Leslie S. Beasley Vidal MD
Armando F. Vidal MD
Patrick J. McMahon MD
Shoulder Injuries
The shoulder is the third most commonly injured joint during athletic activities, after the knee and the ankle. Sports-related injuries of the shoulder may result from a direct traumatic event or repetitive overuse. Any activity that requires arm motion, particularly overhead arm motion such as throwing, may stress the soft tissues surrounding the glenohumeral joint to the point of injury. The shoulder is the most mobile joint in the body partly as a result of minimal containment of the large humeral head by the shallow and smaller glenoid fossa. The trade-off for this mobility is less structural restraint to undesirable and potentially damaging movements. Thus, a fine balance must be struck to maintain full range of shoulder motion and normal glenohumeral joint stability.
Kim DH et al: Shoulder injuries in golf. Am J Sports Med 2004;32(5):1324.
The Shoulder
Anatomy
The glenohumeral joint is a modified ball-and-socket joint. The glenoid fossa is a shallow inverted, comma-shaped, articular surface one-fourth the size of the humeral head. The articular surface of the humeral head is retroverted approximately 30° relative to the transverse axis of the elbow. Because the scapula is oriented anterolaterally about 30° on the thorax, relative to the coronal plane of the body, the face of the glenoid fossa matches the humeral head retroversion. The scapula rotates to direct the glenoid superiorly, inferiorly, medially, or laterally to accommodate changing humeral head positions. As a result, the humeral head is centered in the glenoid throughout most shoulder motions. When this centered position is disturbed, instability may result.
The clavicle articulates medially with the sternum at the sternoclavicular joint and laterally with the acromion of the scapula at the acromioclavicular joint. The clavicle rotates on its long axis and acts as a strut to stabilize the glenohumeral joint, serving as the only bone connecting the appendicular upper extremity to the axial skeleton.
The capsule of the glenohumeral joint may be the most lax of all the major joints, yet in certain positions it makes an important contribution to stability. The capsuloligamentous structures and the glenoid labrum share a common insertion. The anterior capsule is composed of the coracohumeral and superior glenohumeral ligaments, the middle glenohumeral ligament, and the inferior glenohumeral ligament (Figure 5-1). There is a variable relationship between the anterior capsuloligamentous structures and the labrum, such that certain anatomic variations may be associated with joint instability more often than others. For example, an anterosuperior sublabral hole is variably present within the glenohumeral joint, connecting with the subscapularis bursa that lies between the subscapularis tendon and the capsule.
The glenoid labrum acts not only as an attachment site for the capsuloligamentous structures but also as an extension of the articular cavity. Its presence deepens the glenoid socket by nearly 50% and removal of the labrum decreases joint stability to shear stress. In this way, the triangular cross section of the labrum acts as a chock-block to help prevent subluxation.
The muscles around the shoulder may be divided into three functional groups: glenohumeral, thoracohumeral, and those that cross both the shoulder and the elbow.
Four muscles compose the rotator cuff: the supraspinatus, subscapularis, infraspinatus, and teres minor. The supraspinatus originates on the
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posterosuperior scapula, superior to the scapular spine. It passes under the acromion, through the supraspinatus fossa, and inserts on the greater tuberosity with an extended attachment of fibrocartilage. The supraspinatus is active during the entire arc of scapular plane abduction; paralysis of the suprascapular nerve results in an approximately 50% loss of abduction torque. The infraspinatus and the teres minor muscles originate on the posterior scapula, inferior to the scapular spine, and insert on the posterior aspect of the greater tuberosity. Despite their origin below the scapular spine, their tendinous insertions are not separate from the supraspinatus tendon. These muscles function together to externally rotate and extend the humerus. Both account for approximately 80% of external rotation strength in the adducted position. The infraspinatus is more active with the arm at the side, whereas the teres minor activates mainly with the shoulder in 90° of elevation. The subscapularis muscle arises from the anterior scapula and is the only muscle to insert on the lesser tuberosity. The subscapularis is the only anterior component of the rotator cuff and functions to internally rotate and flex the humerus. The tendinous insertion of the subscapularis is continuous with the anterior capsule so that both provide anterior glenohumeral stability.
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Figure 5-1. Ligaments about the shoulder girdle. (Reprinted with permission from McMahon PJ, Skinner HB: Sports medicine. In: Skinner HB (editor): Current Diagnosis & Treatment in Orthopedics, 3rd ed. McGraw-Hill, 2003. ) |
The deltoid is the largest of the glenohumeral muscles. It covers the proximal humerus on a path from its tripennate origin at the clavicle, acromion, and scapular spine to its insertion midway on the humerus at the deltoid tubercle. Abduction of the joint results from activity of the anterior and middle portions. The anterior portion is also a forward flexor. The posterior portion extends the humerus. The deltoid is active throughout the entire arc of glenohumeral abduction; paralysis of the axillary nerve results in a 50% loss of abduction torque. The deltoid muscle can fully abduct the glenohumeral joint with the supraspinatus muscle inactive.
The teres major muscle originates from the inferior angle of the scapula and inserts on the medial lip of the bicipital groove of the humerus, posterior to the insertion of the latissimus dorsi. The axillary nerve and the posterior humeral circumflex artery pass superior to it through the quadrilateral space also bordered by the teres minor, the triceps, and the humerus. It contracts with the latissimus dorsi muscle and the two muscles function as a unit in humeral extension, internal rotation, and adduction.
The pectoralis major and the latissimus dorsi muscles are powerful movers of the shoulder and, hence, contribute to the joint force, which, in turn, usually stabilizes the glenohumeral joint. The pectoralis major muscle arises as a broad sheet of two distinct heads with the lowermost fibers of the sternal head inserting most proximally on the humerus.
Muscles that originate on the thorax contribute to glenohumeral stability, but may have roles in instability as well. When the shoulder is placed in horizontal abduction, similar to the apprehension position, the lowermost fibers of the sternal head of the pectoralis major muscle are stretched to an extreme. Because anterior instability also occurs from forcible horizontal abduction of the shoulder, the humeral head may be pulled out of the glenoid by passive tension in the pectoralis major and latissimus dorsi muscles.
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Both heads of the biceps brachii muscle originate on the scapula. The short head originates from the coracoid, and with the coracobrachialis muscle forms the conjoined tendon. The long head of the biceps originates just superior to the articular margin of the glenoid from the posterosuperior labrum and the supraglenoid tubercle, and is inside the synovial sheath of the glenohumeral joint. It traverses the glenohumeral joint, passing over the anterior aspect of the humeral head to the bicipital groove, where it exits the joint under the transverse humeral ligament.
Its origin on the scapula and insertion of the radius provides the long head of the biceps brachii muscle with the potential to function at both the shoulder and the elbow. Its function at the elbow, as well established, includes both flexion and supination. The role of the active biceps, long considered a depressor of the humeral head, has recently been questioned as electromyographic studies have shown that there is little or no activity of the biceps when elbow motion is controlled. This does not preclude a passive role or an active role associated with elbow motion, as tension in the tendon may then contribute to glenohumeral joint stability.
The axillary artery traverses the axilla, extending from the outer border of the first rib to the lower border of the teres minor muscle, forming the brachial artery. The axillary artery lies deep to the pectoralis muscle, but is crossed in its mid-region by the pectoralis minor tendon, just before the tendon inserts on the coracoid process. The axillary vein travels with the axillary artery, and branches of the axillary artery supply most of the shoulder girdle. The brachial plexus consists of the ventral rami of the fifth through eighth cervical nerves and the first thoracic nerve. This network of nerve fibers begins with the joining of the ventral rami proximally in the neck and continues anteriorly and distally, crossing into the axillary region obliquely underneath the clavicle at about the junction area of the distal one-third and proximal two-thirds. Clavicular fractures in this area may potentially injure the brachial plexus. The plexus then lies inferior to the coracoid process, where its cords form the peripheral nerves that continue down the arm. Muscles of the shoulder girdle are supplied by the nerves arising at all levels of the brachial plexus.
Eberly VC et al: Variation in the glenoid origin of the anteroinferior glenohumeral capsulolabrum. Clin Orthop 2002;400:26.
Enad JG: Bifurcate origin of the long head of the biceps tendon. Arthroscopy 2004;20(10):1081.
Price MR et al: Determining the relationship of the axillary nerve to the shoulder joint capsule from an arthroscopic perspective. J Bone Joint Surg Am 2004;86-A(10):2135.
History & Physical Examination
The history of shoulder complaints must include age, arm dominance, location, intensity, duration, temporal occurrence, aggravating and alleviating factors, radiation of discomfort, level of physical activity, occupation, and the mechanism of injury. Previous responses to treatment will help to characterize their efficacy and establish a pattern of disease or injury progression. The physical examination begins with the patient undressing so that both shoulders are fully exposed. Patients should be examined first in the standing position. The surface anatomy should be checked for asymmetry, atrophy, or external lesions. It is particularly important to examine the supraspinatus and infraspinatus fossae for atrophy. The area of pain should be pointed out by the patient prior to the physician manipulating the shoulder to avoid hurting the patient unnecessarily. A thorough neurovascular examination of the upper extremity should be performed.
Many terms may be used to describe movements of the shoulder joint (Figure 5-2 and Table 5-1). Flexion occurs when the arm begins at the side and elevates in the sagittal plane of the body anteriorly. Extension occurs when the arm starts at the side and elevates in the sagittal plane of the body posteriorly. Adduction occurs when the arm moves toward the midline of the body, with abduction occurring as the arm moves away from the midline of the body. Internal rotation occurs when the arm rotates medially, inward toward the body, and external rotation occurs as the arm rotates laterally or outward from the body. Horizontal adduction occurs as the arm starts at 90° of abduction and adducts forward and medially toward the center of the body, and horizontal abduction occurs as the arm starts at 90° of abduction and moves outward, away from the body. Elevation is the angle made between the thorax and arm, regardless of whether it is in the abduction plane, flexion plane, or in between.
Range of motion of the injured shoulder should be compared with range of motion of the opposite shoulder, along with the strength during abduction and rotation. This should be done both passively and actively. The shoulder should be inspected for any changes in synchrony, such as scapular winging, elevation of the scapula, muscle fasciculations indicating abnormal function, and any other irregular or asymmetric movements of the scapula. Information may be gained on loss of flexibility and instability resulting from muscle imbalance, fibrosis, and tendon, capsular, or ligament
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contractures. Loss of flexibility usually occurs in the capsular tissues of the glenohumeral joint. Sudden pain or clicking may indicate an intraarticular problem. Loss of motion in either internal or external rotation is suggestive of a chronic anterior or posterior dislocation, respectively.
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Figure 5-2. Description of shoulder motion. (Reprinted with permission from McMahon PJ, Skinner HB: Sports medicine. In: Skinner HB (editor): Current Diagnosis & Treatment in Orthopedics, 3rd ed. McGraw-Hill, 2003. ) |
Specific tests are then performed that aid in making the correct diagnosis. The specific tests for instability, impingement syndrome, bicipital tendinitis, and superior capsulolabral/biceps anchor le-sions are discussed below.
Imaging & Other Studies
Many varieties of radiologic views and projections are available to examine shoulder injuries. An initial radiographic evaluation of the shoulder should consist of an anteroposterior view of the glenohumeral joint in both internal and external rotation, and an axillary lateral view. Additional plain radiographic views depend on the underlying pathologic factors. Magnetic resonance imaging (MRI) may be indicated in evaluating rotator cuff disorders recalcitrant to conservative treatment. An MR arthrogram may be useful in detecting labral pathology. Traditional arthrography is rarely indicated because it is invasive and has little or no advantage to MRI. Ultrasonography is also useful in the diagnosis of rotator cuff injury, but it is operator dependent. Electromyographic examination can be useful in identifying shoulder pain of cervical origin.
Arthroscopic Evaluation
Indications for arthroscopic examination of the shoulder include the following:
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Table 5-1. Motion at the shoulder joint. |
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With the patient either in the lateral decubitus or the beach chair position, the arthroscope is inserted into a posterior portal, medial and inferior to the posterolateral corner of the acromion. With visualization of the glenohumeral joint, an anterior portal immediately lateral to the coracoid allows entrance of additional instruments. Distal clavicle excision, removal of loose bodies, and capsular release of adhesive capsulitis can be performed. An additional anterior portal inferior to the first may aid in instability repair with an arthroscopic technique. The arthroscope is then removed from the joint and placed
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into the subacromial bursa. Portals lateral to the acromion allow subacromial decompression and rotator cuff repair to be carried out with arthroscopic techniques.
Examination of shoulder range of motion and stability with the patient under anesthesia is helpful in the diagnosis and treatment of shoulder injuries. This should be performed in the operating room prior to arthroscopy. The steps in arthroscopic examination should then include the following:
Applegate GR et al: Chronic labral tears: value of magnetic resonance arthrography in evaluating the glenoid labrum and labral-bicipital complex. Arthroscopy 2004;20(9):959.
Kaplan LD et al: Internal impingement: findings on magnetic resonance imaging and arthroscopic evaluation. Arthroscopy 2004;20(7):701.
Lee DH et al: The double-density sign: a radiographic finding suggestive of an os acromiale. J Bone Joint Surg Am 2004; 86-A(12):2666
Lindauer KR et al: MR imaging appearance of 180-360 degrees labral tears of the shoulder. Skeletal Radiol 2005;34(2):74.
Magee T et al: Shoulder MR arthrography: which patient group benefits most? Am J Roentgenol 2004;183(4):969.
Middleton WD et al: Sonography of the rotator cuff: analysis of interobserver variability. Am J Roentgenol 2004;183(5):1465.
Porcellini G et al: Arthroscopic treatment of calcifying tendinitis of the shoulder: clinical and ultrasonographic follow-up findings at two to five years. J Shoulder Elbow Surg 2004;13(5):503.
Shoulder Tendon & Muscle Injury
Rotator Cuff Tendon Injuries
Injury to the rotator cuff, a common cause of shoulder pain and disability, has a high prevalence during athletic activities. Injury to the rotator cuff may result in pain, weakness, and decreased range of motion. Symptoms are often worsened by activity, especially when the hand is positioned overhead. Night pain is also common, and many patients complain of awakening after rolling onto the affected shoulder. Although shoulder weakness and decreased range of motion usually result from a rotator cuff tendon tear, pain alone from subacromial bursitis or rotator cuff tendinitis may also be the cause. Each of these entities most often results from impingement syndrome.
Impingement Syndrome
Any prolonged repetitive activity involving overhead motion such as tennis, pitching, golf, or swimming may cause compromise of the space between the humeral head and the coracoacromial arch, which includes the acromion, the coracoacromial ligament, and the coracoid process. Impingement causes microtrauma to the rotator cuff, resulting in local inflammation, edema, cuff softening, pain, and poor function. These problems may even cause greater impingement, producing a continuous vicious cycle (Figure 5-3). This cycle may be precipitated by acute injury to the rotator cuff tendon itself. Blood supply to this tendon is precarious, thus decreasing its capacity for healing.
Essentials of Diagnosis
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Figure 5-3. The cycle of injury and reinjury resulting from rotator cuff impingement. (Reprinted with permission from McMahon PJ, Skinner HB: Sports medicine. In: Skinner HB (editor): Current Diagnosis & Treatment in Orthopedics, 3rd ed. McGraw-Hill, 2003. ) |
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Prevention
Limiting repetitive overhead activities and maintenance of good rotator cuff strength are keys to prevention. Additionally, overall conditioning and stretching and strengthening with careful attention paid to technique can be helpful in minimizing many injuries resulting from overuse.
Clinical Findings
Bursitis of the shoulder refers to an inflammation of the subacromial bursa. It has the mildest signs and symptoms of shoulder impingement. Pain is present with activity involving overhead motion and there is usually no pain or only mild pain with the arm at the side.
Active range of shoulder motion may be limited by pain. No atrophy of the shoulder muscles is present and manual muscle testing demonstrates mild weakness. Passively, when the internally rotated shoulder is moved into forward flexion, the patient will experience discomfort. This is called the Neer impingement sign (Figure 5-4). This pain then resolves and there is a dramatic increase in strength and range of motion with the Neer impingement test (10 mL of lidocaine is injected into the subacromial space).
Radiographic views of the subacromial space such as the supraspinatus outlet view may show a spur on the undersurface of the acromion, causing narrowing of the subacromial space. In recent years, advances in imaging methods such as ultrasonography and MRI have aided in the diagnosis of subacromial bursitis, rotator cuff tendinitis, and rotator cuff tendon tear (Figure 5-5).
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Figure 5-4. Evaluating for impingement of the supraspinatus with the Neer impingement sign. (Reprinted with permission from McMahon PJ, Skinner HB: Sports medicine. In: Skinner HB (editor): Current Diagnosis & Treatment in Orthopedics, 3rd ed. McGraw-Hill, 2003. ) |
Treatment
Treatment for impingement syndrome starts with conservative measures such as activity modification, physical therapy, and oral nonsteroidal antiinflammatory drugs (NSAIDs). Modalities such as heat and cold, iontophoresis or phonophoresis, and microelectric nerve stimulation may also be helpful. Only with normal function of the rotator cuff tendons will glenohumeral mechanics be improved and the impingement syndrome cease. If this treatment fails, a subacromial injection of corticosteroids may be helpful.
Surgical intervention is indicated only after failure of a prolonged conservative treatment program (a minimum of 3 months). If the subacromial space is narrow, shaving the undersurface of the acromion may result in relief of symptoms. This procedure can be done arthroscopically to decrease postoperative discomfort and minimize the complication of deltoid muscle rupture from the acromion.
Prognosis
Most patients respond well to nonoperative management, and those who require surgical decompression are usually able to return to pain-free activities as well.
Essentials of Diagnosis
Prevention
As with subacromial bursitis, limiting repetitive overhead activities and maintenance of good rotator cuff strength are keys to prevention. Additionally, overall conditioning and stretching and strengthening with careful attention paid to technique can be helpful in minimizing many overuse injuries.
Clinical Findings
Of the four rotator cuff muscles, the supraspinatus tendon is most often initially involved. Rotator cuff
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tendinitis also results from impingement syndrome and is characterized by pain with activity involving overhead motion. The patient may occasionally be awakened by pain at night. Active shoulder range of motion is limited by pain. Typically, no atrophy of the shoulder muscles is present and manual muscle testing demonstrates mild weakness. The Neer impingement sign is positive and the pain resolves with a subacromial injection of lidocaine.
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Figure 5-5. MRI demonstrating (A) normal shoulder anatomy and (B) cystic changes at the greater tuberosity with rotator cuff tear. (Reprinted with permission from McMahon PJ, Skinner HB: Sports medicine. In: Skinner HB (editor): Current Diagnosis & Treatment in Orthopedics, 3rd ed. McGraw-Hill, 2003. ) |
Treatment & Prognosis
Radiographic evaluation and treatment are similar to management of subacromial bursitis. An exception is the young athlete with glenohumeral instability and secondary tendinitis. In this case, the instability should be treated first and the rotator cuff tendinitis will then resolve.
Essentials of Diagnosis
Prevention
Maintenance of overall body conditioning with regular stretching and strengthening of the rotator cuff and scapular stabilizing muscles can help prevent rotator cuff injuries.
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Clinical Findings
A rotator cuff tendon tear is characterized by pain with activity involving overhead motion. However, the patient is often awakened at night with pain as well. The athlete with a chronic rotator cuff tear may experience a gradual loss of strength. Pain may be persistent, occurring even when the arm is at the side. Active range of shoulder motion is limited, and if the tear is severe, there will be atrophy of the shoulder muscles. Manual muscle testing demonstrates weakness. The Neer impingement sign is positive and the pain resolves with a subacromial injection of lidocaine. Radiographic evaluation is similar to that for subacromial bursitis and rotator cuff tendinitis.
Treatment
Radiographic evaluation and treatment are similar to subacromial bursitis management. Unlike acute tears, chronic rotator cuff tears often present insidiously, with slow progression from subacromial bursitis to rotator cuff tendinitis and eventual tendon tear. Differentiating severe rotator cuff tendinitis from partial or small full-thickness chronic rotator cuff tears may be difficult.
There are two important considerations in treating an individual with a rotator cuff tear—the current symptoms and the risk of the tear progressing. Although the lesion location and size are helpful in describing a rotator cuff tear, symptoms do not correlate with these factors alone. Some individuals are able to cope with the symptoms of a rotator cuff tear and some may be completely asymptomatic. The severity of symptoms is in-fluenced by a number of other factors including pain tolerance, the acute or chronic nature of the injury, the age and activity level of the individual, humeral head superior migration, shoulder muscle strength, muscle atrophy, fatty changes in the muscle, arthritis, and workman's compensation status.
Rest, rehabilitation, and taking NSAIDs, sometimes for as long as 4–9 months, may relieve symptoms. Range-of-motion and strengthening exercises are recommended, unless they cause significant discomfort. Stengthening the other shoulder muscles may increase the individual's ability to cope with the rotator cuff tear. Avoidance of activities that exacerbate the symptoms, such as activities involving overhead motion, is also recommended. Symptoms of pain, weakness, or decreased range of motion that persist after a nonoperative treatment program has been tried indicate the need for surgical intervention.
Because rotator cuff tears may progress in size over time, immediate repair may be warranted in some at-risk individuals. Both epidemiologic and imaging studies of the general population indicate a high incidence of partial-thickness rotator
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cuff tears at younger ages and full-thickness rotator cuff tears at older ages. The increasing prevalence of rotator cuff injuries in older individuals may be the best evidence that rotator cuff tears progress in severity. Specifically, about 25% of individuals over 60 years of age have a tear and in those over 80 years of age, there is a full-thickness rotator cuff tear in about 50% of individuals. The risk of a rotator cuff tear progressing to a more severe tear cannot currently be predicted, but it is thought to be higher in young, active individuals, partly because they have many more years to sustain an injury.
The thin degenerated tissue of a chronic rotator cuff tear makes surgical repair more difficult than repair of an acute tear. The repair can be accomplished with either an arthroscopic or an open technique. Surgical decompression of the subacromial space to remove spurs should also be considered. Some severe tears may be impossible to repair. This includes tears that are large to massive in size or that involve two or more rotator cuff tendons. Debridement of the rotator cuff and the subacromial spurs may diminish pain in such instances.
Rehabilitation after a repair lasts from 3 months to a year with gradual exercise progression needed to restore normal, or near normal, function and strength. This varies with the size of the tear that was repaired and the type of surgery performed. Typically, immediately after the procedure, passive motion and isometric strengthening exercises start, along with elbow-, hand-, and grip-strengthening exercises. At 6 weeks, the athlete may be able to begin low-intensity active strengthening exercises against gravity. The goals are to bring the athlete to normal strength with a functional, pain-free range of motion.
Prognosis
The prognosis following a rotator cuff tear depends on many factors as described above. There are few specific criteria governing return to sports following rotator cuff injuries. Determining factors must be individualized to the athlete, considering the nature and treatment of the rotator cuff injury as well as the desired sport. Patients must be pain free and have attained full range of motion with near full strength prior to returning to their sport to minimize reinjury.
A partial articular sided tendon avulsion is much more common than a bursal side tear of the rotator cuff. As with other rotator cuff injuries, symptoms may resolve with appropriate physical therapy and analgesics. Yet, some individuals with a partial thickness tear have persistent or recurrent symptoms. If a conservative program of exercises and gradual return to activity do not lead to steady improvement, then further diagnostic evaluation with ultrasonography, MRI, or arthroscopy may be helpful. Whereas repair of the partial-thickness rotator cuff tear may be best in some, debridement of the abnormal cuff may diminish or relieve symptoms in others. Some clinicians use involvement of greater than 50% of the tendon thickness as an indication for repair. Repair necessitates a rehabilitation program similar to that described above for full-thickness rotator cuff tears. Following debridement, immediate resumption of range-of-motion and muscle-strengthening exercises begins. Typically, it requires 6–12 months for an athlete whose sport involves throwing to return to athletics following arthroscopic debridement of a partial-thickness rotator cuff tear.
Klepps S et al: Prospective evaluation of the effect of rotator cuff integrity on the outcome of open rotator cuff repairs. Am J Sports Med 2004;32(7):1716.
Lam F, Mok D: Open repair of massive rotator cuff tears in patients aged sixty-five years or over: is it worthwhile? J Shoulder Elbow Surg 2004;13(5):517.
Millstein ES, Snyder SJ: Arthroscopic evaluation and management of rotator cuff tears. Orthop Clin North Am 2003;34(4):507.
O'Holleran JD et al: Determinants of patient satisfaction with outcome after rotator cuff surgery. J Bone Joint Surg Am 2005;87-A(1):121.
Rebuzzi E et al: Arthroscopic rotator cuff repair in patients older than 60 years. Arthroscopy 2005;21(1):48.
Romeo AA et al: Shoulder scoring scales for the evaluation of rotator cuff repair. Clin Orthop 2004;1(427):107.
Sperling JW et al: Rotator cuff repair in patients fifty years of age and younger. J Bone Joint Surg Am 2004;86-A(10):2212.
Biceps Tendon Injuries
Essentials of Diagnosis
Prevention
Similar to the prevention of rotator cuff injuries, general conditioning and stretching and strengthening before activities can help minimize injury to the biceps tendon.
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Clinical Findings
The long head of the biceps muscle is an intraarticular structure deep in the rotator cuff tendon as it passes under the acromion to its insertion at the top of the glenoid. The same mechanism that initiates symptoms of impingement syndrome in rotator cuff injuries may inflame the tendon of the biceps in its subacromial position, causing bicipital tendinitis.
Tendinitis may also result from subluxation of the tendon out of its groove in the proximal humerus, which occurs with rupture of the transverse ligament. The symptoms of bicipital tendinitis, whether the result of impingement or tendon subluxation, are essentially the same. Pain is localized to the proximal humerus and shoulder joint, with resisted supination of the forearm aggravating the pain. Pain may also occur on manual testing of the elbow flexors and on palpation of the tendon itself. The Yergason test is used to determine instability of the long head of the biceps in its groove.
Treatment
If the tendinitis is associated with shoulder impingement, then therapy aimed at treating the impingement syndrome will relieve the bicipital tendinitis. If subluxation of the tendon within its groove is the cause of the irritation, conservative therapy includes NSAIDs and restriction of activities, followed by a slow resumption of activities after a period of rest. Strengthening of the muscles that assist the biceps in elbow flexion and forearm supination is also beneficial. Steroid injections into the sheath of the biceps tendon are helpful, but they may be hazardous if placed into the substance of the tendon because they will promote tendon degeneration. Persistent symptoms may warrant tenodesis of the biceps tendon directly into the humerus.
Prognosis
Recovery from biceps tenodesis is difficult, and it is doubtful if a competitive athlete could return to peak performance after treatment.
Essentials of Diagnosis
Prevention
Similar to the prevention of rotator cuff injuries, general conditioning and stretching and strengthening before activities can help minimize injury to the biceps tendon.
Clinical Findings
The long head of the biceps tendon may rupture proximally, either from the supraglenoid tubercle of the scapula at the entrance of the bicipital groove proximally, or at the exit of the tunnel at the musculotendinous junction. The muscle mass moves distally, producing a bulging appearance to the arm. Rupture of the long head of the biceps is predictive of a rotator cuff tear. Rupture of the biceps distally at its insertion involves both heads and the muscle mass moves proximally. The mechanism is usually a forceful flexion of the arm and is more common in older athletes, or following direct trauma. Microtears probably serve to render the tendon vulnerable to an acute tearing event. The degree of ecchymosis is dependent on the location of the tear, with avascular areas having less and the musculotendinous junction producing quite a noticeable amount of ecchymosis. Diagnosis is usually easily accomplished, as the deformity is obvious.
Treatment
Surgical treatment of proximal ruptures, if indicated, is usually reserved for younger patients. Open surgical repair leaves a long scar and usually does not completely restore the underlying anatomy. The coiled-up distal end of the tendon is usually found beneath the attachment of the pectoralis major. A correlation exists between proximal biceps tendon rupture and rotator cuff tears in middle-aged and older athletes. Rupture of the distal biceps tendon often warrants surgical repair, due to loss of forearm flexion and supination strength. In this case, the tendon is usually found about 5–6 cm above the elbow joint, and care must be taken to avoid damage to the lateral antebrachial cutaneous nerve.
Prognosis
Athletes are permitted to return to full contact play once they have achieved maximal functional strength and range of elbow motion, which typically occurs 4–6 months following a distal biceps repair.
Cope MR et al: Biceps rupture in body builders: three case reports of rupture of the long head of the biceps at the tendon-labrum junction. J Shoulder Elbow Surg 2004;13(5):580.
Vidal AF et al: Biceps tendon and triceps tendon injuries. Clin Sports Med 2004;23(4):707.
Pectoralis Major Rupture
Essentials of Diagnosis
Prevention
Similar to the prevention of rotator cuff injuries, general conditioning and stretching and strengthening before activities can help minimize injury to the pectoralis major.
Clinical Findings
Rupture of the pectoralis major tendon is an uncommon injury, usually occurring during bench press exercises in weight lifting and caused by sudden unexpected muscle contraction during pulling or lifting. The athlete usually experiences sudden pain and develops local ecchymosis and swelling. As the swelling subsides, a sulcus and deformity may be visible, and the patient notices weakness of the arm in adduction and internal rotation.
Treatment
The rupture may be partial or complete, and nonoperative treatment usually results in satisfactory function for the activities of daily life. Surgery may be considered if the athlete wishes to return to heavy weight lifting.
Prognosis
Athletes are permitted to return to contact sports once they have achieved full strength and range of motion, which typically occurs 6 months following a pectoralis major repair.
Aarimaa V et al: Rupture of the pectoralis major muscle. Am J Sports Med 2004;32(5):1256.
Glenohumeral Joint Instability
To make the correct diagnosis the glenohumeral joint must be tested for anterior, posterior, and inferior instability. Different classifications of glenohumeral joint instability have been proposed, based on etiology, the direction of the instability, or on various combinations. TUBS is an acronym describing instability caused by a traumatic event, which is unidirectional, is associated with a Bankart lesion, and often requires surgical treatment. AMBRI refers to atraumatic, multidirectional instability that may be bilateral and is best treated by rehabilitation. In this classification, the etiology of multidirectional instability is thought to be enlargement of the capsule from either a genetic or microtraumatic origin.
The positive sulcus sign has been used as the diagnostic hallmark for multidirectional instability, but we now know that the sulcus sign is sometimes found in shoulders of asymptomatic individuals with increased laxity. Laxity or joint play is a trait of body constitution that differs from one individual to another. Individuals
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may be loose or tight jointed. A shoulder is hyperlax if the examiner can easily subluxate the humeral head out of the glenoid in the anterior, posterior, and inferior directions without eliciting symptoms. Unfortunately, this makes classification of instability based on etiology, or direction alone, extremely difficult. Instead, classification is best based on the direction of instability that elicits symptoms and the presence or absence of hyperlaxity (Table 5-2).
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Table 5-2. Classification of glenohumeral instability based on the direction of instability and the presence or absence of hyperlaxity. |
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Gerber C, Nyffeler RW: Classification of glenohumeral instability. Clin Orthop 2002;400:65.
Anterior Instability
The apprehension test is performed to assess anterior instability. The test applies an anterior-directed force to the humeral head from the back with the arm in abduction and external rotation (Figure 5-6). A positive test results from the patient's apprehension that the joint will dislocate. This maneuver mimics the position of subluxation, or dislocation, and causes reflex guarding. Conversely, the relocation test is positive if relief is obtained by applying a posterior-directed force to the humeral head (Figure 5-7).
Posterior Instability
No single test has high sensitivity and specificity for posterior instability. The posterior apprehension test is performed by applying a posterior-directed force to the forward flexed and internally rotated shoulder. To perform the circumduction test the patient is instructed to actively move the shoulder in a large circle starting from a flexed, internally rotated and cross-body position, then to forward flexion, then to an abducted and externally rotated position, and lastly to the arm at the side. The examiner stands behind the patient and palpates the posterior shoulder. If positive, the joint
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subluxes in the flexed, internally rotated and cross-body position, and reduces as the shoulder is moved. For the Jahnke test, a posteriorly directed force is applied to the forward flexed shoulder. The shoulder is then moved into the coronal plane as an anterior directed force is applied to the humeral head. A clunk occurs as the humeral head reduces from the subluxed position (Figure 5-8)
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Figure 5-6. The apprehension test for anterior instability. (Reprinted with permission from McMahon PJ, Skinner HB: Sports medicine. In: Skinner HB (editor): Current Diagnosis & Treatment in Orthopedics, 3rd ed. McGraw-Hill, 2003. ) |
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Figure 5-7. The relocation test is positive if relief is obtained by applying a posterior directed force to the humeral head. (Reprinted with permission from McMahon PJ, Skinner HB: Sports medicine. In: Skinner HB (editor): Current Diagnosis & Treatment in Orthopedics, 3rd ed. McGraw-Hill, 2003. ) |
Inferior Instability
The sulcus sign is used to evaluate laxity and inferior instability. The test is performed with the athlete in a sitting position with the arm at the side. A distraction force is applied longitudinally along the humerus. If positive, discomfort or apprehension of instability is experienced as the skin just distal to the lateral acromion hollows out (Figure 5-9).
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Figure 5-8. The Jahnke test for posterior instability. A: A posterior directed force applied to the forward flexed shoulder. B: The shoulder is then moved into the coronal plane as an anterior directed force is applied to the humeral head. A clunk occurs as the humeral head reduces from the subluxed position. [Reprinted with permission from Hawkins RJ, Boker DJ: Clinical evaluation of shoulder problems. In: Rockwood CA et al (editors) The Shoulder. WB Saunders, 1998. ] |
When the shoulder is forced beyond the limit of its normal range of motion, the articular surface of the humeral head may be displaced from the glenoid to varying degrees. The majority of glenohumeral dislocations, or subluxations, are in the anteroinferior direction.
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Figure 5-9. The sulcus sign for inferior instability. With the elbow grasped, inferior traction is applied. Dimpling of the skin below the acromion may be seen. Palpation reveals widening of the subacromial space between the acromion and the humeral head. [Reprinted with permission from Hawkins RJ, Boker DJ: Clinical evaluation of shoulder problems. In: Rockwood CA et al (editors): The Shoulder. WB Saunders, 1998. ] |
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Essentials of Diagnosis
Prevention
Shoulder dislocations are typically the result of an acute traumatic injury. Therefore, although avoiding injury to the shoulder is the best form of prevention, minimizing the risk of dislocation following a blow can be achieved with regular stretching and strengthening of the rotator cuff musculature.
Clinical Findings
Anterior glenohumeral dislocation occurs from either an external rotation, or abduction force on the humerus, a direct posterior blow to the proximal humerus, or a posterolateral blow on the shoulder strong enough to displace the humeral head. The anterior capsule is either stretched or torn within its attachment to the anterior glenoid. The head may be displaced into a subcoracoid, subglenoid, subclavicular, or intrathoracic position. Two major lesions are typically seen in patients with recurrent anterior dislocations (Figure 5-10). First is the Bankart lesion, an anterior capsular injury associated with a tear of the glenoid labrum off the anterior glenoid rim. The Bankart lesion may occur with fractures of the glenoid rim. Such fractures are often minimally displaced, and treatment is usually dictated by the joint instability. The second major lesion associated with recurrent anterior dislocations is the Hill–Sachs lesion, a compression fracture of the posterolateral articular surface of the humeral head. It is created by the sharp edge of the anterior glenoid as the humeral head dislocates over it. When large, both the Bankart and the Hill-Sachs lesions predispose to recurrent dislocations when the arm is placed in abduction and external rotation. If the glenoid rim fracture involves more than 20% of the glenoid diameter, then the joint becomes prone to instability and treatment with open reduction and internal fixation is best. If the fracture is old, or the glenoid rim is worn to a similar level, then corticocancellous bone grafting of the glenoid rim is indicated.
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Figure 5-10. Anatomic lesions associated with shoulder instability. (Reprinted with permission from McMahon PJ, Skinner HB: Sports medicine. In: Skinner HB (editor): Current Diagnosis & Treatment in Orthopedics, 3rd ed. McGraw-Hill, 2003. ) |
Other injuries associated with anterior dislocation may occur. These include avulsion of the greater tuberosity from the humerus, caused by traction from the rotator cuff, and injury to the axillary nerve, which may be stretched or torn. Permanent loss of axillary nerve function results in denervation of the deltoid muscle and loss of sensation over the proximal lateral aspect of the arm. Axillary nerve palsy may also occur during reduction of the dislocation, and therefore should be tested both before and after reduction. The deltoid extension lag sign, described in the section on Axillary Nerve Injury, may be the best way to assess function of this nerve. Lastly, the dead arm syndrome may occur after anterior joint instability. For example, a pitcher may report a sudden inability to throw, with the arm going numb and becoming extremely weak after ball release. The symptoms are transient, resolving within a few seconds to minutes.
Athletes who sustain a shoulder dislocation will try to hold the injured extremity at their side, gripping the forearm with the opposite hand. Most athletes know their shoulder is dislocated, and will immediately seek help. On physical examination of an anterior dislocation, the
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examiner will note a space underneath the acromion where the humeral head should lie and a palpable anterior mass representing the humeral head in the anterior axilla.
Treatment
Acute and recurrent anterior glenohumeral dislocations must be distinguished, as an acute dislocation sustains severe trauma with the increased probability of associated injuries. The recurrent dislocation may occur with minimal trauma, and reduction may be accomplished with much less effort. Anterior dislocations may be reduced by one of several techniques. Longitudinal traction may be exerted on the affected arm with external rotation, followed by internal rotation of the arm. Care must be taken to avoid direct pressure on the neurovascular structures. Another method is to have the patient lie face down on the table and tie or tape a bucket to the injured arm and slowly fill it with water. This allows the musculature around the shoulder to relax from the force of the weight, and effect a spontaneous reduction.
Following reduction of an initial dislocation, the shoulder should be immobilized in internal rotation for 2–6 weeks. Healing will generally take at least 6 weeks. Before returning to athletics, the patient should have normal range of motion without pain and normal strength in the shoulder. Emphasis must be placed on strengthening the rotator cuff muscles to compensate for the laxity of the ligamentous support. When weight training is begun, military press, fly exercises, a narrow grip while bench pressing, and deep shoulder dips must be excluded until considerable time has elapsed and healing is complete.
Recurrent dislocations should be treated with minimal immobilization until the pain subsides, followed by range-of-motion and muscle-strengthening exercises. Many restraining devices are available to help prevent recurrent dislocations during sporting activities, focusing on keeping the arm from going into abduction and external rotation. These orthotics may be effective, but because they limit the athlete's range of shoulder motion, their use is limited for certain competitive activities.
If an athlete has sustained multiple dislocations and is unresponsive to conservative treatment, surgical reconstruction of the shoulder joint may be indicated. The orthopedic literature presents a wide variety of procedures to correct the instability, with most involving repair of the labral defect, and tightening of the anterior capsule and ligamentous structures through an anterior incision (Table 5-3).
For most surgical procedures, aggressive range-of-motion exercises do not start until at least 3 weeks postoperatively. The goal is to have full ab-duction and 90° of external rotation. By 12 weeks, patients have often progressed well into their initial programs and may begin a variety of weight training exercises, avoiding exercises that strain the anterior capsule.
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Table 5-3. Surgical procedures for the treatment of shoulder instability. |
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Prognosis
Young patients are at a high risk for redislocation after a primary traumatic anterior shoulder dislocation if treated conservatively with rehabilitation. Surgical stabilization should be considered in these cases. In general, despite surgical stabilization, patients have up to a 10% chance of redislocation if returning to play in contact sports.
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Essentials of Diagnosis
Prevention
Shoulder dislocations are typically the result of an acute traumatic injury. Therefore, while avoiding injury to the shoulder is the best form of prevention, the risk of dislocation following a blow can be minimized with regular stretching and strengthening of the rotator cuff musculature.
Clinical Findings
Posterior glenohumeral dislocations result from the posterior capsule being torn, stretched, or disrupted from the posterior glenoid. A reverse Hill–Sachs lesion (Figure 5-10) may appear on the anterior articular surface of the humerus. With a posterior dislocation, the subscapularis, or its insertion on the lesser tuberosity, may be injured. Posterior dislocations are often difficult to diagnose, as the patient may have a normal contour to the shoulder or the deltoid of a well-developed athlete may mask signs of a displaced humeral head. The patient holds the injured shoulder in internal rotation and the examiner cannot externally rotate it. Anteroposterior and axillary radiographs must be obtained to diagnose a posterior dislocation.
Treatment
Applying traction in the line of the adducted humerus, with an anterior directed force to the humeral head, reduces a posterior dislocation. Anesthesia often helps decrease the trauma of reduction. Following reduction, the shoulder is immobilized for 2–6 weeks in external rotation and a small amount of abduction. Surgical treatment should be considered if these measures fail to provide the desired results.
Prognosis
Patients with an acute posterior dislocation are often able to return to their sport following a course of rehabilitation emphasizing range-of-motion and rotator cuff strengthening.
Multidirectional Instability
Essentials of Diagnosis
Clinical Findings
Some patients will have instability in both the anterior and posterior directions, which is most often subluxation and not dislocation. This may result in a painful shoulder, especially if rotator cuff strength decreases. The pain is often primarily a result of rotator cuff inflammation, likely from attempts to stabilize the humeral head during activity. Patients may complain of vague symptoms including upper extremity fatigue, discomfort, pain, apprehension, and paresthesias. They may describe frank episodes of instability. Physical examination should include evaluation for signs of generalized hyperlaxity, which include hyperextension of the metacarpophalangeal joints, elbows, and knees and the ability to adduct the thumb to the ipsilateral wrist. Generalized hyperlaxity does not necessarily indicate symptomatic instability of the shoulder. The shoulder examination should include tests for anterior, posterior, and inferior instability as described above. MRI can be a useful adjunct to plain radiographs and may reveal an enlarged axillary pouch and labral or rotator cuff pathology.
Treatment & Prognosis
The mainstay of treatment for multidirectional instability involves a conservative program, which leads to successful results in the vast majority of cases. This includes patient education, modification of activity, and a strengthening program for the rotator cuff and scapular stabilizing muscles.
Brophy RH, Marx RG: Osteoarthritis following shoulder instability. Clin Sports Med 2005;24(1):47.
Good CR, Macgillivray JD: Traumatic shoulder dislocation in the adolescent athlete: advances in surgical treatment. Curr Opin Pediatr 2005;17(1):25.
Kim SH et al: Painful jerk test: a predictor of success in nonoperative treatment of posteroinferior instability of the shoulder. Am J Sports Med 2004;32(8):1849.
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Kim SH et al: Loss of chondrolabral containment of the glenohumeral joint in atraumatic posteroinferior multidirectional instability. J Bone Joint Surg Am 2005;87-A(1):92.
Kirkley A et al: Prospective randomized clinical trial comparing the effectiveness of immediate arthroscopic stabilization versus immobilization and rehabilitation in first traumatic anterior dislocations of the shoulder: long-term evaluation. Ar-throscopy 2005;21(1):55.
Krishnan SG et al: A soft tissue attempt to stabilize the multiply operated glenohumeral joint with multidirectional instability. Clin Orthop 2004;(429):256.
Safran O et al: Posterior humeral avulsion of the glenohumeral ligament as a cause of posterior shoulder instability. A case report. J Bone Joint Surg Am 2004;86-A(12):2732.
Glenoid Labrum Injury
Essentials of Diagnosis
Prevention
As labral injuries can result from repetitive activity or an acute traumatic event, it is important to maintain good strength and flexibility of the shoulder to minimize these injuries.
Clinical Findings
The glenoid labrum is a fibrocartilaginous rim around the glenoid fossa that deepens the socket and provides stability for the humeral head. It is also a connection for the surrounding capsuloligamentous structures. Glenoid labrum tears may occur from repetitive shoulder motion or acute trauma. In the athlete with repeated anterior subluxation of the shoulder, tears of the anteroinferior labrum may occur, leading to progressive instability.
Weight lifters may also develop glenoid labrum tears as a result of repetitive bench pressing and overhead pressing. Weakness in the posterior rotator cuff may aggravate this condition. Tears of the glenoid labrum may also occur from acute trauma such as falling on an outstretched arm, but are also seen in the leading shoulders of golfers and batters when they ground their clubs or bats.
Patients with glenoid labrum injuries may describe pain that interrupts the smooth functioning of the shoulder during specific activities. On examination, they may have discomfort on forced external rotation at 90° of abduction, with the pain typically not increasing as the arm goes into further abduction. Frequently, a labrum disruption may be felt as a “pop” or “click” on forced external rotation. The patient may also experience discomfort on forced horizontal adduction of the shoulder. Manual muscle testing may show associated weakness in the rotator cuff muscles. Diagnostic tests such as a computed tomography (CT) scan and MRI following injection of contrast dye into the shoulder joint may allow early detection of glenoid labrum lesions.
Treatment
Range-of-motion exercises and gradual return to activity are often successful in relieving symptoms. However, if nonoperative management fails, arthroscopic intervention may be indicated to debride a torn, symptomatic labrum. During arthroscopy, care must be taken not to debride the inferior labrum, as this may result in increased anterior shoulder instability escalating the probability of anterior shoulder dislocation. Immediately following surgery, range-of-motion exercises and strengthening training begin.
Prognosis
Usually within 2–3 weeks following arthroscopic debridement, the athlete may begin a throwing program. Baseball pitchers may be ready to throw 3 months postoperatively.
Slap Lesions
The use of shoulder arthroscopy in the diagnosis and treatment of shoulder disorders has led to increased awareness of superior labrum anterior posterior (SLAP) lesions. SLAP lesions involve the origin of the long head of the biceps brachii (biceps anchor) and the superior capsulolabral structures. A type I lesion involves degeneration or fraying of the labrum without instability. Type II lesions are most common, accounting for over 50% of patients with a SLAP lesion, and involve detachment of the superior labrum from the glenoid. A type III lesion involves a bucket-handle tear of the superior labrum with firm attachment of the remainder of the labrum. In type IV lesions attachment to the labrum remains, but there is an associated bucket-handle tear of the labrum that extends into the biceps tendon (Figure 5-11).
Types V–VII SLAP lesions were later added to this initial four-part classification. A type V lesion is an anterior–inferior Bankhart lesion that continues superiorly to include separation of the biceps tendon. A type VI lesion includes a biceps separation with an unstable flap tear of the labrum. Finally, a type VII lesion involves a superior labrum–biceps tendon separation that extends anteriorly beneath the middle glenohumeral ligament.
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Essentials of Diagnosis
Prevention
As labral injuries can result from repetitive activity or an acute traumatic event, it is important to maintain good strength and flexibility of the shoulder to minimize these injuries.
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Figure 5-11. The initial four types of the SLAP lesions include fraying of the superior capsulolabrum (type 1), detachment of the superior capsulolabrum and the biceps anchor (type 2), bucket-handle tearing of the superior capsulolabrum (type 3), and detachment of the superior capsulolabrum and tearing into the biceps anchor (type 4). (Reprinted with permission from McMahon PJ, Skinner HB: Sports medicine. In: Skinner HB (editor): Current Diagnosis & Treatment in Orthopedics, 3rd ed. McGraw-Hill, 2003. ) |
Clinical Findings
Patients present with nonspecific shoulder pain associated with activity. A complicating factor in making the diagnosis is that the majority of SLAP lesions are associated with other shoulder pathology such as rotator cuff tears, acromioclavicular joint pathology, and instability. Less than 28% of SLAP lesions are isolated.
No single test is both sensitive and specific for the diagnosis of SLAP lesions. MR arthrography can be helpful. However, diagnostic arthroscopy remains the best means to definitively diagnose SLAP lesions. The active compression test may prove to be the most useful single provocative maneuver. The internally rotated shoulder is forward flexed to 90° and is then brought across the body in horizontal abduction about 10°. The test is positive if the patient has pain with resisted forward flexion that is relieved by external rotation of the shoulder.
Treatment
Treatment of SLAP lesions can be simplified by noting whether the lesion would contribute to detachment of either the biceps anchor or the anterosuperior capulolabrum. Lesions producing meaningful detachment of the anterior capsuloligamentous structures generally require repair of these structures back to the bony glenoid rim. Lesions producing significant defects extending into the biceps tendon may require biceps tenotomy, with or without tenodesis.
Holtby R, Razmjou H: Accuracy of the Speed's and Yergason's tests in detecting biceps pathology and SLAP lesions: comparison with arthroscopic findings. Arthroscopy 2004; 20(3):231.
Musgrave DS, Rodosky MW: SLAP lesions: current concepts. Am J Sports Med 2001;30(1):29.
Parentis MA et al: Disorders of the superior labrum: review and treatment guidelines. Clin Orthop 2002;400:77.
Shoulder Stiffness
Essentials of Diagnosis
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Prevention
Most patients have some sort of antecedent trauma to their shoulder, be it minimal or severe. Initiating gentle range of motion and strengthening exercises immediately after the traumatic event is essential to minimizing the likelihood of developing shoulder stiffness.
Clinical Findings
Often called adhesive capsulitis or frozen shoulder, shoulder stiffness is a painful condition characterized by significant restriction in both active and passive range of motion. The shoulder is characterized as being stiff when the articular surfaces are normal and the joint is stable, yet there is a restriction in range of motion. Stiffness may also result from pathologic connections between the articular surfaces, soft tissue contracture, bursal adhesions, or a shortened muscle–tendon unit. Often of uncertain etiology, the restrictions of shoulder motion are global. That is, none of the shoulder planes of motion is spared.
Shoulder stiffness may be separated into idiopathic and posttraumatic etiologies. Idiopathic shoulder stiffness is most common in older individuals, especially women between 40 and 60 years of age. Other factors that predispose to idiopathic shoulder stiffness include cervical, cardiac, pulmonary, neoplastic, neurologic, and personality disorders. Patients with diabetes mellitus are also at a high risk of developing shoulder stiffness, with 10–35% of diabetics having restriction of shoulder motion. Diabetics who have been insulin dependent for many years have the greatest incidence and bilateral involvement. The pathophysiology of idiopathic shoulder stiffness remains uncertain, but the pathoanatomy is commonly limited to contracture of the glenohumeral capsule (Figure 5-12). Most prominently involved is the rotator interval, which includes the coracohumeral ligament.
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Figure 5-12. Arthrogram of the shoulder demonstrating the classic findings of adhesive capsulitis. Note the small irregular joint capsule with addition of contrast material. (Reprinted with permission from McMahon PJ, Skinner HB: Sports medicine. In: Skinner HB (editor): Current Diagnosis & Treatment in Orthopedics, 3rd ed. McGraw-Hill, 2003. ) |
Although all patients can recall some traumatic event that preceded their shoulder stiffness, those with distinct trauma such as a prior fracture, rotator cuff tear, or surgical procedure have a posttraumatic etiology. Stiffness after shoulder surgery is typical and usually resolves with time and appropriate rehabilitation. But the shoulder should not be neglected after any surgery about the shoulder girdle. This includes axillary or cervical lymph node dissections, especially when combined with radiation therapy, cardiac catheterization in the axilla, and coronary artery bypass grafting with sternotomy and thoracotomy. All surgeons should be aware that these procedures may result in restricted shoulder motion.
The clinical presentation of idiopathic shoulder stiffness is classically described as having three phases. The first phase is the painful, freezing phase. The pain is typically achy in nature and sudden jolts or attempts at rapid motion exacerbate the chronic discomfort. The pain may begin at night and shoulder motion becomes progressively limited. Patients often hold their arm at their side and in internal rotation with the forearm across
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the belly. They may also be treated for nonspecific shoulder pain with a sling in this position. This inflammatory phase often lasts between 2 and 9 months.
The second phase of progressive stiffness lasts between 3 and 12 months. Stiffness progresses to a point at which shoulder motion is restricted in all planes. Essentially, the shoulder has undergone fibrous arthrodesis. Fortunately, pain progressively decreases from the initial, inflammatory phase. With time, patients are able to use the shoulder with little or no pain, within the restricted range of motion, but attempts to exceed this range are accompanied by pain. The patient's symptoms then plateau. Unfortunately, this phase may be persistent with symptoms lasting for extended periods. In the resolution, or thawing phase, the shoulder slowly and progressively becomes more supple. It can be as short as a month, but typically lasts 1–3 years.
On clinical examination, there is loss of both active and passive range of shoulder motion. Often the first motion to be affected is internal rotation, demonstrated by an inability to bring the arm up the back to the same level as the normal shoulder. Radiographic confirmation of adhesive capsulitis may be done by arthography, which will demonstrate marked reduction in the capacity of the joint. Often the affected shoulder will not take more than 2–3 mL of dye, although normal capacity is 12 mL.
Treatment
Treatment varies, but conservative modalities and progressive range-of-motion exercises seem effective. Range-of-motion exercises for external rotation and abduction will help minimize the length of restriction in motion and dysfunction. Manipulation under anesthesia, long the mainstay of intervention, is being replaced by selective arthroscopic capsular release. Short-term results indicate a quicker return of motion.
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Figure 5-13. Analysis of 1603 shoulder girdle injuries showing the frequency and location of fractures and dislocations. (Reprinted with permission from McMahon PJ, Skinner HB: Sports medicine. In: Skinner HB (editor): Current Diagnosis & Treatment in Orthopedics, 3rd ed. McGraw-Hill, 2003. ) |
Prognosis
Whether treated with rehabilitation alone, or with capsular release, a return of about 80% shoulder range of motion is usual.
Nicholson GP: Arthroscopic capsular release for stiff shoulders: effect of etiology on outcomes. Arthroscopy 2003;19(1):40.
Omari A, Bunker TD: Open surgical release for frozen shoulder: surgical findings and results of the release. J Shoulder Elbow Surg 2001;10(4):353.
Wolf JM, Green A: Influence of comorbidity on self-assessment instrument scores of patients with idiopathic adhesive capsulitis. J Bone Joint Surg Am 2002;84-A(7):1167.
Fractures About the Shoulder
The clavicle is one of the most commonly fractured bones in the body, with direct trauma being the usual cause in athletic events (Figure 5-13). Football, wrestling, and ice hockey are the sports most commonly involved in clavicular fractures, which is not surprising as all three are associated with high-speed contact between players.
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Essentials of Diagnosis
Clinical Findings
Despite the proximity of vital structures, clavicular fractures that occur during athletic activities are rarely associated with neurovascular damage, and accompanying soft tissue disorders are uncommon. The patient will usually give a history of falling in the area of the shoulder or receiving a blow to the clavicle, experiencing immediate pain and an inability to raise the arm. Radiography will usually confirm the clinical impression, and must show the entire clavicle, including the shoulder girdle, upper third of the humerus, and sternal end of the clavicle.
Of clavicular fractures, midclavicular fractures account for 80%, distal fractures for 15%, and proximal fractures for 5%. Most fractures of the shaft of the clavicle heal well. However, some neurovascular complications, such as a tear of the subclavian artery or a brachial plexus injury, are serious, although rare. Therefore, when evaluating and treating clavicular fractures, an initial neurovascular examination is very important. Pulses in the distal part of the upper extremity, strength, and sensation must be carefully evaluated.
Because the clavicle is the only bone structure that fixes the shoulder girdle to the thorax, a fracture through the clavicle causes the shoulder to sag forward and downward. The pull of the sternocleidomastoid muscle may displace the proximal fragment superiorly. These forces tend to hinder the initial reduction and maintenance of reduction. In addition, distal fractures, which are more common in older age groups, may involve tears in the coracoclavicular ligament, which allows the proximal clavicle to ride up superiorly, mimicking an acromioclavicular dislocation. Delayed union is much more common in this type of fracture than in other clavicular fractures.
Treatment
Mid and proximal clavicular fractures are usually treated with a short period of rest, with a sling on the affected side to support the extremity. Immobilization is usually discontinued at 3–4 weeks, and once the clavicular fracture has healed, range-of-motion and strengthening exercises should begin.
Prognosis
Onset of exercises prior to healing may result in nonunion. Athletes should not be allowed to return to play until shoulder strength and range of motion return to preinjury levels. Generally, no special braces or pads are required when the athlete returns to play.
Grassi FS et al: Management of midclavicular fractures: comparison between nonoperative treatment and open intramedullary fixation in 80 patients. J Trauma 2001;50(6):1096.
Robinson CM, Cairns DA: Primary nonoperative treatment of displaced lateral fractures of the clavicle. J Bone Joint Surg Am 2004;86-A(4):778.
Robinson CM et al: Estimating the risk of nonunion following nonoperative treatment of a clavicular fracture. J Bone Joint Surg Am 2004;86-A(7):1359.
Fractures of the proximal humerus, which represent approximately 4–5% of all fractures, are a relatively uncommon sports injury. They most often present in young adolescents with open growth plates or in elderly osteoporotic patients. When they do occur in the athlete, they are typically the result of a high-energy impact injury or are secondary to an underlying pathologic bone condition.
Essentials of Diagnosis
Clinical Findings
The proximal humerus consists of four major bony components: the humeral head, the greater tuberosity, the lesser tuberosity, and the humeral shaft. Fractures, which can occur between any or all of these regions, are traditionally defined by the location and displacement of the fracture fragments (Figure 5-14). The patient
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with a proximal humerus fracture will usually be able to report the mechanism of injury and will complain of pain, swelling, and an inability to use the shoulder. A physical examination will often reveal loss of the normal contour of the shoulder, tenderness about the shoulder, ecchymosis that may extend down to the elbow, and crepitus on attempted range of motion. A thorough neurovascular examination is essential, as brachial plexus and axillary nerve injuries have been reported in association with proximal humerus fractures. Because the axillary nerve is the nerve most commonly injured in these cases, sensation to light touch and pin-prick over the lateral aspect of the upper arm and deltoid muscle function must be tested. An accurate radiographic evaluation is necessary to confirm the type and severity of the fracture and is essential in determining the treatment plan. Anteroposterior and lateral views in the plane of the scapula as well as an axillary view to rule out an associated glenohumeral dislocation are necessary.
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Figure 5-14. Four part classification for fractures of the proximal humerus. AN, anatomic neck; SN, surgical neck; GT, greater tuberosity; LT, lesser tuberosity. [Reprinted with permission from Norris TR, Green A: Proximal humerus fractures and fracture-dislocations. In: Browner BD et al (editors): Skeletal Trauma: Fractures, Dislocation and Ligamentous Injuries. Elsevier, 1998. ] |
Treatment
Most proximal humerus fractures are minimally displaced and can be treated nonoperatively with sling immobilization and early passive range of motion. However, about 20% need to be treated operatively. Many factors contribute to this decision-making process including fracture type and degree of displacement, bone quality, activity level, and associated injuries. Surgical options range from closed reduction and percutaneous pinning to open reduction with internal fixation to humeral head replacement.
Prognosis
For minimally displaced fractures, the prognosis is generally good. Loss of motion is the most common complication. It can take 12–18 months to attain the maximal result, so range-of-motion exercises should be continued for an extended period of time.
Guttmann D et al: Injuries of the proximal humerus in adults. In: Orthopaedic Sports Medicine: Principles and Practice. DeLee JC et al (editors). Saunders, 2003, pp. 1096–1118.
Iannotti JP et al: Nonprosthetic management of proximal humeral fractures. J Bone Joint Surg Am 2003;85:1578.
In young athletes, epiphyseal fractures of the proximal humerus may occur. The separate growth centers of the articular surface, greater tuberosity, and lesser tuberosity coalesce at approximately age 7 years, with the remaining growth plates closing at 20–22 years of age. Therefore, fracture separations may occur at any age until the growth plates have closed. Fortunately, fractures in this area usually do not arrest growth.
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Essentials of Diagnosis
Clinical Findings
Injury can occur to the shoulder in the growing musculoskeletal system of young athletes engaged in sports that involve overhead throwing. Proximal humerus pain associated with widening of the proximal humerus epiphysis, especially while throwing, has been termed “little league shoulder.” Although widening of the proximal humerus epiphysis can be an adaptive change to throwing, when painful it may represent a fracture resulting from overuse.
Treatment
Cessation of throwing is the first step in treatment. Once pain has resolved, range of motion and strengthening exercises can be initiated. Ultimately, throwing can be resumed as long as the patient is pain free.
Dobbs MB et al: Severely displaced proximal humeral epiphyseal fractures. J Pediatr Orthop 2003;23(2):208.
Karatosun V et al: Treatment of displaced, proximal, humeral, epiphyseal fractures with a two-prong splint. J Orthop Trauma 2003;17(8):578.
Acromioclavicular Joint Injury
Essentials of Diagnosis
Prevention
Avoiding activities that may result in a downward blow to the tip of the shoulder is the best way to prevent these injuries.
Clinical Findings
Acromioclavicular dislocations or subluxations, commonly referred to as separations, vary in severity depending on the extent of injury to the stabilizing ligaments and capsule. The typical mechanism of injury is a direct downward blow to the tip of the shoulder. Clinically, pain at the top of the shoulder over the acromioclavicular joint is the predominant symptom, with varying decreases in motion depending on the severity of the injury. The athlete who has sustained this type of injury will typically leave the field holding the arm close to the side.
When checking for instability of the acromioclavicular joint, the examiner should manipulate the midshaft of the clavicle, rather than the acromioclavicular joint to rule out pain from contusion to the acromioclavicular area. For milder acromioclavicular injuries, the patient should put the hand of the affected arm on the opposite shoulder, and the examiner may then gently apply downward pressure at the patient's affected elbow, noting if this maneuver causes pain at the acromioclavicular joint.
Acromioclavicular joint injuries were initially divided into grades I–III (Figure 5-15). Grade I injuries are typically produced by a mild blow causing a partial tear of the acromioclavicular ligament. When the acromioclavicular ligament is completely torn, but the coracoclavicular ligament remains intact, a grade II injury that involves subluxation or partial displacement results. When the force of injury is severe enough to tear the coracoclavicular and acromioclavicular ligaments in addition to the capsule, a grade III injury occurs.
Three additional injuries were later added to the classification. In grade IV injuries, the clavicle is displaced posterior and buttonholed through the fascia of the trapezius muscle. Grade V injuries demonstrate severe inferior displacement of the glenohumeral joint, with the clavicle often 300% superior to the acromion. Lastly, in grade VI injuries the distal end of the clavicle is locked inferior to the coracoid.
Acromioclavicular joint displacement is often obvious on physical examination, but it is best classified by radiography. An anteroposterior radiograph that is aimed 10° cephalad allows visualization of the acromioclavicular joint. A radiograph of the entire upper thorax allows the vertical distance between the coracoid and the clavicle on both the involved and uninvolved sides to be compared. Anteroposterior radiographs with weights applied to the upper extremities are usually unnecessary. An axillary lateral radiograph is also essential for proper classification.
Treatment
Management of acromioclavicular joint injuries depends on their severity. Grade I and grade II injuries may be treated with a sling until discomfort dissipates,
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usually within 2–4 weeks. Next a rehabilitation program starts and normal range of motion and strength to the upper extremity begins to be restored. The treatment of grade III injuries or complete dislocations in athletes is controversial. Although most believe that grade III injuries are best managed nonoperatively, others advocate operative treatment. Grade IV–VI injuries are best treated with open reduction and internal fixation along with reconstruction of the coracoclavicular ligament.
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Figure 5-15. Grades of acromioclavicular (AC) joint separations. A: Type I, partial tear of the AC ligament. B: Type II, complete tear of the AC ligament; the coracoclavicular (CC) ligaments remain intact. C: Type III, disruption of the AC and CC ligaments. (Reprinted with permission from McMahon PJ, Skinner HB: Sports medicine. In: Skinner HB (editor): Current Diagnosis & Treatment in Orthopedics, 3rd ed. McGraw-Hill, 2003. ) |
Nonsurgical treatment may either involve a sling for comfort or an acromioclavicular sling to try to achieve reduction. The device must be fit to apply pressure to the distal clavicle sufficient to afford reduction, but not great enough to compromise the skin. Ice and other modalities are used for an acute acromioclavicular injury to reduce soreness and swelling. Pain is the limiting factor in beginning range-of-motion and isometric muscle-strengthening exercises. It should be used as a guide for gradual initiation and escalation of these physical ther-apy regimes. Isotonic exercises may then follow because isometric exercises are more effective earlier when range of motion is limited.
Before resuming athletic activities, the patient must have full range of pain-free motion and no tenderness upon direct palpation of the acromioclavicular joint or pain when manual traction is applied.
Prognosis
Athletes who do not need to elevate their arms, such as soccer or football players, tend to return to sports earlier than players engaged in sports that require overhead arm activity, such as tennis, baseball, and swimming.
Dumonski M et al: Evaluation and management of acromioclavicular joint injuries. Am J Orthop 2004;33(10):526.
Su EP et al: Using suture anchors for coracoclavicular fixation in treatment of complete acromioclavicular separation. Am J Orthop 2004;33(5):256.
Coracoid Fracture
Fractures of the coracoid process are rare; they are usually seen in professional riflemen and skeet shooters, though they have also been reported in baseball and tennis players. They are identified on radiographs, and conservative treatment, including cessation of activity, usually results in uncomplicated healing after 6–8 weeks.
Sternoclavicular Joint Injury
In the skeletally mature adult athlete, injury to the sternoclavicular joint usually involves the surrounding soft tissue and capsule tearing, leading to subluxation or dislocation. The mechanism of injury is either a blow to the point of the shoulder, which predisposes the athlete to anterior dislocation, or a direct blow to the clavicle or chest with the shoulder in extension, which predisposes the athlete to posterior dislocation. The injury may range from a symptomatic sprain to a complete sternoclavicular dislocation with disruption of the capsule and its restraining ligaments.
Essentials of Diagnosis
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Clinical Findings
The most common type of sternoclavicular dislocation is anterior dislocation. This is recognized clinically by an anterior prominence of the proximal clavicle on the involved side. Radiographic documentation of an anterior sternoclavicular dislocation is difficult because the rib, sternum, and clavicle overlap at the joint, but may be confirmed by oblique views. A CT scan is very sensitive and should be done if the radiograph appears normal but a dislocation is suspected.
Treatment
Although dislocation of the anterior sternoclavicular joint may cause considerable distress initially, the symptoms usually subside rapidly, with no loss of shoulder function. A variety of surgical and nonsurgical approaches have been advocated, but surgery for anterior dislocations often results in significant complications. Closed treatment modalities vary from using a sling to attempted closed reduction, which may be successful initially but is difficult to maintain.
Essentials of Diagnosis
Clinical Findings
Posterior sternoclavicular dislocation is much less common, but is associated with more complications because of the potential for injury to the esophagus, great vessels, and trachea. Presenting symptoms range from mild to moderate pain in the sternoclavicular region to hoarseness, dysphagia, severe respiratory distress, and subcutaneous emphysema from tracheal injury.
Treatment
In most instances, closed reduction of posterior dislocations, if performed early, is successful and stable. To effect reduction, a pillow is placed under the upper back of the supine patient and gentle traction is applied with the shoulder held in 90° of abduction and at maximum extension (Figure 5-16). Rarely, closed reduction under general anesthesia or open reduction is required.
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Figure 5-16. Method for reducing (A) anterior sternoclavicular and (B) posterior sternoclavicular dislocation. (Reprinted with permission from McMahon PJ, Skinner HB: Sports medicine. In: Skinner HB (editor): Current Diagnosis & Treatment in Orthopedics, 3rd ed. McGraw-Hill, 2003. ) |
After reduction, the patient is put in an immobilization splint and is instructed to use ice and oral NSAIDs. Once the joint has healed sufficiently, usually within 2–3 weeks, range-of-motion exercises may begin. Elevation of the arm should not be attempted until 3 weeks after injury.
Medial Clavicular Epiphyseal Fracture
In athletes younger than 25 years of age, sternoclavicular injuries may not result in true dislocations, but rather in fractures through the growth plate of the proximal clavicle. These clavicular epiphyseal fractures may appear clinically as dislocations, particularly if some displacement is present, and may be treated conservatively. Typically, these are not associated with growth deformities, and reduction of the fracture is not needed unless there is severe displacement. Symptomatic treatment for pain
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will usually suffice. Sometimes an adolescent presents with an enlarging mass at the sternoclavicular joint, accompanied by parents with worries of cancer. A careful history reveals trauma several weeks earlier and the mass represents the callus of a healing clavicular epiphyseal fracture that can be demonstrated radiographically.
Battaglia TC et al: Interposition arthroplasty with bone-tendon allograft: a technique for treatment of the unstable sternoclavicular joint. J Orthop Trauma 2005;19(2):124.
Shoulder Neurovascular Injury
Essentials of Diagnosis
Clinical Findings, Treatment, & Prognosis
Brachial plexus injuries are typically caused by a fall on the shoulder as seen in acromioclavicular joint injuries. Most brachial plexus injuries do not involve motor loss and exhibit paresthesias, which resolve in a period of minutes to weeks, although some cases may persist for months or years. Early in the course of the injury, a transient slowing of conduction across the plexus or a mild prolongation of nerve latency may be seen. The “burner” or “stinger” is one of the most common brachial plexus injuries encountered in athletes. The key to diagnosis is a short duration of upper extremity paresthesias and shoulder weakness, with pain-free range of motion of the cervical spine. Players may return to competition after shoulder strength and full, pain-free range of motion have returned.
Rarely, a severe injury will occur (eg, from motorcycle racing). Chronic injuries result in instability of the shoulder that may be treated with trapezius transfer. Arthrodesis is an alternative, initially or after failed muscle transfer.
Safran MR: Nerve injury about the shoulder in athletes. Part 2: Long thoracic nerve, spinal accessory nerve, burners/stingers, thoracic outlet syndrome. Am J Sports Med 2004;32:1063.
Essentials of Diagnosis
Clinical Findings, Treatment, & Prognosis
Traction incidents may cause a long thoracic nerve palsy, with subsequent serratus anterior paralysis and winging of the scapula. Traction and blunt trauma may also cause injury to the spinal accessory nerve, another cause of winging of the scapula. These can be differentiated on physical examination by the position of the scapula. With serratus anterior palsy, the inferior portion of the scapula tends to go medially, whereas the opposite occurs with spinal accessory nerve palsy. Treatment is usually conservative, with return of function in weeks if the nerve has not been divided.
Aquino SL et al: Nerves of the thorax: atlas of normal and pathologic findings. Radiographics 2001;21(5):1275.
Safran MR: Nerve injury about the shoulder in athletes. Part 2: Long thoracic nerve, spinal accessory nerve, burners/ stingers, thoracic outlet syndrome. Am J Sports Med 2004; 32:1063
Essentials of Diagnosis
Clinical Findings, Treatment, & Prognosis
Entrapment of the suprascapular nerve is often associated with activities such as weight lifting, baseball
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pitching, volleyball, and backpacking. Traction and repetitive shoulder use are the mechanisms of injury. Compression of the nerve may occur from entrapment at the anterior suprascapular notch of the scapula or at the level of the spinoglenoid notch. The latter occurs in volleyball players and baseball players and is likely caused by rapid overhead acceleration of the arm. Compression is associated with poorly localized pain and weakness in the posterolateral aspect of the shoulder girdle. This may be followed by atrophy of the supraspinatus or infraspinatus muscles. Eventually, there is weakness of forward flexion and external rotation of the shoulder. The diagnosis is confirmed by electromyography and nerve conduction studies.
Conservative therapy consists of rest, NSAIDs, and physical therapy designed to increase muscular tone and strength. If this is unsuccessful, then surgical exploration is indicated, which may reveal hypertrophy of the transverse scapular ligament, anomalies of the suprascapular notch, and ganglion cysts. Results of surgery vary with the lesion discovered, but many patients return to full function postoperatively.
Safran MR: Nerve injury about the shoulder in athletes. Part 1: Suprascapular nerve and axillary nerve. Am J Sports Med 2004;32:803.
Essentials of Diagnosis
Clinical Findings, Treatment, & Prognosis
This nerve is susceptible to direct frontal blows or surgical procedures. Injury is associated with numbness in the lateral forearm to the base of the thumb and weak to absent biceps muscle function. Most injuries seen in sports are transient and respond to conservative treatment in a matter of days to weeks.
Klepps SJ et al: Anatomic evaluation of the subcoracoid pectoralis muscle transfer in human cadavers. J Shoulder Elbow Surg 2001;10(5):453.
Essentials of Diagnosis
Clinical Findings, Treatment, & Prognosis
The usual mechanism of injury is trauma either by direct blow to the posterior aspect of the shoulder or following dislocation of the shoulder or fracture of the proximal humerus. Axillary nerve injury occurs in many sports such as football, wrestling, gymnastics, mountain climbing, rugby, and baseball. The degree of injury to the nerve varies because the initial presentation may be mild weakness during elevation and abduction of the arm with or without numbness of the lateral arm. The deltoid extension lag sign is indicative of axillary nerve injury. To perform this test the examiner elevates the arm into a position of near full extension, asks the patient to hold the arm in this position, and then releases the arm. If there is complete deltoid paralysis, the arm will drop. For partial nerve injuries, the magnitude of the angular drop, or lag, is an indicator of deltoid strength. Approximately 25% of all dislocated shoulder injuries are associated with axillary nerve traction injuries, which respond well to rest, physical therapy, and time. If recovery is not complete within 3–6 months, surgical intervention is recommended with exploration, utilizing neurolysis or grafting, or both, as necessary. Results of surgery are usually favorable, with sensory recovery occurring before motor recovery.
Steinmann SP, Moran EA: Axillary nerve injury: diagnosis and treatment. J Am Acad Orthop Surg 2001;9(5):328.
Thoracic Outlet Syndrome
Essentials of Diagnosis
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Clinical Findings, Treatment, & Prognosis
The symptoms resulting from thoracic outlet compression may be neurologic, venous, or arterial in nature. Obstruction of the subclavian vein may lead to stiffness, edema, and even thrombosis of the limb. Arterial obstruction may be the result of direct compression and manifests with pallor, coolness, and forearm claudication. Doppler examination reveals changes in arterial and venous flow. Electromyography and nerve conduction studies are also helpful in diagnosis.
Nonoperative treatment is recommended for less severe forms of this syndrome, and once the pain subsides, an exercise program to strengthen the pectoral girdle muscles is beneficial. Special exercises to strengthen the upper and lower trapezius, along with the erector spinae and serratus anterior muscles, yield good results. Correcting poor posture and an ongoing maintenance program are mandatory once improvement is reached. Progression of symptoms or failure of nonoperative treatment is an indication for surgical exploration and correction of the pathologic factors encountered.
Connolly JF, Ganjianpour M: Thoracic outlet syndrome treated by double osteotomy of a clavicular malunion: a case report. J Bone Joint Surg Am 2002;84:437.
Wiesler ER et al: Humeral head fracture-dislocation into the thoracic outlet: case report and review of the literature. J Shoulder Elbow Surg 2004;13(5):576.