Carpal Tunnel Syndrome Medication
- Author: Nigel L Ashworth, MBChB, MSc, FRCPC; Chief Editor: Robert H Meier, III, MD more...
Short (1-2 wk) courses of regular NSAIDs can be of benefit if there is any suggestion of inflammation in the wrist region (eg, flexor tenosynovitis, rheumatoid arthritis). Likewise, if edema is thought to be prominent, then a short course of a mild diuretic may be of benefit.
Nonsteroidal anti-inflammatory drugs
NSAIDs provide pain relief and reduction of inflammation. Reducing inflammation in the structures passing through the carpal tunnel decreases pressure and provides some relief to the compressed nerve.
Naproxen is used for the relief of mild to moderate pain; it inhibits inflammatory reactions and pain by decreasing the activity of cyclo-oxygenase, which is responsible for prostaglandin synthesis.
Diclofenac is one of a series of phenylacetic acids that has demonstrated anti-inflammatory and analgesic properties in pharmacologic studies. It is believed to inhibit the enzyme cyclo-oxygenase, which is essential to the biosynthesis of prostaglandins. Diclofenac can cause hepatotoxicity; hence, liver enzymes should be monitored in the first eight weeks of treatment.
Diclofenac is rapidly absorbed; metabolism occurs in the liver by demethylation, deacetylation, and glucuronide conjugation. The delayed-release, enteric-coated form is diclofenac sodium; the immediate-release form is diclofenac potassium. Diclofenac has relatively low risk for bleeding GI ulcers.
Ibuprofen is the drug of choice (DOC) for patients with mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis. Ibuprofen inhibits cyclo-oxygenase-1 (COX-1) and COX-2 enzymes. This in turn results in decreased formation of prostaglandin precursors.
Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation; inhibits prostaglandin synthesis.
Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeds is clearly less with COX-2 inhibitors than with traditional NSAIDs. Ongoing analysis of cost avoidance of GI bleeds will further define the populations that will find COX-2 inhibitors the most beneficial.
Inhibits primarily COX-2. Considered an inducible isoenzyme, COX-2 is induced during pain and 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 lowest dose of celecoxib for each patient.
Conditions that cause edema may increase pressure in the carpal tunnel. Diuretics may be beneficial in reducing edema.
Inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water, as well as potassium and hydrogen ions.
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