2 Rh IMMUNIZATIONRh haemolytic disease (RHD) is a common condition and affects 1 in 250 live births in Europe and North America although it is much less frequent in other parts of the world such as Asia, where the Rh-negative blood group is uncommon.
3 TRANSPLACENTAL HAEMORRHAGE (TPH) The Rh antigen is limited to the red cell surface and maternal Rh immunization, can, therefore, only take place if fetal red cells cross the placental barrier into the maternal circulation.Occasional breaks in continuity will occur in the placental barrier, during the stress of labour, with consequent admixture of small quantities of maternal and fetal blood.Kleihauer test – citric-phostphate buffer- an elution technique which is capable of detecting very small TPHs of the order of 0.1 ml of fetal blood.
4 DELIVERY:The placenta is subjected to maximal trauma during delivery and it has been deduced that TPH would mainly occur during delivery rather than during the course of pregnancy.
5 ABORTION:TPH occurs after abortion. The risk is greater with induced as compared with spontaneous abortion .TPH of 0.2 ml of fetal blood has been recorded in about 5 percent of abortion.
6 THE NATURAL HISTORY OF Rh IMMUNIZATION The process by which the body responds to an antigen by producing the appropriate antibody is called immunization and there are two types of immunity:a) Humoral immunity – associated with free antibodyb) Cellular immunity – cell bound antibodyRhesus antibodies are humoral antibodies or free antibody1 gm – large, unable to cross the placenta1gG – small, able to cross the placenta andattach itself to Rh positive red cellsleading to haemolytic anaemia
7 IMMUNE RESPONSES ARE: a) Primary – first response to an antigen b) SecondaryFor the D-antigen, the primary response appears afterseveral weeks and is IgM.When exposed to the D- antigen for the second time asecondary immune response takes place. If alreadyprimed, antibody will appear within a few days or ifantibody is already present, the strength will increaserapidly and the antibody will change its character toIgG.Generally, the quantity of antigen required to produce a secondaryimmune response is very much smaller than that required toinitiate the primary immune response.
8 THE IMMUNIZING PREGNANCY: The first pregnancy is usually unaffected by RHD because TPHs of sufficient magnitude to induce primary immunization do not usually take place until delivery.Only about 5 percent of all Rh-negative mothers form antibodies.
9 Reasons:A TPH of sufficient magnitude to induce primary immunization may not take place.50 percent of individuals do not produce Rh antibodies even after a massive TPHReduced chance of immunization if there are no complications of delivery.Vast majority of TPHs after delivery are small and are in the order of about 0.1 ml of fetal blood, but about 0.2% of mothers have larger bleeds of 30 ml or more. The risk of Rh immunization is proportional to the size of the TPH.
10 ABO INCOMPATIBILITYWhen the mother and the baby are ABO incompatible such as an O mother and an A baby any fetal red cell (Group A) entering the maternal circulation (Group O) is destroyed, in an exactly similar way to that occurring in an ABO incompatible blood transfusion.
11 PREGNANCY:TPH does occur during pregnancy but is much less common than following delivery. Most of the bleeds occur in the last trimester when the placenta is degenerating and the barrier may become a little more pervious.
12 COMPLICATIONS:Anything which damages the placenta is liable to increase the risk of TPH. The incidence and magnitude of TPH is therefore increased in: Caesarean section Complicated and difficult deliveries External version Toxaemia Hypertension Amniocentesis
13 ABORTIONS: Rh IMMUNOGLOBULIN Abortions with a gestational age above 14 weeks carry a risk of inducing immunization.Rh IMMUNOGLOBULINThe prevention of RHD is dependent on the fact that, D-positive TPHs can be neutralized by passively administered anti-D antibody (Rh immunoglobulin) taken together with the realization that Rh priming is usually due to a TPH occurring at delivery in the preceeding D-positive pregnancy.
14 FAILURE RATE: About 1 percent of Rh-negative women become immunized after two D-positive pregnancies despitetreatment with Rh immunoglobulina) Those already primed, even though overt antibody is undetectable by present techniques.b) Large TPHs before delivery e.g. epileptic or eclamptic patients.c) Extreme sensitivity to the D-antigen: thus small bleeds will produce primary response.d) Large TPHs after delivery more than the amount that can be taken care of by standard dose of immunoglobulin.e) Failure to give the immunoglobulin – patients who slip through the net.
15 AMNIOCENTESIS AND AMNIOTIC FLUID ANALYSIS. When erythroblastosis fetalis is severe, the amniotic fluid becomes bright yellow from the bilirubin derived from fetal haemolysis. Amniotic fluid bilirubin concentration can be quantified by spectrophotometry by assessing the change in optical density at 450nm ( OD 450)Amniocentesis is started after 24 weeks under continuous ultrasound control.
16 COMPLICATIONS FOLLOWING INTRAUTERINE TRANSFUSION: 1. Premature labour2. Pre-labour ruptured membrane3. Fetal haemorrhage4. Fetal bradycardia5. Failure to obtain a sample6. Increase in maternal iso immunization by inducing feto-maternal haemorrhage
17 MANAGEMENT OF RED BLOOD CELL ISOIMMUNIZATION Pregnancies complicated by clinically relevant maternal RBC antibodies are managed in regional blood transfusion centers and fetal medicine units. These centres maintain expertise in the diverse clinical presentation of these cases, follow them non-invasively and perform invasive tests or therapy as the case requires.
18 Cont. a) Maternal antibody quantification b) Paternal blood group genotypingc) Fetal blood group genotypingd) Ultrasound assessmente) Amniotic fluid spectrophotometryf) Fetal blood samplingg) Fetal blood transfusion
19 ULTRASOUND ASSESSMENT: The severely anaemic fetus is readily identifiable on scan by the detection of skin oedema, ascites, pleural or pericardial effusions, cardiomegaly and an oedematous placenta.Fetal heart rate changes have been noted with severe anaemia. A sinusoidal pattern with the loss of normal baseline variability of the CTG is highly suggestive of severe aneamia.