RH Incompatibilities

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‫‪Rh Disease‬‬

‫‪Dr. Nariman Abdulhassan‬‬


‫اسوي سكرين اذا اكو انتي بدي لل‪ RH‬او ال‪ ABO‬باول مراجعه‬
‫للمريضه و االسبوع ‪ 28‬ووره الوالده واذا صار عندها اي نزف او ردت‬
‫اطيها ‪ IG‬هم الزم اسوي سكرين لالنتي بدي‬
Rh Disease

! Occurs during pregnancy when there is an


incompatibility between the blood types of
the mother and fetus
Blood Types

! A, B, O blood groups are specific types of


proteins found on the surface of RBC’s
! Also found in the cells and other body
fluids (saliva, semen, etc)
! O represents neither protein being present
on RBC
! Possible groups include: A, B, AB, or O
! A, B, O groups most important for
transfusions
Rh Factor

! Proteins (antigens) occurring only on


surface of RBC’s
! Rh + if proteins present
! Rh – if proteins absent
! A+, A-, B+, B-, AB+, AB-, O+, O-
! Most important for pregnancy
! Inheritance is Autosomal Dominant
! 15% Caucasian population is Rh-
Nomenclature

! Correct to say Rh(D) + or –


! Rh blood system has other antigens: C, c,
D, E, e
! D is by far the most common and the only
preventable one
! Weak D (Du) also exists Rhesus
! Also non Rhesus groups such as Kell,
MNS, Duffy (Fy) and Kidd (Jk) exist
Why Does Rh Status Matter?
Fetal RBC cross to maternal circulation

Maternal immune system recognizes foreign


antigens if fetus Rh + and mother Rh –

Antibodies are formed against fetal antigens

Subsequent pregnancy with Rh+ fetus,


immune system activated
and large amounts of Ab formed

IgG Ab cross placenta & attack fetal RBC

Fetal anemia, hydrops, etc


Pathophysiology

! Rh(D) antigen expressed by 30 d GA


! Many cells pass between maternal & fetal
circulation including at least 0.1 ml blood in
most deliveries but generally not sufficient
to activate immune response
! Rh antigen causes > response than most
! B lymphocyte clones recognizing foreign
RBC antigen are formed
Pathophysiology cont…

! Initial IgM followed by IgG in 2 wks- 6 mths


! Memory B lymphocytes activate immune
response in subsequent pregnancy
! IgG Ab cross placenta and attach to fetal
RBC’s ‫وره ما ياشرها االنتي بدي تكتلها املايكروفيج‬

! Cells then sequestered by macrophages in


fetal spleen where they get hemolyzed
! Fetal anemia
Causes of RBC Transfer
Causes of the sensitization ..
‫يعني اسوي سكرين اذا اكو انتي بدي‬
! abortion/ectopic ‫ باول مراجعه‬ABO‫ او ال‬RH‫لل‬
! partial molar pregnancy ‫ ووره الوالده واذا‬28 ‫للمريضه و االسبوع‬
! blighted ovum IG ‫صار عندها اي نزف او ردت اطيها‬
‫هم الزم اسوي سكرين لالنتي بدي‬
! antepartum bleeding
! special procedures (amniocentesis, cordocentesis, CVS)
! external version
! platelet transfusion
! abdominal trauma
! inadvertent transfusion Rh+ blood ‫غير مقصود‬
! postpartum (Rh+baby)
General Screening

! ABO & Rh Ab @ 1st prenatal visit


! @ 28 weeks
! Postpartum
! Antepartum bleeding and before giving any
immune globulin

! Neonatal bloods ABO, Rh, DAT


Gold Standard Test

! Indirect Coombs:
-mix Rh(D)+ cells with maternal serum
-anti-Rh(D) Ab will adhere
-RBC’s then washed & suspended in Coombs
serum (antihuman globulin)
-RBC’s coated with Ab will be agglutinated

! Direct Coombs:
-mix infant’s RBC’s with Coombs serum
-maternal Ab present if cells agglutinate
+ Rh(D) Antibody Screen

! Serial antibody titres q2-4 weeks Middle Cerebral Artery


Dopplers

! If titre ≥1:16 - amniocentesis or MCA


dopplers and more frequent titres (q1-2 wk)
! Critical titre – sig risk hydrops
! ** amnio can be devastating in this setting
! U/S for dating and monitoring
! Correct dates needed for determining
appropriate bili levels (delta OD450)
U/S Parameters

! Non Reliable Parameters:


Placental thickness
Umbilical vein diameter Mcq
Hepatic size
Splenic size
Polyhydramnios
! Visualization of walls of fetal bowel from small
amounts intraabdominal fluid may be 1st sign of
impending hydrops
! U/S reliable for hydrops (ascites, pleural
effusions, skin edema) – Hgb < 70
Mcq ‫يكلي نفوتها‬
Amniocentesis ‫خالل البالسنتا هذا‬
‫غلط‬

! Critical titre/previous affected infant


! Avoid transplacental needle passage Mcq
! Bilirubin correlates with fetal hemolysis
! ∆ optical density of amniotic fluid @ 450nm
on spectral absorption curve
! Data plotted on Liley curve
Liley Curve

! Zone I – fetus very low risk of severe fetal


anemia
! Zone II – mild to moderate fetal hemolysis
! Zone III – severe fetal anemia with high
probability of fetal death 7-10 days

! Liley good after 27 weeks


! 98% sensitive for detecting anemia in
upper zone 2/ zone 3
Middle Cerebral Artery Dopplers

! Measures peak velocity of blood flow


! Anemic fetus preserves O2 delivery to
brain by increasing flow
! Sensitivity of detecting severe anemia
when MCA >1.5 MoM approaches 100%
! Not reliable > 35 weeks GA
Fetus at Risk

! Fetal anemia diagnosed by:


○ amniocentesis
○ cordocentesis
○ ultrasound
hydrops
middle cerebral artery Doppler

! Treatment:
○ intravascular fetal transfusion
○ preterm birth
Infant at Risk

! Diagnosis:
○ history of HDN antibodies?
○ early jaundice < 24 hours
○ cord DAT (“Coomb’s”) positive (due to HDN or
ABO antibodies)
! Treatment:
○ Phototherapy
○ Exchange or Direct blood transfusion
Prevention

! RhoGAM (120mcg or 300mcg)


! Anti-D immune globulin
! Previously 16% Rh(D)- women became
alloimmunized after 2 pregnancies, 2%
with routine PP dose, and 0.1% with added
dose @ 28 wks

It is normal practice to administer anti-D as soon as possible after any potential sensitizing events that may
cause feto-maternal haemorrhage and preferably within 72 hours of exposure to fetal red cells.
Kleihauer-Betke Test

! % fetal RBC in maternal circulation


! Fetal erythrocytes contain Hbg F which is
more resistant to acid elution than HbgA so
after exposure to acid, only fetal cells
remain & can be identified with stain
! 1/1000 deliveries result in fetal hemorrhage
> 30ml
! Risk factors only identify 50%
Kleihauer Calculations
! Fetal red cells = MBV X maternal Hct X % fetal cells in KB
newborn Hct

MBV – maternal blood volume (usually 5000ml)

Fetal cells X 2 = whole blood

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