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Fetal Haemolytic Disease
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Maternal antibodies develop against fetal red blood cells IgG antibodies cross the placenta Haemolysis, anaemia, high-output cardiac failure & death
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Usually a problem with subsequent pregnancies but may occur in the index pregnancy
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Causes ABO – does not usually cause significant haemolytic disease. Anti-Kell – causes fetal bone marrow aplasia. Rhesus – D antigenanti-D c antigenanti-c E antigenanti-E
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Incidence Approx 17% of the population is Rh-ve 10% of women at risk of developing anti-D. Incidence 1/1000 pregnancies
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Predisposing Factors Miscarriage and ectopic pregnancy Invasive procedures ECV Abdominal trauma Antepartum haemorrhage Labour and birth
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Initial exposure Small IgM response Subsequent exposure Large IgG response
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IgG crosses placenta Forms antigen-antibody complex on red cell Red cells phagocytosed Anaemia and haemolysis
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Anaemia Fetal hypoxia Hepatic and cardiac dysfunction Oedema, ascites, pericardial & pleural effusions - HYDROPS
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Haemolysis Increased bilirubin Jaundice postnatally Kernicterus
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Prevention Anti-D after any sensitizing episode after 12 weeks Consider routine prophylaxis
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Management Check antibodies at booking and 3 rd trimester If antibodies present – check antibody levels every 4 weeks to 28 weeks and then 2-weekly to term <4IU/ml – severe disease rare 4-15IU/ml – moderate risk >15IU/ml – 50% risk of severe anaemia
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Check paternal genotype D antigen autosomal dominant Father DD – fetus Rh positive Father d/D – 50% chance that fetus will be Rh+ve
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Measurement of blood velocity in middle cerebral artery. Hyperkinetic circulation correlates with fetal anaemia and need for further treatment.
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Anti-D for sensitising events after 12 weeks. If anti-D antibodies present do not give more anti-D. Serial measurements of Anti-D levels. Observe for signs of fetal anemia – if anemic transfuse or deliver.
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