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NEONATA
L
JAUNDI
CE
By roll no. 91 to 95
Guided by Dr.Dhaval Nayak sir
Zydus Medical College and Hospital, Dahod
Department of Pediatrics
APPROACH
TO
Objectiv
es
• Definition of jaundice
• Types of jaundice
• Causes of neonatal jaundices
• Management of neonatal
jaundice
Neonatal hyperbilirubinemia
Definition :
Jaundice is the yellow color of the skin and sclerae
caused by deposits of bilirubin
1. Increased Bilirubin Load due to a high hemoglobin
concentration.
• The normal newborn infant
• Hemolysis
• Cephalhematoma or bruising , Polycythemia
2. Decreased Bilirubin Conjugation in the liver
3. Defective Bilirubin Excretion
Mechanisms of Neonatal Jaundice
EtiologyOf
Jaundice
CAUS
ES
• Appears after 24 hours
• Total bilirubin rises by less than 5
mg/dl per day
• Maximum intensity by 4th-5th day in
term & 7th day in preterm
• Serum level less than 15 mg / dl
• Clinically not detectable after 14 days
Physiological
Jaundice
Appears within 24 hours of age
• Increase of bilirubin > 5 mg / dl / day
• Serum bilirubin > 15 mg / dl
• Jaundice persisting after 14 days
• Stool clay / white colored and urine
staining yellow
• Direct bilirubin > 2 mg / dl
Pathological
jaundice
Breast milk jaundice
– It is caused by prolonged
increased enterohepatic
circulation of bilirubin
– Bilirubin peaks at 10-15
days of age.
– The level of unconjugated
bilirubin is at 10-30 mg/dL
– If nursing is interrupted for
24 hours, the bilirubin level
falls quickly
Breast-milk jaundice;
is the commonest
cause of Prolonged
jaundice in term
infants
Pathologic
al
Jaundice
Pathological jaundice
1. Appears within 24 hours of age
1. Increase of bilirubin > 5 mg / dl / day
1. Serum bilirubin > 15 mg / dl
1. Jaundice persisting after 14 days
1. Stool clay / white colored and urine staining yellow
1. Direct bilirubin > 2 mg / dl
Conjugated
Bilirubin
Pathological
Unconjugated
Bilirubin (indirect)
Hepati
c
Post-
hepatic
Non-
hemolytic
Hemolyti
c
Pathological
Jaundice
1 Unconjugated (Indirect)
hyperbilirubinemia
1. Hemolysis
• Rh , ABO and other blood group incompatibilities
• spherocytos, elliptocytosis, Alpha thalassemia
• Sepsis ,DIC
• Hematomas
• Polycythemia
2. Non hemolytic
• Breast milk jaundice
• Crigler-Najjar syndrome, types I and II
Pathological jaundice
2-Conjugated
hyperbilirubinemia
1. Hepatic
• Idiopathic neonatal hepatitis
• Infections - TORCH, sepsis
• Inborn errors of metabolism
• Galactosemia
• Tyrosinemia
2. Post hepatic
– Biliary atresia, choledochal
cyst
Common causes of
jaundice
• Physiological
• Blood group
incompatibility
• G6PD deficiency
• Breast milk jaundice
• Cephalhaematoma
• Infections
• Crigler-Najjar syndrome type I - rare
• Complete absence of UDPGT and is characterized by
severe hyperbilirubinemia with the ongoing risk of
kernicterus at any point during an individual's lifespan.
• Currently, liver transplantation is the only definitive
therapy
• Patients with Crigler-Najjar
syndrome type II partial absence of UDPGT
similar to type I but dramatically respond to therapy
with phenobarbital, which is how the diagnosis is made
Risk factors for
jaundice
• J - jaundice within first 24 hrs of life or
premature
• A - a sibling who was jaundiced as neonate
• U - unrecognized hemolysis (ABO)
• N nursing – non-optimal sucking/nursing
• D - deficiency of G6PD , DRUGS , Ceftriaxone,
• I - infection
• C – Cephalhematoma /bruising
• E - East Asian/North Indian
Approach to jaundiced
baby
1. Determine birth weight, gestation and postnatal age
2. Assess clinical condition (well or ill) ,degree of
jaundice
3. Decide whether jaundice is physiological or
pathological
4. Look for evidence of kernicterus in deeply
jaundiced NB
Clinical assessment of
jaundice
Area of body Bilirubin
levels/dlmg
• Face 6
• Upper trunk 9
• Lower trunk & thighs 12
• Arms and lower legs 15
• Palms & soles > 15
High bilirubin level
kernicter
us (Bilirubin Encephalopathy)
Major Clinical Features of Acute Bilirubin
Encephalopathy
• Lethargy
• Poor sucking
• poor or absent Moro's,
• Retrocollis-
opisthotonos
Convulsions
Major clinical features of chronic
bilirubin
encephalopathy
• Athetosis
• Upward gaze
• Sensorineural hearing
loss
• Intellectual deficits, mild
MR
Laboratory tests
• Total & direct bilirubin*
• Blood group and Rh for mother and baby*
• Hematocrit, retic count and peripheral smear*
• G6PD assay
• Coomb’s test
• Sepsis screen
• Liver and thyroid function
• TORCH titers
• Liver scan when conjugated hyperbilirubinemia
• Ultrasonography of the liver and bile ducts in cholestasis
Measurement
of bilirubin by
jaundice
meter
Liver function
tests:
•Aspartate aminotransferase (ASAT or SGOT) and alanine
aminotransferase (ALAT or SGPT) levels are elevated in
hepatocellular disease.
•Alkaline phosphatase and γ -glutamyltransferase (GGT)
levels are often elevated in cholestatic disease.
•A γ -GT/ALAT ratio of more than 1 is strongly suggestive of
biliary obstruction. However, it does not distinguish between
intrahepatic and extrahepatic cholestasis (do ultrasoud)
Reducing substance in urine: is a useful screening test for
galactosemia, provided the infant has received sufficient quantities
of milk.
Other
Tests
• Hearing tests (Brainstem auditory-evoked
potentials) should be obtained in aftermath of
severe neonatal jaundice to exclude
sensorineural hearing loss.
• MRI in kernicterus
Manageme
nt
1. Phototherapy
2. intravenous immune globulin
(IVIG)
3. Exchange transfusion
4. Drugs
Baby under triple unit
intense
phototherapy
Baby under conventional
phototherapy
Baby under triple unit intense
phototherapy
Principle of phototherapy
Native
bilirubin
( water
Insoluble)
450-460nm of
light
`Photo isomers of
bilirubin
(water
Soluble)
Urin
Phototherapy
Technique
• Perform hand wash
• Place baby naked in cradle or incubator
• Fix eye shades
• Keep baby at least 45 cm from lights
• Start phototherapy
• Frequent extra breast feeding every 2
hourly
• Turn baby after each feed
• Temperature record 2 to 4 hourly
• Weight record- daily
• Monitor urine frequency
• Monitor bilirubin level
Side effects of phototherapy
• Increased insensible water loss
• Loose stools
• Skin rash
• Bronze baby syndrome
• Hyperthermia
• May result in hypocalcemia
Intravenous immune
globulin
• IVIG in infants with Rh or ABO isoimmunization
can significantly reduce the need for exchange
transfusions.
• Now IVIG has replaced exchange transfusion as
the second-line treatment in infants with
isoimmune jaundice.
• 1 gm/kg/dose IV
Exchange
transfusion
• Exchange transfusion is
indicated for avoiding bilirubin
neurotoxicity when other
therapeutic modalities have
failed or are not sufficient.
• the procedure may be indicated
in infants with erythroblastosis
who present with severe
anemia, hydrops, or both, even
in the absence of high serum
bilirubin
Phenobarbital (Luminal)
• Hyperbilirubinemia: 3-8 mg/kg/d
PO/IV initially; may increase up to 12
mg/kg/d Not to exceed IV
administration rate of 1 mg/kg/min or
30 mg/min for infants
Remember that:
• Jaundice is the most frequent cause of
admission after
early discharge from nursery.
• It is not physiological if: appear in first 24 hrs,
increases by > 0.5 mg/dL/hr , evidence of
hemolysis, abnormal examination, direct bilirubin is
> 20% of total, or persists
> 3 weeks.
• Jaundice present in the first 24 hrs of life must be
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jaundice-mnb.pptx

  • 1. NEONATA L JAUNDI CE By roll no. 91 to 95 Guided by Dr.Dhaval Nayak sir Zydus Medical College and Hospital, Dahod Department of Pediatrics APPROACH TO
  • 2. Objectiv es • Definition of jaundice • Types of jaundice • Causes of neonatal jaundices • Management of neonatal jaundice
  • 3. Neonatal hyperbilirubinemia Definition : Jaundice is the yellow color of the skin and sclerae caused by deposits of bilirubin
  • 4. 1. Increased Bilirubin Load due to a high hemoglobin concentration. • The normal newborn infant • Hemolysis • Cephalhematoma or bruising , Polycythemia 2. Decreased Bilirubin Conjugation in the liver 3. Defective Bilirubin Excretion Mechanisms of Neonatal Jaundice
  • 7. • Appears after 24 hours • Total bilirubin rises by less than 5 mg/dl per day • Maximum intensity by 4th-5th day in term & 7th day in preterm • Serum level less than 15 mg / dl • Clinically not detectable after 14 days Physiological Jaundice Appears within 24 hours of age • Increase of bilirubin > 5 mg / dl / day • Serum bilirubin > 15 mg / dl • Jaundice persisting after 14 days • Stool clay / white colored and urine staining yellow • Direct bilirubin > 2 mg / dl Pathological jaundice
  • 8. Breast milk jaundice – It is caused by prolonged increased enterohepatic circulation of bilirubin – Bilirubin peaks at 10-15 days of age. – The level of unconjugated bilirubin is at 10-30 mg/dL – If nursing is interrupted for 24 hours, the bilirubin level falls quickly Breast-milk jaundice; is the commonest cause of Prolonged jaundice in term infants
  • 10. Pathological jaundice 1. Appears within 24 hours of age 1. Increase of bilirubin > 5 mg / dl / day 1. Serum bilirubin > 15 mg / dl 1. Jaundice persisting after 14 days 1. Stool clay / white colored and urine staining yellow 1. Direct bilirubin > 2 mg / dl
  • 12. 1 Unconjugated (Indirect) hyperbilirubinemia 1. Hemolysis • Rh , ABO and other blood group incompatibilities • spherocytos, elliptocytosis, Alpha thalassemia • Sepsis ,DIC • Hematomas • Polycythemia 2. Non hemolytic • Breast milk jaundice • Crigler-Najjar syndrome, types I and II Pathological jaundice
  • 13. 2-Conjugated hyperbilirubinemia 1. Hepatic • Idiopathic neonatal hepatitis • Infections - TORCH, sepsis • Inborn errors of metabolism • Galactosemia • Tyrosinemia 2. Post hepatic – Biliary atresia, choledochal cyst
  • 14. Common causes of jaundice • Physiological • Blood group incompatibility • G6PD deficiency • Breast milk jaundice • Cephalhaematoma • Infections
  • 15.
  • 16. • Crigler-Najjar syndrome type I - rare • Complete absence of UDPGT and is characterized by severe hyperbilirubinemia with the ongoing risk of kernicterus at any point during an individual's lifespan. • Currently, liver transplantation is the only definitive therapy • Patients with Crigler-Najjar syndrome type II partial absence of UDPGT similar to type I but dramatically respond to therapy with phenobarbital, which is how the diagnosis is made
  • 17. Risk factors for jaundice • J - jaundice within first 24 hrs of life or premature • A - a sibling who was jaundiced as neonate • U - unrecognized hemolysis (ABO) • N nursing – non-optimal sucking/nursing • D - deficiency of G6PD , DRUGS , Ceftriaxone, • I - infection • C – Cephalhematoma /bruising • E - East Asian/North Indian
  • 18. Approach to jaundiced baby 1. Determine birth weight, gestation and postnatal age 2. Assess clinical condition (well or ill) ,degree of jaundice 3. Decide whether jaundice is physiological or pathological 4. Look for evidence of kernicterus in deeply jaundiced NB
  • 19. Clinical assessment of jaundice Area of body Bilirubin levels/dlmg • Face 6 • Upper trunk 9 • Lower trunk & thighs 12 • Arms and lower legs 15 • Palms & soles > 15
  • 20.
  • 21. High bilirubin level kernicter us (Bilirubin Encephalopathy)
  • 22. Major Clinical Features of Acute Bilirubin Encephalopathy • Lethargy • Poor sucking • poor or absent Moro's, • Retrocollis- opisthotonos Convulsions
  • 23. Major clinical features of chronic bilirubin encephalopathy • Athetosis • Upward gaze • Sensorineural hearing loss • Intellectual deficits, mild MR
  • 24. Laboratory tests • Total & direct bilirubin* • Blood group and Rh for mother and baby* • Hematocrit, retic count and peripheral smear* • G6PD assay • Coomb’s test • Sepsis screen • Liver and thyroid function • TORCH titers • Liver scan when conjugated hyperbilirubinemia • Ultrasonography of the liver and bile ducts in cholestasis
  • 26. Liver function tests: •Aspartate aminotransferase (ASAT or SGOT) and alanine aminotransferase (ALAT or SGPT) levels are elevated in hepatocellular disease. •Alkaline phosphatase and γ -glutamyltransferase (GGT) levels are often elevated in cholestatic disease. •A γ -GT/ALAT ratio of more than 1 is strongly suggestive of biliary obstruction. However, it does not distinguish between intrahepatic and extrahepatic cholestasis (do ultrasoud) Reducing substance in urine: is a useful screening test for galactosemia, provided the infant has received sufficient quantities of milk.
  • 27. Other Tests • Hearing tests (Brainstem auditory-evoked potentials) should be obtained in aftermath of severe neonatal jaundice to exclude sensorineural hearing loss. • MRI in kernicterus
  • 28. Manageme nt 1. Phototherapy 2. intravenous immune globulin (IVIG) 3. Exchange transfusion 4. Drugs
  • 29. Baby under triple unit intense phototherapy Baby under conventional phototherapy Baby under triple unit intense phototherapy
  • 30. Principle of phototherapy Native bilirubin ( water Insoluble) 450-460nm of light `Photo isomers of bilirubin (water Soluble) Urin
  • 31. Phototherapy Technique • Perform hand wash • Place baby naked in cradle or incubator • Fix eye shades • Keep baby at least 45 cm from lights • Start phototherapy • Frequent extra breast feeding every 2 hourly • Turn baby after each feed • Temperature record 2 to 4 hourly • Weight record- daily • Monitor urine frequency • Monitor bilirubin level
  • 32.
  • 33. Side effects of phototherapy • Increased insensible water loss • Loose stools • Skin rash • Bronze baby syndrome • Hyperthermia • May result in hypocalcemia
  • 34. Intravenous immune globulin • IVIG in infants with Rh or ABO isoimmunization can significantly reduce the need for exchange transfusions. • Now IVIG has replaced exchange transfusion as the second-line treatment in infants with isoimmune jaundice. • 1 gm/kg/dose IV
  • 35. Exchange transfusion • Exchange transfusion is indicated for avoiding bilirubin neurotoxicity when other therapeutic modalities have failed or are not sufficient. • the procedure may be indicated in infants with erythroblastosis who present with severe anemia, hydrops, or both, even in the absence of high serum bilirubin
  • 36. Phenobarbital (Luminal) • Hyperbilirubinemia: 3-8 mg/kg/d PO/IV initially; may increase up to 12 mg/kg/d Not to exceed IV administration rate of 1 mg/kg/min or 30 mg/min for infants
  • 37. Remember that: • Jaundice is the most frequent cause of admission after early discharge from nursery. • It is not physiological if: appear in first 24 hrs, increases by > 0.5 mg/dL/hr , evidence of hemolysis, abnormal examination, direct bilirubin is > 20% of total, or persists > 3 weeks. • Jaundice present in the first 24 hrs of life must be