Rh NEGATIVE
PREGNANCY
Dr shweta
Contents
 Introduction.
 Pathophysiology.
 Isoimmunisation.
 Diagnosis.
 Management.
 Effect on fetus.
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.
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.
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.
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.
contd
 Usual fetomaternal Hge- <4ml.
 If no prophylaxis- sensitization in next
pregnancy-16%.
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.
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.
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.
CORD BLOOD TESTS
 Blood grouping and typing.
 Direct Coomb’s test.
 Bilirubin,Hb and haematocrit to detect
haemolysis,anaemia and jaundice.
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.
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.
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.
LARGE FMH
 Traumatic delivery.
 Abruption.
 Manual removal of placenta.
 Stillbirth,IUD.
 Twins.
 Hydrops fetalis.
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.
NONRESPONSE
 Immunologic nonresponder.
 Co-existing ABO incompatibility.
 Insufficient sensitising volume.
FOETAL EFFECT
 Mild effect-haemolytic anaemia of the
newborn.
 Moderate-effect-icterus gravis
neonatorum.
 Severe effect-hydrops foetalis.
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.
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).
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.
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.
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.
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.
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.
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.
TREATMENT OF BABY
 Phototherapy-with blue light with
protection of eye and genitalia from
exposure.
 Phenobarbitone.
 Exchange transfusion.
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.
Conclusion
 Rh negative pregnancy should be
thoroughly investigated to rule out
adverse effects on the mother and the
fetus.
THANK YOU

Rh negative pregnancy

  • 1.
  • 2.
    Contents  Introduction.  Pathophysiology. Isoimmunisation.  Diagnosis.  Management.  Effect on fetus.
  • 3.
    INTRODUCTION  Rh factordiscovered 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 isRh-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 OFTHE 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 fetomaternalHge- <4ml.  If no prophylaxis- sensitization in next pregnancy-16%.
  • 8.
    DIAGNOSIS  Routine bloodgrouping 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 72hours 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  Traumaticdelivery.  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  Mildeffect-haemolytic anaemia of the newborn.  Moderate-effect-icterus gravis neonatorum.  Severe effect-hydrops foetalis.
  • 19.
    CONGENITAL HAEMOLYTIC ANAEMIA  Anaemiadevelops 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  Severehaemolysis.  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 titeror 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 USGguidance.  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/foetalhyrops though a late finding.  Amniocentesis and Liley graph plotting- from 26 weeks.  Middle cerebral artery peak systolic velocity-18 weeks onwards.
  • 26.
    INTRAUTERINE TRANSFUSION  Basedon –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-cordHb<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 negativepregnancy should be thoroughly investigated to rule out adverse effects on the mother and the fetus.
  • 30.