Essentials of Physical Medicine and Rehabilitation: Musculoskeletal Disorders, Pain, and Rehabilitation, 4e [4 ed.] 0323549470, 9780323549479

Packed with practical, up-to-date guidance, Essentials of Physical Medicine and Rehabilitation, 4th Edition, by Walter R

4,232 765 82MB

English Pages 1024 [1014] Year 2018

Report DMCA / Copyright

DOWNLOAD FILE

Polecaj historie

Essentials of Physical Medicine and Rehabilitation: Musculoskeletal Disorders, Pain, and Rehabilitation, 4e [4 ed.]
 0323549470, 9780323549479

Table of contents :
Cover
Essentials of Physical Medicineand Rehabilitation
Copyright
Dedication
Contributors
Preface
Part I: Musculoskeletal Disorders
Section I: Head, Neck, and Upper Back
1 - Cervical Spondylotic Myelopathy
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Anterior Approach
Posterior Approach
Potential Disease Complications
Potential Treatment Complications
2 - Cervical Facet Arthropathy
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
3 - Cervical Degenerative Disease
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
4 - Cervical Dystonia
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
5 - Cervical Radiculopathy
Definition
Symptoms
Physical Examination
Visual Observation
Palpation
Gait Evaluation
Range of Motion (ROM)
Sensory Testing
Deep Tendon Reflexes
Motor Testing
Joint Examination
Special Maneuvering
Lhermitte’s Sign
Adson’s Test and Roos Test
Babinski Response, Hoffmann Sign, and Clonus
Functional Limitations
Diagnostic Studies
X-Ray
Computed Tomography (CT) Scan
MRI
Bone Scans
Nerve Conduction Studies/Electromyography (EMG)
Myelogram
Diagnostic Spinal Injections
Treatment
Initial
Rehabilitation
Procedures
Interlaminar Epidural Steroid Injections (ESIs)
Cervical Selective Nerve Root Block (SNRB)
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
6 - Cervical Sprain or Strain
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
7 - Cervical Spinal Stenosis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Surgery
Technology
Potential Disease Complications
Potential Treatment Complications
8 - Cervicogenic Vertigo
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
9 - Trapezius Strain
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
Section II: Shoulder
10 - Acromioclavicular Injuries
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
11 - Adhesive Capsulitis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
12 - Biceps Tendinopathy
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
13 - Biceps Tendon Rupture
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
14 - Glenohumeral Instability
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Acute Phase (1 to 2 Weeks)
Recovery Phase (2 to 6 Weeks)
Functional Phase (6 Weeks to 6 Months)
Return to Play
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
15 - Labral Tears of the Shoulder
Definition
Symptoms
Superior Labral Anterior-Posterior Tear
Bankart Lesion
Physical Examination
Superior Labral Anterior-Posterior Tear
Bankart Lesion
Functional Limitations
Superior Labral Anterior-Posterior Tear
Bankart Lesion
Diagnostic Studies
Superior Labral Anterior-Posterior Tear
Bankart Lesion
Treatment
Initial
Superior Labral Anterior-Posterior Tear
Bankart Lesion
Rehabilitation
Superior Labral Anterior-Posterior Tear
Bankart Lesion
Procedures
Technology
Surgery
Superior Labral Anterior-Posterior Tear
Bankart Lesion
Potential Disease Complications
Potential Treatment Complications
16 - Rotator Cuff Tendinopathy
Definition
Symptoms
Physical Examination
Inspection
Palpation
Range of Motion
Strength
Special Tests
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Range of Motion and Pain Control
Flexibility and Strengthening
Advanced Strengthening
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
17 - Rotator Cuff Tear
Definition
Symptoms
Physical Examination
Special Tests
Functional Limitations
Diagnostic Studies
Treatment
Non-Operative Treatment
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
18 - Scapular Winging
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
19 - Shoulder Arthritis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
20 - Suprascapular Neuropathy
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
Section III: Elbow and Forearm
21 - Elbow Arthritis
Definition
Inflammatory Arthritis
Osteoarthritis
Symptoms
Physical Examination
Functional Limitations
Diagnostic Testing
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Treatment Complications
22 - Lateral Epicondylitis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
23 - Medial Epicondylitis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
24 - Median Neuropathy
Definition
Pronator Teres Syndrome
Anterior Interosseous Syndrome
Symptoms
Pronator Teres Syndrome
Anterior Interosseous Syndrome
Physical Examination
Pronator Teres Syndrome
Anterior Interosseous Syndrome
Functional Limitations
Pronator Teres Syndrome
Anterior Interosseous Syndrome
Diagnostic Studies
Pronator Teres Syndrome
Anterior Interosseous Syndrome
Treatment
Initial
Pronator Teres Syndrome
Anterior Interosseous Syndrome
Rehabilitation
Pronator Teres Syndrome
Anterior Interosseous Syndrome
Procedures
Technology
Surgery
Pronator Teres Syndrome
Anterior Interosseous Syndrome
Postoperative Rehabilitation36
0 to 1 Week
3 Weeks
Potential Disease Complications
Pronator Teres Syndrome
Anterior Interosseous Syndrome
Potential Treatment Complications
25 - Olecranon Bursitis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
26 - Radial Neuropathy
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
27 - Ulnar Neuropathy (Elbow)
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
Section IV: Hand and Wrist
28 - de Quervain Tenosynovitis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedure
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
29 - Dupuytren Contracture
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
30 - Extensor Tendon Injuries
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Zone I (Mallet Deformity)
Zone II
Zone III (Boutonnière Deformity)
Zone IV
Zone V
Zone VI
Zone VII
Zone VIII
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
31 - Flexor Tendon Injuries
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
32 - Hand and Wrist Ganglia
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
33 - Hand Osteoarthritis
Definition
Symptoms
Physical Examination
Interphalangeal Joints
Metacarpophalangeal Joints
Trapeziometacarpal Joint
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Distal Interphalangeal Joint
Proximal Interphalangeal Joint
Trapeziometacarpal Joint
Potential Disease Complications
Potential Treatment Complications
34 - Hand Rheumatoid Arthritis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Flexor and Extensor Tendon Reconstruction Postoperative Rehabilitation
Metacarpophalangeal Joint Postoperative Rehabilitation
Interphalangeal Joint Postoperative Rehabilitation
Procedures
Technology
Surgery
Extensor Tendon Surgery
Flexor Tendon Surgery
Metacarpophalangeal Joint Surgery
Interphalangeal Joint Surgery
Potential Disease Complications
Potential Treatment Complications
35 - Kienböck Disease
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
36 - Median Neuropathy (Carpal Tunnel Syndrome)
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
37 - Trigger Finger
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
38 - Ulnar Collateral Ligament Sprain
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
39 - Ulnar Neuropathy (Wrist)
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
40 - Wrist Osteoarthritis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
41 - Wrist Rheumatoid Arthritis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
Section V: Mid Back
42 - Thoracic Compression Fracture
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Testing
Treatment
Initial
Rehabilitation
Procedures
Technologies and Devices
Surgery
Potential Disease Complications
Potential Treatment Complications
43 - Thoracic Radiculopathy
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
44 - Thoracic Sprain or Strain
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
Section VI: Low Back
45 - Lumbar Degenerative Disease
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
46 - Lumbar Facet Arthropathy
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
47 - Lumbar Radiculopathy
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Electromyography
Imaging
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
48 - Low Back Strain or Sprain
Definition
Symptoms
Etiology
Axial Pain (Pain Overlying the Lumbosacral Area)
Radicular Pain
Myofascial Pain
Referred Pain
Occult Lesions
Physical Examination
Diagnostic Studies
Treatment
Initial
Rehabilitation
Acupuncture
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
49 - Lumbar Spondylolysis and Spondylolisthesis
Definition
Symptoms
Physical Examination
Diagnostic Studies
Prognosis
Treatment
Initial
Activity Modification
Bracing
Medications
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
50 - Lumbar Spinal Stenosis
Definition
Canal Measurements
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
51 - Sacroiliac Joint Dysfunction
Definition
Symptoms
Physical Examination
Provocative Tests
Gaenslen Test
Patrick Test (Also Called Flexion, Abduction, External Rotation Test)
Gillet Test
POSH Test (Posterior Shear Test)
REAB Test (Resisted Abduction)
Distraction Test (Also Called the Gapping Test)
Compression Test
Yeoman Test
Pressure Over the Sacral Sulcus
Active Straight-Leg Raise
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
Section VII: Pelvis, Hip, and Thigh
52 - Adhesive Capsulitis of the Hip
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Potential Disease Complications
Potential Treatment Complications
53 - Hip Adductor Strain
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
54 - Femoral Neuropathy
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
55 - Hip Osteoarthritis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Corticosteroid Injections
Viscosupplementation Injections
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
56 - Hip Labral Tears
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
57 - Lateral Femoral Cutaneous Neuropathy
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
58 - Piriformis Syndrome
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Testing
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
59 - Pubalgia
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
60 - Quadriceps Contusion
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
61 - Total Hip Replacement
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
62 - Greater Trochanteric Pain Syndrome
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
Section VIII: Knee and Leg
63 - Anterior Cruciate Ligament Sprain
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Acute Phase
Recovery Phase
Functional Phase
Postsurgical Rehabilitation
Return to Play
Objective Testing
Procedures
Technology
Surgery
Potential Complications of Disease
Potential Complications of Treatment
64 - Baker Cyst
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
65 - Knee Chondral Injuries
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
66 - Collateral Ligament Sprain
Definition
Medial Complex Injury and Resultant Instability
Lateral Complex Injury and Resultant Instability
Symptoms
Physical Examination
Functional Limitations
Diagnostic Testing
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
67 - Compartment Syndrome of the Leg
Definition
Acute Compartment Syndrome
Chronic Exertional Compartment Syndrome
Symptoms
Acute Compartment Syndrome
Chronic Exertional Compartment Syndrome
Physical Examination
Acute Compartment Syndrome
Chronic Exertional Compartment Syndrome
Functional Limitations
Acute Compartment Syndrome
Chronic Exertional Compartment Syndrome
Diagnostic Studies
Acute Compartment Syndrome
Chronic Exertional Compartment Syndrome
Treatment
Initial
Acute Compartment Syndrome
Chronic Exertional Compartment Syndrome
Rehabilitation
Acute Compartment Syndrome
Chronic Exertional Compartment Syndrome
Procedures
Technology
Surgery
Acute Compartment Syndrome
Chronic Exertional Compartment Syndrome
Potential Disease Complications
Acute Compartment Syndrome
Chronic Exertional Compartment Syndrome
Potential Treatment Complications
68 - Hamstring Strain
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
69 - Iliotibial Band Syndrome
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
70 - Knee Osteoarthritis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Exercise
Therapeutic Modalities
Adaptive Equipment
Bracing and Footwear
Procedures
Biologics
Technology
Surgery (Table 70.3)
Potential Disease Complications
Potential Treatment Complications
71 - Knee Bursopathy
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complication
Potential Treatment Complications
72 - Meniscal Injuries
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
73 - Patellar Tendinopathy (Jumper’s Knee)
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Testing
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
74 - Patellofemoral Syndrome
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Testing
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
75 - Fibular (Peroneal) Neuropathy
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
76 - Posterior Cruciate Ligament Sprain
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
77 - Quadriceps Tendinopathy
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complication
Potential Treatment Complications
78 - Shin Splints
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
79 - Stress Fractures
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
80 - Total Knee Arthroplasty
Definition
Symptoms
Physical Exam
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Phase One
Phase Two
Phase Three
Phase Four (Final)
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
Section IX: Foot and Ankle
81 - Achilles Tendinopathy
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
82 - Ankle Arthritis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
83 - Ankle Sprain
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
84 - Bunion and Bunionette
Bunion
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
Bunionette
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Procedures
Surgery
Potential Disease Complications
Potential Treatment Complications
85 - Chronic Ankle Instability
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
86 - Foot and Ankle Bursitis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
87 - Hallux Rigidus
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
88 - Hammer Toe
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Postoperative Rehabilitation
Potential Disease Complications
Potential Treatment Complications
89 - Mallet Toe
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
90 - Metatarsalgia
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Surgery
Technology
Potential Disease Complications
Potential Treatment Complications
91 - Morton’s Neuroma
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
92 - Plantar Fasciitis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Testing
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
93 - Posterior Tibial Tendon Dysfunction
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
94 - Tibial Neuropathy (Tarsal Tunnel Syndrome)
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
Part 2: Pain
95 - Abdominal Wall Pain
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
96 - Arachnoiditis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
97 - Chemotherapy-Induced Peripheral Neuropathy
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
98 - Chronic Pain Syndrome
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Patient Education
Mental Health Treatment
Medications
Medical Marijuana
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
99 - Coccydynia
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
100 - Complex Regional Pain Syndrome
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Anti-Inflammatory Medications
Neuropathic Medications
Opioids and N-Methyl-d-Aspartate Receptor Antagonists
Bisphosphonates
Novel Medications
Rehabilitation
Physical and Occupational Therapy
Mirror Therapy
Procedures
Surgery
Technology
Potential Disease Complications
Potential Treatment Complications
101 - Costosternal Syndrome
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Disease Complications
Potential Treatment Complications
102 - Fibromyalgia
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Surgery
Technology
Potential Disease Complications
Potential Treatment Complications
103 - Headaches
Definition
Migraine
Cluster
Tension Type
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Migraine
Cluster
Tension Type
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
104 - Intercostal Neuralgia
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
105 - Myofascial Pain Syndrome
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
106 - Occipital Neuralgia
Definition
Anatomy
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
107 - Pelvic Pain
Definition
Adhesive Disease
Chronic Pelvic Inflammatory Disease
Gastrointestinal: Irritable Bowel Syndrome
Gynecologic: Endometriosis, Uterine Leiomyomas, and Adenomyosis
Musculoskeletal
Pelvic Congestion Syndrome
Urologic
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Myofascial Pelvic Pain Syndrome
Endometriosis
Uterine Leiomyomas
Rehabilitation
Procedures
Surgery
Technology
Potential Disease Complications
Potential Treatment Complications
108 - Phantom Limb Pain
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
109 - Postherpetic Neuralgia
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
110 - Post-Mastectomy Pain Syndrome
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
111 - Post-Thoracotomy Pain Syndrome
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Surgery
Technology
Potential Disease Complications
Potential Treatment Complications
112 - Radiation Fibrosis Syndrome
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
113 - Repetitive Strain Injuries
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technologies and Devices
Surgery
Potential Disease Complications
Potential Treatment Complications
114 - Temporoman­dibular Joint Dysfunction
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
115 - Central Post-Stroke Pain (Thalamic Pain Syndrome)
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Surgery
Technology
Potential Disease Complications
Potential Treatment Complications
116 - Thoracic Outlet Syndrome
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
117 - Tietze Syndrome
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
118 - Trigeminal Neuralgia
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
Part 3: Rehabilitation
119 - Upper Limb Amputations
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Testing
Treatment
Initial
Rehabilitation
Initial Rehabilitation Care
Rehabilitative and Prosthetic Management
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
120 - Lower Limb Amputations
Amputation Levels and Epidemiology
Amputation Surgery
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Revision Surgery
Potential Disease Complications
Potential Treatment Complications
121 - Ankylosing Spondylitis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Pharmacological Treatment
Rehabilitation
Technology
Procedures
Surgery
Potential Disease Complications
Potential Treatment Complications
122 - Burns
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Pain
Pruritus
Wounds
Deep Venous Thrombosis
Hypertrophic Scarring
Contractures
Heterotopic Ossification (see Chapter 131)
Hypermetabolism and Deconditioning
Psychological Comorbidity
Technology
Procedures
Surgery
Potential Disease Complications
Long-term Pain and Pruritus
Hypertrophic Scarring
Contractures
Amputation
Osteophytes and Heterotopic Ossification
Neuropathy
Psychological and Cognitive Complications
Potential Treatment Complications
123 - Cardiac Rehabilitation
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
124 - Cancer-Related Fatigue
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
125 - Cerebral Palsy
Definition
Prevalence
Etiology
Classification
Symptoms
Head, Eyes, Ears, Nose, and Throat
Cardiovascular
Pulmonary
Gastrointestinal and Genitourinary
Musculoskeletal
Neurologic
Other
Physical Examination
Functional Limitations
Diagnostic Studies
Head, Eyes, Ears, Nose, and Throat
Cardiovascular
Pulmonary
Gastrointestinal and Genitourinary
Musculoskeletal
Neurologic
Treatment
Initial
Rehabilitation
Procedures
Surgery
Potential Treatment Complications
Technology
Potential Disease Complications: Aging With Cerebral Palsy
126 - Chronic Fatigue Syndrome
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
127 - Joint Contractures
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
128 - Deep Venous Thrombosis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Deep Venous Thrombosis Treatment
Warfarin
Duration of Anticoagulant Therapy
Management of Recurrent Deep Venous Thrombosis
Treatment of Distal Deep Venous Thrombosis
Treatment of Superficial Venous Thrombosis
Rehabilitation
Procedures
Technology
Surgery or Catheter-Directed Thrombolysis
Potential Disease Complications
Potential Treatment Complications
129 - Diabetic Foot and Peripheral Arterial Disease
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial Risk Factor Modification
Smoking Cessation
Hyperglycemia Management
Hypertension Control
Statin Therapy
Antiplatelet Therapy
Homocysteine Lowering
Influenza Vaccination
Structured Aerobic Exercise
Rehabilitation
Exercise
Foot Care
Skin Ulcers
Procedures
Technology
Cell-Based Therapy
Spinal Cord Stimulation
Intermittent Pneumatic Compression (Arterial Flow Pump)
Surgery
Potential Disease Complications
Potential Treatment Complications
130 - Dysphagia
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Testing
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
131 - Heterotopic Ossification
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Technology and Devices
Potential Disease Complications
Potential Treatment Complications
132 - Lymphedema
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Technologies and Devices
Surgery
Potential Disease Complications
Potential Treatment Complications
133 - Motor Neuron Disease
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Pharmacologic
Symptomatic
Rehabilitation
Exercise
Assistive Technology for Mobility
Pain Management
Dysphagia
Dysarthria
Pulmonary Rehabilitation (see also Chapter 151)
Procedures
Management of Sialorrhea
Gastrostomy Tube
Tracheostomy
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
134 - Movement Disorders
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
135 - Multiple Sclerosis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
136 - Myopathies
Definition
Muscular Dystrophies
Congenital Myopathies
Metabolic Myopathies Including Mitochondrial Myopathies
Inflammatory Myopathies
Drug-Induced and Endocrine Myopathies
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
137 - Neural Tube Defects
Definition
Symptoms
Neurologic
Orthopedic
Urinary
Gastrointestinal
Endocrine
Reproductive
Pulmonary
Cardiovascular
Allergy and Immunology
Dermatology
Nutrition
Psychosocial
Physical Examination
Functional Limitations
Diagnostic Studies
Prenatal
Postnatal
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
138 - Neurogenic Bladder
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Acute Phase and Central Nervous System Shock Phase
Anticholinergic Drugs (Drugs to Increase Bladder Capacity)
Procedures
Botulinum Toxin
Technology
Surgery
Potential Disease Complications
Autonomic Dysreflexia
Potential Treatment Complications
139 - Neurogenic Bowel
Definition
Bowel Innervations and Gastrointestinal Motility
Neurogenic Bowel
Pathophysiology of Constipation in Neurologically Impaired Patients
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Anorectal Dyssynergia
Treatment
Initial
Rehabilitation
Bowel Management after Spinal Cord Injury
Patient Education and Awareness of Risk Factors
Use of Prokinetic Drugs
Procedures
Botulinum Toxin in Gastrointestinal Disorders
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
140 - Osteoarthritis
Definition
Symptoms
Physical Examination
Joint Examination
Neuromuscular and General Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
141 - Osteoporosis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies3-6
Treatment3-6
Initial
Calcium
Vitamin D
Exercise
Smoking Cessation
Fall Prevention
Guidelines for Treatment
Hormone Replacement Therapy
Estrogen Agonist/Antagonists (Formerly Known as Selective Estrogen Receptor Modulators)
Bisphosphonates
Calcitonin
Parathyroid Hormone
Parathyroid Hormone Related Peptide
Denosumab
Rehabilitation
Back Orthoses
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
142 - Parkinson Disease
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
143 - Peripheral Neuropathies
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
144 - Plexopathy—Brachial
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Differential Diagnosis
Etiology of Brachial Plexopathy
Supraclavicular
Birth Trauma
Trauma
Intraoperative Arm Malpositioning
Pancoast Syndrome
Neurogenic Thoracic Outlet
Infraclavicular
Postirradiation
Metastatic Lymphadenopathy
Regional Blocks
Heterotopic Ossification
Retroclavicular
Midclavicular Fractures
Diffuse Localization
Neuralgic Amyotrophy
Hereditary Neuralgic Amyotrophy
Diabetic Cervical Radiculoplexus Neuropathy
Primary Neoplastic Peripheral Nerve Tumors
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
145 - Plexopathy—Lumbosacral
Definition
Etiology
Trauma
Labor and Delivery
Iatrogenic
Oncologic
Diabetic Amyotrophy
Vascular
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Electrodiagnostic Testing
Imaging Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
146 - Polytrauma Rehabilitation
Definition of Polytrauma
History of Polytrauma System of Care
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Imaging
Laboratory
Electrodiagnostics
Neuropsychological Evaluations
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
147 - Postpoliomyelitis Syndrome
Definition
Symptoms
Muscle Weakness
Fatigue
Pain
Respiratory Problems
Swallowing
Cold Intolerance
Physical Examination
Functional Limitations
Diagnostic Studies
Weakness
Fatigue
Pain
Respiratory Problems
Swallowing Problems
Cold Intolerance
Treatment
Initial
Weakness
Fatigue
Pain
Respiratory Problems
Swallowing Problems
Cold Intolerance
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
148 - Postconcussion Symptoms
Definition
Symptoms
Cognition
Headaches
Sleep
Vestibular/Balance Disorder
Other
Physical Examination
Cognition
Psychological
Headaches
Vestibular/Balance Disorder
Visual
Olfactory
Other
Functional Limitations
Diagnostic Testing
Treatment
Initial
Rehabilitation
Psychological
Headaches
Vestibular/Balance Disorder
Cognition
Vocational
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
149 - Pressure Ulcers
Definition
Intrinsic Risk Factors
Extrinsic Risk Factors
Biofilm
Unavoidable Pressure Injuries
Symptoms
Physical Examination
Medical Device–Related Pressure Injury
Mucosal Membrane Pressure Injury
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
150 - Rehabilitation of the Patient with Respiratory Dysfunction
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Organization of a Comprehensive Rehabilitation Program
Therapeutic Interventions
Medications
Counseling and General Medical Care
Nutrition
Retraining of Breathing
Elimination of Airway Secretions
Inspiratory Resistive Exercises
Respiratory Muscle Rest
Supplemental Oxygen Therapy
Exercise
Role of Behavioral Management in Pulmonary Rehabilitation
Physical Aids
The Results of Pulmonary Rehabilitation
Technology
Potential Treatment Complications
151 - Respiratory Management of Neuromuscular Disorders
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
The Intervention Objectives
Goal One: Maintain Pulmonary Compliance, Lung Growth, and Chest-Wall Mobility
Goal Two: Maintain Alveolar Ventilation
Goal Three: Augment Cough Flows
Glossopharyngeal Breathing
Oximetry Monitoring and Feedback Protocol
Technology
Surgery
Long-Term Outcomes
Extubation of Unweanable Patients
Decannulation of Unweanable Patients
Potential Treatment Complications
152 - Rheumatoid Arthritis
Definition
Symptoms
Systemic
Cutaneous
Ophthalmologic
Pulmonary
Neurologic
Cardiac
Physical Examination
Functional Limitations
Diagnostic Studies
Laboratory Evaluation
Imaging
Treatment
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
153 - Scoliosis and Kyphosis
Definitions
Scoliosis
Kyphosis
Symptoms
Scoliosis
Kyphosis
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Scoliosis
Kyphosis
Rehabilitation
Scoliosis
Kyphosis
Procedures
Technology
Scoliosis
Kyphosis
Surgical Treatment
Potential Disease Complications
Potential Treatment Complications
154 - Spasticity
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
155 - Speech and Language Disorders
Definitions
Symptoms
Physical Examination
Aphasia
Apraxia of Speech
Dysarthria
Dysphonia
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Aphasia
Dysarthria
Apraxia of Speech
Dysphonia
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
156 - Spinal Cord Injury (Cervical)
Definition
Symptoms
Physical Examination
Neurologic
Respiratory
Cardiac
Abdomen
Spine
Extremities
Skin
Functional Limitations
Diagnostic Studies
Spinal Imaging
Electrodiagnostic Testing
Urologic Studies
Pulmonary Function
Musculoskeletal Imaging
Treatment
Initial
Rehabilitation
Ongoing Management and Health Maintenance
Respiratory
Cardiovascular
Genitourinary
Gastrointestinal
Skin
Neurologic
Musculoskeletal
Psychosocial
Procedures
Pressure Ulcers
Spasticity
Pain
Technology
Functional Electrical Stimulation
Body Weight-Supported Treadmill Training
Exoskeletons
Brain-computer Interface
Surgery
Spine Surgery
Pressure Ulcers
Spasticity
Motor Function
Bladder Dysfunction
Bowel Dysfunction
Upper Extremity Pain
Post-traumatic Syringomyelia
Potential Disease Complications
Respiratory
Cardiovascular
Genitourinary
Gastrointestinal
Skin
Metabolic and Endocrine
Neurologic
Musculoskeletal
Psychosocial
Potential Treatment Complications
157 - Spinal Cord Injury (Thoracic)
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Skin Management
Pain
Bladder Management
Bowel Management
Mental Health
Sexual and Reproductive Function
Deep Venous Thrombosis
Spasticity Management
Heterotopic Ossification
Osteoporosis
Autonomic Dysreflexia
Respiratory Health
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
158 - Spinal Cord Injury (Lumbosacral)
Definition
Neurologic Versus Skeletal Level of Injury
Symptoms
Physical Examination
Spinal Inspection and Palpation
Evidence of Concurrent Injuries
Neurologic Examination
Sensory Examination
Motor Examination
Neurologic Rectal Examination
Additional Neurologic Examination
Conus Medullaris and Cauda Equina Injuries
Skin Examination
Functional Limitations
Expected Functional Outcomes
Ambulation
Bowel, Bladder, and Sexual Dysfunction
Factors Affecting Functional Outcomes
Diagnostic Studies
Spinal Imaging
Electrodiagnostic Testing
Urologic Studies
Treatment
Initial
Rehabilitation
Bowel Management
Bladder Management
Pain and Spasticity
Pressure Ulcer Prevention
Procedures
Spasticity
Pain
Pressure Ulcers
Technology
Functional Electrical Stimulation of the Lower Extremities
Surgery
Spine
Pressure Ulcers
Upper Extremity Pain
Bladder and Bowel Dysfunction
Post-traumatic Syringomyelia
Potential Disease Complications
Potential Treatment Complications
159 - Stroke
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Exercise
Electrical Stimulation
Dysphagia
Communication
Cognition
Orthoses
Ambulatory Aids and Wheelchairs
Shoulder Subluxation and Pain
Splints and Stretching
Vocational Rehabilitation
Procedures
Technologies and Devices
Surgery
Potential Disease Complications
Potential Treatment Complications
160 - Stroke in Young Adults
Definition
Symptoms
Emotional Effects
Pain
Muscle Stiffness Due to Spasticity
Bladder Dysfunction
Sexual Dysfunction
Fatigue
Physical Examination
Emotional Effects
Pain
Muscle Stiffness Due to Spasticity
Bladder Dysfunction
Sexual Dysfunction
Fatigue
Functional Limitations
Driving
Return to Work
Parenting
Diagnostic Studies
Treatment
Emotional Effects
Initial
Rehabilitation
Pain
Initial
Rehabilitation
Procedures
Surgery
Muscle Stiffness Due to Spasticity
Initial
Rehabilitation
Procedures
Surgery
Bladder Dysfunction
Initial
Rehabilitation
Surgery
Sexual Dysfunction
Fatigue
Initial
Rehabilitation
Technology
Potential Disease Complications
Potential Treatment Complications
161 - Systemic Lupus Erythematosus
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Jaccoud Arthropathy
Increased Risk of Infection
Hypertension
Premature Atherosclerosis
Potential Treatment Complications
162 - Transverse Myelitis
Definition
Symptoms
Physical Examination
Functional Limitations
Diagnostic Studies
Treatment
Initial
Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
163 - Traumatic Brain Injury
Definition
Epidemiology and Pathophysiology
Symptoms
Physical Examination
Functional Limitations
Motor
Behavior
Social
Diagnostic Studies
Imaging Studies
Biomarkers
Functional Assessment Tools
Neuropsychological Testing
Treatment
Initial
Arousal
Attention
Agitation
Memory
Seizures
Spasticity
Rehabilitation
Physical Therapy
Occupational Therapy
Speech Therapy
Vocational Rehabilitation
Procedures
Technology
Surgery
Potential Disease Complications
Potential Treatment Complications
Index
A
B
C
D
E
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
X
Y
Z
IBC

Citation preview

Fourth Edition

Essentials of

Physical Medicine and Rehabilitation Musculoskeletal Disorders, Pain, and Rehabilitation Walter R. Frontera, MD, PhD, MA (Hon.), FRCP Professor Physical Medicine, Rehabilitation, and Sports Medicine Physiology and Biophysics University of Puerto Rico School of Medicine San Juan Puerto Rico

Julie K. Silver, MD Associate Professor and Associate Chair Department of Physical Medicine and Rehabilitation Harvard Medical School Attending Physician, Spaulding Rehabilitation Hospital Clinical Associate, Massachusetts General Hospital Associate in Physiatry, Brigham and Women’s Hospital Boston, Massachusetts

Thomas D. Rizzo, Jr., MD Consultant Physical Medicine and Rehabilitation Mayo Clinic Jacksonville, Florida Assistant Professor College of Medicine Mayo Clinic Rochester, Minnesota

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

ESSENTIALS OF PHYSICAL MEDICINE AND REHABILITATION: MUSCULOSKELETAL DISORDERS, PAIN, AND REHABILITATION, FOURTH EDITION

ISBN: 978-0-323-54947-9

Copyright © 2019 by Elsevier, Inc. All rights reserved. Mayo retains copyright © to Mayo Copyrighted Drawings. 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. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notices Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, 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 practitioners, relying on their own experience and knowledge of their patients, 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 authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Previous editions copyrighted 2015, 2008, and 2002. Library of Congress Control Number: 2018944804

Senior Content Strategist: Kristine Jones Senior Content Development Specialist: Joanie Milnes Publishing Services Manager: Julie Eddy Senior Project Manager: Cindy Thoms Book Designer: Renee Duenow

Printed in China Last digit is the print number: 9 8 7 6 5 4 3 2 1

We dedicate this book to our mentors, teachers, colleagues, and students, who have encouraged us to pursue academic careers with their enthusiasm for knowledge and learning; to our patients, who often are our greatest teachers; and to our families, who support us and provide the foundation for our pursuits. Walter R. Frontera, MD, PhD, MA (Hon.), FRCP Julie K. Silver, MD Thomas D. Rizzo, Jr., MD

Contributors TAYYABA AHMED, DO Physical Medicine and Rehabilitation, Lenox Hill Hospital, New York, New York Pelvic Pain

VENU AKUTHOTA, MD Professor and Chair, Physical Medicine and Rehabilitation, University of Colorado, Denver, Colorado Collateral Ligament Sprain Iliotibial Band Syndrome Meniscal Injuries

JOSEPH T. ALLEVA, MD, MBA Division Head, Division of Physical Medicine and Rehabilitation; Clinical Assistant Professor, University of Chicago, Pritzker School of Medicine, Chicago, Illinois Cervical Sprain or Strain Patellar Tendinopathy (Jumper’s Knee) Patellofemoral Syndrome Piriformis Syndrome

ERIC L. ALTSCHULER, MD, PhD Associate Chief, Residency Program Director, Department of Physical Medicine and Rehabilitation, Metropolitan Hospital Center, New York, New York Complex Regional Pain Syndrome Central Post-Stroke Pain (Thalamic Pain Syndrome)

JOAO E.D. AMADERA, MD, PhD Assistant Professor at the Orthopedic and Traumatology Institute, University of São Spine Center, São Paulo, Brazil Low Back Strain or Sprain Baker Cyst

EDUARDO AMY, MD Assistant Professor, Physical Medicine, Rehabilitation, and Sports Medicine, University of Puerto Rico School of Medicine, San Juan, Puerto Rico Anterior Cruciate Ligament Sprain

OGOCHUKWU AZUH, MD Clinical Lecturer, Physical Medicine and Rehabilitation, University of Michigan, Ann Arbor, Michigan Lumbar Degenerative Disease Temporomandibular Joint Pain

JOHN R. BACH, MD Professor, Department of Physical Medicine and Rehabilitation and Neurology, Rutgers University New Jersey Medical School, Newark, New Jersey Rehabilitation of the Patient with Respiratory Dysfunction Respiratory Management of Neuromuscular Disorders vi

PATRICK J. BACHOURA, MD Department of Physical Medicine and Rehabilitation, Rutgers New Jersey Medical School, Newark, New Jersey Hip Osteoarthritis

LUIS BAERGA-VARELA, MD Assistant Professor, Physical Medicine, Rehabilitation and Sports Medicine, University of Puerto Rico, Rio Piedras, Puerto Rico Knee Bursopathy

LESLIE BAGAY, MD Clinical Assistant Professor, Residency Assistant ­Program Director, Department of Physical Medicine and ­Rehabilitation, Rutgers-Robert Wood Johnson Medical School, JFK Johnson Rehabilitation Institute, Edison, New Jersey Lymphedema

MOON SUK BANG, MD, PhD Department of Rehabilitation Medicine, Seoul National University College of Medicine, Seoul, South Korea Cervical Dystonia Phantom Limb Pain

MATTHEW N. BARTELS, MD, MPH Professor and Chairman, Department of ­Rehabilitation Medicine, Albert Einstein College of Medicine/­ Montefiore Medical Center, Bronx, New York Rehabilitation of the Patient with Respiratory Dysfunction

GERASIMOS BASTAS, MD, PhD Director of Limb Loss Rehabilitation, Assistant Professor, Physical Medicine and Rehabilitation, Vanderbilt ­University Medical Center, Nashville, Tennessee Lower Limb Amputations

KEITH A. BENGTSON, MD Director of Hand Rehabilitation, Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, Minnesota Trigger Finger

TOMMIE BERRY, JR., MD Schwab Rehabilitation Hospital, University of Chicago, Chicago, Illinois Patellar Tendinopathy (Jumper’s Knee)

Contributors

SAURABHA BHATNAGAR, MD Associate Residency Program Director, Physical Medicine and Rehabilitation, Harvard Medical School, Massachusetts General Hospital, Spaulding Rehabilitation Hospital, Boston, Massachusetts Lumbar Degenerative Disease Temporomandibular Joint Pain

DAVID M. BLAUSTEIN, MD Director of Inpatient Rehabilitation Unit and Amputee Program at the Boston VA Healthcare System, Physical Medicine and Rehabilitation, VA Boston Healthcare System, West Roxbury, Massachusetts Knee Osteoarthritis Osteoarthritis

BRENNAN J. BOETTCHER, DO Sports Medicine Fellow, Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, Minnesota Hip Labral Tears

KATH BOGIE, DPhil Associate Professor, Department of Orthopaedics, Case Western Reserve University; Senior Research Scientist, Advanced Platform Technology Center, Louis Stokes Cleveland Department of Veterans Affairs Medical Center, Cleveland, Ohio Pressure Ulcers

KRISTIAN BORG, MD, PhD Professor and Chair, Division of Rehabilitation Medicine, Department of Clinical Sciences, Karolinska Institutet, Danderyd University Hospital, Stockholm, Sweden Myopathies

JOANNE BORG-STEIN, MD Associate Professor and Associate Chair, Chief, Division of Sports and Musculoskeletal Rehabilitation; Associate Director, Harvard/Spaulding Sports Medicine Fellowship, Department of Physical Medicine and Rehabilitation, Harvard Medical School, Boston, Massachusetts Cervicogenic Vertigo Fibromyalgia

HAYLEE E. BORGSTROM, MD, MS Resident Physician, Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital/Harvard Medical School, Boston, Massachusetts Fibromyalgia

GLENDALIZ BOSQUES, MD Associate Professor, Physical Medicine and Rehabilitation, University of Texas - Health Science Center at Houston; Chief, Pediatric Rehabilitation Medicine, TIRR Memorial Hermann, Houston, Texas Neural Tube Defects

vii

MICHELLE E. BRASSIL, MD Resident Physician, Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital/Harvard Medical School, Boston, Massachusetts Cervicogenic Vertigo Sacroiliac Joint Dysfunction Fibromyalgia Burns

JEFFREY S. BRAULT, DO Consultant, Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, Minnesota Extensor Tendon Injuries Flexor Tendon Injuries

DIANE W. BRAZA, MD Professor and Chair, Physical Medicine and Rehabilitation, Medical College of Wisconsin, Milwaukee, Wisconsin Upper Limb Amputations Diabetic Foot and Peripheral Arterial Disease

DAVID P. BROWN, DO Clinical Professor of Medicine, Department of Rehabilitation Medicine, Johnson Rehabilitation Institute, Edison, New Jersey Hand Osteoarthritis

DAVID T. BURKE, MD, MA Professor and Chairman, Rehabilitation Medicine, Emory University School of Medicine, Atlanta, Georgia Median Neuropathy (Carpal Tunnel Syndrome) Traumatic Brain Injury

RONALD ROLF BUTENDIECK, MD Department of Internal Medicine, Division of Rheumatology, Mayo Clinic Florida, Jacksonville, Florida Ankylosing Spondylitis

AARON W. BUTLER, MD Resident Physician, Rehabilitation Medicine, University of Washington, Seattle, Washington Ankle Sprain

KEVIN BYRAM, MD Assistant Professor of Medicine, Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee Rheumatoid Arthritis Systemic Lupus Erythematosus

ALISON L. CABRERA, MD Tennessee Orthopaedic Alliance, Clarksville, Tennessee Knee Chondral Injuries

MELANIE E. CAMPBELL, MS, ATC, FNP-C Orthopedic Nurse Practitioner, Maine Medical Center, Maine Medical Partners Orthopedics and Sports Medicine, Portland, Maine Ankle Arthritis Bunion and Bunionette Hallux Rigidus Posterior Tibial Tendon Dysfunction

viii

Contributors

T. MARK CAMPBELL, MD, MSC, FRCPC Clinician Investigator, Physical Medicine and Rehabilitation, Elisabeth Bruyère, Ottawa, Ontario, Canada Joint Contractures

ALEXIOS G. CARAYANNOPOULOS, DO, MPH Assistant Professor of Neurosurgery, Brown University, Medical Director Comprehensive Spine Center, Division Director Pain and Rehabilitation Medicine, Department of Neurosurgery, Rhode Island Hospital and Newport Hospital, Providence, Rhode Island Thoracic Sprain or Strain

GREGORY T. CARTER, MD, MS Chief Medical Officer, Physiatry, St. Luke’s Rehabilitation Institute; Clinical Professor, Biomedical Sciences, Elson S. Floyd College of Medicine, Washington State University, Spokane, Washington; Clinical Faculty, MEDEX, University of Washington School of Medicine, Seattle, Washington Motor Neuron Disease

ISABEL CHAN, MD Assistant Clinical Professor, Physical Medicine and Rehabilitation, University of Texas Southwestern, Dallas, Texas Pelvic Pain

SOPHIA CHAN, DPT Medical Student, MS-IV, University of New England College of Osteopathic Medicine, Biddeford, Maine Coccydynia Postherpetic Neuralgia

ERIC T. CHEN, MD, MS Physician, Rehabilitation Medicine, University of Washington, Seattle, Washington Adhesive Capsulitis

AMANDA CHEUNG, BSC, MBT Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada Pressure Ulcers

ANDREA CHEVILLE, MD, MSCE Professor, Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, Minnesota Cancer-Related Fatigue

KELVIN CHEW, MBBCH, MSPMED Senior Consultant, Sports Medicine Department, Changi General Hospital, Singapore Greater Trochanteric Pain Syndrome

SALLAYA CHINRATANALAB, MD Assistant Professor of Medicine, Division of Rheumatology and Immunology, Department of Internal Medicine, Vanderbilt University Medical Center, Nashville, Tennessee Rheumatoid Arthritis Systemic Lupus Erythematosus

ELLIA CIAMMAICHELLA, DO, JD Resident Physician, Physical Medicine and Rehabilitation, McGovern Medical School at UT Health in Houston, Houston, Texas Neural Tube Defects

JOHN CIANCA, MD Adjunct Associate Professor, Physical Medicine and Rehabilitation, Baylor College of Medicine; Adjunct Associate Professor, Physical Medicine and Rehabilitation, University of Texas Medical Branch, Houston, Texas Hamstring Strain

DANIEL MICHAEL CLINCHOT, MD Vice Dean for Education, Chair, Biomedical Education and Anatomy, The Ohio State University, Columbus, Ohio Femoral Neuropathy Lateral Femoral Cutaneous Neuropathy

RICARDO E. COLBERG, MD, RMSK Sports Medicine Physician, Physical Medicine and Rehabilitation, Andrews Sports Medicine and Orthopaedic Center, Birmingham, Alabama Hip Adductor Strain

EARL J. CRAIG, MD Clinical Assistant Professor, Department of Physical Medicine and Rehabilitation; Clinical Assistant Professor, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana Femoral Neuropathy Lateral Femoral Cutaneous Neuropathy

LISANNE C. CRUZ, MD, MSC Rehabilitation Medicine, Icahn SOM at Mount Sinai, New York, New York Compartment Syndrome of the Leg

SARA CUCCURULLO, MD Clinical Professor and Chairman, Residency Program Director, Department of Physical Medicine and Rehabilitation, Rutgers Robert Wood Johnson Medical School, Piscataway, New Jersey; Vice President and Medical Director, JFK Johnson Rehabilitation Institute, Edison, New Jersey Abdominal Wall Pain

CHRISTIAN M. CUSTODIO, MD Associate Attending Physiatrist, Rehabilitation Medicine Service, Memorial Sloan Kettering Cancer Center; Associate Clinical Professor, Department of Rehabilitation Medicine, Weill Cornell Medicine, New York, New York Chemotherapy-Induced Peripheral Neuropathy

ALAN M. DAVIS, MD, PhD Associate Professor, Physical Medicine and Rehabilitation, University of Utah School of Medicine, Salt Lake City, Utah Cardiac Rehabilitation

Contributors

DAVID R. DEL TORO, MD Professor, Physical Medicine and Rehabilitation, Medical College of Wisconsin, Milwaukee, Wisconsin Fibular (Peroneal) Neuropathy Tibial Neuropathy (Tarsal Tunnel Syndrome)

LAURENT DELAVAUX, BS, MS, MD Fellow, Physical Medicine and Rehabilitation, JFK Johnson Rehabilitation Institute, Edison, New Jersey Abdominal Wall Pain

FRANCESCA DI FELICE, MD Italian Scientific Spine Institute, Milan, Italy Scoliosis and Kyphosis

JAYNE DONOVAN, MD Clinical Assistant Professor, Rutgers New Jersey Medical School; Clinical Chief of Outpatient Spinal Cord Injury Services, Kessler Institute for Rehabilitation, Newark, New Jersey Olecranon Bursitis

SABRINA DONZELLI, MD Italian Scientific Spine Institute, Milan, Italy Scoliosis and Kyphosis

SUSAN J. DREYER, MD Associate Professor, Orthopaedic Surgery; Associate Professor, Physical Medicine and Rehabilitation, Emory University School of Medicine, Atlanta, Georgia Intercostal Neuralgia

NANCY DUDEK, MD, MED Professor, Medicine, Division of Physical Medicine and Rehabilitation, University of Ottawa, Ottawa, Ontario, Canada Joint Contractures

ISRAEL DUDKIEWICZ, PROFESSOR Chairman, Department of Rehabilitation Medicine, Tel Aviv Medical Center, Tel Aviv, Israel Cervical Spondylotic Myelopathy Cervical Degenerative Disease

SHEILA A. DUGAN, MD Professor, Physical Medicine and Rehabilitation, Rush Medical College, Chicago, Illinois Ulnar Collateral Ligament Sprain Stress Fractures

BLESSEN C. EAPEN, MD Section Chief, Polytrauma Rehabilitation Center, Fellowship Program Director, Brain Injury Medicine, South Texas Veterans Health Care System; Associate Professor, Department of Rehabilitation Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Headaches Occipital Neuralgia Deep Venous Thrombosis Polytrauma Rehabilitation

ix

GEROLD R. EBENBICHLER, MD Physical Medicine and Rehabilitation and Occupational Medicine, Vienna Medical University, General Hospital of Vienna, Vienna, Austria Chronic Fatigue Syndrome

OMAR H. EL ABD, MD Instructor, Physical Medicine and Rehabilitation, Harvard Medical School; Instructor, Physical Medicine and Rehabilitation, Spaulding Rehabilitation, Boston, Massachusetts Low Back Strain or Sprain

MARK I. ELLEN, MD Associate Professor of Physical Medicine and Rehabilitation, Associate Professor of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland Total Knee Arthroplasty

MAURY ELLENBERG, MD Clinical Professor, Physical Medicine and Rehabilitation, Wayne State University School of Medicine, Detroit, Michigan Lumbar Radiculopathy

MICHAEL J. ELLENBERG, MD Rehabilitation Physicians PC, Novi, Michigan Lumbar Radiculopathy

LAUREN ELSON, MD Director of Dance Medicine, Physical Medicine and Rehabilitation, Spaulding Rehabilitation, Harvard University, Charlestown, Massachusetts Post-Mastectomy Pain Syndrome

CHRISTINE ENG, MD Clinical Instructor, Department of Physical Medicine and Rehabilitation, Harvard Medical School, Spaulding Rehabilitation Hospital, Boston, Massachusetts Elbow Arthritis Kienböck Disease

JESSE D. ENNIS, MD, FRCPC Physical Medicine and Rehabilitation, Neurorehabilitation Unit, Victoria General Hospital, Victoria, British Columbia, Canada Spinal Cord Injury (Thoracic)

ERIK ENSRUD, MD Associate Professor, Orthopedics and Rehabilitation, Oregon Health Sciences University, Portland, Oregon Myopathies Plexopathy—Brachial Plexopathy—Lumbosacral

STEVEN ESCALDI, DO Medical Director, Spasticity Management Program, Department of Rehabilitation Medicine, JFK-Johnson Rehabilitation Institute, Edison, New Jersey; Clinical Associate Professor, Rutgers Robert Wood Johnson Medical School, Piscataway, New Jersey Movement Disorders

x

Contributors

STEPHAN M. ESSER, MD Southeast Orthopedic Specialists, Jacksonville, Florida Chronic Ankle Instability

AVITAL FAST, MD Chief, Rehabilitation Services, Tel Aviv Medical Center, Tel Aviv, Israel Cervical Spondylotic Myelopathy Cervical Degenerative Disease

JONATHAN T. FINNOFF, DO Professor, Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, Minnesota Suprascapular Neuropathy Hip Labral Tears

DAVID R. FORBUSH, MD Assistant Professor of Physical Medicine and Rehabilitation, University of Alabama at Birmingham School of Medicine, Birmingham, Alabama Total Knee Arthroplasty

PATRICK M. FOYE, MD Interim Chair and Professor, Physical Medicine and Rehabilitation; Director, Coccyx Pain Center, Rutgers New Jersey Medical School, Newark, New Jersey Hip Osteoarthritis

MICHAEL FREDERICSON, MD Professor, Orthopedics and Sports Medicine, Director, Physical Medicine and Rehabilitation, Sports Medicine Fellowship Director, Primary Care, Sports Medicine, Team Physician, Stanford Intercollegiate Athletics, Stanford University, Redwood City, California Greater Trochanteric Pain Syndrome Knee Chondral Injuries

JOEL E. FRONTERA, MD Associate Professor, Vice Chair for Education and Residency Program Director, Department of Physical Medicine and Rehabilitation, McGovern Medical School at the University of Texas Health Science Center, Houston, Texas Spasticity

WALTER R. FRONTERA, MD, PhD, MA (Hon.), FRCP Professor, Physical Medicine, Rehabilitation and Sports Medicine, Physiology and Biophysics, University of Puerto Rico School of Medicine, San Juan, Puerto Rico Cervical Facet Arthropathy

CHAN GAO, MD, PhD Resident, Department of Physical Medicine and Rehabilitation, Vanderbilt University Medical Center, Nashville, Tennessee Rotator Cuff Tendinopathy Rotator Cuff Tear

YOUHANS GHEBRENDRIAS, MD Assistant Clinical Professor, Physical Medicine and Rehabilitation, University of California Irvine, Orange, California Myofascial Pain Syndrome

MEL B. GLENN, MD Associate Professor, Department of Physical Medicine and Rehabilitation, Harvard Medical School, Boston, Massachusetts; Chief, Brain Injury Division, Department of Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, Charlestown, Massachusetts; Medical Director, NeuroRehabilitation (Massachusetts), Braintree, Massachusetts; Medical Director, Community Rehab Care, Watertown, Massachusetts Postconcussion Symptoms

JENOJ S. GNANA, MD Department of Physical Medicine and Rehabilitation, Rutgers New Jersey Medical School, Newark, New Jersey Hip Osteoarthritis

PETER GONZALEZ, MD Private Practice, Orthopaedic Institute of Central Jersey, Toms River, New Jersey Iliotibial Band Syndrome

THOMAS E. GROOMES, MD Associate Professor, Physical Medicine and Rehabilitation, Vanderbilt University Medical Center, Nashville, Tennessee Total Knee Arthroplasty Heterotopic Ossification

DAWN M. GROSSER, MD Orthopaedic Surgeon, South Texas Bone and Joint, Corpus Christi, Texas Ankle Arthritis Bunion and Bunionette Hallux Rigidus Posterior Tibial Tendon Dysfunction

JONATHAN S. HALPERIN, MD Chief, Physical Medicine and Rehabilitation, Sharp Rees Stealy Medical Group, San Diego, California Quadriceps Tendinopathy

ALEX HAN, BA Medical Student, Physical Medicine and Rehabilitation, Brown University, Providence, Rhode Island Thoracic Sprain or Strain

JOSEPH A. HANAK, MD Clinical Instructor, Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, Charlestown, Massachusetts Tietze Syndrome

TONI J. HANSON, MD Assistant Professor, Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, Minnesota Thoracic Compression Fracture

DAVID E. HARTIGAN, MD Assistant Professor, Orthopedic Surgery, Mayo Clinic Arizona, Phoenix, Arizona Labral Tears of the Shoulder

Contributors

SETH D. HERMAN, MD Director, Brain Injury Medicine Fellowship, Department of Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, Harvard, Boston, Massachusetts Postconcussion Symptoms

JOSEPH E. HERRERA, DO Chairman and Lucy G. Moses Professor, Rehabilitation Medicine, Icahn School of Medicine at Mount Sinai, New York, New York Compartment Syndrome of the Leg

CHESTER HO, MD Professor and Director, Spinal Cord Injury Research Chair, Division of Physical Medicine and Rehabilitation, Department of Medicine, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada Pressure Ulcers

ALICE J. HON, MD Clinical Assistant Professor, University of California – Irvine, VA Long Beach Healthcare System, Long Beach, California Central Post-Stroke Pain (Thalamic Pain Syndrome)

JOAN Y. HOU, MD Staff Physician, Knapp Inpatient Rehabilitation, Department of Physical Medicine and Rehabilitation, Hennepin County Medical Center, Assistant Professor, Department of Rehabilitation Medicine, University of Minnesota, Minneapolis, Minnesota Deep Venous Thrombosis

TIMOTHY HOWARD, MD EmergeOrtho, Wilson, North Carolina Arachnoiditis

RYAN HUBBARD, MD Resident, Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, Minnesota Suprascapular Neuropathy

THOMAS H. HUDGINS, MD Associate Division Head, Division of Physical Medicine and Rehabilitation, NorthShore University Health System, Glenview, Illinois; Assistant Professor, Department of Orthopedics, University of Chicago, Pritzker School of Medicine, Chicago, Illinois Cervical Sprain or Strain Piriformis Syndrome Patellar Tendinopathy (Jumper’s Knee) Patellofemoral Syndrome

KATARZYNA IBANEZ, MD Attending Physiatrist, Department of Neurology, Rehabilitation Service, Memorial Sloan Kettering Cancer Center; Assistant Professor of Rehabilitation Medicine, Weill Cornell Medical College, New York, New York Radiation Fibrosis Syndrome

xi

ZACHARIA ISAAC, MD Director, Interventional Physical Medicine and Rehabilitation, Department of Physical Medicine and Rehabilitation, Harvard Medical School; Medical Director, Comprehensive Spine Care Center, Brigham and Women’s Hospital, Boston, Massachusetts Lumbar Spinal Stenosis Sacroiliac Joint Dysfunction

NITIN B. JAIN, MD, MSPH Associate Professor, Physical Medicine and Rehabilitation, Vanderbilt University Medical Center, Nashville, Tennessee Rotator Cuff Tendinopathy Rotator Cuff Tear

CARLOS A. JARAMILLO, MD, PhD Staff Physician, Polytrauma Rehabilitation Center, South Texas Veterans Health Care System; Clinical and Research Faculty, Geriatric Research, Education and Clinical Center, South Texas Veterans Health Care System; Assistant Professor, Department of Rehabilitation Medicine, University of Texas Health Science Center San Antonio, San Antonio, Texas Headaches Polytrauma Rehabilitation

PRATHAP JAYARAM, MD Assistant Professor; Director of Regenerative Sports Medicine, H. Ben Taub Department of Physical Medicine and Rehabilitation, Department of Orthopedic Surgery, Baylor College of Medicine, Houston, Texas Knee Chondral Injuries

JEFFERY S. JOHNS, MD Associate Professor, Physical Medicine and Rehabilitation, Vanderbilt University Medical Center; Medical Director, Vanderbilt Stallworth Rehabilitation Hospital, Nashville, Tennessee Neurogenic Bladder Neurogenic Bowel

JACLYN JOKI, MD Clinical Assistant Professor, Department of Physical Medicine and Rehabilitation, Rutgers Robert Wood Johnson Medical School, Piscataway, New Jersey; Director of Physical Medicine and Rehabilitation RWJUH, JFK Johnson Rehabilitation Institute, Edison, New Jersey Hand Rheumatoid Arthritis

PRATHAP JACOB JOSEPH, MD Assistant Professor and Vice Chair, Clinical Operations, Department of Physical Medicine and Rehabilitation, UT Health McGovern Medical School, Houston, Texas Metatarsalgia

NANETTE C. JOYCE, DO, MAS Associate Clinical Professor, Physical Medicine and Rehabilitation, University of California, Davis School of Medicine, Sacramento, California Motor Neuron Disease

xii

Contributors

SE HEE JUNG, MD, PhD Associate Professor, Department of Rehabilitation Medicine, Seoul National University Boramae Medical Center, Seoul, Korea Phantom Limb Pain

DANIELLE PERRET KARIMI, MD Associate Clinical Professor, Physical Medicine and Rehabilitation, Associate Clinical Professor, Anesthesiology and Perioperative Care, The University of California Irvine, Orange, California Myofascial Pain Syndrome

JONATHAN KAY, MD Professor of Medicine, Division of Rheumatology, University of Massachusetts Medical School; Director of Clinical Research, Division of Rheumatology, UMass Memorial Medical Center, Worcester, Massachusetts Hand Rheumatoid Arthritis

STUART KIGNER, DPM Podiatrist, Orthopaedic Surgery, Massachusetts General Hospital; Brigham and Women’s Hospital in IgA nephropathy, Boston, Massachusetts Metatarsalgia

TODD A. KILE, MD Consultant, Department of Orthopedic Surgery, Mayo Clinic, Scottsdale, Arizona; Assistant Professor, Mayo Clinic College of Medicine, Rochester, Minnesota Ankle Arthritis Bunion and Bunionette Hallux Rigidus Posterior Tibial Tendon Dysfunction

JOHN C. KING, MD Professor, Rehabilitation Medicine, University of Texas Health Science Center, Medical Director, Reeves Rehabilitation Center, University Health System, San Antonio, Texas Fibular (Peroneal) Neuropathy

HANS E. KNOPP, DO Interventional Spine and Sports Medicine, PC, Middlebury, Connecticut Lumbar Degenerative Disease Temporomandibular Joint Pain

SASHA E. KNOWLTON, MD Cancer Rehabilitation Fellow, Physical Medicine and Rehabilitation, Memorial Sloan Kettering Cancer Center, New York, New York Chemotherapy-Induced Peripheral Neuropathy Trigeminal Neuralgia

JASON H. KORTTE, MS, CCC-SLP Speech-Language Pathologist, Medstar Good Samaritan Hospital, Affiliate Faculty, Loyola University, Baltimore, Maryland Speech and Language Disorders

DANA H. KOTLER, MD Instructor, Physical Medicine and Rehabilitation, Harvard Medical School, Spaulding Rehabilitation Hospital, Newton-Wellesley Hospital, Cambridge, Massachusetts Elbow Arthritis

BRIAN J. KRABAK, MD, MBA Clinical Professor, Rehabilitation, Orthopedics and Sports Medicine, University of Washington and Seattle Children’s Sports Medicine, Seattle, Washington Adhesive Capsulitis Biceps Tendinopathy Ankle Sprain

WYATT KUPPERMAN, DO Schwab Rehabilitation Hospital, University of Chicago, Chicago, Illinois Patellofemoral Syndrome

JENNIFER KURZ, MD Attending Physician, Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital Massachusetts General Hospital; Brigham and Woman’s Hospital, Boston, Massachusetts Costosternal Syndrome

SHI-UK LEE, MD, PhD Department of Rehabilitation Medicine, Seoul National University College of Medicine; Department of Physical Medicine and Rehabilitation, Seoul National University Boramae Medical Center, Seoul, Korea Cervical Dystonia

PAUL LENTO, MD Physical Medicine and Rehabilitation, Sarasota Orthopedic Associates, Florida State University Medical School, Sarasota, Florida Collateral Ligament Sprain Iliotibial Band Syndrome Meniscal Injuries

JAN LEXELL, MD, PhD, DPhil h.c. Department of Neuroscience, Rehabilitation Medicine, University of Uppsala and Uppsala University Hospital, Uppsala, Sweden Postpoliomyelitis Syndrome

PETER A.C. LIM, MD Clinical Professor, Physical Medicine and Rehabilitation, Baylor College of Medicine, Houston, Texas; Adjunct Associate Professor, Medicine, Duke-NUS Medical School; Senior Consultant, Rehabilitation Medicine, Singapore General Hospital, Singapore, Singapore Transverse Myelitis

CINDY Y. LIN, MD Clinical Assistant Professor, Sports and Spine Division, Department of Rehabilitation Medicine, University of Washington Medical Center, Seattle, Washington Greater Trochanteric Pain Syndrome

Contributors

LEI LIN, MD, PhD Clinical Associate Professor, Physical Medicine and Rehabilitation, Rutgers-Robert Wood Johnson Medical School, Edison, New Jersey Thoracic Outlet Syndrome

KARL-AUGUST LINDGREN, MD, PhD ORTON Rehabilitation Centre, Helsinki, Finland Thoracic Outlet Syndrome

UMAR MAHMOOD, MD Kure Pain Management, Stevensville, Maryland Lumbar Spondylolysis and Spondylolisthesis

JUSTIN L. MAKOVICKA, MD Orthopedic Surgery Resident, Mayo Clinic Arizona, Phoenix, Arizona Labral Tears of the Shoulder

STEVEN A. MAKOVITCH, DO Clinical Instructor, Department of Physical Medicine and Rehabilitation, Harvard Medical School, VA Boston Healthcare, Spaulding Rehabilitation Hospital, Boston, Massachusetts Kienböck Disease

VARTGEZ K. MANSOURIAN, MD Assistant Professor, Physical Medicine and Rehabilitation, Vanderbilt University School of Medicine; Medical Director, Stroke Rehabilitation Program, Vanderbilt Stallworth Rehabilitation Hospital, Nashville, Tennessee Stroke in Young Adults

BEN MARSHALL, DO Assistant Professor, Physical Medicine and Rehabilitation, University of Colorado, Aurora, Colorado Collateral Ligament Sprain Meniscal Injuries

JENNIFER N. YACUB MARTIN, MD Assistant Professor, Department of Physical Medicine and Rehabilitation, Clement J. Zablocki VA Medical Center and Medical College of Wisconsin, Milwaukee, Wisconsin Upper Limb Amputations Diabetic Foot and Peripheral Arterial Disease

KOICHIRO MATSUO, DDS, PhD Professor and Chair, Department of Dentistry and Oral-Maxillofacial Surgery, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan Dysphagia

JUAN JOSE MAYA, MD Department of Internal Medicine, Division of Rheumatology, Mayo Clinic Florida, Jacksonville, Florida Ankylosing Spondylitis

xiii

A. SIMONE MAYBIN, MD Department of Physical Medicine and Rehabilitation, Vanderbilt University Medical Center, Nashville, Tennessee Lumbar Facet Arthropathy

DONALD MCGEARY, PhD, ABPP Associate Professor, Department of Psychiatry, Clinical Assistant Professor, Department of Family and Community Medicine, ReACH Scholar, University of Texas Health Science Center at San Antonio, San Antonio, Texas Headaches

KELLY C. MCINNIS, DO Instructor, Physical Medicine and Rehabilitation, Harvard Medical School; Clinical Associate, Physical Medicine and Rehabilitation, Massachusetts General Hospital, Boston, Massachusetts Repetitive Strain Injuries

PETER MELVIN MCINTOSH, MD Assistant Professor, College of Medicine, Mayo Clinic, Rochester, Minnesota; Consultant, Department of Physical Medicine and Rehabilitation, Mayo Clinic Florida, Jacksonville, Florida Scapular Winging Adhesive Capsulitis of the Hip

ALEC L. MELEGER, MD Assistant Professor of Physical Medicine and Rehabilitation, Harvard Medical School, Boston, Massachusetts; Associate Director, Spine Center, Newton-Wellesley Hospital, Newton, Massachusetts Cervical Spinal Stenosis

WILLIAM F. MICHEO, MD Professor and Chair, Sports Medicine Fellowship Director, Department of Physical Medicine, Rehabilitation, and Sports Medicine, University of Puerto Rico, San Juan, Puerto Rico Glenohumeral Instability Anterior Cruciate Ligament Sprain

PAOLO MIMBELLA, MD, MSC McGovern Medical School—UTHealth, Department of Physical Medicine and Rehabilitation; Academic Chief Resident, Baylor/University of Texas, Houston, Texas Hamstring Strain

GERARDO MIRANDA-COMAS, MD Assistant Professor, Rehabilitation Medicine, Sports Medicine Fellowship Director, Icahn School of Medicine at Mount Sinai, New York, New York Glenohumeral Instability

DANIEL P. MONTERO, MD, CAQSM Instructor, Orthopedics, Mayo Clinic Florida, Jacksonville, Florida Hammer Toe

xiv

Contributors

BRITTANY J. MOORE, MD Resident, Physical Medicine and Rehabilitation, Mayo Clinic College of Medicine and Science, Rochester, Minnesota Extensor Tendon Injuries Flexor Tendon Injuries

S. ALI MOSTOUFI, MD Interventional Physiatrist, Spine, Sports, and Regenerative Medicine, New England Spine Care Associates, Cambridge, Massachusetts; Department of Physical Medicine and Rehabilitation, Tufts University School of Medicine, Boston, Massachusetts Cervical Radiculopathy Chronic Pain Syndrome

CHAITANYA S. MUDGAL, MD, MS (Orth), MCh (Orth) Associate Professor in Orthopaedic Surgery, Harvard Medical School, Orthopaedic Hand Service, Massachusetts General Hospital, Boston, Massachusetts Wrist Osteoarthritis Wrist Rheumatoid Arthritis

STEFANO NEGRINI, MD Chair Rehabilitation, Clinical and Experimental Sciences, University of Brescia, Brescia, Italy; Scientific Coordinator Rovato, Fondazione Don Gnocchi, Milan, Italy Scoliosis and Kyphosis

SHANKER NESATHURAI, MD, MPH, FRCPC Professor of Medicine and Division Director of Physical Medicine and Rehabilitation, Michael G. DeGroote School of Medicine, McMaster University; Chief of Physical Medicine and Rehabilitation, Hamilton Health Sciences and St. Joseph’s Healthcare, Hamilton, Ontario, Canada; Lecturer in Physical Medicine and Rehabilitation, Harvard Medical School, Boston, Massachusetts Spinal Cord Injury (Thoracic)

CARINA JOY O’NEILL, DO Medical Director, Physical Medicine and Rehabilitation, Spaulding Rehabilitation, Braintree, Massachusetts; Clinical Instructor, Physical Medicine and Rehabilitation, Harvard Medical School, Boston, Massachusetts de Quervain Tenosynovitis

EZIAMAKA CHIDI OKAFOR, MD Resident, Department of Physical Medicine and Rehabilitation, Harvard Medical School, Boston, Massachusetts Cervical Spinal Stenosis

ANDREA K. ORIGENES Medical Student, Midwestern University College of Osteopathic Medicine, Downers Grove, Illinois Cervical Sprain or Strain

CEDRIC J. ORTIGUERA, MD Assistant Professor, Orthopedic Surgery, Mayo Clinic Florida, Jacksonville, Florida Labral Tears of the Shoulder

MICHAEL D. OSBORNE, MD Consultant, Department of Pain Medicine, Mayo Clinic, Jacksonville, Florida; Assistant Professor, Physical Medicine and Rehabilitation, Mayo Clinic College of Medicine, Rochester, Minnesota Chronic Ankle Instability Arachnoiditis

AJIT B. PAI, MD Chief, Physical Medicine and Rehabilitation Service, Hunter Holmes McGuire VA Medical Center, Richmond, Virginia; Assistant Professor, Physical Medicine and Rehabilitation, Virginia Commonwealth University, Richmond, Virginia Deep Venous Thrombosis

JEFFREY B. PALMER, MD Professor Emeritus, Department of Physical Medicine and Rehabilitation, Johns Hopkins University, Baltimore, Maryland Dysphagia Speech and Language Disorders

SAGAR S. PARIKH, MD Interventional Pain Physician, Pain Fellowship Director, Department of Physical Medicine and Rehabilitation, JFK Johnson Rehabilitation Institute, Edison, New Jersey; Assistant Professor, Physical Medicine and Rehabilitation, Robert Wood Johnson Medical School, Piscataway, New Jersey Abdominal Wall Pain

MARCIN PARTYKA, MD, FRCPC Resident, Physical Medicine and Rehabilitation, Michael G. Degroote School of Medicine, McMaster University, Hamilton, Ontario, Canada Spinal Cord Injury (Thoracic)

ATUL T. PATEL, MD, MHSA Medical Director of Rehabilitation Services, Kansas City Bone and Joint Clinic, PA, Overland Park, Kansas Trapezius Strain Pubalgia

SHAWN A. PATEL, MD Physician, Department of Rehabilitation Medicine, University of Washington, Seattle, Washington Biceps Tendinopathy

NICOLAS PEREZ, MD Fellow, Physical Medicine and Rehabilitation, JFK Johnson Rehabilitation Institute, Edison, New Jersey Abdominal Wall Pain

DWAN PERRY, DO Assistant Professor, Department of Physical Medicine and Rehabilitation, University of Kentucky, Chandler Medical Center, Lexington, Kentucky Quadriceps Contusion

Contributors

EDWARD M. PHILLIPS, MD Assistant Professor, Physical Medicine and Rehabilitation, Harvard Medical School, Boston, Massachusetts; Chief, Physical Medicine and Rehabilitation Service, VA Boston Healthcare System, West Roxbury, Massachusetts; Attending Physician, Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, Charlestown, Massachusetts Knee Osteoarthritis Osteoarthritis

DANIEL C. PIMENTEL, MD, PhD Interventional Physiatrist, Director of Spine Center HCor; Assistant Professor, University of São Paolo, School of Medicine, São Paulo, Brazil Thoracic Radiculopathy

BENEDIKT PLEUHS, BA Clinical Research Assistant, Pediatric Emergency Department, Medical College of Wisconsin, Milwaukee, Wisconsin Cervical Sprain or Strain

THOMAS E. POBRE, MD Director of Outpatient Services, Physical Medicine and Rehabilitation, Nassau University Medical Center, East Meadow, New York Radial Neuropathy

TERRENCE PUGH, MD Assistant Professor, Physical Medicine and Rehabilitation, Carolinas Medical Center; Vice-Chief, Section of Rehabilitation, Supportive Care, Levine Cancer Institute; Associate Director of Oncology Rehabilitation, Physical Medicine and Rehabilitation, Carolinas Rehabilitation, Charlotte, North Carolina Radiation Fibrosis Syndrome

ALISON R. PUTNAM, DO Providence Medical Group Everett, Physiatry, Everett, Washington Iliotibial Band Syndrome

JAMES RAINVILLE, MD Assistant Professor, Part-Time, Department of Physical Medicine and Rehabilitation, Harvard Medical School; Chief, Physical Medicine and Rehabilitation, New England Baptist Hospital, Boston, Massachusetts Lumbar Spondylolysis and Spondylolisthesis

V.S. RAMACHANDRAN, MD, PhD Distinguished Professor, Department of Psychology, University of California, San Diego, La Jolla, California Complex Regional Pain Syndrome

BRIAN E. RICHARDSON, PT Clinical Director, Sports Physical Therapy Residency Program, Vanderbilt University Medical Center, Nashville, Tennessee Rotator Cuff Tendinopathy Rotator Cuff Tear

xv

DAVID RING, MD, PhD Associate Dean for Comprehensive Care, Department of Surgery and Perioperative Care, Dell Medical School— The University of Texas at Austin, Austin, Texas Hand Rheumatoid Arthritis

ALEXANDRA RIVERA-VEGA, MD Staff Physician, Michael E. DeBakey VAMC, Assistant Professor, Department of Physical Medicine and Rehabilitation, Baylor College of Medicine, Houston, Texas Glenohumeral Instability

THOMAS D. RIZZO, JR., MD Consultant, Physical Medicine and Rehabilitation, Mayo Clinic, Jacksonville, Florida; Assistant Professor, College of Medicine, Mayo Clinic, Rochester, Minnesota Acromioclavicular Injuries Total Hip Replacement

RAUL A. ROSARIO-CONCEPIÓN, MD Chief Resident, Physical Medicine and Rehabilitation, University of Puerto Rico School of Medicine, San Juan, Puerto Rico Knee Bursopathy

DARREN C. ROSENBERG, DO Assistant Professor, Physical Medicine and Rehabilitation, Harvard Medical School, Boston, Massachusetts Thoracic Radiculopathy Baker Cyst

ROGER P. ROSSI, DO Professor of Physical Medicine and Rehabilitation, Physical Medicine and Rehabilitation, Rutgers—Robert Wood Johnson/Johnson Rehabilitation Institute, Edison, New Jersey Speech and Language Disorders

SEWARD B. RUTKOVE, MD Professor, Neurology, Harvard Medical School/Beth Israel Deaconess Medical Center, Boston, Massachusetts Peripheral Neuropathies

SUNIL SABHARWAL, MD, MRCP (UK) Associate Professor, Department of Physical Medicine and Rehabilitation, Harvard Medical School; Chief, Spinal Cord Injury, Veterans Affairs Boston Health Care System, Boston, Massachusetts Spinal Cord Injury (Cervical) Spinal Cord Injury (Lumbosacral)

NOURMA SAJID, MD Department of Physical Medicine and Rehabilitation, Rutgers New Jersey Medical School, Newark, New Jersey Hip Osteoarthritis

LUIS A. SANCHEZ, MD Fellow, Department of Physical Medicine, Rehabilitation and Sports Medicine, University of Puerto Rico School of Medicine, San Juan, Puerto Rico Anterior Cruciate Ligament Sprain

xvi

Contributors

FRANCISCO H. SANTIAGO, MD Attending Physician, Physical Medicine and Rehabilitation, Bronx-Lebanon Hospital, Bronx, New York Median Neuropathy Ulnar Neuropathy (Wrist)

DANIELLE SARNO, MD Instructor, Department of Physical Medicine and Rehabilitation, Harvard Medical School, Boston, Massachusetts; Physiatrist, Interventional Pain Management, Department of Neurosurgery, Brigham and Women’s Hospital, Boston, Massachusetts Lumbar Spinal Stenosis

ROBERT J. SCARDINA, DPM Chief and Residency Program Director, Podiatry Service, Massachusetts General Hospital, Boston, Massachusetts Metatarsalgia

BYRON J. SCHNEIDER, MD Assistant Professor, Physical Medicine and Rehabilitation, Vanderbilt University Medical Center, Nashville, Tennessee Lumbar Facet Arthropathy

JEFFREY C. SCHNEIDER, MD Medical Director, Trauma, Burn and Orthopedic Program, Spaulding Rehabilitation Hospital; Assistant Professor, Physical Medicine and Rehabilitation, Harvard Medical School, Boston, Massachusetts Burns

FERNANDO SEPÚLVEDA, MD Assistant Professor, Department of Physical Medicine, Rehabilitation, and Sports Medicine, University of Puerto Rico School of Medicine, San Juan, Puerto Rico Anterior Cruciate Ligament Sprain

JOHN SERGENT, MD Professor of Medicine, Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee Rheumatoid Arthritis Systemic Lupus Erythematosus

DANA SESLIJA, MD, MS Adjunct Professor, Department of Physical Medicine and Rehabilitation, Schulich School of Medicine and Dentistry, Windsor, Ontario, Canada Fibular (Peroneal) Neuropathy Tibial Neuropathy (Tarsal Tunnel Syndrome)

VIVIAN P. SHAH, MD Department of Physical Medicine and Rehabilitation, Rutgers New Jersey Medical School, Newark, New Jersey Hip Osteoarthritis

JYOTI SHARMA, MD Associate, Orthopaedic Surgery Department, Geisinger Health System, Danville, Pennsylvania Wrist Osteoarthritis Wrist Rheumatoid Arthritis

NUTAN SHARMA, MD, PhD Associate Professor, Neurology, Harvard Medical School, Cambridge, Massachusetts; Associate Neurologist, Neurology, Massachusetts General Hospital, Boston, Massachusetts; Associate Neurologist, Neurology, Brigham and Women’s Hospital, Boston, Massachusetts Parkinson Disease

ALEXANDER SHENG, MD Assistant Professor, Sports and Spine, Shirley Ryan AbilityLab, Chicago, Illinois Posterior Cruciate Ligament Sprain

GLENN G. SHI, MD Assistant Professor, Orthopedic Surgery, Mayo Clinic, Jacksonville, Florida Hammer Toe Morton’s Neuroma Plantar Fasciitis

JULIE K. SILVER, MD Associate Professor, Department of Physical Medicine and Rehabilitation, Harvard Medical School; Attending Physician, Spaulding Rehabilitation Hospital; Clinical Associate, Massachusetts General Hospital; Associate in Physiatry, Brigham and Women’s Hospital, Boston, Massachusetts Trigger Finger

CHLOE SLOCUM, MD, MPH Attending Physician, Department of Physical Medicine and Rehabilitation, Spinal Cord Injury Division, Harvard Medical School/Spaulding Rehabilitation Hospital, Boston, Massachusetts Post-Thoracotomy Pain Syndrome

DAVID M. SLOVIK, MD Associate Professor of Medicine, Harvard Medical School; Chief, Division of Endocrinology, Newton-Wellesley Hospital, Newton, Massachusetts; Physician, Endocrine Unit, Massachusetts General Hospital, Boston, Massachusetts Osteoporosis

SOL M. ABREU SOSA, MD Assistant Professor, Physical Medicine and Rehabilitation, Rush Medical College, Chicago, Illinois Ulnar Collateral Ligament Sprain Stress Fractures

KURT SPINDLER, MD Department of Orthopedic Surgery, Cleveland Clinic, Cleveland, Ohio Knee Chondral Injuries

LAUREN SPLITTGERBER, MD Resident Physician, Physical Medicine and Rehabilitation, McGaw Medical Center of Northwestern University/ Shirley Ryan AbilityLab, Chicago, Illinois Posterior Cruciate Ligament Sprain

Contributors

STACY M. STARK, DO Assistant Professor, Vice Chair of Education, Residency Program Director, Department of Physical Medicine and Rehabilitation, Division Chief, Pediatric Rehabilitation Medicine, Medical Director, Rehabilitation Services, Monroe Carell Jr. Children’s Hospital at Vanderbilt, Vanderbilt University Medical Center, Nashville, Tennessee Cerebral Palsy

JOEL STEIN, MD Simon Baruch Professor, Rehabilitation and Regenerative Medicine, Columbia University; Professor, Rehabilitation Medicine, Weill Cornell Medical College; Physiatrist-inChief, Rehabilitation Medicine, NewYork-Presbyterian Hospital, New York, New York Stroke

SONJA K. STILP, MD Private Practice, Boulder, Colorado Iliotibial Band Syndrome

TODD P. STITIK, MD Department of Physical Medicine and Rehabilitation, Rutgers New Jersey Medical School, Newark, New Jersey Hip Osteoarthritis

MICHAEL F. STRETANSKI, DO, AME Medical Director/Fellowship Director, Interventional Pain Management, Interventional Spine and Pain Rehabilitation Center, Mansfield, Ohio; Medical Director, Put-in-Bay Concierge Medical Services, Put-in-Bay, Ohio Biceps Tendon Rupture Shoulder Arthritis Dupuytren Contracture Hand and Wrist Ganglia Shin Splints Achilles Tendinopathy

MICHAEL D. STUBBLEFIELD, MD Associate Attending Physiatrist and Chief, Rehabilitation Service, Department of Neurology, Memorial Sloan Kettering Cancer Center; Associate Professor of Rehabilitation Medicine, Weill Cornell Medical College, New York, New York Radiation Fibrosis Syndrome

BRUNO S. SUBBARAO, DO Medical Director of Polytrauma/Transition and Care Management Programs, Phoenix Veterans Healthcare System, Phoenix, Arizona Occipital Neuralgia

JOHN TALIAFERRO, MD Resident Physician, Orthopaedic Surgery, University of Florida, Jacksonville, Florida Plantar Fasciitis

xvii

REBECCA N. TAPIA, MD Medical Director, Polytrauma Network Site, Polytrauma/ Physical Medicine and Rehabilitation, South Texas Veterans Health Care System, Adjunct Assistant Professor, Department of Rehabilitation Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Polytrauma Rehabilitation

ANN-MARIE THOMAS, MD, PT Assistant Professor, Physical Medicine and Rehabilitation, Harvard Medical School; Staff Physiatrist, Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital; Clinical Associate, Physical Medicine and Rehabilitation, Massachusetts General Hospital; Associate Physiatrist in Medicine, Brigham and Women’s Hospital, Boston, Massachusetts Multiple Sclerosis

JIAXIN TRAN, MD Physical Medicine and Rehabilitation Hospitalist, Madonna Rehabilitation Hospital, Lincoln, Nebraska Complex Regional Pain Syndrome

BIANCA A. TRIBUZIO, DO Staff Physician, Physical Medicine and Rehabilitation, Sharp Rees-Stealy, San Diego, California Quadriceps Tendinopathy

GUY TRUDEL, MD Professor, Medicine, Division of Physical Medicine and Rehabilitation, University of Ottawa, Ottawa, Ontario, Canada Joint Contractures

HEIKKI UUSTAL, MD Attending Physiatrist, Rehabilitation Medicine, JFK Johnson Rehab Institute, Edison, New Jersey; Associate Professor, Medicine, Rutgers Robert Wood Johnson Medical School, Piscataway, New Jersey Mallet Toe

RAMON VALLARINO, JR., MD Attending Physician, Department of Neurosciences, New York Presbyterian Brooklyn Methodist Hospital, Brooklyn, New York Median Neuropathy Ulnar Neuropathy (Wrist)

MONICA VERDUZCO-GUTIERREZ, MD Associate Professor and Vice Chair of Quality, Compliance and Patient Safety, Physical Medicine and Rehabilitation, McGovern Medical School at the University of Texas Health Science Center, Houston, Texas Spasticity

ANKUR VERMA, DO Private Practice, Chicago, Illinois Patellofemoral Syndrome

xviii

Contributors

ARIANA VORA, MD Instructor, Physical Medicine and Rehabilitation, Harvard Medical School; Staff Physiatrist, Physical Medicine and Rehabilitation, Massachusetts General Hospital; Staff Physiatrist, Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, Boston, Massachusetts Coccydynia Postherpetic Neuralgia

MICHAEL C. WAINBERG, MD, MSC Senior Associate Consultant, Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, Minnesota Trigger Finger

ROGER WANG, DO Schwab Rehabilitation Hospital, University of Chicago, Chicago, Illinois Piriformis Syndrome

JAY M. WEISS, MD Medical Director, Long Island Physical Medicine and Rehabilitation, Syosset, New York Lateral Epicondylitis Medial Epicondylitis Ulnar Neuropathy (Elbow)

LYN D. WEISS, MD Chairman and Program Director, Physical Medicine and Rehabilitation, Nassau University Medical Center, East Meadow, New York Lateral Epicondylitis Medial Epicondylitis Radial Neuropathy Ulnar Neuropathy (Elbow)

SARAH A. WELCH, DO, MA Resident Physician, Physical Medicine and Rehabilitation, Vanderbilt University Medical Center, Nashville, Tennessee Cervical Facet Arthropathy

DAVID WEXLER, MD, FRCS(TR&ORTH) Attending, Orthopedics, Maine General Medical Center, Augusta, Maine Ankle Arthritis Bunion and Bunionette Hallux Rigidus Posterior Tibial Tendon Dysfunction

J. MICHAEL WIETING, DO, MEd Associate Dean of Clinical Medicine and Professor of Physical Medicine and Rehabilitation, Lincoln Memorial University-DeBusk College of Osteopathic Medicine, Harrogate, Michigan; Clinical Professor, Department of Physical Medicine and Rehabilitation, Michigan State University-College of Osteopathic Medicine, East Lansing, Michigan Quadriceps Contusion

ALLEN NEIL WILKINS, MD Assistant Clinical Professor, Department of Rehabilitation and Regenerative Medicine, Columbia University College of Physicians and Surgeons; Medical Director, New York Rehabilitation Medicine, New York, New York Foot and Ankle Bursitis

AARON JAY YANG, MD Assistant Professor, Physical Medicine and Rehabilitation, Vanderbilt University Medical Center, Nashville, Tennessee Cervical Facet Arthropathy

FABIO ZAINA, MD Italian Scientific Spine Institute, Milan, Italy Scoliosis and Kyphosis

MEIJUAN ZHAO, MD Assistant Professor, Physical Medicine and Rehabilitation, Harvard Medical School; Staff Physiatrist, Physical Medicine and Rehabilitation, Massachusetts General Hospital, Spaulding Rehabilitation Hospital, Boston, Massachusetts Median Neuropathy (Carpal Tunnel Syndrome)

Preface This book was created with the purpose of discussing a variety of medical conditions that any physiatrist, internist, family physician, orthopedist, rheumatologist, or neurologist will likely encounter in his or her medical practice. We particularly wanted to emphasize the clinical aspects of both musculoskeletal injuries and chronic medical conditions requiring rehabilitation from the perspective of a practitioner in an ambulatory setting. In the second edition we maintained the structure of the book and added an entirely new section on the ambulatory management of conditions associated with pain as a key symptom. The third edition included the ICD-9 and 10 codes as well as some new topics. This, the fourth edition of Essentials of Physical Medicine and Rehabilitation, includes a new section on technology in each of the chapters where recently developed technologies or devices have been added to the therapeutic and rehabilitation strategies. This edition again covers many individual diagnoses in a deliberately succinct and specific format. The first section contains 94 chapters on specific musculoskeletal diagnoses, conveniently organized by anatomic region and in alphabetical order. The second section describes the management of pain in 24 specific conditions and includes a new chapter on abdominal wall pain. The third section covers 45 common medical conditions that are typically chronic and benefit from long-term rehabilitative interventions. Although some of these conditions

require hospitalization, we have tried to focus on the rehabilitation that takes place in an ambulatory setting. Each chapter includes the same sections in the same order (Synonyms, ICD-10 Codes, Definition, Symptoms, Physical Examination, Functional Limitations, Diagnostic Studies, Differential Diagnosis, Treatment [Initial, Rehabilitation, Procedures, and Surgery], Potential Disease Complications, Potential Treatment Complications, and References). It is our hope that physicians in all specialties, rehabilitation providers, and allied health care professionals will find that this book complements the excellent existing rehabilitation textbooks and that it will be an efficient and useful reference tool in the office setting. We are extremely grateful for the hard work of our colleagues who authored these chapters and who represent many different specialties and come from excellent institutions. Their generous support of our work has made this book possible. Finally, we would like to thank our editorial team at Elsevier. Their assistance was invaluable in bringing this ­ book to publication. Walter R. Frontera, MD, PhD, MA (Hon.), FRCP Julie K. Silver, MD Thomas D. Rizzo, Jr., MD

xix

SECTION I

Head, Neck, and Upper Back CHAPTER 1

Cervical Spondylotic Myelopathy Avital Fast, MD Israel Dudkiewicz, MD

Synonyms Cervical radiculitis Degeneration of cervical intervertebral disc Cervical spondylosis without myelopathy Cervical pain

ICD-10 Codes M47.812 Cervical spondylosis without myelopathy or radiculopathy M48.02 Spinal stenosis in cervical region M48.03 Spinal stenosis in cervicothoracic region M50.30 Degeneration of cervical disc M50.32 Degeneration of mid-cervical region M50.33 Degeneration of cervicothoracic region M54.2 Cervical pain M54.12 Cervical radiculitis M54.13 Cervicothoracic radiculitis

Definition Cervical spondylotic myelopathy (CSM) is a frequently encountered entity in middle-aged and elderly patients. The condition affects both men and women. Progressive degeneration of the cervical spine involves the discs, facet joints, joints of Luschka, ligamenta flava, and laminae, leading to gradual encroachment on the spinal canal and spinal cord compromise. CSM has a fairly typical clinical presentation and frequently a progressive and disabling course. As a consequence of aging, the spinal column goes through a cascade of degenerative changes that tend to

affect selective regions of the spine. The cervical spine is affected in most adults, most frequently at the C4-C7 region.1,2 Degeneration of the intervertebral discs triggers a cascade of biochemical and biomechanical changes, leading to decreased disc height, among other changes. As a result, abnormal load distribution in the motion segments causes cervical spondylosis (i.e., facet arthropathy) and neural foraminal narrowing. Disc degeneration also leads to the development of herniations (soft discs), disc calcification, posteriorly directed bone ridges (hard discs), hypertrophy of the facets and the uncinate joints, and ligamenta flava thickening. On occasion, more frequently in Asians but not infrequently in white individuals, the posterior longitudinal ligament and the ligamenta flava ossify.2,3 These degenerative changes narrow the dimensions and change the shape of the cervical spinal canal. In normal adults the anteroposterior diameter of the subaxial cervical spinal canal measures 17 to 18 mm, whereas the spinal cord diameter in the same dimension is approximately 10 mm. Severe CSM gradually decreases the space available for the cord and brings about cord compression in the anterior-posterior axis. Cord compression usually occurs at the discal levels.4-6 The encroaching structures may also compress the anterior spinal artery, resulting in spinal cord ischemia that usually involves several cord segments beyond the actual compression site. Spinal cord changes in the form of demyelination, gliosis, myelomalacia, and eventually severe atrophy may develop.2,4,7-9 Dynamic instability, which can be diagnosed in flexion or extension lateral x-ray views, further complicates matters. Disc degeneration leads to laxity of the supporting ligaments, bringing about anterolisthesis or retrolisthesis in flexion and extension, respectively. This may further compromise the spinal cord and intensify the presenting symptoms.2,4 

Symptoms CSM develops gradually during a lengthy period of months to years. Not infrequently, the patient is unaware of any 3

4

PART 1  MSK Disorders

functional compromise, and the first person to notice that something is amiss may be a close family member. Although pain appears rather early in cervical radiculopathy and alerts the patient to the presence of a problem, this is usually not the case in CSM. A long history of neck discomfort and intermittent pain may frequently be obtained, but these are not prominent at the time of CSM presentation. Most patients have a combination of upper motor neuron symptoms in the lower extremities and lower motor neuron symptoms in the upper extremities.4 Patients frequently present with gait dysfunction resulting from a combination of factors, including ataxia due to impaired joint proprioception, hypertonicity, weakness, muscle control deficiencies, and unexplained falls. Studies have demonstrated that severely myelopathic patients display abnormalities of deep sensation, including vibration and joint position sense, which is attributed to compression of the posterior columns.10,11 Paresthesias and numbness may be frequently mentioned. Compression of the pyramidal and extrapyramidal tracts can lead to spasticity, weakness, and abnormal muscle contractions. These sensory and motor deficits result in an unstable gait. Patients may complain of stiffness in the lower extremities or plain weakness manifesting as foot dragging and tripping.5 Symptoms related to the upper extremities are mostly the result of fine motor coordination deficits. At times, the symptoms in the upper extremities are much more severe than those related to the lower extremities, attesting to central cord compromise.4 Most patients do not have urinary symptoms. However, urinary symptoms (i.e., incontinence) may occasionally develop in patients with long-standing myelopathy.12 As CSM develops in middle-aged and elderly patients, the urinary symptoms may be attributed to aging, comorbidities, and cord compression. Bowel incontinence is rare. 

Physical Examination Because of sensory ataxia, the patient may be observed walking with a wide-based gait. Some resort to a cane to increase the base of support and to enhance safety during ambulation. Patients with severe gait dysfunction frequently require a walker and cannot ambulate without one. Many patients lose the ability to tandem walk. The Romberg test result may become positive. Examination of the lower extremities may reveal muscle atrophy, increased muscle tone, abnormal reflexes—clonus or upgoing toes (Babinski sign)—and abnormalities of position and vibration sense. Muscle fasciculations may be observed. The foot tapping test (number of sole tappings while the heel maintains contact with the floor in 10 seconds) is an easy and useful quantitative tool for lower extremity function in these patients.13 In the upper extremities, weakness and atrophy of the small muscles of the hands may be noted. The patient may have difficulties in fine motor coordination (e.g., unbuttoning the shirt or picking a coin off the table). The patient frequently displays difficulty in performing repetitive opening and closing of the fist. In normal individuals, 20 to 30 repetitions can be performed in 10 seconds. Weakness can occasionally be documented in more proximal muscles and may appear symmetrically. Fasciculations

may appear in the wasted muscles. Hypesthesia, paresthesia, or anesthesia may be documented. On occasion, the sensory findings in the hands are in a glove distribution. As in the lower extremities, the vibration and joint position senses may be disturbed. Hyporeflexia or hyperreflexia may be found. The Hoffmann response may become positive and can be facilitated in early myelopathy by cervical extension.14 In some patients, severe atrophy of all the hand intrinsic muscles is observed.1,5,15-17 The neck range of motion may be limited in all directions. Many patients cannot extend the neck beyond neutral and may feel electric-like sensation radiating down the torso on neck flexion, known as the Lhermitte sign. Often, when a patient stands against the wall, the back of the head stays an inch to several inches away, and the patient is unable to push the head backward to bring it to touch the wall. 

Functional Limitations Patients with CSM have difficulties with activities of daily living. Patients may have difficulties inserting keys, picking up coins, buttoning a shirt, or manipulating small objects. Handwriting may deteriorate. Patients may drop things from the hands and occasionally can complain of numbness affecting the fingers or the palms, mimicking peripheral neuropathy.2,5,16,18,19 They may have problems dressing and undressing. When weakness is a predominant feature, they will be unable to carry heavy objects. Unassisted ambulation may become difficult. The gait is slowed and becomes inefficient. In late stages of CSM, patients may become almost totally disabled and require assistance with most activities of daily living. 

Diagnostic Studies Plain radiographs usually reveal multilevel degenerative disc disease with cervical spondylosis. Dynamic studies (flexion and extension views) may reveal segmental instability with anterolisthesis on flexion and retrolisthesis on extension. In patients with ossification of the posterior longitudinal ligament, the ossified ligament may be detected on lateral plain films. The Torg-Pavlov ratio may help diagnose congenital spinal stenosis. This ratio can be obtained on plain films by dividing the anteroposterior diameter of the vertebral body by the anteroposterior diameter of the spinal canal at that level. The canal diameter can be measured from the posterior wall of the vertebra to the spinolaminar line.20 A ratio of 0.8 or less is indicative of spinal stenosis (Fig. 1.1).21 Magnetic resonance imaging, the study of choice, provides critical information about the extent of stenosis and the condition of the compressed spinal cord. Sagittal and axial cuts clearly show the offending structures (discs, spurs, thickened ligamenta flava) and the cord shape and help to quantify the amount of cord compression. Cord signal changes provide critical information about the extent of cord damage and the prognosis (Fig. 1.2). Increased cord signal on T2-weighted images is abnormal and points to the presence of edema, demyelination, myelomalacia, or gliosis. Decreased cord signal on T1-weighted images may also be observed. Occasionally the increased signal appears as two white dots in T2-weighted images. This is referred to as snake eye appearance (Fig. 1.3). However, these cord signal changes are of

CHAPTER 1  Cervical Spondylotic Myelopathy

5

C2

B

A

A/B ≥ 1

FIG. 1.3  Snake eye appearance on magnetic resonance imaging.

C7

FIG. 1.1 Schematic lateral view of the cervical spine. The canal diameter (A) can be measured by drawing a line between the posterior border of the vertebral body and the spinolaminar line. The vertebral diameter is reflected by line (B). (From Fast A, Goldsher D. Navigating the Adult Spine. New York: Demos Medical Publishing; 2007.)

limited value in predicting functional outcome. A newer magnetic resonance imaging technique, diffusion tensor imaging of the cervical cord, holds considerable promise in predicting the severity of cord injury and may help guide the clinician in deciding when to operate because it may show cord abnormalities before the development of T2 hyperintensity on conventional sequences.22,23 Severe cord atrophy denotes a poor prognosis even when decompressive surgery is performed. Computed tomographic myelography provides fine and detailed information on the amount and location of neural compression and is frequently obtained before surgery. Electrodiagnostic studies play an important role, especially in diabetic patients with peripheral neuropathy, which may confound the clinical diagnosis.  Differential Diagnosis Amyotrophic lateral sclerosis Multifocal motor neuropathy24 Multiple sclerosis Syringomyelia Peripheral neuropathy

Treatment Initial The treatment of CSM depends on the stage in which it is discovered. However, no conservative treatment can be expected to decompress the spinal cord. In the initial stages, patient education is of paramount importance. The patient is instructed to avoid cervical hyperextension. As the cervical spinal canal diameter decreases and the spinal cord diameter increases during cervical hyperextension, this position may lead to further cord compression.25 The patient is advised to drink with a straw and to avoid prolonged overhead activities. 

FIG. 1.2  Sagittal T2-weighted image of the cervical spine showing degenerative disc disease involving the C4-5 and C5-6 intervertebral discs.

Rehabilitation Because the course of CSM may be unpredictable and a significant percentage of patients deteriorate in a slow stepwise

6

PART 1  MSK Disorders

course, close monitoring of the patient’s neurologic condition is indicated. It should be emphasized that treatment should be guided by the clinical symptoms and not the radiologic images because spondylotic changes commonly occur in asymptomatic individuals. Patients with mild CSM may be initially managed conservatively. A biannual detailed neurologic examination and an annual magnetic resonance imaging evaluation are indicated. Special attention should be devoted to the cord cross-sectional area and the cord signal; these are important prognostic factors and may help determine the time of surgery. In the interim, patients should be instructed in static neck exercises. Weak muscles in the upper or lower extremities should be strengthened with progressive resistance exercise techniques. If neck pain or radicular pain becomes an issue, cervical traction, NSAIDs, and analgesic medications may be used. Judicial use of antiinflammatory medications is called for, especially in elderly individuals. Soft cervical collars, which are frequently used (recommended by physicians or obtained by patients without the physician’s recommendations), have no sound scientific basis. Assistive devices, such as a cane or walker, should be provided when ambulation safety is compromised. 

Procedures No existing procedures affect the course or symptoms of cervical myelopathy. 

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery Patients with moderate to severe progressive CSM (unsteady gait, falls, and limited function in the upper extremities) who have significant cord compression or cord signal changes should be referred for decompressive surgery. Potential surgical complications should be mentioned,25 and the patient should be advised that surgery may arrest the myelopathic process but not reverse the cord pathology; thus in patients with advanced disease, status quo ante cannot be expected because the cord changes are irreversible. Two main surgical approaches exist—anterior and posterior. In some patients with severe, advanced multilevel disease, both anterior and posterior surgery may be performed.

Anterior Approach The anterior approach is usually reserved for patients with myelopathy affecting up to three or four spinal levels. This approach allows adequate decompression of “anterior” disease. Anterior disease refers to pathologic changes that are anterior to the spinal cord (e.g., soft disc, hard disc, vertebral body spurs, and ossified posterior longitudinal ligament). Through this approach, the offending structures can be removed without disturbing the spinal cord. The anterior approach allows adequate decompression in patients with cervical kyphotic deformity. The procedure entitled ACDF (anterior cervical decompression and fusion) entails discectomy and corpectomy followed by instrumentation (cage and plate) and bone grafting to ensure proper stabilization. This approach is not indicated in patients whose predominant pathologic process

is posterior to the cord (i.e., hypertrophied ligamentum flavum) or in patients with disease affecting more than four segments, because this may lead to an increased complication rate, including pseudarthrosis.6,17 

Posterior Approach The posterior approach consists of two basic procedures— laminectomy and laminoplasty. It can benefit patients who maintain cervical lordosis because it is expected that following the decompressive procedure the spinal cord will be able to shift posteriorly away from offending anterior pathology. Cervical laminectomy can be easily performed by most spinal surgeons and is less technically demanding than anterior corpectomies are. This approach allows easy access to posteriorly located offending structures such as hypertrophied laminae and ligamenta flava. The main disadvantage of the laminectomy procedure is that it requires stripping of the paraspinal muscles and thus tends to destabilize the cervical spine. This may result in loss of the cervical lordosis or frank kyphotic deformity and instability (stepladder deformity), especially when it is performed over several spinal levels or when the facet joints have to be sacrificed. In multilevel laminectomies, posterior fusion should be performed to stabilize the spine. Laminoplasty, another procedure performed through the posterior approach, has been developed in Japan and addresses some of the shortcomings of laminectomy. Unlike laminectomy, cervical laminoplasty preserves the cervical facets and the laminae. In this procedure, the laminae are hinged away (lifted by an osteotomy) from the site of main pathologic change, resulting in an increase of sagittal canal diameter.26 Unilateral or bilateral hinges can be performed; the bilateral hinge approach allows symmetric expansion of the spinal canal. It is hoped that after posterior decompression, the spinal cord will “migrate” away from the anterior pathologic process, and thus cord decompression will be achieved.17,27 This has been confirmed in magnetic resonance imaging studies after laminoplasty. Regardless of the surgical approach, poor outcome and higher complication rate can be expected in elderly patients with long-standing myelopathy and spinal cord atrophy.28 

Potential Disease Complications Left untreated, a patient with progressive myelopathy may develop quadriplegia and severe disability. Patients may become totally dependent and nonambulatory. In some cases, neurogenic bladder may develop and further compromise the quality of life. 

Potential Treatment Complications Pseudarthrosis, restenosis, spinal instability, postoperative radiculopathy, postoperative kyphotic deformity, dysphagia, and axial pain are among the surgical complications.14 Adjacent level degeneration manifesting in the development of new symptoms occurs in up to 2.9% of ACDF patients per year after surgery and in up to 25% of patients 10 years following surgery.29 The reoperation rate of ACDF ranges from 7% to 9%, especially in elderly diabetic males.30 Another, not infrequent, complication appearing after anterior and posterior surgery is C5 nerve root palsy. It may occur unilaterally or bilaterally and usually resolves.21,31

CHAPTER 1  Cervical Spondylotic Myelopathy

References 1. Heller J. The syndromes of degenerative cervical disease. Orthop Clin North Am. 1992;23:381–394. 2. Nouri A, Tetreault L, Singh A, et al. Degenerative cervical myelopathy. Spine. 2015;40:E675–E693. 3. Machino M, Yukawa Y, Imagama S, et al. Age related and degenerative changes in the osseous anatomy, alignment, and range of motion of the cervical spine. Spine. 2016;41:476–482. 4.  Rao R. Neck pain, cervical radiculopathy, and cervical myelopathy. Pathophysiology, natural history, and clinical evaluation. J Bone Joint Surg Am. 2002;84:1872–1881. 5. Law MD, Bernhardt M, White AA III. Evaluation and management of cervical spondylotic myelopathy. Instr Course Lect. 1995;44:99–110. 6. Truumees E, Herkowitz HN. Cervical spondylotic myelopathy and radiculopathy. Instr Course Lect. 2000;49:339–360. 7. Beattie MS, Manley BT. Tight squeeze, slow burn: inflammation and the aetiology of cervical myelopathy. Brain. 2011;134:1259–1263. 8. Breig A, Turnbull I, Hassler O. Effects of mechanical stresses on the spinal cord in cervical spondylosis. J Neurosurg. 1966;25:45–56. 9. Doppman JL. The mechanism of ischemia in anteroposterior compression of the spinal cord. Invest Radiol. 1975;10:543–551. 10. Takayama H, Muratsu H, Doita M, et al. Impaired joint proprioception in patients with cervical myelopathy. Spine (Phila Pa 1976). 2004;30:83–86. 11. Okuda T, Ochi M, Tanaka N, et al. Knee joint position sense in compressive myelopathy. Spine (Phila Pa 1976). 2006;31:459–462. 12. Misawa T, Kamimura M, Kinoshita T, et al. Neurogenic bladder in patients with cervical compressive myelopathy. J Spinal Disord Tech. 2005;18:315–320. 13. Numasawa T, Ono A, Wada K, et al. Simple foot tapping test as a quantitative objective assessment of cervical myelopathy. Spine (Phila Pa 1976). 2012;37:108–113. 14. Rhee JM, Heflin JA, Hamasaki T, et al. Prevalence of physical signs in cervical myelopathy: a prospective, controlled study. Spine. 2009;34:890–895. 15. Grijalva RA, Hsu FPK, Wycliffe HD, et al. Hoffmann sign: clinical correlation of neurological imaging findings in the cervical spine and brain. Spine. 2015;40:475–479. 16. Nemani VM, Kim HJ, Piaskulkaew, et al. Correlation of cord signal change with physical examination findings in patients with cervical myelopathy. Spine. 2014;40:6–10.

7

17. Edwards CC, Riew D, Anderson PA, et al. Cervical myelopathy: current diagnostic and treatment strategies. Spine J. 2003;3:68–81. 18. Ono K, Ebara S, Fiji T, et al. Myelopathy hand. New clinical signs of cervical cord damage. J Bone Joint Surg Br. 1987;69:215–219. 19. Ebara S, Yonenobu K, Fujiwara K, et al. Myelopathy hand characterized by muscle wasting. A different type of myelopathy hand in patients with cervical spondylosis. Spine (Phila Pa 1976). 1988;13:785–791. 20. Yu M, Tang Y, Liu Z, et al. The morphological and clinical significance of developmental cervical stenosis. Eur Spine J. 2015;24:1583–1589. 21. Taha AMS, Shue J, Lebl D, et al. Considerations for prophylactic surgery in asymptomatic severe cervical stenosis. HSSJ. 2015;11:31–35. 22. Banaszek A, Bladowska J, Szewczyk P, et al. Usefulness of diffusion tensor MR imaging in the assessment of intramedullary changes of the cervical spinal cord in different stages of degenerative spine disease. Eur Spine J. 2014;23:1523–1530. 23. Rajasekaran S, Kanna RM, Chittode VS, et al. Efficacy of diffusion tensor imaging indices in assessing postoperative neural recovery in cervical spondylotic myelopathy. Spine. 2017;42:8–13. 24. Olney RK, Lewis RA, Putnam TD, Campellone JV Jr. Consensus criteria for the diagnosis of multifocal motor neuropathy. Muscle Nerve. 2003;27:117–121. 25. Lauryssen C, Riew KD, Wang JC. Severe cervical stenosis: operative treatment or continued conservative care. SpineLine. 2006:1–25. 26. Simpson AK, Rhee A. Laminoplasty: a review of the evidence and detailed technical guide. Semin Spine Surg. 2014;26:141–147. 27. Chen GD, Lu Q, Sun JJ. Effect and prognostic factors of laminoplasty for cervical myelopathy with an occupying ratio greater than 50%. Spine. 2016;41:378–383. 28. Fehlings M, Smith JS, Kopjar B, et al. Perioperative and delayed complications associated with surgical treatment of cervical spondylotic myelopathy based patients from the AOSpine North America cervical spondylotic myelopathy study. J Neurosurg Spine. 2012;16:425–432. 29. Zhu Y, Zhang B, Liu H, et al. Cervical disc arthroplasty versus anterior cervical discectomy and fusion for incidence of symptomatic adjacent segment disease. Spine. 2016;41:1493–1502. 30. Park MS, Ju YS, Moon SH, et al. Reoperation rates after anterior cervical discectomy and fusion for cervical spondylotic radiculopathy and myelopathy. Spine. 2016;41L:1593–1599. 31. Guzman JZ, Baird EO, Fields AC, et al. C5 nerve root palsy following decompression of the cervical spine. Bone Joint J. 2014;96-B:950–955.

CHAPTER 2

Cervical Facet Arthropathy Aaron Jay Yang, MD Sarah A. Welch, DO, MA Walter R. Frontera, MD, PhD, MA (Hon.), FRCP

Synonyms Facet joint arthritis Facet-mediated pain Facetogenic, pain Spondylosis Z-joint pain Zygapophyseal joint pain Posterior element disorder

ICD-10 Codes M43.02 M47.812 M54.2 M54.02 S13.4

Cervical spondylosis Spondylosis w/o radiculopathy or myelopathy Cervicalgia Facet syndrome (cervical) Neck: Sprain of atlanto-axial (joints), sprain of atlanto-occipital (joints), whiplash injury

Definition The cervical facet joints have long been identified as a potential pain generator for neck pain. The facet joints are located in the posterior portion of the cervical spine and the paired synovial joints articulate between adjacent vertebrae (Fig. 2.1). The coronal oblique orientation of the joints allows greater flexion, extension, and lateral bending of the cervical spine. Cervical facet joint arthropathy is mostly degenerative in nature, although facet joint mediated pain can occur secondary to trauma, acceleration-deceleration injury such as whiplash, or following prior fusion surgery due to adjacent segmental changes. In the case of chronic axial neck pain, the facet joints have been reported to be the primary pain generator in about 25% to 66% of cases.1 In patients with chronic facet-mediated pain, 58% to 88% of patients complained of associated headaches.2-4 Cervical facet joint arthropathy 8

increases with age and in cadaveric studies, the C4-5 level was found to be most frequently affected followed by C3-4, C2-3, C5-6, and C6-7.5 The findings of facet joint arthropathy have been shown to be independent of race and gender.6 However, based on the most clinically affected segments diagnosed by diagnostic blocks, the C2-3 and C5-6 joints were shown to be most commonly affected.2,4,7 In patients who complain of posterior headaches following a whiplash injury, the C2-3 joint has been estimated to be the pain generator in 50% to 53% of patients.3,4 Following trauma, the C5-6 joint has been shown to be the most commonly affected level.2,8 

Symptoms Patients who present with facet-mediated pain secondary to facet arthropathy typically have progressive pain as opposed to acute pain with the main exception being whiplash injuries.9 Patients typically have axial neck pain that is unilateral and does not radiate past the shoulder. Weakness, numbness, or any other neurologic symptom are typically not seen in patients with primary facet-mediated pain, but may occur if there is simultaneous nerve root injury. Pain may worsen with cervical extension and axial rotation. Referral pain patterns arising from the cervical facet joints have been described using noxious stimulation of the joints in asymptomatic subjects that was subsequently validated with diagnostic blocks.10,11 Referral patterns have been described as seen in Fig. 2.2. 

Physical Examination Examination for cervical facet-mediated pain has been shown to be inconsistent, although paraspinal tenderness has been demonstrated to be most correlative with facetmediated pain.12,13 Aside from palpation, examination usually consists of range of motion testing, segmental analysis, and neurologic examination to rule out neurologic impairment. Point tenderness may be associated with exacerbation of symptoms with cervical extension and axial rotation and loss of cervical motion. Manual examination of the joints may be performed with the patient supine. The C2 spinous process can be palpated as the first protuberance below the occiput while the C7 spinous process is the largest and most

CHAPTER 2  Cervical Facet Arthropathy

9

palpable and is fixed in comparison to the relatively mobile C6 spinous process.14 The facet joints may be palpable as hard bony masses about 1.3 to 2.5 cm lateral to the spinous process.9 Unless cervical disc or nerve root disease is also present, the findings of the neurologic examination are otherwise typically normal. 

Functional Limitations Patients may have difficulty with cervical extension and rotation, although they may be limited in all planes due to associated muscle spasm. Patients may complain of difficulty driving due to limited ability to turn their head and may also have interference with various activities of daily living and work tasks that may require rotation of the cervical spine. 

Diagnostic Studies

FIG. 2.1  Lateral fluoroscopic view of the right C2-3 zygapophyseal joint with the needle tip inside the joint. (From Dreyfuss P, Kaplan M, Dreyer SJ. Zygapophyseal joint injection techniques in the spinal axis. In: Lennard TA, ed. Pain Procedures in Clinical Practice, 3rd ed. Philadelphia: Elsevier/Saunders; 2011:373.)

C2-3

C3-4

C4-5

C5-6

C6-7

FIG. 2.2 Distribution of pain following noxious stimulation of the cervical facet joints. (From Dwyer A, Aprill C, Bogduk N. Cervical zygapophyseal joint pain patterns. I: a study in normal volunteers. Spine (Phila Pa 1976). 1990;15(6):453–457.)

Aside from the history and physical examination, the gold standard for diagnosis of cervical facet-mediated pain are fluoroscopically guided medial branch blocks.14 Theoretically, the diagnosis can be confirmed by the alleviation of pain by injecting local anesthetic around the medial branches of the dorsal rami, which supply the nociceptive fibers to the facet joints. However, there is no consensus on what constitutes a positive block as well as whether a single or comparative block should be performed with anesthetics of different durations. False positive rates have been reported to be around 27% to 63% with a single block, thus causing some to advocate for comparative blocks, although this continues to be controversial in the interventional spine community.15,16 Imaging of the facet joints includes plain films, computed tomography (CT), and magnetic resonance imaging (MRI). Disc degeneration has been shown to precede development of facet joint arthropathy.16,17 Population-based studies of patients with neck pain who underwent cervical spine imaging failed to show a correlation of neck pain and facet joint arthropathy in men and women between the ages of 20 and 65.18 Findings on CT and MRI have been unable to predict success with facet joint blocks and radiofrequency denervation, respectively.13,19 Use of bone scintigraphy using single photon emission computed tomography (SPECT) has been studied in predicting a favorable response to facet joint injections in the lumbar spine, although this is not commonly done at this time in the cervical or lumbar spine.20 

Differential Diagnoses Degenerative disc disease Myofascial pain syndrome Internal disc disruption Disc herniation Cervical stenosis Cervical radiculopathy or myelopathy Spondylolysis Tumor Infection Osteoid osteoma

10

PART 1  MSK Disorders

Treatment Initial Initial treatment focuses on education, pain control with nonsteroidal anti-inflammatory drugs, topical creams, ice, stretching, activity modification, and avoidance of activities that exacerbate the pain.21 Soft collars for a short period of time up to 72 hours could be considered, although rarely indicated, and soft tissue massage could also be considered as an adjunct therapy.22 No studies have specifically evaluated conservative therapies for injection-confirmed facet joint pain and the main treatment approaches are extrapolated from studies in patients with non-specific spinal pain.16 

Rehabilitation Rehabilitative approaches focus on decreasing local pain and muscle tension while normalizing range of motion, strengthening the spinal musculature, and addressing biomechanical deficits. Restoring spinal motion helps to improve posture and reduce strain on the paraspinal musculature. Posture reeducation, flexion biased therapy, and stretching tight musculature such as the trapezius muscle may also help to limit strain on the facet joints.22 Modalities such as superficial cryotherapy or heat, therapeutic ultrasound, transcutaneous electrical stimulation, and traction may also be considered, although they have not been shown to affect long-term outcome.23,24 Manual therapies such as myofascial release, soft tissue mobilization, low- and high-velocity manipulations are also considered for facet-mediated pain. In general, alternative therapies such as manipulation and acupuncture are superior to no treatment, but compared to sham treatment or physical exercise, the results have been inconclusive.16 

Procedures The majority of interventional techniques for treating cervical facet-mediated pain are fluoroscopically guided, although ultrasound guidance has been reported.25 Interventional options include intra-articular joint injections, diagnostic medial branch blocks, and therapeutic medial branch radiofrequency denervation. Therapeutic cervical intra-articular facet joint injection with steroids can be considered in patients who have not responded to conservative therapy or to help reduce pain and improve participation in therapy in the subacute phase. However, results in studies have been mixed with success rates in controlled studies varying widely from 35 years or non-athletes >65 years) and is more common than primary biceps tendinitis.1,5 In fact, histopathologic studies reveal a paucity of inflammatory findings in the majority of biceps tendons that are the source of anterior shoulder pain. Rather, chronic degenerative changes are most prominent, similar to other tendinopathies of the body.7 Studies have found that up to 95% of patients with biceps tendinosis have associated rotator cuff disease.8,9 

Symptoms Biceps tendinopathy usually presents with complaints of anterior shoulder pain that is worse with activities involving elbow flexion.2 Pain usually localizes to the bicipital groove with occasional radiation to the arm or deltoid region. Often, pain will also occur with prolonged rest and immobility, particularly at night. The throwing athlete often describes pain during the follow-through of a throwing motion and may feel a “snap” if the tendon subluxes in the groove.4 Attention should be given to onset, duration, and character of the pain. Some individuals present with only complaints of fatigue with shoulder movement. A history of prior trauma, athletic and occupational endeavors, and systemic diseases should be considered in evaluating the shoulder. Patients with accompanying impingement syndrome often complain of a “pinching” sensation with overhead activities and a “toothache” sensation in the lateral proximal arm. Biceps tendinopathy pain can be difficult to differentiate from impingement or rotator cuff syndrome, and these entities commonly coexist.5 

Physical Examination The physical examination begins with careful inspection of the shoulder and neck region. Attention is given to prior scars, structural deformities, posture, and muscle bulk. Determination of the exact location of pain can be helpful for diagnosis. Biceps tendinopathy commonly presents with palpable tenderness over the bicipital groove (Fig. 12.1). Side-to-side comparisons should be made because the tendon is typically slightly tender to direct palpation. Tenderness over the lateral aspect of the shoulder suggests bursitis, rotator cuff tendinopathy, or 59

60

PART 1  MSK Disorders

FIG. 12.1  Palpation of the bicipital groove.

strain of the deltoid muscle. Caution should be used, as the accuracy for palpating the biceps tendon was 5.3% in residents and fellows.10 Range of motion limitation is not seen in isolated biceps tendinopathy, but is often seen in concomitant degenerative joint disease, impingement syndrome, rotator cuff tendinopathy, or adhesive capsulitis. A neurologic examination should be normal, including sensation and deep tendon reflexes. On occasion, strength is limited by pain or disuse. Assessment of the kinetic chain, including scapular stability and spine stabilization, is important. Special tests of the shoulder should be performed routinely. The Speed and Yergason tests (Figs. 12.2 and 12.3) are often used to help evaluate for biceps tendinopathy. Unfortunately, a recent meta-analysis suggests that these tests are not sensitive (Speed = 50% to 63%, Yergason = 14% to 32%) or specific (Speed = 60% to 85%, Yergason = 70% to 89%) for diagnosing biceps tendinopathy.11 Impingement tests and supraspinatus tests will help assess for any concurrent rotator cuff tendinopathy. Other maneuvers to assess for instability (anterior apprehension, anterior-posterior load and shift), labral disease (O’Brien test; see Chapter 15) and acromioclavicular joint arthritis (Scarf or Cross Arm Adduction test; see Chapter 10) should be performed. 

Functional Limitations Biceps tendinopathy may cause patients to limit their activities at home and at work. Limitations may include difficulty with lifting and carrying groceries, garbage bags, and briefcases. Athletics that involve the affected arm, such as swimming, tennis, and throwing sports, may be curtailed. Pain may impair sleep. 

FIG. 12.2  Demonstration of Speed test for bicipital tendinitis. The examiner provides resistance to forward flexion of the shoulder with the elbow in extension and supination of the forearm. Pain is elicited in the intertubercular groove in a positive test result.

FIG. 12.3  Demonstration of Yergason test. The examiner provides resistance against supination of the forearm with the elbow flexed at 90 degrees. The test result is considered positive when pain is produced or intensified in the intertubercular groove.

Diagnostic Studies Biceps tendinopathy is generally diagnosed on a clinical basis, but imaging studies are helpful for excluding other pathologic processes. Plain radiographs are usually normal.1 However, they can show calcifications in the tendon and degenerative disease of the shoulder joint that may

CHAPTER 12  Biceps Tendinopathy

61

Differential Diagnosis

FIG. 12.4  Ultrasound of the biceps tendon. Short-axis view of the biceps tendon shows the tendon (arrow) within the bicipital groove.

predispose to tendinopathy. The Fisk view is used to assess the size of the intertubercular groove. This may help determine whether there is a relative risk for development of recurrent subluxation of the tendon, which is seen in individuals with short and narrow margins of the intertubercular groove.12 Ultrasonography can be an extremely helpful and costeffective way to evaluate the biceps and rotator cuff tendons (Fig 12.4). Ultrasound can detect increased fluid in the biceps tendon sheath and evidence of tendinosis. In addition, ultrasound is highly sensitive and specific for detecting biceps tendon subluxation.13 Research suggests that ultrasound of the shoulder is more accurate in confirming a normal biceps tendon or full-thickness tear, but less accurate in the diagnosis of partial-thickness tears.13,14 Magnetic resonance imaging can detect partial-thickness tendon tears, examine muscle substance, evaluate soft tissue abnormalities and labral disease (magnetic resonance arthrography), and assess for masses. In biceps tendinitis, increased signal intensity is seen on T2-weighted images.14 However, this finding is also seen with partial tears of the tendon. Tendinosis presents with increased tendon thickness and intermediate signal in the surrounding sheath. Arthroscopy is useful in evaluating the intra-articular portion of the biceps tendon but not extra-articular sites of predilection of tendinopathy.15 

Treatment Initial The treatment of biceps tendinopathy involves activity modification, anti-inflammatory measures, and heat and cold modalities.2,4 Overhead activities and lifting are to be avoided initially. Workstation assessment and modification can be helpful for laborers. Evaluation of athletic technique and training adaptations are important in athletes. Nonsteroidal anti-inflammatory drugs can assist with decreasing the pain and inflammation in tendonitis, but do not play a role in tendinosis. Medications to increase blood flow to the tendon (i.e., nitro patches) may play a role in facilitating recovery. Ice is helpful after exercise for minimizing pain.3,4 Moist heat can be useful before activity. Other modalities such as iontophoresis and electrical stimulation have been used, but there are no clinical trials supporting their efficacy. 

Rotator cuff tendinopathy and tears Subacromial/subdeltoid bursitis Labral tear Multidirectional instability of the shoulder Biceps tendon rupture Acromioclavicular joint sprain Glenohumeral or acromioclavicular degenerative joint disease Rheumatoid arthritis Crystalline arthropathy Adhesive capsulitis Cervical spondylosis Cervical radiculopathy Brachial plexopathy Peripheral entrapment neuropathy Referral from visceral organs Diaphragmatic referred pain

Rehabilitation Rehabilitation for biceps tendinopathy is similar to that for rotator cuff tendinopathy (see Chapter 16). Moreover, because biceps tendinopathy rarely occurs in isolation, it is important to rehabilitate the patient by accounting for all of the shoulder disease that is present (e.g., instability, impingement).1,2 Shoulder stretching helps maintain or improve range of motion and is emphasized for all important shoulder movements of abduction, adduction, and internal and external rotation. Posterior capsule stretching is also important, particularly when impingement syndrome is present. Overhead and shoulder abduction activities should be avoided early in treatment because they can exacerbate symptoms. Once full, pain-free active range of motion is achieved, progressive resistance exercises are used to strengthen the dynamic shoulder and spine stabilizers, progressing from static to dynamic exercise as tolerated.4 Eccentric strengthening exercises may be beneficial for biceps tendinopathy, but more research is needed. The exercise program should progress to sportspecific functional activities when appropriate. Athletes may return to play, gradually, when pain is minimal or absent.4 

Procedures Biceps tendon sheath steroid injections are a potentially useful adjunct for biceps tendinitis (Fig. 12.5), but should probably be avoided in cases of tendinosis. The goal of an injection is to diminish pain and inflammation while facilitating the rehabilitation treatment program. It must be used judiciously to avoid weakening of the tendon substance. Ultrasound-guided injections provide better accuracy than unguided injections and fluoroscopy-guided injections, and have fewer complications from injecting the tendon than do unguided injections.16,17 Immediate postinjection care includes icing for 5 to 10 minutes, and the patient may continue to apply ice at home for 15 to 20 minutes, two or three times daily, for several days. The patient should be instructed to avoid heavy lifting or vigorous exercise for 48 to 72 hours after injection. Injection

62

PART 1  MSK Disorders

Potential Disease Complications Progressive biceps tendinopathy and pain can lead to diminished activity, rotator cuff pathology, and adhesive capsulitis. Chronic tendinosis can predispose to proximal biceps tendon rupture. Compensatory problems with other tendons can develop because of their interdependence for proper shoulder movement. The development of myofascial pain of the surrounding shoulder girdle muscles is another common complication in shoulder tendinopathy. 

Potential Treatment Complications The exercise program should be properly supervised initially to prevent aggravation of rotator cuff tendinopathy or impingement. Analgesics and nonsteroidal anti-inflammatory drugs have well-known side effects that most commonly affect the gastric, hepatic, and renal systems. Repeated steroid injections in or near tendons could result in tendon rupture and should be performed under ultrasound guidance whenever possible.

References

FIG. 12.5  Injection technique for the long head of the biceps brachii (ideally performed under ultrasound guidance). Under sterile conditions with use of a 25-gauge, 1½-inch disposable needle and a local anesthetic-corticosteroid combination, the area surrounding the biceps tendon is injected. It is important to bathe the tendon sheath in the preparation rather than to inject the tendon itself. Typically, a 1- to 3-mL aliquot of the mixture is used (e.g., 1 mL of 1% lidocaine mixed with 1 mL of betamethasone). (Reprinted with permission from Lennard TA. Pain procedures in clinical practice. 2nd ed. Philadelphia: Hanley & Belfus; 2000:150.)

of biologics (autologous blood and platelet-rich plasma) is potentially promising, but needs further research to better define its utility. Depending on the concurrent shoulder disease, other injections may also be useful (e.g., subacromial, glenohumeral).18 

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery Surgery is generally not indicated for isolated biceps tendinopathy. However, biceps tenodesis in conjunction with acromioplasty in chronic, refractory cases and in those cases associated with rotator cuff tears or impingement has been found to have good results.19 Tenodesis procedures that incorporate bicipital tunnel decompression have somewhat better outcome measures than those that do not.20 Tenotomy of the long head of the biceps for chronic biceps tendinopathy remains controversial, and long-term results are unknown.19,21 

1. Patton WC, McCluskey GM. Overuse injuries in the upper extremity. Clin Sports Med. 2011;20:439–451. 2. Churgay CA. Diagnosis and treatment of biceps tendinitis and tendinosis. Am Fam Physician. 2009;80(5):470–476. 3. Longo UG, Loppini M, Marineo G, Khan WS, Maffulli N, Denaro V. Tendinopathy of the tendon of the long head of the biceps. Sports Med Arthrosc. 2011;19(4):321–332. Review. 4. Ryu JH, Pedowitz RA. Rehabilitation of biceps tendon disorders in athletes. Clin Sports Med. 2010;29(2):229–246, vii-viii. Review. 5. Snyder GM, Mair SD, Lattermann C. Tendinopathy of the long head of the biceps. Med Sport Sci. 2012;57:76–89. Epub 2011 Oct 4. Review. 6. Pfahler M, Branner S, Refior HJ. The role of the bicipital groove in tendopathy of the long biceps tendon. J Shoulder Elbow Surg. 1999;8:419–424. 7. Streit JJ, Shishani Y, Rodgers M, et al. Tendinopathy of the long head of the biceps tendon: histopathologic analysis of the extra-articular biceps tendon and tenosynovium. Open Access J Sports Med. 2015;6:63–70. 8. Harwood MI, Smith CT. Superior labrum, anterior-posterior lesions and biceps injuries: diagnostic and treatment considerations. Prim Care Clin Office Pract. 2004;31:831–855. 9. Redondo-Alonso L, Chamorro-Moriana G, Jimenez-Rejano JJ, et al. Relationship between chronic pathologies of the supraspinatus tendon and the long head of the biceps tendon: systematic review. BMC Musculoskelet Disord. 2014;15:377. 10. Gazzillo GP, Finnoff JT, Hall MM, Sayeed YA, Smith J. Accuracy of ­palpating the long head of the biceps tendon: an ultrasonographic study. PM R. 2011;3(11):1035–1040. https://doi.org/10.1016/j.pmrj. 2011.02.022. Epub 2011 Jun 25. 11. Hegedus EJ, Goode AP, Cook CE, et al. Which physical examination tests provide clinicians with the most value when examining the shoulder? Update of a systematic review with meta-analysis of individual tests. Br J Sports Med. 2012. 12. Schaeffeler C, Waldt S, Holzapfel K, et al. Lesions of the biceps pulley: diagnostic accuracy of MR arthrography of the shoulder and evaluation of previously described and new diagnostic signs. Radiology. 2012;264(2):504–513. 13. Armstrong A, Teefey SA, Wu T, et al. The efficacy of ultrasound in the diagnosis of long head of the biceps tendon pathology. J Shoulder Elbow Surg. 2006;15(1):7–11. 14. Skendzel JG, Jacobson JA, Carpenter JE, Miller BS. Long head of biceps brachii tendon evaluation: accuracy of preoperative ultrasound. AJR Am J Roentgenol. 2011;197(4):942–948. 15. Saithna A, Longo A, Leiter J, et al. Shoulder arthroscopy does not adequately visualize pathology of the long head of biceps tendon. Orthop J Sports Med. 2016;4(1):2325967115623944. 16. Hashiuchi T, Sakurai G, Morimoto M, Komei T, Takakura Y, Tanaka Y. Accuracy of the biceps tendon sheath injection: ultrasound-guided or unguided injection? A randomized controlled trial. J Shoulder Elbow Surg. 2011;20(7):1069–1073. Epub 2011 Jul 22.

CHAPTER 12  Biceps Tendinopathy

17. Petscavage-Thomas J, Gustas C. Comparison of ultrasound-guided to fluoroscopy-guided biceps tendon sheath therapeutic injection. J Ultrasound Med. 2016;35(10):2217–2221. 18. Elser F, Braun S, Dewing CB, Giphart JE, Millett PJ. Anatomy, function, injuries, and treatment of the long head of the biceps brachii tendon. Arthroscopy. 2011;27(4):581–592. Review. 19. Kelly AM, Drakos MC, Fealy S, et al. Arthroscopic release of the long head of the biceps tendon: functional outcome and clinical results. Am J Sports Med. 2005;33:208–213.

63

20. Taylor SA, Ramkumar PN, Fabricant PD, et al. The clinical impact of bicipital tunnel decompression during long head of the biceps tendon surgery: a systematic review and meta-analysis. Arthroscopy. 2016;32(6): 1155–1164. 21. Slenker NR, Lawson K, Ciccotti MG, Dodson CC, Cohen SB. Biceps tenotomy versus tenodesis: clinical outcomes. Arthroscopy. 2012;28(4):576– 582. Epub 2012 Jan 28. Review.

CHAPTER 13

Biceps Tendon Rupture Michael F. Stretanski, DO, AME

Synonyms Biceps brachii rupture Biceps tear Bicipital strain

ICD-10 Codes M66.821 Rupture of tendon of biceps (upper arm), nontraumatic, right M66.822 Rupture of tendon of biceps (upper arm), nontraumatic, left M66.829 Rupture of tendon of bicep (upper arm), nontraumatic, unspecified

Definition Biceps tendon rupture is either complete or partial disruption of the tendon of the biceps brachii muscle that can occur proximally or distally. The more common proximal ruptures account for 90% to 97% of all biceps ruptures and almost exclusively involve the long head. They are associated with concomitant rotator cuff disease and degenerative joint disease of the shoulder (Fig. 13.1).1 The incidence is 1.2 per 100,000 patients, with a majority on the dominant side of men who smoke and are in the fourth decade of life.2 Most cases involve the long head of the biceps (LHB) brachii and are manifested as a partial or complete avulsion from the superior rim of the anterior glenoid labrum.3 Cadaveric study suggests that the relative avascularity of the LHB tendon may be a risk factor, as seen in many tendons having a “watershed” blood supply. Supplied through its osteotendinous and musculotendinous junctions and, rarely, branches from the anterior circumflex humeral artery traveling in a mesotenon, the LHB tendon has a hypovascular region in the border of two adjacent vascular territories. This region of limited arterial supply, 1.2 to 3 cm from the tendon origin, extends midway through the glenohumeral joint to the proximal intertubercular groove.4 The distal biceps rupture is relatively uncommon and typically occurs in middle-aged men, although acute traumatic ruptures may occur in younger individuals or in anyone engaged in 64

predisposing activities, such as forceful explosive contraction of the biceps. Patients with a distal biceps tendon rupture carry a risk of at least 8% for a rupture on the contralateral side.5 This often develops suddenly with stressing of the flexor mechanism of the elbow. Distal biceps rupture usually occurs as a single traumatic event, such as with heavy lifting; it is often an avulsion of the tendon from the radial tuberosity, but it can also occur as a midsubstance tendon rupture.6 

Symptoms Proximal ruptures are often asymptomatic and are commonly discovered with awareness of distal migration of the biceps brachii muscle mass, or they may occur suddenly by a seemingly trivial event. Often, individuals will note an acute “popping” sensation. The patient often takes one finger and points directly to the bicipital groove when describing the pain. Edema and ecchymosis may be seen with tendon rupture, but also with other regional pathologic processes. The proximal ruptures are typically less painful, but can be preceded by chronic shoulder discomfort.7 An acute distal rupture is often associated with pain at the antecubital fossa that is typically aggravated by resisted elbow flexion. The pain is usually sharp initially but improves with time and is often described as a dull ache.8 Swelling, distal ecchymosis, and proximal migration of the biceps brachii muscle mass accompany this injury with a magnitude dependent on the degree of injury. Younger, healthy patients may often present with a cosmetic rather than a functional complaint. 

Physical Examination As with all musculoskeletal conditions, the physical examination portion of clinical assessment is carried out within the clinical context of functional, not just regional, complaints. Visual inspection of the biceps brachii, including comparison to the contralateral side, is usually the first and most obvious element in the physical examination. Neurosensory, vascular, and even electrodiagnostic medicine exams should be normal. Patients may often present aware of side-to-side changes and may alternate non-dominant for dominant arm activities. Ultrasound assessment of the LHB tendon is now reliable among trained clinicians and is a safe non-invasive modality with virtually no risk that can be incorporated into clinical exam portions of patient

CHAPTER 13  Biceps Tendon Rupture

65

FIG. 13.1  Proximal biceps tendon rupture.

assessment.9 Readers should be aware that as many as 129 shoulder exam maneuvers have been described, many of which overlap or are redundant.9a However, peerreviewed systemic review of combined specific tests, that have been used for decades, has yielded a “3-pack”10 of the O’Brien’s test (downward force distally on the arm while the patient resists with an upward force), throwing test (throwing motion against examiner’s resistance; anterior subluxation may occur), and bicipital tunnel palpation with good inter-rater reliability and possible arthroscopic predictability. Ludington’s test11 is a recommended position in which to observe differences in the contour and shape of the biceps (Fig. 13.2). Diagnosis of complete ruptures is relatively easy; patients often come in aware of the biceps muscle retraction. Partial ruptures exist along a spectrum and can be more difficult to diagnose. The clinician should also assess for the presence of ecchymosis or swelling as a sign of acute injury. Palpation for point tenderness will often reveal pain at the rupture site. An effort should also be made to determine whether the rupture is complete by palpation and observation of the tendon. Thorough assessment of the shoulder and elbow should be made for range of motion and laxity. Yergason and Speed tests were originally intended to examine the long head of biceps, but are also used in conjunction to detect superior labral anteo-posterior (SLAP) lesions of the glenoid labrum. They are accurate for predicting pathology of the biceps/labral complex, but are not very specific to a particular structure. Tests which are used in the assessment of bicipital tendinitis are also recommended (see Chapter 12). Posterior dislocation of the LHB tendon has been reported12 and may share some common physical examination findings, but not muscle retraction. In patients with inconsistent physical examination findings and questionable secondary gains, the American Shoulder and Elbow Surgeons subjective shoulder scale,13 a standardized scale of shoulder function with patient and physician components, has demonstrated acceptable psychometric performance for outcomes assessment in patients

FIG. 13.2  Ludington’s test is performed by having the patient clasp both hands onto or behind the head, allowing the interlocking fingers to support the arms. This action permits maximum relaxation of the biceps tendon in its resting position. The patient then alternately contracts and relaxes the biceps while the clinician palpates the tendon and muscle. In a complete tear, contraction is not felt on the affected side.

with shoulder instability, rotator cuff disease, and glenohumeral arthritis.14 It is important to examine the entire shoulder and to keep in mind that it is a complex, inherently unstable, wellinnervated joint that tends to function, and fail, as a unit; therefore, additional lesions that are the true pain generator may be evident. One study15 looking at shoulder magnetic resonance findings showed no statistical relationship between the level of disability and either biceps tendon rupture or biceps tendinopathy; rather, disability was linked to supraspinatus tendon lesions and bursitis. A thorough neurologic and vascular examination is performed, and findings should be normal in the absence of concomitant problems. Caution should be used with strength testing or end-range motion to avoid worsening of an incomplete tear. 

Functional Limitations The functional limitations are generally relatively minimal with proximal biceps rupture,16 and the patient’s concern is often centered around cosmetic considerations. More significant weakness of elbow flexion and supination is noted after a distal tendon disruption. Pain can be acutely limiting after both situations, but is typically more of a problem in distal rupture. The primary role of the biceps brachii is supination of the forearm. Elbow flexion is functional by the action of the brachialis and brachioradialis. A degree of residual weakness with supination and elbow flexion, particularly after distal tendon rupture, can cause functional impairment for individuals who perform heavy physical labor.17 Fatigue with repetitive work is

66

PART 1  MSK Disorders

also a common complaint with nonsurgically treated distal tendon ruptures.18 The LHB is thought to play a role in anterior stability of the shoulder;19 this is an issue for people who perform overhead activities (such as lifting, filing, and painting), powerlifting (in which the final 10% of strength is crucial), and nonsports activities in which the appearance of symmetry is important (such as modeling or bodybuilding). 

Diagnostic Studies The diagnosis of biceps brachii rupture is often made on a clinical basis alone. Magnetic resonance imaging (MRI) is helpful in confirming the diagnosis and assessing the extent of the injury, but it should be performed in the flexed elbow, abducted shoulder, and forearm supinated (FABS) position to obtain a true longitudinal view;20 it is particularly useful in partial ruptures. MRI studies can also assess concomitant rotator cuff disease. Diagnostic ultrasound has grown in applicability and portability. It may have a role in demonstrating not only proximal, but also distal biceps tendon partial tears, ruptures, bifurcation, subluxation, and the rotator cuff.21 Diagnostic ultrasound may be more cost-effective as an initial screening tool when no surgical injuries are suspected. Imaging of the entire insertion site as well as of elbow structures should be performed in distal ruptures.22 Plain radiographs sometimes show hypertrophic bone formation related to chronic degenerative tendon abnormalities as a predisposition to rupture. Radiographs are also obtained in acute traumatic cases to rule out fractures and to identify developmental variants. Electrodiagnostic medicine consultation for possible peripheral nerve damage should be considered in cases with evidence of lower motor neuron findings or where the distribution of weakness is not fully accounted for by pain. Attention should be paid to median neuropathy at the elbow and, although it is technically difficult, to lateral antebrachial cutaneous nerve studies.  Differential Diagnosis Musculocutaneous neuropathy Rotator cuff disease Brachial plexopathy Pectoralis major muscle rupture Tumor Hematoma Dislocated biceps tendon Cervical radiculopathy Parsonage-Turner syndrome Isolated subscapularis tendon disease

Treatment Initial For most patients, treatment of proximal biceps tears is conservative. Gentle range of motion exercises for prevention of contractures of the elbow and shoulder (adhesive capsulitis) can be started almost immediately. The function of the LHB tendon and its role in glenohumeral

kinematics presently remain only partially understood because of the difficulty of cadaveric and in vivo biomechanical studies. Most treatment and rehabilitation efforts remain evidence based.23 Surgery is rarely necessary because there is little loss of function with this tear, and the cosmetic deformity is generally acceptable without surgical repair. Young athletes or heavy laborers may be the exception; they typically need the lost strength that occurs with loss of the continuity of the biceps tendon.24 Distal tears are more commonly referred to surgery acutely. However, initial treatment of partial distal ruptures consists of splint immobilization in flexion, which should be continued for 3 weeks. This is followed by a gradual return to normal activities. Analgesics, nonsteroidal anti-inflammatory drugs, topical agents (menthol-based or other custom compounded), therapeutic ultrasound, and ice may assist with the swelling and discomfort and facilitate rehabilitation efforts in both proximal and distal ruptures. 

Rehabilitation Nonsurgical treatment includes gentle range of motion exercises of the elbow and shoulder for contracture prevention. Modalities such as iontophoresis and therapeutic ultrasound can be used for pain control and prevention of contraction. Electrical stimulation is largely contraindicated in a partial tear (because of the concern of converting it to a complete tear) and not indicated in a complete tear. Gentle strengthening can typically be done after the acute phase in complete tears that are not going to be repaired because there is little chance of further injury. Partial ruptures can scar and remain in continuity.2 Postoperative rehabilitation for distal biceps rupture repairs consists of immobilization of the elbow in 90 degrees of flexion for 7 to 10 days, followed by the use of a hinged flexion-assist splint with a 30-degree extension block for 8 weeks after surgery. Gentle range of motion and progressive resistance exercises are started initially; unlimited activity is not typically allowed until 5 months postoperatively.25 

Procedures No procedures are performed in the direct treatment of biceps tendon rupture. Musculocutaneous nerve, upper trunk brachial plexus, and stellate ganglion blocks may have a role either perioperatively or palliatively in selected cases. Suprascapular nerve block or subacromial infiltration of local anesthetic may have a role in facilitation of rehabilitation therapies, including maintenance of range of motion and prevention of a secondary adhesive capsulitis. Musculoskeletal physicians in clinical practice often coordinate such local anesthetic infiltrations just before physical or occupational therapy appointments. Caution should be exercised during passive stretching, and even then only by therapists who are familiar with suppression of protective mechanisms, to avoid further soft tissue damage at what may be atypical and asymmetric end-range motion. There may be a role for steroid injection in professional or elite athletes during critical phases of their season. In such cases, the subacromial approach is preferred with avoidance of direct needle entry into the biceps tendon. Pulsed

CHAPTER 13  Biceps Tendon Rupture

radiofrequency of the suprascapular nerve may also have a longer-term role in palliation of pain and has the advantage of not requiring steroid injection. 

Technology Increases in the availability and use of diagnostic ultrasound have made it a widespread modality in diagnosis of labral and tendon ruptures. The increasing popularity and ease of office-based platelet-rich plasma treatments has reflected a trend in treatment of degenerative processes rather than just suppressing the inflammatory component. 

Surgery Surgical treatment, including tendon tear completion and anatomic repair to the radial tuberosity, can yield satisfactory results and appears to provide predictable outcomes.26 Prompt assessment is necessary for complete distal biceps ruptures under consideration for surgical repair because muscle shortening will occur over time. The same is true for proximal ruptures in very active individuals who require maximal upper body strength for their vocation or sport. Optimal surgical outcomes are obtained if treatment occurs within the first 4 weeks after injury. Partial distal ruptures are generally observed nonoperatively until a complete rupture occurs. Several techniques, including the two-incision, buttonhole, and Boyd-Anderson approaches, are used. More recently, a sonographically guided, mini-open technique involving one incision giving access to three peripectoral anatomic zones has been described.27 There seems to be little difference in postoperative functional outcome between tenotomy and tenodesis for LHB lesions.28 In chronic LHB tendon ruptures or for the revision of failed post-surgical LHB ruptures, an open subpectoral LHB tenodesis may be considered.29 The goal of surgical treatment is to restore strength of supination and flexion. For distal repairs, this is typically performed by a two-incision technique involving reinsertion of the biceps tendon to the radial tuberosity.30 A single-incision technique with use of suture anchors in the bicipital tuberosity has shown excellent long-term functional results by the Disabilities of the Arm, Shoulder, and Hand questionnaire.31 Arthroscopists should observe for scuffing, abrasion, or partial tear of the anterior portion biceps tendon, as this “sentinel sign” may suggest coexistent subscapularis rupture that is poorly visualized on CT or MRI and may only become apparent after removal of the anterior part of the biceps sling.32 As with any surgical procedure, revision may be necessary. 

Potential Disease Complications Complications from isolated biceps rupture are relatively rare. Partial tears can become complete tears. Attention should be given to potential contracture formation. Median nerve compression has been reported, presumably to be related to an enlarged synovial bursa associated with a partial distal biceps tendon rupture.33 Isolated antebrachial cutaneous neuropathy, due to traction from the biceps tendon displacing the nerve laterally with alleviation of symptoms after proximal biceps tenodesis, has been reported.34

67

Compartment syndrome has also been reported in proximal biceps rupture in a patient receiving systemic anticoagulation.35 The risk-benefit ratio of discontinuing drugs known to have an association with tendon rupture should be ascertained. Stiffness, contractures, and advanced osteoarthritis are possible with or without surgical intervention, which may lead to functional limitations, impairment, or chronic pain. 

Potential Treatment Complications Anterior shoulder pain attributed to the biceps tendon does not appear to be due to an inflammatory process in most cases. Histologic findings of the extra-articular portion of the LHB tendon and synovial sheath are due to a chronic degenerative process similar to de Quervain’s tenosynovitis.36 This supports the dogma of not using local corticosteroid injection given that treatment’s propensity for tendon rupture. Conversely, platelet-rich plasma has an anabolic effect, which would be expected to have a positive anabolic effect in treating chronic degenerative tendonopathies both of the shoulder and in general.37 Analgesics and nonsteroidal anti-inflammatory drugs have well-known side effects that most commonly affect the gastric, hepatic, and renal systems. Advancement of the extent of the rupture can occur with overly aggressive strengthening measures and passive stretching. The potential for serious surgical complications is most significant with distal rupture because of the important neurovascular structures in that region, including the median and radial nerves and brachial artery and vein. Re-rupture rates with distal repair may be a low as 1.5%, with ruptures being more common in females (3.2%) and bilateral repairs more likely to rupture (7.3%), usually due to poor patient compliance or overzealous therapy,38 However, it would stand to reason that bilateral repair is a more common procedure following bilateral rupture with a systemic etiologic factor (i.e., chronic steroids, quinolones). The complication rate increases with the length of time after rupture that surgery is performed. Proximal radial-ulnar synostosis and heterotopic ossification have also been reported as post-surgical complications, as has humeral fracture after subpectoral biceps tenodesis. The frequencies of re-rupture and nerve complications are both higher for single-incision repairs while the frequency of heterotopic ossification is higher for doubleincision repairs.39

References 1. Branch GL. In: Klein MJ, ed. Biceps rupture med scape drugs & diseases. Physical medicine and rehabilitation; 2017. 2. Safran MR, Graham SM. Distal biceps tendon ruptures: incidence, demographics and the effect of smoking. Clin Orthop Relat Res. 2002;404:275–283. 3. Gilcreest EL. The common syndrome of rupture, dislocation and elongation of the long head of the biceps brachii: an analysis of one hundred cases. Surg Gynecol Obstet. 1934;58:322. 4. Cheng NM, Pan WR, Vally F, et al. The arterial supply of the long head of biceps tendon: anatomical study with implications for tendon rupture. Clin Anat. 2010;23:683–692. 5. Recordon JA, Misur PN, Isaksson F, Poon PC. Endobutton versus transosseous suture repair of distal biceps rupture using the two-incision technique: a comparison series. J Shoulder Elbow Surg. 2015;24(6):928– 933. [Medline].

68

PART 1  MSK Disorders

6. Green JB, Skaife TL, Leslie BM. Bilateral distal biceps tendon ruptures. J Hand Surg Am. 2012;37:120–123. 7. Le Huec JC, Moinard M, Liquois F, Zipoli B. Distal rupture of the tendon of biceps brachii: evaluation by MRI and the results of repair. J Bone Joint Surg Br. 1996;78:767–770. 8. Waugh RI, Hathcock TA, Elliott JL. Ruptures of muscles and tendons: with particular reference of rupture (or elongation of the long tendon) of biceps brachii with report of fifty cases. Surgery. 1949;25:370–392. 9. Bourne MH, Morrey BF. Partial rupture of the distal biceps tendon. Clin Orthop Relat Res. 1991;271:143–148. 9a. Funk L. Shoulder Doc; 2017. https://www.shoulderdoc.co.uk/section/497. 10. Taylor SA, Newman AM, Dawson C, et al. The “3-Pack” examination is critical for comprehensive evaluation of the biceps-labrum complex and the bicipital tunnel: a prospective study. Arthroscopy. 2017;33(1):28–38. 11. Ludington NA. Rupture of the long head of the biceps flexor cubiti muscle. Ann Surg. 1923;77:358–363. 12. Bauer T, Vuillemin A, Hardy P, Rousselin B. Posterior dislocation of the long head of the biceps tendon: a case report. J Shoulder Elbow Surg. 2005;14:557–558. 13. Richards RR, An KN, Bigliani LU, et al. A standardized method for the assessment of shoulder function. J Shoulder Elbow Surg. 1994;3: 347–352. 14. Kocher MS, Horan MP, Briggs KK, et al. Reliability, validity and responsiveness of the American Shoulder and Elbow Surgeons subjective shoulder scale in patients with shoulder instability, rotator cuff disease and glenohumeral arthritis. J Bone Joint Surg Am. 2005;87:2006–2011. 15. Krief OP, Huguet D. Shoulder pain and disability: comparison with MR findings. AJR Am J Roentgenol. 2006;186:1234–1239. 16. Phillips BB, Canale ST, Sisk TD, et al. Ruptures of the proximal biceps tendon in middle-aged patients. Orthop Rev. 1993;22:349–353. 17. Pearl ML, Bessos K, Wong K. Strength deficits related to distal biceps tendon rupture and repair: a case report. Am J Sports Med. 1998;26:295–296. 18. Davison BL, Engber WD, Tigert LJ. Long term evaluation of repaired distal biceps brachii tendon ruptures. Clin Orthop Relat Res. 1996;333:188–191. 19. Warner JJ, McMahon PJ. The role of the long head of the biceps brachii in superior stability of the glenohumeral joint. J Bone Joint Surg Am. 1995;77:366–372. 20. Erickson SJ, Fitzgerald SW, Quinn SF, et al. Long bicipital tendon of the shoulder: normal anatomy and pathologic findings on MR imaging. AJR Am J Roentgenol. 1992;158:1091–1096. 21. Drolet P, Martineau A, Lacroix R, Roy J-S. Reliability of ultrasound evaluation of the long head of the biceps tendon. J Rehab Med. 2016;48(6):554–558. 22. Chew ML, Giuffrè BM. Disorders of the distal biceps brachii tendon. Radiographics. 2005;25:1227–1237. 23. Elser F, Braun S, Dewing CB, et al. Anatomy, function, injuries, and treatment of the long head of the biceps brachii tendon. Arthroscopy. 2011;27:581–592.

24. Hawkins RJ, Kennedy JC. Impingement syndrome in athletes. Am J Sports Med. 1980;8:151–158. 25. Ramsey ML. Distal biceps tendon injuries: diagnosis and management. J Am Acad Orthop Surg. 1999;7:199–207. 26. Behun MA, Geeslin AG, O’Hagan EC, King JC. Partial tears of the distal biceps brachii tendon: a systematic review of surgical outcomes. J Hand Surg Am. 2016;41(7):e175–e189. 27. Bhatia DN, DasGupta B. Surgical correction of the “Popeye biceps” deformity: dual-window approach for combined subpectoral and deltopectoral access and proximal biceps tenodesis. J Hand Surg Am. 2012;37:1917–1924. 28. Gurnani N, van Deurzen DFP, Janmaat VT, van den Bekerom MPJ. Tenotomy or tenodesis for pathology of the long head of the biceps brachii: a systematic review and meta-analysis. Knee Surgery, Sports Traumatol, Arthrosc. 2016;24(12):3765–3771. 29. Euler SA, Horan MP, Ellman MB, Greenspoon JA, Millett PJ. Chronic rupture of the long head of the biceps tendon: comparison of 2-year results following primary versus revision open subpectoral biceps tenodesis. Arch Orthop Trauma Surg. 2016;136(5):657–663 (ISSN: 1434-3916). 30. Boyd HD, Anderson LD. A method for reinsertion of the distal biceps brachii tendon. J Bone Joint Surg Am. 1961;43:1041–1043. 31. McKee MD, Hirji R, Schemitsch EH, et al. Patient-oriented functional outcome after repair of distal biceps tendon ruptures using a singleincision technique. J Shoulder Elbow Surg. 2005;14:302–306. 32. Sahu D, Fullick R, Giannakos A, Lafosse L. Sentinel sign: a sign of biceps tendon which indicates the presence of subscapularis tendon rupture. Knee Surg Sports Traumatol Arthrosc. 2016;24(12):3745–3749. 33. Brogan DM, Bishop AT, Spinner RJ, Shin AY. Shin lateral antebrachial cutaneous neuropathy following the long head of the biceps rupture. J Hand Surg Am. 2012;37:673–676. 34. Richards AM, Moss AL. Biceps rupture in a patient on long-term anticoagulation leading to compartment syndrome and nerve palsies. J Hand Surg Br. 1997;22:411–412. 35. Sears BW, Spencer EE, Getz CL. Humeral fracture following subpectoral biceps tenodesis in 2 active, healthy patients. J Shoulder Elbow Surg. 2011;20:e7–e11. 36. Streit JJ, Shishani Y, Rodgers M, Gobezie R. Tendinopathy of the long head of the biceps tendon: histopathologic analysis of the extraarticular biceps tendon and tenosynovium. Open Access J Sports Med. 2015;6:63–70. 37.  Fitzpatrick J, Bulsara M, Zheng MH. The Effectiveness of platelet-rich plasma in the treatment of tendinopathy. Am J Sports Med. 2016;45(1):226–233. 38. Hinchey JW, Aronowitz JG, Sanchez-Sotelo J, et al. Re-rupture rate of primarily repaired distal biceps tendon injuries. J Shoulder Elbow Surg. 2014;23(6):850–854. 39. Amin Nirav H, Volpi Alex, Sean Lynch T, et al. Complications of distal biceps tendon repair: a meta-analysis of single-incision versus doubleincision surgical technique. Orthop J Sports Med. 2016.

CHAPTER 14

Glenohumeral Instability William F. Micheo, MD Gerardo Miranda-Comas, MD Alexandra Rivera-Vega, MD

Definition

Synonyms Dislocation Subluxation Recurrent dislocation Multidirectional instability

ICD-10 Codes M25.311 M25.312 M25.319 M24.411 M24.412 M24.419 S43.004 S43.005 S43.006 S43.014 S43.015 S43.016 S43.024 S43.025 S43.026 S43.034 S43.035 S43.036

Shoulder instability, right Shoulder instability, left Shoulder instability, unspecified laterality Recurrent shoulder dislocation, right Recurrent shoulder dislocation, left Recurrent shoulder dislocation, unspecified laterality Shoulder dislocation, right Shoulder dislocation, left Shoulder dislocation, unspecified laterality Anterior shoulder dislocation, right Anterior shoulder dislocation, left Anterior shoulder dislocation, unspecified laterality Posterior shoulder dislocation, right Posterior shoulder dislocation, left Posterior shoulder dislocation, unspecified laterality Inferior shoulder dislocation, right Inferior shoulder dislocation, left Inferior shoulder dislocation, unspecified laterality

Shoulder instability represents a spectrum of disorders ranging from shoulder subluxation, in which the humeral head partially slips out of the glenoid fossa, to shoulder dislocation, which is a complete displacement of the humeral head out of the glenoid. It is classified according to direction as anterior, posterior, or multidirectional and on the basis of its frequency, etiology, and degree. Instability can result from macrotrauma, such as shoulder dislocation, or repetitive microtrauma associated with overhead activity, and it can occur without trauma in individuals with generalized ligamentous laxity.1–3 The glenohumeral joint has a high degree of mobility at the expense of stability. Static and dynamic restraints combine to maintain the shoulder in place with overhead activity. Muscle action, particularly of the rotator cuff and scapular stabilizers, is important in maintaining joint congruity in midranges of motion. Static stabilizers, such as the glenohumeral ligaments, the joint capsule, and the glenoid labrum, are important for stability in the extremes of motion.2 Traumatic damage to the shoulder capsule, the glenohumeral ligaments, and the inferior labrum is a result of acute dislocation. Repeated capsular stretch, rotator cuff, and superior labral injuries are associated with overuse injury resulting in anterior instability in athletes who participate in overhead sports. A loose patulous capsule is the primary pathologic change with multidirectional instability, and patients may present with bilateral symptoms.3,4 Shoulder instability affects, in particular, young individuals, females, and athletes, but it may also affect sedentary individuals, with an incidence of 1.7% in the general population.1,5,6 Traumatic instability often occurs when the individual falls on an outstretched, externally rotated, and abducted arm with a resulting anterior dislocation. A blow to the posterior aspect of the externally rotated and abducted arm can also result in anterior dislocation. Posterior dislocation usually results from a fall on the forward flexed and adducted arm or by a direct blow in the posterior direction when the arm is above the shoulder.4 Recurrent shoulder instability after a traumatic dislocation is common, particularly when the initial event happens at a young age. The rate appears to be as high as 72.3% within 5.3 years post-initial injury.7 In these individuals, it may occur repeatedly in association with overhead activity, 69

70

PART 1  MSK Disorders

and it may even happen at night, while changing position in bed, in those with severe instability. The patients may initially require visits to the emergency department or reduction of recurrent dislocation by a team physician, but as the condition becomes more chronic, some may be able to reduce their own dislocations.1 Patients with neurologic problems such as stroke, brachial plexus injury, and severe myopathies may develop shoulder girdle muscle weakness, scapular dysfunction, and resultant shoulder instability. 

Symptoms With atraumatic instability or subluxation, it may be difficult to identify an initial precipitating event. Usually, symptoms result from repetitive activity that places great demands on the dynamic and static stabilizers of the glenohumeral joint, leading to increased translation of the humeral head in overhead sports and occupational activities. Pain is the initial symptom, usually associated with impingement of the rotator cuff under the coracoacromial arch. Patients may also report that the shoulder slips out of the joint or that the arm goes “dead,” and they may report weakness associated with overhead activity.1,2,8 Patients with neurologic injury have pain with motion and shoulder subluxation as well as scapular and shoulder girdle muscle weakness. In the case of a patient with acute shoulder injury, factors to identify include the patient’s age, dexterity or dominant side, sport and position, level of competition, mechanism of injury, and any associated symptoms such as neurologic or functional deficits. 

Physical Examination

FIG. 14.1  In the lift-off test of the subscapularis, the patient places the arm on the lower back area and attempts to forcefully internally rotate against the examiner’s hand. It is important to document first that the patient has enough passive motion to allow the shoulder to be internally rotated away from the lower back area.

Individuals are observed from the anterior, lateral, and posterior positions with the shoulder in on the side of the body as well as with flexion and abduction motion. The shoulder is inspected for deformity, atrophy of surrounding muscles, static and dynamic scapular asymmetry, as well as scapular winging, which may be associated with neurologic injury. Palpation of soft tissue and bone is systematically addressed and includes the four joints that comprise the shoulder complex (sternoclavicular, acromioclavicular, glenohumeral, and scapulothoracic), the rotator cuff muscle-tendon complex, the biceps tendon, and the subacromial region. Passive and active range of motion (ROM) is evaluated. Differences between passive and active motion may be secondary to pain, weakness, or neurologic damage. In the overhead athlete, repeated throwing may lead to an increase in external rotation accompanied by a reduction in internal rotation, while tennis players may present with an isolated glenohumeral internal rotation deficit.9 These changes may be secondary to posterior capsule tightness, humeral torsion, and glenohumeral laxity that may lead to internal or posterior impingement.9 Manual strength testing is performed to identify weakness of specific muscles of the rotator cuff and the scapular stabilizers. The supraspinatus muscle can be tested in the scapular plane with internal rotation or external rotation of the shoulder, and the external rotators are tested with the arm at the side of the body and at 90 degrees of flexion in the scapular plane. The subscapularis muscle can be tested

by the lift-off test, in which the palm of the hand is lifted away from the lower back (Fig. 14.1). The scapular stabilizers, such as the serratus anterior and the rhomboid muscles, can be tested in isolation or by doing wall pushups. Sensory examination of the shoulder girdle is performed to rule out nerve injuries. Testing the shoulder in the position of 90 degrees of forward flexion with internal rotation (Hawkins maneuver) or in extreme forward flexion (until 180 degrees) with the forearm pronated (Neer maneuver) can assess for rotator cuff impingement and may reproduce symptoms of pain (Fig. 14.2).10 Glenohumeral translation testing for ligamentous laxity or symptomatic instability should be documented. Apprehension testing can be performed with the patient sitting, standing, or in the supine position. The shoulder is stressed anteriorly in the position of 90 degrees of abduction and external rotation to reproduce the feeling that the shoulder is coming out of the joint. A relocation maneuver that reduces the symptoms of instability also aids in the diagnosis, increasing diagnostic specificity when combined with a positive apprehension test (Fig. 14.3).8 The causation of posterior shoulder pain (rather than symptoms of instability) with apprehension testing may be associated with internal impingement of the rotator cuff and posterior superior labrum (Fig. 14.4).10–12 Other tests for shoulder laxity include the load and shift maneuver with the arm at the side to document humeral

CHAPTER 14  Glenohumeral Instability

71

A

B FIG. 14.2  Impingement test for impingement against the coracoacromial arch.

head translation in anterior and posterior directions and the sulcus sign to document inferior humeral head laxity. Labral injuries can be evaluated with a combination of tests including the active compression test described by O’Brien and colleagues,12 in which a downward force is applied to the forward flexed, adducted, and internally rotated shoulder to reproduce pain associated with superior labral tears or acromioclavicular joint disease. In the crank test, pain and clicking are reproduced when the shoulder is abducted to 160 degrees and an axial load is placed on the humerus and the arm is internally and externally rotated. Another test is the biceps loading test, in which the patient is asked to supinate the forearm, abduct the shoulder to 90 degrees, flex the elbow to 90 degrees, and externally rotate the arm until apprehensive and the examiner provides resistance against elbow flexion. Pain would suggest a proximal biceps tendinopathy or a labral tear.10–12 

Functional Limitations Impairment includes reduced motion, muscle weakness, and pain that interfere with activities of daily living, such as reaching into cupboards and brushing hair. Athletes, particularly those participating in throwing sports, may experience a decrease in the velocity of their pitches, and tennis players may lose control of their serve. Occupational limitations may include inability to reach or to lift weight above the level of the head or pain with rotation of the arm in a production line. Recurrent instability often leads to avoidance of activities that require abduction and external rotation because of reproduction of symptoms. 

C FIG. 14.3 (A) Apprehension relocation test in supine position with arm in 90 degrees of abduction and maximal external rotation. (B) Reduction of symptoms of apprehension with posteriorly directed force on proximal humerus. (C) Increased symptoms of apprehension or pain with anterior force applied on proximal humerus.

Diagnostic Studies The standard radiographs that are obtained to evaluate the patient with shoulder symptoms include anteroposterior views in external and internal rotation, outlet view, axillary lateral view, and Stryker notch view. These allow an assessment of the greater tuberosity and the shape of the acromion and reveal irregularity of the glenoid or posterior humeral head as well as dysplasia, hypoplasia, or bone loss that can contribute to instability.13

72

PART 1  MSK Disorders

Treatment Initial

FIG. 14.4 Internal impingement test. The arm is abducted to approximately 90 degrees and progressively externally rotated to reproduce pain in the posterior aspect of the shoulder.

Special tests that can also be ordered include arthrography, computed tomographic arthrography, magnetic resonance imaging (MRI), and magnetic resonance arthrography (MRA). These should be ordered to look for rotator cuff or labral abnormalities in the patient who has not responded to treatment. The best diagnostic study in the young athletic population is the MRA, because it allows better evaluation of rotator cuff, glenoid labrum, and glenohumeral ligaments.13 Gadolinium contrast enhancement and modification of the position of the arm for the test appear to increase the sensitivity of MRI in identifying the specific location of capsular or labral pathologic changes associated with recurrent instability and dislocation.13 Musculoskeletal ultrasound (US) allows adequate evaluation of the rotator cuff tendons and evaluation for para­ labral cysts that may suggest labral injury, and the anterior and posterior labrum can be evaluated in a limited fashion.14 The US examination of the posterior labrum can be performed during evaluation of the infraspinatus and teres minor muscles. The anterior labrum along with the capsulolabral complex is seen at the glenoid edge under the subscapularis tendon. Sonographic examination of the inferior labrum is best performed using axillary approach. A crucial part of the sonographic assessment of the labrum is the dynamic examination during rotation of the upper extremity.15 Diagnostic arthroscopy can be used in some cases but is generally not necessary. 

Differential Diagnosis Glenohumeral joint instability Traumatic Atraumatic Multidirectional Rotator cuff tendinopathy Rotator cuff tear or insufficiency Glenoid labral tear Suprascapular neuropathy

Acute management of glenohumeral instability is usually non-operative and includes relative rest, ice, and analgesic or anti-inflammatory medication. Goals at this stage are pain reduction, protection from further injury, and initiation of an early rehabilitation program. If the injury was observed (as often occurs in athletes) and no neurologic or vascular damage is evident on clinical examination, reduction may be attempted. There are multiple techniques that have been described for reduction of an anterior shoulder dislocation. Classic maneuvers include the Stimson and Milch techniques, but more recently the Spaso technique and the Fast, Reliable, and Safe (FARES) method have been described with good outcomes.16,17 The last two are single operator dependent and no sedation is needed. The Spaso technique is performed with the patient lying supine and the operator holds the affected arm around the wrist and applies gentle traction directly upward with a slight external rotation. The FARES method is performed with the patient lying supine and the operator holding the patient’s wrist at neutral position and gently abducting the shoulder while keeping a gentle traction and oscillating vertical movements. When the arm is abducted past 90 degrees, then the arm is gently rotated externally while continuous longitudinal traction, abduction, and vertical oscillating movement are maintained. If fracture or posterior dislocation is suspected, the patient should undergo radiologic evaluation before a reduction is attempted. After the reduction, radiologic studies should be repeated.1,18–20 When acute shoulder dislocations are treated nonoperatively, they are usually managed with 1 to 4 weeks of immobilization in a sling, in which the arm is positioned in internal rotation, followed by an exercise program and gradual return to activity. Several studies have suggested that placement of the arm in a position of external rotation may be more appropriate because of better realignment of anatomic structures and reduction position.18–21 However, this issue still merits further study because there is a lack of randomized controlled studies demonstrating a significant reduction in recurrent dislocation rates or a difference in return to activity levels in comparing the positions of immobilization after reduction or the duration of the postreduction immobilization period.20 

Rehabilitation The rehabilitation of glenohumeral instability should begin as soon as the injury occurs. The goals of nonsurgical management are reduction of pain, restoration of full functional motion, correction of muscle strength deficits, achievement of muscle balance, and return to full activity free of symptoms. The rehabilitation program consists of acute, recovery, and functional phases (Table 14.1).2,3,22

Acute Phase (1 to 2 Weeks) This phase should focus on treatment of tissue injury and clinical signs and symptoms. The goal in this stage is to allow tissue healing while reducing pain and inflammation. Reestablishment of nonpainful active ROM, prevention

CHAPTER 14  Glenohumeral Instability

73

Table 14.1  Glenohumeral Instability Rehabilitation Acute Phase

Recovery Phase

Functional Phase

Therapeutic intervention

Active rest Cryotherapy Electrical stimulation Protected motion Isometric and closed chain exercise to shoulder and scapular muscles General conditioning Nonsteroidal anti-inflammatory drugs

Modalities: superficial heat, ultrasound, electrical stimulation Range of motion exercises, flexibility exercises for posterior capsule Scapular control: closed chain exercises, proprioceptive neuromuscular facilitation patterns Dynamic upper extremity strengthening exercise: isolated rotator cuff exercises Sports-specific exercises: surgical tubing, multiplanar joint exercises, core and lower extremity Gradual return to training

Power and endurance in upper extremities: diagonal and multiplanar motions with tubing, light weights, medicine balls, plyometrics Increased multiple-plane neuromuscular control Maintenance: general flexibility training, strengthening, power and endurance exercise program Sports-specific progression

Criteria for advancement

Pain reduction Recovery of pain-free motion Symptom-free progression of muscle strengthening exercises

Full nonpainful motion Normal scapular stabilizers and rotator cuff strength Correction of posterior capsule inflexibility Symptom-free progression in a sportsspecific program

Normal clinical examination Normal shoulder mechanics Normal kinematic chain integration Completed sports-specific program Normal throwing motion

of shoulder girdle muscle atrophy, reduction of scapular dysfunction, and maintenance of general fitness are addressed. 

Recovery Phase (2 to 6 Weeks) This phase focuses on obtaining normal passive and active glenohumeral ROM, restoring posterior capsule flexibility, improving scapular and rotator cuff muscle strength, and achieving normal core muscle strength and balance. Flexibility training should include the sleeper stretch and the cross arm stretch for posterior shoulder structures; strength training includes exercises for the lower trapezius and serratus anterior muscle. This phase can be started as soon as pain is controlled and the patient can participate in an exercise program without exacerbation of symptoms. Young individuals with symptomatic instability need to progress slowly to the position of shoulder abduction and external rotation. Athletes can progress rapidly through the program and emphasize exercises in functional ranges of motion. Older patients with goals of returning to activities of daily living may require slower progression, particularly if they have significant pain, muscle inhibition, and weakness. Biomechanical and functional deficits including abnormalities in the throwing motion should also be addressed. 

Functional Phase (6 Weeks to 6 Months) This phase focuses on increasing power and endurance of the upper extremities while improving neuromuscular control because a normal sensorimotor system is key in returning to optimal shoulder function.22 Rehabilitation at this stage works on the entire kinematic chain to address specific functional deficits. After the completion of rehabilitation, a continued exercise program with goals of preventing recurrent injury should be instituted for individuals who participate in sports, recreational activities, or work-related tasks in which high demands on the shoulder joint are expected. A training

program that combines flexibility and strengthening exercises with neuromuscular as well as proprioceptive training should be ongoing. Patients with multidirectional instability need to work specifically on strengthening of the scapular stabilizers and balancing the force couples between the rotator cuff and the deltoid muscle. 

Return to Play For the athletic population, there are recommended return to play criteria that include the health status of the athlete, participation risk, and external factors, such as timing in the season and external influences.22 Objective measures that could be considered include normal shoulder ROM. The side differences in internal rotation ROM should be less than 18 degrees, and the difference in total ROM should not be more than 5 degrees.23 Another objective measure to consider is normal muscle strength and balance. In terms of rotator cuff strength, the eccentric external rotation strength should be equal to the isometric internal rotation strength.23 Scapular symmetry should not be used as an objective measure for return to play, since some degree of scapular asymmetry may be normal in some athletes.23 Other measures to consider include pectoralis minor tightness and functional tests, but no clear consensus has been established. 

Procedures If the individual persists with some symptoms of pain secondary to rotator cuff irritation despite an appropriate rehabilitation program, a landmark-guided subacromial injection could be considered (Figs. 14.5 and 14.6). Musculoskeletal US can be useful in guiding injections to the shoulder. Sonographic guidance improves accuracy of injection into the subdeltoid/subacromial bursa, but clinical superiority is still not clear.24 Under sterile conditions,

74

PART 1  MSK Disorders

Lateral Clavicle Acromion

Anterior

Humerus Subacromial injection FIG. 14.5 Approximate surface anatomy (insets) and internal anatomic sites for injection of the glenohumeral joint laterally and anteriorly. See also Fig. 14.6. (From Lennard TA. Physiatric Procedures. Philadelphia: Hanley & Belfus; 1995.)

Clavicle

Acromion

Spine of scapula Scapula Posterior Subacromial injection

Humerus FIG. 14.6  Posterior injection of the glenohumeral joint. (From Lennard TA. Physiatric Procedures. Philadelphia: Hanley & Belfus; 1995.)

with use of a 23- to 25-gauge, 1½-inch disposable needle, inject an anesthetic-corticosteroid preparation by an anterior, posterior, or lateral approach when using a landmarkguided technique. When using US guidance, the bursa is identified in a long axis view inferior to the deltoid muscle, lateral to the acromion and superior to the supraspinatus tendon. The needle is advanced in an in-plane approach until the target is reached. Typically, 3 to 5 mL is injected (e.g., 4 mL of 1% lidocaine and 1 mL of 40 mg/mL triamcinolone or methylprednisolone). Alternatively, the lidocaine may be injected first, followed by the corticosteroid. Postinjection care includes local ice for 5 to 10 minutes. The patient is instructed to ice the shoulder for 15 to 20 minutes three or four times daily for the next few days and to avoid aggressive overhead activities for the following week. Other procedures, such as prolotherapy, plateletrich plasma injections, and stem cells, are becoming more popular, especially in athletes for other musculoskeletal injuries, but the results of use for shoulder instability are still unknown.25 

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery Because of high rates of recurrent instability after conservative treatment in the active athletic population and, in particular, throwers, early surgical intervention is gaining acceptance.26,27 Surgical stabilization in the young and skeletally immature athlete should be considered, because they may be at higher risk for recurrence than previously appreciated. 7 In the individual with recurrent instability, surgical interventions include capsular procedures, such as the capsular shift, and labral as well as rotator cuff procedures, such as debridement and repair.26,28,29 Arthroscopic interventions result in comparable outcomes when they are measured against open surgery, but no “gold standard” method has been established.27 Early arthroscopic repair is becoming widespread because of an apparent reduction in postoperative morbidity that may allow the athlete an early return to function.29-31 For patients without bony injury, arthroscopic Bankart repair is recommended.26,27 For the older patient, initial management should consist of arthroscopic capsulolabral repair.32 Athletes with posterior instability benefit from arthroscopic, rather than open, stabilization procedures using suture anchors to prevent recurrences and revisions.33 More commonly, open Latarjet procedure is recommended when dealing with glenoid bone loss, and arthroscopic techniques are favored for humeral head defects,32 although the former has changed after the introduction of the arthroscopic remplissage technique.34,35 In many instances, these procedures need to be combined for optimal results in the patient, followed by an accelerated rehabilitation program with guidelines like those for the patient treated nonoperatively.31 Rehabilitation protocols are similar for open and arthroscopic techniques. The shoulder is immobilized with an abduction pillow for 4 to 6 weeks, with therapy initiated if stiffness develops. After immobilization, strengthening exercises (similar to nonsurgical protocols) are recommended. If the rehabilitation protocol is successfully completed, the patient is allowed to return to full activity 4 to 6 months after surgery.29,31 

Potential Disease Complications Complications include recurrent instability with overhead activity, pain in the shoulder region, nerve damage, and weakness of the rotator cuff and scapular muscles. These tend to occur more commonly in patients with multidirectional atraumatic instability. Loss of function may include inability to lift overhead and loss of throwing velocity and accuracy. Recurrent episodes of instability in the older individual may also be related to the development of rotator cuff tears.28 

Potential Treatment Complications Analgesics and nonsteroidal anti-inflammatory drugs have well-known side effects that most commonly affect the gastric, hepatic, cardiovascular, and renal systems. Complications of treatment include loss of motion, failure of surgical repair with recurrent instability, and inability to return to previous level of function. Failure of conservative treatment

CHAPTER 14  Glenohumeral Instability

may be associated with incomplete rehabilitation or poor technique. Recurrent dislocation after surgical treatment can be related to not addressing all the sites of pathologic change at the time of the operation.29

References 1. Dumont GD, Russell RD, Robertson WJ. Anterior shoulder instability: a review of pathoanatomy, diagnosis and treatment. Curr Rev Musculoskelet Med. 2011;4(4):200–207. 2. Kibler WB, Kuhn JE, Wilk K, et al. The disabled throwing shoulder: spectrum of pathology-10-year update. Arthroscopy. 2013;29(1):141–161.e26. 3. Eckenrode BJ, Kelley MJ. Kelly JD, 4th. Anatomic and biomechanical fundamentals of the thrower shoulder. Sports Med Arthrosc. 2012;20(1):2–10. 4. Takase K, Yamamoto K. Intraarticular lesions in traumatic anterior shoulder instability: a study based on the results of diagnostic imaging. Acta Orthop. 2005;76(6):854–857. 5. Loud KJ, Micheli LJ. Common athletic injuries in adolescent girls. Curr Opin Pediatr. 2001;13(4):317–322. 6. Wasserlauf BL, Paletta GA Jr . Shoulder disorders in the skeletally immature throwing athlete. Orthop Clin North Am. 2003;34(3):427–437. 7. Zaremski JL, Galloza J, Sepulveda F, Vasilopoulos T, Micheo W, Herman DC. Recurrence and return to play after shoulder instability events in young and adolescent athletes: a systematic review and meta-analysis. Br J Sports Med. 2017;51(3):177–184. 8. Good CR, MacGillivray JD. Traumatic shoulder dislocation in the adolescent athlete: advances in surgical treatment. Curr Opin Pediatr. 2005;17(1):25–29. 9. Myers JB, Laudner KG, Pasquale MR, Bradley JP, Lephart SM. Glenohumeral range of motion deficits and posterior shoulder tightness in throwers with pathologic internal impingement. Am J Sports Med. 2006;34(3):385–391. 10. Pappas GP, Blemker SS, Beaulieu CF, McAdams TR, Whalen ST, Gold GE. In vivo anatomy of the Neer and Hawkins sign positions for shoulder impingement. J Shoulder Elbow Surg. 2006;15(1):40–49. 11. Farber AJ, Castillo R, Clough M, Bahk M, McFarland EG. Clinical assessment of three common tests for traumatic anterior shoulder instability. J Bone Joint Surg Am. 2006;88(7):1467–1474. 12. O’Brien SJ, Pagnani MJ, Fealy S, McGlynn SR, Wilson JB. The active compression test: a new and effective test for diagnosing labral tears and acromioclavicular joint abnormality. Am J Sports Med. 1998;26(5):610–613. 13. Walz DM, Burge AJ, Steinbach L. Imaging of shoulder instability. Semin Musculoskelet Radiol. 2015;19(3):254–268. 14. Jacobson J. Shoulder ultrasound. In: Jacobson J, ed. Fundamentals of Musculoskeletal Ultrasound. 2nd ed. Philadelphia: WB Saunders; 2013:3–71. 15. Krzyzanowski W. The use of ultrasound in the assessment of the glenoid labrum of the glenohumeral joint. Part I: ultrasound anatomy and examination technique. J Ultrason. 2012;12(49):164–177. 16. Ufberg JW, Vilke GM, Chan TC, Harrigan RA. Anterior shoulder dislocations: beyond traction-countertraction. J Emerg Med. 2004;27(3):301–306.

75

17. Maity A, Roy DS, Mondal BC. A prospective randomised clinical trial comparing FARES method with the Eachempati external rotation method for reduction of acute anterior dislocation of shoulder. Injury. 2012;43(7):1066–1070. 18. De Baere T, Delloye C. First-time traumatic anterior dislocation of the shoulder in young adults: the position of the arm during immobilisation revisited. Acta Orthop Belg. 2005;71(5):516–520. 19. Funk L, Smith M. Best evidence topic report. How to immobilise after shoulder dislocation? Emerg Med J. 2005;22(11):814–815. 20. Handoll HH, Hanchard NC, Goodchild L, Feary J. Conservative management following closed reduction of traumatic anterior dislocation of the shoulder. Cochrane Database Syst Rev. 2006;(1):CD004962. 21. Paterson WH, Throckmorton TW, Koester M, Azar FM, Kuhn JE. Position and duration of immobilization after primary anterior shoulder dislocation: a systematic review and meta-analysis of the literature. J Bone Joint Surg Am. 2010;92(18):2924–2933. 22. Cools AM, Borms D, Castelein B, Vanderstukken F, Johansson FR. Evidence-based rehabilitation of athletes with glenohumeral instability. Knee Surg Sports Traumatol Arthrosc. 2016;24(2):382–389. 23. Wilk KE, Macrina LC, Fleisig GS, et al. Correlation of glenohumeral internal rotation deficit and total rotational motion to shoulder injuries in professional baseball pitchers. Am J Sports Med. 2011;39(2):329–335. 24. Finnoff JT, Hall MM, Adams E, et al. American Medical Society for Sports Medicine (AMSSM) position statement: interventional musculoskeletal ultrasound in sports medicine. PM R. 2015;7(2):151–168.e12. 25. Malanga G, Nakamura R. The role of regenerative medicine in the treatment of sports injuries. Phys Med Rehabil Clin N Am. 2014;25(4):881–895. 26. Harris JD, Romeo AA. Arthroscopic management of the contact athlete with instability. Clin Sports Med. 2013;32(4):709–730. 27. Zhang AL, Montgomery SR, Ngo SS, Hame SL, Wang JC, Gamradt SC. Arthroscopic versus open shoulder stabilization: current practice patterns in the United States. Arthroscopy. 2014;30(4):436–443. 28. Porcellini G, Paladini P, Campi F, Paganelli M. Shoulder instability and related rotator cuff tears: arthroscopic findings and treatment in patients aged 40 to 60 years. Arthroscopy. 2006;22(3):270–276. 29. Tauber M, Resch H, Forstner R, Raffl M, Schauer J. Reasons for failure after surgical repair of anterior shoulder instability. J Shoulder Elbow Surg. 2004;13(3):279–285. 30. Harris JD, Gupta AK, Mall NA, et al. Long-term outcomes after Bankart shoulder stabilization. Arthroscopy. 2013;29(5):920–933. 31. Kim SH, Ha KI, Jung MW, Lim MS, Kim YM, Park JH. Accelerated rehabilitation after arthroscopic Bankart repair for selected cases: a prospective randomized clinical study. Arthroscopy. 2003;19(7):722–731. 32. Garcia GH, Taylor SA, Fabricant PD, Dines JS. Shoulder instability management: a survey of the American Shoulder and Elbow Surgeons. Am J Orthop (Belle Mead NJ). 2016;45(3):E91–E97. 33. DeLong JM, Jiang K, Bradley JP. Posterior instability of the shoulder: a systematic review and meta-analysis of clinical outcomes. Am J Sports Med. 2015;43(7):1805–1817. 34. Boileau P, Villalba M, Hery JY, Balg F, Ahrens P, Neyton L. Risk factors for recurrence of shoulder instability after arthroscopic Bankart repair. J Bone Joint Surg Am. 2006;88(8):1755–1763. 35. Rashid MS, Crichton J, Butt U, Akimau PI, Charalambous CP. Arthroscopic “remplissage” for shoulder instability: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2016;24(2):578–584.

CHAPTER 15

Labral Tears of the Shoulder Cedric J. Ortiguera, MD Justin L. Makovicka, MD David E. Hartigan, MD

Synonyms SLAP tears (superior labral anterior-posterior) Soft tissue Bankart lesion Reverse soft tissue Bankart lesion

ICD-10 Codes S43.431 S43.432 S43.439 M75.80

SLAP lesion of right shoulder SLAP lesion of left shoulder SLAP lesion of unspecified shoulder Other shoulder lesions, unspecified shoulder M75.81 Other shoulder lesions, right shoulder M75.82 Other shoulder lesions, left shoulder

Definition The glenoid labrum is a densely fibrous tissue that is located along the periphery of the glenoid portion of the scapula (Fig. 15.1).1 As the outer labrum transitions from the periphery to its articulation with the glenoid, the histology changes from fibrous to a small fibrocartilaginous zone at the junction with the glenoid articular cartilage.2 The labrum increases the height and width of the glenoid while also giving extra depth to the joint. This provides increased stability while still allowing great range of motion.3 The labrum also serves as an attachment point for the long head of the biceps tendon, the glenohumeral ligaments, and the long head of the triceps tendon, forming a periarticular system of fibers that gives the shoulder joint much needed stability.4 The vascular supply to the labrum is from the posterior humeral circumflex artery, the circumflex scapular branch of the subscapular artery, and the suprascapular artery. These arteries come from the periphery of the labrum, making the articular margins of the labrum avascular.2 It has also been shown that the superior labrum has less vascular supply than the inferior labrum. The long head of the 76

biceps tendon has a variable attachment to the labrum and glenoid. Approximately 40% to 60% of biceps tendons originate from the supraglenoid tubercle, and the remaining fibers insert into the labrum.1 The biceps insertion into the labrum is variable, but most commonly is in a more posterior position. Tears can occur in all regions of the labrum. The most studied injury to the labrum is the superior labral anteriorposterior (SLAP) tear. Anterior dislocations of the shoulder can be associated with a disruption of the anteroinferior labrum and anterior band of the inferior glenohumeral ligament, also known as a Bankart lesion. Posterior shoulder instability may result in injury to the posterior band of the inferior glenohumeral ligament as well as the posterior labrum, or a reverse Bankart lesion. Tears can extend to involve multiple regions of the labrum and have other associated injuries. The SLAP tear and Bankart lesion are the most common pathologies seen and for that reason are the focus of this discussion. The most common mechanisms for SLAP tears are forced traction on the shoulder and direct compression. Direct compression can occur in the acute traumatic setting or in the chronic setting typical in the overheadthrowing athlete. Overhead throwers are predisposed to SLAP tears secondary to their adaptive anatomy. They tend to have posterior capsular contractures, loose anterior capsular structures, and a retroverted humeral head, all increasing the amount of external rotation in the shoulder. As a result of these anatomic changes, the arm goes into an extreme externally rotated position while the biceps kinks at its insertion and assumes a more vertical and posterior position. This applies a torsional force to the biceps-labral complex superiorly, resulting in a peelback mechanism on the superior labrum.5,6 Alternatively, as throwers externally rotate in the cocking phase, the rotator cuff may impinge on the posterosuperior glenoid, causing an “internal impingement” and tearing of the labrum.7 Although SLAP lesions are more common in overhead athletes, they also occur in contact sports. A recent study looking at SLAP lesions in professional football players found that offensive linemen have the highest rate of injury when compared to other positions; this is most likely due to the increased contact that is undertaken by this position.8

CHAPTER 15  Labral Tears of the Shoulder

77

Supraspinatus tendon Long head of biceps brachii Infraspinatus m. Sup. glenohumeral lig. Glenoid cavity Sup. recess Articular capsule

Subscapularis m.

Labrum

Mid. glenohumeral lig.

Teres minor m.

Inf. recess Inf. glenohumeral lig. Long head triceps m. Posterior

Anterior

FIG. 15.1  Normal anatomy of the shoulder.

Type I

Type II

Type III

Type IV

FIG. 15.2 Superior labral anterior-posterior tear classification. Type I: degenerative tear of the undersurface of the superior labrum with the biceps anchor intact. Type II: tear of the superior labrum as well as of the biceps anchor. Type III: bucket-handle tear of the superior labrum with biceps anchor intact. Type IV: bucket-handle tear of the superior labrum with extension into biceps tendon.

Classically, SLAP tears are classified into four types, which can then be further modified.9 Most physicians think that the four-class system (Fig. 15.2) is sufficient and that the additional classifications could be placed within these basic types, so it is the preferred classification. Bankart lesions are created by episodes of anterior instability. As the humeral head moves out anteriorly and

inferiorly, anterior damage can occur to the anteroinferior labrum, glenohumeral ligaments, joint capsule, rotator cuff, and possibly neurovascular structures. It has been demonstrated that the Bankart lesion is created about 85% to 97% of the time in anterior dislocations.10,11 This pathologic change is thought to be an important reason for recurrent instability. In addition to increasing the depth and diameter of the glenoid, the labrum and capsule also create a negative pressure that provides stability through the glenohumeral articulation. If the labrum or capsule is injured, such as in the Bankart lesion, this suction seal is lost, and this decreases the stability of the shoulder. Several factors may predispose patients to recurrent instability. These include fracture on the glenoid (bony Bankart) or humeral head (Hill-Sachs lesion), hyperlaxity syndromes, male gender, younger age at initial dislocation, participation in contact or overhead throwing sport, and positive correlation between number of dislocations and risk of future dislocation. Dislocations later in life increase the risk of rotator cuff injury, with tears occurring in nearly 30% of patients older than 40 years and in up to 80% of patients older than 60 years. 

Symptoms Superior Labral Anterior-Posterior Tear A patient with a SLAP tear will most commonly present with symptoms of deep-seated pain, which can be sharp or dull.12 It is usually located deep within the center of the shoulder and can be made worse with overhead activities, pushing heavy objects, lifting, or reaching behind the back. Patients may have mechanical symptoms, such as catching, popping, or grinding with rotation of the shoulder. One study found that in 139 patients demonstrating a SLAP lesion on shoulder arthroscopy, 123 patients (88%) also had other intra-articular lesions, making clinical diagnosis challenging.12

78

PART 1  MSK Disorders

Table 15.1  Common Tests for Diagnosis of Superior Labral Anterior-Posterior Tears Test

Instruction

Indication of Positive Test Result

Active compression (O’Brien) test

Arm is forward flexed to 90 degrees, adducted across the body Patient resists downward force on arm in pronated and supinated position of the forearm

Pain is increased in pronated position

Crank test

Arm is abducted > 100 degrees in the scapular plane; elbow is flexed to 90 degrees Axial force is applied through the humerus onto the glenohumeral joint and the shoulder is rotated (internal and external rotation)

Pain, catching, clicking

Pain provocative test

Patient abducts shoulder to 90 degrees, flexes elbow to 90 degrees, and pronates and supinates the hand

Pain is worse or present only in pronation

Biceps load test

Patient is supine; shoulder is abducted to 90 degrees; elbow is flexed to 90 degrees The shoulder is externally rotated to a point at which the patient feels pain, apprehension, or maximum external rotation; the patient then performs resisted flexion of the elbow

Worsening of pain when resisted elbow flexion is performed

Compression-rotation test

Patient is supine; shoulder is abducted to 90 degrees; elbow is flexed to 90 degrees Axial load is placed on the glenohumeral joint and the humerus is rotated

Pain, catching, clicking, snapping

Anterior slide test

Patient is sitting and places hands on the hips with thumbs facing posterior The examiner places a finger over the anterior shoulder and the other hand pushes up on the humerus superior and anterior; patient is asked to resist

Pain or click

It is essential to obtain a thorough history for trauma to evaluate for traction or compression type injuries, dislocations, and sports (e.g., baseball, football, waterskiing, and tennis) they play that may predispose them to this injury. Overhead throwing athletes may suffer decreased velocity and usually complain of pain in the late cocking and early acceleration phase of throwing. They may have weakness due to pain or secondary to a paralabral cyst compressing the suprascapular nerve. Compression on the nerve at the spinoglenoid notch can cause weakness in external rotation as well as deep posterior shoulder pain. 

Bankart Lesion Symptoms of anterior instability are usually obvious, as the patient states that there has been a dislocation and continues to complain of pain or instability in that shoulder. Sometimes there is not a history of overt dislocation, but instead the patient has multiple episodes of instability without a complete dislocation. The patient will complain of pain and feeling of impending dislocation with the arm in abduction and external rotation. Important historical variables include the patient’s age at first dislocation, need for formal reduction, number of recurrent instability episodes, voluntary instability, and anticipated future sports activities. The most comfortable position for these patients is usually with the arm in adduction and internal rotation. They avoid abduction and external rotation because this is the position that led to the dislocation and it also stresses the injured labrum, inferior glenohumeral ligament, and subscapularis tendon. 

Physical Examination Superior Labral Anterior-Posterior Tear Several clinical tests are designed to assist the clinician in making the SLAP tear diagnosis.13–16 These tests aim to do one of two things: to pinch the torn labrum between the humeral head and the glenoid, causing pain or mechanical symptoms, or to place traction on the biceps tendon (Table 15.1). The tests have had variable ranges of sensitivity and specificity between studies, and thus no single test is considered diagnostic. The most commonly performed test is the O’Brien’s active compression test. This has been shown to be very sensitive, but has poor specificity. Accurate diagnosis requires a careful history to correlate with the examination findings. In many cases, concomitant disease may cloud the physical examination findings.12 On inspection of the shoulder, there may be atrophy of the supraspinatus and infraspinatus muscles. The supraspinatus atrophy is difficult to observe because of the overlying trapezius muscle. The atrophy can occur because of a paralabral cyst that compresses the suprascapular nerve, or it could be secondary to an associated rotator cuff tear. Palpation of the biceps tendon may demonstrate tenderness within the bicipital groove. The range of motion of the shoulder should be preserved, although throwing athletes may have increased external rotation and loss of internal rotation with a resulting glenohumeral internal rotation (GIRD) deficit.5,6 

Bankart Lesion Evaluation for anterior instability may include a number of tests (Table 15.2). After reduction of a dislocation, a

CHAPTER 15  Labral Tears of the Shoulder

79

Table 15.2  Common Tests for Diagnosis of Anterior Instability Test

Instruction

Indication of Positive Test Result

Load and shift

Supine position Arm at 0, 45, 90 degrees of abduction Anterior directed force on the humerus

Increasing translation at higher degrees of abduction indicates that the inferior glenohumeral ligament is compromised Grade 1: increased translation compared with contralateral Grade 2: humeral head translates to the glenoid rim Grade 3: translates over the glenoid rim

Apprehension test (crank)

Supine position Arm brought into 90 degrees of abduction and increasing external rotation

Pain, feeling of impending dislocation, or muscle guarding

Relocation (Jobe) test

Apprehension position with posteriorly directed force on the humeral head

Decreased apprehension or pain

Surprise test

Relocation test with sudden release of posteriorly directed force

Sense of instability or apprehension with release of force

thorough neurovascular examination should be performed to rule out major vessel or brachial plexus injury. In a typical Bankart lesion with anterior instability, patients will often experience apprehension when the arm is brought into abduction and external rotation. Strength should be assessed, looking for axillary or radial nerve palsies as well as rotator cuff disease in the older patient. In a patient older than 40 years who cannot lift the arm after a dislocation, rotator cuff tear is far more common than an axillary nerve palsy.17,18 The surprise test has been shown to be the most accurate test, with a positive predictive value of 98% and a negative predictive value of 78%.19 

Functional Limitations Superior Labral Anterior-Posterior Tear Patients may have difficulty carrying or pushing heavy objects, working overhead, and throwing.1 This pathologic process can often be asymptomatic at rest and symptomatic only with more vigorous activity. SLAP tears often are manifested with a multitude of other shoulder diseases, so limitations may vary according to what else is present in the shoulder along with the SLAP tear.12 

Bankart Lesion Avoidance of the abducted and externally rotated position is required to limit recurrent instability. This may limit many athletic activities, particularly in contact sports and in throwers. Several activities that may lead to recurrent instability in athletes include tackling, overhead throwing, serving in tennis and volleyball, wrestling, and other activities at the extremes of abduction and external rotation. Non-­ athletes also experience recurrent instability in daily activities that bring their shoulders into abduction and external rotation, including placing items on high shelves, lifting weights and working overhead, choking a lawnmower, and countless other activities. Athletes put their arms into this position more often and with much more force, which is why they have a higher rate of recurrent instability compared to non-athletes. 

FIG. 15.3  Coronal magnetic resonance image of a type II superior labral anterior-posterior lesion (SLAP). White arrow indicating fluid tracking between the superior glenoid and superior labrum indicating SLAP lesion.

Diagnostic Studies Superior Labral Anterior-Posterior Tear The initial imaging study for any shoulder pain is plain radiography, including anterior-posterior, scapular anteriorposterior, axillary, and outlet views. There are no typical findings for SLAP tears on radiography, but it is necessary to rule out other sources of pain. Magnetic resonance imaging (MRI) should be the next test obtained for patients with a high clinical likelihood of labral disease (Fig. 15.3). There has been much controversy as to whether high-resolution non-contrast-enhanced MRI or magnetic resonance arthrography (MRA) is the “gold standard” for diagnosis of SLAP lesions.20,21 One metaanalysis showed that MRA is superior to MRI for detection of SLAP lesions.22 This study showed MRA to have both a

80

PART 1  MSK Disorders

FIG. 15.4  Arthroscopic image of the corresponding type II superior labral anterior-posterior lesion from Fig. 15.3.

higher sensitivity (0.87 vs. 0.76) and specificity (0.92 vs. 0.87) of detecting SLAP lesions when compared to MRI. With the high rate of concomitant shoulder injuries, MRI is helpful in showing both intra-articular and extra-articular pathologic changes within the soft tissues. Positioning of the arm in external rotation or abduction and external rotation can improve the ability to accurately diagnose these lesions.23,24 Computed tomographic arthrography may also be used if MRI is contraindicated, but it is less sensitive to other concomitant pathology. Ultrasound may be useful to visualize concomitant disease, such as tears of the rotator cuff and paralabral cyst, but it has poor visualization of the labrum. Arthroscopy is the gold standard for diagnosis of labral disease (Fig. 15.4). Many times the diagnosis is made during arthroscopy after other modalities have failed to make a conclusive diagnosis or if symptoms have persisted despite conservative interventions. 

FIG. 15.5  Axial magnetic resonance image of a Bankart lesion. White arrow indicates fluid tracking between the anterior inferior labrum and anterior inferior glenoid diagnostic for a Bankart lesion.

Differential Diagnosis Impingement syndrome Rotator cuff disease Acromioclavicular joint disease Cervical disc injury Cervical radiculopathy Brachial plexus injury Refractory bicipital tendinitis Multidirectional instability Bony Bankart lesion Humeral avulsion of the glenohumeral ligament Malingering

Treatment Initial

Bankart Lesion

Superior Labral Anterior-Posterior Tear

A complete plain radiography trauma series of the shoulder should be performed to rule out dislocation in the acute setting. This includes true anterior-posterior, anteriorposterior in external and internal rotation, scapular Y lateral, and axillary views. A Velpeau view may be substituted for an axillary view if the patient is unable to abduct their arm. With more chronic instability, additional views could be considered. The West Point view can assist with visualization of the glenoid in an attempt to see bone disruptions of the glenoid rim; a Stryker notch view may better visualize an associated Hill-Sachs lesion of the humeral head. In patients with soft tissue Bankart lesions, the radiographs may be unrevealing. MRI would be the next imaging study conducted (Fig. 15.5). In the acute setting, noncontrast-enhanced MRI is reasonable as the hemarthrosis from the dislocation aids in visualization of the labral process. In the chronic setting, MRA can improve labral imaging. CT scan should be considered in cases with associated bone involvement. 

Overhead-throwing athletes with more than 35 degrees of GIRD deficit have a 60% chance of shoulder injury that requires them to miss games.5 Regular posterior-inferior capsular stretching exercises significantly decrease the rate of shoulder injuries in overhead-throwing athletes5,6 and are now a part of preventive care for baseball players. Initial treatment of a SLAP tear is symptomatic. Nonsteroidal anti-inflammatory medications, cryotherapy, and activity modification are the mainstays of treatment until the acute inflammation and pain subside. A short period of sling immobilization for comfort should be followed by early institution of range of motion exercises, posterior capsular stretching exercises, and then strengthening of the dynamic stabilizers of the shoulder and scapulothoracic articulation. 

Bankart Lesion The Bankart lesion is a result of anterior shoulder instability or dislocation. If the shoulder is dislocated, the initial step in treatment is to reduce the shoulder. Post-reduction

CHAPTER 15  Labral Tears of the Shoulder

radiographs should be obtained and neurovascular status checked. Sling immobilization should be instituted for a short period. Recommendations for the duration of immobilization vary from days to weeks. The position of immobilization is controversial, as immobilization in external rotation has been shown by some to lower the recurrence rate of instability, but it must be instituted immediately after the instability episode.25,26 The most common recommendation is for standard sling immobilization for a period of 1 to 3 weeks. 

Rehabilitation Superior Labral Anterior-Posterior Tear When a SLAP tear is suspected, physical therapy focuses on strengthening the rotator cuff, capsular stretching, range of motion of the glenohumeral joint, and scapular stabilization exercises. One study showed good results with non-operative treatment of SLAP tears consisting of nonsteroidal anti-inflammatory drugs, scapular strengthening, and posterior capsular stretching.27 In this study, 51% of the patients in the study ended up having surgery, but the remainder reported significant pain relief, 100% returned to sports, and 70% returned to pre-injury level. Another study found that non-operative treatment was viable in up to 71.4% of young, active patients at a mean follow-up of 21 months.28 This study noted a higher failure rate of conservative treatment in patients with a history of trauma, mechanical symptoms, or in overhead athletes. Non-operative treatment has also been shown to be effective in high-level professional baseball players. For example, one study demonstrated that a rehabilitation regimen that focuses on scapular dyskinesia and posterior capsular contractures that are associated with GIRD in professional baseball players with SLAP lesions results in a return-to-play rate of 40%.29 These results are comparable to surgical outcomes, so conservative management should be the first-line treatment in all patients with SLAP lesions. Rehabilitation of SLAP lesions in the non-operative setting should address the principles of reducing pain and inflammation, restoring pain-free range of motion (ROM), function and strength of scapular stabilizers and improving overall rotator cuff strength. In SLAP and biceps-related disorders in the overhead athlete, the rehabilitation protocol should also include an exercise program that begins with a low load on the biceps.30 Exercises targeting the trapezius may result in less load on the biceps as opposed to those targeting the serratus anterior.30 Also, exercises with an internal rotation component lead to less load on the biceps. Exercises that follow these principles should be part of the initial regimen and progression made from there. Postoperative rehabilitation after arthroscopic repair involves a 4- to 6-week period of sling immobilization followed by a progressive range of motion and strengthening program. For overhead athletes, a throwing program can begin at 4 months with full return at approximately 7 to 12 months. 

Bankart Lesion After a period of sling immobilization in the acute setting, the patient is progressed through simple passive, activeassisted, and then active range of motion. Once the patient is comfortable with these exercises, the focus shifts to

81

progressive resistance training of the rotator cuff, deltoid, and scapular stabilizers. This should continue until strength and motion are equal bilaterally. The goal is to strengthen the dynamic stabilizers of the glenohumeral joint. Activity modification should be a part of rehabilitation in some patients as well. Avoidance of the activity that led to the dislocation is often reasonable in the older patient, but challenging for the young athlete who would like to return to sport. Other nonsurgical options in addition to physical therapy that can be considered in the patient with anterior instability and a Bankart lesion are bracing and taping. Whereas these modalities are directed at preventing the position of abduction and external rotation or preventing humeral subluxation, neither has been shown to decrease the rate of instability. In the young athlete with first-time dislocation, surgical management is becoming more common as non-operative treatment is not nearly as successful as in a more mature patient population (older than 30 years). Success of nonoperative management is dependent on multiple factors, particularly the age of the patient at first dislocation, athletic activities, associated disease, number of dislocations, and gender. In first-time dislocators older than 30 years, the chance of recurrence is approximately 27%, whereas the patient younger than 30 years has between a 40% and 90% chance of re-dislocation.31 Men typically have a higher rate of recurrence than women, as do athletes involved in throwing or contact sports. An associated pathologic process, such as a bony Bankart lesion, large Hill-Sachs lesion, or rotator cuff tear or avulsion, is also predictive of failure of non-operative treatment. 

Procedures Patients with labral tears can undergo an intra-articular injection with corticosteroid and local anesthetic to help with pain and inflammation. Intra-articular injection should be done in conjunction with the physical therapy as described. This can be done under fluoroscopic or ultrasound guidance or by anatomic landmarks. Aspiration of paralabral cysts causing compression on the suprascapular nerve can be performed with image guidance. This has been shown to provide relief in 60% of patients, although it is usually temporary. Failure to address the primary pathologic process of the labral tear may allow recurrence of the cyst. The role of both platelet-rich plasma and stem cells are currently being researched as adjuvant care for conservative treatment, as well as being used for biologic augmentation for surgical procedures. Their role has yet to be well delineated. 

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery Superior Labral Anterior-Posterior Tear Surgery is indicated once the patient and physician have decided that non-operative measures have not been

82

PART 1  MSK Disorders

adequate. It is generally recommended that patients have a trial of conservative therapy, usually involving at least a 3-month period of physical therapy and medications, before proceeding to the operating room. The following surgical procedures are based on the type of injury: Type I: Gentle débridement of labrum back to stable tissue. Type II: Arthroscopic labral repair with suture anchors. Type III: Arthroscopic débridement of the bucket-handle fragment with repair of any unstable portions of the labral rim. Type IV: Treatment of the biceps disease with débridement, tenotomy, or tenodesis combined with labral repair or débridement. With simple débridement, the patient usually is provided with good pain relief in the short term. About 80% of patients have good relief for the first year or so, but at 2 years or more, this number decreases to near 60%.32,33 Type II SLAP tears are the most commonly encountered, so they are the most studied. Many studies report that 90% of Type II SLAP tears return to sport and approximately 70% to 80% return to pre-injury level. Patients older than 36 years have shown less success with superior labral repair when compared with younger patients.34 Age and workers’ compensation status have been shown to be independent risk factors for increased complications following surgery in these individuals.35 As age increases, postoperative stiffness and reoperation rates increase, while patient satisfaction scores decrease.35 In addition, pain may continue to be generated by the biceps-labral complex in older patients following SLAP repair. In this population, the literature shows that biceps tenotomy and tenodesis are reliable alternatives to SLAP repair, while débridement or tenotomy is favored over SLAP repair when the patient has a concomitant rotator cuff tear.35 Currently, experienced upper extremity surgeons are performing fewer SLAP repairs and the trend has been towards an increase in biceps tenodesis and tenotomy, especially as patient age increases.36 Treatment of a SLAP tear with associated paralabral cyst involves arthroscopic labral repair with or without cyst decompression. Studies show acceptable outcomes with both approaches. 

Bankart Lesion Labral repair with plication of the attenuated capsule is successful in restoring stability (Fig. 15.6). With open or

arthroscopic surgical stabilization, the risk of recurrence compared with conservative treatment is about one fifth that of the non-operative group.37 Modern arthroscopic techniques allow suture anchor fixation of the labrum and capsular plication. Research has demonstrated that open and arthroscopic operations for recurrent shoulder instability have equal quality of life and functional outcome scores at 2-year follow-up. However, the recurrence rate is slightly higher with arthroscopic treatment, likely secondary to less scar tissue formation.38 

Potential Disease Complications SLAP tears result in a decrease in overall shoulder stability as the glenoid labrum is disrupted. This is usually well tolerated, but can lead to episodes of instability and further damage of the labrum, biceps, capsule, and surrounding ligamentous structures. No data exist to suggest that nonoperative management of SLAP tears leads to significant degenerative changes. Bankart lesions are caused by shoulder instability, and the pathologic change that they create increases the chance for further instability. This will create greater attenuation and damage to the tissues around and within the shoulder capsule, which can then cause fracture of the glenoid or the humeral head, possible neurovascular compromise, and increased risk of future glenohumeral arthritis. 

Potential Treatment Complications The risk of taking long-term nonsteroidal anti-inflammatory medication includes damage of the gastric and renal systems. Cyclooxygenase 2 inhibitors avoid some of the gastric complications, but there is a concern for cardiovascular complications, and past medical history should be taken into account. Injection of the glenohumeral joint has a small chance of causing septic arthritis. Non-operative management of SLAP tears has little risk, as conservative management has not been shown to place the shoulder at risk for future deterioration. In the setting of a Bankart tear with anterior instability, recurrent instability episodes do risk further labral, capsular, articular cartilage, and rotator cuff damage. In the younger patient at risk for recurrent instability, this may prompt earlier surgical treatment. Potential surgical complications specific to labral repairs include postoperative stiffness, recurrent tearing, iatrogenic chondral disease, glenoid rim fractures, instability, and posttraumatic arthritis. One study demonstrated increased infection rates, revision rates, and conversion to tenodesis following SLAP repair in patients who use tobacco products.39 As always, patients should be counseled to abstain from tobacco use prior to SLAP repair for at least 8 weeks before surgery.

References

FIG. 15.6  Suture anchor repair of Bankart lesion.

1. Keener JD, Brophy RH. Superior labral tears of the shoulder: pathogenesis, evaluation, and treatment. J Am Acad Orthop Surg. 2009;17:627–637. 2. Cooper DE, Arnoczky SP, O’Brien SJ. Anatomy, histology, and vascularity of the glenoid labrum: an anatomical study. J Bone Joint Surg Am. 1992;74:46–52. 3. Howell SM, Galinat BJ. The glenoid-labral socket: a constrained articular surface. Clin Orthop Relat Res. 1989;243:122–125.

CHAPTER 15  Labral Tears of the Shoulder

4. Huber WP, Putz RV. Periarticular fiber system of the shoulder joint. Arthroscopy. 1997;13:680–691. 5. Burkhart SS, Morgan CD, Kibler WB. Current concepts: the disabled throwing shoulder: spectrum of pathology part I: pathoanatomy and biomechanics. Arthroscopy. 2003;19:404–420. 6. Burkhart SS, Morgan CD, Kibler WB. Current concepts: the disabled throwing shoulder: spectrum of pathology part II: evaluation and treatment of SLAP lesions in throwers. Arthroscopy. 2003;19:531–539. 7. Jobe CM. Posterior superior glenoid impingement: expanded spectrum. Arthroscopy. 1995;11:530–536. 8. Chambers CC, Lynch S, Gibbs DB, et al. Superior labrum anteriorposterior tears in the National Football League. Am J Sports Med. 2016. 9. Snyder SJ, Karzel RP, DelPizzo W. SLAP lesions of the shoulder. Arthroscopy. 1990;6:274–279. 10. Rowe CR, Patel D, Southmayd WW. The Bankart procedure: a long term end-result study. J Bone Joint Surg Am. 1978;10:1–16. 11. Ownes BD, Dickens JF, Kilcoyne KG, Rue JP. The management of mid-season traumatic anterior shoulder instability in athletes. J Am Acad Orthop Surg. 2012;20:518–526. 12. Kim TK, Queale WS, Cosgarea AJ, McFarland EG. Clinical features of the different types of SLAP lesions. An analysis of one hundred and thirty-nine cases. J Bone Joint Surg Am. 2003;85:66–71. 13. Tennent TD, Beach WR, Meyers JF. A review of the special tests associated with shoulder examination. Part II: laxity, instability, and superior labral anterior and posterior (SLAP) lesions. Am J Sports Med. 2003;31:301–307. 14. Berg EE, Ciullo JB. A clinical test for superior glenoid labral or SLAP lesions. Clin J Sport Med. 1998;8:121–123. 15. Kibler WB. Specificity and sensitivity of the anterior slide test in throwing athletes with superior glenoid labral tears. Arthroscopy. 1995;11:296–300. 16. Guanche CA, Jones DC. Clinical testing for tears of the glenoid labrum. Arthroscopy. 2003;19:517–523. 17. Owens BD, Dickens JF, Kilcoyne KG, et al. The management of midseason traumatic anterior shoulder instability in athletes. J Am Acad Orthop Surg. 2012;20:518–526. 18. Neviaser RJ, Neviaser TJ, Neviaser JS. Anterior dislocation of the shoulder and rotator cuff rupture. Clin Orthop Relat Res. 1993;291:103–106. 19. Lo IK, Nonweiler B, Woolfrey M, et al. An evaluation of the apprehension, relocation, and surprise test for anterior shoulder instability. Am J Sports Med. 2004;32:301–307. 20. Major NM, Browne J, Domzalski T, et al. Evaluation of the glenoid labrum with 3-T MRI: is intraarticular contrast necessary? AJR Am J Roentgenol. 2011;196:1139–1144. 21. Phillips JC, Cook C, Beaty S, et al. Validity of noncontrast magnetic resonance imaging in diagnosing superior labrum anterior-posterior tears. J Shoulder Elbow Surg. 2013;22:3–8. 22. Arirachakaran A, Boonard M, Chaijenkij K, et al. A systematic review and meta-analysis of diagnostic test of MRA versus MRI for detection superior labrum anterior to posterior lesions type II-VII. Skeletal Radiol. 2016. 23. Jung JY, Ha DH, Lee SM, et al. Displaceability of SLAP lesion on shoulder MR arthrography with external rotation position. Skeletal Radiol. 2011;40:1047–1055.

83

24. Borrero CG, Casagranda BU, Towers JD, Bradley JP. Magnetic resonance appearance of posterosuperior labral peel back during humeral abduction and external rotation. Skeletal Radiol. 2010;39:19–26. 25. Itoi E, Sashi R, Minagawa H, et al. Position of immobilization after dislocation of the glenohumeral joint: a study with use of MRI. J Bone Joint Surg Am. 2001;83:661–667. 26. Itoi E, Hatakeyama Y, Sato T. Immobilization in external rotation after shoulder dislocation reduces the risk of recurrence: a randomized controlled trial. J Bone Joint Surg Am. 2007;89:1224–2131. 27. Edwards SL, Lee JA, Bell JE, et al. Nonoperative treatment of superior labrum anterior posterior tears. Improvements in pain, function, and quality of life. Am J Sports Med. 2010;38:1456–1461. 28. Jang SH, Seo JG, Jang HS, et al. Predictive factors associated with failure of nonoperative treatment of superior labrum anterior-posterior tears. J Shoulder Elbow Surg. 2016;25:428–434. 29. Fedoriw WW, Ramkumar P, McCulloch PC, et al. Return to play after treatment of superior labral tears in professional baseball players. Am J Sports Med. 2014;42:1155–1160. 30. Cools AM, Borms D, Cottens S, et al. Rehabilitation exercises for athletes with biceps disorders and SLAP lesions: a continuum of exercises with increasing loads on the biceps. Am J Sports Med. 2014;42:1315–1322. 31. Wheeler JH, Ryan JB, Arciero RA, Molinari RN. Arthroscopic versus nonoperative treatment of acute shoulder dislocations in young athletes. Arthroscopy. 1989;5:213–217. 32. Altcheck DW, Warren RF, Wickiewicz TL, et al. Arthroscopic labral debridement: a 3 year follow up study. Am J Sports Med. 1992;20:702–706. 33. Cordasco FA, Steinmann S, Flatow EL, Bigliani LU. Arthroscopic treatment of glenoid labral tears. Am J Sports Med. 1993;21:425–430. 34. Provencher M, McCormick F, Dewing C, et al. A prospective analysis of 179 type 2 superior labrum anterior and posterior repairs: outcomes and factors associated with success and failure. Am J Sports Med. 2013;41:880–886. 35. Erickson J, Lavery K, Monica J, et al. Surgical treatment of symptomatic superior labrum anterior-posterior tears in patients older than 40 years: a systematic review. Am J Sports Med. 2015;43:1274–1282. 36. Patterson BM, Creighton A, Spang JT, et al. Surgical trends in the treatment of superior labrum anterior and posterior lesions of the shoulder: analysis of data from the American Board of Orthopaedic Surgery certification examination database. Am J Sports Med. 2014;42:1904–1910. 37. Hovelius L, Ologsson A, Sandstrom B. Nonoperative treatment of primary anterior shoulder dislocation in patients 40 years of age and younger: a prospective twenty-five-year follow up. J Bone Joint Surg Am. 2008;90:945–952. 38. Mohtadi NG, Chan DS, Hollinshead RM, et al. A randomized clinical trial comparing open and arthroscopic stabilization for recurrent traumatic anterior shoulder instability, two-year follow-up with disease-­specific quality-of-life outcomes. J Bone Joint Surg Am. 2014;96:353–360. 39. Cancienne JM, Brockmeier SF, Werner BC. Tobacco use is associated with increased rates of infection and revision surgery after primary superior labrum anterior and posterior repair. J Shoulder Elbow Surg. 2016;25:1764–1768.

CHAPTER 16

Rotator Cuff Tendinopathy Nitin B. Jain, MD, MSPH Chan Gao, MD, PhD Brian E. Richardson, PT

Synonyms Impingement syndrome Rotator cuff tendinosis

ICD-10 Codes M75.100 Unspecified rotator cuff tear or rupture of unspecified shoulder, not specified as traumatic M75.101 Unspecified rotator cuff tear or rupture of right shoulder, not specified as traumatic M75.102 Unspecified rotator cuff tear or rupture of left shoulder, not specified as traumatic M75.80 Other shoulder lesions, unspecified shoulder M75.81 Other shoulder lesions, right shoulder M75.82 Other shoulder lesions, left shoulder

Definition The rotator cuff is composed of the subscapularis, supraspinatus, infraspinatus, and teres minor muscles and tendons (Figs. 16.1 and 16.2).1 These four muscles originate from the scapula and transition into their respective tendons prior to insertion. The rotator cuff is responsible for abduction (supraspinatus), external rotation (infraspinatus and teres minor), and internal rotation (subscapularis) of the arm.2 In addition, it puts compressive forces on the humeral head, increases joint contact pressure, and centers the humeral head on the glenoid. Each tendon is composed of relatively avascular collagen fibers, so the rotator cuff tendons are the sites of rotator cuff injuries. Because the tendons are relatively avascular, their capacity to heal spontaneously is minimal, resulting in chronic and recurrent symptomatology.3 The supraspinatus tendon is most commonly involved in rotator cuff disease. Rotator cuff disease is a spectrum of disorders that includes subacromial or subdeltoid bursal pathology, rotator cuff tendinopathy, and partial- and full-thickness rotator cuff tears. 84

The term “impingement lesions” was coined by Charles Neer II to describe the impingement of the supraspinatus tendon under the acromion, coracoacromial ligament, and acromioclavicular joint.4 The fibrotic changes seen in rotator cuff tendons and subacromial bursa are caused by repeated episodes of inflammation5; in addition, fibroblastic hyperplasia of tendons (tendinosis) can occur secondary to degeneration from the aging process.6 In chronic rotator cuff tendinopathy, the muscles of the rotator cuff and surrounding scapulothoracic stabilizers may become weak by disuse. Shoulder pain is the third most common musculoskeletal complaint (behind back and knee pain)7 in the United States. The prevalence of shoulder pain ranges from 14% to 34%8,9; each year approximately 1% of the population 45 years and older present with shoulder pain to primary care settings.10 In the United States the direct healthcare expenses attributable to shoulder disorders was estimated to be $7 billion in 2000.11 Rotator cuff disorders are the underlying problems in 65% to 70% of patients with shoulder pain.1,12 

Symptoms Patients usually present with shoulder pain, weakness, and loss of range of motion resulting in impaired shoulder function. Pain may occur with internal and external rotation and may affect daily self-care activities. The patient can be awoken by pain in the shoulder, which impairs sleep. 

Physical Examination The shoulder examination is approached systematically in every patient. It includes inspection, palpation, range of motion, muscle strength testing, and performance of special tests of the shoulder as clinically indicated. 

Inspection The shoulder should be carefully inspected from the anterior, lateral, and posterior positions. Comparison with the contralateral shoulder can be useful. During inspection, assessment of asymmetry of upper body posture, atrophy of the supraspinatus and infraspinatus muscles, scapular winging, and abnormal scapulothoracic rhythm during shoulder elevation are performed. 

CHAPTER 16  Rotator Cuff Tendinopathy

85

Range of Motion f h a e g b d c

i

FIG. 16.1  Anatomy of the anterior rotator cuff. a, Supraspinatus tendon; b, subscapularis tendon; c, long head of biceps brachii tendon; d, long head of biceps brachii tendon sheath; e, greater tuberosity of the humerus; f, acromion; g, coracoid; h, supraspinatus muscle; i, subscapularis muscle. (Reproduced and modified with permission from Primal Pictures Limited.)

Strength

e

a d b

Total active and passive range of motion in all planes and scapulohumeral rhythm should be evaluated (Fig. 16.3). Forward flexion is performed by asking the patient to raise the arm in front of him or her as high as possible with the thumb pointing upward. Maximal total elevation occurs in the plane of the scapula, which lies approximately 30 degrees forward of the coronal plane.2 The impingement syndrome associated with rotator cuff injuries tends to cause pain with elevation between 60 and 120 degrees (painful arc), when the rotator cuff tendons are compressed against the anterior acromion and coracoacromial ligament.13 Abduction is assessed by raising the arm at the side as high as possible while the scapula is held down by the examiner. Glenohumeral external rotation can be assessed at 0 degrees in abduction with 90 degrees of elbow flexion and neutral supination-pronation position of forearm. At 90 degrees of glenohumeral abduction, with 90 degrees of elbow flexion and neutral supination-pronation position of forearm, the external and internal rotation can be measured by moving the forearm upward and downward as much as possible. Internal rotation can also be evaluated by documenting the highest level the patient can reach on his or her back with the dorsum of the thumb. It is helpful to memorize some important bony landmarks: T7 corresponds to the inferior border of scapula and L4 levels at the top of the iliac crest. 

f

c g

FIG. 16.2 Anatomy of the posterior rotator cuff. a, Supraspinatus tendon; b, infraspinatus tendon; c, teres minor tendon; d, greater tuberosity; e, acromion; f, infraspinatus muscle; g, teres minor muscle.

Palpation Tenderness should be evaluated at the greater tuberosity, subacromial bursa, long head of the biceps located in bicipital groove, and acromioclavicular (AC) joint. Muscle atrophy can be assessed by feeling for the loss of muscle bulk and comparison with the contralateral side. 

Muscle strength testing should be done isolating the relevant individual muscles. The precise way to test muscle strength can be performed by using a commercially available device that measures strength in kilograms or pounds, such as a portable handheld dynamometer (Fig. 16.4).2 The patient should be notified that he or she is supposed to push into the device as hard as possible while the examiner resists his or her limb movement. Once the examiner matches the patient’s resistance so that the isometric contraction is achieved, the patient is asked to keep pushing while maintaining the position for 5 seconds. When the 5-second period is up, the examiner can read the numeric value of muscle strength. All measurements should be performed twice on each arm, with a 10-second rest between repetitions. The numeric readings are then averaged for each arm and evaluated for symmetry. To measure external rotation exerted by infraspinatus, the patient is instructed to hold the arm in neutral rotation, elbow at 90 degrees of flexion and thumb directed upward. The dynamometer is placed on the dorsal surface of the distal forearm just proximal to the ulnar styloid process. Abduction exerted by supraspinatus is measured by placing the dynamometers on the distal arm at the lateral humeral epicondyle while the patient is instructed to hold the shoulder at 90 degrees of abduction and 45 degrees of horizontal abduction, elbow fully extended and palms facing down. Internal rotation is exerted predominantly by subscapularis. The patient firstly holds the arm at 90 degrees of forward flexion and elbow at 90 degrees

86

PART 1  MSK Disorders

B

A

C

D

FIG. 16.3  Range of motion testing. (A) Forward flexion. (B) Isolated abduction. (C) External rotation in neutral. (D) External rotation in abduction.

of flexion. The examiner places the dynamometer on the patient’s hand with one hand and supports the patient’s olecranon process with the other hand to ensure only internal rotation moment, and no adduction moment, is produced. 

Special Tests Special tests in general are more applicable to rotator cuff tears. Tests for impingement are described later, and the remaining tests are described in Chapter 17 (Table 16.1). 

Functional Limitations Patients with rotator cuff tendinopathy complain of limitations in the performance of overhead activities, such as throwing a baseball and painting a ceiling, particularly greater than 90 degrees of abduction.16 Pain may also occur with internal and external rotation and may affect daily self-care activities. Women typically have difficulty hooking their bra in back. Work activities, such as filing, hammering overhead, and lifting, can be affected.17 

Diagnostic Studies Imaging studies may be used to confirm the clinician’s diagnosis and to eliminate other possible pathologic processes. Plain films can be useful to assess for fractures, osteoarthritis, and dislocation. The anteroposterior view with internal and external rotation, West Point axillary view, true anteroposterior, and Y views are usually obtained. Calcification can be visualized in plain film in calcified tendinitis of rotator cuff. Magnetic resonance imaging is the study of choice when a patient is not progressing with conservative management or to rule out an alternative pathologic process (e.g., rotator cuff tear). In tendinopathy, magnetic resonance imaging will demonstrate an increased T2-weighted signal within the substance of the tendon.18 Electrodiagnostic studies can be ordered to exclude alternative diagnoses as well (e.g., cervical radiculopathy).19 Ultrasound can also be used in the diagnosis of rotator cuff tendinopathy. Rotator cuff tendinopathy is shown as heterogeneous hypoechoic thickening of the tendon without obvious fibrillar disruption.20 

CHAPTER 16  Rotator Cuff Tendinopathy

87

anti-inflammatory drugs (NSAIDs)27 are aimed at symptomatic relief. There are five basic phases of nonoperative treatment (Table 16.2). These phases often overlap and can be progressed as rapidly as tolerated, but each should be performed for optimal recovery.

Initial A

B

Both oral and topical medications can provide pain relief and help participation in exercise programs. Most commonly used oral medications in rotator cuff disease include NSAIDs, selective cyclooxygenase 2 (COX-2) inhibitor, and acetaminophen.28 COX-2 inhibitor, in comparison to nonselective NSAIDs, has been shown to provide similar improvements in pain and function with noninferior cardiovascular safety and significantly less gastroenterologic and renal adverse effects.29 The efficacy of topical NSAIDs and glyceryl trinitrate in pain reduction in rotator cuff disease has been proven in several clinical studies.30,31 The topical NSAIDs, in the form of patch, foam, gel, or spray, showed no difference in pain reduction compared with systemic NSAIDs and systemic adverse effects compared with placebo.31 

Rehabilitation C FIG. 16.4 Strength testing by using a dynamometer. (A) External rotation. (B) Abduction. (C) Internal rotation.

Differential Diagnosis Nonneurologic Bicipital tendinopathy Labral tear Acromioclavicular sprain Fracture Osteoarthritis Adhesive capsulitis Muscle strain Myofascial pain syndrome or vascular thoracic outlet syndrome Tumor Neurologic Brachial plexus disease, traumatic or atraumatic (e.g., Parsonage-Turner [acute brachial neuritis]) Cervical radiculopathy Neurogenic thoracic outlet syndrome Suprascapular neuropathy

Treatment Nonoperative treatment is recommended for rotator cuff tendinopathy, which includes physical therapy,21,22 and several modalities such as acupuncture, iontophoresis, phonophoresis, transcutaneous electrical nerve stimulation, pulsed electromagnetic field, and ultrasound are also available.23,24 Other nonoperative treatments such as corticosteroid injections,25,26 topical glyceryl trinitrate, and nonsteroidal

Rehabilitation of rotator cuff disorders mainly consists of physical therapy and manual exercise therapy. A rehabilitation prescription should include the number of sets, repetitions, and an intensity at which the specific exercise should be performed. Rehabilitation therapy focuses on restoring normal motion and strength to the shoulder complex, as well as to decrease pain and improve the overall function without surgery. A physical therapy program should be individualized to address the patient’s specific impairments to accomplish these goals. The basic phases of nonoperative management of rotator cuff disorders consist of: range of motion and pain control, flexibility, and strengthening and advanced strengthening. Physical therapy may include treatments such as shoulder stretches, strengthening exercises to the scapular stabilizers and rotator cuff, proprioceptive exercises, joint mobilization techniques, soft tissue mobilization techniques, and modalities to help control pain and inflammation.

Range of Motion and Pain Control During the early stage of rehabilitation, controlling pain and inflammation is important so that the involved tissue may begin to heal, enabling the patient to progress towards an active rehabilitation program. Physical therapy treatment may consist of soft tissue mobilization, passive range of motion, and joint mobilizations to the shoulder to improve mobility and decrease pain in the joint and surrounding tissues. Furthermore, both the cervical spine and thoracic spine should be assessed for soft tissue or joint restrictions. Treatment techniques such as stretches and mobilization techniques may be used because these structures play an important role in the overall mobility of the shoulder complex. The primary goal of this phase is to decrease pain and inflammation to improve mobility and function. There is insufficient evidence to support the use of physical modalities such as electrical stimulation and low-level

PART 1  MSK Disorders

88

Table 16.1  Special Tests for Rotator Cuff Disease Subject Impingement

Test

Procedure

Interpretation

The patient is seated and the examiner stands behind him or her. Scapular rotation is prevented with one hand while the other hand raises the arm in forced forward elevation, causing the greater tuberosity to impinge against the acromion (Fig. 16.5).

The test is positive if the maneuver produces pain.

Hawkin sign14

The examiner forward flexes the humerus to 90 degrees and forcibly internally rotates the shoulder. This maneuver drives the greater tuberosity farther under the coracoacromial ligament.

The test is positive if the maneuver produces pain.

O’Brien sign15

The examiner stands behind the patient. The patient is asked to forward flex the affected arm 90 degrees with the elbow in full extension. The patient then adducts the arm 10–15 degrees medial to the sagittal plane of the body. The arm is internally rotated so that the thumb is pointed downward. The examiner then applies a uniform downward force to the arm. With the arm in the same position, the palm is then fully supinated and the maneuver is repeated.

The test is positive if pain is elicited with the first maneuver and is reduced or eliminated with the second maneuver. Of note, pain or painful clicking described as within the glenohumeral joint itself is also indicative of labral abnormality. Pain localized to the acromioclavicular joint or on top of the shoulder is diagnostic of acromioclavicular joint abnormality.

Neer

sign5

Proprioception and dynamic joint stabilization

laser therapy in the treatment of rotator cuff disorders, and therefore they are not recommended. On the other hand, cryotherapy has been shown to be effective in pain management and controlling inflammation and may be used in the treatment of rotator cuff disorders. Ultrasound can be considered in calcific tendinosis because it has been shown to resolve the calcification and is associated with short-term symptom relief.32 

Sport- or task-specific training

Flexibility and Strengthening

Table 16.2  Treatment Phases for Rotator Cuff Tendinopathy Pain control and reduction of inflammation Restoration of normal shoulder motion, both scapulothoracic and glenohumeral Normalization of strength and dynamic muscle control

FIG. 16.5  Neer sign for impingement syndrome.

Restoring range of motion to the shoulder complex by performing active assisted range of motion exercises such as wand or cane exercises, as well as pulley exercises, may be used at this time. A continued focus on restoring passive range of motion through soft tissue mobilizations, as well as joint mobilizations, may also be performed during this phase. Gentle shoulder stretches should be introduced to stretch those structures that have become tight and guarded due to pain and inflammation. Shoulder self-stretching should focus on the posterior capsule, posterior cuff, and the pectoralis minor muscles. A tight posterior capsule can lead to anterior or superior migration of the humeral head. which in turn, can result in impingement. It is also important to stretch the pectoralis minor muscle as well. Its attachment to the coracoid process on the scapula can cause the scapula to tilt anteriorly, which can lead to muscle imbalances of the lower trapezius and decrease the subacromial space. Strengthening of the scapular muscles should be performed with a focus on middle trapezius, lower trapezius, and serratus anterior muscle groups because they play an important role in controlling the scapula and to normalize scapular mechanics. Strengthening of the rotator cuff musculature may begin during this phase as well. Positioning the arm at 30 degrees of abduction to perform internal rotation and external rotation prevents the “wringing out” effect on the supraspinatus tendon, and it facilitates blood flow to the tendon. The wringing out effect is caused by the humeral head compressing on the articular side of the supraspinatus tendon while the arm is at 0 degrees of adduction. Empty

CHAPTER 16  Rotator Cuff Tendinopathy

89

can exercise with the thumb down and shoulder internally rotated should be avoided because this exercise may cause subacromial impingement. Full can exercises with the thumb up can be performed because this position recruits the supraspinatus better and it is more of a functional position. There are many types of ways to strengthen the scapular stabilizers and the rotator cuff musculature. 

controlled trial of 40 patients, no difference was found between saline and PRP injection at 1 year.41 In contrast, it was reported by another group that PRP achieved a moderate (>50%) improvement in pain syndrome in 81% of patients with rotator cuff tendinopathy refractory to conventional treatments.42 

Advanced Strengthening

Technology

Advanced strengthening of the rotator cuff and the scapular stabilizers should be the focus during the later stages of rehabilitation. Both proprioceptive training and functional rehabilitation may be incorporated during this phase as well. Proprioceptive training is important in retraining the neurologic control of the strengthened muscle groups. Exercises may include both closed chain (e.g. exercises done with the hand in contact with a fixed object) and open chain exercises (e.g. exercises done where the hand is free to move). Functional rehabilitation activities should be geared toward specific activities the patient would like to return to, such as work-related tasks, sport-specific activities, or household activities. 

There is no specific technology for the treatment or rehabilitation of this condition. 

Procedures An injection of lidocaine and corticosteroid is often performed for pain relief.33 The evidence for the use of corticosteroid injections in rotator cuff disorders is variable.34-36 It is difficult to predict a patient’s response to corticosteroid injection, and the failure rate of this procedure was reported around 40%.37 Percutaneous tenotomy can be performed under ultrasound guidance. The needle is localized and placed in and out of the tendon to create small perforations within the damaged tendon. This stimulates the healing response through the inflammatory cascade, enhancing tendon repair. It has been proven safe but not superior to ultrasound-guided subacromial corticosteroid injection.38 Ultrasound-guided percutaneous needle lavage was reported as a safe and cost-effective procedure to reduce pain and calcification in calcified tendinitis.39 in addition, numerous studies supported the use of extracorporeal shock wave therapy to improve pain and range of motion (ROM) in rotator cuff tendinopathy.38 The advent of novel regenerative medicine strategies has shown its promise in treating tendinopathy. Plateletrich plasma (PRP), obtained by gentle centrifugation of whole blood, has been proposed an effective means of facilitating healing of injured tendons because it is rich in platelet-derived growth factors, transforming growth factors, vascular endothelial growth factor, and epithelial growth factor. Current clinical studies evaluating efficacy of PRP are complicated by considerable heterogeneity of tendinopathies, different PRP preparation techniques, and variations in the composition of PRP.40 Therefore we are lacking convincing data to conclude on its clinical efficacy. Low-leveled evidence exists showing the benefit of PRP in alleviating pain and improving function for patients with lateral epicondyle extensor tendinopathy and patellar tendinopathy. Few studies reported the therapeutic outcome of PRP in rotator cuff tendinopathy. In a randomized

Surgery Surgery is generally not indicated in the treatment of rotator cuff tendinopathy unless patients are refractory to nonsurgical treatment and have symptoms for a prolonged period of time. Surgical procedures include arthroscopic or open acromioplasty to alleviate the outlet stenosis.43 Débridement of the tendon and subacromial decompression can also be performed. 

Potential Disease Complications Rotator cuff tendinopathy may progress to a rotator cuff tear, although the clinical implications of this progression are unclear. With prolonged impairment in motion and strength and subtle instability, hooking of the acromion can develop. Adhesive capsulitis may develop with chronic pain and decreased shoulder movement as well.44 

Potential Treatment Complications There are minimal possible complications from nonoperative treatment of rotator cuff tendinopathy. Because NSAIDs are used frequently, one must remain vigilant to their potential side effects (e.g., gastritis, ulcers, renal impairment, bronchospasm). Injections may cause rupture of the diseased tendon.

References 1. Chard MD, Hazleman R, Hazleman BL, et al. Shoulder disorders in the elderly: a community survey [published online March 21, 2004]. Arthritis Rheum. 1991;34(6):766–769. 2. Jain NB, Wilcox RB 3rd, Katz JN, et al. Clinical examination of the rotator cuff [published Online First: 2013/01/22]. PMR. 2013;5(1):45–56. https://doi.org/10.1016/j.pmrj.2012.08.019. 3. Fenwick SA, Hazleman BL, Riley GP. The vasculature and its role in the damaged and healing tendon [published Online First: 2002/07/11]. Arthritis Res. 2002;4(4):252–260. 4. Neer CS 2nd. Anterior acromioplasty for the chronic impingement syndrome in the shoulder: a preliminary report [published Online First: 1972/01/01]. J Bone Joint Surg Am. 1972;54(1):41–50. 5. Neer CS. Impingement lesions. Clin Orthop Relat Res. 1983;173: 70–77. 6. Rathbun JB, Macnab I. The microvascular pattern of the rotator cuff [published Online First: 1970/08/01]. J Bone Joint Surg Br. 1970;52(3):540–553. 7. CDC/NCHS. National Ambulatory Medical Care Survey: 2010 Summary Tables; 2012. http://www.cdc.gov/nchs/ahcd/web_tables. htm#2010. Accessed January 25, 2013. 8. Mitchell C, Adebajo A, Hay E, et al. Shoulder pain: diagnosis and management in primary care [published Online First: 2005/ 11/12]. BMJ. 2005;331(7525):1124–1128. https://doi.org/10.1136/ bmj.331.7525.1124.

90

PART 1  MSK Disorders

9. Speed C. Shoulder pain [published Online First: 2006/04/20]. Clin Evid. 2005;(14):1543–1560. 10. Chen AL, Shapiro JA, Ahn AK, et al. Rotator cuff repair in patients with type I diabetes mellitus [published Online First: 2003/ 10/18]. J Shoulder Elbow Surg. 2003;12(5):416–421. https://doi. org/10.1016/S1058274603001721. 11. Estimates of direct healthcare expenditures among individuals with shoulder dysfunction in the United States. American Society of Shoulder and Elbow Therapists; 2004. http://www.asset-usa.org/Abstracts/Johnson_Crossley_ Oneil_Al-Kakwani.html. 12. Vecchio P, Kavanagh R, Hazleman BL, et al. Shoulder pain in a community-based rheumatology clinic [published Online First: 1995/05/01]. Br J Rheum. 1995;34(5):440–442. 13. Poppen NK, Walker PS. Normal and abnormal motion of the shoulder [published Online First: 1976/03/01]. J Bone Joint Surg Am. 1976;58(2):195–201. 14. Hawkins RJ, Kennedy JC. Impingement syndrome in athletes [published Online First: 1980/05/01]. Am J Sports Med. 1980;8(3):151–158. https://doi.org/10.1177/036354658000800302. 15. O’Brien SJ, Pagnani MJ, Fealy S, et al. The active compression test: a new and effective test for diagnosing labral tears and acromioclavicular joint abnormality [published Online First: 1998/10/24]. Am J Sports Med. 1998;26(5):610–613. https://doi.org/10.1177/ 03635465980260050201. 16. Plancher KD, Litchfield R, Hawkins RJ. Rehabilitation of the shoulder in tennis players [published Online First: 1995/01/01]. Clin Sports Med. 1995;14(1):111–137. 17. Dines DM, Levinson M. The conservative management of the unstable shoulder including rehabilitation [published Online First: 1995/10/01]. Clin Sports Med. 1995;14(4):797–816. 18. Opsha O, Malik A, Baltazar R, et al. MRI of the rotator cuff andinternal derangement [published Online First: 2008/04/05]. Eur J Radiol. 2008;68(1):36–56. https://doi.org/10.1016/j.ejrad.2008.02.018. 19. Plastaras CT, Joshi AB. The electrodiagnostic evaluation of radiculopathy [published Online First: 2011/02/05]. Phys Med Rehabil Clin N Am. 2011;22(1):59–74. https://doi.org/10.1016/j.pmr.2010.10.005. 20. Yablon CM, Bedi A, Morag Y, et al. Ultrasonography of the shoulder with arthroscopic correlation [published Online First: 2013/06/19]. Clin Sports Med. 2013;32(3):391–408. https://doi.org/ 10.1016/j.csm.2013.03.001. 21. Bennell K, Coburn S, Wee E, et al. Efficacy and cost-effectiveness of a physiotherapy program for chronic rotator cuff pathology: a protocol for a randomised, double-blind, placebo-controlled trial [published Online First: 2007/09/01]. BMC Musculoskelet Disord. 2007;8:86. https://doi.org/10.1186/1471-2474-8-86. 22. Kuhn JE. Exercise in the treatment of rotator cuff impingement: a systematic review and a synthesized evidence-based rehabilitation protocol [published Online First: 2008/10/07]. J Shoulder Elbow Surg. 2009;18(1):138–160. https://doi.org/10.1016/j.jse.2008.06.004. 23. Green S, Buchbinder R, Hetrick S. Physiotherapy interventions for shoulder pain [published Online First: 2003/06/14]. Cochrane Database Syst Rev. 2003;(2):CD004258. https://doi.org/ 10.1002/14651858.CD004258. 24. Green S, Buchbinder R, Hetrick S. Acupuncture for shoulder pain [published Online First: 2005/04/23]. Cochrane Database Syst Rev. 2005;(2):CD005319. https://doi.org/10.1002/14651858.CD005319. 25. Gialanella B, Prometti P. Effects of corticosteroids injection in rotator cuff tears. [published Online First: 2011/09/29]. Pain Med. 2011; 12(10):1559–1565. https://doi.org/10.1111/j.1526-4637.2011.01238.x. 26. Buchbinder R, Green S, Youd JM. Corticosteroid injections for shoulder pain [published Online First: 2003/01/22]. Cochrane Database Syst Rev. 2003;(1):CD004016. https://doi.org/10.1002/14651858.CD004016. 27. Pedowitz RA, Yamaguchi K, Ahmad CS, et al. American Academy of Orthopaedic Surgeons clinical practice guideline on: optimizing the management of rotator cuff problems [published Online First: 2012/01/20]. J Bone Joint Surg Am. 2012;94(2):163–167.

28. Itoi E, Tabata S. Conservative treatment of rotator cuff tears [published Online First: 1992/02/01]. Clin Orthop Relat Res. 1992;(275):165–173. 29. Nissen SE, Yeomans ND, Solomon DH, et al. Cardiovascular safety of celecoxib, naproxen, or ibuprofen for arthritis [published Online First: 2016/12/14]. N Engl J Med. 2016;375(26):2519–2529. https://doi.org/10.1056/NEJMoa1611593. 30. Cumpston M, Johnston RV, Wengier L, et al. Topical glyceryl trinitrate for rotator cuff disease [published Online First: 2009/07/10]. Cochrane Database Syst Rev. 2009;(3):Cd006355. https://doi.org/ 10.1002/14651858.CD006355.pub2. 31. Derry S, Moore RA, Rabbie R. Topical NSAIDs for chronic musculoskeletal pain in adults [published Online First: 2012/09/14]. Cochrane Database Syst Rev. 2012;(9):Cd007400. https://doi.org/ 10.1002/14651858.CD007400.pub2. 32. Ebenbichler GR, Erdogmus CB, Resch KL, et al. Ultrasound therapy for calcific tendinitis of the shoulder. N Engl J Med. 1999;340(20):1533– 1538. https://doi.org/10.1056/nejm199905203402002. 33. Mohamadi A, Chan JJ, Claessen FM, et al. Corticosteroid injections give small and transient pain relief in rotator cuff tendinosis: a metaanalysis [published Online First: 2016/07/30]. Clin Orthop Relat Res. 2017;475(1):232–243. https://doi.org/10.1007/s11999-016-5002-1. 34. Mellor SJ, Patel VR. Steroid injections are helpful in rotator cuff tendinopathy [published Online First: 2002/01/05]. BMJ. 2002;324(7328):51. 35. Alvarez CM, Litchfield R, Jackowski D, et al. A prospective, double-blind, randomized clinical trial comparing subacromial injection of betamethasone and xylocaine to xylocaine alone in chronic rotator cuff tendinosis [published Online First: 2005/02/11]. Am J Sports Med. 2005;33(2):255– 262. https://doi.org/10.1177/0363546504267345. 36. Coombes BK, Bisset L, Vicenzino B. Efficacy and safety of corticosteroid injections and other injections for management of tendinopathy: a systematic review of randomised controlled trials [published Online First: 2010/10/26]. Lancet. 2010;376(9754):1751–1767. https://doi.org/10.1016/s0140-6736(10)61160-9. 37. Contreras F, Brown HC, Marx RG. Predictors of success of corticosteroid injection for the management of rotator cuff disease [published Online First: 2014/01/16]. HSSJ. 2013;9(1):2–5. https:// doi.org/10.1007/s11420-012-9316-6. 38. Louwerens JK, Sierevelt IN, van Noort A, et al. Evidence for minimally invasive therapies in the management of chronic calcific tendinopathy of the rotator cuff: a systematic review and meta-analysis [published Online First: 2014/04/30]. J Shoulder Elbow Surg. 2014;23(8):1240–1249. https://doi.org/10.1016/j.jse.2014.02.002. 39. Castillo-González FD, Ramos-Álvarez JJ, Rodríguez-Fabián G, et al. Treatment of the calcific tendinopathy of the rotator cuff by ultrasoundguided percutaneous needle lavage. Two years prospective study. Muscles Ligaments Tendons J. 2014;4(2):220–225. 40. Sheth U, Simunovic N, Klein G, et al. Efficacy of autologous plateletrich plasma use for orthopaedic indications: a meta-analysis [published Online First: 2012/01/14]. J Bone Joint Surg Am. 2012;94(4):298–307. https://doi.org/10.2106/jbjs.k.00154. 41. Kesikburun S, Tan AK, Yilmaz B, et al. Platelet-rich plasma injections in the treatment of chronic rotator cuff tendinopathy: a randomized controlled trial with 1-year follow-up [published Online First: 2013/07/31]. Am J Sports Med. 2013;41(11):2609–2916. https:// doi.org/10.1177/0363546513496542. 42. Mautner K, Colberg RE, Malanga G, et al. Outcomes after ultrasoundguided platelet-rich plasma injections for chronic tendinopathy: a multicenter, retrospective review [published Online First: 2013/02/13]. PMR. 2013;5(3):169–175. https://doi.org/10.1016/j.pmrj.2012.12.010. 43. Azar FMCS, Beaty JH. Campbell’s Operative Orthopaedics. Elsevier; 2017. 44. Harrison AK, Flatow EL. Subacromial impingement syndrome [published Online First: 2011/11/05]. J Am Acad Orthop Surg. 2011;19(11): 701–708.

CHAPTER 17

Rotator Cuff Tear Nitin B. Jain, MD, MSPH Chan Gao, MD, PhD Brian E. Richardson, PT

Synonyms Shoulder tear Torn shoulder

ICD-10 Codes M75.100 Unspecified rotator cuff tear or rupture of unspecified shoulder, nontraumatic M75.101 Unspecified rotator cuff tear or rupture of right shoulder, nontraumatic M75.102 Unspecified rotator cuff tear or rupture of left shoulder, nontraumatic S43.421 Sprain of right rotator cuff S43.422 Sprain of left rotator cuff S43.429 Sprain of unspecified rotator cuff

Definition Shoulder pain is the third most common musculoskeletal complaint (behind back and knee pain) in the United States. In the United States, shoulder symptoms accounted for an estimated 10.7 million ambulatory care visits to physician offices in 2013.1 There were an estimated 272,148 ambulatory rotator cuff surgeries performed in the United States in 2006.2,3 The rotator cuff is composed of supraspinatus, subscapularis, infraspinatus, and teres minor (Fig. 17.1). Rotator cuff tears are categorized as partial- or fullthickness. Rotator cuff tears are measured based on their longitudinal or transverse tear size.4 Rotator cuff tears can occur from a traumatic incident (such as falling off a ladder or motor vehicle accident) or can be secondary to degenerative changes within the tendon. Degenerative rotator cuff tears tend to occur in adults over 40 years of age. In patients with degenerative rotator cuff tears, histological tendon changes such as increased fibroblast cellularity, neovascularity, thinning or loss of collagen matrix, and fatty infiltration have been described.5 In patients with rotator cuff tear, the muscles of the rotator cuff and surrounding scapulothoracic stabilizers may become weak over time. Under these conditions, the muscles can

fatigue early, resulting in altered biomechanics. In patients with a large rotator cuff tear, over time, the humeral head migrates superiorly because of the unopposed action of the deltoid and lack of downward compressive forces from the supraspinatus and infraspinatus.6,7 From this abnormal motion, impingement of the rotator cuff is more likely to occur. It occurs particularly during forward flexion when the anterior portion of the acromion impinges on the supraspinatus tendon. The long head of biceps is often affected in patients with rotator cuff tears. Repetitive trauma resulting from impingement leads to wear of the shoulder joint, commonly involving anterior-superior margin of glenoid bone, and the occurrence of rotator cuff tear arthropathy.8 It was proposed the loss of motion and pathologic change of periarticular structure accelerate the process of bone and cartilage atrophy.9 

Symptoms Patients usually present with shoulder pain, weakness, and loss of range of motion resulting in impaired shoulder function. Pain may occur with internal and external rotation and may affect daily self-care and overhead activities. The patient can be awoken by pain in the shoulder, which impairs sleep. 

Physical Examination The shoulder examination for rotator cuff tears is similar to that for rotator cuff tendinopathy and consists of inspection, palpation, range of motion, and strength testing as described in Chapter 16. It includes inspection, palpation, range of motion, muscle strength testing, and performance of special tests of the shoulder as clinically indicated. 

Special Tests There are more than 25 special tests reported to evaluate the rotator cuff. In this chapter, we describe the ones having been more rigorously assessed for sensitivity and specificity and most useful in clinical practice (Table 17.1).10 Tests for impingement are described in Chapter 16. Testing of the scapula rotators, the trapezius, and the serratus anterior is also important. The serratus anterior can be tested by having the patient lean against a wall; winging of the scapula as the patient pushes against the wall 91

PART 1  MSK Disorders

92

A

B

C

D FIG. 17.1  Special tests for subscapularis. (A) Lift-off test. (B) Belly-press test. (C) Belly-off test. (D) Bear hug test.

Table 17.1  Special Tests for Rotator Cuff Disease Subject Subscapularis (Fig. 17.1)

Test

Procedure

Interpretation

The examiner assists the patient to get in a position where he/she touches their lower back with the arm fully extended and internally rotated.

The test is positive if the patient is unable to lift the dorsum of his hand off his/her back.

Passive lift-off test12

The examiner brings the arm behind the body into maximal internal rotation (around the lower back region and pull it backwards away from the back).

The test is positive if the patient cannot maintain this position.

Belly-press test12

The examiner requests the patient to presses the abdomen with the hand flat and attempts to keep the arm in maximum internal rotation.

A positive test is when the elbow drops back behind the trunk.

Belly-off sign13

The examiner will passively bring the arm of the patient into flexion and maximum internal rotation with the elbow 90 degrees flexed. The elbow of the patient is supported by one hand of the examiner while the other hand brings the arm into maximum internal rotation placing the palm of the hand on the abdomen. The patient is then asked to keep the wrist straight and actively maintain the position of internal rotation as the examiner releases the wrist.

The test is positive if the patient cannot maintain the above position, lag occurs, and the hand lifts off the abdomen.

Bear hug test14

The examiner requests the patient to place the palm of the involved side on the opposite shoulder, extend the fingers (so that the patient could not resist by grabbing the shoulder), and position the elbow anterior to the body. The examiner then asks the patient to hold that position (resisted internal rotation) as the examiner tries to pull the patient’s hand from the shoulder with an external rotation force applied perpendicular to the forearm.

The test is positive if the patient could not hold the hand against the shoulder or if he or she shows weakness of resisted internal rotation of greater than 20% compared with the opposite side.

Lift-off

test11

CHAPTER 17  Rotator Cuff Tear

93

Table 17.1  Special Tests for Rotator Cuff Disease—cont’d Subject

Test

Procedure

Interpretation

Infraspinatus and teres minor (Fig. 17.2)

External rotation lag sign at 0 degree14

The patient is seated on an examination couch with his or her back to the physician. The elbow is passively flexed to 90 degrees, and the shoulder is held at 20 degrees elevation (in the scapular plane) and near maximum external rotation (i.e., maximum external rotation −5 degrees to avoid elastic recoil in the shoulder) by the examiner. The patient is then asked to actively maintain the position of external rotation as the examiner releases the wrist while maintaining support of the limb at the elbow.

The sign is positive when a lag, or angular drop, occurs.

External rotation lag sign at 90 degrees (drop sign)15

The patient is seated on an examination couch with his or her back to the examiner, who holds the affected arm at 90 degrees of elevation (in the scapular plane) and at almost full external rotation, with the elbow flexed at 90 degrees. The patient is asked to actively maintain this position as the physician releases the wrist while supporting the elbow.

The sign is positive if a lag or “drop” occurs. (The maintenance of the position of external rotation of the shoulder is a function mainly of infraspinatus.)

Hornblower’s sign16

The examiner supports the patient’s arm at 90 degrees of abduction in the scapular plane with elbow flexed at 90 degrees. The patient then attempts external rotation of the forearm against resistance of the examiner’s hand.

The test is positive if the patient cannot externally rotate, then he or she assumes a characteristic position.

Jobe test (empty can test)17

It is performed by first assessing the deltoid with the arm at 90 degrees of abduction and neutral rotation. The shoulder is then internally rotated and angled forward 30 degrees; the thumbs should be pointing toward the floor. Manual muscle testing against resistance is performed with the examiner pushing down at the distal forearm.

The test is positive if there is weakness to resistance with the second maneuver as compared with the first maneuver.

Full can test18

With the arm in 90 degrees of elevation in the scapular plane and 45 degrees of external rotation, manual muscle testing against resistance is performed with the examiner pushing down at the distal forearm.

A positive test is when there is weakness to resistance.

Drop arm test10

The examiner abducts the patient’s shoulder to 180 degrees passively and then observes as the patient slowly lowers the arm to the waist.

The test is positive if the arm drops to the side. A positive result indicates a tear of the rotator cuff.

Biceps (Fig. 17.4) Speed test19

The patient flexes his shoulder (elevates it anteriorly) against resistance (from the examiner) while the elbow is extended and the forearm supinated.

The test is positive when pain is localized to the bicipital groove.

Acromioclavicular joint

The patient’s arm forward flexes to 90 degrees, the examiner forcibly adducts the arm across the chest.

If the patient reports pain, it is a positive test.

Supraspinatus (Fig. 17.3)

Cross-chest adduction20

indicates weakness.21 The cervical spine should be examined to assess for pathology. Suprascapular neuropathy results in weakness of the rotator cuff or the scapular stabilizers and can be isolated or accompany a rotator cuff tear.22 

Functional Limitations The greatest limitation that patients complain of is performing overhead activities.23 Patients with rotator cuff tear complain of difficulty with overhead activities (e.g., throwing a baseball, painting a ceiling), greatest above 90 degrees of abduction, secondary to pain or weakness. Internal and external rotation may be compromised and may affect daily self-care activities. Women typically have difficulty hooking the bra in back. Work activities, such as filing, hammering overhead, and lifting, will be affected. The patient can be awakened by pain in the shoulder, which impairs their sleep. 

Diagnostic Studies Imaging studies may be used to confirm the clinician’s diagnosis and to eliminate other possible pathologic processes. Plain films can be useful to assess for fractures, osteoarthritis, and dislocation. The anteroposterior view with internal and external rotation, West Point axillary view, true anteroposterior, and Y views are usually obtained. A tear can be inferred if there is evidence of superior humeral head migration. Magnetic resonance imaging (MRI) is most commonly used to make an imaging diagnosis of rotator cuff tears (Fig. 17.5). The following features are usually assessed on MRI24: Tear Thickness and Size: A full-thickness tear is diagnosed when there is complete disruption of all tendon fibers or when the signal within the cuff tendons is isointense compared with fluid on the T2-weighted

94

PART 1  MSK Disorders

A

C

B

FIG. 17.2  Special tests for infraspinatus and teres minor. (A) External rotation lag sign at neutral position. (B) External rotation lag sign at 90 degrees abduction. (C) Hornblower’s sign.

FIG. 17.3  Jobe (empty can) test for supraspinatus.

images and extended from the articular to the bursal surface on one or more images. A partial-thickness tear is diagnosed when fluid-intensity signal within the tendons is in contact with only one of the surfaces or if there is a discontinuity of some but not all tendon fiber.24 Fatty Infiltration: Fatty infiltration is evaluated based on fatty streaks within the muscle belly observed on a T1weighted oblique sagittal image. It is graded as grade 0, no fat; grade 1, thin streaks of fat; grade 2, less fat than muscle; grade 3, equal amounts of fat and muscle; and grade 4, more fat than muscle. The original study described fatty infiltration based on computed tomography (CT) scan findings.25 However, MRI offers superior resolution of muscle as compared with CT scan and multiple prior studies have used MRI for fatty infiltration grading. Moreover, it is also standard

FIG. 17.4  Speed test for biceps.

clinical practice to use MRI for rotator cuff assessment as opposed to CT scan.26 Muscle Atrophy: Muscle atrophy is graded according to the scale that is based on an oblique sagittal plane in the most lateral image where the coracoid and scapular spine meet the scapular body.27 This position has been found to be easily reproducible. Atrophy is graded as none, mild, moderate, and severe. Although the original study used CT scan for muscle atrophy grading, MRI offers muscle resolution that is better than CT scan. Prior studies have also used MRI for muscle atrophy grading.

CHAPTER 17  Rotator Cuff Tear

A

95

B

FIG. 17.5  Magnetic resonance imaging of rotator cuff tear. (A) Coronal T2-weighted image of rotator cuff shows isointense signal compared with fluid within supraspinatus tendon (arrow) suggesting full-thickness tear. (B) Select sagittal oblique T1-weighted images of the rotator cuff muscle in a study read as grade I fatty infiltration for supraspinatus (arrow) and grade 2 fatty infiltration for infraspinatus (curved arrow).

A

B

Supraspinatus tendon (long axis)

FIG. 17.6  Ultrasound of rotator cuff. (A) Normal supraspinatus tendon is indicated by arrow in the long axis view. (B) Ultrasound guided subacromial/subdeltoid injection in the long axis. Arrow indicates the needle tip. Hollow arrow indicates insertion of supraspinatus tendon in greater trochanter. The hypoechogenic region marked by asterisk is subacromial/subdeltoid bursa.

Tendon Retraction: Tendon retraction in the coronal plane is classified into four stages. A tear is classified as stage I tear if the medial edge of the torn tendon is over the greater tuberosity. Stage II tears exposed the humeral head but did not retract to the glenoid. If the tendon retracted to the glenoid, the tear is classified as Stage III. Stage IV tears are retracted medial to the glenoid.28 MR arthrography is less commonly used to diagnose a rotator cuff tear unless other pathology such as a labral tear is suspected. MRA is an invasive procedure and MRI offers excellent sensitivity and specificity.26 Thus, the incremental benefit of performing a MRA for diagnosing rotator cuff tear is usually outweighed by its invasiveness and added expense.

Electrodiagnostic studies can be ordered to exclude alternative diagnoses as well (e.g., cervical radiculopathy).21 Ultrasound imaging can also be used in the diagnosis of rotator cuff tears (Fig. 17.6A).29 Ultrasonography has gained increasing popularity due to its diagnostic accuracy that is comparable to a MRI30 (Table 17.2) and portability since it can be performed in an office-based setting. Dynamic examination can also be performed using an ultrasound and it is relatively inexpensive as compared with a MRI. The user-dependency of ultrasound is a major limitation. Rotator cuff tears are seen as an area of hypoechogenicity on an ultrasound image. Although there are prior data on the use of ultrasound to assess fatty infiltration, more evidence is needed in this area.

96

PART 1  MSK Disorders

Table 17.2  Accuracy of Diagnostic Imaging for Rotator Cuff Tears Sensitivity

Specificity

Full-Thickness Tear MRI Arthrogram

95%

99%

MRI

92%

93%

Ultrasound

92%

Partial-Thickness Tear MRI Arthrogram

Table 17.3  Summary of AAOS Guidelines for Management of Rotator Cuff Tear AAOS Guidelines Summary on Strength of Evidence for Surgical Treatment of Rotator Cuff Tears Clinical Condition

Treatment

Evidence Strength

94%

Full-thickness tear and asymptomatic

No surgery

Consensus Weak

96%

Chronic full-thickness tear and symptomatic

Surgery

86%

MRI

64%

92%

Acute traumatic cuff tears

Surgery

Weak

US

67%

94%

Irreparable rotator cuff tear

Débridement, partial repair, tendon transfer

Weak

MRI, Magnetic resonance imaging; US, ultrasound

Diagnostic arthroscopy is done in some instances but is not generally necessary.  Differential Diagnosis Nonneurologic Bicipital tendinopathy Labral tear Acromioclavicular sprain Fracture Osteoarthritis Adhesive capsulitis Muscle strain Myofascial pain syndrome or vascular thoracic outlet syndrome Tumor Neurologic Brachial plexus disease, traumatic or atraumatic (e.g., Parsonage-Turner [acute brachial neuritis]) Cervical radiculopathy Neurogenic thoracic outlet syndrome Suprascapular neuropathy

Treatment Individuals with symptomatic rotator cuff disease are typically offered either operative or non-operative treatment.31 Operative repair of cuff tears may be performed by an open approach, arthroscopic assisted (mini-open) technique, or as an arthroscopy only procedure.32 Rotator cuff repairs are now almost exclusively performed arthroscopically. Patients typically wear a sling after surgery and undergo postoperative rehabilitation for 3 to 6 months.33 Non-operative treatment includes physical therapy.34,35 and several modalities such as acupuncture, iontophoresis, phonophoresis, transcutaneous electrical nerve stimulation, pulsed electromagnetic field, and ultrasound are also available.36,37 Other non-operative treatments such as corticosteroid injections,38,39 topical glyceryl trinitrate,40 and nonsteroidal anti-inflammatory drugs (NSAIDs) 31 are aimed at symptomatic relief. Minimal evidence exists regarding operative versus nonoperative, and is best summarized by the AAOS (Table 17.3).31 It is expert opinion that patients with symptomatic acute traumatic tears undergo a rotator cuff repair.31 

AAOS Guidelines Summary on Strength of Evidence for Non-Surgical Treatment of Cuff Tears Rotator cuff tears

Exercise

Inconclusive

Rotator cuff tears

NSAIDs, activity modification, ice, heat, modalities

Inconclusive

Rotator cuff disordersa

Modalities, ice, heat

Inconclusive

Exercise or NSAIDs

Moderate

Rotator cuff

disordersa

aRotator

cuff conditions other than full-thickness tears (partial-thickness tear and tendonitis). NSAIDs, Nonsteroidal anti-inflammatory drugs.

Non-Operative Treatment Non-operative treatment includes pharmacological management and rehabilitation. These treatments have been described in Chapter 16 and are similar for rotator cuff tears.

Procedures An injection of lidocaine and corticosteroid is often performed for pain relief (see Fig. 17.6B).41 The evidence for the use of corticosteroid injections in rotator cuff disorders is variable.42-44 It is difficult to predict a patient’s response to corticosteroid injection, and failure rate of this procedure was reported around 40%.45 In one randomized clinical trial, a single injection of corticosteroid was shown to offer symptomatic relief of both rest and activity pain for 3 months in patients with rotator cuff tear.38 Stem cell–based therapy has emerged as another therapeutic option for tendinopathy. Mesenchymal stem cells (MSCs) are multipotent adult stem cells that can differentiate into osteoblast, tenocyte, chondrocyte, and muscle cells under proper environmental cues. The resource of MSCs is abundant: they can be isolated from different tissues, including bone marrow (bone marrow aspirate), adipose tissue, cartilage, tendon, and synovium.46 MSCs injection was studied to treat lateral epicondyle tendinopathy, patellar tendinopathy, and Achilles tendinopathy with reported success. Injection of bone marrow aspirate in combination with PRP was also shown to improve symptoms of partialthickness rotator cuff tear.47 In the future carefully designed random clinical trials of larger scale are needed to determine the benefit and risk of these novel biological therapeutics. 

CHAPTER 17  Rotator Cuff Tear

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery Early surgical repair is recommended for rotator cuff tear due to acute injury.31 For those without history of acute injury, the indications for surgery are not well defined. If surgery is contemplated, a rotator cuff repair, subacromial decompression, and biceps tenodesis/tenotomy may be considered. Surgical options for irreparable rotator cuff tear include tendon transfers, biceps tenodesis/tenotomy, and reverse shoulder arthroplasty.31 Postoperative rehabilitation aims at improving range of motion and strength in the involved shoulder while allowing the repaired tendon to heal. When approaching the rehabilitation process, it is important to note that the physical therapy guidelines following surgery are a guide to treatment and should be coordinated with the patient’s response to treatment. Communication between the orthopedic surgeon and the rehabilitation professional is important to have a successful outcome. It is important to know the size and location of the tear, tissue quality, and any other procedures performed. All of these factors are important in the success of the rehabilitation. To optimize tendon healing, the patient may be immobilized 4 to 6 weeks. The early stage of rehabilitation is focused on passive range of motion (ROM) and controlling pain and swelling in the joint while protecting the repair. Active assisted ROM may be initiated at 4 to 6 weeks postoperatively followed by active ROM at week 8. Rotator cuff and scapular strengthening may be initiated by week 12 followed by functional exercises in order to return the patient to their prior level of function. 

Potential Disease Complications Partial rotator cuff tears can progress to full-thickness tears, although the clinical relevance of this is unclear. Chronic untreated rotator cuff tears can lead to irreparable rotator cuff tear and shoulder arthropathy.8 

Potential Treatment Complications Analgesics and NSAIDs have well-known side effects that most commonly affect the gastric, hepatic, and renal systems. There are minimal disadvantages to coordinating a rehabilitation program that may improve the patient’s symptoms to a level at which the patient is satisfied and functional. However, an overly aggressive program can progress a partial tear to a complete tear. With surgery, in general, the potential problems include bleeding, infection, worsening of the complaints, and nerve injury.

References 1.  National Ambulatory Medical Care Survey: 2013 State and National Summary Tables. CDC/NCHS; 2013. https://www.cdc.gov/nchs/ ahcd/web_tables.htm#2013. Accessed February 5, 2017. 2. Colvin AC, Egorova N, Harrison AK, et al. National trends in rotator cuff repair [published online Feburary 3, 2012]. J Bone Joint Surg Am. 2012;94(3):227–233. https://doi.org/10.2106/jbjs.j.00739.

97

3. Jain NB, Higgins LD, Losina E, et al. Epidemiology of musculoskeletal upper extremity ambulatory surgery in the United States [published Online First: 2014/01/09]. BMC Musculoskelet Disord. 2014;15:4. https://doi.org/10.1186/1471-2474-15-4 . 4. Gomoll AH, Katz JN, Warner JJ, et al. Rotator cuff disorders: recognition and management among patients with shoulder pain [published Online First: 2004/12/14]. Arthritis Rheum. 2004;50(12):3751–3761. https://doi.org/10.1002/art.20668. 5. Dean BJ, Franklin SL, Carr AJ. A systematic review of the histological and molecular changes in rotator cuff disease [published Online First: 2013/04/24]. Bone & Joint Res. 2012;1(7):158–166. https://doi.org/10.1302/2046-3758.17.2000115. 6. Harryman 2nd DT, Sidles JA, Clark JM, et al. Translation of the humeral head on the glenoid with passive glenohumeral motion [published Online First: 1990/10/01]. J Bone Joint Surg Am. 1990;72(9): 1334–1343. 7. Poppen NK, Walker PS. Normal and abnormal motion of the shoulder [published Online First: 1976/03/01]. J Bone Joint Surg Am. 1976;58(2):195–201. 8. Eajazi A, Kussman S, LeBedis C, et al. Rotator cuff tear arthropathy: pathophysiology, imaging characteristics, and treatment options [published Online First: 2015/10/27]. AJR Am J Roentgenol. 2015;205(5): W502–W511. https://doi.org/10.2214/ajr.14.13815. 9. Visotsky JL, Basamania C, Seebauer L, et al. Cuff tear arthropathy: pathogenesis, classification, and algorithm for treatment [published Online First: 2005/02/05]. J Bone Joint Surg Am. 2004;86-A(suppl 2): 35–40. 10. Jain NB, Wilcox 3rd RB, Katz JN, et al. Clinical examination of the rotator cuff [published Online First: 2013/01/22]. PMR. 2013;5(1):45–56. https://doi.org/10.1016/j.pmrj.2012.08.019. 11. Gerber C, Krushell RJ. Isolated rupture of the tendon of the subscapularis muscle. clinical features in 16 cases [published Online First: 1991/05/01]. J Bone Joint Surg Br. 1991;73(3):389–394. 12. Gerber C, Hersche O, Farron A. Isolated rupture of the subscapularis tendon [published Online First: 1996/07/01]. J Bone Joint Surg Am. 1996;78(7):1015–1023. 13. Scheibel M, Magosch P, Pritsch M, et al. The belly-off sign: a new clinical diagnostic sign for subscapularis lesions [published Online First: 2005/10/18]. Arthroscopy. 2005;21(10):1229–1235. https://doi.org/10.1016/j.arthro.2005.06.021. 14. Barth JR, Burkhart SS, De Beer JF. The bear-hug test: a new and sensitive test for diagnosing a subscapularis tear [published Online First: 2006/10/10]. Arthroscopy. 2006;22(10):1076–1084. https://doi.org/10.1016/j.arthro.2006.05.005. 15. Hertel R, Ballmer FT, Lombert SM, et al. Lag signs in the diagnosis of rotator cuff rupture [published Online First: 1996/07/01]. J Shoulder Elbow Surg. 1996;5(4):307–313. 16. Walch G, Boulahia A, Calderone S, et al. The ‘dropping’ and ‘hornblower’s’ signs in evaluation of rotator-cuff tears [published Online First: 1998/08/12]. J Bone Joint Surg Br. 1998;80(4):624–628. 17. Jobe FW, Jobe CM. Painful athletic injuries of the shoulder [published Online First: 1983/03/01]. Clin Orthop Relat Res. 1983;(173):117–124. 18. Kelly BT, Kadrmas WR, Speer KP. The manual muscle examination for rotator cuff strength. An electromyographic investigation [published Online First: 1996/09/01]. Am J Sports Med. 1996;24(5):581–588. https://doi.org/10.1177/036354659602400504. 19. Crenshaw AH, Kilgore WE. Surgical treatment of bicipital tenosynovitis [published Online First: 1966/12/01]. J Bone Joint Surg Am. 1966;48(8):1496–1502. 20. Silliman JFHR. Clinical examination of the shoulder complex. In: Andrews JRWK, ed. The athlete’s shoulder. New York: Churchill Livingstone; 1994. 21. Malanga GA, Jenp YN, Growney ES, et al. EMG analysis of shoulder positioning in testing and strengthening the supraspinatus [published Online First: 1996/06/01]. Med Sci Sports Exerc. 1996;28(6):661–664. 22. Boykin RE, Friedman DJ, Higgins LD, et al. Suprascapular neuropathy [published Online First: 2010/10/12]. J Bone Joint Surg Am. 2010;92(13):2348–2364. https://doi.org/10.2106/jbjs.i.01743. 23. Plancher KD, Litchfield R, Hawkins RJ. Rehabilitation of the shoulder in tennis players [published Online First: 1995/01/01]. Clin Sports Med. 1995;14(1):111–137. 24. Opsha O, Malik A, Baltazar R, et al. MRI of the rotator cuff and internal derangement [published Online First: 2008/04/05]. Eur J Radiol. 2008;68(1):36–56. https://doi.org/10.1016/j.ejrad.2008.02.018.

98

PART 1  MSK Disorders

25. Goutallier D, Postel JM, Bernageau J, et al. Fatty muscle degeneration in cuff ruptures. Pre- and postoperative evaluation by CT scan [published Online First: 1994/07/01]. Clin Orthop Relat Res. 1994;(304):78–83. 26. Jain NB, Collins J, Newman JS, et al. Reliability of magnetic resonance imaging assessment of rotator cuff: the ROW study. [published Online First: 2014/09/03] PMR. 2015;7(3):245–254.e3; quiz 54. https://doi.org/10.1016/j.pmrj.2014.08.949. 27. Warner JJ, Higgins L, IMt Parsons, et al. Diagnosis and treatment of anterosuperior rotator cuff tears [published Online First: 2001/02/22]. J Shoulder Elbow Surg. 2001;10(1):37–46. https://doi. org/10.1067/mse.2001.112022. 28. Boileau P, Brassart N, Watkinson DJ, et al. Arthroscopic repair of full-thickness tears of the supraspinatus: does the tendon really heal? [published Online First: 2005/06/03] J Bone Joint Surg Am. 2005;87(6):1229–1240. https://doi.org/10.2106/jbjs.d.02035. 29. Moosikasuwan JB, Miller TT, Burke BJ. Rotator cuff tears: clinical, radiographic, and US findings [published Online First: 2005/11/15]. Radiographics. 2005;25(6):1591–1607. https://doi.org/10.1148/rg.256045203. 30. de Jesus JO, Parker L, Frangos AJ, et al. Accuracy of MRI, MR arthrography, and ultrasound in the diagnosis of rotator cuff tears: a metaanalysis [published Online First: 2009/05/22]. AJR Am J Roentgenol. 2009;192(6):1701–1707. https://doi.org/10.2214/ajr.08.1241. 31. Pedowitz RA, Yamaguchi K, Ahmad CS, et al. American Academy of Orthopaedic Surgeons clinical practice guideline on: optimizing the management of rotator cuff problems [published Online First: 2012/01/20]. J Bone Joint Surg Am. 2012;94(2):163–167. 32. Nho SJ, Shindle MK, Sherman SL, et al. Systematic review of arthroscopic rotator cuff repair and mini-open rotator cuff repair [published Online First: 2007/10/31]. J Bone Joint Surg Am. 2007;89(suppl 3):127–136. https://doi.org/10.2106/JBJS.G.00583. 33. van der Meijden OA, Westgard P, Chandler Z, et al. Rehabilitation after arthroscopic rotator cuff repair: current concepts review and evidencebased guidelines [published Online First: 2012/04/25]. Int J Sports Phys Ther. 2012;7(2):197–218. 34. Ainsworth R, Lewis JS. Exercise therapy for the conservative management of full thickness tears of the rotator cuff: a systematic review [published Online First: 2007/02/01]. Br J Sports Med. 2007;41(4):200–210. https://doi.org/10.1136/bjsm.2006.032524. 35. Bennell K, Coburn S, Wee E, et al. Efficacy and cost-effectiveness of a physiotherapy program for chronic rotator cuff pathology: a protocol for a randomised, double-blind, placebo-controlled trial [published Online First: 2007/09/01]. BMC Musculoskelet Disord. 2007;8:86. https://doi.org/10.1186/1471-2474-8-86. 36. Green S, Buchbinder R, Hetrick S. Physiotherapy interventions for shoulder pain [published Online First: 2003/06/14]. Cochrane Database Syst Rev. 2003;(2):CD004258. https://doi.org/ 10.1002/14651858.CD004258.

37. Green S, Buchbinder R, Hetrick S. Acupuncture for shoulder pain [published Online First: 2005/04/23]. Cochrane Database Syst Rev. 2005;(2):CD005319. https://doi.org/10.1002/14651858.CD005319. 38. Gialanella B, Prometti P. Effects of corticosteroids injection in rotator cuff tears [published Online First: 2011/09/29]. Pain Med. 2011;12(10): 1559–1565. https://doi.org/10.1111/j.1526-4637.2011.01238.x. 39. Buchbinder R, Green S, Youd JM. Corticosteroid injections for shoulder pain [published Online First: 2003/01/22]. Cochrane Database Syst Rev. 2003;(1):CD004016. https://doi.org/10.1002/14651858.CD004016. 40. Cumpston M, Johnston RV, Wengier L, et al. Topical glyceryl trinitrate for rotator cuff disease [published Online First: 2009/07/10]. Cochrane Database Syst Rev. 2009;(3):Cd006355. https://doi.org/ 10.1002/14651858.CD006355.pub2. 41. Mohamadi A, Chan JJ, Claessen FM, et al. Corticosteroid injections give small and transient pain relief in rotator cuff tendinosis: a metaanalysis [published Online First: 2016/07/30]. Clin Orthop Relat Res. 2017;475(1):232–243. https://doi.org/10.1007/s11999-016-5002-1. 42. Mellor SJ, Patel VR. Steroid injections are helpful in rotator cuff tendinopathy [published Online First: 2002/01/05]. BMJ. 2002;324(7328):51. 43. Alvarez CM, Litchfield R, Jackowski D, et al. A prospective, doubleblind, randomized clinical trial comparing subacromial injection of betamethasone and xylocaine to xylocaine alone in chronic rotator cuff tendinosis [published Online First: 2005/02/11]. Am J Sports Med. 2005;33(2):255–262. https://doi.org/10.1177/0363546504267345. 44. Coombes BK, Bisset L, Vicenzino B. Efficacy and safety of corticosteroid injections and other injections for management of tendinopathy: a systematic review of randomised controlled trials [published Online First: 2010/10/26]. Lancet. 2010;376(9754):1751–1767. https://doi.org/10.1016/s0140-6736(1061160-9). 45. Contreras F, Brown HC, Marx RG. Predictors of success of corticosteroid injection for the management of rotator cuff disease [published Online First: 2014/01/16]. HSS J. 2013;9(1):2–5. https://doi.org/ 10.1007/s11420-012-9316-6. 46. Randelli P, Randelli F, Ragone V, et al. Regenerative medicine in rotator cuff injuries [published Online First: 2014/09/04]. BioMed Res Int. 2014;2014:129515. https://doi.org/10.1155/2014/129515. 47. Kim SJ, Song DH, Park JW, et al. Effect of bone marrow aspirate concentrate platelet-rich plasma on tendon derived stem cells and rotator cuff tendon tear [published Online First: 2017/01/21]. Cell Transplant. 2017. https://doi.org/10.3727/096368917x694705.

CHAPTER 18

Scapular Winging Peter Melvin McIntosh, MD

Synonyms Scapulothoracic winging Long thoracic nerve palsy Spinal accessory nerve palsy Scapula alata Alar scapula Rucksack palsy

ICD-10 Codes G54.3 G54.5 G56.9

Neuropathy thoracic root Neuralgic amyotrophy Mononeuritis of unspecified upper limb G56.91 Mononeuritis of right upper limb G56.92 Mononeuritis of left upper limb G58.9 Nerve entrapment, unspecified M54.12 Cervical radiculopathy M54.13 Cervicothoracic radiculopathy M62.81 Muscle weakness, generalized

Definition Scapular winging refers to prominence of the vertebral (medial) border of the scapula.1 The inferomedial border can also be rotated or displaced away from the chest wall. This well-defined medical sign was first described by Velpeau in 1837. It is associated with a wide array of medical conditions or injuries that typically result in dysfunction of the scapular stabilizers and rotators and, ultimately, glenohumeral and scapulothoracic biomechanics. Scapular winging is classified as either static or dynamic based on the examination of 25 patients with 23 different causes of scapular winging.1 Static winging is attributable to a fixed deformity in the shoulder girdle, spine, or ribs; it is characteristically present with the patient’s arms at the sides. Dynamic winging is ascribed to a neuromuscular disorder; it is produced by active or resisted movement and is usually absent at rest. Scapular winging has also been classified anatomically according to whether the etiology of the lesion is related to nerve, muscle, bone, or joint disease (Table 18.1). The scapula is a triangular bone that is completely surrounded by muscles and attaches to the clavicle by the

coracoclavicular ligaments and acromioclavicular joint capsule. Motion of the scapula along the chest wall occurs through the action of the muscle groups that originate or insert on the scapula and proximal humerus. These muscles include the rhomboids (major and minor), trapezius, serratus anterior, levator scapulae, and pectoralis minor. The rotator cuff and deltoid muscles are involved with glenohumeral motion. Innervation of these muscle groups includes all the roots of the brachial plexus and several peripheral nerves. Scapular winging may be caused by brachial plexus injuries, but most often is related to a peripheral nerve injury (see Table 18.1). Injury to the long thoracic and spinal accessory nerves with weakness of the serratus anterior and trapezius muscles, respectively, is most commonly associated with scapular winging. The serratus anterior muscle originates on the outer surface and superior border of the upper eighth or ninth ribs and inserts on the costal surface of the medial border of the scapula. It abducts the scapula and rotates it so the glenoid cavity faces cranially and holds the medial border of the scapula against the thorax. The serratus anterior muscle is innervated by the pure motor long thoracic nerve (LTN), which arises from the ventral rami of the fifth, sixth, and seventh cervical roots. The nerve passes through the scalenus medius muscle, beneath the brachial plexus and the clavicle, and over the first rib. It then runs superficially along the lateral aspect of the chest wall to supply all the digitations of the serratus anterior muscles. Because of its long and superficial course, the LTN is susceptible to both traumatic and nontraumatic injuries (Fig. 18.1). The trapezius muscle consists of upper, middle, and lower fibers. The upper fibers originate from the external occipital protuberance, superior nuchal line, nuchal ligament, and spinous process of the seventh cervical vertebra and insert on the lateral clavicle and acromion. The middle fibers arise from the spinous process of the first through fifth thoracic vertebrae and insert on the superior lip of the scapular spine. The lower fibers originate from the spinous process of the sixth through twelfth thoracic vertebrae and insert on the apex of the scapular spine. They are innervated by the pure motor spinal accessory nerve (cranial nerve XI) and afferent fibers from the second through fourth cervical spinal nerves. The root fibers unite to form a common trunk that ascends to enter the intracranial cavity through the foramen magnum. It exits with the vagus nerve through the jugular foramen, pierces the sternocleidomastoid muscle, and descends obliquely across the floor of the posterior triangle of the neck to the trapezius muscle. In the posterior triangle, the nerve lies superficially, covered only by fascia 99

100

PART 1  MSK Disorders

Table 18.1  Etiology of Scapular Winging Characteristic

Nerve

Muscle

Bone

Joint

Site of lesion

LTN2

SA T R

Scapula Clavicle Spine Ribs

GHJ ACJ

SAN3 DSN13 C5-C7 nerve root lesion Brachial plexus lesion4 Traumatic

Acute, repetitive, or chronic compression of LTN, SAN, DSN Trauma or traction injury to LTN, nerve roots, brachial plexus5 Whiplash injury6

Direct muscle injury to SA,8 T, R3,7 Avulsion of SA, T, R RTC disease Sports-related injury7,9

Nonunion Malunion Fractures of scapula,10,11 clavicle, acromion

Glenoid fracture ACJ dislocation Shoulder instability

Congenital, hereditary

Cerebral palsy

Congenital contracture of infraspinatus muscle Agenesis of SA, T, R Duchenne muscular dystrophy FSHD12 Fibrous bands (deltoid)

Scoliosis Craniocleidodysostosis Ollier disease Sprengel deformity

Arthrogryposis multiplex congenita Congenital posterior shoulder dislocation

Degenerative, inflammatory

SLE Neuritis Amyotrophic brachial neuralgia4 Guillain-Barré syndrome14

Toxin exposure Infection Myositis

Iatrogenic

Epidural or general anesthesia Radical neck dissection15 Lymph node biopsy First rib resection16 Radical mastectomy Posterolateral thoracotomy incision Axillary node dissection Anterior spinal surgery17

Postinjection fibrosis (deltoid) Division of SA

Miscellaneous

Vaginal delivery18 Cervical syringomyelia19

Chiropractic manipulations, electrocution, and hemangioma involving subscapular muscle

Abduction-internal rotation contracture from AVN of humeral head Arthropathy

Scapulothoracic bursa Enchondroma Subscapular osteochondroma20-23 Exostoses of rib or scapula

Voluntary posterior shoulder subluxation

ACJ, Acromioclavicular joint; AVN, avascular necrosis; DSN, dorsal scapular nerve; FSHD, facioscapulohumeral muscular dystrophy; GHJ, glenohumeral joint; LTN, long thoracic nerve; R, rhomboid muscles; RTC, rotator cuff muscles; SA, serratus anterior muscle; SAN, spinal accessory nerve; SLE, systemic lupus erythematosus; T, trapezius muscle. From Fiddian NJ, King RJ. The winged scapula. Clin Orthop Relat Res. 1984;185:228–236.

and skin, and is susceptible to injury. Cadaver studies have shown considerable variations in the course and distribution of the spinal accessory nerve in the posterior triangle and in the nerve’s relationship to the borders of the sternocleidomastoid and trapezius muscles.24 The trapezius muscle adducts the scapula (middle fibers), rotates the glenoid cavity upward (upper and lower fibers), and elevates and depresses the scapula. Overall, the trapezius muscles maintain efficient shoulder function by both supporting the shoulder and stabilizing the scapulae (Fig. 18.2). A rare cause of scapular winging is dorsal scapular nerve palsy. The dorsal scapular nerve is a pure motor nerve from the fifth cervical spinal nerve that supplies the rhomboid and levator scapulae muscles. It arises above the upper

trunk of the brachial plexus and passes through the middle scalene muscle on its way to the levator scapulae and rhomboids. The rhomboids (major and minor) adduct and elevate the scapula and rotate it so the glenoid cavity faces caudally. The levator scapulae muscles originate on the transverse process of the first four cervical vertebrae and insert on the medial borders of the scapulae between the superior angle and the root of the spine. They elevate the scapulae and assist in rotation of the glenoid cavity caudally. They are innervated by the dorsal scapular nerve (emanating from the fifth cervical spinal nerve) and the cervical plexus (emanating from the third and fourth cervical spinal nerves) (Fig. 18.3). 

101

CHAPTER 18  Scapular Winging

Levator scapulae Rhomboid minor Rhomboid major

Trapezius upper Trapezius middle

Trapezius lower

FIG. 18.1  Anterolateral view of the right upper chest and shoulder showing the course of the long thoracic nerve and innervation of the serratus anterior muscles. Note the superficial location of the long thoracic nerve. (From the Mayo Foundation for Medical Education and Research. © Mayo Foundation, 2007.)

Sternocleidomastoid muscle Trapezius muscle Spinal accessory nerve

FIG. 18.2  Lateral view of the neck showing the course of the spinal accessory nerve and innervation of the trapezius muscle. (From the Mayo Foundation for Medical Education and Research. © Mayo Foundation, 2007.)

Symptoms A patient’s presenting symptoms depend on the type and chronicity of the injury. Most patients, however, complain of upper back or shoulder pain, muscle fatigue, and weakness

FIG. 18.3 View of upper back showing origins and insertions of rhomboid, levator scapulae, and trapezius muscles. (From the Mayo Foundation for Medical Education and Research. © Mayo Foundation, 2007.)

with use of the shoulder. The diagnosis of scapular winging is made clinically, but can be difficult to make, especially when the presenting symptoms and physical examination direct the practitioner towards more common neck and shoulder conditions.25 A pain profile should be obtained, including onset and duration of pain, location, severity, and quality as well as exacerbating and relieving factors, not only to provide baseline information but also to help develop a differential diagnosis. The patient should also be questioned about hand dominance because the dominant shoulder is usually more muscular but sits lower than the nondominant shoulder. Knowledge of the patient’s age, occupation and hobbies, and current and previous level of functioning may also contribute to the diagnosis and treatment plan. The mechanism of injury in patients with traumatic palsy is important, as are associated findings including muscle spasm, paresthesia, and muscle wasting or weakness.26 The scapular winging of long thoracic neuropathy and serratus anterior muscle weakness must be distinguished from that of a spinal accessory neuropathy and trapezius muscle weakness as well as dorsal scapular neuropathy and rhomboid weakness. Serratus anterior muscle dysfunction is the most common cause of scapular winging. Typically, patients complain of a dull aching pain in the shoulder and periscapular region. The periscapular pain may be related to spasm from unopposed contraction of the other scapular stabilizers in the presence of serratus anterior muscle weakness. There may be “clicking” or “popping” noise emanating from the periscapular area when the patient moves, which is made worse with stressful upper extremity activities. Because the serratus anterior muscle rotates the scapula forward as the arm is abducted or forward flexed above the shoulder level, these movements are affected. Shoulder fatigue and weakness are related to loss of scapular rotation and stabilization.

102

PART 1  MSK Disorders

FIG. 18.4  Winging of the right scapula with forward flexion of the extended arms due to injury of the long thoracic nerve with serratus anterior weakness. Note the upward displacement of the scapula with prominence of the vertebral border and medial displacement of the inferior angle. (From the Mayo Foundation for Medical Education and Research. © Mayo Foundation, 2007.)

FIG. 18.5 Right spinal accessory nerve palsy with trapezius weakness. The neckline is asymmetric, the shoulder droops, and there is lateral displacement of the superior angle of scapula with the glenoid labrum rotated downward. (From the Mayo Foundation for Medical Education and Research. © Mayo Foundation, 2007.)

A cosmetic deformity may occur in the upper back as a result of the winged scapula. It may be apparent at rest, but usually is more obvious on raising of the arm. Patients may find it difficult to sit for prolonged periods with the back resting against a hard surface, such as driving for long periods. With trapezius muscle weakness, the affected shoulder is depressed, and the inferior scapular border rotates laterally, which makes prolonged use of the arm painful and tiresome. Patients often complain of a dull ache around the shoulder girdle and difficulty with overhead activities and heavy lifting, especially with shoulder abduction greater than 90 degrees.26 

Physical Examination The patient should be suitably undressed so that the examiner can observe, both front and back, the normal bone and soft tissue contours of both shoulders and scapulae for symmetry and their relationship to the thorax. The patient’s overall posture is assessed, as are the presence of muscle spasm and trapezius or rhomboid muscle atrophy. Scapulothoracic motion is examined with both passive and active range of motion activities of the shoulder. The different patterns of scapulothoracic movement can assist in the differential diagnosis of scapular winging and are illustrated in Figs. 18.4–18.6.27 A recent prospective study to assess the preferred method of examination for scapular winging found “pushing the wall” was the most popular but least sensitive. Forward lowering of the arms was the most sensitive method.30

FIG. 18.6 Dorsal scapular nerve palsy with rhomboid weakness. There is lateral displacement of the inferior angle of the right scapula that is accentuated when the patient pushes his elbows backward against resistance. Note atrophy of the rhomboid and infraspinatus muscles. (From the Mayo Foundation for Medical Education and Research. © Mayo Foundation, 2007.)

With long thoracic neuropathy and serratus anterior muscle weakness, the cardinal sign is winging of the scapula, in which the vertebral border of the scapula moves away from the posterior chest wall and the inferior angle is rotated toward midline. This scapular winging may be visible with

CHAPTER 18  Scapular Winging

the patient standing normally, but if the weakness is mild, it may be visible only when the patient extends the arm and pushes against a wall in a pushup position (see Fig. 18.4).2,28 Spinal accessory neuropathy and trapezius muscle weakness are usually accompanied by an asymmetric neckline with noticeable shoulder droop when the patient’s arms are unsupported at the sides. On the affected side, deepening of the supraclavicular fossa is evident and shoulder shrug is difficult. With shoulder elevation, the scapula is displaced laterally, rotating downward and outward. There is usually difficulty with shoulder abduction above 90 degrees, more so than with forward flexion. Weakness with attempted shoulder elevation against resistance is characteristic. Normal muscle testing can elicit weakness in the trapezius muscle (see Fig. 18.5).26,29 With weakness of the rhomboids, winging of the scapula is usually minimal. There is lateral displacement of the inferior angle of the scapula that is best accentuated when the patient pushes the elbow backward against resistance or slowly lowers the arms from a forward elevated position. Atrophy of the rhomboids may be present. The scapula is displaced downward and laterally (see Fig. 18.6).29 A complete neurologic and musculoskeletal examination, with manual muscle strength testing and sensory and reflex testing, should be completed to rule out underlying neuromuscular disease processes. In addition, thorough examination of the neck and shoulder with provocative maneuvers should be completed to rule out additional musculoskeletal sources of scapular winging. 

Functional Limitations Functional limitations depend not only on the cause of the scapular winging, but also on the severity of weakness and pain. Difficulty with activities of daily living may be evident as a result of pain, weakness, and altered scapulothoracic and glenohumeral motion. Especially affected are activities that require arm elevation above the level of the shoulder (e.g., brushing hair or teeth or shaving). Recreational and vocational activities such as golf, tennis, and volleyball that entail working or reaching overhead may be affected. Chronic shoulder pain and dysfunction can lead to depression and anxiety, irritability, concentration difficulties, lack of sleep, and chronic fatigue. Overuse of the shoulder and scapular stabilizer muscles can lead to myofascial pain syndromes. 

Diagnostic Studies Plain radiography of the shoulder, cervical spine, chest, and scapulae is recommended as part of the initial evaluation for scapular winging, especially if the cause is not obvious. Plain radiography can help rule out other causes of scapular winging, such as subscapular osteochondroma, avulsion fracture of the scapula, or other primary shoulder and cervical spine disease. With radiographs of the scapula, oblique views are recommended because osteochondroma may be hidden on anteroposterior views There also appears to be a role for high-resolution ultrasound (HRUS) in the evaluation of scapular winging. Progress of HRUS has enabled visualization of small peripheral nerves such as the LTN in anatomical specimens and healthy volunteers.31

103

Computed tomography and magnetic resonance imaging are usually not necessary unless the coexistence of other disease processes is suspected. The patient’s presentation and examination findings are pivotal in deciding whether advanced imaging is necessary. Electromyography and nerve conduction studies are valuable tools clinically to aid in the evaluation of scapular winging. They can assist in localizing injury and disease of peripheral nerves or muscles related to scapular function. These studies can help evaluate patients with abnormal scapulothoracic motion but in whom it cannot be clearly established clinically whether the weakness lies in a particular muscle or in the actions of other muscles acting on the scapula. Serial electromyographic and nerve conduction studies have been used to follow recovery in patients with isolated long thoracic or spinal accessory nerve palsies and to help in decisions of whether to undertake nerve exploration or muscle transfer.25,26 However, caution has been advised in the use of needle electromyographic findings to predict the prognosis and to guide the timing of surgical repair. Long thoracic and spinal accessory neuropathies may be associated with a good prognosis, irrespective of needle electromyographic findings.  Differential Diagnosis39 Rotator cuff disease Shoulder impingement syndromes Glenohumeral instability (especially posterior instability) Acromioclavicular joint disease Shoulder arthritis Adhesive capsulitis Bicipital tendinitis Cervical radiculopathy (especially C5-C7) Suprascapular nerve entrapment Myofascial pain syndromes Scoliosis (associated rib deformities can cause asymptomatic scapular winging on convex side of curve) Sprengel deformity (congenital deformity of shoulder with high-riding and downward-rotated scapula, often confused with scapular winging) Fracture or malunion of clavicle and acromion Tumors of shoulder girdle, lung, or spine

Treatment Initial In most patients, scapular winging is a result of neurapraxic injuries. Fortunately, these types of injuries usually resolve spontaneously within 6 to 9 months after traumatic injury and within 2 years after nontraumatic injuries. In one study,40 traumatic long thoracic and spinal accessory nerve injuries were associated with a poor prognosis compared with nontraumatic neuropathies. Once the diagnosis is made, conservative treatment should be initiated. Some clinicians have recommended a trial of conservative treatment for at least 12 to 24 months to allow adequate time for nerve recovery.26 Pain control may be achieved early with use of an analgesic or an anti-inflammatory medication. Activity modification

104

PART 1  MSK Disorders

is recommended. The patient should avoid precipitating activities and strenuous use of the involved extremity. Physical modalities, such as ice massage, superficial moist heat, and ultrasound, can be applied to help with pain control. Ice massage may additionally help control swelling and relieve associated muscle spasm.29 Immobilization should be a part of the initial management to prevent overstretching of the weakened muscle.32 This can be accomplished with the use of a sling to rest the arm until the patient can recover brace-free shoulder flexion or have reduced pain. In one study, this could be anywhere from 1 to 7 months.33 Long-term use of scapular winging shoulder braces to maintain the position of the scapula against the thorax is controversial. Various shoulder braces and orthotics have been used with mixed results. Some authors7,28 recommend against use of shoulder braces because they are cumbersome, poorly tolerated, and ineffective. Others have advocated their use to protect against muscle overstretching and scapulothoracic overuse.29,32 One author reported successful treatment of a brachial plexus injury and winged scapula with use of Kinesio tape and exercise to facilitate the rotator cuff groups and scapular stabilizers.33 

Rehabilitation Specific treatment varies, depending on the etiology of the scapular winging. In general, range of motion exercises should be initiated early to prevent contractures or adhesive capsulitis, especially if the affected extremity is immobilized. A stretching and strengthening exercise program can be undertaken after pain control is achieved.29 Stretching the scapular stabilizers and shoulder capsules without overstretching the weakened muscle as well as cross-body adduction to stretch the rhomboids is important and should be supervised by a physical therapist. The scapular stabilizer, cervical muscles, and rotator cuff muscle should be strengthened, especially the affected muscle groups. This can be accomplished by passive scapular retraction, such as scapular squeeze. Isometric strengthening exercises can include scapular protraction and retraction, shoulder packing, and shoulder shrugs to strengthen the pectoralis, serratus anterior, rhomboids, upper trapezius, and levator scapulae. Advanced exercises can include specific rotator cuff strengthening as well as shoulder circles with a ball against a wall, stabilizing ball pushups, resistance band pullaparts and pull-downs, and chest presses both standing and lying down. Neuromuscular electrical stimulation may be used to prevent muscle atrophy. Functional glenohumeral and scapulothoracic muscle patterns must be relearned. Progression to an independent structured home exercise program is recommended, but the patient should first be able to perform the exercises appropriately under supervision of a physical therapist. 

Procedures Localized injections are not routinely administered for isolated scapular winging. Injection therapy may be indicated for other coexisting shoulder disease to help with pain control. 

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery Conservative treatment has been recommended for a prolonged period (12 to 24 months) to allow adequate time for recovery before surgical options are considered.25,26,34 Surgery should be considered for patients who do not recover in this time. In patients with penetrating trauma in which the nerve may have been injured, spontaneous recovery is less likely, and early nerve exploration with neurolysis, direct nerve repair, or nerve grafting may be indicated. Surgery may also be indicated if scapular winging appears to have been caused by a surgically treatable lesion (e.g., a subscapular osteochondroma) and the patient is symptomatic or has a cosmetic disfigurement.21,35 In general, surgical options are many but can be divided into two categories: static stabilization procedures and dynamic muscle transfers. Static stabilization procedures involve scapulothoracic fusion and scapulothoracic arthrodesis in which the scapula is fused to the thorax. These procedures may be effective in cases of generalized weakness (e.g., facioscapulohumeral muscular dystrophy) when the patient has disabling pain and functional loss and no transferable muscles.29,34,36,37 They can relieve shoulder fatigue and pain and allow functional abduction and flexion of the upper extremity.12,36 Static stabilization procedures have fallen out of favor for scapular winging related to isolated muscle weakness because the results deteriorate over time with recurrence of winging. The usual incidence of complications associated with some of these procedures is high.29,36 Dynamic muscle transfers have shown better results for correction of scapular winging and restoration of function. Several different muscles have been used in various muscle transfer techniques to provide dynamic control of the scapula and to improve scapulothoracic and glenohumeral motion. Transfer of the sternal head of the pectoralis major muscle to the inferior angle of the scapula with fascia lata autograft reinforcement is the preferred method of treatment for scapular winging related to LTN injury.29,34,38 The surgical procedure of choice for scapular winging related to chronic trapezius muscle dysfunction involves the lateral transfer of the insertions of the levator scapulae and the rhomboid major and minor muscles. This procedure enables the muscles to support the shoulder girdle and to stabilize the scapula.26,29,34 

Potential Disease Complications Disease complications are usually related to scapulothoracic dysfunction as a result of scapular winging. This can contribute to glenohumeral instability and subsequent shoulder range of motion and functional deficits as well as chronic periscapular, upper back, and shoulder pain. Secondary impingement syndromes can result from the muscle dysfunction. Adhesive capsulitis can occur from loss of shoulder mobility and function. Cosmetic deformity is a common result of scapular winging, especially if there is a combined serratus anterior and trapezius muscle weakness. 

CHAPTER 18  Scapular Winging

Potential Treatment Complications Pharmacotherapy can lead to treatment complications. Nonsteroidal anti-inflammatory drugs have well-­ documented adverse effects that most commonly involve the gastrointestinal system. Analgesics may have adverse effects that predominantly involve the hepatorenal system. These complications can be minimized by having a working knowledge of the patient’s ongoing medical problems, current medications, and potential drug interactions. Local injections may cause allergic reactions, infection at the injection site, and, rarely, sepsis. Tendon rupture is a potential complication if inadvertent injection into a tendon occurs. Surgical complications are numerous and include a large, cosmetically unpleasant incision over the shoulder and upper back, postoperative musculoskeletal deformities (e.g., scoliosis), infection, pulmonary complications (e.g., pneumothorax and hemothorax), hardware failure, pseudarthrosis, recurrent winging, and persistent pain.

References 1.  Fiddian NJ, King RJ. The winged scapula. Clin Orthop Relat Res. 1984;185:228–236. 2. Oakes MJ, Sherwood DL. An isolated long thoracic nerve injury in a Navy airman. Mil Med. 2004;169:713–715. 3. Aksoy IA, Schrader SL, Ali MS, et al. Spinal accessory neuropathy associated with deep tissue massage: a case report. J Athl Train. 2009;44:519–526. 4. Parsonage MJ, Turner JW. Neuralgic amyotrophy: the shoulder-girdle syndrome. Lancet. 1948;251:973–978. 5. Lee SG, Kim JH, Lee SY, et al. Winged scapula caused by rhomboideus and trapezius muscles rupture associated with repetitive minor trauma: a case report. J Korean Med Sci. 2006;21:581–584. 6. Bodack MP, Tunkel RS, Marini SG, et al. Spinal accessory nerve palsy as a cause of pain after whiplash injury: case report. J Pain Symptom Manage. 1998;15:321–328. 7. Schultz JS, Leonard JA Jr. Long thoracic neuropathy from athletic activity. Arch Phys Med Rehabil. 1992;73:87–90. 8. Salah S, Migaou H, Belaaj Z, et al. The winged scapula; a muscle rupture or a nerve paralysis? A case series. Ann Phys Rehabil Med. 2016. 59S:e114–e115. 9. Sherman SC, O’Connor M. An unusual cause of shoulder pain: winged scapula. J Emerg Med. 2005;28:329–331. 10. Marsha M, Middleton A, Rangan A. An unusual cause of scapular winging following trauma in an army personnel. J Shoulder Elbow Surg. 2010;19:24–27. 11. Bowen TR, Miller F. Greenstick fracture of the scapula: a cause of scapular winging. J Orthop Trauma. 2006;20:147–149. 12. Rhee YG, Ha JH. Long-term results of scapulothoracic arthrodesis of facioscapulohumeral muscular dystrophy. J Shoulder Elbow Surg. 2006;15:445–450. 13. Argyriou AA, Karanasios P, Makridou A, et al. Dorsal scapular neuropathy causing rhomboid palsy and scapular winging. Jback Musculoskeletal Rehabil. 2015;28(4):883–885. 14. Sivan M, Hasan A. Images in emergency medicine: winged scapula as the presenting symptom of Guillain-Barré syndrome. Emerg Med J. 2009;26:790. 15. Witt RL, Gillis T, Pratt R Jr. Spinal accessory nerve monitoring with clinical outcome measures. Ear Nose Throat J. 2006;85:540–544.

105

16. Wood VE, Frykman GK. Winging of the scapula as a complication of first rib resection: a report of six cases. Clin Orthop Relat Res. 1980;149:160–163. 17. Ameri E, Behtash H, Omidi-Kashani F. Isolated long thoracic nerve paralysis—a rare complication of anterior spinal surgery: a case report. J Med Case Rep. 2009;3:7366. 18. Debeer P, Devlieger R, Brys P, et al. Scapular winging after vaginal delivery. BJOG. 2004;111:758–759. 19. Niedermaier N, Meinck HM, Hartmann M. Cervical syringomyelia at the C7-C8 level presenting with bilateral scapular winging. J Neurol Neurosurg Psychiatry. 2000;68:394–395. 20. Tittal P, Pawar I, Kapoor SK. Pseudo-winging of scapula due to benign lesions of ventral surface of scapula- two unusual causes. J Clin Orthop Trauma. 2015;6(1):30–35. 21. Frost NL, Parada SA, Manoso MW, et al. Scapula osteochondromas treated with surgical excision. Orthopedics. 2010;33:804. 22. Flugstad NA, Sanger JR, Hackbarth DA. Pseudo-winging of the scapula caused by scapular osteochondroma: review of literature and case report. Hand (NY). 2015;10(2):353–356. 23. Scott DA, Alexander JR. Relapsing and remitting scapular winging in a pediatric patient. Am J Phys Med Rehabil. 2010;89:505–508. 24. Symes A, Ellis H. Variations in the surface anatomy of the spinal accessory nerve in the posterior triangle. Surg Radiol Anat. 2005;27:404–408. 25. Srikumaran U, Wells JH, Freehill MT, et al. Scapular winging: a great masquerader of shoulder disorders: AAOS exhibit selection. J Bone Joint Surg Am. 2014;96(14):e122. 26. Wiater JM, Bigliani LU. Spinal accessory nerve injury. Clin Orthop Relat Res. 1999;368:5–16. 27. Tsivgoulis G, Vadikolias K, Courcoutsakis N, et al. Teaching neuroimages: differential diagnosis of scapular winging. Neurology. 2012;78:e109. 28. Warner JJ, Navarro RA. Serratus anterior dysfunction: recognition and treatment. Clin Orthop Relat Res. 1998;349:139–148. 29. Meninger AK, Figuerres BF, Goldberg BA. Scapular winging: an update. J Am Acad Orthop Surg. 2011;19:453–462. 30. Khadilkar SV, Chaudhari CR, Soni G, et al. Is pushing the wall, the best known method for scapular winging, really the best? A comparative analysis of various methods in neuromuscular disorders. J Neurol. Sci. 2015;351(1–2):179–183. 31. Lieba-Samal D, Morgenbesser J, Moritz T, et al. Visualization of the long thoracic nerve using high resolution sonoraphy. Ultraschall Med. 2015;36(3):264–269. 32. Marin R. Scapula winger’s brace: a case series on the management of long thoracic nerve palsy. Arch Phys Med Rehabil. 1998;79:1226–1230. 33. Walsh SF. Treatment of a brachial plexus injury using kinesiotape and exercise. Physiother Theory Pract. 2010;26:490–496. 34. Galano GJ, Bigliani MD, Ahmad CS, Levine WN. Surgical treatment of winged scapula. Clin Orthop Relat Res. 2008;466:652–660. 35. Ziaee MA, Abolghasemian M, Majd ME. Scapulothoracic arthrodesis for winged scapula due to facioscapulohumeral dystrophy (a new technique). Am J Orthop. 2006;35:311–315. 36. Sewell MD, Higgs DS, Al-Hadithy N, et al. The outcome of scapulothoracic fusion for painful winging of the scapula in dystrophic and non-dystrophic conditions. J Bone Joint Surg Br. 2012;94:1253–1259. 37. Jeon IH, Neumann L, Wallace WA. Scapulothoracic fusion for painful winging of the scapula in nondystrophic patients. J Shoulder Elbow Surg. 2005;14:400–406. 38. Streit JJ, Lenarz CJ, Shishani Y, et al. Pectoralis major tendon transfer for the treatment of scapular winging due to long thoracic nerve palsy. J Shoulder Elbow Surg. 2012;21:685–690. 39. Belville RG, Seupaul RA. Winged scapula in the emergency department: a case report and review. J Emerg Med. 2005;29:279–282. 40. Friedenberg SM, Zimprich T, Harper CM. The natural history of long thoracic and spinal accessory neuropathies. Muscle Nerve. 2002; 25:535–539.

CHAPTER 19

Shoulder Arthritis Michael F. Stretanski, DO, AME

Synonyms Glenohumeral arthritis Osteoarthritis Arthritic frozen shoulder

ICD-10 Codes M19.011 M19.012 M19.019 M19.211 M19.212 M19.219 M12.511 M12.512 M12.519 M12.811 M12.812 M12.819

Primary osteoarthritis, right shoulder Primary osteoarthritis, left shoulder Primary osteoarthritis, unspecified shoulder Secondary osteoarthritis, right shoulder Secondary osteoarthritis, left shoulder Secondary osteoarthritis, unspecified shoulder Traumatic arthropathy, right shoulder Traumatic arthropathy, left shoulder Traumatic arthropathy, unspecified shoulder Other specified arthropathies, not elsewhere classified, right shoulder Other specified arthropathies, not elsewhere classified, left shoulder Other specified arthropathies, not elsewhere classified, unspecified shoulder

Definition Osteoarthritis of the glenohumeral joint occurs when there is loss of articular cartilage that results in narrowing of the joint space (Fig. 19.1). Synovitis and osteocartilaginous loose bodies are commonly associated with glenohumeral arthritis. Pathologic distortion of the articular surfaces of the humeral head and glenoid can be due to increasing age, overuse, heredity, or alcoholism. Chronic oral exogenous glucocorticoids account for about 10% of arthroplasties performed annually in the United States; variation exists among practitioners as to what doses are considered 106

“high dose.” Other causation such as intravenous drug use, trauma, Gaucher disease (lipid storage disease), and metabolic disease of bone may also play a role. It is worth noting that the epidemic of intravenous drug use, especially heroin, has resulted in a higher incidence of femoral avascular necrosis (AVN) and while humeral head AVN is not as widely reported, it is certainly a documented etiology.1 In looking at glenohumeral arthritic conditions, one must consider osteonecrosis both as an etiologic entity and as a related endpoint to the disease. Most of the information about osteonecrosis of the humeral head is extrapolated from the research findings of the disorder of the hip.1 The major difference between osteonecrosis of the hip versus the humeral head is that the shoulder bears less weight than the hip. Risk factors are corticosteroid use, radiation therapy, and sickle cell anemia, but its presence in a medically uncomplicated adolescent competitive swimmer2 does seem to suggest that it may be more complex interaction between event and genetic predisposition than previously thought. Shoulder osteoarthritis is most commonly seen beyond the fifth decade and is more common in men. Long-standing complete rotator cuff tears, multidirectional instability from any cause, lymphoma3 (chronic lymphocytic lymphoma or immunocytoma), or prior capsulorrhaphy for anterior instability4 can predispose to glenohumeral arthritis. Acute septic arthritis should not be heedlessly ruled out in the face of severe osteoarthritis,5 especially with a history of intravenous drug use. The medical history should include any history of fracture, dislocation, rotator cuff tear, repetitive motion, metabolic disorder, immunosuppression, chronic glucocorticoid administration, and prior shoulder surgery. 

Symptoms Symptoms include shoulder pain intensified by activity and partially relieved with rest. Pain is usually noted with all shoulder movements. Major restriction of shoulder motion and disuse weakness or pain inhibitory weakness are common and potentially progressive. Resultant adhesive capsulitis may be the primary clinical presentation. Pain is typically restricted to the area of the shoulder and may be felt around the deltoid region, but not typically into the forearm. The pain is generally characterized as dull and aching; however, it may become sharp at the extremes of range of motion and is typically worse in the supine position if attempting to sleep on the arthritic side. Pain may interfere with the sleep-wake cycle and may be worse in the morning, as with all arthritic complaints. Neurologic symptoms, such as numbness and paresthesias, should be absent. 

CHAPTER 19  Shoulder Arthritis

107

FIG. 19.2  Radiograph typical of glenohumeral osteoarthritis.

FIG. 19.1  Osteoarthritis of the shoulder.

Physical Examination Restriction of shoulder range of motion is a major clinical component, especially loss of external rotation and abduction. Both active and passive range of motion is affected in shoulder arthritis, compared to only active motion in rotator cuff tears (passive range is normal in rotator cuff injuries unless adhesive capsulitis is present). Pain increases when the extremes of the restricted motion are reached, and crepitus is common with movement. Tenderness may be present over the anterior rotator cuff and over the posterior joint line. Several well-described tests for examination of the shoulder are commonly used in clinical practice (e.g., Neer, Hawkins-Kennedy, Yergason, painful arc, and compressionrotation test). Pooled sensitivity and specificity range from 53% to 95%, yet meta-analysis has demonstrated that use of any single shoulder examination test to make a diagnosis cannot be unequivocally recommended. Combinations of tests performed by experienced clinicians provide better accuracy, but marginally so. As with all musculoskeletal complaints, the physical exam should be approached in a systematic fashion based on functional, not just regional, complaints. Beginning with observation (e.g., winging, skin atrophy), palpations, neurosensory, active, and passive range of motion, motor, and special tests (apprehension, acromioclavicular shear, Yergason, drop-arm, etc.).6 If acromioclavicular joint osteoarthritis is an accompanying problem, the acromioclavicular joint may be tender. There may be wasting of the muscles surrounding the shoulder because of disuse atrophy. Sensation and deep tendon reflexes should be normal. In patients with inconsistent physical examination findings and questionable secondary gain issues, the American Shoulder and Elbow Surgeons subjective shoulder scale has demonstrated acceptable psychometric performance for outcomes assessment in patients with shoulder instability, rotator cuff disease, and glenohumeral arthritis.7 Additional scoring systems, such as the Hospital for Special Surgery score and the validated Western Ontario Osteoarthritis of the Shoulder Index, may be of clinical or research utility.8 

Functional Limitations The shoulder is richly innervated, so patients may complain of severe pain that limits functional activities. Any activities that require upper extremity strength, endurance, and flexibility can be affected. Most commonly, activities that require reaching overhead in external rotation are limited. These include activities of daily living (such as brushing hair or teeth, donning or doffing upper torso clothes) and activities such as throwing or reaching for items overhead. As with any chronic pain syndrome, sleep may be interrupted; sleep-wake cycle disruption may occur, which affects sleep architecture and hormonal cycles. Situational reactive depression is common. This may lead to amotivational syndromes, poor therapy response, exaggerated pain behaviors, and an overall poor clinical outcome even with good surgical results. 

Diagnostic Studies Routine shoulder radiographs with four views (anteroposterior internal and external rotation, axillary, and scapular Y) are generally sufficient for evaluating loss of articular cartilage and glenohumeral joint space narrowing (Fig. 19.2). Varying degrees of flattening of the humeral head, marginal osteophytes, calcific tendinitis, subchondral cysts in the humeral head and glenoid, sclerotic bone, bone erosion, and humeral head migration may be seen. Specifically, if there is a chronic rotator cuff tear that is contributing to the destruction of the articular cartilage, the humeral head will be seen pressing against the undersurface of the acromion. Associated acromioclavicular joint arthritis can be seen on the anteroposterior view. Conventional magnetic resonance imaging (MRI) is the “gold standard” to assess soft tissues for rotator cuff tear. However, comparison of three-dimensional MRI osseous models have been shown to be statistically equivalent to threedimensional computed tomography (CT),9 suggesting the more economical of the two may be adequate in clinical practice. When more sensitive evaluation of the labrum, capsule, articular cartilage, and glenohumeral ligaments is required or when a partialthickness rotator cuff tear is suspected, magnetic resonance arthrography with intra-articular administration of contrast material may be required to visualize subtle findings. Paralabral cysts (extraneural ganglia), which can result in posterior labral capsular complex tears and cause suprascapular nerve compression, have only been shown to be visualized on MRI.10

108

PART 1  MSK Disorders

CT may have a unique role in finding posterior humeral head subluxation relative to the glenoid in the absence of posterior glenoid erosion.11 A rise in popularity of diagnostic ultrasonography in musculoskeletal medicine is undeniable. The modality may play a role in the diagnosis of full-thickness rotator cuff tear in experienced hands, but significant inter-rater reliability has been called into question,12,13 and diagnostic ultrasonography would play a minimal role in the diagnosis of glenohumeral arthritic conditions. Electrodiagnostic studies help rule out neurologic conditions (e.g., cervical radiculopathy, axillary neuropathy). The sensory irritative component of spinal or peripheral nerve irritation will usually yield a normal result, but H reflexes to median nerve stimulation at the level of the elbow may be suggestive of C5-C6 radiculitis, whereas findings on needle electromyography would be normal. Complete blood counts, coagulation profile, erythrocyte sedimentation rate, and blood cultures may be in order. In addition, the author encourages that any woman with shoulder pain recalcitrant to seemingly appropriate treatment be considered for mammography.  Differential Diagnosis Rotator cuff disease Synovitis Cervical osteoarthritis Shoulder instability Rheumatoid arthritis Cervical radiculopathy Labral degeneration and tear Pseudogout Charcot joint Biceps tendon abnormalities Infection Fracture of the humerus Adhesive capsulitis Parsonage-Turner syndrome Neoplasms Leukemic arthritis Avascular necrosis

Treatment Initial Shoulder arthritis is a chronic condition, but acute exacerbations in pain can be managed conservatively. Nonsteroidal anti-inflammatory drugs or analgesic medications can help with pain and enable rehabilitation. Capsaicin cream, lidocaine patches, ice, or moist heat may be used topically as needed. Gentle stretching exercises help maintain the range of motion and prevent secondary adhesive capsulitis and sequelae of immobility. 

Rehabilitation The shoulder is a complicated structure composed of several joints with both static and dynamic stabilizers that tend to function, and fail, as a unit. A well-designed rehabilitation program must take this into account and treat glenohumeral arthritic conditions within this context. The rehabilitative efforts are dedicated to the restoration of

strength, endurance, and flexibility of the shoulder musculature. Physical or occupational therapy should focus on the upper thoracic, neck, and scapular muscle groups, but address the entire upper extremity kinetic chain, including the rotator cuff, arm, forearm, wrist, and hand. Patients benefit from aquatic therapy and can easily be taught exercises and then transitioned to an independent pool exercise program. In cases of severe rheumatoid arthritis, joint-sparing static exercises may prevent atrophy and maintain strength of dynamic stabilizers of the shoulder without placing undue stress on the remaining articular surfaces. Joint-sparing exercises such as isometric contraction within normal range of motion will strengthen shoulder stabilizers, minimize joint damage, and decrease induction of the inflammatory cascade that often drives arthritic patients to seek health care. The success of flexibility exercises will be determined by the extent of mechanical bone blockade, which in turn is determined by the magnitude of glenohumeral incongruous distortion, presence of loose bodies, and osteophyte formation. Pain control can be assisted with modalities such as ultrasound and iontophoresis, and pre-therapy suprascapular local anesthetic block. Electrical stimulation may have a limited role in posterior shoulder strengthening in patients with poor posture and “rounded shoulders” on examination, but it should not take the place of volitional contraction and not be used routinely across arthritic joints. Although surgical techniques and interventional treatment have progressed, the consensus14 on glenohumeral involvement in rheumatoid arthritis is still that narrowing of the joint space is a turning point indicating a risk of rapid joint destruction, and surgical interventions should be considered before musculoskeletal sequelae are too severe to enable adequate recovery. Postoperative care, depending on the operative intervention, should focus on maintenance of functional range of motion and prevention of adhesive capsulitis, but be balanced with avoidance of dislocation or damage to the repaired labrum or rotator cuff. Patients should undergo preoperative education to understand that postoperative range of motion will be considerably less than in the healthy shoulder. Suprascapular nerve block may have a role in helping the patient tolerate postoperative therapies such as range of motion, but great care should be exercised in handling of the joint. In caring for arthroplasty patients, the Neer protocol for postoperative total shoulder arthroplasty (TSA) rehabilitation is still widely used.15 

Procedures If therapies fail or are impossible because of pain, the patient has several options. Periarticular injections may offer some help to control pain of associated problems, such as subacromial bursitis and rotator cuff tendinopathy. Wide variations exist in local anesthetic doses and techniques; however, steroid dosing does not vary as widely, with methylprednisolone acetate and triamcinolone acetonide being the most commonly used agents. Intra-articular glenohumeral joint injections may also afford some pain relief; however, common dogma is that it may increase joint laxity and seldom has a therapeutic role. The accuracy of intra-articular injections without fluoroscopic guidance is less than perfect at 80%, with the anterior approach being slightly

CHAPTER 19  Shoulder Arthritis

109

Lateral Clavicle Acromion

Anterior

Humerus Glenohumeral injection FIG. 19.3 Approximate surface anatomy (insets) and internal anatomic sites for injection of the glenohumeral joint laterally and anteriorly. (From Lennard TA. Physiatric Procedures in Clinical Practice. Philadelphia, 1995, Hanley & Belfus.)

more accurate than the posterior approach at 50%.16 Injections have not been shown to alter the underlying arthritis pathoanatomy (Fig. 19.3). Great care should be taken in anticoagulated or immunosuppressed patients. Viscosupplementation (Hylan G-F 20) is not approved by the Food and Drug Administration for the glenohumeral joint, but may have an empiric role in comprehensive care of mild osteoarthritis, as has intra-articular phenol lavage, and spinal cord stimulation with leads in the posterior cervical space. The initial setup can be identical for either intra-articular glenohumeral or subacromial injection. With the patient seated with the arm either in the lap or hanging down by the side, the internal rotation and gravity pull of the arm will open the space, leading to the glenohumeral joint or subacromial space. Several approaches have been described. Most commonly for a subacromial injection, the skin entry point is 1 cm inferior to the acromion, and the needle is tracked anteriorly at a lateral-to-medial 45-degree angle in the axial plane and slightly superior (under the acromion). The injectate should flow with minimal resistance into this potential space. If resistance is encountered, the needle should be repositioned to avoid intratendinous injection, which can increase the risk of tendon rupture. For glenohumeral injection, a more inferior and medial approach is used (Fig. 19.4). Post injection care includes awareness of the local anesthetic effects and avoidance of impingement or maneuvers at end range of motion. Patients are cautioned to avoid aggressive activities for the first few days after the injection. If adhesive capsulitis is specifically being treated, a suprascapular nerve block with 5 to 10 mL of 0.25% bupivacaine (Marcaine) with or without epinephrine can be performed immediately before physical therapy appointments to facilitate ROM. Great care is taken in using appropriately trained therapists who are aware of the safe handling of such an anesthetized joint and focus on functionally important range of motion pertinent to accomplishing activities of daily living. Post therapy analgesics may be required. Pulsed radiofrequency of the suprascapular nerve is a simple office-based procedure, and while one study shows a limited 12-week response17 this may be due to use of this technique in isolation rather than as part of a comprehensive rehabilitation and pain program.

FIG. 19.4  Combined subacromial and suprascapular injection. The site is marked for intra-articular glenohumeral injection.

If unacceptable symptoms persist despite conservative treatment, the patient may decide to reduce his or her activity level to minimize pain or proceed with one of several surgical interventions. It is important to inform the patient that with osteoarthritis, regardless of the treatment approach, a return to normal shoulder function, by either rehabilitation or surgery, is not possible. However, pain control and some increased function over preoperative status are usually achievable. 

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery Surgical options include débridement of the glenohumeral joint by open or arthroscopic techniques and hemiarthroplasty or TSA. If reasonable congruity between the humeral head and glenoid is present, good improvement in pain control and some functional improvement can be anticipated with débridement, even in the presence of severe chondromalacia. The glenoid may be amenable to arthroscopic resurfacing with a meniscal allograft.18 Other biologic surfaces include anterior capsule, fascia lata autograft, Achilles tendon allograft, and cartilage-preserving arthroscopic spongioplasty.19 However, inconsistent results and high complication rates are seen, and a trend toward arthroplasty is occurring. Other arthroscopic techniques are successful, provided osteophytes and loose bodies are removed (Fig. 19.5).20 Surgical outcome reporting shows considerable variation between surgical approaches. For example, one particular system had 32 complications in 25 shoulders, with no bilateral complications. Seven shoulders had multiple complications, of which many were not independent events,22 thus making outcome data difficult to interpret. Hemiarthroplasty has considerably higher return-towork rates than TSA and may be indicated in the absence of advanced glenohumeral disease if the glenoid can at least be converted to a smooth concentric surface.21 Shoulder

110

PART 1  MSK Disorders

with sleep, inability to perform work and recreational activities, and reactive depression. Reflex sympathetic dystrophy, isolated nerve injury, or brachial plexopathy may result. 

Potential Treatment Complications

FIG. 19.5 Arthroscopic surgical view of osteoarthritis.

arthroplasty volumes and rates have increased in recent years with both hemiarthroplasty and TSA being successful in the medium term for different glenohumeral diseases across a range of patient ages.23 Hemiarthroplasty may be more appropriate for cuff tear arthroplasties in the elderly with comorbidities. Cuff tear arthroplasty shoulder hemiarthroplasty is a good option for rotator cuff arthropathy in patients with comorbidities and has specifically been suggested as the procedure of choice in moderate to severe glenohumeral arthritis and irreparable rotator cuff tears24; it may have other indications in AVN, glenohumeral chondrolysis, tumor, proximal humeral fracture,25 or complete deltoid denervation with subluxation and secondary osteoarthritis. If major incongruity is present between the humeral head and glenoid, TSA may be indicated.26 While concomitant biceps tenodesis is often performed, and is widely felt to result in better outcomes for shoulder arthroplasty. Recent polymerase chain reaction analysis of harvested long head biceps tendons suggests changes are on the horizon in terms of our comprehension of the role that tendon plays in the arthroplasty population.27 Although it may seem counterintuitive, proprioception improves after TSA over pre-arthroplasty measurements.28 This is important from the standpoint of activities of daily life in osteoarthritic patients. Although a greater risk of more advanced glenohumeral arthritis is associated with arthroscopic procedures that result in limited external rotation,29 arthrodesis may be required for irreversible and non-reconstructible massive rotator cuff tears, tumor, and deltoid muscle denervation as well as for detachment of the deltoid from its origin or to stabilize the glenohumeral joint after many failed attempts at shoulder reconstruction.30 Arthrodesis for failed prosthetic arthroplasty or tumor resection presents additional challenges and additional risk of the complications. Thermal capsulorrhaphy has come in and out of favor, seldom performed and based largely on empiric data that is of more a historical point of interest than clinical practice. 

Potential Disease Complications Disease complications include chronic intractable pain and loss of shoulder range of motion. These result in diminished functional ability to use the arm, disuse weakness, difficulty

Analgesics and nonsteroidal anti-inflammatory drugs have well-known side effects that most commonly affect the gastric, hepatic, and renal systems. Infection, hemarthrosis, and allergic reaction to the medications are rare side effects of injections. Clinicians performing musculoskeletal injections of any type need to be aware of the possibility of inadvertent vascular uptake, which may occur despite negative aspiration for blood, as well as negative observation of passive blood into the needle.31 This can have the most serious acute side effects such as seizure and cardiac events. A reported case of subdeltoid septic bursitis and concomitant systemic infusion of isotretinoin (Accutane)32 should suggest caution in any immunosuppressed patient. Fluid retention or transient hyperglycemia may be seen with a single exogenous glucocorticoid injection. Arthroscopic complications are not common at 2.5% (largely cardiac, thrombotic events and pneumonia), with 2.7% 30-day readmission, but the usual possibilities of neurovascular issues have been reported.33 Inflammatory arthritis, male gender, age, low functional status, and Anesthesia class 3/4 were independent predictors for unplanned 30-day postoperative readmission. Arthrodesis complications include nonunion, malposition, pain associated with prominent hardware, development of complex regional pain syndrome, and periarticular fractures. Arthrodesis after cancer reconstruction has a higher risk of complication.29

References 1. Ozkunt O, Sarıyılmaz K, Sungur M, Ilen F, Dikici F. Bilateral avascular necrosis of the femoral head due to the use of heroin: a case report [published online November 11, 2015]. Int J Surg Case Rep. 2015;17:100–102. https://doi.org/10.1016/j.ijscr.2015.10.042. 2. Zuo J, Sano H, Yamamoto N, et al. Humeral head osteonecrosis in an adolescent amateur swimming athlete: a case report. Sports Med Arthrosc Rehabil Ther Tech. 2012;4:39. 3. Braune C, Rittmeister M, Engels K, Kerschbaumer F. Non-Hodgkin lymphoma (immunocytoma) of low malignancy and arthritis of the glenohumeral joint. Z Orthop Ihre Grenzgeb. 2002;140:199–202 [in German]. 4. Green A, Norris TR. Shoulder arthroplasty for advanced glenohumeral arthritis after anterior instability repair. J Shoulder Elbow Surg. 2001;10:539–545. 5. Bagheri F, Ebrahimzadeh MH, Sharifi SR, Ahmadzadeh-Chabok H, Khajah-Mozaffari J, Fattahi AS. Pathologic dislocation of the shoulder secondary to septic arthritis: a case report. Cases J. 2009;2:9131. https://doi.org/10.1186/1757-1626-2-9131. 6. Rothaermel BJ, DeBerardino TM. Shoulder examination. Medscape Article. Dis/Conditions, Proced. 2015. 7. Kocher MS, Horan MP, Briggs KK, et al. Reliability, validity and responsiveness of the American Shoulder and Elbow Surgeons subjective shoulder scale in patients with shoulder instability, rotator cuff disease and glenohumeral arthritis. J Bone Joint Surg Am. 2005;87:2006–2011. 8. Wright RW, Baumgarten KM. Shoulder outcomes measures. J Am Acad Orthop Surg. 2010;18:436–444. 9. Stillwater L, Koenig J, Maycher B, Davidson M. 3D-MR vs. 3D-CT of the shoulder in patients with glenohumeral instability [published online December 27, 2016]. Skeletal Radiol. 2017;46(3):325–331. https://doi.org/10.1007/s00256-016-2559-4. 10. Spinner RJ, Amrami KK, Kliot M, et al. Suprascapular intraneural ganglia and glenohumeral joint connections. J Neurosurg. 2006;104:551–557. 11. Walch G, Ascani C, Boulahia A, et al. Static posterior subluxation of the humeral head: an unrecognized entity responsible for glenohumeral osteoarthritis in the young adult. J Shoulder Elbow Surg. 2002;11:309–314.

CHAPTER 19  Shoulder Arthritis

12. Naredo E, Miller I, Moragues C, et al. Interobserver reliability in musculoskeletal ultrasonography: results from a “Teach the Teachers” rheumatologist course. Ann Rheum Dis. 2006;65:14–19. 13. O’Connor PJ, Rankine J, Gibbon WW, et al. Interobserver variation in sonography of the painful shoulder. J Clin Ultrasound. 2005;33:53–56. 14. Thomas T, Nol E, Goupille P, et al. The rheumatoid shoulder: current consensus on diagnosis and treatment. Joint Bone Spine. 2006;73:139–143. 15. Wilcox RB, Arslanian LE, Millett P. Rehabilitation following total shoulder arthroplasty. J Orthop Sports Phys Ther. 2005;35:821–836. 16. Sethi PM, El Attrache N. Accuracy of intra-articular injection of the glenohumeral joint: a cadaveric study. Orthopedics. 2006;29:149–152. 17. Liu A, Zhang W, Sun M, Ma C, Yan S. Evidence-based status of pulsed radiofrequency treatment for patients with shoulder pain: a systematic review of randomized controlled trials. Pain Pract. 2016;16:518–525. https://doi.org/10.1111/papr.12310. 18. Lee BK, Vaishnav S, Rick Hatch GF 3rd, Itamura JM. Biologic resurfacing of the glenoid with meniscal allograft: long-term results with minimum 2-year follow-up. J Shoulder Elbow Surg. 2013;22:253–260. 19. Heid A, Dickschas J, Schoeffl V. Cortisone-induced humerus head necrosis in acute myeloid leukemia: cartilage-preserving arthroscopic spongioplasty. Unfallchirurg. 2013;116:180–184 [in German]. 20. Nirschl RP. Arthroscopy in the treatment of glenohumeral osteoarthritis. Presented to the Brazilian Congress of Upper Extremity Surgeons. Brazil: Belo Horizonte; 2000. 21. Hurwit DJ, Liu JN, Garcia GH, et al. A comparative analysis of work-related outcomes after humeral hemiarthroplasty and reverse total shoulder arthroplasty. J Shoulder Elbow Surg. 2017. https://doi. org/10.1016/j.jse.2016.10.004. pii: S1058–2746(16)30535-3. 22. Wright TW, Flurin PH, Crosby L, et al. Total shoulder arthroplasty outcome for treatment of osteoarthritis: a multicenter study using a contemporary implant. Am J Orthop. 2015;44(11):523–526. 23. Sowa B, Thierjung H, Bülhoff M, et al. Functional results of hemi- and total shoulder arthroplasty according to diagnosis and patient age at surgery. Acta Orthop. 2017:1–5. https://doi.org/10.1080/17453674.2017.1280656.

111

24. Laudicina L, D’Ambrosia R. Management of irreparable rotator cuff tears and glenohumeral arthritis. Orthopaedics. 2005;28:382–388. 25. Kancherla VK, Singh A, Anakwenze OA. Management of acute proximal humeral fractures. J Am Acad Orthop Surg. 2017;25(1):42–52. https://doi.org/10.5435/JAAOS-D-15-00240. 26. Lombardo DJ, Khan J, Prey B, Zhang L, Petersen-Fitts GR, Sabesan VJ. Quantitative assessment and characterization of glenoid bone loss in a spectrum of patients with glenohumeral osteoarthritis. Musculoskelet Surg. 2016;100(3):179–185. 27. Kurdziel MD, Moravek JE, Wiater BP, et al. The impact of rotator cuff deficiency on structure, mechanical properties, and gene expression profiles of the long head of the biceps tendon (LHBT): implications for management of the LHBT during primary shoulder arthroplasty [published online May 13, 2015]. J Orthop Res. 2015;33(8):1158–1164. https://doi.org/10.1002/jor.22895. 28. Cuoma F, Birdzell MG, Zuckerman JD. The effect of degenerative arthritis and prosthetic arthroplasty on shoulder proprioception. J Shoulder Elbow Surg. 2005;14:345–348. 29. Brophy RH, Marx RG. Osteoarthritis following shoulder instability. Clin Sports Med. 2005;24:47–56. 30. Safran O, Iannotti JP. Arthrodesis of the shoulder. J Am Acad Orthop Surg. 2006;14:145–153. 31. Stretanski MF, Chopko B. Unintentional vascular uptake in fluoroscopically guided, contrast-confirmed spinal injections: a 1-yr clinical experience and discussion of findings. Am J Phys Med Rehabil. 2005;84(1):30–35. 32. Drezner JA, Sennett BJ. Subacromial/subdeltoid septic bursitis associated with isotretinoin therapy and corticosteroid injection. J Am Board Fam Pract. 2004;17:299–302. 33. Lovy AJ, Keswani A, Beck C, Dowdell JE, Parsons BO. Risk factors for and timing of adverse events after total shoulder arthroplasty. J Shoulder Elbow Surg. 2017. https://doi.org/10.1016/j.jse.2016.10.019. pii: S1058–2746(16)30564-X.

CHAPTER 20

Suprascapular Neuropathy Ryan Hubbard, MD Jonathan T. Finnoff, DO

Synonyms Infraspinatus syndrome Volleyball shoulder Neurogenic shoulder pain Suprascapular nerve rotator cuff compression syndrome

ICD-10 Codes G56.80 Other mononeuritis of unspecified upper limb G56.81 Other mononeuritis of right upper limb G56.82 Other mononeuritis of left upper limb G56.90 Unspecified mononeuritis of unspecified upper limb G56.91 Unspecified mononeuritis of right upper limb G56.92 Unspecified mononeuritis of left upper limb

Definition Suprascapular neuropathy (SN) is defined as a demyelinating or axonal injury to the suprascapular nerve. Once considered a diagnosis of exclusion, SN is now becoming a well-recognized condition stemming from traction or compression of the nerve at some point along its course. Epidemiologic data is limited, but the prevalence of SN in overhead athletes is reportedly between 12% and 33%, and 8% to 100% in patients with massive rotator cuff tears.1-3 To understand the pathophysiology, it is imperative to have a good knowledge of the anatomy (Fig. 20.1). The suprascapular nerve arises from the upper trunk of the brachial plexus and receives contributions mainly from the fifth and sixth cervical nerve roots, with variable contribution from the fourth cervical nerve root. It courses posterolaterally, deep to the trapezius and clavicle, on its way to the suprascapular notch. Here, it passes beneath the superior transverse scapular ligament (STSL), which connects the two borders of the suprascapular notch, to enter the supraspinous fossa.4 112

In 18% to 60% of the population, the anterior coracoscapular ligament (ACSL) lies deep within the anterior portion of the suprascapular notch. Commonly, the suprascapular nerve and vein pass together superior to the ACSL and inferior to the STSL within the suprascapular notch, with the suprascapular artery passing above the STSL.4-7 Within the supraspinous fossa, the suprascapular nerve sends two motor branches to the supraspinatus muscle and receives sensory branches from multiple surrounding structures, including the posterior aspect of the glenohumeral joint, the acromioclavicular joint, the subacromial bursa, the coracohumeral and coracoacromial ligaments, and the overlying skin.8 The nerve then courses inferolaterally around the lateral aspect of the scapular spine. This region is referred to as the spinoglenoid notch, and is a common area of suprascapular nerve compression. Finally, the nerve enters the infraspinous fossa where its terminal motor branches innervate the infraspinatus muscle. The indirect course of the nerve, as well as its passage through two notches, makes it particularly vulnerable to injury. Static forms of compression or traction can stem from anatomic variations, particularly at the suprascapular notch where the STSL or ACSL can hypertrophy or ossify.4,6 Risk of SN is also increased with variations of the suprascapular region such as a bifid or trifid STSL, ACSL, or a small, narrow or shallow suprascapular notch.7,9,10 At the spinoglenoid notch, compression is most frequently due to a space occupying paralabral cyst that develops as a result of a labral tear, and less often from a benign tumor (e.g., lipoma) or hypertrophied spinoglenoid (inferior transverse scapular) ligament.1,2,11 Dynamic forms of SN are often seen in overhead athletes due to tightening of the spinoglenoid ligament during the overhead motion.12 This leads to the so-called “infraspinatus syndrome” since only the infraspinatus is affected. In addition, repetitive overhead movements may lead to muscle and tendon microtrauma (the “sling effect”), causing nerve inflammation and compression. This is most apparent in volleyball players, overhead pitchers, weight lifters, and those who do repetitive overhead motions for their occupation.2,9,13 Less commonly, SN may result from shoulder girdle trauma, glenohumeral joint dislocation, brachial neuritis, iatrogenic injury as a complication of surgery, or large rotator cuff tears.2,3,12,14,15 Three-dimensional mapping of operatively treated scapular fractures has shown extension of the fracture to the spinoglenoid notch in 22% of patients.5 

CHAPTER 20  Suprascapular Neuropathy

Suprascapular nerve and artery

Suprascapular notch and ligament Spinoglenoid notch

113

may demonstrate weakness in abduction or external rotation.4 Weakness may be subtle due to compensatory muscle action. Other special tests should be performed to evaluate for labral pathology, given its association with spinoglenoid notch cysts that can compress the suprascapular nerve. The examiner should also perform a thorough upper extremity neurovascular examination and evaluate the cervical spine and contralateral shoulder. 

Functional Limitations

FIG. 20.1  Posterior view of the scapula demonstrating the course of the suprascapular nerve through the suprascapular and spinoglenoid notches.

Symptoms A range of symptoms may be associated with SN. Patients’ complaints are often similar to those seen with other pathology about the shoulder, including pain, weakness, paresthesia, decreased range of motion, or functional impairment.2 Some patients, however, may present only after recognizing painless atrophy of the scapular musculature.2 SN is therefore difficult to diagnose based on history alone. The pain, when present, can be poorly localized but is often located along the posterolateral shoulder and described as a deep, dull, and burning ache with variable radiation to the arm that is worsened with overhead activity or when sleeping on the affected side.2,4,8 This pain pattern coincides with the diffuse sensory contribution of the suprascapular nerve, as it carries sensory afferents from up to 70% of the shoulder.2,8 For non-traumatic injuries, the onset is typically insidious and night pain is variable. Although less common, trauma can cause SN, and in this case, symptom onset is rapid. Clinicians should have a high index of suspicion in athletes engaged in sports with repetitive overhead motions, particularly volleyball, baseball, tennis, basketball, and swimming. These repetitive overhead motions can lead to suprascapular nerve injury through the previously described mechanism, and can exacerbate symptoms. Furthermore, throwing athletes may experience a decline in throwing velocity or overhead swing (hitting) speed. Athletes may also describe weakness and a sense of fatigue during these activities.8 

Physical Examination A complete physical exam of the shoulder is critical to identify a suprascapular nerve lesion and its underlying etiology. Inspection may demonstrate atrophy in the supraspinatus or infraspinatus fossae.4 Atrophy of the supraspinatus may be difficult to visualize given the bulk of the overlying trapezius. Isolated atrophy of the infraspinatus suggests compression of the nerve at the spinoglenoid notch. Palpation may elicit tenderness along the course of the nerve, particularly at the level of the suprascapular notch, within the supraspinous fossa or at the spinoglenoid notch. The tenderness may be enhanced with horizontal shoulder adduction, which tightens the spinoglenoid ligament. Strength testing

Functional limitations will vary significantly depending on the patient’s activity level. As previously mentioned, overhead athletes may see a decrease in their pitching or throwing velocity or overhead swing speed. Strength deficits are particularly prevalent in volleyball players, where up to 68% have external rotation strength deficits in their hitting arm.16 It should be noted that weakness may be subtle and have limited effect on performance due to compensatory muscle action. In those patients with a proximal neuropathy affecting both the supraspinatus and infraspinatus, functional declines, especially with overhead activities, are more apparent. Non-athletes may have difficulties with overhead activities, such as putting dishes into a high cupboard, or activities that require shoulder external rotation, such as reaching back to put on a jacket. 

Diagnostic Studies A thorough history and physical examination can heighten suspicion for an SN and lead to the initiation of further testing. While standard shoulder radiographs are most often unremarkable, a Stryker notch view can be helpful, as it allows visualization of anatomic variations at the suprascapular notch.8 If bony variations are suspected, three-dimensional computed tomography is helpful to further delineate the anatomy and plan interventions.12 Magnetic resonance imaging allows evaluation of the suprascapular nerve along its course, demonstrating points of tethering or compression. Rotator cuff edema or atrophy may be appreciated, giving a sense of the severity or chronicity of the nerve compression. Magnetic resonance arthrogram is the diagnostic test of choice for labral pathology and will also identify an associated spinoglenoid notch cyst.8,17 Ultrasonography can also identify rotator cuff pathology and paralabral cysts. Electrodiagnostic studies are the gold standard test for confirming the diagnosis of SN and grading the injury severity. A demyelinating injury is suggested by a prolonged distal motor latency when stimulating at Erb’s point and recording over the supraspinatus or infraspinatus on nerve conduction studies. Decreased compound muscle action potential amplitude can be due to conduction block from a demyelinating injury or may represent an axonal injury. Demyelinating and axonal injuries can be differentiated with needle electromyography (EMG). The presence of fibrillation potentials, positive sharp waves, increased motor unit amplitude, duration, and polyphasia, and a decreased recruitment pattern on needle EMG suggest the presence of an axonal injury.2,8,18 A diagnostic suprascapular nerve block can also assist with diagnosing this disorder. The nerve block should be performed with ultrasound or fluoroscopic guidance to ensure

114

PART 1  MSK Disorders

accuracy, with ultrasound-guided injections providing the highest percentage of favorable outcomes.19 Temporary resolution of the patient’s symptoms in response to a suprascapular nerve block confirms the diagnosis of SN.  Differential Diagnosis Rotator cuff tendinopathy or tear Cervical radiculopathy Cervical disc degeneration Brachial plexopathy Subacromial impingement Labral pathology Parsonage-Turner

Treatment Initial An appropriate workup in order to accurately determine the etiology and location of the suprascapular nerve injury is imperative as treatment strategies will vary depending on the precise location and cause of the pathology. In the absence of an identified space-occupying lesion such as a paralabral cyst, the first line of treatment is non-operative. Patients should be instructed to avoid repetitive overhead activities or other exacerbating arm positions. Nonsteroidal anti-inflammatory drugs (NSAIDs) or acetaminophen as well as passive modalities such as application of heat, cold, or iontophoresis can be used for pain relief. As with most shoulder-related pathologies, physical therapy plays an important role in non-operative management. 

Rehabilitation Physical therapy has been demonstrated to be particularly effective when injury to the nerve is the result of a dynamic process, such as in overhead athletes.2,8 One study reported successfully treating 35 of 38 (92%) of competitive volleyball players with isolated atrophy of the infraspinatus, and although the atrophy remained unchanged at long-term follow-up, the patients were asymptomatic.8,20 Early rehabilitation should focus on flexibility of the scapular protractors and elevators such as the pectoralis minor and superior belly of the trapezius. Strengthening should include the scapular stabilizers, with particular attention to the rhomboideus major and minor, inferior and middle bellies of the trapezius, and serratus anterior. The deltoid and rotator cuff should also be strengthened, with a focus on the external rotators. Proprioceptive exercises improve shoulder stability and neuromuscular control. The exercise program should initially avoid positions of abduction and external rotation, and gradually progress to exercises that enter this range of motion as the patient’s symptoms resolve. The final phase of rehabilitation should incorporate sports-specific training in preparation for return to sports. Upon completion of the final phase of supervised rehabilitation, the patient should be transitioned to a home exercise program in order to maintain their therapeutic gains.8 Failure of 6 to 8 months of non-operative treatment should prompt the clinician to pursue further diagnostic studies or consider surgical options.2,8 

Procedures Procedures for management of SN typically serve a diagnostic purpose or provide temporary palliation. Suprascapular nerve blocks, as previously mentioned, can help to localize the pain source. The suprascapular nerve can be blocked at the suprascapular notch or spinoglenoid notch. Due to the deep location and sensitive nature of the suprascapular nerve, image guidance (e.g., fluoroscopy or ultrasound) should be used when performing a suprascapular nerve block.19 If a patient has a paralabral cyst causing suprascapular nerve compression in the spinoglenoid notch, an ultrasoundguided spinoglenoid notch cyst aspiration can be performed. However, this procedure frequently only provides temporary relief as the underlying pathology leading to the cyst (i.e., glenoid labral tear) is not addressed by this procedure.21 Patients with chronic shoulder pain refractory to other treatments may respond to radiofrequency ablation of the suprascapular nerve.19 

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery In the setting of failed non-operative management, surgical intervention has been shown to provide effective pain relief and restoration of function in most patients.2,22 Optimal surgical timing and approach are ongoing areas of debate. The goal of surgery is direct or indirect decompression of the nerve. For isolated SN, direct decompression can be achieved through open or arthroscopic means. The nerve is released at the suprascapular or spinoglenoid notch, depending on the etiology. Some authors have advocated for routinely releasing both the transverse scapular ligament and spinoglenoid ligament in order to optimize the likelihood of a full neurologic recovery.8,23,24 When underlying pathology, such as a paralabral cyst or rotator cuff tear, is present, debate exists as to whether indirect decompression through addressing the primary pathology is sufficient to alleviate the neuropathy or whether concomitant direct nerve decompression is also necessary.1,8,12,23 Further research is required to answer this question. 

Potential Disease Complications Ongoing compression of the suprascapular nerve may lead to permanent muscle weakness and progressive shoulder dysfunction that is usually not reversible when atrophy is significant.8 Given the role of the supraspinatus and infraspinatus in stabilizing the humeral head within the glenoid, one could speculate that rotator cuff arthropathy would be the end result of long-term SN. It has been suggested that earlier surgical decompression may improve the likelihood for restoration of full muscle strength and normalization of shoulder function.8,19,22 

Potential Treatment Complications Patients who are treated with mild oral analgesics such as acetaminophen and NSAIDs are at risk for complications

CHAPTER 20  Suprascapular Neuropathy

associated with these medications such as liver or renal toxicity, or peptic ulcer disease. Suprascapular nerve blocks can result in direct trauma to the suprascapular nerve. The complex anatomy of the suprascapular nerve places it at risk for injury during any surgical approach. Injuries can include nerve traction or nerve laceration. Ongoing pain, continued muscle atrophy, or recurrence can occur despite attempts at treatment.

References 1. Freehill MT, Shi LL, Tompson JD, et al. Suprascapular neuropathy: diagnosis and management. Phys Sportsmed. 2012;40(1):72–83. 2. Hill LJ, Jelsing EJ, Terry MJ, et al. Evaluation, treatment, and outcomes of suprascapular neuropathy: a 5-year review. PM R. 2014;6:774–780. 3. Ahlawat S, Wadhwa V, Belzberg A, et al. Spectrum of suprascapular nerve lesions: normal and abnormal neuromuscular imaging appearances on 3-T MR neurography. AJR. 2015:204. 4. Polguj M, Jedrzejewski K, Podgorski M, et al. A proposal for classification of the superior transverse scapular ligament: variable morphology and its potential influence on suprascapular nerve entrapment. J Shoulder Elbow Surg. 2013;22:1265–1273. 5. Podgorski M, Sibinski M, Majos A, et al. The suprascapular vein: a possible etiology for suprascapular nerve entrapment and risk of complication during procedures around the suprascapular foramen region. Orthop Traumatol Surg Res. 2014;100:515–519. 6. Polguj M, Jedrzejewski K, Majos A, et al. Coexistence of the suprascapular notch and the suprascapular foramen – a rare anatomical variation and a new hypothesis on its formation based on anatomical and radiological studies. Anat Sci Int. 2013;88:156–162. 7. Podgorski M, Topol M, Sibinski M, et al. New parameters describing morphological variations in the suprascapular notch region as potential predictors of suprascapular nerve entrapment. BMC Musculoskelet Disord. 2014;15:396. 8. Moen TC, Babatunde OM, Hsu SH, et al. Suprascapular neuropathy: what does the literature show? J Shoulder Elbow Surg. 2012;21:835–846. 9. Polguj M, Sibinski M, Grzegorzewski A, et al. Morphological and radiological study of ossified superior transverse scapular ligament as potential risk factor of suprascapular nerve entrapment. BioMed Res Int. 2014:2014. 10. Kumar A, Sharma A, Singh P. Anatomical study of the suprascapular notch: quantitative analysis and clinical considerations for suprascapular nerve entrapment. Singapore Med J. 2014;55(1):41–44.

115

11. Doral M, Huri G, Bohacek I, et al. Extra-articular endoscopy. Sports Med Arthrosc Rev. 2014;24(1):29–33. 12. Plancher KD, Luke TA, Peterson RK, et al. Posterior shoulder pain: a dynamic study of the spinoglenoid ligament and treatment with arthroscopic release of the scapular tunnel. Arthroscopy. 2007;23(9):991–998. 13. Clavert P, Thomazeau H. Peri-articular suprascapular neuropathy. Orthop Traumatol Surg Res. 2014;100S:S409–S411. 14. Massimini DF, Singh A, Wells JH, et al. Suprascapular nerve anatomy during shoulder motion: a cadaveric proof of concept study with implications for neurogenic shoulder pain. J Shoulder Elbow Surg. 2013;22:463–470. 15. Beeler S, Ek E, Gerber C. A comparative analysis of fatty infiltration and muscle atrophy in patients with chronic rotator cuff tears and suprascapular neuropathy. J Shoulder Elbow Surg. 2013;22:1537–1546. 16. Lajtai G, Wieser K, Ofner M, et al. Electromyography and nerve conduction velocity for the evaluation of the infraspinatus muscle and the suprascapular nerve in professional beach volleyball players. Am J Sports Med. 2012;40:2303–2308. 17. Collin P, Treseder T, Ladermann A, et al. Neuropathy of the suprascapular nerve and massive rotator cuff tears: a prospective electromyographic study. J Shoulder Elbow Surg. 2014;23:28–34. 18. Buschbacher RM, Weir SK, Bentley JG, et al. Normal motor nerve conduction studies using surface electrode recording from the supraspinatus, infraspinatus, deltoid, and biceps. PM R. 2009;1(2):101–106. 19. Chang K, Hung C, Wu W, et al. Comparison of the effectiveness of suprascapular nerve block with physical therapy, placebo, and intraarticular injection in management of chronic shoulder pain: a metaanalysis of randomized controlled trials. Arch Phys Med Rehabil. 2016;97:1366–1380. 20. Ferretti A, De Carli A, Fontana M. Injury of the suprascapular nerve at the spinoglenoid notch: the natural history of infraspinatus atrophy in volleyball players. Am J Sports Med. 1998;26:759–763. 21. Bathia N, Malanga G. Ultrasound-guided aspiration and corticosteroid injection in the management of a paralabral ganglion cyst. PM R. 2009;1(11):1041–1044. 22. Shah AA, Butler RB, Sung SY, et al. Clinical outcomes of suprascapular nerve decompression. J Shoulder Elbow Surg. 2011;20(6):975–982. 23. Sandow MJ, Hie J. Suprascapular nerve rotator cuff compression syndrome in volleyball players. J Shoulder Elbow Surg. 1998;7:516–521. 24. Savoie F, Zunkiewicz M, Field L. A comparison of functional outcomes in patients undergoing revision arthroscopic repair of massive rotator cuff tears with and without arthroscopic suprascapular nerve release. Open Access J Sports Med. 2016;7:129–134.

SECTION III

Elbow and Forearm

CHAPTER 21

Elbow Arthritis Dana H. Kotler, MD Christine Eng, MD

Synonyms Rheumatoid elbow Primary degenerative arthritis Osteoarthritis of the elbow Post-traumatic arthritis

intermittent pain and mild restriction of motion with minimal changes detectable on radiographs to more advanced stages of arthritis with a limited, painful arc of motion and radiographic demonstration of osteophyte formation, cysts, and loss of joint space. Ultimately these destructive processes may result in complete ankylosis or total instability of the elbow.

Inflammatory Arthritis

ICD-10 Codes M06.821 M06.822 M06.829 M19.021 M19.022 M19.029 M19.221 M19.222 M19.229 M12.521 M12.522 M12.529

Rheumatoid arthritis, right elbow Rheumatoid arthritis, left elbow Rheumatoid arthritis, unspecified elbow Primary osteoarthritis, right elbow Primary osteoarthritis, left elbow Primary osteoarthritis, unspecified elbow Secondary osteoarthritis, right elbow Secondary osteoarthritis, left elbow Secondary osteoarthritis, unspecified elbow Traumatic arthropathy, right elbow Traumatic arthropathy, left elbow Traumatic arthropathy, unspecified elbow

Definition In the simplest of terms, arthritis of the elbow reflects a loss of articular cartilage in the ulnotrochlear and radiocapitellar articulations. Arthritic changes include loss of cartilage and underlying subchondral bone as well as excess bone formation in the form of osteophytes. These changes may result from inflammatory or traumatic disruption of bony architecture, capsule, and ligaments. The spectrum of disease ranges from 116

Inflammatory arthropathies, most commonly rheumatoid arthritis (RA), are the major causes of elbow arthritis. RA is characterized by morning stiffness, symmetric polyarticular involvement (in which the elbow is included), arthritis of hand joints, synovitis and pannus formation, nodule formation, and radiographic changes. These include articular narrowing, periarticular osteoporosis, and progressive joint destruction.1,2 Arthritis of the elbow eventually develops in approximately 20% to 50% of patients with RA.3,4 Initially the patient with RA of the elbow may have only marked synovitis contributing to pain and restricted range of motion, which may improve spontaneously or with disease-modifying treatment. Synovitis can cause distension of the joint, destruction of the annular ligament, and instability of the radial head. Prolonged synovitis is associated with erosion of the articular cartilage, subchondral cyst, and osteophyte formation. This can damage the medial or lateral collateral ligamentous complexes and ultimately weaken the joint capsule and ligamentous supports, resulting in instability.3,4 Other inflammatory conditions affecting the elbow joint are the seronegative spondyloarthropathies (ankylosing spondylitis, psoriatic arthritis, reactive arthritis, and enteropathic arthritis), systemic lupus erythematosus, crystalline arthritis (gout and pseudogout), hemophilic arthritis, and even tuberculous arthritis, each of which has distinguishing features. 

Osteoarthritis Osteoarthritis (OA) is a noninflammatory arthropathy characterized by loss of joint space, development of osteophytes resulting in loss of motion. Initial pain and motion loss typically affects terminal flexion and extension but may also affect pronation and supination. This is related to osteophytes of the

CHAPTER 21  Elbow Arthritis

coronoid and olecranon and their respective fossae.5 Primary OA of the elbow is uncommon, responsible for less than 5% of elbow arthritis,6 and linked to repetitive strenuous arm use. Primary elbow arthritis usually affects the dominant arm of men in their 50s and has been reported in heavy laborers as well as weight lifters and throwing athletes.7 Post-traumatic arthritis is far more common than primary OA and may result from any trauma to the elbow. This includes intra-articular fractures of the elbow, most commonly the distal humerus or radial head. Studies have found a high incidence of arthritis, up to 80%, after internal fixation of distal humeral fractures.8 Similarly, after radial head fracture, the incidence of elbow arthritis is as high as 76% when managed conservatively and 88% to 100% when managed surgically with radial head resection.9 Fractures of the proximal ulna and fracture dislocations have also been associated with the later development of elbow OA.10 Atraumatic OA has been identified in the capitellum, epicondyles, trochlea, and radial head in patients receiving corticosteroid therapy. This can ultimately lead to joint destruction and is often attributed to osteochondrosis, osteonecrosis, and synovial chondromatosis.11,12 In the pediatric population, Panner disease is an osteochondrosis of the capitellum of the elbow that causes pain and stiffness in the affected elbow. It may resemble osteonecrosis but has a much better prognosis.11 Synovial chondromatosis is another rare cause of elbow arthritis.12 

Symptoms As many causes of elbow arthritis are not limited to the elbow joint itself, a thorough history is essential in helping to identify the underlying disease process. Regardless of etiology, the most common complaint associated with elbow arthritis is pain with motion and loss of end-range extension. The severity and characteristics of the pain, presence of stiffness, restriction or pain with motion, mechanical catching, and instability should be clarified. It is crucial to localize the specific affected region of the elbow joint and to distinguish pain at end range or throughout the entire range. Pain throughout the arc of motion implies advanced arthritis. The final stages of arthritis, irrespective of cause, can include severe pain and decreased motion, hindering activities of daily living apart from the cosmetic deformity of a flexed elbow posture. Certain elements in the patient’s history can raise suspicion of specific etiologies including inflammatory arthropathy, post-traumatic arthropathy, primary osteoarthropathy, or septic arthritis. A thorough history should include other organ systems that mostly affect systemic inflammatory diseases such as those causing skin, vision, or genitourinary symptoms. Patients with inflammatory arthritis of the elbow, as in RA, complain of a swollen, painful joint with morning stiffness. Progressive loss of motion or development of joint instability is seen in later stages. Severe pain, swelling, warmth, and limited motion may represent crystalline arthritis of the elbow, but an expedient evaluation to rule out septic arthritis is warranted in such cases. Pain at night or at rest is concerning for an underlying infectious process and should be evaluated carefully. In contrast, post-traumatic or primary OA of the elbow features painful loss of motion but without the significant effusions, warmth, or constant pain associated with synovial inflammation. These patients usually complain of pain at the terminal flexion or extension secondary to osteophyte impingement.

117

A history of occupational activities (such as manual labor) and sports activities that increase demands on the elbow can influence the risk of progression. Previous surgical procedures and any complications should be noted, as well as nonoperative treatments including corticosteroid injection, as intra-articular steroid injections introduce the risk of iatrogenic infection and may cause chondrocyte damage. Patients may also describe neuropathic symptoms related to elbow arthritis. Symptoms of ulnar neuropathy (at the ulnar groove or cubital tunnel) include numbness in the fourth and fifth digits, atrophy of hand intrinsic muscles, clawing, loss of hand dexterity, and aching pain along the ulnar aspect of the forearm. Ulnar nerve symptoms may occur, given the course of the ulnar nerve around the elbow joint and increased risk of entrapment at the elbow or cubital tunnel (see Chapter 27). Compression of the posterior interosseous nerve by rheumatoid synovial hyperplasia can occasionally produce radiating pain to the forearm and the inability to extend the fingers.13 

Physical Examination Physical examination findings of the elbow vary according to the cause and stage of the elbow arthritis. Examination of the elbow starts with inspection for deformity as well as noting the carrying angle. Effusions, synovial thickenings, and erythema are commonly noted in the inflammatory arthropathies during acute flares. The examiner should aim to identify the specific pain generators and maneuvers that trigger pain. Palpation may elicit tenderness specifically over the joint lines, but the patient may also have tenderness over the radial head, olecranon, olecranon bursae, muscles, and tendons attaching around the elbow. Thorough examination of range of motion is crucial. Normal adult elbow range of motion in extension-flexion is from 0 degree to about 150 degrees; pronation averages 75 degrees, and supination averages 85 degrees. A functional range of motion is considered to be 30 to 130 degrees, with 50 degrees of both pronation and supination.14 Primary or post-traumatic arthritis of the elbow results in stiffness, and a flexion contracture is frequently present. Crepitus may be palpable throughout the arc of motion or with forearm rotation. In contrast, RA often leads to restriction in all planes of motion, as the synovitis affects all of the articulating surfaces. Pain, motion restriction, and crepitus worsen as the disease progresses. The range of motion should be monitored at the initial examination and at subsequent follow-up examinations. Wrist and shoulder motion must also be considered, as they come into play in adaptive strategies for patients with restricted elbow motion. Provocative maneuvers for the elbow include assessment of instability or laxity. Recall that RA can result in instability due to destruction of the joint structure, including the capsule and ligaments. This is often perceived by the patient as weakness or mechanical symptoms. Laxity with varus and valgus stress testing or posterior instability may also be seen. In the absence of associated neuropathies, neurologic examination including deep tendon reflexes and sensation are typically normal. Strength of elbow and wrist flexors and extensors may be impaired in long-standing elbow arthritis because of disuse or due to pain. Associated ulnar nerve irritation can lead to pain or a positive Tinel sign over the cubital tunnel. There may be diminished sensation in the fifth digit and ulnar half of the fourth digit (see Chapter 27).

118

PART 1  MSK Disorders

A positive elbow flexion test with paresthesias, provoked by acute flexion of the elbow for 30 to 60 seconds, may also be elicited. Weakness, especially of the hand intrinsic muscles, may also be noted in the presence of associated neuropathies. 

Functional Limitations The elbow functions to position the hand in space. Significant loss of extension can hinder an individual’s ability to interact with the environment. Activities that require nearly full extension, like carrying groceries or briefcases, can become painful. Significant loss of flexion can interfere with activities of daily living, such as eating, shaving, and hygiene. A normal shoulder can compensate well for a lack of pronation, whereas a lack of elbow flexion requires a normal shoulder, wrist, and cervical spine to compensate. There is no simple solution for a significant lack of elbow extension; the body must be moved closer to the desired object. Compensatory mechanisms are often impaired in patients with RA because of involvement of other joints. This magnifies the impact of the elbow arthritis on function. 

Diagnostic Testing Radiographic assessment is usually sufficient for the diagnosis of elbow arthritis, including anteroposterior, lateral, and oblique radiographic views. The radiographs should be inspected for joint space narrowing, osteophyte and cyst formation, bone destruction, evidence of prior injury and healing, hardware integrity, and loose or foreign body. Joint space may appear preserved centrally with osteophytes anteriorly and posteriorly.5 For the rheumatoid patient, the Mayo Clinic radiographic classification of rheumatoid involvement is useful (Table 21.1).2 Dramatic loss of bone is evident as the disease progresses (Fig. 21.1). This pattern of destruction is not seen in patients with post-traumatic or primary OA. Radiographic features in these patients include spurs or osteophytes on the coronoid and olecranon, loose bodies, and narrowing of the coronoid and olecranon fossae (Fig. 21.2). Magnetic resonance imaging is most valuable for confirmation of suspected osteonecrosis or ligamentous injury. Magnetic resonance arthrography or computed tomographic arthrography may help localize suspected loose bodies. Musculoskeletal ultrasound (US) can be used to evaluate for synovitis, bursitis, and enthesitis as well as abnormalities of bony contour resulting from intra-articular erosions. Doppler signal, which can be measured with US, is considered a marker of active inflammatory status.15 For the most part, patients who present with rheumatoid elbow involvement will already have a diagnosis of RA. When isolated inflammatory arthritis of the elbow is suspected, appropriate serologic studies may include analysis of rheumatoid factor, antinuclear antibody, erythrocyte sedimentation rate, anti-CCP, and HLA-B27.16 Elbow aspiration can help rule out a crystalline or infectious cause in patients who present with acute warmth, effusion, and pain without history of trauma or inflammatory arthritis. For patients with neuropathic symptoms, electrodiagnostic testing is useful to evaluate for concurrent or secondary injury of the ulnar, median, radial, or posterior interosseous nerves. Advanced imaging may help identify sites of entrapment of these nerves. 

Table 21.1  Radiographic Classification of Rheumatoid Arthritis2 Grade I

Synovitis with a normal-appearing joint

Grade II

Loss of joint space but maintenance of the subchondral architecture

Grade IIIa

Alteration of the subchondral architecture

Grade IIIb

Alteration of the architecture with deformity

Grade IV

Gross deformity

Morrey B, Adams R. Semiconstrained arthroplasty for the treatment of rheumatoid arthritis of the elbow. J Bone Joint Surg Am. 1992;74(4):479–490.

Differential Diagnosis of Elbow Pain INTRA-ARTICULAR Acute fracture Osteoarthritis (primary or post-traumatic) Inflammatory arthritis Collateral ligament injury, elbow instability Septic arthritis Crystal arthritis  EXTRA-ARTICULAR Medial or lateral elbow tendinopathy/epicondylitis Triceps tendinopathy Olecranon bursitis Soft tissue contracture Median or ulnar nerve compression Cubital tunnel syndrome  REFERRED Cervical radiculopathy PIN entrapment/supinator syndrome Radial tunnel syndrome

Treatment Initial Treatment of elbow arthritis depends on the diagnosis, degree of involvement, functional limitations, and pain. When the elbow is one of several joints actively involved with inflammatory arthritis, the obvious treatment is systemic. Diseasemodifying antirheumatic drugs (DMARDs) have had a dramatic effect in relieving symptoms and retarding the progression of arthritis for many of these patients. In the case of systemic disease, a rheumatology consultation can be beneficial. The initial treatment of an acutely inflamed elbow joint includes rest. A simple sling places the elbow in a relatively comfortable position, but the patient should be encouraged to remove the sling for gentle range-of-motion exercises of the elbow and shoulder several times daily. Icing of the elbow for 15 minutes several times a day for the first few days may be beneficial. Nonoperative treatment of primary OA of the elbow primarily consists of rest, activity modification, and nonsteroidal anti-inflammatory drugs for those without contraindications (e.g., gastrointestinal or renal disease). Oral analgesics may help with pain control. Topical treatments such as diclofenac gel, lidocaine, or capsaicin can be tried as well. Patients who have associated ulnar neuropathic

CHAPTER 21  Elbow Arthritis

A

A

B

B

symptoms should be instructed to avoid direct pressure over the elbow and prolonged elbow flexion. A static night splint that maintains the elbow in about 30 degrees of flexion may help alleviate ulnar nerve symptoms (see Chapter 27). 

Rehabilitation Once the acute inflammation has subsided, physical or occupational therapy may be instituted to regain elbow motion and strength and to educate the patient in activity modification and pain-control measures. Therapy should focus on improving the entire kinetic chain, range of motion, and strength throughout the upper body. Regardless of the degree of elbow arthritis, the goal is to improve function rather than to focus purely on range of motion. Adaptive equipment, such as reachers, can be recommended. Ergonomic workstation equipment may also be useful (e.g., voice-activated computer software, forearm rests).

119

FIG. 21.1 Rheumatoid arthritis. Anteroposterior (A) and lateral (B) elbow radiographs of a 40-year-old woman with long-standing elbow pain. Osteopenia and symmetric joint space narrowing are present. The lateral radiograph demonstrates early bone loss in the ulna. This is categorized as stage IIIa.

FIG. 21.2 Primary degenerative elbow arthritis. Anteroposterior (A) and lateral (B) elbow radiographs of a 52-year-old man with dominant right elbow pain at the extremes of motion. (A) Joint space narrowing and obliteration of the coronoid fossa. (B) Coronoid and olecranon spurs and a large anterior loose body are evident.

Modalities such as US and iontophoresis may help with pain control. Nighttime static, static-progressive, or dynamic extension splinting may be indicated to prevent or treat elbow contractures. Braces may be effective in the setting of instability. In primary OA of the elbow, corrective splinting is not indicated because bone impingement is usually present. Similarly, therapy may aggravate the symptoms and should be ordered judiciously. Again, optimization of motion and mechanics at the shoulder and cervical spine is important in improving function in the patient with limited elbow motion. Rehabilitation is critical to the success of surgical procedures around the elbow. The rheumatoid patient commonly has multiple joint problems that must not be neglected during treatment of the elbow. The shoulder is at particular risk for stiffness. In addition to a successful operation, a motivated patient and a knowledgeable and skillful therapist are necessary to optimize postoperative results. Postoperative rehabilitation is often variable and depends on the specific

120

PART 1  MSK Disorders

Humerus

Radius

Ulna

A

FIG. 21.3  Internal anatomic (A) and approximate surface anatomic (B) lateral views; (C) posterior sites for injection of the elbow laterally and posteriorly. (From Lennard TA. Pain Procedures in Clinical Practice. 2nd ed. Philadelphia: Hanley & Belfus; 2000.)

B

procedure and surgeon’s preference. However, in general, physical or occupational therapy is recommended to restore range of motion and strength. 

Procedures For recalcitrant symptoms, intra-articular steroid injections are effective in relieving the pain associated with synovitis (Fig. 21.3). Intra-articular injections of hyaluronic acid have been shown to provide only short-term relief.17 There is a lack of consensus over anesthetic and corticosteroid dosage, volume, and type. In general, it is reasonable to use about 2 to 5 mL total volume, including 1 mL of steroid and 1 to 4 mL of anesthetic (e.g., 1 mL of 40 mg/mL methylprednisolone and 3 mL of 0.2% ropivacaine). A 25-gauge, 1½-inch needle is adequate for simple injections; for aspirations, a larger 21- to 18-gauge needle may be required. For the palpation-guided injection, the elbow joint is best accessed using a posterolateral approach through the “soft spot,” the center of the triangle formed by the lateral

C

epicondyle, the tip of the olecranon, and radial head. The patient is placed with the elbow between 50 and 90 degrees of flexion. Under sterile conditions, the needle is directed proximally toward the head of the radius and medially into the elbow joint. No resistance should be noted as the needle enters the joint. If an effusion is present, aspiration may be done before the anesthetic-corticosteroid mixture is injected.18 US guidance can improve the accuracy of injections for the elbow,19,20 improve outcomes, and allow for better detection and aspiration of effusions.21 There are several described techniques to access the elbow joint, but most involve either targeting the radiocapitellar joint or the joint space between the olecranon and the trochlea in the posterior elbow lateral to the triceps. For the lateral radiocapitellar approach, the patient is positioned with elbow pronated and flexed to 40 to 90 degrees. The probe is positioned transversely to the radiocapitellar joint. This injection may be done either in plane distal to proximal using a standoff technique or out of plane posterior to anterior using a

CHAPTER 21  Elbow Arthritis

121

FIG. 21.4  Ultrasound-guided injection approaches. Asterisks indicate needle approach, arrows indicates injection target. Left image: lateral approach (C, capitellum; R, radial head). Right image: posterior approach (O, olecranon; H, humerus; TT, triceps tendon; TM, triceps muscle).

walk-down technique (Fig. 21.4).20,22 An alternative posterior approach can be useful in those with joint effusions, which can displace the fat pad posteriorly. The patient is positioned prone, with the arm hanging over the edge of the table and flexed to 90 degrees. The transducer is oriented over the olecranon fossa. Visualization and avoidance of the ulnar nerve is crucial. This injection may be performed using an in-plane lateral-to-medial approach, short axis to the triceps tendon. Alternatively, a proximal-to-distal in-plane approach, with the transducer’s long axis oblique to the triceps myotendinous junction, may be employed.20 Postinjection care may include icing of the elbow for 10 to 20 minutes after the injection and then two or three times daily thereafter. The patient should be informed that the pain may worsen for the first 24 to 36 hours and that the medication may take 1 week to take effect. In general, repeated injections are not recommended. Although there is evidence to suggest that intra-articular steroids at lower doses can improve recovery from damage and increase cell growth, there is growing evidence that larger cumulative doses are associated with gross cartilage damage and chondrotoxicity that could potentially accelerate arthritis.23 Recently there has been increasing interest in regenerative injection options, including the use of platelet-rich plasma or concentrated bone marrow aspirate in treating arthritis in larger joints, particularly for OA. Further study is warranted to determine whether there is any role for regenerative injections in elbow arthritis. Denervation procedures, which have been used effectively in other joints including the wrist and hand, have a potential role in postponing joint replacement surgery, although currently only preliminary data are available.10 

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery Patients with persistent pain after 3 to 6 months of adequate medical therapy are potential candidates for surgery. In assessment of the surgical candidate with primary elbow arthritis, it is important to listen carefully to the patient’s complaints. Selection of an appropriate surgical procedure is based on the location of the arthritis and the patient’s primary complaint. Refractory pain is the best indication

for surgery, as restricted range of motion does not always improve significantly. Many patients are dissatisfied with the simple fact that they cannot fully straighten the elbow, and such patients may not be satisfied with surgery. For humeroradial arthritis, often related to previous fracture or nonunion, radial head resection with interposition has been described. The technique involves interposition of the anconeus muscle into the radiocapitellar articulation underneath the lateral collateral ligament complex.24 In radiohumeral arthropathy without condylar involvement, isolated radial head arthroplasty can improve patients’ pain and function, although it will likely not normalize motion and strength.25 For patients with ulnohumeral arthritis, surgery is indicated in cases of intractable pain and stiffness, although the degree of stiffness dictates the procedure. Intermittent locking or catching, suggestive of a loose body, is often best treated with an elbow arthroscopy. Pain at the extremes of motion, consistent with olecranon and coronoid osteophyte impingement, may be addressed with surgical débridement of the elbow joint. Open surgical techniques have traditionally been performed to remove impinging osteophytes, but more recent arthroscopic advances have enabled surgeons to perform a less invasive débridement with potentially less morbidity. Arthroscopic release involves joint débridement, foreign body extraction, removal of osteophytes, and clearing of the olecranon and coronoid fossae.10,24 For the younger patient with advanced primary elbow arthritis, ulnohumeral distraction interposition arthroplasty or resurfacing arthroplasty with interposition is recommended as an alternative to total joint replacement.26-28 Unlike their rheumatoid counterparts, most of these patients are otherwise healthy, vigorous people who would regularly stress their joint replacement; total elbow arthroplasty (TEA) is therefore avoided. This procedure involves a radical débridement of the joint followed by resurfacing of the joint surfaces with an interposition material, such as autologous fascia lata or allograft Achilles tendon. A hinged external fixator is then applied, which will protect the healing interposition material while simultaneously maintaining elbow stability and permitting motion. In the one relatively large series of distraction interposition arthroplasty,27 pain relief was satisfactory in 69% of patients at an average of 5 years postoperatively. Ulnohumeral arthroplasty is a variation on the OuterbridgeKashiwagi procedure, or olecranon débridement, where osteophytes encroaching on the olecranon and coronoid osteophytes are removed, the joint is débrided, loose bodies are excised, and

122

PART 1  MSK Disorders

a ring of bone is cored from the olecranon and coronoid fossae.6 This procedure is successful at achieving its principal goal— pain relief at the extremes of motion. Despite the only marginal improvements in range of motion, about 85% of patients are satisfied with the results.6,29,30 As expected, the results deteriorate with time as the arthritis progresses. Although the results may be modest, an advantage of interposition arthroplasty is the potential for conversion to TEA, ideally after the age of 60 years.31 TEA is the surgical procedure of last resort, particularly because of prosthesis survival time; it is typically reserved for the sedentary patient above 65 years of age with severe arthritis.32 These patients often complain of pain throughout the arc of motion; radiographs demonstrate advanced arthritis with severe joint space narrowing or joint deformity, where simple removal of the osteophytes is not likely to be successful. This is a reliable procedure for the rheumatoid patient with advanced elbow arthritis.33,34 There are two primary types of elbow prostheses: an unconstrained TEA can be used with competent elbow ligaments and adequate bone stock, versus a constrained TEA, which is used in cases of incompetent elbow ligaments. The Mayo Clinic has reported excellent results with a semiconstrained prosthesis,35 with pain relief in 92% of patients and an average arc of motion of 26 to 130 degrees, with 64 degrees of pronation and 62 degrees of supination. However, a recent analysis of the trends in TEA in the Medicare population found a decline in utilization of TEA for RA, thought to be secondary to improved medical management with DMARDs. A decline in TEA utilization for distal humeral fractures was also seen, possibly related to improved surgical fixation techniques for fracture repair.36 Other nonimplant surgical options include elbow arthrodesis and resection arthroplasty. There is no ideal position for an elbow fusion. The elbow looks more cosmetically appealing when it is relatively straight. However, this position is more or less useless. Consequently elbow arthrodesis is rarely performed, usually in the setting of intractable infection. Resection arthroplasty is an option for a failed TEA. This procedure permits some elbow motion, although the elbow tends to be relatively unstable. For the rheumatoid patient with elbow arthritis, elbow synovectomy and débridement provide predictable shortterm pain relief.37 Interestingly, the results do not necessarily correlate with the severity of the arthritis. The results do, however, deteriorate somewhat over time as the synovitis recurs.38,39 Elbow motion is not necessarily improved by synovectomy; only 40% of patients obtain better motion. A study comparing arthroscopic and open synovectomy demonstrated equivalent results with either technique if the preoperative arc of flexion is greater than 90 degrees.38 For stiff rheumatoid elbows, arthroscopic synovectomy performed better than the open method. 

Potential Treatment Complications Potential surgical complications include infection, wound problems, neurovascular injury, stiffness, recurrent synovitis, triceps disruption, periprosthetic lucency, fracture, and iatrogenic instability. In the primary and post-traumatic osteoarthritic elbow, motion-improving procedures such as ulnohumeral arthroplasty do not halt the inevitable

radiographic progression of the disease. Similarly, synovectomy of the rheumatoid elbow, even if successful in alleviating pain and synovitis, does not reliably prevent further joint destruction. Preoperative ulnar nerve symptoms can occasionally be made worse by surgery. A simultaneous ulnar nerve transposition should be considered in such patients when the preoperative range of motion is limited.30 In an analysis of 473 consecutive elbow arthroscopies, major and temporary minor complications occurred in 0.8% and 11% of patients, respectively.40 The most significant risk factors for development of temporary nerve palsies were RA and contracture. With TEA, wound healing problems, infection, triceps insufficiency, and implant loosening are the principal complications, occurring in approximately 5% to 7% of patients. As a result, most surgeons place lifelong restrictions on highimpact loading (no golf, no lifting of more than 10 lb) to minimize the need for revision surgery.

References 1. Arnett FC, Edworthy SM, Bloch DA, et al. The american rheumatism association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum. 1988;31(3):315–324. 2. Morrey B, Adams R. Semiconstrained arthroplasty for the treatment of rheumatoid arthritis of the elbow. J Bone Joint Surg Am. 1992;74(4):479–490. 3. Kauffman JI, Chen AL, Stuchin S, Di Cesare PE. Surgical management of the rheumatoid elbow. J Am Acad Orthop Surg. 2003;11(2):100–108. 4. Inglis A, Figgie M. Septic and non-traumatic conditions of the elbow: rheumatoid arthritis. In: Morrey BF, ed. The Elbow and its Disorders. 2nd ed. Philadelphia: WB Saunders; 1993:751–766. 5. Wysocki RW, Cohen MS. Primary osteoarthritis and posttraumatic arthritis of the elbow. Hand Clin. 2011;27(2):131–137. 6. Morrey B. Primary degenerative arthritis of the elbow. Treatment by ulnohumeral arthroplasty. Bone Joint J. 1992;74(3):409–413. 7. Stanley D. Prevalence and etiology of symptomatic elbow osteoarthritis. J Shoulder Elbow Surg. 1994;3(6):386–389. 8. Doornberg JN, Van Duijn PJ, Linzel D, et al. Surgical treatment of intra-articular fractures of the distal part of the humerus. J Bone Joint Surg Am. 2007;89(7):1524–1532. 9. Herbertsson P, Josefsson P-O, Hasserius R, Karlsson C, Besjakov J, Karlsson M. Uncomplicated Mason type-II and III fractures of the radial head and neck in adults. J Bone Joint Surg Am. 2004;86(3):569–574. 10. Chammas M. Post-traumatic osteoarthritis of the elbow. Orthop Traumatol Surg Res. 2014;100(1):S15–S24. 11. Le TB, Mont MA, Jones LC, LaPorte DM, Hungerford DS. Atraumatic osteonecrosis of the adult elbow. Clin Orthop Relat Res. 2000;373:141–145. 12. Gramstad GD, Galatz LM. Management of elbow osteoarthritis. J Bone Joint Surg Am. 2006;88(2):421–430. 13. Malipeddi A, Reddy VRM, Kallarackal G, eds. Posterior interosseous nerve palsy: an unusual complication of rheumatoid arthritis: case report and review of the literature. Semin Arthritis Rheum. 2011;40:576–579. 14. Morrey B, Askew L, Chao E. A biomechanical study of normal functional elbow motion. J Bone Joint Surg Am. 1981;63(6):872–877. 15. Uson J, Miguélez-Sánchez R, de los Riscos M, et al. Elbow clinical, ultrasonographic and radiographic study in patients with inflammatory joint diseases. Rheumatol Int. 2016;36(3):377–386. 16. Shen R, Ren X, Jing R, et al. Rheumatoid factor, anti-cyclic citrullinated peptide antibody, C-reactive protein, and erythrocyte sedimentation rate for the clinical diagnosis of rheumatoid arthritis. Lab Med. 2015;46(3):226–229. 17. van Brakel RW, Eygendaal D. Intra-articular injection of hyaluronic acid is not effective for the treatment of post-traumatic osteoarthritis of the elbow. Arthroscopy. 2006;22(11):1199–1203. 18. Tallia AF, Wood UR. Diagnostic and therapeutic injection of the elbow region. Am Fam Physician. 2002;66:2097–2100. 19. Kim TK, Lee JH, Park KD, Lee SC, Ahn J, Park Y. Ultrasound versus palpation guidance for intra-articular injections in patients with degenerative osteoarthritis of the elbow. J Clin Ultrasound. 2013;41(8):479–485.

CHAPTER 21  Elbow Arthritis

20. Sussman WI, Williams CJ, Mautner K. Ultrasound-guided elbow procedures. Phys Med Rehabil Clin N Am. 2016;27(3):573–587. 21. Sibbitt WL, Peisajovich A, Michael AA, et al. Does sonographic needle guidance affect the clinical outcome of intraarticular injections? J Rheumatol. 2009;36(9):1892–1902. 22. Malanga GA, Mautner KR. Atlas of Ultrasound-Guided Musculoskeletal Injections. New York: McGraw-Hill Education; 2014. 23. Wernecke C, Braun HJ, Dragoo JL. The effect of intra-articular corticosteroids on articular cartilage: a systematic review. Orthop J Sports Med. 2015;3(5): 2325967115581163. 24. Sears BW, Puskas GJ, Morrey ME, Sanchez-Sotelo J, Morrey BF. Posttraumatic elbow arthritis in the young adult: evaluation and management. J Am Acad Orthop Surg. 2012;20(11):704–714. 25. Shore BJ, Mozzon JB, MacDermid JC, Faber KJ, King GJ. Chronic posttraumatic elbow disorders treated with metallic radial head arthroplasty. J Bone Joint Surg Am. 2008;90(2):271–280. 26. Gramstad GD, King GJ, O’Driscoll SW, Yamaguchi K. Elbow arthroplasty using a convertible implant. Tech Hand Up Extrem Surg. 2005;9(3):153–163. 27. Cheng S, Morrey B. Treatment of the mobile, painful arthritic elbow by distraction interposition arthroplasty. J Bone Joint Surg Br. 2000;82(2):233–238. 28. Wright P, Froimson A, Morrey B. Interposition arthroplasty of the elbow. The elbow and its disorders. Philadelphia: WB Saunders; 2000:718–730. 29. Wada T, Isogai S, Ishii S, Yamashita T. Débridement arthroplasty for primary osteoarthritis of the elbow. J Bone Joint Surg. 87 (1 suppl 1):95–105. 30. Antuna SA, Morrey BF, Adams RA, O’driscoll SW. Ulnohumeral arthroplasty for primary degenerative arthritis of the elbow. J Bone Joint Surg Am. 2002;84(12):2168–2173.

123

31. Blaine TA, Adams R, Morrey BF. Total elbow arthroplasty after interposition arthroplasty for elbow arthritis. J Bone Joint Surg. 2005;87(2):286–292. 32. Moro JK, King GJ. Total elbow arthroplasty in the treatment of posttraumatic conditions of the elbow. Clin Orthop Relat Res. 2000;370:102–114. 33. Hargreaves D, Emery R. Total elbow replacement in the treatment of rheumatoid disease. Clin Orthop Relat Res. 1999;366:61–71. 34. Ferlic DC. Total elbow arthroplasty for treatment of elbow arthritis. J Shoulder Elbow Surg. 1999;8(4):367–378. 35. Gill DR, Morrey BF. The Coonrad-Morrey total elbow arthroplasty in patients who have rheumatoid arthritis. A ten to fifteen-year follow-up study. J Bone Joint Surg Am. 1998;80(9):1327–1335. 36. Triplet JJ, Kurowicki J, Momoh E, Law TY, Niedzielak T, Levy JC. Trends in total elbow arthroplasty in the Medicare population: a nationwide study of records from 2005 to 2012. J Shoulder Elbow Surg. 2016;25(11):1848–1853. 37. Ferlic DC, Patchett CE, Clayton ML, Freeman AC. Elbow synovectomy in rheumatoid arthritis long-term results. Clin Orthop Relat Res. 1987;220:119–125. 38. Tanaka N, Sakahashi H, Hirose K, Ishima T, Ishii S. Arthroscopic and open synovectomy of the elbow in rheumatoid arthritis. J Bone Joint Surg Am. 2006;88(3):521–525. 39. Horiuchi K, Momohara S, Tomatsu T, Inoue K, Toyama Y. Arthroscopic synovectomy of the elbow in rheumatoid arthritis. J Bone Joint Surg Am. 2002;84(3):342–347. 40. Kelly EW, Morrey BF, O’Driscoll SW. Complications of elbow arthroscopy. J Bone Joint Surg Am. 2001;83(1):25.

CHAPTER 22

Lateral Epicondylitis Lyn D. Weiss, MD Jay M. Weiss, MD

Symptoms

Synonyms

Patients usually report pain in the area just distal to the lateral epicondyle. They may complain of pain radiating proximally or distally. Patients may also complain of pain with wrist or hand movement, such as gripping a doorknob, carrying a briefcase, or shaking hands. Patients occasionally report swelling as well. 

Tendinosis1 Lateral epicondylitis Tennis elbow

ICD-10 Codes M77.10 M77.11 M77.12

Lateral epicondylitis, unspecified elbow Lateral epicondylitis, right elbow Lateral epicondylitis, left elbow

Definition Epicondylitis is a general term used to describe inflammation, pain, or tenderness in the region of the medial or lateral epicondyle of the humerus. The actual nidus of pain and pathologic change has been debated. Lateral epicondylitis implies an inflammatory lesion with degeneration at the tendinous origin of the extensor muscles (the lateral epicondyle of the humerus). The tendon of the extensor carpi radialis brevis muscle is primarily affected. Other muscles that can contribute to the condition are the extensor carpi radialis longus and the extensor digitorum communis. Although the term epicondylitis implies an inflammatory process, inflammatory cells are not identified histologically. Instead, the condition may be secondary to failure of the musculotendinous attachment with resultant fibroplasia,2 termed tendinosis. Other postulated primary lesions include angiofibroblastic tendinosis, periostitis, and enthesitis.3 Overall the focus of injury appears to be the common extensor tendon origin. Symptoms may be related to failure of the repair process.4 Repetitive stress has been implicated as a factor in this condition.5 Overuse from a tennis backhand (especially a one-handed backhand with poor technique) can frequently lead to lateral epicondylitis (hence the term tennis elbow is frequently used synonymously with lateral epicondylitis, regardless of its etiology). Repetitive computer use (especially with a mouse) as well as golf, swimming, and baseball can cause or exacerbate epicondylitis.  124

Physical Examination On examination, the hallmark of epicondylitis is tenderness over the extensor muscle origin. The common origin of the extensor muscles can be located one fingerbreadth below the lateral epicondyle. With lateral epicondylitis, pain is increased with resisted wrist extension, especially with the elbow extended, the forearm pronated, the wrist radially deviated, and the hand in a fist. The middle finger test can also be used to assess for lateral epicondylitis. Here, the proximal interphalangeal joint of the long finger is resisted in extension and pain is elicited over the lateral epicondyle. Swelling is occasionally present. In cases of recalcitrant lateral epicondylitis, the diagnosis of radial nerve entrapment should be considered. The radial nerve can become entrapped just distal to the lateral epicondyle where the nerve pierces the intermuscular septum (between the brachialis and brachioradialis muscles). There may be localized tenderness along the course of the radial nerve around the radial head. Motor and sensory findings are usually absent. 

Functional Limitations The patient may complain of an inability to lift or carry objects on the affected side secondary to increased pain. Typing, using a computer mouse, or working on a keyboard may recreate the pain. Even handshaking or squeezing may be painful in lateral epicondylitis. Athletic activities may cause pain, especially with an acute increase in repetition, poor technique, and equipment changes (frequently with a new racket or restringing). 

Diagnostic Studies The diagnosis is usually made on clinical grounds. Magnetic resonance imaging (MRI), which is particularly useful for soft tissue definition, can be used to assess for tendinitis, tendinosis, degeneration, partial or complete tears, and detachment of the common extensor tendons at the lateral epicondyle.6

CHAPTER 22  Lateral Epicondylitis

125

MRI is rarely needed, however, except in recalcitrant epicondylitis, and it will not alter the treatment significantly in the early stages. The lateral collateral ligament complexes can be evaluated for tears as well as for chronic degeneration and scarring. Ultrasonography has been used to diagnose lateral epicondylitis.7 The common extensor tendon and the radial nerve may appear swollen on the affected side.8 Findings of radial nerve involvement may indicate that the pain was secondary to radial nerve entrapment. Arthrography may be beneficial if capsular defects and associated ligament injuries are suspected. Barring evidence of trauma, early radiographs are of little help in this condition but may be useful in cases of resistant tendinitis and to rule out occult fractures, arthritis, and an osteochondral loose body. 

Differential Diagnosis Posterior interosseous nerve syndrome Bone infection or tumors Ulnar or median neuropathy around the elbow Osteoarthritis Acute calcification around the lateral epicondyle9 Osteochondral loose body Anconeus compartment syndrome10 Triceps tendinitis Degenerative arthrosis11 Elbow synovitis Lateral ligament instability12 Radial head fracture Bursitis Collateral ligament tears Hypertrophic synovial plica13

Treatment Initial Initial treatment consists of relative rest, avoidance of repetitive motions involving the wrist, activity modification to avoid stress on the epicondyle, anti-inflammatory medications, and thermal modalities such as heat and ice for acute pain. Patients who develop lateral epicondylitis from tennis should modify their stroke (especially improving the backhand stroke to ensure that the forearm is in midpronation and the trunk is leaning forward) and their equipment, usually by reducing string tension and enlarging the grip size.5 Frequently a two-handed backhand will relieve the stress sufficiently. In addition, a forearm band (counterforce brace) worn distal to the extensor muscle group origin can be beneficial (Fig. 22.1). The theory behind this device is that it will dissipate forces over a larger area of tissue than the lateral attachment site. Alternatively, the use of wrist immobilization splints may be helpful. A splint set in neutral can be helpful for lateral epicondylitis by relieving the tension on the flexors and extensors of the wrist and fingers. A splint set in 30 to 40 degrees of wrist extension will relieve the tension on the extensor tendons, including the extensor carpi radialis brevis muscle as well as other wrist and finger extensors.14,15 Dynamic extension bracing has also been proposed.16 

FIG. 22.1  Forearm band (counterforce brace) used in patients with lateral epicondylitis.

Rehabilitation Rehabilitation may include physical or occupational therapy. Therapy should include two phases. The first phase is directed at decreasing pain by physical modalities (ultrasound, electrical stimulation, phonophoresis, cortisone iontophoresis,17 myofascial release,18 heat, ice, massage) and decreasing disability (education, reduction of repetitive stress, and preservation of motion). When the patient is pain free, a gradual program is implemented to improve strength and endurance of wrist extensors and stretching. This program must be carefully monitored to permit strengthening of the muscles and work hardening of the tissues without itself causing an overuse situation. The patient should start with static exercises and advance to progressive resistive exercises (with an emphasis on the eccentric phase of the exercise). Thera-Band, light weights, and manual (self) resistance exercises can be used. Work or activity restrictions or modifications may be required for a time. 

Procedures Injections may be useful if therapy and exercise have not provided relief.19,20 Injection of corticosteroid, usually with a local anesthetic, into the area of maximum tenderness (approximately 1 to 5 cm distal to the lateral epicondyle) has been shown to be effective in the shortterm treatment of lateral epicondylitis (Fig. 22.2),21-23 although several studies have questioned the long-term efficacy of these injections.24,25 To confirm the diagnosis, a trial of lidocaine alone may be given. An immediate improvement in grip strength should be noted after injection. Postinjection treatment includes icing of the affected area both immediately (for 5 to 10 minutes) and thereafter (a reasonable regimen is 20 minutes two or three times per day for 2 weeks) and wearing of a wrist splint (particularly for activities that involve wrist movement). The wrist splint should be set in slight extension for lateral epicondylitis. Exacerbating activities are to be avoided. Plateletrich plasma injections have been shown to reduce pain and

126

PART 1  MSK Disorders

Potential Treatment Complications Analgesics and nonsteroidal anti-inflammatory drugs have well-known side effects that most commonly affect the gastric, hepatic, and renal systems. Local steroid injections may increase the risk for disruption of tissue planes, create highpressure tissue necrosis, rupture tendons,1 damage nerves, promote skin depigmentation or atrophy, or cause infection.42

References

FIG. 22.2  Under sterile conditions, with use of a 27-gauge needle and 1 to 2 mL of a local anesthetic combined with 1 to 2 mL of a corticosteroid preparation, inject the solution approximately 1 to 5 cm distal to the lateral epicondyle. The injected materials should flow smoothly. Resistance generally indicates that the solution is being injected directly into the tendon, which should be avoided.

to increase function in patients with lateral epicondylitis to be superior in the intermediate (12 weeks) and long term (6 months to a year).22,23,26-29 However, the optimal concentration of platelets, frequency of application, cell types, and optimal regimen for tissue repair remain unclear.30 Injection of botulinum toxin into the extensor digitorum communis muscles to the third and fourth digits has been reported to be beneficial in chronic treatment– resistant lateral epicondylitis.31,32 Injection of autologous blood has also been shown to improve pain but may pose a higher risk of adverse events.33 There are studies that support acupuncture as an effective modality in the short-term relief of lateral epicondylitis.34-36 Extracorporeal shock wave treatment may also be beneficial.37 A recent study investigated the effectiveness of microtenotomy using a radiofrequency probe in patients with chronic tendinosis of the elbow. Results showed improvement in pain self-reporting.38 In a small study of recalcitrant cases of lateral epicondylitis, pulsed radiofrequency has also been used on the radial nerve (under ultrasound guidance).39 

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery Surgery may be indicated in those patients with continued severe symptoms who do not respond to conservative management. For lateral epicondylitis, surgery is aimed at excision and revitalization of the pathologic tissue in the extensor carpi radialis brevis and release of the muscle origin.40 Pinning may be done if the elbow joint is unstable.41 

Potential Disease Complications Possible long-term complications of untreated epicondylitis include chronic pain, loss of function, and possible elbow contracture. In general, epicondylitis is more easily and successfully treated in the acute phase. 

1. Kraushaar BS, Nirschl RP. Tendinosis of the elbow (tennis elbow): clinical features and findings of histological, immunohistochemical, and electron microscopy studies. J Bone Joint Surg Am. 1999;81:259–278. 2. Nirschl RP, Pettrone FA. Tennis elbow. J Bone Joint Surg Am. 1979;61:832–839. 3. Nirschl RP. Elbow tendinosis/tennis elbow. Clin Sports Med. 1992;11:851–870. 4. Putnam MD, Cohen M. Painful conditions around the elbow. Orthop Clin North Am. 1999;30:109–118. 5. Cassvan A, Weiss LD, Weiss JM, et al. Cumulative trauma disorders. Boston: Butterworth-Heinemann; 1997:123–125. 6. Braddom RL. Physical medicine and rehabilitation. Philadelphia: WB Saunders; 1996:222. 7. Bodor M, Fullerton B. Ultrasonography of the hand, wrist, and elbow. Phys Med Rehabil Clin N Am. 2010;21:509–531. 8. Gürçay E, Karaahmet ÖZ Kara M, et al. Ultrasonographic evaluation of the radial nerves in patients with unilateral refractory lateral epicondylitis. Pain Med. 2016. pii: pnw181. 9. Hughes E. Acute deposition of calcium near the elbow. J Bone Joint Surg Br. 1950;32:30–34. 10. Abrahamsson S, Sollerman C, Soderberg T, et al. Lateral elbow pain caused by anconeus compartment syndrome. Acta Orthop Scand. 1987;58:589–591. 11. Brems JJ. Degenerative joint disease of the elbow. In: Nicholas JA, Hershman EB, eds. The upper extremity in sports medicine. St. Louis: Mosby; 1995:331–335. 12. Morrey BF. Anatomy of the elbow joint. In: Morrey BF, et al., eds. The elbow and its disorders. 2nd ed. Philadelphia: WB Saunders; 1993:16. 13. Kim DH, Gambardella RA, El Attrache NS, et al. Arthroscopic treatment of posterolateral elbow impingement from lateral synovial plicae in throwing athletes and golfers. Am J Sports Med. 2006;34:438–444. 14. Plancher KD. The athletic elbow and wrist, part I. diagnosis and conservative treatment. Clin Sports Med. 1995;15:433–435. 15. Derebery VJ, Devenport JN, Giang GM, Fogarty WT. The effects of splinting on outcomes for epicondylitis. Arch Phys Med Rehabil. 2005;86:1081–1088. 16. Faes M, van den Akker B, de Lint JA, et al. Dynamic extensor brace for lateral epicondylitis. Clin Orthop Relat Res. 2006;442:149–157. 17. Stefanou A, Marshall N, Holdan W, Siddiqui A. A randomized study comparing corticosteroid injection to corticosteroid iontophoresis for lateral epicondylitis. J Hand Surg [Am]. 2012;37:104–109. 18. Ajimsha MS, Chithra S, Thulasyammal RP. Effectiveness of myofascial release in the management of lateral epicondylitis in computer professionals. Arch Phys Med Rehabil. 2012;93:604–609. 19. Murtezani A, Ibraimi Z, Vllasolli TO, et al. Exercise and therapeutic ultrasound compared with corticosteroid injection for chronic lateral epicondylitis: a randomized controlled trial. Ortop Traumatol Rehabil. 2015;17(4):351–357. 20. Coombes BK, Connelly L, Bisset L, et al. Economic evaluation favours physiotherapy but not corticosteroid injection as a first-line intervention for chronic lateral epicondylalgia: evidence from a randomised clinical trial. Br J Sports Med. 2016;50(22):1400–1405. 21. Hay EH, Paterson SM, Lewis M, et al. Pragmatic randomized controlled trial of local corticosteroid injection and naproxen for treatment of lateral epicondylitis of elbow in primary care. BMJ. 1999;319:964–968. 22. Mi B, Liu G, Zhou W, et al. Platelet rich plasma versus steroid on lateral epicondylitis: meta-analysis of randomized clinical trials. Phys Sportsmed. 2017:1–8. 23. Qian X, Lin Q, Wei K, Hu B, Jing P, Wang J. Efficacy and safety of autologous blood products compared with corticosteroid injections in the treatment of lateral epicondylitis: a meta-analysis of randomized controlled trials. PM R. 2016;8(8):780–791.

CHAPTER 22  Lateral Epicondylitis

24. Sirico F, Ricca F, DI Meglio F, et al. Local corticosteroid versus autologous blood injections in lateral epicondylitis: meta-analysis of randomized controlled trials. Eur J Phys Rehabil Med. 2016. 25. Claessen FM, Heesters BA, Chan JJ, et al. A meta-analysis of the effect of corticosteroid injection for enthesopathy of the extensor carpi radialis brevis origin. J Hand Surg Am. 2016;41(10):988–998. 26. Peerbooms JC, Sluimer J, Bruijn DJ, Gosens T. Positive effect of an autologous platelet concentrate in lateral epicondylitis in a double-blind randomized controlled trial: platelet-rich plasma versus corticosteroid injection with a 1-year follow-up. Am J Sports Med. 2010;38:255–262. 27. Gosens T. Ongoing positive effect of platelet-rich plasma versus corticosteroid injection in lateral epicondylitis: a double-blind randomized controlled trial with 2-year follow-up. Am J Sports Med. 2011;39:1200–1208. 28. Hechtman KS, Uribe JW, Botto-vanDemden A, Kiebzak GM. Plateletrich plasma injection reduces pain in patients with recalcitrant epicondylitis. Orthopedics. 2011;34:92. 29. Khaliq A, Khan I, Inam M, et al. Effectiveness of platelets rich plasma versus corticosteroids in lateral epicondylitis. J Pak Med Assoc. 2015;65(11 suppl 3):S100–S104. 30. Halpern BC, Chaudhury S, Rodeo SA. The role of platelet-rich plasma in inducing musculoskeletal tissue healing. HSS J. 2012;8(2):137–145. 31. Morre HH, Keizer SB, van Os JJ. Treatment of chronic tennis elbow with botulinum toxin. Lancet. 1997;349:1746. 32. Wong SM, Jui AC, Tong PY, et al. Treatment of lateral epicondylitis with botulinum toxin: a randomized, double-blind, placebo-controlled trial. Ann Intern Med. 2005;143:793–797. 33. Arirachakaran A, Sukthuayat A, Sisayanarane T, et al. Platelet-rich plasma versus autologous blood versus steroid injection in lateral epicondylitis: systematic review and network meta-analysis. J Orthop Traumatol. 2016;17(2):101–112.

127

34. Trinh KV, Phillips SD, Ho E, Damsma K. Acupuncture for the alleviation of lateral epicondyle pain: a systematic review. Rheumatology (Oxford). 2004;43:1085–1090. 35. Fink M, Wolkenstein E, Luennemann M, et al. Chronic epicondylitis: effects of real and sham acupuncture treatment: a randomised controlled patient- and examiner-blinded long-term trial. Forsch Komplementarmed Klass Naturheilkd. 2002;9:210–215. 36. Fink M, Wolkenstein E, Karst M, Gehrke A. Acupuncture in chronic epicondylitis: a randomized controlled trial. Rheumatology (Oxford). 2002;41:205–209. 37. Gunduz R, Malas FU, Borman P, et al. Physical therapy, corticosteroid injection, and extracorporeal shock wave treatment in lateral epicondylitis. clinical and ultrasonographical comparison. Clin Rheumatol. 2012;31:807–812. 38. Tasto JP, Richmond JM, Cummings JR, et al. Radiofrequency microtenotomy for elbow epicondylitis: midterm results. Am J Orthop (Belle Mead NJ). 2016;45(1):29–33. 39. Oh DS, Kang TH, Kim HJ. Pulsed radiofrequency on radial nerve under ultrasound guidance for treatment of intractable lateral epicondylitis. J Anesth. 2016;30(3):498–502. 40. Organ SW, Nirschl RP, Kraushaar BS, Guidi EJ. Salvage surgery for lateral tennis elbow. Am J Sports Med. 1997;25:746–750. 41. Brown D, Freeman E, Cuccurullo S. Elbow disorders. In: Cuccurullo S, ed. Physical medicine and rehabilitation board review. New York: Demos; 2004:163–173. 42. Nichols AW. Complications associated with the use of corticosteroids in the treatment of athletic injuries [review]. Clin J Sport Med. 2005;15:370–375.

CHAPTER 23

Medial Epicondylitis Lyn D. Weiss, MD Jay M. Weiss, MD

Symptoms

Synonyms Tendinosis1 Medial epicondylitis Pitcher’s elbow Little Leaguer’s elbow Golfer’s elbow

ICD-10 Codes M77.00 M77.01 M77.02

Medial epicondylitis, unspecified elbow Medial epicondylitis, right elbow Medial epicondylitis, left elbow

Definition Epicondylitis is a general term used to describe inflammation, pain, or tenderness in the region of the medial or lateral epicondyle of the humerus. The actual nidus of pain and pathologic change has been debated. Medial epicondylitis implies an inflammatory lesion with degeneration at the origin of the flexor muscles (the medial epicondyle of the humerus). In medial epicondylitis, the tendon of the flexor muscle group is affected (flexor carpi radialis, flexor carpi ulnaris, flexor digitorum superficialis, and palmaris longus). Although the term epicondylitis implies an inflammatory process, inflammatory cells are not identified histologically. Instead, the condition may be secondary to failure of the musculotendinous attachment with resultant fibroplasia,2 termed tendinosis. Other postulated primary lesions include angiofibroblastic tendinosis, periostitis, and enthesitis.3 In children, medial elbow pain may result from repetitive stress on the apophysis of the medial epicondyle’s ossification center (Little Leaguer’s elbow).4 Overall the focus of injury appears to be the muscle origin. Symptoms may be related to failure of the repair process.5 Repetitive stress has been implicated as a factor in this condition.6 Poor throwing mechanics and excessive throwing have been implicated in Little Leaguer’s elbow. Repetitive wrist flexion, as in the trailing arm in a golf swing, can cause medial epicondylitis (hence, the term golfer’s elbow is frequently used for medial epicondylitis regardless of etiology).  128

Patients usually report pain in the area just distal to the medial epicondyle. They may complain of pain radiating proximally or distally. Patients may also complain of pain with wrist or hand movement, such as gripping a doorknob, carrying a briefcase, or shaking hands. They occasionally report swelling as well. Throwing athletes may complain of symptoms during the late cocking or early acceleration phases.7 Patients who spend a lot of time with their forearms supinated (professional slalom water-skiers), may be at increased risk of developing medial epicondylitis.8 

Physical Examination On examination, the hallmark of epicondylitis is tenderness over the flexor muscle’s origin (medial epicondylitis). The origin of the flexor muscles can be located one fingerbreadth below the medial epicondyle. With medial epicondylitis, pain is increased with resisted wrist flexion. There may be localized tenderness along the course of the radial nerve around the radial head. Motor and sensory findings are usually absent. 

Functional Limitations The patient may complain of an inability to lift or to carry objects on the affected side secondary to increased pain. Typing, using a computer mouse, or working on a keyboard may recreate the pain. Even handshaking or hand squeezing may be painful in medial epicondylitis. Athletic activities may cause pain, especially with an acute increase in repetition, poor technique, and equipment changes. 

Diagnostic Studies The diagnosis is usually made on clinical grounds. Magnetic resonance imaging (MRI), which is particularly useful for soft tissue definition, can be used to assess for tendinitis, tendinosis, degeneration, partial tears or complete tears, and detachment of the common flexor at the medial epicondyles.9 MRI is rarely needed, however, except in recalcitrant epicondylitis, and it will not alter the treatment significantly in the early stages. The medial collateral ligament complexes can be evaluated for tears as well as for chronic degeneration and scarring. Ultrasonography has been used to diagnose medial epicondylitis.10,11 Arthrography may be beneficial if capsular defects and associated ligament injuries are suspected. Barring evidence of trauma, early radiographs are of little help in this condition but may be useful in cases of

CHAPTER 23  Medial Epicondylitis

resistant tendinitis and to rule out occult fractures, arthritis, and osteochondral loose bodies. Early radiographic studies (before commencing a rehabilitation program) may be considered in skeletally immature children with elbow pain to rule out growth plate disorders, osteochondritis dissecans, or tears of the ulnar collateral ligament.12 

129

Medial epicondyle

Differential Diagnosis Posterior interosseous nerve syndrome Bone infection or tumors Ulnar neuropathy around the elbow Osteoarthritis Osteochondral loose body Anconeus compartment syndrome13 Triceps tendinitis Degenerative arthrosis14 Elbow synovitis Medial ligament instability15 Radial head fracture Bursitis Collateral ligament tears Hypertrophic synovial plica16

Olecranon

FIG. 23.1  Medial epicondylitis injection.

static exercises and advance to progressive resistive exercises. Thera-Band, light weights, Kinesio taping,19 and manual (self) resistance exercises can be used. Work or activity restrictions or modifications may be required for a time. 

Procedures

Treatment Initial Initial treatment consists of relative rest, avoidance of repetitive motions involving the wrist, activity modification to avoid stress on the epicondyle, nonsteroidal antiinflammatory medications, and thermal modalities such as heat and ice for acute pain. Patients who develop medial epicondylitis from golf should consider modifying their swing to avoid excessive force on wrist flexor muscles. Biomechanical modifications may help to reduce symptoms if the medial epicondylitis is thought to be due to poor pitching technique. In addition, a forearm band (counterforce brace) worn distal to the origin of the flexor muscle group can be beneficial. The theory behind this device is that it will dissipate forces over a larger area of tissue than the medial attachment site.17 Alternatively, the use of wrist immobilization splints may be helpful. A splint set in neutral can be helpful for medial epicondylitis by relieving the tension on the flexors and extensors of the wrist and fingers. Dynamic extension bracing has also been proposed.18 

Rehabilitation Rehabilitation may include physical or occupational therapy. Therapy should include two phases. The first phase is directed at decreasing pain by physical modalities (ultrasound, electrical stimulation, phonophoresis, heat, ice, massage) and decreasing disability (education, reduction of repetitive stress, and preservation of motion). When the patient is pain free, a gradual program is implemented to improve strength and endurance (especially of flexors and pronators7), and it should include stretching. This program must be carefully monitored to permit strengthening of the muscles and work hardening of the tissues without itself causing an overuse situation. The patient should start with

Injections for medial epicondylitis must be used cautiously because of the risk of injury to the ulnar nerve (either by direct injection or by tissue changes that may promote nerve injury). Injection of corticosteroid, usually with a local anesthetic, into the area of maximum tenderness (approximately 1 to 5 cm distal to the medial epicondyle) has been shown to be effective in treatment of epicondylitis (Fig. 23.1).20 To confirm the diagnosis, a trial of lidocaine alone may be given. An immediate improvement in grip strength should be noted after injection. Postinjection treatment includes icing of the affected area both immediately (for 5 to 10 minutes) and thereafter (a reasonable regimen is 20 minutes two or three times per day for 2 weeks) and wearing of a wrist splint (particularly for activities that involve wrist movement). The wrist splint should be set in neutral for medial epicondylitis. Exacerbating activities are to be avoided. Plateletrich plasma injections have been shown to reduce pain and increase function in patients with recalcitrant epicondylitis.20-22 However, the optimal concentration of platelets, frequency of application, cell types, and optimal regimen for tissue repair remain unclear.23 A recent study investigated the effectiveness of microtenotomy using a radiofrequency probe in patients with chronic medial tendinosis of the elbow. Results showed improvement in self-reported pain.20,24 

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery Surgery may be indicated in those patients with continued severe symptoms who do not respond to conservative management. Surgery is aimed at excision and revitalization

130

PART 1  MSK Disorders

of the pathologic tissue and release of the muscle origin.25 Pinning may be done if the elbow joint is unstable.4 Operative treatment for recalcitrant medial epicondylitis has been shown to be effective in restoring function and strength.26,27 

Potential Disease Complications Possible long-term complications of untreated epicondylitis include chronic pain, loss of function, and elbow contracture. Medial epicondylitis may lead to reversible impairment (neurapraxia) of the ulnar nerve.28 In general, epicondylitis is more easily and successfully treated in the acute phase. 

Potential Treatment Complications Analgesics and nonsteroidal anti-inflammatory drugs have well-known side effects that most commonly affect the gastric, hepatic, and renal systems. Local steroid injections may increase the risk for disruption of tissue planes, create high-pressure tissue necrosis, rupture tendons,1 damage nerves, promote skin depigmentation or atrophy, or cause infection.29

References 1. Kraushaar BS, Nirschl RP. Tendinosis of the elbow (tennis elbow): clinical features and findings of histological, immunohistochemical, and electron microscopy studies. J Bone Joint Surg Am. 1999;81:259–278. 2. Nirschl RP, Pettrone FA. Tennis elbow. J Bone Joint Surg Am. 1979;61:832–839. 3. Nirschl RP. Elbow tendinosis/tennis elbow. Clin Sports Med. 1992;11:851–870. 4. Brown D, Freeman E, Cuccurullo S. Elbow disorders. In: Cuccurullo S, ed. Physical medicine and rehabilitation board review. New York: Demos; 2004:163–173. 5. Putnam MD, Cohen M. Painful conditions around the elbow. Orthop Clin North Am. 1999;30:109–118. 6. Cassvan A, Weiss LD, Weiss JM, et al. Cumulative trauma disorders. Boston: Butterworth-Heinemann; 1997:123–125. 7. Amin NH, Kumar NS, Schickendantz MS. Medial epicondylitis: evaluation and management. J Am Acad Orthop Surg. 2015;23(6):348–355. 8. Rosa D, Di Donato SL, Balato G, et al. Supinated forearm is correlated with the onset of medial epicondylitis in professional slalom water-skiers. Muscles Ligaments Tendons J. 2016;6(1):140–146. 9. Braddom RL. Physical medicine and rehabilitation. Philadelphia: WB Saunders; 1996:222.

10. Bodor M, Fullerton B. Ultrasonography of the hand, wrist, and elbow. Phys Med Rehabil Clin N Am. 2010;21:509–531. 11. Park GY, Lee SM, Lee MY. Diagnostic value of ultrasonography for clinical medial epicondylitis. Arch Phys Med Rehabil. 2008;89:732–742. 12. Emery KH. Imaging of sports injuries of the upper extremity in children. Clin Sports Med. 2006;25:543–568. 13. Abrahamsson S, Sollerman C, Soderberg T, et al. Lateral elbow pain caused by anconeus compartment syndrome. Acta Orthop Scand. 1987;58:589–591. 14. Brems JJ. Degenerative joint disease of the elbow. In: Nicholas JA, Hershman EB, eds. The upper extremity in sports medicine. St. Louis: Mosby; 1995:331–335. 15. Morrey BF. Anatomy of the elbow joint. In: Morrey BF, ed. The elbow and its disorders. 2nd ed. Philadelphia: WB Saunders; 1993:16. 16. Kim DH, Gambardella RA, El Attrache NS, et al. Arthroscopic treatment of posterolateral elbow impingement from lateral synovial plicae in throwing athletes and golfers. Am J Sports Med. 2006;34:438–444. 17. Walther M, Kirschner S, Koenig A, et al. Biomechanical evaluation of braces used for the treatment of epicondylitis. J Shoulder Elbow Surg. 2002;11:265–270. 18. Faes M, van den Akker B, de Lint JA, et al. Dynamic extensor brace for lateral epicondylitis. Clin Orthop Relat Res. 2006;442:149–157. 19. Chang HY, Wang CH, Chou KY, Cheng SC. Could forearm kinesio taping improve strength, force sense, and pain in baseball pitchers with medical epicondylitis? Clin J Sport Med. 2012;22:327–333. 20. Amin NH, Kumar NS, Schickendantz MS. Medial epicondylitis: evaluation and management. J Am Acad Orthop Surg. 2015;23(6):348–355. 21. Hechtman KS, Uribe JW, Botto-vanDemden A, Kiebzak GM. Plateletrich plasma injection reduces pain in patients with recalcitrant epicondylitis. Orthopedics. 2011;34:92. 22. 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(11):935–939. 23. Halpern BC, Chaudhury S, Rodeo SA. The role of platelet-rich plasma in inducing musculoskeletal tissue healing. HSS J. 2012;8(2):137–134. 24. Tasto JP, Richmond JM, Cummings JR, et al. Radiofrequency microtenotomy for elbow epicondylitis: midterm results. Am J Orthop (Belle Mead NJ). 2016;45(1):29–3. 25. Organ SW, Nirschl RP, Kraushaar BS, Guidi EJ. Salvage surgery for lateral tennis elbow. Am J Sports Med. 1997;25:746–750. 26. Shahid M, Wu F, Deshmukh SC. Operative treatment improves patient function in recalcitrant medial epicondylitis. Ann R Coll Surg Engl. 2013;95(7):486. 27. Han SH, Lee JK, Kim HJ, Lee SH, Kim JW, Kim TS. The result of surgical treatment of medial epicondylitis: analysis with more than a 5-year follow-up. J Shoulder Elbow Surg. 2016;25(10):1704–1709. 28. Barry NN, McGuire JL. Overuse syndromes in adult athletes. Rheum Dis Clin North Am. 1996;22:515–530. 29. Nichols AW. Complications associated with the use of corticosteroids in the treatment of athletic injuries [review]. Clin J Sport Med. 2005;15:370–375.

CHAPTER 24

Median Neuropathy Francisco H. Santiago, MD Ramon Vallarino Jr., MD

Pronator Teres Syndrome

Synonyms Pronator teres syndrome Pronator syndrome Anterior interosseous syndrome Kiloh-Nevin syndrome

ICD-10 Codes G56.10 G56.11 G56.12

Other lesion of median nerve, unspecified upper limb Other lesion of median nerve, right upper limb Other lesion of median nerve procedure, upper limb

Definition There are three general areas in which the median nerve can become entrapped around the elbow and forearm. Because this chapter mainly deals with entrapment below the elbow and above the wrist, the most proximal and least frequent entrapment is not discussed but merely mentioned. Elbow median nerve entrapment is the compression of the nerve by a dense band of connective tissue called the ligament of Struthers, an aberrant ligament found immediately above the elbow. The topics discussed in this chapter are compression of the median nerve at or immediately below the elbow, where the pronator teres muscle compresses it, and compression distally of a branch of the median nerve—the anterior interosseous nerve. Increased risk for pronator syndrome may be associated with individuals involved in repetitive elbow, wrist, and hand movements, such as chopping wood, playing racket sports, rowing, weight lifting, and throwing. However, pronator syndrome is four times more likely to affect women than men, suggesting that the dominant risk factor is an anatomic anomaly (structural variation) and not overuse. The dominant arm is most likely to be affected, particularly if the individual is heavily muscled (muscle hypertrophy). Pronator syndrome is most commonly diagnosed in individuals between 40 and 50 years of age.1 Pronator syndrome is rare but is the second most common cause of medial nerve compression after carpal tunnel syndrome. Pronator syndrome is responsible for less than 1% of all median nerve entrapment disorders.2 Anterior interosseous syndrome has a similar 1% occurrence rate in median nerve entrapment disorders.3

Pronator teres syndrome4–6 is a symptom complex that is produced where the median nerve crosses the elbow and becomes entrapped as it passes first beneath the lacertus fibrosus—a thick fascial band extending from the biceps tendon to the forearm fascia—then between the two heads (superficial and deep) of the pronator teres muscle and under the edge of the flexor digitorum sublimis (Fig. 24.1). Compression may be related to a local process, such as pronator teres hypertrophy, tenosynovitis, muscle hemorrhage, fascial tear, postoperative scarring, anomalous median artery, giant lipoma, or Schwannoma.6 The median nerve may also be injured by occupational strain, such as carrying a grocery bag or playing a guitar, and by insertion of a catheter.4–16 

Anterior Interosseous Syndrome The anterior interosseous nerve arises from the median nerve 5 to 8 cm distal to the lateral epicondyle.4,7,17 Slightly distal to its course through the pronator teres muscle, the median nerve gives off the anterior interosseous nerve, a purely motor branch (Fig. 24.2). It contains no fibers of superficial sensation but does supply deep pain and proprioception to some deep tissues, including the wrist joint. This nerve may be damaged by direct trauma, forearm fracture, humeral fracture, injection into or blood drawing from the cubital vein, supracondylar fracture, and fibrous bands related to the flexor digitorum superficialis (sublimis) and flexor digitorum profundus muscles. In some patients, it is a component of brachial amyotrophy of the shoulder girdle (proximal fascicular lesion) or related to cytomegalovirus infection or a bronchogenic carcinoma metastasis. The nerve may be partially involved, but in a fully established syndrome, three muscles are weak: the flexor pollicis longus, flexor digitorum profundus to the second and sometimes the third digit, and pronator quadratus.4,7,15–22 

Symptoms Pronator Teres Syndrome In an acute compression with unmistakable symptoms, the diagnosis is relatively simple to establish.5,17 In many cases of intermittent, mild, or partial compression, the signs and symptoms are vague and nondescript. The most common symptom is mild to moderate aching pain in the proximal forearm, sometimes described as tiredness and heaviness. Use of the arm may cause a mild or dull aching pain to become deep or sharp. Repetitive elbow motions are likely to provoke 131

132

PART 1  MSK Disorders

Biceps

Brachial artery Median nerve

Median nerve

Pronator teres

Pronator teres (superficial head)

1

2

Lacertus fibrosus

Radial artery Pronator teres (deep head)

3 FDS arch (sublimis bridge) FDS

FIG. 24.1  The median nerve is shown descending beneath the sublimis bridge after traversing the space between the two heads of the pronator teres. The nerve is compressed at the sublimis bridge. (From Kopell HP, Thompson WA. Pronator syndrome: a confirmed case and its diagnosis. N Engl J Med. 1958;259:713–715.)

symptoms. As the pain intensifies, it may radiate proximally to the elbow or even the shoulder. Paresthesias in the distribution of the median nerve may be reported, but they are generally not as severe or well localized as the complaints in carpal tunnel syndrome. When numbness is a prominent symptom, the complaints may mimic carpal tunnel syndrome. Pronator teres syndrome should be considered as a possibility among patients with carpal tunnel syndrome, especially in severe forms.7,8 However, unlike carpal tunnel syndrome, pronator teres syndrome rarely has nocturnal exacerbation, and the symptoms are not affected by a change of wrist position. 

Anterior Interosseous Syndrome The onset of anterior interosseous syndrome can be related to exertion, or it may be spontaneous. In classic cases of spontaneous anterior interosseous nerve paralysis, there is acute pain in the proximal forearm or arm lasting for hours or days. There may be a history of local trauma or heavy muscle exertion at the onset of pain. As mentioned, the patient may complain of weakness of the forearm muscles innervated by the anterior interosseous nerve. Theoretically, there should be no sensory complaints.6,7 

Biceps brachii Median n. Lacertus fibrosus

Sublimis arch Anterior interosseous n.

Flexor digitorum sublimis

Flexor pollicis longus

Pronator quadratus

Physical Examination Pronator Teres Syndrome Findings may be poorly defined and difficult to substantiate in pronator teres syndrome.5,17 The most important physical finding is tenderness over the proximal forearm. Pressure over the pronator teres muscle produces discomfort and may produce a radiating pain and digital numbness. The symptomatic pronator teres muscle may be firm to palpation compared with the other side. The contour of the forearm may be depressed, caused by the thickening of the lacertus fibrosus. Distinctive findings are weakness of both the intrinsic muscles of the hand supplied by the median nerve and the muscles proximal to the wrist and in the forearm, including tenderness; the Tinel sign over the point of entrapment; and absence of the Phalen sign. Pain may be elicited by pronation of the forearm, elbow flexion, or even contraction of the superficial flexor of the second digit. Sensory examination findings are usually poorly defined but may involve not only the median nerve distribution of

FIG. 24.2  Course of the median nerve and its anterior interosseous branch.

the digits but also the thenar region of the palm because of involvement of the palmar cutaneous branch of the median nerve. Deep tendon reflexes and cervical examination findings should be normal.8,15,16,19–23 

Anterior Interosseous Syndrome To test the muscles innervated by the anterior interosseous nerve,5,17 the clinician braces the metacarpophalangeal joint of the index finger and the patient is asked to flex only the

CHAPTER 24  Median Neuropathy

A

B

distal phalanx. This isolates the action of the flexor digitorum profundus on the terminal phalanx and eliminates the action of the flexor digitorum superficialis. There is no terminal phalanx flexion if the anterior interosseous nerve is injured. Another useful test is to ask the patient to make the “OK” sign.24 In anterior interosseous syndrome, the distal interphalangeal joint cannot be flexed, which results in the index finger’s remaining relatively straight during this test (Fig. 24.3). The patient is asked to forcefully approximate the finger pulps of the first and second digits. The patient with weakness of the flexor pollicis longus and digitorum profundus muscles cannot touch with the pulps of the fingers; instead, the entire volar surfaces of the digits are in contact. This is due to the paralysis of the flexor pollicis longus and flexor digitorum profundus of the second digit. The pronator quadratus is difficult to isolate clinically, but an attempt can be made by flexing the forearm and asking the patient to resist supination. Sensation and deep tendon reflexes should be normal.8,15,16,19–23 

Functional Limitations Pronator Teres Syndrome In pronator teres syndrome, there is clumsiness, loss of dexterity, and a feeling of weakness in the hand. This may lead to functional limitations both at home and at work. Repetitive elbow motions—such as hammering, cleaning fish, serving tennis balls, and rowing—are most likely to provoke symptoms. 

Anterior Interosseous Syndrome As weakness develops in anterior interosseous syndrome, there is loss of dexterity and pinching motion with difficulty in picking up small objects with the first two digits. Activities of daily living, such as buttoning shirts and tying shoelaces, can be impaired. Patients may have difficulty with typing, handwriting, cooking, and so on. 

133

FIG. 24.3 The anterior interosseous nerve innervates the flexor pollicis longus as well as the flexor digitorum profundus to the index and long fingers. (A) It is responsible for flexion of the thumb’s interphalangeal joint and the index finger’s distal interphalangeal joint. (B) An injury to the median nerve high in the forearm or to the anterior interosseous branch of the median nerve results in inability to forcefully flex these joints. (From Concannon MJ. Common Hand Problems in Primary Care. Philadelphia, 1999, Hanley & Belfus.)

Diagnostic Studies Pronator Teres Syndrome Electrodiagnostic testing (nerve conduction studies and electromyography) is the gold standard for confirming pronator teres syndrome.4,25,26 Results of nerve conduction studies may be abnormal in the median nerve distribution; however, the diagnosis may best be established by electromyographic studies demonstrating membrane instability (including increased insertional activity, fibrillation and positive sharp waves at rest, wide- and high-amplitude polyphasics on minimal contraction, and decreased recruitment pattern on maximal contraction) of the median nerve muscles below and above the wrist in the forearm but with sparing of the pronator teres.27,28 Imaging studies (e.g., radiography, computed tomography, hypoechoic swelling by ultrasonography, and magnetic resonance imaging) are used to exclude alternative diagnoses. Magnetic resonance imaging (Bull’s eye sign) and high-resolution ultrasonography (hourglass appearance) may be helpful in diagnosis, although there is no consensus on which is the preferred method.29–35 

Anterior Interosseous Syndrome Electrodiagnostic studies may also help to establish the diagnosis of anterior interosseous syndrome.5 In general, the results of routine motor and sensory studies are normal. The most appropriate technique is surface electrode recording from the pronator quadratus muscle with median nerve stimulation at the antecubital fossa. On electromyography, findings of membrane instability are restricted to the flexor pollicis longus, flexor digitorum profundus (of the second and third digits), and pronator quadratus.12,22 Imaging studies are useful in excluding other diagnoses. Ultrasonography has been used to follow the hourglass-like fascicular constriction, which lessens with relief of motor weakness in treated patients.25–35 

134

PART 1  MSK Disorders

Differential Diagnosis PRONATOR TERES SYNDROME Carpal tunnel syndrome Cervical radiculopathy, particularly lesions affecting C6 or C7 Thoracic outlet syndrome with involvement of the medial cord Elbow arthritis Epicondylitis 

FIG. 24.4  A typical splint used in pronator teres syndrome.

ANTERIOR INTEROSSEOUS SYNDROME Paralytic brachial plexus neuritis Entrapment or rupture of the tendon of the flexor pollicis longus Rupture of the flexor pollicis longus and flexor digitorum profundus

Treatment Initial Pronator Teres Syndrome Treatment is initially conservative, with rest and avoidance of the offending repetitive trauma.7,17 A wrist immobilization splint is applied in 15 degrees of dorsiflexion for 4 to 6 weeks. The patient is instructed in friction massage. Ice and electrical stimulation are instituted three times a week for 10 treatments. The splint is discontinued at a time determined by the physician.36 Nonsteroidal anti-inflammatory drugs may help with pain and inflammation. Analgesics may be used for pain. Low-dose tricyclic antidepressants may be used for pain and to help with sleep. Antiseizure medications are also often used for neuropathic pain (e.g., carba­ mazepine, gabapentin). 

Anterior Interosseous Syndrome Treatment of the anterior interosseous syndrome depends on the cause.5,17 Penetrating wounds require immediate exploration and repair. Impending Volkmann contracture demands immediate decompression. In spontaneous cases associated with specific occupations, a trial of nonoperative therapy is indicated. If spontaneous improvement does not occur by 6 to 8 weeks, consideration should be given to surgical exploration. Conservative management includes avoiding the activity that exacerbates the symptoms. Pharmacologic treatment is similar to that for pronator teres syndrome. 

Rehabilitation Pronator Teres Syndrome A splint that can put the thumb in an abducted, opposed position, such as a C bar or a thumb post–static orthosis, can be used (Fig. 24.4).11,12,14 Taping of the index and middle fingers in a buddy splint to stabilize the lack of distal interphalangeal flexion may be helpful.14 Rehabilitation may include modalities such as ultrasound, electrical stimulation, iontophoresis, phonophoresis, and low-level laser therapy.43 The patient can be instructed in ice massage as well. Once the acute symptoms have subsided, physical or occupational therapy can focus on exercises to improve forearm flexibility, muscle strength responsible for thumb abduction and opposition, and wrist radial flexion. 

FIG. 24.5  A typical splint used in anterior interosseous syndrome.

Anterior Interosseous Syndrome Resting the arm by immobilization in a splint may be tried (Fig. 24.5).37 If the symptoms subside, conservative physical or occupational therapy—including physical modalities as previously described and exercises to improve strength and function of the pronator quadratus, flexor digitorum profundus, and flexor pollicis longus—can be initiated.14 

Procedures In both anterior interosseous and pronator teres syndromes, a median nerve block may be attempted (Figs. 24.6 and 24.7).38 

Technology Low-level laser therapy has been added as an adjunctive physical therapy modality in elbow and wrist pain. Endoscopic procedures have been utilized because of their advantage in using only a small incision. 

Surgery Pronator Teres Syndrome If symptoms fail to resolve, surgical release of the pronator teres muscle and any constricting bands (ligament of Struthers and lacertus fibrosus) should be considered with direct exploration of the area. Traditionally, an S-shaped incision is used to extensively expose the entire median nerve from the forearm to the hand.39 Recent techniques have elucidated the possible advantage of using small-incision endoscopic procedures.40,41 

Anterior Interosseous Syndrome If spontaneous improvement does not occur by 6 to 8 weeks, consideration should be given to surgical exploration. The surgical technique for exploration is exposure of the median nerve directly beneath the pronator teres or separation of this muscle from the flexor carpi radialis, identification of the anterior interosseous nerve, and release of the offending structures.

CHAPTER 24  Median Neuropathy

Median n. Brachial a.

Bicipital aponeurosis

Medial epicondyle Pronator teres m.

135

If surgical decompression was performed and failed to resolve the weakness and after a more proximal fascicular lesion is ruled out, tendon transfers may be considered.39 An endoscopically assisted technique has been tried but without much success at this point because of the depth of the surgical approach and limited view.42 

Postoperative Rehabilitation36 0 to 1 Week Postoperative dressing is removed. Active and gentle passive range-of-motion exercises are initiated for 15 minutes per hour. Desensitization and edema management are instituted. Pronation and elbow extension stretching exercises are instituted four times a day. 

3 Weeks Strengthening is initiated in accordance with the patient’s comfort level using putty, Hand Helper, and Thera-Band. 

FIG. 24.6  Pronator teres nerve block. At the elbow crease, make a mark at the midpoint between the medial epicondyle and the biceps tendon. Then, under sterile conditions, insert a 25-gauge 1½-inch disposable needle into the pronator teres muscle approximately 2 cm below the mark or at the point of maximal tenderness in the muscle. Confirmation of needle placement can be made with a nerve stimulator. Then inject 3 to 5 mL of a corticosteroid-anesthetic solution (e.g., 2 mL of methylprednisolone [40 mg/mL] combined with 2 mL of 1% lidocaine). Postinjection care may include icing for 10 to 15 minutes and splinting of the wrist and forearm in a functional position for a few days. Also, the patient should be cautioned to avoid aggressive use of the arm for at least 1 to 2 weeks. (From Lennard TA. Pain Procedures in Clinical Practice. 2nd ed. Philadelphia, 2000, Hanley & Belfus.)

Potential Disease Complications Pronator Teres Syndrome If the condition is left unresolved, possible disease-related complications include permanent loss of the use of the pinch grasp, lack of wrist flexion, and incessant pain. 

Anterior Interosseous Syndrome If it is allowed to persist, this syndrome will cause inability to perform the pinch grasp, resulting in the functional deficits mentioned previously. 

Potential Treatment Complications Use of anti-inflammatory medications such as nonsteroidal anti-inflammatory drugs can induce gastric, renal, and hepatic side effects. Local steroid injections can induce skin depigmentation, local atrophy, or infection. Surgical complications include infection, bleeding, and injury to surrounding structures.

References

FIG. 24.7 Anterior interosseous nerve block. The anterior interosseous nerve can be blocked by either an anterior or a posterior approach. For the posterior approach, the posterior elbow is exposed and the forearm is placed in neutral. Under sterile conditions with use of a 2-inch, 25-gauge disposable needle, inject 3 to 5 mL of a corticosteroid-anesthetic solution (e.g., 2 mL of methylprednisolone [40 mg/mL] combined with 2 mL of 1% lidocaine) approximately 5 cm distal to the tip of the olecranon. The needle should penetrate about 3.5 to 5 cm toward the biceps tendon’s insertion at the radius. A nerve stimulator is necessary to ensure proper placement. Postinjection care is similar to that of the pronator teres nerve block. (From Lennard TA. Pain Procedures in Clinical Practice. 2nd ed. Philadelphia, 2000, Hanley & Belfus.)

1. Lee MJ, LaStayo PC. Pronator syndrome and other nerve compressions that mimic carpal tunnel syndrome. J Orthop Sports Phys Ther. 2004;34:601–609. 2. Mercier LR. Pronator Syndrome. Ferri’s Clinical Advisor. Philadelphia: Elsevier Mosby; 2010. 3. Sotereanos DG, Sarris I, Gobel F. Pronator and anterior interosseous nerve compression syndromes. In: Berger RA, Weiss AC, eds. Hand Surgery. Philadelphia: Lippincott Williams & Wilkins; 2004:49. 4. Liveson J. Peripheral Neurology—Case Studies in Electrodiagnosis. 2nd ed. Philadelphia: FA Davis; 1991:23–26. 5. Shapiro BE, Preston DC. Entrapment and compressive neuropathies. Med Clin North Am. 2003;87:663–696. 6. Afshar A. Pronator syndrome due to Schwannoma. J Hand Microsurg. 2015;7(1):119–122, Epub 2014 Jan 5. 7. Lee MJ, La Stayo PC. Pronator syndrome and other nerve compressions that mimic carpal tunnel syndrome. J Orthop Sports Phys Ther. 2004;34:601–609. 8. Bilecenoglu B, Uz A, Karalezli N. Possible anatomic structures causing entrapment neuropathies of the median nerve: an anatomic study. Acta Orthop Belg. 2005;71:169–176. 9. Asheghan M, Hollisaz MT, Aghdam AS, Khatibiaghda A. The prevalence of pronator teres among patients with carpal tunnel syndrome: cross-sectional study. Int J Biomed Sci. 2016;12(3):89–94.

136

PART 1  MSK Disorders

10. Hsiao CW, Shih JT, Hung ST. Concurrent carpal tunnel syndrome and pronator syndrome: a retrospective study of 21 cases. Orthop Traumatol Surg Res. 2016;25. 11. Puhaindran ME, Wong HP. A case of anterior interosseous nerve syndrome after peripherally inserted central catheter (PICC) line insertion. Singapore Med J. 2003;44:653–655. 12. Rieck B. Incomplete anterior interosseous syndrome in a guitar player. Handchir Mikrochir Plast Chir. 2005;37:418–422 [in German]. 13. Lederman RJ. Neuromuscular and musculoskeletal problems in instrumental music. Muscle Nerve. 2003;27:549–561. 14. Burke SL, Higgins J, Saunders R, et al. Hand and Upper Extremity Rehabilitation: A Practical Guide. 3rd ed. St. Louis: Elsevier Churchill Livingstone; 2006:87–95. 15. Bromberg MB, Smith AG, eds. Handbook of Peripheral Neuropathy. Boca Raton: Taylor & Francis; 2005:476–478. 16. Valbuena SE, O’Toole GA, Roulot E. Compression of the median nerve in the proximal forearm by a giant lipoma: a case report. J Brachial Plex Peripher Nerve Inj. 2008;3:17. 17. Dawson D, Hallett M, Millender L. Entrapment Neuropathies. 3rd ed. Boston: Little, Brown; 1999:98–109. 18. Aljawder A, Fagi MK, Mohamed A, Alkhalifa F. Anterior interosseous nerve syndrome diagnosis and intraoperative findings, a case report. Int J Surg Case Rep. 2016;21:44–47, Epub 2016 Feb 20. 19. Stewart J, Jablecki C. Median nerve. In: Brown W, Boulton C, Aminoff J, eds. Neuromuscular Function and Disease, Basic Clinical and Electrodiagnostic Aspects. Philadelphia: WB Saunders; 2002:873. 20. Spinner RJ, Amadio PC. Compressive neuropathies of the upper extremities. Clin Plast Surg. 2003;30:158–159. 21. Campbell WW. Proximal Median Neuropathy. Dejong’s the Neurologic Examination. 6th ed. Philadelphia: Lippincott Williams & Wilkins; 2005:553–554. 22. Prescott D, Shapiro B. Proximal median neuropathy. In: Electromyography and Neuromuscular Disorders: Clinical Electrophysiologic Correlations. 2nd ed. Philadelphia: Elsevier; 2005:281–290. 23. Dyck PJ, Thomas PK. Peripheral Neuropathy. Vol. 2. Philadelphia: Elsevier Saunders; 2005:1453–1454. 24. Mackinnon SE. Pathophysiology of nerve compression. Hand Clin. 2002;18:231–241. 25. Bridgeman C, Naidu S, Kothari MJ. Clinical and electrophysiological presentation of pronator syndrome. Electromyogr Clin Neurophysiol. 2007;47:89–92. 26. Dumitru D. Electrodiagnostic Medicine. Philadelphia: Hanley & Belfus; 1994:864–867. 27. Wilbourne AS. Electrodiagnostic examination with peripheral nerve injuries. Clin Plast Surg. 2003;30:150–151.

28. Kimura J. Electrodiagnosis in Diseases of Nerve and Muscle: Principles and Practice. 3rd ed. New York: Oxford University Press; 2001;14–15:719–723. 29. Martinoli C, Bianchi S, Pugliese F, et al. Sonography of entrapment neuropathies in the upper limb (wrist excluded). J Clin Ultrasound. 2004;32:438–450. 30. Jacobson JA, Fessell DP, Lobo Lda G, Yang LJ. Entrapment neuropathies I: upper limb (carpal tunnel excluded). Semin Musculskelet Radiol. 2010;14:473–486. 31. Peer S, Bodner G, eds. High-Resolution Sonography of the Peripheral Nervous System. New York: Springer; 2003. 32. Andreisik G, Crook DW, Burg D, et al. Peripheral neuropathies of the median, radial, and ulnar nerves: MR imaging features. Radiographics. 2006;26:1267–1287. 33. Kim S, Choi JY, Huh YM, et al. Role of magnetic resonance imaging in entrapment and compressive neuropathy—what, where, and how to see the peripheral nerves on the musculoskeletal magnetic resonance image: part 2. Upper extremity. Eur Radiol. 2007;17:509–522. 34. Sneag DB, Saltzman EB, Meister DW, Feinberg JH, Lee SK, Wolfe SW. MRI Bullseye sign: an indicator of peripheral nerve constriction in Parsonage-Turner Syndrome. PTS Muscle Nerve. 2016. 35. Sunogawa T, Nakashima Y, Shinomiya R, Kurumadani H, Adachi N, Ochi M. Correlation between “hourglass-like fascicular constriction” and idiopathic anterior interosseous nerve palsy. Muscle Nerve. 2016. 36. Pronator syndrome therapy. E-hand.com the electronic textbook of hand therapy. American Society for Surgery of the Hand.-01-30-17. 37. Trombly C, ed. Occupational Therapy for Physical Dysfunction. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 1997:556–558. 38. Hunter J, Mackin E, Callahan A, eds. Rehabilitation of the Hand and Upper Extremity. 5th ed. St. Louis: Mosby–Year Book; 2002. 39. Braddom R. Physical Medicine and Rehabilitation. Philadelphia: WB Saunders; 1996:328–329. 40.  Zancolli ER III, Zancolli EP IV, Perotto CJ. New mini-invasive decompression for pronator syndrome. J Hand Surg [Am]. 2012;37: 1706–1710. 41. Lee AK, Khorsandi M, Nurbhai N, et al. Endoscopically assisted decompression for pronator syndrome. J Hand Surg [Am]. 2012;37A:1173–1179. 42. Keiner D, Tschabitscher M, Welschehold S, Oertel J. Anterior interosseus nerve compression: is there a role for endoscopy? Acta Neurochir (Wien). 2011;153:2225–2229. 43. Okuni I, Ushigome N, Harada T, et al. Low level laser therapy for chronic pain of the elbow, wrist and fingers. Laser therapy. 2012;21(1):33–37.

CHAPTER 25

Olecranon Bursitis Jayne Donovan, MD

Synonyms Miner’s elbow Student’s elbow Draftsman’s elbow Plumber’s elbow Dialysis elbow Elbow bursitis

ICD-10 Codes M70.20 M70.21 M70.22

Olecranon bursitis unspecified elbow Olecranon bursitis right elbow Olecranon bursitis left elbow

Definition Olecranon bursitis is a swelling of the subcutaneous, synovium-lined fluid-filled sac located posteriorly over the olecranon process of the ulna and the triceps tendon. The bursa serves as a cushion between the tip of the olecranon and the overlying skin. Because of its location, the olecranon bursa is particularly susceptible to injury and olecranon bursitis is one of the most common forms of superficial bursitis. Olecranon bursitis can be classified as acute, chronic, or septic. The most common etiologies include trauma and pre-existing systemic medical conditions.1 For example, acute bursitis can result from direct trauma, prolonged pressure, or microcrystalline disease. Chronic bursitis is usually secondary to overuse/microtrauma or systemic disorders. Septic olecranon bursitis is almost always associated with trauma and represents approximately 20% of cases.1,2 Trauma can lead to bursitis from a single, direct blow to the elbow or from minor repetitive stress. Trauma is thought to stimulate increased vascularity, resulting in bursal fluid production and fibrin coating of the bursal wall.3 Persons engaged in certain occupations or activities are susceptible to olecranon bursitis due to prolonged pressure or repetitive stress with microtrauma, including auto mechanics, gardeners, plumbers, carpet layers, students, gymnasts, wrestlers, and dart throwers. Interestingly, approximately 7% of hemodialysis patients develop olecranon bursitis.4 Repeated, prolonged positioning of the elbow and anticoagulation appear to be contributing factors. Trauma can also lead to septic olecranon bursitis, allowing for transcutaneous inoculation of the bursa.

Inflammatory causes of olecranon bursitis include systemic diseases such as rheumatoid arthritis, systemic lupus erythematosus, microcrystalline disease, and chondrocalcinosis. Olecranon bursitis is commonly seen in rheumatoid patients, in whom the bursa may communicate with the affected elbow joint. The olecranon bursa is one of the most affected bursae in microcrystalline diseases. In septic olecranon bursitis, the source is most often transcutaneous, with about half of affected individuals having an identifiable break in the skin. Hematogenous seeding is thought to be rare, as the bursa has a limited blood supply.5 When bursal fluid culture samples are positive, Staphylococcus aureus and β-hemolytic Streptococcus are the first and second most common causative agents, respectively.6,7 Resulting sepsis is unusual. There appears to be a seasonal trend, with a peak of staphylococcal septic bursitis during the summer months.8 Many pre-existing diseases are risk factors for septic olecranon bursitis, including microcrystalline diseases, rheumatoid arthritis, diabetes mellitus, uremia, and psoriasis. Alcoholism, injection drug use, and steroid/immunosuppressive therapy are also considered predisposing factors. 

Symptoms A detailed history focusing on presenting symptoms, risk factors (including occupation, hobbies, medical history), recent trauma, and the possibility of infection or neoplasm is key.9 Commonly reported symptoms with olecranon bursitis are swelling, redness, and variable tenderness. These symptoms have been found to be inadequate to differentiate between nonseptic and septic arthritis. However, fever has only been reported in septic bursitis.5,10 Other potential signs of infection include anorexia, lethargy, and night sweats.9 When associated pain is present, patients usually have discomfort when the elbow is flexed beyond 90 degrees secondary to stretching of the bursa and also have trouble resting on the elbow. Neoplasm should be considered on the differential diagnosis and factors including rapid growth, weight loss, history of neoplasms, or failure of initial treatment suggest need for further investigation.9 

Physical Examination The physical examination can vary somewhat, depending on the underlying condition. With acute bursitis, a fluctuant mass is present over the tip of the elbow (Fig. 25.1). With chronic bursitis, the fluctuance may be replaced with a thickened bursa (Fig. 25.2). However, like symptom presentation, differentiating between nonseptic and septic bursitis based on physical exam can be difficult due 137

138

PART 1  MSK Disorders

FIG. 25.1  Atraumatic olecranon bursitis in a 55-year-old woman. A large, fluctuant mass is present.

FIG. 25.3  Lateral radiograph of the elbow in a patient with chronic olecranon bursitis. Note the olecranon spur.

Diagnostic Studies

FIG. 25.2  Chronic gouty olecranon bursitis. The prominence at the tip of the elbow is firm with thinning of the overlying skin.

to significant overlap.5,11 Both conditions may produce tender fluctuance, induration, swelling, warmth, and local erythema. Elbow flexion may be somewhat limited by pain, although not as limited as with septic arthritis of the elbow joint. No pain or changes in range of motion are typically seen with elbow extension. A break in the skin over the elbow and overlying cellulitis are important clues to a potential underlying septic process. In inflammatory cases, pain inhibition may produce mild weakness of elbow flexion and extension. Sensation and distal pulses are unaffected. Examination findings of other joints should also be normal. 

Functional Limitations Functional limitations can vary. Many cases of traumatic olecranon bursitis have minimal associated functional limitations. Patients may note some mild discomfort with direct pressure over the tip of the elbow (e.g., when sitting at a desk or resting the arm on the armrest of a chair or in the car). With crystal-induced and septic bursitis, pain can be more limiting. Patients may have trouble sleeping and have difficulty with most activities of daily living that involve the affected extremity (e.g., dressing, grooming, cleaning, shopping, and carrying packages). 

Although clinical practice varies, many clinicians recommend anteroposterior and lateral radiographs to evaluate for foreign bodies, soft tissue abnormalities, and bony pathology.1,9,11 Plain radiographs may demonstrate an olecranon spur in about one third of cases (Fig. 25.3). Ultrasound can also be considered to help characterize the structure or content of the bursa (such as the size of a fluid collection and any proliferation of the synovium) and potentially identify underlying causes such as loose bodies, gout tophi, or rheumatoid nodules.12 Although there can be considerable overlap in findings, absence of soft tissue enhancement on magnetic resonance imaging is suggestive of nonseptic bursitis.13 Because this is an extra-articular process, imaging studies will not show a joint effusion. In most cases of olecranon bursitis, aspiration of the bursal fluid is indicated to rule out infection and evaluate for a potential microcrystalline disorder.11 If possible, aspiration should be performed under sterile conditions prior to treatment with antibiotic therapy.9 The fluid should be sent for leukocyte count with differential, glucose levels, Gram stain, bacterial culture, and crystal analysis. Additionally, peripheral blood should be analyzed, including complete blood count with differential, C-reactive protein, erythrocyte sedimentation rate, and glucose levels. Peripheral blood cultures should be considered based on clinical presentation, especially in the case of immunocompromised individuals given higher rates of associated bacteremia.1 A positive culture of bursal fluid is the gold standard in the diagnosis of septic olecranon bursitis. Additional test results should be considered collectively, as no single test has been shown to be highly sensitive or specific for early identification of nonseptic versus septic olecranon bursitis.1 Negative Gram stain cannot be relied upon to rule out septic bursitis.1 Aspirate differential is thought to be more valuable than leukocyte count alone. Acute, traumatic bursal fluid typically has a clear, milky, or serosanguineous appearance, with a predominance of monocytes. Infected bursal fluid is usually purulent and contains an increased leukocyte count, with a high percentage of polymorphonuclear cells. Even in the setting of infection, the fluid should be examined under a polarizing microscope because simultaneous infectious and crystal-induced arthritis can occur.14 

CHAPTER 25  Olecranon Bursitis

139

Differential Diagnosis

Procedures

Rheumatoid nodule Lipoma Tophus Elbow synovitis Olecranon spur Neoplasm

Initial needle aspiration can be therapeutic as well as diagnostic and usually reduces symptoms. The elbow is prepared in a sterile fashion. The skin is infiltrated locally with 1% lidocaine. To minimize the risk of persistent drainage after aspiration, it is recommended to insert a long 18-gauge needle at a point well proximal to the tip of the elbow. The bursa should be drained as completely as possible. The fluid should be sent for analysis as mentioned above. Post-injection care includes local icing for 10 to 20 minutes. A sterile compressive dressing is then applied, followed by an anterior plaster splint that maintains the elbow in 60 degrees of flexion. The role of serial aspirations is controversial. Corticosteroid injections into the bursa have been shown to hasten the resolution of traumatic and crystal-induced olecranon bursitis.16 However, treatment with corticosteroids is associated with a higher rate of complications.17 These complications can include infection, skin atrophy, development of a draining sinus tract, and chronic local pain. Consequently, the routine use of steroid injections for olecranon bursitis is not generally recommended. In a recent study, aspiration and aspiration with steroid injection showed no clear treatment advantage over treatment with a short course of NSAIDs and compression. Conservative treatment with compression bandaging and a short course of NSAIDs was suggested.18 

Treatment Initial Treatment of traumatic nonseptic olecranon bursitis begins with prevention of further injury to the involved elbow. An elbow pad provides compression and protects the bursa. The patient should be counseled in ways of protecting the elbow at work and during recreation. After education, conservative treatment with elevation, ice, and nonsteroidal anti-inflammatories (NSAIDs) is recommended.9,11 Traumatic, non-inflammatory bursitis usually resolves with this treatment.15 In suspected cases of septic olecranon bursitis, bursal aspiration is recommended (see the section on procedures) prior to the administration of antibiotics. When cellulitis over the tip of the elbow is present without an obvious collection, empirical treatment with antibiotic therapy to cover penicillin-resistant S. aureus, the most common offender, is recommended. Antibiotic therapy is adjusted based on the culture results. Outpatient cases are observed closely, with any changes in the size of the bursa and the quality of the overlying skin noted. The decision whether to instead use intravenous antibiotics depends on the appearance of the elbow, the signs of systemic illness, and the general health of the patient. Patients with extensive infection or underlying bursal disease, systemic disease, or immunosuppression and outpatients refractory to oral treatment should be treated with an intravenous cephalosporin. In one study, the average duration of intravenous therapy was 4.4 days if symptoms had been present for less than 1 week and 9.2 days if symptoms had been present for longer than 1 week.7 The conversion to oral antibiotics should occur only after consistent improvement is seen in the appearance of the patient and the elbow. 

Rehabilitation Because the process is extra-articular, permanent elbow stiffness is not typically a problem. Physical or occupational therapy for gentle range of motion exercise may be indicated once the bursitis has begun to improve. Extreme flexion should be avoided early on because this position puts tension on the potentially already compromised skin. If prolonged immobilization is necessary in the treatment course, subsequent therapy may include range of motion and strengthening exercises of the arm and forearm. Patients who have traumatic or recurrent olecranon bursitis should be counseled in ways to modify their home and work activities to eliminate irritation to the bursa. This might include the use of ergonomic equipment, such as forearm rests (also called data arms) that do not contact the elbow. In some instances, vocational retraining may be indicated. 

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery Surgery is rarely recommended for acute traumatic olecranon bursitis. Chronic drainage of bursal fluid is the most common indication for surgery.19 Surgical treatment is also considered in nonseptic and septic olecranon bursitis with failed conservative treatment or when complications occur.11 Specifically, in cases of septic olecranon bursitis, surgery is considered if there is no significant improvement with several days of appropriate management or with signs of progressive systemic infection such as fever, serum leukocytosis, hypotension, tachypnea, or change in mental status.9,11,20 Bursectomy is conventionally done through an open technique, although an endoscopic technique is now also being used, which may improve associated wound healing issues.21 Surgery has been found to be significantly less effective for individuals with rheumatoid arthritis compared to non-rheumatoid patients.22 A recent systematic review found surgical management to be less effective and to be associated with higher rates of complications compared to nonsurgical management.17 

Potential Disease Complications Septic bursitis has been traditionally thought to pose the greatest threat with regard to disease complications. If it is neglected, the infection may thin the overlying skin and eventually erode through it. This complication is difficult to manage, often requiring extensive débridement and flap

140

PART 1  MSK Disorders

coverage. Persistent infection can also result in osteomyelitis of the olecranon process. Immunocompromised patients are at risk for sepsis from olecranon bursitis and an increased risk of recurrence.23 Necrotizing fasciitis originating from a septic olecranon bursitis, although rare, may prove to be fatal. 

Potential Treatment Complications Analgesics and NSAIDs have well-known side effects on the gastric, hepatic, and renal systems. Persistent drainage from a synovial fistula is an uncommon complication of aspiration of the olecranon bursa. Complications of steroid injection, as described earlier, can be serious. In addition, wound problems are the major complication associated with surgical treatment of olecranon bursitis. Because of the superficial location of the olecranon and the tenuous blood supply of the overlying skin, wound healing can be difficult. Malnourished and chronically ill patients are especially at risk for surgical complications.

References 1. Reilly D, Kamineni S. Olecranon bursitis. J Shoulder Elbow Surg. 2016;25:158–167. 2. Jaffe L, Fetto JF. Olecranon bursitis. Contemp Orthop. 1984;8:51–56. 3. Canoso JJ. Idiopathic or traumatic olecranon bursitis. Clinical features and bursal fluid analysis. Arthritis Rheum. 1977;20:1213–1216. 4. Irby R, Edwards WM, Gatter RJ. Articular complications of hemotransplantation and chronic renal hemodialysis. Rheumatology. 1975;2:91–99. 5. Garcia-Porrua C, Gonzalez-Gay MA, Ibanez D, Garcia-Pais MJ. The clinical spectrum of severe septic bursitis in north-western Spain: a 10 year study. J Rheumatol. 1999;26:663–667. 6. Zimmerman B III, Mikolich DJ, Ho G. Septic bursitis. Semin Arthritis Rheum. 1995;24:391–410. 7. Ho G Jr, Su EY. Antibiotic therapy of septic bursitis. Arthritis Rheum. 1981;24:905–911. 8. Cea-Pereiro JC, Garcia-Meijide J, Mera-Varela A, Gomez-Reino JJ. A comparison between septic bursitis caused by Staphylococcus aureus and those caused by other organisms. Clin Rheumatol. 2001;20:10–14.

9. Blackwell JR, Hay BA, Alexander MB, Hay SM. Olecranon bursitis: a systematic overview. Shoulder & Elbow. 2014;6:182–190. 10. Laupland KB, Davies HD, Group CHPTPS. Olecranon septic bursitis managed in an ambulatory setting. the calgary home parenteral therapy program study group. Clin Invest Med. 2001;24:171–178. 11. Baumback SF, Lobo CM, Badyine I, et al. Prepatellar and olecranon bursitis: literature review and development of a treatment algorithm. Arch Orthop Trauma Surg. 2014;134:359–370. 12. Blankstein A, Ganel A, Givon U, et al. Ultrasonographic findings in patients with olecranon bursitis. Ultraschall Med. 2006;27:568–571. 13. Floemer F, Morrison WB, Bongartz G, Ledermann HP. MRI characteristics of olecranon bursitis. ARJ Am J Roentgenol. 2004;183:29–35. 14. Gerster JC, Lagier R, Boivin G. Olecranon bursitis related to calcium pyrophosphate dihydrate deposition disease. Arthritis Rheum. 1982;25:989–996. 15. Smith DL, McAfee JH, Lucas LM, et al. Treatment of nonseptic olecranon bursitis. A controlled, blinded prospective trial. Arch Intern Med. 1989;149:2527–2530. 16. Weinstein PS, Canso JJ, Wohlgethan JR. Long-term follow-up of corticosteroid injection for traumatic olecranon bursitis. Ann Rheum Dis. 1984;43:44–46. 17. Sayech ET, Straugh RJ. Treatment of olecranon bursitis: a systematic review. Arch Orthop Trauma Surg. 2014;134:1517–1536. 18. Kim JY, Chung SW, Kim JH, et al. A randomized trial among compression plus nonsteroidal anitinflammatory drugs, aspiration, and aspiration with steroid injection for nonseptic olecranon bursitis. Clin Orthop Relat Res. 2016;474:776–783. 19. Morrey BF. Bursitis. In: Morrey BF, ed. The elbow and its disorders. 3rd ed. Philadelphia: WB Saunders; 2000:901–908. 20. Abzug JM, Chen NC, Jacoby SM. Septic olecranon bursitis. J Hand Surg Am. 2012;37:1253–1253. 21. Rhyou IH, Park KJ, Kim NK, et al. Endoscopic olecranon bursal resection for olecranon bursitis: A comparative study for septic and aseptic olecranon bursitis. J Hand Surg Asian Pac. 2016;21:167–172. 22. Stewart NJ, Manzanares JB, Morrey BF. Surgical treatment of aseptic olecranon bursitis. J Shoulder Elbow Surg. 1997;6:49–54. 23. Perez C, Huttner A, Assal M, et al. Infectious olecranon and patellar bursitis: short-course adjuvant antibiotic therapy is not a risk factor for recurrence in adult hospitalized patients. J Antimicrob Chemother. 2010;65:1008–1014.

CHAPTER 26

Radial Neuropathy Lyn D. Weiss, MD Thomas E. Pobre, MD

Synonyms Radial nerve palsy Radial nerve compression Wrist drop neuropathy Finger or thumb extensor paralysis Saturday night palsy Supinator syndrome Radial tunnel syndrome Cheiralgia paresthetica

ICD-10 Codes G56.30 Lesion of radial nerve, unspecified upper limb G56.31 Lesion of radial nerve, right upper limb G56.32 Lesion of radial nerve, left upper limb

Definition The radial nerve originates from the C5 to T1 roots. These nerve fibers travel along the upper, middle, and lower trunks. They continue as the posterior cord and terminate as the radial nerve. The radial nerve is prone to entrapment in the axilla (crutch palsy), the upper arm (spiral groove), the forearm (posterior interosseous nerve), and the wrist (cheiralgia paresthetica). Radial neuropathies can result from direct nerve trauma, compressive neuropathies, neuritis, or complex humerus fractures.1 In the proximal arm, the radial nerve gives off three sensory branches (posterior cutaneous nerve of the arm, lower lateral cutaneous nerve of the arm, and posterior cutaneous nerve of the forearm). The radial nerve supplies a motor branch to the triceps and anconeus before wrapping around the humerus in the spiral groove, a common site of radial nerve injury. The nerve then supplies motor branches to the brachioradialis, the long head of the extensor carpi radialis, and the supinator. Just distal to the lateral epicondyle, the radial nerve divides into the posterior interosseous

nerve (a motor nerve) and the superficial sensory nerve (a sensory nerve). The posterior interosseous nerve supplies the supinator muscle and then travels under the arcade of Frohse (another potential site of compression) before coursing distally to supply the extensor digitorum communis, extensor digiti minimi, extensor carpi ulnaris, abductor pollicis longus, extensor pollicis longus, extensor pollicis brevis, and extensor indicis proprius. The superficial sensory nerve supplies sensations to the dorsum of the hand, excluding the fifth and ulnar half of the fourth digit, which is supplied by the ulnar nerve (Fig. 26.1). In the hand, the superficial radial nerve further bifurcates into a medial and lateral branch.2 Radial neuropathy is relatively uncommon compared with other compressive neuropathies of the upper limb. A study in 2000 showed that the annual age-standardized rates per 100,000 of new presentations in primary care were 2.97 in men and 1.42 in women for radial neuropathy, 87.8 in men and 192.8 in women for carpal tunnel syndrome, and 25.2 in men and 18.9 in women for ulnar neuropathy.3 

Symptoms Symptoms of radial neuropathy depend on the site of nerve entrapment (Table 26.1).4 In the axilla, the entire radial nerve can be affected. This may be seen in crutch palsy if the patient is improperly using crutches in the axilla, causing compression. With this type of injury, the median, axillary, or suprascapular nerves may also be affected. All radially innervated muscles (including the triceps) as well as sensation in the posterior arm, forearm, and dorsum of the hand may be affected. The radial nerve is especially prone to injury in the spiral groove (also known as Saturday night palsy or honeymooners palsy). The radial nerve may be injured in humeral fractures, either due to the fracture or during operative treatment.5,6 The nerve may also be damaged in the arm during revision of total elbow arthroplasty.7 Symptoms include weakness of all radially innervated muscles except the triceps and sensory changes in the posterior arm and hand. In the forearm, the radial nerve is susceptible to injury as it passes through the supinator muscle and the arcade of Frohse. Because the superficial radial sensory nerve branches before this area of impingement, sensation will be spared. The patient will complain of weakness in the wrist and finger extensors. On occasion, the superficial radial sensory nerve is entrapped at the wrist, usually as 141

PART 1  MSK Disorders

142

a result of lacerations at the wrist or a wristwatch that is too tight. In this situation, the symptoms will be sensory, involving the dorsum of the hand.  Cutaneous innervation

Physical Examination

C5 Post.

Ant.

Radial n.

Post. cut. n. of arm Lower lat. cut. n. of arm

5 6 7 1 2

The findings on physical examination depend on where the injury is along the anatomic course of the nerve. A Tinel sign may be present at the site of compression. Injury in the axilla will lead to weakness in elbow extension, wrist extension, and finger extension. The entire sensory distribution of the radial nerve will be affected. If the injury is in the spiral groove, the examination findings will be the same, except that triceps function will be spared. Radial neurop­ athy in the forearm will usually result in sparing of sensory functions. If the nerve is entrapped in the supinator muscle, supinator strength should be normal. This is because the branch to innervate the supinator muscle is given off proximal to the muscle. The patient will have radial deviation with wrist extension and weakness of finger extensors. Injury to the superficial radial sensory nerve will result in paresthesias or dysesthesias over the radial sensory distribution in the hand. 

Functional Limitations

Post. cut. n. of forearm

Triceps Triceps and anconeus Brachioradialis Extensor carpi radialis longus Post. interosseous n. Extensor carpi radialis brevis Supinator Extensor digitorum Extensor digiti quinti Extensor carpi ulnaris Abductor pollicis longus Extensor pollicis longus and brevis Extensor indicis Dorsal digital n’s

FIG. 26.1  Neural branching of the radial nerve. Its origin in the axilla to the termination of its motor and sensory branches is shown. The inset demonstrates the cutaneous distribution of the various sensory branches of the radial nerve. (From Haymaker W, Woodhall B. Peripheral Nerve Injuries. Philadelphia: WB Saunders; 1953.)

The prognosis for patients with acute compressive radial neuropathies is good.8 Functional limitation depends on the extent of the injury and the level of the lesion. In high radial nerve palsy, wrist and finger extension are impaired. However, the inability to stabilize the wrist in extension leads to the main functional limitation. The loss of the power of the wrist and finger extensors destroys the essential reciprocal tenodesis action vital to the normal grasp and release pattern of the hand and results in ineffective finger flexion function. Activities such as gripping or holding objects will therefore be impaired. The sensory loss associated with radial nerve palsy is of lesser functional consequence compared with that of median or ulnar nerve lesions. Sensory loss is limited to the dorsoradial aspect of the hand, and this leaves the more functionally important palmar surface intact. Pain from posterior interosseous nerve entrapment can be disabling enough to limit the function of the involved extremity. 

Diagnostic Studies Electrodiagnostic testing (electromyography and nerve conduction studies) is the most useful test to assess for radial neuropathies. This test can be used to diagnose, to localize, to prognosticate, and to rule out other nerve injuries. The test is usually performed 3 weeks after the onset of clinical findings.9 At this time, muscle denervation potentials will be observed if axonal injury is present. Radiography and magnetic resonance imaging can be used to rule out a mass (ganglion or tumor)10 or fracture11,12 as the reason for the radial neuropathy. Studies have used ultrasound (Fig. 26.2) to investigate the appearance of the radial nerve in the lateral aspect of the distal upper arm.13–15 The nerve may appear swollen proximal to areas of compression.16 

CHAPTER 26  Radial Neuropathy

143

Table 26.1  Extensor Tendon Compartments—Wrist Muscles

Insertion

Evaluation

Abductor pollicis longus

Dorsal base of thumb metacarpal

Bring thumb out to side

Extensor pollicis brevis

Proximal phalanx of the thumb

Extensor carpi radialis longus Extensor carpi radialis brevis

Dorsal base of index and middle metacarpals

Dorsiflex the wrist with the hand in a fist and apply resistance radially

Extensor pollicis longus

Distal phalanx of the thumb

Hand flat on table Lift only thumb

Extensor digitorum communis

Extensor hood and base of proximal phalanges of the ulnar four digits

Extend fingers with wrist in neutral

Extensor indicis proprius

Extend index finger

Extensor digiti minimi

Proximal phalanx of the little finger

Straighten little finger with other fingers in fist

Extensor carpi ulnaris

Dorsal base of the fifth metacarpal

Wrist extension with ulnar deviation

From American Society for Surgery of the Hand. The Hand: Examination and Diagnosis. New York: Churchill Livingstone; 1983.

Treatment Initial

Brachioradialis muscle

Radial nerve Lateral epicondyle

Radial neuropathies from compression can be managed conservatively in nearly all cases. Elimination of offending factors, such as improper use of crutches, and avoidance of provocative activities are the first steps in the treatment of radial neuropathy. Medications, including tricyclic agents, anticonvulsants, antiarrhythmics, topical solutions, clonidine, and opioids, can be considered for pain management. Nonpharmaceutical treatments, including transcutaneous electrical nerve stimulation and acupuncture, may be considered as adjuvants to medication.21 

Rehabilitation FIG. 26.2  Transverse ultrasound image of the radial nerve in proximity to the humerus just above the elbow. (From Waldman SD. Atlas of Interventional Pain Management. Philadelphia: Elsevier; 2015:244–247.)

Differential Diagnosis Cervical radiculopathy (C6, C7) Brachial neuritis Posterior cord brachial plexopathy Upper or middle trunk brachial plexopathy Extensor tendon rupture Epicondylitis de Quervain tenosynovitis Wrist drop secondary to lead polyneuropathy Posterior interosseous nerve mononeuropathy Peripheral neuropathy Axillary nerve injury Tumor Chondroma17 Hematoma Carpal tunnel syndrome Upper extremity extensor compartment syndrome Ulnar neuropathy Entrapment neuropathy due to chronic injection-induced triceps fibrosis18 Superficial radial neuropathy caused by intravenous injection19 Neuropathy after vascular access cannulation for hemodialysis20

The main goal of rehabilitation is prevention of joint contractures, shortening of the flexor tendons, and overstretching of the extensors while waiting for nerve recovery. This can be achieved by exercises to maintain range of motion, passive stretching, and proper splinting. Functional splinting can make relatively normal use of the hand possible. Dynamic splints use elastic to passively extend the finger at the metacarpophalangeal joints with the wrist immobilized in slight dorsiflexion. This provides stability to the wrist joint, passive extension of the digits by the elastic band, and active flexion of the fingers. A splint designed at the Hand Rehabilitation Center in Chapel Hill, North Carolina, uses a static nylon cord rather than a dynamic rubber band to suspend the proximal phalanges (Fig. 26.3). The design simulates the tenodesis action of the normal grasp-and-release pattern of the hand. Postsurgical release of compression should be immediately followed by exercises to increase or to maintain range of motion and a nerve-gliding program to prevent adhesions. Overly aggressive strengthening should be avoided during reinnervation. In tendon transfers, preoperative strengthening of the muscle to be transferred and postoperative muscle reeducation are vital to the success of the procedure. 

144

PART 1  MSK Disorders

with nerve injury, they are at risk for development of complex regional pain syndrome (reflex sympathetic dystrophy).28 Contractures and chronic pain may develop as well. 

Potential Treatment Complications There are inherent risks with any surgery, including failure to correct the problem, infection, additional deformity, and death. Any injection or surgery involving the wrist should avoid the superficial radial sensory nerve, as this could cause additional paresthesias or dysesthesias.

References

FIG. 26.3 Radial palsy splint with metacarpophalangeal joint extended and flexed.

Procedures Local anesthetic blocks or injections of hydrocortisone can be used,22 but are rarely necessary and have shown only temporary symptomatic relief. Lateral epicondylitis may mimic posterior interosseous nerve entrapment at the elbow. When lateral epicondylitis does not respond to conservative treatment, including injections of the lateral epicondyle, a diagnostic and therapeutic radial nerve injection at the elbow may be indicated.23 

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery Surgical decompression may be required for patients who do not respond to conservative treatment or patients with severe nerve injury. Radial tunnel release has been utilized for compression neuropathies of the posterior interosseous nerve.24 Surgical intervention for anastomosis may be indicated in cases of complete radial injury (neurotmesis). Tendon transfers may be considered in these instances if the surgery is not performed or is not successful.25,26 Care must be exercised to avoid the radial sensory branch during operations involving the wrist.22 Surgery has been noted to be less successful if there are coexisting additional nerve compressions or lateral epicondylitis or if the patient is receiving workers’ compensation.27 

Potential Disease Complications Patients with incomplete recovery may suffer significant functional loss in the upper extremity. Like any patient

1. Lowe JB III, Sen SK, Mackinnon SE. Current approach to radial nerve paralysis. Plast Reconstr Surg. 2002;110:1099–1113. 2. Cho NS, Kim KH, Park BK, et al. Superficial radial sensory neuropathy: medial and lateral branch injury. Muscle Nerve. 2016;53(5):690–693. 3. Latinovic R, Guilliford MC, Hughes RA. Incidence of common compressive neuropathies in primary care. J Neurol Neurosurg Psychiatry. 2006;77:263–265. 4. Silver J. Radial neuropathy. In: Weiss L, Silver J, Weiss J, eds. Easy EMG. New York: Butterworth-Heinemann; 2004:135–139. 5. Reichert P, Wnukiewicz W, Witkowski J, et al. Causes of secondary radial nerve palsy and results of treatment. Med Sci Monit. 2016;22:554–562. 6. Erra C, De Franco P, Granata G, et al. Secondary posterior interosseous nerve lesions associated with humeral fractures. Muscle Nerve. 2016;53(3):375–378. 7. Waitzenegger T, Mansat P, Guillon P, et al. Radial nerve palsy in surgical revision of total elbow arthroplasties: a study of 4 cases and anatomical study, possible aetiologies and prevention. Orthop Traumatol Surg Res. 2015;101(8):903–907. 8. Arnold WD, Krishna VR, Freimer M, et al. Prognosis of acute compressive radial neuropathy. Muscle Nerve. 2012;45:893. 9. Weiss L, Weiss J, Johns J, et al. Neuromuscular rehabilitation and electrodiagnosis: mononeuropathy. Arch Phys Med Rehabil. 2005;86(suppl 1): S3–S10. 10. Bordalo-Rodrigues M, Rosenberg ZS. MR imaging of entrapment neuropathies at the elbow [review]. Magn Reson Imaging Clin N Am. 2004;12:247–263, vi. 11. Ring D, Chin K, Jupiter JB. Radial nerve palsy associated with highenergy humeral shaft fractures. J Hand Surg Am. 2004;29:144–147. 12. Larsen LB, Barfred T. Radial nerve palsy after simple fracture of the humerus. Scand J Plast Reconstr Surg Hand Surg. 2000;34:363–366. 13. Foxall GL. Ultrasound anatomy of the radial nerve in the distal upper arm. Reg Anesth Pain Med. 2007;32:217–220. 14. Cartwright MS, Yoon JS, Lee KH, et al. Diagnostic ultrasound for traumatic radial neuropathy. Am J Phys Med Rehabil. 2011;90:342–343. 15. McCartney CJ, Xu D, Constantinescu C, et al. Ultrasound examination of peripheral nerves in the forearm. Reg Anesth Pain Med. 2007;32:434–439. 16. Choi SJ, Ahn JH, Ryu DS, et al. Ultrasonography for nerve compression syndromes of the upper extremity. Ultrasonography. 2015;34(4):275–291. 17. De Smet L. Posterior interosseous neuropathy due to compression by a soft tissue chondroma of the elbow. Acta Neurol Belg. 2005;105: 86–88. 18. Midroni G, Moulton R. Radial entrapment neuropathy due to chronic injection-induced triceps fibrosis. Muscle Nerve. 2001;24:134–137. 19. Sheu JJ, Yuan RY. Superficial radial neuropathy caused by intravenous injection. Acta Neurol Belg. 1999;99:138–139. 20. Talebi M, Salari B, Ghannadan H, Kakaei F, Azar SA. Nerve conduction changes following arteriovenous fistula construction in hemodialysis patients. Int Urol Nephrol. 2011;43(3):849–853. https://doi.org/10.1007/s11255-010-9740-9. 21. Xu J, Chen XM, Zheng BJ, Wang XR. Electroacupuncture relieves nerve injury-induced pain hypersensitivity via the inhibition of spinal P2X7 receptor-positive microglia. Anesth Analg. 2016;122(3):882–892. 22. Braidwood AS. Superficial radial neuropathy. J Bone Joint Surg Br. 1975;57:380–383. 23. Weiss L, Silver J, Lennard T, Weiss J. Easy injection. Philadelphia: Elsevier; 2007.

CHAPTER 26  Radial Neuropathy

24. Simon Perez C, García Medrano B, Rodriguez Mateos JI, Coco Martin B, Faour Martin O, Martin Ferrero MA. Radial tunnel syndrome: results of surgical decompression by a postero-lateral approach. Int Orthop. 2014;38(10):2129–2135. https://doi.org/10.1007/s00264-014-2441-8. 25. Kozin SH. Tendon transfers for radial and median nerve palsies [review]. J Hand Ther. 2005;18:208–215. 26. Herbison G. Treatment of peripheral neuropathies. Plenary session. Neuropathy: from genes to function. Philadelphia: American Association of Electrodiagnostic Medicine; 2000.

145

27. Lee JT. Long term results of radial tunnel release—the effect of coexisting tennis elbow, multiple compression syndromes and workers’ compensation. J Plast Reconstr Aesthet Surg. 2008;61:1095–1099. 28. Borchers AT, Gershwin ME. Complex regional pain syndrome: a comprehensive and critical review. Autoimmun Rev. 2014;13(3):242–265.

CHAPTER 27

Ulnar Neuropathy (Elbow) Lyn D. Weiss, MD Jay M. Weiss, MD

Synonyms Cubital tunnel syndrome Tardy ulnar palsy Ulnar neuritis Compression of the ulnar nerve

ICD-10 Codes G56.20 G56.21 G56.22

Lesion of ulnar nerve, unspecified upper limb Lesion of ulnar nerve, right upper limb Lesion of ulnar nerve, left upper limb

Definition The ulnar nerve is derived predominantly from the nerve roots of C8 and T1 with a small contribution from C7. The C8 and T1 fibers form the lower trunk of the brachial plexus. The ulnar nerve is the continuation of the medial cord of the brachial plexus at the level of the axilla. Ulnar neuropathy at the elbow is the second most common entrapment neuropathy. Only carpal tunnel syndrome (median neuropathy at the wrist) is more frequent. The ulnar nerve is susceptible to compression at the elbow for several reasons. First, the nerve has a superficial anatomic location at the elbow. Hitting the “funny bone” (ulnar nerve at the elbow) creates an unpleasant sensation that most people have experienced. If the ulnar nerve is susceptible to subluxation, further injury may result. Second, the nerve is prone to repeated trauma from leaning on the elbow or repetitively flexing and extending the elbow. Poorly healing fractures at the elbow may damage this nerve. Finally, and perhaps most important, the ulnar nerve can become entrapped at the arcade of Struthers, in the cubital tunnel (ulnar collateral ligament and aponeurosis between the two heads of the flexor carpi ulnaris; Fig. 27.1), or within the flexor carpi ulnaris muscle. The nerve lengthens and becomes taut with elbow flexion. In addition, there is decreased space in the cubital tunnel in this position. 146

The volume of the cubital tunnel is maximal in extension and can decrease by 50% with elbow flexion.1 The nerve may also become compromised after a distal humerus fracture, either as a direct result of the fracture or because of an altered carrying angle of the elbow and decreased elbow extension (tardy ulnar palsy). Cyclists are prone to traction and compression of the ulnar nerve at both the elbow and the wrist.2 Repetitive or incorrect throwing can lead to damage of the ulnar nerve at the elbow.3 Biomechanical risk factors (repetitive holding of a tool in one position), obesity, and other associated upper extremity work-related musculoskeletal disorders (especially medial epicondylitis and other nerve entrapment disorders) have also been associated with the development of ulnar neuropathy at the elbow.4,5 

Symptoms If the ulnar nerve is entrapped at the elbow, both the dorsal ulnar cutaneous nerve (which arises just proximal to the wrist) and the palmar cutaneous branch of the ulnar nerve will be affected. Patients will therefore complain of numbness or paresthesias in the dorsal and volar aspects of the fifth and ulnar side of the fourth digits. Hand intrinsic muscle weakness may be apparent. In cases of severe ulnar neuropathy, clawing of the fourth and fifth digits (with attempted hand opening) and atrophy of the intrinsic muscles may be noted by the patient (Fig. 27.2). Symptoms may be exacerbated by elbow flexion. Pain may be noted and may radiate proximally or distally. 

Physical Examination The ulnar nerve may be palpable in the posterior condylar groove (posterior to the medial epicondyle) with elbow flexion and extension. A Tinel sign may be present at the elbow; however, it should be considered significant only if the Tinel sign is absent on the nonaffected side. Direct pressure over the ulnar nerve posterior to the medial epicondyle with the elbow in flexion is a sensitive provocative test.6 The ulnar nerve may be felt subluxing with flexion and extension of the elbow. Sensory deficits may be noted in the fifth and ulnar half of the fourth digits. Atrophy of the intrinsic hand muscles and hand weakness may be noted as well (although this is generally seen in more advanced cases). Wartenberg sign (abduction of the fourth and fifth digits) may occur. The

CHAPTER 27  Ulnar Neuropathy (Elbow)

Ulnar nerve Medial epicondyle

Triceps

Ulnar collateral ligament Flexor carpi ulnaris

Flexor carpi ulnaris

FIG. 27.1  The cubital tunnel. (From Bernstein J, ed. Musculoskeletal Medicine. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2003.)

Abnormal

Normal

147

potential amplitude across the elbow) indicates myelin injury, which has a better prognosis.7 These studies can also identify other areas of nerve compression that may accompany ulnar neuropathy at the elbow. Several studies using ultrasound have shown an increased cross-sectional area of the ulnar nerve in patients with ulnar neuropathy at the elbow.8,9 The nerve may appear swollen proximal to areas of compression.10 Magnetic resonance neurography may play a role in the evaluation of ulnar neuropathy at the elbow.11 Radiographs of the elbow with cubital tunnel views can be obtained if fractures, spurs, arthritis, and trauma are suspected. In rare cases, magnetic resonance imaging12 with arthrography may be used to assess for tears in the ulnar collateral ligament or soft tissue disease.  Differential Diagnosis Ulnar neuropathy at a location other than the elbow C8-T1 radiculopathy Brachial plexopathy (usually lower trunk) Thoracic outlet syndrome Elbow fracture Elbow dislocation Medial epicondylitis Carpal tunnel syndrome Ulnar collateral ligament injury Soft tissue disorders at the elbow

Treatment FIG. 27.2 Froment sign. Note prominent atrophy of the intrinsic muscles. (From Weiss L, Silver J, Weiss J, eds. Easy EMG. New York: Butterworth-Heinemann; 2004.)

patient should be tested for Froment sign. Here, a patient is asked to grasp a piece of paper between the thumb and radial side of the second digit. The examiner tries to pull the paper out of the patient’s hand. If the patient has injury to the adductor pollicis muscle (ulnar innervated), the patient will try to compensate by using the median-innervated flexor pollicis longus muscle (see Fig. 27.2). 

Functional Limitations The patient with ulnar neuropathy at the elbow may have poor hand function and complain of dropping things or clumsiness. There may be difficulty with activities of daily living, such as dressing, holding a pen, or using keys. 

Diagnostic Studies Electrodiagnostic studies can help identify, localize, and gauge the severity of an ulnar nerve lesion at the elbow. The findings of abnormal spontaneous potentials (fibrillations and positive sharp waves) in ulnar innervated muscles on needle electromyographic study indicate axonal damage and portend a worse prognosis than with injury to the myelin only. Slowing of the ulnar nerve across the elbow or conduction block (a drop in compound motor action

Initial Treatment initially involves relative rest and protecting the elbow. Elbow pads or night splinting in mild flexion may be beneficial. Treatment should be directed at avoidance of aggravating biomechanical factors, such as leaning on the elbows, prolonged or repetitive elbow flexion, and repetitive valgus stress in throwing. Nonsteroidal anti-inflammatory drugs may also be prescribed. 

Rehabilitation Successful rehabilitation of ulnar neuropathy at the elbow includes identification and correction of biomechanical factors. This may include workstation modifications to decrease the amount of elbow flexion, substitution of headphones for telephone handsets, and use of forearm rests. Often, an elbow pad can be beneficial; the pad protects the ulnar nerve and keeps the elbow in relative extension. A rehabilitation program should include strengthening of forearm pronator and flexor muscles. Flexibility exercises should be instituted to maintain range of motion and to prevent soft tissue tightness. Advanced strengthening, including eccentric and dynamic joint stabilization exercises, can be added.13 

Procedures Procedures are not typically performed to treat ulnar neuropathy at the elbow. 

148

PART 1  MSK Disorders

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery If conservative management has failed or if significant damage to the ulnar nerve is evident, surgery may be considered.14-16 The type of surgery depends on the area of ulnar nerve injury and may involve release of the cubital tunnel, ulnar nerve transposition,17 decompression of the ulnar nerve (open or arthroscopic),18,19 subtotal medial epicondylectomy,20,21 or ulnar collateral ligament repair. Simple decompression and decompression with transposition have been shown to be equally effective in idiopathic ulnar neuropathy at the elbow,22 although decompression with transposition has been associated with more wound infections.23 

Potential Disease Complications If ulnar neuropathy at the elbow is left untreated, complications may include hand weakness, poor coordination, intrinsic muscle atrophy, sensory loss, and pain. In addition, flexion contractures and valgus deformity may develop at the elbow.13 

Potential Treatment Complications The results of surgery depend on the extent of ulnar nerve compression, accuracy of identifying the site of compression, type of procedure, thoroughness of compression release, comorbid factors, degree of prior intrinsic muscle loss, and previous sensory loss.13,24-27 Nonsteroidal antiinflammatory drugs may cause gastric, hepatic, or renal complications.

References 1. Weiss L. Ulnar neuropathy. In: Weiss L, Silver J, Weiss J, eds. Easy EMG. New York: Butterworth-Heinemann; 2004:127–134. 2. Brubacher JW, Leversedge FJ. Ulnar neuropathy in cyclists. Hand Clin. 2017;33(1):199–205. https://doi.org/10.1016/j.hcl.2016.08.015. Review. 3. Aoki M, Takasaki H, Muraki T, et al. Strain on the ulnar nerve at the elbow and wrist during throwing motion. J Bone Joint Surg Am. 2005;87:2508–2514. 4. Descatha A, Leclerc A, Chastang JF, Roquelaure Y, Study Group on Repetitive Work. Incidence of ulnar nerve entrapment at the elbow in repetitive work. Scand J Work Environ Health. 2004;30:234–240.

5. Carter GT, Weiss MD, Friedman AS, et al. Diagnosis and treatment of work-related ulnar neuropathy at the elbow. Phys Med Rehabil Clin N Am. 2015;26(3):513–522. 6. Dy CJ, Mackinnon SE. Ulnar neuropathy: evaluation and management. Curr Rev Musculoskelet Med. 2016;9(2):178–184. 7. Beekman R, Zijlstra W, Visser LH. A novel points system to predict the prognosis of ulnar neuropathy at the elbow. Muscle Nerve. 2016. 8. Beekman R. Ultrasonography in ulnar neuropathy at the elbow: a critical review. Muscle Nerve. 2011;43:627–635. 9. Thoirs K. Ultrasonographic measurements of the ulnar nerve at the elbow: role of confounders. J Ultrasound Med. 2008;27:737–743. 10. Choi SJ, Ahn JH, Ryu DS, et al. Ultrasonography for nerve compression syndromes of the upper extremity. Ultrasonography. 2015;34(4):275–291. 11. Keen NN. Diagnosing ulnar neuropathy at the elbow using magnetic resonance neurography. Skeletal Radiol. 2012;41:401–407. 12. Shen L, Masih S, Patel DB, Matcuk GR Jr. MR anatomy and pathology of the ulnar nerve involving the cubital tunnel and Guyon’s canal. Clin Imaging. 2016;40(2):263–274. 13. Stokes W. Ulnar neuropathy (elbow). In: Frontera W, Silver J, eds. Essentials of physical medicine and rehabilitation. Philadelphia: Hanley & Belfus; 2002:139–142. 14. 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. 15. Nathan PA, Istvan JA, Meadows KD. Intermediate and long-term outcomes following simple decompression of the ulnar nerve at the elbow. Chir Main. 2005;24:29–34. 16. Beekman R, Wokke JH, Schoemaker MC, et al. Ulnar neuropathy at the elbow: follow-up and prognostic factors determining outcome. Neurology. 2004;63:1675–1680. 17. Matei CI, Logigian EL, Shefner JM. Evaluation of patients with recurrent symptoms after ulnar nerve transposition. Muscle Nerve. 2004;30:493–496. 18. 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. 19. Kovachevich R. Arthroscopic ulnar nerve decompression in the setting of elbow osteoarthritis. J Hand Surg Am. 2012;37:663–668. 20. Anglen J. Distal humerus fractures. J Am Acad Orthop Surg. 2005;13:291–297. 21. Popa M, Dubert T. Treatment of cubital tunnel syndrome by frontal partial medial epicondylectomy. A retrospective series of 55 cases. J Hand Surg Br. 2004;29:563–567. 22. Caliandro P, La Torre G, Padua R, Giannini F, Padua L. Treatment for ulnar neuropathy at the elbow. Cochrane Database Syst Rev. 2016. 23. Caliandro P, La Torre G, Padua R, Giannini F, Padua L. Treatment for ulnar neuropathy at the elbow. Cochrane Database Syst Rev. 2016;11. 24. Dellon A. Review of treatment for ulnar nerve entrapment at the elbow. J Hand Surg Am. 1989;14:688–700. 25. Efstathopoulos DG, Themistocleous GS, Papagelopoulos PJ, et al. Outcome of partial medial epicondylectomy for cubital tunnel syndrome. Clin Orthop Relat Res. 2006;444:134–139. 26. 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. 27. 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.

SECTION IV

Hand and Wrist CHAPTER 28

de Quervain Tenosynovitis Carina Joy O’Neill, DO

Synonyms Washerwoman’s sprain1 Stenosing tenosynovitis2 Tenovaginitis3,4 Tendinosis5 Tendinitis6 Peritendinitis6

ICD-10 Codes M65.9 M65.4 M66.131 M66.132 M66.139 M66.141 M66.142 M66.143 M67.20

Synovitis and tenosynovitis, unspecified de Quervain tenosynovitis Rupture of synovium and tendon, right wrist Rupture of synovium and tendon, left wrist Rupture of synovium and tendon, unspecified wrist Rupture of synovium and tendon, right hand Rupture of synovium and tendon, left hand Rupture of synovium and tendon, unspecified hand Other disorders of tendon and synovium, unspecified site

Definition The condition is characterized not by inflammation6 but by thickening of the tendon sheath and most notably by the accumulation of mucopolysaccharide, an indicator of myxoid degeneration. These changes are pathognomonic of the condition and are not seen in control tendon sheaths. The

term stenosing tenovaginitis is a misnomer; de Quervain disease is the result of intrinsic, degenerative mechanisms rather than of extrinsic, inflammatory ones.24 de Quervain tenosynovitis7 is classically defined as a stenosing tenosynovitis of the synovial sheath of tendons of the abductor pollicis longus and extensor pollicis brevis muscles in the first compartment of the wrist due to repetitive use.2 Fritz de Quervain first described this condition in 1895.3 Histologic studies have found that this disorder is characterized by degeneration and thickening of the tendon sheath and that it is not an active inflammatory condition.8 In fact, de Quervain described thickening of the tendon sheath compartment at the distal radial end of the extensor pollicis brevis and abductor longus.3 Extensor triggering, which is manifested by locking in extension, is rare but has also been reported in de Quervain tenosynovitis with a prevalence of 1.3%.1 de Quervain tenosynovitis was linked to repetitive use of the wrist. Many activities have been linked to this condition, including household chores, playing piano, crafting, bowling, and fishing. In more recent years, excessive use of the text-messaging feature on a cellular phone has now also been linked to this painful condition.9 Work related activities such as such as pinching, grasping, pulling, and pushing have been reported in the past as having caused de Quervain tenosynovitis.6 A systemic review and meta-analysis in 2013 questions this common belief that de Quervain is secondary to vocational repetitive use. In a meta-analysis, there was no sufficient scientific evidence confirming a causal relationship between de Quervain tenosynovitis and occupational risk factors.26 For a majority of cases, the onset of de Quervain tenosynovitis is gradual and not associated with a history of acute trauma, although several authors have noted a traumatic etiology, such as falling on the tip of the thumb.6 de Quervain tenosynovitis primarily affects women (gender ratio approximately 10:1) between the ages of 35 and 55 years. There is no predilection for right versus left side, and no racial differences have been observed.6 de Quervain tenosynovitis is associated with pregnancy, the postpartum period, and lactation.25  149

PART 1  MSK Disorders

150

Patients may complain of pain in the lateral wrist during grasp and thumb extension.3 They may also describe pain with palpation over the lateral wrist.10 Symptoms can include swelling and are aggravated by resisted motion of the thumb. Radial deviation and extension can also worsen the pain.25 Symptoms are often gradual in onset and persist for several weeks or months.11 Pain is the most prominent symptom quality, but some patients report stiffness as well. Pain is often described as severe and may be sufficiently intense to render the hand useless.6 Paresthesia in the distribution of the anterior terminal branch superficial radial nerve is uncommon.6 

the moment the thumb is again extended, even if the ulnar abduction is maintained.3 The Eichhoff test is sometimes erroneously called the Finkelstein test. The Brunelli test maintains the wrist in radial deviation while forcibly abducting the thumb3 (Fig. 28.2). Pain over the radial styloid from these provocative stretch maneuvers differentiates de Quervain tenosynovitis from arthritis of the first metacarpal joint.10 Assessment of the first carpometacarpal joint, including range of motion, palpation for tenderness and crepitus, and radiographic investigation, should also be performed because injury to this joint can give a false-positive Finkelstein test result.13,14 Typically, physical examination and history alone are diagnostic.25 

Physical Examination

Functional Limitations

A comprehensive examination of the neck and entire upper extremity should be performed before the wrist examination to rule out radiating pain from a more proximal problem, such as a herniated cervical disc.10 Strength and sensation are expected to be normal in patients with de Quervain tenosynovitis. However, strength, particularly grip and pinch strength, may be decreased from pain or disuse secondary to pain. On examination, the findings of local tenderness and moderate swelling around the radial styloid are likely to be present.11 A positive Finkelstein test result can confirm the diagnosis.12 The Finkelstein test is performed by grasping the patient’s thumb and quickly abducting the hand in ulnar deviation (Fig. 28.1).4 Reproduction of pain is a positive test result. A similar test, described by Eichhoff in 1927, provides ulnar deviation while the patient is flexing the thumb and curling fingers around it. Pain should disappear

Functional impairment is believed to be caused by impaired gliding of the abductor pollicis longus or extensor pollicis brevis tendon through a narrowed fibro-osseous canal.6 Functional impairment of the thumb is a result of mechanical impingement or pain. Activities of daily living, such as dressing, can be impaired. Fastening of buttons often causes significant pain. In addition, household chores can be limited secondary to pain. Limits in recreational activities, such as bowling, fly-fishing, sewing, and knitting, are also seen in de Quervain tenosynovitis. Workers with jobs requiring repetitive motions, such as pushing or pulling in a factory setting, can have pain with work tasks due to de Quervain tenosynovitis. Thus, pain from the condition can have a significant economic impact.6 It is not established, however, that jobs with repetitive motions cause de Quervain tenosynovitis.26 

Symptoms

Diagnostic Studies Tenosynovitis of the wrist is a clinical diagnosis and a positive Finkelstein is pathognomonic, but some authors recommend obtaining a wrist radiograph to rule out other potential causes of wrist pain and may reveal soft tissue swelling.6,27 Ultrasound is accurate at revealing presence and extent of tenosynovitis.27 On ultrasound examination, tenosynovitis is characterized by hypoechoic fluid distending the tendon sheath with inflammatory changes within

A

B FIG. 28.1  Finkelstein test (A) and Eichhoff test (B).

FIG. 28.2  Brunelli test.

CHAPTER 28  de Quervain Tenosynovitis

the tendon (Fig. 28.3).15 Some clinicians report that relief of symptoms after injection of a local anesthetic into the first dorsal compartment is often helpful as a diagnostic tool.6 When clinical findings are nondiagnostic, a bone scan can help confirm the diagnosis.2 Magnetic resonance imaging may demonstrate hypertrophy of the retinaculum that covers the first dorsal compartment of the wrist, thickening of the tendon sheath, hypertrophy and heterogeneous appearance of the tendons, and adjacent inflammatory changes.28 The presence of a septum that divides the first compartment into two subcompartments should be identified, as it may lead to the failure of cortisone-derivative infiltration.28  Differential Diagnosis Carpal joint arthritis Triscaphoid arthritis Rheumatoid arthritis Intersection syndrome Radial nerve injury Ganglion cyst Cervical radiculopathy Scaphoid fracture Carpal tunnel syndrome Radioscaphoid arthritis Kienböck disease Extensor pollicis longus tenosynovitis

151

performed. One study compared splinting with rest and NSAID therapy. Only 14% of patients who were splinted were cured versus 0% with rest and NSAIDs.16 

Rehabilitation The goals of therapy are to reduce pain and to improve function of the affected hand. Classically, therapy includes physical modalities such as ice, heat, transcutaneous electrical nerve stimulation, ultrasound, and iontophoresis.8 In addition, friction massage and active exercises have been employed.8 A thumb spica splint has been used for immobilization as well.17 A thumb spica splint is thought to be an effective way to manage symptoms because it inhibits gliding of the tendon through the abnormal fibro-osseous canal.6 One small, randomized study demonstrated that patients with mild symptoms are more likely to improve with therapy and NSAIDs alone, with the majority of patients with moderate to severe symptoms not responding to therapy.17 Often initial treatment of de Quervain tenosynovitis is injections. Although steroid injection shows better outcomes for de Quervain tenosynovitis, because of the benign profile of physical therapy, it is reasonable to consider these less invasive approaches (such as ice, thumb spica splinting, and NSAIDs) as adjuvants when this disorder is mild and first treated.18 

Procedure

Treatment Initial There is limited evidence that conservative treatment is effective in reducing moderate to severe symptoms of de Quervain tenosynovitis. Some literature has evaluated effectiveness of ice, nonsteroidal anti-inflammatory drugs (NSAIDs), heat, orthoses, strapping, rest, and massage. Available research does not show these techniques to be effective in the treatment of de Quervain tenosynovitis6; however, no randomized controlled study has been

Injection of local anesthetics and corticosteroids, with or without immobilization, became popular in the 1950s.6 It is currently the most frequent treatment modality for patients with de Quervain tenosynovitis. Injection into the first extensor compartment can relieve symptoms (Fig. 28.4). One study described an 83% cure rate with injection.16 In recent years, multiple types of injection techniques have been compared. One study comparing a one-point injection (directed into the first compartment) versus a two-point injection technique (injection corresponding with the paths of both the extensor pollicis brevis and the abductor pollicis longus) showed the latter to

E E R R

A

B

FIG. 28.3  De Quervain disease. Ultrasound images in (A) short axis and (B) long axis to the first extensor wrist tendons show hypoechoic thickening of the tendon sheath (arrowheads) with hypoechoic swelling of the abductor pollicis longus tendon (arrows). E, Extensor pollicis brevis tendon; R, radius. (From Jacobsen JA. Wrist and hand ultrasound. In: Jacobsen JA, ed. Fundamentals of Musculoskeletal Ultrasound. Philadelphia, PA: Elsevier/Saunders; 2013:110–161.e3.)

152

PART 1  MSK Disorders

Potential Disease Complications Pain and reduced hand function is the most cited disease complication. Mechanically, functional impairment is believed to be caused by impaired gliding of the abductor pollicis longus or extensor pollicis brevis tendons because of a narrowed fibro-osseous canal and, in some cases, alterations in the tendons (i.e., gross physical deformity or granulation tissue deposited on their surfaces). Because of friction, the tendon sheath becomes edematous, which can further increase friction. This can eventually lead to fibrosis of the tendon.6 

Potential Treatment Complications FIG. 28.4  The four-point injection technique. The injection is divided into two pairs, with each pair including a proximal and distal injection point corresponding with paths of the extensor pollicis brevis and abductor pollicis longus tendons.

be more beneficial.19 A study evaluating treatment with a four-point injection technique (injecting both the proximal and distal locations for both extensor pollicis brevis and abductor pollicis longus) showed some benefit over the two-point procedure.14 It is essential that corticosteroid enter the compartment of both the extensor pollicis brevis and abductor pollicis longus for the injection to be effective. Many patients have anatomic variations with a septum creating two subcompartments. Incidence of septation of the first compartment reportedly varies in cadaveric studies from 24% to 76%.20,21 Ultrasoundguided injections have reportedly increased improvement after injection to 97%.20 Given the success of injections over therapy, injections remain the first-line treatment of the condition.18 A case report on ultrasound-guided percutaneous needle tenotomy and platelet-rich plasma injection proved effective and may be an option for patients with de Quervain tenosynovitis that is refractory to conservative care.29 

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery Before 1950, surgery was considered the treatment of choice for de Quervain tenosynovitis. Now, with the success of injections, it is reserved for those whose injection therapy fails.22 Surgery involves release of the extensor retinaculum, and either open or endoscopic techniques can be used. Partial resection of the retinaculum can be used as well.23 The patient needs to be instructed to monitor for signs of infection, and limit lifting anything heavier than 1 to 2 pounds in the first 2 weeks. At that time the patient returns to normal daily activities, but still limited from lifting more than 10 pounds until week four. On average, surgical success rates range from 83% to 92%.6 

NSAIDs have well-known side effects that most commonly affect the gastric, hepatic, and renal systems. The most common immediate adverse reaction reported with injection was pain at the injection site (35%), followed by immediate inflammatory flare reaction (10%), temporary radial nerve paresthesia (4%), and vasovagal reaction (4%); 31% had late adverse reactions ranging from minimal skin color lightening to subcutaneous fat atrophy.6 In this study, no post-injection infection, bleeding, or tendon rupture was seen, although this could be possible with any injection. With any type of steroid injection, there is a risk of bleeding. Repeated steroid injections have the potential to weaken the tendon and may cause a tendon rupture. Surgical treatment complications include radial nerve injury, incomplete retinacular release, and tendon subluxation.22

References 1. Alberton GM, High WA, Shin AY, Bishop AT. Extensor triggering in de Quervain’s stenosing tenosynovitis. J Hand Surg Am. 1999;24:1311–1314. 2. Leslie WD. The scintigraphic appearance of de Quervain tenosynovitis. Clin Nucl Med. 2006;31:602–604. 3. Ahuja NK, Chung KC, MD Quervain. (1868-1940): stenosing tendovaginitis at the radial styloid process. J Hand Surg Am. 2004; 29:1164–1170. 4. Finkelstein H. Stenosing tendovaginitis at the radial styloid process. J Bone Joint Surg. 1930;12:509–540. 5. Ashe MC, McCauley T, Khan KM. Tendinopathies in the upper extremity: a paradigm shift. J Hand Ther. 2004;17:329–334. 6. Moore JS. De Quervain’s tenosynovitis: stenosing tenosynovitis of the first dorsal compartment. J Occup Environ Med. 1997;39:990–1002. 7.  http://medical-dictionary.thefreedictionary.com/tenosynovitis. 8. Walker MJ. Manual physical therapy examination and intervention of a patient with radial wrist pain: a case report. J Orthop Sports Phys Ther. 1994;34:761–769. 9. Ashurst JV, Turco DA, Lieb BE. Tenosynovitis caused by texting: an emerging disease. J Am Osteopath Assoc. 2010;110:294–296. 10. Forman TA, Forman SK, Rose NE. A clinical approach to diagnosing wrist pain. Am Fam Physician. 2005;72:1753–1758. 11. Abe Y, Tsue K, Nagai E, et al. Extensor pollicis longus tenosynovitis mimicking de Quervain’s disease because of its course through the first extensor compartment: a report of 2 cases. J Hand Surg Am. 2004;29:225–229. 12. Alexander RD, Catalano LW, Barron OA, Glickel SZ. The extensor pollicis brevis entrapment test in the treatment of de Quervain’s disease. J Hand Surg Am. 2002;27:813–816. 13. Fournier K, Bourbonnais D, Bravo G, et al. Reliability and validity of pinch and thumb strength measurements in de Quervain’s disease. J Hand Ther. 2006;19:2–10. 14. Pagonis T, Ditsios K, Toli P, et al. Improved corticosteroid treatment of recalcitrant de Quervain tenosynovitis with a novel 4-point injection technique. Am J Sports Med. 2011;39:398–403.

CHAPTER 28  de Quervain Tenosynovitis

15. Torriani M, Kattapuram SV. Musculoskeletal ultrasound: an alternative imaging modality for sports-related injuries. Top Magn Reson Imaging. 2003;14:103–111. 16. Richie CA, Briner WW. Corticosteroid injection for treatment of de Quervain’s tenosynovitis: a pooled quantitative literature evaluation. J Am Board Fam Pract. 2003;16:102–106. 17. Lane LB, Boretz RS, Stuchin SA. Treatment of de Quervain’s disease: role of conservative management. J Hand Surg Br. 2001;26: 258–260. 18. Slawson D. Best treatment for de Quervain’s tenosynovitis uncertain. Am Fam Physician. 2003;68:533. 19. Peters-Veluthamaningal C, Winters JC, Groenier KH, Meyboom-De Jong B. Randomised controlled trial of local corticosteroid injections for de Quervain’s tenosynovitis in general practice. BMC Musculoskelet Disord. 2009;10:131. 20. McDermott JD, Ilyas AM, Nazarian LN, Leinberry CF. Ultrasoundguided injections for de Quervain’s tenosynovitis. Clin Orthop Relat Res. 2012;470:1925–1931. 21. Mirzanli C, Ozturk K, Ezenyel CZ, et al. Accuracy of intrasheath injection techniques for de Quervain’s disease: a cadaveric study. J Hand Surg Eur Vol. 2012;37:155–160. 22. Kent TT, Eidelman D, Thomson JG. Patient satisfaction and outcome of surgery for de Quervain’s tenosynovitis. J Hand Surg Am. 1999;24:1071–1077.

153

23. Altay MA, Erturk C, Isikan UE. De Quervain’s disease treatment using partial resection of the extensor retinaculum: a short term results survey. Orthop Traumatol Surg Res. 2011;97:489–493. 24. Clark MT, Lyall HA, Grant JW, et al. The histopathology of de Quervain’s disease. J Hand Surg Br. 1998;23:732–734. 25. Adams JE, Habbu R. Tendinopthies of the hand and wrist. J Am Acad Orthop Surg. 2015;23:741–750. 26. Stahl S, Vida D, Meisner C, et al. Systematic review and meta-analysis on the work-related cause of de Quervain tenosynovitis: a critical appraisal of its recognition as an occupational disease. Plas Reconstr Surg. 2013;132(6):1479–1491. 27. Shuaib W, Mohiuddin Z, Swain FR, Khosa F. Differentiating common causes of radial wrist pain. JAAPA. 2014;27(9):34–36. 28. Cockenpot E, Lefebvre G, Demondion X, Chantelot C, Cotten A. Imaging of sports-related hand and wrist injuries: sport imaging series. Radiology. 2016;279(3):674–692. 29. Peck E, Ely E. Successful treatment of de Quervain tenosynovitis with ultrasound-guided percutaneous needle tenotomy and platelet-­ rich plasma injection: a case presentation. PM R. 2013;5(5):438–441.

CHAPTER 29

Dupuytren Contracture Michael F. Stretanski, DO, AME

Synonyms Dupuytren disease Viking disease Cooper contracture

ICD-10 Code M72.0 Dupuytren contracture (palmar fascial fibromatosis)

Definition Dupuytren disease is a nonmalignant, slowly progressive fibroproliferative disorder causing progressive thickening and shortening of the palmar fascia leading to debilitating and permanent digital contracture. Subsequent flexion contracture usually begins with the fourth and fifth digits on the ulnar side of the hand and may progress to involve metacarpophalangeal (MCP) joints or the proximal interphalangeal (PIP) joints (Fig. 29.1). Dupuytren contracture belongs to the group of fibromatoses that include plantar fibromatosis (Ledderhose disease), penile fibromatosis (Peyronie disease), and fibromatosis of the dorsal PIP joints (Garrod nodes or knuckle pads). The eponym “Cooper contracture” has been suggested for Astley Cooper, who first described and lectured on the entity in 1822, but is seldom referenced in lieu of Baron Dupuytren, Guillaume, personal doctor of Napoleon and Louis XVI, who described the disease in 1833. The primary lesion is a nodule beginning in the palm, presenting initially as a firm, soft tissue mass fixed to both the skin and the deeper fascia. It is characterized histologically by dense, noninflammatory, chaotic cellular tissue and appears on the anterior aspect of the palmar aponeurosis. The key cell response for tissue contraction in Dupuytren disease is thought to be the fibroblast and its differentiation into a myofibroblast.1 This idiopathic activation happens in response to the fibrogenic cytokines interleukin-1, prostaglandin F2, prostaglandin E2, platelet-derived growth factor, connective tissue-derived growth factor, and, most important, transforming growth factor-β and fibroblast growth factor 2. In addition, microRNAs (miRNAs) identified in Dupuytren contracture samples, including miR-29c, miR130b, miR-101, miR-30b, and miR-140-3p, were found to 154

regulate important genes related to the β-catenin pathway: WNT5A, ZIC1, and TGFB1.2 As the nodule extends slowly, it induces shortening and tension on the longitudinal fascial bands of the palmar aponeurosis, resulting in cords of hypertrophied tissue. It is unique among ailments of the hand, and one could conceive of it as a focal autoimmune collagen vascular phenomenon. Dupuytren disease is thought to begin in the overlying dermis. Unlike the nodule, the cord is strikingly different histologically; it contains few or no myofibroblasts and few fibroblasts in a dense collagen matrix with less vascularity. Skin changes are the earliest signs of Dupuytren disease, including thickening of the palmar skin and underlying subcutaneous tissue. Rippling of the skin can occur before the development of a digital flexion deformity.3 A controversy exists as to whether there is a relationship between Dupuytren disease and repetitive microtrauma, but more recent meta-analysis does seem to suggest some degree of occupational correlation with manual work and vibration exposure.5 It is now thought that microruptures, vibration, and trauma are related to development of the contracture. When considering that more than half of male field hockey players in the Netherlands over age 60 have Dupuytren disease, an environmental genetic-predisposition interaction is also supported.6 Cessation of manual labor and immobilization can lead to acceleration of the disease, which has been noted in laborers after retirement.7 A genetic predisposition is thought to be inherited as an autosomal dominant trait on chromosome 16q with variable penetrance of heritable and sporadic forms.9 Family history is often unreliable, as many individuals are unaware they have family members with the disease. Dupuytren disease has been termed “Viking disease”10 because it has a high prevalence in areas that were populated by the Vikings and where the Vikings migrated. Global prevalence is 3% to 6% of the white population, and it is rare in nonwhite populations. Dupuytren disease occurs more commonly in the elderly but tends to be associated with greater functional compromise in younger patients. Women are affected half as often as men.11 There is no relationship to handedness; however, affected individuals tend to complain more frequently about the dominant hand. Other associations with the condition include diabetes mellitus12 (specifically with an increased risk from dietcontrolled diabetes to sulfonylureas to metformin to insulin requiring), BRAF inhibitor treatment (Vemurafenib),13 alcohol consumption,14 cigarette smoking,14,15 human immunodeficiency virus infection,16 and antecedent Colles fracture.

CHAPTER 29  Dupuytren Contracture

FIG. 29.1  Typical appearance of ulnar palmar surface after surgical release; notice scarring and incomplete extension.

Conflicting reports exist of an association with epilepsy, but antiepileptic drugs do not present an increased risk.17 There are potential secondary findings in Dupuytren disease that are rarely seen, but when present suggest a strong Dupuytren diathesis (genetic penetrance of the disease). These findings include knuckle pads (Garrod nodes), plantar fascial disease, and Peyronie disease. The contractile tissue in all of these conditions resembles the pathologic findings of Dupuytren disease in the palm,18 and alterations in the expression of certain gene families, fibroblast to myofibroblast differentiation among others, are similar.19 However, these associated conditions are found in only an estimated 1% or less of patients with Dupuytren disease.20 All patients with the disease have a diathesis, or genetic tendency, towards the disease, making recurrence, bilateral involvement, and need for repeat and or ongoing care likely. Association with these conditions, as well as onset at an early age, and family history suggest the diathesis is strong. Recognition of a strong diathesis is important for planning an appropriate rehabilitation protocol, including long-term follow-up and awareness of possible poor prognosis and likelihood of recurrence with surgical treatment. 

Symptoms Dupuytren disease typically has a painless onset and progression. Decreased range of motion, loss of dexterity, and getting the hand “caught” when trying to place it in one’s pant-pocket are common presenting symptoms. Pain can be a result of concomitant injuries to the hand and fingers that can precede the development or worsening of Dupuytren disease. Abrasions or ecchymosis to the distal interphalangeal and PIP joints of the affected digits may be seen and may be the reason for the initial consultation. With use of the relatively new Dupuytren Disease Scale of Subjective Well-Being of patients’ questionnaire, which covers four areas of the quality of life, there were no differences in quality of life in patients affected in the left or right hand regardless of hand dominance of the patients.21

155

FIG. 29.2  Dupuytren contracture of the ring finger.

The progression of the condition is generally considered to be a result of immobility after an injury in a predisposed individual rather than of the injury itself. Pure sensory symptoms in digits four and five may arise from palmar digital nerves against the relatively inelastic deep transverse metacarpal ligament. 

Physical Examination The most common first sign of Dupuytren disease is a lump in the palm close to the distal palmar crease and in the axis of the ray of the fourth digit (ring finger) (Fig. 29.2). It can also be manifested in the digit, generally over the proximal phalanx. The thumb and index finger are the least affected of the five digits. The nodule can be tender to palpation. In most cases, the skin is closely adherent to the nodule, and movement with tendon excursion often suggests other conditions, such as stenosing tenosynovitis. The condition is more readily apparent when it is manifested in a more advanced stage with palmar nodule, cord, and digital flexion contracture. Conditions associated with this disease include fat pads at the knuckles and evidence of the disease in the plantar fascia. “Swan-neck” deformity as a dorsal variant of Dupuytren disease has been suggested.22 The examination should evaluate the range of motion and kinetic chain of the entire upper limb, including associated adhesive capsulitis, epicondylitis, other tenosynovitis and digital nerve or vascular compromise. Sensory, manual motor, and muscle stretch reflex components of the neurologic examination should be normal. Upper motor neuron findings should be absent. 

Functional Limitations The majority of individuals with this condition have little functional limitation early on. With more advanced contracture, properly opening the palm and grasping can become difficult, making gripping activities such as activities of daily living, opening cans, buttoning shirts, and placing keys in automotive ignitions troublesome. In many cases, the insidious onset allows gradual compensation, and outside observers may notice irregularity during a simple hand shake. 

156

PART 1  MSK Disorders

Diagnostic Studies The diagnosis of Dupuytren disease is generally made on a clinical basis. Biopsy is considered when a palmar soft tissue mass cannot be reliably differentiated from sarcoma.23 The suspicion for sarcoma is higher in a younger individual with no strong evidence of Dupuytren disease because sarcoma is more likely in younger age groups. Unfortunately, histologic differentiation is not always easy because a Dupuytren nodule can appear cellular with mitotic figures and closely resemble an aggressive sarcoma. Blood work relevant to underlying secondary disease (e.g., hemoglobin A1c level, human immunodeficiency virus testing, uric acid level, erythrocyte sedimentation rate) should be entertained. Electrodiagnostic studies are usually normal. However, concomitant median or ulnar neuropathy at the wrist, or compromise of digital nerves, can cause sensory complaints. Dupuytren tissue may compress the palmar digital nerves against the relatively inelastic deep transverse metacarpal ligament.24 Sensory nerve action potentials should be recorded to digit four and not just digit five, with healthy nerves screened for concomitant peripheral neuropathy that may affect postoperative rehabilitation.  Differential Diagnosis Fibroma Lipoma Epithelioid sarcoma Giant cell tumor Neurofibroma Tendon nodules of stenosing tenosynovitis Inclusion cysts Dorsal Dupuytren disease Retinacular ganglions at the A1 pulley Non-Dupuytren palmar fascial disease Tophi

Treatment Initial Many patients who seek consultation for Dupuytren disease are merely looking for reassurance that they do not have a malignant neoplasm and are satisfied to learn that the contracture is not a sign of a more ominous disease. Conventional noninvasive treatment has generally been of little or no value in the prevention of contracture or recurrence in Dupuytren disease. This includes the use of steroid injections, splinting, ultrasound, and nonsteroidal anti-inflammatory medications. Radiotherapy, topical dimethyl sulfoxide, colchicine, and interferon have also been proposed, but lack data demonstrating long-term efficacy. Topical 5-fluorouracil,25 topical imiquimod (Aldara),26 and oral simvastatin27 seem to target the underlying fibroblastic process, but long-term outcome studies do not exist. Traumatic rupture has never gained acceptance as a method of correcting flexion contracture; however, anecdotal reports of individuals correcting their deformity in such a fashion exist,28 but recurrence in true Dupuytren disease would be expected. Continuous passive traction has been proposed by some for severely flexed digit contractures29; however,

this is used as a preoperative adjunctive procedure and not done in isolation. Ergonomic assessment and equipment modification can be of use in some instances with laborers who are functionally limited by contracture. Tobacco abuse or excessive alcohol consumption should be addressed if applicable. 

Rehabilitation Rehabilitation efforts are minimal preoperatively and focus on adaptive equipment recommendations for work and home (e.g., large-handled tools for gripping) as well as accommodation of the deformity and prevention of dislocation or further trauma. Splinting may be done, but there is no evidence that this delays contracture or affects the underlying pathohistologic changes. Continuous passive traction is used along with passive stretching, as with any joint contracture, pre-stretching paraffin bath dips or fluidotherapy may make stretching more effective. Postoperative rehabilitation is needed to facilitate a satisfactory outcome. The length of the rehabilitation generally reflects the invasiveness of the surgical procedure; limited fasciotomies often involve a period of 4 to 6 weeks, whereas more extensive surgery may necessitate a formal rehabilitation process of up to 3 to 6 months. Stretching, splinting in palmar extension, and continuous passive traction in some individuals are used early postoperatively. Strengthening and functional activities are added later, after incision healing. Again, splinting may be an option to prevent recurrence, and adaptive equipment recommendations can help with resumption of functions that involve gripping or repetitive hand use. 

Procedures Debate exists about the role of closed needle fasciotomy (needle aponeurotomy). Despite a recurrence rate of 10% to 20%, compared with surgical recurrence rates of 5% to 10% per year, advantages of cost, faster recovery, ease of performing in an outpatient office setting, lower overall complication rate and suggest it may be a reasonable first-line treatment.30 Controversy exists about the relative effectiveness of injectable collagenase (collagenase Clostridium histolyticum) versus limited fasciectomy and while collagenase provided a more rapid recovery of hand function, fewer adverse events, and better MCP contracture treatment, PIP contractures may do better with limited fasciectomy.31 With having only been approved since 2010, we may be only now starting to see long-term consequences, and Clostridium histolyticum injections may produce a deeply scarred bed and increase the technical difficulty of salvage fasciectomy.32 This should be interpreted within context of the naturally progressive nature of the disease and subsequent palmar fasciectomy results being comparable to those of primary fasciectomy. Anecdotally, Depo-steroid injection into the palmar nodule can be a useful adjunct to flatten the nodule and enable occupational therapies. Concern for potential adverse effect on the underlying flexor tendons and neurovascular bundles should be noted, and can be minimized by being mindful of depth and position of injection. Ultrasound guidance may have a role in any tendon injection, but will not reveal

CHAPTER 29  Dupuytren Contracture

inadvertent vascular uptake. A comparison of miRNAs expressed in Dupuytren’s fascia versus control identified 74 miRNAs with a twofold enrichment in Dupuytren’s tissue, and 32 miRNAs with enrichment in control fascia.33 It is still hoped that this may eventually lead to the development of novel molecular therapy to preferentially target collagens and other extracellular matrix proteins. 

Technology Advances in arthroscopic and needle fasciotomy suggest some evolving technology in the treatment of Dupuytren’s contracture. The increased availability of diagnostic ultrasound may result in earlier diagnosis and screening in individuals with diathesis. 

Surgery Appropriate selection is critical for patients considering surgical treatment. Surgery for Dupuytren contracture generally should be performed on an affected MCP joint if the contracture is 30 degrees or greater.34 The potential for recurrence and worsening after surgery is higher in patients with a strong diathesis. Recurrence is defined as the development of nodules and contracture in the area of previous surgery. Extension is the development of lesions outside of the surgical area where there had previously been no disease. All patients should be made aware that surgery is not curative of this disease and that recurrence and extension are likely at some time. Extensive recurrence is more likely if surgery is performed during the proliferative phase of the condition. Nevertheless, when looking across the spectrum of surgical approaches, up to 79% of patients had “excellent” results at 5-year follow-up.35 Surgical outcomes may be improved by the insertion of an absorbable cellulose implant.36 The goals of surgical treatment, when it is indicated, are to improve function, to reduce deformity, and to prevent recurrence. Surgical indication is generally thought to include digital flexion contracture of the PIP and MCP joints and web space contracture. MCP joint contractures are often fully correctable; however, PIP joint contractures often have residual deformity.37 Multiple surgical procedures have been described for the treatment of Dupuytren contracture. Malingue’s procedure is a modified Z-plasty, making use of Euclidean geometry and avoiding the use of skin grafts or flaps, which may potentially have a lower incidence of reoperation.38 In addition, variations of subcutaneous fasciotomy, fasciectomy, and skin grafting have been used. A controlled randomized trial between the two most common approaches found no statistical difference at 2 years.39 Fewer complications are seen with limited fasciectomy, and this is often the procedure of choice for higher risk patients, for whom temporary relief is a therapeutic goal. A diseased cord arising from the abductor digiti minimi is noted to be present in approximately 25% of cases,40 and it should be released at the time of surgery if it is present. Full-thickness skin grafting has been shown to prevent recurrence41 and is considered in patients with a strong diathesis who have functionally limiting contracture. 

157

Potential Disease Complications In some individuals, the condition can become functionally limiting because of severe contracture. The thumb and index finger tend to be less affected than the other digits. Secondary contracture of the PIP joints can also develop in long-standing deformity. Vascular compromise is rare and more often part of complex regional pain syndrome after surgery. It appears that there is an advantage with axillary block or intravenous regional anesthesia with clonidine over lidocaine alone or general anesthesia in preventing complex regional pain syndrome in patients undergoing Dupuytren surgery.42 

Potential Treatment Complications Overall, recurrence of the disease after surgery is common (∼31%),43 which is not surprising when one considers that surgery does not alter the underlying histopathologic process, and surgery heals by scar formation, which is really just an extension of the underlying disease. Loss of flexion into the palm is particularly disturbing to patients. The presence of thickly calloused hands can result in increased postoperative swelling, leading to longer postoperative follow-up. “Flare reaction” is a postoperative complication in 5% to 10% of patients that occurs 3 to 4 weeks after surgery and is characterized by redness, swelling, pain, and stiffness.43 Complication rates are higher with greater disease severity, in particular PIP joint flexion contracture of 60 degrees or more. Amputation and ray resections are reported complications more common in surgery for recurrences.44 Although women with the disease less frequently meet operative criteria, they are thought to have a higher incidence of complex regional pain syndrome postoperatively.45 Other potential surgical complications are digital hematoma, granulation, scar contracture, inadvertent division of a digital nerve or artery, infection, and graft failure in full-thickness grafting procedures. A potential complication of injection therapy is injury to nearby structures, including the digital artery, nerve, and flexor tendons.

References 1. Cordova A, Tripoli M, Corradino B, et al. Dupuytren’s contracture: an update of biomolecular aspects and therapeutic perspectives. J Hand Surg Br. 2005;30:557–562. 2. Mosakhani N, Guled M, Lahti L, et al. Unique microRNA profile in Dupuytren’s contracture supports deregulation of ß-catenin pathway. Mod Pathol. 2010;23:1544–1552. 3. McFarlane RM. Patterns of the diseased fascia in the fingers in Dupuytren’s contracture. Plast Reconstr Surg. 1974;54:31–44. 4. Deleted in proofs. 5. Descatha A, Jauffret P, Chastang JF, et al. Should we consider Dupuytren’s contracture as work-related? A review and meta-analysis of an old debate. BMC Musculoskelet Disord. 2011;12:96. 6. Boggs W. Dupuytren disease common in older male field hockey players. Br J Sports Med. 2016. 7. Liss GM, Stock SR. Can Dupuytren’s contracture be work-related? Review of the literature. Am J Ind Med. 1996;29:521–532. 8. Deleted in proofs. 9. Hu FZ, Nystrom A, Ahmed A, et al. Mapping of an autosomal dominant gene for Dupuytren’s contracture to chromosome 16q in a Swedish family. Clin Genet. 2005;68(5):424–429. 10. Hueston J. Dupuytren’s contracture and occupation. J Hand Surg Am. 1987;12:657. 11. Yost J, Winters T, Fett HC. Dupuytren’s contracture: a statistical study. Am J Surg. 1955;90:568–572.

158

PART 1  MSK Disorders

12. Geoghegan JM, Forbes J, Clark DI, et al. Dupuytren’s disease risk factors. J Hand Surg Br. 2004;29:423–426. 13. Chan SW, Vorobiof DA. Dupuytren’s contractures associated with the BRAF inhibitor vemurafenib: a case report. J Med Case Reports. 2015;9(158). 14. Godtfredson NS, Lucht H, Prescott E, et al. A prospective study linked both alcohol and tobacco to Dupuytren’s disease. J Clin Epidemiol. 2004;57:858–863. 15. An JS, Southworth SR, Jackson T, et al. Cigarette smoking and Dupuytren’s contracture of the hand. J Hand Surg Am. 1994;19:442. 16. Bower M, Nelson M, Gazzard BG. Dupuytren’s contractures in patients infected with HIV. Br Med J. 1990;300:165. 17. Lund M. Dupuytren’s contracture and epilepsy. Acta Psychiatr Neurol. 1941;16:465–492. 18. Hueston JT. Some observations on knuckle pads. J Hand Surg Br. 1984;9:75. 19. Qian A, Meals RA, Rajfer J, Gonzalez-Cadavid NF. Comparison of gene expression profiles between Peyronie’s disease and Dupuytren’s contracture. Urology. 2004;64:399–404. 20. Cavolo DJ, Sherwood GF. Dupuytren’s disease of the plantar fascia. J Foot Surg. 1982;21:12. 21. Trybus Marek, Bednarek M, Lorkowski J, Teul I. Psychologic aspects of Dupuytren’s disease: a new scale of subjective well-being of patients. Ann Acad Med Stetin. 2011;57(1):31–37. 22. Boyce DE, Tonkin MA. Dorsal Dupuytren’s disease causing a swan-neck deformity. J Hand Surg Br. 2004;29:636–637. 23. Monacelli G, Spagnoli AM, Rizzo MI, et al. Dupuytren’s disease simulated by epithelioid sarcoma with atypical perineural invasion of the median nerve. Case report. G Chir. 2008;29:149–151. 24. Guney F, Yuruten B, Karalezli N. Digital neuropathy of the median and ulnar nerves caused by Dupuytren’s contracture: case report. Neurologist. 2009;15:217–219. 25. Bulstrode NW, Mudera V, McGrouther DA. 5-Fluorouracil selectively inhibits collagen synthesis. Plast Reconstr Surg. 2005;116:209–221. 26. Namazi H. Imiquimod: a potential weapon against Dupuytren contracture. Med Hypotheses. 2006;66:991–992. 27. Namazi H, Emami MJ. Simvastatin may be useful in therapy of Dupuytren contracture. Med Hypotheses. 2006;66:683–684. 28. Sirotakova M, Elliot D. A historical record of traumatic rupture of Dupuytren’s contracture. J Hand Surg Br. 1997;22:198–201. 29. Citron N, Mesina J. The use of skeletal traction in the treatment of severe primary Dupuytren’s disease. J Bone Joint Surg Br. 1998;80: 126–129. 30. Morhart M. Pearls and pitfalls of needle aponeurotomy in Dupuytren’s disease. Plast Reconstr Surg. 2015;135(3):817–825.

31. Zhou C, Hovius SE, Slijper HP, et al. Collagenase clostridium histolyticum versus limited fasciectomy for Dupuytren’s contracture: outcomes from a multicenter propensity score matched study. Plast Reconstr Surg. 2015;136(1):87–97. 32. Eberlin KR, Kobraei EM, Nyame TT, Bloom JM, Upton J III. Salvage palmar fasciectomy after initial treatment with collagenase clostridium histolyticum. Plast Reconstr Surg. 2015;135(6):1000e–1006e. 33. Riester SM, Arsoy D, Camilleri ET, Dudakovic A, Paradise CR, Evans JM. RNA sequencing reveals a depletion of collagen targeting microRNAs in Dupuytren’s disease. BMC Medical Genomics. BMC series – 2015;8:59. 34. Lee S, Gellman H. Surgery for dupuytren contracture medscape update. Orthpedic Surgery. 2015. 35. Khan PS, Iqbal S, Zaroo I, Hayat H. Surgical treatment of Dupuytren’s contracture; results and complications of surgery: our experience. J Hand Microsurg. 2010;2(2):62–66. 36. Degreef I, Tejpar S, De Smet L. Improved postoperative outcome of segmental fasciectomy in Dupuytren disease by insertion of an absorbable cellulose implant. J Plast Recon Surg Hand Surg. 2011;25:157–164. 37. Riolo J, Young VL, Ueda K, Pidgeon L. Dupuytren’s contracture. South Med J. 1991;84:983–996. 38. Apard T, Saint-Cast Y. Malingue’s procedure for digital retraction in Dupuytren’s contracture—principle, modelling and clinical evaluation. Chir Main. 2011;30:31–34. 39. Citron ND, Nunez V. Recurrence after surgery of Dupuytren’s disease: a randomized trial of two skin incisions. J Hand Surg Br. 2005;30:563–566. 40. Meathrel KE, Thoma A. Abductor digiti minimi involvement in Dupuytren’s contracture of the small finger. J Hand Surg Am. 2004;29:510–513. 41. Villani F, Choughri H, Pelissier P. Importance of skin graft in preventing recurrence of Dupuytren’s contracture. Chir Main. 2009;28:349–351. 42. Reuben SS, Pristas R, Dixon D, et al. The incidence of complex regional pain syndrome after fasciectomy for Dupuytren’s contracture: a prospective observational study of four anesthestic techniques. Anesth Analg. 2006;102:499–503. 43. Bulstrode NW, Jemec B, Smith PJ. The complications of Dupuytren’s contracture surgery. J Hand Surg Br. 2005;30:1021–1025. 44. Del Frari B, Estermann D, Piza-Katzer H. Dupuytren’s contracture— surgery of recurrences. Handchir Mikrochir Plast Chir. 2005;37:309–315. 45. Zemel NP, Balcomb TV, Stark HH, et al. Dupuytren’s disease in women: evaluation of long-term results after operation. J Hand Surg Am. 1987;12:1012.

CHAPTER 30

Extensor Tendon Injuries Jeffrey S. Brault, DO Brittany J. Moore, MD

Synonyms

M66.24

Central slip injury Boutonnière deformity Buttonhole deformity Extensor hood injury Extensor sheath injury Mallet finger

M66.241

ICD-10 Codes S66.2 S66.21 S66.22 S66.3 S66.31 S66.32

M20.0 M20.01 M20.011 M20.012 M20.02 M20.021 M20.022

Injury of extensor muscle, fascia, and tendon of thumb at wrist/hand level Strain injury of extensor muscle, fascia, and tendon of thumb at wrist/hand level Laceration of extensor muscle, fascia, and tendon of thumb at wrist/ hand level Injury of extensor muscle, fascia, and tendon of other and unspecified finger at wrist/hand level Strain of extensor muscle, fascia, and tendon of other and unspecified finger at wrist/hand level Laceration of extensor muscle, fascia, and tendon of other and unspecified finger at wrist/hand level Acquired deformities of finger(s) Mallet finger Mallet finger of right finger(s) Mallet finger of left finger(s) Boutonnière deformity Boutonnière deformity of right finger(s) Boutonnière deformity of left finger(s)

M66.242

Spontaneous rupture of extensor tendons, hand Spontaneous rupture of extensor tendons, right hand Spontaneous rupture of extensor tendons, left hand

Definition Extensor tendon injuries occur to the extensor mechanism of the digits, a complex muscle-tendon system formed by the finger and thumb extensors with secondary supports from intrinsic hand musculature and the retinacular system of ligaments throughout the wrist, hand, and digits. These injuries are more common than flexor tendon injuries because of their superficial position and relative lack of soft tissue between them and underlying bone. As a result, extensor tendons are prone to laceration, abrasion, crushing, burns, and bite wounds.1 Demographic data vary per specific injury and are not well documented. Extensor tendon injuries commonly occur from lacerations, fist-to-mouth injuries, and rheumatologic conditions. Extensor tendon injuries result in the inability to extend the finger because of transection of the tendon itself, extensor lag, joint stiffness, or poor pain control. There are eight zones to the extensor mechanism where injury can result in differing pathomechanics (Fig. 30.1).2 

Symptoms Patients typically lose the ability to fully extend the involved finger (Fig. 30.2). Lack of motion may be confined to a single joint or the entire digit based on the site of extensor mechanism injury. Pain in surrounding regions often accompanies loss of motion due to abnormal tissue stresses. Diminished sensation may be present if there is concomitant injury to the dorsal branches of the radial or ulnar nerves. 

Physical Examination Ask if any baseline motion deficits in the digits or hand existed prior to the presenting complaint. Note the resting hand position as well as asymmetry upon active extension 159

160

PART 1  MSK Disorders

from a resting position. Complete extensor tendon disruption creates a resting flexed posture of the unsupported finger; however, this may become more apparent upon attempted activation out of the naturally flexion-biased resting hand position. Evaluate active and passive range of motion at each finger joint, noting presence and amount of extensor lag from neutral. Neurological examination should

assess for injuries to the adjacent dorsal branches of the radial and ulnar nerves. Evaluate light touch and pin prick sensation throughout, with focus on the dorsal aspects of the digits. 

Functional Limitations Functional limitations are manifested as the inability to produce finger extension in preparation for grip or pinch. As a result, writing and manipulation of small objects can be problematic. There may also be difficulty reaching into confined areas, such as pockets, due to the resting flexed digit position with limited ability to extend. 

Diagnostic Studies I II III IV V

Obtain anteroposterior and lateral radiographs of the involved hand and fingers when there is a possibility of bone injury or foreign body in the soft tissues. If clinical suspicion of injury is in question, diagnostic imaging for direct tendon visualization can be performed with ultrasonography or magnetic resonance imaging (MRI). Ultrasonography is an inexpensive alternative to MRI for detection of extensor tendon injuries and has been shown to be more accurate than physical examination or MRI for detection of these injuries.3 Ultrasonography can be particularly helpful for detection of foreign bodies, diagnosis of partial tendon injuries, and dynamic evaluation of extensor tendon function.3–5 

VI

Differential Diagnosis

VII VIII

FIG. 30.1  Zones of extensor tendons. Odd numbers overlie the respective joints, and even numbers overlie areas of intermediate tendon regions.

FIG. 30.2  Extensor tendon disruption of the ring finger resulting in an inability to extend the ring finger. (Modified from Daniels JM II, Zook EG, Lynch JM. Hand and wrist injuries: part I. Nonemergent evaluation. Am Fam Physician. 2004;69:1941–1948.)

Fracture dislocation Joint dislocation Peripheral nerve injury Osteoarthritis Rheumatoid arthritis Trigger finger (stenosing tenosynovitis)

Treatment Initial The treatment protocols for extensor tendon injuries vary by zone, mechanism, and time elapsed since injury. If the disruption of the extensor mechanism is due to laceration, crush injury, burn, or bite, surgical referral is warranted. In open injuries, wound care should be performed. If surgical repair is not immediate, appropriate antibiotics should be initiated, the injured tendon should be promptly irrigated, and primary coverage by skin suturing should be performed to protect the tendon and decrease potential for infection. The surgeon who will be performing the definitive repair should be contacted as soon as possible, ideally prior to skin suturing.6 In general, closed injuries are treated conservatively with splint immobilization, open injuries with less than 50% tendon involvement are managed with skin closure only and splint immobilization, and open injuries with greater than 50% tendon involvement are managed with primary tendon repair and subsequent postoperative splinting. Closed injuries tend to be more common in zones I and II; thus initial

CHAPTER 30  Extensor Tendon Injuries

treatment is with splints. Laceration injuries tend to be more common in zones III through VIII, thus initial treatment with surgery is more common. 

Rehabilitation Splinting can be with static extension splints or early motion splint protocols that aim to reduce adhesion and stiffness. There is no current strong evidence to show significant advantage of early mobilization over traditional static immobilization.7 However, as surgical technique has advanced to create stronger extensor repairs, there has been a shift towards more aggressive postoperative rehabilitation protocols with early motion.2 Early motion splints can be categorized into “short arc motion splints” that passively immobilize the joint while allowing intermittent splint-assisted passive flexion and active extension, “relative motion splints” (also called controlled active mobilization splints) that allow active joint extension while limiting joint flexion, or “dynamic splints” that create passive joint extension with customizable active joint flexion.7–9 Early motion splinting does require close oversight by a skilled therapist to ensure motion occurs in specific protected ranges.

Zone I (Mallet Deformity) Zone I lesions involve the terminal extensor tendon over the distal interphalangeal (DIP) joint. Mechanism of injury is a sudden flexion force applied to a DIP joint that is actively extending. The tendon can tear at its insertion, creating a “soft issue” mallet, or there can be associated avulsion fracture of distal phalanx with tendon injury, creating a “bony” mallet.7,10 Injury produces a characteristic mallet flexion deformity of the DIP joint. The digits most commonly involved are the long, ring, and small fingers of the dominant hand.7 When left untreated,

161

the mallet deformity can lead to DIP joint osteoarthritis or a swan neck deformity with hyperextension of the proximal interphalangeal (PIP) joint.10 Closed injury is treated conservatively with 6 to 8 weeks of continuous immobilization of the DIP joint in full extension to slight hyperextension (0 to 15 degrees).7,10–13 Splinting in full extension may be best suited for bony mallet injuries, whereas mild hyperextension splinting may be best for soft tissue injury.10 Excessive DIP hyperextension should be avoided due to risk of compromising the dorsal skin vascular supply.10 Different types of splint orthoses exist; no specific orthotic has been proven superior.10,13,14 Prefabricated Stack mallet splints have classically been recommended.13 Custom splints may be warranted, particularly in vulnerable population, as there is less risk of developing skin complications when compared to prefabricated splints for management of mallet finger.14 After 6 to 8 weeks of continuous splint immobilization, the splint may be transitioned to nighttime use only for an additional 2 to 4 weeks.7,10 When the splint is removed, the DIP joint should be able to maintain an extended position. A graded home exercise program should be initiated after completion of continuous splint immobilization, with progression from active DIP joint range of motion for the first week, to active and passive motion exercises the subsequent week. Exercises should be performed hourly when awake, 10 repetitions per hour, and through a pain-free range (Table 30.1).11,12 

Zone II Injuries in zone II are often due to a laceration or crush injury to the middle phalanx of the fingers or proximal phalanx of the thumb, with resultant partial or total extensor tendon transection.2 If there is less than 50% tendon involvement, manage with extension splint for

Table 30.1  Extensor Zone Injury Management Overview Injury

Management

Splint

Exercise

Skin Care

Zone I (mallet finger)

Splint only: 50% tendon involvement

6–8 weeks continuous static DIP extension splint Transition to nighttime only static splinting for 2 additional weeks (total 8–10 weeks)

In continuous splint: active flexion and extension of PIP and MCP (hourly) Add active DIP flexion (hourly) with transition to nighttime only splint Add passive DIP flexion (hourly) during second week of nighttime splinting

Remove splint daily to check for skin integrity and hygiene (maintain DIP joint in extension)

Zone II injury

Same as zone I

Same as zone I

Same as zone I

Same as zone I

Zone III injury (boutonnière deformity)

Splint only: 60 degrees, fixed scaphoid rotation (ring sign), capitate migrates proximally

T1: Decreased T2: Variable Possible scapholunate dissociation

III C

Carpal instability

Coronal fracture or fragmentation of the lunate

T1: Decreased T2: Variable

IV

Stiffness with intermittent symptoms after activity (Kienböck Disease Advanced Collapse/KDAC)

Severe lunate collapse, carpal arthritis

T1: Decreased T2: Decreased Chondral loss, articular collapse, and changes of midcarpal and radiocarpal articulations—reactive synovitis and joint effusion

CT, Computed tomography; MRI, magnetic resonance imaging. Data from Lichtman DM, Bain GI. Kienböck’s Disease: Advances in Diagnosis and Treatment. 1st ed. Cham: Springer; 2016. Pientka WF, et al. Clinical presentation, natural history, and classification of Kienböck’s disease. In: Lichtman DM, Bain GI, eds. Kienböck’s Disease: Advances in Diagnosis and Treatment. Cham: Springer International Publishing; 2016:97–109. Lutsky K, Beredjiklian PK. Kienböck disease. J Hand Surg. 2012;37(9):1942–1952. Lichtman DM, Lesley NE, Simmons SP. The classification and treatment of Kienböck’s disease: the state of the art and a look at the future. J Hand Surg (European Vol). 2010;35(7):549–554.

Imaging classification systems, along with clinical and arthroscopic findings, can help guide treatment. The modified Lichtman four-stage classification system is the most widely used today. It utilizes radiographic osseous morphologic characteristics to delineate stages within the natural history of Kienböck disease (Table 35.1; Fig. 35.4). However, basic radiographic findings do not always correlate with degree of symptoms, which contributes to the difficulty in assessing the natural history of this condition. In recent years, an MRI-based classification system has been developed that allows for evaluation of bone marrow perfusion and viability.19 There is also an arthroscopic classification based on the amount of non-functional articular surface of the lunate.20  Differential Diagnosis Posttraumatic lesions (e.g., scaphoid/lunate fracture) Scapholunate ligament injury or dissociation Osteoarthritis Inflammatory arthritis (e.g., rheumatoid arthritis) Preiser disease (avascular necrosis of the scaphoid) Ganglion Intraosseous Wrist sprain Tendinopathy Lunotriquetral synchondrosis Ulnar impaction syndrome

Treatment Initial Management for Kienböck disease is largely surgical, but ultimate treatment decisions should account for the patient’s age, general health, demands on the wrist, lifestyle, and goals. Those with better prognosis may commence a trial of conservative management. Although seen less commonly, prognosis is more favorable in those under 20 years of age and those over 70 years of age.14,21 The skeletally immature under 15 years of age tend to do well with immobilization and can even go on to have revascularization on MRI. These patients can be monitored with MRI to determine if there is need for surgical intervention.3,21 In the elderly, there is a predictable progression to stage IV disease on imaging findings. However, elderly patients clinically do well and respond favorably to conservative treatment.3,22 Adults in the earliest stages of Kienböck disease with intact perfusion, functional articular surfaces, and without lunate collapse, may be initially treated nonoperatively. Unfortunately, most patients with Kienböck disease and abnormal imaging findings will require surgical intervention. 

Rehabilitation Treatment goals target improvement of pain and function. They allow for lunate protection and revascularization.

PART 1 MSK Disorders

188

B

C

A

E

D FIG. 35.4  The stages of Kienböck disease. (A) Stage I. T1-weighted magnetic resonance imaging shows marked signal reduction in the lunate, compatible with loss of blood supply. (B) Stage II. Density changes in the lunate as indicated by sclerosis. Note the ulnar minus variance. (C) Stage IIIA. Collapse of the lunate. There are no fixed carpal derangements. (D) Stage IIIB. Decreased carpal height and proximal migration of the capitate. Note the scaphoid cortical ring sign (arrow). (E) Stage IV. Generalized degenerative changes in the carpus. (From Weinzweig J, ed. Plastic Surgery Secrets. Philadelphia: Hanley & Belfus; 1999:605–606.)

Pain can be treated with analgesics, including nonsteroidal anti-inflammatory drugs. Opioid medications are generally not recommended because of the chronicity of this condition. Conservative treatment starts with activity modification— specifically, reducing strenuous activity with pushing, pulling, twisting, or lifting over 10 pounds. A short period of immobilization with a short arm cast or splint may be helpful. Clear guidelines on immobilization have not been established, but most clinicians opt for an average of 7 weeks in early stages.23 Since Kienböck disease is often treated surgically, data regarding conservative treatment and physical therapy is

lacking. Proposed therapy includes fluidotherapy, ultrasound, range of motion without loading the lunate, tendon glides, and ice.24 Specific physical therapy goals may include reduction of repetitive lunate load by strengthening in unloaded positions, activity modification, retraining wrist movements, and neuromuscular re-education. This currently does not play a large role in conservative treatment. If after 3 months the patient continues to have symptoms or imaging demonstrates progression, surgical treatment should be considered. Postoperatively, therapy plays an important role. This varies depending on type of surgery, but typically the wrist is immobilized for 6 weeks postoperatively until the vascularized graft

CHAPTER 35  Kienböck Disease

189

Table 35.2  Proposed Treatment Based on Modified Lichtman Classification Stages

Description

Treatment

Procedure

0

Pre-Kienböck disease Transient lunate ischemia

Conservative, aimed at lunate protection and unloading

Immobilization with short arm orthosis/cast

I–II

Lunate intact

Trial conservative, then surgical unloading, decompression, revascularization

Immobilization trial, then radial or capitate shortening osteotomy, lunate forage, synovectomy, cancellous bone grafting, radius/ulna core decompression, or vascularized bone graft

III A

Proximal lunate collapse

Lunate reconstruction

Osteochondral graft reconstruction, PRC, lunate replacement, RSL fusion, or SC fusion

III B

Carpal collapse

Stabilize radial column

SC fusion or PRC

III C

Lunate not reconstructible

Lunate salvage

PRC, SC fusion, or RSL fusion

IV

KDAC pancarpal osteoarthritis

Wrist Salvage

Wrist fusion or wrist arthroplasty

KDAC, Kienböck disease advanced collapse; PRC, proximal row carpectomy; RSL, radioscapholunate; SC, scaphocapitate. Data from Lichtman DM, Bain GI. Kienböck’s Disease: Advances in Diagnosis and Treatment. 1st ed. Cham: Springer; 2016. Lichtman DM, Pientka WF, Bain GI. The future of Kienböck’s disease: a new algorithm. In: Lichtman DM, Bain GI, eds. Kienböck’s Disease: Advances in Diagnosis and Treatment. Cham: Springer International Publishing; 2016:307–320.

or fusion has healed. At that point, occupational or physical therapy can effectively begin with gentle range of motion exercises, gradually progressing to strengthening exercises. 

Procedures Intra-articular steroids are of no proven benefit in the management of Kienböck disease, and there is evidence to suggest that long-term systemic corticosteroids may predispose to avascular necrosis.2 

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery The classification systems previously described can help identify the natural history and progression of Kienböck disease and guide surgical treatment (Table 35.2). Lichtman et al. have proposed a new treatment algorithm encompassing the traditional osseous Lichtman classification, the MRI-based perfusion/viability classification, and the arthroscopic articular classification systems.17,25 When initial nonoperative treatment is unsuccessful, surgical lunate unloading, decompression, or revascularization procedures may be indicated in early stages. Lunate unloading procedures include radial shortening osteotomy for ulnar negative variance and capitate shortening osteotomy for neutral or ulnar positive variance. Lunate forage (drilling to relieve venous hypertension), synovectomy, and cancellous bone grafting techniques can be helpful in decompression. Indirect revascularization can be achieved by core decompression of the distal radius and ulna. If the lunate is intact, but with evidence of decreased vascularity, direct revascularization can be performed with pedicle or free vascularized bone graft.17 For those patients in later stages, surgical treatment is a mainstay. In those with localized lunate compromise, lunate reconstruction techniques with vascularized bone grafts may be attempted. This may be technically challenging and time consuming. If the lunate is not reconstructible, then salvage

with lunate replacement or proximal row carpectomy is favored in patients with low demand. In high-demand patients, limited fusion is preferred. These procedures sacrifice motion in an effort to provide pain relief. In later stages with wrist and carpal degeneration, various motion-preserving procedures may be most appropriate. Prior to carpal collapse, specific areas of the wrist can be reconstructed with various excision or fusion techniques, depending on extent of osseous collapse and functional articular surfaces. In the last stages of KDAC, the wrist is not reconstructible and wrist salvage procedures like total wrist fusion or arthroplasty are required. For any of these various procedures, surgeon skill set, equipment, and resources must be considered.17,25 The results of the various procedures are dependent, to some extent, on the stage of the disease. No one surgical treatment method is consistently reliable or is appropriate for all patients. Regardless of the treatment method, patients typically report improvement. In early Kienböck disease, 83% to 90% of patients report improvement in pain after surgery. In the late stages, 63% of patients report pain improvement with nonsurgical management, while 72% to 89% report improvement after surgery.26 

Potential Disease Complications Without surgery, progressive radiographic collapse of the lunate and arthritis of the wrist invariably occur. 

Potential Treatment Complications Analgesics and nonsteroidal anti-inflammatory drugs generally used for symptoms of Kienböck’s Disease have wellknown side effects that most commonly impact the gastric, cardiac, hepatic, and renal systems. In regards to complications of surgical treatment, infection is uncommon after hand surgery.27 Other described surgical complications include nerve injury, decreased grip strength, painful hardware, and stiffness of the wrist and digits. In addition, nonunion after fusion techniques, hardware failure, and secondary arthritis can occur.2 Finally, whether surgery favorably alters the natural history of this rare condition remains unproven.

190

PART 1 MSK Disorders

References 1. Wagner JP, Chung KC. A historical report on Robert Kienböck (1871– 1953) and Kienböck’s disease. J Hand Surg. 2005;30(6):1117–1121. 2. Lichtman DM, Bain GI. 1st ed. Kienböck’s Disease: Advances in Diagnosis and Treatment. Cham: Springer; 2016. 3. Pientka WF, et al. Clinical presentation, natural history, and classification of Kienböck’s disease. In: Lichtman DM, Bain GI, eds. Kienböck’s Disease: Advances in Diagnosis and Treatment. Cham: Springer International Publishing; 2016:97–109. 4. Lichtman DM, Pientka 2nd WF, Bain GI. Kienbock disease: moving forward. J Hand Surg Am. 2016;41(5):630–638. 5. Stahl S, et al. A systematic review of the etiopathogenesis of Kienbock’s disease and a critical appraisal of its recognition as an occupational disease related to hand-arm vibration. BMC Musculoskelet Disord. 2012;13:225. 6. Bain GI, Yeo CJ, Morse LP. Kienbock disease: recent advances in the basic science, assessment and treatment. Hand Surg. 2015;20(3):352–365. 7. Goeminne S, Degreef I, De Smet L. Negative ulnar variance has prognostic value in progression of Kienbock’s disease. Acta Orthop Belg. 2010;76(1):38–41. 8. van Leeuwen WF, et al. Negative ulnar variance and Kienböck disease. J Hand Surg. 2016;41(2):214–218. 9. Afshar A, Aminzadeh-Gohari A, Yekta Z. The association of Kienböck’s disease and ulnar variance in the Iranian population. J Hand Surgery Eur Vol. 2013;38(5):496–499. 10. Stahl S, et al. Critical analysis of causality between negative ulnar variance and Kienbock disease. Plast Reconstr Surg. 2013;132(4):899–909. 11. Lutsky K, Beredjiklian PK. Kienböck disease. J Hand Surg. 2012;37(9):1942–1952. 12. Bain GI, et al. The etiology and pathogenesis of Kienbock disease. J Wrist Surg. 2016;5(4):248–254. 13. Lamas C, et al. The anatomy and vascularity of the lunate: considerations applied to Kienböck’s disease. Chirurgie de la Main. 2007;26(1):13–20.

14. Lichtman DM, Lesley NE, Simmons SP. The classification and treatment of Kienböck’s disease: the state of the art and a look at the future. J Hand Surg Eur Vol. 2010;35(7):549–554. 15. Bain GI, Irisarri C. The etiology of Kienböck’s disease. In: Lichtman DM, Bain GI, eds. Kienböck’s Disease: Advances in Diagnosis and Treatment.Cham: Springer International Publishing; 2016:65–88. 16. Mikkelsen SS, Gelineck J. Poor function after nonoperative treatment of Kienbock’s disease. Acta Orthop Scand. 1987;58(3):241–243. 17. Lichtman DM, Pientka WF, Bain GI. The future of Kienböck’s disease: a new algorithm. In: Lichtman DM, Bain GI, eds. Kienböck’s Disease: Advances in Diagnosis and Treatment.Cham: Springer International Publishing; 2016:307–320. 18. Wang L, Zlatkin MB, Clifford PD. Basic imaging and differential diagnosis of Kienböck’s disease. In: Lichtman DM, Bain GI, eds. Kienböck’s Disease: Advances in Diagnosis and Treatment.Cham: Springer International Publishing; 2016:111–120. 19. Schmitt R, Kalb K. [Imaging in Kienbock’s Disease]. Handchir Mikrochir Plast Chir. 2010;42(3):162–170. 20. Bain GI, Begg M. Arthroscopic assessment and classification of Kienbock’s disease. Tech Hand Up Extrem Surg. 2006;10(1):8–13. 21. Irisarri C, Kalb K, Ribak S. Infantile and juvenile lunatomalacia. J Hand Surg Eur Vol. 2010;35(7):544–548. 22. Taniguchi Y, et al. Kienbock’s disease in elderly patients. J Hand Surg Am. 2003;28(5):779–783. 23. Danoff JR, et al. The management of Kienbock disease: a survey of the ASSH membership. J Wrist Surg. 2015;4(1):43–48. 24. Wollstein R, et al. A hand therapy protocol for the treatment of lunate overload or early Kienbock’s disease. J Hand Ther. 2013;26(3):255– 259; quiz 260. 25. Lichtman DM, Pientka WF II, Bain GI. Kienbock disease: a new algorithm for the 21st century. J Wrist Surg. 2017;6(1):2–10. 26. Innes L, Strauch RJ. Systematic review of the treatment of Kienbock’s disease in its early and late stages. J Hand Surg Am. 2010;35(5):713– 717, 717.e1-4. 27. Goyal KS, et al. The safety of hand and upper-extremity surgical procedures at a freestanding ambulatory surgery center: a review of 28,737 cases. J Bone Joint Surg Am. 2016;98(8):700–704.

CHAPTER 36

Median Neuropathy (Carpal Tunnel Syndrome) Meijuan Zhao, MD David T. Burke, MD, MA

Synonyms Carpal tunnel syndrome Median nerve entrapment at the wrist Median nerve compression

ICD-10 Codes G56.00 Carpal tunnel syndrome, unspecified upper limb G56.01 Carpal tunnel syndrome, right upper limb G56.02 Carpal tunnel syndrome, left upper limb

Definition Carpal tunnel syndrome (CTS), an entrapment neuropathy of the median nerve at the wrist, is the most common compression neuropathy of the upper extremity. This syndrome produces paresthesias, numbness, pain, subjective swelling, and, in advanced cases, muscle atrophy and weakness of the areas innervated by the median nerve. The condition is often bilateral, although the dominant hand tends to be more severely affected. CTS is thought to result from a compression of the median nerve as it passes through the carpal tunnel. The clinical presentation is variable. Whereas there is some variation as to what should be included in this definition, CTS is most often thought to involve sensory changes in the radial 3½ digits of the hand with burning, tingling, numbness, and a subjective sense of swelling. Those affected often first note symptoms at night. In the later stages, complaints include motor weakness in the thenar eminence. It is helpful to think of the carpal tunnel as a structure with four sides, three of which are defined by the carpal bones and the fourth, the “top” of the tunnel, by the transverse carpal ligament (Figs. 36.1 and 36.2). Passing through the tunnel are the median nerve and nine tendons with their synovial sheaths; these include the flexor pollicis longus, the

four flexor digitorum superficialis, and the four flexor digitorum profundus tendons. None of the sides of the tunnel yields well to expansion of the fluid or structures within. Because of this, swelling will increase pressure within the tunnel and may result in compression of the median nerve. CTS occurs more commonly in women than in men, with a prevalence in the general adult population ranging from 2.7% to 5.8%.1,2 It is most common in middle-aged persons between the ages of 30 and 60 years. The older adults may have objective clinical and electrophysiologic evidence of a more severe median nerve entrapment.3 Most cases of CTS are idiopathic with congenital predisposition. Some focal or systemic conditions, such as wrist injury, arthritis, diabetes,4 thyroid disease,5 rheumatoid arthritis, and pregnancy, can increase pressure on the median nerve in the carpal tunnel and contribute to the development of CTS. Increasing BMI is a strong risk factor for CTS6: being overweight increases the risk by 1.5 times, and being obese increases the risk by 2 times.7 High hand or wrist repetition rate is another risk factor for CTS.6 However, the role of computer keyboard or mouse use in contributing to CTS remains controversial. One recent meta-analysis showed no association between keyboard use and CTS,8 while another showed excessive computer use (particularly mouse use) to be a minor risk factor for CTS.9 Prolonged postures in extremes of wrist flexion or extension, repetitive use of the flexor muscles, and exposure to vibration are the primary exposures reported.10–13 The pathophysiologic mechanism of CTS involves a combination of mechanical trauma, increased pressure, and ischemic injury to the median nerve within the carpal tunnel.14 

Symptoms The classic symptoms of CTS include numbness and paresthesias in the radial 3½ fingers (Fig. 36.3). A typical early complaint is awakening in the night with numbness or pain in the fingers. Symptoms during the day are often brought out by activities placing the wrist in substantial flexion or extension or requiring repetitive motion of the structures that traverse the carpal tunnel. Many patients report symptoms outside the distribution of the median nerve as well.15 Numbness and pain in the hand may also be accompanied by volar wrist pain and aching at the forearm. The patient may describe the 191

192

PART 1  MSK Disorders

FIG. 36.1  Radiographic demonstration of the carpal tunnel (for orientation, the hand is in the same position in the radiograph). The carpal tunnel is formed radially, ulnarly, and dorsally by the carpal bones. (From Concannon M. Common Hand Problems in Primary Care. Philadelphia: Hanley & Belfus; 1999.)

FIG. 36.3  Patients with carpal tunnel syndrome complain of numbness or paresthesia within the median nerve distribution (orange area, arrows). (From Concannon M. Common Hand Problems in Primary Care. Philadelphia: Hanley & Belfus; 1999.)

watches, with this sensation fluctuating throughout the day or week. Some patients also report dry skin and cold hands. In the later stages of CTS, the numbness may become constant and motor disturbances more apparent, with complaints of weakness manifested by a functional decrease of strength. Patients may then report dropping objects. 

Physical Examination

FIG. 36.2  The volar carpal ligament (line) forms the roof of the carpal tunnel. This thick, fibrous structure does not yield to expansion, and increased pressure within the carpal tunnel can cause impingement of the median nerve. (From Concannon M. Common Hand Problems in Primary Care. Philadelphia: Hanley & Belfus; 1999.)

symptoms as being positional, with symptoms relieved by the shaking of a hand, often referred to as the flick sign.16 Patients may complain of a sense of swelling in the hands, often noting that they have difficulty wearing jewelry or

A two-point sensory discrimination test is thought to be the most sensitive of the bedside examination techniques. This involves a comparison of the two-point discriminating sensory ability of the median with that of the ulnar nerve distribution of the hand. Careful observation of the hands, comparing the affected side with the unaffected side and comparing the thenar and hypothenar eminences of the same hand, may reveal an increasing asymmetry. Weakness of the thenar intrinsic muscles of the hand can be tested with a dynamometer or clinically by testing abduction of the thumb against resistance. The presence of thenar atrophy is strongly associated with CTS, but absence of thenar atrophy cannot exclude the diagnosis of CTS.6 The more common special tests include the Phalen, the Tinel, and the nerve compression tests. The Phalen test involves a forced flexion at the wrist to 90 degrees for a period of 1 minute; a positive test result reproduces the symptoms

CHAPTER 36  Median Neuropathy (Carpal Tunnel Syndrome)

FIG. 36.4  Phalen test. Patients maximally flex both wrists and hold the position for 1 to 2 minutes. If symptoms of numbness or paresthesia within the median nerve distribution are reproduced, the test result is positive. (From Concannon M. Common Hand Problems in Primary Care. Philadelphia: Hanley & Belfus; 1999.)

of CTS (Fig. 36.4). The reverse Phalen maneuver is the same test completed with forced extension. The Tinel test involves tapping sharply over the volar aspect of the wrist just distal to the distal wrist crease. The test result is positive when a sensory disturbance radiates down the region of the distribution of the median nerve. The nerve compression test involves the placement of two thumbs over the roof of the carpal tunnel, with pressure maintained for 1 minute. The test result is positive if symptoms are reproduced in the area of the distribution of the median nerve. It is not recommended, however, to use the Phalen or Tinel test in isolation to diagnose CTS, as each test alone is poorly associated with ruling-in or ruling-out CTS.6 A review showed an overall estimate of 68% sensitivity and 73% specificity for the Phalen test, 50% sensitivity and 77% specificity for the Tinel test, and 64% sensitivity and 83% specificity for the carpal compression test.17 Two-point discrimination and testing of atrophy or strength of the abductor pollicis brevis proved to be specific but not very sensitive.17 

Functional Limitations Functional limitations of CTS often include difficulty with sleep due to frequent awakenings by the symptoms. Because certain sustained or repetitive motions are difficult, tasks that often become more difficult include driving a car and sustained computer keyboard or mouse use at work. The later symptom of weakness in the thenar eminence may result in difficulty maintaining grip. Profound CTS may result in functional limitations, such as the inability to tie one’s shoes, to button shirts, and to put a key in a lock. 

Diagnostic Studies Whereas CTS is a syndrome rather than a singular finding, it is often suggested that the “gold standard” test of CTS is electrodiagnostic testing. Electromyography and nerve conduction studies can confirm the diagnosis, determine

193

the severity (if any) of nerve damage, guide and measure the effect of treatment, and rule out other conditions such as radiculopathy, polyneuropathy, and brachial plexopathy. Ultrasound studies, which reveal an enlarged median nerve, may assist with the diagnosis.18 Typically, the ultrasound examination may show flattening of the nerve within the tunnel and enlargement of the nerve proximal and distal to the tunnel. Pooling of recent articles seems to confirm that sonography using cross-sectional area of the median nerve could not be an alternative to electrodiagnostic testing for diagnosis of CTS, but could give complementary results. Limitations to ultrasound use include examiner experience, dependent intra-rater reliability in measurement of the median nerve,19 and a lack of consensus in diagnostic thresholds and ideal locations for ultrasound measurement.6 Though ultrasound should not be used routinely in diagnosis of CTS,6 ultrasound examination should be considered in doubtful cases or secondary cases of CTS.20 Others have advocated the diagnostic injection of corticosteroids or bupivacaine into the carpal tunnel. If the injection is accompanied by a relief of symptoms, it provides diagnostic evidence of CTS.21 A wrist radiograph may be helpful if a fracture or degenerative joint disease is suspected. Blood tests should be ordered if underlying rheumatologic disease or endocrine disturbance is suspected. These include fasting blood glucose concentration, erythrocyte sedimentation rate, thyroid function, and rheumatoid factor. MRI is not sensitive for a diagnosis of CTS and is not routinely recommended.6 

Differential Diagnosis Cervical radiculopathy in C5 to T1 distribution Brachial plexopathy Proximal median neuropathy Ulnar or radial neuropathy Generalized neuropathy Arthritis of carpometacarpal joint of thumb de Quervain tenosynovitis Tendinitis of the flexor carpi radialis Raynaud phenomenon Hand-arm vibration syndrome Arthritis of the wrist Gout

Treatment Initial Once the diagnosis is established, treatment should begin with conservative management in patients with mild disease. Nighttime wrist splinting (Fig. 36.5) in a neutral position may help reduce or completely relieve CTS symptoms. Wrist splinting in neutral position may be more effective than in 20-degree extension in the short term.22 Fulltime use, if tolerable, has been shown to provide greater improvement of symptoms and electrophysiologic measures than night-only use.23 Compliance with full-time use is more difficult.23 Strong evidence supports the use of wrist splints6 and most patients will achieve maximal symptom

194

PART 1  MSK Disorders

FIG. 36.5  Wrist splint in neutral position.

relief through splinting within 2 to 3 weeks. If current treatment fails to resolve symptoms within 2 to 7 weeks, another nonsurgical treatment or surgery is suggested.24 Nonsteroidal anti-inflammatory drugs are frequently prescribed as an adjunct to wrist splinting. However, studies have demonstrated that nonsteroidal anti-inflammatory drugs, vitamin B6, and diuretics are often no more effective than placebo in relieving the symptoms of CTS.6,22 The use of oral steroids (prednisone in doses of 20 mg daily for the first week and 10 mg daily for the second week,25 or prednisolone at 25 mg daily for 10 days26) has proved to be of some benefit, although not as impressive as the results noted through injection.26 However, the effectiveness of oral or injected steroids was not maintained in the long term.22 Underlying conditions, such as hypothyroidism, rheumatoid arthritis, or diabetes, should be treated. Frequent periods of rest of the wrist should be prescribed, especially when vocational activities involve sustained positioning or repetitive and forceful flexion or extension of the wrist. Ice after periods of use may be effective for symptom relief. Positioning of the body while a task is being performed should be reviewed to relieve unnecessary strain as necessary motions are performed. 

Rehabilitation Rehabilitation must address the patterns of hand use, which exacerbate the symptoms of CTS in many individuals. Lifestyle modifications, including decreasing repetitive activity and using ergonomic devices, have been traditionally advocated but have inconsistent evidence to support their effectiveness. Occupational therapists can be helpful in instructing flexion and extension stretching of the wrist and forearm. Although many therapists advocate strengthening as part of a treatment program, aggressive strengthening exercises should be avoided until symptom relief is nearly complete. Icing after long periods of use has been advocated to reduce the pain and swelling. In addition, it is important that patients be instructed in a program of general physical conditioning; generalized deconditioning exacerbates the symptoms of CTS.27 There is evidence that ketoprofen phonophoresis may reduce pain, as compared to placebo.6 Limited data exists to suggest that therapeutic ultrasound is more effective than placebo.6

FIG. 36.6  Preferred method for ulna bursa injection. Needle puncture is just ulnar to the palmaris longus tendon. The circle is over the pisiform bone. (From Lennard TA. Pain Procedures in Clinical Practice. 2nd ed. Philadelphia: Hanley & Belfus; 2000.)

Magnet therapy did not show significant improvement in treating CTS, and it is not recommended to use magnet therapy for the treatment of CTS.6 There is no evidence for the effectiveness of postoperative splinting.6 It is suggested that the wrist not be immobilized postoperatively after routine carpal tunnel surgery.6 Active motion of the hand and wrist should start immediately postoperatively to prevent joint stiffness and to ensure adequate glide of the tendons and median nerve in the carpal tunnel. Routine supervised therapy and home programs are equally effective in the immediate postoperative period.6 Passive range of motion should be initiated at least 4 weeks postoperatively for mobilization of stiff joints and tendons. Strengthening is initiated at 3 to 4 weeks as wounds heal and inflammation resolves.28 On average, postsurgical patients were able to return to driving in 9 days, to activities of daily living in 13 days, and to work in 17 days.29 

Procedures The patient can also be treated with corticosteroid injections into the carpal tunnel. Steroid injections are strongly associated with improved patient reported outcomes.6 A number of authors have suggested various injection techniques to avoid direct injury to the median nerve.30–33 For injection into the carpal tunnel (Fig. 36.6), 1 mL of steroid (triamcinolone, 40 mg/mL) can be injected under sterile conditions. For delivery, one should use a ⅝-inch, 27-gauge needle, placing the needle proximally to the distal wrist crease and ulnar to the palmaris longus tendon. The needle should be directed dorsally and angled at 30 degrees to a depth of about ⅝ inch (the length of the needle) or contact with a flexor tendon. Slowly inject 1 mL of the corticosteroid.

CHAPTER 36  Median Neuropathy (Carpal Tunnel Syndrome)

Anesthetics are not typically used in this injection unless for diagnostic verification. In individuals lacking a palmaris longus tendon (about 2% to 20% of the population), the needle can be placed midpoint between the ulna and radial styloid process. The injection will increase the volume of fluid within the carpal tunnel and thus may exacerbate the discomfort for a few hours; relief is expected within the 24 to 48 hours after injection. Although effectiveness is primarily short term, corticosteroid injection may be particularly useful to control the pain and to reduce symptoms for patients wishing to delay surgical treatment. Both ultrasound-guided and blind steroid injections are effective in treating CTS. Though ultrasound-guided carpal tunnel injection has been reported to be more effective than conventional blind, palpation-guided injection,34–36 the exact role of ultrasound guidance for carpal tunnel injection is still arguable.37 

Technology Low-level laser therapy, also called cold laser therapy, is a physiotherapy modality that uses lower level red and near-infrared light to exert apparently anti-inflammatory and analgesic effects. Low-level laser therapy may be used for mild to moderate CTS, with one recent meta-analysis showing that laser therapy improves grip strength, but has no effect on functional status, pain reduction, or motor electrodiagnostic evaluations.38 

Surgery Carpal tunnel release surgery should be considered in patients with symptoms that do not respond to conservative measures and for whom electrodiagnostic testing clearly confirms median neuropathy at the wrist. Surgery or another nonsurgical treatment is suggested when the current treatment fails to resolve symptoms within 2 to 7 weeks.24 Six weeks to 3 months of conservative treatment is reasonable in patients with mild disease.39 Early surgery is indicated when there are signs of atrophy or muscle weakness. The optimal timing of surgery in the natural history of CTS has not been established, although timing is an important factor for total recovery after surgery. A long-lasting compression could result in irreversible axonal damage, which would not improve despite surgical intervention.22 Surgical treatment has been shown to lead to better outcome than nonsurgical treatment.6 Surgery is also more effective than nonsurgical treatment at improving electrophysiological measures.40 The primary reason for a poor result is an error in diagnosis. The open release of the transverse carpal ligament represents the standard procedure and can be performed by dividing the transverse carpal ligament through a small open wrist incision. The reliability of and good visualization provided by the open technique continue to make it the preferred operation for many hand surgeons, with a 2011 survey of hand surgeons finding that 52% used only open release, 36% used mostly endoscopic release, and 12% used both.41 The endoscopic techniques were introduced in the late 1980s to be minimally invasive and to prevent palmar scarring. Both methods have equal efficacy and provide excellent outcomes in relieving symptoms of CTS,6,42,43 with

195

satisfaction rates up to 90%. Potential benefits of the endoscopic technique, including a more rapid functional recovery, reduced scar tenderness, and earlier return to work,43–46 must be weighed against the technique’s increased cost and higher complication rate.42,43 

Potential Disease Complications As with any insult to a peripheral nerve, untreated CTS may result in chronic sensory disturbance or motor impairment in the area serviced by the median nerve. It is important that the clinician be wary of this and not allow the nerve disturbance to progress to permanent nerve damage. 

Potential Treatment Complications Although oral analgesics may be important for symptomatic relief early in the stages of CTS, gastric, renal, and hepatic complications of nonsteroidal anti-inflammatory drugs should be monitored. Complications from local corticosteroid injections include infection, bleeding, skin depigmentation, skin and fat atrophy, potential for tendon rupture, and potential for injury to the median nerve at the time of injection. Surgical complications have been noted to be few in the literature. These include accidental transection of the median nerve, with permanent loss of function distal to the transection. In addition, some have suggested that endoscopic surgery might damage the Berrettini branch of the median nerve, a sensory branch.47 Whereas complications of surgical intervention are thought to be relatively infrequent, a number have been reported. The most common complication of surgical intervention is the incomplete sectioning of the transverse carpal ligament. Other potential complications include injury to the median nerve, palmar cutaneous branch, recurrent motor branch, and superficial palmar arch; hypertrophied or thickened scar due to inappropriate incision; tendon adhesions because of wound hematoma; recurrence because of repair of the ligament; bowstringing of flexor tendons; malposition of the median nerve; inappropriate separation of the nerve fibers from surrounding scars; pillar pain; and reflex sympathetic dystrophy.

References 1. de Krom MC, Knipschild PG, Kester AD, et al. Carpal tunnel syndrome, prevalence in the general population. J Clin Epidemiol. 1992;45:373–376. 2. Atroshi I, Gummesson C, Johnsson R, et al. Prevalence of carpal tunnel syndrome in a general population. JAMA. 1999;282:153–158. 3. Blumenthal S, Herskovitz S, Verghese J. Carpal tunnel syndrome in older adults. Muscle Nerve. 2006;34:78–83. 4. Pourmemari MH, Shiri R. Diabetes as a risk factor for carpal tunnel syndrome: a systematic review and meta-analysis. Diabet Med. 2016;33:10–16. 5. Shiri R. Hypothyroidism and carpal tunnel syndrome: a meta-analysis. Muscle Nerve. 2014;50:879–883. 6. American Academy of Orthopaedic Surgeons. Management of carpal tunnel syndrome. Evidence-based clinical practice guideline. www.aaos. org/ctsguideline. Published February 29, 2016. 7. Shiri R, Pourmemari MH, Falah-Hassani K, et al. The effect of excess body mass on the risk of carpal tunnel syndrome: a meta-analysis of 58 studies. Obes Rev. 2015;16:1094–1104. 8. Mediouni Z, de Roquemaurel A, Dumontier C, et al. Is carpal tunnel syndrome related to computer exposure at work? A review and metaanalysis. J Occup Environ Med. 2014;56:204–208. 9. Shiri R, Falah-Hassani KJ. Computer use and carpal tunnel syndrome: a meta-analysis. Neurol Sci. 2015;349:15–19.

196

PART 1  MSK Disorders

10. Chell J, Stevens A, Davis TR. Work practices and histopathological changes in the tenosynovium and flexor retinaculum in carpal tunnel syndrome in women. J Bone Joint Surg Am. 1999;81:868–870. 11. Martin S. Carpal tunnel syndrome: a job-related risk. Am Pharm. 1991;31:21–24. 12. Nathan PA, Meadows KD, Doyle LS. Occupation as a risk factor for impaired sensory conduction of the median nerve at the carpal tunnel. J Hand Surg Br. 1988;13:167–170. 13. Pelmear PL, Taylor W. Carpal tunnel syndrome and hand-arm vibration syndrome. A diagnostic enigma. Arch Neurol. 1994;51:416–420. 14. Ibrahim I, Khan WS, Goddard N, Smitham P. Carpal tunnel syndrome: a review of the recent literature. Open Orthop J. 2012;6:69–76. 15. Stevens JC, Smith BE, Weaver AL, et al. Symptoms of 100 patients with electromyographically verified carpal tunnel syndrome. Muscle Nerve. 1999;22:1448–1456. 16. Pryse-Phillips WE. Validation of a diagnostic sign in carpal tunnel syndrome. J Neurol Neurosurg Psychiatry. 1984;47:870–872. 17. MacDermid JC, Wessel J. Clinical diagnosis of carpal tunnel syndrome: a systematic review. J Hand Ther. 2004;17:309–319. 18. Cartwright MS, Hobson-Webb LD, Boon AJ, et al. Evidence-based guideline: neuromuscular ultrasound for the diagnosis of carpal tunnel syndrome. Muscle Nerve. 2012;46:287–293. 19. Fowler JR, Hirsch D, Kruse K. The reliability of ultrasound measurements of the median nerve at the carpal tunnel inlet. J Hand Surg Am. 2015;40(10):1992–1995. 20. Descatha A, Huard L, Aubert F, et al. Meta-analysis on the performance of sonography for the diagnosis of carpal tunnel syndrome. Semin Arthritis Rheum. 2012;41:914–922. 21. Phalen GS. The carpal tunnel syndrome—clinical evaluation of 598 hands. Clin Orthop. 1972;83:29–40. 22. Huisstede BM, Hoogvliet P, Randsdorp MS, et al. Carpal tunnel syndrome. Part I: effectiveness of nonsurgical treatments—a systemic review. Arch Phys Med Rehabil. 2010;91:981–1004. 23. Walker WC, Metzler M, Cifu DX, et al. Neutral wrist splinting in carpal tunnel syndrome: a comparison of night-only versus full-time wear instruction. Arch Phys Med Rehabil. 2000;81:424–429. 24. Keith MW, Masear V, Chung KC, et al. American Academy of Orthopaedic Surgeons. American Academy of Orthopaedic Surgeons clinical practice guideline on the treatment of carpal tunnel syndrome. J Bone Joint Surg Am. 2010;92:218–219. 25. Herskovitz S, Berger AR. Low-dose, short-term oral prednisone in the treatment of carpal tunnel syndrome. Neurology. 1995;45:1923–1925. 26. Wong SM, Hui AC, Tang A. Local vs systemic corticosteroids in the treatment of carpal tunnel syndrome. Neurology. 2001;56:1565–1567. 27. Nathan PA, Keniston RC. Carpal tunnel syndrome and its relation to general physical condition. Hand Clin. 1993;9:253–261. 28. Hayes EP, Carney K, Wolf J, et al. Carpal tunnel syndrome. In: Hunter JM, Mackin EJ, Callahan AD, eds. Rehabilitation of the hand and upper extremity. 5th ed. St. Louis: Mosby; 2002:643. 29. Acharya AD, Auchincloss JM. Return to functional hand use and work following open carpal tunnel surgery. J Hand Surg Br. 2005;30:607–610.

30. Frederick HA, Carter PR, Littler T. Injection injuries to the median and ulnar nerves at the wrist. J Hand Surg Am. 1992;17:645–647. 31. Kay NR, Marshall PD. A safe, reliable method of carpal tunnel injection. J Hand Surg Am. 1992;17:1160–1161. 32. Racasan O, Dubert T. The safest location for steroid injection in the treatment of carpal tunnel syndrome. J Hand Surg Br. 2005;30:412–414. 33. Hui AC, Wong S, Leung CH, et al. A randomized controlled trial of surgery vs steroid injection for carpal tunnel syndrome. Neurology. 2005;64:2074–2078. 34. Chavez-Chiang NR, Delea SL, Sibbitt WL Jr, et al. Outcomes and costeffectiveness of carpal tunnel injections using sonographic needle guidance. Arthritis Rheum. 2010;62:S677, 1626. 35. Lee JY, Park Y, Park KD, et al. Effectiveness of ultrasound-guided carpal tunnel injection using in-plane ulnar approach: a prospective, randomized, single-blinded study. Medicine (Baltimore). 2014;93(29):e350. 36. Ustün N1, Tok F, Yagz AE, et al. Ultrasound-guided vs. blind steroid injections in carpal tunnel syndrome: a single-blind randomized prospective study. Am J Phys Med Rehabil. 2013;92(11):999–1004. 37. Goldberg G, Wollstein R, Chimes GP. Carpal tunnel injection: with or without ultrasound guidance? PM R. 2011;3:976–981. 38. Bekhet AH, Ragab B, Abushouk AI, et al. Efficacy of low-level laser therapy in carpal tunnel syndrome management: a systematic review and meta-analysis. Lasers Med Sci. 2017. https://doi.org/10.1007/ s10103-017-2234-6. 39. Shrivastava N, Szabo RM. Decision making in upper extremity entrapment neuropathies. J Musculoskelet Med. 2008;25:278–289. 40. Andreu JL, Ly-Pen D, Millan I, et al. Local injection versus surgery in carpal tunnel syndrome: neurophysiologic outcomes of a randomized clinical trial. Clin Neurophysiol. 2014;125:1479–1484. 41. Leinberry CF, Rivlin M, Maltenfort M, et al. Treatment of carpal tunnel syndrome by members of the American Society for Surgery of the Hand: a 25-year perspective. J Hand Surg Am. 2012;37:1997–2003. 42. Mintalucci DJ, Leinberry CF Jr. Open versus endoscopic carpal tunnel release. Orthop Clin North Am. 2012;43:431–437. 43. Atroshi I, Hofer M, Larsson GU, et al. Extended follow-up of a randomized clinical trial of open vs endoscopic release surgery for carpal tunnel syndrome. JAMA. 2015;314:1399–1401. 44. Sayegh ET, Strauch RJ. Open versus endoscopic carpal tunnel release: a meta-analysis of randomized controlled trials. Clin Orthop Relat Res. 2015;473:1120–1132. 45. Vasiliadis HS, Georgoulas P, Shrier I, et al. Endoscopic release for carpal tunnel syndrome. Cochrane Database Syst Rev. 2014;1:CD008265. 46. Chen L, Duan X, Huang X, et al. Effectiveness and safety of endoscopic versus open carpal tunnel decompression. Arch Orthop Trauma Surg. 2014;134:585–593. 47. Stancic MF, Micovic V, Potocnjak M. The anatomy of the Berrettini branch: implications for carpal tunnel release. J Neurosurg. 1999;91:1027–1030.

CHAPTER 37

Trigger Finger Michael C. Wainberg, MD, MSc Keith A. Bengtson, MD Julie K. Silver, MD

Synonyms Stenosing tenosynovitis Digital flexor tenosynovitis Locked finger

ICD-10 Code M65.30 Trigger finger, unspecified finger

Definition Trigger finger is the snapping, triggering, or locking of the finger as it is flexed and extended. Thickening and disproportionate narrowing of the retinacular sheath relative to its flexor tendons occur due to hypertrophy and fibrocartilaginous metaplasia at the tendon-pulley interface.1 While known as stenosing tenosynovitis, tenovaginitis is a more accurate term as the histopathologic changes localize to the retinacular sheath and peritendinous tissue rather than the tenosynovium. Normal tendon glide is most prominently affected at the A1 pulley where there is greater angulation of the tendon as it enters the pulley system. Trigger finger is thought to arise from high pressures at the proximal edge of the A1 pulley, the most common site of triggering, at the level of the metacarpal head (Fig. 37.1).2 The thumb (33%) and the ring finger (27%) are most commonly affected in adults, but 90% of pediatric trigger fingers involve the thumbs, 25% of which are bilateral.2 Pediatric trigger thumb occurs more frequently as a result of focal enlargement of the flexor pollicis longus, but no definite ultrasound abnormality of the A1 pulley has been noted.3 Primary idiopathic trigger finger is more common while secondary trigger finger is associated with diabetes mellitus, rheumatoid arthritis, hypothyroidism, histiocytosis, amyloidosis, and gout.2 Incidence is generally thought to be 2% in the general population, more common in women and in patients with diabetes (7%) and rheumatoid arthritis.4–6 The relationship of trigger finger to repetitive trauma has been cited in the literature; however, the exact mechanism of this correlation is still open to debate.5,7 Rarely, it is due to acute trauma or space-occupying lesions.8,9 

Symptoms Patients may initially note clicking or catching in the finger with some limitation in range of motion, or locking of the digit in flexion that is overcome with forceful voluntary effort or passive assistance. As the stenosis increases, complaints of pain typically develop in the proximal interphalangeal (PIP) joint of the finger, rather than in the true anatomic location of the problem—about the metacarpophalangeal (MCP) joint. Some individuals may report swelling or stiffness in the fingers, particularly in the morning. Involvement of multiple fingers can be seen in patients with rheumatoid arthritis or diabetes.4,5 In one study, patients complained of pain with motion with trigger thumb whereas with trigger finger, they complained primarily of triggering and loss of range of motion.10 

Physical Examination The essential element in the physical examination is the localization of the disorder at the level of the MCP joint. There is palpable tenderness and sometimes a tender nodule or crepitus over the volar aspect of the metacarpal head. Swelling of the finger may also be noted. Opening and closing of the hand actively produces a painful clicking as the inflamed tendon passes through a constricted sheath. With chronic triggering, the patient may have interphalangeal joint flexion contractures.11 In the absence of comorbidities such as carpal tunnel syndrome or diabetic neuropathy, neurologic examination should be normal except in severe cases associated with disuse weakness or atrophy. Trigger finger has been graded as mild crepitus in a non-triggering digit (type 0), uneven movement in a nontriggering digit (type I), actively correctable triggering (type II), passively correctable triggering (type III), and fixed deformity (type IV).12 

Functional Limitations Functional limitations include difficulty with grasping and fine manipulation of objects due to pain, locking, or both. Fine motor problems may include difficulty with inserting a key into a lock, typing, or buttoning a shirt. Gross motor skills may include limitation in gripping a steering wheel or in grasping tools at home or at work. Joint contracture at the 197

198

PART 1  MSK Disorders

Nodule Tendon sheath

Tendon sheath

Nodules

FIG. 37.1  The flexor tendon nodule catches under the annular ligament and produces the snapping or triggering sensation.

MCP joint as well as the proximal and distal interphalangeal joints are noted in the triggering digit.11 Patients note lower perceived quality of life and activity level, with reduced hand strength and dexterity.13 

Diagnostic Studies This is a clinical diagnosis. Patients without a history of injury or inflammatory arthritis do not need routine radiographs.14 Magnetic resonance imaging can confirm tenosynovitis of the flexor sheath, but this offers minimal advantage over clinical diagnosis.15 Alternatively, a diagnostic ultrasound examination can show tendon nodules, tenosynovitis, and active triggering at the level of the A1 pulley. 

Differential Diagnosis • Dupuytren disease • Ganglion of the tendon sheath (retinacular cyst) • Tumor of the tendon sheath (giant cell tumor or spaceoccupying lesion, such as an amyloidosis) • Rheumatoid arthritis or other diagnoses associated with secondary trigger finger

Treatment Initial The goal of treatment is to restore the normal gliding of the tendon through the pulley system. This can often be achieved with conservative treatment. Initial noninvasive care includes activity modification, adaptive equipment, anti-inflammatories and splinting. When clinically appropriate, nonsteroidal anti-inflammatory drugs can be administered orally or transdermally.16,17 Progression to a local steroid injection is often based on the severity of the patient’s symptoms (more severe symptoms generally respond better to injections), required or target activity level (e.g., someone who needs to return to work as quickly as possible), and the preference of the patient and clinician. Many types of splints are advocated including MCP joint at 0 degrees18 or at 10 to 15 degrees of flexion with the PIP and distal interphalangeal joints free, for up to 6 weeks continuously.16 Alternatively, the DIP may be immobilized with MCP, PIP, or DIP splinting providing lasting clinical success in up to 87% of patients, although less so in the thumbs.19–21 Splinting can decrease loss of time from work.20 A novel splint with NSAID microneedle delivery has been developed.17 Padded gloves provides protection and can decrease inflammation by avoiding direct trauma. 

CHAPTER 37  Trigger Finger

199

FIG. 37.2  Under sterile conditions with use of a 27-gauge, 5/8-inch needle, a 2- to 3-mL aliquot of a local anesthetic and steroid mixture (e.g., 1 mL of 1% lidocaine mixed with 1 mL [40 mg] of methylprednisolone) is injected into the palm at the level of the distal palmar crease, which directly overlies the tendon. Before cleaning of the area to be injected, palpate for the nodule to localize exactly where the injection should be placed.

Rehabilitation Rehabilitation may include treatment with an occupational or physical therapist experienced in the treatment of hand problems.18 Supervised therapy may be useful in the following scenarios: when a patient has lost significant strength, range of motion, or function from not using the hand or from prolonged splinting; when modalities such as ultrasound and iontophoresis are recommended to reduce inflammation; and when a customized splint is deemed to be necessary. Therapy should focus on increasing function and decreasing inflammation and pain. This can be done by techniques such as ice massage, contrast baths, paraffin, ultrasound, and iontophoresis with local steroid use. A custom splint may fit better and permit better function at work than a prefabricated splint.22 Range of motion, strength, and function can be improved through supervised therapy before surgery and postoperatively.11 

Procedures When symptoms persist or are more functionally limiting, a local corticosteroid injection combined with local anesthetic (Fig. 37.2) is indicated.16,23 Post-procedure care frequently includes splinting and relative protection for 1 week. Single injection to the A1 pulley has demonstrated symptom resolution in 54% to 73% of patients at 1 year24,25 along with decrease in pulley thickness and tendon thickness.26 Repeat injection is safe and effective with incremental benefit,27 though longer duration symptoms required greater number of injections.28 Corticosteroid injection is less effective with involvement of multiple digits or when the condition has persisted longer than 4 months.29 Diminishing response to injection is suggested to be due to the inability of corticosteroids to reverse the established fibrocartilaginous metaplasia.16

Sonography is helpful for localization and in the presence of anatomic variants, though recent studies did not observe superior clinical benefits with ultrasound-guided injections.30 Betamethasone sodium phosphate is frequently recommended (water soluble, lower risk of tenosynovitis and fat necrosis) along with studies employing triamcinolone and methylprednisolone; however, clinical superiority of one corticosteroid preparation over another is unclear.16,27,31 In addition to corticosteroids, studies of intrasheath hyaluronic acid32 and diclofenac33 have demonstrated clinical benefit. 

Technology New custom microneedle splints fabricated using 3-D printing for drug delivery and splinting have been recently reported,17 awaiting clinical studies to assess clinical efficacy. 

Surgery In adults, steroid injections should be tried for most trigger finger cases before surgery is considered. However, surgical intervention is highly successful for conservative treatment failures and should be considered for patients desiring quick and definitive relief16,34 from this disorder. Individuals with diabetes, rheumatoid arthritis, multiple joint involvement, and younger age at onset are more likely to require surgery.4,35 There are two general types of surgery for this condition: the standard open operative release of the A1 pulley and the percutaneous A1 pulley release procedure. A recent metaanalysis notes improving success rates of percutaneous trigger finger release to 94% and suggests better outcomes with ultrasound guidance.36 Both surgical procedures are generally effective and carry a relatively low risk of complications.11,34

200

PART 1  MSK Disorders

From a cost-of-care perspective, an algorithm of noninvasive care, up to two corticosteroid injections, and subsequent surgical intervention is recommended.37 

Potential Disease Complications Disease-related complications are rare and could include permanent loss of range of motion from development of a contracture in the affected finger, most commonly at the PIP joint.11 More rarely, chronic intractable pain may develop despite treatment. 

Potential Treatment Complications Treatment-related complications from nonsteroidal antiinflammatory drugs are well known and include gastric, renal, and hepatic side effects. Complications from local corticosteroid injections include skin depigmentation, dermatitis, subcutaneous fat atrophy, digit necrosis, tendon rupture, digital sensory nerve injury, and infection.31,38 Possible surgical complications include infection, nerve injury, and flexor tendon bowstringing.39,40

References 1. Spirig A, Juon B, Banz Y, Rieben R, Vogelin E. Correlation between sonographic and in vivo measurement of A1 pulleys in trigger fingers. Ultrasound Med Biol. 2016;42:1482–1490. 2. Akhtar S, Bradley MJ, Quinton DN, Burke FD. Management and referral for trigger finger/thumb. BMJ. 2005;331:30–33. 3. Verma M, Craig CL, DiPietro MA, et al. Serial ultrasound evaluation of pediatric trigger thumb. J Pediatr Orthop. 2013;33:309–313. 4. Stahl S, Kanter Y, Karnielli E. Outcome of trigger finger treatment in diabetes. J Diabetes Complications. 1997;11:287–290. 5. Gray RG, Gottlieb NL. Hand flexor tenosynovitis in rheumatoid arthritis. Prevalence, distribution, and associated rheumatic features. Arthritis Rheum. 1977;20:1003–1008. 6. Schubert C, Hui-Chou HG, See AP, Deune EG. Corticosteroid injection therapy for trigger finger or thumb: a retrospective review of 577 digits. Hand. 2013;8:439–444. 7. Moore SJ. Flexor tendon entrapment of the digits (trigger finger and trigger thumb). J Occup Environ Med. 2000;42:526–545. 8. Schwaiger K, Ensat F, Neureiter D, Wechselberger G, Hladik M. Trigger finger caused by extraskeletal chondroma. Hand Surg. 2017;42:e51–e55. 9. Fujiwara M. A case of trigger finger following partial laceration of flexor digitorum superficialis and review of the literature. Arch Orthop Trauma Surg. 2005;125:430–432. 10. Moriya K, Uchiyama T, Kawaji Y. Comparison of the surgical outcomes for trigger finger and trigger thumb: preliminary results. Hand Surg. 2005;10:83–86. 11. Lu SC, Kuo LC, Hsu HY, Jou IM, Sun YN, Su FC. Finger movement function after ultrasound-guided percutaneous pulley release for trigger finger: effect of postoperative rehabilitation. Arch Phys Med Rehabil. 2015;96:91–97. 12. Quinnell RC. Conservative management of trigger finger. Practitioner. 1980;224:187–190. 13. Langer D, Maeir A, Michailevich M, Applebaum Y, Luria S. Using international classification of functioning to examine the impact of trigger finger. Disabil Rehabil. 2016;38:2530–2537. 14. Katzman BM, Steinberg DR, Bozentka DJ, et al. Utility of obtaining radiographs in patients with trigger finger. Am J Orthop. 1999;28:703–705. 15. Gottlieb NL. Digital flexor tenosynovitis: diagnosis and clinical significance. J Rheumatol. 1991;18:954–955.

16. Ryzewicz M, Wolf JM. Trigger digits: principles, management, and complications. J Hand Surg Am. 2006;31:135–146. 17. Lim SH, Ng JY, Kang L. Three-dimensional printing of a microneedle array on personalized curved surfaces for dual-pronged treatment of trigger finger. Biofabrication. 2017;9:015010. 18. Huisstede BMA, Hoogvliet P, Coert JH, Fride´n J for the European HANDGUIDE Group. Multidisciplinary consensus guideline for managing trigger finger: results from the European HANDGUIDE study. Phys Ther. 2014;94:1421–1433. 19. Patel MR, Bassini L. Trigger fingers and thumb: when to splint, inject, or operate. J Hand Surg Am. 1992;17:110–113. 20. Rodgers JA, McCarthy JA, Tiedeman JJ. Functional distal interphalangeal joint splinting for trigger finger in laborers: a review and cadaver investigation. Orthopedics. 1998;21:305–309, discussion 309–310. 21. Valdes K. A retrospective review to determine the long-term efficacy of orthotic devices for trigger finger. J Hand Ther. 2012;25:89–95, quiz 96. 22. Colbourn J, Heath N, Manary S, Pacifico D. Effectiveness of splinting for the treatment of trigger finger. J Hand Ther. 2008;21:336–343. 23. Benson LS, Ptaszek AJ. Injection versus surgery in the treatment of trigger finger. J Hand Surg Am. 1997;22:138–144. 24. Peters-Veluthamaningal C, Winters JC, Groenier KH, Jong BM. Corticosteroid injections effective for trigger finger in adults in general practice: a double-blinded randomised placebo controlled trial. Ann Rheum Dis. 2008;67:1262–1266. 25. Castellanos J, Munoz-Mahamud E, Dominguez E, Del Amo P, Izquierdo O, Fillat P. Long-term effectiveness of corticosteroid injections for trigger finger and thumb. J Hand Surg Am. 2015;40:121–126. 26. Shinomiya R, Sunagawa T, Nakashima Y, Yoshizuka M, Adachi N. Impact of corticosteroid injection site on the treatment success rate of trigger finger: a prospective study comparing ultrasound-guided true intra-sheath and true extra-sheath injections. Ultrasound Med Biol. 2016;42:2203–2208. 27. Dardas AZ, VandenBerg J, Shen T, Gelberman RH, Calfee RP. Longterm effectiveness of repeat corticosteroid injections for trigger finger. J Hand Surg Am. 2017;42:227–235. 28. Golas AR, Marcus LR, Reiffel RS. Management of stenosing flexor tenosynovitis: maximizing nonoperative success without increasing morbidity. Plast Reconstr Surg. 2016;137:557–562. 29. Newport ML, Lane LB, Stuchin SA. Treatment of trigger finger by steroid injection. J Hand Surg Am. 1990;15:748–750. 30. Cecen GS, Gulabi D, Saglam F, Tanju NU, Bekler HI. Corticosteroid injection for trigger finger: blinded or ultrasound-guided injection? Arch Orthop Trauma Surg. 2015;135:125–131. 31. Sawaizumi T, Nanno M, Ito H. Intrasheath triamcinolone injection for the treatment of trigger digits in adult. Hand Surg. 2005;10:37–42. 32. Liu DH, Tsai MW, Lin SH, et al. Ultrasound-guided hyaluronic acid injections for trigger finger: a double-blinded, randomized controlled trial. Arch Phys Med Rehabil. 2015;96:2120–2127. 33. Shakeel H, Ahmad S. Steroid injection versus NSAID injection for trigger finger: a comparative study of early outcomes. J Hand Surg. 2012;37A:1319–1323. 34. Turowski GA, Zdankiewicz PD, Thomson JG. The results of surgical treatment of trigger finger. J Hand Surg Am. 1997;22:145–149. 35. Rozental TD, Zurakowski D, Blazar PE. Trigger finger: prognostic indicators of recurrence following corticosteroid injection. J Bone Joint Surg Am. 2008;90:1665–1672. 36. Zhao JG, Kan SL, Zhao L, et al. Percutaneous first annular pulley release for trigger digits: a systematic review and meta-analysis of current evidence. J Hand Surg Am. 2014;39:2192–2202. 37. Kerrigan CL, Stanwix MG. Using evidence to minimize the cost of trigger finger care. J Hand Surg. 2009;34A:997–1005. 38. Fitzgerald BT, Hofmeister EP, Fan RA, Thompson MA. Delayed flexor digitorum superficialis and profundus ruptures in a trigger finger after a steroid injection: a case report. J Hand Surg Am. 2005;30:479–482. 39. Thorpe AP. Results of surgery for trigger finger. J Hand Surg Br. 1988;13:199–201. 40. Heithoff SJ, Millender LH, Helman J. Bowstringing as a complication of trigger finger release. J Hand Surg Am. 1988;13:567–570.

CHAPTER 38

Ulnar Collateral Ligament Sprain Sheila A. Dugan, MD Sol M. Abreu Sosa, MD

Synonyms Skier’s thumb Ulnar collateral ligament tear or rupture Gamekeeper’s thumb Break-dancer’s thumb Stener lesion1 (ruptured, displaced ulnar collateral ligament with interposed adductor aponeurosis)

ICD-10 Codes S63.90 S63.91 S63.92

Sprain of unspecified part of unspecified wrist and hand Sprain of unspecified part of right wrist and hand Sprain of unspecified part of left wrist and hand

Definition The ulnar collateral ligament (UCL) complex includes the ulnar proper collateral ligament and the ulnar accessory collateral ligament.1 These ligaments are located deep to the adductor aponeurosis of the thumb and stabilize the first metacarpophalangeal (MCP) joint. Tears can occur if a valgus force is applied to an abducted first MCP joint.2 A lesion of the UCL is commonly called skier’s thumb. Acute injuries can occur when the strap on a ski pole forcibly abducts the thumb. In the United States, estimates for skiing injuries are three or four per 1000 skier-hours; thumb injuries account for about 10% of skiing injuries.3 A study of downhill skiing found that thumb injuries accounted for 17% of skiing injuries, second only to knee injuries.4 Three fourths of the thumb injuries were UCL sprains. UCL injury in football players may be related to falls or blocking. Other sports involving ball handling or equipment with repetitive abduction forces to the thumb, like basketball or lacrosse, can cause injury to the UCL. UCL injuries may be accompanied by avulsion fractures. Complete tears can fold back proximally when they are ruptured distally and become interposed between the adductor

aponeurosis.1 This injury is known as the Stener lesion and has been described as a complication of complete UCL tears, with a frequency ranging from 33% to 80%.5 Chronic ligamentous laxity is more common in occupational conditions associated with repetitive stresses to the thumb. The term gamekeeper’s thumb was coined in the mid-1950s to describe an occupational injury of Scottish gamekeepers.6 The term is also used for acute injuries to the UCL. Rupture of the thumb MCP joint UCL represents one of the most common ligamentous injuries of the hand. Failure to recognize the injuries or to treat them appropriately can lead to instability, pain, and weakness of the joint.7 

Symptoms Patients report pain and instability of the thumb joint. In the acute injury setting, patients can often recall the instant of injury. If the UCL is ruptured, patients report swelling and hematoma formation; pain may be minimal with complete tears. When pain is present, it can cause thumb weakness and reduced function. Numbness and paresthesias are not typical findings. 

Physical Examination The physical examination begins with the uninvolved thumb, noting the individual’s normal range of motion and stability. Palpate to determine the point of maximal tenderness, assessing for distal tenderness; if the ligament is torn, it tears distally off the proximal phalanx. Initially, the examiner may be able to detect a knot at the site of ligament disruption. Laxity of the UCL is the key finding on examination. Ligament injuries are graded as follows: grade I sprains, local injury without loss of integrity; grade II sprains, local injury with partial loss of integrity, but end-feel is present; and grade III sprains, complete tear with loss of integrity and end-feel (Fig. 38.1). Passive abduction can be painful, especially in acute grade I and grade II sprains. The UCL should be tested with the first MCP joint in extension and flexion to evaluate all bands. The excursion is compared with the uninjured side. Testing for disruption of the ulnar proper collateral ligament is done with the thumb flexed to 90 degrees.1 With the thumb in 201

202

PART 1  MSK Disorders

contraindicated in the acute stage of injury or on the basis of the extent of injury. In the setting of high-level or professional sports competition, the clinical decision to allow an athlete to compete with appropriate splinting or casting is based on severity of symptoms, with the caveat that the potential for worsening of the injury exists. 

Diagnostic Studies

FIG. 38.1  Skier’s thumb. The ulnar collateral ligament to the metacarpophalangeal joint is disrupted by an abduction force. (Reprinted with permission from Mellion MB. Office Sports Medicine. 2nd ed. Philadelphia: Hanley & Belfus; 1996:228.)

extension, a false-negative finding may result. The stability of the joint will not be impaired even if the ulnar proper collateral ligament is torn because of the taut ulnar accessory ligament in extension. To avoid a false interpretation, the examiner must prevent MCP rotation by grasping the thumb proximal to the joint. If there is more than 30 degrees of laxity (or 15 degrees more laxity than on the non-injured side), rupture of the proper collateral ligament is likely. The thumb is then positioned in extension for repeat valgus stress testing. If valgus laxity is less than 30 degrees (or 15 degrees less than on the non-injured side), the accessory collateral ligament is intact. If valgus laxity is greater than 30 degrees (or 15 degrees more than on the non-injured side), the accessory collateral ligament is also ruptured.7 A displaced fracture is a contraindication to stress testing. The fracture presents with swelling or discoloration on the ulnar side of the first MCP joint and tenderness along the base of the proximal phalanx. Some authors recommend that conventional radiographs be obtained before stressing of the UCL to determine whether a large undisplaced fracture is present because stress testing could cause displacement.8 More than 3 mm of volar subluxation of the proximal phalanx indicates gross instability. The patient may be unable to pinch. Pain may limit the complete examination and lead to underestimation of injury extent. Infiltration of local anesthetic around the injury site can reduce discomfort and improve the accuracy of the examination.9 Avulsion fracture represents a special class of collateral ligament injury. It cannot be graded I to III because technically the ligament is not torn. However, it still deserves mention because fracture can compromise the bone ligament stabilization complex and lead to chronic symptoms. 

Functional Limitations Individuals describe difficulty with pinching activities (e.g., turning a key in a lock). Injuries affecting the dominant hand can have an impact on many fine motor manipulations, such as buttoning or retrieving objects from one’s pocket. Injuries affecting the nondominant hand can impair bilateral hand activities requiring stabilization of small objects. Sports performance can be reduced with dominant hand injuries, and skiing, ball handling, or equipment use may be

Whereas clinical examination is the mainstay of diagnosis, imaging studies are useful in the setting of uncertain diagnosis.10 A plain radiograph is essential to rule out an avulsion fracture of the base of the ulnar side of the proximal phalanx. A stress film with the thumb in abduction is occasionally useful and should be compared with the uninjured side. UCL rupture presents with an angle greater than 35 degrees. Magnetic resonance imaging has greater than 90% sensitivity and specificity for UCL tears but is expensive and not always required.11 Ultrasonography has been used as a less expensive means of diagnosing UCL tears, but controversy exists as to whether it is useful or fraught with pitfalls.10,12–14 However, a retrospective review of ultrasound study from 17 surgically proven displaced full-thickness UCL tears identified the following ultrasound criteria for 100% accuracy in the diagnosis of displaced full thickness UCL tear: lack of UCL fibers and presence of a heterogeneous mass like abnormality proximal to the MCP joint of the thumb. Such displaced UCL tears were most often located proximal to the leading edge of the adductor aponeurosis rather than superficially.15,16 Standardized ultrasound technique, which includes dynamic imaging, should be a consideration when the ultrasound examination is performed for this diagnosis.15 Review of the literature on US examination of UCL tears shows an overall sensitivity of 76%, specificity of 81% accuracy, positive predictive value of 74% and a negative predictive value of 87%.16 Ultrasound may be more cost effective if an experienced musculoskeletal ultrasonographer is available to perform the examination; if not, MRI should be obtained.17  Differential Diagnosis Radial collateral ligament sprain or rupture First MCP joint dislocation with or without volar plate injury Thumb fracture-dislocation (Bennett fracture)

Treatment Initial Pain and edema are managed with ice, nonsteroidal antiinflammatory drugs, and rest. Initial treatment of a firstdegree (grade I) UCL sprain is taping for activity. Initial treatment of an incomplete (grade II) UCL sprain involves immobilization in a thumb spica cast for 3 to 6 weeks with the thumb slightly abducted. Injuries involving nondisplaced or small avulsion fractures associated with an incomplete UCL tear can also be managed nonsurgically and may require a longer course of immobilization. The cast may be extended to include the wrist for greater stability.18 An alpine splint allows

CHAPTER 38  Ulnar Collateral Ligament Sprain

203

interphalangeal flexion while prohibiting abduction and extension of the first MCP joint.19 A study of 63 cases of nonoperative and postsurgical patients compared short arm plaster cast immobilization with functional splinting that prevented ulnar and radial deviation of the thumb; there was no difference between the two groups in regard to stability, thumb range of motion or strength, and length of sick leave after an average follow-up of 15 months.20 Even slightly displaced avulsion fractures without complete UCL rupture tended to do well with immobilization in a study of 30 patients; those with larger bone fragments and larger initial rotation of the fragment were more likely to have residual symptoms.21 Grade III injuries require surgical repair unless surgery is contraindicated for other reasons. Prompt referral for surgical consultation is recommended to maximize ligament positioning for reattachment. Failure to refer promptly or misdiagnosis of a complete tear can result in a less favorable outcome, including a Stener lesion.5 

Rehabilitation Physical or occupational therapy is important in the rehabilitation management of UCL sprains. Therapists who have completed special training and are certified hand therapists (often called CHTs) can be great resources. Range of motion of the unaffected joints of the arm, especially the interphalangeal joint of the thumb, must be maintained. Grade I and grade II are appropriate for nonoperative treatment like rehabilitation because they are considered stable injuries.16 In the setting of a grade I sprain, after a short course of relative rest and taping, therapy may be required to restore strength to the pre-injury level. In grade II sprains, a volar splint replaces the cast after 3 to 6 weeks. Splints may be custom molded by the therapist. They can be removed for daily active range of motion exercises. Passive range of motion and isometric strength training are initiated once pain at rest has resolved, and the patient is progressed to concentric exercise after about 8 weeks for nonsurgical lesions and 10 to 12 weeks for postsurgical lesions. Prophylactic taping is appropriate for transitioning back to sports-specific activity (Fig. 38.2). Postsurgical rehabilitation is less aggressive with avoidance of strengthening, especially a power pinch, for 8 weeks postoperatively.22 Protected early postoperative range of motion is indicated.23 Full activity after grade II tears with or without nondisplaced avulsion fractures begins at 10 to 12 weeks compared with 12 to 16 weeks for surgically repaired injuries.24 

Procedures There are no specific nonsurgical procedures performed for this injury. 

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery Early direct repair is required in the setting of a ruptured UCL (grade III) injury. Grade II and grade III injuries resulting in severe instability, displaced fractures, or intra-articular

FIG. 38.2  Taping technique to protect the ulnar collateral ligament.

fragments are also surgical candidates. Surgery is indicated in the setting of gross instability.25 Surgery is also indicated if the thumb is unstable in extension (more than 30 degrees of laxity or 15 or more degrees of laxity than on the noninjured side), which indicates a complete rupture is present and ligament displacement is likely.8 Acute, complete ruptures of the UCL ligament less than 3 to 6 weeks old are generally treated with repair of the anatomic ligament. If the native tissue is lacking either length or quality, reconstruction should be necessary just as it happens with chronic tear, including bone-retinaculum-bone reconstruction.26 A cadaveric study where a model of thumb UCL fracture avulsion was created demonstrated that hook plate construct or approach was superior to suture anchor construct for fixation of thumb MCP joint UCL fracture-avulsion with regard to load to failure.27 Tension wiring is used to fixate avulsions; open reduction may be required for large displaced avulsion defects. Surgical approaches that improve stability are the focus of new techniques.28,29 Surgical repair is considered the gold standard of treatment, but postoperative immobilization causes partial stiffness. A randomized prospective study carried out in 30 consecutive patients treated with surgery compared a regular spica splint to a modified spica splint post operation. The researchers concluded that surgical repair combined with the new functional splint was effective, safe, and well tolerated.30 However, postoperative immobilization is being reconsidered. A cadaver study concluded that a controlled active motion therapy protocol after suture anchor repair of a ruptured UCL is safe from a biomechanical point of view.31 The techniques for reconstruction of chronic UCL injuries involve either dynamic or static procedures. Dynamic procedures use musculotendinous units to stabilize the MCP joint by pulling the proximal phalanx ulnarward. Static procedures use free tendon grafts through bone tunnels or pull-out sutures to reconstruct the proper and

204

PART 1  MSK Disorders

accessory collateral ligaments. Static procedures have gained in popularity, as they allow for ligament reconstruction and preservation of existing thumb function, whereas dynamic procedures require the removal of existing muscle units and do not restore the anatomy of the UCL.31 

Potential Disease Complications Disease complications include chronic laxity with associated functional limitations, pain, and inability to pinch; premature arthritis and persistent pain in the first MCP joint; and decreased range of motion of the thumb. 

Potential Treatment Complications Analgesics and nonsteroidal anti-inflammatory drugs have well-known side effects that most commonly affect the gastric, renal, and hepatic systems. Prolonged splinting can lead to loss of range of motion of the joint and weakness and atrophy of the surrounding joints, depending on the extent of the injury and the length of time spent in a splint. Surgical risks include nonunion of avulsed fragments and the typical infrequent surgical complications, such as infection and bleeding. Surgery can result in persistent numbness on the ulnar aspect of the thumb. A neuropraxia secondary to injury of the radial sensory nerve from either swelling or intraoperative traction is the most common nerve injury and usually resolves spontaneously.8

References 1. Stener B. Displacement of the ruptured ulnar collateral ligament of the metacarpophalangeal joint of the thumb. A clinical and anatomical study. J Bone Joint Surg Br. 1962;44:869–879. 2. McCue FC, Hussamy OD, Gieck JH. Hand and wrist injuries. In: Zachazewski JE, Magee DJ, Quillen WS, eds. Athletic Injuries and Rehabilitation. Philadelphia: WB Saunders; 1996:589–599. 3. Schneider T. Snow skiing injuries. Aust Fam Physician. 2003;32:499–502. 4. Enqkvist O, Balkfors B, Lindsjo U. Thumb injuries in downhill skiing. Int J Sports Med. 1982;3:50–55. 5. Louis DS, Huebner JJ, Hankin FM. Rupture and displacement of the ulnar collateral ligament of the metacarpophalangeal joint of the thumb. Preoperative diagnosis. J Bone Joint Surg Am. 1986;68:1320–1326. 6. Campbell CS. Gamekeeper’s thumb. J Bone Joint Surg Br. 1955;37: 148–149. 7. Heyman P. Injuries to the ulnar collateral ligament of the thumb metacarpophalangeal joint. J Am Acad Orthop Surg. 1997;5:224–229. 8. Kibler WB, Press JM. Rehabilitation of the wrist and hand. In: Kibler WB, Herring SA, Press JM, eds. Functional rehabilitation of sports and musculoskeletal injuries. Gaithersburg: MD:Aspen; 1998:186–187. 9. Cooper JG, Johnstone AJ, Hider P, Ardagh MW. Local anaesthetic infiltration increases the accuracy of assessment of ulnar collateral ligament injuries. Emerg Med Australas. 2005;17:132–136. 10. Koslowsky TC, Mader K, Gausepohl T, et al. Ultrasonographic stress test of the metacarpophalangeal joint of the thumb. Clin Orthop Relat Res. 2004;427:115–119.

11. Plancher KD, Ho CP, Cofield SS, et al. Role of MR imaging in the management of “skier’s thumb” injuries. Magn Reson Imaging Clin North Am. 1999;7:73–84. 12. Hergan K, Mittler C, Oser W. Pitfalls in sonography of the gamekeeper’s thumb. Eur Radiol. 1997;7:65–69. 13. Susic D, Hansen BR, Hansen TB. Ultrasonography may be misleading in the diagnosis of ruptured and dislocated ulnar collateral ligaments of the thumb. Scand J Plast Reconstr Surg Hand Surg. 1999;33: 319–320. 14. Schnur DP, DeLone FX, McClellan RM, et al. Ultrasound: a powerful tool in the diagnosis of ulnar collateral ligament injuries of the thumb. Ann Plast Surg. 2002;49:19–22. 15. Melville D, Jacobson JA, Haase S, Brandon C, Brigido MK, Fessell D. Ultrasound of displaced ulnar collateral ligament tears of the thumb: the Stener lesion revisted. Skeletal Radiol. 2013;42(5):667–673. 16. Papandrea RF, Fowler T. Injury at the thumb UCL: is there a Stener lesion? J Hand Surg AM. 2008;33:1882–1884. 17. Avery DM, Caggiano NM, Matulio KS. Ulnar collateral ligament of the thumb. Orthop Clin North Am. 2015;46(2):281–292. 18. Reid DC, ed. Sports injury assessment and rehabilitation. New York: Churchill Livingstone; 1992:1089–1092. 19. Moutet F, Guinard D, Corcella D. Ligament injuries of the first metacarpophalangeal joint. In: Bruser P, Gilbert A, eds. Finger bone and joint injuries. London: Martin Dunitz; 1999:207–211. 20. Kuz JE, Husband JB, Tokar N, McPherson SA. Outcome of avulsion fractures of the ulnar base of the proximal phalanx of the thumb treated nonsurgically. J Hand Surg Am. 1999;24:275–282. 21. Sollerman C, Abrahamsson SO, Lundborg G, Adalbert K. Functional splinting versus plaster cast for ruptures of the ulnar collateral ligament of the thumb. A prospective randomized study of 63 cases. Acta Orthop Scand. 1991;62:524–526. 22. Neviaser RJ. Collateral ligament injuries of the thumb metacarpophalangeal joint. In: Strickland JW, Rettig AC, eds. Hand injuries in athletes. Philadelphia: WB Saunders; 1992:95–105. 23. Firoozbakhsh K, Yi IS, Moneim MS, et al. A study of ulnar collateral ligament of the thumb metacarpophalangeal joint. Clin Orthop Relat Res. 2002;403:240–247. 24. Brown AP. Ulnar collateral ligament injury of the thumb. In: Clark GL, Wilgis EF, Aiello B, et al., eds. Hand rehabilitation: a practical guide. 2nd ed. New York: Churchill Livingstone; 1997:369–375. 25. Jackson M, McQueen MM. Gamekeeper’s thumb: a quantitative evaluation of acute surgical repair. Injury. 1994;25:21–23. 26. Shin EH, Drake ML, Parks BG, Means Jr KR. Hook plate versus suture anchor fixation for thumb ulnar collateral ligament fracture- avulsion: a cadaver study. J Hand Surg Am. 2016;41(2). Epub 2015 Dec 22. 27. Carlsen BT, Moran SL. Thumb trauma: Bennett fractures, Rolando fractures, and ulnar collateral ligament injuries. J Hand Surg Am. 2009;34(5):945–952. 28. Lee SK, Kubiak EN, Liporace FA, et al. Fixation of tendon grafts for collateral ligament reconstructions: a cadaveric biomechanical study. J Hand Surg Am. 2005;30:1051–1055. 29. Lee SK, Kubiak EN, Lawler E, et al. Thumb metacarpophalangeal ulnar collateral ligament injuries: a biomechanical simulation study of four static reconstructions. J Hand Surg Am. 2005;30:1056–1060. 30. Rocchi L, Merolli A, Morini A, Motelone G, Foti C. A modified spiccasplint in post operative early motion management of skier thumb lesion: a randomized clinical trial. Eur J Phys Rehabil Medic. 2014;50(1):49– 57. Epub 2013 Nov 4. 31. Ritting AW, Baldwin PC, Rodner CM. Ulnar collateral ligament injury of the thumb metacarpophalangeal joint. Clin J Sport Med. 2010;20(2):106–112.

CHAPTER 39

Ulnar Neuropathy (Wrist) Ramon Vallarino Jr., MD Francisco H. Santiago, MD

Synonym Guyon canal entrapment

ICD-10 Codes G56.20 G56.21 G56.22

Lesion of ulnar nerve, unspecified upper limb Lesion of ulnar nerve, right upper limb Lesion of ulnar nerve, left upper limb

Definition Entrapment neuropathy of the ulnar nerve can be encountered at the wrist in a canal formed by the pisiform and the hamate and its hook (the piso-hamate hiatus). These are connected by an aponeurosis that forms the ceiling of the Guyon canal (Fig. 39.1). This canal generally contains the ulnar nerve and the ulnar artery and vein. The following three types of lesions can be encountered.1 Type I affects the trunk of the ulnar nerve proximally in the Guyon canal and involves both the motor and sensory fibers. This is the most commonly seen lesion. Type II affects only the deep (motor) branch distally in the Guyon canal and may spare the abductor digiti quinti, depending on the location of its branching. A further classification is type IIa (still pure motor), in which all the hypothenar muscles are spared because of a lesion distal to their neurologic branching. Type III affects only the superficial branch of the ulnar nerve, which provides sensation to the volar aspect of the fourth and fifth fingers and the hypothenar eminence. There is sparing of all motor function, although the palmaris brevis is affected in some cases. This is the least common lesion encountered. This injury is commonly seen in bicycle riders and people who use a cane improperly because they place excessive weight on the proximal hypothenar area at the canal of Guyon and therefore are predisposed to distal ulnar nerve traumatic injury, especially affecting the deep ulnar motor branch (type II).2,3 The positioning of the biker’s wrist on the handlebars has been shown via magnetic resonance

imaging (MRI) to make a statistical difference in terms of the measured distance between the hook of the hamate and the superficial and deep branches of the ulnar nerve in the Guyon canal, especially with hyperextension and ulnar ­deviation.4 This information may be of use in the future in the ergonomic design of handlebars. Entrapment at the Guyon canal has also been associated with prolonged, repetitive occupational use of tools, such as pliers and screwdrivers.2 With the advancement of endoscopic carpal tunnel release during the past few years, there have been reports of both adverse and favorable consequences to the ulnar nerve at the Guyon canal, which is very close anatomically. There have been inadvertent injuries to the ulnar nerve as well as documented decompression and improvement of nerve conduction.5,6 Other rare causes have been reported in the literature. These include fracture of the hook of the hamate, ganglion cyst formation, tortuous or thrombosed ulnar artery aneurysm (hypothenar hammer syndrome), osteoarthritis or osteochondromatosis of the pisotriquetral joint, anomalous variation of abductor digiti minimi, schwannomas, aberrant fibrous band, and idiopathic.7–10 Of 250 wrists studied by 3 Tesla MRI assessment, it was noted that anatomy of the Guyon canal was normal in 168 (67.2%) wrists; 73 (29.2%) wrists presented with anatomic variations, and 9 (3.6%) wrists had derangements with clinical and radiologic features attributed to Guyon canal syndrome, making this a rare condition.11 

Symptoms Signs and symptoms can vary greatly and depend on which part of the ulnar nerve and its terminal branches are affected and where along the Guyon canal itself the compression occurs (Table 39.1). It is of great importance to be able to differentiate entrapment of the ulnar nerve at the wrist from entrapment at the elbow, which occurs far more commonly. The two clinical findings that confirm the diagnosis of Guyon canal entrapment instead of ulnar entrapment at the elbow are (1) sparing of the dorsal ulnar cutaneous sensory distribution in the hand and (2) sparing of function of the flexor carpi ulnaris and the two medial heads of the flexor digitorum profundus (Figs. 39.2 and 39.3). Otherwise, the symptoms in both conditions are generally similar and may include hand 205

PART 1 MSK Disorders

206

intrinsic muscle weakness and atrophy, numbness in the fourth and fifth fingers, hand pain, and sometimes severely decreased function. 

Physical Examination

Hook of hamate

Zone 2

Zone 3 Zone 1 Pisiform

FIG. 39.1  Distal ulnar tunnel (Guyon canal) showing the three zones of entrapment. Lesions in zone 1 give motor and sensory symptoms, lesions in zone 2 cause motor deficits, and lesions in zone 3 create sensory deficits.

Table 39.1  Volar Forearm and Hand: Ulnar Nerve Muscle

Action

Flexor carpi ulnaris

Flexes wrist, ulnarly deviates

Flexor digitorum profundus

Flexes distal interphalangeal joint (fourth and fifth)

Abductor digiti quintia

Analogous to dorsal interosseous

Flexor digiti quintia,b

Analogous to dorsal interosseous

Opponens digiti quintia,b

Flexes and supinates fifth metacarpal

Volar interosseia

Adduct fingers, weak flexion metacarpophalangeal

Dorsal interosseia,b

Abduct fingers, weak flexion metacarpophalangeal

Lumbricals (ring and fifth)a,b

Coordinate movement of fingers; extend interphalangeal joints; flex metacarpophalangeal joints

Adductor pollicisa

Adducts thumb toward index finger

Lumbricals (ring, small)a

Coordinate movement of fingers; extend interphalangeal joints; flex metacarpophalangeal joints

aHand

intrinsic muscles. mass.

bHypothenar

Careful examination of the hand and a thorough knowledge of the anatomy of motor and sensory distribution of ulnar nerve branches are required to determine the location of the lesion. Except for the five muscles innervated by the median nerve (abductor pollicis brevis, opponens pollicis, flexor pollicis brevis superficial head, and first two lumbricals), the ulnar nerve supplies every other intrinsic muscle in the hand. Classically, there is notable atrophy of the first web space due to denervation of the first dorsal interosseous muscle (Fig. 39.4). In lesions involving the motor branches where the compression is in the proximal aspect of the Guyon canal, there will be weakness and eventually atrophy of the interossei, the adductor pollicis, the fourth and fifth lumbricals, and the deep head of the flexor pollicis brevis. The palmaris brevis, abductor digiti quinti, opponens digiti quinti, and flexor digiti quinti may be involved or spared, depending on the level of the lesion. Sensory examination in all but type II, in which the compression of the ulnar nerve is at the level of the lower wrist, reveals decreased sensation of the volar aspect of the hypothenar eminence and the fourth and fifth fingers (with splitting of the fourth in most patients). There is always sparing of the sensation of the dorsum of the hand medially because it is innervated by the dorsal ulnar cutaneous branch of the ulnar nerve, which branches off the forearm proximal to the Guyon canal.1 The ulnar claw (hyperextension of the fourth and fifth metacarpophalangeal joints with flexion of the interphalangeal joints) seen in more proximal lesions may be more pronounced because of preserved function of the two medial heads of the flexor digitorum profundus. This creates flexion that is unopposed by the weakened interossei and lumbricals.1,12 The flexor carpi ulnaris has normal strength. All the signs of intrinsic hand muscle weakness that are seen in more proximal ulnar nerve lesions, such as the Froment paper sign, are also found in Guyon canal entrapment affecting the motor nerve fibers (Fig. 39.5).13 Grip strength is invariably reduced in these patients when the motor branches of the ulnar nerve are affected.14 Type III is the least common and involves pure sensory loss from the compression of the superficial branch at the distal aspect of the Guyon canal. The clinician must always consider that there may be possible variations in distal sensory innervation, as both imaging and cadaveric studies have demonstrated anastomoses within the ulnar branches themselves and with the distal sensory branches of the median nerve (up to 57% in the latest study). This consideration is of paramount importance when planning a surgical approach.11,15,16 

Functional Limitations Functional loss can vary from isolated decreased sensation in the affected region to severe weakness and pain with impaired hand movement and dexterity. As can be anticipated, lesions affecting motor nerve fibers are functionally more severe than those affecting only sensory nerve fibers.

CHAPTER 39  Ulnar Neuropathy (Wrist)

A

207

B

FIG. 39.2  (A) The flexor carpi ulnaris functions as a wrist flexor and an ulnar deviator. (B) It can be tested by the patient’s forcefully flexing (arrow) and ulnarly deviating the wrist. The clinician palpates the tendon while the patient performs this maneuver. (From Concannon MD. Common Hand Problems in Primary Care. Philadelphia: Hanley & Belfus; 1999.)

The patient may have trouble holding objects and performing many activities of daily living, such as daily household chores, grooming, and dressing. Vocationally, individuals may not be able to perform the basic requirements of their jobs (e.g., operating a computer or cash register, carpentry work). This can be functionally devastating. 

Diagnostic Studies The cause of the clinical lesion suspected after careful history and physical examination can be investigated with the use of imaging techniques. Plain radiographs could reveal a fracture of the hamate or other carpal bones as well as of the metacarpals and the distal radius, especially if there has been a traumatic injury. MRI11 and computed tomography (multislice spiral computed tomographic angiography, multidetector computed tomography) can be helpful if a fracture, angioleiomyoma, tortuous ulnar artery, pseudoaneurysm of the ulnar artery, lipoma, or ganglion cyst is suspected.17–21 As technology and accuracy of ultrasound equipment have advanced, there are now reports of the

use of conventional and color duplex sonography to diagnose conditions such as thrombosed aneurysm of the ulnar artery.22,23 Nerve conduction study and electromyography are helpful in confirming the diagnosis and the classification as well as in determining the severity of the lesion and the prognosis for functional recovery. Ulnar nerve entrapment in the Guyon canal may be due to recurrent carpal tunnel syndrome.5 As a rule, the dorsal ulnar cutaneous sensory nerve action potential is normal compared with the unaffected side.5 Abnormalities in both sensory and motor conduction studies are seen in type I. The ulnar sensory nerve action potential recorded from the fifth finger is normal in type II, and an isolated abnormality is encountered in type III. The compound muscle action potential of the abductor digiti quinti is normal in types IIa and III. For this reason, it is important to perform motor studies recording from more distal muscles, such as the first dorsal interosseous.23 Motor conduction studies should include stimulation across the elbow to rule out a lesion there, as it is far more common. Furthermore, ulnar nerve stimulation at the palm, after the

208

PART 1 MSK Disorders

A

B

FIG. 39.3  (A) Flexor digitorum profundi (arrows). (B) These tendons can be tested by the patient’s flexing the distal phalanx while the clinician blocks the middle phalanx from flexing. (From Concannon MD. Common Hand Problems in Primary Care. Philadelphia: Hanley & Belfus; 1999.)

FIG. 39.4 It is not unusual for patients with ulnar neuropathy to present with signs of muscle atrophy. It is most noticeable at the first web space, where atrophy of the first dorsal interosseous muscle leaves a hollow between the thumb and the index rays (arrow). (From Concannon MD. Common Hand Problems in Primary Care. Philadelphia: Hanley & Belfus; 1999.)

FIG. 39.5  Ulnar nerve lesion. A patient with an ulnar nerve lesion is asked to pull a piece of paper apart with both hands. Note that the affected side (right hand) uses the flexor pollicis longus muscle to prevent the paper from slipping out of the hand, thus substituting for the adductor pollicis muscle and generating the Froment sign. (From Haymaker W, Woodhall B. Peripheral Nerve Injuries. Philadelphia: WB Saunders; 1953.)

CHAPTER 39  Ulnar Neuropathy (Wrist)

209

traditional stimulation at the wrist and across the elbow, can be useful in sorting out the location of the compression and which fascicles are affected.24 Care must be taken not to overstimulate because median nerve-innervated muscles are very close (i.e., lumbricals 1 and 2), and their volumeconducted compound muscle action potentials could confuse the diagnosis. A “neurographic” palmaris brevis sign has been described in type II ulnar neuropathy at the wrist.25 This consists of a positive wave preceding the delayed abductor digiti minimi motor response, presumably caused by volume-conducted depolarization of a spared palmaris brevis muscle. Needle electromyography helps in documenting axonal loss, determining severity of the lesion to allow prognosis for recovery, and more precisely localizing a lesion for an accurate classification. The flexor carpi ulnaris and the ulnar heads of the flexor digitorum profundus should be completely spared in a lesion at the Guyon canal.26  Differential Diagnosis27 Ulnar neuropathy at the elbow (or elsewhere) Thoracic outlet syndrome (typically lower trunk or medial cord) Cervical radiculopathy at C8-T1 Motor neuron disease Superior sulcus tumor (affecting the medial cord of the plexus) Camptodactyly (an unusual developmental condition with a claw deformity)

Treatment Initial Initial treatment involves rest and avoidance of trauma (especially if occupational or repetitive causes are suspected). Ergonomic and postural adjustments can be effective in these cases. The use of nonsteroidal anti-inflammatory drugs in cases in which an inflammatory component is suspected can also be beneficial. Analgesics may help control pain. Low-dose tricyclic antidepressants may be used both for pain and to help with sleep. More recently, the use of antiepileptic medications for neuropathic pain syndromes has been increasing because of good efficacy. Prefabricated wrist splints may be beneficial and are often prescribed for night use. For individuals who continue their sport or work activities, padded, shock-absorbent gloves may be useful (e.g., for cyclists, jackhammer users). 

Rehabilitation A program of physical or occupational therapy performed by a skilled hand therapist can help obtain functional range of motion and strength of the interossei and lumbrical muscles. Instruction of the patient in a daily routine of home exercises should be done early in the diagnosis. Static splinting (often done as a custom orthosis) with an ulnar gutter will ensure rest of the affected area. In more severe cases, the use of static or dynamic orthotic devices may be considered to improve the patient’s functional level. Weakness in the ulnar claw deformity can be corrected to improve grasp with the use of a dorsal metacarpophalangeal block (lumbrical bar) to the fourth and fifth fingers with a soft strap over the palmar aspect.28

FIG. 39.6  Approaches for two ulnar nerve blocks. The needle with syringe attached demonstrates the puncture for block at the Guyon canal. The circle is over the pisiform bone, and the solid mark is over the hook of the hamate. The second needle demonstrates the puncture site for an ulnar nerve block at the wrist, ulnar approach. (From Lennard TA. Pain Procedures in Clinical Practice. 2nd ed. Philadelphia: Hanley & Belfus; 2000.)

A work site evaluation may be beneficial as well. Ergonomic adaptations can prove helpful to individuals with ulnar nerve entrapment at the wrist (e.g., switching to a foot computer mouse or voice-activated computer software). 

Procedures Injections into the Guyon canal may be tried if a compressive entrapment neuropathy is suspected and generally provide symptomatic relief (Fig. 39.6).2 Under sterile conditions, with use of a 25-gauge, 11/2inch disposable needle, a mixture of corticosteroid and 1% or 2% lidocaine totaling no more than 1 mL is injected into the distal wrist crease to the radial side of the pisiform bone; the needle is angled sharply distally so that its tip lies just ulnar to the palpable hook of the hamate.2,29 With the advent of ultrasound-guided injections it is possible to inject the canal of Guyon with added precision.30 Postinjection care includes ensuring hemostasis immediately after the procedure, local icing for 5 to 10 minutes, and instructions to the patient to rest the affected limb during the next 48 hours. 

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery Surgery is recommended when there is a fracture of the hook of the hamate or of the pisiform or a tortuous ulnar artery that causes neurologic compromise as well as with any space-occupying lesion that causes compression of the ulnar nerve and the resulting clinical signs. Ganglion cyst,

210

PART 1 MSK Disorders

masses, and piso-hamate arthritis are also indications for surgical treatment. Surgery in general involves exploration, excision of the hook of hamate or pisiform (if fractured), repair of the ulnar artery as necessary, excision of any mass, decompression, and neurolysis of the ulnar nerve.2,7 Experience and a sound knowledge of the possible anatomic variations (i.e., muscles, fibrous bands) and the arborization patterns of the ulnar artery in the Guyon canal are of great importance in promoting a positive outcome when surgery is medically necessary.9,31 There have been reports of endoscopic surgery being performed at the Guyon canal, but the procedure has been found to be suboptimal at this time.32 Preoperatively, the patient is educated about the expected clinical course after nerve release. The patient is warned about incisional tenderness for 8 to 12 weeks postoperatively. Nighttime numbness, weakness, or clumsiness will resolve gradually, and recovery may be incomplete. For days 0 to 5, the patient is instructed in isolated tendon glide exercises for all digits. No heavy resistance activities are permitted for 6 weeks after surgery. From 1 to 6 weeks, active range of motion of the wrist, edema control, scar massage, and desensitization are initiated when the incision is made accessible. From 6 to 12 weeks, progressive strengthening exercises are initiated.33 

Potential Disease Complications The severity and type of lesion of the ulnar nerve at the wrist will ultimately determine the complications. Severe motor axon loss will cause profound weakness and atrophy of ulnar-innervated muscles in the hand and render the patient unable to perform even simple tasks because of lack of vital grip strength. Some patients also have chronic pain in the affected hand, which can be severely debilitating, perhaps inciting a complex regional pain syndrome, and it can predispose them to further problems, such as depression and drug dependency. 

Potential Treatment Complications The use of nonsteroidal anti-inflammatory drugs should be carefully monitored because there are potential side effects, including gastrointestinal distress and cardiac, renal, and hepatic disease. Low-dose tricyclic antidepressants are generally well tolerated but may cause fatigue, so they are usually prescribed for use in the evening. Injection complications include injury to a blood vessel or nerve, infection, and allergic reaction to the medication used. Complications after surgery include infection, wound dehiscence, recurrence, and, rarely, complex regional pain syndrome.

References 1. Dumitru D. Electrodiagnostic Medicine. Philadelphia: Hanley & Belfus; 1995:887–891. 2. Dawson D, Hallet M, Millender L. Entrapment Neuropathies. 2nd ed. Boston: Little, Brown; 1990:193–195. 3. Akuthota V, Plastaras C, Lindberg K, et al. The effect of long-distance bicycling on ulnar and median nerves: an electrodiagnostic evaluation of cyclist palsy. Am J Sports Med. 2005;33:1224–1230. 4. Rauch A, Teixeira PA, Gillet R, et al. Analysis of the position of the branches of the ulnar nerve in Guyon’s canal using high-resolution MRI in positions adopted by cyclists. Surg Radiol Anat. 2016;38(7):793–799.

5. Ozdemir O, Calisaneller T, Gulsen S, Caner H. Ulnar nerve entrapment in Guyon’s canal due to recurrent carpal tunnel syndrome: case report. Turk Neurosurg. 2011;21:435–437. 6. Mondelli M, Ginanneschi F, Rossi A. Evidence of improvement in distal conduction of ulnar nerve sensory fibers after carpal tunnel release. Neurosurgery. 2009;65:696–700. 7. Murata K, Shih JT, Tsai TM. Causes of ulnar tunnel syndrome: a retrospective study of 31 subjects. J Hand Surg Am. 2003;28:647–651. 8. Harvie P, Patel N, Ostlere SJ. Prevalence of epidemiological variation of anomalous muscles at Guyon’s canal. J Hand Surg Br. 2004;29:26–29. 9. Bozkurt MC, Tajil SM, Ozcakal L, et al. Anatomical variations as potential risk factors for ulnar tunnel syndrome: a cadaveric study. Clin Anat. 2005;18:274–280. 10. Jose RM, Bragg T, Srivata S. Ulnar nerve compression in Guyon’s canal in the presence of a tortuous ulnar artery. J Hand Surg Br. 2006;31:200–202. 11. Pierre-Jerome C, Moncayo V, Terk MR. The Guyon’s canal in perspective: 3-T MRI assessment of the normal anatomy, the anatomical variations and Guyon’s canal syndrome. Surg Radiol Anat. 2011;33:897–903. 12. Liveson JA, Spielholz NI. Peripheral Neurology: Case Studies in ElectroDiagnosis. Philadelphia: FA Davis; 1991:162–165. 13. Haymaker W, Woodhall B. Peripheral Nerve Injuries. Philadelphia: WB Saunders; 1953. 14. Snider RK. Essentials of Musculoskeletal Care. Rosemont, IL: American Academy of Orthopaedic Surgeons; 1997:260–262. 15. Depukat P, Henry B, Popieluszko P, et al. Anatomical variability and histological structure of the ulnar nerve in the Guyon’s canal. Arch Orthop Trauma Surg. 2017;137(2):277–283. 16. Sulaiman S, Soames R, Lamb C. Ulnar nerve cutaneous distribution in the palm: application to surgery of the hand. Clin Anat. 2015;28(8):1022–1028. 17. Jeong C, Kim HN, Park IJ. Compression of the ulnar nerve in Guyon’s canal by an angioleiomyoma. J Hand Surg Eur Vol. 2010;35:594–595. 18. Stocker RL, Kosak D. Compression of the ulnar nerve at Guyon’s canal by a pseudoaneurysm of the ulnar artery. Handchir Mikrochir Plast Chir. 2012;44:51–54. 19. Ozdemir O, Calisaneller T, Genimez A, et al. Ulnar nerve entrapment in Guyon’s canal due to lipoma. J Neurosurg Sci. 2010;54:125–127. 20. Blum AG, Zabel JP, Kohlman R, et al. Pathologic conditions of the hypothenar eminence: evaluation with multidetector CT and MR imaging. Radiographics. 2006;26:1021–1044. 21. Coulier B, Goffin D, Malbecq S, Mairy Y. Colour duplex sonographic and multislice spiral CT angiographic diagnosis of ulnar artery aneurysm in hypothenar hammer syndrome. JBR-BTR. 2003;86:211–214. 22. Peeters EY, Nieboer KH, Osteaux MM. Sonography of the normal ulnar nerve at Guyon’s canal and of the common peroneal nerve dorsal to the fibular head. J Clin Ultrasound. 2004;32:375–380. 23. Witmer B, DiBenedetto M, Kang CG. An improved approach to the evaluation of the deep branch of the ulnar nerve. Electromyogr Clin Neurophysiol. 2002;42:485–493. 24. Wee AS. Ulnar nerve stimulation at the palm in diagnosing ulnar nerve entrapment. Electromyogr Clin Neurophysiol. 2005;45:47–51. 25. Morini A, Della Sala WS, Bianchini G, et al. ‘Neurographic’ palmaris brevis sign in type II degrees ulnar neuropathy at the wrist. Clin Neurophysiol. 2005;116:43–48. 26. Kim DJ, Kalantri A, Guha S, Wainapel SF. Dorsal cutaneous nerve conduction: diagnostic aid in ulnar neuropathy. Arch Neurol. 1981;38:321–322. 27. Patil JJP. Entrapment neuropathy. In: O’Young BJ, Young MA, Stiens SA, eds. Physical Medicine and Rehabilitation Secrets. 2nd ed. Philadelphia: Hanley & Belfus; 2002:144–150. 28. Irani KD. Upper limb orthoses. In: Braddom RL, ed. Physical Medicine and Rehabilitation. Philadelphia: WB Saunders; 1996:328–330. 29. Mauldin CC, Brooks DW. Arm, forearm, and hand blocks. In: Lennard TA, ed. Physiatric Procedures. Philadelphia: Hanley & Belfus; 1995:145–146. 30. Meng S, Tihofer I, Grisold W, Weninger WJ. Ultrasound Med Biol. 2015;41(8):2119–2124. 31. Murata K, Tamaj M, Gupta A. Anatomic study of arborization patterns of the ulnar artery in Guyon’s canal. J Hand Surg Am. 2006;31:258–263. 32. Noszczyk BH, Zdybek P. Feasibility and limitations of endoscopy in Guyon’s canal. Wideochir Inne Tech Maloinwazyjne. 2014;9(3):387–392. 33. Ulnar nerve Guyon’s canal therapy. E-hand.com The Electronic Textbook of Hand Therapy. American Society for Surgery of the Hand; December 2016.

CHAPTER 40

Wrist Osteoarthritis Chaitanya S. Mudgal, MD, MS (Orth), MCh (Orth) Jyoti Sharma, MD

Synonyms Degenerative arthritis of the wrist Osteoarthritis of the wrist Post-traumatic arthritis of the wrist SLAC wrist SNAC wrist

ICD-10 Codes M19.031 M19.032 M19.039

Primary osteoarthrosis, right wrist Primary osteoarthrosis, left wrist Primary osteoarthrosis, unspecified wrist M19.231 Secondary osteoarthrosis, right wrist M19.232 Secondary osteoarthrosis, left wrist M19.239 Secondary osteoarthrosis, unspecified wrist M12.531 Traumatic arthropathy, right wrist M12.532 Traumatic arthropathy, left wrist M12.539 Traumatic arthropathy, unspecified wrist M24.831 Other specific joint derangement, of right wrist, not elsewhere classified M24.832 Other specific joint derangement, of left wrist, not elsewhere classified M24.839 Other specific joint derangement, un­speci­fied wrist, not elsewhere classified M25.431 Effusion, right wrist M25.432 Effusion, left wrist M25.439 Effusion, unspecified wrist M25.531 Pain in right wrist M25.532 Pain in left wrist M25.539 Pain in unspecified wrist S63.501 Unspecified sprain of right wrist S63.502 Unspecified sprain of left wrist S63.509 Unspecified sprain of unspecified wrist Add the appropriate seventh character to category 63 for the episode of care.

Definition Primary osteoarthritis (OA) of the wrist refers to the painful degeneration of the articular surfaces that make up the wrist joint due to non-inflammatory arthritides. It commonly affects the joints between the distal radius and the proximal row of carpal bones. Symptoms include pain, swelling, stiffness, and crepitation. Radiographs will reveal different degrees of joint space narrowing, cyst formation, subchondral sclerosis, and osteophyte formation. OA in the wrist is rare. The Framingham study showed a 9-year incidence of only 1% of radiographically significant wrist OA in women, and 1.7% in men. These rates are significantly lower than the rates of thumb basal joint OA (30%), distal interphalangeal (DIP) joint arthritis (28% to 35% in patients over the age of 40), and radiographic hand OA in patients 80 years and older (90% to 100%).1 Secondary OA of the wrist joint is the most common form of wrist OA,2 most commonly resulting from posttraumatic conditions, such as distal radius fractures, carpal fractures, and carpal instability. Rare conditions that may cause secondary wrist OA include idiopathic osteonecrosis of the lunate (Kienböck disease) and the scaphoid (Preiser disease). Distal radius fractures that have healed inappropriately (malunited) can also be the cause (Fig. 40.1). Malunion occurs in approximately 23% of nonsurgically and 11% of operatively treated distal radius fractures.3 In considering malunited fractures of the distal radius, abnormal parameters that have been shown to be associated with wrist arthritis include the following: on an anteroposterior radiograph, an intra-articular step-off of more than 2 mm and radial shortening of more than 5 mm; or on the lateral radiograph, a dorsal angulation of more than 10 degrees. Articular step-off followed by loss of height have been found to be the two most important factors associated with wrist arthritis out of these parameters.4–6 Carpal fractures that fail to heal, particularly of the scaphoid, can also be the cause of arthritis.7 This bone is predisposed to nonunions biologically because of its fragile vascular supply and biomechanically on account of the shear forces it encounters.8,9 Other factors associated with nonunions include fracture displacement, fracture location, and delay in initiation of treatment.10,11 Features of a scaphoid nonunion that appear to be associated with arthritis are the displacement of the cartilaginous surfaces and the loss of carpal stability.12,13 Both of these lead to abnormal loading of the cartilage and consequently to ensuing arthritis. This pattern of arthritis is known as scaphoid nonunion advanced collapse (SNAC). 211

212

PART 1  MSK Disorders

A

B

FIG. 40.1  Anteroposterior (A) and lateral (B) plain radiographs of wrist osteoarthritis secondary to a malunited wrist fracture. Note the dorsal angulation of the distal articular surface and the reduced joint space. This patient also had significant osteopenia secondary to pain-induced lack of use.

A

B

FIG. 40.2  Anteroposterior (A) and lateral (B) plain radiographs of wrist osteoarthritis secondary to scapholunate advanced collapse, stage 2. Note the increased scapholunate space and the sclerosis of the radioscaphoid joint. Early osteophytes are clearly seen on the radial border of the scaphoid. The lateral view shows dorsal osteophytes as well as the dorsally angled lunate.

Carpal instability can also result in uneven loading of the articular surfaces and subsequent arthritis (Fig. 40.2).14 The most common form of carpal instability is scapholunate dissociation.15 It consists of a disruption of the interosseous ligament between the scaphoid and lunate. The resultant abnormal biomechanics lead to abnormal loading and subsequent arthritis, a pattern known as scapholunate advanced collapse (SLAC).1 

Symptoms Wrist pain is the presenting symptom in the overwhelming majority of patients. For the most part, this pain is of insidious onset, although many patients will recall a particular

event that brought it to their attention. It is diffusely located across the dorsum of the wrist. It may be activity related and may bear little correlation to radiographic findings. Patients may also report inability to do their daily activities because of weakness, but on further questioning, this weakness is often secondary to pain. Pain tends to be intermittent and waxes and wanes over time. Another presenting symptom is stiffness, particularly in flexion and extension of the wrist. Pronation and supination are usually not affected, unless the arthritic process is extensive and also involves the distal radioulnar joint. In some patients, motion may be associated with a clicking sensation or with audible crepitation. Complaints about cosmetic

CHAPTER 40  Wrist Osteoarthritis

deformity are also common, particularly after distal radius fractures that have healed with an inappropriate alignment. Swelling is commonly noted by patients. This swelling is essentially a representation of the malunited fracture, but in patients with advanced arthritis irrespective of the etiology, it may represent synovial hypertrophy or osteophyte formation. In this situation, the swelling tends to be located in the dorsoradial region of the wrist. 

Physical Examination In general, comparison of the affected side with the contralateral extremity, if it is not involved, is useful to appreciate changes in the affected limb. Examination of the wrist includes a thorough examination of the entire upper limb, starting with the shoulder. Other sources of joint pain and loss of motion should be noted. Visual inspection of the wrist and upper extremity can reveal swelling and deformity, if present. Next, motion, strength, and sensory function should be tested. In wrist OA, the most obvious finding may be loss of motion. Normal range of motion of the wrist joint includes approximately 80 degrees of flexion, 60 degrees of extension, 20 degrees of radial deviation, and 40 degrees of ulnar deviation.16 Loss of grip strength may be evident, especially in patients with decreased radial inclination, which theoretically affects the function of the finger flexors biomechanically due to a change in the position of the carpal tunnel, through which the finger flexors run.3 The strength of the abductor pollicis brevis is tested by asking the patient to palmarly abduct the thumb against resistance. Similarly, the strength of the first dorsal interosseus muscle should be checked by asking the patient to radially deviate the index finger against resistance. These tests evaluate for motor deficits of the median nerve and ulnar nerve, respectively. Sensation should also be compared with the opposite side. Whereas static two-point discrimination is an excellent way to test sensation in the office, a more precise evaluation of early sensory deficits can be performed by graduated Semmes-Weinstein monofilaments. Frequently, this test requires a referral to occupational therapists who perform it. Next, the wrist is palpated for evidence of tenderness or masses, such as cysts. Tenderness just distal to Lister tubercle may be a sign of pathologic change at the scapho­ lunate joint, including scapholunate dissociation, Kienböck disease, or synovitis of the radiocarpal joint. Tenderness at the anatomic snuffbox may indicate a scaphoid fracture or nonunion, and in early SNAC, this may be the site of radioscaphoid degeneration. In the presence of pancarpal arthritis, the tenderness is usually diffuse. Provocative maneuvers should also be performed to check for signs of carpal instability. The scaphoid shift test of Watson evaluates for scapholunate instability.17 In this test, the examiner places a thumb volarly on the patient’s scaphoid tubercle, and the rest of the fingers wrap around the wrist to lie dorsally over the proximal pole of the scaphoid. As the wrist is taken from ulnar deviation to radial deviation, the thumb will apply pressure on the scaphoid tubercle and force the scaphoid to sublux out of its fossa dorsally in ligamentously lax patients as well as in those with frank scapholunate instability. Once pressure from the thumb is released, the scaphoid will then shift back into its fossa and is accompanied by pain experienced by the patient.

213

At times, an audible or palpable clunk will be appreciated as the scaphoid reduces. This finding is best demonstrated in patients who have ligamentous laxity or in patients with recent injuries. Patients who have chronic injuries often develop sufficient fibrosis to prevent subluxation of the scaphoid out of its fossa. However, they often still have pain that is reproduced with this maneuver. Comparison with the unaffected side is essential, especially if the patient has evidence of generalized ligamentous laxity. 

Functional Limitations The majority of the limitations in wrist arthritis arise from a lack of motion. A range of motion from 10 degrees of flexion to 15 degrees of extension is required for activities involving personal care.18 The loss of motion mainly affects activities of daily living such as washing one’s back, fastening a brassiere, and writing. Eating, drinking, and using a telephone require 35 degrees of extension. However, learned compensatory maneuvers can allow most activities of daily living to be accomplished with as little as 5 degrees of flexion and 6 degrees of extension.19 

Diagnostic Studies The initial evaluation of the arthritic wrist includes standard posteroanterior, lateral, and pronated oblique radiographs. In the posteroanterior view, any evidence of arthritis between the radius and proximal row of carpal bones or between the proximal and distal rows should be noted. Radiographic features that indicate an arthritic process include reduction or loss of joint space, osteophyte formation, cyst formation in periarticular regions, and loss of normal bony alignment (see Fig. 40.2). Injury to the scapholunate ligament is evidenced by a space between the scaphoid and the lunate greater than 2 mm and a cortical ring sign of the scaphoid.15 Sclerosis or collapse of the lunate is consistent with Kienböck disease.20 The lateral view can reveal signs of carpal instability, such as a dorsally or palmarly oriented lunate. In the lateral view, an angle between the long axes of the scaphoid and the lunate in excess of 60 degrees is also consistent with scapholunate dissociation. The oblique view will often demonstrate the site of a scaphoid nonunion. Although it may be possible to make a diagnosis of scapholunate dissociation on plain radiographs, some patients can often have bilateral scapho­ lunate distances and angles in excess of normal limits. It is therefore critical to obtain contralateral radiographs before a diagnosis of scapholunate injury is made. Patterns of arthritic progression in SLAC and SNAC wrists have been classified into three stages. In a SLAC wrist, stage 1 involves arthritis between the radial styloid and the distal pole of the scaphoid; stage 2 results in reduction or loss of joint space between the radius and the proximal pole of the scaphoid; and stage 3 indicates capito­ lunate degeneration with proximal migration of the capitate between the scaphoid and lunate. In a SNAC wrist, stage 1 and stage 3 are similar to those in a SLAC wrist. However, in stage 2, there is degenerative change between the distal pole of the scaphoid and capitate. Other imaging modalities are not necessary for the diagnosis of OA. Computed tomography is sometimes used to evaluate the alignment of the scaphoid fragments in cases of

214

PART 1  MSK Disorders

nonunion and the amount of collapse of the lunate in Kienböck disease. Magnetic resonance imaging is occasionally used to evaluate the vascularity of the scaphoid proximal pole and lunate in scaphoid nonunions and Kienböck disease, respectively.20,21 Wrist arthroscopy offers the optimal ability to assess the condition of the articular cartilage; however, this assessment can be made from plain radiographs or at the time of surgical reconstruction of the wrist. 

Differential Diagnosis Acute fracture Septic arthritis Crystalline arthritis Carpal tunnel syndrome Rheumatoid arthritis de Quervain tenosynovitis

were better liked by patients in one recent study.22 Nonsteroidal anti-inflammatory drugs can also provide significant pain relief, particularly during periods of acute exacerbation of symptoms. Long-term use of nonsteroidal anti-inflammatory drugs is not indicated. Some randomized clinical trials have shown that turmeric, the active ingredient of which is known as curcumin, has benefits in inflammation reduction and consequently pain reduction in patients suffering from arthritis.23 Periodic application of ice, especially during periods of acute symptom exacerbation, can be of help, as can topical agents such as over-the-counter creams and gels. On occasion, in patients with radioscaphoid arthritis (SNAC), inclusion of the thumb in a custom-made orthoplast thumb spica splint may provide better pain relief. Use of magnetic and copper bracelets has not been shown to be effective in clinical trials.24 Prior to the initiation of any pharmacologic treatment, the patient should always consult his or her primary care physician. 

Rehabilitation

Treatment Initial OA of the wrist is a condition that has usually been present for a significant amount of time. However, it is not uncommon for symptoms to be of a short duration, and they can often be manifested after seemingly trivial trauma. It is important for the physician to establish good rapport with the patient during several visits so that the pathophysiologic changes of the process can be emphasized to the patient. This becomes even more important in situations involving workers’ compensation or litigation or both. It is also important for the patient to understand that the condition cannot be reversed and that the symptoms are likely to be cyclic. Patients must understand that over time, the condition may worsen radiographically; however, it is impossible to predict the rate of clinical progression or severity of symptoms that might ensue. Many patients present with symptoms of wrist OA that are not severe enough to be limiting, but enough to be noticed. These patients are often looking for reassurance about their condition. If they are able to do all the activities that they want to do, surgical intervention is not needed. They should not refrain from doing their activities in fear that they may accelerate the condition; there is no scientific evidence to substantiate this concern. This approach offers the least amount of risk to the patient. Other patients may prefer to have some symptom reduction, particularly during episodes of acute worsening, despite some inconvenience or small risks. An overthe-counter wrist splint with a volar metal stabilizing bar (cock-up splint) can be a small inconvenience; however, by virtue of immobilizing the wrist, it can provide great symptom relief during daily activities. This metal bar can be contoured to place the wrist in the neutral position rather than in extension, as most splints of this nature tend to do. The neutral position appears to be better tolerated by patients and affords better compliance with splint wear. Both overthe-counter and custom-made splints have been shown to relieve pain and improve function and grip strength. Custom splints, however, provided more of these improvements and

Once the acute inflammation phase has passed, most patients are able to resume most activities. Some may complain of persistent lack of motion or strength. These patients may benefit from a home exercise program for range of motion and strengthening directed by an occupational therapist. Modalities such as fluidotherapy may help with range of motion by decreasing pain. Static progressive splinting is usually not recommended to improve range of motion because there is often a bony block to motion, due to altered anatomy or osteophytes or both. It is always important to understand that therapy itself may worsen symptoms, especially passive stretching exercises. Active range of motion and active-assisted range of motion exercises are better tolerated by patients, and some patients may be better off without any formal rehabilitation. 

Procedures Nonsurgical procedures, including corticosteroid injections, may be indicated for wrist OA, although they appear to have a greater use in crystalline and inflammatory arthritides. Hyaluronan injections for OA have been studied in other joints, including the thumb carpometacarpal joint, with potentially beneficial results; however, their use in the wrist is still considered experimental.25 Typically, all injections around the wrist should be done utilizing an aseptic technique with a 25-gauge, 11⁄2-inch needle and a mixture of a nonprecipitating, water-soluble steroid preparation that is injected along with 2 mL of 1% lidocaine. The radiocarpal joint can be injected from the dorsal aspect approximately 1 cm distal to Lister tubercle, with the needle angled proximally about 10 degrees to account for the slight volar tilt of the distal radius articular surface. This is done with the wrist in the neutral position. Gentle longitudinal traction by an assistant can help widen the joint space, which may be reduced due to the disease. An alternative radiocarpal injection site is the ulnar wrist, just palmar to the extensor carpi ulnaris tendon at the level of the ulnar styloid process. With strict aseptic technique, a 25-gauge, 11⁄2-inch needle is inserted into the ulnocarpal space, just distal to the ulnar styloid, just dorsal or volar to the easily

CHAPTER 40  Wrist Osteoarthritis

A

215

B

FIG. 40.3  Anteroposterior (A) and lateral (B) plain radiographs of a patient after she underwent a proximal row carpectomy. A terminal radial styloidectomy has also been performed to reduce impingement of the trapezium on the tip of the radius. Note how well the capitate articulates with the lunate fossa of the distal radius.

palpable tendon of the extensor carpi ulnaris. The needle must be angled proximally by 20 to 30 degrees to enter the space between the ulnar carpus and the head of the ulna. It is important to ascertain that the injectate flows freely. Any resistance indicates a need to reposition the needle appropriately. Alternatively, the injection may be performed by fluoroscopic guidance with the help of a mini image intensifier or with ultrasound guidance, if either is available in the office. If a midcarpal injection is required, this is best done through the dorsal aspect, under fluoroscopic guidance, with injection into the space at the center of the lunatetriquetrum-hamate-capitate region. 

Pisiform

Hamate Capitate

Radio-lunate ligament

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Radio-scapho capitate ligament

Surgery

FIG. 40.4  An intraoperative photograph of the patient seen in Fig. 40.3, during a proximal row carpectomy, to show healthy articular cartilage over the head of the capitate.

The goal of surgery in an osteoarthritic wrist is pain relief. Surgical procedures for OA can be divided into motionsparing procedures and fusions (arthrodesis). However, even motion-sparing procedures often result in significant loss of motion. This is very important in patients who have almost no motion preoperatively. These patients will not benefit from motion-sparing procedures and are better served with total wrist fusions. The decision to proceed with surgery should not be made until nonsurgical means have been tried for an adequate time, which usually amounts to a period of 3 to 6 months. In some patients who are going to have a total wrist fusion, before a decision is made about surgery, it is useful to apply a well-molded fiberglass short arm cast for 2 weeks to accustom the patient to the lack of wrist motion.

Motion-sparing procedures include proximal row carpectomy (PRC), total wrist arthroplasty and limited intercarpal fusions with scaphoid excision. The excision of the scaphoid is essential because 95% of wrist arthritis involves the scaphoid.2 PRC involves removal of the scaphoid, lunate, and triquetrum. The capitate then articulates with the radius through the lunate fossa (Fig. 40.3). Wrist stability is maintained by preserving the volar wrist ligaments. As a prerequisite for this procedure, the lunate fossa of the radius and the articular surface over the head of the capitate must be healthy and free of degenerative change (Fig. 40.4). The main advantages of this procedure is that it does not involve any fusions and it more closely resembles normal

216

PART 1  MSK Disorders

A

B

FIG. 40.5  (A) and (B) Postoperative function 6 months after a proximal row carpectomy. The patient has recovered nearly a 100-degree arc of motion and has no pain.

A

B

FIG. 40.6  Anteroposterior (A) and lateral (B) postoperative radiographs after scaphoid excision and four-bone fusion have been performed.

wrist kinematics when compared to other procedures, such as a four-corner fusion.35 After a short period of postoperative casting, patients are allowed to start moving the wrist as early as 3 weeks after surgery. Most patients are able to attain a flexion-extension arc of 60 to 80 degrees and 60% to 80% of the grip strength of the uninvolved side (Fig. 40.5).26,27 This procedure is appropriate for the early stages of SLAC and SNAC arthritis. Some surgeons have attempted to extend the indications for PRC in the setting of capitate head cartilage loss or lunate fossa arthritis by suggesting interposition of soft tissue allo- or autograft or osteochondral autograft to the capitate from the excised carpal bones.28–30 Indications for total wrist arthroplasty have expanded from end-stage rheumatoid arthritis, to include post-traumatic OA, end-stage primary OA, and Kienböck disease. Patients are permanently discouraged from heavy lifting after arthroplasty surgery, but can otherwise return to full activity after a 2- to 3- month period of splinting in 30 to 40 degrees of extension to prevent flexion contracture. Shortterm results have been encouraging with significant pain relief, maintaining grip strength of 60% of the uninvolved

side, preservation of motion, and even an increase in radial deviation in one study.31,32 Total wrist arthroplasty is not recommended in people younger than 50 years of age, heavy laborers, or those dependent on walking aids. The durability of total wrist arthroplasty especially in patients with noninflammatory arthritides remains unclear. The most common limited intercarpal fusion is known as the four-corner or four-bone fusion. It involves creating a fusion mass between the lunate, triquetrum, capitate, and hamate. The scaphoid is excised. The prerequisite for this procedure is an intact joint between the radius and the lunate. A theoretical advantage of this procedure over a PRC is that it maintains carpal height, leading to a better grip strength (Fig. 40.6). However, this has not been shown to be the case in larger studies comparing these two procedures.33 The flexionextension arc of wrist motion is also not significantly different between these two procedures.34 Theoretical disadvantages of a four-corner fusion include protracted immobilization until fusion is confirmed (usually 8 weeks) and the possibility of needing a secondary operative procedure to remove hardware (Fig. 40.7). The risks of nonunion and hardware failure also exist. This procedure is also appropriate for the early

CHAPTER 40  Wrist Osteoarthritis

A

217

B

FIG. 40.7  Anteroposterior (A) and lateral (B) postoperative radiographs. A mature four-bone fusion after a secondary procedure to remove the pins seen in Fig. 40.6. To avoid the second operative procedure, some may elect to leave the pins percutaneous and to remove them during an office visit. Newer implants have also been developed for this procedure that do not necessarily mandate removal (headless screws, staples, and contoured plates).

stages of SLAC and SNAC arthritis and is usually preferred in the younger patient population versus a PRC, which carries a higher risk of further future arthritis development.35 Newer options involving limited fusions of the lunate and capitate with scaphoidectomy are also being studied as viable options for SLAC and SNAC wrists with advanced collapse. Fewer fusion surfaces are required for healing and no significant changes in mobility and carpal alignment have been seen.36 Patients with severe arthritis that involves not only the radiocarpal joint but also the joint between the proximal and distal carpal rows (midcarpal joint) are better served with total wrist fusion. This procedure is also beneficial in patients who present preoperatively with minimal or no wrist motion. It involves a fusion between the radius, proximal row, and distal row of carpal bones (or between the radius and distal row of carpal bones, as a PRC can be done in conjunction with a wrist arthrodesis to reduce the number of surfaces that require healing). The wrist is protected with a splint or cast for 4 to 6 weeks. Most patients are able to attain a grip strength that is 60% to 80% of the opposite side.33 A successful fusion abolishes the flexion-extension arc of wrist motion and, more important, can be effective in obtaining pain relief. However, the lost motion makes it difficult for patients to position the hand in tight spaces and can affect perineal care.34 In these patients, the loss of motion does not appear to have an adverse functional impact because most of these patients have significant reduction of motion at the time of presentation. The pain relief provided by this procedure, however, can have a positive impact on functional outcome to a significant degree. Pronation and supination are unaffected. This procedure is appropriate for the advanced stages of SLAC and SNAC arthritis (Fig. 40.8). Wrist denervation, which does not address the OA directly but acts as a palliative option, was proposed in 1966 by Wilhelm.37 The procedure involves ablation of sensory branches of local nerves to the wrist capsule without addressing any bony deformity. Since then, others have modified the approach and have also suggested partial denervations. Pain relief can be as high as 80% to 100%.

A

B FIG. 40.8 Anteroposterior (A) and lateral (B) postoperative radiographs after a total wrist arthrodesis with a contoured plate and screws. In the anteroposterior radiograph, it is evident that the wrist is in mild ulnar deviation; in the lateral radiograph, the wrist appears to be in mild dorsiflexion. This is the optimal position for hand function in such patients. The patient also underwent excision of the distal ulna.

218

PART 1  MSK Disorders

The major benefit of denervation is that all the above options remain at the surgeon’s disposal should bony procedures become necessary. Despite early concerns, the wrist does not undergo Charcot arthropathy after denervation.38,39 

Potential Disease Complications Wrist OA that progresses to advanced stages results in severely painful limitations of motion. Patients are unable to do their activities of daily living because any load across the arthritic wrist joint results in pain. The pain and stiffness can also inhibit the ability of the patient to position the hand in space. Rarely, osteophytes occurring over the dorsal aspect of the distal radius and the distal radioulnar joint can cause attritional ruptures of extensor tendons. 

Potential Treatment Complications Nonsteroidal anti-inflammatory medicines carry risks to the cardiovascular, gastric, renal, and hepatic systems. For these reasons, these medications are typically used for short periods. Surgery exposes the patient to significant risks from anesthesia, infection, nerve injury, and tendon injury. Fusions carry the risk of nonunion and malunion as well as that of hardware complications, such as prominence of the hardware, tendon irritation, and metal sensitivity. Motionsparing procedures can eventually lead to further degenerative disease and in the presence of symptoms may require further surgery, which most commonly consists of a total wrist fusion. Total wrist arthroplasties can be complicated by infection, loosening, wound issues, hardware failure, instability, dislocation, tendon rupture, and impingement with complication rates varying from 9% to 75%. Survival rates of total wrist arthroplasty in a Norwegian study ranged from 57% to 78% at 5 years, and were as high as 71% at 10 years, depending on the implant and preoperative diagnosis.32

References 1. Haugen IK, Englund M, Aliabadi P, et al. Prevalence, incidence and progression of hand ostoearthiris in the general population: the Framingham Osteoarthritis Study. Ann Rheum Dis. 2011;70:1581–1586. 2. Watson HK, Ballet FL. The SLAC wrist: scapholunate advanced collapse pattern of degenerative arthritis. J Hand Surg Am. 1984;9:358–365. 3. Lodha SJ, Wysocki RW, Cohen MS. Malunions of the distal radius. In: Chung K, ed. Hand Surgery Update V: Hand, Elbow, and Shoulder. Am Soc Surg Hand. 2011:125–137. 4. Knirk JL, Jupiter JB. Intra-articular fractures of the distal end of the radius in young adults. J Bone Joint Surg Am. 1986;68:647–659. 5. Aro HT, Koivunen T. Minor axial shortening of the radius affects outcome of Colles’ fracture treatment. J Hand Surg Am. 1991;16:392–398. 6. Gliatis JD, Plessas SJ, Davis TR. Outcome of distal radial fractures in young adults. J Hand Surg Br. 2000;25:535–543. 7. Ruby LK, Stinson J, Belsky MR. The natural history of scaphoid non-union. A review of fifty-five cases. J Bone Joint Surg Am. 1985;67:428–432. 8. Gelberman RH, Menon J. The vascularity of the scaphoid bone. J Hand Surg Am. 1980;5:508–513. 9. Slade JF III, Dodds SD. Minimally invasive management of scaphoid nonunions. Clin Orthop Relat Res. 2006;445:108–119. 10. Cooney WP, Linscheid RL, Dobyns JH. Scaphoid fractures. Problems associated with nonunion and avascular necrosis. Orthop Clin North Am. 1984;15:381–391. 11. Osterman AL, Mikulics M. Scaphoid nonunion. Hand Clin. 1988;4:437–455.

12. Lindstrom G, Nystrom A. Incidence of post-traumatic arthrosis after primary healing of scaphoid fractures: a clinical and radiological study. J Hand Surg Br. 1990;15:11–13. 13. Mack GR, Bosse MJ, Gelberman RH, Yu E. The natural history of scaphoid non-union. J Bone Joint Surg Am. 1984;66:504–509. 14. 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. 15. Walsh JJ, Berger RA, Cooney WP. Current status of scapholunate interosseous ligament injuries. J Am Acad Orthop Surg. 2002;10:32–42. 16. Ryu J, Cooney WP III, Askew LJ, et al. Functional ranges of motion of the wrist joint. J Hand Surg Am. 1991;16:409–419. 17. Watson HK, Weinzweig J. Physical examination of the wrist. Hand Clin. 1997;13:17–34. 18. Brumfield RH, Champoux JA. A biomechanical study of normal functional wrist motion. Clin Orthop Relat Res. 1984;187:23–25. 19. Nissen KL. Symposium on cerebral palsy (orthopaedic section). Proc R Soc Med. 1951;44:87–90. 20. Allan CH, Joshi A, Lichtman DM. Kienböck’s disease: diagnosis and treatment. J Am Acad Orthop Surg. 2001;9:128–136. 21. Simonian PT, Trumble TE. Scaphoid nonunion. J Am Acad Orthop Surg. 1994;2:185–191. 22. Thiele J, Nimmo R, Rowell W, Quinn A, Jones G. A randomized single blind crossover trial comparing leather and commercial wrist splints for treating chronic wrist pain in adults. BMC Musculoskeletal Disorders. 2009;10:129–136. 23. Daily JW, Yang M, Park S. Efficacy of tumeric extracts and curcumin for alleviating the symptoms of joint arthritis: a systematic review and meta-analysis of randomized clinical trials. J Med Food. 2016;19:717–729. 24. Richmond SJ, Brown SR, Campion PD, et al. Therapeutic effects of magnetic and copper bracelets in osteoarthritis: a randomized placebocontrolled crossover trial. Complement Ther Med. 2009;17:249–256. 25. Mandl LA, Hotchkiss RN, Adler RS, et al. Injectable hyaluronan for the treatment of carpometacarpal osteoarthritis: an open label pilot trial. Curr Med Res Opin. 2009;25:2103–2108. 26. Imbriglia JE, Broudy AS, Hagberg WC, McKernan D. Proximal row carpectomy: clinical evaluation. J Hand Surg Am. 1990;15:426–430. 27. Cohen MS, Kozin SH. Degenerative arthritis of the wrist: proximal row carpectomy versus scaphoid excision and four-corner arthrodesis. J Hand Surg Am. 2001;26:94–104. 28. Kwon BC, Choi SJ, Shin J, Baek GH. Proximal row carpectomy with capsular interposition arthroplasty for advanced arthritis of the wrist. J Bone Joint Surg Br. 2009;91-B:1601–1606. 29. Santos Carneiro R, Dias CE, Baptista CM. Proximal row carpectomy with allograft scaffold interposition arthroplasty. Tech Hand Surg. 2011;15:253–256. 30. Dang J, Nydick J, Polikandriotis JA, Stone J. Proximal row carpectomy with capitate osteochondral autograft transplantation. Tech Hand Up Extrem Surg. 2012;16(2):67–71. 31. Nydick JA, Greeberg SM, Stone JD, Williams B, Polikandriotis JA, Hess AV. Clinical outcomes of total wrist arthroplasty. J Hand Surg. 2012;37(A):1580–1584. 32. Krukhaug Y, Lie SA, Havelin LI, Furnes O, Hove LM. Results of 189 wrist replacements, a report from the Norwegian Arthroplasty Register. Acta Orthpaedica. 2011;82(4):405–409. 33. Bolano LE, Green DP. Wrist arthrodesis in post-traumatic arthritis: a comparison of two methods. J Hand Surg Am. 1993;18:786–791. 34. Weiss AC, Wiedeman G Jr, Quenzer D, et al. Upper extremity function after wrist arthrodesis. J Hand Surg Am. 1995;20:813–817. 35. Wolff AL, Garg R, Kraszewski AP, et al. Surgical treatments for scapho­ lunate advanced collapse wrist: kinematics and functional performance. J Hand Surg. 2015;40:1547–1553. 36. Chahla J, Schon JM, Olleac R, et al. Stage III advanced wrist collapse treatment options: a cadaveric study. J Wrist Surg. 2016;5:265–272. 37. Wilhelm A. Denervation of the wrist. Hefte Unfallheilkd. 1965;81:109–114. 38. Schweizer A, von Kanel O, Kammer E, Meuli-Simmen C. Longterm follow-up evaluation of denervation of the wrist. J Hand Surg. 2006;31A:559–564. 39. Braga-Silva J, Roman JA, Padoin AV. Wrist denervation for painful conditions of the wrist. J Hand Surg. 2011;36A:961–966.

CHAPTER 41

Wrist Rheumatoid Arthritis Chaitanya S. Mudgal, MD, MS (Orth), MCh (Orth) Jyoti Sharma, MD

Synonyms Rheumatoid wrist Synovitis of the wrist Tenosynovitis of the wrist

Rheumatoid synovial hypertrophyICD-10 Codes M06.831 M06.832 M06.839 M24.831 M24.832 M24.839 M25.531 M25.532 M25.539 M67.331 M67.332 M67.339 M65.9 M21.90

Rheumatoid arthritis, right wrist Rheumatoid arthritis, left wrist Rheumatoid arthritis, unspecified wrist Other specific joint derangement, of right wrist, not elsewhere classified Other specific joint derangement, of left wrist, not elsewhere classified Other specific joint derangement, unspecified wrist, not elsewhere classified Pain in right wrist Pain in left wrist Pain in unspecified wrist Transient synovitis, right wrist Transient synovitis, left wrist Transient synovitis, unspecified wrist Synovitis and tenosynovitis, unspecified Unspecified acquired deformity of unspecified limb

Definition Rheumatoid arthritis (RA) is a systemic autoimmune disorder involving the synovial joint lining and is characterized by chronic symmetric erosive synovitis. It has been estimated that 1% to 2% of the world’s population is affected by this disorder. Women are affected more frequently, with a ratio

of 2.5:1. The cause of rheumatoid arthritis is thought to be multifactorial, including both genetic and environmental factors. The diagnostic criteria for RA include symptomatology (morning stiffness, symmetric joint swelling, and skin nodules), laboratory tests, and radiographic findings. The wrist is among the most commonly involved peripheral joints; more than 65% of patients have some wrist symptoms within 2 years of diagnosis, increasing to more than 90% by 10 years. Of patients with wrist involvement, 95% have bilateral involvement.1–5 The inflamed and hypertrophied synovial tissue is responsible for the destruction of adjacent tissues and resultant deformities. The cascade of events that lead to articular cartilage damage is a T-cell mediated autoimmune process mediated by the HLA-II locus.4,5 The synovium is infiltrated by destructive molecules, resulting in thickening and proliferation of the synovium, chemotactic attraction of polymorphonuclear cells, and release of lysosomal enzymes and free oxygen radicals by the polymorphonuclear cells, which destroy joint cartilage. The wrist articulation can be divided into three compartments, all of which are lined by synovium and therefore involved in rheumatoid arthritis: the radiocarpal, midcarpal, and distal radioulnar joints. Cartilage loss from both degradation and synovial proliferation contribute to ligamentous laxity of the extrinsic and intrinsic wrist ligaments. The laxity around the wrist leads to the classic rheumatoid deformities of carpal supination and ulnar translocation. The normally stout volar radioscaphocapitate ligament and the dorsal radiotriquetral ligament, which are important stabilizers of the carpus in relation to the distal radius, are stretched, resulting in ulnar translocation of the carpus. Laxity of the volar radioscaphocapitate ligament also leads to loss of the ligamentous support to the waist of the scaphoid and weakening of the intrinsic scapholunate ligament. The scaphoid responds by adopting a flexed posture, and this is accompanied by radial deviation of the hand at the radiocarpal articulation. The bony carpus supinates and subluxes palmarly and ulnarly; thus the ulna is left relatively prominent on the dorsal aspect of the wrist, a condition sometimes referred to as the caput ulnae syndrome.5–7 The secondary effect of carpal supination is subluxation of the extensor carpi ulnaris tendon in a volar direction to the point that it no longer functions effectively as a wrist extensor. The bony architecture of the wrist is affected secondarily, in that the inflammatory 219

220

PART 1  MSK Disorders

A

B

C

FIG. 41.1  (A) Appearance of the wrist in early rheumatoid arthritis. Note the swelling around the ulnar head. (B) The synovial hypertrophy around the head of the ulna and distal radioulnar joint is appreciated in profile. There is also an early radial deviation of the hand at the wrist. (C) The prominence of the ulnar head is compounded by the subluxation and supination of the carpus, creating an appearance of an abrupt change in contour from the wrist to the hand.

A

B

C

FIG. 41.2  (A) Synovitis around the distal end of the ulna may be manifested with swelling just volar to the ulnar styloid, as in this patient. (B) and (C) Loss of motion in early rheumatoid disease of the wrist, as in this patient, is often a manifestation of the synovitis and pain associated with it rather than a true joint destruction.

cascade also stimulates bone-resorbing osteoclasts, which cause subchondral and periarticular osteopenia. Areas of the wrist that display vascular penetration into bone or contain significant synovial folds, such as the radial attachment of the radioscaphocapitate ligament (the most radial of the volar radiocarpal ligaments), the waist of the scaphoid, and the base of the ulnar styloid (prestyloid recess), are the most common sites of progressive synovitis. The results of chronic erosive changes in these areas are bone spicules that can abrade and weaken tendons passing in their immediate vicinity, ultimately causing tendon rupture and functional deterioration. The extensor tendons to the small finger and ring finger (Vaughn-Jackson syndrome)8 rupture at the level of the ulnar head (see caput ulnae syndrome) and the flexor tendon of the thumb at the level of the scaphoid tubercle (Mannerfelt syndrome)9 are the most commonly involved. In addition to mechanical abrasion, the extensor tendons are enclosed in a sheath of synovium at the wrist, which makes them susceptible to the damaging changes of synovial hypertrophy that are commonly seen in rheumatoid arthritis. The synovial proliferation causes changes in tendons, of both an ischemic and inflammatory nature, which make them susceptible to weakening and eventual rupture and dysfunction. 

Symptoms Three distinct areas of the wrist can be the source of symptoms from rheumatoid disease: the distal radioulnar joint, the radiocarpal joint, and the extensor tendons. However, symptoms

can originate as far proximal as the cervical spine or involve the shoulder and the elbow. Joint-related symptoms in early disease include swelling and pain, with morning stiffness as a classic characteristic. Loss of motion in the early stages usually results from synovial hypertrophy and pain. Progressive loss of motion is seen with disease progression and represents articular destruction. The distal radioulnar joint can be painful because of inflammation within the joint, and it can be a source of decreased forearm rotation (Figs. 41.1 and 41.2). Later stages of the disease usually are manifested with complaints of severe pain, decreased motion, aesthetic appearance, and difficulties in performing activities of daily living. Erosive changes are more strongly associated with changes in subjective disability than joint space narrowing.10 Tenosynovitis of the tendons traversing the dorsal wrist can often manifest as a painless swelling. Patients with advanced rheumatoid disease in the wrist or those unresponsive to medical management may present with loss of extension of the digits at the metacarpophalangeal joints or with inability to flex the thumb at the interphalangeal articulation. These findings result from extensor digitorum communis tendon ruptures over the dorsal aspect of the wrist or a rupture of the flexor pollicis longus over the volar scaphoid, respectively, as described above. Deformity of the wrist and hand is often the most concerning factor for patients and is attributable to the progressive carpal rotation and translocation discussed earlier, coupled with the extensor tendon imbalance accentuated at the metacarpophalangeal joints of the hand, which causes ulnar drift of the digits. Compensatory ulnar deviation (in response to the

CHAPTER 41  Wrist Rheumatoid Arthritis

radial deviation of the wrist) occurs at the metacarpophalangeal joints, and it can often be the presenting symptom in undiagnosed or untreated patients. Symptoms of median nerve compression and dysfunction (altered or absent sensation primarily in the radially sided digits and night pain and paresthesias in the hand) can be associated with rheumatoid arthritis as well, though the prevalence is likely similar to the general population.11 This is primarily due to hypertrophy of the tenosynovium around the flexor tendons within the confined space of the carpal canal, with resulting compression of the median nerve. Vascular damage of the peripheral nerve (rheumatoid neurop­ athy) may also contribute to symptomatology.12 

221

TABLE 41.1  Larsen Radiographic Staging of Rheumatoid Arthritis Larsen Score

Radiographic Status

0

No changes, normal joint

1

Periarticular swelling, osteoporosis, slight narrowing

2

Erosion and mild joint space narrowing

3

Moderate destructive joint space narrowing

4

End-stage destruction, preservation of articular surface

5

Mutilating disease, destruction of normal articular surfaces

Physical Examination Keeping in mind the three primary locations of rheumatoid involvement in the wrist, careful physical examination can help identify the sources of pain and dysfunction and plan a course of treatment. Swelling around the ulnar styloid and loss of wrist extension secondary to extensor carpi ulnaris subluxation indicate early wrist involvement. Dorsal wrist swelling is commonly present and can be due to radiocarpal synovitis, tenosynovitis, or a combination of the two processes. An inflamed synovial membrane surrounding the radiocarpal joint is usually tender to palpation, but there can be surprisingly little swelling on examination if it is confined only to the dorsal capsule. Swelling that is related to the joint usually does not display movement with passive motion of the digits. However, tenosynovitis which visibly affects the extensors more commonly, is typically painless and nontender, and moves with tendon excursion as the digits are moved. Distal radioulnar joint involvement is confirmed with tenderness to palpation, pain, crepitation, limitation of forearm rotation, and prominence of the ulnar head, indicating subluxation or dislocation. If the ulnar border of the hand and carpus are in straight alignment with the ulna, it is indicative of radial deviation and carpal supination. As mentioned previously, ulnar drift of the digits at the metacarpophalangeal joints often accompanies this. It is important to examine the individual function and integrity of the tendons of the digits, primarily the extensor tendons and flexor pollicis longus tendon, to identify any attritional ruptures that may be present. Examination for provocative signs of carpal tunnel syndrome includes eliciting of a Tinel sign over the carpal canal, reproduction or worsening of numbness in the digits with compression over the proximal edge of the canal at the distal wrist crease (Durkan test), or flexion of the wrist (Phalen test). Abductor pollicis brevis atrophy may be seen in the thenar region of the hand. A careful neurologic examination may detect decreased light touch sensibility in the thumb, index, middle, and radial aspects of the ring finger if there is advanced median nerve dysfunction. Consideration should be given to the possibility of more proximal (cervical spine) causes of symptoms. If there is significant synovitis of the radiocapitellar joint proximally, there can be posterior interosseous nerve dysfunction as well. This is manifested during the wrist and hand examination as the inability to extend the thumb and digits and, to some extent, the wrist. This finding, however, needs to be differentiated from tendon rupture or subluxation at the level of the metacarpophalangeal joints. Checking the tenodesis test of the digits can help differentiate the two separate pathologies. This test involves passively flexing

the wrist and observing for digital extension, which indicates intact extensor tendons. Strength testing may be diminished because of pain from synovitis, muscle atrophy, or the inability to contract a muscle secondary to tendon rupture. 

Functional Limitations Rheumatoid patients often have shoulder, elbow, and hand involvement and an abnormal wrist, which leads to significant limitations in activities of daily living. Because the distal radioulnar joint is important in allowing functional forearm rotation and in helping position the hand in space, advanced synovitis of this joint causing pain and fixed deformity can have a severe impact on a patient’s daily functional activity. Functional difficulties that are commonly experienced by these patients include activities of lifting, carrying, and sustained or repetitive grasp. Whereas a loss of pronation may be compensated for by shoulder abduction and internal rotation, compensating for supination loss is very difficult. This can lead to difficulty in opening doors and turning keys. Simple acts such as receiving change during shopping can be compromised by reduced supination. Furthermore, in patients with shoulder involvement, the freedom of compensatory motion at the shoulder can be severely limited, compounding the functional limitations imposed on the patient’s function by limitation of forearm rotation. 

Diagnostic Studies In patients in whom rheumatoid arthritis is suspected clinically, appropriate diagnostic serologic tests may include rheumatoid factor, antinuclear antibody, HLA-B27, sedimentation rate, and anticitrulline antibody assay. These tests are performed in conjunction with a consultation by a rheumatologist or an internist experienced in the care of rheumatoid disease. Plain radiographs of the wrist that include posterioranterior, lateral, and oblique views allow thorough examination of the radiocarpal, midcarpal, and distal radioulnar joints. Specifically, a supinated oblique view13 should be closely inspected for early changes consistent with rheumatoid synovitis. The earliest changes are symmetric soft tissue swelling and juxta-articular osteopenia. Radiographic staging can be performed as well (Table 41.1).14 Although a majority of patients already have a diagnosis of rheumatoid arthritis when seen by an orthopedic surgeon

222

PART 1  MSK Disorders

A

A

B FIG. 41.3 (A) and (B) Radiographs (of the patient in Fig. 41.2) in early rheumatoid disease of the wrist show bone erosions in areas of synovitis, such as around the ulnar styloid and distal radioulnar joint. There are also early erosive changes in the scapholunate articulation. The soft tissue swelling and deformity around the distal ulna are easily appreciated. These radiographs represent Larsen stage 2 disease.

due to progressively worsening hand deformities, radiographic examination occasionally detects the earliest signs of the disease in areas of the wrist where there is a concentration of synovitis. Wrist pain or swelling can be signs of this synovitis and early rheumatoid changes to the hand and wrist. Radiographic changes include erosions at the base of the ulnar styloid, the sigmoid notch of the distal radius, and the waist of the scaphoid and isolated joint space narrowing of the capitolunate joint seen on the posteroanterior view (Figs. 41.3 and 41.4). Ulnar translocation of the carpus can also be seen on this view. The lateral radiograph can show small bone spikes protruding palmarly, usually from the scaphoid. Late radiographic changes include pancompartmental loss of joint spaces and large subchondral erosions (Fig. 41.5).15 Although radiographic findings may not always correlate well with clinical findings, the information

B FIG. 41.4 (A) As the disease advances, cystic changes in the radioscaphoid articulation, reduction in joint space, and osteophyte formation are clearly seen in this radiograph of stage 3 disease. (B) Radiographic appearance in stage 3 of persistent synovitis around the ulnar head and distal radioulnar joint, which leads to destruction of the ulnar head and osteophyte formation, both of which can contribute to extensor tendon attrition and rupture. There is ulnar translocation of the carpus best appreciated by the ulnar displacement of the lunate.

gained from plain radiographs can be important in influencing which procedures will be of most benefit in patients with poor medical disease control. Significant joint subluxation, bone loss, relative ulnar length, and ulnar translocation can help determine which procedure best serves a patient. Advanced imaging techniques such as magnetic resonance imaging and computed tomography are not usually helpful in evaluation or planning for surgery. Electrodiagnostic studies are recommended if neurologic symptoms are present. 

CHAPTER 41  Wrist Rheumatoid Arthritis

223

Treatment Initial The monitored use of disease-modifying antirheumatic drugs (DMARDs) has dramatically improved control of the disease, especially with early, aggressive treatment. The medical treatment consists of three categories of drugs: nonsteroidal antiinflammatory agents, corticosteroids, and disease-modifying drugs (both nonbiologic [i.e., methotrexate] and biologic [i.e., tumor necrosis factor inhibitors]).4 The details of medical treatment are beyond the scope of this chapter. Management of local disease depends on several factors, such as severity of disease, functional limitations, pain, and cosmetic deformity. The patient’s education, nutrition, and psychological health should be maximized. Acutely painful, inflamed wrists are best managed with rest, immobilization, and oral anti-inflammatory agents. Splints available over-the-counter may be ill-suited for this population of patients because the material cannot mold to altered anatomic contours. In such cases, a custom-made, forearm-based, volar resting splint that holds the wrist in the neutral position will provide support and comfort and is likely to be worn with greater compliance. Splints serve to stabilize joints that are subjected to subluxation forces and to improve grip when it is impaired by pain. However, splinting should be treated as a comfort measure and is not effective for preventing deformity as a result of progression of the disease.16 

A

Rehabilitation

B FIG. 41.5  (A) and (B) In advanced disease (stage 4), there is complete loss of joint space affecting the entire wrist, profuse osteophyte formation best appreciated in the lateral view, and deformation and dorsal dislocation of the ulnar head.

Differential Diagnosis Posttraumatic arthritis Chronic scapholunate advanced collapse Septic arthritis Septic tenosynovitis Wrist instability Carpal tunnel syndrome Gout

Occupational therapy can provide potential pain control measures, activity modification education, custom splinting, and exercises for range of motion, tendon gliding, and strengthening. A home exercise program can be developed to improve function and strength, if the disease is under adequate medical control.16 In patients affected with local tenosynovitis of the extensor aspect and unwilling to have an injection, a trial of iontophoresis may prove beneficial. In patients with large amounts of subcutaneous adipose tissue, iontophoresis may be of limited efficacy in joints or periarticular structures. Studies on the effects of hot and cold in patients with rheumatoid arthritis show benefits in pain, joint stiffness, and strength but do not prove the superiority of one modality over the other.17 Paraffin baths and moist heat packs are used to improve joint motion and pain, allowing improved activity tolerance. The results with paraffin baths are superior when they are combined with exercise programs.18 Hydrotherapy can be an adjunct to many treatment programs, primarily for the purpose of decreasing muscle tension and reducing pain. Physical therapy particularly focusing on shoulder and elbow range of motion to position the hand in space may be of benefit if multiple joints are affected and symptomatic. Improvement of shoulder and elbow function is important because it is difficult to position a hand in space with a painful, stiff joint proximal to it. Potentially the most critical role of rehabilitative therapy is in the postoperative period. It is then that patients particularly require monitored splinting, improvement in range of motion and strength, and edema control. 

224

PART 1  MSK Disorders

Procedures Intra-articular cortisone injections are effective in alleviating wrist pain due to synovitis. Typically all injections around the wrist should be done by aseptic technique with a 25-gauge, 1½-inch needle and a mixture of a steroid preparation, which is injected along with 1% lidocaine. The radiocarpal joint can be injected from the dorsal aspect approximately 1 cm distal to Lister tubercle, with the needle angled proximally about 10 degrees to account for the slight volar tilt of the distal radius articular surface. This is done with the wrist in the neutral position. Gentle longitudinal traction by an assistant can help widen the joint space, which may be reduced on account of the disease. An alternative radiocarpal injection site is the ulnar wrist, just dorsal or volar to the easily palpable extensor carpi ulnaris tendon at the level of the ulnar styloid process. The needle must be angled proximally by 20 to 30 degrees to enter the space between the ulnar carpus and the head of the ulna. It is important to ascertain that the injectate flows freely. Any resistance indicates a need to reposition the needle appropriately. Alternatively the injection may be performed with imaging guidance such as a mini image intensifier or ultrasound, if available in the office. If a midcarpal injection is required, this is done through the dorsal aspect, under fluoroscopic guidance, with injection into the space at the center of the lunatetriquetrum-hamate-capitate region. Injections into the carpal tunnel are usually performed at the level of the distal wrist crease with the needle introduced just ulnar to the palmaris longus, which in most patients is just palmar to the median nerve and therefore protects it at this level. In patients who do not display clinical evidence of a palmaris longus, carpal tunnel injections are not recommended. To treat associated carpal tunnel syndrome, patients should be issued a splint that maintains the wrist in the neutral position, primarily for nighttime use. Steroid injection into the carpal canal is an option, but the risks of possible attritional tendon rupture need to be discussed with the patient. Thorough knowledge of local anatomy is essential before an injection into the carpal tunnel is attempted. More important, alteration of local anatomy (and therefore altered location of the median nerve) must be considered very carefully before a carpal tunnel injection in patients with rheumatoid arthritis. Patients must be counseled about the postinjection period. It is not uncommon for patients to experience some increase in local discomfort for 24 to 36 hours after the injection. Use

of the splint is recommended during this time, and icing of the area may also be of benefit. In our experience, most steroid injections take a few days to have a therapeutic effect. Because of the deleterious effect that corticosteroids can have on articular cartilage by transient inhibition of chondrocyte synthesis, repeated intra-articular injections should be minimized if there is no radiographic sign of advanced cartilage wear. Contrary to popularly held misconceptions, there is no published data limiting the number of steroid injections. On the other hand, in advanced disease, when joint surgery in inevitable, there is no contraindication to repeat injections that have proved beneficial to a patient. 

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery The indications for operative treatment of the rheumatoid wrist include one or more of the following: disabling pain and chronic synovitis not relieved by a minimum of 4 to 6 months of adequate medical and nonoperative measures, deformity and instability that limit hand function, tendon rupture, and nerve compression. Deformity alone is rarely an indication for surgery. It is not uncommon to see patients with significant deformities demonstrate excellent function with the use of compensatory maneuvers in the absence of pain. Corrective surgery in these patients is ill-advised. Surgical procedures can be divided into those involving bone and those involving soft tissue (Table 41.2).19 On occasion, a bony procedure will be combined with a soft tissue procedure in the same setting. Synovectomy involves the removal of the inflamed, thickened joint lining from the radiocarpal, and distal radioulnar joints, and is best performed for the painful joint that demonstrates little or no radiographic evidence of joint destruction. Tenosynovectomy involves débridement of the tissue around involved tendons in the hope of avoiding future attritional tendon ruptures. Patients best suited for these procedures have relatively good medical disease control, no fixed joint deformity, and minimal radiographic changes. If tendon rupture has already occurred, most commonly over the distal ulna, the procedure of choice is some form of tendon transfer, usually combined with resection of the ulnar head (Darrach procedure).20 Primary tendon repair is not indicated or possible in most cases because of the poor tissue quality

TABLE 41.2  Wrightington Classification of Rheumatic Disease Wrightington Grade

Radiographic Findings

Surgical Therapy

1

• Preservation of wrist architecture • Periarticular cysts, osteoporosis

Synovectomy

2

• Preservation of radioscaphoid joint • Ulnar translocation, flexion of lunate or scaphoid, or radiolunate joint involvement

Darrach procedure, tendon rebalancing, partial arthrodesis

3

• Preservation of radius architecture • Intracarpal arthritis, radioscaphoid joint arthritis, or volar subluxation of carpus

Arthroplasty versus arthrodesis

4

• Loss of radius bone stock

Arthrodesis

CHAPTER 41  Wrist Rheumatoid Arthritis

and extensive loss of tendon tissue in the zone of rupture. Depending on the number of tendons ruptured, it is possible to transfer the ruptured distal tendon into a neighboring healthier tendon or to transfer a more distant tendon, such as the extensor indicis proprius or superficial flexor tendon, into the affected tendon. Bony procedures include resection arthroplasty, resurfacing arthroplasty, and limited or complete wrist fusions. Resection arthroplasty, such as the Darrach procedure in which the distal ulna is resected, is beneficial in the setting of distal ulnar impingement on the carpus or for distal radioulnar joint disease. It may also prevent tendon rupture of the extensor tendons on the dorsum of the prominent ulnar head. However, in some instances, it may further ulnarly translocate the carpus and therefore should be combined with a radiolunate arthrodesis in patients with weak ligamentous support where this is a concern (see below). An alternate treatment for debilitating distal radio-ulnar joint pain is the Sauve-Kapandji procedure in which the distal ulna is fused to the distal radius, along with a distal ulnar osteotomy. This osteotomy is essentially a resection of a small segment of bone proximal to the fused distal radioulnar joint to construct a “false joint,” or pseudarthrosis, through which the patient may be able to rotate the forearm. Excellent pain relief has been demonstrated in rheumatoid patients with this procedure.21,22 Although this procedure is better at preventing ulnar translocation, nonunion of the arthrodesis site is an issue, particularly in RA patients with poor bone stock. To address the radiocarpal joint two options exist: wrist resurfacing arthroplasty or fusion. The arthroplasty requires the resection of a portion of the distal radius and carpus and insertion of an implant usually made of a metallic component with a polyethylene spacer. It is generally restricted to patients with low functional demands who have bilateral rheumatoid wrist disease and require some motion in one wrist if the other wrist is fused. It is most effective in patients who have good bone stock, relatively good alignment, and intact extensor tendons. The benefits of the arthroplasty include maintenance of range of motion as well as pain relief. Although some studies show promising results with wrist arthroplasty,23–28 other long-term studies show loosening in half to two-thirds of the population29,30 with removal in 25% to 40%. Fusion, or arthrodesis, procedures to eliminate pain due to significantly degenerative joints are well described.31–36 However, depending on the nature of the fusion, these lead to a partial or complete loss of wrist motion. Limited fusions are described of the radiolunate joint or the radioscapholunate joint.37 The potential benefit of limited fusions is some sparing of wrist motion, which can occur through the articulations that remain unfused, and this sparing of some motion can be critical to overall function in this group of patients. In each of these procedures, the midcarpal joint must be well preserved. Total wrist fusion is a reliable, safe, and well-established procedure for relieving pain and providing a stable wrist that improves hand function but without range of motion of the radiocarpal joint.31,32,34 Success rates of 65% to 85% have been shown in terms of eliminating or significantly improving wrist pain.34 For advanced wrist rheumatoid disease, it has become the most common bone procedure. Fusion can be accomplished either with a contoured dorsal plate fixed to the wrist by screws or with one or more large intraosseous pins placed across

225

the wrist (Fig. 41.6). The intraosseous pins are usually placed through the second or third metacarpal or through both, across the wrist into the medullary canal of the radius. Ideally the wrist is fused in slight extension to

A

B FIG. 41.6  (A) and (B) Radiographs depicting a total wrist arthrodesis with use of a contoured plate and screws. Note that the distal end of the ulna has also been excised (Darrach procedure). The polyarthritic nature of the disease process is emphasized by the metacarpophalangeal joint arthroplasties in the fingers and a metacarpophalangeal arthrodesis of the thumb.

226

PART 1  MSK Disorders

allow improved grip strength. However, if both wrists are to be fused, one may consider fusing one in slight flexion and the other in slight extension to allow for functional differences.5 High rates of fusion and a 15% rate of symptomatic hardware removal have been described.31 Consideration of the quality of the overlying soft tissue is necessary when deciding on a fusion technique, as more soft tissue dissection is necessary for the plate and may result in wound complications. If significant median nerve compression exists, an extended open carpal tunnel release is typically performed through a palmar incision. Flexor tenosynovectomy is performed in conjunction with the carpal tunnel release in RA patients, given the high incidence of synovial proliferation, which contributes to median nerve compression.38 

Potential Disease Complications Rheumatoid arthritis is a chronic, progressive disease that can cause significant upper extremity disability at many locations by stiffness or instability from the shoulder to the hand. If wrist involvement becomes advanced, this contributes to problems with motion, pain, stiffness, and nerve compression. Extensor and flexor tendon rupture is a common scenario in rheumatoid disease and can complicate management. During the course of their disease, the majority of patients with rheumatoid disease will lose some functional capacity, and about half will develop disabling disease that requires significant physical dependence on adaptive measures for performance of the activities of daily living. Occupational therapists and social workers play roles in obtaining and using aids and appliances, such as special grips and alterations of household appliances, to maximize the patient’s function. 

Potential Treatment Complications Systemic complications from the medical treatment of rheumatoid arthritis with current DMARDs are beyond the scope of this chapter. Analgesics and nonsteroidal antiinflammatory medications have well-known side effects that can affect the cardiac, gastric, renal, and hepatic systems. Intra-articular corticosteroid injections involve a very small risk of infection as well as cumulative cartilage injury from repeated exposure to steroid. Surgical complications can result from wound healing problems, infection, neurovascular injury, recurrent synovitis, recurrent tendon rupture, persistent joint instability, and implant loosening or failure. To some extent, meticulous surgical technique and judicious management of medications affecting wound healing and immunity, such as methotrexate and systemic steroids, may reduce the frequency of complications.

References 1. Hämäläinen M, Kammonen M, Lehtimäki M, et al. Epidemiology of wrist involvement in rheumatoid arthritis. Rheumatology. 1992;17:1–7. 2. Lee SK, Hausman MR. Management of the distal radioulnar joint in rheumatoid arthritis. Hand Clin. 2005;21:577–589. 3. Papp SR, Athwal GS, Pichora DR. The rheumatoid wrist. J Am Acad Orthop Surg. 2006;14:65–77. 4. Chung k, Pushman G. Current concepts in the management of rheumatoid hand. J Hand Surg. 2011;36A:736–747.

5. Trieb K. Treatment of the wrist in rheumatoid arthritis. J Hand Surg. 2008;33A:113–123. 6. Bäckdahl M. The caput ulnae syndrome in rheumatoid arthritis. A study of morphology, abnormal anatomy and clinical picture. Acta Rheumatol Scand Suppl. 1963;5:1–75. 7. Hsueh JH, Liu WC, Yang KC, et al. Spontaneous extensor tendon rupture in the rheumatoid wrist: risk factors and preventative role of extended tenosynovectomy. Ann Plast Surg. 2016;76:S41–S47. 8. Vaughan-Jackson OJ. Rupture of extensor tendons by attrition at the inferior radio-ulnar joint: report of two cases. J Bone Joint Surg Br. 1948;30:528–530. 9. Mannerfelt L, Norman O. Attrition ruptures of flexor tendons in rheumatoid arthritis caused by bony spurs in the carpal tunnel: a clinical and radiological study. J Bone Joint Surg Br. 1969;51:270–277. 10. Koevoets R, Dirven L, Klarenbeek NB, et al. Insights in the relationship of joint space narrowing versus erosive joint damage and physical functioning of patients with RA. Ann Rheum Dis. 2012;30. 11. Sakthiswary R, Singh R. Has the median nerve involvement in rheumatoid arthritis been overemphasized? Rev Bras Reumatol. 2016. https://doi.org/10.1016/j.rbr.2016.07.002. 12. Muramatsu K, Tanaka H, Taguchi T. Peripheral neuropathies of the forearm and hand in rheumatoid arthritis: diagnosis and options for treatment. Rheumatol Int. 2008;28:951–957. 13. Nørgaard F. Earliest roentgenological changes in polyarthritis of the rheumatoid type: rheumatoid arthritis. Radiology. 1965;85:325–329. 14. Larsen A, Dale K, Eek M, et al. Radiographic evaluation of rheumatoid arthritis by standard reference films. J Hand Surg Am. 1983;8:667–669. 15. Resnick D. Rheumatoid arthritis of the wrist: the compartmental approach. Med Radiogr Photogr. 1976;52:50–88. 16. Heine PJ, Williams MA, Williamson E, et al. Development and delivery of an exercise intervention for rheumatoid arthritis; strengthening and stretching for rheumatoid arthritis of the hand (SARAH) trial. Physiotherapy. 2012;90(2):121–130. 17. Adams J, Burridge J, Mullee M, Hammond A, Cooper C. The clinical effectiveness of static resting splints in early rheumatoid arthritis: a randomized controlled trial. Rheumatology. 2008;47:1548–1553. 18. Michlovitz SL. The use of heat and cold in the management of rheumatic diseases. In: Michlovitz S, ed. Thermal Agents in Rehabilitation. 2nd ed. Philadelphia: FA Davis; 1990:158–174. 19. Hodgson SP, Stanley JK, Muirhead A. The Wrightington classification of rheumatoid wrist X-rays: a guide to surgical management. J Hand Surg Br. 1989;14:451–455. 20. Darrach W. Partial excision of lower shaft of ulnar for deformity following Colle’s fracture. Ann Surg. 1913;57:764–765. 21. Vincent KA, Szabo RM, Agee JM. The Sauvé-Kapandji procedure for reconstruction of the rheumatoid distal radioulnar joint. J Hand Surg Am. 1993;18:978–983. 22. Fujita S, Masada K, Takeuchi E, et al. Modified Sauvé-Kapandji procedure for disorders of the distal radioulnar joint in patients with rheumatoid arthritis. J Bone Joint Surg Am. 2005;87:134–139. 23. Cobb TK, Beckenbaugh RD. Biaxial total-wrist arthroplasty. J Hand Surg Am. 1996;21:1011–1021. 24. Bosco JA, Bynum DK, Bowers WH. Long-term outcome of Volz total wrist arthroplasties. J Arthroplasty. 1994;9:25–31. 25. Anderson MC, Adams BD. Total wrist arthroplasty. Hand Clin. 2005;21:621–630. 26. Nydick JA, Greenberg SM, Stone JD, Williams B, Polikandriotis JA, Hess AV. Clinical outcomes of total wrist arthroplasty. J Hand Surg. 2012;37A:1580–1584. 27. Ferreres A, Lluch A, del Valle M. Universal total wrist arthroplasy: midterm follow-up study. J Hand Surg. 2011;36A:967–973. 28. Badge R, Kailash K, Dickson DR, et al. Medium-term outcomes of the Universal-2 total wrist arthroplasty in patients with rheumatoid arthritis. Bone Joint J. 2016;98:1642–1647. 29. Ward C, Kuhl T, Adams BD. Five to ten year outcomes of the Universal total wrist arthroplasty in patients with rheumatoid arthritis. J Bone Joint Surg. 2011;93A:914–919. 30. van Harlingen D, Heesterbeek PJC, de Vos MJ. High rate of complications and radiographic loosening of the biaxial total wrist arthroplasty in rheumatoid arthritis. Acta Orthopaedica. 2011;82:721–726. 31. Barbier O, Saels P, Rombouts JJ, et al. Long-term functional results of wrist arthrodesis in rheumatoid arthritis. J Hand Surg Br. 1999;24:27–31. 32. Jebson PJ, Adams BD. Wrist arthrodesis: review of current technique. J Am Acad Orthop Surg. 2001;9:53–60.

CHAPTER 41  Wrist Rheumatoid Arthritis

33. Meads BM, Scougall PJ, Hargreaves IC. Wrist arthrodesis using a Synthes wrist fusion plate. J Hand Surg Br. 2003;28:571–574. 34. Ishikawa H, Murasawa A, Nakazono K. Long-term follow-up study of radiocarpal arthrodesis for the rheumatoid wrist. J Hand Surg Am. 2005;30:658–666. 35. Solem H, Berg NJ, Finsen V. Long term results of arthrodesis of the wrist: a 6-15 year follow up of 35 patients. Scand J Plast Reconstr Surg Hand Surg. 2006;40:175–178.

227

36. Rauhaniemi J, Tiusanen H, Sipola E. Total wrist fusion: a study of 115 patients. J Hand Surg Br. 2005;30:217–219. 37. Motomiya M, Iwasaki N, Minami A, et al. Clinical and radiological results of radiolunate arthrodesis for rheumatoid arthritis: 22 wrist followed for an average of 7 years. J Hand Surg Am. 2013;38:1484–1491. 38. Muramatsu K, Tanaka H, Taguchi T. Peripheral neuropathies of the forearm and hand in rheumatoid arthritis: diagnosis and options for treatment. Rheumatol Int. 2008;28:951–957.

SECTION V

Mid Back

CHAPTER 42

Thoracic Compression Fracture Toni J. Hanson, MD

Synonyms Thoracic compression fracture Dorsal compression fracture Wedge compression Vertebral crush fracture

ICD-10 Codes M84.40 S22.009

Pathological fracture, unspecified site Unspecified fracture of unspecified thoracic vertebra Add seventh character (A—initial encounter closed fracture, B—initial encounter open fracture, D—subsequent encounter fracture with routine healing, G—subsequent encounter fracture with delayed healing, K—subsequent encounter fracture with nonunion, S—sequela)

Definition A compression fracture is caused by forces transmitted along the vertebral body. The ligaments are intact, and compression fractures are usually stable (Fig. 42.1).1 Compression fractures in the thoracic vertebrae are commonly seen in osteoporosis with decreased bone mineral density. They may be asymptomatic and diagnosed incidentally on radiography. Such fractures may occur with trivial trauma and are usually stable.2,3 Pathologic vertebral fractures may occur with metastatic cancer (commonly from lung, breast, or prostate), as well as with other processes affecting vertebrae. Trauma, such as a fall from a height or a motor vehicle accident, can also result in thoracic compression fracture. Considerable force is required to fracture healthy vertebrae, which are resistant to compression. In such cases, the force required to produce 228

a fracture may cause extension of fracture components into the spinal canal with neurologic findings. There may be evidence of additional trauma, such as calcaneal fractures from a fall. Multiple thoracic compression fractures, as seen with osteoporosis, can produce a kyphotic deformity.4–6 An estimated 1.5 million vertebral compression fractures occur annually in the United States, with 25% of postmenopausal women affected in their lifetime. Estimates indicate that there are 44 million persons with osteoporosis and 34 million with low bone mass in the United States.7 Existence of vertebral compression fracture increases the risk of future vertebral compression fractures (with one fracture, there is a 5-fold increase; with two or more fractures, there is a 12-fold increase).8 

Symptoms Pain in the thoracic spine over the affected vertebrae is the usual hallmark of the presentation. It may be severe, sharp, exacerbated with movement, and decreased with rest. Severe pain may last 2 to 3 weeks and then decrease during 6 to 8 weeks, but pain may persist for months. Acute fractures in osteoporosis, however, may result in little discomfort or poor localization.9 In osteoporotic fractures, the mid and lower thoracic vertebrae are typically affected. A good history and physical examination are essential, as there may be indicators of a more ominous underlying pathologic process.10,11 

Physical Examination Tenderness with palpation or percussion over the affected region of the thoracic vertebrae is the primary finding on physical examination. Spinal movements also produce pain. Kyphotic deformity, loss of height, and impingement of the lower ribs on the superior iliac crest may be present in the patient who has had multiple prior compression fractures. Neurologic examination below the level of the fracture is recommended to assess for presence of reflex

CHAPTER 42  Thoracic Compression Fracture

229

resonance imaging, may also elucidate further detail (see Fig. 42.2B).16 Percutaneous needle biopsy of the affected vertebral body can be helpful diagnostically in selected cases. Laboratory tests are obtained as appropriate. These include a complete blood count and sedimentation rate or C-reactive protein level (which are nonspecific but sensitive indicators of an occult infection or inflammatory disease). Serum alkaline phosphatase, serum and urine protein electrophoresis, and other laboratory tests are beneficial when a malignant neoplasm is suspected. Diagnostic testing is directed, as appropriate, on the basis of the entire clinical presentation, including secondary causes of osteoporosis. Bone densitometry can be performed when the patient is improved clinically.  Differential Diagnosis

FIG. 42.1  Thoracic compression fracture with reduction in anterior vertebral height and wedging of the vertebrae.

changes, pathologic reflexes such as Babinski sign, and sensory alterations. Sacral segments can be assessed through evaluation of rectal tone, volitional sphincter control, anal wink, and pinprick if there is concern about bowel and bladder function.12 It is also important to assess the patient’s gait for stability. Comorbid neurologic and orthopedic conditions may contribute to gait dysfunction and fall risk.13,14 

Functional Limitations Functional limitations in a patient with an acute painful thoracic compression fracture can be significant. The patient may experience loss of mobility and independence in activities of daily living and household activities, and there may be an impact on social, avocational, vocational, and psychological functioning. In patients with severe symptoms, hospitalization may be necessary.15 

Diagnostic Testing Anteroposterior and lateral radiographs of the thoracic spine can confirm the clinical impression of a thoracic compression fracture. On radiographic examination in a thoracic compression fracture, the height of the affected vertebrae is reduced, generally in a wedge-shaped fashion, with anterior height less than posterior vertebral height. In osteoporosis, biconcave deformities can also be noted on spinal radiographs (Fig. 42.2A). A bone scan may help localize (but not necessarily determine the etiology of) processes such as metastatic cancer, occult fracture, and infection. Spinal imaging, such as computed tomography or magnetic

Thoracic sprain Thoracic radiculopathy Thoracic disc herniation Metastatic malignant disease Primary spine malignant neoplasm (uncommon, most frequently multiple myeloma)17 Benign spinal tumors Infection, osteomyelitis (rare)18 Inflammatory arthritis Musculoskeletal pain, other Referred pain (pancreatic cancer, abdominal aortic aneurysm)

Treatment Initial Initial treatment consists of activity modification, including limited bed rest. Cushioning with use of a mattress overlay (such as an egg crate) can also be helpful. Bed rest should be limited to only a few days to prevent vascular, cardiopulmonary, and cutaneous complications, and to avoid further bone loss, deconditioning, and functional decline. Proper transitional body mechanics with use of a spinal orthotic to minimize spinal stress and pain is recommended. Pharmacologic agents, including oral analgesics, muscle relaxants, and anti-inflammatory medications, as appropriate to the patient, are helpful. Agents such as tramadol 50 mg (one or two every 4 to 6 hours, not exceeding eight per day), acetaminophen 300 mg/codeine 30 mg (one or two every 4 to 6 hours), and controlled-release oxycodone CR (10 or 20 mg every 12 hours) may be considered. Acetaminophen dose should not exceed 3 g/day. Muscle relaxants such as cyclobenzaprine, 10 mg three times daily, may be helpful initially with muscle spasm. A variety of nonsteroidal anti-inflammatory drugs, including celecoxib (Celebrex, a cyclooxygenase 2 inhibitor), can be considered, depending on the patient. Calcitonin (one spray daily, alternating nostrils, providing 200 IU per spray) has also been used for painful osteoporotic fractures.19 Stool softeners and laxatives may be necessary to reduce strain with bowel movements and constipation, particularly with narcotic analgesics. Selection of pharmacologic agents must factor in the age, comorbidities, and clinical status of the patient.

230

PART 1  MSK Disorders

C

A

B FIG. 42.2  (A) Anteroposterior and lateral radiographs demonstrating thoracic compression fracture (arrow). (B) Magnetic resonance images demonstrating T1 (left) and T2 (right) appearance of a thoracic compression fracture. (C) Anteroposterior and lateral radiographs demonstrating appearance of vertebrae after vertebroplasty. (Courtesy Kent R. Theilen, MD, Mayo Clinic, Rochester, Minnesota.)

Avoidance of spinal motion, especially flexion, by appropriate body mechanics (such as log rolling in bed) and spinal bracing is helpful. There are a variety of spinal orthoses that reduce spinal flexion (Fig. 42.3). They must be properly fitted.20,21 A lumbosacral orthosis may be sufficient for a low thoracic fracture. A thoracolumbosacral orthosis is used frequently (see Fig. 42.3A–D). If a greater degree of fracture immobilization is required, an off-the-shelf orthosis (see Fig. 42.3E) or a custom-molded body jacket may be fitted by an orthotist. Proper diagnosis and treatment of underlying contributors to the thoracic compression fracture are necessary.22,23 Most thoracic compression fractures will heal with symptomatic improvement in 4 to 6 weeks.24,25 

Rehabilitation Physical therapy is helpful to assist with gentle mobilization of the patient by employing proper body mechanics, optimizing transfer techniques, and training with gait aids (such as a wheeled walker) to reduce biomechanical stresses on the spine and to ensure gait safety.26 Pain-relieving modalities, such as therapeutic heat or cold, and transcutaneous

electrical stimulation may also be employed. Exercise should not increase spinal symptoms and should be implemented at the appropriate juncture. In addition to proper body mechanics and postural training emphasizing spinal extension and avoidance of flexion, spinal extensor muscle strengthening, limb muscle strengthening, stretching to muscle groups (such as the chest, hips, and lower extremity muscles), and deep breathing exercises may also be indicated. Weight-bearing exercises for bone health, balance, and fall prevention are also important.27 Proper footwear, with cushioning inserts, can also be helpful. Occupational therapy can help the patient with activities of daily living, reinforce proper spinal ergonomics, address equipment needs, and prevent falls. Successful rehabilitation is targeted at increasing the patient’s comfort, decreasing deformity, and decreasing resultant disability and is individualized to address specific patient needs.28–30 

Procedures Invasive procedures are generally not necessary. Percutaneous vertebroplasty or kyphoplasty with use of polymethyl methacrylate may be helpful to reduce fracture pain, to

CHAPTER 42  Thoracic Compression Fracture

C

B

A

D

231

E

FIG. 42.3  (A) Cruciform anterior spinal hyperextension brace (to limit flexion). (B) Three-point sagittal hyperextension brace (to limit flexion). (C) Thoracolumbosacral orthosis, anterior view. (D) Thoracolumbosacral orthosis, posterior view. (E) Off-the-shelf molded spinal orthosis with Velcro closures.

reinforce thoracic vertebral strength, and to improve function; with kyphoplasty, some potential restoration of vertebral height has been reported (see Fig. 42.2C).26,31 Patients with imaging evidence of an acute or a subacute thoracic fracture who have correlating pain, who fail to

improve with conservative management, and who are without contraindications may be candidates for such interventional procedures.32,33 In two randomized controlled trials, no beneficial effect was noted in vertebroplasty versus sham.32,34

232

PART 1  MSK Disorders

A

B

C FIG. 42.4  (A) and (B) Magnetic resonance imaging demonstrating sagittal T1 and sagittal STIR appearance of a thoracic compression fracture. (C) Computed tomography fluoroscopic guided thoracic facet injection (axial thoracic image).

Structural changes in the vertebral body with compression fractures can alter biomechanical forces on the associated facet joints (Fig. 42.4A and B).35 Bilateral fluoroscopically guided intraarticular facet joint injections performed in the superior and inferior thoracic facets (see Fig. 42.4C) can be helpful. Facet joint medical branch blocks and radiofrequency ablation procedures can also be beneficial for facet mediated pain in thoracic spinal compression fractures. 

Technologies and Devices There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery Surgery is rarely necessary. Surgical stabilization can be considered in patients with continued severe pain after compression fracture as a result of nonunion of the fracture, in patients with spinal instability, or if neurologic complications occur. Referral to a spine surgeon is recommended in these cases for further assessment.36 

Potential Disease Complications Neurologic complications, including nerve or spinal cord compromise, as well as orthopedic complications with continued pain, nonunion, and instability can occur. Underlying

CHAPTER 42  Thoracic Compression Fracture

primary disease (e.g., metastatic thoracic compression) needs to be addressed. Patients with severe kyphosis may experience cardiopulmonary dysfunction. Severe kyphosis may also result in rib impingement on the iliac bones, producing further symptoms. Severe pain accompanying a fracture may further limit deep breathing and increase the risk of pulmonary complications, such as pneumonia. Progressive spinal deformity may produce secondary pain generators. The patient may have progressive levels of dependency as a result. 

Potential Treatment Complications Side effects with medications, particularly nonsteroidal anti-inflammatory drugs as well as narcotic medications, can occur. It is important to select medications appropriate for individual patients.37 There may be difficulty with the use of spinal orthotics, such as intolerance in patients with gastroesophageal reflux disease. Kyphotic patients frequently do not tolerate orthoses, and fitting is a problem. Complications of vertebroplasty or kyphoplasty can include infection, bleeding, fracture (in the treated or adjacent vertebrae), and systemic issues such as embolism. Cement leaks into surrounding tissues with spinal cord, spinal nerve, or vascular compression can occur.38 Surgery can result in many complications, not only from general anesthesia risks but also from infection, bleeding, or thromboembolism. Poor mechanical strength of bone, as in osteoporosis with paucity of dense lamellar and cortical bone, may result in suboptimal surgical outcome.

Acknowledgments The author thanks Dr. Kent Thielen and Dr. Timothy Maus for the interventional radiology case studies, Sara Harstad for orthotic modeling, and Pamela Harders for secretarial support.

References 1. Bezel E, Stillerman C. The Thoracic Spine. St. Louis: Quality Medical Publishers; 1999:20. 2. Toh E, Yerby S, Bay B. The behavior of thoracic trabecular bone during flexion. J Exp Clin Med. 2005;30:163–170. 3. Toyone T, Tanaka T, Wada Y, Kamikawa K. Changes in vertebral wedging rate between supine and standing position and its association with back pain: a prospective study in patients with osteoporotic vertebral compression fractures. Spine. 2006;31:2963–2966. 4. Kesson M, Atkins E. The thoracic spine. In: Kesson M, Atkins E, eds. Orthopaedic Medicine: a Practical Approach. Boston: ButterworthHeinemann; 1998:262–281. 5. McRae R. The thoracic and lumbar spine. In: Parkinson M, ed. Pocketbook of Orthopaedics and Fractures. vol. 1. London: Churchill Livingstone/Harcourt; 1999:79–105. 6. Dandy D, Edwards D. Disorders of the spine. In: Dandy D, Edwards D, eds. Essential Orthopaedics and Trauma. New York: Churchill Livingstone; 1998:431–451. 7. Qaseem A, Snow V, Shekelle P, et al. Pharmacologic treatment of low bone density or osteoporosis to prevent fractures: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2008;149:404–415. 8. Marshall D, Johnell O, Wedel H. Meta-analysis of how well measures of bone mineral density predict occurrence of osteoporotic fractures. BMJ. 1996;18:1254–1259. 9. Bonner F, Chesnut C, Fitzsimmons A, Lindsay R. Osteoporosis. In: DeLisa J, Gans BM, eds. Rehabilitation Medicine: Principles and Practice. 3rd ed. Philadelphia: Lippincott-Raven; 1998:1453–1475. 10. Van de Velde T. Disorders of the thoracic spine: non-disc lesions. In: Ombregt L, ed. A System of Orthopaedic Medicine. Philadelphia: WB Saunders; 1995:455–469.

233

11. Errico T, Stecker S, Kostuik J. Thoracic pain syndromes. In: Frymoyer J, ed. The Adult Spine: Principles and Practices. 2nd ed. Philadelphia: Lippincott-Raven; 1997:1623–1637. 12. Huston C, Pitt D, Lane C. Strategies for treating osteoporosis and its neurologic complications. Appl Neurol. 2005;1. 13. Hu S, Carlson G, Tribus C. Disorders, diseases, and injuries of the spine. In: Skinner H, ed. Current Diagnosis and Treatment in Orthopedics. 2nd ed. New York: Lane Medical Books/McGraw-Hill; 2000:177–246. 14. Pattavina C. Diagnostic imaging. In: Hart R, ed. Handbook of Orthopaedic Emergencies. Philadelphia: Lippincott-Raven; 1999:32–47, 116– 126; 127–140. 15. Goldstein T. Treatment of common problems of the spine. In: Goldstein T, ed. Geriatric Orthopaedics: Rehabilitative Management of Common Problems. 2nd ed. Gaithersburg, Md: Aspen Publications; 1999:211–232. 16. Bisese J. Compression fracture secondary to underlying metastasis. In: Bolger E, Ramos-Englis M, eds. Spinal MRI: a Teaching File Approach. New York: McGraw-Hill; 1992:73–129. 17. Heller J, Pedlow F. Tumors of the spine. In: Garfin S, Vaccaro AR, eds. Orthopaedic Knowledge Update. Spine. Rosemont, Ill: American Academy of Orthopaedic Surgeons; 1997:235–256. 18. Levine M, Heller J. Spinal infections. In: Garfin S, Vaccaro A, eds. Orthopaedic Knowledge Update. Spine. Rosemont, Ill: American Academy of Orthopaedic Surgeons; 1997:257–271. 19. Kim D, Vaccaro A. Osteoporotic compression fractures of the spine; current options and considerations for treatment. Spine. 2006;6:479–487. 20. Saunders H. Spinal orthotics. In: Saunders R, ed. Evaluation, Treatment and Prevention of Musculoskeletal Disorders. vol. 1. Bloomington, Minn: Educational Opportunities; 1993:285–296. 21. Bussel M, Merritt J, Fenwick L. Spinal orthoses. In: Redford J, ed. Orthotics Clinical Practice and Rehabilitation Technology. New York: Churchill Livingstone; 1995:71–101. 22. Khosla S, Bilezikian J, Dempster D, et al. Benefits and risks of bisphosphonate therapy for osteoporosis. J Clin Endocrinol Metab. 2012;97:2272–2282. 23. Mura M, Drake M, Mullan R, et al. Clinical review. Comparative effectiveness of drug treatments to prevent fragility fractures: a systematic review and network meta-analysis. J Clin Endocrinol Metab. 2012;97:1871–1880. 24. Brunton S, Carmichael B, Gold D. Vertebral compression fractures in primary care. J Fam Pract. 2005;54:781–788. 25. Old J, Calvert M. Vertebral compression fractures in the elderly. Am Fam Physician. 2004;69:111–116. 26. Rehabilitation of Patients With Osteoporosis-Related Fractures. Washington, DC: National Osteoporosis Foundation; 2003:4. 27. Sinaki M. Critical appraisal of physical rehabilitation measures after osteoporosis vertebral fracture. Osteoporos Int. 2003;14:773–779. 28. Browngoehl L. Osteoporosis. In: Grabois M, Garrison SJ, Hart KA, Lehmkuhl LD, eds. Physical Medicine and rehabilitation: the Complete Approach. Malden, Mass: Blackwell Science; 2000:1565–1577. 29. Eilbert W. Long-term care and rehabilitation of orthopaedic injuries. In: Hart R, Rittenberry TJ, Uehara DT, eds. Handbook of Orthopaedic Emergencies. Philadelphia: Lippincott-Raven; 1999:127–138. 30. Barr J, Barr M, Lemley T, McCann R. Percutaneous vertebroplasty for pain relief and spinal stabilization. Spine. 2000;25:923–928. 31. Kostuik J, Heggeness M. Surgery of the osteoporotic spine. In: Frymoyer J, ed. The Adult Spine: Principles and Practice. 2nd ed. Philadelphia: Lippincott-Raven; 1997:1639–1664. 32. Kallmes D, Comstock B, Heagerty P, et al. A randomized controlled trial of vertebroplasty for osteoporotic spine fractures. N Engl J Med. 2009;361:569–579. 33. Rad A, Gray L, Sinaki M, Kallmes D. Role of physical activity in new onset fractures after percutaneous vertebroplasty. Acta Radiol. 2011;52:1020–1023. 34. Buchbinder R, Osborne R, Ebeling P, et al. A randomized trial of vertebroplasty for painful osteoporotic vertebral fractures. N Engl J Med. 2009;361:557–568. 35. Mitra R, Huy D, Alamin T, Cheng I. Facet pain in thoracic compression fractures. Pain Med. 2010;11(11):1674–1677. 36. McCarthy J, Davis A. Diagnosis and management of vertebral compression fractures. Am Fam Physician. 2016;94(1):44–50. 37. Snell E, Scarpone M. Orthopaedic issues in aging. In: Baratz M, Watson AD, Imbriglia JE, eds. Orthopaedic Surgery: the Essentials. New York: Thieme; 1999:865–870. 38. Khosla A, Diehn F, Rad A, Kallmes D. Neither subendplate cement deposition nor cement leakage into the disk space during vertebroplasty significantly affects patient outcomes. Radiology. 2012;264:180–186.

CHAPTER 43

Thoracic Radiculopathy Darren C. Rosenberg, DO Daniel C. Pimentel, MD, PhD

Synonyms Thoracic radiculitis Thoracic disc herniation

ICD-10 Code M54.14

Radiculopathy, thoracic region

radiculopathy is neoplastic compression. Primary spine tumors are rare, although the spine is a frequent metastasis site (4% to 15%) of primary solid tumors, such as breast, lung, and prostate cancer.6 Regarding spine metastasis, the thoracic spine is the most commonly affected (70%), followed by lumbar (20%) and cervical (10%).7 Finally, other less common causes that may lead to thoracic radiculopathy include scoliosis, inflammation induced by herpes zoster, and tuberculosis.5 

Symptoms Definition Thoracic radiculopathy is a painful syndrome caused by mechanical compression, chemical irritation, or metabolic abnormalities of a thoracic spinal nerve root. Thoracic disc herniations are estimated to occur in approximately 12% to 37% of the population and are more often asymptomatic. Its incidence is equal between men and women.1,2 It accounts for less than 2% of all spinal disc surgeries and 0.15% to 4% of all symptomatic spinal disc herniations.3 The majority of thoracic disc herniations (35%) occur between the levels of T8 and T12, with a peak (20%) at T11-T12. Most patients (90%) present clinically between the fourth and seventh decades of life; 33% present between the ages of 40 and 49 years. Approximately 33% of thoracic disc protrusions are lateral, preferentially encroaching on the spinal nerve root. The remainder are central or central lateral, resulting primarily in various degrees of spinal cord compression. Synovial cysts, although rare in the thoracic spine (0.06% of patients requiring decompressive surgery), may also be responsible for foraminal encroachment. These tend to be more common at the lower thoracic levels.4 Natural degenerative forces and trauma are generally thought to be the most important factors in the etiology of mechanical thoracic radiculopathy. Foraminal stenosis from bone encroachment may also cause compression of the exiting nerve root and radicular symptoms. The most common cause of thoracic radiculopathy is a metabolic condition: diabetes mellitus. It often results in multilevel disease.4,5 This may occur at any age but often appears with other neuropathic symptoms due to injury to the blood supply to the nerve root. Another etiology that should be considered a possible cause of thoracic 234

Most patients (67%) present with complaints of “band-like” chest pain (Fig. 43.1). The second most common symptom (16%) is lower extremity pain.8 Injury to nerve roots T2-3 may be manifested as axillary or midscapular pain. Injury to nerve roots T7-T12 may be manifested as vague and poorly localized abdominal pain.9 Abdominal wall bulging due to weakness of local muscles may also suggest thoracic radiculopathy.10 Less common symptoms such as mastalgia can occur due to thoracic radiculopathy.11 Unlike thoracic radiculopathy, spinal cord compression produces upper motor neuron signs and symptoms consistent with myelopathy. Therefore examiners should pay close attention to the presence of motor impairment, hyperreflexia and spasticity, sensory impairment, and bowel and bladder dysfunction. The last may be caused by T11-T12 lesions damaging the conus medullaris or cauda equina.12 Thus in thoracic radiculopathy, pain—localized, axial, or radicular—is the primary complaint in 76% of patients. It is also important to include in the history any trauma (present in 37% of patients)13 or risk factors for non-neurologic causes of chest wall or abdominal pain. Thoracic compression fractures that may mimic the symptoms of thoracic radiculopathy may be seen in young people with acute trauma, particularly falls, regardless of whether they land on their feet. In older people (particularly women with a history of osteopenia or osteoporosis) or in individuals who have prolonged history of steroid use, a compression fracture should be considered. Because thoracic radiculopathy is not common, it is important in nontraumatic cases to be suspicious of more serious pathologic processes, such as infection or cancer. Therefore a history of weight loss, decreased appetite, immunosuppressive factors, fever, chills, or previous malignant disease should be elicited.14,15 

CHAPTER 43  Thoracic Radiculopathy

235

cardiopulmonary system, abdominal organs, and skin should be performed, particularly in individuals who have sustained trauma or relevant comorbidities. 

Functional Limitations The pain produced by thoracic radiculopathy often limits an individual’s movement and activity. Patients may be limited in activities such as dressing and bathing and other activities that include trunk movements, such as putting on shoes. Work activities may be restricted, such as lifting, climbing, and stooping. Even sedentary workers may be so uncomfortable that they are not able to perform their jobs. Anorexia may result from pain in the abdominal region. 

Diagnostic Studies

FIG. 43.1  Typical pain pattern in a thoracic radiculopathy.

Physical Examination The physical examination may show only limitations of range of motion—particularly trunk rotation, flexion, and extension—generally due to pain. In traumatic cases, location of ecchymosis or abrasions should be noted. Range of motion testing should not be done repeatedly if an acute spinal fracture is suspected. Careful palpation for tenderness over the thoracic spinous and transverse processes, as well as over the ribs and intercostal spaces, is critical in localizing the involved level. Pain with percussion over the vertebral bodies should alert the clinician to the possibility of a vertebral fracture. On the other hand, uncommon symptoms in the lower limbs, such as pain, reflex changes, spasticity, and weakness, can be a result of spinal cord compression by thoracic disc herniation,17 although this phenomenon is seldom observed. Physical examination in diagnosis of thoracic radiculop­ athy has a modest accuracy and reliability because there is difficulty in testing strength of possibly affected muscles (such as paraspinal, intercostal, and abdominal muscles) in isolation,18 although it is crucial for ruling out other possible causes of pain or neurologic abnormalities. In addition, sensation may be abnormal in a dermatomal pattern. This will direct the examiner to more closely evaluate the involved level. Any abnormalities of the spine should be noted, including scoliosis, which is best detected when the patient flexes forward. A thorough examination of the

Because of the low incidence of thoracic radiculopathy and the possibility of serious disease (e.g., tumor), the clinician should have a low threshold for ordering imaging studies in patients with persistent (more than 2 to 4 weeks) thoracic pain of unknown origin. Magnetic resonance imaging remains the imaging study of choice to evaluate the soft tissue structures of the thoracic spine. Computed tomography and computed tomographic myelography are alternatives if magnetic resonance imaging cannot be obtained. The electromyographic evaluation of thoracic radiculopathy can be challenging because of the limited techniques available and the lack of easily accessible muscles representing a myotomal nerve root distribution. The muscles most commonly tested are the paraspinals, intercostals, and abdominals. The risk of pneumothorax is 8.8% when investigating intercostal nerve conduction, which discourages many practitioners from using the technique.16 The clinician must investigate multiple levels of the thoracic spine to best localize the lesion. Techniques for intercostal somatosensory evoked potentials have also been shown to isolate individual nerve root levels.9 In patients who have sustained trauma, plain radiographs are advised as a primary approach to rule out fractures and spinal instability.  Differential Diagnosis SPINAL DIAGNOSES Compression fracture Malignant neoplasm (primary or metastatic) Pott disease (tuberculosis of the spine) Other infectious causes Spondylosis Spinal stenosis Facet syndrome Degenerative disc disease Disc displacement (bulging, protrusion, herniation) Spine deformities (scoliosis, kyphosis) Herpes zoster  EXTRASPINAL DIAGNOSES Intercostal neuralgia Myofascial trigger point Enthesopathy (ligament or tendon) Costovertebral joint dysfunction Costotransverse ligament sprain

236

PART 1  MSK Disorders

Rib fracture Angina Myocardial infarction Aortic aneurysm Cholecystitis Pyelonephritis Peptic ulcer disease Esophageal disorders Mastalgia Pleuritis Pulmonary embolism Adiposis dolorosa

Treatment Initial Pain control is important early in the disease course. Patients should be advised to avoid activities that cause increased pain and to avoid heavy lifting. Nonsteroidal antiinflammatory drugs are often the first line of treatment and help control pain and inflammation. Oral steroids can be powerful anti-inflammatory medications and are typically used in the acute stages. This is generally done by starting at a moderate to high dose and tapering during several days. For example, a methylprednisolone (Medrol) dose pack is a prepackaged prescription that contains 21 pills. Each pill is 4 mg of Solu-Medrol. The pills are taken during the course of 6 days. On the first day, six tablets are taken, and then the dose is decreased by one pill each day. Both non-narcotic and narcotic analgesics may be used to control pain, as well as muscle relaxants. In subacute or chronic cases, other medications may be tried, such as tricyclic antidepressants and anticonvulsants (e.g., gabapentin and carbamazepine), which have been effective in treating symptoms of neuropathic origin.19,20 Moist heat or ice can be used, as tolerated, for pain. Transcutaneous electrical nerve stimulation units may also help with pain.21 

Rehabilitation Physical therapy can be used initially to assist with pain control. Modalities such as ultrasound and electrical stimulation may reduce pain and improve mobility,22 although no physical modality provides long-term relief or alters the long-term course of the disease.23 The main goal of physical therapy is to progress with spine stabilization exercises, back and abdominal strengthening,24 and a trial of mechanical spine traction.25 Some patients may benefit from a thoracolumbar brace to reduce segmental spine movement,26 although it should be carefully used because of possible postural muscle weakness that can result from long-term use. Conservative management tends to provide significant pain relief and functional improvement in 77% of cases.2 Patients with significant spinal instability documented by imaging studies should be referred to a spine surgeon. In addition, physical therapy should address postural retraining, particularly for individuals with habitually poor posture. Work sites can be evaluated, if indicated. All sedentary workers should be counseled on proper seating, including use of a well-fitting adjustable chair with a lumbar support. More active workers should be advised on

appropriate lifting techniques and avoidance of unnecessary trunk rotation. Finally, physical therapy can focus on improving biomechanical factors that may play a role in abnormal loads on the thoracic spine. These include flexibility exercises for tight hamstring muscles and orthotics for pes planus (flat feet). 

Procedures Transforaminal injections can have both diagnostic and therapeutic purposes.27 They have been shown to significantly reduce radiating pain.28 This is done under fluoroscopic guidance to minimize risk of injury to the lung and to ensure the accuracy of the level of injection. 

Technology There is no specific technology for the treatment or rehabilitation of this condition. 

Surgery Thoracoscopic microsurgical excision of herniated thoracic discs has been shown to have excellent outcomes with less surgical time, less blood loss, fewer postoperative complications, and shorter hospitalizations than more traditional and invasive surgical approaches.29,30 Traditionally, mechanical causes of thoracic radiculopathy have been treated with posterior laminectomy, lateral costotransversectomy, or anterior discectomy by a transthoracic approach. In a cohort study with 167 patients who underwent thoracoscopic discectomy, 79% reported a good or excellent outcome regarding pain improvement, and 80% reported good or excellent outcome for motor function.31 Within the past few years several new surgical approaches to thoracic spine discs have been developed. Treatments such as microendoscopic discectomy, when well indicated, can provide excellent results with less morbidity. Other novel minimally invasive surgical procedures for the condition include microscopic discectomy and mini-open lateral approach.32 

Potential Disease Complications If it is left untreated, thoracic radiculopathy can result in chronic pain and its associated comorbidities. Progressive thoracic spinal cord compression, if unrecognized, can lead to paraparesis, neurogenic bowel and bladder, and spasticity. 

Potential Treatment Complications Analgesics and nonsteroidal anti-inflammatory drugs have well-known side effects that most commonly affect the gastric, hepatic, and renal systems. Care should be taken with use of steroids in diabetic patients because they may elevate blood glucose levels. In patients with uncontrolled diabetes who present with thoracic radiculopathy, glucose control should be attempted, although extremely elevated serum glucose levels have not been proved to cause the diabetic form of thoracic radiculopathy. Because of the risk of gastric ulceration, steroids are not typically used

CHAPTER 43  Thoracic Radiculopathy

simultaneously with nonsteroidal anti-inflammatory drugs. Rarely, short-term oral steroid use may produce avascular necrosis of the hip. Tricyclic antidepressants may cause dry mouth and urinary retention. Along with anticonvulsants, they may also cause sedation. On occasion, physical therapy may exacerbate symptoms. The risks of invasive pain procedures and surgery, including bleeding, infection, further neurologic compromise, and mainly pain33 are well documented.

References 1. Elhadi AM, Zehri AH, Zaidi HA, et al. Surgical efficacy of minimally invasive thoracic discectomy. J Clin Neurosci. 2015;22(11): 1708–1713. 2. Brown CW, Deffer PA JR, Akmakjian J, et al. The natural history of thoracic disc herniation. Spine (Phila Pa 1976). 1992;17:S97–S102. 3. Leininger B, Bronfort G, Evans R, Reiter T. Spinal manipulation or mobilization for radiculopathy: a systematic review. Phys Med Rehabil Clin N Am. 2011;22:105–125. 4. Cohen-Gadol AA, White JB, Lynch JJ, et al. Synovial cysts of the thoracic spine. J Neurosurg Spine. 2004;1:52–57. 5. Derby R, Chen Y, Lee SH, Seo KS, Kim BJ. Non-surgical interventional treatment of cervical and thoracic radiculopathies. Pain Physician. 2004;7(3):389–394. 6. Hayat MJ, Howlader N, Reichman ME, Edwards BK. Cancer statistics, trends, and multiple primary cancer analyses from the Surveillance, Epidemiology, and End Results (SEER) Program. Oncologist. 2007;12:20–37. 7. Spinazze S, Caraceni A, Schrijvers D. Epidural spinal cord compression. Crit Rev Oncol Hematol. 2005;56:397–406. 8. Bicknell J, Johnson S. Widespread electromyographic abnormalities in spinal muscles in cancer, disc disease, and diabetes. Univ Mich Med Center J. 1976;42:124–127. 9. Rubin DI, Shuster EA. Axillary pain as a heralding sign of neoplasm involving the upper thoracic root. Neurology. 2006;66:1760–1762. 10. Streib EW, Sun SF, Paustian FF, et al. Diabetic thoracic radiculopathy: electrodiagnostic study. Muscle Nerve. 1986;9:548–553. 11. Pirti O, Barlas AM, Kuru S, et al. Mastalgia due to degenerative changes of the spine. Adv Clin Exp Med. 2016;25(5):895–900. 12. Tokuhashi Y, Matsuzaki H, Uematsu Y, Oda H. Symptoms of thoracolumbar junction disc herniation. Spine (Phila Pa 1976). 2001;26:E512–E518. 13. Stillerman CB, Chen TC, Couldwell WT, et al. Experience in the surgical management of 82 symptomatic herniated thoracic discs and review of the literature. J Neurosurg. 1998;88:623–633. 14. Koes BW, van Tulder MW, Ostelo R, Kim Burton A, Waddell G. Clinical guidelines for the management of low back pain in primary care: an international comparison. Spine (Phila Pa 1976). 2001;26(22): 2504–2513.

237

15. Choi HE, Shin MH, Jo GY, Kim JY. Thoracic radiculopathy due to rare causes. Ann Rehabil Med. 2016;40(3):534–539. 16. Johnson ER, Powell J, Caldwell J, et al. Intercostal nerve conduction and posterior rhizotomy in the diagnosis and treatment of thoracic radiculopathy. J Neurol Neurosurg Psychiatry. 1974;37:330–332. 17. Ueda Y, Kawahara N, Murakami H, et al. Thoracic disk herniation with paraparesis treated with transthoracic microdiskectomy in a 14-yearold girl. Orthopedics. 2012;35:e774–e777. 18. O’Connor RC, Andary MT, Russo RB, DeLano M. Thoracic radiculopathy. Phys Med Rehabil Clin N Am. 2002;13:623–644, viii. 19. Kasimcan O, Kaptan H. Efficacy of gabapentin for radiculopathy caused by lumbar spinal stenosis and lumbar disk hernia. Neurol Med Chir (Tokyo). 2010;50:1070–1073. 20. Selph S, Carson S, Fu R, et al. Drug class review: neuropathic pain: final update 1 report [Internet]. Drug Class Reviews. 2011. 21. Plastaras CT, Schran S, Kim N, et al. Complementary and alternative treatment for neck pain: chiropractic, acupuncture, TENS, massage, yoga, Tai Chi, and Feldenkrais. Phys Med Rehabil Clin N Am. 2011;22:521–537. 22. Iversen MD. Rehabilitation interventions for pain and disability in osteoarthritis. Am J Nurs. 2012;112:S32–S37. 23. O’Connor RC, Andary MT, Russo RB, DeLano M. Thoracic radiculopathy. Phys Med Rehabil Clin N Am. 2002;13(3):623–644. 24. Kennedy DJ, Noh MY. The role of core stabilization in lumbosacral radiculopathy. Phys Med Rehabil Clin N Am. 2011;22:91–103. 25. Hahne AJ, Ford JJ, McMeeken JM. Conservative management of lumbar disc herniation with associated radiculopathy: a systematic review. Spine (Phila Pa 1976). 2010;35:E488–E504. 26. Agabegi SS, Asghar FA, Herkowitz HN. Spinal orthoses. J Am Acad Orthop Surg. 2010;18:657–667. 27. Manchikanti L., Boswell M.V., Singh V., et al. Comprehensive evidencebased guidelines for interventional techniques in the management of chronic spinal pain. Pain Physician. 2009;12:699–802. 28. Kaye AD, Manchikanti L., Abdi S., et al. Efficacy of epidural injections in managing chronic spinal pain: a best evidence synthesis. Pain Physician. 2015;18(6):E939–E1004. 29. Wait SD, Fox DA Jr, Kenny KJ, Dickman CA. Thoracoscopic resection of symptomatic herniated thoracic discs: clinical results in 121 patients. Spine (Phila Pa 1976). 2012;37:35–40. 30. Rosenthal D, Dickman CA. Thoracoscopic microsurgical excision of herniated thoracic discs. J Neurosurg. 1998;89:224–235. 31. Quint U, Bordon G, Preissl I, et al. Thoracoscopic treatment for single level symptomatic thoracic disc herniation: a prospective followed cohort study in a group of 167 consecutive cases. Eur Spine J. 2012;21:637–645. 32. Snyder LA, Smith ZA, Dahdaleh NS, Fessler RG. Minimally invasive treatment of thoracic disc herniations. Neurosurg Clin N Am. 2014;25(2):271–277. 33. Bayman EO, Brennan TJ. Incidence and severity of chronic pain at 3 and 6 months after thoracotomy: meta-analysis. J Pain. 2014;15(9):887–897.

CHAPTER 44

Thoracic Sprain or Strain Alexios G. Carayannopoulos, DO, MPH Alex Han, BA

Synonyms Thoracic sprain Pulled upper back Mid-back pain Benign thoracic pain

ICD-10 Codes S23.3 S39.012 M40.04 M47.814 M51 M53.2X4 M54.6

Sprain of ligaments of thoracic spine Strain of muscle, fascia and tendon of lower back Postural kyphosis, thoracic region Spondylosis, thoracic region Thoracic, thoracolumbar, and lumbosacral intervertebral disc disorders Spinal instabilities, thoracic region Pain in thoracic spine

Definition Thoracic strain or sprain refers to the acute or subacute onset of pain in the region of the thoracic spine due to soft tissue injury, including muscles, ligaments, tendons, and fascia, of an otherwise normal back (Fig. 44.1). Sprain relates to injury in ligament fibers without total rupture, whereas strain is an overstretching or overexertion of some part of the musculature.1 Because the thoracic cage is unified by the overlying fascia, thoracic sprain or strain can translate into pain throughout the thoracic spine. Although the scientific literature on musculoskeletal pain in the cervical and lumbar spine is abundant, similar information about pain in the thoracic region is sparse because of its lower prevalence.2 A systematic review found that thoracic spine pain is more common in female patients and in child and adolescent populations, compared with adults.3 In the general population, the lifetime prevalence of having experienced musculoskeletal pain in the thoracic spine is 17% in contrast to 57% in the low back and 40% in the neck.4 Therefore observation and characterization of such lesions are minimal, subsequently limiting the potential to improve treatment methods for thoracic sprain and 238

strain disorders. Moreover, pain felt in the thoracic spine is often referred from the cervical spine, mistakenly giving the impression that the incidence is higher.5 Thoracic strain or sprain may be the indirect result of disc lesions, which have been reported to be evenly distributed in incidence between the sexes and are most common in patients in their third to fifth decades of life.6 Muscles adjacent to the injured disc tend to become tight in response to the local inflammatory process, which may jeopardize the local muscle equilibrium, possibly leading to ligament strains and muscle sprains in the thoracic region. Other structures that may lead to strain or sprain in the mid back due to the same inflammatory process are the thoracic facet joints and the nerve roots.7 As with most nonspecific mechanical disorders of the cervical and lumbar regions, the natural progression in the majority of patients with nonspecific thoracic strain or sprain is resolution within 1 to 6 months.8 The thoracic spine is the least mobile area of the vertebral column secondary to the length of the transverse processes, the presence of costovertebral joints, the decrease in disc height compared with the lumbar spine, and the presence of the rib cage.9 Movements that occur in the thoracic spine include rotation with flexion or extension. Thoracic sprain and strain injuries can occur in all age groups, but there is an increased prevalence among patients of working age.10 Intrinsic mechanisms include bone disease as well as alteration of normal spine or upper extremity biomechanics. This includes cervical or thoracic deformity from neuromuscular or spinal disease as well as shoulder or scapular dysfunction. The most common intrinsic cause of thoracic strain, however, is poor posture or excessive sitting. Scheuermann disease in the young and osteoporosis in the elderly may contribute to development of poor posture, potentially leading to kyphosis and compression deformities seen in these patients (Fig. 44.2).11 Poor posture is often manifested as excessive protraction or drooping of the neck and shoulders as well as decreased lumbar lordosis or “flat back.” With the classic “slouched position” encountered in children and adolescents and often carried on through adulthood, there is excessive flexion of the thoracic spine with a decrease in rotation and extension.12 Postural alterations promote increased thoracic kyphosis, resulting in the “flexed posture.” Excessive flexion results in excessive strain on the “core,” including the small intrinsic muscles of the spine, the long paraspinal muscles, and the abdominal and rib cage muscles. Excessive flexion can

CHAPTER 44  Thoracic Sprain or Strain

239

Extrinsic or environmental mechanisms include repetitive strain, trauma, and obesity. In female patients, larger breasts have been associated with thoracic pain. Women with macromastia, or breast hypertrophy, were found to have significantly increased thoracic spine pain on the Numeric Rating Scale as compared with women with average breast size.13,14 Additional risk factors include occupational and recreational activities characterized by repetitive motions, such as lifting, twisting, and bending. Occupations requiring manual labor or extended periods of sitting are predisposed to a higher incidence of such disorders.15 Traumatic causes include falls, violence, and accidents leading to vertebral fractures, chest wall contusions, or flail chest. 

Symptoms

FIG. 44.1 Coronal magnetic resonance imaging of hyperflexion injury of thoracic spine leading to paraspinal hematoma (arrows). (From Goldstein SJ. Hyperflexion injury of the thoracic spine [Med Pix®].; 2007. Accessed January 2017.)

Patients typically report pain in the mid back, which may be related to upper extremity or neck movements. Symptoms may be exacerbated by deep breathing, coughing, rotation of the thoracic spine, or prolonged standing or sitting. The pain can be generalized in the mid back area or focal. If it is focal, it is usually described as a “knot,” which is deep and aching. It may radiate to the anterior chest wall, abdomen, upper limb, cervical spine, or lumbosacral spine and may be accentuated with movement of the upper extremity or neck. The location of pain in mechanical disorders of the thoracic spine is either central (symmetric) or unilateral (asymmetric).5 Other symptoms include muscle spasm, tightness, and stiffness, as well as pain or decreased range of motion in the mid back, low back, neck, or shoulder. 

Physical Examination

FIG. 44.2 Plain film of Scheuermann kyphosis of the mid-thoracic spine. (From Modzelewski LN. Scheuermann kyphosis [MedPix®]. ; 2007. Accessed January 2017.)

increase the risk of rib stress fractures as well as costovertebral joint irritation. This can cause referral of pain to the chest wall with subsequent development of trigger points in the erector spinae, levator scapulae, rhomboids, trapezius, and latissimus dorsi. Poor motion in extension and rotation can place an increased load on nearby structures, such as the lumbar or cervical spine and shoulders.

The essential finding in the physical examination of thoracic sprain or strain is thoracic muscle spasm with normal neurologic examination findings. Pain may be exacerbated when the patient lifts the arms overhead, extends backward, or rotates. Rib motion may be restricted and may be assessed by examining diaphragmatic excursion of the chest wall during respiration. This is accomplished by placing hands on the upper and lower chest wall and looking for symmetry and rhythm of movement. The upper ribs usually move in a bucket-handle motion, whereas the lower ribs move in a pump-handle motion. Restriction of specific ribs can be assessed by examining individual rib movements with respiration. The position of comfort is usually flexion, but this is the position that should be avoided. Sensation and reflex examination findings should be normal. A finding of lower extremity weakness or neurologic deficit on physical examination suggests an alternative diagnosis and may warrant further investigation.16 As the thoracic cage and spine are the anchors for the upper limbs, the thoracic spine influences and is influenced by active and resisted movement of the extremities, cranium, and lumbar and cervical spine.17 Therefore a careful spinal and shoulder examination is essential to rule out restrictive movements, obvious deformity, soft tissue asymmetry, and skin changes (that may be seen in infection or tumor). Detailed examination of other

240

PART 1 MSK Disorders

organ systems is important because thoracic pain can be referred. Examination includes static and dynamic assessment of posture. The patient should be observed in relaxed stance with the shirt removed. Viewing is from the posterior, lateral, and anterior perspectives, and deviations from an ideal posture are noted.17 With dynamic assessment, it is important to provoke the patient’s symptoms by moving and stressing the structures from which pain is thought to originate. In addition, the presence of deformities and the site of pain and tenderness are noted. Pain is often felt between the scapulae, around the lower border of the scapula, and centrally in the area between T1 and T7. Thoracic spine landmarks include the sternoclavicular joint (T1), superior angle (T2), and inferior angle (T7) of the scapula, sternal angle (T4), and xiphoid process (T9). Much of the pain felt in the thoracic area, however, has been shown to originate in the cervical spine. Pain in the region above an imaginary line drawn between the inferior borders of the scapulae is most likely secondary to the cervical region—mainly lower cervical facet joints.18 

Functional Limitations Functional limitations include difficulty with bending, lifting, and overhead activities, such as throwing and reaching. These limitations affect both active and sedentary workers. Activities of daily living, such as upper extremity bathing and dressing, might be affected. General mobility may be impaired. As most sports-related or leisure activities involve use of the upper extremity, extension, or rotation of the thorax, athletic participation and functional capacity may be limited as well. 

Diagnostic Studies Thoracic sprain and strain injuries are typically diagnosed on the basis of the history and physical examination. No tests are usually necessary during the first 4 weeks of symptoms if the injury is nontraumatic. If there is suspicion of tumor (night pain, constitutional symptoms), infection (fever, chills, malaise), or fracture (focal tenderness with history of trauma or fall), earlier and more complete investigation is warranted (Fig. 44.3; see Chapter 42). Plain film x-rays should be ordered initially if the injury is associated with recent trauma or malignant disease. Magnetic resonance imaging is the study of choice in considering thoracic malignant neoplasia and osteoporotic compression fracture or when the patient has unilateral localized thoracic pain with sensory-motor deficits to rule out a thoracic disc herniation with consequent radiculopathy.19 A computed tomographic scan, ultrasonography, or triple-phase bone scan can identify bone abnormalities if magnetic resonance imaging is contraindicated. Magnetic resonance imaging, however, can detect abnormalities unrelated to the patient’s symptoms because many people who do not have pain have abnormal imaging findings.20 This fact emphasizes the importance of a meticulous clinical evaluation of patients with thoracic pain. 

FIG. 44.3 Magnetic resonance imaging of thoracic vertebral fracture secondary to osteomyelitis. (From Brelsford MA. Vertebral fracture secondary to osteomyelitis [MedPix®]. ; 2006. Accessed January 2017.)

Differential Diagnosis SPINAL DIAGNOSES Sprain or strain Thoracic radiculopathy Facet joint arthropathy Structural rib dysfunction Spinal stenosis Scheuermann disease Ankylosing spondylosis Discitis Osteopenia or osteoporosis Vertebral fracture (trauma, insufficiency, pathologic) Scoliosis or kyphosis Spinal cord tumor  EXTRASPINAL DIAGNOSES Malignancy (gastrointestinal, renal, cardiopulmonary) Aortic aneurysm Coronary artery disease or congestive heart failure Peptic ulcer disease Pancreatitis Cholecystitis Nephrolithiasis Hiatal hernia Macromastia Shingles

Treatment Initial The initial treatment of a thoracic sprain or strain injury generally involves the use of cold packs to decrease pain and edema during the first 48 hours after the injury. Thereafter the application of moist heat to reduce pain and muscle spasm is indicated. Bed rest for up to 48 hours may be

CHAPTER 44  Thoracic Sprain or Strain

beneficial, but prolonged bed rest is discouraged because it can lead to muscle weakness. Relative rest by avoidance of activities that exacerbate pain is preferable to complete bed rest. Temporary use of a rib binder or elastic wrap may reduce pain as well as increase activity tolerance and mobility. A short course of nonsteroidal anti-inflammatory drugs, acetaminophen, muscle relaxants, or topical anesthetics such as lidocaine patches may be beneficial. Opioids are generally not necessary. There has also been growing interest in the use of compounded or combined topical analgesics, which may provide more rapid onset of pain relief through multiple mechanisms of action as well as a more desirable side effect profile compared to oral, parenteral, or intrathecal analgesics.21 

Rehabilitation Most acute thoracic sprain or strain injuries will heal spontaneously with rest and physical modalities used at home, such as ice, heating pad, and massage. Body mechanics and postural training are important aspects of the rehabilitation program for thoracic sprain or strain.22,23 A focus on correct posture at work, during leisure activities, and while driving is important. In the car, patients can use a lumbar roll to promote proper posture; at work, patients are advised to sit upright at the computer in an adjustable, comfortable chair with adequate monitor adjustment. The monitor should be adjusted to align with the keyboard at a height that aligns the first row of text with eye level. Finally, the correct depth should be achieved in a way that the user does not need to lean forward to comfortably read.24 Other workplace modifications include forearm seat rests to support the arms, foot rests, and the use of a telephone earpiece or headset to prevent neck and upper thoracic strain. For patients with abnormally flexed or slouched posture, household modifications can be made that might help encourage extension and subsequently decrease pain. These include pillows or lumbar rolls on chairs and replacement of sagging mattresses with firm bedding. Also, use of paper plates and lightweight cookware in the kitchen and reassignment of objects in overhead cabinets to areas that are more accessible can help if lifting or reaching is painful. If pain persists beyond several weeks, physical therapy may be indicated. In general, physical therapy will apply movements that centralize, reduce, or diminish the patient’s symptoms while discouraging movements that peripheralize or increase the patient’s symptoms.5 In most cases, an active approach that encourages stretching and strengthening exercises is preferred to a more passive approach. To correct sitting posture, patients are advised to continue to use the lumbar roll in all sitting environments. To correct standing posture, patients are shown how to normalize lumbar curvature and to move the lower part of the spine backward while at the same time moving the upper spine forward, raising the chest, and retracting the head and neck. To correct lying posture, patients should use a firm mattress as previously indicated. In the case of patients who experience more pain in the thoracic spine when lying in bed, this advice often leads to worsening of the symptoms rather than a resolution. In these patients, advice should be given to deliberately sag the mattress by placing pillows under each end of the mattress so that it becomes dished. In this manner, the thoracic kyphosis

241

is not forced into the extended range while lying supine, and the removal of this stress allows a comfortable night’s sleep. Long-term goals, however, still include improvement in extension range of motion.5 After a formal physical therapy program is completed, a home exercise or gym regimen is essential and should be prescribed and individualized for all patients to maintain progress made during physical therapy. Exercises at home are aimed at improvement in flexibility of the thoracic spine and may include extension in lying, standing, and sitting performed six to eight times throughout the day. In addition, alternating arm and leg lifts and active trunk extension in the prone position should be performed. Finally, regular stretching to improve extension and rotation with trigger pointing can decrease muscle tension over the affected muscles. A thoracic wedge, which is designed to increase extension range of motion, can be used. The wedge is a hard piece of molded plastic or rubber with a wedge cut out to accommodate the spine. The patient lies on the ground with the wedge placed in between the shoulder blades and is instructed to arch over it. Alternatively, two tennis balls can be taped together for the same effect. These exercises can be done before regular stretching to increase excursion. Regular massage therapy can maintain flexibility and prevent tightening from more frequent exercise. At the gym, progressive dynamic movements such as rowing, latissimus pull-downs, pull-ups, and an abdominal core strengthening program should be emphasized. Instruction in proper positioning and technique should be provided to prevent further injury. Use of a “physio-ball” at home or at the gym can facilitate trunk extension as well as abdominal stretching and strengthening to increase overall conditioning of the thoracic cage and core musculature. This can be done in conjunction with use of exercise bands with progressive resistance to facilitate stretching of the arms and shoulders with mild strengthening of the shoulder, arm, and core muscles. Finally, a pool program can be prescribed. Swimming strokes such as the crawl, backstroke, and butterfly emphasize extension and can be very useful to prevent or to correct a flexion bias. With the crawl, patients are instructed to breathe on both sides to prevent unilateral strain in the neck and upper thoracic spine. 

Procedures Dry needling and trigger point injections may help reduce focal pain caused by taut bands of muscle, allowing the patient to exercise to restore range of motion, to correct postural imbalance, and to increase strength and balance of the dysfunctional segment.25,26 Acupuncture can be used for local as well as for systemic treatment. Finally, botulinum toxin type A has been used for specific muscles, including rhomboids, trapezius, levator scapulae, and serratus, which often contribute to thoracic strain and sprain. A systematic review of seven trials assessing the use of botulinum toxin type A for treatment of thoracic myofascial pain found inconclusive evidence regarding its efficacy.27 Two studies found that botulinum toxin type A treatment improved pain levels and quality of life measures, but the majority of studies found no significant benefit compared to placebo.28,29 Additional electrostimulation treatment modalities for myofascial pain syndrome that can be applied in thoracic

242

PART 1 MSK Disorders

sprain or strain cases include intramuscular electrical stimulation, transcutaneous electrical nerve stimulation, and extracorporeal shock wave therapy. These may be effective alternatives to needling or medication infusion.25,30 

Technology Spinal cord stimulation (SCS) has recently emerged as a treatment modality for refractory chronic thoracic pain, and operates by delivering low-level electrical stimulation to the spinal epidural space to interfere with direct transmission of pain signals.31 Neuromodulation approaches such as SCS may be particularly useful for cases of neuropathic pain or when analgesic medication is ineffective; however, a retrospective review of 172 patients who underwent thoracic SCS placement found a postoperative complication of thoracic radiculopathy in 15 of the patients.32 Recent advancements in orthoses include a novel thoracic support used as part of an Active Lumbar Support vehicle seat designed to better accommodate occupational equipment, as well as the use of nonrigid thoracolumbosacral orthoses to slow the progression of deformity in scoliosis patients and better support the spine.33,34 Finally, a novel portable spinal monitor has been developed that provides real-time measurements that correlate strongly with digital fluoroscopy and can be easily used in nonlaboratory settings to assess changes in posture.35 

Surgery Surgery is not usually indicated unless focal disc herniation with neurologic abnormalities such as radiculopathy (see Chapter 43) is found or if there is instability of particular spinal segments from fracture or dislocation. For women with macromastia, reduction mammaplasty may help improve posture and reduce or eliminate musculoskeletal spinal pain.36,37 

Potential Disease Complications Thoracic sprain and strain injuries can occasionally develop into myofascial pain syndromes. Prolonged inactivity due to these injuries may predispose patients to weight gain, bone density loss, and loss of flexibility and muscle strength. 

Potential Treatment Complications Possible complications include gastrointestinal side effects from nonsteroidal anti-inflammatory drugs. Other possible complications include somnolence or confusion from muscle relaxants; addiction from narcotics; bleeding, infection, postinjection soreness, and pneumothorax from trigger point injections; excessive weakness and development of antibodies from botulinum toxin; and temporary posttreatment exacerbation of pain from manual medicine or electrostimulation therapy.38

References 1.  Sprains and strains, MeSH (Medical Subject Headings). National Center for Biotechnology Information, U.S. National Library of Medicine. 2012. http://www.ncbi.nlm.nih.gov/mesh/68013180. Access Date, January 2017. 2. Johansson MS, Jensen Stochkendahl M, Hartvigsen J, et al. Incidence and prognosis of mid-back pain in the general population: a systematic review. Eur J Pain. 2017;21:20–28.

3. Briggs AM, Smith AJ, Straker LM, Bragge P. Thoracic spine pain in the general population: prevalence, incidence and associated factors in children, adolescents, and adults: a systematic review. BMC Musculoskelet Disord. 2009;10:77. 4. Leboeuf-Yde C, Nielsen J, Kyvik KO, et al. Pain in the lumbar, thoracic or cervical regions: do age and gender matter? A population-based study of 34,902 Danish twins 20-71 years of age. BMC Musculoskelet Disord. 2009;10:39. 5. McKenzie RA, May S. The Cervical and Thoracic Spine: Mechanical Diagnosis and Therapy. 2nd ed. Waikanae, NZ: Spinal Publications Ltd; 2006. 6. Russell T. Thoracic intervertebral disc protrusion: experience of 67 cases and review of the literature. Br J Neurosurg. 1989;3:153–160. 7. Manchikanti L, Helm S, Singh V, et al. An algorithmic approach for clinical management of chronic spinal pain. Pain Physician. 2009;12:E225–E264. 8. Malmivaara A, Hakkinen U, Aro T, et al. The treatment of acute low back pain—bed rest, exercises, or ordinary activity? N Engl J Med. 1995;332:351–355. 9. White AA, Panjabi MM. Clinical Biomechanics of the Spine. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 1990. 10. Choi BC, Levitsky M, Lloyd RD, Stones IM. Patterns and risk factors for sprains and strain in Ontario, Canada 1990: an analysis of the Workplace Health and Safety Agency database. J Occup Environ Med. 1996;38:379–389. 11. Katzman WB, Wanek L, Shepherd JA, et al. Age-related hyperkyphosis: its causes, consequences, and management. J Orthop Sports Phys Ther. 2010;40:352–360. 12. Mirbagheri S, Rahmani-Rasa A, Farmani F, et al. Evaluating kyphosis and lordosis in students by using a flexible ruler and their relationship with severity and frequency of thoracic and lumbar pain. Asian Spine J. 2015;9:416–422. 13. Spencer L, Briffa K. Breast size, thoracic kyphosis & thoracic spine pain–association & relevance of bra fitting in post-menopausal women: a correlational study. Chiropr Man Therap. 2013;21:20. 14. Fernandes PM, Sabino Neto M, Veiga DF, et al. Back pain: an assessment in breast hypertrophy patients. Acta Ortop Bras. 2007;15:227–230. 15. Manchikanti L, Singh V, Datta S, et al. Comprehensive review of epidemiology, scope, and impact of spinal pain. Pain Physician. 2009;12:E35–E70. 16. Choi HE, Shin MH, Jo GY, et al. Thoracic radiculopathy due to rare causes. Ann Rehabil Med. 2016;40:534–539. 17. Kendall FP, McCreary EK, Provance PG, et al. Muscles: Testing and Function, With Posture and Pain. 5th ed. Philadelphia: Lippincott Williams & Wilkins; 2005. 18. Louw A, Schmidt SG. Chronic pain and the thoracic spine. J Man Manip Ther. 2015;23:162–168. 19. Splendiani A, Bruno F, Patriarca L, et al. Thoracic spine trauma: advanced imaging modality. Radiol Med. 2016;121:780–792. 20. Elliott JM, Flynn TW, Al-Najjar A, et al. The pearls and pitfalls of magnetic resonance imaging for the spine. J Orthop Sports Phys Ther. 2011;41:848–860. 21. Safaeian P, Mattie R, Hahn M, et al. Novel treatment of radicular pain with a multi-mechanistic combination topical agent: a case series and literature review. Anesth Pain Med. 2016;6:e33322. 22. Richmond J. Multi-factorial causative model for back pain management; relating causative factors and mechanisms to injury presentations and designing time- and cost effective treatment thereof. Med Hypotheses. 2012;79:232–240. 23. Yoo WG. Effect of thoracic stretching, thoracic extension exercise and exercises for cervical and scapular posture on thoracic kyphosis angle and upper thoracic pain. J Phys Ther Sci. 2013;25:1509–1510. 24. Bleecker ML, Celio MA, Barnes SK. A medical-ergonomic program for symptomatic keyboard/mouse users. J Occup Environ Med. 2011;53:562–568. 25. Rock JM, Rainey CE. Treatment of nonspecific thoracic spine pain with trigger point dry needling and intramuscular electrical stimulation: a case series. Int J Sports Phys Ther. 2014;9:699–711. 26. Fernandez-de-las-Penas C, Layton M, Dommerholt J. Dry needling for the management of thoracic spine pain. J Man Manip Ther. 2015;23:147–153. 27. Desai MJ, Shkolnikova T, Nava A, et al. A critical appraisal of the evidence for botulinum toxin type A in the treatment of cervico-thoracic myofascial pain syndrome. Pain Pract. 2014;14:185–195. 28. Gobel H, Heinze A, Reichel G, et al. Dysport myofascial pain study group. Efficacy and safety of a single botulinum type-A toxin complex treatment (Dysport) for the relief of upper back myofascial pain syndrome: results from a randomized double-blind placebo-controlled multicenter study. Pain. 2006;125:82–88.

CHAPTER 44  Thoracic Sprain or Strain

29. Lew HL, Lee EH, Castaneda A, et al. Therapeutic use of botulinum toxin type A in treating neck and upper-back pain of myofascial origin: a pilot study. Arch Phys Med Rehabil. 2008;89:75–80. 30. Gleitz M, Hornig K. Trigger points—diagnosis and treatment concepts with special reference to extracorporeal shockwaves. Orthopade. 2012;41:113–125. 31. Wolter T. Spinal cord stimulation for neuropathic pain: current perspectives. J Pain Res. 2014;7:651–653. 32. Mammis A, Bonsignore C, Mogilner AY. Thoracic radiculopathy following spinal cord stimulator placement: case series. Neuromodulation. 2013;16:443–447. 33. Gruevski KM, Holmes MW, Gooyers CE, et al. Lumbar postures, seat interface pressures and discomfort responses to a novel thoracic support for police officers during prolonged simulated driving exposures. Appl Ergon. 2016;52:160–168.

243

34. Gammon SR, Mehlman CT, Chan W, et al. A comparison of thoracolumbosacral orthoses and SpineCor treatment of adolescent idiopathic scoliosis patients using the Scoliosis Research Society standardized criteria. J Pediatr Orthop. 2010;30:531–538. 35. O’Sullivan K, Verschueren S, Pans S, et al. Validation of a novel spinal posture monitor: comparison with digital videofluoroscopy. Eur Spine J. 2012;21:2633–2639. 36. Goulart R, Detanico D, Vasconcellos RP, et al. Reduction mammoplasty improves body posture and decreases the perception of pain. Can J Plast Surg. 2013;21:29–32. 37. Singh KA, Losken A. Additional benefits of reduction mammaplasty: a systematic review of the literature. Plast Reconstr Surg. 2012;129:562–570. 38. Rompe JD, Segal NA, Cacchio A, et al. Home training, local corticosteroid injection, or radial shock wave therapy for greater trochanter pain syndrome. Am J Sports Med. 2009;37:1981–1990.

SECTION VI

Low Back

CHAPTER 45

Lumbar Degenerative Disease Saurabha Bhatnagar, MD Ogochukwu Azuh, MD Hans E. Knopp, DO

Synonyms Osteoarthritis of the spine Spondylosis Lumbar arthritis Degenerative joint disease of the spine Degenerative disc disease

ICD-10 Codes M47.817 M47.899 M51.36 M51.37 M54.5

Spondylosis without myelopathy or radiculopathy, lumbosacral region Other spondylosis, site unspecified Other intervertebral disc degeneration, lumbar region Other intervertebral disc degeneration, lumbosacral region Low back pain

Definition Low back pain (LBP), also known as lumbago, is a common condition that according to observational studies occurs in about 80% of people.1 In the United States, respondents of a survey of adults 18 and over by the National Center for Health Statistics revealed that LBP was the most common type of pain (28.1%) when compared to severe headache or migraine (16.6%) and neck pain (14.6%).2 Normal aging is a key component of the degenerative spine process and at times both are hard to differentiate. As such, literature has shown an increased prevalence in spine 244

degeneration with age in asymptomatic individuals. When comparing prevalence estimates of degenerative spine imaging findings in asymptomatic patients aged 30 and aged 80, disc degeneration (52% vs. 96%, respectively), disc bulge (40% vs. 84%), facet degeneration (9% vs. 83%), and spondylolisthesis (5% vs. 50%) increased with age.3 With age, all anatomic components of the spine are affected: bone, muscles, discs, ligaments, and joints. As a result of the alteration of the “spinal structural equilibrium,” this can lead to spinal instability, clinical syndromes, restricted range of motion (ROM), pain, and in worst cases, disability. The three-joint complex is the functional unit of the lumbar spine and comprises two consecutive vertebrae, the intervertebral disc, and the zygapophyseal (facet) joint (Fig. 45.1). The lumbar disc can be separated into three components: the nucleus pulposus, annulus fibrosus, and cartilaginous endplates. When axial forces are placed upon the nucleus, it distributes the tensile forces via the annulus and the endplates. The degeneration of the intervertebral discs has been thought to be the catalyst leading to secondary degeneration of the surrounding spinal elements. Degeneration of the discs has been shown to be nutrition-related. The main source of nutrition to the intervertebral discs is derived from the cartilaginous endplates and as one ages, permeability of the nutritional gradient from endplates decreases as well as blood supply. An imbalance between extracellular matrix synthesis and degradation occurs, which leads to loss of disc structure and function. There is histological evidence showing cracks and microfractures in the cartilaginous endplates, concentric tears (cleft formation) in the nucleus pulposus, and radial tears in the annulus fibrosus.4 The intervertebral discs receive innervation anteriorly and laterally from the gray ramus communicans and posteriorly from the sinuvertebral nerve, with a majority of free nerve endings found in the outer third of the annulus.5

CHAPTER 45  Lumbar Degenerative Disease

POSTERIOR JOINTS

THREE-JOINT COMPLEX

INTERVERTEBRAL DISC CIRCUMFERENTIAL TEARS

SYNOVIAL REACTION CARTILAGE DESTRUCTION

HERNIATION

RADIAL TEARS INTERNAL DISRUPTION

OSTEOPHYTE FORMATION CAPSULAR LAXITY

INSTABILITY

LOSS OF DISC HEIGHT

SUBLUXATION

LATERAL NERVE ENTRAPMENT

DISC RESORPTION

ENLARGMENT ARTICULAR

ONE-LEVEL CENTRAL STENOSIS

PROCESS (AND LAMINA)

245

OSTEOPHYTES AT BACK OF VERTEBRAL BODIES

EFFECT OF RECURRENT STRAINS AT LEVELS ABOVE AND BELOW ORIGINAL LESION MULTILEVEL DEGENERATIVE LESIONS MULTILEVEL SPINAL STENOSIS FIG. 45.1  (Modified from Araghi A, Ohnmeiss DD. Natural history of the degenerative cascade. In: Yue JJ, ed. The Comprehensive Treatment of the Aging Spine: Minimally Invasive and Advanced Techniques. Philadelphia: Saunders/Elsevier; 2011:22.) The three-joint complex is the functional unit of the lumbar spine. The interdependence of each component is evident when they are subjected to biomechanical changes. Outlined is a sequence of degeneration.

With age, collagen content within the nucleus increases and the junction between the nucleus and the annulus becomes less demarcated. Thus tears in the annulus lead to degeneration, prolapse, extrusion, and then sequestration, which can all be sources of pain. As the mechanical load on the spine is altered, forces are distributed through the surrounding facet joints which, depending on one’s position, are responsible for 10% to 30% of lumbar weight bearing.5 These joints are diarthrodial synovial joints and, like all synovial joints, are subjected to degradation of cartilage, subchondral bone sclerosis, osteoporosis, osteophyte formation, and inflammation. This results in facet hypertrophy and, with increased repeated mechanical ­loading, can lead to joint laxity, subluxation, and narrowing of the lateral recess. In concert with disc height loss, it can then lead to central canal stenosis. Other bony elements of the spine (i.e., vertebral bodies, endplates, spinous and transverse processes) also undergo this degeneration process. The ligamentum flavum is a ligament that runs from C2 to S1, connecting lamina of adjacent vertebrae together. It is 80% elastin and 20% collagen and occupies the posterior lateral borders of the spinal canal. Aging causes ligament hypertrophy and in association with disc degeneration leads to bucking, seen as thickness on imaging. This results in spinal canal narrowing and can lead to compression of neural elements. The cause of ligamentum flavum hypertrophy is unknown, but has been postulated to be due to age-related fibrosis secondary to a decrease in elastin-to-collagen ratio.6 The spine is surrounded by a “core” group of muscles that aid in maintaining stability and equilibrium. These muscles are the abdominals (mostly transversus abdominis), diaphragm and pelvic floor muscles, erector spinae, and spinal multifidi.

As time passes, a degenerative myopathy occurs which contributes to the alteration of vector forces upon the spine, thereby shifting it out of equilibrium. An example of this is seen in primary camptocormia, also referred to as bent spine syndrome, relating to primary idiopathic axial myopathy.7,8 The most commonly involved lumbar levels are L4-L5 and L5-S1, as they undergo the most torsion and compressive forces during activity. Factors contributing to lumbar degeneration include environmental (diabetes mellitus, smoking, obesity), occupational (jobs with repetitive bending, stooping, prolonged sitting or vibratory stress), and psychosocial (stress, anxiety, depression), which can contribute to the perception of LBP).9,10 

Symptoms As previously described, lumbar degenerative disease is associated with the normal aging process. Findings on imaging such as intervertebral disc degeneration, facet joint osteoarthritis, spondylolysis, spondylolisthesis, spinal stenosis, and degenerative changes in paraspinal muscles are also seen in asymptomatic individuals. Approximately one third of individuals with substantial abnormalities on magnetic resonance imaging do not manifest any clinical symptoms.11,12 For those with symptoms, common complaints range from acute to chronic LBP. Onset can range from days to months. Positioning such as lumbar flexion, extension, rotation or lateral bending, or lumbar palpation can exacerbate symptoms. Pain with flexion, coughing, sneezing, or Valsalva can be associated with disc disease. Pain quality can be sharp, dull, achy, or shock-like. Severity can range from mild to severe. Pain can be localized at a specific region, as the patient will be

246

PART 1  MSK Disorders

able to point to exact location; or it can radiate locally or to a distant site. The presence of stiffness in the morning could be due to osteoarthritis. However, atypical symptoms of pain at night, fever, and recent weight loss could be due to malignancy or infection. Alleviating factors such as forward bending could signify compression of neural elements. Leakage of pain-related neuropeptides (e.g., substance P) from the disc secondary to annulus tears to surrounding free nerve endings or onto the nearby dorsal root ganglion can cause pain.5 Clinicians should also inquire about psychological symptoms such as anxiety, depression, or sleep disturbance as contributing factor symptoms. 

Physical Examination Many structures comprise the spinal element; therefore a physical examination should be geared toward discerning one of the five most common sources of LBP: discogenic, facet arthropathy or instability, radiculopathy or neural compression, myofascial or soft tissue, and psychogenic. Although usually found alone, they can also be found in combination. Hence, the goal of the physical examination is to narrow one’s differential diagnosis to lead to more cost effective testing and therapeutic strategies (Table 45.1). Paramount to any physical examination is inspection. In order to gain a sense of patient disability, one must observe the patient, paying close attention to posture, shape of spine (kyphosis, scoliosis, lordosis, back flattening), musculature (atrophy or spasms), skin (midline dimple or tuft of hair), ambulation, and facial expression. Lumbosacral spine movement should be assessed by flexion, extension, rotation, and lateral bending to each side. Hip and sacroiliac (SI) joints should also be tested, as pain from these areas can be referred (e.g., FABER, Gillet, Yeoman, and Gaenslen tests).13 A complete examination includes inspection of the lower extremities and a neurologic examination. Manual muscle strength testing, sensory (dermatomes), and proprioception testing should be performed. Functional muscle testing should also be performed. This can include gait analysis, body weighted squats, tandem walking, and walking/standing on tiptoes and heel. Deep tendon reflex testing (patellar tendon [L3, L4], hamstring tendon [L5], Achilles tendon [S1]) is of utmost importance, as subtle asymmetries could be the only finding on exams. Proprioception (dorsal columns), Babinski, and clonus (upper motor neuron findings) should also be checked. Of note, once the ankle reflex is lost, in half the cases, it does not return. Therefore in new cases of lower back pain, the absence of this reflex alone does not confirm recent root conduction impairment.13 Specialized specific tests for lower back syndromes can also be employed, including straight-leg raising, femoral stretch test, dural tension test, and Schober’s test. For patients in whom psychological factors are thought to contribute to their pain,14 Wadell et al. created a list of nonorganic signs of back pain. (Table 45.2). 

Functional Limitations Functional limitations are restrictions that prevent one from fully performing activities of daily living (ADL) from physical or mental causes and can lead to disability. This tends to affect one’s occupation, leisurely activities, hobbies, sports, and physical exercise. Although most patients complain of

back pain and stiffness, the functional limitations associated with lumbar degenerative disease depend on the structure that is affected. For example, if pathology is discogenic in origin, patients may have difficulty with forward bending, squatting, bending, and twisting. Those with pathology of the facet joint will have limitations with extension, side bending, standing, and walking down stairs. People with central spinal stenosis and stenosis of the lateral recess have difficulty with prolonged walking or standing, with relief coming from sitting and forward bending.13 Patients with ligamentous and myofascial pathology complain of pain that is associated with prolonged postural stress (e.g., standing or physical activity). Psychogenic pathology often involves complaints of pain out of proportion to physical examination, failure of multiple treatment remedies and associated complaints of anxiety or depression surrounding the inability to manage pain. 

Diagnostic Studies Radiography of the spine is usually the first imaging acquired due to its low cost and relative speed of acquisition. However, plain radiographs have a limited role, as difficulty in interpretation can lead to a high false-positive rate.15 The Eastern Association for the Surgery of Trauma, as an example, eliminates plain radiographs from their algorithm for the screening for thoracolumbar spinal injuries in blunt trauma.16 Anteroposterior (AP) and lateral radiographic views are the standard views performed. AP views can detect misalignment such as in scoliosis and spinal process misalignment indicative of rational injury from unilateral facet dislocation. Lateral views can evaluate disc height, spondylolisthesis, osteoarthritis, spondylosis, vertebral compression fractures, and facet arthropathy (Fig. 45.2). With oblique radiographic views, the patient (or x-ray tube) is angled between 30 and 45 degrees, allowing visualization of the facet joints, neural foramen, and pars interarticularis. It can show spondylolysis and facet pathology. Although flexion-extension radiographs are more common to the cervical region, they can still be performed in the lumbar region with the main goal of assessing ligament and spinal column instability in a dynamic spine. Magnetic resonance imaging (MRI) is the imaging modality of choice when examining the spinal cord, neural elements of the lumbar spine, ligaments, surrounding muscle, and soft tissue. MRI can detect canal and lateral recess stenosis, tumors, infection, hematomas, osteomyelitis, disc degeneration, and facet arthropathy.16,17 If one suspects pathology from a vascular etiology such as arteriovenous malformation or fistula, a magnetic resonance angiogram (MRA) can be performed. Computer tomography (CT) is the ideal imaging modality when assessing bony structures of the spine, as it demonstrates fractures of bony elements (transverse process, spinous process, pars interarticularis, vertebra), and dislocations (facet joints). Myelography is invasive and rarely used. This study involves injection of a contrast medium into the spinal canal to delineate the spinal cord and nerve root using real time radiography (fluoroscope) or CT and can detect location of neural impingement in the neural foramina and lateral recess, spinal cord injury, tumors, or cysts. Myelography may be the only method to evaluate patients who have a contraindication to MRI such as ferromagnetic implants. CT, when used in conjunction with myelography, is more

CHAPTER 45  Lumbar Degenerative Disease

247

Table 45.1  Pseudospine Pain: Diagnostic Keys Condition

Diagnostic Keys

Vascular

Abdominal aortic aneurysm

Gynecologic

Endometriosis

Older than 50 years Abdominal and back pain Pulsatile abdominal mass Women of reproductive age Cyclic pelvic and back pain Young, sexually active women Systemically ill (fever, chills) Discharge, dysuria Missed period Abdominal or pelvic pain Positive pregnancy test result Men older than 30 years Dysuria Low back and perineal pain Flank and groin pain Hematuria Abdominal pain radiating to back Systemic signs (fever, nausea, vomiting) Elevated serum amylase Abdominal pain radiating to back Young to middle-aged women Widespread pain Multiple tender points Disrupted sleep, fatigue Normal radiographs and laboratory values Older than 50–60 years Hip or shoulder girdle pain and stiffness Elevated erythrocyte sedimentation rate Dramatic response to low-dose prednisone Younger men (ankylosing spondylitis, Reiter syndrome) Lower lumbosacral pain Morning stiffness (“gel”) Improvement with activity Radiographic sacroiliitis Older than 50–60 years Thoracolumbar stiffness or pain Flowing anterior vertebral calcification Buttock and leg pain Pain on resisted hip external rotation and abduction Transgluteal or transrectal tenderness Age 12–15 years Thoracic or thoracolumbar pain Increased fixed thoracic kyphosis 3 or more wedged vertebrae with endplate irregularities Pain or tenderness over greater trochanter Back pain Uneven shoulders, scapular prominence Paravertebral hump with forward flexion Women older than 60 years Severe acute thoracic pain (fracture) Severe weight-bearing pelvic pain (fracture) Aching, dull thoracic pain; relieved in supine position (mechanical) Loss of height, increased thoracic kyphosis Diffuse skeletal pain or tenderness Increased alkaline phosphatase Bone pain: low back, pelvic, tibia Increased alkaline phosphatase Characteristic radiographic appearance Older than 50 years Diffuse leg pain, worse at night Proximal muscle weakness Older than 50 years Back pain unrelieved by positional change—night pain Previous history of malignant disease Elevated erythrocyte sedimentation rate

Pelvic inflammatory disease Ectopic pregnancy Genitourinary

Prostatitis Nephrolithiasis

Gastrointestinal

Pancreatitis

Rheumatologic

Penetrating or perforated duodenal ulcer Fibromyalgia

Polymyalgia rheumatica

Seronegative spondyloarthropathies (ankylosing spondylitis, Reiter syndrome, psoriatic, enteropathic)

Diffuse idiopathic skeletal hyperostosis (Forestier disease) Piriformis syndrome Scheuermann kyphosis

Trochanteric bursitis, gluteal fasciitis Adult scoliosis Metabolic

Osteoporosis

Osteomalacia Paget disease Diabetic polyradiculopathy Malignant neoplasia

Modified from Mazanec D. Pseudospine pain: conditions that mimic spine pain. In: Cole AJ, Herring SA, eds. The Low Back Pain Handbook. Philadelphia: Hanley & Belfus; 1997.

248

PART 1  MSK Disorders

Table 45.2  Waddell Signs Five Nonorganic Physical Signs Are Described by Waddell Tenderness

Nonorganic tenderness may be either superficial or nonanatomic. Superficial tenderness can be elicited by lightly pinching over a wide area of lumbar skin. Nonanatomic pain is described as deep tenderness felt over a wide area rather than localized to one structure.

Simulation test

This is usually based on movement that produces pain. Two examples are axial loading, in which low back pain is reported on vertical loading over the standing patient’s skull by the clinician’s hands, and rotation, in which back pain is reported when the shoulder and pelvis are passively rotated in the same plane as the patient stands relaxed with feet together.

Distraction test

If a positive physical finding is demonstrated in a routine manner, this finding is checked while the patient’s attention is distracted. Straight-leg raising is the most useful distraction test. There are several variations to this test; most commonly, however, straight-leg raise is done in the supine position and then, while the patient is distracted, in the sitting position. This is commonly referred to as the flip test. However, one should keep in mind that biomechanically, the two positions are very different.

Regional disturbances

Regional disturbances involve a widespread area, such as an entire quarter or half of the body. The essential feature of this nonorganic physical sign is divergence of the pain beyond the accepted neuroanatomy. Examples include giveaway weakness in many muscle groups manually tested and sensory disturbances, such as diminished sensation to light touch, pinprick, or vibration, that do not follow a dermatomal pattern. Again, care must be taken not to mistake multiple root involvement for regional disturbance.

Overreaction

Waddell reported that overreaction during the examination may take the form of disproportionate verbalization, facial expression, muscle tension, tremor, collapsing, and even profuse sweating. Analysis of multiple nonorganic signs showed that overreaction was the single most important nonorganic physical sign. However, this sign is also the most influenced by the subjectivity of the observer.

Modified from Geraci MC Jr, Alleva JT. Physical examination of the spine and its functional kinetic chain. In: Cole AJ, Herring SA, eds. The Low Back Pain Handbook. Philadelphia: Hanley & Belfus; 1997.

A

B

FIG. 45.2  Chronic degenerative changes—plain film. (A) On a coned-down lateral film, the L4-L5 motion segment shows a vacuum phenomenon in the disc (large arrow), endplate remodeling with large anterior spurs (curved arrows), and grade I retrolisthesis (open arrow). (B) A standing lateral film shows multilevel degenerative disc disease with large posterior spurs, small anterior osteophytes, endplate remodeling, and moderately severe disc space narrowing at L2-L3, L3-L4, and L4-L5. (From Cole AJ, Herzog RJ. The lumbar spine: imaging options. In: Cole AJ, Herring SA, eds. The Low Back Pain Handbook. Philadelphia: Hanley & Belfus; 1997.)

useful than MRI in determining the degree of spinal stenosis at a given level and when specific lumbar segment localization is needed to perform decompressive surgery.17 Discography or discogram is a procedure in which contrast medium is injected into the nucleus pulposus to discern the

cause of discogenic pain. A normal disc can receive between 1 and 1.5 mL of contrast. If greater than 2 mL of contrast is injected, then degenerative disc disease is likely. During the provocative injection procedure, localization of pathologic disc degeneration (i.e., nucleus or annulus tears, fissures, or

CHAPTER 45  Lumbar Degenerative Disease

Table 45.3  Goals in Rehabilitation of Musculoskeletal Injury Acute Phase

Recovery Phase

Functional Phase

Treat clinical symptoms

Allow tissue healing

Correct abnormal biomechanics

Protect injured tissue

Restore normal strength and flexibility

Prevent recurrent injury

Modified from Micheo W, López-Acevedo CE. Medical rehabilitation— lumbar axial pain. In: Slipman CW, ed. Interventional Spine: An Algorithmic Approach. London: Elsevier Health Sciences; 2007:993.

disc protrusion) can be confirmed if pain is reproduced. The sinuvertebral nerve is thought to carry nociceptive sensation to the intervertebral disc. Hence, exploratory studies with blockade of the nerve as an alternative means of diagnosing pain of discogenic origin have been performed.18 Electrodiagnostic studies can be an adjunctive tool for patients in whom physical exam and imaging findings are equivocal and the diagnosis remains a conundrum. Electromyography is specific in diagnosing spinal stenosis and can detect neuromuscular disease that can mimic spinal stenosis.19 

Treatment Initial Studies have shown approximately 90% of people who develop acute LBP experience a resolution of the symptoms within 6 weeks.1,15 Hence, the physician’s main goal during the initial patient encounter should be one of reassurance and education regarding the pathophysiology and natural course of lower back pain. Anti-inflammatory medications should be the mainstay of pharmacological therapy and should be given on a time-contingent basis instead of a paincontingent basis.1 Muscle relaxants, heat and cold modalities, myofascial release, and a physical therapy regimen or exercise prescription should be trialed. Opioid dependency is an important consideration when prescribing these medications, and limiting their use for those with severe symptoms is recommended. There are numerous guidelines that suggest using safe prescribing habits (e.g., a maximum 7-day supply on prescriptions for opioids when issued to an adult for the first time). One should avoid restriction of activities (e.g., work or bed rest), as this leads to prolonged immobility. For those with psychological causes contributing to pain (e.g., sleep disturbances), medications such as melatonin, trazodone, or ramelteon could be employed. 

Rehabilitation The mainstay of rehabilitation, whether through physical or occupational therapy, should be patient education about their disease process, recognizing patterns of back pain and incorporation of exercise, and therapeutic modalities to achieve their goal. Spinal rehabilitation can be approached by delineating three separate phases: acute phase, recovery phase, and functional phase.20 Each phase has a specific goal, which must be met prior to progression to the next phase (Table 45.3).

249

The acute phase of rehabilitation treatment should focus on gradual introduction to therapy by low-level activity and eliminating factors of non-compliance (i.e., symptom control). The goal of this phase is reduction of pain and inflammation, healing of injured tissue, and prevention of further tissue injury. Primarily, one starts by educating the patient about spine biomechanics and identifying one’s neutral spine position. From there, incorporate spine stabilization ­exercise via isometric and static exercises and gradual pain-free ROM exercise. Cryotherapy, transcutaneous nerve stimulation (TENS), massage, or electro-acupuncture can be incorporated at this stage. Acupuncture can be individualized to the cause of a patient’s biomechanical m ­ isalignment and can specifically target paraspinal or quadratus lumborum muscle spasms. After achieving pain-free range of motion, promotion to the recovery phase is warranted. Trying to restore the biomechanical relationships between normal and injured tissue highlights this stage. Emphasis is placed on physical activity during ADL tasks despite existence of pain, focusing on core strengthening, flexion-extension exercises, high exercise repetitions, dynamic flexibility in different planes, and progression of stabilization exercises from stable to unstable surfaces. Anti-inflammatory medications, analgesics, acupuncture, heat therapy, ultrasound, and TENS can be used at this stage. The goal of the functional phase is restoration of function for ADLs and biomechanical motion associated to workrelated activities. This is accomplished by eccentric loading of the spine through complete lumbar ROM exercises and the use of aggressive quota-based exercise programs. After one progresses successfully through the three phases, the focus of therapy is prevention of disability and building upon the foundation one has achieved from the rehabilitation process. This is achieved by promoting and managing healthy lifestyles through exercise and stressing independence from medical treatment. For those who fail therapy or have complaints of persistent pain and disability, it is best to refer them, if available and feasible, to a multidisciplinary care pain program. 

Procedures For those who fail conservative therapy and may benefit from a procedure, the general rule is to start from minimally invasive (e.g., local trigger point injections or “dry needling”) with progression to more invasive options. Local injections can be both diagnostic and therapeutic. Fluoroscopy with use of contrast medium has become the standard method of choice.21 Diagnostic techniques include epidural steroid injections, facet or sacroiliac joint blocks, and provocative discograms as mentioned previously. Therapeutic procedures include caudal, transforaminal, and interlaminar epidural injections; percutaneous and endoscopic spinal adhesiolysis; facet joint interarticular injections and medial branch neurotomy; sacroiliac joint blocks or radiofrequency neurotomy; intradiscal electrothermal therapy (IDET); intrathecal drug administration systems; and spinal cord stimulators.22 Epidural steroid injections are the most commonly performed procedure, with studies showing its benefit in temporary relief of radicular symptoms,23 the thought being that local infiltration of steroid will aid in reduction of

250

PART 1  MSK Disorders

inflammation. Recent case reports have questioned the uses of particulate steroid due to risk of paralysis with inadvertent intra-arterial injection.24 To show the efficacy of use of non-particulate steroid, Kennedy et al. showed that transforaminal epidural injection with dexamethasone does not have major differences when compared with triamcinolone. The facet (zygapophyseal joint) is a synovial joint and is innervated by the medial and articular branch of each lumbar dorsal ramus.25 When pathology is suspected, anesthesia can be obtained via intra-articular joint injection or local anesthetic blockade of medial branches (as articular branches are too small to be accurately targeted). This process can act as a diagnostic test to confirm the facet as the pain generator, paving the way for a more permanent medial branch neurotomy by radiofrequency ablation.26 Since the 1970s, minimally invasive intradiscal therapies such as chemonucleolysis, laser therapy, and percutaneous or endoscopic disc compression have been employed. The use of intradiscal steroid injection is debated, due to risk of discitis, and thermal application to the posterior annulus via intradiscal catheter (IDET) demonstrates favorable outcome, but only with stringent patient selection.27 Intradiscal oxygen-ozone (O2-O3) chemonucleolysis is an effective treatment procedure for neural compression secondary to bulging or herniated disc. The thought is that injection leads to dehydration of the disc, leading to decreased bulging or herniation of the disc tissue, enhanced tissue oxygenation, and anti-inflammatory effects.28,29 A new arena in therapeutic strategies for intervertebral disc and vertebral cartilage is the use of mesenchymal stem cells for repair and degeneration.30 Bone morphogenic protein, juvenile chondrocytes, and fibrin adhesives have also been trialed as other methods to decrease inflammation and slow the degenerative spine process. 

Technology For patients who progress to chronic intractable lumbar pain, new technology in the form of spinal cord stimulation is becoming frequently used. This technology works under the principle of neuromodulation via electrical stimulation of dorsal column, established in 1967.31 The electrical current alters pain processing by masking the sensation of pain, instead inducing a comfortable tingling or paresthesia.32 New technology is emerging for the stimulation of the dorsal root ganglion, which is a highly targeted form of neuromodulation. 

Surgery After failure of conservative and procedural management and after psychological and mental issues have been addressed, surgical treatment next becomes a viable alternative. A randomized controlled multicenter study with 2-year follow-up comparing lumbar fusion to nonsurgical treatment for chronic LBP found lumbar fusion to be significantly superior to nonsurgical treatment in improvement of pain and disability.33 Although the surgical management of lower back pain is constantly under debate, this study showed positive outcomes in a well-defined surgical group. Lumbar arthrodesis (fusion) has long been thought to be the “gold standard” of surgical management of lumbar

degenerative disc disease.34 The rationale of removing the nociceptive load by removal of the diseased disc material and then fusion of the selected segment to decrease motion of the already sensitized segment is the basis for treatment. The three main fusion techniques are posterolateral fusion, interbody fusion, and a 360-degree circumferential fusion, also known as a combination of interbody and posterolateral fusion. Posterolateral fusion targets only the posterior elements while interbody fusion can be performed via anterior or posterior approach. Minimally invasive spine surgery allows access to the spine with minimal disruption of skin and muscle, allowing for decreased intraoperative blood loss, postoperative pain, reoperation rates, hospital length of stay, and faster return to work.35 Lumbar disc arthroplasty (“artificial disc”) recently utilized in the United States after decades of use in Europe has proven a viable option for those looking to preserve lumbar motion instead of the restrictive nature of fusion. Even though there have been studies showing satisfaction of use, there still appears to be no conclusive evidence showing its long-term superiority in level I studies.34 

Potential Disease Complications As stated previously, lumbar degenerative disease is part of the normal aging process. This is evidenced by imaging studies of asymptomatic individuals showing some level of degeneration. However, for patients who are symptomatic, the process begins by advanced segmental degeneration via loss of disc height, osseous degeneration, neural compression (i.e., spinal stenosis, radiculopathy), and neurogenic claudication that leads to functional limitation. For those who suffer acute lower back pain, approximately 90% of pain resolves within 6 weeks. However, for those whose pain is unremitting, they can further go on to develop chronic pain. For individuals with persistent neurological deficits, emphasis is made on quick diagnosis and prompt treatment to prevent permanent neurologic loss. The incidence of mental disorders, whether it be anxiety, depression, or somatoform disorders, is high in patients with chronic pain. Therefore it is important to identify this cohort in order to target them for multidisciplinary care involving behavioral psychology or psychiatry. 

Potential Treatment Complications When considering treatment, whether it is medication, noninvasive, or surgical, no one has completely benign aftereffects. Upon initiating medication use, one always has to check the safety profile. Anti-inflammatory medications have been shown to have gastric, hepatic, and renal side effects. A common complaint for patients taking muscle relaxants is sedation. Heat and cold therapy can cause localized tissue injury if applied for too long or at extreme temperatures. Opioid therapy can cause overdose and dependence. Spinal injections can be complicated by dural puncture, spinal headache, cortisone flare, hypoglycemia, and rarely, hematoma, infection, intra-arterial cannulation, or neurological injury. For those undergoing surgery, appropriate patient selection is important. Surgical complications include vascular complications depending on approach,

CHAPTER 45  Lumbar Degenerative Disease

hematoma, dural tears, epidural fibrosis, postoperative ileus, implant loosening, infection, and spinal cord injury. Medical complications from surgery could be acute kidney injury, urinary retention, urinary tract infection, and pneumonia. It is vital to find the appropriate diagnosis and to educate the patient about the pathophysiology. Discussion of the risk versus benefit and potential complications before initiation of treatment is important.

References 1. University of Michigan Health System. Acute Low Back Pain: UMHS Low Back Pain Guideline Update. 2010. http://www.med.umich.edu/ 1info/FHP/practiceguides/back/back.pdf. Accessed July 12, 2018. 2. U.S. Department of Health and Human Services. National Center for Health Statistics. Chartbook With Special Feature on Racial and Ethnic Health Disparities, 39th ed. N.P.: U.S. Government Printing Office; 2015. 3. Brinjikji W, Luetmer PH, Comstock B, et al. Systematic literature review of imaging features of spinal degeneration in asymptomatic populations. AJNR Am J Neuroradiol. 2014;36(4):811–816. 4. Boos N, Weissbach S, Rohrbach H, et al. Classification of agerelated changes in lumbar intervertebral discs. Spine. 2002;27(23): 2631–2644. 5. Araghi A, Ohnmeiss DD. Natural history of the degenerative cascade. In: Yue JJ, ed. The Comprehensive Treatment of the Aging Spine: Minimally Invasive and Advanced Techniques. Philadelphia: Saunders/Elsevier; 2011:20–24. 6. Altinkaya N, Yildirim T, Demir S, et al. Factors associated with the thickness of the ligamentum flavum: is ligamentum flavum thickening due to hypertrophy or buckling? Spine. 2011;36(16):E1093–E1097. 7. Benoist M. Natural history of the aging spine. Eur Spine J. 2003;12:4–7. 8. Lenoir T, Guedj N, Boulu P, et al. Camptocormia: the bent spine syndrome, an update. Eur Spine J. 2010;19(8):1229–1237. 9. Fraser RD, Bleasel JF, Moskowitz RW. Spinal degeneration: pathogenesis and medical management. In: Frymoyer JW, ed. The Adult Spine: Principles and Practice, 2nd ed. Philadelphia: Lippincott-Raven; 1997:735–759. 10. Hoy D, Brooks P, Blyth F, et al. The epidemiology of low back pain. Best Pract Res Clin Rheumatol. 2010;24(6):769–781. 11. Kalichman L, Kim DH, Li L, et al. Computed tomography-evaluated features of spinal degeneration: prevalence, intercorrelation, and association with self-reported low back pain. Spine J. 2010;10(3):200–208. 12. 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. 13. Ombregt L. Clinical examination of the lumbar spine. In: Ombregt L, ed. A System of Orthopaedic Medicine. Edinburgh: Churchill Livingstone Elsevier; 2013:491–522. 14. Waddell G, McCulloch JA, Kummel E, et al. Nonorganic physical signs in low-back pain. Spine (Phila Pa 1976). 1980;5:117–125. 15. Humphreys CS. Neuroimaging in low back pain. Am Fam Physician. 2002;65(11):2299–2306. 16. Sixta S, Moore FO, Ditillo MF, et al. Screening for thoracolumbar spinal injuries in blunt trauma. J Trauma Acute Care Surg. 2012;73:S326–S332.

251

17. Siemund R, Thurnher M, Sundgren PC. How to image patients with spine pain. Eur J Radiol. 2015;84(5):757–764. 18. Schliessbach J, Siegenthaler A, Heini P, et al. Blockade of the sinuvertebral nerve for the diagnosis of lumbar diskogenic pain: an exploratory study. Anesth Analg. 2010;111:204–206. 19. Haig A, Tong HC, Yamakawa KSJ, et al. The sensitivity and specificity of electrodiagnostic testing for the clinical syndrome of lumbar spinal stenosis. Spine. 2005;30(23):2667–2676. 20. Micheo W, López-Acevedo CE. Medical rehabilitation - lumbar axial pain. In: Slipman CW ed. Interventional Spine: An Algorithmic Approach. London: Elsevier Health Sciences; 2007:991–999. 21. O’Neill C, Derby R, Kenderes L. Precision injection techniques for diagnosis and treatment of lumbar disc disease [review]. Semin Spine Surg. 1999;11:104–118. 22. Boswell MV, Shah RV, Everett CR, et al. Interventional techniques in the management of chronic spinal pain: evidence based practice guidelines. Pain Physician. 2005;8:1–47. 23. Carette S, Leclaire R, Marcoux S, et al. Epidural corticosteroid injections for sciatica due to herniated nucleus pulposus. N Engl J Med. 1997;336:1634–1640. 24. Kennedy DJ, Plastaras C, Casey E, et al. Comparative effectiveness of lumbar transforaminal epidural steroid injections with particulate versus nonparticulate corticosteroids for lumbar radicular pain due to intervertebral disc herniation: a prospective, randomized, double-blind trial. Pain Medicine. 2014;15(4):548–555. 25. Lau P, Mercer S, Govind J, et al. The surgical anatomy of lumbar medial branch neurotomy (facet denervation). Pain Medicine. 2004;5(3):289–298. 26. Dreyfuss P, Halbrook B, Pauza K, et al. Efficacy and validity of radiofrequency neurotomy for chronic lumbar zygapophysial joint pain. Spine. 2000;25:1270–1277. 27. Lu Y, Guzman JZ, Purmessur D, et al. Nonoperative management of discogenic back pain. Spine. 2014;39(16):1314–1324. 28. Dall’olio M, Princiotta C, Cirillo L, et al. Oxygen-ozone therapy for herniated lumbar disc in patients with subacute partial motor weakness due to nerve root compression: the first 13 cases. Interv Neuroradiol. 2014;20:547–554. 29. Perri M, Marsecano C, Varrassi M, et al. Indications and efficacy of O2O3 intradiscal versus steroid intraforaminal injection in different types of disco vertebral pathologies: a prospective randomized double-blind trial with 517 patients. Radiol Med. 2015;121:463–471. 30. Richardson SM, Kalamegam G, Pushparaj PN, et al. Mesenchymal stem cells in regenerative medicine: focus on articular cartilage and intervertebral disc regeneration. Methods. 2016;99:69–80. 31. Shealy CN, Mortimer JT, Reswick JB. Electrical inhibition of pain by stimulation of the dorsal columns: preliminary clinical report. Anesth Analg. 1967;46(4):489–491. 32. Verrills P, Sinclair C, Barnard A. A review of spinal cord stimulation systems for chronic pain. J Pain Res. 2016;9:481–492. 33. Fritzell P, Hägg O, Wessberg P, et al. 2001 Volvo award winner in clinical studies: lumbar fusion versus nonsurgical treatment for chronic low back pain. Spine. 2001;26(23):2521–2532. 34. Lee YC, Zotti MGT, Osti LO. Operative management of lumbar degenerative disc disease. Asian Spine J. 2016;10(4):801–819. 35. Perez-Cruet MJ, Hussain NS, White GZ, et al. Quality-of-life outcomes with minimally invasive transforaminal lumbar interbody fusion based on long-term analysis of 304 consecutive patients. Spine. 2014;39(3):E191–E198.

CHAPTER 46

Lumbar Facet Arthropathy Byron J. Schneider, MD A. Simone Maybin, MD

Synonyms Facet joint pain Facet joint arthritis Zygapophyseal joint pain Z-joint pain Lumbar spondylosis Facet syndrome Posterior element disorder

ICD-10 Codes M47.817 M47.899 M54.5

Spondylosis without myelopathy or radiculopathy, lumbosacral region Other spondylosis, site unspecified Low back pain

Definition Lumbar facet joints (zygapophyseal joints, z-joints) are formed by the articulation of the inferior and superior articular facets of adjacent vertebrae. The synovial capsule of facet joints receives nociceptive innervation via the medial branches of the dorsal rami (Fig. 46.1).1 The point prevalence of low back pain in the United States is 8.1%,2 with lumbar facet pain as the cause between 10% and 40% of the time.3,4 Facet arthropathy refers to any acquired, traumatic, or degenerative process that changes the normal function or anatomy of a lumbar facet joint. The most common cause of lumbar facet arthropathy is osteoarthritis,5 which is most common at L4-L5 and associated with advancing age and intervertebral disc degeneration at L5.6 These findings are independent of race and sex.7 Segmental degenerative changes including facet arthropathy are very common after lumbar disc surgery.8 These are accompanied by facet joint pain in 8% of patients after lumbar disc surgery.9 Other causes of lumbar arthropathy include rheumatologic conditions such as ankylosing spondylitis and biomechanical abnormalities such as asymmetric alignment of the joints (facet tropism). In patients with low back pain, 252

lumbar facet joints may be a primary source of pain, but may also be painful concomitantly with other lumbar spine pathology. 

Symptoms In general, facet arthropathy can result in low back pain. However, specific clinical features have not been found to reliably differentiate facet joint pain from other causes of low back pain.10 Patients may complain of generalized or paramidline spinal pain. Pain may be well localized; however, localization of pain to the low back, buttocks, and leg is a nonspecific finding in patients with low back pain.11 Surprisingly, pain referred below the knee is neither less nor more prevalent in patients with facet joint pain.10 

Physical Examination A detailed examination of the lumbar spine and a lower extremity neurologic examination are considered standard procedure for any patient presenting with low back pain. The physical examination can be helpful in elevating the clinician’s level of suspicion for the diagnosis of lumbar facet pain. The examination starts with simple observation of the patient’s gait, posture, movement patterns, and range of motion. Generalized and segmental spinal palpation is followed by a detailed neurologic examination for sensation, reflexes, tone, and strength. In the absence of coexisting pathologic processes, such as lumbar radiculopathy, strength, sensation, and deep tendon reflexes should be normal. Provocation maneuvers should also be performed. Facet pain may be reproduced with extension and rotation (facet loading maneuver). Pain with lumbar extension may also be present. Other physical exam maneuvers may be performed to assess for alternate pain generators that refer pain to the low back, for example, performing Flexion Abduction External Rotation test to evaluate for sacroiliac joint pain. Neural tension tests such as the straight leg raise can be performed to rule out superimposed lumbar radicular pain that might accompany a facet disorder. Typically, in isolated cases of lumbar facet disorders, this maneuver does not provoke radiating symptoms into the lower extremity, but may cause low back pain. That said, no single exam or combination of exam maneuvers has been shown to be a valid diagnostic tool for diagnosing lumbar facet pain.4,12,13 

CHAPTER 46  Lumbar Facet Arthropathy

253

FIG. 46.1  Cadaveric dissection showing the lumbar facet joints and innervation via the medial branches of the dorsal rami. dr, Dorsal ramus; mal, mamillo-accessory ligament; mb, medial branch; sap, superior articular process; tp, transverse process.  (Image reproduced with permission from International Spine Intervention Society. Lumbar medial branch blocks. In: Bogduk N, ed. Practice Guidelines for Spinal Diagnostic and Treatment Procedures. 2nd ed. San Francisco: International Spine Intervention Society; 2013).

Functional Limitations Because of the location of lumbar facet joints in the posterior column of the spine axis, symptoms are aggravated by extension-based activities. Patients may describe this as pain worse with standing or lying prone and alleviated by sitting. Functionally, this may also be experienced as difficulties with prolonged standing or walking during work or recreation activities, twisting motions during sports, and lying in bed. 

Diagnostic Studies Abnormalities seen in the facet joints on routine imaging such as x-ray or computed tomography do not correlate with symptomatically painful joints.14 Limited evidence exists that abnormalities seen on single photon emission computed tomography (SPECT) may predict painful z-joints that respond to intra-articular steroid injections.15 More recently, abnormalities seen in lumbar facet joints on short tau inversion recovery magnetic resonance imaging (MRI) sequences and fat-saturated MRI sequences have been correlated with symptomatic facet arthropathy.16 Facet inflammation on MRI has also been correlated with serum inflammatory markers in patients with ankylosing spondylitis.17 Recall that the lumbar facet joints are innervated by the medial branches of the dorsal rami above and below the joint space (Fig. 46.2).1 Accurately anesthetizing these nerves via fluoroscopy has been experimentally proven to block pain arising from the facet joints.18 Accordingly, fluoroscopy-guided medial branch blocks (MBBs) are considered the “gold standard” for the diagnosis of a painful lumbar facet joint.19 A single MBB has an unacceptably high false positive rate, however, so to

ensure accuracy, dual MBBs are recommended.19 In this paradigm, an MBB is performed twice, each time with an anesthetic of different duration of action. If a patient fails to achieve relief in either case, ideally for a time consistent with the local anesthetic used, the result of the test is considered negative. In general, the patient must be experiencing his or her typical pain prior to the procedure. Careful documentation of the patient’s pre- and post-procedure pain level is then required to determine what degree of pain relief was achieved after this injection and for how long this lasted.  Differential Diagnosis Lumbar discogenic pain Spondylolysis Mobile spondylolisthesis Proximal lumbar radicular pain Sacroiliac joint dysfunction Somatic referred hip pain Fibromyalgia

Treatment Initial Initial treatment for low back pain commonly involves medication. For noninvasive treatment options, such as medication or physical therapy, most literature does not specify between specific causes of low back pain and only evaluates these treatment options as they pertain to “nonspecific low back pain.” Such studies must also be considered within the context of an already favorable natural history of most cases

254

PART 1  MSK Disorders

Inflexion L3 mb

mp Inflexion

L4 mb

mp Inflexion

L5 dr

A

B

FIG. 46.2  Oblique view of the lumbar spine showing the target points for medial branch blocks targeting the L3-L4 and L4-L5 facet joints. The white dotted lines represent the course of the target nerve. dr, Dorsal ramus; mb, medial branch; mp, mammillary process. (Image reproduced with permission from International Spine Intervention Society. Lumbar medial branch blocks. In: Bogduk N, ed. Practice Guidelines for Spinal Diagnostic and Treatment Procedures. 2nd ed. San Francisco: International Spine Intervention Society; 2013.)

of low back pain. Given these limitations, it is often difficult to properly interpret the outcomes of these studies. Medication choices include acetaminophen, muscle relaxants, nonsteroidal anti-inflammatory drugs (NSAIDs), and opioids. Oral acetaminophen has been shown to have no effect on recovery time from an acute episode of low back pain compared to placebo.20 Evidence in support of topical NSAIDs is also limited.21 Oral NSAIDs have been found to be both superior to placebo, but equal to acetaminophen in treating low back pain.22 In the acute setting, the addition of cyclobenzaprine or oxycodone with acetaminophen to prescribing naproxen (an NSAID) did not result in differences in pain or function at 1 week.23 The heterogeneity in outcomes seen in these studies is likely at least in part due to the nonspecific design of studies that includes many heterogeneous etiologies of low back pain.24 Accordingly, often medications with more favorable side-effect profiles are preferentially used. Opioids should be used with great caution due to the high risk of addiction and overdose. Recent Centers for Disease Control and Prevention (CDC) guidelines state that, in cases of non-cancer or non-palliative care such as low back pain, non-opioid pharmacologic therapy is preferred.25 Moreover, if opioids are to be used, three days or less is often sufficient, with use beyond seven days rarely indicated.25 

Rehabilitation In addition to oral medication, initial treatment for low back pain also frequently incorporates physical therapy. Physical therapy entails a variety of modalities including pain control (e.g., ice, heat), traction, instruction in body mechanics, flexibility training (including hamstring stretching), articular mobilization techniques, core strengthening, generalized conditioning, and restoration of normal movement patterns. It may be helpful to assess the biomechanics

of specific activities (e.g., sitting at a desk, carpentry work, driving, running, cycling). In theory, this may result in decreased severity or frequency of recurrent episodes of pain by optimizing the underlying forces at the affected joint. Outcome literature on physical therapy for the treatment of low back pain is variable. This again is likely due to heterogeneous patient groups being included in nonspecific studies. That said, some of the best supporting evidence is for early outpatient physical therapy for the treatment of acute low back pain.26 There is no evidence suggesting benefit for inpatient rehabilitation in the treatment of isolated facet joint-mediated low back pain. 

Procedures Fluoroscopic-guided facet targeted injections are a potential treatment option for lumbar facet pain, usually after oral medications and therapy have been attempted and failed to provide adequate relief. The evidence in support of intraarticular lumbar facet steroid injections is very limited.27 The best evidence that exists in support of intra-articular lumbar facet steroid injections utilizes SPECT imaging to identify patients with lumbar facet pain.15,27 One comparative study also suggests that intra-articular steroid injections may be as effective as radiofrequency neurotomy (RFN) targeting the lumbar facet joints.28 Ultrasound guidance for intra-articular facet injections is also an emerging option, though additional evidence is still needed.29 The best available evidence on the treatment of lumbar facet pain supports the use of RFN.19 RFN uses radiofrequency to transmit heat energy at the tip of an electrode. When applied to a nerve, this results in neurolysis via protein denaturing and cellular membrane disruption. RFN requires technical precision in order to generate lesions that capture the target nerve. For example, electrodes must be placed parallelly to the target as opposed to

CHAPTER 46  Lumbar Facet Arthropathy

255

patients in the study reported at least 50% relief of their back pain after 2 years of treatment with high-frequency SCS.34 

Surgery Surgical spinal fusion may be performed for axial low back pain, most commonly in the setting of suspected discogenic pain. Some studies have found that the majority of patients undergoing lumbar spinal fusion also have evidence of secondary facet arthropathy.35 However, facet arthropathy is not a primary indication for lumbar spinal fusion, and some suggest it is actually a contraindication.35 

Potential Disease Complications

FIG. 46.3  Oblique fluoroscopic image of a radiofrequency electrode placed in the location of the left L2 medial branch as it courses along the sulcus formed between the superior articular process and transverse process of the L3 vertebral body. *Note the position of the electrode inferior to this targeting the L3 medial branch is not yet in final position. (Image courtesy Byron J. Schneider, MD.)

perpendicularly (Fig. 46.3); procedure details are published elsewhere.19 RFN is not necessarily curative, as intact cell bodies remain capable of axonal regeneration. However, average relief is greater than 1 year.30 If symptoms return, repeat RFN will often re-institute relief obtained from the initial treatment.30 Randomized controlled studies have shown RFN to result in statistically and clinically significant reductions in pain and function compared to placebo procedure for up to 1 year.31 Under ideal conditions, including selection of patients via dual controlled MBBs, up to 60% of patients can expect at least 90% reduction in pain and 87% of patients can expect at least 60% reduction in pain at 12 months.32 Other studies have corroborated this, demonstrating that in addition to pain relief, greater than 50% of patients can expect at least 80% pain relief, restoration of activities of daily living, return to work, and no additional health care needs related to back pain.30 Studies with average follow up of greater than 3 years have shown continued benefit of lumbar RFN.33 

Technology Spinal cord stimulators (SCS) have traditionally been indicated in the treatment of chronic post-operative lumbar radicular pain. Recent evidence has suggested high frequency SCS may also be effective in treating axial low back pain.34 In this study, 80% of the patients in the study had a history of lumbar surgery, and 41% of patients also had a diagnosis of spondylosis, although only 15% had a specific diagnosis of lumbar facet arthropathy; 76.5% of all

The potential complications related to facet arthropathy are dependent on the etiology of arthropathy. Extremely rare causes of arthropathy such as infection or malignancy can potentially have life-threatening complications. On the other hand, most cases of facet arthropathy are degenerative in nature,5 which can be progressive and may result in chronic low back pain if untreated. In general, however, very few patients that initially present with low back pain develop chronic low back pain.36 Facet joints osteophytes may result in subarticular stenosis or foraminal stenosis. They may also combine with other degenerative processes such as disc degeneration or ligamentum flavum hypertrophy to result in central canal stenosis. Lumbar stenosis can then result in radiculopathy with associated neurologic deficits. 

Potential Treatment Complications Serious complications related to the treatment of lumbar facet can be due to medication use or spine interventions. In general, 1% to 2% of NSAID users experience a serious gastrointestinal complication such as bleeding and hospitalization.37 Other NSAID-related complications include cardiovascular and renal complications. Opioid-related deaths in the United States have increased over 200% to a rate of 9/100,000 people since 2000 and have become a national epidemic.38 Intervention-based procedures inherently carry risks of relatively minor complications such as minor bleeding or bruising, procedure-related discomfort, and vasovagal reactions.39 Intra-articular steroid injections also carry with them related side effects from corticosteroids. RFN carries with it potential complications such as inadvertent nerve damage. In the closed claims database from the American Society of Anesthesiologists that spanned from 1970 to 1999, only four claims were attributed to RFN.40 When proper technique is used for lumbar facet RFN, no serious complications have been reported.19

References 1. Bogduk N. The innervation of the lumbar spine. Spine. 1983;8(3): 286–293. 2. Johannes CB, Le TK, Zhou X, Johnston JA, Dworkin RH. The prevalence of chronic pain in United States adults: results of an Internetbased survey. J Pain. 2010;11(11):1230–1239. 3. DePalma MJ, Ketchum JM, Saullo T. What is the source of chronic low back pain and does age play a role? Pain Med. 2011;12(2):224–233.

256

PART 1  MSK Disorders

4. Schwarzer AC, Wang SC, Bogduk N, McNaught PJ, Laurent R. Prevalence and clinical features of lumbar zygapophysial joint pain: a study in an Australian population with chronic low back pain. Ann Rheum Dis. 1995;54(2):100–106. 5.  de Vlam K, Mielants H, Verstaete KL, Veys EM. The zygapophyseal joint determines morphology of the enthesophyte. J Rheumatol. 2000;27(7):1732–1739. 6. Eubanks JD, Lee MJ, Cassinelli E, Ahn NU. Prevalence of lumbar facet arthrosis and its relationship to age, sex, and race: an anatomic study of cadaveric specimens. Spine. 2007;32(19):2058–2062. 7. Li J, Muehleman C, Abe Y, Masuda K. Prevalence of facet joint degeneration in association with intervertebral joint degeneration in a sample of organ donors. J Orthop Res. 2011;29(8):1267–1274. 8. Ebenbichler GR, Leitgeb J, Amtmann G, König F, Schernthaner M, Resch K-L, et al. Degeneration and instability and the relation to patients’ function late after lumbar disc surgery: data from a 12-year follow-up. Am J Phys Med Rehabil. 2016;95(12):871–879. 9. Steib K, Proescholdt M, Brawanski A, Lange M, Schlaier J, Schebesch K-M. Predictors of facet joint syndrome after lumbar disc surgery. J Clin Neurosci. 2012;19(3):418–422. 10. Schwarzer AC, Aprill CN, Derby R, Fortin J, Kine G, Bogduk N. Clinical features of patients with pain stemming from the lumbar zygapophysial joints. is the lumbar facet syndrome a clinical entity? Spine. 1994;19(10):1132–1137. 11. Mooney V, Robertson J. The facet syndrome. Clin Orthop. 1976;(115): 149–156. 12. Schwarzer AC, Aprill CN, Derby R, Fortin J, Kine G, Bogduk N. Clinical features of patients with pain stemming from the lumbar zygapophysial joints. Is the lumbar facet syndrome a clinical entity? Spine. 1994;19(10):1132–1137. 13. Hancock MJ, Maher CG, Latimer J, et al. Systematic review of tests to identify the disc, SIJ or facet joint as the source of low back pain. Eur Spine J. 2007;16(10):1539–1550. 14. Schwarzer AC, Wang SC, O’Driscoll D, Harrington T, Bogduk N, Laurent R. The ability of computed tomography to identify a painful zygapophysial joint in patients with chronic low back pain. Spine. 1995;20(8):907–912. 15. Ackerman WE III, Ahmad M. Pain relief with intraarticular or medial branch nerve blocks in patients with positive lumbar facet joint SPECT imaging: a 12-week outcome study. South Med J. 2008;101(9):931–934. 16. Czervionke LF, Fenton DS. Fat-saturated MR imaging in the detection of inflammatory facet arthropathy (facet synovitis) in the lumbar spine. Pain Med. 2008;9(4):400–406. 17. Lee S, Lee JY, Hwang JH, Shin JH, Kim T-H, Kim S-K. Clinical importance of inflammatory facet joints of the spine in ankylosing spondylitis: a magnetic resonance imaging study. Scand J Rheumatol. 2016;45(6):491–498. 18. Kaplan M, Dreyfuss P, Halbrook B, Bogduk N. The ability of lumbar medial branch blocks to anesthetize the zygapophysial joint. a physiologic challenge. Spine. 1998;23(17):1847–1852. 19. Bogduk N. Practice Guidelines for Spinal Diagnostic and Treatment Procedures. 2nd ed. San Francisco; 2013. 20. Williams CM, Maher CG, Latimer J, Day RO, et al. Efficacy of paracetamol for acute low-back pain: a double-blind, randomised controlled trial. Lancet. 2014;384(9954):1586–1596. 21. Haroutiunian S, Drennan DA, Lipman AG. Topical NSAID therapy for musculoskeletal pain. Pain Med. 2010;11(4):535–549. 22. Roelofs PDDM, Deyo RA, Koes BW, Scholten RJPM, van Tulder MW. Nonsteroidal anti-inflammatory drugs for low back pain: an updated Cochrane review. Spine. 2008;33(16):1766–1774.

23. Friedman BW, Dym AA, Davitt M, et al. Naproxen with cyclobenzaprine, oxycodone/acetaminophen, or placebo for treating acute low back pain: a randomized clinical trial. JAMA. 2015;314(15):1572–1580. 24. Schneider BJ, Kennedy DJ, Kumbhare D. Second-order peer reviews of clinically relevant articles for the physiatrist: naproxen with cyclobenzaprine, oxycodone/acetaminophen, or placebo to treating acute low back pain: a randomized clinical trial. Am J Phys Med Rehabil. 2016. 25. Dowell D, Haegerich TM, Chou RCDC. Guideline for prescribing opioids for chronic pain-United States, 2016. JAMA. 2016. 26. Gellhorn AC, Chan L, Martin B, Friedly J. Management patterns in acute low back pain: the role of physical therapy. Spine. 2012;37(9):775–782. 27. Schneider B, Levin JA. Narrative review of intra-articular zygapophysial steroid injections for lumbar zygapophysial-mediated pain. Curr Phys Med Rehabil Rep. 2016;2(4):108–116. 28. Lakemeier S, Lind M, Schultz W, Fuchs-Winkelmann S, Timmesfeld N, Foelsch C, et al. A comparison of intraarticular lumbar facet joint steroid injections and lumbar facet joint radiofrequency denervation in the treatment of low back pain: a randomized, controlled, double-blind trial. Anesth Analg. 2013;117(1):228–235. 29. Wu T, Zhao W-H, Dong Y, Song H-X, Li J-H. Effectiveness of ultrasound-guided versus fluoroscopy or computed tomography scanning guidance in lumbar facet joint injections in adults with facet joint syndrome: a meta-analysis of controlled trials. Arch Phys Med Rehabil. 2016;97(9):1558–1563. 30. MacVicar J, Borowczyk JM, MacVicar AM, Loughnan BM, Bogduk N. Lumbar medial branch radiofrequency neurotomy in New Zealand. Pain Med. 2013;14(5):639–645. 31. Tekin I, Mirzai H, Ok G, Erbuyun K, Vatansever D. A comparison of conventional and pulsed radiofrequency denervation in the treatment of chronic facet joint pain. Clin J Pain. 2007;23(6):524–529. 32. Dreyfuss P, Halbrook B, Pauza K, Joshi A, McLarty J, Bogduk N. Efficacy and validity of radiofrequency neurotomy for chronic lumbar zygapophysial joint pain. Spine. 2000;25(10):1270–1277. 33. McCormick ZL, Marshall B, Walker J, McCarthy R, Walega DR. Longterm function, pain and medication use outcomes of radiofrequency ablation for lumbar facet syndrome. Int J Anesth Anesthesiol. 2015;2(2). 34. Kapural L, Yu C, Doust MW, et al. Comparison of 10-kHz highfrequency and traditional low-frequency spinal cord stimulation for the treatment of chronic back and leg pain: 24-month results from a multicenter, randomized, controlled pivotal trial. Neurosurgery. 2016;79(5):667–677. 35. Wong DA, Annesser B, Birney T, et al. Incidence of contraindications to total disc arthroplasty: a retrospective review of 100 consecutive fusion patients with a specific analysis of facet arthrosis. Spine J. 2007;7(1):5–11. 36. Carey TS, Garrett JM, Jackman AM. Beyond the good prognosis. Examination of an inception cohort of patients with chronic low back pain. Spine. 2000;25(1):115–120. 37. Sostres C, Gargallo CJ, Lanas A. Nonsteroidal anti-inflammatory drugs and upper and lower gastrointestinal mucosal damage. Arthritis Res Ther. 2013;15(Suppl 3):S3. 38. Rudd RA, Aleshire N, Zibbell JE, Gladden RM. Increases in drug and opioid overdose deaths–United States, 2000-2014. MMWR Morb Mortal Wkly Rep. 2016;64(50–51):1378–1382. 39. Kennedy DJ, Schneider B, Casey E, et al. Vasovagal rates in flouroscopically guided interventional procedures: a study of over 8,000 injections. Pain Med Malden Mass. 2013;14(12):1854–1859. 40. Fitzgibbon DR, Posner KL, Domino KB, et al. Chronic pain management: American Society of Anesthesiologists closed claims project. Anesthesiology. 2004;100(1):98–105.

CHAPTER 47

Lumbar Radiculopathy Michael J. Ellenberg, MD Maury Ellenberg, MD

Synonyms Lumbar radiculitis Sciatica Pinched nerve Herniated nucleus pulposus with nerve root irritation

ICD-10 Codes M54.16 Radiculopathy, lumbar region M51.9 Unspecified thoracic, thoracolumbar, lumbosacral intervertebral disc disorder

Definition Lumbar radiculopathy refers to a pathologic process involving the lumbar nerve roots. Lumbar radiculitis refers to an irritation or inflammation of a nerve root. These terms should not be confused with disc herniation, which is a displacement of the lumbar disc from its anatomic location between the vertebrae (often into the spinal canal) (Fig. 47.1). Although lumbar radiculopathy is often caused by a herniated lumbar disc, this is not invariably the case. Many pathologic processes, such as bone encroachment, tumors, and metabolic disorders (e.g., diabetes) can also result in lumbar radiculopathy. It is of utmost significance that disc herniation is often an incidental finding on imaging of the lumbar spine of asymptomatic individuals.1 Therefore, without a clear correlation with the history and physical examination, imaging studies alone can be more misleading than beneficial. When disc herniation results in radiculopathy, the precise cause of the pain is not fully understood. The two possibilities are mechanical compression and inflammation. It has been demonstrated that in a “nonirritated” nerve, mechanical stimulus rarely leads to pain. In contrast, an “irritated” nerve usually results in pain. Furthermore, inflammatory mediators have experimentally been shown to cause radicular pain in the absence of compression.2 It is likely that both factors may be at work individually or together in any given patient. As a result of the imaging findings in asymptomatic individuals and the

various causes of pain in radiculopathy, it should be no surprise that disc herniations and nerve root compression can be present in asymptomatic patients1 and that patients can have radiculopathy without visible disc herniations or nerve root compression.3 The prevalence of lumbar radiculopathy in the general population varies from 2.2% to 8%, depending on the study, and the incidence ranges from 0.7% to 9.6%.4,5 In patients with radiculopathy, one study found a higher incidence in men (67%), with the highest prevalence in individuals 45 to 65 years old,6 and an association with obesity and smoking as well as a correlation with occupations requiring very heavy physical activity. 

Symptoms The most common symptom in lumbar radiculopathy is pain, which may vary in severity and location. The pain may be severe and is often exacerbated or precipitated by standing, sitting, coughing, and sneezing. The location of the pain depends on the nerve root involved, with a great deal of overlap among the dermatomes. Most commonly, S1 radiculopathy produces posterior thigh and calf pain; L5, buttocks and anterolateral leg pain; L4, anterior thigh, anterior or medial knee, and medial leg pain; and L3, groin pain. The patient usually cannot pinpoint the precise onset of pain. Location of pain at onset may be in the back; however, by the time the patient is evaluated, the pain may be present only in the buttocks or limb. Paresthesias are also common and occur in the dermatomal distribution of the involved nerve root (rarely is the sensory loss complete). On occasion, the patient may present with complaints of weakness. Rarely, there is bladder and bowel involvement, which may manifest as urinary retention or bowel incontinence. 

Physical Examination The most important elements in the evaluation of lumbar radiculopathy are the history and physical examination.7 A thorough musculoskeletal and peripheral neurologic examination should be performed. Examine the back for asymmetry or a shift over one side of the pelvis. Evaluate back motion and see whether radicular symptoms (pain radiating to an extremity) in the distribution of the patient’s complaints are produced. In an L5 or S1 radiculopathy, 257

258

PART 1  MSK Disorders

forward flexion of the back while standing is equivalent to a straight-leg raising test and may produce pain in the buttock or posterior thigh. In an L4 or L3 radiculopathy, extension may produce groin or anterior thigh pain. Manual muscle testing is a vital part of the examination for radiculopathy. The major muscle weakness in relation to the nerve root involved is as follows: L3, hip flexors; L4, knee extensors and hip adductors; L5, hip abductors, knee flexors, ankle dorsiflexors, foot evertors, foot inverters, and great toe extensor; S1, ankle plantar flexors (Table 47.1). Try to detect weakness in the distribution of two peripheral nerves arising from the same nerve root. Proximal muscle weakness in the appropriate nerve root distribution is useful in distinguishing bilateral radiculopathy from peripheral neuropathy. The straight-leg raising test can be performed with the patient sitting or supine. The lower limb while extended is raised by the examiner, and the test result is positive if the

Third lumbar vertebra Normal disc Herniated nucleus pulposus impinging on spinal nerve

patient complains of pain in the extremity (not the back), typically in a specific nerve root distribution. If pain occurs only in the back, this is not a positive straight-leg raising test, and therefore not an indicator of radiculopathy and is most often seen with nonspecific low back pain. On occasion, the process of lumbar radiculopathy may start with low back pain, and several days or weeks later, the symptom of pain will occur in the lower limb. It is possible that the initial process of nucleus pulposus rupture through the annulus may result in the initial back pain, but the pathogenesis is not completely known at this time. Compare side to side to confirm a positive response to the straight-leg raise test as opposed to the pain associated with passive hamstring stretch. Rectal examination and perianal and inguinal sensory testing should be done if there is history of bowel or bladder incontinence or retention or recent onset of erectile dysfunction. Waddell signs are a group of indicators that a nonorganic process is interfering with the accuracy of the physical examination. The signs are superficial tenderness; simulation—axial loading or rotation of the head causing complaints of back pain; distraction—sitting straight-leg raising versus supine; regional disturbance—weakness or sensory loss in a region of the body that is in a nonanatomic distribution; and overreaction—what is described commonly as excessive pain behavior. These signs are often present in patients with compensation, litigation, or psycho-emotional issues.8 Evaluation for presence of Waddell signs should be a routine part of the examination in patients with pain complaints, particularly if they are long-standing or the history reveals that some of the above mentioned issues are present. 

Functional Limitations

Sacrum FIG. 47.1  A herniated disc.

The functional limitations depend on the severity of the symptoms and weakness. Limitations usually occur because of pain, but may occasionally occur because of weakness. Standing and walking may be limited, and sitting tolerance is often decreased. Patients with an L4 radiculopathy are at risk of falling down stairs if the involved leg is their “trailing” (power) leg on the stairs. They would also have difficulty ascending stairs or rising from a seated position, depending on the degree of weakness (although that is not as dangerous as descending stairs). Patients with a severe S1 radiculopathy will be unable to run because of calf weakness, even when the

Table 47.1  Diagnosis of Lumbar Radiculopathy Nerve Root

Pain Radiation

Gait Deviation

Motor Weakness

Sensory Loss

Reflex Loss

L3

Groin and inner thigh

Sometimes antalgic

Hip flexion

Anteromedial thigh

Patellar (variable)

L4

Anterior thigh or knee, or upper medial leg

Sometimes antalgic Difficulty rising onto a stool or chair with one leg

Knee extension, hip flexion and adduction

Lateral or anterior thigh, medial leg, and knee

Patellar

L5

Buttocks, anterior or lateral leg, dorsal foot

Difficulty heel walking; if more severe, then foot slap or steppage gait Trendelenburg gait

Ankle dorsiflexion, foot eversion and inversion, toe extension, hip abduction

Posterolateral thigh, anterolateral leg, and mid-dorsal foot

Medial hamstring (variable)

S1

Posterior thigh, calf, plantar foot

Difficulty toe walking or cannot rise on toes 20 times

Foot plantar flexion

Posterior thigh and calf, lateral and plantar foot

Achilles

CHAPTER 47  Lumbar Radiculopathy

pain resolves until the calf muscle strength returns. Patients with L5 radiculopathy may catch the foot on curbs or, if weakness is severe, on the ground. They may require a brace (ankle dorsiflexion assist). In patients with acute radiculop­ athy that is severe, the pain will usually preclude them from a whole range of activities—household, recreation, and work. In the majority of patients, once the acute process is ameliorated, they can return to most activities except for heavy household and work activity. After about 3 to 6 months, they can return to all activities unless there is residual weakness, in which case they would be functionally limited as noted before, depending on the level of the radiculopathy. 

Diagnostic Studies Diagnostic testing takes two forms: one to corroborate the diagnosis and the second to determine the etiology. For simple cases, despite the current “rush toward imaging,” diagnostic testing is usually not needed and the clinical picture can guide the treatment. A history that includes trauma, cancer, bacterial infection, human immunodeficiency virus infection, or diabetes would be an indication for earlier diagnostic testing. 

Electromyography Electromyography and nerve conduction studies, when performed by an individual well versed in the diagnosis of neuromuscular disorders, can be valuable in the diagnosis of lumbar radiculopathy. They can also help with differential diagnoses and in clarifying the diagnosis in patients whose physical examination is not reliable. Electromyography has the advantage over imaging techniques of high specificity, and recordings will rarely be abnormal in asymptomatic individuals.9 Electrodiagnostic studies, however, do not give direct information about the cause of the radiculopathy. 

Imaging Imaging techniques in relation to lumbar radiculopathy usually refer to lumbosacral spine radiography, computed tomography (CT) scan, and magnetic resonance imaging (MRI). Plain radiography can be useful to exclude traumatic bone injury or metastatic disease. It allows visualization of the disc space but not the contents of the spinal canal or the nerve roots. CT and MRI allow visualization of the disc, spinal canal, and nerve roots (Fig. 47.2). There is a high incidence of abnormal findings in asymptomatic people, with rates of disc herniation ranging from 21% in the 20- to 39-year age group to 37.5% in the 60- to 80-year age group.2 In fact, in one study, only 36% of asymptomatic individuals had normal discs at all levels. In other words, it is “normal” to have some disc abnormality, which occurs as part of normal aging.1 To be meaningful, CT and MRI must clearly correlate with the clinical findings. Perform these studies if tumor is suspected or surgery is contemplated. They also may be useful in precisely locating pathologic changes for transforaminal epidural steroid injection. The most accurate study is MRI, and gadolinium enhancement is not needed unless a tumor is suspected or the patient has undergone prior surgery. Gadolinium enhancement is useful postsurgically to distinguish disc herniation from scar tissue. 

259

Differential Diagnosis Trochanteric bursitis Anserine bursitis Hamstring strain Lumbosacral plexopathy Diabetic amyotrophy Sciatic neuropathy Tibial neuropathy Peroneal neuropathy Femoral neuropathy Hip osteoarthritis Sacroiliitis Avascular necrosis of the hip Pelvic stress fracture Occult hip fracture Shin splints Lateral femoral cutaneous neuropathy (meralgia paresthetica) Spinal stenosis Cauda equina syndrome Demyelinating disorder Lumbar facet syndrome Piriformis syndrome Transient migratory regional osteoporosis

Treatment Initial The treatment goal is to reduce inflammation and thereby relieve the pain and allow resolution of the radiculopathy, regardless of the underlying anatomic abnormalities. Bed rest, which had been the mainstay of nonoperative treatment, is now recommended only for symptom control. In previous studies, bed rest has not been shown to have an effect on the final outcome of the disorder.10 As long as patients avoid aggravating activities or bending or lifting, which tend to increase intradiscal pressure, they can carry on most everyday activities. Use nonsteroidal anti-inflammatory drugs (NSAIDs) to help reduce inflammation and to provide pain relief. NSAIDs have been shown to be effective in acute low back pain.11 However, a review that included pooling of three randomized clinical trials using NSAIDs showed no effectiveness over placebo in acute lumbar radiculopathy.20 It is still reasonable to give NSAIDs a short trial in acute lumbar radiculopathy for pain relief, although they will not shorten the course of the disorder. The use of oral steroids remains controversial and has not passed the scrutiny of well-controlled studies, even in acute low back pain. In a recent meta-analysis of the use of NSAIDS, corticosteroids, tricyclic antidepressants, and anticonvulsants, although the pooled data showed no efficacy with any of these medications over placebo in chronic radiculopathy,13 there was one study that found short-term efficacy for gabapentin.14 There were two studies in patients with acute radiculopathy in which oral corticosteroids seemed to be effective in the short-term treatment of radicular pain.13 Other medications, such as cyclobenzaprine, metaxalone, methocarbamol, and chlorzoxazone, some of which may have effectiveness in acute low back pain, have not been shown to be effective in acute radiculopathy.15 Clinically, for acute radiculopathy, there are several options. If the pain is severe, early epidural steroid injection

260

PART 1  MSK Disorders

C A

B

D

E FIG. 47.2  (A) Normal disc. Note the concave posterior margin of the disc (arrows). (B) Bulging disc. Image from a computed tomography (CT) myelogram shows the broad-based margin of the bulging disc (arrows) pushing on the anterior thecal sac. (C) Left posterior disc herniation (arrow). (D) Right posterior disc herniation. The abnormal soft tissue from the herniated disc is seen in the right lateral recess on this CT myelogram (arrow). Note the normally opacified nerve root sheath on the contralateral side (open arrow). (E) Herniated discs L4-L5 and L5-S1; the L4-L5 herniation is the larger of the two. There is posterior displacement of the low-signal posterior longitudinal ligament (arrow). (From Barckhausen RR, Math KR. Lumbar spine diseases. In: Katz DS, Math KR, Groskin SA, eds. Radiology Secrets. Philadelphia: Hanley & Belfus; 1998.)

(see the section on procedures) and testing with imaging and electromyography are reasonable. Another option is oral steroids, such as methylprednisolone (Medrol) dose pack, and the use of opioids for short-term pain control. For more chronic radicular pain, it would be reasonable to try anticonvulsants, such as gabapentin, or a combination of gabapentin and a tricyclic antidepressant, such as amitriptyline or nortriptyline. Start treatment with a low dose and titrate up gradually to determine the lowest effective dose. Opioids may be used for pain relief, although their effectiveness is suboptimal in neuropathic pain, with some suggestion that they should be used only in severe cases.16 There is less concern for addiction in acute care of patients who have not demonstrated past addictive behavior. Nevertheless, the practitioner should follow all protocols such as signing an opioid agreement, and if opioids are used for more than a few weeks, initiating urine testing. It is

clear now that opioid dependency and addiction favors no age barriers or socioeconomic status and has reached epidemic proportions. This should not preclude use in acute pain conditions with proper precautions and protocols, but extreme diligence must be taken when prescribing these medications, especially in the elderly. There is a large range of side effects and the number of yearly deaths from drug overdoses now exceed those from motor vehicle accidents.34-36 Opioids for acute radiculopathy have limited effectiveness. As a consequence use should be limited and no more than 60-80 morphine equivalents should be used a day. Usually just 30 or 40 short term should suffice. Opioid options are short acting hydrocodone or oxycodone. For more severe pain, use a long-acting opioid, such as oxycodone (OxyContin) or MS Contin, and for breakthrough pain, use a shorter acting opioid, such as hydrocodone, oxycodone, or short-acting morphine. These treatments

CHAPTER 47  Lumbar Radiculopathy

should be short term to avoid the risks of dependency or addiction. There seems to be no efficacy of opioids versus placebo for symptom relief or decrease in disability in chronic radiculopathy.17 Although there was some clinical suggestion that pregabalin or other anticonvulsants were effective in lumbar or cervical radiculopathy, a recent prospective randomized placebo controlled study did not show any efficacy over placebo.37 This was, however, a very small study and definitive determination of efficacy will have to await more robust studies. 

Rehabilitation With an acute painful radiculopathy, it is generally best to wait for some of the acute stage to subside before ordering physical therapy. In a longer standing problem, therapy may be the best first approach. Physical methods are a useful adjunct to the medication treatment. Various methods, which include flexion and extension exercises (often called a lumbosacral stabilization program), have been tried. Whatever method is used, if radicular pain is produced, the exercises should be stopped. After the radiculopathy resolves, the patient should be prescribed a proper exercise regimen to improve flexibility and muscle strength. Lumbar stabilization exercises, core muscle strengthening, and remaining active may be the most effective of the various methods studied carefully in lumbar radiculopathy. One study showed no effectiveness of lumbar traction.18 Other modalities, such as transcutaneous electrical nerve stimulation, acupuncture, massage, and manipulation, are not well studied with randomized clinical trials in lumbar radiculopathy.3 Because they are not likely to cause injury, they can be given a short trial. The manipulation should be done cautiously. 

Procedures Epidural steroid injections are beneficial in acute radiculopathy in patients with or without disc herniation.18 The results in chronic radiculopathy are less convincing. The most effective technique and material to be used for epidural steroid injection are controversial.19,20 Some literature suggests that either steroid preparations or local anesthetics are superior to placebo for long-term effects. Short-term effects, however, favored the steroid group.20,21 Some studies show that transforaminal epidural steroid injections have a marginally greater improvement in pain scores compared with lumbar epidural steroid injections. However, on the basis of the preferred safety profile, greater procedural comfort of lumbar epidural steroid injections, and nearly equal functional gains of the two procedures, a reasonable clinical approach is to attempt a lumbar epidural steroid injection initially and then, in the absence of significant improvement or resolution in 2 weeks, to attempt a transforaminal epidural steroid injection.19 Whereas the scientific literature shows that the effects of these interventions are relatively short-lived,19 the intervention is beneficial because it limits opiate use19 and referral for surgical management. These procedures should be performed under fluoroscopic guidance,22 in order to optimize the likelihood of placing the injectate within the epidural space. It is advisable to perform one injection and to re-evaluate the patient

261

in 1 or 2 weeks to determine whether further injections are required. It is not appropriate to perform a “series of three injections.” On the other hand, a maximum of three injections could be performed for any one episode of radiculop­ athy. It is reasonable to repeat this procedure for recurrent episodes of radiculopathy after 3 to 6 months. Nonoperative treatment allows resolution of the radiculopathy in up to 90% of cases.12,23 More interestingly, studies have demonstrated that when radiculopathy is the result of disc herniation, the actual herniation will resolve in the majority of cases, and even when the herniation remains, the symptoms often will still abate.24-26 

Technology There is no new specific technology for the treatment or rehabilitation of this condition. 

Surgery Surgery is appropriate under two conditions. First, surgery is performed on an emergency basis when a patient presents with a central disc herniation with bowel and bladder incontinence or retention and bilateral lower extremity weakness. In this very rare condition, a neurosurgeon or orthopedic spine surgeon must be consulted immediately and the patient operated on, preferably within 6 hours. Second, surgery is an option if a patient continues to have pain that limits function after an adequate trial of nonoperative treatment. Patient selection is extremely important to achieve a good surgical outcome. The best outcomes occur in patients with single-level root involvement; with pain experienced more in the limb than in the back; and when an anatomic abnormality on imaging corresponds to the patient’s symptoms, physical examination findings, and electromyographic findings in patients without psychological or secondary gain issues.26,27 A recent update of a Cochrane review on the subject of surgery versus conservative care concluded that in selected patients, surgery can provide faster relief, but there remains no convincing evidence of a difference in long-term outcomes.28 The type of surgery depends on the cause of the radiculopathy. For cases of disc herniation, simple laminectomy and discectomy suffice; there seems to be no difference between the standard, microdiscectomy, and newer minimally invasive procedures on outcome or time to return to activity.25 Fusion should be avoided in these instances. With spinal stenosis, a more extensive laminectomy with foraminotomy may be needed. Fusion should be reserved for the relatively infrequent case of well-demonstrated spinal instability together with radiculopathy or if the surgical procedure will result in spinal instability.38 One study30 suggested that fusion is needed in the case of spondylolisthesis. Two recent studies addressed this issue, both published in the April 14, 2016 edition of the New England Journal of Medicine.39,40 The studies both showed no difference in disability between laminectomy and fusion. One study (60 patients) used the SF-36 as the primary outcome and showed a small but statistically significant difference favoring fusion. The larger trial with primary endpoint of Oswestry disability index and 6-minute walk test showed no difference. Both showed very significant increased cost, hospital stay, and morbidity with the fusion procedure. 

262

PART 1  MSK Disorders

Table 47.2  Suggested Duration of Discontinuation of Various Medications Prior to Performance of Epidural Injections Trade Name

Generic Name

Hold Time

Re-Start Time

Aggrastat

Tirofiban

8h

2h

Aggrenox

ASA/Dipyridamole

7 days

Same day

Arixtra

Fondaparinux

3 days

24 h

Check Platelet/CBC

Aspirin >325 mg if greater than 1000 mg

Acetylsalicylic acid

7 days 10 days

Same day

ASA ASA Anacin—400 mg | Ecotrin 325 mg Ascriptin—325 mg | Excedrin—250 mg Bayer—325 mg | Fiorinal—325 mg may continue aspirin 81 mg

Brilinta

Ticagrelor

5 days

Same day

Coumadin

Warfarin

5 days

Same day

Effient

Prasugrel

10 days

Same day

Eliquis

Apixaban

5 days

24 h

Elmiron

Pentosan Polysulfate Sodium

5 days

Same day

Fragmin

Dalteparin

24 h

24 h

Avoid, Check Platelet/CBC

Lovenox

Enoxaparin

24 h

Same day

Check CBC

Miradon

Anisindione

24–72 h

Same day

Check PT

Heparin (5000 units)

Heparin

12 h

24 h

Permole Persantine

Dipyridamole

3 days

Same day

Plavix

Clopidogrel

7 days

Same day

Pletal

Cilostazol

7 days

Same day

Pradaxa

Dabigatran

5 days

24 h

Ticlid

Ticlopidine

14 days

2h

Trental

Pentoxifylline

7 days

Same day

Xarelto

Rivaroxaban

5 days

Next day

Avoid, Check Platelet/CBC

Check PT/INR, INR must be 420 Tibial F wave and soleus H reflex latencies after exercise21,22

Can evaluate for peripheral neuropathy and entrapments as well as progression of neurologic impairment Can rule out other neuromuscular disease

Significant interpretation bias May be difficult to differentiate lumbar spinal stenosis from other multiroot diseases (e.g., arachnoiditis) Patient discomfort or pain Expensive and time-consuming

Abnormal study in 78%–97% of patients with stenosis Paraspinal mapping electromyography score > 4: specificity 100% and sensitivity 30%

for patients with lumbar spinal stenosis, modalities have no additional effect to exercise and that surgery leads to better long-term (2 years) outcomes for pain and disability, but not walking distance, than physical therapy.22 General recommendations include relative rest (avoidance of pain-exacerbating activities while staying active to minimize deconditioning) and a flexion-biased exercise program, including inclined treadmill and exercise bicycle. Flexion biasing increases the cross-sectional area of the spinal canal compared with exercises performed in neutral or

extension, thereby maximizing activity tolerance.23 One case series24 reported on three patients who demonstrated significant improvements in pain and function at 18 months after undergoing specialized physical therapy programs that included spinal manipulation, flexion and rotation spine mobilization exercises, hip joint mobilization, hip flexor stretching, muscle retraining (lower abdominal, gluteal, and calf muscles), body weight-supported ambulation, and daily walking with properly prescribed orthotics. Physicians and therapists must be aware of any medical comorbidities, such

CHAPTER 50  Lumbar Spinal Stenosis

as cardiovascular and pulmonary disease, osteoporosis, cognitive deficits, and other musculoskeletal or neuromuscular conditions, which may have an impact on therapy tolerance. A retrospective analysis of predictors of walking performance and walking capacity showed that body mass index, pain, female sex, and age predict walking performance and capacity in people with lumbar spinal stenosis, those with low back pain without lumbar spinal stenosis, and asymptomatic control subjects. The authors of this analysis concluded that obesity and pain are modifiable predictors of walking deficits that could be targets for future intervention studies aimed at increasing walking performance and capacity in both the low back pain and lumbar spinal stenosis populations.25 Body weight-supported ambulation acts to decrease the axial loading of the spine to increase the cross-sectional area of the neural foramina, and studies have provided some support of this strategy.26 Based on a case series, a wheeled walker set to induce lumbosacral flexion was reported to improve walking and reduce pain in most patients (about 70%).27 

Procedures According to the North American Spine Society evidencebased recommendations, interlaminar epidural steroid injections may provide short-term (2 weeks to 6 months) symptom relief in patients with neurogenic claudication or radiculopathy due to degenerative lumbar spinal stenosis, but there is conflicting evidence for long-term (21.5 to 24 months) efficacy.28 One systemic review29 concluded that for interlaminar, transforaminal, and caudal epidural steroid injections, there is strong evidence for short-term relief and limited to moderate evidence for long-term relief of lumbar radicular pain. A number of studies have cited short-term success rates of 71% to 80%30,31 and long-term success rates of 32% to 75%.30,32 Furthermore, symptomatic management with epidural steroid injections may delay surgery an average of 13 to 28 months.33,34 A randomized controlled trial revealed that patients with lumbar central spinal stenosis received significant pain relief and their Oswestry disability index scores improved after receiving lumbar interlaminar injections with or without steroids.35 In another study evaluating the short-term effects of transforaminal epidural steroid injection for degenerative lumbar scoliosis combined with spinal stenosis, the researchers found that the Oswestry disability index showed a significantly greater improvement in the steroid group compared to the lidocaine group. The authors concluded that the findings suggest that fluoroscopic transforaminal epidural steroid injections may be an effective nonsurgical treatment option for patients with degenerative lumbar scoliosis combined with spinal stenosis and radicular pain.36 In a multicenter, double-blind study of fluoroscopically guided epidural injections for lumbar spinal stenosis, there were no significant differences between patients assigned to glucocorticoids plus lidocaine and those assigned to lidocaine alone with respect to pain-related functional disability or pain intensity at 6 weeks. Patients in both treatment groups had decreased pain and improved function. At 3 weeks, the glucocorticoid-lidocaine group had greater improvement than the lidocaine-alone group, but the differences were clinically insignificant.37

281

In general, epidural steroid injections can be considered a safe and reasonable therapeutic option for symptomatic management before surgical intervention is pursued. 

Technology Currently there is no specific technology for the treatment or rehabilitation of this condition. 

Surgery Lumbar spinal stenosis is the most common reason for spinal surgery in patients over 65 years.38 Patients with persistent symptoms despite conservative measures may benefit from surgical treatment. Randomized trials comparing surgical decompression with nonsurgical management have suggested that surgery leads to more rapid resolution of symptoms, but the high rate of crossover has been a limitation.39 A key feature in the selection of patients is ensuring that the symptoms indeed arise from nerve root compression. Screening for depression also is important. A prospective clinical study of lumbar spinal stenosis patients who underwent surgery found at 2-year follow-up that patients with depressive symptoms had poorer surgical outcomes than those with normal mood.40 Surgery generally consists of decompressive laminectomy with medial facetectomy. The decompressive laminectomy relieves central canal stenosis; the medial facetectomy and dissection along the lateral recesses decompress areas of foraminal stenosis. The Maine Lumbar Spine Study prospectively examined the outcome of initial surgical versus nonsurgical treatment in 148 patients out to 10 years. The benefits from surgery diminished over time, although improvements in leg pain and back-related functional status were maintained. Rates of improvement in low back pain and leg pain at 1 year ranged from 77% to 79% in the surgery group and 42% to 45% in the nonsurgical group. At 8- to 10-year follow-up, the rates dropped to 53% to 67% in the surgery group and remained essentially stable at 41% to 50% in the nonsurgical group.41 The Spine Patient Outcomes Research Trial (SPORT) compared the 4-year and 8-year outcomes of patients who underwent surgical management of lumbar spinal stenosis with the outcomes of those who received nonoperative care.42,43 In this prospective randomized trial with a concurrent observational cohort study, surgical candidates with at least 12 weeks of symptoms and confirmatory imaging were enrolled in a randomized cohort or observational cohort. At 2-year follow-up and at 4-year follow-up, intention-totreat analysis showed significant improvement in SF-36 bodily pain and Oswestry disability index from baseline in the surgical group compared with the nonsurgical group. In addition, comparative effectiveness evidence for defined diagnostic groups from the SPORT showed good value for surgery compared with nonoperative care measured at 4 years. The study also found that patients with predominant leg pain improved significantly more with surgery than did patients with predominant low back pain. However, patients with predominant low back pain still improved significantly more with surgery than with nonoperative treatment.42 Between 4 and 8 years, patients with symptomatic

282

PART 1  MSK Disorders

spinal stenosis showed diminishing benefits of surgery in as-treated analyses of the randomized group, whereas outcomes in the observational group remained stable. At 8-year follow-up, the intention-to-treat analysis found no significant difference between surgical or nonoperative treatment. The authors note that these results must be viewed in the context of high rates of nonadherence to the assigned treatment as this mixing of treatments generally biases treatment effect estimates towards the null.43 

Potential Disease Complications The natural history of lumbar spinal stenosis is not well understood, but existing literature seems to indicate that most cases do not lead to significant deterioration. One study followed 19 patients with moderate stenosis who did not undergo surgery. Approximately 70% of these patients had stable to improved symptoms at mean follow-up of 49 months.44 The nonsurgical management of the SPORT also demonstrated stable pain and functional outcomes even at 8 years follow-up.43 In patients with worsening symptomatic stenosis, there may be a progressive increase in back or leg pain and a decrease in walking tolerance. Loss of lower extremity sensation may increase risk of falls. Severe stenosis may lead to a neurogenic bladder, especially in patients with narrowed dural sac anteroposterior diameter. Cauda equina syndrome is a rare but serious complication, in which case emergent surgical decompression is generally required. 

Potential Treatment Complications Exacerbation of symptoms is possible, particularly with functional restoration programs that may attempt to condition patients to painful activities through safe repetition of pain-inducing motions. In addition, patients with significant comorbidities, such as cardiopulmonary disease, are at risk for activity-induced adverse events. Complications from medication use include liver toxicity with acetaminophen; gastritis, gastrointestinal bleeds, renal toxicity, and platelet inhibition with nonsteroidal anti-inflammatory drugs; increased risk of cardiovascular events with some cyclooxygenase 2 inhibitors; nausea and lowering of seizure threshold with tramadol; anticholinergic effects including dry mouth and urinary retention with tricyclic antidepressants; sedation, ataxia, and other cognitive side effects with anticonvulsants (although gabapentin and pregabalin are relatively safe); and sedation, constipation, urinary retention, tolerance, and central pain sensitization with opioids. Adverse gastrointestinal events related to nonsteroidal anti-inflammatory drugs can be minimized with the use of a cyclooxygenase 2 inhibitor or concomitant use of a gastroprotective agent, such as a proton pump inhibitor or H2 blocker.45 Quantified data on complications associated with nonsurgical interventional procedures, including epidural steroid injections, are limited. A retrospective study of 207 patients receiving transforaminal epidural steroid injections46 reported the following adverse events: transient nonpositional headaches that resolved within 24 hours (3.1%), increased back pain (2.4%), facial flushing (1.2%), increased leg pain (0.6%), vasovagal reaction (0.3%), increased blood glucose concentration in an insulin-dependent diabetic

(0.3%), and intraoperative hypertension (0.3%). Other potential complications are infection at the injection site, dural puncture potentially with associated spinal headache, chemical or infectious meningitis, epidural hematoma, intravascular penetration, anaphylaxis, and nerve root or spinal cord injury leading to paresis or paralysis.47 Complications of decompressive surgery include infection (0.5% to 3%), epidural hematoma, vascular injury (0.02%), thromboembolism including pulmonary embolism (0.5%), dural tears (70%) Age (>40 years)30 Prolonged immobilization of a joint15 Coronary artery disease17 Autoimmune disorders After hip surgery Intra-articular loose bodies Osteoid osteoma Synovial chondromatosis Osteoarthritis Dupuytren contracture Elevated C-reactive protein level, positive HLA-B27/serum IgA level Myocardial infarction Pulmonary tuberculosis Bronchitis Stroke with hemiparesis

anteriorly and extends along the intertrochanteric line and along the femoral neck posteriorly and inferiorly. The fibrous capsule is reinforced by the pubofemoral, ischiofemoral, and iliofemoral ligaments, which are considered thickening of the fibrous capsule and help stabilize the hip joint. The capsular fiber consists of both superficial bands and deep bands. The deep circular bands from the iliofemoral ligament form the zona orbicularis, which divides the synovial cavity into medial and lateral recesses. The hip joint is dynamically stabilized by numerous muscles. Neviaser introduced the term adhesive capsulitis and described pathologic changes in the synovium and subsynovium.3 Evidence supports the hypothesis that the underlying pathologic process involves synovial inflammation with reactive capsular fibrosis, thus making adhesive capsulitis both an inflammatory and a fibrosing condition.3 The histologic changes of adhesive capsulitis seen in the hip are similar to those in the shoulder. There is chronic inflammatory reaction in the capsule and synovium with subsequent adherence to the femoral neck.2,5 Biopsy tissue shows evidence of edematous, fibrotic synovial tissue with partial or complete loss of synovial lining.2 Many authors acknowledge that adhesive capsulitis is a relatively common clinical syndrome when it occurs in the shoulders (2% to 5% of the general population) but is infrequently described in other joints, such as the wrist, hip, and ankles.7 

Symptoms The diagnosis of hip adhesive capsulitis is based on clinical findings of decreased passive and active range of motion in all planes of the hip joint, with no abnormal radiographic findings.9 The patient may describe gradual onset

of stiffness with hip movements, resulting in difficulty in crossing the leg or sitting in certain positions. Patients may describe difficulty with lower extremity dressing, such as putting on socks, or with hygiene, such as clipping of toenails. Pain is usually a presenting symptom, especially with extreme external rotation or abduction, and is usually the reason for seeking medical evaluation. Gait difficulty may or may not be present, but it is usually not to the severity that a gait aid is required. The diagnosis of hip adhesive capsulitis is rarely made, possibly because the hip joint can sustain range of motion loss without significant disability, whereas even a mild loss of motion in the shoulders can result in significant difficulty with performance of routine activities of daily living.7–9 

Physical Examination Hip pain can be caused by different intra-articular and extra-articular structures. Differentiating the specific pathologic structures can be challenging, but it is critical for appropriate medical management. The history, physical examination, and adjuvant imaging are crucial in identifying the source of pain. In patients with adhesive capsulitis of the hip, the clinical examination findings may be minimal. The patient may or may not exhibit an antalgic gait pattern. The neuromuscular and neurovascular examination findings are usually unremarkable. The back examination is usually benign, unless there is a concomitant spinal condition. Provocative maneuvers of the hip joint (i.e., Stinchfield and FABERE tests) may generate nonspecific groin discomfort. The hallmark finding on physical examination is limitation of range of motion of the hip joint in all planes (flexion-extension, internal and external rotation, and abduction-adduction).10 

Functional Limitations Functional limitations may differ, depending on the severity of pain and range of motion deficits. Difficulty with activities of daily living is limited to the lower extremities. This can be manifested as difficulty with lower extremity dressing, such as donning or doffing pants, socks, or shoes. There is difficulty in crossing one leg over the other, or sitting in a tailor’s position. There may be difficulty in sleeping on one side or the other or standing with the hip externally rotated and abducted. There may be difficulty with prolonged sitting or driving a car, especially if a manual shift is used. The onset of pain and inflammation causes reflex inhibition of the muscles around the joint, which can subsequently lead to loss of mobility and compensatory abnormal movement of the joint. If gait pattern is affected, recreational and vocational activities that require prolonged ambulation can be affected (i.e., golfing, tennis, or power walking for exercise). With time, there is resolution of pain, but residual range of motion deficits and limitation of function can remain. This persistent loss of mobility and dysfunction can lead to psychosocial issues, such as irritability, depression and anxiety, and disordered sleep patterns. 

CHAPTER 52  Adhesive Capsulitis of the Hip

Anterior superior iliac spine Anterior inferior iliac spine

Iliofemoral ligament (Y ligament of Bigelow)

Greater trochanter

Superior pubic ramus

293

Pubofemoral ligament

Intertrochanteric line Lesser trochanter Inferior pubic ramus

Lunate (articular) surface of acetabulum Articular cartilage Greater trochanter

Anterior superior iliac spine Anterior inferior iliac spine Ligament of head of femur (cut) Iliopubic eminence

Head of femur Neck of femur Intertrochanteric line

Acetabular labrum (fibrocartilaginous) Transverse acetabular ligament Ischial tuberosity Lesser trochanter

FIG. 52.1  Hip joint. Normal anatomy and fibrous capsule.

Diagnostic Studies Laboratory studies are important in the initial evaluation of intra-articular hip abnormalities. They help assess for autoimmune and rheumatologic conditions. The results of laboratory studies, including blood cell counts, electrolyte values, chemistry panels, acute phase reactants, and rheumatologic screening studies (such as antinuclear antibodies, double-stranded DNA, rheumatoid factor, and HLA-B27 antibodies), are usually normal in patients with adhesive capsulitis of the hip. Multiple imaging modalities are available to assess the pelvis and hip joint and surrounding soft tissues. Conventional radiography, including anteroposterior views, remains the initial imaging modality of choice in assessing patients with groin pain and dysfunction. These studies, however, are of limited value if there is internal derangement as the cause of hip pain, because findings are typically normal in those circumstances. In hip adhesive capsulitis, results of these studies are usually normal except for possible diffuse osteopenia, most likely related to pain and decreased range of motion from underlying disease.11 Griffiths and

colleagues reported on a series of patients who had adhesive capsulitis of the hips related to mild trauma or repetitive activity. In all of the patients, the conventional radiographs were unremarkable.6 Bone scans can show increased uptake in the areas of osteopenia, but this is usually nonspecific. Focal accumulation of radionuclide reflects an alteration of balanced bone turnover due to changes in bone blood flow and can occur in several conditions. Ultrasonography of the hip has been widely accepted as a useful diagnostic tool in patients with a wide range of acute and chronic conditions affecting the hip or limited range of motion. It allows evaluation of different anatomic and pathologic structures, such as joint recess, bursa, tendons, and muscles. It also allows evaluation of the osseous structures of the joint, ischial tuberosity, and greater trochanter. It is useful for guided procedures in the hip joint and periarticular soft tissue under direct visualization.12 Ultrasonography has considerable advantages over computed tomography (CT) and magnetic resonance imaging (MRI); these include absence of radiation, good visualization

294

PART 1  MSK Disorders

FIG. 52.2  Coronal image from magnetic resonance arthrography of the hip depicting a small-volume joint with tight joint capsule. Very small recesses of the hip joint, compatible with adhesive capsulitis, are demonstrated (arrows).

of the joint cavity, quantification of soft tissue abnormalities, multiple joint scanning, and rapid side-to-side anatomic comparison. It also has relatively low cost, good patient compliance, and dynamic real-time study of multiple planes. Direct contact with the patient allows maneuvers that elicit symptoms to be evaluated while the study is being performed. Direct ultrasonographic visualization offers the possibility of guided procedures in the hip joint and periarticular soft tissues. The limited size and number of acoustic windows make detailed examination of some structures extremely difficult (i.e., femoral cartilage and hip capsule).13 It is not recommended for evaluation of hip adhesive capsulitis, in which there is retraction of the fibrous joint capsule with little or no fluid in the synovial space. Supplemental imaging with CT or MRI is often used to further evaluate the pelvis and hip to rule out the presence of simple, nondisplaced avulsion to complex fractures and to assess for displacement, comminution, and locations of fragments. MRI is helpful in diagnosis of occult injuries and stress fractures and in the evaluation of the soft tissue and musculature of the pelvis and hip.11,14 In adhesive capsulitis, CT scans are usually unremarkable and MRI shows capsular thickening with little or no fluid in the synovial space. If the clinical examination or a nonarthrographic CT or MRI study suggests a possible labral or intra-articular hip disease, direct magnetic resonance arthrography (MRA) is performed.15 Computed tomographic or MRA is the preferred examination for evaluation of the joint capsule, labrum, and articular cartilage. Intra-articular needle placement is confirmed under fluoroscopic guidance before 15 mL of 1:200 dilution of a gadolinium contrast agent and normal saline is injected into the joint. Characteristic arthroscopic findings show a hip joint with low volume and loss of normal recesses, high intracapsular pressure, and a thick capsule (Figs. 52.2 and 52.3). Joo retrospectively evaluated MRAs of patients with clinical suspicion of idiopathic adhesive capsulitis of the hip and compared with normal controls. Capsular thickness was measured in both populations with resultant statistically significant

FIG. 52.3 Coronal image from computed tomographic arthrography of the hip showing a small-volume joint with tight joint capsule. Areas of capsule rupture and extra-articular contrast material are demonstrated (arrowheads).

increase in the mean thickness of the joint capsule superiorly and posteriorly in the idiopathic adhesive capsulitis group.17 There is usually reduction of intra-articular capacity of at least one-third ( 30 mm Hg • 5 minutes after exercise > 20 mm Hg A large systematic review found that pre-exercise, means values ranged from 7.4 to 50.7 mm Hg for CECS patients and 5.7 to 12 mm Hg for controls; 1-minute post exercise timing interval showed values ranging from 34 to 55.4 mm Hg and 9 to 19 mm Hg in CECS patients and controls, respectively. The authors concluded that levels above the highest reported value for controls (27.5 mm Hg) along with a good history should be regarded as highly suggestive of CECS.8 It is important that the patient’s symptoms correlate with the compartment in which there is elevated pressure. Pressure should increase in the symptomatic compartment with exercise and remain elevated for an abnormal time.8 Values for posterior compartments are more controversial. Normal resting pressures are less than 10 mm Hg, and values should return to resting levels after 1 to 2 minutes of exercise.14 Drawbacks to measurement of pressures include the following: • They are invasive and can be complicated by bleeding or infection. • Because of the anatomy, it is difficult to test the deep posterior compartment. • Pressures are dependent on the position of the leg and the technique used, so strict standards should be followed. • It is time-consuming because each compartment must be tested separately, and all compartments should be tested because multiple areas are often involved. • It is often difficult for patients to exercise with the catheter in place. Because of these drawbacks, alternative tests to confirm the diagnosis are sometimes used. Magnetic resonance imaging done before and after exercise can show increased signal intensity throughout the affected compartment in the T2-weighted images after exercise in patients with compartment syndrome.20,21 Alternatively, near-infrared spectroscopy has been used as well. This method measures the hemoglobin saturation of tissues.8 In cases of CECS, there is de-oxygenation of muscle during exercise and delayed re-oxygenation after exercise. Failure of the compartment to return to baseline within 25 minutes after exercise is diagnostic of CECS.10 Although near-infrared spectroscopy seems to be helpful in patients with anterior compartment syndrome, light absorption may be altered in deeper compartments, and therefore it is more difficult to monitor the pressure in these deeper compartments.8 Other methods include thallium stress testing and nuclear magnetic

ATMG

Fib

TP

Tib

FIG. 67.4 Ultrasound marker placement for anterior compartment thickness measurement using ultrasound in patients at rest. (From Rajasekaran S, Beavis C, Aly AR, Leswick D. The utility of ultrasound in detecting anterior compartment thickness change in chronic exertional compartment syndrome: a pilot study. Clin J Sport Med. 2013;23(4):305–311.)

resonance spectroscopy, which may also be helpful in the diagnosis of CECS.8 Triple-phase bone scan and single-photon emission computed tomography scans can be used to rule out other conditions in the differential diagnosis, such as medial tibial stress syndrome or stress fractures.10 More recently, ultrasound has been studied as a point of care diagnostic tool used to diagnose CECS. One pilot study showed that the mean anterior compartment thickness (ACT) in patients with CECS versus control subjects significantly increased after exertion at 0.5 minutes, 2.5 minutes, and 4.5 minutes.22 The authors concluded that ultrasonography reveals a significant increase in ACT in patients with CECS of the anterior leg compartment (Fig 67.4).  Differential Diagnosis ACUTE COMPARTMENT SYNDROME Arterial occlusion Severe muscle trauma Neuropraxia of the common, deep, or superficial peroneal or tibial nerve Deep venous thrombosis Cellulitis Fracture  CHRONIC EXERTIONAL COMPARTMENT SYNDROME Tibial or fibular stress fractures Medial tibial stress syndrome or shin splints Atherosclerosis with vascular claudication Popliteal artery compression from aberrant insertion of the medial gastrocnemius Muscle hyper-development causing compression of the popliteal artery Cystic adventitial disease23

Treatment Initial Acute Compartment Syndrome If the differential pressure is less than 30 mm Hg, treatment of ACS is surgical fasciotomy.17 In cases in which the

CHAPTER 67  Compartment Syndrome of the Leg

375

differential pressure remains above 30 mm Hg, it has been shown to be safe to observe those patients with serial pressure measurements.24 

Chronic Exertional Compartment Syndrome For CECS, the initial treatment consists of rest, ice, and nonsteroidal anti-inflammatory drugs. Counseling the patient to avoid running on hard surfaces, to use orthotics to control pronation, and to wear running shoes with the appropriate amount of cushion and a flared heel is important.7 At least a 6-week course of rehabilitation should be initiated to monitor improvement in function and a decrease in pain.25 Surgery is usually reserved for symptoms persisting beyond 6 to 12 weeks, despite conservative therapy.12 

A

Rehabilitation Acute Compartment Syndrome The rehabilitation of ACS is limited to the post-fasciotomy stage. Rehabilitation depends on the extent of the injury. Proper skin care for either the open area left to close by secondary intent or the skin grafts that have been applied is imperative. An ankle-foot orthosis to correct footdrop is often needed. Physical therapy is needed for gentle range of motion exercises to prevent contractures and should begin as soon after surgery as possible and as allowed by wound healing issues. Other measures include strengthening muscles that may be only partially affected and gait training, possibly with an assistive device. There is no scientific literature to support any specific rehabilitation protocols, and so programs should be individualized on the basis of the particular patient’s needs. If the patient has deficits in activities of daily living, such as dressing or transfers, occupational therapy may be helpful in addressing these areas. 

Chronic Exertional Compartment Syndrome Controversy exists about the success of conservative treatment of CECS.7 Current recommendations are based on the initial use of PRICE (protection, rest, ice, compression, and elevation), with progression to reestablishing range of motion and soft tissue mobility, incorporating stretching, nerve gliding techniques, strengthening exercises, and biomechanical analysis of the patient during sport-specific activity.26 Evaluating and identifying the underlying cause, such as excessive pronation, are important in considering the rehabilitation course. Treatment of excessive pronation includes establishing normal muscle lengths throughout the kinetic chain, especially stretching the gastrocnemius and posterior tibialis, and strengthening the anterior tibialis.27 Shoe orthoses to address excessive pronation may also be helpful. Training errors, such as rapid increases in intensity or duration, are addressed and corrected. In addition, soft tissue mobilization and manipulation techniques, including massage, myofascial stretching, and taping, may increase fascial compliance. This would address the proposed pathophysiologic process involving increased fascial thickness, stiffness, and increased pressure.26 A recent case report of an Olympic level triathlon who opted out of surgery describes successful recovery and return to sport after 3.5 months of physical therapy using the Functional Manual Therapy Approach.28 This approach addressed myofascial restrictions, neuromuscular function and motor control deficits, and resulted in improvements lasting through to the 3-year follow-up.28

Lateral leaf compartment

PROX

DIST

B FIG. 67.5  A, An 18-gauge needle entering the skin under ultrasound guidance to fenestrate the anterior compartment of the lower leg. B, Long axis ultrasound image of the needle fenestrating the left lateral compartment of the lower leg. Facia, (arrow head), needle tip, (arrow). PROX, proximal; DIST, distal. (From Finnoff JT, Rajasekaran S. Ultrasound-guided, percutaneous needle fascial fenestration for the treatment of chronic exertional compartment syndrome: a ca