Download Fetal-Haemolytic

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