ABO incompatibilities are present in ~20% of all pregnancies, however only 5-10% of newborns are symptomatic. The highest risk is with type O mothers and type A or B newborns.
The highest risk for ABO incompatibility involves blood type O mothers and blood type A or B newborns.
The presence of pre-existing maternal antibodies (anti-A or anti-B IgG) are able to cross the placenta and can result in hemolysis in the fetus. As these pre-existing antibodies are present even if sensitization has not occurred, hemolysis can commence even during the first pregnancy.
Neonatal hemolytic anemia can occur due to the hemolysis of RBCs in the fetus. The anti-A or anti-B antibodies from the mother may cross the placenta and start binding to fetal RBCs, tagging them for lysis. Overall though, ABO incompatibility usually has a significantly milder course of disease compared to Rh incompatibility.
ABO hemolytic disease often presents asymptomatically, but if the number of lysed RBCs is significant, findings like anemia, hyperbilirubinemia, and jaundice may occur.
Mild neonatal jaundice can present at birth or within 24 hours after birth.
If there are signs of hemolysis postnatally, a Coombs test can be conducted. ABO incompatibilities will have a mostly negative or weakly positive Coombs test because macrophages will phagocytose most antibody-bound RBCs so very little agglutination occurs.
Postnatal treatment includes phototherapy and, if necessary, transfusion with RBCs can be used to address hyperbilirubinemia. Additionally, iron supplementation can ameliorate the symptoms of neonatal hemolytic anemia.
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