This document provides an overview of neonatal jaundice, including its epidemiology, pathophysiology, etiology, clinical presentation, management, and complications. Key points include: - Neonatal jaundice is common, occurring in 50-80% of newborns, and is usually harmless. It is caused by elevated bilirubin levels in the blood. - Jaundice can be physiological or pathological. The causes and management differ depending on whether the elevated bilirubin is conjugated or unconjugated. - Evaluation involves clinical exam, bilirubin levels, and other tests to determine the underlying cause. Management includes phototherapy, exchange transfusion, or pharmacotherapy depending on

1. 1
NEONATAL JAUNDICE
BY
DR. AYODELE, NOSRULLAH S
FMC, BIRNIN KEBBI

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

3. INTRODUCTION
 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 1,2
 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
3

4. INTRODUCTION
 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
4

5. EPIDEMIOLOGY
 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
5

6. EPIDEMIOLOGY
 Incidence varies with ethnicity and geography, higher
in East Asians and American Indians and lower in
Africans 3
 Incidence is higher in populations living at high
altitudes 3
 Risk of developing significant neonatal jaundice is
higher in male infants 3
 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%). 4
6

7. TYPES OF 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 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

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
10
 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
 Causes of pathological jaundice
 Unconjugated hyperbilirubinemia (hemolytic/non-hemolytic)
 Conjugated hyperbilirubinemia (hepatic / post hepatic)
11

12. AETIOLOGY
 Hemolytic causes of pathological jaundice
(Unconjugated)
12
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
 Non hemolytic causes of pathological jaundice
(Unconjugated)
 Breast milk jaundice
 Criggler Najjar syndrome types I and II
 Gilbert syndrome
 Hypothyroidism
13

14. AETIOLOGY
 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
14

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

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

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 18

19. EXAMINATION
 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
19

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

21. INVESTIGATIONS
 Bilirubin measurement
 Serum (total and direct)
 Transcutaneous (bilirubinometer/icterometer) 5
 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
 Liver function test (AST/ALT, ALP/GGT)
21

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

23. TRANSCUTANEOUS
MEASUREMENT OF BILIRUBIN
 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
23

24. SUMMARY OF EVALUATION
Nelson Textbooks of Paediatrics

25. JAUNDICE ASSOCIATED WITH
BREAST-FEEDING
25
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,reduced
caloric intake,glucose water
supplement

26. TREATMENT OF UNCONJUGATED
HYPERBILIRUBINEMIA
 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
26

27. PHOTOTHERAPY (PT)
 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 2
 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 4
27

28. PHOTOTHERAPY
 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 -
28

29. PHOTOTHERAPY
 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
29

30. PHOTOTHERAPY
 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
 Watch for side effects
30

31. PHOTOTHERAPY
 Complications
31
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)
 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
32

33. EXCHANGE BLOOD
TRANSFUSION
 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
33

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
34

35. EXCHANGE BLOOD
TRANSFUSION
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.
35

36. EXCHANGE BLOOD
TRANSFUSION
 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.
36

37. PHARMACOTHERAPY
 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
37

38. PHARMACOTHERAPY
 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
38

39. KERNICTERUS
 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
39

40. KERNICTERUS
 By pathologic criteria, it develops in 30% of infants (all
gestational ages) with untreated hemolytic disease and
bilirubin levels >25-30 mg/dL 2
 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
40

41. KERNICTERUS
 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
41

42. KERNICTERUS
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
42

43. KERNICTERUS
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
43

44. TREATMENT OF CONJUGATED
HYPERBILIRUBINAEMIA
 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)
44

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
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. 47

48. REFERENCES
1. https://www.nhs.uk/conditions/jaundice-newborn/HS. Accessed on
26/2/2018
2. Kliegman, Robert, Richard E. Behrman, and Waldo E. Nelson. Nelson
textbook of pediatrics. 20th edition (2016).
3. https://emedicine.medscape.com/article/974786-overview#a6.
Accessed on 26/2/2018
4. Azubuike JC, Nkanginieme KE. Paediatrics and child health in a tropical
region. 2nd edition. African Educational Services;. Pp 163-170
5. Krishnasamy M, Bakri R, Bilirubinometer t. Non-invasive, hand held
transcutaneous bilirubinometer. Health Technology Assessment Section,
Medical Development Division Ministry of Health Malaysia. 2009
6. Kaplana M. Neonatal jaundice. Manipal Teaching Hospital. Powerpoint
presentation. Accessible online at: www.slideshare.net
7. Ogunlesi TA, Ogunfowora OB. Predictors of acute bilirubin
encephalopathy among Nigerian term babies with moderate-to severe
hyperbilirubinaemia. J Trop Pediatr 2011;57:80–6.
8. Ogunfowora OB. Neonatal Jaundice. OOUTH Sagamu. 2009
48

49. 49
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