The increasing number of case reports on neurologic sequelae related to hyp
erbilirubinaemia may represent a re-emergence of kernicterus in the industr
ialized world. However, not much has been written about infants who survive
d extreme levels of serum bilirubin without neurologic damage. We present t
hree cases of extreme neonatal hyperbilirubinaemia, all with peak serum bil
irubin levels > 600 mu mol/L. Two of the infants developed neurologic seque
lae, but the third infant did not. In contrast to the two with sequelae. th
e infant without sequelae was female, had a positive Coombs' test, less cli
nical signs compatible with bilirubin encephalopathy, and a shorter exposur
e to serum bilirubin values > 400 mu moL/L.
Conclusion: The basic mechanism of bilirubin neurotoxicity remains unknown,
and it is not clear why some infants do not develop neurologic injury at s
erum bilirubin levels at which others do. We speculate that a comparison be
tween patients with sequelae and those without may yield important informat
ion.