The Role of Phototherapy in the Crash-Cart Approach to Extreme Neonatal Jaundice

Extreme neonatal jaundice occurs infrequently but carries a high risk of permanent sequelae (kernicterus) when it does. Rapid therapeutic intervention has the potential to reduce this risk in some infants. Several case reports of infants with acute intermediate to advanced bilirubin encephalopathy shows that reversal may be possible. Phototherapy can be instituted at the flip of a switch, whereas other therapeutic measures necessarily involve delays. Therefore, high-intensity phototherapy must be regarded as an emergency measure in infants presenting with extreme jaundice and even more so in the presence of neurological symptoms. The principal and well-described effect of phototherapy involves conversion of bilirubin IXα (z, z) to more polar isomers, which are excreted in bile and urine. When care is taken to maximize the spectral power of phototherapy lights, and whenever possible with measures added to reduce the enterohepatic circulation of bilirubin, very rapid reductions in total serum bilirubin levels are possible. A hypothesis has been advanced that conversion of bilirubin to more polar photoisomers, which can reach relative concentrations of 20%-25% of total serum bilirubin within 1-2 hours, might have a direct neuroprotective effect. This theory posits that because polar molecules generally require a transporter to cross the blood–brain barrier, bilirubin photoisomers should be less prone to enter the brain. Although this theory has some support in in vitro toxicity studies, the evidence is controversial. Until further experimental support can be gained, photoconversion of bilirubin does not constitute a viable argument against instituting further measures against bilirubin neurotoxicity, such as intravenous immune globulin (when indicated) and exchange transfusion. Conversely, neither is the state of evidence an argument against immediate and effective phototherapy in the medical emergency of extreme neonatal jaundice.