NEONATAL JAUNDICE

1. Neonatal Jaundice

2. All babies have a transient rise in serum
bilirubin but only about 75% are visibly
jaundiced.
Jaundice is clinically detectable when the
serum bilirubin levels are >85 μmol/L
(5 mg/dl).
It refers to yellow discolouration of the skin
and sclera caused by the accumulation of
bilirubin in the skin & mucous membrane.

4. Physiological Jaundice In Babies
Due to
excessive
bilirubin
production
(higher
haemoglobin
content
Shorter red
blood cell life
span in
newborn
babies)
Poor bilirubin
clearance
(liver
immaturity)
Usually
appears two
to four days
after birth,
resolving
after one to
two weeks
(three weeks
if preterm)
Not
associated
with
underlying
disease and is
usually benign

5. Physiological Jaundice
Total serum bilirubin
(TSB) level usually
rises in full-term
infants to a peak of 6
to 8 mg/dL by 3 days
of age and then falls.
A rise to 12mg/dL is
in the physiologic
range.
In premature infants,
the peak may be 10
to 12 mg/dL on the
fifth day of life,
possibly rising over 15
mg/dL without any
specific abnormality
of bilirubin
metabolism.
Levels under 2mg/dL
may not be seen until
one month of age in
both full term and
premature infants.
The baby has an
immature liver,
bilirubin is processed
slower. The jaundice
first appears at 2 to 3
days of age. It usually
disappears by 1 to 2
weeks of age and the
levels of bilirubin are
harmless.

6. Advise for physiological jaundice:
 The parents should be explained about the benign nature of jaundice.
 The mother should be encouraged to breast-feed frequently. The newborn
should be exclusively breast-fed with no top feeds, water or dextrose
water.
 Mother should be told to bring the baby to the hospital if the baby looks
too yellow or yellow discoloration of the skin beyond the legs .
 Any newborn discharged prior to 72 hours of life should be evaluated
again in the next 48 hours for adequacy of breast-feeding and
progression of jaundice.
 Clinical judgment should be used in determining follow-up. Earlier or more
frequent
 follow-up should be provided for those who have risk factors for
hyperbilirubinemia

7. Risks of Severe NNJ
Prematurity Low birth weight
Jaundice in the
first 24 hours of
life
Mother with blood
group O or rhesus
negative
G6PD deficiency
Rapid rise of total
serum
bilirubin6mg/dL/day
(130 μmol/day )
Sepsis
Lactation failure
in exclusive
breastfeeding
cephalhaematoma or
bruises
Babies of diabetic
mothers
Family history of
severe NNJ in
siblings

8. Approach to an infant with jaundice
• Age of onset.
• Previous infants with NNJ, kernicterus, neonatal
death, G6PD deficiency.
• Mother’s blood group (from antenatal history).
• Gestation
• Presence of abnormal symptoms such as apnoea,
difficulty in feeding, feed
• Intolerance and temperature instability.
History
• General condition, gestation and weight, signs of
sepsis, hydration status.
• Signs of kernicterus: lethargy, hypotonia, seizure,
opisthotonus, high pitch cry.
• Pallor, plethora, cephalhaematoma, subaponeurotic
haemorrhage.
Signs of intrauterine infection e.g. petechiae,
hepatosplenomegaly.
Cephalo-caudal progression of severity of jaundice.
Physical
examination

9. METHODS OF DETECTING JAUNDICE AND
ASSESSING ITS SEVERITY
1. Total Serum Bilirubin
 TSB measurement is the gold standard for detecting and determining the level of hyperbilirubinaemia.
2. Transcutaneous bilirubinometer (TcB)
 The transcutaneous bilirubinometer is a hand-held device that measures the amount of bilirubin in the
skin.
 showed a significant correlation (r ranging from 0.75 to 0.95) between bilirubin measurements taken by
TcBs (BiliCheck and JM 103), with TSB measurements, in both term and preterm babies.
3. Visual assessment
 assessment of the extent and severity of yellow discolouration of the skin. It is performed by blanching
the skin with slight finger pressure and noting the underlying colour of the skin.
 Jaundice is usually visible when bilirubin levels are about 5 - 7 mg/dL (86 - 120 μmol/L) and progresses
from head to toe as the level of bilirubin rises.
 Kramer’s rule describes the relationship between serum bilirubin levels and the progression of skin
discolouration

16. Total Serum Bilirubin levels mg/dL (μmol/L)
Low risk
≥38wkandwell
Medium risk
≥ 38 wk + risk factors or 35 to <38 wk and
well
High risk
35to<38wk + risk factors
Intensive
phototherapy
ET
Intensive
phototherapy
ET
Intensive
phototherapy
ET
<24*
24 12 (200) 19 (325) 10 (170) 17 (290) 8 (135) 15 (255)
48 15 (255) 22 (375) 13 (220) 19 (325) 11 (185) 17 (290)
72 18 (305) 24 (410) 15 (255) 21 (360) 13 (220) 18.5 (315)
96 20 (340) 25 (425) 17 (290) 22.5 (380) 14 (240) 19 (325)
>96 21 (360) 25 (425) 18 (305) 22.5 (380) 15 (255) 19 (325)
Note:
• Start conventional phototherapy at TSB 3 mg/dL (50 μmol/L) below the
levels for intensive phototherapy.
• Risk factors – isoimmune hemolytic disease; G6PD deficiency, hypoxic-
ischemic encephalopathy, significant lethargy, temperature instability, sepsis, acidosis or albumin < 3.0 g/dL
* Infants jaundiced at < 24 hours of life are not considered healthy and require further evaluation.

17. Management
 Phototherapy is the mainstay treatment in NNJ.
 Phototherapy works by changing bilirubin into a compound
that can be broken down and excreted by the body via the
urine and feces.
 Certain wavelengths of light can change bilirubin into two
other compounds, called lumirubin and photobilirubin.
 These light wavelengths can be produced by fluorescent
lights.
 When they penetrate the skin, they convert the bilirubin
into its isomers, which can be removed from the body
without the involvement of the liver.

18. Phototheraphy
 Type of phototherapy
 LED phototherapy
 In two meta-analyses, phototherapy based
on LED and non-LED
 light sources showed similar clinical
efficacy as measured by duration of
phototherapy and rate of decline of TSB in
term and late preterm babies.
 In preterm babies, the use of LED has a
similar rate of decline but significantly
shorter duration of phototherapy
compared with a non- LED light

19.  Fibreoptic phototherapy
 Fibreoptic phototherapy units
are less commonly used
compared with
conventional/LED
phototherapy.
 Common fibreoptic
phototherapy units used in
studies Include Biliblanket and
Wallaby II.

20. Complication
Acute Bilirubin Encephalopathy (ABE)
 ABE results in changes of mental (behavioural) status
and muscle tone
 during the neonatal period when the baby is having
hyperbilirubinaemia.
 These include drowsiness, poor feeding and hypotonia
followed by hypertonia affecting extensor muscles in
particular, resulting in retrocollis and opisthotonos.

21. Classic Kernicterus
May be seen in babies who survive from ABE
• The manifestations of ABE include:
➢ dystonia
➢ athetoid cerebral palsy
➢ paralysis of upward gaze
➢ sensorineural hearing loss
• Post-mortem icteric (yellow) staining of the
basal ganglia, specifically the globus pallidus is
the hallmark of this condition

23. Bilirubin-Induced Neurologic Dysfunction
(BIND)
BIND is a wider spectrum of disorders that not only includes
classic kernicterus and ABE, but also less severe forms of
neuropathy, including
➢ auditory neuropathy
➢ fine and gross motor incoordination
➢ gait abnormalities
➢ fine tremors
➢ exaggerated extrapyramidal reflexes and behavioural
problems

25.  Babies with acute bilirubin encephalopathy should have
long-term follow-up to monitor for neurodevelopmental
sequelae.
 Term and late preterm babies with TSB > 20mg/dL (342
μmol/L)or exchange transfusions should have Auditory
Brainstem Response (ABR􏰈 testing done within the first
three months of life. If the ABR is abnormal,
neurodevelopmental follow-up should be continued.
 Healthy term and late preterm babies with non-
haemolytic hyperbilirubinaemia and TSB <25mg/dL (428
μmol/L) may be followed-up at the primary care level.
 Preterm babies with jaundice should be followed-up for
neurodevelopmental sequelae as per follow-up plans for
all preterm babies.

26. Exchange transfusion (ET) is indicated for
severe hyperbilirubinaemia.
 Introduction
 Indicated when the TSB is above the recommended levels
 There are various methods used in performing ET. These include femoral vein (FV),
umbilical vein (UV), umbilical artery/vein (UA/V) and peripheral artery (radial
artery)/peripheral vein.
 Indications
 Double volume exchange
• Blood exchange transfusion to lower serum bilirubin level and reduce the
risk of brain damage associated with kernicterus.
• Hyperammonimia
• To remove bacterial toxins in septicaemia.
• To correct life-threatening electrolyte and fluid disorders in acute renal
failure.
 Partial exchange transfusion
• To correct polycythaemia with hyperviscosity.
• To correct severe anaemia without hypovolaemia.

27.  Type of Blood to be used
 • Rh isoimmunisation: ABO compatible, Rh negative blood.
• Other conditions: Cross-match with baby and mother’s blood.
• In Emergencies if Blood type unkown (rarely): ‘O’ Rh negative blood.
 Post ET Management
 Maintain intensive phototherapy. • Monitor vital signs:
 Hourly for 4 - 6 hours, and 4 hourly subsequently.
Monitor capillary blood sugar: Hourly for 2 hours following ET.
 Check serum Bilirubin: 4 - 6 hours after ET.
 Follow-up
 Long term follow-up to monitor hearing and neurodevelopmental
assessment.

28. Prolonged
Jaundice
Visible jaundice (or
serum bilirubin SB
>85 μmol/L) that
persists beyond 14
days of life in a
term infant or 21
days in a preterm
infant
Unconjugated
hyperbilirubinaemia
Admit if infant is unwell. Otherwise follow-up until jaundice resolves.
Important investigations: Thyroid function, urine FEME and C&S,
urine for reducing sugar, FBC, reticulocyte count, peripheral
blood film, G6PD screening.
• Exclude urinary tract infection and hypothyroidism.
• Congenital hypothyroidism is a Neonatal Emergency. (Check
Screening TSH result if done at birth). •
• Breast milk Jaundice is a diagnosis of exclusion. Infant must be
well, gaining weight appropriately, breast-feeds well and stool is
yellow.
Conjugated
Hyperbilirubinaemia
Pale stools/ dark urine, raised conjugated bilirubin (>15% total or
>15umol/l)Causes include :
Congenital obstruction and malformation of the biliary system
(e.g biliary atresia, choledochal cyst and bile duct stenosis)
Idiopathic neonatal hepatitis
Infection (e.g Hepatitis B, TORCH)
Metabolic disorders (e.g galactosemia, Alpha-1 antitrypsin
deficiency, gylcogen storage disease)

30. Thank You

31.  ALGORITHM ON MANAGEMENT OF NEONATAL JAUNDICE *If jaundice persists
beyond 14 days in term babies and 21 days in preterm babies, further
evaluation for prolonged jaundice is needed. G6PD Deficiency Jaundice Yes No
Admit and observe Phototherapy ± ET Jaundice resolved Monitor as scheduled
Discharge and follow-up Assess risk factors Need admission Monitor as
scheduled* Need treatment Jaundice resolved Yes N

32.  ALGORITHM ON MANAGEMENT OF NEONATAL JAUNDICE *If jaundice persists
beyond 14 days in term babies and 21 days in preterm babies, further
evaluation for prolonged jaundice is needed. G6PD Deficiency Jaundice Yes No
Admit and observe Phototherapy ± ET Jaundice resolved Monitor as scheduled
Discharge and follow-up Assess risk factors Need admission Monitor as
scheduled* Need treatment Jaundice resolved Yes N