Even in term fetuses, hepatic maturation is not complete, and thus some unconjugated bilirubin-either albumin bound or free-is cleared by placental transfer to be conjugated in the maternal liver (Chap. 7, p. 135). Fetal protection from unconjugated bilirubin is lost after delivery if not cleared rapidly. Because clearance is totally dependent on neonatal hepatic function, varying degrees of neonatal hyperbilirubinemia result. Even in the mature newborn, serum bilirubin levels usually rise for 3 to 4 days to reach up to 10 mg/ dL. After this, concentrations usually fall rapidly. In one large study, 1 to 2 percent of neonates delivered at 35 weeks' gestation or later had a maximum serum bilirubin level >20 mg/ dL (Eggert, 2006). Concomitant glucose-6-phosphate deiciency worsens hyperbilirubinemia (Chang, 2017). In approximately 15 percent of term newborns, bilirubin levels cause clinically visible skin yellowing termed physiological jaundice (Burke, 2009). As expected, in preterm neonates, the bilirubin elevation is greater and more prolonged.
Excessive serum bilirubin levels can be neurotoxic for newborns (Dijk, 2012; Watchko, 2013). he pathogenesis is complex, and toxicity has two forms. Acute bilirubin encephalopathy is encountered in the irst days of life and is characterized by hypotonia, poor feeding, lethargy, and abnormal auditory-evoked responses (Kaplan, 2011). Immediate recognition and treatment'will usually mitigate progressive neurotoxicity. he chronic form is termed kernicterus. With this, neurotoxicity follows bilirubin deposition and staining of the basal ganglia and hippocampus and is further characterized by profound neuronal degeneration. Survivors have spasticity, muscular incoordination, and varying degrees of mental deiciencies (Frank, 2017). Although there is a positive correlation between kernicterus and unconjugated bilirubin levels above 18 to 20 mg/dL, it can develop at much lower concentrations, especially in very preterm neonates (Sgro, 2011). Continuing hemolysis is a risk factor for kernicterus (EI Houchi, 2017; Vandborg, 2012).
Various forms of phototherapy are used to prevent and treat neonatal hyperbilirubinemia (Ree, 2017). These «bili-lights" emit a spectrum of 460 to 490 nm, which augments bilirubin oxidation to enhance its renal clearance and lower serum levels. Sunlight iltered to remove ultraviolet light has been used in resource-poor countries (Slusher, 2015). Light that penetrates the skin also increases peripheral blood low, which further enhances photo-oxidation. It is problematic that available devices are not standardized (Bhutani, 2011). Another advantage is that exchange transfusions are seldom required with phototherapy. Studies in both preterm and term newborns attest to phototherapy eicacy (Watchko, 2013). A Neonatal Research Network study reported that aggressive phototherapy in low-birthweight neonates reduced rates of neurodevelopmental impairment (Newman, 2006). Similar reductions were reported from Canada after implementation of 2007 guidelines (Sgro, 2016).