The overhead throwing motion is an intricate, highly coordinated musculoskeletal sequence placing multidirectional and supraphysiological forces on the shoulder. The repetitive and highly demanding action results in adaptive structural changes allowing the athlete to effectively perform the overhead athletic motions; however, this is often at the expense of the normal kinematics of 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 posterior (SLAP) tears, and rotator cuff tears.1–9 Because of the continued prevalence of injury in this athletic population, it is important to understand the biomechanics of throwing, how to physically evaluate and work-up these athletes, and subsequently determine the best treatment options.
PHASES OF THROWING
The overhead pitching motion is classically divided into 6 phases. Although variations can exist between players, these aspects of pitching represent phases that are common to all pitching motions (Fig. 1).10
The windup begins with the initial movement of the lead leg and culminates with its elevation to its highest point. During this phase, the lower extremities prepare a stable base for energy transfer via an essential center of gravity over the back leg to generate the most momentum in subsequent phases. The risk of injury to the shoulder is relatively low during this phase.10 The early cocking phase begins once the lead leg reaches its maximum height and ends when the lead foot contacts the pitching mound. Trunk stability is critical as the stride requires balance and control. The deltoid, supraspinatus, and infraspinatus activate during the late portion of this phase to externally rotate the shoulder.10 The late cocking phase occurs between lead foot contact and the point of maximal external rotation of the throwing shoulder. The scapula is brought into a position of retraction, the elbow flexes, and the humerus undergoes additional abduction and extreme external rotation. As the shoulder approaches maximum external rotation, the subscapularis, pectoralis major, and latissimus dorsi are eccentrically contracting and applying a stabilizing anterior force to the glenohumeral joint. Hyperexternal rotation at the glenohumeral joint allows the accelerating forces to act over a longer distance, allowing greater elastic energy transfer to the ball during acceleration, and thus greater velocity.10 The acceleration phase is defined as the time between maximum external rotation of the shoulder and ball release. The scapula protracts as the humerus undergoes horizontal adduction and internal rotation. The subscapularis, pectoralis major, and latissimus dorsi reaches maximum activity during this phase to produce internal rotation of the humerus. The deceleration phase occurs between ball release and maximum humeral internal rotation and elbow extension. This is often considered the most violent and dangerous phase of the pitching motion, as it results in the greatest joint loading during throwing. During deceleration, excessive distraction and shear forces are placed on the glenohumeral joint. Any energy not imparted through the ball is dissipated through the shoulder, resulting in significant eccentric loading of the posterior rotator cuff musculature.1,10–12 During deceleration, there is also marked biceps and brachialis activity to decelerate the rapidly extending elbow. Follow-through proceeds with the body continuing to move forward with the arm until motion has ceased.10
MECHANISM OF INJURY
A variety of mechanisms are associated with the development of shoulder pathology in overhead throwing athletes. Although all of these mechanisms likely contribute to shoulder pain/injury of the shoulder, different theories exist regarding the primary etiology. Common to these mechanisms, however, is the association with the late cocking (early acceleration) and the deceleration phases of throwing. The extremes of motion and forces at the shoulder during these 2 phases can lead to both physiological and pathologic alterations in anatomy and kinematics. One of these well-reported pathologic alterations is GIRD. This deficit in motion is concerning as it has been reported to be associated with injury by numerous authors. The repetitive loading of the posterior shoulder during deceleration can lead to posteroinferior capsular hypertrophy and contracture, resulting in limited internal rotation. It is defined as the difference between the nonthrowing and throwing shoulder internal rotation at 90 degrees of abduction. Although there is no unanimous agreement on a threshold number for diagnosis, differences >18 degrees should cause alert.2,9,13 Debate continues as to which is more concerning, GIRD or a deficit in total range of motion between the shoulders.
Walch et al8 first described another mechanism of injury in tennis players, known as internal impingement. Internal impingement is defined as pathologic contact between the posterosuperior glenoid labrum and articular-sided rotator cuff and greater tuberosity. Although internal impingement is commonly a normal physiological phenomenon in overhead athletes, the presence of GIRD causes a posterosuperior shift of the humeral head, which can accentuate the internal impingement of the involved structures and lead to partial articular-sided rotator cuff tears (PASTA) or SLAP tears.2,4,6,13–17 Although not statistically significant, Keller et al17 reported in a systematic review that GIRD resulted in a trend toward increased risk of shoulder injury. In addition, scapular positioning and kinematics may contribute to internal impingement and shoulder injuries, as well. Fatigue of the scapular stabilizers can lead to dyskinesia and altered overhead mechanics. Burkhart et al2,18 described a constellation of findings known as the “SICK scapula” and theorized this to be the primary contributor to the development of SLAP lesions and PASTA tears.
On the contrary, Jobe and colleagues theorized that anterior capsuloligamentous laxity is the central contributing factor to the development of pathologic internal impingement. This theory suggests with late cocking, the humeral head translates anteriorly, resulting in increased tension on the rotator cuff and abrasion on the superior glenoid.19 This theory is supported by a cadaveric study showing that excessive shoulder external rotation results in significantly increased anterior-inferior glenohumeral ligament length (30% increase in length).20 Thus, it is important to have an understanding of all the potential mechanisms which could lead to pathologic lesions in the throwing shoulder.
A detailed history is critical to narrowing the differential diagnosis in the overhead athlete. This includes the location of pain, neurological symptoms, exacerbating/mitigating factors, any trauma or inciting event, duration and frequency of symptoms, history of shoulder problems or injury, and any previous treatments or surgeries. In addition, pitching specific information is pertinent to obtain including; type of pitcher (starting or relief), types of pitches (which ones cause pain), phase of throwing during which 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.2 The athlete usually relates this discomfort to the late cocking or early acceleration phase of the throwing sequence, when the arm begins to move forward. At this point, the thrower feels a sudden sharp pain, the arm “goes dead,” and the athlete is unable to effectively perform.2 Athletes with superior labral pathology can experience varying degrees of mechanical symptoms, including catching, locking, snapping, or shoulder instability, depending on the type and size of the SLAP lesion.
A comprehensive physical examination with both routine and specific examination maneuvers is important in differentiating between the potential different shoulder pathologies in the overhead thrower. The athlete should always be evaluated with the shirt off allowing visual inspection for signs of bruising, muscular atrophy, swelling, discoloration of fingers or nails, and resting scapular abnormalities.2,18 “SICK” scapular syndrome is characterized by scapular malposition, inferior-medial border prominence, coracoid tenderness to palpation, and scapular dyskinesis (Fig. 2).
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 accentuation of abnormal symmetry between sides. Thorough active and passive range of motion with testing of both arms can raise suspicion for subacromial impingement, internal impingement, and/or rotator cuff pathology. Comparison of internal and external rotation of the shoulder at 90 degrees of abduction between shoulders is critical. Patients with GIRD can present with significantly increased external rotation and significantly decreased internal rotation and it remains paramount to compare the overall total range of motion of each shoulder (Fig. 3). Cross body adduction and latissimus dorsi range of motion 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.
After the routine examination is completed, more provocative tests for overhead athletes are performed. Examination of the superior labrum is most commonly conducted with the O’Brien’s active compression test.21 The athlete’s shoulder is positioned in 90 degrees of forward flexion, 20 degrees of horizontal adduction, and maximum internal rotation. The examiner applies a downward force, asking the athlete to resist. The extremity is then externally rotated with the palm facing upward and the maneuver is repeated. Reproduction of pain during internal rotation with decreased pain during external rotation represents a positive test.21 SLAP pathology is also evaluated using the Mayo Shear (dynamic labral shear)22 and the Savoie et al23 described tests. The senior author stresses the performance of all tests to aid in this diagnosis. In addition, 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 the Adson tests.24
Imaging evaluation of the shoulder in the overhead throwing athlete should begin with plain radiographs. In the musculoskeletally immature athlete, bilateral shoulders should be imaged for comparison of the physes. In addition, radiographs can reveal subtle signs of pathology such as calcification along the posterior glenoid (Bennett’s lesion).25 Wright and Paletta26 reported a prevalence of 22% for Bennett’s lesions in 55 major league baseball players, which can be associated with pain and GIRD.27–29 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, and/or erosions of the posterosuperior glenoid rim.26,30,31 Ultrasonography has been shown to be an effective tool in diagnosing partial and full-thickness rotator cuff tears; however, this is highly operator-dependent and has relatively poor diagnostic value if it is not performed well.32 Magnetic resonanc imaging (MRI) has become the predominant form of imaging utilized for shoulder injuries in the overhead athlete. It has been found to be highly accurate for the diagnosis of rotator cuff abnormalities, SLAP lesions, as well as other capsulolabral pathology. Bhatnagar and colleagues correlated MRI with arthroscopy for various shoulder pathologies in 39 patients and found that it was very accurate for the diagnosis of rotator cuff tears (90% accuracy), osteochondral defects (100% accuracy), and Bankart lesions (90% accuracy). The accuracy for the diagnosis of SLAP tears was moderate (70% accuracy) and had poor sensitivity to detect SLAP tears (sensitivity=0.15).33 Performing the MR with arthrography has also been utilized with very good accuracy and sensitivity, and particularly is beneficial in the diagnosis of SLAP lesions.34 Waldt et al34 examined 68 SLAP lesions and reported MR arthrography had an overall sensitivity of 82% and a specificity of 98%. Magee35 also reported on the diagnostic value of MR arthrography and showed significantly increased sensitivity for detection of partial-thickness articular surface supraspinatus tears, anterior labral tears, and SLAP tears compared with conventional MRI. It is important to note, rotator cuff pathology and other glenohumeral abnormalities are commonly demonstrated on advanced imaging in the overhead throwing athlete, yet most are asymptomatic. Connor and colleagues reported on 20 asymptomatic overhead athletes, 8 of whom (40%) were found to have partial or full-thickness rotator cuff tears in their dominant shoulders. None of the athletes interviewed 5 years later had any subjective symptoms or required any evaluation or treatment for shoulder-related problems during the study period.36
SICK scapula is characterized by scapular malposition, inferior-medial border prominence, coracoid tenderness, and scapular dyskinesis. Treatment for the SICK scapula syndrome is typically nonoperative and is focused on scapular rehabilitation. Initially, the thrower is restricted from all throwing and begun on a regimented daily strengthening and stretching program for all the scapular stabilizer muscles.37 The anterior tightness (coracoid tenderness) is treated by placing a rolled towel between the shoulder blades of the supine patient and steadily pushing posteriorly on the shoulders to stretch the pectoralis minor. Strengthening the SICK scapula consists of exercises to regain control of scapular motion, neuromuscular control, and positioning with closed chain exercises. When the affected scapula is ≥50% improved in position from its initial pathologic position and the thrower is asymptomatic, an interval throwing program is initiated. He/she continues the scapular program until the scapula is symmetric with the other side. At that time, return to sport and unrestricted throwing is allowed and the thrower is encouraged to perform an every-other-day scapular muscle strengthening maintenance program to prevent recurrence. In the 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 >1 year, all successfully returned to asymptomatic throwing at their preinjury level of performance by 4 months.2,18,37
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 in 4 weeks of a regular stretching program.4,38 The importance of a consistent stretching program and frequent monitoring cannot be understated, as multiple studies have showed significant changes in shoulder range of motion after a single start, as well as after a single season.39–41 Fortunately, 90% of throwers with symptomatic GIRD will respond positively to a posterior capsular stretching program and improve GIRD to an acceptable level.2 In athletes with GIRD that is refractory to posterior capsular stretching, arthroscopic posterior capsular release has been described with good results. Codding et al42 reported that 10 of 13 overhead athletes with symptomatic GIRD were able to return to their previous level of play after arthroscopic posterior-inferior capsular release. However, with associated pathology addressed at same time as posterior capsular release, Van Kleunen et al43 reported very poor results with only 6 of 17 athletes (35%) returning to their preinjury level of performance.
Pathologic Internal Impingement
As discussed above, internal impingement of the shoulder occurs when a pitcher’s repetitive overhead throwing motion results in anatomic adaptations of the glenohumeral joint and its surrounding structures. These include humeral retrotorsion and posterior capsular contracture that result in posterosuperior shift in the humeral head. With these anatomic adaptations, the normal physiological contact between the posterosuperior glenoid and the greater tuberosity during late cocking can result in pathologic internal impingement of the posterosuperior labrum and rotator cuff.4,8 Pathologic internal impingement can present as signs/symptoms of rotator cuff and/or superior labral pathology.4 Treatment should be initiated with nonoperative management including throwing cessation/rest, ice, anti-inflammatory medications, and physical therapy with an emphasis on rebalancing the scapula and correcting GIRD. Physical therapy will be 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 those athletes with refractory symptoms despite nonoperative treatment for 4 to 6 months and would address the particular structural abnormality which is not allowing a return to throwing (see the Bennett lesion section).
In throwers, and often associated with GIRD and internal impingement, is the presence of a Bennett lesion. Originally defined as a bony spur/exostosis at the posteroinferior glenoid, the Bennett lesion has also been described/identified at the posterosuperior and direct posterior areas of the glenoid25–29,44,45 (Fig. 4).
Several hypotheses have been proposed to explain the mechanisms causing the Bennett lesion. Suggested causes include traction on the posterior joint capsule or triceps tendon during the follow-through phase of throwing, posterior impingement of the humeral head on the glenoid in the late cocking phase, and/or a wringing action during the acceleration phase of throwing.25,27–29
Many overhead throwing athletes have been found to have Bennett lesions, which are commonly asymptomatic.26 However, a Bennett lesion can become symptomatic and affect throwing ability, especially if this bony exostosis is fragmented or avulsed from its attachment.46 Possible causes of pain include local irritation of the joint capsule and/or axillary nerve by the bony spur, nonunion of fracture fragments, and internal impingement. Diagnosing a patient with a painful Bennett lesion can be difficult as they are commonly associated with other capsulolabral and rotator cuff abnormalities. However, multiple diagnostic criteria have been discussed: (1) detection of a bony spur at the posterior glenoid rim on plain radiographs; (2) posterior shoulder pain during throwing, especially in the follow-through phase; (3) tenderness at the posteroinferior aspect of the glenohumeral joint; and (4) reduction of throwing pain by an injection of lidocaine into the Bennett lesion.46,47 Although treatment of symptomatic Bennett lesions is controversial with no current consensus, multiple studies have performed arthroscopic removal of the Bennett lesion, as well as treatment of associated pathology with favorable results.29,47
Burkhart and Morgan proposed that the “peel-back mechanism” may contribute to the development of type II SLAP lesions. Because of extreme abduction and external rotation during late cocking, the force vector of the biceps shifts to a more vertical and posterior direction and can result in torsional “peel back” and acute avulsion of the labrum from the bone.48 Nonoperative treatment is the initial and desired management as described above for internal impingement. Secondary to “fair” results in this population, only after exhausting appropriate and focused conservative management should surgical intervention be considered. Sayde et al49 performed a systematic review regarding type 2 SLAP repairs and reported only 63% of overhead athletes return to their previous level of performance. Neri and colleagues 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 level of competition if both the SLAP tear was repaired and the cuff tear debrided.50 Gilliam and colleagues reported of the 216 baseball players who underwent SLAP repair, with only 64% able to return to at least the same level of competition. Importantly, 59% of pitchers versus 76% of position players reached the same level of return showing the differences based on position.51 Although debate exists, current technical recommendations while performing a SLAP repair in throws includes staying posterior to the biceps and addressing the most posterior aspect of the lesion. A trans-rotator cuff approach can be utilized safely if needed in this population.52 In addition, it is critical to not overconstrain the labrum, suggesting the use of polydioxanone suture rather than heavy nonabsorbable suture. Furthermore, postoperative immobilization in an external rotation brace may assist in regaining motion for effective throwing (Fig. 5).
Rotator Cuff Tears
Rotator cuff pathology is common in overhead throwing athletes, yet most are asymptomatic. Connor and colleagues reported on 20 asymptomatic overhead athletes, 8 of whom (40%) were found to have partial or full-thickness rotator cuff tears in their dominant shoulders. None of the athletes interviewed 5 years later had any subjective symptoms or required any evaluation or treatment for shoulder-related problems during the study period.36 Furthermore, Mchugh et al53 examined 69 high school baseball pitchers and reported significant supraspinatus weakness and catabolic rotator cuff changes associated with high pitch volume. Again, the same conservative management program described for internal impingement should be initiated. When surgical intervention is required, is the outcomes show a drastic difference between the results of debridement versus repair. Reynolds et al54 reported on 67 pitchers who underwent debridement of small partial-thickness rotator cuff tears in overhead athletes and 76% were able to return to pitching at the professional level. Andrews et al55 reported 85% good-to-excellent results with debridement of partial-thickness tears in 34 overhead athletes with an average of 13-month follow-up. However, Mazoue and Andrews56 reported only 2 (1 pitcher and 1 position player) of 16 professional baseball players (17%) were able to return to an elite level of baseball following mini-open rotator cuff repair for full-thickness tears. Furthermore, Dines and colleagues reported on 6 MLB pitchers who underwent full-thickness rotator cuff repairs. Although they reported a return to play rate of 83%, the player’s demonstrated a decreased return to performance rate with a significantly decreased mean number of innings pitched compared with preinjury (1806.5 innings vs. 183.7 innings).57 Thus, it is critical to not treat the overhead athlete with a RTC tear with the same techniqueswhich may be utilized in the majority of the population.
Shoulder injuries in the throwing athlete can occur secondary to altered motion and kinematics coupled with the supraphysiological forces involved in the overhead throwing action. A thorough history and physical examination is critical to help narrow the differential diagnosis and assist in planning a comprehensive diagnostic work-up. An exhaustive and focused nonoperative treatment plan should be performed before attempting surgical intervention as studies have showed only fair results in this patient population.
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