Describe the epidemiology.
Sex: ♀ = ♂
Incidence: up to 9% of patients with cholelithiasis [1]
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.
What is the most common cause?
Choledocholithiasis (most common)
List other causes.
Biliary strictures
Congenital
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.)
Acute pancreatitis
Periampullary duodenal diverticulum
Contamination of bile with intestinal contents
Manipulation of the biliary tract (e.g., papillotomy, stent placement, ERCP, liver transplantation)
Biliary-enteric fistula
What are the pathognomic features?
Charcot cholangitis triad (25–70% of patients present with all three features
Reynolds pentad
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)
High fever
Jaundice (least common feature)
Describe the reynolds pentad.
Charcot cholangitis triad PLUS hypotension and mental status changes
Reynolds pentad is associated with significant morbidity/mortality.
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