NEONATAL JAUNDICE

PROLONGED JAUNDICE
By
MOHD ZAMIR GHOUSE
 DEFINITION

 Jaundice is a visible manifestation of chemical

hyperbilirubinemia due to imbalance of production and
excretion of bilirubin.

 Becomes apparent on skin when serum bilirubin reaches

more than 5mg/dL.

 Almost all neonates (60% term and 80% preterm) will have
bilirubin greater than 5mg/dL in the first week of life.
 Bilirubin physiology

Heme oxygenase
HEME BILIVERDIN

Biliverdin reductase

BILIRUBIN
 Classification
• Bilirubin metabolism

Increased Production Decreased Excretion Combined

• Blood group • Increased • Sepsis
imcompatibilities enterohepatic • Intrauterine infection
• Extravascular blood in circulation • Cirrhosis
bony tissues • Breast feeding
• Polycythemia • Inborn errors of
• RBC abnormalities metabolism
(hemoglobinopathies, • Hormones and drugs
membrane and • Hepatic
enzyme defects) hypoperfusion
• Induction of labor • Cholestatic syndromes
• Obstruction of the
biliary tree
• Prematurity
• Time of onset

<24 hrs • Hemolytic disease of newborn (ABO, Rh, G6PD)

• Sepsis

24- •
•
•
Physiological
Polycythemia
Extravassation of blood
72hrs • Increased enterohepatic circulation

• Breast milk jaundice

>72hrs •
•
Metabolic disorders (eg. hypothyrodism)
Extra hepatic biliary atresia
• Unconjugated or Conjugated

Unconjugate • Increased lysis of RBCs

• Decreased hepatic uptake and
d conjugation
(indirect) • Increased entero hepatic reabsorption

Conjugated • Hepatocellular diseases

• Biliary tree abnormalities
(direct)

*Unconjugated hyperbilirubinemia elevation beyond 30mg/dL may cause

kernicterus
 Kernicterus
Severe unconjugated hyperbilirubinemia (>30mg/dL) causes yellow staining
Severe unconjugated hyperbilirubinemia (>30mg/dL) causes yellow staining
of certain regions of the brain particularly
o ofbasal
certain regions of the brain particularly
o basalganglia
ganglia
o hippocampus
o hippocampus
o cerebellum
o cerebellum
o nuclei
o nucleiofofthe floor of the fourth ventricle
the floor of the fourth ventricle
Clinical signs of kernicterus :
o Clinical signs of kernicterus :
o Sluggishmoro
Sluggish reflex
moro reflex
o Opisthotonus
o Opisthotonus
o Hypotonia
o Hypotonia
o Vomiting
o Vomiting
o High
o Highpitched cry
pitched cry
o Seizures
o Seizures
o Hyperpyrexia
o Hyperpyrexia
o Paresis
o Paresisofofgaze
gaze
 ‘Physiological’ Jaundice

First appears between 24-72 hours of age

First appears between 24-72 hours of age
Maximum intensity seen on 4-5ththday in term
Maximum intensity seen on 4-5 day in term
and
and77thday
th
dayininpreterm
pretermneonates
neonates
Does not exceed 12mg/dL
Does not exceed 12mg/dL
Clinically undetectable after 14 days
Clinically undetectable after 14 days
Baby should be monitored for signs of
Baby should be monitored for signs of
worsening
worseningjaundice
jaundice
 Pathological jaundice

Development before 36 hours of age

Development before 36 hours of age
Persistent beyond 10 days of age
Persistent beyond 10 days of age
Serum bilirubin greater than 12mg/dL
Serum bilirubin greater than 12mg/dL
Elevation of direct reacting fraction of bilirubin
Elevation of direct reacting fraction of bilirubin
(30%
(30%ofofTSB
TSBatatany
anytime)
time)
 Approach to jaundiced neonates

1. Time of onset of jaundice

1. Time of onset of jaundice
2. Review maternal and perinatal history
2. Review maternal and perinatal history
3. Physical examination
3. Physical examination
4. Laboratory tests
4. Laboratory tests
 Visual Assessment
Skin becomes jaundiced in a cephalocaudal manner.

Lower trunk Palms and

Head and neck Upper trunk
and thighs soles
• 4-8mg/dL • 5-12mg/dL • 8-16mg/dL • >15mg/dL

This is of approximate value based on kramer’s rule, it is advised to monitor

hyperbilirubinemia by laboratory tests
 Investigations
 Total serum bilirubin
 Total serum bilirubin
 Unconjugated and conjugated fractions of bilirubin
 Unconjugated and conjugated fractions of bilirubin
 Infant’s blood group and maternal blood group
 Infant’s blood group and maternal blood group
 Direct coombs’ test
 Direct coombs’ test
 G6PD status
 G6PD status
 Full blood count
 Full blood count
 Reticulocyte count
 Reticulocyte count
 Peripheral blood film
 Peripheral blood film
 Blood culture, urine FEME
 Blood culture, urine FEME
 Management

Prevention of • Early and frequent feeding

hyperbilirubinemia • Adequate hydration

Reduction of • Phototherapy
bilirubin • Exchange transfusion
 Phototherapy
 Allowing bilirubin to be excreted into bile without the usual requirement for
hepatic glucoronidation

456nm blue light 4z, 15E-bilirubin

Native bilirubin 4z, 15E-bilirubin
Native bilirubin &
( 4Z, 15Z-Bilirubin) &
( 4Z, 15Z-Bilirubin) Lumirubin
Lumirubin
Insoluble Soluble and excreted via bile
 Exchanged Transfusion

 Exchange transfusion is the most rapid method to acutely lower the serum
bilirubin concentration.

 Indicated in cases of bilirubin concentration >25mg/dL for more than 48hours

despite adequate phototherapy.

 In cases of hemolytic disease or inborn errors of bilirubin metabolism

 Possible high risk of kernicterus

 Volume double exchange (80ml/kg x weight x 2)

 Prolonged jaundice

Causes of prolonged jaundice :

Crigler Najjar syndrome
Breast milk jaundice
Hypothyrodism
Pyloric stenosis
Ongoing hemolysis (eg.malaria)
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