Maternal-foetal compatibility must be ensured for the development of a healthy foetus. Practically, the rule of compatibility is that there must not be clogging or agglutination between the red blood cells (RBCs) of the donor and the antibodies in the blood of the recipient. Negligence to this rule results in a hypersensitivity reaction that lyse foreign cells. This includes massive hemolysis of the recipient’s red blood cells which leads to systemic shock and kidney failure and then death which is common.
Hence, it is necessary to be cautious of one’s blood type and Rhesus status especially in transfusion and child bearing. Rhesus factor or D antigen,another red blood cell antigen of major medical or clinical importance was first observed in rabbits inoculated with RBCs of Rhesus monkeys. Surprisingly, the antigen produced antibodies that reacted with the RBC of humans. The – or + signs that appear immediately after your blood type is your Rhesus status. Examples; A+ this means that the rhesus antigen is present in the individual with the blood type A. Same goes with B+,AB+, O+
O- this depicts the absence of the rhesus antigen, likewise in A-, B- and AB-
However,unlike the ABO antigen,the rhesus factor can only be sensitized via transfusion and placenta sensitization which occurs during child birth. Rhesus factor is the major cause of erythroblastosis fetalis.
How is erythroblastosis fetalis triggered ?
Erythroblastosis fetalis, hemolytic disease of the newborn occurs when a mother is Rh- while the foetus is Rh+. The RBCs of the foetus find their way into the mother’s circulation and tthe detachment of of the placenta during delivery creates room for foetal blood to enter the mother’s bloodstream as well. Here, the immune system detects the foreign Rh factor on the foetal RBCs, hence is sensitized by producing antibodies and memory cells. The first Rhesus positive child is usually not affected as the reaction comes very late that the child is born before the sensitization completes. However, subsequent foetus will have this hemolytic disease because the immune system of the mother has been sensitized. And the memory cells will keep reminding the system that the foetus is a foreign body and therefore should be attacked. With subsequent pregnancies,the foetus is at risk when the maternal anti rhesus antibodies cross the placenta into the foetal circulation where they bind to foetal RBCs and cause lysis. Symptoms seen in babies with these diseases are enlarged spleen and liver, anaemia and jaundice. However, it is worthy to note that these reactions occur late in pregnancy and therefore can be curbed to avoid subsequent complications.
Prevention is better than cure, you know. Here, a careful insight on the family history is of immense help. If both parents are Rh-, there won’t be any complication as the child will be Rh- too,so free of risk. But if the father is Rh+,the chances of the child’s safety is 50% or 100% depending on the father’s exact genetic make up. So,if there is possibility that the child is Rh+, the mother must be passively immunized by antiserum containing antibodies against the Rh antigen. Such antiserum is RhoGAM, it is introduced into the mother at 28 to 32 weeks and again immediately after delivery to prevent sensitization caused by placenta detachment.
Note that anti-Rh antibody such as RhoGAM must be used for each pregnancy that involves an Rhesus positive foetus. It is ineffective if the mother has been previously or already sensitized by a prior Rh+ foetus or an incorrect blood transfusion. This can be discovered by a serological test.
One should align oneself to the importance of these antigens ,ABO and Rhesus factor when it comes to the issue of blood compatibility.