Venous thrombosis is the least common cause of AMI, accounting for 5% of all cases. Risk factors for venous thrombosis include age, hypercoagulable state, and intra-abdominal trauma or infection. The superior mesenteric vein is affected most often. ^1,4,6

The clinical presentation of AMI can be quite varied, usually based on etiology.⁴ Embolic disease typically causes acute pain that is maximal at onset with diarrhea. Thrombosis usually causes postprandial pain over several days, associated with anorexia and weight loss. Both nonocclusive and venous disease processes are subacute or even chronic.

Most patients with AMI are elderly, but nonocclusive and venous disease can occur in younger patients in the setting of shock, digoxin therapy, and oral contraceptive use.

Many symptoms are nonspecific and occur with early disease, prior to transmural involvement and peritoneal irritation.

Ruotolo et al. report that only a third of patients with AMI present with nausea, vomiting, or diarrhea.³ Up to 25% will have a positive fecal occult blood test,⁷ but this, too, is not a specific finding.

The late findings of AMI include marked abdominal distention, shock, and peritoneal irritation, signaling infarction, and perforation.³

No single laboratory test is sufficiently sensitive or specific for the diagnosis of AMI.⁵ Pooled estimates of accuracy for abnormal lab tests are white blood cell count (sensitivity 80%, specificity 50%), amylase (42%, 68%), pH (38%, 84%), and base excess (74%, 42%).

The d-isomer of lactate, made by bacteria (l-isomer by humans), was thought to be indicative of bacterial translocation. However, pooled sensitivity was no better than 82% and specificity only 48%.⁸

The major role of abdominal X-ray is to exclude other causes of acute abdominal pain.⁵ In fact, abnormal findings on a plain film of the abdomen are nonspecific, indicative of late-stage presentation and associated with high mortality rates.5 The classic finding of bowel wall thickening and thumbprint sign (suggestive of thickened edematous mucosal folds) occurs in less than 40% of patients at presentation.⁹

Oral contrast enhanced computed tomography (CT) also has been investigated for the diagnosis of AMI. The diagnostic criteria employed relied on late findings such as intramural gas, portal venous gas, focal lack of bowel-wall enhancement, and liver or splenic infarcts. Reported sensitivity and specificity of CT are 64% and 92%, respectively.¹⁰