- Case Report
- Open Access
Spontaeneous subacute portomesenteric venous thrombosis: a case report
© Mushtaque et al; licensee BioMed Central Ltd. 2008
- Received: 28 May 2008
- Accepted: 27 August 2008
- Published: 27 August 2008
Although uncommon and often asymptomatic, portal venous thrombosis can have catastrophic consequences for the individual it afflicts, particularly when the process propagates to involve the superior mesenteric vein. Familiarity with the condition's pathogenesis and presentation however permits early diagnosis and allows aggressive conservative management to achieve a successful outcome. Here we describe the successful outcome of such management for a 42-year-old male patient who developed this condition spontaneously.
- Portal Vein
- Esophageal Varix
- Portal Vein Thrombosis
- Superior Mesenteric Vein
- Portal Hypertensive Gastropathy
Portomesenteric ischemia accounts for approximately 5–15% of all cases of mesenteric ischemia and has been associated with mortality rates of 20–50% [1, 2]. Recent thrombosis of the portal vein may be asymptomatic or else may be associated with a systemic inflammatory syndrome with or without signs of intestinal ischemia. Old thrombosis of the portal vein is usually only recognizable on imaging by the demonstration of its cavernous transformation. Such a "portal cavernoma" refers to venous collateralization around the portal vein which develops in response to occlusion of the extrahepatic portal system and which partially maintains hepatopedal blood flow . It has been previously shown that the interval between obstruction of the portal vein and the cavernous transformation is approximately 5 weeks . These multiple, millimetric veins tends to occur predominantly around the suprapancreatic part of the common bile duct and may result in cholestasis due to the resulting angulation and even stenosis of the duct . The main complication however of chronic portal vein thrombosis is gastrointestinal bleeding due to rupture of esophageal varices or portal hypertensive gastropathy. Although less frequent, intestinal necrosis may occur due to thrombotic extension that can result in obstruction of the superior mesenteric vein. The cause of thrombosis may be either a general prothrombotic state (e.g. myeloproliferative syndrome, antiphospholipid syndrome, antithrombin deficiency, protein C or S deficiencies, or factor gene mutations) or intraabdominal inflammation (including pancreatitis and inflammatory bowel disease). Furthermore, portal vein occlusion has been reported to occur after abdominal surgery (in particular splenectomy).
Although surgery may be required when venous gangrene of the intestine occurs, early diagnosis may allow successful conservative management with anticoagulation. Although thrombolysis has been recently proposed , heparinization remains the first-line treatment. For this, unfractionated heparin infusion is preferable to fractionated subtypes because of its shorter half-life and ease of reversibility. Upper gastrointestinal bleeding risk can be prevented by beta-adrenergic blockade, endoscopic ligation, or endoscopic sclerosis of varices. Because the risk of disease progression persists early after initiation of therapy, a low threshold for operative exploration is required during conservative management. In the long-term, permanent anticoagulant treatment is recommended when a permanent prothrombotic state exists, even in patients who have a history of gastrointestinal bleeding.
Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
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