Although neonatal jaundice is usually a self limited condition, in exceptional circumstances, extreme hyperbilirubinaemia, with its devastating potential of irreversible brain damage due to bilirubin encephalopathy or kernicterus, may occur. For the most part, kernicterus should nowadays be a preventable condition; however, cases continue to occur. The reasons for the persistence of kernicterus are undoubtedly multifactorial. One factor may have been an opinion which evolved at the beginning of the 1990s that in some cases higher serum total bilirubin (STB) concentrations could be allowed than were previously acceptable. At about the same time a new phenomenon developed: that of earlier and earlier discharge of the mother-infant dyad. The potential consequences of discharge at or even earlier than 24 hours are that in many instances lactation may not yet be established, jaundice may often not have become manifest, to say nothing of reaching its peak, and associated illnesses may not yet have declared themselves. Additional factors included discharge of borderline premature neonates of 35–37 weeks gestation as if they were born at term, and failure of physicians to abide by the guidelines for the detection of hyperbilirubinaemia and prevention of kernicterus published by the American Academy of Pediatrics (AAP) in 1994.¹ During the last 15 years, cases of kernicterus were reported not only from the United States,² but also, although to a lesser extent, from other industrialised countries, including Canada, Denmark, Holland, and New Zealand.³ The myth that haemolysis was a prerequisite for kernicterus was disproved.⁴ By the year 2001 the number of cases of kernicterus reported was sufficient for the AAP to publish a warning cautioning paediatricians of the potential of kernicterus and the dangers of hyperbilirubinaemia.⁵

In response to the continuing occurrence of cases of kernicterus, the AAP has recently …