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Neonatal Jaundice 2023
Neonatal Jaundice 2023
Neonatal Jaundice 2023
OBJECTIVES
Introduction
Causes of neonatal hyperbilirubinemia especially indirect
Clinical Presentations
complications
Investigations
Management of hyperbilirubinemia in neonates
GIZAW T.(MSC IN MATERNITY AND NEONATOLOGY) April 6, 2024 1
NEONATAL JAUNDICE…
Introduction
⚫ It is a yellowish discoloration of the skin and/or sclera due to elevated serum
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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)
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
Increased enterohepatic
Circulation
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
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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
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PHOTOTHERAPY…
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PHOTOTHERAPY …
The latter is the product of a reversible reaction and is excreted in bile
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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
exchange transfusion.
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MONITORING
Monitor RBS every 30-60 minutes during the procedure and 2-4 hourly for
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MONITORING
Najjar syndrome.
◘ High dose of IV immunoglobulin.
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)
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REFERENCE