ABO incompatibility is the single, most common form of isoimmune hemolytic anemia in the Western world, occurring in 12% to 15% of all pregnancies (Roberts, 2008). The condition occurs when the maternal blood type differs from the fetal blood type. Most commonly, the condition arises in a blood type O mother who carries a blood type A or B fetus, although it can present in a blood type A or B mother who carries a fetus of a different blood type. In 3% to 4% of these pregnancies, maternal red blood cells (RBCs) cross the placenta and interact with fetal cells triggering complications, including anemia and hyperbilirubinemia (Basu, Kaur, & Kaur, 2011).
ABO incompatibility is one of the hemolytic anemias. Because of the antenatal administration of RhoGAM (anti-D gamma globulin), Rh isoimmunization decreases, leading to ABO incompatibility, one of the most common causes of hemolytic disease.
Blood types are assigned to correspond to the surface antigen on the RBC. Type A blood carries A-antigens on the surface of the RBC along with anti-B antibodies. Type B blood carries B-antigens on the surface along with anti-A antibodies. Type AB blood carries both A- and B-antigens on the surface, but neither anti-A nor anti-B antibodies. Finally, type O blood carries neither A- nor B-antigens, but both anti-A and anti-B antibodies. Each blood type recognizes cells from the same type when they encounter corresponding antigens that match their own. Conversely, antibodies mobilize, clump, and hemolyze blood cells that carry antigens different from their own.
The reason why type O blood is the universal donor is that it carries no antigens to trigger hemolysis and rejection. The mother with type O blood has no antigens on the surface of her RBCs and so the fetus with a dissimilar blood type will not hemolyze maternal cells. However, her blood does carry anti-A and anti-B antibodies. When O negative cells of the mother cross into fetal circulation, the anti-A and anti-B antibodies they carry attack and hemolyze fetal cells, which lowers the RBC count and elevates the levels of waste products, including bilirubin. This is the mechanism by which ABO incompatibility leads to anemia and hyperbilirubinemia.
Actual, symptomatic hemolytic disease (HD) occurs in less than 1% of infants affected by ABO incompatibility. The primary symptom is hyperbilirubinemia 114and the presentation is generally mild, particularly if the Coombs direct antibody test (DAT) is negative.
Bilirubin causes jaundice, which is easily visible to the eye. However, visualization is an unreliable indicator of the severity of the disease or the risk. For this reason, routine screening is important, especially for infants with deeply pigmented skin (American Academy of Pediatrics Subcommittee on Hyperbilirubinemia, 2004).
Infants with ABO incompatibility should be closely monitored and their bilirubin levels plotted to determine their level of risk for hyperbilirubinemia. Diagnosis of ABO incompatibility can be quickly established shortly after birth. A blood type and DAT should be determined for all infants born to mothers with blood type O. Infants found to have a blood type of A or B, who also have a positive DAT, have a confirmed diagnosis of ABO incompatibility. However, a positive test does not indicate that severe hyperbilirubinemia will develop. It is important and necessary to evaluate the risk of HD. Serial bilirubin levels, a complete blood count (CBC), reticulocyte count, and a history of a sibling who was treated for significant hyperbilirubinemia are all predictors of HD (Bhat & Kumar, 2014).