Neonatal Jaundice

Sahisnuta Basnet
 PHYSIOLOGY
• Destruction of circulating senescent
RBC accounts for 75% of daily bilirubin
production
• Rest 25%- turnover of nonHb heme
proteins and destruction of immature
&ineffective RBC
• 1gm of Hb-35 mg bilirubin amounting
to 6-10 mg/kg/day of bilirubin
 Physiology
• Bilirubin is from breakdown of hemoglobin
• Unconjugated bilirubin transported to liver
– Bound to albumin because insoluble in water
• Transported into hepatocyte & conjugated
• Primarily bound to ligandin within the cell & this
prevents the backflow into circulation
– With glucuronic acid → now water soluble
(by action of uridine diphosphate gluconoryl
transferase)
• Secreted into bile
• In ileum & colon, converted to
urobilinogen
• Excreted from urine as urobilin
• Excreted from feces as stercobilin
Bilirubin Metabolism

Unconjugated
Glucuronyl Transferase

(Bilirubin Diglucuronide)
 Why do newborns
develop jaundice?
 Increased production (↑RBC mass, so ↑ed hemolysis
 Fetus is in a hypoxic environment – high Hb
 Postnatal rise in PO2
 Decrease in erythropoietin prodn.
 Destruction of excess Hb.

 Decreased conjugation(immature liver enzyme

system)
 Neonatal RBC lesser life span (60-90days)
 Increased entero-hepatic circulation – sterile gut
• Enterohepatic Circulation:
– Sterile intestines of neonate is rich in
glucoronidase
– This enzyme splits bilirubin glucoronide
to bilirubin and glucoronic acid
– Unconjugated bilirubin again reabsorbed
through the portal circulation
 PHYSIOLOGICAL JAUNDICE
• Seen both in term and preterms
• Self limiting
• Develops after 24 hours
• Peaks by day 4- 5 in terms and day 7-8 in
preterms
• Peak levels -12mg/dl in term & 15mg/dl in
preterm
• Gradually subsides by 10-14 days
• No Treatment necessary
 PATHOLOGICAL JAUNDICE
Suspect if...
• Jaundice in first 24 hours
• rise of >5mg/24 hours or
0.5mg/dl/hour
• Jaundice beyond physiological limits
• Conjugated bilirubin >2mg/dl
• Persists beyond 2 weeks
• Signs of underlying illness
 Etiology
• Early Jaundice (jaundice within 10days
of life)
– A. Within first 2 days of life:
– Hemolytic disease of NB
Rh incompatibility
ABO incompatibility
– G-6PD deficiency
– Congenital spherocytosis
– Sepsis
• B. Within 3-10 days of life
– Physiological jaundice
– Prematurity
– Hypoglycemia
– Acidosis
– Sepsis
– Congenital hemolytic anemia
– Crigler Najjar & Gilberts syndrome
– Galactosemia
– Cephalhematoma
– Subcutaneous bruising
– Drugs:
• Prolonged Jaundice (jaundice at more than 10 days of
life)
• A. Prolonged Unconjugated hyperbilirubinemia
breast milk jaundice
breast feeding jaundice
sepsis
hypothyroidism
galactosemia
infantile pyloric stenosis
persisting hemolysis
hemoglobinopathies
drugs: erythromycin , chloramphenicol
• Pronged conjugated hyperbilirubinemia
– 1. intrahepatic cholestasis
• A. Infections:
– Septicemia
– UTI
– Hepatitis
– STORCH infections
• B. Metabolic
– Galactosemia
– Alpha 1 antitrypsin deficiency
– MPS
– Gauchers disease
– Cystic Fibrosis
• 3. Endrocrine
– Hypothyroidism
– Hypoparathyroidism
– Hypopituiterism

4. Total parental nutrition

5. Drugs: sulphonamides
6. Intrahepatic bile duct disease
7. Idiopathic neonatal hepatitis
• B. Extra hepatic cholestasis
– Biliary atresia
– Choledochal cyst
– Bile duct stenosis
 Breast Feeding Jaundice
Breast Feeding Jaundice
• Misnomer
• Higher levels on day 4 compared to
formula fed babies due decreased
intake of milk
• This leads to increased
enterohepatic circulation
 Breast milk jaundice
Breast Milk Jaundice
• By day 7, instead of usual fall in bilirubin
level, bilirubin level continues to rise
• May sometimes reach 20-30mg/dl by 2nd -3rd
wk of life
• gradually returns to normal by 4-12 weeks
• Exact mech unknown, but thought to be
due to factors in breast milk ( a
glucoronidase in breast milk) interfering
with bilirubin conjugation or metabolism
• If breast feeding is stopped for 48hours ,
bilirubin level will fall rapidly
• Rebound increase after resumption of
feeding of 2-3mg/dl
• Chance of reoccurance in future
pregnancies: 70%
 CLINICAL EVALUATION
• History to rule out other causes
• Careful physical examination
• Dermal progression of jaundice
• Icterometer
• Transcutaneous bilirubinometer
• Laboratory investigations
 Cramer’s Index
• Face ~ 4-6 mg %
• Chest and Upper abdomen ~ 8-10
mg %
• Lower abdomen and thighs ~ 12-14
mg%
• Fore arms and legs ~ 15-18
mg %
• Palms and soles ~ 15-20 mg %
 Lab Investigations
• Hemoglobin, PCV
• Peripheral smear examination
• Coombs’ test
• Reticulocyte count
• Blood group and Rh typing
• Bilirubin level – Total / Direct & Indirect
• Special tests –
– STORCH titres - Thyroid function tests
– Metabolic work up - Sepsis screen
– USG / X ray abdomen
 Approach
• Age at appearance

<24 hrs 24hrs – 2 weeks >2 weeks

Incompatibilities Direct Indirect sepsis
Sepsis IEM
Thyroid

Sepsis Hemolytic Non hemolytic

Hypothyroid Rh / ABO Cephalhematoma
Obstructive Enzyme defects Polycythemia
Syndromic Membrane defects
Laboratory Evaluation of Term Newborn with Jaundice
MANAGEMENT

• Phototherapy
• Drugs
• Exchange
transfusion
 Indications for Phototherapy
• TSB > 15 mg % in term
• TSB > 12 mg% in preterm
• TSB > 5 mg% within 24 hours
• Adjuvant to exchange transfusion
• VLBW with Perinatal risk factors
• Precautions
– Cover the eyes and Genitals
– Supplemental hydration
– Watch for side effects
 PHOTOTHERAPY
• Blue light (425-475 nm)
• Fibreoptic blankets or overhead banks
• As close as possible ( 25cm)
• Continuos therapy-interruptions for
feeding allowed
Mechanism Of Phototherapy

Conversion of insoluble Bilirubin into

soluble bilirubin
– Photo-isomerization: natural isomer
ofunconjugated bilirubin is converted to
less toxic polar isomer which diffuses
into blood & excreted into bile without
need of conjugation
– Structural isomerization: of bilirubin into
lumirubin & is excreted into bile and
urine without conjugation
– Photo-oxidation: bilirubin converted to
small polar products which are excreted
in urine
Phototherapy Complications

• Dehydration: insensible water loss is

increased
• Hypothermia: particularly in winters
• Increased frequency of greenish
stools: ↑ed bile salts and
unconjugated bilirubin in bowel
• Retinal damage
• Bronze baby: when PT given with direct
hyperbilirubinemia
• Testicular damage: mutations, sister
chromatid exchange, DNA strand breaks
• Hampering of materno-fetal bonding
 DRUGS
• Phenobarbitone
-induces liver ezymes: useful for Crigler Najjar
Syndrome Type II
• Metalloporphyrins
-inhibits heme oxygenase and therefore
conversion of biliverdin to bilirubin
• IVIG: may be used in hemolytic anemia
• Oral agar
• Albumin infusions
THANK YOU