Fetal erythroblastosis

Erythroblastosis fetalis is a hemolytic anemia in the fetus or neonate caused by transplacental transfer of maternal antibodies to fetal red blood cells. The disorder usually results from incompatibility between maternal and fetal blood groups, often the Rh0(D) antigen. [ 1 ] Diagnosis begins with prenatal screening of maternal antigens and antibodies, and may also require paternal testing, serial maternal antibody titers, and fetal testing. Treatment should include intrauterine transfusion in the fetus or exchange transfusion in the neonate. Intrauterine immunoglobulin injection has been used to prevent Rh0(D) in women at risk. [ 2 ]

Causes fetal erythroblastosis

Traditionally, fetal erythroblastosis is the result of Rh0(D) incompatibility, which can develop when a woman with Rh-negative blood is impregnated by a man with Rh-positive blood and the resulting fetus has Rh-positive blood. Other maternal-fetal incompatibilities that can cause fetal erythroblastosis include Kell, Duffy, Kidd, MNSs, Luteran, Diego, Xg, P, Ee, and Cc and other antigen systems. ABO blood group incompatibility does not cause fetal erythroblastosis.

Fetal red blood cells cross the placenta into the maternal circulation throughout pregnancy. The migration is greatest at delivery or termination of pregnancy; feto-maternal hemorrhage may occur with maternal abdominal trauma. In women who have Rh-negative blood and are carrying a fetus with Rh-positive blood, fetal red blood cells stimulate the production of antibodies against maternal Rh antigens (isoimmunization); the mechanism is the same when other antigen systems are involved.

In subsequent pregnancies, maternal antibodies cross the placenta and destroy fetal red blood cells, causing anemia, hypoalbuminemia, and possibly hypersystolic heart failure or intrauterine death.

Anemia stimulates the fetal bone marrow to produce and release immature red blood cells (erythroblasts) into the fetal peripheral circulation (erythroblastosis fetalis). Hemolysis results in elevated bilirubin levels in the newborn, which causes neonatal bilirubin encephalopathy. Isoimmunization in pregnant women is usually asymptomatic.

Diagnostics fetal erythroblastosis

At the first prenatal visit, all women have a blood sample taken for Rh status. If the woman is Rh negative, the paternal blood type and zygosity (if paternity is determined) are determined. If the blood is Rh positive, the mother's Rh antibody titer is measured at 26–28 weeks. If titers are positive only at dilutions less than 1:32 (or below the local blood bank's cutoff values), titers are measured more frequently. If titers are around 1:32 (or above the local laboratory's cutoff values), mean fetal cerebral artery blood flow is measured at 12-week intervals depending on the titers and the patient's history; the goal is to detect heart failure. If fetal blood flow is elevated for gestational age, percutaneous umbilical cord blood sampling (if anemia is suspected) or spectrophotometric bilirubin levels in amniotic fluid obtained by amniocentesis should be measured every 2 weeks. If paternity is known and the father is likely to be heterozygous for RhO(D), the fetal Rh identity is determined from the cells in the amniotic fluid. If fetal blood is Rh negative or if mean cerebral artery blood flow or amniotic fluid bilirubin levels remain normal, the pregnancy can be continued to term without treatment. If fetal blood is Rh positive or Rh identity is unknown and if mean cerebral artery blood flow or amniotic fluid bilirubin levels are elevated, the fetus may be transfused by a specialist in a facility equipped to manage pregnancies with risk factors, assuming fetal anemia. Transfusions are needed every 12 weeks until fetal lung maturity is achieved (usually 32-34 weeks) and delivery is possible. Corticosteroids are needed before the first transfusion if the pregnancy is 24 weeks or more.

[ 3 ], [ 4 ], [ 5 ], [ 6 ]

Treatment fetal erythroblastosis

Delivery should be as atraumatic as possible. Manual removal of the placenta should be avoided because it may cause fetal cells to enter the maternal circulation. Newborns with erythroblastosis are immediately evaluated by a pediatrician to determine the need for exchange transfusion.

Prevention

Sensitization in the mother and antibody production due to Rh incompatibility can be prevented by the administration of RhO(D) immunoglobulin. This preparation contains high titers of anti-Rh antibodies that neutralize Rh-positive fetal erythrocytes. Since the intensity of fetal-maternal exchange and the likelihood of sensitization increase toward the end of pregnancy, preparation is carried out within 72 hours before the end of any pregnancy, regardless of its end (delivery, abortion, treatment of ectopic pregnancy ). The standard dose of the preparation is 300 mcg.

An immune rosette test may be used to rule out significant fetomaternal hemorrhage, and if positive, the Kleihauer-Betke (acid elution) test measures the amount of fetal blood in the maternal circulation. If fetomaternal hemorrhage is massive (>30 mL of total blood), additional injections (up to five doses of 300 mcg within 24 hours) are needed. Treatment late in pregnancy is sometimes ineffective because sensitization may have begun earlier in pregnancy. Therefore, at approximately 28 weeks, all pregnant women with Rh-negative blood and no history of sensitization also receive a dose of immunoglobulin. Because there is no risk in using RhO(D) immunoglobulin in sensitized women, the injection can be given when blood is drawn for titer measurement at 28 weeks. Some experts recommend a second dose if delivery has not occurred by 40 weeks. Rh0(D) immunoglobulin should also be given after any episode of vaginal bleeding and after amniocentesis or chorionic villus sampling. Anti-IL antibodies persist for more than 3 months after a single dose.