Anterior Apprehension and Relocation Tests

These are tests for anterior glenohumeral joint instability. The patient is placed in the supine position. The examiner abducts the patient’s shoulder 90 degrees and flexes the elbow 90 degrees. The examiner uses one hand to slowly externally rotate the patient’s humerus using the patient’s forearm as the lever. At the same time, the examiner’s other hand is placed posterior to the patient’s proximal humerus and exerts an anteriorly directed force on the humeral head. The test result is considered positive if the patient indicates a feeling of impending anterior dislocation. If the examiner removes the hand from behind the proximal humerus and places it over the anterior proximal humerus and then exerts a posteriorly directed force, and the patient subsequently reports a reduction in apprehension, then a positive relocation test has occurred.¹⁰¹

Posterior Apprehension Test

This test evaluates posterior glenohumeral joint stability. The patient’s affected shoulder is forward flexed to 90 degrees and then maximally internally rotated. A posteriorly directed force is then placed on the patient’s elbow by the examiner. A positive test result causes a 50% or greater posterior translation of the humeral head or a feeling of apprehension in the patient.¹⁰¹

Sulcus Sign

The sulcus sign is used to evaluate inferior glenohumeral joint instability. The patient is seated or standing with the arm relaxed in shoulder adduction. The patient’s forearm is grasped by the examiner, and a distal traction force is placed through the patient’s arm. In the presence of inferior instability, a sulcus will develop between the humeral head and the acromion.¹⁰¹

O’Brien Test

This test evaluates for acromioclavicular (AC) joint and labral abnormalities. The shoulder is flexed to 90 degrees with the elbow fully extended. The arm is then adducted 15 degrees, and the shoulder is internally rotated so that the patient’s thumb is pointing down. The examiner applies a downward force against the arm, which the patient is instructed to resist. The shoulder is then externally rotated so that the patient’s palm is facing up, and the examiner applies a downward force on the patient’s arm, which the patient is instructed to resist. A positive test result is indicated by pain during the first part of the maneuver with the patient’s thumb pointing down, which is then lessened or eliminated when the patient resists a downward force with the palm facing up. Pain in the region of the AC joint indicates AC pathology, whereas pain or painful clicking deep inside the shoulder suggests labral pathology.¹²⁸

Horizontal Adduction Test

The shoulder is passively flexed to 90 degrees and then horizontally adducted across the chest. Pain located in the region of the AC joint suggests AC joint pathology, whereas posterior shoulder pain suggests posterior capsular tightness.¹⁰⁵

Speed’s Test

This test is for biceps tendonitis. The patient’s shoulder is forward flexed to 90 degrees with the elbow fully extended and the palm facing up. The examiner applies a downward force against the patient’s active resistance. Pain in the region of the bicipital groove suggests bicipital tendonitis.¹⁰¹

Yergason’s Test

With the patient’s arm at the side, the elbow is flexed to 90 degrees and the forearm is pronated. The patient then tries to simultaneously supinate the forearm and externally rotate the shoulder against the examiner’s resistance. This test can provoke bicipital region pain in patients with bicipital tendonitis, and a painful “pop” in patients with bicipital tendon instability.¹⁰¹

Neer-Walsh Impingement Test

The patient’s shoulder is internally rotated while at the side. The examiner passively forward flexes the patient’s shoulder to 180 degrees while maintaining internal rotation. Pain in the subacromial area suggests rotator cuff tendonitis.¹⁰¹

Hawkins-Kennedy Impingement Test

The patient’s shoulder and elbow are each passively flexed to 90 degrees, respectively. The examiner then grasps the patient’s forearm, stabilizes the patient’s scapulothoracic joint, and uses the forearm as a lever arm to internally rotate the glenohumeral joint. A positive test result is indicated by pain in the subacromial region occurring with the internal rotation.¹⁰¹

Drop Arm Test

The examiner passively abducts the patient’s shoulder 90 degrees. The patient is then asked to slowly lower the arm back to the side. A positive test result is indicated by pain and an inability to slowly lower the arm to the side, suggesting a rotator cuff tear.¹⁰¹

Cozen’s Test

The patient is asked to fully extend the elbow, pronate the forearm, and make a fist. The examiner then resists the patient’s attempt to extend and radially deviate the wrist. Pain over the lateral epicondyle represents a positive test result and suggests the presence of lateral epicondylitis.⁹⁹

Ligamentous Instability Test

The examiner flexes the patient’s elbow 20 to 30 degrees and stabilizes the patient’s arm by placing a hand at the elbow and a hand on the distal forearm. Varus and valgus forces are placed across the elbow by the examiner to test the stability of the radial and ulnar collateral ligaments (UCL), respectively.⁹⁹

Finkelstein Test

This test is used to detect tenosynovitis of the extensor pollicis brevis and abductor pollicis longus tendons (de Quervain’s tenosynovitis). The patient makes a fist with the thumb inside the fingers, and the examiner passively deviates the wrist in an ulnar direction. A positive test result causes pain in the affected tendons.¹⁰⁰

Watson Test

This test assesses scapholunate stability. The patient’s wrist begins in an ulnarly deviated position. The examiner places a dorsally directed force against the proximal volar pole of the scaphoid. The examiner then radially deviates the wrist while continuing to place the same force against the scaphoid. A “pop” or subluxation of the scaphoid indicates a positive test result.¹⁰⁰

Sternoclavicular Joint Sprains

Sternoclavicular joint dislocations account for less than 1% of all joint dislocations. Two thirds of sternoclavicular joint dislocations occur anteriorly, whereas one third of dislocations occur posteriorly. The etiology is usually traumatic.³⁸

The diagnosis of sternoclavicular joint injuries is made with an accurate history, physical examination, and radiologic evaluation. Anterior sternoclavicular joint injuries can cause the medial end of the clavicle to become more prominent, whereas posterior joint injuries typically have more pain with a less prominent medial clavicular end. Posterior dislocations can also be associated with vascular compromise to the ipsilateral upper limb, neck and upper limb venous congestion, difficulty breathing, or difficulty swallowing.

Ligament injuries are commonly graded on a scale of 1 to 3 (Table 38-1).³⁸ The presence of tenderness at the sternoclavicular joint without subluxation or dislocation indicates a grade 1 injury; tenderness with subluxation indicates a grade 2 injury; and tenderness with associated dislocation indicates a grade 3 injury.¹⁹⁰

Table 38-1 Ligamentous Injury Grading Scale

The radiologic evaluation of sternoclavicular joint injuries includes an anteroposterior radiograph of the chest or sternoclavicular joint and a serendipity view, which involves a 40-degree cephalic tilt view of the sternoclavicular joints (Figure 38-1).¹⁵⁷ Often standard radiographs leave the diagnosis in question, and computed tomography (CT) scan is frequently used for definitive evaluation of sternoclavicular joint injuries.

FIGURE 38-1 The serendipity view of the sternoclavicular joints.

The treatment of grade 1 and 2 injuries is nonoperative and involves the application of the previously described rehabilitation principles. Sling immobilization can be used for comfort and protection during the acute rehabilitation phase. Activity can progress as tolerated with an anticipated return to activity after 1 to 2 weeks for a grade 1 injury and 4 to 6 weeks for a grade 2 injury.

Grade 3 sternoclavicular joint sprains frequently can be treated nonoperatively as described for grade 1 and 2 injuries.⁴¹ Those that remain unstable postreduction, however, might require surgical intervention.¹⁹⁰ Because complications frequently arise with grade 3 posterior dislocations, a thorough evaluation to rule out pulmonary or vascular damage should be undertaken. If mediastinal compression is present, posterior grade 3 dislocations require immediate surgical intervention.¹⁹⁰ Because of the significant risk of vascular complications, posterior sternoclavicular joint dislocations should be reduced in the hospital setting with a vascular surgeon present.

Clavicle Fractures

A majority of clavicular fractures occur in childhood and adults less than 25 years of age. Eighty percent of clavicular fractures occur in the middle third of the clavicle, whereas approximately 15% occur in the lateral one third and 5% in the medial one third. Most clavicular fractures occur as a result of a direct blow to the point of the shoulder, but a small percentage occur from a fall onto an outstretched arm.¹⁷

Most patients know when they have fractured their clavicle. It is important to rule out associated neurovascular and pulmonary injuries during the physical examination and radiologic evaluation. Routine anteroposterior radiographs of the clavicle are usually adequate for visualization of clavicular middle third fractures. For proximal third fractures, the addition of a serendipity view is often used. When a lateral third fracture is suspected, a 15-degree cephalic tilt anteroposterior view centered on the AC joint using a soft tissue technique (Zanca view) and an axillary lateral view are usually diagnostic when combined with anteroposterior radiographs. Occasionally, CT scanning is required for more definitive evaluation.¹⁷

If the fracture has good alignment, partial immobilization is the treatment of choice using an immobilization device such as a sling or figure-of-eight bandage. If 15 to 20 mm of shortening occurs as a result of displacement, surgical intervention should be considered.¹⁴³ Other common indications for surgical intervention include displaced fractures with tissue interposition between the fracture ends, open fractures, neurovascular compromise, tenting of the skin over the fracture site that might lead to tissue necrosis, and displaced fractures located in the lateral third of the clavicle.¹⁷

Acromioclavicular Joint Sprains

AC joint sprains account for only 9% of all shoulder injuries, are most frequent in males in their third decade of life, and are usually partial rather than complete sprains.¹⁰⁵ Most injuries occur as a result of direct trauma from a fall or blow to the acromion. Physical examination demonstrates point tenderness, a positive horizontal adduction test, and a positive O’Brien test.

Rockwood¹⁵⁸ classified AC joint sprains into six types (Figure 38-2). Type 1 sprains involve a mild injury to the AC ligaments, and radiologic evaluation is normal. Type 2 injuries involve the complete disruption of the AC ligaments but with intact coracoclavicular ligaments. Radiographs might demonstrate clavicular elevation relative to the acromion but less than 25% displacement. Type 3 sprains result in the complete disruption of the AC and coracoclavicular ligaments, but the deltotrapezial fascia remains intact. Radiographs reveal a 25% to 100% increase in the coracoclavicular interspace relative to the normal shoulder. Type 4 sprains involve complete disruption of the coracoclavicular and AC ligaments, with posterior displacement of the distal clavicle into the trapezius muscle. In type 5 sprains, the coracoclavicular and AC ligaments are fully disrupted along with a rupture of the deltotrapezial fascia. This results in an increase in the coracoclavicular interspace to greater than 100% of the normal shoulder. Type 6 sprains involve complete disruption of the coracoclavicular and AC ligaments, as well as the deltotrapezial muscular attachments, with displacement of the distal clavicle below the acromion or the coracoid process.

FIGURE 38-2 The Rockwood classification of acromioclavicular joint sprains.

Radiographic evaluation of the AC joint should include anteroposterior and lateral views of the AC joint, and a Zanca view. Stress views do not provide additional clinically useful information.¹⁰⁵

Type 1, 2, and 3 AC joint sprains are usually treated nonoperatively, using the previously described principles of rehabilitation. A brief period of sling immobilization might be required for pain control. Indications for surgical intervention for type 3 sprains include persistent pain or unsatisfactory cosmetic results. Some authors advocate operative treatment of type 3 sprains in heavy laborers and athletes who participate in sports that place a high demand on the upper limbs,^30,89,141 but the current literature favors nonoperative treatment for type 3 sprains because of the similar outcomes between operative and nonoperative management and higher complication rates after operative intervention.¹⁷¹ Type 4, 5, or 6 sprains require surgical treatment.¹⁰⁵

Intraarticular AC joint fractures are treated similarly to type 1 through 3 AC joint sprains, unless the injury is open or involves neurovascular compromise. Posttraumatic arthrosis in the AC joint can occur. Persistent pain, despite an appropriate nonoperative treatment program, necessitates surgical resection of the distal clavicle.¹⁰⁵

Osteolysis of the Distal Clavicle

Repetitive overload of the distal clavicle can result in osteolysis. Young weight lifters who perform a significant amount of bench press and military press lifts are the most susceptible to this condition.²⁶ The athlete usually presents with gradual onset of AC joint pain that is increased with overhead presses or bench press, particularly when the bar is lowered all the way to the chest because this results in a significant sheer stress to the AC joint. It frequently occurs bilaterally.¹⁶⁷

Radiographic evaluation is the same as for AC joint injuries. The pathologic changes found on radiographs include distal clavicular subchondral bone loss and cystic changes. Widening of the AC joint can occur in late stages. Bone scans are positive during active disease and can be used to confirm the diagnosis.¹⁰⁵

Nonoperative treatment of distal clavicular osteolysis involves avoidance of the aggravating activities, and application of the previously discussed rehabilitation principles. Occasionally, AC joint intraarticular corticosteroid injections can assist in pain control. For many athletes, however, activity modification is not practical or does not result in significant pain relief. In those athletes who fail to improve with nonoperative measures or are unable to adequately modify their activities, distal clavicular resection is the surgical procedure of choice.¹⁶⁷

Scapulothoracic Crepitus

Multiple authors have reported the occurrence of pathologic sounds at the scapulothoracic joint, often referred to as a snapping scapula or scapular crepitus.^116,140,144 The three primary types of sound that can occur at this joint include a gentle friction sound, a louder grating sound, and a loud snapping. Although the gentle friction sound is probably physiologic, a loud grating sound suggests soft tissue disease such as bursitis, fibrotic muscle, muscular atrophy, or anomalous muscular insertions.¹¹⁶ Occasionally an excessive thoracic kyphosis or thoracic scoliosis can cause pathologic crepitus at the scapulothoracic articulation. Scapulothoracic dyskinesis or scapular winging can also cause painful friction between the scapula and the thorax.⁸⁴ A loud snapping sound is frequently caused by bony pathology such as an osteophyte, a rib or scapular osteochondroma, hooked superomedial angle of the scapula, or malunion of rib fractures.^117,140,154

The physical examination of individuals with symptomatic scapulothoracic crepitus or snapping should include localization of pain and crepitus or snapping through palpation, evaluation of scapulothoracic mechanics for quality and quantity of scapulothoracic motion, and a neurologic examination of the upper limb. Electrodiagnostic studies should be used when nerve injury is suspected. Tangential and anteroposterior radiographic evaluation of the scapula might identify osseous causes of the scapular crepitus or snapping. The radiologic workup might require further evaluation by CT or magnetic resonance imaging (MRI) for selected cases.

Treatment is warranted when the scapular snapping or crepitus is symptomatic. Nonoperative treatment involves correction of biomechanical deficits such as scapulothoracic dyskinesis, strength and flexibility imbalances, and poor posture. Soft tissue mobilization, NSAIDs, and local modalities might assist in pain control. An injection of corticosteroids into the painful area has been advocated by some authors,^33,106 but caution must be exercised because complications such as pneumothorax can occur. For those who fail to improve with nonoperative measures, several surgical procedures have been described for treatment of this condition.¹⁰⁶

Rotator Cuff Tendonitis and Impingement

Injuries to the rotator cuff are common. Although macrotrauma can cause rotator cuff injuries, repetitive microtrauma and outlet impingement between the acromion and greater tuberosity of the humerus are more common.¹¹⁵ Neer categorized this type of rotator cuff injury into three stages.¹²² Stage 1 injuries involved inflammation and edema in the rotator cuff. Stage 2 rotator cuff injuries had progressed to fibrosis and tendonitis. When a partial or complete rotator cuff tear occurred, this was considered a stage 3 injury. In the overhead athlete, underlying instability patterns of the glenohumeral joint with associated excessive translation of the humeral head frequently led to outlet impingement and rotator cuff disease.⁶

On cadaveric examination, Bigliani²¹ found a relationship between the acromial shape and the presence of rotator cuff tears. He classified the acromions into three types (Figure 38-3). Type 1 acromions were relatively flat, whereas type 2 acromions demonstrated a curve, and type 3 acromions were hooked. The incidence of rotator cuff tears increased as the acromion progressed from a type 1 to a type 3 shape. This was presumably related to the greater outlet impingement of the rotator cuff caused by an increasing acromial curve.

FIGURE 38-3 A, Type 1 acromion. B, Type 3 acromion.

A phenomenon referred to as internal impingement has recently been reported in young overhead athletes.^40,184 When the arm is abducted 90 degrees and maximally externally rotated, there is contact between the undersurface of the rotator cuff and the posterosuperior glenoid rim. This is augmented by anterior glenohumeral joint instability and posterior glenohumeral joint capsular tightness. Internal impingement causes pathologic changes to the undersurface of the rotator cuff.

Impingement can be primary or secondary. Examples of causative factors leading to primary impingement include a hooked acromion or a thick coracoacromial ligament. Secondary impingement has many causes, including glenohumeral joint instability, weak scapular stabilizers, or scapulothoracic dyskinesis and instability.^66,67 Lack of adequate scapular control or weakness in the scapular stabilizers can lead to poor scapular positioning during arm elevation. This can result in an acromion that does not retract during overhead activities, creating secondary impingement. Regardless of whether the impingement is primary or secondary, the underlying cause must be determined to formulate an appropriate treatment program.

Rotator cuff microtrauma can also be caused by “eccentric overload” of the shoulder external rotators during the deceleration phase of throwing.

Microvascular studies of the rotator cuff have found a hypovascular zone in the leading edge of the supraspinatus tendon during shoulder adduction compared with shoulder abduction and on the articular compared with bursal surface of the supraspinatus.^97,149 These hypovascular areas have been implicated as a cause of rotator cuff degeneration and correlate with the higher incidence of articular-sided partial-thickness tears of the rotator cuff.

Patients with rotator cuff injuries frequently note anterior or lateral shoulder pain that occurs with overhead activity and also at night while trying to sleep. Symptoms such as stiffness, weakness, and catching might also be present. It is important to try to elicit any symptoms of underlying glenohumeral joint instability such as numbness, tingling, feelings of subluxation, or previous “dead arm” episodes.

The physical examination of patients with suspected rotator cuff pathology should include an evaluation of the cervical spine because problems originating in the cervical spine frequently refer symptoms to the shoulder. During inspection, the examiner should be sure to assess for proper scapulothoracic mechanics. Strength testing of the rotator cuff muscles can detect weakness as a result of a rotator cuff tear or pain inhibition caused by tendonitis or tendinosis. The Neer-Walsh and Hawkins-Kennedy impingement tests should be performed. Elimination of the pain provoked by impingement testing after injection of 10 mL of 1% lidocaine into the subacromial space confirms the diagnosis of impingement.

The examination of individuals with suspected rotator cuff pathology should also include maneuvers to detect underlying glenohumeral joint instability. The anterior apprehension test can be used to detect both anterior instability of the glenohumeral joint and also internal impingement. If the patient has a sensation of anterior apprehension during the test that is relieved with the relocation test, then there is likely anterior instability. If, however, there is pain in the posterior aspect of the shoulder during the anterior apprehension test that is relieved with the relocation test, then internal impingement is occurring.

Radiographic evaluation of patients with suspected rotator cuff pathology should include anteroposterior, supraspinatus outlet, and axillary radiographs. Anteroposterior radiographs should be performed in the neutral, external, and internal rotation positions to adequately visualize the glenohumeral joint and the greater and lesser tuberosities. Large rotator cuff tears can be indicated by an acromiohumeral distance of less than 7 mm and sclerosis on the undersurface of the acromion. The supraspinatus outlet view allows for categorization of the acromion type and will reveal AC joint osteophytes. Double-contrast arthrograms identify full-thickness rotator cuff tears, partial-thickness articular surface tears, and biceps tendon pathology. Bursal surface and intrasubstance partial-thickness rotator cuff tears are poorly evaluated with this technique. Ultrasound and MRI have high levels of sensitivity and specificity for rotator cuff pathology.^13,73

Nonoperative treatment should include application of the previously described rehabilitation principles. Strengthening exercises for the scapular stabilizing muscles rather than the rotator cuff should be emphasized in the acute rehabilitation stage. Specifically, strengthening muscles that retract and depress the scapula (e.g., serratus anterior and inferior trapezius) and stretching muscles that protract and elevate the scapula (e.g., pectoralis minor and upper trapezius) reduce impingement. Posterior glenohumeral joint capsular tightness should be corrected, particularly in patients with internal impingement. It is imperative to reestablish normal scapulothoracic kinematics through neuromuscular retraining. This can begin once shoulder ROM is pain-free. Rotator cuff muscle strengthening should begin with closed chain exercises to promote stability and proprioception. Open chain exercises can be used to correct strength imbalances, such as weakness of the shoulder external rotators relative to the internal rotators. Some patients benefit from a subacromial corticosteroid injection, although studies of corticosteroid injections have shown mixed results.^68,112,121 Patients recalcitrant to these measures might benefit from extracorporeal shock-wave therapy or, if calcific tendonitis is present, ultrasound-guided percutaneous lavage and aspiration of the calcification.^42,130 If the patient fails to respond to the above measures, surgical evaluation should be considered.

Patients who have sustained an acute full-thickness rotator cuff tear should receive early surgical intervention to maximize their postoperative recovery potential. If the rotator cuff tear is chronic or degenerative, an initial trial of nonoperative rehabilitation measures can be used with the goal of restoring the patient to a functional level. In the young or active subgroups, however, nonoperative measures frequently fail to restore the patient to an adequate level of function, and surgical intervention is required.

Long Head of the Biceps Tendon Strains

Rupture of the long head of the biceps brachii tendon usually occurs in patients more than 40 years of age with a prolonged history of outlet impingement and rotator cuff disease. The patient frequently experiences a “pop” at the time of the injury, which often occurs during lifting or pulling activities. Some patients, however, just present with a painless retraction of the biceps distally resulting in an exaggeration of the biceps muscle contour. Pain can occur with an acute rupture but is not usually a factor in chronic cases. Because rupture of the long head of the biceps brachii tendon results in a loss of approximately 8% of elbow flexion strength and 21% of supination strength,¹⁰³ function is not significantly affected in most individuals.

This injury is best evaluated radiographically with MRI or ultrasound, which demonstrate the biceps tendon’s absence in the bicipital groove.

Treatment in patients more than 40 years of age who are relatively sedentary includes sling immobilization for comfort and application of the rehabilitation principles previously described. Strengthening exercises of the rotator cuff, shoulder girdle, and arm musculature should be undertaken when the patient is able to tolerate it. This allows for maximal restoration of function.

In younger or physically active patients, early surgical intervention might be warranted. Mariani et al.¹⁰³ reported that 93% of the surgically treated patients and 63% of the nonsurgically treated patients were able to return to full work capacity.

Pectoralis Major Strain

Pectoralis major muscle strains are most commonly seen in athletes who perform forceful shoulder adduction and/or internal rotation against resistance, such as weight lifters and football players.¹¹⁰ Pectoralis muscular strains can be categorized into three grades, with grade 1 being minimal muscle disruption and grade 3 a complete rupture. The strain can be located in the muscle belly, musculotendinous junction, or tendon.

Pectoralis major muscle strains are characterized by sudden pain in the pectoral region during a forceful shoulder adduction or internal rotation. Chest wall and proximal anterior arm region edema and ecchymosis can develop, and the anterior axillary fold often demonstrates a visible defect when the shoulder is abducted 90 degrees. The defect in the muscle can also be palpated on examination. Weakness and pain with shoulder adduction and internal rotation are usually present. Radiographs are normal, but ultrasound or MRI examinations can demonstrate the injury.

Treatment is conservative for grade 1 or grade 2 strains, intramuscular grade 3 strain, or rupture from the sternal or clavicular origins. Conservative treatment should use the previously described rehabilitation principles.

If the patient sustains a complete rupture of the pectoralis major tendon at the humeral insertion, nonathletes can undergo a conservative treatment program if they are willing to accept permanent shoulder adduction and internal rotation weakness. In athletes and those who wish to improve their postinjury strength potential, however, surgical intervention is needed.

Glenohumeral Joint Instability

The glenohumeral joint is a diathroidal joint with a rather large humeral head in relation to the small glenoid fossa. This anatomic relationship allows for the significant mobility seen in the glenohumeral joint but comes at the price of poor bony stability. Glenohumeral joint stability is provided by a combination of static and dynamic stabilizers.

The static stabilizers of the glenohumeral joint include the bony congruence between the humeral head and the glenoid fossa, the glenoid labrum, the negative intraarticular pressure, the glenohumeral joint capsule, and the glenohumeral ligaments.¹

The dynamic stabilizers of the glenohumeral joint include the scapular stabilizing muscles, the rotator cuff muscles, and the long head of the biceps.⁹⁰ The importance of optimal scapular function for glenohumeral joint stability cannot be overemphasized. The scapular stabilizing muscles orient the scapula properly in relation to the humerus for optimal static and dynamic stability of the glenohumeral joint and stabilize the scapula during glenohumeral joint movements.⁵¹ The primary scapular stabilizing muscles include the serratus anterior, trapezius, pectoralis minor, rhomboideus minor and major, latissimus dorsi, and levator scapulae.⁵¹

The rotator cuff muscles include the supraspinatus, infraspinatus, subscapularis, and teres minor. These muscles contribute to dynamic glenohumeral joint stability through a number of mechanisms. Concavity compression, first described by Lippitt et al.,⁹⁵ refers to the compressive forces placed on the glenohumeral joint during rotator cuff muscle co-contractions. These forces press the humeral head into the glenoid fossa, center the humeral head within the glenoid fossa, and help resist glenohumeral translation. Because the glenohumeral ligaments are lax in the midranges of glenohumeral joint motion, coordinated rotator cuff muscle contraction and concavity compression are particularly important mechanisms for glenohumeral joint stability in these ranges.⁹⁰

At the distal insertion of the rotator cuff muscles on the humerus, there is an intertwining of the joint capsule with the rotator cuff tendons. With rotator cuff muscle contraction, it is possible that the glenohumeral joint capsule develops tension and increases in stiffness, consequently acting as a dynamic musculoligamentous stabilizing system.⁹⁰

The rotator cuff muscles also provide glenohumeral joint stability through passive muscle tension and act as barriers to glenohumeral joint translation during active motion.^25,31 The subscapularis appears to be an especially important stabilizer for both anterior and posterior glenohumeral joint stability.^22,43

Proprioception and neuromuscular control refer to the mechanism by which the position and movements of the shoulder girdle are sensed (proprioception), processed, and result in an appropriate motor response (neuromuscular control).¹²⁰ Glenohumeral joint instability is often associated with a concomitant decrement in proprioception.⁹³ The abnormal proprioception is restored after surgical correction of the joint instability, suggesting that one of the mechanisms causing proprioceptive deficits in unstable glenohumeral joints is a lack of appropriate capsuloligamentous tension.⁹⁴

The classification of glenohumeral joint instability includes the degree, frequency, etiology, and direction of instability.¹⁴ The degree includes dislocation, subluxation, or microinstability. A dislocation implies that the humeral head is disassociated from the glenoid fossa and often requires manual reduction. A subluxation occurs when the humeral head translates to the edge of the glenoid, beyond normal physiologic limits, followed by self-reduction. Microinstability is due to excessive capsular laxity, is multidirectional, and is frequently associated with internal impingement of the rotator cuff.¹⁴

The frequency of instability can be either acute or chronic.¹⁴ Acute instability involves a new injury resulting in subluxation or dislocation of the glenohumeral joint. Chronic instability refers to repetitive instability episodes.

The etiology of glenohumeral joint instability can be traumatic or atraumatic.¹⁴ Unidirectional instability is frequently caused by a traumatic event resulting in disruption of the glenohumeral joint. Atraumatic instability refers to glenohumeral joint instability resulting from congenital capsular laxity or repetitive microtrauma. Atraumatic instability can be subclassified into voluntary and involuntary categories. Voluntary instability refers to an individual who volitionally subluxes or dislocates his or her glenohumeral joint, whereas those with involuntary instability do not. Some patients with voluntary instability have associated psychologic pathology, which often portends a poor outcome if surgical stabilization is performed.¹⁶¹

Glenohumeral joint instability can be unidirectional or multidirectional. Unidirectional instability refers to instability only in one direction. The most frequent type of unidirectional instability is traumatic anterior instability.¹⁴ Multidirectional instability is instability in two or more directions and is usually due to congenital capsular laxity or chronic repetitive microtrauma.¹⁴

Traumatic anterior glenohumeral dislocation frequently tears the anterior–inferior glenohumeral joint capsule (e.g., the middle glenohumeral ligament and/or anterior band of the inferior glenohumeral ligament [IGHL]) and avulses the anterior–inferior glenoid labrum with or without some underlying bone from the glenoid rim.⁹⁰ The latter of these two entities is frequently referred to as a Bankart lesion.¹⁶ Other anatomic lesions that contribute to anterior glenohumeral joint instability include humeral avulsion of the glenohumeral ligament, superior labral anterior to posterior (SLAP) lesions, injury to the rotator interval, or rotator cuff tears (particularly to the subscapularis muscle).⁹⁰ Acute anterior glenohumeral joint dislocations are also frequently associated with a compression fracture of the posterolateral aspect of the humeral head, referred to as a Hill-Sachs defect.¹⁶³

Inferior glenohumeral joint instability typically does not occur in isolation. Causes of inferior glenohumeral joint instability, however, include capsuloligamentous laxity, absence of the glenoid fossa upward tilt, and lesions to the rotator interval, IGHL, superior glenohumeral ligament (SGHL), coracohumeral ligament (CHL), and the inferior glenoid labrum.

Congenital glenoid hypoplasia or excessive glenoid or humeral retroversion has been reported to contribute to posterior glenohumeral joint instability. The more common lesions that lead to posterior glenohumeral joint instability, however, include excessive capsuloligamentous laxity, or an injury to the rotator interval, SGHL, posterior band of the IGHL, coracohumeral (CHL), or subscapularis muscle.⁹ A tear of the posterior inferior glenoid labrum causing separation from the glenoid fossa rim, often referred to as a “reverse Bankart lesion,” or a fracture of the posterior inferior glenoid fossa rim can also cause posterior glenohumeral joint instability.^9,146 A “reverse Hill-Sachs defect” can also be present, representing an impaction fracture of the anterior humeral head.^9,146

Multidirectional instability can be caused by primary or secondary capsuloligamentous laxity. It is frequently seen bilaterally and can be accompanied by generalized ligamentous laxity.¹⁴ Recurrent unilateral joint instability occasionally stretches the glenohumeral capsuloligamentous structures to the point that multidirectional instability develops secondarily.¹⁴ Another possible cause for secondary multidirectional instability is the presence of an underlying connective tissue disorder such as Marfan or Ehlers-Danlos syndromes.¹⁴

Although many patients with glenohumeral joint instability have vague symptoms, common complaints of patients with shoulder instability include pain, popping, catching, locking, an unstable sensation, stiffness, and swelling.¹⁸ A history of acute trauma or chronic, repetitive microtrauma should be obtained. Some patients might have a history of glenohumeral joint dislocation, and the examiner should find out the direction of dislocation, the duration of the dislocation, whether it has recurred, and whether it required manual reduction or spontaneously reduced. Subluxation episodes are commonly associated with a burning or aching dead feeling in the arm. Repetitive overhead activities such as baseball pitching can cause enough microtrauma to lead to symptomatic laxity.¹⁸ Patients should be asked whether they or their family members have a history of generalized ligamentous laxity or connective tissue disorders.

The physical examination should include inspection, palpation, glenohumeral joint ROM, analysis of scapulothoracic kinesis, upper limb strength, sensation (including proprioception), reflex evaluations, and special tests for glenohumeral joint instability.

The most common initial radiographic views for the evaluation of glenohumeral joint instability include the anteroposterior shoulder view, axillary lateral view, and scapular “Y” view.¹⁴ The anteroposterior view allows visualization of the osseous structures of the shoulder, including the scapula, clavicle, upper ribs, humeral head, and glenoid rim.¹⁶³ With internal rotation, the anteroposterior view can also allow visualization of a Hill-Sachs defect.¹⁶³ The scapular Y view can help in the assessment of glenohumeral joint alignment after acute dislocations.¹⁶³ The axillary lateral view can assess anterior or posterior subluxation or dislocation, as well as fractures of the anterior or posterior glenoid rim.¹⁶³ Other specialized views include the Garth view and the West Point view, both of which are useful in the detection of Bankart fractures. The Stryker Notch view can be used for evaluation of Hill-Sachs defects and stress views for the documentation of the degree of glenohumeral joint instability.¹⁶³Magnetic resonance arthrography provides optimal visualization of the labrum, cartilage, and joint capsule. Imaging of nondisplaced injuries to the IGHL and anteroinferior glenoid labrum is improved by placing the arm in an abducted and externally rotated position.

The treatment options for glenohumeral joint instability and dislocation include nonoperative and operative approaches. After glenohumeral joint subluxation episodes and in patients with multidirectional instability or unidirectional posterior or inferior instability, a comprehensive rehabilitation program that addresses kinetic chain deficits, scapulothoracic mechanics, and shoulder girdle strength, flexibility, and neuromuscular control is appropriate. Operative intervention should be considered only in those patients who have failed to improve after a comprehensive nonoperative treatment program.

For patients with glenohumeral joint instability, the strengthening program should begin with closed chain exercises that promote co-contraction of the glenohumeral joint–stabilizing musculature. The patient can eventually progress to functional open chain exercises as stability is achieved. Proprioceptive closed and open chain exercises are also important to recoordinate the stabilizing shoulder girdle musculature and attain engrams that respond appropriately to a dynamically changing environment.

For patients who have suffered a first-time traumatic anterior glenohumeral joint dislocation, the decision between a trial of nonoperative treatment versus immediate surgical stabilization is more controversial. In the older, less active patient, nonoperative management frequently is successful.³ In the younger, more active patient involved in contact sports, studies have shown a very high redislocation rate in those treated nonoperatively compared with those receiving early operative intervention.^11,12,85,173

Regardless of whether a patient opts for early surgical intervention, closed reduction confirmed by radiologic examination should be performed on all patients who sustain an acute glenohumeral joint dislocation that does not spontaneously reduce. Radiologic studies should be performed in two planes, such as anteroposterior with the humerus in internal rotation and axillary lateral views, to confirm relocation and exclude an associated fracture.¹⁶³ Sensory testing over the deltoid muscle is important to rule out an associated axillary nerve injury.¹⁴

Standard sling immobilization can be used for comfort but does not change future redislocation rates.^71,72,166 If initiated within the first 24 hours postinjury, 3 weeks of shoulder immobilization with the humerus externally rotated 30 degrees can reduce the risk of recurrent dislocation by nearly 100%, but the benefits of this type of immobilization are not statistically significant if begun after the first day.^75–78 The previously described shoulder instability rehabilitation program can be used to treat patients who opt for nonoperative treatment of their shoulder dislocation.

Adhesive Capsulitis

Adhesive capsulitis, or “frozen shoulder,” is characterized by painful, restricted shoulder ROM in patients with normal radiographs.^61,123 Adhesive capsulitis occurs in approximately 2% to 5% of the general population, is 2 to 4 times more common in women than men, and is most frequently seen in individuals between 40 and 60 years of age.^27,35

Adhesive capsulitis is usually an idiopathic condition but can be associated with diabetes mellitus, inflammatory arthritis, trauma, prolonged immobilization, thyroid disease, cerebrovascular accident, myocardial infarction, or autoimmune disease. Pathologic evaluation can reveal perivascular inflammation, but the predominant abnormality is fibroblastic proliferation with increased collagen and nodular band formation.²⁷

Adhesive capsulitis has been divided into four stages (Table 38-2).⁶⁴ Stage 1 occurs for the first 1 to 3 months and involves pain with shoulder movements but no significant glenohumeral joint ROM restriction when examined under anesthesia. In stage 2, the “freezing stage,” symptoms have been present for 3 to 9 months and are characterized by pain with shoulder motion and progressive glenohumeral joint ROM restriction in forward flexion, abduction, and internal and external rotation. During stage 3, or the “frozen stage,” symptoms have been present for 9 to 15 months and include a significant reduction in pain but maintenance of the restricted glenohumeral joint ROM. In stage 4, frequently referred to as the “thawing stage,” symptoms have been present for approximately 15 to 24 months and ROM gradually improves.

Table 38-2 Stages of Adhesive Capsulitis

Routine radiographic evaluation is usually normal, but glenohumeral joint arthrography typically shows a significant reduction in the capsular volume.

Treatment during stages 1 and 2 of adhesive capsulitis includes physical modalities, analgesics, and activity modification to reduce pain and inflammation. Up to three intraarticular corticosteroid injections can be used during stages 1 and 2 of adhesive capsulitis to reduce inflammation and pain, facilitate rehabilitation, and shorten the duration of this condition.^64,165 Postural retraining to reduce kyphotic posture and forward humeral positioning should be undertaken. Aggressive ROM exercises should be avoided until the patient’s pain has been adequately controlled.¹⁷⁸ Otherwise, the patient’s symptoms can worsen, leading the patient to immobilize his or her shoulder, thus resulting in a further loss of shoulder ROM. Early in the rehabilitation process, however, passive joint glides and nonpainful passive ROM exercises might be beneficial. Early scapular stability exercises and closed chain rotator cuff exercises can be instituted. As the patient’s symptoms improve, active-assisted and active ROM activities can be added, along with open chain and proprioceptive exercises. Most patients will have restoration of normal function over a 12- to 14-month period.^63,118 In patients who do not improve after 6 months of nonoperative treatment, more aggressive treatments such as capsular hydrodilatation, manipulation under anesthesia, and arthroscopic lysis of adhesions can be considered.^∗