Superior Labral Lesions 

The glenoid labrum is a triangular fibrocartilaginous structure that serves to deepen the glenoid. While tears of the anteroinferior labrum have long been known to be associated with significant shoulder pathology, injuries of the superior labrum have really only been appreciated as a potential pathologic lesion since the advent of shoulder arthroscopy. The superior labrum often has a more meniscoid attachment to the glenoid rim compared with the remainder of the labrum and therefore may be more susceptible to both degenerative and traumatic lesions. It also serves as part of the origin of the long head of the biceps. Injuries to the superior labral biceps complex can compromise the biceps anchor. Furthermore, the repetitive tensile force exerted by the biceps on the superior labrum likely contributes to poor healing of superior labral tears.^[1]

An image depicting superior labral tears can be seen below.

Superior labrum tears were first described by Andrews.^[2] In a study that reviewed their experience in 73 throwing athletes, the authors identified tears of the labrum involving the anterosuperior aspect near the origin of the biceps tendon. They attributed this lesion to the biceps tendon being pulled off the labrum as a result of force generated during the throwing motion. Snyder et al coined the term SLAP to denote a superior labrum, anterior and posterior lesion to describe a more extensive injury.^[3] A SLAP lesion as described by Snyder involves a tear of the superior labrum, which starts posteriorly and extends anteriorly to include the anchor of the biceps tendon to the superior labrum. The injuries were subdivided into 4 types (I-IV).

Similar to Andrew's findings, a subset of patients who reported a traction injury were identified. However, the majority of patients related a history of a compressive injury to the shoulder secondary to a fall on an outstretched arm in a flexed and abducted position.

Initial operative treatment of superior labral (labrum) lesions consisted of debridement only. This therapy is appropriate for type I and type III lesions, as well as for some type IV lesions, in which the biceps anchor is intact. However, in type II and in type IV lesions in which the biceps anchor is unstable, debridement alone yields poor results.

Early attempts at arthroscopic fixation used a metal staple. This technique was discontinued because of concerns for chondral injury as well as the need for a second surgery for staple removal. For similar reasons, techniques involving a metal screw are no longer used. A transglenoid technique similar in concept to a transglenoid technique for a Bankart repair has been described; however, this is technically difficult and has fallen out of favor. Good results were initially reported with use of a bioabsorbable tack. However, complications, including implant breakage with resultant particulate debris and a foreign body reaction, have been reported.

Suture anchors loaded with nonabsorbable suture is the preferred method of fixation.

Superior labral (labrum) lesions can cause painful mechanical symptoms and difficulty with overhead activities whether they be athletic or those of daily living. SLAP (superior labrum, anterior and posterior) lesions (see image below), as opposed to occult anterior instability, are likely the underlying cause of the so-called dead arm syndrome in throwing athletes. Regardless of whether injuries to the superior labrum biceps complex are secondary to a throwing or nonthrowing etiology, they can be a source of considerable disability for the patient.

These injuries are difficult to diagnose on physical examination because the findings are often nonspecific and demonstrate considerable overlap with those of other etiologies of shoulder pain. Similarly, both nonenhanced MRI and magnetic resonance arthrography have variable accuracy in determining if a SLAP lesion is present. At times, the only definitive way to diagnose a SLAP lesion is with a diagnostic arthroscopy. Even so, a thorough understanding of the normal anatomy and biomechanics of the superior labral biceps complex, as well as commonly observed normal anatomic variants, is mandatory to ensure appropriate surgical stabilization and to avoid unnecessary repair of the superior labrum.^{[4, 5]}

Snyder classified superior labral tears into 4 types.^[3] A type I lesion is characterized by significant fraying of the labrum, but the biceps anchor is intact. A type II lesion is a tear of the superior labrum that results in instability of the biceps anchor. Significant fraying of the labrum occurs as is observed in type I tears; in addition, the superior labrum and associated biceps anchor is stripped away from the superior glenoid. A type III lesion describes a bucket-handle tear of the superior labrum. The central portion of the superior labrum is torn and usually displaced into the joint. The peripheral attachment of the labrum is intact, and the biceps anchor is usually stable. A bucket-handle tear of the superior labrum also characterizes a type IV lesion; however, the tear also propagates to a variable degree into the biceps tendon. Modifications have been made to the original classification.

Morgan and Burkhart subdivided the type II lesions into anterior type II, posterior type II, and combined type II, referring to the tear involving the labrum both anterior and posterior to the biceps anchor.^[6]

Maffet et al expanded the classification to include types V, VI, and VII.^[7] A type V SLAP refers to a Bankart lesion that extends superiorly to include the superior labrum and biceps anchor. A type VI lesion has a flap tear of either the anterior or posterior superior labrum with an associated type II tear. A type VII lesion describes a tear of the superior labrum that includes the middle glenohumeral ligament. Type II lesions are by far the most common and are also the source of the greatest diagnostic difficulty.

Frequency

Superior labral (labrum) lesions are unusual. The reported prevalence in patients undergoing shoulder arthroscopy has ranged from 3.9-6%. In the largest series reported, SLAP (superior labrum, anterior and posterior) lesions represented 6% of 2375 patients who underwent shoulder arthroscopy. The average age was noted to be 38 years, and 91% of the patients were male. The reported incidence of types I-IV is variable, with type II lesions being the most common. Type I lesions have been reported to account for 9.5-21% of all cases; type II, 41-55%; type III, 6-33%; and type IV, 3-15%.

When considering the etiology of superior labral (labrum) lesions, it is useful to divide them into the 2 broad categories of traction and compression injuries. A compression injury is usually secondary to a fall on an outstretched arm that is in an abducted and slightly flexed position. This can result in a compressive load to the superior labrum with a resultant tear. A direct blow to the shoulder has also been found to be a contributing factor for SLAP (superior labrum, anterior and posterior) lesions. Traction injuries can be secondary to a sudden pull in an inferior direction such as occurs when an individual loses hold of a heavy object. An overhead traction force, as when individuals attempt to catch themselves from falling from a height, can also result in a superior labral injury.

Clearly, engaging in throwing sports can predispose one to developing a SLAP lesion. The exact mechanism of this is somewhat controversial. In Andrews' original 1985 study, traction force placed on the superior labrum by the biceps tendon in the follow-through phase of the throwing motion was thought to be responsible for creating a SLAP lesion.^[2] The hypothesis was that the eccentric contraction of the biceps necessary to decelerate the elbow resulted in the biceps tendon detaching portions of the glenoid labrum. However, recent studies suggest that the forces generated during the late cocking phase are in fact the predominant factor. The peel-back phenomena as described by Burkhart and Morgan,^[8] along with shear forces generated by a tight posteroinferior capsule, are thought to be major contributing factors to developing a type II SLAP or variants thereof.

The presence of a peel-back sign can be demonstrated arthroscopically. The arm is placed into 70-90° of abduction and then progressively externally rotated. In this position, the biceps vector is now more posteriorly and vertically oriented. To accommodate this, the base of the biceps twists. A torsional load is transmitted to the superior labrum, and if the posterosuperior labrum and biceps anchor is incompetent, medial displacement of the superior labral biceps complex occurs. If more than 5 mm of the posterosuperior glenoid is uncovered or the biceps root at the level of the supraglenoid tubercle is uncovered, a posterior type II SLAP is present.

As already noted, posterior capsule tightness is thought to play an important role in the development of SLAP lesions. Almost all high-demand throwers develop a posterior capsular contracture with limitation of internal rotation. This tight posteroinferior capsule is thought to result in obligatory superior translation of the humeral head when the arm is in abduction and external rotation and as a result exposes the superior labrum to large shear forces. This increased shear force is most pronounced at the same time the peel-back forces are at their maximum, increasing the likelihood of a SLAP lesion developing.

To accurately classify superior labral (labrum) lesions, one must be aware of normal anatomy, including the many normal variants that are observed. The biceps tendon origin is divided roughly in half between the supraglenoid tubercle and the superior labrum. Vangsness et al demonstrated that, 55% of the time, the labral insertion is entirely or mostly into the posterior labrum.^[9] Only a small percentage (approximately 8%) have a predominant anterior insertion. The remainder, approximately 37%, have equal insertions to the anterior and posterior labrum.

Cooper et al in their anatomic study noted that the superior portion of the labrum had a distinctly different morphology than the inferior labrum.^[10] The superior and anterosuperior portions were found to be loosely attached to the glenoid rim through thin connective tissue that easily stretched. This is similar to that of the meniscus of the knee. In contrast, the inferior labrum has a firm attachment through thick inelastic fibers and appears as a firm immobile extension of the glenoid articular cartilage. The 12-o'clock position was the only location on the glenoid rim where the hyaline articular cartilage extended over the rim of the glenoid. The biceps tendon inserts into the supraglenoid tubercle, which is 5 mm medial to the glenoid rim. This, along with the often meniscoid attachment of the superior labrum, results in a sublabral recess.

This should not be mistaken for a type II SLAP (superior labrum, anterior and posterior) lesion. As reported by DePalma, a sublabral recess may be present in up to 50% of individuals older than 20 years.^[11] This incidence increases with patient age. More than 95% of the specimens in DePalma's study obtained from patients in the seventh and eighth decades of life were found to have a sublabral recess.

The middle glenohumeral ligament can sometimes insert directly into the superior labrum as a large thick cordlike structure (ie, the so-called Buford complex). In these cases, the anterosuperior labrum is absent. The Buford complex is not pathologic and should not be stabilized because to do so would markedly restrict external rotation. A sublabral foramen can be observed where the anterosuperior labrum, from approximately the 1- to 3-o'clock position in a right shoulder, is loosely attached or not attached at all to the glenoid rim. Again, this is not pathologic and should not be stabilized. To do so would result in a significant loss of external rotation.

Histologically, the superior labrum is composed of fibrocartilage. This is composed of type II cartilage in a relatively acellular matrix with occasional interspersed elastin fibrils. This is in contrast to the hyaline cartilage of the glenoid and the dense fibrous glenohumeral capsule. Branches of the suprascapular, circumflex scapular, and posterior humeral circumflex supply the labrum. Periosteal and capsular vessels supply the labrum throughout its periphery. No vessels enter the labrum from the underlying bone. In general, the superior and anterosuperior labrum have less vascularity than other portions of the labrum.

On a biomechanical level, incompetence of the superior labrum and biceps anchor has been shown to have a deleterious effect on anterior glenohumeral stability. Rodosky et al compared anterior glenohumeral stability in specimens with an intact superior labrum with those with a SLAP lesion in a cadaver study.^[12] They demonstrated that the presence of a SLAP lesion decreased the torsional resistance by 11-19%, as compared with the intact shoulder, as it was placed in the abducted and externally rotated position. The inferior glenohumeral ligament was subject to significantly increased strain (increase by >100%) in the presence of a SLAP lesion.

Pagnani and Deng et al in another cadaver study demonstrated that a SLAP lesion results in significant increases in both anterior-posterior and superior-inferior translations.^[13] At 45° of elevation, a 6-mm increase was noted in anterior translation with the arm in neutral rotation and a 6.3-mm increase in translation in internal rotation occurred.

Several other studies have examined the strain changes in the superior labrum and biceps anchor with different positions of the throwing motion. Pradhan et al found that a significant increase in strain in the anterior and posterior portions of the superior labrum only occurs when the arm is in maximum external rotation as found in the late cocking phase. Furthermore, the strain in the posterior portion of the superior labrum was significantly higher than that of the anterior portion.^[14]

Kuhn et al supported these findings with their study of failure patterns of the biceps superior labral complex.^[15] They found that failure was significantly more likely in the late cocking position as compared to the early acceleration position. In the late cocking position, 9 of 10 specimens demonstrated failure of the biceps superior labral complex. In contrast, of the 10 paired specimens that were tested in the early acceleration position, only 2 had failure of the biceps superior labral complex. The load to failure was found to be significantly less in the late cocking position than in the early acceleration position. Of the 5 patients that developed type II SLAP lesions, 4 of these occurred in the late cocking positions.

These studies emphasize the important role the biceps superior labral complex likely plays in anterior shoulder stability. An unstable SLAP lesion found in the course of a Bankart repair should be stabilized. The important role of the posterior portion of the superior labrum likely reflects the fact that the biceps tendon attachment is usually posterior-dominant as demonstrated in a study by Vangsness et al.^[9] In repairing SLAP lesions, particular attention should be given to ensuring the posterior aspect is well stabilized.

Patients with superior labral (labrum) lesions often present describing a poorly defined pain that is posterior in location. They can also describe a painful popping and clicking similar to mechanical symptoms associated with a meniscal tear. Nonthrowing individuals may report a history of a fall either on an outstretched arm or in which a direct impact on the shoulder occurred. A history of a sudden deceleration injury, such as occurs when one loses control of a heavy object that is being carried, may be present. In a throwing athlete, a discrete injury with no prodromal period may be reported. In contrast, the athlete may not recall a specific injury and merely report a prodromal phase consisting of some mild posterior pain with a sense of posterior tightness.

The patient's range of motion should be carefully assessed, especially in the throwing athlete.^[16] Throwers often develop a loss of internal rotation in abduction. This loss of internal rotation with tightness of the posteroinferior capsule is thought to be a risk factor for the development of a SLAP (superior labrum, anterior and posterior) lesion. One should be especially cognizant of this entity in an individual who presents with loss of internal rotation at the expense of a 180° arc of motion with the arm abducted 90°. Burkhart and Morgan postulated that this finding defines a shoulder at risk of developing a type II SLAP lesion and the dead arm syndrome.^[17]

An acute SLAP lesion, especially a posterior type II lesion, can manifest as posterior shoulder pain in abduction and external rotation, decreased throwing velocity, and easy fatigability. This symptom complex has been labeled the dead arm syndrome. Multiple physical examination tests for a SLAP lesion have been described; however, correlation with arthroscopic findings has been poor. Furthermore follow-up studies by independent investigators have been unable to reproduce the high sensitivities, specificities, and positive-predictive values reported by the authors who originally described the tests.^[18]

In Snyder's initial report describing SLAP lesions, he used the biceps tension (Speed) test and the compression rotation test.^[3] The Speed sign is positive when pain is elicited with resisted flexion of the fully supinated arm with the elbow extended and the arm flexed to 90°. The compression-rotation sign is performed with the patient supine, the shoulder elevated to 90°, and the elbow flexed to 90°. An axial load is then applied to the humerus to compress the glenohumeral joint, and the arm is rotated. Pain as well as mechanical symptoms elicited during this test are considered positive test results. Multiple other tests have been described.^[19]

The O'Brien sign, or the active-compression test, is elicited by first placing the arm in 90° of forward flexion and 10° of adduction.^{[20, 21, 22]} The arm is then fully internally rotated into the thumbs-down position. The patient is then asked to resist downward pressure to the arm that is applied by the examiner. Differentiate deep-seated shoulder pain from that localized to the anterosuperior aspect of the shoulder because the latter is associated with acromioclavicular (AC) joint pathology. The test is then conducted again but with the arm in full supination; the pain should be decreased in this position as compared with the initial position for the test result to be considered positive. A positive Speed test as well as a positive O'Brien sign is thought to be consistent with an anterior type II SLAP tear.

Kibler described the anterior slide test to help diagnose anterior SLAP lesions.^[23] The patient is instructed to place both hands on the hips. The examiner stabilizes the scapula with one hand over the acromion. The other hand is used to axially load the humerus in anterior and superior direction. Pain with this motion is considered to be positive for an anterior based SLAP lesion.

Kim et al described the biceps tension test II.^[24] The shoulder is placed in 120° of abduction and full external rotation, and the elbow is flexed to 90° and fully supinated. The patient is then instructed to flex against resistance. Pain with this is consistent with a SLAP lesion. Kim et al also described the biceps tension test I to help determine the presence of a SLAP lesion in the patient with unidirectional anterior instability. An anterior apprehension test is first performed, which in this subgroup of patients is positive for instability. Resisted elbow flexion with the arm fully supinated should decrease the sensation of instability if the biceps superior labral complex is intact. In the presence of a SLAP lesion, no alleviation of the instability sensation occurs.

The Jobe relocation test has been used to help diagnose posterior type II SLAP lesions.^[25] The patient is placed in the supine position. The arm is placed in 90° of abduction and maximum external rotation. Pain in this position that is alleviated with a posteriorly directed force to the proximal humerus is consistent with a posterior type II lesion. Differentiate the sensation of pain in this test as opposed to that of instability found in an anteriorly unstable shoulder. Patients with type III and type IV lesions are more likely to report mechanical symptoms, although eliciting these on physical examination is often difficult.^[26]

Despite the multitude of described tests for a SLAP lesion, none has proven to be reliable to date. Follow-up independent studies have demonstrated poor sensitivities, specificities, and positive predictive values.^[27]

Check for rotator cuff impingement signs on examination.^[28] The prevalence of rotator cuff tears, either partial or full-thickness, in patients with SLAP lesions has been noted to be in the 30-40% range.

Surgical treatment of superior labral (labrum) lesions is indicated in patients with persistent symptoms despite 3 months of nonoperative treatment. These patients should have persistent posterior shoulder pain, with or without mechanical symptoms, and findings on physical examination consistent with a SLAP lesion and ideally have supportive MRI findings. However, note that physical findings as well as MRI findings are often equivocal. If a high clinical suspicion exists, with the patient continuing to be symptomatic after an appropriate amount of conservative treatment, then strong consideration should be given to diagnostic arthroscopy.

See Etiology and Pathophysiology.

See Etiology and Pathophysiology.