Pathogenesis of Mesenteric Venous Thrombosis

Mesenteric venous thrombosis is classified as either primary or secondary. When an etiologic factor is found, patients are said to have secondary mesenteric venous thrombosis (Table 1). The proportion of patients with primary, or idiopathic, mesenteric venous thrombosis continues to decline as our ability to diagnose inherited thrombotic disorders5 and to recognize hypercoagulable states6 improves.

Currently, an etiologic factor can be identified in about three quarters of patients. The most common causes are prothrombotic states due to heritable or acquired disorders of coagulation or to cancer, intraabdominal inflammatory conditions, the postoperative state, and cirrhosis and portal hypertension. Oral-contraceptive use accounts for 9 to 18 percent of the episodes of mesenteric venous thrombosis in young women.5,7 Although certain hypercoagulable disorders such as resistance to activated protein C and prothrombin mutations can be identified by molecular methods, the use of plasma measurements to diagnose protein C, protein S, and antithrombin III deficiencies can result in errors because plasma levels of these proteins can be falsely low in the presence of acute thrombosis.


Table 1. Causes of Mesenteric Venous Thrombosis.

Mesenteric venous thrombosis appears to be a manifestation of a hypercoagulable state resulting from or exacerbated by an event such as pancreatitis or surgery. The clinical manifestations depend largely on the extent of the thrombus, the size of the vessel or vessels involved, and the depth of bowel-wall ischemia. When ischemia is restricted to the mucosa, the manifestations consist of abdominal pain and diarrhea; transmural ischemia leads to necrosis, with gastrointestinal bleeding, perforation, and peritonitis.

The location of the thrombus may be determined on the basis of the underlying cause. Thrombosis due to intraabdominal causes starts in the larger vessels at the site of compression and then progresses peripherally to involve the smaller venous arcades and arcuate channels. In contrast, thrombosis due to underlying prothrombotic states begins in the small vessels and progresses to involve the larger vessels. Occlusion of the venae rectae and the intramural vessels interferes with venous drainage, with subsequent hemorrhagic infarction of the involved bowel segment. The transition from ischemic to normal bowel is usually gradual, unlike that seen with arterial occlusion.