Wednesday, 26 April 2023

 

                        SLAP Lesion


                                 Dr. KS Dhillon


Introduction

Superior labral anterior to posterior (SLAP) lesions are a subset of complex shoulder pain pathologies. SLAP lesions are usually seen in young laborers, overhead athletes, and middle-aged manual laborers [1]. Andrews was the first to describe superior labral pathologies in 1985. Snyder later coined the term “SLAP lesion” because of the location and characteristic tear patterns [1,2]. Initially, Snyder developed the 4-subtype classification of these lesions.  In decades that followed other groups including Morgan et al and Maffet et al [3,4] further subdivided the SLAP classification to ultimately delineate ten different types of SLAP tear patterns. This included combined SLAP and Bankart-type lesions seen in specific associative patterns.

There have been advances in contemporary diagnostic capabilities.  Arthroscopic management techniques have led to evolving management paradigms. SLAP tears are commonly seen in various patient populations with varying degrees of actual clinical relevance. There is increasing evidence that SLAP tears are frequently seen on MRI of the shoulder in asymptomatic overhead athletes. Hence, clinicians should remain cognizant of the known clinical ambiguity that may be present with SLAP lesions recognized in isolation or in association with other shoulder pathology.


Etiology

The etiology underlying the various SLAP tear presentations is multifactorial. It remains a topic of debate and controversy. Patients with symptomatic SLAP tears will complain of acute onset of shoulder pain and mechanical symptoms such as popping, locking, or catching with shoulder movements.

There are various etiologies for SLAP lesions. Acute traumatic SLAP lesions result from trauma. The traumatic injuries occur following acute index events based on one of the following mechanisms:[2] 

  • Compression-type injuries. Classically advocated by Snyder. His original case series from 1990 reported that about half of the patient presentations were following a fall onto an outstretched arm with the arm in varying degrees of shoulder abduction.

  • Traction-type injuries. Occur due to sudden jerking movements or after lifting heavy objects. Can also occur after an unexpected pull on the arm

  • Combined-type injuries


Attritional SLAP Injuries occur by a peel-back mechanism. The overhead athlete is more likely to present with attritional SLAP injuries. The SLAP tears present with insidious onset and 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 arm 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 some debate about 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 peel-back mechanism implicates the late-cocking phase of throwing, while the deceleration phase of throwing would theoretically implicate more traction-based mechanisms. Cadaveric studies have shown that SLAP tears are more likely to occur with the shoulder in a forward-flexed position than positions in extension [7].

Degenerative SLAP tears can develop secondary to the normal wear and tear as seen in patients with advanced age.  Degenerative SLAP tears often affect overhead laborers over the age of 40 years [8].

There are 8 types of SLAP tears [9]:

  • Type I SLAP Tear - There is degenerative fraying at the free edge of the labrum. The insertion to the superior glenoid remains intact.

  • Type II SLAP Tear- This is caused by an acute injury. The labrum and the long head of the biceps tendon (LHBT) are torn and avulsed off the glenoid cavity. The avulsed area is now devoid of cartilage in the zone of injury.

  • Type III SLAP Tear- There is a “bucket-handle” pattern. The labral insertion of LHBT is left unaffected. This is the rarest form.

  • Type IV SLAP Tear- “Type III plus anterior shoulder instability”. There is Type III tear pattern plus extension into the LHBT. Often seen in association with shoulder instability and anterior labral tears.

  • Type V Slap Tear- “Type II plus anterior shoulder instability.”

  • Type VI Slap Tear- The incidence is unknown. The tear pattern involves larger superior labral flaps without detachment of the LHBT insertion.

  • Type VII Slap Tear- Type II SLAP tear pattern plus middle and inferior glenohumeral ligament compromise. Tear pattern is seen in the setting of complex shoulder instability.

  • Type VIII Slap Tear- Type II SLAP tear pattern plus additional cartilage injury adjacent to the bicipital footplate


Epidemiology

There are limitations in the ability to accurately report the definitive epidemiological trends as the contemporary recognition and diagnosis of SLAP injuries remain debated [10,11]. The literature on the incidence of clinical diagnosis of SLAP lesions and the incidence of SLAP repairs remains limited. There is a paucity of high-quality studies reporting the epidemiologic data and surgical management trends [12]. 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 of SLAP lesions is present in the 20 to 29 year-old and 40 to 49 year-old age groups [15]. Furthermore, we now know that SLAP lesions commonly occur in asymptomatic overhead athletes [16,17]. Most physicians now recognize that these asymptomatic “tears” are adaptive changes in high-level, experienced overhead throwers [18].

With the advent of magnetic resonance imaging (MRI), SLAP tears became a more frequent diagnosis. However, the ideal treatment of SLAP tears was never fully elucidated. Increasing recognition of SLAP injuries brought about an increased incidence of SLAP repair rates.

Snyder’s group [2] 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 increased rate of SLAP repairs performed at many institutions.

Weber et al [12] searched the American Board of Orthopaedic Surgery (ABOS) Part II database and they found that SLAP repairs increased over the study period from 9.4% to 10.1% for the years 2003 through 2008.  

A study by Onyekwelu et al [19] done in 2012 showed a rising incidence of arthroscopic SLAP repair rates within New York State from 2002 to 2010. They noted a 464% increase in the number of SLAP repairs. The case volume jumped from 765 to 4313 annual SLAP repairs. 

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. Clinicians began reporting on the critical importance of differentiating younger, active patient populations under the age of 40 years and overhead athletes from older patients over the age of 40 years with degenerative SLAP tears secondary to repetitive overhead manual laborer occupations [20].

In 2016, Erickson et al [8] reported that an institutional trend from 2004 to 2014 showed decreasing rates of SLAP repairs performed. Furthermore, the age of patients operated on for SLAP tears was decreasing. The majority of SLAP repairs being performed by the latter half of the study were limited to mostly Type II SLAP tears.

A study by Waterman et al [11] in 2015 showed that 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%.

The contemporary consensus regarding SLAP tears is that they account for 80% to 90% of labral pathology in the stable shoulder. They are typically seen in association with other shoulder pathologies and rarely present in isolation [21]. SLAP tears account for approximately 1% to 3% of injuries presenting to sports medicine centers. SLAP tears are present in approximately 6% of shoulder arthroscopy procedures [2,2,22].


Pathophysiology

Variability in the anatomy of the biceps anchor and tendinous origin leads to varying levels of strain on the superior labrum [23]. Vangsness et al [24]  described four types of attachment patterns of the long head of the biceps tendon (LHBT) to the superior glenoid rim and the superior labrum.  These four types were described based on the observation of 105 cadaveric shoulder specimens:

  • Posterior, complete – 22%

  • Posterior, dominant – 33%

  • Equal (anterior and posterior) – 37%

  • Anterior, complete – 8%

Tuoheti et al [25] later, further clarified these attachment types and included their relationships with the glenoid attachment of the glenohumeral ligaments. Their study included over 100 shoulder cadaver specimens. The attachment sites clarified the findings from the previous study:

  • Posterior, complete – 28%

  • Posterior, dominant – 56%

  • Equal (anterior and posterior) – 16%

  • Anterior, complete – 0%

This latter study is the contemporary consensus agreement regarding the LHBT attachment patterns [25].

Another 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 22 weeks of pregnancy. It persists throughout childhood and into adulthood [26].

A sublabral hole or sublabral foramen is located at the 12 to 2 o’clock position [27]. It is the anatomic manifestation of a congenital failure of fusion of the labrum that attaches to the glenoid with a smooth margin or a medial slip [28]. The Buford complex is a congenitally absent anterosuperior labrum plus a thickened cord-like middle glenohumeral ligament [27].


Histopathology

Alpantaki et al [29] had previously demonstrated that the tendon of the long head of the biceps contains a complex network of sensory and sympathetic nerve fibers. Previous reports have emphasized that the LHBT is a potentially dominant source of anterior shoulder pain [30,31].

Boesmueller et al [32] histologically characterized the most proximal extent of the LHBT, specifically the neurofilament distribution, as the tendon transitions into the superior labral complex. The authors showed via immunohistochemical staining that there is an inhomogeneous distribution of nerve endings and sympathetic nerve fibers throughout the superior labral complex. The anterior part of the superior labrum and the labral region anterior to the LHBT origin have the highest density of these fibers.

This may have a potential impact on patients experiencing persistent pain following various types of SLAP repairs.  


History and Physical Examination

A comprehensive history is required when a patient presents with acute or chronic shoulder pain.  SLAP tears may present with other shoulder pathologies. History should be obtained to help differentiate SLAP tears from other shoulder injuries.

Pertinent elements in history taking to elucidate the nature of a potential SLAP tear or other associated shoulder injuries include [33,34,35]:


  • Acute onset of “deep” shoulder pain.

  • Mechanical symptoms such as popping, locking, and catching with various movements and activity

  • History of any sudden, jerking force to the shoulder with associated   pain

  • History of or current episodes of shoulder instability

  • History of or current sport-specific participation including the level of competition (e.g., professional, collegiate, recreational). Common SLAP-provoking sports include but are not limited to overhead sports (volleyball, baseball pitchers, javelin, swimming). History or current manual/physical laborer occupations.

Characteristics of LHBT-associated pathologies may include any combination of the following:

  • Atraumatic insidious onset of anterior shoulder pain

  • Exacerbation of symptoms with overhead activities

  • Pain radiating from the shoulder down the anterior arm 

  • Clicking or audible popping

  • Pain at rest and at night

A thorough history includes a detailed account of the patient’s occupational history and current status of employment, hand dominance, and history of injury to the shoulder and/or neck.


Physical Examination [36,37,38,39,40]

A neck and cervical spine examination is carried out to exclude 

co-existing cervical radiculopathy. Observation of muscular symmetry, neck posturing, palpable tenderness, and movements is carried out. Spurling maneuver, myelopathic testing, reflex testing, and a comprehensive neurovascular examination is done.

Shoulder examination has to be carried out. The examiners should observe and compare both shoulders. The examiner has to look for asymmetry, scapular posturing, muscle bulk comparison, or any atrophic changes. The skin is observed for the presence of surgical scars, lacerations, other scars, erythema, or induration. Patients with chronic instability will almost always exhibit at least a mild degree of shoulder asymmetry. The deltoid muscle often shows atrophy in patients with chronic dislocations. 

An anterior fullness can be felt in patients with chronic anterior instability. The posterior shoulder when viewed from the patient's side will be relatively flat relative to the anterior fullness. Chronic anterior and posterior instability patients may also exhibit corresponding posterior and anterior acromial prominences. 

While performing an examination scapulothoracic motion and scapular winging should also be evaluated during active and passive motion of the shoulder. 

The active and passive ROM are both recorded. The movements may be limited on initial follow-up in the clinic after an acute instability event or the setting of any complex instability case. 

In patients with chronic anterior instability, the status of the axillary nerve must be determined. Chronic dislocators usually exhibit normal deltoid function and internal and external rotator strength. Testing of the supraspinatus muscle can be difficult when the passive ROM is limited. Evidence of significant muscular weakness may indicate an underlying associated neurologic deficit. 

A detailed sensory examination is carried out in all patients with acute and chronic instability. The motor function of the elbow, wrist, and hand should be carried out to exclude the possibility of a brachial plexus injury associated with the dislocation. 


Provocative Examination Testing [36,37,38,39]:

Level I and II studies suggest that a combination of specific tests such as the Speed’s test and uppercut test is recommended for the clinical detection of biceps tendon lesions. Recent studies have reported on the diagnostic accuracy of these tests: 

Speed’s Test [41,42,36]:

A positive test consists of pain elicited in the bicipital groove when the patient attempts to forward elevate the shoulder against resistance with the elbow slightly flexed and the forearm supinated. The sensitivity of this test is 32% and the specificity is 75%.

Uppercut Test [43]:

The involved shoulder is placed in neutral position, the elbow is flexed to 90 degrees, the forearm is supinated, and the patient makes a fist.  The examiner then instructs the patient to perform a boxing “uppercut” punch while placing the hand over the patient’s fist to resist the upward motion. A positive test is pain or a painful pop over the anterior shoulder near the bicipital groove region. The sensitivity of this test is 73% and the specificity is 78%.

Yergason’s Test [42] [37]:

The patient's arm is stabilized against the trunk, and the elbow is flexed to 90 degrees with the forearm pronated. The examiner resists supination while the patient also externally rotates the arm against resistance. A positive test is if the patient reports pain over the bicipital groove and/or subluxation of the LHB tendon occurs. The sensitivity of the test is 43% and the specificity is 79%.

Bear-Hug Test [43]:

The patient places the hand on the contralateral (normal) shoulder in a self-hug position. The palm is on the anterior aspect of the contralateral shoulder and the elbow is flexed to 90 degrees. The examiner applies a perpendicular external rotational force to try and lift the patient’s hand off the shoulder.  A positive test is when the patient cannot hold the hand against the shoulder as the examiner applies an external rotation force.

The sensitivity of the test is 79% and the specificity is 60%.

Belly Press Test [43,39]:

The patient’s arm is at 90 degrees of elbow flexion, and IR testing is performed by the patient by pressing the palm of his/her hand against the belly, bringing the elbow in front of the plane of the trunk. The examiner supports the elbow, and a positive test occurs if the elbow does not maintain this position upon the examiner removing the supportive force.

The sensitivity of this test is 31% and the specificity is 85%.

O’Brien/Active Compression Test [36,43]:

With the patient standing the arm is positioned at 90 degrees of forward flexion, 10 degrees of adduction, and internally rotated so the thumb points toward the floor. The examiner then places his/her hand over the patient’s elbow while instructing the patient to resist the examiner’s downward force applied to the arm. This maneuver is then repeated with the patient’s arm now rotated, so the palm faces the ceiling. The test is positive if there is pain located at the joint line during the initial maneuver (thumb down/internal rotation) in conjunction with reported improvement or elimination of the pain during the subsequent maneuver (palm up/external rotation). The sensitivity of the test is 38% and the specificity is 61%.

Anterior Slide Test [44] [36]:

The patient stands with his/her hand placed on the ipsilateral hip with the thumb pointing posteriorly. The examiner places one hand on the elbow and the other hand on the joint line of the shoulder. An axial load is then applied in an anterosuperior direction from the elbow to the shoulder. The test is positive if there is pain or a painful click on the anterior or posterior joint line. The sensitivity of this test is 10% and the specificity is 82%.

Supine Resistance Test [45]:

The patient lies supine on the exam table with his/her arms resting in full abduction with the forearm and hand supported by the table and the palm facing upward.  The examiner applies a downward resistive force just distal to the elbow while asking the patient to perform a throwing motion. The test is positive if it elicits pain deep inside the shoulder joint or at the shoulder's dorsal aspect along the joint line during the resisted movement. The sensitivity of the test is 80% and the specificity of the test is 69%.

Mayo Shear Test (also known as the Modified O’Driscoll Test or the Modified Dynamic Labral Shear Test [46]:

The patient stands with his/her arm flexed 90 degrees at the elbow and abducts the shoulder in the scapular plane to above 120 degrees. The examiner applies external rotation until resistance is appreciated. The examiner then applies a shear force through the shoulder joint by maintaining external rotation and horizontal abduction and lowering the arm from 120 to 60 degrees of abduction. The test is positive if there is reproduction of the pain and/or a painful click or catch in the joint line along the posterior joint line between 120 and 90 degrees of abduction. The sensitivity of the test is 80%.


Evaluation

Radiographic imaging has to be done for all patients with acute or chronic shoulder pain.

A true anteroposterior (AP) image of the glenohumeral joint also known as the “Grashey” view is done. This true AP image is taken with the patient rotated between 30 and 45 degrees off the cassette in the coronal plane. Otherwise the beam can be rotated while the patient is neutral in the coronal plane. Other views include the axillary lateral view and “scapular Y”/outlet views.

MRI and MR arthrography (MRA) are commonly used imaging modalities to diagnose a SLAP lesion. Intra-articular contrast media, articular effusion and arm traction, and external rotation, improve the sensitivity of the MRI to determine a SLAP lesion. The utilization of MRA may promote the overdiagnosis of asymptomatic (or clinically irrelevant) SLAP lesions. The variations of labral anatomy visible on MRI in asymptomatic overhead throwers should prompt caution before concluding that the labrum is the cause of the patient’s pain [18].

Schwartzberg et al [47] reported MRI documented SLAP lesions in up to 72% of middle-aged, asymptomatic individuals. It is important to keep in mind that other shoulder pathologies, such as shoulder impingement, rotator cuff syndrome, LHBT tendinopathy, and acromioclavicular arthritis, are all common pain generators in the middle-aged population [38,39]. This concept can also be applied to the young, athletic population as well. An MRI analysis of professional handball players demonstrated abnormalities in 93% of shoulders, with only 37% being symptomatic [48].


Treatment 

Asymptomatic tears should be observed and need no treatment. Those causing symptoms may need surgery. Depending on the type of SLAP tear pattern and the presence or absence of other associated shoulder pathologies, the recommended surgical technique may vary. For the vast majority of SLAP lesions, the initial management is conservative.

Nonoperative management modalities include the use of anti-inflammatory medications, cryotherapy, rest, and activity modification.

The aim of physical therapy (PT) modalities is to treat any underlying pathologic shoulder biomechanics that may have been present at baseline before the injury. Shoulder girdle proprioceptive training is beneficial to prevent re-injury. 

Scapulothoracic dyskinesia can result from an imbalance of the shoulder girdle muscles and static/dynamic glenohumeral joint stabilizers. Posterior shoulder joint capsular contractures have to be addressed with stretching and strengthening exercises. 

There are several reports on high-level overhead throwers that have demonstrated equivalent outcomes regarding return to play and return to play performance in athletes managed with operative versus nonoperative modalities. The nonoperative PT regimens focused on correcting 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 surgical treatment would be required. 

Operative treatment is considered in tandem while keeping in mind the patient's age, concomitant pathologies, functional requirements, occupational demands, and sport-specific goals.

Some authors have proposed surgical treatment algorithms depending on the type of SLAP lesion identified on advanced imaging, clinical exam, and intraoperative arthroscopy [41]. It is important to determine whether the labrum alone is responsible for the patient’s symptoms and whether restoring the labral attachment and biceps root to the glenoid will be useful. It is important to know how to treat a SLAP tear in the presence of other concomitant shoulder injuries. In older patients with or without rotator cuff repair, the repair of the SLAP correlates with inferior results compared to intentional neglect or performing a bicep tenodesis/tenotomy with regards to stiffness, persistent pain, and the need for revision surgery [18]. In younger patients presenting with shoulder instability, the SLAP injury may be present and contributing to symptoms, especially in the presence of an acute anterior and/or posterior labral tear.

The following algorithm has been previously proposed [41]:

  • Type I SLAP tear- Surgical treatment by arthroscopic debridement.

  • Type II SLAP tear- The arthroscopic criterion for a type II SLAP lesion includes the ability to demonstrate with an arthroscopic probe the separation of the superior labrum from the supraglenoid cartilage rim. Burkhart previously demonstrated a ‘‘peel-back’’ sign during arthroscopy [50]. The arm traction is released and brought into an abducted/externally rotated position. In cases of a positive peel-back sign, the biceps anchor assumes a more vertical and posterior angle that is dynamically visible. The surgical treatment for SLAP II is SLAP repair with/without biceps tenotomy/tenodesis.

  • Type III SLAP tear- Surgical treatment includes SLAP repair or resection. The bucket-handle tear of the superior labrum is resected,  with the repair of the SLAP complex if needed.

  • Type IV SLAP tear- Surgical treatment is needed. If less than 50% of the biceps tendon is affected, SLAP repair or resection is done. If more than 50% of the biceps tendon is affected, tenotomy or tenodesis is done.

  • Type V Slap tear- Surgical treatment includes a Bankart repair plus SLAP repair.

  • Type VI Slap tear- Surgical treatment includes SLAP repair or resection.

  • Type VII Slap tear- Surgical treatment includes suture/anchor fixation of anterosuperior labrum plus SLAP repair.

  • Type VIII Slap tear- Surgical treatment includes SLAP repair versus biceps tenotomy/tenodesis and gentle debridement of any cartilage or chondral unstable flap.  


Multiple SLAP repair techniques have been described. A wide array of implant options are available. Some authors have advocated the use of simple versus mattress sutures and the option for knotless fixation devices to minimize the risk of having bulky knots that can create symptoms postoperatively [51,52].

After confirming the diagnosis of a SLAP tear, a shaver can be used to resect unstable flaps of tissue that are irreparable. Glenoid neck preparation is done with a tissue elevator, rasp, and/or shaver. The Neviaser portal is often utilized. The appropriate anchor placement depends on the predominant region of instability in the superior labral-biceps tendon complex.


Differential Diagnosis

Shoulder pain is common and the differential diagnosis is extensive. SLAP tears can occur in isolation but are usually associated with other shoulder pathology. This makes identifying SLAP tears difficult. A few common shoulder diagnoses that may be confused with SLAP tears include the following, listed in order of decreasing likelihood: 

●Rotator cuff tendinopathy or partial tear – Patients with SLAP tears can have rotator cuff pathology as well. However, patients with rotator cuff pathology usually have signs of anterior shoulder impingement and night pain, which are usually absent in patients with isolated SLAP tears. Intra-articular symptoms, such as catching or clunking, are uncommon with isolated rotator cuff pathology. Weakness with shoulder abduction or external rotation and a positive painful arc test are more frequently seen with rotator cuff problems. Articular-sided supraspinatus tears lie close to the biceps tendon and can mimic SLAP tears. Ultrasound is very useful for identifying tendinopathy and partial or complete rotator cuff tears. A normal ultrasound in patients with significant shoulder symptoms makes SLAP lesion a strong possibility. 

●Shoulder impingement syndrome (SIS) – SIS generally causes persistent, vague anterior shoulder pain with overhead motions. SIS like rotator cuff pathology, typically does not produce intra-articular symptoms. Patients with SIS who do not improve with rehabilitation may have an underlying SLAP tear. 

●Biceps tear or tendinopathy – The close proximity of the proximal biceps tendon insertion and the glenoid labrum make it possible for patients to have bicipital tendon pathology and SLAP tears at the same time. Anterior shoulder pain is a common complaint with both these conditions. Biceps tendon pathology typically does not cause intra-articular symptoms. Proximal biceps tendon tears are rare in younger patients and they can create a notable deformity of the muscle called Popeye deformity.  Complete or partial tears of the biceps tendon are easily identified on ultrasound. Maneuvers commonly used to elicit pain from a SLAP tear, such as active compression and compression-rotation tests typically do not produce pain in those with isolated biceps tendon pathology. Patients who continue to experience anterior shoulder pain despite rehabilitation of the biceps tendon may have an associated SLAP tear. 

Entrapment of the long head of the biceps tendon, due to an anatomic variant called an hourglass biceps, can produce the symptoms and signs of a SLAP tear [53]. In such patients, a hypertrophic intra-articular portion of the biceps tendon becomes entrapped in the glenohumeral joint when the shoulder is abducted and the elbow flexed at the same time. This can produce a mechanical block within the glenohumeral joint producing signs that mimic intra-articular labral pathology. This can only be seen during arthroscopy and the intra-articular portion of the long head of the biceps tendon has to be excised to prevent recurrence.

●Glenohumeral osteoarthritis – SLAP tears and glenohumeral osteoarthritis can both produce anterior shoulder pain. Patients with these conditions may experience reduced shoulder motion and pain with overhead activities. Night time pain is common with osteoarthritis but not with SLAP lesions. Glenohumeral osteoarthritis is easily seen on plain radiographs of the shoulder, whereas patients with an isolated SLAP tear typically have normal radiographs.

●Multidirectional shoulder instability – A SLAP tear can produce symptoms of shoulder instability, especially after a traumatic dislocation. In general, however, patients with SLAP tears do not complain of shoulder instability symptoms or transient neurologic symptoms. Multidirectional instability involves laxity in all directions of humeral motion including anterior, inferior, and posterior, whereas SLAP tears may in rare instances be associated with anterior laxity only. 


Prognosis

There are no level I and II studies in the literature on the outcomes following arthroscopic type II SLAP repairs. Most studies in the literature report overall favorable results and good outcomes in the appropriately selected patients [54,55,56]. There are a number of authors who reported good results in athletes, including those with sport-specific overhead demand requirements [57].

Inferior outcomes have been demonstrated following revision arthroscopic SLAP repairs and in high-level professional overhead athletes [58]. Professional baseball pitchers generally demonstrate relatively inferior outcomes regarding return to play and return to prior performance level.   Superior outcomes have been in fact reported in this particular subset of athletic patients following non-surgical management alone [49,58].


Complications

It is important to discuss the risk factors for revision surgery with the patients. There are risks of continued pain, stiffness, dysfunction, and the potential need for further surgery in the future. Taylor et al in a 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 [59]. The risk factors include:

  • Age greater than 40 years

  • Female gender

  • Obesity

  • Smoking

  • Presence of concomitant LHBT tendinitis or tendinosis: The odds ratio for revision surgery was 5.1 in the setting of LHBT tearing/fraying. The odds ratio for revision surgery was 3.5 in the setting of LHBT tendinitis alone.


Postoperative and Rehabilitation Care

Sling immobilization is done until 4 weeks postoperative. Early shoulder pendulum exercises and periscapular muscle activation exercises are carried out. Passive and active-assisted forward elevation is encouraged.  Extremes of abduction and external rotation is avoided.

At weeks 4 to 6 postoperative active ROM exercises are started. Extremes of abduction and external rotation are avoided.

At weeks 6 to 12 postoperative functional exercises and light strengthening exercises can be incorporated. Beyond 6 to 8 weeks biceps resistance exercises are started. Resisted elbow flexion, and resisted forearm supination exercises can be incorporated.

At week 12 and beyond advance strength, ROM, and sport-specific exercises can be started. Around 6 months return to sport is allowed.


Conclusions

Knowledge of the relevant anatomy, pathogenesis, clinical presentation, and treatment of the spectrum of injuries involving the superior glenoid labrum and biceps origin is required for treating the patient with a SLAP tear. Despite the vast amount of literature regarding SLAP lesions, their clinical diagnosis remains challenging for several reasons. The clinical outcomes following surgical treatment of SLAP tears vary depending on the method of treatment, associated pathology, and patient characteristics. Biceps tenodesis has been receiving increasing attention as a form of treatment for SLAP tears.


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