Chronic Mesenteric Ischaemia

Chronic mesenteric ischaemia is insufficient intestinal blood flow during increased metabolic demand, most commonly caused by atherosclerotic stenosis of the superior mesenteric and coeliac arteries.

Extensive collateral circulation means symptoms usually develop only when perfusion reserve becomes significantly impaired. Symptomatic disease is important because continued weight loss and malnutrition are common and plaque thrombosis can cause acute on chronic mesenteric ischaemia.

A symptomatic isolated stenosis of approximately 70% or more may be clinically relevant. In multivessel disease, a superior mesenteric artery stenosis of approximately 50% or more may be clinically significant when symptoms are convincing.

The typical syndrome is postprandial epigastric or central abdominal pain beginning after food intake and lasting from tens of minutes to several hours.

Progressive food avoidance produces weight loss. Weight loss greater than 5% with typical postprandial symptoms should increase suspicion substantially. Diarrhoea, nausea and early satiety may accompany the syndrome.

The classical triad of postprandial pain, weight loss and abdominal bruit has poor sensitivity. Its absence does not exclude disease.

Sudden intensification of chronic symptoms, continuous pain or development of tenderness should trigger immediate assessment for acute thrombosis.

CT angiography: first line anatomical investigation; defines coeliac and superior mesenteric artery disease and guides revascularisation planning. Contrast enhanced MR angiography is appropriate when CT contrast cannot be used.

Duplex ultrasound can screen for proximal arterial stenosis in experienced centres but a positive result requires definitive cross sectional vascular imaging.

Chronic mesenteric ischaemia should not be diagnosed from an incidental stenosis alone. Correlate arterial disease with a compatible symptom complex and exclude competing gastrointestinal causes.

Symptomatic atherosclerotic chronic mesenteric ischaemia requires revascularisation rather than nutritional treatment alone.

Do not delay revascularisation solely to achieve weight restoration. The postprandial perfusion deficit is the reason the patient cannot maintain nutrition.

Endovascular revascularisation is generally preferred because of lower early procedural morbidity. Angioplasty with stenting is preferred over angioplasty alone for atherosclerotic mesenteric lesions. When one vessel is targeted, the superior mesenteric artery is the priority vessel.

Open mesenteric bypass remains appropriate in fit patients with anatomy unsuitable for endovascular treatment, failed endovascular therapy or durable reconstruction requirements.

After mesenteric artery stenting, a practical antiplatelet regimen is:

Aspirin 75 to 100 mg orally once daily plus clopidogrel 75 mg orally once daily for at least 1 month, followed by lifelong single antiplatelet therapy, usually aspirin.

Patients already requiring therapeutic anticoagulation generally need only one additional antiplatelet agent for approximately 4 weeks after stenting rather than prolonged triple therapy.

Treat the systemic atherosclerotic disease aggressively with smoking cessation, blood pressure control, diabetes management and high intensity lipid lowering therapy according to cardiovascular prevention targets. Secondary cardiovascular prevention should begin as soon as atherosclerotic chronic mesenteric ischaemia is diagnosed.

Recurrent postprandial symptoms after treatment should prompt evaluation for restenosis using duplex ultrasound or CT angiography.