Hemolytic disease of the Fetus & Newborn Flashcards
Hemolytic disease of the fetus
premature RBC destruction results in disease varying from mild anemia to death in utero
(bilirubin is processed by mama liver)
worry about anemia
hemolytic disease of the newborn
RBC destruction results in anemia & elevated levels of bilirubin in new born
the placenta
exchange site for oxygen, nutrients, & waste
barrier between mother & baby circulations & reduces exposure to foreign antigens
prevents fetal cells from entering mom’s circulation
when does sensitization of the mother occur?
anytime fetal RBCs enter mother’s circulation:
delivery, amniocentesis, chorionic villi sampling, spontaneous/induced abortion
ectopic pregnancy
abdominal trauma
requirements for HDFN to occur
mother must have developed antibody
fetus must posses the antigen
antigen must be well developed at birth
greatest threat of hemolytic disease of the fetus
cardiac failure due to uncompensated anemia
greatest threat of hemolytic disease of the newborn
premature baby liver that does not produced glucuronyl transferase to conjugate indirect bilirubin & can cross blood-brain barrier to bind to CNS tissues = kernicterus, deafness, mental retardation or death
3 classes of HDFN
- RhD
- ABO
- non-anti-D alloantibody-mediated
RhD HDFN
anti-D responsible for most severe cases of HDFN
anti-D #1 cause of death in HDFN
ABO HDFN
most common HDFN
most cases are subclinical & do not need treatment
A/B substances in fetal tissues & secretions neutralize most maternal antibodies
large portion of anti-A/B are IgM; IgG are low titer
group A baby & group O mommy
ABO HDFN
group O make an anti-A,B antibody that is IgG
can affect first pregnancy
cutoff for hyperbilirubinemia in infants
> 5 mg/dL
second most common cause of HDFN
anti-c antibody & can be in combination with anti-D
3rd most common cause of HDFN
anti-K
Kell HDFN
kell is expressed on RBC precursors!!!!
HDN is MUCH more severe when due to kell antibodies bc they target precursors & lead to SEVERE anemia
prenatal work up
D neg mothers need to be IDed
mothers with IgG antibodies capable of causing HDFN need to be IDed
no testing for ABO HDFN
& antibody titration if necessary
antibody titration
predict HDFN; titer done early in pregnancy & repeated every 4-6 weeks & specimen is frozen
two-dilution rise in titer is an indication for further monitoring
critical titer of antibody?
> 16
this is high enough to affect the fetus
Doppler ultrasonography
measures blood velocity
rate is inversely proportional to hgb (faster during anemia)
lower resistance when there are fewer cells
postnatal work up
- mother is Rh neg- need to know about Rhogam doses
2. when HDFN is suspected
postnatal mother tests
type & screen
if RhD pos - done
if RhD neg test baby
postnatal baby tests
type & screen
if child is RhD neg-> weak D test
if child is RhD neg & mother has anti-D-> perform elution
if child is RhD pos & mother has no anti-D then test for fetal maternal hemorrhage
Fetal maternal hemorrhage screen
determine if >20ml of RhD pos fetal blood is in RhD neg mother
neg result: 1 unit of rhogam
pos result: multiple units of rhogam
Kleihauer-Betke test
quantifies all fetal cells in mother’s circulation
acid elution of peripheral blood smear
Hgb F is acid stable
hgb A is acid soluble
gold standard assay for fetal maternal hemorrhage
flow cytometry!!
immunophenotype RBCs
testing on infants with suspected HDN
ABO/D only forward type
antibody screen
DAT - if positive then elution
importance of DAT
if infant RBCs are DAT positive, then the antibody MUST have come from the mother
only need IgG not polyspecific
RhIG
concentrate of anti-D IgG prepared from pools of human plasma (sensitized to D antigen on RBCs during their lives)
prevent sensitization
prevention of RhD HDFN
after RhD neg woman gives birth to a RhD pos child she must receive at least one dose of RhIG
one dose of RhIG covers how many ml of whole blood & how many mls of packed blood
30 mL whole blood
15 ml of fetal RBCs
1st dose of RhIG at how many weeks?
28 weeks
ATDP
anti-D passive
anti-D antibody will show up in women who have recently been given RhIG (only in gel/capture methods)
Cordocentesis
transfusion into the umbilical vein group O, RhD neg crossmatch compatible with maternal serum CMV negative hemoglobin S negative irradiated <7 days old blood
sunlight
treatment for mild hyperbilirubinemia
photo-oxidizes bilirubin
excreted in urine
bili-bed
treatment for moderate hyperbilirubinemia
exposure to blue light
photoisomerizes bilirubin so it can be excreted w/o conjugation in the liver
excreted in the bile
exchange transfusion
remove a volume of whole blood from baby & add in the same volume of PRBCs
treat severe bilirubinemia
removes some bilirubin & antibody
removes sensitized RBCs
bilirubin & child weight
bilirubin is more toxic the smaller the child
ABO HDFN
most common HDFN
most cases are subclinical & do not need treatment
A/B substances in fetal tissues & secretions neutralize most maternal antibodies
large portion of anti-A/B are IgM; IgG are low titer
