Rhesus D and Haemolytic disease of the newborn

Epidemiology

  • With advances in Rh D immunisation, haemolytic disease of the newborn is now extremely rare

Background

  • Rhesus antigens are just one of several proteins that can be expressed on red blood cells.  These are genetically predetermined, i.e. you inherit proteins from either parent.
  • In the case of Rhesus, the rhesus D protein can be particularly antigenic and will cause an immune response to occur.
  • If a mum who is Rhesus D -ve carries a child that is Rhesus D +ve, there is a risk that a small amount of foetal blood will cross into the maternal circulation (foeto-maternal haemorrhage, or FMH)
    • This usually occurs in the third trimester/during childbirth
    • The mother’s immune system mounts an immune response and produces anti-D antibodies- once sensitisation has occurred it is irreversible
  • If this is the first pregnancy, then this is not usually a problem for either mother or child.  However, in subsequent pregancies, the immune response will be greater and more rapid.  The result can be destruction of the foetal RBCs and a severe/fatal foetal anaemia.  This can result in neonatal jaundice (secondary to haemolysis)

Risk Factors for FMH

  • Traumatic delivery (inc C-section)
  • Manual removal of the placenta
  • Stillbirths/miscarriage
  • Abdominal trauma during the third trimester
  • Multiple pregnancy

Antenatal screening

  • All pregnant women will have their Rhesus status checked and whether they have antibodies already
    • the latter can be tested with an indirect Coombe’s Test
      • mother’s serum (containing IgG) can be added to Rh+ve RBCs, then added to anti-human IgG which will cause agglutination (only if patient sample is positive for Anti-D
  • Antenatal ultrasound will look for features of hydrops fetalis and foetal anaemia
    • e.g. by doppler USS looking at the middle cerebral artery
    • If there are any concerns, foetal blood sampling could also be done
      • anaemia, abnormal RBCs and a high reticulocyte count are features of anaemia

Presentation after birth

  • In up to 50% of cases, babies may be born normal.  Babies typically develop symptoms within the first 24 hours
    • jaundice (including yellow amniotic fluid and vermix (‘gunk’ on baby’s skin))
    • hepatosplenomegaly
    • hypoglycaemia
    • hydrops fetalis
      • IMPORTANT: babies who appear normal but have identified rhesus incompatibility should be closely observed for up to 2 months
  • Severe disease may result in still birth or require intensive resuscitation

Prevention

  • Rh-ve mothers should be offered an injection of Anti-D antibody at 28 weeks, or when she has any invasive obstetric procedure (e.g. amniocentesis), or if she has any significant risk factors (e.g. abdominal trauma); and finally after delivery
    • This works by binding to the baby’s blood antigens before the mother can mount an immune response

Management of HDN

In utero

  • If the baby is anaemic (confirmed by blood test), transfusion directly to the foetus (via the umbilical vein) with O- cells should be given at around 16-18 weeks
  • These babies should be delivered early (37/8 weeks) if no complications, (earlier- down to 32 weeks, if complications)

 

Post-natal

    • Transfusion may be required
    • Phototherapy for jaundice
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