Medial Gastrocnemius Strain Medication

Updated: May 22, 2023
  • Author: Anthony J Saglimbeni, MD; Chief Editor: Sherwin SW Ho, MD  more...
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Medication Summary

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 newer 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.



Class Summary

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

Class Summary

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.



Class Summary

Nonsteroidal anti-inflammatory agents (NSAIDs) inhibit prostaglandin synthesis resulting in decreased inflammation and pain.

Naproxen (Aleve, Anaprox, Naprosyn)

Naproxen is used for relief of mild to moderate pain; it inhibits inflammatory reactions and pain by decreasing activity of cyclo-oxygenase, which results in a decrease of prostaglandin synthesis.

Indomethacin (Indocin)

Indomethacin inhibits the synthesis of prostaglandins in body tissues by inhibiting at least 2 cyclooxygenase isoenzymes, cyclooxygenase-1 (COX-1) and -2 (COX-2). It may inhibit chemotaxis, may alter lymphocyte activity, may decrease proinflammatory cytokine activity, and may inhibit neutrophil aggregation. These effects may contribute to its anti-inflammatory activity.