A 76-year-old Caucasian man presented with acute onset of intense periumbilical abdominal pain associated with nonbloody diarrhea. His past medical history was significant for portal vein thrombosis diagnosed 2 years earlier. At that time thrombophilia workup was unremarkable except for JAK2 V617F mutation. Subsequent bone marrow studies showed no evidence of myeloproliferative disease (MPD). Other comorbidities included coronary artery disease, atrial fibrillation, hypertension, and dyslipidemia. His Coumadin treatment was interrupted 1 week prior to the admission for a tooth extraction and was not resumed. His vital signs were normal except for mild tachycardia. The abdominal pain was severe and seemed to be out of proportion to the physical findings. The abdomen was soft with predominantly midline tenderness and mild guarding. The remainder of the physical examination was unremarkable.

Comprehensive laboratory evaluation was only remarkable for an elevated white blood cell (WBC) count to 21,000 cells per cubic millimeter with normal differential. Contrast-enhanced computed tomographic (CT) scan of the abdomen showed acute superior mesenteric vein (SMV) thrombosis, thickening of small bowel loops, and presence of collateral vessels at the porta hepatis (Figures 50-1,50-2 50-3).

Adequate anticoagulation was achieved with unfractionated heparin. However, the following day his abdominal pain was worse and WBC count increased to 34,000 per cubic millimeter. An exploratory laparotomy revealed an ischemic ileum that necessitated a small bowel resection with primary anastomosis. After a prolonged hospitalization, the patient recovered and was discharged home on Coumadin.

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  Mesenteric venous thrombosis (MVT) refers to thrombosis of the splanchnic veins draining the intestine (superior mesenteric, inferior mesenteric, portal, and splenic veins).

  
  
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  Venous obstruction induces bowel edema and distension that ultimately impedes the arterial inflow leading to intestinal ischemia.

  
  
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  JW Elliot first recognized MVT as a cause of intestinal ischemia in 1895.

  
  
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  The high-mortality rates formerly encountered in patients with MVT have been attributed to its insidious course, late presentation, and missed diagnosis.

  
  
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  Wide availability of CT venography (CTV) and magnetic resonance venography (MRV) has led to a decline in the mortality rates from acute MVT from early diagnosis.¹

  
  
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  The SMV, which drains the small intestine, cecum, ascending colon, and transverse colon, is most commonly affected, whereas the inferior mesenteric vein (IMV) draining the descending colon, the sigmoid colon, and the rectum is rarely involved.

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  The average age of presentation ranges from 45 to 60 years with an overall slightly higher male gender predominance.^2,3

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  MVT can be primary (without any underlying etiology) or secondary.

  
  
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  Numerous causes of secondary MVT have been identified (Table 50-1).⁴

  
  
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  The extent of the thrombotic event, rate of thrombus expansion, size of the vessel involved, and the depth of intestinal wall ischemia determine the degree of intestinal injury.

  
  
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  Ischemic injury restricted to mucosa leads to abdominal pain and diarrhea, while transmural ischemia or necrosis can lead to gastrointestinal bleeding and peritonitis.

  
  
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  Hypercoagulable states lead to thrombosis arising in the small veins (intramural venules, vasa recta, and venous arcades), which then propagates to involve the large veins. In contrast, thrombosis due to intra-abdominal causes (such as surgery or pancreatitis) begins in the large veins and then progresses distally to the small veins.

  
  
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  Contrary to arterial causes of bowel ischemia, the transition from ischemic segment to normal bowel is usually gradual with no clear demarcation separating viable and nonviable tissues.