4.4 Biceps

The long head of the biceps tendon (LHB) is an enigmatic structure but is also an important cause of shoulder symptoms. Though its anatomy is well described, understanding of its surrounding restraints and structures such as the rotator interval are still being evaluated. More problematically for surgeons its function is still hotly debated, and poorly defined, leading to contention regarding potential surgical treatment.

This chapter will attempt to clarify the current understanding of the role and pathology of the LHB at the shoulder, and propose treatment strategies that are appropriate for the available evidence, and attainable for modern arthroscopic treatment modalities.

The LHB arises from the supraglenoid tubercle and the superior glenoid labrum. Its origin is, however, variable, and most anatomical studies have shown the labral origin to be more common. The intra-articular course is extrasynovial, and it exits the glenohumeral joint via the intertubercular (bicipital) groove, between the lesser and greater tuberosities, and carries a synovial reflection down within this groove.

At the point of exit from the joint a complex set of restraints exist. The ‘biceps sling’ comprising the superior glenohumeral ligament (SGHL), anterior band of the coracohumeral ligament, and capsule of the rotator interval, forms the anterior (or medial) restraint. The leading edge of the supraspinatus (anterior column) forms the posterior restraint. Failure of any of these structures may lead to instability. The course of the tendon within the bicipital groove is constrained, and vulnerable to many pathological abnormalities. At the inferior limit of the groove it passes beneath the tendon of the pectoralis major, before merging into the lateral muscle belly.

The intra-articular course of the tendon is oblique, variable depending on shoulder rotation and elevation, and is subject to significant shearing forces, which predispose the tendon to pathological changes.

The primary function of the biceps is at the elbow as a flexor and forearm supinator. The function of the long head at the shoulder is still unclear. Evolutionary change has rendered the LHB less functional at the shoulder in humans, and anatomical, biomechanical, neurophysiological, and radiological studies have produced conflicting results. The LHB contributes to 7–10% of abduction strength, but only with the humerus in external rotation. The head depressor effect of the LHB is also minimal, though more interest has recently been focused on its role as a secondary anterior stabilizer in the unstable shoulder.

The clinical evaluation of LHB pathology is notoriously imprecise. Unfortunately current imaging investigations are only moderately more accurate, truly leaving dynamic arthroscopic diagnosis the gold standard investigation.

Clinical evaluation of the shoulder has been dealt with in Chapter 4.1, but there are certain specific points regarding diagnosis of LHB pathology that warrant further attention.

The history, typically, is of well-located, anterior shoulder pain that the patient can point to at the bicipital groove. This pain may radiate down the arm, along the biceps muscle belly, but can extend as far as the hand, usually along the radial border of the forearm towards the thumb. This referred pain needs to be distinguished from radicular pain of cervical origin. The painful clunk of a subluxing tendon is quite specific, but is an infrequent symptom. SLAP (superior labral tear from anterior to posterior) lesions may present with deep-seated pain on certain activities, or with pain associated with instability, or shoulder pain in a young patient with negative clinical signs of rotator cuff pathology.

Palpation of the tendon in the bicipital groove, classically described with the arm in 10 degrees of internal rotation, is a useful sign, but correlation with the contralateral shoulder is important. Clinical tests such as Speed’s test, Yergason’s test, and biceps instability test, are poorly validated, and a recent paper has reported sensitivity and specificity of 50–67% for palpation and Speed’s tests in the diagnosis of partial thickness tears.

The clinical diagnosis of SLAP lesions is no easier. Many tests have been proposed, and many variations exist, the most widely defined being the O’Brien active compression test and the Biceps Load II. The AERS (abduction external rotation supination), Mayo shear, anterior superior SLAP test, and biceps tension tests are also commonly used.

Plain radiography has a limited role in the diagnosis of LHB pathology. The two views that may show bony changes associated with arthritis, malunion of fractures, and loose bodies are the anteroposterior in external rotation and the Fisk view, an axial view centred on the bicipital groove.

Arthrography and computed tomography arthrography were the first imaging techniques to visualize the intra-articular tendon, but these have been largely superseded by ultrasound (US) and magnetic resonance imaging (MRI).

Both MRI and US can demonstrate the entire LHB tendon from origin to the musculotendinous junction, and gross pathology such as dislocation and rupture are well shown by both modalities. The spatial resolution, and dynamic capability of modern US now provides advantages in diagnosing partial tears, subtle dynamic instability, and the hourglass lesion. Unfortunately, studies have still only reported moderate accuracy of MRI (37% concordance with arthroscopic findings) and US (49% sensitivity). These findings are largely due to both techniques being poor at demonstrating partial thickness tears, which usually occur on the deep surface of the tendon.

As an intra-articular, but extrasynovial structure, the LHB is prone to tenosynovitis. The tendon is also subject to significant shearing forces in its oblique course though the glenohumeral joint. The forces acting on the tendon vary with arm position, notably rotation and elevation, though in the majority of functional positions the tendon bears upon the medial wall of the groove, that is, the lesser tuberosity and the biceps sling. Tenosynovitis is, by definition, an inflammatory condition and is reversible in the majority with conservative measures.

Tendinosis represents irreversible degenerate change within the tendon. This is commonly seen in association with subacromial impingement and degenerate rotator cuff disease. Progressive degenerate change may lead to ‘hypertrophy’, ‘atrophy’, and partial tendon tears and eventually rupture. Though the link between tendinosis and pain is less clear, partial thickness tears are often symptomatic and cause mechanical symptoms in the shoulder. These tears are usually on the deep surface of the tendon, often at the entry to the bicipital groove or within the groove itself, and therefore interfere with the smooth gliding of the tendon over the biceps pulley and within the groove.

Rupture of the LHB, often termed ‘spontaneous’, is a well-recognized clinical entity, producing the characteristic ‘Popeye’ sign of the descended lateral muscle belly. Males in their fifties and sixties, often with manual occupations, are most frequently affected, and often have no or only a short history of preceding symptoms. The rupture itself often heralds the resolution of symptoms, and many ruptures therefore never present to orthopaedic surgeons. The cosmetic deformity is also usually well tolerated in this patient population.

The functional deficit produced by rupture (and also by surgical tenotomy) is again only demonstrable at the elbow, with a loss of 20% of forearm supination strength and 8–20% of elbow flexion strength. This deficit is generally well tolerated in the elderly, but in the sporting population and manual workers may be more significant.

The ‘hourglass biceps’ is a term describing mechanical entrapment of an enlarged or hypertrophic tendon within the glenohumeral joint on elevation. It is analogous to the bucket-handle meniscal tear or the triggering of a flexor tendon in the hand, leading to a loss of active and passive movement. The LHB glides passively into the bicipital groove on elevation of the arm, but enlargement of the tendon can block this excursion, and the tendon buckles and impinges between the humeral head and the superior glenoid. This leads to a loss of the terminal 10–20 degrees of elevation, often with associated discomfort. With time, tendon delamination and tears occur, though this phenomenon may also cause progressive damage to the tendon restraints, and tendon instability.

Dislocation of the LHB was the first recognized pathology of the LHB described in the first part of the nineteenth century. It remains one of the most common indications for surgical treatment of the LHB. Instability may be dynamic, defined as subluxation, or static, as in a fixed dislocation. The majority of instability is medial (anterior), though posterior (lateral) instability may occur with dislocations and supraspinatus tears. The failure of the biceps sling allows medial displacement of the tendon, which in turn causes abrasion of the LHB on the subscapularis tendon, first recognized by Walch as the ‘hidden lesion’, of a LHB dislocation and partial thickness, deep surface subscapularis tear.

Medial biceps instability has been classified by Walch (Figure 4.4.1) and may occur anterior to the subscapularis (the least common), into the substance of the tendon (partial subscapularis tear), or beneath the tendon a condition that has to be associated with a full thickness subscapularis tear.

The importance of lesser grades of instability is also now appreciated, especially in sporting injuries, and has been described to be present in up to 45% of arthroscopies for rotator cuff tears.

Isolated LHB pathology is particularly important in the athlete. The overhead and throwing athlete are particularly vulnerable and instability, partial tears, and SLAP lesions are all common.

Anterosuperior internal impingement (ASI) is a novel diagnosis that has been brought to light by dynamic arthroscopic studies. At arthroscopy, abrasion is seen on the anterosuperior labrum, just in front of the biceps origin with a corresponding ‘kissing’ lesion at the LHB pulley. It is thought that these two structures shear against each other in the follow through phase of throwing when the arm is in adduction and internal rotation and rapidly decelerating. It is commonly seen in sports injuries but how to manage it remains contentious. At the present state of knowledge, the use of a sports physiotherapist to change the pattern of follow through may be the best management, but it is unpredictable.

Another common condition in the athlete is posterosuperior impingement (PSI). This is a complex syndrome involving repetitive forced contact between the deep surface of the supraspinatus and posterior labrum and may lead to posterosuperior labral fraying, tears, and deep surface cuff pathology. A tight posterior capsule, anterior capsular laxity, and instability have all been implicated in its pathogenesis.

It was only following the advent of shoulder arthroscopy that lesions of the superior labrum and biceps anchor were recognized. Snyder first described the ‘SLAP’ lesion in 1990, in relation to the throwing athlete, and it is now recognized as an important cause of shoulder dysfunction, and a common indication for surgery.

Snyder described four types of lesion, and although these have been expanded to include many subtypes and associated instability lesions, the original classification still describes the four major types of lesion well (Figure 4.4.2).

SLAP lesions may be produced either by the acceleration or deceleration phases of the throwing movement, as well as compression injuries with proximal displacement of the humeral head. There is also an overlap with anterior instability and superior extension of the classical Bankart lesion as well as posterosuperior impingement, which may lead to posterior SLAP lesions.

Type I SLAP lesions describe degenerative fraying of the superior labrum. They may be found prematurely in athletes, or in association with the normal ageing process. Anterosuperior fraying is most common in ageing, while posterosuperior fraying raises the possibility of PSI. Type II lesions are the most common lesions requiring surgical intervention. True bicipital/labral avulsions must be carefully distinguished from a mobile meniscoid labrum, which is a normal variant. Type III lesions are less common and the type IV lesion poses particular decision-making difficulties with respect to repair of the entire complex or labral repair and LHB tenodesis.

The primary indications for surgical intervention in biceps pathology are mechanical lesion such as instability, entrapment, and partial tendon tears. Secondary indications are refractory pain due to tenosynovitis and early tendinopathy, and treatment of concurrent rotator cuff disease, instability, and arthritis. Determining the relative contribution of the LHB to shoulder pain is difficult, but careful arthroscopic evaluation can prevent surgical failures due to missed LHB pathology.

A LHB rupture in a young patient or manual worker may also be an indication for early surgery, which should be performed within 6 weeks of rupture to be successful and restore strength.

As loss of the LHB from the shoulder has little, or no, consequences on shoulder function there are few contraindications for surgical intervention. Unnecessary intervention obviously subjects patients to the risk of the surgical procedure, but the possibility of neglecting bicipital pain must always be considered.

One contraindication to tenotomy is in the pseudoparalytic arm with anterosuperior escape due to a large rotator cuff tear. In this situation, active elevation will not be restored with a simple tenotomy. Tenotomy is also contraindicated in young active patients where a tenodesis should always be performed.

Arthroscopic biceps tenotomy is the simplest, most reliable, and probably most common surgical intervention to the LHB. Releasing the tendon close to its origin allows the tendon to retract outside the glenohumeral joint, and will relieve bicipital symptoms at the shoulder effectively. This technique was popularized in the 1990s in Europe, and many studies have confirmed its effectiveness The limitations of this procedure are the cosmetic deformity often produced, a small incidence of persistent muscle belly cramping on activity, and the loss of elbow flexion and supination strength. It is of interest that not everyone who undergoes surgical tenotomy shows the cosmetic ‘Popeye’ sign after surgery. This is either due to the tendon still being held by vinculae, or, more commonly, a hypertrophied tendon retracts into the sulcus but then gets trapped there like a cork in a bottle.

Open tenodesis was historically the treatment of choice for bicipital pathology. Many techniques were described, and many more have recently been described as arthroscopic techniques. There are broadly three groups of techniques: soft tissue techniques using suture fixation of the tendon to other tendons or the transverse humeral ligament; fixation of the tendon to bone using sutures and anchors; and fixation of the tendon within the bone of the proximal humerus (Figure 4.4.3). The first technique is evidently the simplest, and the last the most mechanically secure.

The different classes of SLAP lesion require different surgical approaches. Type I lesions do not require intervention, or merely debridement if found in association with other pathology. Type II lesions require repair of both the superior labrum and biceps anchor. This is usually achieved with suture anchors placed anterior and posterior to the LHB origin. Type III lesions can usually be excised, though an attempt to repair very peripheral tears may be indicated. Finally the treatment of type IV tears will depend on the extent of damage to the biceps tendon itself. A combination of excision and repair may be used for the labral portion of the tear, and the decision between LHB tendon repair or tenodesis will depend on the extent of bicipital involvement both in terms of percentage cross-sectional tearing and extent of tear propagation along the length of the LHB.

The results of surgery to the biceps tendon are difficult to assess due to the majority of series including associated rotator cuff repair, subacromial decompression, debridement, and stabilization procedures. There are a few papers, however, where isolated tenotomy, tenodesis, and SLAP repairs have been reported.

Isolated athroscopic tenotomy in patients with irreparable rotator cuff tears has been reported, with good results. Poor function of the teres minor is, however, associated with poorer results. Manou and colleagues in a small series showed that complementary acromioplasty did not confer additional benefit and Walch confirmed this finding if the preoperative acromiohumeral distance is less than 7mm. Indeed, a large cuff tear is a contraindication to releasing the coracoacromial ligament with anterior acromioplasty as this may lead to anterosuperior escape.

The results of isolated tenodesis have been reported both in the presence of advanced rotator cuff disease and for isolated LHB pathology. For the former group the results of tenodesis appear equivalent to tenotomy, and for the latter group 77% of patients could return to their sporting activities.

The published results of SLAP repair have been favourable but more variable. The heterogenicity of lesions, associated pathology, and different surgical approaches makes interpretation of the literature difficult.

There are certain conditions, or procedures, apart from rotator cuff disease that warrants attention to the LHB.

Primary glenohumeral osteoarthritis commonly produces LHB symptoms. Osteophytes in the groove, loose bodies, and joint effusions may all cause symptoms. Intra-articular injections may be partially effective by addressing symptoms generated by the LHB. Both in arthroscopic treatment of early osteoarthritis and during joint replacement addressing the LHB by tenotomy or tenodesis is recommended.

The rational for treatment of the LHB in fractures and their fixation is similar to that of osteoarthritis. The LHB is frequently damaged at the level of the fracture and any degree of malunion affecting the bicipital groove, usually at its superior or inferior boundaries, will lead to poor gliding properties of the tendon. Persistent anterior shoulder pain following malunion should alert the surgeon to possible LHB pathology, and LHB tenodesis at the time of fracture surgery should always be considered.

The LHB is a fascinating structure. Recognition of its importance in generating shoulder symptoms is currently high, and much new research is emerging.

Further understanding of its role at the shoulder and clarification of the basic science of its pathology is needed before consensus on its treatment will be reached. Future advances will include further development of imaging techniques, particularly US, and scientific clinical results will guide treatment options, in particular in terms of surgical technique. Reconstructive procedures to stabilize the unstable tendon, and potentially repair tendon tears, which have to date proved unsuccessful, would be a great advance, and with the advance of arthroscopic techniques will hopefully be realistic goals in the near future.