NEONATAL JAUNDICE

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:

Where does bilirubin come from?

34mg bilirubin

being produced

from 1gm of Hb3

• 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

PHYSIOLOGICAL MECHANISMS OF NEONATAL JAUNDICE

CLINICAL ASSESSMENT OF 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.

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.

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:

PHYSIOLOGICAL JAUNDICE 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.

PATHOLOGICAL JAUNDICE

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….

CAUSES OF 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.

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.

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.

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.

BILIRUBIN ENCEPHALOPATHY

Risk of bilirubi

n toxicit

y depend on :

Serum bilirubi

n levels,

Gestational age,

Underlying cause

of jaundice,

Other co-

morbid conditio

ns

Factors predisposing to

bilirubin toxicity include :

Acidosis, Birth asphyxia,

Pyogenic meningitis, Intracranial hemorrhag

e,

Drugs displacing bilirubin

from albumin.

PREDISPOSING FACTORS:

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”.

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

CLINICAL FEATURES:

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

WORKUP FOR PATHOLOGICAL JAUNDICE

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