Neonatal Jaundice 2023

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NEONATAL JAUNDICE

OBJECTIVES
Introduction
Causes of neonatal hyperbilirubinemia especially indirect
 Clinical Presentations
 complications
Investigations
Management of hyperbilirubinemia in neonates
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NEONATAL JAUNDICE…
Introduction
⚫ It is a yellowish discoloration of the skin and/or sclera due to elevated serum

or plasma bilirubin (hyperbilirubinemia).


⚫ In newborns jaundice appears when total bilirubin (TB) is more than 7

mg /dl and almost 97 % healthy full term babies have


biochemical hyperbilirubinemia.
⚫ It could be physiologic or pathologic
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BILIARY SYSTEM
Bilirubin--conjugation RBC-HB-
BILIVERDIN

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Urobilinogen
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Stercobilin
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Zebenay.W( MSc(PCHN), MPH(Nutrition), Assistant
Professor)
BLOOD
Stercobilin
CELLS Urobilin
excreted in feces
Hemoglobin excreted in urine

Globin
Urobilinogen
Heme
O2 formed by bacteria KIDNEY
reabsorbed
Heme oxygenase INTESTINE into blood
CO

se on
Biliverdin IX via bile duct to intestines

i da c o r
gl u
NADPH
Biliverdin Bilirubin diglucuronide
reductase (water-soluble)

NADP+ 2 UDP-glucuronic acid


Indirect (unconj.) Bilirubin
(water-insoluble) LIVER
Bilirubin via blood
(water-insoluble) to the liver

Catabolism of hemoglobin
PHYSIOLOGY OF BILIRUBIN METABOLISM
• Haemoglobin biliverdin unconjugated bilirubin
• Unconjugate bilirubin Albumin liver combines with
glucuronic acid, sulfate, others
• Transferase enzyme (UDPGT) conjugated bilirubin
• Conjugated bilirubin bacteria urobilinogen excreted via
feaces (stercoblin), kidney (urobilin)

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Physiology of bilirubin metabolism…
⚫ Hemoglobin----Biliverdin-----Bilirubin---Uptake in the liver---
Conjugation----Excretion
⚫ Unconjugated bilirubin (indirect) is toxic to the brain
⚫ Unconjugated bilirubin cross blood brain barrier
⚫ Conjugated bilirubin (direct bilirubin) is non toxic to the brain and not
cross blood brain barrier
⚫ Conjugated bilirubin is toxic to the liver
⚫ Conjugated bilirubin is polar and water soluble
⚫ Conjugated bilirubin is not neurotoxic but indicates a potentially serious
disorder
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MECHANISM OF PHYSIOLOGIC JAUNDICE
Increased rbc’s

Shortened rbc lifespan

Immature hepatic uptake


& conjugation

Increased enterohepatic
Circulation

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PHYSIOLOGICAL AND PATHOLOGICAL JAUNDICE
No Features Physiologic Pathological Jaundice
Jaundice
1 Clinical onset of jaundice (after >24 hrs <24 hrs
birth)
2 Jaundice still clinically visible Term < 8 days Term ≥8 days
(day after birth) Preterm < 14 days Preterm > 14 days
3 Peak TSB Term < 12 mg/dl Term > 12 mg/dl
Preterm < 15 mg/dl Preterm > 15 mg/dl
4 Rise in TSB < 5mg/dl/24 hrs > 5mg/dl/24 hrs
5 Conjugated serum bilirubin level <2mg/dl >2mg/dl or 15 % of
TB

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CAUSE OF PHYSIOLOGIC JAUNDICE
Increased bilirubin production
Increased fetal RBC value
Shorter life span of RBC(70-90days)
Increased enterohepatic circulation
Increased beta glucoronidase activity
Decreased hepatic uptake, conjugation and excretion
Y protein (ligandin) is diminished
UDP-Glucuronyl transferase enzyme activity is decreased
CAUSES OF PATHOLOGIC BILIRUBIN
I. Increased bilirubine production

 Hemolytic anemia
 Hematoma
 Polycythemia
 Gut obstructions, pylor stenosis, ileus
 Infections
CAUSES OF PATHOLOGIC BILIRUBIN…
II. Hereditary disorders of bilirubin metabolism
 Crigler-Najjar syndrome (absence of UGT activity)
 Gilbert’s syndrome
III. Acquired unconjugated hyperbilirubinemia
 Breast feeding
 Brest milk
 Hypothyroidism
 Lucey-Driscoll syndrome
CLINICAL MANIFESTATIONS

◘ Yellowish discoloration of sclera, skin, mucus membranes

◘ A newborn may present with signs of biluribin encephalopathy.

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NEONATOLOGY) April 6, 2024

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RISK FACTORS FOR BILIRUBIN ENCEPHALOPATHY
◘ Prematurity
◘ Metabolic acidosis,
◘ Hypoglycemia,
◘ Sepsis,
◘ Temperature instability,
◘ Significant lethargy
◘ Low serum albumin

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INVESTIGATIONS
.
 Total bilirubin  Reticulocyte production

 Direct and indirect bilirubin index(RPI)


 Maternal and neontal blood  Serum albumin level
 albumin to bilirubin ratio
group and RH
 Direct/indirect Coombs test  Liver function test (LFT)

 Hemoglobin (Hgb) or  Septic work up.

hematocrit (HCT)  Abdominal ultrasound with


 Peripheral RBC morphology indication
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Treatment modalities
Phototherapy
◘ Bilirubin absorbs light in blue range wave length (425-475
nm) MOA
 Structural-isomerization (Cyclization)-to Limirubin.
Most important method due to fast reaction and irreversibility
 Photo-isomerization from 4z, 15z to (4z, 15e) but it is
reversible back to it’s original isoform
 Photo oxidation- Least important form as it is a slow process

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PHOTOTHERAPY…

 Bilirubin absorbs light maximally in the blue range.

 Bilirubin in the skin absorbs light energy, which by photo-isomerization

converts the toxic native unconjugated 4Z,15Z-bilirubin into the


unconjugated configurational isomer 4Z,15E- bilirubin.
 4Z,15Z-bilirubin phototherapy 4Z,15E bilirubin

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PHOTOTHERAPY …
 The latter is the product of a reversible reaction and is excreted in bile

without any need for conjugation.


 Phototherapy also converts native bilirubin, by an irreversible reaction, to the

structural isomer lumirubin, which is excreted by the kidneys in the


unconjugated state.
 Phototherapy is indicated only after the presence of pathologic
hyperbilirubinemia has been established.
 The basic cause or causes of the jaundice should be treated concomitantly.
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RADIANT PHOTOTHERAPY

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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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EXCHANGE TRANSFUSION
 The most important and effective method
 Umbilical vein catheterization
 Double volume blood exchange (2x80ml/kg)
 The procedure washes 87% of the total blood
 Reduces jaundice by 40-60% of pre-exchange level
 It removes bilirubin, hemolyzed blood, Igs and bacteria

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DOUBLE VOLUME EXCHANGE TRANSFUSION
 The amount of blood volume to be exchanged is equivalent to
2x the blood volume of the baby (85ml/kg )
 Use fresh blood less than 7 days old
 Do procedure after umbilical catheterization using aseptic
technique
 Heparinize the catheter
 The amount of blood to be removed at a time is 5ml to 20
ml
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TYPE OF BLOOD TO BE TRANSFUSED
 Rh hemolytic disease

⚫ give blood group compatible to the baby and RH of the mother.

 ABO hemolytic disease

⚫ give blood group of the mother and Rh compatible to the newborn

 O negative blood is the most preferred type of blood for

exchange transfusion.

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MONITORING

 Strictly monitor the vital signs during the procedure.

 Determine post transfusion HCT 4-6 hours after the procedure.

 Determine bilirubin 4 hourly after the procedure.

 Monitor RBS every 30-60 minutes during the procedure and 2-4 hourly for

the first 24 hours after procedure.

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MONITORING

◘ Calcium gluconate slowly via a peripheral vein under strict

cardiac monitoring after every 100ml of blood is


exchanged.
◘ Cloxacillin 50mg/Kg bid for 2- 3 days and gentamicin

5mg/kg BID for 2-3 days.


◘ Keep baby NPO for 3 hours before and after procedure
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OTHER TREATMENT MODALITIES

◘ Phenobarbital 5 mg/kg to stimulate liver enzyme in Crigler –

Najjar syndrome.
◘ High dose of IV immunoglobulin.

◘ In case of breast milk jaundice discontinuation of breast milk for

48 hrs

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COMPLICATIONS OF HYPERBILIRUBINAMIA
1. Acute bilirubin encephalopathy has three phases
◘ Phase -I
⚫1st – 2 Days of Age
⚫Poor motor reflex, high pitched cry, Decreased tone, lethargy, poor feeding
◘ Phase-II
⚫ middle of 1st week
⚫Hypertonia, seizure and depressed sensorium, fever, opisthotonos
posturing, paralysis of upward gazing.
◘ Phase -III
⚫after 1week of age Hypertonia decreases, hearing and visual
abnormality, poor feeding.,
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COMPLICATIONS
2. Chronic bilirubin encephalopathy (Kernicterus)

◘ Choreoathetoid cerebral palsy

◘ Upward gaze palsy

◘ Sensorineural hearing loss

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REFERENCE

• Nelson Text book 19 edition


• Manual of neonatal care 6th edition
• Fanaroff and marthin’s neonatal and perinatal medicine 8th ed
THANK YOU!

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