Erythrobalstosis Fetalis

Bawa-an, Ephraim Fritz Z.

DEFINITION

a hemolytic disease of the fetus and newborn that

occurs when the immune system of an Rh-negative
mother produces antibodies to an antigen in the
blood of an Rh-positive fetus which cross the
placenta and destroy fetal erythrocytes and that is
characterized by an increase in circulating
erythroblasts and by jaundice
Etiologoy

When a mother who is pregnant with a baby whose

blood type is incompatible with the baby's,
antibodies in the mother's blood may cross the
placenta and attack the baby's red blood cells.
This causes anemia in the baby. If it is severe enough,
it can cause the baby to die before birth
Pathophysiology

Fetal 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 150 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.
Signs and Sypmtoms

Jaundice: This occurs due to the deposition of bilirubin (breakdown

product of hemoglobin from RBC) in the skin and the whites of the
eyes. This imparts a yellowish color to these structures.
Hemolytic Anemia: This occurs due to the destruction of RBCs.
Untreated anemia can cause heart failure, enlarged liver and/or
spleen, generalized swelling and respiratory distress.
Kernicterus: This occurs due to the deposition of bilirubin in the
brain and spinal cord. This can lead to nerve cell
degeneration, hearing loss, mental retardation, and even death.
Hydrops Fetalis: This is the severest form of the disease in
newborns and is characterized by extreme edema (abnormal
accumulation of serous fluid) in unusual places like the abdominal
cavity, heart and lungs. This can lead to congestive heart failure as
the extra fluid causes increased pressure on the heart, reducing its
pumping ability. Moreover, fluid accumulation in the lungs prevents
normal breathing, because the lungs cannot expand fully.
Treatment and Prevention

Treatment
Fetal blood transfusions
Delivery at 32 to 35 wk
If fetal blood is Rh negative or if middle cerebral artery 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 wk until fetal
lung maturity is confirmed (usually at 32 to 35 wk), when delivery should be done. Corticosteroids should be given
before the first transfusion if the pregnancy is > 24 wk, possibly > 23 wk.
Neonates with erythroblastosis are immediately evaluated by a pediatrician to determine need for exchange
transfusion (see Perinatal Anemia : Exchange transfusion).
Prevention
Prevention involves giving the Rh-negative mother
Rh0(D) immune globulin at 28 wk gestation and within 72 h of pregnancy termination
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 Rh0(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 h after termination of each pregnancy, whether by delivery, abortion, or treatment
of ectopic pregnancy. The standard dose is 300 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 test results indicate fetomaternal hemorrhage is massive (> 30
mL whole blood), additional injections (300 mcg for every 30 mL of fetal whole blood, up to 5 doses within 24 h)
are necessary.
Diagnostic Tests

Blood Tests
Indirect Coombs test is done on the mothers blood if she is found to be
Rh-, during the antenatal visit and the father is Rh+. It measures the
number of antibodies in the maternal blood. If the Rh mother does not
have antibodies during initial testing, then she will be tested again at 18 to
20 weeks of pregnancy and again at 26 to 27 weeks. If anti-Rh antibodies
are detected at any of these time-points, then treatment is initiated.
Direct Coombs test is carried out on the fetal blood sample which
measures the level of maternal antibodies attached to the babys RBCs.
This test is done if the fetus shows features of anemia and jaundice.
Tests to determine fetal blood counts to check for anemia and serum bilirubin
levels to check for jaundice.
In another scenario, the baby may develop jaundice after birth, in spite of the
fact that there is no Rh incompatibility. Under these circumstances, the
symptoms can be attributed to ABO incompatibility. However, the
symptoms are much milder than in case of Rh incompatibility.
Nursing Intervention

Screen all pregnant women for blood type, Rh type, anti-

Rh0(D), and other antibodies that can cause
erythroblastosis fetalis.
If women are at risk, measure antibody levels and middle
cerebral artery blood flow periodically.
Treat erythroblastosis fetalis with intrauterine fetal blood
transfusions as needed and delivery as soon as fetal lung
maturity is confirmed.
Give Rh0(D) immune globulin at 28 wk gestation and
within 72 h of pregnancy termination to women at risk of
sensitization.