History
To an extent, all types of acute mesenteric ischemia (AMI) present similarly. However, there are some differences in clinical appearance for each type (see below), which may be diagnostically useful. The most important finding is pain that is disproportionate to physical examination findings. Typically, pain is moderate to severe, diffuse, nonlocalized, constant, and sometimes colicky.
Onset varies from type to type. Nausea and vomiting are found in 75% of affected patients. Anorexia and diarrhea progressing to obstipation are also common. Abdominal distention and gastrointestinal (GI) bleeding are the primary symptoms in as many as 25% of patients. Pain may be unresponsive to opioids. As the bowel becomes gangrenous, rectal bleeding and signs of sepsis (eg, tachycardia, tachypnea, hypotension, fever, and altered mental status) develop. A review of systems, looking for risk factors of AMI, should be performed.
If not properly and rapidly treated, AMI has a catastrophic outcome. Accordingly, it should be considered in any patient with abdominal pain disproportionate to physical findings, gut emptying in the form of vomiting or diarrhea, and the presence of risk factors, especially age older than 60 years.
Acute mesenteric arterial embolism
Of all the types of AMI, acute mesenteric arterial embolism (AMAE; ie, embolic AMI) typically has the most abrupt and painful presentation as a consequence of the rapid onset of occlusion and the inability to form additional collateral circulation. It has been described as abdominal apoplexy and is sometimes referred to as a “bowel attack.”
Often, vomiting and diarrhea (gut emptying) are observed. Patients are usually found to have a source of embolization. Because most emboli are of cardiac origin, patients often have atrial fibrillation or a recent myocardial infarction (MI) with mural thrombus. Infrequently, patients may report a history of valvular heart disease or a previous embolic episode.
Acute mesenteric arterial thrombosis
Acute mesenteric arterial thrombosis (AMAT; ie, thrombotic AMI) typically develops when an artery already partially blocked by atherosclerosis becomes completely occluded.
A patient with AMAT presents with severe abdominal pain. He or she may give a history of postprandial pain, typically occurring 10-20 minutes after eating and lasting as long as 1-3 hours (abdominal angina). The pain is diffuse, and the patient may report frank blood in the stool. Symptoms worsen over time.
Typically, these patients typically have a history of atherosclerotic disease at other sites, such as coronary artery disease (CAD), cerebrovascular disease, recent MI, peripheral artery disease (PAD; especially aortoiliac occlusive disease), or a history of aortic reconstruction. They may have a long history of smoking or uncontrolled diabetes mellitus. Weight loss, “food fear,” early satiety, and altered bowel habits may be present.
The precipitating event that initiates AMAT may be a sudden drop in cardiac output from acute MI or congestive heart failure (CHF) or a ruptured plaque. Dehydration from vomiting or diarrhea due to an unrelated illness may also precipitate AMAT. As a consequence of the massive shifts in fluid volume and the hypercoagulable state, patients in surgical intensive care are especially prone to developing arterial thrombosis.
Compared with patients who have AMAE, patients who have AMAT have undergone a more gradual progression of arterial occlusion and frequently have a better collateral supply. Their bowel viability is better preserved, which means that the presentation is often less severe than would be the case with AMAE. Symptoms tend to be less intense and of more gradual onset.
Nonocclusive mesenteric ischemia
Nonocclusive mesenteric ischemia (NOMI) occurs more frequently in older patients. Often, these elderly patients are already in an intensive care unit (ICU) with acute respiratory failure or severe hypotension from cardiogenic or septic shock, or else they are taking vasopressive drugs. Historically, many were taking digitalis (which is seldom prescribed nowadays in the United States).
Symptoms typically develop over several days, and patients may have experienced a prodrome consisting of malaise and vague abdominal discomfort. When infarction occurs, the clinical condition of the ICU patient deteriorates with no apparent reason. Patients may report increased pain associated with vomiting. They may become hypotensive and tachycardic, with loose bloody stool.
Mesenteric venous thrombosis
Mesenteric venous thrombosis (MVT) is often observed in a much younger patient population than other types of AMI are. MVT patients can present with an acute or subacute abdominal pain syndrome related to involvement of the small intestine rather than the colon.
The symptoms of MVT are frequently less dramatic than those of other types of AMI, with a more insidious onset. Diagnosis can be even more difficult than for other AMI types, in that MVT symptoms may have been present for weeks before being noticed or reported (27% have symptoms for >30 days). Typical symptoms of MVT may have been experienced for a prolonged period with gradual worsening (eg, vague abdominal discomfort evolving over 7-10 days).
Many patients have a history of one or more of risk factors for hypercoagulability. These include oral contraceptive use, congenital hypercoagulable states, deep vein thrombosis (DVT), pulmonary embolism (PE), liver disease, cancer, and portacaval surgery. Patients presenting with pancreatitis or signs of intra-abdominal infection should be considered predisposed to developing MVT.
Physical Examination
The different etiologies notwithstanding, physical examination findings are generally similar in patients with AMI. The characteristic feature of this syndrome is a relatively normal abdominal examination in the face of severe abdominal pain. The main distinction to be made with respect to physical findings is between early and late presentations.
Early in the course of AMI, in the absence of peritonitis, physical signs are few and nonspecific. Tenderness is minimal to nonexistent. The abdomen may be distended. Stool may be positive for blood.
Peritoneal signs develop late, when infarction with necrosis or perforation occurs. Tenderness becomes severe and may indicate the location of the infarcted bowel segment. A palpable tender mass may be present. Bowel sounds range from hyperactive to absent. Voluntary and involuntary guarding appears.
Fever, hypotension, tachycardia, tachypnea, and altered mental status are observed. Foul breath may be noted with bowel infarction, from the putrefaction of undigested alimentary material accumulated proximal to the pathologic site. Paracentesis may demonstrate bloody peritoneal fluid; however, this occurs after bowel infarction and therefore is a late sign.
Signs reflecting risk factors for AMI may be noted. Patients with AMAE may have atrial fibrillation or heart murmurs. Those with AMAT or NOMI may have an abdominal murmur or the scar from an abdominal aortic repair with or without reimplantation of the superior mesenteric artery (SMA). Those with MVT may have evidence of tumor, cirrhosis, DVT, or recent abdominal surgery.
Complications
The following are potential complications of AMI:
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Bowel necrosis necessitating bowel resection
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Sepsis and septic shock
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Multiple organ dysfunction syndrome (MODS)
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Death
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Pneumatosis intestinalis (black stripes of air) in advanced acute mesenteric ischemia (AMI) with gangrenous bowel.
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CT scan (with contrast) of nonocclusive mesenteric ischemia with resulting bowel wall edema (arrows).
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Aortogram showing narrowing of superior mesenteric artery.
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Radiograph showing bowel spasm (early sign of ischemia).
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Gas in colon wall (typical of advanced ischemia).
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Ischemia stricture.
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Thumbprinting of bowel, characteristic of mesenteric artery ischemia.
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Pathologic findings 2 hours after bowel ischemia starts.
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Microscopic findings 24 hours after ischemia starts.
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Gross specimen showing hemorrhagic dead bowel after resection from patient with acute mesenteric ischemia.
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Pneumatosis intestinalis, one of few radiographic findings in patients with mesenteric ischemia.
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Diagnosis and treatment of intestinal ischemia (mesenteric venous thrombosis and major nonembolic arterial occlusion). Solid lines indicate accepted management plan; dashed lines indicate alternate management plan. DVT=deep vein thrombosis; SMA=superior mesenteric artery. Adapted from Gastroenterology. 2000 May;118(5):954-68.
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Diagnosis and treatment of intestinal ischemia (minor arterial occlusion or embolus, major embolus, and splanchnic vasoconstriction without occlusion). Solid lines indicate accepted management plan; dashed lines indicate alternate management plan. DVT=deep vein thrombosis; SMA=superior mesenteric artery. Adapted from Gastroenterology. 2000 May;118(5):954-68.
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Management of colon ischemia. Solid lines indicate accepted management plan; dashed lines indicate alternative management plan. BE=barium enema; NPO—nil per os (nothing by mouth); PLC=protein-losing colopathy; IBD=inflammatory bowel disease. Adapted from Gastroenterology. 2000 May;118(5):954-68.
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Complete aortic occlusion (Leriche syndrome) with acute embolism of superior mesenteric artery.
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Gross specimen of dead bowel.
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Meandering artery (radiographic sign of preexisting bowel ischemia).
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CT scan demonstrating thrombosis of superior mesenteric vein.
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CT scan demonstrating thrombosis of portal vein.
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CT scan demonstrating cavernous change of superior mesenteric vein as consequence of venous thrombosis.
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Mesenteric venous air (red arrows) and free intraperitoneal air (white arrow.) Mesenteric venous air is common finding in advanced acute mesenteric ischemia. Courtesy of Brandon Dessecker, MD, Melanie Nukula, MD, and Robert Marx, DO.
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Pronounced portal venous air seen within liver (red arrow), as well as free intraperitoneal air (white arrow) and pneumatosis intestinalis throughout bowel wall, which are classic findings for advanced acute mesenteric ischemia. Courtesy of Brandon Dessecker, MD, Melanie Nukula, MD, and Robert Marx, DO.