Human red blood cells contain protein molecules (antigens) in their cell membranes that determine the blood type of an individual. There are several kinds of antigens present on human red blood cells, as well as the Rh antigen. People with the Rh antigen are distinguished with a blood type ending in a plus (+); those without the Rh antigen have a minus (-) in their blood type.
Rh disease occurs when an Rh-negative mother is exposed to Rh-positive fetal blood and develops antibodies. During pregnancy, and especially during labor and delivery, some of the fetus's Rh-positive red blood cells get into the mother's (Rh -) bloodstream. Higher passage of fetal cells is observed in women who have undergone amniocentesis and other invasive diagnostic procedures, and in women with placental anomalies. This triggering of the mother's immune response is referred to as sensitization, or isoimmunization. In pregnancies occurring after exposure (usually not in the first pregnancy), maternal antibodies may lyse (disintegrate) the red blood cells of an Rh-positive fetus, leading to red blood cell destruction and fetal anemia. In the case of Rh, the predominant maternal antibody belongs to the G type (igG) which can freely cross the placenta and enter the fetal circulation. The consequent anemia may be so profound that the fetus may die in the uterus. Reacting to the anemia, the fetal bone marrow may release immature red blood cells (erythroblasts) into the fetal peripheral circulation, causing erythroblastosis fetalis. After birth, affected newborns may develop kernicterus. At any further pregnancy, the Rh incompatibility mechanism tends to be accelerated.
Since 1968, there has been a treatment that can prevent Rh disease. Without prophylaxis (preventative treatment), about one in six Rh negative women who deliver a Rh positive infant will develop anti-Rh antibodies from fetomaternal hemorrhage occurring either during pregnancy or at delivery. No universal policy exists for postnatal prophylaxis. The standard dose of anti-D immunoglobulin varies in different countries. In the USA, it is standard practice for Rh- patients who deliver Rh+ infants to receive an intramuscular dose of Rh immune globulin within 72 hours after delivery. With this treatment, the risk of subsequent sensitization deceases from about 15% to 2%. However, in spite of the routine use of gammaglobulin for both antepartum and postpartum immunoprophylaxis, severe fetal Rh alloimmunization continues to be a serious medical problem. In the presence of severe fetal anemia, early intervention appears to offer substantial improvement in clinical outcome.
Prenatal antibody screening is recommended for all pregnant women at their first prenatal visit. Repeat antibody screening at 24-28 weeks gestation is recommended for unsensitized Rh-negative mothers. The goals of antepartum care are to accurately screen the pregnant woman for Rh incompatibility and sensitization, to start appropriate therapeutic interventions as quickly as possible, and to deliver a mature fetus who has not yet developed severe hemolysis.
Frequent blood tests (indirect Coombs' tests) are obtained from the mother, starting at 16 to 20 weeks' gestation. These tests identify the presence of Rh-positive antibodies in maternal blood. When the antibody titer rises to 1:16 or greater, the fetus should be monitored by amniocentesis, cordocentesis, or the delta optical density 450 test. Administration of a dose of Rh immune globulin to Rh- patients at 28 weeks was found to reduce the risk of sensitization to about 0.2%.
The early diagnosis of fetal Rh status represents the best approach for the management of the disease, and a promising non-invasive detection of incompatibility seems now possible by means of the polymerase chain reaction (PCR) analysis of cell-free fetal DNA circulating in the mother's blood.
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