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.³ 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.⁴ 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.⁵

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 ⁶ was associated with 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 “microinstability” as a result of repetitive forces in an abducted and maximally externally rotated position. Paley and colleagues ⁷ and Conway⁸ 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.⁹ Other studies have confirmed symptomatic internal impingement without anterior instability and a lack of laxity between throwing and nonthrowing shoulders in pitchers.¹⁰

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.² The authors noted that the resulting glenohumeral internal rotation deficit (GIRD) is the hallmark of the at-risk throwing shoulder. Other studies have confirmed the high prevalence of GIRD in throwing shoulders, its increased association with shoulder pathology, and resolution of symptoms with correction of GIRD.^2,11,12 However, there is evidence contrary to this idea as well. Huffman and colleagues, the same group that performed the biomechanical study that initially supported GIRD, revised their model in 2006 and showed that obligate translation with simulated posterior capsular contracture was in fact anterior and inferior and occurred during follow-through and not cocking.¹³ In addition, GIRD has been noted to be present in 40% of asymptomatic throwers.¹⁴ 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

History and Physical Examination

The dysfunctional throwing shoulder may manifest classically with posterior shoulder pain at the cocking phase of the throwing motion or during follow-through. Some patients, however, may describe a loss of control or velocity or the feeling of a “dead arm.” The physical examination may reveal tenderness to palpation, increased external rotation with decreased internal rotation,¹⁵ instability or laxity, and positive posterior impingement test results,¹⁶ as well as more traditional impingement signs. Decreased internal rotation of more than 20 degrees compared with the contralateral side, especially in the setting of a decreased total arc of motion, is suggestive of GIRD (Fig. 7-1) and should raise the suspicion for the examiner. With this increased suspicion, the examiner must pay particular attention to the core strength of the athlete, the scapula, and associated shoulder pathology. SICK scapula syndrome (scapular malposition, inferior medial border prominence, coracoid pain and malposition, and dyskinesis of scapular movement), or scapular dyskinesia, usually manifests with static and dynamic scapular malposition evident when the patient is asked to repeatedly raise and lower the arms or engage the dynamic stabilizers of the scapula.¹⁷ Associated pathology such as shoulder microinstability, as evidenced by a positive result on relocation test for pain, superior labral tears suspected with a positive active compression test result, and pain with a sleeper stretch are all keys to the physical examination.