Chronic intestinal ischemia results from atherosclerotic occlusive lesions at the origins of the superior mesenteric artery (SMA), celiac artery, and inferior mesenteric artery (IMA). Because of collateral flow via the middle colic artery branch of the SMA and the ascending colic artery of the IMA, the superior and inferior pancreaticoduodenal arteries, and the superior and inferior hemorrhoidal arteries, bowel ischemia does not occur until two of the three main visceral arteries are diseased severely. In fact, almost 30% of patients with peripheral vascular disease have asymptomatic occlusive disease of the mesenteric arteries. Symptoms consist of postprandial epigastric pain, and at later stages, food avoidance (sitophobia), resulting in weight loss. Chronic intestinal ischemia is a diagnosis of exclusion, derived after a negative workup for peptic ulcer disease, gastroesophageal reflux, pancreatitis, irritable bowel syndrome, and malignancy. A suggestive history in a person over 45 years of age who appears chronically ill, has risk factors for arterial occlusive disease, and has no other identifiable cause for abdominal symptoms is an indication for arteriography. Intravenous hydration must be provided to avoid acute bowel ischemia from catheter-induced or contrast-associated arterial spasm. Surgical or endovascular management is directed toward restoration of antegrade visceral arterial flow. Transaortic endarterectomy and mesenteric artery bypass are associated with a 5-9% mortality rate and a 10-25% recurrence rate at long-term follow-up. A higher recurrence rate is observed with stenting of short-segment lesions; these patients require routine angiographic follow-up. Survivors have an unexpectedly good long-term life expectancy.

Celiac axis compression syndrome (stenosis of the celiac artery caused by external compression of the arcuate ligament) has been described as a variant of chronic mesenteric ischemia. As an isolated entity, it is occasionally associated with cramping abdominal pain, nausea, vomiting, and diarrhea. Division of the arcuate ligament may be combined with celiac artery dilation. The pathophysiological basis for this disease remains elusive.

Acute intestinal ischemia may result from (1) embolic occlusion of a visceral branch of the abdominal aorta, generally in patients with mitral valvular disease, atrial fibrillation, or left ventricular mural thrombus; (2) thrombosis of an atherosclerotic mesenteric vessel; (3) low-flow or shock state due to cardiac failure or arterial spasm induced by ergot or cocaine intoxication; or (4) postcoarctectomy syndrome, producing nonocclusive mesenteric vascular insufficiency. Emboli are responsible for almost half of all cases. Symptoms include sudden onset of severe epigastric and periumbilical abdominal pain with minimal appreciable findings on abdominal examination (“pain out of proportion to physical findings”) and a high leukocyte count. Lactic acidosis, hypotension, and abdominal distention indicate bowel infarction. Mortality approaches 80% despite aggressive surgical management.

Visceral angiography can be performed in the stable patient; duplex ultrasound is of less diagnostic value in this setting. Mesenteric thrombosis causes occlusion at the origin of the vessel, while emboli most often lodge within the superior mesenteric artery usually at the first jejunal branch. In hypoperfusion-related mesenteric ischemia, the vessels are pruned but patent. Angiography also allows delivery of catheter-directed therapy: thrombolytics (alteplase, 0.5-1 mg/h) for thrombotic disease or vasodilators (papaverine, 30-60 mg/h) for nonocclusive disease. Broad-spectrum antibiotics are administered to all patients. Embolic disease, acidosis, hemodynamic instability, or severe or progressive abdominal pain mandate emergent laparotomy. Mesenteric flow is first reestablished with thomboembolectomy or bypass, and the bowel resection margins are then determined by gross inspection or examination with fluorescein. A second-look operation is planned if any bowel is of questionable viability at the close of the case.

Mesenteric vein occlusion is responsible for 5-15% of cases of acute mesenteric ischemia. Risk factors include hypercoagulable state (malignancy; protein C, protein S, or antithrombin III deficiency; presence of anticardiolipin or antiphospholipid antibody; polycythemia vera), intra-abdominal sepsis, previous splenectomy or portal angiography or sclerotherapy, portal hypertension, and cirrhosis. Diagnosis is made by contrast-enhanced abdominal CT scan or arterial portography. Patients should be treated with long-term anticoagulation. Surgery is reserved for those suspected of having bowel infarction and consists of bowel resection and occasionally venous thrombectomy. In some cases, percutaneous transhepatic administration of thrombolytics has been successful.

Ischemic colitis can develop as a result of acute or chronic colonic ischemia and is characterized by bouts of crampy lower abdominal pain and mild -  often bloody -  diarrhea. This picture may be indistinguishable from inflammatory bowel disease. Colonoscopy reveals segmental inflammatory changes, most prominent in the watershed areas of the rectosigmoid junction and splenic flexure. Conservative management is usually adequate. Surgery may be indicated for progressive symptoms or stricture formation.

Edwards MS et al: Acute occlusive mesenteric ischemia: surgical management and outcomes. Ann Vasc Surg 2003;17:72.

Kasirajan K et al: Chronic mesenteric ischemia: open surgery versus percutaneous angioplasty and stenting. J Vasc Surg 2001;33:63.