Management of the throwing shoulder

Introduction

The throwing shoulder continues to be a challenge to manage and treat. The demands placed on the shoulder by overhead athletes produce a unique pathophysiology most evident in elite throwers. The throwing shoulder exerts up to 7000 degrees/sec rotational velocity, reportedly the fastest movement in sports. As a result, throwing shoulders have been noted to exhibit adaptations including increased external rotation, decreased internal rotation, increased humeral and glenoid retroversion, and anterior capsular laxity. The combination of these demands and adaptations has created common pathologic lesions in the shoulder such as partial-thickness articular rotator cuff tears, anterior capsular laxity and pseudolaxity, posterior-inferior capsular contracture, posterior and posterosuperior labral injury, biceps tendon pathology, and scapular dyskinesis.

One of the most difficult challenges in treating the disabled throwing shoulder is understanding the difference between pathologic entity and required adaptation. A “fix everything” approach may well lead to a shoulder that cannot return to the same level of throwing. It is therefore critical that the surgeon use a cautious approach to preoperative evaluation, meticulous surgical technique, and a comprehensive postoperative rehabilitation program in the athlete who hopes to return to such a demanding activity.

Pathology

Multiple theories about the cause of the dysfunctional throwing shoulder have been presented throughout the years. In 1959, Bennett described a posteroinferior glenoid exostosis as the inciting pathology for pain in the professional pitcher secondary to repetitive traction on the posterior capsule and triceps tendon. This theory has since fallen out of favor, although his focus on the posterior capsule would lay the foundation for future work in treating the throwing shoulder.

Neer described impingement syndrome in 1972, and for a time this was considered a likely cause of the dysfunctional throwing shoulder. The patient’s complaints and physical examination findings had much overlap with those of impingement, and it was clear that the rotator cuff was often involved. However, Tibone and colleagues in 1985 reported on a series of shoulders treated with acromioplasty for impingement, including the shoulders of 18 throwers. Despite good pain relief, only 4 of the 18 returned to throwing.

In the 1990s, Jobe introduced the concept of secondary impingement, which proposed that anterior shoulder instability brought on by repetitive stretching of the anterior capsule was the cause of the impingement. Jobe’s 1991 article reported excellent pain relief, but return to throwing remained elusive.

By the late 1990s, arthroscopy had become an important adjunctive tool in evaluating the throwing shoulder. At that time both Jobe and Walch separately described impingement of the cuff on the posterosuperior glenoid or “internal impingement.” Jobe continued to attribute it to anterior laxity or “micro instability” as a result of repetitive forces in an abducted and maximally externally rotated position. Paley and colleagues and Conway both demonstrated that anterior instability was very common in throwers and contributed to internal impingement.

However, Walch reported on arthroscopic examination of 16 throwers with internal impingement but no instability, and described the visualization of the rotator cuff impinging in an abducted and externally rotated position leading to partial-thickness cuff tears and posterior capsular lesions. Other studies have confirmed symptomatic internal impingement without anterior instability and a lack of laxity between throwing and nonthrowing shoulders in pitchers.

In 2003, Burkhart and colleagues reported that internal impingement is actually a physiologic occurrence and that contracture of the posteroinferior capsule shifting the humerus posterosuperiorly is the primary pathology in the disabled throwing shoulder. However, there is evidence contrary to this idea as well. Huffman and colleagues showed that obligate translation with simulated posterior capsular contracture was in fact anterior and inferior and occurred during follow-through and not cocking thus implicating a traction mechanism of injury rather than impingement. Regardless of the mechanism, the resulting glenohumeral internal rotation deficit (GIRD) was identified as the hallmark of the at-risk throwing shoulder. Other studies confirmed the high prevalence of GIRD in throwing shoulders, its increased association with shoulder pathology, and the resolution of symptoms with correction of GIRD. ^{, ,} However, GIRD has been noted to be present in 40% of asymptomatic throwers, and more recently a 2018 study found GIRD was no longer present when it was corrected for humeral head retrotorsion. Furthermore, recent studies have shown professional baseball pitchers with less humeral retrotorsion were at greater risk of a shoulder injury and had more severe shoulder injuries than those with more humeral retrotorsion. ^, In fact, the disabled throwing shoulder may well be caused by a spectrum of conditions resulting from the adaptations required when variable anatomy and physiology are subjected to the extreme demands of throwing an object beyond physiologic limits.

Preoperative considerations