Neonatal Jaundice

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Neonatal Jaundice

• Neonatal Ward
• Dr. Ziyu Hua

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Classification of neonatal jaundice
Physiological jaundice
Pathological jaundice
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Etiology of physiological jaundice
In the first few days after birth, haemoglobulin
concentration falls rapidly.
Red cell life span of newborn infants is 70 days
which is much shorter than that of adults(120
days).
Hepatic bilirubin metabolism is less efficiency.
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Jaundice is important as
A sign of another disorder, e.g. infection,
hemolysis
Kernicterus a severe complication of neonatal
jaundice, indirect bilirubin (UB) deposited in
the brain (basal ganglia).
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Warning
There are no bilirubin levels which are known to
be safe or which will definitely cause
kernicterus.
Infants who experience severe hypoxia,
hypothermia or any serious illness may be
susceptible to damage from hyperbilirubinemia.
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Severity of jaundice
The jaundice starts on the head and face, spreads
down the trunk and limbs.
How to measure
Observation by eye blanching the skin
Transcutaneous jaundice meter
Blood sample minibilirubin meter
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Gestation
Preterm infants may be damaged by a lower
bilirubin level than term infants.
Age from birth is important, higher tolerance
with increasing age.
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Rate of change
Rate of rise tends to be linear until reaching
plateau.
Rapid rise with increasing harm.
Serial measurement of serum bilirubin, suitable
intervention when necessary.
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Etiology of pathological jaundice
Age of onset is a useful guide to likely cause of
jaundice.
Within 24 hrs
During 24 hrs to 2 wks
After 2 wks
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Jaundice within 24 hrs of age
Hemolytic disorders UB, rise rapidly, high level
Rhesus hemolytic disease jaundice, anemia,
hydrops, hepatosplenomegaly antenatal identify,
fetal therapy.
ABO incompatibility less severe, more common,
slight or without anemia, peak in the first
1272hrs.
G6PD deficiency epidemiology some drugs,
infection, hypoxia.
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Jaundice within 24 hrs of age
Hemolytic disorders
Spherocytosis less common, family history
spherocytes found on the blood film.
Congenital infection conjugated bilirubin, other
abnormal clinical signs.
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Jaundice at 24 hrs to 2 wks of age
Physiological jaundice
Infection unconjugated hyperbilirubinemia
abnormal metabolism of bilirubin pneumonia,
sepsis, hepatitis, urinary tract infection.
Other causes bruising, polycythaemia (venous
hematocrit gt65) Crigler-Najjar syndrome
(inherited deficiency of enzyme glucuronyl
transferase)
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Jaundice at 24 hrs to 2 wks of age
Breast milk jaundice prolonged, unconjugated
hyperbilirubinemia unknown cause declined
bilirubin with interruption of breast-feeding
may be harmless.
It is unnecessary to stop breast-feeding when
breast milk jaundice is diagnosed.
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Jaundice at gt2 wks of age(persistent)
Unconjugated hyperbilirubinemia
Infection, particularly of urinary tract.
Congenital hypothyroidism neonatal biochemical
screening clinical manifestations (constipation,
dry skin, coarse facies, hypotonia)
Breast milk jaundice most common, 15 affected
disappears by 3-4 wks of age.
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Jaundice at gt2 wks of age(persistent)
Conjugated hyperbilirubinemia
Neonatal hepatitis syndrome(TORCH), biliary
atresia
Dark urine and unpigmented pale stools
Biliary atresia should be diagnosed as soon as
possible.
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Management
No study could prove that supplement with water
or dextrose solution would reduce jaundice.
Effective treatments
Phototherapy, intense phototherapy
Exchange transfusion
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Phototherapy
Overhead light, blanket, and both of them
Blue light wavelength 450nm, visible
Photodegradation UB is converted into a
water-soluble pigment, harmless, excreted in urine
Side effects
Uncomfortable eyes, retinal damage in animal,
dehydration, rash, diarrhoea, abnormal
temperature
Phototherapy should not be used indiscriminately.
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Exchange transfusion(ET)
Indications
Bilirubin rises to the dangerous level
Continues to rise above the recommended level in
spite of intensive phototherapy.
Transfusion via cord vessels, peripheral vessels
Blood volume twice infants blood volume
It should be consider seriously whether to use ET.