ABO incompatibility in newborns is a condition that arises when a mother and her developing baby have incompatible blood types within the ABO blood group system. This incompatibility causes the mother’s immune system to produce antibodies that react against the baby’s red blood cells. This reaction leads to the destruction of the infant’s red blood cells, resulting in a type of anemia and jaundice. ABO incompatibility is generally much milder than other forms of blood group incompatibility, such as Rh disease, but still requires careful monitoring after birth.
Understanding Blood Group Interactions
The ABO blood group system is based on the presence or absence of specific molecules, called antigens, on the surface of red blood cells. Individuals with type A blood have A antigens, those with type B have B antigens, type AB have both, while type O individuals have neither. A person’s immune system naturally produces antibodies against the antigens they lack.
The incompatibility occurs most often when a mother has type O blood and the baby has type A or type B blood. The antibodies that cause a reaction are of the Immunoglobulin G (IgG) class, which are small enough to pass through the placenta into the fetal circulation. Once these maternal IgG antibodies cross the placenta, they bind to the incompatible antigens on the baby’s red blood cells, marking them for destruction in a process called hemolysis. This destruction begins in the uterus, but the effects become clinically apparent after birth.
How ABO Incompatibility Affects Newborns
The primary clinical consequence of red blood cell destruction is hyperbilirubinemia, an excessive buildup of bilirubin in the baby’s blood. Bilirubin is a yellow waste product created when hemoglobin, the oxygen-carrying component of red blood cells, is broken down. The rapid rate of hemolysis overwhelms the newborn’s liver, which is not yet mature enough to efficiently process and excrete the large amount of bilirubin produced.
This buildup quickly manifests as neonatal jaundice, a yellowish discoloration of the skin and whites of the eyes, which typically appears within the first 24 hours of life. The jaundice associated with this condition tends to increase more rapidly than the common non-hemolytic physiologic jaundice. Ongoing red blood cell destruction also leads to a mild form of hemolytic anemia.
A rare but serious complication of untreated severe hyperbilirubinemia is a condition called kernicterus, which is a type of brain damage caused by bilirubin crossing the blood-brain barrier.
Identifying Risk and Diagnosing the Condition
Identifying the risk for ABO incompatibility begins during routine prenatal screening, where the mother’s blood is typed, and an antibody screen is performed. Mothers with type O blood are flagged as being at risk, though the severity of the condition cannot be accurately predicted based on maternal antibody levels alone.
The definitive diagnosis is typically made shortly after birth when the newborn develops jaundice or is identified as high-risk. A Direct Antiglobulin Test (DAT), also known as a Direct Coombs test, is performed on the infant’s cord blood or peripheral blood. A positive DAT confirms that maternal antibodies are coating the baby’s red blood cells, indicating an immune reaction.
In addition to the DAT, the infant’s blood type is determined, and bilirubin levels are repeatedly measured to monitor the rate of increase. The presence of a positive DAT in a type A or B infant born to a type O mother, coupled with rising bilirubin levels, confirms the diagnosis of hemolytic disease of the newborn due to ABO incompatibility.
Managing and Treating the Effects
The primary goal of managing ABO incompatibility is to reduce the concentration of circulating bilirubin to prevent kernicterus. For most newborns, the standard intervention is phototherapy, or light treatment. This involves placing the infant under special blue lights that emit light at a specific wavelength.
The light energy works by changing the structure of the unconjugated bilirubin molecules in the skin, converting them into water-soluble isomers. These new forms can be excreted more easily in the baby’s urine and stool, lowering the overall level of bilirubin in the blood.
If bilirubin levels are rising quickly or remain dangerously high despite intensive phototherapy, more aggressive treatments may be required. Intravenous immunoglobulin (IVIG) can be administered to slow the destruction of red blood cells by blocking the maternal antibodies in the baby’s circulation. For the most severe cases, an exchange transfusion may be necessary, a procedure where a small amount of the baby’s blood is sequentially removed and replaced with donor blood.