Abstract

Although the prevalence of mesenteric artery stenoses (MAS) is high, symptomatic chronic mesenteric ischemia (CMI) is rare. The collateral network in the mesenteric circulation, a remnant of the extensive embryonal vascular network, serves to prevent most cases of ischemia. This explains the high incidence of MAS and relative rarity of cases of CMI. The number of affected vessels is the major determinant in CMI development. Most subjects with single vessel mesenteric stenosis do not develop ischemic complaints. Our experience is that most subjects with CA and SMA stenoses with abdominal complaints have CMI. A special mention should be made on patients with median arcuate ligament compression (MALS). There is ongoing debate whether the intermittent compression, caused by respiration movement, can cause ischemic complaints. The arguments pro and con treatment of MALS will be discussed. The clinical presentation of CMI consists of postprandial pain, weight loss, and an adapted eating pattern caused by fear of eating. In end-stage disease more continuous pain, diarrhea or a dyspepsia-like presentation can be observed.Workup of patients suspected for CMI consists of three elements: the anamnesis, the vascular anatomy and proof of ischemia. The main modalities to establish mesenteric vessel patency are duplex ultrasound, CT angiography or MR angiography. Assessing actual ischemia is still challenging, with only tonometry and visual light spectroscopy as tested candidates.Treatment consists of limiting metabolic demand, treatment of the atherosclerotic process and endovascular or operative revascularisation. Metabolic demand can be reduced by using smaller and more frequent meals, proton pump inhibition. Treatment of the atherosclerotic process consists of cessation of smoking, treatment of dyslipidemia, hypertension, hyperglycaemia, and medication with trombocyte aggregation inhibitors.

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