INTRODUCTION

Platelets play a vital role in the maintenance of normal hemostatic activity. Accordingly, for patients with low platelet counts (thrombocytopenia) or impaired platelet function, platelet transfusion can be of significant value in preventing and treating hemorrhage. (See "Overview of hemostasis".)

Although many patients respond appropriately when transfused with platelets, less than adequate results tend to be the rule rather than the exception [1], leading to an increased risk of morbidity and mortality [2]. Published reports have cited an incidence of refractoriness to platelet transfusion of 15 to 25 percent in the hematology/oncology patient population utilizing leukocyte-reduced blood products and even higher rates during the pre-leukocyte-reduction era [3-6]. (See "Clinical and laboratory aspects of platelet transfusion therapy".)

The numerous factors associated with poor recovery and survival of transfused platelets, and the diagnosis, management, and prevention of alloimmune refractoriness to platelet transfusion will be reviewed here. General issues related to platelet transfusion are discussed separately. (See "Clinical and laboratory aspects of platelet transfusion therapy".)

ETIOLOGY

Refractoriness to platelet transfusion can be separated into non-immune and immune causes (table 1).

• Approximately two-thirds of refractory episodes are due to non-immune causes, such as sepsis, fever, bleeding, splenomegaly, disseminated intravascular coagulation (DIC), hepatic sinusoidal obstruction syndrome (hepatic veno-occlusive disease), graft-versus-host disease (GVHD) and medications [3,7].
• Twenty percent of cases have a combination of both immune and non-immune causes.
• Immune causes account for the remaining minority of cases and include alloimmunization to HLA and/or platelet-specific antigens.