Chronic mesenteric ischemia (CMI) usually results from long-standing atherosclerotic disease of 2 or more mesenteric vessels.  Other nonatheromatous causes of CMI include the vasculitides, such as Takayasu arteritis. Symptoms are caused by the gradual reduction in blood flow to the intestine.  (See Presentation.)
In 1958, Shaw and Maynard described the first thromboendarterectomy of the superior mesenteric artery (SMA) for the treatment of both acute mesenteric ischemia (AMI) and CMI. Several other surgical procedures have since been attempted, ranging from reimplantation of the visceral branch into the adjacent aorta to using an autogenous vein graft. In 1972, Stoney and Wylie introduced transaortic visceral thromboendarterectomy and aortovisceral bypass, which have proved to be highly effective techniques.
Since the introduction of endovascular treatment in 1980, there has been an increase in the use of this modality. (See Treatment.) A systematic literature review from 2013 showed that endovascular treatment was used in 50.48% of cases between 2001 and 2010, compared with 22.3% between 1986 and 2000. 
Mastery of the anatomy of the mesenteric vessels is essential to management of CMI, though the wide array of vascular variations can make such mastery difficult to achieve. The primary vessels supplying the mesentery are as follows:
Celiac trunk (also referred to as the celiac artery or celiac axis) - Foregut
SMA - Midgut
Inferior mesenteric artery (IMA) - Hindgut
The celiac trunk arises from the ventral surface of the aorta at the T12-L1 vertebral body. It courses anteroinferiorly before branching into the common hepatic, splenic, and left gastric arteries. Numerous variations have been observed, but further discussion of these is beyond the scope of this article.
The hepatic artery gives off the gastroduodenal artery, which branches further into the right gastroepiploic artery and the anterosuperior and posterosuperior pancreaticoduodenal arteries. The right gastroepiploic artery communicates with the left gastroepiploic artery, which is an immediate branch of the splenic artery. The anterosuperior and posterosuperior pancreaticoduodenal arteries communicate with the corresponding inferior branches from the SMA.
The splenic artery gives off the left gastroepiploic artery and the dorsal pancreatic artery, which supplies the body and tail of the pancreas and communicates with the anterosuperior pancreaticoduodenal and gastroduodenal arteries and, sometimes, the middle colic artery or SMA.
The left gastric artery communicates with the right gastric artery along the posterior aspect of the lesser curvature of the stomach.
The celiac trunk supplies most of the blood to the lower esophagus, stomach, duodenum, liver, pancreas, and spleen.
The SMA comes off of the ventral aorta and gives off the inferior pancreaticoduodenal artery and the ileocolic, middle colic, right colic, jejunal, and ileal branches.
The inferior pancreaticoduodenal artery gives rise to the corresponding anteroinferior and posteroinferior branches, which anastomose with their superior counterparts (see above). This communication is an important connection that helps maintain bowel perfusion in the setting of mesenteric ischemia.
The ileocolic artery supplies the ileum, cecum, and ascending colon, whereas the middle colic artery supplies the transverse colon and communicates with the IMA. The right colic artery typically branches at the same level as the middle colic artery. The right and middle colic arteries are important suppliers of blood to the marginal artery of Drummond and give rise to the terminal vasa recta, which provide blood to the colon.
The IMA is the smallest mesenteric vessel and comes off the anterior aorta. It provides blood to the distal transverse, descending, and sigmoid colon, as well as to the rectum.
Many communications with the SMA exist within the mesentery, and rectal branches offer communication of the visceral blood supply with the common blood supply.
The watershed area, near the splenic flexure, is thought to be more susceptible to ischemia secondary to poor arterial flow. Because this area is poorly developed, it has an increased propensity for ischemia.
Because of the multiple areas of potential collateral flow in the mesenteric system, at least 2 of the 3 main vessels must be occluded to produce CMI.
In more than 95% of patients, the process driving mesenteric ischemia is diffuse atherosclerotic disease, which decreases the flow of blood to the bowel. As the atherosclerotic disease progresses, symptoms worsen. 
The interconnections between the celiac trunk, the SMA, and the IMA often permit easy compensation if stenotic lesions develop in 1 of these 3 vessels. Usually, therefore, at least 2 of the 3 major visceral vessels must be occluded or narrowed for CMI to develop. CMI with intestinal malperfusion is rarely seen in clinical practice, but when it does occur, it represents a serious and complex vascular disorder.
Although the pathophysiologic mechanism by which ischemia produces pain is still not completely understood, current physiologic understanding of splanchnic perfusion suggests a key role for the splanchnic circulation in the regulation of cardiovascular homeostasis.
In situations such as critical illness, major surgery, and exercise (all of which are characterized by increased demands on the circulation to maintain tissue oxygen delivery), gastrointestinal (GI) perfusion is often compromised earlier than other vascular beds are. Perhaps more important, this relative hypoperfusion often outlasts the period of the hypovolemic insult or low-flow state. [5, 6, 7]
Conditions less frequently involved in the pathogenesis of CMI are celiac artery compression syndrome (CACS; also known as median arcuate ligament syndrome [MALS]) and fibromuscular dysplasia (FMD). CACS entails external compression of the celiac trunk by the median arcuate ligament or the celiac ganglion. 
Factors that predispose to atherosclerosis are associated with increased risk for CMI. These include the following:
Hypercholesterolemia (although patients may present with hypocholesterolemia because of their chronic malnourished state)
When the arterial lumen is narrowed secondary to atherosclerosis, any increase in intestinal demand (as in eating) or decrease in intestinal supply (as in hypovolemia) can result in severe abdominal pain and possibly infarction. The risk factors for atherosclerosis are therefore pertinent to the development of CMI.
CMI is a rare diagnosis. In 1997, Moawad and Gewertz searched 20 years of literature and found only 330 cases.  In 2013, Pecoraro et al included 1795 cases in their systematic review of 25 years of literature.  Because many cases are not reported, the true prevalence could be much higher. Autopsy studies support this possibility, with findings of stenosis in as many as 30% of selected patients with a history of abdominal pain. No differences in frequency have been reported in various regions of the world.
CMI generally occurs in patients older than 60 years. Most studies have found it to be more prevalent in females than in males.
CMI, by itself, does not represent an important cause of mortality. When death does occur in patients with CMI, it could be related to mesenteric ischemia or to cardiac or other nonrelated causes (eg, cancer). Complications such as acute thrombosis or embolism are significant causes of increased mortality.
Patients with CMI often present with malnutrition secondary to their fear of postprandial abdominal pain. These patients may have a prolonged hospital course as a consequence of their chronically malnourished state.
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