Acute Mesenteric Ischemia: Epidemiology, Pathophysiology, Clinical Evaluation, and Management

Arterial Embolism

Historically, arterial embolism was considered the common pathophysiology of acute mesenteric ischemia, accounting for 40% to 50% of cases. ^, Nearly one-third of patients with a mesenteric embolus have had an antecedent embolic event, most commonly arising from a cardiac source including atrial tachyarrhythmia, low ejection fraction (congestive heart failure, cardiomyopathy), recent myocardial infarction, and ventricular aneurysm, while as high as 68% of patients have synchronous embolisms in other locations. ^{, ,} Although less common than a cardiac source, proximal arterial sources, such as in instances of a cardiac valvular disease, endocarditis, aortic aneurysm or mural thrombi, and recent catheter-based angiography may also be sources of embolization.

Due to the oblique angle of the SMA origin from the visceral aortic segment, thromboembolism most commonly lodges in the SMA, specifically in the proximal SMA, just beyond the first few jejunal branches as the SMA tapers. However embolization to the celiac artery may also cause mesenteric symptoms, particularly in patients with chronic SMA disease. A minority (15%) may lodge at the SMA origin, but 50% lodge distal to the middle colic artery, ^, creating a classic pattern of ischemia that spares the first portion of the small intestine and the ascending colon ( Fig. 133.1 ). Atheroembolic emboli, in contrast, tend to be smaller and therefore lodge in the more distal mesenteric circulation; as a result, they affect bowel perfusion less often and in more localized areas.

Arterial Thrombosis

In patients with a thrombotic etiology, acute-on-chronic presentation is common and occurs when an arterial thrombosis is superimposed on pre-existing severe atherosclerotic disease. While historical data noted arterial embolism to be the most common cause of acute mesenteric ischemia, recent studies have suggested that in situ thrombosis of chronic lesions may now account for greater than 50% of cases of acute mesenteric ischemia. Autopsy studies have shown that up to 29% of people have significant stenosis in at least one mesenteric artery, including 60% of patients older than 80 years of age. In those with peripheral vascular disease, the incidence may be as high as 27%. In acute-on-chronic ischemia, the presentation of bowel infarction may be more insidious in onset due to a pre-existing collateral network that maintains viability until an event such as a small embolism or hypotension results in occlusion of a critically stenotic vessel or collateral.

Patients with previous intervention for mesenteric ischemia are also at heightened risk for thrombotic complications. These include patients who have in-stent restenosis or hyperplasia of a previous bypass graft. While immediate endovascular failures – including distal embolization, vessel perforation, dissection, stent migration, and thrombosis – result in higher mortality, morbidity, and longer hospital length of stay, late occlusion may also occur in patients treated for chronic mesenteric ischemia who have developed restenosis or intimal hyperplasia over time. For these reasons, short- and long-term follow-up is critical for maintaining the patency of both open- and endovascular-treated vessels.

Nonocclusive Mesenteric Ischemia

Mesenteric vasospasm, usually in the distribution of the SMA, is the sine qua non of Nonocclusive Mesenteric Ischemia (NOMI). This form of AMI accounts for approximately 20% of presentations, but carries the highest mortality rates. NOMI is morbid due to its difficulty to diagnose and treat and because of its frequent association with multisystem organ failure. ^, Initial descriptions were in postmortem observations of small intestinal gangrene in patients who had shown no evidence of arterial or venous occlusive disease. NOMI is frequently described in patients with severe cardiac failure, and while concomitant visceral atherosclerosis may be present, the underlying etiology is related to vasospasm. These observations formed the basis for the hypothesis that cardiac failure, peripheral hypoxemia, paradoxical splanchnic vasospasm, and reperfusion injury may all contribute to the development of NOMI. Perhaps resulting from excessive sympathetic activity during cardiogenic shock or hypovolemia, the vasospasm represents a homeostatic mechanism that attempts to maintain cardiac and cerebral perfusion at the expense of visceral and peripheral organs. Vasopressin and angiotensin are the likely neurohormonal mediators of this process. In the current era, vasoactive medications such as epinephrine, norepinephrine, and vasopressin have also been associated with the development of NOMI. Once mesenteric vasospasm is initiated, it may persist even after correcting the initiating event. Although intestinal auto-regulation may initially offset reductions in blood flow, the auto-regulatory capacity is exceeded after several hours.

Clinical Presentation

Patients presenting with acute mesenteric ischemia often have vague abdominal symptoms. These may include diffuse abdominal pain, nausea and vomiting, melena, and generalized malaise. Tenderness to palpation typically does not occur until transmural ischemia has developed, causing peritoneal irritation. Once patients have bowel necrosis they may present with tachycardia, hypotension, fever, and other signs of systemic sepsis. For patients who present with embolism, the onset is often more abrupt with rapid clinical decline due to the lack of an established collateral circulation. In contrast, patients with a thrombotic etiology may present with an insidious development and progression of symptomatology as a result of a developed collateral network. The subacute presentation may start days or weeks before the final acute insult that prompts the patient to seek medical attention. Patients may have abdominal pain, distention, diarrhea, acidosis, sepsis, or gastrointestinal bleeding. NOMI patients have the most unpredictable presentation and typically present with a protracted clinical course. These patients are often critically ill and being treated for concurrent organ failure or were found to be ill at home for days prior to presentation, making history difficult to obtain. In these patients, systemic sepsis, laboratory abnormalities, and abdominal pain and distention may be the initial clues to the underlying diagnosis of acute mesenteric ischemia; however, imaging is necessary to evaluate for occlusive flow and definitive cause.

The signs and symptoms of acute mesenteric ischemia can easily be mistaken for other, more common intra-abdominal pathologies such as pancreatitis, cholecystitis, appendicitis, diverticulitis, or bowel obstruction, and early diagnosis may be missed in up to 60% of patients. ^, Delays in diagnosis and treatment remain the greatest challenge to reducing morbidity and mortality for all forms of mesenteric ischemia. It has been shown that survival decreases from approximately 50% to 30% when the diagnosis of SMA embolism is made more than 24 hours after the onset of symptoms. A high index of suspicion in the setting of a compatible history and physical examination serves as a cornerstone of prompt treatment. Once it is suspected, the clinician should quickly move to appropriate imaging to confirm the diagnosis and proceed to the operating room.