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Neonatal Hyperbilirubinemia
Yanyan Ni, MD
Division of Neonatology
The Children's Hospital,
Zhejiang University School of Medicine
INTRODUCTION
Hyperbilirubinemia is a common and, in most cases, benign

problem in neonates.
The jaundice results from the accumulation of

unconjugated, nonpolar, lipid-soluble bilirubin pigment in
the skin. .
INTRODUCTION
ETIOLOGY
Cause of hyperbilirubinemia
1.Increased bilirubin production
• Hemolytic disease(most common cause)
•Erythrocyte biochemical abnormalities (G-6-PD dehydrogenase/pyruvate
kinase deficiencies/abnormal erythrocyte morphology)
2.Decreased bilirubin clearance
• Mutations in the gene that encodes UGT1A1 decrease bilirubin
conjugation, reducing hepatic clearance and increasing serum TB levels.
• Gilbert syndrome
• others
3.Increased enterohepatic circulation
• Breastfeeding failure jaundice(insufficient intake slower bilirubin
elimination and increased enterohepatic circulation)
•Breast milk jaundice (occurs in about 2.4% of all infants)
CLINICAL MANIFESTATIONS
Lethargy
poor feeding
without treatment kernicterus

PHYSIOLOGIC JAUNDICE (ICTERUS
NEONATORUM)
normal indirect bilirubin in umbilical cord serum
1-3 mg/dL
rises at a rate of < 5 mg/dL/24 hr
jaundice becomes visible on the 2nd or 3rd day, usually

peaking between the 2nd and 4th days and decreasing
between the 5th and 7th days of life.
Risk designation of term and near-term well newborns based
on their hour-specific serum bilirubin values
DETERMINATION OF CAUSES
In general, a search to determine the cause of jaundice should be

made if
(1)it appears in the first 24-36 hr of life,
(2) serum bilirubin is rising at a rate faster than 5 mg/dL/24 hr,
(3) serum bilirubin is > 12 mg/dL in a full-term infant (especially

in the absence of risk factors) or 10-14 mg/dL in a preterm infant,
(4) jaundice persists after 10-14 days of life,
Or (5) direct bilirubin fraction is > 2 mg/dL at any time.

PATHOLOGIC HYPERBILIRUBINEMIA
bilirubin-induced neurologic dysfunction (BIND)
The development of kernicterus (bilirubin encephalopathy)

depends on the level of indirect bilirubin, duration of
exposure to bilirubin elevation, the cause of jaundice, and
the infant’s well-being.
HEMOLYTIC DISEASE OF THE NEWBORN CAUSED BY BLOOD
GROUP A AND B INCOMPATIBILITY
ABO incompatibility is the most common cause of hemolytic disease of

the newborn.
Major blood group incompatibility between the mother and fetus generally
results in milder disease than Rh incompatibility does.
KERNICTERUS
Kernicterus, or bilirubin encephalopathy, is a neurologic

syndrome resulting from the deposition of unconjugated
(indirect) bilirubin in the basal ganglia and brainstem nuclei.
KERNICTERUS
CLINICAL FEATURES OF KERNICTERUS
TREATMENT OF HYPERBILIRUBINEMIA
Phototherapy
exchange transfusion
PHOTOTHERAPY
Clinical jaundice and indirect hyperbilirubinemia are

reduced by exposure to a high intensity of light in the visible
spectrum.
Bilirubin absorbs light maximally in the blue range (420-470

nm).
Bilirubin in the skin absorbs light energy, causing several

photochemical reactions.
PHOTOTHERAPY
PHOTOTHERAPY
Complications
loose stools dehydration
Rash hypothermia from exposure
overheating bronze baby syndrome

PHOTOTHERAPY
Guidelines for phototherapy in hospitalized infants of ≥ 35 weeks of gestation.

PHOTOTHERAPY
EXCHANGE TRANSFUSION
Double-volume exchange transfusion is performed if

intensive phototherapy has failed to reduce bilirubin
levels to a safe range and if the risk of kernicterus
exceeds the risk of the procedure.
Guidelines for exchange transfusion in hospitalized infants of ≥ 35 weeks of gestation.

SUMMARY
Although bilirubin may have a physiologic role as an antioxidant,

hyperbilirubinemia is potentially neurotoxic.
Neonatal hyperbilirubinemia may be caused or increased by any factor that

affects the metabolism of bilirubin.
Infants with severe hyperbilirubinemia may present with lethargy and poor
feeding and, without treatment, can progress to acute bilirubin encephalopathy
(kernicterus).
Phototherapy and, if it is unsuccessful, exchange transfusion remain the

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Neonatal Hyperbilirubinemia

Hyperbilirubinemia is a common and, in most cases, benign

The jaundice results from the accumulation of

without treatment kernicterus

rises at a rate of < 5 mg/dL/24 hr

jaundice becomes visible on the 2nd or 3rd day, usually

In general, a search to determine the cause of jaundice should be

(1)it appears in the first 24-36 hr of life,

(2) serum bilirubin is rising at a rate faster than 5 mg/dL/24 hr,

(3) serum bilirubin is > 12 mg/dL in a full-term infant (especially

(4) jaundice persists after 10-14 days of life,

Or (5) direct bilirubin fraction is > 2 mg/dL at any time.

bilirubin-induced neurologic dysfunction (BIND)

The development of kernicterus (bilirubin encephalopathy)

ABO incompatibility is the most common cause of hemolytic disease of

Kernicterus, or bilirubin encephalopathy, is a neurologic

Clinical jaundice and indirect hyperbilirubinemia are

Bilirubin absorbs light maximally in the blue range (420-470

Bilirubin in the skin absorbs light energy, causing several

loose stools dehydration

Rash hypothermia from exposure

overheating bronze baby syndrome

Guidelines for phototherapy in hospitalized infants of ≥ 35 weeks of gestation.

Double-volume exchange transfusion is performed if

Guidelines for exchange transfusion in hospitalized infants of ≥ 35 weeks of gestation.

Although bilirubin may have a physiologic role as an antioxidant,

Neonatal hyperbilirubinemia may be caused or increased by any factor that

Phototherapy and, if it is unsuccessful, exchange transfusion remain the

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