Pathogenesis

Placental transfer of fetal cells—^maternal circulation is maximal at delivery; the condition does not usually present in the firstborn (Note: ABO incompatibility is an exception). Previous maternal transfusion, abortion, amniocentesis, chorionic villus sampling (CVS) or obstetric manipulations can cause antibody formation. Maternal IgG crosses placenta, reacts with Ag +ve fetal RBCs.

Rh HDN classically presents as jaundice in first 24h of life.

Mild HDN may go unnoticed and presents as persistent hyper-bilirubinaemia or late anaemia weeks after birth.

Severe HDN may result in a macerated fetus, fresh stillbirth or severely anaemic, grossly oedematous infant (hydrops fetalis) with hepato-splenomegaly 2° to compensatory extramedullary haemopoiesis in utero.

440 Kernicterus: Neurological damage secondary to bilirubin deposition in the brain, depends on a number of factors including the unconjugated bilirubin level, maturity of the baby, the use of interacting drugs.

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