Veno-occlusive mesenteric ischemia

Changed by Ayush Goel, 13 Aug 2014

Updates to Article Attributes

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Acute superior mesenteric vein thrombosis is one of the less common causes of intestinal ischaemia. 

For a general discussion refer to intestinal ischaemia

Epidemiology

Compared to acute superior mesenteric artery occlusion or ischaemia secondary to small bowel obstruction, acute superior mesenteric vein thrombosis is uncommon, accounting for only 5-15% of all cases of acute mesenteric ischemia 1-3. Often despite thrombosis of the SMV, small bowel necrosis does not occur 1, presumably due to persistent arterial supply and some venous drainage via collaterals.  

The majority of cases are considered secondary to an identifiable underlying condition, including 1-3

  • hypercoagulable states
    • malignancy
    • polycythemia vera
    • protein C and protein S deficiency
    • antithrombin III deficiency
  • recent abdominal surgery
  • intra-abdominal or systemic sepsis
  • portal hypertension
  • mechanical narrowing due to adjacent malignancy

Approximately 20-40% of cases have not clear precipitant and are considered idiopathic 3

Clinical presentation

Acute superior mesenteric vein thrombosis presents vaguely as an acute abdomen with gradually worsening diffuse, colicky abdominal pain, associated with distention, and symptoms may have been present for a few days 2-3. Heme-positive stool may also be present 3. As ischaemia progresses, eventual necrosis, perforation, sepsis and shock ensue. 

Pathology

As the superior mesenteric vein thrombosis, back pressure builds as arterial supply to the bowel is uninterrupted. This leads to bowel wall oedema (and thus bowel wall thickening) and possible intramural haemorrhage (leading to hyperdense bowel wall) 1. Depending on the how complete occlusion is, and whether or not collateral drainage is available, the combination of back pressure, and bowel wall thickening can lead to inadequate tissue perfusion leading to intestinal ischaemia, infarction and eventual necrosis 1

Radiographic features

Imaging is the only reliable way of making the diagnosis, especially as clinical presentation is vague. CT is the most accurate test available to us at present, with excellent sensitivity (up to 100%). Ultrasound and catheter mesenteric angiography are reported to have approximately 70% sensitivity 3 but in practice are infrequently requested as a first line investigation, unless the presentation suggests another diagnosis (e.g. cholecystitis). 

CT
Technique

For a discussion on CT technique refer to intestinal ischaemia article. 

Findings

The findings in superior mesenteric vein thrombosis include 1:

  • bowel wall
    • typically thickened 
      • most common finding
      • 8-9mm (usually <15mm)
      • normal wall is 3-4mm
    • density (variable)
      • hypo-attenuating due to oedema
      • hyperdense wall on non-contrast images (due to intramural haemorrhage)
    • enhancement (variable)
      • absent once infarcted (more common in arterial occlusion)
      • hyper-enhancement or target appearance 
      • prolonged enhancement
    • pneumatosis intestinalis (transmural infarction)
  • dilated and fluid filled lumen
  • filling defect in the superior mesenteric vein and branches (seen in 90% of cases)
  • mesenteric congestion and stranding
  • ascites

Treatment and prognosis

Traditionally management has been surgical, with assessment of the small bowel for necrosis +/- resection, followed by anti-coagulation. This has a reported mortality rate of 7-20% 2-3, which although still high, is much better than the 92-100% mortality with non-operative management 3

Surgery is clearly still required in patients with intestinal infarction, however in patients where this has not yet occursoccurred, endovascular thombolysis / thrombectomy is also an option in selected cases 2-3. Thrombolytic agents can be introduced via either via superior mesenteric artery catheter or a transhepatic transportal retrograde approach, whereas mechanic clot lysis can only be achieved via a retrograde transhepatic venous approach 2.  

Probably the safest way to directly access the portal circulation is via a transjugular / transhepatic approach (similar to the initial steps of a TIPS). Direct transhepatic approach have also been performed but are associated with greater risk of haemorrhage 5

Complications

Complications include 3:

  • surgical complications
    • abscess / anastomosis breakdown
    • short bowel syndrome
  • recurrent mesenteric thrombosis: 14%, usually within 6 weeks

Differential diagnosis

If superior mesenteric vein thrombus / filling defect can be identified then no differential diagnosis exists. In cases where a filling defect cannot be identified then the differential diagnosis is essentially that of bowel wall thickening and includes:

  • -<li><a title="Portal hypertension" href="/articles/portal_hypertension">portal hypertension</a></li>
  • +<li><a href="/articles/portal-hypertension">portal hypertension</a></li>
  • -</ul><h4>Treatment and prognosis</h4><p>Traditionally management has been surgical, with assessment of the small bowel for necrosis +/- resection, followed by anti-coagulation. This has a reported mortality rate of 7-20% <sup>2-3</sup>, which although still high, is much better than the 92-100% mortality with non-operative management <sup>3</sup>. </p><p>Surgery is clearly still required in patients with intestinal infarction, however in patients where this has not yet occurs, endovascular thombolysis / thrombectomy is also an option in selected cases <sup>2-3</sup>. Thrombolytic agents can be introduced via either via superior mesenteric artery catheter or a transhepatic transportal retrograde approach, whereas mechanic clot lysis can only be achieved via a retrograde transhepatic venous approach <sup>2</sup>.  </p><p>Probably the safest way to directly access the portal circulation is via a transjugular / transhepatic approach (similar to the initial steps of a <a href="/articles/transjugular-intrahepatic-portosystemic-shunt">TIPS</a>). Direct transhepatic approach have also been performed but are associated with greater risk of haemorrhage <sup>5</sup>. </p><h5>Complications</h5><p>Complications include <sup>3</sup>:</p><ul>
  • +</ul><h4>Treatment and prognosis</h4><p>Traditionally management has been surgical, with assessment of the small bowel for necrosis +/- resection, followed by anti-coagulation. This has a reported mortality rate of 7-20% <sup>2-3</sup>, which although still high, is much better than the 92-100% mortality with non-operative management <sup>3</sup>. </p><p>Surgery is clearly still required in patients with intestinal infarction, however in patients where this has not yet occurred, endovascular thombolysis / thrombectomy is also an option <sup>2-3</sup>. Thrombolytic agents can be introduced via either via superior mesenteric artery catheter or a transhepatic transportal retrograde approach, whereas mechanic clot lysis can only be achieved via a retrograde transhepatic venous approach <sup>2</sup>.  </p><p>Probably the safest way to directly access the portal circulation is via a transjugular / transhepatic approach (similar to the initial steps of a <a href="/articles/transjugular-intrahepatic-portosystemic-shunt">TIPS</a>). Direct transhepatic approach have also been performed but are associated with greater risk of haemorrhage <sup>5</sup>. </p><h5>Complications</h5><p>Complications include <sup>3</sup>:</p><ul>
  • -<li><a href="/articles/typhilitis">typhilitis</a></li>
  • +<li><a href="/articles/typhlitis">typhilitis</a></li>

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