blood type incompatibility

8/3/2019 Blood Type Incompatibility

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Blood TypeBlood TypeIncompatibilityIncompatibilityBlood TypeBlood TypeIncompatibilityIncompatibility

RH & ABORH & ABO

Rebecca Jo HelmreichRebecca Jo Helmreich



Rh incompatibility RH+ fetal cells (Rh antigen)

enter the blood circulation of an

RH- mother

² through breaks in the maternal-fetal circulation 1st IgM antibodies are formed, followed by IgG antibodies

capable of crossing the placenta

IgG Antibodies cross to fetus

coat fetal RBC·s and hemolysis occurs Mild = >erythropoiesis HbF = compensates Severe = >anemia ² hydrops fetalis from CHF--Death



Hemolytic Disease of the

Newborn Red cells of a fetus or neonate are destroyed by IgG antibodies produced

by the mother

Maternal IgG antibody directed against fetal RBCantigen

Antibody production stimulated throughpregnancy or transfusion

Most often, fetal cells enter maternal circulation at birth as placenta separates from uterus (fetal maternal

hemorrhage)

Occasionally during pregnancy itself IgG molecules cross the placenta and sensitize

fetal red cells



Pathogenesis Antibody-coated RBCs removed from fetal

circulation by spleen and liver ² anemia may result.

In response to anemia, Fetal bone marrow increases erythocytosis ² (HbF)

immature red cells are released into fetal circulation

Rate of hemolysis after birth decreases,

because there is no additional antibody enteringinfant·s circulation



Continued Pathogenesis Hemolysis results in production of bilirubin

In utero, excreted by mother

(transported across placenta, conjugated in maternalliver)

After birth, infant liver is unable toconjugate bilirubin so unable to excrete

(deficiency in glucuronyl transferase) Bilirubin can cause kernicterus.



Rh HDN Anti-D causes most cases of severe HDN

² Importance of anti-D has decreasedsubstantially, due to introduction of Rh immune

globulin (RHOGham) Women usually sensitized after first Rh-

postive pregnancy but may occur anytimemixing of blood

Rh neg women with ABO-incompatible, Rh postivefetus have decreased risk of Rhsensitization



Diagnosis History & Physical

History of previous abortion, blood transfusion, orinfant with jaundice

Kleihauer-Betke test: to determine amount of fetal blood inmaternal circulation & determine the dose of Rh immune globulinwhen large maternal-fetal bleed is suspected

Blood:² Blood group, Rh factor, (RH- not a problem if father also RH-)

² serial antibody screening Indirect Coomb·s test: ? Rh- mother has developed antibodies to the Rh

antigen Direct Coomb·s test: on infant·s blood after birth to identify maternalantibodies attached to fetal RBC·s



Nursing Diagnosis &

Evaluation Nsg. Dx

Risk for injury

Deficient Knowledge

Anxiety

Evaluation The client delivers a healthy infant with negative

direct Coombs· test

The client receives RhoGam to prevent maternalantibody formation that might complicate futurepregnancies



Interventions Provide support and education

Have carry an Rh-negative identification card & informthat may need RhoGam with future reproductive events

Ultrasound Evaluate fetus for amniotic fluid volume, fetal size, development

of edema or >heart

Fetal well being FHT monitoring (sinusoidal FHT = >anemia); Biophysical profile Middle cerebral artery (MCA) Doppler = detect anemia close to

term Early delivery with phototherapy and possible exchange

transfusion PRN



Prevention ² Rh HDN

Concentrate of IgG anti-D preparedfrom pooled human plasma

Protects women from sensitizationduring pregnancy and after deliveryof a Rh positive infant



Guidelines for RhIG All doses within 72 hours of delivery or procedure Women should not already be sensitized to D

antigen 50 mg (IM) dose up to 12th week gestation for: Abortion Miscarriage

Termination of ectopic pregnancy



Guidelines for RhIG 300 mg dose

² 28 weeks of gestation² After amniocentesis (repeat if procedures are >21 days apart)² After any procedure that can cause fetal-maternal

hemorrhage (communication of blood between mom & fetus) After delivery of Rh-positive infant 120 mg dose

² Termination of pregnancy after 12th week gestation² Amniocentesis² Other manipulations after 34th week of gestation

² Delivery of Rh-positive infant



Postnatal Testing for

?HDN Mother·s blood

² ABO

² Rh including Du if negative² Indirect antiglobulin test (antibody

screen) and ID if positive

² If ID is positive for IgG, do hemoglobinand bili on baby



Postnatal Testing for

?HDN Cord Blood

² ABO-

² Rh including Du if negative



Treatment for HDN In Utero

Intrauterine transfusion

Postpartum ² lower bilirubin levels² Phototherapy

² Exchange transfusion



Blood selection for Intrauterineand

Exchange Transfusions Group O (or ABO-compatible) Rh negative RBCs that are Dry packed and reconstituted with

AB fresh frozen plasma

Less than 7 days after collection CMV negative (or leukoreduced) Gamma irradiated Hemoglobin S negative

Negative for offending antibody Crossmatched with maternal serum



ABO HDN

Most common cause Anti-A and anti-B in group B and A persons are mostly IgM; in group O persons, partially IgG

Mild HDN in 1 in 150 births Reasons not severe

² A and B antigens not fully developed at birth² Smaller number of A and B antigenic sites on fetal RBCs

² A and B antigens also on tissues ² combine with maternalantibody

blood type incompatibility

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