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.
Diagnosis & workup
Diagnostics & workup: - Order cell-free fetal DNA (cffDNA) from maternal blood to determine fetal Rh(D) status non-invasively - Order serial indirect Coombs with anti-D antibody titers monthly until 24 weeks, then every 2 weeks - Order MCA Doppler peak systolic velocity (PSV) every 1-2 weeks when titers reach critical threshold (≥1:16) - Interpret MCA PSV: >1.5 multiples of the median (MoM) indicates moderate-to-severe fetal anemia - Order amniocentesis for delta OD450 (Liley curve) if MCA Doppler is equivocal - Order percutaneous umbilical blood sampling (cordocentesis) to directly measure fetal hematocrit before intrauterine transfusion - Order serial fetal ultrasound for signs of hydrops: ascites, pleural effusion, skin edema, placentomegaly, polyhydramnios - Order cord blood at delivery: type, Rh, direct Coombs, bilirubin, hemoglobin, reticulocyte count