The Rhesus (Rh) factor is an antigen carried on red blood cells of 83% of the population, these people are said to be Rhesus positive. The 17% of the population who do not have this antigen are said to be Rhesus negative. Those who are Rh positive carry the D antigen.
When there is Rhesus incompatibility between a mother and her fetus, hemolytic disease of the new born may occur. This incompatibility occurs when the mother is Rh negative and her fetus is Rh positive, having inherited the gene for the Rhesus factor from his father.
An individual who is Rh negative does not naturally carry antibodies to the Rhesus factor. If by some means Rh positive red blood cells enter her circulation they alert the immune system and antibodies may be produced in order to destroy the foreign protein.
There is normally no mixing of fetal and maternal blood during pregnancy and labour but when the placenta begins to separate and the chorionic villi tear, the risk of a fetomaternal transfusion increases.
The first encounter may not result in actual antibody formation but the woman will be sensetised; on a second encounter, antibodies are produced in abundance. Once formed, these antibodies are permanent.
Other occasions on which a fetomaternal transfusion may occur are at abortion, amniocentesis, external cephalic version or ante partum haemorrhage.
There are three ways of preventing a woman from producing
· avoiding transfusion of Rh positive blood
· prevention of avoidable fetomaternal transfusion
· administration of anti- D immunoglobulin
Even if a small amount of Rh positive blood introduced in to the circulation of a Rh negative person will result in sensitization. Rh positive blood should never be administered if the individual’s blood group is unknown and whenever possible cross matching should be undertaken prior to blood transfusion.
This will coat the fetal red cells that contain Ag and destroy them before the woman’s immune system has time to recognize the foreign protein and react to it. The immunoglobulin must be given with in 72 hours of the leak if it is to be effective.
The normal dose of anti-D immunoglobulin is 500 IU after delivery or following an abortion which takes place after 20 week’s gestation. In case of earlier abortion, 250 IU is given.
The possible courses of action are:
· To allow pregnancy to continue but to repeat the amniocentesis at intervals in order to assess bilirubin levels. If the bilirubin level rises, intervention may be necessary
· To deliver the fetus if it is dangerous to continue pregnancy
· To administer an intra-uterine transfusion to the fetus in order to prolong life until he is mature enough to survive.
Immediately the baby is born, the cord must be clamped in order to prevent any further Rhesus antibodies from entering the circulation.
Transference of maternal Rh antibodies to the fetus during pregnancy will result in haemolysis and consequently in anemia and jaundice.
The degree of haemolysis and the number of maternal antibodies remaining in his circulation determine the condition of the baby.
This arises when haemolysis is minimal. It causes anemia of slow onset but little jaundice. The liver and spleen are enlarged. The baby’s haemoglobin level must be monitored and if necessary a small transfusion of 30ml packed cells is given.
Haemolysis has been taking place in the fetus and the baby is born with a low haemoglobin level. After delivery the baby can not cope with the large amount of bilirubin from red cell breakdown and he rapidly becomes jaundiced.
Treatment must restore the haemoglobin level, reduce the bilirubin level and remove maternal Rh antibodies.
This condition is one of congestive heart failure due to gross haemolytic anaemia. At birth the baby is extremely pale, has sever oedema and ascites and may be stillborn.
All babies whose mothers have Rh antibodies should be transferred to a eonatal intensive care unit.
In this condition the mother is blood group 0 and the baby is group A or B. The mother has naturally occurring antibodies anti-A anti-B. These are of type Igm and are too large to cross the placenta. If the immune system produces small antibodies (IgG) similar to anti-A and anti-B, these will be able to cross the placenta and become attached to fetal red cells and destroy them. The condition may affect the first born as much as asubsquent child.
The jaundice is usually mild but may appear with in the first 24 hours of life. If this happens, blood must be taken for grouping and coombs’ test. Bilirubin levels are estimated. Treatment depends on the serum biurubin level and its rate of rise.
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