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.[4] In the US, 20 to 25 million people are estimated to have gallstones, and approximately 750,000 cholecystectomies are performed annually.[5] The prevalence rates are relatively low in Africa and Asia.[6] Most patients with gallstones do not develop symptoms. About 1% to 2% of people with asymptomatic gallstones become symptomatic each year.[7][8][9][10] Acute cholecystitis occurs in about 10% of symptomatic patients.[11] It is 3 times more common in women than in men up to the age of 50 years, and is about 1.5 times more common in women than in men thereafter.[3] 

Acute acalculous cholecystitis accounts for 5% to 14% of cases of acute cholecystitis.[3] The incidence is higher in the intensive-care population, particularly in patients in burn and trauma units.

Risk factors

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gallstones

Gallstones cause 90% of cases, by becoming impacted within the cystic duct, leading to gallbladder inflammation.[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.[6]

severe illness

Factors leading to biliary tract disease in critically ill patients include gallbladder dysmotility, gallbladder ischaemia, and total parenteral nutrition.[6] Vascular compromise, especially in critically ill patients who experience episodes of hypotension, is thought to be a contributing factor.[17] Recent severe illness, including trauma and burns, puts the patient at risk of acalculous cholecystitis.

total parenteral nutrition (TPN)

Fasting causes gallbladder hypomotility. Prolonged TPN causes gallbladder stasis, biliary sludge, and gallstones due to decreased gallbladder emptying. Around 60% of patients receiving TPN exhibit sludge after only 3 weeks.[6] It is thought that bile stasis leads to accumulation of toxic agents in the gallbladder lumen, causing gallbladder mucosa damage.[17]

diabetes

There is an increased risk of gallbladder disease in people with diabetes.[20]

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physical inactivity

Risk factor for developing gallstones.

low fibre intake

Risk factor for developing gallstones.

trauma

Related to bile stasis, ischaemia, bacterial infection, sepsis, and activation of factor XII.[18]

severe burns

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.[19]

ceftriaxone

Secreted into bile; can precipitate with calcium, forming biliary sludge and stones.[6]

ciclosporin

Can decrease bile acid secretion, which may predispose to sludge or stone formation.[11]

hepatic arterial embolisation

Ischaemia occurs 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.[21]

infections

Cytomegalovirus, Cryptosporidium, and Salmonella typhi can infect the biliary system and produce cholecystitis. Can occur in HIV-positive patients as part of the spectrum of AIDS-related cholangiopathy due to infections with microsporidia species.

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