Extreme neonatal hyperbilirubinaemia in refugee and migrant populations: retrospective cohort

Abstract

ObjectiveTo describe neonatal survival and long-term neurological outcome in neonatal hyperbilirubinaemia (NH) with extreme serum bilirubin (SBR) values.DesignRetrospective chart review, a one-off neurodevelopmental evaluation.SettingSpecial care baby unit in a refugee camp and clinics for migrant populations at the Thailand–Myanmar border with phototherapy facilities but limited access to exchange transfusion (ET).PatientsNeonates ≥28 weeks of gestational age with extreme SBR values and/or acute neurological symptoms, neurodevelopment evaluation conducted at 23–97 months of age.Main outcome measuresNeonatal mortality rate, prevalence of acute bilirubin encephalopathy (ABE) signs, prevalence of delayed development scores based on the Griffiths Mental Development Scale (GMDS).ResultsFrom 2009 to 2014, 1946 neonates were diagnosed with jaundice; 129 (6.6%) had extreme SBR values during NH (extreme NH). In this group, the median peak SBR was 430 (IQR 371–487) µmol/L and the prevalence of ABE was 28.2%. Extreme NH-related mortality was 10.9% (14/129). Median percentile GMDS general score of 37 survivors of extreme NH was poor: 11 (2–42). ‘Performance’, ‘practical reasoning’ and ‘hearing and language’ domains were most affected. Four (10.8%) extreme NH survivors had normal development scores (≥50th centile). Two (5.4%) developed the most severe form of kernicterus spectrum disorders.ConclusionIn this limited-resource setting, poor neonatal survival and neurodevelopmental outcomes, after extreme NH, were high. Early identification and adequate treatment of NH where ET is not readily available are key to minimising the risk of extreme SBR values or neurological symptoms.

High levels of pathological jaundice in the first 24 hours and neonatal hyperbilirubinaemia in an epidemiological cohort study on the Thailand-Myanmar border

“…As far as we are aware this study represents the first report of a high proportion (26%) of pathological NH in the first 24 hours of life in a resource-limited setting: all preterm neonates <35 weeks of gestation developed NH, and all within the first 24 h. The high rate of NH in four of five neonates born at 35 to 37 weeks of gestation, half of whom developed this within 24 h, is a more unusual pattern but is partially recognized by both American Academy of Pediatrics and the NICE guidelines. Premature neonates are at higher risk of developing severe NH and developing acute neurological sequelae [ 33 ]. Early screening is therefore paramount to avoid delaying the start of PT and thus reducing the risk of bilirubin-induced neurological dysfunction; as in this study, the value of the first TSB screening done at 24 h of life or earlier was already above the gestational-age adjusted PT threshold in nearly all preterm neonates.…”

Diagnostics Value of Quantitative Magnetic Resonance Imaging (MRI) in Neonatal Acute Bilirubin Encephalopathy

“…Acute bilirubin encephalopathy can cause irreversible brain damage, including movement disorders of dystonia and choreoathetosis, sensorineural hearing loss, oculomotor paresis, and tooth enamel dysplasia. 25,26 This has significant consequence for the life quality of neonates and imposes psychological and economic burden on the affected families and the society at large. The estimated incidence of acute bilirubin encephalopathy is approximately 1.2 to 1.3 per 100 000 neonates, whereas the incidence is higher in low-income and middle-income countries.…”