Prolonged neonatal jaundice and phototherapy mechanisms
THE CONTEXT
The passage defines prolonged jaundice in term infants, outlines its evaluation, and explains how phototherapy promotes bilirubin elimination.
Prolonged jaundice
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Prolonged jaundice is significant jaundice of approximately 10 mg/dL persisting beyond three weeks in a term baby.
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Common causes include inadequate feeding, breast milk jaundice, extravasated blood such as cephalohematoma, ongoing hemolytic disease, G6PD deficiency, and hypothyroidism.
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Assess urine and stool color and measure direct bilirubin to rule out cholestasis.
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Dark urine or significant jaundice warrants investigation for cholestasis, ongoing hemolysis including a G6PD screen, hypothyroidism, and urinary tract infection.
Principles of phototherapy
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Phototherapy is the mainstay of treatment for neonatal hyperbilirubinemia. It converts insoluble unconjugated bilirubin into soluble isomers that can be excreted in urine and feces.
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Blue-green light at 460–490 nm is effective; light sources with high irradiance in this range are more effective.
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Bilirubin must be present in the skin for phototherapy to work, so the passage states that prophylactic phototherapy has no role.
Mechanisms and relative contributions
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Configurational isomerization converts bilirubin Z-isomers to E-isomers immediately on light exposure. This reaction is reversible as bilirubin reaches the bile duct.
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After 8–12 hours of phototherapy, these non-toxic E-isomers account for about 25% of total serum bilirubin. Their slow excretion makes this a less significant mechanism for lowering total serum bilirubin.
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Structural isomerization irreversibly converts bilirubin to lumirubin. Although lumirubin forms only 2–6% of total serum bilirubin, its rapid excretion makes this the main mechanism of the phototherapy-induced decline.
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The response is directly proportional to the dose of phototherapy.
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Photo-oxidation is a minor reaction that generates photoproducts excreted in urine.