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Cholecystitis is the inflammation of the gall bladder wall, usually as a response to cystic duct obstruction by a gall stone. It is subdivided into acute or chronic depending on the timeline, and acute cholecystitis is further subdivided into calculous and acalculous. Usually, cholecystitis is defined by fever, an elevated white blood cell (WBC) count, and a thickened gall bladder on ultrasound.

Acute cholecystitis

Acute calculous cholecystitis accounts for 90% of acute cholecystitis cases. In this type of cholecystitis, the obstruction of the cystic duct by a stone results in chemical irritation and inflammation. Increased pressure within the gall bladder compresses blood vessels, reducing blood flow and resulting in ischemia. Intestinal bacteria can be cultured from the bile in 80% of cases within 2 days of onset of symptoms, and may have a primary role.

Edema, congestion, hemorrhage, and acute inflammation are all present. There may also be necrosis and peritoneal exudate. If the lumen is full of pus, this is empyema. If there is transmural necrosis, it is gangrenous cholecystitis, which presents a high risk of perforation.

In most patients (85%), there is spontaneous recovery with movement of the stone, though the condition frequently recurs.

Acute acalculous cholecystitis accounts for 10% of acute cholecystitis cases. It is usually seen after major non-biliary surgery and in critically ill patients. The pathogenesis is probably multifactorial, involving bile stasis, increased bile viscosity, and decreased blood flow.

The gross and microscopic features are similar to acute calculous cholecystitis, except there is a higher incidence of gangrene and perforation. Therefore, morbidity and mortality are greater.

Chronic cholecystitis

Chronic cholecystitis may or may not have a history of acute cholecystitis. Gall stones, present in 95%, are thought to result in low grade chronic inflammation with eventual fibrosis, and loss of function. Bacteria are cultured in 20-30% of cases, though the significance of this is unknown. Microscopically, chronic inflammation and fibrosis are seen, often with mucosal changes (metaplasia).