Acute Mesenteric Ischemia

Acute mesenteric ischemia (AMI) is a life-threatening vascular emergency that requires early diagnosis and intervention to adequately restore mesenteric blood flow and prevent fatal bowel necrosis. Causes include arterial embolus, which occurs most frequently (40%–50%), arterial thrombosis (20%–30%), venous obstruction (5%–18%) and nonobstructive causes (20%–30%). Clinical signs vary considerably and are nonspecific. Patients present with severe abdominal pain that is initially out of proportion to any physical findings. Risk factors and clinical course differ according to underlying physiopathology.

Arterial embolism occurs in patients with cardiac conditions that predispose to emboli (thrombi, tachyarrhythmia), but can also complicate aortic catheterization procedures. Onset of symptoms is rapid, with intense and unrelenting abdominal pain that is disproportionate to physical examination findings. Associated symptoms include nausea and diarrhea, with bloody stools in some cases. Symptoms related to emboli in other locations are not uncommon. Patients who develop acute abdominal pain after arterial interventions in which catheters traverse the visceral aorta or who have arrhythmias (e.g., atrial fibrillation) or recent myocardial infarction should be suspected of having AMI.

The typical clinical trial for an acute embolic superior mesenteric artery (SMA) occlusion is (1) severe abdominal pain with minimal findings on examination (pain out of proportion to clinical signs), (2) bowel emptying, and (3) the presence of a source of embolus, most often atrial fibrillation. The often sudden onset of abdominal pain (phase 1; reversible ischemia) may decrease in intensity (phase 2), followed by an increase in abdominal pain associated with clinical deterioration and progression toward generalized peritonitis (phase 3; irreversible ischemia).

Arterial thrombosis occurs in patients at risk for atherosclerosis at areas of severe atherosclerotic narrowing, most often where the SMA and celiac artery originate from the aorta. Occlusive atherosclerotic lesions in the SMA are clinically more important, compared with those in the celiac artery. Thrombosis can also complicate aortic aneurysm or dissection. In most cases, onset of symptoms is insidious, sometimes preceded by symptoms of chronic mesenteric ischemia (e.g., intermittent postprandial abdominal pain, food avoidance, weight loss). Patients often have evidence of atherosclerotic occlusive disease elsewhere, such as coronary or peripheral artery disease. The frequency with which chronic intestinal ischemia progresses to AMI, presumably by acute-on-chronic thrombosis, is unknown.5

AMI as a complication of aortic dissection is discussed elsewhere in this book.

Mesenteric venous thrombosis (MVT) often affects much younger patients, many of whom have a history of one or more risk factors for hypercoagulability. Symptoms may present later than acute arterial thrombosis, sometimes after as long as 30 days, and are frequently less dramatic.

Inflammation or other local factors contribute to thrombus formation in large mesenteric veins, whereas systemic hypercoagulability is more likely to be responsible for thrombus formation in smaller vessels.

Nonocclusive mesenteric ischemia (NOMI) generally occurs in older patients who have severe clinical conditions and splanchnic vasoconstriction; these patients are sometimes unable to express abdominal pain. In the intensive care unit setting, acute respiratory distress syndrome or severe hypotension from cardiogenic or septic shock may precede NOMI. Here, AMI is the result of severe and prolonged intestinal arterial vasospasm. Symptoms typically develop over several days and patients may have experienced malaise and vague abdominal discomfort. The diagnosis is more often made when infarction occurs: patients develop increased pain associated with vomiting and may become hypotensive and tachycardic, with loose bloody stools. In this setting, the diagnosis is highly probable, especially if patency of the superior mesenteric vein (SMV) has been demonstrated.

NOMI should be suspected in patients receiving vasoconstrictive substances and medications (e.g., cocaine, ergot, vasopressin, and norepinephrine) who develop abdominal pain requiring vasopressor support and evidence of multiorgan dysfunction. (Recommendation 1B).

It should also be suspected in patients who develop abdominal pain after coarctation repair or surgical revascularization for intestinal ischemia due to arterial obstruction.

AMI is an uncommon cause of acute abdominal pain (<1% among abdominal emergencies, according to Bergan et al.).

The diagnosis should be considered in patients with the following risk factors: age older than 60 years, previous history of vascular disease or valvular heart disease, cardiac arrhythmia, emboli, hypotension, recent heart failure, or hypercoagulability.

In occlusive AMI, overall symptoms on admission are nonspecific, from abdominal pain and nausea to hematochezia and discomfort.

Because of the nonspecific symptoms, the MVT is often mistakenly assumed to be due to other causes, e.g., postoperative discomfort or exacerbation of inflammatory bowel disease

There are no laboratory markers that are sufficiently accurate to identify the presence or absence of ischemic or necrotic bowel, although elevated serum L-lactate and D-dimer results may assist. (Recommendation 1B) In acute occlusive AMI, laboratory evaluation most frequently shows leukocytosis (90%) and lactic acidosis (88%). The serum amylase value is elevated in approximately 50% of patients; approximately 25% of patients have occult blood in the stool.

There is no single specific marker that is sensitive or specific for the diagnostic of MVT. Profound leukocytosis (>20,000 cells/μL) may be the only initial laboratory abnormality. Even if laboratory results are not definitive, they may help to corroborate clinical suspicion if a diagnosis of MVT is considered.

The diagnosis of AMI must be rapidly confirmed by a sensitive and specific imaging technique.

Conventional plain x-ray films often show nonspecific dilated bowel loops. They have limited diagnostic value in evaluating AMI, although signs of intestinal perforation and/or infarction may be seen. (Recommendation 1B). A negative x-ray does not exclude an AMI.

Ultrasonography is not an appropriate tool for suspected AMI. Bowel paralysis associated with acute intestinal ischemia precludes accurate Doppler ultrasound scanning in many patients. Although proximal occlusive lesions of the visceral arteries can be identified, distal occlusions cannot be visualized.

Computed tomographic angiography (CTA) is the current diagnostic modality of choice and should be performed as soon as possible for any patient suspected of having AMI. (Recommendation 1A). It allows the detection of thrombi and/or emboli into the SMA trunk or branches and of intestinal ischemic signs such as pneumatosis intestinalis, portalis, and/or pneumoperitoneum in occlusive AMI ( Fig. 28.1 A–B ).

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(A), (B) Computed tomographic angiography showing acute thrombosis of superior mesenteric and portal veins in a patient with worsening abdominal pain, treated by intensive intravenous heparin therapy because of a contraindication to thrombolysis.

The characteristic finding for MVT is a filling defect within the mesenteric vein. Other nonspecific findings include liver or splenic infarcts, focal lack of bowel-wall enhancement, bowel-wall thickening, indistinct bowel margins, ascites, and a thickened mesentery. The sensitivity and specificity of CTA in the arterial and venous phases are 93% and 100%, respectively.

Finally, digital subtraction angiography (DSA) is accurate for the diagnosis and characterization of occlusive AMI, but has been superseded by CTA, which facilitates the diagnosis of occlusive AMI and MVT. DSA is a diagnostic method that can differentiate occlusive, embolic, and thrombotic mesenteric arterial lesions from nonocclusive AMI. However, DSA is seldom used for diagnostic purposes alone. If endovascular revascularization seems to be possible, angiography must be performed without delay because revascularization must be undertaken early at the reversible ischemic stage, before bowel infarction supervenes (the common endpoint of all etiologic processes), which is characterized by onset of signs of peritoneal irritation.