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Hyperbilirubinemia is a condition when blood bilirubin level crosses a threshold allowing bilirubin – a catabolic breakdown byproduct produced from hemoglobin – to cross the blood-brain barrier. Consequently, infants with hyperbilirubinemia are susceptible to near and long-term brain damage, e.g., cerebral palsy, as bilirubin is a neurotoxin.

Neonatal Phototherapy

Newborn babies have high hemoglobin content in their blood as it was necessary to transport oxygen to them when they were a fetus. Immediately following birth, air is available more easily as they start to breathe air. Coupled with reduced need of hemoglobin, the short life span of red blood cells in the neonatal phase, and reduce liver uptake, bilirubin starts building in the body for every neonate. This buildup is most noticeable in up to 60% of term and 80% of preterm neonates in the second day after birth [1].

Phototherapy is the most common form of treatment provided to jaundiced neonates. The light delivered by phototherapy equipment breakdown the non-polar bilirubin, which cannot be eliminated from the body easily, into water-soluble products that are cleared through urine and stool. The most common form of non-polar bilirubin in the body is called ZZ Bilirubin due to its chemical structure. Photoirradiation of ZZ bilirubin triggers two isomerization reactions [2,3] to occur: (a) an irreversible structural isomerization reaction that produces EE cyclobilirubin, EZ cyclobilirubin, and few others collectively known as lumirubin; (b) a reversible configurational isomerization reaction that yields ZE Bilirubin.

In humans, structural isomerization plays a significant role in bilirubin elimination as configurational isomers have a rate lamination on their removal. Moreover, the configurational isomerization reaction, unlike its counterpart, reaches an equilibrium state known as photo-stabilization state after which the rate of its production does not increase with treatment light intensity. It has been concluded by many researchers [4- 8], through clinical validation, that the efficacy of phototherapy treatment could be improved by tapping into the rate dependence of structural isomers on treatment intensity.

Albeit, the rate also depends on the wavelength of treatment light and body surface coverage. In conclusion, the efficacy of phototherapy in neonates can be increased to quickly reduce the risk posed by bilirubin neurotoxicity by increasing their body surface coverage and treatment light intensity from an appropriate light source with specified peak wavelength and bandwidth according AAP & FDA norms.


1.    Newman, T. B., Easterling, M. J., Goldman, E. S., &Stevenson, D. K. (1990). Laboratory evaluation of jaundice in newborns:frequency, cost, and yield. American Journal of Diseases of Children, 144(3),364-368.

2.    Ennever, J. F., Sobel, M., Mcdonagh, A. F., &Speck, W. T. (1984). Phototherapy for neonatal jaundice: in vitro comparison oflight sources. Pediatric research, 18(7), 667.

3.    Ennever, J. F., Costarino, A. T., Polin, R. A., &Speck, W. T. (1987). Rapid clearance of a structural isomer of bilirubin duringphototherapy. The Journal of clinical investigation, 79(6), 1674-1678.

4.    Sweeting, J. (1987). Bilirubin and lumirubin in thenewborn. Gastroenterology, 93(6), 1443-1444.

5.    Kirk, J. M. (2008). Neonatal jaundice: a criticalreview of the role and practice of bilirubin analysis. Annals of clinicalbiochemistry, 45(5), 452-462.

6.    Itoh, S., Okada, H., Kuboi, T., & Kusaka, T.(2017). Phototherapy for neonatal hyperbilirubinemia. Pediatrics International,59(9), 959-966.

7.    Lamola, A. A. (2016). A pharmacologic view ofphototherapy. Clinics in perinatology, 43(2), 259-276.

8.    Vandborg, P. K., Hansen, B. M., Greisen, G., &Ebbesen, F. (2012). Dose-response relationship of phototherapy forhyperbilirubinemia. Pediatrics, peds-2011.