This document discusses neonatal jaundice, including its definition, etiology, bilirubin production and metabolism, types of hyperbilirubinemia, causes, clinical features, kernicterus, and treatment options. Neonatal jaundice is caused by increased bilirubin levels and results in a yellowish skin and eye discoloration. Bilirubin is produced from the breakdown of hemoglobin. Treatment depends on the type and severity of hyperbilirubinemia, and may include phototherapy, exchange blood transfusions, or medications to increase bilirubin clearance from the liver.

1. DR JALO I
NEONATAL JAUNDICE

2. DEFINITION
 Yellowish discoloration of the sclera of the eyes
and mucous membranes
 It is due to increased levels of serum bilirubin
 Bilirubin is derived mainly from breakdown of
haemoglobin

3. ETIOLOGY
 Increase load of bilirubin to be metabolized
 Damage or reduction in the activity of transferase
enzyme
 Competition for or blockage of the transferase
enzyme
 Reduction of bilirubin uptake by the liver
 Insufficient bilirubin excretion
 Increased enterohepatic circulation

4. BILIRUBIN PRODUCTION
 Bilirubin is the end product of catabolism of
heam, derived principally from circulating
haemoglobin
 1gm of haemoglobin gives 35g of bilirubin
 About 75% of bilirubin is derived from catabolism
of haemoglobin
 About 25% of bilirubin is derived from tissue
haemoproteins . (Cytochromes catalases)

5. CONVERSION OF HAEM TO
BILIRUBIN

6. BILIRUBIN METABOLISM
HEAM......haem oxygenase...........BILIVERDIN
BILIVERDIN....biliver reductase.......BILIRUBIN
BILIRUBIN......ligadin (Y)..........SERUM.......LIVER
UNCONJ.......glu transferase.....CONJ BILIRUBIN

7. UNCONJUGATED
HYPERBILIRUBINEMIA
(HEAMOLYSIS)
 Blood group incompatibilities( ABO, Rhesus)
 Deficiency of red cell enzymes (G6PD, Hexokinase,
pyruvate kinase)
 Congenital red cell membrane defects
(eliptocytosis,spherocytosis)
 Infections – Neonatal septicaemia
 Haemolytic agents (Naphthalene, Menepthone)
 Extravasated blood (cephalhaematoma , IVH)

8. UNCONJUGATED
HYPERBILIRUBINEMIA
(DEFECTIVE CONJUGATION)
 Crigler Najjar syndrome
 Breast milk jaundice
 Familial neonatal hyperbilirubinemia
 Hypothyroidism

9. UNCONJUGATED
HYPERBILIRUBINEMIA- OTHERS
 Down’s syndrome
 Infants of diabetic mothers
 prematurity

10. CAUSES OF CONJUGATED
HYPERBILIRUBINEMIA
 INFECTION
 Toxoplasmosis, CMV, Hepatitis B, Rubella
 Giant cell hepatitis
 BIOCHEMICAL/METABOLIC
 Galactosemia, alfa-1-antitripsin deficiency, Roto’s & Dubin
Johnson syndrome
 Hypothyroidism, tyrosinosis
 CONGENITAL OBLITERATION
 Congenital biliary atresia, Choledochal cyst, Bile duct stenosis
 Inspissated bile duct syndrome
 OTHERS
 Hypoxia, shock and TPN

11. PHYSIOLOGIC JAUNDICE
 This usually appears 2-3rd day of life
 Peaks to 5-6mg/dl on 4th day
 Bilirubin levels not more than 12mg/dl
 Returns to below 2mg/dl on the 7- 10th day
 It is a diagnosis of exclusion

12. BREAST FEEDING
JAUNDICE
Early unconjugated hyperbilirubinemia.
• Believed to be due to decreased PO
• Onset 2-4 days; peaks at 3-6 days (>12.0)
• Returns to < 3.0 at greater than 3 weeks
• Prevalence is ~ 12% in BF infants

13. BREAST FEEDING
JANDICE (CONT)
• Is it good for infants?? Bilirubin
is antioxidant.
• No evidence of increased BR
production in BF infants
• BF infants receive fewer
calories in first few days vs.
formula

14. BREAST MILK JAUNDICE
• Late unconjugated
hyperbilirubinemia
• Onset 4-7 days; peak 5-15 days (>
10.0)
• Returns to < 3.0 at greater than 9
weeks
• Prevalence is 2-4% of BF infants

15. Breast Milk Jaundice
Possible Etiologies:
–Inhibition of hepatic excretion
• factors in milk? Pregnanediol, FAs, lipase
–Intestinal Readsorption
• Delayed passage of meconium
• Sterile GI: no conversion to urobilinogen
• -glucuronidase: “unconjugates” BR

16. COMMONLY USED ICTEROGENIC
AGENTS

17. PATHOLOGICAL JAUNDICE
 Jaundice appearing in the first 24hrs of life
 Total serum bilirubin >12mg/dl
 Serum bilirubin increasing by >0.5mg/dl/hr
 Serum bilirubin increasing by >5mg/dl/day
 Conjugated bilirubin >2mg/dl
 Clinical jaundice persisting for more than 2 weeks
 Presence of evidence of haemolysis

18. CLINICAL FEATURES
 Jaundice may appear any time during neonatal period
 Jaundice begins on the face and as the level
increases, progress to the abdomen and feet
 Unconjugated bilirubin appears bright yellow or
orange
 Conjugated bilirubin appears greenish or muddy
yellow
 Infants usually lethargic and feed poorly
 Signs of primary disease.(sepsis, galactosemia etc)

19. KREMER RULE FOR ESTIMATION
OF NNJ
Zone SBR mmol/L
 1 = 100 mmol/L
 2 = 150 mmol/L
 3 = 200 mmol/L
 4 = 250 mmol/L
 5 > 250 mmol/L

20. KERNICTERUS- BILIRUBIN
ENCEPALOPATHY
 Unbound bilirubin crosses the blood brain barrier and
causes toxic damage to brain cells of the basal
ganglia,hippocampus, substantia nigra, geniculate
body and cranial nerve nuclei.
 It is not known at what serum bilirubin concentration
or under what circumstance significant brain damage
occurs
 1/3 of infants with HD and bilirubin >25-30 will
develop acute bilirubin encephalopathy
 At autopsy 2 1% of hyperbirubinemic preterm babies
have bilirubin encephalopathy

21. STAGE I
• Lethargy
• Hypotonia
• Irritability
• Poor Moro reflex
• Poor oral intake
• High pitched cry
• Emesis

22. STAGE II
 Hypertonia arching
 Opisthotonic posturing
 High pitched cry
 Convulsions

23. STAGE III
 Evolves over several weeks or months
 Present with varying degrees of dystonia
 Choreoarthetoid cerebral palsy
 Mental retardation
 Auditory abnormalities, gauze palsies

24. Bilirubin-Induced Neurologic Dysfunction
Score (BIND score); Johnson et al
BIND
Score
Stage IA
Early Subtle Signs
(Score 1)
Stage IB
Early Subtle Signs
(Score 2)
Stage II
Semi-Coma,
Apnea,
Convulsions
(Score 3)
Mental
Status
Tone slightly  Tone mod or 
depending
On arousal state;
Mild neck arching
Tone markedly  or 
depending; Opisthotonic
posturing; Back bends;
Bicycling movements
Cry Hi pitched Shrill, Very
Hi pitched
Piercing,
Shrill
Inconsolable
Suck Normal Weak/Poor Absent

25. Laboratory Evaluation of Neonatal
Hypybilirubinaemia
Urine Tests:
• Routine urinalysis, (including
protein and reducing substances)
• Urine culture
• Bilirubin and urobilinogen
• Amino acid screening

26. Laboratory Workup (contd.)
• Reticulocyte count
• RBC morphology
• Platelets count; clotting test
• White blood cell count
• Erythrocyte sedimentation rate
• Serology (specific IgM antibodies - TORCHES)
• Carboxyhaemoglobin level
• Hepatitis-associated antigens
• Alpha1-anti-trypsin concentration

27. Treatment of Unconjugated
Hyperbilirubinaemia
 Observation/monitoring
• Increase fluids/oral intake
• Phototherapy
• Exchange blood transfusion
• Phenobarbitone
• Antibiotics for suspected sepsis
• Supportive therapy

28. PHOTOTHERPY – INDICATION
 Prevention of hyperbilirubinaemia in preterm
babies (VLBW)
 Treatment of moderate hyperbilirubinemia
 Post EBT

29. Factors Affecting Efficacy of
phototherapy
 The spectrum of light delivered by the phototherapy
unit. Because of the optical properties of bilirubin
and skin, the most effective wavelengths are in the
blue-green spectrum
 The power output of the phototherapy light and flux
of light energy incident on the infant, expressed as
irradiance (watts per square meter). When measured
over a specific portion of the spectrum (e.g, the blue
spectrum, approximately 425 to 475 nm), it is called
the spectral irradiance and is measured in
µW/cm2/nm
 The surface area of the infant exposed to
phototherapy.

30. Standard/Intensive
Phototherapy
The overhead standard phototherapy unit,
delivered only 9 to 10 μW/cm2 per nanometer
- the bilirubin level decreased by only 6% (1
mg/dl)/24 hours
While intensive phototherapy produced an
irradiance of 35 μW/cm2 per nanometer -
produced an average decline of 43% (7.4
mg/dL) in 24 hours (from about 17 to 10
mg/dL)

31. Intensive/Therapeutic
Phototherapy
‘Intensive phototherapy’ is defined
as irradiance of 30 µW/cm2/nm or
higher in the 430- to 490-nm band
delivered to as much of the
infant’s surface area as possible.

32. PHOTOTHERAPY –
COMPLICATIONS
 Increased fluid lost with risk of dehydration
 Damage to the retina and gonads
 Skin damage – rashes, bronze baby syndrome
 Increase incidence of PDA
 Loose stools

33. PHARMACOTHERAPY
 Augments uptake of bilirubin by hepatic cells
 It increases the activity of UDPG-T enzyme
 Use of tin-mesoporphyrin to inhibit the production
of haeme oxygenase has shown some promise
but not yet in routine clinical use.

34. EXCHANGE BLOOD
TRANSFUSSION - INDICATION
 Serum bilirubin levels >20mg/dl in term infants
 Serum bilirubin levels > 15mg/dl in preterm
 In haemolytic disease - > 10mg/dl 24hrs of life
 >15mg/dl 48hrs of live
 >20mg/dl any age
 >5mg/dl/24hrs
 Technique of EBT

35. COMPLICATIONS OF EBT
 Catheter: gut perforation, cardiac arrythymias, NEC and liver cirrhosis
 Infection: HIV, Hepatitis, malaria
 Transfusion reactions
 Embolism
 Haemodynamic: hypo hyper vol
 Metabolic: Hypocalcaemia, hypoglycaemia, hypomagnesemia,
acid/base
imbalance
 hypothermia

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