Diagnosis and treatment of hemolytic disease of the fetus and newborn (HDFN) have seen significant advancements in recent decades. Since 1940, when the Rh blood group was identified, doctors have a deeper understanding of the causes of HDFN. This, in turn, led to progress in the prevention, early detection and timely management of HDFN.
HDFN is a rare red blood cell disease that occurs as a result of a mismatch of blood groupBlood group A classification of blood based on inherited markers found on red blood cells. The ABO and Rh blood groups are most common in HDFN. (ABO) or blood type (Rhesus (RhRh factor A protein or antigen found on red blood cells. When an Rh-negative mother carries an Rh-positive fetus, her immune system may make antibodies that attack the fetus' red blood cells.)), between the mother and fetus. If untreated, this incompatibility will allow the mother’s red blood cells to cross the placenta and attack her baby’s red blood cells, leading to anemiaAnemia A condition that occurs when the body doesn’t have enough healthy red blood cells to carry oxygen to its tissues. In HDFN, anemia occurs when maternal antibodies destroy fetal red blood cells. and other more severe outcomes for the fetus or newborn, including death.
History of HDFN
First reported in 1609 by a French midwife, Louise Bourgeois, little was known of HDFN until the 1940s. Before 1945, for example, up to 50% of fetuses with Rh-HDFN died. At the start of the 1970s, the systematic administration of anti-D immunoprophylaxis to Rh(D)-negative women was introduced, reducing HDFN fetal mortality to 2%-3%. Since then, the care of babies affected by HDFN has continued to progress, leading to better outcomes.
Recent improvements
With the advent of routine prenatal blood tests (group and blood screen), pregnant women at risk for HDFN also receive better care. Screening identifies the blood type and if there is a need for Rh-D immunoprophylaxis. Women who are Rh(D)-negative will be monitored more closely and will receive the Rh immune globulin at 28 weeks gestation, and again within 72 hours of delivery. Women who are affected by ABO incompatibility will also be monitored more carefully throughout their pregnancy, particularly in the case of fetal-maternal hemorrhage.
Regular antibodyAntibody A protein made by the immune system that recognizes and attacks foreign substances, such as bacteria, or in HDFN, fetal red blood cells carrying incompatible antigens. testing will be done to determine if the pregnant mother has developed antibodiesAntibody A protein made by the immune system that recognizes and attacks foreign substances, such as bacteria, or in HDFN, fetal red blood cells carrying incompatible antigens. to her baby’s blood. If positive, the antibody levels will be assessed and monitored, with a close eye kept on the fetus for symptoms of HDFN. If a fetus develops HDFN, prompt treatment such as the administration of intravenous immunoglobulin or intrauterine transfusions may be considered.
With the benefit of preventative measures, early diagnosis and prompt treatment of the fetus affected by HDFN, care of the newborn post-delivery is now often less critical. PhototherapyPhototherapy A treatment that uses special blue light to help newborns break down bilirubin and prevent kernicterus. is the first-line treatment for jaundiceJaundice A common symptom of HDFN, jaundice is caused by excess bilirubin and is characterized by a yellow tint to the skin or eyes., followed by blood transfusions for severe anemia and jaundice.
Rare, but still present
Despite the improvements demonstrated in the prevention, diagnosis and care of babies affected by HDFN, in utero and post-delivery, HDFN continues to occur in approximately 1695 of 100,000 live births in the US.
This may be the case for any of the following reasons:
- Anti-D immunization during pregnancy.
- No anti-D immunoprophylaxis administered during pregnancy.
- An insufficient dose of anti-D immunoprophylaxis administered during pregnancy.
- Error in initial blood typing in prenatal blood screening.
- Error in transfusion therapy.
