The evaluation and management of platelet refractoriness and alloimmunization

Abstract

T HE ARREST of hemorrhage associated with an increase in the patient's platelet count after blood transfusion was first reported by Duke in 1910.' It was not until the 1960s that clinical studies showed that therapeutic platelet transfusions decreased fatal hemorrhagic complications in thrombocytopenic patients2 and that prophylactic platelet transfusions reduced episodes of bleeding.3 More recent reports have suggested that a threshold of I O,OOO/~ for prophylactic platelet transfusion is equivalent to 20,OOO/~ in the absence of additional complicating clinical factors such as platelet dysfunction, associated coagulopathy, or primary defects of vascular integrity.4.5 The hemostatic benefit of platelet transfusion is presumably mediated through an increase in the posttransfusion platelet count above a target level, and clai!s that platelet transfusion may be beneficial even in the absence of such an increase are not commonly accepted.