Increased platelet destruction in infancy and childhood.

The number of platelets in the peripheral blood of healthy children, full-term, and premature infants falls into the same range as that of adults. Thrombocytopenia, defined as a platelet count of less than 150,000/mm(<150 × 10/L), may be due to decreased production, splenic sequestration, or increased platelet destruction. The following is a review of disorders involving the last mechanism, all of which have the common feature of reduced autologous platelet survival. Excluded from current considerations are inherited disorders in which the survival of allogenic platelets is normal and bleeding is mainly due to diminished platelet production, e.g., Wiskott-Aldrich syndrome, or a defect in platelet function, e.g., Bernard-Soulier syndrome. Destructive thrombocytopenias may be classified on the basis of pathogenesis: these are either immune mediated, nonimmune mediated, or a combination of both. The immune thrombocytopenias may be further divided into disorders of primary type in which there are no identifiable underlying disease processes (e.g., childhood idiopathic thrombocytopenia and neonatal immune thrombocytopenias) and disorders of secondary type in which the thrombocytopenia is associated with an identifiable insult (e.g., secondary autoimmune disorders and drugs). The nonimmune thrombocytopenias include a large group of disorders in which the increased platelet destruction is either surface mediated, e.g., hemolytic-uremic syndrome (HUS), thrombin mediated, e.g., disseminated intravascular coagulation and giant hemangioma, or caused by multiple factors, e.g., necrotizing enterocolitis, hemolytic anemia, exchange transfusion, phototherapy, intrauterine growth retardation, congenital polycythemia, hypoxia, and deficiency of plasma