Published online Aug 16, 2021. doi: 10.12998/wjcc.v9.i23.6674
Peer-review started: March 28, 2021
First decision: April 28, 2021
Revised: May 8, 2021
Accepted: July 5, 2021
Article in press: July 5, 2021
Published online: August 16, 2021
Processing time: 130 Days and 5.4 Hours
Acute acalculous cholecystitis (AAC) is an inflammation of the gallbladder not associated with the presence of gallstones. It usually occurs in critically ill patients but it has also been implicated as a cause of cholecystitis in previously healthy individuals. In this subgroup of patients, infectious causes comprise the primary etiology. We, herein, discuss the pathophysiological mechanisms involved in AAC, focusing on the infectious causes. AAC associated with critical medical conditions is caused by bile stasis and gallbladder ischemia. Several mechanisms are reported to be involved in AAC in patients without underlying critical illness including direct invasion of the gallbladder epithelial cells, gallbladder vasculitis, obstruction of the biliary tree, and sequestration. We emphasize that multiple pathogenic mechanisms may concurrently contribute to the development of AAC in varying degrees. Awareness of the implicated pathogens is essential since it will allow a more focused examination of the histopathological specimens. In conclusion, additional research and a high degree of clinical suspicion are needed to clarify the complex spectrum of mechanisms that are involved in the pathogenesis of AAC.
Core Tip: The most important mechanisms involved in acute acalculous cholecystitis in patients without underlying critical illness are direct invasion of the gallbladder epithelial cells, gallbladder vasculitis, obstruction of the biliary tree, and sequestration. Awareness of the implicated pathogens is essential since it will allow a more focused examination of the histopathological specimens.