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PATHOPHYSIOLOGY OF CHOLANGITIS

Presence of biliary tract obstruction or stricture eg. choledocholithiasis Increase in intraluminal pressure causes dilatation Occlude vascular supply causing ischemia Predispose to bacterial infection from retrograde ascent

Release of inflammatory mediators eg. PG

Inflammatory exudate & bile stasis

PROGRESSION TO ASCENDING CHOLANGITIS


Infection in CBD extends proximally to intrahepatic duct system (biliary canaliculi, hepatic veins & peri-hepatic lymphatics)
Go into acute suppurative cholangitis and systemic bacteremia as bacteria escape hepatic sinusoids Present as Charcots triad ( RUQ pain, fever and jaundice) or Reynolds pentad with altered mental status and signs of sepsis

EPIDEMIOLOGY
Relatively uncommon (1% develop secondary to cholelithiasis) 1-3% develop after ERCP due to poor biliary drainage Median age is from 50-60 years old Equal distribution for M & F

RISK FACTORS
Age > 50 years old Presence of cholelithiasis/ choledocholithiasis Benign stricture Malignant stricture Post-procedure injury Hx of Sclerosing Cholangitis HIV or parasitic infections

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