- Also called:
- hemolytic disease of the newborn
erythroblastosis fetalis
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What is erythroblastosis fetalis?
Erythroblastosis fetalis is a type of anemia where a mother's immune system attacks the red blood cells of her fetus due to blood group incompatibility. This occurs when the fetus inherits a blood factor from the father that the mother lacks.
The most severe form arises when an Rh-negative mother carries an Rh-positive fetus. During pregnancy or, more likely, delivery, fetal red blood cells enter the mother's bloodstream, causing her to produce antibodies. These antibodies can cross the placenta and destroy the fetus's red blood cells. Symptoms range from mild anemia to severe complications like jaundice, enlarged liver and spleen, or even fetal death. Extreme cases can result in hydrops fetalis, characterized by edema and heart failure.
Rh immunoglobulin injections can prevent the mother's sensitization, thus protecting future Rh-positive fetuses. Other treatments, like intrauterine transfusions, are available if the fetus is at risk.
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Why does erythroblastosis fetalis occur in newborns?
Erythroblastosis fetalis occurs when a mother's immune system attacks the red blood cells of her fetus due to blood group incompatibility. This typically happens when an Rh-negative mother carries an Rh-positive fetus, inheriting the Rh factor from the father, which the mother lacks.
During pregnancy, fetal red blood cells can cross the placenta and enter the mother's bloodstream, especially during delivery. This exposure can trigger the mother's immune system to produce antibodies against the Rh factor. These antibodies can then cross the placenta in subsequent pregnancies and destroy the red blood cells of an Rh-positive fetus, leading to erythroblastosis fetalis. The severity ranges from mild anemia to fetal death.
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What role do blood types play in erythroblastosis fetalis?
Erythroblastosis fetalis arises from blood group incompatibility between a mother and her fetus. The Rh and ABO systems are most associated with this condition.
Rh incompatibility occurs when an Rh-negative mother carries an Rh-positive fetus, leading to the mother's immune system producing antibodies against the Rh factor. These antibodies can cross the placenta and destroy the fetal red blood cells.
ABO incompatibility is more common but generally less severe, except when the fetus is type A and the mother is type O. In such cases, ABO antibodies can cause hemolysis (destruction of red blood cells) in the fetus.
The severity varies, ranging from mild anemia to fetal death. However, treatments like Rh immunoglobulin injections have greatly reduced its incidence.7 Britannica SourcesCreated from Britannica articles using AI. AI can make mistakes, so verify using Britannica articles. -
How does a mother's immune system cause erythroblastosis fetalis?
Erythroblastosis fetalis arises from an incompatibility between the blood of a mother and her fetus. It typically occurs when an Rh-negative mother carries an Rh-positive fetus, inheriting the Rh factor from the father, which the mother lacks. During pregnancy, fetal red blood cells cross the placenta, entering the mother's bloodstream. This triggers the mother's immune system to produce antibodies against the Rh factor. These antibodies then cross the placenta and destroy the red blood cells of the Rh-positive fetus, leading to anemia and other complications. Administering anti-Rh serum to the mother promptly after delivery can prevent sensitization and protect future Rh-positive fetuses.
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What are the symptoms of erythroblastosis fetalis in affected babies?
Erythroblastosis fetalis arises from blood group incompatibility between a mother and her fetus, where the mother's immune system attacks the fetus's red blood cells. Symptoms range from mild to severe, sometimes causing fetal or newborn death.
Affected babies can exhibit anemia, indicated by many immature red blood cells (erythroblasts) in their circulation. Jaundice may occur from a buildup of bilirubin, a hemoglobin breakdown product. Enlargement of the liver and spleen are also typical. In severe cases, hydrops fetalis can occur, with extreme edema and congestive heart failure, often resulting in death without an exchange transfusion. Brain damage and neurological deficits can also occur.
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How can erythroblastosis fetalis be prevented or treated?
Erythroblastosis fetalis, a hemolytic disease in newborns, happens when a mother's immune system attacks the fetus' red blood cells due to blood group incompatibility. Prevention primarily involves administering anti-Rh serum (Rh immunoglobulin) to Rh-negative mothers after delivering an Rh-positive child. This destroys fetal red blood cells in the mother's circulation before she becomes sensitized, protecting future Rh-positive fetuses.
Treatment varies based on severity. Mild cases may only require monitoring. More severe cases might need exchange transfusions, replacing the infant's Rh-positive blood with Rh-negative blood. In utero transfusions can be performed if the fetus is at risk. These treatments, along with Rh immunoglobulin, have greatly reduced erythroblastosis fetalis incidence in developed countries.
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erythroblastosis fetalis, type of anemia in which the red blood cells (erythrocytes) of a fetus are destroyed in a maternal immune reaction resulting from a blood group incompatibility between the fetus and its mother. This incompatibility arises when the fetus inherits a certain blood factor from the father that is absent in the mother. Symptoms of erythroblastosis fetalis range from mild to severe; death of the fetus or newborn sometimes results.
Two blood group systems, Rh and ABO, primarily are associated with erythroblastosis fetalis. The Rh system is responsible for the most severe form of the disease, which can occur when an Rh-negative woman (a woman whose blood cells lack the Rh factor) conceives an Rh-positive fetus. Sensitization of the mother’s immune system (immunization) occurs when fetal red blood cells that carry the Rh factor (an antigen in this context) cross the placental barrier and enter the mother’s bloodstream. They stimulate the production of antibodies, some of which pass across the placenta into fetal circulation and lyse, or break apart, the red blood cells of the fetus (hemolysis).
It is rare for a mother to become sensitized during the course of her first Rh-positive pregnancy because the amount of fetal Rh antigen that enters maternal circulation is insufficient to cause sensitization; usually only during labour will exposure be significant. However, because Rh sensitivity is likely to develop during labour, the risk of the disease developing in subsequent Rh-positive pregnancies increases. The risk can be reduced if the mother receives injections of Rh immunoglobulin, which destroys fetal red blood cells in her bloodstream, during her first pregnancy. The fetus also is protected from Rh hemolytic disease if an ABO blood group incompatibility exists concurrently; protection is conferred by ABO antibodies, which destroy fetal blood cells in the maternal circulation before the mother develops Rh sensitivity. Fetal-maternal incompatibilities within the ABO blood group alone are more common than those of the Rh type, but the immune reaction is usually much less severe, unless the fetus is type A and the mother type O.
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The severity of erythroblastosis fetalis varies depending on the degree of hemolysis. Symptoms include anemia, with the presence of many immature red blood cells (erythroblasts) in the circulation; jaundice, resulting from a buildup of bilirubin (a breakdown product of hemoglobin from red blood cells); and an enlarged liver and spleen. In its mildest form, the disease manifests only as slight anemia with no other complications; in its most extreme form, the fetus dies in utero. Hydrops fetalis, which is characterized by extreme edema (abnormal accumulation of serous fluid) and congestive heart failure, is the most severe form of the disease in newborns. Usually the infant dies, unless an exchange transfusion in which the Rh-positive blood of the infant is replaced by Rh-negative blood is successful. A complication of erythroblastosis fetalis is kernicterus, which is caused by deposition of bilirubin in the brain. Hearing loss, mental retardation, or death may result. Nevertheless, many procedures are available to avert these consequences. If it is determined that the fetus is at risk for erythroblastosis fetalis, amniocentesis can be used to measure bilirubin concentrations and predict the severity of the disease. If levels are elevated, intrauterine transfusions of Rh-negative blood can be given until premature delivery can be induced. These measures, together with the use of Rh immunoglobulin, have almost eliminated the incidence of erythroblastosis fetalis in developed countries.