Analgesic Agents
Class Summary
Pain control is essential to quality patient care. Analgesics ensure patient comfort and have sedating properties, which are beneficial for patients who have sustained trauma or injuries.
Acetaminophen (Tylenol, FeverAll, Aspirin Free Anacin)
Acetaminophen is the drug of choice for pain in patients with documented hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants.
Nonsteroidal Anti-Inflammatory Drugs
Class Summary
NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action may include inhibition of cyclooxygenase 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 (Naprosyn, Aleve, Naprelan, Anaprox)
Naproxen is indicated for relief of mild to moderate pain. This agent inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.
Ketorolac
Ketorolac is an intravenously administered NSAID and a very powerful analgesic. It inhibits prostaglandin synthesis by decreasing activity of the enzyme cyclooxygenase, which results in decreased formation of prostaglandin precursors. In turn, this results in reduced inflammation.
Aspirin (Anacin, Ascriptin, Bayer Aspirin)
Aspirin treats mild to moderate pain. It inhibits prostaglandin synthesis, which prevents formation of platelet-aggregating thromboxane A2.
Ibuprofen (Advil, Motrin)
Ibuprofen is usually the drug of choice for treatment of mild to moderate pain, if no contraindications exist. It inhibits inflammatory reactions and pain by decreasing the activity of the enzyme cyclo-oxygenase, resulting in inhibition of prostaglandin synthesis.
Celecoxib (Celebrex)
Unlike nonselective NSAIDs, which inhibit both cyclooxygenase-1 (COX-1) and COX-2, celecoxib primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme that is induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations celecoxib does not inhibit COX-1; thus GI toxicity may be decreased.
Although the higher cost of celecoxib can be a drawback, the incidence of costly and potentially fatal GI bleeds is clearly less with this agent than it is 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. Seek the lowest dose of celecoxib for each patient.
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An illustration that depicts measurement of compartment pressures in the forearm.
