Neonatal Jaundice

Jaundice is a relatively common occurance in human infants. As in adults, jaundice is due to elevated blood concentrations of bilirubin (hyperbilirubinemia). There are at least two significant processes that predispose normal infants to jaundice:

• The rate of bilirubin production is higher in infants than adults because their red blood cells have a shorter half-life and turn over more rapidly.
• Infants have a relatively limited ability to conjugate bilirubin, and conjugation in the liver is necessary for efficient elimination.

Additionally, there are a number of pathologic conditions that can result in neonatal jaundice. Examples include:

• Conditions that cause accelerated destruction of red cells, which can occur as a result of immune-mediated hemolysis, certain enzyme deficiencies, or structural abnormalities in red cells.
• Increased intestinal absorption of bilirubin, which blunts the infant's ability to eliminate this waste product. Infants that fail to feed well are often deficient in the types of intestinal bacteria that metabolize bilirubin, and in such cases, significant amounts of bilirubin of reabsorbed into blood.
• Genetic defects in hepatic uptake of bilirubin (e.g. Gilbert's syndrome) or deficiency in the enzyme necessary for conjugating bilirubin (uridine diphosphate glucuronosyltransferase).

A large majority of cases of neonatal hyperbilirubinemia are mild and resolve over the first few weeks of life. However, persistently high concentrations of bilirubin can be dangerous. Elevated levels of bilirubin interfere with a number of cellular processes, and may be neurotoxic. Kernicterus is a serious and life-threatening form of neonatal jaundice that reflects the toxicity of bilirubin to the central nervous system. Kernicterus, in both acute and chronic forms, is manifest by a variety of neurologic and cognitive deficits ranging from poor suckling and seizures to low IQ. Clearly, this disorder should be treated without delay.

The standard treatment for neonatal jaundice is phototherapy. Affected infants are placed under lights, and photons are absorbed by bilirubin as it circulates in skin capillaries. This energy transfer results in conversion of bilirubin to lumirubin and other products which, in contrast to bilirubin, are more water-soluble and readily excreted. The rate of bilirubin elimination depends upon both the wavelength of light used and its dose. Blue light (460 to 490 nm) is the most effective, but such light causes eye strain in those monitoring the baby, making it difficult to detect other conditions such as cyanosis. The most frequently used form of phototherapy is standard fluorescent white light.

In severe cases of neonatal jaundice, another effective treatment is exchange transfusion. In this procedure, small amounts of blood (and hence bilirubin) are removed from the baby and replaced with donor blood; this procedure is repeated until roughly twice the blood volume has been replaced. Exchange transfusion also eliminates antibodies against red blood cells, which may be the inciting factor in development of hyperbilirubinemia.

Neonatal jaundice almost certainly occurs in animals other than humans, but, by it self, is not recognized as a significant disorder. Immune-mediated hemolytic anemias are relatively common in foals, calves and piglets, and may lead to jaundice. However, the most serious aspect of this disease is the anemia, rather than jaundice per se.

References and Reviews

• Dennery PA, Seidman DS, Stevenson DK: Neonatal hyperbilirubinemia. New Eng J Med 344:581, 2001.
• Ennever JF: Blue light, green light, white light, more light: treatment of neonatal jaundice. Clin Perinatol 17:467, 1990.
• Maisels MJ, McDonagh AF. Phototherapy for neonatal jaundice. New Eng J Med 358:920-928, 2008.
• Newman TB, Liljestrand P, Jeremy RJ, etc. Outcomes among newborns with total serum bilirubin levels of 25 mg per deciliter or more. New Eng J Med 354:1889, 2006.

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