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Acute acalculous cholecystitis due to infectious causes
Ioulia Markaki1, Afroditi Konsoula2, Lamprini Markaki3
1Department of Emergency, General Hospital of Kythira "Trifyllio", Kythira 80200, Greece.
Insights
Acute acalculous cholecystitis (AAC), gallbladder inflammation without stones, can stem from infections in healthy individuals. Understanding these infectious mechanisms is crucial for diagnosis and treatment.
Area of Science:
- Gastroenterology
- Pathophysiology
- Infectious Diseases
Background:
- Acute acalculous cholecystitis (AAC) is gallbladder inflammation without gallstones.
- AAC typically affects critically ill patients but can occur in healthy individuals.
- Infectious etiologies are primary drivers of AAC in non-critically ill patients.
Purpose of the Study:
- To discuss the pathophysiological mechanisms of AAC.
- To focus on infectious causes of AAC.
- To highlight the importance of pathogen identification in AAC.
Main Methods:
- Review of pathophysiological mechanisms of AAC.
- Focus on infectious etiologies.
- Discussion of contributing factors like bile stasis, ischemia, and direct invasion.
Main Results:
- AAC in critically ill patients involves bile stasis and gallbladder ischemia.
- In non-critically ill patients, AAC mechanisms include epithelial cell invasion, vasculitis, biliary obstruction, and sequestration.
- Multiple pathogenic mechanisms can contribute concurrently to AAC.
Conclusions:
- Infectious causes are key in AAC among healthy individuals.
- Awareness of pathogens aids histopathological examination.
- Further research and clinical suspicion are needed to understand AAC pathogenesis.
Abstract:
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.
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