Impairment of platelet function is well recognized in the neonate. The abnormalities include a reduction in platelet factor 3 activity and availability, a reduction in the release of nonmetabolic storage pool ADP and ATP, and platelet factor 4 following stimulation, decreased adhesiveness, and impaired aggregation with ADP, epinephrine, collagen, and thrombin. Whether the cause of the platelet abnormality and the impairment in platelet secretion is due to a “storage pool deficiency” or an “aspirin-like defect” has been unclear. However, recent data suggests that the neonatal platelet possesses neither a significant deficiency in prostaglandin synthesis nor a significant decrease in storage pool adenine nucleotides. The abnormalities noted appear most likely to be due to a membrane-related phenomenon.