Alcohol Abuse and Unusual Abdominal Pain in a 49-Year-Old

Gregory Taylor, DO; Michael Semple, DO; Matthew Warpinski, DO


October 02, 2020

Many risk factors for MVT are recognized, including direct injury (eg, abdominal trauma, splenectomy, intra-abdominal inflammatory processes), venous congestion/stasis (eg, congestive heart failure, portal hypertension, cirrhosis), and hypercoagulable conditions (eg, protein C/S deficiency, antithrombin III deficiency, factor V Leiden mutation, pancreatic/colon carcinoma, oral contraceptive use, polycythemia vera, heparin-induced thrombocytopenia, lupus anticoagulant/anti-phospholipid syndrome).[4] In pancreatitis, the pathogenesis involves local venous congestion/stasis and spasm, with mass effect from the inflamed pancreas and damage to the wall of the veins by pancreatic enzymes.[5]

Acute occlusion of the mesenteric vein results in increased resistance within the mesenteric venous bed, leading to decreased perfusion pressure.[3] As flow stagnates in the mesenteric vein, increased venous pressure results in an efflux of fluid into the tissues, leading to bowel-wall edema. If the clinical progression continues, venous return from the bowel wall is completely occluded, and the end result is bowel ischemia.[3] Integrity of the bowel mucosa is lost and bacteria can translocate, leading to lactic acidosis, sepsis, multiorgan failure, and eventually death.[2]

MVT can occur acutely, subacutely, or chronically. The clinical features vary, depending on the location of the thrombus within the splanchnic vasculature.[3] Acute MVT, similar to other forms of acute mesenteric ischemia, presents most often as a colicky periumbilical pain that is often out of proportion to the physical examination findings. However, the onset of venous thrombosis, compared with arterial thrombosis, is often less sudden and dull, with as many as 75% of patients presenting after 2 days of abdominal pain.[3]

Alternatively, chronic mesenteric venous thrombosis often presents with portal hypertension and variceal hemorrhage.[2] In general, peritoneal signs are absent, unless the venous thrombosis goes untreated and the bowel becomes ischemic, in which case peritoneal signs develop.

In a retrospective study, 31 patients diagnosed with MVT from 1985-1999 were reviewed.[4] Approximately 84% of patients presented with abdominal pain, with 16% presenting with peritoneal signs. Common overall symptoms included diarrhea (42%), nausea and vomiting (32%), lower gastrointestinal bleeding (19%), fatigue (16%), and upper gastrointestinal bleeding (10%). Furthermore, only 22 patients were initially treated with heparin. Five patients were found to have peritonitis and underwent exploratory laparotomy, with the ultimate goal to prevent or limit gangrenous bowel, with an additional five patients later undergoing surgery for the development of ischemic bowel. Seven of the 31 patients died within 30 days, secondary to complications from infarcted bowel and multisystemic organ failure. Overall, 19 of the 24 survivors were treated with long-term anticoagulation, with 88% of those surviving long-term.

Differentiating between ischemia secondary to MVT and ischemia secondary to a mesenteric arterial thrombosis is important. MVT presents in the setting of thrombophilia or an inflammatory abdominal process, whereas mesenteric arterial ischemia presents in the setting of cardiac disease, low-flow states, and atrial fibrillation.[1] Similar to all forms of mesenteric ischemia, no clinical features are specific to MVT. As such, a clinician must have a high index of suspicion in order to make an early diagnosis and avoid the complications of an undiagnosed MVT.


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