1. Rh NEGATIVE PREGNANCY

2. The individual having the antigen on the human red cells is called Rh positive and in whom it is not present is called Rh negative. Incidence : In India 5% to 10% South India 5% North India 10% In general 60% of Rh Positive men are heterozygous and 40% are homozygous Overall Rh Negative women have the chance of having an Rh positive fetus is 60% irrespective of father’s genotype.

3. Mechanism of antibody formation in the mother Antibody formation occurs by iso immunization, which is defined as the production of immune antibodies in an individual in response to an antigen derived from another individual of the same species provided first one lacks the antigen. This occurs in two stages Sensitisation Sensitisation Immunisation Immunisation In ABO - blood groups naturally occurring anti-A, anti-B antibodies are present in the serum. But in Rh group there is no such naturally occurring antibodies. So for the first time when Rh positive fetal red cells enter mother’s blood, they remain in the circulation for their remaining life span. There after they are removed by the reticulo-endothelial tissues and are broken down with liberation of antigen which triggers the iso immunization. Since it takes as long as 6 months for detectable antibodies to develop the immunization in 1st pregnancy is unlikely. If the feto-maternal bleed is less than 0.1 ml the anti body production sufficient to produce iso immunization is unlikely

4. The main effect of Rh antibodies is on the baby in the form of hemolytic disease of the new born. If the baby is Rh positive and the mother is Rh negative, in the sensitized mother the antibody becomes attached to the antigen on the surface of fetal erythrocytes. The effected fetal cells are rapidly removed from the circulation by the RE system. Depending upon the degree of agglutination and destruction of the fetal red cells various types of fetal hemolytic diseases appear. They are Congenital anemia of new born Congenital anemia of new born Icterus gravis Neonatorum Icterus gravis Neonatorum Hydrops fetalis Hydrops fetalis

5. Congenital anemia of new born: It is the mildest form of the disease where hemolysis is going on slowly. The destruction of the red cells continues up to six weeks after which the antibodies are not available for hemolysis. So the neonate may require blood transfusion for its survival. Icterus gravis Neonatorum : The baby is born alive without evidence of jaundice but soon develops it with in 24 hrs of birth. If Bilirubin level rises to the critical level of 20 mg/100ml then Bilirubin crosses the blood brain barrier to damage the basal nuclei of the brain producing clinical manifestations of Kernicterus and may require exchange transfusion. Hydrops fetalis: Excessive destruction of the fetal RBC leads to severe anemia, tissue anoxaemia and metabolic acidosis. These have got adverse effects on the fetal heart, brain and on the placenta. Hyperplasia of the placental tissue occurs in an effort to increase the transfer of oxygen. Hyperplasia of the placental tissue occurs in an effort to increase the transfer of oxygen. As a result of fetal anoxaemia there is damage to the liver leading to hypoproteinemia which is responsible for generalized oedema ascites and hydrothorax. Fetal death occurs sooner or later due to cardiac failure. Baby is either still born or macerated and even if it is born alive dies soon after. As a result of fetal anoxaemia there is damage to the liver leading to hypoproteinemia which is responsible for generalized oedema ascites and hydrothorax. Fetal death occurs sooner or later due to cardiac failure. Baby is either still born or macerated and even if it is born alive dies soon after.

6. Affection in the mother Increased incidence of pre-eclampsia, Polyhydramnios Big size of the baby Hypofibrinogenemia due to prolonged retention of dead fetus. Maternal syndrome or mirror syndrome with generalized oedema proteinurea and pruritis. Repeated still births Repeated abortions.

7. Past history History of previous transfusions History of previous normal fetus and in Subsequent pregnancies fetus presenting as hemolytic diseases of new born. History of receiving Anti D after delivery Signs Generalised oedema PIH Jaundice may be present Pruritis On abdominal examination Polyhydramnios may be present. Size of the uterus may be more than the expected. In case of a intra-uterine death of fetus FHS absent.