Labral Injury and Posterior Impingement in Elite Tennis Players

  • Giovanni Di Giacomo
  • Nicola de Gasperis


The repetition of the abduction-external rotation movement of the arm during the overhead action carries an increased risk of overloading various structures around the shoulder. Pathologic contact between the posterior margin of the glenoid and the articular surface of posterosuperior rotator cuff tendons is known as posterior internal impingement. The chronic repeated compression or impingement leads to articular tears of the rotator cuff tendons as well as lesion of the superior labrum. Every overhead athlete requires a training program that strengthens all elements of the kinetic chain of the throwing motion. Patients with mild symptoms and early phases of the disorder need active rest, including a complete break from throwing along with physical therapy. Conservative management of SLAP lesions is often the first line of treatment. However, frequently, rehabilitation is unsuccessful; therefore, surgical intervention is often warranted to repair the labral lesion while addressing any concomitant pathology.

14.1 Introduction

The shoulder is the most mobile joint in the human body. Its anatomical design provides stability allowing a wide range of motion in all directions. This leads to a fragile equilibrium between stability and mobility, especially in the tennis player, who is trying to generate as much energy as possible for the serving motion. The repetition of the abduction-external rotation movement of the arm during the overhead action carries an increased risk of overloading various structures around the shoulder. The cause of shoulder pain in the overhead athlete is very difficult to identify and diagnose. Pathologic contact between the posterior margin of the glenoid and the articular surface of posterosuperior rotator cuff tendons is known as posterior internal impingement (PII) [1, 2, 3]. Young overhead athletes, continuously performing high velocity throwing actions over the years, usually go to specific osseous and soft tissue adaptations. Adaptive anatomic changes in throwers athletes that can lead to internal impingement include glenohumeral internal rotation deficit (GIRD), increased humeral and glenoid retroversion, acquired glenohumeral anterior-posterior instability, scapular weakness, and concomitant rotator cuff weakness. The chronic repeated compression or impingement leads to articular tears of the rotator cuff tendons as well as lesion of the superior labrum (SLAP lesions).

14.2 Biomechanical Aspects and Pathomechanics of Posterior Impingement and Labral Injuries in Tennis Players

To understand the function of the shoulder in the tennis serve, it is important to consider all aspects that contribute to this action. To create an optimal service motion with maximum power release, an intact kinetic chain function, a normal scapular function, and intact dynamic and static stabilizers of the shoulder are necessary. During the serve, the shoulder is part of a kinetic energy chain, in which the body is considered as a linked system of articulated segments, each part contributing to the final energy needed for hitting the ball. All segments (leg, hip, trunk, shoulder, elbow, and wrist) of the kinetic chain have to be in perfect shape to be able to transfer a sufficient level of energy to produce an effective serve. The kinetic chain allows generation, summation, and transfer of forces from the legs to the hand. Breakage of a link in the proximal part of the chain will lead to a higher demand on the more distally located segments. From this mechanism, it is clear that the more distal parts of the kinetic chain (shoulder, elbow, and wrist) are more susceptible to overuse and injury than the proximal parts [4]. The scapula has a key role in the function of the shoulder. It acts as a stable base for the humeral head during the overhead motion. It also has to move around the thoracic wall while the arm moves from early cocking to late cocking and follow-through (retraction/protraction) and has to move in an upward direction (rotation) in order to clear the acromion from the moving humeral head. Finally, it forms a stable base for the intrinsic and extrinsic muscles that control arm motion and the position of the scapula against the thorax. Fine-tuning of scapular motion is provided by coupling of muscle action (serratus anterior, upper and lower trapezius, latissimus dorsi, and the rhomboideus muscles). Dysfunction of these muscles leads to scapular dyskinesis, caused by inflexibility, weakness, and imbalance of the muscles. This dysfunction can be either primary through direct injury of the muscles or secondary as a result of pain-induced muscular inhibition [5, 6]. The term “SICK scapula” was introduced to describe a pathological state of the scapula, characterized by scapular malposition, inferior medial border prominence, coracoid pain and malposition, and kinesis abnormalities of the scapula. This syndrome, characterized by a drooping shoulder, is often seen in overhead athletes and is thought to contribute to the development of shoulder injuries. In most tennis players, such an abnormal position of the scapula can be detected. Although it seems that the affected shoulder has a lower position compared with the healthy side, actually there is scapular malposition consisting of forward tilting and protraction. According to Kibler [7], this clinical picture is associated with anterior coracoid-based pain, posterosuperior localized pain, and pain at the superolateral side of the shoulder (subacromial space, acromioclavicular joint). The role of the capsulolabral complex in the development of a shoulder injury remains a topic of debate. The most important function of the ligaments is to limit the range of motion of the shoulder joint. At the beginning of abduction-external rotation, it is mainly the dynamic stabilizers that keep the shoulder in a central position in the glenoid socket. At the end of the range of motion, the ligamentous structures become more important. At maximal abduction and external rotation, the inferior glenohumeral ligament (IGHL) is taut and limits further movement [8]. In the IGHL, a distinctive reinforcement is present, called the anterior band, which moves in front of the humeral head, providing a restraint to anterior and inferior displacement. Behind this, the posterior part of the IGHL shifts in front of the posterior side of the humeral head in abduction and internal rotation, protecting the head against posterior displacement. This dynamic interplay of the ligaments means that, in the overhead athlete, the shoulder is often susceptible to injury. Several explanations have been developed to clarify the pathogenesis of shoulder injuries in overhead athletes. As mentioned above, one explanation is that the repetitive nature of the serve causes microtrauma of the anterior capsule. Elongation of the ligaments may be responsible for subtle instability. The anterior displacement of the humeral head shifts the center of rotation to a more anterior position. This probably brings, in abduction and external rotation (ABER) position, the greater tuberosity and rotator cuff tendons close to the posterior glenoid, causing posterior internal impingement (PII) [9]. Although PII occurs in healthy shoulders, it can become pathological in the tennis player. PII is characterized by pain in the posterior aspect of the glenohumeral joint of overhead-throwing athletes during the late cocking phase of the throw, where the arm is in a position of full external rotation and abduction of at least 90°. The pain is due to a compression of the supraspinatus and infraspinatus tendons by the posteriorly rotated greater tuberosity of the humeral head against the posterosuperior portion of the glenoid. This occurs when the humeral shaft moves posteriorly beyond the plane of the scapular body during the cocking phase of throwing [10]. In this phase, if the scapular body and the humeral shaft fail to remain on the same plane of movement, rotator cuff tendons could remain between the humeral head and the glenoid rim causing PII. Another common finding in tennis players is a change in the rotational arc of the shoulder. Usually, there is an increase in external rotation and a decrease in internal rotation caused by posteroinferior capsular contracture [11, 12]. It has been suggested that there is an association of glenohumeral internal rotation deficit (GIRD) with the development of shoulder injuries [13]. If the limitation of internal rotation exceeds the gain in external rotation, resulting in a decrease in rotational arc (>10% of the contralateral side), the shoulder is susceptible to injury [7]. The stiffness and shortening of the posterior structures have consequences for stabilization of the shoulder during abduction and external rotation (Fig. 14.1). According to O’Brien et al., the IGHL is the most important stabilizing capsular component in the shoulder (anterior band in abduction-external rotation; posterior band in internal rotation) [14]. In the position of abduction and external rotation of the shoulder, the posterior IGHL is positioned under the humeral head. In the case of a functionally shortened posterior IGHL, a posterosuperior directed force exists, shifting the center of rotation of the shoulder to a more posterosuperior location. This posterosuperior shift can lead to anatomical lesions of the labral complex (SLAP lesion).
Fig. 14.1

Arthroscopic view of posterior capsule inflammation

14.3 Posterior Impingement

During the late cocking phase of throwing, the shoulder reaches a maximum external rotation of 170°–180°, while abduction is maintained at 90°–100°. In this ABER position, Walch et al. were the first to note that contact of the rotator cuff occurs between the greater tuberosity and the posterosuperior labrum [1]. This was called posterior internal impingement (PII). Following MRI studies showed that this contact is a physiological phenomenon and may occur in shoulders of normal individuals during the ABER position [15, 16]. However, as a result of the throwing biomechanics and the structural adaptations which occur in shoulders of these athletes, this contact is intensified and leads to pathological PII. This clinical syndrome is characterized by posterosuperior pain and glenohumeral joint dysfunction. Athletes participating overhead sports like tennis, baseball, water polo, and javelin are particularly at risk in developing PII. In these athletes, the pathological shift of the axis of glenohumeral joint contact/rotation occurs as the arm is brought in ABER position during the throwing or serving action, which leads to a no more physiological posterosuperior impingement [17]. There are two different theories which offer a biomechanical explanation for the change in the contact/rotational axis of the glenohumeral joint. In an earlier theory, Jobe postulated that anterior capsuloligamentous structures fail as a result of microtrauma caused by the repeated excessive strain occurring during the late cocking phase of throwing [3]. The injured anterior capsular structures are then less able to contain the humeral head leading to a posterior displacement of the contact point between the humeral head and glenoid which ultimately accentuates the contact of the rotator cuff between the posterosuperior labrum and the greater tuberosity in ABER position. In a more recent study, Burkhart proposed that the posteroinferior capsular contraction, caused by frequent microtrauma subsequent to repetitive distraction and rotational forces during the follow-through phase, was the initial mechanism of the glenohumeral contact point shift [11]. This theory is in line with the major clinical finding in patients with PII which is a glenohumeral internal rotational deficit (GIRD) [18]. Burkhart’s theory also offers an explanation for the physiological adaptations in throwers as well as the pathologies commonly associated with PII. The new glenohumeral point of contact allows greater external rotation. This external rotation gain arises from the increased clearance of the greater tuberosity over the glenoid during rotation as well as a decrease in the cam effect of the anterior capsule. The thrower is then subject to rotator cuff tears due to a combination of impingement and increased torsional and shearing forces resulting from the fibers overtwisting. The increased external rotation in the late cocking phase of throwing also creates more torsional stress upon the biceps anchor leading to a greater risk of SLAP lesion [19]. Shear stress and impingement could result in posterosuperior labral tears. Young throwing athletes have an increased number and frequency of smaller labral tears [19]. It is important to note that abnormal MRI findings do not necessarily correlate with the existence of pain or the likelihood of developing PII in the throwing shoulder. Halbrect et al. noted abnormal MRI findings indicating potential pathological PII in asymptomatic shoulders of throwing athletes [16].Their study raises the suggestion that MRI findings may manifest prior to the clinical picture of pathological PII (Fig. 14.2a, b). The presentation of PII can be classified into three stages [3]. In stage 1 the athlete complains of poor throwing or serving performance and discomfort in warming up when the shoulder is placed in the ABER position. In stage 2 the thrower is able to localize pain to the posterior aspect of the shoulder during the late cocking phase. Stage 3 is described as the persistence of symptoms after the end of the rehabilitation program.
Fig. 14.2

(a) MRI axial view of a professional tennis player showing posterior impingement signs on the humeral head and on the posterior-superior aspect of the glenoid. (b) MRI frontal view of a professional tennis player showing SLAP lesion signs

14.4 Clinical Evaluation and Treatment of Posterior Impingement

Internal impingement typically affects young to middle-aged adults; in most major case 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 [20, 21, 22, 23]. The majority of patients who have been identified with internal impingement are overhead athletes [24, 25]. Most patients present with a progressive decrease in throwing velocity or a loss of control and performance [10, 26, 27]. Chronic, diffuse posterior shoulder girdle pain is common in terms of the presenting complaint, but the pain may be localized to the joint line. 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 [28, 29]. Alternatively, patients may also have instability symptoms, such as apprehension or the sensation of subluxation with the arm in an abduction and external rotation position. Burkhart et al. reported an 80% rate of anterior coracoid pain in their series of 96 athletes with a disabled throwing shoulder, rather than isolated posterior shoulder pain, described as the most common presenting symptom [5]. Posterior glenohumeral joint line tenderness, increased external rotation, and decreased internal rotation (GIRD) are the most common physical examination findings in throwing athletes. With regard to concomitant increased external rotation, Myers et al. recently emphasized that throwers with pathological internal impingement exhibiting significantly increased posterior shoulder tightness and glenohumeral internal rotation deficits do not necessarily gain significantly increased external rotation [18]. In addition, scapular dyskinesis is a commonly reported finding. Characteristic features include a prominent inferior medial border of the scapula and the appearance of an inferiorly dropped throwing shoulder compared to the non-throwing side [30]. Meister et al. 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 [31]. 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. The sensitivity and specificity of the posterior impingement sign were 75.5% and 85%, respectively. MRI is considered the gold standard in the work-up of any young patient presenting with shoulder pain [9]. MR findings in internal impingement include articular-sided partial-thickness rotator cuff tears of the supraspinatus, infraspinatus, or both tendons and posterior or superior labral lesions [32]. The tears of the rotator cuff tendons are usually small and involve the articular surface. In addition, these athletes often present with associated posterosuperior labral abnormalities. Cysts and impaction deformity are also seen at the posterior greater tuberosity and can increase diagnostic confidence in the diagnosis of internal impingement. The vast majority of shoulder injuries in throwers should initially be treated with a conservative, nonoperative regime. Only significant structural injuries such as an acute rotator cuff tear, dislocation, or SLAP lesion deserve early surgical intervention. Every overhead athlete requires a training program that strengthens all elements of the kinetic chain of the throwing motion. Patients with mild symptoms and early phases of the disorder need active rest, including a complete break from throwing along with physical therapy. Anti-inflammatory measures to “cool down” the irritated shoulder can be beneficial in accelerating the rehabilitation process. This includes nonsteroidal anti-inflammatory drugs (NSAIDs) and occasionally a corticosteroid injection. Athletes with longer-lasting problems need a rehabilitation program emphasizing dynamic stability, rotator cuff strengthening, capsular stretching, and a scapular stabilization program [5, 33, 34]. Rehabilitation program Phase 1: the primary aims of the rehabilitation program are aimed at allowing the injured tissue to heal, modification of activity, decreasing pain and inflammation, on the re-establishment of a baseline dynamic stability, correction of the muscle balance, and restoration of proprioception. In addition, the athlete’s activities (such as throwing and exercises) must be modified to a pain-free level. Active-assisted motion exercises may be used to normalize shoulder motion, particularly shoulder internal rotation and horizontal adduction. The thrower should also perform specific stretches and flexibility exercises for the benefit of the posterior capsule and rotator cuff muscles. Rehabilitation program Phase 2: the primary goals are to intensify the strengthening program, continue to improve flexibility, and facilitate neuromuscular control. During this phase, the rehabilitation program is progressed to more aggressive isotonic strengthening activities with emphasis on restoration of the muscle balance. Selective muscle activation is also used to restore muscle balance and symmetry. Contractures of the posterior structures, the pectoralis minor muscle, and the short head of the biceps muscle also contribute to a glenohumeral internal rotation deficit and increase the anterior tilting of the scapula. Borstad et al. found the “sleeper stretch” to be effective for a stretch on the posterior aspect of the shoulder [35]. Several authors have emphasized the importance of scapular muscle strength and neuromuscular control as a contribution to normal shoulder function [30]. Isotonic exercise techniques are used to strengthen the scapular muscles. Overhead-throwing athletes often exhibit external rotator muscle weakness. Also during this second rehabilitation phase, the overhead-throwing athlete is instructed to perform core-strengthening exercises for the abdominal and lower back musculature. In addition, the athlete should perform lower extremity strengthening and participate in a running program including jogging and sprints. Upper extremity stretching exercises are continued as needed to maintain soft tissue flexibility. Rehabilitation program Phase 3: the goals are to initiate aggressive strengthening drills, enhance power and endurance, perform functional drills, and gradually initiate throwing activities. Dynamic stabilization drills are also performed to enhance proprioception and neuromuscular control. An interval throwing program may be initiated in this phase of rehabilitation. Rehabilitation program Phase 4: this phase usually involves progression of the interval throwing program as well as neuromuscular maintenance. The goal is to return to the full throwing velocity over the course of 3 months. To prevent the effects of overtraining or throwing, it is essential to instruct the athlete what to do through specific exercises throughout the year. A lack of improvement after 3 months, or an inability to return to competition within 6 months, constitutes failure of the nonoperative conservative management and thus should result in an additional diagnostic testing, and, if necessary, operative intervention should be considered. The following arthroscopic examination is performed in terms of a systematic review of the entire shoulder. The surgeon should carefully evaluate the entire shoulder and look for evidence of instability in the biceps tendon, biceps anchor, labrum, capsule, rotator interval, and the rotator cuff insertion. Surgical intervention should be directed toward specific pathological lesions believed to correspond to the patient’s symptoms or play a role in the complex pathophysiology of internal impingement. Despite this treatment, up to 90% of the patients can be expected to have persistent pain, although to a lesser degree, while playing tennis. Furthermore, only 50% of tennis players with posterosuperior glenoid impingement surgically treated can be expected to return to tennis at their preinjury level [25].

14.5 Labral Injury (SLAP Lesion)

The labrum is a fibrous structure strongly attached around the edge of the glenoid that increases the contact surface area between the glenoid and the humeral head [36]. The glenoid labrum enhances shoulder stability reducing humeral head translation, increasing the “concavity-compression” effect between the humeral head and the glenoid, increasing the overall depth of the glenoid fossa, and contributing to the stabilizing effect of the long head of the biceps anchor [36, 37, 38, 39, 40, 41]. The superior labrum is rather loose and mobile and has a “meniscal-like” aspect, while the inferior labrum appears rounded and more tightly attached to the glenoid rim. The labrum is attached to the lateral portion of the biceps anchor superiorly. Additionally, approximately 50% of the fibers of the long head of the biceps originate from the superior labrum, and the remaining fibers originate from the superior glenoid tubercle. There are several injury mechanisms that are speculated to be responsible for creating SLAP lesions. These mechanisms range from single traumatic events to repetitive microtraumatic injuries. Repetitive overhead activity is maybe the most common mechanism of injury responsible for producing SLAP injuries. Andrews et al. originally described the detachment of the superior labrum in a subset of throwing athletes in 1985 [42]. Later Snyder et al. introduced the term SLAP lesion—indicating an injury located within the superior labrum extending anterior to posterior [43]. They originally classified these lesions into four distinct categories based on the type of lesion present, emphasizing that this lesion may disrupt the origin of the long head of the biceps. Over time, modifications have been made to the initial classification system such that ten different types of SLAP tears have now been identified [44, 45, 46, 47, 48]. Andrews et al. first hypothesized that SLAP pathology in overhead-throwing athletes was the result of the high eccentric activity of the biceps during the arm deceleration and follow-through phases of the overhead throw [42, 49]. Burkhart et al. and Morgan et al. have hypothesized a “peel back” mechanism that produces SLAP lesion in the overhead athlete. They suggest that when the shoulder is placed in a position of abduction and maximal external rotation, the rotation produces a twist at the base of the biceps, transmitting torsional force to the anchor [48, 50]. Furthermore, Jobe and Walch et al. have also demonstrated that when the arm is in a maximally externally rotated position, there is contact between the posterior-superior labral lesions and the rotator cuff [1, 3]. A recent study conducted at the authors’ research center simulated each of these mechanisms using cadaveric models [40]. Nine pairs of cadaveric shoulders were loaded to biceps anchor complex failure in either a position of simulated in-line loading (similar to the deceleration phase of throwing) or simulated peel back mechanism (similar to the cocking phase of overhead throwing). Results showed that seven of eight of the in-line loading group failed in the midsubstance of the biceps tendon with one of eight fracturing at the supraglenoid tubercle. However, all eight of the simulated peel back group failures resulted in a type II SLAP lesion. The ultimate strength of the biceps anchor was significantly different when the two loading techniques were compared. The biceps anchor demonstrated significantly higher ultimate strength with the in-line loading (508 N) as opposed to the ultimate strength seen during the peel back loading mechanism (202 N). In theory, SLAP lesions most likely occur in overhead athletes from a combination of these two previously described forces. The eccentric biceps activity during deceleration may serve to weaken the biceps-labrum complex, while the torsional peel back force may result in the posterosuperior detachment of the labral anchor. Several authors have also reported a strong correlation between SLAP lesions and glenohumeral instability. Normal biceps function and glenohumeral stability are dependent on a stable superior labrum and biceps anchor. Pagnani et al. found that a complete lesion of the superior portion of the labrum large enough to destabilize the insertion of the biceps was associated with significant increases in anterior-posterior and superior-inferior glenohumeral translation [37]. Reinold et al. reported that in a series of 130 overhead athletes with symptomatic hyperlaxity undergoing thermal-assisted capsular shrinkage (TACS) of the glenohumeral joint, 69% exhibited superior labral degeneration, while 35% had type II SLAP lesions [51]. Furthermore, Kim et al. reported that maximal biceps activity occurred when the shoulder was abducted to 90° and externally rotated to 120° in patients with anterior instability [52]. Because this position is remarkably similar to the cocking position of the overhand throwing motion, the finding of instability may cause or facilitate the progression of internal impingement (impingement of the infraspinatus on the posterosuperior glenoid rim) in the overhead athlete.

Although this tear pattern has been described and studied for quite some time, the ideal treatment of these injuries remains elusive. Indications for operative repair remain unclear with increasing reports of complications and suboptimal outcomes within the literature [53, 54]. With the knowledge that degenerative changes of the superior labrum occur commonly with age and improvements in magnetic resonance imaging quality, SLAP tears are becoming a more frequent diagnosis. Zhang et al. recently reviewed the demographic trends of SLAP repairs in the United States using a publicly available database and found that the number of SLAP repairs significantly increased over time from 2004 to 2009 [55]. This increase in the number of diagnosed SLAP tears that are treated with arthroscopic repair is interesting because the ideal treatment for SLAP tears has not been elucidated and several studies have shown increasing risk of complications and poor outcomes with inability to return to sport particularly in overhead-throwing athletes.

14.6 Clinical Evaluation and Treatment of SLAP Lesion

Clinical examination is essential to establishing the potential presence of glenoid labral pathology. Clinical examination to detect SLAP lesions is often difficult because of the common presence of concomitant pathology in patients presenting with this type of condition. Mileski and Snyder reported that 29% of their patients with SLAP lesions exhibited partial-thickness rotator cuff tears, 11% complete rotator cuff tears, and 22% Bankart lesions of the anterior glenoid [56]. Kim et al. prospectively analyzed the clinical features of different types of SLAP lesion as they vary with patient population in 139 cases [57]. They demonstrated that type I SLAP lesions are typically associated with rotator cuff pathology, while type III and IV lesions are associated with traumatic instability. They also note that injuries presenting concomitant with type II SLAP lesions vary by patient age, with older patients presenting more often with rotator cuff pathology and younger patients instability. Pain complaints are typically intermittent and are most frequently associated with overhead activity. Overhead athletes typically report a loss of velocity and accuracy along with general uneasiness of the shoulder. Probably the most predictive subjective complaint in the athlete is the inability to perform sporting activities at a high level. The physical examination should include a complete evaluation of bilateral passive and active range of glenohumeral motion with particular emphasis placed on determining the presence, persistence, and behavior of any painful arc of motion. A wide variety of potentially useful special test maneuvers have been described to help determine the presence of labral pathology in an overhead thrower, including the active compression test, the biceps load test, the biceps load test II, the pain provocation test, the resisted supination and external rotation test, the pronated load test, and the modified dynamic labral shear test [52, 58, 59, 60, 61, 62]. Several authors also recommend MR enhanced arthrography in order to detect SLAP lesions, but its reliability for the diagnosis is disputed [63, 64, 65, 66]. Nevertheless definitive diagnosis of SLAP lesion requires arthroscopy. Conservative management of SLAP lesions is often the first line of treatment and has been shown to be successful. Edwards et al. showed that 10 of 15 overhead throwers with a known SLAP lesion who were treated with nonoperative management were able to return to play at the same level or better [67]. However, frequently, rehabilitation is unsuccessful; therefore, surgical intervention is often warranted to repair the labral lesion while addressing any concomitant pathology. Treatment in these patients remains somewhat controversial [68, 69, 70, 71]. Not all SLAP tears require surgical intervention, and approximately 70–80% of patients who undergo surgical fixation can expect to return to their previous sports [44, 67, 72, 73, 74]. The marginal benefits of SLAP repair surgery have led some surgeons to consider biceps tenodesis as an alternative procedure [73, 75, 76, 77, 78, 79]. Several open and arthroscopic tenodesis techniques have been described, but none of them seem to be superior to another. To date the literature does not provide evidence to support one technique over the other, and there are advantages to each procedure. The lack of physical exam maneuvers and diagnostic tests to reliably diagnose SLAP tears has led to a significant increase in the number of SLAP repairs performed in the United States [55]. Most SLAP repairs are performed for type II SLAP tears (Figs. 14.3 and 14.4). The outcomes following debridement (without repair) of unstable type II and IV SLAP lesions have been poor, and thus these two types of lesions should be repaired in order to restore the normal anatomy [80]. In the presence of a type II SLAP lesion, the superior labrum should be reattached to the glenoid and the biceps anchor stabilized. The type II lesion is often stabilized utilizing suture anchors. Treatment of type IV SLAP lesions is generally based on the extent to which the biceps anchor is involved. When biceps involvement is less than approximately 30% of the entire anchor, the torn tissue is typically resected and the superior labrum reattached. If the biceps tear is more substantial, a side-to-side repair of the biceps tendon, in addition to reattachment of the superior labrum, is generally performed. However, if the biceps tear is extensive enough to substantially alter the biceps origin, a biceps tenodesis or tenotomy is more practical than a direct repair. Weber et al. recently reviewed data from the American Board of Orthopaedic Surgery Part II Database from 2003 to 2007 to determine the incidence rates, complications, and outcomes for SLAP repairs [53]. The most concerning conclusion was that only 26.3% of patients stated that they were pain-free, whereas only 13.1% rated their function as normal. Recently, multiple authors have reported outcomes of SLAP repairs as unpredictable [53, 54]. Provencher et al. reviewed 179 patients who underwent repair for a type II SLAP tear [81]. At a mean follow-up of 40.4 months, 37% were classified as a failure, and 28% underwent a revision. This study also found that the only risk factor that significantly increased a patient’s risk of failure was age more than 36. Similarly, Boileau et al. found that 60% of patients who underwent repair for a type II SLAP tear were disappointed because of persistent pain and only 20% were able to return to sports at their preinjury level [73]. This was in comparison to a group of patients who underwent arthroscopic biceps tenodesis for a type II SLAP tear and showed a 93% satisfaction rate and an 87% return to the previous level of sport. Erickson et al. showed that the number of biceps tenodeses significantly increased over time, whereas that of SLAP repairs significantly decreased over time [82]. Although some argue that SLAP repairs restore arm function better than biceps tenodesis, Chalmers et al. proved this to be inaccurate [75]. The authors evaluated 18 pitchers (7 uninjured controls, 6 after a SLAP repair, and 5 after a subpectoral biceps tenodesis) and found that pitchers who underwent a SLAP repair had altered patterns of thoracic rotation compared with the controls and pitchers who had undergone a biceps tenodesis. Laughlin et al. similarly found altered mechanics in 13 collegiate and professional pitchers who underwent SLAP repairs compared with a group of control pitchers [83]. Therefore, in high-level athletes, biceps tenodesis is a reliable option compared with SLAP repair. Because overtreatment of SLAP tears may result in increased complications such as stiffness, persistent pain, and need for revision surgery, the future treatment of SLAP tears will likely see an increase in biceps tenodesis and a decrease in SLAP repairs based on the outcomes reported in the literature and the high risk of failure and complications seen with SLAP repairs.
Fig. 14.3

Arthroscopic view of a type II SLAP lesion

Fig. 14.4

Arthroscopic view of a type II SLAP lesion repair


The vast majority of shoulder injuries in overhead athletes should initially be approached with a conservative treatment. Only significant structural injuries deserve early surgical intervention. Every overhead athlete requires a training program that strengthens all elements of the kinetic chain of the throwing motion. Further investigation is needed to help determine which patients are likely to succeed with nonoperative treatment and those who will predictably do well with surgical repair. Most clinical studies on this topic are from single institutions and lack the power necessary to definitively draw conclusions about the superiority of specific management options.


  1. 1.
    Walch G, Boileau P, Noel E, Donell ST. Impingement of the deep surface of the supraspinatus tendon on the posterosuperior glenoid rim: an arthroscopic study. J Shoulder Elb Surg. 1992;1:238–45.CrossRefGoogle Scholar
  2. 2.
    Walch G, Liotard JP, Boileau P, Noel E. Posterosuperior glenoid impingement. Another shoulder impingement. Rev Chir Orthop Reparatrice Appar Mot. 1991;77:571–4.PubMedGoogle Scholar
  3. 3.
    Jobe CM. Posterior superior glenoid impingement: expanded spectrum. Arthroscopy. 1995;11:530–6.CrossRefGoogle Scholar
  4. 4.
    Van der Hoeven H, Kibler WB. Shoulder injuries in tennis players. Br J Sports Med. 2006;40:435–40. Scholar
  5. 5.
    Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology. Part III: The SICK scapula, scapular dyskinesis, the kinetic chain, and rehabilitation. Arthroscopy. 2003;19:641–61. S074980630300389X.CrossRefGoogle Scholar
  6. 6.
    Burkhart SS, Morgan CD, Kibler WB. Shoulder injuries in overhead athletes. The “dead arm” revisited. Clin Sports Med. 2000;19:125–58.CrossRefGoogle Scholar
  7. 7.
    Kibler WB. The role of the scapula in athletic shoulder function. Am J Sports Med. 1998;26:325–37.CrossRefGoogle Scholar
  8. 8.
    Gagey OJ, Gagey N. The hyperabduction test: an assessment of the laxity of the inferior glenohumeral ligament. J Bone Joint Surg Br. 2001;83:69–74.CrossRefGoogle Scholar
  9. 9.
    Heyworth BE, Williams RJ III. Internal impingement of the shoulder. Am J Sports Med. 2009;37:1024–37. Scholar
  10. 10.
    Cools AM, Declercq G, Cagnie B, Cambier D, Witvrouw E. Internal impingement in the tennis player: rehabilitation guidelines. Br J Sports Med. 2008;42:165–71. Scholar
  11. 11.
    Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology. Part I: Pathoanatomy and biomechanics. Arthroscopy. 2003;19:404–20.CrossRefGoogle Scholar
  12. 12.
    Jobe CM. Superior glenoid impingement. Current concepts. Clin Orthop Relat Res. 1996;330:98–107.CrossRefGoogle Scholar
  13. 13.
    Myers JB, Laudner KG, Pasquale MR, et al. Posterior capsular tightness in throwers with internal impingement. Presented at the Annual Meeting of Orthopaedic Surgeons, February 23–27; 2005.Google Scholar
  14. 14.
    O’Brien SJ, Neves MC, Arnoczky SP, et al. The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med. 1990;18:449–56.CrossRefGoogle Scholar
  15. 15.
    Gold GE, Pappas GP, Blemker SS, et al. Abduction and external rotation in shoulder impingement: an open MR study on healthy volunteers-initial experience. Radiology. 2007;244:815–22.CrossRefGoogle Scholar
  16. 16.
    Halbrect JL, Tirman P, Atkin D. Internal impingement of the shoulder: comparison of findings between the throwing and non-throwing shoulders of college baseball players. Arthroscopy. 1999;15:253–8.CrossRefGoogle Scholar
  17. 17.
    Fessa CK, Peduto A, Linklater J, Tirman P. Posterosuperior glenoid internal impingement of the shoulder in the overhead athlete: pathogenesis, clinical features and MR imaging findings. J Med Imaging Radiat Oncol. 2015;59:182–7. Scholar
  18. 18.
    Myers JB, Laudner KG, Pasquale MR, Bradley JP, Lephart SM. Glenohumeral range of motion deficits and posterior shoulder tightness in throwers with pathologic internal impingement. Am J Sports Med. 2006;34:385–91. Scholar
  19. 19.
    Jbara M, Chen Q, Marten P, Morcos M, Beltran J. Shoulder MR arthrography: how, why, when. Radiol Clin N Am. 2005;43:683–92.CrossRefGoogle Scholar
  20. 20.
    Braun S, Kokmeyer D, Millett PJ. Shoulder injuries in the throwing athlete. J Bone Joint Surg Am. 2009;91:966–78. Scholar
  21. 21.
    Struhl S. Anterior internal impingement: an arthroscopic observation. Arthroscopy. 2002;18:2–7. S0749806302767625.CrossRefGoogle Scholar
  22. 22.
    Tirman PF, Smith ED, Stoller DW, Fritz RC. Shoulder imaging in athletes. Semin Musculoskelet Radiol. 2004;8:29–40. Scholar
  23. 23.
    Kirchhoff C, Imhoff AB. Posterosuperior and anterosuperior impingement of the shoulder in overhead athletes - evolving concepts. Inter Orthop (SICOT). 2010;34:1049–58. Scholar
  24. 24.
    Werner SL, Guido JA Jr, Stewart GW, McNeice RP, VanDyke T, Jones DG. Relationships between throwing mechanics and shoulder distraction in collegiate baseball pitchers. J Shoulder Elb Surg. 2007;16:37–42. Scholar
  25. 25.
    Sonnery-Cottet B, Edwards TB, Noel E, Walch G. Results of arthroscopic treatment of posterosuperior glenoid impingement in tennis players. Am J Sports Med. 2002;30:227–32.CrossRefGoogle Scholar
  26. 26.
    Cools AM, Cambier D, Witvrouw EE. Screening the athlete’s shoulder for impingement symptoms: a clinical reasoning algorithm for early detection of shoulder pathology. Br J Sports Med. 2008;42:628–35. Scholar
  27. 27.
    Curtis AS, Deshmukh R. Throwing injuries: diagnosis and treatment. Arthroscopy. 2003;19(Suppl 1):80–5. Scholar
  28. 28.
    Fleisig GS, Andrews JR, Dillman CJ, Escamilla RF. Kinetics of baseball pitching with implications about injury mechanisms. Am J Sports Med. 1995;23:233–9.CrossRefGoogle Scholar
  29. 29.
    Gerber C, Sebesta A. Impingement of the deep surface of the subscapularis tendon and the reflection pulley on the anterosuperior glenoid rim: a preliminary report. J Shoulder Elb Surg. 2000;9:483–90. Scholar
  30. 30.
    Kibler WB. Scapular involvement in impingement: signs and symptoms. Instr Course Lect. 2006;55:35–43.PubMedGoogle Scholar
  31. 31.
    Meister K. Internal impingement in the shoulder of the overhand athlete: pathophysiology, diagnosis, and treatment. Am J Orthop. 2000;29:433–8.PubMedGoogle Scholar
  32. 32.
    Wörtler K. Shoulder injuries in overhead sports. Radiologe. 2010;50(5):453–9.CrossRefGoogle Scholar
  33. 33.
    Wilk KE, Meister K, Andrews JR. Current concepts in the rehabilitation of the overhead throwing athlete. Am J Sports Med. 2002;30:136–51.CrossRefGoogle Scholar
  34. 34.
    Manske RC, Grant-Nierman M, Lucas B. Shoulder posterior internal impingement in the overhead athlete. Int J Sports Phys Ther. 2013;8(2):194–204.PubMedPubMedCentralGoogle Scholar
  35. 35.
    Borstad JD, Ludewig PM. Comparison of scapular kinematics between elevation and lowering of the arm in the scapular plane. Clin Biomech. 2002;17:650–9. S0268003302001365.CrossRefGoogle Scholar
  36. 36.
    Cooper DE, Arnoczky SP, O’Brien SJ, Warren RF, Di Carlo E, Allen AA. Anatomy, histology, and vascularity of the glenoid labrum. An anatomical study. J Bone Joint Surg Am. 1992;74(1):46–52.CrossRefGoogle Scholar
  37. 37.
    Pagnani MJ, Deng XH, Warren RF, Torzilli PA, Altchek DW. Effect of lesions of the superior portion of the glenoid labrum on glenohumeral translation. J Bone Joint Surg Am. 1995;77(7):1003–10.CrossRefGoogle Scholar
  38. 38.
    Wilk KE, Arrigo CA. Current concepts in the rehabilitation of the athletic shoulder. J Orthop Sports Phys Ther. 1993;18(1):365–78.CrossRefGoogle Scholar
  39. 39.
    Wilk KE, Arrigo CA, Andrews JR. Current concepts: the stabilizing structures of the glenohumeral joint. J Orthop Sports Phys Ther. 1997;25(6):364–79.CrossRefGoogle Scholar
  40. 40.
    Shepard MF, Dugas JR, Zeng N, Andrews JR. Differences in the ultimate strength of the biceps anchor and the generation of type II superior labral anterior posterior lesions in a cadaveric model. Am J Sports Med. 2004;32(5):1197–201.CrossRefGoogle Scholar
  41. 41.
    Wilk KE, Andrews JR, Arrigo CA. The physical examination of the glenohumeral joint: emphasis on the stabilizing structures. J Orthop Sports Phys Ther. 1997;25(6):380–9.CrossRefGoogle Scholar
  42. 42.
    Andrews JR, Carson WG Jr, McLeod WD. Glenoid labrum tears related to the long head of the biceps. Am J Sports Med. 1985;13(5):337–41.CrossRefGoogle Scholar
  43. 43.
    Snyder SJ, Karzel RP, Del Pizzo W, Ferkel RD, Friedman MJ. SLAP lesions of the shoulder. Arthroscopy. 1990;6(4):274–9.CrossRefGoogle Scholar
  44. 44.
    Knesek M, Skendzel JG, Dines JS, Altchek DW, Allen AA, Bedi A. Diagnosis and management of superior labral anterior posterior tears in throwing athletes. Am J Sports Med. 2013;41:444–60. Scholar
  45. 45.
    Powell SE, Nord KD, Ryu RKN. The diagnosis, classification, and treatment of SLAP lesions. Oper Tech Sports Med. 2004;12:99–110.CrossRefGoogle Scholar
  46. 46.
    Gartsman GM, Hammerman SM. Superior labrum, anterior and posterior lesions. When and how to treat them. Clin Sports Med. 2000;19(1):115–24.CrossRefGoogle Scholar
  47. 47.
    Maffet MW, Gartsman GM, Moseley B. Superior labrum-biceps tendon complex lesions of the shoulder. Am J Sports Med. 1995;23(1):93–8.CrossRefGoogle Scholar
  48. 48.
    Morgan CD, Burkhart SS, Palmeri M, Gillespie M. Type II SLAP lesions: three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy. 1998;14(6):553–65.CrossRefGoogle Scholar
  49. 49.
    Andrews JR, Broussard TS, Carson WG. Arthroscopy of the shoulder in the management of partial tears of the rotator cuff: a preliminary report. Arthroscopy. 1985;1(2):117–22.CrossRefGoogle Scholar
  50. 50.
    Burkhart SS, Morgan CD. The peel-back mechanism: its role in producing and extending posterior type II SLAP lesions and its effect on SLAP repair rehabilitation. Arthroscopy. 1998;14(6):637–40.CrossRefGoogle Scholar
  51. 51.
    Reinold MM, Wilk KE, Hooks TR, Dugas JR, Andrews JR. Thermal-assisted capsular shrinkage of the glenohumeral joint in overhead athletes: a 15- to 47-month follow-up. J Orthop Sports Phys Ther. 2003;33(8):455–67.CrossRefGoogle Scholar
  52. 52.
    Kim SH, Ha KI, Ahn JH, Kim SH, Choi HJ. Biceps load test II: a clinical test for SLAP lesions of the shoulder. Arthroscopy. 2001;17(2):160–4.CrossRefGoogle Scholar
  53. 53.
    Weber SC, Martin DF, Seiler JG III, Harrast JJ. Superior labrum anterior and posterior lesions of the shoulder: incidence rates, complications, and outcomes as reported by American Board of Orthopedic Surgery. Part II candidates. Am J Sports Med. 2012;40:1538–43.CrossRefGoogle Scholar
  54. 54.
    Erickson J, Lavery K, Monica J, Gatt C, Dhawan A. Surgical treatment of symptomatic superior labrum anterior-posterior tears in patients older than 40 years: a systematic review. Am J Sports Med. 2015;43:1274–82.CrossRefGoogle Scholar
  55. 55.
    Zhang AL, Kreulen C, Ngo SS, Hame SL, Wang JC, Gamradt SC. Demographic trends in arthroscopic SLAP repair in the United States. Am J Sports Med. 2012;40:1144–7.CrossRefGoogle Scholar
  56. 56.
    Mileski RA, Snyder SJ. Superior labral lesions in the shoulder: pathoanatomy and surgical management. J Am Acad Orthop Surg. 1998;6(2):121–31.CrossRefGoogle Scholar
  57. 57.
    Kim TK, Queale WS, Cosgarea AJ, McFarland EG. Clinical features of the different types of SLAP lesions: an analysis of one hundred and thirty-nine cases. J Bone Joint Surg Am. 2003;85-A(1):66–71.CrossRefGoogle Scholar
  58. 58.
    O’Brien SJ, Pagnani MJ, Fealy S, McGlynn SR, Wilson JB. The active compression test: a new and effective test for diagnosing labral tears and acromioclavicular joint abnormality. Am J Sports Med. 1998;26(5):610–3.CrossRefGoogle Scholar
  59. 59.
    Kim SH, Ha KI, Han KY. Biceps load test: a clinical test for superior labrum anterior and posterior lesions in shoulders with recurrent anterior dislocations. Am J Sports Med. 1999;27(3):300–3.CrossRefGoogle Scholar
  60. 60.
    Mimori K, Muneta T, Nakagawa T, Shinomiya K. A new pain provocation test for superior labral tears of the shoulder. Am J Sports Med. 1999;27(2):137–42.CrossRefGoogle Scholar
  61. 61.
    Myers TH, Zemanovic JR, Andrews JR. The resisted supination external rotation test: a new test for the diagnosis of superior labral anterior posterior lesions. Am J Sports Med. 2005;33(9):1315–20.CrossRefGoogle Scholar
  62. 62.
    Kibler WB, Sciascia AD, Hester P, Dome D, Jacobs C. Clinical utility of traditional and new tests in the diagnosis of biceps tendon injuries and superior labrum anterior and posterior lesions in the shoulder. Am J Sports Med. 2009;37(9):1840–7. Scholar
  63. 63.
    Bencardino JT, Beltran J, Rosenberg ZS, Rokito A, Schmahmann S, Mota J, et al. Superior labrum anterior-posterior lesions: diagnosis with MR arthrography of the shoulder. Radiology. 2000;214(1):267–71.CrossRefGoogle Scholar
  64. 64.
    Nam EK, Snyder SJ. The diagnosis and treatment of superior labrum, anterior and posterior (SLAP) lesions. Am J Sports Med. 2003;31(5):798–810.CrossRefGoogle Scholar
  65. 65.
    Green MR, Christensen KP. Magnetic resonance imaging of the glenoid labrum in anterior shoulder instability. Am J Sports Med. 1994;22(4):493–8.CrossRefGoogle Scholar
  66. 66.
    Liu SH, Henry MH, Nuccion SL. A prospective evaluation of a new physical examination in predicting glenoid labral tears. Am J Sports Med. 1996;24(6):721–5.PubMedGoogle Scholar
  67. 67.
    Edwards SL, Lee JA, Bell JE, Packer JD, Ahmad CS, Levine WN, et al. Nonoperative treatment of superior labrum anterior posterior tears: improvements in pain, function, and quality of life. Am J Sports Med. 2010;38(7):1456–61. Scholar
  68. 68.
    Bedi A, Allen AA. Superior labral lesions anterior to posterior - evaluation and arthroscopic management. Clin Sports Med. 2008;27:607–30. Scholar
  69. 69.
    Keener JD, Brophy RH. Superior labral tears of the shoulder: pathogenesis, evaluation, and treatment. J Am Acad Orthop Surg. 2009;17:627–37.CrossRefGoogle Scholar
  70. 70.
    McCormick F, Bhatia S, Chalmers P, Gupta A, Verma N, Romeo AA. The management of type II superior labral anterior to posterior injuries. Orthop Clin North Am. 2014;45:121–8. Scholar
  71. 71.
    Kibler WB, Sciascia A. Current practice for the surgical treatment of SLAP lesions: a systematic review. Arthroscopy. 2016;32(4):669–83. Scholar
  72. 72.
    Steinhaus ME, Makhni EC, Lieber AC, Kahlenberg CA, Gulotta LV, Romeo AA, Verma NN. Variable reporting of functional outcomes and return to play in superior labrum anterior and posterior tear. J Shoulder Elb Surg. 2016;25(11):1896–905. Scholar
  73. 73.
    Boileau P, Parratte S, Chuinard C, Roussanne Y, Shia D, Bicknell R. Arthroscopic treatment of isolated type II SLAP lesions: biceps tenodesis as an alternative to reinsertion. Am J Sports Med. 2009;37:929–36. Scholar
  74. 74.
    Voos JE, Pearle AD, Mattern CJ, Cordasco FA, Allen AA, Warren RF. Outcomes of combined arthroscopic rotator cuff and labral repair. Am J Sports Med. 2007;35:1174–9. Scholar
  75. 75.
    Chalmers PN, Trombley R, Cip J, Monson B, Forsythe B, Nicholson GP, et al. Postoperative restoration of upper extremity motion and neuromuscular control during the overhand pitch: evaluation of tenodesis and repair for superior labral anterior-posterior tears. Am J Sports Med. 2014;42:2825–36. Scholar
  76. 76.
    Denard PJ, Lädermann A, Parsley BK, Burkhart SS. Arthroscopic biceps tenodesis compared with repair of isolated type II SLAP lesions in patients older than 35 years. Orthopedics. 2014;37:e292–7. Scholar
  77. 77.
    Ek ET, Shi LL, Tompson JD, Freehill MT, Warner JJ. Surgical treatment of isolated type II superior labrum anterior-posterior (SLAP) lesions: repair versus biceps tenodesis. J Shoulder Elb Surg. 2014;23:1059–65. Scholar
  78. 78.
    Gottschalk MB, Karas SG, Ghattas TN, Burdette R. Subpectoral biceps tenodesis for the treatment of type II and IVsuperior labral anterior and posterior lesions. Am J Sports Med. 2014;42:2128–35. Scholar
  79. 79.
    Tayrose GA, Karas SG, Bosco J. Biceps tenodesis for type II SLAP tears. Bull Hosp Jt Dis (2013). 2015;73:116–21.Google Scholar
  80. 80.
    Altchek DW, Warren RF, Wickiewicz TL, Ortiz G. Arthroscopic labral debridement. A three-year follow-up study. Am J Sports Med. 1992;20(6):702–6.CrossRefGoogle Scholar
  81. 81.
    Provencher MT, McCormick F, Dewing C, McIntire S, Solomon D. A prospective analysis of 179 type 2 superior labrum anterior and posterior repairs: outcomes and factors associated with success and failure. Am J Sports Med. 2013;41:880–6.CrossRefGoogle Scholar
  82. 82.
    Erickson BJ, Jain A, Abrams GD, Nicholson GP, Cole BJ, Romeo AA, Verma NN. SLAP lesions: trends in treatment. Arthroscopy. 2016;32(6):976–81. Scholar
  83. 83.
    Laughlin WA, Fleisig GS, Scillia AJ, Aune KT, Cain EL Jr, Dugas JR. Deficiencies in pitching biomechanics in baseball players with a history of superior labrum anterior posterior repair. Am J Sports Med. 2014;42:2837–41.CrossRefGoogle Scholar

Copyright information

© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  • Giovanni Di Giacomo
    • 1
  • Nicola de Gasperis
    • 2
  1. 1.Department of Orthopaedics and TraumaConcordia HospitalRomeItaly
  2. 2.Concordia Hospital for Special SurgeryRomeItaly

Personalised recommendations