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The American Journal of Sports Medicine http://ajs.sagepub.com/ Internal Impingement of the Shoulder Benton E. Heyworth and Riley J. Williams III Am J Sports Med 2009 37: 1024 originally published online December 4, 2008 DOI: 10.1177/0363546508324966 The online version of this article can be found at: http://ajs.sagepub.com/content/37/5/1024 Published by: http://www.sagepublications.com On behalf of: American Orthopaedic Society for Sports Medicine Additional services and information for The American Journal of Sports Medicine can be found at: Email Alerts: http://ajs.sagepub.com/cgi/alerts Subscriptions: http://ajs.sagepub.com/subscriptions Reprints: http://www.sagepub.com/journalsReprints.nav Permissions: http://www.sagepub.com/journalsPermissions.nav Downloaded from ajs.sagepub.com by Valentin Schroyen on June 25, 2009 Clinical Sports Medicine Update Internal Impingement of the Shoulder Benton E. Heyworth, MD, and Riley J. Williams III,* MD From the Hospital for Special Surgery, New York, New York Internal impingement of the shoulder is a pathologic condition characterized by excessive or repetitive contact of the greater tuberosity of the humeral head with the posterosuperior aspect of the glenoid when the arm is abducted and externally rotated. This arm positioning leads to rotator cuff and glenoid labrum impingement by the bony structures of the glenohumeral joint. Although some degree of contact between these structures occurs under normal conditions, to date most of the orthopaedic literature has focused on internal impingement as a disease state that affects overhead athletes and is characterized by the development of articular-sided rotator cuff tears and posterosuperior labral lesions. The precise cause of these impingement lesions remains unclear. However, it is believed that varying degrees of glenohumeral instability, posterior capsular contracture, and scapular dyskinesis may play a role in the development of symptomatic internal impingement. The purpose of this article is to review the pathomechanics, clinical complaints, physical examination findings, and imaging findings that are associated with internal impingement. The results of treatment will be reviewed, and a diagnostic and therapeutic algorithm for the management of internal impingement is presented. Keywords: internal impingement; glenoid impingement; throwing athlete; throwing shoulder anterior infraspinatus tendon by the posterosuperior glenoid margin. This phenomenon, which is distinct from subacromial impingement syndrome, is known as internal impingement, or posterior glenoid impingement.35 This review will describe the biomechanical and etiologic factors pertinent to the development of internal impingement. In addition, the anatomic structures involved in the constellation of internal impingement lesions and the clinical presentation of affected patients will be discussed. We will also present a systematic diagnostic approach to physical examination, radiologic imaging, and intraoperative assessment that should assist the clinician in treating this malady. Finally, the published literature on the treatment and outcomes of internal impingement will be explored in an effort to establish a therapeutic algorithm for the management of this condition. Internal impingement of the shoulder is a condition characterized by excessive or repetitive contact of the greater tuberosity of the humeral head with the posterosuperior aspect of the glenoid when the arm is abducted and externally rotated; this leads to impingement of the rotator cuff and labrum. Although there is some controversy regarding whether this described “internal impingement” is a normal or pathologic condition, it has most often been described as a chronic, pathologic condition that is associated with throwing and other repetitive, overhead athletic activities. However, internal impingement has been described in nonathletes as well.35,80 Findings typical of internal impingement include articular-sided partialthickness rotator cuff tears and posterosuperior or posterior labral fraying or tears. Posterior shoulder pain in throwers was first described by Bennett in 1959.6 However, it was Lombardo et al48 who identified the late cocking phase of the thrower’s motion as a possible cause of posterior shoulder pain in this group of athletes. Andrews et al2 have been credited with describing the association of superior labrum anterior and posterior (SLAP) tears with partial-thickness rotator cuff tears in throwers, based on work published in 1985.3 In 1992, Walch et al80 and Jobe and Sidles (unpublished data, 1992) separately described impingement of the undersurface (deep layer) of the posterior supraspinatus tendon and/or the ANATOMIC AND BIOMECHANICAL CONSIDERATIONS Orthopaedic surgeons’ understanding of the biomechanical and etiologic forces involved in the development of internal impingement of the shoulder has evolved in a gradual, stepwise fashion, but remains incomplete. This is partially due to the limited patient population in which the condition arises, and also because of the variety of pathologic findings that have been reported. Unlike “external” or “subacromial” impingement, most often simply called “impingement syndrome,”59 there is not a single pathophysiologic process at work in the painful throwing shoulder. Internal impingement syndrome is thought to be fundamentally more complex and multifactorial in nature. Bennett,6 in 1959, published observations on the range of elbow and shoulder injuries seen in baseball pitchers *Address correspondence to Riley J. Williams III, MD, Hospital for Special Surgery, 535 East 70th St, New York, NY 10021 (e-mail: [email protected]). No potential conflict of interest declared. The American Journal of Sports Medicine, Vol. 37, No. 5 DOI: 10.1177/0363546508324966 © 2009 American Orthopaedic Society for Sports Medicine Downloaded from ajs.sagepub.com by Valentin Schroyen on June 25, 2009 1024 Internal Impingement of the Shoulder Vol. 37, No. 5, 2009 that were well ahead of his time. His focus on the common, although variable, development of a posteroinferior glenoid exostosis opened the door for future investigators to explore the phenomenon of posterior shoulder pain in throwers more completely. Interestingly, he believed this bony lesion to be secondary to repetitive traction of the posterior capsular structures and traction of the triceps origin.6 Most subsequent reports have refuted the association between the triceps and the bony exostosis lesion or Bennett lesion, as it is most commonly called.27,54 Bennett also described articular-sided fraying of a superficially intact supraspinatus tendon as a typical finding, but he thought that it was related to anterior shoulder pain and not glenoid impingement.6 In 1992, Walch et al80 published a landmark article in which 30 athletes were assessed for shoulder pain. Of the original 30 athletes, 17 individuals (16 of whom were throwing athletes) underwent an arthroscopic shoulder examination; typical findings included the presence of posterior labral lesions and articular surface rotator cuff tears, in the absence of Bankart or SLAP tears. The authors differentiated the labral lesions in their series from SLAP lesions that extended anterior to the biceps anchor at the supraglenoid tubercle, concluding that internal impingement may be responsible for a subset of patients with isolated posterior SLAP tears. In each case, direct arthroscopic observation was made of impingement of the posterior aspect of the humeral head on the posterosuperior rim of the glenoid. This area of impingement corresponded precisely with the location of the rotator cuff and labral lesions when the arm was brought into the abducted, externally rotated throwing position. These findings paralleled those of Jobe and Sidles (unpublished data, 1992), who in the same year presented the results of patients with similar arthroscopic and MRI findings. Jobe and Sidles also used cadaveric shoulders to study the mechanism by which these observed lesions might occur. They suggested that the positioning of the arm versus the glenoid during the throwing motion results in the interposition of the rotator cuff between the glenolabral complex and the humeral head. The principal difference between the potential origins of internal impingement, as suggested by Jobe versus Walch and colleagues, revolves around the role of glenohumeral translation in causing the rotator cuff and labral changes noted in the throwing athlete. Walch et al80 distinguished the pathomechanics of internal impingement from those of anterior instability, excluding patients with any signs of instability from their series. Jobe and Sidles (unpublished data 1992) reasoned that the spectrum of pathologic anterior laxity resulting from hyperangulation of the humerus in the throwing motion was integrally related to the onset of internal impingement.37 Studies by Andrews et al2,4 and Bigliani et al9 have suggested that glenohumeral joint laxity is a common finding in throwing athletes. Such a finding would facilitate anterior humeral head translation and ultimately cause the entrapment of the junction of the posterior supraspinatus and anterior infraspinatus tendons between the humeral head and posterior glenoid, as occurs in internal impingement. Paley et al64 contended that anterior instability is actually the most significant factor 1025 in the development of internal impingement. Conway22 also noted that “anterior glenohumeral instability almost certainly contributes to internal impingement.” A high frequency of anterior instability in throwing athletes has been supported by other studies as well.38,39,44 Paley et al64 cite the combination of repetitive microtrauma and subsequent attenuation of the anterior glenohumeral ligament complex (static restraints), and fatigue or desynchrony of the dynamic stabilizers of the glenohumeral and scapulothoracic articulations, as the precipitating mechanisms that allow abnormal anterior humeral head translation relative to the glenoid surface in some throwers. Overhead athletes, by definition, commonly position the arm in the maximally abducted and externally rotated position; this arm position causes anterior translation of the humeral head and rotator-cuff impingement on the posterior glenoid rim. The potential role of anterior instability in the origin of internal impingement is further substantiated by the common findings of Bankart lesions, anterior labral fraying, and SLAP tears seen in throwing athletes.64 Some authors have suggested that the slightly lower rates of internal impingement lesions seen in the series by Walch et al80 are explained by the fact that the volleyball and tennis players in that study did not mimic the degree of repetition or force of the overhead motion that was characteristic of the studied professional overhand throwers.64 However, this interpretation is confounded by an additional study of 25 tennis players performed by Sonnery-Cottet et al,73 who reported that no patients demonstrated signs of anterior instability, but all were found to have symptomatic internal impingement lesions. In addition, a more recent study from Borsa et al,10 using ultrasound and instrumented graded stress technique to assess glenohumeral translation and rotation in pitchers, found no difference in translation between throwing and nonthrowing shoulders and no correlation between translation and rotational range of motion. These findings supported the results of another stress radiography study that demonstrated no significant side-to-side differences in pitchers’ 2 shoulders.26 Although these studies challenge the notion that anterior instability in the throwing shoulder plays a role in internal impingement, they were performed only on asymptomatic overhead athletes, not on those with pathologic internal impingement. It is notable that several authors23,33,35,80 have contended that patients with significant degrees of subluxation or frank dislocation are actually protected against internal impingement. These investigators point out that the abnormal position of the humerus relative to the glenoid in severe instability actually precludes impingement between the greater tuberosity and posterosuperior glenoid. The fact that nonpathologic interposition of the rotator cuff and posterosuperior labrum between the glenoid rim and greater tuberosity, which some authors will refer to as internal impingement, occurs in throwers and nonthrowers alike has become a well-accepted concept. Cadaveric, MRI, and arthroscopic studies have consistently shown that contact of the rotator cuff on the posterosuperior labrum is a normal, physiologic occurrence.12,14-16,25,33,50 In fact, Burkhart12 has contended that the loss of “internal Downloaded from ajs.sagepub.com by Valentin Schroyen on June 25, 2009 1026 Heyworth and Williams The American Journal of Sports Medicine Figure 1. Line drawing illustrates impingement of the greater tuberosity on the posterosuperior glenoid rim, with the interposed articular side of the rotator cuff and the posterosuperior labrum, which are prone to inflammation, fraying, or tears. impingement” is actually pathologic, in that the absence of this normal restraint to hyperextension of the humeral head in the throwing motion can lead to SLAP tears, fatigue failure of the rotator cuff, and “dead-arm syndrome.” In 2003, Burkhart et al14 meticulously described the biomechanics of how a loss of internal rotation, or development of a glenohumeral internal rotation deficit (GIRD), could initiate the central pathophysiologic cascade in the throwing shoulder. They describe the first step in this cascade as the development of a contracture of the posterior band of the inferior glenohumeral ligament (PIGHL) and posteroinferior capsule. As shown by O’Brien et al,61 the PIGHL and anterior inferior glenohumeral ligament normally act as individual but reciprocating cables balancing the humeral head in the center of the glenoid, in the glenoid bare spot, when the arm is in abduction. Burkhart et al14 contend that a contracture of the PIGHL, commonly seen in pitchers, acts as a tether to normal glenohumeral rotation, shifting the normal, central contact point of glenohumeral articulation in a posterosuperior direction, which can lead to a greater arc of external rotation occurring before the normal contact of internal impingement. Moreover, they suggested that this shift decreases the beneficial “cam effect” that the humeral head and proximal humeral calcar exert on the anteroinferior capsule, by occupying space and tensioning the capsule when the arm is in abduction. Collectively, these changes lead to an increase in the pathologic “peel-back mechanism,” in which the vector of the biceps in the cocking position transmits heightened torsional loads on the posterosuperior labrum, leading to SLAP tears. The authors cite the reduced cam effect, as well as posterior and anteroposterior type II SLAP tears (ie, disruption of the labral ring), as the likely causes of perceived instability and positive “drive-through sign” (in which the arthroscope can be moved from the inferior to superior aspect of the joint without significant resistance) commonly seen in throwers. Notably, they distinguish this common state of “pseudolaxity” seen in both symptomatic and asymptomatic young throwers from the rarer, pathologic state of hyperextension and/or true anterior instability in older athletes, which may be associated with subluxation and tearing of the anterior capsuloligamentous complex.14 They therefore recommend a posterior capsular stretching program as the initial and most critical therapeutic intervention in most symptomatic throwers, citing 90% success rate with such a regimen. The rare thrower who does not respond may be a candidate for arthroscopic posteroinferior capsular release and possibly a repair of the SLAP lesion. Burkhart et al15 also describe a constellation of findings they refer to as scapular malposition, inferior medial border prominence, coracoid pain and malposition, and dyskinesis of scapular movement, which they call “SICK scapula syndrome,” as a critical part of the disabled throwing shoulder. They believe this muscle overuse fatigue syndrome causes protraction of the scapula, which in turn leads to malposition of the glenoid and, ultimately, increased tensile loads on the anterior capsule and posterosuperior labrum. They believe this increase in loads can exacerbate the pathologic cascade responsible, in most cases, for dead-arm syndrome in throwers.15 Although Burkhart et al believe that internal impingement is a normal occurrence in all people, including throwers, other investigators37,52,53,57 have proposed that the increased frequency and force with which external rotation and abduction occurs in some throwing athletes explain the development of internal impingement as a pathologic condition. Jobe35 proposed that 2 different extremes of positions or motions in throwers could cause the constellation of injuries seen in internal impingement, specifically either direct forward elevation, as replicated during the Neer test, or abduction–external rotation, as performed in throwing (Figure 1). There may, in fact, be 3 different forms of internal impingement. Mithöfer et al57 suggested that the first form is the most commonly described infraspinatus contact against the posterosuperior glenoid and labrum. The second mode of internal impingement occurs when the supraspinatus rubs against the posterior labrum in the midacceleration phase of the throw, as detailed by Jobe.36 The third form of the condition, labeled “anterior impingement” by Struhl,75 involves a partial undersurface supraspinatus tear resulting from impingement between the anterior humeral head and anterosuperior glenoid and labrum during forward flexion of the arm. Struhl’s series of 10 patients from the general population (not elite athletes) had an average age of 37 years, suggesting a significantly younger population affected than that described in subacromial impingement series. Downloaded from ajs.sagepub.com by Valentin Schroyen on June 25, 2009 Internal Impingement of the Shoulder Vol. 37, No. 5, 2009 Figure 2. Arthroscopic view from the posterior portal demonstrates an articular-sided, partial-thickness tear of the infraspinatus tendon at the myotendinous junction (arrow) and corresponding posterosuperior labral fraying (triangle). Other anatomic factors may also play a role in the development of internal impingement. Abnormally high glenoid anteversion or abnormally low humeral head retroversion may be predisposing factors.72,80 However, although Walch et al80 noted decreased retroversion in the majority of patients in their original series, 2 of 17 patients had normal retroversion, leading the authors to conclude only that such an anatomic anomaly could be a contributing factor. This theory was later tested by the same group in a study by Riand et al,72 who performed humeral derotational osteotomy with a concurrent subscapularis shortening myorrhaphy in 20 throwing athletes who had persistent posterior shoulder pain after arthroscopic debridement of impingement lesions. The mean increase in humeral retroversion was 29°. At a mean follow-up of 3.8 years, 55% had returned to their sport at their premorbid level, 25% had returned to their sport at a lower level, and 15% discontinued throwing secondary to pain. Although the authors reported no signs of anterior instability in any patient preoperatively, 3 of the 4 surgeries they termed as “failures” were performed on patients demonstrating “hyperlaxity,” with a positive sulcus sign preoperatively. The authors also reported the arthroscopic findings from the surgeries that had been performed an average of 8 months before the osteotomy. Undersurface rotator cuff tears had been noted in 100% of patients, posterosuperior labral lesions in 80% of patients, and posterosuperior humeral head osteochondral lesions in 30% of patients. However, the details of the arthroscopic debridement performed for these lesions are not provided.72 It has been suggested that excessive traction of the rotator cuff tendon during the late cocking phase is the critical etiologic factor in the development of articular rotator cuff tears in throwing athletes.2 Other authors64 have refuted 1027 Figure 3. Oblique coronal magnetic resonance image demonstrates a high-grade, delaminating, articular-sided partial tear of the supraspinatus tendon (arrow) in an overhead athlete. (Courtesy of the Hospital for Special Surgery Department of Radiology.) this mechanism based on the relative preservation of the subscapularis tendon, which undergoes similar tensile forces in the throwing motion but rarely demonstrates injury in this patient population. Few investigators have distinguished between the rotator cuff injury that can occur at the myotendinous junction of the anterior infraspinatus at the level of the joint line (Figure 2) from the more distal site of insertion of the supraspinatus on the lesser tuberosity (Figure 3). We believe the former represents the site of actual impingement, in which the cuff is interposed or pinched between the tuberosity and glenoid in the extremes of abduction and external rotation, but this lesion typically consists of minor pathologic changes, usually in the form of fraying. This finding is often encountered when the arthroscope is first introduced in the posterior portal, and can obscure visualization of the joint until simple, minor debridement is performed. More extensive repair is rarely necessary. A second, distinct type of rotator cuff lesion in throwers occurs at the deep, posterior aspect of the footprint in the form of a delaminating, articular-sided supraspinatus tear of varying thickness. We believe this lesion develops as a result of the combination of repetitive eccentric loading, as initially proposed by Andrews et al,2 and the development over time of excessive shear and torsional forces with external rotation, as elaborated upon by Burkhart et al.14 In addition to the posterosuperior labrum and rotator cuff, injury to a number of other structures in the shoulder have been associated with pathologic internal impingement. Jobe35 has suggested that as many as 5 anatomic structures are at risk: the posterior superior labrum, the rotator cuff tendon (articular surface), the greater tuberosity, the inferior glenohumeral ligament (IGHL) complex, and the posterior superior glenoid. He noted that the majority of patients with internal impingement have more than 1 of the 5 structures injured at the time of arthroscopic assessment, underscoring the importance of a thorough diagnostic arthroscopic assessment of the shoulder joint in the setting of suspected internal impingement or in Downloaded from ajs.sagepub.com by Valentin Schroyen on June 25, 2009 1028 Heyworth and Williams The American Journal of Sports Medicine cases in which a typical internal impingement lesion is unexpectedly detected.35 Unlike Bukhart et al,14 who suggest the PIGHL is the chief culprit in the disabled throwing shoulder, Jobe identified the anterior IGHL complex as the structure uniquely injured by tension forces in internal impingement, as it is draped over the prominence of the articular surface of the humeral head when the arm is in extremes of either forward elevation or combined abduction-external rotation. As the fibers at the apex of this bulge undergo maximal stress, stretch and eventual attenuation of the fibers can occur, leading to anterior IGHL injury.35 Repetitive microtrauma to the bony greater tuberosity or the posterosuperior rim of the glenoid may represent extremes of the spectrum of injury caused by the abducted, externally rotated position associated with internal impingement,35 but even cases of fracture of these structures have been reported in some series.34,35,80 Although osteochondral lesions of the humeral head have also been described, it is likely these occur from a similar mechanism to greater tuberosity changes, with subtle variations in anatomy or the throwing motion accounting for a different site of humeral head contact with the glenoid rim. Because some series of internal impingement patients have demonstrated low rates of calcification or ossification in the region of the posteroinferior glenoid,80 often labeled a Bennett lesion, it remains unclear whether the finding is a significant pathologic component of internal impingement. Also, because such lesions have been demonstrated variably as osteophytes in contiguity with the posteroinferior glenoid rim83 or as calcifications within the joint capsule,27,54 the PIGHL, or the triceps tendon origin,6,63 speculation continues regarding their true pathophysiology. Although a range of theories have been proposed about the biomechanical and pathophysiologic role of internal impingement, it seems clear that the causes of the disabled throwing shoulder are multifactorial. We believe that anterior subluxation of the humeral head that is associated with gross or microinstability—whether arising from anterior capsular stretch or any disruption of the labral ring— likely exacerbates internal impingement, but is not a prerequisite to its occurrence. The cardinal lesions of internal impingement, articular-sided rotator cuff tears and posterosuperior labral lesions, have been shown to occur in association with a number of other findings, most importantly GIRD and SICK scapula syndrome, but also posterior humeral head lesions, posterior glenoid bony injury, and more rarely Bankart and IGHL lesions. More biomechanical and clinical research is needed before a complete understanding and reconciliation of the varying theories of the pathomechanics of injury is developed. Below, we will discuss the spectrum of clinical presentation in patients with internal impingement, and the diagnostic tools used to evaluate and differentiate the treatable features and their associated intra-articular findings. CLINICAL PRESENTATION AND DIAGNOSIS Patient Demographics and Clinical Presentation Because of the constellation of findings that characterize internal impingement and the strong association with other pathologic lesions of shoulder, the incidence of the condition, in isolation, has not been established. Internal impingement typically affects young to middle-aged adults; in most major series of internal impingement, patients are under 40 years of age and participate in activities involving repetitive abducting and externally rotating arm motions or positions. The majority of patients who have been identified with internal impingement are overhead athletes. For example, the first major series by Walch et al80 consisted primarily of volleyball and tennis players. However, in a recent series of 75 recreational athletes (with the exception of 1 professional tennis player) treated for partial-thickness rotator cuff tears, 55 patients were found to have concurrent SLAP tears, suggesting the possibility of a high prevalence of internal impingement lesions outside of the elite athletic population.11 The largest athletic group studied with internal impingement has been the throwing athlete, particularly baseball players. Most patients present with a progressive decrease in throwing velocity or loss of control and performance. Chronic, diffuse posterior shoulder girdle pain is commonly the presenting complaint, but the pain may be localized to the joint line.57 Jobe36 classified three stages in the clinical presentation of internal impingement. Stage I is characterized by complaints of stiffness, with pain occurring specifically in the late cocking and early acceleration phases. Progression to significant posterior joint-line pain with activity characterizes stage II. Stage III is defined as failure to improve with conservative means. Interestingly, there are series in which a substantial number of studied patients were not throwing athletes or even athletes at all. These patients are more likely than throwers to have acute posterior shoulder pain following an injury rather than progressive, chronic pain. In one series,35 Jobe reported on 6 of 11 patients treated for internal impingement who were not throwing athletes. The series included acute (8 patients) and chronic (3 patients) injury mechanisms, with varying degrees of arm abduction, elevation, and external rotation.35 Typically, the injuries were sustained with the arm in full forward elevation or abduction with external rotation. One patient in this series was a forklift driver, whose trunk underwent repetitive extremes of rotation to allow the patient to drive in reverse while the arm rested on the steering wheel.35 Despite posterior shoulder pain being the most common complaint among patients with internal impingement, patients may also present with symptoms similar to those associated with classic rotator cuff disease. Younger patients with such symptoms, particularly throwing athletes, should raise the clinician’s index of suspicion for internal impingement. In fact, some authors have identified internal impingement as the leading cause of rotator cuff lesions in athletes.23 Alternatively, patients may also have instability symptoms, such as apprehension or the sensation of subluxation with the arm in a position of abduction and external rotation. However, as previously mentioned, those with moderate to severe degrees of instability may actually be protected against the lesions typical of internal impingement because the abnormal position of the humerus, relative to the glenoid, prevents impingement between the greater tuberosity and posterior superior Downloaded from ajs.sagepub.com by Valentin Schroyen on June 25, 2009 Internal Impingement of the Shoulder Vol. 37, No. 5, 2009 At-Risk Sports/Activities - Baseball - Other throwing athletes (waterpolo, football) - Tennis - Squash - Other racquet sports (racquetball) - Volleyball - Forklift driver Other isolated conditions that may present similarly to internal impingement - Anterior instability - Full thickness rotator cuff tear - SLAP tear - Subacromial impingement History or physical examination suspicious for internal impingement MRI signs of internal impingement Treat other condition MRI signs of internal impingement - Articular-sided partial thickness posterior supraspinatus or infraspinatus rotator cuff tear (RCT) - Posterosuperior glenoid labral lesion (fraying, tearing, detachment) Nonoperative Treatment Principles of nonoperative treatment - Rest (remove from competition) - Physical therapy (aggressive posterior capsular stretching, periscapular strengthening) - Anti-inflammatory medications (NSAIDs) Examination under anesthesia (bilateral EUA in adduction and 90° abduction before sterile draping) Physical examination signs of internal impingement - Posterior impingement sign - Relocation sign - Posterior glenohumeral joint line tenderness MRI No MRI signs of internal impingement 1029 Resolution of symptoms No resolution of symptoms Continued, progressive rehabilitation, Return to competition Operative treatment (examination under anesthesia, diagnostic arthroscopy) 1+ Ant Instability No capsular intervention 2+ Ant Instability Consider capsular plication 3+ Ant Instability Capsular plication IR Defecit Posterior capsular release RCT Debridement (partial) vs repair (full) Posterosuperior labral lesion Debridement (fraying, tearing) vs repair (frank detachment or posterior instability) Diagnostic arthroscopy Intervention-specific postoperative rehabilitation, return to competition Continued, progressive rehabilitation, Return to competition Figure 4. An algorithmic approach to diagnosis and treatment of internal impingement. MRI, magnetic resonance imaging; SICK scapula syndrome, a constellation of findings consisting of scapular malposition, inferior medial border prominence, coracoid pain and malposition, and dyskinesis of scapular movement; SLAP, superior labrum anterior and posterior. glenoid.23,35,80 Notably, Burkhart et al,16 in their series of 96 athletes with a disabled throwing shoulder, reported an 80% rate of anterior corocoid pain, rather than isolated posterior shoulder pain, as the most common presenting symptom. However, this cohort was throwers designated with SICK scapula syndrome, which they specifically differentiate from those with pathologic internal impingement. Thus the diagnosis of internal impingement based on history alone is extremely difficult, and symptoms tend to be variable and fairly nonspecific. Although nonthrowing Downloaded from ajs.sagepub.com by Valentin Schroyen on June 25, 2009 1030 Heyworth and Williams The American Journal of Sports Medicine athletes and nonathletes may be affected by internal impingement, the vast majority of patients studied with this condition have been high-level throwers with posterosuperior shoulder pain. As throwing requires maximal abduction and external rotation, this athletic activity provides the most replicable model of the disease. Older patients are more likely to have concurrent shoulder conditions, such as subacromial impingement or glenohumeral arthrosis, and the workup should be directed to ruling out diagnoses other than internal impingement. A summary of the sports and activities that have been associated with internal impingement are listed within Figure 4. Physical Examination Findings Posterior glenohumeral joint line tenderness, increased external rotation, and decreased internal rotation are the most common physical examination findings in throwing athletes. However, all patients suspected of internal impingement should be evaluated with a complete shoulder examination due to the high rate of other shoulder conditions associated with internal impingement. In addition to documentation of bilateral active and passive motion of the shoulders, testing for SLAP lesions, “classic” impingement signs such as the Neer and Hawkins tests, cross-body adduction tests, and instability testing should be performed. Despite significant controversy regarding the validity of various physical examination maneuvers for detecting SLAP tears,24,30,51,68,81 because superoposterior labral tears represent a cardinal feature of pathologic internal impingement, performing some combination of these tests is generally indicated. O’Brien et al62 reported 100% sensitivity and 98.5% specificity for the “active compression test,” although other authors have not replicated these findings.74 Liu et al47 published sensitivity and specificity rates of 91% and 94%, respectively, for the “crank test.” Speed’s test is also commonly used for assessment of SLAP tears,58 but may be positive with biceps lesions distal to the labral insertion.7 Kim et al43 described 2 different “biceps load tests,” the first with greater than 90% sensitivity and specificity in patients with concurrent anterior instability and the second geared toward patients with isolated SLAP tears.42 A number of additional tests, including the “clunk test” of Andrews et al,3 Kibler’s anterior slide test,41 the “SLAPrehension test,”8 and, most recently, the supine flexion resistance test,24 have been advocated by various authors. However, a small number of physical examination tests designed to specifically test for internal impingement rather than SLAP tears have also emerged. Meister et al55 investigated the ability of a single maneuver, referred to as the “posterior impingement sign,” to detect the presence of articular-sided rotator cuff tears and posterior labrum lesions. They prospectively enrolled 69 overhead athletes with a mean age of 22.7 years who presented with posterior shoulder pain. The subjects were tested for the presence of deep posterior shoulder pain when the arm was brought into a position similar to that noted during the late cocking phase of throwing—abduction to 90° to 110°, extension to 10° to 15°, and maximal external rotation. The sensitivity and specificity of the posterior impingement sign were 75.5% and 85%, respectively. When the 21 patients who had sustained contact injuries were excluded in a stratified analysis, the sensitivity improved to 95% and the specificity improved to 100%. Notably, all patients with noncontact injuries with a positive test had arthroscopic findings amenable to surgical treatment. The authors concluded that the test was extremely useful in identifying operable internal impingement lesions in younger overhead athletes.55 As such, the clinician should carefully investigate the injury mechanism in this subset of patients. Jobe and his associates suggested that the relocation test could be used to identify internal impingement as well.23,35 With the arm in an abducted and maximally externally rotated position (in throwers, sometimes up to 140°), the internal impingement patient would experience posterior shoulder pain that was relieved with a posteriorly directed force on the proximal humerus. The pain is thought to be secondary to impingement of the rotator cuff and posterosuperior labrum between the greater tuberosity and the glenoid. This finding is distinct from the uncomfortable feeling of apprehension and anterior shoulder pain noted in patients with true anterior shoulder instability, who also experience relief with a posteriorly directed force. The findings of Paley et al64 support the use of this maneuver as well; these investigators reported that, among patients with a positive relocation test on physical examination, 100% had evidence of shoulder joint injury that was suggestive of internal impingement: undersurface rotator cuff tears, posterior labral tears, and osteochondral lesions. Jobe35 also reported 7 positive relocation tests in his series of 11 internal impingement patients who did not sustain their injuries from throwing sports. Mithöfer et al57 reported that subacromial impingement tests are usually negative in patients with known internal impingement, although conflicting results have been reported by other authors. For example, one study reported that over 25% of the 41 professional throwing athletes evaluated arthroscopically had demonstated a positive Neer or Hawkins sign.64 However, the significance of this finding is questionable, given that acromioplasty has not been demonstrated to lead to predictable rates of return to sport in overhead athletes.76 The active compression test may be positive in patients with internal impingement, given the high frequency of superior labral lesions seen in patients with the condition. As previously mentioned, a glenohumeral internal rotation deficit, marked by a loss of greater than 30° to 40° of internal rotation relative to the expected gain in external rotation, compared with the contralateral side, is an overwhelmingly common physical examination finding in symptomatic throwers. For example, Burkhart et al14 reported the presence of GIRD in 100% of a series of 124 symptomatic baseball pitchers found to have a type II SLAP tear arthroscopically.14 In addition, scapular protraction, caused by SICK scapula syndrome and associated with scapular dyskinesis, is a commonly reported finding by the same investigators.15 Characteristic features include a prominent inferior medial border of the scapula Downloaded from ajs.sagepub.com by Valentin Schroyen on June 25, 2009 Internal Impingement of the Shoulder Vol. 37, No. 5, 2009 and the appearance that the throwing shoulder is drooped inferior compared with the nonthrowing side. In our experience, GIRD is a common finding in symptomatic throwers, while appreciable changes in the appearance of the scapula are relatively rare. A summary of the physical examination findings most commonly associated with internal impingement are listed within Figure 4. Radiographic Findings Radiographic evaluation of patients with signs and symptoms of internal impingement should include standard AP, axillary, scapular Y, West Point, and Stryker notch views of the shoulder. Four radiographic findings that have been described in association with internal impingement include (1) exostosis of the posteroinferior glenoid rim, also known as a Bennett lesion; (2) sclerotic changes of the greater tuberosity; (3) posterior humeral head osteochondral lesions or cystic “geodes”; and (4) rounding of the posterior glenoid rim. It should be noted that radiographic findings may often be minimal or normal in patients with internal impingement. There is much controversy surrounding the cause and significance of the Bennett lesion. Bennett first described this finding as the presence of an ossific deposit in the area of the posterior glenoid, which he believed was secondary to traction of the triceps tendon on its bony origin. He observed this finding exclusively in baseball players, noting “I do not believe one sees [this] in other people.”6 Ozaki et al,63 who supported the notion of posterior glenoid rim overgrowth secondary to a traction epiphysitis of the triceps origin, identified the exostosis in 5 of 7 throwers, all of whom had pain in the late cocking phase of the throw. However, several studies have refuted the association between the Bennett lesion and the triceps origin.27,54 Ferrari et al27 reported on 7 competitive baseball pitchers with posteroinferior ossific lesions, none of which was in the region of the triceps tendon. This conclusion was also supported by a larger series of Meister et al,54 who cited no involvement of the triceps origin. The authors recommended use of the Stryker notch view for assessment of the posterior exostosis or osteophyte. In their series of 22 throwers with Bennett lesions, 21 patients also had undersurface tearing of the rotator cuff (typical of internal impingement). Thus, while the presence of a Bennett lesion may be somewhat specific, it is by no means sensitive for internal impingement. For example, in their series of 17 athletes with posterior shoulder pain, Walch et al80 reported that abnormalities in the posterior border of the glenoid, such as the presence of a Bennett lesion, were seen in only 6% of patients. Wright et al84 used a “modified Bennett view,” with the x-ray tube angled 5° cephalad and the arm abducted 45°, to assess the asymptomatic throwing shoulders of a large cohort of professional baseball players. The authors found the prevalence of inferior glenoid osteophytes to be 60%, but did not specify whether these were considered true Bennett lesions. This represents a follow-up of a study from Wright and Paletta,83 who previously showed the prevalence of Bennett lesions to be 22% in 55 asymptomatic professional baseball pitchers. The authors suggest that this 1031 may not represent a pathologic finding, and therefore stress the importance of identifying concomitant sources of posterior shoulder pain when this lesion is seen. Ferrari et al27 contend that the structures seen in the region of the posteroinferior glenoid are actually extra-articular calcification, based on their review of MRI examinations, CT arthrography studies, and arthroscopic evaluations of the joint. The authors noted no osseous lesions in any of their patients. Thus, while Bennett proposed that overgrowth of the posteroinferior glenoid represented an osteophytic extension of the glenoid rim itself, Ferrari et al suggested that the calcific changes in the region may instead be due to repetitive traction of the posterior capsule and PIGHL during the extremes of the throwing motion.27 Other studies have supported these findings as well.48,60 Greater tuberosity changes are also commonly found on the radiographs of internal impingement patients. Mithöfer et al57 stressed the importance of assessing the greater tuberosity for sclerotic and cystic changes; these findings are present in approximately half of patients with internal impingement. Likewise, Walch et al80 noted sclerosis of the greater tuberosity in 8 of 17 patients. Interestingly, a recent radiographic study analyzing 57 asymptomatic professional baseball pitchers demonstrated that cystic changes in the humeral head were present in 39% of shoulders imaged.84 Similar to the Bennett lesion, this finding may not be indicative of pathologic changes, but simply a common finding in the throwing shoulder. Walch et al80 noted a second characteristic finding— posterior humeral head geodes—in 8 of their 17 patients. This likely corresponds to the osteochondral defects detected arthroscopically by Paley et al.64 These authors contend that such a lesion is similar in nature to a HillSachs lesion but is found more superiorly, near the insertion of the supraspinatus tendon. Interestingly, they report that 2 patients in their series had osteochondral lesions of the humeral head in conjunction with posterosuperior labral damage, but no undersurface fraying of the rotator cuff. They suggest that a small subset of throwers may have impingement simply between the humeral head and glenoid at slightly greater degrees of abduction, such that the supraspinatus tendon may actually avoid interposition and be free of injury from impingement.64 Another finding that may be seen in radiographs of internal impingement patients is rounding or remodeling of the posterior glenoid rim, although MRI (axial plane) is the optimal modality to appreciate this phenomenon (Figure 5). One study57 reported this feature in one-third of patients with internal impingement. The finding of bony remodeling is more common in skeletally immature throwers, in whom a process of chronic abnormal impingement will lead to a rounded appearance in the posterior glenoid. MRI Findings Although meticulous inspection of radiographs for typical findings of internal impingement is critical, MRI remains the gold standard for workup of any young patient with shoulder pain, particularly throwers with posterior shoulder pain. When labral lesions are suspected, many authors Downloaded from ajs.sagepub.com by Valentin Schroyen on June 25, 2009 1032 Heyworth and Williams The American Journal of Sports Medicine Figure 5. Axial magnetic resonance image demonstrates posterior glenoid remodeling (black arrow) and associated labral degeneration (white arrow) in a 16-year-old baseball pitcher. (Courtesy of the Hospital for Special Surgery Department of Radiology.) advocate the use of magnetic resonance arthrography with either gadolinium contrast material or saline to better identify labral tears and other lesions.17,18,65-67,77-79 However, Potter and coworkers have demonstrated that noncontrast MRI demonstrates equivalent or superior sensitivity and specificity rates, when the appropriate pulse sequences are used.19,20,31,32 Despite these findings, magnetic resonance arthrograms are commonly used at many centers. Typical MRI findings in internal impingement include articular-sided partial-thickness rotator cuff tears of the supraspinatus, infraspinatus, or both, and posterior or superior labral lesions. Bennett lesions, humeral head osteochondral lesions or cysts, and posterior glenoid bony lesions have also been reported at high rates. Several studies have shown that shoulder MRI is effective in diagnosing rotator cuff lesions, glenoid labral lesions, and injuries to the labral capsuloligamentous complex in throwing athletes.19,20,33 Interestingly, Halbrecht et al33 performed noncontrast MRI of the shoulder in a position of abduction and external rotation in the throwing and nonthrowing arms of 10 asymptomatic college baseball players. Because contact between the rotator cuff and posterosuperior glenolabral complex was seen in all shoulders, the authors concluded that this was a normal physiologic occurrence. However, in 4 of 10 of the throwing shoulders, signal changes suggestive of tendinosis or delamination were seen in the rotator cuff. Moreover, 3 of the 10 throwing shoulders demonstrated labral tears with adjacent paralabral cysts that extended towards the spinoglenoid notch. None of these findings were noted in the nonthrowing shoulders. Given the high rate of findings in asymptomatic patients, the authors urged caution when considering treatment of throwing athletes based on abnormal MRI findings.33 Similar conclusions were drawn by Miniaci et al,56 who identified abnormalities of the labrum in 79% of bilateral shoulders imaged by MRI in 14 asymptomatic professional baseball pitchers. However, these investigators found no difference in the appearance of supraspinatus and infraspinatus tendons between the throwing and nonthrowing shoulders imaged. In contrast, Connor et al21 reported that 40% of dominant shoulders in a series of 20 asymptomatic elite overhead athletes had partial-thickness or full-thickness rotator cuff tears, compared with 0% in nondominant shoulders. Likewise, MRI allowed for identification of Bennett lesions in 25% of dominant shoulders, compared with none in nondominant shoulders. Although Miniaci et al56 identified no clear Bennett lesions in any of the shoulders imaged in their series, they suggested that the enthesopathic features seen in the posterior glenoid labrum of the 4 pitchers with internal rotation deficits may have represented pre–Bennetttype lesions. When Kaplan et al40 attempted to correlate MRI and arthroscopic findings in 9 patients who underwent surgery for a diagnosis of symptomatic internal impingement, they showed that all 9 athletes had posterosuperior labral lesions (fraying in 8 cases, frank tearing in 1 case) that had been diagnosed preoperatively with MRI. In addition, cystic changes in the posterosuperior aspect of the humeral head beneath the insertion of the infraspinatus tendon were seen in 8 cases by MRI. There was 1 additional case of moderate chondrosis in the central to posterior aspect of the humeral head articular surface. Arthroscopy confirmed the humeral head findings in each of these cases. While no rotator cuff tears had been identified with MRI in the 5 athletes in whom articular-sided partial thickness rotator cuff tears were seen arthroscopically, mild to moderate tendinopathy of the rotator cuff had been documented in all patients by MRI.40 A summary of the MRI findings that are most commonly associated with internal impingement are listed within Figure 4. Both MRI and radiographs should be used in conjunction with physical examination findings to establish a diagnosis of internal impingement. However, as a number of studies have shown, most of the described findings may also be seen in the asymptomatic shoulder. Thus all the features of the patient’s clinical picture must be considered as a whole, with consideration of age, profession, patient activity level, symptom severity, degree of disability, and the effects of the condition on athletic performance and activities of daily living. TREATMENT AND RESULTS Nonoperative Treatment As with most nontraumatic injuries of the shoulder, conservative care should be attempted in patients with a diagnosis of internal impingement before surgical intervention is considered. Rest, cryotherapy, oral anti-inflammatory medications, and physical therapy are the cornerstones of nonoperative treatment. Because studies have reported high rates of GIRD in throwers with shoulder pain, exercises should focus on posterior capsular stretching if a capsular contracture or GIRD is noted on physical examination.14 One group of authors theorized that 90% of throwers could reduce GIRD to an “acceptable” level within 2 weeks of initiation of a series of posterior capsular stretches, Downloaded from ajs.sagepub.com by Valentin Schroyen on June 25, 2009 Internal Impingement of the Shoulder Vol. 37, No. 5, 2009 1033 TABLE 1 Table Used for Documentation of Findings of Examination Under Anesthesia for Patients With Internal Impingementa Right Shoulder Position/Provocative Test ROM/Test Result IR in 0° abduction ER in 0° abduction IR in 90° abduction ER in 90° abduction Sulcus sign (+, –) Anterior instability (1+, 2+, 3+) Posterior instability (1+, 2+, 3+) Left Shoulder Position/Provocative Test ROM/Test Result IR in 0° abduction ER in 0° abduction IR in 90° abduction ER in 90° abduction Sulcus sign (+,–) Anterior instability (1+, 2+, 3+) Posterior instability (1+, 2+, 3+) a ROM, range of motion; IR, internal rotation; ER, external rotation labeled “sleeper stretches.” In addition, strengthening of the periscapular musculature and rotator cuff is generally indicated to improve scapular stabilization and to minimize hyperextension and external rotation of the glenohumeral joint. Burkhart et al15 reported a 100% rate of return to preinjury level of throwing by 4 months in 96 overhead athletes treated for isolated SICK scapula with scapular muscular rehabilitation. When scapular dyskinesis is part of the spectrum of findings that can accompany pathologic internal impingement, symptomatic improvement may be expected. Another author reported the use of a similar regimen in all internal impingement patients except those with concurrent greater tuberosity fractures, citing failure to improve with these exercises as an indication for surgery.35 Approach to Surgical Management Indications for surgery include the failure to improve with conservative measures or inability to return to competitive play despite a prolonged rehabilitation protocol geared toward correction or resolution of the pathologic findings suggested by the physical examination and the imaging. Tibone et al76 demonstrated that acromioplasty is associated with low rates of return to competitive sports in throwing athletes. Therefore, subacromial decompression should be reserved for failure of primary arthroscopic interventions focused on the lesions of internal impingement in individuals with persistent signs of subacromial impingement. Mithöfer et al57 also suggested that internal impingement represents a relative contraindication to acromioplasty. Other investigators73 have supported this nihilistic approach to subacromial decompression in overhead athletes, with 1 team of authors characterizing classic impingement, if present, as a “secondary phenomenon.”1 However, subacromial bursectomy may be warranted in cases where substantial degrees of subacromial inflammation and bursitis are noted at the time of surgery1; subacromial bursectomy is frequently performed in throwing athletes by some clincians.71 The operative approach to patients with signs and symptoms of internal impingement should be pursued in a deliberate, methodical fashion. Because physical findings in the awake patient may be confusing in symptomatic throwing shoulders, the final therapeutic plan depends on the specific findings of the examination under anesthesia (EUA) and the diagnostic arthroscopy. Surgical intervention should be directed toward specific pathologic lesions that are believed to correspond to the patient’s symptoms or play a role in the complex pathophysiology of internal impingement. A graphic representation of the recommended algorithmic approach to diagnosis and management of internal impingement syndrome is represented in Figure 4. Examination under anesthesia must be performed before operative treatment of internal impingement is pursued. In most instances, bilateral EUA before surgical draping should be performed, even if regional anesthesia with sedation is used. The recommended components of a routine EUA for a patient with suspected internal impingement is shown in Table 1. The clinician must in all cases assess the glenohumeral joint for range of motion. Moreover, because of the importance of identifying even subtle degrees of subluxation, meticulous attention should be paid to the results of instability testing and the detection of a sulcus sign. While some aspects of the examination process listed in Table 1 may be performed routinely with arthroscopic shoulder surgeries, reliance on a systematic and exhaustive approach at the EUA stage provides critical information for evidence-based selection of surgical interventions over reliance upon dogmatic principles, given the often variable and sometimes confusing constellation of arthroscopic findings associated with internal impingement and the throwing shoulder. Findings on Diagnostic Arthroscopy and Treatment of Intra-articular Lesions Although preoperative planning based on physical examination and MRI findings is recommended, surgeons should perform a comprehensive diagnostic arthroscopy when approaching an internal impingement patient. Below we describe the results reported in the literature related to each of the major findings associated with internal impingement. Rotator Cuff Tears. Articular-sided rotator cuff tears are the most commonly seen lesions in patients with internal impingement. In the first major series reported from the Kerlan-Jobe Institute, 100% of a series of 41 throwing Downloaded from ajs.sagepub.com by Valentin Schroyen on June 25, 2009 1034 Heyworth and Williams The American Journal of Sports Medicine athletes showed abnormal contact between the posterosuperior glenoid rim and the rotator cuff when the arm was placed in the position of the “relocation test”; 93% of these patients were noted to have undersurface fraying of the rotator cuff.64 In another series reported by Walch et al,80 76% of patients were found to have undersurface rotator cuff tears and 71% were found to have posterosuperior labral fraying. Although few authors distinguish between the types of rotator cuff lesions that are associated with internal impingement, we believe the fraying often seen at the musculotendinous junction of the anterior infraspinatus generally warrants only minimal debridement; these lesions are not typically full thickness. More distal, articular-sided tears near the supraspinatus footprint may be more severe, particularly in older throwers, and may therefore necessitate repair. Despite the dearth of literature investigating management of rotator cuff pathology in elite athletes, we believe that the criteria used in nonathletes—debridement for small, partial-thickness (less than 50%) lesions and repair for tears that are greater than 50% of tendon thickness—represent a reasonable guide for overhead athletes as well. Some authors have advocated either partial articular-side tendon avulsion (PASTA) repair (side-to-side repair of the articular-sided supraspinatus tear and abrasion of the humeral head insertion point), or completion of the partial tear, followed by routine single or double-row repair with suture anchors.49,57 While repair remains an option for high-grade lesions of the rotator cuff, the literature suggests that most authors have not advocated repair. Sonnery-Cottet et al73 followed 25 tennis players with internal impingement for a mean of 3.8 years after arthroscopic debridement alone of articular-sided rotator cuff tears and posterosuperior labral lesions, reporting an 82% satisfaction rate. Notably, however, 20 of 22 patients who returned to sport complained of persistent pain with participation. Reynolds et al71 recently reported on 82 competitive pitchers who had undergone debridement of small, partial-thickness rotator cuff tears, noting an 82% rate of return to play. However, 45% of patients were unable to return to their previous level of play. Moreover, the reported rate of 45% may represent an overestimate, given that follow-up was obtained in only 41% of the total series. Among other confounding factors was a 96% rate of concomitant pathologic lesions in these patients, suggesting that isolated cuff tears are exceedingly rare in competitive throwers. Careful assessment of partial rotator cuff lesions is recommended with meticulous inspection for the presence of other lesions. Labral Tears. The glenoid labrum is typically injured or abnormal in patients with internal impingement. In a series of 41 overhead athletes studied by Paley et al,64 88% of throwing athletes demonstrated posterior superior labral changes. Interestingly, they showed that anterior labral fraying was present in 36% of patients as well. Notably, the authors distinguished the posterosuperior labral changes from frank SLAP tears, which they reported in only 10% of their series. This is in contrast to Andrews et al,2 who reported superior glenoid tears in 36 of 36 throwing athletes investigated. Likewise, other authors have reported rates of 70% posterosuperior labral detachment in symptomatic overhead athletes, with evidence for fraying or degenerative changes in 80%.57 Controversy exists regarding how substantial an etiologic role labral tears may have in throwers’ symptoms. Burkhart et al contend that type II SLAP lesions are the most common pathologic entities associated with symptomatic throwing shoulders, and reported an 87% return to preinjury function for 2 seasons or more in competitive throwers who underwent arthroscopic SLAP repair.14,58 Other authors have supported the notion of SLAP tears contributing to anterior pseudolaxity.5 The real frequency of clinically significant SLAP tears in patients with internal impingement is not known. However, the superior labrum should always be assessed, and we believe significant detachments of the superior labrum in young, athletic patients should be addressed with suture-anchor repair before considering operative treatment of anterior glenohumeral laxity. Interestingly, growing evidence suggests that for older or less active patients, and perhaps in the setting of revision surgery as well, labral repair, particularly for type II SLAP lesions, may be no better than debridement alone or biceps tenotomy or tenodesis, particularly when a concomitant rotator cuff lesion is seen and addressed with debridement.28 Although some authors have reported good results with biceps tenodesis for overhead athletes with anterior shoulder pain diagnosed as corocoid impingement syndrome,69 we believe that biceps tenodesis and tenotomy are rarely indicated in the young, athletic population with internal impingement, particularly elite throwers. Anterior Laxity and Instability. The prevalence and role of anterior laxity and instability in patients with internal impingement has not yet been fully established. Walch et al80 reported no cases of anterior instability in a 17-patient series of individuals with internal impingement. However, the authors did not report on the interventions performed in these patients or provide information on clinical follow-up. In another series,54 10 of 22 patients diagnosed with internal impingement were also found to have anterior instability. Only 55% of these patients, who were treated with rotator cuff and labral debridement alone, returned to their premorbid level of throwing 1 year postoperatively. In another series of patients with anterior instability with concurrent undersurface rotator cuff tears and posterior labral tears, treated only with debridement of the cuff and labral lesions,70 the authors reported only a 25% rate of return to sports and 37% satisfaction rate. Paley et al64 suggest that because of the high rate of anterior instability seen in throwing athletes in their studies, anterior capsulolabral reconstruction should be considered in conjunction with arthroscopic treatment of posterior impingement lesions. The authors cite previous supportive studies,38 which have suggested high rates of return to competitive play in throwers undergoing anterior capsulolabral reconstruction. Others have suggested that open anterior capsular repair may be the preferred treatment in some throwing athletes with signs of instability.1 In contrast, Levitz et al46 reported on treatment of internal impingement with use of thermal capsulorrhaphy as an adjunct to debridement of undersurface rotator cuff tears and labral debridement. At 30 months after arthroscopic surgery, 90% of throwing athletes treated with the combined technique Downloaded from ajs.sagepub.com by Valentin Schroyen on June 25, 2009 Internal Impingement of the Shoulder Vol. 37, No. 5, 2009 had returned to play, compared with 67% of patients treated with rotator cuff and labral debridement only. This investigation underscores the concept that addressing anterior microinstability may improve outcome in this patient population. However, based on more recent studies regarding the range of complications associated with the use of thermal capsulorrhaphy,29,45,82 we believe that arthroscopic suture capsulorrhaphy should be favored over thermal capsulorrhaphy for treatment of anterior microinstability or gross instability, which should be noted at the time of the examination under anesthesia, and can be executed by simply plicating the tissues of the anterior IGHL to the anterior labrum. Alternatively, suture anchors based at the anteroinferior glenoid can also be used to achieve the same end. In all cases, the instability phenomena noted during EUA should be eliminated after this portion of the procedure. Posterior Capsular Contracture. While some authors have emphasized treatment of anterior instability in throwers with internal impingement, Burkhart et al contend that contracture of the PIGHL and posterior capsule, resulting in GIRD, is the initial etiologic lesion responsible for the development of SLAP tears in the disabled throwing shoulder.12-16 Accordingly, they have advocated specific posterior capsular stretching exercises, called “sleeper stretches,” as first-line treatment for most symptomatic throwers and as a preventive measure for active pitchers to prevent dead-arm syndrome.14-16 The authors suggest that while rates of failure of these conservative measures are exceedingly low, particularly in younger pitchers, arthroscopic posteroinferior capsular release may be performed in conjunction with SLAP repairs in older pitchers who do not respond to stretching. We believe that GIRD is likely a commonly overlooked condition in symptomatic throwers and advocate a rigorous physical therapy regimen, with consideration of capsular release following diagnostic arthroscopy if nonoperative treatment fails. Humeral Head Lesions. As abnormalities of the humeral head are common in internal impingement, the humeral head should be taken through a full range of motion and assessed for chondral damage and osteochondral lesions. Osteochondral lesions in patients with internal impingement are most frequently encountered on posterior aspect of the humeral head, near the insertion of the posterior edge of the supraspinatus tendon. Unstable lesions may be debrided.57 One group of authors64 reported osteochondral lesions of the humeral head in 17% of 41 throwing athletes who underwent arthroscopy. The authors differentiated these lesions from Hill-Sachs lesions, noting them to be more superior, adjacent to the insertion of the supraspinatus insertion, and all smaller than 1 cm in diameter. Although most of the osteochondral findings consisted of grade II and grade III changes, there was 1 full-thickness cartilage defect in their series. In our experience, debridement of humeral head lesions is rarely necessary. Bony Glenoid Lesions. Although it is generally understood that mild posterior glenoid rounding or remodeling may be seen and is not amenable to operative treatment, the role of surgery to address Bennett lesions and similar bony posterior glenoid lesions remains an area of controversy. 1035 Interestingly, while Ferrari et al27 contend that such lesions require no operative treatment, Yoneda et al85 reported on a series of 16 patients with Bennett lesions who underwent arthroscopic debridement or “Bennettplasty.” The described surgical technique, which involves detachment (and subsequent repair) of the posteroinferior capsule for access to the lesion, supports the suggestion that such lesions are extracapsular. However, in contrast to Ferrari’s conclusion that the Bennett lesion represents an ossification of the posterior capsular soft tissues, the authors demonstrated that the bony overgrowth was contiguous with the glenoid in all cases.85 Although 88% of the patients in the series by Yoneda et al were satisfied at a minimum of 1 year after the procedure, most patients had soft tissue procedures (including bursectomy, rotator cuff debridement, Bankart repair, biceps and labral complex debridement or repair) performed concurrently, thus confounding any definitive conclusions about the efficacy of arthroscopic debridement of Bennett lesions. Meister et al54 were the first to report on arthroscopic resection of Bennett lesions, but performed such an intervention on only half of the 22 patients in whom such findings were detected preoperatively. The remaining patients underwent associated soft tissue treatments, the most common of which was debridement of partial-thickness tears of the rotator cuff. The authors concluded that when an exostotic lesion is seen in conjunction with posterior shoulder pain, arthroscopic debridement is appropriate, particularly when the lesion is larger than 100 mm2 in total size.54 Despite some supportive literature, we have typically not found debridement of posterior glenoid exostoses a useful tool in treating overhead athletes with internal impingement. SUMMARY Although the understanding of internal impingement as a unique condition of the shoulder continues to evolve, cadaveric, biomechanical, and clinical studies suggest that its cause is multifactorial and that a variety of anatomic structures are involved. Nevertheless, it seems clear that the thrower’s shoulder is particularly at risk for the development of internal impingement due to the repetitive and forceful nature of the overhead throw and its requirement that the arm be in the abducted and externally rotated position. Articular-sided, partial-thickness lesions at the musculotendinous junction of the infraspinatus tendon or at the distal insertion of the supraspinatus tendon, posterosuperior labral tears, and a loss of glenohumeral internal rotation are the hallmark findings of this condition. While physical examination findings alone seldom establish the diagnosis, posterior joint line tenderness, the posterior impingement sign, and the relocation sign should raise one’s index of suspicion for internal impingement. There are several commonly identified radiographic and MRI findings in patients with internal impingement, but the high frequency of similar abnormal findings in asymptomatic throwers makes correlation of such findings with clinical symptoms essential. A systematic approach to Downloaded from ajs.sagepub.com by Valentin Schroyen on June 25, 2009 1036 Heyworth and Williams The American Journal of Sports Medicine treatment of all sources of pathologic abnormalities that combines thoughtful consideration of patient complaints, imaging studies, findings from examination under anesthesia, and diagnostic arthroscopy provides optimal results. However, outcomes data on patients with a specific diagnosis of internal impingement remain sparse and additional research efforts are warranted. ACKNOWLEDGMENT The authors thank Dr Hollis Potter for her assistance with the preparation of this manuscript. REFERENCES 1. Altchek DW, Dines DM. Shoulder injuries in the throwing athlete. 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