Epidemiology
The distribution and incidence of acute cholecystitis follow that of cholelithiasis because of the close relationship between the two.
Cholelithiasis occurs in approximately 15% of adults.[5] In the US, more than 20 million people are estimated to have gallstones, and approximately 750,000 cholecystectomies are performed annually.[6] The prevalence rates are relatively low in Africa and Asia.[7] Most patients with gallstones do not develop symptoms. About 1% to 2% of people with asymptomatic gallstones become symptomatic each year and up to 20% will develop symptoms within 20 years.[8][9][10] Forty percent of those that do develop symptoms (8% of those with initially asymptomatic gallstones) will present with complications such as cholecystitis or pancreatitis.[11]
Acute cholecystitis occurs in about 1% to 3% of patients with symptomatic gallstones.[12][4] It is more common in females than males, most likely due to gallstones being more prevalent in females.[13]
Acute acalculous cholecystitis accounts for up to 10 of cases of acute cholecystitis.[4][2] The incidence is higher in the intensive-care population, particularly in patients in burn and trauma units.
Risk factors
Gallstones cause 90% of cases, by becoming impacted within the cystic duct, leading to gallbladder inflammation.[4][3] Gallstones become more common with age in both genders. Studies have indicated an increased frequency of gallstone disease in families, twins, and relatives of gallstone patients.[7]
Factors leading to biliary tract disease in critically ill patients include gallbladder dysmotility, gallbladder ischaemia, and total parenteral nutrition.[7] Vascular compromise, especially in critically ill patients who experience episodes of hypotension, is thought to be a contributing factor.[19] Recent severe illness, including trauma and burns, puts the patient at risk of acalculous cholecystitis.
Fasting causes gallbladder hypomotility. Prolonged TPN causes gallbladder stasis, biliary sludge, and gallstones due to decreased gallbladder emptying. In one study of 23 patients receiving TPN, 6% exhibited sludge after only 3 weeks, 50% after 4-6 weeks, and 100% after 6 weeks of TPN.[20] It is thought that bile stasis leads to accumulation of toxic agents in the gallbladder lumen, causing gallbladder mucosa damage.[19]
There is an increased risk of gallbladder disease in people with diabetes.[21]
Changes in weight (gaining or losing) pose a risk for developing gallstones, being active reduces the risk.[22]
Risk factor for developing gallstones.[23]
Related to bile stasis, ischaemia, bacterial infection, sepsis, and activation of factor XII.[24]
Patients with extensive burns commonly have multiple risk factors for developing acalculous cholecystitis, such as sepsis, dehydration, total parenteral nutrition use, and positive pressure ventilation.[25]
GLP-1 receptor agonists have been associated with acute cholecystitis, cholangitis and pancreatitis.[26]
Ischaemia can occur as a primary event (e.g., small vessel vasculitis) or as a complication of hepatic chemoembolisation, such as inadvertent embolisation of the cystic artery causing acalculous acute cholecystitis.[28]
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