Splanchnic venous thrombosis



Splanchnic venous thrombosis involves thrombosis in the mesenteric, splenic, or portal veins, with or without the hepatic veins.



The superior mesenteric and splenic veins join to form the portal vein, which supplies up to 75% of blood to the liver. 



The incidence is estimated to be between 1 to 4 cases per million people.



The Budd-Chiari syndrome, hepatic venous thrombosis, is the least common manifestation of splanchnic venous thrombosis, with an incidence of 0.5 to 1 case per million people per year .



They most common sites of splancnic vein thrombosis are  the portal vein (77%) and the mesenteric vein (44%).



Splanchnic venous thrombosis


causes intestinal infarction distinct from mesenteric arterial occlusion.



Mesenteric venous thrombosis accounts for 5% to 15% of all intestinal ischemic events.



Etiology of splanchnic venous thrombosis is divided into localized and systemic causes. 



Local causes include:  cirrhosis, solid cancer such as hepatocellular carcinoma or gastric and pancreatic adenocarcinomas, inflammatory disorders of the abdomen such as inflammatory bowel disease and diverticulitis, and abdominal surgery. 



Systemic causes include inherited and acquired thrombophilic conditions: Inherited factors may include the factor V Leiden mutation and the prothrombin gene mutation 20210A; acquired thrombophilic causes include myeloproliferative neoplasms especially with positive JAK2 mutation, the antiphospholipid antibody syndrome, paroxysmal nocturnal hemoglobinuria, hormonal therapy, and abdominal malignancy.



Idiopathic splanchnic thrombosis  accounts for about 15% to 27% of cases.



The most common local causes are liver cirrhosis (27.8%) and solid cancer (22.7%.



Myeloproliferative neoplasms are the leading systemic cause  of splanchnic thrombosis.



Factor V Leiden is more associated with Budd-Chiari syndrome while the prothrombin gene mutation has a stronger association with portal venous thrombosis.



Clots seen in larger vessels are usually due to intra-abdominal causes.



With thrombophilic the thrombosis often begins in smaller vessels and progresses to involve larger vessels.



The most prominent feature of mesenteric ischemia, of arterial or venous type, is abdominal pain out of proportion to the physical exam.



Splanchnic venous thrombosis can be acute, subacute, or chronic.



With acute splanchnic venous thrombosis, abdominal pain begins suddenly and is associated with a risk of bowel infarction and peritonitis. 



The subacute form of splanchnic venous thrombosis is  characterized by abdominal pain lasting for days to weeks without bowel infarction. 



Pain in acute and subacute thrombosis is mid-abdominal and colicky.



With acute Budd-Chiari syndrome there is an associated ascites and hepatic necrosis.



Patients with  chronic splanchnic venous thrombosis may not exhibit pain, but  develop extensive venous collateral circulation, and are at risk for complications such as bleeding esophageal varices.



Patients  with  chronic splanchnic venous thrombosis can develop fever, guarding, and rebound tenderness and progress to bowel infarction and peritonitis.



An abdominal CT scan is the best test for diagnosing splanchnic venous thrombosis. 



Abdominal CT findings include: acute thrombus will appear as a central lucency in the mesenteric vein, and enlargement of the superior mesenteric vein.



If abdominal CT or MRI reveal developed collateral circulation in the mesentery and retroperitoneum, the thrombosis has been present for more than a few weeks.



Ultrasound usefulness in splanchnic venous thrombosis is limited by overlying bowel gas.



Doppler ultrasound has a sensitivity of about 90% for the diagnosis of Budd-Chiari syndrome and portal venous thrombosis. 



Anticoagulation is recommended for all patients with splanchnic venous thrombosis for at least 3 months.



Longer treatment is proposed in patients with permanent thrombotic conditions and a low bleeding risk.



Extended anticoagulation is recommended for cancer-associated thromboembolism.



Anticoagulation for patients with acute portal venous thrombosis and Budd-Chiari syndrome is recommended for at least 3 months. 



Where permanent risk factors or clot extension into the mesenteric veins exist, patients should receive anticoagulation indefinitely, as with patients with Budd-Chiari syndrome.



Thrombolytic therapy is for  patients with severe symptoms, such as mesenteric venous thrombosis with ischemia, and a low risk of bleeding .



Direct oral anticoagulant drugs have the potential to make splanchnic venous thrombosis treatment easier.



The risk for both thrombosis recurrence and bleeding is higher in patients with portal venous thrombosis than in patients with isolated mesenteric venous thrombosis. 



Anticoagulation therapy may improve survival, decrease the recurrence rate, and improve recanalization. 



The recanalization in portal venous thrombosis may prevent subsequent development of portal hypertension.







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