- Hemolytic disease of the fetus and newborn is an immune reaction of the mother’s blood against the blood group factor on the fetus RBCs.
- When RhoGAM (Rh immune globulin) became available in the 1960’s to treat isoimmunization in Rh-negative women, the incidence of hemolytic disease in the fetus and newborn dropped significantly.
- Hemolytic disease occurs most frequently when the mother does not have the Rh factor present in her blood but the fetus has this factor. Another common cause of hemolytic disease is ABO incompatibility. In most cases of ABO incompatibility, the mother has blood type O and the fetus has blood type A. It may also occur when the fetus has blood type B or AB.
- Hemolysis is occasionally caused by maternal anemias, such as thalassemia or from other blood group antigens (anti-D).
- This disorder occurs when the fetus has a blood group antigen that the mother does not posses. The mother’s body forms an antibody against that particular blood group antigen, and hemolysis begins. The process of antibody formation is called maternal sensitization.
- The fetus has resulting anemia from the hemolysis of blood cells. The fetus compensates by producing large numbers of immature erythrocytes, a condition known as erythroblastosis fetalis, hemolytic disease of the newborn, or hydrops fetalis. Hydrops refers to the edema and fetalis refers to the lethal state of the infant.
- In Rh incompatibility, the hemolysis usually begins in utero. It may not affect the first pregnancy but all pregnancies that follow will experience this problem. In ABO incompatibility, the hemolysis does not usually does not usually begin until the birth of the newborn.
1. Clinical manifestations
- The hemolytic response in ABO incompatibility usually begins at birth with a resulting newborn jaundice.
- Rh incompatibility may lead to:
- Hydramnios in the mother
- Excess bilirubin levels in the amniotic fluid.
- Varying degrees of hemolytic anemia (erythroblastosis) in the fetus. If the condition is left unmanaged, 25% of affected infants may die or suffer permanent brain damage.
2. Laboratory and diagnostic study findings
- The indirect Coombs test can aid in the search for agglutination of Rh-positive RBCs to determine if antibodies are present.
- Amniocentesis is used to determine optical density and estimate fetal hemolysis. Spectrophotometer readings are made of the amniotic fluid collected. The readings are obtained to determine fluid density. They are plotted on a graph and correlated with gestational age. The amount of bilirubin resulting from the hemolysis of red blood cells can then be estimated.
- An antibody titer should be drawn at the first prenatal visit on all Rh-negative women. It should also be drawn at 28 and 36 weeks of pregnancy and again at delivery or abortion. The normal value is 0. The result is usually reported as a ratio; normal is 1:8. If the titer is absent or minimal (1:8), no therapy is needed. A rising titer indicates the need for RhoGAM and vigilant monitoring of fetal well-being.
1. Administer RhoGAm to the unsensitized Rh-negative client as appropriate
- Administer RhoGAM at 28 weeks’ gestation, even when titers are negative, or after any invasive procedure, such as amniocentesis. RhoGAM protects against the effects of early transplacental hemorrhage (as recommended by the American College of Gynecologists).
- When the Rh-negative mother is in labor, crossmatch for RhoGAM, which must given within 72 hours of delivery of the newborn.
2. Provide management for the sensitized Rh-negative mother and Rh-positive fetus.
- Focus management of the sensitized Rh-negative mother on close monitoring of fetal well-being, as reflected by Rh titers, amniocentesis results, and sonography.
- If there is evidence of erythroblastosis, notify the perineal team of the possibility for delivery of a compromised newborn.
3. Provide management for ABO incompatibility.