MEDIAL EPICONDYLITIS

MEDIAL EPICONDYLITIS

Medial epicondylitis (ME) is an overuse injury affecting the flexor-pronator muscle origin at the anterior medial epicondyle of the humerus.

ME is often discussed in conjunction with lateral epicondylitis (LE), which occurs much more frequently. ME is the most common cause of medial elbow pain, although the clinician is likely to see at least 5 cases of LE for every case of ME.

Patients who develop medial elbow pain appreciate their physician's knowledge of the subtle differences in the diagnosis and treatment of the 2 disorders.

PATHOPHYSIOLOGY

ME involves primarily the flexor-pronator muscles (ie, pronator teres, flexor carpi radialis, palmaris longus) at their origin on the anterior medial epicondyle.

Less often, ME also affects the flexor carpi ulnaris and flexor digitorum superficialis. Repetitive stress at the musculotendinous junction and its origin at the epicondyle leads to tendinitis in its most acute form and to tendinosis in its more chronic form.

In addition, an ulnar neuropraxia caused by compression of the ulnar nerve in or around the medial epicondylar groove has been estimated to occur in up to 50% of ME cases.

The tendinosis that occurs is primarily the result of failure of the damaged tendon to heal.

Microscopic examination of the involved tissue shows granulation tissue, fibrovascular and fibrocartilaginous tissue, tendon microfragmentation, calcification, and necrosis.

Histologically, damage to the involved tendons has been described as angiofibroblastic hyperplasia tendinosis and fibrillary degeneration of collagen.

A simple, acute inflammatory reaction is noted to be a much less common finding than are the previously described tendinosis changes.

SEX

A male-to-female ratio of 2:1 has been reported.

AGE

Peak incidence is in patients aged 20-49 years, but ME is also seen in teens and older adults, especially if they engage in hobbies, jobs, or sports activities that make them prone to overuse injuries.

CLINICAL

HISTORY

ME is characterized by pain over the medial epicondyle. Pain worsens with wrist flexion and forearm pronation activities. Patients may report discomfort even when simply shaking hands with someone.

Up to 50% of patients with ME complain of occasional or constant numbness and/or tingling sensation that radiates into their fourth and fifth fingers, suggesting involvement of the ulnar nerve.

The patient's history may include the occurrence of an acute injury as a result, for instance, of taking a divot in golf, throwing a pitch in baseball, or hitting a hard serve in tennis.

PHYSICAL

Tenderness with palpation over the anterior aspect of the medial epicondyle is the most consistent finding.

Other characteristics of ME include the following:

• Typically, pain is reproduced with resisted wrist flexion or resisted forearm pronation.

• Occasionally, the area of tenderness extends approximately 1 inch toward the proximal flexor-pronator muscle mass just distal to the epicondyle.

• The range of motion of the elbow and wrist is usually within normal limits.

• Patients may have symptoms of an ulnar neuropathy (eg, decreased sensation in the ulnar nerve distribution, a positive elbow-flexion test, a positive Tinel sign). In more severe cases, decreased sensation is associated with intrinsic weakness; intrinsic muscle atrophy may be noted.

CAUSES

The causes of ME include the following:

• The condition can result from the repetitive use of flexor-pronator muscles, especially with valgus stress at the medial epicondyle.

• The onset can be related to the patient's occupation (if, for example, his/her job requires repetitive actions, such as the consistent use of a screwdriver or hammer).

• ME's onset can accompany acute injury.

• An excessive topspin in tennis, excessive grip tension, improper pitching techniques in baseball, and an improper golf swing are common sports-related causes of ME.

DIAGNOSIS

LABORATORY STUDIES

• Laboratory studies are generally not indicated in ME.

IMAGING STUDIES

• A radiograph of the elbow is often performed to rule out associated lesions (eg, loose bodies, bony avulsion, osteoarthritis). Typically, anteroposterior and lateral films are adequate.

• Oblique views are needed if loose bodies are suggested upon examination or because of a catching or clicking sensation described by the patient.

• Valgus stress radiographs should be obtained if medial instability is suggested.

• Magnetic resonance imaging (MRI) may be helpful in looking for the characteristic pathology that is seen in chronic cases of ME; MRI also permits assessment of the medial collateral ligament and ulnar nerve.  Although in most cases an MRI scan is not necessary, it should be considered in individuals with atypical symptoms or in patients who are not responsive to conservative measures.

• Research suggests that ultrasonography also is useful for the diagnosis of ME. In a prospective, single-blind study, Park et al found that ultrasonographic findings were positive in 20 of 21 elbows with ME and were negative in 23 of 25 elbows without ME. According to the investigators, the sensitivity, specificity, accuracy, positive predictive value, and negative predictive value of ultrasonography in the diagnosis of clinical ME were, respectively, 95.2%, 92%, 93.5%, 90.9%, and 95.8%. They therefore recommended that ultrasonography be considered as an initial imaging modality in the evaluation of ME.

OTHER TESTS

• If ulnar nerve involvement is suggested, a nerve conduction study and electromyography should be performed.

TREATMENT

PHYSICAL THERAPY

The physician may recommend that the patient with ME receive physical or occupational therapy.

The discipline of therapy usually depends on the type of facility available, the accessibility of therapists, and physician preference.

The proper means of treatment for ME are discussed below, in the Occupational Therapy section.

OCCUPATIONAL THERAPY

Treatment begins with rest, ice, compression, and bracing, to decrease pain and inflammation.

One to 6 weeks of relative rest of the affected muscles and tendons is typically advised, until discomfort subsides.

Icing is employed for 5-10 minutes, 4-6 times per day and is particularly important if a patient presents after an acute event. Patients should be instructed to avoid icing over the ulnar nerve.

Compression with a medial counterforce brace (ie, a tennis elbow splint) with a pad placed anteromedially on the proximal forearm over the flexor-pronator mass is routine. Discontinue if symptoms of an ulnar neuropathy worsen.

In addition, if the symptoms are severe, brace with a wrist splint worn in the neutral position in order to rest the wrist flexors.

In milder cases, a counterbalance brace may be used alone instead of a rigid splint; this limits extremes of motion while allowing some movement for functional activities.

In the case of ulnar nerve involvement, a nighttime elbow extension splint should be considered. The splint is made in 30-45 º of elbow flexion. A daytime elbow pad also may be useful, by limiting additional trauma to the nerve.

After the patient's initial discomfort has subsided, a rehabilitation program with an occupational therapist should be initiated for muscle/tendon reconditioning.

Begin with gentle stretching and add gradual strengthening of the flexor-pronator muscles, as the patient tolerates. Follow this with functional activities and with patient education aimed at avoiding re-injury. 

The patient should be advised to perform very slow stretching exercises 10-15 times to warm up muscles and increase flexibility, before doing any strengthening exercises or functional activities.

Strengthening begins slowly with isometrics and progresses to eccentric exercises, with a gradual increase in resistance. Take care to cut back on exercises if they cause a recurrence of symptoms. Icing for 5-10 minutes after exercise is reasonable, especially if the patient reports pain in the affected area following exercise.

Concomitant modalities may include ultrasound, iontophoresis, phonophoresis, and transcutaneous electrical nerve stimulation, and low-energy, extracorporeal shock-wave therapy. Successful relief from symptoms is variable. Shock-wave therapy has been shown to be less effective for ME than it is for LE.

SURGICAL INTERVENTION

Epicondylar debridement is rarely indicated but has proven to be effective in cases in which conservative treatment has failed. In addition, the ulnar nerve may be decompressed surgically.

OTHER TREATMENT

If conservative measures fail, injection with local anesthetic and steroid to the point of maximal tenderness is appropriate.

Special care should be taken to avoid injection directly into the tendon or the ulnar nerve. If concern for dislocation of the ulnar nerve exists, the injection should be performed with the elbow extended or semiflexed.

The number of injections should be limited to 3 to decrease the risk of tendon atrophy or rupture. Short-term relief of discomfort with cortisone injection may be expected, but a complete rehabilitation program, as previously described, is a more effective and long-lasting way to treat ME.

MEDICATION

Nonsteroidal anti-inflammatory drugs (NSAIDs), taken orally, are the medicines of choice for ME to help control pain and any associated inflammation.

NSAIDs are used on average only for the first 7-10 days of the treatment period. For the patient, taking these medications with food may help to decrease the possible gastrointestinal side effects.

NONSTEROIDAL ANTI-INFLAMMATORY DRUGS

NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclo-oxygenase activity and prostaglandin synthesis.

Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions. 

IBUPROFEN (Motrin, Advil, Nuprin)

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

Adult: 400 mg PO q4-6h, 600 mg PO q6h, or 800 mg PO q8h; 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

(Consult pediatrician)

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

Pregnancy category D in third trimester of pregnancy; caution in congestive heart failure, hypertension, decreased renal and hepatic function, anticoagulation abnormalities, or during anticoagulant therapy 

NAPROXEN (Naprosyn, Aleve, Naprelan, Anaprox)

For the relief of mild to moderate pain; naproxen inhibits inflammatory reactions and pain by decreasing the activity of cyclo-oxygenase, which is responsible for prostaglandin synthesis

Adult: 500 mg PO bid; not to exceed 1.25 g/d

Pediatric:

<2 years: Not established

>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d (Consult pediatrician)

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

Pregnancy category D in third trimester of pregnancy; acute renal insufficiency; interstitial nephritis; hyperkalemia; hyponatremia and renal papillary necrosis may occur; patients with pre-existing renal disease or compromised renal perfusion, risk of 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 the drug 

ETODOLAC (Lodine, Lodine XL)

For relief of mild to moderate pain; etodolac inhibits inflammatory reactions and pain by decreasing the activity of cyclo-oxygenase, which is responsible for prostaglandin synthesis.

Adult: 200-400 mg PO q8h prn; not to exceed 1200 mg/d.