Hemolytic Disease of the Newborn(redirected from Erythroblastosis, fetal)
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Hemolytic Disease of the Newborn
(erythroblastosis fetalis; erythroblasts are immature forms of erythrocytes), a disease manifested at birth or shortly thereafter and generally caused by incompatibility of the mother’s blood with that of the fetus with respect to the rhesus (Rh) factor. The disease may occur in the edematous form (the most severe) and the icteric form, as well as in the form of congenital anemia. The icteric form is the most common. Jaundice, which often ends in death, has long been known. However, its cause (hemolytic disease) was not discovered until the period 1937 to 1940, when the Austrian physician K. Landsteiner and the American physician A. Wiener found in the erythrocytes of 85 percent of the persons examined a peculiar substance also present in all monkeys of the rhesus breed. The substance was therefore called the rhesus (Rh) factor.
If a woman whose blood does not contain the Rh factor (Rh-negative) is made pregnant by her Rh-positive husband and the fetus inherits the Rh-positive blood of the father, the number of Rh-antibodies gradually increases in the mother’s blood. Passing through the placenta into the fetus’ blood, these antibodies destroy the fetus’ erythrocytes and later the newborn’s erythrocytes. Hemolytic disease of newborns may also occur in case of blood group incompatibility between the parents, when the infant inherits the father’s blood group. In such cases the mother usually has the 1(0) group while the infant has the 11(A) or III(B) group. If the mother and infant have Rh-incompatible blood, hemolytic disease usually develops in children born from the second, third, and subsequent pregnancies, because the amount of Rh-antibodies in the mother increases slowly. However, the disease may also develop in a child born from the first pregnancy if the mother received a blood transfusion during pregnancy or was injected intramuscularly with blood regardless of its Rh factor. Hemolytic disease occurs on the average in two to five out of 1,000 newborns. Previous abortions promote the development of the severe form of hemolytic disease. An abortion performed during the first pregnancy results in the formation of antibodies and increases the possibility that hemolytic disease will develop.
The icteric form of hemolytic disease of the newborn is characterized by the early appearance of jaundice (during the first hours or days after birth), with rapid intensification of the jaundice on the following days. (So-called physiological jaundice of the newborn, which is observed in healthy children, usually appears three to four days after birth.) The jaundice is caused by the escape into blood plasma of bilirubin, which is formed after destruction of the infant’s erythrocytes. The infant’s condition usually deteriorates on the following days. Anemia intensifies, the child becomes sluggish, sucks poorly, and often develops spasms associated with disorders of the nervous system. Children who had hemolytic disease in the severe icteric form sometimes lag in development if they are inadequately treated. In cases of the edematous form of hemolytic disease of the newborn (general congenital edema of the fetus), the fetus is generally born prematurely or is stillborn, or it dies a few hours after birth. Symptoms of the disease are edema of the skin and subcutaneous tissue, accumulation of fluid in the chest and abdominal cavities, enlarged liver and spleen, and pronounced anemia. The main symptom of the mildest form of hemolytic disease—congenital anemia of the newborn—is skin pallor associated with a small amount of hemoglobin and erythrocytes. The course of this form of the disease is usually favorable and, if treated promptly, ends in recovery.
Treatment involves exchange transfusion (replacement of 70 to 80 percent of the infant’s blood with the blood of a Rh-negative donor). This procedure is sometimes repeated and is performed in the first 24 hours after birth to remove as quickly as possible from the newborn’s body both the toxic products formed after destruction of the erythrocytes and the Rh-antibodies. Drugs that improve liver function are prescribed. During the first two weeks children with hemolytic disease are usually fed milk drawn from another woman, because at this time the mother’s milk contains Rh-antibodies that are harmful to the infant. The infant is switched to its mother’s milk as soon as the antibodies disappear. Children suffering from hemolytic disease need good care and proper feeding.
Prevention includes the examination of the blood of all pregnant women to determine whether they are Rh-negative and should be registered in the women’s consultation service. Rh-antibodies are measured once a month, and more often if necessary, in Rh-negative pregnant women. It is important to protect the pregnancy. If antibodies are found, longer intervals between pregnancies are recommended, because the antibody titer increases with each succeeding pregnancy. Every child born to a mother with Rh-negative blood should be carefully observed and examined without fail within a few hours after birth for the presence of] bilirubin and the Rh factor in the blood, and its blood group should be determined.
REFERENCESPoliakova, G. P. “Gemoliticheskaia bolezn’ novorozhdennogo.” In Mnogotomnoe rukovodstvo po akusherstvu i ginekologii. Moscow, 1964. Vol. 3, book 2, pp. 809-27.
Gemoliticheskaia bolezn’ novorozhdennogo (collection of articles). Leningrad, 1958.
I. A. SHTERN