Hemolytic disease of the newborn

Syndrome/definition/pathophysiology/epidemiology Hemolytic disease of the newborn (HDN) is also known as erythroblastosis fetalis, isoimmunization, or blood group incompatibility HDN occurs when fetal red blood cells (RBCs), which possess an antigen that the mother lacks, cross the placenta into the maternal circulation, where they stimulate antibody production. The antibodies return to the fetal circulation and result in RBC destruction Rhesus positive (+) denotes presence of the D antigen. The number of antigenic sites on RBCs varies with the genotype, and the prevalence of the genotype varies with the population. In the USA, Rhesus-negative (d/d) individuals comprise 15% of Whites, 5.5% of African Americans, and <1% of Asians. A sensitized Rhesus-negative mother produces anti-Rh IgG antibodies which cross the placenta. Risk factors for antibody production include prior miscarriage or abortion, second (or later) pregnancies, maternal toxemia, paternal zygosity (D/D rather than D/d), and amount of antigen load With maternal blood types A and B, isoimmunization does not occur because the naturally occurring antibodies (anti-A and -B) are IgM, not IgG. In type-O mothers, the antibodies are predominantly IgG, cross the placenta, and can cause hemolysis in the fetus. The association of a type-A or B fetus with a type-O mother occurs in ~15% of pregnancies. However, HDN occurs in only 3%, is severe in only 1%, and <1:1000 require exchange transfusion. Unlike Rh, ABO disease can occur in first pregnancies, because anti-A and anti-B antibodies are found early in life from exposure to A- or B-like antigens present in many foods and bacteria