Intro, Disease Process, Classification & Pathogenesis
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| Hemolytic disease of the newborn is? | destruction of RBCs of the fetus & neonate by AB produced by the mother
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| Th mother is stimulated to produce ABs by? | curent or previous pregnancies or by transfusion
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| HDN is most commonly caused by | anti-D and other Rh blood group ABs
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| During pregnancy there is fetomaternal hemorrhage | which are RBCs from fetus enter the mothers circulation, 0.1ml
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| Mother forms antibodies against | paternal antigens
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| IgG antibodies cross placenta | and bind to fetal RBCs
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| D hemolytic disease | caused by anti-D alone or in combo with anit-C or anti-E
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| Other hemolytic disease | caused by other Rh ABs or blood group ABS, anti-K, anti-c
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| ABO hemolytic disease | usually caused by anti-A,B in O women
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| FHM occurs in # of pregnancy | 75%, usually immediately after delivery
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| Other causes of FHM | amniocentesis, abortion, chorionic villus sampling, cordocentesis,etopic preg, blunt trauma to abdomen
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| Since advent of Rh immune globulin | < 1% of D neg mothers exhibit immunization
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| Incidence of 'D' HDN = | 18% in untreated D neg mothers of D pos infants
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| Prevalance of non-anti-D HDN = | <0.3%
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| Transfusion of D pos red cell products | to women of child bearing age should be avoided
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| IF D pos transfusion necessary | then Rh IG prophylacic treatment
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| Hemolysis & Erythropoiesis | Maternal IgG AB attaches on fetal RBCs; AB/AG complex removed by macrophages in spleen; fetal bone marrow & hempietic tissue in liver & spleen increase RBC production
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| Anemia | moderate to severe depending on #RBCs destroyed; severe anemia may lead to hydrops fetalis from enlarged liver and spleen;
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| Anemia cont | RBC destruction continues after birth as long as maternal AB in system
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| Hydrops fetalis | severe edema, effusions, ascites
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| Bilirubnemia | RBC lysis casuse release of HgB which is metabolized into indirect bikirubin; then may be transported across placenta & conjugated in maternal liver to direct bilirubin & then excreted
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| Bilirubnemia cont | total bili elevated in fetal serum & amniotic fluid, but not harmful; after birth, accumulation of indirect bili to toxic levels & can cause brain damage
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