RH INCOMPATIBILITY.pptx. Rh

RH INCOMPATIBILITY

1. RH INCOMPATIBILITY PRESENTED BY – RIYA KANDWAL BSC (N) VII SEM

2. INTRODUCTION OF RH FACTOR The resus factor gets its name from experiments conducted in 1937 by scientists KARL LANDSTEINER and alexander s. weiner . Their experiments involved rabbits which, when injected with the RHESUS monkey’s red blood cells, produced an antigen that is present in the red blood cells of many humans.

3. The genotype is determined by the inheritance of 3 pairs of closely linked allelic genes situated on chromosomes 9 named as D/d C/c E/e ( fisher- race theory )

4. RH- BLOOD GROUPING SYSTEM First demonstrated in rhesus monkey. Blood groups are Classified as Rh positive and Rh negative. The Rh factor, Rh- usually refers specifically to the presence or absence of antigen – D . There are two alleles, or genetic variants, of the antigen : D and d. A person who is Rh- has two recessive traits, dd. Anyone who has at least one D- DD or Dd – is Rh+.

5. Rh Type and Pregnancy A person’s Rh type is generally most relevant with respect to pregnancies. If the pregnant woman and her husband are Rh negative, there is no reasons to worry about Rh incompatibility. If she is Rh negative and her husband is Rh positive, the baby will inherit the father’s blood type, creating incompatibility between mother and her fetus. If some of the fetal blood gets into mother’s blood stream, her body will produce antibodies.

6. These antibodies could pass back through the placenta and harm the developing baby’s red blood cells, causing very mild to very serious anemia in the fetus . DEFINITION : Rh incompatibility is a condition which develops when a pregnant woman have a rh negative blood and the baby in her womb has Rh positive blood. Develops Rh incompatibility Also called “ hemolytic disease of newborn’s . ”

7. Causes Of Rh Incompatibility mother’s Rh negative blood : when th e Rh negative mother carries on Rh positive fetus. previous exposure to rh negative blood : through previous pregnancy, blood transfusions, or other. Fetal blood cells enter mother’s blood- stream : during pregnancy, childbirth , or medical procedures.

8. RH SENSITIZATION

9. TYPES OF ANTIBODIES TYPES OF ANTIBODIES ARE FORMED : IGM : this type of antibody is the first to appear in the maternal circulation and agglutations red cells containing D when suspended in saline. Igm being larger molecules cannot pass through the placental barrier and is not harmful to the fetus. IgG : it is also called incomplete or blocking antibody. It will agglutinate the red cells containing D only when suspended in 20% albumin. Because of its small molecular size, it can cross the placental barrier and cause damage to the fetus. It appears at the later period than does the IgM antibody. It is important to recognize the preponderance of one or the other type of antibody than the actual level of the titer.

10. CLINICAL MANIFESTATION

11. Pathophysiology of rh incompatibility In first pregnancy Father RhD + First newborn Rhd + safe but mother Mother RhD – RhD – is now sensitized to Rh-D Fetus RhD + antigen fetal – maternal blood transfer during labour

12. Rapid production of IgG anti D by mother Maternal IgG anti D crosses placenta IgG anti D attaches to fetal RBC and marks them for destruction Fetal or newborn hemolytic anemia Increased bilirubin , CNS damage (Kernicterus) ,death IN SECOND PREGNANCY

13. Investigation for Rh incompatibility Blood test : blood testing for Rh and ABO grouping should be done at the first antenatal visit . If the woman is found Rh negative ,Rh grouping of the husband is to be done . If husband is found to be Rh-positive ,further investigation are to be carried out. Obstetric history : If woman is a primigravida with no previous history of blood transfusion ,it is quite unlikely that the baby will be affected. In a parous woman ,a detailed obstetric history has to be taken. Example: History of stillbirth ,neonatal death due to jaundice ,etc . Also enquire about the administration of anti–D immunoglobulin following delievery or abortion.

14. Antibody detection : In all cases of Rh negative woman irrespective of blood grouping and parity ,IgG antibody is detected by indirect Coombs test. Quantitative estimation of IgG antibody should be done at weekly interval. Sudden rise in the titer from 1:8 to 1:256 is very much suggestive of fetal affection. Some centers consider the titer of 1:6 or antibody level >10 IU/ml as a critical one. Critical titer means anti-D antibody level that causes hydrops fetalis . Doppler ultrasound : Serial Doppler study of middle cerebral artery (MCA) peak systolic velocity (PSV) is the main predictor for fetal anemia. A value>1.5 multiples of the median ( MoMs ) for the corresponding gestational age predicts moderate to severe fetal anemia.

15. Amniocentesis : Amniocentesis and estimation of bilirubin in the amniotic fluid by spectrophotometer predict the severity of fetal hemolysis. The optical density of the liquor containing the bilirubin pigment is observed at 250-700 nm wavelength. In the presence of bilirubin ,there is ‘deviation bulge’ peaking at 450nm wavelength. For any given period of gestation, the height Of spectrophotometric ‘deviation bulge’ at OD450 falls within one of the three zones when plotted on liley’s chart. Interpretations: Liley’s zone 1(low zone): The fetus is unlikely to be affected and the pregnancy can be continued to term.

16. 2. Liley’s zone 2(mid zone) : Repeat amniocentesis by 2 weeks Value upward Cordocentesis hematocrit <30% Intrauterine transfusion to raise hematocrit 40-45%. Preterm delivery after 34 weeks. 3. Liley’s zone 3( high zone) : Fetus is severely affected and death is imminent. Pregnancy >34 weeks Delivery . Pregnancy <34 weeks Cordocentesis Hematocrit <30% Intrauterine transfusion to raise hematocrit 40-45% . Preterm delivery after 34 weeks .

17. Prevention To prevention active immunizations : Rh anti-D immunoglobulin (IgG)300 microgram is administered. IM to the mother during pregnancy . 72 hours following delivery or abortions. To prevent or minimize fetomaternal bleeding : use precautions during cesarean section to prevent blood spilling into peritoneal cavity and while removing placenta. Prophylactic ergometrine with delivery of the anterior shoulder should preferably be withheld.

18. Amniocentesis should be done after sonographic localizations of the placenta to prevent its injury. Avoid external versions in Rh – negative pregnancy. Manual removal of placenta should be done gently. Avoid abdominal palpation in case of placental abruption ( abruptio placentae ) To avoid mismatched transfusions .

19. ANTI –D PROPHYLAXIS

20. PLAN OF DELIVERY Unimmunized mothers : In cases where there is no detectable antibody found during pregnancy, an expectant is followed till term . Tendency of pregnancy to overrun the expected date should not be allowed . Immunized mothers : As mentioned previously, whenever there is evidence of hemolytic process in the fetus in utero , the patient should be shifted to an equipped center specialized to deal with Rh problems. An intensive neonatal care unit, arrangements for exchange transfusion and an expert neonatologist are the basic requirements to tackle the affected babies.

21. Delivery is to be done in all cases of immunized mothers with evidences of hemolysis in utero. The following factors are to be considered as to when terminate the pregnancy : Previous history of stillbirth with father being homozygous. Sudden rise in maternal antibody titer The optical density difference at 450 nm wavelength as plotted on Liley’s chart Doppler and ultrasound features of fetal affection .

22. In mild affection , the pregnancy may be continued up to 38 weeks and then termination is to be done . In severe affection ,It is reasonable to terminate the pregnancy around 34 weeks after maternal steroid administration . In every case of premature termination before 34 weeks ,it is desirable to confirm the fetal lung maturation by measuring the L:S ratio in the amniotic fluid. In a specialized center where there is severe affection before 34weeks ,intrauterine fetal transfusion (intraperitoneal or intravascular)is done to continued pregnancy beyond 34 weeks.

23. Methods of delivery : Amniotomy ( low rupture of the membranes) is quite effective , if termination is done near term. Vaginal prostaglandin gel could be used to make the cervix ripe. Cesarean section : In cases when termination has to be done prematurely (say 34-37 weeks ),the cervix will be unfavorable and considering the severity of affection and urgency of termination ,cesarean section is a safe procedure .

24. Care during delivery : Vaginal delivery : Careful fetal monitoring is to be done to detect at the earliest , evidences of distress Prophylactic ergometrine during second stage should be withheld Gentle handling of the uterus in the third stage To take care of postpartum hemorrhage .

25. Cesarean section : To avoid spillage of blood into the peritoneal cavity Routine manual removal of placenta should be withheld. Clamping the umbilical cord: In either methods ,the cord is to be clamped as quickly as possible to minimize even minute amount of antibody to cross to the fetus from the mother. The cord should be kept long (15-20cm ) for exchange transfusion ,if required . Collection of cord blood for investigation : cord blood sample is to be taken from the placental end of the cut cord . The cord should not be squeezed to prevent contamination

26. with Wharton’s jelly . About 5ml ,of blood (2ml oxalated and 3ml ,clotted ) should be collected for the following tests: Clotted blood : ABO and Rh grouping ,reticulocyte count ,direct Coombs test and serum bilirubin . Oxalated blood : Hemoglobin estimation and blood smear for presence of immature RBC .

27. EXCHANGE TRANSFUSION IN THE NEWBORN Exchange transfusion is a life saving procedure in severly affected hemolytic disease of the fetus and newborn (HDFN). With the advent of wider use prophylactic anti – D immunoglobulin. Less and less problem babies are born and through exchange transfusions, the incidence of kernicterus has also been reduced. Indications : rh positive with direct coomb’s test positive babies having Cord blood bilirubin level more than 4 mg /dl and hemo -globin level is less than 11g /dl . Rising rare of bilirubin is over 1 mg / dl/ hour despite phototherapy.

28. Total bilirubin level 20 mg /dl or more. Objectives: to stop hemolysis, and bilirubin production. to correct anemia and to improve congestive cardiac failure of the neonates. To remove the circulatory antibodies. To remove sensitized RBCs. To eliminate the circulatory bilirubin production. While about 80 -90 % of the fetal blood is exchanged during the procedure, transfusions of Rh – negative blood cannot alter the Rh – factor of the baby’s blood. The replacement temporarily help to tide over the crisis from anemia and hyperbilirubinemia for about 2 weeks. Thereafter, the baby is quite capable to get rid of the maternal antibodies by protecting sufficiently his own Rh-positive blood.

29. Nature and amount of blood transfused – Blood for exchange should be Rh –Negative whole blood with the same blood ABO grouping to that of the baby , otherwise group ‘O’ . The blood should be cross matched with the mother’s serum or with the infant’s serum . The blood should be collected relatively fresh (<7days old ). The amount is about 160mL/Kg body weight of the baby. Adjuvant therapy : Phototherapy : phototherapy is to be continued for 24 hours . Phototherapy (blue or blue green light of 420-470 nm wavelength ) degrades bilirubin by photo-oxidation and structural isomerization ( lumibilirubin ). Bilirubin is converted to less toxic polar isomer .these products are water soluble and therefore readily excreted in the bile and urine . Ultraviolet light should be screened out and the baby’s eyes should be protected by dark glasses .

30. 2) Photochemical reactions convert bilirubin to less toxic and water-soluble polar isomer or to lumirubin. 3) Antibiotics should be administered for 3-5 days .