Acute mesenteric ischemia (AMI) refers to a group of disease entities whose clinical features are caused by inadequate blood flow and tissue oxygenation to the small bowel and mesentery. The lack of sufficient oxygenation can be caused by occlusive or nonocclusive obstructions in either the venous or arterial system.¹

The overall incidence of AMI is estimated at 12.9 per 100,000 person-years.² It is reported that AMI represents 0.1% of all hospital admissions and 1% of all admissions for acute abdomen in the elderly population.3 These admission statistics are increasing due to the aging population, heightened awareness of diagnosis, and improved survival of patients with cardiac disease.^3,4

The overall mortality is extremely high at 60%-80%.4 Mortality is dependent on stage at presentation. If a patient presents prior to intestinal infarction, mortality is about 50%; after infarction, mortality is 62%-93%.4 Despite technological and therapeutic advances, overall mortality has not changed significantly in the past few decades.¹ However, early diagnosis and intervention prior to intestinal infarction is associated with improved mortality.⁵

The pathogenesis of AMI begins when impairment of microcirculation caused by blood vessel obstruction, constriction, or congestion leads to activation of inflammatory cells, endothelial cells, and platelets. This results in increased inflammatory cytokine production and cell permeability.

Damage to the microcirculation can cause local irreversible intestinal necrosis and translocation of gut bacteria, as well as systemic injuries such as disseminated intravascular coagulation (DIC) and systemic inflammatory response syndrome (SIRS). Reperfusion injury is a common feature of AMI, where restoration of oxygenation to ischemic tissue leads to the generation of free radicals and subsequent damage to cell membranes.⁶

The spectrum of AMI can be divided into four subtypes based on etiology: embolic, thrombotic, nonocclusive, and venous.

Mesenteric arterial embolism is the most common, accounting for almost half of all cases of AMI.4 Risk factors associated with arterial embolism include age, dysrhythmias (especially atrial fibrillation), myocardial infarction, rheumatic heart disease, aortic aneurysm, cardiac surgery, angiography, and endocarditis.

Mesenteric arterial thrombosis is the underlying etiology in 20% of all AMI cases.⁴ The major risk factor is severe atherosclerosis.^1,4,6 The superior mesenteric artery (SMA) is the most common site of both embolic and thrombotic disease. Nonocclusive disease is caused by low-flow states, such as heart failure or shock, and accounts for 25% of all AMI cases.

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

CT angiography has emerged as the diagnostic gold standard for AMI. Early reports demonstrated that an optimal sensitivity and specificity can be achieved utilizing this technique (96% and 94%, respectively).¹¹ Multiple recent reports have confirmed these findings¹² and a recently published meta-analysis showed a pooled sensitivity of 93% and a pooled specificity of 96%,13 suggesting CT angiography may be used as the first-line imaging method.

Duplex ultrasound also was studied for the diagnosis of AMI. Although sensitive in detecting proximal occlusive disease, it was found to be of little aid in detecting occlusive emboli beyond the proximal main vessel or in nonocclusive disease.

Magnetic resonance (MR) angiography has comparable accuracy to CT angiography in diagnosing AMI.¹⁴ The advantage of MR over CT is avoidance of allergy and nephrotoxicity from contrast dye. The major limitations of MR include availability, technical difficulty, and the amount of postacquisition processing of images, which delays the diagnosis.

Conventional angiography is the historical diagnostic gold standard. This modality is now being replaced by CT angiography. The primary advantage of conventional angiography is the ability to simultaneously diagnose and intervene therapeutically. The limitations of conventional angiography are lack of universal availability, the invasive nature of the study, and the potential for complications.

As more nonsurgical treatment options for AMI are being explored (e.g., directed thrombolytics and vasodilators), the role of conventional angiography is becoming increasingly important.¹⁵

Initial treatment of AMI includes active resuscitation, aggressive hydration, and treatment of the underlying etiology. Secondary treatment goals should be to reduce any associated vasospasm, prevent propagation of blood clot, and minimize the potential for reperfusion injury.¹⁵

Fluid repletion is important, as most patients will present with at least moderate dehydration, and the clinical course may be complicated by hypotension from septic shock.⁸

Broad-spectrum antibiotics should be initiated early to target gram-negative and anaerobic bacteria.⁸ Vasopressors can worsen oxygen delivery to the splanchnic circulation and should be minimized, if at all possible.¹⁵ If no contraindication to anticoagulation exists, a heparin infusion should be initiated to minimize thrombus formation and propagation.

Early consultation with interventional radiology and surgery is necessary for definitive management.

Endovascular interventions in hemodynamically stable patients include angioplasty, arterial stenting, aspiration embolectomy, and directed SMA thrombolysis.

Vasodilators are employed to reduce vasospasm. Specific agents include papaverine (a phosphodiesterase inhibitor) and glucagon. Papaverine’s standard dose is 30-60 mg/h via direct angiography catheter. Patients with peritoneal signs or concern for perforated bowel should prompt immediate surgical consultation. However, attempts at revascularization should precede surgical intervention when the clinical situation allows.⁸

Laparotomy is required for all patients who have evidence of any threatened bowel.¹⁵

Other surgical approaches include open embolectomy, thromboendarterectomy, and mesenteric artery bypass.

Acute mesenteric ischemia is a difficult clinical problem in part because of varying underlying etiologies and difficulty establishing the diagnosis.

A high index of suspicion is required, given the notable lack of simple, noninvasive testing available to confirm or exclude the diagnosis.

Early recognition and initiation of management are especially important given the high morbidity and mortality related to delay in diagnosis.

Suspect AMI in the elderly patient with a history of cardiac disease who presents with abdominal pain.

References

1. O’Keefe KP and Sanson TG. Mesenteric ischemia. In: Adams JG, et al. Emergency Medicine, 2008, p. 331.
2. Acosta S. Epidemiology of mesenteric vascular disease. Semin Vasc Surg 2010 Mar;23(1):4-8.
3. Ruotolo RA, et al. Mesenteric ischemia in the elderly. Clin Geriatr Med 1999;15(3):527-57.
4. Oldenburg WA, et al. Acute mesenteric ischemia. Arch Intern Med 2004;164:1054-62.
5. Brandt LJ and Boley SJ. AGA technical review on intestinal ischemia. Gastroenterology 2000;118:954-68.
6. Yasuhara H. Acute mesenteric ischemia: The challenge of gastroenterology. Surg Today 2005;35:185-95.
7. Hendrickson M and Naparst TR. Abdominal surgical emergencies in the elderly. Emerg Med Clinic North Am 2003;21:937-69.
8. Evennett NJ, et al. Systematic review and pooled estimates for the diagnostic accuracy of serological markers for intestinal ischemia. World J Surg 2009;33:1374-83.
9. Berland T and Oldenburg WA. Acute mesenteric ischemia. Curr Gastroenterol Rep 2008;10(3):341-6.
10. Taourel PG, et al. Acute mesenteric ischemia: Diagnosis with contrast-enhanced CT. Radiology 1996;199(3):632-6.
11. Kirkpatrick ID, et al. Biphasic CT with mesenteric CT angiography in the evaluation of acute mesenteric ischemia. Radiology 2003;229(1):91-8.
12. Ofer A, et al. Multidetector CT angiography in the evaluation of acute mesenteric ischemia. Eur Radiol 2009 Jan;19(1):24-30.
13. Menke J. Diagnostic accuracy of multidetector CT in acute mesenteric ischemia: systematic review and meta-analysis. Radiology 2010;256(1):93-101.
14. Chow LC, et al. A comprehensive approach to MR imaging of mesenteric ischemia. Abdom Imaging 2002;27:507-16.
15. Wyers MC. Acute mesenteric ischemia: Diagnostic approach and surgical treatment. Semin Vasc Surg 2010;23(1):9-20.