniscus can perform the same job with the same orientation. Sometimes it is hard to place the plugs exactly: many meniscal transplants have concomitant ACL grafts, and the room for plugs is limited. Occasionally, the allograft was badly sized and the allograft is too big or too small for the knee. It would appear that way if the meniscus is not getting to the edge of the joint (too small) or looks redundant.

CHONDRAL STIMULATION Description With the ability to see inside the knee joint, first with arthrotomy and arthrography and now with arthroscopy and MRI, we are identifying subtle abnormalities that might have previously gone undetected or tolerated. One of these abnormalities is articular chondral injuries that can cause pain, catching, clicking, or locking. The simplest treatment for a chondral injury, and one that can be performed at the time of arthroscopy without preparation, is to make holes in the subchondral bone, promoting bleeding. The blood fills the chondral defect and promotes the creation of reparative cartilage (usually fibrocartilage rather than articular cartilage). Chondroplasty involves smoothing the chondral edges and base of a chondral lesion.When the chondral abnormality extends to bone, stimulating bleeding is done by techniques called picking, abrasion arthroplasty, drilling, and microfracture, which are the same from an imaging standpoint.11

Indications, Contraindications, Purpose, and Underlying Mechanics Chondral stimulation by making the subchondral bone bleed is performed for small (