PHYSIOLOGICAL JAUNDICE

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PHYSIOLOGICAL JAUNDICE

• Learning Outcomes
• The students will at the end of the session be
  able to
• Understand the aetiology of physiological
  jaundice
• Appreciate the dangers associated with jaundice
• Evaluate the management treatment for
  neonatal jaundice     
•  

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What is Jaundice?
A yellow discolouration of the skin, sclera and
mucous membrane due to an increase in the serum
bilirubin level. This becomes clinically evident
when serum bilirubin reaches about 80-100
?mol/l.

• Physiological jaundice usually
• peaks 48-72 hours
• disappears by 1 week
• does not present before 24 hours

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• Incidence
• Preterm infants 80
• 30 50 of term infants in first week of life

• 10 will require phototherapy

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• Aetiology of Physiological Jaundice
• Hb in neonate 18-19g/dl and in adult 11-14g/dl
• Breakdown of excess RBCs (Haemoglobin is a
  constituent of RBC) 
• Hb broken into
• globin - a protein that is conserved and utilised
• haem - cannot be used
• ? degraded and excreted

Bilirubin is a product of this degradation It
causes yellow staining of the tissues
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• The bilirubin first formed is UNCONJUGATED FAT
  SOLUBLE.
• It cannot be excreted in bile or urine
•  Unconjugated Bilirubin
•  - travels in plasma, bound to albumin.
• - enters the liver cells with the aid of Y Z
  carrier proteins
• - becomes conjugated with glucoronic acid
• The reaction is catalysed by an enzyme
  ?Glucuronyl Transferase

Hypoxia or hypothermia may compromise bilirubin
conjugation
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Conjugated Bilirubin is water soluble  It is
excreted through the biliary tree into the gut.
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• Conjugated bilirubin is further catabolised by
  intestinal flora into
• urobilinogen
• stercobilin
• It forms a major component of bile in
  faeces.(This gives the characteristic orange
  colour to faeces.)
• A small amount is passed in the urine

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• Conjugated Bilirubin is unstable
• Why?
• Due to
• the relatively alkaline environment of the
  duodenum jejunum
• specific enzymes eg beta glucuronidase
• ? Converts back into unconjugated bilirubin.
•  

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When deconjugated in the intestine  the
bilirubin is absorbed across the intestinal
mucosa and returned to the circulation and the
portal venous system CONJUGATION HAS TO TAKE
PLACE ALL OVER AGAIN
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• Physiological Factors Associated with
  Physiological Jaundice
• Hb level is higher than required
• RBC have shorter life
• Hepatic Immaturity
• - reduced glucuronyl transferase activity
• - reduced active uptake of UB
• - reduced intracellular transport system
• - reduced active secretion of CB
• - large enterohepatic circulation of bilirubin
  to add to the load of UB in the hepatocyte

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Other Factors That Can Contribute To
Physiological Jaundice
Drugs eg antibiotics (penicillin) Bruises Caput Ce
phalhaematoma Hypoxia /asphyxia Hypoglycaemia
Hypothermia
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• INVESTIGATIONS
• Assessment of skin and sclera colour
• Clinical history of mother/family
• History of labour ?bruising / cephal haematoma
  /birth trauma
• Blood group rhesus factor
• Feeding pattern
• Infection
• G6PD 

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• Drugs
• Serum bilirubin ? conjugated/unconjugated
  (Icterometer)
• Hb
• Reticulocyte count ( raised levels in cases of
  haemolysis) 

Danger of Jaundice - KERNICTERUS!!!
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• Care of Baby
• Early feeding/ Nutrition/ Hydration
• Increase frequency of breast feeding
• Neutral thermal environment
• Prevent hypoglycaemia and hypoxia
• Avoid constipation

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May require Phototherapy Conventional or
Fibro-optic blankets - converts fat soluble to
water soluble bilirubin ? When to commence
phototherapy
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Management of Jaundice

• ?Feeding
• SBR levels- invasive!! (? icterometer)
• - pain
• - infection
• Phototherapy
• - to maintain levels below 340 mmols/l
• (others argue 500mmol/l)

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Care of Baby Requiring Phototherapy

• Hygiene (sore buttocks)
• Eye pads
• Serum bilirubin levels
• Parent infant attachment

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Problems with phototherapy

• Hypothermia
• Hyperthermia
• Rashes
• Gastro-intestinal upset
• Dehydration
• Isolation
• Interfere with breastfeeding

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Other Types of Jaundice
1.Haemolytic - ABO Incompatability - Rhesus
Incompatability - Polycythaemia - Extravasation
of blood - Septicaemia - Glucose 6-Phosphate
Dehydrogenase Deficiency - Spherocytosis
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2. Reduced Albumin Binding Capacity - drugs,
hypoxia, hypothermia, acidosis,
hypoalbuminaemia 3. Defective
Conjugation - infection, breast feeding, inborn
errors of metabolism 4. Breast milk
jaundice - progressive increase in bilirubin
from day 4, peaks at 10-15 days of life
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5. Obstructive Jaundice   - obstruction to the
flow of bile - bilirubin is conjugated normally,
but become reabsorbed into the blood - water
soluble, therefore circulates to kidneys
colouring urine dark yellowish brown - stools
remain pale no risk of kernicterus
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• References
• Al-Alaiyan (1996) Fiberoptic, conventional and
  combination phototherapy for treatment of
  nonhaemolytic hyperbilirubinemia in neonates
  http//www.kfshrc.edu.sa/annals/166/96-036.html
  Date accessed 20/10/2000
•  Blackburn (1995) Hyperbilinemia Neonatal
  Jaundice. Neonatal Network (October) 14 7 15
• Coe L (1999) Pathology physiology of neonatal
  jaundice BJM April p 240-243
• College of Family Physicians of Canada (1999)
  Approach to the management of
  hyperbilirubinemia in term newborn infants
  paeditrics Child Health 4(2) 161-164
  http//www.cps.ca/english/statements/FN/fn98-02.ht
  m date accessed 20/10/00
•  

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• Hey (1995) Phototherapy fresh light on a murky
  subject.Midirs Midwifery Digest (Sept ) 53 256-
•  Hey (1995)Neonatal jaundice-how much do we
  really know? Midirs Midwifery Digest (March) 5
  14-
•  Robertson (1993) Neonatal jaundice. Mechanisms
  diagnosis. Modern Midwife. Sept/Oct p28