What is Jaundice?
Bilirubin synthesis, transport, and excretion. Abbreviations: RBC, erythrocytes; RE, reticuloendothelial. Adapted from Hyperbilirubenimia, Watson, 2009.
A baby shown with jaundice on the left, note the yellow tone to the skin. The same baby after treatment on the right.
Establishing “risk zones” for the prediction of hyperbilirubinemia in newborns. This nomogram is based on hour-specific bilirubin values obtained from 2,840 well newborns >36 weeks gestational age whose birthweights were >2,000 g or >35 weeks gestational age whose birthweights were >2,500 g. The serum bilirubin concentration was measured before discharge. The risk zone in which the value fell predicted the likelihood of a subsequent bilirubin level exceeding the 95th percentile.
As early as 1724, neonatal jaundice, or hyperbilirubinemia, has been observed in newborns. Today, approximately 60% of newborns and 80% of preterm infants develop hyperbilirubinemia, making this the most common condition requiring evaluation and treatment in newborns. Jaundice results from the deposition of bilirubin, a substance formed during the hemolysis of red blood cells, in the skin and mucous membranes. This deposition causes a yellowing of the skin and eyes, which is the most common symptom of jaundice. This deposition is often of little consequence; however, it has potentially devastating, permanent effects if ignored.
Health Complications from Jaundice
Hyperbilirubinemia is known to have severe neurological effects, some permanent and some reversible. This occurs when toxic, unconjugated bilirubin crosses the blood-brain barrier and settles primarily in the basal ganglia, central and peripheral auditory pathways, hippocampus, subthalamic nuclei, midbrain, and cerebellum. This results in TSB concentrations greater than 20 mg/dL. The two major neurological risk factors are bilirubin encephalopathy and kernicterus. Acute bilirubin encephalopathy occurs in three phases during the first few weeks after birth:
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Slight stupor (lethargy), slight hypotonia (scarcity of movement), poor sucking, and a slightly high-pitched cry
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Moderate stupor, hypertonia of extensor muscles, minimal feeding, seizures, high-pitched cry, and fever
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Deep stupor to coma, hypertonia
If bilirubin levels are not reduced during the first postnatal week, the infant can have permanent neurological damage, known as kernicterus. It occurs in two phases during the first postnatal year:
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Hypotonia, active deep-tendon flexes, neck reflexes, and delayed motor skills
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Cerebral palsy, tremors, an upward gaze, hearing loss, cognitive impairment, and ballismus (violent, involuntary movement of limbs)
Treatment Methods
The primary goal for effective and efficient management of neonatal hyperbilirubinemia is to prevent long-lasting, life altering effects. The American Academy of Pediatrics (AAP) has existing guidelines for preventative clinical strategies. These safety recommendations are geared toward safely and cost-effectively distinguishing babies who are most likely to have a benign experience with newborn jaundice from those in whom the course is less predictable or potentially unsafe. This common condition can usually be resolved without treatment. However, in some infants, jaundice indicates underlying pathological conditions that must be identified. If bilirubin levels necessitate it, treatment for jaundice involves phototherapy and/or exchange transfusion of donor blood. The suggested intervention based on the severity of hyperbilirubinemia is summarized below:
Severe hyperbilirubinemia at three days of age |
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TSB Level |
Intervention |
|
> 75th Percentile |
<14 mg/dL |
Nutritional Support |
> 95th Percentile |
>17 mg/dL |
Intensive Phototherapy at home or in the hospital |
> 98th Percentile |
>20 mg/dL |
Intensive Phototherapy in hospital |
> 99.9th Percentile |
>25 mg/dL |
Intensive Phototherapy and prepare for exchange transfusion |
> 99.99th Percentile |
>30 mg/dL |
Intensive Phototherapy and perform exchange transfusion |
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