neontal joudice is is a yellowish discoloration of the skin, sclerae, mucous membranes and nails. Hyperbilirubinemia is a common and, in most cases, benign problem in neonates.

1. Neonatal jaundice
Learning objectives
At the end of the training, the students will be able to:
 Define jaundice
 Differentiate between physiologic and pathologic
jaundice
 Identify the causes of jaundice
 Describe the complications of neonatal jaundice.
 Recall investigation and management of jaundice
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2. Introduction
Bilirubin is Yellow pigment, Anti-oxidative agent :to
avoid oxygen toxicity in the days after birth.
Bilirubin can be
1. Unconjugated bilirubin = Indirect bilirubin.
2. Conjugated bilirubin = Direct bilirubin.
Normal value of Bilirubin :–
Total Bilirubin <1.5mg/dl,
direct Bilirubin 0.2-0.4 mg/dl and
indirect Bilirubin 0.4-0.8mg/dl.
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3. Mechanism of Biluribin
Located in
spleen ,liver
,all nucleated
cells
CO
 Hepaticuptake=>
 Conjugation Bilirubin +
glucuronic acid=bilirubin di
and monoglucuronides=>
 Biliary excretion-intestine
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conserved
Exhaled
Current pediatrics diagnosis & treatment 18th edition).3

4. Mechanism of Biluribin
 Sources of bilirubin in the body: Heme -containing
proteins (cytochromes and catalase) and hemoglobin
 Hepatic uptake – Circulating bilirubin, which is bound
to albumin, is transported to the liver. Bilirubin
dissociates from albumin and is taken up by hepatocytes,
where it is processed for excretion.
 Conjugation –In hepatocytes, uridine
diphosphogluconurate glucuronosyltransferase (UGT)
catalyzes the conjugation of bilirubin with glucuronic
acid, producing bilirubin diglucuronides and, to a lesser
degree, bilirubin monoglucuronides.
 Conjugated bilirubin, which is more water-soluble
than unconjugated bilirubin, is excreted in bile
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5. Mechanism of Biluribin…
 In the presence of normal gut flora, the conjugated
bilirubin is metabolized further to stercobilins and
excreted in the stool.
 At birth ,many flora absent, very little conjugated
bilirubin is reduced to urobilin.
 Infants have beta-glucuronidase in the intestinal
mucosa, which deconjugates the conjugated
bilirubin. =>
 Unconjugated bilirubin can be reabsorbed and recycled
into the circulation, a process known as the
"enterohepatic circulation of bilirubin“=> Jaundice.
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6. Neonatal jaundice
 Definition: Hyperbilirubinemia refers to an excessive
level of accumulated bilirubin in the blood and is
characterized by jaundice.
 Jaundice is a yellowish discoloration of the skin,
sclerae, mucous membranes and nails.
 Hyperbilirubinemia is a common and, in most cases,
benign problem in neonates.
 However, untreated severe indirect hyperbilirubinemia
is potentially neurotoxic, and
 conjugated-direct hyperbilirubinemia often signifies a
serious hepatic or systemic illness.
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7. CONJUGATED
HYPERBILIRUBINEMIA
Neonatal jaundice associated with a rise in
conjugated bilirubin
It is indicative of a defect or insufficiency
in bile secretion,
 biliary flow, or both and
is always pathologic.
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8. Neonatal jaundice
 In newborns, jaundice appears when total bilirubin (TB)
is more than 7 mg /dl and almost 97 % healthy full term
babies have biochemical hyperbilirubinemia.
Neonatal jaundice can be classified as
 physiologic or
 pathologic
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10. 1. Physiologic Jaundice (Icterus Neonatorum)
 Under normal circumstances, the level of indirect-reacting
bilirubin in umbilical cord serum is 1–3 mg/dL and
 rises at a rate of less than 5 mg/dL/24 hr; thus,
 jaundice becomes visible on the 2nd–3rd day,
 usually peaking between the 2nd and 4th days at 5–6 mg/dL and
decreasing to below 2 mg/dL between the 5th and 7th days of life.
 Jaundice associated with these changes is designated
“physiologic” and is believed to be the result of increased
bilirubin production after the breakdown of fetal red blood cells
combined with transient limitation in the conjugation of bilirubin
by the liver.
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11. 2. Pathological Jaundice…
Usually appears within 24hrs of birth and
characterized by a rapid rise in serum bilirubin
and prolonged jaundice
Features of pathological jaundice
Clinical jaundice appears within 24hrs of life
Increase in bilirubin >5mg/dl per day
Total bilirubin >12mg/dl
Persistence of clinical jaundice for 7-10 days
in term and 2wks in preterm infants
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12. Jaundice Associated with Breast-Feeding
There are two types of jaundice in breastfed babies:
1. breastfeeding jaundice; and
 It is the result of the baby not receiving enough milk to
lower their bilirubin levels.
 usually occurs in the first week of life
 This causes the bilirubin to be reabsorbed into the
intestines and keep the levels elevated which triggers
jaundice.
 A baby's meconium (early bowel movements) are also
essential to helping remove bilirubin, and inadequate
milk supply delays the passage of meconium.
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13. Jaundice Associated with Breast-Feeding
2. Breast Milk Jaundice
Occurs in about 2% of breast fed term infants
 Usually after the 7th day of life.
Maximum concentration can reach as high as 10
to 30 mg/dl during the 2nd to 3rd week of life.
Gradually decreases even if the baby is
continued on breast feeding may persist for 3
to10 weeks at lower levels
 It drops fast if breast feeding is stopped for a
short period of time
Cause is not known but may be due to the
presence of glucornidase in breast milk.
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14. Features differentiating Physiological
jaundice from Pathological Jaundice
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15. Causes of Jaundice:
 Isoimmunization: RH incompatibility, ABO incompatibility,
Other blood group incompatibility
 Infection: Bacterial, viral, protozoal
 Sequestered blood: Subgaleal hemorrhage, cephalhematoma,
ecchymosis, hemangioma
 Erythrocyte biochemical defect: G6PD deficiency, Hexokinase
deficiency
 Structural abnormalities of erythrocytes: Hereditary
spherocytosis, elliptocytosis
 Disorder of hepatic uptake: Gilbert syndrome
 Disorder of conjugation: Crigler-Najjar syndrome (absence of
UGT activity)
 Hypothyroidism: Disorder of enterohepatic circulation
(associated with breast feeding practice)
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16. Clinical manifestations
 A newborn presents with yellowish discoloration of
sclera, skin, mucus membranes
 Depending on severity and time of presentation a
newborn may present with signs of bilirubin
encephalopathy
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17. Complications of hyperbilirubinemia
1. Acute bilirubin encephalopathy is an early bilirubin
toxicity, which is transient and reversible. If it is not
recognized or untreated, it may progress to permanent
neurologic impairment-Kernicterus.
Acute bilirubin encephalopathy has three phases
 Phase -1 ( 1st – 2 Days Of Age): Poor motor reflex,
high pitched cry, Decreased tone, lethargy, poor feeding
 Phase- 2 (middle of 1st week age): Hypertonia, seizure
and depressed sensorium, fever, opisthotonos posturing,
paralysis of upward gazing.
 Phase -3 (after 1week of age): Hypertonia decreases,
Hearing and visual abnormality, poor feeding, Athetosis
and seizure may also occur
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18. Kernicterus
 Kernicterus, or bilirubin encephalopathy, is a
neurologic syndrome resulting from the deposition of
un conjugated bilirubin in the basal ganglia and
brainstem nuclei
 Kern icterus =bilirubin in kern-the nuclear component
of brain .
 The pathogenesis of kernicterus is multi factorial
 The precise blood level above which indirect-reacting
bilirubin or free bilirubin will be toxic for an individual
infant is unpredictable(variable)
 In previously healthy, predominantly breast-fed term
infants, kernicterus has developed when bilirubin levels
exceed 20- 30 mg/dL.
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19. KERNICTERUS
 Because unconjugated bilirubin are lipid soluble and
toxic,it can crosses the blood-brain barrier and it will
penetrates neuronal and glial membrane thus cause
neurotoxicity.
 Patients surviving kernicterus have severe permanent
neurologic symptoms such as
 Choreoathetos
 Spasticity
 Muscular rigidity
 Ataxia
 Deafness(Sensorineural hearing loss
 Upward gaze palsy
 Mental retardation 29
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20. Risk factors aggravate bilirubin
encephalopathy
 Prematurity
 Metabolic acidosis,
 Hypoglycaemia,
 Sepsis,
 Temperature instability,
 Significant lethargy
 Low serum albumin
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21. Potentially preventable causes of kernicterus
 Early discharge (<48 hr) with no early follow-up)
 Failure to check the bilirubin level
 Failure to recognize the presence of risk factors for
hyper bilirubinemia
 Underestimating the severity of jaundice by clinical
(i.e., visual) assessment.
 Lack of concern regarding the presence of jaundice
 Delay in measuring the serum bilirubin level despite
marked jaundice or delay in initiating phototherapy in
the presence of elevated bilirubin levels and
 Failure to respond to parental concern regarding
jaundice, poor feeding, or lethargy
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22. Investigations
 Total bilirubin
 Direct and indirect bilirubin
 Maternal blood group and RH type
 Neonatal blood group and RH type
 Direct/indirect Coombs test
 Haemoglobin (Hgb) or haematocrit (HCT)
 Peripheral RBC morphology
 Reticulocyte production index(RPI)
 Serum albumin level and albumin to bilirubin ratio
 Liver function test (LFT)
 Septic work up.
 Abdominal ultrasound with indication.
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23. Therapeutic Management
 Purposes: reduce level of serum bilirubin and
prevent bilirubin toxicity
 Prevention of hyperbilirubinemia: early feeds,
adequate hydration
 Reduction of bilirubin levels: phototherapy, exchange
transfusion,
 Drugs Use of Phenobarbital promote liver enzymes
and protein synthesis.
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24. Management of Unconjugated Hyperbilirubinemia:
The main goal of treatment is to avoid acute and
chronic bilirubin encephalopathy.
Principles of mx are
 Avoid any drug that interfere bilirubin metabolism ex-
anti convulsant
 Correct any thing making CNS susceptible (hypoxia,
hypoglycemia, acidosis)
 Give adequate feeding
 Lower serum bilirubin by:
1. Phototherapy
2. Exchange transfusion
3. Other medical managements
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25. Management of Unconjugated Hyperbilirubinemia:
1. Phototherapy
 It is the mainstay of treatment
 It is indicated for excessive unconjugated
hyperbilirubinemia
 It acts by photoisomerization, structural isomerization,
and photooxidation.
 It is not a substitute for exchange transfusion if
exchange transfusion indicated.
 Intensive phototherapy is preferred if available.
 Infant should get adequate feeding.
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26. Indications for phototherapy
Phototherapy is started quickly, at lower bilirubin
levels in infants:
Who are smaller or preterm
Who are sick particularly with hemolysis
In whom jaundice appears within 12-24hrs
Bilirubin levels indicating phototherapy are:
 17-22mg/dl for term infants who become jaundiced
after 48hrs
 8-10mg/dl for preterm infants >1500gm
 5-8mg/dl for preterm infants <1500gm
 Declining serum bilirubin levels below 13mg/dl are
generally accepted as necessary for stopping
phototherapy.
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27. Bhutani curve: phototherapy indication in hospitalized infants of 35 or
more weeks’ gestation
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28. Precaution/care for the new born during
phototherapy
 Cover the baby’s eye and put diaper with maximum
body surface area being exposed.
 The distance b/n the light source & the baby should be <
40 cm.
 The position should be changed every 2hrs from supine
to prone.
 Measure weight daily and increase fluid intake by 25 %
 Give a bolus of fluid with N/S 20ml/kg if bilirubin
remains high
 Discontinue phototherapy and remove eye patches at
least once per 8 hour shift or at the time of feeding
 Monitor fluid and electrolyte status
 Monitor temperature
 Determine TSB 6 hourly
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29. Babies under phototherapy
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30. Side effects of phototherapy
 Insensible water loss
 Watery and frequent stool
 Retinal damage
 Erythema and increased blood flow
 Bronze baby syndrome (with increased CB)
 Low calcium level (in preterm)
 Interferes with maternal infant bonding
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31. 2. Double Volume Exchange Transfusion
 Most effective and reliable method of reducing bilirubin
level there by reduce the risk of brain damage and
kernicterus
 Can also help treat sever anemia
 The amount of blood volume to be exchanged is
equivalent to 2x the blood volume of the baby (85ml/kg )
 One double volume exchange transfusion lowers serum
bilirubin to half pre exchange value.
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32. Double Volume Exchange Transfusion
Objective of ET
To prevent a rise in bilirubin to toxic level when
phototherapy fails
To correct anemia and improve heart failure in
hydropic infants with haemolytic disease.
To stop hemolysis and bilirubin production by
removing antibody and
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33. Double Volume Exchange transfusion
 Blood for ET should be as fresh as possible(< 7 days)
 Blood should be gradually warmed and maintained at a
temperature between 35 and 37°C throughout ET
 Type of blood used .
 If there is Rh haemolytic disease – give blood group
compatible to the baby and RH to the mother.
Note: - O negative blood is the most preferable
type for exchange transfusion
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34. Bhutani curve: Exchange transfusion in infants of 35 or more weeks’ gestation
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35. Indications
 Hydrops fetalis
• Cord Hgb < 11gm/dl and Cord TSB >5 mg/dl
• Hgb level 11 - 13 g/dL, and Rate of rise of TSB >
0.5mg/dl/hr despite phototherapy .
 Rate of rise of TSB > 5mg /24hrs despite phototherapy.
 The bilirubin level is rising 1 mg/dL/hour despite
phototherapy.
 Any TSB > 12 mg in the 1st 24 hrs
 Any TSB >20 mg In the neonatal period or it appears
that it will reach 20 mg/dL at the rate it is rising
Repeat exchanges are done for the same indications as
the initial exchange.
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36. Preparation of infant
 Ensure pulse, temperature and respiration are
stabilized and maintained.
 Continue feeding the child and omit only the LAST
feed before exchange transfusion.
 The infant’s stomach should be emptied before
transfusion to prevent aspiration,
 If needed, empty gastric content by doing NG
aspiration before exchange transfusion.
 Check resuscitation equipment.
 Set a peripheral IV line.
 Get a signed informed consent from parent (mortality
from ET is 1%).
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37. The procedure of Double Volume ET
 Do procedure after umbilical catheterization using aseptic
technique .
 Heparinize the catheter (instill heparin to the tube) before
starting the procedure.
 Strictly monitor the vital signs during the procedure.
 Monitor RBS every 30-60 minutes during the procedure
and 2-4 hourly for the first 24 hours after procedure.
 Administer 1ml/kg of Calcium gluconate slowly via a
peripheral vein under strict cardiac monitoring after
100ml of blood is exchanged.
 Administer prophylactic dose of Cloxacillin 50mg/Kg bid
for 2- 3 days and gentamicin 5mg/kg BID for 2-3 days.
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38. procedure….
The exchange
• Should be carried out over a 45-60 min period,
• Usually volume taken out and given will be to 20 ml at a time
but 5-10 mL may be indicated for sick and premature infants.
• Exchange should start with removal of blood
• The patient’s blood is slowly drawn out & an equal amount of
fresh, prewarmed blood, plasma or physiologic saline is
transfused.
• The cycle is repeated until a predetermined volume of blood has
been replaced
• The goal should be an iso volumetric
• If child anemic (Hb < 15) give an extra volume of blood at the
end, leaving a positive balance).
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40. Post exchange
 Give vitamin K 1mg
 Repeat all medications which the baby was receiving
 Monitor V/S ½ hrly for the first two hrs
 Watch for bleeding from umblical stump
 Continue photo therapy
 Check for blood sugar, TSB And HCT 2-4 hourly for
the first 24 hours after procedure
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41. Complications of ET
1. Catheter related
• Infection
• Hemorrhage
• Portal and splenic vein thrombosis
• Air embolism
2. Hemodynamic problems
• Overload cardiac failure
• Hypo volaemic shock
• Arrhythmia (Catheter tip near sinus node in Rt.
Atria)
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42. Complications of ET
Electrolyte imbalance
• Hyperkalemia (old blood)
• Hypocalcaemia
• Increase or decrease Blood glucose
• Acidosis (sometimes late alkalosis due to breakdown of
citrate)
• Tissue hypoxia (old blood )
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43. Follow-up
• Serial follow up of Serum bilirubin level till
discharge and then 2 days after discharge
• For infant who had exchange transfusion, follow-
up for 2 years
• Assess every time for the late complications
• Signs of deafness
• Cerebral palsy and
• Mental retardation
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44. 3. Other treatment modalities
 High dose of IV immunoglobulin.
 In case of Breast milk jaundice, discontinuation of
breast milk for 1-3days usually causes a prompt
decline but still controversial.
 where as in breast-feeding (breast-feeding failure)
jaundice increase the amount of feeding.
 Administration of medication based on the cause.
e.g Phenobarbital 5 mg/kg to stimulate liver enzyme
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45. • Thank you
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