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disease of the newborn or rhesus disease
Haemolytic disease of the newborn (HDN) is caused when the blood group of the mother and baby are not compatible. Anti-D prophylaxis and advances in neonatal care have reduced the frequency of HDN to 1 in 21,000 births.
People can belong to one of four blood groups, A, B, AB and O, which are carried on the red blood cells. The other important difference in people’s blood is called rhesus factor, which is also found in the red blood cells. People who are rhesus positive have a substance known as D antigen on the surface of their red blood cells. People who are rhesus negative do not have the D antigen on their blood cells.
During pregnancy and childbirth the rhesus factor D can have an important role to play when a RhD-negative mother is expecting a RhD-positive baby. The placenta acts as a barrier between the red blood cells of the mother and baby. However, sometimes small amounts of the baby’s blood can cross over into the mother’s blood stream.
If any of the blood cells from a RhD-positive baby get into the blood of a RhD-negative woman, she will react to the D antigen in the baby’s blood as though it is a foreign substance and will produce antibodies. This is called ‘rhesus sensitisation’.
As a general rule, the first child that triggers this sensitisation does not suffer any adverse consequences, as it will already have been born by the time antibodies have developed. However, if the woman goes on to become pregnant with a second RhD-positive child, maternal anti-D IgG antibodies cross placenta, attach to RhD antigens on foetal red blood cells (RBC), these RBC are seen as ‘foreign’ by the foetal immune system and destroyed ‘haemolysed’. This is called ‘haemolytic disease of the newborn’.
Haemolytic Disease of the Newborn can be mild but can also lead to jaundice, brain damage or even the death of the child depending on the rate and severity of haemolysis. With further RhD-positive children, the antibody reaction becomes faster and more serious.
HDN may be mild, moderate or severe depending on the rate of haemolysis and the ability of the baby to make new RBCs. This is reflected in the severity of the resulting anaemia and jaundice and further complications.
Anaemia: As RBCs are haemolysed/broken down, the baby responds by trying to make more RBCs very quickly in the bone marrow, liver and spleen to compensate, causing these organs to enlarge (hepatosplenomegaly). An increase in immature RBCs (erythroblasts) is seen (erythroblastosis) with anaemia.
Jaundice: RBC haemolysis releases haemoglobin from the RBC, then converts haemoglobin to bilirubin which may cause jaundice.
• Before delivery this may be mostly removed by the placenta and foetal bilirubin levels may remain low.
• After birth, the neonate’s immature liver is unable to metabolise the increased bilirubin and levels increase leading to jaundice.
Further complications: Depend on the rate, severity and duration of haemolysis and the foetus/neonate’s ability to respond to this.
• Hydrops foetalis – severe HDN leading to swollen foetal tissue (usually fatal in utero or soon after birth).
• Kernicterus – increasing bilirubin (highly neurotoxic) levels may enter the brain to cause death or permanent brain damage in survivors.
For more information about Haemolytic Disease of the Newborn please contact your Healthcare Professional