Abstract

ABSTRACT: The bleeding time is prolonged in anemic patients independent of their platelet count and is shortened by elevating the hematocrit. It is theorized that an increase in circulating red blood cells increases platelet radial movement and interaction with endothelium. Platelet dysfunction in uremia is well known but poorly understood. Anemia is one contributory factor; others may involve storage pool deficiency, increased vessel wall prostaglandin production, and abnormal platelet arachidonic acid metabolism. Ameliorating anemia with red blood cell transfusions has been shown to shorten the bleeding time without affecting other platelet function values. Recently, recombinant human erythropoietin has been shown to shorten the bleeding time, with a parallel rise in hematocrit level to 30%. Clinicians should be aware that a diminished hematocrit may contribute to the bleeding tendency already present in patients with thrombocytopenia.