RHESUS ISO-IMMUNIZATION

1. RHESUS ISO-IMMUNIZATION Dr. Ahmed Al Harbi Consultant Obstetrician & Gynecologist

2. TWO WAYS OF BLOOD GROUP 1. Blood group (O, A, B, AB) 2.Rhesus system – C, D and ED antigens When fetal red cells pass across to the maternal circulation, as they do to a greater or lesser extend during pregnancy, sensitization of the maternal immune system to these fetal 'foreign' red blood cells may occur.

3. TWO WAYS OF BLOOD GROUP ABO blood group iso-immunization may occur when the mother is blood group O and the baby is blood group A or B. Anti-A and anti-B antibodies are present in the maternal circulation naturally, and hence do not require prior sensitization in order to be produced. This means that ABO incompatibility may occur in a first pregnancy.

4. TWO WAYS OF BLOOD GROUP In this situation, anti-A or anti-B antibodies pass to the fetal circulation, causing fetal haemolysis and anaemia. ABO incompatibility causes mild haemolytic disease of the baby, but may sometimes explain unexpected jaundice in an otherwise healthy term infant. The D antigen is associated most commonly with severe haemolytic fetal disease. This can only occur if the mother is D rhesus negative and the baby is D rhesus positive.

5. THE AETIOLOGY OF RHESUS DISEASE Rhesus disease does not affect a first pregnancy. The mother must have exposure to D rhesus-positive fetal cells in a previous pregnancy and then developed and immune response that has lain dormant until a following pregnancy of a D rhesus-positive baby. IgG antibodies cross from the mother to the fetal circulation.

6. POTENTIAL SENSITIZING EVENTS FOR RHESUS DISEASE Miscarriage Termination of pregnancy Antepartum haemorrhage Invasive prenatal testing (chorionvillus sampling, amniocentesis and cordocentesis) Delivery

7. POTENTIAL SENSITIZING EVENTS FOR RHESUS DISEASE

8. THE GENETICS OF RHESUS DISEASE Rhesus-negative mother, rhesus-negative father (homozygote) Rhesus-negative mother, rhesus-positive father (heterozygote) Rhesus-negative mother, rhesus-positive father (homozygote)

9. THE GENETICS OF RHESUS DISEASE

10. ANTIBODIES ASSOCIATED WITH HAEMOLYTIC DISEASE ABO Rhesus (C, D, E) Kell Duffy c (know as 'little c') S

11. PREVENTING RHESUS ISO-IMMUNIZATION The intramuscular administration of anti-D immunoglobulins to a mother, preferably within 72 hours of exposure to fetal red cells. The exact dose is determined by the gestation at which sensitization has occurred and the size of the feto-maternal haemorrhage. A Kleihauer is a test of maternal blood to determined the proportion of fetal cells present (relying on their ability to resist denaturation by alcohol or acid); it will allow calculation of the amount of extra anti-D immunoglobulin required should a large transfusion have occurred. Rhesus-negative women are given anti-D at 28 and/or 34 weeks routinely.

12. PREVENTING RHESUS ISO-IMMUNIZATION The intramuscular administration of anti-D immunoglobulins to a mother, preferably within 72 hours of exposure to fetal red cells. The exact dose is determined by the gestation at which sensitization has occurred and the size of the feto-maternal haemorrhage. A Kleihauer is a test of maternal blood to determined the proportion of fetal cells present (relying on their ability to resist denaturation by alcohol or acid); it will allow calculation of the amount of extra anti-D immunoglobulin required should a large transfusion have occurred. Rhesus-negative women are given anti-D at 28 and/or 34 weeks routinely.

13. SIGNS OF FETAL ANAEMIA Polyhydramnios Enlarged fetal heart Ascites and pericardial effusions Hyperdynamic fetal circulation (can be detected by Doppler ultrasound by measuring increased velocities in the middle cerebral artery or aorta). Reduced fetal movements Abnormal CTG with reduced variability, eventually a 'sinusoidal' trace.

14. THE SPECTRUM OF RHESUS DISEASE (Mildest)…  Normal delivery at term; mild jaundice requiring phototherapy Preterm delivery of an anaemic fetus requiring exchange transfusion Delivery of fetus at 34 weeks following fortnightly blood transfusion from 26 weeks gestation. Stillbirth or neonatal death due to rhesus (earlier gestation=worse prognosis) ….(Severest).

15. THE MANAGEMENT OF RHESUS DISEASE 1.The woman is D rhesus negative, as is her partner. There is therefore no chance of rhesus disease. 2.The woman is D rhesus negative and her partner is rhesus positive. She has no D rhesus antibodies and it is either her first pregnancy or she has not had a pregnancy previously affected by D rhesus disease. Monitor atypical antibody levels at booking, 24 and 36 weeks. 3.The woman is D rhesus negative and she has been sensitized to the D rhesus antigen, manifesting itself in an adverse pregnancy outcome. Once a woman is sensitized to the D rhesus antigen, no amount of anti-D will ever turn back the clock. In this situation, there is therefore no role whatsoever for anti-D.

16. BLOOD TRANSFUSION Blood may be given to the baby by a needle introduced through the mother's abdomen. Blood is given either intravascularly (into the umbilical vein or heart) or intraperitoneally. Blood transfused to the fetus must be: - concentrated (Hb normally 22-24g/dL) - cytomegalovirus negative - rhesus negative - irradiated (to reduce the risk of graft-versus-host disease)

17. BLOOD TRANSFUSION If the baby is known to be anaemic or has had multiple transfusions, a neonatologist must be present at delivery should exchange transfusion be required. Blood must therefore always be ready for the delivery. All babies born to rhesus-negative women should have cord blood taken at delivery for a blood count, blood group and indirect Coomb's test.

18. END OF PRESENTATION THANK YOU