Only a few blood group antigens pose no fetal risk. Lewis antibodies-Lea and Leb, as well as I antibodies, are cold agglutinins. They are predominantly IgVl and are not expressed on fetal red cells (American College of Obstetricians and Gynecologists, 2016). Another antibody that does not cause fetal hemolysis is Duy group B-Fl.
Kell Alloimmunization. Approximately 90 percent of nonHispanic white Americans and up to 98 percent of African Americans are Kell negative. Kell type is not routinely determined. Transfusion history is important, as nearly 90 percent of Kell sensitization cases result from transfusion with Kellpositive blood. .
Kell sensitization may develop more rapidly and may be more severe than with sensitization to D and other blood group antigens. his is because Kell antibodies attach to erythrocyte precursors in the fetal bone marrow, thereby impairing the normal hemopoietic response to anemia. With fewer erythrocytes produced, there is less hemolysis, and severe anemia may not be predicted by the maternal Kell antibody titer. One option is to use a lower critical titer-l:8-for Kell sensitization (Moise, 2012). he American College of Obstetricians and Gynecologists (2016) has recommended that antibody titers not be used to monitor Kell-sensitized pregnancies.
Incompatibility for the major blood group antigens A and B is the most common cause of hemolytic disease in newborns, but it does not cause appreciable hemolysis in the fetus. Approxi mately 20 percent of newborns have ABO blood group incom patibility, yet only 5 percent are afected clinically. And in such cases, the resulting anemia is typically mild.
The condition difers from CDE incompatibility in several respects. First, ABO incompatibility is often seen in firstborn neonates, whereas sensitization to other blood group antigens is not. This is because most group 0 women have developed antiA and anti-B isoagglutinins before pregnancy from exposure to bacteria displaying similar antigens. Second, ABO alloimmunization rarely becomes more severe in successive pregnancies. Last, ABO incompatibility is considered a pediatric diseaserarely of obstetrical concern. his is because most anti-A and anti-B antibodies are IgM and do not cross the placenta. Fetal red cells also have fewer A and B antigenic sites than adult cells and are thus less immunogenic.
Consequently, fetal surveillance and early delivery are not indicated in pregnancies with prior ABO incompatibility. Careful neonatal observation is essential, however, because hyperbilirubinemia may require treatment with phototherapy or occasionally transfusion (Chap. 33, p. 626).
• Management of the Alloimmunized
An estimated 25 to 30 percent of fetuses from D-alloimmunized pregnancies will have mild-to-moderate hemolytic anemia. And without treatment, up to 25 percent will develop hydrops (Tannirandorn, 1990). If alloimmunization is detected and the titer is below the critical value, the titer is generally repeated every 4 weeks for the duration of the pregnancy (American College of Obstetricians and Gynecologists, 2016). Importantly, if a prior pregnancy was complicated by alloimmunization, serial titer assessment is not indicated, and the pregnancy is assumed to be at risk regardless of titer. Management of such pregnancies is discussed subsequently. In any pregnancy in which an antibody titer has reached a critical value, there is no beneit to repeating it. The pregnancy is at risk even if the titer drops, and further evaluation is still required.