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    Rhisoimmunization2 191008035506

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    vijetha gmc
    This document discusses Rh isoimmunization, which occurs when an Rh-negative mother is sensitized to Rh-positive fetal red blood cells during pregnancy. This can lead to hemolytic disease of the fetus and newborn in subsequent pregnancies. The key aspects covered are: 1) Rh isoimmunization occurs when an Rh-negative mother is first sensitized during a pregnancy with an Rh-positive baby, followed by the development of IgG antibodies during later pregnancies that can destroy Rh-positive fetal red blood cells. 2) Fetal complications range from mild anemia to severe hydrops fetalis depending on antibody titer levels. Management involves monitoring antibody titers, fetal assessment including Doppler ultrasound, and

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    Rhisoimmunization2 191008035506

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    vijetha gmc
    48 views50 pages
    This document discusses Rh isoimmunization, which occurs when an Rh-negative mother is sensitized to Rh-positive fetal red blood cells during pregnancy. This can lead to hemolytic disease of the fetus and newborn in subsequent pregnancies. The key aspects covered are: 1) Rh isoimmunization occurs when an Rh-negative mother is first sensitized during a pregnancy with an Rh-positive baby, followed by the development of IgG antibodies during later pregnancies that can destroy Rh-positive fetal red blood cells. 2) Fetal complications range from mild anemia to severe hydrops fetalis depending on antibody titer levels. Management involves monitoring antibody titers, fetal assessment including Doppler ultrasound, and

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    rhisoimmunization2-191008035506

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    This document discusses Rh isoimmunization, which occurs when an Rh-negative mother is sensitized to Rh-positive fetal red blood cells during pregnancy. This can lead to hemolytic disease of the fetus and newborn in subsequent pregnancies. The key aspects covered are: 1) Rh isoimmunization occurs when an Rh-negative mother is first sensitized during a pregnancy with an Rh-positive baby, followed by the development of IgG antibodies during later pregnancies that can destroy Rh-positive fetal red blood cells. 2) Fetal complications range from mild anemia to severe hydrops fetalis depending on antibody titer levels. Management involves monitoring antibody titers, fetal assessment including Doppler ultrasound, and

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    48 views50 pages

    Rhisoimmunization2 191008035506

    Uploaded by

    vijetha gmc
    This document discusses Rh isoimmunization, which occurs when an Rh-negative mother is sensitized to Rh-positive fetal red blood cells during pregnancy. This can lead to hemolytic disease of the fetus and newborn in subsequent pregnancies. The key aspects covered are: 1) Rh isoimmunization occurs when an Rh-negative mother is first sensitized during a pregnancy with an Rh-positive baby, followed by the development of IgG antibodies during later pregnancies that can destroy Rh-positive fetal red blood cells. 2) Fetal complications range from mild anemia to severe hydrops fetalis depending on antibody titer levels. Management involves monitoring antibody titers, fetal assessment including Doppler ultrasound, and

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    RH ISO IMMUNIZATION

    RH ALLO IMMUNIZATION

    RH NEGATIVE COMPLICATING
    PREGNANCY
    Rh- antigen
    • Rh- system – LANDSTEINER – 1940
    • Rhesus blood group antigens – C, c, D, E, e
    • Short arm of chromosome 1
    • RH (D) – most immunogenic
    • Person lacking D-antigen called Rh-ve
    • Lewis and Kell
    • 38th day after conception
    • INDIA- incidence =8-10%
    RH ISOIMMUNIZATION = MAJOR CAUSE OF HEMOLYTIC
    DISEASE OF FETUS AND NEWBORN (HDFN)
    PATHOGENESIS

    FETOMATERNAL
    HEMORRHAGE
    FIRST PREGNANCY – SENSITIZING PREGNANCY

    MOST FMH OCCURS DURING DELIVERY

    Weak IgM response

    First baby is not affected


    Fetal effects of isoimmunization –
    non severe
    SUBSEQUENT PREGNANCY – SENSITIZED PREGNANCY

    RH POSITIVE FETUS – FMH occurs

    AMNESTIC IgG RESPONSE

    FETAL CELL HEMOLYSIS


    •Congenital anemia of newborn
    •Hydrops fetalis
    •Fetal Hyperbilirubinemia / ICTERUS GRAVIS NEONATORUM

    OUTCOME WORSENS WITH EVERY PREGNANCY


     Rh Antibodies
    CRITICAL AMOUNT = 0.1 ml
     Antibodies Coated Red Cells

     Destruction of Fetal Cells by Fetal RES

     Fetal Anemia

     Fetal Hypoxia and Stimulation of Erythropoitin

     Extra Medullary red Cells Synthesis

     Hepato spleenomegally

     Hepatic Cell Failure

     Hypoproteinemia, Increased Intrahepatic


    Pressure, Portal hypertension

    Ascitis , Edema, hypoxia, Placental


    Thickness, Polyhydramnios, Pericardial
    effusion
    GRAND MOTHER THEORY
    FETO MATERNAL HEMORRHAGE
    • Abortion, ectopic pregnancy, molar pregnancy
    • Cordocentesis, amniocentesis, chorionic villus
    sampling
    • Attempted version
    5% - First trimester
    • Manual removal of placenta 46% - third trimester
    • Trauma Maximum (75%) at time of delivery

    • Antepartum hemorrhage
    • Vaginal delivery, cesarean section, forceps delivery -
    <3ml
    • Placental abruption
    • Blood transfusion
    Risk of sensitization in relation to
    volume of FMH
    Volume of FMH Risk of
    (mL) sensitization (%)
    0.1 3
    0.2-1 25
    >5 65
    ABO INCOMPATIBILITY PROTECTIVE
    • ABO incompatibility – most common
    • HEMOLYTIC DISEASE in newborn
    • Very mild anemia
    • IGM antibodies – do not cross placenta
    • Fetal red cells have fewer A and B antigenic sites than
    adult cells- less immunogenic
     Red blood cells is easily destroyed, so not
    reaching enough immunological component
    to cause antibody response and reaction.
     The risk of sensitization after ABO
    incompatible pregnancy is only 2%.

    If ABO is compatible:

    Rh+ fetal cells  remain in circulation (life


    span) until removed by (R.E.S)  destroyed
     liberating antigen (D)  isoimmunization
    Macroph.Antigen
    Mother
    Presenting Cell Group “O” Rh Negative
    T-Hellper
    Anti - A Anti - B

    B-cell

    Anti-D
    Placenta

    A Rh positive B Rh
    “O” Rh positive Positive
    Infant
    FETAL EFFECTS OF ISOIMMUNIZATION
    •Fetal anemia USG
    •Hydrops fetalis
    •Fetal Hyperbilirubinemia
    HEMOLYTIC DISEASE OF FETUS AND NEWBORN
    • Hemolysis tolerated by fetus
    •Mild anemia and jaundice at birth
    •Usually resolves without treatment

    • increased circulating bilirubin cleared by placenta


    •After birth bilirubin not cleared by immature liver
    • hyperbilirunbinemia  Kernicterus
    •Moderate anemia – post natal treatment required

    • severe fetal anemia


    •Hepatosplenomegaly
    •Erthryoblasts in circulation
    •Liver dysfunction
    •Fetal cardiac failure
    •Fetal hydrops – stillbirth, neonatal
    death
    SIGNS OF FETAL ANEMIA
    • Polyhydramnios
    • Hyperplacentosis- as an effort to increase the
    transfer of oxygen but available fetal red cells
    • Fetal ascites
    • Hepatosplenomegaly
    • Increased right atrial size
    • Foetal hydrops(generalised edema)
    Hydrops Fetalis
    •Ground glass placenta
    •Ascites HALO SIGN

    •Pleural effusion

    •Pericardial effusion

    •Buddha posture

    •Halo sign – subcutaneous


    edema of scalp

    •MCA PSV >1.5 MoM


    FETAL DEATH = due to cardiac failure
    MATERNAL EFFECTS OF Rh
    ALLOIMMUNISATION
    • Hyper placentosis – pre eclampsia
    • Cordocentesis ,amniocentesis complications
    MATERNAL MIRROR SYNDROME
    Ballantyne
    syndrome

    Swollen baby
    Swollen placenta
    Swollen mother !
    ROUTINE ANTENATAL MANAGEMENT
    OF NORMAL SINGLETON PREGNANCY
    BABY

    MOTHER
    DETERMINING FETAL Rh factor
    • Non invasive fetal testing for Rh D gene
    • Cell – free fetal DNA (cfDNA) in maternal
    plasma
    SCREENING OF ALLO IMMUNISATION
    • In the first pregnancy:
     At first booking
     20 weeks
     28 weeks
    • In subsequent pregnancies
    previous pregnancy with no or mild hemolytic disease
    1. At first booking
    2. Every 4-6 weeks subsequently
     Previous pregnancy with severe hemolytic disease
    1. Titre not required
    2. Testing for fetal anemia beginning from 16-18 weeks
    ICT = NEGATIVE

    NO ISOIMMUNIZATION AT PRESENT

    AIM:
    Minimizing chances of FMH
    Preventing alloimmunization – Anti D

    ANTI – D
    •28 weeks of gestation – ICT NEGATIVE
    •within 72 hours of delivery – RH POSITIVE FETUS -DCT
    NEGATIVE - atleast within 13 days
    ANTI – D
    •IgG antibody

    •Binds to fetal RBCs and prevent


    stimulation of maternal immune
    system

    •POLYCLONAL (MOST COMMON)

    •300mcg = 15 ml of fetal RBCs


    = 30 ml of fetal blood

    •50 mcg = 2.5 ml of fetal RBCs

    •Half life = 16-24 days

    •IM – Deltoid/ Anterolateral aspect


    of thigh
    Dose of Anti D ≈ Amount of FMH
    KLEIHAUER BETKE TEST / ACID ELUTION TEST
    • Sample: Maternal blood
    • Principle : HbF is more resistant to acid elution than HbA
    MBV x maternal Hct x %fetal cells in KB
    Fetal blood volume = ---------------------------------------------------------
    Newborn Hct
    • 100mcg of Anti D neutralise 4ml of fetomaternal blood

    Flow cytometry
    Maternal red cells/ ghost
    cells

    Dark red fetal cells


    FETO MATERNAL HEMORRHAGE
    Indications Recommended Dose (mcg)
    First trimester abortion/ 50
    MTP
    First trimester ectopic 50
    pregnancy
    Second trimester 300
    abortion/MTP
    Second trimester 300
    300 mcg = 1500IU
    amniocentesis
    Prophylaxis at 28 weeks 300

    After delivery 300


    ICT = POSITIVE

    Rh ISOIMMUNIZED PREGNANCY

    Assess Antibody titre


    CRITICAL TITRE = 1:16
    < 1:16 > 1:16
    MONITOR
    FETAL
    ANEMIA
    ICT EVERY 4 WEEKS
    < 1.5 MoM >1.5 MoM

    >34 weeks >34 weeks

    FETAL BLOOD
    DELIVER SAMPLING

    HEMATOCRIT <30% HEMATOCRIT >30%

    WEEKLY FBS, depending


    on MCA-PSV
    SERIAL AMNIOCENTESIS AND LILEY
    CURVE
    • Hemolysis  high levels of bilirubin into
    amniotic fluid
    • Amniocentesis done
    • Amount of bilirubin is quantitated by
    spectrophotometrically measuring delta
    optical density (∆OD 450nm wavelength)
    LILEY’S CHART
    Serial Amniocentesis

    Lily zone I Upper Zone II Zone III


    Lower Zone II Hydramnios & Hydrops

    Repeat
    Fetal blood sampling
    Amniocentesis every
    2-4 weeks
    Fetal Fetal
    hematocrit<30% hematocrit>30%
    Delivery at OR near term

    Intrauterine
    Transfusion
    Repeat Amniocentesis in 7 Follow with fetal
    days or FBS Blood sampling
    & USG
    Hct < 30% Hct > 30%

    DELIVERY
    Intrauterine Repeat Sampling
    WHEN LUNG
    Transfusion 7 to 14 days
    MATURE
    Suggested management after amniocentesis for ΔO D 450
    FETAL MIDDLE CEREBRAL ARTERY
    PEAK SYSTOLIC VELOCITY
    • Presently used Fetal anemia
    Normal
    INTRA UTERINE TRANSFUSION
    • HCT <30%
    • O Negative
    • Crossmatched with mother’s blood
    • Tightly packed to achieve hematocrit of 75-85%

    ROUTES

    INTRA- INTRA-
    VASCULAR PERITONEAL

    Intra hepatic
    Umbilical vein at Diaphragmatic
    portion of umbilical
    cord insertion lymphatics
    vein
    INTRA UTERINE TRANSFUSION
    MANAGEMENT DURING DELIVERY

    Indication for LSCS:

     Severe form of hemolytic


    infant disease in the term
    or 34-35 weeks after
    previous antenatal
    prevention of fetal hyaline
    membranes syndrome;
    Measures to be taken during LSCS
     prevent spillage of blood from the placenta
    to into the peritoneal cavity.
     Spontaneous delivery of placenta using
    control cord traction without squeezing the
    uterus.
    Avoid avulsions of the cord.
    Vaginal delivery in Rh-
    isoimmunization
     undergo delivery in
    the term of 37-38
    weeks of gestation.
     Induction of labor is
    performed by
    prostaglandin (in the
    case of “unripe”
    uterine cervix) or by
    intravenous oxytocin
    infusion
    administration (in the
    case of “ripe” uterine
    cervix).
    Vaginal delivery in Rh-isoimmunization
     During labor:
     No fundal pushing in 1st or 2nd stage of labor.
     Withhold inj methergin after ant. shoulder delivery.
     Early cord clamping and no milking.
     No uterine massage or squeeze in 3rd stage.
     Let the placenta to be delivered spontaneous to
    avoid avulsions of the cord.
     Protect the vaginal and perineal wounds and
    laceration from being exposed to the fetal blood spilled
    from cord
     At birth
     Maternal blood

    a. antibodies by indirect Comb's test ( ICT )..

    b. fetal red blood cells in maternal circulation


     Cord blood sample ( Neonatal blood sample ) for
    a. antibodies by Direct Comb's test ( DCT )
    b. Infant blood group and rh-typing.
    c. Infant bilirubin level
    d. Infant Hb & Hct level
    Management of sensitized
    newborn
    Mild anemia (Hb <14gm/dl,
    cord bilirubin>4 mg/dl)---
    Phototherapy
    -Moderate to severe----
    Exchange
    transfusion.
    -Mild Hydrops improves in
    88% of cases
    -Severe hydrops—Mortality is
    39%

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