Neonatal jaundice, or hyperbilirubinemia, refers to excessive levels of bilirubin in the blood of newborns which can cause jaundice and if levels get too high can potentially lead to bilirubin deposits in the brain causing permanent neurological damage known as kernicterus; the document discusses the definition, causes, clinical assessment, management including phototherapy and exchange transfusion, and prevention of neonatal jaundice.

1. Neonatal Jaundice
Dr. Karuppiah Pandi

2. Neonatal Jaundice
(Hyperbilirubinemia)
Definition: Hyperbilirubinemia refers,
excessive level of bilirubin in the blood.
Characterized by jaundice, a yellowish
discoloration of the skin, sclera, mucous
membranes and nails.

3. Visible form of bilirubinemia
Adult sclera >2mg / dl
Newborn skin >5mg /dl
Unconjugated = Indirect
Conjugated = Direct bilirubin.

4. •Why am I learning this?
•Is it important?

5. Why?
Jaundice more common in newborn
Full term infants: at least 60%.
Preterm infants: over 80%.
6-10% require phototherapy/ other
therapeutic options.

6. Is it important?
Most Importantly…
Kernicterus: Unconjugated bilirubin deposits
in the brain = Yellow staining + degenerative
lesions

7. Hyperbilirubinemia & Clinical
Outcomes
Deposits in
skin and
mucous
membranes
Unconjugated
bilirubin
deposits in
the brain
Permanent
neuronal
damage
JAUNDICE
ACUTE BILIRUBIN
ENCEPHALOPATHY
KERNICTERUS

8. Kernicterus:
*Bilirubin deposits typically in basal ganglia,
hippocampus, substantia nigra, etc.

9. Clinical Symptoms:
• Acute Bilirubin Encephalopathy/Kernicterus:
• Irritability, jitteriness, increased high-pitched crying
• Lethargy and poor feeding
• Back arching
• Apnea
• Seizures
• Long-term: Choreoathetoid CP, upward gaze palsy,
SN hearing loss, dental dysplasia

10. Stages of Kernicterus
I :- Unable to suck, hypotonia, lethargy
II :- Seizures, opisthotonus, spasticity
III :- Spasticity, shrill cry, apnea and seizures
IV :- Athetosis, deafness, up gaze palsy, dental
dysplasia and mental retardation

11. Causes of jaundice based on age at
onset Within 24 hours
a. Hemolytic disease of new born
a. Rh incompatibility
b. ABO incompatibility
b. Intra uterine infection
a. Toxoplasmosis, CMV, Rubella
c. Deficiency of red cell enzyme
a. G6PD deficiency, pyruvate kinase deficiency
d. Others

12. Onset- 24 to 72 hours of life
• Physiological jaundice
• Can be aggravated & prolonged by
i. Immaturity
ii. Cephalhematoma
iii. Birth asphyxia
iv. Hypothermia
v. Breast feeding
vi. infection

13. Onset – after 72 hours of age
a. Septicemia
b. EHBA
c. Breast milk jaundice
d. Metabolic causes
i. Galactosemia
ii. Tyrosinemia
iii. Hereditary fructosemia
iv. Gilbert syndrome
v. Organic acidemia

14. Physiological versus pathological
jaundice
Physiological jaundice
• Jaundice due to physiological immaturity of
neonates to handle increased bilirubin
production.
Pathological jaundice
• When TSB concentrations are not in
‘physiological jaundice’ range

16. Why does physiological jaundice develop?
Increased RBC’s
(Polycythemia)
Shortened RBC lifespan
Immature hepatic
uptake &
conjugation
Increased enterohepatic
Circulation

17. Physiological versus pathological
jaundice
PHYSIOLOGICAL PATHOLOGICAL
Onset More than 24 hours Less than 24 hours
Duration Term - <2 wks
Preterm- <3 wks
Term - >2 wks
Preterm- >3 wks
Serum bilirubin
concentration
Raise < 0.2 mg/dl/hr or
< 5 mg/dl / day
Raise > 0.2 mg/dl/hr or > 5
mg/dl / day
TSB < 15mg/dl > 15mg/dl
Involvement of palm
and soles
No Yes
Signs of acute bilirubin
encephalopathy
No Yes
Direct bilirubin Less than 2mg/ dl more than 2 mg/dl

18. Bhutani Curve- phototherapy

19. Bhutani Curve- Exchange transfusion

20. Causes of pathological jaundice
Common causes:
 Haemolysis:
Blood group incompatibility - ABO, Rh and minor
Enzyme deficiencies- G6PD deficiency
Decreased conjugation
Prematurity
Increased enterohepatic circulation
Breastfeeding jaundice, GI obstruction
Extravasated blood
Cephalhematoma, extensive bruising etc

21. Risk factors for jaundice
JAUNDICE
J - jaundice within first 24 hrs of life
A - a sibling who was jaundiced as neonate
U - unrecognized haemolysis
N – non-optimal sucking/nursing
D - deficiency of G6PD
I – infection
C – Cephalhematoma /bruising
E - East Asian/North Indian

22. Where do you look for jaundice in
newborn
1. Forehead
2. Tip of nose
3. Chest
4. Knee
5. Palms and soles

23. Clinical assessment of jaundice
• Visual inspection of jaundice
1. Examine the baby in bright natural light or
white fluorescent light. No yellow or off
white background
2. Make sure the baby is naked
3. Examine blanched skin and gums
4. Note the extent of jaundice (Kramer’s rule)
5. Depth of jaundice (degree of yellowness)

24. Kramer’s rule

25. Kramer’s rule
Zone 1= 5mg/dl
Zone 2 = 5-10 mg/dl
Zone 3 = 10-12 mg/dl
Zone 4 = 15mg/dl
Zone 5 = >15mg/dl

26. Measurement of serum bilirubin
Transcutaneus bilirubinometry (TcB)
• Advantage:
• Reduce invasive blood test
• Disadvantage:
• Costly,
• unreliable- less than 35 weeks, during initial 24 hr of
age & TSB more than 14mg/dl
• Measured by using multiple wave length
analysis

27. Measurement of TSB
Indications
i. Jaundice in first 24 hour
ii. Beyond 24 hr: if visually assessed jaundice more
than 15 mg/dL
iii. If you are unsure about visual assessment
iv. During phototherapy, for monitoring progress and
after phototherapy
Methods:
i. Biochemical: High performance liquid
chromatography (HPLC)
ii. Micro method: Based on spectrophotometry

28. Questions
1. Name four modality of treatment for
jaundice?
2. What are the lights used in phototherapy?
3. Which is the best light for phototherapy?
4. Can babies with jaundice shown in sunlight?

29. Management of Indirect Hyperbilirubinemia
• Careful assessment and monitoring
– Visual assessment
– Blood level monitoring per
hospital protocol at 24 hr of life
or sooner as indicated
– Interpretation of risk levels and
need for treatment
• Phototherapy
• IVIg
• Exchange Transfusions
• Phenobarbital

30. Therapeutic Management
Purposes: reduce level of serum bilirubin and prevent
bilirubin toxicity
Modalities :
1. Phototherapy- Reduction of bilirubin levels
2. Exchange transfusion- Reduction of bilirubin levels
3. IV IG- prevent- Lysis of RBC’s by blocking immune
mediated antibody
4. Metalloporphyrin tin/ zinc- Prevent breakdown of Hb
by heme oxidase
5. Phenobarbitone/ UDCA- Conjugation of bilirubin

31. Phototherapy
Safe and effective method for treatment of
neonatal jaundice
Bilirubin absorbs light maximum at 420-460
nm

32. Phototherapy

33. Mechanism of Action
• Conversion of insoluble Bilirubin into soluble
bilirubin Excretion of bilirubin
1. Photo- isomerisation
2. Structural isomerisation
3. Photo- oxidation

34. Photo-isomerisation
Reversible reaction.
Conversion of insoluble, toxic form Z
isomer non toxic polar (water soluble) E
isomer diffuses into the blood 
excreted easily into bile

35. Structural isomerisation
Irreversible reaction
Bilirubin  lumirubin
Rapidly excreted in bile and urine
Main responsible for phototherapy induce
decline of TSB
Reduction of bilirubin directly proportional to
dose of phototherapy

36. Photo-oxidation
Minor reaction
Photo-oxidation of Bilirubin to water soluble
polymers
Colourless by product
Riboflavin- catalyze the dermal photo-
oxidation

37. Phototherapy

38. Indications for Phototherapy
TSB > 18 mg % in term
TSB > 15 mg% in preterm
Adjuvant to exchange transfusion
Prophylactic PT
- ELBW
- Extreme preterm babies,
- Bruised babies
- Babies with DCT positivity
- Babies whose mother is ICT positive

39. Procedure
 Best is narrow spectral blue lights (425- 475nm)
 White lamps (380-700nm)
 Distance from skin – 45cm
 Intensive PT – 15-20 cm
 Shield eyes & genitalia
 Change position once in every 2-4 hrs
 Level to be checked every 10-12 hrs
 Frequent temperature monitoring & daily
weight check

41. Side Effects
Immediate:
i. Loose stools
ii. Dehydration
iii. Hypo or hyperthermia
iv. Rashes
v. Bronze baby syndrome
Late:
i. Risk of skin malignancies
ii. Damage to intracellular DNA
iii. Retinal damage
iv. Testicular damage

42. Exchange transfusion
• The procedure involves the incremental
removal of the patient's blood and
simultaneous replacement with fresh donor
blood, saline or plasma
• Indications- infants with Rh isoimmunnisation
include:
i. Cord bilirubin 5mg/ dl or more
ii. Cord Hb 10g/ dl or less

43. Exchange transfusion
• Complications
• Hypocalcaemia and Hypomagnesaemia - Citrate in
CPD blood
• Hypoglycaemia
• Metabolic alkalosis or acidosis
• Hyperkelemia
• CVS: overload and arrhythmias
• Infections: HBV HIV
• Haemolysis
• Hypothermia, NEC.

44. Prevention
Breastfeeding

45. Case #1:
• FT baby girl born at 40 weeks
to primi mother
• BW 3200 g; APGAR 8,9
• Pregnancy and delivery
without complications
• Currently DOL #2 (48h of life)
• Nurses noted that she looks
like this and call you to the
Well-Baby Nursery to evaluate
her:

46. Case #1:
• What else would you want to know?
– How is she feeding? How is it going?
– Is she stooling and voiding? How often?
– What is her current weight?
– How is she doing otherwise?
– Does she have any risk factors?
– Has she had her TcB checked?
– Has she had blood bilirubin levels checked?

47. Case #1:
• Her mother is breastfeeding her. She thinks it is
going well but this is her first baby and she is not
sure if her milk is in yet. She is feeding for 20
minutes every 4 hours.
• Voided once and stooled several times since birth.
• Current weight is 2850 g (about 11% less than BW).
• She seems less active and is sleeping more today.
• No known risk factors. Mother and baby are both
B positive.
• Total/direct bilirubin is 18/1 mg/dL.

48. Case #1:
• What is your working diagnosis?
– BREASTFEEDING JAUNDICE

49. Case #1:
• What would you do
next?
– Initiate phototherapy
– Monitor serial
bilirubin levels
– Encourage increased
frequency of feedings
(q 2-3h ATC) and
consider
supplementation prn
– Request lactation
consult
Bhutani Curve: Phototherapy Indication

50. Breast feeding jaundice Breast milk jaundice
Incidence 5-10 % of newborn 2- 4 % of newborn
Etiology & pathogenesis Decrease intake of breast milk
leads to increased enterohepatic
circulation
Due to unknown( substance
in breast milk blocks
destruction of bilirubin
Day of appearance Similar to physiological jaundice 4 to 7 days of age
Duration of jaundice Less than 3 weeks 3 – 10 weeks. Bilirubin level
may reach upto 20-30 mg/dl
Treatment Adequate breast feeding Not harmful
Aggravating factors Dehydration Nil

51. Case #2:
• Late pre-term baby boy born
at 35 weeks
• BW 2500g; Apgars 8,9
• Pregnancy and delivery
without complications
• Currently DOL #1 (12 h of life)
• Nurses noted that he looks
like this and called you into
Room 1 to evaluate him:

52. Case #2:
• What else would you want to know?
– How is he feeding? How is it going?
– Is he stooling and voiding? How often?
– What is his current weight?
– How is he doing otherwise?
– Does he have any risk factors?
– Has he had his TcB checked?
– Has he had blood bilirubin levels checked?

53. Case #2:
• He is taking Neosure formula 2 ounces q 2-3 hours.
• Voided twice and stooled several times since birth.
• Current weight is 2500 g (same as BW).
• He is less active and sleeping more today.
• Mother is O positive and baby is A positive.
• Total/direct bilirubin is 18/1 mg/dL.
• Coombs positive.

54. Case #2:
• What is your working diagnosis?
– ABO INCOMPATIBILITY

55. Case #2:
• What would you do next?
– Exchange transfusion
Bhutani Curve: Phototherapy Indication Exchange Transfusion Indication

56. Prolonged jaundice
• Definition :
• Persistence of significant jaundice for more
than 2 weeks in term
or
More than 3 weeks in preterm babies

57. Causes of prolonged jaundice
Common:
i. Inadequacy of breast feeding
ii. Breast milk jaundice
iii. Cholestasis
Rare causes:
i. Hypothyroidism
ii. Criggler-Najjar syndrome
iii. GI obstruction due to malrotation
iv. Gilbert syndrome

58. Summary:
• Hyperbilirubinemia is a common and potential
serious issue in neonates
• Important to recognize and diagnose early in order
to initiate prompt treatment when possible