Bicipital Tendonitis

Article Author:
Matthew Varacallo
Article Editor:
Scott Mair
Updated:
12/2/2018 12:49:22 PM
PubMed Link:
Bicipital Tendonitis

Introduction

The long head of the biceps (LHB) brachii tendon originates at the supraglenoid tubercle and superior glenoid labrum. Its labral origin is mostly posterior in over half of cases. Inside the joint, the tendon is extrasynovial and passes obliquely heading toward the bicipital groove. The LHB tendon distally joins the short head of the biceps (SHB) tendon as both transitions into their respective muscle bellies in the central third of the upper arm, and after crossing the volar aspect of the elbow, inserts on the radial tuberosity and medial forearm fascia. The latter occurs via the bicipital aponeurosis.[1]

The blood supply to the LHB tendon occurs via the anterior humeral circumflex artery. Two critical areas of avascularity of the LHB tendon have been demonstrated to be located on the deep undersurface of the tendon in the groove, and proximally near its insertion at the superior glenoid.[2]

The bicipital groove is an anatomic landmark that sits between the greater and lesser tuberosities and serves as a critical location of proximal biceps stability. The soft tissue components of the groove create a tendoligamentous sling to support the LHB tendon and include portions of the rotator cuff muscles (subscapularis and supraspinatus), coracohumeral ligament (CHL), and the superior glenohumeral ligament (SGHL).[2]

Biomechanically, the LHBT has a controversial role in the dynamic stability of the shoulder joint. It has been demonstrated, mostly in biomechanical cadaveric-based studies and animal models, that the tendon at least plays a passive stabilizing role in the shoulder. Neer proposed in the 1970s that the LHBTs stabilizing role varied depending on the position of the elbow.[3] Several subsequent studies refuted the theory that the LHBT played any active shoulder stabilizing effect.  Jobe and Perry evaluated the activation of the biceps during the throwing motion in athletes. The authors reported the peak muscle stimulation occurred in relation to elbow flexion and forearm deceleration, with very little proximal biceps activity during the earlier phases of throwing.[4][5][6]

Thus, in most healthy patient populations, the LHBT plays a negligible role in the dynamic stability of the shoulder. The main function of the biceps muscle is forearm supination and elbow flexion. The biceps also contributes 10% of the total power in shoulder abduction when the arm is in external rotation.[2]

Etiology

Biceps tendonitis describes a clinical condition of inflammatory tenosynovitis most commonly affecting the tendinous portion of the LHB as it travels within the bicipital groove in the proximal humerus.  The continuum of clinical pathology ranges from acute inflammatory tendinitis to degenerative tendinopathy.

Primary bicipital tendinitis is much less common than cases where it is associated with concomitant primary shoulder pathologies (i.e., secondary cases). The etiologies for primary bicipital tendinitis are not well understood compared to the more common secondary presentations. A particular subset of patients with primary, isolated biceps tendinitis is recognized in the younger, athletic population.  Provocative sports include baseball, softball, and volleyball. Beyond this aforementioned athletic cohort, there are only a few case reports in the literature highlighting patients presenting with spontaneous LHB tendon ruptures secondary to medical comorbidities.

Secondary cases are much more common and have been described in the literature with increasing frequency dating back to at least the early 1980s.  In 1982, Neviaser et al. demonstrated the relationship between increasing LHB tendon inflammatory changes with increasing severity of rotator cuff (RC) tendinopathy. Other associated shoulder pathologies include[2][7][8]:

  • Rotator cuff tendinitis and tendinopathy
  • Subscapularis injuries
  • LHB tendon instability/dislocation
    • Often seen in association with subscapularis injuries/tears
  • Direct or indirect trauma
  • Inflammatory conditions
  •  Internal impingement of the shoulder (“Thrower’s” shoulder)
    • Glenohumeral internal rotation deficit (GIRD)
    • Superior labral lesions (the “peel-back” mechanism)
  • External impingement/Subacromial impingement syndrome (EI/SIS)
  • Glenohumeral arthritis

Epidemiology

Primary LHB tendinitis represents about 5% of cases of proximal biceps pathology. Although much less common, primary isolated cases are typically observed in young athletes participating in baseball, softball, volleyball, gymnastics, and/or swimming.[8][9][10]

The vast majority of cases are seen in association with the aforementioned shoulder pathologies. Most commonly, LHB tendinopathy occurs in association with RC pathology, EI/SIS, or in tandem with subscapularis injuries. In the setting of RC tears, 90% of cases demonstrated concomitant LHB tendinopathy, and 45% of cases had additional LHB instability.[11][12]

Pathophysiology

Tendinopathic Cascade[2]

The pathophysiology of LHB tendinitis/tendinopathy begins with the early stages of tenosynovitis and inflammation secondary to repetitive traction, friction, and shoulder rotation. Inflammation develops early on in the tendinous portion in the bicipital groove. The tendon increases in diameter secondary to swelling and/or associated hemorrhage, further compromising the tendon as it becomes mechanically irritated in its confined space.

The resultant increased pressure and specific sites of traction predispose the tendon to pathologic shear forces. In addition, the sheath of the biceps tendon is a direct extension of the synovial lining of the glenohumeral joint. Thus, concomitant or pre-existing RC pathology can directly compromise the LHB tendon itself.  In the early stages of the disease, the LHB tendon remains mobile in the bicipital groove.

As the pathophysiology escalates, there is an ensuing LHB sheath thickening, fibrosis, and vascular compromise. The LHB tendon undergoes degenerative changes and associated scarring, fibrosis, and adhesions eventually compromise LHB tendon mobility. In effect, the tendon becomes pathologically “anchored” in the groove, further exacerbating the potential points of traction and overall increases shear forces experienced by the LHB tendon along its course.

In advanced, end-stage conditions the LHB tendon can eventually rupture at its origin near the superior glenoid tubercle, or as it exits the bicipital groove near its musculotendinous junction.

Overhead Throwing[8][9][10]

During an overhead throw, such as pitching in baseball, the thrower’s shoulder is brought into a position of maximum shoulder abduction and external rotation during the late cocking phase. Biceps injuries occur in this position secondary to the peel-back phenomenon.  Subsequently, the biceps muscle eccentrically contracts to decelerate elbow extension during the follow-through phase of throwing.

Histopathology

The degree of histologic severity of LHB tendon disease states does not correlate with the degree of pathology demonstrated on either MRI or from direct intra-operative inspection. Furthermore, other studies suggest that the duration of symptoms does not correlate with the histologic severity. Also, the more proximal zones of the LHB tendon (i.e., the intra-articular and bicipital groove portions) consistently demonstrate higher histologic grades of tendinopathy compared to tissue specimens examined from more distal LHB tendon zones.[13][14][15]

While histologic grading of the severity of tendinopathic changes remains separate from the clinical presentation and MRI- and/or intra-operative findings, there are some noteworthy pathologic patterns associated with increasing grades of severity of tendinopathy.[13][14][15]

Grade 0

  • Tenocytes are normal in appearance
  • Myxoid degenerative material not present
  • Collagen remains arranged in tight, cohesive bundles
  • Blood vessels arranged inconspicuously between collagen bundles

Grade I

  • Tenocytes are rounded
  • Myxoid degenerative material present in small amounts between collagen bundles
  • Collagen remains arranged in discrete bundles, but slight separation between bundles becomes apparent
  • Capillary clustering is evident (< 1 cluster per ten high-power fields)

Grade II

  • Tenocytes are rounded and enlarged
  • Myxoid degenerative material evident in moderate to large amounts
  • Collagen bundles lose discrete organization as the separation between individual fibers and bundles increases
  • Capillary clustering is increases (1 to 2 clusters per ten high-power fields)

Grade III

  • Tenocytes are rounded and enlarged with abundant cytoplasm and lacuna
  • Myxoid degenerative material abundant
  • Collagen disorganized, loss of microarchitecture
  • Capillary clustering is increased (>2 clusters per ten high-power fields)

Other changes associated with tendinopathy:

  • Tenosynovium
    • Irrespective of histologic grade of tendinopathy, the surrounding bicipital sheath/synovium demonstrates varying degrees of synovial hypertrophy, hyperplasia, and proliferation
  • Low-grade degenerative tendinopathy:
    • Total cellularity (cell density, cells/ mm): minimal increase
    • Apoptotic index (% relative to total number of cells counted): minimal increase
  • Moderate grade degenerative tendinopathy:
    • Total cellularity (cell density, cells/ mm): peak increase
    • Apoptotic index (% relative to total number of cells counted): moderate increase
  • Severe grade degenerative tendinopathy:
    • Total cellularity (cell density, cells/ mm): decreases
    • Apoptotic index (% relative to total number of cells counted): peak increase

Histologic studies have consistently reported that irrespective of patient age, severity of symptoms, and duration of symptoms, acute inflammatory changes are rarely evident upon histologic specimen analysis.

History and Physical

A comprehensive history should be obtained by clinicians evaluating patients presenting with acute or chronic shoulder pain. Characteristics of proximal biceps tendinitis include the following:

  • Atraumatic, insidious onset of anterior shoulder pain
  • Symptom exacerbation with overhead activities
  • Pain radiating down the anterior arm from the shoulder
  • Clicking or audible popping can be reported in the setting of proximal biceps instability
  • Pain at rest, pain at night
  • History or current sports, especially baseball, volleyball, and other overhead sports
  • History or current manual/physical laborer occupations

In addition, a thorough history includes a detailed account of the patient’s occupational history and current status of employment, hand dominance, history of injury/trauma to the shoulder(s) and/or neck, and any relevant surgical history.

C-Spine /Neck Exam[16]

Co-existing cervical radiculopathy should be ruled out in any situation where neck and/or shoulder pathology is in consideration. Observation of neck posturing, muscular symmetry, a palpable tenderness, and active/passive ROM should be evaluated. Special tests that are helpful in this regard include the Spurling maneuver, myelopathic testing, reflex testing, and a comprehensive neurovascular exam.

Shoulder Exam[17][18][19][20][21]

Clinicians must observe the overall shoulder girdle to assess symmetry, shoulder posturing, and overall muscle bulk and symmetry. Scapular winging should also be ruled out. The skin should be observed for the presence of any previous surgical incisions, lacerations, scars, erythema or induration. In the setting of proximal biceps pathology, especially in traumatic or spontaneous LHB tendon ruptures, patients will typically exhibit significant ecchymosis in the upper arm over the area of the biceps brachii muscle itself, and an associated “Popeye” deformity is characteristic for a complete rupture. The latter is more readily appreciated in fit or thin patients and can be a more subtle finding in patients with a large body habitus. Thus, a comparison to the contralateral extremity is helpful.

After the observational component of the physical examination, active and passive ROM are documented. In the setting of both primary and secondary proximal biceps tendinitis cases, full ROM should be observed. In the absence of advanced glenohumeral arthritic changes, limited passive ROM is considered diagnostic for adhesive capsulitis.

The clinician can assess motor strength grading for C5 to T1 nerve roots in addition to specific RC muscle strength testing. Specifically, RC strength and/or pathology can be assessed via the following examinations: 

Proximal Biceps Provocative Testing[22]

There are a multitude of focused physical examination maneuvers reported in the literature. Specific physical examination maneuvers target either LHB pathology localized to the bicipital groove or more proximally near the tendons origin at the supraglenoid tubercle. It is important to differentiate LHBT associated pain from other associated shoulder pathologies, including pain secondary to AC joint pathologies[23]

Bicipital groove palpation

Direct palpation over the patient’s bicipital groove elicits a painful response in the setting of pathology.

Speed test

A positive test consists of pain elicited in the bicipital groove when the patient attempts to forward elevate the shoulder against examiner resistance; the elbow is slightly flexed, and the forearm is supinated.

Upper cut test 

The involved shoulder is positioned at neutral, the elbow is flexed to 90 degrees, the forearm is supinated, and the patient makes a fist. The examiner instructs the patient to perform a boxing “uppercut” punch while placing his or her hand over the patient’s fist to resist the upward motion. A positive test is when the patient experiences pain or a painful pop over the anterior shoulder near the bicipital groove region.

Yergason test

The arm is stabilized against the patient’s trunk, and the elbow is flexed to 90 degrees with the forearm pronated. The examiner manually resists supination while the patient also externally rotated the arm against resistance. A positive test is noted if the patient reports pain over the bicipital groove and/or subluxation of the LHB tendon.

In addition to eliciting bicipital groove pathology, the clinician should also attempt to examine for possible associated labral and/or rotator cuff pathologies.

AC Joint Provocative Testing[24][25]

Observation and direct palpation

Patients presenting with chronic AC joint pain and/or arthritic pathology often will have clinically obvious AC joint hypertrophy that can be appreciated solely with observation and/or direct palpation over the joint. 

Cross body adduction 

The examiner may find it helpful to directly localize the AC joint with direct palpation. Subsequently, the examiner brings the shoulder into about 90 degrees of flexion in front of the plane of the scapula, and a positive test includes patient-reported symptom reproduction as the arm is brought into cross-body adduction positions. The physician should be able to discern the exact location of pain reproduction with the cross body adduction maneuvers.

Superior Labrum Anterior-Posterior (SLAP) lesions

O’Brien test/Active Compression test

The patient is standing, and the arm of interest is positioned at 90 degrees of forward flexion, 10 degrees of adduction, and internally rotated so the thumb points toward the floor. The examiner places his or 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 repeated with the patient’s arm rotated, so the palm faces the ceiling. A positive test is denoted by 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).

Anterior slide test

The patient stands with the hand of the involved arm on the ipsilateral hip with the thumb pointing posteriorly. The examiner places one hand on the joint line of the shoulder and the other hand on the elbow. The examiner then applies an axial load in an anterosuperior direction from the elbow to the shoulder. A positive test includes pain or a painful click on the anterior or posterior joint line.

Modified O’Driscoll test /Modified dynamic labral shear test

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

Rotator Cuff Muscle Testing

Supraspinatus (SS)

  • Jobe test: A positive test is pain/weakness with resisted downward pressure while the patient’s shoulder is at 90 degrees of forward flexion and abduction in the scapular plane with the thumb pointing toward the floor. 
  • Drop arm test: the patient’s shoulder is brought into a position of 90 degrees of shoulder abduction in the scapular plane. The examiner initially supports the limb and then instructs the patient to slowly adduct the arm to the side of the body. A positive test includes the patient’s inability to maintain the abducted position of the shoulder and/or an inability to adduct the arm to the side of the trunk in a controlled manner.

Infraspinatus (IS)

  • Strength testing: This is performed while the shoulder is positioned against the side of the trunk, the elbow is flexed to 90 degrees, and the patient is asked to externally rotate (ER) the arm while the examiner resists this movement.
  • External rotation lag sign: The examiner positions the patient’s shoulder in the same position, and while holding the wrist, the arm is brought into maximum ER. The test is positive if the patient’s shoulder drifts into internal rotation (IR) once the examiner removes the supportive ER force at the wrist.

Teres Minor (TM)

  • Strength testing: This is performed while the shoulder positioned at 90 degrees of abduction and the elbow is also flexed to 90 degrees. Teres minor (TM) is best isolated for strength testing in this position while ER is resisted by the examiner.
  • Hornblower sign: The examiner positions the shoulder in the same position and maximally ERs the shoulder under support. A positive test occurs when the patient is unable to hold this position, and the arm drifts into IR once the examiner removes the supportive ER force.

Subscapularis (SubSc)

  • IR lag sign: The examiner passively brings the patient’s shoulder behind the trunk (about 20 degrees of extension) with the elbow flexed to 90 degrees. The examiner passively IRs the shoulder by lifting the dorsum of the handoff of the patient’s back while supporting the elbow and wrist. A positive test occurs when the patient is unable to maintain this position once the examiner releases support at the wrist (i.e., the arm is not maintained in IR, and the dorsum of the hand drifts toward the back)
  • Passive ER ROM: A partial or complete tear of the subscapularis (SubSc) can manifest as an increase in passive ER compared to the contralateral shoulder.
  • Lift-off test: This test is more sensitive/specific for lower SubSc pathology.  In the same position as the IR lag sign position, the examiner places the patient’s dorsum of the hand against the lower back and then resists the patient’s ability to lift the dorsum of the hand away from the lower back.
  • Belly press: This test is more sensitive/specific for upper subscapularis pathology. The examiner has the patient’s arm at 90 degrees of elbow flexion, and IR testing is performed by the patient pressing the palm of his/her hand against the belly, bringing the elbow in front of the plane of the trunk. The elbow is initially supported by the examiner, and a positive test occurs if the elbow is not maintained in this position upon the examiner removing the supportive force.

External impingement/SIS

  • Neer impingement sign: Positive test occurs if the patient reports pain with passive shoulder forward flexion beyond 90 degrees.
  • Neer impingement test: Positive test occurs after a subacromial injection is given by the examiner and the patient reports improved symptoms upon repeating the forced passive forward flexion beyond 90 degrees.
  • Hawkins test: Positive test occurs with the examiner passively positioning the shoulder and elbow at 90 degrees of flexion in front of the body – the patient will report pain when the examiner passively IR’s the shoulder. 

Internal impingement

  • Internal impingement test: The patient is placed in a supine position, and the shoulder is brought into terminal abduction and external rotation. A positive test consists of the reproduction of the patient’s pain.

Evaluation

Radiographic imaging should be obtained in all patients with acute or chronic shoulder pain.

Radiographs[2]

Recommended imaging includes a true anteroposterior (AP) image of the glenohumeral joint (i.e., the “Grashey” view). The true AP image is taken with the patient rotated between 30 and 45 degrees offset the cassette in the coronal plane. Alternatively, the beam can be rotated while the patient remains neutral in the coronal plane. The distance between the acromion and the humeral head (i.e., the acromiohumeral interval) can be calculated. A normal interval is between 7 and 14 mm, and this interval is decreased in cases of advanced degenerative arthritis and RCA. Other standard views include the lateral (or “scapular Y”) view and an axillary view.

Routine radiographs are recommended, but in the majority of cases of LHB tendinitis without coexisting pathologies, these will be normal.

Ultrasound (US)[2]

Ultrasound (US) is highly operator-dependent but is often touted as a fast, cost-effective tool for diagnosing LHB tendon pathology.  Characteristic findings include tendon thickening, tenosynovitis/hypertrophy of the synovial sheath, and fluid surrounding the tendon in the groove. The ability to perform a dynamic examination increases the sensitivity and specificity for detecting subtle instability. The diagnostic accuracy of ultrasound in detecting LHB pathology ranges from 50% to 96% (sensitivity) and 98% to 100% (specificity) when compared to magnetic resonance arthrography (MRA).

Magnetic Resonance Imaging (MRI)/Magnetic Resonance Arthrography (MRA)[2]

Magnetic resonance imaging (MRI) is useful in evaluating the LHB tendon, bicipital groove, and any fluid or edema that may be indicative of pathology. MRI is most beneficial in delineating other associated shoulder pathologies; however, there is poor concordance with MRI-suspected pathology, intra-operative findings, and/or histologic grades of biceps tendinopathy. 

MRI is useful in evaluating the LHB tendon’s position in the bicipital groove. Absence of the tendon within the groove would suggest subluxation and/or dislocation. In these cases, careful attention should be paid to evaluating for concomitant subscapularis pathology. Other associated shoulder pathologies and rotator cuff integrity can also be evaluated with MRI. Other common sources of acute or chronic shoulder pain can be evaluated on MRI, including subdeltoid and/or subacromial bursitis, acromioclavicular (AC) joint pathology, and morphology.  A systematic approach to reviewing shoulder MRIs is important, especially when correlating the MRI findings with the patient reported symptoms and clinical examination.

The addition of IV-contrast dye (MR arthrography) is sensitive but only moderately specific for LHB tendon pathology.  While a standard MRI series can be valuable in detecting fluid surrounding the LHB tendon as it courses in the bicipital groove, the administration of the dye serves as a confounding variable that inherently limits the specificity of this pathologic finding.

Treatment / Management

Nonoperative Management

The initial management of LHB tendinopathy is nonsurgical. A period of rest and activity modification is beneficial in the acute setting, coupled with nonsteroidal anti-inflammatory drugs (NSAIDs).

Physical therapy[2]

Successful physical therapy regimens target the underlying source(s) contributing to the LHB tendon pathology. Potential factors predisposing to biceps-related shoulder injuries include glenohumeral internal rotation deficit (GIRD) in overhead-throwing athletes/baseball pitchers, poor trunk control, scapular dyskinesia, and internal impingement.

Strengthening protocols should focus on restoring muscle balance across the shoulder girdle, including rotator cuff and periscapular muscle strengthening programs. Focused stretching on the anterior shoulder structures, including pectoralis minor, should also be considered. Other modalities such as dry needling have demonstrated promise in preliminary animal studies.

Injections[26][27][27][28]

Corticosteroid injections are considered in the setting of persistent symptoms despite the aforementioned therapies. There is some controversy with respect to the type of technique used (ultrasound-guided versus blind injection) and exact location utilized for the injection (subacromial, intra-articular, bicipital groove/sheath).  Theoretically, in the setting of concomitant shoulder pathologies, an intra-articular injection would also reach the LHB tendon in the bicipital groove, as the sheath is contiguous with the glenohumeral joint synovial tissue.

Direct injection is targeted to the sheath itself, and not the LHB tendon directly. Although not definitively documented, an intratendinous LHB tendon injection may predispose the patient to tendon rupture. In a 2011 randomized controlled trial (RCT) comparing injection accuracy (with post-injection CT imaging to confirm injection placement by location) of ultrasound-guided versus blind bicipital sheath injections at its location in the groove.  Potential injection location results included (1) solely in the tendon sheath, (2) inside the tendon, in the tendon sheath, and surrounding (but outside) the tendon sheath, and (3) confined to only the area outside the tendon sheath. The ultrasound-guided injections resulted in 87% accuracy for injecting the tendon sheath alone (location "1"). By stark contrast, the blind injection was accurate only 27% of the time, and one-third of the time the tendon itself and the entire bicipital sheath was missed altogether.

Surgical Management

For the purposes of this review, the management of SLAP injuries will not be discussed.

Indications for surgical management include:

  • Intra-operative findings of an inflamed tendon (i.e., the “lipstick” lesion), significant fraying, tearing, or hypertrophy
  • Partial-thickness tears of the LHB tendon (>25 to 50%)
  • Medial LHB subluxation
  • LHB subluxation with associated subscapularis tear, or bicipital groove soft tissue compromise

Surgical Techniques

Biceps tenotomy[2]

  • Provides reproducible results in terms of pain relief
  • Minimal post-operative rehabilitation

The technique involves an initial diagnostic arthroscopy. The glenohumeral joint is inspected for any co-existing clinical pathology. The biceps tendon is examined under direct traction to visually inspect the intertubercular groove portion, which is a prime location of pathology. Next, a probe is used to evaluate the LHB tendon stability in the bicipital groove. Stability can be further assessed by internally rotating the arm and evaluating for any medial/inferior subluxation of the LHB tendon. In the setting of LHB tendon instability, this maneuver will lead to tendon entrapment within the joint. The entrapment is relieved with external rotation of the arm.

Arthroscopic inspection of the tendon allows for estimation of the relative percentage of the LHB tendon that is compromised. A popular classification system utilized for the intra-operative grade corresponding to the degree of LHB tendon macroscopic pathology is the Lafosse grading scale[29]:

  • Grade 0: Normal tendon
  • Grade 1: Minor lesion (partial, localized areas of tendon erosion/fraying, focal areas affect <50% of the tendon width)
  • Grade 2: Major lesion (extensive tendon loss, compromising >50% of the tendon width)

Some surgeons solely debride the tendon in the setting of <50% tendinous compromise. Arthroscopic biceps tenotomy is performed by releasing the tendon as close as possible to the superior labrum. As long as the tendon is free from intimate soft tissue adhesions to surrounding structures, the tendon should retract distally toward the bicipital groove. If adhesions are present, all efforts should be made to mobilize the tendon in order to allow for retraction following the tenotomy. In cases where the LHB tendon is particularly hypertrophic and scarred to other soft tissue structures in the joint, this serves as a potential source of postoperative pain.

 Biceps tenodesis[2][30][2]

  • Preferred technique in younger patients, athletes, laborers, and those patients specifically concerned with postoperative cosmetic deformity
  • Optimizes the length-tension relationship of the biceps muscle; mitigates postoperative risk of muscle atrophy, fatigue, and cramping

Various locations for the tenodesis itself, in addition to fixation technique, used provide equivalent results in terms of patient satisfaction and clinical outcomes. Following a standard diagnostic arthroscopy, a spinal needle is used to “tag” the tendon near its entrance into the bicipital groove. Once this is tagged with fiberwire, the tenotomy is performed, and the residual “stump” is shaved back to the superior labrum.

Next, the arthroscope is taken into the subacromial space, and the tagging sutures help localize the residual LHB tendons location. The bicipital groove is then opened up with a cautery device until the LHB tendon is visualized. Following mobilization of the tendon to the medial aspect of the bicipital groove, the osseous groove is cleared of all soft tissue in preparation for fixation. One technique involves interference screw placement approximately 1cm distal to the superior extent of the groove. During the fixation of the tendon, care is taken to utilize an arthroscopic grasper to maintain ideal tension on the proximal extent of the LHB tendon. Once fixation is complete, any residual tendon that remains prominent from the fixation point is carefully resected.

An alternative to the arthroscopic (or suprapectoral) tenodesis procedure is the open subpectoral approach. Several studies have compared outcomes between the all-arthroscopic and open subpectoral approaches. Although advocates for the latter approach cite the theoretical advantage of being able to completely remove the LHB tendon from the bicipital groove, the majority of studies report similar patient-reported outcomes and no difference in patient-reported pain scores.

Differential Diagnosis

The differential diagnosis for chronic shoulder pain includes several etiologies:

Impingement

  • External/SIS
  • Subcoracoid
  • Calcific tendonitis
  • Internal (including SLAP lesions, GIRD, little league shoulder, posterior labral tears)

RC pathology 

  • Partial- versus full-thickness tears (PTTs versus FTTs)
  • RCA

Degenerative

  • Advanced DJD, often associated with RCA
  • Glenohumeral arthritis
  • Adhesive capsulitis
  • Avascular necrosis (AVN)
  • Scapulothoracic crepitus

Proximal biceps

  • Subluxation–often seen in association with SubSc injuries
  • Tendonitis and tendinopathy

AC joint conditions

  • AC separation
  • Distal clavicle osteolysis
  • AC arthritis

Instability 

  • Unidirectional instability–seen in association with an inciting event/dislocation (anterior, posterior, inferior)
  • Multidirectional instability (MDI)
  • Associated labral injuries/pathology

Neurovascular conditions

  • Suprascapular neuropathy–can be associated with paralabral cyst at the spinoglenoid notch
  • Scapular winging–medial or lateral
  • Brachial neuritis
  • Thoracic outlet syndrome (TOS)
  • Quadrilateral space syndrome

Other conditions

  • Scapulothoracic dyskinesia
  • Os acromiale
  • Muscle ruptures (pectoralis major, deltoid, latissimus dorsi)
  • Fracture (acute injury or pain resulting from long-standing deformity, malunion, or nonunion)

Prognosis

Patients with persistent, debilitating symptoms in the setting of known proximal biceps tendon pathology are good surgical candidates for either a tenotomy or tenodesis procedure. 

The literature demonstrates a high level of patient satisfaction and patient-reported pain and overall outcome scores at long-term follow-up. A 2017 study of > 100 patients that were 1-year out from surgical arthroscopy procedures with concomitant biceps tenotomy revealed that > 90% of patients were “satisfied” or “very satisfied” with their outcome. In addition, 95% stated that they would have the same surgery again.[31] Similar positive results are demonstrated in studies following biceps tenodesis patients at long-term follow-up. In addition, the majority of reports have noted no appreciable difference between tenotomy and tenodesis patients with respect to elbow flexion and forearm supination strength recovery.[32]

Complications

The approximate rates of the most common postoperative surgical complications relative to each procedure[2][32]:

Biceps Tenotomy

  • Cosmetic (“Popeye”) deformity: 10% to 70%
  • Muscle spasm/cramping: 15% to 25%
  • Biceps pain: 10% to 20%

Biceps Tenodesis

  • Groove pain: 0% to 25% 
  • Cosmetic (“Popeye”) deformity: 10% to 15%
  • Muscle spasm/cramping: 5% to 10%
  • Biceps pain: 5% to 10%
  • Humeral shaft fracture
    • Recent case reports have described spiral humeral fractures after SPBT performed with an 8-mm interference screw, raising concern for possible increased fracture susceptibility when the humerus is stressed with torsional load.[33][34]

Postoperative and Rehabilitation Care

For isolated biceps procedures, typical postoperative protocols are as follows:

Biceps Tenotomy

Rehab phases

  • Sling use for 1 to 2 weeks
  • Active ROM begins at 2 to 4 weeks post-op; sling discontinued
  • Strengthening begins at 4 to 6 weeks post-op 

Return to work/activity

  • Patients typically can resume light work by 3 to 4 weeks post-op
  • Depending on occupational demands, return to full duty ranges from 1 to 3 months after surgery
  • Most patients return to unrestricted activities at 3 to 4 months postoperatively 

Biceps Tenodesis

Rehab phases

  • Sling use for 3 to 4 weeks
  • Initial period includes passive elbow ROM and grip strengthening
  • Avoid active elbow flexion and forearm supination until the 6-week mark
  • Goal of achieving full active and passive shoulder ROM by 6 weeks

Return to work

  • Patients typically can resume light work by 3 to 4 weeks postop
  • Depending on occupational demands, return to full duty ranges from 2 months to 4 months from surgery
  • Most patients return to unrestricted activities at 3 to 4 months postoperatively

Consultations

The majority of patients with LHB tendinitis can be managed nonoperatively. Consideration for referral should be in the setting of persistent pain/symptoms despite 6 to 8 weeks of nonoperative management. In addition, referral for the appropriate physical therapy program focused on correcting any existing muscular imbalances about the shoulder girdle, including scapular dyskinesia.

In the management of young athletes, consideration should be given for early referral to a sports medicine physician experienced in managing these types of shoulder pathologies. Again, as most biceps-related shoulder pathologies can be managed nonoperatively, referral to an orthopedic surgeon for surgical management should be considered in any of the following scenarios:

  • Persistent/worsening symptoms despite PT/NSAIDs/activity modification/injections
  • Diagnostic imaging confirming evidence of tendon subluxation and/or dislocation
  • In the setting of either post-operative “Popeye” deformity, failed biceps tenodesis techniques, or spontaneous rupture, referral to a surgeon with experience in correcting the deformity should be considered

Deterrence and Patient Education

Patients should be educated on the possible etiologies and concomitant shoulder pathologies seen in association with proximal biceps pathologies. A point of emphasis should be given to including any LHB tendon pathology that may be seen in association with other known shoulder pathologies. For example, a patient should be not only educated on the injury affecting the rotator cuff itself, but also the potential for co-existing injury to the biceps tendon. Discussion,  especially with older patient populations, should include that the planned concomitant procedure (i.e., the tenotomy or tenodesis procedure) may or may not occur. By doing this, the patient’s postoperative expectations can be adequately managed before performing surgery.

Enhancing Healthcare Team Outcomes

Long head of the biceps (LHB) tendon pathologies span a clinical spectrum, from acute tendinitis to chronic degenerative tendinopathy and spontaneous tendon rupture. In athletic populations, the physician must coordinate and work in tandem with his or her physical therapists to ensure the athletes potential; co-existing shoulder girdle risk factors are addressed appropriately. In throwers, it is critical to recognize that poor trunk control, scapular dyskinesia, shoulder girdle atrophy, and muscular imbalances all can contribute to the proximal biceps tendinitis. Thus, the comprehensive management of these injuries often involves head coaches and athletic trainers in the athletic populations, all the way to general practitioners, geriatricians, sports medicine primary care physicians, and orthopedic surgery sports medicine specialists.

Failed nonoperative management is an indication for proceeding with surgical treatment. Other indications for surgery include:

  • Partial-thickness tears of the LHB tendon (> 25% to 50%)
  • Medial LHB tendon subluxation/dislocation
  • LHB tendon subluxation/dislocation with associated bicipital groove soft tissue stabilizer injury; also may or may not include injuries to the subscapularis muscle/tendon

The two most common surgical techniques employed include biceps tenodesis and biceps tenotomy procedures. The literature demonstrates equivalent outcomes between each type of procedure, and both techniques yield a high rate of patient satisfaction and clinical outcomes at long-term follow-up with each type of procedure. (Level I)