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Diagnosis and management of superior labrum anterior posterior lesions in overhead athletes
  1. Geoffrey D Abrams,
  2. Marc R Safran
  1. Department of Orthopaedic Surgery, Stanford University, Redwood City, California, USA
  1. Correspondence to Professor Marc R Safran, Department of Orthopaedic Surgery, Stanford University, 450 Broadway Street, M/C 6342, Redwood City, CA 94063, USA; msafran{at}stanford.edu

Abstract

Shoulder pain is a common complaint in overhead athletes, and superior labrum anterior posterior (SLAP) lesions are a common cause of this pain. The pathological cascade which results in the SLAP lesion consists of a combination of posterior inferior capsular tightness and scapular dyskinesis, resulting in a ‘peel back’ phenomenon at the biceps anchor and leading to the SLAP tear. Physical exam tests vary in their sensitivity and specificity in detecting SLAP lesions, so MRI is helpful in demonstrating the anatomical alteration. Treatment can be conservative, with posterior inferior capsular stretching and scapular open and closed chain exercises. Many SLAP lesions in overhead athletes require surgical treatment that involves repair of the labrum back to the glenoid. Treatment of concomitant injuries such as rotator cuff tears and Bankart lesions in conjunction with the SLAP repair may be necessary.

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Introduction

Overhead athletes place tremendous stress on the soft tissue and osseous structures of the glenohumeral (GH) joint.1 Shoulder motion has been shown to be altered among those participating in baseball,2,,7 tennis,8 9 swimming10 and other overhead activity sports.11 These varied mobility patterns are thought to arise from structural changes in the GH ligaments, labrum, muscles and osseous structures as an adaptation to long-term overhead activity sports participation.12 13 These structural changes can lead to alterations in motions and forces at the GH joint. These alterations may place stress on the labrum, with resulting injury and decreased performance.

Labral lesions and anatomy

Anatomically, the labrum serves as the glenoid attachment for the GH ligaments and for the long head of the biceps tendon. The glenoid labrum surrounds the glenoid, functionally deepening it, increasing the surface area of contact with the humeral head and thus resisting translation of the humeral head relative to the glenoid by functioning as a buttress. It has been characterised as a washer, capable of deforming and modifying loads and pressure at the joint.

There is anatomical variability in the superior labral complex. One variant consists of an absent anterior superior labral complex associated with a prominent ‘cord-like’ middle GH ligament, the socalled Buford complex.14 Bents and Skeete reported an incidence of the Buford complex of 2.5% in an active military population.15 The anterosuperior labrum also has an inconsistent attachment to the glenoid, with half of the cadaveric specimens demonstrating the long head of the biceps originating from the supraglenoid tubercle and the other half from the superior labral complex.16 Others have identified a sublabral foramen as being a normal variant in 3% of shoulders.17

History and classification

Andrews et al first reported on superior labral lesions in throwing athletes, and this was followed by similar case reports in other overhead athletes.18,,20 The term ‘SLAP’ (superior labrum anterior posterior) was later coined by Snyder et al, who reported an incidence of 6% in more than 2000 arthroscopic shoulder cases and also presented a classification system which included four types.21 22 It has been recognised that type II SLAP lesions, where the superior labrum and biceps anchor are detached from the glenoid rim, are the most common type in overhead athletes as well as non-athletes.22,,25 Morgan et al presented a subclassification of type II SLAP lesions: anterior, posterior and combined anterior posterior.25

Choi and Kim have presented a further type II variant in which the superior labral complex pathology is accompanied by articular cartilage avulsion and loose bodies.26 Others have subsequently expanded on the initial classification system with a total of 10 types having been reported.27 28 There is no evidence, however, that classification beyond the initial four types reported by Snyder has influenced treatment or understanding of SLAP lesions.29

Pathophysiology

When SLAP lesions were initially reported, it was hypothesised that the eccentric forces placed on the long head of the biceps during the follow-through phase of throwing contributed to SLAP tears.18 This concept was developed from earlier work which showed the biceps muscle to have peak activity during the deceleration phase of the throwing motion.30 Kuhn et al, however, reported that failure of the biceps superior labral complex occurred during the late cocking phase of throwing rather than deceleration.31 Furthermore, peak biceps activity reaches only 44% of maximum voluntary contraction during follow-through, which would seem inadequate to generate a SLAP lesion.32

It has been recognised that athletes who do repetitive overhead activities, especially tennis and baseball players, develop asymmetries in the ranges of internal and external rotation. This is usually characterised as an increase in external rotation that is associated with a similar decrease in internal rotation, leaving the total arc of rotation symmetrical.33,,35

This increase in external rotation has been attributed to a variety of factors and is a subject of controversy. These theories range from anterior capsule laxity36 37 allowing anterior superior migration of the humeral head, 36 38 an expansion of the internal impingement concept originally described by Walch et al,39 to bony changes in glenoid and humeral retroversion accentuating anterior laxity.35 40 Consensus cannot be attained on whether the osseous changes noted contribute wholly or partially to the increase in external rotation.7 41 However, absolute loss of internal rotation in the face of increased external rotation has also been identified with a resulting decrease in total arc of motion. Side-to-side asymmetries of greater than 11°,42 18°25 43 or 25°4 have been associated with shoulder injury, mainly labral tears, and have been termed glenohumeral internal rotation deficit (GIRD).4

The exact causation of GIRD is unclear. Humeral retroversion has been demonstrated to change internal rotation by 12–15°,35 44 but these alterations will not change after puberty and do not explain the 40° asymmetries frequently seen in injured athletes.4 Chronic exposure to tensile forces has been theorised to create thickening of the posterior capsule,4 and acute changes have been attributed to muscular forces.43

It has been shown that a tight posterior capsule leads to anterosuperior or posterosuperior migration of the humeral head.4 24 25 45,,47 Morgan expanded on this concept to theorise that the posterior inferior glenohumeral ligament (IGHL) becomes contracted in response to eccentric loads exerted on it during the follow-through phase of overhead activities.4 This contracted posterior IGHL causes a shift in the centre point of the humeral articulation with the glenoid to a more posterior superior location during abduction and external rotation (figure 1).4 45 This tight posterior capsuloligamentous complex also may lead to internal impingement of the labrum between the posterior superior aspect of the glenoid and the humerus, and lead to degenerative changes. However, some note that posterosuperior impingement is normal in the abducted and externally rotated position and that anterior instability did not correlate with MRI evidence of internal impingement.48

Figure 1

Change in glenohumeral centre of rotation with posterior inferior glenohumeral ligament (PIGHL) contracture. (A) Equal tensioning on the anterior inferior glenohumeral ligament (AIGHL) and PIGHL allows the centre of rotation to be near the glenoid bare spot. (B) Contraction of the PIGHL causes a posterior superior shift in the centre of rotation, allowing the greater tuberosity to clear a larger arc of external rotation before internal impingement occurs (utilised from Burkhart et al4).

This GH shift, however, causes redundancy in the anterior inferior capsule through the cam effect, allowing the range of motion to shift even more towards external rotation4 and that the anterior instability mentioned above36 37 is more a function of this posterior superior GH shift and not a pathological change in the anterior capsule.4 48 Further evidence for this overall theory was provided by biomechanical studies which determined that the long head of the biceps and labral complex contribute to stability of the shoulder by increasing the shoulder's resistance to torsional forces in the throwing position.49,,54

With this shift towards greater maximal external rotation, sheer forces at the biceps anchor and posterior superior labral attachment are increased.4 24 25 As the arm is brought into abduction and external rotation, the biceps assumes a more vertical and posterior position. This shift in angle produces a posterior vector change as well as a twist at the base of the biceps which results in increases in torsional force, or ‘peel back,’ to the labrum (figure 2).4 Without secure attachment or with repetitive stress, type II SLAP lesions can result.

Figure 2

‘Peel-back’ mechanism. (A) Superior view of the biceps labral complex in the resting position. (B) View of the biceps labral complex in the abducted and externally rotated position (from Burkhart et al4).

The biomechanical alterations that contribute to increased labral injury risk are exacerbated by alterations in scapular position and motion, which create scapular protraction and increased glenoid antetilting. This creates a situation where the scapula is moving into internal rotation as the humerus is moving into external rotation. The altered position at rest has been termed Scapular malposition/Inferior medial border prominence/Coracoid pain/dysKinesis (SICK) scapula.55 The altered motion in association with arm motion is termed scapular dyskinesis.56 These alterations are produced by muscle inflexibility, muscle imbalance and disordered muscle activat ion alterat ions, which create an abnor mal posit ion of excessive scapular protraction at rest and an altered motion of decreased scapular retraction and decreased acromial elevation during cocking and early acceleration phases.55 This excessive scapular protraction increases GH angulation outside the normal range of motion, causing excessive posterior compression and anterior tension, and therefore increasing the risk of injury not only to the posterior superior labrum but also to the undersurface of the posterior supraspinatus tendon and anterior inferior capsular structures. This increased GH angulation may also increase humeral external rotation during the late cocking and acceleration, further intensifying the ‘peel back’ effect.55

History and physical exam

Symptomatic type II SLAP lesions are common in the dominant arm of young high-performance overhead athletes.1 57 Athletes may often report pain and a gradual loss of function, such as decreased throwing or serving velocity, in the affected shoulder. They may also complain of intermittent clicking or mechanical symptoms in the shoulder, particularly during the cocking phase.29 An acute traumatic injury to the shoulder, such as a fall on an outstretched arm, may also be responsible for a SLAP tear.1 58

Many clinical tests to detect the presence of labral tears have been described, and vary considerably in their sensitivity and specificity, and it may be that a combination of tests are more helpful than a single test.42 59,,71 Hegedus et al concluded that, ‘Currently, almost without exception, there is a lack of clarity with regard to whether common (orthopaedic special tests) used in clinical examination are useful in differentially diagnosing pathologies of the shoulder.’72 Generally, most subsequent studies to evaluate the sensitivity and/or specificity of techniques to diagnose SLAP lesions fail to achieve the results of the initial publication describing the test, and currently, no single clinical test can be considered the gold standard to detect SLAP lesions with regard to sensitivity or specificity.

GH rotation must be evaluated carefully to make sure that only GH rotation is accurately measured. The most effective method is to place the patient supine, place the arm in the scapular plane at 90° of GH abduction and use two examiners. One stabilises the scapula by placing the hand over the coracoid and acromion, and the other measures the range of achieved motion using a bubble goniometer centred at the olecranon (a regular goniometer or inclinometer may also be used). The patient moves the arm in rotation to tightness against the stabilised scapula, with no forcing by the examiner or patient.

Examination of the scapula is also an important part of the physical exam in overhead athletes presenting with shoulder pain. The hallmark feature of SICK scapular syndrome is asymmetrical malposition of the scapula on the dominant side, with the dominant shoulder appearing lower than the contralateral shoulder with a prominent inferior medial border of the scapula and the superior border and acromion less prominent (figure 3). Anteriorly, the coracoid tilts inferiorly, causing tightness in the pectoralis minor and short head of the biceps. For athletes with isolated SICK scapular syndrome, the most common complaint is anterior shoulder pain in the area of the coracoid followed by posterior superior scapular pain with or without radiation into the paraspinous neck region.55

Figure 3

(A) Professional right-handed baseball pitcher with a scapular malposition/inferior medial border prominence/coracoid pain/ dyskinesis right scapula viewed from posterior. (B) Apparent inferior position of the lateral clavicle caused by scapular protraction, viewed from the anterior (from Burkhart et al55).

Dynamic exam of the scapula can be reliably performed by clinical observation of scapular motion with arm elevation. Studies have documented that prominence of the medial scapular border in patients with shoulder symptoms is correlated with biomechanically determined dyskinesis and is clinically reliable enough to be used as the basis for the determination of the presence or absence of dyskinesis.73,,75 The exam is conducted by having the patients raise and lower the arms in forward flexion three to five times with a three to five pound weight in the hands. Medial border prominence on the affected side is recorded ‘yes’ (prominence detected) or ‘no’ (prominence not detected). For a ‘yes,’ further evaluation for the multiple proximal or distal causes should be done.76

Other helpful exam tests include the corrective manoeuvres, the scapular assistance tests and scapular retraction test (SRT). These help determine scapular contribution to shoulder symptoms.77 For a labral tear, the SRT, by positioning the glenoid in a less antetilted position, often decreases the internal impingement and posterior shear that creates pain. In these patients, rehabilitation to improve scapular retraction is a key point in both non-operative and postoperative treatment.

Imaging

Imaging of patients with shoulder pain and suspected SLAP lesions begins with high-quality orthogonal plain radiographs of the shoulder. While SLAP lesions are not seen on plain films, radiographs may demonstrate concomitant pathology.

The gold standard for identifying labral pathology, however, remains MRI, particularly MR arthrography, demonstrating over 90% sensitivity and specificity for detecting SLAP tears.29 78,,82 SLAP tears are best appreciated on coronal oblique sequences in which the clefts between the labrum and glenoid fill with contrast (figure 4). The physician must be aware of normal anatomical variants, such as the Buford complex and isolated sublabral foramen. Also, many overhead athletes will demonstrate MRI evidence of SLAP injury in the absence of symptoms. The MRI findings must be used in conjunction with the history, physical exam and functional limitations, to make the accurate diagnosis of labral injury.

Figure 4

MR arthrogram T2-weighted coronal oblique sequence demonstrating a superior labrum anterior–posterior lesion, with irregular extension of joint fluid.

Non-operative treatment

The time at which the athlete is at greatest risk for progression of shoulder pathology is when GIRD exceeds the external rotation gain.83 It is at this point when GH rotation begins to translate the humeral head posterior superiorly in abduction and external rotation because of the tightened posterior IGHL.4 45 It has been reported that non-surgical management can be successful in treating posterior capsular tightness with obvious improvement and/or elimination of internal impingement.4 84

Stretching of the posterior inferior capsule may be accomplished by the ‘sleeper stretch’ in which the patient lies on their side and flexes both the elbow and shoulder to 90° while the shoulder is passively internally rotated4 (figure 5), shoulder cross-body adduction with forward elevation74 (figure 6), capsular mobilisation85 or towel/racquet stretches.86

Figure 5

Sleeper stretch: the patient lies on their side with the elbow and shoulder at 90° of flexion while passively internal rotation of the shoulder is performed.

Figure 6

Posterior inferior capsular stretching with shoulder crossbody adduction and forward elevation.

Approximately 10% of overhead athletes will not respond to stretching exercises.4 Those failing the stretching regimen are almost exclusively athletes who have been performing overhead activities for years, have severe GIRD and have longstanding symptoms likely also related to intracapsular pathology such as type II SLAP lesions.4

In addition to stretching of the posterior capsule, a strengthening programme for the rotator cuff and scapular stabilisers should be included as part of the physical therapy regimen. For the scapula, closed chain exercises to address protraction, retraction, elevation/depression and retraction, internal rotation and elevation, and external rotation and depression are initially begun prior to open chain exercises.55 87 Anterior or pectoralis minor tightness can be addressed by placing a roll between the shoulder blades while the patient lies supine.55

In a recent investigation of professional baseball players, pitchers enrolled for more than 3 years in an internal rotation stretching programme had greater internal rotation and overall range of motion than those enrolled for a shorter period of time.88 Kibler prospectively evaluated high-level tennis players for 2 years and divided them into two groups.86 One group performed daily posterior inferior capsular stretching to minimise GIRD, and the other group did not stretch.Over the study period, the stretching group had significantly greater internal rotation and a 38% decrease in incidence of shoulder problems as compared with the control group. Also, manually stretching professional baseball players on a daily basis to minimise GIRD during the course of three seasons, one author reported no innings lost, no intra-articular problems and no surgical interventions among this cohort.4

Arthroscopic diagnosis

Current surgical arthroscopic technique calls for creation of standard posterior viewing portal for diagnostic arthroscopy. Evaluation of the biceps anchor labral complex should be done with a probe, as it may appear normal with only visualisation.83 According to Burkhart et al, the arthroscopic diagnostic sign for a SLAP lesion is the ‘peel-back’ sign, or detachment of the biceps and superior labrum complex medially over the edge of the glenoid in the abducted and externally rotated position.83 One must note that the ‘peel-back’ sign may not be present in isolated anterior type II SLAP lesions.

Other finding such as a displaceable biceps root or superior sublabral sulcus depth greater than 5 mm may be present.83 A sublabral sulcus is a normal variant where the caudal portion of the base of the superior labrum is not attached to the superior glenoid near the insertion of the long head of the biceps tendon.89 However, articular cartilage is usually noted superiorly on the glenoid extending to the biceps–labral insertion. If the sublabral sulcus is greater than 5 mm or if the labral attachments are tenuous, the physician must recognise the possibility of a SLAP lesion.83 In addition, a positive ‘drive through’ sign, where the arthroscope can be easily ‘driven through’ the joint from superior to inferior, may be present. This has previously been recognised as a sign of anterior instability,90 91 and its association with SLAP lesion pseudolaxity is debated.4 91 This laxity may be due to the contribution of the biceps and superior labral complex to overall GH stability.49 50 52 54 90

Surgical Technique

Exact operative technique, patient positioning and arthroscopic access varies between surgeons. This surgery may be performed with the patient in the beach chair position or lateral, and with two or three portals (trans rotator cuff or not), and is based on surgeon preference, as no one approach has been shown superior.83 92,,96

Early treatment of SLAP lesions mostly consisted of arthroscopic debridement, but the surgical results with this technique were inconsistent.21 97 98 As such, surgical fixation of SLAP lesions has become the standard, and has evolved in the last 15 years, with multiple fixation techniques used including transosseous sutures, staples, screws, arthroscopic sutures and bioabsorbable tacks.21 51 94 95 99,,105 Bioabsorbable tacks have fallen out of favour due to complications with this fixation type.99 106 107 The current approach to type II SLAP lesions favours arthroscopic surgical repair with bioabsorbable anchors loaded with non-absorbable sutures.83 92 108 109 Knotless suture anchors are also available, but these demonstrate decreased biomechanical strength for type II SLAP repairs versus standard suture anchors,110 even though ultimate pullout strength was noted to be higher in certain knotless anchor systems.111

The current technique calls for positioning of the anchor at the articular margin at a 45° angle to the osseous surface. Lehtinen et al used cadavers to find that glenoid bone stock was greatest at the most superior portion of the glenoid rim and was therefore the most appropriate location for suture anchor placement.112 The same study found bone stock to decrease as one moved posteriorly towards the 10:30 position upon the glenoid rim.

There have been a number of biomechanical evaluations on a variety of suture anchor locations and suture configurations.68 113 114 One investigation found simple suture configuration to be superior to mattress type113 while another found that one anterior and one posterior simple suture configuration was equivalent to two posterior simple sutures in resisting ‘peel-back’ forces.68 However, other investigators demonstrated an advantage of mattress type sutures as compared with one- and two-point fixation with simple sutures when a type II SLAP lesion was subjected to cyclic traction.114 As the results of suture anchor placement and suture type are varied, most authors prefer to pass simple translabral loop sutures utilising a variety of arthroscopic knots.83 92 One author argues that the most critical component of the construct to resisting peel-back forces is to position a tight suture loop just posterior to the root of the biceps, with the loop attached to a suture anchor placed beneath the root of the biceps.83 Care must be taken not to restrict the normal motion of the biceps as the arm goes into external rotation. Tethering and kinking of the biceps may restrict this key motion and decrease the ability to achieve full cocking.

Following repair, the ‘peel-back’ test and ‘drive through’ signs are repeated. If the ‘drive through’ sign remains positive after appropriate fixation of the SLAP lesion, consideration should be given to capsular tightening.83 Morgan recommends plication of the anterior IGHL if external rotation is greater than 130° with the shoulder in 90° of abduction and posterior inferior capsular releases in overhead athletes who did not respond to preoperative stretching regimens for loss of internal rotation.83 At this time, there are no reported trials of combining these procedures with SLAP repair.

Surgical outcomes

Snyder et al have published one of the largest retrospective reviews on the results of arthroscopic SLAP repair, demonstrating that 80% of lesions repaired with suture anchors had healed lesions at repeat arthroscopy.21 In treating SLAP lesions in overhead athletes, Morgan et al reported an 87% success rate in return of throwers to preinjury levels.25 O'Brien et al published outcomes at an average of 4 years following repair of isolated type II lesions and found that overall satisfaction was high, and 16 of 31 patients were able to return to their preinjury level of sporting activity.95 Kim and colleagues reported an overall return to preinjury function of 91%; however, those participating in overhead sports had significantly lower shoulder scores and rates of return to play than the less active cohort when the SLAP lesion was repaired with suture anchors.94 More recently, Brockmeier et al reported results of a prospective series of outcomes for patients with type II lesions treated with arthroscopic suture anchor fixation.92 He found significant improvement in two shoulder function rating scales, and 74% of competitive athletes were able to return to their preinjury level of competition.

Treatment of combined pathology

Patients diagnosed as having SLAP lesions often have other forms of associated GH pathology.17 21 104 Snyder et al reported that of 140 patients with arthroscopically diagnosed SLAP lesions, 81% had other associated shoulder lesions, with 47% having a positive impingement test preoperatively and 39% having rotator cuff signs.21 Others showed that arthroscopically confirmed type II SLAP lesions were associated with Bankart lesions in patients 40 years or younger, and supraspinatus tear and humeral head osteoarthritis was associated with SLAP lesions in those patients over 40 years of age.17 Interestingly, type I SLAP lesions were associated with rotator cuff disease, while types III and IV lesions were associated with traumatic instability.17

Despite these findings, many surgeons are reluctant to perform type II SLAP repair with subacromial decompression or other procedures because of concerns related to shoulder stiffness. Coleman et al recently reported that combined type II SLAP repair and acromioplasty had outcomes comparable with those undergoing isolated SLAP repair, and furthermore, the combined procedure appeared to prevent residual clinical impingement.100 A group from the same institution also reported on combined rotator cuff repair with either SLAP or Bankart lesion repair and also found that arthroscopic treatment of both lesions led to good clinical outcomes.115

Summary

Type II SLAP lesions due to repetitive overhead activities are the most common cause of shoulder pathology in the overhead athlete. While controversy exists as to whether impingement or a pathological cascade resulting from posterior IGHL contracture and scapular dyskinesis is the cause of the pathology, it is generally agreed that a posterior capsular stretching and scapular strengthening regimen can reduce the risk of SLAP lesions. Arthroscopic treatment with suture anchor fixation is the most effective surgical management. While return to sports in young competitive overhead athletes undergoing shoulder surgery for various diagnoses generally results in a return to play of about 67%, return to sports after SLAP repair approaches 90% in many series. Repair of SLAP lesions with combined rotator cuff or other labral pathologies has also been shown to have good clinical outcomes.

What is already known on this topic

  • There is much information published about superior labrum anterior posterior lesions, which occurs more commonly in overhead athletes, such as tennis players and baseball players. However, there is much confusion about the published information. Further, the evaluation and treatment continues to evolve confounding clinicians.

What this study adds

  • This is a comprehensive review of superior labrum anterior posterior (SLAP) lesions in the tennis player. This manuscript provides a concise synthesis of current information to help the clinician remain current on the concepts of pathoaetiology, evaluation and treatment of SLAP lesions.

References

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Footnotes

  • Detail has been removed from this case description/these case descriptions to ensure anonymity. The editors and reviewers have seen the detailed information available and are satisfied that the information backs up the case the authors are making.

  • Competing interests None.

  • Provenance and peer review Commissioned; not externally peer reviewed.