Fetal Erythroblastosis

The fetal erythroblastosis is a hemolytic anemia of fetuses (or newborn as erythroblastosis neonatorum), which is caused by a transplacental crossing maternal antibodies to fetal erythrocytes. The disease usually results from an incompatibility between maternal and fetal blood type, often Rh0 (D) antigens. The diagnostic begins with a prenatal maternal antigen-antibody screening, and may also require a paternal screening, a repeated measurement of the maternal antibody titer and an examination of the fetuses. The treatment involves, in some cases, intrauterine fetal transfusion or neonatal exchange transfusion. Women with appropriate risk receive preventive injection of Rh0 (D) immunoglobulin.

Fetal erythroblastosis results traditionally from a Rh0 (D) -Inkompatibilität that can develop when a woman with Rh-negative blood of a man with Rh-positive blood is pregnant and a child with Rh-positive blood receives (Perinatal Anemia: hemolysis). Other fetomaternal incompatibilities that can cause fetal erythroblastosis are Kell, Duffy, Kidd, MNSs-, Lutheran-, Diego-, XG, P, Ee and Cc antigen systems and other antigens. Incompatibility of the AB0 blood group does not cause fetal erythroblastosis.

The fetal erythroblastosis is a hemolytic anemia of fetuses (or newborn as erythroblastosis neonatorum), which is caused by a transplacental crossing maternal antibodies to fetal erythrocytes. The disease usually results from an incompatibility between maternal and fetal blood type, often Rh0 (D) antigens. The diagnostic begins with a prenatal maternal antigen-antibody screening, and may also require a paternal screening, a repeated measurement of the maternal antibody titer and an examination of the fetuses. The treatment involves, in some cases, intrauterine fetal transfusion or neonatal exchange transfusion. Women with appropriate risk receive preventive injection of Rh0 (D) immunoglobulin. Fetal erythroblastosis results traditionally from a Rh0 (D) -Inkompatibilität that can develop when a woman with Rh-negative blood of a man with Rh-positive blood is pregnant and a child with Rh-positive blood receives (Perinatal Anemia: hemolysis). Other fetomaternal incompatibilities that can cause fetal erythroblastosis are Kell, Duffy, Kidd, MNSs-, Lutheran-, Diego-, XG, P, Ee and Cc antigen systems and other antigens. Incompatibility of the AB0 blood group does not cause fetal erythroblastosis. Pathophysiology Fetal erythrocytes usually occur during pregnancy through the placenta into the maternal circulation. The crossing is the time of birth or at the end of pregnancy is greatest. A conversion of large amounts (. Eg 10 to 150 ml) is considered significant fetomaternal hemorrhage; this can occur after trauma and sometimes after childbirth or termination of pregnancy. In pregnant women with Rh-negative blood, carrying a fetus with Rh-positive blood, the fetal red blood cells stimulate the maternal antibody production against Rh antigens. The stronger the fetomaternal circulation, the more antibodies are produced. The mechanism is the same when other antigen systems are involved; However, a Kell-antibody incompatibility suppressed directly erythropoiesis in the bone marrow. Other reasons for the formation of maternal anti-Rh antibodies are injected with needles contaminated with Rh-positive blood, and inadvertent transfusion of Rh-positive blood. During the initial sensitizing pregnancy, no complications develop; in subsequent pregnancies, however, the maternal antibodies cross the placenta and fetal red blood cells lyse, resulting in anemia, hypoalbuminemia, and possibly heart failure result from an increased cardiac output or fetal death. The anemia stimulates the fetal bone marrow to increased production and release of immature red blood cells (erythroblasts) in the peripheral fetal circulation (fetal erythroblastosis). Hemolysis caused finally increased in the newborns levels of indirect bilirubin, which leads to kernicterus (Kernicterus). Normally, a isoimmunization does not cause symptoms in the pregnant woman. Diagnostic determination of blood group and Rh factors of mother and reflex antibody screening Serial antibody titer determination and blood flow measurements of the middle cerebral artery are at risk pregnancies during the first screening in all women’s blood type, Rhesus factor and anti-Rh0 (D) – and other antibodies determines that are formed in response to antigens and may cause fetal erythroblastosis (reflex antibody screening). can cause the women Rh negative and positive for anti-Rh0 (D) or another antibody that fetal erythroblastosis, blood type and zygosity of the father are determined (in confirmed paternity). If he has Rh-negative blood and is negative for the antigen corresponding to the antibody that was identified at the parent, no further testing is required. If he has Rh-positive blood or the antigen of the maternal anti-Rh antibody titer is measured. If the titers are positive, but below the value, referred to by the laboratory as critical (usually 1: 8 to 1:32), that every 2 to 4 weeks will be measured after 20 weeks, we exceeded the critical value, is measured depending on the initial blood flow measurement and patient medical history, at intervals of 1-2 weeks, the blood flow in the fetal cerebral artery. The aim is to identify heart failure at increased cardiac output at an early stage, which indicates a high risk of anemia. An increased blood flow for gestational age should require a prompt percutaneous umbilical blood sampling in order to obtain a sample of the fetal blood; but because this method can lead to complications, the decision to treat is sometimes done without sampling. If the paternity secured and the father probably heterozygous for Rh0 (D), the fetal Rhesus factor is determined. If the fetal blood Rh-positive or of unknown status and flow of the middle cerebral artery is increased, there is probably a fetal anemia. Fetal blood transfusions treatment confinement between the 32th-35th SSW When the fetal blood is Rh-negative or of blood flow in the middle cerebral artery is normal, then the pregnant woman can remain untreated by the deadline. If fetal anemia is suspected, the fetus can by a specialist in a clinic that is set up for the care of high-risk pregnancies, intrauterine intravascular transfusion are given. These transfusions take place every 1-2 weeks until the fetal lung maturity is secured (usually in the 32nd-35th week of pregnancy) should be carried out and the birth. During pregnancy> 24 weeks, possibly> 23 weeks, should be administered before the first transfusion corticosteroids. (.. Editor’s note .: In Germany, the diagnosis and treatment of fetal erythroblastosis is regulated by the maternity guidelines.) Newborns with a erythroblastosis must be immediately examined by a pediatrician, so he can decide on the need for exchange transfusion (Perinatal Anemia: exchange transfusion ). Prevention Prevention includes giving following the Rh-negative mother: Rh0 (D) immunoglobulin in the 28th week of pregnancy and within 72 hours after completion of pregnancy Birth is as gentle as possible. A manual removal of the placenta should be avoided because it could be pushed into the maternal circulation, fetal cells. A maternal sensitization and antibody production by Rh incompatibility can be prevented by administration of Rh0 (D) immunoglobulin to the patient. This product contains high titers of anti-Rh antibodies neutralize the fetal Rh-positive red blood cells. Since the fetomaternal exchange and the likelihood of sensitization at the end of pregnancy are highest, the preparation is 72 hours after the termination of any pregnancy, it is given by birth, miscarriage or treatment of ectopic pregnancy. The standard dose is 300 micrograms i.m. To exclude a significant fetomaternal bleeding, z. B. performed a rosette test. With positive results, a Kleihauer Bethke test (acid elution) can determine the amount of fetal blood in maternal circulation. If the test indicates that the fetomaternal inflow of blood is massive (> 30 ml total blood volume), additional injections (300 micrograms up to 5 doses per 30 ml of fetal whole blood within 24 hours) are required. For exclusive gift after the birth or at the end of pregnancy, treatment is sometimes ineffective because the sensitization may already take place at an earlier stage of pregnancy. Therefore, all Rh-negative pregnant women who have not undergone any sensitization, dosed at about the 28th week of pregnancy is. Some experts recommend a second dose if it is up to the 40th SSW not come to birth. Rh0 (D) immune globulin should also be added after each phase of vaginal bleeding and after amniocentesis or chorionic villus sampling. After a dose of anti-Rh antibodies> 3 months persist. Summary Most fetal erythrocytes enter the circulation of the mother (which is a highest risk of maternal sensitization) than after childbirth or termination of pregnancy. In all pregnant women blood type, Rh factor, anti-Rh0 (D) should – and other antibodies to be determined, which may cause fetal erythroblastosis. Is an increased risk before, the antibody title, and the blood flow in the middle cerebral artery are measured at regular intervals. The fetal erythroblastosis is treated as needed with intrauterine blood transfusion and with a delivery once the fetal lung maturity is confirmed. In women at risk for sensitization Rh0 (D) immunoglobulin in the 28th week of pregnancy and within 72 hours after termination of pregnancy is given.

Health Life Media Team

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