eMedicine Specialties > Sports Medicine > Shoulder

Superior Labrum Lesions

Author: Riley J Williams III, MD, Associate Professor, Department of Orthopedic Surgery, Hospital for Special Surgery, Weill Cornell Medical College; Director, HSS Institute for Cartilage Repair
Coauthor(s): Frank A Petrigliano, MD, Orthopaedic Surgery Resident, Department of Orthopaedic Surgery, University of California Los Angeles
Contributor Information and Disclosures

Updated: Mar 15, 2008

Introduction

Background

Before the use of shoulder arthroscopy and magnetic resonance imaging (MRI) in the diagnosis and management of shoulder problems, glenoid labrum lesions were underappreciated. More specifically, superior labrum lesions about the insertion of the long biceps tendon were typically were noted or managed using standard open surgical techniques. An improved understanding of the surgical anatomy and the biomechanical contributions of the superior labrum have demonstrated its significance in shoulder stability and its role in the pathogenesis of shoulder pain.

Andrews et al published a study that examined glenoid labrum lesions related to the long head of the biceps (LHB) in 73 throwing athletes.1  The authors observed that the LHB was contiguous with the superior labrum and that most of these patients had avulsed the anterosuperior labrum off the glenoid in conjunction with the biceps tendon. Subsequently, Snyder et al defined the pattern of superior labral injury in 27 patients who were described as having superior labrum anterior posterior (SLAP) lesions.2 The authors described the SLAP lesion as a labral detachment originating posterior to the long biceps insertion and extending anteriorly. These lesions were subsequently categorized as types I-IV, as follows:

SLAP classification2

  • Type I: The glenoid labrum demonstrates degenerative changes and fraying at the edges but remains firmly attached to the glenoid rim. No avulsion of the biceps tendon is present (see Image 1, upper left).
  • Type II: Degenerative changes and fraying are present in type II lesions. The glenoid labrum is detached completely from the anterosuperior to the posterosuperior glenoid rim. This portion of the labrum is lifted by the long biceps tendon, and the attachment of the biceps tendon is unstable (see Image 1, lower right).
  • Type III: With type III lesions, the free margin of the superior labrum is displaced into the joint (bucket handle), whereas the labral attachment to the glenoid rim and biceps tendon remains intact. The insertion of the biceps tendon is not unstable (see Image 2, upper left).
  • Type IV: The superior portion of the labrum is displaced into the joint (bucket handle) in type IV lesions. In contrast to type III tears, the long biceps tendon is also affected, involving partial rupture in the direction of the fibers (see Image 2, lower right).

Superior labral pathology is now recognized as a potential sources of considerable pain and disability in active patients. The goal of this article is to familiarize the reader with the anatomy, pathophysiology, diagnosis, and management of labral tears of the superior glenoid.

For excellent patient education materials, see eMedicine's Hand, Wrist, Elbow, and Shoulder Center and the patient education articles Rotator Cuff Injury and Shoulder Separation.

Related eMedicine topics:
Multidirectional Glenohumeral Instability
Posterior Glenohumeral Instability
Rotator Cuff Injury
Superior Labral Lesions [in the Orthopedic Surgery section]

Related Medscape topics:
Resource Center Exercise and Sports Medicine
Resource Center Pain Management: Pharmacologic Approaches
American Orthopaedic Society for Sports Medicine 31st Annual Meeting-NSAIDs and Physical Therapy Effective for Superior Labral Tears

Frequency

United States

Snyder et al reported the result of over 140 patients who were treated operatively for superior labral lesions.3  The authors noted a 6% incidence of SLAP lesions in persons undergoing shoulder arthroscopy for all diagnoses over an 8-year period. The percentages of the types of SLAP lesions encountered were as follows: type I, 21%; type II, 55%; type III, 9%; type IV, 10%; and complex lesions, 5%. Associated lesions included Bankart lesions (22%) and lesions of the rotator cuff (11%). Only 28% of SLAP lesions were found without associated pathology.

Kim et al reported that of 544 shoulder arthroscopy procedures, 139 (26%) demonstrated a SLAP lesion.4 Of the SLAP lesions, 103 (74%) were type I, 29 (21%) were type II, 1 (0.7%) was type III, and 6 (4%) were type IV. Most (123) of the SLAP lesions were found to be associated with other intra-articular lesions.

Most recently, Kampa and Clasper evaluated the presentation and incidence of SLAP lesions in military and civilian populations.5 Of 178 patients who underwent arthroscopy for complaints of either pain, instability, or pain and instability, 39 (22%) SLAP lesions were found. According to the Snyder classification (see Introduction, SLAP classification), 20.5% were type I, 69.3% were type II, 5.1% were type III, and 5.1% were type IV. The authors found that patients with a history of trauma or symptoms of instability were more likely to have a SLAP lesion than patients presenting with atraumatic etiologies. Military patients also had a higher incidence of these lesions relative to civilian patients.

Collectively, these data suggest that patients who suffer traumatic injuries of the shoulder are at increased risk for sustaining an injury to the superior labrum, and that the severity of the resulting lesion is variable. Traumatic SLAP lesions are often associated with other intra-articular shoulder injuries, and the examining physician must have a high index of suspicion for coexisting pathology.

Functional Anatomy

Grossly, the glenoid labrum surrounds the entire circumference of the glenoid surface. Moseley and Overgaard6 in 1962 and Detrisac and Johnson7 in 1986 described the labrum as a redundant fold of capsular (fibrous) tissue. Superiorly, the labrum is contiguous with the tendon insertion of the LHB as it attaches to the supraglenoid tubercle. The anterior labrum fibers may insert into the middle glenohumeral ligament (joint capsule). The superior labrum is more meniscuslike in structure because its fibers are loosely attached to the glenoid rim and may overlap the superior glenoid surface, whereas the inferior labrum is attached more tightly to the glenoid rim and is typically round in appearance.

The entire labral complex is attached at all points to either the bony glenoid rim or joint capsule about the glenoid, except in the anterosuperior margin. A sublabral foramen is present in most individuals; this labral foramen may be confused on MRI or at arthroscopy with a labral tear.

The Buford complex represents another anatomic variant and is described as a cordlike thickening of the middle glenohumeral ligament and absence of the anterosuperior labrum. This anatomic finding must be recognized as a normal variant because attempts to repair or debride this region may result in abnormal capsular constraint, shoulder stiffness, or glenohumeral instability. Interestingly, a retrospective review suggested that the presence of a Buford complex may correlate with the presence of a SLAP lesion in patients.8

Histology

Cooper et al examined the anatomy and histology of the glenoid labrum.9  The authors noted an existing fibrocartilaginous transition zone at the superior glenoid margin between the fibrocartilaginous labrum and the hyaline cartilage of the glenoid surface. This study also confirmed the gross observation that the superior labrum fibers insert directly into the fibers of the LHB, distal to the biceps insertion into the supraglenoid tubercle. Histologic examination also revealed that the labrum consists of densely packed collagen bundles and fibrochondrocytes.

The primary labrum vascular supply originates from the suprascapular, circumflex scapular, and posterior humeral circumflex arteries. Only the periphery of the labrum appears to be vascularized, and no contribution to the labral blood supply is derived from the underlying bone. Prodromos et al observed that fetal and newborn shoulders possess an extensive blood supply throughout the labrum, whereas adult specimens have only sparse peripheral vasculature.10 Apparently, labral vascularity, much like the meniscus, recedes with advanced age.

As previously mentioned, the LHB brachii muscle is also anatomically important in the discussion of SLAP lesions (see Introduction, Background). This LHB tendon arises from the supraglenoid tubercle, and fibers from the superior labrum attach to the biceps tendon in this region. Following the examination of over 100 cadaver specimens, Vangsness et al estimated that approximately 50% of the biceps tendon originates from the superior labrum11 . The most common labral origin of the biceps is the posterior-superior region.

Sport-Specific Biomechanics

Long before the advent of shoulder arthroscopy, labral tears were described in association with anterior shoulder subluxation and dislocation, suggesting a role for the labrum in glenohumeral stability maintenance. McGlynn and Caspari described the intra-articular findings of subluxating shoulders noted at the time of arthroscopy.12 As suggested by previous studies, fraying, tearing, or detachment of the glenoid labrum was a common finding in this group of 19 unstable shoulders.

In defining the relevant factors contributing to anterior shoulder stability, Turkel et al noted that the inferior glenohumeral ligament, which attaches to the glenoid via the labrum, is essential in preventing anterior shoulder instability.13 The glenoid labrum increases the area and depth of the glenoid cavity, contributing to articular stability of the glenohumeral joint. The labrum has been suggested to act as a chock block to the humeral head as it attempts to translate anteriorly or posteriorly upon the glenoid surface.

Andrews et al demonstrated that superior labrum lesions were observed in a group of overhead throwing athletes who underwent arthroscopic examination of the shoulder.1 On the basis of observed lesions in this group of athletes, the authors suggested that the biceps tendon is subjected to large forces during the act of throwing. Intraoperative stimulation of the biceps during arthroscopic shoulder surgery also revealed that the LHB tends to pull the labrum off the superior glenoid rim (especially in the presence of a SLAP lesion). Therefore, excessive forces generated by the biceps tendon during overhead throwing activities may lead to the generation of superior labral tears.

In a study from the University of Pittsburgh, Rodosky et al analyzed the role of the LHB and superior labrum in anterior shoulder instability.14 A dynamic cadaveric shoulder model was used to simulate the forces of the late-cocking phase of the throwing motion. Strain gauges were placed in the inferior glenohumeral ligaments of 7 nonembalmed cadaver shoulders. Tests of anterior glenohumeral translation were made with and without the presence of superior labral lesions (analogous type II lesions). Varying forces were applied to the biceps tendon (0-100% extrapolated maximum force) in all tested specimens.

In normal shoulders (ie, no SLAP lesion), peak torque increased 22% and peak torsional rigidity increased 32% in shoulders with maximal biceps (loading versus unloaded shoulders).14 In shoulders with a simulated SLAP lesion and no biceps loading, the observed peak torque was 12% lower than that of normal specimens, and a 120% increase in inferior glenohumeral ligament strain was observed. In shoulders with simulated SLAP lesions and 100% biceps loading, the observed peak torque was 7% lower than that of normal specimens. Torsional rigidity was also decreased by the creation of a SLAP lesion with and without biceps loading. In this study, torsional rigidity represented a measure of the tested shoulder to resist rotational forces.

In another study, Pagnani et al examined the effect of superior glenoid labrum lesions on glenohumeral translation.15 In this cadaveric study, the investigators applied sequential anterior, posterior, superior, and inferior forces of 50 Newtons (N) to the proximal humerus. A 22-N compressive force was also applied. During the application of the described loads, a 55-N force was applied to the LHB tendon. The shoulders were tested in 7 positions of glenohumeral elevation and rotation. Each specimen was tested with a normal superior labral complex, a partial superior labral tear, and a complete tear (including the biceps insertion on the supraglenoid tubercle).

The authors found that a partial tear of the superior labrum had no significant effect upon superoinferior or anteroposterior translation15 ; however, the creation of a complete SLAP lesion resulted in significant increases in anterior and inferior translation at all arm elevations. Increased glenohumeral translation persisted even after the application of a 55-N force to the biceps tendon. Pagnani et al suggested that the LHB tends to stabilize the joint by generating joint compressive forces and by acting as a physical restraint to translation.

These data suggest that in external rotation and abduction, the forces generated by the biceps muscle result in an increase in torsional rigidity. These findings suggest that increased loads applied to the biceps tendon may protect the shoulder from anterior subluxation during the throwing motion.

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Elbow and Forearm Overuse Injuries
Overuse Injury
Rotator Cuff Injury

Related Medscape topic:
Resource Center Exercise and Sports Medicine

Clinical

History

The initial evaluation of an individual with a suspected SLAP lesion should include a thorough review of the patient's activities, history of previous shoulder injuries, subsequent interventions, and aggravating factors. The majority of SLAP lesions occur in conjunction with other shoulder disorders, making the diagnosis difficult to establish.

  • Nonspecific shoulder pain with overhead or cross-body activities is the most common presenting symptom of patients with SLAP lesions. Reports of popping, clicking, or catching at the shoulder joint are common. Patients may describe a deep, vague pain within the shoulder joint in association with weakness or stiffness. Additionally, symptoms of instability may be present if the tear extends into the anterior ligament and labrum, resulting in a Bankart lesion.
  • The patient's history may reveal a traction injury or a direct blow to the shoulder area proper. A fall onto an outstretched arm may also cause a SLAP lesion. Compression (direct blow) injuries are most often traumatic in nature and can be sustained during a fall onto the affected extremity. Overhead throwing athletes may also be prone to the development of SLAP lesions because of the repetitive traction forces of the throwing motion. In many of these cases, no antecedent injury or activity is reported.

Physical

Patients suspected of having a labral tear or SLAP lesion should undergo a thorough physical examination of the cervical spine, shoulder girdle, and upper extremity.

  • The physical examination should assess range of motion (ROM), glenohumeral stability, muscular strength, and neurologic function. Unfortunately, no single physical sign or test is specific for the detection of a SLAP lesion, and a diagnosis based solely upon the patient's history and the physical examination findings remains difficult. Some studies have advocated certain maneuvers that, when considered with other diagnostic modalities (eg, history, imaging), may be highly suggestive of labral pathology.
  • Note that commonly performed diagnostic maneuvers often elicit positive findings in patients with superior labral tears; thus, attention to detail is necessary when documenting physical findings. Associated lesions (eg, rotator cuff tears, instability) may produce confusing signs during the physical examination; thus, the correlation of all findings with information from the history and imaging studies is recommended.
    • The Speed biceps tension test (also Speed's test, biceps tendon test) may be useful in detecting SLAP lesions. This test is performed with the patient's forearm in maximal supination and the elbow extended. Then, the examiner resists active glenohumeral flexion, which may result in pain in the patient when the biceps attachment site is injured or inflamed.
    • Field and Savoie described the compression rotation test wherein the patient is placed in a lateral position and the affected arm is held in 90° of abduction.16 Pain is noted with internal and external rotation of the arm.
    • The O'Brien active compression test (also O'Brien sign, active compression test) is often utilized to detect labral pathology.17 This maneuver is performed with the examiner standing behind the patient. The patient stands upright with the affected arm flexed 90° and adducted 15° medial to the sagittal plane of the body. With the arm internally rotated (thumb down), the examiner places a downward force on the arm. Pain is localized to the shoulder joint or acromioclavicular (AC) joint. The test is then repeated with the forearm in maximal supination.
      • A positive test result is recorded when pain is decreased by the second maneuver. Superficial pain is correlated with AC joint pathology, whereas a deep pain or click is correlated with labral abnormalities in 94% of the patients studied.17
    • Kibler described the anterior slide test to help diagnose anterior SLAP lesions. The patient is instructed to place both hands on the hips.18 The examiner stabilizes the scapula of the affected side with one hand over the acromion. The other hand is used to axially load the humerus in the anterior and superior direction. Pain with this motion is considered to be a positive result for an anterior-based SLAP lesion.
    • Kim et al (2003) described the biceps load test II.4 With the patient supine, the affected arm is flexed to 120° and maximally externally rotated, with the elbow at 90° of flexion. If pain is elicited with resisted elbow flexion, the test finding is positive. The authors stated a sensitivity of 89.7% and specificity of 96.9% in detecting SLAP lesions.
    • In a study by Kim et al (2007), the authors described the passive compression test to assess for SLAP lesions.19  The patient is asked to lie down in a lateral position with the affected shoulder up and the physician standing behind the patient. The physician stabilizes the patient’s affected shoulder by holding the AC joint and controls the patient’s elbow with the other hand. The examiner rotates the patient’s shoulder externally with 30° of abduction and then pushes the arm proximally while extending the arm, which results in passive compression of the superior labrum onto the glenoid.
      • The test finding is considered positive if pain or a painful click is elicited in the glenohumeral joint.  The sensitivity of this test was reported to be 81.8%, and the specificity was 85.7%.
    • It should be noted that patients may also demonstrate a positive Neer (pain with passive forward elevation of the affected arm) or Hawkins sign (pain with passive internal rotation of the affected arm at 90° of flexion) in the presence of superior labral pathology.
  • Parentis et al completed a prospective study aimed at determining the most effective provocative maneuver with which to diagnose type I and II SLAP lesions.20 The 2 most sensitive tests for type II SLAP lesions were found to be the active compression (65.2%) and Hawkins test (65.2%). None of the sensitive tests were highly specific for type I or type II lesions.
    • Swaringen et al reported that electromyographic analysis of physical examination tests for type II SLAP lesions demonstrated that the active compression test and biceps tension test had significantly higher electromyographic signals relative to other tests, and consequently, maneuvers which maximize muscle activation transmitted through the LHB may be the best to identify type II SLAP lesions.21

Causes

In a series, Snyder et al reported that a compressive force or traction injury to the affected extremity was the most common mechanism of injury.2 However, in 21% of these patients, the etiology of the SLAP lesion was insidious. Moreover, most throwing athletes examined by Andrews et al did not report a distinct traumatic event.1 Thus, although an isolated injury may cause a labral injury, SLAP lesions may also occur as a result of the repetitive microtrauma that is associated with the overhead throwing motion.

Numerous authors have described a peel-back method for the development of SLAP II lesions. When the shoulder is in an abducted and externally rotated position, the biceps tendon is thought to assume a more vertical and posteriorly directed posture, which transmits a force to the superior labrum and causes it to peel off of the glenoid. Grossman et al supported this hypothesis in a cadaveric model.22 A contracted posterior capsule and resulting internal rotation deficiency, which is commonly observed in overhead throwing athletes, may translate the humeral head anteriorly, further aggravating the patient's symptoms.

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Elbow and Forearm Overuse Injuries
Overuse Injury
Rotator Cuff Injury

Related Medscape topic:
Resource Center Exercise and Sports Medicine

More on Superior Labrum Lesions

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Differential Diagnoses & Workup: Superior Labrum Lesions
Treatment & Medication: Superior Labrum Lesions
Follow-up: Superior Labrum Lesions
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References

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Further Reading

Keywords

superior labrum anterior-posterior lesion, SLAP lesion, superior glenoid lesion, anterior to posterior lesion of the superior labrum, anterior-to-posterior lesion of the superior labrum, shoulder instability, labral repair, posterior labral repair, capsulolabral complex, capsulolabral repair, Bankart lesion, Buford complex

Contributor Information and Disclosures

Author

Riley J Williams III, MD, Associate Professor, Department of Orthopedic Surgery, Hospital for Special Surgery, Weill Cornell Medical College; Director, HSS Institute for Cartilage Repair
Riley J Williams III, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American College of Sports Medicine, American Orthopaedic Society for Sports Medicine, and Medical Society of the State of New York
Disclosure: Nothing to disclose.

Coauthor(s)

Frank A Petrigliano, MD, Orthopaedic Surgery Resident, Department of Orthopaedic Surgery, University of California Los Angeles
Frank A Petrigliano, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons
Disclosure: Nothing to disclose.

Medical Editor

Gerard A Malanga, MD, Founder and Director, New Jersey Sports Medicine Institute; Director of Pain Management, Overlook Hospital; Director of Sports Medicine, Sports Medicine Fellowship Director, Mountainside Hospital; Clinical Chief, Rehabilitation Medicine and Electrodiagnosis, St Michael's Medical Center; Medical Director, Consultant, Horizon Healthcare Worker's Compensation Services, Blue Cross and Blue Shield Worker's Compensation
Gerard A Malanga, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, North American Spine Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Henry T Goitz, MD, Chief, Sports Medicine, Associate Professor, Department of Orthopaedic Surgery, Medical College of Ohio
Henry T Goitz, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons and American Orthopaedic Society for Sports Medicine
Disclosure: Nothing to disclose.

CME Editor

Jon B Whitehurst, MD, Clinical Instructor of Surgery, University of Illinois College of Medicine; Partner and Executive Board Member, Rockford Orthopedic Associates; Orthopedic Chairman, Rockford Memorial Hospital
Jon B Whitehurst, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.

Chief Editor

Craig C Young, MD, Professor, Departments of Orthopedic Surgery and Community and Family Medicine, Medical Director of Sports Medicine, Sports Medicine Fellowship Director, Medical College of Wisconsin
Craig C Young, MD is a member of the following medical societies: American Academy of Family Physicians, American College of Sports Medicine, American Medical Society for Sports Medicine, Phi Beta Kappa, and Wilderness Medical Society
Disclosure: Nothing to disclose.

 
 
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