Mesenteric venous thrombosis (MVT) is a disorder in which a local blood coagulation impairs the venous return of the bowel. Primary mesenteric venous thrombosis is considered spontaneous and idiopathic, while secondary mesenteric venous thrombosis arises from an underlying disease or risk factor. This condition can lead to venous engorgement and mesenteric ischemia and accounts for 5% to 15% of all mesenteric ischemic events. Thrombosis commonly involves the superior mesenteric vein, but rarely the inferior mesenteric vein. Delayed detection or treatment of mesenteric venous thrombosis allows intestinal infarction to develop, which can be life-threatening. Although mesenteric venous thrombosis is a relatively rare condition, mortality remains high due to nonspecific symptoms, delayed diagnosis, and insufficient clinician awareness.
Mesenteric venous thrombosis is considered primary when there is no etiology or predisposing factor. Primary mesenteric venous thrombosis represents 0% to 49% of all mesenteric venous thrombosis cases and has declined with increased index of suspicion and improved diagnosis of hypercoagulation disorders. Characteristic risk factors cause secondary mesenteric venous thrombosis.
Various conditions can lead to mesenteric venous thrombosis with many patients experiencing a multifactorial origin of thrombosis. Unlike arterial thrombosis, mesenteric venous thrombosis usually occurs with thrombophilia. Prothrombotic states and primary hypercoagulable states are the most common causes of secondary mesenteric venous thrombosis. Specific hypercoagulable states are identified in 60% to 75% of patients with mesenteric venous thrombosis. These include heparin-induced thrombocytopenia, essential thrombocythemia, post-splenectomy thrombocytosis, polycythemia vera and neoplastic disorders. Combined mesenteric and portal venous thrombosis are more often associated with non-systemic pathologies, such as local abdominal inflammatory conditions (e.g., inflammatory bowel disease, pancreatitis, diverticulitis), myeloproliferative neoplasms, and malignancies (e.g., hepatocellular carcinoma, pancreatic adenocarcinoma).
Genetic abnormalities also contribute to venous thrombosis and primary hypercoagulable states. These include defects in antithrombotic proteins (antithrombin III, protein C, protein S) and increased prothrombotic protein (e.g., activated protein C resistance, G20210A prothrombin gene mutation).
Despite being a relatively rare condition with low incidence, mesenteric venous thrombosis has increased in prevalence over the last 2 decades since the advent of computerized tomography (CT). However, mesenteric venous thrombosis is often not suspected in many patients, which underestimates its incidence. Acute mesenteric venous thrombosis causes 6% to 9% of all mesenteric ischemia cases. It accounts for 1 in 5000-15,000 in-patient admissions and 1 in 1000 emergency department admissions. Computed tomography identifies approximately 90% of mesenteric venous thrombosis cases. Although mortality remains high (19% to 23%), there has been an increase in earlier mesenteric venous thrombosis recognition without laparotomy since abdominal imaging has become more common. In general, mesenteric venous thrombosis is more common in males and individuals 40 to 60 years of age.
The location of the venous thrombus in relation to the mesenteric circulation and the existence of any collateral circulation are important factors in predicting bowel ischemia and intestinal infarction. Various underlying risk factors influence the location of the thrombus. Thrombosis can originate in different locations, such as the vena rectae or other major veins, and can arise from prothrombotic states, vessel wall injury, and venous stasis. Patients with mesenteric venous thrombosis that involve small, more distal venous branches tend to be at a higher risk for developing bowel infarction. Mesenteric venous thrombosis should be suspected when patients with previous thrombotic episodes or coagulopathy present with acute abdominal symptoms.
For unknown reasons, the superior mesenteric vein is more often involved than the inferior mesenteric vein. Inferior mesenteric thrombosis accounts for up to 11% of mesenteric venous thrombosis cases.
A patient with acute mesenteric venous thrombosis presents with a sudden onset of nonspecific symptoms, including abdominal pain, nausea, and vomiting. Abdominal pain is typically the dominant symptom, with severe pain in the mid-abdomen. Other abdominal signs, including tenderness, distention, and ascites may occur. If not treated, the abdominal pain will worsen as peritonitis develops. This indicates intestinal infarction, which is seen in one to two-thirds of mesenteric venous thrombosis patients. Unlike in arterial ischemia, the evolution from normal to an ischemic bowel is gradual in mesenteric venous thrombosis. Subacute mesenteric venous thrombosis patients experience symptoms over days to weeks. The average duration of symptoms varies from 6 to 14 days.
Chronic mesenteric venous thrombosis patients are often asymptomatic with a diagnosis of mesenteric venous thrombosis resulting from incidental findings or portal hypertension. Chronic mesenteric venous thrombosis is differentiated from acute mesenteric venous thrombosis by the existence of collateral venous circulation and cavernoma around the thrombosed vein. Chronic mesenteric venous thrombosis accounts for approximately 20% to 40% of total mesenteric venous thrombosis cases and rarely causes intestinal infarction.
The most informative evaluation for suspected mesenteric venous thrombosis is abdominal imaging. Radiographs are noninvasive and show abnormalities in 50% to 75% of cases. However, they only show evidence of bowel ischemia in less than 5% of cases. CT with contrast medium is the ideal diagnostic tool; its accuracy is approximately 90% for mesenteric venous thrombosis. Bowel wall thickening, thickened mesentery, and ascites which are all indicative of intestinal ischemia can be observed.
Routine laboratory testing is not helpful for a mesenteric venous thrombosis diagnosis. Although blood screening can be performed for thrombophilic factors, there are no accurate plasma biomarkers for early detection of intestinal ischemia. Elevated levels of L-lactate dehydrogenase, D-lactate and L-lactate have been observed in systemic and portal circulation in late-stage intestinal ischemia. These findings suggest an increase in anaerobic glycolysis and intestinal mucosa permeability. Amylase levels can also be elevated with bowel ischemia, but levels higher than 1000 U/L would suggest pancreatitis instead. Abdominal Doppler ultrasonography can detect thrombosis in larger veins but is unable to visualize smaller vena recta.
The objectives of mesenteric venous thrombosis treatment are to prevent bowel infarction and to avoid recurrent thrombosis in the future. Previously, the initial treatment method was surgery, such as intravenous thrombectomy with thrombolysis. However, more contemporary approaches mainly involve anticoagulation therapy, and adequate follow-up, which are less invasive and have shown to produce better patient outcomes. Heparin should be administered as soon as the diagnosis of mesenteric venous thrombosis is established. Once the patient improves, invasive procedures are no longer necessary, and warfarin therapy is introduced. Patients with known reversible conditions complete anticoagulation for approximately 6 months. Patients with prothrombotic states with unknown etiology continue lifelong anticoagulation.
For acute mesenteric venous thrombosis, management includes pain control, bowel rest, and fluid and electrolyte replacement. Red blood cell transfusion may be required for gastrointestinal bleeding. Broad-spectrum antibiotics for gram-negative and anaerobic organisms should be given to patients with septic thrombophlebitis of the mesenteric vein or superimposed sepsis due to bacterial translocation from bowel infarction.
If intestinal infarction is impending or peritoneal signs are present, urgent surgical consultation is warranted. The standard surgical intervention includes exploratory laparotomy with possible bowel resection with or without immediate re-establishment of bowel continuity depending on the amount of peritoneal contamination and the hemodynamic stability of the patient. Second look laparotomy may be required before final abdominal wall closure to assess bowel for continued ischemia further. Efforts are made to conserve as much bowel as possible. Patients at risk for bowel infarction without peritonitis can be treated with interventional radiology. This can include vasodilator therapy with papaverine infusion with or without thrombolytics if the mesenteric vein is not obstructed fully. Those properly treated tend to have a good prognosis in the long term.