Patients with chronic mesenteric ischemia usually present to their primary care physician or gastroenterologist with abdominal pain and/or weight loss. There are no specific characteristics related to the pain, although it tends to occur in the midepigastric region and can radiate through to the back. The pain usually develops within 15 to 30 minutes after eating and can persist for 1 to 3 hours. The pain may progress along the spectrum from postprandial pain associated only with certain food types to a persistent unremitting character, although the latter is worrisome for acute mesenteric ischemia and bowel infarction. Patients develop adaptive strategies to minimize or reduce the pain, with the net effect that they avoid eating and ultimately lose weight. This behavior has been termed “food fear.” The weight loss associated with chronic mesenteric ischemia is due to an inadequate caloric intake rather than intestinal malabsorption. The mean pre-operative weight loss reported from several large clinical series has been between 20 and 30 pounds. Unfortunately, there are no characteristic bowel habits associated with chronic mesenteric ischemia, with some patients complaining of constipation due to poor oral intake and others complaining of immediate postprandial diarrhea.

Patients with chronic mesenteric ischemia are fairly characteristic, and the diagnosis is usually suggested by their general appearance. The typical patient is a cachectic middle-aged woman with a strong smoking history. Indeed, chronic mesenteric ischemia is one of the few cardiovascular disorders that is more common in women. Physical examination is not particularly enlightening, with the exception of the patients’ appearance, although patients frequently have evidence of systemic vascular disease and may have abdominal bruits. However, the absence of systemic vascular disease does not rule out the diagnosis, because patients may have isolated central aortic occlusive disease.

Although patients with chronic mesenteric ischemia present with abdominal pain and weight loss, the associated differential diagnosis is extensive and includes an intra-abdominal malignancy first and foremost on the list. Each patient should undergo an appropriate diagnostic workup, with this working diagnosis including an abdominal/pelvic CAT scan, an esophagogastroduodenoscopy (EGD), a colonoscopy, and an abdominal ultrasound. Most patients undergo this extensive diagnostic workup before being diagnosed and referred to a vascular surgeon. Notably, the average diagnostic delay usually exceeds a calendar year and includes almost three diagnostic tests and/or operative procedures. Gastric ulcers are frequently found on EGD and are incorrectly attributed to be the cause of the pain and weight loss. These are likely sequelae of gastric ischemia and are almost pathognomonic for chronic mesenteric ischemia.

The diagnosis of chronic mesenteric ischemia requires a confirmatory imaging study in addition to the appropriate clinical scenario. Duplex ultrasound is an excellent screening tool for visceral artery occlusive disease, with sensitivities and specificities relative to contrast arteriography of >80%. Peak systolic and end diastolic flow velocities of >275 cm/sec and >45 cm/sec, respectively, in the superior mesenteric artery have been reported to correspond to a >70% stenosis. Similarly, peak systolic and end diastolic flow velocities of >200 cm/sec and >55 cm/sec, respectively, in the celiac axis have been reported to correspond to the same degree of stenosis. However, it is imperative that each institution establish its own duplex criteria for these significant stenoses relative to standard arteriography. Unfortunately, mesenteric duplex ultrasound has several limitations. It is technically challenging, operator dependent, and not universally available. Furthermore, the examination is complicated by the deep location of the vessels, respiratory variation, the strict need for a Doppler angle of 60°, and presence of intra-abdominal gas. Standard contrast arteriography is the definitive imaging test and serves to confirm the duplex findings, plan the operative procedure, and affords an opportunity for intervention. Both magnetic resonance and CT arteriography have the potential to replace duplex ultrasound and contrast arteriography in the future, although their current role remains undefined.

The pathogenesis of chronic mesenteric ischemia is the inability to achieve postprandial hyperemic intestinal blood flow. Intestinal blood flow normally increases after eating with the maximal increase after 30 to 90 minutes. This hyperemic response lasts between 4 and 6 hours and varies with the size and composition of the meal. In the presence of hemodynamically significant stenoses, this postprandial hyperemic response is attenuated, and this leads to a relative imbalance between the tissue supply/demand for oxygen and other metabolites with the development of postprandial pain or mesenteric angina.

There is an extensive collateral network between the visceral and internal iliac arteries, which functions to maintain intestinal blood flow despite the presence of a hemodynamically significant stenosis. The celiac axis and superior mesenteric artery collateralize through the superior (celiac axis) and inferior (SMA) pancreaticoduodenal arteries, while the superior and inferior mesenteric arteries collateralize through both marginal artery of Drummond and the meandering artery. The latter is the most significant collateral and connects the ascending branch of the left colic with the middle branch of the middle colic. It lies at the base of the mesentery and is at risk of being ligated during exposure of the infrarenal aorta. The inferior mesenteric artery communicates with the internal iliac artery via the hemorrhoidal branches. Significant occlusive disease in two of the three visceral vessels is usually required before patients become symptomatic; however, this is not an absolute requirement, and patients may have isolated single vessel disease. Notably, the overwhelming majority of patients undergoing open surgical revascularization have significant disease in both the celiac axis and superior mesenteric artery.

Atherosclerosis is the leading cause of the visceral artery occlusive disease that leads to chronic mesenteric ischemia, although a variety of other causes, including fibromuscular disease, aortic dissections, neurofibromatosis, rheumatoid arthritis, Takayasu arteritis, radiation injury, Buerger disease, systemic lupus, and drugs (e.g., cocaine, ergots), have been incriminated. Patients with visceral artery occlusive disease often have concomitant renal artery occlusive disease in a pattern consistent with central aortic disease. However, it should be emphasized that visceral artery occlusive disease is relatively common in contrast to mesenteric ischemia. Autopsy studies have found that up to 10% of individuals have a ≥50% stenosis in one of the visceral vessels, while approximately 25% of those undergoing arteriography before peripheral arterial reconstruction have a >50% stenosis of the superior mesenteric artery or celiac axis.

All patients with chronic mesenteric ischemia should undergo revascularization, because the natural history is death from inanition or bowel infarction. Admittedly, the natural history has not been well defined, because patients usually undergo revascularization after diagnosis and, therefore, there is no untreated control group. There is no role for chronic parenteral alimentation and noninterventional therapies, even in relatively high-risk patients. The role of revascularization in patients with asymptomatic visceral artery occlusive disease remains unresolved. Several reports have suggested that patients with severe occlusive disease in all three visceral vessels and those undergoing aortic reconstruction represent a high-risk group for bowel infarction and consideration should be given for revascularization.

The optimal means of revascularization for patients with chronic mesenteric ischemia has been debated for the past few decades. The pivotal questions are the type of revascularization (endovascular vs. open) and the type/configuration of open revascularization. Endovascular treatment has a tremendous amount of appeal because it is less invasive and has the potential to reduce morbidity, mortality, length of hospital stay, and cost. However, the long-term outcome remains unclear. Antegrade bypass from the supraceliac aorta and retrograde bypass from the infrarenal aorta/common iliac artery are the most common open, surgical procedures. The advantages of the antegrade bypass include the direct course of the graft that maintains antegrade flow and the fact that the supraceliac aorta is usually uninvolved with atherosclerosis. The advantages of the retrograde bypass include its relative ease/simplicity and the lower incidence of hemodynamic instability and distal embolization with the infrarenal aortic/ iliac clamp application. The major disadvantage of the retrograde bypass is the obligatory course of the graft and its potential to kink.

The peri-operative and long-term outcomes after both open and endovascular revascularization for patients with chronic mesenteric ischemia are shown in Tables 38-1 and 38-2. Despite the heterogeneity of the patient populations and the treatments, several conclusions can be reached. The technical and immediate clinical success rates for endovascular treatment of visceral artery occlusive lesions are both quite good. Similarly, both the mortality and complication rates appeared to be lower for the endovascular treatment. Admittedly, the ranges for the mortality and complication rates were similar for the open and endovascular treatments, although the adverse outcomes in the endovascular group appeared to cluster at the lower end of the range and the magnitude of the complications was lower. The long-term clinical success, graft patency, and patient survival after open revascularization as objectively documented with either the life table or Kaplan-Meier method are all quite good. The same outcome measures are poorly documented after endovascular treatment, although the limited data suggest that these long-term measures are comparable.

The pre-operative evaluation before mesenteric bypass is comparable to that for other major vascular surgical procedures. All active medical conditions should be optimized, although extensive medical workups are unnecessary given the relative sense of urgency associated with the underlying problem. Similarly, extensive cardiac evaluations are likely unnecessary and should be dictated by the patient’s underlying symptoms, with catheterization reserved for patients with either unstable angina and/or a change in their anginal pattern. Operative planning is facilitated by a visceral arteriogram, although this is usually the definitive diagnostic study. A CAT scan of the supraceliac aorta should be obtained prior to antegrade bypass to assure that it is a suitable inflow site. Ankle-brachial indices and vein surveys of the saphenous and superficial femoral veins are routinely obtained to quantify the level of lower-extremity arterial occlusive disease and to identify all available autogenous conduits in the event that a prosthetic conduit is contraindicated. Patients with minimal postprandial pain are allowed to continue to eat, although they are counseled to avoid large meals or types of food that exacerbate their symptoms, while patients with continuous abdominal pain are made nothing per mouth (NPO) with the exception of medications. Patients hospitalized during the pre-operative period are started on total parenteral nutrition; however, the operative intervention is not delayed in an attempt to replete the nutritional stores. A mechanical bowel preparation is not used due to the theoretical concerns of precipitating acute mesenteric ischemia.

The pre-operative evaluation before endovascular revascularization is essentially the same as before mesenteric bypass. Indeed, patients should be prepared to undergo emergent, open revascularization if a complication should arise, although this is unusual. Patients with a contrast allergy should be treated with an appropriate
steroid preparation, while patients with elevated serum creatinine levels considered candidates for standard contrast (serum creatinine 1.5 to 2.0 mg/dL) should receive gentle hydration and acetylcysteine or sodium bicarbonate.