Compared with anterior shoulder instability, posterior instability is relatively uncommon, occurring in 2% to 10% of cases. Electrocution and convulsive seizures are rare causes of posterior shoulder dislocation reported in the general population. More commonly, a posteriorly directed blow to an adducted, internally rotated, and forward-flexed upper extremity is classically described as the sentinel traumatic event. However, recurrent or locked posterior shoulder dislocations from macrotrauma are exceedingly rare in the athletic population. Instead, athletes typically present with posterior shoulder instability as a result of repetitive microtrauma, which can occur in multiple arm positions and under a variety of loading conditions. In 1952, McLaughlin first acknowledged the existence of a wide clinical spectrum of posterior shoulder instability, ranging from locked posterior dislocation to the often subclinical recurrent posterior subluxation (RPS).
Background
In athletics, RPS has been observed in overhead throwers, baseball hitters, golfers, tennis players, butterfly and freestyle swimmers, paddling sport athletes, weightlifters, rugby players, and football linemen, among others. The etiology of RPS is repetitive microtrauma, most commonly leading to posterior capsular attenuation and a labral tear. Overhead throwers with RPS are a subset worthy of specific mention, because they have a complex mechanism of injury involving pathology associated with the abducted and externally rotated (ABER) shoulder position, high forces across the glenohumeral joint with the throwing motion, and adaptive structural changes over time; these factors can result in an atypical combination of posterior capsular contracture and posterosuperior labral tear, a clinical variant that will be discussed in detail. Regardless of the sport, athletes with RPS often present with ambiguous complaints of diffuse pain and shoulder fatigue without a distinct injury, which often makes elucidation of the underlying pathology and diagnosis a challenge.
A thorough history and physical examination, coupled with specific imaging studies, are required to determine the exact pathogenesis of and appropriate treatment options for RPS. With increased clinical awareness, imaging advances such as the magnetic resonance arthrogram (MRA), and the development of specific provocative physical examination tests, the rate of identification of RPS in the athletic population is improving. Several variables that must be considered during the workup include mechanism of injury (true posterior traumatic dislocation versus repetitive microtrauma versus an acute or chronic subluxation), the specific direction of instability (posterior versus posteroinferior or posterosuperior), and the pattern of instability (unidirectional or multidirectional), because these factors will ultimately affect treatment and outcome.
Successful treatment of RPS begins with thorough identification of all of the structural abnormalities present in the affected shoulder, which can include any combination of the labrum, capsule, supporting ligaments, and rotator cuff. Over time, posterior glenohumeral stabilization has evolved from various open procedures to an anatomic-based arthroscopic approach, which allows for enhanced identification and repair of intraarticular pathology including posterior capsular laxity, complete or incomplete detachment of the posterior capsulolabral complex, and inferior capsular tears. Although postoperative results are generally good to excellent after stabilization for RPS, room for improvement exists, particularly with regard to return of the overhead thrower to a preinjury level of competition. Accordingly, research continues on both the biomechanical and clinical fronts to further refine our diagnostic and treatment approaches to RPS.
Pathogenesis
The pathogenesis of RPS varies among athletes, in direct relationship to the particular repetitive stresses placed on the posterior structures of the glenohumeral joint during competition and training. For example, the follow-through phase of throwing, the pull-through phase in swimming, the tennis backhand stroke, and the golf or baseball backswing can all lead to RPS. Similarly, activities such as push-ups, bench press weightlifting, and blocking in football linemen all place direct stress on the posterior capsulolabral complex of the shoulder, potentially resulting in RPS. Given the enormous spectrum of arm positions that athletes use in both contact and noncontact sports worldwide, it can only be assumed that numerous other mechanisms similarly place the shoulder at risk for RPS.
The posterior labrum, capsule, and posterior band of the inferior glenohumeral ligament (IGHL) are the primary stabilizers to posterior translation of the humeral head, particularly between 45 degrees and 90 degrees of glenohumeral abduction. The posterior capsule is delineated by the area between the intraarticular portion of the biceps tendon and the posterior band of the IGHL. It is the thinnest segment of the shoulder capsule and is devoid of any supporting ligamentous structures, thus making it prone to attenuation from applied stress. It has been postulated that athletes such as overhead throwers, tennis players, and swimmers experience shoulder pain that is associated with progressive laxity of the posterior capsule and fatigue of the static and dynamic stabilizers. Recurrent posterior subluxation can lead to plastic deformation of the posterior capsule and a patulous posteroinferior capsular pouch with an associated increased joint volume. After a traumatic posterior subluxation or dislocation, athletes may sustain a capsulolabral detachment know as a reverse Bankart tear, further contributing to recurrent instability and symptoms; this injury pattern has been observed in overhead throwers ( Figs. 47-1 and 47-2 ).
Many authors have reported an elaborate role of the anterior IGHL and shoulder capsule in preventing posterior instability, which varies with shoulder position and applied forces. Warren and colleagues studied the static restraints to posterior translation with the arm in the vulnerable position of shoulder flexion and internal rotation. Transection of the infraspinatus, teres minor, and entire posterior capsule was insufficient to produce posterior dislocation; however, when the anterosuperior capsule and superior glenohumeral ligament (SGHL) were transected, a posterior dislocation would develop. This observation led to the development of the circle concept, which proposed that dislocation in one direction requires capsular damage on both the same side and the opposite side of the joint. A biomechanical study by Cole and colleagues has revealed that the rotator interval and SGHL provide static glenohumeral stability by limiting inferior and posterior joint translations with the arm adducted. Similarly, in a biomechanical study of 16 shoulders, Wellmann and colleagues concluded that a lesion of the rotator interval contributed to increased inferior glenohumeral translation, which may play a role in posteroinferior instability of the shoulder. However, recent work by Provencher and colleagues has demonstrated that although rotator interval closure is associated with a predictable loss of external rotation, it has no effect on reducing the posterior instability of the glenohumeral joint. Similarly, other cadaveric studies have challenged the concept of injury to anterior structures, including the rotator interval, in a posteriorly dislocated shoulder. Thus it appears that rotator interval closure is potentially not clinically indicated in the athlete with unidirectional posterior instability and may actually have a deleterious affect on overhead throwers who rely on functioning in the ABER position.
Muscular forces surrounding the shoulder, namely from the deltoid and rotator cuff, also contribute greatly to the dynamic concavity compression effect on the humeral head within the glenoid. Of the rotator cuff muscles, the subscapularis provides the most resistance to posterior translation of the shoulder, acting as a dynamic supporter of the action of the posterior band of the IGHL. This relationship is of particular interest in overhead throwers such as baseball pitchers, who position the shoulder in the ABER position during the cocking phases of throwing. In one cadaveric study examining the effect of rotator cuff imbalance on the development of a labral tear, it was concluded that decreased subscapularis muscle strength in the position simulating the late cocking phase of throwing motion results in increased maximum glenohumeral external rotation and increased glenohumeral contact pressure. It was inferred from these findings that throwers who experience subscapularis fatigue from repetitive throwing may be more susceptible to these forces and a resultant type II superior labral anterior posterior (SLAP) tear. In our clinical experience with both throwers and nonthrowers, we have found that type II SLAP tears can propagate posteroinferiorly around the glenoid rim, resulting in the type VIII SLAP tear and symptomatic RPS.
Although a full understanding of the pathology contributing to decreased performance in the elite throwing athlete has yet to be established, an evidence-based biomechanical model regarding RPS is taking shape. It is known that the humeral head possesses an oblong (cam) shape because of the presence of the greater and lesser tuberosities. In the ABER position, the anterior band of the IGHL becomes taut because it is draped over the anteroinferior aspect of the eccentrically positioned humeral head, providing a check-rein against excessive external rotation in that position. In pitchers, it is known that increased glenohumeral external rotation is favored at the expense of internal rotation in an effort to prime the late cocking phase of throwing, primarily because an enhanced late cocking phase leads to more rapid internal humeral rotation in follow-through and increased pitch velocity. Chronic use of the shoulder in this manner, with external rotation priming, ultimately results in a glenohumeral internal rotation deficit (GIRD), which manifests structurally as a posterior capsular contracture.
Burkhart and colleagues have postulated that the cam effect of the humerus is overcome by the thrower, who, by developing a posterior capsular contracture, shifts the rotational fulcrum posterosuperiorly; this shift of the rotational fulcrum allows the cam-shaped humeral head to clear the anteroinferior labroligamentous restraints and achieve more external rotation in abduction. With this adaptation, it is believed that the posterior and posterosuperior glenohumeral restraints in overhead throwers are susceptible to repetitive microtrauma events during the follow-through phase with the shoulder in the adducted, flexed, and internally rotated position. Throwers who have GIRD are thought to experience repetitive microtrauma after ball release, resulting in progressive tearing of the superior and potentially the posterior labrum ( Fig. 47-3 ).
The resultant posteroinferior capsular thickening from contracture associated with GIRD has been visualized on MR examinations of throwing athletes. In addition, dynamic MRA has shown that throwing athletes who have painful posterior shoulder instability and commonly perform with the shoulder in the ABER position experience a phenomenon described as posterosuperior labral “peel back.” During the peel-back event, when the arm is placed in the ABER position during MRA, the detached posterosuperior labral tissue is seen separating from and moving medially to the glenoid rim, thus reinforcing the postulated cause-and-effect relationship between the ABER position and RPS. This dynamic phenomenon can also be visualized arthroscopically with the arm in the ABER position.
Not all throwing athletes demonstrate concurrent findings of GIRD and posterior labral tear, which highlights the complexity of the pathogenesis of RPS in this population. It has been observed that some adaptive changes can occur in the throwing shoulder without negative consequence, whereas other athletes reach a tipping point that may lead to symptoms. After approximately 25 degrees of GIRD, the posterosuperior shift in the glenohumeral center of rotation ceases to be adaptive and instead leads to pathologic shearing forces on the posterosuperior labrum and rotator cuff. In effect, the excessive external rotation in the ABER position exposes the posterosuperior labrum, the long head of the biceps tendon, and undersurface rotator cuff tendons to large rotatory lever arm forces, resulting in the peel-back phenomenon. Additionally, the posterosuperior shift of the humeral head in the ABER position has been found to result in a relative redundancy of the anteroinferior capsuloligamentous complex. The relative redundancy in the anteroinferior shoulder capsule is caused by a decrease in the cam effect of the proximal humerus and may have clinical implications in the pathophysiology of the disabled throwing shoulder. However, it should be recognized that this relative redundancy is a secondary anterior pseudolaxity, with the primary pathology being a tight posteroinferior capsule.
With a continuously evolving understanding of posterior shoulder instability, treatment options are formulated. The clinical presentation of posterosuperior labral tear in combination with posteroinferior capsular contracture in throwing athletes differs from the spectrum of pathology seen in offensive linemen, weightlifters and athletes who are frequently subjected to repetitive high loads with the arm in the forward flexed and adducted position. In the latter athletes, these high shearing forces on the posterior labrum result in labral tear, posterior capsular laxity, and capsular redundancy that is best treated with arthroscopic posterior labral repair and additional posterior capsular plication as indicated. On the contrary, when GIRD and RPS are present in the overhead thrower, stretching of the posteroinferior capsular contracture by way of “sleeper stretches” is a more appropriate initial treatment. Additionally, subscapularis muscle strengthening may play a role. Ultimately, arthroscopic posterior labral repair with optional posterior capsular release can be performed to treat recalcitrant symptoms in the thrower with GIRD and RPS. In these cases, the GIRD is typically successfully treated preoperatively with stretching, and the associated capsulolabral avulsion is treated with arthroscopic repair; in rare cases of recalcitrant GIRD, a limited capsular release is performed concomitantly during surgery.
Of additional importance is the identification and treatment of scapular dyskinesia, which has variable clinical implications. Scapular winging can act as a compensatory mechanism to prevent posterior subluxation of the humeral head in some patients, although in other patients scapular winging is thought to be the primary etiology of subluxation. According to a study of eight elite golfers with posterior shoulder instability, fatigue developed in the serratus anterior muscle during competitive play, possibly contributing to scapulothoracic asynchrony and the combination of posterior shoulder instability and subacromial impingement. Further study of the relationship between scapular mechanics and shoulder stability is warranted. Typically, a periscapular muscle-strengthening program is incorporated into the physical therapy protocol for RPS to account for the possible contribution of scapular dyskinesia to symptoms.
Finally, “batter’s shoulder” was initially described by Dines and colleagues as a cause of RPS in baseball hitters. This syndrome affects the lead shoulder during a baseball swing as dynamic posterior pulling forces approach 500 Newtons, resulting in a posterior labral tear. Typically the nondominant arm is affected, resulting in pain with batting. It has been inferred that golfers may experience a similar mechanism of injury, and one can infer that any athlete with a similar follow-through type motion after swinging is at risk.
History
Patients with RPS often have vague or nonspecific symptoms that make the clinical diagnosis difficult to elucidate. Complaints can include any combination of activity-related pain, perceived weakness, mechanical sensations such as crepitus, and intermittent subluxation episodes. Additionally, loss of motion in certain planes can be reported by persons in whom capsular contracture has developed.
Physical Examination
Physical examination of the shoulder of a person suspected of having RPS begins with inspection, focusing on asymmetry, scapular dysrhythmia, and muscular atrophy. Pollock and Bigliani noted that two thirds of athletes who ultimately required surgery presented with reports of difficulty in using the shoulder outside of sports, particularly with the arm above the horizontal. An inquiry should also be made regarding mechanical symptoms, because one study found that 90% of patients with symptomatic RPS noted clicking or crepitation with motion. Often this crepitus can be reproduced during examination and is due to discrete posterior capsulolabral pathology.
A skin dimple over the posteromedial deltoid of both shoulders has been found to be 62% sensitive and 92% specific in correlating with posterior instability. Tenderness to palpation as a result of inflammation is next assessed at the posterior glenohumeral joint line, greater tuberosity, and biceps tendon. A majority of patients with posterior instability have been found to have posterior joint line tenderness, likely as a result of posterior synovitis or posterior rotator cuff tendinosis secondary to multiple episodes of instability.
Multiple methods are used to assess range of motion (ROM) of both shoulders. With the patient standing, measurements are taken of forward elevation, abduction in the scapular plane, external rotation with the arm at the side, and internal rotation behind the back to the highest vertebral level. With the patient supine, the arm is abducted 90 degrees, the scapula is stabilized, and internal and external glenohumeral rotation are measured. These supine measurements are compared with the contralateral shoulder and are used to calculate the total arc of rotation (i.e., total external rotation plus total internal rotation) and GIRD (the side-to-side difference in internal rotation).
Strength testing is performed bilaterally, with a focus on the rotator cuff musculature, and graded on a 5-point scale as follows: Grade 0, no muscle contraction is detectable; grade 1, a contraction can be seen or palpated but strength is insufficient to move the joint at all; grade 2, the muscle can move the joint if the limb is oriented so that the force of gravity is eliminated; grade 3, the muscle can move the joint against the force of gravity, but not against any additional applied force; grade 4, the muscle can move the joint against the force of gravity and additional applied force but is not believed to be normal; and grade 5, the muscle strength is considered normal. The majority of athletes with RPS who are tested have grade 4 or 5 strength.
Supraspinatus strength is tested with a downward force while the arm is abducted 90 degrees in the scapular plane, also known as the empty can test. Strength in the infraspinatus and teres minor muscles is assessed with resisted external rotation with the arm adducted and the elbow flexed 90 degrees. Subtle weakness can be detected in side-to-side comparisons if the posterior rotator cuff has sustained damage. Lastly, subscapularis strength is tested with the lumbar lift-off, belly-press, and bear-hug tests.
Glenohumeral stability is assessed for both shoulders with the patient supine, and the differences between the two are documented. The load-and-shift maneuver is performed with the arm held in 90 degrees of abduction and neutral rotation. In this position a moderate axial load is applied to the glenohumeral joint in combination, first with an anterior force, in an attempt to translate the humeral head over the anterior glenoid rim. The test is repeated with a posterior-directed force ( Fig. 47-4 ). Anterior and posterior laxity are quantified as 0 for a humeral head that does not translate to the glenoid rim, 1+ for a humeral head that translates to but does not translate over the glenoid rim, 2+ for a humeral head that translates over the glenoid rim but spontaneously reduces, and 3+ for a humeral head that translates over the glenoid rim and does not spontaneously reduce.
To assess for excessive IGHL and SGHL laxity, a sulcus test is performed by applying longitudinal traction with the arm adducted and in neutral rotation, with the patient seated. The test is repeated in 30 degrees of external rotation. Laxity is quantified as 1+ for an acromiohumeral distance less than 1 cm, 2+ for an acromiohumeral distance between 1 and 2 cm, or 3+ for an acromiohumeral distance greater than 2 cm. A 3+ sulcus sign that remains 2+ or greater in 30 degrees of external rotation is considered pathognomonic for multidirectional instability (MDI). The implications of a patient who has RPS and concomitant MDI pertain to the potential need to address the rotator interval and the posterior capsulolabral complex for successful glenohumeral stabilization.
Generalized ligamentous laxity also may contribute to MDI and thus should be graded on the 9-point Beighton scale with the following tests: (1) the ability to hyperextend the elbows beyond 10 degrees (1 point for each extremity); (2) the ability to passively touch the thumb to the adjacent forearm with the wrist in flexion (1 point for each extremity); (3) the ability to passively hyperextend the small finger metacarpophalangeal joint more than 90 degrees (1 point for each extremity); (4) the ability to hyperextend the knees beyond 10 degrees (1 point for each extremity); and (5) the ability to touch the palms to the floor with the feet together (1 point). Patients who score 5 points or more on the Beighton scale are considered ligamentously lax.
A number of specialized tests have been devised to further elucidate capsulolabral pathology in the shoulder. The jerk test is used to assess posterior stability in the seated position. The medial border of the scapula is stabilized with one hand, and the other hand applies a posteriorly directed force to the 90 degrees forward-flexed, adducted, and internally rotated arm. The test is positive if posterior subluxation or dislocation of the humeral head occurs while simultaneously reproducing the symptoms of pain and apprehension; variable sensitivity of the jerk test has been reported.
The Kim test can also aid in the diagnosis of posterior and posteroinferior shoulder instability. With the patient seated, the arm is placed in 90 degrees of abduction in the scapular plane and an axial load is applied. The arm is subsequently forward elevated an additional 45 degrees and a posteroinferior vector is placed on the glenohumeral joint. Kim and colleagues concluded that the test is positive with a sudden onset of posterior subluxation with pain. This test, in combination with the jerk test, was found to be 97% sensitive in detecting a posteroinferior labral lesion. The authors also found that patients who experienced pain with the Kim test were more likely to require operative interventionto alleviate their symptoms than were patients who did not experience pain.
The circumduction test is particularly useful in persons with higher grades of chronic posterior instability and is performed with the patient seated. With the elbow in full extension, the arm is brought into 90 degrees degrees of forward elevation and slight adduction. Similar to the jerk test, a posteriorly directed load is applied, which subluxates, or possibly dislocates, the humeral head posteriorly. The arm is then circumducted with a combination of abduction and extension until the head reduces into the glenoid. A positive test results in a palpable and typically audible “clunk” as the posteriorly subluxated head reduces into the glenoid. In patients with chronic posterior instability, this test can often be performed without pain or muscle guarding.
In some cases of RPS, particularly involving overhead throwers, a posterior labral tear is associated with a superior labral tear, resulting in the type VIII SLAP tear. Accordingly, when examining a shoulder in which RPS is suspected, the active compression (O’Brien) test for superior labral pathology should also be performed. For this test, the patient is seated and the arm is forward elevated 90 degrees, adducted 10 degrees, and internally rotated with the elbow extended. A downward force is placed on the arm. A positive test is confirmed when deep pain within the shoulder joint elicited in this position does not occur in the same position with the arm externally rotated and the same force applied. Care must be taken to differentiate deep shoulder pain with this test, which is suggestive of superior labral pathology, from pain at the acromioclavicular joint, which can result in a false-positive test.
Impingement signs may also be positive in patients with RPS and should be sought during physical examination. Secondary subacromial and even subcoracoid impingement is not uncommon in persons with RPS but is typically due to underlying scapular dyskinesia as opposed to true outlet impingement. Similarly, stress-related changes in the posterior rotator cuff can manifest as a secondary impingement syndrome in some cases, and if it is of sufficient severity, it can potentially warrant treatment.
Imaging
Three radiographs of the shoulder are routinely obtained for the workup of RPS: (1) an anteroposterior view in the plane of the scapula; (2) an axillary view; and (3) a scapular Y lateral view. In most patients with RPS, radiographic images are normal, although in some cases a posterior glenoid lesion or impaction of the anterior humeral head (a reverse Hill-Sachs lesion) can be visualized. The axillary view is specifically useful for analyzing the glenoid version, and together with computed tomography (CT), can provide valuable osseous detail in posttraumatic or chronic cases. In rare instances, a fracture of the lesser tuberosity will provide evidence of a previous posterior dislocation. Additionally, the West Point radiographic view can be useful in detecting fractures of the glenoid rim or subtle ectopic bone formation around the glenoid.
MRA is the most sensitive diagnostic test for identifying lesions of the posterior labrum and capsule. Specific MRA findings indicative of posterior shoulder instability include posterior translation of the humeral head relative to the glenoid, posterior labrocapsular avulsion, posterior labral tear or splitting, discrete posterior capsular tears or rents, reverse humeral avulsion of the glenohumeral ligaments, posterior labrum periosteal sleeve avulsion, and subscapularis tendon avulsion ( Fig. 47-5 ).
The Kim classification is used to specifically describe posterior labral tear morphology as follows: type I, incomplete detachment; type II (the Kim lesion), a concealed complete detachment; type III, chondrolabral erosion; and type IV, a flap tear of the posteroinferior labrum ( Figs. 47-6, 47-7, and 47-8 ). The Kim lesion appears arthroscopically as a crack at the junction of the posteroinferior glenoid articular cartilage and labrum, through which a complete detachment of the deeper labrum from the glenoid rim can be identified ( Fig. 47-7 ).
In further work by Kim and colleagues, 33 shoulders with atraumatic posterior instability were studied with MRA to examine chondrolabral changes. Compared with age-matched normal shoulders, the affected shoulders had a glenoid that was more shallow, with more osseous and chondrolabral retroversion present in the middle and inferior glenoid ( Fig. 47-9 ). The study was not able to determine whether these changes were etiologic or pathologic, but nonetheless they should be sought when diagnosing posterior instability of the shoulder. Similar findings were presented in a 2006 study by Bradley and colleagues in which MRA of 48 shoulders with RPS revealed increased chondrolabral retroversion (10.7 degrees vs. 5.5 degrees) and increased glenoid bony retroversion (7.1 degrees vs. 3.5 degrees) compared with control subjects (n = 20 patients). More recent data by Bradley and colleagues has revealed that 16 baseball pitchers with RPS who were examined with MRA had even higher chondrolabral retroversion (11.5 degrees) and glenoid bony retroversion (8.4 degrees). Additionally, Tung and Hou found that in 24 patients with RPS, MRA revealed more posterior humeral head translation, posterior labral tears, and posterior labrocapsular avulsions compared with healthy control subjects.
As a supplementary test, dynamic MRA can be performed, as previously discussed, to demonstrate labral peel-back in the ABER position, which is consistent with a posterosuperior labral tear. This finding has been most commonly seen in overhead throwers, who often present with concomitant posterior and superior labral tears in the type VIII SLAP morphology. Finally, in our practice the use of CT is limited to cases in which a significant amount of bony glenoid retroversion is suspected and an accurate measurement is desired when considering operative intervention.
Decision-Making Principles
A variety of operative and nonoperative treatment methods for posterior shoulder instability have been described. Rehabilitation with an emphasis on strengthening the rotator cuff, posterior deltoid, and periscapular muscles is frequently the first line of treatment and may allow an athlete to return to the preinjury level of sport. It is recommended that this physical therapy protocol be maintained for a minimum of 6 months to decrease an athlete’s functional disability. Previous studies have reported subjective improvement in up to 70% of athletes with this protocol. Objectively, the RPS is typically not completely eliminated, but the functional disability during athletics is improved sufficiently to allow participation in sport without significant problems. If an athlete is not able to return to the preinjury level of competition, operative treatment is a reasonable option. Therapy has traditionally been more effective in patients who have an atraumatic cause of RPS as opposed to those with generalized ligamentous laxity or who have experienced a discrete traumatic event.
Thorough knowledge of an athlete’s sport, position, and training regimen is critical in deducing the pathogenesis and specific pathology associated with RPS. Based on this information, treatment options may ultimately include labral debridement, labral repair, posterior capsular release, posterior capsular plication, or some combination of these procedures.
Treatment Options
Many operative procedures have been described for the treatment of posterior instability. Overall, the results of surgical treatment of posterior instability have been less consistent compared with those for anterior instability, particularly in overhead throwers. Although in general clinical data on attempted posterior shoulder stabilization is relatively scarce, several noteworthy studies have been produced in the past decade. Overall, trends of a transition from open to arthroscopic repair and from nonanatomic to anatomic reconstruction have been noted. However, the findings in the literature are difficult to compare because of multiple confounding variables, including differing causes of instability (RPS vs. traumatic dislocation), patterns of instability (unidirectional posterior vs. MDI), surgical techniques (open vs. arthroscopic), patient populations (athletic vs. nonathletic; throwers vs. nonthrowers), postoperative rehabilitation protocols, postoperative functional demands (return to work, sport, or neither) and definitions of clinical success and failure.
Historically, a number of open procedures for posterior shoulder stabilization have been performed that have involved patients of wide demographics, variable patterns of instability, and differing levels of athletic competition. These procedures have included the reverse Putti-Platt procedure, biceps tendon transfer, subscapularis transfer, infraspinatus advancement, posterior opening glenoid wedge osteotomy, proximal humeral rotational osteotomy, bone block augmentation of the posterior glenoid or acromion, posterior staple capsulorrhaphy, allograft reconstruction, capsulolabral reconstruction, and open capsular shift. Scapinelli found that an inverted scapular spine bone graft to the posterior border of the acromion to treat recurrent posterior shoulder instability in 10 shoulders resulted in 100% success at 9.5-year follow-up. However, a biomechanical study has shown that posterior bone block repair capsulorrhaphy overcorrects posterior translation and does not restore inferior glenohumeral stability. Notable soft tissue tightening procedures have included the reverse Putti-Platt procedure and the Boyd and Sisk procedure of rerouting the long head of the biceps tendon to the posterior glenoid. In 1980, Neer and Foster reported good results in their description of a laterally based posterior capsular shift to tighten a patulous posteroinferior capsule. Similarly, numerous investigators have attempted a medially based posterior capsular shift for posterior capsular tightening. Misamore and Facibene reported on 14 patients with traumatic unidirectional posterior instability who were treated with an open posterior capsulorrhaphy and were evaluated at mean follow-up of 45 months. Based on Rowe grading criteria, 13 of 14 patients were found to have excellent results and 12 of 14 patients returned to their preinjury level of athletic competition.
In further pursuit of anatomic-based repair, Rhee and colleagues presented a review of 33 shoulders for which open, deltoid-saving posterior capsulolabral reconstruction was performed for recurrent posterior instability. At 25-month follow-up, four patients (13.3%) had recurrent instability. Wolf and colleagues presented similar findings in a retrospective review of 44 shoulders after open posterior glenohumeral stabilization; the recurrence rate was 19%, with poor results in patients older than 37 years and in those with chondral damage.
Because of interest in minimizing iatrogenic surgical trauma, arthroscopic techniques for the treatment of shoulder instability have been implemented and have been increasing in popularity. Arthroscopic thermal capsulorrhaphy has been used to treat shoulder instability with mixed results. Bisson presented results of 14 shoulders with unidirectional posterior instability without labral detachment that were treated with thermal capsulorrhaphy; at 2-year follow-up, it was found that treatment failed in three patients (21%). D’Alessandro and colleagues found that 37% of patients who underwent thermal capsulorrhaphy for anterior, anteroinferior, or multidirectional shoulder instability had unsatisfactory results based on American Shoulder and Elbow Surgeons (ASES) scores at 2- to 5-year follow-up, lending additional skepticism to the reliability of this surgical technique. Miniaci and McBirnie presented similar disappointing results in another study of 19 shoulders with MDI that were treated with thermal capsulorrhaphy; nine patients (47%) had recurrent instability an average of 9 months after surgery, five patients (26%) had stiffness, and four patients (21%) had neurologic complications. Accordingly, we presently do not advocate thermal capsulorrhaphy for the treatment of RPS because of the variable response patients have demonstrated to thermal energy.
Over time an evolution to arthroscopic capsulolabral repair for RPS has occurred. This anatomic procedure is minimally invasive and is our preferred method of treatment. Our indications for surgery include failure of the procedure after 6 or more months of physical therapy, a large labral tear on MRA, chondrolabral retroversion greater than 10 degrees, reverse humeral avulsion of the glenohumeral ligaments or discrete posterior capsular tear, or an inability to return to sport or activity at the preinjury level.
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