A b s t r a c tThe use ofRh immune globulin (RhIG) The binding of maternal anti-D to the fetal RBCs often leads to extravascular hemolysis that ranges from minimal to extreme and this, in part, determines the severity of HDN. At its worst, the anemia leads to fetal hepatosplenomegaly, hydrops fetalis, heart failure, and death in utero or soon after birth.2 Infants who survive are at risk for the development of kernicterus and resultant neuronal damage.There is a dose-dependent relationship between the volume of Rh-positive RBCs to which the Rh-negative person is exposed and the incidence of Rh immunization, with volumes as small as 0.1 mL resulting in antibody formation.3 Consequently, the degree of fetomatemal hemorrhage (FMH) is an important consideration in the maternal development of anti-D. During a normal first-trimester pregnancy, approximately 3% of women have detectable fetal RBCs in their circulation, although, typically, this is less than 0.1 mL. 4 As pregnancy progresses, the frequency and volume of fetal RBCs in the maternal circulation increases, with 12% of women in the second trimester and 45% of women in the third trimester having detectable fetal RBCs in their circulation. 4 At the time of delivery, up to 50% of women delivering an ABO-compatible infant will have demonstrable circulating fetal RBCs. 5 Therefore, the major immunizing event for Rh-negative women occurs late in pregnancy and primarily at the time of delivery when