Managing patients with acute type A aortic dissection and mesenteric malperfusion syndrome: A 20-year experience.

Abstract

To assess outcomes of endovascular reperfusion followed by delayed open aortic repair for stable patients with acute type A aortic dissection and mesenteric malperfusion syndrome (mesMPS). Among 602 patients with acute type A aortic dissection who presented to our center from 1996 to 2017, all 82 (14%) with mesMPS underwent upfront endovascular fenestration/stenting. Primary outcomes were in-hospital mortality and long-term survival. Patients with acute type A aortic dissection with no malperfusion syndrome of any organ (n = 419) served as controls. In-hospital mortality of all comers with mesMPS was 39%. After endovascular fenestration/stenting, 20 mesMPS patients (24%) died from organ failure and 11 patients (13%) died from aortic rupture before open aortic repair, 47 patients (58%) underwent aortic repair, and 4 patients (5%) survived without open repair. No patients died from aortic rupture during the second decade (2008-2017). The significant risk factors for death from organ failure after endovascular reperfusion were acute stroke (odds ratio, 23; 95% confidence interval, 4-144; P = .0008), gross bowel necrosis at laparotomy (odds ratio, 7; 95% confidence interval, 1.4-34; P = .016), and serum lactate ≥6 mmol/L (odds ratio, 13.5; 95% confidence interval, 2-97; P = .0097). There was no significant difference in operative mortality (2.1% vs 7.5%; P = .50) or long-term survival between patients with mesMPS who underwent open aortic repair after recovering from mesMPS and patients with no malperfusion syndrome. In patients with acute type A aortic dissection with mesMPS, endovascular fenestration/stenting, and delayed open aortic repair achieved favorable short- and long-term outcomes. Surgeons should consider correcting mesenteric malperfusion before undertaking open aortic repair in patients with mesMPS, especially those with acute stroke, gross bowel necrosis at laparotomy, or serum lactate ≥6 mmol/L.