A 46-year-old woman comes to the emergency department due to 3 days of persistent upper abdominal pain, nausea, and vomiting. The patient has had similar pain in the past, especially after fatty meals, which resolved spontaneously within several hours. Temperature is 38.6 C (101.5 F), blood pressure is 110/65 mm Hg, and pulse is 98/min. BMI is 33 kg/m². Physical examination is notable for severe right upper quadrant tenderness. Leukocyte count is 21,000/mm³. Laparoscopic surgery is performed and reveals an erythematous, distended gallbladder with patchy necrosis. Which of the following events most likely initiated this patient's condition?

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This patient likely has acute calculous cholecystitis, an acute inflammation of the gallbladder initiated by gallstone obstruction of the cystic duct. Patients typically present with persistent right upper quadrant pain, fever, and leukocytosis. Examination classically shows Murphy sign, an inspiratory pause elicited by pain during deep palpation of the right upper quadrant. Symptoms are often preceded by transient episodes of abdominal pain and nausea after fatty meals due to temporary cystic duct obstruction (biliary colic). Persistent gallbladder outflow obstruction promotes hydrolysis of luminal lecithins to lysolecithins, which disrupts the protective mucus layer. The luminal epithelium is then exposed to the detergent action of the bile salts, resulting in chemical irritation and prostaglandin release. Inflammation of the mucosa and deeper tissues causes gallbladder hypomotility. The increasing distension and internal pressure within the gallbladder eventually result in ischemia. Finally, bacteria (eg, Escherichia coli, Enterococcus, Klebsiella, Enterobacter) invade the injured and necrotic gallbladder wall, causing an infection (Choice A). (Choices B and D) The gallbladder is vulnerable to ischemic injury as the cystic artery lacks collateral circulation. Although inflammation/edema of the gallbladder may compromise blood flow, ischemic disruption of the mucosal layer is usually the next to last step in the pathogenesis of acute calculous cholecystitis. Gallbladder ischemia is not typically caused by cystic artery thrombosis. (Choice E) Lecithin hydrolysis and mucosal damage occur after gallbladder outflow obstruction in the pathogenesis of acute calculous cholecystitis. Educational objective: Acute calculous cholecystitis is an acute inflammation of the gallbladder initiated by gallstone obstruction of the cystic duct. Subsequent steps in pathogenesis include mucosal disruption by lysolecithins, bile salt irritation of the luminal epithelium, prostaglandin release with transmural inflammation, gallbladder hypomotility, increased intraluminal pressure causing ischemia, and bacterial invasion. __________ References: Acute cholecystitis. (http://www.ncbi.nlm.nih.gov/pubmed/12242178)

A 46-Year-Old Woman Comes to the Emergency Department Due to 3