A condition in which the red blood cells of the fetus are destroyed because antibodies in the mother’s blood react against them.
A potentially serious disease of the newborn, characterized by haemolytic anaemia (excessive destruction of red blood cells) and jaundice. If severe, it may be obvious before birth because the baby becomes very oedematous and develops heart failure so-called hydrops fetalis. It may become noticeable on the first day of life as jaundice and anaemia. The disease is due to blood-group incompatibility between the mother and baby, the commonest type being rhesus incompatibility. In this condition a rhesus-negative mother’s immune system has already been sensitized to produce rhesus antibodies, either by the previous delivery of a rhesus-positive baby, a miscarriage or a mismatched blood transfusion. These antibodies cross over into the fetal circulation and attack any of the fetal red blood cells which contain the rhesus antigen on their surface (that is, if the baby happens to be rhesus positive), causing the red cells to break open haemolysis.
Haemolytic disease of the newborn is a condition where excessive destruction of red blood cells occurs in the fetus and newborn due to antibodies produced by the mother. It is most commonly caused by Rhesus (Rh) incompatibility. This happens when a mother with Rh-negative blood, who has been exposed to Rh-positive blood through previous births, miscarriages, abortions, or amniocentesis, becomes pregnant with a baby having Rh-positive blood. However, the occurrence of haemolytic disease has become rare since the implementation of routine preventive treatment for Rh-negative women during pregnancy.
In mild cases of the disease, the newborn baby may experience slight jaundice within the first 24 hours of life, resulting from an excess of the bile pigment bilirubin in the blood, along with mild anemia. However, in more severe instances, the bilirubin levels in the blood may rise to dangerous levels, posing a risk of kernicterus—a type of brain damage. Severely affected babies can exhibit marked anemia while still in the uterus, leading to swelling (hydrops fetalis) and, in many cases, stillbirth.
In mild cases, no treatment is required. However, in more severe situations, the goal is to deliver the baby before the anemia becomes critical, typically inducing labor between 35 to 39 weeks of gestation. If delivering the baby is not safe at that stage, fetal blood transfusions might be necessary to address the condition.
Following birth, phototherapy, a light treatment that converts bilirubin in the skin into a water-soluble form for easier excretion from the body, can be used to reduce jaundice. In more severe cases, an exchange blood transfusion may be necessary.