Mesenteric Venous Thrombosis 

Mesenteric venous thrombosis (also known as visceral venous thrombosis) is a rare but lethal form of mesenteric ischemia (see the image below). Antonio Hodgson first described mesenteric ischemia in the latter part of the 15th century. In 1895, Elliot first described mesenteric venous thrombosis as a cause of mesenteric ischemia. By the turn of the 19th century, many review articles and texts were describing the recent advances in the characterization and treatment of mesenteric ischemia, particularly venous thrombosis. In 1935, Warren and Eberhard reported that intestinal infarction resulted from ischemia due to venous thrombosis, and they reported a mortality rate of 34% in patients with venous thrombosis after resection. Unfortunately, despite improvements in therapy, this mortality rate still holds.

Mesenteric venous thrombosis is an insidious disease with a high mortality rate typically attributed to the long delay in diagnosis. Patients with this condition benefit from rapid diagnosis and expedient surgical therapy.^[1]

Mesenteric venous thrombosis is one of many causes of mesenteric ischemia, and the mechanism has been well described. Once treated, patients with this condition have a fairly good prognosis, and long-term outcomes are good if patients receive long-term anticoagulant therapy.

Frequency

Mesenteric venous thrombosis accounts for approximately 10-15% of all cases of mesenteric ischemia. This accounts for 0.006% of hospital admissions. Venous thrombosis is found in approximately 0.001% of patients who undergo exploratory laparotomy.

The risk of acute mesenteric venous thrombosis increases in patients with hypercoagulable states (eg, polycythemia vera, protein C and S deficiencies,^[2] )^[3] visceral infection, portal hypertension, perforated viscus, blunt abdominal trauma, malignancy, previous abdominal surgery (open or laparoscopic), or pancreatitis and in patients who smoke. Women taking oral contraceptives are also at increased risk of venous thrombosis. Patients who have undergone splenectomy,^{[4, 5, 6]} colectomy, and Roux-en-Y gastric bypass^{[7, 8]} are at increased risk of subsequent portal venous thrombosis, which rarely results in bowel infarction. A CT scan demonstrating mesenteric venous thrombosis is shown below. Malignancy may cause thrombosis because of a hypercoagulable state or by direct extension of the tumor. The most common cause seems to be intra-abdominal sepsis. No underlying cause is found in 25-50% of patients diagnosed with mesenteric venous thrombosis.

While the mesenteric arterial system may carry 25-40% of the cardiac output at one time, the venous system typically carries 30%. The mechanism that causes ischemia is a massive influx of fluid into the bowel wall and lumen, resulting in systemic hypovolemia and hemoconcentration. Resulting bowel edema and decreased outflow of blood secondary to venous thrombosis impede the inflow of arterial blood, which leads to bowel ischemia. While bowel ischemia is detrimental to the patient, the resulting multiple organ system failure actually accounts for the increased mortality rate.

In a study of mortality factors in 31 patients with mesenteric venous thrombosis, Abu-Daff et al determined that 30-day mortality in these patients was strongly linked to colonic involvement in ischemia and to short-bowel syndrome.^[9] Lack of anticoagulation also may have been a factor. Five-year mortality, according to the investigators, was primarily related to short-bowel syndrome.

Patients with mesenteric venous thrombosis have an insidious onset of symptoms described as vague abdominal discomfort that typically evolve over 7-10 days.

Patients may have a condition that predisposes them to a hypercoagulable state, which may be elicited by taking a thorough history. Cancer, polycythemia vera, or a history of deep vein thrombosis or pulmonary embolus are important risk factors that should be elicited from the history. Patients presenting with pancreatitis or signs of intra-abdominal infection should be considered predisposed to developing mesenteric venous thrombosis.

Patients may have a distended abdomen and guaiac-positive stool samples. If the patient has an underlying intra-abdominal infection, peritoneal signs may be elicited and a palpable abdominal mass may be felt. As with acute mesenteric ischemia, patients may report pain disproportionate to that normally elicited during a physical examination.

Paracentesis may demonstrate bloody peritoneal fluid; however, this occurs after bowel infarction and, therefore, is a late sign.

Unfortunately, laboratory examinations are not much help for confirming the diagnosis of venous thrombosis. Laboratory studies help more to suggest, rather than exclude, the diagnosis. Requisite laboratory studies include prothrombin time (PT), activated partial thromboplastin time (aPTT), complete blood count (CBC, which may reveal leukocytosis and/or hemoconcentration), and chemistries (which may show metabolic acidosis). Leukocytosis and acidosis are the most specific laboratory findings in patients with ischemia. Unfortunately, they are late findings. Evaluate patients for protein C and S deficiencies; antithrombin III deficiency; and abnormalities in lupus anticoagulant, anticardiolipin antibody, and platelet aggregation.

Obtain chest films and electrocardiograms (ECGs). Additionally, computed tomography (CT) scanning and angiography have proven equally reliable in helping confirm the diagnosis of acute venous occlusion, although some researchers consider CT scanning to be the diagnostic test of choice.^[10] A CT scan of the abdomen may show an enlarged mesenteric or portal vein with sharp definition of the venous wall and low density within the vein. An arteriogram may show vasospasm, contrast in the bowel lumen, nonvisualized venous system, reflux of contrast into the aorta, and finally, absent flow to necrotic bowel areas. A duplex scan of the mesenteric vessels is beneficial only if used early.

Despite all of these diagnostic indicators, the diagnosis of venous thrombosis is usually confirmed during laparotomy or autopsy. Only after other causes of a hypercoagulable state have been excluded can a patient be considered to have idiopathic venous thrombosis.

Indications for surgery in patients with acute mesenteric venous thrombosis include signs of peritonitis, possible bowel infarction,^[11] and hemodynamic instability.

Mastery of the anatomy of the mesenteric vessels is key to understanding and treating patients with mesenteric ischemia. The endless array of vascular variations can make this difficult. The celiac axis, the superior mesenteric artery, and the inferior mesenteric artery supply the foregut, midgut, and hindgut, respectively.

The anatomy of the arterial system is described in detail in the eMedicine topics Mesenteric Artery Ischemia and Mesenteric Artery Thrombosis.

The venous system, for the most part, parallels the arterial system. The superior mesenteric vein (SMV) is formed by the jejunal, ileal, ileocolic, right colic, and middle colic veins, which drain the small intestine, cecum, ascending colon, and transverse colon. The right gastroepiploic vein drains the stomach to the SMV, while the inferior pancreaticoduodenal vein drains the pancreas and duodenum. The inferior mesenteric vein drains the descending colon, the sigmoid colon, and the rectum through the left colic vein, the sigmoid branches, and the superior rectal vein, respectively. The inferior mesenteric vein joins the splenic vein, which then joins the SMV to form the portal vein, which enters the liver.

If bowel infarction is probable, acute mesenteric thrombosis is a surgical emergency and should be treated without hesitation.