Erythroblastosis fetalis is a historical term for a serious condition that can affect unborn babies and newborns. This blood disorder involves the destruction of a baby’s red blood cells by antibodies from the mother.
Defining Erythroblastosis Fetalis
Erythroblastosis fetalis is now more commonly known as Hemolytic Disease of the Fetus and Newborn (HDFN). This immune-mediated disorder occurs when a pregnant mother’s antibodies cross the placenta and attack the baby’s red blood cells, leading to their destruction. The severity of HDFN can range from mild to very severe.
Immune System Origins
The primary cause of HDFN is Rh incompatibility, where an Rh-negative mother carries an Rh-positive baby. Red blood cells have markers called antigens, including the Rh factor. If an Rh-negative mother is exposed to Rh-positive red blood cells, her immune system may produce antibodies against them. This sensitization typically occurs during a first pregnancy, miscarriage, abortion, or at birth when the baby’s blood mixes with the mother’s.
Once sensitized, the mother’s immune system retains these antibodies. In subsequent pregnancies with an Rh-positive baby, these maternal antibodies can cross the placenta and target the baby’s Rh-positive red blood cells, causing their destruction. While Rh incompatibility is the most significant cause of severe HDFN, other blood group incompatibilities can also lead to the condition. ABO incompatibility, for example, is common but usually results in milder forms of HDFN compared to Rh incompatibility.
Consequences for Fetal and Infant Health
The destruction of red blood cells in HDFN leads to several health complications. A primary consequence is anemia, a low level of red blood cells, impairing the baby’s ability to carry oxygen. The baby’s body attempts to compensate for this blood cell loss by producing more red blood cells rapidly, often in organs like the liver and spleen, leading to their enlargement. These newly produced red blood cells are often immature and less effective, exacerbating the anemia.
As red blood cells break down, they release bilirubin, a yellowish waste product. High levels of bilirubin cause jaundice, characterized by yellowing of the skin and eyes. If bilirubin levels become excessively high and remain untreated, it can lead to kernicterus, a severe form of brain damage. In the most severe cases, the fetus can develop hydrops fetalis, a life-threatening condition marked by severe swelling and fluid accumulation, often due to heart failure.
Medical Approaches and Prevention
Detecting HDFN typically begins with maternal blood tests early in pregnancy to determine Rh type and screen for antibodies. If antibodies are detected, further monitoring may involve ultrasounds and Doppler scans to assess the baby’s condition, including signs of anemia or organ enlargement. Amniocentesis might also be used to examine amniotic fluid for signs of the condition.
Treatment for HDFN can occur both before and after birth. For severe cases during pregnancy, intrauterine blood transfusions may be performed. After birth, phototherapy is a common treatment for jaundice, using special lights to help the baby’s body break down and excrete bilirubin. In more severe post-birth cases of anemia or high bilirubin, exchange transfusions may be necessary to replace the baby’s affected blood with healthy donor blood.
A key advancement in preventing HDFN is the administration of Rho(D) immune globulin, commonly known as RhoGAM. This medication prevents an Rh-negative mother’s immune system from developing antibodies against Rh-positive red blood cells. RhoGAM is typically given around the 28th week of pregnancy and again within 72 hours after the birth of an Rh-positive baby, or after events that could cause maternal-fetal blood mixing, such as miscarriage or certain prenatal procedures. This preventive measure has significantly reduced the incidence of severe Rh-induced HDFN.