This document provides an outline and overview of neonatal jaundice. It discusses the epidemiology, bilirubin metabolism, causes (physiological and pathological), clinical presentation, management including phototherapy and exchange blood transfusion, complications and prevention of neonatal jaundice. Neonatal jaundice is a common condition seen in newborns due to elevated bilirubin levels that can cause yellowing of the skin if not properly managed.

1. NEONATAL JAUNDICE
1
Preparedby
Abdulghani jaafar

2. OUTLINE
2
 INTRODUCTION
 EPIDEMIOLOGY
 BILIRUBIN METABOLISM/PATHOPHYSIOLOGY
 AETIOLOGY
 CLINICAL PRESENTATION
 MANAGEMENT
 COMPLICATIONS
 PREVENTION
 SUMMARY
 CONCLUSION

3. INTRODUCTION
3
 Neonatal jaundice is the yellowish discoloration of the eyes,
skin and mucous membranes in the first month of life due to
elevated level of bilirubin in the blood
 It is a common and, in most cases, harmless problem in
neonates
 It may present with other symptoms like
 yellowing of the palms or
 dark, yellow urine – a newborn baby's urine should be
colourless
 pale-coloured stool – should be yellow or orange

4. INTRODUCTION
4
 The yellow discoloration may be as a result of elevation of
either the uncongugated or conjugated bilirubin
 Bilirubin may have a physiologic role as an antioxidant but
elevations of indirect, unconjugated
bilirubin are potentially neurotoxic.
 Even though the conjugated form is not neurotoxic, direct
hyperbilirubinemia indicates a potentially serious hepatic
disorders or a systemic illness
 Poor management can result into either death or serious
neurological problems

5. EPIDEMIOLOGY
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 Neonatal jaundice first been described in a Chinese
textbook 1000 years ago
 In 1875, Orth first described yellow staining of the
brain, in a pattern later referred to by Schmorl as
kernicterus
 It is extremely common because almost every
newborn develops an unconjugated serum bilirubin
level of more than 30 µmol/L (1.8 mg/dL) during the
first week of life

6. EPIDEMIOLOGY
6
 Incidence varies with ethnicity and geography, higher in East
Asians and American Indians and lower in Africans
 Incidence is higher in populations living at high
altitudes
 Risk of developing significant neonatal jaundice is higher in
male infants
 Generally, the prevalence in hospital practice is estimated at
between 50-80%, being more common in preterm (about
80%) than in term infants (about 50%).

7. TYPES OF JAUNDICE
• 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 12-15 mg / dl
• Clinically not detectable after 14 days
• Resolves without treatment
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
• Urine staining yellow, staining clothes
• Direct bilirubin > 2 mg / dl
• Signs of underlying illness
Pathological
Jaundice
7

8. Cytochrome, calatases
Rate limiting step. activated by physiological
stressors like hypothermia, acidosis, hypoxia and
infections.
Bound to albumin
BILIRUBIN METABOLISM

9. BILIRUBIN METABOLISM (Lippincott Illustrated Reviews Biochemistry 6th Edition(

10. AETIOLOGY
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 The cause of jaundice can be either physiologic or
pathologic
 Causes of physiological jaundice
1. Decreased RBC survival <90 days, increased RBC vol /Kg,
polycythemia of NB
2. Poor hepatic uptake due to immature liver - decreased ligandin
or Y- protein
3. Increased enterohepatic circulation due to
 high level of intestinal beta-glucuronidase
 delayed colonization by bacteria
 decreased gut motility

11. AETIOLOGY
11
 Causes of pathological jaundice
 Unconjugated hyperbilirubinemia )hemolytic/non-hemolytic(
 Conjugated hyperbilirubinemia (hepatic / post hepatic(

12. AETIOLOGY
12
 Hemolytic causes of pathological jaundice( Unconjugated(
Coomb test positive Coomb test negative
ABO incompatibility RBC membrane defect
)Spherocytosis, elliptocytosis(
Rh incompatibility RBC enzyme defect (G6PD(
Hemoglobinopathies
Sepsis
DIC
Hematomas
Polycythaemia
Drugs (diazepam, oxytoci)

13. AETIOLOGY
13
 Non hemolytic causes of pathological jaundice
)Unconjugated(
 Breast milk jaundice
 Criggler Najjar syndrome types I and II
 Gilbert syndrome
 Hypothyroidism

14. AETIOLOGY
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 Causes of Pathological jaundice (conjugated(
1. Hepatic
 Idiopathic neonatal hepatitis
 Dubin Johnson syndrome
 Rotor’s syndrome
 Infections –TORCH, sepsis
 Inborn errors of metabolism (galactosemia, tyrosinemia(
2. Post hepatic
 Biliary atresia
 Bile duct stenosis
 Choledochal cyst

15. AETIOLOGY
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 Common causes of jaundice in our environment
 Physiological
 Blood group incompatibility
 G6PD deficiency
 Breast milk jaundice
 Sepsis
 Cephalhematoma

16. CLINICAL PRESENTATION
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 Yellowness of the eyes or body
 Fever
 Vomiting
 Inability to suck
 Features of failure to thrive
 Abdominal distention
 Passage of pale stool

17. MANAGEMENT
17

18. HISTORY
 Biodata
 Onset / duration /progression
 Color of urine/stool
 Vomiting
 Feeding history
 Loss of weight
 Maternal history
 Antenatal –booking, illnesses, infections
 Drugs – sulfa, NSAIDs, herbals
 Medical history – blood group, hemolytic diseases, liver disease,
recurrent jaundice
 Family history – siblings with jaundice, familial jaundice, liver disease
 Birth history – trauma, cord clamping
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19. EXAMINATION
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 Examine for jaundice (bright yellow/orange or
greenish/muddy yellow)
 Jaundice usually becomes apparent in a cephalocaudal
progression, starting on the face and progressing to the
abdomen and then the feet, as serum levels increase.
 Kramer’s Index
1. Face-4-6 mg/dl
2. Chest &Upper trunk – 8-10 mg/dl
3. Lower abdomen,thigh-12 -14mg/dl
4. Forearms &lower legs -15 -18 mg/dl
5. Palms & sloes->15-20 mg/dl

20. EXAMINATION
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 Pallor
 Dehydration
 Weight loss
 Fever or hypothermia
 Hepato/splenomegaly
 Evidence of birth trauma or injuries
 Evidence of Kernicterus

21. INVESTIGATIONS
 Bilirubin measurement
 Serum (total and direct)
 Transcutaneous (bilirubinometer/icterometer(
 Full blood count and blood smear
 Hemoglobin concentration
 Reticulocyte count
 Blood group
 Coombs test
 Urinalysis – reducing substances
 urine m/c/s
 Electrolyte, urea and creatinine
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 Liver function test (AST/ALT, ALP/GGT(

22. INVESTIGATIONS
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 G6PD assay
 Ultrasound scan
 Thyroid function tests

23. TRANSCUTANEOUS
MEASUREMENT OF BILIRUBIN
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 Eligibility of babies for TcB estimation:
1. Babies ≥ 38 week gestation visibly jaundiced after 24 hrs of
age until 14 days
2. Babies 34 – 37+6 weeks gestation who are ≥ 72 hrs old until
14 days
3. Babies not on phototherapy
 Contraindications
1. Infants with pathological Jaundice
2. Babies less than 24 hrs old
3. Babies on phototherapy or undergone phototherapy /exchange
transfusion

24. SUMMARY OF EVALUATION
Nelson Textbooks of Paediatrics

25. JAUNDICE ASSOCIATED
WITH BREAST-FEEDING
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Breast milk jaundice Breastfeeding jaundice
2% of breastfed infants 13% of breastfed infants
Occurs after 7th day Occurs within 1 week
Max may be up to10-30mg/dl May reach >12mg/dl
Peaks at 2-3 weeks
SB falls gradually if
breastfeeding stops
Responds to phototherapy Responds to frequent
breastfeeding
Aetiology not clear
Associated with glucuronidase
in milk
Cause: decreased milk
intake,dehydration,reduce
d caloric intake,glucose
water supplement

26. TREATMENT OF UNCONJUGATED
HYPERBILIRUBINEMIA
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 Aim of treatment
1. Reduce the incidence of severe hyperbilirubinaemia
2. Prevent bilirubin encephalopathy (kernicterus(
 Modalities include
1. Phototherapy
2. Exchange blood transfusion
3. Pharmacotherapy

27. PHOTOTHERAPY (PT)
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 Is the use of high intensity light energy to reduce
bilirubin levels on the skin surface
 Light is used in the white, blue, turquoise, and green
wavelengths
 Bilirubin absorbs light maximally in the blue range
from 420-470nm
 It is useful in the prevention and/or treatment of
moderate hyperbilirubinaemia.
 When adequately delivered, should lower bilirubin by
1-2mg/dl over 4-6 hours

28. PHOTOTHERAPY
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 Mechanism of action - conversion of insoluble
bilirubin into soluble bilirubin
1. Structural isomerization - conv to lumirubin -rapidly
excreted in bile and urine
2. Photoisomerization – converts bilirubin (4Z,15Z) to
soluble isomers (e.g 4Z15E) without conjugation and
excreted into bile
3. Photooxidation -

29. PHOTOTHERAPY
29
 Indications
 TSB > 15 mg/dl in term
 TSB > 12 mg/dl in preterm
 TSB > 5 mg/dl within 24 hours
 Adjuvant to exchange transfusion
 Prophylactic PT – ELBW, bruised babies, hemolytic disease of
NB,VLBW with perinatal risk factors
 Contraindications
 Porphyria
 Conjugated hyperbilirubinaemia – Bronze baby syndrome
 Unconjugated hyperbilirubinaemia (20mg/dl or >)Diseases with
hypersensitivity to light

30. PHOTOTHERAPY
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 Watch for side effects
 Procedure/precautions
 Distance from skin – 45cm , Intensive PT – 15-20 cm
 Space of 5-8cm between phototherapy unit & incubator
 Double surface PT – can be given by fiber-optic blankets
(biliblankets)
 Distant child from other not needing PT
 Cover the eyes and Genitals
 Change position once in every 2-4 hrs
 Level to be checked every 10-20 hrs
 Frequent temperature monitoring
 Supplemental hydration(10-25ml/kg/day(
 Daily weight check

31. PHOTOTHERAPY

Complications
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Early Late
Loose stools Skin malignancy
Dehydration Damage to DNA
Skin rashes Patent ductus arteriosus
Hyperpigmentation Gonadal damage
Upsets maternal
infant interactions
(bond)
Retinal damage
Hyperthermia Disturbance of circadian rhythm
Bronze baby syndrome

32. EXCHANGE BLOOD TRANSFUSION (EBT)
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 Done to rapidly lower the serum bilirubin concentration
and/or prevent further rise
 Indications
 Unconjugated hyperbilirubinemia of 20mg/dl and above in term or 15mg/dl
and above LBW in preterm
 Serum bilirubin level up to 10mg/kg for other preterms
 Bilirubin level rising rapidly up to 5mg/dl/day
 Serum bilirubin >10mg/dl on the first day of life or 15mg/dl at 48hrs of life
 Clinical signs of kernicterus
 Others -severe anaemia, DIC

33. EXCHANGE BLOOD TRANSFUSION
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 Technique – commonly “push-pull” method using
umbilical vein catheter
 Choice of blood – heparinized, fresh whole blood preferred
(also used – ACD or CPD can also be used(
 Quantity – twice the blood volume of the patient
(160-170ml/kg), over 60-90min.
 Blood is exchanged in aliquots of 5,10 or 20ml, or smaller
volumes for small infants
 Priming the infant by infusion of 1 mg/kg of salt-poor
albumin a few hours before EBT increases efficiency

34. EXCHANGE BLOOD
TRANSFUSION
 Procedure
 Take vital signs
 Empty the stomach – prevents aspiration
 Ensure right blood is available
 Maintain asepsis
 Catheterize umbilical vein and secure in place
 Take pre EBT PCV and serum bilirubin
 Exchange blood in aliquots and document
 Give 1ml of 10%calcium gluconate after every 100ml slowly
and listen to the heart alongside
 Take post EBT PCV and serum bilirubin
 Replace all drugs given earlier if not time for next dose
 Prevent hypoglycaemia – 200mg/kg of IV glucose
 Adjuvant phototherapy
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35. EXCHANGE BLOOD
TRANSFUSION
35
Complications of EBT
 Complications of catheterization
 Gut perforation and peritonitis
 Wrong position of tip of catheter (may excite cardiac
arrhythmia if in the right atrium(
 Necrotizing enterocolitis
 Liver cirrhosis (long-term complications(
 Complications of blood transfusion
 Transmission of infection (malaria, hepatitis B, HIV(
 Transfusion reactions (immediate and delayed(
 Thromboembolism.

36. EXCHANGE BLOOD
TRANSFUSION
36
 Complications EBT itself
 Haemodynamic changes following the push-pull process
(hypovolaemia, hypervolaemia(Electrolyte changes
(hyperkalaemia, hypocalcaemia, hypomagnesaemia
 Acid/base imbalance
 Changes in cerebral blood flow.

37. PHARMACOTHERAPY
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 Not routine used because of ineffectiveness
 Phenobartitone
 augments hepatic uptake of bilirubin and increases the
activity of glucuronyl-transferase (UDPG-T) enzyme
 Takes 48-72 hrs to reach therapeutic level
 Dose 5-8mg/kg/day
 Side effect – sedates, difficult to assess baby
 Useful in Criggler Najar disease

38. PHARMACOTHERAPY
38
 Metalloprotoporphyrins (eg tin mesoporphirin(
 are competitive inhibitors of heme oxygenase
 Experimental – showing prospects
 Oral agar (e.g Cholesteramine(
 Decreases enterohepatic circulation
 Albumin infusion
 Increases albumin binding to bilirubin for easy transport
 Intravenous immunoglobulin
 Used for infants with Rh or ABO isoimmunization
 Inhibits haemolysis
 Dose = 0.5-1 gm/kg/dose IV, repeat in 12hrs

39. KERNICTERUS
39
 Is the pathologic diagnosis referring to the yellow
staining of the brain caused by bilirubin deposition
associated with neuronal necrosis and gliosis
 It is a direct consequence of very high level of
unconjugated bilirubin
 The parts of the brain commonly affected
 Basal ganglia
 Brain stem nuclei
 Cerebellar neclei
 Hippocampus
 Anterior horn cells of the spinal cord

40. KERNICTERUS
40
 By pathologic criteria, it develops in 30% of infants (all gestational ages)
with untreated hemolytic disease and bilirubin levels >25-30 mg/dL
 Overt neurologic signs have a grave prognosis
 More than 75% of infants die, and 80% of affected survivors have
bilateral choreoathetosis with involuntary muscle spasms

41. KERNICTERUS
41
 It manifests clinically as acute or chronic encephalopathy
 The acute is characterized by 3 phases
 PHASE 1: hypotonia, lethargy, high pitched cry and poor suck, loss of Moro
reflex (D1-3)
 PHASE 2: hypertonia, opisthotonus, rigidity, oculogyric crisis, retrocollis,
fever, seizures. (middle of first week). Those who survive develop chronic
bilirubin encephalopathy
 PHASE 3: Hypotonia replaces hypertonia after first week

42. KERNICTERUS
42
Chronic encephalopathy manifests as
 1st year
 hypotonia,
 active deep tendon reflexes,
 obligatory tonic neck reflexes,
 delayed motor skills
 After 1st yr:
 movement disorders (choreoathetosis, ballismus, tremor(,
 upward gaze,
 sensorineural hearing loss

43. KERNICTERUS
43
Treatment:
 Treatment of hyperbilirubinaemia
 Counselling/training the parents on coping with the sequale
 Management of feeding difficulty
 Physiotherapy for limitation of disability
 Speech and language therapy (SALT(
 Follow up appointments

44. TREATMENT OF CONJUGATED
HYPERBILIRUBINAEMIA
44
 Mainly supportive
 Parenteral vitamin k
 Vitamin A and D supplementation – prevents rickets
 Diet – low fat, medium chain triglyceride
 Phenobarbitone – helps bile exceretion
 Surgery may be needed (not usually in the neonatal period(

45. PREVENTION
 This entails prevention of neonatal jaundice,
treatment and prevention of its complications when it
occurs
 Follows the three levels of prevention
1. Health promotion (primary)- educate the masses about it and
how to prevent, lifestyle modification
2. Specific protection(primary)- identify risks and institute
preventive measures
3. Early diagnosis and adequate treatment (secondary)–
identify and treat jaundice promptly
4. Limitation of disability (tertiary) - physiotherapy
5. Rehabilitation (tertiary) – integration of the baby and the
mother into the community
45

46. SUMMARY
 Jaundice presents with yellowness of the skin and
mucous membranes
 The cause can be physiological or pathological due to
abnormalities in bilirubin metabolism
 Unconjugated bilirubin is neurotoxic to the brain and
hence needs urgent attention
 Prompt diagnosis and management helps to prevent severity
and complications like kernicterus
 Modalities of treatment include phototherapy, EBT
and pharmacotherapy
46

47. CONCLUSION
O Neonatal jaundice still contributes significantly to
neonatal morbidity, mortality and long-term handicap
especially in the developing countries. This is made
worse by ignorance on the part of parents and health
workers which contributes to delay in seeking proper
medical care.
However, education at Primary Health Care level, prompt
diagnosis and referral to appropriate specialist will go a long
way to prevent the jaundice-associated problems early so that
death is averted and the child will have a good quality of life.
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