HDFN & RhIg Flashcards
HDFN
- maternal red cell antibodies (IgG) crss placenta and attach to fetal cells causing hemolysis
- anemia in fetu
- increase in erythropoiesis (Erythroblastosis fetalis)
- mild to severe depending on antibody identity and concentration
factors of maternal Ab production (5)
- amount of blood (0.5 mL vs 25 mL
- immunogenicity of antigen (D vs Fya)
- previous exposure (primary vs secondary)
- maternal immune response (responder vs. non-responder)
- ABO compatibility
severe cases of HDFN (in utero)
- profound anemia
- hepatosplenomegaly
- hypoproteinemia
- cardiovascular failure (heart enlarged bc decrease in RBC mass)
- “Hydrops fetalis” severe edema = infant dies in utero
severe cases of HDFN (postpartum)
- anemia
- hyperbilirubinemia
> unconjugated bilirubin increases = Kernicterus - hemolysis continues postpartum
kernicterus
brain damage
- unconjugated bilirubin crossed BBB
- cerebral palsy-like effect
why don’t we see jaundice in fetus?
bc bilirubin in amniotic ac ad mom is getting rid of it so jaundice only seen in newborn
these blood groups are not associated with HDFN
Lewis
P
I (babies = i)
most common blood group associated with HDFN
ABO
- mild or subclinical
- first pregnancy can be affected
- IgG ABO antibodies (anti-A,B)
disease at birth for ABO HDFN
- no anemia or mild
- no jaundice, but bilirubin increases
- spherocytes on smear
What is RhIg?
- human source anti-D
> acquired from pooled plasma with anti-D
> anion exchange column chromatography
> solvent detergent (destroys lipid enveloped viruses) and ultrafiltration steps (removes non-enveloped viruses)
> lyophilized
how is RhIg delivered?
intravenous (IV) or intramuscular (IM)
mechanism of action RhIg
used for prevention of anti-D production in pregnancy when given to Rh neg females
mechanism of RhIg is not fully understood but may involve inhibiting the adaptive immune system by: (3)
- masking epitope of D antigen
- increasing rate of removal of D pos infant cells by opsonization (removal by spleen)
- FcyRIIB receptor inhibition of B cells
who gets RhIg? and when?
- given to Rh neg females without active anti-D
- 28 weeks gestation (26-32 weeks)
> removes any Rh pos fetal cells that enter maternal circulation prior to delivery - <72 hrs post-delivery of Rh pos or wk D pos infant
> removes fetal cells from circulation at time of delivery - additional dose may be given throughout pregnancy (amniocentesis, trauma, incomplete/therapeutic abortion)
standard dose RhIg
- 300 ug
- 1-300 ug will clear: 30 mL whole blood; 15 mL packed cells
** additional vials may be needed depending on size of bleed **
prior to RhIg, what was the only treatment for jaundice babies?
phototherapy
RhIg effectiveness
- 15% of white women are Rh neg
- no RhIg given = anti-D production = 12-13%
- 1 dose postnatal = 1%
- 28 wk and postnatal dose = 0.1%
half-life of RhIg
23-26 days
- may be detected up to 8 weeks in patients following injection (passive anti-D) and can interfere with PRETRANSFUSION testing
T or F. RhIg is not effective when active anti-D is present
T! it’s a prevention strategy so if it’s made… can’t remove it
T or F. RhIg prevents antibody production to other blood group antigens
F! you can still make anti-c, -kell, etc.
does passive anti-D harm the fetus?
no because given at last few weeks of pregnancy so risk is low and titre goes down eventually
other uses of RhIg
- Rh incompatible transfusions
> may be given to Rh neg females of child-bearing potential <45y who received Rh pos blood (emergency, error, Rh pos platelets) - treatment for idiopathic thrombocytopenic purpura (ITP)
> given to non-splenectomized Rh pos patients as an alternative to IVIg
prenatal testing follow up when antibody screen is positive
- Ab ID with panel
- perform titration
- antigen type mother and father
- verbal report to physician: antibody screen, ID, and titre
T or F. Level of Ab titre may not correspond to disease severity in infant
T
even though mom has a high Ab titre of anti-D, fetus could still be Rh neg
