Hemolytic Disease Of The Newborn

Hemolytic disease of the newborn is also known as fetal erythroblastosis. It is a dangerous form of neonatal jaundice that is associated with different blood groups of mother and the child.


Neonatal jaundice is a common condition in many newborns. It is caused by the breakdown of fetal red blood cells as they are replaced by new ones. Degraded erythrocytes release hemoglobin that is processed to a pigment known as bilirubin, which can discolor the skin and mucous membranes yellow.


In hemolytic disease of the newborn, however, this cell decay is much more serious. Usually, it is caused by a mismatch between Rh factor of the mother and the child. The Rh factor indicates presence of a particular structure (antigen D) in the membranes of the erythrocytes.


In Rh positive (Rh +) people this structure is present, while in Rh-negative (Rh -) it is not.


The body of Rh-negative individuals does not know the D antigen and upon contact with Rh-positive blood it forms antibodies targeting it and destroying erythrocytes of the Rh-positive person. And this is the problem of hemolytic disease of the newborns. If a Rh-negative woman has her first child with an Rh-positive father, there is a chance that this child will be also Rh-positive (i.e. there is mother-child Rh incompatibility). The blood circulation of the mother and child are separated and their blood does not mix. During the childbirth, however, the mother’s and child’s blood mix. It makes no problem to the child but in mother’s body the immune system encounters Rh positive red blood cells, evaluates them foreign and forms antibodies that are able to cross the placental barrier. If such this woman has another Rh-positive baby, the antibodies penetrate through placenta and destroy the fetal blood cells. As long the baby is in the womb, the released bilirubin is taken away by placenta and degraded by mother’s liver. After the birth, the newborn suffers from prolonged erythrocytes destruction by remaining mother’s antibodies but the newborn’s body is no longer able to cope with overproduction of bilirubin.


Note: Rh negative woman can create the above-mentioned antibodies not only during delivery of a Rh-positive baby, but also during abortion of Rh-positive fetus, or by transfusion of Rh-positive blood.

What does this mean?

  • The main risk is when a Rh-negative mother has a Rh-positive fetus
  • First child is usually not in danger, but the others are.
  • The disease does not manifest prenatally, but shortly after birth


Hemolytic disease of the newborn manifests with jaundice (yellow skin and mucous membranes) of the newborn. High concentration of produced bilirubin can penetrate into the brain and cause its permanent damage. In acute phase, it manifests with cramps, eating disorders and disturbances of consciousness. Severe forms may be even fatal. Chronic symptoms include mental retardation and movement disorders due to irreversible brain damage. Damage of the newborn’s brain by bilirubin is technically known as kernicterus. In adults, this can not happen, as the mature brain has a barrier that prevents the bilirubin entrance. In addition to the brain damage, massive breakdown of newborn’s red blood cells may cause severe anemia and heart failure. Liver tissue gets enlarged as it desperately tries to process the bilirubin.


In addition to jaundice, the serum concentration of bilirubin is high and laboratory signs of anemia may be present. The Rh incompatibility may be also proven by simple blood test of both the mother and newborn. Presence of the above-mentioned antibodies in child’s blood is another way of confirmation.


When the Rh-negative woman has faced the Rh-positive blood (typically during the first delivery of a Rh-positive baby), it is possible to immediately administer an artificially produced antibodies against the Rh factor. These antibodies quickly destroy any Rh positive red blood cells that penetrated in woman’s circulatory system and so the immune system does not have time to create its own antibodies. The artificial antibodies degrade in a short time.


The treatment is similar to the therapeutic management of severe neonatal jaundice, i.e. phototherapy and exchange transfusions (see more in relevant text).


Jiri Stefanek, MD  Author of texts: Jiri Stefanek, MD
 Contact: jiri.stefanek@seznam.cz
 Sources: basic text sources