Acute calculous cholecystitis initially results from chemical irritation and inflammation of the gallbladder wall due to obstruction of bile outflow. Gallbladder injury in the setting of bile obstruction stems from several sources, including: phospholipases derived from the mucosa hydrolyze biliary lecithin to lysolecithin, which is toxic to the mucosa; the normally protective glycoprotein mucous layer is disrupted, exposing the mucosal epithelium to the detergent action of bile salts.; prostaglandins released within the wall of the distended gallbladder enhance mucosal and mural inflammation; and distention and increased intraluminal pressure may compromise blood flow to the mucosa. All of these effects occur in the absence of bacterial infection, which may be superimposed later.
Between 5% and 12% of gallbladders removed for acute cholecystitis contain no gallstones. Most cases occur in seriously ill patients. Some of the most common predisposing insults are as follows:
Severe trauma (e.g., from motor vehicle crashes)
Other contributing factors include dehydration, gallbladder stasis and sludging, vascular compromise, and bacterial contamination.
Chronic cholecystitis may be the sequel to repeated bouts of acute cholecystitis, but in most instances it develops without any antecedent history of acute attacks. Like acute cholecystitis, it is almost always associated with gallstones. However, gallstones do not seem to be an essential part of the initiation of inflammation or the development of pain, because chronic acalculous cholecystitis causes symptoms and morphologic alterations similar to those seen in the calculous form. Rather, supersaturation of bile appears to predispose to both chronic inflammation and, in most instances, stone formation. Microorganisms, usually E. coli and enterococci, can be cultured from the bile in only about one-third of cases. Unlike acute calculous cholecystitis, obstruction of gallbladder outflow by stones is not requisite in chronic cholecystitis. Most gallbladders removed at elective surgery for gallstones show features of chronic cholecystitis, making it likely that biliary symptoms emerge after long-term coexistence of gallstones and low-grade inflammation.
MORPHOLOGYInacute cholecystitis, thegallbladderusuallyisenlargedandtense,andhasabrightredorblotchy,violaceouscolor,thelatterimpartedbysubserosalhemorrhages.Theserosafrequentlyiscoveredbyafibrinousor,inseverecases,afibrinopurulentexudate.In90%ofcases,stonesarepresent,oftenobstructingtheneckofthegallbladderorthecysticduct.Thegallbladderlumenisfilledwithcloudyorturbidbilethatmaycontainfibrin,blood,andpus.Whenthecontainedexudateismostlypus,theconditionisreferredtoasempyema of the gallbladder. Inmildcases,thegallbladderwallisthickened,edematous,andhyperemic.Inmoreseverecases,thegallbladderwallisgreen-blackandnecrotic—aconditiontermedgangrenous cholecystitis. Onhistologicexamination,theinflammatoryreactionsarenotdistinctiveandconsistofsomecombinationoftheusualpatternsofacuteinflammation(i.e.,edema,leukocyticinfiltration,vascularcongestion,abscessformation,gangrenousnecrosis).