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Does Rh incompatibility cause any problems?

Q: Can a female having Rh negative marry a male having Rh positive? Will it cause any problem during child-birth?

A:The Rh (rhesus) factor is a protein (antigen) present on the surface of red blood cells (RBCs). As it was first discovered in the rhesus monkey, it has been so named. Individuals carrying this antigen are called Rh-positive (Rh+) blood group type while those lacking it are Rh-negative (Rh-). Rh incompatibility (or Rh disease) is a state in which a woman with Rh-negative blood group is exposed to Rh-positive RBCs leading to the formation of antibodies against this protein (called Rh antibodies). This process of Rh sensitisation can occur when an Rh-negative woman is carrying an Rh-positive baby or if an Rh-negative woman receives blood transfusion containing Rh-positive cells. In either case, her immune system is exposed to the Rh antigen (which is ‘foreign’ to her body) and begins producing Rh antibodies. The problem of Rh incompatibility is of clinical importance only in a pregnant woman or if blood transfusion is required. These circulating antibodies in a woman’s blood are otherwise harmless. Rh incompatibility can commonly cause haemolytic transfusion reaction (HTR) in the woman (when she receives Rh+ blood) or haemolytic disease of the newborn (HDN) in which the baby’s red cells are destroyed resulting in anaemia and jaundice. During pregnancy and delivery, red cells from the baby enter the mother’s circulation (feto-maternal haemorrhage). In most pregnancies the transplacental haemorrhage is less than 0.1 ml but women can get sensitised as a result of this small undetectable fetomaternal haemorrhage. If the exposure is significant, the mother gets sensitised and begins to produce antibodies. HDN results as once these antibodies are made in the mother, they can cross the placenta into the developing baby’s circulation and destroy the baby’s RBCs, which are Rh-positive leading to anaemia and jaundice in the baby. Delivery is the usual time when sensitisation occurs, and thus first-born babies are usually unaffected, as antibodies have not yet formed in the mother. The clinical features of HDN depend on the titre (levels) and affinity of maternal anti-D antibodies. In most cases the baby may have severe anaemia, jaundice, oedema and hepatosplenomegaly but rarely in severe cases, the baby may develop hydrops foetalis, which is a fatal condition. The diagnostic evaluation includes maternal prenatal ABO and Rh typing, and an antibody screen. Depending on the results of the antibody screen, maternal antibody titres, and paternal and/or fetal RBC phenotyping are performed. If fetal RBC express the antigen against which maternal alloimmunisation has occurred, the pregnancy is then followed by measuring serial maternal antibody titres and abdominal sonograms. Following birth, there is usually the presence of erythroblasts, high reticulocyte count and a positive direct antiglobulin test (DAT) in cord blood and a positive indirect antiglobulin test (IAT) in maternal blood. Most institutions give human anti-D immune globulin (Rh IgG) antenatally to Rh-negative pregnant women. If a woman has been already sensitised, she needs to get the antibody titres estimated and be closely monitored during pregnancy. Babies born to such mothers too may require specialised neonatal care. Pregnant mothers should have regular indirect antiglobulin tests. As a guide, anti-D antibody levels < 0.2 mg/ml require no action while higher levels require action; levels > 2.0 mg/ml typically are associated with severe disease. Prevention is now carried out with anti-D Ig (intramuscular within 72 hours of delivery) in all Rh-negative mothers giving birth to an Rh-positive child. A Kleihauer test for foetal haemoglobin can be used as a guide for the dose of anti-D Ig to be administered.

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