• Hadley Cadot, Michael D Addis, Peter L Faries, Alfio Carroccio, James A Burks, Edwin C Gravereaux, Nicholas J Morrissey, Victoria Teodorescu, Salvatore Sparacino, Larry H Hollier, and Michael L Marin.
• Department of Surgery, Mount Sinai School of Medicine, New York, New York 10029-6501, USA.
• Am Surg. 2002 Oct 1;68(10):839-43; discussion 843-4.

AbstractThe incidence of acute cholecystitis complicating standard abdominal aortic aneurysm (AAA) repair has been reported between 0.3 and 18 per cent. This has prompted considerable debate regarding the management of cholelithiasis discovered incidentally during open aortic reconstruction. This study seeks to determine the incidence of cholelithiasis and acute cholecystitis after endovascular AAA repair and evaluate options for management. Between February 1996 and October 2001 492 patients underwent endovascular AAA repair. All the procedures were performed in the operating room under fluoroscopic guidance. Epidural (98.9%), local (0.5%), or general (1.7%) anesthesia was used during these cases. The incidence of cholelithiasis and acute cholecystitis was evaluated by CT scan and abdominal ultrasound. Serum measurements of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total and direct bilirubin, and amylase were performed and clinical assessment was conducted at 1, 6, and 12 months postoperatively and annually thereafter. The mean age of these patients was 76.6 years; 84% were male. Comorbid medical conditions were present in all patients (average 3.5 conditions/patient). Follow-up ranged from 2 to 35 months (mean 12.8 months). Endovascular stent graft deployment was successful in 486 of the 492 patients (98.8%). Six patients were converted to standard open repair because of inability to achieve successful endovascular aneurysm repair. The perioperative major morbidity rate was 14.9 per cent. Minor morbidity rate was 8.5 per cent. The perioperative mortality rate was 1.9 per cent. No deaths were related to biliary disease. Cholelithiasis was identified in 64 (13%) patients preoperatively. One of 64 patients with a prior Billroth II reconstruction for peptic ulcer disease developed jaundice 8 days after AAA repair as a result of choledocholithiasis that required surgical repair. One patient without gallstones developed acute acalculous cholecystitis on postoperative day 16 as determined on pathologic analysis of the gallbladder. A third patient who had gallstones identified on preoperative CT scan developed calculous cholecystitis 16 months after endovascular AAA repair. These two patients underwent uncomplicated laparoscopic cholecystectomy and recovered uneventfully. The incidence of postoperative symptomatic cholelithiasis is 1.6 per cent (one of 64). The incidence of postoperative acute cholecystitis was 0.2 per cent (one of 486) and was unrelated to the presence of gallstones. The incidence of delayed symptomatic cholelithiasis was 1.6 per cent (one of 64). Endovascular repair of AAA does not appear to predispose the patient to the development of symptomatic cholelithiasis during the perioperative period. Therefore a preoperative or intraoperative diagnosis of cholelithiasis does not necessitate cholecystectomy in the setting of planned endovascular AAA repair. Patients who develop cholecystitis after endovascular AAA repair may be effectively treated by standard laparoscopic techniques.

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