© Springer-Verlag France 2015
Cyril Mauffrey and David J. Hak (eds.)Passport for the Orthopedic Boards and FRCS Examination10.1007/978-2-8178-0475-0_31Shoulder
(1)
Department of Orthopedic Surgery, Center for Shoulder, Elbow and Sports Medicine, New York Presbyterian/Columbia University Medical Center, New York, NY, USA
1 AC Joint Arthritis
Take-Home Message
Radiographic evidence of AC joint arthritis must be correlated with clinical evidence of pain at the AC joint.
Lidocaine injection test is highly specific for AC joint pathology and predicts success if surgery is indicated.
Nonoperative management including activity modification is effective.
Fastest return to full activity with arthroscopic techniques, but comparable long-term outcomes versus open surgery.
Definition
Degeneration of the acromioclavicular joint (ACJ) that causes pain and disability in the shoulder
Etiology
Primary osteoarthritis: degeneration secondary to large forces across the small joint surface area
Radiographic evidence of degeneration in the ACJ does not necessarily mean it is symptomatic. Sixty percent of elderly individuals have ACJ arthritis, but this is often asymptomatic.
Post-traumatic arthritis: superficial joint susceptible to trauma, associated with AC separations
Distal clavicle osteolysis: secondary to repetitive stress (weight lifting; “weight lifter’s shoulder”)
Pathophysiology
ACJ is a diarthrodial joint susceptible to degeneration and begins in the second decade.
Arthritis characterized by sclerosis, osteophyte formation, subchondral cysts, and joint space narrowing.
Distal clavicle osteolysis bone shows microscopic fractures, osteopenia, subchondral cysts, and distal clavicle erosions.
Radiographs
Standard shoulder radiographs inadequate.
Zanca view highlights the distal clavicle and AC joint.
Normal ACJ space in young patient is 1–3 mm, but >60 years 0.5 mm.
Distal clavicle osteolysis radiographs show relative osteopenia, loss of subchondral bone, increased size of the distal clavicle, and widening of joint space.
Stress views not routinely used. Bone scan helpful in middle-age active patient with pain but no radiographic changes.
MRI has low specificity but high sensitivity and must correlate to physical exam. Reactive bone edema in the distal clavicle/acromion (best seen on T2 images) best predictor of symptomatic AC joint.
Classification
No true classification.
Understanding etiology is key to determining treatment (primary OA, post-traumatic arthritis, distal clavicle osteolysis).
Treatment
Treatment success directly related to ability of physician to distinguish AC joint pain from other sources of pain (subacromial, biceps, glenohumeral)
Selective AC joint anesthetic injection helpful to improve diagnostic accuracy
Nonoperative
Activity modification (avoid inciting activity); if symptomatic during bench press exercise, encourage patient to decrease maximal weight to relieve symptoms.
Heat therapy, NSAIDs.
Intra-articular corticosteroid injections.
Physical therapy (limited success unless coexistent impingement or restricted shoulder motion), rotator cuff strengthening.
Recommended minimum 6 months of nonoperative treatment prior to surgery.
Operative
Success of distal clavicle resection predicted by pain relief with intra-articular anesthetic injection.
Regardless of technique used, resect 1 cm bone and ensure smooth distal clavicle from anterior to posterior ensuring no residual abutment (especially posterosuperior corner if performed arthroscopically).
Outcomes are excellent for open or arthroscopic techniques and differ mainly in postoperative limitations (arthroscopic techniques enable faster return to activity).
Distal clavicle resection contraindicated if history of AC separation higher than grade II.
Preferential ligament preservation important – maintenance of superior AC joint capsule improves joint stability.
High failure rate in workmen’s compensation patients or those undergoing litigation.
Open distal clavicle resection
Open distal clavicle resection allows for direct joint inspection to ensure no further impingement, preferred if open cuff repair is being performed.
Potential for weakness in the deltoid and trapezius which also delays return to sport.
Minimal shoulder motion allowed × 3 weeks, resistance exercises initiated at 6 weeks, and return to overhead activity at 3 months.
Arthroscopic resection with subacromial approach or superior approach
Arthroscopic technique is technically more demanding and takes longer than open procedure.
Subacromial approach can be performed in conjunction with subacromial decompression for impingement.
Direct superior approach potentially avoids injury to the ACJ capsule and is preferred for distal clavicle osteolysis but is more difficult than subacromial approach if small joint space.
Both techniques allow immediate return to work, with sling for comfort for 2–3 days followed by permitted use of arm for ADLs, and for beginning of overhead activity after 3 weeks with return to full activity after 1–2 months.
Complications
Inadequate resection is the most common cause of surgical failure, usually due to posterior distal clavicle abutment on the acromion, often seen as technical cause of failure in arthroscopic techniques secondary to uneven resection.
Weakness or failure of deltoid/trapezius repair after open distal clavicle resection.
If the ACJ is unstable, then poorer prognosis, conoid excision during surgery, or history of injury allows for increased mediolateral motion increasing chance for ACJ abutment and symptoms.
If pain is not due to ACJ arthritis, then any surgical approach will fail to relieve pain, avoided by the use of lidocaine injection test.
Bibliography
1.
Hossain S, Jacobs LG, Hashmi R. The long-term effectiveness of steroid injections in primary acromioclavicular joint arthritis: a five-year prospective study. J Shoulder Elbow Surg. 2008;17(4):535–8. Epub 2008/03/25.
2.
Mall NA, Foley E, Chalmers PN, Cole BJ, Romeo AA, Bach BR, Jr. Degenerative joint disease of the acromioclavicular joint: a review. Am J Sports Med. 2013;41(11):2684–92. Epub 2013/05/08.
3.
Rabalais RD, McCarty E. Surgical treatment of symptomatic acromioclavicular joint problems: a systematic review. Clin Orthop Relat Res. 2007;455:30–7. Epub 2006/12/13.
4.
Shubin Stein BE, Ahmad CS, Pfaff CH, Bigliani LU, Levine WN. A comparison of magnetic resonance imaging findings of the acromioclavicular joint in symptomatic versus asymptomatic patients. J Shoulder Elbow Surg. 2006;15(1):56–9. Epub 2006/01/18.
2 Subacromial Impingement
Take-Home Message
Etiology of this disease is debated (extrinsic versus intrinsic causes) and is likely multifactorial.
Nonoperative treatment (steroid injections and physical therapy) often successful as first-line treatment.
Operative intervention is controversial with regard to open versus arthroscopic, bursectomy alone or in conjunction with acromioplasty, and amount of acromioplasty; all operative treatments appear to show clinical improvement in literature.
Definition
Compression of the contents of the subacromial space (rotator cuff tendons, bursa) by the anterior acromion, coracoacromial ligament, and acromioclavicular joint
Etiology
Debate between primary causes of subacromial impingement, extrinsic versus intrinsic causes.
Extrinsic causes: repetitive impingement of the humeral head and rotator cuff against the coracoacromial ligament causes bursitis and tendinopathy of the rotator cuff which further incites acromial spur formation on the anterolateral band.
Intrinsic causes: partial versus full-thickness cuff tears (or weakness) increase in incidence with age due to natural degeneration versus traumatic tears leading to superior migration of the humeral head and glenohumeral joint narrowing the subacromial space and directly causing impingement of the greater tuberosity on the acromion and coracoacromial ligament which causes spur formation and tuberosity erosion.
Pathophysiology
Bursitis, tendinopathy
Acromial spur formation on the anterolateral band of the coracoacromial ligament
Bursal-sided partial-thickness tears versus full-thickness tears of the supraspinatus
Superior migration of the humeral head in the joint
Secondary impingement: caused by underlying glenohumeral instability (decompression surgery will fail if not recognized)
Radiographs
AP shoulder, true AP (Grashey view), scapular Y view (outlet), and axillary radiographs.
Typical changes include AC joint osteophyte formation inferiorly, acromial enthesophytes, subchondral cysts, or sclerosis in the humeral head around the greater tuberosity.
Decreased acromiohumeral index (normal 7–8 mm).
Outlet visualizes acromial morphology described by Bigliani et al.
Axillary view shows the os acromiale (unfused acromial ossification center).
MRI shows rotator cuff tears and degeneration and subacromial bursitis (thickness >3 mm, increased bursal fluid).
Classification
Bigliani et al. described acromion morphology as seen on supraspinatus outlet view.
Type I: flat
Type II: curved
Type III: hooked, associated with impingement, highest incidence of rotator cuff tears
Neer stages of impingement based on rotator cuff tendinopathy
Stage I: edema and hemorrhage of the bursa and cuff, patient <25 years old, reversible
Stage II: fibrosis and tendinitis of the cuff, patient 25–40 years old, activity-related pain
Stage III: AC spur and partial or complete cuff tear, patient >40 years old
Two stages of impingement by Neer
Outlet impingement: coracoacromial arch impinges on the supraspinatus outlet.
Non-outlet impingement: due to thickening or hypertrophy of the rotator cuff tendons or bursa.
Treatment
Operative and nonoperative management strategies equally efficacious
Nonoperative
Activity modification
Physical therapy shown to help improve pain and shoulder function, but no improvements in range of motion or strength noted; maximal improvement out to 1 year
Subacromial injection with corticosteroid (NSAIDs inferior), notable improvement after 6 weeks
Operative
Indicated after 6-month failed trial of nonoperative therapies
Open anterior acromioplasty (Neer) versus arthroscopic subacromial decompression
Arthroscopic technique shown to have fast return to work and fewer days in the hospital although equally efficacious.
Open technique allows for direct cuff repair if necessary.
Bursectomy alone versus anterior acromioplasty with bursectomy highly debated with both techniques showing decreased pain and improvements in functional scores
Avoid coracoacromial ligament resection if massive tear
Complications
Persistent pain, often secondary to incorrect initial diagnosis.
If irreparable rotator cuff tear, excessive debridement of the coracoacromial ligament will lead to superior migration of the humeral head.
Inadequate bone resection can lead to recurrent symptoms, whereas excessive bone resection can predispose to acromial fractures.
Typical risks of arthroscopic portal creation includes injury to the suprascapular and axillary nerves.
Bibliography
1.
Bigliani LU, Levine WN. Subacromial impingement syndrome. J Bone Joint Surg Am. 1997;79(12):1854–68. Epub 1997/12/31.
2.
Bigliani LU, Morrison DS, April EW. The morphology of the acromion and its relationship to rotator cuff tears. Orthop Trans. 1986;10:228.
3.
Davis AD, Kakar S, Moros C, Kaye EK, Schepsis AA, Voloshin I. Arthroscopic versus open acromioplasty: a meta-analysis. Am J Sports Med. 2010;38(3):613–8. Epub 2009/02/04.
4.
Neer CS, 2nd. Anterior acromioplasty for the chronic impingement syndrome in the shoulder: a preliminary report. J Bone Joint Surg Am. 1972;54(1):41–50. Epub 1972/01/01.
5.
Neer CS, 2nd. Impingement lesions. Clin Orthop Relat Res. 1983(173):70–7. Epub 1983/03/01.
6.
Neer CS. Shoulder reconstruction. Philadelphia: Saunders; 1990. xi, 551 p.
3 Calcific Tendinopathy
Take-Home Message
Calcium deposition in the rotator cuff tendon with unknown etiology, the supraspinatus is the most common location.
Prevailing theory of reactive formation of calcium stages: pre-calcific, calcific (formative, resting, resorptive), and post-calcific.
Acute pain in resorptive phase often resolves spontaneously with supportive care.
Chronic pain in formative phase requires surgical intervention or extracorporeal shock-wave therapy.
Definition
Self-limiting cell-mediated calcification within and around the living tendon followed by spontaneous phagocytic resorption and reconstitution of the normal viable tendon
Etiology
Controversial mechanism with causative agent thought to be tissue hypoxia and local tissue pressure, no proven direct cause.
Incidence 1.5× female versus male and increased if HLA-A1 antigen positive or coexistent insulin-dependent diabetes (30 %) (diabetics most likely to be asymptomatic), typically 30- to 50-year olds.
Eighty percent occurrence in the supraspinatus, 25 % have rotator cuff tear.
Pathophysiology
Calcium deposition within the tendon substrate causes cell-mediated inflammatory response which causes acute pain and secondarily leads to bursitis and thickening of the rotator cuff with secondary subacromial impingement.
Degenerative calcification: tendon fiber degeneration mainly in the hypovascular zone manifests as tendonitis, and age-related wear leads to tenocyte necrosis with intracellular accumulation of calcium which leads to tendon calcification.
This theory has mainly been rejected as there is no noted increased incidence of this disease as patients age despite increasing number with rotator cuff pathology.
Reactive calcification: prevailing theory, 3 stages, no definitive time course for each phase
Pre-calcific stage: fibrocartilaginous metaplasia of tenocytes turning into chondrocytes, painless
Calcific stage: 3 phases
Formative: calcium crystal deposits form foci within tendon separated by fibrocartilage, chalk-like, ± pain
Resting: no further calcium deposition and no evidence of inflammation, ± pain
Resorptive: inflammatory cell-mediated reaction with increased vascularity around deposits with infiltration of macrophages and multinucleated giant cells, notable calcium deposit phagocytosis, form creamy calcium-containing pasty material that increases the intra-tendinous pressure, ++PAINFUL
Post-calcific stage: granulation tissue and remodeling with type III collagen replacing type I collagen, notable tendon healing, ± pain
Radiographs
Plain film AP (evaluate supraspinatus, most common), internal (infraspinatus/teres minor) and external rotation (subscapularis), scapular Y (impingement) to localize calcium deposits
CT helpful to confirm location of deposits as these can be difficult to see in plain films
MRI useful for diagnosis of coexistent rotator cuff tear and subacromial bursitis or tendon edema
Classification
DePalma and Kruper
Type I: resorptive phase, acute pain, fluffy-appearing deposits with poorly defined periphery with overlying streaks at the site where calcium deposits ruptured from the tendon into the subacromial bursa
Type II: formative phase, subacute or chronic pain, discrete homogeneous calcium deposits with uniform density and well-defined periphery
Gärtner: evaluates appearance of calcium deposits on radiographs
Type I: homogeneous, defined borders
Type II: heterogeneous with sharp outline OR homogeneous without defined border
Type III: cloudy and translucent
Treatment
Nonoperative
Physical therapy to maintain shoulder motion
NSAIDs have unclear, unproven benefit.
Subacromial corticosteroid injections.
Needle lavage to release intra-tendinous pressure.
Extracorporeal shock-wave therapy (ESWT).
Operative
Open versus arthroscopic tendon debridement ± rotator cuff repair (if indicated)
Resorptive Phase (Gärtner III)
Spontaneous healing although length of time to heal varies; acute symptoms typically improve after 3–5 weeks, but time for complete resolution of radiographic appearance of calcium deposits ranges 3–10 years in 33 % of patients.
Nonoperative therapy predominates with steroid injections for pain control and to decrease inflammation, needle lavage to decrease intra-tendinous pressure, and physical therapy to maintain motion.
No indication for ESWT or surgery.
Formative Phase (Gärtner I/II)
Uncommon for symptoms to resolve with nonoperative management
ESWT proven efficacious at high energy to target calcium deposits, best outcomes when combined with needle lavage
Open or arthroscopic calcium deposit excision indicated if symptomatic, arthroscopic methods preferable
Recovery is longer if surgery is needed to allow for tendon healing, but this allows for rotator cuff repair if present.
Debate as to the level of aggressiveness with calcium debridement, if subacromial decompression is indicated and if it is necessary to explore the glenohumeral joint.
Complications
Hematomas noted after ESWT
Risk of creating a rotator cuff tear during arthroscopic or open calcium excision
Secondary shoulder stiffness
Typical risks of open shoulder surgery or arthroscopy
Bibliography
1.
Cacchio A, Paoloni M, Barile A, Don R, De Paulis F, Calvisi V, et al. Effectiveness of radial shock-wave therapy for calcific tendinitis of the shoulder: single-blind, randomized clinical study. Phys Ther. 2006;86(5):672–82.
2.
Galasso O, Amelio E, Riccelli DA, Gasparini G. Short-term outcomes of extracorporeal shock wave therapy for the treatment of chronic non-calcific tendinopathy of the supraspinatus: a double-blind, randomized, placebo-controlled trial. BMC Musculoskelet Disord. 2012;13:86
3.
Le Goff B, Berthelot JM, Guillot P, Glémarec J, Maugars Y. Assessment of calcific tendonitis of rotator cuff by ultrasonography: comparison between symptomatic and asymptomatic shoulders. Joint Bone Spine. 2010;77(3):258–63.
4.
Rizzello G, Franceschi F, Longo UG, Ruzzini L, Meloni MC, Spiezia F, et al. Arthroscopic management of calcific tendinopathy of the shoulder: do we need to remove all the deposit? Bull NYU Hosp Jt Dis. 2009;67(4):330–3.
5.
Seil R, Litzenburger H, Kohn D, Rupp S. Arthroscopic treatment of chronically painful calcifying tendinitis of the supraspinatus tendon. Arthroscopy. 2006;22(5):521–7.
4 Rotator Cuff Tear
Take-Home Message
Result of extrinsic and intrinsic factors, impingement, and age-related degeneration.
Partial
Bursal sided
Articular sided
Full-thickness tear classification (Cofield, North America)
Small <1 cm
Medium 1–<3 cm
Large 3–<5 cm
Massive ≥5 cm
Ellman classification is most commonly used to describe size and location of tear.
Low-grade partial-thickness tears (<50 % thickness) can be debrided, while high-grade tears (>50 % thickness) or acute tears in young patients should be repaired.
Full-thickness tears treated with primary repair may be amenable to direct tendon-to-bone healing or may require interval slide, marginal convergence techniques.
Massive tear repair can be performed – negative prognostic factors include muscle atrophy (Goutallier 3 and 4 bad), level of retraction, and proximal humeral migration.
Definition
Partial or complete detachment of one or more of the four muscle-tendon units (supraspinatus, infraspinatus, teres minor, subscapularis) that mobilize and dynamically stabilize the humeral head within the glenohumeral joint
Etiology
Multifactorial with extrinsic and intrinsic causes that exacerbate one another
Extrinsic: acromioclavicular impingement or shoulder instability or trauma can cause tears that cause tendon degeneration that exacerbates disease and can also cause bursitis and tendon inflammation which worsens impingement and disease progression.
Intrinsic: normal aging, tendon overuse, and eccentric muscle loading leads to degeneration which can further cause glenohumeral instability and impingement leading to further tearing.
Extrinsic causes (impingement) typically first show bursal-sided partial-thickness tears or intra-tendinous tears, while intrinsic causes lead to articular-sided tears.
Known hypovascular zone near insertion of the supraspinatus predominantly in articular side may predispose to articular side tears.
Common disease (not all symptomatic) with increasing incidence in elderly; unilateral rotator cuff tear and >65 years old associated with 50 % incidence of bilateral rotator cuff tear.
Unclear in literature as to the natural history of partial-thickness tear progression, thought that partial-thickness tears increase strain on middle and bursal segments, which may lead tear progression.
Spinoglenoid notch cysts may cause impingement of suprascapular nerve and impaired function of the infraspinatus which may masquerade as cuff tear.
Pathophysiology
Partial or full thickness; small, medium, large, or massive tears.
Inflammation and tendon swelling.
Loss of dynamic stability of the glenohumeral joint with poor coordination of the rotator cuff muscles and deltoid.
Irreversible fatty atrophy and interfibrous fat infiltration of the rotator cuff muscle occur around 4 months after tear occurs.
Cysts can form at cuff insertion if complete tear occurs.
Articular-sided tears 2–3× are more common than bursal-sided tears.
Overhead-throwing athletes usually present with partial-thickness tears on articular side of the supraspinatus and infraspinatus tendon.
Radiographs
AP, scapular Y, and axillary views to evaluate joint for degenerative changes, subacromial spurs, cystic changes in the humeral head (suggests cuff tear), instability with superior migration of head, decreased acromiohumeral distance.
Ultrasound helpful to dynamically test cuff and evaluate for tears.
MRI/MRA is the most sensitive and specific; is the best method of visualizing size and shape of the tear, partial versus full thickness, and amount of retraction; and can also evaluate muscle atrophy; T2 images are the most useful; must confirm tear on coronal and sagittal views.
Shoulder in abduction and external rotation improves accuracy.
Classification
Tear size description: small, <1 cm; medium, 1–3 cm; large, 3–5 cm; massive, ≥5 cm or involving 2 or more tendons
Ellman classification system of partial-thickness rotator cuff tears describes size of tear and location
Size: I = < 3 mm (<25 % thickness), II = 3–6 mm (25–50 % thickness), III = >6 mm (>50 % thickness)
Location: A = articular surface, B = bursal surface, C = interstitial
Geometric classification (Davidson and Burkhart) guides treatment based on MRI findings
Type 1: crescent shaped, short and wide tear, mobile in medial/lateral direction, amenable to direct tendon-to-bone repair
Type 2: U shaped or L shaped, long and narrow, mobile in anterior/posterior direction, treat with marginal convergence
Type 3: massive contracted tear, long and wide, treated with interval slide technique and/or partial repair
Type 4: rotator cuff arthropathy, glenohumeral arthrosis and loss of acromiohumeral space, requires joint arthroplasty (see subsection on “Rotator Cuff Arthropathy”)
Goutallier classification: grading scheme to classify cuff muscle atrophy and assess potential ability to repair cuff, best assessed on sagittal T1 images
Grade 0 = normal
Grade 1 = some fatty streaks
Grade 2 = more muscle than fat
Grade 3 = equal muscle and fat
Grade 4 = more fat than muscle
Treatment
Nonoperative
Useful in patients with minimal risk of progression to irreversible muscle/tendon changes (intact cuff with tendinitis especially associated with subacromial bursitis or impingement, small partial-thickness tears)
Activity modification, avoid repeated forward flexion >90°
Physical therapy, exercises to increase mobility and strengthen rotator cuff and periscapular musculature and improve shoulder stability
Oral NSAIDs
Subacromial or glenohumeral glucocorticoid or NSAID injections
Operative
Any surgical repair where rotator cuff is re-approximated to the footprint takes 2–3 months to achieve biologic healing.
Arthroscopic versus mini-open repair techniques used, historically open approaches were used.
Partial-thickness rotator cuff tear
Debridement alone for low-demand patient with articular side tear <50 % tendon thickness with viable surrounding tissue.
Debridement with acromioplasty and subacromial decompression if bursal-sided tear and signs of mechanical impingement.
Tendon repair for manual laborer/athlete if bursal sided and >30 % thickness, acute repair better than delayed in this case.
PASTA (partial articular-sided supraspinatus tendon avulsion) tears should be repaired if >7 mm footprint is involved (violates >50 % footprint); however, this should be performed with great caution in overhead athletes as the tear is likely adaptive.Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
