Arterial Bypass for Chronic Mesenteric Ischemia

Chronic mesenteric ischemia (CMI) is a relatively rare, potentially lethal, and often misdiagnosed condition caused by fixed stenosis or occlusion of the proximal splanchnic arteries. It is estimated to account for less than 1 in 100,000 hospital admissions in the United States. The earliest description of CMI as a clinical disorder dates to the early 20th century, but it was Dunphy who in 1936 recognized the association of mesenteric ischemic symptoms with atherosclerosis of the mesenteric arteries.

Chronic mesenteric ischemia is caused by atherosclerotic occlusive disease in 90% to 95% of patients. A minority of cases are secondary to arterial fibrodysplasia, external compression (median arcuate ligament syndrome), Takayasu’s disease and other vasculitides, dissection, embolic disease, drug effect (digitalis, cocaine), and radiation. Atherosclerotic plaque typically involves the ostium of the mesenteric arteries. Patients often manifest advanced systemic atherosclerosis at a relatively young age in their fifth or sixth decade, and women are afflicted three to four times more commonly than men.

The estimated prevalence of anatomically significant mesenteric arterial occlusive disease is quite high, with stenoses or occlusions of the splanchnic arteries found in up to one fifth of autopsies, aortograms, or vascular ultrasound examinations performed in atherosclerotic populations. Only a minority of patients with documented greater than 50% stenosis of the celiac artery or superior mesenteric artery (SMA) develop symptoms of intestinal ischemia during the following years, lending a relatively benign natural history to asymptomatic splanchnic arterial occlusive disease. There is little correlation between significant occlusive disease in the mesenteric vessels and clinical symptoms of chronic intestinal angina. This lack of correlation between significant anatomic splanchnic arterial stenoses and symptoms is related to variations in the rich collateral network connecting the three vascular territories responsible for intestinal perfusion.

The small and large bowel receives 10% to 15% of the cardiac output at rest, but postprandial flow increases up to 35% of the cardiac output, with 70% of the mesenteric blood flow supplying the intestinal mucosa and submucosa. Multiple collateral pathways can develop between the main vessels to compensate for stenosis in any given mesenteric artery. In certain cases the absence of a collateral network caused by previous surgical intervention or anatomic variation can result in symptomatic visceral ischemia with single-vessel disease.