the best i could come up with on obstructive jaundice

1. PATHOPHYSIOLOGY
OF OBSTRUCTIVE
JAUNDICE
DR. VIGNESH KUMAR
AMBEDKAR HOSPITAL

2. Contents
 Metabolism
 Effect on systems
 Symptomatology
 The why behind it

3. Jaundice
 “jaune” in french = yellow
 Normal bile secretion 600-1200ml/day
 Bilirubin 250-350mg/day
 Types of jaundice
 Van der Bergh test /
Photospectrometry
 Scleral icterus is evident at 2.5mg/dl,
and cutaneous/mucous membrane
icterus at 6mg/dl

4. Hemoglobin catabolism

5. Bilirubin metabolism

6. Bile salt metabolism

7. Systemic effects
 Hepatobiliary
◦ Normal biliary pressures 7-14 cm H₂O
◦ As the pressure in the biliary tree
increase, the cholangiolymphatic reflux
and cholangiovenous reflux come into
play l/t systemic toxicity
◦ As biliary pressure increases (30 cm
H₂O), the bile secretion completely stops
◦ Reflux into space of disse and hepatic
sinusoids resulting in an inflammatory
response followed by increased
fibrogenesis

8. Cholangiolymphatic and
cholangiovenous reflux
Greenfield's surgery

9. Systemic effects
 Cardiovascular
◦ decreased cardiac contractility; reduced
left ventricular pressures; impaired
response to β- agonistic drugs; decreased
peripheral vascular resistance
 Renal
◦ depressed cardiac function; hypovolemia;
endotoxemia may l/t renal impairment

10. Systemic effects
 Immunity
◦ increased bacterial translocation from the
gut in the setting of bile duct obstruction
 Wound healing
◦ Delayed wound healing and a high
incidence of wound dehiscence and
incisional hernia have been observed in
patients undergoing surgery to relieve
obstructive jaundice

11. Symptomatology
 Pruritis
 Clay coloured
stools
 High coloured urine
 RUQ pain
 Icterus
 Steatorrhoea
 Bleeding tendency
 f/o fat soluble
vitamin deficiency
 Anorexia
 Fever
 Nausea / vomiting
 High grade fever
with chills
 Weight loss
 Systemic
endotoxemia
 f/o liver cell failure

12. The why behind it all
 Pruritis
◦ Bile salts reflux back into plasma, l/t mast
cell degranulation in the skin
 Clay coloured stools
◦ Conjugated bilirubin does not reach the
gut, no sterco/urobilin, stools devoid of
yellow colour
 High coloured urine
◦ Conjugated bilirubin (soluble) diffuses into
plasma, is filtered by kidney

13. The why behind it all (cont.)
 RUQ pain and tenderness
◦ Stasis of bile in ducts l/t inflammatory
response causing pain
◦ Elicited as tenderness (irritation of parietal
peritoneum) and palpable lump (omentum)
 Biliary colic
◦ A misnomer as CBD in most individuals does
not contain muscle layers
◦ Stasis leads to release of inflammatory
mediators (phospholipase A₂ and
prostaglandins)

14. The why behind it all (cont.)
 Steatorrhoea
◦ Fat does not get absorbed without bile
salt (micelle formation)
 Bleeding tendency
◦ Vitamin K deficiency l/t prolonged PT
 Deficiency of fat soluble vitamins
◦ Deficiency of vitamins A,D,E,K and their
manifestations

15. The why behind it all (cont.)
 Icterus
◦ Bilirubin has a high affinity for elastin that
is abundant in sclera and skin
 Fever
◦ Release of TNF alpha and IL-1d/t
inflammatory response
◦ Local PG activity in anterior hypothalamus
 Nausea / Vomiting
◦ Gut irritation and vagal stimulation d/t pain

16. The why behind it all (cont.)
 Anorexia
◦ IL-1 effects on satiety centre
 Weight loss
◦ IL-1 increases production of IL-2 and TH-
2 cells, l/t skeletal muscle proteolysis and
thereby weight loss

17. The why behind it all (cont.)
 High grade fever with chills
◦ Stasis leads to ascending bile infection
 Systemic endotoxemia
◦ elevated intraductal pressure in the bile
duct allows translocation of bacteria or
endotoxin into the vascular and lymphatic
system (cholangio-venous/lymphatic
reflux)
 Courvoisier’s law

18. The why behind it all (cont.)
 Features of liver cell failure
◦ Portal hypertension
◦ Ascitis
◦ Gynaecomastia
◦ Vascular spider naevi
◦ Palmar erythema
◦ Testicular atrophy
◦ Dupuytrens contracture
◦ KF ring
◦ Flapping tremors
◦ Fetor hepaticus
◦ Hepatic encephalopathy