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.