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Pertinent family history includes the presence of a first-degree relative with
history of jaundice or anemia, and racial or ethnic origin associated with a
hematologic disorder.
Physical Examination
The general appearance and vital signs of the patient will help guide the clinician
as to the likelihood of a serious underlying condition such as bacterial sepsis.
Hydration status should be ascertained. Hepatomegaly may indicate underlying
liver dysfunction. Splenomegaly may be found in hypersplenic states or patients
with hemolytic anemia. Neurologic examination should include evaluation for
signs of ABE: hypotonia, irritability, retrocollis, opisthotonos, high-pitched cry,
and coma. Pallor may indicate concomitant anemia. Presence of a
cephalohematoma or large areas of ecchymosis may suggest extravascular
hemolysis as the cause of hyperbilirubinemia.
Clinical examination of jaundice involves close inspection of the sclera and
skin under adequate light, applying gentle pressure with one finger to facilitate
examination of color. In neonates, jaundice progresses in a cephalocaudal
direction from the face to the trunk and extremities, and finally to the palms and
soles. In neonates, visual assessment of jaundice has been found to correlate
poorly with serum bilirubin measurement, with great interobserver variability
noted.
The acute neurologic manifestations of the neurotoxic effects of bilirubin are
known as ABE, the term recommended by the American Academy of Pediatrics
(AAP). ABE may be reversible if identified in the early phase, when clinical
findings may be subtle and include sleepiness, hypotonia, and/or a high-pitched
cry. Later phases include lethargy, irritability, retrocollis, opisthotonos, seizures,
apnea, and coma. Death is typically due to respiratory failure or intractable
seizures.
Additional Studies
The total and fractionated (direct and indirect) serum bilirubin level should