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 case report. PM R. 2016;8(3):286–290.)

If a fasciotomy is done for CECS, postsurgical rehabilitation should follow. Weight bearing is permitted as tolerated, and gentle range of motion exercises are begun 1 to 2 days postoperatively. Strengthening and gradual return to activity begin at 1 to 2 weeks. Full return to activity such as running usually takes 8 to 12 weeks.29 

Procedures Procedures are not typically done in ACS except to measure compartmental pressures. The urgency for surgery often negates the possibility of more conservative procedures in ACS, whereas in CECS, less invasive procedures may be of benefit. A recent case report demonstrated successful treatment of bilateral anterior and lateral compartment CECS in an 18-year-old college athlete with ultrasound-guided, percutaneous needle fascial fenestration (Fig 67.5).30 The athlete was able to return to full, unrestricted activity in 1 week post procedure. Per the authors’ conclusions, ultrasound-guided fascial fenestration warrants further investigation to determine its role in the treatment of CECS because of the minimally invasive nature of this treatment, the rapid return to sports, and the potential for cost savings.30 

376

PART 1  MSK Disorders

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

Surgery Acute Compartment Syndrome Fasciotomy should be performed for ACS as soon as possible. Large longitudinal incisions are often made in the affected compartment and can be left open to close gradually, or splitthickness skin grafts are applied. Results of the surgery are variable and depend on the length of time of ischemia and other injuries involved.31 The surgical technique of fasciotomy, however, is evolving. More recently, endoscopic techniques have been developed to decrease complications from tissue manipulation and lessen the risk of wound complications.32 This technique allows for a subcutaneous fasciotomy of the anterior and lateral compartment, but is limited for the deeper compartments.10,12 Controversy exists as to whether all four compartments need to be released in cases of ACS. One study showed that release of only the anterior compartment had equivalent results to release of the anterior and lateral compartments.33 If treatment is delayed for more than 12 hours, it is assumed that permanent damage has occurred to the muscles and nerves in the involved compartment. Late reconstruction procedures can be done, if necessary, to correct muscle contractures or to perform tendon transfers for footdrop.31 

Chronic Exertional Compartment Syndrome Fasciotomy is also the mainstay for surgical treatment of CECS.7 The surgical techniques employed for the treatment of CECS differ from those used in managing ACS. Namely, rather than opening all compartments, only those with symptoms or with evidence of high pressures are treated.34 Several studies have found that the anterior and lateral compartments can be safely and completely released with a subcutaneous endoscopic approach.32,34-36 Similarly, minimally invasive surgical fasciotomies employing a single incision approach have proven to be safe and effective in the management of CECS.37-39 Results of surgery are usually good, with average success rates of 81% to 100% as defined by a decrease in symptoms and a return to sports.33,40 Despite these modifications, endoscopic fasciotomy requires specialized surgical equipment and training and minimally invasive surgeries have a higher risk of neurovascular compromise34 unless larger incisions are made to improve tissue exposure. It has been suggested that ultrasound guidance can be used in lieu of endoscopic and minimally invasive techniques as a way of limiting tissue disruption, increasing visibility of neurovascular structure, and eliminating the need for expensive and specialized surgical equipment.41 A cadaveric study demonstrated that ultrasound-guided fasciotomy of the anterior and lateral leg compartment can be safely performed with fasciotomy length comparable to a surgical fasciotomy.42 Similarly, a study of young athletes with CECS who underwent ultrasound-guided fasciotomy found that all patients (n = 7) had a decrease in pain, and all except 1 returned to pre-symptomatic exercise levels with a median return to play of 35 days.41 With further research needed, ultrasound guidance may offer a safe and effective compartmental release that minimizes soft tissue complications and the promise of a faster return to physical activity. 

Potential Disease Complications Acute Compartment Syndrome In ACS, ischemia of less than 4 hours usually does not cause permanent damage. If ischemia lasts more than 12 hours, severe damage is expected. Ischemia of 4 to 12 hours can also cause significant damage, including muscle necrosis, muscle contractures, loss of nerve function, infection, gangrene, myoglobinuria, and renal failure. Amputation of the affected limb is sometimes necessary, and even death may occur from the systemic effects of necrosis or infection.1,3,7 Recurrence has also been known to develop. Calcific myonecrosis can also be a late side effect.43 

Chronic Exertional Compartment Syndrome If CECS is left untreated, it may become acute in presentation and result in irreversible sequelae.12 

Potential Treatment Complications There are potentially serious complications associated with ACS fasciotomy. Mortality rates are 11% to 15%, and serious morbidity is common, including amputation rates of 10% to 20% and diminished limb function in 27%.44 Incomplete fasciotomy occurs when the fascial openings are not adequate to permit complete decompression of the compartment. In one study, recurrence of compartment syndrome due to incomplete fasciotomy was 13%,45 commonly when skin and fascial openings were too small. Some complications may also occur after fasciotomy, including infections, hematomas, fascial adhesions, swelling, lymphocele, and hemorrhage of the leg.34 Injury to the superficial peroneal is thought to occur as frequently as in 6% of patients undergoing emergent leg fasciotomy for trauma.46 Additionally, single leg incisions are thought to limit visualization, leaving the peroneal nerve and artery vulnerable to injury. CECS fasciotomy is a less extensive surgery on a healthier population. Complications are uncommon, but can include bleeding or hematoma, infection, deep venous thrombosis, wound infection, lymphocele, and nerve injury, particularly to the superficial peroneal nerve. Most patients report unlimited exercise after fasciotomy; however, about 4% report mild symptoms associated with nerve injury and persistent ankle pain.34 Case series report a recurrence rate of 3% to 20%.34 The most common reasons for recurrence are excessive scar tissue formation, causing the compartment to become tight again, and inadequate fascial release due to limited fascial incision length. A case series exploring the outcome of repeated fasciotomy for recurrence of symptoms reported that 70% of patients had good or excellent outcomes.47 One potential long-term complication of fasciotomy is an increased risk for development of chronic venous insufficiency caused by the loss of the calf musculovenous pump.48

References 1. Swain R, Ross D. Lower extremity compartment syndrome. When to suspect acute or chronic pressure buildup. Postgrad Med. 1999;105: 159–162, 165, 168. 2. Horgan AF, Geddes S, Finlay IG. Lloyd-Davies position with Trendelenburg—a disaster waiting to happen? Dis Colon Rectum. 1999;42: 916–919. discussion 919–920.

CHAPTER 67  Compartment Syndrome of the Leg

3. Gulli B, Templeman D. Compartment syndrome of the lower extremity. Orthop Clin North Am. 1994;25:677–684. 4. Woolley SL, Smith DR. Acute compartment syndrome secondary to diabetic muscle infarction: case report and literature review. Eur J Emerg Med. 2006;13:113–116. 5. Beraldo S, Dodds SR. Lower limb acute compartment syndrome after colorectal surgery in prolonged lithotomy position. Dis Colon Rectum. 2006;49:1772. 6. Simms MS, Terry TR. Well leg compartment syndrome after pelvic and perineal surgery in the lithotomy position. Postgrad Med J. 2005;81(958):534–636. 7. DeLee JC, Drez D. Orthopaedic Sports Medicine: Principles and Practice. Philadelphia: WB Saunders; 2002:1612–1619. 8. Aweid O, Buono A, Malliaras P, et al. Systematic review and recommendations for intracompartmental pressure monitoring in diagnosing chronic exertional compartment syndrome of the leg. Clin J Sport Med. 2012;22:356–370. 9. Edwards PH Jr, Wright ML, Hartman JF. A practical approach for the differential diagnosis of chronic leg pain in the athlete. Am J Sports Med. 2005;33:1241–1249. 10. George C, Hutchinson M. Chronic exertional compartment syndrome. Clin Sports Med. 2012;31:307–319. 11. Newton EJ, Love J. Acute complications of extremity trauma. Emerg Med Clin North Am. 2007;25:751. 12. Murdock M, Murdock M. Compartment syndrome: a review of the literature. Clin Podiatr Med Surg. 2012;29:301–310. 13. Mars M, Hadley GP. Failure of pulse oximetry in the assessment of raised limb intracompartmental pressure. Injury. 1994;25:379–381. 14. Reneman RS. The anterior and the lateral compartmental syndrome of the leg due to intensive use of the muscles. Clin Orthop Relat Res. 1975;113:69–80. 15. Bong MR, Polatsch DB, Jazrawi LM, Rokito AS. Chronic exertional compartment syndrome: diagnosis and management. Bull Hosp Jt Dis. 2005;62:77. 16. Elliott KG, Johnstone AJ. Diagnosing acute compartment syndrome. J Bone Joint Surg Br. 2003;85:625–632. 17. Ozkayin N, Aktuglu K. Absolute compartment pressure versus differential pressure for the diagnosis of compartment syndrome in tibial fractures. Int Orthop. 2005;29(6):396–401. 18. White TO, Howell GE, Will EM, et al. Elevated intramuscular compartment pressures do not influence outcome after tibial fracture. J Trauma. 2003;55:1133–1138. 19. Rominger MB, Lukosch CJ, Bachmann GF. MR imaging of compartment syndrome of the lower leg: a case control study. Eur Radiol. 2004;14:1432–1439. 20. Lauder TD, Stuart MJ, Amrami KK, Felmlee JP. Exertional compartment syndrome and the role of magnetic resonance imaging. Am J Phys Med Rehabil. 2002;81:315–319. 21. Van den Brand JG, Nelson T, Verleisdonk EJ, van der Werken C. The diagnostic value of intracompartmental pressure measurement, magnetic resonance imaging, and near-infrared spectroscopy in chronic exertional compartment syndrome: a prospective study in 50 patients. Am J Sports Med. 2005;33:699–704. 22. 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. 23. Ni Mhuircheartaigh N, Kavanagh E, O’Donohoe M, Eustace S. Pseudo compartment syndrome of the calf in an athlete secondary to cystic adventitial disease of the popliteal artery. Br J Sports Med. 2005;39: e36. 24. McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures. The pressure threshold for decompression. J Bone Joint Surg Br. 1996;78:99–104. 25. Meulekamp MZ, Sauter W, Buitenhuis M, Mert A, van der Wurff P. Short-term results of a rehabilitation program for service members with lower leg pain and the evaluation of patient characteristics. Mil Med. 2016;181(9):1081–1087.

377

26. Schubert A. Exertional compartment syndrome: review of the literature and proposed rehabilitation guidelines following surgical release. Int J Sports Phys Ther. 2011;6:126–141. 27. Blackman PG, Simmons LR, Crossley KM. Treatment of chronic exertional anterior compartment syndrome with massage: a pilot study. Clin J Sport Med. 1998;8:14–17. 28. Collins CK, Gilden B. A non-operative approach to the management of chronic exertional compartment syndrome in a triathlete: a case report. Int J Sports Phys Ther. 2016;11(7):1160–1176. 29. Schepsis AA, Gill SS, Foster TA. Fasciotomy for exertional anterior compartment syndrome: is lateral compartment release necessary? Am J Sports Med. 1999;27:430–435. 30. Finnoff JT, Rajasekaran S. Ultrasound-guided, percutaneous needle fascial fenestration for the treatment of chronic exertional compartment syndrome: a case report. PM R. 2016;8(3):286–290. 31. Finkelstein JA, Hunter GA, Hu RW. Lower limb compartment syndrome: course after delayed fasciotomy. J Trauma. 1996;40:342–344. 32. Schepsis AA, Martini D, Corbett M. Surgical management of exertional compartment syndrome of the lower leg. Long-term followup. Am J Sports Med. 1993;21:811–817. 33. de Fijter WM, Scheltinga MR, Luiting MG. Minimally invasive fasciotomy in chronic exertional compartment syndrome and fascial hernias of the anterior lower leg: short and long term results. Mil Med. 2006;171(5):399. 34. Leversedge FJ, Casey PJ, Seiler JG, Xerogeanes JW. Endoscopically assisted fasciotomy: description of technique and in vitro assessment of lower-leg compartment decompression. Am J Sports Med. 2002;30:272–278. 35. Wittstein J, Moorman CT III, Levin LS. Endoscopic compartment release for chronic exertional compartment syndrome: surgical technique and results. Am J Sports Med. 2010;38:1661–1666. 36. Knight JR, Daniels M, Robertson W. Endoscopic compartment release for chronic exertional compartment syndrome. Arthrosc Tech. 2013;2:187–190. 37. Bramante C, Gandolfo L, Bosco V. Minimally invasive fasciotomy in the treatment of chronic exertional anterior compartment syndrome of the leg: personal technique. Chir Ital. 2008;60:711–715. 38. Maffulli N, Loppini M, Spiezia F, et al. Single minimal incision fasciotomy for chronic exertional compartment syndrome of the lower leg. J Orthop Surg Res. 2016;11:61–68. 39. Drexlet M, Rutenberg TF, Rozen N, et al. Single minimal incision fasciotomy for the treatment of chronic exertional compartment syndrome: outcomes and complications. Arch Orthop Trauma Surg. 2017;137(1):73–79. 40. Balius R, Bong DA, Ardebol J, Pedret C, Codina D, Dalmau A. Ultrasound-guided fasciotomy for anterior chronic exertional compartment syndrome of the leg. J Ultraound Med. 2016;35(4):823–829. 41. Lueders DR, Sellon JL, Smith J, Finnoff JT. Ultrasound-guided fasciotomy for chronic exertional compartment syndrome: a cadaveric study. PM R. 2016:1–8. 42. Packer JD, Day MS, Nguyen JT, et al. Functional outcomes and patient satisfaction after fasciotomy for chronic exertional compartment syndrome. Am J Sports Med. 2013;41:430–436. 43. Snyder BJ, Oliva A, Buncke HJ. Calcific myonecrosis following compartment syndrome: report of two cases, review of the literature, and recommendations for treatment. J Trauma. 1995;39:792–795. 44. Heemskerk J, Kitslaar P. Acute compartment syndrome of the lower leg: retrospective study on prevalence, technique, and outcome of fasciotomies. World J Surg. 2003;27:744–747. 45. Jensen SL, Sandermann J. Compartment syndrome and fasciotomy in vascular surgery. Eur J Vasc Endovasc Surg. 1997;13(1):48–53. 46. Kashuk JL, Moore EE, Pinski S, et al. Lower extremity compartment syndrome in the acute care surgery paradigm: safety lessons learned. Patient SAf Surg. 2009;3(1):11–17. 47. Schepsis AA, Fitzgerald M, Nicoletta R. Revision surgery for exertional anterior compartment syndrome of the lower leg: technique, findings, and results. Am J Sports Med. 2005;33:1040–1047. 48. Singh N, Sidawy AN, Bottoni CR, et al. Physiological changes in venous hemodynamics associated with elective fasciotomy. Ann Vasc Surg. 2006;20:301–305.

CHAPTER 68

Hamstring Strain John Cianca, MD Paolo Mimbella, MD, MSc

Synonyms Hamstring contusion Hamstring pull Hamstring tear Hamstring avulsion Delayed-onset muscle soreness of the posterior thigh Stretch-induced injury to the hamstring Posterior thigh injury Hamstring tendinopathy

ICD-10 Codes S76.309A S76.319A S73.199A M76.899 S76.399A S76.392A S76.391A

Hamstring injury Hamstring strain, tear Hamstring sprain Hamstring tendonitis at origin Avulsion of hamstring muscle Avulsion of left hamstring muscle Avulsion of right hamstring muscle

Definition The hamstrings are some of the most commonly injured muscles, particularly in athletes. Hamstring strains increase in incidence with age and have been reported most commonly in athletes participating in American football, soccer, and sports that require sprinting. Although most hamstring injuries occur in practice (∼68%), the rate of in-competition injury is twice as high.1 The hamstrings consist of three muscles. The biceps femoris originates on the ischium (long head) and femoral shaft (short head) and jointly attaches on the fibular head, making up the lateral portion of the hamstrings. The semitendinosus and semimembranosus both originate on the ischial tuberosity and insert on the medial tibia. Hamstring strains constitute a range of injuries from delayed-onset muscle soreness, to partial tears, to complete rupture of the muscle-tendon unit.2 These injuries can be acute, subacute, or chronic in nature and can occur from direct or indirect forces. Direct forces refer to lacerations and contusions. Complete avulsion of the proximal hamstring origin from the ischial tuberosity has been described, most commonly in water-skiers.3-5 They may occur more 378

frequently in the skeletally immature or the aging individual with less than optimal fitness when forced hip flexion is sustained while the knee remains in complete extension. Most hamstring injuries, however, occur from indirect forces with exertional use of the muscles, such as running, sprinting, and hurdling. The majority of these injuries occur at the myotendinous junction during eccentric actions when the muscle lengthens while developing force, most commonly in the biceps femoris.4 Their primary eccentric action as functional decelerators of stride, especially for directional change, places them at increased risk for strain. Other reported risk factors for hamstring strain are insufficient hamstring flexibility, insufficient warm-up, strength imbalance between the hamstrings and quadriceps, imbalances between contralateral hamstrings, increases in training volume/speed, and fatigue. However, the greatest risk factor for hamstring strain is previous hamstring strain.7 Hamstring strains can occur in a variety of patients, from young to old, and from the “weekend warrior” to the elite athlete. Hamstring tendinopathy is the product of overuse and occurs silently over time. It can be acute or chronic and, similar to hamstring strain, is very common. Soreness proximally at the ischial tuberosity with sitting or after activity is a common complaint. There is no recollection of an injury, unlike acute strains. Despite the lack of an identifiable triggering event, there is often significant disability produced (Fig. 68.1A and B). The hamstrings are multi-joint muscles that act over two articulations. Like other biarticular muscle groups, such as the Rectus femoris, the gastrocnemius, and the biceps brachii, the hamstrings are more susceptible to injury than single-joint action muscles. The hamstrings cross the hip and knee joint (with the exception of the short head of the biceps femoris). During the latter part of the swing phase of gait, the hamstrings act eccentrically to decelerate knee extension. At heel strike, the hamstrings act concentrically to assist in hip extension. During running, this rapid change in function puts the muscle at risk for injury; the higher the running speed and angular velocity, the greater the forces at heel strike and therefore myofibril lengthening.8,9 Any large strength imbalance between the larger and stronger quadriceps and the hamstrings will also put the posterior thigh muscles at a disadvantage. In general, if one muscle in an agonist-antagonist couple is significantly more powerful than the other, a vigorous contraction may result in strain of the weaker unit. This is especially true during co-contraction. Any factor that adversely affects neuromuscular coordination during running, such as lack of proper neuromuscular and motion-specific warm-up, poor training, or muscle fatigue with subsequent breakdown in technique, may result in a strain injury.

CHAPTER 68  Hamstring Strain

A

379

B

FIG. 68.1  Hamstring tendinopathy at the origin with enlargement and hypoechogenicity of the tendon along with cortical changes at the enthesis. (A) Short-axis view of the conjoint tendon of the hamstring origin. (B) Long-axis view of the conjoint tendon of the hamstring origin. CJT, Conjoined tendon; IT, ischial tuberosity; arrowheads, areas of tendinopathy.

STUMP

Semimembranosus

prox

L Thigh

FIG. 68.2  Short-axis view of the distal muscle belly of the short head of the biceps femoris showing a small area of hypoechogenicity and loss of normal muscle architecture consistent with a grade I muscle tear. LHBF, Long head biceps femoris, SHBF, short head biceps femoris; arrowheads, area of disrupted muscle fibers.

Hamstring strains can be divided into three grades according to their severity: 1. Grade I, or first-degree, strain: mild strain with minimal muscle damage (less than 5% of muscle fiber disruption). There is associated pain but little or no loss of muscle strength (Fig. 68.2). 2. Grade II, or second-degree, strain: moderate strain with more severe partial tearing of the muscle but no complete disruption of the myotendinous unit. Pain is present with loss of knee flexion strength. 3. Grade III, or third-degree, strain: complete tearing of the myotendinous unit. This injury presents with severe pain and marked loss of knee flexion strength (Fig. 68.3).2,10 Avulsion of the hamstrings tendon from its origin on the ischium or distally from the tibia or fibula is not graded like the classic myotendinous strains. These injuries are usually complete or partial avulsion injuries and can be described roentgenographically as such. 

FIG. 68.3 Grade III tear of the semimembranosus muscle demonstrated on an “extended field of view” sonograph. Arrows, Terminal fibers of the torn semimembranosus representing the residual distal stump of the muscle; Prox, proximal.

Symptoms At the time of injury, patients typically report a sudden, sharp pain in the back of the thigh. Some describe a “popping” or tearing sensation. There is generalized pain and point tenderness at the site of injury. The patient may complain of tightness, weakness, and impaired range of motion. Depending on the severity of the injury, the individual may or may not be able to continue activity and occasionally is unable to bear weight on the affected limb. Swelling and ecchymosis are variable and may be delayed for several days. The ecchymosis may descend and manifest at the distal thigh, posterior knee, calf, or ankle as blood tracks down the disrupted fascial layer. In absence of this discreet finding, it is doubtful that a structural hamstring injury has occurred. As with any pathological process, a differential list should arise in the mind of the clinician. For example, if the complaint is of localized soreness at the origin of the hamstring that is persistent despite inactivity, hamstring tendinopathy should be considered. Commonly, this condition is most bothersome with sitting. At times, the patient may complain of symptoms of numbness, tingling, and distal extremity weakness. If these are present, further

380

PART 1  MSK Disorders

SN

SM

ST

BF

FIG. 68.4  Axial magnetic resonance image demonstrating injury to the semitendinosus (ST), semimembranosus (SM), and biceps femoris (BF) muscles. The sciatic nerve (SN) is shown anterior to the muscles and within the hematoma of injury.

investigation into a sciatic neuropathy is warranted. Complete tears and proximal hamstring avulsion injuries can also cause a large hematoma or scar tissue that compresses the sciatic nerve,10,11 although this is relatively uncommon. Of less consequence, rapid increases in training volumes or patterns, especially in the previously untrained subject, can lead to hamstring injury with delayed-onset muscle soreness. This is thought to be the result of microscopic damage followed by a local inflammatory response.12 In these instances, there is no recall of an acute injury. The symptoms arise after the activity has concluded, and typically 24 to 48 hours post exercise.13 

Physical Examination The physical examination begins with assessment of gait abnormalities. Patients with hamstring injuries often have a shortened walking gait or running stride associated with an antalgic gait. Swelling and ecchymosis may not be detectable for several days after the initial injury, and the amount of bleeding depends on the severity of the strain. As previously explained, blood can track through fascial planes in a hamstring strain and result in ecchymosis distal to the site of injury.14 The posterior thigh is inspected for visible defects and deformity, asymmetry, swelling, and ecchymosis. The entire length of the hamstrings should be palpated, including the proximal origin near the ischial tuberosity and distal insertions at the posterior knee. A palpable defect in the posterior thigh indicates a more severe injury with possible complete rupture of the muscle. A soft tissue defect with distal bulging may increase suspicion of a retracted muscle belly and possibly indicate a partial or complete rupture. Neurologic examination findings should be normal except for strength testing of the hamstring group and in rare cases when there is an associated sciatic nerve irritation. In these cases, there may be weakness, particularly notable in plantar flexion, and loss of the affected Achilles reflex. 

Functional Limitations Most patients sustaining a hamstring strain have no residual deficits and return to their previous level of function. However, others may experience difficulty with walking or running, time lost from occupation, and delayed return to sports. Hamstring strains heal slowly and are at high risk for re-injury if return to activity is too early. In the recovery process, active and passive range of motion of the hamstrings should be tested and compared with the contralateral side. Range of motion of the knee can be measured with the hip at 90 degrees in the supine position or sitting position. Deficits in knee and hip range of motion are common, and the point at which pain limits range of motion should be noted. Concentric and eccentric muscle strength testing of the hamstrings should also be performed with the patient both sitting and prone. Weakness of knee flexion and hip extension is common. With severe injuries, it may take up to 1 year for patients to resume pre-injury activities. In some cases of complete ruptures, patients never return to the previous level of function.15 

Diagnostic Studies Hamstring strain is typically a clinical diagnosis. However, moderate and severe cases may warrant diagnostic imaging. If the injury localizes near the origin of the hamstrings, plain radiographs may help identify irregularities of the hip, such as a bony avulsion of the ischial tuberosity. Patients at extremes of age, including the adolescent and elderly, are especially at risk due to bone quality. Other radiographic findings may include ectopic calcification consistent with chronic myositis ossificans or advanced tendinopathy.6,16 Musculoskeletal ultrasound (US) and magnetic resonance imaging may be used to determine the degree of injury and to identify complete proximal avulsion injuries (Fig. 68.4). In the acute phase, sonographic examination of the hamstrings is a practical and cost-effective modality. The advantages of US are low cost, portability, visualization

CHAPTER 68  Hamstring Strain

381

L Hamstring

FIG. 68.5  Grades II to III tear of the proximal semitendinosus (ST) at the level of the conjoint tendon demonstrating separation of the conjoint tendon and retraction of the ST muscle. The space between the + signs is a 6.26 cm gap within the conjoint tendon filled with blood and edema. SN, Sciatic nerve.

and differentiation of soft tissues, and the ability to dynamically assess structures (Fig. 68.5). Although the accuracy of assessment is dependent on the skill of the sonographer, the findings of this particular injury are often dramatic enough for easy identification by even a novice sonographer. Neither MRI nor US have demonstrated usefulness for determining return to play (Fig. 68.6).17,18 

A

Differential Diagnosis Lumbosacral radiculopathy Hamstring syndrome Radiculopathy Bone avulsion or apophysitis of the ischial tuberosity Hip osteoarthritis Sacroiliac joint dysfunction Ischiogluteal bursitis (weaver’s bottom) Sciatic nerve injury Stress fracture in the pelvis, femoral neck, or femoral shaft Adductor group strain Pelvic floor dysfunction Chronic exertional compartment syndrome of posterior thigh Piriformis syndrome

Tear

B

Treatment Initial The primary goal of treatment for a hamstring strain is return to prior level of function (or performance in the athlete) and minimization of risk for re-injury.19 Initial management of a hamstring strain consists of the PRICE principle (protection, rest, ice, compression, and elevation). Relative rest, but not complete immobilization, and protection may involve weight bearing as tolerated or, with higher-grade injuries (grade II or grade III injuries), cane or crutch walking. Ambulatory aids help prevent tissue irritation and the resulting inflammation, both of which prolong

FIG. 68.6  (A) Grade III tear of the semimembranosus (SM). The retracted muscle is demonstrated to the right of the image while the middle of the image shows an area of blood and edema and the left side of the image reveals disorganized and retracted fibers of the SM. (B) Longitudinal tear of the conjoint tendon seen in Fig. 68.5A, showing retraction laterally of the biceps femoris fibers and medially of the semitendinosus (ST) fibers. BF, Biceps femoris, tear, separated fibers of the conjoint tendon and edematous fluid within the void created by the tear.

recovery. Assistive devices should be used until the patient can walk in a normal heel-toe, non-antalgic gait. The use of cryotherapy as a means of pain control and for mitigation of excessive inflammation has advantages over nonsteroidal anti-inflammatory drugs, given the localized effect of ice

382

PART 1  MSK Disorders

FIG. 68.7 Stretching the hamstring fully requires the hip to be at 90 degrees with the ankle dorsiflexed. Forceful stretching should be avoided.

and potential complications/contraindications of NSAIDs. Compression by taping or elastic wrapping of the thigh combined with elevation reduces hemorrhage, thereby helping control edema and pain. NSAIDs and other analgesics are commonly used to limit inflammation and for pain control in the first few days. However, care should be taken not to overuse nonsteroidals, either acutely or over the long term, as gastric, renal, hematologic, and medication interaction effects are well documented. Aggressive soft-tissue mobilization at the site of pain should be avoided for at least 5 days because this may exacerbate the inflammatory response. 

Rehabilitation The elements of a hamstring rehabilitation program involve a pain-free progression of stretching, strengthening, and sports-specific activities. In the acute phase, pain-free range of motion should be achieved as soon as possible to optimize a return to full function and prevent further losses of range of motion. Patients should start with pain-free active range of motion and progress to pain-free passive range of motion and gentle stretching. For a full stretch of the hamstring muscle to be achieved, the hip must be flexed to 90 degrees and the knee fully extended. This stretch is best achieved in the supine position; a towel can facilitate hamstring lengthening (Fig. 68.7). It is also critical to improve flexibility throughout the spine and lower extremities. Strengthening can begin when the patient achieves full active stretch without pain. It is best to start with static contractions, such as multiple-angle submaximal isometric exercises.20 Once these are performed at 100% effort without pain, the patient may progress to isotonic exercise, such as prone hamstring strengthening and isokinetic exercise if available. These concentric strength exercises are followed by eccentric strength exercises and finally sport-specific activities as tolerated. There are a variety of methods to engage eccentric strengthening, some more challenging than others. Examples of eccentric training include Nordic hamstring exercises, straight-leg windmills, straight-leg dead lift, and flywheel training.21 Return to sport criteria includes: no pain with palpation, full and equal bilateral strength with both concentric and eccentric actions, no kinesiophobia,22 and the ability to perform sport-specific movements with no pain at full intensity. Hamstring-quadriceps strength ratio should be symmetric as well.8 Hamstring flexibility

should be a focus of the rehabilitation process to prevent reinjury and contracture. However, as mentioned, in the initial phase, aggressive flexibility training should be avoided, as this may contribute to prolonged recovery.22 Aerobic conditioning should continue throughout the rehabilitation process. Bicycling without toe clips (toe clips increase use of hamstrings), swimming or jogging in a pool, and upper body ergometry are recommended. Rehabilitation programs incorporating progressive agility and trunk stabilization exercising have been shown to decrease re-injury rates.23 It is critical to educate patients about how to prevent recurrent hamstring injuries. This includes a good warm-up period before engaging in sports. Full return to play must be gradual because the risk of recurrent injury is high. Recall that the greatest risk factor for a hamstring strain is a prior strain. Those with prior hamstring strain are 2 to 6 times more likely to suffer another strain.24 In addition, training errors, such as an abrupt switch to a hard surface or an increase in training intensity, should be avoided. Correcting underlying biomechanical/kinetic chain insufficiencies is an important consideration during the reintegration of normal activities. 

Procedures Procedures are not typically performed in common hamstring strain injuries. Direct intramuscular glucocorticoid injections are not recommended. These medications may degrade tendons and increase the risk of complete rupture.25 However, the use of platelet-rich plasma to aid in the recovery of high hamstring strains continues to gain popularity.26 Results of these procedures along with needling, stem cells, and autologous blood injections are mixed and more research is warranted.27,28 Given the rich vascular supply to the hamstrings, an injury excluding the complete rupture of one of the hamstring muscles, diligent attention to recovery, rehabilitation, and reintegration techniques will typically allow for complete recovery. 

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

Surgery Routine hamstring strains do not require surgical intervention and respond well to a conservative rehabilitation program. However, in the case of complete hamstring avulsion from the ischial tuberosity or even complete mid-substance tear, surgical repair is recommended because of the residual loss of power and function in non-operatively treated patients.3,4,29 Surgical neurolysis may also be recommended for the rare complication of symptomatic scarring around the sciatic nerve.10,11 If a high-grade strain or complete tear is suspected, MRI is indicated and a consultation to an orthopedic surgeon will likely be warranted. 

Potential Disease Complications The most common complication of hamstring strain is recurrent injury. Loss of hamstring flexibility and strength

CHAPTER 68  Hamstring Strain

as well as neuromuscular coordination put the patient at risk for re-injury, especially if the return to activity is before full recovery. The high injury recurrence rate has mainly been attributed to return to play before full strength is regained in the lengthened hamstring position.30 Two cases of posterior thigh compartment syndrome have been reported with complete hamstring tears, one resulting from injury alone and one complicated by anticoagulation therapy.31,32 As previously mentioned, higher-grade hamstring tears can also result in substantial scar formation around the sciatic nerve within the posterior thigh. Patients may present with radicular-type symptoms ranging from sensory paresthesias to footdrop, although it is once again stressed that this is a rare occurrence. Patients with chronic complete hamstring avulsion off the ischial tuberosity may complain of pain, weakness, and cramping as well as difficulty in running and walking and poor leg control, especially walking downhill.4 

Potential Treatment Complications Nonsteroidal anti-inflammatory drugs are known to have gastrointestinal, renal, and hepatic side effects. There has been concern with the long-term use of NSAIDs potentially contributing to delayed healing, weakened tissue, impaired function, and progression of a pre-existing injury.33 There is a paucity of high-quality evidence governing NSAID prescription34; however, a short-term (no greater than 7 days) use of NSAIDs or pain relievers early in the treatment of hamstring injury for pain control is reasonable, if no contraindications are present. Ultrasound therapy and application of heat should be avoided in the acute treatment of high-degree strains, especially if hematoma formation is suspected, to prevent further hemorrhage from occurring.32 Potential complications of surgical repair of an avulsion fracture include sensation loss along the incision site and postoperative sciatica.35

References 1. Dalton SL, Kerr ZY, Dompier TP. Epidemiology of hamstring strains in 25 NCAA sports in the 2009-2010 and 2013-2014 academic years. Am J Sports Med. 2015;43(11):2671. 2. Kujala UM, Orava S, Järvinen M. Hamstring injuries: current trends in treatment and prevention. Sports Med. 1997;23:397–404. 3. Brewer BJ. Athletic injuries; musculotendinous unit. Clin Orthop. 1962;23:30–38. 4. Blasier RB, Morawa LG. Complete rupture of the hamstring origin from a water skiing injury. Am J Sports Med. 1990;18:435–437. 5. Wood DG, Packham I, Trikha SP, Linklater J. Avulsion of the proximal hamstring origin. J Bone Joint Surg Am. 2008;90(11):2365–2374. 6. Morris AF. Sports Medicine: Prevention of Athletic Injuries. Dubuque: William C. Brown Publishers; 1984:162–163. 7. Hägglund M, Waldén M, Ekstrand J. Previous injury as a risk factor for injury in elite football: a prospective study over two consecutive seasons. Br J Sports Med. 2006;40(9):767–772. 8. Young JL, Laskowski ER, Rock M. Thigh injuries in athletes. Mayo Clin Proc. 1993;68:1099–1106. 9. Agre JC. Hamstring injuries: proposed aetiological factors, prevention, and treatment. Sports Med. 1985;2:21–33.

383

10. Street CC, Burks RT. Chronic complete hamstring avulsion causing foot drop. Am J Sports Med. 2000;28:1–3. 11. Hernesman SC, Hoch AZ, Vetter CS, Young CC. Foot drop in a marathon runner from chronic complete hamstring tear. Clin J Sport Med. 2003;13:365–368. 12. Brockett CL, Morgan DL, Proske U. Predicting hamstring strain injury in elite athletes. Med Sci Sports Exerc. 2004;36:379–387. 13. Costello JT, Baker PR, Minett GM, Bieuzen F, Stewart IB, Bleakley C. Whole-body cryotherapy (extreme cold air exposure) for preventing and treating muscle soreness after exercise in adults. Cochrane Database Syst Rev. 2015;(9): CD010789. 14. Best TM. Soft-tissue injuries and muscle tears. Clin Sports Med. 1997;16:419–434. 15. Salley PI, Friedman RL, Coogan PG, et al. Hamstring muscle injuries among water skiers: functional outcome and prevention. Am J Sports Med. 1996;24:130–136. 16. Zarins B, Ciullo JV. Acute muscle and tendon injuries in athletes. Clin Sports Med. 1983;2:167–182. 17. Petersen J, Thorborg K, Nielsen MB, et al. The diagnostic and prognostic value of ultrasonography in soccer players with acute hamstring injuries. Am J Sports Med. 2014;42(2):399–404. 18. De Vos RJ, Reurink G, Goudswaard GJ, Moen MH, Weir A, Tol JL. Clinical findings just after return to play predict hamstring re-injury, but baseline MRI findings do not. Br J Sports Med. 2014;48(18):1377–1384. 19. Heiderscheit BC, Sherry MA, Silder AC, Chumanov ES, Thelen DG. Hamstring strain injuries: recommendations for diagnosis, rehabilitation, and injury prevention. J Orthop Sports Phys Ther. 2012;40(2):67–81. 20. Worrel TW. Factors associated with hamstring injuries: an approach to treatment and preventative measures. Sports Med. 1994;17:338–345. 21. Opar D, Williams M, Shield A. Hamstring strain injuries. Sports Med. 2012;42:209–226. 22. Sherry MA, Johnston T, Heiderscheit BC. Rehabilitation of acute hamstring strain injuries. Clin Sports Med. 2015;34:263–284. 23. Ali K, Leland M. Hamstring strains and tears in the athlete. Clin Sports Med. 2012;31:263–272. 24. Freckelton G, Pizzari T. Risk factors for hamstring muscle strain injury in sport: a systematic review and meta-analysis. Br J Sports Med. 2013;47(6):351–358. 25. Tempfer H, Gehwolf R, Lehner C, Wagner A. Effects of crystalline glucocorticoid triamcinolone acetonide on cultured human supraspinatus tendon cells. Acta Orthop. 2009;80(3):357–362. 26. Sherry MA, Best TM. A comparison of 2 rehabilitation programs in the treatment of acute hamstring strains. J Orthop Sports Phys Ther. 2004;34:116–125. 27. Hamilton B, Tol JL, Almusa E, et al. Platelet rich plasma does not enhance return to play in hamstring injuries: a randomized controlled trial. Br J Sports Med. 2015;49(14):943–950. 28. A Hamid MS, Mohamed Ali MR, Yusof A, George J, Lee LP. Platelet rich plasma injections for the treatment of hamstring injuries: a randomized controlled trial. Am J Sports Med. 2014;42(10):2410–2418. 29. Cross MG, Vandersluis R, Wood D, Banff M. Surgical repair of chronic complete hamstring tendon rupture in the adult patient. Am J Sports Med. 1998;26:785–788. 30. Schmitt B, Tim T, McHugh M. Hamstring injury rehabilitation and prevention of reinjury using lengthened state eccentric training: a new concept. Int J Sports Phys Ther. 2012;7:333–341. 31. Oseto MC, Edwards JC, Acus RW. Posterior thigh compartment syndrome associated with hamstring avulsion and chronic anticoagulation therapy. Orthopedics. 2004;27:229–230. 32. Kwong Y, Patel J. Spontaneous complete hamstring avulsion causing posterior thigh compartment syndrome. Br J Sports Med. 2006;40:723–724. 33. Almekinders LC. Anti-inflammatory treatment of muscular injuries in sport. An update of recent studies. Sports Med. 1999;28(6):383. 34. Ziltener JL, Leal L, Fournier PE. Non-steroidal anti-inflammatory drugs for athletes: an update. Ann Phys Rehabil Med. 2010;53(4):278–288. 35. Birmingham P, Muller M, Wickiewicz T, et al. Functional outcome after repair of proximal hamstring avulsions. J Bone Joint Surg Am. 2011;93:1819–1826.

CHAPTER 69

Iliotibial Band Syndrome Venu Akuthota, MD Sonja K. Stilp, MD Paul Lento, MD Peter Gonzalez, MD Alison R. Putnam, DO

Synonyms Iliotibial band friction syndrome Iliotibial tract friction syndrome Snapping hip

ICD-10 Codes M24.851 M24852 M24.859 M76.30 M76.31 M76.32

Joint derangement of the right hip, not elsewhere classified (snapping hip) Joint derangement of the left hip, not elsewhere classified (snapping hip) Joint derangement of unspecified hip, not elsewhere classified (snapping hip) Iliotibial band syndrome, unspecified leg Iliotibial band syndrome, right leg Iliotibial band syndrome, left leg

Definition The iliotibial band (ITB) is a dense fascia on the lateral aspect of the knee and hip. Fascial contributions from the gluteus maximus, gluteus medius, and tensor fascia lata (TFL) are the proximal origin of the ITB (Fig. 69.1).1 Proximal attachment includes the iliac tubercle or iliac crest.2,3 In the distal thigh, the ITB attaches to the linea aspera and the upper edge of the lateral femoral epicondyle.3 After passing over the lateral femoral epicondyle, it separates into two components.4 The iliotibial tract of the distal ITB attaches to Gerdy tubercle of the anterolateral proximal tibia. The iliopatellar band of the ITB has aponeurotic connections to the patella and the vastus lateralis.4 Other distal attachments include the biceps femoris, lateral patellar retinaculum, and the patellar tendon.4,5 An anatomic pouch can be found underlying the posterior ITB at the level of the lateral femoral epicondyle.6 Controversy exists as to whether this 384

pouch is a bursa, a synovial extension of the knee joint, or degenerative tissue.6,7 Others have reported that a highly innervated fat pad overlies the lateral femoral epicondyle.8 Iliotibial band syndrome (ITBS) or ITB friction syndrome is an overuse injury typically referring to lateral knee pain as a result of impingement of the distal ITB over the lateral femoral epicondyle. Less commonly, ITBS may refer to hip pain associated with movement of the ITB across the greater trochanter. This chapter deals primarily with distal ITBS. The suspected pain generator in ITBS is as controversial as the anatomy around the lateral epicondyle. It has been postulated to be bursitis, synovitis, or irritation of the fat pad, posterior fibers of the ITB, or periosteum.3,5,8–11 Although the anatomic pain generator may not be fully known, pain at the distal aspect of the ITB is thought to be caused by the fibers of the ITB passing over the lateral femoral epicondyle with knee flexion and extension.5,10 Friction has been implicated as the most important factor in ITBS.7,10 Maximum friction occurs when the posterior fibers of the ITB pass over the lateral femoral epicondyle at 20 to 30 degrees of knee flexion, the putative “impingement zone.”7 Repeated knee flexion and extension, particularly with increased running mileage per week, creates friction and has been shown to predispose an individual to lateral knee pain.7,10 ITBS is the most common cause of lateral knee pain in runners.5 Friction has been shown to play a role in cycling activities as well. Cycling-induced ITBS is thought to result from the repetitive activity of cycling, as less time is spent in the impingement zone than during running activities.10 Other authors have theorized that pain is due not only to friction but also to compression of the fat pad between the ITB and the lateral femoral epicondyle. The compression of the fat pad was found to be greatest at 30 degrees of flexion, similar to previous reports, and increased with internal rotation of the tibia during knee flexion.5,8 Several factors may increase the risk of developing ITBS. Although it has not been extensively studied, poor neuromuscular control appears to be an important modifiable risk factor for ITBS. Weakness of hip abductors has been implicated in ITBS.5 However, difference in strength of hip abduction was not found in a study of 10 runners with

CHAPTER 69  Iliotibial Band Syndrome

Greater trochanter

Iliotibial band

385

recreational runners with history of ITBS.1,15 Strengthening of the gluteus medius and TFL, decelerators of the valgus-­internal rotation vectors at the knee, has been shown to reduce symptoms of ITBS.9 Lack of dynamic flexibility, particularly of the ITB, has been implicated with ITB injury susceptibility.5,14,18,19 Yet, no research study to date has revealed a correlation between ITB tightness and ITB injury. Theoretically, however, tightness of the ITB or its constituent muscles increases impingement of the ITB on the lateral femoral epicondyle.7 Other risk factors that may be attenuated with proper shoe wear or foot orthoses include excessive foot-ankle pronation and supination.5,15 Training errors have also been highlighted as increasing the risk of ITBS, such as rapid changes in training routine, hill training, striding, and excessive mileage.5,11 Increased ground reaction force, as with running in old shoes, may also increase frictional forces at the knee and exacerbate symptoms.7 Intrinsic or non-modifiable factors, such as bone malalignment or a wide distal ITB, may contribute to the development of ITBS.19 

Symptoms

FIG. 69.1 Anatomy of the iliotibial band, which can cause “snapping” as it slips anteriorly and posteriorly over the prominent greater trochanter.

ITBS compared to controls.12 Specifically, neuromuscular control is needed to attenuate the valgus-internal rotation vectors at the knee after heel strike. If appropriate control is not available, the ITB may have an abrupt increase in tension at its insertion site.9,13,14 Increased hip adduction and knee internal rotation has been noted in female runners, suggesting increased ITBS strain as a mechanism of injury.14 Increased foot inversion, maximum knee flexion, and knee internal rotation were noted during an exhaustive run in recreational runners with history of ITBS.15 Peak rearfoot eversion, knee internal rotation angle, and hip adduction angle were increased in 35 female runners with history of ITBS compared to matched controls.16 Contradictory results were found in a study of 18 runners with ITBS compared to controls. Results indicated decreased hip adduction in those with ITBS, though they were found to have a lack of “coordination” defined as earlier hip flexion and knee flexion.17 It has been noted that the strain rate of the ITB during stance phase was increased in female runners who developed ITBS compared to healthy age-matched controls as well as increased ITBS strain in

Symptoms of ITBS occur typically at the lateral femoral epicondyle but may emanate from the distal attachment of the ITB at Gerdy tubercle on the tibia.5,11 Individuals present with sharp or burning lateral knee pain that is aggravated during repetitive activity. This pain may radiate up into the lateral thigh or down to Gerdy tubercle.20 Runners often describe a specific, reproducible time when the symptoms commence.21 Pain usually subsides after a run; however, in severe cases, persistent pain may cause symptoms in walking or stairs.22 Runners also note more pain with downhill running because of the increased time spent in the impingement zone.7,22 Paradoxically, runners state that faster running and sprinting often does not produce pain. Fast running allows the athlete to spend more time in knee angles greater than 30 degrees.7 Cyclists present with rhythmic, stabbing pain with pedaling. Specifically, they complain of pain at the end of the downstroke or the beginning of the upstroke.20 Bikers with improper saddle height and cleat position may experience greater symptoms.20,23 ITBS symptoms may also occur as a lateral snapping hip. An external or lateral snapping hip occurs as the ITB rapidly passes anteriorly over the greater trochanter as the femur passes from extension to flexion.24 Athletes, particularly dancers, sometimes experience an audible painful snap on landing in poor turnout (decreased external rotation at the hip) and with excessive anterior pelvic tilt.25 

Physical Examination Physical examination begins with a screening examination of the joints above and below the site of injury. Hip girdle examination includes an assessment for joint range of motion, asymmetries, and muscle strength (particularly hip abductors).9,26 The modified Thomas and Ober tests are used to assess flexibility of the ITB and related musculature at the hip and knee (Figs. 69.2 and 69.3).5,11,27 A recent laboratory study revealed that when the Ober test and modified Ober test were performed on cadavers after ITB transection, no changes in thigh adduction occurred.

386

PART 1  MSK Disorders

FIG. 69.2  Thomas test to assess hip flexion contracture. The patient lies supine while the clinician flexes one of the patient’s hips, bringing the knee to the chest to flatten the lumbar spine. The patient holds the flexed knee and hip against the chest. If there is a flexion contracture of the hip, the patient’s other leg will rise off the table.

However, after the transection of the gluteus medius/ minimus and hip joint capsule with intact ITB, there was a significant change in hip adduction suggesting that the Ober test assesses structures other than the ITB.28 The knee examination includes palpation, patellar accessory motion,29 and the Noble compression test (Fig. 69.4).7 Knee tenderness is noted either at the lateral femoral epicondyle (above the lateral joint line) or at Gerdy tubercle. Palpatory examination should also include a thorough assessment for myofascial restrictions and trigger points along the lateral thigh musculature.21,22 On rare occasion, ITB swelling and crepitus accompany tenderness. Pain can also be elicited by the Noble compression test.5 Other conditions are effectively ruled out by performing a relevant physical examination. The foot and ankle examination is particularly useful in the determination of gastrocnemius-soleus inflexibility, subtalar motion restrictions, and specific foot type (e.g., forefoot varus). Finally, a biomechanical assessment of sports-specific activity can be done. Walkers and runners are observed for abnormalities such as excessive foot-ankle pronation, inability to attenuate shock at the knee, or Trendelenburg gait at the pelvis.22,23,30 Bicyclers are observed for proper foot placement on the pedal, saddle height, and knee angles with pedaling revolution.23 Dancers can be observed performing rond de jambe or grand plié for proper turnout and pelvic stabilization.25 The findings of the neurologic examination, including strength, sensation, and reflexes, are typically normal. Strength may be affected by disuse or guarding due to pain, particularly in the hip abductors and external rotators. 

Functional Limitations ITBS pain usually restricts athletes from their sports activity but does not typically cause limitations of daily activities. Yet, a vicious circle is set forth in which biomechanical deficits (e.g., gluteal weakness and ITB tightness) cause ITB tissue injury with resultant functional adaptations to avoid the pain of the tissue injury (e.g., external rotation of the hip).31 

A

B

C FIG. 69.3 Ober test to assess contracture of the iliotibial band. The patient is side lying with the lower leg flexed at the hip and knee. The clinician passively abducts and extends the patient’s upper leg with the knee straight (A) or flexed to 90 degrees (C). The test result is positive if the leg remains abducted and does not fall to the table (B).

Diagnostic Studies Imaging has a limited role in ITBS because it is usually a clinical diagnosis. Radiographs are rarely helpful.11 Diagnostic ultrasound can be used to measure ITB thickness for

CHAPTER 69  Iliotibial Band Syndrome

387

corticosteroid injection in the initial stages.21,22 As well, modalities such as ice, ice massage, ultrasound, iontophoresis, and phonophoresis can be helpful in the early period to reduce early inflammation and pain.5,10,22 It is critical early on to address the biomechanical cause of ITB injury.22  Differential Diagnosis

30°

FIG. 69.4  Noble compression test to determine whether there is iliotibial band friction at the knee. The patient lies supine, and the knee is flexed to 90 degrees (the hip flexes as well). The clinician applies pressure with the thumb at the lateral femoral epicondyle while the patient slowly extends the knee. The test result is positive if the patient complains of severe pain over the lateral femoral epicondyle at 30 degrees.

which normal values have been determined in uninjured subjects.32 In a diagnostic ultrasound study, fluid anterior and deep to the ITB was found to be present in 100% in asymptomatic recreational runners.33 In follow-up to this study, the lateral synovial recess was found to be the source of the fluid on cadaver evaluation of iatrogenic knee effusion, and it was opined that synovial irritation may contribute to pain at the lateral knee and ITBS.34 When definitive diagnosis is needed or other diagnoses need to be excluded, magnetic resonance imaging may show a thickened ITB, peri-ITB edema (high intensity on axial T2-weighted images), or fluid deep to the ITB.8,33 

Treatment Initial Acute-phase treatment is akin to that of other musculoskeletal injuries. Relative rest consists of activity modification, particularly with restriction of those activities that exacerbate the pain symptoms.5,22 In most instances, this does not mean a complete cessation of activity. The clinician needs to emphasize the positive aspects of relative rest and provide alternative training regimens. The ITB can be relatively offloaded if an individual can keep his or her activity below the threshold of pain. Frequently, this can be achieved by simply decreasing intensity or training duration. Medications such as nonsteroidal anti-inflammatory drugs may help reduce pain and inflammation in the first few weeks of injury. If swelling is present, some authors advocate a local

ITB: HIP Hip joint disease Meralgia paresthetica Trochanteric bursitis Internal snapping hip Referred or radicular pain from lumbar spine Primary myofascial pain  ITB: KNEE Popliteus tendinitis Lateral collateral ligament injury Lateral hamstring strain Lateral meniscus tear Patellofemoral pain Common peroneal nerve injury Fabella syndrome Lateral plica Stress fracture Primary myofascial pain ITB, Iliotibial band.

Rehabilitation Ultrasound, phonophoresis, iontophoresis, and electrical stimulation may also be used to reduce early inflammation and pain.22 The subacute phase of rehabilitation addresses the biomechanical deficits found on physical examination. Typically, flexibility deficits are seen in the ITB, iliopsoas, quadriceps, and gastrocnemius-soleus.21,22 Incorporating flexibility and strengthening into the rehabilitation treatment is often recommended.5,12,22 Proper stretching addresses all three planes and incorporates proximal and distal musculotendinous fibers. In a study of the relative effectiveness of three commonly prescribed standing ITB stretches, the authors concluded that when overhead arm extension is added to the standing ITB stretch, the ITB length and average external adduction moments could be increased.18 This stretch is performed standing with the symptomatic leg extended and adducted across the uninvolved leg. The subject laterally flexes the trunk toward the contralateral side and extends both arms overhead (Fig. 69.5). A study evaluated the effectiveness of the Ober test (see Fig. 69.3) and the modified Ober test in stretching the ITB and the most distal component, the iliotibial tract. The modified test is performed the same as the Ober test except the knee remains extended at 0 degrees. The investigators used ultrasonography to assess the soft tissue changes of the iliotibial tract and concluded that both tests are effective in the initial stages of stretching. However, the modified Ober test may afford a greater stretch of the iliotibial tract of the ITB when additional adduction of the hip is allowed.35 In a cadaveric study, there was limited ability to lengthen the ITB with modified Ober, and hip flexion, adduction, and external rotation with knee flexion (HIP) compared to control (straight leg raise), though the HIP test

388

PART 1  MSK Disorders

ITB stretch

FIG. 69.6  Distal iliotibial band injection technique at the lateral epicondyle of the femur.

FIG. 69.5  Iliotibial band (ITB) stretch.

had significantly greater strain. In another limb of the same study, they found minimal change in length with isometric contraction of the TFL, concluding that focus should be stretching the muscular component of the ITB complex.3 Some muscle groups do not respond to stretch unless myofascial and joint restrictions are concomitantly addressed by experienced therapists or by self-administered techniques.21,22 In a systematic review, one study of transverse friction massage was not found to be beneficial.10 Proper facilitation of hip girdle musculature can be achieved by addressing antagonistic tight structures, such as tight hip flexors or anterior hip capsule.27 In conjunction with a flexibility and joint mobilization program, strengthening of weak or inhibited muscles can be started. Strengthening regimens ultimately need to move away from the plinth to more functional activities, such as single squats and lunges, with an emphasis on proper pelvic and core stabilization.22,26 Finally, the maintenance phase focuses on returning patients to their respective activities with confidence in their functional abilities. In this phase, athletes are ideally observed or videotaped in their sporting environment. Frequently, runners have form deviations that lead to uncontrolled valgus-internal rotation of the knee. These abnormalities include excessive pronation, inability to shock attenuate at the knee, and Trendelenburg frontal plane gait at the pelvis.22,23,30 A meta-analysis of cross sectional studies of the biomechanical risk factors associated with ITB syndrome in runners found that females with ITB syndrome have increased peak knee internal rotation and trunk ipsilateral flexion during stance.36 Based on a systematic review of ITB literature through 2011, the authors concluded that abnormal biomechanics of the foot or tibia are not likely increasing tensioning of the ITB, and suggest a more proximal cause.30 Supporting this, there are two studies done by the same group investigating ITB stiffness

in both two- and three-dimensional postural changes. In the first, two-dimensional study, ITB stiffness was significantly increased with pelvic and trunk inclination opposite the standing leg (which increases hip adduction angle and hip adduction moment at the hip and knee). In the following, three-dimensional study, ITB stiffness increased with hip adduction, external rotation, and extension.37 In regard to hip extension, this contradicts other findings noting that hip flexion increased ITB stiffness. This was thought to be related to TFL activation with different positions (weight bearing and non-weight bearing) and cadavers versus live subjects.37 Foot orthoses have also been advocated for runners with lower limb injuries. Their benefit is as yet empirical. Cyclists can often correct their ITB problems with equipment and bicycle adjustments.23 Dancers performing rond de jambe or grand plié can be cued on maintaining turnout and neutral pelvic position.27 After sports-specific adjustments have been made, athletes need to be reintroduced to activity gradually and individually. 

Procedures Corticosteroid injections may be performed at different locations along the ITB. Injection into the anatomic pouch at the lateral femoral epicondyle is a relatively simple procedure and is advocated for patients with persistent pain and swelling (Fig. 69.6).21 A mixture of anesthetic (e.g., 1 mL of 1% lidocaine) and long-acting steroid (e.g., 1 mL of betamethasone) is instilled to the affected site. A randomized controlled study evaluating the efficacy of corticosteroid injections in runners with acute symptoms of ITB-mediated pain showed that runners in the injection group experienced less pain during running activities.38 Steroid injections should be repeated only if adequate relief is obtained after the initial injection. Patients can return to play as their pain allows. 

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

CHAPTER 69  Iliotibial Band Syndrome

Surgery Surgical treatment of ITBS is rarely needed. Surgery involves excision of the posterior half of the ITB where it passes over the lateral femoral epicondyle, z lengthening, or removal of the underlying putative bursa utilizing open or endoscopic techniques.11,39,40 These procedures appear to have mixed results and should be contemplated only for patients who have exhausted all other options, including a comprehensive rehabilitation program as previously outlined. 

Potential Disease Complications If ITBS is not properly addressed, biomechanical adaptations can occur.30,31 Chronic pain, leading to progressive disability, is a potential complication. 

Potential Treatment Complications Rehabilitation complications are rare. Nonsteroidal antiinflammatory drugs and analgesics have well-known side effects that may affect gastrointestinal, hepatic, or renal function. Corticosteroid injections have the potential complications of infection, depigmentation of skin, and flare of symptoms at the site of injection. Surgical procedures for ITBS carry inherent risks. Postoperative infection and other standard risks should be explained to patients before surgical interventions. Overall, interventional procedures for the ITB carry few risks or complications.

References 1. Hamill J, Miller R, Noehren B, Davis I. A prospective study of iliotibial band strain in runners. Clin Biomech. 2008;23(8):1018–1025. 2. Sher I, Umans H, Downie SA, Tobin K, Arora R, Olson TR. Proximal iliotibial band syndrome: what is it and where is it? Skelet Radiol. 2011;40(12):1553–1556. https://doi.org/10.1007/s00256-011-1168-5. 3. Falvey EC, Clark R a, Franklyn-Miller A, Bryanta L, Briggs C, McCrory PR. Iliotibial band syndrome: an examination of the evidence behind a number of treatment options. Scand J Med Sci Sport. 2010;20(4):580–587. https://doi.org/10.1111/j.1600-0838.2009.00968.x. 4. Terry G. The anatomy of the iliopatellar band and iliotibial tract. Am J Sport Med. 1986;14(1):39–45. 5. Baker RL, Souza RB, Fredericson M. Iliotibial band syndrome: soft tissue and biomechanical factors in evaluation and treatment. PM R. 2011;3(6):550–561. https://doi.org/10.1016/j.pmrj.2011.01.002. 6. Nemeth WC, Sanders BL. The lateral synovial recess of the knee: anatomy and role in chronic Iliotibial band friction syndrome. Arthroscopy. 1996;12(5):574–580. 7. Orchard JW, Fricker PA, Abuda T, Mason BR. Biomechanics of iliotibial band friction syndrome in runners. Am J Sport Med. 1996;24(3): 375–379. 8. Fairclough J, Hayashi K, Toumi H, et al. The functional anatomy of the iliotibial band during flexion and extension of the knee: implications for understanding iliotibial band syndrome. J Anat. 2006;208(3):309–316. https://doi.org/10.1111/j.1469-7580.2006.00531.x. 9. Fredericson M, Cookingham CL, Chaudharia M, Dowdell BC, Oestreicher N, Sahrmann SA. Hip abductor weakness in distance runners with iliotibial band syndrome. Clin J Sport Med. 2000;10(3): 169–175. 10. Ellis R, Hing W, Reid D. Iliotibial band friction syndrome–a systematic review. Man Ther. 2007;12(3):200–208. https://doi.org/10.1016/j. math.2006.08.004. 11. Strauss E, Kim S, Calcei J, Park D. Iliotibial band syndrome: evaluation and management. J Am Acad Orthop Surg. 2011;16:728–736. 12. Grau S, Krauss I, Maiwald C, Best R, Horstmann T. Hip abductor weakness is not the cause for iliotibial band syndrome. Int J Sport Med. 2008;29(7):579–583. https://doi.org/10.1055/s-2007-989323.

389

13. Powers CM. The influence of abnormal hip mechanics on knee injury: a biomechanical perspective. J Orthop Sport Phys Ther. 2010;40(2): 42–51. https://doi.org/10.2519/jospt.2010.3337. 14. Noehren B, Davis I, Hamill J. ASB clinical biomechanics award winner 2006 prospective study of the biomechanical factors associated with iliotibial band syndrome. Clin Biomech. 2007;22(9):951–956. https:// doi.org/10.1016/j.clinbiomech.2007.07.001. 15. Miller RH, Lowry JL, Meardon SA, Gillette JC. Lower extremity mechanics of iliotibial band syndrome during an exhaustive run. Gait Posture. 2007;26(3):407–413. https://doi.org/10.1016/j. gaitpost.2006.10.007. 16. Ferber R, Noehren B, Hamill J, Davis IS. Competitive female runners with a history of iliotibial band syndrome demonstrate atypical hip and knee kinematics. J Orthop Sport Phys Ther. 2010;40(2):52–58. https:// doi.org/10.2519/jospt.2010.3028. 17. Grau S, Krauss I, Maiwald C, Axmann D, Horstmann T, Best R. Kinematic classification of iliotibial band syndrome in runners. Scand J Med Sci Sport. 2011;21(2):184–189. https://doi. org/10.1111/j.1600-0838.2009.01045.x. 18. Fredericson M, White JJ, MacMahon JM, Andriacchi TP. Quantitative analysis of the relative effectiveness of 3 iliotibial band stretches. Arch Phys Med Rehabil. 2002;83(5):589–592. https://doi.org/10.1053/ apmr.2002.31606. 19. Lavine R. Iliotibial band friction syndrome. Curr Rev Musculoskelet Med. 2010;3:18–22. https://doi.org/10.1007/s12178-010-9061-8. 20. Holmes J, Pruitt A, Whalen N. Lower extremity overuse in bicycling. Clin Sport Med. 1994;13:187–205. 21. Fredericson M, Guillet M, Debenedictis L. Quick solutions for iliotibial band syndrome. Phys Sport. 2000;28(2):53–68. 22. Fredericson M, Wolf C. Iliotibial band syndrome in runners: innovations in treatment. Sport Med. 2005;35(5):451–459. 23. Baker RL, Souza RB, Fredericson M. Iliotibial band syndrome: soft tissue and biomechanical factors in evaluation and treatment. PM R. 2011;3(6):550–561. https://doi.org/10.1016/j.pmrj.2011.01.002. 24. Allen W, Cope R. Coxa saltans: the snapping hip revisited. J Am Acad Orthop Surg. 1995;3(5):303–308. 25. Khan K, Brown J, Way S. Overuse injuries in classical ballet. Sport Med. 1995;19:341–357. 26. Geraci MC, Brown W. Evidence-based treatment of hip and pelvic injuries in runners. Phys Med Rehabil Clin N Am. 2005;16(3):711–747. https://doi.org/10.1016/j.pmr.2005.02.004. 27. Geraci MC. Rehabilitation of the hip, pelvis, and thigh. In: Kibler W, Herring S, Press J, eds. Functional Rehabilitation of Sports and Musculoskeletal Injuries. Gathersburg; 1998:216–243. 28. Willett G, Keim S, Lomneth C, Shostrom V. An anatomic investigation of the ober test. Am J Sports Med. 2016;44(3):696–701. 29. Puniello MS. Iliotibial band tightness and medial patellar glide in patients with patellofemoral dysfunction. J Orthop Sport Phys Ther. 1993;17(3):144–148. 30. Louw M, Deary C. The biomechanical variables involved in the aetiology of iliotibial band syndrome in distance runners - a systematic review of the literature. Phys Ther Sport. 2014;15(1):64–75. https:// doi.org/10.1016/j.ptsp.2013.07.002. 31. Press J, Herring S, Kibler W. Rehabilitation of the combatant with musculoskeletal disorders. In: Dillingham T, Belandres P, eds. Rehabilitation of the Injured Combatant. Washington, DC: Office of the Surgeon General; 1999:353–415. 32. Gyaran IA, Spiezia F, Hudson Z, Maffulli N. Sonographic measurement of iliotibial band thickness: an observational study in healthy adult volunteers. Knee Surg Sport Traumatol Arthrosc. 2011;19(3):458–461. https://doi.org/10.1007/s00167-010-1269-z. 33. Jelsing EJ, Finnoff J, Levy B, Smith J. The prevalence of fluid associated with the iliotibial band in asymptomatic recreational runners: an ultrasonographic study. PM R. 2013;5(7):563–567. 34. Jelsing EJ, Maida E, Finnoff JT, Smith J. The source of fluid deep to the iliotibial band: documentation of a potential intra-articular source. PM R. 2014;6(2):134–138. 35. Wang T-G, Jan M-H, Lin K-H, Wang H-K. Assessment of stretching of the iliotibial tract with Ober and modified Ober tests: an ultrasonographic study. Arch Phys Med Rehabil. 2006;87(10):1407–1411. 36. Aderem J, Louw QA. UK DRAFFT - A Randomised Controlled Trial of Percutaneous Fixation with Kirschner Wires Versus Volar Locking-Plate Fixation in the Treatment of Adult Patients with a Dorsally Displaced Fracture of the Distal Radius; 2011.

390

PART 1  MSK Disorders

37. Tateuchi H, Shiratori S, Ichihashi N. The effect of three-dimensional postural change on shear elastic modulus of the iliotibial band. J Electromyogr Kinesiol. 2016;28:137–142. https://doi.org/10.1016/j. jelekin.2016.04.006. 38. Gunter P, Schwellnus MP. Local corticosteroid injection in iliotibial band friction syndrome in runners: a randomised controlled trial. Br J Sport Med. 2004;38(3):269–272. https://doi.org/10.1136/ bjsm.2003.000283.

39. Hariri S, Savidge ET, Reinold MM, Zachazewski J, Gill TJ. Treatment of recalcitrant iliotibial band friction syndrome with open iliotibial band bursectomy: indications, technique, and clinical outcomes. Am J Sport Med. 2009;37(7):1417–1424. https://doi. org/10.1177/0363546509332039. 40. Ilizaliturri VMJ, Camacho-Galindo J. Endoscopic treatment of snapping hips, iliotibial band, and iliopsoas tendon. Sport Med Arthrosc Rev. 2010;18(2):120–127.

CHAPTER 70

Knee Osteoarthritis David M. Blaustein, MD Edward M. Phillips, MD

Synonyms Degenerative joint disease of the knee joint Degenerative arthritis Joint destruction of the knee Osteoarthrosis

ICD-10 Codes M17.0 M17.10 M17.11 M17.12 M17.4 M17.5 M12.561 M12.562 M12.569

Bilateral primary osteoarthritis of knee Unilateral primary osteoarthritis, unspecified knee Unilateral primary osteoarthritis, right knee Unilateral primary osteoarthritis, left knee Other bilateral secondary osteoarthritis of knee Other unilateral secondary osteoarthritis of knee Traumatic arthropathy, right knee Traumatic arthropathy, left knee Traumatic arthropathy, unspecified knee

Definition Osteoarthritis (OA) is steadily becoming the most common cause of disability for the middle-aged and has become the most common cause of disability for those older than 65 years.1 The knee joint is the most common site for lower extremity OA.2 It is estimated that nearly half of all adults will have symptomatic knee OA in their lifetimes.3 In addition to the growing population of elderly patients with knee OA, an increasing number of former athletes with previous knee injuries may experience post-traumatic knee OA. OA of the knee results from mechanical and idiopathic factors. Although OA is now known to be a complex condition involving the entire joint, the hallmark of OA is the alteration of the balance between degradation and synthesis of articular cartilage and subchondral bone. OA can involve any or all of the three major knee compartments: medial, patellofemoral, or lateral. The medial

compartment is most often involved, leading to medial joint space collapse and thus to a genu varum (bowleg) deformity. Lateral compartment involvement may lead to a genu valgum (knock-knee) deformity. Arthritis in one compartment may, through altered biomechanical stress patterns, eventually lead to involvement of another compartment. OA affects all structures within and around a joint. Hyaline articular cartilage is lost. Bone remodeling occurs, with capsular stretching and weakness of periarticular muscles. Synovitis is present in some cases and ligamentous laxity occurs. Lesions in the bone marrow may also develop. OA often involves the joint in a nonuniform and focal manner. Localized areas of loss of cartilage can increase focal stress across the joint, leading to further cartilage loss. With a large enough area of cartilage loss or with bone remodeling, the joint becomes tilted, and malalignment develops. Malalignment is the most potent risk factor for structural deterioration of the knee joint.4 By further increasing the degree of focal loading, malalignment creates a vicious circle of joint damage that ultimately can lead to joint failure. The role of obesity as a risk factor for knee OA has been well documented. A large, population-based prospective study found that the risk for knee OA was seven times greater for people with a body mass index of 30 or higher compared with those with a body mass index below 25.5 Moreover, women (of average height) who lost 5 kg of weight reduced their risk of symptomatic knee OA by 50%.6 Sports injuries and vigorous physical activity are considered to be important risk factors in knee OA. Athletes who take part in high-impact sports, such as soccer, ice hockey, and football, have an increased risk of knee OA.7 Knee OA is common in those performing heavy physical work, especially if this involves knee bending, squatting, kneeling, or repetitive use of joints.8 It is unclear if the association of knee OA with these work-related activities is secondary to the nature of the work or the increased likelihood of injury. 

Symptoms Knee OA is characterized by joint pain, tenderness, decreased range of motion, crepitus, occasional effusion, and inflammation of varying degrees. Initial OA symptoms are generally minimal, given the gradual and insidious onset of the condition. Pain typically occurs around the knee, particularly during weight bearing, tending to worsen later in the day and decreasing with rest. With progression of the disease, pain can persist even at rest. Pain may also radiate to adjacent sites, as OA indirectly alters the biomechanics 391

392

PART 1  MSK Disorders

of other anatomic structures such as ligaments, muscles, nerves, and veins. Joint stiffness may occur after periods of inactivity, such as after awakening in the morning or prolonged sitting. Patients often report higher pain levels in the morning, but usually for less than 30 minutes. Patients often experience limitation of movement because of joint stiffness or swelling. Many patients report a “locking” or a “catching” sensation (actual knee locking is often associated with meniscal tear [see Chapter 72]), which is probably due to a variety of causes, including debris from degenerated cartilage or meniscus in the joint known as a “loose body,” increased adhesiveness of the relatively rough articular surfaces, muscle weakness, and even tissue inflammation. Stiffness can discourage mobility. This initiates a cycle that results in deconditioning, decreased function, and increased pain. Barometric changes, such as those associated with damp, rainy weather, will often increase pain intensity.9 Patients often note that their knees “give way” or feel unstable at times. 

Physical Examination Examination of the patient includes testing for various possible causes of knee pain. Therefore the entire limb, from the hip to the ankle, along with the opposite limb, is examined. It is important to look for quadriceps weakness or atrophy, knee and hip flexion contractures, and foot abnormalities such as excessive pronation. Gait should be observed for presence of a limp, functional limb length discrepancy (with the arthritic limb often being shorter due to knee flexion contracture from OA), or buckling. Genu varum or valgum is often better appreciated when the patient is standing. The affected knee should be compared with the contralateral uninvolved knee. Knee examination may reveal decreased knee extension or flexion secondary to effusion or osteophytes (both of which may be palpable). Osteophytes along the femoral condyles may be palpated, especially along the medial distal femur. Palpation may reveal patellar or parapatellar tenderness. Crepitation, resulting from juxtaposition of roughened cartilage surfaces, may be appreciated along the joint line when the knee is flexed or extended. A mild effusion and tenderness may be appreciated along the medial joint line or at the pes anserine bursa. Ligament testing may reveal laxity of the collateral or cruciate ligaments. Lateral subluxation of the patella may be found in patients with genu valgum (Table 70.1). Another clue on examination that the patient probably has knee OA is the finding of visible bone enlargements (exostoses) of the fingers. The findings of the neurologic examination are typically normal, with the exception of decreased muscle strength, particularly in the quadriceps, due to disuse or guarding secondary to pain. 

Functional Limitations Individuals with knee arthritis may describe deficits in their ability to transfer from sit to stand, particularly from a low chair or in and out of a car. In addition, ascending and descending stairs, gait speed, and ability to walk long distances may be compromised. 

Table 70.1  Typical Physical Examination Findings in Knee Osteoarthritis Inspection

Bone hypertrophy Varus deformity from preferential medial compartment involvement

Palpation

Increased warmth Joint effusion Joint line tenderness

Range of motion

Painful knee flexion Decreased joint flexion secondary to pain Crepitus (coarse)

Joint stability

Mediolateral instability

Diagnostic Studies OA is diagnosed clinically on the basis of history and physical examination. Imaging, however, can be used to confirm the diagnosis and to rule out other conditions. Radiographic changes include joint space narrowing, subchondral sclerosis, and bone cysts in weight-bearing regions of the joint and osteophytes in low-pressure areas, especially along the marginal regions of the joint. Joint space narrowing is the initial finding, followed by subchondral sclerosis, then by osteophytes, and finally by cysts with sclerotic margins (known as synovial cysts, subchondral cysts, subarticular pseudocysts, or necrotic pseudocysts). Radiographic evidence of OA is not well correlated with symptoms; however, the presence of osteophytes and subchondral sclerosis had a strong association with knee pain, whereas the absence or presence of joint space narrowing was not associated with pain.10 Knee pain severity was a more important determinant of functional impairment than radiographic severity of OA.11 Indications for plain x-ray films include trauma, effusion, symptoms not readily explainable by physical examination findings, severe pain, presurgical planning, and failure of conservative management. Recommended films are weight-bearing (standing) anteroposterior, lateral, and patellar views. Radiographs taken during weight bearing with the knee in full extension and partial flexion may reveal a constellation of findings associated with OA, including asymmetric narrowing of the joint space (typically medial compartment), osteophytes, sclerosis, and subchondral cysts (Fig. 70.1). A Merchant view specifically evaluates the patellofemoral space and patellar tilt. Non-weight-bearing lateral views may help in the evaluation of the patellofemoral and tibiofemoral joint spaces. Tunnel views can help visualize loose osteochondral bodies. Magnetic resonance imaging (MRI) usually adds little but cost to the evaluation of OA of the knee. Although it may reveal early OA changes, MRI is not indicated in the initial evaluation of older persons with chronic knee pain. MRI may detect incidental findings, such as meniscal tears, that are common in middle-aged and older adults with and without knee pain. Musculoskeletal ultrasonography (MUS) has potential for detecting bone erosions, synovitis, tendon disease, and enthesopathy. It has a number of distinct advantages over MRI, including good patient

CHAPTER 70  Knee Osteoarthritis

393

tolerability and ability to scan multiple joints in a short time. Although there is not an abundance of data, there are now several studies showing good reliability and validity of MUS in detecting knee OA.12 However, there remains limited data describing standardized scanning methodology and standardized definitions of ultrasound pathologic changes. Laboratory test results are typically normal, but analysis may be undertaken, especially for elderly patients, to establish a baseline (e.g., blood urea nitrogen concentration, creatinine concentration, or liver function tests before use of nonsteroidal anti-inflammatory drugs or acetaminophen) or to exclude other conditions such as rheumatoid arthritis. Synovial fluid analysis should not be undertaken unless destructive, crystalline, or septic arthritis is suspected.  Differential Diagnosis Common Causes of Knee Pain by Age Group Children and adolescents

Adults

Older adults

Patellar subluxation Osgood-Schlatter disease Patellar tendinitis/patellofemoral pain Referred pain (e.g., slipped capital femoral epiphysis) Osteochondritis dissecans Subchondral fracture Genetic or congenital defect Septic arthritis Tumor Patellofemoral pain syndrome (chondromalacia patellae) Medial plica syndrome Pes anserine bursitis Trauma: ligamentous sprains Meniscal tear Inflammatory arthropathy: rheumatoid arthritis, Reiter syndrome Septic arthritis Midlumbar radiculopathy Tumor OA Crystal-induced inflammatory arthropathy: gout, pseudogout Rheumatoid arthritis Popliteal cyst Tumor

Differential Diagnosis of Knee Pain by Anatomic Site Anterior knee Patellar subluxation or dislocation/ten­ pain dinitis Jumper’s knee Tibial apophysitis (Osgood-Schlatter lesion) Quadricep tendinitis Patellofemoral pain syndrome (chondromalacia patellae) Medial knee Medial collateral ligament sprain pain Medial meniscal tear Pes anserine bursitis Medial plica syndrome Lateral knee Lateral collateral ligament sprain pain Lateral meniscal tear Iliotibial band tendinitis Posterior knee Popliteal cyst (Baker cyst) pain Posterior cruciate ligament injury OA, Osteoarthritis.

FIG. 70.1  Knee radiograph demonstrating osteophytes (arrows) and medial joint space narrowing consistent with degenerative arthritis. (From West SG. Rheumatology Secrets. Philadelphia: Hanley & Belfus; 1997.)

Treatment Initial The PRICE regimen may help provide initial relief for patients in pain: protection with limited weight bearing by using a cane or modification of exercise to reduce stress; relative rest (or taking adequate rests throughout the day, avoiding prolonged standing, climbing of stairs, kneeling, deep knee bending); ice (applied while the skin is protected with a towel for up to 15 minutes at a time several times a day; note, however, that some patients with chronic pain may find better relief with moist heat); compression (if swelling exists, wrapping with an elastic bandage or a sleeve may help); and elevation (may help diminish swelling, if it is present). There are a wide variety of initial treatment options for knee arthritis. Current guidelines put forth by the American College of Rheumatology suggest the use of acetaminophen as a first-line therapy for OA,13 followed by oral and topical nonsteroidal anti-inflammatory drugs. Prior recommendations of topical capsaicin cream and nutritional intervention, such as glucosamine sulfate and chondroitin sulfate, are no longer in place. Orthotics and footwear modifications are also included in the list of treatment options and are discussed further in the next section. 

Rehabilitation Exercise Exercise is the mainstay of non-pharmacologic and nonsurgical treatment of knee OA. A recent meta-analysis showed exercise to be equally effective to oral analgesics in knee OA.14 Randomized studies definitively support the benefits of exercise (even if it is home based) on pain, function, and quality of life in patients with knee OA.15 Because there is currently no cure for OA, most research continues to evaluate the use of exercise as a treatment to alleviate symptoms of the disease and to enhance functional capacity. Exercise programs for knee OA typically consist of (1) lower extremity stretching, (2) lower extremity strengthening focusing on the quadriceps but also with attention to

394

PART 1  MSK Disorders

the hamstrings and hip muscles, (3) aerobic conditioning with a stationary bike, treadmill, water aerobics, or elliptical trainer, and (4) balance and proprioceptive exercises or perturbation exercises. Although isotonic, isometric, isokinetic, and aerobic exercise have all been shown to improve pain, disability, and walking speed, there are conflicting findings on the superiority of one over another with no general consensus.16 The exact amount of resistance and number of repetitions has not been quantified for the treatment of knee OA, but one recent meta-analysis showed that individuals with knee OA who followed the American College of Sports Medicine guidelines for strengthening achieved greater gains in lower extremity strength than individuals who didn’t follow these guidelines. The suggested guidelines consist of using an external load greater than 40% of one repetition maximum for 8 to 12 repetitions in 2 to 4 sets.17 It is important to understand the waxing and waning nature of arthritis symptoms in the knee and be flexible in adjusting the resistance used based upon pain and episodic arthritic flares. For patients with greater pain, this can be done with static exercise such as isometric quad sets or aquatic exercise programs. Closed kinetic chain exercises such as lunges and wall slides are preferable to open chain exercises, as they allow more controlled motion at the knee. The resistance should slowly be increased with time if possible and use of ice should be employed to manage pain during treatment. Exercise bicycles and walking should be recommended to enhance aerobic capacity. Deep knee bends in the presence of effusion should be avoided. Particular attention must be paid to strengthening of the medial quadriceps in patients with genu valgum who have lateral subluxation of the patella. Maintaining activity is critical to maintaining function. Even those patients scheduled for total knee arthroplasty should pursue static and dynamic strengthening as well as cardiovascular conditioning preoperatively to ease postoperative rehabilitation.18 Newer approaches are being employed in the treatment of OA, including Tai Chi, which was shown to be equally effective to standardized PT in a recent randomized trial,19 and whole body vibration (WBV). This latter technique has patients stand on a vibrating plate, which in turn is purported to stimulate muscles and tendons and improve neuromuscular performance. No quality randomized trials have been done yet on the effect of WBV on knee OA.20 

Therapeutic Modalities Transcutaneous electrical nerve stimulation, the application of an electrical current through the skin with the aim of pain modulation, is a frequently used modality in knee OA. Although this is a popular treatment option, research supporting its efficacy is lacking.21 Additional therapeutic modalities, such as electrical stimulation or massage, may also be used. Therapists may also review postural alignment and joint positioning techniques, especially for when the patient is sleeping. In particular, the use of a pillow under bent knees, much favored by many patients when they are supine, should be avoided because resulting knee flexion contractures, even if small, can significantly increase stresses on the knee during gait. Stretching of the hamstrings and quadriceps may also prove

beneficial. Patients should be counseled against prolonged wearing of high heels, which is associated with medial knee OA.22

Adaptive Equipment Adaptive equipment, such as a cane or walker, can reduce hip or knee loading, thereby reducing pain. It may also reduce fall risk in patients with impaired balance. Proper training in the use of a cane is important because it reduces joint loading in the contralateral hip but amplifies forces in the ipsilateral hip. 

Bracing and Footwear The basic rationale for a knee brace for unicompartmental knee OA is to improve function by reducing the patient’s symptoms. This can be accomplished, in theory, by reducing the biomechanical load on the affected compartment of the knee. A review of the published literature on knee bracing for OA points out limitations of clinical trials to date, but acknowledges limited evidence for improvement in pain and function in patients using OA braces.23 In patients with OA and varus malalignment of the knees, a shoe wedge (thicker laterally) moves the center of loading laterally during walking, a change that extends from foot to knee, lessening medial load across the knee. Although such modifications to footwear decrease varus malalignment, studies show no reduction in pain compared with a neutral insert in patients with medial compartment knee OA.23 Tilting or malalignment of the patella may cause patellofemoral pain. Patellar realignment with the use of braces or tape to pull the patella back into the trochlear sulcus of the femur or to reduce its tilt may lessen pain. In clinical trials with tape to reposition the patella into the sulcus without tilt, knee pain, range of motion, and proprioception was improved compared to placebo.24 However, patients may find it difficult to apply tape, and skin irritation is common. Commercial patellar braces are also available, but their efficacy has not been studied formally. Heel lifts or built-up shoes may be required in the presence of leg length discrepancy to prevent compensatory knee flexion gait on the longer side. In the presence of knee deformity, therapists can also evaluate for altered biomechanics (e.g., genu varum may lead to femoral internal torsion, resulting in compensatory external rotation of the tibia, which predisposes the patient to increased arthritic changes). Therapists can also visit the homes and workplaces of patients to suggest adjustments, such as raised toilet seats, grab bars, reachers, and the like. 

Procedures Intra-articular corticosteroid injections may help in reduction of local inflammation and improvement of symptoms. Hence, selection of patients with suspected knee inflammation tends to yield a better response to these injections. The response is generally rapid, but may not be sustained in the longer term. A systematic review of intra-articular corticosteroid injections demonstrated evidence of pain reduction up to six weeks following injection.25 Because the corticosteroid is delivered directly, systemic toxicity is minimized. Although intra-articular corticosteroid injections have not

CHAPTER 70  Knee Osteoarthritis

Table 70.2  Minimizing Potential Side Effects of Intra-articular Corticosteroid Injection Side Effect

Ways to Minimize Risk

Systemic effects

Avoid high doses and multiple simultaneous injections; use accurate injection techniques

Tendon rupture, fat atrophy, muscle wasting, skin pigment changes

Avoid misdirected injections. Consider musculoskeletal ultrasound for guidance

Septic arthritis

Use sterile technique; withhold therapy in at-risk patients

Nerve and blood vessel damage

Use accurate injection techniques

Postinjection symptom flare or synovitis

Avoid the same preparation for future injections

Flushing

Avoid high doses

Anaphylaxis

Take careful drug allergy history

Steroid arthropathy

Avoid high doses and overly frequent injections

Synovial cavity

Patella

395

available in several forms with different molecular weights. The rationale for using viscosupplementation is to impart protective properties to synovial fluid, including shock absorption, energy dissipation, and lubrication of the articular cartilage surface. Hyaluronate can be administered in a series of three weekly injections (2-mL vials or prefilled syringes) or in higher volume single-injection form. Treatments are typically repeated two to three times per year. Clinical trials of viscosupplementation have demonstrated limited efficacy in pain relief.26 Compared with corticosteroid injection, the effect of hyaluronic acid appears to be less dramatic but more durable. In a meta-analysis comparing both interventions, hyaluronic acid was less effective for pain relief in the first 4 weeks after injection. By week 4, the two approaches had equal efficacy. Beyond week 8, hyaluronic acid had a greater effect.27 Side effects included local inflammation and increased pain at the injection site. There is no evidence that hyaluronan injection in humans alters biologic processes or progression of cartilage damage. The hyaluronic acid is injected into the knee in the same manner as the intra-articular steroid is administered. Patients should be told that they may not see any clinical improvement until up to five weeks following injection(s). There is no evidence that one brand of a viscosupplement is superior to another in terms of efficacy.28 Acupuncture, a technique in existence for thousands of years, has gained renewed interest as a treatment of OA; however, there is conflicting evidence regarding its effectiveness in treatment of knee OA. A meta-analysis showed that sham acupuncture had the same effect as acupuncture and therefore a placebo effect is felt to be playing a role.29 The ACR conditionally recommends the use of acupuncture in chronic moderate to severe OA when surgical intervention is not possible.

Biologics

FIG. 70.2  Location for needle insertion.

been shown to cause cartilage damage, they are generally not given >3 times per year. Given the short-term effect and limitation on injection frequency, corticosteroid injection is most often used as an adjunctive therapy for acute or severe symptom flares. Table 70.2 lists potential systemic side effects of corticosteroid injections. Administration of steroids through iontophoresis may be an alternative for patients hesitant to undergo injections. Intra-articular knee injections can be done using six different approaches, including medial and lateral suprapatellar, medial and lateral mid patellar, and medial and lateral anterior patellar. The latter two approaches are performed with the knee in a flexed position and the former approaches with the knee extended. Learning two different approaches is optimal since arthritic changes may be asymmetric, making it more difficult to enter a region of the joint with more prominent joint space narrowing or osteophytes. An alternative entry point is then available to the clinician performing the injection. Fig. 70.2 details one injection technique. Viscosupplementation with hyaluronic acid, available as naturally occurring hyaluronan, is now commercially

The use of PRP injections for various musculoskeletal injuries has expanded over the past two decades and knee OA is among the leading diagnoses that this procedure has been used to treat. The procedure involves drawing a patient’s blood and spinning it down in a centrifuge to separate out platelets from other blood products, including plasma. A small amount of autologous plasma is combined with these highly concentrated platelets in a solution that is subsequently injected into degenerated joints or tendons. Platelets contain various growth factors and cytokines that are thought to jumpstart the healing process and promote tissue regeneration in several ways, including stimulating cell replication, promoting angiogenesis, and stimulating the inflammatory cascade in chronic musculoskeletal conditions.30 A recent meta-analysis of PRP injections in the treatment of knee OA looked at 10 randomized trials showing that PRP and viscosupplementation had similar therapeutic effect 6 months postinjection, but that PRP had superior pain relief and functional improvement 1 year postinjection.31 Although these early findings are promising, further studies need to be done to confirm the efficacy of this procedure. PRP injections are not covered by insurance and no specific indications have been identified for its use. In general, this procedure is more effective in mild to moderate OA and has been used when all other conservative treatment for OA has been ineffective or when knee replacement surgery is contraindicated. 

396

PART 1  MSK Disorders

Table 70.3  Surgical Options for Osteoarthritis of the Knee Established Techniques

Indications

Outcome

Arthroscopic débridement

Meniscal signs and symptoms Synovitis Osteophytic impingement Catching or locking caused by loose bodies

Most reports show improvement in 50% to 80% of patients; however, results deteriorate with time

Osteotomy of the proximal tibia or distal femur

Predominantly medial compartment involvement

Recovery is prolonged Relief of symptoms often incomplete

Unicompartmental knee replacement

Predominantly medial compartment involvement Minimal lateral compartment disease No major anterior knee pain Stable knee joint Correctable varus deformity Fixed flexion deformity of less than 10 degrees

Survivorship rate for implants of 90% at 20 years

Patellofemoral replacement

Isolated patellofemoral joint involvement

Results have been variable

Total knee replacement

Tricompartmental disease

Survival rates of between 84% and 98% at 15 years

Technology While total knee replacement (TKR) remains the mainstay for severe multicompartmental DJD, advances in patellofemoral arthroplasties may help younger patients with isolated patellofemoral arthritis avoid the more radical procedure. If patients are screened carefully to ensure that the patellofemoral arthritis is indeed the source of symptoms, then patellofemoral replacement is a viable option. Firstgeneration patellofemoral arthroplasties had high failure rates due to patellar maltracking, with the main long-term complication being progression of tibiofemoral joint arthritis. However, more contemporary designs have addressed the tracking issues and have resulted in improved short- and mid-term outcomes. The durability of these prostheses remains uncertain, however, and longer-term studies are lacking.32 

Surgery (Table 70.3) Arthroscopic débridement includes lavage and the removal of loose bodies, debris, mobile fragments of articular cartilage, unstable torn menisci, and impinging osteophytes. However, it is clear from the literature that drilling, abrasion chondroplasty, microfracture, saucerization, notchplasty, osteophyte removal, synovectomy, and arthrolysis are also performed simultaneously in many clinical series. Patients who have a short history and a sudden onset of mechanical symptoms and also have knee effusions are likely to do best.33 Meniscal symptoms and signs, synovitis or synovial impingement, osteophytic impingement, and catching or locking caused by loose bodies favor a good outcome. Significant instability and malalignment are poor prognostic factors. Patients who have radiographic signs of advanced degeneration are unlikely to benefit.34 Although arthroscopic surgery has been widely used for OA of the knee, scientific evidence to support its efficacy is lacking. Most of the orthopedic literature supporting its use is based on retrospective studies. However, in a randomized, controlled trial, arthroscopic surgery for OA of

the knee provided no additional benefit to optimized physical and medical therapies.35 Up to a quarter of patients with knee OA have predominant involvement of the medial compartment. The surgical options for such patients who are younger and active remain somewhat controversial and include medial unicompartmental knee replacement (UKR), proximal tibial or distal femoral osteotomy, and TKR (see Chapter 80). Osteotomy is a less drastic measure than knee replacement, as it preserves the knee joint and is often favored by younger, active patients with unicompartmental symptoms. In osteotomy, a wedge-shaped piece of bone is removed from either the femur or tibia to bring the knee joint back into a more physiologic alignment. This procedure moves the weight-bearing axis to the less damaged compartment. Recovery is prolonged and relief of symptoms often incomplete, but osteotomy may delay or even avoid the need for TKR.36 Successful treatment could allow a return to sport. The risks specific to this surgery depend on the technique and include nonunion at the osteotomy site, common peroneal nerve injury, pain from the proximal tibiofibular joint, and overcorrection or undercorrection of the deformity. An ongoing debate within the orthopedic community concerns the relative merits of high tibial osteotomy compared with UKR in younger patients. A meta-analysis comparing these two procedures did not show significant benefit of one method over another,37 although UKR patients tend to recover more quickly and have better knee motion. UKR has now become an accepted treatment for older patients with medial compartment arthritis. The prerequisites for a UKR include stability of the joint, correctable varus deformity, fixed flexion deformity of less than 10 degrees, and minimal lateral compartment disease. The results of UKR in lateral compartment disease have yet to be fully determined. Wear of the polyethylene prosthesis in UKR is also an issue, but the ability to retain the anterior and posterior cruciate ligaments is an advantage that UKR has over TKR.38 TKRs, with a quarter-century track record, have generally provided most patients with good

CHAPTER 70  Knee Osteoarthritis

pain relief. Severe chondromalacia may necessitate patellectomy (patella excision). Knee arthrodesis (fusion) today is generally reserved for patients in whom knee replacement surgery fails and are of relatively younger age with higher functional levels and poor knee extension. Other less commonly used surgical options, such as synovectomy and small prostheses (to correct deformity), are also possible. 

Potential Disease Complications Progressive knee OA may result in reduced mobility and the general systemic complications of immobility and deconditioning. Antalgic gait can result in contralateral hip disease (e.g., greater trochanteric bursitis). The risk of falls will be increased by decreased mobility at the knee. Complaints of chronic pain may result from the initial knee OA if it is inadequately treated. 

Potential Treatment Complications Complications of anti-inflammatory medication and steroid injections are well known. Infection is a rare but possible result of joint injection or surgery. Cryotherapy or heat therapy can, of course, lead to frostbite or burns. Hyaluronic acid injections may result in localized transient pain or effusion. Arthroscopy may damage the articular surface membrane, thus initiating damage to uninvolved cartilage. Excessive arthroscopic scraping has sometimes been associated with persistent pain. The possibility of infection and deep venous thrombosis (DVT) and the small but real possibility of intraoperative mortality limit the use of surgery to a lastline option. There is still debate regarding routine perioperative use of anticoagulation and it has been suggested that this decision be tailored to the individual patient’s risk factors. One recent large population-based case control study confirmed the higher risk of DVT after knee arthroscopy and showed ligament reconstruction further increases risk of DVT. Low-molecular-weight heparin was not found to decrease DVT risk.39 Mechanical wear and prosthesis loosening, especially for cemented prostheses, often lead to the need for revision after a decade or so.

References 1. Bashaw RT, Tingstad EM. Rehabilitation of the osteoarthritic patient: focus on the knee. Clin Sports Med. 2005;24:101–131. 2. Hootman J, Bolen J, Helmick C, Langmaid G. Prevalence of doctor-diagnosed arthritis and arthritis-attributable activity limitation—United States, 2003-2005. MMWR Morb Mortal Wkly Rep. 2006;55:1089–1092. 3. Murphy L, Schwartz TA, Helmick CG, et al. Lifetime risk of symptomatic knee osteoarthritis. Arthritis Rheum. 2008;59:1207–1213. 4. Sharma L, Song J, Felson DT, et al. The role of knee alignment in disease progression and functional decline in knee osteoarthritis. JAMA. 2001;286:188–195. 5. Toivanen AT, Heliövaara M, Impivaara O, et al. Obesity, physically demanding work and traumatic knee injury are major risk factors for knee osteoarthritis—a population-based study with a follow-up of 22 years. Rheumatology (Oxford). 2010;49:308–314. 6. Pai Y-C, Rymer WZ, Chang RW, et al. Effect of age and osteoarthritis on knee proprioception. Arthritis Rheum. 1997;40:2260–2265. 7. Driban J, Hootman JM, Sitler MR, Harris KP, Cattano NM. Is participation in certain sports associated with knee arthritis? A systematic review. J Athl Train. 2017;52(6):497–506. 8. Hunter DJ, March L, Sambrook PN. Knee osteoarthritis: the influence of environmental factors. Clin Exp Rheumatol. 2002;20: 93–100.

397

9. McAlindon T, Formica M, Schmid CH, Fletcher J. Changes in barometric pressure and ambient temperature influence osteoarthritis pain. Am J Med. 2007;120(5):429–434. 10. Szebenyi B, Hollander AP, Dieppe P, Quilty B, Duddy J, Clarke S, Kirwan JR. Associations between pain, function and radiographic features in osteoarthritis of the knee. Arthritis Rheum. 2006;54(1):230–235. 11. Bruyere O, Honore A, Giacovelli G, et al. Radiologic features poorly predict clinical outcomes in knee osteoarthritis. Scand J Rheumatol. 2002;31:13–16. 12. Razek AAKA, El-Basyouni SR. Ultrasound of knee osteoarthritis: interobserver agreement and correlation with Western Ontario and MacMaster Universities Osteoarthritis. Clin Rheumatol. 2016;35(4): 997–1001. 13. Hochberg MC, Altman RD, April RT, et al. American College of Rhematology 2012 recommendations for the use of nonpharmacologic and pharmacologic therapies in osteoarthritis of the hand, hip, and knee. Arthritis Care Res. 2012;64(4):465–474. 14. Henriksen M, Hansen JB, Klokker L, Bliddal H, Christensen R. Comparable effects of exercise and analgesics for pain secondary to knee osteoarthritis:a meta-analysis of trials included in Cochrane systematic reviews. J Comp Eff Res. 2016;5(4):417–431. 15. Fransen M, McConnell S, Harmer AR, Van der Esch M, Simic M, Bennell KL. Exercise for osteoarthritis of the knee. Cochrane Database Syst Rev. 2015;1:CD004376. 16. Huang MH, Lin YS, Yang RC, Lee CL. A comparison of various therapeutic exercises on the functional status of patients with knee osteoarthritis. Semin Arthritis Rheum. 2003;32(6):398–406. 17. Bartholdy C, Juhl C, Christensen R, Lund H, Zhang W, Henriksen M. Comparing clinical outcomes of exercise interventions according to the American College of Sports Medicine guidelines for strength training to other types of exercise in knee osteoarthritis: a systematic review and meta-analyses. Osteoarthr Cartil. 2016;24:S483–S484. 18. Swank AM, Kachelman JB, Bibeau W, et al. Prehabilitation before total knee arthroplasty increases strength and function in older adults with severe osteoarthritis. J Strength Cond Res. 2011;25:318–325. 19. Wang C, Schmid CH, Iversen MD, et al. Comparative effectiveness of Tai Chi versus physical therapy for knee osteoarthritis: a randomized trial. Ann Intern Med. 2016;165(2):77–86. 20. Xin L, Wang XQ, Chen BL, Huang LY, Liu Y. Whole body vibration exercise for knee osteoarthritis: a systematic review and meta-analysis. Evid Based Complement Alternat Med. 2015;2015:758147. 21. Palmer S, Domaille M, Cramp F, et al. Transcutaneous electrical nerve stimultion as an adjunct to education and exercise for knee osteoarthritis: a randomized controlled trial. Arthritis Care Res. 2014;66(3):387–394. 22. Kerrigan D, Todd M, O’Reilly P. Knee osteoarthritis and high heeled shoes. Lancet. 1998;351:1399–1401. 23. Duivenvoorden T, Brouwer RW, van Raaij TM, Verhagen AP, Verhaar JA, Bierma-Zeinstra SM. Braces and orthoses for osteoarthritis of the knee. Cochrane Database Syst Rev. 2015;3:CD004020. 24. Cho HY1, Yoon YW. Kinesio taping improves pain, range of motion and proprioception in older patients with knee osteoarthritis: a randomized controlled trial. Am J Phys Med Rehabil. 2016;95(1):e7–8. 25. da Costa, Bruno R, Jüni P. Intra-articular corticosteroids for osteoarthritis of the knee. JAMA. 2016;316(24):2671–2672. 26. Rutjes AW, Jüni P, da Costa BR, et al. Viscosupplementation for osteoarthritis of the knee: a systematic review and meta-analysis. Ann Intern Med. 2012;157:180–191. 27. Bannuru RR, Natov NS, Obadan IE, et al. Therapeutic trajectory of hyaluronic acid versus corticosteroids in the treatment of knee osteoarthritis: a systematic review and meta-analysis. Arthritis Rheum. 2009;61:1704–1711. 28. Gigis I, Fotiadis E, Nenopoulos A, Tsitas K, Hatzokos I. Comparison of two different molecular weight intra-articular injections of hyaluronic acid for the treatment of knee osteoarthritis. Hippokratia. 2106;20(1):26–31. 29. Manheimer E, Linde K, Lao L, Bouter LM, Berman BM. Meta-analysis: acupuncture for osteoarthritis of the knee. Ann Intern Med. 2007;146(12):868–877. 30. Sampson S, Gerhardt M, Mandelbaum B. Platelet rich plasma injection grafts for musculoskeletal injuries: a review. Curr Rev Musculoskelet Med. 2008;1(3):165–174. 31. Dai WL, Zhou AG, Zhang H, Zhang J. Efficacy of platelet–rich plasma in the treatment of knee osteoarthritis arthroscopy. Arthroscopy. 2017;33(3):659–670. 32. Lustig S. Patellofemoral arthroplasty. Orthop Traumatol Surg Res. 2014;100(1):S35–43.

398

PART 1  MSK Disorders

33. Day B. The indications for arthroscopic débridement for osteoarthritis of the knee. Orthop Clin North Am. 2005;36:413–417. 34. Felson DT, Buckwalter J. Débridement and lavage for osteoarthritis of the knee. N Engl J Med. 2002;347:132–133. 35. Kirkley A, Birmingham TB, Litchfield RB, et al. A randomized trial of arthroscopic surgery for osteoarthritis of the knee. N Engl J Med. 2008;359:1097–1107. 36. Bonasia DE, Governale G, Spolaore S, Rossi R, Amendola A. High tibial osteotomy. Curr Rev Musculoskelet Med. 2014;7(4):292–301.

37. Fu D, Li G, Chen K, Zhao Y, Hua Y, Cai Z. Comparison of high tibial osteotomy and unicompartmental knee arthroplasty in the treatment of unicompartmental osteoarthritis. J Arthroplasty. 2013;28(5):759–765. 38. Parratee S, Argenson JN, Pearce O, Pauly V, Auquier P, Aubaniac JM. Medial unicompartmental knee replacement in the under-50s. Bone Joint J. 2009;91(3):351–356. 39. van Adrichem RA, Nelissen RG, Schipper IB, Rosendaal FR, Cannegieter SC. Risk of venous thrombosis after arthroscopy of the knee: results from a large population-based case-control study. J Thromb Haemost. 2015;13(8):1441–1448.

CHAPTER 71

Knee Bursopathy Luis Baerga-Varela, MD Raul A. Rosario-Concepión, MD

ICD-10 Codes M71.561 Bursitis, not elsewhere classified, right knee M71.562 Bursitis, not elsewhere classified, left knee M71.569 Bursitis, not elsewhere classified, unspecified knee M71.80 Other Specified bursopathies, unspecified site M71.861 Other Specified bursopathies, right knee M71.862 Other Specified bursopathies, right knee M71.869 Other Specified bursopathies, unspecified knee M71.9 Bursopathy, unspecified M76.40 Tibial collateral bursitis, unspecified leg M76.41 Tibial collateral bursitis, right leg M76.42 Tibial collateral bursitis, left leg M70.40 Prepatellar bursitis, unspecified knee M70.41 Prepatellar bursitis, right knee M70.42 Prepatellar bursitis, left knee M70.50 Other bursitis of knee, unspecified knee M70.51 Other bursitis of knee, right knee M70.52 Other bursitis of knee, left knee M71.161 Other infective bursitis, right knee M71.162 Other infective bursitis, left knee M71.169 Other infective bursitis, unspecified knee M06.261 Rheumatoid bursitis, right knee M06.262 Rheumatoid bursitis, left knee M06.269 Rheumatoid bursitis, unspecified knee

Definition A bursa is a closed sac filled with synovial fluid. Traditionally, bursitis has been the preferred term for a painful bursa. Recently, the term bursopathy has been adopted by many since the presence of acute inflammation cannot be determined clinically.1 Similar terminology has been adopted in the description of tendon pathologies, preferring the term tendinopathy to tendinitis. For discussion purposes, we will

continue to use the term bursopathy, even though the term bursitis is more commonly seen in the literature. The knee has 11 bursae whose principal function is to reduce friction between two tissues, such as tendons, ligaments, and bone. The location of bursae in the knee can be divided into 4 regions: anterior, medial, lateral, and posterior. Anterior region The anterior knee includes the suprapatellar bursa or recess, the prepatellar bursa, and the deep and superficial infrapatellar bursa.2-5 The suprapatellar bursa is a superior recess of the knee joint deep to the quadriceps femoris tendon and anterior to the intercondylar fossa.3,5 The prepatellar bursa is located subcutaneously, anterior to the patella.2,3 The superficial infrapatellar bursa can be found anteriorly to the tibial tubercle and the deep infrapatellar bursa between the posterior aspect of the distal patellar tendon and the anterior tibia.2,3,5 Posterior region The posterior knee includes the gastrocnemio-semimembranosus bursa and the popliteus bursa.2,3,5 At the distal aspect of the tendon sheath of the popliteus muscle is the popliteus bursa which, on occasions, communicates with the tibiofibular joint.2,5 The gastrocnemio-semimembranosus bursa is located between the semimembranosus tendon, the medial head of the gastrocnemius, and medial femoral condyle.3,4 A valvular communication from the joint capsule to the gastrocnemius-semimembranosus bursa is a common anatomical variant. Joint fluid extrusion through this communication into the bursa can result in a popliteal cyst, also known as a Baker cyst.6,7 Lateral region On the lateral knee we can find the iliotibial bursa3-5 and the lateral collateral ligament-biceps femoris bursa.3,5 The iliotibial bursa is located between the iliotibial band and the lateral femoral condyle. The lateral collateral ligament-biceps femoris bursa lies superficially to the lateral collateral ligament and deep in the anterior arm of the long head of the biceps femoris muscle.3 Medial region The pes anserine bursa, the semimembranosus-tibial collateral ligament bursa, and the medial collateral ligament (MCL) bursa are found in the medial region.2-5,8 The pes anserine bursa is found between the upper medial aspect of the tibia and the conjoined tendon of the pes anserinus muscles.9 The MCL bursa is located between the two layers of the MCL.2 The semimembranosus-tibial collateral ligament bursa is present posterior and superior to the pes anserine bursa between the semimembranosus tendon and MCL.1,2  399

PART 1  MSK Disorders

400

Pes anserine bursopathy presents with pain and tenderness at the pes anserine tendon insertion at the upper medial tibia.9 It may result from direct trauma or repetitive friction movement of the tendon.12 It is more commonly found in females with obesity, osteoarthritis, valgus deformity, pes planus, diabetes mellitus, and rheumatoid arthritis.9,12 Medial collateral bursopathy presents as medial knee pain reproduced by palpation and valgus stress13 and must be differentiated from other etiologies like pes anserine bursopathy, tear of the medial meniscus, MCL injury, semimembranosus bursopathy, or medial plica syndrome. It may be seen in sports that require horse and motorcycle riding due to the friction at the medial knee.14 The semimembranosus-tibial collateral ligament bursopathy can be found as primary pathology or associated with a semimembranosus tendinopathy. The main symptom is medial knee pain, which can be difficult to differentiate from other pathologies involving the medial knee. Ultrasound imaging has been useful in identifying the semimembranosus bursa.1,15 

A

Physical Examination A complete knee examination should be performed and include inspection, palpation, ROM, ligament stability, knee special tests, and neurologic examination in order to rule out other pathologies. The knee must be inspected for swelling, muscle atrophy, effusion, erythema, and warmth. Anatomically guided palpation may show tenderness over the affected bursa. A thorough hip and lumbar spine exam should also be performed to rule out referred pain from the hip or spine. 

B FIG. 71.1 Prepatellar bursopathy (housemaid’s knee). (A) Patient with prepatellar bursopathy secondary to trauma. (B) Sonographic evaluation of fluid-filled prepatellar bursa (arrow).

Symptoms In patients with knee bursopathies, the most common complaints are local knee pain, swelling, and tenderness in the area of the affected bursa. The symptoms may or may not be associated with ROM limitation, or antalgic gait. The presence of fever suggests a septic bursitis, especially with a history of penetrating trauma.10 Prepatellar bursopathy (housemaid’s knee) presents as pain and swelling anterior to the patella after direct trauma or overuse. It is frequently seen in specific occupational workers who must frequently crawl or kneel, such as carpenters, housemaids, gardeners, and roofers,10 although infrequently, it may also be seen in systemic diseases like gout, rheumatoid arthritis, systemic lupus erythematosus, and uremia.2,10 Superficial infrapatellar bursopathy (vicar’s knee) presents secondary to overuse of the knee extension mechanism with swelling and pain inferiorly to the patella (Fig. 71.1). Deep infrapatellar bursopathy is characterized in jumpers, runners, and juvenile idiopathic arthritis.2,11

Functional Limitations Knee bursopathies can affect different aspects of the patient’s functionality, including mobility and activities of daily living. As previously discussed, knee bursopathies can be associated with specific physical and occupational activities like kneeling, crawling, and climbing that may limit vocational, recreational, and sporting activities. 

Diagnostic Studies Knee bursopathies are clinical diagnoses, based on a complete history and physical examination. Imaging studies may be useful to differentiate a bursopathy from an underlying tendinopathy or other pathology. Plain x-rays can be used to rule out degenerative changes, bone fractures, or tumors in the presence of clinical suspicion. Ultrasound is considered an effective, inexpensive, and accessible modality that can be part of the diagnostic evaluation of the superficial knee, allowing for visualization and evaluation of pathologic bursae.1,12,16-18 It can be very useful in the differentiation of bursopathy from other soft tissue pathologies. MRI may be necessary for evaluation of intra-articular structures like menisci, ligaments, and cartilage.2 If septic bursitis is suspected, blood samples and bursa aspiration for evaluation and culture are indicated.10 

CHAPTER 71  Knee Bursopathy

List of Differential Diagnosis Tendinopathy Arthritis (osteoarthritis, rheumatoid arthritis, psoriatic arthritis, gout) Meniscal tear Collateral ligament sprain or tear Fractures (patellar, tibial plateau, insufficiency) Avascular necrosis Infection (e.g., septic knee) Tumor

401

efficacy of sonographically guided bursal infiltrations versus palpation-guided injection is still limited. There has been an increasing trend in the use of regenerative medicine therapies to treat chronic musculoskeletal pathologies. At the time this chapter was written, only one study was found describing the use of platelet-rich plasma for the treatment of pes anserine bursopathy.22 Currently, there is not enough evidence to suggest regenerative treatments as standard therapy in knee bursopathy. 

Technology

Treatment Initial Initial treatment should include PRICE (protection, relative rest, ice, compression, and elevation).10 The use of nonsteroidal anti-inflammatory medications can be useful for pain management and inflammation control as initial treatment. In septic bursitis and infection, oral antibiotic treatment is necessary. The majority of infections are secondary to Staphylococcus aureus. If systemic symptoms are present, hospitalization may be indicated for IV antibiotic therapy.10 

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

Surgery Surgical procedures are usually not indicated. In the event of refractory septic bursitis with poor response to intravenous antibiotics and conservative treatment, surgical treatment is considered. The principal surgical approach is drainage.10 Traditionally, open cleaning and débridement is performed, but there is also some evidence for endoscopic bursectomy.23,24 Long-term results of bursectomy have not been studied. 

Rehabilitation

Potential Disease Complication

First, a stretching and strengthening program should be used to correct any predisposing biomechanical imbalances. Special care must be given to quadriceps, hamstrings, gastrocnemius, hip adductors, and the iliotibial band. Evaluation and treatment of the kinetic chain as well as activity-specific rehabilitation should be considered. Occupational therapy can help modify activities that cause symptomatology, especially by avoiding further knee trauma or overuse. There is limited evidence on the use of physical modalities, showing positive results with superficial heat, ultrasound, and electrical stimulation in one study.19 If used, it should be used in conjunction with strengthening and stretching exercises. Kinesiotaping may be helpful in the treatment of pes anserine bursopathy.20 

If not promptly treated, knee bursopathy can cause chronic pain, which in turn can cause inhibitory weakness, disuse muscle atrophy, deconditioning, and gait problems, especially in the geriatric population. 

Procedures Bursal aspiration and infiltration can be considered for acute pain relief. The mixture of local anesthetic and corticosteroids may be considered for acute bursopathies with a suspected inflammatory component. It can be used after poor response to conservative management, for rapid pain relief, and to improve rehabilitation tolerance. Risk of bleeding is low; therefore anticoagulation and antiplatelet medications do not need to be held prior to aspiration or infiltration. Absolute contraindications to injection include bacteremia, sepsis, local skin infection, and articular fractures.21 Relative contraindications are uncontrolled hyperglycemia and supratherapeutic international normalized ratio (INR ) level. If infection or coagulopathy are clinically suspected, labs including CBC, PT, PTT and INR should be obtained prior to injection. Recent evidence shows that ultrasound-guided bursal infiltrations of the knee result in improved accuracy over landmark-based techniques.1,12,13 Evidence of increased

Potential Treatment Complications Complications may arise from oral medications, intra-bursae injections, or physical modalities. One of the principal side effects of nonsteroidal antiinflammatory drugs is gastric ulcers. For this reason, NSAIDs are only recommended for a short period of time. In addition, renal, cardiovascular, and hepatic side-effect profiles must be taken into consideration. Serious complications with corticosteroid infiltration are rare.21 Excessive use of corticosteroids may result in osteoporosis, Cushingoid syndrome, or avascular necrosis. However, as with any infiltration, steroid injections may result in drug hypersensitivity, infection, nerve injury, tendon rupture, and lipoatrophy. Special consideration must be taken to maintain glycemic control in diabetic patients. Some patients may develop post-injection flares that may last for 2 to 3 days, for which orientation about post-corticosteroid injection flares must be given.21 Basic precautions during physical modality application should be taken to prevent therapy-related complications. Possible complications of bursectomy include wound healing problems, chronic scar pain, hypoesthesia, and recurrence.10

References 1. Onishi K, Sellon J, Smith J. Sonographically guided semimembranosus bursa injection: technique and validation. PM R. 2016;8:51–57. 2. Steinbach L, Stevens K. Imaging of cysts and bursae about the knee. Radiol Clin North Am. 2013;51:433–454. 3. Draghi F, Corti R, Urciuoli L, et al. Knee bursitis: a sonographic evaluation. J Ultrasound. 2015;18:251–257.

402

PART 1  MSK Disorders

4. Chatra P. Bursae around the knee joints. Indian J Radiol Imaging. 2012;22:27. 5. Chhabra A, Cerniglia CA. Bursae, cysts and cyst-like lesions about the knee. J Am Osteopath Coll Radiol. 2013;2:2–13. 6. Cao Y, Jones G, Han W, et al. Popliteal cysts and sub gastrocnemius bursitis are associated with knee symptoms and structural abnormalities in older adults: a cross-sectional study. Arthritis Res Ther. 2014;16(2):R59. 7. Frush TJ, Noyes FR. Baker’s cyst: diagnostic and surgical considerations. Sports Health. 2015;7(4):359–365. 8. Pedersen R. The medial and posteromedial ligamentous and capsular structures of the knee: review of anatomy and relevant imaging findings. Semin Musculoskelet Radiol. 2016;20(01):12–25. 9. Lee J, Kim K, Jeong Y, et al. Pes anserinus and anserine bursa: anatomical study. Anat Cell Biol. 2014;47(2):127. 10. Baumbach S, Lobo C, Badyine I, et al. Prepatellar and olecranon bursitis: literature review and development of a treatment algorithm. Arch Orthop Trauma Surg. 2013;134(3):359–370. 11. Alqanatish J, Petty R, Houghton K, et al. Infrapatellar bursitis in children with juvenile idiopathic arthritis: a case series. Clin Rheumatol. 2010;30(2):263–267. 12. Finnoff J, Nutz D, Henning P, et al. Accuracy of ultrasound-guided versus unguided pes anserinus bursa injections. PM R. 2010;2(8):732–739. 13. Jose J, Schallert E, Lesniak B. Sonographically guided therapeutic injection for primary medial (tibial) collateral bursitis. J Ultrasound Med. 2011;30(2):257–261. 14. McCarthy C, McNally E. The MRI appearance of cystic lesions around the knee. Skeletal Radiol. 2004;33(4):187–209.

15. De Maeseneer M, Marcelis S, Boulet C, et al. Ultrasound of the knee with emphasis on the detailed anatomy of anterior, medial, and lateral structures. Skeletal Radiol. 2014;43(8):1025–1039. 16. Toktas H, Dundar U, Adar S, et al. Ultrasonographic assessment of pes anserinus tendon and pes anserinus tendinitis bursitis syndrome in patients with knee osteoarthritis. Mod Rheumatol. 2014;25(1):128–133. 17. Uysal F, Akbal A, Gökmen F, et al. Prevalence of pes anserine bursitis in symptomatic osteoarthritis patients: an ultrasonographic prospective study. Clin Rheumatol. 2014;34(3):529–533. 18. Imani F, Rahimzadeh P, Abolhasan Gharehdag F, et al. Sonoanatomic variation of pes anserine bursa. Korean J Pain. 2013;26(3):249. 19. Sarifakioglu B, Afsar S, Yalbuzdag S, et al. Comparison of the efficacy of physical therapy and corticosteroid injection in the treatment of pes anserine tendino-bursitis. J Phys Ther Sci. 2016;28(7):1993–1997. 20. Homayouni K, Foruzi S, Kalhori F. Effects of kinesiotaping versus nonsteroidal anti-inflammatory drugs and physical therapy for treatment of pes anserinus tendino-bursitis: a randomized comparative clinical trial. Phys Sportsmed. 2016;44(3):252–256. 21. Freire V, Bureau N. Injectable corticosteroids: take precautions and use caution. Semin Musculoskelet Radiol. 2016;20(05):401–408. 22. Rowicki K, Płomiński J, Bachta A. Evaluation of the effectiveness of platelet rich plasma in treatment of chronic pes anserinus pain syndrome. Ortop Traumatol Rehabil. 2014;16(3):307–318. 23. Dillon J, Freedman I, Tan J, et al. Endoscopic bursectomy for the treatment of septic pre-patellar bursitis: a case series. Arch Orthop Trauma Surg. 2012;132(7):921–925. 24. Huang YW. Endoscopic treatment of prepatellar bursitis. Int Orthop. 2010;35(3):355–358.

CHAPTER 72

Meniscal Injuries Paul Lento, MD Ben Marshall, DO Venu Akuthota, MD

Synonyms Cartilage tears Locked knee

ICD-10 Codes M23.300 Other meniscus derangements, unspecified lateral meniscus, right knee M23.301 Other meniscus derangements, unspecified lateral meniscus, left knee M23.302 Other meniscus derangements, unspecified lateral meniscus, unspecified knee M23.303 Other meniscus derangements, unspecified medial meniscus, right knee M23.304 Other meniscus derangements, unspecified medial meniscus, left knee M23.305 Other meniscus derangements, unspecified medial meniscus, unspecified knee M23.306 Other meniscus derangements, unspecified meniscus, right knee M23.307 Other meniscus derangements, unspecified meniscus, left knee M23.309 Other meniscus derangements, unspecified meniscus, unspecified knee S83.251 Bucket-handle tear of lateral meniscus, current injury, right knee S83.252 Bucket-handle tear of lateral meniscus, current injury, left knee S83.259 Bucket-handle tear of lateral meniscus, current injury, unspecified knee Add seventh character to S83 for episode of care M23.341 Meniscus derangements, anterior horn of lateral meniscus, right knee M23.342 Meniscus derangements, anterior horn of lateral meniscus, left knee

M23.349 Meniscus derangements, anterior horn of lateral meniscus, unspecified knee M23.351 Meniscus derangements, posterior horn of lateral meniscus, right knee M23.352 Meniscus derangements, posterior horn of lateral meniscus, left knee M23.359 Meniscus derangements, posterior horn of lateral meniscus, unspecified knee M23.361 Other meniscus derangements, other lateral meniscus, right knee M23.362 Other meniscus derangements, other lateral meniscus, left knee M23.369 Other meniscus derangements, other lateral meniscus, unspecified knee S83.241 Other tear of medial meniscus, current injury, right knee S83.242 Other tear of medial meniscus, current injury, left knee S83.249 Other tear of medial meniscus, current injury, unspecified knee S83.281 Other tear of lateral meniscus, current injury, right knee S83.282 Other tear of lateral meniscus, current injury, left knee S83.289 Other tear of lateral meniscus, current injury, unspecified knee

Definition The menisci serve important roles in maintaining proper joint health, stability, and function.1 The anatomy of the medial and lateral menisci helps explain functional biomechanics. Viewed from above, the medial meniscus appears C-shaped and the lateral meniscus appears O-shaped (Fig. 72.1).1 Each meniscus is thick and convex at its periphery (the horns), but becomes thin and concave at its center. This contouring serves to provide a larger area for the rounded femoral condyles and the relatively flat tibia. Menisci do not move in isolation. They are connected by ligaments to each other anteriorly and to the anterior cruciate ligament, the patella, the femur, and the tibia.2,3 The medial meniscus is less mobile than the lateral meniscus. This is due to its firm connections to the knee joint capsule and the medial collateral ligament. This decreased mobility, in conjunction with the fact that the medial 403

404

PART 1  MSK Disorders

Transverse ligament Medial meniscus Anterior cruciate ligament

Lateral meniscus

Medial collateral ligament Posterior cruciate ligament

Ligament of Wrisberg FIG. 72.1  Superior view of medial and lateral menisci.

meniscus is wider posteriorly, is cited as the usual reason for the higher incidence of tears within the medial meniscus than within the lateral meniscus.1 The semimembranosus muscle (through attachments from the joint capsule) helps retract the medial meniscus posteriorly, serving to avoid entrapment and injury to the medial meniscus as the knee is flexed.3 The lateral meniscus is not as adherent to the joint capsule. Unlike the medial meniscus, the lateral meniscus does not attach to its respective collateral ligament. The posterolateral aspect of the lateral meniscus is separated from the capsule by the popliteus tendon. Therefore the lateral meniscus is more mobile than the medial meniscus.1,3 The attachment of the popliteus tendon to the posterolateral meniscus ensures dynamic retraction of the lateral meniscus when the knee internally rotates to return out of the screwhome mechanism, as one proceeds into flexion out of a fully extended and locked knee.2 Therefore both the medial and the lateral menisci, by having attachments to muscle structures, share a common mechanism that helps avoid injury. The architecture of the vascular supply to the meniscus has important implications for healing.1,4 Capillaries penetrate the menisci from the periphery to provide nourishment. After 18 months of age, as weight bearing increases, the blood supply to the central part of the menisci recedes. In fact, research has shown that eventually only the peripheral 10% to 30% of the menisci, or the red zone, receives this capillary network (Fig. 72.2).5 Therefore the central and internal portion, or white zone, of these fibrocartilaginous structures becomes avascular with age, relying on nutrition received through diffusion from the synovial fluid. Because of this vascular arrangement, the peripheral meniscus is more likely to heal than are the central and posterolateral aspects.4 The primary, but not sole function, of the menisci is to distribute forces across the knee joint and to enhance stability.1,6-8 Multiple studies have shown that the ability of the joint to transmit loads is significantly reduced if the meniscus is partially or wholly removed.1,6,7,9 There was a seminal article published in 1948 suggesting that the menisci are vital in protecting the articular surfaces.10 It reported that

White zone

Red/ white Red zone zone

FIG. 72.2  Vascular zones of the meniscus. Tears within the red zone have a higher healing potential.

individuals who had undergone total meniscectomies demonstrated premature osteoarthritis. Meniscal tears are classified by their complexity, plane of rupture, direction, location, and overall shape. Tears are commonly defined as vertical, horizontal, longitudinal, or oblique in relation to the tibial surface (Fig. 72.3).11 Most meniscal tears in young patients will be verticallongitudinal, whereas horizontal cleavage tears are more

CHAPTER 72  Meniscal Injuries

Longitudinal

Degenerative

Flap tear

Horizontal

Radial

FIG. 72.3  Types of meniscal tears. Longitudinal

FIG. 72.4  Bucket-handle type of meniscal tear.

commonly found in older patients.12 The bucket-handle tear is the most common type of vertical (or longitudinal) tear (Fig. 72.4).13 Tears are also described as complete, full-thickness, or partial tears. Complete, full-thickness tears are so named as they extend from the tibial to femoral surfaces. In addition, medial meniscus tears outnumber lateral meniscus tears from 2:1 to 5:1.14,15 Meniscal injuries may result from an acute injury or from gradual degeneration with aging.16 Vertical tears (e.g., bucket-handle tears) tend to occur acutely in individuals 20 to 30 years of age and are usually located in the posterior two thirds of the meniscus.13,17 Sports commonly associated with meniscal injuries are soccer, football, basketball, baseball, wrestling, skiing, rugby, and lacrosse. Injury commonly occurs when an axial load is transmitted through a flexed or extended knee that is simultaneously rotating.16 Degenerative tears, in contrast, are usually horizontal and are seen in older individuals with concomitant degenerative joint changes.13,18 On the basis of arthroscopic examination, the majority of acute peripheral meniscal injuries are associated with some degree of occult anterior cruciate ligament laxity.19 In addition, true anterior cruciate ligament tears are associated

405

with lesions of the posterior horns of the menisci.19 Lateral meniscal tears appear to occur with more frequency with acute anterior cruciate ligament injuries, whereas medial meniscal tears have a higher incidence with chronic anterior cruciate ligament injuries. With chronic anterior cruciate ligament injuries, the medial meniscus may be more frequently damaged because its posterior horn serves as an important secondary stabilizer of anterior-posterior instability.20 Finally, meniscal architecture appears to be mostly unchanged between male and female knees with the notable exception of larger average volumes in male menisci. Meniscal degenerative patterns do vary between the genders, however, with males tending to preferentially wear on the medial side and females the lateral. This has been theorized to be more associated with biomechanical differences imposed by the hip girdle and not intrinsic to the knee itself.1,3 

Symptoms The history will help diagnose a meniscal injury 75% of the time.12 Young patients who experience meniscal tears will recall the mechanism of injury 80% to 90% of the time and may report a “pop” or a “snap” at the time of injury. Deep knee bending activities are often painful, and mechanical locking may be present in 30% of patients.21 Bucket-handle tears should be suspected in cases of mechanical locking with loss of full extension.16 If locking is reported approximately 1 day after the injury, this may be due to “pseudolocking,” which results from hamstring contracture.14 Knee hemarthrosis may also occur acutely, especially if the vascularized, peripheral portion of the meniscus is involved. In fact, 20% of all acute traumatic knee hemarthroses are caused by isolated meniscal injury.22 More typically, however, knee swelling occurs approximately 1 day later as the meniscal tear causes mechanical irritation within the intraarticular space, creating a reactive effusion. Typically, this effusion is secondary to a lesion in the central portion of the meniscus.16 In contrast, degenerative meniscal tears are not usually associated with a history of trauma. In fact, the mechanism of injury, which may not be reported by the patient, can be simple daily activities, such as rising from a chair and pivoting on a planted foot.16 Patients with degenerative tears often also report recurrent knee swelling, particularly after activity. 

Physical Examination Physical examination aids the accurate diagnosis of a meniscal injury in 70% of patients.23 Gait evaluation may reveal an antalgic gait with decreased stance phase and knee extension on the symptomatic side.22 A knee effusion is observed in about half of individuals with a known meniscal tear.24 Quadriceps atrophy may be noted a few weeks after injury. Palpation of the joint line frequently results in tenderness. Posteromedial or lateral tenderness is most suggestive of a meniscal tear.12 The result of a “bounce home” test may be positive. This test result is positive when pain or mechanical blocking is appreciated as the patient’s knee is passively forced into full extension.14 The result of the McMurray test is positive 58% of the time in the presence of a tear, but

406

PART 1  MSK Disorders

A

B

C

FIG. 72.5  McMurray test. (A) Starting position for testing of the medial meniscus. The knee is acutely flexed, with the foot and tibia in external rotation. (B) Starting position for testing of the lateral meniscus. The knee is acutely flexed, and the foot and tibia are internally rotated. (C) Ending position for the lateral meniscus. The knee is brought into extension while rotation is maintained. Ending position for the medial meniscus is the same but with the external rotation. If pain or a “clunk” is elicited, the test result is considered positive. (From Mellion MB. Office Sports Medicine, 2nd ed. Philadelphia: Hanley & Belfus; 1996.)

is also reported to be positive in 5% of normal individuals (Fig. 72.5).13 The Apley compression test is an insensitive indicator of meniscal injury. With this test, the prone knee is flexed to 90 degrees and an axial load is applied (Fig. 72.6). A painful response is considered a confirmatory test result with a reported sensitivity of 45%.22 A dynamic functional test known as the Thessaly maneuver can detect a meniscal tear. This maneuver is performed while the patient stands with the affected knee flexed at either 5 degrees or 20 degrees and internally or externally rotates the body. The test result is considered suggestive of a meniscal tear if there is reproduction of joint line discomfort or if clicking or locking is noted.24 Prospective studies have suggested a sensitivity and specificity similar to other special tests possibly with a greater capacity to predict lateral tears.25 No singular meniscal provocation test has been shown to be predictive of meniscal injury compared with findings on arthroscopy or magnetic resonance imaging (MRI).25 Physical examination findings become even less reliable in patients with concomitant anterior cruciate ligament deficiencies.14,23 Neurologic examination findings, including sensation and deep tendon reflexes, should be normal unless there is associated guarding due to pain or diffuse weakness, particularly with knee extension (quadriceps muscle inhibition). 

Functional Limitations Patients with meniscal injuries may have difficulty with deep knee bending activities, such as traversing stairs, squatting, or toileting. In addition, jogging, running, and even walking may become problematic, particularly if any rotational component is involved. Laborers who repetitively squat may report mechanical locking with loss of full knee extension on rising. 

Diagnostic Studies Standing plain radiographs are usually normal in isolated meniscal injuries. Presence of osteoarthritis, as with degenerative meniscal tears, can be detected with weight-bearing anteroposterior and lateral knee films. With nondegenerative tears, MRI is the favored imaging modality; however, meniscal tears can be present in asymptomatic individuals with increasing likelihood with increased age.12,26 Sagittal views demonstrate the anterior and posterior horns of the menisci; coronal

FIG. 72.6  Apley compression test. The patient is prone. The examiner applies pressure on the sole of the foot toward the examination table. The tibia is internally and externally rotated. (From Mellion MB. Office Sports Medicine, 2nd ed. Philadelphia: Hanley & Belfus; 1996.)

images can be vital in diagnosis of bucket-handle and parrotbeak tears.1,14 There are three grades of meniscal injury as determined by the location of T2 signal intensity within the black cartilage. By definition, only grade 3 tears qualify as true meniscal tears; however, a few grade 2 lesions seen on MRI will be found to be true tears on arthroscopy (Fig. 72.7).27 With use of arthroscopy as the “gold standard,” the sensitivity of MRI varies from 64% to 95%, with an accuracy of 83% to 93%.16 MRI appears to have a false-positive rate of 10%.1,22 A 5% false-negative rate is also reported and may be due to missed tears at the meniscosynovial junction.28 Ultrasonography has also been used to diagnose meniscal tears, traditionally with lower specificity and sensitivity compared with MRI, although improvements in technology and physician training have significantly enhanced its utility in recent years.29 Interestingly, despite the recent accessibility and advancement in ultrasonography and MRI, clinical examination by experienced physicians is cheaper and appears to be as accurate as MRI for the diagnosis of meniscal tears.29,30 However, MRI may be particularly helpful when history and physical examination findings are equivocal and the physician is required to establish an expedient diagnosis, particularly if surgery is being considered.13,21 

CHAPTER 72  Meniscal Injuries

A

B

407

C

FIG. 72.7  Magnetic resonance imaging grading of meniscal tears. (A) Poorly defined “globular” zone of increased signal intensity (arrow), corresponding to grade 1 change. (B) Linear zone of hyperintensity (arrow) not communicating with the articular surfaces, corresponding to grade 2 change. (C) Linear band of hyperintensity (arrow) communicating with both articular surfaces, corresponding to grade 3 change, that is, a complete tear. (From Mellion MB. Office Sports Medicine, 2nd ed. Philadelphia: Hanley & Belfus; 1996.)

Differential Diagnosis Anterior or posterior cruciate ligament tear Medial collateral ligament tear Osteoarthritis Plica syndromes Popliteal tendinitis Osteochondritic lesions Loose bodies Patellofemoral pain Fat pad impingement syndrome Inflammatory arthritis Physeal fracture Tumors

Treatment Initial The truly locked knee resulting from a meniscal tear should be reduced within 24 hours of injury. Otherwise, acute tears of the meniscus may initially be treated with rest, ice, and compression, with weight bearing as tolerated. Patients may need to use crutches acutely. A knee splint may be applied for comfort of the patient, particularly in unstable knees with underlying ligamentous injury.21 Analgesics such as acetaminophen or opioids can be used for pain. Nonsteroidal anti-inflammatory drugs can be used for pain and inflammation. Arthrocentesis can be performed (ideally in the first 24 to 48 hours) for both diagnostic and treatment purposes when there is a significant effusion. 

Rehabilitation Not all meniscal injuries necessitate surgical intervention or resection. In fact, some meniscal lesions have gradual resolution of symptoms during a 6-week period and may have normal function by 3 months.11 Types of tears that may be treated with nonsurgical measures include partial-thickness

longitudinal (vertical) tears, small ( Physical Medicine and Rehabilitation Medscape; 2016. 5. Scott A, Zwerver J, Grewal N. Lipids, adiposity and tendinopathy: is there a mechanistic link? Critical review. Br J Sports Med. 2015;49(15):984–988. 6. Pingel J, Fredberg U, Qvortrup K, et al. Local biochemical and morphological differences in human Achilles tendinopathy. BMC Musculoskelet Disord. 2012;13:53. 7. Kraushaar B, Nirschl R. 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. 8. Kawtharani F, Masrouha KZ, Afeiche N. Bilateral Achilles tendon ruptures associated with ciprofloxacin use in the setting of minimal change disease: case report and review of the literature. J Foot Ankle Surg. 2016;55(2):276–278. 9. Spoendlin J, Layton JB, Mundkur M, Meier CR. The risk of Achilles or biceps tendon rupture in new statin users: a propensity score-matched sequential cohort study. Drug Saf. 2016;39(12):1229–1237. 10. Nirschl R. Surgical considerations of ankle injuries. In: O’Connor F, Wilder R, eds. The Complete Book of Running Medicine. New York: McGraw-Hill; 2001. 11. Stretanski MF, Weber GJ. Medical and rehabilitation issues in classical ballet. Am J Phys Med. 2002;81:383–391. 12. Siu WL, Chan CH, Lam CH, Lee CM, Ying M. Sonographic evaluation of the effect of long-term exercise on Achilles tendon stiffness using shear wave elastography. J Sci Med Sport. 2016;19(11):883–887. 13. Finni T, Hodgson JA, Lai AM, et al. Muscle synergism during isometric plantarflexion in Achilles tendon rupture patients and in normal subjects revealed by velocity-encoded cine phase-contrast MRI. Clin Biomech (Bristol, Avon). 2006;21:67–74. 14. Wagnon R, Akayi M. Post-surgical Achilles tendon and correlation with functional outcome: a review of 40 cases. J Radiol. 2005;86(Pt 1):1783–1787. 15. Fouré A. New imaging methods for non-invasive assessment of mechanical, structural, and biochemical properties of human Achilles tendon: a mini review. Front Physiol. 2016;7:324. 16.  Nefeli T, van Dieën JH, Coppieters MW. Central pain processing is altered in people with Achilles endinopathy. Br J Sports Med. 2016;50(16):1004–1007. 17. Rompe JD, Nafe B, Furia JP, Maffulli N. Eccentric loading, shockwave treatment, or a wait-and-see policy for tendinopathy of the main body of tendo achillis: a randomized controlled trial. Am J Sports Med. 2007;35:374–383. 18. van Sterkenburg MN, de Jonge MC, Sierevelt IN, van Dijk CN. Less promising results with sclerosing ethoxysclerol injections for midportion Achilles tendinopathy: a retrospective study. Am J Sports Med. 2010;38:2226–2232. 19. Paoloni JA, Appleyard RC, Nelson J, Murrell GA. Topical glyceryl trinitrate treatment of chronic noninsertional Achilles tendinopathy. A randomized, double-blind, placebo-controlled trial. J Bone Joint Surg Am. 2004;86:916–922.

CHAPTER 81  Achilles Tendinopathy

20. Sartorio F, Zanetta A, Ferriero G, Bravini E, Vercelli S. The EdUReP approach plus manual therapy for the management of insertional Achilles tendinopathy. J Sports Med Phys Fitness. 2018;58(5):664–668. 21. Wu PT, Jou IM, Kuo LC, Su FC. Intratendinous injection of hyaluronate induces acute inflammation: a possible detrimental effect. PLoS One. 2016;11(5):e0155424. 22. Gentile P, De Angelis B, Agovino A, et al. Use of platelet rich plasma and hyaluronic acid in the treatment of complications of Achilles tendon reconstruction. World J Plast Surg. 2016;5(2):124–132. 23. Gaulke R, Krettek C. Tendinopathies of the foot and ankle: evidence for the origin, diagnostics and therapy. Unfallchirurg. 2017;120(3):205–213. 24. Huisman E, Guy P, Scott A. Vancouver data supports a weak association between tendon pathology and serum lipid profiles. Br J Sports Ed. 2016;50:1485–1486. 25. Weinert-Aplin RA, Bull AM, McGregor AH. Orthotic heel wedges do not alter hindfoot kinematics and Achilles tendon force during level and inclined walking in healthy individuals. J Appl Biomech. 2016;32(2):160–170. 26. Wiegerinck JI, van Dijk NC. Treatment of midportion Achilles tendinopathy: an evidence-based overview. Knee Surg Sports Traumatol. Arthrosc. 2016;24(7):2103–2111. 27. Chiu TC, Ngo HC, Lau LW, et al. An investigation of the immediate effect of static stretching on the morphology and stiffness of Achilles tendon in dominant and non-dominant legs. PLoS One. 2016;11(4):e0154443. 28. Peltonen J, Cronin NJ, Stenroth L, Finni T, Avela J. Achilles tendon stiffness is unchanged one hour after a marathon. J Exp Biol. 2012;215(Pt 20):3665–3671. 29. Waugh CM, Morrissey D, Jones E, Riley GP, Langberg H, Screen HR. In vivo biological response to extracorporeal shockwave therapy in human tendinopathy. Eur Cell Mater. 2015;29:268–280; discussion 280. 30. Yeung CK, Guo X, Ng YF. Pulsed ultrasound treatment accelerates the repair of Achilles tendon rupture in rats. J Orthop Res. 2006;24:193–201.

455

31. Salate AC, Barbosa G, Gaspar P, et al. Effect of in-Ga-Al-P diode laser irradiation on angiogenesis in partial ruptures of Achilles tendon in rats. Photomed Laser Surg. 2005;23:470–475. 32. Steyaert AE, Burssens PJ, Vercruysse CW, et al. The effects of substance P on the biomechanic properties of ruptured rat Achilles’ tendon. Arch Phys Med Rehabil. 2006;87:254–258. 33. Barata P, Cervaens M, Resende R, et al. Hyperbaric oxygen effects on sports injuries. Ther Adv Musculoskelet Dis. 2011;3:111–121. 34. Chen TM, Rozen WM, Pan WR, Ashton MW, Richardson MD, Taylor GI. The arterial anatomy of the Achilles tendon: anatomical study and clinical implications. Clin Anat. 2009;22(3):377–385. 35. Kuskucu M, Mahirogullari M, Solakoglu C, et al. Treatment of rupture of the Achilles tendon with fibrin sealant. Foot Ankle Int. 2005;26:826–831. 36. Sorrenti SJ. Achilles tendon rupture: effect of early mobilization in rehabilitation after surgical repair. Foot Ankle Int. 2006;27:407–410. 37. Rompe JD, Furia JP, Maffulli N. Mid-portion Achilles tendinopathy— current options for treatment. Disabil Rehabil. 2008;30:1666–1676. 38. Maffulli N, Longo UG, Maffulli GD, et al. Achilles tendon ruptures in elite athletes. Foot Ankle Int. 2011;32:9–15. 39. Maes R, Copin G, Averous C. Is percutaneous repair of the Achilles tendon a safe technique? A study of 124 cases. Acta Orthop Belg. 2006;72:179–183. 40. Hunt KJ, Cohen BE, Davis WH, Anderson RB, Jones CP. Surgical treatment of insertional Achilles tendinopathy with or without flexor hallucis longus tendon transfer: a prospective, randomized study. Foot Ankle Int. 2015;36(9):998–1005. 41. Majewski M, Rohrbach M, Czaja S, Ochsner P. Avoiding sural nerve injuries during percutaneous Achilles tendon repair. Am J Sports Med. 2006;34:793–798.

CHAPTER 82

Ankle Arthritis David Wexler, MD, FRCS (Tr & Orth) Melanie E. Campbell, MS, ATC, RNFA, FNP-C Dawn M. Grosser, MD Todd A. Kile, MD

Symptoms

Synonym Degenerative joint disease of the ankle

ICD-10 Codes M19.071 M19.072 M19.079 M19.271 M19.272 M19.279 M12.571 M12.572 M12.579

Primary osteoarthritis, right ankle and foot Primary osteoarthritis, left ankle and foot Primary osteoarthritis, unspecified ankle and foot Secondary osteoarthritis, right ankle and foot Secondary osteoarthritis, left ankle and foot Secondary osteoarthritis, unspecified ankle and foot Traumatic arthropathy, right ankle and foot Traumatic arthropathy, left ankle and foot Traumatic arthropathy, unspecified ankle and foot

Definition Ankle arthritis is degeneration of the cartilage within the tibiotalar joint that can result from a wide range of causes, most commonly post-traumatic degenerative joint disease. An acute injury or trauma sustained a number of years before presentation, or less severe, repetitive, minor injuries sustained during a longer period, can lead to a slow but progressive destruction of the articular cartilage, resulting in degenerative joint disease.1 Other common types are primary osteoarthritis, inflammatory arthritis (including rheumatoid, psoriatic, and gouty), and septic arthritis. Osteoarthritis is usually less inflammatory than rheumatoid arthritis, but can also involve many joints simultaneously.  456

As with arthritis of any joint, the presenting symptoms are pain (which may be variable at different times of the day and exacerbated by activity), swelling, stiffness, and progressive deformity.1 The ankle may be stiff on initial weight bearing; this improves after walking a while, but then worsens with too much ambulatory activity. The pain is often relieved with rest. Pieces of the cartilage can break off, forming a loose body, and the joint can “lock” or “catch,” sticking in one position and causing acute, excruciating pain until the loose body moves from between the two irregular joint surfaces. Another symptom is that of “giving way” or instability of the joint, which may be a result of surrounding muscle weakness or ligamentous laxity. With progression of the arthritis, night pain can become a major complaint. 

Physical Examination Swelling, pain, and increased temperature on palpation may be present. The pain is usually maximal along the anterior talocrural joint line and is typically chronic and progressive. If the patient’s other ankle is normal, it is important to compare the two. Assessing the overall alignment of the entire lower extremities, including the knees, is important. Deformity and reduced range of motion in plantar flexion and dorsiflexion (normal: up to 20 degrees of dorsiflexion and 45 degrees of plantar flexion) may be seen. The patient may exhibit an antalgic gait or a limp. Therefore gait pattern should be evaluated to determine if there are any abnormal loading patterns as the foot strikes the ground. Acute arthritis is manifested very differently. Onset is rapid with associated warmth, erythema, swelling, and severe pain with passive range of motion and may be accompanied by constitutional symptoms such as fever and rigors. It is appropriate to examine the other joints in the lower limb, particularly the knee. The findings on neurovascular examination are typically normal. Decreased sensation in the lower limb raises the possibility of a Charcot joint causing a destructive arthropathy (see Chapter 129). 

Functional Limitations Pain with walking distances and difficulty in negotiating stairs or inclines are particular functional disabilities. Even prolonged standing can become intolerable with advanced

CHAPTER 82  Ankle Arthritis

FIG. 82.1  Lateral ankle X-ray demonstrating osteoarthritis showing significant reduction of joint space, sclerosis (whitening of the bone), and osteophyte (bone spur formation).

joint deterioration. Night pain can lead to disturbance of sleep. Patients will typically adjust their activities or eliminate many of them, particularly exercising, because of pain. 

Diagnostic Studies Plain anteroposterior and lateral standing radiographs provide sufficient information in the later stages of the disease (Figs. 82.1 and 82.2). Magnetic resonance imaging may show damage to articular cartilage and a joint effusion earlier in the course of the disease. In assessment of the radiographs, attention should also be paid to the other joints in the hindfoot because these will affect management options. Generalized bone density and alignment should also be noted. In some cases, patients present with varying degrees of degeneration of other adjacent joints, such as the subtalar joint or the knee. By performing differential blocks (i.e., isolated ankle block or subtalar block) with local anesthetic under radiographic control, the clinician may determine which of these joints are symptomatic. A bone scan might be of assistance. In acute presentations, complete blood cell count with a white blood cell count differential, serum urate concentration, and possible joint needle aspiration can help clarify the diagnosis.  Differential Diagnosis Edema (e.g., edema secondary to congestive cardiac failure) Subtalar joint degenerative disease Posterior tibial tenosynovitis Osteochondral defect Fracture Osteonecrosis

457

FIG. 82.2  Anteroposterior weight-bearing comparative ankle X-rays demonstrating a normal left ankle but severe osteoarthritis of the right ankle also showing significant reduction of joint space, sclerosis (whitening of the bone), and osteophyte (bone spur) formation. On this view, there is also subchondral cyst formation and varus malalignment (the talus or ankle bone is tilted towards the midline).

Treatment Initial Initial treatment focuses on pain relief and minimizing inflammation. Nonsteroidal anti-inflammatory drugs or simple analgesics are used to alleviate the pain. Prefabricated orthoses, ranging from flexible neoprene braces and lace-up or wraparound ankle supports to more rigid braces or walking boots, can be prescribed to enhance stability and to reduce movement in the ankle joint, thus reducing pain levels. 

Rehabilitation A custom-molded rigid ankle-foot orthosis fabricated by a skilled orthotist along with a rocker-bottom modification to the shoe (which can be accomplished by most cobblers) can provide dramatic pain relief for most patients with ankle arthritis. A physical therapist can instruct a patient in the proper technique for use of a walking stick or cane in the opposite hand. This is a simple but effective aid in reducing the forces across the ankle joint when the patient is ambulatory. Mobilization, stretching techniques, and range of movement exercises may help alleviate pain and stiffness. Non– weight-bearing exercises are important, and if it is accessible, hydrotherapy has been shown to be an extremely useful and productive adjunct. Distraction and gliding mobilization techniques improve range of movement. Strengthening of surrounding muscle groups and proprioceptive rehabilitation will enhance stability. 

Procedures Other than the blocks that are performed to determine the location of the pathologic changes in confusing cases, injections are not typically done for ankle arthritis. Corticosteroid

458

PART 1  MSK Disorders

FIG. 82.4  Weight-bearing lateral X-ray of a total ankle replacement. FIG. 82.3  Weight-bearing anteroposterior X-ray of a total ankle replacement.

injection is generally of only limited duration, and steroids are chondrotoxic (cause cartilage damage). However, they can provide excellent temporary pain relief in patients with joints at end-stage disease. Viscosupplementation injections (as used in the management of knee arthritis) are still experimental and not recommended at this time. 

efficacy of arthrodesis and total joint arthroplasty.8,9,13 Selection of patients is of paramount importance; those with high expectations and demands (hiking, tennis, running) may be better served with a more predictable, stable fusion than with a replacement that has a high likelihood of failure and need of revision. 

Technology

Potential Disease Complications

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

Progressive immobility, permanent loss of motion of the ankle joint, bone collapse leading to leg length discrepancy, and chronic intractable pain can result from ankle arthritis. 

Surgery Surgery is indicated in patients who fail to respond to nonoperative management and especially in those with unremitting pain. In the earlier stages of arthritis, an arthroscopic washout and cartilage débridement of the ankle joint may provide significant improvement in pain levels. As the disease progresses, more extensive surgery is required. Many different variations and techniques of fusion have been described, ranging from minimally invasive arthroscopic arthrodesis to open fusion with hardware.1–6 Distraction arthroplasty (application of an external fixator for a period of time) is an alternative to ankle arthrodesis or total ankle arthroplasty in a younger patient and it has shown some promising results. Total ankle joint replacement (arthroplasty) has been an alternative to ankle fusion since the 1970s in certain select populations of patients (Figs. 82.3 and 82.4). It has undergone a series of alterations because the earlier generation models were prone to failure and unpredictable results.7,13 Currently, there are more than five different total ankle replacement systems being utilized in the United States. In recent times, there have been significant advances in and ongoing research comparing

Potential Treatment Complications Analgesics and nonsteroidal anti-inflammatory drugs have well-known side effects that most commonly affect the gastric, hepatic, and renal systems. Arthroscopy can be complicated by nerve damage or, rarely, septic arthritis. On occasion, with arthrodesis, fusion can fail to occur.10 An alteration in gait is common.11 Arthroplasty complications include infection, thromboembolism, bone collapse, implant wear and loosening, impingement of soft tissues, and arthrofibrosis.13 Ankle distraction arthroplasty complications include superficial pin site infections, pin breakage, premature loosening, posterior tibial neuropraxia, and heel numbness.12

References 1. Richardson EG. Arthrodesis of ankle, knee and hip. In: Canale ST, ed. Campbell’s Operative Orthopaedics, 9th ed. St. Louis: Mosby; 1988:165–182. 2. Thordarson DB. Ankle and hindfoot arthritis: fusion techniques. In: Craig EV, ed. Clinical Orthopaedics. Philadelphia: Lippincott Williams & Wilkins; 1999:883–890. 3. Mann RA, Van Manen JW, Wapner K, Martin J. Ankle fusion. Clin Orthop. 1991;268:49–55.

CHAPTER 82  Ankle Arthritis

4. Morgan CD, Henke JA, Bailey RW, Kaufer H. Long-term results of tibiotalar arthrodesis. J Bone Joint Surg Am. 1985;67:546–550. 5. Kile TA. Ankle arthrodesis. In: Morrey B, ed. Reconstructive Surgery of the Joints, 2nd ed. New York: Churchill Livingstone; 1996:1771–1787. 6. Kile TA, Donnelly RE, Gehrke JC, et al. Tibiotalocalcaneal arthrodesis with an intramedullary device. Foot Ankle. 1994;15:669–673. 7. McGuire MR, Kyle RF, Gustilo RB, Premer RF. Comparative analysis of ankle arthroplasty versus ankle arthrodesis. Clin Orthop Relat Res. 1988;226:174–181. 8. Haddad SL, Coetzee JC, Estok R, et al. Intermediate and long-term outcomes of total ankle arthroplasty and ankle arthrodesis: a systematic review of the literature. J Bone Joint Surg Am. 2007;89:1899–1905. 9. Cracchiolo A III, DeOrio JK. Design features of current total ankle replacements: implants and instrumentation. J Am Acad Orthop Surg. 2008;16:530–540.

459

10. Smith RW. Ankle arthrodesis. In: Thompson RC, Johnson KA, eds. Master Techniques in Orthopaedic Surgery. The Foot and Ankle. Philadelphia: Raven Press; 1994:467–482. 11. Mazur JM, Schwartz E, Simon SR. Ankle arthrodesis: long-term followup with gait analysis. J Bone Joint Surg Am. 1979;61:964–975. 12. Bernstein M, Reidler J, Fragomen A, Rozbruch SR. Ankle distraction arthroplasty: indications, technique, and outcomes. J Am Acad Orthop Surg. 2017;25(2):89–99. 13. Saltzman CL, Mann RA, et al. Prospective controlled trial of STAR total ankle replacement versus ankle fusion: initial results. Foot Ankle Int. 2009;30(7):579–596.

CHAPTER 83

Ankle Sprain Brian J. Krabak, MD, MBA Aaron W. Butler, MD

Synonym Inversion sprain

ICD 10 codes S93.401 Sprain of unspecified ligament of right ankle S93.402 Sprain of unspecified ligament of left ankle S93.409 Sprain of unspecified ligament of unspecified ankle S93.601 Unspecified sprain of right foot S93.602 Unspecified sprain of left foot S93.609 Unspecified sprain of unspecified foot

during several weeks to months, depending upon the grade of injury. It is estimated that 20% to 40% of ankle sprains result in chronic sequelae.8 An ankle sprain that does not heal may be caused by injuries to other structures and will necessitate further investigation for other causes. The exact structure torn will depend upon the mechanism of injury. The most common mechanism of injury involves foot supination and inversion resulting in a tear of the lateral ankle structures (primarily the ATFL). An eversion stress to the foot or ankle will tear the medial structures (deltoid ligament), and ankle dorsiflexion with external rotation will lead to a syndesmotic injury.7,9 Ligamentous injuries are categorized into three grada­tions: Grade I is a partial tear without laxity and only mild edema. Grade II is a partial tear with mild laxity and moderate pain, swelling, tenderness, and instability. Grade III is a complete rupture resulting in considerable swelling, increased pain, significant laxity, and often an unstable joint (Fig. 83.2). 

Definition

Symptoms

Ankle sprain involves stretching or tearing of the ligaments of the ankle. Ankle injuries are a common cause of morbidity in the general and athletic population, with an estimated 25,000 ankle sprains requiring medical care in the United States per day.1 Between the ages of 15 and 24 years, ankle sprains are slightly more likely to occur in males than females (incidence ratio of 1.04) and nine times more likely to occur in younger than older individuals.2 However, a recent metaanalysis showed that overall, females have a higher incidence than males (13.6 vs. 6.94 per 1000 exposures).3 In the high school athlete, there are an average of 5.23 ankle injuries per 10,000 athlete exposures, most often due to traumatic ligament injuries involving boys’ basketball, girls’ basketball, and boys’ football.4 In the collegiate athlete, ankle sprains represent 15% of all athletic injuries and account for almost 25% of injuries of men’s and women’s collegiate basketball and women’s volleyball athletes.5,6 Eighty-five percent of all ankle sprains occur on the lateral aspect of the ankle, involving the anterior talofibular ligament (ATFL) and calcaneofibular ligament (CFL) (Fig. 83.1).7 Another 5% to 10% are syndesmotic injuries or high ankle sprains, which involve a partial tear of the distal anterior tibiofibular ligament. Identification of syndesmotic sprains is important, as they may have a prolonged recovery compared to milder lateral ankle sprains, and are more likely to require surgery. Only 5% of all ankle sprains involve the medial aspect of the ankle, as the strong medial deltoid ligament is quite resistant to tearing. Most ankle sprains will recover

Acutely, the injured patient will report pain, swelling, and tenderness over the injured ligaments. Some patients report a “pop” at the time of injury. Initially, they may have difficulty weight bearing on the injured ankle and with subsequent ambulation. They may report some ecchymosis over the first 24 to 48 hours. There may be sensory symptoms in the sural, superficial, or deep peroneal nerve’s distribution. Decreased function and range of motion along with instability are reported more often in grade II and grade III injuries. 

460

Physical Examination Inspection of the ankle will reveal edema and sometimes ecchymosis around the area of injury, depending upon the extent of injury. Range of motion of the ankle joint may be limited by associated swelling and pain. Reduced dorsiflexion may predispose the joint to an ankle sprain.10 Palpation should include the ATFL and CFLs, syndesmotic area, and medial deltoid ligament. In addition, the examiner should palpate the distal fibula, medial malleolus, base of the fifth metatarsal, cuboid, and lateral process of the talus (to assess for a possible snowboarder’s fracture), and epiphyseal areas to assess for any potential fractures.11,12 The patient should be examined for strength deficits or reflex abnormalities, which could reveal concurrent injury. Although uncommon, ankle inversion injuries are sometimes associated with peroneal nerve injury and may result in sensory changes on the

CHAPTER 83  Ankle Sprain

461

Anterior talofibular ligament Posterior talofibular ligament Calcaneofibular ligament

FIG. 83.1  Ligaments of the lateral ankle.

FIG. 83.3  Anterior drawer test of the ankle. (From Brinker MR, Miller MD. Fundamentals of Orthopaedics. Philadelphia: Saunders; 1999.) FIG. 83.2  Grade III ankle sprain with a complete tear of the anterior talofibular ligament.

dorsum of the foot (superficial peroneal nerve) or the first web space (deep peroneal nerve). Deep peroneal nerve injury could result in decreased strength in dorsiflexion and eversion. If a fracture is not suspected, single leg balance could be tested to assess the extent of proprioceptive compromise. Ankle stability should be examined through a variety of tests and compared with the non-injured side to assess the amount of abnormal translation in the joint. The anterior drawer test of the ankle (Fig. 83.3) will assess the integrity of the ATFL. It is performed by plantar flexing the ankle to approximately 30 degrees and applying an anterior force to the calcaneus while

stabilizing the tibia with the other hand. Increased translation compared with the other side implies injury to the ATFL. Studies in cadavers suggest the test is quite accurate in detecting abnormal lateral ankle motion with 100% sensitivity and 75% specificity.13,14 The talar tilt test (Fig. 83.4) is performed with the ankle a neutral position and assesses the integrity of the CFL.14 The squeeze test (Fig. 83.5) is used to diagnose a syndesmotic injury. It is performed by squeezing the proximal fibula and tibia at the midcalf and causes pain over the syndesmotic area. Similarly, the external rotation stress test is performed by placing the ankle in a neutral position and externally rotating the tibia, leading to pain in the syndesmotic region.15 Unfortunately, several studies have demonstrated

462

PART 1  MSK Disorders

poor correlation between clinical stress test results and the degree of ligamentous disruption.16 

Functional Limitations The patient may have difficulty in walking secondary to pain and swelling. Proprioception and balance on the injured ankle will be abnormal, as noted by greater difficulty with single-leg standing on the injured leg.17 The athlete will have difficulty with return to play until swelling and pain have diminished and rehabilitation is nearly completed. Incomplete recovery or inadequate rehabilitation may predispose the patient to reinjury.18 Of note, the single-leg balance test can be helpful in predicting which athletes may sustain an ankle injury over the course of the upcoming season.19 Chronic ankle sprains can result in mechanical instability, with objective instability or laxity noted on examination in all patients.20 

Diagnostic Studies Standard anteroposterior, mortise (Fig. 83.6), and lateral radiographs should be considered in cases in which there is tenderness over the lateral malleolus, ankle joint, syndesmosis, or other bony structure to rule out an underlying fracture.7,11 The Ottawa ankle rules (Fig. 83.7) were developed

FIG. 83.4  The talar tilt (inversion stress) test of the ankle.

and validated to clarify the indications for these ankle radiographs. The rules recommend imaging when there is tenderness along the lower 6 cm posterior edge or top of the lateral or medial malleolus, the navicular, the base of the fifth metatarsal, and an inability to bear weight immediately post injury and in the emergency room. Adherence to these rules has shown a 30% reduction in x-ray utilization while missing no major fractures.11,12 At 4 to 6 weeks, a slowly healing lateral ankle injury without significant pain resolution or improvement should be evaluated radiographically, especially if an initial radiograph was not obtained. A magnetic resonance imaging scan can help identify the soft tissue disease as well as evaluate the osteochondral joint surface when the ankle does not heal despite adequate rehabilitation. Osteochondral injuries may not be seen immediately, but occur later especially in cases with chronic instability. Stress radiographs are optional and have questionable reliability because of the great range of normal joint movement.21 Ultrasound may be utilized to further evaluate the soft tissue structures of the ankle, including ligament injury and associated

FIG. 83.5  The squeeze test detects tears of the syndesmosis. The test result is positive when squeezing of the midcalf produces pain in the distal interosseous membrane and syndesmosis.

CHAPTER 83  Ankle Sprain

tendon subluxation. Advantages of ultrasound include the lack of radiation and relatively low cost.22 A study comparing ultrasonography findings to operative findings in 120 patients with chronic lateral ankle ligament injury showed the sensitivity, specificity, and accuracy of ultrasonography to be 98.9%, 96.2%, and 84.2%, respectively, for injury to the ATFL and 93.8%, 90.9%, and 83.3%, respectively, for injury to the CFL.23  Differential Diagnosis High ankle sprain, syndesmotic sprain Osteochondral fracture of the talar dome Neurapraxia of the common, superficial, or deep peroneal nerve Fracture of the lateral process of the talus (snowboarder’s fracture) Avulsion or fracture of the tip of the fibula Fracture of the base of the fifth metatarsal Peroneal tendon injury Subtalar joint instability Posterior impingement or fracture of the os trigonum

463

Treatment Initial Protection, relative rest, ice, compression, and elevation (PRICE) are the proposed mainstay of initial treatment and are introduced immediately.24 However, there appears to be insufficient evidence to determine the true effectiveness of rest, ice, compression, and elevation for acute ankle sprains.25 It intuitively makes sense to utilize crutches if weight bearing causes pain. The crutches can be discontinued as ambulatory pain declines (usually in 2 to 3 days). Grade II and Grade III sprains may require longer use of assistive devices. Patients should be cautioned to avoid hanging the ankle in a plantar flexed position because it may stretch the injured ATFL. Positioning in maximum dorsiflexion also minimizes resultant joint effusion. Plastic removable walking cast boots or air splints are occasionally used in higher-grade injuries until pain-free weight bearing is achieved. This may be utilized for weeks to months, depending on the extent of injury. Caution should be taken with prolonged immobilization, as a systematic review of randomized controlled trials suggests that prolonged immobilization (more than 4 weeks) is less effective than early functional treatment.26 Local ice applications for 20 to 30 minutes three or four times daily combined with compression immediately after injury is effective in decreasing edema, pain, and dysfunction. Nonsteroidal anti-inflammatory drugs may be employed to decrease pain and inflammation. Other therapeutic modalities including diathermy, electrotherapy, and therapeutic ultrasound have not been shown to be effective. 

Rehabilitation

FIG. 83.6  X-ray (mortise view) of the ankle. (A) Posterior edge or tip of lateral malleolus

The rehabilitation of ankle sprains has moved toward earlier mobilization in hopes of minimizing swelling, decreasing pain, and preventing chronic ankle problems.27,28 Active range of motion in all planes is initially performed without resistance as soon as tolerated. Dorsiflexion and eversion strengthening can be started with static exercises and progress to concentric and eccentric exercises with tubing when the patient tolerates pain-free weight bearing. Double-leg toe raises should progress to single-leg toe raises and can be done in water if they are not tolerated on land. Endurance and lower extremity muscle strengthening exercises are incorporated and increased as tolerated by the patient. Proprioception training can start in (B) Posterior edge or tip of medial malleolus

Malleolar zone 6 cm

Midfoot zone

6 cm

(C) Base of 5th metatarsal

(D) Navicular

Lateral view

Medial view

FIG. 83.7  Ottawa ankle rules. (From Derksen RJ, Knijnenberg LM, Fransen G, et al. Diagnostic performance of the Bernese vs. Ottawa ankle rules: results of a randomised controlled trial. Injury. 2015;46(8):1645–1649.)

464

PART 1  MSK Disorders

a seated position and then advance to standing balance exercises. Standing exercises begin with single-leg stance while swinging the raised leg. Then, single-leg squats are required. Finally, exercises progress to single-leg stance and functional or sport-specific activity, such as dribbling, catching, or kicking. A randomized study comparing PRICE therapy with early mobilization in patients with grade I or II ankle sprains reported better functional recovery in the first 2 weeks post injury in the early mobilization groups. There were no long-term differences at 16 weeks and reinjury rate was the same for both groups.27 A supervised program appeared to provide better results than a conventional home program.29 Several studies have highlighted the importance of proprioceptive training on early recovery from ankle sprains and chronic functional instability (such as circular wobble board training or walking on different surfaces). A prospective cohort study of volleyball players demonstrated a 21% reduction in ankle sprains the first year and 49% reduction the second year in athletes who performed balance exercises.30 In addition, they reported fewer recurrent ankle sprains, and patients with more than one sprain benefited the most. A systematic review showed that proprioceptive and balance training does in fact improve recovery acutely, and can reduce recurrence rates of injury.31 Therefore, proprioceptive and balance exercises should be incorporated into the rehabilitation program as soon as possible. A recent meta-analysis analyzing ankle sprain prevention programs in soccer players showed that interventions that utilized neuromuscular, proprioceptive, strengthening, and stretching exercises showed a protective effect (relative risk of 0.60).32 The use of orthotic bracing is somewhat controversial. Earlier studies have suggested that bracing and taping may decrease recurrent injury rates in the previously injured ankle, but they have not been shown to be effective in athletes without a prior injury.33,34 A prospective randomized study of 182 patients with first-time grade I and grade II ankle ligament sprains showed that treatment with the air stirrup brace combined with an elastic wrap provided earlier return to pre-injury function than with use of the air stirrup brace alone, an elastic wrap alone, or a walking cast for 10 days.33 Interestingly, a more recent meta-analysis suggests the use of an ankle brace or ankle tape has no effect on enhancing proprioception in individuals with recurrent ankle sprains or who have functional ankle instability.35 These studies suggest that the decrease in injury rates is due to something other than enhanced proprioception of the ankle. Despite these findings, many athletes will consider utilizing a brace to prevent a recurrent sprain. A prospective randomized study suggested that use of ankle braces in healthy competitive recreational soccer players did not significantly affect performance in speed, agility, or kicking accuracy.36 The authors proposed the need for future studies to investigate the impact on athletes with ankle injuries. 

Procedures Regenerative techniques, such as platelet-rich plasma (PRP), are emerging treatment options for soft tissue

injuries. These injections have received increased attention in recent years, especially among elite and professional athletes. PRP therapy involves an injection of a high concentration of platelets from a patient’s own blood to the site of injury. This is thought to enhance healing and tissue regeneration due to release of immunologically active proteins. The efficacy of PRP treatment is controversial. A small randomized controlled trial comparing PRP to standard treatment in patients presenting to the emergency department with acute ankle injuries did not show significant benefit in either function or pain.37 Further studies are needed to determine the clinical utility of PRP as an intervention for ankle sprains. 

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

Surgery Surgery is rare for ankle sprains. Most grade III ankle sprains with complete tears of the ATFL and instability are not treated surgically unless they result in chronic instability.38 If necessary, surgical repair may be completed after the sports season and is usually successful. Reconstruction of the lateral ankle ligaments involves anatomic reconstruction of the ligament (modified Brostrom) and tendon weaving through the fibula (Watson-Jones, Chrisman-Snook).39 The direct repair of the ligament, even years after the injury, can be highly successful. Despite the various techniques, an extensive literature review did not demonstrate evidence of benefit from surgical repair and recommended against surgery for acute lateral ligament complex injuries, regardless of severity.40,41 

Potential Disease Complications Recurrent sprains may lead to both mechanical (gross laxity) and functional (giving way) instability. The patient may present with undiagnosed secondary sources of pain, and these must be sought (see the box on “Differential Diagnosis”). Chronic intractable pain is another potential complication. 

Potential Treatment Complications Lack of recognition of and the prevalence of subacute sequelae in ankle sprains may lead to under-treatment and subsequent chronic pain or instability. Nonsteroidal antiinflammatory drugs may cause gastric, hepatic, or renal complications. Prolonged immobilization can lead to inflexibility, muscle atrophy, and longer time loss from work or sport. Return to work, sport, or activity before adequate healing and rehabilitation may result in chronic pain and giving way (functional instability) and gross laxity (mechanical instability). As noted, the heat and contrast baths should be avoided during the acute stage of injury, as these modalities could promote swelling and bleeding. Finally, surgical complications could include joint injection, loss of range of motion, and compromised gait.

CHAPTER 83  Ankle Sprain

References 1. Kerr ZY, Collins CL, Fields SK, Comstock RD. Epidemiology of player–player contact injuries among US high school athletes, 20052009. Clin Pediatr (Phila). 2011;50(7):594–603. 2. Waterman BR, Owens BD, Davey S, Zacchilli MA, Belmont PJ Jr. The epidemiology of ankle sprains in the United States. J Bone Joint Surg Am. 2010;92(13):2279–2284. 3. Doherty C, Delahunt E, Caulfield B, Hertel J, Ryan J, Bleakley C. The incidence and prevalence of ankle sprain injury: a systematic review and meta-analysis of prospective epidemiological studies. Sports Med. 2014;44(1):123–140. 4. Nelson AJ, Collins CL, Yard EE, Fields SK, Comstock RD. Ankle injuries among United States high school sports athletes, 2005-2006. J Athl Train. 2007;42(3):381–387. 5. Hootman JM, Dick R, Agel J. Epidemiology of collegiate injuries for 15 sports: summary and recommendations for injury prevention initiatives. J Athl Train. 2007;42(2):311–319. Review. 6. Beynnon BD, Vacek PM, Murphy D, et al. First-time inversion ankle ligament trauma: the effects of sex, level of competition, and sport on incidence of injury. Am J Sports Med. 2005;33:1485–1491. 7. Safran MR, Benedetti RS, Bartolozzi AR 3rd, Mandelbaum BR. Lateral ankle sprains: a comprehensive review. part 1: etiology, pathoanatomy, histopathogenesis, and diagnosis. Med Sci Sports Exerc. 1999;31(suppl 7):S429–S437. 8. Rodriguez-Merchan EC. Chronic ankle instability: diagnosis and treatment. Arch Orthop Trauma Surg. 2012;132(2):211–219. Epub 2011 Nov 5. Review. 9. Tiemstra JD. Update on acute ankle sprains. Am Fam Physician. 2012;85(12):1170–1176. 10. de Noronha M, Refshauge KM, Herbert RD, et al. Do voluntary strength, range of motion, or postural sway predict occurrence of lateral ankle sprain? Br J Sports Med. 2006;40:824–828. 11. Jenkin M, Sitler MR, Kelly JD. Clinical usefulness of the Ottawa Ankle Rules for detecting fractures of the ankle and midfoot. J Athl Train. 2010;45(5):480–482. 12. Bachmann LM, Kolb E, Koller MT, et al. Accuracy of Ottawa ankle rules to exclude fractures of the ankle and mid-foot: systematic review. BMJ. 2003;326:417. 13. Bahr R, Pena F, Shine J, et al. Mechanics of the anterior drawer and talar tilt tests. A cadaveric study of lateral ligament injuries of the ankle. Acta Orthop Scand. 1997;68:435–441. 14. Phisitkul P, Chaichankul C, Sripongsai R, Prasitdamrong I, Tengtrakulcharoen P, Suarchawaratana S. Accuracy of anterolateral drawer test in lateral ankle instability: a cadaveric study. Foot Ankle Int. 2009;30(7):690–695. 15. Hertel J, Denegar C, Monroe M, Stokes W. Talocrural and subtalar joint instability after lateral ankle sprain. Med Sci Sports Exerc. 1999;31:1501–1507. 16. Fujii T, Luo ZP, Kitaoka HB, An KN. The manual stress test may not be sufficient to differentiate ankle ligament injuries. Clin Biomech (Bristol, Avon). 2000;15:619–623. 17. Docherty CL, Valovich McLeod TC, Shultz SJ. Postural control deficits in participants with functional ankle instability as measured by the balance error scoring system. Clin J Sport Med. 2006;16:203–208. 18. Ross SE, Guskiewicz KM. Examination of static and dynamic postural stability in individuals with functionally stable and unstable ankles. Clin J Sport Med. 2004;14:332–338. 19. Trojian TH, McKeag DB. Single leg balance test to identify risk of ankle sprains. Br J Sports Med. 2006;40:610–613. 20. Hubbard TJ, Hertel J. Mechanical contributions to chronic lateral ankle instability. Sports Med. 2006;36:263–277. 21. Hubbard TJ, Kaminski TW, Vander Griend RA, Kovaleski JE. Quantitative assessment of mechanical laxity in the functionally unstable ankle. Med Sci Sports Exerc. 2004;36:760–766. 22. Guillodo Y, Varache S, Saraux A. Value of ultrasonography for detecting ligament damage in athletes with chronic ankle instability compared to computed arthrotomography. Foot Ankle Spec. 2010;3(6):331–334.

465

23. Cheng Y, Cai Y, Wang Y. Value of ultrasonography for detecting chronic injury of the lateral ligaments of the ankle joint compared with ultrasonography findings. Br J Radiol. 2014;87(1033):20130406. 24. van den Bekerom MP, Kerkhoffs GM, McCollum GA, Calder JD, van Dijk CN. Management of acute lateral ankle ligament injury in the athlete. Knee Surg Sports Traumatol Arthrosc. 2013;21(6):1390–1395. 25. van den Bekerom MP, Struijs PA, Blankevoort L, Welling L, Van Dijk CN, Kerkhoffs GM. What is the evidence for rest, ice, compression, and elevation therapy in the treatment of ankle sprains in adults? J Athl Train. 2012;47(4):435–443. 26. Kerkhoffs GM, Rowe BH, Assendelft WJ, Kelly K, Struijs PA, van Dijk CN. Immobilisation and functional treatment for acute lateral ankle ligament injuries in adults. Cochrane Database Syst Rev. 2002;(3):CD003762. Review. 27. Bleakley CM, O’Connor SR, Tully MA, et al. Effect of accelerated rehabilitation on function after ankle sprain: randomized controlled trial. BMJ. 2010;340:c1964. 28. Kerkhoffs GM, van den Bekerom M, Elders LA, et al. Diagnosis, treatment and prevention of ankle sprains: an evidence-based clinical guideline. Br J Sports Med. 2012;46(12):854–860. 29. Van Rijn RM, van Ochten J, Luijsterburg PAJ, van Middelkoop M, Koes BW, Bierma-Zeinstra SMA. Effectiveness of additional supervised exercises compared with conventional treatment alone in patients with acute lateral ankle sprains: systematic review. BMJ. 2010;341:c5688. 30. Bahr R, Bahr IA. Incidence of acute volleyball injuries: a prospective cohort study of injury mechanisms and risk factors. Scand J Med Sci Sports. 1997;7:166–171. 31. McKeon PO, Hertel J. Systematic review of postural control and lateral ankle instability, part II: is balance training clinically effective? J Athl Train. 2008;43(3):305–315. 32. Grimm NL, Jacobs JC Jr, Kim J, Amendola A, Shea KG. Ankle injury prevention programs for soccer athletes are protective: a level-I metaanalysis. J Bone Joint Surg Am. 2016;98(17):1436–1443. 33. Beynnon BD, Renstrom PA, Haugh L, et al. A prospective, randomized clinical investigation of the treatment of first-time ankle sprains. Am J Sports Med. 2006;34:1401–1412. 34. Olmsted LC, Vela LI, Denegar CR, Hertel J. Prophylactic ankle taping and bracing: a numbers-needed-to-treat and cost-benefit analysis. J Athl Train. 2004;39:95–100. 35. Raymond J, Nicholson LL, Hiller CE, Refshauge KM. The effect of ankle taping or bracing on proprioception in functional ankle instability: a systematic review and meta-analysis. Med Sci Med Sport. 2012;15(5):386–392. 36. Putnam AR, Bandolin SN, Krabak BJ. Impact of ankle bracing on skill performance in recreational soccer players. PM R. 2012;4(8):574–579. 37. Rowden A, Dominici P, D’Orazio J, Manur R, Deitch K, Simpson S, et al. Double-blind, randomized, placebo-controlled study evaluating the use of platelet-rich plasma therapy (PRP) for acute ankle sprains in the emergency department. J Emerg Med. 2015;49(4):546–551. 38. Petersen W, Rembitzki IV, Koppenburg AG, Ellermann A, Liebau C, Bruggemann GP, et al. Treatment of acute ankle ligament injuries: a systematic review. Arch Orthop Trauma Surg. 2013;133(8):1129–1141. 39. Liu SH, Baker CL. Comparison of lateral ankle ligamentous reconstruction procedures. Am J Sports Med. 1992;20:594–600. 40. Kerkhoffs GM, Handoll HH, de Bie R, Rowe BH, Struijs PA. Surgical versus conservative treatment for acute injuries of the lateral ligament complex of the ankle in adults. Cochrane Database Syst Rev. 2007;(2):CD000380. Review. 41. Chaudhry H, Simunovic N, Petrisor B. Cochrane in CORR (R): surgical versus conservative treatment for acute injuries of the lateral ligament complex of the ankle in adults (review). Clin Orthop Relat Res. 2015;473(1):17–22.

CHAPTER 84

Bunion and Bunionette David Wexler, MD, FRCS (Tr & Orth) Melanie E. Campbell, MS, ATC, RNFA, FNP-C Dawn M. Grosser, MD Todd A. Kile, MD

Synonyms Hallux valgus Lateral deviation of the great toe

ICD-9 Codes 727.1 727.1 735.0

Bunion Bunionette Hallux valgus (acquired)

ICD-10 Codes M20.10 Hallux valgus (acquired), unspecified foot M20.11 Hallux valgus (acquired), right foot M20.12 Hallux valgus (acquired), left foot

Bunion Definition The term bunion stems from the Latin word bunio, which means “turnip,” an image suggestive of an apparent growth or enlargement around the joint. The medical term for this is hallux valgus. There is no similar Latin term for the fifth toe, so a similar process involving the fifth metatarsophalangeal (MTP) joint is called a bunionette. Hallux valgus is a common deformity of the forefoot and the most common deformity of the first MTP, often causing pain (Figs. 84.1 and 84.2). The pathophysiologic process stems from both the proximal phalanx and the metatarsal bone. The proximal phalanx deviates laterally on the head of the first metatarsal, exacerbated by the pull of the adductor hallucis muscle. The lateral capsule becomes contracted, and the medial structures are attenuated. The metatarsal deviates medially, but the underlying sesamoids remain in their relationship to the second metatarsal, thus creating dissociation of the metatarsal-sesamoid complex. As these two processes occur together, the pull of the abductor hallucis 466

moves more plantarward and the pull of the extensor tendon moves laterally, causing pronation and further lateral deviation of the great toe, respectively. As the metatarsal head becomes more uncovered, a prominent medial eminence, or bunion, is apparent. There is a bursa between the metatarsal head and the skin that may become inflamed and painful. Depending on the amount of axial rotation of the first metatarsal and pronation of the toe, the first ray becomes dysfunctional, leading to increased weight bearing on the more lateral metatarsal heads and “transfer metatarsalgia,” causing pain under the plantar aspect of the forefoot.1 The etiology of hallux valgus is multifactorial and can be either intrinsic or extrinsic.2 The intrinsic causes are essentially genetic and are related to hypermobility of the first ray (hallux metatarsal) at its articulation with the medial cuneiform. Ligamentous laxity (e.g., Marfan syndrome, Ehlers-Danlos syndrome) can lead to this deformity as well as to variations in the shape of the metatarsal head (i.e., a rounder head is less stable than a flat one). Another contributing factor is metatarsus primus varus, or medial deviation of the first metatarsal, which is thought to be associated with a juvenile bunion.3 Pes planus and first metatarsal length have also been evaluated for their contribution to hallux valgus, but findings are equivocal.4 The principal extrinsic cause is inappropriate, nonconforming footwear, with abnormal valgus forces creating deformity.5 This is particularly notable in women who wear high-heeled shoes with narrow toe boxes. The ratio of hallux valgus between women and men has been reported to be 15:1.6 

Symptoms Presenting symptoms can vary. The patient may complain only of a painless prominent medial eminence. However, more commonly, there will be pain that is worse when constrictive shoes are worn and relieved by walking barefoot or with open-toed shoes. If there is significant arthritis, patients may have pain throughout range of motion of the MTP joint while walking. The bunion may become red and inflamed as the bursa enlarges and overlying skin becomes abraded by the shoe. The patient will have difficulty finding comfortable shoes. As the hallux deviates into increased valgus, it tends to impinge on the medial aspect of the pulp of the second toe, causing pressure and soreness.7 

CHAPTER 84  Bunion and Bunionette

467

Bunion

FIG. 84.3  Standing anteroposterior radiograph of both feet in a patient with bilateral hallux valgus. This is more pronounced on the left. Note also the lateral deviation of the sesamoid bones.

FIG. 84.1  Anatomy of a bunion.

metatarsal heads—may also be seen even without a callus. Passive extension of the hallux MTP joint will reveal possible limitation of range of motion (normally approximately 70 degrees). This may indicate concomitant degenerative joint disease of the MTP joint. Mobility of the hallux at the first metatarsal medial cuneiform joint is assessed in relation to the second ray. Hammertoes are commonly noted as a consequence of the crowding in the shoe by the great toe. Depending on the patient’s medical history (e.g., diabetes), the neuromuscular evaluation is important to assess for any vibratory loss, two-point discrimination loss, or other indications of neurologic compromise. Otherwise, the neurologic examination findings should be normal. 

Functional Limitations Limitations are principally in walking long distances and wearing shoes with a narrow toe box or high heels for prolonged periods. As hallux valgus progresses, arthritis may become a component and lead to stiffness and pain with any activity (biking, hiking, walking short distances, or even standing). 

Diagnostic Studies

FIG. 84.2  Clinical photograph demonstrating a bunion or hallux valgus deformity. Note also the pronation of the digit.

Physical Examination There is generally an obvious medial enlargement overlying the metatarsal head, with occasional signs of inflammation (bursitis). The great toe will be laterally deviated, and with progression of deformity, it will be pronated (axially rotated). There may be splaying of the forefoot and callosities visible under the metatarsal heads of the lesser toes. Metatarsalgia—tenderness under the

Weight-bearing plain radiographs will provide most of the necessary information. The anteroposterior view (Fig. 84.3) demonstrates the angle (Fig. 84.4) between the first and second metatarsals (intermetatarsal angle). The congruency of the first MTP joint can also be assessed for any evidence of arthritis. These all have a bearing on any proposed surgery.8,9  Differential Diagnosis Gout Hallux rigidus Rheumatoid arthritis Infection

468

PART 1  MSK Disorders

first MTP joint and strengthening of the intrinsic muscles of the foot, which may improve symptoms, as well as focus on gait training.11 Distraction techniques like varus stretching or toe spacers may also be useful.  Hallux valgus angle (normal 1 inch) small-gauge needles should be avoided because long, thin needles can easily bend once they are inserted into the muscle, and the tip can inadvertently puncture the pleura. Rather, short (101°F (>38.3°C); • abnormal cervical or vaginal mucopurulent discharge; • presence of abundant numbers of WBC on saline microscopy of vaginal fluid; • elevated erythrocyte sedimentation rate; • elevated C-reactive protein; and • laboratory documentation of cervical infection with Neisseria gonorrhoeae or Chlamydia trachomatis.10 

Gastrointestinal: Irritable Bowel Syndrome Irritable bowel syndrome is a common functional bowel disorder of uncertain etiology characterized by a chronic, relapsing pattern of abdominopelvic pain and altered bowel habits in the absence of an organic cause. Although not all patients with this disorder seek treatment, the estimated prevalence is 14.1% in North America with about only 3.3% diagnosed medically.11 The abdominal and pelvic pain is usually crampy in nature and varies in location, often exacerbated by emotional stress and eating habits and relieved by defecation. The Rome III criteria are used to diagnose irritable bowel syndrome, and patients must have two of the following: pain relieved with defecation; onset of pain associated with a change in frequency of stool; or onset associated with a change in form (appearance) of stool.12 

Gynecologic: Endometriosis, Uterine Leiomyomas, and Adenomyosis Endometriosis is a common gynecologic condition affecting women of reproductive age. It is characterized by the presence of endometrial tissue that is found outside of the uterus. It often affects the ovaries, fallopian tubes, ureter, peritoneum, bowel, bladder, and in rare cases the lungs, cesarean section scars, appendectomy scars, and episiotomies.13 The extrauterine endometrial implants respond to the hormonal stimuli in the same way as intrauterine endometrium does, causing cyclic bleeding in the sensitive tissues of the peritoneum, ovaries, fallopian tubes, and elsewhere. This process can lead to formation of pelvic adhesions, scar tissue, and endometriomas. This disorder is found in 10% to 15% of women of reproductive age, in 25% to 40% of women undergoing treatment for infertility, and noted in 33% of women who have undergone laparoscopy for CPP. Risk factors include early menarche, short menstrual cycles (C8 pattern of motor axon involvement. Other common motor complaints include progressive inability to use the hand and loss of dexterity. Sensory complaints are relatively minor; most patients have long history of intermittent aching and paresthesias in a lower plexus (particularly T1) distribution.6 In contrast, disputed neurogenic thoracic outlet syndrome most commonly presents with pain and paresthesias. It may involve the lower plexus or upper plexus. The associated sensori­ motor abnormalities have a C8 and/or T1 distribution for the lower plexus type, and C5 and/or C6 distribution for the upper plexus type.15 Coldness, easy fatigability, ischemia of a finger or a hand, and pallor on elevation are considered to be symptoms of arterial origin. Swelling, discoloration, and a heavy feeling in the hand are considered to be symptoms of venous origin. Swelling, hyperesthesia, discoloration, and a feeling of alternate cold and warm could also be signs of complex regional pain syndrome. Traumatic thoracic outlet syndrome commonly presents with pain at the trauma site, frequently radiating into the upper extremity in the medial cord distribution. Traction on the stellate ganglion has also been considered a possible cause of pain in these patients.12 In general, in the absence of peripheral emboli, most “vascular symptoms” or “Raynaud phenomena” probably result from irritation of the sympathetic nerves rather than from compression of the subclavian artery in the thoracic outlet. A common feature of the symptoms is their intermittence and provocation by use of the arm above shoulder level. Aggravation of the symptoms often occurs after rather than during exercise. 

Physical Examination The diagnosis of thoracic outlet syndrome is a clinical one based on a detailed history and physical examination. Many of these patients have some psychological complaints, and a thorough clinical examination including a logical explanation for the symptoms will often reduce the psychic burden. The physical examination starts with an inspection of the neck, shoulders, and upper extremities. Color, muscle

CHAPTER 116  Thoracic Outlet Syndrome

atrophy, edema, temperature, and nails are examined. This requires the patient to be examined with the shirt off. The cervical spine is then examined to exclude symptoms of cervical origin caused by a cervical disc or spondylarthrotic intervertebral foramen. A typical pain radiculation in C5 to C8 distribution indicates that a nerve root irritation is present. A local distribution of pain with neck extension indicates a facet joint problem. A neurologic examination is performed to include sensory testing, muscle strength testing (C5-C8), and reflexes. Tinel sign is tested to exclude carpal tunnel syndrome. Palpation of the median, ulnar, and radial nerves from the axilla to the hand may reveal tenderness. Almost all clinical tests used in the examination of the patient with thoracic outlet syndrome aim to provoke the symptoms felt by the patient, presuming that the compressing structure may be provoked to irritate the neurovascular bundle in the area of the thoracic outlet during the test. These maneuvers are unreliable in general.16 A clinical test in extensive use is the Adson test.17 With the patient sitting, hands resting on the thighs, both radial pulses are simultaneously palpated. During forced inspiration, hyperextension of the neck, and turning of the head to the affected side, the radial pulse is palpated for obliteration, and auscultation is done for supraclavicular bruit. The test has changed during the years. In 1927, when Adson described his test, the vascular changes were considered to be pathognomonic of thoracic outlet syndrome. Later, neurologic changes occurred more frequently than vascular ones, and these can be detected better when the head is rotated to the contralateral rather than the ipsilateral side, as initially described. Radial pulse obliteration or subclavian bruit is found in 69% of normal patients.18 All studies clearly indicate that pulse obliteration with the arm and head in various positions is a normal finding and has no relation to thoracic outlet syndrome. In the hyperabduction test, symptoms are reproduced by hyperabduction of the arm. However, more than 80% of normal individuals experience obliteration of the radial pulse during this test.19 In the exaggerated military maneuver, also called Eden test, symptoms are reproduced by pulling back the acromioclavicular joint in an exaggerated military “attention” position. The neurovascular structures could be compressed between the first rib and the clavicle, without any anatomic predisposing factors. This maneuver is also referred to as the costoclavicular test. Arterial compression is found in 60% of asymptomatic individuals by this test. In the abduction-external rotation test, also called Roos test or elevated arm stress test (EAST), the hands are in the “stick up” position and are then repeatedly opened and closed for 3 minutes. Roos10 considered the symptoms to be due to both arterial and brachial plexus compression and referred to this procedure as a claudication test; he was later convinced that thoracic outlet syndrome was neurologic rather than vascular in origin but claimed that the EAST procedure was the most reliable procedure. Roos has also claimed that the EAST procedure has great specificity, with a positive result in thoracic outlet syndrome but generally negative results in carpal tunnel syndrome and cervical radiculopathy. However, in a

635

controlled study, it was found that the EAST procedure is an excellent test for carpal tunnel syndrome; the result is positive in 92% of patients with carpal tunnel syndrome and in 74% of normal controls.20 Positional compression during these tests is a common phenomenon in normal subjects, and diminishing of the pulse in Adson test, the costoclavicular maneuver, and the hyperabduction test is considered to be a normal finding rather than a pathologic one. None of these tests unequivocally establishes the presence or absence of thoracic outlet syndrome. Ribbe and colleagues21 used a “thoracic outlet syndrome index” to establish the diagnosis of thoracic outlet syndrome. According to these authors, a patient with thoracic outlet syndrome should have at least three of the following four symptoms or signs: 1. A history of aggravation of symptoms with the arm in the elevated position 2. A history of paresthesia in the segments C8-T1 3. Tenderness over the brachial plexus supraclavicularly 4. A positive “hands-up” (abduction-external rotation) test result Because all of these provocative maneuvers are unreliable, one should examine the function of the thoracic upper aperture. The function of the upper thoracic aperture should be analyzed with the cervical rotation-lateral flexion test.22 The test is carried out as follows. The neutrally positioned cervical spine is first passively and maximally rotated away from the side being examined and then, in this position, gently flexed as far as possible, moving the ear toward the chest. This is done in both directions. A restriction blocking the lateral flexion part of the movement indicates a positive test result; a free movement indicates a negative test result (Fig. 116.3). This test indicates an abnormal function of the upper thoracic aperture. The test is indicative of a subluxation of the first rib at the costotransverse joint. The test has been used to identify patients who did not gain from surgery23 as well as in a 2-year follow-up study after conservative treatment.24 In the surgery series,23 it was hypothesized that the remaining stump of the first rib was subluxated and that is why the symptoms persisted after surgery. The importance of the length of the remaining stump has also been stressed by other authors.25,26 It is mandatory to analyze the function of the upper thoracic aperture and not rely only on provocative maneuvers that may lead to unnecessary surgical interventions. 

Functional Limitations The patients with symptoms of thoracic outlet syndrome have difficulty in working over the horizontal level, such as cleaning windows and putting up draperies. Static work, such as working with a keyboard, may be difficult because of paresthesias and difficulty in controlling the movements of the arm. Many patients cannot “rely” on the hand. Sleep is disturbed because of pain and tingling after exertion during the day. 

Diagnostic Studies Radiologic examination in the thoracic outlet syndrome can detect cervical ribs, bone anomalies of the first or

636

PART 2 Pain

A

B

FIG. 116.3  The performance of the cervical rotation-lateral flexion test. (A) The head is rotated away from the side to be examined. (B) In this position, the neck is tilted forward, bringing the ear toward the chest. If this movement is restricted, the test result is considered positive and is indicative of a malfunction of the first rib. A normal free movement indicates a negative test result. (Reproduced with permission of Kustannus Oy Duodecim.)

second ribs, a prominent C7 transverse process, tumors, or the “droopy shoulder” syndrome. The incidence of arterial compression of clinical significance is extremely low, and less invasive Doppler ultrasound (duplex) has generally replaced conventional more invasive arteriography. Duplex may detect vessel narrowing, occlusion, arterial thrombosis, or poststenotic aneurysms.27 Computed tomography (CT) angiography generates a more detailed assessment of the vascular abnormalities. When these procedures demonstrate reduced arterial blood flows, they are confirmatory. The evaluation of venous thoracic outlet syndrome is established by clinical and imaging features. Venous ultrasound (with color duplex imaging) is the study of choice. CT and CT venography are used when ultrasound is unrevealing, but they are associated with radiation exposure and bone-related image degradation. Contrast-enhanced magnetic resonance imaging with magnetic resonance venography is the most helpful study to define the extent and chronicity of the thrombosis.28 The diagnosis of traumatic neurovascular thoracic outlet syndrome is relatively straightforward. Chest radiographs and axial views of the clavicle identify the fracture and vascular Doppler imaging delineates the vascular abnormalities. Nerve involvement is better identified by electrodiagnostic testing performed after day 21.14 The major studies used to diagnose true neurogenic thoracic outlet syndrome are electrodiagnostic testing and radiologic imaging. The characteristic electrodiagnostic features in true neurogenic thoracic outlet syndrome reflect a chronic axon loss process that affects the lower portion of the brachial plexus and disproportionately involves the T1 more than the C8 sensory and motor fibers.14 The appropriate evaluation for disputed thoracic outlet syndrome includes electrodiagnostic testing to rule out true neurogenic origin and imaging studies to identify any anatomical abnormalities. When vascular features suggest arterial, venous, or traumatic thoracic outlet syndrome, vascular imaging studies are necessary. 

Differential Diagnosis Advanced carpal tunnel syndrome C8, T1 radiculopathy Multiple sclerosis Syringomyelia Glenohumeral instability Tumors of the cervical spine Pancoast tumor Myofascial pain syndrome in the cervical region Trapezius strain Elbow and forearm overuse injuries Acromioclavicular joint injury Shoulder impingement syndrome

Treatment Initial After the thorough clinical examination and detailed history, what the examining physician suspects to be the origin of the symptoms must be explained to the patient. Good pain management, not only using pain medications but also taking into account sleeping hygiene, is important. A multiprofessional team should be consulted so that all therapy modalities are taken into account. This includes physiatrists, physiotherapists, occupational therapists, social workers, and psychologists; also, there must be a possibility to consult specialists in neurology and psychiatry, thoracic surgeons, and neurosurgeons. The optimal treatment regimen for venous thoracic outlet syndrome must be individualized. When venous thoracic outlet syndrome is suspected, treatment includes anticoagulation and symptom resolution (bed rest, limb elevation, warm compresses, and analgesics). Thrombolysis is performed after the diagnosis is confirmed, and it is most successful when started within 1 week of presentation.29 Surgical decompression is usually reserved for patients with hypercoagulable disorders with a compressive lesion.30 Long-term anticoagulation is started following decompressive surgery.

CHAPTER 116  Thoracic Outlet Syndrome

A

637

B

FIG. 116.4  Normal function of the first ribs and the upper aperture can be achieved by activation of the scalene muscles by the patient. (A) The patient first activates the anterior scalene muscles by pressing the forehead against the palm, with the cervical spine being all the time in a neutral position. (B) The middle scalene muscles are activated by pressing sidewards against the palm. The exercises are done five or six times for a duration of 5 seconds each and with about 15 seconds between the exercises. The exercises are done on both sides. (Reproduced with permission of Kustannus Oy Duodecim.)

The appropriate management for traumatic thoracic outlet syndrome is dictated by lesion severity and the specific vascular, clavicular, and nerve injuries. The vascular injuries usually require immediate surgical intervention. With incomplete nerve injury, conservative treatment is indicated, which includes neuropathic pain medication and appropriate braces.31 Physical therapy focuses on range of motion and stretching; strengthening is also employed. Disputed thoracic outlet syndrome should be considered a cervicoscapular pain syndrome and is best managed conservatively.31 Physical therapy should identify the patient’s postural abnormalities and muscle imbalance, educate the patient regarding proper postures, and initiate a stretching program targeting the pathologically shortened muscles. 

Rehabilitation The best outcome in the case of patients with all forms of thoracic outlet syndrome requires involvement of specialists in rehabilitation medicine, orthopedics, vascular surgery, and physical therapists. Chandra et al.32 studied 41 competitive athletes suffering thoracic outlet syndrome who went through a mandatory thoracic outlet syndromespecific physical therapy designed to mimic relaxation of the thoracic outlet; surgery was offered to those who exhibited modest improvement after thoracic outlet syndrome-specific physical therapy. They found thoracic outlet syndrome-specific physical therapy and ultimately surgery both resulted in an 81% likelihood of return to sport. Nine patients who had symptoms for shorter periods (less than

3 months) continued with physical therapy; seven of those nine patients (78%) were able to return to their sport, even though they had not undergone surgery. The authors also found the continued improvement in symptoms with time after surgery with postoperative conditioning and strengthening therapy. Thompson et al.33 reported 13 established Major League Baseball (MLB) pitchers underwent an operation and 10.8 ± 1.5 months of postoperative physical therapy for neurogenic thoracic outlet syndrome. Ten of the 13 pitchers (77%) returned to MLB. The authors believed that thoracic outlet decompression coupled with an ample period of postoperative rehabilitation can provide effective treatment for professional athletes with careers threatened by neurogenic thoracic outlet syndrome. The exercises that aim to activate the anterior, middle, and posterior scalene muscles are the most important part (Fig. 116.4). These exercises have been shown to correct any malfunction of the first ribs, thus normalizing the function of the upper thoracic aperture and enabling normal movement of the first ribs. Stretching of the muscles of the shoulder girdle involves the upper part of the trapezius muscles, the sternocleidomastoid muscles, the levator scapulae, and the small pectoral muscle. Strengthening exercises for the anterior serratus muscle should be included, thus enhancing the stability of the scapula. Nerve gliding exercises are used to restore the mobility of the nerves. It is mandatory that physiotherapists, psychologists, occupational therapists, and social workers be consulted during the whole process. The patients should be observed for a long time because relapses are common.

638

PART 2 Pain

If symptoms persist despite restored function, the differential diagnosis should be reviewed. The fact that conservative treatment is tedious and relapses are common should not be considered a reason for surgical intervention. Surgery is a viable option only if there are signs of significant motor loss, atrophy, or vascular thrombosis. Psychosocial aspects should always be taken into account. It is important to evaluate the degree of disability that thoracic outlet syndrome symptoms cause in relation to the patient’s life situation and psychosocial abilities. There is a link between the workplace and the individual in the pathogenesis and course of thoracic outlet syndrome. The role of occupational factors must be considered, and it is therefore important to assess the workplace. 

Procedures Kim et al.34 compared the effect of steroid injection and daily exercise program for 2 weeks among patients with suspected neurogenic thoracic outlet syndrome on clinical examination without abnormalities in the electrodiagnostic test. Twenty patients received 0.5 mL of 20 mg triamcinolone injection into each belly of the anterior and middle scalene muscles under ultrasound guidance; another 20 patients were taught to do daily self-exercise comprising stretching to alleviate muscle spasm and tightness, and to avoid a posture that might aggravate the symptoms. Changes of paresthesia using visual analog scale (VAS) scores revealed a significant decrease of VAS after treatment compared with baseline in both groups. VAS was reduced by 90% (18 of 20) after injection, and 25% (5 of 20) after stretching exercise. 

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

Surgery True neurogenic thoracic outlet syndrome is always treated surgically with band sectioning and the C7 bony anomaly removal via supraclavicular approach.31 Patients suffering from arterial thoracic outlet syndrome who present with acute arterial compromise must be treated to restore distal arterial flow. Surgical decompression of the vessel and removal of the responsible compressive structure was first performed in the 1800s. Surgical repair is required when an aneurysm is identified. Bypass procedure to restore blood flow is indicated when a thrombosed aneurysm or artery is noted. Supraclavicular approach is used when subclavian artery reconstruction is required.8,27 Botulinum chemodenervation of the scalene muscles has been found useful in alleviating symptoms in patients with thoracic outlet syndrome, especially if they are waiting for definitive surgical decompression. However, a randomized trial showed that chemodenervation did not result in clinically or statistically significant improvement in pain, paresthesias, or function in a population with thoracic outlet syndrome.35 

Potential Disease Complications It is very important to detect those patients with post-traumatic thoracic outlet syndrome. These may present with worsening of the symptoms, such as a decrease in muscle strength, increase of pain, and tingling in the radicular territory, as well as unspecific disturbances such as dizziness and face pain. In the case of these patients, one must consider surgical options.36 It has been said that true neurogenic thoracic outlet syndrome is rare. Over-diagnosis of this syndrome results from a failure to realize that a wide range of symptoms occur regularly in patients with advanced carpal tunnel syndrome or C8, T1 radiculopathies and that these are commonly outside the anatomic distribution of the median nerve. The failure to recognize this can reinforce abnormal behavior in patients, particularly when they are subjected to unnecessary brachial plexus or ulnar nerve surgery undertaken without neurophysiologic identification of an appropriate neurogenic abnormality.37 If they are not dealt with correctly, these patients will suffer for long periods with more than one symptom. These may include muscle atrophy, swelling in the supraclavicular fossa, abnormal posture, and tendency to faint with certain movements. The leading symptom is numbness and clumsiness of the hand, but pain in the occiput-shoulder area is an important symptom too.38 These may worsen without proper therapy. 

Potential Treatment Complications Surgery for thoracic outlet syndrome is not as innocuous as it was once thought. Dale39 found that more than half of those who reported performing the surgery had encountered brachial plexus injuries severe enough to produce clinical weakness, nearly one fifth of which were permanent. Large numbers of failed thoracic outlet syndrome surgeries have been reported during the last decades. Brachial plexus lesions, infections, and cases of life-threatening hemorrhage have been published. Even deaths have been reported. Franklin and colleagues40 reported that 60% of workers were still work disabled 1 year after thoracic outlet syndrome decompression surgery.

References 1. Klaassen Z, Sorenson E, Tubbs RS, et al. Thoracic outlet syndrome: a neurological and vascular disorders. Clin Anat. 2014;27:724–732. 2. Kuhn JE, Lebus VGF, Bible JE. Thoracic outlet syndrome. J Am Acad Orthop Surg. 2015;23:222–232. 3. Moore R, Wei LY. Thoracic outlet syndrome. Vasc Med. 2015;20: 182–189. 4. Lindblad B, Tengborn L, Bergqvist D. Deep vein thrombosis of the axillary-subclavian veins: epidemiology data, effects of different types of treatment and late sequelae. Eur J Vasc Surg. 1988;2:161–165. 5. Mall NA, Van Thiel GS, Heard WM, et al. Paget-Schroetter syndrome: a review of effort thrombosis of the upper extremity from a sports medicine prospective. Am J Sports Med. 2012;5:353–356. 6. Ferrante MA. The thoracic outlet syndrome. Muscle Nerve. 2012;45: 780–795. 7. Wilbourn AJ. The most commonly asked questions about thoracic outlet syndrome. Neurologist. 2001;7:309–312. 8. Daniels B, Michaud L, Sease F Jr, et al. Arterial thoracic outlet syndrome. Curr Sports Med Rep. 2014;13:75–80. 9. Della SD, Naraka A, Bonnard C. Late lesions of the brachial plexus after fracture of the clavicle. Ann Hand Surg. 1991;10:531–540. 10. Roos DB. Historical perspectives and anatomic considerations. Semin Thorac Cardiovasc Surg. 1996;8:183–189.

CHAPTER 116  Thoracic Outlet Syndrome

11. Chang KZ, Likes K, Davis K, et al. The significance of cervical ribs in thoracic outlet syndrome. J Vasc Surg. 2013;57:771–775. 12. Schulman J. Brachial neuralgia. Arch Phys Med Rehabil. 1949;30:150–153. 13. Lindgren KA, Leino E. Subluxation of the first rib: a possible thoracic outlet syndrome mechanism. Arch Phys Med Rehabil. 1988;69:692–695. 14. Tsao BE, Ferrente MA, Wilbourn AJ, et al. Electrodiagnostic features of true neurogenic thoracic outlet syndrome. Muscle Nerve. 2014;49:724–727. 15. Leffert RD. Thoracic outlet syndrome. J Am Acad Orthop Surg. 1994;2: 317–325. 16. Nord KM, Kapoor P, Fisher J, et al. False positive rate of thoracic outlet syndrome diagnostic maneuvers. Electromyogr Clin Neurophysiol. 2008;48:67–74. 17. Adson AW, Coffey JR. Cervical rib: a method of anterior approach for relief of symptoms by division of the scalenus anticus. Ann Surg. 1927;85:839–857. 18. Gilroy J, Meyer JS. Compression of the subclavian artery as a cause of ischaemic brachial neuropathy. Brain. 1963;86:733–746. 19. Wright IS. The neurovascular syndrome produced by hyperabduction of the arms. Am Heart J. 1945;29:1–29. 20. Costigan DA, Wilbourn AJ. The elevated arm stress test: specificity in the diagnosis of the thoracic outlet syndrome. Neurology. 1985;35(suppl 1):74–75. 21. Ribbe E, Lindgren S, Norgren L. Clinical diagnosis of thoracic outlet syndrome—evaluation of patients with cervicobrachial symptoms. Man Med. 1986;2:82–85. 22. Lindgren KA, Leino E, Manninen H. Cervical rotation lateral flexion test in brachialgia. Arch Phys Med Rehabil. 1992;73:735–737. 23. Lindgren KA. Reasons for failures in the surgical treatment of thoracic outlet syndrome. Muscle Nerve. 1995;18:1484–1486. 24. Lindgren KA. Conservative treatment of thoracic outlet syndrome: a 2-year follow-up. Arch Phys Med Rehabil. 1997;78:373–378. 25. Geven LI, Smit AJ, Ebels T. Vascular thoracic outlet syndrome. Longer posterior rib stump causes poor outcome. Eur J Cardiothorac Surg. 2006;30:232–236. 26. Mingoli A, Sapienza P, di Marzo L, et al. Role of first rib stump length in recurrent neurogenic thoracic outlet syndrome. Am J Surg. 2005;190:156.

639

27. Aljabri B, Al-Omran M. Surgical management of vascular thoracic outlet syndrome: BA teaching hospital experience. Ann Vasc Dis. 2013;6:74–79. 28. Demodion X, Bacqueville E, Paul C, et al. Thoracic outlet: assessment with MRI imaging in asymptomatic and symptomatic populations. Radiology. 2003;227(2):461–468. 29. Divi V, Proctor MC, Axelrod DA, et al. Thoracic outlet decompression for subclavian vein obstruction: experience in 71 patients. Arch Surg. 2005;140:54–57. 30. Guzzo JL, Chang K, Desmos J, et al. Preoperative thrombolysis and venoplasty affords no benefit in patency following first rib resection and scalenectomy for subacute and chronic subclavian vein thrombosis. J Vasc Surg. 2010;52:658–662. 31. Wilbourn AJ. Thoracic outlet syndrome. Neurol Clin. 1999;17:477–497. 32. Chandra V, little C, Leii JT. Thoracic outlet syndrome in high performance athletes. J Vasc Surg. 2014;60(4):1012–1018. 33. Thompson RW, Dawkins C, Vemuri C, et al. Performance metric in professional baseball pitchers before and after surgical treatment for neurogenic thoracic outlet syndrome. Ann Vasc Surg. 2017;39:216–227. 34. Kim YW, Yoon SY, Park YB, et al. Comparison between steroid injection and stretching exercise on the scalene of patients with upper extremity paresthesia: randomized cross-over study. Yonsei Med J. 2016;57(2):490–495. 35. Finlayson HC, O’Connor RJ, Brasher PM, et al. Botulinum toxin injection for management of thoracic outlet syndrome: a double-blind, randomized, controlled trial. Pain. 2011;152:2023–2028. 36. Alexandre A, Coro L, Azuelos A, et al. Thoracic outlet syndrome due to hyperextension-hyperflexion cervical injury. Acta Neurochir Suppl. 2005;92:21–24. 37. Burke D. Symptoms of thoracic outlet syndrome in women with carpal tunnel syndrome. Clin Neurophysiol. 2006;117:930–931. 38. Muizelaar JP, Zwienenberg-Lee M. When it is not cervical radiculopathy: thoracic outlet syndrome—a prospective study on diagnosis and treatment. Clin Neurosurg. 2005;52:243–249. 39. Dale WA. Thoracic outlet compression syndrome. Critique in 1982. Arch Surg. 1982;117:1437–1445. 40. Franklin GM, Fulton-Kehoe D, Bradley C, et al. Outcome of surgery for thoracic outlet syndrome in Washington state workers’ compensation. Neurology. 2000;54:1252–1257.

CHAPTER 117

Tietze Syndrome Joseph A. Hanak, MD

Synonyms Parasternal chondrodynia Costochondral junction syndrome Thoracochondralgia Chondropathia tuberosa Costal chondritis

ICD-10 Code M94.0 Chondrocostal junction syndrome (Tietze)

Recurrent functional overloading or microtrauma to the costal cartilages from severe coughing, heavy manual work, and sudden movement of the rib cage as well as malnutrition, sprain of the intra-articular sternocostal ligament, and respiratory tract infections may influence the development of Tietze syndrome.2,5,6,8–10,13,16 Costal swelling may be due to focal enlargement,4,7 ventral angulation or irregular calcification of the affected costal cartilage,4,21 and thickening of overlying muscle.21,22 Tietze syndrome may mimic a variety of life-threatening clinical entities4,6,16 and must be considered in the differential diagnosis of any painful mass in the parasternal area. Clinical awareness of this syndrome and of its benign course may minimize performance of invasive diagnostic procedures.14 

Symptoms Definition Tietze syndrome is a benign, non-suppurative inflammatory localized painful swelling of the upper costal cartilages, a self-limited condition of unknown etiology.1–11 It affects the costochondral, costosternal, or sternoclavicular joints.2,5–7,9 The manubriosternal and xiphisternal joints are less frequently affected.5,10 First described in 1921 by German surgeon Alexander Tietze in Breslau, it is different from the costosternal syndrome.5–13 Tietze syndrome is a rare cause of benign anterior chest wall pain associated with local swelling of the involved costal cartilages (Fig. 117.1).5,6,13 It is different from costochondritis, in that its prevalence is rare, there is local swelling, the second and third junctions are most commonly affected, it occurs more frequently in the younger population, and is usually unilateral and only at one site. It is typically described in young adults and is a disease of the second and third decades of life.10,13 Although it is not common, Tietze syndrome may also appear in children, infants,10,14 and elderly people.15 It affects both men and women in a 1:1 ratio.4–6,9,10,16 Lesions are unilateral and single in more than 80% of patients,4,10 and the second and third costal cartilages are most commonly involved.1,4,6,9–13 Costosternal syndrome (see Chapter 101) is different from Tietze syndrome, is also a frequent cause of benign anterior chest wall pain, and is not associated with a local swelling of the involved costal cartilages.5–13 Costosternal syndrome usually occurs during and after the fourth decade of life, more frequently in women in a rate of 2 to 3:1.9,10 Multiple costal cartilages are involved in 90% of patients with costosternal syndrome.5,9,10 Chest pain is experienced by 20% to 40% of the general population at some point during their lifetime.17–20 The pathogenesis of Tietze syndrome is unknown.1–4,6,8–10 640

Clinical manifestations include the sudden or gradual onset of pain of variable intensity3,4,10,16 in the upper anterior chest wall in association with a fusiform and tender swelling of the involved costal cartilage.4,16 Despite descriptions that pain may radiate to the shoulder, arm, and neck,3,4,13 its distribution usually occurs within the segment innervated by the afferent fibers carrying the painful impulse.2 It is often aggravated by motion of the thoracic wall, sneezing, coughing, deep breathing, bending, exertion,1–8,16 and lying prone or over the affected side.10 Some patients report inability to find a comfortable position in bed and have pain on turning over in the bed.1 Weather change, anxiety, worry, and fatigue may exacerbate the pain.4 Symptoms are usually unilateral with no preferential side,3 but was found to be present often on the patient’s dominant side in a case series.23 There is no reported association with sternotomy. Common primary aggravating factors reported were any activity that caused heavy breathing and/or end-range horizontal abduction and adduction of the shoulder.23 Clinicians evaluating patients with chest pain should have a high suspicion for cardiac etiology, and symptoms such as shortness of breath, chest pressure, and nausea/vomiting should be documented and expeditiously evaluated to rule out life-threatening conditions. 

Physical Examination On physical examination, a slight firm swelling is noted at the involved site.1–4,16 Systemic manifestations4,6,10,14,16 and inflammation are usually absent,1,4,5,7,10,16 but there may be local heat.16 Pain is reproduced with active protraction or retraction of the shoulder, deep inspiration, and elevation of the arm (Fig. 117.2).13 A unique

CHAPTER 117  Tietze Syndrome

FIG. 117.1  Schematic representation of the area of Tietze syndrome (costal cartilage, costosternal and costochondral joints) and anatomic relations with the mediastinal structures and other anterior chest wall structures.

641

Pectoralis minor muscle Sternum

Costal Pectoralis cartilage major muscle

Functional Limitations The disability produced by Tietze syndrome is usually minor, although it can be severe, with activity restriction involving the trunk and upper limbs. Activities such as lifting, bathing, ironing, combing and brushing hair, and other activities of daily living can be problematic. Patients who have physically vigorous jobs may need to be put on light duty for weeks and avoid physical efforts of the upper limbs and trunk.1 Functional limitations may also be due to chronic pain24; however, even of those patients who continue to have pain after 1 year, most lead a life without disability. It has been shown that the biomechanics of the thoracic vertebrae and rib cage are interdependent, which assists with directed interventions to these regions.23  FIG. 117.2  Reproduction of the spontaneous pain complaint during arm elevation in a patient diagnosed with Tietze syndrome.

visible, spherical, non-suppurative tender tumor of elastic-hard and pasty consistency can be palpated, usually over the second and third costochondral joints. Local palpation with firm pressure over the localized tender swelling reproduces the spontaneous pain complaint (Fig. 117.3).13 Physical examination findings of the musculoskeletal and neurologic systems of reported cases from the literature are usually normal except for the local findings.4–6,14,16,22 Muscle strength and upper limb range of motion may be decreased because of pain. Dermatomal and subcutaneous hyperalgesia (Fig. 117.4) and hyperemia (Fig. 117.5) may be present in the involved thoracic spinal segments. The adjacent intercostal,13 sternal, and pectoralis major and minor muscles may be tender to palpation.15 Patients can have increased tightness and/or guarding in the pectoralis major/minor and upper trapezius muscle, with greater tone on the involved side.23 

Diagnostic Studies Diagnosis of Tietze syndrome is essentially made on a clinical basis: anterior chest wall pain confirmed by palpation of a tender swelling at the second or third costochondral junction that reproduces the patient’s complaint in the absence of another definite diagnosis.3–5,7–9,12,16 Results of laboratory analysis, including inflammatory and immunologic parameters, are usually normal.4–9,16 Some cases may show a slight increase in the erythrocyte sedimentation rate.7,14,16 Chest, rib, and sternum plain films and conventional tomograms of the costochondral junction are generally normal.6,21,24 Plain radiographs may show cartilage enlargement on tangential views, chondral calcification, irregularities at the joint surface, osteosclerosis, and presence of osteophytes at the costal joint. However, these radiographic changes may also be found in physiologic costochondral calcifications.25 Plain radiographs are therefore mainly indicated to rule out occult bone diseases including tumors, low-grade infections, tender fat or lipomas, chest wall contusion, and congenital deformity.4,13,21 Tuberculosis, chondroma, and chondrosarcoma are mostly located at the costochondral junction.21

642

PART 2 Pain

FIG. 117.3 Local palpation with firm pressure over the localized tender swelling reproduces the spontaneous pain complaint.

FIG. 117.4 Subcutaneous hyperalgesia during the pinch and roll maneuver at the thoracic level.

FIG. 117.6  Comparison of the ultrasonographic findings of the affected costochondral joint (left) and the nonaffected contralateral joint (right) in an 82-year-old woman diagnosed with Tietze syndrome. The affected costochondral joint appears with a discrete increased size and as a nonhomogeneous hyperechoic cartilage with dotty, hyperreflective echoes and broad posterior acoustic shadows. (Courtesy Marcelo Bordalo Rodrigues.)

FIG. 117.5  Hyperemia localized at the involved thoracic spinal segments after the pinch and roll maneuver.

Ultrasonographic findings of the affected costochondral joints are characterized by an increase of the size of the affected costal cartilage compared with the contralateral symmetric joint and normal age- and gender-matched controls (Fig. 117.6).26 There is also a nonhomogeneous increase in the echogenicity in the diseased cartilage, with dotty, hyperreflective echoes and intense broad posterior acoustic shadow.26 The normal ultrasonographic picture of the costal cartilage (Fig. 117.7) is manifested as a hypoechoic oval area with the absence of posterior acoustic

CHAPTER 117  Tietze Syndrome

Sternum Costal arch

643

in the subchondral bone; and intense gadolinium uptake in the areas of thickened cartilage, in the subchondral bone marrow, or in capsule and ligaments.32 Magnetic resonance imaging is also indicated if an occult mass is suspected.9,13 Magnetic resonance imaging allows differentiation of cartilage and bone abnormalities. The histopathologic characteristics of costal cartilage in Tietze syndrome are usually normal16 or nonspecific.3,6,7,16 These characteristics include increased vascularity and degenerative changes with patchy loss of ground substance leading to a fibrillar appearance.6,28,29 Degenerative changes occur with the formation of clefts, which may undergo calcification.1,28,33  Differential Diagnosis

FIG. 117.7  Normal ultrasonographic appearance of the costal cartilage. The normal costal cartilage appears as the homogeneous hypoechoic oval area between the sternum and the costal arch. (Courtesy Marcelo Bordalo Rodrigues.)

shadows in the longitudinal scans, and it appears as a ribbonshaped homogeneous hypoechogenicity in the transverse scan with no posterior acoustic shadowing. Computed tomography of the chest is an effective noninvasive means of imaging costal cartilage and adjacent structures in patients with Tietze syndrome.22,26,27 Costal cartilage is normally symmetric in size and orientation at any level and is normally oriented along the horizontal axis.22 Cartilage density is uniform and greater than that of the overlying muscle but less than calcium density. Reported computed tomographic abnormalities of patients with Tietze syndrome include focal enlargement of the involved costal cartilage,6,22,27 ventral angulations,6,14,15,27 swelling or irregular calcification of the affected costal cartilage,22,27 perichondral soft tissue swelling, and periarticular bone sclerosis.5,28 Computed tomography scan is useful to exclude other possible causes of chest wall or thoracic mass,6 such as malignant lymphoma22,29 and mediastinal carcinoma.30 Fluorodeoxyglucose-positron emission tomography can also be used in the differential diagnosis with malignant neoplasms.31 Asymmetric thickening of the pectoralis major muscle simulating a chest wall mass can also be excluded.21 Planar bone scanning with technetium Tc 99 usually reveals intense tracer uptake, but the findings are not specific.4,6,16,25,28 Bone scintigraphy allows the precise localization of the involved joint6 and the delineation of the number of involved joints; it should be considered to rule out occult fractures of the ribs and sternum in cases of local trauma.13 Pinhole skeletal scintigraphy seems to enhance diagnostic specificity, and this is able to show a characteristic appearance of a drumstick-like pattern in acute cases and a C- or inverted C-shaped uptake in the chronically affected costal cartilage.25 Magnetic resonance imaging of the costosternal and sternoclavicular joints usually shows thickening at the site of complaint; focal or widespread increased signal intensities of affected cartilage on both T2-weighted and short T1 inversion recovery or fat-saturated images; bone marrow edema

ANTERIOR CHEST WALL PAIN OF LOCAL ORIGIN Costosternal syndrome Trauma: dislocation and fractures of the ribs, sternum, clavicle, costal cartilage, costochondral, or sternoclavicular joint Arthritis: osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, Reiter syndrome, psoriatic arthritis, SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, osteitis), gout Infection: osteomyelitis, low-grade infection of the costal cartilage (tuberculosis, syphilis, typhoid and paratyphoid infections, blastomycosis, actinomycosis, brucellosis) Tumors of the costochondral cartilages Benign: chondroma, multiple exostoses, lipomas Malignant neoplasms: Hodgkin and non-Hodgkin lymphoma,34 metastatic bone diseases (carcinoma of breast, lung, thyroid, kidney, or prostate), multiple myeloma, plasmacytoma, thymoma, chondrosarcoma Myofascial pain syndrome at the anterior chest wall: sternal, pectoralis major, pectoralis minor, scalene, sternocleidomastoid (sternal head), subclavius, iliocostalis cervicis muscles Other: slipping rib syndrome, condensing osteitis of the clavicle, congenital sternoclavicular malformations, xiphoidalgia syndrome, T1-T12 radiculopathy, intercostal neuritis (postherpetic neuralgia)  ANTERIOR CHEST WALL PAIN OF VISCERAL ORIGIN Cardiac: myocardial infarction, angina pectoris, stenocardia Pulmonary: pneumonia, pulmonary embolism, pleurisy, lung abscess, atelectasis, spontaneous pneumothorax Breast: cyclic breast pain, duct ectasia, breast carcinoma Abdominal: peptic duodenal ulcer, epigastric hernia, gastritis or pancreatitis, acute cholecystitis, diffuse peritonitis

Treatment Initial Treatment is symptomatic because the pathogenesis of the disease is still unclear.3,4,6,15,16 The natural history of patients diagnosed with true Tietze syndrome is, in general, good and benign because of the self-limited characteristic of the condition. In the majority of cases, pain disappears spontaneously within a few weeks and swelling in a few months16 without treatment.9 Symptoms may be exacerbated after manual work and severe cough. During this period, the use of an elastic rib belt may also provide symptomatic relief and help protect the costosternal joints from additional trauma.9,13 Initial treatment of the pain and functional disability associated with Tietze syndrome should

644

PART 2 Pain

include simple oral analgesics such as acetaminophen, oral or topical nonsteroidal anti-inflammatory drugs (NSAIDs) alone6,9,12,15 or in combination with codeine5,8,9,16 or tramadol. Although the use of opiates is described in the literature, it is important to prescribe them with caution as there is the potential for addiction and the risk may outweigh the benefit. Tricyclic antidepressants are helpful in reducing reports of pain in patients with chest pain and normal coronary arteries.35 Reassurance about the benign nature of the disorder and the diagnosis of a non–life-threatening but real and wellrecognized musculoskeletal pain disease can often by itself reduce the anxiety and fears and lead to symptomatic pain relief.2–5,8–12,16,35 Avoidance of iatrogenic worries is usually helpful.35 Removal of aggravating and perpetuating factors (including physical efforts of the upper limbs and trunk, chronic cough, and bronchospasm) and improved nutrition are also important.1,5,8,9,15 In one report, human calcitonin was given for a course of 1 month to five women diagnosed with Tietze syndrome who had intense pain not relieved by conventional treatment.36 Three patients reported complete remission of symptoms and imaging findings, and symptoms improved in two patients with disappearance of pain. At this time, only a single research trial exists that supports stretching as an intervention using the visual analog scale for an outcome.23,37 

Rehabilitation Physical modalities including local superficial heat for 20 minutes, two or three times a day, and ice for 10 to 15 minutes, three or four times a day, can be performed until symptoms are improved.3,13,15 Heat and cold are equally effective, and the choice of modality relies on the patient’s preference and tolerance. Transcutaneous electrical nerve stimulation and electroacupuncture may be applied over the painful area.15 Gentle, pain-free range of motion exercises should be introduced as soon as tolerated.13 Vigorous exercises should be avoided if they exacerbate the patient’s symptoms.13 Proper posture during sitting or working activities should be restored.5,8,9 Inactivation of associated pectoralis major trigger points followed by relaxation and stretching exercises with relaxation of the involved muscles may also be helpful. Stretching exercises of the pectoralis major muscle, such as the standing pushup in the corner for 10 seconds, repeated for 1 or 2 minutes several times a day, may be helpful.8,37 Vapocoolant spray applied to the involved areas may also relieve chest wall pain.8 Patients should be instructed to avoid improper posture or repetitive misuse of chest wall muscles.8 Psychological and psychopharmacologic treatment should be considered for patients with continuing symptoms and disability, especially if these are associated with abnormal health beliefs, depressed mood, panic attacks, or other symptoms such as fatigue or palpitations.35 Both cognitive-behavioral therapy and selective reuptake inhibitors have been shown to be effective.36 Manual therapy and thoracic flexion/extension selfmobilization timed with breathing as well as thoracic flexion/extension with unilateral rotation self-mobilization timed with breathing have been beneficial treatments.23 

Procedures Most patients respond to NSAIDs, heat, and activity modification. Electroacupuncture may be applied by introducing the acupuncture disposable needle over the skin points of lower electrical skin resistance that are located within the involved spinal segments. Galvanic or faradic low-frequency electrical currents are applied at the inserted needle.15 Administration of corticosteroids by iontophoresis may provide more prolonged pain relief.12 For patients who do not respond to the initial and rehabilitation treatment modalities, local anesthetic2,4,6 and steroid injection can be performed as the next symptom control maneuver.2,5,6,8,9,12,13,16,26 Injection of the costal cartilage is performed by placing the patient in the supine position.13,26 Proper preparation with antiseptic solution of the skin overlying the affected costal cartilage is carried out with isopropyl alcohol and soluble iodine solution to swab the injection site.26 The exact position for injection is identified by clinical and ultrasonographic examination.26 The injection site is the point of maximum tenderness by palpation or the point of maximum cartilaginous hypertrophy by ultrasonographic examination. A refrigerant spray may be used to anesthetize the overlying skin before the needle is inserted. There should be limited resistance to injection. If significant resistance is found, the needle should be withdrawn slightly and repositioned until the injection proceeds with only limited resistance. This procedure should be repeated for each affected joint. After the needle is removed, a sterile pressure dressing and ice pack are placed at the injection site. Local steroid injections associated with local anesthetics have shown good therapeutic results. There is an average of 82% decrease in the size of the affected costal cartilage 1 week after the local anesthetic and steroid injection, and the posterior acoustic shadowing is absent.26 Clinical examination of the injected patients detected complete resolution and substantial improvement of signs and symptoms of pain and swelling. This shows a strong correlation between clinical changes and ultrasonographic findings in patients with Tietze syndrome. An intercostal nerve block performed 1.5 to 2 inches proximal to the costochondral joint of the affected level provides even longer lasting pain relief and is indicated if other measures are not effective.12 Prolotherapy was compared to conservative treatment, was shown to be performed safely and is a method with a favorable long-term treatment for Tietze syndrome. It may be the ideal procedure for patients with drug side effects and adverse events, especially for those with limited liver and kidney reserve or significant comorbidities.38 

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

Surgery Surgical procedures are rarely necessary and indicated only if the symptomatic conservative measures fail to alleviate symptoms. Surgical excision of the localized involved cartilage can be performed in severe and refractory cases.9 Costosternal or

CHAPTER 117  Tietze Syndrome

sternoclavicular arthrodesis may be performed if conservative measures fail to provide satisfactory results. 

Potential Disease Complications Tietze syndrome is a benign condition and rarely presents complications. It is self-limited with spontaneous recovery of the pain after a few weeks or several months1,3,4,16 to 1 year in the majority of cases. Swelling may persist for months16 to years.4 The course of this condition is characterized by periods of recurrence and improvement.1,3,4,15 

Potential Treatment Complications The systemic complications of NSAIDs are well known and most commonly affect the gastric, hepatic, and renal systems. The major complication of the local steroid combined with local anesthetic injections is pneumothorax if the needle is placed too laterally or deeply and invades the pleural space.13 Cardiac tamponade as well as an iatrogenic infection, although rare, can occur if, respectively, the needle is placed in the direction of the heart and strict aseptic techniques are not performed. The possibility of trauma to the contents of the mediastinum remains another possibility. This complication can be greatly decreased if the clinician pays close attention to accurate needle placement or performs the injection with ultrasound guidance.26

References 1. Geddes AK. Tietze’s syndrome. Can Med Assoc J. 1945;53:571–573. 2. Wehrmacher WH. The painful anterior chest wall syndromes. Med Clin North Am. 1958;38:111–118. 3. Kayser HL. Tietze’s syndrome: a review of the literature. Am J Med. 1956;21:982–989. 4. Levey GS, Calabro JJ. Tietze’s syndrome: report of two cases and review of the literature. Arthritis Rheum. 1962;5:261–269. 5. Fam AG, Smythe HA. Musculoskeletal chest wall pain. CMAJ. 1985;133:379–389. 6. Boehme MW, Scherbaum WA, Pfeiffer EF. Tietze’s syndrome—a chameleon under the thoracic abdominal pain syndrome. Klin Wochenschr. 1988;66:1142–1145. 7. Jurik AG, Graudal H. Sternocostal joint swelling—clinical Tietze’s syndrome. Report of sixteen cases and review of the literature. Scand J Rheumatol. 1988;17:33–42. 8. Semble EL, Wise CM. Chest pain: a rheumatologists perspective. South Med J. 1988;81:64–68. 9. Aeschlimann A, Kahn MF. Tietze’s syndrome: a critical review. Clin Exp Rheumatol. 1990;8:407–412. 10. Bonica JJ, Sola AF. Chest pain caused by other disorders. In: Bonica JJ, ed. The Management of Pain. II. Philadelphia: Lea & Febiger; 1990:1114–1145. 11. Fam AC. Approach to musculoskeletal chest wall pain. Prim Care. 1988;15(4):767–782. 12. Jensen S. Musculoskeletal causes of chest pain. Austral Fam Physician. 2001;30:834–839.

645

13. Waldman SD. Tietze’s syndrome. In: Waldman SD, ed. Atlas of Common Pain Syndromes. Philadelphia: WB Saunders; 2002:158–160. 14. Mukamel M, Kornreich L, Horev G, et al. Tietze’s syndrome in children and infants (clinical and laboratory observations). J Pediatr. 1997;131:774–775. 15. Imamura ST, Imamura M. Síndrome de Tietze. In: Cossermelli W, ed. Terapêutica Em Reumatologia. São Paulo: Lemos Editorial. 2000:773–777. 16. Hiramuro-Shoji F, Wirth MA, Rockwood CA. Atraumatic conditions of the sternoclavicular joint. J Shoulder Elbow Surg. 2003;12:79–88. 17. Brattberg G, Parker MG, Thorslund M. A longitudinal study of pain; reported pain from middle age to old age. Clin J Pain. 1997;3:144–149. 18. Eslick GD, Jones MP, Talley NJ. Non-cardiac chest pain: prevalence, risk factors, impact and consulting—a population-based study. Aliment Pharmacol Ther. 2003;17:1115–1124. 19. Lock GR 3rd, Talley NJ, Fett SLL, et al. Prevalence and clinical spectrum of gastroesophageal reflux: a population-based study in Olmsted County, Minnesota. Gastroenterology. 1997;112:1448–1456. 20. Moran B, Bryan S, Farrar T, et al. Diagnostic evaluation of nontraumatic chest pain in athletes. Curr Sports Med Rep. 2017;16(2):84-94. 21. Jurik AG, Justesen T, Graudal H. Radiographic findings in patients with clinical Tietze syndrome. Skeletal Radiol. 1987;16:517–523. 22. Edelstein G, Levitt RG, Slaker DP, et al. Computed tomography of Tietze syndrome. J Comput Assist Tomogr. 1984;8:20–23. 23. Zaruba RA, Wilson E. Impairment based examination and treatment of costochondritis: a case series. Int J Sports Phys Ther. 2017;12(3):458–467. 24. Mayou RA, Bass C, Hart G, et al. Can clinical assessment of chest pain be made more therapeutic? Q J Med. 2000;93:805–811. 25. Yang W, Bahk YW, Chung SK, et al. Pinhole skeletal scintigraphic manifestations of Tietze’s disease. Eur J Nucl Med. 1994;21:947–952. 26. Kamel M, Kotob H. Ultrasonographic assessment of local steroid injection in Tietze’s syndrome. Br J Rheumatol. 1997;36:547–550. 27. Edelstein G, Levitt RG, Slaker DP, et al. CT observation of rib anomalies: spectrum of findings. J Comput Assist Tomogr. 1985;9:65–72. 28. Honda N, Machida K, Mamiya T, et al. Scintigraphic and CT findings of Tietze’s syndrome: report of a case and review of the literature. Clin Nucl Med. 1989;14:606–609. 29. Fioravanti A, Tofi C, Volterrani L, et al. Malignant lymphoma mimicking Tietze’s syndrome. Arthritis Rheum. 2002;47:229–230. 30. Thongngarm T, Lemos LB, Lawhon N, et al. Malignant tumor with chest wall pain mimicking Tietze’s syndrome. Clin Rheumatol. 2001;20:276–278. 31. Mathew AS, El-Haddad G, Lilien DL, Takalkar AM. Costosternal chondrodynia simulating recurrent breast cancer unveiled by FDG PET. Clin Nucl Med. 2008;33:330–332. 32. Volterrani L, Mazzei MA, Giordano N, et al. Magnetic resonance imaging in Tietze’s syndrome. Clin Exp Rheumatol. 2008;26:848–853. 33. Cameron HU, Fornasier VL. Tietze’s syndrome. J Clin Pathol. 1974;27:960–962. 34. Jeon IH, Jeong WJ, Yi JH, et al. Non-Hodgkin’s lymphoma at the medial clavicular head mimicking Tietze syndrome. Rheumatol Int. 2012;32:2531–2534. 35. Bass C, Mayou R. ABC of psychological medicine. Chest pain. BMJ. 2002;325:588–591. 36. Ricevuti G. Effects of human calcitonin on pain in the treatment of Tietze’s syndrome. Clin Ther. 1985;7:669–673. 37. Rovetta G, Sessarego P, Monteforte P. Stretching exercises for costochondritis pain. G Ital Med Lav Ergon. 2009;31:169–171. 38. Senturk E, Sahin E, Serter S. Prolotherapy: an effective therapy for Tietze syndrome. J Back Musculoskelet Rehabil. 2017;30:975-978.

CHAPTER 118

Trigeminal Neuralgia Sasha E. Knowlton, MD

Synonyms Tic douloureux Cranial neuralgia Facial pain Facial neuralgia Trifacial neuralgia

ICD-10 Code G50.0

Trigeminal neuralgia, tic douloureux, trifacial neuralgia, syndrome of paroxysmal facial pain

Definition Trigeminal neuralgia is defined as pain in the distribution of at least one of the fifth cranial nerve distributions, usually occurring in the maxillary or mandibular branches.1–3 Pain associated with trigeminal neuralgia can last for a variable amount of time and frequency and between attacks, patients are usually pain-free.1 Triggers for a pain attack, also known as a paroxysm, can include eating, brushing the teeth, light touch to the face, or talking.1,2 Trigeminal neuralgia is a relatively rare disorder and in one systematic review, the prevalence was 0.03% to 0.3%.3 Older investigation determined the overall incidence of trigeminal neuralgia to be 4.3 per 100,000 people with a slightly higher rate for women (5.9/100,000) than men (3.4/100,000).4 Women are generally more likely affected than men, with most cases occurring in individuals 40 years or older.3,4 The trigeminal nerve is the largest cranial nerve and originates in the brainstem with one motor nucleus and three sensory nuclei.5 There are three divisions of the fifth cranial nerve, known as the ophthalmic (V1), maxillary (V2), and mandibular (V3) branches. The three branches of the trigeminal nerve form from the trigeminal, or Gasserian, ganglion.5 At the root entry zone where central myelin changes to peripheral myelin, the trigeminal nerve is thought to be susceptible to vascular compression, resulting in trigeminal neuralgia.5  646

Symptoms Trigeminal neuralgia is a painful unilateral condition occurring in one of the three branch distributions of the trigeminal nerve. The pain is paroxysmal with sudden onset and termination of pain episodes.1,6 The episodes can be brief, lasting only a few seconds, or can last up to 2 minutes and are stabbing, sharp, shooting, and electric shock in quality.1,6 The pain episodes can be induced by mechanical stimuli such as a light touch or a breeze or by movements such as smiling or applying makeup.1,2,6 The symptoms may be accompanied by trigger zones, weight loss, poor quality of life or depression, and may lessen with improving sleep hygiene.7 Occasionally patients may have ongoing background pain or autonomic features such as congestion or lacrimation.2 Red flags for trigeminal neuralgia that constitute a further in-depth workup include deafness, optic neuritis, age less than 40, a family history of multiple sclerosis, a history of skin or oral lesions, sensory changes, or poor response to treatment.2 If these symptoms are present, a primary process may be the etiology and a diagnostic workup should be performed. 

Physical Examination Diagnosing trigeminal neuralgia is based primarily on symptom description. In cases of primary trigeminal neuralgia, the physical and neurologic examinations usually do not reveal any abnormalities.7 However, a full neurologic examination, including the cranial nerves, should be performed in order to rule out secondary causes of trigeminal neuralgia such as a tumor or multiple sclerosis.2,7 Additionally, physical examination of the oral cavity, dentition, and trigeminal nerve distribution should be performed to rule out other diseases as well, which can present with secondary trigeminal neuralgia.2 

Functional Limitations In general, there are no impairments associated with trigeminal neuralgia. However, the pain from this entity may result in significant limitation in several activities of daily living. For example, during exacerbations, patients may be functionally incapacitated because of pain and may be unable to perform activities such as combing their hair, chewing food, or shaving.7 Talking on the telephone may be painful and

CHAPTER 118  Trigeminal Neuralgia

wearing glasses or makeup may not be possible. Essentially any activity that involves contact with the face may become difficult or impossible. 

Diagnostic Studies The International Headache Society has defined diagnostic criteria for trigeminal neuralgia, which include (1) the presence of three or more attacks of unilateral facial pain that (2) occur in a division of the trigeminal nerve with no radiation outside of the trigeminal nerve distribution and (3) the pain has to have at least three of the following characteristics: recurring paroxysmal attacks lasting a fraction of a second to 2 minutes; severe intensity; electric shocklike, shooting, stabbing or sharp in quality; precipitated by innocuous stimuli and not occurring as the result of another disorder.8,9 Practitioners should possess a low threshold to perform imaging of the brain in suspected cases of trigeminal neuralgia.10 Patients should undergo a brain magnetic resonance imaging (MRI) with and without contrast if they are younger, have abnormal “red flag” symptoms, or if they do not respond to standard medication treatment.2,10 MRI with gadolinium has sensitivity in demonstrating multiple sclerosis and enhancement of the trigeminal nerve in addition to identifying masses or lesions in the intracranial and extracranial areas along the trigeminal nerve pathway.2 While MRI may be able to detect vascular compression of the trigeminal nerve in the setting of primary trigeminal neuralgia, this study is not typically indicated.2 Neurophysiologic testing of the trigeminal reflex has been proposed as a reliable test for the diagnosis of trigeminal neuralgia.9,11 Additional studies that may aid in the diagnosis of trigeminal neuralgia may be other radiographs such as intraoral x-rays when the trigeminal neuralgia is suspected to be secondary to another cause.10 

Treatment Initial Trigeminal neuralgia is generally treatable with pharmacotherapy, procedures, or surgical treatment. However, it can progress to become a chronic intractable pain syndrome in refractory cases. Carbamazepine and oxcarbazepine are typically used as the first-line agents to treat trigeminal neuralgia.9 Older studies demonstrated the effectiveness of carbamazepine in treating the pain of trigeminal neuralgia in the short and long term.12,13 Carbamazepine has been recommended as the initial drug of choice for trigeminal neuralgia, but is associated with Stevens-Johnson syndrome and other potentially serious side effects.1,12 Although carbamazepine can reduce the frequency and intensity of painful episodes, oxcarbazepine has a more favorable side effect profile.9,14 Oxcarbazepine is a derivative of carbamazepine and can effectively treat trigeminal neuralgia.15 Appropriate monitoring of labs should be performed when prescribing these medications. In cases where carbamazepine or oxcarbazepine are ineffective, not tolerated, or contraindicated, clinicians can try other medications. However, there is less research in this area.14 Alternative medications to try in trigeminal neuralgia

647

include baclofen (which can be useful in cases of multiple sclerosis), gabapentin, or lamotrigine; evaluation of the risks and benefits of each medication should be performed on a case-by-case basis.1,14 Overall, evidence is lacking for the routine use of baclofen, gabapentin, and lamotrigine in the treatment of trigeminal neuralgia.14 A recent Cochrane review determined there to be insufficient evidence to demonstrate that non-antiepileptic medications such as tizanidine are effective in treating trigeminal neuralgia.16 Pharmacologic therapy with nonsteroidal anti-inflammatory agents, acetaminophen, tricyclic antidepressants, and serotonin-norepinephrine reuptake inhibitors may be useful. Other suggested drugs with very limited investigation include phenytoin, clonazepam, valproate, topiramate, and intravenous lidocaine.17 One study showed that intranasal lidocaine administered by a metered-dose spray produced acute but temporary analgesia in patients with second-division trigeminal neuralgia.18 

Rehabilitation Trigeminal neuralgia can be approached from a rehabilitative perspective by classifying it as a type of neuropathic pain. Modalities such as hot and cold packs, electric stimulation such as transcutaneous electric nerve stimulation, and neurostimulation techniques such as transcranial magnetic stimulation can be trialed in trigeminal neuralgia.19 Speech therapy may be indicated to help with oral motor deficits that affect speech or swallowing. As part of the rehabilitation program, the use of cognitive behavioral therapy, relaxation therapy, and increasing exercise can be trialed to assist with neuropathic pain management.19 Adaptive equipment, such as a modified telephone earset, may be recommended to avoid triggering a paroxysm. General chronic pain rehabilitation approaches may also be useful, such as improved sleep hygiene, low-intensity aerobic exercise, biofeedback, cognitive-behavioral therapy, and relaxation techniques. Acupuncture may also have a role in the management of trigeminal neuralgia.19,20 Rehabilitation programs may need to be adjusted pending response to medication, nonsurgical, or surgical procedures. If pain recurs, medications may need to be restarted, a procedure may need to be repeated, or a different treatment strategy may need to be conducted. If trigeminal neuralgia is secondary to an underlying disease or disorder, treating the primary pathology is important to address from the medical and rehabilitative standpoints. 

Procedures When medical management does not adequately provide pain control for trigeminal neuralgia, patients should be referred for procedural consultation.1,7 There are a number of procedures and surgical techniques that have been investigated to date to treat medically refractory pain associated with trigeminal neuralgia. The selection of a particular intervention should be performed on a case-by-case basis, which includes patient preference, high-risk elderly patients, or prior failed treatments.2,7,10,21 Percutaneous neurosurgical techniques, such as radiofrequency thermocoagulation, balloon compression, or glycerol injection into the trigeminal cistern provide immediate

648

PART 2 Pain

but short-duration pain relief with typically excellent initial response rates.1,9,10,21 Patients can experience side effects from these procedures, including facial numbness, masseter weakness, pain, dysesthesias, trigeminal and other cranial nerve dysfunction, and vagal instability in addition to carotid injury and intracranial infection.1,9,10,21 Radiofrequency thermocoagulation targets the trigeminal nerve and root, resulting in destruction of pain-mediating fibers under fluoroscopic guidance, and has improved results when used conventionally compared to a pulsed manner; overall, there is significant initial pain relief post-procedure, though the pain can recur.9,21,22 Balloon compression, which is also performed under fluoroscopic guidance, causes compression of the affected ganglion and has a decompression-like effect post-procedure; while there is significant pain relief immediately, there is no standardization of the procedure.9,21 Glycerol gangliolysis under fluoroscopy results in trigeminal neuronal destruction with significant pain relief post-procedure, and patients often experience sensory changes during the procedure.9,21 

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

Surgery Microvascular decompression aims to relieve the trigeminal nerve from vascular compression, often from the superior cerebellar artery, anterior inferior cerebellar artery, or the superior petrosal veins.21 Microvascular decompression may have excellent immediate and long-term pain relief outcomes and by some is considered the “gold standard” surgery for managing trigeminal neuralgia in the appropriate patient population.1,9,10,23 The most common side effect of microvascular decompression is ipsilateral hearing loss.1 Another operative technique in treating trigeminal neuralgia is stereotactic radiosurgery, commonly in the form of Gamma Knife radiosurgery. Gamma Knife radiosurgery uses a focused dose of radiation as an alternative for microvascular decompression and results in significant pain relief.9,21 Gamma Knife radiosurgery using a dose range of 70 to 90 Gy to target the trigeminal nerve is a safe and effective tool for managing trigeminal neuralgia pain in the short and long term.24 Gamma Knife radiosurgery does not have immediate pain-relieving effects and numbness is a common side effect.1,9 While patients may have long-term pain relief, relapse is possible; however, repeat Gamma Knife radiosurgery does provide additional pain relief.25 

Potential Disease Complications Trigeminal neuralgia is treatable with the medications, procedures, and surgeries listed above; however, it can progress to become a chronic intractable pain syndrome. In refractory cases, the treating clinician must consider other diagnoses or facial pain syndromes. 

Potential Treatment Complications All of the medications listed (carbamazepine and oxcarbaze­ pine as first-line agents) are associated with a number of

potential side effects such as Stevens-Johnson syndrome.1,9,12,14 Close laboratory monitoring should be performed, including a complete blood count and chemistry panel on a regular basis. The procedures listed above have adverse effects, as do the surgical interventions; appropriate counseling of patients regarding the risks and benefits of each is important to perform prior to treatment.1,9,10,21,22

References 1. Zakrzewska JM, Linskey ME. Summaries of BMJ clinical evidence: trigeminal neuralgia. BMJ. 2015;350:h1238. 2. Zakrzewska JM, Linskey ME. Clinical review: trigeminal neuralgia. BMJ. 2014;348:g474. 3. Porto de Toledo I, Conti Reus J, Fernandes M, et al. Prevalence of trigeminal neuralgia: a systematic review. JADA. 2016;147(7):570–576. 4. Katusic S, Beard M, Bergstralh E, Kurland LT. Incidence and clinical features of trigeminal neuralgia, Rochester, Minnesota, 1945-1984. Ann Neurol. 1990;27(1):89–95. 5. Woolfall P, Coulthard A. Trigeminal nerve: anatomy and pathology. Br J Radiol. 2001;74:458–467. 6. Cruccu G, Finnerup NB, Jensen TS, et al. Trigeminal neuralgia: new classification and diagnostic grading for practice and research. Neurology. 2016;87:220–228. 7. van Kleef M, van Genderen WE, Narouze S, et al. 1. Trigeminal neuralgia. Pain Practice. 2009;9(4):252–259. 8.  Headache Classification Committee of the International Headache Society (HIS). The International Classification of Headache Disorders, 3rd ed. (beta version). Cephalagia. 2013;33(9):629–808. 9. Montano N, Conforti G, Di Bonaventura RD, et al. Advances in diagnosis and treatment of trigeminal neuralgia. Ther Clin Risk Manag. 2015;11:289–299. 10. Bennetto L, Patel NK, Guller G. Clinical review: trigeminal neuralgia and its management. BMJ. 2007;334:201–205. 11. Cruccu G, Sommer C, Anand P, et al. EFNS guidelines on neuropathic pain assessment: revised 2009. Eur J Neurol. 2010;17:1010–1018. 12. Cambell FG, Graham JG, Zilkha KJ. Clinical trial of carbazepine (Tegretol) in trigeminal neuralgia. J Neurol Neurosurg Psychiat. 1966;29:265–267. 13. Taylor JC, Brauer S, Espir ML. Long-term treatment of trigeminal neuralgia with carbamazepine. Postgrad Med J. 1981;57:16–18. 14. Zakrzewska JM, Linskey ME. Trigeminal neuralgia. BMJ Clin Evid. 2014;2014. pii: 1207. 15. Zakrzewska JM, Patsalos PN. Oxcarbazepine: a new drug in the management of intractable trigeminal neuralgia. J Neurol Neurosurg Psychiatry. 1989;52:472–476. 16. Zhang J, Yang M, Zhou M, He L, Chen N, Zakrzewska JM. Nonantiepileptic drugs for trigeminal neuralgia. Cochrane Database Syst Rev. 2013;(12):CD004029. 17. Sindrup SH, Jensen TS. Pharmacotherapy of trigeminal neuralgia. Clin J Pain. 2002;18:22–27. 18. Kanai A, Suzuki A, Kobayashi M, Hoka S. Intranasal lidocaine 8% spray for second-division trigeminal neuralgia. Br J Anaesth. 2006;97:559–563. 19. Akyuz G, Kenis O. Physical therapy modalities and rehabilitation techniques in the treatment of neuropathic pain. Int J Phys Med Rehabil. 2013;1:4. 20. Zakrzewska J, Linskey M. Trigeminal neuralgia. BMJ Clin Evid. 2009;3:1207. 21. Punyani SR, Jasuja VR. Trigeminal neuralgia: an insight into the current treatment modalities. J Oral Biol Craniofacial Res. 2012;2(3):188–197. 22. Erdine S, Ozyalcin NS, Cimen A, et al. Comparison of pulsed radiofrequency with conventional radiofrequency in the treatment of idiopathic trigeminal neuralgia. Eur J Pain. 2007;11:309–313. 23. Burchiel KJ. Trigeminal neuralgia: new evidence for origins and surgical treatment. Clin Neurosurg. 2016;63(1):52–55. 24. Regis J, Tuleasca C, Resseguier N, et al. Long-term safety and efficacy of gamma knife surgery in classical trigeminal neuralgia: a 497-patient historical cohort study. J Neurosurg. 2016;124:1079–1087. 25. Helis CA, Lucas JT, Bourland JD, et al. Repeat radiosurgery for trigeminal neuralgia. Neurosurgery. 2015;77:755–761.

CHAPTER 119

Upper Limb Amputations Diane W. Braza, MD Jennifer N. Yacub Martin, MD

Synonyms

S68.112

Hand amputations Below-elbow amputations Above-elbow amputations

S68.113 S68.114

ICD-9 Codes 886 886.0 886.1 887 887.0 887.1 887.2 887.3 887.4 887.5 887.6 887.7 905.9 997.60

Traumatic amputation of other finger(s) (complete) (partial) Without mention of complication Amputated finger, complicated Traumatic amputation of arm and hand (complete) (partial) Unilateral, below elbow, without mention of complication Unilateral, below elbow, complicated Unilateral, at or above elbow, without mention of complication Unilateral, at or above elbow, complicated Unilateral, level not specified, without mention of complication Unilateral, level not specified, complicated Bilateral (any level), without mention of complication Bilateral (any level), complicated Late effect of traumatic amputation Amputation stump complication, unspecified

S68.115 S68.116 S68.117 S68.118 S68.119 S68.120 S68.121 S68.122 S68.123

ICD-10 Codes

S68.124

S68.110

S68.125

S68.111

Complete traumatic metacarpophalangeal amputation of right index finger Complete traumatic metacarpophalangeal amputation of left index finger

S68.126 S68.127

Complete traumatic metacarpophalangeal amputation of right middle finger Complete traumatic metacarpophalangeal amputation of left middle finger Complete traumatic metacarpophalangeal amputation of right ring finger Complete traumatic metacarpophalangeal amputation of left ring finger Complete traumatic metacarpophalangeal amputation of right little finger Complete traumatic metacarpophalangeal amputation of left little finger Complete traumatic metacarpophalangeal amputation of other finger Complete traumatic metacarpophalangeal amputation of unspecified finger Partial traumatic metacarpophalangeal amputation of right index finger Partial traumatic metacarpophalangeal amputation of left index finger Partial traumatic metacarpophalangeal amputation of right middle finger Partial traumatic metacarpophalangeal amputation of left middle finger Partial traumatic metacarpophalangeal amputation of right ring finger Partial traumatic metacarpophalangeal amputation of left ring finger Partial traumatic metacarpophalangeal amputation of right little finger Partial traumatic metacarpophalangeal amputation of left little finger 651

652

PART 3 Rehabilitation

S68.128

Partial traumatic metacarpophalangeal amputation of other finger

S68.129

Partial traumatic metacarpophalangeal amputation of unspecified finger Complete traumatic amputation of right shoulder and upper arm, level unspecified Complete traumatic amputation of left shoulder and upper arm, level unspecified Complete traumatic amputation of unspecified shoulder and upper arm, level unspecified Partial traumatic amputation of right shoulder and upper arm, level unspecified Partial traumatic amputation of left shoulder and upper arm, level unspecified Partial traumatic amputation of unspecified shoulder and upper arm, level unspecified Complete traumatic amputation at elbow level, right arm Complete traumatic amputation at elbow level, left arm Complete traumatic amputation at elbow level, unspecified arm Partial traumatic amputation at elbow level, right arm Partial traumatic amputation at elbow level, left arm Partial traumatic amputation at elbow level, unspecified arm Complete traumatic amputation at level between elbow and wrist, right arm Complete traumatic amputation at level between elbow and wrist, left arm Complete traumatic amputation at level between elbow and wrist, unspecified arm Unspecified complication of amputation stump Other injury of unspecified body region Neuroma of amputation stump, unspecified extremity Neuroma of amputation stump, right upper extremity Neuroma of amputation stump, left upper extremity Neuroma of amputation stump, right lower extremity Neuroma of amputation stump, left lower extremity Infection of amputation stump, unspecified extremity

S48.911 S48.912 S48.919 S48.921 S48.922 S48.929 S58.011 S58.012 S58.019 S58.021 S58.022 S58.029 S58.111 S58.122 S58.119 T87.9 T14.8 T87.30 T87.31 T87.32 T87.33 T87.34 T87.40

Z44.9 Z44.011 Z44.012 Z44.019 Z44.021 Z44.022 Z44.029

Encounter for fitting and adjustment of unspecified external prosthetic device Encounter for fitting and adjustment of complete right artificial arm Encounter for fitting and adjustment of complete left artificial arm Encounter for fitting and adjustment of complete artificial unspecified arm Encounter for fitting and adjustment of partial artificial right arm Encounter for fitting and adjustment of partial artificial left arm Encounter for fitting and adjustment of partial artificial unspecified arm

Definition Upper limb amputations are devastating occurrences for individuals, with profound functional and vocational consequences. In the United States, overall, there are approximately 1.7 million people living with a limb loss, or approximately 1 of every 200 people.1 In contrast to lower limb loss, upper extremity amputation is much less frequent, affecting approximately 41,000 persons, or about 3% of the US amputee population.2 The etiologies for limb loss are also different. The primary reason for upper limb loss in adults is trauma; cancer is the next most common cause.2–5 Other causes of upper limb loss include infections, burns, and congenital deformities. Dysvascular disease, a frequent cause of lower limb amputations, is primarily related to diabetes and peripheral arterial diseases; lower extremity dysvacular amputations occur in 45 per 100,000 individuals and disproportionately affect minority individuals.3,4 Dysvascular disease rarely affects the upper limbs. The rates for traumatic amputations have declined over the last four decades,3 probably because of changing work force patterns and greater concerns for industrial occupational safety. Finger amputations are the most common of upper limb amputations and mostly involve single digits. Upper limb amputations from trauma occur at a rate of 3.8 individuals per 100,000; finger amputations are the most common (2.8 per 100,000). Hand amputations from trauma occur at a rate of 0.02 per 100,000.3 Excluding finger amputations, traumatic transradial (forearm) and transhumeral (humerus) are the most common upper limb amputations. In an analysis of the National Trauma database between the years 2000 and 2004, upper limb amputations were more likely to be seen than lower limb amputations in motor vehicle crashes. Motorcyclists and pedestrians were more likely to sustain a lower limb amputation.6 Machinery, power tools (involving saws or blades), explosions, selfinflicted injury, and assaults are among the most common reasons for traumatic upper limb amputations.6 Men are at far greater risk for traumatic amputation than women are, demonstrating about 6.6 times the female rate for minor amputations of the finger and hand.4

CHAPTER 119  Upper Limb Amputations

As a result of wars in Afghanistan and Iraq, the number of catastrophic injuries due to explosive devices has increased.7 Traumatic amputation is the major reason for upper extremity loss in the military.7 As of July 2011, 14% of major limb loss sustained in Operation New Dawn, Operation Iraqi Freedom, and Operation Enduring Freedom involved the upper extremity.6 Between October 1, 2001 and July 30, 2011 there were 225 active military who suffered upper extremity amputations.6 Of those 225, 11 (7%) were isolated bilateral upper extremity amputees.6 Transradial amputations were the most common upper extremity amputation levels (47%) and elbow disarticulations were the least common (2.1%).6 Electrical burn is an uncommon cause of upper extremity amputation. Heating causes coagulative necrosis, and the passage of the electrical current through the tissues causes disruption of cell membranes.8 Limb loss from trauma occurs at a rate of 0.1 per 100,000.3 Limb amputations that result from malignant neoplasms have declined approximately 42% from 1988 to 1996.3 Their rates of occurrence are lower than for trauma, with an upper limb loss rate in 1996 of 0.09 per 100,000.3 These rates of upper limb amputations are lower than the incidence rates of lower limb dysvascular amputations due to diabetes and peripheral arterial diseases, which occur in 45 per 100,000 individuals and disproportionately affect minority individuals.3,7 As of September 2010, there were 1219 major limb and 399 partial limb amputations.6 Rates of prosthetic rejection are high among upper limb amputees.7 Persons sustaining upper limb amputations present complex rehabilitative needs that are ideally best managed in a rehabilitation center with therapists, prosthetists, and physicians possessing specialized knowledge and experience. Proper rehabilitation and a comfortable and functional prosthesis will facilitate functional restoration. Vocational counseling and vocational retraining are vital aspects of any program, as this condition often afflicts young, vocationally productive persons, primarily men. A continuum of care is vital to successful rehabilitation. Patients must be transitioned effectively from the inpatient postsurgical unit, sometimes to an inpatient rehabilitation unit, and always to a long-term outpatient rehabilitation and prosthetic program. 

Symptoms Congenital upper limb amputees may report no specific symptoms except the lack of full upper extremity function. In contrast, traumatic upper limb amputees may describe phantom pain (pain perceived in the missing part of the limb) or phantom sensation (nonpainful perceptions of the missing part of the limb). Discomfort with prosthetic fit or skin breakdown on the residual limb may be reported in prosthetic users. 

Physical Examination Upper limb amputees require a thorough musculoskeletal examination that includes muscle strength testing, sensory testing, and examination of the contralateral limb. Examination of the residual limb should assess for areas of skin breakdown, redness, painful neuroma, and volume changes

653

that could affect prosthetic fit. Persons with traumatic amputations of the upper limb can have brachial plexus injuries or rotator cuff tears that weaken the residual upper limb muscles. Insensate skin can predispose a patient to breakdown at the site of contact with a prosthesis. Joint range of motion should be assessed. In particular, the scapulothoracic motion is important, as protraction of the scapulae provides the force for a dual-control cable system for body-powered prostheses. Reduced elbow or shoulder range of motion from heterotopic ossification, joint capsule contracture, or muscle contracture can impede maximum recovery of function or use of a prosthesis. 

Functional Limitations An upper limb amputee’s functional status depends on the level of amputation. Persons with finger loss (not including the thumb) are quite functional without a prosthesis. Persons with thumb amputations lose the ability to grip large objects as well as fine motor skills that require opposition with another finger. Reconstructive surgery by pollicization with another remaining finger dramatically improves hand function. Transradial and transhumeral amputees lose hand function and have limitations in basic and higher-level activities of daily living, such as dressing. Jang and colleagues9 surveyed upper extremity amputees regarding the impact on activities of daily living. Subjects reported difficulty with complex tasks and either changed jobs or became unemployed. The most common difficulties in daily living were lacing shoes, using scissors, and removing bottle tops.9 Upper limb amputees frequently sustain new vocational limitations that can preclude return to their previous work activities. Most persons can adapt to almost all basic daily activities with use of the intact contralateral hand and upper limb. Prosthetic devices may or may not improve function. Some amputees find upper limb prosthetic devices cumbersome, discarding their use altogether. Datta and colleagues10 found a 73.2% return to work rate after upper limb amputation, although 66.6% had to change jobs. The overall rejection rate of the prosthesis in this study population of predominantly traumatic upper limb amputees was about 34%. The vast majority used the prosthesis primarily for cosmesis; 25% of patients reported that the prosthesis was beneficial for driving, and a small proportion used it for employment and recreational activities. Some amputees require a specialized prosthesis to continue their specific work-related activities. Recreational activities such as golf, tennis, and other sports can often be accomplished with the use of adaptive prosthetic devices designed for these specific purposes. Return after amputation to such enjoyable pursuits can be quite therapeutic. 

Diagnostic Testing No special diagnostic testing is generally required beyond a careful physical examination. If there is weakness of the limb, electrodiagnostic testing may clarify whether a plexopathy is also present. Radiographs may be necessary to evaluate for osteomyelitis, heterotopic ossification, or a bone spur in the distal limb causing poor prosthetic fit. If

654

PART 3 Rehabilitation

myoelectric prostheses are considered, electromyographic signals and voluntary control of key muscles can be tested by a specialized therapist to determine if such control is possible and to train the amputee to independently use these potential control muscles. 

Treatment Initial Management of persons with upper limb amputations involves a continuum of care.3,11–15 This begins with provision of preoperative information when the amputation is elective, as in the case of cancer. The overriding concern in planning the amputation is to save all possible length, particularly the elbow joint. This preserves elbow flexion and prevents the need for a dual-control cable system. The early input of a physiatrist, nurse, and physical or occupational therapist with expertise in this area is highly advantageous. Early involvement of the rehabilitation team can provide helpful information about prosthetic options, the rehabilitation continuum, and what can be expected after amputation (such as phantom sensations). 

Rehabilitation Initial Rehabilitation Care Immediately after amputation, the primary goals are wound healing, edema control, and prevention of contractures and deconditioning. Persons sustaining upper limb amputations due to trauma or cancer generally have normal underlying blood supply, and most surgical sites can readily heal. Edema is prevented by use of a shrinker sock, elastic bandage wrapping with a figure-of-eight technique that provides pressure distally without choking the limb, or a rigid dressing system. In sophisticated centers, immediate postoperative prosthesis fitting in the operating room is implemented. The immediate postoperative prosthesis is placed over the limb after padding of the skin with soft dressings. The immediate postoperative prosthesis accommodates surgical drains yet prevents the formation of edema. Prosthetic components can be attached to the immediate postoperative prosthesis and early training implemented. Postoperative early identification and treatment of adherent scar tissue are important. Scar can form between skin, muscle, and bone. These adherences can cause pain when muscles are contracted or a joint is moved during operation of the prosthesis.16 Amputation of a limb can lead to phantom sensations, telescoping, residual limb pain (RLP), and phantom pain.12 Phantom sensations are very common, defined as nonpainful physical perceptions that occur after a traumatic or surgical amputation. Telescoping is the perception of progressive shortening of the phantom body part resulting in the sensation that the distal part of the limb is becoming more proximal.12 RLP, or stump pain, is pain localized to the residual body part following amputation. Fortunately, disabling phantom pain, described as a painful unpleasant sensation in the distribution of the missing or deafferentated body part, decreases often in frequency, duration, and severity during the first 6 months.12 Despite the many

interventions used for phantom pain, there are no uniformly effective treatments.12–14 Medication, physical therapy, psychologic interventions, and alternative therapies such as acupuncture must be tried in a rational fashion to determine the most effective intervention. Physical modalities such as ultrasound, vibration, transcutaneous electrical nerve stimulation unit, physical manipulation, and massage of the residual limb may provide relief.12 Fitting of a comfortable prosthesis can often help reduce these painful sensations. Case series and one randomized controlled double-blind study have been published supporting the use of botulinum toxin A (BTX-A) in management of residual limb and phantom pain [#25-Intiso 2015]. The case series followed outcomes for up to 3 months and reported. Neuromodulating medications, such as antidepressants and antiepileptics (gabapentin and pregabalin), are frequently used with variable results.12,14 Beta blockers (propranolol and atenolol) have been found to be somewhat effective in treating phantom pain.12 If patients require cardiac or hypertension medications, the choice of a beta blocker may serve two purposes for these amputees with phantom pain. Topical capsaicin is often prescribed for localized pain. For cramping pain or flexor spasticity, baclofen or clonazepam may be effective.12 Opiates may be effective for these problems in the short term when other methods fail to relieve phantom pain.12,14 Most amputees with phantom pain have intermittent severe pain that can be treated with small doses on an as-needed basis of a short-acting opiate, such as oxycodone. For the few patients with severe, unremitting, phantom and RLP, referral to a specialized pain center is suggested. Case series and one randomized controlled double-blind study have been published supporting the use of botulinum toxin A (BTX-A) in management of residual limb and phantom pain.18 The case series followed outcomes for up to 3 months and reported significant relief in pain, reduction in medication use, improved tolerance of prosthetic wear, and no side effects.18 The only randomized, double-blind pilot study included 14 amputees with intractable phantom limb pain (PLP) and RLP. In this study, BTX-A injection was compared to lidocaine/depo medrol. Both groups were injected into the muscles, subcutaneous tissues, and neuroma. Neither injection provided improvement in PLP; however, both resulted in immediate improvements of RLP: P = .002 and P = .06 for BTX-A and lidocaine/depo medrol, respectively; and pain tolerance: P = .01 and P = .07 for BTX-A and lidocaine/depo medrol, respectively. The treatment effect was noted to last for 6 months in both groups and no side effects were observed.17 

Rehabilitative and Prosthetic Management Prevention of contractures in the residual limb and prevention of generalized deconditioning are important goals of early rehabilitation. Any other injuries, as are common in persons sustaining severe trauma, should be identified and rehabilitation efforts directed at their remediation. For body-powered prostheses, scapulothoracic motion provides power through a cable system to operate the prosthesis. Therefore, to optimize function, therapeutic exercise to optimize shoulder range of motion and scapular stabilization is important. Likewise, elbow contractures or shoulder contractures or capsulitis will severely impede maximal

CHAPTER 119  Upper Limb Amputations

prosthetic use, and these problems should be aggressively addressed. Early training in activity of daily living skills should be pursued as well. Therapies should be directed toward amelioration of weakness through exercises or of contractures through active-assisted range of motion exercises and prolonged stretching. A detailed discussion of prosthetic devices is beyond the scope of this chapter, and consultation with a skilled prosthetist and physiatrist is desirable. Prostheses can serve a cosmetic (passive) role or a functional role, or both. In general, there are two types: body-powered and myoelectric devices.3,15 Body-powered prostheses enable an amputee to harness residual body movements to generate controlled movement and force of a terminal device. Body-powered devices are usually less cosmetic and associated with limited range of motion and limited prehensile strength, yet they are less expensive and much more durable. Myoelectric prostheses are controlled by electrical signals generated in muscles from the remaining residual limb or shoulder girdle. Myoelectric prosthetic devices extract signals from remaining muscles under voluntary control to activate and to control drive motors in the prosthesis.18 These devices are expensive, and special prosthetic skills are required to fabricate and to maintain them, but they are generally more cosmetic in appearance and well suited for selected patients. Prosthetic functional outcomes depend on an individual’s goals related to cosmesis, function, and psychological factors.16 Prosthetic prescription should also consider an individual’s level of cognitive functioning and ability to learn to operate a device. Skin breakdown can occur over bone prominences, where there are skin grafts, or where skin is adherent to underlying bone. Alteration of the prosthetic socket and suspension systems or temporary discontinuation of prosthetic use until the skin has healed may be necessary. To meet the needs of military amputees, the Defense Advanced Research Projects Agency (DARPA) has funded development of two advanced upper limb prosthetic solutions. One of the technologies uses neural control; the other, DEKA arm, uses a “strap and go” system that can be controlled by noninvasive means.5 Implementation of advanced technology requires a coordinated approach using multiple members of the rehabilitation team. Success is largely contingent on the availability of highly trained and specialized personnel to fit and train amputees and resources to pay for these services.5 Telemedicine may help overcome some of these barriers. The field of upper extremity prosthetics is changing with the development of implantable neurologic sensing devices and targeted muscle innervation (TMR). Targeted motor reinnervation incorporates the transfer of residual peripheral nerves into muscles in or near the residual limb, with subsequent reinnervation of those muscles. By use of these surface electromyographic signals that relate directly to the original function of the limb, control of the externally powered prosthesis occurs.18 Multidextrous terminal devices may soon be available.16 

Procedures Most procedures related to the care of upper extremity amputees focus on pain management techniques, such as injection of local anesthetic around a painful neuroma,

655

nerve blocks, massage, or chiropractic manipulation. Acupuncture, hypnosis, and biofeedback have also been used in the management of PLP with variable success.14 

Technology To date, the most advanced upper extremity prosthetic devices on the market include: Michelangelo hand, BeBionic hand, i-Digit quantum, i-limb quantum, and i-limb. These prostheses exhibit a variety of features, including individual moving fingers, changing grip strength, and articulating hands. Functional outcomes of prosthetic fitting largely depend on a stable stump-socket connection; therefore, some research efforts have been focused on technologic improvements to this interface by using subcutaneous osseointegration implants.19 The goal of this device is to improve pressure distribution and increase loading surface while maintaining rotational stability. While hopeful in decreasing rejections rates associated with upper limb prosthetics, the use of this device does run a significant risk of infection.6,19 There are currently upper extremity prosthetics that use either implantable neurologic sensing devices or TMR. Targeted motor reinnervation is an invasive procedure that builds on the technology used in myoelectric, in which residual peripheral nerves are used to reinnervate muscles in or near the residual limb.21 For example, the median nerve innervates the hand flexors, so by “reinnervating” the pectoralis major muscle with the median nerve, the prosthetic user is now able to stimulate the “natural” nerve used to close the hand, making prosthetic use more intuitive.7,20 While research has shown these implantations to be successful, they are awaiting clinical trials by the US Food and Drug Administration (FDA). Emerging prosthetic research is investigating the use of brain-computer interface (BCI) technologies. The goal of this technology is to bridge the brain and outside world with the hopes of creating highly dexterous prosthetic limbs or exoskeleton assistive devices.21 Initial studies investigated invasive BCI options that perform activities in a single dimension. While impressive in their performance, invasive options carry the risks associated with surgical procedures and chronic implantation of electrodes in cortical areas. To eliminate these risks, Meng et al. investigated the efficacy of noninvasive electroencephalogram-based BCI. They were able to demonstrate control of a robotic arm to reach and grasp and move objects located in a constrained 3D space using the noninvasive BCI technology. To meet the needs of military amputees, the DARPA has funded development of two advanced upper limb prosthetic solutions. One uses neural control (TMR) and the other uses a “strap and go” system that can be controlled by non-invasive (e.g., foot control) methods.23,5 In 2014, the FDA approved the DARPA-funded Life Under Kinetic Evolution (LUKE) arm, which features vibratory stimulation and pneumatic pressure pads for sensory feedback and is planned to be available to both military and civilian persons in 2017. Specific programs within DARPA include Revolutionizing Prosthetics, Reliable Neural-Interface Technology, and Hand Proprioception and Touch Interfaces. These programs are focused on the development of peripheral and central

656

PART 3 Rehabilitation

nervous system interfaces. These interfaces are focused on developing prostheses that provide tactile and proprioceptive feedback to the user in addition to providing motor commands to the prosthesis. In a 2016 demonstration, DARPA was able to showcase upper extremity prosthetic technology that provided 100% accuracy in sensory feedback from a prosthetic device to a live human. This feedback was provided by the use of four microelectrode arrays implanted into the the motor and sensory cortex of the brain. Further research and development is being done on this project with the hopes of an FDA-approved Hand Proprioception and Touch Interfaces prosthesis system by 2019.2 One of the technologies uses neural control; the other, DEKA arm, uses a “strap and go” system that can be controlled by noninvasive means.5 Implementation of advanced technology requires a coordinated approach using multiple members of the rehabilitation team. Success is largely contingent on the availability of highly trained and specialized personnel to fit and train amputees and resources to pay for these services.5 Telemedicine may help overcome some of these barriers. The field of upper extremity prosthetics is changing with the development of implantable neurologic sensing devices and TMR. Targeted motor reinnervation incorporates the transfer of residual peripheral nerves into muscles in or near the residual limb, with subsequent reinnervation of those muscles. By use of these surface electromyographic signals that relate directly to the original function of the limb, control of the externally powered prosthesis occurs.19 Multidextrous terminal devices may soon be available.17 

Surgery Revision surgeries are sometimes necessary to remove bone spurs that interfere with prosthetic fitting. A well-healed surgical site with good distal soft tissue coverage of the bone end is an optimal result that facilitates prosthetic use. In addition, surgical treatment of adherent scar tissue may be necessary to improve function of a prosthesis. In a study of combat-related upper extremity amputations, 42% underwent revision surgery. The most common indications for revision surgery, in order of decreasing frequency, are heterotopic ossification excision, wound infection, neuroma excision, wound dehiscence, scar revision, and contracture release. In the group that underwent revision surgery, regular prosthesis use increased from 19% before the revision to 87% after it.22 

Potential Disease Complications As a result of the upper limb amputation, RLP, including severe phantom pain, can occur. Joint contractures can develop in the remaining part of the limb, as can frozen shoulder and adhesive capsulitis. This is a particular concern with coexistent peripheral nerve or brachial plexus injury. Self-reported musculoskeletal pain is more frequent in upper limb amputees than in controls, frequently located in the neck, upper back, and shoulder region.23 Depression brought on by the difficulties of adjusting to limb loss is reported. Psychological counseling and support groups incorporating peer support are valuable resources. 

Potential Treatment Complications Surgical complications include postoperative wound infections and postoperative failure of the surgical wounds to heal. Neuroma formation can occur after transection of a nerve. Burying the nerve ending under large soft tissue masses may reduce the likelihood of neuroma irritation. Many medications used in the treatment of phantom pain associated with amputations have potential side effects, including dry mouth, constipation, weight gain, mental cloudiness, cardiovascular effects, and addiction. The side effect profiles vary by the medication class and dosage. Skin breakdown from a poorly fitting prosthesis can occur. This can be aggravated by hyperhidrosis, folliculitis, or poor hygiene. Overuse injuries in the non-amputated limb reportedly are higher than expected in the normal population.10 These include repetitive strain-type injuries due to the individual’s performing certain tasks with poor body posture and ergonomics.24

References 1.  National Limb Loss Information Center. Amputation statistics by cause. Limb loss in the United States. NLLIC fact sheet; 2008. http://www.amputee-coalition.org/fact_sheets/amp_stats_cause.pdf [accessed 07.10.12]. Limb Loss Statistics. Amputee Coalition. http:// www.amputee-coalition.org/resources/limb-loss-statistics/[accessed 03.14.17]. 2. Ziegler-Graham K, MacKenzie EJ, Ephraim PL, et al. Estimating the prevalence of limb loss in the United States: 2005–2050. Arch Phys Med Rehabil. 2008;89:422–429. 3. Dillingham TR, Pezzin LE, MacKenzie EJ. Limb amputation and limb deficiency: epidemiology and recent trends in the United States. South Med J. 2002;95:875–883. 4. Dillingham TR, Pezzin LE, MacKenzie EJ. Racial differences in the incidence of limb loss secondary to peripheral vascular disease: a population-based study. Arch Phys Med Rehabil. 2002;83:1252–1257. 5. Dillingham TR, Pezzin LE, MacKenzie EJ. Incidence, acute care length of stay, and discharge to rehabilitation of traumatic amputee patients: an epidemiologic study. Arch Phys Med Rehabil. 1998;79:279–287. 6. Barmparas G, Inaba K, Teixeira P, et al. Epidemiology of post-­traumatic limb amputation: a national trauma databank analysis. Am Surg. 2010; 76:1214–1222. 7. Resnik L, Meucci MR, Lieberman-Klinger S, et al. Advanced upper limb prosthetic devices: implications for upper limb prosthetic rehabilitation. Arch Phys Med Rehabil. 2012;93:710–717. 8. Tarim A, Ezer A. Electrical burn is still a major risk factor for amputations. Burns. 2013;39:354–357. 9. Jang CH, Yang HE, Yang HE, et al. A survey on activities of daily living and occupations of upper extremity amputees. Ann Rehabil Med. 2011;35:907–921. 10. Datta D, Selvarajah K, Davey N. Functional outcome of patients with proximal upper limb deficiency—acquired and congenital. Clin Rehabil. 2004;18:172–177. 11. Nelson VS, Flood KM, Bryant PR, et al. Limb deficiency and prosthetic management. 1. Decision making in prosthetic prescription and management. Arch Phys Med Rehabil. 2006;87:S3–S9. 12. Bartels K, Cohen SP, Raja SN. Postamputation pain. In: Benzon, Raja, Liu, Fishman, Cohen, eds. Essentials of Pain Medicine, 3rd ed. Elsevier; 2011. 13. Roberts TL, Pasquina PF, Nelson VS, et al. Limb deficiency and prosthetic management. 4. Comorbidities associated with limb loss. Arch Phys Med Rehabil. 2006;87:S21–S27. 14. Hanley MA, Ehde DM, Campbell KM, et al. Self-reported treatments used for lower-limb phantom pain: descriptive findings. Arch Phys Med Rehabil. 2006;87:270–277. 15. Dillingham TR. Rehabilitation of the upper limb amputee. In: Dill­ ingham TR, Belandres P, eds. Rehabilitation of the Injured Combatant. Washington, DC: Office of the Surgeon General; 1998:33–77. 16. Lake C, Dodson R. Progressive upper limb prosthetics. Phys Med Rehabil Clin N Am. 2006;17:49–72.

CHAPTER 119  Upper Limb Amputations

17. Intiso D, Basciani M, et al. Botulinum toxin type A for the treatment of neuropathic pain in neuro-rehabilitation. Toxins (Basel). 2015;7(7):2454–2480. 18. Dawson M, Carey J, Fahimi F. Myoelectric training systems. Expert Rev Med Devices. 2011;8:581–589. 19. Salminger S, Gradischar A, et al. Attachment of upper arm prostheses with a subcutaneous osseointegrated implant in transhumeral amputees. Prosthet Orthot Int. 2016. 20. Ovadia S, Askari M. Upper extremity amputation and prosthetics. Semin Plast Surg. 2015;29:55–61. 21. Meng J, Zhang S, et al. Noninvasive electroencephalogram based control of a robotic arm for reach and grasp tasks. Scientific Reports. 2016;6:38565.

657

22. Kuiken T. Targeted reinnervation for improved prosthetic function. Phys Med Rehabil Clin N Am. 2006;17:1–13. updated information with new publication- Ovadia 2015. 23. Defense Advanced Research Projects Agency. https://www.darpa.mil/ news-events/2016-10-13. 24. Jones LE, Davidson JH. Save the arm: a study of problems in the remaining arm of unilateral upper limb amputees. Prosthet Orthot Int. 1999;23:55–58. 25. Ostlie K, Franklin RJ, Skjeldal OH, et al. Musculoskeletal pain and overuse syndromes in adult acquired major upper-limb amputees. Arch Phys Med Rehabil. 2011;92:1967–1973.

CHAPTER 120

Lower Limb Amputations Gerasimos Bastas, MD, PhD

Synonyms Below-knee amputation—transtibial amputation Above-knee amputation—transfemoral amputation Stump—residual limb or residuum

ICD-10 Codes G54.7 G54.6 R26.2 S98.131 S98.141 S88.911 S88.921 S88.111 S88.121 S88.011 S88.021 T87.40 T87.33 T87.34 Z44.9 Z89.511 Z89.611 Z89.612

658

Phantom limb syndrome with pain Phantom limb syndrome without pain Difficulty walking Complete traumatic amputation of one right lesser toe Partial traumatic amputation of one right lesser toe Complete traumatic amputation of right lower leg, level unspecified Partial traumatic amputation of right lower leg, level unspecified Complete traumatic amputation at level between knee and ankle, right lower leg Partial traumatic amputation at level between knee and ankle, right lower leg Complete traumatic amputation at knee level, right lower leg Partial traumatic amputation at knee level, right lower leg Infection of amputation stump, unspecified extremity Neuroma of amputation stump, right lower extremity Neuroma of amputation stump, left lower extremity Encounter for fitting and adjustment of unspecified external prosthetic device Acquired absence of right leg below knee Acquired absence of right leg above knee (Above codes ending in 1 can be changed to end in 2 to designate left side involvement, e.g., Acquired absence of left leg above knee.)

Amputation Levels and Epidemiology Amputation levels are designated by eponymous procedures and descriptive terms. These are: partial toe (any part of a toe), toe disarticulation (at metatarsophalangeal joint), ray resection (toe and its associated metatarsal), transmetatarsal (at midsection of the metatarsal), tarsometatarsal disarticulation (Lisfranc), midtarsal (Chopart), calcaneotibial arthrodesis (Boyd or Pirigoff amputations depending on surgical approach), and ankle or foot disarticulation (Syme’s resection of distal fibula and medial tibial malleolus to level of inferior tibial articular surface, with distal reattachment of the heel pad). The terms below- and above-knee, though still in use, are more aptly respectively designated as transtibial and transfemoral. Knee and hip disarticulations occur through the respective joints. Hemipelvectomy involves the resection of a lower limb with variable resection of the hemipelvis (hindquarter). Hemicorporectomy is a resection below L4-L5. In 2005, an estimated 975,000 persons in the United States were living with lower limb loss.1 Vascular conditions account for most amputations (54%), with two thirds having a secondary diagnosis of diabetes.2 Over half of dysvascular amputations are major (transfemoral, 25.8%; transtibial, 27.6%),2,3 with 42.8% involving more distal levels (partial foot, ray, toes). Most occur in people aged 60 years and older. In the United States, there are approximately 82,000 non-traumatic, diabetes-related lower limb amputations annually.3 Trauma is the next most common cause (22%), followed by tumors (5%). In children aged 10 to 20 years, neoplasm is the most common cause. Men outnumber women 2.1:1 for disease-related and 7.2:1 for traumarelated limb loss.4 The global incidence of lower limb loss is estimated at 5.8 to 31 per 100,000 in the total population, with significant variation existing based on regional reporting differences.5 

Amputation Surgery Knowledge of surgical approaches permits better assessment of postoperative complications and prognostication of outcomes. In older techniques, resected muscles simply retracted and atrophied, positing problems for prosthetic ambulation and skin integrity. Newer techniques employ myoplastic or osteomyoplastic (myodesis) approaches. Myoplasties involve muscle-to-muscle attachment across fascial layers over the end of a transected bone, preventing unopposed contracture and atrophy, and preserving some muscle action for socket control. They are indicated

CHAPTER 120  Lower Limb Amputations

in dysvascular cases to ensure distal muscle tissue viability. Osteomyoplasties anchor resected muscles at distal ends of long transected bones, improving control over their movement, leading to better socket tolerance and control. At the transtibial level, the anterior distal tibia should be beveled and the fibula should be resected (2 to 2.5 cm) more proximally than the tibia. Relative motion between tibia and fibula (known as “chopsticking”) in a socket may be uncomfortable and injurious. The Ertl osteomyoplasty6 attempts to control this by creating a tibiofibular synostotic bridge, purported to promote end weight-bearing on the residuum. Attention is paid to closure of osseous intramedullary canals and treatment of neurovascular structures to decrease arteriovenous formations and entrapment of nerve stumps in scar tissue. Aspects of this procedure can be applied, wholly or in part, to other levels. For the patient with little ambulatory potential, a knee disarticulation merits consideration over a transtibial amputation, decreasing long-term risk of knee flexion contractures and skin breakdown.7 In a patient with good ambulatory potential, a knee disarticulation may also merit consideration over a transfemoral amputation as initial surgery or revision from a lower level.8 The Mazet procedure involves resection of the distal femoral condyles, partial appropriation of the patella in the intercondylar space, and distal myodesis of the thigh musculature. It preserves distal weight-bearing and a longer lever arm, leading to improved stability and propulsion. Surgical planning for hip disarticulation and hemipelvectomy levels must ensure adequate musculocutaneous coverage of the amputation site for comfortable socket use. 

Symptoms Post-amputation symptoms may include pain, phantom limb sensations, phantom pain, and delayed recurrence of residuum pain. Patients may report uncomfortable socket use, residuum skin breakdown, worsening walking ability, and falls. Surgical site pain is common and should resolve within a few weeks of surgery. Incidence of chronic residuum pain has been reported between 10% and 25%. Several conditions cause residual limb pain including, but not limited to, edema, ischemia, radiculopathy, sympathetic pain, neuromas, osteomyelitis, bone spurs, bony overgrowth, heterotopic ossification, soft-tissue inflammation (stump bursitis), and fluid collections. Phantom limb sensation is the perception of paresthetic or dysesthetic symptoms (tingling, prickling, numbness, heaviness, formication, itching) in that part of the limb that has been removed. Their frequency and intensity subside in the first year following surgery, aided by stump desensitization and initiation of shrinker and socket use. Patients typically describe intermittent, non-debilitating, phantom sensations thereafter. Some may experience a “telescoping” phenomenon, described as the perception that the extremity (i.e., the foot) is moving closer to the amputation site, occasionally in non-anatomic angles or positions. Phantom limb pain is a distressingly painful perception in the absent body part. Patients may describe it as cramping, stabbing, burning, or icy cold. The reported incidence varies from 0.5% to 100% owing to differences in study methods and population. Recent studies suggest that up to 85% of people with amputations will experience phantom pain at

659

some time.9 Newer studies are beginning to implicate the dorsal root ganglion as contributory to the maintenance of phantom limb pain from ectopic action of axotomized primary afferent neurons in this location.10 Low back or intact lower limb pain may follow a period of ambulation with an inappropriately fitting or aligned prosthesis, stemming from gait deviations. 

Physical Examination A patient’s cognitive ability to safely use and manage a prosthesis (involving hygiene, troubleshooting fit, and device maintenance) must be determined. Upper limb dexterity is examined for ability to independently don/doff and operate the prosthesis; noted impairments may influence the choice of suspension method, prosthesis controls, and of other assistive devices. Both lower limbs must be evaluated for strength, range of motion, deformities, or dynamic instability of joints and skin integrity. Muscle strength graded at least 4/5 is required for safe ambulation. Passive and dynamic malalignments in standing and walking should be assessed for scoliosis or lordosis of the spine, pelvic position (lateral or anterior tilt), and intact limb ankle hyperpronation or pes planus. Contractures, in either lower limb, result from stiffening changes to periarticular connective tissue structures such as ligaments or from muscle shortening, compromising joint range of motion. Functional contractures result from sustained positioning, when joints are not taken through their full range of motion. For example, knee and hip flexion contractures may result from prolonged habitual sitting. Mechanical contractures result from unopposed muscle action. For instance, the transfemoral amputee may develop hip flexion and abduction contractures from the unopposed action of those firmly attached muscles against the resected and weakened hip adductors and hamstrings. Flexion contractures of up to 20 degrees at the knee (for the transtibial residuum) or hip (at the transfemoral level) can be accommodated in the prosthetic socket alignment; greater contractures make prosthetic fitting more challenging and ambulation less safe. Absence of contractures is related to better success in prosthetic ambulation.11 Postoperatively, non-healing incisions are manifestations of ischemia, underlying hematoma, or abscess. Sutures may be removed to facilitate evacuation of an abscess or hematoma. Expressible purulent discharge should prompt imaging evaluation (with an appropriate modality) to assess extent of underlying involvement. Gram stain and culture should only be sent if samples can be acquired under the strictest aseptic technique. Probing of tracts by long-tipped cotton swabs should be avoided, to decrease risk of delivering surface contaminants to deeper tissues, unless performed following thorough cleansing of the wound surface. In the mature residuum, adherent scar tissue may lead to poor socket tolerance. Residuum skin breakdown in a prosthesis user results from pressure or shear forces. Motion of the residuum against the socket wall or brim causes shear that can separate epidermal and dermal layers, manifesting serous or serosanguinous blisters. Non-blanchable erythema over a bony prominence is a pressure sore until proved otherwise. Sustained increased focal pressure may progress slowly through skin callousing and fissuring, or quickly

660

PART 3 Rehabilitation

through deep tissue injury and overlying skin compromise. It is important to examine the prosthetic socket and other components such as liners for corresponding wear and alleviating or offending modifications fashioned by the prosthetist or patient. The prosthesis should not be worn until lesions are healed and appropriate adjustments to the socket have been made. Bruising of the distal residuum is indicative of poor fit, with increased contact at the bottom of the socket. Conversely, a choke phenomenon may occur whereby proximal constriction prevents the residuum to fully enter the socket, leading to lack of total contact distally. Lack of distal contact, with negative pressure between residuum and socket, leads to impaired venous and/or lymphatic outflow, chronic lymphedema, and subsequent formation of verrucous plaque hyperplasia. The latter carries a risk for secondary ulceration and infection. Verrucous plaques do not require harsh chemical, biochemical, or mechanical débridement, and are reversible when gentle compression (by appropriate shrinker or liner) and total contact with the socket is restored. Skin conditions affecting the residuum can also include, but are not limited to, contact dermatitis (to cleanser, skin product, or prosthetic material), bacterial folliculitis or cellulitis, ingrown hairs, dermatomycosis, and viral infections (molluscum contagiosum). Residuum pain without signs or symptoms of infection should be evaluated for neuroma (palpation and percussion along the anatomic course of the peripheral nerves). Skin breakdown without congruent pain symptoms should prompt evaluation of the level and quality of sensation in the residual limb (to fine touch, temperature, and deep pressure). Unexpected deformity of bone, firmness with painful or painless palpation of periosseous soft tissues, should all prompt radiographic evaluation for spurs or heterotopic ossification. Gait evaluation should be performed with the prosthesis and other assistive devices, as necessary, to ensure safety. Observational gait analysis should note deviations during stance, weight transfer, and limb advancement phases for intact and prosthetic limb. Apparent gait deviations should be correlated with physical exam findings and communicated to the prosthetist to help guide modifications, and to the physical therapist for individualized attention to functional gait impairments and balance retraining. History of falls should prompt evaluation of other systems such as vision, balance, other neurologic or musculoskeletal impairments, and of prosthesis malfunction. 

Functional Limitations Functional limitations are largely dependent on the premorbid status of the individual. An otherwise healthy person with traumatic unilateral lower limb loss will experience a prosthetic ambulation energetic cost increase of 15% with loss at the ankle, 25% to 33% at the transtibial level (50% if bilateral), 75% at the transfemoral level, and 110% to 200% at the hip disarticulation/hemipelvectomy level. In the diabetic or dysvascular amputee, the metabolic cost of ambulation may increase by another 25% to 40% at each respective level.2,11 Older individuals with multiple cardiovascular and pulmonary comorbidities should be encouraged to pursue

functional independence by optimizing wheelchair mobility and transfers when there is inadequate physiologic reserve, or cardiac safety margin, to ambulate with an assistive device.12 Individuals with significantly impaired cardiac output may not be prosthetic candidates, as the increased demands of prosthetic ambulation11 cause obligate increases in cardiac output that may be poorly tolerated. Coronary artery calcification scores were very high in amputees compared with Framingham Risk Score-matched control groups. This suggested moderate to extensive coronary artery disease in more than two thirds of amputees studied. It may be prudent to evaluate amputees for asymptomatic coronary artery disease and consider prophylactic revascularization.13 Individuals with preexisting amputations who undergo coronary artery bypass grafting will not be able to use an assistive device postoperatively (maintenance of sternal precautions), and alternate mobility options (e.g., power wheelchair) should be considered. The individual with new amputation secondary to peripheral vascular disease may require cardiac evaluation to establish parameters for an exercise prescription. Safety and fall concerns may arise from visual, vestibular, proprioceptive system impairments, deconditioning of muscles and reflexes affecting postural stability, autonomic dysfunction, pharmacologic side effects, prosthesis misalignment or malfunction, and quality of prosthetic fitting. Functional limitations due to pain are associated with decreased participation in activities of daily living. In general, phantom sensations are seldom debilitating, whereas phantom pain can be severely limiting, preventing participation in pre-prosthetic rehabilitation and prosthesis use. The ambulatory prosthesis user may develop gait deviations to accommodate poor fitting or to decrease pain persisting in device use out of necessity. Rates of clinical depression range from 18% to 35% among amputees. Depression should be differentiated from the grief response and postoperative adjustment period.14 

Diagnostic Studies Residual limb pain should be initially assessed with plain radiographs if bone spurs or heterotopic ossification are suspected. High-resolution ultrasound is preferred for initial work-up of soft tissue abnormalities. Magnetic resonance imaging is reserved for cases when initial imaging and clinical findings are equivocal.15 The individual with phantom limb pain may benefit from diagnostic as well as therapeutic sympathetic nerve block. On occasion, electrodiagnostic studies are helpful to differentiate symptoms of radiculopathy or offer other localizing insights for the cause of phantom pain. In the young amputee, it is occasionally necessary to obtain plain radiographs of the residuum to assess for bone overgrowth (typically evident on inspection, with radiograph confirming extent of overgrowth). 

Treatment Initial Initial treatment focuses on edema control and shaping of the residuum, wound healing, prevention of contractures,

CHAPTER 120  Lower Limb Amputations

661

Table 120.1  Treatment Options for Edema Control Treatment Options

Advantages

Disadvantages

Above-knee cast

Prevents knee flexion contracture Provides protection No patient “skill” or management necessary to remove Very low cost

Bulky, awkward, heavy to move Unable to visualize wound Unable to remove Potential for skin breakdown

Residuum “shrinker”

Easy to don and doff Enables visualization of wound Accustoms individual to use of a sock Provides shaping of residual limb

Cost—may need to be replaced after stump has begun to shrink

Rigid removable dressing (Fig. 120.1)

Excellent for preparing residual limb for eventual prosthesis Fosters patient’s independence in assessing need for stump socks Good edema management Provides some soft tissue protection Able to view wound

Therapist, physician, and prosthetist must be skilled in fabrication Potential for skin breakdown if applied incorrectly

Elastic bandage (ACE wrap)

Easily available Able to visualize wound Accommodates all shapes and sizes Good edema control

Requires excellent dexterity for patient to don and doff Potential for shear injury if wrap unravels Must be reapplied multiple times a day secondary to potential loosening

In a transtibial amputee

In a transfemoral amputee Residuum shrinker, elastic bandage

Same advantages and disadvantages as described for transtibial amputee

and pain management. Options for edema control are listed in Table 120.1.16,17 Selection of appropriate measures rests on postoperative setting of care and the patient’s and/or caretaker’s insight and ability to demonstrate safe, meaningful use. Patients should be educated about contracture avoidance practices and proper positioning. Education and reassurance of the patient and ongoing tactile input (i.e., massaging the distal residual limb) enhance accommodation to phantom sensations. There are many proposed treatments of phantom pain; however, there is no one definitive treatment that seems to work best. Initial pharmacologic intervention includes non-narcotic and narcotic analgesics; nonsteroidal anti-inflammatory drugs; anticonvulsants and membrane stabilizers, particularly gabapentin, duloxetine, and pregabalin; and tricyclic antidepressants.14 Mirror therapy has shown limited generalized effectiveness in mitigating phantom sensations and pain.18 It involves placing a mirror between a patient’s lower limbs, while the patient focuses intently and moves the reflected intact limb. The approach purports to exploit the brain’s preference to prioritize visual over proprioceptive feedback concerning limb positioning. As such, the artificial visual feedback may make it possible to “move” or “unclench” a phantom limb from a perceived painful position. Mirror therapy may, therefore, have some application in patients who report uncomfortable or sustained non-anatomic positioning of their phantom limb. 

Rehabilitation Pre-prosthetic training focuses on functional independence in mobility and self-care from the ambulatory (single limb)

FIG. 120.1  Application of the removable rigid dressing. (From Lennard TA. Pain Procedures in Clinical Practice, 2nd ed. Philadelphia: Hanley & Belfus; 2000.)

or wheelchair level, avoidance of hip and knee contractures, and residual limb healing and desensitization. With the incision healed, the patient can be instructed to perform scar mobilization to reduce the presence of adherent scar tissue. Firm tapping of the entire residuum helps with desensitization and promotes readiness for initial socket fitting. Edema control and maturation of residuum size and shape in the

662

PART 3 Rehabilitation

Table 120.2  K Levels

Procedures

K0 (level 0)

Does not have the ability or potential to ambulate or to transfer safely with or without assistance, and a prosthesis does not enhance the quality of life or mobility

K1 (level 1)

Has the ability or potential to use a prosthesis for transfers or ambulation on level surfaces at fixed cadence—typical of the limited and unlimited household walker

Treatment of phantom pain includes sympathetic blocks, typically performed under fluoroscopic guidance. Symptomatic neuromas may manifest 1 to 12 months or even several years after amputation as focal soft tissue masses with reproducible pain on palpation. Local anesthetic injection may provide pain relief. Surgical resection is an option but can result in a new (painful) neuroma.22 

K2 (level 2)

Has the ability or potential for ambulation with the ability to traverse low-level environmental barriers, such as curbs, stairs, or uneven surfaces—typical of the limited community walker

K3 (level 3)

Has the ability or potential for walking with variable cadence—typical of the community walker who is able to traverse most environmental barriers and may have vocational, therapeutic, or exercise activity that demands prosthetic use beyond simple walking

K4 (level 4)

Has the ability or potential for prosthetic use that exceeds basic walking skills, exhibiting high impact, stress, or energy levels—typical of the prosthetic demands of the child, active adult, or athlete

months following amputation can continue with appropriately sized prosthetic shrinkers or liners. A description of prostheses is beyond the scope of this chapter; however, the reader is referred to one of several texts on prosthetic components and prescription.19,20 K levels are used by Medicare to determine an individual’s functional potential and thus to justify prosthetic components (Table 120.2). When the prosthesis has been fabricated, an outpatient appointment with the ordering physician is scheduled for attendance by the patient and the prosthetist. A basic evaluation of the fit of the prosthesis is conducted, and referral for physical therapy that focuses on prosthetic training is made at that time, or adjustments to the prosthesis are made. The patient must be taught how to don and doff the prosthesis as well as when to add socks for a better fit (if compatible with suspension method used). The patient should be educated to routinely inspect the skin of the residuum (often done best with a long-handled mirror). Physical therapy for the lower limb prosthesis user has to include education on contracture avoidance, maintenance of core flexibility and strength, lower limb flexibility and strength, as well as prosthetic gait and balance retraining. The creation of a home exercise program addressing all of these items is strongly advised prior to discharge from physical therapy. Occupational therapy consists of identifying necessary equipment (e.g., toilet safety frame, tub transfer bench) and establishing independence in self-care from the wheelchair or ambulation with the intact limb. Occupational therapy should also be ordered when the patient receives the prosthesis to establish independence in self-care, particularly with lower body dressing, toileting, and homemaking while the prosthesis is worn. The majority (80.5%) of lower limb prosthesis users are able to return to automobile driving 3.8 months after amputation. People with right-sided amputations may need vehicle modifications (40%) or may switch to a left-foot driving style.21 

Technology Transdermal osseointegrated prostheses are being actively explored as a direct suspension/fixation approach of prosthetic components to the residual appendicular skeleton, obviating the need for prosthetic sockets.23 A single- or double-stage procedure introduces a threaded titanium implant in the residual bony diaphysis (femur or tibia), exiting distally through a transdermal stoma. Typical prosthetic components are directly appended to specialized external connectors of the osseointegrated implant. Periprosthetic (bony) loosening and deep and superficial infections remain significant concerns, with the procedure currently investigated in and indicated for select patient subpopulations. Ongoing clinical trials, basic research, and further technology development efforts are needed and are underway. 

Revision Surgery Surgery is indicated if the residuum is compromised from ischemia or infection. Hamstring releases have a limited or no role because they would inhibit the ability to walk. There does not appear to be any role for surgical stump revision for treatment of phantom pain. There are few data to promote dorsal root entry zone ablation, dorsal rhizotomy, dorsal column tractotomy, thalamotomy, or cortical resection in the treatment of phantom pain. A small trial to surgically treat phantom pain locally was performed, with splitting of the sciatic nerve and a sling fashion reconnection of the two parts proximal to the popliteal fossa. Of 15 patients, 14 reported that the procedure was “very helpful.”22 In 10% to 30% of cases with congenital limb absence/ difference, bone overgrowth may occur during developmental growth spurts, which must be addressed surgically. Long-term planning may include preemptive resection or ablation of complicating osseous growth plates. In the adult with an acquired amputation, development of painful bone spurs may warrant surgical intervention after prosthetic accommodations to socket fitting and alignment have been attempted without symptomatic alleviation. 

Potential Disease Complications The most common complications are surgical incision dehiscence, most often from infection, ischemia, or direct trauma. Conservative management with antibiotics (after a culture specimen is obtained) and local wound care is reasonable. Increasing wound necrosis, foul drainage, and fever or chills warrant re-evaluation by the surgeon.

CHAPTER 120  Lower Limb Amputations

Other complications may involve cardiac ischemia as a previously inactive individual begins using up to 100% more energy for gait training.11 A reasonable guideline for gait training is assessment of an individual’s ability to ambulate with the intact lower extremity with crutches or other assistive device. A person who cannot endure to safely hopambulate short distances on one foot using an assistive device is likely not a candidate for prosthetic ambulation. Major limb amputations continue to result in significant morbidity and mortality. One-year survival for dysvascular and diabetic individuals is 50.6% for transfemoral amputees and 74.5% for transtibial amputees. Five-year survival is 22.5% and 37.8% (survival in end-stage renal disease is as low as 14% at 5 years after amputation).2,3 

Potential Treatment Complications Skin breakdown is the most common complication with prosthesis use. Patients should be instructed to inspect the residuum daily and immediately report signs of persistent, nonblanchable erythema. Stopping prosthesis use is advised until assessment and socket modifications are made. Medications should be reviewed for appropriate dosing, as well as possible side effects and drug interactions. Patients may report symptoms of musculoskeletal repetitive stress injuries from gait deviations. Non-optimized prosthetic ambulation can predispose lower limb amputees to gait deviations with asymmetric and poorly controlled forces through the kinematic chain, promoting secondary musculoskeletal degeneration.

References 1. Esquenazi A, Yoo SK. Epidemiology and assessment lower limb amputations. Knowledgenow.com. Published November 7, 2012. Accessed February 19, 2014. 2. Ziegler-Graham K, MacKenzie EJ, Ephraim PL, et al. Estimating the prevalence of limb loss in the United States: 2005-2050. Arch Phys Med Rehabil. 2008;89:422–429. 3. Dillingham TR, Pezzin LE, MacKenzie EJ. Limb amputation and limb deficiency: epidemiology and recent trends in the United States. South Med J. 2002;95:875–883. 4. Leonard EI, McAnelly RD, Lomba M, Faulker VW. Lower limb prosthesis in physical medicine and rehabilitation. In: Braddom RL, ed. Physical Medicine and Rehabilitation, 2nd ed. Philadelphia: WB Saunders; 2000:279–310.

663

5. Moxey PW, Gogalniceanu P, Hinchliffe RJ, et al. Lower extremity amputations–a review of global variability in incidence. Diabet Med. 2011;28(10):1144–1153. 6. Talyor BC, Poka A. Osteomyoplastic transtibial amputation: the Ertl technique. J Am Acad Orthop Surg. 2016;24(4):259–265. 7. Albino FP, Seidel R, Attinger CE, et al. Through knee amputation: technique modifications and surgical outcomes. Arch Plast Surg. 2014;41(5):562–570. 8. Morse BC, Sull DL, Taylor SM, et al. Through-knee amputation in patients with peripheral arterial disease: a review of 50 cases. J Vasc Surg. 2008;48(3):638–643. 9. Ehde DM, Czerniecki JM, Smith DG, et al. Chronic phantom sensations, phantom pain, residual limb pain, and other regional pain after lower limb amputation. Arch Phys Med Rehabil. 2000;81:1039–1044. 10. Vaso A, Adahan HM, Gjika A, et al. Peripheral nervous system origin of phantom limb pain. Pain. 2014;155(7):1384–1391. 11. Friedan RA, Brar AK, Esquinazi A. Fitting an older patient with medical comorbidities with a lower limb prosthesis. PM R. 2012;4:59–64. 12. Morgenroth DC, Czerniecki JM. The complexities surrounding decisions related to prosthetic fitting in elderly dysvascular amputees [letter]. PM R. 2012;4:540–542. 13. Nallegowda M, Lee E, Brandstater M, et al. Amputation and cardiac comorbidity: analysis of severity of cardiac risk. PM R. 2012;4:657–666. 14. Roberts TL, Pasquina PF, Nelson VS, et al. Limb deficiency and prosthetic management. 4. Comorbidities associated with limb loss. Arch Phys Med Rehabil. 2006;87:S21–S27. 15. Subedi N, Heire P, Ali SI, et al. Multimodality imaging review of the post-amputation stump pain. Br J Radiol. 2016;89:20160572. 16. Mueller MS. Comparison of rigid removable dressings and elastic bandages in preprosthetic management of patients with below-knee amputations. Phys Ther. 1982;62:1438–1441. 17. Wu Y, Krick H. Rigid removable dressings for below knee amputees. Clin Prosthet Orthot. 1987;11:33–44. 18. Barbin J, Seetha V, Perennou D, et al. The effects of mirror therapy on pain and motor control of phantom limb in amputees: a systematic review. Ann Phys Rehabil Med. 2016;59S:e149. 19. Nelson VS, Flood KM, Bryant PR, et al. Limb deficiency and prosthetic management. 1. Decision making in prosthetic prescription and management. Arch Phys Med Rehabil. 2006;87:S3–S9. 20. Walsh NE, Bosker G, Santa Maria D. Upper and lower extremity prosthetics. In: Frontera WR, ed. DeLisa’s Physical Medicine and Rehabilitation: Principles and Practice, 5th ed. Philadelphia: Lippincott Williams & Wilkins; 2010:2017–2049. 21. Boulias C, Meikle B, Pauley T, Devlin M. Return to driving after lower extremity amputation. Arch Phys Med Rehabil. 2006;87:1183–1188. 22. Prantl L, Schreml S, Heine N, et al. Surgical treatment of chronic phantom limb sensation and limb pain after lower limb amputation. Plast Reconstr Surg. 2006;118:1562–1572. 23. Monument MJ, Lerman DM, Randall RL. Novel applications of osseointegration in orthopedic limb salvage surgery. Orthop Clin North Am. 2015;46(1):77–87.

CHAPTER 121

Ankylosing Spondylitis Ronald Rolf Butendieck, MD Juan Jose Maya, MD

Synonyms Seronegative spondyloarthropathy Seronegative arthritis Seronegative spondyloarthritides HLA-B27 associated spondyloarthropathy

ICD-10 Codes M45.0 Ankylosing spondylitis of multiple sites in spine M45.1 Ankylosing spondylitis of occipito-atlantoaxial region M45.2 Ankylosing spondylitis of cervical region M45.3 Ankylosing spondylitis of cervicothoracic region M45.4 Ankylosing spondylitis of thoracic region M45.5 Ankylosing spondylitis of thoracolumbar region M45.6 Ankylosing spondylitis of lumbar region M45.7 Ankylosing spondylitis of lumbosacral region M45.8 Ankylosing spondylitis of sacral and sacrococcygeal region M45.9 Ankylosing spondylitis of unspecified sites in spine

Definition Ankylosing spondylitis (AS) is a chronic inflammatory arthritis characterized by sacroiliitis, enthesitis (inflammation of the soft tissues attaching tendons, ligaments, and joint capsules to bone), and a marked propensity for sacroiliac joint (SJ) and spinal fusion. This arthritis is part of the spondyloarthritis (SpA) family of diseases, which have similar clinical, genetic, and immunologic features; however, AS has universal involvement with SJ inflammation or fusion, and more prevalent spinal ankylosis. Peripheral involvement is less common in AS, but paravertebral ligaments and 664

attachments of the Achilles tendon and plantar fascia are occasionally affected. Peripheral joints can also be involved in the more severe forms of the disease or when the patient has a younger age of onset.1 The onset of symptoms of AS is usually in late adolescence or early adulthood, and there is a 3:1 male predilection. AS is not associated with the presence of rheumatoid factor, anticyclic citrullinated peptide antibody, or antinuclear antibodies (ANA), although there is a genetic association with the HLA-B27 histocompatibility antigen. Approximately 90% of AS patients express the HLA-B27 genotype; however, this marker is not useful for screening, as only 5% of individuals with the HLA-B27 genotype develop AS.2 There are various classification criteria for AS, including the Modified New York Criteria for AS, the European Spondyloarthritis Study Group criteria for SpA, and the Amor criteria for SpA3 that have a role in epidemiologic studies, therapeutic trials, and other forms of clinical research. These classification criteria mainly rely on radiographic features; however, these may take years to develop and therefore potentially exclude patients with early manifestations.1 Consequently, the Assessment in Ankylosing Spondylitis (ASAS) classification of SpA included the term “nonradiographic axial SpA,” which gave magnetic resonance imaging (MRI) a significant role in the classification and diagnosis of AS and SpA.4 

Symptoms Inflammatory spondyloarthropathies should be suspected in any young adult patient who complains of insidious onset, progressively worsening, dull, thoracolumbar or lumbosacral back pain. Other characteristics that should raise suspicion for inflammatory-mediated axial disease include: back pain that improves with exercise, no improvement with rest, beneficial response to nonsteroidal anti-inflammatory medications, and pain during the night.5 AS can have a variable presentation, but sacroiliac pain is a common complaint accompanied by progressive morning stiffness and prolonged stiffness after inactivity. Tendon and ligament attachment sites may become painful and swollen, and one third of patients may develop hip or shoulder pain. Pleuritic chest pain and inflammatory eye disease (uveitis) tend to be late symptoms of more severe disease.6 Neurologic symptoms, such as paresthesia and motor weakness, are usually absent. 

CHAPTER 121  Ankylosing Spondylitis

665

A

B FIG. 121.1  Gaenslen test. (A) With the patient in side-lying position, the clinician extends the test leg. (B) With the patient supine, the test leg is extended over the edge of the table. Pain in the sacroiliac joints indicates a positive test result.

Physical Examination In addition to a complete physical exam, the evaluation of a patient with AS should focus on three regions: entheses, peripheral joints, and axial joints. The most typical findings on physical examination include signs of decreased spine mobility, sacroiliac pain, and pain at sites of ligament and tendon attachments. On palpation, the spine, lower paraspinal muscles, and SJs may be tender. Palpation of extremities demonstrates pain at entheses sites, particularly around the heel (e.g., calcaneal enthesitis) and knee (i.e., tibial tuberosity). The Gaenslen test may be positive (Fig. 121.1), and a Flexion Abduction External Rotation or Patrick test might also be abnormal, suggesting SI joint pathology.7 Peripheral joint swelling and pain with decreased range of motion (ROM) can be seen in 25% to 30% of patients. A discolored and edematous iris with circumferential corneal congestion occurs in iritis and anterior uveitis. The neurologic evaluation is typically normal with regard to motor, sensory, and reflex

examination findings. Weakness may be noted, but it is usually associated with pain, loss of mobility, or disuse. Tests of spinal mobility including the modified Schober test, finger to floor distance, cervical rotation, occiput or tragus to wall distance, and chest expansion should be performed on every visit. The modified Schober test is performed with the patient initially standing in erect position. The examiner identifies the posterosuperior iliac crest line (i.e., lumbosacral junction) and makes two midline marks, one 10 cm above the iliac crest line and one 5 cm below the iliac crest line. The patient is then instructed to perform forward trunk flexion while the examiner measures the distance between the two marks (Fig. 121.2A–C). Normal spinal mobility is indicated by an increase of more than 5 cm or a total distance greater than 20 cm, whereby an increase less than this would suggest limited lumbar spine mobility. The inability to touch the occiput to the wall while standing against it and the inability to expand the chest by more than 3 cm in full inhalation are late findings in the disease.8 

PART 3 Rehabilitation

666

A

B

C

FIG. 121.2  (A) Identification of sacral dimples and midline mark. (B) Markings at 10 cm above and 5 cm below the midline mark. (C) Measurement between upper and lower marks as patient’s back is maximally flexed. A distance of 21 cm or more indicates normal lumbar spine flexion.

Functional Limitations The functional limitations of the patient with AS are typically related to spine pain and immobility. The three best predictors of decreased spinal mobility are cervical rotation, modified Schober test, and finger to floor distance, although these measurements have not correlated with patients’ assessment of disease activity.8,9 Early in the disease process, decreased spine ROM is secondary to back pain and muscle spasms, and most dysfunction is mild and self-limited, typically improving with treatment. In severe disease, limitations from hip flexion contractures, thoracic kyphosis, and loss of cervical rotation decrease patients’ ability to view activities in front of them and side to side. The most commonly reported activity limitations are interrupted sleeping, turning the head while driving, carrying groceries, and having energy for social activities.10 Limitations in chest wall motion lead to a reliance on diaphragmatic breathing and a secondary drop in aerobic capacity. Pain, posture, and functional impairments can also significantly impact sexual relationships.11 The Bath Ankylosing Spondylitis Functional Index and the Dougados Functional Index are functional assessment tools used by clinicians specializing in the care of patients with AS to measure daily function.12–14 Past studies have shown approximately 90% of patients with AS remain employed, although evidence suggests up to one third of patients experience some form of employment disruption due to pain and physical limitations.6,9,15 

Diagnostic Studies There is a well-documented lag time between initial onset of symptoms and diagnosis that ranges from 7 to 11 years. Given the lack of specific signs and symptoms for early AS, a high level of suspicion is required in young patients presenting with back pain. Laboratory investigation should include inflammatory markers: erythrocyte sedimentation rate and C-reactive protein. Approximately 40% of patients with AS will have normal inflammatory markers, but the elevation

FIG. 121.3  Bamboo spine.

of acute phase reactants can indicate severity, responsiveness to treatment, peripheral joint involvement, or extraarticular disease. HLA-B27 is present in 90% of patients with AS, and the absence of this histocompatibility complex genotype suggests milder disease with a better prognosis. Rheumatoid factor and ANA are usually absent.14,16 Spine and pelvis radiographs are the standard imaging modalities in diagnosis and assessment of disease, although computed tomography (CT) and MRI are more sensitive for detecting bony changes, especially early in the disease course.17 Spine radiographs show ossification of spinal ligaments and apophyseal joints, sclerosis, and syndesmophytes, with eventual ankylosis that leads to the classic bamboo spine appearance (Fig. 121.3). Pelvic (sacroiliac +

CHAPTER 121  Ankylosing Spondylitis

hip) radiographs demonstrate symmetric involvement of the SJs with bone erosions, sclerosis, and blurring of the subchondral bone plate, eventually progressing to complete ankylosis. Based on modified New York Criteria for AS, radiographic features of moderate bilateral sacroiliitis or moderate to severe unilateral sacroiliitis plus one clinical feature are required for definite diagnosis of AS. Additional radiographic findings include bone erosions at entheses, symmetric and concentric joint narrowing, and subchondral sclerosis of the hip joints with ankylosis in severe disease. Once initial radiographs are abnormal, further radiographic progression correlates with worsening results of the modified Schober test, although it is recommended that assessment of spinal mobility be used as a proxy for radiographic evaluation.18 Early CT imaging findings demonstrate pseudo-widening of the SJs followed by sclerosis, narrowing, and ankylosis. Sonography with power Doppler can be used to diagnose enthesitis and can also be particularly useful to guide therapeutic interventions and follow disease progression.19,20 MRI is considered the most sensitive imaging modality for recognizing early involvement in AS, since it can identify active disease in the SJs and spine. Active AS findings in the SI joints include juxta-articular bone marrow edema, enhancement of the bone marrow and the joint space after contrast medium administration; chronic changes include bone erosions, sclerosis, periarticular fatty tissue accumulation, bone spurs, and ankyloses. Active spine lesions include spondylitis, spondylodiscitis and arthritis of the facet, costovertebral and costotransverse joints, and structural changes such as bone erosions, focal fat infiltration, bone spurs (syndesmophytes), and/or ankylosis. Enthesitis is also common and may affect the interspinousinal and supraspinous ligaments as well as the interosseous ligaments in the retroarticular space of the SJs.21  Differential Diagnosis Rheumatoid arthritis Other seronegative spondyloarthropathies Reactive arthritis (formerly Reiter’s syndrome) Psoriatic arthritis Enteropathic spondylitis Behçet syndrome Diffuse idiopathic skeletal hyperostosis Epidural abscess and other spine infections

Treatment The goals of treatment of AS are to reduce symptoms, maintain spinal flexibility and normal posture, reduce functional limitations, maintain work ability, and decrease disease complications. Different groups, including the European League Against Rheumatism and the ASAS, and most recently the American College of Rheumatology/Spondylitis Association of America/Spondyloarthritis Research and Treatment Network (ACR/SAA/SRTN), have published guidelines on the management of AS. These guidelines include concurrent medical, rehabilitation, and surgical treatment to achieve these goals.1,22–24 However, given the variable presentation and progression of symptoms in each

667

patient, an individualized program tailored to the patient’s specific needs is necessary.

Pharmacological Treatment The mainstays of treatment for AS have been nonsteroidal anti-inflammatory drugs (NSAIDs) and exercise, with the additional use of slow-acting antirheumatic drugs (SAARDs) in patients with peripheral arthritis. Over the past 20 years, however, the availability of tumor necrosis factor inhibitors (TNFi) and other biologic agents has greatly improved the treatment of AS. NSAIDs provide symptomatic relief and have been shown to slow radiographic progression in patients with AS.25–27 The ACR/SAA/SRTN guidelines recommend treatment with continuous dosing of NSAIDs for patients with active AS, and intermittent for stable AS. Continuous dosing has shown only marginal increase in side effects. No specific NSAID is recommended, and the choice should be based on individual therapeutic response, compliance, and side effects.1,23,26,28 Biologics have revolutionized the treatment of rheumatologic diseases29; specifically, tumor necrosis factor alpha inhibitors (TNFi) (etanercept, infliximab, adalimumab, certolizumab, and golimumab) have demonstrated significant clinical effectiveness in the treatment of AS.24 In patients with active AS despite treatment with an NSAID, treatment with TNFi is strongly recommended. The choice of TNFi is based on individual therapeutic response and other factors such as concomitant inflammatory bowel disease or uveitis, in which case TNFi monoclonal antibodies are recommended over etanercept. The ACR/SAA/SRTN guidelines do not recommend the use of non-TNFi, since studies have failed to demonstrate significant treatment response of AS to rituximab, tocilizumab, and abatacept;1 however, secukinumab (Il-17A inhibitor) recently demonstrated significant reduction in the signs and symptoms of AS, and was given FDA approval for the treatment of AS.30 Ustekinumab (Il-12 and 23 antagonist) and apremilast (phosphodiesterase 4 inhibitor), which have been approved for psoriatic arthritis, are also being studied for AS, but so far only ustekinumab has shown reduction in the signs and symptoms of AS.31,32 Other SAARDs have shown limited efficacy and are not generally recommended in the treatment of AS, except when TNFi are contraindicated. Sulfasalazine is an alternative to TNFi, and has shown some benefit in peripheral disease, inflammatory bowel disease, and psoriasis.24,33 Injections with glucocorticoids may be an option to treat arthritis and enthesitis, but short-term high dose oral glucocorticoids (prednisolone 50 mg/day) may have a very modest effect on signs and symptoms in patients with axial disease and should not be used long-term.34 Pamidronate, when it is used to treat associated osteoporosis, may also decrease AS disease progression.35 

Rehabilitation The benefits of exercise for patients with AS are well-­ documented36 and the ACR/SAA/SRTN guidelines strongly recommend treatment with physical therapy.1 Individualized programs should include activities to optimize aerobic

668

PART 3 Rehabilitation

capacity, flexibility, and pulmonary function.37 Hip ROM increases with regular stretching incorporating the contraction-relaxation-stretching technique. Strengthening of back and hip extensors should follow the flexibility exercises. Aerobic activities may maintain chest expansion. However, an exercise stress test should be considered before an aerobic program if aortic insufficiency is suspected.38 Despite the well-documented benefits of exercise programs, patients with AS are poorly compliant and, not surprisingly, the benefits of these programs are lost once the exercise is discontinued. There is no evidence that a particular type of exercise is superior to another, although specific exercise programs that target strengthening and flexibility of shortened muscle chains involved in opposing gravity show promise over conventional programs that stretch and strengthen muscles individually.39 One particular area that has clearly shown benefit is the setting in which the program is performed: a physical therapy supervised group is superior to a home exercise program and both are superior to no intervention for improvements in pain, function, mobility, and patient global assessment;36,40,41 ROM and aerobic water-based exercises have demonstrated significant improvement in pain score and quality of life of the patients with AS compared with home-based exercise.42 Spa therapy and balneotherapy can be safely recommended and have shown moderate benefit for treatment of pain and improving patients’ assessment of disease activity.43 Splinting and spinal orthoses have a limited use, since modifying forces in ossified spines can lead to injury, but foot orthotics can help with calcaneal enthesopathies and orthotic devices for postural unleveling can improve the ability to perform activities of daily living.44 There are no data to support or refute the use of diet, education, or self-help groups,23 but formal self-management education, instruction of patients in the nature, treatments, and prognosis of AS is an important aspect of good clinical care. No studies were found that examined the effectiveness of fall evaluations or fall counseling in patients with AS. Because falls can lead to spinal fractures and devastating neurologic consequences in some patients, fall evaluation and counseling is recommended for patients with osteoporosis, extensive spinal fusion, postural instability, or concomitant neurologic or musculoskeletal diseases that affect balance. Due to the absence of evidence of benefit and some evidence of significant harm, chiropractic spinal manipulation with high-velocity thrusts is not recommended in patients with AS who have spinal fusion or advanced spinal osteoporosis.1 

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

Procedures Periarticular corticosteroid injections and fluoroscopically guided SJ injections may have a role during NSAID-resistant flares or when NSAIDs are contraindicated.45 Local injections for enthesopathies may be effective, but peritendon injections of Achilles, patellar, and quadriceps tendons should be avoided.1 

Surgery Hip and knee arthroplasties are effective for patients with intractable pain, limitations in mobility, and poor quality of life. Early referral to an orthopedic surgeon should be considered, as joint replacement is optimal before progression to ankylosis. Age is not considered a limiting factor as young patients have fared well, with long-term studies demonstrating that greater than 50% of patients exceed 20 years with their prosthesis.46,47 Spinal osteotomy is an option for patients with severe kyphosis to improve horizontal vision and balance, although there is an increase in the risk of neurological injury.19,48 

Potential Disease Complications Potential complications include iritis or uveitis, inflammatory bowel disease, aortic insufficiency, and aortic root dilatation.49 Osteoporosis (best evaluated with bone densitometry of the femur) is common and increases the risk of spine fracture and associated neurologic injury after relatively minor trauma.50,51 Some evidence suggests that there is an increased morbidity and mortality secondary to cardiovascular disease in patients with AS.52 

Potential Treatment Complications Pharmacologic treatment options for AS are not devoid of side effects, and some of the most significant ones include: gastrointestinal and renal side effects with NSAIDs53; osteoporosis, diabetes, glaucoma, and cataracts with corticosteroids; and demyelinating diseases and increased risk of serious infections (including re-activation of latent tuberculosis and hepatitis B) with biologic therapy. Surgical procedures also have risks: total hip arthroplasty increases the risk of anterior dislocations, while spinal osteotomy carries the risk of paralysis and an increase in the mortality rate of up to 4%.48

References 1. Ward MM, et al. American College of Rheumatology/Spondylitis Association of America/Spondyloarthritis Research and Treatment Network 2015 recommendations for the treatment of ankylosing spondylitis and nonradiographic axial spondyloarthritis. Arthritis Rheumatol. 2016;68:282–298. 2. Reveille JD. Major histocompatibility genes and ankylosing spondylitis. Best Pract Res Clin Rheumatol. 2006;20(3):601–609. 3. Van Tubergen A, et al. Diagnosis and classification in spondyloarthritis: identifying a chameleon. Nat Rev Rheumatol. 2012;8:253–261. 4. Rudwaleit M, et al. The development of assessment of spondyloarthritis international society classification criteria for axial spondyloarthritis (part II): validation and final selection. Ann Rheum Dis. 2009;68:777–783. 5. Sieper J, et al. New criteria for inflammatory back pain in patients with chronic back pain: a real patient exercise by experts from the Assessment of SpondyloArthritis international Society (ASAS). Ann Rheum Dis. 2009;68(6):784–788. 6. Ozgul A, et al. Effect of ankylosing spondylitis on health-related quality of life and different aspects of social life in young patients. Clin Rheumatol. 2006;25(2):168–174. 7. Bagwell JJ, et al. The reliability of FABER test hip range of motion measurements. Int J Sports Phys Ther. 2016;11(7):1101–1105. 8. Haywood KL, et al. Spinal mobility in ankylosing spondylitis: reliability, validity and responsiveness. Rheumatol. 2004;43(6):750–757. 9. Dalyan M, et al. Disability in ankylosing spondylitis. Disabil Rehabil. 1999;21(2):74–79.

CHAPTER 121  Ankylosing Spondylitis

10. Dagfinrud H, et al. Impact of functional impairment in ankylosing spondylitis: impairment, activity limitation, and participation restrictions. J Rheumatol. 2005;32(3):516–523. 11. Healey EL, et al. Ankylosing spondylitis and its impact on sexual relationships. Rheumatol. 2009;48(11):1378–1381. 12. Calin A, et al. A new approach to defining functional ability in ankylosing spondylitis: the development of the Bath ankylosing spondylitis functional index. J Rheumatol. 1994;21(12):2281–2285. 13. Dougados M, et al. Evaluation of a functional index and an articular index in ankylosing spondylitis. J Rheumatol. 1988;15(2):302–307. 14. Zochling J, Braun J, van der Heijde D. Assessments in ankylosing spondylitis. Best Pract Res Clin Rheumatol. 2006;20(3):521–537. 15. Fabreguet I, et al. Assessment of work instability in spondyloarthritis: a cross-sectional study using the ankylosing spondylitis work instability scale. Rheumatol. 2012;51(2):333–337. 16. Feldtkeller E, et al. Age at disease onset and diagnosis delay in HLAB27 negative vs. positive patients with ankylosing spondylitis. Rheumatol Int. 2003;23(2):61–66. 17. Braun J, van der Heijde D. Imaging and scoring in ankylosing spondylitis. Best Pract Res Clin Rheumatol. 2002;16(4):573–604. 18. Wanders A, et al. Association between radiographic damage of the spine and spinal mobility for individual patients with ankylosing spondylitis: can assessment of spinal mobility be a proxy for radiographic evaluation? Ann Rheum Dis. 2005;64(7):988–994. 19. Aydin SZ, et al. Monitoring Achilles enthesitis in ankylosing spondylitis during TNF-alpha antagonist therapy: an ultrasound study. Rheumatol. 2010;49(3):578–582. 20. Spadaro A, et al. Clinical and ultrasonography assessment of peripheral enthesitis in ankylosing spondylitis. Rheumatol. 2011;50(11):2080–2086. 21. Østergaard M, et al. Imaging in ankylosing spondylitis. Ther Adv Musculoskelet Dis. 2012;4(4):301–311. 22. Zochling J, et al. ASAS/EULAR recommendations for the management of ankylosing spondylitis. Ann Rheum Dis. 2006;65(4):442–452. 23. van den Berg R, et al. First update of the current evidence for the management of ankylosing spondylitis with non-pharmacological treatment and non-biologic drugs: a systematic literature review for the ASAS/ EULAR management recommendations in ankylosing spondylitis. Rheumatol. 2012;51(8):1388–1396. 24. Baraliakos X, et al. Update of the literature review on treatment with biologics as a basis for the first update of the ASAS/EULAR management recommendations of ankylosing spondylitis. Rheumatol. 2012;51(8):1378–1387. 25. Zochling J, et al. Current evidence for the management of ankylosing spondylitis: a systematic literature review for the ASAS/EULAR management recommendations in ankylosing spondylitis. Ann Rheum Dis. 2006;65(4):423–432. 26. Wanders A, et al. Nonsteroidal antiinflammatory drugs reduce radiographic progression in patients with ankylosing spondylitis: a randomized clinical trial. Arthritis Rheum. 2005;52(6):1756–1765. 27. Kroon F, et al. Continuous NSAID use reverts the effects of inflammation on radiographic progression in patients with ankylosing spondylitis. Ann Rheum Dis. 2012;71(10):1623–1629. 28. Koehler L, Kuipers JG, Zeidler H. Managing seronegative spondarthritides. Rheumatol. 2000;39(4):360–368. 29. Khan MA. Ankylosing spondylitis and related spondyloarthropathies: the dramatic advances in the past decade. Rheumatol. 2011;50(4):637–639. 30. Baeten D, et al. Secukinumab, an interleukin-17A inhibitor, in ankylosing spondylitis. N Engl J Med. 2015;373(26):2534–2548. 31. Poddubnyy D, et al. Ustekinumab for the treatment of patients with active ankylosing spondylitis: results of a 28-week, prospective, open-label, proof-of-concept study (TOPAS). Ann Rheum Dis. 2014;73(5):817–823.

669

32.  Study of apremilast to treat subjects with active ankylosing spondylitis (POSTURE), 2016. https://clinicaltrials.gov/ct2/show/ NCT01583374. Accessed January 2017. 33. Clegg DO, Reda DJ, Abdellatif M. Comparison of sulfasalazine and placebo for the treatment of axial and peripheral articular manifestations of the seronegative spondylarthropathies: a department of veterans affairs cooperative study. Arthritis Rheum. 1999;42(11):2325–2329. 34. Van der Heijde D, Ramiro S, Landewé R, et al. 2016 update of the ASAS-EULAR management recommendations for axial spondyloarthritis. Ann Rheum Dis. 2017;76:978–991. 35. Haibel H, et al. Treatment of active ankylosing spondylitis with pamidronate. Rheumatol. 2003;42(8):1018–1020. 36. Dagfinrud H, Kvien TK, Hagen KB. Physiotherapy interventions for ankylosing spondylitis. Cochrane Database Syst Rev. 2008;(1):CD002822. 37. Sweeney S, Taylor G, Calin A. The effect of a home based exercise intervention package on outcome in ankylosing spondylitis: a randomized controlled trial. J Rheumatol. 2002;29(4):763–736. 38. Ince G, et al. Effects of a multimodal exercise program for people with ankylosing spondylitis. Phys Ther. 2006;86(7):924–935. 39. Fernandez-de-Las-Penas C, et al. One-year follow-up of two exercise interventions for the management of patients with ankylosing spondylitis: a randomized controlled trial. Am J Phys Med Rehabil. 2006;85(7):559–567. 40. Passalent LA. Physiotherapy for ankylosing spondylitis: evidence and application. Curr Opin Rheumatol. 2011;23(2):142–147. 41. Passalent LA, et al. Exercise in ankylosing spondylitis: discrepancies between recommendations and reality. J Rheumatol. 2010;37(4): 835–841. 42. Dundar U, et al. Effect of aquatic exercise on ankylosing spondylitis: a randomized controlled trial. Rheumatol Int. 2014;34(11):1505–1511. 43. Aydemir K, et al. The effects of balneotherapy on disease activity, functional status, pulmonary function and quality of life in patients with ankylosing spondylitis. Acta Reumatol Port. 2010;35(5):441–446. 44. Lipton JA, Mitchell LJ. J Am Osteopath Assoc. 2014;114:125–128. 45. Luukkainen R, et al. Periarticular corticosteroid treatment of the sacroiliac joint in patients with seronegative spondylarthropathy. Clin Exp Rheumatol. 1999;17(1):88–90. 46. Sweeney S, et al. Total hip arthroplasty in ankylosing spondylitis: outcome in 340 patients. J Rheumatol. 2001;28(8):1862–1866. 47. Joshi AB, et al. Total hip arthroplasty in ankylosing spondylitis: an analysis of 181 hips. J Arthroplasty. 2002;17(4):427–433. 48. Van Royen BJ, De Gast A. Lumbar osteotomy for correction of thoracolumbar kyphotic deformity in ankylosing spondylitis. A structured review of three methods of treatment. Ann Rheum Dis. 1999;58(7): 399–406. 49. Lautermann D, Braun J. Ankylosing spondylitis–cardiac manifestations. Clin Exp Rheumatol. 2002;20(6 suppl 28):S11–S15. 50. Waldman SK, et al. Diagnosing and managing spinal injury in patients with ankylosing spondylitis. J Emerg Med. 2013;44(4):e315–e319. 51. Robinson Y, Sanden B, Olerud C. Increased occurrence of spinal fractures related to ankylosing spondylitis: a prospective 22-year cohort study in 17,764 patients from a national registry in Sweden. Patient Saf Surg. 2013;7(1):2. 52. Papagoras C, Voulgari PV, Drosos AA. Atherosclerosis and cardiovascular disease in the spondyloarthritides, particularly ankylosing spondylitis and psoriatic arthritis. Clin Exp Rheumatol. 2013;31(4):612–620. 53. Zochling J, et al. Nonsteroidal anti-inflammatory drug use in ankylosing spondylitis–a population-based survey. Clin Rheumatol. 2006;25(6):794–800.

CHAPTER 122

Burns Jeffrey C. Schneider, MD Michelle E. Brassil, MD

Synonyms Thermal injury Late effects of burn injury Burn contracture Hypertrophic scarring from burns

ICD-10 Codes T20.00XS Late effect of burn of unspecified degree of head, face, and neck, unspecified site T20.07XS Late effect of burn of unspecified degree of neck T26.40XS Late effect of burn of unspecified eye and adnexa, part unspecified T26.41XS Late effect of burn of right eye and adnexa, part unspecified T26.42XS Late effect of burn of left eye and adnexa, part unspecified T30.0 Burn of unspecified body region, unspecified degree (Note: This code is not for inpatient use.) Burns have to be coded by location and then degree (see section T20-T25) I96 Gangrene, not elsewhere classified

Definition A burn is an injury to the skin or other organic tissue caused by extreme heat, flame, contact with heated objects, or chemicals. There are approximately 486,000 burn injuries requiring medical treatment and 40,000 burn hospitalizations, including 30,000 at burn centers, in the United States each year.1 Adult burn injury patients are most likely to be young (average age at injury for adults is 42 years) and male (68% to 75%).1 Most burns in adults result from fire or flame injuries (43% to 61%).1 Other causes of burns that are also commonly reported include scald, contact, grease, electrical, and chemical injuries.1 Burns usually happen in the home (73%), but also occur in the workplace (8%) or as a result of motor vehicle accidents (5%).1 For children, 670

scald injuries are the most common cause and occur more frequently in children younger than 5 years. Additionally, there are disproportionally more scald and inhalation injuries in minority populations. Although there are 3275 estimated deaths from fire and burns annually in the United States,1 the incidence of burns has decreased dramatically in the past 50 years. In addition, mortality from burn injury has been greatly reduced. A 2014 report demonstrated that half of patients who experience a 90% total body surface area (TBSA) burn survive; in contrast, in the 1940s, only a 20% TBSA burn accounted for a 50% survival rate. These dramatic improvements in survival rates are related to advancements in surgical interventions, systemic antibiotics, critical care support, and the development of comprehensive burn centers (Table 122.1).2 Survival of patients admitted to burn centers is estimated to be 97%.1 Once survival is ensured, medical management and treatment of burn injury currently focuses on wound healing, management of complications, and rehabilitation. 

Symptoms The symptoms of burn injury are directly related to the depth, size, and location of the injury. As expected, nociceptive pain is a major symptom of burn injury. Involvement of nerve endings in the dermal layer may also result in impaired or altered sensations causing neuropathic pain. Burn pain varies greatly from patient to patient, shows substantial fluctuation over time, and can be unpredictable because of the complex interaction of physiologic, psychosocial, and premorbid behavior issues. Pruritus is common in the acute period and is linked to both the chronic inflammatory state and altered pain pathways of burns. It has been reported that prevalence rates of post-burn pruritus in adults can be as high as 93%, with the most severe symptoms reported in the first months after wound closure. Risk factors associated with pruritis intensity include younger age, dry skin, and raised or thick scars.3 Deep partial-thickness and full-thickness burns interrupt the function of skin appendages. Damaged skin appendages may include the apocrine sweat glands, resulting in dry, friable skin that does not heal well and is susceptible to infection. Additionally, body temperature regulation may be compromised, with research showing how a burn patient’s rise in core body temperature following exercise is directly related to the amount of skin grafted.4

CHAPTER 122 Burns

671

Table 122.1  Criteria for Referral to a Burn Center Burn Injuries That Should be Referred to a Burn Center Partial-thickness burns greater than 10% of the total body surface area Burns that involve the face, hands, feet, genitalia, perineum, or major joints Third-degree burns in any age group Electrical burns, including lightning injury Chemical burns Inhalation injury Burn injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality Any patient with burns and concomitant trauma (such as fractures) in which the burn injury poses the greatest risk of morbidity or mortality Burned children in hospitals without qualified personnel or equipment for the care of children Burn injury in patients who will require special social, emotional, or rehabilitative intervention From American College of Surgeons, Committee on Trauma. Guidelines for the operation of burn centers. Resources for Optimal Care of the Injured Patient. Chicago, IL: American College of Surgeons; 2006.

Other symptoms are related to the multitude of other burn complications that will be discussed in detail in the section titled, “Potential Disease Complications.” 

Physical Examination A thorough physical examination is necessary to assess the burn itself as well as resulting complications. The evaluation should begin with an examination of the skin for burn location and depth, sensation, and signs of infection. Determination of burn depth allows categorization of wound severity. The current burn classification system includes four categories of varying depth: superficial, superficial and deep, partial thickness, and full thickness. Superficial injuries, traditionally known as first-degree burns, solely affect the epidermal layer. The category of second-degree burns is divided into superficial and deep partial-thickness burns. Superficial partial-thickness burns interrupt the epidermis and superficial (papillary) dermis. These often have good vascular supply and are painful with a pink or red and sometimes blistered appearance. Deep partial-thickness burns extend into the deep (reticular) dermis and damage skin appendages, which affects some degree of sensory and apocrine function. Fullthickness burns, also called third-degree burns, affect the entire epidermal and dermal layers and result in complete loss of skin appendages. Deep partial-thickness and fullthickness burns usually have poor blood flow and can be painless and appear less red. Severe injuries also may penetrate to the muscle, tendon, and bone. Such deep injuries, classified as fourth-degree burns, are not part of the newer anatomic classification system (Fig. 122.1 and Table 122.2). The depth of burn is an important factor in determining acute management of wounds. Burn surgeons often classify burns as superficial wounds, which heal by conservative management, or deep wounds, which require surgical intervention. Clinical assessment is the most widely used technique

Hair follicle Sweat gland Epidermis Basal layer

Dermis

Burn depth 1°

2°

Fat

3°

Muscle

4°

FIG. 122.1 Diagram of skin anatomy with subdivisions by degree of burn.

to evaluate burn wound depth and severity. Because of the evolving nature of burn wounds in the first few days after injury, monitoring the progression of the wound over time allows one to best assess its ultimate anatomic classification and management plan. Postoperative burn wounds should also be closely watched in the rehabilitation setting. Postoperative wound evaluation includes inspection of grafts for hematoma, seroma, infections, and areas of graft loss. After skin grafting, and as the skin matures, one should monitor for signs of hypertrophic scarring, which initially appears as erythematous, raised, and hardened skin. A complete neurologic examination including an assessment of motor and sensory function, reflexes, and cognition should also be performed. Immediately after injury or surgery, the sensory examination is primarily limited to light touch modality because of pain. However, after wound closure, the sensory examination enables one to evaluate for small- and large-fiber neuropathies. Deep burn wounds may involve the vascular supply and affect wound healing. A pertinent vascular examination includes assessment of peripheral pulses of the involved extremities. Because contractures are a common complication, the musculoskeletal examination should assess not only strength, but also joint range of motion and deformities. The motor examination of joints crossed by a deep partialthickness or full-thickness burn should not be performed until after skin graft “take” is ensured, usually within a week after grafting. Note that burn patients may have significant weakness from deconditioning and loss of muscle mass. A complete cardiac and pulmonary examination should be performed with particular attention to signs of respiratory complications and hypermetabolic state. Psychiatric examination should include a thorough screening for signs of sleep disturbance, depression, anxiety, substance abuse, and post-traumatic stress. Patients who exhibit symptoms of a major psychiatric disorder should receive a complete psychiatric evaluation. 

672

PART 3 Rehabilitation

Table 122.2  Burn Severity Classifications Classic Classification

New Classification

Appearance and Symptoms

Course and Treatment

First degree (epidermis)

Superficial thickness

Erythematous; dry, mildly swollen; blanches with pressure; painful

Exfoliation; heals spontaneously in 1 week; no scarring

Second degree (dermis)

Superficial partial thickness

Blistering; moist, weeping; blanches with pressure; painful

Reepithelialization in 7–20 days

Deep partial thickness

No blisters; wet or waxy dry; variable color; less painful; at risk for conversion to full thickness because of marginal blood supply

Reepithelialization in weeks to months; skin grafting may speed recovery; associated with scarring

Third degree (all of dermis and epidermis)

Full thickness

White waxy to leathery gray to charred black; insensate to pain; does not blanch to pressure

Reepithelialization does not occur; requires skin grafting; associated with scarring

Fourth degree (extends to muscle, bone, tendon)

—

Black (eschar); exposed bones, ligaments, tendons

May require amputation or extensive deep débridement

Functional Limitations Functional limitations are directly related to the severity and location of the burn and related complications. Those with burns to the upper extremities may experience impairments in activities of daily living, fine motor tasks, and occupational activities. Burns to the lower extremities may result in impairments in mobility and higher-level exercise and sport activities. Small burns to sensitive areas such as the face, including the eyes, ears, nose, or mouth, and genitals may result in significant impairments in vision, hearing, smell, taste, feeding, and reproduction. An important component of post-burn function, especially with the improvement in burn survival rate, is community and work reintegration. Factors associated with delayed return to work include increased hospital length of stay, electrical etiology, injury at work, and the need for inpatient rehabilitation. Further barriers for work reintegration include pain, neurologic issues, and impaired mobility.5 A burn-specific computer adapted test has been proposed that measures multiple dimensions of social participation and may prove helpful in future research of this topic.6 

Diagnostic Studies Many different diagnostic tests are useful in the initial assessment of the burn patient. These may include tests to assess wound depth. The “gold standard” of burn depth analysis is biopsy with histologic assessment, but this is not common practice. Techniques using laser Doppler imaging, thermography, vital dyes, ultrasonography, and confocal laser scanning microscopes have been suggested for wound depth assessment, but these methods are not routinely used clinically. Bronchoscopic evaluation of the airway as well as serum carboxyhemoglobin level are used to assess for inhalation injury. In the rehabilitation setting, diagnostic tests are targeted toward short- and long-term sequelae of burns. Doppler ultrasound is the recommended screening technique for detection of deep venous thrombosis given its high specificity and sensitivity. D-dimer has not been shown to be efficacious in deep vein thrombosis (DVT) screening in burn patients, with

one study showing specificity of 20% and positive predictive value of 5%.7 Plain radiographs are used to evaluate for abnormal bone and joint changes, such as bone growth deformity in children, osteophytes, or joint subluxation and dislocation. Plain films are also used to evaluate heterotopic ossification (HO) but may not demonstrate findings until 3 weeks (see Chapter 131).8 HO is diagnosed as early as 7 days after formation with a triple-phase bone scan. The aberrant ossification is visualized by increased uptake in the third phase of the scan. For patients with signs or symptoms of peripheral nerve injury, nerve conduction study and electromyography are used for the diagnosis of neuropathy.  Differential Diagnosis Thermal injury Electrical burns Chemical burns Radiation burns Scalding

Treatment Initial The initial management of the severely burned patient focuses on the ABCs: airway, breathing, and circulation. Aggressive fluid resuscitation to compensate for insensible fluid losses is a mainstay of acute management. However, scientific studies have shown that overresuscitation is a complication with grave consequences, including extremity and abdominal compartment syndrome, respiratory failure, and ocular hypertension.9 Other principles of initial management include maintenance of clean and protected wounds, use of antimicrobial agents and infection prevention, emergent relief of ischemic compression by fasciotomy or escharotomy, and early excision and grafting of open wounds. A detailed review of the rapid advances in acute management of burn injuries is beyond the scope of this chapter. 

CHAPTER 122 Burns

Rehabilitation Rehabilitation of burn patients is a complex process. The most common and significant issues are discussed in this section.

Pain Pain management after burn injury is an integral part of rehabilitation. Background nociceptive pain from the injury itself and exacerbations of pain from therapy, dressing changes, débridement, and other procedures can cause significant discomfort. Long-acting opioid pain medications are commonly used to treat background pain. Premedication with short-acting opioid analgesics before dressing changes or procedures and for breakthrough pain is standard of care. Opioid agonist-antagonist drugs (e.g., nalbuphine and butorphanol) have been shown to be effective in treating burn-related pain, but research is limited.10 Given the growing awareness of opioid abuse in society, a plan for tapering these addictive medications and utilizing adjuvant medications and nonpharmacologic strategies is an important component of pain management strategy. Even nonsteroidal anti-inflammatory drugs and acetaminophen can be valuable for pain control in combination with opioids.11 Antidepressants, anticonvulsants, and clonidine have been proposed as potential analgesic agents, but have yet to been studied in burn patients specifically.10 Multiple studies have demonstrated a reduction of pain scores with the following techniques: massage, hypnosis, multimodal distraction techniques, and cognitive-behavioral techniques.10 Additionally, off-the-shelf virtual reality and music therapy have both been shown to reduce acute pain intensity during wound care procedures.10 Clinicians should note that pain is often a multifactorial experience and therefore should make extended efforts to treat all possible contributing factors, including pruritus, neuropathy, anxiety, sleep disturbance, depression, and post-traumatic stress. 

Pruritus Moisturizing is encouraged for treatment of pruritus; not only do emollients such as aloe vera and lanolin help improve skin quality, but massaging may provide itch relief by the gate theory and desensitization of the skin.12 Studies have also shown that topical treatments with colloidal oatmeal, liquid paraffin, eutectic mixture of local anesthetics application, and doxepin cream can be effective for symptom management. A mainstay of treatment is antihistamines. Histamine is found in abundance in burn wounds and is implicated as a primary mediator of pruritus. Selective H1 and H2 antihistamines are generally preferred to nonspecific antihistamines for their limited side effect profile. The use of cetirizine and cimetidine was also shown to be more effective than diphenhydramine and placebo in treatment of post-burn pruritus.12 However, the effect of any antihistamine is often limited. A study of 35 adult patients using diphenhydramine, hydroxyzine, and chlorpheniramine showed similar effect with complete relief in only 20%, partial relief in 60%, and no relief in 20% of patients.13 Gabapentin has been shown in studies to relieve pruritus, both as monotherapy and in combination with

673

antihistamines. It is thought to have anti-pruritic effects by blocking post-synaptic calcium channels and inhibiting neurotransmitter synthesis. A comparative study of gabapentin, cetirizine, and the combination of the two in 60 patients showed significantly better results in the gabapentin group and the combination group compared with the cetirizineonly group.14 Similarly, a double-blinded randomized placebo controlled study (n = 80) compared pregabalin to cetirizine, a combination of both, and placebo. The pregabalin and combination groups both showed a reduction in itch for almost 95% of participants.15 Other agents including ondansetron, paroxetine, and naltrexone have shown potential usefulness as adjunctive treatments. Biofeedback therapy and psychological support may attenuate symptoms. Modalities including laser treatment, massage, and transcutaneous electrical nerve stimulation have also demonstrated positive results and may be useful.16–18 A recent prospective study performed reported positive preliminary results with the use of botulinum toxin injection, but this treatment is still under investigation.19 

Wounds The goal of wound care is to provide a moist, clean environment for reduced bacterial colonization and re-epithelialization. Silver-based dressings are the cornerstone of wound management because silver ions have broad antimicroorganism activity. Silver sulfadiazine is the best known and most widely used silver-based agent for burns. More recent research suggests that new dressings that elute nanocrystalline silver have better antimicrobial activity, including against methicillin-resistant Staphylococcus aureus.20 These dressings allow longer intervals between dressing changes and increase the patient’s comfort. Hydrofiber dressings are another new dressing type that may be less painful and are commonly used for exudative burns.21 There has also been increasing interest in honey. Several clinical trials comparing honey with traditional dressing in minor burns showed shorter healing times.20 In general, there are many dressing options, and dressing selection should take into account knowledge and familiarity of the health care providers. 

Deep Venous Thrombosis A randomized control trial by Ahuja et al. supports routine chemoprophylaxis with low molecular weight heparin (0.5 mg/kg twice daily, max 60 mg/daily) for DVT prevention in burn patients.22,23 

Hypertrophic Scarring Compression garments are considered standard of care for treatment of hypertrophic scars. Such garments are initiated with closure of wounds. Initially, pressure wrappings are applied around the affected areas with plastic elastic (ACE), cotton elastic (Tubigrip), or adhesive elastic (Coban) bandages. As edema resolves, the scarred area assumes a more stable shape, and custom-made pressure garments are then fitted. These garments are usually recommended to be worn 23 hours per day for up to 1 to 2 years after a burn. Compliance with this schedule is difficult for many patients. The efficacy of this treatment has not been established, but a number of studies show some improvement in clinical appearance in patients with moderate or severe scarring.24 Silicone gel sheeting is also considered first-line treatment, and a

674

PART 3 Rehabilitation

systematic review recently published further supports their use for immature epithelialized burn wounds at high risk for hypertrophic scarring.25 Other adjunctive therapies for scarring include laser treatment, intense pulsed light, steroids, exercise, and injection of fat, but there is little evidence surrounding each of these modalities.26 

Contractures Positioning and splinting are used to prevent development of contractures and to maximize joint function. Preventive treatment ideally begins on admission to the intensive care unit. The optimal position to minimize contracture development is depicted in Fig. 122.2. Particular attention is given to burns that cross joints and exposed tendons. Such joints are at high risk for contracture development. A system of cutaneous functional units (CFUs) has been created based on the fact that the amount of skin involved in joint movement extends far beyond the immediate proximity of the joint creases themselves. For example, the CFUs for the action of neck extension include the skin from the sternal notch to the pubic bone. The CFU system helps determine the areas of damaged skin, both proximal and distal, that could potentially contribute to joint contractures.27 This system may be helpful in promoting contracture prevention techniques in these high-risk areas, such as empirical splinting and ranging of joints. Range of motion exercises can begin immediately if the patient has not undergone skin grafting and usually within 1 week after grafting so as not to interfere with graft take. Once a contracture develops, rehabilitation interventions such as splinting, positioning, range of motion exercises, and serial casting have been shown to prevent worsening of the contracture and to improve joint motion.28 

Heterotopic Ossification (see Chapter 131) Conservative treatments include positioning and range of motion exercises. Medications such as nonsteroidal

Abduction, external rotation

Extension/hyperextension

Supination 90°

Straight alignment

No external rotation, no flexion 20° Straight

Dorsiflexion

FIG. 122.2  Optimal positioning to prevent burn contractures.

anti-inflammatory drugs or bisphosphonates and radiation therapy are efficacious in the prevention of HO in other disease populations (e.g., spinal cord injury and hip arthroplasty). Their use can be considered, but studies have not examined their effect in burn patients. A scoring system was recently developed to stratify risk of developing HO at time of admission to rehabilitation. The scoring system is based upon the following significant predictors of HO: TBSA, and the need for grafting of the arm, head/neck and trunk. This scoring system can help identify high-risk burn patients suitable for diagnostic testing and interventional HO prophylaxis trials.29 

Hypermetabolism and Deconditioning After severe burns, survivors often experience a hypermetabolic state with increased catabolism and loss of lean body and bone mass. Meeting nutritional needs, often under the guidance of a dietitian, is an important part of burn care. Enteral feeding may be needed in the acute setting for effective nutrition. Consideration should also be given to nutritional supplementation including vitamins C and D, zinc, and thiamine. Propanolol is one of the most studied drugs in the management of stress response to burns. A randomized control study showed that long-term treatment with propanolol (for 1 year post injury) improved peripheral lean body mass in the first 6 months after injury compared with placebo.30 Oxandrolone, an anabolic steroid, has been shown in multiple randomized controlled trials, with up to 1 year of use, to increase muscle protein synthesis and weight gain and to decrease hospital length of stay.31 There have been mixed results on the use of recombinant human growth hormone in regards to its efficacy and safety in adult populations; thus, more studies are needed.32 Because of prolonged hospitalization and the loss of muscle, burn survivors are often severely deconditioned. Long-term exercise training programs are needed for return to premorbid functional level. Aerobic and progressive resistance training programs have been shown to be efficacious in improving aerobic capacity (including peak oxygen consumption) and strength, respectively.33 

Psychological Comorbidity There is limited research validating treatment of depression, acute stress disorder, post-traumatic stress disorder, and sleep disorders specifically in the burn population. One small study suggests that sertraline may be useful in preventing post-traumatic stress disorder in burned children.34 Another study validated the use of escitalopram in adult burn patients for the treatment of depression.35 Regardless of the limited research specific to burn patients, a large body of evidence documents the efficacy of both pharmacologic and nonpharmacologic treatments of these disorders in other populations, and psychological conditions in burn patients should be addressed on the basis of these guidelines. Treatment of the burn-injured patient ideally involves collaboration with a mental health team to assist in the diagnosis and treatment of these problems. 

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

CHAPTER 122 Burns

Procedures Extracorporeal shock wave therapy (ESWT) is said to promote perfusion, increase angiogenesis, and accelerate burn wound healing and may have a role in improving pliability and appearance of post-burn scarring.36 Initial studies demonstrate a beneficial effect of ESWT on scar pain.37 In preliminary studies, ablative fractional CO2 laser treatment demonstrated both objective improvements in scar appearance and subjective improvements in patient quality of life.38 

Surgery Excision and grafting of open wounds are ideally performed within 1 week of injury in clinically stable patients. The goal is to remove necrotic and inflamed tissue for promotion of physiologic wound closure. Studies have shown that early excision and grafting minimizes fluid loss, reduces metabolic demand, and decreases the risk of infection and sepsis.39 There are many techniques for grafting. Most commonly, partial-thickness burns are treated with split- and full-thickness grafts of epidermis and superficial (papillary) dermis harvested from a nonaffected area (autograft). For larger wounds, mesh grafts or tissue expanders may be used. Allograft, dermal substitutes, cultured epithelial autograft, and Meek technique for micrografts can be used for extensive burns with minimal viable tissue. Deeper burns may require excision and coverage with skin, muscle, or myocutaneous flaps, but these may lead to great deformity. In spite of aggressive rehabilitation after a burn injury, significant contractures may still develop. Surgical release of the contracted joint is indicated when there are significant functional impairments despite appropriate conservative treatment. However, a recent review showed that there is no definitive evidence supporting surgical correction for contractures.40 Surgical resection of heterotopic bone is indicated if it results in nerve entrapment or significant joint impairment despite a course of conservative treatment. Scarring, disfigurement, and other cosmetic concerns are addressed with reconstructive surgical efforts. Severely burned patients may undergo multiple surgeries during the span of years after their injury. Planning of the myriad of possible procedures is a task that should involve multiple members of the burn team, including the patient and his or her family, physiatrist, surgeon, therapists, and mental health professionals. 

Potential Disease Complications Long-term Pain and Pruritus Hypersensitivity can be a chronic consequence of burn injury regardless of the severity of the burn. Patients with long-term severe pain and depression are associated with lower physical function at 2 years after injury.41 This should be taken into account for rehabilitation, return to work, and community integration. Chronic itch, defined as itch after all phases of wound healing have completed, is quite common as well, with reports in up to 67% to 73% of patients.42 Regular monitoring

675

with use of standardized measures is recommended. The visual analog scale, numeric pain rating scale, and 5-D scale for itching are useful in assessing symptoms and treatment response. 

Hypertrophic Scarring Hypertrophic scarring is common (as high as 70%) among those severely burned and is more prevalent among darker pigmented individuals.43 When it crosses a joint, it may result in deformities and contractures, leading to psychological, functional, and cosmetic impact.15 

Contractures Contractures are a common and significant complication of burn injury. They result in cosmetic deformity as well as decreased joint range of motion and function. Contractures are most common at the shoulder, elbow, and knee. Length of stay, inhalation injury, and extent of burn are associated with increased incidence and severity of contracture.44 Contractures of the hand most commonly occur at the wrist but may involve the metacarpophalangeal (MCP), proximal interphalangeal, and distal interphalangeal joints of all digits. Burns of the dorsal surface of the hands and feet may contract, resulting in joint hyperextension. Prolonged hyperextension places the joint at risk for subluxation. This condition is most common at the MCP and metatarsophalangeal. Predictors of hand contracture development include concomitant medical problems, TBSA grafted, and presence of hand burn and hand grafting.45 Similarly, dislocations of the hip and shoulder joints can occur. Finally, contractures over the spine may result in postural changes, such as scoliosis or kyphosis. 

Amputation Severe deep injury of extremities can require amputations of nonviable limbs. Amputations are most commonly associated with electrical injury. Low-voltage ( 40 years Obesity Varicose veins Prolonged immobilization Pregnancy High-dose estrogen therapy Tamoxifen Bevacizumab Previous deep venous thrombosis

Thrombophilia Antithrombin III, protein C, protein S deficiency Antiphospholipid antibody, lupus anticoagulant Malignant disease Major medical illness Trauma Spinal cord injury Paralysis

Pelvic surgery Lower limb orthopedic surgery Neurosurgery

Modified from Sokolof J, Knight R. Deep venous thrombosis. In: Frontera WR, Silver JK, Rizzo TD Jr, eds. Essentials of Physical Medicine and Rehabilitation, 2nd ed. Philadelphia: WB Saunders; 2008.

risk for development of DVT are advanced age, morbid obesity, varicose veins, prolonged immobility, pregnancy, malignant disease, stroke, inflammatory bowel disease, congestive heart failure, and previous DVT. Certain hereditary conditions may also predispose to development of DVT, such as deficiencies in protein C and protein S and familial thrombophilia. Acquired deficiencies of the natural anticoagulant system include antibodies directed against antiphospholipid and heterozygous factor V Leiden mutations.1 Patients can be categorized according to their risk for development of DVT2 on the basis of the type of surgical procedure, with orthopedic patients carrying the highest risk3 (Table 128.2). It is believed that orthopedic procedures carry such a high risk for DVT because the mechanical destruction of bone marrow during most orthopedic procedures causes intravasation of marrow cells and cell fragments and elevations of plasma tissue factor.4 Plasma tissue factor is a potent trigger of blood clotting.5 It is found in high concentrations in bone marrow and the adventitia surrounding the major blood vessels and the brain. Surgical trauma to these structures places neurosurgical patients at great risk for development of DVT. Following neurosurgery, the incidence of DVT has been reported to be as high as 50%.6 Risk factors that increase the rates of DVT in neurosurgery patients include intracranial surgery, malignant tumors, duration of the surgery, and presence of paresis or paralysis of the lower limbs.7 Patients can remain in a hypercoagulable state up to 5 weeks postoperatively.8 In addition to surgical patients, victims of orthopedic and neurologic trauma are at great risk for development of DVT, especially if long bone fracture or paralysis is sustained. Patients who suffer injury to the spinal cord are at high risk for DVT because of stasis and hypercoagulability. 

Symptoms Venous thrombosis often occurs asymptomatically. Symptoms of DVT may include ipsilateral lower extremity edema, fever, extremity warmth, and pain. Symptoms do not rule in or rule out DVT, but they can serve as a trigger for further diagnostic inquiry. 

712

PART 3 Rehabilitation

Table 128.2  Risk Categories of Venous Thromboembolism in Surgical Patients Without Prophylaxis Risk Category

Calf DVT

Proximal DVT

Fatal PE

High Major orthopedic surgery of the lower limb Major general surgery in patients > 40 years with cancer or recent DVT or PE Multiple trauma Thrombophilia Moderate General surgery in patients > 40 years that lasts 30 minutes or more without additional risk factors General surgery in patients < 40 years receiving estrogen or with a history of DVT or PE Emergency cesarean section in women > 35 years Low Minor surgery (i.e., < 30 minutes in patients > 40 years without additional risk factors) Uncomplicated surgery in patients < 40 years without additional risk factors

40%–80%

10%–30%

1%–5%

10%–40%

2%–10%

0.1%–0.8%

1.40) and may also be used to assess perfusion in patients with suspected critical limb ischemia (CLI).15,24 Arterial imaging (duplex ultrasound, computed tomography angiography, magnetic resonance angiogram, or invasive angiography) is generally reserved for highly symptomatic patients in whom revascularization is being considered.24 The 2016 American Heart Association/American College of Cardiology Guideline on the management of lower extremity PAD24 recommends resting ABIs to establish the diagnosis of lower extremity PAD in patients with exertional leg symptoms, non-healing wounds, age ≥ 65 years, those with other risk factors for atherosclerosis (HTN, DM, smoking history, hyperlipidemia), or known forms of atherosclerosis. If a person complains of numbness in the legs or feet or has low back pain, electrodiagnostic testing should be conducted to identify whether peripheral polyneuropathy is present or whether lumbosacral radiculopathy is responsible for these symptoms. Nerve conduction study findings may include reduced sensory and motor amplitude, latencies, and slowed conduction velocity. Electromyographic findings in radiculopathy include increased insertional activity, abnormal spontaneous activity, and changes in motor unit morphology; when these electromyographic findings are seen in a myotomal pattern, this suggests radiculopathy.  Differential Diagnosis NONVASCULAR Neurogenic claudication from lumbar spinal stenosis Calf pain due to S1 radiculopathy Foot pain due to plantar fasciitis Symptomatic Baker cyst Ankle or knee pain due to osteoarthritis Pain in legs and feet due to polyneuropathy Arthritis of the hips Restless legs syndrome  VASCULAR Arterial embolus Deep venous thrombosis Thromboangiitis obliterans (Buerger disease)

CHAPTER 129  Diabetic Foot and Peripheral Arterial Disease

Treatment Initial Risk Factor Modification Smoking Cessation Cigarette smoking is the most important risk factor for development of PAD.25 Observational studies have demonstrated that the risk of death, myocardial infarction, and amputation is substantially greater in those individuals with PAD who continue to smoke.25 The risk of smoking for vascular disease is even greater for women than men.25 Intense smoking cessation programs have been shown to be more effective than minimal intervention programs. Intense programs can include verbal advice from a physician to quit, in-person counselor sessions to discuss cognitive-behavioral therapy and pharmacologic options, and a friend or family support system. Minimal intervention programs often include physician verbal advice to quit and providing patients with resources to explore on their own. 

Hyperglycemia Management The presence of PAD is 20% to 30% higher in diabetics than in the general population.15 Poor glycemic control has been associated with a higher prevalence of PAD and risk of adverse outcomes.26 Goals for hemoglobin A1c are typically less than 7%. With each percent increase above 7%, there is an associated 28% increased risk of PAD.26 

Hypertension Control Management of blood pressure is required. Desired BP range is BP < 140/90, or 40 cm H2O), ultimately results in deterioration of renal function and should therefore be addressed actively, even if renal function is normal.11 

Rehabilitation Patients at risk for degenerative neurogenic bladders, particularly those with (or at risk for) sensory neurop­ athies (e.g., diabetic patients), should have a timed voiding schedule to prevent overdistention and progression to bladder areflexia. A 24-hour voiding diary, including fluid intake, time and quantity voided, and postvoid residual (by catheterization or ultrasound evaluation) should be recorded periodically. These patients should void every 6 hours, void again immediately after the first void, and adjust their fluid intake and voiding frequency according to the voiding diary. Patients with diabetes should be careful to maintain good glycemic control, not only for global prevention of related degenerative disease but also to prevent osmotic diuresis. Most neurogenic bladder lesions are associated with impaired bowel function. Fecal impaction and obstructed constipation may also cause mechanical obstruction to the passage of urine. Further, many of the medications used to reduce bladder contractility, particularly the anticholinergics, exacerbate bowel motility dysfunction. It is therefore important that these patients be routinely prescribed highfiber diets, stool softeners (e.g., docusate), laxatives (e.g.,

BP 106 60

B

psyllium), and suppositories (e.g., bisacodyl) and undergo digital stimulation either daily or every other day. Digital stimulation is best performed after either a meal or coffee or tea to take advantage of the gastrocolic reflex. The Credé method (suprapubic pressure) alone can lead to high intravesical pressures and even vesicoureteral reflux. Such pressure, or persistent tapping of the suprapubic region for 2 minutes at a time, should be performed only when methods to relieve bladder outlet obstruction have been ensured. This should not be performed in patients with active DSD and detrusor hyperreflexia because it will only exacerbate already high bladder pressures, and urine will not be completely evacuated.

Acute Phase and Central Nervous System Shock Phase This phase usually lasts days to weeks. The bladder is areflexic during this period, and adequate bladder drainage should be secured to prevent the areflexic bladder from developing overdistention and myogenic failure. Indwelling continuous Foley catheterization (14 F) is the easiest way to ensure bladder drainage. Alternatively, intermittent catheterization may be performed (after the initial phase of diuresis) and, when it is used from the onset, reduces the incidence of infection and stone disease.12 Patients do need training or assistance in self-catheterization. Rehabilitation nurses and occupational therapists may also be involved in this educational process. Catheterization is performed every 4 to 6 hours and fluid is restricted to a maximum of 2 L per day, if possible. The frequency of catheterization should be adjusted so that residuals are no more than 300 to 400 mL. For patients with a hyperreflexic bladder, long-term intermittent catheterization requires mitigation of the detrusor reflex with anticholinergics (see Table 138.2). 

Anticholinergic Drugs (Drugs to Increase Bladder Capacity) In humans, the bladder (detrusor muscle) has muscarinic receptors (M2 and M3 receptors). M3 receptors compared with M2 receptors are small in number, but are mainly responsible for bladder contraction. The antimuscarinic drugs listed in Table 138.2 are currently available to modulate detrusor hyperreflexia, to increase bladder capacity, and to reduce bladder voiding pressures. Dry mouth and

CHAPTER 138  Neurogenic Bladder

constipation are major problems for compliance of patients with most of these medications because of the widespread existence of M3 receptors, particularly in the salivary glands. Comparative studies of the non-selective antimuscarinic agents have found similar efficacy; however, most are slightly better tolerated than oxybutynin.13 The American Urology Association advises to use extended release formulations of these medications in order to reduce side effects. Oxybutynin, tolterodine, and trospium are currently available in extended release formulations.14 Except for trospium chloride, most of the other antimuscarinic drugs shown in Table 138.2 are tertiary amines and cross the blood-brain barrier, enhancing the centrally-acting anticholinergic factor. There is a growing body of evidence that chronic use of anticholinergic medications is associated with an increased risk for dementia.15 Mirabegron, a selective β3-receptor agonist that causes detrusor fundus relaxation, is a relatively newer pharmaceutical alternative for patients failing to respond to anticholinergic therapy in the able-bodied idiopathic overactive bladder population.16 Mirabegron has been shown to be efficacious in the overactive bladder population, while having significantly fewer lower incidence of side effects than the antimuscarinic medications.14 Although further studies are needed, early reports indicate that mirabegron is efficacious in the SCI population as well.13 

Procedures Another alternative to long-term management of bladder drainage is placement of a suprapubic catheter. This is preferable to chronic transurethral catheterization because it eliminates the risk of urethral or meatal erosion and is less often the cause of epididymitis or orchitis. Urinary tract infections, however, are just as likely, and these catheters require changing once a month. They are best placed either in the operating room under cystoscopic guidance or, better, through suprapubic incision to ascertain that the catheter ultimately resides as superiorly as possible, far from the bladder neck. This helps prevent irritation at the bladder neck, which often causes reflex bladder contractions, particularly if the catheter balloon (also in an indwelling Foley catheter) drops down into the posterior urethra.

Botulinum Toxin Patients with neurogenic overactive bladder failing to respond to anticholinergic therapy may benefit from periodic administration of intravesical botulinum toxin A (BoNT/A). Its purported mechanism of action is the inhibition of release of acetylcholine at the presynaptic cholinergic junction,17 which effectively suppresses detrusor contraction.18 Although BoNT/A is commercially available as onabotulinumtoxinA (oBoNT/A) and abobotulinumtoxinA, only oBoNT/A has FDA approval for this indication in adult patients with subcervical SCI.13 oBoNT/A is typically administered by submucosal injection cystoscopically in 0.5-1.0-mL aliquots. Although the maximum FDA-recommended total dose for this indication is 200 units, slightly higher dosing is common. oBoNT/A is efficacious and safe in patients with neurogenic detrusor overactivity and incontinence, with clinical benefits lasting 6 to 16 months after injection.13,19

783

oBoNT/A reduced incontinence episodes and improved quality of life in patients with multiple sclerosis and in patients with SCI.19 After oBoNT/A injection, postvoid residuals may be significantly elevated in a dose-dependent fashion; a third of patients had urinary retention and required intermittent catheterization.19 Another drawback of this agent is need for repeated treatment periodically. Rarely, generalized weakness, difficulty in swallowing, or dysarthria ensues, although these side effects reverse spontaneously in several weeks.20 The combination of oBoNT/A and antimuscarinics does not appear to offer additional benefit. Urethral injection of oBoNT/A is also being explored as a possible treatment for DSD. This is currently an off-label use, but positive outcomes have been reported.13 

Technology A variety of electrical stimulation techniques have been developed and are currently under investigation to improve and control bladder function following SCI. These include sacral anterior root stimulation (which requires a concomitant posterior rhizotomy to treat DSD and neurogenic detrusor overactivity), sacral nerve stimulation, percutaneous tibial nerve stimulation, and pudendal nerve stimulation. These procedures have proven to have variable efficacy for the ablebodied population, and the potential role and utility for treatment of the neurogenic bladder remains unclear.21 

Surgery Transurethral sphincterotomy has been used in suprasacral lesions in the past and has fallen into disfavor because of intraoperative and delayed bleeding potential. Use of a laser in a contact mode causes virtually no intraoperative bleeding.22 This procedure results in incontinence postoperatively and requires the use of an external condom catheter. There are rare circumstances in which bladder management has aggravated renal function, evidenced by recurrent ascending urinary tract infections or a bladder that is too contracted to store sufficient volumes. Some patients find it socially unacceptable to be incontinent and are willing to perform intermittent self-catheterization, but their body habitus precludes them from this. In such cases, there are certain reconstructive options that should be considered. An incontinent urinary diversion with a stoma in abdomen that drains urine into a bag may be performed. Cystectomy may be combined with this procedure or the bladder may be left in situ with a small risk of pyocystis. In patients willing and able to perform intermittent self-catheterization, the most common reconstructive alternative is an augmentation cystoplasty. The bladder is augmented by a segment of ileum, and the ureters remain in their native locations. Bladder pressure is reduced and capacity increased, thus protecting the upper tracts from side effects of high-pressure bladder. The drainage of urine is performed by intermittent self-catheterization. This procedure may be combined with an artificial urinary sphincter in patients with incompetent sphincter.11 For bladders that have low pressures and good compliance but leak through fixed sphincters, the Mitrofanoff and bladder neck closure may be an excellent option. Spina

784

PART 3 Rehabilitation

bifida patients with conus lesions might be good candidates for this procedure. However, consideration and discussion must be given to the high incidence of complications such as stomal stenosis, leakage, and conduit stricture.23 Egress through the bladder neck is eliminated, and the appendix is interposed between the bladder and the umbilicus where it is opened. In the common event that the bladder has poor compliance, an ileal bladder augmentation will raise bladder volume and lower bladder pressure. Patients would then catheterize their augmented bladders through the umbilicus. 

Potential Disease Complications Urinary tract infections (UTIs), kidney stones, and autonomic dysreflexia are common disease complications associated with neurogenic bladder. Social isolation due to incontinence may lead to depression. Patients with SCI who have a UTI may lack traditional symptomatology.24 Fevers, chills, back pain, suprapubic pain, dysuria, frequency, increased spasticity, and/or testicular swelling in the setting of positive urine cultures should be regarded as a urinary tract infection. Patients without overt symptoms of pyelonephritis, prostatitis, epididymitis-orchitis, or cystitis are more difficult to diagnose, particularly if they have an indwelling catheter or are being managed by intermittent catheterization. Those using catheters are virtually always colonized with bacteria, and the injudicious use of antibiotics will only select out resistant strains. Clean intermittent catheterization or condom catheter utilization result in less frequent UTIs than indwelling catheters.24 Factors indicating a need for treatment include urinary lithiasis, as this is most often related to infection, and pyuria in the setting of bacteriuria. Urine pH should be checked periodically; pH above 7 is invariably associated with infection from urea-splitting organisms, which may lead to struvite stone formation. Patients with DSD or urinary retention of any kind should have the bladder drained expeditiously with a fresh Foley catheter during the course of their treatment to ascertain good egress of infected urine. If prostatitis is suspected, transurethral insertion of a Foley catheter is relatively contraindicated, and drainage should be ensured suprapubically. Although improved bladder knowledge and care has resulted in fewer upper tract problems, care must also be taken to avoid and identify complications such as pyelonephritis, hydronephrosis, and renal failure.24

Autonomic Dysreflexia The lack of control of widespread sympathetic activity below the spinal lesion (T6-T8) is the key factor in the management of autonomic dysreflexia. Noxious stimuli, such as overdistention of the bladder, should be reversed immediately by catheter drainage. Consideration of procedures for patients at risk (spinal lesions above T6) should include spinal anesthesia, use of ganglion blockers, and use of adrenergic blockers. In the acute episode, if reversal of the noxious stimulus fails to control blood pressure and symptoms, vasodilating medications such as nitropaste may be required. Note should be made that normal systolic blood pressure for an

individual with a spinal cord injury is commonly less than 100 mm Hg. The chronic form of this syndrome is often related to active DSD, and methods aimed at control of this phenomenon, pharmacologically or via a procedure such as transurethral sphincterotomy, may alleviate the patient of autonomic dysreflexia.22 

Potential Treatment Complications Attention to hygiene is paramount in the prevention of urinary tract infections in the spinal cord-injured population. Those requiring Foley catheter or condom catheter drainage should have them changed regularly and utilize appropriate catheter monitoring and cleansing to minimize risk of infection, skin breakdown, or urethral erosion (in the case of an indwelling catheter). Leg bags should be routinely disinfected and then washed well with running water. Wheelchair seat cushions and covers should be changed and/or cleaned, and the patient should take a shower daily to reduce colony counts at the perineum. The possible role for suppressive or prophylactic antibiotics remains unclear. Several other methods of reducing UTIs in the able-bodied population have also proven ineffective or with mixed results in the SCI population. These include cranberry, D-mannose, ascorbic acid, and methenamine salts.24 Stoma care after urostomy is a source of great consternation for many who have it because of frequent appliance leaks and skin irritation. Also, the stoma must be situated properly on the abdomen according to the patient’s habitus and positioning in the wheelchair. Bladder augmentations of any kind are susceptible to perforations and life-threatening infections (as much as 10%). These patients have a 3% chance of small bowel obstruction from adhesions during their lifetime. Chronic indwelling Foley catheters carry the potential for urinary infection, meatal erosion, epididymitisorchitis, stone disease, and urethral fistula. In women, the urethra becomes patulous in time and incontinence ensues with or without a catheter.

Acknowledgment We would like to acknowledge and thank Ayal M. Kaynan, MD, FACS; Meena Agarwal, MD, PhD, MS, Dip Urol, FRCS, FRCS(Urol); and Inder Perkash, MD, FRCS, FACS, who were the authors of this chapter in the previous text edition. Their writing and contribution was the framework and basis of this chapter update.

References 1. Wein AJ, Dmochowski RR. Neuromuscular dysfunction of the lower urinary tract. In: Wein AJ, Kavoussi LR, Novick AC, et al., eds. Campbell-Walsh Urology, 10th ed. Philadelphia: Saunders Elsevier; 2011:351–358. 2. Bradley WE, Timm GW, Scott FB. Innervation of the detrusor muscle and urethra. Urol Clin North Am. 1974;1:3–27. 3. Denny-Brown D, Robertson EG. On the physiology of micturition. Brain. 1933;56:149. 4. Igawa Y. Discussion: functional role of M1, M2, and M3 muscarinic receptors in overactive bladder. Urology. 2000;55(suppl 5A):47–49. 5. Gosling JA, Dixon JS. The structure and innervation of smooth muscle in the wall of the bladder neck and proximal urethra. Br J Urol. 1975;47:549–558. 6. Kavia RB, Dasgupta R, Fowler CJ. Functional imaging and the central control of the bladder [review]. J Comp Neurol. 2005;493:27–32.

CHAPTER 138  Neurogenic Bladder

7. Khan A, Hertanu J, Yang WC, et al. Predictive correlation of urodynamic dysfunction and brain injury after cerebrovascular accident. J Urol. 1981;126:86–88. 8. Sakakibara R, Hattori T, Uchiyama T, Yamanishi TJ. Videourodynamic and sphincter motor unit potential analyses in Parkinson’s disease and multiple system atrophy. J Neurol Neurosurg Psychiatry. 2001;71:600–606. 9. Burney TL, Senapti M, Desai S, et al. Acute cerebrovascular accident and lower urinary tract dysfunction: a prospective correlation of the site of brain injury with urodynamic findings. J Urol. 1996;156:1748–1750. 10. Perkash I, Friedland GW. Posterior ledge at the bladder neck: crucial diagnostic role of ultrasonography. Urol Radiol. 1986;8:175–183. 11. Linsenmeyer TA. Neurogenic bladder following spinal cord injury. In: Kirshblum S, Campagnolo DI, eds. Spinal Cord Medicine, 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2011:224–228. 12. Guttman L, Frankel H. The value of intermittent catheterization in early management of traumatic paraplegia and tetraplegia. Paraplegia. 1966;4:63–84. 13. Wyndaele JJ. The management of neurogenic lower urinary tract dysfunction after spinal cord injury. Nat Rev Urol. 2016;13(12): 705–714. 14. Scott K, Dmochowski RR, Padmanabhan P. Delivery methods for drugs used in the treatment of overactive bladder. Expert Opin Drug Deliv. 2016;13(3):361–371. 15. Gray SL, Anderson ML, Dublin S, et al. Cumulative use of strong anticholinergics and incident dementia: a prospective cohort study. JAMA Intern Med. 2015;175(3):401–407.

785

16. Otsuki H, Kosaka T, Nakamura K, et al. β3-Adrenoceptor agonist mirabegron is effective for overactive bladder that is unresponsive to antimuscarinic treatment or is related to benign prostatic hyperplasia in men. Int Urol Nephrol. 2013;45:53–60. 17. Simpson LL. Molecular pharmacology of botulinum toxin and tetanus toxin. Annu Rev Pharmacol Toxicol. 1986;26:427–453. 18. Nitti VW. Botulinum toxin for the treatment of idiopathic and neurogenic overactive bladder: state of the art. Rev Urol. 2006;8:198–208. 19. Herschorn S, Gajewski J, Ethans K, et al. Efficacy of botulinum toxin A injection for neurogenic detrusor overactivity and urinary incontinence: a randomized, double-blind trial. J Urol. 2011;185:2229–2235. 20. Stoehrer M, Wolff A, Kramer G, et al. Treatment of neurogenic detrusor overactivity with botulinum toxin A: the first seven years. Urol Int. 2009;83:379–385. 21. McGee MJ, Amundsen CL, Grill WM. Electrical stimulation for the treatment of lower urinary tract dysfunction after spinal cord injury. J Spinal Cord Med. 2015;38(2):135–146. 22. Perkash I. Transrectal sphincterotomy provides significant relief in autonomic dysreflexia in spinal cord injured patients: long term follow up results. J Urol. 2007;177:1026–1029. 23. Faure A, et al. Bladder continent catheterizable conduit (the mitrofanoff procedure): long-term issues that should not be underestimated. J Pediatr Surg. 2016. https://doi.org/10.1016/j.jpedsurg.2016.09.054. 24. Jahromi MS, Mure A, Gomez CS. UTIs in patients with neurogenic bladder. Curr Urol Rep. 2014;15(433):1–7.

CHAPTER 139

Neurogenic Bowel Jeffery S. Johns, MD

Synonyms None

ICD-10 Code K59.2 Neurogenic bowel

Definition A neurogenic bowel has been defined as “a life-altering impairment of gastrointestinal and anorectal function resulting from a lesion of the nervous system that can lead to life-threatening complications.”1 Neurologic dysfunction results in several gastrointestinal end-organ problems, including prolonged colonic transit time, reduced anorectal sensibility, and lack of voluntary control of the external anal sphincter associated with a dyssynergic response. These problems have an extensive impact on quality of life and frequently affect individuals with neurologic conditions, including spinal cord injury (SCI), multiple sclerosis (MS), cerebral palsy, spina bifida, stroke, and Parkinson disease.2 The quality and severity of colorectal dysfunction following an SCI depends on the degree of completeness and level of the SCI.3,4 Severity of bowel dysfunction after SCI correlates with high level of lesion, increased degree of completeness of injury, and longer duration of injury.5 As many as 95% of individuals with SCI may need some intervention to initiate defecation, and bowel dysfunction has been reported to affect lifestyle or life activities in 41% to 61% of persons living with SCI.1

Bowel Innervations and Gastrointestinal Motility Unlike the bladder, small and large bowels have a large degree of intrinsic regulation via the intrinsic enteric nervous system (ENS). The ENS is composed of the submucosal plexus and the myenteric plexus, which are located between the circular and longitudinal layers of smooth muscle in the wall of the intestines. The submucosal plexus regulates mucosal secretion and blood flow, while the myenteric plexus coordinates intestinal motility.6 The colon also receives extrinsic innervation from somatic as well as parasympathetic and sympathetic nerves. The vagus nerve arises intracranially and provides parasympathetic innervations 786

from the esophagus to the splenic flexure of the colon, modulating the ENS to increase colonic motility.6 The vagus nerve is spared in spinal cord lesions (Fig. 139.1). The pelvic nerve carries parasympathetic fibers from S2-S4 to the descending colon and rectum. Some pelvic nerve branches travel proximally and innervate the transverse and ascending colon.7 Sympathetic innervations are supplied by the superior and inferior mesenteric (T9-T12) and hypogastric (T12L2) nerves. This sympathetic system modulates the ENS to decrease colonic contractions.6 The somatic pudendal nerve (S2-S4) innervates the pelvic floor. Peristaltic waves travel both toward and away from the ileocecal valve in the ascending colon, but in the descending colon, the waves travel mainly to push the contents to the anus.5 The motility of the colon is performed by three primary mechanisms: myogenic, chemical, and neurogenic. The myogenic transmission of signals occurs between enteric smooth muscle cells that are interconnected by gap junctions, which produce transmission from cell to cell. Most intestinal muscle displays autorhythmicity that causes colonic wall contractions.5 Chemical control is through the activity of neurotransmitters and hormones. The chemicals influence the promotion or inhibition of contractions through the action of the central nervous system or autonomic nervous system or by direct action on muscle cells. This activity can be triggered by luminal stimuli that are detected by nerves through epithelial intermediation. Epithelial enterochromaffin cells act as sensory transducers that activate the mucosal processes of both intrinsic and extrinsic primary afferent neurons through their release of 5-hydroxytryptamine (5-HT). Intrinsic primary afferent neurons are present in both the submucosal and myenteric plexuses. Peristaltic and secretory reflexes are initiated by submucosal intrinsic primary afferent neurons, which are stimulated by 5-HT acting at 5-HT1P receptors. Serotonergic transmission within the ENS and the activation of myenteric intrinsic primary afferent neurons are 5-HT3 mediated.7 Signaling to the central nervous system is also predominantly 5-HT3 mediated. The gut is thus the only organ that can display reflexes and integrate neuronal activity even when it is isolated from the central nervous system. The neurogenic mechanism of colonic control is through the ENS, which coordinates all segmental motility and some propagated movement. A 2017 study documented the important interconnection between the intrinsic and extrinsic nervous systems of the intestines by demonstrating that impaired extrinsic innervation results in major neuromuscular alterations of the colon. These include loss of myenteric neurons, decreased nerve

CHAPTER 139  Neurogenic Bowel

787

Aging patients Senile dementia Alzheimer disease Parkinsonism Cerebrovascular accidents Detrusor hyperreflexia

Sympathetic hypogastric T12-L2

Minimal bowel impairment

Pelvic floor dyssynergia • Detrusorsphincter Spinal cord lesion dyssynergia

Below pons Pelvic parasympathetic n.

• Reflex bladder Rectosigmoid and left colon

Bladder S2

Cauda equina and conus injury

• Mixed lesion • Areflexia ±

S3 S4

External urethral sphincter Anal ext. sphincter

Pudendal n. (voluntary)

fiber density in the myenteric plexus, and disruption of the network of signaling cells around the myenteric plexus.6 Normal defecation is the result of a complex interaction between muscles, nerves, and central nervous system. For normal defecation, there must be a mass movement of colonic contents associated with relaxation of internal and external anal sphincters. The colon absorbs fluids, electrolytes, and short-chain fatty acids; provides for growth of symbiotic bacteria; secretes mucus for lubrication of feces; and slowly propels stool toward the anus.8 The contents in the distal colon are retained until bowel evacuation. Transport of contents may take 12 to 30 hours from the ileocecal valve to the rectum.4 

Neurogenic Bowel A neurogenic bowel occurs when there is a dysfunction of the colon or rectosigmoid due to impaired extrinsic nervous control.1,9,10 The ENS remains intact after an SCI. However, depending on the level of the injury, different bowel problems and complications may arise. The lower motor neuron bowel syndrome or areflexic bowel results from a lesion affecting the parasympathetic cell bodies in the conus medullaris, cauda equina lesions, or damage to the pelvic nerves. No spinal cord-mediated peristalsis occurs, and there is slow stool propulsion. Only the myenteric plexus coordinates segmental colonic peristalsis, and a dryer, rounder stool shape occurs. Because of the denervated external anal sphincter, there is increased risk for incontinence. The levator ani muscles lack tone, and this reduces the rectal angle and causes the lumen of the rectum to open. A lesion above the conus medullaris causes an upper motor neuron bowel syndrome or hyperreflexic bowel. There is increased colonic wall and anal tone. The voluntary

FIG. 139.1 Important central neural control of the pelvic organs and resultant dysfunctions after denervation. (Modified with permission from Zafar Khan.)

control of the external anal sphincter is lacking, and the sphincter remains tight, thereby retaining stool. The nerve connections between the spinal cord and the colon, however, remain intact; therefore, there is reflex coordination and stool propulsion. These changes result in constipation and fecal retention at least in part owing to the hyperactivity of the external anal sphincter. 

Pathophysiology of Constipation in Neurologically Impaired Patients In neurogenic bowel, constipation is usually a major consequence.1,9,10 The pathophysiologic mechanisms of constipation are obstructed defecation, weak abdominal muscles, impaired rectal sensation, and delayed colonic transit time. Both incomplete and complete lesions can cause obstructed defecation or fecal incontinence.11 The mechanism for fecal incontinence is due to areflexic or atonic anal sphincter, uninhibited rectal contractions, poor rectal sensibility, and lack of anal sphincter tone and contraction (conus and cauda equina lesions). During attempts to defecate, in some able-bodied persons with chronic constipation, there is also an inappropriate contraction (or failed relaxation) of the puborectalis and of the external anal sphincter muscles. This paradoxical contraction of the pelvic floor musculature during straining at defecation is also called pelvic floor dysfunction11,12 or pelvic floor dyssynergic response. This is not a true dyssynergia because patients can learn to relax the pelvic floor musculature with biofeedback to manage functional obstructed defecation. This dyssynergic response, therefore, needs to be distinguished from true detrusor anal sphincter dyssynergia due to neurologic impairment, in which biofeedback may not have any role for the functional improvement. 

788

PART 3 Rehabilitation

Symptoms Neurogenic bowel results in a wide spectrum of gastrointestinal symptoms: incontinence, constipation, hemorrhoids, abdominal pain, abdominal bloating, fecal impaction, rectal bleeding, rectal prolapse, anal fissure, nausea, autonomic dysreflexia, and prolonged evacuation. These symptoms and/or the fear of these symptoms negatively impact quality of life and may lead to social isolation. Hospitalization for an intestinal complication such as constipation, volvulus, impaction, or megacolon is twice as frequent in individuals with a neurogenic bowel versus those without this condition.2 

Physical Examination For the management of neurogenic bowel, an individual evaluation13,14 is important with a careful rectal examination and anorectal neurologic testing to document degree of neurologic impairment. A neurologic examination can reveal the extent of the nerve damage and the completeness of SCI. The abdomen should be inspected and palpated for distention, palpable fecal masses, increased abdominal muscle tone indicative of spasticity, and bowel sounds. The rectal examination can provide information about external anal sphincter tone, stool in the rectal vault, presence of hemorrhoids, cystocele in women, or masses, and it assesses the tone and ability to produce voluntary contraction of the puborectalis muscles. The bulbocavernosus reflex assesses the integrity of the local spinal reflex arc; its absence, along with poor anal tone, indicates a conus or cauda equina lesion (lower motor neuron). It is also important to assess the patient’s strength in the upper and lower extremities, hand function, sitting balance, and ability to transfer; the length of the patient’s arms, legs, and trunk; and the patient’s weight. These factors are helpful to determine whether the patient can perform his or her own bowel program or whether assistance will be needed. People with tetraplegia are more likely to need assistance than are people with paraplegia. 

Functional Limitations There is some degree of loss of voluntary control for bowel evacuation, constipation, unpredicted incontinence, abdominal distention, and associated discomfort, depending on the degree and level of completeness of the neurologic lesion. The occurrence and/or fear of unplanned or uncontrolled bowel evacuation can lead to social isolation, significant vocational challenges, and depression. 

Diagnostic Studies Colonic motor activity comprises four main components: myoelectric activity,15 phasic contractile activity, tonic contractile activity, and intraluminal transit. Specific methods are available for the assessment of each separate component, but no single investigation gives information about all four types of activity. In current clinical practice, evaluation of colonic motor function is almost exclusively limited to assessment of intraluminal pressure and transit time.16,17 Although the direct assessment of colonic contractile

activity can be achieved through colonic manometry, this procedure is only slowly gaining clinical acceptance, notably in children. Other novel methods are also available; two techniques exist for the routine assessment of colonic (or whole gut) transit, both of which involve irradiation of the subjects: radiopaque markers18 and radionuclide scintigraphy.19 Wireless (telemetric) motility capsules20 with magnetic markers to obviate irradiation are currently being tried, but they need further validation before being incorporated into general clinical practice. Together with assessment of rectal evacuation and rectal sensation, studies of colonic transit should form the cornerstone of investigation of chronic idiopathic constipation in patients with functional or partial neurologic impairment. These investigations have led to the conceptualization of constipation in three broad and overlapping categories: normal-transit constipation, slow-transit constipation, and evacuation disorders.

Anorectal Dyssynergia For the precise diagnosis of anorectal dyssynergia, particularly in incomplete or functional lesions, anorectal manometry along with simultaneous electromyography of the external anal sphincter is important to distinguish between functional constipation12,21 and obstructed constipation due to a neurologic lesion. It is also important to evaluate impairment due to an incomplete lesion (e.g., MS, pudendal nerve lesion after childbirth, lumbar disc disease, back injury, or spinal tumor). Defecography, nerve stimulation and pudendal latency, ultrasonography, and magnetic resonance imaging may also be required for better understanding of gastrointestinal dysfunction. Defecography detects structural abnormalities and assesses functional information on the movement of the pelvic floor and the organs that it supports; conversely, excessive descent (descending perineum syndrome) can also be a pathophysiologic mechanism of constipation. Defecography can also help complement anorectal manometry studies in ruling out slow transit and other causes of constipation. Magnetic resonance imaging or pelvic floor sonography can further complement the studies. 

Treatment Initial The 2014 Cochrane review describes an effective management program for neurogenic bowel management as involving the “modulation of stool consistency, promotion of stool transit through the bowel, and effective reflex or manual evacuation of the stool from the rectum at an appropriate time and place.”2 Unless there is an associated acute abdomen, the small bowel and the bulk of the colon are functional and are not paralyzed. Management of bowel evacuation will also depend on level of SCI. In cauda equina lesions and also during the shock phase after SCI, there is a flaccid bowel; the management generally involves manual removal (disimpaction) of stool and use of a suppository. Digital stimulation may also be helpful with intact bulbocavernosus reflex. In patients with a supraconal lesion with spastic bowel, routine use of

CHAPTER 139  Neurogenic Bowel

stool softeners, suppository insertion, and digital stimulation help evacuation of the fecal matter. Digital stimulation for 20 to 30 minutes with and without suppository usually evokes bowel evacuation. 

Rehabilitation Bowel Management after Spinal Cord Injury In the rehabilitation of an individual with an SCI, adequate bowel evacuation in less than 60 minutes is an ideal goal; however, many patients require significantly longer. It is therefore important to individualize the bowel program for adequate evacuation on the basis of the neurologic and physical status with a set time, diet control, and digital stimulation with or without a glycerin suppository.1 Additional help to regulate the bowel with bulking agents by increasing water content (e.g., psyllium) or stool softeners by increasing water penetration of stool (e.g., docusate) has been useful in children. Iso-osmotic laxative (e.g., polyethylene glycol) and osmotic laxative (e.g., lactulose) are also widely used to help individualize the bowel program. The addition of bisacodyl to aid myoelectric propagation activity, transit in the ascending colon, and rectal tone in humans has been studied. Bisacodyl has been widely prescribed for the management of neurogenic bowel.22 The dosage is normally 5 or 10 mg, but up to 30 mg can be taken for complete cleansing of the bowel before a procedure. If it is taken at the maximum dosage, there will likely be a sudden, extremely powerful, uncontrollable bowel movement, and so precautions should be taken. When it is administered rectally in suppository form, it is usually effective in 15 to 60 minutes. Total bowel care time, time to flatus, and defecation can all be significantly reduced by using bisacodyl suppositories that are vegetable oil based rather than polyethylene glycol-based.23 Two suppositories can be inserted at once if a very strong, purgative, enema-like result is needed. A few hours after the initial evacuation, there can be a secondary action that will continue as long as there is unexpelled bisacodyl present in the rectum. For design of the bowel program, a variety of factors need to be considered. Is this an upper motor neuron or lower motor neuron bowel dysfunction? Is it a complete or an incomplete lesion? Is this associated with anorectal dyssynergia? A detailed history is needed to find out any bowel problems antedating the SCI, such as diabetes, irritable bowel syndrome, lactose intolerance, inflammatory bowel disease, or past rectal bleeding. These disorders may affect the management and choice of medications used in the bowel regimen. Other medications frequently used by patients with SCI for other problems, such as anticholinergics for treatment of neurogenic bladder, antidepressants, narcotics, and antispasticity medications, also affect the bowel. Additionally, the person’s dietary habits and the amount of fluid intake need to be documented as part of bowel management. It is helpful to evaluate psychosocial and family circumstances to provide guidelines to modify convenient timing for the bowel program and to develop rehabilitation strategies through diet, pelvic floor exercises, abdominal massage, and biofeedback, which have been found to be of benefit in some individuals with MS.2 

789

Patient Education and Awareness of Risk Factors It is critical to develop a comprehensive, individualized, and structured education program for prevention of incontinence, bowel accidents, and skin breakdown during sitting on a toilet seat. There are flaws in commode-shower chair design, as reported by consumers, which increase the risk of falls during transfers and risk of pressure ulcers due to inadequate padding as well as the long duration of the bowel care process. It is also important to identify other risk factors for negative outcomes: colonic overdistention, irritable bowel syndrome, bladder dysfunction, or autonomic dysreflexia in high spinal cord lesions. The current and most frequently used neurogenic bowel management strategies in some persons with only digital stimulation or a suppository insertion may be associated with incomplete evacuation, some incontinence, increased risk of pressure-induced tissue damage resulting from longer duration of commode sitting, and more damage to the mucosal tissue than with other methods available to persons with SCI. The use of the docusate mini enema may be an option in neurogenic bowel management because it has been shown to reduce the occurrence of bowel incontinence; it reduces the duration of commode sitting and thus reduces the risk of pressure ulcers, and it does not cause inflammation or seepage of the mucosal lining of the lower bowel.24 All of these may improve quality of life and social and community integration of persons with SCI. Phosphate enemas and other large volume enemas may be needed to help fecal impaction, but these are not recommended for ongoing or routine management.25 

Use of Prokinetic Drugs When conservative management is not effective, prokinetic agents, such as cisapride, prucalopride, metoclopramide, neostigmine, and fampridine, have been used for the treatment of chronic constipation in spinal cord–injured patients. They need to be used carefully for their side effects and have been suggested for consideration only for severe cases resistant to bowel program modification.1 Serious cardiac arrhythmias including ventricular tachycardia, fibrillation, and QT prolongation have been reported in patients taking cisapride. Cisapride has therefore been removed from the US market.26–28 The gastro-prokinetic effects make metoclopramide useful in the treatment of gastric stasis and in gastroesophageal reflux disease. Because of the risk of tardive dyskinesia with chronic or high-dose use of the drug, the US Food and Drug Administration recommends that metoclopramide be used for short-term treatment, preferably less than 12 weeks 28; in 2009, it required all manufacturers of metoclopramide to issue a black box warning.28 Given as an intramuscular injection, neostigmine and glycopyrrolate have been shown to speed bowel care time without significant adverse effects.29 

Procedures Botulinum Toxin in Gastrointestinal Disorders Botulinum neurotoxin inhibits contraction of gastrointestinal smooth muscles and sphincters; it has also been shown that the neurotoxin blocks cholinergic nerve endings in the autonomic nervous system, but it seems not to block noradrenergic responses mediated by nitric oxide. This

790

PART 3 Rehabilitation

has attracted use of botulinum neurotoxin for overactive smooth muscles, such as the anal sphincters for treatment of anal fissure and the lower esophageal sphincter for treatment of esophageal achalasia.30 It is critical to appreciate the anatomic and functional organization of the denervation of the gastrointestinal tract for neuropathic bowel dysfunctions, particularly in patients with long-term constipation and incomplete bowel evacuation for whom a bowel rehabilitation program has failed. Botulinum neurotoxin may help with an early resolution of obstruction by controlling the pelvic floor dyssynergic response and preventing back pressure effects on the rectosigmoid and colon. So far, few placebo-controlled trials have been performed despite widespread use of the toxin for the past 10 years. Botulinum toxin appears to be safe, and side effects are uncommon. The short-term efficacy of intrasphincteric injection of botulinum neurotoxin in achalasia is now well established. The US Food and Drug Administration has not approved botulinum toxin for any of these conditions. 

Technology Surface electrical stimulation of the abdominal wall muscles via electrodes embedded in an abdominal belt can decrease colonic transit time and total bowel care time.25 Sacral nerve stimulation for neurogenic bowel management is not commonly used for this primary purpose; however, data from lower levels of evidence (pre-post studies) have found improved bowel function and quality of life as well as fewer episodes of autonomic dysreflexia.25 Further study is needed before this intervention can be recommended on a larger scale for neurogenic bowel.2,25 

Surgery Although not commonly performed, several alternate interventions are available to allow enemas to be delivered antegrade rather than retrograde. These include the Malone antegrade continence enema (ACE), which can be done via open incision or alternate minimally invasive techniques; the Monti ACE, which utilizes an ileal tube rather than the Malone’s appendiceal conduit; and the Chait procedure, which some consider to be a minimally invasive version of the Monti ACE. Toileting times are significantly reduced following Malone ACE, and stomal stenosis is the most common complication. The Chait procedure decreases soiling frequency and has produced good patient satisfaction. Perioperative complications of the Chait include intraabdominal or subcutaneous abscess, and long-term complications include leakage of liquid stool around the catheter with associated cellulitis. Patient selection is paramount to success of ACE in general and for determining which procedure may be best.25 Fecal diversion via colostomy is a reliable alternative in severe and refractory cases of neurogenic bowel or in the setting of severe non-healing sacral pressure injuries. It may also be utilized to simplify care for some individuals who require significant assistance with their bowel care. Colostomy has been associated with good patient satisfaction, decreased time spent on bowel care, and fewer hospitalizations related to bowel dysfunction. Complications include

stomal stenosis, bowel obstruction, parastomal hernia, breakdown, and dermatitis.25 The use of common and validated scoring systems, such as the Neurogenic Bowel Dysfunction score and those found in the International Bowel Function data sets,31,32 will be helpful if they are implemented so that comparison of results and meta-analyses may be conducted to further our knowledge on the treatment and management of neurogenic bowel after SCI. 

Potential Disease Complications In spinal cord lesions above T6 level, one of the serious complications is autonomic dysreflexia. It usually accompanies poor bladder drainage or impacted fecal matter in the rectum. It needs immediate attention with gentle bowel evacuation after lidocaine jelly (4%) insertion in the rectum and use of pharmacologic agents to control blood pressure.1 In a slow-transit bowel, marked abdominal distention with chronic constipation and dilated colon further aggravates bowel evacuation. A barium contrast enema will delineate an obstructing lesion, if it is present, or may reveal a huge colon with redundant bowel. Although this finding will not delineate the specific cause, it will indicate the magnitude of the anatomic abnormality. If the impaction is located more proximally in the bowel, oral stimulants, such as magnesium citrate solution or bisacodyl tablets, may be required. Caution in the use of oral medication is needed if a bowel obstruction is suspected, as intestinal perforation could result. The decision to proceed with colonoscopy depends on the individual’s clinical history and findings as well as on whether the physician is satisfied with the results of the contrast enema. To clear the contrast material and to prevent constipation, oral laxatives and frequent bowel care should be used for a few days after studies that require barium.1 Fecal incontinence can lead to overgrowth of microorganisms around the anus, which weakens the skin, and skin sores can develop. Also, sitting on inadequately padded bowel care seat for a long time without frequent pressure relief could result in pressure injury. Hemorrhoids occur frequently2 and may become more symptomatic as they increase in size; they may be exacerbated by physical interventions, such as suppositories, enemas, or digital stimulation, to regulate the bowels in individuals with SCI. When hemorrhoids become clinically significant, they may cause pain (if sensation is present), bleeding, mucus incontinence secondary to prolapsed mucosa, or symptoms of autonomic dysreflexia. Persistent bleeding and autonomic dysreflexia that are not responsive to changes in bowel care routine are indications for consideration of banding33 or hemorrhoidectomy. 

Potential Treatment Complications In 27% of spinal cord–injured patients, chronic gastrointestinal problems appeared usually 5 to 10 years after the initial injury, suggesting that these problems are acquired and may therefore be avoided by the adoption of certain chronic care routines to manage obstructed constipation with anal stretch, high-fiber diet, and adequate fluid intake.34 Chronic use of stimulant laxatives can lead to damage of the myenteric plexus with aggravated colonic dysmotility.

CHAPTER 139  Neurogenic Bowel

Acknowledgment We would like to acknowledge and thank Inder Perkash, MD, FRCS, FACS and Meena Agarwal, MD, PhD, MS, Dip Urol, FRCS, FRCS(Urol) who were the authors of this chapter in the previous text edition. Their writing and contribution was the framework and basis of this chapter update.

References 1. Consortium for Spinal Cord Medicine. Neurogenic Bowel Management in Adults with Spinal Cord Injury. Washington, DC: Paralyzed Veterans of America; 1998:8–9. 2. Coggrave M, Norton C, Cody JD. Management of faecal incontinence and constipation in adults with central neurological diseases. Cochrane Database Syst Rev. 2014;1:CD002115. 3. Krassioukov A, Eng JJ, Claxton G, et al. SCIRE Research Team. Neurogenic bowel management after spinal cord injury: a systematic review of the evidence. Spinal Cord. 2010;48:718–733. 4. Menardo G, Bausano G, Corazziari E, et al. Large-bowel transit in paraplegic patients. Dis Colon Rectum. 1987;30:924–928. 5. Bassotti G, Germani U, Morelli A. Human colonic motility: physiological aspects. Int J Colorectal Dis. 1995;10:173–180. 6. den Braber-Ymker M, Lammens M, van Putten MJ, Nagtegaal ID. The enteric nervous system and the musculature of the colon are altered in patients with spina bifida and spinal cord injury. Virchows Arch. 2017. [Epub ahead of print]. 7. Glatzle J, Sternini C, Robin C, et al. Expression of 5-HT3 receptors in the rat gastrointestinal tract. Gastroenterology. 2002;123:217–226. 8. Stephen AM, Cummings JH. The microbial contribution to human faecal mass. J Med Microbiol. 1980;13:45–56. 9. Staas WE Jr Cioschi HS. Neurogenic bowel dysfunction: critical review. Phys Rehabil Med. 1989:11–21. 10. Benevento BT, Sipski ML. Neurogenic bladder, neurogenic bowel, and sexual dysfunction in people with spinal cord injury. Phys Ther. 2002;82:601–612. 11. Vallès M, Mearin F. Pathophysiology of bowel dysfunction in patients with motor incomplete spinal cord injury: comparison with patients with motor complete spinal cord injury. Dis Colon Rectum. 2009;52:1589–1597. 12. Diagnosis, pathophysiology and treatment: a multinational consensus. In: Drossman DA, Corazziari E, Talley NJ, et al., eds. ROME II. The Functional Gastrointestinal Disorders, 2nd ed. McLean, VA: Degnon Associates; 2000. 13. Stiens SA, Bergman SB, Goetz LL. Neurogenic bowel dysfunction after spinal cord injury: clinical evaluation and rehabilitative management. Arch Phys Med Rehabil. 1997;78(suppl.):S86–S102. 14. Liu CW, Huang CC, Chen CH, et al. Prediction of severe neurogenic bowel dysfunction in persons with spinal cord injury. Spinal Cord. 2010;48:554–559. 15. Frexinos J, Bueno L, Fioramonti J. Diurnal changes in myoelectric spiking activity of the human colon. Gastroenterology. 1985;88(Pt 1):1104–1110.

791

16. Scott SM. Manometric techniques for the evaluation of colonic motor activity: current status. Neurogastroenterol Motil. 2003;15:483–513. 17. Camilleri M, Bharucha AE, di Lorenzo C, et al. American Neurogastroenterology and Motility Society consensus statement on intraluminal measurement of gastrointestinal and colonic motility in clinical practice. Dig Dis Sci. 1985;30:289–294. 18. Murcia MN, Stone JM, Chang PJ, Perkash I. Colonic transit time in spinal cord–injured patients. Invest Radiol. 1990;25:109–112. 19. Stivland T, Camilleri M, Vassallo M, et al. Scintigraphic measurement of regional gut transit in idiopathic constipation. Gastroenterology. 1991;101:107–115. 20. Rao SS, Kuo B, McCallum RW, et al. Investigation of colonic and whole-gut transit with wireless motility capsule and radiopaque markers in constipation. Clin Gastroenterol Hepatol. 2009;7:537–544. 21. Levi R, Hultling C, Nash MS, Seiger A. The Stockholm spinal cord injury study: 1. Medical problems in a regional SCI population. Paraplegia. 1995;33:308–315. 22. Stiens SA, Luttrel W, Binard JE. Polyethylene glycol versus vegetable oil based bisacodyl suppositories to initiate side-lying bowel care: a clinical trial in persons with spinal cord injury. Spinal Cord. 1998;36: 777–781. 23. Yi Z, Jie C, Wenyi Z, Bin X, Hongzhu J. Comparison of efficacies of vegetable oil based and polyethylene glycol based bisacodyl suppositories in treating patients with neurogenic bowel dysfunction after spinal cord injury: a meta-analysis. Turk J Gastroenterol. 2014;25(5): 488–492. 24. Amir I, Sharma R, Bauman WA, Korsten MA. Bowel care for individuals with spinal cord injury: comparison of four approaches. J Spinal Cord Med. 1998;21:21–24. 25. Gor RA, Katorski JR, Elliott SP. Medical and surgical management of neurogenic bowel. Curr Opin Urol. 2016;26(4):369–375. 26. Walker AM, Szneke P, Weatherby LB, et al. The risk of serious cardiac arrhythmias among cisapride users in the United Kingdom and Canada. Am J Med. 1999;107:356–362. 27. Hennessy S, Leonard CE, Newcomb C, et al. Cisapride and ventricular arrhythmia. Br J Clin Pharmacol. 2008;66:375–385. 28. U.S. Food and Drug Administration. FDA requires boxed warning and risk mitigation strategy for metoclopramide-containing drugs [press release]. 2009. 29. Hughes M. Bowel management in spinal cord injury patients. Clin Colon Rectal Surg. 2014;27(3):113–115. 30. Vittal H, Pasricha PF. Botulinum toxin for gastrointestinal disorders: therapy and mechanisms. Neurotox Res. 2006;9:149–159. 31. Krogh K, Perkash I, Stiens SA, Biering-Sørensen F. International bowel function basic spinal cord injury data set. Spinal Cord. 2009;47:230–234. 32. Krogh K, Perkash I, Stiens SA, Biering-Sørensen F. International bowel function extended spinal cord injury data set. Spinal Cord. 2009;47: 235–241. 33. Cosman BC, Stone JM, Perkash I. Gastrointestinal complications of chronic spinal cord injury. J Am Paraplegia Soc. 1991;14:175–181. 34. Stone JM, Nino-Murcia M, Wolfe VA, Perkash I. Chronic gastrointestinal problems in spinal cord injury patients: a prospective analysis. Am J Gastroenterol. 1990;85:1114–1119.

CHAPTER 140

Osteoarthritis David M. Blaustein, MD Edward M. Phillips, MD

Synonym Degenerative joint disease

ICD-10 Codes M15.9 Generalized osteoarthritis M19.91 Primary osteoarthritis, unspecified site M19.93 Secondary osteoarthritis, unspecified site M19.90 Unspecified osteoarthritis, unspecified site M12.50 Traumatic arthropathy, unspecified M12.9 Arthropathy, unspecified

Definition Osteoarthritis (OA) is generally considered to comprise a family of degenerative joint disorders characterized by specific clinical and radiographic findings. OA is the most prevalent chronic joint disease and has become the most common cause of walking disability in older adults in the United States.1,2 It is estimated1 that almost 31 million adults have clinical OA, and the total cost for all arthritis, including OA, is more than 2% of the US gross domestic product.2 With the aging of the population and the higher incidence of obesity, the disease burden of OA is likely to continue to increase; it is projected that by 2020 it will be the fourth leading cause of disability globally.2,3 OA has traditionally been thought of as the “wear and tear” form of arthritis limited to cartilage degeneration. It is actually a complex combination of genetic, metabolic, biomechanical, and biochemical joint changes that can involve the entire joint and surrounding tissues. The sequence in which joint structures are affected can vary, but the hallmark of OA is the early failure of normal cartilage remodeling causing cartilage degeneration (Fig. 140.1) in response to stress or injury.4 More recent evidence implicates bone changes and synovial inflammation as also integral to the pathologic process of OA.4 As a whole, OA is characterized by the degradation and loss of articular cartilage, hypertrophic bone changes with osteophyte formation, subchondral bone remodeling appearing as sclerosis or cysts, chronic synovitis or inflammation of the synovial membrane, and 792

pathology of the joint capsule and surrounding ligaments/ tendons.4 Joint involvement in OA has a predilection for weightbearing joints. Common sites of involvement are the hips, knees, hands, feet, and spine. Less common sites of involvement are the ankles, wrists, shoulders, elbows, and sacroiliac joints. Secondary arthritis may become manifest with an atypical pattern of joint involvement. OA can be classified into two groups: primary and secondary. Primary or idiopathic OA can be localized or generalized. Localized OA usually involves a single joint; generalized OA is the involvement of three or more joints. Secondary OA is due to a specific condition known to cause or to worsen the development of OA (Table 140.1). Multiple risk factors have been linked to the development of OA (Table 140.2). Systemic factors include age, gender, genetics, bone mineral density, and body weight. Age is one of the strongest risk factors for OA.2 Female gender is associated with higher prevalence of symptomatic knee, hip, and hand OA.2 Heritable genetic traits of OA are complex and not felt to be due to a defect in a single gene; instead, more recent studies support a polygenic inheritance pattern. Some genetic markers strongly implicated in OA include the GDF5 gene in chromosome 7q22.5 There is a relationship between bone mineral density and OA.6 Overweight individuals are shown to be at greater risk for OA, especially in weight-bearing joints like the knee.7 However, metabolic factors related to obesity have been implicated in the development of OA—a finding based on the association of obesity and OA of a non-weight-bearing joint such as the hand.8 Other studies have associated OA with metabolic factors such as type 2 diabetes, hypertension, and hyperlipidemia, with one study showing diabetes to be a factor in the progression of narrowing of the knee joint space in men with established OA.9 Although there has been discussion regarding the role of vitamin deficiencies, there is no consensus regarding the effect of vitamin supplementation in OA. More recent studies have shown vitamin B complex to improve knee pain in OA.10 Local biomechanical factors implicated in OA include previous joint injury, joint malalignment, anatomic variation or abnormalities in bone, and muscle weakness. Those with previous injury have a 15% greater lifetime risk of symptomatic knee OA.7 Lower extremity malalignment may be associated with greater radiographic knee OA. Bone abnormalities such as acetabular dysplasia are associated with a greater incidence of hip OA.11 Muscle weakness, specifically of the knee extensor muscles, predicts knee OA in

CHAPTER 140 Osteoarthritis

793

Psychosocial dysfunction Depression

Decreased activity • Recreational • Vocational • Sexual

Pain Genetic and biochemical changes • Cytokines • Prostaglandins • Nitric oxide • Collagenase • Free radicals Abnormal loading and increased biomechanical stress

Inflammation Effusion

Disuse of joint or limb

Physiologic impairment • Musculoskeletal • Cardiovascular • Pulmonary

Cartilage degeneration Altered joint geometry and biomechanics

Medical comorbidities (CAD, CHF, COPD)

Weakness Atrophy Loss of motion Proprioceptive loss

Disability • Vocational • Recreational • Sexual • Self-care

Altered limb biomechanics • Gait disturbance • Impaired protective responses FIG. 140.1  Model of multifactorial process of degeneration, pain, psychosocial and physiologic dysfunction, and disability that may occur in osteoarthritis. CAD, Coronary artery disease; CHF, congestive heart failure; COPD, chronic obstructive pulmonary disease.

Table 140.1  Causes of Secondary Osteoarthritis

Symptoms

Bone and joint disorders, such as osteonecrosis and Paget’s disease Calcium crystal deposition disorders Congenital or developmental disorders, for example, hip dysplasia Endocrine disorders, such as acromegaly and hypothyroidism Infectious diseases, such as septic arthritis Inflammatory arthritis, such as rheumatoid arthritis Metabolic disorders Neuropathic disorders, such as diabetes mellitus and Charcot arthropathy Trauma

Patients usually complain of pain, stiffness, reduced movement, and swelling in the affected joints, which is exacerbated with activity and relieved by rest. Pain at rest or at night suggests severe disease or another diagnosis. Earlymorning stiffness, if present, typically lasts for less than 30 minutes. Joint tenderness and crepitus on movement may also be present. Swelling may be due to bone deformity, such as osteophyte formation, or an effusion caused by an accumulation of synovial fluid. Systemic symptoms are absent. In early disease, pain is usually gradual in onset and mild in intensity. Pain is typically self-limited or intermittent and tends to worsen as the day progresses. Patients with advanced disease may describe a sense of grinding or locking with joint motion and buckling or instability of joints during demanding tasks. Periarticular muscle pain may be prominent. Patients may complain of fatigue if biomechanical changes lead to increased energy requirements for activities of daily living. Overuse of muscle groups can lead to the development of pain syndromes in other parts of the musculoskeletal system. 

Table 140.2  Major Risk Factors for the Development of Osteoarthritis Systemic Factors Age Bone mineral density Gender Genetics Obesity Biomechanical Factors Joint injury Joint malalignment Bone variation or abnormality Muscle weakness

most cohorts of women.2 Historical data have correlated certain sporting activities with OA of specific joints, but there is no conclusive evidence, and the studies that have been done have many confounders that make interpretation inconclusive.2 

Physical Examination Joint Examination The diagnosis of OA involves assessment of the affected joints for common clinical features (Table 140.3). These usually include tenderness, bone enlargement, and malalignment. Osteophytes, joint-surface irregularity, or chronic disuse may also result in decreased range of motion, pain, effusion, and crepitus. Locking during range of motion may suggest loose bodies, floating cartilage fragments in the joint, or meniscal

794

PART 3 Rehabilitation

Table 140.3  Clinical Features of an Osteoarthritic Joint Tenderness to palpation Bone enlargement Malalignment Joint effusion or swelling Crepitus Periarticular muscle spasm, atrophy, or weakness Decreased, painful range of motion

tears. Joint contracture can result from holding a joint in slight flexion, which is less painful for inflamed or swollen joints. There may be secondary abnormalities in joints above or below the primarily involved joint. Joints must be assessed bilaterally because asymptomatic joints may also have abnormal findings. 

Neuromuscular and General Examination A thorough musculoskeletal examination should include inspection, palpation of soft tissues surrounding the joint of interest, and assessment of both muscle strength and flexibility. First, gait should be observed. There may be an ant­ algic gait or a slow gait pattern because of pain in a specific joint. If the patient uses a cane, appropriate use of the cane should be assessed during gait. Both functional strength and manual muscle testing should be performed. Periarticular muscle atrophy and weakness may be present in chronic OA, but functional tests like sit-to-stand testing, which often provokes pain in OA of the knee and hip, may be more informative. Palpation and dynamic testing of soft tissues may differentiate pain from tendinopathy or bursitis from OA. Joint-specific provocative maneuvers may help to isolate the source in symptomatic patients with poorly localized pain. A careful neurologic examination should be performed to make sure that pain is not due to nerve impingement or a neuropathic process. Clinicians may also consider performing a general examination. Evaluation of other systems may also help to differentiate primary OA from secondary OA due to a systemic process. Because obesity is the most important modifiable risk factor for OA, assessment of the patient’s body mass index is essential. 

Functional Limitations Functional limitations will depend on the joints affected by OA. Patients with disease in the hips and knees will have impairments in mobility, locomotion, and activities of daily living involving the lower body. For example, loss of hip external rotation commonly seen in OA can impair one’s ability to sit cross-legged and therefore impact lower extremity dressing. Patients may complain of increasing difficulty with ascending and descending stairs, walking, making chair or toileting transfers, and lower body dressing and grooming. Degeneration in the shoulders or hands limits vocational and recreational activities, selfcare, and upper body activities of daily living. Patients may initially have trouble with using the computer or lifting boxes, which then progresses to difficulties with

activities of daily living like feeding, grooming, bathing, and dressing. OA of the spine can result in limitations with all mobility. 

Diagnostic Studies Although imaging studies are not needed to confirm the diagnosis, plain radiographs may help to elucidate the severity of joint damage and progression of OA. The classic findings include asymmetric joint space narrowing without periarticular joint erosions, osteophytes at joint margins, subchondral sclerosis, and subchondral cyst formation. There is a well-demonstrated discordance between x-ray findings and symptoms in OA. Asymptomatic individuals, particularly the elderly, may have significant radiographic disease, whereas severe pain and dysfunction can occur in the setting of limited radiologic changes. Computed tomography scans, ultrasonography, and magnetic resonance imaging (MRI) are typically not needed for the evaluation of OA but can be helpful in providing better visualization not only for the evaluation of OA severity but also for the identification of other pathologic tissue processes and diagnosis. MRI in particular can identify early OA changes such as cartilage defects before they are seen on routine x-rays. Routine laboratory test results should be normal, and laboratory testing is usually not needed in uncomplicated cases of OA. If laboratory tests are available, clinicians should take care in interpreting the results. There is a high prevalence of laboratory abnormalities in elderly people, such as a raised erythrocyte sedimentation rate or anemia because of comorbid conditions. Autoimmune markers may be useful to differentiate OA from other musculoskeletal disorders such as inflammatory arthritides. Joint aspiration should be pursued in patients with significant joint effusion or inflammation. Analysis of joint fluid can be helpful in ruling out a crystal deposition disease such as gout or pseudogout, inflammatory arthritis, or infectious arthritis. In contrast to other arthritides, synovial fluid in OA is usually clear, with normal viscosity and leukocyte counts typically less than 1500 to 2000/mm3. 

Differential Diagnosis Inflammatory arthritis, rheumatoid arthritis, systemic lupus erythematosus, polymyalgia rheumatica Soft tissue disorders, bursitis, tendinitis, overuse injury/sprain, ligamentous injury Neoplasm Fibromyalgia Crystal-induced arthropathy, gout, pseudogout Seronegative spondyloarthopathies, ankylosing spondylitis, psoriatic arthritis Infectious/septic joint, Lyme disease, osteomyelitis, reactive arthritis (Reiter syndrome) Bone disorders, occult fracture, osteochondral defect Cartilage disorders, chondromalacia, tears Vascular disorders, deep venous thrombosis, aseptic necrosis Neuropathic disorders, complex regional pain syndrome, Charcot joint, radiculopathy, neuropathy

CHAPTER 140 Osteoarthritis

Treatment Initial The major principles of OA management involve relieving pain and other symptoms as well as maximizing joint function and quality of life. Initial treatment should include both pharmacologic and nonpharmacologic rehabilitation modalities. Here we provide a broad overview of major concepts. Site-specific management of OA is discussed in more detail in other chapters. No pharmacologic intervention has been shown conclusively to alter disease progression in OA. A number of topical and oral medications have been used to alleviate symptoms and improve functional status. Topical treatment of OA includes nonsteroidal anti-inflammatory drugs (NSAIDs), capsaicin, rubefacients, and opioids. Several treatment guidelines have recommend topical NSAIDs as a first-line OA treatment, especially in elderly patients, in whom drug safety and tolerability are significant concerns.12,13 However, oral acetaminophen is still recommended by the American College of Rheumatology (ACR) as a first-line medication for hip and knee OA.13 Topical NSAIDs are significantly more effective than placebo in treating chronic musculoskeletal conditions such as OA, with some studies showing them to be as effective to oral NSAIDs.14 Treatment recommendations will likely emerge to use these medications earlier and more often in the course of OA.15 Topical diclofenac is the only NSAID approved for use by the US Food and Drug Administration.14 Topical NSAIDs are recommended over oral NSAIDs by the ACR for the treatment of hand OA in patients above 75 years of age.13 Topical capsaicin cream has also been shown to reduce pain in joints affected by OA. This derivative of cayenne pepper causes the exuberant release and depletion of substance P, which diminishes pain transmission from C fibers. Limited data from controlled trials have shown improvements in OA pain with capsaicin, and its use is recommended by the ACR and the Osteoarthritis Research Society International as an adjunct or additional treatment for OA of the hand and knee.12,13 Topical rubefacients containing salicylate or nicotinate esters are available without a prescription for the treatment of musculoskeletal pain. They are thought to produce counterirritation and vasodilation of the skin for pain relief. Although earlier studies showed that they may be efficacious in the treatment of acute musculoskeletal pain in the short term (1 week), research on effectiveness is lacking.16 The ACR conditionally recommends the topical cream trolamine salicylate as a treatment of hand OA.13 Although there may be some pain relief, use of transdermal opioids is not routinely recommended because of the potential negative effects of opioid use. Oral agents often discussed in the treatment of OA include acetaminophen, NSAIDs, opioids and opioid-like medications, serotoninnorepinephrine reuptake inhibitors, and glucosamine and chondroitin. Acetaminophen and NSAIDs are typically considered first-line oral agents. These medications, whenever possible, should be prescribed on a symptomatic basis rather than on a schedule.12,13 Acetaminophen is the preferred initial oral agent with a maximum dose of 3 g/day in divided doses, particularly if there is no suspicion of joint inflammation. Although NSAIDs are more efficacious than acetaminophen, effects were modest and associated with greater rates of adverse gastrointestinal effects.17 No

795

NSAID has been shown to be superior to another in the treatment of OA; because of the variable responses and differing chemical structures of these compounds, it is reasonable to try two to three different NSAIDs before moving on to a different class of medication. Tramadol not only acts as a weak opioid but also modulates serotonin and norepinephrine levels. Common dosing of tramadol is 50 mg slow release every 12 hours as needed. Studies have demonstrated that tramadol mildly improves pain and function in OA patients, but it was often noted that adverse effects led patients to discontinue this medication.18 Tramadol alone or in combination with acetaminophen is conditionally recommended by the ACR in the treatment of OA of several joints after a trial of acetaminophen and NSAIDs.13 Although tramadol is thought to have a lower abuse potential than other opioids, there is evidence of a potential for dependence at higher doses; this should be considered when prescribing this medication for a chronic condition.19 Despite the recent opioid epidemic, the use of opioid medications in OA remains a common practice. The risk/ benefit ratio of prescribing these medications should always be weighed. Although opioids can improve pain and function in patients with OA, there is a high rate of adverse events and the withdrawal of patients from treatment. A recent systematic review comparing pain reduction of NSAIDs and opioids for knee OA showed similar results. Opioids therefore should be considered a second-line treatment at best, even when OA pain is severe.20 The ACR recommends the use of opioids only for patients who are either not willing to undergo or have contraindications to total knee arthroplasty after medical therapy has failed.13 Duloxetine is a serotonin-norepinephrine reuptake inhibitor that is conditionally recommended by the ACR for the treatment of knee OA.13 In multiple randomized controlled trials, patients with knee OA treated with duloxetine, typically at doses of 60 mg/day, were more likely to experience an improvement in outcome, pain, and function.21 Significant attention has focused on the use of supplements such as chondroitin and glucosamine in OA. The preponderance of evidence has failed to show a significant benefit in pain reduction with these substances.20,21 The ACR conditionally recommends against the use of chondroitin and glucosamine in knee OA and hip OA.13 However, these supplements have a low risk profile and they are still widely used. Patients considering the use of glucosamine or chondroitin should be advised to stop them after 6 months if no improvement is noted. Other treatments of OA include turmeric, avocado soybean unsaponifiables, rosehip powder, and diacerein. One recent meta-analysis suggested that turmeric and curcuminenriched extracts improve pain in OA, but larger-scale, higherquality studies should be done to confirm these findings.24 

Rehabilitation A comprehensive rehabilitative approach is important and effective in promoting wellness and reducing disability in patients with OA. This holistic approach is particularly important if multiple joints are involved. Self-management interventions and programs foster the active participation of patients and are thought to be key

796

PART 3 Rehabilitation

elements of chronic disease management. These programs provide education and experiential skills not only in disease management but also in mental and social well-being. Studies have demonstrated that these interventions reduce pain, improve health behaviors, and reduce use of health care resources in patients with chronic pain and arthritis.25 Group-based self-management programs are often available through a local chapter of the Arthritis Foundation and are conditionally recommended by the ACR for patients with hip and knee OA.13 Lifestyle changes like exercise and weight loss are an integral part of the rehabilitation of arthritic patients and may slow the progression of OA.26 There is significant evidence that physical activity is important in patients with OA. Both aerobic and muscle strengthening exercises seem to be beneficial in terms of improving pain, function, and quality of life.27–30 There is robust evidence that land-based therapeutic exercises have at least short-term benefit on pain reduction in knee OA; this benefit is sustained for a minimum of 2 to 6 months following cessation of the program, and there is moderate-quality evidence for benefit in physical function.30 Similar findings were seen for hip OA but to a slightly lesser extent.29 Therapeutic exercises should include joint-protection techniques, stretching and range-of-motion exercises, muscle strengthening, and aerobic exercises. Weight loss is important in overweight patients with OA. A meta-analysis of weight reduction in patients with knee OA showed improved physical ability with a weight loss of more than 5% within a 20-week period.31 The ACR strongly recommends land-based cardiovascular (aerobic) and resistance exercises, aquatic exercises, Tai Chi, and weight loss (in overweight individuals) for patients with OA of the hip and knee.13 Clinical experience suggests that cold, heat, and manual therapy can be helpful in decreasing pain and increasing mobility. Thermal agents and manual therapy in combination with supervised exercise are also recommended by the ACR.13 Braces and splints may be helpful for symptomatic relief in certain joints. There are conflicting data on the effectiveness of knee bracing.34 One recent meta-analysis showed that knee bracing had little to no clinical effect on pain, knee function, or quality of life.32 However, other studies have shown some benefit from unloading valgus braces on patients with medial compartment arthritis. Many patients experience side effects such as discomfort due to poor fit, skin irritation, or sweating and thus stop using these braces.33 Splints may be useful for OA of the thumb.35 The ACR recommends splinting for patients with hand OA, specifically of the trapeziometacarpal joint (first CMC joint), but offers no recommendations on knee bracing.13 The wearing of a thumb-base OA splint at night has been shown to decrease pain and possibly decrease disability.36 Orthotic wedged insoles and medially directed patellar taping may be helpful for knee OA to off-load the joint or to improve biomechanics. Patellar taping affords effective short-term relief of pain with patellofemoral arthritis.37 Adaptive equipment, such as a cane or walker, can be used if necessary by patients with impaired balance to prevent falls or for pain reduction by decreasing joint loading. In the setting of significant functional impairments, therapists

can provide assistive devices that help with feeding, grooming, dressing, and other activities of daily living. The use of transcutaneous electrical nerve stimulation is supported by a few small short-term trials. Systematic review of the data has been inconclusive.38 For most patients in these studies, pain relief was experienced only during active use of the device. Nevertheless, transcutaneous electrical nerve stimulation is conditionally recommended by the ACR for knee OA.13 Ultrasound appears to have no proven benefit in the treatment of OA. Acupuncture is also recommended for the treatment of chronic moderate to severe pain in knee OA. Overall there is evidence that acupuncture can be effective as adjunctive therapy for reducing pain and improving function in patients with knee OA.39 A recent meta-analysis of two to three sessions per week of acupuncture in the treatment of chronic knee OA showed significant benefits in long- and shortterm function but only short-term improvement in pain.40 

Procedures Intra-articular corticosteroid injection is conditionally recommended by the ACR for patients with painful knee or hip OA who do not have a satisfactory clinical response to full-dose acetaminophen.13 The short-term effect of intra-articular corticosteroid injection has been well demonstrated in meta-analyses and is routinely used in the treatment of OA.41 There is clinically significant improved pain relief and patient global assessment compared with placebo injections, with the effects typically lasting up to 6 weeks postinjection.41 Most clinical studies have looked at relatively lower doses of intra-articular corticosteroids (40 mg of triamcinolone or methylprednisolone), whereas there is evidence that higher doses (>50 mg of methylprednisolone) afford greater benefit for longer periods of time.42 Intra-articular injections of hyaluronic acid (viscosupplementation) are conditionally recommended by the ACR for people 75 years of age or older with knee OA but are not routinely recommended for OA of other joints.13 Although conflicting evidence exists, multiple meta-analyses of randomized controlled trials suggest that there is a benefit in comparison with intra-articular placebo injection or noninterventional control.43 The clinical significance is difficult to determine and may be irrelevant. In comparison with glucocorticoid injections, hyaluronic acid injections had greater benefit between 5 and 13 weeks after injection, but this was not sustained over a longer term.43 Botulinum toxin A is thought to inhibit the release of transmitters involved in nociception. A recent prospective randomized controlled trial of botulinum toxin A showed it to be beneficial in controlling pain and improving function in short- and long-term follow-up.44 Regenerative medicine has gained popularity over the past few years, and a branch of this emerging field involves the regeneration of cartilage, muscle, and bone using mesenchymal stem cells (MSCs). The role of MSCs is to maintain and repair their endogenous tissues, and they have therefore generated immense interest as therapeutic agents in arthritic conditions. These adult pluripotent cells can be found in several human tissues but are primarily extracted from bone marrow and adipose tissue, and the cells can be expanded in number by being placed in various growth factors and then

CHAPTER 140 Osteoarthritis

injected into arthritic joints or damaged muscles/tendons. A recent review of 18 clinical trials of the use of MSCs in the treatment of knee OA found that MSC treatment was effective up to 2 years posttreatment even when compared with efficacy at 3 to 6 months.45 Although MSC treatment is a promising option for OA patients, it should be noted that MSCs are not currently FDA-approved and that more practical knowledge must be obtained regarding dosing and patient selection. Preliminary studies seem to indicate that patients with mild to moderate OA are ideal candidates for MSC treatment; patients with more advanced OA were less responsive.46 

Technology There is no specific technology for the treatment and rehabilitation of OA.

Surgery In patients for whom pain and loss of mobility are disabling despite conservative management, orthopedic consultation should be obtained to assess the risks and benefits of surgery. Surgical interventions performed for OA include arthroscopic lavage and débridement, osteotomy, joint fusion, joint distraction, and arthroplasty. Joint replacement surgery or total joint arthroplasty is a mainstay of surgical OA treatment. Protocols for total joint arthroplasty include different approaches and minimally invasive techniques. A systematic review of hip replacement surgery trials concluded that in 70% of subjects, pain and function scores were rated good or excellent 10 years postoperatively.47 Observational studies have suggested that better outcomes are associated with patients between the ages of 45 and 75 years; who weigh less than 70 kg; who have good social support, a higher educational level, and lower preoperative morbidity.48 Similar favorable results have been achieved in total knee replacement for OA. In both hip and knee joint replacements, early inpatient rehabilitation after arthroplasty has been shown to reduce hospital stays and cost of care in older patients with medical comorbidities.49 A systematic review of arthroscopic lavage and débridement in OA showed no short- or long-term benefit compared with placebo, and it is not advised.50 Osteotomy has been used to correct biomechanics and unload areas of high stress, with some success. Fusion may be helpful in situations where joint replacement is not appropriate. Joint distraction or distraction arthroplasty is increasingly performed for ankle OA to avoid fusion and maintain range of motion. Hip joint resurfacing is an effective alternative to total arthroplasty in severe hip OA,51 but patellar resurfacing is not recommended in knee pain, for which no benefit has been shown.52 

Potential Disease Complications Potential complications of OA include chronic pain, muscle weakness, decreased range of motion, limited physical function, inability to participate in work or the community, and loss of self-care skills. 

797

Potential Treatment Complications The safety profile of topical OA medications is generally good. Topical NSAIDs, capsaicin, and rubefacients may cause increased local adverse events (mostly mild skin reactions such as redness, burning pain, and itching). It is worthwhile to caution patients that they may experience increased pain when beginning such therapy. Oral analgesics including acetaminophen and NSAIDs have well-known side effects that most commonly involve the gastric, hepatic, and renal systems. Although the use of acetaminophen is associated with only mild side effects for the most part, it does carry a significant risk of hepatic toxicity. NSAIDs are known to have both gastrointestinal toxicity and nephrotoxicity and are associated with increased risk of myocardial infarction, stroke, and erectile dysfunction. In patients with high gastrointestinal risk for ulceration and bleeding, a cyclooxygenase-2 inhibitor or NSAID with concurrent use of a proton pump inhibitor may be considered. Until recently, it was thought that selective cyclooxygenase-2 inhibitors (celecoxib) carried a greater cardiovascular risk; however, a recent study comparing celecoxib with nonselective cyclooxygenase-1 inhibitors, naproxen, and ibuprofen showed no increased risk of heart failure, myocardial infaction (MI), or stroke with celecoxib.53 The most common adverse reactions to tramadol and opioids are nausea, vomiting, itching, sweating, constipation, and drowsiness. Drug addiction and dependence with both are widely reported. All intra-articular injections usually have mild side effects but, like any such procedure, may result in bleeding, infection, local irritation, and pain. Studies have clearly documented the adverse effects or events associated with total arthroplasty. Intraoperative complications include fracture, nerve injury, vascular injury, and cement-related hypotension. Postoperative complications of total joint arthroplasty include thromboembolism, dislocation, osteolysis, aseptic loosening, implant failure or fracture, and heterotopic ossification. Aseptic loosening, implant failure, and fractures are often painful and require surgical revision.

References 1. Cisternas M, Murphy L, Sacks JJ, et al. Alternative methods for defining osteoarthritis and the impact on estimating prevalence in a US population-based survey. Arthritis Care Res (Hoboken). 2016;68(5):574–580. 2. Lawrence RC, Felson DT, Helmick CG, et al. Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part II. Arthritis Rheum. 2008;58:26–35. 3. Woolf AD, Pfleger B. Burden of major musculoskeletal conditions. Bull World Health Organ. 2003;81:9. 4. Cucchiarini M, de Girolamo L, Filardo G, et al. Basic science of osteoarthritis. J Exp Orthop. 2016;3(1):22. 5. Chapman K, Valdes AM. Genetic factors in OA pathogenesis. Bone. 2012;51:258–264. 6. Nevitt MC, Zhang Y, Javaid MK, et al. High systemic bone mineral density increases the risk of incident knee OA and joint space narrowing, but not radiographic progression of existing knee OA: the MOST study. Ann Rheum Dis. 2010;69:163–168. 7. Blagojevic M, Jinks C, Jeffery A, et al. Risk factors for onset of osteoarthritis of the knee in older adults: a systematic review and meta-analysis. Osteoarthritis Cartilage. 2010;18:24–33. 8. Sellam J, Berenbaum F. Is osteoarthritis a metabolic disease? Joint Bone Spine. 2013;80(6):568–573. 9.  Eymard F, Parsons C, Edwards MH, et al. Diabetes is a risk factor for knee osteoarthritis progression. Osteoarthritis Cartilage. 2015;23(6):851–859.

798

PART 3 Rehabilitation

10. Morteza D. Comparative effectiveness of B and E vitamins with diclofenac in reducing pain due to osteoarthritis of the knee. Med Arch. 2015;69(2):103–106. 11. Reijman M, Hazes JM, Pols HA, et al. Acetabular dysplasia predicts incident osteoarthritis of the hip: the Rotterdam study. Arthritis Rheum. 2005;52:787–793. 12. Arnstein PM. Evolution of topical NSAIDs in the guidelines for treatment of osteoarthritis in elderly patients. Drugs Aging. 2012;29:523–531. 13. Hochberg MC, Altman RD, April KT, et al. American College of Rheumatology 2012 recommendations for the use of nonpharmacologic and pharmacologic therapies in osteoarthritis of the hand, hip, and knee. Arthritis Care Res (Hoboken). 2012;64:465–474. 14. Rannou F, Pelletier JP, Martel-Pelletier J. Efficacy and safety of topical NSAIDs in the management of osteoarthritis: evidence from real-life setting trials and surveys. Semin Arthritis Rheum. 2016;45(4):S18–S21. 15. Balmaceda CM. Evolving guidelines in the use of topical nonsteroidal anti-inflammatory drugs in the treatment of osteoarthritis. BMC Musculoskelet Disord. 2014. 16. Derry S, Matthews PRL, Wiffen PJ, Moore RA. Salicylate-containing rubefacients for acute and chronic musculoskeletal pain in adults. Cochrane Database Syst Rev. 2014;(11):CD007403. 17. Nagai J, Uesawa Y, Shimamura R. Characterization of the adverse effects induced by acetaminophen and nonsteroidal anti-inflammatory drugs based on the analysis of the Japanese Adverse Drug Event Report Database. Clin J Pain. 2017;33(8):667–675. 18. Cepeda MS, Camargo F, Zea C, et al. Tramadol for osteoarthritis. Cochrane Database Syst Rev. 2006;3:CD005522. 19. Zhang H, Liu Z. The investigation of tramadol dependence with no history of substance abuse: a cross-sectional survey of spontaneously reported cases in Guangzhou City. China Biomedical Res Int. 2013. Article ID 283425. 20. Smith SR, Deshpande BR, Collins JE, et al. Comparative pain reduction of oral non-steroidal anti-inflammatory drugs and opioids for knee osteoarthritis: systemic analytic review. Osteoarthritis Cartilage. 2016;24(6):962–972. 21. Hochberg MC, Wohlreich M, Gaynor P, et al. Clinically relevant outcomes based on analysis of pooled data from 2 trials of duloxetine in patients with knee osteoarthritis. J Rheumatol. 2012;39:352–358. 22. Deleted in page proofs. 23. Deleted in page proofs. 24. Daily JW, Yang M, Park S. Efficacy of turmeric 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(8):717–729. 25. Lorig KR, Sobel DS, Stewart AL, et al. Evidence suggesting that a chronic disease self-management program can improve health status while reducing hospitalization: a randomized trial. Med Care. 1999;37:5–14. 26. Svege I, Nordsletten L, Fernandes L, et al. Exercise therapy may postpone total hip relplacemtent surgery in patients with hip osteoarthritis: a long-term follow-up of a randomized trial. Ann Rheum Dis. 2013. 27. Pelland L, Brosseau L, Wells G, et al. Efficacy of strengthening exercises for osteoarthritis (Part I): a meta-analysis. Phys Ther Rev. 2004;9:77–108. 28. Loew L, Brosseau L, Wells GA, et al. Ottawa panel evidence-based clinical practice guidelines for aerobic walking programs in the management of osteoarthritis. Arch Phys Med Rehabil. 2012;93:1269–1285. 29. Fransen M, McConnell S, Hernandez-Molina G, et al. Exercise for osteoarthritis of the hip. Cochrane Database Syst Rev. 2014;4:CD007912. 30. Fransen M, McConnell S, Harmer AR. Exercise for osteoarthritis of the knee. Cochrane Database Syst Rev. 2015;1:CD004376.

31. Christensen R, Bartels EM, Astrup A, Bliddal H. Effect of weight reduction in obese patients with knee osteoarthritis: a systematic review and meta-analysis. Ann Rheum Dis. 2007;66:433–439. 32. Duivienvoorden T, Brouwer RW, van Raaij TM, et al. Braces and orthoses for treating osteoarthritis of the knee. Cochrane Database Syst Rev. 2015;3:CD004020. 33. Moyer R, Birmingham T, Marriott K, et al. A systematic review and meta-analysis of biomechanical and clinical effects of valgus knee bracing. Osteoarthritis Cartilage. 2014;22:S457. 34. Brouwer RW, Jakma TS, Verhagen AP, et al. Braces and orthoses for treating osteoarthritis of the knee. Cochrane Database Syst Rev. 2005;1:CD004020. 35. Rannou F, Dimet J, Boutron I, et al. Splint for base-of-thumb osteoarthritis: a randomized trial. Ann Intern Med. 2009;150:661–669. 36. Beaudreuil J. Orthoses for osteoarthritis: a narrative review. Ann Phys Rehabil Med. 2017;60(2):102–106. 37. Crossley K, Marino G, Macilquham M, et al. The effect of patellar tape on patellar malalignment associated with patellofemoral osteoarthritis. J Sci Med Sport. 2009;12:S68. 38. Rutjes AW, Nüesch E, Sterchi R, et al. Transcutaneous electrostimulation for osteoarthritis of the knee. Cochrane Database Syst Rev. 2009;4:CD002823. 39. Hochberg M, Lixing L, Bausell B, et al. Traditional Chinese acupuncture is effective as adjunctive therapy in patients with osteoarthritis of the knee [abstract]. Arthritis Rheum. 2004;50:S644. 40. Lin X, Huang K, Zhu G. The effects of acupuncture on chronic knee pain due to osteoarthritis, a meta-analysis. J Bone Joint Surg Am. 2016;98(18):1578–1585. 41. da Costa BR, Hari R, Juni P. Intra-articular corticosteroids for osteoarthritis of the knee. JAMA. 2016;(24):316. 42. David T Felson. Intra-articular corticosteroids and knee osteoarthritis interpreting different meta-analyses. JAMA. 2016;316(24):2607–2608. 43. Bellamy N, Campbell J, Robinson V, et al. Viscosupplementation for the treatment of osteoarthritis of the knee. Cochrane Database Syst Rev. 2006;2:CD005321. 44. Hsieh L-F, Wu C-W, Chou C-C, et al. Effects of botulinum toxin landmark-guided intra-articular injection in subjects with knee osteoarthritis. PM R. 2016;8(12):1127–1135. 45. Cui GH, Wand YY, Li CJ, et al. Efficacy of mesenchymal stem cells in treating patients with osteoarthritis of the knee: a meta-analysis. Exp Ther Med. 2016;12(5):3390–3400. 46. Afizah H, Hui JHP. Mesenchymal stem cell therapy for osteoarthritis. J Clin Orthopaed Trauma. 2016;7(3):177–182. 47. Faulkner A, Kennedy LG, Baxter K, et al. Effectiveness of hip prostheses in primary total hip replacement: a critical review of evidence and an economic model. Health Technol Assess. 1998;2:1–33. 48. Young NL, Cheah D, Waddell JP, et al. Patient characteristics that affect the outcome of total hip arthroplasty: a review. Can J Surg. 1998;41:188–195. 49. Munin MC, Rudy TE, Glynn NW, et al. Early inpatient rehabilitation after elective hip and knee arthroplasty. JAMA. 1998;279:847–852. 50. Laupattarakasem W, Laopaiboon M, Laupattarakasem P, et al. Arthroscopic debridement for knee osteoarthritis. Cochrane Database Syst Rev. 2008;1:CD005118. 51. Smith TO, Nichols R, Donell ST, et al. The clinical and radiological outcomes of hip resurfacing versus total hip arthroplasty: a meta-­ analysis and systematic review. Acta Orthop. 2010;81:684–695. 52. Pavlou G, Meyer C, Leonidou A, et al. Patellar resurfacing in total knee arthroplasty: does design matter? A meta-analysis of 7075 cases. J Bone Joint Surg Am. 2011;93:1301–1309. 53. Nissen S, Yeomans N, et al. Cardiovascular safety of celecoxib, naproxen or ibuprofen for arthritis. N Engl J Med. 2016;375(26):2519–2529.

CHAPTER 141

Osteoporosis David M. Slovik, MD

Synonyms Thin bones Brittle bones

ICD-10 Code M81.0

Age-related osteoporosis without current pathological fracture

Definition Osteoporosis is a skeletal disorder characterized by compromised bone strength predisposing a person to an increased risk for fracture. Bone strength primarily reflects the integration of bone density and bone quality. Bone quality refers to factors such as microarchitectural changes, bone turnover, collagen structure, damage accumulation (e.g., microfractures), and degree of mineralization.1 Osteoporosis can also be defined according to the World Health Organization criteria on the basis of bone mineral density and bone mineral content measurements (see section on Diagnostic Studies). Osteoporosis is the most common metabolic bone disease. The National Osteoporosis Foundation estimates that at least 10 million Americans have osteoporosis and another 34 million have decreased bone mass, putting them at increased risk for osteoporosis and fractures. Of the 10 million, 8 million are women and 2 million are men. Annually in the United States, more than 1.5 million fractures attributable to osteoporosis occur, including approximately 750,000 vertebral, 300,000 hip, and 250,000 wrist fractures. About one out of every two Caucasian women will experience an osteoporotic-related fracture in her lifetime as well as approximately one in five men. The annual cost of caring for osteoporosis-related fractures in the United States is in excess of $16 billion. In addition, there is a 15% to 25% excess mortality within the first year after a hip fracture. Recent trends suggest that femur neck osteoporosis in older US adults was higher than in the past and the previous trend in decreasing hip fractures may have stopped.2 

Symptoms Osteoporosis is a silent disease until a fracture occurs. Pain and deformity are usually present at the site of fracture. Vertebral fractures often occur with little trauma, such as

coughing, lifting, or bending over. Acute back pain may be related to a vertebral compression fracture, with pain localized to the fracture site or in a radicular distribution. New back pain or chronic back pain in a patient with osteoporosis and prior vertebral fractures may be related to new fractures, muscle spasm, or other causes. With vertebral fractures, even if they are asymptomatic, there may be a gradual loss of height and the development of a kyphosis. Breathing may be difficult, and early satiety and bloating—a sensation of fullness and dyspepsia—may develop because of less room in the abdominal cavity. 

Physical Examination In evaluating patients with osteoporosis, it is important to diagnose treatable and reversible causes and to assess the risk factors for development of osteoporosis and osteoporotic fractures. Table 141.1 lists common causes of osteoporosis. Table 141.2 lists risk factors for osteoporosis. The physical examination focuses on findings suggestive of secondary causes of osteoporosis (e.g., hyperthyroidism and Cushing syndrome). One should also examine areas previously involved with fractures (e.g., back, hip, and wrist) to assess for deformity and limitation of function. A baseline measurement of height should be obtained and reevaluated at subsequent visits, preferably using a wall-mounted stadiometer. Localized vertebral tenderness may be present from fracture, paravertebral muscle spasm, or exaggerated thoracic kyphosis. The findings of the neurologic examination looking for any deficits due to vertebral fracture are usually normal. 

Functional Limitations Functional limitations are related to the type of fracture and its long-term consequences. With vertebral fractures, the functional limitation may initially be related to the acute pain and inability to move. The chronic limitations may be related to loss of height, chronic back pain, difficulty in moving, abdominal distention, and difficulty in breathing. The functional limitations after a hip fracture are related to the decreased functional mobility, often the need for long-term use of assistive devices, the lack of independence, and the long-term need for assistive care. An assistive device will be needed permanently for ambulation by 50% of people with a hip fracture, and two thirds will lose some of their ability to perform ordinary daily activities. Wrist fractures usually heal completely, but some people have chronic pain, deformity, and functional limitations.  799

800

PART 3 Rehabilitation

Table 141.1  Common Causes of Osteoporosis

Diagnostic Studies3-6

Age Related Postmenopausal

Bone density measurements are the standard for assessment of risk, diagnosis, and long-term management of patients with osteoporosis. Bone density measurement is often essential to make management decisions. Available techniques include dual-energy x-ray absorptiometry (DEXA), quantitative computed tomography (QCT), and quantitative ultrasonography. DEXA, although it is not as sensitive as QCT for detection of early trabecular bone loss, is the method of choice for measurement of bone mineral density because of its good precision, low radiation dose, and fast examination time. Bone mineral density testing should be based on an individual’s fracture risk profile and skeletal health assessment. It should be performed only if the results will influence a treatment decision. Bone mineral density testing should be considered on the basis of the National Osteoporosis Foundation guidelines, as follows3: • Women age 65 and older and men age 70 and older, regardless of clinical risk factors • Younger postmenopausal women and men age 50 to 69 about whom you have concern based on their clinical risk factor profile • Adults who have a fracture after age 50 • Adults with a condition (e.g., rheumatoid arthritis) or taking a medication (e.g., glucocorticoids in a daily dose of 5 mg or more for >3 months) associated with low bone mass or bone loss • Anyone being considered for pharmacologic therapy for osteoporosis •  Anyone being treated for osteoporosis, to monitor treatment effect • Anyone not receiving therapy in whom evidence of bone loss would lead to treatment • Postmenopausal women discontinuing estrogen Bone mineral density is reported by T and Z scores (Table 141.3). The T score compares an individual’s bone mineral density with the mean value for young normal individuals expressed as a standard deviation (SD); the Z score compares the values to age- and sex-matched adults. • Normal: a T score value for bone mineral density or bone mineral content that is not more than 1 SD below the young adult mean value. • Low bone mass (osteopenia): a T score value for bone mineral density or bone mineral content that lies between 1.0 and 2.5 SDs below the young adult mean value. • Osteoporosis: a T score value for bone mineral density or bone mineral content that is 2.5 SDs or more below the young adult mean value. The lower the T score, the higher the risk for subsequent fractures. However, the score will not predict who will fracture because other factors come into play (e.g., fall velocity,

Senile Endocrine and Metabolic Related Hypogonadism Hyperthyroidism Primary hyperparathyroidism Adrenal-cortical hormone excess Diabetes mellitus, type 1 Hypercalciuria Genetics and Collagen Disorders Osteogenesis imperfecta Ehlers-danlos syndrome Homocystinuria Marfan syndrome Hematologic Disorders Multiple myeloma Systemic mastocytosis Thalassemia Drug Related Glucocorticoids Thyroid hormone excess Chemotherapy, immunosuppressants Anticonvulsant drugs Aromatase inhibitors Androgen deprivation therapy (men) Proton pump inhibitors Selective serotonin reuptake inhibitors Thiazolidinediones Miscellaneous Rheumatoid arthritis Immobilization Organ transplantation

Table 141.2  Risk Factors for Osteoporosis Advanced age Female Small-boned, thin women White and Asian women Estrogen deficiency Personal history of fracture as adult Fracture in first-degree family members Inactivity Low calcium intake Cigarette smoking

Table 141.3  Bone Mineral Density Reporting

Alcoholism

T score

Medications such as glucocorticoids, excessive thyroid hormone, chemotherapy and immunosuppressants, antiseizure drugs, aromatase inhibitors; androgen deprivation therapy in men

SDs above or below peak bone mass in young, normal, sex-matched adults

Z score

SDs above or below age- and sex-matched adults

SDs, Standard deviations.

CHAPTER 141 Osteoporosis

type of fall, direction of fall, and protective padding). A low Z score may suggest excessive bone loss due to secondary causes of osteoporosis. Specific laboratory tests are obtained to exclude secondary causes of osteoporosis in the differential diagnosis of osteoporosis. The general laboratory tests include a complete blood count, chemistry profile including calcium and phosphorus, liver and kidney tests, and parathyroid hormone and thyroid-stimulating hormone concentrations. Because of the high prevalence of vitamin D deficiency in the adult population, especially elderly individuals, a serum 25-hydroxyvitamin D level should be obtained. A 24-hour collection of urine for calcium and creatinine measurement is also helpful. In selected patients, a serum and urine protein electrophoresis, tissue transglutaminase antibodies, and urinary free cortisol should be obtained. Blood and urine test results are usually normal in uncomplicated cases of osteoporosis. After a fracture, the alkaline phosphatase activity may be elevated. Biochemical markers of bone turnover, including urine N-telopeptide and serum C-telopeptide, may be helpful in selective patients to assess for bone turnover and whether someone is responding to treatment.  Differential Diagnosis Common causes of osteoporosis are listed in Table 141.1.

801

Table 141.4  Treatment Options Nonpharmacologic Intervention Calcium Vitamin D Exercise Smoking cessation Fall prevention Pharmacologic Agents Hormone replacement therapy Estrogen agonist/antagonists (Selective estrogen receptor modulators)  Raloxifene (Evista) Conjugated estrogen/bazedoxifene (Duavee) Bisphosphonates  Alendronate (Fosamax)  Risedronate (Actonel)  Ibandronate (Boniva)  Zoledronic acid (Reclast) Calcitonin (Miacalcin and Fortical nasal sprays) Teriparatide (Forteo) Abaloparatide (Tymlos) Denosumab (Prolia)

Treatment3-6 Initial

Table 141.5  Osteoporosis Prevention Guidelines

The initial approach to the prevention and treatment of osteoporosis involves non-pharmacologic interventions and, in appropriate patients, the use of various pharmacologic agents (Table 141.4). Prevention and treatment guidelines are presented in Tables 141.5 and 141.6.

Hormone replacement therapy for menopausal symptoms

Calcium Adequate calcium is important for all age groups. Epidemiologic studies suggest that long-standing dietary calcium deficiency can result in lower bone mass. The average dietary calcium intake in postmenopausal women is less than 600 mg/day. Several studies have shown that calcium supplementation along with vitamin D, especially in the elderly, may slow bone loss and reduce vertebral and nonvertebral fracture rates.7,8 A total calcium intake of 1200 to 1300 mg/day is recommended for postmenopausal women.9 It is best to achieve this primarily by consumption of foods that have a high calcium content, such as milk and dairy products and calcium-fortified foods, especially yogurt. Calcium supplementation is often required, especially in elderly individuals. Calcium carbonate supplements have the highest calcium content, but may cause abdominal discomfort with bloating and constipation and are better absorbed when they are taken with foods. Calcium citrate preparations are generally better absorbed and are not dependent on gastric acid. A recent meta-analysis has reported that calcium intake within tolerable levels, defined as 2000 to 2500 mg/day, is not associated with cardiovascular disease risk in generally healthy adults.10,11 

Raloxifene, 60 mg/day Conjugated estrogens/bazedoxifene; conjugated estrogen 0.45 mg and bazedoxifene 20 mg daily Alendronate, 5 mg/day or 35 mg once weekly by mouth (prevention dose) Risedronate, 5 mg/day or 35 mg weekly or 150 mg monthly by mouth Ibandronate, 2.5 mg daily or 150 mg monthly by mouth Zoledronic acid, 5 mg intravenously every other year

Vitamin D Vitamin D insufficiency and deficiency are common in postmenopausal women, especially in those who have sustained a hip fracture and those who are chronically ill, housebound, institutionalized, and poorly nourished.9,12 Vitamin D improves muscle strength and balance and reduces the risk of falling. There may also be other unproven nonskeletal beneficial effects. A dose of 800 to 1000 IU/day (from supplements, multivitamins, and other sources) should be administered to prevent vitamin D deficiency. Some require higher amounts. Many calcium supplements now also contain vitamin D. Maintaining a serum 25-hydroxyvitamin D level of more than 30 ng/mL (70 nmol/L) is suggested by many experts, although the US National Academy of Medicine suggests levels above 20 ng/mL. 

802

PART 3 Rehabilitation

Table 141.6  Osteoporosis Treatment Guidelines

Guidelines for Treatment

Alendronate, 10 mg/day or 70 mg once weekly (treatment dose)

The guidelines for treatment of postmenopausal women based on National Osteoporosis Foundation recommendations are as follows: • Hip or spine fracture • T score—2.5 or below at the spine, femoral neck, or total hip • T score—between 1.0 and 2.5 and high 10-year fracture risk by the US-adapted World Health Organization Fracture Risk Assessment Calculator. Treat if 10-year risk is 3% or more for hip fractures or 20% or more for major osteoporosis-related fractures.16 

Risedronate, 5 mg/day or 35 mg weekly or 150 mg monthly by mouth Ibandronate, 2.5 mg/day or 150 mg monthly orally; 3 mg intravenously every 3 months Zoledronic acid, 5 mg intravenously yearly Raloxifene, 60 mg/day Calcitonin (nasal spray), 200 units once daily Teriparatide, 20 μg subcutaneously daily for 2 years Abaloparatide 80 μg subcutaneously daily for 2 years Denosumab, 60 mg subcutaneously every 6 months

Exercise There is significant evidence that dynamic weight-bearing and strength training exercises are beneficial to bone in helping achieve peak bone mass and preserving bone later in life.13 Bone adapts to physical and mechanical loads placed on it by altering its mass and strength. This occurs either by the direct impact from the weight-bearing activity or by the action of muscle attached to bone. Exercising can also help strengthen back muscles, improve balance, lessen the likelihood of falling, and give one a sense of well-being.14 Back extension exercises and abdominal strengthening exercises are helpful. However, acute stresses to the back, such as trunk flexion, side-bending, high impact, and heavy weights, should be avoided to lessen the likelihood of injury and fracture. A proper exercise program should be established and may require working with a physical therapist or an exercise trainer. Older postmenopausal women and even the frail elderly can tolerate and potentially show improvements in muscle strength and bone mineral density in response to strength training and resistive exercise programs. The exercise regimen should also be adjusted to their medical status. 

Smoking Cessation A 5% to 10% reduction in bone density has been seen in women who smoked one pack per day in adulthood. Therefore, it is recommended that physicians aggressively pursue smoking cessation in their treatment plans. 

Fall Prevention Many factors can lead to falls, including poor vision, frailty, medication (especially narcotic pain medications, hypotensive agents, and psychotropic drugs), and balance disturbances.15 Each area needs to be assessed appropriately. Prevention measures include keeping rooms free from clutter and having good lighting. Advise patients to wear supportive shoes, to be aware of thresholds, and to avoid slippery floors; rugs should be tacked down. Grab bars are useful in the bathroom. A portable telephone and a personal alarm activator are helpful, and someone should check on the individual regularly. 

Hormone Replacement Therapy Hormone replacement therapy can be used in the short-term management of postmenopausal women with symptoms of estrogen deficiency, including hot flashes, memory deficits, urinary frequency, and vaginal dryness. Long-term hormone replacement therapy can slow bone loss and lower the incidence of fractures.17 In the Women’s Health Initiative (WHI) study with estrogen and progestin, there was a 34% reduction in the incidence of vertebral and hip fractures. However, there was an increase in breast cancer, coronary heart disease, stroke, and thromboembolic disease.18 The mean age of patients in the WHI was 63 years. A reanalysis from the WHI showed no increase in coronary heart disease risk in women when hormone replacement therapy was started within 10 years of the onset of menopause.19 Significant controversy still exists about the results of the WHI. Estrogen is approved for the prevention of osteoporosis, but not for treatment. The major reason to use hormone replacement therapy is to treat menopausal symptoms. The lowest dose of estrogen and progesterone should be used to effectively relieve these symptoms. Women who have had a hysterectomy should be given estrogen alone. A progestin should be added to the estrogen regimen if the uterus is still present. 

Estrogen Agonist/Antagonists (Formerly Known as Selective Estrogen Receptor Modulators) Estrogen agonist/antagonists are synthetic compounds that have both estrogen-agonistic and estrogen-antagonistic properties. Raloxifene is approved by the Food and Drug Administration (FDA) for the prevention and treatment of osteoporosis at an oral dose of 60 mg daily. Raloxifene is also approved for the reduction in risk of invasive breast cancer in postmenopausal women with osteoporosis and in postmenopausal women at high risk of invasive breast cancer. Raloxifene reduces new vertebral fractures by 40% to 50%, but not the risk of nonspine fractures.20 Raloxifene acts as an anti-estrogen on breast tissue and reduces the risk of invasive breast cancer similar to the reduction by tamoxifen. It does not produce uterine hypertrophy and does not significantly affect the risk of coronary heart disease. Raloxifene has no beneficial effects on menopausal symptoms and may increase hot flashes and the risk of deep venous thrombosis. A combination of conjugated estrogen with bazedoxifene (a SERM) is approved for the treatment of menopausal symptoms and prevention of osteoporosis.21 

CHAPTER 141 Osteoporosis

Bisphosphonates The bisphosphonates are a group of compounds related chemically to pyrophosphate. They are characterized by a P-C-P structure. Changes in the side chains affect the binding and potency of the bisphosphonates. They are potent inhibitors of osteoclastic bone resorption. Alendronate was the first approved by the FDA in 1995 for the prevention and treatment of postmenopausal osteoporosis. Alendronate is also approved for the treatment of glucocorticoid-induced osteoporosis and osteoporosis in men. In postmenopausal women, the dose for prevention is 5 mg/day or 35 mg once weekly; the dose for treatment is 10 mg/day or 70 mg once weekly. Alendronate significantly increases bone mineral density at various sites. In addition, there is a significant decrease in the incidence of vertebral, hip, and wrist fractures as well as painful vertebral fractures, hospitalization days, and other measurements of functional impairment.22 Risedronate is approved by the FDA for the prevention and treatment of postmenopausal osteoporosis with an oral dose of 5 mg daily, 35 mg weekly, or 150 mg monthly. Studies have shown an increase in bone mineral density at various sites along with a decrease in vertebral and nonvertebral fractures.23 Risedronate is also approved for the prevention and treatment of glucocorticoid-induced osteoporosis and osteoporosis in men. Ibandronate is approved by the FDA for the prevention and treatment of postmenopausal osteoporosis. The oral dose is either 2.5 mg daily or 150 mg monthly. An intravenous preparation is also available for the treatment of postmenopausal osteoporosis in a dose of 3 mg intravenously every 3 months. Studies have shown an increase in bone density and a reduction in vertebral fractures.24 The bisphosphonates are poorly absorbed and must be given on an empty stomach to maximize their absorption. Alendronate and risedronate must be taken at least 30 minutes (ibandronate, 60 minutes) before the first food, beverage, or medication with a full glass of plain water, and patients should not lie down for at least 30 minutes (ibandronate, 60 minutes) to avoid the potential upper gastrointestinal side effects, especially of esophagitis. Patients with a history of reflux should not be given these medications. Zoledronic acid is approved by the FDA for the treatment of postmenopausal osteoporosis, osteoporosis in men, and glucocorticoid-induced osteoporosis and after surgical repair of hip fracture. It is administered as a onceyearly infusion of 5 mg, usually over 15 to 20 minutes. It significantly reduces spine, hip, and nonhip fractures and increases bone density.25 It is also approved for the prevention of postmenopausal osteoporosis with a 5 mg infusion once every 2 years. The major side effects with the intravenous bisphosphonates are the acute phase symptoms, including fever, muscle and joint pains, influenza-like symptoms, and headache. These usually last for no more than 24 to 72 hours. These symptoms have been reported in 32% of patients with the first infusion, in 7% after the second yearly infusion, and in 3% after the third infusion of zoledronic acid. Very uncommon but serious adverse complications from long-term use of the bisphosphonates include osteonecrosis of the jaw26,27 and atypical femur

803

fractures.2,28 Osteonecrosis of the jaw has been reported primarily in cancer patients who receive bisphosphonates for skeletal metastases at a dose much higher than the dose given for osteoporosis. 

Calcitonin Synthetic salmon calcitonin given parenterally by injection and nasal spray is approved for the treatment of postmenopausal osteoporosis. The injectable calcitonin is given as 100 units daily subcutaneously or intramuscularly. The nasal spray of calcitonin is approved in a dose of 200 units (one spray) daily. A reduction in new vertebral fractures but not in hip or nonvertebral fractures has been reported.29 Occasional nasal irritation or headache may be seen with the nasal spray. A mild short-term analgesic effect can be seen. 

Parathyroid Hormone As long ago as the late 1920s, there was evidence that parathyroid extract, administered in an intermittent once-a-day injection, stimulated osteoblast activity in animal models. This is in contrast to bone loss seen with chronic elevations in parathyroid hormone in primary hyperparathyroidism. After human parathyroid hormone was sequenced in the early 1970s, clinical studies with use of the 1-34 aminoterminal fragment started. Early results in osteoporosis trials showed increases in bone accretion, calcium balance, and trabecular bone volume with normal skeletal architecture. In the multicenter trial of recombinant human parathyroid hormone 1-34 fragment (teriparatide), 20 μg administered subcutaneously daily produced an increase in vertebral and hip bone density and a 55% reduction in vertebral fracture risk.30 Teriparatide is generally well tolerated with occasional leg cramps, nausea, and dizziness. It has to be selfadministered for up to 2 years by use of a 31-gauge needle and a prefilled syringe with a 28-day supply of medication. Until very recently it was the only anabolic agent available (in contrast to the antiresorptive agents) and is approved for the treatment of postmenopausal women with osteoporosis who are at high risk for fracture. It is also approved for treatment of osteoporosis in men and glucocorticoidinduced osteoporosis. In rats given teriparatide in doses up to 60 times the exposure in humans, there was an increase in osteosarcoma, which was dose and duration dependent. Thus, teriparatide should not be administered to patients who have an increased baseline risk for osteosarcoma, including patients with Paget disease of bone, those with unexplained elevated alkaline phosphatase, and those who have received prior external beam or implant radiation therapy involving the skeleton. It is suggested the cumulative use of teriparatide and abaloparatide should not exceed two years in a patient’s lifetime. 

Parathyroid Hormone Related Peptide Abaloparatide (human parathyroid human related peptide 1-34 fragment; PTHrP[1-34]) was recently approved for the treatment of postmenopausal women with osteoporosis at high risk for fracture. It is an anabolic agent and reduces the risk of vertebral and nonvertebral fractures. It is a selfadministered injection of 80 μg subcutaneously once daily. It is generally well tolerated and adverse effects include

804

PART 3 Rehabilitation

dizziness, nausea, and headache. As with teriparatide, in rats there was a dose-dependent increase in the incidence of osteosarcoma. It thus should not be given to individuals at increased risk for osteosarcoma, as noted above in the teriparatide section. In addition, it is suggested the cumulative use of teriparatide and abaloparatide should not exceed two years in a patient’s lifetime.31 

Denosumab Denosumab is a human monoclonal antibody directed against RANKL, a cytokine mediator responsible for accelerating osteoclast formation. It is approved for the treatment of postmenopausal osteoporosis at high risk for fractures and osteoporosis in men. It is also approved to treat bone loss in women with breast cancer receiving aromatase inhibitor treatment and to treat bone loss in men receiving gonadotropin-reducing hormone treatment for prostate cancer. The dose is 60 mg subcutaneously every 6 months. Reductions in spine, hip, and nonspine fractures are seen, and there is an increase in bone density. Side effects include a small increase in serious infection, such as skin infections. It is not affected by renal function and can be given to patients with reduced renal function.32 

Rehabilitation Rehabilitation efforts in osteoporosis should commence long before a fracture. Either a physical or occupational therapist can be involved in assessing the patient’s home to make sure it is safe and to decrease the risk of falls. Specialized equipment, such as grab bars for the bathroom and hand-held reachers for high cupboards, can be very helpful. It is important to educate patients about keeping the floors clear of clutter and throw rugs. Small pets also can be a hazard underfoot. Therapists can assess whether the patient would be safer ambulating with an assistive device (e.g., cane or walker) in the home and community. It is important for all assistive devices to be appropriately prescribed and fitted for the patient. Finally, patients need instructions about how to exercise to improve strength, flexibility, and balance. All of these activities can help prevent falls, and weight-bearing strengthening exercises may also improve bone density. In patients with a hip fracture or other disabling fracture, a multidisciplinary-coordinated team approach involving the physician, therapists, and other rehabilitation specialists (e.g., nurse, social worker) is necessary for the patient to regain maximal function and to lead a productive life. The initial rehabilitation program also involves pain control, bowel and bladder care, and maintenance of skin integrity. The team, in addition to working on a program involving bed mobility, transfers, gait activities, safety precautions, and activities of daily living, must be cognizant of the medical problems in each patient. After an acute rehabilitation stay, some patients may need an additional stay in a transitional setting on their way to eventually going home or else require long-term placement. For those able to go home, the team needs to teach the patient a home exercise program, to order appropriate equipment, and to arrange for continued therapy, either at home or in an outpatient setting.

Back Orthoses Back orthoses may be helpful, especially in the short term, to get patients out of bed and ambulatory so they can participate in activities. Back orthoses, however, can be very uncomfortable and often are not tolerated. Long-term use should be discouraged unless it helps the patient in functional activities and with control of pain. 

Procedures Other than surgery for fracture repair, procedures are generally not needed in the management of osteoporosis. Two procedures—vertebroplasty and kyphoplasty—are available to stabilize vertebral fractures and to alleviate pain. 

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

Surgery The preferred treatment of hip fracture and some other fractures is surgical repair and stabilization. 

Potential Disease Complications As bone density decreases, the risk for sustaining a fracture increases. Osteoporosis is asymptomatic until a fracture occurs. Thereafter, all complications are related to the problems from these fractures, to the surgery (if it is required), to the multiple medical problems and to the recuperative period, and eventually to the loss of function and independence. After vertebral fractures, acute pain may limit mobility. Bed rest and narcotic analgesics may be necessary. Severe constipation and urinary retention may ensue. Chronically, patients may suffer from severe back pain and have respiratory problems, abdominal distention, bloating, and constipation. Many patients who wear a back brace complain about the discomfort and difficulty in using it. 

Potential Treatment Complications The complications of treatment can be related either to the surgical repair of the fracture and the recuperative phase or to medications used to prevent or to treat osteoporosis. Most osteoporotic fractures occur in older patients and result in loss of function and loss of independence and the need for long-term care. Because surgery is required to repair a hip fracture, complications from surgery, anesthesia, bed rest, and pain medications (often narcotics) are common. Pneumonia, phlebitis, urinary tract infection, constipation, and respiratory problems also are frequent. Complications from drug therapy for osteoporosis include the following: potential increase in breast cancer (estrogen), heart disease (estrogen), clotting and thromboembolic problems (estrogen, raloxifene), and endometrial cancer (in those using only estrogen); hot flashes (raloxifene); upper gastrointestinal symptoms and esophagitis from oral alendronate, risedronate, and ibandronate; fever, muscle and joint aches, and influenza-like symptoms from

CHAPTER 141 Osteoporosis

intravenous ibandronate and zoledronic acid; osteonecrosis of the jaw and atypical femur fractures with long-term bisphosphonates; running nose and headache from calcitonin; and transient mild hypercalcemia with teriparatide and abaloparatide and a small increase in infections with denosumab.

References 1. NIH consensus development panel on osteoporosis prevention, diagnosis, and therapy. osteoporosis prevention, diagnosis, and therapy. JAMA. 2001;285:785–795. 2. Looker AC, Srafrazi Isfahani N, Fan B, Shepherd JA. Trends in osteoporosis and low bone mass in older US adults, 2005-2006 through 2013-2014. Osteoporos Int. 2017;28(6):1979–1988. 3. Cosman F, de Beur SJ, Leboff MS, et al. Clinician’s guide to prevention and treatment of osteoporosis. Osteoporos Int. 2014;25:2359–2381. 4. Watts NB, Bilezikian JP, Camacho PM, et al. American Association of Clinical Endocrinologists medical guidelines for clinical practice for the diagnosis and treatment of postmenopausal osteoporosis. Endocr Pract. 2010;16:1–37. 5. Camacho PM, Petak SM, Binkley N, et al. American Association of Clinical Endocrinologists and American College of Endocrinology clinical practice guidelines for the diagnosis and treatment of postmenopausal osteoporosis-2016: executive summary. Endocr Pract. 2016;22:1111–1118. full report 22 (suppl 4) 1–42. 6. Black DM, Rosen CJ. Postmenopausal osteoporosis. N Engl J Med. 2016;374:254–262. 7. Dawson-Hughes B, Harris SS, Krall EA, Dallal GE. Effect of calcium and vitamin D supplementation on bone density in men and women 65 years of age or older. N Engl J Med. 1997;337:670–676. 8. Weaver CM, Alexander DD, Boushey CJ, et al. Calcium plus vitamin D supplementation and risk of fractures: an updated metaanalysis from the national osteoporosis foundation. Osteoporos Int. 2016;27:367–376. 9. Ross AC, Manson JE, Abrams SA, et al. The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know. J Clin Endocrinol Metab. 2011;96:53–58. 10. Chung M, Tang AM, Fu Z, et al. Calcium intake and cardiovascular disease risk: an updated systemic review and meta-analysis. Ann Intern Med. 2016;165:856–866. 11. Kopecky SL, Bauer DC, Gulati M, et al. Lack of evidence linking calcium with or without vitamin D supplementation to cardiovascular disease in generally healthy adults: a clinical guideline from the National Osteoporosis Foundation and the American Society for Preventive Cardiology. Ann Intern Med. 2016;165:867–868. 12. Rosen CJ. Vitamin D, insufficiency. N Engl J Med. 2011;364:248–254. 13. Slovik DM. Osteoporosis. In: Frontera WF, Slovik DM, Dawson DM, eds. Exercise in Rehabilitation Medicine, 2nd ed. Champaign, IL: Human Kinetics; 2006:221–248. 14. Nelson ME, Wernick S. Strong Women, Strong Bones. updated ed. New York: Putnam Penguin; 2006. 15. Greenspan SL, Myers ER, Kiel DP, et al. Fall direction, bone mineral density, and function: risk factors for hip fracture in frail nursing home elderly. Am J Med. 1998;104:539–545. 16. FRAX algorithm. www.shef.ac.uk/FRAX. Also available at www.NOF.org.

805

17. The North American Menopause Society. Management of osteoporosis in postmenopausal women: 2010 position statement of the North American Menopause Society. Menopause. 2010;17:25–54. 18. Rossouw JE, Anderson GL, Prentice RL, et al. Writing Group for the Women’s Health Initiative Investigation. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results from the Women’s Health Initiative randomized controlled trial. JAMA. 2002;288:321–333. 19. Rossouw JE, Prentice RL, Manson JE, et al. Postmenopausal hormone therapy and risk of cardiovascular disease by age and years since menopause. JAMA. 2007;297:1465–1477. 20. Ettinger B, Black DM, Mitlak BH, et al. Multiple outcomes of raloxifene evaluation (MORE) investigators. Reduction of vertebral fracture risk in postmenopausal women with osteoporosis treated with raloxifene: results from a 3-year randomized clinical trial. JAMA. 1999;282:637–645. 21. Gallagher JC, Palacios S, Ryan KA, et al. Effect of conjugated estrogens/bazedoxifene on postmenopausal bone loss: pooled analysis of two randomized trials. Menopause. 2016;23:1083–1091. 22. Black DM, Cummings SR, Karpf DB, et al. Randomized trial of effect of alendronate on risk of fracture in women with existing vertebral fractures. Lancet. 1996;348:1535–1541. 23. Harris ST, Watts NB, Genant HK, et al. Vertebral efficacy with risedronate therapy (VERT) study group, et al. Effects of risedronate treatment on vertebral and nonvertebral fractures in women with postmenopausal osteoporosis: a randomized, controlled trial. JAMA. 1999;282:1344–1352. 24. Chesnut CH, Skag A, Christiansen C, et al. Effects of oral ibandronate administered daily or intermittently on fracture risk in postmenopausal osteoporosis. J Bone Miner Res. 2004;19:1241–1249. 25. Black DM, Delmas PD, Eastell R, et al. Once-yearly zoledronic acid for treatment of postmenopausal osteoporosis. N Engl J Med. 2007;356:1809–1822. 26. Khan AA, Morrison A, Hanley DA, et al. Diagnosis and management of osteonecrosis of the jaw: a systematic review and international consensus. J Bone Miner Res. 2015;30:3–23. 27. Hellstein JW, Adler RA, Edwards B, et al. Managing the care of patients receiving antiresorptive therapy for prevention and treatment of osteoporosis. Recommendations from the American Dental Association Council on Scientific Affairs. J Am Dent Assoc. 2011;142:1243–1251. 28. Shane E, Burr D, Abrahamsen B, et al. Atypical subtrochanteric and diaphyseal femoral fractures: second report of a task force of the American Society for Bone and Mineral Research. J Bone Miner Res. 2014;29:1–23. 29. Chesnut CH, Silverman S, Andriano K, et al. PROOF Study Group. A randomized trial of nasal spray salmon calcitonin in postmenopausal women with established osteoporosis: the prevent recurrence of osteoporotic fractures study. Am J Med. 2000;109:267–276. 30. Neer RM, Arnaud CD, Zanchetta JR, et al. Effect of parathyroid hormone1-34 on fractures and bone mineral density in postmenopausal women with osteoporosis. N Engl J Med. 2001;344:1434–1441. 31. Miller PD, Hattersley G, Juel Riis B, et al. Effect of abaloparatide vs placebo on new vertebral fractures in postmenopausal women with osteoporosis: a randomized clinical trial. JAMA. 2016;316:722–733. 32. Cummings SR, Marten JS, McClung MR, et al. Denosumab for prevention of fractures in postmenopausal women with osteoporosis. N Engl J Med. 2009;361:756–765.

CHAPTER 142

Parkinson Disease Nutan Sharma, MD, PhD

Synonyms Shaking palsy Paralysis agitans Idiopathic parkinsonism

ICD-10 Codes G20 G25.0 G23.9

Parkinson disease Essential tremor Degenerative disease of basal ganglia, unspecified G23.1 Progressive supranuclear palsy G90.3 Multisystem degeneration of the autonomic nervous system G31.85 Corticobasal degeneration G31.8 Lewy body dementia

Definition Parkinson disease (PD) is a chronic, progressive neurodegenerative disease. On pathologic examination, it is characterized by preferential degeneration of dopaminergic neurons in the substantia nigra pars compacta and the presence of cytoplasmic inclusions known as Lewy bodies. Clinically, it is characterized by a resting tremor, bradykinesia, and rigidity. It is important to distinguish PD from the disorders that are known collectively as the Parkinson-plus syndromes. These are relatively rare disorders that share some of the features of PD, such as rigidity and bradykinesia. However, the Parkinson-plus syndromes do not respond to medical treatment and have some unique clinical features as well. The prevalence of PD has been estimated in greater than 80 studies conducted around the world. The most consistent finding is that PD is an age-related disease. Between the ages of 50 and 59, the prevalence is estimated at 273 per 100,000, whereas between 70 and 79 the prevalence is estimated at 2700 per 100,000.1 Some studies have reported a higher prevalence of PD in men, whereas other studies have not. The genetic contribution to the development of PD is an area of intense study. A variety of gene mutations have been identified, in family studies, that can cause PD.1 Seven disease-causing mutations have been identified, including alpha-synuclein, leucine-rich repeat kinase 2 (LRRK2), Parkin, PTEN-induced putative kinase-1 (PINK1), DJ-1, 806

ATPase type 13A2 (ATP3A2), and glucocerebrosidase. To date, monogenic causes of PD account for about 5% of all PD cases, inherited in either an autosomal dominant or autosomal recessive pattern. The most common monogenic cause of PD is mutations in the LRKK2 gene, which have been associated with 1% of sporadic PD cases and 4% of hereditary parkinsonism cases.2 Environmental risk factors are also thought to play a role in the pathogenesis of PD. Numerous studies have focused on the risk of pesticide and heavy metal exposure to the development of PD. Whereas the methodology used varies in different studies, in those with an occupational exposure to pesticides or heavy metals, the data have been mixed, indicating either an increased risk of developing PD or no increased risk.1 

Symptoms The most common initial manifestations of PD are unilateral rest tremor and bradykinesia. The resting tremor is suppressed by either purposeful movement or sleep and exacerbated by anxiety. The bradykinesia may produce a sensation of stiffness in the affected arm or leg. Pain is also a part of PD. An aching pain in the initially affected limb may first be attributed to bursitis or arthritis. Less common presenting complaints include gait difficulty and fatigue. It is not uncommon for one of these features to be present for months or even years before others develop. As the disease progresses, there is marked difficulty in both initiating and terminating movement. There is difficulty in rising from a seated position, particularly when one is seated in a sofa or chair without armrests. The unilateral rest tremor and bradykinesia become bilateral. Handwriting becomes smaller and more difficult to read. Friends and family members often complain that the patient’s speech is more difficult to understand, particularly on the telephone. The symptom of a softer voice with a decline in enunciation is known as hypophonia. 

Physical Examination The most distinctive clinical feature is the rest tremor. It is typically present in a single upper extremity early in the course of the disease. As the disease progresses, the resting tremor may spread to both the ipsilateral lower limb and the contralateral limbs. Examination of motor tone reveals cogwheel rigidity in the affected limb. Motor strength, however, remains unaffected. Additional features that must be evaluated in an examination include rapid, repetitive limb movements and gait. Examination of repetitive movements of the fingers, entire

CHAPTER 142  Parkinson Disease

hand or foot will reveal bradykinesia and decreased amplitude and accuracy of finger tapping or toe tapping movements in the affected limb. Examination of gait will reveal decreased arm swing on the affected side, smaller steps, and an inability to pivot turn. Typically, patients make several steps to complete a turn because of some degree of postural instability. Deep tendon reflexes and sensation are not affected in PD. In advanced PD, loss of postural reflexes becomes evident. Individuals are unable to maintain balance when turning. Other manifestations of advanced PD include episodes of frozen gait and dysphagia. There is also a spectrum of cognitive impairment in PD, extending from minimal cognitive impairment (MCI) to PD with dementia (PDD). MCI is defined as a gradual decline in cognitive function, identified by the patient or caregiver, that does not interfere significantly with functional independence.3 PDD is dementia with a slowly progressive course of cognitive impairment that most prominently affects attention, executive, and visuospatial functions.4 In examination of someone who is taking medication for PD, it is important to record the time at which the last dose of medication was taken relative to the time at which the examination occurs. Medications for PD are particularly good at ameliorating the rest tremor and bradykinesia, particularly in the early stages of the disease. Typically, the rest tremor will subside for 1 to 3 hours after the last dose of medication. Other features, such as poor hand writing, hypophonia, and loss of postural reflexes, do not respond to oral medication. 

Functional Limitations Functional limitations depend on which symptoms are most prominent in a particular patient. Early in the course of PD, the sole limitation may be in one’s ability to write legibly. Affected individuals are still able to perform activities of daily living, although they may prefer to use the unaffected limb for tasks such as shaving and dressing. Although the rest tremor may result in a feeling of self-consciousness or embarrassment, it does not affect one’s independence, as it is suppressed with purposeful movement. As the disease progresses, the ability to perform fine motor skills declines, and difficulty with standing and gait develops. An individual will have difficulty in buttoning a shirt or tying shoelaces. More time will be required to stand and initiate gait. Postural instability with a tendency to retropulse also develops. Thus, patients have difficulty in climbing stairs and walking safely and quickly. Slowed reaction times may also affect one’s ability to drive safely. Decisions about whether someone should drive are often difficult and must be made on an individual basis. Marked hypophonia may make speaking on the telephone difficult as well. As the voice becomes more affected, dysphagia is likely to develop. One aspect of PD that has historically gotten little attention is the effect it has on sexual activity. Men may experience erectile dysfunction and difficulty with ejaculation as part of the autonomic dysfunction found in PD. Women may experience inadequate lubrication and a tendency to urinate during sex secondary to autonomic dysfunction. In both genders, hypersexuality may be seen as a side effect of treatment with dopamine agonists.5

807

In end-stage PD, limitations include marked dysphagia and severe abnormalities of gait that require both devices and one or two persons for assistance. At this stage, help is necessary for all activities of daily living as well. 

Diagnostic Studies PD is a clinical diagnosis. Conventional laboratory investigations do not contribute to the diagnosis or management of PD. Computed tomography and magnetic resonance imaging scans of the brain do not reveal any consistent abnormalities. Recently a dopamine transporter radioligand has become available for clinical use in single-photon emission computed tomography scanning to assist in the evaluation of those with suspected PD. The scan is known as a DaTSCAN, and a recent analysis demonstrates that it does not provide greater accuracy than a clinical diagnosis, based on history and examination of a patient.6  Differential Diagnosis The differential diagnosis includes essential tremor and several diseases known collectively as the Parkinson-plus syndromes: Lewy body dementia, progressive supranuclear palsy, multiple system atrophy, and corticobasal degeneration. Condition

Symptoms

Essential tremor

An involuntary, rhythmic tremor of a body part, most commonly affecting arms and hands but can also involve head, voice, tongue, trunk, or legs

Lewy body dementia

Motor symptoms of PD with rapidly progressive dementia within the first year. Visual hallucinations are common

Progressive supranuclear palsy

Bradykinesia, rigidity, frequent falls early in disease course, rest tremor, and inability to voluntarily move the eyes upward

Multiple system atrophy

Bradykinesia, rigidity, ataxia, and autonomic dysfunction (flushing, palpitations, nausea, vomiting)

Corticobasal degeneration

Bradykinesia, rigidity, inability to coordinate purposeful movements (apraxia), and sense that limbs are not one’s own (alien limb syndrome)

PD, Parkinson disease.

Treatment Initial The decision to initiate medical treatment is based on the degree of disability and discomfort that the patient is experiencing. Six classes of drugs are used to treat PD (summarized in Table 142.1). The selection of a particular drug depends on the patient’s main complaint, which is usually either a rest tremor or bradykinesia. There is no evidence to suggest that expediting or delaying the onset of treatment for PD has any effect on the overall course of the disease. However, it is clear that those who do not receive treatment and are bradykinetic are at greater risk of falling and injuring themselves.

808

PART 3 Rehabilitation

Table 142.1  Classes of Antiparkinson Medications, Mechanisms of Action, Beneficial Effects, and Side Effects Drug Class

Specific Agents

Mechanism of Action

Effective for

Side Effects

Anticholinergic

Benztropine

Muscarinic receptor blocker

Tremor, rigidity

Dry mouth, blurred vision, constipation, urinary retention, confusion, hallucinations, impaired concentration

Antiviral

Amantadine

Promotes synthesis and release of dopamine

Tremor, rigidity, akinesia

Leg edema, livedo reticularis, confusion, hallucinations

Dopamine replacement

Levodopa (oral and intestinal forms)

Converted to dopamine

Tremor, rigidity, akinesia, freezing

Nausea, diarrhea, confusion, hallucinations

Dopamine agonists (D1 and D2)

Bromocriptine, pergolide, apomorphine

Dopamine analogues that bind to D1 and D2 receptors

Rigidity, akinesia

Leg edema, nausea, confusion, hallucinations

Dopamine agonists (D2)

Ropinirole, pramipexole

Dopamine analogues that bind to D2 receptors

Rigidity, akinesia

Leg edema, sleep attacks, nausea, confusion, hallucinations

Monoamine oxidase B inhibitors

Selegiline, rasagiline

Inhibit the metabolism of dopamine

Mild reduction in “wearing off” from levodopa

Nausea, hallucinations, confusion

Inhibits the metabolism of dopamine

Mild reduction in “wearing off” from levodopa

Dyskinesia, nausea, diarrhea

Catechol O-methyl­ Entacapone transferase inhibitor

Anticholinergic agents are the oldest class of medications used in PD. They are most effective in reducing the rest tremor and rigidity associated with PD. However, the side effects associated with anticholinergic agents typically limit their usefulness. Amantadine is also used in the treatment of PD. Amantadine produces a limited improvement in akinesia, rigidity, and tremor. Dopamine replacement remains the cornerstone of antiparkinson therapy. Levodopa is the natural precursor to dopamine and is converted to dopamine by the enzyme aromatic amino acid decarboxylase. To ensure that adequate levels of levodopa reach the central nervous system, levodopa is administered simultaneously with a peripheral decarboxylase inhibitor. In the United States, the most commonly used peripheral decarboxylase inhibitor is carbidopa. Levodopa is most effective in reducing tremor, rigidity, and akinesia. The most common side effects, seen with the onset of treatment, are nausea, abdominal cramping, and diarrhea. Long-term treatment with levodopa is associated with three types of complications: hourly fluctuations in motor state, dyskinesias, and a variety of psychiatric complaints including hallucinations and confusion. However, it is not clear whether the motor fluctuations are due to the levodopa treatment alone, the disease progression alone, or a complex interplay of imperfect dopamine replacement and the inexorable progression of disease. In summary, current evidence supports the use of dopamine replacement as soon as the symptoms of PD become troublesome to the individual patient. There is no evidence that supports withholding of treatment to minimize long-term motor complications. Two relatively new medications are available for the amelioration of motor complications: levodopa-carbidopa intestinal gel (LCIG) and subcutaneous injections of apomorphine. LCIG is administered via a percutaneous endoscopic gastrostomy with a jejunal extension tube (PEG-J). The medication is then administered, via a pump, into the PEG-J, resulting in reduced time in the ‘off ’ stage without

an increase in dyskinesias.7 Apomorphine is particularly helpful in the morning. A daily injection has been shown to reduce the time before symptoms are ameliorated, allowing patients to move more easily and perform the activities of daily living.8 Dopamine agonists, which directly stimulate dopamine receptors, are also used in the treatment of PD. These agents can be used either as an adjunct to levodopa therapy or as monotherapy. The older dopamine agonists, which are relatively nonspecific and exert their effects at both D1 and D2 receptors, are bromocriptine and pergolide. In comparison to the side effects seen with levodopa, there is a lower frequency of dyskinesias and a higher frequency of confusion and hallucinations. The newer dopamine agonists pramipexole and ropinirole are more specific for D2 receptors. These newer agents have been reported to cause daytime somnolence, peripheral edema, and impulse control disorders.9 All dopamine agonists can cause orthostatic hypotension, particularly when they are first introduced. It is best to start with a small dose of medication at bedtime and then slowly increase the total daily dose. Inhibitors of dopamine metabolism are also used in the medical treatment of PD. Both selegiline and rasagiline inhibit monoamine oxidase B, which metabolizes dopamine in the central nervous system. Thus, inhibitors of monoamine oxidase B are thought to improve an individual’s response to levodopa by alleviating the motor fluctuations that are seen with long-term levodopa treatment. Another agent that inhibits the metabolism of dopamine is entacapone. Entacapone inhibits catechol O-methyltransferase in the periphery. Entacapone is administered in conjunction with levodopa and, by inhibiting peripheral catechol O-methyltransferase activity, increases the amount of levodopa that reaches the central nervous system. The benefits of entacapone treatment include a reduction in total daily levodopa dose and an improvement in the length of time of maximum mobility.10 

CHAPTER 142  Parkinson Disease

809

Rehabilitation

Technology

The clinical pathologic process seen in PD reveals that patients tend to become more passive, less active, and less motivated as the disease progresses. The benefits to physical and occupational therapy are thus more far reaching than a simple improvement in motor function. The physical benefits include improvement in muscle strength and tone as well as maintenance of an adequate range of motion in the joints. The psychological benefits include enlistment of the patient as an active participant in treatment and provision of a sense of mastery over the effects of PD. Both physical therapy and occupational therapy focus on mobility, the use of adaptive equipment, and safety in both the home and community. Because the symptoms of PD gradually worsen over time, individuals can benefit from periodic physical training throughout the course of their illness. The training may take place either through community-based programs that are more readily accessible for those who live far from an academic center or home-based programs for those who cannot easily travel. An emphasis on gait training is particularly helpful to prevent falls and injury. Gait training typically involves training an individual to be conscious of taking a longer stride and putting the foot down with each step. Another method is to use visual cues to maintain a regular size for each step. For example, one can put strips of masking tape on the floor, at a regular interval that is comfortable for one’s height, weight, and gender. As PD progresses, episodes of frozen gait, in which the feet seem to be stuck to the floor, occur. Freezing episodes can be broken by multiple techniques, such as visualizing that one is stepping over an imaginary line on the floor, counting in a rhythmic cadence, or marching in place. Occupational therapy is particularly helpful in recommending adaptive devices or establishing new routines that allow people with PD to continue to live independently. For example, the use of a long-handled shoehorn eliminates the need to bend over and thus reduces the risk that a person with PD will fall while getting dressed. Other examples of adaptive equipment are a firmly secured grab bar in the bathtub and a relatively high toilet seat with armrests to minimize the risk of freezing while on the toilet. Speech therapy plays a critical role for those PD patients who suffer from communication difficulties. Although dysarthria is difficult to treat, hypophonia can be overcome with training. Specifically, the Lee Silverman Voice Treatment program has been shown to be effective in improving both the volume and clarity of speech in those with PD.11 Swallow evaluation and therapy are also helpful in the treatment of dysphagia, which occurs as PD progresses. 

A common source of frustration for those with PD is that others cannot hear them easily. Fortunately, there are several methods for overcoming that problem. Applications, commonly known as ‘apps,’ that can be downloaded onto portable electronic devices, such as cell phones and tablets, can be utilized to convert text into speech. For those who prefer to use their natural voice, rather than an artificial voice, portable voice amplifiers are readily available. For those who experience episodes of frozen gait, new walkers with a laser beam provide a visual cue that allows patients to “step over” the laser beam and resume walking. 

Procedures Feeding tubes are sometimes used in individuals who have severe end-stage PD. Some patients elect hospice care, without artificial feeding at that point. Individuals who do get feeding tubes may need to have medication doses adjusted (e.g., carbidopa-levodopa will now bypass the esophagus and have a shortened time to onset of action). 

Surgery Although a large number of medications are available for the treatment of early and moderately advanced PD, they are of limited efficacy in those with advanced PD. Several surgical procedures are currently available for those with advanced PD. These procedures consist of either creation of a permanent lesion or insertion of an electrical stimulator in a specific nucleus of the brain. Thalamotomy consists of introduction of a lesion in the ventral intermediate nucleus of the thalamus. Thalamotomy has been reported to produce a reduction in tremor of the contralateral limb in 85% of the patients who were treated. Thalamotomy is recommended in PD patients with an asymmetric, severe, medically intractable tremor. Unilateral pallidotomy consists of introduction of a lesion in the globus pallidus. The most striking benefits are a reduction in contralateral drug-induced dyskinesias, contralateral tremor, bradykinesia, and rigidity. Unilateral pallidotomy is recommended in PD patients with bradykinesia, rigidity, and tremor who experience significant drug-induced dyskinesia despite optimal medical therapy. However, data regarding the long-term cognitive effects of unilateral pallidotomy are limited and varied in their findings.12,13 Thus, neuropsychological evaluation is recommended in all patients both before and after surgery. Deep brain stimulation (DBS) for Parkinson disease consists of high-frequency electrical stimulation in either the globus pallidus or the subthalamic nucleus. DBS requires surgery, in which the source of electrical stimulation is placed subcutaneously in the chest wall and the leads to which it is attached are placed in one of the locations listed. The advantage of DBS is that the degree of electrical stimulation can be easily adjusted, externally, once the DBS unit is in place. In contrast, both thalamotomy and pallidotomy result in permanent, fixed lesions in the brain. DBS of the ventral intermediate nucleus of the thalamus is effective in the treatment of a severe and disabling tremor that is unresponsive to medical therapy, with reports of approximately 80% improvement in tremor 5 years after DBS implantation.14 DBS of the globus pallidus results in a marked reduction in dyskinesia. There are also improvements in bradykinesia, speech, gait, rigidity, and tremor. DBS of the subthalamic nucleus also results in marked improvement in tremor, akinesia, gait, and postural stability.15 

810

PART 3 Rehabilitation

Potential Disease Complications Depression is found in approximately 35% of those with PD.16 It may be difficult to distinguish true depression from the apathy associated with PD. The crucial factor is to determine whether the patient has a true disturbance of mood, with loss of interest, sleep disturbance, and sometimes suicidal thoughts. The reasons for depression in PD are a subject of debate. There is a suspicion that the pathologic process of PD itself may predispose to depression. Regardless of the cause, recognition and treatment of depression may have a significant impact on the overall disability caused by the illness. Many PD patients have been treated safely and effectively with selective serotonin reuptake inhibitors, such as fluoxetine and paroxetine. Tricyclic antidepressants can be used, although their anticholinergic properties may limit their effectiveness. Gastrointestinal complications also occur in PD. Dysphagia is typically due to poor control of the muscles of both mastication and the oropharynx. Soft food is easier to eat, and antiparkinson medication improves swallowing. Constipation is a frequent complaint in those with PD. Treatment includes increase in physical activity; discontinuation of anticholinergic drugs; and maintenance of a diet with intake of adequate fluids, fruit, vegetables, fiber, and lactulose (10 to 20 g daily). 

Potential Treatment Complications The motor complications seen with pharmacologic treatment are divided into two categories: fluctuations (off state) and levodopa-induced dyskinesias. The off state consists of a return of the signs and symptoms of PD: bradykinesia, tremor, and rigidity. Patients may also experience anxiety, dysphoria, or panic during an off state. The development of levodopa-induced dyskinesias appears to be related to the degree of dopamine receptor super-sensitivity. As PD progresses, there is an increasing loss of dopamine receptors. This results in an increased sensitivity of the remaining dopamine receptors to dopamine itself. Thus, there is a greater chance for development of dyskinesias at a given dose of levodopa. Treatment options are to lower each dose of levodopa but with an increase in the frequency with which it is taken; to add or to increase the dose of a dopamine agonist while the dose of levodopa is decreased; and to add amantadine, which has been shown to be an anti-dyskinetic agent in some patients.17 There are potential complications to each of these solutions; reducing each dose of levodopa while increasing the frequency of

doses (e.g., once every 2 hours) is a difficult schedule for a patient to maintain, adding or increasing the dose of dopamine agonist may result in compulsive behaviors (shopping, gambling, hypersexuality), excessive daytime sleepiness, and peripheral edema; amantadine may cause confusion. An alternative is to treat those who continue to experience an improvement in their mobility with levodopa but develop dyskinesias that become more pronounced as the day progresses with DBS.

References 1. Wirdefeldt K, Adami H, Cole P, et al. Epidemiology and etiology of Parkinson’s disease: a review of the evidence. Eur J Epidemiol. 2011;26:S1–S58. 2. Lee A, Gilbert RM. Epidemiology of Parkinson disease. Neurol Clin. 2016:955–965. 3. Litvan I, Goldman JG, Troster AI, et al. Diagnostic criteria for mild cognitive impairment in Parkinson’s disease: Movement Disorder Society Task Force guidelines. Mov Disord. 2012;27:349–356. 4. Goetz CG, Emre M, Dubois B. Parkinson’s disease dementia: definitions, guidelines and research perspectives in diagnosis. Ann Neurol. 2008;64:S81–S92. 5. Bronner G, Vodusek DB. Management of sexual dysfunction in Parkinson’s disease. Ther Adv Neurol Disord. 2011;4:375–383. 6. de la Fuente-Fernandez. Role of DaTSCAN and clinical diagnosis in Parkinson disease. Neurology. 2012;78:696–701. 7. Wirdefeldt K, Odin P, Nyholm D. Levodopa-carbidopa intestinal gel in patients with Parkinson’s disease: a systematic review. CNS Drugs. 2016;30:381–404. 8. Isaacson S, Lew M, Ondo W, Hubble J, Clinch T, Pagan F. Apomorphine subcutaneous injection for management of morning akinesia in Parkinson’s disease. Mov Disord Clin Pract. 2017;4:78–83. 9. Antonini A, Tolosa E, Mizuno Y, Yamamoto M, Poewe WH. A reassessment of risks and benefits of dopamine agonists in Parkinson’s disease. Lancet Neurol. 2009;8:929–937. 10. Fox SH, Katzenschlager R, Lim SY, et al. The Movement Disorder Society evidence-based medicine review update: treatments for the motor symptoms of Parkinson’s disease. Mov Disord. 2011;(suppl 3):S2–S41. 11. Sapir S, Spielman JL, Ramig LO, Story BH, Fox C. Effects of intensive voice treatment (the Lee Silverman Voice Treatment [LSVT]) on vowel articulation in dysarthric individuals with idiopathic Parkinson disease: acoustic and perceptual findings. J Speech Lang Hear Res. 2007;50:899–912. 12. Alegret M, Valldeoriola F, Tolosa E, et al. Cognitive effects of unilateral posteroventral pallidotomy: a 4-year follow-up study. Mov Disord. 2003;18(3):323–328. 13. Strutt AM, Lai EC, Jankovic J, et al. Five year follow-up of unilateral posteroventral pallidotomy in Parkinson’s disease. Surg Neurol. 2009;71:551–558. 14. Pahwa R, Lyons KE, Wilkinson SB, et al. Long-term evaluation of deep brain stimulation of the thalamus. J Neurosurg. 2006;104:506–512. 15. Walter BL, Vitek JL. Surgical treatment for Parkinson’s disease. Lancet Neurol. 2004;3:719–728. 16. Aarsland D, Pahlhagen S, Ballard CG, et al. Depression in Parkinson’s disease – epidemiology, mechanisms and management. Nat Rev Neurol. 2011;8:35–47. 17. Hubsher G, Haider M, Okun MS. Amantadine: the journey from fighting flu to treating Parkinson disease. Neurol. 2012;78:1096–1099.

CHAPTER 143

Peripheral Neuropathies Seward B. Rutkove, MD

Synonyms Polyneuropathies Neuropathies

ICD-10 Codes G60.8 G60.3 M35.9 [G63] E11.42 D49.9 [G63] G62.9 G62.1 G62.0 G62.2

Hereditary and idiopathic neuropathies Idiopathic progressive neuropathy Polyneuropathy in collagen vascular disease Type 2 diabetes mellitus with diabetic polyneuropathy Polyneuropathy in malignant disease Polyneuropathy, unspecified Alcoholic polyneuropathy Drug-induced polyneuropathy Polyneuropathy due to other toxic agents

Definition Peripheral neuropathies are a collection of disorders characterized by the generalized dysfunction of peripheral nerves. This group of diseases is heterogeneous, including those that predominantly affect the nerve axon, others that primarily affect the myelin sheath, and still others that involve both parts of the nerve simultaneously. In addition, some peripheral neuropathies affect only small, unmyelinated fibers, whereas others predominantly involve only large myelinated ones. Table 143.1 contains a list of the most frequently encountered forms of peripheral neuropathy. Peripheral neuropathy is common; one Italian study suggested a prevalence of about 3.5% in the general population.1 In diabetes, one study demonstrated clinical peripheral neuropathy affecting 8.3% of individuals compared with a control population, in whom 2.1% of individuals were

affected.2 After 10 years, 41.9% of the diabetic patients had peripheral neuropathy, compared with 6% of the control subjects. Defining peripheral neuropathy remains no simple task; however, a formal case definition for distal symmetric polyneuropathy (the most common form) has been developed.3 This definition uses a combination of symptoms, signs, and electrodiagnostic testing results to formulate an ordinal ranking system to identify the likelihood of the disease in a given patient. Although it is a useful tool for future research studies, the necessity of applying such a complex approach underscores the difficulty in attempting to define peripheral neuropathy in any simple fashion. 

Symptoms Patients with peripheral neuropathy present with a number of specific sensory complaints, including decreased sensation that is often associated with pain, tingling (paresthesias), and burning. They may complain of a “sock-like” feeling in their feet or that their feet are persistently cold. Some patients, usually with more advanced disease, will note atrophy of the intrinsic foot muscles and some weakness, especially with the development of partial footdrop. Walking difficulties usually also develop once sensation is significantly impaired. Sensory symptoms in the hand (paresthesias and reduced tactile sensation) usually develop once an axonal peripheral neuropathy has progressed up to about the level of the knees. In patients with generalized demyelinating peripheral neuropathies, more generalized symptoms of weakness and sensory loss are often present, although distally predominant paresthesias often occur. History taking should include a detailed review of current and past medical issues, review of systems, and any exposure to toxins (Table 143.2). 

Physical Examination The physical examination demonstrates distinct abnormalities that depend on the form of peripheral neuropathy present. Most commonly, patients present with a sensorimotor axonal peripheral neuropathy. In this condition, decreased sensation to pinprick, vibration, light touch, and temperature may be identified distally in the lower extremities with normal sensation more proximally. Some weakness of toe or foot extension and flexion may also be apparent. Deep 811

812

PART 3 Rehabilitation

Table 143.1  Specific Disorders of Peripheral Nerves Predominantly Axonal Disorders Diabetic neuropathy Alcoholic neuropathy Medication-related neuropathy (e.g., due to metronidazole, colchicine, nitrofurantoin, isoniazid) Systemic disease–related neuropathy (e.g., chronic renal failure, inflammatory bowel disease, connective tissue disease) Thyroid neuropathy Heavy metal toxic neuropathy (lead, arsenic, cadmium) Porphyric neuropathy Paraneoplastic neuropathy Syphilitic, Lyme neuropathy Sarcoid neuropathy Human immunodeficiency virus–related neuropathy Hereditary neuropathies (Charcot-Marie-Tooth type 2; familial amyloid; mitochondrial) Critical illness neuropathy Predominantly Demyelinating Disorders Idiopathic CIDP CIDP associated with monoclonal proteins Antimyelin-associated glycoprotein neuropathy (a form of CIDP) Human immunodeficiency virus–associated CIDP Idiopathic Guillain-Barré syndrome Guillain-Barré syndrome secondary to known etiology (e.g., influenza, Campylobacter jejuni, Zika) Hereditary (Charcot-Marie-Tooth types 1 and 3) CIDP, Chronic inflammatory demyelinating polyradiculoneuropathy.

tendon reflexes will be hypoactive distally (e.g., ankle jerks decreased relative to knee jerks). In patients with acquired demyelinating peripheral neuropathy, the examination may demonstrate marked generalized weakness with some abnormal sensory findings, usually including decreased joint position sense. In this disorder, deep tendon reflexes may be reduced or diffusely absent. Patients with hereditary demyelinating polyneuropathies may demonstrate distal muscle atrophy in the feet and lower legs. Such patients may develop a pes cavus foot deformity, in which the foot is foreshortened and has a very high arch. A “champagne bottle” appearance to the legs (where muscle atrophy of the lower leg, especially of the calf, is prominent) may also be present. As any peripheral neuropathy progresses, lower extremity sensory loss may lead to gait unsteadiness, and upper extremity sensory loss may decrease hand dexterity. 

Functional Limitations Patients with peripheral neuropathy face a number of potential functional limitations. In those individuals with a distal axonal peripheral neuropathy, limitations usually include problems with gait and unsteadiness, especially as the neuropathy progresses. If pain is a prominent symptom, activities of daily living may be compromised to some extent. Pain may also be prominent at night, interfering with sleep. In those patients with very advanced axonal peripheral neuropathy or demyelinating forms, such as hereditary Charcot-Marie-Tooth disease, weakness can produce major functional limitations, restricting the patient’s walking ability and in some

Table 143.2  Toxins Producing Peripheral Nerve Degeneration Industrial Chemicals Affect peripheral nervous system preferentially Lead Acrylamide Organophosphates Thallium Some effects on central nervous system Carbon disulfide Methylmercury Methyl bromide Large amounts required Arsenic Trichloroethylene Tetrachloroethane 2,4-Dichlorophenoxyacetic acid (2,4-D) Pentachlorophenol DDT Some effects on other than nervous tissue Carbon tetrachloride Carbon monoxide Pharmaceutical Substances Arsenic Arsenic-based chemicals Clioquinol Disulfiram Gold Hydralazine Nitrofurantoin Phenytoin Sulfonamides Thalidomide Thallium Vincristine Modified from Gilliatt RW. Recent advances in the pathophysiology of nerve conduction. In: Desmedt JE, ed. New Developments in Electromyography and Clinical Neurophysiology. Basel: Karger; 1973:2–18.

cases leading to dyspnea and nocturnal hypoventilation. In patients with some chronic forms of demyelinating polyneuropathy, weakness of both proximal and distal muscles can become severe, limiting the performance of many activities of daily living. Sensory deficits can limit one’s ability to button shirts, to zip pants, to turn a key in a lock, to tie shoelaces, to type on a computer, or to use a smartphone. 

Diagnostic Studies Electrodiagnostic studies (including electromyography and nerve conduction studies) remain the most important first tests in the evaluation of polyneuropathy.5 Nerve conduction studies assist in determination of whether the peripheral neuropathy is mainly demyelinating, axonal, or mixed (Figs. 143.1 and 143.2) by evaluation of the amplitude and conduction velocities of the motor and sensory responses obtained.6 In axonal neuropathies, amplitudes are reduced and conduction velocities are relatively normal; in demyelinating neuropathies, amplitudes are generally preserved but conduction velocities are decreased; in mixed neuropathies, a combination of reduced amplitude and conduction velocities is present. In small-fiber neuropathies, nerve conduction

CHAPTER 143  Peripheral Neuropathies

813

Table 143.3  Serologic Testing in Peripheral Neuropathy Baseline Testing Vitamin B12 Thyroid-stimulating hormone Rapid plasma reagin (or VDRL test) Serum glucose Serum hemoglobin A1c Antinuclear antibody Erythrocyte sedimentation rate Serum protein electrophoresis Urine protein electrophoresis

Normal

Segmental demyelination

Axonal degeneration

FIG. 143.1  Types of peripheral nerve damage.

Some Additional Tests, Depending on Clinical Suspicion Serum protein immunophoresis 24-Hour urine collection for heavy metals 24-Hour urine collection for porphyrins Glucose tolerance testing Human immunodeficiency virus infection testing Anti-Ro, anti-La antibodies (Sjögren syndrome) Anti-Hu antibody (paraneoplastic neuropathy) Additional antibody testing in certain demyelinating disorders Antimyelin-associated glycoprotein Serologic testing for primary post-infectious cause (e.g., Campylobacter, Zika) Genetic testing (for disorders such as familial amyloidosis, Charcot-Marie-Tooth disease) VDRL, Venereal Disease Research Laboratory.

Cell body

Myelin sheath

Axon

Dendrites

FIG. 143.2 Schematic representation of a motor nerve extending from a cell body to the muscle it innervates.

studies are generally normal. Likewise, nerve conduction studies help to determine the severity of the process as well, with more severe conditions showing lower response amplitudes and/or slower conduction velocities. Although needle electromyography plays a more limited role in the diagnosis of peripheral neuropathy, a gradient of reinnervation, in which distal muscles are most abnormal and proximal muscles less affected, helps to determine the degree of motor involvement. In addition, needle electromyography may assist in determining whether a superimposed problem, such as polyradiculopathy, is also present. In general, a number of serologic tests are also performed to identify the cause of the peripheral neuropathy. These are outlined in Table 143.3.

Additional workup is occasionally necessary. Sural nerve biopsy can be useful for determining the cause of the polyneuropathy for some conditions that are difficult to diagnose, such as amyloid neuropathy, as well as some other unusual forms of peripheral neuropathy. The analysis of cutaneous sensory fibers through the use of skin biopsy to identify the presence of peripheral neuropathy involving only small, unmyelinated fibers is now also routinely performed to assist with the diagnosis of idiopathic smallfiber neuropathy or that associated with certain conditions, such as amyloid.7 On occasion, muscle biopsy may be helpful in this regard as well, because vasculitic abnormalities or amyloid can also be identified in skeletal muscle. Lumbar puncture may aid in the determination of whether an acquired demyelinating peripheral neuropathy is present by the identification of a very elevated cerebrospinal fluid protein concentration in the presence of a normal number of white cells (so-called albuminocytologic dissociation). Autonomic testing—such as quantitative sudomotor axon reflex texting, tilt-table testing, and heart rate variability to deep breathing—can also be helpful in delineating involvement of the autonomic nervous system in the neuropathic process.8 Ultrasound imaging can also be useful in evaluating for thickened nerves, which are most commonly seen in autoimmune and hereditary demyelinating neuropathies.9 Ultrasound can also be useful in helping to identify superimposed compression or entrapment neuropathies.10  Differential Diagnosis Myelopathy (spinal cord compression) Lumbosacral polyradiculopathy (lumbar stenosis) Mononeuropathy multiplex

814

PART 3 Rehabilitation

Treatment Initial If a cause of the axonal peripheral neuropathy is known or identified (which generally is achieved about 80% of the time), treatment geared toward the underlying disorder itself might help to slow progression of the polyneuropathy. For example, improved glucose control can help to improve neuronal function in diabetic neuropathy.11 Likewise, in those people with a neuropathy secondary to toxin exposure, such as alcoholic neuropathy, decreased exposure to the toxin may be helpful. In patients with axonal peripheral neuropathies, treatment is usually symptom-based, with efforts to reduce pain and dysesthesias. A number of drugs have proved useful in this regard.12 The tricyclic antidepressants remain most effective (generally nortriptyline or amitriptyline, starting with 10 mg at bedtime and increasing as needed until improvement occurs). Gabapentin (starting at a dose of 100 to 300 mg three times daily) has also gained wide acceptance as a first-line therapy in the treatment of this disorder.13 Duloxetine and pregabalin, though specifically approved for diabetic neuropathy, can be useful in a variety of peripheral neuropathies. Duloxetine can be dosed at 30–60 mg daily and pregabalin at 50–100 mg three times per day,14,15 However, it is not clear that either of these agents is more efficacious than previously available and more inexpensive medications.16 The serotonin reuptake inhibitor venlafaxine has also been studied, but a recent Cochrane review did not find convincing evidence of its efficacy.17 In patients in whom these measures prove of limited value, the use of long-acting narcotic agents may occasionally be necessary. Cannabinoids, including medical marijuana and tetrahydrocannabinol, can also be useful supplements for treating neuropathic pain.18 In patients with certain forms of demyelinating peripheral neuropathy (such as chronic inflammatory demyelinating polyradiculoneuropathy), immunosuppressive or immunomodulating therapies can make a dramatic difference in the patient’s symptoms and level of function. Drugs including corticosteroids, azathioprine, cyclosporine, and cyclophosphamide can be used.19 Intravenous immune globulin and plasmapheresis are also widely used in this group of disorders.20,21 Rituximab is also finding wider use.22 Finally, in all patients with distal sensory loss due to peripheral neuropathy, and especially in those with diabetic peripheral neuropathy, regular podiatric care is extremely important in preventing the development of serious foot complications, such as ulcerations.23 

Rehabilitation Physical therapy may be recommended to improve mobility, muscle strength, and balance. In patients with moderate to severe peripheral neuropathy, gait training may consist of balance exercise and use of an assistive device, such as a cane or walker. Either a physical or occupational therapist can review precautions to prevent falls (e.g., avoiding throw rugs in the home or using a chair in the bath or shower). Some patients may benefit from an ankle-foot orthosis. However, in patients with compromised sensation, monitoring of the skin to prevent breakdown when a brace is

used is critical. Patients can be taught to self-monitor their skin with use of a long-handled mirror to check the bottoms of their feet. Custom shoes (e.g., extra depth and width) may be beneficial, as can custom shoe orthoses. In patients with more advanced peripheral neuropathy, adaptive equipment—such as elastic shoelaces, wide-grip handles for cookware and utensils, and shoehorns—can be provided. In advanced neuropathy, evaluation by an occupational therapist may also be useful in helping to maximize upper extremity function. If pain is an issue, therapeutic modalities may be used to alleviate the pain. These may include instruction on the use of transcutaneous electrical nerve stimulation, paraffin baths, and the like. It is important to caution the patient with impaired sensation not to use any heat or ice that may cause burns or frostbite. Individuals with impaired vascular status should also be advised not to use ice because of its vasoconstrictive effects. 

Procedures Patients with peripheral neuropathy are generally at increased risk for the development of superimposed compressive neuropathies, such as carpal tunnel syndrome, which can be challenging to diagnose.24 Treatment with local corticosteroid injections can be helpful for this problem (see Chapter 36). 

Technology Specialized equipment such as voice-activated computer software, car driving adaptations, and environmental control units may be useful. 

Surgery Surgery may be necessary for some associated conditions, including severe carpal tunnel syndrome, but it is usually more relevant to patients who develop infections of the distal lower extremities and require amputations. Other, less severe distal leg problems may also develop, requiring orthopedic or podiatric surgery. Although lower extremity nerve-release surgeries are sometimes performed in the hope of treating neuropathic symptoms,25 there is little evidence to support the use of these procedures to treat peripheral neuropathy.26 

Potential Disease Complications A number of potential foot complications can occur, including persistent intractable pain, skin ulcerations, and foot trauma, possibly leading to amputation. Serious trauma secondary to increased gait unsteadiness is another potential problem. Finally, depression due to immobility and persistent pain also often plays a role in patients with more advanced peripheral neuropathy. 

Potential Treatment Complications The tricyclic antidepressants and other pain medications have the potential side effect of drowsiness. Dry mouth, constipation, and urinary retention also occur commonly

CHAPTER 143  Peripheral Neuropathies

with the tricyclic antidepressants. Side effects of duloxetine include dizziness, nausea, and constipation. Side effects of pregabalin include dizziness and somnolence. Addiction remains a major concern with narcotic use. Treatment of the autoimmune peripheral neuropathies poses significant risk, given the inherent toxicity of the medications employed. Patients using immunosuppressive medications are at increased risk for infection, malignant neoplasia, anemia, and multiple other side effects (e.g., liver toxicity with azathioprine, renal failure with intravenous immune globulin, hemorrhagic cystitis with cyclophosphamide). Skin breakdown can occur with improper bracing.

References 1. Italian General Practitioner Study Group. Chronic symmetric symptomatic polyneuropathy in the elderly: a field screening investigation in two Italian regions. Neurology. 1995;45:1832–1836. 2. Partanen J, Niskanen L, Lehtinen J, et al. Natural history of peripheral neuropathy in patients with non–insulin dependent diabetes mellitus. N Engl J Med. 1995;333:89–94. 3. England JD, Gronseth GS, Franklin G, et al. American Academy of Neurology, American Association of Electrodiagnostic Medicine, American Academy of Physical Medicine and Rehabilitation. Distal symmetric polyneuropathy: a definition for clinical research: report of the American Academy of neurology, the American Association of Electrodiagnostic Medicine, and the American Academy of Physical Medicine and Rehabilitation. Neurology. 2005;64:199–207. 4. Deleted in page proofs. 5. Karvelas K, Rydberg L, Oswald M. Electrodiagnostics and clinical correlates in acquired polyneuropathies. PM R. 2013;5:S56–S62. 6. Albers J. Clinical neurophysiology of generalized polyneuropathy. J Clin Neurophysiol. 1993;10:149–166. 7. Lauria G, Merkies IS, Faber CG. Small fibre neuropathy. Curr Opin Neurol. 2012;25:542–549. 8. England JD, Gronseth GS, Franklin G, et al. American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Academy of Physical Medicine and Rehabilitation. Practice parameter: the evaluation of distal symmetric polyneuropathy: the role of autonomic testing, nerve biopsy, and skin biopsy (an evidence-based review). Report of the American Academy of Neurology, the American Association of Neuromuscular and Electrodiagnostic Medicine, and the American Academy of Physical Medicine and Rehabilitation. PM R. 2009;1:14–22. 9. Goedee HS, van der Pol WL, van Asseldonk JH, et al. Diagnostic value of sonography in treatment-naive chronic inflammatory neuropathies. Neurology. 2017;88:143–151.

815

10. Cartwright MS, Walker FO. Neuromuscular ultrasound in common entrapment neuropathies. Muscle Nerve. 2013;48:696–704. 11. Ang L, Jaiswal M, Martin C, Pop-Busui R. Glucose control and diabetic neuropathy: lessons from recent large clinical trials. Curr Diab Rep. 2014;14:528. 12. Sindrup S, Jensen T. Pharmacologic treatment of pain in polyneuropathy. Neurology. 2000;55:915–920. 13. Moore RA, Wiffen PJ, Derry S, Toelle T, Rice AS. Gabapentin for chronic neuropathic pain and fibromyalgia in adults. Cochrane Database Syst Rev. 2014;27:CD007938. 14. Raskin J, Pritchett YL, Wang F, et al. A double-blind, randomized multicenter trial comparing duloxetine with placebo in the management of diabetic peripheral neuropathic pain. Pain Med. 2005;6: 346–356. 15. Shneker BF, McAuley JW. Pregabalin: a new neuromodulator with broad therapeutic indications. Ann Pharmacother. 2005;39:2029–2037. 16. Tesfaye S, Selvarajah D. Advances in the epidemiology, pathogenesis and management of diabetic peripheral neuropathy. Diabetes Metab Res Rev. 2012;28(suppl 1):8–14. 17. Gallagher HC, Gallagher RM, Butler M, et al. Venlafaxine for neuropathic pain in adults. Cochrane Database Syst Rev. 2015;8:CD011091. 18. Deshpande A, Mailis-Gagnon A, Zoheiry N, Lakha SF. Efficacy and adverse effects of medical marijuana for chronic noncancer pain: systematic review of randomized controlled trials. Can Fam Physician. August 2015;61:e372–e381. 19. Oaklander AL, Lunn MP, Hughes RA, van Schaik IN, Frost C, Chalk CH. Treatments for chronic inflammatory demyelinating polyradiculoneuropathy (CIDP): an overview of systematic reviews. Cochrane Database Syst Rev. 2017;13:CD010369. 20. Hahn A, Bolton C, Zochodne D, Feasby T. Intravenous immunoglobulin treatment in chronic inflammatory demyelinating polyneuropathy. Brain. 1996;119:1067–1077. 21. Hahn A, Bolton C, Pillay N, et al. Plasma-exchange therapy in chronic inflammatory demyelinating polyneuropathy. Brain. 1996;119:1055–1066. 22. Querol L, Rojas-García R, Diaz-Manera J, et al. I. Rituximab in treatment-resistant CIDP with antibodies against paranodal proteins. Neurol Neuroimmunol Neuroinflamm. 2015;2:e149. 23. Boulton AJ. What you can’t feel can hurt you. J Vasc Surg. 2010;52(supp l): 28S–30S. 24. Gazioglu S, Boz C, Cakmak VA. Electrodiagnosis of carpal tunnel syndrome in patients with diabetic polyneuropathy. Clin Neurophysiol. 2011;122:1463–1469. 25. Aszmann OC, Kress KM, Dellon AL. Results of decompression of peripheral nerves in diabetics: a prospective, blinded study. Plast Reconstr Surg. 2001;108:1452–1453. 26. Chaudhry V, Russell J, Belzberg A. Decompressive surgery of lower limbs for symmetrical diabetic peripheral neuropathy. Cochrane Database Syst Rev. 2008;3:CD006152.

CHAPTER 144

Plexopathy— Brachial Erik Ensrud, MD

Synonyms Brachial plexopathy Neuralgic amyotrophy Parsonage-Turner syndrome Brachial amyotrophy Idiopathic shoulder girdle neuropathy Brachial plexitis Erb palsy Klumpke palsy

ICD-10 Codes G54.0 G54.5 M54.10 M54.11

Brachial plexus disorders Neuralgic amyotrophy Radiculopathy, site unspecified Radiculopathy, occipito-atlanto-axial region M54.12 Radiculopathy, cervical region M54.13 Radiculopathy, cervicothoracic region M54.14 Radiculopathy, thoracic region P14.0 Erb paralysis due to birth injury P14.1 Klumpke paralysis due to birth injury P14.3 Other brachial plexus birth injuries P14.9 Birth injury to peripheral nervous system, unspecified P15.9 Birth injury, unspecified

Definition Brachial plexopathy is the pathologic dysfunction of the brachial plexus, a complex peripheral nerve structure in the proximal upper extremity. The brachial plexus starts just outside the spinal cord in the lower neck and extends to the axilla. The total average brachial plexus length is approximately 6 inches.1 The plexus is divided into five sections: roots, trunks, divisions, cords, and branches or terminal nerves. The spinal nerves C5 through T1 classically supply anterior primary rami of the nerve roots, which then form the plexus. Variations in nerve root supply that involve other nerve roots are said to be expanded. When the C4 nerve 816

root also supplies the brachial plexus and the T1 contribution is minimal, the plexus is called prefixed. When the T2 nerve root supplies the brachial plexus and the C5 contribution is minimal, the plexus is said to be postfixed.2 The nerve roots combine to form the trunks behind the clavicle. There are three trunks: the upper, middle, and lower. The upper is formed from the C5 and C6 nerve roots, the middle is a continuation of C7, and the lower is formed from C8 and T1. The trunks then divide behind the clavicle into anterior and posterior divisions. Just inferior to the clavicle the divisions coalesce into cords. The cords travel along the axillary artery, just inferior to the clavicle, and are named for their spatial relationship to the artery. The posterior cord is formed from the union of the three posterior divisions. The lateral cord is formed by the union of the anterior divisions of the upper and middle trunks. The medial cord is the continuation of the anterior division of the lower trunk. Nerve branches are the most distal elements of the brachial plexus and are the major nerves of the upper extremity. These branches begin in the distal axilla and—except for the median nerve, which is formed by contributions from the medial and lateral cords—are continuations of the cords. There are also numerous peripheral nerves that arise directly from the roots, trunks, and cords (Fig. 144.1). Brachial plexopathy can be due to wide-ranging causes, including idiopathic, iatrogenic, autoimmune, traumatic, neoplastic, and hereditary conditions. It can occur in any age group; but other than when it is secondary to obstetric trauma, it usually occurs in individuals between the ages of 30 and 70 years. Men are affected two to three times as often as are women; the reason for this may be their more frequent participation in vigorous athletic activities that can lead to trauma. About half of the cases have no identified precipitating event; in others, brachial plexopathy follows an antecedent infection, trauma, surgery, or immunization. 

Symptoms Brachial plexopathy can cause symptoms of pain, weakness, and numbness, both at the level of the brachial plexus and distally in the supplied upper extremity. The area of pain and other symptoms correlates with the portion of the brachial plexus involved and the specific nerve elements from that area. Depending on the cause of the plexopathy, symptom onset can range from sudden to insidious. Because of the complex muscle suspension of the shoulder joint, chronic brachial plexopathy may result in glenohumeral subluxation

CHAPTER 144 Plexopathy—Brachial

817

Roots

Divisions Posterior (P)

Trunks Upper (U) Middle (M) Lower (L)

4

4

5

Cords Lateral (L) Posterior (P) Medial (M)

5 6

6 7

U M Branches Radial n. (R) Median n. (M) Ulnar n. (U)

AA

P

P P A

L

8 1

7

Dorsal scapular n. N. to subclavius Suprascapular n.

1 Long thoracic n. Bridge Upper subscapular n. Thoracodorsal n. Lower subscapular n.

L P M

Medial pectoral n. Lateral pectoral n. Axillary n. Medial brachial cutaneous n.

R M

Medial antebrachial cutaneous n.

U

Musculocutaneous n.

FIG. 144.1  The brachial plexus. The clinician must be able to visualize this structure in performing electrodiagnostic examinations so that an appropriate number of muscles and nerves are sampled to localize a lesion. (From Dumitru D, Amato A, Zwarts M. Electrodiagnostic Medicine, 2nd ed. Philadelphia: Hanley & Belfus; 2002.)

and instability due to stretching of the shoulder capsule. Brachial plexopathy usually does not cause prominent neck pain. Some brachial plexopathies may occur bilaterally and therefore cause symptoms in both upper extremities. 

Physical Examination The physical examination of the brachial plexus for brachial plexopathy must be thorough because of the complexity of the plexus’s structure and function. The shoulder girdle and entire extremity must be exposed during examination to allow close inspection of muscle bulk and fasciculations. Assessment of atrophy of muscles is often assisted by sideto-side comparisons. Muscle strength examination must be thorough and include proximal muscles not commonly tested, such as the infraspinatus, supraspinatus, rhomboids, and serratus anterior. Sensory testing must also be thorough, with both dermatomal and peripheral nerve sensory distributions examined. A musculoskeletal examination of the

shoulder joint is helpful; joint disease can be both a possible primary cause of pain and a secondary effect of plexopathy. Shoulder range of motion and signs of tendinosis as well as reflexes must be assessed. The lack of pain exacerbation with neck movement and multiroot distribution of sensory or motor deficits can help to distinguish brachial plexopathy from cervical radiculopathy, which more commonly affects a single root.3 It is often not possible to determine the exact location of a brachial plexus lesion by physical examination, but the examination is usually helpful in focusing electrodiagnostic and radiologic testing. 

Functional Limitations The proximal shoulder muscles, distal muscles involved in fine finger movements, or the entire extremity can be weak or numb depending on which part of the brachial plexus is involved: the upper plexus, the lower plexus, or the entire plexus. Activities of daily living, such as dressing, feeding, and

818

PART 3 Rehabilitation

grooming, can be significantly affected. These impairments in nerve function can result in disabilities in many activities, including computer use, writing, and driving. Brachial plexopathy secondary to birth trauma may subsequently cause difficulty for children and teens with sports and other recreational activities. 

Diagnostic Studies Electromyography (EMG) can be helpful in localizing the pathologic area in brachial plexopathy as well as in determining the severity of axonal injury and the potential for recovery. However, many brachial plexopathies cannot be definitely localized by EMG because of subtle findings encountered with incomplete nerve injury and the complexity of plexus-related innervation. The nerve conduction and needle EMG assessment is best directed by both symptoms and physical examination findings. Both nerve conduction studies and needle EMG are required for complete assessment. Sensory nerve conduction studies can help in localization by the pattern of abnormalities seen and in judging injury severity based on reductions of amplitudes or absence of potentials. The nerve conduction study may not detect abnormality if the lesion is mild in severity or too recent to allow axonal degeneration. The following five basic sensory nerve conduction studies are suggested as a screen for brachial plexus evaluation: lateral antebrachial cutaneous, median recording from the thumb, median recording from the index finger, superficial radial, and ulnar recording from the little finger.2 The presence of fibrillation potentials in EMG is particularly sensitive for motor axon loss and helps localize the site of lesions. The choice of muscles sampled on EMG is usually focused on the area of interest, but other areas are also included for the exclusion of wider disease. It is important to include paraspinal muscles of the relevant areas to investigate the possibility of radiculopathy (paraspinals are supplied by the posterior primary rami of the nerve roots, which do not supply the brachial plexus). EMG evaluation of the brachial plexus is complex and best performed by experienced electromyographers. Radiologic studies of the plexus are helpful to evaluate the severity of trauma, presence of mass lesions, and inflammation of the brachial plexus nerve elements.4 Magnetic resonance imaging (MRI), particularly MR neurography, has become the study of choice in the evaluation of traumatic brachial plexus injuries.5 More than 80% of traumatic nerve root avulsions will show pseudomeningoceles, which are tears in the meningeal sheath surrounding the nerve roots that allow extravasation of cerebrospinal fluid into nearby tissues. They appear bright on T2-weighted images. MRI is also the most useful study for evaluation of other causes of brachial plexopathy, such as tumors, both secondary and primary.6 An early MRI sign in Pancoast tumor is obliteration of the interscalene fat pad, which is best visualized on coronal T1-weighted MRI.7 Inflammatory changes in the brachial plexus may be visualized with MRI, including brachial neuralgic amyotrophy.8 Computed tomography myelography is increasingly becoming the study of choice in the preoperative evaluation of infants with obstetric brachial plexopathy, given its usefulness in identifying nerve root avulsion, which affects operative interventions.9,10

Musculoskeletal ultrasonography has been used in the evaluation of suspected neoplastic brachial plexop­ athy. Sonography may identify the neoplastic lesion as a hypoechoic mass or present evidence consistent with a compressive lesion, such as segmental neuronal swelling of the involved portion of the brachial plexus.11 Chest radiographs are valuable for the evaluation of diaphragmatic paralysis in traumatic brachial plexopathy, which usually indicates an irreparable lesion of the brachial plexus.12  Differential Diagnosis Generalized peripheral neuropathy Focal peripheral neuropathy Cervical radiculopathy Motor neuron disorder Neuromuscular junction disorder Myopathy Spinal cord injury Stroke Complex regional pain syndrome

Differential Diagnosis Etiology of Brachial Plexopathy It is helpful to approach the differential diagnosis of brachial plexopathy by the common causes in the different anatomic regions where the brachial plexus is affected. The anatomic areas of interest are the supraclavicular, retroclavicular, and infraclavicular. There are also causes of brachial plexopathy that tend to produce more diffuse plexus injury.

Supraclavicular Birth Trauma Lateral deviation of the head and neck to free the infant’s shoulder during both vaginal delivery and cesarean section can lead to stretch injury of the upper brachial plexus. Such injuries can also occur from in utero causes, including compression of the fetal shoulder by the maternal symphysis pubis or sacral promontory as well as by uterine anomalies that result in abnormally elevated intrauterine pressures.13 The incidence of brachial plexopathy from birth trauma is 0.4 to 4 per 1000 live births.14 It is called Erb palsy when the C5-C6 nerve roots are affected, resulting primarily in proximal arm weakness. When the C8-T1 roots are affected, the results are hand weakness, called Klumpke paralysis. 

Trauma Most commonly, trauma involves the upper plexus and is especially seen with closed traction, as in “burner” or “stinger” sports injuries (sudden separation of the shoulder and head due to contact) and pressure from backpack straps (“rucksack palsy”). The roots can be stretched but remain continuous or they may tear or avulse from the spinal cord. More direct trauma, such as from a stab or gunshot wound, can affect any portion of the plexus, but the supraclavicular portion is the most susceptible. 

CHAPTER 144 Plexopathy—Brachial

Intraoperative Arm Malpositioning Postoperative brachial plexopathy may result from malpositioning of the arm during surgery.15 

Pancoast Syndrome An apical lung tumor (usually small cell carcinoma) can extend into the supraclavicular brachial plexus, often manifesting with shoulder pain.16 

Neurogenic Thoracic Outlet This syndrome is a rare condition in which a fibrous band extends from the lower cervical spine (cervical rib or transverse process) to the first rib. The T1 fibers are deflected and injured further by this fibrous band more than the C8 fibers are. 

Infraclavicular Postirradiation Radiation therapy directed at the axillary lymph nodes can result in brachial plexopathy, which can occur months to years after radiation therapy. EMG studies may reveal evidence of conduction block and classic myokymia. 

Metastatic Lymphadenopathy A secondary neoplastic injury is usually due to compression from enlargement of involved axillary lymph nodes. 

Regional Blocks Infraclavicular brachial plexus injury has been identified as a complication of axillary regional blocks.17 

Heterotopic Ossification The growing mass of heterotopic ossification about the shoulder can envelop and compromise the brachial plexus.18 In midclavicular fractures, brachial plexopathy can be secondary to the initial trauma and also result from the development of heterotopic ossification.18 

Retroclavicular Midclavicular Fractures In midclavicular fractures, retroclavicular brachial plexop­ athy can be secondary to the initial trauma but can also result late from exuberant callus compression of the brachial plexus.18 Retroclavicular brachial plexopathy, however, is rare and most often occurs in the context of more widespread plexopathy. 

Diffuse Localization Neuralgic Amyotrophy Also called Parsonage-Turner syndrome, brachial amyotrophy, idiopathic shoulder girdle neuropathy,19 and brachial plexitis, neuralgic amyotrophy is a well-described syndrome of idiopathic monophasic brachial plexopathy that was characterized by a large case series.20 The initial symptom is onset during a few hours of severe continuous proximal upper extremity pain, which occurred in 90% of patients in this case series. After the onset of pain, weakness of the extremity usually develops within 2 weeks. Whereas sensory symptoms in the affected extremity are usually less

819

pronounced than pain and weakness, they occur in 70% of patients. Pain decreases first, with an average pain duration of 28 days. Motor recovery begins within 6 months in most patients and with significant functional improvement; but in this case series, more than 70% of patients still had at least mild weakness detected on thorough strength examination at 3 years after weakness onset. Neuralgic amyotrophy can involve any part of the brachial plexus but tends to affect the upper plexus; 49% of patients have shoulder–proximal arm involvement. The true incidence of neuralgic amyotrophy may be much higher than previously thought, with a recent study showing an incidence rate of 1 per 1000.21 

Hereditary Neuralgic Amyotrophy This is a similar condition to neuralgic amyotrophy but with a known genetic etiology and septin 9 (SEPT9) mutations that can be identified with a commercially available test.22 

Diabetic Cervical Radiculoplexus Neuropathy Distinct from neuralgic amyotrophy is the recently described diabetic cervical radiculoplexus neuropathy.23 This condition is associated with type 2 diabetes mellitus. Patients initially develop pain in the upper limb, often acutely, followed later by weakness and sensory changes, such as paresthesias, dysesthesias, or numbness. Associated autonomic symptoms (orthostasis, sudomotor changes) are common, as is weight loss. Electrodiagnosis reveals predominantly axonal neuropathy, whereas biopsy findings of involved nerves show axonal degeneration, ischemic injury, and perivascular inflammation. The condition is typically monophasic with improvement, but 21% of patients demonstrated recurrence.23 

Primary Neoplastic Peripheral Nerve Tumors Local primary peripheral nerve tumors can cause brachial plexopathies that occur anywhere in the brachial plexus, but they are rare and usually benign. Benign tumors are typically nerve sheath tumors, either schwannomas or neurofibromas (associated with neurofibromatosis type 1), and cause painless sensory loss and weakness.2 In contrast, malignant peripheral nerve tumors in the brachial plexus tend to be painful.24,25 

Treatment Initial The treatment of brachial plexopathy must be customized to the individual patient and the cause of the brachial plexopathy. Pain can be the most disabling symptom but is usually effectively treated with neuropathic pain medications; these include gabapentin and tricyclic antidepressants and analgesics such as tramadol and opiates in cases of severe pain. Dosing is usually at the higher end of accepted ranges (such as gabapentin at 600 mg three times daily) because of the severe pain of acute plexopathy, although the duration of therapy may be brief. Patients with neuralgic amyotrophy have been shown to have marked improvement in long-term outcome and decreased pain when a 14-day course of prednisolone was started within 1 month of symptom onset.26 

820

PART 3 Rehabilitation

Rehabilitation

Potential Treatment Complications

When the muscles of the shoulder girdle are involved, therapy focused on positioning and shoulder range of motion can prevent secondary complications, such as adhesive capsulitis.27 A focused program of physical and occupational therapy for patients with neuralgic amyotrophy can facilitate improvements in activity and performance.28 Occupational therapy is often indicated when weakness from brachial plexopathy results in loss of function. Adaptive aids, such as a shoulder sling to help reduce imbalance from proximal arm weakness from brachial plexopathy, can be helpful when indicated. Vocational rehabilitation may be indicated when the resultant disability from weakness affects the patient’s ability to perform in the job setting. 

Stretching and range-of-motion exercises for avoidance or treatment of contractures can acutely exacerbate neuropathic pain. Care to avoid shoulder impingement during range-ofmotion exercises is important because of weak rotator cuff muscles. Insensate limbs become more susceptible to heat injuries, as by hot packs or therapeutic ultrasound. Medicines used for brachial plexopathy pain can have side effects specific to the particular medicine used. Surgery for brachial plexopathy may result in nerve or vascular injury.

Procedures Brachial plexus blocks are rarely used but are possible for the treatment of severe pain from metastatic brachial plexopathy or severe acute brachial plexopathy. Increasingly, botulinum toxin injection, combined with surgery, serial casting, and physical and occupational therapy are used to treat and prevent shoulder and forearm pronation contractures as well as to optimize elbow range of motion in infants with obstetric brachial plexus injury.29 However, botulinum use in this setting has yet to be tested in randomized controlled trials. 

Technology No specific new or recent technologies are used in the treatment or rehabilitation of these patients. 

Surgery Surgery is an option in cases of traumatic plexopathy but has had variable results. Surgical techniques such as nerve grafting, free muscle transfer, neurolysis, and neurotization are used. Surgeons who use these techniques frequently differ considerably in their approach to them, making conclusions about their efficacy difficult. Surgery is an option in brachial plexus birth injuries, usually when persistent severe motor deficits are present after 3 to 8 months of age. A case series found improvement in surgically treated patients on a shoulder motion scale.30 The location of injury affects selection of patients for surgery and surgical outcome. For example, postganglionic nerve root avulsion injuries may do better with earlier surgery.31 Preganglionic avulsions are difficult to repair, but direct implantation into the spinal cord may help some patients.32 

Potential Disease Complications Weakness from brachial plexopathy can result in joint instability or in joint and musculotendinous contractures of upper extremity joints. There is a high incidence of long-term persistent pain and impairments in persons with neuralgic amyotrophy.33 Secondary depression can be due to pain and loss of function. Insensate limbs are at risk for trauma neglect, infection, and amputation. 

References 1. Slinghuff CL Jr, Terzis CK, Edgerton MT. The quantitative microanatomy of the brachial plexus in man: reconstructive relevance. In: Terzis JK, ed. Microreconstruction of Nerve Injuries. Philadelphia: WB Saunders; 1987:285–324. 2. Ferrante MA. Brachial plexopathies: classification, causes, and consequences. Muscle Nerve. 2004;30:547–568. 3. Mamula CJ, Erhard RE, Piva SR. Cervical radiculopathy or ParsonageTurner syndrome: differential diagnosis of a patient with neck and upper extremity symptoms. J Orthop Sports Phys Ther. 2005;35:659–664. 4. Castillo M. Imaging the anatomy of the brachial plexus: review and selfassessment module. AJR Am J Roentgenol. 2005;185:S196–S204. 5. Upadhyaya V, Upadhyaya DN, Kumar A, Gujral RB. MR neurography in traumatic brachial plexopathy. Eur J Radiol. 2015;84(5):927–932. 6. Saifuddin A. Imaging tumors of the brachial plexus. Skeletal Radiol. 2003;32:375–387. 7. Huang JH, Zagoul K, Zager EL. Surgical management of brachial plexus tumors. Surg Neurol. 2004;61:372–378. 8. Lieba-Samal D, Jenqojan S, Kasprian G, et al. Neuroimaging of classic neuralgic amyotrophy. Muscle Nerve. 2016;54(6):1079–1085. 9. Steens SCA, Pondaag W, Malessy MJA, Verbist BM. Obstetric brachial plexus lesions: CT myelography. Neuroradiology. 2011;259:508–515. 10. VanderHave KL, Bovid K, Alpert H, et al. Utility of electrodiagnostic testing and computed tomography myelography in the preoperative evaluation of neonatal brachial plexus injury. J Neurosurg Pediatr. 2012;9:283–289. 11. Lapegue F, Faruch-Bilfeld M, Deomdion X, et al. Ultrasonography of the brachial plexus, normal appearance and practical applications. Diagn Interv Imaging. 2014;95(3):259–275. 12. Belzberg AJ, Dorsi MJ, Strom PB, Moriarty JL. Surgical repair of brachial plexus injury: a multinational survey of experienced peripheral nerve surgeons. J Neurosurg. 2004;101:365–376. 13. Doumouchtsis SK, Arulkumaran S. Are all brachial plexus injuries caused by shoulder dystocia? Obstet Gynecol Surv. 2009;64:615–623. 14. Hale HB, Bae DS, Waters PM. Current concepts in the management of brachial plexus birth palsy. J Hand Surg Am. 2010;35:322–331. 15. Wilbourn AJ. Iatrogenic nerve injuries. Neurol Clin. 1998;16:55–82. 16. Huehnergarth KV, Lipsky BA. Superior pulmonary sulcus tumor with Pancoast syndrome. Mayo Clin Proc. 2004;79:1268. 17. Tsao BE, Wilbourn AJ. Infraclavicular brachial plexus injury following axillary regional block. Muscle Nerve. 2004;30:44–48. 18. England JD, Tiel RL. AAEM case report 33: costoclavicular mass syndrome. American Association of Electrodiagnostic Medicine. Muscle Nerve. 1999;22:412–418. 19. Weaver K, Kraft GH. Idiopathic shoulder girdle neuropathy. Phys Med Rehabil Clin N Am. 2001;12:353–364. 20. van Alfen N, van Engelen BG. The clinical spectrum of neuralgic amyotrophy in 246 cases. Brain. 2006;129(Pt 2):438–450. 21. van Alfen N, vanEijk JJ, Ennik T, et al. Incidence of neuralgic amyotrophy (Parsonage-Turner syndrome) in a primary care setting-a prospective cohort study. PLoS One. 2015;10(5):e0128361. 22. Collie AM, Landsverk ML, Russo E, et al. Non-recurrent SEPT9 duplications cause hereditary neuralgic amyotrophy. J Med Genet. 2010;47(9):601–607. 23. Massie R, Mauermann M, Staff N, et al. Diabetic cervical radiculoplexus neuropathy: a distinct syndrome expanding the spectrum of diabetic radiculoplexus neuropathies. Brain. 2012;135:3074–3088. 24. Park JK. Peripheral nerve tumors. In: Samuels MA, Feske SK, eds. Office Practice of Neurology, 2nd ed. Philadelphia: Churchill Livingstone; 2003: 1118–1121.

CHAPTER 144 Plexopathy—Brachial

25. Pacelli J, Whitaker C. Brachial plexopathy due to malignant peripheral nerve sheath tumor in neurofibromatosis type 1: case report and subject review. Muscle Nerve. 2006;33:697–700. 26. van Eijk JJ, van Alfen N, Berrevoets M, et al. Evaluation of prednisolone treatment in the acute phase of neuralgic amyotrophy: an observational study. J Neurol Neurosurg Psychiatry. 2009;80(10):1120–1124. 27. Langer JS, Sueoka SS, Wang AA. The importance of shoulder external rotation in activities of daily living: improving outcomes in traumatic brachial plexus palsy. J Hand Surg Am. 2012;37:1430–1436. 28. Ijspeert J, Janssen RM, Murgia A, et al. Efficacy of combined physical and occupational therapy in patients with subacute neuralgic amyotrophy. Neurorehabilitation. 2013;33(4):657–665. 29. Gobets D, Beckerman H, de Groot V, et al. Indications and effects of botulinum toxin A for obstetric brachial plexus injury: a systematic literature review. Dev Med Child Neurol. 2010;52:517–528.

821

30. Grossman JA, DiTaranto P, Yaylali I, et al. Shoulder function following late neurolysis and bypass grafting for upper brachial plexus birth injuries. J Hand Surg Br. 2004;29:356–358. 31. Waters PM. Update on management of pediatric brachial plexus palsy. J Pediatr Orthop B. 2005;14:233–244. 32. Bertelli JA, Ghizoni MF. Brachial plexus avulsion injury repairs with nerve transfers and nerve grafts directly implanted into the spinal cord yield partial recovery of shoulder and elbow movements. Neurosurgery. 2003;52:1385–1389. 33. Cup EH, Ijspeert J, Janssen RJ, et al. Residual complaints after neuralgic amyotrophy. Arch Phys Med Rehabil. 2013;94(1):67–73.

CHAPTER 145

Plexopathy— Lumbosacral Erick Ensrud, MD

Synonyms Lumbosacral plexitis Neuralgic amyotrophy of the lumbosacral plexus Lumbosacral plexus neuropathy Lumbosacral radiculoplexus neuropathy Diabetic amyotrophy

ICD-10 Codes G54.1 G54.8 G54.9

Lumbosacral plexus disorders Other nerve root and plexus disorders Nerve root and plexus disorder, unspecified S34.21 Injury of nerve root of lumbar spine S34.22 Injury of nerve root of sacral spine S34.4 Injury of lumbosacral plexus M54.15 Radiculopathy, thoracolumbar region M54.16 Radiculopathy, lumbar region M54.17 Radiculopathy, lumbosacral region M54.18 Radiculopathy, sacral and sacrococcygeal region Add seventh character for episode of care (S—late effects)

Definition Lumbosacral plexopathy is an injury to or involvement of one or more nerves that combine to form or branch from the lumbosacral plexus. This involvement is distal to the root level. The lumbar plexus originates from the first, second, third, and fourth lumbar nerves (Fig. 145.1). The fourth lumbar nerve makes a contribution to both the lumbar and the sacral plexus. There is typically a small communication from the 12th thoracic nerve as well. As in the brachial plexus, these nerve roots divide into the dorsal rami and the ventral rami as they exit through the intervertebral foramina. The dorsal or posterior rami innervate the paraspinal muscles and supply nearby cutaneous sensation. The ventral or anterior rami of the lumbar plexus form the motor and 822

sensory nerves to the anterior and medial sides of the thigh and the sensation on the medial aspect of the leg and foot. The undivided anterior primary rami of the lumbar and sacral nerves also carry postganglionic sympathetic fibers that are mainly responsible for vasoregulation of the lower extremities. The branches of the lumbar plexus include the iliohypogastric, ilioinguinal, genitofemoral, femoral, lateral femoral cutaneous, and obturator nerves.1 The lumbar portion of the plexus lies just anterior to the psoas muscle.2 The sacral plexus innervates the muscles of the buttocks, posterior thigh, and leg below the knee and the skin of the posterior thigh and leg, lateral leg, foot, and perineum. It is formed from the lumbosacral trunk to include L5 and a portion of L4 as well as the S1 to S3 (or S4) nerve roots (Fig. 145.2). The anterior primary rami of S2 and S3 nerve roots carry parasympathetic fibers that mainly control the urinary bladder and anal sphincters. The triangular sacral plexus lies on the anterior surface of the sacrum, in the immediate vicinity of the sacroiliac joint and lateral to the cervix or prostate.1 The branches of the sacral plexus include the superior and inferior gluteal nerves; the posterior cutaneous nerves of the thigh; the lumbosacral trunk, which becomes the sciatic nerve with both tibial and peroneal divisions; and the pudendal nerve.

Etiology Lumbosacral plexopathy has been recognized as a clinical entity or complication in a variety of surgical procedures, trauma, and obstetric surgery or delivery and as a clinical finding or sequela in treatment of pelvic tumors. 

Trauma Traumatic pelvic fractures have a 30.8% incidence of lumbosacral plexus injury.3,4 The incidence and severity of traumatic lumbosacral plexopathy increase with the number of pelvic fracture sites and fracture instability.4 Sacral fractures have become recognized as essential in pelvic trauma because of their high association with lumbosacral nerve deficits.5 This can have a profound influence on prognosis and level of functional recovery.3,6 The more common sacral fractures are typically the compression or avulsion fractures of the sacral ala, which can occur in lateral compression and anteroposterior compression pelvic fractures.7 Fractures of the sacral neuroforamina or midline sacral fractures may

Terminal branches

Divisions (Posterior shaded)

Iliohypogastric nerve (T12, L1)

Branches

Plexus roots From anterior primary divisions T12

(Inconstant)

Iliac branch L1

Hypogastric branch *

Ilioinguinal nerve (L1) Genitofemoral nerve (L1, L2)

L2

Lumboinguinal branch External spermatic branch

*

L3

Lateral femoral cutaneous nerve (L2, L3)

*

L4 *

To psoas muscles

L5 Femoral nerve (L2, L3, L4) *Branches to intertransversarii and quadratus lumborum muscles

Obturator nerve (L2, L3, L4)

Lumbosacral trunk (to sacral plexus)

FIG. 145.1  The lumbar plexus and its peripheral terminal branches. The shaded portions represent the posterior divisions of the ventral primary rami; those not shaded are either the ventral primary rami or their anterior branches. In this diagram, the nerve to the psoas major arises from the femoral nerve as opposed to directly from the spinal nerve region. (From de Groot J, Chusid JG. Correlative Neuroanatomy, 21st ed. Norwalk, CT: Appleton & Lange; 1991.)

Terminal and collateral branches

Divisions (Posterior [shaded] and anterior)

Plexus roots From anterior primary divisions

(To lumbar plexus)

Branches from posterior divisions Superior gluteal nerve (L4, L5, S1)

L4

(Lumbosacral trunk)

Branch to piriformis (S1, S2)

L5

Inferior gluteal nerve (L5, S1, S2) * S1

Branches from both anterior and posterior divisions

*

Posterior femoral cutaneous nerve (S1, S2, S3)

S2

S3 Sciatic nerve

(To pudendal plexus)

Inferior medial clunial nerve (S2, S3) Common peroneal nerve

Tibial nerve

(To hamstring muscles)

Branches from anterior divisions Branch to quadratus femoris and gemellus inferior muscles (L4, L5, S1) Branch to obturator internus and gemellus superior muscles (L5, S1, S2)

FIG. 145.2  Schematic representation of the sacral plexus. The shaded portions signify the posterior divisions of the ventral primary rami; the unshaded aspects are the anterior branches of the ventral primary rami. (From de Groot J, Chausid JG. Correlative Neuroanatomy, 21st ed. Norwalk, CT: Appleton & Lange; 1991.)

824

PART 3 Rehabilitation

also occur. Fractures of the sacrum can increase the incidence of neurologic injury in pelvic trauma to between 34% and 50% because of its proximity to the sacral nerve roots.7 Gunshot wounds and motor vehicle accidents have long been recognized as potential causes of lumbosacral plexus injuries. In a retrospective comparison of patterns of lumbosacral plexus injury in motor vehicle crashes and gunshot wounds, individuals with gunshot wounds had a greater chance of involvement of the upper portion of the plexus in comparison with individuals who sustained a motor vehicle crash. Lower plexus injuries were more common in victims of motor vehicle accidents as opposed to gunshot wounds.8 Finally, trauma is a common cause of retroperitoneal hemorrhage, which can injure the lumbosacral plexus. 

Labor and Delivery The lumbosacral plexus may be compressed as a complication of labor and delivery. The incidence of neurologic injury reported in the literature for postpartum sensory and motor dysfunction is relatively low at 0.008% to 0.5%.9,10 Factors associated with nerve injury were nulliparity and a prolonged second stage of labor; assisted vacuum or forceps vaginal delivery also had some positive association. Women with nerve injury spent more time pushing in the semiFowler lithotomy position. During the second stage of labor, direct pressure of the fetal head may compress the lumbosacral plexus against the pelvic rim, which can result in nerve injury.11,12 Fortunately postpartum lumbosacral plexopathy has a good prognosis. 

Iatrogenic Gynecologic surgery is thought to be one of the most common causes of femoral nerve injury (see Chapter 54) and lumbosacral plexus nerve injuries. Abdominal hysterectomy is the surgical procedure most frequently implicated.13,14 The mechanisms of neurologic injury that have been identified include improper placement or positioning of selfretaining or fixed retractors, incorrect positioning of the patient in lithotomy position preoperatively or prolonged lithotomy positioning without repositioning, and radical surgical dissection resulting in autonomic nerve disruption.15 Lumbosacral injury has also been noted after appendectomy and inguinal herniorrhaphy. Patients who are thin, diabetic, or elderly are at increased risk for such an injury. Injury to the lumbosacral plexus with clinical findings occurs in up to 10% of hip replacement procedures, and injury that is subclinical but detected electromyographically occurred in up to 70% of these patients.16 In individuals receiving anticoagulant therapy or with acquired or congenital coagulopathies, retroperitoneal hemorrhage causing lumbosacral plexopathy may occur with no precipitating injury.17,18 Retroperitoneal hematoma has also been documented as a rare but potentially serious complication after cardiac catheterization.19,20 In a review of 9585 femoral artery catheterizations, a reported retroperitoneal hematoma rate of 0.5% occurred. In patients undergoing stent placement, there was evidence of lumbar plexopathy involving the femoral, obturator, and lateral femoral cutaneous nerves; this condition was typically completely reversible.21,22 Femoral vein catheterization for dialysis has also

been documented as a cause of hemorrhagic complications and retroperitoneal hemorrhage.23 Case reports have also identified patients sustaining lumbosacral plexopathy after aortoiliac bypass grafting for abdominal aortic aneurysm. The proposed mechanism for this rare complication, with fewer than 80 patients reported in the literature, is neural ischemia secondary to interruption of the blood supply to the lumbosacral plexus or caudal portion of the spinal cord.24,25 

Oncologic Both pelvic malignant neoplasms and treatment of pelvic tumors can damage the lumbosacral plexus. Lumbosacral radiculopathy is most common with gynecologic tumors, sarcomas, and lymphomas. Neoplastic plexop­ athy is characterized by severe and unrelenting pain, typically followed by weakness and sensory disturbances.26 Pelvic radiation therapy may cause a delayed lumbosacral plexopathy that can occur 3 months to 22 years after completion of treatment; the median amount of time from the completion of treatment to onset of symptoms is about 5 years.27-29 Chemotherapeutic agents can also cause symptoms of lumbosacral radiculopathy. Cisplatin, 5-fluorouracil, mitomycin C, and bleomycin have been implicated in the majority of these plexopathies.2 Metastatic or tumor extension into the lumbosacral plexus and malignant psoas syndrome have been described in the literature. Malignant psoas syndrome was first reported in 1990. It is characterized by proximal lumbosacral plexopathy, painful fixed flexion of the ipsilateral hip, and radiologic or pathologic evidence of ipsilateral psoas major muscle malignant involvement.2 

Diabetic Amyotrophy Diabetic and nondiabetic lumbosacral radiculoplexus neuropathies have been documented. Diabetic lumbosacral radiculoplexus neuropathy is a subacute, painful, asymmetric lower limb neuropathy that is associated with significant weight loss (at least 10 lb), type 2 diabetes mellitus, and a relatively recent diagnosis of diabetes with relatively good glucose control.30 The underlying pathophysiologic mechanism is thought to be immune-mediated with microvasculitis of the nerve rather than a metabolic issue caused by diabetes; nondiabetic lumbosacral radiculoplexus neuropathy has also been documented with similar clinical and pathophysiologic features.30-34 The similar clinical symptoms, findings, and response to treatment suggest that the metabolic changes from diabetes may not be the cause of these symptoms, although impaired glucose tolerance has been noted in nondiabetic lumbosacral radiculoplexus neuropathy.32 

Vascular Vascular causes of lumbosacral plexopathies may include diabetic amyotrophy and connective tissue diseases that may be associated with vasculitis, such as systemic lupus erythematosus, rheumatoid arthritis, and polyarteritis nodosa.35 If a vascular cause is suspected, the aorta and iliac vessels must be evaluated for disease or occlusion.36 

CHAPTER 145 Plexopathy—Lumbosacral

Symptoms Plexopathies may vary considerably in their presentation, depending on the location and degree of involvement. Lumbosacral plexopathy often begins with leg pain radiating to the low back and buttocks and progressing posterolaterally down the leg, soon followed by symptoms of numbness and weakness. Lumbosacral plexus injuries are often associated with a footdrop and sensory changes to the top of the foot. A plexopathy involving the upper lumbar roots may primarily be manifested by femoral and obturator nerve symptoms. Femoral nerve injury typically is manifested with iliopsoas or quadriceps weakness, and there may be sensory deficits over the anterior and medial thigh as well as the anterior medial aspect of the leg.13 Obturator injury has also been seen in upper plexus injuries with weakness of the hip adductors10 and sensory changes in the upper medial thigh. Diabetic plexopathy typically starts as an identifiable onset of asymmetric lower extremity symptoms that most typically involve the thigh and hip with pain that progresses to include weakness, which then becomes the main disabling symptom. In a few months, this usually evolves into bilateral symmetric weakness and pain with distal as well as proximal involvement. Although motor findings are prominent, sensory and autonomic nerves have also been shown to be involved.29 Bowel and bladder injuries tend to occur in cases in which there is bilateral sacral root involvement. Sexual dysfunction has been documented in both bilateral and unilateral sacral injuries and pelvic trauma. Lumbosacral plexus injuries are much more common in pelvic and sacral fractures but have been documented in acetabular fractures and midshaft femoral fractures as well.3,6,26 

Physical Examination Clinical examination to evaluate for a lumbosacral plexop­ athy involves neurologic assessment including the testing of motor strength, sensory function, muscle stretch reflexes, tone, and bowel and bladder function. The pattern of sensory loss, asymmetric reflexes, or weakness is suggestive of multiple nerve or root level involvement. It is important to differentiate a suspected plexus injury from single root level involvement, suggesting a radiculopathy, or more generalized nerve changes consistent with peripheral neuropathy. A detailed examination of both lower limbs—including skin sensory testing of all dermatomes, manual muscle testing of all myotomes, and examination of the patellar and Achilles deep tendon reflexes—can reveal neurologic deficits that can aid in this differentiation. In addition, it may be necessary to evaluate lower sacral involvement by physical examining the tone of a patient’s external anal sphincter, particularly if complaints include bowel and bladder incontinence. Edema or swelling in one lower extremity may be suggestive of a pelvic mass or lumbosacral plexus involvement rather than a more global peripheral neuropathy or possible retroperitoneal hematoma or pelvic malignant neoplasm.2 

Functional Limitations Functional limitations depend on which portions of the lumbar or lumbosacral plexus have been injured and the

825

severity of the injury. Patients frequently present with some type of difficulty with mobility and ambulation. Activities such as transferring from one surface to another, rising from a chair, ambulation, grooming, bathing, dressing, and cooking may potentially be affected. These functional limitations may have far-reaching consequences on an individual’s ability to live independently and to continue in his or her chosen vocation. 

Diagnostic Studies Electrodiagnostic Testing The electrodiagnostic evaluation of lumbosacral plexopathy is one of the most effective tools available for differentiating a specific pattern and severity of nerve involvement. Guided by a focused history and physical examination, the skilled electromyographer can use testing of both proximal and distal sensory and motor nerves as well as muscle needle examination to determine whether there is radicular involvement, lumbar or lumbosacral plexus involvement with multiple nerves involved but no paraspinal involvement, or a more generalized picture consistent with a peripheral neuropathy. Testing for upper lumbar plexopathy may include studies of the lateral femoral cutaneous nerve, saphenous nerve, posterior femoral cutaneous sensory nerve, and femoral motor nerve. Side-to-side comparison is recommended to assess for asymmetry in these technically challenging studies. Sensory involvement without motor involvement suggests a lesion distal to the dorsal root ganglion. Studies to evaluate the lumbosacral plexus and lumbosacral roots include sural and superficial peroneal sensory studies, H reflex, and peroneal and tibial motor conduction studies. Depending on the timing of the injury, nerve conduction studies can demonstrate a decrease in amplitude for the sensory nerve action potentials starting at 5 to 6 days and for compound muscle action potentials starting at 2 to 4 days.37 The needle electromyographic examination is likely to be the most useful electrodiagnostic technique.37 Careful examination of the proximal and distal musculature demonstrates a pattern of muscle membrane instability in more than one peripheral nerve from different root levels without involvement of the paraspinal muscles. The pattern of muscle membrane instability indicates whether the injury appears to be a neurapraxia with conduction block, axon­ otmesis, or neurotmesis with wallerian degeneration and a poor prognosis for reinnervation. Increased insertional activity may be seen in the involved musculature after 7 to 8 days, with positive waves and fibrillations starting at 10 to 30 days but being most prominent at 21 to 30 days after injury.37 Decreased recruitment is noted immediately after injury, and this may be the only change on needle electromyographic examination in the first few days if the nerve is partially intact. 

Imaging Studies Computed tomography and positron emission tomography can be useful in determining the presence of a structural mass in the pelvic region. Computed tomographic scans, along with abdominal ultrasonography, may be used to diagnose a retroperitoneal hemorrhage. Both computed

826

PART 3 Rehabilitation

tomographic scanning and magnetic resonance imaging have been used to evaluate the lumbosacral plexus. Magnetic resonance imaging has been found to be more sensitive than computed tomography for diagnosis of cancer-related lumbosacral plexopathy.38 High-resolution magnetic resonance neurography with T1-weighted fast spin echo and fat-saturated T2-weighted fast spin echo has been increasingly used to study the lumbosacral plexus and the sciatic nerve.39,40 Plain radiographs are useful as a screening tool for suspected aneurysms or malignant disease.  Differential Diagnosis Spinal cord injury Cauda equina injury Lumbosacral nerve root injury Multiple peripheral nerve injuries Anterior horn cell diseases Myopathies Occlusion of the aorta

Treatment Initial Initial treatment is based on both the presenting symptoms and the cause of the lumbosacral plexopathy. For example, many obstetric lumbosacral plexus symptoms are treated conservatively. Pelvic masses or a retroperitoneal hemorrhage may require surgical or medical intervention. Neoplastic or radiation-based plexopathy symptoms may need specific medical management, chemotherapy, or possibly surgery. If edema control is necessary, leg elevation and compressive stockings may be of some benefit. Medication for neuropathic pain might include gabapentin, duloxetine, or pregabalin. Tricyclic antidepressants may also be helpful. Opioids and nonsteroidal anti-inflammatory drugs may also provide pain relief. Use of nonsteroidal anti-inflammatory drugs is contraindicated, however, when hemorrhage is suspected. Various immunomodulation therapies for diabetic amyotrophy— including corticosteroids, cyclophosphamide, intravenous immune globulin, and plasmapheresis—have been described in a number of case series. One series showed particularly marked improvement in pain within days of a methylprednisolone dose.40 However, no randomized double-blind trials have been published and a systematic review of the evidence for immunotherapy in diabetic amyotrophy was equivocal.41 

Rehabilitation Rehabilitation aims to maximize mobility and functional independence. The goals of rehabilitation are preservation of joint range of motion and flexibility, joint protection, and pain management; these goals depend on a good physical examination to determine what neurologic and functional deficits are present. One of the primary rehabilitation concerns in an individual with nerve involvement in the lumbar or lumbosacral plexus is safe mobility and ambulation. The patient should be evaluated for the need for an assistive device such as a cane or a walker to facilitate ambulation. Patients with significant footdrop impairing gait benefit from prescription of ankle-foot orthoses, with dorsiflexion assist as an option.

Energy conservation techniques and the care of insensate feet are key treatment tools. Symptoms of lumbosacral plexopathy may be subtle and difficult to appreciate in a clinical setting. Physicians need to address potentially sensitive issues such as work limitations, sexual functioning, and sensory changes in the pelvic and inguinal areas. 

Procedures Sympathetic nerve blocks and chemodenervation have both been used to ameliorate pain. This can be both diagnostic and treatment oriented in helping to confirm the suspected diagnosis. Sacral nerve stimulation has been evaluated for adjunctive treatment of lumbosacral plexopathy, but further research is required for its effectiveness to be determined.17 

Technology No specific new or recent technology is available for the treatment or rehabilitation of this condition. 

Surgery Lumbosacral plexus injuries associated with pelvic or sacral fractures or with gynecologic surgery are often treated conservatively,13 although it has been documented that long-term sequelae can occur. Nerve reconstruction including nerve grafting has been reported in an attempt to restore some lower extremity function.42 Microsurgical treatment of lumbosacral plexopathies for neurolysis and nerve grafting has been used in the retroperitoneal space. In a series of 15 cases, the muscles that benefited the most from surgery were the gluteal and femoral innervated muscles. The more distal musculature did not seem to show much benefit.43 Whereas motor improvement is an important consideration, pain is often extremely debilitating in patients with a lumbosacral plexopathy and may block or limit rehabilitation. Pain relief is one of the major goals of surgical intervention. Surgical resection of a tumor may also be indicated in certain cases with lumbosacral plexopathy.26 

Potential Disease Complications Potential complications of lumbosacral plexopathy include joint contractures, limited mobility, weakness, falls secondary to weakness or sensory loss, bowel or bladder incontinence, diminished or absent sensation, skin breakdown, sexual dysfunction, and significant decrease in functional independence from these complications. The rare complication of complex regional pain syndrome type II has also been reported.44 

Potential Treatment Complications Treatment complications may include skin breakdown under orthoses and increased weakness if the rehabilitation program is too aggressive. Medication side effects are dizziness, somnolence, gastrointestinal irritation, and ataxia due to anticonvulsants; dry mouth, urinary retention, and atrioventricular conduction block due to tricyclic antidepressants; and dependence, dizziness, somnolence, and constipation due to opioid pain medications. Nonsteroidal anti-inflammatory drugs and analgesics can also have significant side effects that affect the gastrointestinal and renal systems as well as the liver.

CHAPTER 145 Plexopathy—Lumbosacral

References 1. Moore KL, Dalley AF, eds. Clinically Oriented Anatomy, 4th ed. Philadelphia: Lippincott Williams & Wilkins; 1999. 2. Agar M, Broadbent A, Chye R. The management of malignant psoas syndrome: case reports and literature review. J Pain Symptom Manage. 2004;28:282–293. 3. Kutsy RL, Robinson LR, Routt ML. Lumbosacral plexopathy in pelvic trauma. Muscle Nerve. 2000;23:1757–1760. 4. Jang D-H, Byun SH, Jeon SY, Lee SJ. The relationship between lumbosacral plexopathy and pelvic fractures. Am J Phys Med Rehabil. 2011;90:707–712. 5. Medelman JP. Fractures of the sacrum: their incidence in fractures of the pelvis. Am J Roentgenol Radium Ther Nucl Med. 1939;42:100–103. 6. Gibbons KJ, Soloniuk DS, Razack N. Neurological injury and patterns of sacral fractures. J Neurosurg. 1990;72:889–893. 7. Bellabarba C, Stewart JD, Ricci WM, et al. Midline sagittal sacral fractures in anterior-posterior compression pelvic ring injuries. J Orthop Trauma. 2003;17:32–37. 8. Chiou-Tan FY, Kemp K, Elfenbaum M, et al. Lumbosacral plexopathy in gunshot wounds and motor vehicle accidents: comparison of electrophysiologic findings. Am J Phys Med Rehabil. 2001;80:280–285. 9. Holdcroft A, Gibberd FB, Hargrove RL, et al. Neurological complications associated with pregnancy. Br J Anaesth. 1995;75:522–526. 10. Wong CA, Scavone BM, Dugan S, et al. Incidence of postpartum lumbosacral spine and lower extremity nerve injuries. Obstet Gynecol. 2003;101:279–288. 11. Dawson DM, Krarup C. Perioperative nerve lesions. Arch Neurol. 1989;46:1355–1360. 12. Richard A, Vellieux G, Benlifla JL, et al. Good prognosis of postpartum lower limb sensorimotor deficit: a combined clinical, electrophysiological, and radiological follow-up. J Neurol. 2017;264(3):529–540. 13. Irvin W, Andersen W, Taylor P, et al. Minimizing the risk of neurologic injury in gynecologic surgery. Obstet Gynecol. 2004;103:374–382. 14. Fardin P, Benettello P, Negrin P. Iatrogenic femoral neuropathy. Considerations on its prognosis. Electromyogr Clin Neurophysiol. 1980;20: 153–155. 15. Whiteside JL, Barber MD, Walters MD, et al. Anatomy of ilioinguinal and iliohypogastric nerves in relation to trocar placement and low transverse incisions. Am J Obstet Gynecol. 2003;189:1574–1578; discussion 1578. 16. Solheim LF, Hagen R. Femoral and sciatic neuropathies after total hip arthroplasty. Acta Orthop Scand. 1980;51:531–534. 17. Chad DA, Bradley WG. Lumbosacral plexopathy. Semin Neurol. 1987;7:97–107. 18. Rajashekhar RP, Herbison GJ. Lumbosacral plexopathy caused by retroperitoneal hemorrhage: report of two cases. Arch Phys Med Rehabil. 1974;55:91–93. 19. Ozcakar L, Sivri A, Aydinli M, et al. Lumbosacral plexopathy as the harbinger of a silent retroperitoneal hematoma. South Med J. 2003;96:109–110. 20. Kent KC, Moscucci M, Mansour KA, et al. Retroperitoneal hematoma after cardiac catheterization: prevalence, risk factors, and optimal management. J Vasc Surg. 1994;20:905–910; discussion 910–913. 21. Lumsden AB, Miller JM, Kosinski AS, et al. A prospective evaluation of surgically treated groin complications following percutaneous cardiac procedures. Am Surg. 1994;60:132–137. 22. Kent KC, Moscucci M, Gallagher SG, et al. Neuropathy after cardiac catheterization: incidence, clinical patterns, and long-term outcome. J Vasc Surg. 1994;19:1008–1013; discussion 1013–1014. 23. Kaymak B, Ozcakar L, Cetin A, et al. Bilateral lumbosacral plexopathy after femoral vein dialysis: synopsis of a case. Joint Bone Spine. 2004;71:347–348.

827

24. Adbelhamid MF, Sandler D, Awad RW. Ischaemic lumbosacral plexopathy following aorto-iliac bypass graft: case report and review of literature. Ann R Coll Surg Engl. 2007;89:W12–W13. 25. Abdellaoui A, West NJ, Tomlinson MA, et al. Lower limb paralysis from ischaemic neuropathy of the lumbosacral plexus following aorto-iliac procedures. Interact Cardiovasc Thorac Surg. 2007;6:501–502. 26. Jaeckle KA. Neurological manifestations of neoplastic and radiationinduced plexopathies. Semin Neurol. 2004;24:385–393. 27. Georgiou A, Grigsby PW, Perez CA. Radiation induced lumbosacral plexopathy in gynecologic tumors: clinical findings and dosimetric analysis. Int J Radiat Oncol Biol Phys. 1993;26:479–482. 28. Taphoorn MJB, Bromberg JEC. Neurological effects of therapeutic irradiation. Continuum: lifelong learning in neurology. Neuro Oncol. 2005;11:93–115. 29. Thomas JE, Cascino TL, Earle JD. Differential diagnosis between radiation and tumor plexopathy of the pelvis. Neurology. 1985;35: 1–7. 30. Fann A. Plexopathy—lumbosacral. In: Frontera WR, Silver JK, eds. Essentials of Physical Medicine and Rehabilitation. Philadelphia: Hanley & Belfus; 2001:671. 31. Dyck PJB, Windebank AJ. Diabetic and nondiabetic lumbosacral radiculoplexus neuropathies: new insights into pathophysiology and treatment. Muscle Nerve. 2002;25:477–491. 32. Dyck PJB, Norell JE, Dyck PJ. Non-diabetic lumbosacral radiculoplexus neuropathy: natural history, outcome and comparison with the diabetic variety. Brain. 2001;124:1197–1207. 33. Kelkar P, Hammer-White S. Impaired glucose tolerance in nondiabetic lumbosacral radiculoplexus neuropathy letter. Muscle Nerve. 2005;31:273–274. 34. Zochodne DW, Isaac D, Jones C. Failure of immunotherapy to prevent, arrest, or reverse diabetic lumbosacral plexopathy. Acta Neurol Scand. 2003;107:299–301. 35. Dumitru D, Zwarts MJ. Lumbosacral plexopathies and proximal mononeuropathies. In: Dumitru D, Amato A, Zwarts M, eds. Electrodiagnostic Medicine, 2nd ed. Philadelphia: Hanley & Belfus; 2002: 777–836. 36. van Alfen N, van Engelen BG. Lumbosacral plexus neuropathy: a case report and review of the literature. Clin Neurol Neurosurg. 1997;99: 138–141. 37. Strakowski JA. Electrodiagnosis of plexopathy. PM R. 2013;(suppl5): S50–S55. 38. Taylor BV, Kimmel DW, Krecke KN, et al. Magnetic resonance imaging in cancer-related lumbosacral plexopathy. Mayo Clin Proc. 1997;72: 823–829. 39. Robbins NM, Shah V, Benedetti N, et al. Magnetic resonance neurography in the diagnosis of neuropathies in the lumbosacral pleus: a pictorial review. Clin Imaging. 2016;40(6):1118–1130. 40. Kilfoyle D, Kelkar P, Parry GJ. Pulsed methylprednisolone is a safe and effective treatment for diabetic amyotrophy. J Clin Neuromuscul Dis. 2003;4(4):168–170. 41. Chan YC, Lo YL, Chan ES. Immunotherapy for diabetic amyotrophy. Cochrane Database Syst Rev. 2017;7:CD006521. https://doi. org/10.1002/14651858.CD006521.pub4. 42. Tung TH, Martin DZ, Novak CB, et al. Nerve reconstruction in lumbosacral plexopathy. Case report and review of the literature. J Neurosurg. 2005;102(suppl):86–91. 43. Alexandre A, Coro L, Azuelos A. Microsurgical treatment of lumbosacral plexus injuries abstract. Acta Neurochir Suppl. 2005;92: 53–59. 44. Gallo AC, Codispoti VT. Complex regional pain syndrome type II associated with lumbosacral plexopathy: a case report. Pain Med. 2010;11: 1834–1836.

CHAPTER 146

Polytrauma Rehabilitation Carlos A. Jaramillo, MD, PhD Rebecca N. Tapia, MD Blessen C. Eapen, MD

Synonyms

S06.30

Blast injury Multiple injuries Multiple trauma

S06.9.x

ICD-10 Codes Acute Injuries S02.0xx Fractures of vault of skull—requires a seventh character for type of encounter and healing S02.1 Fractures of base of skull—requires two digits and a seventh character S06.0 Concussion—requires two digits and a seventh character S06.1 Traumatic cerebral edema—requires two digits and a seventh character S06.2 Diffuse traumatic brain injury—requires two digits and a seventh character S06.30 Unspecified focal traumatic brain injury—requires an additional digit and a seventh character S06.31 Contusion and laceration of right cerebrum—requires an additional digit and a seventh character S06.32 Contusion and laceration of left cerebrum—requires an additional digit and a seventh character S06.33 Contusion and laceration of cerebrum unspecified—requires an additional digit and a seventh character S06.9.x Unspecified intracranial injury (TBI NOS)—requires an additional digit and a seventh character

Late Effect Codes or Sequelae S06.2

828

Diffuse traumatic brain injury—requires two digits and a seventh character of S

Focal traumatic brain injury—requires an additional digit and a seventh character of S Unspecified intracranial injury (TBI NOS) —requires an additional digit and a seventh character of S

War Operations Y36.20

Blast wave

Symptoms Involving Cognitive Function and Awareness R41.840 R41.841 R41.842 R41.843 R41.844 R41.89

Attention and concentration deficit Cognitive communication deficit Visuospatial deficit Psychomotor deficit Frontal lobe and executive function deficit Other signs and symptoms involving cognitive functions and awareness

Physical Effects of Traumatic Brain Injury G44.301 Post-traumatic headache, unspecified intractable G44.309 Post-traumatic headache, unspecified not intractable G44.321 Chronic post-traumatic headache, unspecified intractable G44.329 Chronic post-traumatic headache, unspecified not intractable R42 Dizziness R43.0 Loss of smell (anosmia) R43.8 Other disturbance of smell and taste R47.82 Fluency disorder conditions classified elsewhere R47.81 Slurred speech R56.1 Post-traumatic seizures

CHAPTER 146  Polytrauma Rehabilitation

Definition of Polytrauma Within the field of rehabilitation medicine, polytrauma has been defined as “two or more injuries, one of which may be life threatening, sustained in the same incident that affect multiple body parts or organ systems and result in physical, cognitive, psychological, or psychosocial impairments and functional disability.”1 Given the nature of the exposure (motor vehicle collision, blast, fall, blunt trauma, assault, etc.) it is likely that traumatic brain injury (TBI) occurred and in severe cases could dictate the entire course of rehabilitation. Thus, there has been increased focus on intracranial injuries as part of polytrauma. Other conditions commonly seen as part of polytrauma include amputations, wounds, spinal cord and musculoskeletal injuries, burns, acute and chronic pain (general prevalence of 81.5% in Iraq and Afghanistan veterans), auditory or visual impairments, post-traumatic stress disorder (general prevalence of 68.2% in Iraq and Afghanistan veterans), and other mental health diagnoses.2 Because of the heterogeneity of injuries and potential causes, it is difficult to estimate the true incidence of polytrauma. However, both military and civilian settings TBI tracking systems have been established and for the former, the US Department of Defense (DoD) has found that over 370,000 TBI of different severities have been diagnosed since the year 2000.3 Many of the individuals who sustained a TBI will have other associated traumatic injuries, so a better understanding of the incidence and prevalence of polytrauma will continue to emerge. TBI is a heterogeneous condition spanning from experiencing a brief episode of confusion after external trauma all the way to catastrophic injury and death (see Chapters 148 and 163). Table 146.1 demonstrates the formal definitions of TBI based on 2016 VA/DoD Clinical Practice Guidelines; however, it is important to note that these definitions relate to immediate metrics (such as duration of loss of consciousness) and are not representative of current level of function. Should the patient meet criteria in more than one category of severity, the higher severity level is assigned.4

History of Polytrauma System of Care Coordinated national trauma care systems are quite rare, with only nine documented systems existing in high-income countries.5 Military trauma care in the United States has been greatly accelerated in the past decade, producing efforts to establish a national trauma care system pairing military and civilian organizations to develop common best practices, data standards, research, and workflow across the continuum.6 As service members began returning from the war in the early 2000s, it became apparent that a comprehensive rehabilitation system would be needed to ensure these individuals were returned to their maximum level of function and quality of life. These patients presented with complex medical, rehabilitation, and psychosocial needs that proved challenging to meet in the existing DoD and VA rehabilitation system. Legislation enacted in 2004 directed the Veterans Health Administration (VHA) to establish a continuum of care centered around TBI and other conditions associated with war exposures including extremity

829

Table 146.1  VA/DoD Definitions of Traumatic Brain Injury Criteria

Mild

Moderate

Severe

Structural imaging

Normal

Normal or abnormal

Normal or abnormal

Loss of consciousness (LOC)

0–30 min

>30 min and 24 h

Alteration of consciousness/mental state (AOC)a

up to 24 h

>24 h; severity based on other criteria

Post-traumatic amnesia (PTA)

0–1 day

>1 and 7 days

Glasgow Coma Scale (GCS) (best available score in first 24 h)

13–15

9–12

90%. • Systolic blood pressure >100, 60, 60 years Coagulation disorder or anticoagulation Trauma above the clavicle with clinical signs of skull fracture Continued post-traumatic amnesia or retrograde amnesia longer than 30 min Unclear mechanism of injury or intoxication with drug or alcohol

Left

The use of biomarkers to assess the magnitude of total brain injury and to localize brain injury is promising, though with little routine clinical use. These markers may prove to be useful in patients with mild TBI with otherwise normal imaging findings, as well as in patients whose injury severity cannot be accurately assessed because of confounders mentioned previously. Important cognition-related biomarkers include acetylcholine, glutamate, dopamine, serotonin (5-HT), gammaaminobutyric acid, substance P (SP), amyloid-β (Aβ), and neurotrophic protein S100B. These may soon be of clinical use as an adjunct to neuroimaging in the early assessment of primary and evolving damage in traumatic and ischemic brain injury.25,26 

Functional Assessment Tools

Table 163.2  Risk Factors for Intracranial Complications

FIG. 163.1  Diffusion tensor imaging in traumatic brain injury: loss of white matter tract fibers after traumatic brain injury (right) compared with an age-matched control (left). (From Maas AI, Menon DK. Traumatic brain injury: rethinking ideas and approaches. Lancet Neurol. 2012;11:12–13.)

the functional limitations caused by the injury. In patients with otherwise normal findings on neuroimaging, diffusion tensor imaging is emerging as a potential diagnostic tool for mild brain injury, as it can detect white matter microstructure changes (Fig. 163.1).21,22 Despite the potential of new imaging techniques, TBI remains primarily a clinical diagnosis.23,24 At the time of outpatient follow-up, it may be necessary to remind the patient and his or her caregivers of the extreme limitations of these diagnostic studies and to focus on that patient’s functional abilities as the more important measure of the extent of the injury. In general, follow-up radiologic examinations are useful tools only if the patient has excessively slow progress or has demonstrated a decline in function. These may be helpful in determining new or expanding lesions. Otherwise, these are generally of limited utility. 

Superior Anterior

Posterior Inferior

Right

One of the best diagnostic tools is the Glasgow Coma Scale, which is used for the initial evaluation of the severity of the patient’s injury (see Table 163.1). A review of this initial score will help in the determination of the extent of the injury and thus with prognostication. Later, as a review of function in the outpatient setting, progress can be measured by the Disability Rating Scale. Post-traumatic amnesia is important for prognostication as well and can be assessed by the Galveston Orientation and Amnesia Test. For the current level of functional recovery to be characterized, the Rancho Los Amigos Scale is helpful in the assessment of the patient’s awareness and interaction with the environment. 

CHAPTER 163  Traumatic Brain Injury

Neuropsychological Testing This battery of tests, performed by a neuropsychologist, is the best means of determining the full spectrum of cognitive, affective, and emotional function of the individual. This may be completed before discharge from inpatient rehabilitation and should be repeated when a change in function needs to be documented. This testing may provide the clinician with critical information needed to understand the ability of the patient to progress toward more independence or responsibility at home or at work. This also may be a critical assessment tool for the documentation of the injury for insurance and/or legal purposes.  Differential Diagnosis Anoxic brain injury Metabolic encephalopathy Affective disorder Depression Whiplash-associated disorder

Treatment Initial The initial focus of treating a patient with a TBI is to reduce the magnitude of the secondary injury. If the initial injury is of sufficient severity, CT or MRI may be helpful in determining the need for surgical intervention. The scans are reviewed for signs of excessive bleeding, edema, and shifting of the brain. If these signs are absent, medical intervention addresses the possible secondary injury that may result. Although it is still unclear as to how long a window of opportunity exists to affect the extent of secondary injury processes, it is generally accepted that this opportunity is likely to occur within the time of the initial acute hospitalization.5 For this reason, there is little opportunity to affect this process in the outpatient setting. Initially, metabolic issues such as blood pressure, electrolytes, hydration and nutrition, infectious processes, sleep disturbances including sleep apnea, and medications need to be addressed. Any imbalance in these may inhibit the function of the surviving brain tissue. Hydration and nutrition should be well maintained. An individual with a brain injury may be unable or unwilling to take nutrients by mouth, and this may necessitate either intravenous or direct gastrointestinal feedings. This may be a significant issue well into the post-acute phase of recovery. A survey for possible infectious processes should include, at a minimum, the pulmonary and genitourinary systems. Even infections that a clinician may otherwise label subclinical can disrupt the function of a damaged brain. For this reason, such infections should be treated as potentially symptomatic. A number of medications can have undesired negative effects among those with a brain injury. These need to be reviewed carefully to eliminate any that may interfere with cognitive function. The list is long, but the most common offenders include antiseizure medications, antihypertensive medications, antispasticity medications, neuroleptics,

963

sedatives, hypnotics, and gastrointestinal medications. Some of these may be unnecessary, whereas others may have less disruptive alternatives. In addition to neuropsychological testing of the cognitive performance of the patient, psychological services are important in the assessment and treatment of affective disorders, which may include depression, apathy, and posttraumatic stress disorder. It is important to consider psychology services as being useful for the family and support system, as the stress on these individuals may be tremendous. Psychologists and behavior specialists may be helpful for the intervention into behavior issues.

Arousal Arousal will fluctuate throughout the day for a person with brain injury. Fatigue may become a long-standing problem. Frequent rests and naps may be needed, even at more than 1 year after injury. Pharmacologic interventions may be initiated for hypoarousal and excessive fatigue. These include amantadine, bromocriptine, carbidopa/levodopa, methylphenidate, modafinil, atomoxetine, amphetamine, nortriptyline, and protriptyline.27 In a double-blind clinical trial, amantadine has been shown to accelerate the pace of functional recovery in patients with severe brain injury.28 

Attention Neuropharmacologic agents for attention are similar to those used for arousal. These include neurostimulants, such as methylphenidate, modafinil, and atomoxetine, and dopaminergic agents, including amantadine, bromocriptine, and carbidopa/levodopa. Antidepressants include a long list of mixed as well as selective serotonin reuptake inhibitors; these will be especially useful if there is an element of depression interfering with cognition. 

Agitation Because agitation is a common and often troubling issue among those recovering from a TBI, a careful selection of pharmacologic agents is important to prevent injury, to allow focus on rehabilitation, and to reduce the stress on caregivers. In general, the agents that are preferred will help control behavior, while producing the least disruption of cognition. Because benzodiazepines are thought to have the potential of interfering with the recovery of the injured brain, these are often not recommended in the early stages of recovery. Other medications are therefore used as first-line agents. As an anxiolytic, buspirone seems preferable. A clinician may use antiseizure medications as a mood stabilizer (e.g., divalproex sodium, carbamazepine), newer antipsychotic medications (e.g., risperidone, quetiapine), beta blockers (e.g., propranolol), and antidepressants for anxious or agitated patients. Because poor attention to the environment may result in behavioral agitation, medications such as amantadine and methylphenidate should also be considered as useful agents. 

Memory Because memory requires both arousal and attention, the medications previously discussed for improved attention may ­produce improvements in the ability to learn. In addition, there have been limited reports of positive results through

964

PART 3 Rehabilitation

the use of donepezil, memantine, rivastigmine, and other similar drugs. Memory can also be enhanced through the use of compensatory strategies and services. Speech pathologists can be useful for the introduction of and training in some of these strategies. There are portable electronic devices that can be preprogrammed with important information, and these memory aids can be frequently updated for individuals whose TBI may interfere with the ability to program the electronic memory aids. 

Seizures There is a reasonable body of literature to suggest that the use of antiseizure medications is not warranted if no seizure occurs within the first week after the brain injury. If the patient experiences a seizure after 1 week, the use of anticonvulsant agents may be needed for an extended time until the patient is seizure free for a period of 2 to 5 years; the patient is then to be reevaluated and managed per standard guidelines for patients with new-onset seizures.29,30 Recommended agents depend on seizure type and usually include carbamazepine, valproic acid, and gabapentin. 

Spasticity Spasticity is a common problem among patients with brain injury (see Chapter 154). Patients may also have hyperactive muscle stretch reflexes and clonus. If these problems are not addressed, early contracture of joints may result. The modified Ashworth scale can be used to measure the degree of spasticity. As a first step of intervention, the clinician should look to reduce noxious stimuli, including anything that may produce pain. Infectious issues, positioning, and seating should be addressed as potential offenders. Stretching should be initiated and may necessitate serial casting and splinting. If medications are needed, these may include tizanidine, clonidine, dantrolene, diazepam, and baclofen. All of these agents have potential side effects and should be used judiciously. Dantrolene is unique in its lack of central effect, but often results in acute liver dysfunction. 

Rehabilitation The rehabilitation of patients with brain injury begins during the acute stage of treatment when the risks of secondary brain injury are the greatest. After the acute phase, it is important that the clinician reviews the potential pharmacologic management and combine this with an interdisciplinary group of therapies, depending on the specific deficits of the patient. Studies have suggested that early admission to a dedicated inpatient brain rehabilitation unit is associated with reduced overall cost as well as improved outcome.31

Physical Therapy Physical therapy is important for the restoration of range of motion of the lower extremities and, if needed, through the use of serial casting. This may be aided by neurolysis or blocks at the neuromuscular junction. Later, issues of wheelchair preparation and propulsion may be important for those with sufficient impairment of mobility. Ambulation training with the appropriate assistive device should be frequently reviewed as the patient progresses with ambulation. Ambulation may be complicated by dizziness and balance issues, even among those with mild injuries.

Safety must always be considered because the patient with TBI may be endangered by impulsivity or poor planning and judgment. 

Occupational Therapy Occupational therapy addresses the preservation of joints when a lack of strength or an excess in tone or spasticity threatens a joint. As strength and ataxia are often issues in the first year, these should be addressed individually. The issues of self-care, including daily activities such as dressing, bathing, and grooming, must be addressed and emphasize the need for a planning strategy for the patient. Cooking and driving evaluations may be needed to advise the patient before his or her return to the home. 

Speech Therapy Early in the care of the patient, the ability to swallow safely needs to be evaluated (see Chapter 130). In addition, the speech pathologist, ideally working with the neuropsychologist, can identify focal cognitive needs of the patient and address these over a length of time. These often involve memory strategies, such as mnemonic training, and pragmatics, which focus on the contextual and social aspects of communication skills. Published cognitive training studies have supported the efficacy of cognitive-based interventions on overall cognition, verbal memory, and executive function.32–35 These strategies, as a part of a comprehensive cognitive rehabilitation program, may enhance a partial restoration of focal activities in regions of the brain associated with memory, such as the hippocampus.36 

Vocational Rehabilitation Many patients will have difficulty in returning to their previous level of employment. Vocational rehabilitation counselors can evaluate a patient’s skills and determine the need for training. 

Procedures For spasticity, local injections may be preferable to oral medications. These may include nerve root blocks, nerve blocks, motor unit blocks (all with phenol), and neuromuscular junction blocks (with botulinum toxin). When spasticity is severe and not responsive to these interventions, an intrathecal pump may be considered for continuous infusion of baclofen into the cerebrospinal fluid (refer to Chapter 154). 

Technology Portable memory aids are often used to assist patients with TBI. These have long included portable electronic devices. With the widespread use and acceptance of smart phones, these devices are increasingly used as memory aides, wayfinding using GPS, and auditory feedback. Despite its promise, there is still no universally accepted use of this technology.38 

Surgery Patients with new-onset hydrocephalus may need a shunt placed to reduce the pressure load at the brain. If

CHAPTER 163  Traumatic Brain Injury

965

Table 163.3  Medications Frequently Used in Traumatic Brain Injury Symptoms

Medication

Initial Dose

End Dose

Arousal

Amantadine

50 mg, 8 am and 2 pm

100 mg, 8 am and 2 pm

Bromocriptinea

1.25 mg, 8 am and 2 pm

5.0 mg, 8 am and 2 pm

Carbidopa/levodopaa

10 mg/100 mg tid

50 mg/100 mg tid

Methylphenidate

2.5 mg, am and 2 pm

20 mg, am and 2 pm

Modafinil

100 mg qd

100 mg, 8 am and 2 pm

Dextroamphetamine

5 mg qd

30 mg, am and 2 pm

Methylphenidate

2.5 mg, am and 2 pm

20 mg, am and 2 pm

Adderall

5 mg bid

20 mg bid

Modafinil

100 mg, am

100 mg, am and pm

Amantadine

100 mg, am

150 mg, am and 2 pm

Bromocriptinea

1.25 mg, am

50 mg, 8 am and 2 pm

Carbidopa/levodopaa

10 mg/100 mg tid

50 mg/100 mg tid

Sertraline

50 mg qd

200 mg qd

Citalopram

20 mg qd

40 mg qd

Donepezil

2.5 mg qd

5 mg bid

Memantine

5 mg qd

10 mg qd

Atomoxetine

20 mg qd

60 mg qd

Buspirone

7.5 mg bid

30 mg bid

Carbamazepine

200 mg bid

600 mg bid

Risperidone

1 mg bid

6 mg/day

Morphine

10 mg q4h

10 mg q4h

Propranolol

10 mg qd

Limited by heart rate and blood pressure

Quetiapine

25 mg qd

800 mg qd

Donepezil

5 mg

10 mg

Memantine

5 mg

10 mg bid

Attention

Agitation

Memory

aLimited

by hypotension.

medications and other measures fail to control spasticity and contractures result, surgery may be an option. If joint contractures occur, a surgical release may be indicated. 

Potential Disease Complications Seizures can result from a TBI. The risk is highest early after the injury but persists for years. Soon after the injury, patients are at risk for aspiration pneumonia and, if swallowing is impaired, for malnutrition and dehydration. Sleep apnea is a frequent early issue. If not treated, it may exacerbate the symptoms of the TBI. Continuous positive airway pressure may be an effective treatment. As with all trauma patients, there is a risk for deep venous thrombosis (see Chapter 128). This must be treated with prophylactic low-dose unfractionated heparin, low-molecular-weight heparin, or mechanical prophylaxis with pneumatic compression devices.37 

Potential Treatment Complications Medications that are used to treat attention and arousal may lead to excess arousal and agitation. This may also be

manifested as somatic complaints or delirium. Medications for agitation and seizures may slow the patient’s recovery over time and may reduce the patient’s function while the medications are taken. Refer to Table 163.3.

References 1. Taylor CA, Bell JM, Breiding MJ, Xu L. Traumatic brain injury–related emergency department visits, hospitalizations, and deaths—United States, 2007 and 2013. MMWR Surveill Summ. 2017;66(SS-9):1–16. 2. Hyder A, et al. The impact of traumatic brain injuries: a global perspective. Neurorehabilittion. 2007;22:341–353. 3. CDC grand rounds: reducing severe traumatic brain injury in the United States. Morb Mortal Wkly. 2013;62(27):549–552. 4. Redelmeier DA, Tibshirani RJ, Evans L. Traffic-law enforcement and risk of death from motor-vehicle crashes: case-crossover study. Lancet. 2003;361:2177–2182. 5. Langlois JA, Rutland-Brown W, Wald MM. The epidemiology and impact of traumatic brain injury: a brief overview. J Head Trauma Rehabil. 2006;21:375–378. 6. Maas AI, Stocchetti N, Bullock R. Moderate and severe traumatic brain injury in adults. Lancet Neurol. 2008;7:728–741. 7. McGinn M, et al. Pathophysiology of traumatic brain injury. Neurosurg Clin N Am. 2016;27:397–407. 8. Yuen TJ, Browne KD, Iwata A, Smith DH. Sodium channelopathy induced by mild axonal trauma worsens outcome after a repeat injury. J Neurosci Res. 2009;87:3620–3625.

966

PART 3 Rehabilitation

9. Mondello S, Muller U, Jeromin A, et al. Blood-based diagnostics of traumatic brain injuries. Expert Rev Mol Diagn. 2011;11:65–78. 10. Carney N, Totten AM, O’Reilly C, et al. Guidelines for the management of severe traumatic brain injury, fourth edition. Neurosurgery. 2017;80(1):6–15. 11. Gennarelli TA, Champion HR, Sacco WJ, et al. Mortality of patients with head injury and extracranial injury treated in trauma centers. J Trauma. 1989;29(9):12-1–12–2. 12. Fernandez-Ortega JF, Prieto-Palomino MA, Garcia-Caballero M, et al. Paroxysmal sympathetic hyperactivity after traumatic brain injury: clinical and prognostic implications. J Neurotrauma. 2012;29:1364–1370. 13. Englander J, Bushnik T, Oggins J, Katznelson L. Fatigue after traumatic brain injury: association with neuroendocrine, sleep, depression and other factors. Brain Inj. 2010;24:1379–1388. 14. Holly LT, Kelly DF, Counelis GJ, et al. Cervical spine trauma associated with moderate and severe head injury: incidence, risk factors, and injury characteristics. J Neurosurg. 2002;96(suppl):285–291. 15. Paiva WS, Oliveira AM, Andrade AF, et al. Spinal cord injury and its association with blunt head trauma. Int J Gen Med. 2011;4:613–615. 16. Arango-Lasprilla JC, Ketchum JM, Dezfulian T, et al. Predictors of marital stability 2 years following traumatic brain injury. Brain Inj. 2008;22:565–574. 17. Murray GD, Butcher I, McHugh GS, et al. Multivariable prognostic analysis in traumatic brain injury: results from the IMPACT study. J Neurotrauma. 2007;24:329–337. 18. Smits M, Dippel DW, Steyerberg EW, et al. Predicting intracranial traumatic findings on computed tomography in patients with minor head injury: the CHIP prediction rule. Ann Intern Med. 2007;146:397–405. 19. Vos PE, Battistin L, Birbamer G, et al. EFNS guideline on mild traumatic brain injury: report of an EFNS task force. Eur J Neurol. 2002;9:207–219. 20. Ebell MH. Computed tomography after minor head injury. Am Fam Physician. 2006;73:2205–2207. 21. Bigler ED, Bazarian JJ. Diffusion tensor imaging: a biomarker for mild traumatic brain injury? Neurology. 2010;74:626–627. 22. Maas AI, Menon DK. Traumatic brain injury: rethinking ideas and approaches. Lancet Neurol. 2012;11:12–13. 23. Mac Donald CL, Johnson AM, Cooper D, et al. Detection of blastrelated traumatic brain injury in U.S. military personnel. N Engl J Med. 2011;364:2091–2100. 24. Aoki Y, Inokuchi R, Gunshin M, et al. Diffusion tensor imaging studies of mild traumatic brain injury: a meta-analysis. J Neurol Neurosurg Psychiatry. 2012;83:870–876.

25. Kochanek PM, Berger RP, Bayir H, et al. Biomarkers of primary and evolving damage in traumatic and ischemic brain injury: diagnosis, prognosis, probing mechanisms, and therapeutic decision making. Curr Opin Crit Care. 2008;14:135–141. 26. Zhao-Liang D, et al. Biomarkers of cognitive dysfunction in traumatic brain injury. J Neural Transm. 2014;121(1):79–90. 27. Gordon WA, Zafonte R, Cicerone K, et al. Traumatic brain injury rehabilitation: state of the science. Am J Phys Med Rehabil. 2006;85:343–382. 28. Giacino JT, Whyte J, Bagiella E, et al. Placebo-controlled trial of amantadine for severe traumatic brain injury. N Engl J Med. 2012;366:819–826. 29. Bratton SL, Chestnut RM, Ghajar J, et al. Guidelines for the management of severe traumatic brain injury. XIII. Antiseizure prophylaxis. J Neurotrauma. 2007;24(suppl 1):S83–S86. 30. Hixson JD. Stopping antiepileptic drugs: when and why? Curr Treat Options Neurol. 2010;12:434–442. 31. Cardenas DD, Haselkorn JK, McElligott JM, Gnatz SM. A bibliography of cost-effectiveness practices in physical medicine and rehabilitation: AAPM&R white paper. Arch Phys Med Rehabil. 2001;82:711–719. 32. Stringer AY. Ecologically-oriented neurorehabilitation of memory: robustness of outcome across diagnosis and severity. Brain Inj. 2011;25:169–178. 33. Carney N, Chesnut RM, Maynard H, et al. Summary report: evidence for the effectiveness of rehabilitation for persons with traumatic brain injury. J Head Trauma Rehabil. 1999;14:176–188. 34. Cicerone KD, Dahlberg C, Malec JF, et al. Evidence-based cognitive rehabilitation: updated review of the literature from 1998 through 2002. Arch Phys Med Rehabil. 2005;86:1681–1692. 35. Cicerone KD, Dahlberg C, Kalmar K, et al. Evidence-based cognitive rehabilitation: recommendations for clinical practice. Arch Phys Med Rehabil. 2000;81:1596–1615. 36. Hampstead BM, Stringer AY, Stilla RF, et al. Mnemonic strategy training partially restores hippocampal activity in patients with mild cognitive impairment. Hippocampus. 2012;22:1652–1658. 37. Theriault T, Thochette M, Goupil V, et al. Thromboprophylaxis adherence to the ninth edition of the American College of Chest Physicians antithrombotic guidelines in a tertiary care centre: a cross-sectional study. J Eval Clin Pract. 2016;22(6):956–961. 38. Wong D, et al. Smartphones as assistive technology following traumatic brain inury: a preliminary study of what helps and what hinders. Disability Rehabil. 2016:1–8.

Index A

Abatacept, in rheumatoid arthritis, 880t–881t Abdomen, in cervical spinal cord injury, physical examination of, 906 Abdominal cutaneous nerve entrapment syndrome (ACNES), 517 Abdominal pain, algorhythmic thought process to, 519f Abdominal wall nerve entrapment syndrome. See Abdominal wall pain Abdominal wall pain, 515–522 definition of, 517–518 diagnostic studies for, 519 differential diagnosis of, 519b functional limitations in, 519 physical examination of, 518–519 potential disease complications of, 521 potential treatment complications of, 521 procedures for, 520–521 rehabilitation for, 520 symptoms of, 518 treatment of, 519–521 Abduction-external rotation test, in thoracic outlet syndrome, 635 Abduction stress test, 367, 367f Abductor pollicis brevis, strength testing of, 213 Abductor pollicis longus, 143t Abobotulinumtoxin A, 892, 893t Abortive therapy for cluster headache, 563 for migraine, 563 Above-elbow amputations. See Upper limb amputations Above-knee amputation-transfemoral amputation. See Lower limb amputations Acetabular fossa, 291 Acetabular labrum, 315 Acetabulum, 291 Acetaminophen for cervical spinal stenosis, 36 for costosternal syndrome, 552 for hand osteoarthritis, 175–176 for hip osteoarthritis, 309 for knee osteoarthritis, 393 for lumbar facet arthropathy, 254 for lumbar spinal stenosis, 279 for meniscal injuries, 407 for myofascial pain syndrome, 575 for spondylolysis and spondylolisthesis, 274–275 for stress fractures, 440–441 for thoracic compression fractures, 229–230 for thoracic sprain or strain, 240–241 Achilles reflex, in hamstring strain, 380 Achilles tendinopathy, 451–455 definition of, 451 diagnostic studies for, 452 differential diagnosis of, 453b

Achilles tendinopathy (Continued) disease complications of, 454 functional limitations in, 452 physical examination of, 452, 452f symptoms of, 451–452 treatment of, 453–454 Achilles tendinosis. See Achilles tendinopathy Achillodynia. See Bursitis, foot and ankle ACL-deficient knee. See Anterior cruciate ligament (ACL); sprain of Acquired brain injury. See Traumatic brain injury Acromioclavicular injuries, 46–52 definition of, 46 diagnostic studies for, 48–49, 49f differential diagnosis of, 49b functional limitations in, 48 grades of, 47t physical examination of, 47–49 potential disease complications of, 51 potential treatment complications of, 51 symptoms of, 46–47 treatment of, 47t, 49–51 Acromioclavicular (AC) joint, 46 normal anatomy of, 47f osteoarthritis of, 107 tests for, 92t–93t Acromioclavicular resisted extension test, 47–48 Acromioclavicular separation. See Acromioclavicular injuries Active compression test, 70–71 for acromioclavicular injuries, 47, 48f Active mobilization techniques, in hip adhesive capsulitis, 295 Active straight-leg raise, in sacroiliac joint dysfunction, 287 Activities of daily living after hip replacement, 341 in joint contractures, 706t Activity modification, for spondylolysis and spondylolisthesis, 274 Acupuncture for chronic fatigue syndrome, 702 for fibromyalgia, 558 for low back strain or sprain, 267 for osteoarthritis, 796 for thoracic sprain or strain, 241 for trapezius strain, 44 Acute compartment syndrome, 371 diagnostic studies for, 373 functional limitations in, 372–373 initial treatment of, 374–375 physical examination of, 372 potential disease complications of, 376 potential treatment complications of, 376 rehabilitation for, 375 surgery for, 376 Acute low back pain. See Low back strain or sprain

Acute therapy, for tension-type headache, 563 Acyclovir, in postherpetic neuralgia, 601 Adaptive equipment, for knee osteoarthritis, 394 Adduction stress test, for lateral collateral ligament injury, 367, 367f Adductor strain, of hip, 297–302 complications of, 301 definition of, 297–298, 298f, 298t diagnostic studies for, 299, 299f differential diagnosis of, 299b functional limitations in, 298–299 physical examination of, 298 symptoms of, 298 treatment of, 300–301 Adenomyosis, pelvic pain and, 588 Adhesive capsulitis, 53–58, 54f–56f, 55b diseases and conditions associated with secondary, 54t of hip, 291–296, 292t, 293f, 294b–295b post-mastectomy pain syndrome and, 606 rotator cuff tendinopathy and, 89 stages of, 53, 54t Adhesive disease, pelvic pain and, 587 Adjunct medications, for chronic pain syndrome, 535t Adjunctive diagnostic testing, of chronic ankle instability, 472 Adson’s test, for cervical radiculopathy, 25, 24f Adult scoliosis, 247t Adult spinal deformity (ASD), 882 Adult spinal muscular atrophy, 740 Aerobic exercise, for chronic pain syndrome, 536 Aging with cerebral palsy, 695 in lumbar degenerative disease, 244 Agitation, medications used for, 963, 965t Airway secretions, elimination of, in pulmonary rehabilitation (PR), 862–863 Alar scapula. See Scapular winging Alarm clock headache. See Cluster headache Albert disease. See Bursitis, foot and ankle Albuminocytologic dissociation, 813 Alendronate, for osteoporosis, 803 Alkaline phosphatase, in heterotopic ossification, 731–732 Allen test, 171, 171f Allis sign, in cerebral palsy, 692–693, 693t Alopecia, in systemic lupus erythematosus, 946 Alprazolam, for trapezius strain, 44 Alveolar ventilation, maintaining, in neuromuscular disorders, 870 Amantadine, for Parkinson disease, 808, 808t, 810 Ambulation after hip replacement, 341 in ankle sprain, 460 in lower limb amputations, 658–659

Note: Page numbers followed by “f ” indicate figures and “t” indicate tables “b” indicate boxes. 967

968

Index

Ambulation (Continued) in lumbosacral spinal cord injury, 927 in mallet toe, 490 in stress fractures, 440–441 Ambulatory aids, in treatment, of stroke, 935 American College of Rheumatology, preliminary diagnostic criteria for fibromyalgia, 555, 556t American Heart Association, cardiac diet recommendations, 680, 680t American Shoulder and Elbow Surgeons subjective shoulder scale, biceps tendon rupture and, 65 American Spinal Injury Association Impairment Scale, for cervical spinal cord injury, 902, 903t Amitriptyline in central post-stroke pain, 630 in intercostal neuralgia, 569 in occipital neuralgia, 585t Amniocentesis, for neural tube defects, 773 Amputations in burns, 675 levels and epidemiology, 658 lower limb, 658–663, 661f, 661t–662t surgery, 658–659 upper limb, 649–657 Amyotrophic lateral sclerosis, 740. See also Motor neuron disease. pharmacologic management of, 745t pulmonary function testing in, 741t Amyotrophy diabetic, 824 neuralgic, 819 Anal manometry testing, in coccydynia, 540 Anal sphincter, voluntary contraction of, 778 Analgesia, for post-thoracotomy pain syndrome, 609 Analgesics for Achilles tendinopathy, 453 for ankle arthritis, 457 for biceps tendinopathy, 62 for biceps tendon rupture, 66–67 for bunion, 468 for chronic pain syndrome, 535t for flexor tendon injuries, 168 for glenohumeral instability, 72, 74–75 for hand and wrist ganglia, 173 for Kienböck disease, 189 for lateral epicondylitis, 126 for meniscal injuries, 407 non-narcotic, hand osteoarthritis and, 176 for olecranon bursitis, 140 oral for lumbar spinal stenosis, 279 for thoracic compression fractures, 229–230 for thoracic radiculopathy, 236 for shin splints, 436 topical, for thoracic sprain or strain, 240–241 for trapezius strain, 44 Anarthria, 895–896 Anemia cancer-related fatigue and, 686 hip replacement and, 344 pressure ulcer and, 853 Anencephaly. See Neural tube defects Anesthesia, manipulation under, hip adhesive capsulitis and, 295 Anesthetic agents, for spondylolysis or spondylolisthesis, 274

Anesthetic injection, 348 for acromioclavicular injuries, 50 for cervicogenic vertigo, 40 for costosternal syndrome, 554 for lateral femoral cutaneous neuropathy, 323, 323f for sacroiliac joint dysfunction, 287–288 Anesthetic-steroid injection, for tibial neuropathy, 512 Anesthetics, topical, for thoracic sprain or strain, 240–241 Angiography, in heterotopic ossification, 731–732 Angle of trunk rotation (ATR), 884 Ankle. See also Foot (feet) anatomy of, 476f arthritis of, 456–459, 457f–458f, 457b bursitis of, 475–481, 476f, 476t–477t chronic instability of. See Chronic ankle instability iliotibial band syndrome in, 386 sprain of, 460–465, 461f–463f, 463b Ankle-brachial index, 719 Ankle-foot orthosis (AFO) in ankle arthritis, 457 in peroneal (fibular) neuropathy, 420, 422 Ankle pain, 471 Ankle plantar flexors, stretching of, 479f Ankle reflex, loss of, lumbar degenerative disease and, 246 Ankylosing spondylitis, 664–669 complications of, 668 definition of, 664 diagnostic studies for, 666–667, 666f differential diagnosis of, 667b functional limitations in, 666 physical examination of, 665, 665f–666f symptoms of, 664 treatment of, 667–668 Ankylosis. See Joint contractures of hip joint. See Adhesive capsulitis, of hip of sacroiliac joint. See Sacroiliac joint, dysfunction of Anomic aphasia, 896t Anorectal dyssynergia, 788 Antebrachial cutaneous neuropathy, biceps tendon rupture and, 67 Anterior apprehension test, 60 Anterior compartment, of leg, 372, 372f Anterior compartment thickness (ACT), in chronic exertional compartment syndrome, 374 Anterior cruciate ligament (ACL), 350, 424 reconstruction of, 353, 353f sprain of, 350–357, 351f–352f, 351b, 353t–354t Anterior cruciate ligament (ACL) tear. See Anterior cruciate ligament (ACL), sprain of Anterior discectomy, in thoracic radiculopathy, 236 Anterior disease, in cervical spondylotic myelopathy, 6 Anterior drawer test, 367 for ankle sprain, 461–462, 461f for anterior cruciate ligament tear, 351, 352f Anterior hip impingement test, for hip labral tears, 315–316, 316f Anterior interosseous nerve block, 135f Anterior interosseous syndrome, 131, 132f. See also Median neuropathy diagnostic studies for, 133 differential diagnosis of, 134b functional limitations in, 133 initial treatment of, 134

Anterior interosseous syndrome (Continued) physical examination of, 132–133, 133f potential disease complications of, 135 rehabilitation for, 134, 134f symptoms of, 132 Anterior knee pain. See Patellofemoral syndrome Anterior metatarsalgia. See Metatarsalgia Anterior or medial tibial pain syndrome. See Compartment syndrome, of leg Anterior-posterior load and shift, 60 Anterior talofibular ligament (ATFL), 460, 461f Anterocollis, 18 Anti-cyclic citrullinated protein antibodies (ACPAs), 878 Anti-inflammatory medications for complex regional pain syndrome, 545 for lumbar degenerative disease, 249 for transverse myelitis, 956 Anticholinergics for multiple sclerosis, 760–761 for neurogenic bladder, 780t, 782–783 for Parkinson disease, 753, 808, 808t for post-stroke symptoms, 933t Anticoagulant therapy, for deep venous thrombosis, 716 Anticonvulsants for arachnoiditis, 525 for complex regional pain syndrome, 545 for fibromyalgia, 557 for intercostal neuralgia, 569 for lumbar radiculopathy, 259 for occipital neuralgia, 583 for peroneal (fibular) neuropathy, 421 for phantom limb pain, 597 for post-stroke symptoms, 933t for repetitive strain injuries, 622 for thoracic radiculopathy, 236 for trapezius strain, 44 Antidepressants for arachnoiditis, 525, 525t for chronic fatigue syndrome, 701 for chronic pain syndrome, 535t for complex regional pain syndrome, 545 for fibromyalgia, 557 for intercostal neuralgia, 569 for lumbar spinal stenosis, 279 for motor neuron disease, 744 for occipital neuralgia, 583–585, 585t for peripheral neuropathies, 814 for phantom limb pain, 597 for post-mastectomy pain syndrome, 606 for radiation fibrosis syndrome, 615–616 for repetitive strain injuries, 621–622 for trapezius strain, 44 tricyclic. See Tricyclic antidepressants Antihistamines, for burns, 673 Antimalarials in rheumatoid arthritis, 880t–881t in systemic lupus erythematosus, 950t Antiplatelet therapy, in peripheral arterial disease, 721 Antispasticity, for post-stroke symptoms, 933t Anxiety, motor neuron disease and, 744 Anxiolytics, for chronic pain syndrome, 535t, 537 Aortic aneurysm, abdominal, 247t Apex localization, 885 Aphasia, 895, 896t differential diagnosis of, 898b physical examination of, 897 rehabilitation for, 899 Apixaban, for deep venous thrombosis, 714–715

Index

Apley compression test, in meniscal injuries, 405–406, 406f Apprehension test, 70, 71f Apraxia of speech, 895, 896t differential diagnosis of, 898b physical examination of, 897 rehabilitation for, 899–900 Arachnoiditis, 523–528, 524t definition of, 523 diagnostic studies for, 524 differential diagnosis of, 524b functional limitations in, 523–524 physical examination of, 523 potential disease complications of, 527 potential treatment complications of, 527 procedures for, 525–526 rehabilitation for, 525 symptoms of, 523 treatment of, 525–527 Arachnoiditis ossificans, 527 Arcuate sign, 368, 369f Areflexic bowel, 787 ArmeoPower system, 934f Arnold-Chiari type II malformation, neural tube defects and, 773f, 774–775 Arnold neuralgia. See Occipital neuralgia Arousal, medications used for, 963, 965t Arterial insufficiency. See Foot, diabetic; Peripheral arterial disease Arthritic frozen shoulder. See Shoulder, arthritis of Arthritis. See also Osteoarthritis. basic principles of management of, 176t elbow, 116–123 diagnostic testing for, 118, 118t, 119f functional limitations in, 118 physical examination of, 117–118 symptoms of, 117 treatment of, 118–122 septic, acute, 106 shoulder. See Shoulder; arthritis of Arthritis mutilans, 183, 183f Arthrocentesis for anterior cruciate ligament sprain, 352 for meniscal injuries, 407 for posterior cruciate ligament sprain, 428 Arthrodesis in costosternal syndrome, 554 in hammer toe, 488 in hand osteoarthritis, 177 knee, 396–397 lumbar, for lumbar degenerative disease, 250 in mallet toe, 491–492 in wrist osteoarthritis, 215, 217f in wrist rheumatoid arthritis, 225, 225f Arthrofibrosis. See also Joint contractures in knee chondral injuries and, 365 Arthrography in adhesive capsulitis, 54–55, 55f in Baker cyst, 359 in chronic ankle instability, 472f in glenohumeral instability, 72 in lateral epicondylitis, 124–125 in medial epicondylitis, 128–129 Arthropathy, lumbar facet, 252–256, 253f Arthroplasty in ankle arthritis, 458 in ankylosing spondylitis, 668 in cervical degenerative disease, 15 disc in cervical radiculopathy, 27 in lumbar degenerative disease, 250 in hand osteoarthritis, 177 hip joint, 338 in hip osteoarthritis, 312

Arthroplasty (Continued) in Kienböck disease, 189 in mallet toe, 491–492 in osteoarthritis, 797 in shoulder arthritis, 109 total elbow, 122 total hip, 337–338 approaches to, precautions associated with, 340t components of, 342–343, 343f goals of rehabilitation after, 340, 341t total knee, 443–450, 446t, 447f–448f total wrist, in wrist osteoarthritis, 216 in wrist rheumatoid arthritis, 225 Arthroscopic débridement, for knee osteoarthritis, 396, 396t Arthroscopy in ankle arthritis, 458 in biceps tendinopathy, 61 in glenohumeral instability, 72 in knee osteoarthritis, 397 in rotator cuff tear, 96 in shoulder arthritis, 109, 110f in superior labral anterior-posterior (SLAP) tears, 80, 80f in wrist osteoarthritis, 213–214 Arthrotomy, medial parapatellar, in total knee arthroplasty, 447 Articular cartilage disorder. See Knee, chondral injuries Ashworth scale, 759 in cerebral palsy, 693 Aspiration in Baker cyst, 360 bursal, 401 of ganglion cyst, 171–172 knee joint, in anterior cruciate ligament sprain, 355 in quadriceps contusion, 334 Assistive devices for cerebral palsy, 695 for cervical spinal stenosis, 36 for cervical spondylotic myelopathy, 6 for hamstring strain, 381–382 for multiple sclerosis, 761–762 for myopathy, 768 for osteoarthritis, 796 for peripheral neuropathies, 814 Ataxia, 751 dysarthria, 897t multiple sclerosis and, 762 Athetosis, 751 Athletic hernia. See Pubalgia Athletic pubalgia. See Pubalgia Atlanto-occipital instability or subluxation, in rheumatoid arthritis, 876–877 Atraumatic osteolysis of the distal clavicle. See Acromioclavicular injuries Attention, medications used for, 963, 965t Atypical chest pain. See Costosternal syndrome Autologous chondrocyte implantation (ACI), 364–365 Autolytic débridement, for pressure ulcers, 857 Autonomic cephalgia. See Cluster headache Autonomic dysreflexia, 906t in neurogenic bladder, 784 in thoracic spinal cord injury, treatment of, 920–921 Autonomic testing, in peripheral neuropathies, 813 Avascular necrosis of femoral head classification, 950t of lunate. See Kienböck disease

969

Avoidance behavior, in chronic fatigue syndrome, 698–699 Avulsion, of hamstring tendon, 379, 383 Avulsion fractures, posterior cruciate ligament, 428 Awaji-shima revised El Escorial criteria, 742, 742t Azathioprine, for systemic lupus erythematosus, 950t

B

Babinski response, in cervical radiculopathy, 25 Babinski sign in cervical spinal stenosis, 34 in cervical spondylotic myelopathy, 4 Back orthoses, for osteoporosis, 804 Back pain, 525. See also Low back strain or sprain axial, 265 in lumbar degenerative disease, 244 myofascial, 265 occult lesions, 265 radicular, 265 referred, 265 in scapular winging, 101 in spondylolysis or spondylolisthesis, 270, 274 Baclofen for multiple sclerosis, 760, 762 for neurogenic bladder, 780t for spasticity, 891, 892t for trigeminal neuralgia, 647 Baker cyst, 358–361, 359f, 359b Balance testing, in chronic ankle instability, 471 Bald spots, in systemic lupus erythematosus, 946 Ball of foot pain. See Metatarsalgia Ballismus, 751 Bamboo spine appearance, 666–667, 666f Bankart lesion, 76 diagnostic studies for, 80, 80f functional limitations in, 79 initial treatment of, 80–81 physical examination of, 78–79, 79t potential disease complications of, 82 rehabilitation for, 81 surgery for, 82 suture anchor repair of, 82f symptoms of, 78 Baricitinib, in rheumatoid arthritis, 880t–881t Barlow maneuver, in cerebral palsy, 693t Barometric changes, in knee osteoarthritis, 392 Bates-Jensen Wound Assessment Tool, for pressure ulcers, 852 Baxter nerve, 510 Bear hug test, 92f, 92t–93t Bed rest joint contractures and, 706f for lumbar radiculopathy, 259 for thoracic sprain or strain, 240–241 Bedsores. See Pressure ulcers Behavior limitations, in traumatic brain injury, 961 Belimumab, for systemic lupus erythematosus, 949, 950t Belly-off sign, 92t–93t Belly-press test, 92f, 92t–93t Below-elbow amputations. See Upper limb amputations

970

Index

Below-knee amputation-transtibial amputation. See Lower limb amputations Benign headaches. See Headaches Benign thoracic pain. See Thoracic sprain or strain Bent-knee prosthesis, 707f Benzodiazepines for amyotrophic lateral sclerosis, 744 for central post-stroke pain, 630 for multiple sclerosis, 760 for neurogenic bladder, 780t for spasticity, 891, 892t Bernhardt-Roth syndrome. See Lateral femoral cutaneous neuropathy Beta blockers, for upper limb amputations, 654 Betamethasone sodium phosphate, 199 Bethanechol, for areflexic bladder, 780t Biceps, tests for, 92t–93t, 94f Biceps brachii rupture. See Biceps tendon rupture Biceps femoris, 378, 379f Biceps loading test, 70–71 Biceps rupture. See Biceps tendon rupture Biceps tendinopathy, 59–63 definition of, 59 diagnostic studies for, 60–61, 61f differential diagnosis of, 61b functional limitations in, 60 physical examination of, 59–60, 60f potential disease complications of, 62 potential treatment complications of, 62 symptoms of, 59 treatment of, 61–62 Biceps tendinosis. See Biceps tendinopathy Biceps tendon rupture, 64–68 definition of, 64 diagnostic studies for, 66 differential diagnosis of, 66b functional limitations in, 65–66 physical examination of, 64–65, 65f potential disease complications of, 67 potential treatment complications of, 67 proximal, 64, 65f symptoms of, 64 treatment of, 66–67 Biceps tenodesis, in biceps tendinopathy, 62 Bicipital groove, palpation of, 59–60, 60f Bicipital strain. See Biceps tendon rupture Bicipital tendinitis. See Biceps tendinopathy Bicipital tenosynovitis. See Biceps tendinopathy Bicycle ergometer protocols, in cardiac rehabilitation, 679 Bier block, for complex regional pain syndrome, 547 Bilevel positive airway pressure, for motor neuron disease, 747 Biofeedback for dysphagia, 727 for phantom limb pain, 597 therapy, for burns, 673 Biofilms, in pressure ulcers, 850 Biomarkers, in traumatic brain injury, 962 Biomechanics, altered, causes of, 415t Biopsy in myopathy, 767 in peripheral neuropathies, 813 in pressure ulcer, 853 Bipolar hemiarthroplasty. See Total hip replacement Bisacodyl for bowel management, 919t for neurogenic bowel, 789

Bisphosphonate-related stress fractures, 441 Bisphosphonates for complex regional pain syndrome, 545–546 for heterotopic ossification, 732 for osteoporosis, 803 for stress fracture, 439 Bladder areflexic, 778 control of, 777 incontinence, in pressure ulcer, 850 management in lumbosacral spinal cord injury, 928 in thoracic spinal cord injury, 918 neurogenic, 777–785 differential diagnosis of, 782b functional limitations in, 779 pharmacologic action on, 780t physical examination of, 778 symptoms of, 777–778 treatment of, 782–784 Bladder dysfunction after stroke, in young adults, 939 initial treatment of, 943 physical examination of, 940 rehabilitation and, 943 surgery for, 943 cervical spinal cord injury and, 913 lumbosacral spinal cord injury and, 927, 929 multiple sclerosis and, 760–761 Parkinson disease and, 778 Blast injury. See Polytrauma, rehabilitation for Blood clot. See Deep venous thrombosis Blood flow pressure ulcer formation and, 850 in repetitive strain injuries, 618–619 Blood pressure, in foot, 721 Body-powered prostheses, 655 Body weight-supported treadmill training, for cervical spinal cord injury, 912 Bone mineral density in postpoliomyelitis syndrome, 839 reporting, 800t Bone-patellar tendon-bone (BTB) graft, for anterior cruciate ligament sprain, 354–355 Bone scan in ankle arthritis, 457 in cancer-related fatigue, 685 in cervical radiculopathy, 26 in coccydynia, 540 in hip adhesive capsulitis, 293 in quadriceps contusion, 334 in Tietze syndrome, 643 Bone scintigraphy in spondylolysis and spondylolisthesis, 271 in Tietze syndrome, 643 “Bone spurs”, 482 Borg scale of perceived exertion, 681, 682f Botulinum toxin in cervical dystonia, 19 injection in cerebral palsy, 694–695 in cervicogenic vertigo, 40 in coccydynia, 541 in motor neuron disease, 754 in myofascial pain syndrome, 577 in piriformis syndrome, 327 in radiation fibrosis syndrome, 616 in multiple sclerosis, 762 in neurogenic bladder, 780t, 783 in neurogenic bowel, 789–790 in spasticity, 893t

Botulinum toxin A in patellofemoral syndrome, 416 in thoracic sprain or strain, 241 in upper limb amputations, 654 Bouchard node, 174 “Bounce home” test, in meniscal injuries, 405–406 Boutonnière deformity, 161t–162t, 162. See also Extensor tendon injuries in rheumatoid arthritis, 179, 877f surgery for, 183 Bowel areflexic, 787 dysfunction cervical spinal cord injury and, 913 lumbosacral spinal cord injury and, 927, 929 multiple sclerosis and, 761 function of, impaired, neurogenic bladder and, 782 incontinence, in pressure ulcer, 850 innervations of, 786–787 management in lumbosacral spinal cord injury, 928 in neural tube defects, 774 in thoracic spinal cord injury, 918–919, 919t neurogenic, 786–791 definition of, 786–787 diagnostic studies for, 788 disease complications in, 790 functional limitations in, 788 physical examination of, 788 symptoms of, 788 treatment complications in, 790–791 treatment of, 788–790 slow-transit, 790 Brace for ankle sprain, 464 for chronic ankle instability, 473 for quadriceps contusion, 334 for scapular winging, 104 for scoliosis, 887 for shin splints, 436 for thoracic compression fractures, 231f for transverse myelitis, 958 Brace protection, for meniscal injuries, 408 Brachial amyotrophy. See Brachial plexopathy Brachial plexitis. See Brachial plexopathy Brachial plexopathy, 816–821, 818b Brachial plexus, 633, 634f, 816, 817f Brachioradialis reflex testing, for cervical radiculopathy, 24f Bracing for knee osteoarthritis, 394 for spondylolysis and spondylolisthesis, 274 Braden Scale, 851 Bragard sign, in low back strain or sprain, 266t Brain attack. See Stroke Brain-computer interface for cervical spinal cord injury, 912 for upper limb amputations, 655 Brainstem dysfunction, in neural tube defects, 770 Break-dancer’s thumb. See Ulnar collateral ligament sprain Breast cancer, lymphedema in, 738 Breathing, retraining of, in pulmonary rehabilitation (PR), 862 Brittle bones. See Osteoporosis Broca aphasia, 896t Bromocriptine, for Parkinson disease, 808, 808t Bruce protocol, in cardiac rehabilitation, 679

Index

Brunelli test, 150f Bucket-handle tear, 404–405, 405f Bulbocavernosus reflex, 788 Bunion, 466–470 definition of, 466, 467f diagnostic studies for, 467, 467f–468f differential diagnosis of, 467b disease complications of, 468 functional limitations in, 467 physical examination of, 467 symptoms of, 466 treatment of, 468 Bunionectomy, 495 Bunionette, 466–470 definition of, 468–469 diagnostic studies for, 469, 469f disease complications of, 469 functional limitations in, 469 physical examination of, 469 symptoms of, 469 treatment of, 469 Bupropion, for cardiac rehabilitation, 679–680 Burns, 670–677 complications of, 675–676 definition of, 670, 671t diagnostic studies for, 672 differential diagnosis of, 672b electrical, upper limb amputations and, 653 functional limitations in, 672 physical examination of, 671, 671f, 672t symptoms of, 670–671 treatment of, 672–675 Bursa, 399 Bursectomy, 348–349 Bursitis, 467 foot and ankle, 475–481, 476f, 476t–479t, 478b olecranon, 137–140, 138f, 139b septic, 480 trochanteric, 247t, 346 Bursopathy, knee, 399–402 definition of, 399 diagnostic studies for, 400 differential diagnosis of, 401b disease complications of, 401 functional limitations in, 400 physical examination of, 400 symptoms of, 400, 400f treatment of, 401 Buttonhole deformity. See Extensor tendon injuries

C

C-reactive protein, in heterotopic ossification, 732 C2 neuralgia. See Occipital neuralgia C7 radiculopathy, 22 Calcaneofibular ligament, 460, 461f Calcaneus altus. See Bursitis; foot and ankle Calcification, in trochanteric bursitis, 347 Calcitonin for osteoporosis, 803 for thoracic compression fractures, 229–230 for Tietze syndrome, 644 Calcium in osteoporosis, 801 in stress fractures, 439 Calf, edema of, 712 Calf hypertension. See Compartment syndrome, of leg Canal measurements, in lumbar spinal stenosis, 277–278

Canalith repositioning maneuvers, for postconcussion symptoms, 846 Cancer breast, 738 lumbosacral plexopathy with, 825–826 lymphedema with, 735 Cancer-related fatigue, 684–688 complications of, 687–688 definition of, 684 diagnostic studies for, 685–686 differential diagnosis of, 686b functional limitations in, 685 physical examination of, 685 symptoms of, 684–685 treatment of, 686–687 Cannabis, smoked, 535–536 Capsaicin for intercostal neuralgia, 569 for knee osteoarthritis, 393 for post-mastectomy pain syndrome, 606 for postherpetic neuralgia, 601–602 Capsulitis. See also Joint contractures adhesive, 53–58 Caput ulnae syndrome, 219–220 Carbamazepine for femoral neuropathy, 305 for lateral femoral cutaneous neuropathy, 323 for occipital neuralgia, 585t for phantom limb pain, 597 for trigeminal neuralgia, 647 Cardiac rehabilitation, 678–683 complications of, 682–683 definition of, 678 diagnostic studies for, 679 functional limitations in, 679 physical examination of, 678–679 symptoms of, 678 treatment of, 679–682 Cardiac tamponade, in Tietze syndrome, 645 Cardiovascular disease, rehabilitation in, 678, 680t Cardiovascular system, in cervical spinal cord injury disease complications in, 913 ongoing management and health maintenance in, 909–910 physical examination of, 906, 906t Carisoprodol, for cervicogenic vertigo, 40 Carnett test, 589 for abdominal wall pain, 518 Carnitine, for myopathy, 767 Carpal cyst. See Ganglion cyst Carpal instability, in wrist osteoarthritis, 212 Carpal tunnel release, 195 Carpal tunnel syndrome, 13, 191–196, 192f–194f, 193b in wrist rheumatoid arthritis, 221 Cartilage tears. See Meniscal injuries Cast above-knee, in lower limb amputation, 661t in joint contractures, 706–708, 707f in posterior tibial tendon dysfunction, 508 in ulnar collateral ligament sprain, 202–203 Catechol O-methyltransferase, in Parkinson disease, 808 Catheter-directed thrombolysis, for deep venous thrombosis, 717 Catheterization femoral artery, 824 in neurogenic bladder, 782 suprapubic, 783

971

Cauda equina injuries, in lumbosacral spinal cord injury, 926 Cauda equina lesions, neurogenic bowel and, 787 Caudal regression syndrome. See Neural tube defects Causalgia. See Complex regional pain syndrome (CRPS) Celecoxib in occipital neuralgia, 585t in thoracic compression fractures, 229–230 Cell-based therapy, in peripheral arterial disease, 722 Central pain. See Central post-stroke pain Central post-stroke pain, 629–632 definition of, 629 diagnostic studies for, 630 differential diagnosis of, 630b functional limitations in, 630 physical examination of, 629–630 potential disease complications of, 631 potential treatment complications of, 631 symptoms of, 629 treatment of, 630–631 Central slip injury. See Extensor tendon injuries Centre for Sleep and Chronobiology Sleep Assessment Questionnaire, 700 Cerebellar tremor, 751–752 Cerebral infarction. See Stroke, in young adults Cerebral palsy (CP), 689–696 complications of, 695 definition of, 689–690 diagnostic studies for, 693–694 functional limitations in, 693 physical examination of, 692–693, 692t–693t symptoms of, 690–692 treatment of, 694–695 Cerebral venous thrombosis. See Stroke, in young adults Cerebrovascular accident. See Stroke Cervical collar for cervical radiculopathy, 26 for cervical spinal stenosis, 35–36 for spondylotic myelopathy, 6 Cervical disc disease, with radiculopathy. See Radiculopathy, cervical Cervical dystonia, 17–21, 752 definition of, 17 diagnostic studies for, 18 differential diagnosis of, 20b functional limitations in, 18 physical examination of, 18 potential disease complications of, 20 potential treatment complications of, 20 radiation induced, 613–614 symptoms of, 17–18 treatment of, 18–20 Cervical migraine. See Occipital neuralgia Cervical musculature, fibromyalgia of, 620f Cervical myalgia. See Cervical spine, sprain/ strain of Cervical myelopathy, 33. See also Cervical spine; stenosis of Cervical neuritis. See Radiculopathy, cervical Cervical pain. See Cervical spondylotic myelopathy Cervical radiculitis. See Cervical spondylotic myelopathy; Radiculopathy, cervical Cervical rib syndrome. See Thoracic outlet syndrome Cervical rotation-lateral flexion test, 635, 636f

972

Index

Cervical spinal cord injury, 902–915 American Spinal Injury Association Impairment Scale for, 902, 903t definition of, 902 diagnostic studies for, 907 differential diagnosis of, 907b disease complications in, 913–914 electrodiagnostic testing in, 907 equipments needed in, 909t functional limitations in, 907, 907t–908t International Spinal Cord Injury Pain Classification, 902, 904t musculoskeletal imaging in, 907 ongoing management and health maintenance, 909–912 physical examination of, 904–907, 904t–905t abdomen, 906 cardiac, 906, 906t extremities, 907 neurologic, 904–905, 905f–906f respiratory, 905 skin, 907 spine, 906 potential treatment complications of, 914, 914t pulmonary function in, 907 spinal imaging in, 907 symptoms of, 902, 903t–904t treatment of, 907–913 urologic studies in, 907 Cervical spinal nerves, 22 Cervical spine aging-related changes in, 3, 12 anatomy, 22 canal diameter in, 3, 5f degenerative disease of, 12–16 definition of, 12 diagnostic studies for, 14 differential diagnosis of, 14b functional limitations in, 14 physical examination of, 13–14, 13t potential disease complications of, 15 potential treatment complications of, 16 symptoms of, 12–13 treatment of, 14–15 examination of, in rotator cuff tear, 91 facet arthropathy of, 8–11, 9f definition of, 8 diagnostic studies for, 9 differential diagnosis of, 9b functional limitations in, 9 physical examination of, 8–9 potential disease complications of, 11 potential treatment complications of, 11 symptoms of, 8 treatment of, 10–11 facet joints of, 8 neurocentral joints of, 12 palpation of in facet arthropathy, 8–9 in radiculopathy, 23 radiculopathy of, 22–28 sprain/strain of, 29–32 definition of, 29 diagnostic studies for, 30, 30f differential diagnosis of, 30b physical examination of, 30, 30f potential disease complications of, 31 potential treatment complications of, 31 symptoms of, 29, 30f treatment of, 30–31 stenosis of, 33–38, 34f definition of, 33 diagnostic studies for, 34–35, 34f differential diagnosis of, 35b

Cervical spine (Continued) functional limitations in, 34 physical examination of, 33–34 potential disease complications of, 37 potential treatment complications of, 37 symptoms of, 33 treatment of, 35–37 traction on, in radiculopathy, 26 Cervical spondylosis with myelopathy. See Cervical spine, degenerative disease of without myelopathy. See Cervical spondylotic myelopathy Cervical spondylotic myelopathy, 1–7. See also Cervical spine, stenosis of definition of, 3 diagnostic studies for, 4–5 differential diagnosis of, 5b functional limitations in, 4 physical examination of, 4 potential disease complications of, 6 potential treatment complications of, 6 symptoms of, 3–4 treatment of, 5–6 Cervical traction for cervical degenerative disease, 15 for cervical spinal stenosis, 36 for degenerative disease, 15 Cervical vertigo. See Cervicogenic vertigo Cervicogenic dizziness, 40. See also Cervicogenic vertigo Cervicogenic vertigo, 39–42 definition of, 39 diagnostic studies for, 40 differential diagnosis of, 40b functional limitations in, 39 physical examination of, 39 potential disease complications of, 41 potential treatment complications of, 41 symptoms of, 39 treatment of, 40 Cervicothoracic ganglion block, in complex regional pain syndrome, 546–547 Cervicothoracic muscle atrophy, 614f Cetirizine, for burns, 673 Change in voice. See Dysphonia Cheiralgia paresthetica. See Radial neuropathy Chemical neurolysis with phenol, for spasticity, 892 Chemodenervation with botulinum toxin, for spasticity, 892 Chemotherapy-induced peripheral neuropathy (CIPN), 529–532, 530t definition of, 529 diagnostic studies for, 530–531 differential diagnoses of, 530b functional limitations in, 530 physical examination of, 530 potential disease complications of, 532 potential treatment complications of, 532 procedures for, 531–532 rehabilitation for, 531 symptoms of, 529 treatment of, 531–532 Chest pain in cardiac rehabilitation, 678 causes of, 568t in intercostal neuralgia, 566 Chest radiography, in systemic lupus erythematosus, 948 Chest-wall mobility, maintaining, in neuromuscular disorders, 869–870 Chickenpox, 600–601 Chlorzoxazone, for lumbar radiculopathy, 259

Choking, in dysphagia, 724 Chondral injuries, knee, 362–365, 363f, 364b, 365f Chondroitin, in osteoarthritis, 795 Chondroitin sulfate, for knee osteoarthritis, 393 Chondromalacia of medial or lateral compartments of the knee. See Knee, chondral injuries Chondromalacia patella. See Knee, chondral injuries; Patellofemoral syndrome (PFS) Chondropathia tuberosa. See Tietze syndrome Chorea, 751 Chronic abdominal wall syndrome. See Abdominal wall pain Chronic ankle instability, 471–474, 472b Chronic exertional compartment syndrome, 371 diagnostic studies for, 374 functional limitations in, 373 initial treatment of, 375 physical examination of, 372 potential disease complications of, 376 potential treatment complications of, 376 rehabilitation for, 375 Chronic fatigue and immune dysfunction syndrome. See Chronic fatigue syndrome Chronic fatigue syndrome, 697–703, 699t, 700f, 701t, 701b Chronic leptomeningitis. See Arachnoiditis Chronic nonvisceral abdominal pain. See Abdominal wall pain Chronic obstructive pulmonary disease (COPD), 860. See also Pulmonary rehabilitation (PR) therapeutic prescription for, 862t Chronic pain, 544 Chronic pain syndrome, 533–537, 534t–535t, 534b. See also Pain Chronic pelvic inflammatory disease, 588 Chronic pelvic pain (CPP), 587 Chronic tenosynovitis. See Posterior tibial tendon dysfunction Chronic wrist pain, hand and wrist ganglia and, 173 Cimetidine, for burns, 673 Claudication, intermittent, 720 Claw toe. See Mallet toe Claw toe syndrome. See Mallet toe Clonazepam, for trigeminal neuralgia, 647 Closed injuries, in femoral neuropathy, 304t Closed kinetic chain exercises for anterior cruciate ligament sprain, 353 for knee osteoarthritis, 394 Cluster headache, 561 treatment of, 563 “Coasting” effect, 529 Cobb angle, 885 Coccyalgia. See Coccydynia Coccydynia, 538–542, 539f definition of, 538 diagnostic studies for, 540, 540f differential diagnosis of, 540b functional limitations in, 540 physical examination of, 539–540 potential disease complications of, 541 potential treatment complications of, 541 procedures for, 541 rehabilitation for, 540–541 symptoms of, 538–539 treatment of, 540–541 Coccygeal subluxation, 539f Coccygectomy, 541 Coccygodynia. See Coccydynia

Index

Cock-up splint in hand and wrist ganglia, 172 in wrist osteoarthritis, 214 Cognition in postconcussion symptoms, 842–843, 846 treatment of, stroke and, 935 Cognitive-behavioral therapy for chronic fatigue syndrome, 702 for myofascial pain syndrome, 576 for postconcussion symptoms, 845 Cognitive behavioral therapy, for abdominal wall pain, 519–520 Cognitive deficits/impairments, in cancerrelated fatigue, 685 Cognitive difficulties, in polytrauma rehabilitation, 830 Cognitive dysfunction, in multiple sclerosis, 758, 761 Cognitive impairments in burns, 676 in chronic fatigue syndrome, 698 Cold intolerance, in postpoliomyelitis syndrome, 836–838 Cold laser therapy. See Low-level laser therapy Collateral ligament sprain, 366–370, 367f, 368b Colon motility of, 786 motor activity of, 788 Common peroneal nerve palsy (CPNP), in total knee arthroplasty, 449 Communication, in treatment, of stroke, 934 Compartment syndrome, 333–334 acute, 371 anterior, 374 in biceps tendon rupture, 67 chronic exertional, 371 differential diagnosis of, 374 of leg, 371–377, 374b physical examination of, 372, 372f posterior, 374 posterior, thigh, 383 shin splints and, 434 Compensatory ulnar deviation, in wrist rheumatoid arthritis, 220–221 Complementary medicine, for chronic fatigue syndrome, 702 Complex regional pain syndrome (CRPS), 543–548 definition of, 543–544 diagnostic studies for, 544–545 differential diagnosis of, 545b functional limitations in, 544 physical examination of, 544 potential disease complications of, 547 potential treatment complications of, 547 procedures for, 546–547 rehabilitation for, 546 symptoms of, 544 treatment of, 545–547 Compression of tibial nerve. See Tibial neuropathy of ulnar nerve. See Ulnar neuropathy, elbow Compression devices, in deep venous thrombosis prophylaxis, 714 Compression fracture, thoracic, 228–233, 229f definition of, 228 diagnostic testing of, 229, 230f differential diagnosis of, 229b functional limitations in, 229 physical examination of, 228–229

Compression fracture, thoracic (Continued) potential disease complications of, 232–233 potential treatment complications of, 233 procedures for, 230–232, 231f–232f symptoms of, 228 treatment of, 229–232 Compression garments, for scars, 673–674 Compression neuropathy of the fibular nerve. See Peroneal (fibular) neuropathy Compression test active, 70–71 for acromioclavicular injuries, 47, 48f in sacroiliac joint dysfunction, 287 Computed tomographic arthrography in glenohumeral instability, 72 in hip adhesive capsulitis, 294, 294f Computed tomographic myelography in cervical degenerative disease, 14 in cervical spinal stenosis, 35 in cervical spondylotic myelopathy, 5 in lumbar spinal stenosis, 280t in thoracic radiculopathy, 235 Computed tomography (CT) in ankylosing spondylitis, 667 in brachial plexopathy, 818 in cerebral palsy, 694 in cervical degenerative disease, 14 in cervical facet arthropathy, 9 in cervical radiculopathy, 25 in chronic ankle instability, 472 in heterotopic ossification, 731, 733 in Kienböck disease, 186 in lumbar degenerative disease, 246 in lumbar radiculopathy, 259, 260f in lumbar spinal stenosis, 280t in lumbosacral plexopathy, 825–826 in occipital neuralgia, 582 in piriformis syndrome, 325–326 in polytrauma, 831 in post-thoracotomy pain syndrome, 609 in postconcussion symptoms, 841 in radiation fibrosis syndrome, 614 in sacroiliac joint dysfunction, 287 in scapular winging, 103 in shoulder arthritis, 108 in spondylosis, 271, 272f in stress fractures, 440 in systemic lupus erythematosus, 948 in thoracic radiculopathy, 235 in Tietze syndrome, 643 in wrist osteoarthritis, 213–214 in wrist rheumatoid arthritis, 222 Computer-driven isokinetic dynamometers, in repetitive strain injuries, 620 Concurrent injuries, lumbosacral spinal cord injury and, 925 Concussions, 841, 961. See also Postconcussion symptoms Conduction aphasia, 896t Congenital myopathies, 765, 766t Constipation in cerebral palsy, 690, 694 in multiple sclerosis, 758, 761 in Parkinson disease, 810 pathophysiology of, 787 Constraint-induced aphasia therapy (CIAT), for speech and language disorders, 900 Continuous noninvasive ventilatory support (CNVS), 870f Continuous passive motion (CPM) devices, in total knee arthroplasty, 445 Contraceptive pill, oral, pelvic pain, 593 Contracted toe. See Mallet toe Contractures in burns, 674–675, 674f

973

Dupuytren, 154–158, 155f hip flexion, 338, 339f of hip joint. See Adhesive capsulitis, of hip joint, 704–709 bed rest and, 706f complications of, 708 definition of, 704–705, 705f–706f, 705t diagnostic studies for, 707 differential diagnosis of, 707b functional limitations in, 706–707 physical examination of, 706, 707f sequelae of, 709b spinal cord injury and, 705 symptoms of, 705, 706t treatment of, 707–708 in lower limb amputations, 659 prevention of, in upper limb amputations, 654–655 Contrast bath, in arachnoiditis, 525 Contrast venography, in deep venous thrombosis, 712–713, 713f Controlled-release oxycodone CR, for thoracic compression fractures, 229–230 Contusion, quadriceps, 333–336 Conus medullaris, in lumbosacral spinal cord injury, 926 Cooper contracture. See Dupuytren contracture Coronary artery disease, in rheumatoid arthritis, 877 Coronary heart disease, rehabilitation in, 678 Corticosteroids administration of, for Tietze syndrome, 644 for complex regional pain syndrome, 545 for hand rheumatoid arthritis, 181 infiltration with, in intercostal neuralgia, 570 injection of for abdominal wall pain, 520 for adhesive capsulitis, 55–57 for ankle arthritis, 457–458 for ankylosing spondylitis, 668 for carpal tunnel syndrome, 193, 194f for chronic ankle instability, 473 for foot and ankle bursitis, 480 for glenohumeral instability, 73–74 for hammer toe, 487–488 for hand osteoarthritis, 176 for hip adductor strain, 300–301 for hip adhesive capsulitis, 295 for hip osteoarthritis, 310, 310f–311f for iliotibial band syndrome, 388–389, 388f for knee osteoarthritis, 394–395 for Morton’s neuroma, 499 for olecranon bursitis, 139 for osteoarthritis, 796 for piriformis syndrome, 326–327, 327f for pubalgia, 331 for quadriceps tendinopathy, 433 for rotator cuff tear, 96 for rotator cuff tendinopathy, 89 for trigger finger, 199, 199f for ulnar neuropathy, 209 for wrist osteoarthritis, 214 for lateral femoral cutaneous neuropathy, 323 for lumbar radiculopathy, 259 complications from, 262 for multiple sclerosis, 762 oral for carpal tunnel syndrome, 194 for femoral neuropathy, 305 for median neuropathy, 194 for trochanteric bursitis, 348

974

Index

Corticotropin-releasing hormone, in fibromyalgia, 573 Cortisone injections, for wrist rheumatoid arthritis, 224 Costal chondritis. See Tietze syndrome Costochondral junction syndrome. See Tietze syndrome Costochondritis, 549, 550t stretching exercises for, 553, 553f Costoclavicular syndrome. See Thoracic outlet syndrome Costoclavicular test, in thoracic outlet syndrome, 635 Costosternal arthrodesis, 554 Costosternal syndrome, 549–554, 640 Cough flows, augmentation of, in neuromuscular disorders, 870–871 Coughing, in dysphagia, 724 Counseling, in pulmonary rehabilitation (PR), 862 Counterforce bracing, in Achilles tendinopathy, 453 Coxarthrosis. See Hip, osteoarthritis of Cranial neuralgia. See Trigeminal neuralgia Craniorachischisis. See Neural tube defects Creatine kinase in heterotopic ossification, 732 myopathies and, 765 Credé maneuver, 910t Credé method, 782 Crest pads, in mallet toe, 491 Cross-body adduction test, for acromioclavicular injuries, 47 Crossed straight-leg raise, in low back strain or sprain, 266t “Crossover sign”, in hip adductor strain, 298 “Crowing rooster”, 551, 551f Cruciate ligament anterior, 350, 424 posterior, 424 avulsion fractures, 428 injuries, classification of, 425t reconstruction of, 429 sprain, 424–430 Cryotherapy in intercostal neuralgia, 570 in knee osteoarthritis, 397 Cubital tunnel, 147f Cubital tunnel syndrome. See Ulnar neuropathy; elbow Cucumber heel. See Bursitis, foot and ankle “Cullen sign”, for abdominal wall pain, 519 Curvature of the spine/back. See Scoliosis Curve rigidity, 884 Curved spine/back. See Scoliosis Cushion, for pressure ulcers, 853 Custom-molded rigid ankle-foot orthosis, in ankle arthritis, 457 Cutaneous nerves, anterior and lateral, 518f Cycling-induced ITBS, 384 Cyclobenzaprine in cervicogenic vertigo, 40 in fibromyalgia, 557 in lumbar facet arthropathy, 254 in lumbar radiculopathy, 259 in myofascial pain syndrome, 575 in thoracic compression fractures, 229–230 Cyclooxygenase 2 inhibitors in acromioclavicular injuries, 51 in occipital neuralgia, 585t Cyclophosphamide in rheumatoid arthritis, 880t–881t in systemic lupus erythematosus, 950t in transverse myelitis, 956

Cystoscopy in neural tube defects, 773 in neurogenic bladder, 781 Cysts Baker, 358–361, 359f, 359b ganglion of hand and wrist, 169 hand osteoarthritis and, 174 mucous, 169, 170f, 171 occult, 169 paralabral, suprascapular neuropathy and, 114 popliteal, 358 retinacular, 169, 170f, 171 synovial, 169

D

D-dimer assay, in deep venous thrombosis, 713 Dabigatran, for deep venous thrombosis, 714–715 Dantrolene for multiple sclerosis, 762 for neurogenic bladder, 780t for spasticity, 891, 892t Darifenacin, 780t Darrach procedure, 224–225, 225f DaTSCAN, in Parkinson disease, 807 Daytime drowsiness, in cervical spinal cord injury, 903t–904t de Quervain tenosynovitis, 149–153 diagnostic studies for, 150–151, 151f differential diagnosis of, 151b functional limitations in, 150 physical examination of, 150f potential disease complications of, 152 potential treatment complications of, 152 symptoms of, 150 treatment of, 151–152, 152f Débridement in ankle arthritis, 458 in hip labral tears, 319 in pressure ulcers, 857 in shoulder arthritis, 109 Decannulation, of unweanable patients, neuromuscular disorders and, 873 Decompressive surgery, for cervical spondylotic myelopathy, 6 Decubitus ulcers, 849 Deep brain stimulation (DBS) for cervical dystonia, 20 for motor neuron disease, 755 Deep infrapatellar bursopathy, 400 Deep posterior compartment, of leg, 372, 372f Deep tendon reflex testing, for lumbar degenerative disease, 246 Deep venous thrombosis, 710–718 in burns, 673 complications of, 717, 717f definition of, 711, 711t–712t diagnostic studies for, 712–713, 712t, 713f differential diagnosis of, 714b distal, 716 functional limitations in, 712 hip replacement and, 344 physical examination of, 712 recurrent, 716 superficial, 716 symptoms of, 711 in thoracic spinal cord injury, treatment of, 920 in total knee arthroplasty, 449 treatment of, 714, 715t

Defecation, 787 Defecography, 788 Defense Advanced Research Projects Agency (DARPA), 655 Deformities, in hand rheumatoid arthritis, 179 Degenerative arthritis. See Osteoarthritis of knee. See Osteoarthritis, knee of wrist. See Osteoarthritis, wrist Degenerative disease lumbar, 244–251 in wrist osteoarthritis, 218 Degenerative hip joint. See Hip, osteoarthritis of Degenerative joint disease, 307. See also Osteoarthritis of the ankle. See Ankle, arthritis of of the first metatarsophalangeal joint. See Hallux rigidus of the knee joint. See Osteoarthritis, knee Deglutition disorder. See Dysphagia Delayed-onset muscle soreness of the posterior thigh. See Hamstring; strain of Delayed radiation myelopathy, in transverse myelitis, 955t Dementia, in Parkinson disease, 807 Denosumab, for osteoporosis, 804 Depression in cardiac rehabilitation, 680 in cerebral palsy, 692 in Parkinson disease, 810 in postconcussion symptoms, 843 reactive, motor neuron disease and, 744 Derangement, internal, knee, unspecified. See Knee, chondral injuries Dermal sinus. See Neural tube defects Desensitization, in post-mastectomy pain syndrome, 606 Detrusor hyperactivity, 762 Detrusor-sphincter dyssynergia, 760–761, 778, 779f, 782f Diabetes, pressure ulcer and, 853 Diabetes mellitus lumbosacral plexopathy in, 824 peripheral arterial disease in, 719 thoracic radiculopathy and, 234 Diabetic amyotrophy, 824. See also Femoral neuropathy Diabetic cervical radiculoplexus neuropathy, 819 Diabetic plexopathy, 825 Diabetic polyradiculopathy, 247t Diagnostic spinal injections, for cervical radiculopathy, 26 Diagnostic testing, in piriformis syndrome, 325–326 Diagnostic ultrasound, in biceps tendon rupture, 66 Dialysis elbow. See Olecranon bursitis Diarrhea in cervical spinal cord injury, 903t–904t in multiple sclerosis, 761 Diastematomyelia. See Neural tube defects Diazepam for spasticity, 892t for trapezius strain, 44 Diclofenac, topical, in osteoarthritis, 795 Diet in cardiac rehabilitation, 680 in dysphagia, 725 Diffuse axonal injury. See Traumatic brain injury Diffuse idiopathic skeletal hyperostosis, 247t Diffuse periarticular osteopenia, in hand rheumatoid arthritis, 180

Index

Diffusion tensor imaging, in traumatic brain injury, 962f Diffusion-weighted sequences, for cervical spinal stenosis, 35 Digital flexor tenosynovitis. See Trigger finger Digital stereophotogrammetry systems, for pressure ulcers, 852 Diplomyelia. See Neural tube defects Direct oral anticoagulants (DOACs), for deep venous thrombosis, 714–715 Disabilities of the Arm, Shoulder, and Hand (DASH) questionnaire, 620 biceps tendon rupture and, 67 Disability Rating Scale, 962 Disabling fracture, rehabilitation for, 804 Disc herniation of, 257, 258f lesions of, thoracic sprain or strain, 238 Disc arthroplasty in cervical radiculopathy, 27 in lumbar degenerative disease, 250 Disc degeneration, in cervical degenerative disease, 12 Discectomy, for cervical radiculopathy, 27 Discography for cervical degenerative disease, 14 for cervical radiculopathy, 25 for lumbar degenerative disease and, 248–249 Disease-modifying antirheumatic drugs (DMARDs), 118 for hand rheumatoid arthritis, 180 for wrist rheumatoid arthritis, 223 Dislocation, shoulder. See Glenohumeral instability Disseminated sclerosis. See Multiple sclerosis Distal metatarsal metaphyseal osteotomy (DMMO), 495 Distraction arthroplasty, in ankle arthritis, 458 Distraction test, in sacroiliac joint dysfunction, 287 Dix-Hallpike test, for cervicogenic vertigo, 39 Dizziness, cervicogenic, 40 DMPK gene, 766 Docusate sodium, for bowel management, 919t Dopamine replacement, in Parkinson disease, 808, 808t Dorsal column stimulation, in arachnoiditis, 525 Dorsal compression fracture. See Compression fracture, thoracic Dorsal dynamic protection splint, in flexor tendon injuries, 167f Dorsal enteric fistula. See Neural tube defects Dorsal rhizotomy in cerebral palsy, 695 in occipital neuralgia, 583–584 Dorsal scapular nerve palsy, 100, 102f Dorsum rotundum. See Kyphosis Double-bundle reconstruction, of posterior cruciate ligament, 429 Double crush syndrome, 13 Dowager’s hump. See Kyphosis Draftsman’s elbow. See Olecranon bursitis Drawer test, 493–494 anterior, 367 for ankle sprain, 461–462, 461f for anterior cruciate ligament tear, 351, 352f posterior, for posterior cruciate ligament sprain, 425–426, 426f

Dressing hip replacement and, 341 for lower limb amputation, 661f, 661t Driving lower limb amputations and, 662 stroke and, 941 Drop arm test, 92t–93t Dropped head syndrome, 612–613 Drug-induced myopathies, 765 Drugs peripheral neuropathies and, 814 prokinetic, in neurogenic bowel, 789 Dry needling for thoracic sprain or strain, 241 for trapezius strain, 44 Dual-energy x-ray absorptiometry, 800 Duloxetine for arachnoiditis, 525, 525t for cervical degenerative disease, 14–15 for chemotherapy-induced peripheral neuropathy, 531 for intercostal neuralgia, 569 for osteoarthritis, 795 for radiation fibrosis syndrome, 615–616 Duodenal ulcer, penetrating or perforated, 247t Dupuytren contracture, 154–158, 155f diagnostic studies for, 156 differential diagnosis of, 156b functional limitations in, 155 physical examination of, 155, 155f potential disease complications of, 157 potential treatment complications of, 157 symptoms of, 155 treatment of, 156–157 Dupuytren disease. See Dupuytren contracture Durkan test, 221 Dynamic extension bracing, for medial epicondylitis, 129 Dynamic posterior shift test, in posterior cruciate ligament sprain, 426 Dynamic winging, 99 Dynasplint Trismus System, in radiation fibrosis syndrome, 616 Dysarthria, 895–896, 896t classification of, 897t differential diagnosis of, 898b in motor neuron disease, 746–747 in multiple sclerosis, 759 physical examination of, 897 rehabilitation for, 899 Dysesthetic pain, 566 Dysfunction, posterior tibial tendon, 506–509 Dyskinesias. See Movement disorders Dyspareunia, 589 Dyspepsia, in hip labral tears, 320 Dysphagia, 724–728 causes of, 725t in cerebral palsy, 690 differential diagnosis of, 725b disease complications of, 727 functional limitations in, 725 in motor neuron disease, 746 for multiple sclerosis, 762 physical examination of, 724 principal treatments of, 726t in stroke, management of, 934 symptoms of, 724, 725t treatment complications of, 727 Dysphasia. See Aphasia Dysphonia, 896, 896t differential diagnosis of, 898b in dysphagia, 724 physical examination of, 897

975

Dysphonia (Continued) in postpoliomyelitis syndrome, 836 rehabilitation for, 900 Dyspnea in cancer-related fatigue, 685 in cardiac rehabilitation, 678–679 Dysreflexia, autonomic, 906t in neurogenic bladder, 784 Dyssynergia, anorectal, 788 Dystonias, 751 Dysvascular disease, upper limb amputations and, 652

E

Ecchymosis, in hamstring strain, 379 Echocardiography, for systemic lupus erythematosus, 948 Ectopic pregnancy, 247t Edema. See also Lymphedema calf, 712 lower limb amputations and, 660–661, 661t in systemic lupus erythematosus, 946 Eden test, in thoracic outlet syndrome, 635 Edoxaban, for deep venous thrombosis, 714–715 Effusions, in rheumatoid arthritis, 878 Eichhoff test, 150f El Escorial criteria, 742, 742t Elastic bandage, for lower limb amputation, 661f Elbow arthritis of, 116–123, 118t, 119f–121f bursitis. See Olecranon bursitis golfer’s, 128 immobilization of, in biceps tendon rupture, 66 ulnar neuropathy at, 146–148, 147f Elbow pain, differential diagnosis of, 118b Electrical activity, in myofascial pain syndrome, 572 Electrical burn, upper limb amputations and, 653 Electrical nerve stimulation, for osteoarthritis, 796 Electrical stimulation in arachnoiditis, 525 in biceps tendinopathy, 61 in biceps tendon rupture, 66 in cervical sprain/strain, 31 in lateral femoral cutaneous neuropathy, 323 in neurogenic bladder, 783 in occipital neuralgia, 584f in Parkinson disease, 809 in pressure ulcers, 857 in shin splints, 436 in stroke, 934 Electroacupuncture, for Tietze syndrome, 644 Electrodiagnostic medicine study (EDX), in hand and wrist ganglia, 171 Electrodiagnostic studies in cervical degenerative disease, 14 in cervical spondylotic myelopathy, 5 in femoral neuropathy, 304–305 in hip osteoarthritis, 309 in postpoliomyelitis syndrome, 836 in rotator cuff tendinopathy, 86 in shin splints, 435–436 in shoulder arthritis, 108 in suprascapular neuropathy, 113 Electrodiagnostic testing in carpal tunnel syndrome, 193 in lumbosacral plexopathy, 825 in peripheral neuropathies, 811 in tibial neuropathy, 512

976

Index

Electrodiagnostics, in lumbar spinal stenosis, 280t Electroencephalography in complex regional pain syndrome, 544 in polytrauma rehabilitation, 831 Electromyography (EMG) in brachial plexopathy, 818 in carpal tunnel syndrome, 193 in cervical dystonia, 19, 19t in cervical radiculopathy, 26 in dysphagia, 725 in femoral neuropathy, 304–305 in lateral femoral cutaneous neuropathy, 322 in lumbar degenerative disease, 249 in lumbar radiculopathy, 259 in lumbosacral plexopathy, 825 in Morton’s neuroma, 498 in myopathy, 767 needle in Achilles tendinopathy, 452 in peroneal (fibular) neuropathy, 421 in peripheral neuropathies, 812–813 in plantar fasciitis, 502–503 in polytrauma, 831 in radiation fibrosis syndrome, 614 in scapular winging, 103 in ulnar neuropathy, 207–209 Elephantiasis, 738 Elevated arm stress test (EAST), 635 Embolectomy, for deep venous thrombosis, 717 Emotional effects, of stroke, in young adults, 938 initial treatment of, 942 physical examination of, 940 rehabilitation and, 942 Emotional incontinence, for amyotrophic lateral sclerosis, 744 Encephalocele. See Neural tube defects End-plate noise, 572 Endocrine myopathies, 765 Endocrine system, in cervical spinal cord injury, disease complications in, 913 Endometriosis, 247t pelvic pain and, 588, 593 Endoscopy, in dysphagia, 727 Entacapone, in Parkinson disease, 808, 808t Enthesitis, 667 Entrapment neuropathy of tibial nerve. See Tibial neuropathy Enzymatic débridement, for pressure ulcers, 857 Epicondylitis, 124 Epidural steroid injection for lumbar degenerative disease, 249–250 for lumbar radiculopathy, 259–261 complications from, 262–263 Epigastric pain, in systemic lupus erythematosus, 946 Episcleritis, in rheumatoid arthritis, 876 Epithelial enterochromaffin cells, 786 Epworth Sleepiness Scale questionnaire, 700 Equinocavovarus deformity, 691, 691f Equinoplanovalgus deformity, 691, 691f Equinus deformity, 691, 691f Erb palsy, 818 Ergonomic accessories, for cervicogenic vertigo, 40 Ergonomics adaptation, in coccydynia, 540 in repetitive strain injuries, 622 Esophagectomy, in dysphagia, 727 Esophagoscopy, in dysphagia, 725 Esophagus, dilation of, 727

Etidronate disodium, in heterotopic ossification, 733 Eugeroics, for post-stroke symptoms, 933t Eutectic mixture of local anesthetics (EMLA), in intercostal neuralgia, 569 Exercise(s) in Achilles tendinopathy, 453 in acromioclavicular injuries, 50 in adhesive capsulitis, 56f, 57 after hip replacement, 341 in ankle sprain, 463–464 in ankylosing spondylitis, 667–668 in arachnoiditis, 525 in biceps tendinopathy, 61 in biceps tendon rupture, 66 in brachial plexopathy, 820 in burns, 674 in cancer-related fatigue, 686 in cardiac rehabilitation, 681t–682t in cervical degenerative disease, 15 in cervical sprain/strain, 31 in chronic ankle instability, 473 in chronic fatigue syndrome, 702 in chronic pain syndrome, 536 in collateral ligament sprain, 368–369 in dysphagia, 725, 727f in femoral neuropathy, 305–306 in fibromyalgia, 557 in foot and ankle bursitis, 478 in hammer toe, 487 in hamstring strain, 382 in hand osteoarthritis, 175–176 in heterotopic ossification, 733 in hip adductor strain, 300 in hip adhesive capsulitis, 295 in hip labral tears, 319 in hip osteoarthritis, 309, 312 in knee chondral injuries, 364 in knee osteoarthritis, 393–394 in low back strain or sprain, 267 in mallet toe, 491 in meniscal injuries, 407–408 in metatarsalgia, 495 in migraine, 563 in motor neuron disease, 744–746 in myofascial pain syndrome, 574 in myopathy, 767 in occipital neuralgia, 583 in osteoporosis, 802 in Parkinson disease, 754 in patellar tendinopathy, 411–412 in patellofemoral syndrome, 415–416 in peripheral arterial disease, 721 in peroneal (fibular) neuropathy, 422 in post-thoracotomy pain syndrome, 610 in posterior cruciate ligament sprain, 428 in posterior tibial tendon dysfunction, 508 in postpoliomyelitis syndrome, 839 in pulmonary rehabilitation (PR), 863–864 in quadriceps contusion, 335 in quadriceps tendinopathy, 433 in rotator cuff tear, 97 in rotator cuff tendinopathy, 87 in scapular winging, 104 in shin splints, 436 in shoulder arthritis, 108 in spondylolysis and spondylolisthesis, 274 in stroke, 933–934, 934f in suprascapular neuropathy, 114 in temporomandibular joint dysfunction, 626 testing, in cardiac rehabilitation, 679, 681 in thoracic outlet syndrome, 638 in thoracic sprain or strain, 241 in tibial neuropathy, 512 in Tietze syndrome, 644

Exercise(s) (Continued) in trigeminal neuralgia, 647 in ulnar collateral ligament sprain, 203 in ulnar neuropathy, 209 in wrist osteoarthritis, 214 Exercise-induced compartment syndrome. See Compartment syndrome, of leg Exercise-induced menstrual abnormalities, 439 Exogenous glucocorticoid injection, in Achilles tendinopathy, 453 Exoskeletons, for cervical spinal cord injury, 912 Extensor carpi radialis brevis, 143t Extensor carpi radialis longus, 143t Extensor carpi ulnaris, 143t Extensor digiti minimi, 143t Extensor digitorum communis, 143t Extensor digitorum longus lengthening, 488 Extensor hood injury. See Extensor tendon injuries Extensor indicis proprius, 143t Extensor pollicis brevis, 143t Extensor pollicis longus, 143t Extensor sheath injury. See Extensor tendon injuries Extensor tendon compartments, 143t Extensor tendon injuries, 159–164, 160f diagnostic studies for, 160 differential diagnosis of, 160b functional limitations in, 160 physical examination of, 159–160 potential disease complications of, 163 potential treatment complications of, 163 symptoms of, 159, 160f treatment of, 160–163, 161t–162t zone I, 161 zone II, 161–162 zone III, 162 zone IV, 162 zone V, 162–163, 163f zone VI, 163 zone VII, 163 zone VIII, 163 Extensor tendon surgery, for hand rheumatoid arthritis, 182 Extensor tenosynovitis, in hand rheumatoid arthritis, 179, 182 External cooling, for spasticity, 891 External rotation recurvatum test, 367, 368f Extracorporeal shockwave therapy (ESWT) for greater trochanteric pain syndrome, 348 for hip adductor strain, 301 in patient with Morton’s neuroma, 499 for plantar fasciitis, 504 Extrapyramidal disease. See Movement disorders Extremities, in cervical spinal cord injury, physical examination of, 907 Extubation, of unweanable patients, neuromuscular disorders and, 873, 873t

F

FABER maneuver, in hip osteoarthritis, 308, 308f FABER test, 286, 286f for hip adductor strain, 298 for hip labral tears, 315–316 in low back strain or sprain, 266t Facet examination, for cervical radiculopathy, 24 Facet joint arthritis. See Cervical spine; facet arthropathy of; Lumbar facet arthropathy

Index

Facet joint pain. See Lumbar facet arthropathy Facet joints, 245, 250 lumbar, arthropathy of, 252–256, 253f Facet-mediated pain. See Cervical spine, facet arthropathy of Facet syndrome. See Lumbar facet arthropathy Facetogenic pain. See Cervical spine; facet arthropathy of Facial neuralgia. See Trigeminal neuralgia Facial pain. See Trigeminal neuralgia FAIR testing, 326t Falls in postpoliomyelitis syndrome, 839 prevention of, in osteoporosis, 802 Famciclovir, in postherpetic neuralgia, 601 Familial lymphedema. See Lymphedema Far-out syndrome, 277–278 Fasciitis gluteal, 247t plantar, 501–505 Fasciotomy for acute compartment syndrome, 376 for chronic exertional compartment syndrome, 376 endoscopic, 376 ultrasound-guided percutaneous, for chronic exertional compartment syndrome, 375, 375f Fast, Reliable, and Safe (FARES) method, 72 Fat-suppressed magnetic resonance imaging, in shin splints, 435 Fatigue after stroke, in young adults, 939–940 initial treatment of, 943 physical examination of, 940–941 rehabilitation and, 943 cancer-related, 684–688, 686b in cervical spinal cord injury, 903t–904t chronic, 697–703, 699t, 700f, 701t, 701b in multiple sclerosis, 758, 761, 761t in postpoliomyelitis syndrome, 835, 837 Fatigue fractures. See Stress fractures Fecal incontinence, in neurogenic bowel, 790 Feedback protocol, in neuromuscular disorders, 872 Feeding in dysphagia, 727 in motor neuron disease, 746 in Parkinson disease, 809 Femoral artery catheterization, 824 Femoral articulation, 291 Femoral component, loose, in total hip replacement, 340f Femoral nerve, 303 anatomy of, 304f injury to, 824–825 sensory innervation of, 304f traction on, 305f Femoral neuropathy, 303–306 complications of, 306 definition of, 303, 304f, 304t diagnostic studies for, 304–305 differential diagnosis of, 305b functional limitations in, 303–304 physical examination of, 303, 305f symptoms of, 303 treatment of, 305–306 Femoral stress fractures, 439, 439f–440f Femoroacetabular impingement (FAI), 315 cam type, 315, 316f, 317, 318f pincer type, 315, 316f–317f, 317 Femoroacetabular joint, 307 Fesoterodine, 780t

Fever, in cervical spinal cord injury, 903t–904t 18F-fluorodeoxyglucose positron emission tomography/computed tomography, for cervical dystonia, 19 “Fibro fog”, 556 Fibroids, 588 Fibromyalgia, 247t, 555–559, 573. See also Trapezius strain. of cervical musculature, 620f criteria, revised, 556t definition of, 555 diagnostic studies for, 556 differential diagnosis of, 556b functional limitations in, 556 initial treatment of, 556–557 pharmacologic management of, 557 physical examination of, 555–556 potential disease complications of, 558 potential treatment complications of, 558 procedures for, 557–558 rehabilitation for, 557 Symptom Severity Scale for, 556t symptoms of, 555 Widespread Pain Index for, 556t Fibrositis. See Fibromyalgia; Myofascial pain syndrome (MPS); Trapezius strain Fibrous capsule, 291–292 Fibrous sacrococcygeal symphysis, 538 Fibular (peroneal) mononeuropathy. See Peroneal (fibular) neuropathy Fibular palsy. See Peroneal (fibular) neuropathy Filariasis, 735 Filum terminale lipoma. See Neural tube defects Finger, trigger, 197–200, 198f–199f, 198b Finger escape sign, in cervical spinal stenosis, 33–34 Finger or thumb extensor paralysis. See Radial neuropathy Finkelstein test, 150–151, 150f Fisk view, in biceps tendinopathy, 60–61 Flaccid dysarthria, 897t Flat palpation technique, in myofascial pain syndrome, 573–574, 574f Flatfoot deformity, adult acquired. See Posterior tibial tendon dysfunction Flexibility, in rotator cuff tendinopathy, 88–89 Flexion Abduction External Rotation test, for lumbar facet arthropathy, 252 Flexion contracture hip, 338, 339f of proximal interphalangeal joint. See Hammer toe Flexor carpi ulnaris, 206, 207f Flexor digitorum longus contracture, 486 Flexor digitorum profundus, 208f in flexor tendon injuries, 165 Flexor profundus tendon, 166f Flexor tendon injuries, 165–168, 166f–167f, 167b Flexor tendon laceration or rupture. See Flexor tendon injuries Flexor tendon surgery, for hand rheumatoid arthritis, 182 Flexor tendons, zones of, 165, 166f Flexor tenosynovitis, in hand rheumatoid arthritis, 182 Floating ulnar head, in hand rheumatoid arthritis, 183 Fluid balance, in pressure ulcers, 850

977

Fluid-filled sac of fibrous tissue. See Bursitis, foot and ankle Fluidotherapy, for wrist osteoarthritis, 214 Fluorescent antibody testing, in postherpetic neuralgia, 600 Focal sclerosis. See Multiple sclerosis Fondaparinux, in deep venous thrombosis prophylaxis, 714 Foot (feet). See also Ankle bursae, 475 bursitis of, 475–481, 476f, 476t–477t care of, in peripheral arterial disease, 722 diabetic, 719–723 disorders of, in cerebral palsy, 691, 691f iliotibial band syndrome in, 386 ulcer of in diabetes, 719 in tibial neuropathy, 513 Foot orthotics, for ankylosing spondylitis, 668 Footdrop, in peroneal (fibular) neuropathy, 419–420 Footwear, for knee osteoarthritis, 394 Foraminal stenosis, 277 Foraminotomy for cervical degenerative disease, 15 for cervical radiculopathy, 27 Forearm band (counterforce brace) for lateral epicondylitis, 125f for medial epicondylitis, 129 Forestier disease, 247t Foucher sign, in Baker cyst, 358 Four-corner or four-bone fusion, in wrist osteoarthritis, 216–217, 216f–217f Four-point injection technique, for de Quervain tenosynovitis, 152f Fractures in acromioclavicular injuries, 50 avulsion, posterior cruciate ligament, 428 bisphosphonate-related stress, 441 compression, thoracic, 228–233 femoral stress, 439, 439f–440f hip, 799, 804 metatarsal stress, 440–441 midclavicular, 819 midshaft tibial stress, 440–441 navicular, 440–441 osteoporotic, 804 sacral, 822–824 thoracic compression, 228–233 wrist, 799 Freiberg sign, 326t Friction, in iliotibial band syndrome, 384 Froment sign, 147f, 206 Frozen hip. See Adhesive capsulitis, of hip Frozen shoulder. See Adhesive capsulitis Full can test, 92t–93t Full spine x-rays, for spinal deformities, 885 Fulminant shingles, 600 Functional assessment tool, in traumatic brain injury, 962 Functional electrical stimulation (FES) for cervical spinal cord injury, 912 of lower extremities, 929 for transverse myelitis, 957 Functional instability, 471 Functional Manual Therapy Approach, in chronic exertional compartment syndrome, 375 Functional muscle testing, for lumbar degenerative disease, 246 “Functional” rehabilitation program, in patellofemoral syndrome, 416–417, 416f–417f

978

G

Index

G-EO System, for transverse myelitis, 957 Gabapentin for arachnoiditis, 525, 525t for central post-stroke pain, 630 for cervical degenerative disease, 14–15 for chemotherapy-induced peripheral neuropathy, 531 for femoral neuropathy, 305 for intercostal neuralgia, 569 for lateral femoral cutaneous neuropathy, 323 for lumbar radiculopathy, 259–260 in multiple sclerosis, 760 for occipital neuralgia, 585t for peripheral neuropathies, 814 for phantom limb pain, 597 for post-mastectomy pain syndrome, 606 for post-thoracotomy pain syndrome, 609–610 for postherpetic neuralgia, 601–602 for pruritus, 673 for repetitive strain injuries, 621 for tibial neuropathy, 512 for trigeminal neuralgia, 647 Gaenslen maneuver, in low back strain or sprain, 266t Gaenslen test in ankylosing spondylitis, 665, 665f in sacroiliac joint dysfunction, 286, 286f Gait antalgic, in hip osteoarthritis, 308 in cerebral palsy, 692–693 in femoral neuropathy, 306 in hip disease, 338 in knee osteoarthritis, 392 in lower limb amputations, 660 in osteoarthritis, 794 in Parkinson disease, 806–807, 809 Gait dysfunction, in cervical spondylotic myelopathy, 4 Gait evaluation, for cervical radiculopathy, 23 Galant reflex, in cerebral palsy, 693 Galeazzi maneuver, 693t Galeazzi sign, 692–693 Galveston Orientation and Amnesia Test, 962 Gamekeeper’s thumb, 201 Gamma Knife radiosurgery, for trigeminal neuralgia, 648 Ganglia, of hand and wrist, 169–173, 172b Ganglion cyst of hand and wrist, 169 hand osteoarthritis and, 174 Gapping test, in sacroiliac joint dysfunction, 287 Gastric ulceration, in hip labral tears, 320 Gastrointestinal motility, 786–787, 787f Gastrointestinal system, in cervical spinal cord injury disease complications in, 913 ongoing management and health maintenance in, 911 Gastrostomy tube, for motor neuron disease, 747 General medical care, in pulmonary rehabilitation (PR), 862 Generalized Anxiety Disorder (GAD-7) screen, 686 Genetic testing, in myopathy, 767 Genitourinary system, in cervical spinal cord injury disease complications in, 913 ongoing management and health maintenance in, 910–911, 910t

Geste antagoniste, 17, 19 Gibbus deformity. See Kyphosis Gillet test, in sacroiliac joint dysfunction, 286 Gilmore’s groin. See Pubalgia Glandular sac. See Bursitis, foot and ankle Glasgow Coma Scale, 961–962, 961t Glenohumeral arthritis. See Shoulder, arthritis of Glenohumeral instability, 69–75, 73t definition of, 69–70 diagnostic studies for, 71–72 differential diagnosis of, 72b functional limitations in, 71 physical examination of, 70–71, 70f–72f potential disease complications of, 74 potential treatment complications of, 74–75 symptoms of, 70 treatment of, 72–74 Glenohumeral joint anatomy of, 53, 54f injection of, 73–74, 74f osteoarthritis of, 106, 107f Glenoid labrum, 76 Global aphasia, 896t Glossopharyngeal breathing, in neuromuscular disorders, 871–872, 871f Glucocorticoids in rheumatoid arthritis, 880t–881t for systemic lupus erythematosus, 950t Glucosamine, in osteoarthritis, 795 Glucosamine sulfate, for knee osteoarthritis, 393 Gluteal fasciitis, 247t Gluteus medius tendinopathy. See Greater trochanteric pain syndrome Glycosylated hemoglobin (HbA1c) level, in cardiac rehabilitation, 679 Golfer’s elbow, 128. See also Medial epicondylitis Gonadotropin-releasing hormone (GnRH) agonists, pelvic pain, 593 Goniometer, in joint contractures, 706, 707f Gracilis syndrome. See Pubalgia Graft, in anterior cruciate ligament tear, 355 Greater trochanter, anatomy of, 347f Greater trochanteric pain syndrome, 346–349, 347f–348f, 347b Groin, anatomic layers of, 330f Groin pain. See Pubalgia Groin pull. See Pubalgia Groin strain. See Hip; adductor strain of; Pubalgia Gross Motor Functional Classification System, 692, 692t Gunshot wounds, lumbosacral plexopathy with, 824 Guyon canal corticosteroid injection in, 209 entrapment. See Ulnar neuropathy; wrist ulnar nerve entrapment in, 205, 206f

H

H reflexes, 325–326 in Achilles tendinopathy, 452 Haglund deformity, 475. See also Foot (feet), bursitis of. Hallux rigidus, 482–485, 483f diagnostic studies for, 482–483 differential diagnosis of, 483b functional limitations in, 482 physical examination of, 482 potential disease complications of, 484

Hallux rigidus (Continued) potential treatment complications of, 484, 484f rehabilitation for, 483 surgery for, 483–484, 484f symptoms of, 482 Hallux valgus, 466, 467f. See also Bunion angle of, 468f etiology of, 466 Hammer toe, 486–489, 487f. See also Mallet toe definition of, 486 diagnostic studies for, 487 differential diagnosis of, 487b functional limitations in, 487 physical examination of, 486–487 postoperative rehabilitation for, 488 potential disease complications of, 488 potential treatment complications of, 488–489 procedures for, 487–488 rehabilitation for, 487 surgery for, 488, 488f symptoms of, 486 treatment of, 487–488 Hammer toe syndrome. See Hammer toe; Mallet toe Hamstring complete tear of, 379 injuries to, prevention of, 382 range of motion of, 380 strain of, 378–383, 379f, 381b grades of, 379, 379f stretching of, 382, 382f tendinopathy of, 378, 379f tightness of, 379 Hamstring avulsion. See Hamstring, strain of Hamstring contusion. See Hamstring, strain of Hamstring pull. See Hamstring, strain of Hamstring tear. See Hamstring, strain of Hand flexor tendons of, 166 ganglia, 169–173, 172b rheumatoid arthritis, 179–184, 180f, 180b in thoracic outlet syndrome, 634, 634f Hand amputations. See Upper limb amputations Hand grip-and-release test, for cervical spinal stenosis, 33–34 Hand osteoarthritis, 174–178, 175f, 175b Haptic Walker, for transverse myelitis, 957 Hatchet-shaped heel. See Bursitis, foot and ankle Hawkin sign, 88t Hawkins maneuver, 70 Head injury. See Traumatic brain injury Headaches, 560–565 in cervical spinal cord injury, 903t–904t cluster, 561 definition of, 560–561 diagnostic studies for, 562 differential diagnosis of, 562b functional limitations in, 562 initial treatment of, 562–563 physical examination of, 561–562 in postconcussion symptoms, 842–843 potential disease complications of, 564 potential treatment complications of, 564 procedures for, 564 rehabilitation for, 563–564 surgery for, 564 technology for, 564 tension-type, 561 Heart disease, rehabilitation in, 678

Index

Heat and cold modalities, for lumbar degenerative disease, 249 Heat therapy for cervical degenerative disease, 15 for piriformis syndrome, 326 Heberden nodes, 174, 175f, 308 Heel cord tendinitis. See Achilles tendinopathy Heel lifts, in bursitis, 478 Heel pain, 501 Heel spur syndrome. See Plantar fasciitis Heel wedge, for chronic ankle instability, 473 Hemarthrosis, for posterior cruciate ligament sprain, 428 Hematoma intermuscular, in quadriceps contusion, 334 retroperitoneal, 824 Hematuria, in cervical spinal cord injury, 903t–904t Hemiarthroplasty, hip, 338 Hemiballismus, 751 Hemimyelocele. See Neural tube defects Hemimyelomeningocele. See Neural tube defects Hemorrhage intracerebral. See Stroke, in young adults retroperitoneal, 825–826 Hemorrhoids, in neurogenic bowel, 790 Heparin, in total knee arthroplasty, 445 Herniated nucleus pulposus with nerve root irritation. See Lumbar radiculopathy Herniography, 331 Herpes zoster, 599 Herpes zoster ophthalmicus, 600 Herpes zoster oticus, 600 Heterotopic ossification, 729–734, 730f, 730t in biceps tendon rupture, 67 in brachial plexopathy, 819 in burns, 674–675 diagnostic studies for, 731–732, 731f differential diagnosis of, 732b disease complications of, 733 functional limitations in, 731 physical examination of, 730–731 symptoms of, 730 in thoracic spinal cord injury, treatment of, 920 treatment complications of, 733–734 treatment of, 732–733 High-prow heel. See Bursitis, foot and ankle Hip adductor strain of, 297–302, 298f–299f, 298t, 299b adhesive capsulitis of, 291–296, 292t, 293f, 294b–295b fracture of, 799, 804 hemiarthroplasty, 312, 338 injections, in hip labral tears, 319 labral tears of, 315–320, 316f–318f, 317b definition of, 315 osteoarthritis of, 307–314, 308f–312f, 309b replacement of, 337–345. See also Total hip replacement ambulation after, 341 anemia and, 344 Hip adductor muscles, 297, 298f Hip adductor tendinitis/tendinopathy. See Hip; adductor strain of Hip bursitis. See Greater trochanteric pain syndrome Hip degenerative joint disease. See Hip, osteoarthritis of

Hip pocket neuropathy. See Piriformis syndrome Histamine cephalgia. See Cluster headache HLA-B27, 664, 666 HLA-B27 associated spondyloarthropathy. See Ankylosing spondylitis Hoarseness. See Dysphonia Hodgkin lymphoma, 613f–614f Hoffmann sign in cervical radiculopathy, 25 in cervical spinal stenosis, 33–34 Homocysteine, peripheral arterial disease and, 721 Horizontal flexion test, 550, 550f Hormonal therapy, pelvic pain, 593 Hormone replacement therapy, for osteoporosis, 802 Hornblower’s sign, 92t–93t, 94f Housemaid’s knee, 400, 400f “Hover test”, for abdominal wall pain, 519 Humeroscapular fibrositis. See Adhesive capsulitis Humpback. See Kyphosis Hunchback. See Kyphosis Huntington chorea, 752 Hutchinson sign, 600 Hyaluronan injections, for wrist osteoarthritis, 214 Hyaluronate, injection of, in hand osteoarthritis, 176 Hydrocele spinalis. See Neural tube defects Hydrocephalus, symptoms of, 770 Hydrocodone, for lumbar radiculopathy, 260–261 Hydrofiber dressings, for burns, 673 Hydrotherapy, for wrist rheumatoid arthritis, 223 Hydroxychloroquine for hand rheumatoid arthritis, 180 for systemic lupus erythematosus, 949 Hyperabduction test, in thoracic outlet syndrome, 635 Hyperbaric oxygen therapy, 722 Hyperemia, in Tietze syndrome, 642f Hyperkinetic disorders, 750 Hyperkinetic dysarthria, 897t Hyperkyphosis (HK), 882 Hypermetabolism, and deconditioning, in burns, 674 Hypernasality. See Dysphonia Hyperreflexia, 24 Hypertension control of, 721 in neural tube defects, 771 in systemic lupus erythematosus, 950 Hypertrophic scarring, in burns, 673–675 Hypertrophy, tissue, in knee chondral injuries and, 365 Hypnosis, in myofascial pain syndrome, 576 Hypokinetic dysarthria, 897t Hypokinetic problems, 750 Hyponasality. See Dysphonia Hypophonia, in Parkinson disease, 806 Hypotension, in chemotherapy-induced peripheral neuropathy, 529 Hypothalamic-pituitary dysfunction, neural tube defects and, 775 Hysterectomy, in pelvic pain, 593–594

I

Ibandronate, for osteoporosis, 803 Ice massage, for acromioclavicular injuries, 49 Iceland disease. See Chronic fatigue syndrome

979

Idiopathic osteonecrosis, lower extremity, in shin splints, 434–435 Idiopathic parkinsonism. See Parkinson disease Idiopathic pulmonary fibrosis, 861f Idiopathic shoulder girdle neuropathy. See Brachial plexopathy Idiopathic torsion dystonia. See Cervical dystonia Iliac gapping test, in low back strain or sprain, 266t Iliopsoas impingement, 344 Iliotibial band (ITB), 384 anatomy of, 385f injection technique in, 388f stretch of, 388f Iliotibial band friction syndrome. See Iliotibial band syndrome (ITBS) Iliotibial band release, 348–349 Iliotibial band syndrome (ITBS), 384–390 definition of, 384–385, 385f diagnostic studies for, 386–387 differential diagnosis of, 387b disease complications of, 389 functional limitations in, 386 physical examination of, 385–386, 386f–387f symptoms of, 385 treatment of, 387–389 Iliotibial tract friction syndrome. See Iliotibial band syndrome (ITBS) Imaging studies in polytrauma, 831 in traumatic brain injury, 962 Imipramine, in occipital neuralgia, 585t Immunoglobulin, intravenous for complex regional pain syndrome, 546 for postpoliomyelitis syndrome, 837 Immunoglobulin G antibodies, in transverse myelitis, 954 Impaired vision, in multiple sclerosis, 757 Impedance plethysmography, in deep venous thrombosis, 713 Impingement syndrome. See also Rotator cuff, tendinopathy of Neer sign for, 88f Impingement test, 70, 71f internal, 70, 72f Incobotulinumtoxin A, 892, 893t Increased muscle tone. See Spasticity Indwelling catheterization (urethral or suprapubic), 910t Indwelling continuous Foley catheterization, in neurogenic bladder, 782 Infantile paralysis, 834 Infection lymphedema and, 738 in systemic lupus erythematosus, 950 Infiltration, bursal, 401 Inflammatory arthritis. See also Rheumatoid arthritis. elbow, 116 Inflammatory myopathies, 765, 766t Inflammatory spondyloarthropathies, in ankylosing spondylitis, 664 Infrapatellar bursopathy, 400 Infraspinatus, tests for, 92t–93t, 94f Infraspinatus syndrome, 112. See also Suprascapular neuropathy Inguinal canal, posterior wall of, 329, 330f Injection in hand osteoarthritis, 177f in Tietze syndrome, 644 Inspiratory resistive exercises, in pulmonary rehabilitation (PR), 863 Insufficiency fractures. See Stress fractures

980

Index

Insular sclerosis. See Multiple sclerosis Intention tremor, 751 Intercostal nerve, 566, 567f, 570f Intercostal nerve block in costosternal syndrome, 553 in Tietze syndrome, 644 Intercostal nerve pain. See Intercostal neuralgia Intercostal neuralgia, 566–571, 567f, 568t, 568b, 570f in post-thoracotomy pain, 608 Intercostal neuroma. See Intercostal neuralgia Intercostobrachial nerve, in post-mastectomy pain syndrome, 604 Interdigital nerve compression syndrome. See Morton’s neuroma Interdigital neuroma. See Morton’s neuroma Interdisciplinary team, composition of, 832 Interferon, in multiple sclerosis, 762 Interlaminar epidural steroid injections for cervical radiculopathy, 27 for cervical spinal stenosis, 36 Intermetatarsal bursitis. See Bursitis, foot and ankle Intermetatarsal nerve entrapment, plantar, 495 Intermetatarsal neuroma. See Morton’s neuroma Intermittent catheterization, 910t Intermittent claudication, 720 Intermittent pneumatic compression, 722 in deep venous thrombosis, 714 in total knee arthroplasty, 445 International Association for the Study of Pain, 566 International Classification of Functioning, Disability, and Health (ICF), 908–909 chronic fatigue syndrome and, 700 International Myelodysplasia Study Group, criteria for assigning motor levels, 772t International Spinal Cord Injury Pain Classification, 902, 904t International Standards for Neurological Classification of Spinal Cord Injury, 24 International Workshop on Definition and Classification of CP, 689 Interphalangeal joints in hand rheumatoid arthritis, postoperative rehabilitation for, 181–182 osteoarthritis of, 174, 175f distal, 175f, 177 proximal, treatment of, 177 Interstitial cystitis (IC), 589 Intervertebral disc disorder, with myelopathy. See Cervical spine, degenerative disease of Intervertebral discs, degeneration of, 3 Intra-articular facet joint injection, for cervical facet arthropathy, 10 Intra-articular glenohumeral injection, 108–109, 109f Intra-articular injection, in costosternal syndrome, 553, 553f Intra-articular knee injections, for knee osteoarthritis, 395 Intracerebral hemorrhage. See Stroke, in young adults Intracranial complications, in traumatic brain injury, 962t Intractable pain. See Chronic pain syndrome Intrathecal baclofen pump, for spasticity, 892 Inversion sprain. See Ankle, sprain of Iontophoresis for biceps tendinopathy, 61 for biceps tendon rupture, 66 Irritable bowel syndrome, 588

J

Jaccoud arthropathy, in systemic lupus erythematosus, 950 Janus kinase inhibitors, in rheumatoid arthritis, 880t–881t Japanese Orthopaedic Association (JOA) classification system, of cervical spinal stenosis, 36 Jersey finger, 166f. See also Flexor tendon injuries Jobe test (empty can test), 92t–93t, 94f Joint aspiration, in osteoarthritis, 794 Joint contractures, 704–709 complications of, 708 definition of, 704–705, 705f–706f, 705t diagnostic studies for, 707 differential diagnosis of, 707b functional limitations in, 706–707 physical examination of, 706, 707f sequelae of, 709b symptoms of, 705, 706t treatment of, 707–708 Joint destruction. See Osteoarthritis Joint examination, for cervical radiculopathy, 24 Joint fluid, analysis of, in osteoarthritis, 794 Joint stiffness, in knee osteoarthritis, 392 Jumper’s knee, 410–413

K

Kelikian push-up test, 486 Kennedy disease, 740 Keratoconjunctivitis sicca, in rheumatoid arthritis, 876 Ketamine, in phantom limb pain, 597 Ketoprofen phonophoresis, in carpal tunnel syndrome, 194 Kienböck disease, 185–190, 186f, 187b, 213–214 hand and wrist ganglia and, 171–172 stages of, 187, 187t, 188f treatment of, 189t Kienböck disease advanced collapse (KDAC), 186 Kiloh-Nevin syndrome. See Median neuropathy Kinesiophobia, in chronic fatigue syndrome, 698–699 Klumpke paralysis, 818 Knee anterior cruciate ligament sprain and, 350–357 Baker cyst, 358–361, 359f, 359b chondral injuries, 362–365 iliotibial band syndrome in, 384–386 posterior cruciate ligament sprain of, 424–430 Knee bend exercise, 416f Knee bursopathy, 399–402 Knee joint, aspiration of, in anterior cruciate ligament sprain, 355 Knee ligamentous injuries. See Collateral ligament sprain Knee osteoarthritis, 391–398 Knee valgus or varus instability or insufficiency. See Collateral ligament sprain Knobby heel. See Bursitis, foot and ankle KT-1000 arthrometer, in posterior cruciate ligament sprain, 427 Kyphoplasty, percutaneous, in thoracic compression fractures, 230–231

Kyphosis, 882–889 definition of, 882, 883f diagnostic studies for, 885, 886f differential diagnosis of, 885b disease complications in, 888 functional limitations in, 884–885 neural tube defects and, 775 physical examination of, 884 symptoms of, 884 treatment of, 886–888

L

Labor, lumbosacral plexopathy with, 824 Labral tears of hip, 315–320 of shoulder, 76–83, 77f, 78t–79t, 79f–80f, 80b, 82f Labrum, acetabular, 315 Lachman test, 351, 351f posterior, in posterior cruciate ligament sprain, 426 Laminectomy for cervical spondylotic myelopathy, 6 for lumbar spinal stenosis, 281 Laminoplasty, for cervical spondylotic myelopathy, 6 Laminotomy, for cervical degenerative disease, 15 Lamotrigine for central post-stroke pain, 630 for phantom limb pain, 597 for trigeminal neuralgia, 647 Laparoscopy, for pelvic pain diagnosis, 592 Lasègue sign, 326t in low back strain or sprain, 266t Late effects of burn injury. See Burns Late effects of poliomyelitis. See Postpoliomyelitis syndrome Late effects of radiation. See Radiation fibrosis syndrome Lateral collateral ligament (LCL), 366, 367f Lateral compartment, of leg, 372, 372f Lateral epicondylitis, 124–127 diagnostic studies for, 124–125 differential diagnosis of, 125b functional limitations in, 124 physical examination of, 124 potential disease complications of, 126 potential treatment complications of, 126 symptoms of, 124 treatment of, 125–126, 125f–126f Lateral femoral cutaneous nerve, 321, 322f Lateral femoral cutaneous neuropathy, 321–324 complications of, 324 definition of, 321, 322f, 322t diagnostic studies for, 322–323 differential diagnosis of, 323b functional limitations in, 322 physical examination of, 321–322 symptoms of, 321 treatment of, 323–324, 323f Lateral medullary infarction, 726f Lateral meniscus, 403–404, 404f Lateral popliteal neuropathy. See Peroneal (fibular) neuropathy Laterocollis, 18, 18f Laterolisthesis, 270 Latex allergy, in neural tube defects, 771 Latissimus dorsi, in post-thoracotomy pain, 610 Laxatives, for thoracic compression fractures, 229–230 Leflunomide, for rheumatoid arthritis, 880t–881t hand, 180

Index

Leg pain, lumbar spinal stenosis and, 278 Leg swelling, unilateral, in cervical spinal cord injury, 903t–904t Leiomyomas, uterine, pelvic pain and, 588, 593–594 Lesser metatarsalgia. See Metatarsalgia Lesser toe deformity. See Hammer toe; Mallet toe Levator ani syndrome, in coccydynia, 538–539 Levator scapulae muscles, 100, 101f Levodopa, for Parkinson disease, 752–753, 808, 808t, 810 Levodopa-induced dyskinesias, in Parkinson disease, 810 Lhermitte sign in cervical radiculopathy, 25 in cervical spinal stenosis, 33–34 in cervical spondylotic myelopathy, 4 in multiple sclerosis, 757 Lhermitte’s phenomenon, 530 Lidocaine for abdominal wall pain, 519 for adhesive capsulitis, 57 for coccydynia, 540–541 for complex regional pain syndrome, 546 injection of for rotator cuff tear, 96 for rotator cuff tendinopathy, 89 for post-mastectomy pain syndrome, 606 for postherpetic neuralgia, 601–602 for trigeminal neuralgia, 647 for wrist arthritis, 214 for wrist rheumatoid arthritis, 224 Lidoderm, for intercostal neuralgia, 569 Lifestyle modification for cluster headache, 563 for migraine, 563 for tension-type headache, 563 LifeViz system, for pressure ulcers, 852f Lift-off test, 70, 70f, 92f, 92t–93t Ligamentous injuries, gradations of, 460, 461f Ligamentous laxity, 466 Ligamentum flavum, 245 Lipedema, in lymphedema, 736 Lipoma with dural involvement. See Neural tube defects Lipomyelomeningocele. See Neural tube defects Lipomyeloschisis. See Neural tube defects Little disease. See Cerebral palsy (CP) Little Leaguer’s elbow, 128. See also Medial epicondylitis Load and shift maneuver, 70–71 Local anesthetic injection for bunion, 468 for posterior tibial tendon dysfunction, 508 for spasticity, 892 Locked finger. See Trigger finger Locked knee. See Meniscal injuries Locomotor training (LT), for cervical spinal cord injury, 912 Long thoracic nerve, injury in, 99, 102f Long thoracic nerve palsy. See Scapular winging Loose body in ankle arthritis, 456 of the knee. See Knee, chondral injuries Lordosis, and neural tube defects, 775 Lou Gehrig’s disease. See Motor neuron disease

Low back pain. See also Lumbar spine, stenosis of in lumbar degenerative disease, 244 Low back strain or sprain, 264–268, 265t–266t, 267b Low-level laser therapy for carpal tunnel syndrome, 195 for median neuropathy, 134 Low-molecular-weight heparin (LMWH), 714–715, 715t Lower extremity idiopathic osteonecrosis, in shin splints, 434–435 Lower limb amputations, 658–663 amputation levels and epidemiology of, 658 complications of, 662–663 diagnostic studies for, 660 functional limitations in, 660 physical examination of, 659–660 surgery for, 658–659 symptoms of, 659 treatment of, 660–662, 661f, 661t–662t Lower limb functional electric stimulation (FES), 929 Lower motor neuron bowel syndrome, 787 Lubricated single-digit examination, 590 Ludington test, 65, 65f Lumbar arthritis. See Lumbar degenerative disease Lumbar arthrodesis, for lumbar degenerative disease, 250 Lumbar degenerative disease, 244–251, 245f, 247t, 248f, 249t aging and, 244 definition of, 244–245 diagnostic studies for, 246–249 functional limitations in, 246 physical examination of, 246 potential disease complications of, 250 potential treatment complications of, 250–251 symptoms of, 245–246 treatment of, 249–250 Waddell signs in, 248t Lumbar disc arthroplasty, for lumbar degenerative disease, 250 Lumbar facet arthropathy, 252–256, 253f definition of, 252 diagnostic studies for, 253, 254f differential diagnosis of, 253b functional limitations in, 253 physical examination of, 252 potential disease complications of, 255 potential treatment complications of, 255 symptoms of, 252 treatment of, 253–255 Lumbar plexus, 822, 823f Lumbar puncture, in transverse myelitis, 955 Lumbar radiculitis, 257. See also Lumbar radiculopathy; Lumbar spine; stenosis of Lumbar radiculopathy, 257–263, 258f, 258t, 262t definition of, 257 diagnostic studies for, 259 differential diagnosis of, 259b electromyography of, 259 functional limitations in, 258–259 imaging of, 259 physical examination of, 257–258 potential disease complications of, 262 potential treatment complications of, 262–263 symptoms of, 257 treatment of, 259–261 Waddell signs, 258

981

Lumbar spine normal anatomic structures of, 278f spondylolisthesis of, 269–276, 270f–273f, 273b spondylolysis of, 269–276, 270f–273f, 273b stenosis of, 277–283, 278t, 279b, 280t Lumbar spondylosis. See Lumbar facet arthropathy Lumbar strain or sprain, 264 Lumbar sympathetic block, for complex regional pain syndrome, 546–547 Lumbosacral myotomes, muscle groups for, 926t Lumbosacral orthosis, for thoracic compression fractures, 229–230, 231f Lumbosacral plexitis. See Lumbosacral plexopathy Lumbosacral plexopathy, 822–827, 826b Lumbosacral radiculoplexus neuropathy. See Lumbosacral plexopathy Lumbosacral spinal cord injury, 924–930 definition of, 924 diagnostic studies for, 927–928 differential diagnosis of, 928b disease complications in, 929 electrodiagnostic testing for, 928 functional limitations in, 926–927, 927t neurologic versus skeletal level, 924, 925f physical examination of, 925–926 spinal imaging in, 927–928 symptoms of, 924–925 treatment of, 928–929 urologic studies in, 928 Lumbosacral spinal fibrosis. See Arachnoiditis Lumbosacral spinal segments, sensory points for, 926t Lumbosacral stabilization program, for lumbar radiculopathy, 261 Lunate avascular necrosis of. See Kienböck disease revascularization of, 189 Lunate osteomalacia or osteonecrosis. See Kienböck disease Lunatomalacia. See Kienböck disease Lung disease, pulmonary rehabilitation for patients with, 860 Lung growth, maintaining, in neuromuscular disorders, 869–870 Lunge exercise, 416f Lupus. See Systemic lupus erythematosus Lupus erythematosus. See Systemic lupus erythematosus Luschka, joint of, 12, 13f Lymphadenopathy, metastatic, 819 Lymphatic examination, in post-mastectomy pain syndrome, 604–605 Lymphatic system, 735, 736f Lymphedema, 733, 735–739, 736f diagnostic studies for, 737 differential diagnosis of, 737b disease complications of, 738 functional limitations in, 736, 736t, 737f malignant, 735 physical examination of, 736, 736t post-mastectomy, 735 symptoms of, 735–736 treatment complications of, 738 treatment of, 737–738

M

Magnesium, intravenous, for complex regional pain syndrome, 546 Magnetic resonance angiography, for cervicogenic vertigo, 40

982

Index

Magnetic resonance arthrography in chronic ankle instability, 472 in glenohumeral instability, 72 in hip adhesive capsulitis, 294, 294f in hip labral tears, 317, 318f in rotator cuff tear, 95 in suprascapular neuropathy, 113 Magnetic resonance elastography, for trapezius strain, 44 Magnetic resonance imaging (MRI) in Achilles tendinopathy, 452 in acromioclavicular injuries, 49 in acute compartment syndrome, 373 in adhesive capsulitis, 54–55, 55f in amyotrophic lateral sclerosis, 742 in ankle arthritis, 457 in ankle sprain, 462–463 in ankylosing spondylitis, 667 in anterior cruciate ligament tear, 351 in arachnoiditis, 523, 524f in Bankart lesion, 80, 80f in biceps tendinopathy, 61 in biceps tendon rupture, 66 in brachial plexopathy, 818 in cerebral palsy, 694 in cervical degenerative disease, 14, 14f in cervical dystonia, 18 in cervical facet arthropathy, 9 in cervical radiculopathy, 26 in cervical spinal stenosis, 34–35, 34f–35f in cervical spondylotic myelopathy, 4–5, 5f in cervical sprain/strain, 30 in cervicogenic vertigo, 40 in chronic ankle instability, 472 in chronic fatigue syndrome, 697 in coccydynia, 540 in complex regional pain syndrome, 545 fat-suppressed, in shin splints, 435 in glenohumeral instability, 72 in hamstring strain, 380–381, 380f in hand and wrist ganglia, 171–172 in hand osteoarthritis, 175 in hand rheumatoid arthritis, 180 in hip adductor strain, 299, 299f in hip adhesive capsulitis, 294 in hip disease, 338–340 in hip osteoarthritis, 308–309 in intercostal neuralgia, 568 in Kienböck disease, 186, 186f, 188f in knee bursopathy, 400 in knee chondral injuries, 363–364 in knee osteoarthritis, 392–393 in lateral epicondylitis, 124–125 in low back strain or sprain, 266–267 in lumbar degenerative disease, 246 in lumbar facet arthropathy, 253 in lumbar radiculopathy, 259, 260f in lumbar spinal stenosis, 280t in lumbosacral plexopathy, 825–826 in medial epicondylitis, 128–129 in meniscal injuries, 406, 407f in metatarsalgia, 494 in misaligned coccygeal fracture, 539f in Morton’s neuroma, 498 in multiple sclerosis, 759 in neural tube defects, 773, 773f in occipital neuralgia, 582 in patellar tendinopathy, 411 in piriformis syndrome, 325–326 in polytrauma, 831 in posterior cruciate ligament sprain, 427, 427f in posterior tibial tendon dysfunction, 507 in pubalgia, 331 in quadriceps contusion, 334 in radiation fibrosis syndrome, 614, 615f

Magnetic resonance imaging (MRI) (Continued) in repetitive strain injuries, 621 in rotator cuff tear, 93, 95f in rotator cuff tendinopathy, 86 in sacroiliac joint dysfunction, 287 in scapular winging, 103 in shin splints, 435–436 in shoulder arthritis, 107 in spondylolysis and spondylolisthesis, 272–273, 273f in stress fractures, 440 in superior labral anterior-posterior (SLAP) tears, 79–80, 79f in suprascapular neuropathy, 113 in systemic lupus erythematosus, 948 in thoracic outlet syndrome, 636 in thoracic radiculopathy, 235 in thoracic sprain and strain, 240, 240f in tibial neuropathy, 512 in Tietze syndrome, 643 in total knee arthroplasty, 444 in transverse myelitis, 954, 954f in trigeminal neuralgia, 647 in trigger finger, 198 in trochanteric bursitis, 347 in ulnar collateral ligament sprain, 202 in ulnar neuropathy, 205 in wrist osteoarthritis, 213–214 in wrist rheumatoid arthritis, 222 Magnetic resonance neurography in femoral neuropathy, 305 in ulnar neuropathy (elbow), 147 Magnetic resonance venography, in deep venous thrombosis, 713 Maine Lumbar Spine Study, 281 Malalignment, in knee osteoarthritis, 391 Malignant neoplasms, cancer-related fatigue and, 685 Malleolar bursitis, 476, 477t Mallet finger, 161t–162t. See also Extensor tendon injuries Mallet toe, 490–492, 491f definition of, 490 diagnostic studies for, 490–491 differential diagnosis of, 491b functional limitations in, 490 physical examination of, 490 potential disease complications of, 492 potential treatment complications of, 492 procedures for, 491, 491f rehabilitation for, 491 surgery for, 491–492 symptoms of, 490 treatment of, 491–492 Mallet toe syndrome. See Mallet toe Malnutrition, pressure ulcers and, 853, 855 Maltracking. See Patellofemoral syndrome (PFS) Manipulation, in total knee arthroplasty, 445 Manipulative therapy, in chronic pain syndrome, 536 Mannerfelt syndrome, 180, 220 Manometry, in dysphagia, 725 Manual Ability Classification System, 692, 692t Manual muscle testing, for lumbar radiculopathy, 258 Manual therapy for cervical facet arthropathy, 10 for cervical sprain/strain, 31 for cervicogenic vertigo, 40 for occipital neuralgia, 583 March fractures. See Stress fractures Mastectomy, pain after, 604

Mastodynia. See Post-mastectomy pain syndrome Matrix metalloprotease, 850 McConnell’s taping method, in patellofemoral syndrome, 415–416 McMurray test in anterior cruciate ligament sprain, 351 in meniscal injuries, 405–406, 406f Medial branch blocks (MBBs) for cervical facet arthropathy, 10 for lumbar facet arthropathy, 253 Medial collateral bursopathy, 400 Medial collateral ligament (MCL), 366, 367f injury to, 366 Medial epicondylitis, 128–130 diagnostic studies for, 128–129 differential diagnosis of, 129b functional limitations in, 128 physical examination of, 128 potential disease complications of, 130 potential treatment complications of, 130 symptoms of, 128 treatment of, 129–130, 129f Medial epicondylitis injection, 129f Medial meniscus, 403–404, 404f Medial parapatellar arthrotomy, in total knee arthroplasty, 447 Medial tibial periostalgia. See Shin splints Medial tibial stress syndrome. See Shin splints Median nerve block, for median neuropathy, 134 Median nerve compression. See also Median neuropathy in biceps tendon rupture, 67 in wrist rheumatoid arthritis, 221 Median nerve entrapment, at wrist. See Median neuropathy Median neuropathy, 131–136 diagnostic studies for, 133 differential diagnosis of, 134b functional limitations in, 133 physical examination of, 132–133 potential disease complications of, 135 potential treatment complications of, 135 symptoms of, 131–132 treatment of, 134–135 wrist, 191–196, 192f–194f, 193b Medical marijuana, for chronic pain syndrome, 535–536 Medications in chronic pain syndrome, 535 in pulmonary rehabilitation (PR), 861 Melatonin, in postconcussion symptoms, 845–846 Melodic intonation therapy (MIT), for speech and language disorders, 900 Memory, medications used for, 963–964, 965t Meninges, 523 Meningocele. See Neural tube defects Meniscal injuries, 403–409 definition of, 403–405, 404f–405f diagnostic studies for, 406, 407f differential diagnosis of, 407b disease complications of, 408 functional limitations in, 406 physical examination of, 405–406, 406f symptoms of, 405 treatment of, 407–408 Meniscectomy, for meniscal injuries, 407 Menisci, 403 vascular zones of, 404f Meniscofemoral ligaments, intact, for posterior cruciate ligament sprain, 428

Index

Mental health, in thoracic spinal cord injury, treatment of, 919 Mental health treatment, in chronic pain syndrome, 535 Mental status examination, for chronic fatigue syndrome, 698 Meralgia paresthetica. See Lateral femoral cutaneous neuropathy Mesenchymal stem cells, for lumbar degenerative disease, 250 Metabolic myopathies, 765, 766t Metabolic system, in cervical spinal cord injury, disease complications in, 913 Metacarpophalangeal joints in hand rheumatoid arthritis, postoperative rehabilitation for, 181 osteoarthritis of, 175 Metatarsal bone, 466 Metatarsal bursitis, 476, 477t Metatarsal heads, 493–494, 494f Metatarsal pad, 495f Metatarsal stress fractures, 440–441 Metatarsalgia, 467, 493–497 definition of, 493 diagnostic studies for, 494 differential diagnosis of, 494b functional limitations in, 494 hammer toe and, 486 physical examination of, 493–494 potential disease complications of, 495 potential treatment complications of, 496 rehabilitation for, 495 surgery for, 495 symptoms of, 493 treatment of, 494–495 Metatarsophalangeal (MTP) joint, 493 loss of articular cartilage from, 482 palpation of, 497 synovitis, 493 Metaxalone, for lumbar radiculopathy, 259 Methocarbamol, for lumbar radiculopathy, 259 Methotrexate for rheumatoid arthritis, 880t–881t hand, 179–181 wrist, 223 for systemic lupus erythematosus, 950t Methylprednisolone for cervical degenerative disease, 14–15 for cervical sprain/strain, 31 intrathecal, for postherpetic neuralgia, 602 for lumbar radiculopathy, 259–260 for thoracic radiculopathy, 236 Metoclopramide, for bowel management, 919t Mexiletine, in occipital neuralgia, 585t Microfracture, in knee chondral injuries, 364–365, 365f Microtrauma, in quadriceps tendinopathy, 431 Micturition reflex, 777 Mid-back pain. See Thoracic sprain or strain Midclavicular fractures, 819 Midshaft tibial stress fractures, 440–441 Midvastus approach, in total knee arthroplasty, 447 Migraine, 560–561 with aura, 560–561, 561t treatment of, 563 without aura, 560–561, 561t Migrainous neuralgia. See Cluster headache Mild traumatic brain injury (mTBI), 841 Milnacipran, for intercostal neuralgia, 569 Mindfulness meditation, in myofascial pain syndrome, 576 Miner’s elbow. See Olecranon bursitis

Minimal cognitive impairment, in Parkinson disease, 807 Minimal joint space (MJS), 308 Minimally invasive surgery (MIS), in total knee arthroplasty, 447 Minnesota Multiphasic Personality Inventory, 534 Mirror therapy for complex regional pain syndrome, 546, 546f for phantom limb pain, 597 Mitochondrial myopathies, 765, 766t Mixed dysarthria, 897t Mobility, assistive technology for, in motor neuron disease, 746 Modified Ashworth Scale, for spasticity, 891, 891t, 940t Modified Brostrom, 464 Modified Milwaukee brace, in kyphosis, 888 Modified Ober test, in iliotibial band syndrome, 387–388 Modified Spurling maneuver, for cervical radiculopathy, 25, 25f Moist heat, for thoracic sprain or strain, 240–241 Moist heat packs, for wrist rheumatoid arthritis, 223 Montreal Cognitive Assessment, for postconcussion symptoms, 843 Mood, changes in, concussion and, 830 Mood and affect disorders, in chronic pain syndrome, 533 Mood stabilizers, for chronic pain syndrome, 535t Morton, Thomas, 497 Morton’s extension orthotic devices, 483 Morton’s neuralgia. See Morton’s neuroma Morton’s neuroma, 497–500, 498f definition of, 497 diagnostic studies for, 498 differential diagnosis of, 498b functional limitations in, 498 physical examination of, 497, 498f potential disease complications of, 499 potential treatment complications of, 499 procedures for, 498–499 rehabilitation for, 498 surgery for, 499, 499f symptoms of, 497 treatment of, 498–499 Motion-sparing procedures, in wrist osteoarthritis, 215–216 Motor deficits, in cervical spondylotic myelopathy, 4 Motor examination, in lumbosacral spinal cord injury, 926, 926t Motor function, in cervical spinal cord injury, surgery for, 912 Motor imagery, in phantom limb pain, 597 Motor limitations, in traumatic brain injury, 961 Motor nerve fiber cell bodies, in chemotherapy-induced peripheral neuropathy, 529 Motor neuron disease, 740–749, 741t diagnostic studies for, 742, 742t–744t differential diagnosis of, 742b–743b disease complications of, 748 functional limitations in, 741–742 physical examination of, 741 symptoms of, 741 treatment complications of, 748 treatment of, 743 Motor neurons, 834 Motor speech disorders, 895

983

Motor testing, for cervical radiculopathy, 24, 24t Movement disorders, 750–756 diagnostic studies for, 752 differential diagnosis of, 752b disease complications in, 755 functional limitations in, 752 physical examination of, 751–752 symptoms of, 750–751 treatment complications in, 755 treatment of, 752–755, 753f Mucous cyst, 169, 170f, 171 Mulder’s click test, 497 Multidirectional instability, shoulder. See Glenohumeral instability Multiple concussions, 846 Multiple injuries. See Polytrauma, rehabilitation for Multiple myeloma, cancer-related fatigue and, 685 Multiple rehabilitation protocols, for meniscal injuries, 407–408 Multiple sclerosis, 757–764, 761t complications of, 762 diagnostic criteria for, 758t diagnostic studies for, 759 differential diagnosis of, 760b functional limitations in, 759 physical examination of, 758–759 symptoms of, 757–758, 758t transverse myelitis and, 955t treatment of, 760–762 Multiple trauma. See Polytrauma, rehabilitation for Muscle atrophy, in ulnar neuropathy, 208f Muscle contraction headache. See Tensiontype headache Muscle relaxants for cervicogenic vertigo, 40 for chronic pain syndrome, 537 for low back strain or sprain, 267 for lumbar degenerative disease, 249 for lumbar facet arthropathy, 254 for lumbar spinal stenosis, 279 for multiple sclerosis, 760 for myofascial pain syndrome, 575 for radiation fibrosis syndrome, 615–616 for thoracic compression fractures, 229–230 for thoracic sprain or strain, 240–241 for trapezius strain, 44 Muscle stiffness due to spasticity, in stroke, in young adults, 938–939 initial treatment of, 942 physical examination of, 940, 940t procedures for, 942–943 rehabilitation and, 942 surgery for, 943 Muscle transfers, in scapular winging, 104 Muscle weakness, in postpoliomyelitis syndrome, 835–837 Muscular dystrophies, 765, 766t Musculoskeletal examination in chronic fatigue syndrome, 698 in post-mastectomy pain syndrome, 604–605 Musculoskeletal system, in cervical spinal cord injury disease complications in, 913 ongoing management and health maintenance in, 912 Musculoskeletal ultrasonography (MUS), in knee osteoarthritis, 392–393 Musculoskeletal ultrasound in glenohumeral instability, 72 in hamstring strain, 380–381, 381f

984

Index

Myalgic encephalomyelitis. See Chronic fatigue syndrome Mycophenolate mofetil, for systemic lupus erythematosus, 950t Myelitis, transverse, 952–959 Myelo-radiculo-plexo-neuro-myopathy. See Radiation fibrosis syndrome Myelocele. See Neural tube defects Myelocystocele. See Neural tube defects Myelodysplasia. See Neural tube defects Myelography for cervical radiculopathy, 26 for cervical spinal stenosis, 34–35 for lumbar degenerative disease, 246–248 for lumbar spinal stenosis, 280t Myelomeningocele. See also Neural tube defects. clinical presentation and functional considerations of, 770t Myelopathy, cervical, 33 spondylotic, 1–7 Myelopathy hand, in cervical spinal stenosis, 33–34 Myocardial infarction, rehabilitation after, 678 Myoclonus, 751 Myoelectric prosthetic devices, 655 Myofascial pain syndrome (MPS), 43, 572–580, 574b. See also Abdominal wall pain. Myofascial pelvic pain, 588, 593 Myofascial shoulder pain. See Trapezius strain Myofascial trigger points, 572, 573f in cervicogenic vertigo, 39 Myofasciitis. See Trapezius strain Myogelosis. See Myofascial pain syndrome (MPS) Myomas, 588 Myopathies, 765–768, 766t, 767b Myositis ossificans. See Heterotopic ossification Myotonic dystrophy (MD 1), 766 Myotonic syndromes, 766, 766t

N

N-methyl-D-aspartate receptor antagonists activity, for arachnoiditis, 525 for complex regional pain syndrome, 545 for phantom limb pain, 597 Naproxen, for lumbar facet arthropathy, 254 Narcotics for chronic pain syndrome, 537 for femoral neuropathy, 305 for intercostal neuralgia, 569 for lateral femoral cutaneous neuropathy, 323 for spondylolysis and spondylolisthesis, 275 Nasal noninvasive positive pressure ventilation support, 872f Nash and Moe method, in vertebral rotation, 885 National Cancer Institute Common Terminology Criteria for Adverse Events, 530t National Comprehensive Cancer Network, cancer-related fatigue and, 684 National Osteoporosis Foundation guidelines, for bone mineral density testing, 800 National Trauma database, 652 Navicular fractures, 440–441 Near-infrared spectroscopy, in chronic exertional compartment syndrome, 374

Neck, range of motion, in cervical spondylotic myelopathy, 4 Necrosis, avascular, of lunate. See Kienböck disease Needle electromyography in Achilles tendinopathy, 452 in peroneal (fibular) neuropathy, 421 Neer maneuver, 70 Neer sign, 88f, 88t Nephrolithiasis, 247t Nerve block in adhesive capsulitis, 57 in biceps tendon rupture, 66–67 in lower limb amputations, 660 in lumbosacral plexopathy, 826 in multiple sclerosis, 762 in occipital neuralgia, 583, 583f in phantom limb pain, 597 in suprascapular neuropathy, 113–114 sympathetic, in postherpetic neuralgia, 602 in ulnar neuropathy, 209f Nerve compression test, in carpal tunnel syndrome, 192–193 Nerve conduction studies in brachial plexopathy, 818 in carpal tunnel syndrome, 193 in cervical radiculopathy, 26 in femoral neuropathy, 304–305 in lumbosacral plexopathy, 825 in myopathies, 767 in peripheral neuropathies, 812–813, 813f in peroneal (fibular) neuropathy, 421 in scapular winging, 103 in shin splints, 435–436 in ulnar neuropathy, 207–209 Nerve conduction velocity studies, for Morton’s neuroma, 498 Nerve entrapment, in rheumatoid arthritis, 876–877 Nerve grafting, in lumbosacral plexopathy, 826 Nerve roots, in cervical radiculopathy, 22 Neural tension tests, for lumbar facet arthropathy, 252 Neural tube defects, 769–776, 770t, 773f allergy in, 771 definition of, 769 dermatology in, 771 diagnostic studies for, 773 differential diagnosis of, 773b disease complications in, 774–775 functional limitations in, 771–772, 772t immunology in, 771 nutrition in, 771 physical examination of, 771 symptoms of, 769–771 cardiovascular, 771 endocrine, 771 gastrointestinal, 771 neurological, 770 orthopedic, 770–771 pulmonary, 771 reproductive, 771 urinary, 771 treatment complications in, 775 treatment of, 773–774 Neuralgia intercostal, 566–571, 567f, 568t, 570f occipital, 581–586, 582f, 584f, 585t postherpetic, 599–603 trigeminal, 646–648 Neuralgic amyotrophy, 819 of lumbosacral plexus. See Lumbosacral plexopathy

Neurasthenia. See Chronic fatigue syndrome Neurenteric cyst. See Neural tube defects Neuro-algodystrophy. See Complex regional pain syndrome (CRPS) Neurocompression test, for cervical sprain/ strain, 30 Neuroendocrine testing, 844 Neurogenic bladder, 777–785 differential diagnosis of, 782b functional limitations in, 779 and neural tube defects, 774 pharmacologic action on, 780t physical examination of, 778 symptoms of, 777–778 treatment of, 782–784 Neurogenic bowel, 786–791 definition of, 786–787 diagnostic studies for, 788 disease complications in, 790 functional limitations in, 788 physical examination of, 788 symptoms of, 788 treatment complications in, 790–791 treatment of, 788–790 Neurogenic claudication, 278. See also Lumbar spine, stenosis of Neurogenic heterotopic ossification. See Heterotopic ossification Neurogenic ossifying fibromyositis. See Heterotopic ossification Neurogenic osteoma. See Heterotopic ossification Neurogenic shoulder pain. See Suprascapular neuropathy Neurogenic thoracic outlet, 819 Neurologic examination in lumbosacral spinal cord injury, 926 in post-mastectomy pain syndrome, 604–605 Neurologic rectal examination, in lumbosacral spinal cord injury, 926 Neurologic system, in cervical spinal cord injury disease complications in, 913 ongoing management and health maintenance in, 911–912, 911t physical examination of, 904–905, 905f–906f Neuroma Morton’s, 497–500, 498f postamputation, 660 Neuromodulation, in complex regional pain syndrome, 545 Neuromuscular disorders, respiratory management of, 868–875 definition in, 868 diagnostic studies for, 869 functional limitations in, 869 long-term outcomes of, 870f–872f, 872–873 decannulation of unweanable patients, 873 extubation of unweanable patients, 873, 873t physical examination of, 868 symptoms of, 868 treatment complications in, 873–874 treatment in, 869–872 alveolar ventilation, maintaining, 870 cough flows, augmentation of, 870–871 glossopharyngeal breathing in, 871–872, 871f intervention objectives, 869 oximetry monitoring and feedback protocol in, 872

Index

Neuromuscular disorders, respiratory management of (Continued) pulmonary compliance, lung growth, and chest-wall mobility, maintaining, 869–870 Neuromyelitis optica (Devic’s disease), in transverse myelitis, 954 Neuropathic bladder. See Neurogenic bladder Neuropathic medications, for complex regional pain syndrome, 545 Neuropathic pain, 531, 566 Neuropathy. See also Chemotherapy-induced peripheral neuropathy (CIPN) in burns, 675–676 lateral femoral cutaneous, 321–324, 322f–323f, 322t, 323b peroneal (fibular), 419–423, 420f–421f, 421b radial, 141–145, 142f–144f, 143t, 143b suprascapular. See Suprascapular neuropathy ulnar, wrist, 205–210, 206f–209f, 206t, 209b Neuropeptides, pain-related, leakage of, 246 Neuroprostheses, for transverse myelitis, 957 Neuropsychological evaluations, in polytrauma, 831–832 Neuropsychological testing, for traumatic brain injury, 963 Neurotologic test battery, for cervicogenic vertigo, 40 Neurotoxicity. See Chemotherapy-induced peripheral neuropathy (CIPN) Neurovascular compression, 633 Nighttime wrist splinting, in carpal tunnel syndrome, 193–194, 194f Nitro patches, in biceps tendinopathy, 61 Nitroglycerin, topical, in Achilles tendinopathy, 453 No man’s land, tendon injury, 165 Noble compression test, 386, 387f Nodules flexor tendon, 198f subcutaneous, in rheumatoid arthritis, 876 Non-weight bearing status, in stress fractures, 440–441 Nonarticular rheumatism. See Trapezius strain Noninvasive positive pressure ventilation (NIPPV), in motor neuron disease, 747 Nonmalignant headache disorder. See Headaches Nonne-Milroy-Meige syndrome. See Lymphedema Nonpharmacologic treatment for cluster headache, 563 for migraine, 563 for tension-type headache, 563 Nonspecific work-related upper limb disorders, 618 Nonsteroidal anti-inflammatory drugs (NSAIDs) in Achilles tendinopathy, 453 in acromioclavicular injuries, 49 in adhesive capsulitis, 57 in ankle arthritis, 457 in ankle sprain, 463 in ankylosing spondylitis, 667 in arachnoiditis, 525 in biceps tendinopathy, 61–62 in biceps tendon rupture, 66–67 in bunion, 468 in carpal tunnel syndrome, 193–194 in cervical radiculopathy, 26

Nonsteroidal anti-inflammatory drugs (NSAIDs) (Continued) in cervical spinal stenosis, 36 in cervicogenic vertigo, 40 in chronic pain syndrome, 537 in costosternal syndrome, 552 in femoral neuropathy, 305 in fibromyalgia, 557 in flexor tendon injuries, 168 in glenohumeral instability, 74–75 in hallux rigidus, 483 in hamstring strain, 381–382 in hand and wrist ganglia, 173 in hand osteoarthritis, 177 in hand rheumatoid arthritis, 181, 183 in heterotopic ossification, 733 in hip adductor strain, 300 in iliotibial band syndrome, 387, 389 in Kienböck disease, 189 in knee bursopathy, 401 in knee osteoarthritis, 393 in lateral epicondylitis, 126 in lateral femoral cutaneous neuropathy, 323 in low back strain or sprain, 267 in lumbar facet arthropathy, 254 in lumbar radiculopathy, 259 complications from, 262 in lumbar spinal stenosis, 279 in median neuropathy, 193–194 in meniscal injuries, 407 in myofascial pain syndrome, 575 in occipital neuralgia, 583–585, 585t in olecranon bursitis, 140 in osteoarthritis, 795 in pelvic pain, 592 in posterior cruciate ligament sprain, 428 in postherpetic neuralgia, 602 in pubalgia, 331 in quadriceps tendinopathy, 433 in radiation fibrosis syndrome, 615–616 in repetitive strain injuries, 621 in rheumatoid arthritis, 880t–881t in rotator cuff tendinopathy, 87, 89 in sacroiliac joint dysfunction, 288 in shin splints, 436 in spondylolysis and spondylolisthesis, 274 in stress fractures, 440–441 in systemic lupus erythematosus, 950t in thoracic compression fractures, 229–230 in thoracic radiculopathy, 236 in thoracic sprain or strain, 240–241 in tibial neuropathy, 512 in Tietze syndrome, 643 in trigger finger, 200 in ulnar neuropathy, 209–210 in wrist osteoarthritis, 214, 218 in wrist rheumatoid arthritis, 223, 226 Nonsteroidal anti-inflammatory therapy, for plantar fasciitis, 503 Nonvertiginous dizziness, 843 Nortriptyline, in occipital neuralgia, 585t Novel medications, for complex regional pain syndrome, 546 NPUAP Pressure Ulcer Scale for Healing (PUSH Tool), for pressure ulcers, 852 Numbness in carpal tunnel syndrome, 191–192, 192f in cervical spinal cord injury, 903t–904t Nurick scale, in cervical spinal stenosis, 36, 37t Nutrition, in pulmonary rehabilitation (PR), 862 Nutritional status, in motor neuron disease, 746

O

985

Ober test, in iliotibial band syndrome, 385–386, 386f Obesity knee osteoarthritis and, 391 in neural tube defects, 771 O’Brien sign, 88t O’Brien test, 60, 70–71 Occipital headache. See Occipital neuralgia Occipital myalgia-neuralgia syndrome. See Occipital neuralgia Occipital nerve, 581 anatomy of, 582f blockade of, 583 stimulation of, 584, 584f Occipital neuralgia, 581–586, 582f, 582b–583b, 584f, 585t Occipital neuritis. See Occipital neuralgia Occipital neuropathy. See Occipital neuralgia “Occult” cyst, 169 Occupational overuse, 618 Occupational therapy in acromioclavicular injuries, 50 in brachial plexopathy, 820 in cerebral palsy, 694 in cervical spinal stenosis, 36 in cervicogenic vertigo, 40 in complex regional pain syndrome, 546 in knee bursopathy, 401 in lower limb amputations, 662 in Parkinson disease, 809 in trapezius strain, 44 in traumatic brain injury, 964 in wrist rheumatoid arthritis, 223 Off-the-shell orthosis, in thoracic compression fracture, 231f Olecranon bursitis, 137–140 diagnostic studies for, 138, 138f differential diagnosis of, 139b functional limitations in, 138 physical examination of, 137–138, 138f potential disease complications of, 139–140 potential treatment complications of, 140 symptoms of, 137 treatment of, 139 Olfactory nerve, in postconcussion symptoms, 844 Oligoclonal bands, in transverse myelitis, 955 Olivopontocerebellar degeneration, 751 Onabotulinum toxin A, 892, 893t injections, in headaches, 564 Ondansetron, for cervicogenic vertigo, 40 One-legged hop test, in stress fractures, 439 Open injuries, in femoral neuropathy, 304t “Opera glass hands” deformity. See Arthritis mutilans Ophthalmic zoster, 600 Opiates in post-mastectomy pain syndrome, 605–606 in post-thoracotomy pain, 609 in upper limb amputations, 654 Opioids for arachnoiditis, 525 for burns, 673 for cancer pain, 687 for central post-stroke pain, 630 for chronic pain syndrome, 537 for complex regional pain syndrome, 545 for fibromyalgia, 557 for low back strain or sprain, 267 for lumbar degenerative disease, 249 for lumbar facet arthropathy, 254 for lumbar radiculopathy, 260–261 complications from, 262 for lumbar spinal stenosis, 279

986

Index

Opioids (Continued) for meniscal injuries, 407 for radiation fibrosis syndrome, 615–616 for total knee arthroplasty, 444–445 Optic neuritis, from ophthalmic zoster, 602 Oral antispasticity medications, 891, 892t Oral bisphosphonate treatment, 839 Oral contraceptive pill, pelvic pain, 593 Oral-motor control, in cerebral palsy, 690 Oral ulcerations, in systemic lupus erythematosus, 945–946 Orbital apex syndrome, 602 Ordinary headache. See Tension-type headache Orthosis for ankle arthritis, 457 back, for osteoporosis, 804 for bunion, 468 foot, for tibial neuropathy, 512 for hand rheumatoid arthritis, 181 for peroneal (fibular) neuropathy, 422 for shin splints, 436 spinal, for thoracic compression fractures, 229–230, 231f for thoracic compression fractures, 229–230 treatment of, stroke and, 935 Orthostatic intolerance, in chronic fatigue syndrome, 698 Orthotic devices in radiation fibrosis syndrome, 615 in spasticity, 891 Orthotics functional, in hammer toe, 487 in transverse myelitis, 958 Ortolani maneuver, in cerebral palsy, 693t Osgood-Schlatter disease, 410 Ossifying fibromyopathy. See Heterotopic ossification Osteitis pubis, 331. See also Pubalgia Osteoarthritis, 792–798, 793f acromioclavicular. See Acromioclavicular injuries clinical features of, 794t collateral ligament sprain and, 369 definition of, 792–793 diagnostic studies for, 794 differential diagnosis of, 794b elbow, 116–117 of the first metatarsophalangeal joint. See Hallux rigidus functional limitations in, 794 of the great toe. See Hallux rigidus hand, 174–178, 175f, 175b knee, 391–398 definition of, 391 diagnostic studies for, 392–393, 393f disease complications of, 397 functional limitations in, 392 initial treatment of, 393 physical examination of, 392, 392t procedures for, 394–395, 395f, 395t rehabilitation for, 393–394 surgery for, 396–397, 396t symptoms of, 391–392 treatment complications in, 397 physical examination of, 793–794 risk factors for, 793t secondary, 211, 792, 793t shoulder. See Shoulder, arthritis of of the spine. See Lumbar degenerative disease symptoms of, 793 treatment of, 795–797 wrist, 211–218, 212f, 214b, 215f–216f secondary to malunited wrist fracture, 211, 212f

Osteoarthrosis. See Osteoarthritis, knee Osteochondral autograft transfer (OAT), for knee chondral injuries, 364–365 Osteochondritis dissecans. See Knee, chondral injuries Osteodystrophy. See Complex regional pain syndrome (CRPS) Osteomalacia, 247t Osteophytes in burns, 675 formation in wrist osteoarthritis, 212–213 of hallux rigidus, 482 in knee osteoarthritis, 392 Osteoporosis, 238, 247t, 799–805 in ankylosing spondylitis, 668 causes of, 800t diagnostic studies for, 800–801, 800t differential diagnosis of, 801b disease complications of, 804 functional limitations in, 799 physical examination of, 799, 800t risk factors for, 800t symptoms of, 799 in thoracic spinal cord injury, treatment of, 920 treatment complications of, 804–805 treatment of, 801–804, 801t–802t Osteotomy for ankylosing spondylitis, 668 for knee osteoarthritis, 396, 396t for osteoarthritis, 797 for posterior tibial tendon dysfunction, 508 Ottawa ankle rules, 462, 463f Outerbridge classification, of cartilage lesions, 362, 363f Overuse syndromes, 618 Oxandrolone, for burns, 674 Oxcarbazepine, for trigeminal neuralgia, 647 Oximetry monitoring, in neuromuscular disorders, 872 Oxybutynin, 780t Oxycodone for lumbar facet arthropathy, 254 for lumbar radiculopathy, 260–261 Oxygen therapy, supplemental, in pulmonary rehabilitation (PR), 863

P

Pace sign, 325, 326t Paget disease, 247t Pain, 533 abdominal wall, 515–522 in Achilles tendinopathy, 451–452 acromioclavicular. See Acromioclavicular injuries in ankle arthritis, 456 antecubital fossa, in biceps tendon rupture, 64 in anterior chest wall, 549 in anterior cruciate ligament sprain, 351 in arachnoiditis, 523 around metatarsal heads. See Metatarsalgia in Bankart lesion, 78 behaviors, in chronic pain syndrome, 533 in brachial plexopathy, 816–817 in bunion, 466 in burns, 670, 673, 675 central post-stroke pain, 629 in cerebral palsy, 690 cervical. See Cervical spine; facet arthropathy of in cervical dystonia, 18 in cervical spinal cord injury, 903t–904t

Pain (Continued) treatment of, 912 upper extremity, surgery for, 913 in chemotherapy-induced peripheral neuropathy, 529 chest wall, 549, 566 chronic. See Chronic pain syndrome in chronic ankle instability, 471 in chronic fatigue syndrome, 698 coccygeal, 538 complex regional, 543–548 control, in rotator cuff tendinopathy, 87–88 in femoral neuropathy, 303 in fibromyalgia, 556 foot in posterior tibial tendon dysfunction, 507 in tibial neuropathy, 510–511 forefoot, in metatarsalgia, 493 groin, in hip labral tears, 315 in hallux rigidus, 482 in hammer toe, 486 hand in carpal tunnel syndrome, 191–192 in rheumatoid arthritis, 179 in headache, 561 in hip adductor strain, 298 in hip adhesive capsulitis, 293 in hip disease, 338 in hip osteoarthritis, 307–308 knee chondral injuries, 363 in collateral ligament sprain, 367 differential diagnosis of, 393b in iliotibial band syndrome, 384–385 in osteoarthritis, 392 in patellar tendinopathy, 410 in quadriceps tendinopathy, 431 in lateral femoral cutaneous neuropathy, 321 leg in lumbar spinal stenosis, 278 in lumbosacral plexopathy, 825 in lumbar facet arthropathy, 252 in lumbar radiculopathy, 257 in lumbosacral spinal cord injury rehabilitation for, 928–929 treatment of, 929 upper extremity, surgery for, 929 in mallet toe, 490 management of, in motor neuron disease, 746 in multiple sclerosis, 757, 759t, 761 in myofascial trigger points, 572 in myopathies, 766 neck in cervical degenerative disease, 12 in cervical radiculopathy, 22 in cervical spinal stenosis, 33 in cervical sprain/strain, 29, 30f in cervicogenic vertigo, 39 prevalence of, 12 neuropathic, 612–613 in osteoarthritis, 793 in osteoporosis, 799 in Parkinson disease, 806 patterns of, in thoracic radiculopathy, 235f pelvic, 587–595 chronic, 587 myofascial, 588, 593 in peripheral arterial disease, 719 in peripheral neuropathies, 811, 814 peritrochanteric, 346 phantom limb, 596–598, 659 in piriformis syndrome, 325

Index

Pain (Continued) in plantar fasciitis, 501 plantar forefoot, 493 post-mastectomy pain syndrome, 604–607 in post-thoracotomy pain syndrome, 608–611 in postherpetic neuralgia, 599 in postpoliomyelitis syndrome, 835, 837–838 pseudospine, 247t in pubalgia, 329 in quadriceps contusion, 333 refractory knee, after total knee arthroplasty, 443 in repetitive strain injuries, 619–620 residual limb, in upper limb amputations, 654 sacroiliac joint. See Sacroiliac joint, dysfunction of shoulder in adhesive capsulitis, 53–54 in biceps tendinopathy, 59 in glenohumeral instability, 70 in rotator cuff tear, 91 in rotator cuff tendinopathy, 84 in scapular winging, 101 in shoulder arthritis, 106 in suprascapular neuropathy, 113 in SLAP tear, 77 in stress fractures, 439 in stroke, in young adults, 938, 939t initial treatment of, 942 physical examination of, 940 procedures for, 942 rehabilitation and, 942 surgery for, 942 in thoracic compression fracture, 228 in thoracic outlet syndrome, 634 in thoracic spinal cord injury, treatment of, 918 in thoracic sprain or strain, 240 in Tietze syndrome, 640–641, 641f–642f in trapezius strain, 43 treatment of, stroke and, 935 in trigeminal neuralgia, 646 in ulnar collateral ligament sprain, 201 wrist in wrist osteoarthritis, 212 in wrist rheumatoid arthritis, 221–222 Pain-relieving modalities, for thoracic compression fracture, 230 Painful phantom sensation. See Phantom limb pain Painful xiphoid syndrome, 551 Pallidotomy, in Parkinson disease, 809 Palmar grasp response, in cerebral palsy, 693 Palmar oblique ligament, reconstruction of, hand osteoarthritis and, 177 Palmaris brevis sign, “neurographic”, 207–209 Palpation, in plantar fasciitis, 501 Palpation technique, flat, in myofascial pain syndrome, 573–574, 574f Pamidronate, for ankylosing spondylitis, 667 Pancoast syndrome, 819 Pancreatitis, 247t Panner disease, 117 “Paper pull-out test”, 493–494 Paraffin baths, for wrist rheumatoid arthritis, 223 Parainfectious myelopathy, in transverse myelitis, 955t Paralabral cyst, suprascapular neuropathy and, 114 Paralysis, infantile, 834 Paralysis agitans. See Parkinson disease

Paraneoplastic dysfunction. See Cancerrelated fatigue Paraosteoarthropathy. See Heterotopic ossification Paraplegia. See Lumbosacral spinal cord injury; Thoracic spinal cord injury heterotopic ossification in. See Heterotopic ossification Parasternal chondrodynia. See Tietze syndrome Parasympathetic nerves, 777 Parathyroid hormone, for osteoporosis, 803 Parenting, stroke and, 941 Paresthesias in carpal tunnel syndrome, 191–192, 192f in cervical radiculopathy, 23 in chronic fatigue syndrome, 698 in lumbar radiculopathy, 257 in multiple sclerosis, 757 Parkinson disease, 806–810 definition of, 806 diagnostic studies for, 807 differential diagnosis of, 807b disease complications in, 755, 810 functional limitations in, 807 physical examination of, 806–807 symptoms of, 750–751, 806 treatment of, 752–755, 753f, 807–809 urinary dysfunction in, 778 “Parkinsonism pugilistica”, 751 Paroxysmal pain, 566 Pars interarticularis, defect in, 269. See also Lumbar spine, spondylolisthesis of Parsonage-Turner syndrome. See Brachial plexopathy Partial rupture of the patellar ligament. See Patellar tendinopathy Passive joint mobilization (PJM), for cervicogenic vertigo, 40 Passive mobilization techniques, for hip adhesive capsulitis, 295 Passive range-of-motion exercises, for spasticity, 891 Patella, Q angle of, 415, 415f Patella clunk syndrome, 449 Patellalgia. See Patellofemoral syndrome (PFS) Patellar apicitis. See Patellar tendinopathy Patellar pain. See Patellofemoral syndrome (PFS) Patellar tendinitis. See Patellar tendinopathy Patellar tendinopathy, 410–413, 412f definition of, 410 diagnostic testing for, 411 differential diagnosis of, 411b disease complications of, 412 functional limitations in, 411 physical examination of, 411 symptoms of, 410–411 treatment of, 411–412 Patellar tendinosis. See Patellar tendinopathy Patellofemoral arthralgia. See Patellofemoral syndrome (PFS) Patellofemoral replacement, for knee osteoarthritis, 396, 396t Patellofemoral syndrome (PFS), 414–418, 415f–417f, 415t definition of, 414 diagnostic testing for, 415 differential diagnosis of, 416b disease complications of, 417 functional limitations in, 415 physical examination of, 414–415 symptoms of, 414 treatment of, 415–417

987

Pathognomonic sign, of scoliosis, 884 Patient education, in chronic pain syndrome, 535 Patient Health Questionnaire-9 (PHQ-9), 686, 843 Patrick test, 286, 286f in hip labral tears, 315–316 in hip osteoarthritis, 308, 308f in low back strain or sprain, 266t Paxinos sign, in acromioclavicular injuries, 48, 49f Pectineus syndrome. See Pubalgia Pellegrini-Stieda disease, 369 Pelvic congestion syndrome, pelvic pain and, 589 Pelvic examination, in neurogenic bladder, 778 Pelvic inflammatory disease, 247t Pelvic nerve, 786 Pelvic pain, 587–595 chronic, 587 definition of, 587 diagnostic studies for, 592 differential diagnosis of, 592b functional limitations in, 591 initial treatment of, 592–594 myofascial, 588, 593 physical examination of, 589–590, 590f–591f potential disease complications of, 594 potential treatment complications of, 595 procedures for, 594 rehabilitation for, 594 symptoms of, 589 Pelvic rock, in low back strain or sprain, 266t Pelvic tension myalgia. See Coccydynia Pelvic tumors, 824 Pendulum exercise, for adhesive capsulitis, 56f, 57 Penn Spasm Frequency Scale, for spasticity, 891, 891t Perceived exertion, 681, 682f Percutaneous endoscopic gastrostomy, for motor neuron disease, 747 Percutaneous laser disk decompression (PLDD), for cervicogenic vertigo, 40 Percutaneous transluminal angioplasty, 722 Perdriolle Torsiometer, 885 Pergolide, for Parkinson disease, 808, 808t Periarthritis of the shoulder. See Adhesive capsulitis Periarticular adhesions. See Adhesive capsulitis Periarticular ossification. See Heterotopic ossification Pericardiocentesis, for cancer-related fatigue, 687 Perineural fibroma. See Morton’s neuroma Periostitis. See Shin splints Peripheral arterial disease, 719–723 diagnostic studies for, 720 differential diagnosis of, 720b disease complications of, 722–723 functional limitations in, 720 physical examination of, 720 symptoms of, 719–720 treatment complications of, 723 treatment of, 721–722, 721t Peripheral nerves disorders of, 812t tumors of, 819 Peripheral neuropathies, 811–815 axonal, 811–812, 814 chemotherapy-induced, 529–532, 530t definition of, 811 demyelinating, 812

988

Index

Peripheral neuropathies (Continued) diagnostic studies for, 812–813, 813f, 813t differential diagnosis of, 813b disease complications of, 814 functional limitations in, 812 physical examination of, 811–812 symptoms of, 811 treatment complications of, 814–815 treatment of, 814 Peripheral polyneuropathy, in diabetes, 720 Peritendinitis. See de Quervain tenosynovitis Peritendinosis. See Achilles tendinopathy Peroneal nerve palsy, common, in total knee arthroplasty, 449 Peroneal (fibular) neuropathy, 419–423 definition of, 419, 420f diagnostic studies for, 421 differential diagnosis of, 421b disease complications of, 422 functional limitations in, 420 physical examination of, 420, 420f–421f symptoms of, 419–420 treatment of, 421–422 Pes anserine bursopathy, 400 Pes planus, asymmetric. See Posterior tibial tendon dysfunction Phalen test, 192–193, 193f, 221 Phantom breast pain. See Post-mastectomy pain syndrome Phantom limb pain, 596–598, 597t, 598b, 659 Phantom limb sensation, 659 Phantom limb syndrome. See Phantom limb pain Phantom pain. See Phantom limb pain Phenol, injection, for cerebral palsy, 694–695 Phenytoin, for trigeminal neuralgia, 647 Phlebolymphedema, 735 Phlebothrombosis. See Deep venous thrombosis Phonation, 896 Phosphodiesterase type 5 inhibitors, for post-stroke symptoms, 933t Photosensitivity, in systemic lupus erythematosus, 945–946 Physical aids, in pulmonary rehabilitation (PR), 865 Physical modalities, for Tietze syndrome, 644 Physical therapy in acromioclavicular injuries, 50 in cervical spinal stenosis, 36 in complex regional pain syndrome, 546 in greater trochanteric pain syndrome, 348 in lumbar facet arthropathy, 254 in thoracic compression fracture, 230 in thoracic radiculopathy, 236 in thoracic sprain or strain, 241 in trapezius strain, 44 in traumatic brain injury, 964 in wrist rheumatoid arthritis, 223 Physiotherapeutic Scoliosis Specific Exercises (PSSE), 887 “Piano Key Sign”, in hand rheumatoid arthritis, 183 Pinched nerve. See Lumbar radiculopathy Pinhole skeletal scintigraphy, in Tietze syndrome, 643 Piriformis muscle, 325, 326f Piriformis sign, 326t Piriformis syndrome, 247t, 325–328 definition of, 325 diagnostic testing for, 325–326 differential diagnosis of, 326b functional limitations with, 325

Piriformis syndrome (Continued) initial treatment of, 326 physical examination of, 325, 326t potential disease complications of, 327 potential treatment complications of, 327 procedures for, 326–327, 327f rehabilitation for, 326 surgery for, 327 symptoms of, 325 treatment of, 326–327 Pitcher’s elbow. See Medial epicondylitis Pivot shift test, 351, 352f “Place and hold” therapy, in flexor tendon injuries, 168 Plain myelography, in lumbar spinal stenosis, 280t Plain radiographs in shin splints, 435 in systemic lupus erythematosus, 948 in total knee arthroplasty, 444 weight-bearing, in bunion, 467 Plantar fasciitis, 501–505, 502f definition of, 501 diagnostic testing of, 502–503, 503f differential diagnosis of, 503b functional limitations in, 501–502 physical examination of, 501 potential disease complications of, 504 potential treatment complications of, 504 procedures for, 504 rehabilitation for, 503–504 symptoms of, 501 treatment of, 503–504 Plantar fasciosis. See Plantar fasciitis Plantar forefoot pain. See Metatarsalgia Plantar plate tear, hammertoe with, 494f Plastic removable walking cast boots, 463 Platelet-rich plasma (PRP) for hamstring strain, 382 for hand and wrist ganglia, 172 for hip adductor strain, 300–301 for meniscal injuries, 408 for rotator cuff tendinopathy, 89 Platinum agents, 529 Pleural effusions, in rheumatoid arthritis, 876 Pleuritic chest pain, in systemic lupus erythematosus, 946 Pleuritis, in rheumatoid arthritis, 876 Pleurocentesis, for cancer-related fatigue, 687 Plexopathy brachial, 816–821, 818b diabetic, 825 lumbosacral, 822–827, 826b neoplastic, 824 Plumber’s elbow. See Olecranon bursitis Plumbline, 884 Plyometrics, in shin splints, 436 Pneumatic leg brace, for stress fractures, 441 Pneumothorax, in Tietze syndrome, 645 Poliomyelitis, 834 Poliomyelitis sequelae. See Postpoliomyelitis syndrome Polyethylene glycol, for bowel management, 919t Polymerase chain reaction (PCR) technique, in transverse myelitis, 954–955 Polymyalgia rheumatica, 247t Polymyographic electromyography (pEMG), for cervical dystonia, 19 Polyneuropathies. See Peripheral neuropathies Polyradiculopathy, diabetic, 247t Polysomnography, in postconcussion symptoms, 844

Polytrauma definition of, 829 distribution of, 830f impairments in, examples of, 831t potential disease complications of, 832, 833t potential treatment complications of, 833, 833t rehabilitation for, 828–833 system of care for, history of, 829 technology for, 832 Poor circulation. See Foot, diabetic; Peripheral arterial disease Popliteal angle maneuver, 692–693, 693t Popliteal cysts, 358 Popliteal vein, deep venous thrombosis of, 713f Portable memory aids, for traumatic brain injury, 964 POSH test, for sacroiliac joint dysfunction, 286–287 Positioning, in joint contractures, 708 Positron emission tomography, in cancerrelated fatigue, 685 Post-axillary dissection pain. See Postmastectomy pain syndrome Post-exertional malaise, in chronic fatigue syndrome, 698 Post-mastectomy lymphedema. See Lymphedema Post-mastectomy pain syndrome, 604–607 anatomy relevant to, 605 definition of, 604 diagnostic studies for, 605 differential diagnosis of, 605b functional limitations in, 605 initial treatment of, 605–606 physical examination of, 604–605 potential disease complications of, 606 potential treatment complications of, 606 procedures for, 606 rehabilitation for, 606 surgery for, 606 symptoms of, 604 Post-stroke shoulder pain, 939t Post-thoracotomy pain syndrome (PTPS), 608–611 complications of, 610 definition of, 608 diagnostic studies for, 609 differential diagnosis of, 609b factors associated with, 609t functional limitations in, 608–609 initial treatment of, 609 physical examination of, 608 potential disease complications of, 610 potential treatment complications of, 610 procedures for, 610 rehabilitation for, 609–610 symptoms of, 608 Post-thrombotic syndrome, 717 Post-traumatic arthritis. See Elbow, arthritis of of wrist. See Osteoarthritis; wrist Post-traumatic dystrophy. See Complex regional pain syndrome (CRPS) Post-traumatic osteoporosis. See Complex regional pain syndrome (CRPS) Post-traumatic syringomyelia in cervical spinal cord injury, surgery for, 913 in lumbosacral spinal cord injury, surgery for, 929 Post-viral fatigue syndrome. See Chronic fatigue syndrome

Index

Postconcussion symptoms, 841–848, 842f, 844b, 845t Postconcussive disorders. See Postconcussion symptoms Posterior compartment deep, of leg, 372, 372f superficial, of leg, 372, 372f Posterior cruciate ligament (PCL), 424 avulsion fractures, 428 injuries, classification of, 425t reconstruction of, 429 sprain of, 424–430, 425f–427f, 426t, 427b Posterior cruciate ligament tear. See Posterior cruciate ligament (PCL), sprain of Posterior drawer test, for posterior cruciate ligament sprain, 425–426, 426f Posterior element disorder. See Cervical spine, facet arthropathy of, Lumbar facet arthropathy Posterior hip impingement test, for hip labral tears, 315–316 Posterior interosseous nerve dysfunction, in wrist rheumatoid arthritis, 221 Posterior Lachman test, in posterior cruciate ligament sprain, 426 Posterior sag test, in posterior cruciate ligament sprain, 426, 426f Posterior shear test, for sacroiliac joint dysfunction, 286–287 Posterior tarsal tunnel syndrome. See Tibial neuropathy Posterior thigh injury. See Hamstring, strain of Posterior tibial nerve entrapment. See Tibial neuropathy Posterior tibial tendon dysfunction, 506–509 definition of, 506 diagnostic studies for, 507 differential diagnosis of, 507b functional limitations in, 507 physical examination of, 506–507 potential disease complications of, 508 potential treatment complications of, 508 procedures for, 508 rehabilitation for, 508 symptoms of, 506 treatment of, 508 Posteroanterior radiograph, for spinal deformities, 885 Postherpetic neuralgia, 599–603, 600b Postpolio. See Postpoliomyelitis syndrome Postpoliomyelitis syndrome, 834–840, 835t, 837b, 838f Postural kyphosis. See Kyphosis Posture head, 19, 19t poor, 238 static and dynamic assessment of, 240 Pramipexole, in Parkinson disease, 808, 808t Prealbumin concentration, in pressure ulcers, 853 Prednisone, for cervical degenerative disease, 14–15 Preemptive analgesia, in post-thoracotomy pain syndrome, 609 Pregabalin in arachnoiditis, 525, 525t in cervical degenerative disease, 14–15 in chemotherapy-induced peripheral neuropathy, 531 in fibromyalgia, 557 in intercostal neuralgia, 569 in multiple sclerosis, 760 in occipital neuralgia, 585t in postherpetic neuralgia, 601–602 in radiation fibrosis syndrome, 615–616 Preganglionic sympathetic neurons, 777

Pregnancy, ectopic, 247t Preiser disease, 211 Premature atherosclerosis, in systemic lupus erythematosus, 950 Prepatellar bursopathy, 400, 400f Pressure, at sacral sulcus, in low back strain or sprain, 266t Pressure over the sacral sulcus, in sacroiliac joint dysfunction, 287 Pressure sores. See also Pressure ulcers in joint contractures, 708 Pressure ulcers, 849–859, 850t, 852f, 853b, 854f–855f in cervical spinal cord injury surgery for, 912 treatment of, 912 in lumbosacral spinal cord injury prevention of, 929 surgery for, 929 treatment of, 929 PRICE (protection, rest, ice, compression, and elevation) for ankle sprain, 463 for chronic exertional compartment syndrome, 375 for collateral ligament sprain, 368 for knee bursopathy, 401 for knee osteoarthritis, 393 for posterior cruciate ligament sprain, 428 for stress fractures, 440–441 Primary adamantinoma, 434 Primary degenerative arthritis. See Elbow, arthritis of Primary lateral sclerosis, 740 Primary lymphedema. See Lymphedema Primary progressive aphasia, 895 Proctalgia fugax, 539 Progestin, pelvic pain, 593 Progressive bulbar palsy, 740 Progressive muscular atrophy, 740 Progressive supranuclear palsy, 751 Prokinetic drugs, in neurogenic bowel, 789 Prolotherapy for chronic ankle instability, 473 for coccydynia, 541 for sacroiliac joint dysfunction, 288 Pronator syndrome. See Median neuropathy Pronator teres nerve block, 135f Pronator teres syndrome, 131, 132f. See also Median neuropathy diagnostic studies for, 133 differential diagnosis of, 134b functional limitations in, 133 initial treatment of, 134 physical examination of, 132 potential disease complications of, 135 rehabilitation for, 134, 134f symptoms of, 131–132 Prophylactic therapy for cluster headache, 563 for migraine, 563 for tension-type headache, 563 Prophylaxis, in deep venous thrombosis, 714 Propiverine, 780t Propranolol, for essential tremor, 753 Proprioceptive drills, in posterior tibial tendon dysfunction, 508 Proprioceptive exercises in hip labral tears, 318 in suprascapular neuropathy, 114 Proprioceptive neuromuscular facilitation, for quadriceps contusion, 335 Proprioceptive training in ankle sprain, 464 in chronic ankle instability, 473 in rotator cuff tendinopathy, 89

989

Prostatitis, 247t Prosthesis bent-knee, 707f in lower limb amputations, 659, 662, 662t in phantom limb pain, 597 in total knee arthroplasty, 447, 448f in upper limb amputations, 653 Protein depletion, in pressure ulcers, 850 Provocative maneuvers, 620 for lumbar facet arthropathy, 252 for wrist osteoarthritis, 213 Prow beak deformity. See Bursitis, foot and ankle Proximal phalanx osteotomy, of hallux rigidus, 483–484 Proximal radial-ulnar synostosis, in biceps tendon rupture, 67 Proximal row carpectomy, in wrist osteoarthritis, 215–216, 215f–216f Pruritus, in burns, 670, 673, 675 Pseudobulbar affect, in motor neuron disease, 744 Pseudoclaudication, 278. See also Lumbar spine, stenosis of Pseudodystonia, 18 Pseudospine pain, 247t Psoas syndrome, 824 Psychological approach, in myofascial pain syndrome, 575 Psychological comorbidity, in burns, 674 Psychological complaints, in chronic fatigue syndrome, 698 Psychological complications, in burns, 676 Psychological counseling, in postconcussion symptoms, 845 Psychological examination, for chronic fatigue syndrome, 698 Psychological interventions, in chronic pain syndrome, 535 Psychological treatment, for Tietze syndrome, 644 Psychopharmacologic treatment, for Tietze syndrome, 644 Psychosocial system, in cervical spinal cord injury disease complications in, 914 ongoing management and health maintenance in, 912 Psychostimulants, in postconcussion symptoms, 846 Psyllium powder, for bowel management, 919t Pubalgia, 329–332 definition of, 329 diagnostic studies for, 331 differential diagnosis of, 331b functional limitations with, 331 physical examination of, 329–331 potential disease complications of, 331 potential treatment complications of, 331 symptoms of, 329 treatment of, 331 Puborectalis syndrome. See Coccydynia Pudendal nerves, 777 “Pulled muscle” in the low back. See Low back strain or sprain Pulled upper back. See Thoracic sprain or strain Pulmonary compliance, maintaining, in neuromuscular disorders, 869–870 Pulmonary rehabilitation (PR) behavioral management in, 865 definition of, 860 diagnostic studies for, 860–861, 861t functional limitations in, 860 for motor neuron disease, 747

990

Index

Pulmonary rehabilitation (PR) (Continued) organization of comprehensive rehabilitation program, 861 physical examination of, 860 in post-thoracotomy pain syndrome, 610 result of, 865 symptoms in, 860 therapeutic interventions in, 861–865 airway secretions, elimination of, 862–863 counseling and general medical care, 862 exercise, 863–864 inspiratory resistive exercises, 863 medications, 861 nutrition, 862 physical aids, 865 respiratory muscle rest, 863 retraining of breathing, 862 supplemental oxygen therapy, 863 treatment complications in, 865 treatment in, 861–865 Pulsed radiofrequency, for coccydynia, 541 Pump bump, 475

Q

Q angle, 415, 415f Quadriceps active test, in posterior cruciate ligament sprain, 426, 426f Quadriceps contusion, 333–336 definition of, 333 diagnostic studies for, 334 differential diagnosis of, 334b functional limitations with, 334 initial treatment of, 334–335 physical examination of, 333–334 potential disease complications of, 335 potential treatment complications of, 335 procedures for, 335 rehabilitation for, 335 surgery for, 335 symptoms of, 333 Quadriceps tendinitis. See Patellar tendinopathy Quadriceps tendinopathy, 431–433, 431b, 432f–433f Quadriceps tendinosis. See Quadriceps tendinopathy Quadriceps tendon, 431 anatomy of, 432f rupture of, 333–334 ultrasound image of, 433f Quadriceps testings, 303 Quadriplegia. See Cervical spinal cord injury

R

Radial deviation, in wrist rheumatoid arthritis, 220–221 Radial nerve compression. See Radial neuropathy Radial nerve palsy. See Radial neuropathy Radial neuropathy, 141–145, 142f diagnostic studies for, 142, 143f differential diagnosis of, 143b functional limitations in, 142 physical examination of, 142 potential disease complications of, 144 potential treatment complications of, 144 symptoms of, 141–142, 143t treatment of, 143–144, 144f Radial palsy splint, 144f Radial pulse, in thoracic outlet syndrome, 635 Radial shortening, in Kienböck disease, 189

Radial tunnel syndrome. See Radial neuropathy Radiation fibrosis syndrome, 612–617, 613f–614f, 615b Radiation fields, used to treat Hodgkin lymphoma, 613f Radiation-induced cervical dystonia. See Radiation fibrosis syndrome Radiation therapy for cancer-related fatigue, 687 for heterotopic ossification, 733 Radiculitis, lumbar, 257 Radiculopathy cervical, 22–28 lumbar, 257–263, 258f, 258t thoracic, 234–237 Radiculoplexus neuropathy, lumbosacral, 824 Radiofrequency denervation, for cervical facet arthropathy, 10, 10f Radiofrequency neurotomy (RFN) for lumbar facet arthropathy, 254, 255f for sacroiliac joint dysfunction, 288 Radiofrequency thermocoagulation, for trigeminal neuralgia, 647–648 Radiographic grading scales, in stress fractures, 440 Radiography in adhesive capsulitis, 54–55 in ankle arthritis, 457, 457f in ankylosing spondylitis, 666–667 in anterior cruciate ligament sprain, 351 in biceps tendinopathy, 60–61 in biceps tendon rupture, 66 in carpal tunnel syndrome, 192f, 193 in cervical degenerative disease, 14 in cervical dystonia, 18 in cervical spondylotic myelopathy, 4 in cervical sprain/strain, 30, 30f in cervicogenic vertigo, 40 chest, in systemic lupus erythematosus, 948 in chronic ankle instability, 472 in coccydynia, 539f, 540 in collateral ligament sprain, 368 in complex regional pain syndrome, 545 in costosternal syndrome, 552 in flexor tendon injuries, 167 in foot and ankle bursitis, 477, 477t in glenohumeral instability, 71 in hallux rigidus, 482 in hamstring strain, 380–381 in hand and wrist ganglia, 171–172 in hand osteoarthritis, 175 in hand rheumatoid arthritis, 180, 181f in heterotopic ossification, 730, 730f in hip adhesive capsulitis, 293 in hip disease, 338–340, 339f–340f in hip labral tears, 317 in hip osteoarthritis, 308, 309f in Kienböck disease, 186, 186f in knee osteoarthritis, 392, 393f in lumbar degenerative disease, 246, 248f in lumbar radiculopathy, 259 in lumbar spinal stenosis, 280t in mallet toe, 490–491 in meniscal injuries, 406 in Morton’s neuroma, 498 in osteoarthritis, 794 in patellar tendinopathy, 411 pelvis, in pubalgia, 331 in polytrauma, 831 in post-thoracotomy pain syndrome, 609 in postconcussion symptoms, 844 in posterior tibial tendon dysfunction, 507, 507f in postpoliomyelitis syndrome, 837

Radiography (Continued) in quadriceps contusion, 334 in radiation fibrosis syndrome, 614 in repetitive strain injuries, 621 in scapular winging, 103 in shoulder arthritis, 107, 107f in spondylolysis, 271, 271f in thoracic compression fractures, 229, 230f in thoracic outlet syndrome, 636 in thoracic radiculopathy, 235 in Tietze syndrome, 641 in ulnar collateral ligament sprain, 202 in ulnar neuropathy, 207 in wrist osteoarthritis, 213, 215f, 217f in wrist rheumatoid arthritis, 221, 222f–223f Radiologic studies, in brachial plexopathy, 818 Radionuclide bone scanning, in shin splints, 435 Raimondi method, in vertebral rotation, 885 Raloxifene, for osteoporosis, 802 Ramisectomy, for cervical dystonia, 20 Ramsay Hunt syndrome, 600 Rancho Los Amigos Scale, 962 Range of motion (ROM) in ankle arthritis, 456 in ankle sprain, 463–464 cervical spine, in radiculopathy, 23 in chronic ankle instability, 473 in femoral neuropathy, 306 in hamstring strain, 382 hip, 329–331 adductor strain, 300 labral tears of, 318 osteoarthritis of, 308 joint, contractures, 706t knee in meniscal injuries, 407–408 in total knee arthroplasty, 444t, 447 in mallet toe, 490 in post-thoracotomy pain syndrome, 605, 610 in quadriceps tendon, 333 shoulder in acromioclavicular injuries, 47 in adhesive capsulitis, 53–54 in biceps tendinopathy, 59–60 in glenohumeral instability, 70 in rotator cuff tear, 91 in rotator cuff tendinopathy, 85, 86f in shoulder arthritis, 107 in thoracic radiculopathy, 235 in wrist osteoarthritis, 213–214 Range of motion (ROM) testing, for cervicogenic vertigo, 39 Rasagiline, in Parkinson disease, 808, 808t Raynaud phenomenon, in systemic lupus erythematosus, 946 REAB test, in sacroiliac joint dysfunction, 287 Reactive depression, motor neuron disease and, 744 Reconstruction, of anterior cruciate ligament (ACL), 353, 353f Recreational therapist, 536 Rectal bleeding, in cervical spinal cord injury, 903t–904t Rectus abdominis, 330f Rectus abdominis nerve syndrome. See Abdominal wall pain Recurrent dislocation, shoulder. See Glenohumeral instability Referral pain patterns, in cervical facet arthropathy, 8, 9f

Index

Reflex(es) Achilles, in hamstring strain, 380 ankle, loss of, lumbar degenerative disease and, 246 bulbocavernosus, 788 in cerebral palsy, 693 in cervical radiculopathy, 24, 24f, 24t micturition, 777 in multiple sclerosis, 759 Reflex myoclonus, 751 Reflex sympathetic dystrophy, 543 Reflex voiding, 910t Refrigerant spray, in Tietze syndrome, 644 Regional blocks, 819 Rehabilitation cardiac, 678–683, 680t–682t for pubalgia, 331 in respiratory dysfunction, 860–867 Relative stenosis, 277–278 Relaxation, for cardiac rehabilitation, 680 Relocation maneuver, 70 Renal ultrasonography, for systemic lupus erythematosus, 948 Repetitive strain injuries, 618–623, 619f–620f, 621b trapezius, 43 Repetitive stress injury. See Trapezius strain Reproductive function, in thoracic spinal cord injury, treatment of, 919–920 Resection arthroplasty, in wrist rheumatoid arthritis, 225 Residual limb pain, 659 Residuum “shrinker”, for lower limb amputation, 661t Resisted abduction, in sacroiliac joint dysfunction, 287 Respiratory dysfunction, rehabilitation in, 860–867 Respiratory failure in motor neuron disease, 741, 747 in multiple sclerosis, 762 Respiratory muscle rest, in pulmonary rehabilitation (PR), 863 Respiratory problems, in postpoliomyelitis syndrome, 836–838 Respiratory system, in cervical spinal cord injury disease complications in, 913 ongoing management and health maintenance in, 909 physical examination of, 905 Restrictive lung disease, in neural tube defects, 771 Restrictive pulmonary disease, myopathies and, 768 Retinacular cyst, 169, 170f, 171 Retroachilles bursitis, 476, 477t Retrocalcaneal bursitis, 476, 477t Retrocollis, 18 Retrolisthesis, 270 Return to work, stroke and, 941 Revascularization procedures, in Kienböck disease, 189 Reverse Phalen maneuver, 192–193 Reverse pivot shift test, in posterior cruciate ligament sprain, 426 Reverse soft tissue Bankart lesion. See Labral tears; of shoulder Reverse straight-leg raise, in low back strain or sprain, 266t Revision arthroplasty. See Total hip replacement Revision knee arthroplasty. See Total knee arthroplasty (TKA) Revision surgery, for lower limb amputations, 662

Rheumatism. See Rheumatoid arthritis Rheumatoid arthritis, 876–881 2010 ACR/EULAR classification criteria, 876, 877t definition of, 876 diagnostic studies for, 878–879 differential diagnosis of, 879b disease complications of, 880 functional limitations in, 878 of hand, 179–184, 180f, 180b imaging of, 878–879, 878f laboratory evaluation of, 878 Larsen radiographic staging of, 221t physical examination of, 877–878, 877f procedures for, 879–880 radiographic classification of, 118t rehabilitation for, 879 symptoms of, 876–877 treatment of, 879 complications in, 880, 880t–881t of wrist, 219–227, 220f, 222f–223f, 223b Rheumatoid elbow. See Elbow, arthritis of Rheumatoid factor (RF), 878 Rheumatoid nodules, 876 Rheumatoid wrist. See Wrist, rheumatoid arthritis of Rhizotomy dorsal, in cerebral palsy, 695 in occipital neuralgia, 583–584 Rhomboids, 100, 101f Ribs cervical, 633 first, 633–635, 636f Rigid dressing, for lower limb amputation, 661f, 661t Riluzole, for amyotrophic lateral sclerosis, 743 RimabotulinumtoxinB, 892, 893t Risedronate, for osteoporosis, 803 Risser scale, 885 Rituximab, for rheumatoid arthritis, 880t–881t hand, 180–181 Rivaroxaban, for deep venous thrombosis, 714–715 Robot-assisted upper limb exercise therapy, 934f Robotic assisted gait training devices, for transverse myelitis, 957 Rocker-bottom shoes, for stress fractures, 441 Rome III criteria, 588 Roos test for cervical radiculopathy, 25 for thoracic outlet syndrome, 635 Root tension signs, in low back strain or sprain, 266t Ropinirole, in Parkinson disease, 808, 808t Rotational torticollis, 18, 18f Rotator cuff, 91 anatomy of, 84, 85f impingement test of, 70, 72f tear of, 91–98, 92f, 92t–93t, 94f–95f, 96t, 96b tendinopathy of, 84–90, 85f–88f, 87b, 88t Rotator cuff tendinosis. See Rotator cuff, tendinopathy of Rotterdam CT score, 962 Roundback. See Kyphosis Royal Free disease. See Chronic fatigue syndrome Rucksack palsy. See Scapular winging

S

991

Sacral fractures, 822–824 Sacral nerve stimulation, in neurogenic bladder, 783 Sacral plexus, 822, 823f Sacral sulcus,pressure over, in sacroiliac joint dysfunction, 287 Sacroiliac joint, 284, 285f compression, in low back strain or sprain, 266t dysfunction of, 284–290, 286f–287f, 288b Sacroiliac joint injury. See Sacroiliac joint, dysfunction of Sacroiliac joint instability. See Sacroiliac joint, dysfunction of Sacroiliac joint syndrome. See Sacroiliac joint, dysfunction of Sacroiliac subluxation. See Sacroiliac joint, dysfunction of Sag test, posterior, in posterior cruciate ligament sprain, 426, 426f Saline, injection of, for adhesive capsulitis, 57 Saturday night palsy. See Radial neuropathy Sauve-Kapandji procedure, in wrist rheumatoid arthritis, 225 Scalene muscle activation of, 637, 637f botulinum chemodenervation of, 638 Scalenus anticus syndrome. See Thoracic outlet syndrome Scaphoid nonunion advanced collapse (SNAC), 211 Scaphoid shift test of Watson, 213 Scapholunate advanced collapse (SLAC), 212, 212f Scapholunate dissociation, in wrist osteoarthritis, 212 Scapula, 99 Scapula alata. See Scapular winging Scapular dyskinesis, 47, 48f Scapular winging, 99–105 definition of, 99–100, 100t, 101f diagnostic studies for, 103 differential diagnosis of, 103b functional limitations in, 103 physical examination of, 102–103, 102f potential disease complications of, 104 potential treatment complications of, 105 symptoms of, 101–102 Scapulothoracic winging. See Scapular winging Scar, in post-thoracotomy pain, 610 Scarf or cross arm adduction test, 60 Scarring, hypertrophic, in burns, 673–675 Scheuermann disease, 238, 239f Scheuermann kyphosis, 247t Schober test, 665 Sciatic nerve, 325, 326f Sciatic neuropathy, 325 Sciatica. See Lumbar radiculopathy Scientific Exercises Approach to Scoliosis (SEAS), 887 Scleritis, in rheumatoid arthritis, 876 Scoliometer, 884 Scoliosis, 882–889 adult, 247t definition of, 882 diagnostic studies for, 885, 886f differential diagnosis of, 885b disease complications in, 888 functional limitations in, 884–885 idiopathic, classification of, 883t and neural tube defects, 774–775 physical examination of, 884 symptoms of, 884 treatment of, 886–888

992

Index

Second impact syndrome, 846 Secondary lymphedema. See Lymphedema Secondary metatarsalgia, 493 Sedating agents, in postconcussion symptoms, 845–846 Segmental spinal dysgenesis. See Neural tube defects Seizures cerebral palsy and, 692 in traumatic brain injury, treatment of, 964 Selective estrogen receptor modulators, for osteoporosis, 802 Selective nerve root block (SNRB), for cervical radiculopathy, 27 Selective serotonin reuptake inhibitors for motor neuron disease, 744 for post-stroke symptoms, 933t Selegiline, in Parkinson disease, 808, 808t Self-reported Impairments in Persons with late effects of Polio (SIPP), 839 Semimembranosus-tibial collateral ligament bursopathy, 400 Semmes-Weinstein monofilaments, 213 Senile tremor, 751–752 Senna, for bowel management, 919t Sensation, in diabetic foot, 720 Sensory changes, in cervical degenerative disease, 13–14, 13t Sensory deficits in cervical spondylotic myelopathy, 4 in peroneal (fibular) neuropathy, 420, 420f Sensory discrimination training, in phantom limb pain, 597 Sensory examination in lumbosacral spinal cord injury, 926, 926t in ulnar neuropathy, 206 Sensory function, in lateral femoral cutaneous neuropathy, 321 Sensory nerve conduction studies, in brachial plexopathy, 818 Sensory nerves, in chemotherapy-induced peripheral neuropathy, 529 Sensory testing in cervical radiculopathy, 23, 23f in post-mastectomy pain syndrome, 604–605 Sensory tricks, in dystonia, 754 Separated shoulder. See Acromioclavicular injuries Septic arthritis, acute, 106 Seronegative arthritis. See Ankylosing spondylitis Seronegative spondyloarthritides. See Ankylosing spondylitis Seronegative spondyloarthropathies, 247t. See also Ankylosing spondylitis. Serotonin-norepinephrine reuptake inhibitors, for chronic pain syndrome, 537 Serratus anterior muscle, 99, 101f dysfunction of, 101 in post-thoracotomy pain, 610 Sexual activity in cardiac rehabilitation, 680 in Parkinson disease, 807 Sexual dysfunction in lumbosacral spinal cord injury, 927 in multiple sclerosis, 758, 761 in stroke, in young adults, 939 physical examination of, 940 treatment of, 943 Sexual function, in thoracic spinal cord injury, treatment of, 919–920 Shaker exercise, 727f

Shaking palsy. See Parkinson disease Sharp débridement, for pressure ulcers, 857 Shin splints, 434–437, 435f, 436b Shingles, 599–600 Shock-absorbing insert, 438–439 Shock wave treatment, repetitive lowenergy, in Achilles tendinopathy, 453 Shoe(s) for bunion, 467 for foot and ankle bursitis, 478 for hallux rigidus, 482 for hammer toe, 487 for mallet toe, 491 for metatarsalgia, 493–494 for shin splints, 436 Short arc motion, in flexor tendon injuries, 168 Short T1 inversion recovery (STIR) sequences, in stress fractures, 440 Shortness of breath, in cervical spinal cord injury, 903t–904t Shoulder adhesive capsulitis of, 53–58 arthritis of, 106–111, 107f, 108b, 109f–110f dislocation of, 69 instability of, 69 labral tears of, 76–83 normal anatomy of, 77f osteoarthritis of, 106, 107f rehabilitation for, in post-mastectomy pain syndrome, 606 stretching, in biceps tendinopathy, 61 subluxation of, 69 treatment, stroke and, 935 tear. See Rotator cuff, tear of Shoulder dysfunction, in post-thoracotomy pain, 610 Shoulder-hand syndrome. See Complex regional pain syndrome (CRPS) Shy-Drager syndrome, 751 Sialorrhea, in motor neuron disease, 744, 747 Sick headache. See Migraine Silicone gel sheeting, for burns, 673–674 Silver sulfadiazine, for burns, 673 Single-leg balance test, in ankle sprain, 462 Single-photon emission computed tomography (SPECT), 544 in cervical facet arthropathy, 9 in lumbar facet arthropathy, 253 in spondylolysis and spondylolisthesis, 271–272, 272f Sitting root test, in low back strain or sprain, 266t Skeletal muscle weakness, in motor neuron disease, 744–745 Skier’s thumb, 201, 202f Skin anatomy of, 671f in cervical spinal cord injury disease complications in, 913 ongoing management and health maintenance in, 911 physical examination of, 907 in lower limb amputations, 659–660 in lumbosacral spinal cord injury, examination of, 926 management, in thoracic spinal cord injury, 918 pressure ulcers of, 849 Skin grafts in burns, 675 in pressure ulcers, 857 SLE. See Systemic lupus erythematosus

Sleep changes in, concussion and, 830 in postconcussion symptoms, 843 Sleep disorders, in chronic pain syndrome, 533–534 Sleep disturbances in cerebral palsy, 692 in chronic fatigue syndrome, 698 in chronic pain syndrome, 535 Sleep interventions, for migraine, 563 Sling in acromioclavicular injuries, 50 in glenohumeral instability, 72 in scapular winging, 104 Slipped rib syndrome, 551 Slit and wick catheters, 373, 373f Slow-transit bowel, 790 Slurred speech. See Dysarthria Smoked cannabis, 535–536 Smoking cessation in cardiac rehabilitation, 679–680 in osteoporosis, 802 Snapping hip. See Iliotibial band syndrome (ITBS) Social limitations, in traumatic brain injury, 961–962 Soft tissue Bankart lesion. See Labral tears, of shoulder Soft-tissue mobilization, for hamstring strain, 381–382 Solifenacin, 780t Somatosensory-evoked potentials, for lateral femoral cutaneous neuropathy, 322–323 Somatosensory information, distribution pattern of, 618 Spasmodic torticollis, 17. See also Cervical dystonia Spaso technique, 72 Spastic dysarthria, 897t Spastic dystonia. See Spasticity Spasticity, 692, 890–894 in cervical spinal cord injury surgery for, 912 treatment of, 912 definition of, 890 diagnostic studies for, 891, 891t differential diagnosis of, 891b disease complications of, 892–893 functional limitations in, 890–891 increased, in cervical spinal cord injury, 903t–904t joint contractures and, 704, 706 in lumbosacral spinal cord injury rehabilitation for, 928–929 treatment of, 929 management, in thoracic spinal cord injury, 920 in motor neuron disease, 744 in multiple sclerosis, 757, 760 muscle stiffness due to, in stroke, in young adults, 938–939 initial treatment of, 942 physical examination of, 940, 940t procedures for, 942–943 rehabilitation and, 942 surgery for, 943 in neural tube defects, 774 physical examination of, 890 symptoms of, 890 in traumatic brain injury, treatment of, 964 treatment of, 891–892 complications in, 893 Speculum examination, pelvic pain, 590 Speech, in Parkinson disease, 809

Index

Speech and language disorders, 895–901 definition of, 895–896, 896t diagnostic studies for, 898 differential diagnosis of, 898b disease complications in, 900 functional limitations in, 897–898 physical examination of, 896–897 symptoms of, 896 treatment of, 898–900 Speech dysfunction, in multiple sclerosis, 759 Speech therapy, for traumatic brain injury, 964 Speed test, 65, 92t–93t, 94f for biceps tendinopathy, 60, 60f Spermatic cord, 330f Sphincterotomy, transurethral, 783 Spina bifida (occulta, aperta, manifesta/ cystica). See Neural tube defects Spinal accessory nerve, 99, 101f Spinal accessory nerve palsy. See Scapular winging Spinal accessory neuropathy, 103 Spinal adhesive arachnoiditis. See Arachnoiditis Spinal claudication. See Lumbar spine, stenosis of Spinal cord compression, symptomatic, 33 Spinal cord infarct, in transverse myelitis, 955t Spinal cord injury bowel management after, 789 cervical, 902–915 abdomen examination, 906 American Spinal Injury Association Impairment Scale for, 902, 903t cardiac examination, 906, 906t definition of, 902 diagnostic studies for, 907 differential diagnosis of, 907b disease complications in, 913–914 electrodiagnostic testing in, 907 equipments needed in, 909t extremities examination, 907 functional limitations in, 907, 907t–908t International Spinal Cord Injury Pain Classification, 902, 904t musculoskeletal imaging in, 907 neurologic examination, 904–905, 905f–906f ongoing management and health maintenance, 909–912 physical examination of, 904–907, 904t–905t potential treatment complications of, 914, 914t pulmonary function in, 907 respiratory examination, 905 skin examination, 907 spinal imaging in, 907 spine examination, 906 symptoms of, 902, 903t–904t treatment of, 907–913 urologic studies in, 907 enteric nervous system after, 786 etiology of, 917f lumbosacral, 924–930 definition of, 924 diagnostic studies for, 927–928 differential diagnosis of, 928b disease complications in, 929 electrodiagnostic testing for, 928 functional limitations in, 926–927, 927t neurologic versus skeletal level, 924, 925f

Spinal cord injury (Continued) physical examination of, 925–926 spinal imaging in, 927–928 symptoms of, 924–925 treatment of, 928–929 urologic studies in, 928 management of, 874t thoracic, 916–923 definition of, 916, 917f diagnostic studies for, 917–918 differential diagnosis of, 918b disease complications in, 922 functional limitations in, 917 physical examination of, 917 symptoms of, 916–917 treatment of, 918–922 Spinal cord lesions, neurogenic bladder and, 778 Spinal cord stimulation (SCS) in arachnoiditis, 525, 526f in chemotherapy-induced peripheral neuropathy, 532 in lumbar degenerative disease, 250 in lumbar facet arthropathy, 255 in peripheral arterial disease, 722 in postherpetic neuralgia, 603 in thoracic sprain or strain, 242 Spinal dysraphism. See Neural tube defects Spinal fusion, for lumbar facet arthropathy, 255 Spinal manipulation, in occipital neuralgia, 583 Spinal muscular atrophy, 740 Spinal orthosis, for thoracic compression fractures, 229–230, 231f Spinal stenosis, cervical. See Cervical spine, degenerative disease of; Cervical spine, stenosis of Spine in cervical spinal cord injury physical examination of, 906 surgery for, 912 in lumbosacral spinal cord injury inspection and palpation of, 925 surgery for, 929 muscles surrounding, 245 thoracic, 238 Spine Patient Outcomes Research Trial, 281–282 Spine surgery, minimally invasive, for lumbar degenerative disease, 250 Spinobulbar muscular atrophy (Kennedy disease). See Motor neuron disease Spinoglenoid notch, 112 Splenomegaly, in systemic lupus erythematosus, 947–948 Splints in Achilles tendinopathy, 453 in biceps tendon rupture, 66 in carpal tunnel syndrome, 193–194, 194f in contractures, 674 in flexor tendon injuries, 167, 167f in hand osteoarthritis, 176 in hand rheumatoid arthritis, 181, 182f in joint contractures, 708 in Kienböck disease, 188 in median neuropathy, 193–194, 194f in osteoarthritis, 796 in peroneal (fibular) neuropathy, 422 in plantar fasciitis, 503 in temporomandibular joint dysfunction, 627 in treatment, of stroke, 935 in trigger finger, 198 in ulnar collateral ligament sprain, 202–203

993

Splints (Continued) in ulnar neuropathy, 209 in wrist osteoarthritis, 214 in wrist rheumatoid arthritis, 223 Split notochord syndrome. See Neural tube defects Spondylitis, ankylosing, 664–669 Spondylolisthesis etiology of, 269–270 of lumbar spine, 269–276, 270f–273f, 273b Spondylolysis, of lumbar spine, 269–276, 270f–273f, 273b Spondylosis. See also Cervical spine, facet arthropathy of; Lumbar degenerative disease cervical, 3 Spontaneous myoclonus, 751 Sport-specific drills, in chronic ankle instability, 473 Sports, stepwise return to, in postconcussion symptoms, 845t Sports hernia. See Pubalgia Sprain ankle, 460–465 of anterior cruciate ligament, 350–357, 351f–352f, 351b, 353t–354t cervical, 29–32 collateral ligament, 366–370, 367f, 368b low back, 264–268, 265t–266t, 267b of posterior cruciate ligament, 424–430, 425f–427f, 426t, 427b sacroiliac joint. See Sacroiliac joint, dysfunction of thoracic, 238–243 ulnar collateral ligament, 201–204, 202f–203f, 202b Spurling maneuver, 582 for cervical radiculopathy, 25, 25f for low back strain or sprain, 266t Spurling sign, in cervical spinal stenosis, 33–34 Spurling test, for cervical degenerative disease, 13 Squeeze test, in ankle sprain, 461–462, 462f Standing cable column, 417f Static progressive splinting, in wrist osteoarthritis, 214 Static tremor, 750–751 Static winging, 99 Statin therapy, in peripheral arterial disease, 721 Steel shanks, for stress fractures, 441 Steinert disease, 766 Stellate ganglion block, in complex regional pain syndrome, 546–547 Stener lesion, 201 Stenosing tenosynovitis. See de Quervain tenosynovitis; Trigger finger Stenosis of cervical spine, 33–38, 34f lumbar spinal, 277–283, 278t, 279b Step-down exercise, 416f Stereotactic radiosurgery, for trigeminal neuralgia, 648 Sternoclavicular arthrodesis, 554 Steroids in cervical degenerative disease, 14–15 injection of in biceps tendinopathy, 61–62, 62f in bunion, 468 in posterior tibial tendon dysfunction, 508 in postherpetic neuralgia, 602 in tibial neuropathy, 513

994

Index

Steroids (Continued) in lateral femoral cutaneous neuropathy, 323, 323f oral in lumbar radiculopathy, 259–260 in thoracic radiculopathy, 236 Stiff and painful shoulder. See Adhesive capsulitis Stiffness in rheumatoid arthritis, 179 in wrist osteoarthritis, 212–213 Stimulants, for post-stroke symptoms, 933t Stinchfield’s test, for hip labral tears, 315–316 Stoma, care of, after urostomy, 784 Stool incontinence, in neural tube defects, 771 Stool softeners, for thoracic compression fractures, 229–230 Straight-leg raise active, in sacroiliac joint dysfunction, 287 in low back strain or sprain, 266t in lumbar radiculopathy, 258 Strain cervical, 29–32 hamstring, 378–383, 381b complete tear of, 379 grades of, 379, 379f hip adductor, 297–302 injuries, repetitive, 618–623, 619f–620f low back, 264–268, 265t–266t, 267b sacroiliac joint. See Sacroiliac joint, dysfunction of thoracic, 238–243 trapezius, 43–45 Strength testing manual, in glenohumeral instability, 70 in rotator cuff tendinopathy, 85–86, 87f Strengthening in rotator cuff tear, 97 in rotator cuff tendinopathy, 88–89 in scapular winging, 104 in suprascapular neuropathy, 114 Stress fractures, 438–442 bisphosphonate-related, 441 definition of, 438–439 diagnostic studies for, 440 differential diagnosis of, 440b disease complications of, 441 femoral, 439, 439f–440f functional limitations in, 440 metatarsal, 440–441 midshaft tibial, 440–441 physical examination of, 439–440 surgery for, 441 symptoms of, 439 treatment of, 440–441 Stress radiographs, in posterior cruciate ligament sprain, 427 “Stress response”, in myofascial pain syndrome, 576 Stretch-induced injury to the hamstring. See Hamstring, strain of Stretching for joint contractures, 708 for spasticity, 891 in treatment, of stroke, 935 Stroke, 931–936, 932b, 933t in young adults, 937–944, 941b Stryker notch view, in glenohumeral instability, 71 Student’s elbow. See Olecranon bursitis Stump-residual limb or residuum. See Lower limb amputations Subcutaneous botulinum toxin A injection, in postherpetic neuralgia, 602 Subcutaneous hyperalgesia, in Tietze syndrome, 642f

Subcutaneous nodules, in rheumatoid arthritis, 876 Subluxation, shoulder. See Glenohumeral instability Subscapularis lift-off test of, 70, 70f strength testing for, 85–86 tests for, 92f, 92t–93t Substance P, in fibromyalgia, 573 Subvastus approach, in total knee arthroplasty, 447 Sudeck atrophy. See Complex regional pain syndrome (CRPS) Sudeck syndrome. See Complex regional pain syndrome (CRPS) Suicide headache. See Cluster headache Sulfasalazine in hand rheumatoid arthritis, 180 in rheumatoid arthritis, 880t–881t Superficial infrapatellar bursopathy, 400 Superficial posterior compartment, of leg, 372, 372f Superior labral anterior-posterior (SLAP) tears, 76 classification of, 77f diagnostic studies for, 79–80, 79f–80f functional limitations in, 79 initial treatment of, 80 physical examination of, 78, 78t potential disease complications of, 82 rehabilitation for, 81 surgery for, 81–82 symptoms of, 77–78 Supinator syndrome. See Radial neuropathy Supplemental oxygen for motor neuron disease, 747 for pulmonary rehabilitation (PR), 863 Suprapubic pressure, 782 Suprascapular nerve, 112, 113f block, 113–114 Suprascapular nerve rotator cuff compression syndrome. See Suprascapular neuropathy Suprascapular neuropathy, 112–115 definition of, 112, 113f diagnostic studies for, 113–114 differential diagnosis of, 114b functional limitations in, 113 physical examination of, 113 potential disease complications of, 114 potential treatment complications of, 114–115 symptoms of, 113 treatment of, 114 Supraspinatus strength testing for, 85–86 tests for, 92t–93t, 94f Sural nerve biopsy, 813 Sustained hip flexion, in low back strain or sprain, 266t Sustained natural apophyseal glides (SNAG), for cervicogenic vertigo, 40 Swallowing in motor neuron disease, 746 in multiple sclerosis, 758, 762 in postpoliomyelitis syndrome, 836–838 Swallowing disorder. See Dysphagia Swallowing impairment. See Dysphagia Swan-neck deformities in hand rheumatoid arthritis, 179 surgery for, 183 reversible, in systemic lupus erythematosus, 947f in rheumatoid arthritis, 877f splinting, 182f Sweater finger. See Flexor tendon injuries

Swelling in Tietze syndrome, 640 in wrist osteoarthritis, 212–213 in wrist rheumatoid arthritis, 221 Swimming, for thoracic sprain or strain, 241 Sympathetic nerve blocks in lumbosacral plexopathy, 826 in postherpetic neuralgia, 602 Sympathetically maintained pain. See Complex regional pain syndrome (CRPS) Symptom Severity Scale, 556t Symptomatic torsion dystonia. See Cervical dystonia Synovectomy, in wrist rheumatoid arthritis, 224–225 Synovial chondromatosis, 117 Synovial cyst, 169 Synovial fluid, in osteoarthritis, 794 Synovial hypertrophy, in wrist osteoarthritis, 212–213 Synovitis in hand rheumatoid arthritis, 179–180 in wrist rheumatoid arthritis, 220f Systemic disease pressure ulcers and, 850 in transverse myelitis, 955t Systemic exercise intolerance disease. See Chronic fatigue syndrome Systemic lupus erythematosus (SLE), 945–951 definition of, 945 diagnostic studies for, 948–949 differential diagnosis of, 949b disease complications in, 950 functional limitations in, 948 laboratory testing in, 948t organ involvement in, 947t physical examination of, 946–948, 947f procedures for, 949 rehabilitation for, 949 symptoms of, 945–946 Systemic Lupus International Collaborating Clinics, classification criteria for, 945, 946t treatment of, 949–950 complications in, 950, 950t Systemic Lupus International Collaborating Clinics, classification criteria for systemic lupus erythematosus, 945, 946t

T

Tactile stimulation, in phantom limb pain, 597 Tadalafil, for complex regional pain syndrome, 546 Tailor’s bunion, 468–469 Talar tilt test, in ankle sprain, 461–462, 462f Taping McConnell’s, in patellofemoral syndrome, 415–416 in ulnar collateral ligament sprain, 203f Tardieu rating scale, in cerebral palsy, 693 Tardive dyskinesia, 751 treatment of, 753–754 Tardy ulnar palsy. See Ulnar neuropathy, elbow Tarsal tunnel syndrome (TTS), 510, 511f Task-specific tremor, 753 Tasks, sport-specific activities, in rotator cuff tendinopathy, 89 Taxanes, 529 Technetium Tc 99m diphosphonate bone scanning, in stress fractures, 440

Index

Temperature, in complex regional pain syndrome, 544 Temporomandibular disorder. See Temporomandibular joint (TMJ), dysfunction of Temporomandibular joint (TMJ), 624 anatomy of, 625f in closed position, 625f dysfunction of, 624–628, 626b medial displacement of, 626f replacement, 627f Tenderness, knee, in iliotibial band syndrome, 386 Tendinitis. See de Quervain tenosynovitis hip adductor. See Hip, adductor strain of Tendinopathy Achilles, 451–455 biceps, 59–63 hip adductor. See Hip, adductor strain of patellar, 410–413 quadriceps, 431–433 rotator cuff, 84–90 Tendinosis, 84, 124. See also de Quervain tenosynovitis; Lateral epicondylitis; Medial epicondylitis in posterior tibial tendon dysfunction507 quadriceps. See Quadriceps tendinopathy Tendo Achilles bursitis. See Bursitis, foot and ankle Tendon injury, zones of, 165, 166f Tendon reconstruction, flexor and extensor, for hand rheumatoid arthritis, 181 Tendon transfer surgery, for posterior tibial tendon dysfunction, 508 for transverse myelitis, 958 Tennis elbow. See Lateral epicondylitis Tenosynovectomy in hand rheumatoid arthritis, 182 in posterior tibial tendon dysfunction, 508 in wrist rheumatoid arthritis, 224–226 Tenosynovitis in posterior tibial tendon dysfunction, 507 in wrist rheumatoid arthritis, 220–221 Tenovaginitis. See de Quervain tenosynovitis Tension neck ache. See Trapezius strain Tension-type headache, 561 treatment of, 563 Teres minor, tests for, 92t–93t, 94f Teriparatide, for osteoporosis, 803 Tethered cord syndrome, 770, 774 Tetraplegia, 902 Thalamic pain syndrome. See Central poststroke pain Thalamotomy, in Parkinson disease, 809 Thenar atrophy, in carpal tunnel syndrome, 192 TheraBite Jaw Motion Rehabilitation System, in radiation fibrosis syndrome, 616 Therapeutic ultrasound for biceps tendon rupture, 66 for spasticity, 891 Thermal capsulorrhaphy, in shoulder arthritis, 110 Thermal injury. See Burns Thessaly maneuver, in meniscal injuries, 405–406 Thin bones. See Osteoporosis Third occipital headache. See Occipital neuralgia Thomas maneuver, 692–693, 693t Thomas test in iliotibial band syndrome, 385–386, 386f in total hip replacement, 338, 339f

Thompson test, in Achilles tendinopathy, 452, 452f Thoracentesis, for cardiac rehabilitation, 682 Thoracic compression fracture. See Compression fracture, thoracic Thoracic disc herniation, in thoracic radiculopathy, 234 Thoracic epidural anesthesia, in postthoracotomy pain, 609–610 Thoracic outlet syndrome, 633–639, 634f, 636f–637f, 636b index, 635 Thoracic radiculitis. See Thoracic radiculopathy Thoracic radiculopathy, 234–237 definition of, 234 diagnostic studies for, 235 differential diagnosis of, 235b–236b functional limitations in, 235 pain pattern in, 235f physical examination of, 235 potential disease complications of, 236 potential treatment complications of, 236–237 symptoms of, 234 treatment of, 236 Thoracic spinal cord injury, 916–923 definition of, 916, 917f diagnostic studies for, 917–918 differential diagnosis of, 918b disease complications in, 922 functional limitations in, 917 physical examination of, 917 symptoms of, 916–917 treatment of, 918–922 Thoracic spine compression fracture of, 228–233 examination of, intercostal neuralgia vs., 567 imaging of, in post-mastectomy pain syndrome, 605 Thoracic sprain or strain, 238–243, 239f definition of, 238–239 diagnostic studies for, 240, 240f differential diagnosis of, 240b extrinsic or environmental mechanisms of, 239 functional limitations in, 240 physical examination of, 239–240 potential disease complications of, 242 potential treatment complications of, 242 symptoms of, 239 treatment of, 240–242 Thoracic wedge, for thoracic sprain or strain, 241 Thoracochondralgia. See Tietze syndrome Thoracotomy, 608 Three-phase bone scan, 731, 731f Three-point sagittal hyperextension brace, in thoracic compression fracture, 231f Thrombectomy, for deep venous thrombosis, 717 Thrombolytic therapy, for deep venous thrombosis, 715–716 Thrombophlebitis. See Deep venous thrombosis Thromboprophylaxis, after hip arthroplasty, 289, 312 Thumb gamekeeper’s, 201 Skier’s, 201, 202f Tibial mononeuropathy at ankle. See Tibial neuropathy Tibial nerve, transplanting, for peroneal (fibular) neuropathy, 422

995

Tibial neuropathy, 510–514, 511f definition of, 510 diagnostic studies for, 512 differential diagnosis of, 512b functional limitations in, 511 physical examination of, 511, 511f potential disease complications of, 513 potential treatment complications of, 513 procedures for, 512 rehabilitation for, 512 symptoms of, 510–511 treatment of, 512–513 Tic douloureux. See Trigeminal neuralgia Tics, 751, 753 Tietze syndrome, 549, 550t, 640–645 complications of, 645 definition of, 640, 641f diagnostic studies for, 641–643 differential diagnosis of, 643b functional limitations in, 641 physical examination of, 640–641, 641f–642f symptoms of, 640 treatment of, 643–645 Tight filum terminale. See Neural tube defects Tinel sign, 146–147 in tibial neuropathy, 511, 512f in wrist rheumatoid arthritis, 221 Tinel test, 192–193 Tissue hypertrophy, in knee chondral injuries and, 365 Tizanidine for multiple sclerosis, 760 for spasticity, 891, 892t for trapezius strain, 44 Tocilizumab for hand rheumatoid arthritis, 180–181 for rheumatoid arthritis, 880t–881t Toe(s) hammer, 486–489, 487f mallet, 490–492, 491f Tofacitinib for hand rheumatoid arthritis, 180–181 for rheumatoid arthritis, 880t–881t Tolterodine, 780t Topical rubefacients, in osteoarthritis, 795 Topiramate, 846 for trigeminal neuralgia, 647 Torg-Pavlov ratio, in cervical spondylotic myelopathy, 4 Torg ratio, in cervical spinal stenosis, 35 Torn shoulder. See Rotator cuff, tear of Torticollis, 752 rotational, 18, 18f spasmodic, 17 Total ankle joint replacement, in ankle arthritis, 458, 458f Total elbow arthroplasty (TEA), 122 Total hip arthroplasty, 337–338 approaches to, precautions associated with, 340t components of, 342–343, 343f goals of rehabilitation after, 340, 341t Total hip replacement, 337–345, 340f dislocation and, 339f sport participation recommendations and associated levels of, 341, 342t Total knee arthroplasty (TKA), 443–450, 446t, 447f–448f Total knee implant. See Total knee arthroplasty (TKA) Total knee replacement. See also Total knee arthroplasty (TKA) for knee osteoarthritis, 396, 396t

996

Index

Total wrist arthrodesis in wrist osteoarthritis, 217f in wrist rheumatoid arthritis, 225f Total wrist arthroplasty, in wrist osteoarthritis, 215–216, 218 indications for, 216 Total wrist fusion in wrist osteoarthritis, 215, 217 in wrist rheumatoid arthritis, 225 Tourette syndrome, 751 Toxins, peripheral neuropathies and, 812t Tracheostomy, for motor neuron disease, 747–748 Traction, cervical for cervical degenerative disease, 15 for cervical spinal stenosis, 36 for degenerative disease, 15 Tram-tracking, in deep venous thrombosis, 713f Tramadol for fibromyalgia, 557 for low back strain or sprain, 267 for osteoarthritis, 795 for thoracic compression fractures, 229–230 Transcortical mixed aphasia, 896t Transcortical motor aphasia, 896t Transcortical sensory aphasia, 896t Transcranial direct current stimulation (tDCS), for speech and language disorders, 900 Transcranial magnetic stimulation (TMS), for speech and language disorders, 900 Transcutaneous electrical nerve stimulation (TENS), 520 in chronic pain syndrome, 536 in costosternal syndrome, 552 in knee osteoarthritis, 394 in phantom limb pain, 597 in postherpetic neuralgia, 602 Transcutaneous nerve stimulation, for lateral femoral cutaneous neuropathy, 323 Transducer-tipped probe, 373, 373f Transforaminal epidural steroid injections, for cervical spinal stenosis, 36 Transrectal linear array ultrasonography, in neurogenic bladder, 780 Transurethral sphincterotomy, 783 Transverse myelitis, 952–959 definition of, 952–953 diagnostic studies for, 954–955, 954f, 955t disease complications in, 958 functional limitations in, 953–954 idiopathic acute, criteria for diagnosis of, 955t physical examination of, 953 reported causes of, 956t symptoms of, 953 treatment of, 955–958 Trapeziometacarpal joint, osteoarthritis of, 175, 177 Trapezius muscle, 99–100, 101f weakness of, 103 Trapezius myositis. See Trapezius strain Trapezius strain, 43–45 definition of, 43 diagnostic studies for, 44 differential diagnosis of, 44b functional limitations in, 43 physical examination of, 43 potential disease complications of, 45 potential treatment complications of, 45 symptoms of, 43 treatment of, 44

Trauma in brachial plexopathy, 818 possibility of, in Tietze syndrome, 645 Traumatic amputation, upper limb amputations and, 653 Traumatic brain injury, 829, 829t, 960–966 agitation of, 960–961 definition of, 960–961 diagnostic studies for, 962–963 differential diagnosis of, 963b disease complications in, 965 distribution of, 830f functional limitations in, 961–962 medications used in, 965t physical examination of, 961 supervision in, 832 symptoms of, 961, 961t treatment of, 963–965 Traumatic Coma Data Bank classification, 962 Traumatic quadriceps strain. See Quadriceps contusion Traumatic tension in muscles. See Compartment syndrome, of leg Treadmill testing, in cardiac rehabilitation, 679 Tremor, 750–751 essential, 750 in multiple sclerosis, 757, 762 in Parkinson disease, 806 Trendelenburg sign, 338, 338f, 347 Tricyclic antidepressants for arachnoiditis, 525, 525t for cervical sprain/strain, 31 for cervicogenic vertigo, 40 for chemotherapy-induced peripheral neuropathy, 532 for intercostal neuralgia, 569 for lumbar radiculopathy, 259 for motor neuron disease, 744 for occipital neuralgia, 583–585, 585t for peripheral neuropathies, 814 for peroneal (fibular) neuropathy, 421 for phantom limb pain, 597 for post-mastectomy pain syndrome, 606 for radiation fibrosis syndrome, 615–616 for repetitive strain injuries, 621–622 for thoracic radiculopathy, 236 for Tietze syndrome, 643 for ulnar neuropathy, 209 Trifacial neuralgia. See Trigeminal neuralgia Trigeminal nerve, 646 Trigeminal neuralgia, 646–648 complications of, 648 definition of, 646 diagnostic studies for, 647 functional limitations in, 646–647 physical examination of, 646 symptoms of, 646 treatment of, 647–648 Trigger finger, 197–200, 198f–199f, 198b Trigger point(s), in myofascial pain syndrome, 572, 573f Trigger point injections for cervical sprain/strain, 31 for cervicogenic vertigo, 40, 41f for fibromyalgia, 557 for hip adductor strain, 300–301 for hip adhesive capsulitis, 295 for myofascial pain syndrome, 574–575 for radiation fibrosis syndrome, 616 for temporomandibular joint dysfunction, 626 for thoracic sprain or strain, 241 for trapezius strain, 44 Trismus, 613–614, 614f

Trochanteric bursitis, 247t, 346. See also Greater trochanteric pain syndrome. Trospium, 780t Tumor necrosis factor, in rheumatoid arthritis, 880t–881t Tumor necrosis factor alpha inhibitors (TNFi), for ankylosing spondylitis, 667 Tumor necrosis factor antagonists, in hand rheumatoid arthritis, 183 Tumor necrosis factor inhibitors, for wrist rheumatoid arthritis, 223 Two-point discrimination in flexor tendon injuries, 166 in wrist osteoarthritis, 213 Two-point sensory discrimination test, 192

U

Ulcer(s) foot in diabetes, 719 in tibial neuropathy, 513 oral, in systemic lupus erythematosus, 945–946 pressure, 849–859, 850t, 852f, 853b, 854f–855f skin, in diabetes, 719, 722 Ulna bursa injection, in carpal tunnel syndrome, 194f Ulnar claw, 206 Ulnar collateral ligament (UCL) complex, 201 Ulnar collateral ligament sprain, 201–204, 202f–203f, 202b Ulnar collateral ligament tear or rupture. See Ulnar collateral ligament sprain Ulnar nerve, 206t lesion, 208f Ulnar neuritis. See Ulnar neuropathy; elbow Ulnar neuropathy elbow, 146–148, 147f diagnostic studies for, 147 differential diagnosis of, 147b functional limitations in, 147 physical examination of, 146–147, 147f potential disease complications of, 148 potential treatment complications of, 148 symptoms of, 146 treatment of, 147–148 wrist, 205–210, 206f–209f, 206t, 209b Ulnohumeral arthroplasty, 121–122 Ultrasonography (US) in abdominal wall pain, 520 in Achilles tendinopathy, 452 in acromioclavicular injuries, 49, 51f in adhesive capsulitis, 54–55 in Baker cyst, 359–360 in biceps tendinopathy, 61, 61f in brachial plexopathy, 818 in carpal tunnel syndrome, 193 in cerebral palsy, 694 in cervical sprain/strain, 30 in chronic exertional compartment syndrome, 374, 374f in deep venous thrombosis, 713 in flexor tendon injuries, 167 in hand and wrist ganglia, 171–172 in hand osteoarthritis, 175 in hand rheumatoid arthritis, 180 in heterotopic ossification, 731–732 in hip adhesive capsulitis, 293 in iliotibial band syndrome, 387–388 in knee bursopathy, 400 in lateral epicondylitis, 124–125 in medial epicondylitis, 128–129

Index

Ultrasonography (US) (Continued) in metatarsalgia, 494 in Morton’s neuroma, 498 of muscle tears, 552, 552f in osteoporosis, 800 in patellar tendinopathy, 411 in piriformis syndrome, 326–327 in plantar fasciitis, 502–503 in posterior cruciate ligament sprain, 427 in posterior tibial tendon dysfunction, 507 in pubalgia, 331 in quadriceps contusion, 334 in rotator cuff tear, 95, 95f in tibial neuropathy, 512 in Tietze syndrome, 642–643, 642f–643f in trapezius strain, 44 in trigger finger, 198 in trochanteric bursitis, 347, 348f in ulnar collateral ligament sprain, 202 Ultrasound-guided bursal infiltrations, of knee, 401 Ultrasound therapy in hip adductor strain, 299, 299f in joint contractures, 708 in trigger finger, 199 Unfractionated heparin (UFH), 714 Unicompartmental knee arthroplasty. See Total knee arthroplasty (TKA) Unicompartmental knee replacement, for knee osteoarthritis, 396, 396t Unipolar hemiarthroplasty. See Total hip replacement Unloader hip brace, for hip osteoarthritis, 311–312, 312f Unweanable patients decannulation of, 873 extubation of, 873, 873t Upper limb amputations, 649–657 complications of, 656 definition of, 652–653 diagnostic testing for, 653–654 functional limitations in, 653 physical examination of, 653 symptoms of, 653 treatment of, 654–656 Upper motor neuron bowel syndrome, 787 Urethral sphincter, 777 Urinary tract infections in neural tube defects, 771 in neurogenic bladder, 784 Urodynamic testing, in neurogenic bladder, 781, 781f Uterine leiomyomas, pelvic pain and, 588, 593–594

V

Vacuum-assisted closure, for pressure ulcers, 857 Vagus nerve, 786 Valacyclovir, in postherpetic neuralgia, 601 Valganciclovir, for chronic fatigue syndrome, 701 Valleix phenomenon, 511 Valproate, for trigeminal neuralgia, 647 Valsalva maneuver, 910t Valvular inflammation, in rheumatoid arthritis, 877 Vapocoolant spray, in Tietze syndrome, 644 Varicella zoster virus, 599 infection, 599 Vascular claudication. See Foot, diabetic; Peripheral arterial disease

Vascular headache. See Migraine Vascular parkinsonism, 751 Vastus medialis obliquus (VMO), strengthening of, for patellofemoral syndrome, 417 Vaughn-Jackson syndrome, 220 in hand rheumatoid arthritis, 180 Vena caval filters, for deep venous thrombosis, 717 Venlafaxine, in intercostal neuralgia, 569 Venous thromboembolism. See Deep venous thrombosis Venous thrombosis, cancer-related fatigue and, 685 Venous ultrasonography, in deep venous thrombosis, 713 Ventilation, in myopathy, 768 Vertebral crush fracture. See Compression fracture; thoracic Vertebroplasty, for thoracic compression fractures, 230–231 Vertigo cervicogenic, 39–42 in postconcussion syndrome, 842–843 Vestibular/balance disorder, in postconcussion symptoms, 843, 846 Vestibular rehabilitation therapy (VRT) for cervicogenic vertigo, 40 for postconcussion symptoms, 846 Vicar’s knee, 400 “Vicious cycle” theory, 887 Videofluorographic swallowing study, 725 Videofluorography, in dysphagia, 725 Viking disease. See Dupuytren contracture Vinca alkaloids, 529 Virchow triad, 711 Viscosupplementation injections for ankle arthritis, 457–458 for hip osteoarthritis, 311 for knee osteoarthritis, 395 Vision disorders, in cerebral palsy, 690 Visual disorientation, in postconcussion symptoms, 844 Visual observation, for cervical radiculopathy, 23 Vitamin D in osteoporosis, 801 in stress fractures, 438–439 Vocational rehabilitation for stroke, 935 for traumatic brain injury, 964 Voice disturbance. See Dysphonia Voiding, patterns of, 778, 779t Volar carpal ligament, 192f Volkmann ischemia. See Compartment syndrome; of leg Volleyball shoulder. See Suprascapular neuropathy

W

Waddell signs in lumbar degenerative disease, 248t in lumbar radiculopathy, 258 WalkAide, for transverse myelitis, 957 Wallet neuritis. See Piriformis syndrome Warfarin in deep venous thrombosis, 716 prophylaxis, 714 in total knee arthroplasty, 445 Washerwoman’s sprain. See de Quervain tenosynovitis Weak ankle. See Chronic ankle instability

997

Weakness, in cervical spinal cord injury, 903t–904t Wedge compression. See Compression fracture, thoracic Weight training, in post-mastectomy pain syndrome, 606 Weil osteotomy, 488 of metatarsalgia, 495 Well leg compartment syndrome, 371 Wells prediction rules, in deep venous thrombosis, 712, 712t Wernicke aphasia, 896t Wheelchairs for transverse myelitis, 957 in treatment, of stroke, 935 Whiplash injury, 8, 29. See also Cervical spine, sprain/strain of Widespread Pain Index, 556t Wilson disease, 18 Winter heel. See Bursitis, foot and ankle Women’s Health Initiative (WHI) study, 802 Wound bed preparation, for pressure ulcers, 855f Wounds, from burns, 673 Wrightington classification, of rheumatic disease, 224t Wrist de Quervain tenosynovitis of, 149–153 extensor tendon compartments of, 143t fracture of, 799 ganglia of, 169–173, 172b dorsal, 170f volar, 169, 170f osteoarthritis of, 211–218, 212f, 214b, 215f–216f secondary to malunited wrist fracture, 211, 212f rheumatoid arthritis of, 219–227, 220f, 222f–223f, 223b Wrist denervation, in wrist osteoarthritis, 217–218 Wrist drop neuropathy. See Radial neuropathy

X

X-ray for acromioclavicular injuries, 48 for cervical radiculopathy, 25 for cervical spinal stenosis, 34–35 for thoracic sprain and strain, 240

Y

Yeoman test in low back strain or sprain, 266t in sacroiliac joint dysfunction, 287, 287f Yergason test, 60, 60f, 65 Yuppie flu. See Chronic fatigue syndrome

Z

Z-joint pain. See Lumbar facet arthropathy Z-point pain. See Cervical spine, facet arthropathy of Zoledronic acid, in osteoporosis, 803 Zolpidem, in postconcussion symptoms, 845–846 Zygapophyseal joint, 250 Zygapophyseal joint pain. See Cervical spine, facet arthropathy of, Lumbar facet arthropathy