A 52-year-old woman presents to the emergency department with severe right upper quadrant pain radiating to the right shoulder, nausea, and vomiting for 8 hours following a fatty meal. On examination, she has a fever of 38.5°C, RUQ tenderness with guarding, and a positive Murphy's sign. Ultrasound of the abdomen shows the findings marked as **B** in the diagram. Which of the following best describes the pathophysiological mechanism underlying the acute inflammation seen in this case?
A. Direct bacterial invasion of the gallbladder wall by enteric organisms without preceding stone impaction
B. Sustained cystic duct obstruction by an impacted gallstone leading to mucosal injury and release of phospholipase, which hydrolyzes biliary lecithin into toxic lysolecithin
C. Chronic irritation of the gallbladder mucosa by cholesterol crystals without any mechanical obstruction
D. Acute ischemia of the gallbladder wall due to vasculitis in a critically ill patient
Explanation
Why sustained cystic duct obstruction with phospholipase-mediated injury is right
The clinical presentation (severe RUQ pain >4–6 hours after fatty meal, fever, positive Murphy's sign, leukocytosis) combined with ultrasound findings of B — acute calculous cholecystitis with gallstone, wall thickening, pericholecystic fluid, and positive Murphy's sign — defines acute calculous cholecystitis. The Tokyo Guidelines TG18 and Sabiston 21e confirm that >90% of acute cholecystitis is acute calculous cholecystitis caused by sustained obstruction of the cystic duct by an impacted gallstone at the gallbladder neck or Hartmann's pouch. The trapped bile under pressure causes mucosal injury, releasing phospholipase A2, which hydrolyzes biliary lecithin into toxic lysolecithin — the key initiating mechanism of acute inflammation. Secondary bacterial superinfection (E. coli, Klebsiella, Enterococcus) develops in ~50% within 48 hours, explaining the fever and leukocytosis.
Why each distractor is wrong
Direct bacterial invasion without stone obstruction: This describes acalculous cholecystitis, which accounts for only ~10% of acute cholecystitis and occurs in critically ill patients (ICU, sepsis, major surgery, TPN), not in an ambulatory patient with a clear precipitant (fatty meal) and imaging evidence of a stone.
Acute ischemia in a critically ill patient: This is the mechanism of acalculous cholecystitis due to gallbladder ischemia and gangrene in septic or post-operative patients. The patient in this case is not critically ill and has a visible gallstone on ultrasound, making acute calculous cholecystitis the diagnosis.
Chronic irritation by cholesterol crystals without obstruction: This describes chronic cholecystitis (marked as A in the diagram), which presents with chronic intermittent symptoms and wall thickening alone without acute inflammation, pericholecystic fluid, or positive Murphy's sign.
