Chapter 24: Alterations of Hematologic Function in Children

Anemia represents the most prevalent pediatric blood disorder and develops through either decreased erythrocyte production or accelerated destruction; iron deficiency anemia constitutes the leading nutritional deficiency globally and disproportionately impacts infants, toddlers, and adolescents through mechanisms including inadequate dietary intake, intestinal malabsorption, occult hemorrhage, and parasitic infection, with untreated disease resulting in impaired physical growth, cognitive dysfunction, and behavioral disturbance. Hemolytic disease of the fetus and newborn arises from maternal-fetal blood group incompatibility when maternal immunoglobulin G antibodies traverse the placental barrier and lyse fetal erythrocytes, precipitating severe anemia, unconjugated hyperbilirubinemia, bilirubin encephalopathy, generalized edema, and fetal death in severe presentations; widespread use of Rh immune globulin has substantially diminished the incidence of rhesus-mediated disease. Inherited hemoglobinopathies including sickle cell disease and thalassemias cause chronic hemolysis and tissue damage through abnormal hemoglobin structure or deficient globin chain synthesis, respectively, requiring multimodal therapeutic approaches encompassing pharmacologic agents, transfusion protocols, iron chelation, and potentially curative stem cell transplantation. Coagulation disorders such as hemophilias A, B, and C result from inherited deficiencies of specific clotting factors and predispose to spontaneous hemorrhage and joint degeneration, while immune thrombocytopenia represents the most common acquired platelet disorder in pediatric populations and typically emerges following viral infection. Hematologic malignancies, predominantly acute lymphoblastic leukemia and acute myeloid leukemia, constitute the most frequent childhood cancers and present with pancytopenia-related symptoms, lymphadenopathy, and potential central nervous system involvement; pediatric lymphomas including Burkitt, lymphoblastic, and Hodgkin variants require intensive chemotherapy and may incorporate targeted biologic agents to optimize survival while minimizing treatment-related toxicity.