Venous Thrombosis Within the Splanchnic Circulation

Mesenteric vein thrombosis was first recognized by Eliot a century ago and was more completely described by Warren and Eberhard as early as 1935. The underlying pathophysiology and treatment options have only been well delineated during the last few decades. Understanding has been confounded by the fact that clinical presentations range widely from acute life-threatening bowel ischemia to very subtle chronic symptoms, depending on the pace of thrombosis and the specific vein segments involved. The initial classification of primary or secondary disease, based on the presence or absence of known etiologic factors, actually added very little to the clinical decision making. The development of more exact serologic testing for genetic markers of hypercoagulable states and the increasing specificity of tomographic imaging of intraabdominal inflammation suggest that the vast majority of cases are, in fact, secondary to such specific processes. Hence, a more rational classification system has evolved that separates hematologic causes from nonhematologic disorders such as intraperitoneal inflammatory disease, low-flow states, and dehydration.

Mesenteric vein thrombosis with or without portal vein extension, isolated portal vein thrombosis, splenic vein thrombosis, and hepatic vein occlusion (Budd–Chiari syndrome) represent the four major categories of this disease entity.

The intestinal venous drainage follows a well-derived route, with venae rectae forming larger veins that drain blood from the small intestine and proximal colon into the ileocolic, right colic, and middle colic vessels. These collectively flow into the superior mesenteric vein (SMV), which joins with the splenic vein to form the portal vein. The portal vein drains blood into the liver and ultimately into the inferior vena cava through the hepatic veins.