- 90% to 95% of cases of cholecystitis are calculous in origin.
- 5% to 10% of the cases and is acalculous cholecystitis more common in critically ill trauma, burn, and sepsis patients and individuals with cardiac, diabetic, and acquired immunodeficiency syndrome conditions.This type is higher incidence of gangrene, emphysematous infection, perforation, and mortality
Stagnation of bile and resultant infection from an impacted gallstone was
once thought to be the main pathophysiology in the development of cholecystitis.
However, studies investigating bile cultures have shown that only 15% to 30% of
patients undergoing cholecystectomy for cholecystitis have positive bile
cultures. This indicates that inflammation of the gallbladder is
not simply an infectious process but rather a multifactorial series of events
that are initiated by gallstone obstruction of the cystic duct. A well-described
“ball-valve” mechanism has been attributed to the characteristic pain. Initially, a gallstone
impacts at the neck of the gallbladder leading to obstruction and wall edema.
This leads to the formation of lysolecithin, a mucosal toxin. Prostaglandin
synthesis increases and amplifies the inflammatory response. The edema and
inflammation can then result in the lifting of the gallbladder wall away from
the stone, thereby disimpacting the stone and effecting drainage through the
cystic duct. In most patients this series of events plays through and
conservative management is effective. In some patients, however, disimpaction
does not occur, and this results in continued cystic duct obstruction and leads
to venous congestion, gallbladder ischemia, biliary stasis, and a systemic
inflammatory response that necessitates operative intervention.
Anatomic relationships of the gallbladder
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