Early prediction of adverse outcomes in infants with acute bilirubin encephalopathy.

Wenqing Kang,Wen Li,Changlian Zhu,Dapeng Liu,Yanchao Cheng,Rui Li,Bangli Xu,Xiao Yuan,Juan Song,Yaodong Zhang,Falin Xu

doi:10.1002/acn3.51077

Abstract

ObjectiveAcute bilirubin encephalopathy (ABE) remains one of the important causes of neonatal mortality and child disability, early identification, and intervention which could improve outcomes. The purpose of this study was to evaluate early predictors of adverse outcomes in infants with ABE.MethodsNewborns of gestational age ≥ 35 weeks and diagnosed with ABE were included in the study. Bilirubin‐induced neurological dysfunction (BIND) score, total serum bilirubin (TSB) peak value, and serum albumin levels were determined. Adverse outcomes were defined as death or survival with auditory dysfunction and/or cerebral palsy.ResultsEighty‐two infants were eligible for recruitment in the study. The outcome data from 76 ABE infants (92%) were used for analysis, of which 25 infants got adverse outcomes and 51 live a normal life. Univariate analysis for BIND score, TSB peak value, bilirubin–albumin ratio (B/A), albumin level, abnormal AABR, and neonatal sepsis was performed to elucidate the association with adverse outcomes. Bivariate logistic regression analysis showed B/A (OR 10.48, 95%CI: 1.55–70.81, P = 0.02) and BIND score (OR 3.68, 95%CI: 1.39–9.72, P = 0.01) were correlated with adverse outcomes. ROC curve analysis showed that B/A (≥8.9 mg/g), BIND score (≥6) could predict adverse outcomes of ABE separately; B/A in conjunction with BIND score could increase prediction sensitivity to 100%.InterpretationBoth B/A and BIND score can be used to predict adverse outcomes of ABE, and the combination of the two parameters can increase prediction sensitivity significantly.

Highlights

Studies have revealed that increased levels of bilirubin is detrimental for nervous system, especially damage the basal ganglia, cerebellum, and brainstem, resulting in acute bilirubin encephalopathy (ABE).[1,2] Acute bilirubin encephalopathy (ABE) in neonates is a significant cause of death or lifelong disability, including cerebral palsy (CP)[3,4] and auditory disorders.[5]
We focused on the above-mentioned biochemical profile, and on magnetic resonance imaging (MRI), automated auditory brainstem response (AABR), and clinical assessment such as Bilirubin-induced neurological dysfunction (BIND) scores, to determine the early predictors of adverse outcomes in ABE
Twelve severe ABE infants died of ABE during hospitalization (4 with ABO hemolysis, 3 with Rh hemolysis, 4 with sepsis, 1 with ABO hemolysis and sepsis), and 13 infants turned out with poor outcome (4 cases with hearing disabilities, 1 with CP, and 8 with both hearing disability and CP)

Summary

Introduction

Studies have revealed that increased levels of bilirubin is detrimental for nervous system, especially damage the basal ganglia, cerebellum, and brainstem, resulting in acute bilirubin encephalopathy (ABE).[1,2] ABE in neonates is a significant cause of death or lifelong disability, including cerebral palsy (CP)[3,4] and auditory disorders.[5]. Studies have revealed that increased levels of bilirubin is detrimental for nervous system, especially damage the basal ganglia, cerebellum, and brainstem, resulting in acute bilirubin encephalopathy (ABE).[1,2]. ABE in neonates is a significant cause of death or lifelong disability, including cerebral palsy (CP)[3,4] and auditory disorders.[5]. Incidence of ABE has decreased in the developed countries; ABE morbidity is still high in the developing countries. In Nigeria, 159 cases of ABE were diagnosed in 1040 patients who were a 2020 The Authors. Predicting Outcome in Acute Bilirubin Encephalopathy admitted for treatment of jaundice (15.3%).[6]. In China, 348 ABE cases were reported across 33 tertiary care referral centers, accounting for about 4.8% of the total number of newborns admitted in 2012.7

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Results

Conclusion