Abstract
Acute acalculous cholecystitis was observed to increase in frequency between 1950 and 1979, an increase that was statistically significant. The greatest part of this increase occurred between 1965 and 1979. Acute acalculous cholecystitis was also found to be associated with a higher mortality rate, more than twice that of acute calculous cholecystitis. Acute acalculous cholecystitis occurred in a variety of clinical settings including bacterial sepsis, severe trauma including surgical trauma and burns, multiple transfusions, and severe debilitation. The lesion in the gallbladder consists of intense injury of blood vessels in the muscularis and serosa similar to those induced experimentally by in vivo activation of factor XII dependent pathways. Possibly because of the intensity of vascular injury, acute acalculous cholecystitis with minimal clinical manifestations may rapidly progress to gangrene with perforation. Undelayed surgical treatment, which has become more widely accepted over the past 50 years, is essential. It may have also contributed to the increased recognition of this clinical entity.
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