What do Doctors call this Condition – Erythroblastosis fetalis
What is this Condition?
When the fetus’s blood is incompatible with the mother’s, the mother produces antibodies against the fetus’s red blood cells. Intrauterine transfusions with human Rh(D) immune human globulin can save 40% of fetuses with this disorder. However, in severe, untreated blood incompatibility, the prognosis is poor, especially if kernicterus (infiltration of parts of the brain and spinal cord with bilirubin) develops. About 70% of these infants die, usually within the first week of life; survivors inevitably develop severe nervous system damage.
What Causes it?
Blood incompatibility between mother and fetus usually results from Rh isoimmunization – a condition that develops in approximately 7% of all pregnancies in the United States. Until treatment with human Rh(D) immune human globulin became available, this condition was an important cause of kernicterus and neonatal death.
During her first pregnancy, a woman with Rh-negative blood factors becomes sensitized (during delivery or abortion) by exposure to Rh-positive fetal blood factors inherited from the father. In the next pregnancy that produces an Rh-positive fetus, increasing amounts of maternal anti-Rh-positive antibodies cross the placental barrier, attach to Rh-positive cells in the fetal blood, and destroy them.
To compensate for this, the fetus steps up the production of new red blood cells, which are attacked in their turn. Escalating red cell destruction releases large amounts of unconjugated bilirubin (a red cell component), which the fetal liver cannot properly process and excrete.
ABO incompatibility, another form of blood incompatibility between mother and fetus, is less severe.
What are its Symptoms?
An infant with this incompatibility disorder has liver problems. Jaundice (resulting from the fetal liver’s failure to process bilirubin from the destroyed red cells) doesn’t usually appear at birth but may occur 30 minutes to 24 hours later. A mildly affected infant is pale and has a mildly to moderately enlarged liver and spleen. Severely affected infants who survive birth usually have pallor, swelling, small reddish skin spots, an enlarged liver and spleen, grunting respirations, abnormal breath sounds, poor muscle tone, nervous system unresponsiveness, possible heart murmurs, a bile-stained umbilical cord, and yellow or meconium-stained amniotic fluid.
How is it Diagnosed?
Diagnostic evaluation considers both prenatal and neonatal findings.
Important factors to consider are:
• maternal history (for blood incompatibility-related stillbirths, abortions, previously affected children, or previous anti-Rh blood levels)
• blood typing and screening
• father’s blood test results
• history of blood transfusion.
Other diagnostic tests that provide important information include amniotic fluid analysis and X-ray studies.
How is it Treated?
Treatment depends on the degree of maternal sensitization and the effects of hemolytic disease on the fetus or newborn .
• Intrauterine-intraperitoneal blood transfusion is performed when amniotic fluid analysis suggests that the fetus is severely affected and that delivery is inappropriate because the fetus will be premature. A transabdominal puncture under fluoroscopy into the fetal peritoneal cavity allows infusion of group 0, Rh-negative blood. This may be repeated every 2 weeks until the fetus is mature enough for delivery.
• Planned delivery is usually done 2 to 4 weeks before term date, depending on maternal history, serologic tests, and amniocentesis results; labor may be induced from the 34th to 38th week of gestation. During labor, the fetus should be monitored electronically; capillary blood scalp sampling determines acid-base balance. Any indication of fetal distress calls for an immediate cesarean delivery .
• The newborn’s serum bilirubin levels are brought down by phenobarbital administered during the last 5 to 6 weeks of pregnancy; or by an albumin infusion, which helps bind bilirubin; or by phototherapy with ultraviolet light .
• Administration of human Rh(D) immune globulin can provide passive immunization, which prevents maternal Rh isoimmunization in Rh-negative women. However, it’s ineffective if sensitization has already resulted from a previous pregnancy, abortion, or transfusion.