neonatalalloimmuunihemoliosta

Neonatal alloimmune hemolysis is a condition in which maternal IgG antibodies directed against fetal red blood cell antigens cross the placenta and cause destruction of fetal or newborn red blood cells. It most commonly arises from incompatibilities such as Rh(D) but other antigens, including Kell, Duffy, Kidd, E and c, can be involved. It is a form of hemolytic disease of the fetus and newborn.

The underlying mechanism involves maternal exposure to fetal red cell antigens, which leads to the production of alloantibodies. These IgG antibodies cross the placenta during pregnancy, bind to fetal red blood cells, and trigger their removal by splenic macrophages. This results in fetal anemia and increased bilirubin production, which may cause jaundice after birth and, in severe cases, hydrops fetalis.

Clinical features vary from fetal anemia and hydrops to postnatal jaundice and anemia. In the newborn, signs can include pallor, rapid heart rate, enlarged liver or spleen, and jaundice that appears within the first days of life. Laboratory findings typically show a positive direct Coombs test in the newborn, maternal antibodies in the indirect Coombs test, reticulocytosis, and elevated unconjugated bilirubin.

Diagnosis relies on maternal antibody screening and identification of specific alloantibodies, along with testing of the newborn. Monitoring during pregnancy may include Doppler ultrasound assessment of fetal anemia, and management after birth focuses on controlling hyperbilirubinemia and correcting anemia.

Prevention involves RhD immune prophylaxis for Rh-negative mothers and routine prenatal antibody screening to detect clinically significant alloantibodies. With timely detection and appropriate treatment, outcomes are generally favorable, though severe cases can lead to hydrops fetalis or long-term complications from extreme hyperbilirubinemia.