Introduction
The past few decades have seen a rapid shift in our understanding of the anatomy and pathology of the biceps and superior labrum. Today’s clinical and basic science literature suggests that these two structures are interdependent; therefore modern nomenclature refers to conditions of these structures as afflictions of the biceps-labral complex (BLC). Successful surgical intervention for BLC disease is predicated on a comprehensive understanding of the relevant anatomy, a history of the injuries and aggravating activities, clinical examination maneuvers, utility of imaging, and diagnostic injections to ensure the appropriate selection and application of specific surgical techniques.
Traditionally held beliefs that the long head of the biceps tendon (LHBT) and superior labrum should be considered independently have been challenged by evidence in both the clinical and basic science domains. , The new approach is based on an enhanced understanding of the clinically relevant anatomy, pathoanatomy, and biomechanical considerations. For example, Provencher et al. and others have described successful salvage of failed superior labrum anterior-to-posterior (SLAP) repairs with open subpectoral biceps tenodesis. The etiology of a failed SLAP repair is likely multifactorial ( Fig. 9.1 ) and may result from technical errors, nonadherence to postoperative rehabilitation guidelines, kinematic deficiencies, biologic factors that impair healing, or perhaps concomitant unrecognized extra-articular bicipital tunnel syndrome. , It is also possible that patients with failed SLAP repair had developed symptoms from a biceps problem as opposed to pathology of the superior labrum or perhaps from inappropriate “SLAP repair” due to the surgeon’s failure to recognize a normal anatomic variant such as a recessed attachment or meniscoid type of superior labrum.
Dozens of surgical procedures have been described to address symptomatic BLC disease. These have included labral repairs, biceps debridement, tenotomy, and a variety of tenodesis techniques. SLAP repairs vary with regard to suture anchor selection, suture configuration, and instrument access. Techniques for biceps tenodesis tend to vary with respect to location (proximal vs. distal), type (bony vs. soft tissue), bicipital tunnel (decompressing vs. nondecompressing), and the hardware used (suture only, anchors, buttons, and/or interference screws). The sheer number of surgical techniques described in the literature reflects an ongoing and evolving quest for an optimal surgical solution to BLC disease.
This chapter is structured to present a comprehensive view of the BLC, the clinically relevant anatomic considerations, pathoanatomy, common surgical techniques, and our evidence-based algorithm for the selection of patient-specific interventions.
Anatomy of the biceps-labral complex
The BLC has three clinically relevant zones: inside, junction, and bicipital tunnel ( Fig. 9.2 ). Inside includes the superior labrum and the biceps anchor. Junction includes the intra-articular portion of the LHBT, which is visualized during standard glenohumeral arthroscopy and its stabilizing pulley. Bicipital tunnel represents the extra-articular segment of LHBT extending from the articular margin through the subpectoral region inclusive of its fibro-osseous confinement. , An understanding the normal anatomy, pathoanatomy, and the limitations of diagnostic arthroscopy of these three zones is imperative to develop an accurate diagnosis and treatment algorithm.
Biceps-labral complex inside
The inside (see Fig. 9.2 B) represents the labrum and the proximal biceps anchor, which previously would have been considered the superior labrum separate from the LHBT. Careful consideration must be given to distinguishing between normal anatomic variations and pathologic lesions during glenohumeral arthroscopy. Thorough diagnostic arthroscopy includes probe retraction of the labrum and the arthroscopic active compression test (ACT). The inside pathology tends to be readily identifiable during diagnostic arthroscopy.
Inside the biceps-labral complex: Normal anatomy
The triangle-shaped collagenous glenoid labrum connects circumferentially to the glenoid to deepen the shallow fossa without altering its radius of curvature. It is approximately 4 to 6 mm wide and 4 mm thick and is intimately associated with capsular ligaments and the LHBT anchor. Labral vascularity emanates from an anastomotic network receiving contributions from the suprascapular, anterior humeral circumflex, and posterior humeral circumflex arteries without any direct vascularity emanating from the glenoid bone. Of particular interest is the superior labrum, which has limited inherent healing potential due to its relative vascular deprivation.
It is particularly important to note that the superior labrum shows great variability in its attachment morphology. One variation is a meniscoid type of loose attachment, which consists of thin elastic connective tissue as opposed to a more firm inelastic tissue in the case of the inferior labrum. Normally there is a synovial reflection at the superior aspect of the glenoid deep to the superior labrum, which is of variable depth and has been confused with a type II SLAP tear. Our experience is that meniscoid superior labra are frequently reported by radiologists as SLAP tears. Stoller also reported variations in superior labral attachment, with type 1 representing a solid attachment to the glenoid rim and types 2 and 3 separated by a small synovium-lined recess. The depth of the recess serves to differentiate between the two. The meniscoid superior labrum is represented by redundant labrum with a deep synovial reflection without tearing of its attachment. The mobility of the meniscoid labrum is due to the lack of robust attachment to the superior glenoid near the biceps anchor and should be considered when the labrum falls over the underlying glenoid at the 12 o’clock position. In a series of 472 cases, findings from magnetic resonance imaging (MRI) supported the diagnosis of a meniscoid superior labrum in 48 (10.2%) cases. An additional noncontrast MRI study performed by Connell et al. included a prospective evaluation of 104 patients with suspected labral lesions who subsequently went on to arthroscopic surgery. The investigators found that noncontrast MRI has a sensitivity of 98%, specificity of 89.5%, and accuracy of 95.7% for detecting superior labral lesions. According to a 2016 study by Natsis et al., rates of labral meniscal folds have been noted to be present in up to 62.7% of arthroscopies. The evaluation noted that these folds were more frequently present at the 2 o’clock position in right shoulders and the 10 o’clock position in left shoulders, correlating with the anterosuperior aspect of the labrum. Rispoli et al. identified a 2.6- to 7.3-mm overlap of the labrum onto the bony surface of the glenoid. This is a variation of normal anatomy and should not be mistaken for a SLAP tear. A mobile and loosely attached superior labrum should not be considered abnormal unless there is a definitive detachment and the tear is visible.
The LHBT anchor attaches to both the superior glenoid labrum and the supraglenoid tubercle at the 12 o’clock position approximately 5 mm medial to the superior edge of the glenoid rim. There is a particularly intimate association between the LHBT and the glenoid labrum, with blending of fibers. Vangsness et al. evaluated the biceps anchor in 105 cadaveric specimens and demonstrated that the LHBT was attached to the supraglenoid tubercle in 50% of the specimens and only to the superior labrum in the remaining specimens. They described four types of biceps attachments to the glenoid labrum: attached entirely to the posterior labrum (type I), predominately posterior with some anterior labral attachment (type II), attached equally to the anterior and posterior labrum (type III), and a mostly anterior labral contribution (type IV). Grossly, the majority of biceps tendons that originate from the superior labrum do so posterior to the supraglenoid tubercle (type I or II). , The fibers of the LHBT and glenoid labrum blend in this region regardless of their gross appearance. Another cadaveric study determined that 83% of the LHBT origins were either entirely posterior (28%) or posterior dominant (55%).
Variant anatomy of the biceps brachii has been well described in the literature; however, intra-articular variants of the LHBT are relatively rare. A single large series of shoulder arthroscopies reported on 3000 arthroscopies and noted an intra-articular variance rate of 1.9%. Several variations of normal anatomy—such as sublabral foramen and Buford complex—have been described and must be differentiated from pathologic lesions at arthroscopy. , The Buford complex is a variation marked by a lack of anterosuperior labrum; a cordlike middle glenohumeral ligament arises from the base of the biceps tendon and attaches to the capsule. The reported incidence of the Buford complex was 1.5% in a series comprising 200 patients. A more common variant is the sublabral foramen, in which a well-defined hole is visible beneath the anterosuperior labrum in 12% of patients; the authors found an associated cordlike middle glenohumeral ligament in most of these holes. Fixation of either of these variants is not advisable as it produces a significant loss of external rotation. Variations of the biceps anchor have been described, including a mesotendon that is freely movable and unattached to the rotator cuff, an adherent type LHBT where the LHBT is attached to the supraspinatus and/or labrum, congenital absence, extra-articular origin, and others.
Additional, though less common, intra-articular variants include vincula of the biceps tendon, which is described as small bands of tissue attached to the undersurface of the cuff that span across the joint, ultimately exiting the glenohumeral joint while accompanying the biceps into the bicipital tunnel. In 1992, Johnson et al. reported finding vincula in 24.3% of their series of 411 shoulder arthroscopies. They reported up to four vincula in a single shoulder and found younger age to be a significant predictor for the presence of vincula. More recent reports of intra-articular variants have noted a trifurcate origin of the LHBT, with origins arising from the supraspinatus tendon, superior labrum, and rotator interval.
Biceps-labral complex inside: Pathologic lesions
In 1985, Andrews and colleagues first described injury to the anterosuperior labrum near the origin of the LHBT in overhead throwing athletes. Later, in 1990, Snyder et al. coined the term SLAP lesion to describe tearing of the intra-articular origin of the biceps tendon. Since then, this term has universally been accepted and used to describe a spectrum of injuries affecting the biceps tendon anchor and the surrounding glenoid labrum. The etiology of SLAP tears is often debated and likely multifactorial, with humeral head translation (i.e., the “push off mechanism”) and eccentric traction from the biceps tendon (i.e., the “pull off mechanism”) being the most commonly proposed mechanisms. The physical demands placed on the shoulder during athletic activity likely influences the mechanism of SLAP tear development in each athlete. Hwang et al. showed that humeral head translation had a greater effect on superior glenoid labral strain than did biceps tension, which supports the notion that SLAP tears result primarily from superior migration of the humeral head rather than biceps tension. Patzer et al. suggested, based on their cadaveric study, that SLAP repair improves glenohumeral stability as long as the LHBT remains in continuity. If the biceps was tenotomized, then subsequent SLAP repair had no impact on the glenohumeral translation. Strauss et al. used a cadaveric model to demonstrate that type II SLAP tears increased glenohumeral translation in all directions and that biceps tenodesis in the setting of type II SLAP did not magnify glenohumeral instability induced by the type II SLAP tear. Although their results suggested that biceps tenodesis as a treatment for type II SLAP would not adversely affect stability, concomitant superior labral repair in throwing athletes may be considered in an effort to restore stability.
Snyder’s classification for types I to IV SLAP tears remains the most widely recognized ( Fig. 9.3 ) :
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Type I lesions are characterized by marked fraying and a degenerative appearance of the superior labrum. The labrum remains firmly attached to the glenoid with an intact biceps anchor attachment. These lesions are commonly seen in a middle-aged population and may be asymptomatic. Surgical treatment is debridement and not surgical repair.
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Type II lesions are defined by visible detachment of the biceps anchor from the supraglenoid tubercle. These lesions must be carefully distinguished from biceps anchors with normal meniscal variant attachments (as discussed earlier). Although mobile on probing, the meniscal variant will reveal normal articular cartilage beneath the anchor, which is contiguous with the smooth synovial lining of the biceps anchor. Pathologic findings include inflammatory tissue under the anchor and an anchor that can be lifted off the glenoid. These lesions require surgical repair versus biceps tenodesis depending on clinical findings and patient age. We advocate for SLAP repair in the setting of an unstable SLAP tear with an acute or traumatic onset of symptoms when clinical findings suggest the absence of hidden extra-articular bicipital tunnel disease (either negative bicipital tunnel tenderness or negative O’Brien sign). Furthermore, though not a definitive factor in decision making, we consider the patient’s age in deciding on SLAP repair versus biceps tenodesis. Provencher and colleagues suggested that patients over the age of 36 years had a significantly higher failure of SLAP repairs; thus biceps tenodesis may be preferable in this demographic.
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Type III lesions consist of a bucket-handle tear of the biceps anchor and a normal biceps tendon and anchor attachment. Mechanical locking can occur from mobile fragments of the flap and is treated with debridement of the loose fragment.
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Type IV lesions include a bucket-handle tear of the superior labrum that extends into the biceps tendon and/or the anchor. These lesions can cause mechanical symptoms and may be treated with debridement and/or repair or biceps tenodesis, again depending on clinical examination findings and the patient’s age.
Several others have modified Snyder’s original classification. Morgan subclassified type II lesions based on the predominant area of instability under the biceps anchor. Type IIA lesions have an anterosuperior lesion, IIB lesions have a posterosuperior lesion, and IIC lesions have combined anterior and posterior lesions ( Fig. 9.4 ). Maffet et al. expanded the classification to include types V to VII. Type V includes a Bankart lesion with separation of the biceps anchor, type VI adds an unstable flap tear of the labrum to a biceps anchor separation, and type VII has a biceps anchor separation that continued beneath the middle glenohumeral ligament. Nord added types VIII to X, a SLAP tear with posterior extension to the inferior glenoid; type IX, a circumferential labral detachment; and type X was a SLAP tear with a bridge of normal labrum immediately posterior, followed by a posteroinferior labral tear. Pfahler et al. suggested that SLAP tears may normally occur during the aging process, with fissuring reported in the fourth decade and spontaneous detachments occurring in the seventh decade and beyond. The biceps anchor and anterosuperior labrum were the most common sites for detachment.
In addition to the superior labral tears, inside lesions include dynamic incarceration and medial biceps chondromalacia ( Fig. 9.5 ). Incarceration of the LHBT between the humeral head and the glenoid fossa may occur in a subset of patients. Verma et al. described a subset of symptomatic patients who had arthroscopically normal LHBT but demonstrated incarceration of the tendon between the glenoid and humeral head when the arm was positioned in forward flexion and internal rotation (i.e., mimicking the ACT, or O’Brien sign) as viewed from the standard posterior portal (see Fig. 9.5 ). We believe that the ACT should be part of routine diagnostic arthroscopy in any patient with preoperative BLC symptoms. Certainly incarceration is not in and of itself pathologic, but it may become symptomatic. In our clinical experience, patients who incarcerate the LHBT often do so bilaterally. Therefore we suggest performing the ACT bilaterally during preoperative evaluation. Discomfort deep within the shoulder produced by this test on the unaffected contralateral shoulder may indicate that the patient is an incarcerator. In a patient with a SLAP tear who is also an incarcerator, even a perfectly performed SLAP repair may inadequately address the pathology and leave the patient with persistent symptoms. In such a situation, we recommend that biceps tenodesis should be preferred over a SLAP repair.
We define medial biceps chondromalacia as attritional chondral wear along the anteromedial aspect of the humeral head’s articular surface due to chronic incarceration of the LHBT between the humeral head and the glenoid (see Fig. 9.5 C). It corresponds to the area of contact between the LHBT and the humeral head during a positive arthroscopic ACT. Other authors have observed this phenomenon at the articular margin deep to the LHBT in what we call junctional chondromalacia (described later in this chapter). Sistermann reported “a biceps tendon footprint” in 16% of 118 shoulder arthroscopies, which had a strong correlation with biceps synovitis, multidirectional instability, and rotator cuff tears. As discussed later, biceps chondromalacia presents in two distinct locations: medial and junctional ( Fig. 9.6 ).
In order to assess the diagnostic accuracy of MRI for biceps chondromalacia, our group compared preoperative MRI evaluation for three groups of patients who underwent shoulder arthroscopy ( Figs. 9.7 and 9.8 ). Group 1 had symptomatic BLC disease with grossly visible biceps chondromalacia at arthroscopy. Group 2 had symptomatic BLC disease without grossly visualized biceps chondromalacia at arthroscopy. Group 3 served as a control population and consisted of patients with an asymptomatic BLC who underwent an anterior arthroscopic stabilization procedure. Preoperative MRI radiographs of each patient were reviewed by a radiologist trained in musculoskeletal examinations and blinded to all clinical and intraoperative data looking for evidence of biceps chondromalacia. MRI evidence of cartilage loss, subchondral signal changes, and proximal biceps signal abnormalities were significantly different between the three groups. The results demonstrated very good sensitivity (61% to 82%) as well as moderate positive (51% to 53%) and negative (58% to 67%) predictive value for arthroscopically confirmed biceps chondromalacia. Interestingly, the two symptomatic groups (groups 1 and 2) demonstrated similar MRI evidence of biceps chondromalacia regardless of whether a lesion was evident at arthroscopy. These two groups differed significantly from the control population. Therefore the aforementioned MRI features served as an excellent diagnostic tool for the identification of symptomatic BLC disease (groups 1 or 2) with sensitivity 60% to 84%, specificity 48% to 66%, positive predictive value (PPV) of 76% to 78%, and negative predictive value (NPV) of 46% to 64%.
Biceps-labral complex junction
The “junction” represents the intra-articular segment of LHBT and its constraining biceps pulley. Junctional pathology can be identified during standard diagnostic glenohumeral arthroscopy (see Fig. 9.5 D–F).
Biceps-labral complex junction: Normal anatomy
The LHBT has an average length of 99 to 138 mm from its origin at the supraglenoid tubercle to the musculotendinous junction , , and an average intra-articular and extra-articular diameter of 6.6 mm and 5.1 to 6 mm, respectively. , Braun et al. reported an average 6-mm diameter of LHBT at arthroscopy in their series comprising more than 200 patients. Excursion of 19 mm occurs during normal glenohumeral motion. Its blood supply emanates from superior labral tributaries proximally and ascending branches of the anterior humeral circumflex artery distally as well as from the vincular attachments. Therefore there is a hypovascular zone or watershed region present 12 to 30 mm from the LHBT origin, which corresponds with the segment of tendon that crosses the articular margin and is marked by a particular susceptibility to rupture.
Alpantaki et al. demonstrated an extensive sensory and sympathetic network within the LHBT, which was densest within the proximal segment of the tendon, thus supportive of the widely accepted notion that LHBT can be a source of pain in a variety of shoulder pathologies. A follow-up study also identified neural cell adhesion molecules that play an important role in nociception within several samples of LHBT harvested from six patients who underwent shoulder surgery. Tosounidis et al. used immunohistochemical analysis and identified increased sympathetic innervation of the LHBT and alpha-1 adrenergic receptors in patients with acute (proximal humeral fracture) and chronic pathology (rotator cuff disease) compared with cadaveric controls.
Intra-articular delivery of the LHBT during glenohumeral arthroscopy with a probe is considered the gold standard diagnostic modality for the discovery of pathologic lesions with ideal arm positioning in 30 degrees forward flexion, 40 degrees abduction, and 90 degrees of elbow flexion. Several studies have reported the limitation of the diagnostic arthroscopic pull test for visualization of the LHBT ( Fig. 9.9 ). The average LHBT excursion afforded by arthroscopic pull test was only 15 to 19 mm in cadaveric studies , and 14 mm in vivo.
The biceps pulley is a capsuloligamentous stabilizing complex formed by coalescing fibers from the superior glenohumeral ligament (SGHL), the coracohumeral ligament (CHL), and contributions from the subscapularis and supraspinatus tendons ( Fig. 9.10 ). Together, these structures stabilize the LHBT as it turns 35 to 40 degrees along the articular margin en route to its extra-articular course. The CHL stretches from the coracoid process to the greater tuberosity and partially to the lesser tuberosity; it is an inferior stabilizer of the glenohumeral joint. The SGHL originates with or just anterior to the origin of the long head of the biceps and consists of oblique and direct fibers arising from the supraglenoid tubercle and labrum, respectively; they course in parallel with the biceps tendon and insert onto the fovea capitis just superior to the lesser tuberosity. Some fibers continue to insert into the base of the bicipital groove, whereas the remainder contribute to the transverse humeral ligament.
Braun et al. defined the arthroscopic anatomy of the biceps pulley as having an anteromedial biceps reflection pulley and a posterolateral biceps reflection pulley, either of which may be compromised. In their series of 207 patients who underwent shoulder arthroscopy for a wide variety of indications, 32% had a pulley tear, which was highly associated with proximal LHBT instability/subluxation. Interestingly, there were only slightly more anteromedial pulley lesions than posteromedial ones. The average age of patients with pulley tears was 13 years greater than those without and there was a significant association of pulley lesions with rotator cuff tears and SLAP tears. Biceps excursion at the level of the biceps pulley is 10 to 13 mm; the highest shear forces occur with the patient’s arm in internal rotation, with the arm at the side, and forward flexion with the humerus in either internal or neutral rotation. These cadaveric findings suggest a vulnerability of the biceps pulley to injury due to increased shear stress sustained in the aforementioned positions as well as attritional abrasion secondary to repeated excursion of the LHBT against the pulley.
A full understanding of the intra-articular anatomy of the biceps would not be complete without a discussion of the rotator interval and its contribution to the biceps pulley. The rotator interval is a distinct anatomic structure within the glenohumeral joint that was first described by Neer in 1970 to describe the anterosuperior space in the rotator cuff between the supraspinatus and subscapularis tendons. Since that time, basic science and clinical studies have advanced our understanding of this distinct anatomic structure, which is now defined as a quadrangular structure at the anterosuperior aspect of the glenohumeral joint bound by the coracoid process medially, the transverse humeral ligament laterally, with the superior margin of the subscapularis tendon and the anterior margin of the supraspinatus tendon representing the inferior and superior borders, respectively. Structures within the rotator interval include the CHL, the SGHL, the glenohumeral capsule, and the biceps tendon.
Biceps-labral complex junction: Pathologic lesions
Partial and complete tears of the LHBT are common, particularly those along the articular margin, which is approximately 2.5 cm from the origin and is a vascular watershed region. Boileau et al. described an “hourglass biceps” lesion in which the tendon hypertrophy occurs proximal to the bicipital groove and causes symptoms related to entrapment of the tendon within the glenohumeral joint. The hypertrophied biceps is often associated with rotator cuff disease and becomes unable to slide within the bicipital groove. This pathology presents in much the same way as a biceps tendon that is fixed to the groove owing to soft tissue adhesions; it can lead to mechanical symptoms from entrapment of the tendon during forward elevation. This can cause persistent pain during motion and potentially also chronic subluxation of the biceps tendon within the groove. Furthermore, Moon et al. reported that 79% of proximal arthroscopically visualized LHBT tears propagated distally into the bicipital tunnel and were often accompanied by extensive tenosynovitis.
In their cadaveric study (see Fig. 9.10 ), Taylor et al. demonstrated that on standard diagnostic arthroscopy, the pull test was able to visualize only 78% and 55% of the LHBT relative to the inferior margin of the subscapularis tendon (bicipital tunnel zone 1) and the proximal margin of the pectoralis major tendon (PMPM) (bicipital tunnel zone 2), respectively. In a study by Gilmer et al., diagnostic arthroscopy with inclusion of the pull test was able to visualize 30 mm (range, 15 to 45 mm) of LHBT compared with 95 mm (75 to 130 mm) during open subpectoral biceps tenodesis in a series of patients who underwent open subpectoral biceps tenodesis for BLC disease. Others have drawn similar conclusions regarding the diagnostic limitations of arthroscopy for visualizing the full extent of clinical pathology. Gilmer et al. showed that diagnostic arthroscopy identified only 67% of pathology and tended to underestimate the extent of the injury in up to 56% of patients.
It is important to note that junctional lesions occur not only in isolation but may also occur concomitantly with lesions in other zones. For example, nearly 50% of patients with a junctional lesion also had a hidden bicipital tunnel lesion ( Fig. 9.11 ). As will be evident later, disease and hidden bicipital tunnel disease occurring concomitantly play an important role in surgical decision making.
Lesions of the biceps pulley described by Bennett produce proximal LHBT instability. The investigators identified resulting instability in 165 patients who underwent shoulder arthroscopy for subscapularis tears (28%) and rotator interval lesions (19%). Several signs of interval/pulley insufficiency have been described in the imaging literature; these include displacement of the LHBT relative to the subscapularis tendon on oblique sagittal images, medial subluxation of the LHBT on axial images, discontinuity of the SGHL, and the presence of biceps tendinopathy. Overall, MR arthrography has demonstrated a high sensitivity (82% to 89%) and specificity (87% to 98%) for the detection of pulley lesions.
The term junctional biceps chondromalacia was coined to describe attritional wear of the humeral head below the LHBT along the articular margin. Other authors have recognized this phenomenon as well, though by different names. Sistermann reported on a “biceps tendon footprint,” which was observed in 16% of 118 shoulder arthroscopies, identifying a high correlation with biceps synovitis, MDI, and rotator cuff tears. Byram et al. identified a group of patients with humeral head abrasion below the intra-articular portion of the LHBT, and 33 of the 127 patients in their retrospective series had humeral head abrasions. Although this lesion was most common among patients with failed SLAP repairs, it was also seen in the presence of other biceps pathologies. Chondral lesions on the humeral head below the LHBT, called “bicipital chondral prints,” were observed in 78% of 182 patients with SLAP tears (type I excluded) ; the association was independent of the patient’s age or type of trauma. Furthermore, in a follow-up study, the authors found that a SLAP lesion tends to increase the anterior and anteroinferior translation and is associated with greater LHBT tension.
Biceps-labral complex bicipital tunnel
Taylor et al. recently defined the “bicipital tunnel” as the extra-articular segment of LHBT and its fibro-osseous enclosure extending from the articular margin through the subpectoral region. The bicipital tunnel has been subdivided into three distinct zones ( Fig. 9.12 ). It is a closed space that commonly harbors lesions that are hidden during standard diagnostic glenohumeral arthroscopy ( Fig. 9.13 ). Patients with bicipital tunnel disease producing bicipital tunnel syndrome who undergo proximal BLC surgical techniques may remain symptomatic owing to residual distal lesions.
Biceps-labral complex tunnel: Normal anatomy
Zone 1 is the osseous bicipital groove defined proximally by the aperture created by the biceps pulley at the articular margin and distally by the distal margin of the subscapularis (DMSS). Although the osseous morphology of zone 1 has been described as widely variable, Cone et al. reported the average medial wall angle to be 56 degrees, depth to be 4.3 mm, proximal width to be 8.8 mm, and middle width to be 5.4 mm. Nearly a third of their specimens had gross osteophytic changes.
The constraining roof of zone 1 can be described as the “transverse humeral ligament,” although this term was debunked after recent cadaveric studies suggested that this ligament is actually the coalescence of fibers from the subscapularis and CHL medially, the supraspinatus laterally, and the falciform ligament inferiorly. Gleason et al. used cadavers to show that the transverse humeral ligament consisted of a continuation of the superficial fibers of the subscapularis tendon that stretches over the intertubercular groove and meshed with longitudinal fibers from the supraspinatus and the CHL. MacDonald et al. reported similar findings among 85 cadaveric specimens. They demonstrated subscapularis fibers extending deep to the LHBT along the floor of the groove in approximately one-third of their specimens. Taylor et al. identified a deep osseous morphology of zone 1, which is covered by periosteum and extending fibers of the subscapularis tendon. In keeping with previous reports, the authors identified synovium in all specimens. They also found that the roof (transverse humeral ligament) was formed by a meshwork of subscapularis, supraspinatus, and falciform fibers. Interestingly, when proximal extension of the falciform ligament was present (33% of specimens), the fibers were oriented perpendicularly (parallel to the LHBT).
Zone 2, referred to as “no man’s land,” is defined proximally by the DMSS and distally by the PMPM ( Fig. 9.14 ). Identification of offending lesions in zone 2 is particularly challenging owing to its relative invisibility from arthroscopic visualization above and from open subpectoral exposure below. The osseous morphology of the floor is that of a shallow trough with overlying periosteum and proximal expansion of latissimus dorsi fibers and distal expansion of subscapularis fibers. In zone 2, the roof is made up of fibers from the bicipital sheath and the falciform ligament. Previous reports have suggested that the falciform ligament was the bicipital sheath ; however, recent histologic evaluation clearly demonstrates that the bicipital sheath and falciform ligament are independent structures with perpendicularly oriented fibers. The falciform ligament is an expansion of the sternocostal head of the pectoralis major but has substantial variability with regard to the location of fibers, its proximal extension, and thickness. The authors also demonstrated that 67% of specimens had synovium in zone 2, which stands in contrast to the traditional notion of a synovial reflection in the groove (zone 1).
Zone 3 is the subpectoral region, which begins at the PMPM. The osseous floor here is predominately flat and is covered by periosteum and fibers of the latissimus dorsi. The roof of zone 3 is formed by the PMPM, which inserts on the humerus lateral to the LHBT. Importantly, the medial enclosure of the LHBT here consists of loose areolar connective tissue and was shown to have significantly increased percent empty tunnel (% ET), as determined by cross-sectional quantitative analysis, in contrast to that in zones 1 and 2, which had similarly constrained % ET. As a consequence, space-occupying lesions such as scar, osteophytes, and loose bodies likely have less of a clinical impact in zone 3 than they do in zones 1 and 2.
Biceps-labral complex tunnel: Pathologic lesions (bicipital tunnel syndrome)
The bicipital tunnel commonly harbors lesions in chronically symptomatic patients and conceals them from standard glenohumeral arthroscopic evaluation. Such lesions confer a diagnosis of bicipital tunnel syndrome as described by Taylor et al., with a reported prevalence of up to 47% ( Fig. 9.15 ). Gilmer et al. reported that the bicipital tunnel concealed 33% of BLC lesions and that glenohumeral arthroscopy frequently underestimated the magnitude of the pathology. Recently, Moon et al. found that 79% of proximally identified LHBT tears propagated distally into the bicipital tunnel and were accompanied by dense synovitis.
According to Taylor et al., bicipital tunnel disease includes a wide variety of lesions including loose bodies, scar, partial LHBT tears, osseous stenosis, osteophytes, instability, synovitis, and inflamed vincula (see Fig. 9.15 ). In their retrospective evaluation of 277 patients, 47% of patients had bicipital tunnel syndrome. The most common lesion was adhesion/scar (22%), followed by instability (11%), bony stenosis (8%), LHBT partial tearing (6%), loose bodies (4%), and inflamed vincula (3%). Scar and adhesion formation in zones 1 and 2 of the bicipital tunnel are most prevalent. McGahan et al. demonstrated that such simulated adhesions produce a 47.3-degree loss of glenohumeral internal rotation.
We believe that several anatomic features—namely the dense connective tissue sheath, presence of synovium, and functional bottleneck imposed by the PMPM—contribute to the pathogenesis of bicipital tunnel syndrome. First, the dense connective tissue sheath encloses the tunnel in zones 1 and 2, thus rendering it particularly vulnerable to synovial hypertrophy, scar formation, osteophytes, and loose bodies. Second, the synovial extension exists further than previously thought. We identified it in zone 2 in the majority of specimens and even in zone 3 in one specimen. Therefore synovitis may occur more distally than previously thought in areas hidden from traditional arthroscopic view. Finally, PMPM defines the transition from zones 2 to 3 of the bicipital tunnel and is particularly important because it forms a bottleneck for many lesions such as loose bodies and synovitis, which migrate distally but cannot decompress into the subpectoralis region (zone 3), and tend to aggregate in zone 2. ,
History, physical examination, and imaging techniques
The role of pain attributed to the proximal biceps remains a commonly observed and intensely investigated topic within orthopedic medicine. Documented case reports and investigations regarding disorders of the biceps tendon can be traced back as far as 1694 and continue to be acknowledged and investigated today. The difficulty related to the proper evaluation and diagnosis of true BLC injury continues to be intensely scrutinized as it is challenging to distinguish from other disorders of the shoulder. Concomitant disorders such as arthritis, subacromial bursitis, intertubercular grove injury, degenerative processes, osteitis, SLAP tears, subluxation and dislocation, or impingement syndrome as it relates to rotator cuff tears can mimic the symptoms of biceps-related pain and may mask the true source of discomfort. Further complicating this issue is the variable presentation of BLC symptoms that may coexist with the previously mentioned comorbidities. , Many patients present with a history of progressive anterior shoulder pain and limited function, commonly from repetitive overhead activities. Factors associated with biceps pathology include anteromedial pain in the region of the bicipital groove, which may radiate down the biceps muscle belly. A careful history should also include questioning regarding any signs of biceps instability, which may present with mechanical symptoms of popping, clunking, snapping, or subjective instability. The most common mechanisms of injury are trauma and overuse. Trauma often occurs from a fall on an outstretched arm, from lifting a heavy object overhead, or from traction injury in throwers. Overuse can occur from repetitive overhead actions during either sports participation or manual labor.
Current methods of evaluating disease specific to the proximal biceps include physical examination techniques, ultrasound, MRI, diagnostic injections, and visualization under arthroscopy. Many physical exam techniques have been described over the years and include the Speed test, Yergason sign, biceps instability test, Ludington test, DeAnquin test, Lippmann test, and Heuter sign. Palpation of the anterior bicipital groove for tenderness may also be performed, but identification of the biceps can be difficult owing to the overlying deltoid muscle. Findings of these exams can also be compared before and after injection of a local anesthetic into the bicipital groove or the glenohumeral joint to evaluate for pain relief. Despite the abundance of techniques, a reproducible and reliable examination to localize biceps disease has not been identified. In addition, multiple histologic investigations report that the macroscopic appearance of the proximal biceps may not accurately reflect tendinopathy. ,
Despite the challenges, physical examination remains the mainstay diagnostic modality ( Fig. 9.16 ). The preferred physical exam approach demands the “three-pack” examination, which includes palpation of the bicipital tunnel, throwing test, and ACT (O’Brien sign). In a prospective study by our group, 145 patients were evaluated with sensitivity, specificity, PPV, and NPV for the three-pack examination as well as the more traditional tests (Speed, Yergason, and Jobe). The three-pack tests were highly sensitive (73% to 98%) but less specific (46% to 79%) for BLC disease in all three locations (inside, junction, and tunnel) than the traditional tests, which were less sensitive (20% to 67%), but more specific (83% to 100%) for BLC disease in all three locations ( Fig. 9.17 ). Of particular importance for the choice of surgical technique, palpation and the O’Brien sign were highly sensitive (97.8% and 95.7%, respectively) for hidden bicipital tunnel disease and had a high NPV (96.4% and 92.6%, respectively), which, if negative, essentially would allow the surgeon to rule out bicipital tunnel disease. The Speed and Yergason tests, conversely, were poorly sensitive but had high specificity (86.7% and 97.9%, respectively) and PPV (76% and 92.3%, respectively), suggesting that a positive examination should prompt the selection of a bicipital tunnel decompressing tenodesis technique.
