Superior labral anterior to posterior (SLAP) lesions constitute a recognized clinical subset of complex shoulder pain pathologies. SLAP lesions demonstrate a predilection for young laborers, overhead athletes, and middle-aged manual laborers.[1] In 1985, Andrews first described superior labral pathologies, and Snyder later coined the term “SLAP lesion” because of the location and characteristic tear extension patterns.[1][2] Snyder developed the initial 4-subtype classification of these lesions. In the ensuing decades, other groups including Morgan et al.[3] and Maffet et al.[4] further subdivided the SLAP classification schemes to ultimately delineate ten different types of SLAP tear patterns, including combined SLAP- and Bankart-type injuries seen in specific associative patterns.
Advances in contemporary diagnostic capabilities and arthroscopic management techniques have led to evolving management paradigms since the original descriptions of SLAP-type lesions. These injuries are not solely limited to young throwing athletes as originally described, and SLAP tears commonly can be seen in various patient populations with varying degrees of actual clinical relevance. There is increasing evidence that SLAP tears are frequently present on MRI in asymptomatic overhead athletes. Thus, clinicians should remain cognizant of the known clinical ambiguity that may present with SLAP lesions recognized in isolation or association with other shoulder pathology.
The specific etiology underlying the various SLAP tear presentations is multifactorial and remains a topic of debate and controversy. Regardless of the underlying etiology, patients presenting with symptomatic SLAP tears will commonly report the acute onset of deep shoulder pain accompanied by mechanical symptoms such as popping, locking, or catching with various shoulder movements.
Acute traumatic SLAP lesions
Traumatic injuries commonly occur following acute, index events based on one of the following mechanisms:[2]
Attritional SLAP injuries
Peel-back mechanism
Compared to the acute, traumatic SLAP injuries, the overhead athlete is more likely to present with attritional-based etiologies. In these scenarios, SLAP tears present with the insidious onset and progressive deep shoulder pain in young athletes with the arm in the abduction and external rotation position during the late-cocking phase of throwing. In this position, the force on the biceps coupled with the posterior glide of the humerus results in the peeling off of the posterosuperior quadrant of the glenoid and posterior labrum.[5]
There remains debate regarding whether the so-called peel-back mechanism versus the deceleration phase of throwing is most responsible for the pathologic forces driving SLAP tears in overhead athletes.[6] The former implicates the late-cocking phase of throwing while the latter would theoretically implicate more traction-based mechanisms. Cadaveric studies have demonstrated SLAP tears are more likely to occur with the shoulder in a forward flexed position compared to positions in extension.[7]
Degenerative SLAP lesions
Degenerative SLAP tears can develop secondary to the normal “wear-and-tear” patterns seen in patients with advanced age. Degenerative SLAP tears often affect overhead laborers with increasing degrees of association in patients over 40 years old[8]
Types I – VIII[9]
It is important to appreciate the limitations in our ability to accurately report the definitive epidemiological trends as the contemporary recognition and diagnosis of SLAP injuries remains debated.[10][11] Furthermore, the respective incidence rates for the clinical diagnosis of SLAP lesions and the incidence of SLAP repairs remains limited given the paucity of available high-quality studies reporting available epidemiologic data and surgical management trends.[12] These concepts are further realized by the fact that a formal diagnosis code was not available until 2001, and it took until 2003 to institute a separate Current Procedural Terminology (CPT) code: 29807.[13][14]
The highest incidence rates of SLAP lesions present in the 20- to 29-year-old and 40- to 49-year-old age groups.[15] Additionally, we now recognize that SLAP lesions commonly occur in asymptomatic overhead athletes.[16][17] Analogous to meniscal cleavage planes, many Major League Baseball (MLB) team physicians now recognize these asymptomatic “tears” as adaptive changes in high-level, experienced overhead throwers and MLB pitchers.[18]
As our knowledge evolved over time with improvements in magnetic resonance imaging (MRI) quality, SLAP tears subsequently became a more frequent diagnosis. However, the ideal treatment of SLAP tears was never fully elucidated, and thus the increasing recognition of SLAP injuries brought about an increased incidence of SLAP repair rates across institutions.
The rise of SLAP repair rates
While Snyder’s group reported that SLAP repairs represent about 3% of shoulder cases in a large tertiary referral center, ensuing studies from the first decade of the 2000s reported a consistent rise in the overall increasing rate of SLAP repairs performed at many other institutions. Weber et al. reported surprising trends after mining the American Board of Orthopaedic Surgery (ABOS) Part II database. The ABOS database houses the collection of International Classification of Diseases, Tenth Revision (ICD-10) and CPT coding across eligible ABOS Part II candidates during their respective board collection periods. The authors noted an increase in the SLAP repair rate to greater than 10% of shoulder cases reported by the year 2008.[12]
Similarly, a 2012 study reported the rising incidence of arthroscopic SLAP repair rates within New York State from 2002 to 2010, noting a 464% increase in the number of SLAP repairs. This increase constituted a jump in case volume reporting from 765 to 4313 annual SLAP repairs. This increase translated to a population-based increased incidence rate from 4 per 100000 patients in 2002 to 22.3 per 100000 patients in 2010.[19]
The fall of SLAP repair rates
As our knowledge regarding the actual clinical significance of SLAP tear presentations continued to evolve from 2010 and beyond, the initial rise in the incidence rate of SLAP repairs performed reached its peak before subsequently declining over the last decade. Moreover, clinicians began reporting on the critical importance of differentiating younger, active patient populations (e.g., under 40 years old) and overhead athletes from the older patients (e.g., over 40 years old) with degenerative SLAP tears secondary to repetitive overhead manual laborer occupations.[20]
Erickson et al. reported in 2016 that an institutional trend from 2004 to 2014 (including four fellowship-trained orthopedic surgeons) revealed decreasing rates of total SLAP repairs performed. Further, the age of patients operated on for SLAP tears was decreasing, and the majority of SLAP repairs still being performed by the latter half of the study were limited to mostly Type II SLAP tears.[8]
A 2015 study investigated the adjusted incidence rates of SLAP tears as reported in the Defense Medical Epidemiological Database between 2002 and 2009. The adjusted annual incidence rate for SLAP lesions increased from 0.31 cases per 1000 person-years in 2002 to 1.88 cases per 1000 person-years in 2009, with an average annual increase of just over 20% during the study period.[11]
Despite the aforementioned limitations, the contemporary consensus regarding SLAP tears is that they account for 80% to 90% of labral pathology in the stable shoulder, although they are typically seen in association with other shoulder pathologies and rarely present in isolation.[21] Furthermore, SLAP tears account for approximately 1% to 3% of injuries presenting to sports medicine referral centers, and SLAP tears are present in approximately 6% of shoulder arthroscopy procedures.[2][21][22]
Anchor Anatomy
Variability in the anatomy of the biceps anchor and tendinous origin translates to varying levels of strain on the superior labrum[23]. Vangsness et al. initially described four types of attachments patterns of the long head of the biceps tendon (LHBT) to the superior glenoid rim and the superior labrum.[24] These four types were described based on macroscopic observation of 105 cadaveric shoulder specimens:
Tuoheti et al.[25] later clarified these attachment types and included their relationships with the glenoid attachment of the glenohumeral ligaments. Moreover, the macroscopic attachment types correlated to the specimen histologic sectioning observed in sagittal section. In this study (also studying over 100 shoulder cadaver specimens), the attachment sites clarified the findings from the previous study:
The latter study is the contemporary consensus agreement regarding the LHBT attachment patterns.[25]
Sublabral variations
Another potential nidus predisposing certain patients to SLAP tears is the presence of a sublabral recess (or sublabral sulcus). The recess/sulcus can be present during fetal development as early as by 22 weeks in pregnancy, persisting throughout childhood and into adulthood.[26]
In contrast, a sublabral hole or sublabral foramen,[27] is typically located at the 12 to 2 o’clock position and is the anatomic manifestation of a congenital failure of fusion of the labrum which attaches to the glenoid with a smooth margin or a medial slip.[28]
Finally, the Buford complex is a congenitally absent anterosuperior labrum plus a thickened cord-like middle glenohumeral ligament.[27]
Alpantaki et al. previously demonstrated that the tendon of the long head of the biceps contains a complex network of sensory and sympathetic nerve fibers.[29] Previous reports have emphasized the LHBT as a potentially dominant source of anterior shoulder pain at clinical presentation.[30][31]
Boesmueller recently histologically characterized the most proximal extent of the LHBT, specifically the neurofilament distribution as the tendon transitions into the superior labral complex. The authors demonstrated via immunohistochemical staining that there is an inhomogeneous distribution of nerve endings and sympathetic nerve fibers throughout the superior labral complex. Interestingly enough, the anterior aspect of the superior labrum and the labral region anterior to the LHBT origin has the highest density of these fibers.[32]
This factor may have a potential impact on patients experiencing persistent pain following various types of SLAP repairs. More research is necessary regarding the histologic characterization of the superior labrum-LHBT complex.
Clinicians should obtain a comprehensive history should when evaluating patients presenting with acute or chronic shoulder pain. SLAP tears may present in a relatively nonspecific fashion and association with other shoulder pathologies. Clinicians should inquire regarding certain elements in history taking that may help differentiate SLAP tears from other shoulder injuries.
Pertinent elements in history taking to best elucidate the nature of a potential SLAP tear (or other associated shoulder injuries) include[33][34][35]
Characteristics of LHBT-associated pathologies have been previously described and may include any combination of the following:
In addition, a thorough history includes a detailed account of the patient’s occupational history and current status of employment, hand dominance, history of injury/trauma to the shoulder(s) and/or neck, and any relevant surgical history.
Physical Examination Pearl [36][37][38][39][40]
C-spine / neck exam
Co-existing cervical radiculopathy should be ruled out in any situation where neck and/or shoulder pathology is in consideration. Observation of neck posturing, muscular symmetry, palpable tenderness, and active/passive ROM should undergo evaluation. Special tests that are helpful in this regard include the Spurling maneuver, myelopathic testing, reflex testing, and a comprehensive neurovascular exam.
Shoulder exam
Examiners should observe and compare bilateral shoulder girdles for any notable asymmetry, scapular posturing, and muscle bulk comparison or any atrophic changes. The skin should be observed for the presence of any previous surgical incisions, lacerations, scars, erythema, or induration.
Chronic instability patients will almost always exhibit at least a mild degree of asymmetry. The deltoid muscle often demonstrates atrophy in chronic dislocators. The findings can be rather subtle, especially in obese patients.
In the setting of chronic anterior instability, the clinician may be able to appreciate a palpable anterior fullness. Upon observation, the posterior shoulder (when viewed from the side of the patient) will be relatively flat relative to the anterior fullness. Chronic anterior and posterior instability patients may also exhibit corresponding posterior and anterior acromial prominences, respectively.
Scapulothoracic motion and scapular winging should also be evaluated during active and passive motion.
Following the observational component of the physical examination, the active and passive ROM are both documented; this may be limited in the setting of initial follow-up in the clinic after an acute instability event, or the setting of any complex instability case, especially in the setting of glenoid bone loss.
In the setting of chronic anterior instability, the clinician should attempt to assess the current status of the axillary nerve, although chronic dislocators often exhibit normal deltoid function as well as internal and external rotator strength. Specific testing of the supraspinatus muscle can be difficult when passive ROM is limited. Any evidence of significant muscular weakness may hint at an underlying associated neurologic deficit.
A detailed sensory examination should take place in all acute and chronic instability patients. In addition to axillary nerve function, motor function of the elbow, wrist, and hand should undergo an assessment to rule out the possibility of a brachial plexus injury associated with the dislocation. Distal pulses should be assessed at the wrist as well.
Older patients and in the setting of suspected concomitant shoulder pathologies (e.g., rotator cuff injuries or biceps tendon pathology), specialized testing for these pathologies also merit consideration.
Provocative examination testing/maneuver:[36][37][38][39]
The available evidence of level I and II studies in the recent literature suggests that a combination of specific tests such as the Speed’s and uppercut test is recommended for the clinical detection of biceps tendon lesions. Recent studies have reported on the diagnostic accuracy of specific tests concerning diagnosing SLAP tears:
Uppercut test:[43]
Bear-Hug test:[43]
O’Brien/Active Compression test:[43][36]
Supine Resistance test:[45]
Mayo Shear test (also known as the Modified O’Driscoll test or the Modified dynamic labral shear test:[46]
Radiographic imaging is necessary for all patients with acute or chronic shoulder pain.
Radiographs
Clinicians should obtain a true anteroposterior (AP) image of the glenohumeral joint (also known as the “Grashey” view). The true AP image is taken with the patient rotated between 30 and 45 degrees offset the cassette in the coronal plane. The beam can otherwise be rotated while the patient is neutral in the coronal plane. Other standard views include the axillary lateral view and “scapular Y”/outlet views.
Advanced imaging
MRI and MR arthrography (MRA) are commonly used imaging modalities to detect a SLAP lesion. Intra-articular contrast media and articular effusion, as well as arm traction and external rotation, improve the sensitivity of the MRI to determine a SLAP lesion. Clinicians should keep in mind the utilization of MRA may promote the overdiagnosis of asymptomatic (or clinically irrelevant) SLAP lesions and thus exercise best clinical judgment in ordering specific advanced imaging modalities. The endemic rate of variations of labral anatomy visible on MRI in asymptomatic overhead throwers should prompt caution before concluding that the labrum is the source of the patient’s pain.[18]
Schwartzberg reported MRI documented SLAP lesions can be present in up to 72% of middle-aged, asymptomatic patients.[47] Moreover, it is important to recognize that other shoulder pathologies, such as shoulder impingement (external or internal), rotator cuff syndrome, LHBT tendinopathy, acromioclavicular (AC) arthritis are all common pain generators in the middle-age population.[39][38] Thus, the inadvertent focus given to a potential SLAP lesion may be either overappreciated or misdirected. As mentioned, this concept can also be applied to the young, athletic population as well. In 2005, an MRI analysis of professional handball players demonstrated abnormalities in 93% of shoulders with only 37% being symptomatic.[48]
It is essential to understand that not all SLAP tears are created equal. Clinicians should focus on the potential relevance of the SLAP lesion as it attributes to the specific patient’s pain and dysfunction. Asymptomatic tears should be observed. Those that are potentially contributing to patient-reported symptoms may require surgery, and depending on the particular SLAP tear pattern and the presence (or absence) of other associated shoulder pathologies, the recommended surgical technique(s) may vary. Moreover, for the vast majority of SLAP injuries, the initial management is nonoperative.
Nonoperative management modalities
Anti-inflammatory medications, cryotherapy/cooling/ice application, rest and activity modification
An initial period of rest following the acute (or acute-on-chronic) injury should be implemented in all patients. In the appropriate patient, the use of NSAIDs and cryotherapy device/ice pack application can be beneficial for pain control. Athletes and overhead laborers should also be placed on a restricted sport-specific timeline protocol, and manual laborers should receive appropriate occupational modifications.
Physical therapy
The goal of physical therapy (PT) modalities should be to treat any underlying pathologic shoulder biomechanics that may have been present at baseline before the acute injury. Also, shoulder girdle proprioceptive training is beneficial to help prevent re-injury.
Scapulothoracic dyskinesia may result from any degree of imbalance of the shoulder girdle muscles and static/dynamic glenohumeral joint stabilizers. In addition, posterior shoulder joint capsular contractures should be addressed with various stretching and strengthening programs. Utilizing dedicated formal PT regimens can help ensure each “SLAP tear” diagnosis is most appropriately managed to help mitigate the risks of inferior patient outcomes.
Multiple reports on high-level (i.e., professional) overhead throwers have demonstrated equivalent outcomes regarding return to play and return to play performance in athletes managed with operative versus nonoperative modalities alone. Nonoperative PT regiments focused on correcting for scapular dyskinesia and glenohumeral internal rotation deficit (GIRD).[49]
If the non-operative therapy fails and symptoms persist that prevent sports activities or activities of daily living, then this would indicate the need for operative treatment.
Surgical management
After exhausting nonoperative treatment modalities, operative management is considered in tandem while keeping in mind each patient’s age, concomitant pathologies, functional requirements, occupational demands, and sport-specific goals.
Several authors have proposed surgical treatment algorithms depending on the specific type of SLAP lesion identified on advanced imaging, clinical exam, and during intraoperative arthroscopy.[41] It is critical to discern whether the labrum alone is responsible for the patient’s symptoms and whether restoring the labral attachment and biceps root to the glenoid will help. In addition, understanding how to treat a SLAP tear in the setting of other concomitant injuries is imperative. For example, in older patients with or without rotator cuff repair, the repair of the SLAP correlates with inferior results in comparison to intentional neglect or performing a bicep tenodesis/tenotomy regarding stiffness, persistent pain and need for revision surgery.[18] However, in younger patients presenting with shoulder instability, the SLAP injury may be present and contributing to symptoms, especially in the setting of an acute anterior and/or posterior labral tear. The following algorithm has been previously proposed[41]
SLAP repair technique
Multiple SLAP repair techniques have been previously described. Also, a wide array of implant options are available depending on surgeon preference. Previous authors have advocated for the use of simple versus mattress sutures and the option for knotless fixation devices to minimize the risk of having a bulky knot create symptoms postoperatively.[51][52]
After probing to confirm the diagnosis of a SLAP tear, a shaver can be used to resect unstable flaps of tissue that are deemed irreparable. Glenoid neck preparation is with a tissue elevator, rasp, and/or shaver instrument. The Neviaser portal is often utilized and established under direct visualization once confirming the appropriate trajectory are achieved. The determination of appropriate anchor placement depends on the predominant region of instability regarding the superior labral-biceps tendon complex.
The differential diagnosis for chronic shoulder pain includes several etiologies:
Impingement
RC pathology
Degenerative
Proximal biceps
AC joint conditions
Instability
Neurovascular conditions
Other conditions
Although Level I and II studies in the literature are lacking regarding outcomes following arthroscopic type II SLAP repairs, most studies report overall favorable results and good outcomes in the appropriately selected patients.[53][54][55] A number of authors report good results in athletes, including those with sport-specific overhead demand requirements.[56]
Clinicians should recognize that inferior outcomes have been demonstrated in the literature following revision arthroscopic SLAP repairs and in high-level (i.e. professional) overhead athletes.[57] Professional baseball pitchers demonstrate relatively inferior outcomes in terms of return to play and return to prior performance level. In fact, superior outcomes have been reported in this particular subset of athletic patients following non-surgical management alone.[49][57]
Risk factors for revision surgery are critical in discussing overall patient expectations and discussing the risks of continued pain, stiffness, dysfunction, and the potential need for further surgery in the future. A 2017 level III case-control study highlighted the potential risk factors for revision surgery following SLAP repair, with the inclusion of nearly 5000 patients in the database query[58]
Weeks 0 to 4 to 6 postop
Weeks 4 to 6 postop
Weeks 6 to 12 postop
Week 12 and beyond
Primary care sports medicine specialists experienced in managing SLAP tears nonoperatively. Given the clinical complexity of SLAP injuries and concomitant shoulder pathologies, early consultation with an orthopedic surgeon is encouraged.
Patients presenting with concerns over a potential SLAP tear should receive education regarding the contemporary clinical knowledge we now have regarding these injuries. Moreover, patients will often present with an MRI final report stating a SLAP tear was present on imaging. In these clinical scenarios especially, the recommendation is to reassure the patient and educate them regarding the high incidence rate of “incidental” or “clinically irrelevant” SLAP injuries and detailed and focused attention should be given to appropriately delineating the extent of all potential underlying shoulder girdle pathologies.
SLAP lesions first gained recognition in the 1980s. Over the last two decades, our knowledge and appreciation of SLAP tear recognition, diagnosis, treatment, and potential surgical management has evolved dramatically. There is an increasing body of literature evidence now recognizing that appropriate patient selection is critical, and management must consider a multitude of factors include the patient’s age, activity level, sport-specific requirements, occupational demands, and expectations of a good to excellent outcome. A team approach, involving clinicians, therapists, and nurses will provide the best results. [Level II-III]
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