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 then 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.

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.

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.

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 that 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 that 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 that 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.

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.

Speed 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.

Yergason 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.

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.

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.

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.

Cozen 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.

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.

Finkelstein Test

This test is used to detect tenosynovitis of the extensor pollicis brevis and abductor pollicis longus tendons (de Quervain 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.

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.

Acromioclavicular Joint Sprains

AC joint sprains account for only 9% of all shoulder injuries, are most frequent in men in their third decade of life, and are usually partial rather than complete sprains. 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.

Rockwood classified AC joint sprains into six types ( Figure 35-1 ). 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.

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 (anteroposterior projection with 15-degree cephalic tilt). Stress views do not provide additional clinically useful information.

Type 1, 2, and 3 AC joint sprains are usually treated nonoperatively, with 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, but the current literature favors nonoperative treatment for type 3 sprains. Type 4, 5, or 6 sprains require surgical treatment.

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. On cadaveric examination, Bigliani et al. found a relation between the acromial shape and the presence of rotator cuff tears. He classified the acromions into three types ( Figure 35-2 ). 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.

A, Type 1 acromion. B, Type 3 acromion.

Microvascular studies of the rotator cuff have found a hypovascular zone in the articular surface of the leading edge of the supraspinatus tendon. This hypovascular area has been implicated as a cause of rotator cuff degeneration and correlates with the higher incidence of articular-sided partial-thickness tears in the anterior aspect of the supraspinatus tendon.

Subacromial, or “outlet,” 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, scapulothoracic dyskinesis, and instability. Lack of adequate scapular control or weakness in the scapular stabilizers can lead to inadequate acromial retraction 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.

Another form of impingement, internal impingement, can occur in overhead athletes. 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.

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 magnetic resonance imaging (MRI) have higher levels of sensitivity and specificity for rotator cuff pathology than radiographs.

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. 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. 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.

Glenohumeral Joint Instability

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. The dynamic stabilizers of the glenohumeral joint include the scapular stabilizing and rotator cuff muscles, and the long head of the biceps. 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. The primary scapular stabilizing muscles include the serratus anterior, trapezius, pectoralis minor, rhomboideus minor and major, latissimus dorsi, and levator scapulae.

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., refers to the compressive forces placed on the glenohumeral joint during rotator cuff muscle cocontractions. 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.

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.

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

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). Glenohumeral joint instability is often associated with a concomitant decrement in proprioception. 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.

The classification of glenohumeral joint instability includes the degree, frequency, etiology, and direction of instability. 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 attributable to excessive capsular laxity, is multidirectional, and is frequently associated with internal impingement of the rotator cuff.

The frequency of instability can be either acute or chronic. 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. Unidirectional instability is frequently caused by a traumatic event resulting in disruption of the glenohumeral joint. Atraumatic instability is attributable to 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 psychological pathology, which often portends a poor outcome if surgical stabilization is performed.

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. Multidirectional instability is instability in two or more directions and is usually caused by congenital capsular laxity or chronic repetitive microtrauma.

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. The latter of these two entities is frequently referred to as a Bankart lesion. 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.

Inferior glenohumeral joint instability typically does not occur in isolation. Causes of inferior glenohumeral joint instability include capsuloligamentous laxity or injury and absence of the glenoid fossa upward tilt.

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 injury, or injury to the subscapularis tendon. 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. A “reverse Hill-Sachs defect” can also be present, representing an impaction fracture of the anterior humeral head.

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

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. 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. 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. The anteroposterior view allows visualization of the osseous structures of the shoulder, including the scapula, clavicle, upper ribs, humeral head, and glenoid rim. With internal rotation, the anteroposterior view can also allow visualization of a Hill-Sachs defect. The scapular Y view can help in the assessment of glenohumeral joint alignment after acute dislocations. The axillary lateral view can assess anterior or posterior subluxation or dislocation, as well as fractures of the anterior or posterior glenoid rim. 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. Magnetic 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 cocontraction 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. 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.

Regardless of whether or not 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 and axillary lateral views, to confirm relocation and exclude an associated fracture. Sensory testing over the deltoid muscle is important to rule out an associated axillary nerve injury.

Standard sling immobilization can be used for comfort but does not change future redislocation rates. Immobilization in shoulder external rotation does not appear to reduce redislocation rates. 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. 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.

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.

Adhesive capsulitis has been divided into four stages ( Table 35-1 ). 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 35-1

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