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Query: UMLS:C0008325 (cholecystitis)
 3,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is ample evidence from this retrospective comparison to indicate that emphysematous cholecystitis does merit clinical distinction apart from acute cholecystitis. It is an acute infection of the gallbladder caused by a specific group of bacteria that may be aided by some aspect of local ischemia. Cholelithiasis does not seem to be a major factor in the pathogenesis of emphysematous cholecystitis, and this, in association with some dependence upon ischemia, may account for the predominance of this disease in males rather than females. Gangrene is a common feature of the pathologic process, and thus it is not surprising that the diagnosis of emphysematous cholecystitis implies a risk of gallbladder perforation that is five times that expected from ordinary acute cholecystitis. The key to identifying this disease is the plain abdominal roentgenogram which in most instances will make the diagnosis and provide an impetus for early operative intervention.
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PMID:A comparative appraisal of emphysematous cholecystitis. 17 53

Temporary ischemia of the gall bladder was induced in rabbits by ligation of the gall bladder artery with silk. Histological examination revealed vascular disorders, such as hyperemia, blood stasis and focal hemorrhages. Electron microscopic studies showed the presence of increased number dark epithelial cells, expansion of intercellular area, loosening of the basal membrane and defects in it with invagination of the epithelial cells into the submucous layer. The most striking changes were discovered after a thrice-repeated 30-minute occlusion of the gall bladder artery. The degree of destructive changes proved to depend on the number of stimulated spasms (occlusions) and not on the duration of ischemia. This gives grounds to believe that multiple circulatory disorders participated in the complicated pathogenesis of cholecystitis.
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PMID:[Ultrastructural changes in the gallbladder mucous membrane during temporary experimental ischemia]. 127 60

Ischemia is one mechanism implicated in the pathogenesis of acute acalculous cholecystitis. Gallbladder specimen arteriography was performed to define the comparative status of cystic artery runoff in the macroscopically normal gallbladder (n = 10), in acute gallstone-associated cholecystitis (n = 10), and in acute acalculous cholecystitis (n = 7). Standardized film exposure and quantity of contrast medium administered permitted objective intergroup comparison. Compared to the macroscopically normal gallbladder, specimens of acute gallstone-associated cholecystitis exhibited arterial dilatation and extensive venous filling. In contrast, multiple arterial occlusions, with absent or minimal venous filling, were consistent features of acute acalculous cholecystitis; the degree of arteriographic abnormality for acute acalculous cholecystitis corresponded to the severity of gallbladder pathologic findings. Small vessel occlusion, on the basis of low splanchnic flow or intravascular coagulation, may be a fundamental element in the pathogenesis of acute acalculous cholecystitis.
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PMID:Small vessel occlusion in acute acalculous cholecystitis. 173 86

To elucidate the pathogenesis of acute acalculous cholecystitis, the gallbladder was subjected to ischemia-reperfusion by simultaneously occluding the middle hepatic artery and the superior mesenteric vein in dogs, and the degree of inflammation and biochemical changes in the gallbladder mucosa were studied by varying the duration of ischemia or reperfusion. Ischemia alone did not induce cholecystitis either macroscopically and histologically, although it increased phospholipase A2 (PLA2) activity, content of lipid peroxide, and superoxide dismutase (SOD) activity in the mucosa with prolongation of the ischemic time. Cholecystitis was produced in all animals by 45-min ischemia followed by 90-min reperfusion as the shortest ischemia and reperfusion times. In this model, prolongation of the ischemic time increased the area of mucosal inflammation horizontally with increases of the PLA2 activity, content of lipid peroxide, and SOD activity, whereas by prolonging the reperfusion time the inflammation area spread deeper vertically toward the serosal side with significant increase in the mucosal PLA2 activity, content of lipid peroxide, and SOD activity. These results revealed that ischemia-reperfusion plays an important role in the pathogenesis of acute acalculous cholecystitis, causing the generation of free radicals and the activation of membrane-bound PLA2.
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PMID:Experimental study on the pathogenesis of acute acalculous cholecystitis, with special reference to the roles of microcirculatory disturbances, free radicals and membrane-bound phospholipase A2. 175 95

Acute acalculous cholecystitis is a virulent disease of uncertain etiology observed most commonly in critically ill patients. Although the precise mechanism is unknown, the most commonly postulated theories regarding its pathogenesis are bile stasis, sepsis, and ischemia. The role of ischemia in this process, whose etiology is multifactorial, has been difficult to elucidate. Consequently, we report two patients who developed acute acalculous cholecystitis without apparent risk for the disease other than severe visceral atherosclerosis. Both patients had symptomatic mesenteric vascular disease requiring revascularization and developed fulminant acalculous cholecystitis temporally related to exacerbation of their visceral ischemia. These cases suggest that patients with visceral atherosclerosis may be at increased risk for acute acalculous cholecystitis, perhaps due to impaired mucosal resistance when other factors, such as bile statis and sepsis, are also present.
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PMID:Does visceral ischemia play a role in the pathogenesis of acute acalculous cholecystitis? 230 85

The authors report the surgical management of 19 patients with chronic intestinal ischemia over the last ten years. There were 11 women and 8 men (mean age 59 years). Most patients (13/19) suffered from widespread generalized atheromatosis. Fifteen patients had symptoms which were mostly aspecific and insidious in onset. In 8 cases, there was previous misdiagnosis when pain was considered as peptic ulcer or cholecystitis, which explains a mean delay of 18 months between the onset of symptoms and angiographic evidence of coeliomesenteric stenosis. Four patients were asymptomatic and underwent a prophylactic splanchnic revascularization during aorto-iliac or aorto-renal surgery. Obstructive lesions were limited to one single digestive artery in 9 patients, 2 arteries in 7 patients and all 3 arteries in 3 patients. Twenty-two operations for coeliomesenteric revascularization were performed: 16 venous bypasses, 1 prosthetic bypass, 6 thrombendarterectomies, and 5 arterial reimplantations. Nine bypasses were retrograde versus 8 anterograde. A mean of 1.5 visceral arteries was revascularized per patient. Complete revascularization of all 3 splanchnic vessels was obtained in 73% of the cases. Operative mortality (30 days) was 16% (3 cases). Mean follow-up is 3 years. There was no single late mesenteric infarction. Four patients died of non-related causes (3 cardiac, 1 cerebrovascular), and 84% of the survivors are completely symptom free since the operation.
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PMID:[Surgical treatment of chronic mesenteric ischemia]. 248 11

Acute acalculous cholecystitis is common, accounting for 5% to 10% of cases of acute cholecystitis. Although originally attributed to stasis and inspissated bile with subsequent obstruction of the cystic duct, acalculous cholecystitis has more recently been attributed to gallbladder ischemia from such conditions as hypotension or vasculitis. However, a significant number of cases of acute acalculous cholecystitis occur with no obvious cause. This report notes acute acalculous cholecystitis, diagnosed in 12 patients from 1982 to 1987, that was apparently precipitated by initiation of antibiotic therapy. Histologic sections of these gallbladders each disclosed a massive eosinophilic infiltrate. Two of the patients had identical signs, symptoms, and abnormal laboratory values during a previous course of erythromycin. These findings subsided when the antibiotic therapy was discontinued. We hypothesize that a significant cause of acute acalculous cholecystitis may be a hypersensitivity reaction to concurrent antibiotic therapy. Such patients should have antibiotic therapy halted or altered, which, it is hoped, will result in resolution of symptoms and avoidance of unnecessary laparotomy.
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PMID:Acalculous hypersensitivity cholecystitis: hypothesis of a new clinicopathologic entity. 318 4

Posttraumatic acute cholecystitis is an often unrecognized and potentially fatal complication seen among patients hospitalized for trauma, and differs in etiology from cholecystitis which develops de novo. The cause, although not yet clearly defined, is believed to be related to bile stasis, ischemia, bacterial infection, sepsis, the activation of factor XII, and the Shwarzman reaction. A case is described in which a 53-year-old man with pelvic fractures developed acute acalculous cholecystitis and died of multiple organ failure 3 weeks following cholecystectomy. The histopathological findings are also reported; these are most likely attributed to the Shwarzman reaction or the activation of the factor XII pathways. There has been a tendency to regard posttraumatic acute acalculous cholecystitis as induced by trauma, and calculous as mere coincidence. We believe, however, that it is not calculous but histopathological findings that determine whether acute cholecystitis following trauma was more than coincidence or just mere coincidence. Although progress in clinical care has improved the chances of survival of severely traumatized patients, posttraumatic acute cholecystitis has been increasing in frequency. We cannot be careful enough in judging the relationship of this fatal complication to the initial trauma.
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PMID:Posttraumatic acute cholecystitis. Relationship to the initial trauma. 360 14

Extrahepatic manifestations due to an immunologic response to a surface antigen of hepatitis B virus have been identified. These include a serum sicknesslike syndrome and a necrotizing vasculitis. The latter is far more important and in indistinguishable histologically from nonhepatitis related polyarteritis. At least 90 cases have been reported in the decade since 1970, and five are added here. The necrotizing vasculitis syndrome results from fibrinoid necrosis and inflammation of small and medium-sized arterial walls recognizable angiographically by arterial microaneurysms and often by visceral infarction and hemorrhage. Renal failure is common and often associated with pulmonary edema. Gastrointestinal symptoms are a prominent feature due to bowel ischemia. Infarction and perforation are significant causes of morbidity and mortality. Necrotizing vasculitis is also one cause of pancreatitis and of cholecystitis. Plain films, contrast studies, computed tomography, and sonography have been shown to be useful in the recognition of these complications.
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PMID:Radiologic recognition of extrahepatic manifestations of hepatitis B antigenemia. 611 55

Nine cases of acute acalculous cholecystitis were diagnosed in the surgical intensive care unit at Hartford Hospital during a 2 year period after abdominal, cardiovascular, and traumatic surgery. A tender mass in the right upper quadrant was suggestive but not diagnostic of the condition. Hyperamylasemia was seen in all patients. Ultrasonography is the most useful diagnostic tool; serial studies reveal progressive gallbladder dilatation and edema. Tube cholecystostomy was used in five patients and cholecystectomy in four. Cholecystostomy led to resolution of the inflammatory process in all five patients. Cholecystectomy should be reserved for those patients with extensive gallbladder necrosis. Six of the nine patients in the series died, all from multiple systems failure with concomitant sepsis. Hypotension is probably central to the development of acute acalculous cholecystitis. In the face of elevated intraluminal gallbladder pressure caused by ampullary edema and increased bile viscosity, hypotension may result in mucosal ischemia and necrosis with subsequent bacterial colonization. Acute acalculous cholecystitis represents another organ failure in critically ill patients who are experiencing progressive failure of multiple organ systems. An aggressive approach to the manifestations of organ failure, including acalculous cholecystitis, must be employed.
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PMID:Acute acalculous cholecystitis in the critically ill patient. 618 83


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