Explain how hemolytic disease of the newborn may result from Rh incompatibility and describe its possible consequences.

Outline:

·        Rh blood groups

·        Rh immune response

·        Causes and consequences of hemolytic disease of newborn

·        Prevention and treatment

Essay:

            Along with the O-A-B blood group system, the Rh system is important in the transfusion of blood. In the O-A-B system, the agglutinins responsible for causing transfusion reactions develop spontaneously, whereas in the Rh system, spontaneous agglutinins almost never occur. Instead, the person must first be massively exposed to an Rh antigen, usually by transfusion of blood or a mother’s having a baby who has the antigen, before enough agglutinins to cause a significant transfusion reaction will develop.

            There are six common types of Rh antigens, each of which is called an Rh factor. The type D antigen is widely prevalent in the population and considerably more antigenic than the other Rh antigens. Anyone who has antigen D is Rh positive, whereas a person who does not have type D antigen is Rh negative.

            When red blood cells containing Rh factor are injected into a Rh-negative person, anti-Rh agglutinins develop slowly. If an Rh-negative person has never been exposed to Rh-positive blood, transfusion of Rh-positive blood into that person causes no immediate reaction. However, in some of these people, anti-Rh antibodies develop in sufficient quantities during the next 2 to 4 weeks to cause agglutination of the transfused cells that are still circulating in the blood. These cells are then hemolyzed by the tissue macrophage system. Thus, a delayed transfusion occurs, although it is usually mild. On subsequent transfusion of Rh-positive blood into the same person, who is now immunized against the Rh factor, the transfusion reaction is greatly enhanced and can become severe.

            Hemolytic disease of the newborn, or erythroblastosis fetalis, is a disease of the fetus and neonate characterized by agglutination and phagocytosis of the red blood cells. It arises when an Rh-negative mother carries an Rh-positive fetus. Small amounts of fetal blood leak into the maternal circulation at the time of delivery, and some mothers develop significant titers of anti-Rh agglutinins during the postpartum period. During the next pregnancy, the mother’s agglutinins cross the placenta to the fetus. When anti-Rh agglutinins cross the placenta to an Rh-positive fetus, they can cause hemolysis. If hemolysis in the fetus is severe, the infant may die in utero or may develop anemia, severe jaundice, and edema. The hemopoietic tissues of the infant attempt to replace the hemolyzed red blood cells. The liver and spleen become greatly enlarged and produce red blood cells so rapidly that many early forms are emptied into the circulatory system. Children who barely survive the anemia exhibit permanent mental impairment or damage to the motor areas of the brain as a result of Kernicterus, a neurologic syndrome in which bile pigments are deposited in the basal ganglia, causing their destruction.

            The usual treatment for erythroblastosis fetalis is to replace the neonate’s blood with Rh-negative blood. About 400 mililiters of Rh-negative blood is infused over a period of 1.5 o more hours while the neonate’s own Rh-positive blood is being removed. This procedure may be repeated several times during the first few weeks of life, mainly to keep the bilirubin level low and thereby prevent kernicterus.

            Since sensitization of Rh-negative mothers by carrying an Rh-positive fetus generally occurs at birth, the first child is usually normal. However, hemolytic disease occurs in about 17% of the Rh-positive fetuses born to Rh-negative mothers who have previously been pregnant one or more times with Rh-positive fetuses. It is usually possible to prevent sensitization from occurring the first time by administering a single dose of anti-Rh antibodies in the form of Rh immune globulin during the postpartum period.