BICEPS TENDINOPATHY

BICEPS TENDINOPATHY

Biceps tendinopathy describes pain and tenderness in the region of the biceps tendon. The biceps musculotendinous junction is particularly susceptible to overuse injuries, especially in individuals performing repetitive lifting activities.

This condition is often diagnosed incorrectly and confused with rotator cuff tendinopathy. Biceps tendinopathy is rarely seen in isolation. It coexists with other pathologies of the shoulder, including rotator cuff tendinopathy and tears, shoulder instability, and imbalances of the dynamic stabilizers. 

Among patients with biceps tendinopathy, 95% have "impingement syndrome" as their primary diagnosis.

PATHOPHYSIOLOGY

Historically, all disorders of the biceps tendon have been termed biceps tendinitis. Evidence suggests that degenerative changes in the tendon occur without inflammation.

In acute cases, an inflammatory pathology may still be a valid explanation of biceps tendon pain.

Tendinitis describes inflammation of the tendon and the paratendon. This is usually caused by chronic overload, which leads to microscopic tears in the tendon, triggering an inflammatory response.

Peritendinitis is the inflammation of the paratendon or tendon sheath. This usually occurs as a result of a direct injury or irritation in which the tendon rubs over a bony prominence; this is referred to as a tenosynovitis. Tendinosis is a histological definition describing degenerative changes in the tendon.

Macroscopic evaluation of a degenerative tendon reveals disorganized tissue that is soft and yellow or brown (mucoid degeneration).

The microscopic appearance reveals degenerative changes to collagen with fibrosis. Inflammatory mediators are not usually present in tendinosis.

Most injuries of more than 3 months involve only a minimal amount of persistent inflammation, with tendinosis being a greater component of the injury.

The term tendinopathy refers to the clinical presentation of a symptomatic tendon. The underlying pathology, degenerative or inflammatory, is not considered in this definition.

Three etiologies of tendinopathy have been described, as follows:

• Mechanical theory - This theory states that repetitive loading of the tendon results in microscopic degeneration. Fibroplasia occurs within the tendon, resulting in scar tissue.

• Vascular theory - According to this theory, tendon degeneration occurs as a result of focal areas of vascular compromise.

• Neural modulation - The newest of the 3 theories, this focuses on the assumption that tendinopathy results from neurally mediated mast cell degranulation and the release of substance P.

More studies are needed to more clearly understand the relationship between the peripheral nervous system and tendinopathies.

Knowing the anatomy of the biceps brachii muscle is important in understanding biceps tendinopathy.

The biceps brachii has 2 heads.

The short head arises from the tip of the coracoid process of the scapula.

The long head arises from the supraglenoid tubercle of the scapula, and the superior labrum runs through the intertubercular groove between the greater and lesser tubercles of the humerus.

Proximally, the long head of the biceps acts as a shoulder stabilizer through depression of the humeral head.

The 2 heads join together in the distal arm to form 1 strong tendon, which inserts on the radial tuberosity on the upper end of the radius. Distally, the tendon gives off the bicipital aponeurosis (an expansion that blends with the flexor forearm muscles, extending to the ulna).

The biceps brachii is innervated by the musculocutaneous nerve (C5, C6).

The actions of the biceps brachii muscle are flexion of the elbow, supination of the forearm, humeral head depression, and shoulder flexion (short head primarily).

FREQUENCY

Biceps tendinopathy is a common condition, but the exact frequency is unknown.

CLINICAL

HISTORY

The diagnosis of biceps tendinopathy is primarily clinical.

Patient history suggests the diagnosis.

Characteristics of the condition are as follows: 

• Pain is reported in the region of the anterior shoulder located over the bicipital groove, occasionally radiating down to the elbow.

• The pain is aggravated by activities that require shoulder flexion, forearm supination, and/or elbow flexion.

• Pain is usually exacerbated by the initiation of activity.

• Some patients describe fatigue with shoulder movements.

• The symptoms are alleviated by rest, ice, massage, stretching, and sometimes heat.

• Night pain is not uncommon.

PHYSICAL

Physical examination for biceps tendinopathy includes the following:

• Inspection - Muscle bulk of the shoulder girdle, anatomical abnormalities, posture

• Palpation - For tenderness over the biceps tendon in the bicipital groove; compare side to side (because there is often tenderness in asymptomatic patients)

• Range of motion (ROM) - Passive and active ROM of the shoulder in forward flexion, extension, abduction, adduction, internal and external rotation

• Neurologic testing - Muscle strength, sensation, and deep tendon reflexes; strength testing possibly limited by pain

• Special biceps tests

  • Speed test 1 - With the forearm in the supinated position and the elbow fully extended, the patient attempts to flex the arm (forward flexion at the shoulder) against the resistance provided by the examiner. Tenderness in the bicipital groove is considered a positive test result and is indicative of bicipital tendinitis.

  • Speed test 2 - This test is a variation on Speed test 1. Test 2 may be performed by having the patient forward-flex the arm to 90 º while the examiner tries to move the patient's arm into extension against resistance provided by the patient. A positive test result is indicated by discomfort or pain in the bicipital groove.

  • Yergason test - The patient's elbow is flexed to 90 º and is stabilized against the thoracic cage, with the forearm pronated; the examiner resists supination while the patient also laterally rotates the arm against resistance. The test is considered positive if the patient experiences discomfort or pain in the bicipital groove or if the tendon pops out of the groove.

  • Gilchrist test - The patient lifts a 5-pound weight overhead with an externally rotated arm and slowly lowers it to the lateral horizontal position. Discomfort or pain in the bicipital groove is considered a positive test result.

  • Lippman test - With the patient's arm flexed to 90 º, the examiner palpates the biceps tendon 3 inches (7.6 cm) below the glenohumeral joint and moves the biceps tendon from side to side. Pain and a palpable displacement of the tendon from its groove indicate tenosynovitis with instability of the biceps tendon.

• Other tests - Tests for associated rotator cuff, labral, and acromioclavicular joint pathology are as follows:

  • Impingement tests include the Hawkins-Kennedy test and the Neer test.

  • Acromioclavicular joint tests include the cross-body adduction test.

  • Labral tests include the O'Brien test, the anterior slide test, and the Clunk test.

CAUSES

Biceps tendinopathy can result from the following causes:

• Poor lifting techniques

• Chronic, repetitive upper extremity activities (shoulder/elbow flexion)

• Impingement syndrome

• Rotator cuff pathology

• Biceps subluxation

• Shoulder girdle muscle imbalances

• Poor posture

• Overload (usually eccentrically)

• Lack of flexibility/capsular tightness

• Direct trauma

• Multidirectional shoulder instability

• Calcifications of the tendon

• Osteoarthritis and spurring

• Anatomical abnormalities (eg, variations of the bicipital groove, fractures, first rib subluxations)

DIAGNOSIS

LABORATORY STUDIES

• No laboratory studies are necessary for the diagnosis of biceps tendinopathy.

IMAGING STUDIES

• In patients with biceps tendinopathy, plain radiography may show calcifications in the biceps tendon or demonstrate associated degeneration in the glenohumeral or acromioclavicular joint. Fisk views help to evaluate the size of the biceps groove. Short, narrow margins of the groove may predispose the patient to biceps tendon subluxations.

• Ultrasonography can be used to assess the dynamic function of the biceps tendon. It is also useful for diagnosing biceps ruptures or instability.

• Magnetic resonance imaging (MRI) is performed to rule out shoulder pathology (eg, rotator cuff tear, labral tears, biceps rupture). MRI may show signal changes in the biceps tendon that indicate pathology.

OTHER TESTS

• Diagnostic local anesthetic infiltration of the region of the bicipital groove may help to clarify the source of the nociception. If an alternate diagnosis is suggested, other tests can be performed.

• Electromyography (EMG) or nerve conduction studies (NCSs) are performed to rule out mononeuropathy, brachial plexopathy, and cervical radiculopathy.

TREATMENT

PHYSICAL THERAPY

The components of a physical therapy program, as follows, are coordinated with various stages of the bicipital tendinopathy:

v  Immediate

§  Initiate rest, ice, compression, and elevation (RICE) therapy.

§  Avoid activity that aggravates the condition.

v  Subacute

§  Physical therapy should involve soft-tissue therapy with transverse gliding of the tendon and cross-friction massage.

§  Electrical stimulation and/or ultrasonography may be beneficial if symptoms interfere with therapeutic exercise.

§  Apply moist heat to help facilitate stretching and reduce pain.

§  If the shoulder is stable, perform ROM exercises for the shoulder, including gradual stretching of the biceps tendon. Other activities include circumduction, pendulum, 2-hand rod swinging, and lateral/front finger wall walking.

§  Progress to resistive exercises as symptoms subside. Isometrics progress to concentric exercises, then to eccentric exercises, and finally to sport-specific exercises. Eccentric loading in the management of tendinopathies of other muscle groups has shown promise in reversing some degenerative changes.

§  Closed kinetic chain exercises are generally started first, with open kinetic chain exercises initiated later with sport-specific activities.

§  Perform proprioceptive shoulder exercises with a Swiss ball.

§  Address biomechanical factors that may be contributing to the biceps tendinopathy.

v  Long term

§  Continue physical therapy as described.

§  Avoid aggravating factors.

§  Look for other causes or predisposing factors, such as bony abnormalities, labral pathology, and radiculopathy.

OCCUPATIONAL THERAPY

The occupational therapist should instruct the patient with biceps tendinopathy in the use of the appropriate adaptive equipment, in work simplification strategies, in ergonomic modifications, in the stretching of the appropriate shoulder girdle musculature, and in the strengthening program that will eventually be undertaken.

COMPLICATIONS

Possible complications that can develop from biceps tendinopathy include the following:

• Recurrent anterior shoulder pain

• Biceps rupture

• Weakness

• Maladaptive compensation strategies by the individual, causing other ailments

SURGICAL INTERVENTION

• Surgery is rarely necessary, but it may be required in patients with refractory cases associated with persistent pain that has not responded to any other treatment.

• Surgery often involves decompression of the musculotendinous structure through tenolysis, using arthroscopic or open surgical technique.

OTHER TREATMENT

• Injection with anesthetic and corticosteroid into the biceps tendon sheath may be helpful. This can be performed under ultrasonographic guidance to ensure correct placement of the medication. Avoid direct injection into the biceps tendon.

• Myofascial trigger point injections in the scapular stabilizer muscles may be beneficial. This technique uses an injection with dilute local anesthetic.

• Manipulation may be helpful, especially for first-rib abnormalities that contribute to the syndrome.

• Lithotripsy (extracorporeal shock wave therapy) has been under study for Achilles and patellar tendinopathy, with promising results. No studies related to biceps tendinopathy have been published.

MEDICATION

Nonsteroidal anti-inflammatory drugs (NSAIDs) may be used to manage acute symptoms of pain and stiffness. No apparent advantage is noted with regard to the use of one agent over another.

Liniments, including NSAID and capsaicin creams, may be considered. Acetaminophen may be used for analgesia.

NONSTEROIDAL ANTI-INFLAMMATORY DRUGS

NSAIDs are most commonly used for the relief of mild to moderate pain. Although the effects in the treatment of pain tend to be patient specific, ibuprofen is usually the drug of choice (DOC) for initial therapy.

Other options include fenoprofen, flurbiprofen, mefenamic acid, ketoprofen, indomethacin, and piroxicam. Celebrex, a cyclooxygenase-2 (COX-2) inhibitor, may also be used, although its efficacy is not greater. An improved adverse-effect profile is controversial. 

IBUPROFEN (Ibuprin, Advil, Motrin)

DOC for mild to moderate pain. Ibuprofen inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Adult: 200-400 mg PO q4-6h while symptoms persist; not to exceed 3.2 g/d

Pediatric:

<6 months: Not established

6 months to 12 years: 4-10 mg/kg/dose PO tid/qid

>12 years: Administer as in adults

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy 

NAPROXEN (Anaprox, Naprelan, Naprosyn)

For relief of mild to moderate pain. Naproxen inhibits inflammatory reactions and pain by decreasing the activity of COX, which is responsible for prostaglandin synthesis.

Adult: 375-500 mg PO bid

Pediatric:

<2 years: Not recommended

>2 years: 10 mg/kg/d PO in divided doses

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in patients with syndrome of ASA, nasal polyps, and asthma; acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug 

KETOPROFEN (Oruvail, Orudis, Actron)

For relief of mild to moderate pain and inflammation. Small dosages of ketoprofen are indicated initially in patients with small body size, in elderly patients, and in patients with renal or liver disease. Doses >75 mg do not increase the therapeutic effects. Administer high doses with caution and closely observe the patient for a response.

Adult: 25-50 mg PO q6-8h prn; not to exceed 300 mg/d

Pediatric:

<3 months: Not established

3 months to 12 years: 0.1–1 mg/kg PO q6-8h

>12 years: Administer as in adults

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy 

CELECOXIB (Celebrex)

Primarily inhibits COX-2. COX-2, which is considered an inducible isoenzyme, is induced by pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity.

At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, the incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, may be decreased in comparison with nonselective NSAIDs.

Seek the lowest dose for each patient.

Celecoxib neutralizes circulating myelin antibodies through anti-idiotypic antibodies; down-regulates proinflammatory cytokines, including INF-gamma; blocks Fc receptors on macrophages; suppresses inducer T and B cells and augments suppressor T cells; blocks complement cascade; promotes remyelination; and may increase CSF IgG (10%).

Celecoxib has a sulfonamide chain and is primarily dependent on cytochrome P450 enzymes (hepatic enzymes) for metabolism.

Adult: 200-400 mg/d PO qd or divided bid

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

May cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, conditions predisposing to fluid retention; caution in severe heart failure and hyponatremia because may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; caution in the presence of existing controlled infections; evaluate therapy when symptoms or lab results suggest liver dysfunction

ANALGESICS

Pain control is essential for quality patient care. Analgesics ensure patient comfort and have sedating properties, which are beneficial for patients with tendinitis. 

ACETAMINOPHEN (Tylenol, Panadol, Aspirin Free Anacin)

DOC for pain in patients with documented hypersensitivity to aspirin, NSAIDs, those who have been diagnosed with upper GI disease, and patients on oral anticoagulants.

Adult: 325-650 mg PO q4-6h or 1,000 mg tid/qid; not to exceed 4 g/d

Pediatric:

<12 years: 10-15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d

>12 years: 325-650 mg PO q4h; not to exceed 5 doses in 24 h

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

In chronic alcoholics, various dose levels of acetaminophen can cause hepatotoxicity; severe or recurrent pain or high or continued fever may indicate a serious illness 

CAPSAICIN (Dolorac, Capsin, Zostrix)

Derived from plants of the Solanaceae family. Capsaicin may render skin and joints insensitive to pain by depleting substance P in peripheral sensory neurons.

Adult:

Cream: Apply to skin tid/qid for 3-4 consecutive wk and evaluate efficacy (not to exceed 4 applications/d).