The throwing shoulder can sustain injuries to the capsulolabral complex, the biceps labral complex and the rotator cuff tendons. The complex mechanisms associated with the pathomechanics must be understood to appropriately, diagnose and treat the athlete.
KeywordsBiceps Labral Complex Injuries, Glenohumeral Internal Rotation Deficit (GIRD), Labral Tears, Rotator Cuff Injuries, Superior Labral Anterior Posterior (SLAP) tears, Throwing Shoulder
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.
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 ( ).
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 ( ).
Imaging evaluation of the shoulder in overhead thrower athletes should begin with plain radiographs. In musculoskeletally immature athletes, bilateral shoulders should be imaged for comparison of the physes. Additionally, radiographs can reveal subtle signs of pathology such as calcification along the posterior glenoid (Bennett lesion) ( ). reported an incidental finding prevalence of 22% for Bennett lesions in 55 Major League Baseball players, but it can be associated with pain and GIRD ( ). In addition, radiographs can reveal other pathology associated with GIRD and internal impingement such as cystic changes of the posterosuperior humeral head, sclerosis of the greater tuberosity, or erosions of the posterosuperior glenoid rim ( ). Ultrasonography has been shown to be an effective tool in diagnosing partial- and full-thickness rotator cuff tears, but this is highly operator dependent and has relatively poor diagnostic value if it is not performed well ( ). Magnetic resonance imaging (MRI) has become the predominant form of imaging used for shoulder injuries in the overhead athlete. It has been found to be highly accurate for the diagnosis of soft tissue abnormalities. correlated MRI with arthroscopy for various shoulder pathologies in 39 patients and found it very accurate for the diagnosis of rotator cuff tears, osteochondral defects, and Bankart lesions. Performing the MR with arthrography has also been used with very good accuracy and sensitivity and particularly is beneficial in the diagnosis of SLAP lesions. examined 68 SLAP lesions and reported that MR arthrography had an overall sensitivity of 82% and a specificity of 98%. also reported on the diagnostic value of MR arthrography and demonstrated significantly increased sensitivity for detection of partial-thickness articular surface supraspinatus tears, anterior labral tears, and SLAP tears compared with conventional MRI.
Workup and Indications for Surgery
Treatment for the SICK scapula syndrome is nonoperative and focused on scapular rehabilitation. Initially, the thrower is restricted from all throwing and begun on a regimented daily strengthening and stretching program emphasizing the scapular stabilizer muscles. This includes exercises to regain control of scapular protraction, retraction, depression, elevation, and rotation with closed chain exercises. Additionally, stretching of the pectoralis minor is performed. When the affected scapula is 50% or more improved in position from its initial pathologic position and the thrower is asymptomatic, an interval throwing program is initiated. The scapular program is continued until the scapula is symmetric with the other side. At that time, return to sport and unrestricted throwing are allowed, and the thrower is encouraged to maintain an every-other-day scapular muscle strengthening program to prevent recurrence. In a compliant overhead athlete, the 50% repositioned scapula can be attained within 2 to 3 weeks, with complete scapular symmetry with the contralateral side being attained by 3 months. Of the 96 overhead athletes treated for this syndrome and followed up for more than 1 year, all successfully returned to asymptomatic throwing at their preinjury levels of performance by 4 months ( ).
Glenohumeral Internal Rotation Deficit
Nonoperative rehabilitation is the frontline treatment for GIRD with emphasis on posterior capsular stretching. Sleeper and cross-body adduction stretches are critical and have been shown to improve shoulder internal rotation and horizontal adduction ( ). The importance of a consistent stretching program and frequent monitoring cannot be understated because multiple studies have demonstrated significant changes in shoulder ROM after a single start, as well as after a single season ( ). Fortunately, 90% of throwers with symptomatic GIRD will respond positively to a posterior capsular stretching program and improve GIRD to an acceptable level ( ). In cases of refractory GIRD, arthroscopic posterior capsular release has been described with good results. reported 10 of 13 overhead athletes with symptomatic GIRD were able to return to their prior level of play after arthroscopic posterior-inferior capsular release. However, with associated pathology addressed at the same time as posterior capsular release, reported very poor results with only 6 of 17 athletes (35%) returning to their preinjury levels of performance.
Pathologic Internal Impingement
Pathologic internal impingement can present as signs and symptoms of rotator cuff or superior labral pathology. Treatment should be initiated with nonoperative management, including throwing cessation or rest, ice, antiinflammatory medications, and physical therapy targeted at posterior capsular stretching and strengthening of the rotator cuff and periscapular musculature stabilization and rebalancing. When symptoms improve, throwers are to follow a regimented interval throwing program before return to play. Operative intervention is reserved for athletes with refractory symptoms despite nonoperative treatment for 4 to 6 months and would address the particular structural abnormality that is not allowing a return to throwing.
Nonoperative treatment is the initial management as described earlier for internal impingement. Secondary to “fair” results in this population, only after exhausting appropriate and focused conservative management should surgical intervention be considered. performed a systematic review regarding type 2 SLAP repairs and reported that only 63% of overhead athletes return to their prior level of performance. described 23 elite overhead athletes with concomitant type 2 SLAP tears and partial-thickness rotator cuff tears and reported that only 57% of the athletes were able to return to their preinjury levels of competition if both the SLAP tear was repaired and the cuff tear debrided. Technical factors in SLAP repair of throwers include staying posterior to the biceps and ensuring the most posterior aspect of the lesion has been addressed. A trans–rotator cuff approach can be used safely if needed in this population ( ). Additionally, it is important to not overconstrain the labrum, and thus polydioxanone (PDS) suture could potentially be a better option than heavy nonabsorbable suture ( Fig. 22.3 ).