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Rh NEGATIVE PREGNANCY Dr shweta

Rh negative pregnancy

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Page 1: Rh negative pregnancy

Rh NEGATIVE PREGNANCYDr shweta

Page 2: Rh negative pregnancy

Contents

Introduction. Pathophysiology. Isoimmunisation. Diagnosis. Management. Effect on fetus.

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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.

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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.

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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.

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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.

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contd Usual fetomaternal Hge- <4ml.

If no prophylaxis- sensitization in next pregnancy-16%.

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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.

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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.

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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.

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CORD BLOOD TESTS Blood grouping and typing. Direct Coomb’s test. Bilirubin,Hb and haematocrit to detect

haemolysis,anaemia and jaundice.

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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.

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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.

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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.

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

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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.

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

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FOETAL EFFECT Mild effect-haemolytic anaemia of the

newborn. Moderate-effect-icterus gravis

neonatorum. Severe effect-hydrops foetalis.

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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.

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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).

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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.

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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.

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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.

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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.

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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.

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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.

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TREATMENT OF BABY Phototherapy-with blue light with

protection of eye and genitalia from exposure.

Phenobarbitone. Exchange transfusion.

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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.

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Conclusion

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

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THANK YOU