Neurological complications of neonatal hyperbilirubinemia in Eastern India

Abstract Background: Neonatal hyperbilirubinemia (NH) affects up to 60%–80% of term and near-term infants and, when severe or delayed in treatment, can progress to acute bilirubin encephalopathy or permanent kernicterus. In Eastern India, late recognition and limited resources exacerbate the risk of lasting neurodevelopmental injury. Objectives: To determine the neurologic outcomes in NH neonates from Eastern India, identify key risk factors, and evaluate the impact of therapeutic interventions. Materials and Methods: We performed a 24-month prospective observational study at a tertiary-care center, enrolling preterm, term, and near-term neonates with total serum bilirubin ≥15 mg/dL. Neurologic assessments comprised bilirubin-induced neurologic dysfunction (BIND) scoring, brain imaging (ultrasound/magnetic resonance imaging), brainstem evoked response audiometry, and developmental screening at 6 months. Results: Hemolytic factors—glucose-6-phosphate dehydrogenase deficiency (18%), ABO blood group (14%), and positive direct Coombs test (16%)—were linked to significantly higher peak bilirubin ( P < 0.01) and greater exchange transfusion (ET) rates ( P < 0.001). In multivariable models, ET (odds ratio [OR]: 0.24; 95% confidence intervals [CI]: 0.10–0.60), higher peak bilirubin (OR: 0.88 per mg/dL; 95% CI: 0.82–0.95), baseline tone abnormalities (OR: 0.35; 95% CI: 0.16–0.77), and sepsis (OR: 0.42; 95% CI: 0.18–0.99) independently predicted poor BIND score improvement. Low 5 min Apgar (<7) and acidosis were the sole predictors of congenital anomalies. Peak bilirubin (OR: 1.10; 95% CI: 1.04–1.16), ET (OR: 3.88; 95% CI: 1.36–11.06), delayed feeding (OR: 2.73; 95% CI: 1.08–6.92), and congenital anomaly (OR: 4.52; 95% CI: 1.29–15.80) independently increased odds of abnormal neurodiagnostic findings. Conclusion: Early identification of risk factors and treatment was needed to mitigate irreversible neurologic damage.