Diagnosis and management of hyperbilirubinemia in the term neonate: for a safer first week

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Scope of neonatal hyperbilirubinemia

Over 60% of the 3.5 million healthy babies admitted to well-baby nurseries in the United States will develop jaundice and be diagnosed with hyperbilirubinemia during the first week after birth. About 25% of these well babies who have TSB levels above the 75th percentile or with postnatal age in hours will be classified as being at high risk for developing TSB above the 95th percentile (severe hyperbilirubinemia). At this point, most babies are about 96 hours old, have already been discharged

The hour-specific bilirubin nomogram

The hour-specific bilirubin nomogram (Fig. 1) provides a more appropriate understanding of the magnitude of hyperbilirubinemia in the contexts of postnatal age in hours and the percentile level as defined for healthy infants. It was developed using bilirubin data from term and near-term infants who did not have evidence of hemolytic disease or other illness requiring neonatal intensive care unit (NICU) admission [4], [12]. This nomogram was not specifically designed to be used in premature

Clinical manifestations of neonatal hyperbilirubinemia

Serial observations of the clinical manifestations of jaundice and hyperbilirubinemia indicate two patterns from a management perspective, irrespective of the specific etiology of hyperbilirubinemia. Early-onset severe hyperbilirubinemia is generally associated with increased bilirubin production, whereas late-onset hyperbilirubinemia is likely to be associated with delayed bilirubin elimination that may or may not be complicated with increased bilirubin production. Both are described below in

Clinical management of neonatal hyperbilirubinemia

The primary goal for effective and efficient management of neonatal hyperbilirubinemia is to prevent ABE. Of the preventive clinical strategies, implementation of either the existing AAP guidelines or those enhanced by a system-based approach may be used. There are no comparative studies of these two approaches thus far, and both are likely to be effective, provided all babies are screened before discharge and uniformly followed postdischarge. We have practiced and implemented a system-based

Predischarge management

A system-based approach (Table 2) addresses parental education, clinical recognition of jaundice, and predischarge risk assessment with multidisciplinary strategies to

  • Recognize the clinical significance of jaundice within the first 24 hours after birth

  • Recognize the limitations of visual recognition of jaundice

  • Recognize and document clinical jaundice and document severity of hyperbilirubinemia by a bilirubin measurement before discharge from the hospital

  • Ensure postdischarge follow-up based on

“Crash-cart” approach to ABE in babies who have severe hyperbilirubinemia

Once specific signs of ABE are recognized, the goal of therapy is a prompt, expeditious, and safe reduction of the bilirubin load. Strategies to accomplish this have also been detailed in the AAP Practice Parameters [13]. Our “crash-cart” approach is based on the following considerations:

  • 1.

    Presently, only an exchange transfusion can accomplish rapid and effective clearance of bilirubin in a symptomatic neonate to minimize brain damage.

  • 2.

    The risk of a performing an exchange transfusion (in

Long-term follow-up

The authors recommend that all babies who have TSB levels above 25 mg/dL, those who receive an exchange transfusion, those who have had ABR abnormalities (even transient), and those who manifested the intermediate (or more) clinical signs of ABE should be followed during infancy and childhood until school age. The clinical follow-up should include a neurologic and neurodevelopmental evaluation (especially for extrapyramidal function and for processing disorders) as well as auditory neuropathy.

Summary

Bilirubin-induced neurologic dysfunction can occur in term and near-term healthy babies. The term babies who are unwell, the preterm neonates, and the infants who have multiple comorbidities constitute a group vulnerable to bilirubin neurotoxicity. The current resources for clinical interventions that can drastically and efficiently reduce the increased bilirubin load—intensive phototherapy and exchange transfusions—are available for use in those infants who have excessive hyperbilirubinemia

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