Neonatal jaundice is one of the most common conditions in newborns. It is caused by high levels of bilirubin in the blood which causes yellowing of the skin. Physiological jaundice is common and appears after 24 hours, peaks by days 3-5, and resolves by 14 days without treatment. Pathological jaundice appears within 24 hours and requires treatment. Proper assessment includes history, physical exam, and lab tests to determine severity and risk of complications like acute bilirubin encephalopathy. Treatment may include phototherapy or exchange transfusion in severe cases. Close monitoring is important to prevent bilirubin neurotoxicity in newborns.

1. NEONATAL JAUNDICE
YEE WEI HOONG
121303147
31B (L1)
1

2. DEFINITION
• Jaundice is a yellowish discolouration of
skin, sclerae, mucous membranes & nails
from accumulation of bilirubin.
• Hyperbilirubinemia refers to an excessive
level of bilirubin in blood.
2

3. Neonatal Jaundice
• One of the most common medical
conditions in newborn babies
• All babies have transient rise in
serum bilirubin, but only 75% are
visibly jaundiced.
• Jaundice is clinically detectable when
serum bilirubin levels are >5mg/dL
(85 umol/L)
• Jaundice is more common in Asian 3

4. Day 1 Day 7 Day 14/21
PATHOLOGICAL
jaundice
PHYSIOLOGICAL
jaundice
PROLONGED
jaundice
Time Frame for
Jaundice
4

5. CLASSIFICATIONS
• Physiological
1. Appears after 24hrs
2. Maximum intensity by 3rd -5th day in term, 7th day in
preterm
3. TSB <15mg/dL (<255umol/L)
4. Not detectable clinically after 14days
5. No underlying cause
6. Disappears spontaneously
• Pathological
1. Appears within 24hrs of age
2. Serum bilirubin level increase >6mg/dl/day
3. TSB >20mg/dL(340umol/dL)
4. Conjugated/Direct bilirubin >2mg/dL(34umoLdL) 5

6. Pathophysiology of Physiological
Jaundice
1. Decreased erythrocyte life span (80 to 90 days) in a full
term infant
2. Increased erythrocyte volume
3. Increased bilirubin load on the hepatic cell
4. Defective uptake from plasma into liver cell – decreased
ligandin
5. Defective conjugation - relatively low activity of the
enzyme glucuronosyltransferase which normally converts
unconjugated bilirubin to conjugated bilirubin
6. Low conversion of bilirubin to urobilinogen by the
intestinal flora resulting in higher entero-hepatic
circulation
7. Decreased excretion 6

7.  RBC vol &  RBC survival
 Bil monoglucoronide
 Bil Diglucoronide
UCB
ProductionTransport
Uptake
Excretion
Conjugatio
n
 ineffective erythropoiesis &  haem
turnover
Non availability of
albumin binding sites
Defective conjugation
 Ligandin
Decreased
excretion
 gut motility
Poor
evacuation
 beta glucoronidase,  intestinal
bacteria
 BILIRUBIN load
Defective uptake from
plasma
 Entero-hepatic
circulation
Bilirubin Load Causing
Jaundice in Newborn
7

8. CAUSES OF PATHOLOGICAL
JAUNDICE
1. Haemolytic disease of newborn: Rh, ABO &
minor group (anti-Kell, Duffy)
incompatibility
2. Infections: Intrauterine infection
(Bacterial, viral)
3. Membrane defects: Spherocytosis,
elliptocytosis
4. RBC enzyme defects: G6PD deficiency,
pyruvate kinase deficiency
5. Polycythemia
8

9. NNJ & Mother’s Knowledge
• A Malaysian study found that less
than 50% of the mothers had good
knowledge & awareness about the
risks & complications of NNJ.1
9
1. Boo NY, et al. Med J Malaysia. 2011 Aug;66(3):239-243

10. MONITORING
• Extract (1) from Malaysia CPG :
10

11. MONITORING
• Extract (2) from Malaysia CPG :
11

12. MONITORING
• Extract (3) from Malaysia CPG :
12
82. Division of Family Health Development, Ministry of Health. Integrated Plan for Detection and
Management of Neonatal Jaundice. Putrajaya: MoH; 2009

13. MONITORING
• Extract (4) from Malaysia CPG :
13

14. P.P.A.P Physiological, Pathological
and Prolonged
14
Physiological
Jaundice
Pathological
Jaundice
Prolonged
jaundice
Starts within 24
hours
Starts after 24 hours;
usually disappear by
14th day
Jaundice lasting >14
days
MIX &
MATCH!!!

15. Maybe Previous Q was too
easy…Try This Pulak.
In the development of physiological NNJ, there is:
a.decreased bilirubin load F
b.defective uptake of bilirubin from
plasma
T
c.defective conjugation T
d.increased excretion F
e.decreased entero-hepatic circulation F
15

16. Three Components of
Assessment
• History
• Physical Examination
• Lab Investigations
*Phototherapy must always be started
while awaiting further assessment &
investigation
16

17. Objectives of Proper Assessment
(History, Physical Examination, Lab
Investigations)
17
End Point
Prevention of
bilirubin
neurotoxicity
(acute/
chronic)
To identify
Risk Factors
(for severe NNJ
and neurotoxicity)
Severity of
NNJ
(level of SB or
extent of
hemolysis)
Complications
(signs of ABE)
To decide on
Management
(phototherapy,
exchange
transfusion)
Follow-up
(ABR, MRI,
development)
But not at the cost of overinvestigating or overtreating low risk
babies

18. 1. Risk Factor Identification
18

19. 2. ASSESSMENT OF
SEVERITY
• Visual assessment
• Transcutaneous measurement
• Analysis of blood serum
19

20. VISUAL ASESSMENT-
KRAMER’s RULE
Kramer’s rule describes the relationship
between serum bilirubin levels & the
progression of skin discolouration
20

21. Transcutaneous
bilirubinometer (TcB)
• The transcutaneous bilirubinometer is a hand-held
device that measures the amount of bilirubin in the
skin.
Bilicheck (Philips)
Does not require any disposable material & less time consuming
JM 103 (Draeger)
21

22. Serum Bilirubin (SB)
Measurement
• Gold standard for detecting & determining the
level of hyperbilirubinaemia.
• May be estimated on either a capillary or a
venous blood sample.
• Blood sample should be analysed as soon as
possible & should be shielded from light during
transport (exposure to light rapidly &
significantly decreases bilirubin).
• Remove phototherapy prior to sample collection.
22

23. CPG says…
23

24. 3. Assessing
Complications
24

25. Dangers of Hyperbilirubinemia
• If untreated, it will lead to acute & chronic bilirubin
encephalopathy, eventually kernicterus.
• C/F:
 Refusal of feeds, shrill cry, setting sun sign, convulsions,
retrocollis & opisthotonus
 Sluggish Moro’s response, lethargy, poor feeding
 Preterm – Non specific. Die due to apnoeic attacks
 Infancy – Athetoid cerebral palsy, choreo-athetosis, brownish
staining of teeth, dental dysplasia, deafness, paralysis of upward
gaze, intellectual retardation & learning disabilities
25

26. 26
Images taken from: Vinod K, et al. Bilirubin Neurotoxicity in Preterm Infants: Risk and Prevention. J
Clin Neonatol. 2013 Apr-Jun; 2(2): 61–69.

27. Acute Bilirubin
Encephalopathy (ABE)
• ABE: Changes of mental (behavioural)
status & muscle tone during the neonatal
period when the baby is having
hyperbilirubinaemia.
• Identifying & Monitoring of ABE:
• Term Babies: Use BIND Score
• Preterm Babies: Difficult, as signs are subtle.
Auditory Brainstem Response (ABR) could be
used.
27

28. BIND
Score
28

29. Indications for Referral to
Hospital
• Jaundice within 24hours of life
• All babies that require phototherapy
• Jaundice below umbilicus
• Jaundice extending to soles and feet
• Rapid increase of bilirubin level (>0.5mg/h)
• Diagnosed with G6PD deficiency
• Haemolytic disorder
• Symptoms and signs of sepsis
29

30. Investigations
• *Total serum bilirubin
• *G6PD status
• Others as indicated:
-infant’s blood group
-Maternal blood group
-Direct coombs’ test (indicated in day 1 jaundice and
severe jaundice)
-FBC, reticulocyte count, peripheral blood smear
-Blood culture, urine microscopy, and culture (infection
30

31. TREATMENT
1. Phototherapy
• Light with wavelenght of 450nm convert
unconjugated bilirubin into harmless water soluble
pigment excreted predominantly in the urine
2. Exchange Transfusion
• Twice the infant’s blood volume 2x80ml/kg is
exchange
3. IVIG (Intravenous immunoglobulin)
• high dose IVIG (0.5-1 gm/kg over 2hours) reduce the need for ET in Rh
and ABO hemolytic disease
• Give as early as possible in hemolytic disease with positive Coomb’s test or
when the serum bilirubin increasing despite intensive phototherapy.
31

32. Hmm…Final Q
• Following vessels can be utilised for
exchange transfusion, except:
A. Femoral Vein
B. Umbilical Artery
C. Umbilical Vein
D. Subclavian Vein
E. Peripheral Artery
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33. Measures to Prevent Severe
Neonatal Jaundice
• Promote & support breastfeeding.
• Advise a frequency of 8 to 10 feedings per day
• Formula milk for term infants should be 1 to 2 ounce every 2 to
3 hrs in the 1st week.
• If phototherapy in infants with hemolytic jaundice is initiated
early and discontinue before infant 3-4 days old, must monitor
for rebound jaundice and adequacy of breast feeding within the
next 24-48 hours.
• Routine supplements with water or dextrose water will not help
prevent hyperbilirubinemia
33

34. Follow up
• All infant discharge < 48hrs after birth should be
monitor in ambulatory setting or at home
• Infants with risk factors for severe neonatal
jaundice, early follow up is a must to detect
rebound jaundice
• Infant with hemolytic diseases not requiring ET
should be closely followed up for anemia until risk
of ongoing hemolysis is minimal.
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35. REFERENCES
1. Malaysia Clinical Practice Guidelines:
Management of Neonatal Jaundice, 2nd
edition, 2014.
2. Paediatric Protocol. 3rd ed: KKM,2015
3. Tom Lissauer, Illustrated TextBook of
Paediatrics, 4th ed.2012
4. Nelson essential of pediatrics.
5. http://emedicine.medscape.com/article/9
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