Bilirubin Screening and Management of Hyperbilirubinemia
This document does not represent a comprehensive review of relevant information or recommendations included in the Clinical Practice Guideline released by the American Academy of Pediatrics (AAP) Subcommittee of Pediatrics. It is only meant to be a quick summary/reference of useful points coupled with our approach to bilirubin screening at LPCH. For the complete guideline visit the AAP link below.
Bilirubin Basics
- Bilirubin is derived from proteins that contain heme
- Biggest source is breakdown of from red blood cells
- Heme is broken down to biliverdin, which is reduced to bilirubin (in the process, CO is produced)
- Measurement of exhaled CO is an indication of ongoing hemolysis
Major Risk Factors for Developing Hyperbilirubinemia
- Predischarge TSB in High Risk zone on Bhutani nomogram
- Jaundice observed in the first 24 hours
- ABO incompatibility with positive direct Coombs, other known helmolytic disease
- Gestational age 35-36 weeks
- Previous sibling received phototherapy
- Cephalohematoma or significant bruising
- Exclusive breastfeeding, especially if not nursing well and excessive weight loss
- East Asian race
Use of Nomograms and Guidelines
- Nomograms help assess risk for developing hyperbilirubinemia and help arrange appropriate follow-up
- There is now good data and an accepted nomogram for assessing risk based on bilirubin level (Bhutani, 1999)
- Clinical Guidelines for screening and management are available from the AAP (July 2004)
- Early jaundice (age < 24h) still has a broad differential and requires workup, despite the ease of initiating management with phototherapy
Bilirubin Screening
- Screening policies that are widely used do not have good evidence for predicting hyperbilirubinemia (eg. screening babies of all O+ moms)
- Total Serum Bilirubin is inexpensive (<$2) and thus has a good cost/benefit ratio
- Technology will ultimately allow us to determine ongoing hemolysis with exhaled CO