Platelet function can be abnormally increased, as in association with acute vascular events, or defective, as in a variety of clinical settings. Acquired platelet dysfunction may occur at any age and range in severity from mild to life-threatening haemorrhages. Diagnostic work-up of platelet disorders requires meticulous evaluation of medical history, specifically of any drugs interfering with platelet function, careful clinical examination and a staged laboratory protocol to assess the underlying platelet defect(s). To identify hyperactive platelets ex vivo, costly procedures may be required using flow cytometry and distict
epitope-specific
monoclonal antibodies. Currently, this approach can be recommended for research purposes only. Drugs represent the most common cause of platelet dysfunction in our overmedicated society. While
aspirin, clopigogrel (more recently also
prasugrel) and
integrin αIIbβ3 (GPIIb-IIIa) receptor antagonists (
abciximab,
eptifibatide and
tirofiban) are well-known prototypes of
antiplatelet drugs, other widely used agents (e.g. nonsteroidal anti-inflammatory drugs,
antibiotics,
serotonin reuptake inhibitors and volume expanders) can also impair platelet function and thus cause or aggravate
hemorrhages. Identification of individual patients with pre-existing
hemostatic defects remains crucial (i) to prevent
bleeding complications, (ii) to manage symptoms adequately, (iii) to minimize the risk from invasive procedures, and (iv) to avoid unnecassary exposure to blood products. Screening for platelet dysfunction can be performed by point-of-care testing followed by platelet aggregometry in response to various agonists. While mild
bleeding episodes due to antiplatelet
therapy can be managed by withdrawal of the drug(s), severe
hemorrhages may require immediate
platelet transfusions. Apart from that, the prohemostatic armamentarium is limited to
desmopressin,
antifibrinolytic agents, and
recombinant factor VIIa.