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More than 85% of newborns develop some degree of jaundice during the first days of life. Often a benign condition, the yellowish discolouration of the skin, sclerae, and mucous membranes in newborn infants is caused by unconjugated hyperbilirubinaemia, which may result from increased production of bilirubin, limited ability to conjugate bilirubin, and/or slow hepatic-enteric clearance of bilirubin.1 A small proportion of newborns develops extreme hyperbilirubinaemia, that is, a total serum bilirubin (TSB) level of 25 mg/dL (428 µmol/L) or more. When it is not timely recognised or treated, extreme unconjugated hyperbilirubinaemia may lead to acute bilirubin encephalopathy. This in turn carries a risk of developing a spectrum of long-term neurological sequelae known as kernicterus spectrum disorders (KSD), encompassing ‘classical kernicterus’ but also milder forms of permanent brain damage caused by bilirubin neurotoxicity.1 2 Worldwide, it is estimated that extreme hyperbilirubinaemia affects at least 481 000 late-preterm and term newborn infants annually, resulting in 114 000 deaths and more than 63 000 survivors with moderate or severe long-term disability.1 3 More than 75% of affected infants live in low-income and lower-middle-income countries. Moreover, in South Asia severe hyperbilirubinaemia is the seventh leading cause of neonatal mortality.1
When timely recognised, clinically significant hyperbilirubinaemia can be treated with conventional phototherapy and in more severe cases exchange transfusion, thus reducing the risk of KSD. Relatively uncommon in high-income countries, exchange transfusions …
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