Introduction
Prevalence
The prevalence of mesenteric arterial stenoses is much more common than is the clinical manifestation of chronic mesenteric ischemia (CMI), likely due to the rich vascular communication among the three mesenteric vessels. CMI is twice as common in women than men. Asymptomatic mesenteric stenosis was documented angiographically in 40% of patients with an abdominal aortic aneurysm, 29% with aortoiliac obstructive disease, and in 25% of patients with peripheral arterial disease of the lower extremities. In a healthy group of elderly individuals (>65 years) ultrasound imaging found a 17.5% prevalence of asymptomatic (>70%) stenosis of at least one mesenteric artery. Symptomatic CMI is uncommon, accounting for less than 2% of all atheromatous revascularization procedures, and it is usually the consequence of atherosclerotic disease involving aorto-ostial stenosis of the celiac, superior mesenteric, and/or inferior mesenteric arteries often in the context of concomitant atherosclerotic disease of the aorta.
Etiology
Classical teaching suggests that CMI occurs when only one of three mesenteric arteries (celiac, superior mesenteric, and inferior mesenteric) remains patent due to the rich collateral supply and the most commonly intervened on vessel is the superior mesenteric artery. Causes of CMI include vascular conditions such as fibromuscular dysplasia, Takayasu disease, Buerger disease, radiation and autoimmune arteritis, and aortic dissection, but atherosclerosis is the predominant (>95%) cause of clinical mesenteric arterial stenosis. The median arcuate syndrome, also called the celiac axis compression syndrome, can occur if the origin of the celiac trunk arising from the aorta is extrinsically compressed by the arcuate ligament of the diaphragm. This can cause significant, sometimes critical, stenosis of this vessel.
Natural History
The natural history of asymptomatic mesenteric artery stenosis is that clinical symptoms do not develop in the majority of patients. Abdominal angiography was performed in 980 patients, demonstrating >50% stenosis of at least one mesenteric artery in 82 patients. After 2.6 years of follow-up, CMI developed in only 4 (4.9%) of the 82 patients, and these individuals all had involvement of all three mesenteric arteries.
The natural history of patients with symptomatic CMI is that between 20% and 50% of patients will progress to develop acute mesenteric ischemia. The remaining patients continue to suffer chronic postprandial abdominal pain, weight loss, and emaciation.
Diagnosis
Clinical Presentation
The classical symptoms of CMI include abdominal pain triggered by food ingestion and accompanied by significant unexplained weight loss ( Table 21-1 ). The abdominal pain is often periumbilical and described as dull aching or sometimes as “crampy” and begins within 1 hour after food ingestion and subsides 1 to 2 hours later. Many patients develop a “fear of food” and decrease their caloric intake, resulting in unintended weight loss. It is not unusual for patients with classic CMI to present with a 20- to 40-pound weight loss. Significant weight loss often helps to differentiate patients with functional bowel symptoms from those with CMI.
Typical symptoms Post-prandial abdominal pain Fear of food Weight loss (>20 pounds) | 78% |
Ischemic gastropathy Nausea, vomiting Fullness Abdominal pain Right upper quadrant discomfort Weight loss | 14% |
Ischemic colitis Abdominal pain Gastrointestinal bleeding Hematochezia | 8% |
Ischemic gastropathy, ischemic colitis, and malabsorption are less common manifestations of CMI. Ischemic gastropathy usually manifests as nausea, vomiting, fullness, right upper quadrant discomfort, abdominal pain, and weight loss. Ischemic colitis presents with abdominal pain, gastrointestinal bleeding, and/or hematochezia. The diagnosis may be delayed as patients may be referred for a malignancy evaluation for weight loss. However, evidence of significant stenosis of two or more mesenteric vessels in conjunction with endoscopic findings of bowel ischemia should prompt the diagnosis. CMI may occur in single mesenteric artery disease particularly after surgery if mesenteric collaterals have been disrupted.
CMI often masquerades as a severe functional bowel syndrome. In a series of 59 patients with CMI from the Ochsner Clinic a typical presentation was found in 78%, with the remainder presenting with ischemic gastropathy or ischemic colitis in the remaining 22% of patients. The diagnosis of CMI is based upon symptoms of bowel ischemia in the presence of hemodynamically significant stenoses in more than one mesenteric artery. Due to the difficulty in making this diagnosis, a multidisciplinary team approach is encouraged. On physical examination patients with CMI may have an abdominal bruit localized in the epigastrium, and they may have other signs of peripheral vascular disease.
Imaging
Duplex ultrasonography, as well as cross-sectional imaging with computed tomographic angiography (CTA), and magnetic resonance angiography (MRA), are adequate to establish the presence of mesenteric arterial stenosis.
Invasive angiography remains the gold standard for visualizing the mesenteric arterial tree. Visualization of the mesenteric vessels requires a lateral aortogram ( Figure 21-1 ). The anterior-posterior aortogram may reveal the arc of Riolan, an engorged collateral connecting the inferior mesenteric artery (IMA) to the superior mesenteric artery (SMA) and indicative of proximal mesenteric artery disease. Invasive angiography is used less frequently for screening, but is recommended for patients with an inconclusive noninvasive imaging study or in whom revascularization therapy is being considered.
Management of Chronic Mesenteric Ischemia
Medical Therapy
Patients with asymptomatic CMI should be treated as other patients with atherosclerotic vascular disease with aggressive multimodality therapy to treat risk factors including lipid-lowering therapy with a statin drug, smoking cessation, blood pressure control, diabetes control, and treated with aspirin antiplatelet therapy. In addition, treatment with digoxin should be avoided due to the detrimental actions of digoxin in the splanchnic circulation causing vasoconstriction and ischemia.
Current guideline recommendations are that patients with symptomatic CMI should be evaluated for revascularization. Without revascularization they will have progression of their disease and risk the development of acute myocardial infarction (AMI), inanition, and death.
Catheter-Based Endovascular Therapy
Catheter-based endovascular revascularization techniques are preferred to open surgery due to their lower procedural morbidity ( Figure 21-2 ). Endovascular therapies may be repeated if necessary, generally without increased patient risk compared with the first procedure, and prior angioplasty does not preclude surgery if required at a later date.