Describe the epidemiology.
Sex: ♀ = ♂
Incidence: up to 9% of patients with cholelithiasis 
Peak incidence: 50–60 years
Describe the pathophysiology.
Biliary tract obstruction → bile stasis with increased intraductal pressure → bacterial translocation into the bile ducts → bacterial infection ascends the biliary tract (even into the hepatic ducts)
High intraductal pressure also causes bacterial translocation from bile into the systemic circulation, resulting in bacteremia, which can progress to sepsis, septic shock, and MODS without timely management.
List other causes.
Infectious (e.g., HIV)
Inflammatory (e.g., primary sclerosing cholangitis, IgG4-related sclerosing cholangitis)
Iatrogenic (e.g., ERCP, stent placement)
Malignant obstruction (e.g., due to cholangiocarcinoma, pancreatic cancer, etc)
Extrinsic compression (e.g., Mirizzi syndrome)
Parasitic infection (e.g., liver fluke, hydatid cyst, Ascaris spp.)
Periampullary duodenal diverticulum
Contamination of bile with intestinal contents
Manipulation of the biliary tract (e.g., papillotomy, stent placement, ERCP, liver transplantation)
What are the pathognomic features?
Charcot cholangitis triad (25–70% of patients present with all three features
Features of sepsis, septic shock, and multiorgan dysfunction may be present, depending on the severity of disease at
What is the charcot cholangitis triad?
Abdominal pain (most commonly RUQ)
Jaundice (least common feature)