Hyperbilirubinemia
Answer: C
Neonatal jaundice may be pathologic or benign. Jaundice occurring in the first 24 hours is pathologic until proven otherwise. A more common scenario for emergency physicians is an otherwise well child who develops jaundice at home or worsens from discharge. A deliberate approach to these newborns is important to assess the risk of hyperbilirubinemia and its sequelae.
Newborn infants invariably have higher bilirubin levels than adults for three reasons: a) bilirubin production is 2-3 times higher than in adults (neonatal hematocrit is higher, and fetal red blood cells have a shorter lifespan); b) the liver is immature, and enzymes for breakdown are lacking; and c) neonates have an increased enterohepatic circulation.
A thorough history and physical examination are essential in the evaluation of these infants. Important historical features to elicit are gestational age (this will directly impact management), difficulty feeding, volume status, history of fever, medications given to the infant or taken by the mother (if breastfeeding), and family history of G6PD deficiency or other blood dyscrasias. Every newborn who comes to the ED should have a careful and detailed head-to-toe exam; in this case, the examiner should look for general appearance, evidence of cephalohematoma (which may be a cause of recirculating bilirubin), ecchymosis, trauma, volume status, and splenomegaly. Jaundice readily appears clinically around total bilirubin levels of 5 mg/dL, begins at the head, and progresses caudally as the bilirubin level increases. (A special note in dark-skinned children is that the yellow tinge may be difficult to appreciate. Mucous membranes and the palms and soles are good places to look if the general exam is not revealing.) The take home point here is that occult trauma, early sepsis, or unrecognized congenital conditions may be missed if not carefully considered.
The feared consequence to severe hyperbilirubinemia in this age group is bilirubin-induced neurologic dysfunction (BIND), which can occur when toxic levels of bilirubin cross the blood-brain barrier and “bind” to brain tissue. This can result in acute bilirubin encephalopathy; its chronic sequela is kernicterus.
For the emergency physician, the clinical questions are: 1) is the child well appearing? (special attention to volume status), 2) what is the gestational age?, and 3) are there risk factors for severe hyperbilirubinemia needing intervention? Risk factors include blood dyscrasias such as isoimmune hemolytic disease, G6PD deficiency, history of a previous sibling’s needing phototherapy, and East Asian race.
The Bhutani nomogram (below) shows guidelines for newborns 35 weeks or greater in gestation. It describes low, medium, and high risk, depending on gestational age, hour of life, and presence of risk factors.
Although rapid rise in total bilirubin in house (>0.2 mg/dL/hour) is a risk factor, serial testing in the ED is not warranted, as it rarely aids in decision making (A).
It is important to obtain a careful birth history, including time of delivery, as illustrated by the nomogram (C).
A child with markedly high bilirubin levels will need phototherapy to aid in conjugation of bilirubin; they can also readily become dehydrated. However, in this case, the child is low risk: he is well appearing, euvolemic, and has a reassuring history and physical examination and total bilirubin level (B, D). A low-risk child may safely go home with close follow up in 24-48 hours and strict return precautions, with special emphasis on volume status/adequate urine output. Family education and reassurance will help to alleviate parental stress; breastfeeding should be encouraged in outpatients (regardless of bilirubin level).
Reference (including nomogram)
Subcommittee on Hyperbilirubinemia et al. Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation. Pediatrics 2004;114:297-316
Neonatal jaundice may be pathologic or benign. Jaundice occurring in the first 24 hours is pathologic until proven otherwise. A more common scenario for emergency physicians is an otherwise well child who develops jaundice at home or worsens from discharge. A deliberate approach to these newborns is important to assess the risk of hyperbilirubinemia and its sequelae.
Newborn infants invariably have higher bilirubin levels than adults for three reasons: a) bilirubin production is 2-3 times higher than in adults (neonatal hematocrit is higher, and fetal red blood cells have a shorter lifespan); b) the liver is immature, and enzymes for breakdown are lacking; and c) neonates have an increased enterohepatic circulation.
A thorough history and physical examination are essential in the evaluation of these infants. Important historical features to elicit are gestational age (this will directly impact management), difficulty feeding, volume status, history of fever, medications given to the infant or taken by the mother (if breastfeeding), and family history of G6PD deficiency or other blood dyscrasias. Every newborn who comes to the ED should have a careful and detailed head-to-toe exam; in this case, the examiner should look for general appearance, evidence of cephalohematoma (which may be a cause of recirculating bilirubin), ecchymosis, trauma, volume status, and splenomegaly. Jaundice readily appears clinically around total bilirubin levels of 5 mg/dL, begins at the head, and progresses caudally as the bilirubin level increases. (A special note in dark-skinned children is that the yellow tinge may be difficult to appreciate. Mucous membranes and the palms and soles are good places to look if the general exam is not revealing.) The take home point here is that occult trauma, early sepsis, or unrecognized congenital conditions may be missed if not carefully considered.
The feared consequence to severe hyperbilirubinemia in this age group is bilirubin-induced neurologic dysfunction (BIND), which can occur when toxic levels of bilirubin cross the blood-brain barrier and “bind” to brain tissue. This can result in acute bilirubin encephalopathy; its chronic sequela is kernicterus.
For the emergency physician, the clinical questions are: 1) is the child well appearing? (special attention to volume status), 2) what is the gestational age?, and 3) are there risk factors for severe hyperbilirubinemia needing intervention? Risk factors include blood dyscrasias such as isoimmune hemolytic disease, G6PD deficiency, history of a previous sibling’s needing phototherapy, and East Asian race.
The Bhutani nomogram (below) shows guidelines for newborns 35 weeks or greater in gestation. It describes low, medium, and high risk, depending on gestational age, hour of life, and presence of risk factors.
Although rapid rise in total bilirubin in house (>0.2 mg/dL/hour) is a risk factor, serial testing in the ED is not warranted, as it rarely aids in decision making (A).
It is important to obtain a careful birth history, including time of delivery, as illustrated by the nomogram (C).
A child with markedly high bilirubin levels will need phototherapy to aid in conjugation of bilirubin; they can also readily become dehydrated. However, in this case, the child is low risk: he is well appearing, euvolemic, and has a reassuring history and physical examination and total bilirubin level (B, D). A low-risk child may safely go home with close follow up in 24-48 hours and strict return precautions, with special emphasis on volume status/adequate urine output. Family education and reassurance will help to alleviate parental stress; breastfeeding should be encouraged in outpatients (regardless of bilirubin level).
Reference (including nomogram)
Subcommittee on Hyperbilirubinemia et al. Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation. Pediatrics 2004;114:297-316
