Medication Summary
The standard choice for medication is nonsteroidal anti-inflammatory drugs (NSAIDs). These medications not only provide analgesia but also can decrease some of the mediators of inflammation. When to administer NSAIDs to achieve the most beneficial effect is debated. One argument is to administer them immediately following injury to avoid side effects that may interfere with muscle remodeling and repair. The other argument is to delay use until 2-4 days after the injury, so they do not interfere with the chemotaxis required for the laying down of new muscle fibers. No consensus has been reached on which approach to timing yields the best outcome.
Nonsteroidal anti-inflammatory drugs
Class Summary
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.
Naproxen (Anaprox, Naprelan, Naprosyn)
Available in both a regular and delayed-release form.
Ibuprofen (Motrin, Ibuprin)
DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
Ketoprofen (Orudis, Actron)
For relief of mild to moderate pain and inflammation. Small doses initially are indicated in small and elderly patients and in those with renal or liver disease. Doses over 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patient for response.
COX-2 inhibitors
Class Summary
Cyclooxygenase 2 (COX-2) inhibitors have a lower incidence of GI bleeding as compared with other NSAIDs, although there is still a risk involved. They should be considered for use in patients with a history of GI bleed or those who have a high risk for a bleed.
Celecoxib (Celebrex)
Primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme, 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 incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, may be decreased when compared to nonselective NSAIDs. Seek lowest dose for each patient.
Neutralizes circulating myelin antibodies through anti-idiotypic antibodies; down-regulates pro-inflammatory 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; may increase CSF IgG (10%).
Has a sulfonamide chain and is primarily dependent upon cytochrome P450 enzymes (a hepatic enzyme) for metabolism.
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Normal sagittal alignment permits the knee to lock in full extension, aided by powerful quadriceps and an intact extensor mechanism. The ground reaction force passes anterior to the "center of rotation" of the knee, while the posterior cruciate ligament, posterior capsule, hamstrings, and gastrocnemius provide a tension band effect.
