eMedicine Specialties > Sports Medicine > Lower Limb

Medial Gastrocnemius Strain: Treatment & Medication

Author: Anthony J Saglimbeni, MD, Staff Physician, Family Practice Residency, President, South Bay Sports and Preventive Medicine Associates; Private Practice; Team Internist, San Francisco Giants; Team Internist, West Valley College; Team Physician, Bellarmine College Prep; Team Physician, Presentation High School
Contributor Information and Disclosures

Updated: Aug 6, 2009

Treatment

Acute Phase

Rehabilitation Program

Physical Therapy

Initial treatment of a medial calf injury includes relative rest, ice, compression, elevation (RICE), and early weight bearing, as tolerated. The initial treatment should continue for 24-72 hours. Ice therapy is best instituted over a damp elastic wrap, which also provides compression. Preventing the limb from hanging dependently prevents further swelling. The use of crutches with a feathering gait and bilateral heel lifts is indicated if normal gait is compromised. Active foot and ankle ROM can be carried out if there is pain-free ROM.

Medical Issues/Complications

Pain management should include analgesics as indicated. Caution should be used with nonsteroidal anti-inflammatory drugs (NSAIDs) during the acute injury phase, as these agents can predispose the patient to increased bleeding and hematoma formation in the initial days after an injury. Theoretically, cyclooxygenase-2 (COX-2) inhibitors may provide pain control without the risk of bleeding in acute injuries, which is a concern with traditional NSAIDs.

Other Treatment

Ankle/foot bracing should be used to keep the ankle in a position of maximal tolerable dorsiflexion. Studies have shown an increased rate of healing with this intervention.

Recovery Phase

Rehabilitation Program

Physical Therapy

Ice therapy and active resistance dorsiflexion exercises can be undertaken until the athlete is pain free. Then, light plantar flexion exercises against resistance are initiated. Progression of therapy includes reduction in heel-lift height and gradual introduction of stationary cycling, leg presses, and heel raises. At this stage, ultrasonography, used with or without phonophoresis, and muscle stimulation are also applicable. Massage techniques can help with the removal of interstitial fluid. Apply compression dressing from the metatarsal heads to the gastrocnemius for the first 2 weeks. Partial weight-bearing ambulation should begin as soon as tolerable to maximize the contact of the sole of the foot to the ground, then progress to increased cyclic loading, advanced proprioception and balance training, and eventual full weight-bearing ambulation, with dynamic change of speed and direction as tolerable.

Maintenance Phase

Rehabilitation Program

Physical Therapy

Once the athlete is pain free with full and symmetric ROM and full strength is regained, sports-specific activities can be resumed. Strengthening and stretching of the injured area should continue for several months to overcome the increased risk for reinjury due to the deposition of scar tissue that is involved in the healing process.

Medication

Medications are directed at maintaining patient comfort in what can be a very painful injury of the medial head of the gastrocnemius. Clinicians must carefully consider pain therapy in the first 48 hours, as decreased platelet activity may result in increased bleeding and larger hematoma formation—with resultant effects on healing.

The simplest, yet least powerful of the recommended analgesics is acetaminophen. Typical doses of 1000-1300 mg, 3-4 times daily can be used as needed. This agent does not affect platelet function but may not greatly control pain.

To gain better pain control, more potent analgesics can be used, such as NSAIDs or an acetaminophen/narcotic combination. As referred to above (see Medical Issues/Complications in the Treatment, Acute Phase section), NSAIDs may enhance bleeding shortly after the injury has occurred. These agents are also likely to cause symptoms of gastrointestinal (GI) discomfort, and they can result in mucosal injury and even bleeding ulcers. On the other hand, opioid analgesic agents may cause GI side effects but not result in bleeding issues; these medications are generally better at pain control, but opioid analgesics have the possible complication of addiction or abuse.

Opioid medications come in various forms and various dosages. An alternative to the above medications is to use a newer NSAID from the COX-2 inhibitor class. The new COX-2 inhibitor drugs affect inflammation in a more specific manner by not affecting the prostaglandins that can cause the above side effects; these agents have also been shown to provide equianalgesia to the traditional NSAIDs.

Analgesics

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet (ie, decrease pulmonary secretions, open the airways), and have sedating properties, which are beneficial for patients who have sustained trauma or injuries.

Acetaminophen (Tylenol, Feverall)

DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants. No benefit as an anti-inflammatory agent. No effect on platelet function.

Acetaminophen with codeine 300/30 (Tylenol #3)

First-line agent for moderate to severe pain. Has no anti-inflammatory benefit. With the combination of a narcotic and acetaminophen, pain control is much better than acetaminophen alone.

Cyclooxygenase-2 (COX-2) inhibitors

COX-2 inhibitors promote control of moderate pain and anti-inflammatory effects, especially in patients who have sensitivity to the traditional NSAIDs. Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeding is clearly less with COX-2 inhibitors than with the traditional NSAIDs. Ongoing analysis of the cost avoidance of GI bleeding will further define the populations that will benefit from the use of COX-2 inhibitors.

Celecoxib (Celebrex)

Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme during pain and with inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus GI toxicity may be decreased. Seek the lowest dose of celecoxib for each patient.

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