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The shoulder joint is composed of four articulations: the sternoclavicular, acromioclavicular, glenohumeral, and scapulothoracic that work together to allow smooth shoulder function. Together, they allow the shoulder joint to have the greatest range of motion of any joint in the body, and the relationship between these articulations must be considered when treating shoulder dysfunction. Normal function of the shoulder is a balance between mobility and stability. In addition to the four articulations, mobility is allowed by the “large ball–small socket” bony arrangement and the voluminous glenohumeral joint capsule, which does not restrict movement until the extremes of motion. The bony anatomy contributes little to stability and has been compared with a golf ball on a tee. The glenoid is encircled by the labrum, composed of dense fibrocartilaginous tissue, which increases the depth of the socket by 50% around the humeral head and increases stability. The glenoid articular surface and the labrum combine to create a socket that is approximately 9 mm deep in the superoinferior direction and 5 mm deep in the anteroposterior direction. Adding the glenoid labrum increases the glenoid surface to 75% of the humeral head vertically and 57% horizontally. Biomechanical testing of cadaver shoulder specimens showed that the labrum affects the distribution of contact stresses when a compressive load is applied to the shoulder at 90 degrees of abduction. Because there is very little bony constraint to the shoulder, most of the stability is provided by the surrounding muscles and ligaments.
The ligamentous constraints are the primary stabilizers at extremes of motion. The superior glenohumeral ligament is the primary restraint to inferior humeral subluxation in 0 degrees of abduction and is the primary stabilizer to anterior and posterior stress in the same position. Tightening of the rotator interval (which includes the superior glenohumeral ligament) decreases posterior and inferior translation. The middle glenohumeral ligament limits external rotation when the arm is in the lower and middle ranges of abduction but has little effect when the arm is in 90 degrees of abduction. The inferior glenohumeral ligament is composed of an anterior band that is quite thick, a posterior band that is less thick and distinct, and a thinner intervening axillary pouch, creating a hammock-type sling . With external rotation, the hammock slides anteriorly and superiorly, the anterior band tightens, and the posterior band fans out. With internal rotation, the opposite occurs. The anteroinferior glenohumeral ligament complex is the main stabilizer to anterior and posterior stresses when the shoulder is abducted 45 degrees or more.
The muscles of the shoulder joint can be divided into intrinsic and extrinsic groups. The extrinsic muscles primarily control movement of the scapula and include the rhomboids, levator scapulae, trapezius, and serratus anterior. The intrinsic muscles control the glenohumeral joint and include the rotator cuff muscles (subscapularis, supraspinatus, infraspinatus, and teres minor), the deltoid, the pectoralis major, the teres major, the latissimus dorsi, and the biceps brachii. The muscular constraints work in several ways to provide stability. First, they dynamically position the scapula to place the glenoid opposite the humeral head as the shoulder moves. Rowe compared the relationship to a “ball on a seal’s nose.” As the ball (humerus) moves, the seal (scapula and glenoid) moves to maintain the balanced relationship. Second, whereas ligaments work in a static fashion to limit translation and rotation, their stiffness and torsional rigidity are increased with concomitant muscle activity. Rotator cuff activity and biceps activity have been shown to stiffen the capsule and decrease glenohumeral translation. Third, intrinsic and extrinsic muscle groups serve as fine tuners of motion and power movers by working in “force couples.” The force couples control and direct the force through the joint, contributing to stability. The most important such force couple involves the subscapularis and posterior rotator cuff. Together, these muscles provide a compressive force that centers the humeral head in the glenoid cavity and explains why some patients with massive superior rotator cuff tears can have remarkably well-preserved overhead activity. In particular, the teres minor has often been viewed as a minor contributor to rotator cuff function; however, there has been heightened attention to its contribution, particularly when the other cuff tendons fail.
The tendinous insertions of the rotator cuff muscles, the articular capsule, the coracohumeral ligament, and the glenohumeral ligament complex blend into a confluent sheet before insertion into the humeral tuberosities. The tendons of the infraspinatus and supraspinatus muscles join approximately 15 mm proximal to their insertion and cannot be readily separated by blunt dissection. The infraspinatus and teres minor fuse near their musculotendinous junctions. The supraspinatus and subscapularis tendons join as a sheath that surrounds the biceps tendon at the entrance of the bicipital groove. The roof of this sheath consists of a portion of the supraspinatus tendon, and a sheet of the subscapularis tendon forms the floor. This relationship is relevant to the frequent coexistence of subscapularis tendon tears with lesions and/or instability of the long head of the biceps. The coracohumeral ligament is a thick band of fibrous tissue extending from the coracoid process along the surface of the capsule to the tuberosities between the supraspinatus and subscapularis tendons. The ligament is deep to the tendinous insertion of the cuff and blends with the capsule and supraspinatus tendon to form part of the roof of the biceps sheath. A 1-cm wide thickening of fibrous tissue extends posteriorly from the coracohumeral ligament origin on the coracoid to the posterior margin of the infraspinatus. This band is an extension of the coracohumeral ligament and travels between the capsule and the cuff tendons. A sheet of fibrous tissue from the coracohumeral ligament origin also extends posterolaterally to form a sheet over the superficial supraspinatus and infraspinatus tendon insertions.
Histologic studies of the supraspinatus and infraspinatus tendons identified five distinct layers. The most superficial layer (layer one) contains large arterioles and comprises fibers from the coracohumeral ligament. This layer is 1 mm thick and contains fibers that are oriented obliquely to the long axis of the muscle bellies. Layer two is 3 to 5 mm thick and represents the direct tendinous insertion into the tuberosities. Large bundles (1 to 2 mm in diameter) of densely packed parallel tendon fibers compose layer two. The subscapularis tendinous insertion exhibits a similar structure, with collagen fiber bundles that parallel the long axis of the muscle and splay before insertion. A group of bundles from the subscapularis joins with fibers of the supraspinatus to serve as the floor of the biceps sheath, and the roof of the biceps sheath is formed by fibers from layer two of the supraspinatus. Layer three is approximately 3 mm thick and comprises smaller bundles of collagen with a less uniform orientation than in layer two. Fibers within this layer travel at 45-degree angles to one another to form an interdigitating meshwork that contributes to the fusion of the cuff tendon insertion. Layer four comprises loose connective tissue and thick collagen bands that merge with the coracohumeral ligament at the most anterior border of the supraspinatus. Layer five (2 mm thick) represents the shoulder capsule and includes a sheet of interwoven collagen extending from the glenoid labrum to the humerus.
The insertion site of the rotator cuff tendon at the greater tuberosity often is referred to as the “footprint.” Dugas et al. examined 20 normal cadaver rotator cuff specimens and mapped the footprint using a three-space digitizer. The mean medial-to-lateral insertion widths of the supraspinatus, infraspinatus, teres minor, and subscapularis tendons were 12.7 mm, 13.4 mm, 11.4 mm, and 17.9 mm, respectively. The mean minimal medial-to-lateral insertion width of the entire rotator cuff insertion occurred at the midportion of the supraspinatus and was 14.7 mm. The articular surface-to-tendon insertion distance was less than 1 mm along the anterior 2.1 cm of the supraspinatus-infraspinatus insertion. This distance progressively increased to a mean distance of 13.9 mm at the most inferior aspect of the teres minor insertion. The mean anteroposterior distances of the supraspinatus, infraspinatus, teres minor, and subscapularis insertions were noted to be 1.63 cm, 1.64 cm, 2.07 cm, and 2.43 cm, respectively.
An additional important concept relative to the rotator cuff is the rotator cable and rotator crescent. Viewed best from the articular side, the rotator cable is a thick bundle that acts as a suspensory support mechanism to bear forces applied to the rotator cuff ( Fig. 46.1 ). In turn, it offloads and protects the rotator crescent. Rotator cuff tears involving the cable are believed to correlate more with pain than others.
The rotator interval is defined as the triangular area in the anterior and superior shoulder where no rotator cuff tendons are present. As such, the interval is bounded by the supraspinatus superiorly, the subscapularis inferiorly, and the coracoid medially. The apex of the triangle is marked laterally by the transverse humeral ligament. The coracohumeral ligament, biceps tendon, and superior glenohumeral ligament are found in the rotator interval. The rotator interval is altered in pathologic states and has been found to be contracted in patients with adhesive capsulitis and expanded in those with shoulder instability.
The coracoacromial arch lies superior to the glenohumeral joint and is composed of the coracoid and the anterior acromion, which are spanned by the coracoacromial ligament. The distal clavicle usually is considered to be part of the arch as well. The rotator cuff tendons, the subacromial bursa, the biceps tendon, and the proximal humerus all pass beneath this arch. Any acquired or congenital process that narrows the space available for these structures can cause mechanical impingement. The coracoacromial arch also serves as a restraint to superior proximal humeral migration, and its disruption is considered the final step in the cascade of events culminating in anterosuperior escape in advanced degenerative shoulder disorders associated with massive rotator cuff tears. In escape, the humeral head dislocates anteriorly and superiorly with attempted forward elevation of the shoulder. As a result, the humeral head comes to rest in a palpable and visible position in the subcutaneous tissues.
Evaluation of a painful shoulder is challenging for several reasons. Different clinical conditions, such as the various impingement syndromes, rotator cuff tears (partial and complete), calcific tendinitis, adhesive capsulitis, and nerve entrapment syndromes, have similar histories, pain patterns, and findings on physical examination. All of these conditions can cause pain, weakness, and loss of motion of the affected extremity. The pain, usually exacerbated by overhead activities, is worse with active rather than passive motion and may awaken the patient from sleep. Pain may be referred to the area of the deltoid insertion. On physical examination, it often is impossible to reliably establish which structure in the shoulder is causing the pain because of the close anatomic proximity of these structures. Many tests are sensitive for detecting shoulder pathology but are not specific. Many conditions are painful with the same provocative maneuvers. Palpation is of limited benefit, especially in muscular or heavy patients. It is impossible to palpate the labrum or capsule, and although some authors have claimed to be able to palpate rotator cuff tears, we have not had that experience other than in very thin patients. Clicks and crepitus in the shoulder are not specific for any one pathologic condition, and often the reverberating quality of these clicks makes them unreliable for localization.
Although the physical examination often is inconclusive, it is an essential component of the evaluation of a patient with a painful shoulder and helps eliminate other potential causes of referred pain to the shoulder, such as disorders of the cervical spine (herniated disc, spondylosis, brachial plexopathy), chest cavity (Pancoast tumor, upper lobe pneumonia), breasts, axillary area, and abdomen (diaphragmatic irritation, gallbladder dysfunction).
The physical examination begins with inspection. The patient should be undressed above the waist. Women may cover up in a fashion similar to a strapless dress. This exposure allows observation of the anterior and the posterior aspects of the shoulder. Comparison of the shoulders may reveal subtle atrophy, swelling, or deformity. Ecchymosis may suggest contusions or ruptures of structures such as the rotator cuff or the long head of the biceps tendon. Palpation of the superficial bony structures may identify a painful acromioclavicular joint, sternoclavicular joint, clavicle, or acromion. Palpation elsewhere around the shoulder may suggest potential sources of pain, but as previously mentioned this is not often specific. The joints above and below the area of pain should be examined; for the shoulder, the joint above is the cervical spine. Indeed, 5% of patients presenting with the chief complaint of shoulder pain will be found to have an isolated cervical spine disorder. Therefore, a neurovascular examination of both upper extremities should be included along with an assessment of motor strength. Range of motion is determined actively and passively, noting painful arcs and tendencies to substitute muscle function.
More than 100 tests have been described for detecting shoulder instability, tendinitis, and tears of the rotator cuff, with varying degrees of accuracy. In an exhaustive review of the literature, Hegedus et al. determined that no single physical examination test can be used to make an unequivocal diagnosis; combinations of tests provide only marginally better accuracy. The following tests are ones that we frequently use and are designed either to reproduce symptoms or to produce pain suggesting impingement of the rotator cuff or tendinitis.
Neer first described the impingement test in 1972 ( Fig. 46.2A ). With the patient seated, the examiner raises the affected arm in forced forward elevation while stabilizing the scapula, causing the greater tuberosity to impinge against the acromion. This maneuver produces pain with impingement lesions of all stages. It also produces pain in many other shoulder conditions, such as adhesive capsulitis, osteoarthritis, calcific tendinitis, and bone lesions. Neer also described the impingement test with the use of a subacromial injection of 10 mL of 1% lidocaine (Xylocaine). Pain caused by impingement usually is significantly reduced or eliminated, but pain caused by other conditions (with the exception perhaps of calcific tendinitis) is not relieved. One study revealed sensitivity for the impingement sign of 75% for bursitis and 88% for cuff abnormalities, with specificities of 48% and 51%. The positive predictive values were 36% and 40%, and the negative predictive values were 83% and 89%. The test was positive, however, in 25% of patients with Bankart lesions, 46% of patients with superior labral anterior and posterior lesions, and 69% of patients with acromioclavicular arthritis.
Hawkins and Kennedy described their test in 1980 as an alternative to the Neer test, but they did not believe that it was as reliable ( Fig. 46.2B ). The test is performed by forward flexing the humerus to 90 degrees and forcibly internally rotating the shoulder. This maneuver drives the greater tuberosity farther under the coracoacromial ligament, reproducing the impingement pain. Sensitivities of 92% for bursitis and 88% for cuff abnormalities were found in 85 consecutive patients, with specificities of 44% and 43%. The positive predictive values were 39% and 37%, and the negative predictive values were 93.1% and 90%. The test was positive, however, in 31% of patients with Bankart lesions, 69% of patients with superior labral anterior and posterior lesions, and 94% of patients with acromioclavicular joint arthritis.
Jobe described the “supraspinatus test” in 1983 ( Fig. 46.2C ). The test is performed by placing the shoulder in 90 degrees of abduction and 30 degrees of forward flexion and internally rotated so that the thumb is pointing toward the floor. Muscle testing against resistance shows weakness or insufficiency of the supraspinatus owing to a tear or pain associated with rotator cuff impingement.
Zaslav described a test to differentiate between internal and classic outlet impingement ( Fig. 46. 2 D ). The test is performed with the patient seated and the examiner standing behind the patient. The patient’s arm is positioned in 90 degrees of abduction in the coronal plane and approximately 80 degrees of external rotation. A manual isometric muscle test is performed for external rotation and compared with one for internal rotation in the same position. If a patient with a positive impingement sign has good strength in external rotation and weakness in internal rotation, the test is positive. A positive internal rotation resistance stress test suggests internal impingement, and a negative test (more weakness in external rotation) suggests classic outlet impingement. Zaslav reported a sensitivity of 88%, specificity of 96%, positive predictive value of 88%, and negative predictive value of 94%. All of the patients tested had been selected, however, because they had a previous positive Neer impingement test, resulting in a population of “impingers” rather than a population with unconfirmed shoulder abnormalities.
This test, described by O’Brien for diagnosis of labral tears and acromioclavicular joint abnormalities, is performed with the physician standing behind the patient and asking the patient to forward flex the affected arm 90 degrees with the elbow in full extension. The arm is then adducted 10 to 15 degrees medial to the sagittal plane of the body and is internally rotated so that the thumb points downward. The examiner then applies a uniform downward force to the arm. With the arm in the same position, the palm is then fully supinated and the maneuver is repeated. The test is considered positive if pain is elicited with the first maneuver and is reduced or eliminated with the second maneuver. Pain localized to the acromioclavicular joint or on top of the shoulder is diagnostic of acromioclavicular abnormality. Pain or painful clicking described as inside the glenohumeral joint itself is indicative of labral abnormality. O’Brien et al. compared the physical examination findings to those identified on MRI or at surgery in 318 patients. The active compression test for labral abnormality revealed a sensitivity of 100%, a specificity of 98.5%, a positive predictive value of 100%, and a negative predictive value of 100%. For the acromioclavicular joint, the data revealed a sensitivity of 100%, a specificity of 95.2%, a positive predictive value of 91.5%, and a negative predictive value of 100%.
O’Driscoll described the dynamic labral shear test to reproduce the shearing mechanism that can cause a superior labrum tear anterior and posterior (SLAP); it is reported to yield reliable results that isolate a SLAP lesion’s causal role in symptoms and impaired function. The test is performed with the patient supine with the affected arm relaxed off the side of the examining table; the scapula is supported by the table, but the humerus is free. To test the right shoulder, the examiner flexes the right elbow 90 degrees and grasps the olecranon and distal humerus. The shoulder is passively rotated externally to its natural limit with the force of gravity alone pulling down on the forearm (approximately 90 degrees); the elbow is then dropped back into its natural limit of horizontal abduction (toward the floor), and the shoulder is passively elevated and depressed while horizontal abduction and external rotation are maintained. During elevation of the shoulder, the magnitude of horizontal abduction will vary and must be permitted to do so without constraint. The degree of external rotation also will vary throughout the arc of elevation and must be unconstrained. While the shoulder is being elevated, the examiner’s right hand is kept on the acromion to stabilize the scapula and to detect any palpable click transmitted through the bony structures ( Fig. 46.3 ). Usually the click will be felt by the left hand on the olecranon, as well as the distal humerus. After full overhead elevation, the entire motion is reversed and the arm is brought down to the side while the natural limits of shoulder external rotation and horizontal abduction are maintained. The test is considered positive if the patient’s deep pain at the posterior glenohumeral joint is reproduced by the test through an arc from approximately 90 degrees to 120 degrees; it is considered negative if it is not painful in this range or it does not reproduce the patient’s pain. The test can also be performed with the patient sitting or standing, and we have found this to be reliable in the clinical setting. Cheung and O’Driscoll reported sensitivity for diagnosis of a type II SLAP lesion of 86%, which was as good as MRI with gadolinium and better than MRI without gadolinium contrast dye. Kibler et al. found a sensitivity of 72%, specificity of 98%, accuracy of 97%, positive predictive value of 97%, and negative predictive value of 77% for detecting labral disease with this test.
This test is performed with the patient sitting with the arm in 90 degrees of abduction. The examiner holds the elbow and lateral aspect of the proximal arm, and applies a strong axial loading force ( Fig. 46.4A ). While the arm is elevated 45 degrees diagonally upward, downward and backward force is applied to the proximal arm ( Fig. 46.4B ). A sudden onset of posterior shoulder pain indicates a positive test result, regardless of accompanying posterior clunk of the humeral head. Because it is important to apply a firm axial compression force to the glenoid surface by the humeral head, having the patient sit against the back of a chair rather than on a stool provides a good countersupport of the axial loading in the involved arm.
In both a study by Kim et al. and a systematic review, the Kim test was found to have a sensitivity of 80% and specificity of 94%. When the jerk test was used in combination with the Kim test, sensitivity increased to 97%.
The jerk test is highly sensitive and specific for a posterior labral tear. It is performed with the patient sitting. While the examiner holds the scapula with one hand, the patient’s arm is abducted 90 degrees and internally rotated 90 degrees. An axial force is applied with the examiner’s other hand holding the patient’s elbow ( Fig. 46.5A ), and a simultaneous horizontal adduction force is applied ( Fig. 46.5B ). A sharp pain, with or without posterior clunk or click, suggests a positive test result.
With the patient supine, the examiner places the patient’s shoulder in 120 degrees of abduction, the elbow in 90 degrees of flexion, and the forearm in supination, and then externally rotates the shoulder ( Fig. 46.6 ). The patient then flexes his or her elbow, and any pain while the examiner resists elbow flexion is a positive test. Reported sensitivity of the biceps load II test is 90%, specificity 97%, positive-predictive value 92%, and negative-predictive value 95%.
The Gerber test is designed to identify impingement between the rotator cuff and the coracoid process ( Fig. 46. 2 E ). It is performed in a manner similar to the Hawkins-Kennedy impingement test. The arm is forward flexed 90 degrees and adducted 10 to 20 degrees across the body to bring the lesser tuberosity into contact with the coracoid. Pain with the maneuver indicates coracoid impingement.
Jobe described a combination test in 1989 to distinguish between primary impingement and secondary impingement owing to subtle anterior instability ( Fig. 46. 2 F ). With the patient supine, the arm is abducted 90 degrees and externally rotated, which produces pain from impingement. Application of a posteriorly directed force to the humeral head, relocating it in the glenoid, does not change the pain in patients with primary impingement but relieves the pain in patients with instability (subluxation) and secondary impingement, who tolerate maximal external rotation with the humeral head maintained in a reduced position. Evaluation of this test concluded that pain in the position of 90 degrees of abduction and 90 degrees of external rotation could be caused by a variety of disorders and would be diminished by a posteriorly directed force.
In 1966, Crenshaw and Kilgore described a test they attributed to Speed ( Fig. 46.2G ). The Speed test is performed by having the patient forward flex the shoulder to 90 degrees with the elbow extended and the forearm supinated. Resistance is applied to the forearm, and a positive result produces pain localized to the bicipital groove. In an arthroscopic analysis that included biceps tendinitis and superior labral anterior and posterior lesions as positive findings, Bennett found that the Speed test had a sensitivity of 90% and a specificity of 14%. The positive predictive value was 23%, and the negative predictive value was 83%. A study in 2005 showed the following values: sensitivity 38%, specificity 83%, positive predictive value 81%, and negative predictive value 43%.
Yergason described the “supination sign” in 1931 ( Fig. 46.2H ). The elbow is flexed to 90 degrees, and the forearm is pronated. The patient attempts to supinate the forearm actively against resistance applied by the examiner at the patient’s wrist. Pain localized to the bicipital groove indicates inflammation of the long head of the biceps. Yergason noted that this test may be negative with partial or complete rupture of the supraspinatus tendon.
Park et al. evaluated eight impingement tests ( Table 46.1 ) in 552 patients and determined that if the Hawkins-Kennedy sign, the painful arc sign, and the infraspinatus muscle (Jobe) test all were positive, the likelihood of a patient having an impingement syndrome of some degree was greater than 95%; if these three tests all were negative, the likelihood of impingement syndrome was less than 24%.
Test | Sensitivity (%) | Specificity (%) | Positive Predictive Value (%) | Negative Predictive Value (%) | Overall Accuracy (%) |
---|---|---|---|---|---|
Neer sign | 68 | 68.7 | 80.4 | 53.2 | 68.3 |
Hawkins-Kennedy sign | 71.5 | 66.3 | 79.7 | 55.7 | 69.7 |
Painful arc sign | 73.5 | 81.1 | 88.2 | 61.5 | 76.1 |
Supraspinatus (Jobe) muscle test | 44.1 | 89.5 | 88.4 | 46.8 | 60.2 |
Speed test | 38.3 | 83.3 | 80.5 | 42.9 | 54.4 |
Cross-body adduction test | 38.3 | 83.3 | 80.5 | 42.9 | 54.4 |
Drop-arm test | 26.9 | 88.4 | 81 | 39.7 | 48.6 |
Infraspinatus muscle test | 41.6 | 90.1 | 90.6 | 45.8 | 58.7 |
The tests described next ( Fig. 46.7 ) are designed to assess rotator cuff integrity and fall into two types: tests that determine whether a movement can be undertaken actively and tests that determine whether a passive position can be maintained (the lag signs). The main finding on physical examination of patients with full-thickness tears depends on which tendons are torn, what percentage of the tendon width is torn, and the duration for which the tendons have been torn. During an examination of a patient with pain, it may be difficult to determine if weakness is caused by the pain or to a torn tendon. Weakness with pain should be interpreted with caution and not be assumed to indicate a full-thickness tear.
In 1991, Gerber and Krushell described the lift-off test for detection of an isolated rupture of the subscapularis tendon ( Fig. 46.7A ). With the patient seated or standing, the arm is internally rotated, and the dorsum of the hand is placed against the lower back. If the patient is unable to lift the dorsum of the hand off the back, the test is positive. Electromyography has confirmed that the subscapularis muscle is maximally active with the hand in the midlumbar position and with resistance applied.
Gerber et al. described the belly press test for patients who have decreased internal rotation ( Fig. 46.7B ). In this test, the patient presses the abdomen with the flat of the hand and attempts to keep the arm in maximal internal rotation. If active internal rotation is strong, the elbow does not drop backward, meaning it remains in front of the trunk. If the strength of the subscapularis is impaired, maximal internal rotation cannot be maintained, the patient feels weakness, and the elbow drops back behind the trunk. The patient exerts pressure on the abdomen by extending the shoulder, rather than by internally rotating it. Other investigators have noted that when the subscapularis tendon is torn, patients tend to flex the wrist to press against the abdomen and are unable to hold the elbow forward.
The bear-hug test is performed with the patient’s palm of the involved side placed on the opposite shoulder with fingers extended ( Fig. 46.8A ) and the elbow positioned anterior to the body. The patient is asked to hold that position (resisted internal rotation), and the examiner tries to pull the patient’s hand from the shoulder with an external rotation force applied perpendicular to the forearm ( Fig. 46.8B ). The test is considered positive if the patient is unable to hold the hand against the shoulder or if he or she shows weakness of resisted internal rotation of more than 20% compared with the opposite side. If strength is comparable to that of the opposite side, without any pain, the test is considered negative. A painful bear-hug test without weakness is considered negative.
The external rotation stress test is intended to test the integrity of the external rotators of the shoulder, specifically the infraspinatus and the teres minor ( Fig. 46.7C ). With the patient’s arms by his or her side in neutral flexion and abduction, the shoulders are externally rotated 45 to 60 degrees. The examiner applies force against the dorsum of the hands, attempting to rotate the shoulders internally back to neutral while the patient is asked to resist. Pain and weakness suggest inflammation or tearing of the infraspinatus or the teres minor or both.
The external rotation lag sign test is designed to test the integrity of the supraspinatus and infraspinatus tendons ( Fig. 46.7D ). The patient is seated with his or her back to the examiner. The elbow is passively flexed to 90 degrees, and the shoulder is held at 20 degrees of elevation and near maximal external rotation (maximal external rotation –5 degrees to avoid elastic recoil in the shoulder) by the examiner. The patient is asked to maintain the position of external rotation actively as the examiner releases the wrist, while maintaining support of the arm at the elbow. The sign is positive when a lag, or angular drop, occurs. As with all tests, performance and interpretation are complicated by pathologic changes in the passive range of motion. The external rotation lag sign of more than 40 degrees has been shown to have a sensitivity of 100% and a specificity of 92%.
The Patte sign is used to determine the strength of the teres minor. With the patient standing, the examiner elevates the patient’s arm to 90 degrees in the scapular plane and flexes the elbow to 90 degrees ( Fig. 46.9 ). The patient is then asked to laterally rotate the shoulder. Weakness and/or pain constitutes a positive test. This sign was reported to have a sensitivity of 93% to 100% and a specificity of 72% to 93%.
The drop sign is intended to test the integrity of the infraspinatus ( Fig. 46.7E ). The patient is seated with his or her back to the examiner. The affected arm is held at 90 degrees of elevation in the scapular plane and at almost full external rotation with the elbow flexed at 90 degrees. The patient is asked to maintain this position actively as the examiner releases the wrist while supporting the elbow, which is mainly a function of the infraspinatus. The sign is positive if a lag or “drop” occurs. The drop sign has a reported sensitivity of 87% and specificity of 88%.
The internal rotation lag sign test is designed to test the integrity of the subscapularis tendon ( Fig. 46.7F ). The patient is seated with his or her back to the examiner. The affected arm is held by the examiner in almost maximal internal rotation. The elbow is flexed to 90 degrees, and the shoulder is held at 20 degrees of elevation and 20 degrees of extension. The dorsum of the hand is passively lifted away from the lumbar region until almost full internal rotation is reached. The patient is asked to maintain this position actively as the examiner releases the wrist while maintaining support at the elbow. The sign is positive when a lag occurs.
Plain radiographs should be obtained for initial evaluation of a patient with shoulder pain. The radiographs should be made in two planes, preferably at right angles to each other, and should include an anteroposterior view, axillary lateral view, and supraspinatus outlet view. Anteroposterior radiographs can be made with the shoulder in neutral, internal rotation, or external rotation with advantages to each view. The internal rotation view is useful for detecting Hill-Sachs lesions, and the external rotation view provides a good view of the greater tuberosity and proximal humeral physis in skeletally immature patients. A true anteroposterior radiograph of the glenohumeral joint (also known as the Grashey view) provides the best evaluation of the articular cartilage of the glenoid and the humeral head. The axillary lateral view has the advantage of showing the anatomy of the glenoid rim, the acromion, the coracoid, and the proximal humerus. An outlet view assists in the evaluation of patients with rotator cuff disease. This view is a lateral view of the scapula with the tube angled 10 degrees caudad. On this radiograph, the acromion can be classified into one of three types (flat, curved, or hooked). An association between a hooked acromion and rotator cuff disease has been shown, but the causal relationship between the two has not been established. This classification of the acromion also is subject to poor agreement between observers, and slight changes in how the radiographs are made may alter the classification of the acromial shape. Radiographs may reveal exostoses, greater tuberosity cysts or sclerosis, and subacromial sclerosis (sourcil sign), which indicate chronic cuff tears. Calcific deposits to the rotator cuff are consistent with calcific tendinitis. In addition, superior migration of the humeral head with narrowing of the acromiohumeral space to less than 7 mm suggests a rotator cuff tear, and a space less than 5 mm suggests a massive tear. A Stryker notch view is helpful to evaluate for Hill-Sachs lesions, and a West Point view is used to evaluate bony Bankart lesions.
Further imaging can assist with the diagnosis. Traditionally, an arthrogram has been used to document full-thickness rotator cuff tears. Leakage of contrast material into the subacromial and subdeltoid spaces after injection into the glenohumeral joint indicates a full-thickness tear. Tendinopathy or even partial-thickness tears are difficult, however, if not impossible, to diagnose with an arthrogram. The arthrogram does not provide any additional information, such as the size of the tear or the condition of the rotator cuff muscles. Arthrography is still useful for patients in whom MRI is contraindicated, such as patients with a pacemaker, cerebral aneurysm clip, intraocular metal, or recent cardiac stents. Arthrography can be combined with MRI to improve the diagnostic accuracy when evaluating rotator cuff repairs for failure or retears in which it is difficult to differentiate scar tissue from tendon, as well as for evaluation of entities such as labral tears, Bankart and reverse-Bankart lesions, and SLAP lesions, when additional information is needed for treatment decision-making.
MRI is currently the most commonly used test for evaluation of a rotator cuff pathologic process. It is highly accurate and shows detailed anatomic information, including the size of rotator cuff tears and the status of the rotator cuff muscles. In addition, partial tears and tendinopathy are well visualized by MRI. A patient with symptoms of subacromial impingement may show increased signal in the infraspinatus tendon on T2-weighted MRI consistent with tendinopathy; increased fluid in the subacromial bursa also is a sign of subacromial impingement. MR images typically are made in several orientations, including coronal oblique, sagittal oblique, and axial. Coronal oblique MR images assist in evaluating the supraspinatus tendon and muscle, delineating the extent of retraction and the size and quality of the supraspinatus muscle. Fatty replacement of the supraspinatus muscle and the supraspinatus fossa indicates chronic pathology. The size of the supraspinatus tear in the anterior and posterior direction can be determined by noting the tear on sequential images. The sagittal oblique images show the anterior and posterior extent of supraspinatus tearing and the quality of all of the rotator cuff muscles. Axial images are used to show the condition of the biceps tendon and of the subscapularis and infraspinatus tendons and muscles. One potential disadvantage of MRI is the significant potential for false-positive findings. Consequently, MRI findings should always be correlated with clinical findings. Another potential problem with MRI is overuse; specific indications rarely have been discussed. Patients with an insidious onset of shoulder pain and dysfunction do not require MRI evaluation until appropriate nonoperative treatment has failed. Patients for whom surgery is not a consideration do not need MRI unless there are concerns about another pathologic entity, such as an infection or neoplasm.
Ultrasound scanning has been reported to have a sensitivity of 58% to 100%, a specificity of 85% to 100%, and an overall accuracy of 80% to 94% in the detection of rotator cuff tears. In a comparison of MRI and ultrasound assessment of rotator cuff healing in 61 patients, ultrasound had 80% sensitivity and 98% specificity using MRI as the reference. A Cochrane Database Review concluded that MRI, MR arthrography, and ultrasound all have good diagnostic accuracy, and any could be used equally for detection of full-thickness tears in patients with shoulder pain for whom surgery is being considered, especially those with full-thickness tears; however, both MRI and ultrasound appear to have poor sensitivity for detecting partial-thickness tears. Advantages of ultrasonography over other imaging methods are that it is rapid, noninvasive, and inexpensive; a disadvantage is that the accuracy of ultrasound evaluation is highly dependent on the experience of the ultrasonographer and on the quality of the equipment used. Dynamic ultrasound also can be useful in confirming shoulder impingement syndrome, assessing glenohumeral laxity, and identifying biceps tendon pathology.
Current understanding of impingement syndrome has evolved considerably since Jarjavay’s first description of subacromial bursitis in 1867. Codman, in 1931, was the first to note that many patients with inability to abduct the arm had incomplete or complete ruptures of the supraspinatus tendon, rather than primary bursal problems. In 1972, Neer described impingement syndrome characterized by a ridge of proliferative spurs and excrescences on the undersurface of the anterior process of the acromion, apparently caused by repeated impingement of the rotator cuff and the humeral head with traction of the coracoacromial ligament. Neer also noted that the anterior third of the acromion and its anterior lip seemed to be the offending structure in most cases. He introduced the concept of a continuum of impingement syndrome ( Box 46.1 ). The supraspinatus insertion into the greater tuberosity that passes beneath the coracoacromial arch during forward flexion of the shoulder is susceptible to impingement ( Fig. 46.10 ). Neer also described the temporary relief of pain with subacromial injection of lidocaine as a diagnostic test, now known as the impingement test , which is helpful in differentiating purely impingement-type symptoms from other pathologic processes.
Typical age of patient: <25 years old
Differential diagnosis: subluxation, acromioclavicular joint arthritis
Clinical course: reversible
Treatment: conservative
Typical age of patient: 25-40 years old
Differential diagnosis: frozen shoulder, calcium deposits
Clinical course: recurrent pain with activity
Treatment: consider bursectomy or division of coracoacromial ligament
Typical age of patient: >40 years old
Differential diagnosis: cervical radiculitis, neoplasm
Clinical course: progressive disability
Treatment: anterior acromioplasty, rotator cuff repair
The natural history of impingement syndrome remains unclear. In a group of 63 patients with subacromial impingement without rotator cuff tears who were evaluated 8 years after diagnosis, 44% had a relapsing course with asymptomatic periods between recurrences, 25% had no recurrences, and 30% had a chronic course. Of those with a chronic course, 37% eventually required surgery. Younger age, lower body mass index (BMI), more functional capacity, shorter symptomatic period, reversible changes on MRI, and higher Constant and American Shoulder and Elbow Surgeons (ASES) Standardized Shoulder Assessment scores at the first evaluation were good prognostic factors.
Since Neer’s original description, the concept of impingement syndrome has evolved to encompass four types of impingement: (1) primary impingement, (2) secondary impingement, (3) subcoracoid impingement, and (4) internal impingement. Primary impingement is subcategorized further into intrinsic and extrinsic types. Primary impingement is the classic version and occurs without any other contributing pathology. Secondary impingement occurs when there is instability of the glenohumeral joint allowing translation of the humeral head, typically anteriorly, resulting in contact of the rotator cuff against the coracoacromial arch. When the structures passing beneath the coracoacromial arch become enlarged resulting in abutment against the arch, the cause of the impingement is considered to be intrinsic. Examples of this condition include thickening of the rotator cuff, calcium deposits within the rotator cuff, and thickening of the subacromial bursa. Extrinsic impingement occurs when the space available for the rotator cuff is diminished; examples include subacromial spurring, acromial fracture or pathologic os acromiale, osteophytes off the undersurface of the acromioclavicular joint, and exostoses at the greater tuberosity.
Acromial morphology has been implicated as contributing to impingement. Bigliani, Morrison, and April described three types of acromion morphology ( Fig. 46.11 ) and noted an increase in rotator cuff tears with type III, or hooked, acromions. In a cadaver study of 140 shoulders, one third had full-thickness tears of the rotator cuff, 73% of which were in shoulders with type III acromions. A more recent comparison of patients with full-thickness supraspinatus tendon tears or subacromial impingement to a control group found that a low lateral acromial angle and a large lateral extension of the acromion were associated with a higher occurrence of impingement and rotator cuff tears. An extremely hooked anterior acromion with a slope of more than 43 degrees and a lateral acromial angle of less than 70 degrees occurred only in patients with rotator cuff tears. Patients with less slope to their acromion have been reported to have a propensity toward impingement because of subacromial stenosis. A cadaver study showed significantly lower angles in shoulders with rotator cuff tears than in shoulders with intact cuffs. A study investigating the association between kyphosis, subacromial impingement syndrome, and a reduction in shoulder elevation found a significant association between impingement and reduced shoulder elevation. The authors suggested that kyphosis might influence the development of impingement indirectly by reducing shoulder elevation because of restriction of thoracic spine extension and scapular dyskinesis. Based on these observations, the recommended treatment for impingement syndrome has been anterior acromioplasty to remove the offending structure.
Recently, numerous calculations of distances, angles, and slopes about the shoulder have been described that are based on measurements on radiographs and MRIs. These are attempts to provide objective support for the clinical diagnosis of impingement syndrome and to predict the presence or risk of development of a rotator cuff tear. Most measurements require precise shoulder positioning to be accurate and clinically helpful. The efficacy of these measurements has not been proven. Sasiponganan et al. correlated radiographic measurements of acromial index, lateral acromion angle, subacromial space on AP and Y-views, acromial anterior and lateral downsloping, and MRI findings of rotator cuff pathology. Studying 140 MRIs in 137 women, they concluded that subacromial impingement anatomy characteristics have no significant associations with supraspinatus or infraspinatus tears in symptomatic women. Balke et al. studied 136 patients with arthroscopic rotator cuff repair to determine if acromial morphology in degenerative supraspinatus tendon tears differs from that with traumatic tears. On preoperative radiographs, they evaluated Bigliani type, acromial slope, acromiohumeral distance, lateral acromial angle, acromion index, and critical shoulder angle ( Fig. 46.12 ). They found that shoulders with degenerative tears had a narrower subacromial space, a larger lateral extension, and a steeper angulation of the acromion than traumatic tears.
Gumina et al. presented an intriguing study attempting to determine the relative role of genetics or external forces in determining the subacromial space width. They studied 29 pairs of twins, both monozygotic and dizygotic, and measured the acromiohumeral space on MRI scans. The intraclass correlation coefficient was substantially higher for monozygotic than for dizygotic twins, indicating a high degree of concordance of the acromiohumeral distance in pairs of individuals who shared 100% of their genes. There were no differences among subjects in different job categories. They concluded that the acromiohumeral distance is mainly genetically determined and only marginally influenced by external factors.
Other investigators have suggested that the shape of the acromion and the coracoacromial ligament are not the primary problems, but rather that intrinsic rotator cuff degeneration is the primary cause with subacromial changes occurring secondarily. Senescence of the tendon fibroblasts with resulting disruption of the tendon architecture is a common finding in the rotator cuff with aging. Age-related degenerative changes, including decreased cellularity, fascicular thinning and disruption, accumulation of granulation tissue, and dystrophic calcification, all have been noted and are likely irreversible. A zone of relative hypovascularity also is present on the articular surface of the rotator cuff. Differential shear stress within the tendon layers also has been cited as a cause of the disruption of the tendon fibers. Others have suggested that the rotator cuff tendons may fail in tension as a result of throwing a baseball or other overhead sports. Intrinsic degeneration leads to loss of the force couples, causing superior humeral head translation and impingement. As support for their theory of impingement as a secondary phenomenon, these authors cited the improvement of symptoms after rehabilitation (capsular stretching and rotator cuff strengthening). They recommended minimal or no acromioplasty at the time of surgery for rotator cuff repair and repair of the coracoacromial ligament rather than excision. Several systematic reviews and meta-analyses have failed to find differences in pain, function, and time to recovery between patients treated nonoperatively and those treated with acromioplasty. In addition, excision of the ligament is losing favor because of the potential for anterior and superior subluxation of the humeral head from underneath the acromion (anterior-superior escape) when the rotator cuff tear is irreparable or the repair fails and the ligament restraint is gone. A study of practice patterns in rotator cuff repair identified a trend toward increased arthroscopic rotator cuff repair without subacromial decompression and a decrease in isolated subacromial decompression.
In their study to identify shoulder motions that cause subacromial impingement, Park et al. measured the vertical displacement and peak strain of the coracoacromial ligament. They found that forward flexion, horizontal abduction, and internal rotation with the arm at 90 degrees of abduction showed higher vertical displacement and peak strain of the coracoacromial ligament, causing subacromial impingement. They recommended that patients with impingement syndrome or a repaired rotator cuff avoid these shoulder motions.
In 1909, Goldthwait first described pain in the shoulder caused by contact between the rotator cuff and the coracoid process. Gerber et al. suggested that this painful contact might be caused by a prominent coracoid, for which there may be numerous reasons, including idiopathic and iatrogenic conditions. The iatrogenic form was most common in their series, and it was found in patients who had undergone a Trillat osteotomy of the coracoid for the treatment of anterior instability. In their series of 475 patients with rotator cuff tears, Park et al. identified subcoracoid impingement in 13%; of 110 with subscapularis tears, 56% had subcoracoid impingement. Among patients with subacromial impingement but no rotator cuff tears, 41% had subcoracoid impingement. This entity has not been studied extensively, and it remains a diagnosis of exclusion.
Physical findings attributed to this condition include tenderness over the coracoid and a positive coracoid impingement test (see Fig. 46.2E ). An injection of lidocaine into the subcoracoid region similar to the Neer impingement test (see Fig. 46.2A ) has been used to evaluate patients for coracoid impingement. Relief of pain suggests the diagnosis, but the proximity of multiple structures in the subcoracoid region, including the glenohumeral joint itself, makes the accuracy of these injections questionable. CT has been used in the diagnosis of coracoid impingement; a suggested distance of 6.8 mm between the coracoid tip and the closest portion of the proximal humerus indicates impingement. For suspected impingement, open or arthroscopic coracoplasty has been recommended. A comparison of outcomes between patients with arthroscopic coracoplasty and those without found a significant increase in internal rotation in the treated group, especially in those with large to massive rotator cuff tears. We have no experience with this procedure.
In this condition, internal contact of the rotator cuff occurs with the posterosuperior aspect of the glenoid when the arm is abducted, extended, and externally rotated as in the cocked position of the throwing motion. This contact probably is a normal phenomenon but becomes pathologic in certain patients. It often occurs in throwers who have lost internal rotation of the shoulder. This loss causes the center of rotation of the humeral head to move upward so that the contact between the rotator cuff and the biceps tendon attachments increases. Several cadaver studies have attempted to identify factors related to the development of internal impingement. One such study determined that increased capsular laxity significantly increased horizontal abduction and contact pressure in the glenohumeral joint, resulting in impingement of the supraspinatus and infraspinatus tendons and posterosuperior labrum between the greater tuberosity and glenoid. In contrast, another cadaver study found that excessive posteroinferior capsular tightness caused forceful internal impingement of the shoulder at maximal external rotation, whereas another identified increased internal scapular rotation and decreased upward scapular rotation as significantly increasing glenohumeral contact pressure and the area of impingement of the rotator cuff. Arthroscopic findings include partial rotator cuff tears, posterior and superior labral tears, and anterior shoulder laxity. Early in the course of the condition, aggressive physical therapy with attention to regaining internal rotation and rotator cuff strengthening is often successful. Arthroscopic management of this problem is discussed in Chapter 52 .
The initial treatment of a patient with tendinopathy caused by classic primary extrinsic impingement is a well-planned and well-executed nonoperative regimen, including anti-inflammatory medications and one or at most two subacromial cortisone injections. Hyaluronic acid injections have been suggested to improve results, but a comparison of hyaluronic acid injections (51 patients) with corticosteroid (53 patients) or placebo injections (55 patients) found no benefit from hyaluronic acid injections; corticosteroid injections produced a significant reduction in pain in the short term (3 to 12 weeks), but in the long term the placebo injection produced the best results. Platelet-rich plasma (PRP) has been offered as a treatment for subacromial impingement, but a single-blinded randomized controlled trial comparing PRP to exercise therapy found that both were effective in reducing pain and disability. Medical treatment is followed by a physical therapy program focusing on stretching for full shoulder motion and strengthening the rotator cuff. A scapular motor control retraining protocol was reported to be successful in relieving symptoms in young patients. If the patient fails to respond after 3 to 4 months of conservative therapy, operative intervention may be indicated and should be directed to the specific lesion. Significantly greater improvements in Constant scores have been reported for patients with a positive Hawkins-Kennedy sign in the neutral position, and positive Neer and Jobe tests compared with those with negative signs. Patients with four positive tests out of the five studied (Neer, Hawkins-Kennedy in neutral and in abduction, Jobe empty can, and painful arc) had greater improvement than those with three or fewer positive test results.
Arthroscopic or open acromioplasty when indicated is the surgical treatment of choice for external impingement syndrome. The reported results of open anterior acromioplasty vary widely. In more than 20 large series of open acromioplasties, the overall success rate was approximately 85%. Failures were related to incorrect diagnosis, technical inadequacy, and other complications. For acromioplasty to be successful, impingement must be the cause of the pain and a thorough history and physical examination are necessary. Acromioclavicular arthritis, glenohumeral arthritis, subtle shoulder instability in throwing athletes, early adhesive capsulitis, and fibromyalgia all can present diagnostic dilemmas. Cervical spondylosis with nerve root irritation and suprascapular nerve injury also can mimic the symptoms associated with an impingement syndrome.
Recently, studies have questioned the superiority of acromioplasty over physical rehabilitation. Ketola et al. randomized 140 patients into a structured exercise program or an arthroscopic acromioplasty group that also did the therapy postoperatively. At follow-up, there were no statistically significant differences in either the amount of perforating ruptures of the supraspinatus tendon or in the changes in muscle volume at 5 years. Kolk et al. in a double-blind randomized clinical trial compared arthroscopic bursectomy alone with bursectomy combined with acromioplasty. Forty-three patients were examined at a median of 12 years postoperatively. Based on Constant score, Simple Shoulder test score, visual analog scale (VAS) pain score, and VAS shoulder function score, there were no relevant additional effects of arthroscopic acromioplasty on bursectomy alone with respect to clinical outcomes or rotator cuff integrity at 12 years follow-up. Paavola et al. compared arthroscopic acromioplasty, diagnostic arthroscopy, and physical therapy. There were no differences between acromioplasty and diagnostic arthroscopy at 2 years, and the differences between acromioplasty and therapy did not reach a minimum clinically important difference.
Technical inadequacy has been implicated as a cause of failed acromioplasties. Adequate bone must be removed to alleviate outlet stenosis. Inadequate bone removal seems to occur more often in arthroscopic than open acromioplasties. In addition to the anterior lip, the portion of the acromion anterior to the anterior clavicular border must be removed to obtain optimal results. Original technical descriptions called for resecting and removing a portion of the coracoacromial ligament to prevent the cut edge from scarring back to the acromion. Our current practice is to release the ligament. We believe that the ligament can be part of the pathologic process and anticipate that it would heal back to the acromion, restoring the coracoacromial arch and preventing anterosuperior subluxation of the humeral head.
We use arthroscopic and occasionally open techniques. We believe that either open or arthroscopic acromioplasty is satisfactory if the main principles of the original procedure as described by Neer are kept in mind, as follows:
Release (but not resection) of the coracoacromial ligament
Removal of the anterior lip and lateral edge of the acromion
Removal of part of the acromion anterior to the anterior border of the clavicle
Removal of the distal 1 to 1.5 cm of clavicle if significant degenerative changes are found
Place the patient in a semi-upright position with the head elevated 30 to 35 degrees (beach chair position). Place a towel or an intravenous bag medial to the scapula to stabilize it. This degree of head elevation usually places the superior acromial surface perpendicular to the floor, allowing the acromial osteotomy to be made perpendicular to the floor. Drape the arm free to permit shoulder rotation.
Outline the bony contour of the shoulder, including the lateral acromial border, coracoid, and acromioclavicular joint.
Outline the proposed skin incision along the Langer line 4 to 6 cm long and infiltrate it with 10 mL of 1:500,000 epinephrine to minimize bleeding.
Make the incision from lateral to the anterior acromion toward the coracoid and just lateral to it ( Fig. 46.13 ).
After mobilization of the subcutaneous tissue, identify the raphe between the anterior and middle deltoid and split it from a point 5 cm or less distal to the acromial border (to avoid axillary nerve injury) toward the anterolateral acromion ( Fig. 46.14A ).
The deltoid can be left attached or can be detached from the corner of the acromion, depending on the surgeon’s preference. We prefer to leave the deltoid attached initially, detaching it later if the procedure warrants.
To use this approach, elevate a flap of deltoid with its periosteal attachment and the periosteal attachment of the trapezius approximately 2 cm onto the superior acromial surface ( Fig. 46.14B ).
Carry this medially as far as the acromioclavicular joint (the anterior capsule of which usually is included in the flap) and 1 cm along the lateral acromion. Occasionally, these periosteal attachments are tenuous after elevation, and the deltoid must be detached, to be secured later to the acromion through drill holes. We have found that using electrocautery with a Bovie needle for elevation usually ensures thicker flaps.
The importance of correct deltoid detachment cannot be overemphasized. A secure cuff of tissue must be maintained for later defect closure or reattachment to the acromion. Without secure deltoid attachment, the results of the acromioplasty would be compromised by lack of deltoid function.
After completing the anterior limb of the elevation, resect the coracoacromial ligament. We use the electrocautery for this as well because the acromial branch of the coracoacromial artery is contained within the ligament, and electrocautery allows exposure of the entire subacromial space.
With the subacromial space exposed, resect the bursa along with all adhesions and soft-tissue coverage from the acromial undersurface. The bursa can be quite thick and easily mistaken for the rotator cuff tendon. The bursa can be identified by its continuity with the acromial undersurface and its unilaminar appearance, as opposed to the multilaminar appearance of the rotator cuff. Clark and Harryman showed five distinct layers with multiple interdigitations in the cuff tendons.
After bursal resection, use an oscillating saw or rongeur to remove the portion of the acromion that projects anterior to the anterior border of the clavicle ( Fig. 46.14C ). This removes a portion of the offending acromial hook and squares off the surface, allowing easier completion of the acromioplasty with an oscillating saw or an osteotome. We prefer an oscillating saw for this portion of the procedure because it affords more control than an osteotome, which may propagate a fracture line into the posterior acromion.
Begin the osteotomy at the anterosuperior aspect of the acromion and continue it through the junction of the anterior and middle thirds of the acromion, including the entire anterior acromion from medial to lateral.
Use a curved, blunt Hohmann or malleable retractor to depress the humeral head and protect the cuff during this portion of the procedure.
Smooth out any rough surfaces with a rasp.
Palpate the acromioclavicular joint undersurface and remove any bony spurs.
If severe degenerative changes are present, resect the distal 1.0 to 1.5 cm of the lateral clavicle. Preoperative radiographs and symptoms should indicate the necessity of this additional procedure, and it should not be done routinely.
If the clavicle is resected, leave the superior acromioclavicular capsule intact to make deltoid repair in this area easier. Do not extend the clavicular cut beyond 1.5 cm to avoid violating the coracoclavicular ligaments and making the distal clavicle unstable.
Carefully inspect the entire rotator cuff for tears before closure. The area just proximal to the supraspinatus insertion is the most common site for tears. Palpate this area for thinning, which may indicate a partial-thickness tear on the articular side.
If preoperative studies show extreme degeneration without fresh tearing, resection of the diseased tendon and direct repair or suturing to a trough in bone should be considered (see Technique 46.2).
Internally and externally rotate the shoulder to allow inspection of the entire bursal surface of the cuff.
Copiously irrigate the area to remove all debris from the subacromial space.
Suture the deltoid periosteum from side to side or, if necessary, through drill holes into the acromion with nonabsorbable sutures, ensuring that the reattachment is secure. The repair of the deltoid to the acromion through drill holes has become our preferred method of repair.
Close the wound in layers in routine fashion.
The arm is supported by a sling. Pendulum exercises are started the day after surgery. Passive abduction and internal and external rotation exercises are started at the end of 1 week. At 3 weeks, active exercises are begun. The sling is discarded as soon as the patient feels comfortable.
Complications after acromioplasty include, but are not limited to, infection, seroma formation, hematoma, synovial fistula, biceps rupture, pulmonary embolus, acromial fracture, and complex regional pain syndrome. Poor patient motivation, poor rehabilitation compliance, or a poorly designed rehabilitation program also can lead to failure because of continued pain and stiffness. Bouchard et al. cited co-planing and workers’ compensation claims as poor prognostic indicators.
Without question, the worst common complication is loss of anterior deltoid function, which is caused by either axillary nerve injury or detachment of the deltoid from the acromion. Loss of anterior deltoid function produces a poor outcome despite technically adequate bone work and ligament resection. Very little can be done to restore function to a detached, retracted deltoid. Because deltoid detachment, retraction, and scarring are much more common after the “deltoid on” approach, we recommend suturing to the acromion with heavy sutures whenever tissue is unavailable for direct side-to-side repair.
Although some patients present with a sudden onset of symptoms following an acute shoulder injury, most patients with a pathologic condition of the rotator cuff have insidious onset of progressive pain and weakness, with concomitant loss of active motion. Pain usually is present at night and may be referred to the area of the deltoid insertion. Passive motion initially remains full until pain limits active motion enough to cause development of adhesive capsulitis. Most patients cannot recall a specific traumatic incident referable to the onset of problems. Treatment recommendations are based on the patient’s age, symptoms, and activity demands, and the natural history of rotator cuff tears.
The natural history of rotator cuff tears is not always predictable. On the one hand, many patients with full-thickness rotator cuff tears are asymptomatic or respond well to nonoperative treatment. On the other hand, studies indicate that some previously asymptomatic tears become symptomatic and some tears progress in size and become irreparable. Rotator cuff pathology is a common problem, and cadaver anatomic studies have reported rotator cuff tears in 30% to 50% of specimens, suggesting that they may be part of the normal aging process.
Full-thickness rotator cuff tears are compatible with normal function. In 1962, McLaughlin advanced five reasons to avoid early repair of the average rupture: (1) at least 25% of cadaver shoulders had a torn or degenerated cuff; (2) 50% of patients recovered spontaneously; (3) immediate repair had no advantages because rupture always occurred in diseased tendon; (4) results of early and late repair were the same; and (5) early diagnosis was difficult. Resolution of symptoms has been reported in 33% to 90% of patients treated nonoperatively, and we recommend nonoperative treatment initially for elderly patients or patients with low activity with suspected rotator cuff tears. Patients without pain or limitation of activities of daily living also should be treated nonoperatively. When the decision to treat nonoperatively is made, treatment should be instituted promptly and aggressively. The duration of symptoms seems to correlate inversely with the long-term success of nonoperative management because patients with symptoms for longer than 6 months had poorer outcomes.
The natural history of rotator cuff tears is not always predictable. When counseling a patient with a rotator cuff tear, the surgeon must remember that some asymptomatic tears become symptomatic and some tears do progress in size. A study of patients with bilateral rotator cuff tears found that, although all patients were asymptomatic on one side at presentation, at follow-up more than half had developed symptoms in the previously asymptomatic side. Medium-size tears have been shown to be at high risk of progression, whereas partial tears or small full-thickness tears appear to have little risk of early development of irreparable damage . The presence of rotator cuff disease has been shown to correlate with age; after the age of 66 years, there is a 50% likelihood of bilateral tears. Duration of symptoms also has been correlated with severity of rotator cuff disease: the longer the symptoms, the more extensive the fatty degeneration of the torn rotator cuff muscle. A retrospective review of 1688 patients with rotator cuff tears determined that moderate supraspinatus fatty infiltration appeared an average of 3 years after the onset of symptoms and that severe fatty infiltration appeared at an average of 5 years after the onset of symptoms. In an ultrasound study of 105 rotator cuff repairs, patients with intact repairs of large tears had outcomes that were equal to those in patients with small tears. As the size of the recurrent defect increased, the strength, motion, and function decreased. A more recent study confirmed these results in a group of patients aged 65 years or older: those with healed tears after surgery had function comparable to patients of a similar age without tears and better than that of patients with untreated tears. These findings indicate that early operative intervention, when most tears are small and less degeneration of the muscle has occurred, improves outcomes.
Loss of continuity of the rotator cuff can be described in several ways, including acute and chronic , partial or full thickness , and traumatic or degenerative. It is important to differentiate between the different types to plan appropriate treatment. Full-thickness rotator cuff tears also are classified based on their size ( Box 46.2 ). The most common size classification (Cofield) is based on the largest dimension of the tear. Tears also can be classified according to the number of tendons involved. In addition, the extent of tendon retraction and tissue quality are important features not generally accounted for by classification schemes. Chronic tears can be classified based on the percentage of fatty infiltration of the muscle belly as seen on MRI or CT. Goutallier et al. proposed five stages of fatty degeneration. The presence and degree of fatty infiltration and atrophy of the muscle affect the success of the repair. Partial-thickness tears have been described by location, grade, and tear area (in mm 2 ). We have found it easier to classify partial tendon tears as involving less or more than 50% of the depth of the tendon and base treatment on this distinction.
Small tear: <1 cm
Medium tear: 1 to <3 cm
Large tear: 3 to <5 cm
Massive tear: ≥5 cm
Partial-thickness tears may be articular-sided, bursal-sided, or intratendinous. The true incidence of partial-thickness tears is unknown. Most of the information is from cadaver studies, which reflect an older population; the true incidence in young overhead-throwing athletes is unknown. Among partial-thickness tears, cadaver studies indicate that intratendinous tears are more common than articular-sided or bursal-sided tears, whereas a clinical study found that articular-sided tears constituted 91% of all partial-thickness tears in a population of young athletes. This discrepancy between cadaver and clinical studies may result because intratendinous tears are more difficult to diagnose with arthroscopy, MRI, or ultrasound than are bursal-sided or articular-sided tears. The true prevalence of partial-thickness tears is likely to be greater than that currently documented in the literature. In a systematic review of the literature, Lazarides et al. determined that among young patients with rotator cuff tears, most had full-thickness traumatic tears, but in a subgroup of elite throwers, most tears were partial-thickness tears resulting from chronic overuse.
The natural history of partial-thickness tears is not fully known. Imaging and clinical studies have suggested that partial-thickness tears progress in as many as 80% of patients.
For partial-thickness rotator cuff tears, a nonoperative program that includes activity modification, stretching and strengthening exercises, and antiinflammatory medication is appropriate as initial treatment. Operative management is indicated if conservative management fails. Arthroscopic evaluation is required to determine the extent of the lesion, and subacromial decompression is indicated when outlet impingement is present. The causes of the tear should be treated at the time of surgery. Debridement or repair of partial-thickness rotator cuff tears depends on the degree of the tear and the activity level and age of the patient. We currently perform arthroscopic debridement of partial-thickness tears when they are found on inspection during arthroscopic acromioplasty. If a lesion involves less than 50% of cuff thickness, acromioplasty and debridement are sufficient treatment. If a tear is longer or thicker, elliptical excision of the diseased tendon and repair are indicated. Good results have been reported with arthroscopic repair of bursal-side partial-thickness tears.
The results of nonoperative treatment of partial-thickness tears are unknown because no long-term follow-up studies using a standardized treatment protocol on a well-defined uniform patient population exist in the literature. Excellent and good results after arthroscopic debridement have been reported in from 80% to 90% of patients, with improvements in pain, function, active forward flexion, and strength. Studies also have shown no significant difference in outcome between patients with full-thickness and patients with partial-thickness tears or between patients with partial-thickness tears less than 50% of tendon thickness and patients without any tears.
The primary goal of operative management of rotator cuff tears is pain relief, and this is accomplished with predictable results. Improvement of function is a secondary but important consideration. Functional improvement is not as predictable as pain relief and depends on the age of the patient, the age and size of the tear (which suggests the quality of the tissue and the condition of the muscle), and the postoperative rehabilitation program. In elderly patients or patients with low activity, we attempt a course of conservative treatment (8 to 12 weeks). If there is a positive response, the nonoperative approach may be continued, but if there is no improvement, we proceed to surgery to minimize the atrophy of the rotator cuff musculature. Surgery is appropriate for an acute rotator cuff injury in a young patient or in an older patient (60 to 70 years old) with a defined injury who suddenly is unable to rotate the arm externally against resistance. In our experience, these patients usually have an excellent return of strength and function. Surgery is contraindicated in patients with rotator cuff tears and concomitant stiffness (secondary to adhesive capsulitis). Any significant preoperative stiffness must be corrected before rotator cuff repair to avoid severe postoperative stiffness. It is imperative that nearly full motion be regained before surgical intervention to prevent severe postoperative stiffness.
The clinical results of rotator cuff repair in symptomatic patients who have been followed for 10 years are good to excellent in a high percentage of cases, even though rerupture of the cuff occurs in 20% to 65%. In four large series (Hawkins et al., Neer et al., Ellman et al., and Cofield et al.) that included 476 patients, success rates ranged from 78% to 86%, with excellent or good results reported in 383 (80%) of the 476 patients. In a review of several series of rotator cuff repairs, overall pain relief was obtained in 87% of patients, with a 77% patient satisfaction rate. Most repair failures have been found to occur within the first 2 years after surgery; if the repair survives this initial period, its 10-year survival is likely. Our results with rotator cuff repair are similar, achieving pain control and return of function in approximately 80% of patients. Outcomes of repair generally are better in patients younger than 60 years of age, although clinical results often are good despite poor imaging results. Factors consistently found to be associated with failed repair include age of 65 years or older, large and massive tears (>3 cm), moderate to severe muscle atrophy, more than 50% fatty infiltration of the involved cuff, tear retraction of more than 2.5 cm, and diabetes. Some newer studies, however, have challenged these traditional risk factors. In a comparison of 40 patients older than 70 years and 40 patients younger than 50 years, Moraiti et al. found that functional gain was similar, even though healing was more frequent in younger patients. Although increasing age may predict a diminished healing environment, many studies have demonstrated excellent outcomes in older patients. Chung et al. reported that tendinosis severity assessed by preoperative MRI was the only factor associated with failure to heal in their 55 patients (mean age, 58 years), and Inderhaug et al. identified preoperative use of NSAIDs, long-standing symptoms before surgery, and nonacute onset of symptoms as predictors of inferior long-term outcomes in 147 patients. Other studies have noted that preoperative range of motion, obesity, fatty infiltration, or cuff retraction were not supported as prognostic factors for quality of life after arthroscopic rotator cuff repair. These conflicting reports emphasize the importance of careful preoperative evaluation and specific treatment plans tailored for the individual patient.
Several investigators have compared the results of decompression alone with repair and found much better results with repair. Satisfactory outcomes after decompression have ranged from 8% to 59%, and results have been reported to deteriorate over time. Most rotator cuff tears are now approached arthroscopically. The tear and size can be confirmed, and other intraarticular pathology can be treated. A decision can be made to treat the tear arthroscopically, or arthroscopically assisted (mini-open), or to convert to an open procedure. We currently believe that arthroscopic-assisted or arthroscopic repair is appropriate for partial-thickness and small to medium and some large full-thickness rotator cuff tears. Proposed advantages of arthroscopic repair include access for glenohumeral inspection and treatment of intraarticular lesions, no deltoid detachment, less soft-tissue dissection, and smaller incisions. Arthroscopic techniques can reliably assess rotator cuff tear size, tendon quality, tendon mobility, and suture anchor placement. A recent meta-analysis of randomized controlled trials comparing arthroscopic to mini-open repairs found no differences in surgery time, functional outcome scores, VAS pain scores, or functional outcomes. For the arthroscopic repair technique, see Chapter 52 .
An arthroscopic-plus-open technique has been described for combined tears of the subscapularis, supraspinatus, and infraspinatus tendons. Repair of the posterosuperior rotator cuff is done arthroscopically, followed by open repair of the subscapularis tendon. Cited advantages of this method include an ability to treat concomitant pathology, relative ease of repair, and creation of a strong, reliable construct.
Open rotator cuff repairs also can be done through a miniarthrotomy deltoid-splitting approach (see Technique 1.95.
Perform an anterior acromioplasty as described in Technique 46.1. This is an important part of rotator cuff surgery, and the results of repair without decompression are not as good as the results using the combined procedure.
After standard acromioplasty, evaluate the rotator cuff tear carefully.
Perform a subacromial bursectomy. Protect the biceps tendon unless biceps pathology is present; if so, a proximal biceps tendon release or tenodesis (see Technique 52.10) is indicated.
Tears usually begin at the supraspinatus insertion, and the end retracts into its fossa under the acromioclavicular joint. Most tears not only are transverse but also have a longitudinal component, making them oval or triangular. All but the smallest tears need to be advanced anteriorly and laterally, not just laterally, to restore anatomic position and correct muscle-tendon unit length. In tears of more than 2 to 3 cm, the infraspinatus tendon is involved as well.
When the defect has been identified and its size approximated, attention is turned to the repair itself. Typically some degree of mobilization is necessary.
Begin mobilization posteriorly with the infraspinatus, using a blunt probe or a finger to release adhesions inside and outside the joint ( Fig. 46.15A and B ). Do not dissect below the level of the teres minor to avoid injury to the axillary nerve in the quadrangular space or the suprascapular nerve in the area of the spinoglenoid notch near the inferior border of the supraspinatus fossa.
Continue mobilization anteriorly to the supraspinatus. If necessary, more exposure can be gained by resecting the distal 1.0 to 1.5 cm of the clavicle at the acromioclavicular joint, but this should not be done unless concomitant acromioclavicular arthrosis exists. Release of the coracohumeral ligament in this area allows further mobilization of the supraspinatus laterally.
If the supraspinatus and infraspinatus tendons are retracted so far that adequate length cannot be obtained with tendon mobilization, incise the capsule at its insertion into the glenoid labrum ( Fig. 46.15C and D ). If necessary, carry this incision from the 8-o’clock position posterior to the 4-o’clock position posterior.
The use of a second posterior incision over the scapular spine to increase mobilization has been described, but we have no experience with this technique.
Debride the end of the mobilized tendon to obtain a raw edge, taking care not to confuse the tendon with the overlying bursa. The goals of mobilization are to obtain tissue of adequate strength, to position it anatomically for repair without damage to innervation and without compromise of deltoid function, and to decompress the subacromial space to prevent further mechanical impingement on repaired cuff tissue. When these goals are accomplished, the actual repair can be performed. We believe that the best results are obtained with the double-row technique, suturing the tendon to bone in a cancellous trough in combination with suture anchor fixation. This reduces tension on the primary trough repair. Using transosseous tunnels through the greater tuberosity increases the surface area of tendon-to-bone healing, which more closely restores the anatomic footprint.
With No. 2 nonabsorbable suture, use a double loop technique, superior to inferior and inferior to superior in a horizontal mattress manner. Place the sutures 5 to 10 mm from the free edge of the tear. This helps push the tendon down into the trough.
Use a rongeur or burr to create a 3 mm wide shallow trough running the length of the exposed bone of the greater tuberosity ( Fig. 46.15E ) to accommodate the thickness of the supraspinatus and infraspinatus tendons.
Place two or three rotator cuff suture anchors immediately medial to the trough at a 45-degree angle and pass the suture through the rotator cuff tendon 5 mm medial to the sutures in the free end of the tendon.
Drill holes for sutures 2 to 3 cm distal to the trough, and connect them to the trough using a No. 5 Mayo needle, a towel clip, or a specialized instrument (Concept, Largo, FL; Fig. 46.15F ). Take care not to fracture the thin cortical bone in this area, which may be osteoporotic. Space the holes at least 1 to 2 cm apart on the cortical humeral surface to give an adequate surface over which to tie the knots.
Tie the suture of the anchor down on top of the tendon with four or five knots to prevent impingement of the suture material. The use of strong sutures rather than Kocher clamps or hemostats to pull on the tendon while suturing avoids crush injury to the tendon. We occasionally make longitudinal incisions along the extremes of the free tendon edge to allow placement of the tendon in the trough; these can be sutured before closure.
Next secure the sutures from the suture anchors over the tendon, completing the double-row repair ( Fig. 46.15G ).
Most repairs are done with the shoulder in 0 degrees of abduction.
If the lateral humeral cortex is fractured during tying down of the suture or construction of the suture tunnel, the anchors can be used as a salvage procedure. The anchors reportedly have adequate holding power in cancellous bone and are reasonable alternatives in problematic situations. Use these sutures for additional leverage when tying down the trough sutures and tie them on top of the tendon with four knots to prevent impingement of the suture material.
If the anterior deltoid has been detached, reattach it through 2-mm drill holes in the acromion and/or by periosteal repair.
Close the wounds in the same manner as for open acromioplasty.
Postoperative protocols are based on the size of the tear, condition of the tissue, and stability of the repair. The evidence supporting early motion protocols over immobilization is contradictory. After standard repair, a low-profile pillow sling is worn for 6 weeks. It is removed for assisted exercises in flexion and external rotation to avoid adhesions, disuse atrophy, and disruption of the repairs. The repair is weakest at 3 weeks, and tendon strength is less than at the time of surgery for the first 3 months after surgery. Empirically, we advance to isometric exercises of external rotation at 6 weeks, and at 12 weeks active motion is permitted. Patients are cautioned that overaggressive use of the extremity can lead to disruption of the repair for 6 to 12 months, depending on the size of the repair and the quality of the tissue and repair.
Cordasco and Bigliani identified five factors that improved results of operative treatment of large and massive rotator cuff tears:
Adequate subacromial decompression
Maintaining the integrity of the deltoid origin
Mobilizing torn tendons and performing an interval slide when indicated
Repairing tendons to bone
Carefully supervising and staging postoperative rehabilitation
In the ideal repair, the arm can be brought down to the patient’s side without tension on the repair. Occasionally, despite the most diligent efforts to mobilize the tendons, tension remains on the repaired tendons. For these difficult problems, there are few options. If the tendon can be brought to the bony trough with the arm in abduction, the repair is completed and the shoulder is immobilized in an abduction orthosis for 6 weeks to permit tendon-to-bone healing. There are many problems with this technique, but we still believe it to be an option for certain patients.
Excessive tension at the repair that results in suture cutting through the tendon is believed to be the most common mechanism of failure of rotator cuff repair. The choice of suture type and technique can improve repair strength, as can decreasing the postoperative activity level. The latter option, however, has a significant problem with patient compliance. It is difficult to enforce the use of an abduction splint for 6 weeks because of problems with hygiene, comfort, and driving. Without early movement, adhesive capsulitis is likely and may produce a poorer result than the original tear and loss of collagen strength caused by immobilization. Overall results are consistent with improved pain relief and function; however, a decrease in range of motion and muscle strength may remain.
In an effort to decrease tension and increase strength and thus improve the rate and quality of biologic healing of rotator cuff repairs, a number of augmentation methods have been developed, including autografts (biceps, subscapularis, teres minor, latissimus dorsi, coracoacromial ligament), allografts (tendon, ligament, freeze-dried rotator cuff graft), xenografts, and synthetic grafts. The most frequently used augmentation methods involve scaffold devices, which have been developed from polylactic acid, poly(lactide- co -glycolide), and polytetrafluoroethylene; extracellular matrix (ECM) from human, porcine, bovine, and equine sources ( Table 46.2 ); chitin; and chitosan-hyaluronan. Most of the published studies describe animal or biomechanical research involving ECM, with only a limited number of follow-up studies in human patients; these studies have reported mixed results in surgical outcomes and complication rates. Several studies, including one prospective comparative study, have reported improvements in outcomes after repairs of massive and recurrent rotator cuff tears with ECM augmentation, whereas others have found no significant improvement in outcomes. Other series have shown better results with synthetic patch augmentation than with biologic patch augmentation (retear rates of 17% and 51%, respectively). Studies of the use of a porcine xenograft scaffold have found not only worse outcomes with the scaffold but also severe postoperative inflammatory reactions requiring open debridement.
Product | Type | Source | Manufacturer |
---|---|---|---|
Restore | SIS | Porcine | DePuy Orthopaedics (Warsaw, IN) |
CuffPatch | SIS (crosslinked) | Porcine | Organogenesis (Canton, MA) |
GraftJacket | Dermis | Human | Wright Medical Technology (Arlington, TN) |
Conexa | Dermis | Porcine | Tornier (Edina, MN) |
TissueMend | Dermis (fetal) | Bovine | Stryker Orthopaedics (Mahwah, NJ) |
Zimmer Collagen Repair | Dermis (crosslinked) | Porcine | Zimmer (Warsaw, IN) |
Bio-Blanket | Dermis (crosslinked) | Bovine | Kensey Nash (Exton, PA) |
OrthADPAT Bioimplant | Pericardium (crosslinked) | Equine | Pegasus Biologics (Irvine, CA) |
Synthetic Scaffold Devices | |||
SoftMesh Soft Tissue Reinforcement | Poly(urethane urea) | Biomet Sports Medicine (Warsaw, IN) | |
X-Repair | Poly- l -lactide | Synthasome (San Diego, CA) |
A number of factors influence the extent to which a scaffold device can augment the mechanical properties of a tendon repair, including the mechanical and suture retention properties and the surgical methods of scaffold application (e.g., the number, type, and location of fixation sutures; pretensioning of the scaffold at the time of repair). A study using an analytical model for rotator cuff repairs determined that 70% to 80% of the load is distributed to the tendon after repair, with 20% to 30% of the load carried by the augmentation device. The host response and remodeling of biologic scaffolds also are affected by the species and tissue of origin and the processing and sterilization methods used in preparing the scaffold. Because of the scarcity of clinical data on which to base indications for the use of biologic scaffolds, Derwin et al. developed a grading system that correlates tear size, geometry, and ability to be repaired to the appropriate use of ECM scaffolds ( Table 46.3 ). We have limited experience with the use of ECM augmentation.
Grade | Tear Characteristics | Current Treatment(S) | Outcomes | Indication |
---|---|---|---|---|
VI | Massive, retracted irreparable tear with intraarticular pathology | Open reverse total shoulder replacement (aggressive) | Adequate, but limited function | Not indicated |
V | Large, massive tear (3-5 cm, 2-3 tendons); not repairable (unable to reappose to tuberosity with low tension) | Open or arthroscopic attempt at repair, muscle transfer, debridement, and/or partial repair | High failure rate (≥50% retear and/or low outcome scores) | Interpositional in selected patients |
IV | Large, massive tear (3-5 cm, 2-3 tendons); repairable | Open or arthroscopic repair | Moderate failure rate (≥30% retear rate, 85% pain free but function reduced) | Augmentation |
III | Small to medium tear (<3 cm, 1 tendon) | Arthroscopic repair | Moderate failure rate (5%-10% retear rate; 85% pain free but >50% with reduced function) | Augmentation |
II | Partial-thickness tear (>50% of articular or bursal surface) | Arthroscopic decompression/debridement or repair with acromioplasty | 40% failure within 5 years with debridement only; 95% heal when repaired | Not indicated |
I | Partial-thickness tear (<50% of articular or bursal surface) | Arthroscopic decompression/debridement or repair with acromioplasty | 95% heal when repaired | Not indicated |
Molecular and cellular studies have targeted the tendon-bone interfaces, researching the use of growth factors and cell-coated scaffolds to improve healing. The delivery of transforming growth factor-β3 with an injectable calcium-phosphate matrix was reported to improve healing in a rat model, whereas other studies in a rat model found that application of mesenchymal stem cells genetically modified to overexpress bone morphogenetic protein-13 (BMP-13) did not improve healing, but that stem cells modified to overexpress the developmental gene MT1-MMP produced more fibrocartilage at the interface and improved biomechanical strength. Heringou et al. compared outcomes in rotator cuff tears with and without the use of mesenchymal stem cells and found significant improvements in healing time and substantial improvement in tendon integrity at 10 years after surgery.
In the late 1990s and early 2000s, platelet-rich plasma (PRP), which had been used successfully for many years in other medical specialties, became a popular treatment modality for a variety of orthopaedic conditions, including acute soft-tissue injuries and chronic tendinopathy. PRP is defined as a “volume of plasma that has a platelet count above the baseline of whole blood”; however, PRP preparations can vary markedly according to the amount of blood used and the efficacy of platelet recovery, the presence or absence of white or red blood cells, the activation of platelets with thrombin, and the level of fibrin production. The effect of PRP on healing also differs with different musculoskeletal structures, adding to the difficulty of determining its efficacy. Most studies of the efficacy of PRP in rotator cuff healing have found no benefit regarding retear rates or clinical outcomes. Five meta-analyses and two randomized controlled trials all reached the same conclusion: PRP does not improve early tendon-bone healing or functional recovery. Two comparative studies of leukocyte-plate-rich plasma (L-PRP) found no improvement in the quality of tendon healing or clinical outcomes with the use of L-PRP. A randomized comparison, however, found that PRP significantly decreased the rate of retears and increased the cross-sectional area of the supraspinatus in repair of large to massive rotator cuff repairs; there was no significant difference in clinical outcomes at 1 year.
Occasionally, despite the surgeon’s best efforts and the use of all techniques of mobilization, some tears are so large or retracted, or both, that an anatomic repair is impossible. In this situation, several options are available, none of which is ideal. The two repair options are nonanatomic repair or partial repair. Muscle transfers or slides are another option. The final option is simple debridement.
McLaughlin described suturing the tendon to a trough in bone at whatever point it could be advanced onto the humeral head ( Fig. 46.16 ). This may be more proximal (approximately 2 cm) through the anterior neck area. Although this repair allows a watertight closure, the mechanical advantage of the muscle-tendon unit is lost with this much proximal advancement. Partial repair of massive rotator cuff tears has been proposed to assist in closing large defects and as an alternative to debridement only or tendon transfers. The initial step is a side-to-side tendon repair that results in “marginal convergence” toward the greater tuberosity, which decreases the strain at the free margin of the rotator cuff tear, enhancing the mechanics of the construct. A combination of the tendon-to-tendon repair with tendon-to-bone repair can result in a functional rotator cuff. Partial repair has been shown to be superior to debridement, tendon transfers, and tendon augmentation procedures for the treatment of massive irreparable rotator cuff tears.
Tendon transfers for the treatment of irreparable rotator cuff tears may involve transfer of rotator cuff tendons or other muscle-tendon units. Cofield described subscapularis tendon transposition to fill large gaps in the supraspinatus insertion ( Fig. 46.17 ). The flap is created by separating the outer portion of the subscapularis from the inner capsular portion. It is detached from the lesser tuberosity and mobilized superiorly to cover the humeral head. Other surgeons prefer to use the upper half of the subscapularis tendon by separating it from the anterior capsule and transferring it superiorly. This repair results in great tension in abduction and external rotation and disrupts the subscapularis force couple, which could prove detrimental to shoulder function.
For anterosuperior tears involving the subscapularis and the supraspinatus, transfer of the pectoralis major has been described. The coracoacromial arch should be intact. The technique involves sharply releasing the sternocostal portion of the pectoralis major from its common insertion site on the humerus and bluntly dissecting it from the more superficial clavicular head. Care should be taken not to injure its nerve supply. The sternocostal head is passed deep to the clavicular head and underneath the conjoined tendon to the lesser tuberosity. The musculocutaneous nerve should be identified and protected; the tendon is passed superficial to the nerve. Passing the tendon beneath the conjoined tendon improves the posterior and inferior vectors of the transferred tendon. This transfer also is indicated for treatment of anterior soft-tissue deficiencies and instability after shoulder arthroplasty.
For posterosuperior tears involving the infraspinatus and supraspinatus, the latissimus dorsi has been transferred. Clinically small but statistically significant gains can be expected in motion and strength. Factors reported to be associated with better clinical results include better preoperative function in active forward flexion and external rotation and synchronous in-phase contraction of the transferred latissimus dorsi by electromyography; poor shoulder function and generalized muscle weakness before surgery have been correlated with a poor clinical result. Patients with unsatisfactory results after this procedure may be clinically worse than they were preoperatively.
Transfer of the subcoracoid pectoralis major has been reported for patients with anterosuperior subluxation associated with massive rotator cuff tears, with approximately 80% satisfactory results. Other muscles used for transfer include the teres minor, deltoid, and trapezius, but these are used infrequently and are associated with compromised function. We have no experience with this technique.
Others have used free grafts (autologous or autogenous), such as the intrinsic portion of the biceps, the coracoacromial ligament, and fascia lata, or synthetics to augment or replace deficient rotator cuff tendon. There are few published reports of results, and most are not encouraging; however, successful closure of 14 massive cuff defects was reported with the use of a “tendon patch” fashioned from the long head of the biceps tendon. The disadvantages of the synthetic material are the potential for foreign body reaction to synthetics and tissue rejection. Such materials do not replace the atrophic and weakened rotator cuff musculature present with chronic massive tears.
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