Acute acalculous cholecystitis (AAC) represents cholecystitis without gallstones, occurring in approximately 5-10% of all cases of acute cholecystitis in adults. Several risk factors have been recognized, while infectious diseases can be a cause of cholecystitis in otherwise healthy people. Coronavirus disease 2019 (COVID-19) is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has spread worldwide, leading to an unprecedented pandemic. The virus enters cells through the binding of the spike protein to angiotensin-converting enzyme 2 (ACE2) receptors expressed in many human tissues, including the epithelial cells of the gastrointestinal (GI) tract, and this explains the symptoms emanating from the digestive system. Acute cholecystitis has been reported in patients with COVID-19. The purpose of this review is to provide a detailed analysis of the current literature on the pathogenesis, diagnosis, management, and outcomes of AAC in patients with COVID-19.

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.

In Switzerland, the preferred mode of treatment for hydatid liver disease caused by Echinococcus granulosus is surgery, giving us the opportunity for a retrospective histopathologic study of 17 consecutive liver resections. We focused on the occurrence of satellite cysts and of biliary fistulas and their effects on bile ducts. Of 17 patients, 6 (35%) had one or more satellite cysts, to be distinguished from internal daughter cysts. Small areas of fibrinoid necrosis within the fibrous pericyst, a surprisingly constant histologic finding, offer a simple explanation for the occurrence of such satellite cysts as well as for the development of biliary fistulas. Large fistulas with gross drainage of cyst contents into bile ducts were present in 5 patients (30%). The accompanying cholangitis was distinctly granulomatous in 2 of them, an observation rarely mentioned in the literature. All 5 patients with large fistulas also had chronic sclerosing cholangitis and dilatation of smaller bile ducts, in all probability the result of chronic cyst fluid leakage through preexisting, clinically silent smaller fistulas. Dilatation of small bile ducts is rightly considered a precursor sign for large fistulas. Awareness of the histopathology of these complications facilitates the interpretation of ultrasound and radiologic imaging, sheds light on their pathogenesis, and may influence the choice of treatment.