➢ Posterior shoulder instability in athletes is usually the result of direct trauma during contact sports, repetitive microtrauma, and rarely, atraumatic causes.
➢ Computed tomography and magnetic resonance arthrography are the most sensitive imaging studies to identify posterior shoulder lesions.
➢ Certain athletes have characteristic physical examination and imaging findings, including positive jerk and Kim tests, that are indicative of posterior shoulder abnormality.
➢ Posterior arthroscopic capsulolabral reconstruction, although not as effective as anterior arthroscopic capsulolabral reconstruction, can still lead to a high rate of return to play.
➢ Open stabilization may be necessary for athletes with recurrent instability that has failed to respond to prior arthroscopic treatment or those who have substantial osseous injuries.
➢ Glenoid bone-block augmentation may be necessary for patients with recurrent dislocations associated with erosive glenoid changes or osseous deficiencies involving >25% of the glenoid.
Posterior instability represents up to 10% of all cases of shoulder instability1. In athletes, posterior instability can result from a single traumatic injury, repetitive microtrauma, or, rarely, atraumatic instability. The demands on the athlete’s shoulder, especially in contact or overhead throwing sports, can be dramatic, and, as a result, the managing orthopaedic surgeon must understand the complexities of such an injury complex. Participation in contact sports may result in an increased risk for the development of traumatic posterior instability. In overhead athletes, posterior instability can result from repetitive microtrauma sustained from an early age, which can be further exacerbated with the increase in year-round play.
Anatomy and Biomechanics of Shoulder Injury
The static stabilizers of the glenohumeral joint include the glenoid and the humeral head, the capsulolabral complex, the articular surface, and the glenohumeral ligaments. Anatomic alterations of the retroversion of the osseous and chondrolabral portions of the glenoid have been shown to be associated with posterior shoulder instability2. Cadaveric studies of the superior, middle, and inferior portions of the posterior capsule, which includes the posterior band of the inferior glenohumeral ligament (PIGHL), were shown to be thinner than the anterior band of the inferior glenohumeral ligament (AIGHL)3. These different inherent properties, in theory, can lead to reduced biomechanical performance of the posterior aspect of the shoulder. In addition, as shown in anatomic dissections and biomechanical tests, the posterior band of the inferior glenohumeral ligament may not be found consistently as a discrete structure and has different viscoelastic properties compared with the anterior band of this ligament4-6. The posterior band of the inferior glenohumeral ligament provides most of the posterior stability when the arm is in adduction, internal rotation, and flexion7. The rotator interval contribution as a static stabilizer is by limiting posterior and inferior translation while the arm is in an adducted position; however, it likely plays a lesser role when the arm is in the provocative position for posterior instability (flexion, adduction, and internal rotation)8.
The dynamic stabilizers of the glenohumeral joint include the periscapular muscles, the long head of the biceps, and the rotator cuff muscles, especially the subscapularis, which acts as the primary dynamic stabilizer by preventing posterior translation of the humeral head9. The infraspinatus and teres minor muscles also act as posterior compressors and stabilize the joint during internal rotation during the first half of abduction10.
Unlike anterior instability, recurrent posterior instability is more commonly the result of repetitive microtrauma as opposed to acute traumatic dislocation11,12. Certain athletes are more susceptible to the development of posterior shoulder lesions, including contact athletes (football linemen, hockey players, wrestlers, rugby players, boxers, etc.), weight-lifters, overhead athletes (pitchers, tennis players, volleyball players, swimmers, etc.), and rowers1,13-20. When the arm is placed in a flexed, adducted, and internally rotated position, as in the blocking position seen in football linemen, the posterior band of the inferior glenohumeral ligament is under maximum tension. Stretching of the capsule and the posterior band of the inferior glenohumeral ligament beyond their initial resting length in this position has been shown to be a potential cause of both posterior shoulder instability and multidirectional instability21,22. Biomechanical studies have also shown that the posterior capsule and the posterior band of the inferior glenohumeral ligament may be permanently deformed as a result of repetitive low-strain cyclic loading (e.g., repetitive microtrauma) and that recurrent posteroinferior subluxation of the humeral head can lead to plastic deformation of the capsule23-25.
History and Physical Examination
Athletes with posterior instability typically describe a decrease in performance and strength and even recurrent apprehension or actual episodes of dislocation and/or subluxation when using the affected extremity. Specific complaints can include decreased pitching velocity, pain while blocking (e.g., as in offensive and defensive linemen), and increased fatigue while working out (e.g., during push-ups and bench presses). In patients with acute trauma, it is important to establish the position of the arm and the direction of the external force during the incident. In many cases, the incident involves shoulder subluxation or dislocation or hard, direct contact with the arm in a flexed, adducted, and internally rotated position. Rarely, a player could have a seizure with a subsequent dislocation. Football players and wrestlers are the athletes with the highest risk of developing posttraumatic posterior shoulder instability as a result of either making contact with another player or landing on the playing surface26,27. Patients with posterior instability resulting from repetitive microtrauma typically have more insidious complaints and symptoms. Therefore, a detailed history to derive which activities and positions of the shoulder provoke pain is imperative.
A thorough physical examination is important in order to provide a comprehensive assessment of the athlete’s shoulder and should include a cervical spine examination. Both shoulders should always be evaluated for comparison and should be clearly visible to the clinician. During the inspection of the shoulder, atrophy of the periscapular musculature should be noted. Von Raebrox et al. described the posterior subacromial dimple as a unique sign with 67% sensitivity and 92% specificity for recurrent posterior dislocations28. A careful evaluation of scapular positioning and motion should be performed, especially in the throwing athlete. Palpation of the posterior aspect of the glenohumeral joint and surrounding structures may elicit pain and may be indicative of a pathological process. Passive and active range-of-motion and strength testing should be performed to detect any associated injuries. The physician should be aware of athletes with an acquired laxity that allows them a functional range of motion to play their sport at an elite level.
Provocative maneuvers to elicit the direction of instability are important. A sulcus sign is measured by generating a downward force on the shoulder with the arm adducted at the side in neutral rotation. Translation of >2 cm is considered indicative of inferior instability in a patient with symptoms29. Maneuvers specific to posterior instability include the jerk, Kim, and load-and-shift tests (Fig. 1). Kim et al. retrospectively evaluated the clinical importance of a painful jerk test in comparison with a painless jerk test and found a painful test to be 90% sensitive and 85% specific for posterior labral lesions30. More importantly, the patients with a painful jerk test had a much higher rate of failure with nonoperative treatment in comparison with those who had a painless jerk test (p < 0.01)30. In a follow-up study, Kim et al. determined that, by itself, the Kim test was 80% sensitive and 94% specific for detecting posteroinferior labral tears, whereas the jerk test was 73% sensitive and 98% specific31. However, when the Kim test was combined with the jerk test, the overall sensitivity improved to 97%31.
A series of radiographs (including anteroposterior, axillary lateral, and scapular-Y views) should be ordered. Useful information about osseous abnormalities, traumatic lesions, or overuse injuries (e.g., reverse osseous Bankart, reverse Hill-Sachs, and Bennett lesions) can be obtained from radiographs. Modified views, such as a West Point axillary lateral view or a Stryker notch view, can be useful for a more careful assessment of the joint and glenoid itself. Other specialized views, such as the Bennett view (a 5° cephalad-angled view with the shoulder in 45° of abduction), can be used to assess the Bennett lesion (an osseous spur of the posteroinferior glenoid rim) and other posterior osteophytes.
Radiographs can highlight the general state of the extremity, especially in athletes with repetitive motion and stress to the shoulder. Wright et al. reported on the variability of radiographic findings in the shoulders and elbows of fifty-seven asymptomatic pitchers for the St. Louis Cardinals during spring training and found a correlation between the number of innings pitched and radiographic findings in the distal aspect of the clavicle and the acromion, but not in the glenoid32.
Computed tomography (CT) is useful for evaluating osseous abnormalities and for preoperative planning in cases of severe osseous injury requiring internal fixation or deficiency requiring bone-grafting. CT scanning can identify pathological lesions such as reverse osseous Bankart lesions and reverse Hill-Sachs lesions, can quantify glenoid bone loss, and can help to evaluate glenoid hypoplasia or version abnormalities in cases of atraumatic instability.
Magnetic resonance imaging (MRI) is the most useful imaging study for evaluating the posterior part of the labrum, capsule, and other soft-tissue structures of the shoulder. Chandnani et al. compared CT arthrography, noncontrast MRI, and magnetic resonance arthrography (MRA) for the detection of labral abnormalities and found MRA to be the most sensitive for detecting detached labral fragments (96%) and labral degeneration (56%)33. For posterior labral tears, noncontrast MRI was found to be 74% sensitive34. In two other studies evaluating the diagnostic accuracy of a 3-T MRI in relation to arthroscopic findings, the sensitivity for posterior labral tears improved from 78% to 89%35 and from 84% to 95%36 when contrast medium was used. Lesniak et al. evaluated the preseason MRI scans of twenty-one dominant shoulders in Major League Baseball pitchers and found that thirteen shoulders (62%) had either an anterior or a posterior labral tear37.
Pathoanatomy and Imaging Findings of Lesions Common to Posterior Instability
Posterior instability is commonly associated with the presence of posterior labral lesions; however, the prevalence of posterior labral tears varies greatly in patients with posterior shoulder instability and in some cases such tears are not found (Table I).
Traumatic shoulder instability occurs as a result of a forceful event during contact sports that usually leads to a shoulder dislocation or subluxation event. Patients may develop different variations of posterior labral lesions but do not usually develop recurrent posterior instability as the result of a single traumatic event.
Reverse Soft-Tissue or Osseous Bankart, Reverse Hill-Sachs, and Glenolabral Articular Disruption (GLAD) Lesions
The reverse Bankart or osseous Bankart lesion is a posteroinferior labral tear with or without an osseous component that occurs as a result of an acute traumatic dislocation or repetitive dislocations. The reverse Bankart lesion usually does not exhibit the same type of displacement as seen with anterior Bankart lesions38.
A reverse Hill-Sachs lesion can be associated with the same acute traumatic posterior dislocation. Such lesions are usually located along the anterior and superomedial portions of the humeral head and may be associated with extensive anterior cartilaginous damage39. The lesion may articulate with the glenoid when the humerus is in a position of flexion, adduction, and internal rotation40. If a reverse Hill-Sachs lesion is present and a recurrent dislocation is sustained, the lesion on the humerus may become locked on the glenoid. While osseous abnormality is less common in athletes, contact athletes with a posterior dislocation are the most likely to have osseous lesions41-43. Mair et al. observed that posterior labral detachment does not necessarily have to coincide with capsular tears in contact athletes15. Robinson et al. reported an 18% rate of recurrent dislocations in a study of 112 cases of acute traumatic posterior dislocation. They found that an age of less than forty years, injuries associated with seizures, and large reverse Hill-Sachs lesions measuring >1.5 cm3 were predictive of recurrence44.
Reverse Bankart (Fig. 2), osseous Bankart, and reverse Hill-Sachs lesions are commonly found on MRI scans after posterior dislocations. Saupe et al., in a study of thirty-six patients with acute traumatic posterior shoulder dislocations, reported that thirty-one patients (86%) had a reverse Hill-Sachs lesion, twenty-one (58%) had a reverse Bankart lesion, and eleven (31%) had a reverse osseous Bankart lesion41. The degree of bone involvement in a reverse osseous Bankart lesion can be quantified with CT imaging of the shoulder (Fig. 3), which has been shown to be highly sensitive for glenoid bone loss45. A quantification method for anterior Bankart lesions using three-dimensional CT was described by Chuang et al. and accurately predicted the need for bone-grafting in patients with osseous Bankart lesions46. In a head-to-head comparison between CT and MRI, the correlation between CT and arthroscopy was slightly better than that between MRI and arthroscopy for quantifying anterior glenoid bone loss47. However, to our knowledge, there has been no definitive work using the same radiographic methods to specifically assess and quantify posterior glenoid bone loss.
Neviaser first described GLAD (glenolabral articular disruption) lesions in association with anterior inferior labral tears48. Like anterior GLAD lesions, posterior GLAD lesions can be seen on MRI in association with a posterior labral tear (Fig. 2), with variable disruption of the articular cartilage. Usually, the posterior GLAD lesion is located at the 7 o’clock to 9 o’clock region (right shoulder) of the glenoid49.
Posterior Labrocapsular Periosteal Sleeve Avulsion Lesions
Posterior labrocapsular periosteal sleeve avulsion (POLPSA) is the counterpart to the anterior labroligamentous periosteal sleeve avulsion (ALPSA) lesion seen in association with anterior instability. The posterior labrum is avulsed from the glenoid with a sleeve of intact periosteum, creating a patulous posterior capsule with redundant volume and resultant laxity. Posterior labrocapsular periosteal sleeve avulsion lesions commonly occur as a result of posterior dislocations.
In the study by Saupe et al., the posterior labrocapsular periosteal sleeve avulsion lesion was found on the MRI scans of ten (28%) of thirty-six shoulders after a first-time posterior dislocation41. In a case series of six athletes, Yu et al. reported that the posterior labrocapsular periosteal sleeve avulsion lesion was variable in size and structurally different from a reverse Bankart lesion on MRI scans and arthroscopic images50.
Posterior Humeral Avulsion of Glenohumeral Ligaments
Posterior humeral avulsion of the glenohumeral ligaments (also referred to as the PHAGL lesion, reverse HAGL lesion, or avulsion of the posterior band of the inferior glenohumeral ligament from the humerus), with a reported rate of 7% (five of seventy-three), is rare in comparison with anterior HAGL lesions and is almost exclusively seen in association with acute traumatic posterior dislocations or subluxations or a direct blow to a flexed, adducted, internally rotated arm during sports51,52. In contrast, anterior humeral avulsion of the glenohumeral ligaments usually occurs in association with a hyperabducted and externally rotated arm, typical of anterior instability injuries53.
MRA can be useful for identifying these lesions and can show either a classic disruption of the capsulolabral complex from the humerus, an osseous avulsion from the humerus, or a floating lesion resulting from a combined labroligamentous avulsion51,52. The redundancy of the posterior capsule can also allow leakage of fluid or contrast medium into the posterior soft tissues or down the humeral shaft, both which can be seen on MRI or MRA49. Diagnosing posterior humeral avulsion of the glenohumeral ligaments requires a high index of suspicion during the preoperative work-up. Castagna et al. described their experience with nine athletes and reported seeing the lesion exclusively on MRI scans during a retrospective analysis after arthroscopy confirmed the lesion54. Recently, Smith et al. described a variant involving an osseous PHAGL lesion associated with a teres minor tendon avulsion in a sixteen-year-old baseball player55.
Repetitive microtrauma arises from chronic loading of the shoulder in provocative positions, which usually results in recurrent posterior instability. The accumulation of microtrauma usually is focused on the posteroinferior part of the labrum and can lead to capsular stretching, which may become permanent.
Kim et al. classified the MRA findings of posteroinferior labral lesions into three types based on correlation with arthroscopy findings: Type I (separation without displacement), Type II (incomplete avulsion), and Type III (loss of labral contour)56. The Kim lesion was described as an incomplete and concealed avulsion of the posteroinferior aspect of the labrum from the glenoid articular cartilage without complete detachment of the labrum, most consistent with what Kim et al. originally described as a Type-II lesion57. The injury was proposed to occur through repetitive microtrauma (rim-loading) resulting from submaximal, posteriorly directed forces that occur at the posteroinferior aspect of the labrum and create marginal cracks that do not involve the chondrolabral junction56. Additional important findings that Kim et al. associated with posteroinferior multidirectional instability were a posterior capsular redundancy, loss of glenoid height, and associated chondrolabral retroversion (mean, 7.0°) in all MRA-staged Type-II and III lesions58. Therefore, MRA findings of an incomplete avulsion with accompanying loss of labral height or contour and chondrolabral retroversion are pathognomonic signs for a Kim lesion. Smark et al. recently compared the MRA imaging for patients with arthroscopically confirmed Kim lesions with those for a control group of patients with shoulder abnormalities other than posterior lesions and calculated that MRA had a sensitivity of 86% and a specificity of 75% for detecting Kim lesions59. They also determined the interobserver reliability of MRA for detecting and classifying Kim lesions to be good and fair, respectively59.
The Bennett lesion is extra-articular calcification adjacent to the attachment of the posterior band of the inferior glenohumeral ligament that is found almost exclusively in baseball players. It has been proposed that this type of lesion develops as a result of traction on the posteroinferior aspect of the capsule and the posterior band of the inferior glenohumeral ligament during the deceleration/follow-through phase of pitching16. Bennett lesions have been characterized as “painful” if they fit a set of four requirements: a spur at the posterior glenoid rim, posterior shoulder pain while throwing, tenderness of the posteroinferior aspect of the joint, and decreased pain with a guided lidocaine injection into the Bennett lesion60. Ferrari et al reported on Bennett lesions in one college and six professional pitchers and found a strong correlation, during arthroscopy, between accompanying posterior labral tears and undersurface rotator cuff tears61. Miniaci et al. evaluated the MRI scans for fourteen asymptomatic professional pitchers and found that four (29%) had Bennett lesions; interestingly, all four had a higher internal rotation deficit than the other pitchers in the study62. Wright and Paletta studied fifty-five Major League Baseball pitchers and found that twelve (22%) had Bennett lesions on radiographs63. Connor et al. reported similar findings in a study of twelve college pitchers and eight professional tennis players, in which five (25%) of twenty asymptomatic dominant shoulders had Bennett lesions on MRI64. Nakagawa et al., in a series of five athletes, described a radiographic variant of the traditional Bennett lesion in which the lesion was located more posterosuperiorly as a mobile osteophyte65. Yu et al. proposed that Bennett lesions could arise from posterior labrocapsular periosteal sleeve avulsion lesions over time as a result of chronic changes to the posteroinferior aspect of the capsule50.
Batters are subject to repetitive microtrauma and can develop “batter shoulder.” A large amount of force is generated at the shoulders during a baseball swing. The combination of counterforce from the bat striking the ball and the activation of additional dynamic stabilizers during contact with the ball can partially offset these forces. When a pitch is missed, a larger percentage of the posteriorly directed force exerted by the lead shoulder during follow-through is transferred to the posterior aspect of the capsulolabral complex66. This force is believed to be greatest when missing an outside pitch because the increased abduction angle of the lead shoulder leads to greater shear forces across the joint67. These increased shear forces can lead to posterior capsular laxity or a posteroinferior labral tear. Despite the repetitive microtrauma, there is typically an acute episode during which the athlete first notices a feeling of instability with subluxation of the shoulder, although there is rarely a true dislocation event.
Type-VIII Superior Labrum Anterior Posterior (SLAP) Tear
Although a distinct entity from true posterior instability lesions, the Type-VIII SLAP tear is important to discuss as a generator of posterior shoulder pain and instability68. This lesion is a Type-II SLAP tear with posterior extension to the 6 o’clock to 7 o’clock area (right shoulder), with likely involvement of the posterior band of the inferior glenohumeral ligament. However, Type-VIII SLAP tears are not clinically well studied. Seroyer et al., in what we believe to be the only such study to date, reported the outcomes for thirteen athletes who underwent operative treatment of Type-VIII SLAP lesions68. The majority of athletes played contact sports, and the authors attributed the development of this lesion to likely repetitive microtrauma stressing the posterior aspect of the capsulolabral complex after the development of a Type-II SLAP tear. The authors reported improvement in terms of the mean ASES (American Shoulder and Elbow Surgeons) score, pain, range of motion, instability, and strength at a minimum of two years after arthroscopic labral repair.
Atraumatic Instability and Variations of Glenoid Morphology
Atraumatic instability is still a poorly understood concept and is attributed to inherent ligamentous laxity and morphological variations. For patients with recurrent posterior instability secondary to repetitive microtrauma or atraumatic instability, it is important to thoroughly evaluate the glenoid morphology and version. Glenoid hypoplasia or dysplasia and adaptive changes leading to excessive retroversion in athletes, especially during overhead throwing sports, should be evaluated with appropriate imaging. Normal glenoid version is, on the average, in slight retroversion (2° to 4°), with a variable range (10° of anteversion to 10° of retroversion)69,70. Measurement of version can be subdivided into glenoid osseous version and chondrolabral version. Kim et al. measured chondrolabral version at the inferior one-third of the glenoid at the posteroinferior labral junction and showed a significant difference in chondrolabral retroversion between patients with Type-II and III tears and the control group (p = 0.021)58. Bradley et al., in a study of 100 shoulders (ninety-one athletes) with posterior instability, evaluated the MRA scans of forty-eight shoulders and reported that these shoulders had significantly greater chondrolabral version (10.7° compared with 5.5°; p < 0.001) and osseous glenoid version (7.1° compared with 3.5°; p = 0.008) than the control group14. Drakos et al. and Crockett et al. evaluated professional pitchers and compared them with control groups, assessing dominant and nondominant arms, and showed significant differences in glenoid version and other osseous structural adaptations71,72. Harper et al. reported a 14% prevalence of glenoid dysplasia in a series of >100 consecutive shoulder MRAs and found posterior labral tears in 64% of patients with moderate to severe glenoid deficiency73. Even patients with mild glenoid changes had a higher rate of posterior labral tears in comparison with a control group of unaffected patients73. Owens et al., in a study of 714 young athletes, showed that increased glenoid retroversion (mean, 17.7°) was a significant risk factor (p < 0.0001) for posterior shoulder instability74.
Conservative therapies include guided rehabilitation focusing on strengthening exercises and range of motion. If conservative therapy fails or there is a need for operative treatment based on absolute or relative indications, then operative treatment can be divided into two broad groups: soft-tissue repair and osseous stabilization.
The majority of patients who present with posterior instability resulting from soft-tissue lesions should undergo a trial of physical therapy and rehabilitation. The purpose of therapy is to strengthen all of the periscapular and rotator cuff muscles while emphasizing the importance of scapulothoracic mechanics20,75. If conservative therapy fails, it still will aid in postoperative rehabilitation. Athletes should be informed that all aggravating activities should be discontinued and that they should refrain from playing or practicing. Burkhead and Rockwood showed successful outcomes for 94% (fifteen) of sixteen patients with atraumatic posterior instability who were managed with a conservative rehabilitation program75. However, this rate decreased to 36% (four of eleven) for patients with a known traumatic history and osseous defects75. Kim et al. evaluated the outcomes of nonoperative treatment for patients with posteroinferior instability and found a significantly higher rate of failure for patients with a painful jerk test as compared with those with a painless jerk test (86% [thirty of thirty-five] compared with 7% [four of fifty-four]; p < 0.001)30.
Indications for Operative Treatment
The indications for operative treatment of posterior instability depend on numerous factors. For the athlete, failed conservative treatment, especially with continued or recurrent posterior instability and pain, is an indication for operative treatment. When evaluating candidates for operative treatment, it is important to consider the athlete’s personal expectations, the current level of play and performance, the history with regard to failed conservative management, and the findings on imaging studies.
The cultural shift from open to arthroscopic treatment has advanced as a result of improved technology and technique whereby the majority of these procedures can now be done arthroscopically. Large posterior labral tears, especially those associated with failed therapy and posterior instability, can all be treated arthroscopically unless open glenoid treatment (e.g., glenoid osteotomy or bone augmentation) is needed. Certain posttraumatic posterior fracture-dislocations can be treated arthroscopically with suture anchor fixation if <25% of the glenoid surface is involved (Fig. 4). Although this quantification is predominantly applicable in cases of anterior instability, it is a good guide with which to manage glenoid deficiencies. Burkhart et al. described an arthroscopic quantification of glenoid bone loss with the anterior, posterior, and inferior margins being approximately 11 mm from the bare spot (Fig. 5)76.
Open stabilization procedures are indicated for patients with recurrent posterior instability for whom conservative therapy and arthroscopic stabilization have failed and for a certain subset of contact athletes who have recurrent posterior instability resulting from repetitive microtrauma that may benefit from a posterior capsulotenodesis and who have a concurrent need for posterior glenoid bone-block augmentation.
Open posterior bone-block augmentation is indicated in cases of preexisting glenoid abnormalities associated with instability, failed conservative treatment, involuntary recurrent posterior instability secondary to trauma (Fig. 6), recurrent posterior instability with progressive glenoid erosion, and failed arthroscopic treatment of reverse osseous Bankart lesions or glenoid rim fractures leading to recurrent posterior instability and erosive glenoid changes.
Detailed reviews of outcomes for arthroscopic and open stabilization and glenoid bone augmentation are shown in Table I, Table II, and Table III. Batter shoulder and the Bennett lesion are discussed separately below.
Wanich et al. reported the outcomes for fourteen baseball players (four professional, six college, four high school), twelve of whom were managed operatively with posterior labral repair (ten) or debridement (two)77. Of the twelve operatively managed patients, ten were found to have Type-III lesions (chondrolabral disruption). Eleven of these twelve patients returned to batting by 5.9 months postoperatively and to play by 6.5 months postoperatively. The two nonoperatively managed players returned to play within one month; however, imaging did not reveal any obvious posterior lesions.
Wright and Paletta found that twelve (22%) of fifty-five asymptomatic Major League pitchers had a Bennett lesion and reported no need for operative intervention at any time in their careers63. Multiple studies have investigated the operative treatment of Bennett lesions61,78,79. However, a majority of patients who have had either open or arthroscopic resection of the glenoid exostosis have required treatment of other posterior capsulolabral or intra-articular abnormalities, with mixed outcomes61,78,79. Yoneda et al. followed sixteen baseball players with painful Bennett lesions and other shoulder abnormalities60. Eleven players returned to baseball, and ten players had a complete resolution of throwing pain; however, none of the patients had an isolated Bennett lesion, confounding the conclusions that can be derived from this study60. On the basis of the available evidence, it is hard to determine whether resection of symptomatic Bennett lesions can definitively lead to improvement in terms of throwing pain and performance. Painless Bennett lesions that are discovered incidentally should be treated conservatively.
Posterior shoulder instability is uncommon and not understood or treated as frequently as cases of anterior shoulder instability. For active patients, especially athletes, it can lead to disability, pain, and a decrease in performance and play. Nonoperative treatment should be the first line of therapy in the majority of cases. However, if nonoperative treatment fails, or a patient has a severe enough injury with the appropriate indications, then arthroscopic or open stabilization procedures can be performed. As more information on this patient population is gained, a better understanding of how best to diagnose and manage these patients will develop.
Source of Funding: No external funds were received in support of this study.
Investigation performed at the Division of Sports Medicine, Department of Orthopaedic Surgery, Allegheny General Hospital, Pittsburgh, Pennsylvania
Disclosure: None of the authors received payments or services, either directly or indirectly (i.e., via his or her institution), from a third party in support of any aspect of this work. One or more of the authors, or his or her institution, has had a financial relationship, in the thirty-six months prior to submission of this work, with an entity in the biomedical arena that could be perceived to influence or have the potential to influence what is written in this work. No author has had any other relationships, or has engaged in any other activities, that could be perceived to influence or have the potential to influence what is written in this work. The complete Disclosures of Potential Conflicts of Interest submitted by authors are always provided with the online version of the article.
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