Hemolytic Disease of The Newborn
Hemolytic disease of the newborn, formerly known as erythroblastosis fetalis, affects the fetus and neonate. It stems from an incompatibility of fetal and maternal blood, resulting in maternal antibody activity against fetal red blood cells (RBCs).
Intrauterine transfusions can save 40% of fetuses with this problem. In severe, untreated hemolytic disease of the newborn, the prognosis is poor, especially if kernicterus develops. About 70% of these infants die, usually within the first week of life; survivors inevitably develop pronounced neurologic damage.
ABO incompatibility, another form of fetomaternal incompatibility, can also occur and can lead to hemolytic disease of the newborn.
Although more than 60 RBC antigens can stimulate antibody formation, hemolytic disease of the newborn usually results from Rh isoimmunization, a condition that develops in about 7% of all pregnancies in the United States.
During her first pregnancy (whether it ends in delivery or abortion), an Rh-negative female becomes sensitized by exposure to Rh-positive fetal blood antigens inherited from the father. A female may also become sensitized by receiving blood transfusions with alien Rh antigens, causing agglutinins to develop. This sensitization is the result of inadequate doses of Rho(D) immune globulin (human) or from failure to receive Rho(D) immune globulin after significant fetal-maternal leakage from abruptio placentae.
Subsequent pregnancy with an Rh-positive fetus causes increasing amounts of maternal agglutinating antibodies to cross the placental barrier, attach to Rh-positive cells in the fetus, and cause hemolysis and anemia in the fetus. To compensate for this, the fetus produces more RBCs and erythroblasts (immature RBCs) appear in the fetal circulation. Extensive hemolysis results in the release of large amounts of unconjugated bilirubin, which the liver is unable to conjugate and excrete, causing hyperbilirubinemia and hemolytic anemia in the fetus. Before the development of Rho(D) immune globulin, this condition was a major cause of kernicterus and neonatal death.
The following are the most common symptoms of hemolytic disease of the newborn. However, each baby may experience symptoms differently. Some of the symptoms of Hemolytic disease of the newborn include:
Diagnostic tests are performed on the mother and the neonate. The father may also be tested for blood group, Rh factor , and Rh zygosity.
The choice of treatment depends on the degree of maternal sensitization and hemolytic effects on the fetus or neonate.
Intrauterine transfusion is performed on a fetus When amniotic fluid analysis suggests that the fetus is severely affected and delivery is inappropriate because of fetal immaturity. The mother is admitted to the labor and delivery area and monitored closely. She is given a tocolytic agent I.V. to inhibit contractions, and ultrasonography is performed to locate the umbilical vein of the fetus. Then, using a procedure called percutaneous umbilical blood sampling, a needle is inserted into the umbilical vein and a blood sample is taken to identify fetal blood type, measure hemoglobin levels and hematocrit, and obtain other pertinent information. If the fetal blood sample verifies anemia, a blood transfusion of O-negative blood in utero can take place through the sampling needle. This procedure may be repeated periodically (about every 2 weeks) until the fetus is mature enough for delivery.
Planned delivery usually is done 2 to 4 weeks before term date, depending on maternal history, serologic tests, and amniocentesis; labor may be induced from the 34th to 38th week of gestation. During labor, the fetus should be monitored electronically; capillary blood sampling (from the scalp) determines acid-base balance. Any indication of fetal distress necessitates immediate cesarean delivery.
Phenobarbital administered during the last 5 to 6 weeks of gestation may lower serum bilirubin levels in the neonate.
An exchange transfusion removes antibody-coated RBCs and prevents hyperbilirubinemia through removal of the infant's blood and replacement with fresh group O Rh-negative blood. Albumin infusion binds bilirubin, reducing the risk of hyperbilirubinemia. Phototherapy by exposure to ultraviolet light reduces bilirubin levels.
Administration of gamma globulin that contains anti-Rh-positive antibody (Rho[D]) can provide passive immunization, which prevents maternal Rh isoimmunization in Rh-negative females. However, it's ineffective if sensitization has already resulted from a previous pregnancy, abortion, or transfusion.
Neonatal therapy for hydrops fetalis consists of maintaining ventilation by intubation, oxygenation, and mechanical assistance, when necessary, and removing excess fluid to relieve ascites and respiratory distress. Other appropriate measures include an exchange transfusion and maintenance of the neonate's body temperature.
Administration of Rho(D) immune globulin (human) to an unsensitized Rh-negative mother as soon as possible after the birth of an Rh-positive infant or after a spontaneous or elective abortion prevents complications in subsequent pregnancies.
The following patients should be screened for Rh isoimmunization or irregular antibodies:
Fortunately, HDN is a very preventable disease. Because of the advances in prenatal care, nearly all women with Rh negative blood are identified in early pregnancy by blood testing. If a mother is Rh negative and has not been sensitized, she is usually given a drug called Rh immunoglobulin (RhIg), also known as RhoGAM. This is a specially developed blood product that can prevent an Rh negative mother's antibodies from being able to react to Rh positive cells. Many women are given RhoGAM around the 28th week of pregnancy. After the baby is born, a woman should receive a second dose of the drug within 72 hours.
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