Elsevier

Clinics in Perinatology

Volume 27, Issue 1, 1 March 2000, Pages 171-179
Clinics in Perinatology

BILIRUBIN AND JAUNDICE IN THE MICROPREMIE

https://doi.org/10.1016/S0095-5108(05)70012-9Get rights and content

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BACKGROUND

Treatment protocols for severe hyperbilirubinemia secondary to Rh incompatibility accompanied and even preceded the development of modern neonatal intensive care. Preterm delivery and respiratory distress were often features of the perinatal management of the fetus and newborn with severe Rh-incompatible hemolytic disease. Respiratory distress syndrome, sepsis, profound anemia, and cardiovascular instability were all part of the clinical spectrum of Rh disease, especially following planned

PHYSIOLOGY OF BILIRUBIN PRODUCTION AND DISPOSAL IN LOW–BIRTH WEIGHT INFANTS

Several developmental and clinical characteristics of the very low–birth weight infant may alter bilirubin production and disposal.

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    The shorter half-life of fetal versus adult red cells, and an apparent tendency toward low-grade hemolysis in some very low–birth weight infants.

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    Delay in feeding, an important substrate for bulk intestinal flow and bacterial colonization in the term infant.

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    A lower serum albumin concentration.5 Although adequate for transport of bilirubin to the liver at normal

Developmental Aspects of Neonatal Preterm Jaundice

Does benign neonatal hyperbilirubinemia (i.e., physiologic jaundice) have a physiologic function? It may be appropriate to consider circulating bilirubin in the neonate as something more than only a waste product capable of damaging the brain. Bilirubin may be an antioxidant of physiologic importance.14, 15 A number of in vitro and in vivo studies demonstrate antioxidant properties of both bound and unbound bilirubin and its immediate precursors and metabolites at physiologic (i.e., nanomolar

DIAGNOSIS OF HYPERBILIRUBINEMIA IN THE MICROPREMIE

As noted previously, the clinical course of physiologic bilirubin elevation in the micropremie may be prolonged or exaggerated by accelerated red cell breakdown and lingering hepatic immaturity. With increasing survival of infants in the range of 750 g, it is now more difficult than it ever was to specify what circulating concentrations of indirect bilirubin are too high or potentially harmful in the micropremie. Early in their nursery course, plasma indirect bilirubin in the tiny premature

PREVENTION AND TREATMENT OF HYPERBILIRUBINEMIA IN VERY LOW–BIRTH WEIGHT INFANTS

Most clinicians prefer to deal with the problem of hyperbilirubinemia in very low–birth weight and extremely low–birth weight infants proactively, by early institution of phototherapy. Protocols that existed years ago giving weight-related criteria for exchange transfusion in preterm infants have been informally modified to include weight-related criteria for the early institution of phototherapy. The basic approach to treatment is as follows:

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    Phototherapy

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      Requires cutaneous

OUTCOMES

Postmortem bilirubin staining in the central nervous system of low–birth weight infants has markedly decreased or even disappeared from autopsy series since the time when low–bilirubin kernicterus was considered a significant clinical problem. In neurodevelopmental follow-up studies of very low–birth weight infants, the serum bilirubin concentration or its management have not yet emerged as significant independent variables affecting long-term neurodevelopmental outcome, and bilirubin appears

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Adress reprint requests to William J. Cashore, MD, Department of Pediatrics, Women and Infants Hospital of Rhode Island, 101 Dudley Street, Providence, RI 02905–2401

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