Rh negative pregnancy

1. Rh NEGATIVE
PREGNANCY
Dr shweta

2. Contents
 Introduction.
 Pathophysiology.
 Isoimmunisation.
 Diagnosis.
 Management.
 Effect on fetus.

3. INTRODUCTION
 Rh factor discovered by Landsteiner in
1937.
 Protein antigen of red cell membrane.
 5% of pregnancies are Rh-ve.
 Inherited as Mendelian dominant.
 common cause of perinatal mortality in
babies of Rh-ve mothers.

4. PATHOPHYSIOLOGY
 Mother is Rh-ve with a Rh+ve foetus.
 Mother is having anti Rh antibodies.
 Antibodies cross placenta to foetus.
 Foetal Rh+ve red blood cells get
hemolysed.
 Foetus suffers from severe anaemia
leading to cardiac failure,oedema and
death.

5. CAUSES FOR ISOIMMUNISATION
OF THE MOTHER
 Previous Rh+ve fetus with isoimmunisation
due to foeto-maternal haemorrhage.
 May be full term delivery, abortion,
ectopic or partial mole.
 Previous Rh+ve blood transfusion.

6. ISOIMMUNISATION
 Cause-foetomaternal haemorrhage.
 Maternal blood produces large number of
antibodies in response to small amount of
foetal blood.
 Amount of foetal blood required to cause
isoimmunisation-0.1ml.
 Antibodies thus formed in maternal blood
stays lifelong.

7. contd
 Usual fetomaternal Hge- <4ml.
 If no prophylaxis- sensitization in next
pregnancy-16%.

8. DIAGNOSIS
 Routine blood grouping and typing for all
antenatal mothers on 1st
visit.
 If Rh-ve-, husband’s blood group.
 If negative-normal pregnancy.
 If positive-indirect Coomb’s test to look for
isoimmunisation at 24 weeks.
 If negative for antibodies-treat as
nonisoimmunised Rh-ve pregnancy.

9. INDIRECT COOMB’S TEST(ICT)
 Done in Rh-ve antenatal mothers with a
Rh+ve husband.
 Timing-24 weeks.
 Detects incomplete IgG antibodies which
can cross placenta.
 Done with Coomb’s serum containing
antiglobulin antibodies.

10. MANAGEMENT OF ICT-VE
 Anti D prophylaxis-at 28 weeks.
 After delivery if needed.
 Prevent anaemia.
 Arrange donors before delivery.
 Ensuring availability of blood in bank.
 Quick clamping of cord.
 Send cord blood for testing.
 Neonatal care facility.

11. CORD BLOOD TESTS
 Blood grouping and typing.
 Direct Coomb’s test.
 Bilirubin,Hb and haematocrit to detect
haemolysis,anaemia and jaundice.

12. ANTI D PROPHYLAXIS
 Anti D immunoglobulin is administered to
neutralise the Rh+ve blood which enters maternal
circulation.
 Sensitisation in next reduced to 1.6% compared to
16% if not given.
 These antibodies disappear from blood within
some time.

13. TIMING
 Within 72 hours of delivery if baby blood
group is Rh+ve and DCT-ve.
 After 1st
trimester pregnancy loss.
 After invasive procedures-
amniocentesis,chorionic villus
sampling,cordocentesis.
 Antenatal-at 28 weeks.
 Also in 2nd
,3rd
trimester APH,ECV.

14. DOSE AND ROUTE
 Route-intramuscular injection.
 Dose-300µgm of anti D immunoglubulin.
 Neutralises 15ml of foetal RBC or 30ml of
blood.
 Higher dose required for larger FMH.
 Assessed by Kleihauer Betke test.

15. LARGE FMH
 Traumatic delivery.
 Abruption.
 Manual removal of placenta.
 Stillbirth,IUD.
 Twins.
 Hydrops fetalis.

16. KLEIHAUER BETKE TEST
 To assess amount of FMH.
 Acid elution test which detects foetal
haemoglobin.
 Amount of foetal blood in ml=
maternal blood vol x maternal hct X KB
cells/ fetal hct.

17. NONRESPONSE
 Immunologic nonresponder.
 Co-existing ABO incompatibility.
 Insufficient sensitising volume.

18. FOETAL EFFECT
 Mild effect-haemolytic anaemia of the
newborn.
 Moderate-effect-icterus gravis
neonatorum.
 Severe effect-hydrops foetalis.

19. CONGENITAL HAEMOLYTIC
ANAEMIA
 Anaemia develops slowly in first few
weeks.
 Jaundice is not evident.
 Haemolysis continues for 6 weeks after
which antibodies cease to exist.

20. ICTERUS GRAVIS NEONATORUM
 Baby not jaundiced at birth.
 Develops so within 24 hours.
 Effect starts after cord clamping as
excretion through placenta stops and
premature liver enzymes.
 If serum bilirubin >20mg/dl-crosses blood
brain barrier-kernicterus(damage of basal
ganglia).

21. HYDROPS FOETALIS
 Severe haemolysis.
 Anaemia causes heart failure.
 Compensatory placental hyperplasia.
 Liver damage causing hypoprotinemia
 Oedema,hydrothorax,ascites.
 Stillborn or dies soon after.
 USG-Buddha foetus-for scalp edema.

22. MANAGEMENT OF
ISOIMMUNISED PREGNANCY
 Critical titer of Ab-1:16 to 1:32.
 If ICT +ve-titer at 1st
visit-monthly.
 If below critical level-deliver at term.
 If >CL-if mature lungs-delivery.
 If immature lungs-glucocorticoids.
 If below 36weeks-amniocentesis and
bilirubin estimation.

23. Contd
 High titer or multiple isoimmunised
pregnancy or previous history of EF-
amniocentesis,bilirubin estimation at
OD450.
 Plot it in Liley’s graph as zones 1,2 or 3 with
zone 3 as most severe.
 Zone1-deliver at term.
 Zone 2-repeat titer after 2 weeks.
 Zone 3-cordocentesis and IUT.

24. CORDOCENTESIS
 Under USG guidance.
 0.5 to 2 ml collected from umbilical vein.
 Risk of abortion,preterm labour,IUD.
 Test for foetal haematocrit and bilirubin.

25. FOETAL MONITORING
 USG-polyhydramnios/foetal hyrops
though a late finding.
 Amniocentesis and Liley graph plotting-
from 26 weeks.
 Middle cerebral artery peak systolic
velocity-18 weeks onwards.

26. INTRAUTERINE TRANSFUSION
 Based on –Hct,amniocentesis or MCA-
PCV.
 Route-intravascular(portal/umbilical
vein),intraperitoneal.
 Blood-fresh O-ve packed cells.
 Amount based on gestational age or
Nicolaide’s formula.

27. TREATMENT OF BABY
 Phototherapy-with blue light with
protection of eye and genitalia from
exposure.
 Phenobarbitone.
 Exchange transfusion.

28. EXCHANGE TRANSFUSION
 INDICATIONS-cord Hb<10gm/dl
cord bil>5mg/dl
rising rate>1mg/dl/hr
 Aim –to correct anaemia,to remove
antibodies and bilirubin.
 Route-umbilical vein by push and pull
technique.
 Watch for hypoglycemia,
hypocalcimea,metabolic acidosis.

29. Conclusion
 Rh negative pregnancy should be
thoroughly investigated to rule out
adverse effects on the mother and the
fetus.

30. THANK YOU