It is for this entity that percutaneous treatment of mesenteric vascular disease is most frequently employed. As mentioned, due to the various anastomotic pathways (Table 33.3) that allow single-vessel disease to be well tolerated, chronic intestinal ischemia most commonly results from multivessel disease of the mesenteric vessels. In nine reports of 244 cases of chronic mesenteric ischemia published in the 1980s and 1990s, 91 % of cases involved 2-vessel disease, 55 % involved 3-vessel disease, and 9 % had single-vessel disease (7 % SMA, 2 % celiac) by catheter-based angiography [15]. Though uncommon, single-vessel mesenteric disease can result in symptomatic chronic intestinal ischemia in the presence of insufficient collateral reserve. Individuals with prior abdominal surgery are particularly susceptible to disrupted collateral supply. Culprit atherosclerotic lesions most commonly affect the ostium of the mesenteric vessels and are frequently heavily calcified.

Several imaging modalities facilitate the diagnosis of chronic mesenteric ischemia due to atherosclerosis and have largely replaced the need for diagnostic invasive angiography for this disease. Doppler ultrasonography is an excellent modality in the diagnosis of obstructive atherosclerotic disease of the celiac and superior mesenteric arteries provided the study is performed by a skilled technician and the patient’s body habitus is not prohibitive [15, 17]. Due to the proximal nature of typical atherosclerotic stenoses, computed tomographic angiography and magnetic resonance angiography are also accurate imaging tools. Though superior in its imaging resolution, catheter-based angiography is not a first-line diagnostic test for chronic intestinal ischemia due to a relatively higher rate of vascular complications than other imaging tests and due to the exposure to iodinated contrast and radiation as compared to duplex ultrasonography or magnetic resonance angiography. It should be emphasized that the presence of obstructive lesions on any of these modalities is not sufficient to make the diagnosis of chronic intestinal ischemia; rather, the presence of suggestive clinical symptoms is also necessary. Thus, catheter-based angiography – with an inclination for endovascular treatment – is typically reserved for the patient with suggestive symptoms of chronic mesenteric ischemia in addition to evidence of severe obstructive disease on a less-invasive imaging modality.

Asymptomatic mesenteric atherosclerosis is thought to have a relatively high prevalence but a benign natural history. In a population-based study of 553 elderly individuals, the prevalence of single-vessel mesenteric obstructive disease was 17 % by duplex ultrasonography [18]. The favorable prognosis of asymptomatic mesenteric atherosclerotic disease is largely based on a report from the Cardiovascular Health Study; however, this report suffered from incomplete follow-up [18]. Nonetheless, it is generally accepted that medical therapy, in the absence of revascularization, is warranted for asymptomatic patients [6].

For patients with symptoms and weight loss thought to be due to obstructive, atherosclerotic mesenteric disease, revascularization is warranted. No randomized trials have been conducted comparing the various treatment options of chronic intestinal ischemia due to atherosclerotic disease. Surgical revascularization was 1st done in 1958 [19]. Options include bypass, endarterectomy, and reimplantation. Bypass choices include single-vessel versus multivessel revascularization, prosthetic versus venous conduits, and antegrade (from the supraceliac aorta) versus retrograde (from the internal iliac arteries) approaches [15]. Depending on the study, perioperative mortality has ranged from 0 to 16 %, and reported recurrence rates have varied widely from 0 to 26 % over 3–12 years [8].

Feasible, percutaneous revascularization is generally preferred over surgical revascularization due to the morbidity associated with surgery in the typically elderly population with this disease. However, certain patient subsets are more appropriate for surgery, including those with concomitant aneurysmal disease in need of repair and those with flush occlusions of the culprit mesenteric vessel(s) [6]. The technical aspects of endovascular therapy and its evidence base are discussed later in this chapter.

Less than 10 % of cases of chronic intestinal ischemia are due to nonatherosclerotic diseases, which are summarized in Table 33.4 [16]. In general, catheter-based angiography is employed more frequently for the diagnosis of fibromuscular dysplasia and vasculitis than for atherosclerotic disease due to involvement of mid and distal mesenteric vessels by these nonatherosclerotic diseases and consequently the need for an imaging modality with higher resolution. There is minimal literature to assist with decision-making regarding revascularization for chronic intestinal ischemia in fibromuscular dysplasia and vasculitis. In the absence of such evidence, extrapolation of data from intervention in other arterial beds seems appropriate. Thus, for chronic intestinal ischemia due to fibromuscular dysplasia, measurement of pressure gradients to assess severity of stenoses and angioplasty alone without stenting should be considered as is done for renal artery interventions for this disorder [20]. Also, endovascular therapy for chronic mesenteric ischemia due to vasculitis should be performed in the chronic fibrotic stage, rather than the active inflammatory stage, to improve durability of the intervention.

Median arcuate ligament syndrome is a controversial entity that refers to compression of the celiac trunk by the arcuate ligament of the diaphragm in the presence of symptoms of chronic mesenteric ischemia and in the absence of alternative etiologies. The stenosis is dynamic, becoming more severe in expiration when the diaphragm moves upward. Duplex ultrasonography shows elevated peak systolic velocities during expiration. CT angiography shows a focal, ostial narrowing with an acutely downward-going proximal segment forming a classic “hooked” appearance [21, 22].

Celiac artery compression by the arcuate ligament occurs not infrequently in the absence of symptoms [23]. Thus, establishing a cause-and-effect relationship between this finding and symptoms is challenging and likely only possible if symptoms improve after revascularization. However, given the uncertain benefit, the indication for revascularization is often suspect. If revascularization is pursued, surgical release of compression with or without celiac trunk revascularization is recommended [6]. Laparoscopic release with or without endovascular revascularization has been described as a minimally invasive option ([24]. It is important for the interventionalist not to mistake this syndrome with atherosclerotic disease of the celiac artery.

Acute mesenteric ischemia can result from arterial occlusion, nonocclusive mesenteric ischemia, or venous thrombosis. Arterial occlusion most commonly results from thromboembolism, which accounts for 30–50 % of cases of acute mesenteric ischemia. In situ thrombosis is another common cause of arterial occlusion, contributing to 25–30 % of cases of acute mesenteric ischemia. Less common causes of acute mesenteric arterial occlusion are atheroembolism and dissection [5, 10, 14]. Nonocclusive mesenteric ischemia (NOMI) refers to a state of low cardiac output accompanied by profound mesenteric vasoconstriction in the absence of focal mesenteric arterial obstruction. This entity is responsible for 20–30 % of acute mesenteric ischemia cases [10]. It can also be due to intense mesenteric vasospasm from ergotamines, digoxin, cocaine, amphetamine, or vasopressor agents without reduced cardiac output [4]. Venous thrombosis of the celiac and/or superior mesenteric veins is typically seen in conditions predisposing to deep venous thrombosis – such as protein C deficiency, protein S deficiency, factor V Leiden, and prothrombin gene mutation – and is reported to account for 15–20 % of acute intestinal ischemia [10, 30]. Other risk factors for mesenteric venous thrombosis include pancreatitis, recent intra-abdominal surgery, and cirrhosis [30].

Regardless of etiology, patients with acute mesenteric ischemia present with severe abdominal pain that is classically out of proportion to physical findings. Other symptoms include nausea, vomiting, diarrhea, and gastrointestinal bleeding. On physical exam, a rigid abdomen indicates peritonitis from perforation of necrotic bowel. Such a finding is critical in the early evaluation of this disease as it indicates the need for emergent surgery, the absence of which carries a high mortality rate [4]. Melena may also be present, though the absence of heme-positive stools cannot rule out acute intestinal ischemia [4]. Lactic acidosis is common, but an elevated lactate is nonspecific.

In all comers with acute intestinal ischemia, the median age is 70 years and 2/3 are women [4]. There may be clinical features that suggest a precise etiology in patients presenting with acute mesenteric ischemia, and recognition of these clues can facilitate appropriate initial workup and management. For example, potential sources of thrombotic or atherosclerotic embolism should be sought (e.g., atrial fibrillation, severe left ventricular dysfunction, aortic atheroma, and a recent arterial catheterization procedure), particularly in the nonanticoagulated patient. These patients may also have evidence of embolization elsewhere, causing acute stroke or acute limb ischemia. A history of chronic intestinal ischemic symptoms suggests in situ atherothrombosis as the etiology of acute intestinal ischemia. Critical illness, hypotension from any cause, and certain offending medications (vasopressors, digoxin, ergotamines) are risk factors for NOMI. Finally, a known hypercoagulable state and pancreatitis may be present in patients with mesenteric venous thrombosis.