I. Osteoarthritis
A. Epidemiology/overview
1. Primary osteoarthritis (OA)—Cause is unknown
2. Secondary OA
a. Trauma
b. Instability
c. Prior surgery
B. Pathoanatomy—Primary OA of the shoulder
1. Posterior glenoid wear and posterior humeral head subluxation occur in up to 45% of shoulders affected by primary OA.
2. The anterior soft tissues (eg, anterior capsule and subscapularis) become contracted, limiting external rotation.
3. Joint space narrowing and periarticular osteophyte formation occur most commonly on the inferior aspects of the humeral head ("goat's beard").
4. Rotator cuff tears are rarely associated with primary OA (5% to 10%).
C. Evaluation
1. History
a. Common symptoms include pain (with activity and at night), decreased motion, and loss of function.
b. Any history of previous trauma, instability, or prior joint surgery (causes of secondary OA)
2. Physical examination—Visual inspection
a. Anterior flattening secondary to posterior subluxation may be seen.
Young W. Kwon, MD, PhD, is a consultant for or employee of Exactech.
b. Common findings include limited range of motion (especially external rotation), crepitus, and pain with motion.
3. Imaging
a. Radiographs
i. AP, true AP, and axillary views should be obtained.
ii. Findings include joint space narrowing, subchondral sclerosis, and osteophytes about the glenoid and humeral head (
Figure 1).
iii. Axillary view—Posterior glenoid erosion, humeral head subluxation (
Figure 2)
[Figure 1. AP radiograph of an osteoarthritic glenohumeral joint with subchondral sclerosis, cyst formation, humeral head flattening, and osteophyte formation.]
[Figure 2. Axillary radiograph of the shoulder showing posterior glenoid erosion and posterior subluxation of the humeral head, which are commonly seen in osteoarthritis.]
b. CT is the study of choice for evaluating glenoid bony changes and to aid in preoperative planning.
c. MRI—Not necessary, but can provide information about the rotator cuff.
D. Classification—Walch and associates identified three types of glenoid morphology that are associated with primary glenohumeral OA (
Figure 3).
1. Type A—Concentric wear with no subluxation (59%)
2. Type B—A biconcave glenoid with asymmetric wear of the posterior glenoid rim and posterior humeral subluxation (32%)
3. Type C—Glenoid retroversion >25° and posterior humeral subluxation (9%)
E. Treatment
1. Nonsurgical
a. Medications—Nonsteroidal anti-inflammatory drugs (NSAIDs)
b. Intra-articular corticosteroid injection
c. Physical therapy
d. The role of viscosupplementation is unproven.
2. Surgical
a. Indications
i. No response to nonsurgical treatment
ii. Symptoms associated with significant disability
[Figure 3. Classification of glenoid morphology associated with primary glenohumeral OA. A1, Minor erosion. A2, Major erosion. B1, Narrowing of the posterior joint space, subchondral sclerosis, and osteophytes. B2, A posterior wear with a bioconcave aspect to the glenoid. C, Glenoid retroversion of more than 25%, regardless of the erosion.]
b. Arthroscopic debridement
i. The role of arthroscopy is controversial and has limited applicability.
ii. It is best indicated for concentric glenoids, preserved motion, and some maintained joint space.
c. Hemiarthroplasty
i. Hemiarthoplasty is indicated for large, irreparable rotator-cuff tears or when there is inadequate bone stock to support a glenoid prosthesis.
ii. Outcomes are improved in shoulders with concentric glenoids.
iii. Biologic resurfacing of the glenoid may be considered for young patients (indications are evolving).
d. Total shoulder arthroplasty (TSA)
i. TSA with cemented, all-polyethylene glenoid resurfacing is the standard of care for OA.
ii. TSA provides reliable pain relief and range of motion.
iii. 10-year survival rate is 93%.
iv. Contraindications include active infection, nonfunctioning deltoid, nonfunctioning or insufficient rotator cuff, irreparable rotator cuff tears, brachial plexus palsy, and severe glenoid bone loss.
v. "Rocking horse" phenomenon—Loosening of the glenoid prosthesis in the presence of an irreparable rotator cuff tear.
e. Arthrodesis
i. Indications—Rarely indicated for OA, arthrodesis may be appropriate for patients with deltoid and rotator cuff deficiencies.
ii. The optimal positioning for shoulder arthrodesis is 30° flexion, 30° internal rotation, and 30° of abduction.
F. Pearls and pitfalls
1. The average retroversion is 19° in relation to the forearm.
a. Posterior glenoid erosion can usually be corrected by eccentrically reaming the anterior glenoid rim.
b. Cement should not be used to compensate for glenoid bone loss.
2. Radiolucency around the glenoid component is a common finding, but it does not always correlate with clinical failure.
3. Appropriate sizing and alignment of the humeral prosthesis are important.
a. Avoid overstuffing the joint with an oversized humeral head, as this can cause increased joint reaction forces and tension on the rotator cuff.
b. Avoid valgus positioning of the humeral stem in the canal.
c. The top of the humeral head should be approximately 5 to 8 mm superior to the top of the greater tuberosity.
d. Rarely, posterior capsular imbrication may be needed to restore appropriate soft-tissue tension.
4. Anterior soft-tissue contracture
a. Release rotator interval
b. Release anterior and inferior capsule
c. 360° subscapularis release
5. Subscapularis function must be restored for optimal outcome; may consider lesser tuberosity osteotomy for improved healing.
II. Inflammatory Arthritis
A. Epidemiology/overview
1. Rheumatoid arthritis (RA) is the most prevalent form of inflammatory arthritis affecting the shoulder.
2. 91% of patients with RA for more than 5 years develop shoulder symptoms.
3. Other less common forms of inflammatory arthritis include spondyloarthropathies, disorders of connective tissue (eg, systemic lupus erythematosus), psoriatic arthritis, and crystalline deposition disorders.
B. Pathoanatomy
1. RA is a systemic autoimmune disorder that can affect multiple joints.
2. Erosive pannus formation within the joint and the release of inflammatory cytokines lead to cartilage damage, bone resorption, and soft-tissue degradation.
3. Patients with RA may have concomitant rotator cuff tears.
a. Up to 75% of patients with RA eventually develop rotator cuff pathology.
b. 25% to 30% of patients have full-thickness tears at the time of surgery.
C. Evaluation
1. History
a. Generalized fatigue, pain in other joints, fever, and weight loss
b. Pain, swelling, progressive loss of motion, and weakness are commonly seen in the affected shoulder.
2. Physical examination
a. Common findings include localized warmth, limited range of motion, crepitus, and weakness.
b. Periscapular atrophy may be noted if there is a rotator cuff tear.
c. Sternoclavicular or acromioclavicular joint tenderness occurs in about one third of patients with glenohumeral arthritis.
3. Laboratory evaluation
a. A complete blood cell count, erythrocyte sedimentation rate, C-reactive protein level, uric acid level, rheumatoid factor, serum complement, human leukocyte antigen-B27 screening, and antinuclear antibody titer are helpful in making a diagnosis.
b. Arthrocentesis may be helpful in the setting of an acutely painful shoulder to rule out septic arthritis and crystalline arthropathies. Fluid tests include cell count, Gram stain, culture, and crystal analysis.
i. Milwaukee shoulder (calcium hydroxyapatite crystalline arthropathy)—Aspirates contain blood-tinged fluid with debris, hydroxyapatite crystals, and inflammatory cells with a preponderance of monocytes. Diagnosis
[
Figure 4. AP radiographs showing changes associated with RA. A, Early changes of rheumatoid disease. Osteopenia (with minimal articular degenerative changes) and superior migration of the humeral head (consistent with rotator cuff compromise) are present. B, Intermediate changes of symmetric glenohumeral joint space loss and early cyst formation. C, As the disease progresses, more extensive erosions are evident around the humeral head and glenoid; progressive glenoid bone loss results in medialization of the humeral head. The superior migration of the humeral head indicates progressive rotator cuff deterioration. D, Extensive articular destruction, or arthritis mutilans, reflects end-stage changes with extensive erosions and bone loss.]
is confirmed by positive staining of the crystals with alizarin red.
ii. Gout (deposition of sodium urate crystals) is characterized by negatively birefringent, needle-shaped crystals.
iii. Pseudogout (the deposition of calcium pyrophosphate dihydrate crystals) is characterized by positively birefringent, rhomboid-shaped crystals.
4. Imaging
a. Radiographs (Figure 4)
i. Classic radiographic findings for RA of the shoulder include osteopenia (earliest radiographic sign), marginal erosions, and cyst formation.
ii. Inflammatory arthritis is characterized by concentric joint space narrowing and medial glenoid wear.
iii. Large, irreparable rotator cuff tears may lead to proximal migration of the humeral head.
b. CT scans should be obtained when large bony defects are present.
c. MRI is useful for evaluating the integrity of the rotator cuff tendons.
d. A preoperative radiographic examination of the cervical spine is mandatory for patients with RA, to assess cervical stability before intubation.
D. Classification—Neer identified three types of shoulder RA based on radiographic findings.
1. Dry—Joint space narrowing, subchondral cysts, erosions with marginal osteophytes
2. Wet—Marginal erosions (sometimes quite extreme) and a "pointed" contour of the proximal humerus
3. Resorptive—Rapid bone and cartilage loss with centralization (medialization to the level of the coracoid process) of the glenohumeral joint
E. Treatment
1. Nonsurgical
a. Medications
i. Disease-modifying antirheumatic drugs
ii. NSAIDs
b. Limited intra-articular corticosteroid injections
c. Physical therapy may be helpful for preserving motion.
2. Surgical
a. Preoperative radiographic examination of the cervical spine is mandatory for patients with RA, to assess cervical stability before intubation.
b. Synovectomy
i. Synovectomy may be appropriate for patients with active synovitis and mild articular involvement; it is most beneficial during the early stages of RA, before joint destruction.
ii. The duration and efficacy of pain relief depend on the severity of the disease.
iii. Arthroscopic synovectomy is performed more commonly than open synovectomy.
iv. If the rotator cuff tendon is deficient, the coracoacromial arch must be preserved to prevent anterosuperior escape of the humeral head.
c. Hemiarthroplasty—Indicated for large, irreparable rotator cuff tears or when there is inadequate bone stock to support a glenoid prosthesis.
d. Total shoulder arthroplasty
i. Sufficient bone stock to support a glenoid prosthesis must be present.
ii. The rotator cuff must be intact or have a small (<2 cm) tear that is repairable.
iii. Contraindications include active infection, nonfunctioning deltoid, nonfunctioning or insufficient rotator cuff, irreparable rotator cuff tears, brachial plexus palsy, and severe glenoid bone loss.
iv. Overall outcome is good to excellent, but slightly inferior to outcome in patients with OA.
F. Pearls and pitfalls
1. Significant medialization of the joint (to the level of the coracoid process) may erode enough glenoid bone to preclude reaming and the insertion of a glenoid prosthesis.
2. In patients with RA, osteopenia leads to a significantly higher risk for intraoperative iatrogenic fractures.
3. Care must be taken when implanting the prosthesis to avoid intraoperative fractures.
4. A long-stem humeral prosthesis should be avoided in patients with RA, because elbow arthroplasty may be necessary in the future.
5. In patients with RA, TSA (if possible) results in better outcomes than hemiarthroplasty.
III. Osteonecrosis
A. Epidemiology/overview
1. Posttraumatic osteonecrosis
a. Four-part fracture-dislocations are associated with osteonecrosis in nearly 100% of patients.
b. Displaced four-part fractures are associated with osteonecrosis in 45% of patients.
c. Valgus-impacted four-part fractures have a much lower incidence (approximately 11%).
d. Three-part fractures are associated with osteonecrosis in 14% of patients.
2. Atraumatic osteonecrosis
a. The humeral head is the second most common site of atraumatic osteonecrosis. The femoral head is the most common.
b. Systemic corticosteroid use is the most common cause of atraumatic osteonecrosis. The estimated incidence of atraumatic osteonecrosis after corticosteroid use is 5% to 25%.
c. Atraumatic osteonecrosis is also associated with alcohol abuse, sickle-cell disease, Caisson disease, Gaucher disease, and systemic lupus erythematosus.
[
Figure 5. Posttraumatic osteonecrosis. A, AP view. B, Axillary view. C, Photograph of surgical specimen demonstrating subchondral collapse.]
B. Pathoanatomy
1. The common final pathway is blood flow insufficiency, leading to death of cells within the bony matrix.
2. During subsequent bone resorption and remodeling, microfracture and subchondral bone collapse may lead to joint incongruity and arthritic changes.
3. Blood supply to the humeral head
a. The main supply is from the ascending branch of the anterior circumflex artery, which runs in the lateral bicipital groove and becomes intraosseous as the arcuate artery.
b. A lesser contribution is made by the posterior humeral circumflex artery, which runs along the posteromedial aspect of the humeral neck (to also supply the humeral head).
C. Evaluation
1. History
a. Common symptoms include pain, loss of motion, crepitus, and weakness.
b. The onset of symptoms is commonly insidious, which often causes a delay in the patient seeking treatment and in the establishment of a diagnosis.
c. A history of risk factors including prior surgery, fractures, alcohol abuse, corticosteroid use, and diving may be elicited.
2. Physical examination—Similar to examination for arthritis; common findings include limited range of motion, crepitus, and weakness in the rotator cuff and deltoid.
3. Imaging
a. Radiographs—The most common initial site for osteonecrotic lesions is the superior middle portion of the humeral head, deep to the articular cartilage. This area can be visualized best in an AP view of the shoulder with the arm in neutral external rotation (Figure 5).
b. MRI is the preferred imaging method; its sensitivity in detecting early osteonecrosis is nearly 100%.
D. Classification—The Cruess system (
Figure 6)
E. Treatment
1. Nonsurgical
a. Medications for pain relief
b. Physical therapy
c. Activity modifications with restriction of overhead activities and manual labor
2. Surgical
a. Core decompression
i. Indicated for patients with stage I and stage II disease; one study reported successful results in 94% to 88% of patients with stage I or stage II disease, respectively.
ii. Clinical experience of core decompression in the humeral head is limited.
b. Hemiarthroplasty—May be appropriate for patients with stage III or stage IV disease.
c. The role of vacscularized bone grafting for osteonecrosis of the humeral head is unclear.
d. For stage V disease, TSA must be considered.
[Figure 6. The Cruess classification system for osteonecrosis. There are five stages, based on radiographic appearance. In stage I, changes are not visible on plain radiographs but can be detected on MRI. In stage II, sclerotic bone can be seen on plain radiographs. In stage III, a subchondral fracture (crescent sign) can be seen on radiographs. Stage IV is characterized by collapse of the humeral head and joint incongruity that does not affect the glenoid. In stage V, there are arthritic changes in the glenoid.]
F. Pearls and pitfalls
1. Once osteonecrosis-related subchondral collapse occurs, arthroplasty is the most reliable treatment option.
2. After osteonecrosis of the humeral head has been established, other joints should be examined for osteonecrosis, especially the femoral head.
IV. Complications of Total Shoulder Arthroplasty
A. Loosening
1. Humeral stem loosening
a. Uncommon in OA; always rule out infection as a cause.
b. Can occur in RA or osteonecrosis
2. Glenoid loosening
a. Most common cause of TSA failure; it accounts for approximately 30% of revisions in the setting of primary OA.
b. Can occur in RA or osteonecrosis
c. Radiographic signs of glenoid lucency do not always correlate with clinical failure.
B. Infection
1. Early infection (<6 weeks after surgery) without evidence of prosthetic loosening may be treated with open irrigation and debridement.
2. Late infection is best treated by removal of the prosthesis, intravenous antibiotics, and staged reconstruction.
C. Failure of subscapularis healing
D. Postoperative stiffness
E. Neurologic injury
1. The axillary nerve is the most commonly injured nerve.
2. The musculocutaneous nerve can also be injured during the placement of retractors under the conjoint tendon.
F. Intraoperative fracture—In patients with RA, osteopenia leads to a significantly higher risk for intra-operative iatrogenic fractures.
Top Testing Facts
Osteoarthritis
1. In primary OA of the shoulder, glenoid erosion typically occurs posteriorly.
2. Anterior capsule and subscapularis contractures are common in primary OA.
3. Rotator cuff tears are rarely associated with primary OA (5% to 10%).
4. Hemiarthroplasty is indicated for large, irreparable rotator cuff tears or when there is inadequate bone stock to support a glenoid prosthesis.
5. In TSA, rotator cuff insufficiency may lead to a "rocking horse" phenomenon that prematurely loosens the glenoid component.
6. Glenoid loosening is the most common cause of TSA failure; it accounts for approximately 30% of revisions in the setting of primary OA.
7. Optimal positioning for shoulder arthrodesis is 30° flexion, 30° internal rotation, and 30° of abduction.
Inflammatory Arthritis
1. Patients with RA may have concomitant rotator cuff tears. Up to 75% of patients with RA eventually develop rotator cuff pathology; 25% to 30% of patients have full-thickness tears at the time of surgery.
2. Inflammatory arthritis is characterized by concentric joint space narrowing and medial glenoid wear.
3. Large, irreparable rotator cuff tears may lead to proximal migration of the humeral head.
4. A preoperative radiographic examination of the cervical spine is mandatory for patients with RA, to assess cervical stability before intubation.
5. An irreparable rotator cuff tear is a contraindication for TSA.
6. In patients with RA, osteopenia leads to a significantly higher risk for intraoperative iatrogenic fractures.
7. Significant medialization of the joint (to the level of the coracoid process) may erode enough glenoid bone to preclude reaming and the insertion of a glenoid prosthesis.
8. Synovectomy is most beneficial during the early stages of RA, before joint destruction.
9. A long-stem humeral prosthesis should be avoided in patients with RA, because elbow arthroplasty may be necessary in the future.
10. In patients with RA, TSA (if possible) results in better outcomes than hemiarthroplasty.
Osteonecrosis
1. Osteonecrosis can have a posttraumatic or an atraumatic cause.
2. The humeral head is the second most common site of atraumatic osteonecrosis. The femoral head is the most common.
3. Systemic corticosteroid use is the most common cause of atraumatic osteonecrosis. The estimated incidence of atraumatic osteonecrosis after corticosteroid use is 5% to 25%.
4. Disruption of the blood supply to the humeral head, primarily from the ascending branch of the anterior circumflex artery, is the most common cause of post-traumatic osteonecrosis.
5. The most common initial site for osteonecrotic lesions is the superior middle portion of the humeral head, deep to the articular cartilage. This area can be visualized best in an AP view of the shoulder with the arm in neutral external rotation.
6. MRI is the preferred imaging method; its sensitivity in detecting early osteonecrosis is nearly 100%.
7. Once osteonecrosis-related subchondral collapse occurs, arthroplasty is the most reliable treatment option.
Bibliography
Cameron BD: Clinical diagnosis and imaging, in Williams GR Jr, Yamaguchi K, Ramsey ML, Galatz LM (eds): Shoulder and Elbow Arthroplasty. Philadelphia, PA, Lippincott, 2005, pp 59-74.
Castagna A, Giombini A, Vinanti G, Massazza G, Pigozzi F: Arthroscopic treatment of shoulder ochronotic arthropathy: A case report and review of literature. Knee Surg Sports Traumatol Arthrosc2006;14:176-181.
Chen AL, Joseph TM, Zuckerman JD: Rheumatoid arthritis of the shoulder. J Am Acad Orthop Surg 2003;11:12-24.
Edwards TB, Kadakia NR, Boulahia A, et al: A comparison of hemiarthroplasty and total shoulder arthroplasty in the treatment of primary glenohumeral osteoarthritis: Results of a multicenter study. J Shoulder Elbow Surg 2003;12:207-213.
Gartsman GM, Roddey TS, Hammerman SM: Shoulder arthroplasty with or without resurfacing of the glenoid in patients who have osteoarthritis. J Bone Joint Surg Am 2000; 82:26-34.
Iannotti JP, Norris TR: Influence of preoperative factors on outcome of shoulder arthroplasty for glenohumeral osteoarthritis. J Bone Joint Surg Am 2003;85:251-258.
Matsen FA III, Rockwood CA Jr, Wirth MA, Lippitt SB, Parsons M: Glenohumeral arthritis and its management, in Rock-wood CA Jr, Matsen FA III, Wirth MA, Lippitt SB (eds): The Shoulder.Philadelphia, PA, WB Saunders, 2004, pp 879-1007.
Sarris I, Weiser R, Sotereanos DG: Pathogenesis and treatment of osteonecrosis of the shoulder. Orthop Clin North Am 2004;35:397-404.
Smith CA, Williams GR Jr: Replacement arthroplasty in glenohumeral arthritis: Intact or reparable rotator cuff, in Williams GR Jr, Yamaguchi K, Ramsey ML, Galatz LM (eds): Shoulder and Elbow Arthroplasty. Philadelphia, PA, Lippincott, 2005, pp 75-103.
Trail IA: Replacement arthroplasty in synovial-based arthritis, in Williams GR Jr, Yamaguchi K, Ramsey ML, Galatz LM (eds): Shoulder and Elbow Arthroplasty. Philadelphia, PA, Lippincott, 2005, pp 115-129.
Walch G, Badet R, Boulahia A, Khoury A: Morphologic study of the glenoid in primary glenohumeral osteoarthritis. J Arthroplasty 1999;14:756-760.
Wijgman AJ, Roolker W, Patt TW, Raaymakers ELFB, Marthi RK: Fixation of three and four part fractures of the proximal part of the humerus. J Bone Joint Surg Am 2002;84: 1919-1925.