bb HDFN

Hemolytic disease

destruction of rbcs of a fetus and/or neonate by antibodies produced by the mother

percentage of HDFN caused by antibodies in the mother directed against Rh(D)

95%

rbcs of a fetus are destroyed by

antibodies produced by the mother’s immune system

antibodies that are efficient in crossing the placenta

IgG 1 and IgG 3

when do fetal rbcs enter the maternal circulation

during gestation and delivery when the placenta separates from the uteruspe

percentage of pregnancies that are ABO incompatible that cause HDFN

20%

leading cause of maternal alloimmunization

previous pregnancy with fetomaternal hemorrhage

what blood group of fetus affects group O mothers

group A or group B infants

other specificities associated with HDFN

anti K, E, C, c, e, Fya, Fyb, Jka, Jkb, S, s, and U

what rbc antigen is most antigenic

D antigen

what non RH system antibodies are considered to be most clinically significant in HDFN

anti-kell

fetal rbc destruction and the resulting anemia stimulate the fetal bone marrow to produce rbcs at an accelerated rate

greatest concern to the fetus in utero

anemia

what occurs during erythroblastosis fetalis

immature fetal rbcs (erythroblasts) are released into the circulation

hepatosplenomegaly results from extramedullary hematopoiesis

what occurs during hydrops fetalis

severe anemia and hypoproteinemia lead to development of high output cardiac failure with generalized edema, effusions, and ascites

the result of RBC destruction which releases hemoglobin causes what

rbc destruction releases hemoglobin which is metabolized to bilirubin

what does the maternal liver metabolize

unconjugated bilirubin

can the newborn liver process unconjugated bilirubin

no, not adequately

what levels of indirect bilirubin can reach toxicity levels & affect infants brain

more than 18 to 20mg/dl

infant brain bilirubin toxicity due to

kernicterus

postnatal diagnosis includes

• transfusion/pregnancy histories i.e. alloantibodies, previous births, still birth, miscarriages, abortion, newborns w HDFn

• developing of jaundice within 12 to 48 hrs after birth

• positive DAT (cord or neonatal RBCs)

• negative DAT with infant jaundice requires other causes of jaundice should be investigated

  • ABO and Rh

how to differentiate IgG from IgM alloantibody

with sulfhydryl reagents like dithiothretiol for certain alloantibodies such as antiM

antibody titration

relative concentration of all antibodies capable of cossing the placenta and causeing HDFN is determined by antibody titration

the measurement of the fetal MCA-PSV with color doppler ultrasonogrpahy can reliably predict anemia in the fetus

how early can amniocentesis or chorionic villus sampling be performed to determine D antigen gene

10-12 weeks gestation

intervention in the form of intrauterine transfusion becomes necessary when one or more of these conditions exists

• MCA-PSV indicates anemia

• fetal hydrops on ultrasound

• fetal hgb less than 10g/dl

• amniotic fluid OD 450nm results are high

  • risks and benefits of intrauterine transfusion must be weighed and evaluated

management of the infant includes

cord blood testin: ABO, RhD, DAT, elution

ABO/Rh testing and DAT on cord blood

a 2 volume exchange removes 80-90% of infant sensitized rbc, maternal antibody, and 50% of bilirubin

infant blood needed in the presence of maternal antibodies to a high prevalence antigen could include

anti U, Kpb, Jsb, k, Vel

when is phototherapy used

• mild HDFN

• after delivery to help w hyperbilirubinemia

• done at 460-490 nm to change bilirubin to isomers and decrease toxicity

  • UV fluorescent light metabilizes bilirubin

steps included for prevention during selection of blood for intrauterine and neonatal transfusion

• most facilities use group O rbcs for intrauterine and neonatal transfusions

• rbcs must be antigen negative for mothers antibodies

• donors are CMV negative

  • blood units less than 7 days old from collection are used

regular dose vial of RhIG in the U.S. contains sufficient anti D to protect against how much packed rbcs or whole blood

15mL of packed rbcs or 30ml of whole blood

test used to determine volume of fetal hemorrhage

kleinhauer betke test

RhIG is prepared from what

pooled human plasma from individual who have made anti D

dose for RhIG

comes in 50mg dose and a 300mg dose

300mg protects against alloimmunization to the D antigen after exposure to 15ml of fetal red cell or 30ml of fetal whole blood

how much RhIG is administered at 28 weeks gestation to D negative, weak D negative mothers

300mg dose

how much RhIG is administered at 12 weeks

50mg micro dose

other situations where RhIG is used

• abortion, miscarriage, termination of ectopic pregnancy

• if after 12 weeks gestation, give 300mg dose

  • can also be used for abdominal trauma, following amniocentesis/cordocentesis or antepartum hemorrhage

how much RhIG is given postpartum and when

300mg within 72hrs of delivery to D neg/weak D mothers

what is included in the evaluation for postpartum FMH and dosage of RhIG

maternal sample screened fro FMH with rosette test, can detect >10ml of fetal red cell

if test is positive: KB test or flow cytometry assessment performed and calculate FMH

if negative: give single vial of RhIG