Use Of Aspirin And Nonsteroidal Antiinflammatory Drugs

Table 211:3, depicts many of the commonly used drugs that can affect platelet function. Of these, the most commonly used are aspirin and the NSAIDs, which will be discussed in more detail.

Aspirin inhibits platelet function by acetylating and irreversibly inactivating platelet cyclooxygenase. Normally, platelet cyclooxygenase allows the formation of endoperoxides and thromboxanes, which stimulate platelet aggregation. This effect can be seen with as little as 80 mg aspirin per day and can continue for as long as 7 to 10 days after the aspirin is stopped, until the affected platelets are replaced by new platelets. The clinical significance of aspirin ingestion and bleeding is usually minimal except in some surgeries, cardiothoracic, plastic, and neurosurgery, where small amounts of blood loss are crucial, and in patients with underlying bleeding disorders (congenital or acquired) such as von Willebrand's disease, hemophilia, liver disease, uremia, or heavy ethanol ingestion. Chronic aspirin ingestion can lead to gastrointestinal blood loss; however, this is primarily from the direct effect of aspirin on the gastric mucosa. Platelet transfusion is the only acute treatment to overcome the platelet dysfunction induced by aspirin but this is rarely required.

The NSAIDs such as ibuprofen, indomethacin, and naproxen reversibly inhibit platelet cyclooxygenase. Inhibition of platelet cyclooxygenase occurs only as long as there is active drug in the circulation. The transient defect in platelet aggregation usually lasts less than 24 h. An exception is the drug piroxicam, which has a 2-day half-life; the resultant platelet dysfunction may be present for days. NSAIDs can be safely used in patients with hemophilia.

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