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Rare disorder characterized by development of a gray-brown discoloration that may persist for months in neonates undergoing phototherapy for neonatal hyperbilirubinemia.

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Neonatal Jaundice.

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None.

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Combination of hepatocellular dysfunction and increased bilirubin products from photodestruction during phototherapy. The exact source of the pigment is unknown; it may be a photoisomer of natural bilirubin. Phototherapy with bilirubin acts as a catalyst, forming photoproducts from copper-bound porphyrins, causing skin discoloration.

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Age and clinical course (appearance of the discoloration with the use of phototherapy), liver biopsy (hepatocellular dysfunction with decreased excretion of bile constituents and photooxidation products at the level of bile canaliculi). Causative factor for the hyperbilirubinemia should be determined by appropriate tests.

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Discoloration usually improves over time. Outcome usually is benign in cases where the hyperbilirubinemia is caused by icterus neonatorum, although the prognosis depends on the causative liver disease. Risk of bilirubin encephalopathy may be increased.

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Exclude other causes of discoloration (e.g., cyanosis, gray baby syndrome from chloramphenicol overdose). Evaluate severity of hepatic dysfunction and determine the underlying cause of impairment. Kernicterus should be excluded and appropriate treatment instituted (exchange transfusion, phenobarbital). Preoperative investigations should include a complete blood count, liver function tests, coagulation studies, arterial blood gas analysis, urea, and creatinine.

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Anesthetic issues related to neonatal period should be considered (immaturity of various systems, differences in pharmacokinetics and pharmacodynamics). Adequate hydration should be maintained in patients with significant hyperbilirubinemia to prevent development of renal failure. Administer vitamin K. If prothrombin time is abnormal, clotting factors should be available. Hypotension should be avoided to minimize the reduction in hepatic perfusion. Anesthetic management of the neonate must take into account the causative factor for the development of hyperbilirubinemia. The perioperative risk is significantly increased in the presence of kernicterus. Factors known to precipitate seizures in neonates should be avoided (e.g., hypoxia, hypercarbia, hyponatremia, hypoglycemia).

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Hepatocellular dysfunction prolongs the elimination half-life of drugs excreted via the biliary system (e.g., pancuronium, vecuronium). Atracurium or cisatracurium is the drug of choice for paralysis. Halothane should be avoided in view of a theoretical risk of hepatitis, especially since sevoflurane is available for inhalational induction. Anesthetic agents that are proconvulsants should be avoided.

Ashley JR, Littler CM, Burgdorf WH, et al: Bronze baby syndrome. J Am Acad Dermatol 12:325, 1985.  [PubMed: 3973126]
Bertini G, Dani C, Fonda C, et al. Bronze baby syndrome and the risk of kernicterus. Acta Paediatr 94:968, 2005.  [PubMed: 16188824]
Rubaltelli FF, Da Riol R, D'Amore ES, Jori G: The bronze baby syndrome: evidence of increased tissue concentration of copper porphyrins. Acta Paediatr 85:381, 1996.  [PubMed: 8696003]

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