Acquired Platelet Dysfunction
(See also Overview of Platelet Disorders.)
Acquired abnormalities of platelet function are very common. Causes include
Acquired platelet dysfunction is suspected and diagnosed when unusual or prolonged bleeding is observed and other possible diagnoses (eg, thrombocytopenia, coagulation abnormalities) have been eliminated. Platelet aggregation studies are unnecessary.
Drugs
Aspirin, other NSAIDs, inhibitors of the platelet P2Y12 adenosine diphosphate (ADP) receptor (eg, clopidogrel, prasugrel, ticagrelor), and glycoprotein IIb/IIIa receptor inhibitors (eg, abciximab, eptifibatide, tirofiban) may induce platelet dysfunction. Sometimes this effect is incidental (eg, when the drugs are used to relieve pain and inflammation) and sometimes therapeutic (eg, when aspirin or the P2Y12 inhibitors are used for prevention of stroke or coronary thrombosis).
Aspirin and NSAIDs prevent cyclooxygenase-mediated production of thromboxane A2. This effect can last 5 to 7 days. Aspirin modestly increases bleeding in healthy people but may markedly increase bleeding in older patients and those with underlying platelet dysfunction or a severe coagulation disturbance (eg, patients receiving heparin, patients with severe hemophilia). Clopidogrel, prasugrel, and ticagrelor all can markedly reduce platelet function and increase bleeding.
A number of other drugs can also cause platelet dysfunction (1).
Systemic disorders
Many disorders (eg, myeloproliferative neoplasms, myelodysplastic disorders, uremia, macroglobulinemia, multiple myeloma, cirrhosis, systemic lupus erythematosus) can impair platelet function.
Uremia prolongs bleeding via unknown mechanisms. If bleeding is observed clinically in uremic patients, bleeding may be reduced with vigorous dialysis, cryoprecipitate administration, or desmopressin infusion. If necessary, increasing the hemoglobin concentration to > 10 g/dL by transfusion or by giving erythropoietin also reduces bleeding.
Cardiopulmonary bypass
As blood circulates through a pump oxygenator during cardiopulmonary bypass, platelets may become dysfunctional, prolonging bleeding. The mechanism appears to be activation of fibrinolysis on the platelet surface with resultant loss of the glycoprotein Ib/IX binding site for von Willebrand factor. Regardless of platelet count, patients who bleed excessively after cardiopulmonary bypass are often transfused with platelets. Giving an antifibrinolytic agent during bypass may preserve platelet function and reduce the need for transfusion.
General reference
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Scharf RE: Drugs that affect platelet function. Semin Thromb Hemost 38(8): 865–883, 2012. doi: 10.1055/s-0032-1328881 Epub 2012 Oct 30.
