Epidemiology, Mechanism of Injury, History and Physical Examination, Imaging, Workup, and Indications for Surgery

Introduction

The overhead throwing motion is an intricate, highly coordinated musculoskeletal sequence placing multidirectional and supraphysiologic forces on the shoulder. In fact, the angular velocity during pitching represents the fastest human movement recorded ( ). This repetitive and highly demanding action results in adaptive structural changes permitting the shoulder to effectively perform overhead athletic motions but potentially at the expense of normal kinematics at the glenohumeral joint. Abnormal kinematics coupled with altered motion could result in a variety of pathologic changes and injuries at the shoulder including scapular dyskinesia, glenohumeral internal rotation deficit (GIRD), superior labral anterior and posterior (SLAP) tears, and rotator cuff tears ( ). Because of the increasing prevalence of injury in this athletic population, it is important to understand the pathogenesis and biomechanics of throwing, how to evaluate and further workup these athletes, and subsequently how to determine the best treatment options.

Mechanism of Injury

To understand the pathology most often encountered in the throwing shoulder, a firm understanding of the biomechanics of the phases of throwing is essential. The overhead throwing motion requires the transfer of kinetic energy from the lower extremities, through the trunk, and into the pitching extremity to generate the optimal velocity on the ball. Although the pitching motion can vary among players, it is classically divided into six phases originally described by ( Fig. 22.1 ).

The two phases most commonly associated with shoulder pathology are the late cocking (early acceleration) and the deceleration phases. The extremes of motion and forces borne by the shoulder in these phases is expected but can lead to altered anatomy and kinematics, resulting in injury. The repetitive loading of the posterior shoulder during deceleration can lead to posteroinferior capsular hypertrophy, thickening, and contracture. This can lead to GIRD (nonthrowing–throwing shoulder internal rotation at 90 degrees of abduction). Although there is no unanimous agreement on a threshold number for diagnosis, differences greater than 18 degrees should cause alert ( ). Perhaps more important is the difference in total range of motion (ROM) between shoulders.

described the pathologic contact between the posterosuperior glenoid labrum and the articular-sided rotator cuff and greater tuberosity during late cocking known as “internal impingement” in tennis players. Although numerous publications have determined internal impingement to be a normal phenomenon in overhead throwers ( ), the presence of GIRD causes the humeral head to shift more posterior and superior ( ). This can accentuate the internal impingement, potentially leading to partial articular-sided rotator cuff tears (PASTA) or SLAP tears. Secondary to the significant distractive forces across the glenohumeral joint during deceleration, which are resisted by tensile forces in the rotator cuff and biceps tendon, these same injuries could occur via abrasion, delamination, and degeneration ( ).

described the constellation of findings known as the “SICK scapula” and believe its presence to be the cause of SLAP lesions and PASTA tears. However, theorized that anterior capsuloligamentous laxity is the central contributing factor to the development of pathologic internal impingement. This theory suggests that with late cocking, the humeral head translates anteriorly, resulting in increased tension on the rotator cuff and its abrasion on the superior glenoid ( ). This theory is supported by a cadaveric study demonstrating that excessive shoulder external rotation results in significantly increased anterior-inferior glenohumeral ligament length (30% increase in length) ( ). Thus, it is important to have an understanding of all the potential mechanisms that could lead to pathologic lesions in the throwing shoulder.

History

Obtaining a detailed history is critical to narrowing the differential diagnosis. Important questions regarding an overhead athlete include the location of pain, neurologic symptoms, exacerbating and mitigating factors, any trauma or inciting event, duration of symptoms, frequency of symptoms, history of shoulder problems or injury, and any previous treatments or surgeries. Additionally, pitching-specific questions should also be asked, including type of pitcher (starting or relief), types of pitches (which ones cause pain), phase of throwing when symptoms occur, number of innings pitched, number of games, and amount of rest over the past year without throwing. Often the athlete will describe symptoms of a “dead arm,” which is defined as any pathologic shoulder condition in which the thrower is unable to throw with preinjury velocity and control because of a combination of pain and subjective unease in the shoulder ( ).

Physical Examination

A comprehensive physical examination with both routine and special physical examination maneuvers is important in differentiating among different shoulder pathologies in overhead throwing athletes. The athlete should always be evaluated with the shirt off, allowing visual inspection for signs of bruising, muscular atrophy, swelling, discoloration of the fingers or nails, and scapular abnormalities ( ). SICK scapular syndrome is characterized by scapular malposition, inferior medial border prominence, coracoid tenderness to palpation, and scapular dyskinesis. Thorough palpation should be performed of the humeral head, joint line (posterior), bicipital groove, coracoid, and scapula. Repeated forward flexion can aid in diagnosing scapular dyskinesia via fatigue or abnormal symmetry between sides. Thorough active and passive ROM with testing of both arms can raise suspicion for subacromial impingement, internal impingement, or rotator cuff pathology. Specific attention should be paid to comparing internal and external rotation of the shoulder at 90 degrees of shoulder abduction between shoulders. Patients with GIRD can present with significantly increased external rotation and significantly decreased internal rotation, and it remains paramount to compare the overall ROM of each shoulder ( Fig. 22.2 ). Cross-body adduction and latissimus ROM should be compared between sides as well. Trunk and core strength, symmetry, and stability should be routinely assessed. A baseline comprehensive major muscle and rotator cuff examination should be performed in all patients.

Focused provocative tests are performed with suspicion of particular diagnoses. Provocative examination of the superior labrum is most commonly conducted with the O’Brien active compression test ( ), the Mayo shear (dynamic labral shear) ( ), and the test described by with the arm abducted in the 90-degree scapular plane with the palm up and a downward force placed against resistance on the wrist in a posterior-inferior direction. Pain secondary to shifting in an anterior-superior direction indicates a positive test result. Additionally, in throwers, a comprehensive neurovascular examination should be performed routinely as thoracic outlet syndrome can be overlooked in this population. This includes the ROOS, Wright, and Adson tests ( ).