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Nonocclusive mesenteric ischemia

David A Tendler, MD
J Thomas Lamont, MD
Section Editors
John F Eidt, MD
Joseph L Mills, Sr, MD
Deputy Editor
Kathryn A Collins, MD, PhD, FACS


Acute mesenteric ischemia refers to the sudden onset of intestinal hypoperfusion, which can be due to a nonocclusive reduction of arterial blood flow. Nonocclusive arterial hypoperfusion is most commonly due to primary splanchnic vasoconstriction. Nonocclusive mesenteric ischemia was first described by Ende in patients with heart failure [1]. The majority of cases involve spasm of branches of the superior mesenteric artery (SMA) supplying the small intestine and proximal colon. Early diagnosis is based upon a high index of clinical suspicion in patients with risk factors, but often requires arteriography to firmly establish the diagnosis. Nonocclusive mesenteric ischemia is less common than in the past, and when it occurs, it is managed by reversal of inciting factors, including cessation of vasoconstrictive medicines, correction of the underlying cause of hypoperfusion (if possible), and anticoagulation to limit arterial thrombosis. Selective infusion of the SMA with papaverine or other vasodilator is an option, but is uncommonly performed today.

Nonocclusive mesenteric ischemia will be reviewed here. Acute and chronic mesenteric arterial occlusion affecting the small intestine, and colonic ischemia are discussed separately. (See "Overview of intestinal ischemia in adults" and "Mesenteric venous thrombosis in adults" and "Chronic mesenteric ischemia" and "Colonic ischemia".)


The circulation to the small intestines is derived primarily from the superior mesenteric artery (SMA) and inferior mesenteric artery (IMA) (figure 1 and figure 2). The venous drainage parallels the arterial circulation and drains into the portal venous system (figure 3 and figure 4). An extensive collateral circulation (figure 5) protects the intestines from transient periods of inadequate perfusion [2,3].


Ischemic injury to the intestine develops when delivery of oxygen and nutrients are insufficient for cellular metabolism. The likelihood of developing intestinal ischemia depends upon the adequacy of systemic perfusion and collateral circulation, the number and caliber of mesenteric vessels that are affected, and the duration of the ischemic insult. The intestine is able to compensate for approximately a 75 percent acute reduction in mesenteric blood flow for up to 12 hours without substantial injury, in part because of increased oxygen extraction [4].

The pathogenesis of nonocclusive mesenteric ischemia is related to a homeostatic mechanism that maintains cardiac and cerebral blood flow at the expense of the splanchnic and peripheral circulation [5-7]. Vasopressin and angiotensin are likely the neurohormonal mediators of this phenomenon. Spasm may also be triggered by vasoactive and cardiotonic drugs [5,8]. The normal physiology of the intestine and response to ischemia are discussed in more detail elsewhere.


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Literature review current through: Sep 2016. | This topic last updated: Jun 30, 2014.
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