Hemolytic disease of the newborn (HDN) is a blood disorder in a fetus or newborn infant. In some infants, it can be fatal.
Normally, red blood cells (RBCs) last for about 120 days in the body. In this disorder, RBCs in the blood are destroyed quickly and thus do not last as long.
During pregnancy, RBCs from the unborn baby can cross into the mother's blood through the placenta. HDN occurs when the immune system of the mother sees a baby's RBCs as foreign. Antibodies then develop against the baby's RBCs. These antibodies attack the RBCs in the baby's blood and cause them to break down too early.
HDN may develop when a mother and her unborn baby have different blood types. The types are based on small substances (antigens) on the surface of the blood cells.
There is more than one way in which the unborn baby's blood type may not match the mother's.
HDN can destroy the newborn baby's blood cells very quickly, which can cause symptoms such as:
Signs of HDN include:
Which tests are done depends on the type of blood group incompatibility and the severity of symptoms, but may include:
Infants with HDN may be treated with:
The severity of this condition can vary. Some babies have no symptoms. In other cases, problems such as hydrops can cause the baby to die before, or shortly after, birth. Severe HDN may be treated before birth by intrauterine blood transfusions.
The most severe form of this disease, which is caused by Rh incompatibility, can be prevented if the mother is tested during pregnancy. If needed, she is given a shot of a medicine called RhoGAM at certain times during and after her pregnancy. If you have had a baby with this disease, talk with your health care provider if you plan to have another baby.
Reviewed By: Kimberly G. Lee, MD, MSc, IBCLC, Clinical Professor of Pediatrics, Division of Neonatology, Medical University of South Carolina, Charleston, SC. Review provided by VeriMed Healthcare Network. Also reviewed by David Zieve, MD, MHA, Medical Director, Brenda Conaway, Editorial Director, and the A.D.A.M. Editorial team.