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    RH Negative Pregnancy: DR Shweta

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    ZaenNias
    This document discusses Rh negative pregnancy and its management. It begins by introducing Rh factor and its role in isoimmunization. When an Rh negative mother is pregnant with an Rh positive baby, fetomaternal hemorrhage can cause the mother's immune system to produce anti-Rh antibodies. These antibodies can then cross the placenta and destroy the baby's red blood cells, causing hemolytic disease of the newborn. The document outlines methods for diagnosis, monitoring, and treatment which aim to prevent isoimmunization through anti-D prophylaxis and manage its effects through techniques like amniocentesis, intrauterine transfusions if needed. Close monitoring and individualized care are important for optimizing outcomes for

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    RH Negative Pregnancy: DR Shweta

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    ZaenNias
    62 views30 pages
    This document discusses Rh negative pregnancy and its management. It begins by introducing Rh factor and its role in isoimmunization. When an Rh negative mother is pregnant with an Rh positive baby, fetomaternal hemorrhage can cause the mother's immune system to produce anti-Rh antibodies. These antibodies can then cross the placenta and destroy the baby's red blood cells, causing hemolytic disease of the newborn. The document outlines methods for diagnosis, monitoring, and treatment which aim to prevent isoimmunization through anti-D prophylaxis and manage its effects through techniques like amniocentesis, intrauterine transfusions if needed. Close monitoring and individualized care are important for optimizing outcomes for

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    This document discusses Rh negative pregnancy and its management. It begins by introducing Rh factor and its role in isoimmunization. When an Rh negative mother is pregnant with an Rh positive baby, fetomaternal hemorrhage can cause the mother's immune system to produce anti-Rh antibodies. These antibodies can then cross the placenta and destroy the baby's red blood cells, causing hemolytic disease of the newborn. The document outlines methods for diagnosis, monitoring, and treatment which aim to prevent isoimmunization through anti-D prophylaxis and manage its effects through techniques like amniocentesis, intrauterine transfusions if needed. Close monitoring and individualized care are important for optimizing outcomes for

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    62 views30 pages

    RH Negative Pregnancy: DR Shweta

    Uploaded by

    ZaenNias
    This document discusses Rh negative pregnancy and its management. It begins by introducing Rh factor and its role in isoimmunization. When an Rh negative mother is pregnant with an Rh positive baby, fetomaternal hemorrhage can cause the mother's immune system to produce anti-Rh antibodies. These antibodies can then cross the placenta and destroy the baby's red blood cells, causing hemolytic disease of the newborn. The document outlines methods for diagnosis, monitoring, and treatment which aim to prevent isoimmunization through anti-D prophylaxis and manage its effects through techniques like amniocentesis, intrauterine transfusions if needed. Close monitoring and individualized care are important for optimizing outcomes for

    Copyright:

    © All Rights Reserved
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    of 30

    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

     PreviousRh+ve fetus with isoimmunisation


    due to foeto-maternal haemorrhage.

     Maybe 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
     Routineblood grouping and typing for all
    antenatal mothers on 1st visit.

     If Rh-ve-, husband’s blood group.

     If negative-normal pregnancy.

     Ifpositive-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
     AntiD 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.

     Theseantibodies 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

     Toassess 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

     Mildeffect-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

     Rhnegative pregnancy should be


    thoroughly investigated to rule out
    adverse effects on the mother and the
    fetus.
    THANK YOU

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