INTRODUCTION
Chemical hyperbilirubinemia, defined as total serum bilirubin (TSB) ≥2.0 mg/dL, is virtually universal in newborns during the 1st week of life. Neonates characteristically do not appear jaundiced until TSB exceeds 5 to 7 mg/ dL.[1] Neonatal hyperbilirubinemia (NNH) is an important cause of preventable brain damage among infants. Emerging current practices like early hospital discharges have led to a rise in the rate of preventable neurodevelopmental sequelae resulting from untreated NNH.
By pathologic criteria, Kernicterus develops in 30% of infants with bilirubin levels >25-30 mg/dL[1]. In clinical setting, kernicterus denotes the chronic and permanent sequelae of bilirubin toxicity. Acute Bilirubin Encephalopathy is the clinical manifestation of bilirubin toxicity in neonatal period. It has been well recognized that once “Acute Bilirubin Encephalopathy” develops babies sustain varying degree of neurodevelopmental sequelae. Hyperbilirubinemia in term infants has been associated with abnormalities in Brainstem Auditory Evoked Responses (BERA), cry characteristics, and neurobehavioral measures. There has been conflicting evidence regarding the proportionate association of peak serum bilirubin with the future neurodevelopmental delay. The level of bilirubin associated with toxicity in healthy term or preterm infants is uncertain and appears to vary among infants and in different clinical circumstances [2-4].
This study was aimed to assess the association between neonatal peak total serum bilirubin levels and the neurodevelopmental outcome at 6 months of age in healthy term infants with NNH. The study also aimed to assess changes if any, in auditory evoked responses of neonates with hyperbilirubinemia.