INTRODUCTION

A qualitative abnormality of platelet function should be considered in patients with mucocutaneous bleeding and normal platelet counts. An investigation for an acquired platelet disorder should commence when there is no family history – defined as no known bleeding disorder among first-degree relatives – and no laboratory evidence for von Willebrand disease (VWD). In contrast to congenital platelet disorders, which are rare, acquired disorders of platelet function are encountered commonly in hematology practice. Their clinical significance is defined almost exclusively by the patient encounter and, particularly in the intensive or coronary care unit setting, the impact of platelet dysfunction on clinical bleeding or bleeding risk is difficult to extricate from the complex coagulopathies that sometimes arise in the setting of multiorgan failure, sepsis, and treatment of acute coronary syndromes with several antithrombotic drugs.

A variety of medications and systemic diseases have been implicated in the pathophysiology of platelet dysfunction. Antiplatelet drugs are the most common cause, but uremia, hepatic cirrhosis, myeloma, myelo-proliferative disorders, and cardiopulmonary bypass have long been recognized as clinical situations in which platelet dysfunction contributes to bleeding. Such recognition is the first step needed to correct the hemostatic defect, as it then directs an effective treatment–such as platelet transfusion, hemodialysis, or administration of a nonspecific hemostatic drug.