Acalculous Gangrenous Cholecystitis in Absence of Typical Risk Factors

Abstract

Acute acalculous cholecystitis (AAC) is typically seen as a complication in severely ill, hospitalized patients. We report a case of acute gangrenous acalculous cholecystitis in an outpatient. 47-year-old African-American male presented with acute onset of epigastric abdominal discomfort and multiple episodes of vomiting persisting over one day. He denied having any fever or chills, change in bowel habits, dysphagia, weight loss, change in appetite, blood in stools, recent travel history or NSAID/alcohol use. He had a history of hypertension and hyperlipidemia. On exam, he was afebrile, BP 100/60 mmhg, HR 110 /min. He had tenderness in the epigastrium and right upper quadrant of his abdomen. Murphy's sign was positive. The initial blood tests including liver function tests and lipase were normal except for an elevated white cell count. An US of RUQ was obtained revealed, gall bladder wall thickening along with edema and pericholecystitc fluid collection. No gall stones were seen. Blood cultures were obtained, and the patient was started on antibiotics empirically. A HIDA scan revealed no uptake of contrast in the gall bladder one hour after contrast admission, confirming the diagnosis of AAC. Surgery was consulted and cholecystectomy was performed. Removed gall bladder appeared inflamed with early signs of gangrene. Acute acalculous cholecystitis (AAC) is defined as inflammation of the gall bladder without presence of gallstones. It is typically seen in severely medically or surgically ill, hospitalized patients. Altthough not common, cases of AAC in out patients with no significant risk factors have been reported. Physical examination and laboratory data are often unreliable in diagnosis of AAC, and diagnosis mainly rests on imaging studies. AAC has an extremely fulminant course leading to gall bladder gangrene in 50% of patients and perforation in 10 % of patients. Even with treatment, the mortality rate is about 30%. Hence, early diagnosis and treatment are warranted. In very few patients, atherosclerosis-causing changes in microcirculation of gall bladder, atherosclerotic changes can leading to ischemia at cellular level, thereby causing inflammation have been postulated to be causing AAC. Our patient presented in the outpatient setting and was diagnosed to have acute gangrenous acalculous cholecystitis. Given the high mortality rates AAC should be kept in dfferentials even in the outpatient settings.