Haemolytic Disease of Newborn in Hematology Aspect

Hematology

1. HDFN DR AHMAD ARIF CHE ISMAIL TRANSFUSION MEDICINE SPECIALIST HRPZ ii

2. CASE STUDY G2P1 @ 32w POG, late booker blood group 0 RhD –ve What do you want to know?

3. CASE STUDY CONT Antibody screening +ve Antibody identification – antiD detected AntiD titre 1: 1024 Should start RhIg? When to repeat antibody titre? How frequent? Who to refer? What else to do?

4. HDFN - OUTLINE INTRO CAUSES ANTEPARTUM POSTPARTUM TREATMENT

5. INTRO ASH Hemolytic disease of the fetus and newborn (HDFN) affects 3- 80/100000 patients per year It is due to maternal blood group antibodies that cause fetal red cell destruction

6. INTRO This process leads to fetal anemia, and in severe cases can progress to edema, ascites, heart failure, and death.

7. INTRO Late 1960s – HDFN was a common neonatal problem by Rh(D) alloimmunization Associated with morbidity & mortality Early 1970 – introduction Rh Immune Globulin (Rh Ig or anti-D) Reduced D alloimmunization by 90% Prevalence of Rh negative in Msia??

8. AS FETUS In pregnancy – placenta serves as barrier between mom & fetal circulation

9. During delivery /abd trauma 🡪placenta separated from uterus 🡪 RBC escape into mom circulation (FMH)🡪RBC carry diff ag 🡪 stimulate IR 🡪 IgG ab produced -🡪 subsequent pregnancy 🡪IgG ab cross placenta 🡪 ab bind to fetal ag 🡪 RBC destruction by macrophages in fetal L/S 🡪indirect bilirubin across placenta🡪bilirubin excreted by mom liver 🡪more destruction hence baby more anemic 🡪 L/S enlarged as erythropoeisis ++ 🡪untreated, heart failure 🡪HF

10. AS NEONATE After delivery , RBC destruction cont 🡪 bilirubin released (previously in utero, mom liver help to excrete ) 🡪 newborn liver unable to conjugate ID bilirubin 🡪 binding capacity to albumin exceeded 🡪 bilirubin binds to tissues 🡪jaundice

11. FETUS , HDFN is caused by hypoxic effect of anemia During pregnancy , bilirubin crosses placenta & removed by mother’s liver NEWBORN , HDFN is caused by toxic effects of anemia & hyperbilirubinaemia In newborn because of liver immaturity, plasma bilirubin will increased

12. HDFN IMMUNE MEDIATED DESTRUCTIION Antibodies causing HDFN – D/ABO/other ab Passive transfer of IgG is most active in third trimester IgG autoantibodies can also cause HDFN D antigen is extraordinarily immunogenic & induce high affinity anti-D IgG- major cause of HDFN

13. GOOGLE BBG

14. ANTEPARTUM MANAGEMENT All pregnant women should have testing performed a)Blood grouping (ABO, RhD) b)Antibody screening Prevention of alloimmunization a)Primary b)Secondary

15. POTENTIALLY SENSITISING EVENTS IN PREGNANCY Amniocentesis, chorionic villus biopsy and cordocentesis Antepartum haemorrhage/Uterine (PV) bleeding in pregnancy External cephalic version Abdominal trauma (sharp/blunt, open/closed) Ectopic pregnancy Evacuation of molar pregnancy Intrauterine death and stillbirth In‐utero therapeutic interventions (transfusion, surgery, insertion of shunts, laser) Miscarriage, threatened miscarriage Therapeutic termination of pregnancy Delivery – normal, instrumental or Caesarean section Intra‐operative cell salvage

16. All pregnant women should have testing performed a)Blood grouping (ABO, RhD) b)Antibody screening Prevention of alloimmunization a)Primary b)Secondary

17. PREVENTION OF HDFN Primary prevention Focuses on prevention of maternal alloimmunization in the first pregnancy. Policy by transfusion services to provide compatible red cell transfusions to females of child bearing potential.

18. SECONDARY PREVENTION RhD immune globulin (RhIg) is available Prevent naïve RhD-negative immune systems from synthesizing anti-D antibody after exposure to small amounts of RhD antigen The risk of an RhD-negative mother becoming allosensitized can be reduced to from 16% to 0.1% by the appropriate administration of RhIg. (M.Delaney, 2015 )

19. RhIg is typically administered at 2 time points during pregnancy. a)The first dose at 28 weeks gestation b)The second dose after delivery of an RhD-positive infant. The 28 week dose reduces the rate of allosensitization to RhD from 1.5% (antenatal administration only) to 0.1%.

20. MANAGEMENT OF ALLOIMMUNIZED MOTHER – DAMAGE CONTROL Antibody titre need to be monitored 1:16-32 are commonly used to indicate critical level At 16-24 weeks, or when a critical antibody titer is reached, fetal anemia is monitored using Middle cerebral artery (MCA) Doppler velocity measurements every 2 weeks Weekly fetal monitoring eg ultrasound and fetal heart rate

21. If fetal anemia becomes moderate to severe as indicated by Doppler ultrasound measurements exceeding 1.5 Invasive testing via cordocentesis is done to determine fetal hematocrit. If the fetus has not reached an acceptable gestational age for delivery, and the hematocrit level is 30%, intrauterine transfusion is usually indicated

22. POSTPARTUM MANAGEMENT OF HDFN

23. MONITORING OF NEWBORN Intrauterine transfusion suppress fetal erythropoiesis Very few require postpartum exchanged transfusion However late anemia is common Neonates need follow up with monitoring hemoglobin, FBP, reticulocyte count & bilirubin

24. HDFN TREATMENT Phototherapy – oxidized unconjugated bilirubin, excreted in urine IVIg – control the hemolysis Exchange transfusion if phototherapy fail

25. CONCLUSION Although HDFN can be fatal, advances in diagnosis & treatment & prevention has made it controllable Postpartum management includes treatment of hyperbilirubinaemia & anemia Exchange transfusion , IVIg and intensive phototheraphy among available

26. IKLAN

27. B LOOD DONATION RATE DEVELOPED COUNTRY 5-8% MALAYSIA 2.2% (22 per 1000) KELANTAN 1.7% (17 per 1000) HRPZ STAF < 2% WHY 3