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Neonatal Jaundice

The first 300 words of the full text of this article appear below.

	Objectives

 
After reviewing this article, readers should be able to:

1. Understand the metabolism of bilirubin.
   
2. Describe the factors that place an infant at risk for developing severe hyperbilirubinemia.
   
3. Describe the physiologic mechanisms that result in neonatal jaundice.
   
4. List the common causes of indirect hyperbilirubinemia in the newborn.
   
5. Delineate the criteria for diagnosing ABO hemolytic disease.
   
6. Discuss the major clinical features of acute bilirubin encephalopathy and chronic bilirubin encephalopathy (kernicterus).
   
7. List the key elements of the American Academy of Pediatrics guidelines for the management of hyperbilirubinemia.
   
8. Describe the factors that affect the dosage and efficacy of phototherapy.
   

	Case Report

 
A 23-year-old primiparous mother delivered a 36 weeks’ gestation male infant following an uncomplicated pregnancy. The infant initially had some difficulty latching on for breastfeeding, but subsequently appeared to nurse adequately, although his nursing quality was considered "fair." At age 25 hours, he appeared slightly jaundiced, and his bilirubin concentration was 7.5 mg/dL (128.3 mcmol/L). He was discharged at age 30 hours, with a follow-up visit scheduled for 1 week after discharge. On postnatal day 5, at about 4:30 PM, the mother called the pediatrician’s office because her infant was not nursing well and was becoming increasingly sleepy. On questioning, she also reported that he had become more jaundiced over the previous 2 days. The mother was given an appointment to see the pediatrician the following morning. Examination in the office revealed a markedly jaundiced infant who had a high-pitched cry and intermittently arched his back. His total serum bilirubin (TSB) concentration was 36.5 mg/dL (624.2 mcmol/L). He was admitted to the hospital, and an immediate exchange transfusion was performed. Neurologic evaluation at age 18 months showed profound neuromotor delay, choreoathetoid movements, an upward gaze paresis, and a sensorineural hearing loss.

This infant had acute bilirubin encephalopathy and eventually developed chronic bilirubin encephalopathy . . . [Full Text of this Article]

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This article has been cited by other articles:

				J. Profit, A. J. Cambric-Hargrove, K. O. Tittle, K. Pietz, and A. R. Stark Delayed Pediatric Office Follow-up of Newborns After Birth Hospitalization Pediatrics, August 1, 2009; 124(2): 548 - 554. [Abstract] [Full Text] [PDF]