Although the pathophysiology of acute acalculous cholecystitis is not clear cut, many hypotheses have been proposed. Visceral hypoperfusion of the gallbladder may lead to ischemia in critically ill hypotensive patients. Narcotics such as morphine, which are used in the intensive care unit (ICU), may lead to biliary stasis and sphincter of Oddi spasm, causing gallbladder distention and possible ischemia. In the fasting state, the gallbladder may not contract, and when it does contract against a sludge-filled cystic duct, as may occur with initiation of oral feeding after a period of fasting, acute acalculous cholecystitis may occur secondary to the increase in intraluminal pressure. Lack of neurohumoral stimuli may occur in the biliary tract in the fasting state with a decrease in gastrointestinal secretion which may lead to an increase in bile viscosity and concentration, an increase in water absorption, or an increase in mucin secretion. This may lead to acute acalculous cholecystitis.

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