Case Presentation: Chronic mesenteric ischemia (CMI) is defined as a gradual reduction of perfusion to the bowels. While bowel infarction is the primary concern with CMI, there may be a relationship between CMI and acute acalculous cholecystitis (AAC). We present the case of a 60-year old female with acute onset right upper quadrant (RUQ) abdominal pain. The patient had an identical episode a few months ago that self-resolved. She also had a one year history of epigastric abdominal pain, food aversion, and unintentional weight loss. Previous workup had revealed thrombus of the proximal superior mesenteric artery (SMA).Physical exam demonstrated RUQ tenderness and a positive Murphy’s sign. Pertinent lab findings included alkaline phosphatase of 200. Remaining liver enzymes were normal. Computed tomography (CT) abdomen pelvis and RUQ ultrasound revealed a distended gallbladder (GB) with mild wall thickening, pericholecystic inflammatory fat stranding, internal sludge, and re-demonstration of prior SMA thrombosis. HIDA scan was unremarkable. A multidisciplinary clinical decision opted for SMA angiography with stenting, holding off on cholecystectomy given the interpretation that the GB was hydropic but not profoundly inflamed. Due to difficulty gaining distal access, the procedure was converted to an open approach, revealing a grossly necrotic gallbladder without stones. SMA endarterectomy and open cholecystectomy ensued, with pathology demonstrating acute gangrenous cholecystitis. Postoperative course was uncomplicated.
Discussion: AAC is a rare phenomenon that most often presents in critically ill patients. Dramatic weight loss, long hospital stays, major surgery, and trauma predispose patients to GB stasis. The continuous build-up of intraluminal pressure and bacterial colonization leads to GB ischemia and inflammation. Emerging evidence hints at a possible relationship between CMI and AAC. Previous case reports have shown that AAC may develop as a result of worsening mesenteric ischemia. A seven-year study analyzing AAC patients found that 72% had significant vascular disease. AAC has also been speculated to be a presenting sign of life-threatening mesenteric ischemia in the elderly. In patients with severe symptoms of mesenteric ischemia, clinicians should remain aware that AAC can develop. AAC in the setting of mesenteric ischemia is primarily treated with emergent cholecystectomy. This raises the question: does emergent mesenteric revascularization also need to be attempted in these patients? As previously discussed, AAC diagnosed in conjunction with mesenteric ischemia, may be a marker to impending bowel infarction. Therefore, it may be valuable to attempt revascularization efforts immediately following cholecystectomy.
Conclusions: This case seeks to explore the relationship between CMI and AAC. Severe CMI may lead to AAC, and AAC may indicate impending bowel infarction. Understanding this relationship has implications for clinical management and warrants further investigation.