Included in this category of platelet defects are those factors that are external to the platelet and that are nonimmune, such as drug-related platelet abnormalities, extrinsic platelet abnormalities, or as a sequel to an underlying disorder. Of all the drugs that affect platelet function, aspirin is the most popular. Ingestion of aspirin irreversibly inhibits cyclooxygenase (COX-1 inhibitors) by inhibiting the formation of prostaglandin synthesis. Both of these chemicals are necessary for the production of thromboxane A2, a potent platelet aggregator. Without the production of proper amount of thromboxane A2, platelet aggregation is impaired. This effect lasts for the entire life span of the platelet, 7 to 10 days, and patients on aspirin will show a prolonged bleeding time. Patients should be queried about their aspirin use or use of aspirin-containing products prior to any surgical event, elective or nonelective, to avoid any unexpected bleeding complications. The effect of aspirin on platelets is fairly rapid, occurring 45 minutes after ingestion.22 Additionally, aspirin as an antiplatelet agent is used as a preventive for patients susceptible to strokes, heart attacks, or other cardiovascular events. Other drugs such as NSAIDs and the class of COX-2 inhibitors such as naproxen and ibuprofen may affect platelet function. Certain antiplatelet agents such as ticlopidine and clopidogrel inhibit fibrinogen binding to GP IIb and IIIa. The plasma expander dextran also alters platelet function. The coating of platelets with dextran gives an antiplatelet effect by inhibiting the action of the platelet membrane and its surface receptors.
Platelet function may also be impaired by plasma conditions that are less than favorable to the platelet. In most cases, disorders in platelets are secondary to the main disorder but may not be present in the initial presentation. Conditions that may lead to disturbed platelet function include uremia due to renal disease and the paraproteinemias such as multiple myeloma and Waldenstrom's macroglobulinemia. The pathophysiol-ogy involved in the platelet defect in these acquired disorders is not clear-cut. Patients with renal disease are
known to exhibit purpura (Fig. 16.2), epistaxis, and hemorrhage at times. A few of the factors involved in platelet dysfunction in uremia include decreased thromboxane synthesis, decreased adhesion, decreased platelet release, and decreased aggregation. Most of these patients will undergo peritoneal or hemodialysis, which usually improves platelet function.
Multiple myeloma and Waldenstrom's macroglob-ulinemia represent a group of plasma cell disorders in which a normal immunoglobulin is produced in excess leading to hyperviscosity syndrome and a parapro-teinemia. Platelets circulating in abnormal amounts of protein are unable to fully participate in the activation of coagulation factors and in the fibrin formation. Patients will show a prolonged bleeding time and may show postoperative bleeding and ecchymoses. Table 16.5 displays a list of drugs that affect platelet function.
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