Pathophysiology
Clinical meaning
Rh alloimmunization triggers a Type II hypersensitivity reaction in which maternal IgG anti-D antibodies cross the placenta and opsonize fetal Rh-positive erythrocytes. These opsonized cells are destroyed by Fc receptor-bearing macrophages in the fetal spleen and liver (extravascular hemolysis). Fetal anemia triggers compensatory extramedullary hematopoiesis in the liver and spleen (hepatosplenomegaly), while hyperbilirubinemia from hemolysis causes unconjugated bilirubin accumulation. In utero, unconjugated bilirubin is cleared by the placenta; after birth, it rapidly rises, potentially causing kernicterus (bilirubin encephalopathy). Severe anemia leads to high-output cardiac failure, hypoalbuminemia from impaired hepatic protein synthesis, and hydrops fetalis (effusions, ascites, generalized edema). The clinician must manage the alloimmunized pregnancy with serial antibody titers, MCA Doppler surveillance, coordinate intrauterine transfusion when indicated, and manage neonatal hemolytic disease with phototherapy, IVIG, and possible exchange transfusion.