Six cases of kernicterus in term and near-term infants, diagnosed in Denmark between 1994 and 1998, are reported from the University Hospital of Aalborg. These reports contrast with a complete absence of cases in Denmark for the previous 20 years. The etiology of the hyperbilirubinemia was spherocytosis, galactosemia, A-0 blood type incompatibility in 2, and unknown in 2. The maximum plasma total bilirubin concentrations were 531-745 mcmol/L. Causes listed for the re-emergence of cases of kernicterus include the following: 1) a decreased awareness of signs of kernicterus; 2) premature discharge of infants from the maternity ward; 3) breast-feeding associated jaundice; 4) difficulty in recognition of jaundice in some ethnic patient groups. The following preventive measures are considered: a) alert healthcare workers to the risks of bilirubin encephalopathy; b) instruct mothers more fully before discharge; c) more liberal use of infant formula supplements; d) lower plasma bilirubin limits for phototherapy and exchange transfusion; e) screen all term and near-term infants; f) use skin jaundice detection device that corrects for melanin content. [1]

COMMENT. A recent increase in the cases of kernicterus in term or nearterm infants in Denmark has raised concerns regarding the primary and secondary healthcare recognition and management of the problem. A larger prospective study of infants with elevated bilirubin levels should be performed prior to considering a population-based screening program.

Prediction and prevention of hyperbilirubinemia is currently a concern in the USA [2]. The predictors of extreme neonatal hyperbilirubinemia (> or = to 428 mcmol/L) determined in 11 Northern California Kaiser Permanente hospitals and a cohort of >51,000 term newborns included the following: 1) family history of jaundice in a newborn; 2) exclusive breastfeeding; 3) cephalhematoma. No case of kernicterus was diagnosed.

Diagnosis of kernicterus. The characteristic neurological findings of kernicterus (athetosis, impaired vertical gaze, and auditory loss or imperception) may not evolve until 4 years of age. In the neonatal period, the diagnosis is suspected when an infant with hyperbilirubinemia becomes drowsy, hypertonic and opisthotonic, the Moro reflex is absent, and the cry abnormal. Clonic convulsions occur in about 10% of cases. Early classic references to kernicterus as a form of cerebral palsy are by Byers RK, Paine RS, and Crothers B [3] and Perlstein MA (Charles C Thomas, 1961).