Hemolytic Disease of the Newborn
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A hemolytic anemia in newborns due to the destruction of fetal and newborn RBCs by maternal antibodies passively transferred across the placenta; primarily related to ABO blood group or RhD incompatibility
- ABO incompatibility
- Occurs in 12% of first pregnancies
- Only 10–20% become significantly jaundiced, requiring phototherapy.
- Rh incompatibility
- Incidence of Rh hemolytic disease: 6–7/1,000 live births
- Prevalence of RhD positive (RhD+) fetus in RhD negative (Rh−) mother: 15%
- RhD(−) status in 15% of white, 7–8% of black and Hispanic, and 2% of Asian persons
- 48–55% are heterozygous (Dd)
- 35–45% are homozygous (DD)
- Of all Rh-sensitized pregnancies:
- 9% require intrauterine transfusion.
- 10% are delivered early and require newborn exchange transfusion.
- 31% require treatment after a full-term delivery.
- 50% require no treatment.
- Type O mother pregnant with either type A, B, or AB fetus
- RhD(−) mother becomes pregnant with an RhD(+) fetus; D-antigen is inherited from the father.
- Omitted or failed RhIG (anti-D) prophylaxis
- Only a fraction of women at risk develop antibodies.
- Rh incompatibility: RhIG is given to an RhD(−) woman after any exposure to RhD(+) blood.
- RhIG is also known by trade names RhoGAM and HyperRHO.
- Given at 28 weeks, 34 weeks (prophylaxis), and within 72 hours of birth, or following, for example, amniocentesis, abortion, antepartum bleeds
- No prophylaxis for HDN caused by other blood group incompatibilities.
- Isoimmunization—general principles:
- Passage of fetal RBCs into maternal circulation occurs as a result of asymptomatic transplacental hemorrhage.
- Initial sensitization of mother from fetomaternal hemorrhage can occur with placental abruption, abortion, ectopic pregnancy, or procedures (CVS, amniocentesis, or cordocentesis).
- Exposure triggers maternal immune response (anti-D antibodies).
- Maternal IgG antibodies (Ab) cross the placenta and bind to fetal RBCs. Coated RBCs are then destroyed in the reticuloendothelial system, primarily the spleen.
- Isoimmunization may lead to hyperbilirubinemia, severe anemia, and potentially hydrops.
- Extramedullary hematopoiesis in the fetal liver and spleen is a response to severe fetal anemia, leading to hepatosplenomegaly.
- ABO isoimmunization
- Occurs in type O mothers with a type A or B fetus; clinically a milder hemolysis compared to Rh incompatibility and rarely requires intervention
- 1% of type O mothers have high titers of IgG Ab against both A and B that cross the placenta and cause HDN.
- Hemolysis due to anti-A is more common.
- Hemolysis due to anti-B can be more severe and may require exchange transfusion in the newborn.
- Rh isoimmunization
- Passage of RhD(+) fetal RBCs which cross the placenta into the circulation of an Rh(−) mother
- RhD(−) state is the absence of D antigens on RBCs.
- Decreased risk of RhD sensitization of mother if fetus is also ABO incompatible
- Rh isoimmunization rarely occurs in first pregnancy.
- Fetomaternal hemorrhage, usually asymptomatic, with maternal immune response to foreign fetal RBC antigens
- Most common systems involved: ABO blood group antigens, with mild HDN, and RhD antigens, with more severe HDN
- 1% of cases involve other RBC antigens, such as Kell, Kidd, Duffy, or MNS blood groups.