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Mesenteric venous thrombosis in adults

David A Tendler, MD
J Thomas Lamont, MD
Peter Grubel, 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, one cause of which can be mesenteric venous occlusion. Mesenteric venous thrombosis can present acutely or in a subacute or chronic manner. At one time, acute mesenteric venous thrombosis was thought to be the principal cause of acute mesenteric ischemia; however, with increasing recognition of and differentiation from the occlusive and nonocclusive forms of acute arterial mesenteric ischemia, the proportion of cases attributed to mesenteric venous thrombosis has decreased to approximately 10 percent of all cases of acute mesenteric ischemia [1].

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


The venous drainage parallels the arterial circulation and drains into the portal venous system (figure 1 and figure 2). The anatomy of the intestinal circulation, normal physiology of the intestine, and response to ischemia are discussed in detail elsewhere. (See "Overview of intestinal ischemia in adults", section on 'Collateral circulation' and "Overview of intestinal ischemia in adults", section on 'Intestinal vascular anatomy' and "Overview of intestinal ischemia in adults", section on 'Physiology and mechanisms of ischemia'.)

Pathophysiology — Venous thrombosis is predominantly a result of stagnation of blood flow, vascular injury, and hypercoagulability (ie, Virchow's triad). Local factors (eg, splenectomy, pancreatitis) appear to be associated with initial thrombus formation in the large veins, whereas systemic hypercoagulable states (eg, protein C deficiency) lead to thrombosis initiated in the intramural venules, vasa recta, and venous arcades [2]. Mesenteric vein thrombosis almost always involves the distal small intestine (superior mesenteric venous drainage) and rarely involves the colon (inferior mesenteric venous drainage) [3]. The anatomic site of involvement in acute mesenteric venous thrombosis is most often ileum (64 to 83 percent) or jejunum (50 to 81 percent), followed by colon (14 percent) and duodenum (4 to 8 percent) [4,5]. The inferior mesenteric venous distribution is less commonly involved for reasons that are poorly understood but possibly related to collateral flow through the internal iliac system, rectal venous plexus, or systemic circulation via the left renal vein, splenic vein, and hemiazygous veins, though this is unproven [6-9].

Acute thrombotic occlusion of one or more mesenteric veins reduces perfusion pressure due to increased resistance in the mesenteric venous bed. As flow stagnates, increased venous pressure leads to efflux of fluid into the tissues, causing profound bowel wall edema, which can lead to submucosal hemorrhage. If the venous arcades and vasa recta are involved and venous return from the bowel wall is completely occluded, bowel infarction will occur [6]. However, not all cases of mesenteric venous thrombosis are associated with intestinal infarction. In animal models, gradual occlusion of the superior mesenteric vein is associated with the development of collateral venous drainage without ischemic damage [10]. Chronic mesenteric venous thrombosis often features dilated venous collaterals, which can bleed, due to elevated venous pressures [11]. Many patients with chronic mesenteric venous thrombosis also exhibit portal vein thrombosis. (See "Chronic portal vein thrombosis in adults: Clinical manifestations, diagnosis, and management".)

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