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Impingement: Secondary

Individuals with shoulder instability or other underlying pathology can develop significant abnormal mechanics that can lead to rotator cuff functional disability, eventual fatigue and loss of humeral head containment. When this occurs, rather than the coracoacromial arch moving toward the cuff, the cuff migrates cephalad as containment is compromised.

In addition to articular-sided internal impingement-type
rotator cuff tearing, secondary changes, including traction spurring of the CA ligament and abrasive changes of the bursal aspect of the cuff can be encountered.

Several investigators have described partial articular-sided rotator cuff tears resulting from internal impingement. This entity represents contact between the undersurface of the cuff and the posterior-superior glenoid and labrum. There exist a plethora of potential causes for internal impingement including physiologic to pathologic change from repetitive intra-articular contact, torsional forces created by loss of humeral head retroversion, ligamentous insufficiency and abnormal mechanics, especially with regard to scapular dyskinesia. These patients are younger, and often complain of pain localizing to the posterior shoulder.

They also complain of early fatigue and loss of control in the throwing motion. Fatigue of the dynamic stabilizers and excessive external rotation secondary to overstretching of the anterior capsule may predispose individuals to development of internal impingement. A subset of patients, usually baseball pitchers, develop a glenohumeral internal rotation deficit (GIRD syndrome) with a significant loss of internal rotation on the affected side.

This contracture initiates a cascade of kinematic abnormalities that can result in increased torsional strain within the cuff, labral abnormalities and tertiary capsular insufficiency, all implicated in the secondary articular-sided partial cuff tears. In later stages, the ability to discriminate between primary and secondary impingement may be challenging.

Even if a primary instability is present and treatment is directed toward correcting the primary pathology, consideration of subacromial debridement up to and including bony resection must be considered as part of the overall treatment regimen if changes such as bursal-sided cuff tearing and fraying of the coaracoacromial ligament are witnessed.

The real challenge for the clinician is to carefully evaluate these patients to assign the correct diagnosis before proceeding with surgical treatment. Performing a subacromial decompression without treating instability in those with underlying symptomatic shoulder laxity can serve to worsen the degree of instability.

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