PHYSIOLOGICAL JAUNDICE.ppt

ppt

1. PHYSIOLOGICAL JAUNDICE
Learning Outcomes:
The students will at the end of the session be
able to:
a)Understand the aetiology of physiological
jaundice
b)Appreciate the dangers associated with
jaundice
c)Evaluate the management & treatment
for neonatal jaundice

2. 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.
What is Jaundice?
Physiological jaundice usually
•peaks 48-72 hours
•disappears by 1 week
•does not present before 24 hours

3. Incidence:
•Preterm infants –80%
•30 –50 % of term infants in first week of
life
•10% will require phototherapy

4. Aetiology of Physiological Jaundice
Hb in neonate =18-19g/dl andinadult =11-14g/dl
Breakdown of excess RBCs (Haemoglobin is a
constituent of RBC)
Hb broken into:
(i)globin -a protein that is conserved and utilised
(ii)haem -cannot be used
degraded and excreted
Bilirubin is a product of this degradation
It causes yellow staining of the tissues

5. The bilirubin first formed isUNCONJUGATED & 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 conjugatedwith glucoronic acid
The reaction is catalysed by an enzyme Glucuronyl
Transferase
Hypoxia or hypothermia may compromise
bilirubin conjugation

6. Conjugated Bilirubin is water soluble
It is excreted through the biliary tree into the gut.

7. Conjugated bilirubin is further catabolised by intestinal flora into:
i.urobilinogen
ii.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

8. Conjugated Bilirubin is unstable
Why?
Due to :
1)the relatively alkaline environment of the duodenum &
jejunum
2)specific enzymes eg beta glucuronidase
Converts back into unconjugated bilirubin.

9. 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

10. Physiological Factors Associated with Physiological
Jaundice
1)Hb level is higher than required
2)RBC have shorter life
3)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

11. Drugs eg antibiotics (penicillin)
Bruises
Caput
Cephalhaematoma
Hypoxia /asphyxia
Hypoglycaemia
Hypothermia
Other Factors That Can Contribute To
Physiological Jaundice

12. 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

13. •Drugs
•Serum bilirubin ? conjugated/unconjugated
(Icterometer)
•Hb
•Reticulocyte count ( raised levels in cases of
haemolysis)
Danger of Jaundice -KERNICTERUS!!!

14. Care of Baby
•Early feeding/ Nutrition/ Hydration
•Increase frequency of breast feeding
•Neutral thermal environment
•Prevent hypoglycaemia and hypoxia
•Avoid constipation

15. May require Phototherapy
Conventional or Fibro-optic blankets
-converts fat soluble to water soluble bilirubin
? When to commence phototherapy

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

17. •Hygiene (sore buttocks)
•Eye pads
•Serum bilirubin levels
•Parent infant attachment
Care of Baby Requiring Phototherapy

18. Problems with phototherapy
•Hypothermia
•Hyperthermia
•Rashes
•Gastro-intestinal upset
•Dehydration
•Isolation
•Interfere with breastfeeding

19. Other Types of Jaundice:
1.Haemolytic
-ABO Incompatability
-Rhesus Incompatability
-Polycythaemia
-Extravasation of blood
-Septicaemia
-Glucose 6-Phosphate Dehydrogenase Deficiency
-Spherocytosis

20. 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

21. 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

22. 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.htmlDate
accessed 20/10/2000
•Blackburn (1995) Hyperbilinemia & Neonatal Jaundice. Neonatal
Network(October) 14: 7 15
•Coe L (1999) Pathology & physiology of neonatal jaundice BJMApril
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.htmdate accessed
20/10/00

23. •Hey (1995) Phototherapy: fresh light on a murky subject.Midirs
Midwifery Digest(Sept ) 5:3; 256-
•Hey (1995)Neonatal jaundice-how much do we really know?
Midirs Midwifery Digest(March) 5: 1;4-
•Robertson (1993) Neonatal jaundice. Mechanisms & diagnosis.
Modern Midwife. Sept/Oct: p28