Incidence and causes of severe neonatal hyperbilirubinemia in Canada

Maisels and Newman’s commentary (CMAJ 2006;175:599) accurately pointed out some difficulties in interpretation of data from our recent article1. There is no doubt that due to the inherent nature in which studies are conducted through surveillance programs incompleteness of data collection can lead to an underestimation of the number of index cases and limit our ability to thoroughly analyze the underlying etiologies. Despite these limitations, our study has shown that severe hyperbilirubinemia continues to occur in Canada and that the majority of infants that were discharged home were subsequently readmitted shortly after leaving the hospital. This raises the concern that at the time of initial discharge health care providers are missing an opportunity to prevent severe hyperbilirubinemia. Although recommendations from the AAP2 have recently been published, they are currently not being followed or are impractical to apply for these patients.

Introducing routine screening tests (serum bilirubin, blood group and Coombs’ testing) in order to prevent severe hyperbilirubinemia may have financial implications including longer hospital stays for neonates. Given the impact of introducing these investigations, it is of paramount importance to understand the burden of illness that severe hyperbilirubinemia and its complications cause in Canada, namely bilirubin -induced neurological dysfunction (BIND) and kernicterus. Newman and Maisels state that kernicterus is estimated to be infrequent, anywhere from 1:100,000 to 1:50,000 live births. They acknowledge however that this is based on very little research data. They reference a Danish study3 that estimated the incidence of kernicterus at 1:50,000 to 1:60,000. It is important to note that this was by no means a systematic review of their population, and was based on case reports in a relatively homogenous population. In our study 50.4% of the infants reported were born to non- caucasian mothers1. Ethnicity may be one of the contributing factor responsible for severe hyperbilirubinemia secondary to a higher incidence of Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency in these populations and a delay in recognition of jaundice due to the babies darker pigmentation.

We believe that careful assessment of newborns at the time of discharge is helpful, and consideration of blood group incompatibility and risk of G6PD deficiency would be helpful in planning investigations prior to discharge such as serum bilirubin as well as appropriate follow-up in order to prevent neonatal hyperbilirubinemia, readmission to hospital and possible neurological complications. A more accurate estimate of kernicterus is of paramount importance in order to justify cord blood testing and the measurement of serum bilirubin at the time an infant is discharged from hospital.

REFERENCES 1. Sgro M, Campbell DM, Shah V. Incidence and causes of severe neonatal hyperbilirubinemia in Canada. CMAJ 2006;175(6):587-90. 2. American Academy of Pediatrics Clinical practice guideline: management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics 2004;114(1):297-316. 3. Ebbesen F. Recurrence of kernicterus in term and near-term infants in Denmark. Acta Paediatr 2000;89(10):1213-7.

Michael Sgro Douglas Campbell Department of Pediatrics St. Michael's Hospital Toronto, Ont. Vibhuti Shah Mount Sinai Department of Pediatrics Toronto, Ont.

Conflict of Interest:

None declared