PATHOPHYSIOLOGY OF OBSTRUCTIVE JAUNDICE DR. VIGNESH KUMAR AMBEDKAR HOSPITAL
Aug 15, 2015
PATHOPHYSIOLOGY OF OBSTRUCTIVE
JAUNDICE
DR. VIGNESH KUMARAMBEDKAR HOSPITAL
ContentsMetabolismEffect on systemsSymptomatology The why behind it
Jaundice “jaune” in french = yellowNormal bile secretion 600-
1200ml/dayBilirubin 250-350mg/dayTypes of jaundiceVan der Bergh test /
PhotospectrometryScleral icterus is evident at
2.5mg/dl, and cutaneous/mucous membrane icterus at 6mg/dl
Hemoglobin catabolism
Bilirubin metabolism
Bile salt metabolism
Systemic effectsHepatobiliary
◦ 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
Greenfield's surgery
Cholangiolymphatic and cholangiovenous reflux
Systemic effectsCardiovascular
◦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
Systemic effectsImmunity
◦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
Symptomatology PruritisClay coloured
stoolsHigh coloured
urineRUQ painIcterus Steatorrhoea Bleeding
tendencyf/o fat soluble
vitamin deficiency
AnorexiaFeverNausea /
vomitingHigh grade fever
with chillsWeight lossSystemic
endotoxemiaf/o liver cell
failure
The why behind it allPruritis
◦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
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)
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
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
hypothalamusNausea / Vomiting
◦Gut irritation and vagal stimulation d/t pain
The why behind it all (cont.)Anorexia
◦IL-1 effects on satiety centreWeight loss
◦IL-1 increases production of IL-2 and TH-2 cells, l/t skeletal muscle proteolysis and thereby weight loss
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
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