18.1 Introduction

Internal impingement describes the pathologic contact between the posterosuperior glenoid and the articular side of the rotator cuff, resulting in a constellation of symptoms that most frequently affect overhead throwing athletes. ^{1 , 2} The overhead athlete’s shoulder is exposed to repetitive activities at the extremes of the functional arc of motion under high loading conditions, which may result in both osseous and soft-tissue adaptations. ^{3 – 8} The contributions of Neer, Jobe, Walch, and others have improved our understanding of internal impingement. ^{1 , 2 , 5 , 9 – 12}

While the biomechanical pathogenesis of internal impingement has been debated, current thinking suggests that symptomatic internal impingement is multifactorial, involving physiologic shoulder remodeling, posterior capsular contracture, and scapular dyskinesis. ^{13 , 14} The overhead athletes’ performance is related in part to the adaptive changes that develop in response to their repetitive overhead activities. Baseball pitchers have been shown to possess a maximum internal rotation velocity of upward of 7,000 deg/s. Such velocity is achieved by expanding the arc of rotation, in this case, increasing external rotation in the late-cocking phase of throwing. Several adaptations develop in the throwing shoulder to optimize velocity—increased glenohumeral external rotation, increased humeral head and glenoid retroversion, and anterior capsular laxity. ^{2 , 3 , 6 , 7 , 15 , 16} Consequently, numerous compensatory and sometimes pathologic anatomic changes may occur, including anterior instability and posterior capsular contracture. Both of these factors are believed to contribute to the pathogenesis of internal impingement.

Due to repetitive overuse, throwers may develop posterior shoulder muscle fatigue and weakness. This includes fatigue and weakness of the rotator cuff and periscapular stabilizers. A glenohumeral distraction force of up to 1.5 times the body weight is produced during the deceleration phase of the throwing motion. This enormous distraction moment is counterbalanced by posterior shoulder muscle contraction at ball release. In the setting of posterior muscle weakness, this distraction force is counteracted by the posteroinferior aspect of the capsule, resulting in capsular thickening and contracture, and a subsequent glenohumeral internal rotation deficit. A posterior capsular contracture has been demonstrated to shift the glenohumeral contact point posteriorly and superiorly, thereby significantly decreasing shoulder internal rotation in the abducted and externally rotated position. ^{17 , 18}

Edelson and Teitz ¹⁹ posited that violent deceleration of the arm in the follow-through phase of throwing causes abrasive degeneration of the rotator cuff on the posterosuperior aspect of the glenoid. Burkhart and Morgan, ²⁰ on the other hand, proposed that the superior and posterior translation of the humeral head contact point on the glenoid reduces the cam effect of the humeral head and permits supraphysiological external rotation. This, they believe, exposes the rotator cuff to a hypertwist mechanism with large shear stresses, ultimately leading to failure.

Posterior capsular contracture produces a functional lengthening of the anterior capsule ²⁰ that may contribute to a subtle anterior instability, or microinstability. It is not surprising, then, that glenohumeral joint laxity is a common finding in throwers. ^{21 , 22} Some authors ¹⁶ believe that this microinstability is critical to the development of symptoms in internal impingement, while others ^{1 , 4 , 13} suggest that subtle instability is protective against symptomatic internal impingement. Either way, determining the difference between adaptive and pathologic laxity is a challenging task. Determining this difference, along with assessing for other associated conditions, is critical to the evaluation of shoulder pain in the overhead athlete.

18.2 Clinical Assessment

Internal impingement describes a spectrum of associated conditions, including partial- and full-thickness rotator cuff tears, anterior and posterior capsular injury, labral tears, humeral head chondromalacia, and biceps lesions. ^{4 , 5 , 19 , 20 , 23 – 25} A thorough history, therefore, is particularly important to making an accurate diagnosis. Most commonly, the athlete reports posterior shoulder pain, which worsens at the late-cocking phase of throwing. Throwers may also note shoulder stiffness, the need for a prolonged warm-up, and a decline in performance, as manifested by loss of control or decreased pitch velocity. Jobe developed a classification system for internal impingement based on clinical presentation ( Table 18.1 ).

Often, the dominant shoulder has 10 to 15 degrees more external rotation, 10 to 15 degrees less internal rotation, and greater muscular development compared to the nondominant shoulder. ⁶ The scapulae should be evaluated for positioning, dyskinesias, and winging. Patients with internal impingement may also have asymmetric microinstability. Distinguishing between pathologic and adaptive laxity, however, may be difficult. However, we have found the “relocation” test to be an extraordinarily sensitive sign for pathologic anterior instability in throwers. Symptoms reflective of “dead arm,” shoulder weakness after throwing, or a subjective sense of a slipping shoulder may indicate pathologic microinstability. Apprehension in 90 degrees of abduction and external rotation is not uncommon. While the posterior impingement test is frequently positive, ²⁵ the impingement sign as described by Neer ¹¹ is typically absent.

Rotator cuff strength should be assessed. Rotator cuff pathology may range from undersurface fraying and partial articular-sided tears to full-thickness tears. The infraspinatus is most commonly involved; therefore, assessment of external rotation strength is critical. As mentioned earlier, internal impingement often occurs in the setting of concomitant injuries, including superior labral anterior and posterior (SLAP) and biceps lesions, bursal-sided rotator cuff tears, and tendinitis, and the patient should be examined accordingly.

18.3 Radiographic Evaluation

Standard radiographs, including internal and external rotation anteroposterior, scapular Y, axillary, and West Point views, are obtained. Radiographs are most often normal, but may show a “Bennett lesion” (exostosis of the posteroinferior glenoid rim), greater tuberosity sclerosis, posterohumeral osteochondral cysts, and rounding of the posterior glenoid rim. ^{26 , 27}

MRI is critical to a thorough radiographic evaluation. MRI has a high sensitivity for rotator cuff, labral, and capsular pathology. We prefer a noncontrast MRI, as it has demonstrated to have equivalent or superior sensitivity to MR arthrogram when specific pulse sequences are employed. ²⁸ Common MRI findings in patients with internal impingement are partial-thickness articular-sided rotator cuff tears, posterosuperior labral tears, and cystic changes in the posterior humeral head ^{24 , 29} ( Fig. 18.1 ). Patients may also display a Bennett lesion, posterior capsular contracture and thickening at the level of the posterior band of the inferior glenohumeral ligament, and subchondral fracture and possible remodeling of the posterosuperior glenoid. ¹⁵ In particularly severe cases, this remodeling may produce narrowing of the spinoglenoid notch adjacent to the suprascapular neurovascular bundle. As MRI may reveal lesions that are asymptomatic, radiologic findings must be correlated with clinical signs and symptoms. Halbrecht et al ⁴ found that 4 of 10 collegiate baseball players had abnormal signal change in the rotator cuff tendons despite the absence of symptoms. Other studies have also shown that MRI findings do not always correlate with the athlete’s symptoms. ^{30 , 31}

While CT may be useful in assessing humeral and glenoid version, CT is rarely used for the evaluation of internal impingement of the shoulder.

18.4 Treatment

18.5 Operative Treatment

18.6 Surgical Technique

The goal of surgery is to treat only the pathologic entities without changing the osseous and soft-tissue adaptations required to throw at maximal velocity. Operative management includes a comprehensive diagnostic arthroscopy, labral debridement versus repair, biceps-labral complex debridement versus repair, rotator cuff debridement versus repair, and appropriate treatment of other associated lesions, if necessary.

18.6.1 Anesthesia and Positioning

Patients are administered sedation and a regional nerve block (intrascalene, supraclavicular). Patients are placed in a modified beach-chair position with a beanbag at the medial border of the scapula, which serves to elevate the ipsilateral trunk and allow maximal clearance posterior to the shoulder ( Fig. 18.2 ). The position is a slight modification of the usual beach-chair position in that the patient is more upright and the acromion is parallel to the floor. A sterile articulated arm holder is used to aid in arm positioning throughout the procedure. Prophylactic antibiotics are given and the skin is cleaned with ChloraPrep.

Related posts:

Part I Rotator Cuff/Biceps Part I Rotator Cuff/Biceps 7 Arthroscopic Subscapularis Repair 14 Open Suprapectoral Biceps Tenodesis 15 Open Subpectoral Biceps Tenodesis 5 Arthroscopic Rotator Cuff Repair

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