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    Rhesus Isoimmunisation

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    Muwanga faizo
    1. Rhesus isoimmunization occurs when a Rh-negative mother is exposed to Rh-positive fetal blood cells during pregnancy or delivery, leading to the production of Rh antibodies. 2. These Rh antibodies can then cross the placenta in subsequent pregnancies and destroy Rh-positive fetal red blood cells, causing fetal anemia or even death. 3. Management involves prophylactic anti-D immunoglobulin administration after potential fetal maternal hemorrhage to prevent isoimmunization, antibody screening during pregnancy, and treatment depending on antibody titers which may include amniocentesis, fetal transfusions, or early delivery.

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    Rhesus Isoimmunisation

    Uploaded by

    Muwanga faizo
    21 views27 pages
    1. Rhesus isoimmunization occurs when a Rh-negative mother is exposed to Rh-positive fetal blood cells during pregnancy or delivery, leading to the production of Rh antibodies. 2. These Rh antibodies can then cross the placenta in subsequent pregnancies and destroy Rh-positive fetal red blood cells, causing fetal anemia or even death. 3. Management involves prophylactic anti-D immunoglobulin administration after potential fetal maternal hemorrhage to prevent isoimmunization, antibody screening during pregnancy, and treatment depending on antibody titers which may include amniocentesis, fetal transfusions, or early delivery.

    Original Description:

    Haematology

    Original Title

    4. RHESUS ISOIMMUNISATION

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    1. Rhesus isoimmunization occurs when a Rh-negative mother is exposed to Rh-positive fetal blood cells during pregnancy or delivery, leading to the production of Rh antibodies. 2. These Rh antibodies can then cross the placenta in subsequent pregnancies and destroy Rh-positive fetal red blood cells, causing fetal anemia or even death. 3. Management involves prophylactic anti-D immunoglobulin administration after potential fetal maternal hemorrhage to prevent isoimmunization, antibody screening during pregnancy, and treatment depending on antibody titers which may include amniocentesis, fetal transfusions, or early delivery.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    21 views27 pages

    Rhesus Isoimmunisation

    Uploaded by

    Muwanga faizo
    1. Rhesus isoimmunization occurs when a Rh-negative mother is exposed to Rh-positive fetal blood cells during pregnancy or delivery, leading to the production of Rh antibodies. 2. These Rh antibodies can then cross the placenta in subsequent pregnancies and destroy Rh-positive fetal red blood cells, causing fetal anemia or even death. 3. Management involves prophylactic anti-D immunoglobulin administration after potential fetal maternal hemorrhage to prevent isoimmunization, antibody screening during pregnancy, and treatment depending on antibody titers which may include amniocentesis, fetal transfusions, or early delivery.

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    “Rhesus Isoimmunization”

    1
    Blood groups (1900):
    Antigens: Antibodies:
    O (45%) AntiA+Anti B
    A (40%) Anti B
    B (10%) Anti A
    AB (5%)

    A and B : dominant
    O : recessive

    2
    Rhesus factor (1940):
    Agglutinogen (C,D,E) mainly D
    C,D,E dominant antigen
    d,e recessive antigen

    3
    - Rh positive about 85%( homozygous (DD)
    (35%), or heterozygous (Dd) (50%)‚
    - Rh negative about 15%
    - Incidence of Rh -ve in far east is about 1%
    Examples of Rh factor: (CDe=R1) , (Cde=r)
    (cDE=R2)
    Other systems:kell-antikell,luther,Duffy,etc .

    4
    So in response to introduction of foreign protein
    (antigen)--- production of antibody to neu-
    tralize the antigen .
    In ABO and other non Rh-incompatibility: It
    usually causes mild anaemia, mainly as
    there is no intrapartum boosting .
    In Rhesus isoimmunization: mainly (D), but C,E
    can produce antibodies

    5
    Feto-maternal haemorrhage: during pregnancy leakage of fetal cells in
    the maternal circulation {(Rh+ve) fetal cells in Rh-ve maternal circula-
    tion} .
    Examples:
    -spontaneous abortion
    - Induced abortion
    - APH
    - E.C.V.
    - Cordocentesis, CVS, amniocentesis
     - severe preeclampsia
    -Ectopic pregnancy
     - Caesarean section
     - Manual removal or placenta
    - Silent feto-maternal hage.

    6
    Development of Rhesus antibodies: depends
    on factors
    1- Inborn ability to respond
    2- protection if ABO incompatible1\10
    3- Strength of Rh antigen stimumlus (CDe=R1)
    4- Volume of leaking feta blood (0.25ml)
    IgM (7 days) doesn’t cross placenta, then IgG
    21 days - crosses placenta )

    7
    1- If ABO is incompatible:
    Red blood cells is easily destroyed, so not
    reaching enough immunological component
    to cause antibody response and reaction

    8
    1. Cleared by
    Macrophage Mother
    2. Plasma Primary Response
    stem cells
    •6 wks to 6 M.
    •IGM.

    IGM antibodies
    Placental

    The First Pregnancy is not Affected


    9
    Macroph. antigen
    Presenting cell Mother
    T- helper cell Secondary Response

    •Small amount
    B cell •Rapid
    •IgG
    IgG
    Anti - D
    Placental

    10 Fetal Anemia
    2-If ABO is compatible:
    Rh (+ve) fetal cells - remain in circulation (life span)
    until removed by (R.E.S)- destroyed - liberating
    antigen (D)- isoimmunization.
    It takes time:
    1st pregnancy is almost always not affected:
    1% (during labour or 3rd stage),
    10% 6 months after delivery,
    and15% by the 2nd pregnancy

    11
    12
    Mild Cases:
    fetal (RBC) destruction - from anti.D (IgG): -- anaemia--
    compensating haemopoiesis - excess of unconjugated biliru-
    bin .
    Severe Cases:
    excessive destruction of fetal (RBC) - severe anaemia - hy-
    poxia the tissues - cardiac or circulatory failure --gener-
    alized oedema -(H.Failure)-- ascitis - I.U.FDeath

    When excess of unconjugated bilirubin >(310-350 mol/L) - It


    passes brain barrier (kernicterus)  permanent neurological
    and mental disorders .

    13
    Kleihauer-Betke: technique:
    (acid elution test) to measure amount of feto-maternal
    haemorrhage
    If 0.1- 0.25ml of fetal blood leakes (critical volume) this
    will produce isoimmunization represented by 5 fetal
    cells in 50 low power microscopic field of peripheral
    maternal blood .
    So 1ml is represented by 20 fetal cells

    14
    Fetal and Neonatal Effects:

    - Haemolytic anaemia of newborn Hb 14-18g/dl


    - Icterus gravis neonaturm Hb 10-14g/dl
    - Hydrops fetalis (Erythroblastosis fetalis)

    15
    Management :

    I) Prophylaxis

    1-Prevention of Rhesus isoimmunization: Anti D (RhoD IgG)


    Standard dose for > 20w, and ½ standard dose for <20weeks
    Given within 72hours of the incident
    SD: I.M. injection: 500 iu = 100 ugm (UK), SD in USA
    300ugm=1500iu
    - 1500iu =300 ugm - neutralize 15ml ,
    - 500 iu = 100 ugm=neutralize 5ml (4ml + 1ml) ,
    4ml = 4x20 f.cells = 80 fetal cells

    16
    Management
    K-B test if large amount of leaking - another s.d if
    mother is Rh -ve, baby Rh +ve with no isoimmu-
    nization (checked by indirect or direct coomb’s test)

    2-A.P administration of anti D:


    S.d. at 28w or at 28 and 36w will reduce Rh isoimmu-
    nization

    17
    Management:

    II) - 1- Antibody Screening: for all pregnant


    women in ANC for irregular antibodies
    (mainly for Rhesus Negative women) then
    start at 20w , and every 4 weeks

    18
    Management
    2-Management following detection of Rh antibodies
    - Should be treated in specialized centres
    - Quantitative measures of antibodies + husband geno-
    type
    - Repeat titration (indirect coomb’s , detecting of an-
    tibodies) titre or specific enzymes for antibodies IU
    - Amniocentesis once necessary
    - Obstetrical management based on timing of I.U
    trans-fusion (Now cordocentesis + fetoscopy) ver-
    sus delivery

    19
    Management
    3-Amniocentesis: should be performed under ultra-
    sound guidance if titre > 1\16 = 0.5-1 ugm = > 2.5-5
    I.U
    - timing: 1st amniocentesis 10 weeks before previous
    IUFD
    - Start from 20-22 weeks, 2-4 weekly or more frequent
    if needed
    - Amniotic fluid analysis : spectrophotometry: optical
    density at the height of optical density deviation at
    wave length 450 nM.

    20
    cordocentesis

    21
    Management:

    IU transfusion (cordocentesis, in the past in-


    traperitoneal transfusion) versus delivery of
    the baby:
    - Using Lily’s chart
    - Prediction chart (Queenan curve)
    - Whitefield’s action line

    22
    Liley’ chart

    23
    Whitefield’ action line

    24
    Management

    - Alternatively follow up with doppler study for


    the fetal middle cerebral artery.

    Prognosis depends on :Obst. history, paternal


    genotype, mat. history (blood transfusion, an-
    tibody titre) amniocentesis results.

    Delivery: Vaginal versus Cs

    25
    Management

    Intensive plasmaphoresis: when severe cases antici-


    pated,using continous flow cell seperator, as
    early as 12 w
    Postnatal management: for the neonate
    - direct coomb’s test, Bl.gp,Rh type, Hb, bilirubin .
    - Mild cases: phototherapy - correction of acidosis
    - Severe cases :exchange transfusion

    26
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