introduction, physiology, pathology, causes, clinical features, predisposing factors of neonatal jaundice.

1. NEONATAL
JAUNDICE

2. Physiological jaundice occurs in nearly two- thirds of
newborns, with excellent out come.
 However, serum bilirubin levels can exceed
physiological limits, leads to brain damage.
 The normal term newborn produces about 6-
10mg/kg/day of bilirubin.
 In adults 3 to 4 mg/kg/day of bilirubin is produced.
INTRODUCTION:

3. Where does bilirubin come from?
34mg bilirubin
being produced
from 1gm of Hb3

4. •Higher erythrocyte
mass.
• Shorter RBC lifespan.
• Increased turnover of
nonhaemoglobin
heme proteins.
Increased
Bilirubin
Production
•Defective uptake.
• Defective
conjugation.
Reduced
Hepatic
Metabolism
• High levels of
intestinal beta-
glucuronidase.
• Paucity of intestinal
bacteria.
• Dec. gut motility.
Increased
Enteroheptic
Circulation
PHYSIOLOGICALMECHANISMSOF NEONATAL
JAUNDICE

5. CLINICALASSESSMENTOF JAUNDICE
 In newborns, the jaundice is detected by blanching the skin
with fingers, revealing the yellow staining of skin and
subcutaneous tissues.
 Jaundice is seen first in the face at serum bilirubin levels of 5
to 6 mg/dl & then progresses in a cephalo-caudal manner
to the trunk and extremities
 It is difficult to detect jaundice in eyes of a newborn as
unlike adults, neonates keep their eyes shut because of
physiological photophobia.

6.  Kramer described the
approximate serum bilirubin level
with the level of skin
discoloration.
 Once palms and soles are
distinctly yellow stained, serum
bilirubin exceeds 15 mg/dl.
 After phototherapy is started,
skin gets bleached and it
becomes difficult to assess
jaundice clinically.

7.  This device measures the
intensity of yellow staining of skin
and subcutaneous tissues.
 The value is displayed as either
transcutaneous bilirubin index or
a bilirubin levels.
 It is a good screening method.
 TRANSCUTANEOUS BILIRUBINOMETRY:

8. PHYSIOLOGICALJAUNDICE
 It appears on second or third day of life, rises at a
rate less than 5 mg/dl/day
 Peaks at 4 or 5 days of age; spontaneously
disappears by day 10-14 days of life.
 It is always indirect reacting hyperbilirubinemia &
serum bilirubin levels do not exceed 15 mg/dl.
 Term infants with physiological jaundice do not
require any treatment and outcome is excellent.

9. PATHOLOGICALJAUNDICE
 Jaundice appears on day 1 of age.
 Persists beyond 2 weeks.
 Rise in serum bilirubin level is more than 0.5
mg/dl/hour.
 Conjugated serum bilirubin is >2 mg/dl or
>20% of total bilirubin.
 Associated with signs of illness ++
Suspect if….

10. CAUSESOF JAUNDICE
Jaundice
appearing within
24hrs of age
•Hemolytic diseases of
newborn.
•Intrauterine infections.
•G-6PD deficiency.
•Hereditary
spherocytosis.
•Crigler-Najjar
syndrome.
•Alpha-thalassemia.
Jaundice
appearing b/w 24
& 72hrs of age
• Physiological.
• Septicemia.
• Polycythemia.
• Concealed
hemorrhages
Jaundice
appearing after
72hrs
• Septicemia.
• Idiopathic jaundice.
• Hypothyroidism.
• Metabolic disorders.

11.  BREASTMILK JAUNDICE:
 Breastmilk jaundice is a misnomer since no
factor in breastmilk has consistently been
shown to be causative of jaundice in
neonates and this terminology should be
better avoided.
o Diagnosis:
 It is suspected in breastfed neonates
whose physiological jaundice fails to
decline after first week of birth
 And persists beyond two weeks of birth.

12. o MANAGEMENT OF BREASTMILK
JAUNDICE:
 Phototherapy is indicated, if serum bilirubin
exceeds 20 mg/dl.
 Exchange transfusions, if serum bilirubin
reaches 25-30 mg/dl.
 Temporary interruption of breastfeeding
may be followed by fall in serum bilirubin
values.
 However, in majority of cases the jaundice
can be managed without need of
stopping breastfeeding.

13.  Severe Unconjugated hyperbilirubinemia
can result in neuronal damage.
 Acute bilirubin encephalopathy refers to
clinical manifestations of bilirubin toxicity.
 The term Kernicterus is reserved for chronic
& permanent sequelae of bilirubin toxicity.
 This condition is characterized by
- Yellow staining of basal ganglia & brain
stem nuclei.
- Involves diffuse neuronal damage.
BILIRUBINENCEPHALOPATHY

14. Risk of
bilirubin
toxicity
depend
on :
Serum
bilirubin
levels,
Gestational
age,
Underlying
cause of
jaundice,
Other co-
morbid
conditions
Factors
predisposi
ng to
bilirubin
toxicity
include :
Acidosis,
Birth
asphyxia,
Pyogenic
meningitis,
Intracranial
hemorrhage,
Drugs
displacing
bilirubin from
albumin.
PREDISPOSINGFACTORS:

15.  What is the highest bilirubin value that is safe?
 In term neonates with hemolytic disease, kernicterus rarely
occurs with bilirubin levels lower than 20 mg/dl.
 In case of non-hemolytic jaundice, serum bilirubin levels up to
25 mg/dl are generally safe.
 However in premature babies, brain damage may occur at
lower bilirubin levels, so called “LOW BILIRUBIN KERNICTRUS”.

16. Early phase(1-2
days):
Poor sucking,
Hypotonia,
lethargy.,
High pitched cry,
Loss of Moro reflex
Intermediate
phase(3-7 days):
Hypertonia.
Opisthotonus,
Retrocollis, bulging
of anterior fontanel,
Fever, seizures
Advanced
phase(>1 week):
Pronounced
opisthotonus,
Apnea, seizures,
coma, death.
Chronic phase(1st
year):
Hypotonia, brisk
tendon reflexes.
After 1st year:
Choreoathetosis,
tremors, dental
dysplasia, mental
retardation
CLINICALFEATURES:

17. Review maternal &
perinatal history:
Age of onset of
jaundice,
Color of urine and
feces,
Maternal illness during
pregnancy,
Delay in meconium
passage,
Difficulty in breast
feeding
Physical
examination:
Excessive weight loss,
Signs of dehydration,
Pallor hemolysis,
TORCH infections,
Prematurity,
Sepsis,
Hepatosplenomegaly,
Laboratory tests:
Total serum bilirubin,
Blood group & Rh of
mother & baby,
Direct coomb’s test,
Hematocrit,
Sepsis screen,
Thyroid profile,
TORCH titres
WORKUPFORPATHOLOGICALJAUNDICE

18. Thank u