ERITROBLASTOSIS FETALIS ADALAH PDF

Erythroblastosis fetalis is hemolytic anemia in the fetus or neonate, as erythroblastosis neonatorum caused by transplacental transmission of maternal antibodies to fetal red blood cells. The disorder usually results from incompatibility between maternal and fetal blood groups, often Rho D antigens. Diagnosis begins with prenatal maternal antigenic and antibody screening and may require paternal screening, serial measurement of maternal antibody titers, and fetal testing. Treatment may involve intrauterine fetal transfusion or neonatal exchange transfusion.

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Erythroblastosis fetalis is hemolytic anemia in the fetus or neonate, as erythroblastosis neonatorum caused by transplacental transmission of maternal antibodies to fetal red blood cells. The disorder usually results from incompatibility between maternal and fetal blood groups, often Rho D antigens. Diagnosis begins with prenatal maternal antigenic and antibody screening and may require paternal screening, serial measurement of maternal antibody titers, and fetal testing.

Treatment may involve intrauterine fetal transfusion or neonatal exchange transfusion. Prevention is Rho D immune globulin injection for women who are Rh-negative.

Erythroblastosis fetalis classically results from Rho D incompatibility, which may develop when a woman with Rh-negative blood is impregnated by a man with Rh-positive blood and conceives a fetus with Rh-positive blood, sometimes resulting in hemolysis. Incompatibilities of ABO blood types do not cause erythroblastosis fetalis. Fetal red blood cells RBCs normally move across the placenta to the maternal circulation throughout pregnancy.

Movement is greatest at delivery or termination of pregnancy. Movement of large volumes eg, 10 to mL is considered significant fetomaternal hemorrhage; it can occur after trauma and sometimes after delivery or termination of pregnancy.

In women who have Rh-negative blood and who are carrying a fetus with Rh-positive blood, fetal RBCs stimulate maternal antibody production against the Rh antigens. The larger the fetomaternal hemorrhage, the more antibodies produced. The mechanism is the same when other antigen systems are involved; however, Kell antibody incompatibility also directly suppresses RBC production in bone marrow.

Other causes of maternal anti-Rh antibody production include injection with needles contaminated with Rh-positive blood and inadvertent transfusion of Rh-positive blood. No complications develop during the initial sensitizing pregnancy; however, in subsequent pregnancies, maternal antibodies cross the placenta and lyse fetal RBCs, causing anemia, hypoalbuminemia, and possibly high-output heart failure or fetal death.

Anemia stimulates fetal bone marrow to produce and release immature RBCs erythroblasts into fetal peripheral circulation erythroblastosis fetalis. Hemolysis results in elevated indirect bilirubin levels in neonates, causing kernicterus.

Usually, isoimmunization does not cause symptoms in pregnant women. Serial antibody level measurements and middle cerebral artery blood flow measurements for pregnancies considered at risk. At the first prenatal visit, all women are screened for blood type, Rh type, and anti-Rho D and other antibodies that are formed in response to antigens and that can cause erythroblastosis fetalis reflex antibody screening.

If he has Rh-negative blood and is negative for the antigen corresponding to the antibody identified in the mother, no further testing is necessary. If he has Rh-positive blood or has the antigen, maternal anti-Rh antibody titers are measured. If titers are positive but less than a laboratory-specific critical value usually to , they are measured every 2 to 4 weeks after 20 weeks. If the critical value is exceeded, fetal middle cerebral artery MCA blood flow is measured at intervals of 1 to 2 weeks depending on the initial blood flow result and patient history; the purpose is to detect high-output heart failure, indicating high risk of anemia.

Elevated blood flow for gestational age should prompt consideration of percutaneous umbilical blood sampling and intrauterine blood transfusion. If fetal blood is Rh positive or status is unknown and if MCA blood flow is elevated, fetal anemia is likely. This test is available in North America. If fetal blood is Rh negative or if MCA blood flow remains normal, pregnancy can continue to term untreated.

If fetal anemia is likely, the fetus can be given intravascular intrauterine blood transfusions by a specialist at an institution equipped to care for high-risk pregnancies. Transfusions occur every 1 to 2 weeks, usually until 32 to 35 weeks. During that time period, delivery may be recommended if there is continuing evidence of severe fetal anemia based on MCA blood flow.

The woman may continue to term delivery if there is no evidence of severe fetal anemia based on MCA blood flow. Neonates with erythroblastosis are immediately evaluated by a pediatrician to determine need for exchange transfusion.

Prevention involves giving the Rh-negative mother Rho D immune globulin at the following times:. Delivery should be as atraumatic as possible. Manual removal of the placenta should be avoided because it may force fetal cells into maternal circulation. Maternal sensitization and antibody production due to Rh incompatibility can be prevented by giving the woman Rho D immune globulin.

This preparation contains high titers of anti-Rh antibodies, which neutralize Rh-positive fetal RBCs. Because fetomaternal transfer and likelihood of sensitization is greatest at termination of pregnancy, the preparation is given within 72 hours after termination of each pregnancy, whether by delivery, abortion, or treatment of ectopic pregnancy. The standard dose is mcg IM. A rosette test can be used to rule out significant fetomaternal hemorrhage, and if results are positive, a Kleihauer-Betke acid elution test can measure the amount of fetal blood in the maternal circulation.

If given only after delivery or termination of pregnancy, treatment is occasionally ineffective because sensitization can occur earlier during pregnancy. Therefore, at about 28 weeks, all pregnant women with Rh-negative blood and no known prior sensitization are given a dose of Rho D immune globulin. Some experts recommend a 2nd dose if delivery has not occurred by 40 weeks. Rho D immune globulin should also be given after any episode of vaginal bleeding and after amniocentesis or chorionic villus sampling.

The largest number of fetal RBCs move to the maternal circulation resulting in the greatest risk of maternal sensitization after delivery or termination of pregnancy. Screen all pregnant women for blood type, Rh type, anti-Rho D , and other antibodies that can cause erythroblastosis fetalis.

If women are at risk, measure antibody levels and, if needed, middle cerebral artery blood flow periodically. Treat erythroblastosis fetalis with intrauterine fetal blood transfusions as needed and, if severe fetal anemia is detected, delivery at 32 to 35 weeks, depending on the clinical situation. Give Rho D immune globulin at 28 weeks gestation and within 72 hours of pregnancy termination to women at risk of sensitization.

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Erythroblastosis Fetalis

When a woman and her unborn baby carry different Rh protein factors, they have an Rh incompatibility. A blood test can determine your Rh status. If an…. An ABO incompatibility reaction can occur if you receive the wrong type of blood during a blood transfusion.

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Hemolytic disease of the newborn

Erythroblastosis fetalis , also called hemolytic disease of the newborn , 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. 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.

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