Fig. 22.1
Anatomy of the glenoid cavity showing the superior labral complex, anterior, posterior, and inferior
Anatomical variations are common in the anterior labral region and should be distinguished from pathological conditions. Variations include a sublabral foramen [12] or absence of the anterior labrum, both of which are commonly associated with a robust middle glenohumeral ligament (Buford complex) present in 1.5% of people [13, 14] (Fig. 22.3).
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Fig. 22.3
Anatomical variations of the labral complex. Above: foramen sublabral. Below: Buford complex (medial glenohumeral ligament in rope entering the base of the long biceps cable and hypoplastic anterior labrum)
The glenoid labrum is the fibrocartilage of the shoulder joint. It comprises three sides and one edge: the superficial side is free and responsive to the humeral head; the articular side adheres to the edge of the glenoid cavity; and the peripheral side is in continuity with the joint capsule (providing vascularization) and the shoulder ligament insertion. The axial edge is free. The form varies according to the region: the articular side does not adhere to the edge of the glenoid cavity in the superior region, where it is free (meniscus-like aspect); it is wide and voluminous and adheres to the edge of the glenoid cavity in the inferior and posterior region (region of the inferior glenohumeral ligament insertion), on which the strongest forces act. The insertion of the long head of the biceps tendon is to both the supraglenoid tubercle and the superior part of the labrum. The proportion and orientation of biceps fibers connected to the labrum vary greatly between individuals [9].
22.2 Biomechanics
The labrum has several functions and three in particular: it increases the contact area between the humeral head and scapula, by 2 mm anteroposteriorly and 4.5 mm supero-inferiorly; it contributes to the “viscoelastic piston” effect, maintaining −32 mmHg intra-articular negative pressure; this is especially effective against traction stress and, to a lesser extent, against shear stress; it provides the insertion for stabilizing structures (capsule and glenohumeral ligaments), as a fibrous “crossroad” [15]. Labrum and ligaments are in synergy in a genuine complex, each structure’s contribution varying with the position of the limb: in abduction and external rotation (ABER), the inferior glenohumeral ligament (IGHL) absorbs 51% of the stress, the superior glenohumeral ligament (SGHL) 22%, and the MGHL 9% [16].
Biomechanical studies have sought to elucidate the function of an intact superior labrum/biceps complex and confirm the pathogenesis of injuries [17]. The function of the biceps is controversial and many authors have looked at this. The long head of the biceps tendon (LHBT) is felt to act as a humeral head depressor, aiding in glenohumeral compression and anterior and posterior glenohumeral stabilization and can limit external rotation [18, 19]. Giphart et al., however, found that there was no significant effect of the LHBT on glenohumeral kinematics [20].
A variety of mechanisms of injury are proposed in the pathogenesis of SLAP lesions, especially traction tension loads on the arm, compressive forces, and repeated microtrauma in throwing athletes. During the overhead throwing motion in the baseball pitch, SLAP lesions are often seen in the late and deceleration phase [21]. The increased lateral rotation in this late stage creates an increase in torsional stress in the insertion of the biceps, resulting in the dynamic peel-back mechanism and injury to the posterosuperior labrum [22]. In the last decade, understanding of the biomechanics and pathophysiology of the athletic shoulder has significantly improved. Especially in overhead athletes and throwers, several pathologic mechanisms have been identified which could not be explained by the traditional concepts of instability and impingement. Glenohumeral instability and posterior capsule contracture are believed to play a crucial role in the etiology of the painful athletic shoulder. Instability and contractures related to sports are frequently underappreciated. These may initiate a vicious cycle of secondary internal impingement, muscular dysfunction, and damage to intra-articular structures. The results can be devastating and may even end the athlete’s career [23].
The term “instability” constitutes a spectrum of disorders, which includes hyperlaxity, subluxation, and dislocation. Principally, glenohumeral instability can be classified according to its etiology, degree, frequency, and direction. The classic categorization of affected individuals into two groups with traumatic and atraumatic instability represented by the mnemonics TUBS (traumatic, unidirectional, Bankart lesion, surgical treatment) and AMBRII (atraumatic, multidirectional, bilateral, rehabilitation, inferior capsular shift, rotator interval closure) has been supplemented by a further grouping that is mainly comprised of overhead athletes with so-called micro-instability (microtraumatic instability) and that has been labeled with the acronym AIOS (acquired instability in overstressed shoulder). However, it should be emphasized that congenital or acquired hyperlaxity, micro-instability, and traumatic instability can overlap particularly in athletes engaged in overhead sports [24, 25].
22.3 Mechanism of Trauma
Snyder et al. [6] described the most common mechanisms of SLAP lesions as compression injuries of the upper limb and traction injuries of the superior labrum biceps tendon complex with the shoulder in hyperextension. A three-part series of articles by Burkhart and colleagues looked at the association of kinetic chain disorders and scapular dyskinesia on SLAP injuries. The peel-back mechanism is associated with SLAP tears, with associated posteroinferior contraction and migration of rotation from the center toward the posterosuperior portion of the glenohumeral joint. With associated anteroinferior relaxation, there is a change in the biceps vector and elevated shearing in peel-back forces during the throwing cycle [21, 22, 26, 27].
Traumatic glenohumeral instability is also implicated as an associated etiology. It is typically initiated by a specific traumatic event, followed by other episodes of dislocation or subluxation usually in an anteroinferior direction when a sudden force overwhelms the anterior capsular structures. This occurs while the athlete’s arm is in an abducted, externally rotated, and extended position. The resulting combination of injuries represents the source of chronic instability, particularly those involving the inferior glenohumeral ligament (IGHL). Most studies agree that the IGHL is the most important passive stabilizer of the shoulder joint [28, 29]. The IGHL is formed by an anterior and a posterior band, which represents a thickening of the capsule connecting the inferior labrum to the glenoid and the humeral neck. The anteroinferior labrum and the anterior band of the IGHL together form the anteroinferior labro-ligamentous complex. The labrum is thought to serve as an insertion site for the IGHL and to provide stability to the glenohumeral joint by deepening the glenoid fossa [30]. Although generally common in contact collision sports, this type of instability is rarely observed in throwers or overhead athletes. When present, however, this type of instability can cause secondary damage to the rotator cuff and the superior and posterior labrum [31].
According to Soslowsky et al., inferior subluxation of the shoulder resulted in type II SLAP lesions [32]. Lo and Burkhart concluded that anterior lesions led to injuries of the superior and posterior labrum, because a history of trauma was observed in shoulders when they were positioned in abduction and external rotation [33]. They believe that recurrent anteroinferior instability is mainly responsible for the SLAP lesions.
These authors also suggest that more extensive lesions are a result of an increased number of dislocations, secondary to progression of a simple injury. However, this is not always the case, since extensive lesions have also been noted with low numbers of dislocations in the presence of high-energy trauma [34]. Durban et al. suggest that the severity of the lesions is a result of the initial high-energy trauma leading to the anterior shoulder instability with SLAP lesions [35]. Therefore, primary lesions of complex labral tears, such as type V SLAP lesions, should be examined thoroughly.
22.4 Classification
In 1985, Andrews postulated that a SLAP lesion, an anteroposterior tear of the superior labrum, was caused by overloading and traction of the long head of the biceps tendon during the follow-through phase of throwing [1]. Snyder categorized SLAP lesions into four types and suggested that type II SLAP lesions were the most common injuries and were primarily responsible for pain and restricted mobility of the shoulder joint in overhead athletes [6]. Maffet then added more types to this classification, because 38% of the SLAP lesion patients did not fall into the classification by Snyder. The authors use the Morgan and Maffet modifications [7] (Figs. 22.4, 22.5, 22.6, 22.7, and 22.8):
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Type I: Lip fibrillation with a local degeneration. Commonly seen in middle-aged, usually asymptomatic
Type II: More common. Detachment of the upper lip/biceps glenoid complex with an abnormal mobility. Important to differentiate the meniscoid appearance and the medial insertion of the glenoid lip (usually symptomatic). Subdivided into types A (anterior), B (predominantly posterior), and C (combined)
Type III: Bucket handle injury with an intact biceps. May cause mechanical symptoms depending on the size of the lesion
Type IV: Bucket handle injury extending into the biceps tendon
Type V: Association with Bankart lesion
Type VI: SLAP with an unstable labrum flap
Type VII: Association with the middle glenohumeral ligament injury
Type VIII: Association with a posterior labrum injury
Type IX: Circumferential labral injury (360°)
Type X: Association with a superior glenohumeral ligament injury
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Fig. 22.4
Snyder classification of the four types of injury. (a) type I; (b) type II; (c) type III; (d) type IV
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Fig. 22.5
SLAP lesions: classification according to Snyder. (a) Type I: Lip fibrillation. (b) Type II: Detachment of the upper lip/biceps glenoid complex. (c) Type III: Bucket handle injury with an intact biceps. (d) Type IV: Bucket handle injury extending into the biceps tendon (LBC labral-bicipital complex, HH humeral head, G glenoid)
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Fig. 22.6
Four types of SLAP. Coronal oblique MRI with arrows pointing superior labrum lesions types I to IV. Type I: Lip fibrillation. Type II: Detachment of the upper lip/biceps glenoid complex. Type III: Bucket handle injury with an intact biceps. Type IV: Bucket handle injury extending into the biceps tendon. HH humeral head, G glenoid (From: Woertler and Waldt [62])
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Fig. 22.7
Type V to type X SLAP lesions (BT biceps tendon, G glenoid, SGHL superior glenohumeral ligament, MGHL medium glenohumeral ligament, IGHL inferior glenohumeral ligament, SS supraspinal, IS infraspinal, T teres minor)
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Fig. 22.8
Types V to X of SLAP (Maffet-Morgan modification) seen in MR arthrogram, pointed by the arrows. Type V: Association with Bankart lesion. Type VI: SLAP with an unstable labrum flap. Type VII: Association with the middle glenohumeral ligament injury. Type VIII: Association with the posterior labrum injury. Type IX: Circumferential labral injury (360°). Type X: Association with superior glenohumeral ligament injury. HH humeral head, G glenoid, SS supraspinal muscle, C coracoid process (From: Woertler and Waldt [62])
22.5 History and Physical Exam
A complete clinical history with detailed mechanism of trauma description is essential. Symptoms associated with Bankart lesions typically do not include chronic pain but rather functional limitations that arise from symptoms of instability. In contrast, SLAP lesions frequently present with pain. We believe the combination of both lesions involves a great degree of energy with the arm in abduction and external rotation, where simultaneously the biceps labral complex is subjected to shear and torsional forces.
There are many tests that have been described in the literature. These include O’Brien’s test, Speed’s test, Yergason’s test, pain provocation test, biceps load test, biceps load test type II, crank test, and many more. Recent literature [36] has looked at a combination of tests to get the optimal sensitivity and specificity. And these often involve the combination of O’Brien’s, Hawkin’s, Speed’s, Neer’s, and Jobe’s test. High specificity tests include pain provocation and Yergason’s test. The authors feel that a combination of several tests is optimal for an accurate diagnosis.
The use of SLAP tests and assessments for traumatic anterior instability in combination with radiologic imaging can improve accuracy, but arthroscopy is the gold standard for both diagnosis and treatment of SLAP tears [37].
22.6 Radiological Evaluation
The high diagnostic accuracy of magnetic resonance (MR) arthrography in the detection of labro-ligamentous lesions has been demonstrated in several studies with a sensitivity of 88–96% and a specificity of 91–98% [38]. For the detection of lesions of the superior, middle, and inferior glenohumeral ligaments, Chandnani and coworkers reported sensitivities and specificities of 88–100% [39]. The sensitivities and specificities of unenhanced MR imaging for the diagnosis of labro-ligamentous injuries vary widely in the literature. A direct comparison with MR arthrography has not yet been performed in a larger series. The role of standard MR imaging in the diagnostic work-up of shoulder instability is questionable, particularly in regard to chronic cases and the identification of associated pathology. The advantages of MR arthrography result from capsular distension with separation of anatomic structures and improved delineation of tears following introduction of contrast media. MR arthrography thereby allows a more confident identification of pathology from the common anatomic variations of labral morphology, as well as the congenital variants of the glenohumeral ligaments and the labro-ligamentous unit, such as the Buford complex. MR arthrography (MRA) is the current gold standard imaging method to detect SLAP tears [39, 40].
We can clearly see a SLAP type II lesion in association with a Bankart lesion using MR arthrography (Fig. 22.9).
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Fig. 22.9
SLAP type II lesion in association with a Bankart lesion in traumatic anterior glenohumeral instability. (a) Coronal oblique fat-suppressed T1-weighted MR arthrogram shows superior extension of contrast media into the superior labrum and biceps anchor (arrowhead). (b) Corresponding sagittal oblique MR arthrogram reveals tearing of the entire anterior labrum (arrowheads) extending from inferior to superior. (c, d) Corresponding transverse MR arthrograms demonstrate detachment of the anterior labrum that continues as a classic Bankart lesion anteroinferiorly (arrows) (From: Woertler and Waldt [62])
22.7 Treatment
22.7.1 Conservative Treatment
Nonoperative treatment continues to have a role for patients who have mild symptoms and/or with contraindications to a surgical procedure. Nonoperative treatment usually focuses on associated shoulder injuries and the results of clinical examination. The aim of therapy is capsular mobilization, rotator cuff strengthening, scapular and humeral head stabilization, and the use of nonsteroidal anti-inflammatory drug (NSAID) medications [37, 41]. There is no study, which the authors are aware of, that investigates the effectiveness of conservative treatment with SLAP lesions.
22.7.2 Operative Treatment
Although the exact contribution of the biceps and superior labrum to anterior shoulder stability is unclear, several authors have noted that SLAP lesions can contribute to glenohumeral joint instability. Rodosky et al., in a biomechanical study, found that superior labral detachment placed increased strain on the inferior glenohumeral ligament and decreased the shoulder’s resistance to torsional forces [42]. They considered superior labral detachment to be detrimental to anterior shoulder stability. Pagnani et al. in 1995 showed significantly increased anteroposterior and supero-inferior glenohumeral translation when the insertion of the biceps was destabilized [43]. In their analysis of 139 cases of SLAP tears, Kim et al. noted that type III and type IV lesions were significantly associated with a Bankart lesion and a high-demand occupation [25]. Similarly, Snyder et al. noted that 43% of their patients with type IV SLAP tears had a concurrent Bankart lesion [11]. When confronted with a combined Bankart and type IV SLAP lesion, we make an effort to repair all pathoanatomy present including the superior labrum and biceps tendon split to preserve its stabilizing function.
Some authors believe that reattachment of concomitant SLAP lesions depends on the age and functional demand of the patient, noting that biceps tenodesis or tenotomy had varied results. Most studies show that with combined repairs, there is a significant difference in ranges of motion, functional scores, and recurrence rates when compared to an isolated Bankart repair [44, 45]. However, other authors have noted several limitations especially in external rotation among those who underwent the combined procedure [46].
The treatment of LHBT pathology lies along a spectrum ranging from simple debridement to tenotomy to one of many procedures developed for tenodesis. The decision to perform a tenodesis versus primary SLAP repair has evolved over recent years as the rate of SLAP repair has declined in response to discouraging outcomes in some patient populations. The location of tenodesis remains a topic of controversy, as does the debate between arthroscopic and open techniques.
In cases where the biceps tendon is involved and/or the SLAP tear is very degenerative and has a low potential for healing, a biceps tenotomy or tenodesis has been more recently recommended, rather than a SLAP repair [47]. Additionally it has been shown that operative treatments of SLAP tears that involve debridement were often unsuccessful [48, 49].
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