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Chapter 37: Acute Mesenteric Ischemia

Susan Natalie Eisert; Michael R. Go

GENERAL CONSIDERATIONS AND HISTORY

Introduction

Acute mesenteric ischemia (AMI) is caused by a decrease in blood flow to the intestines such that perfusion no longer meets their metabolic demands.1 This leads to gut ischemia, necrosis, sepsis, and if left untreated, certain death. The incidence of AMI is low; it occurs in 3-5 individuals per 100,000 population and accounts for only 0.09% to 0.2% of all acute admissions to the ED.2 Yet the mortality rate is high and directly correlated to the time to diagnosis and treatment. Thus, a high index of suspicion is required. A delay in diagnosis of more than 24 hours from onset increases mortality from 50% to 70%.3 AMI can be categorized into four types: embolic, thrombotic, nonocclusive mesenteric ischemia (NOMI), or mesenteric venous thrombosis (MVT). Rare causes of AMI include arterial dissection, vasculitis, or aneurysm. Table 37-1 provides a general overview of the four most common types of AMI, while the flow chart in Figure 37-1 depicts the general paradigms for workup and treatment for each respective category, and can be used as a visual guide throughout this chapter.

FIGURE 37-1

Work-up and treatment algorithm for AMI, going from left to right. Note alternative pathways for “high suspicion for bowel necrosis” designated with the red text, as compared to “low suspicion for bowel necrosis” as designated with the green text, for each type of mesenteric ischemia. AMI, acute mesenteric ischemia; MVT, mesenteric venous thrombosis; NOMI, nonocclusive mesenteric ischemia; SMA, superior mesenteric artery.

A flowchart shows the steps to manage acute mesenteric Ischemia (AMI). "The information presented is as follows. Suspicion of AMI leads to history and CT angiogram. History and CT angiogram lead to MVT, NOMI, Thrombotic AMI, and embolic AMI. MVT leads to anticoagulation. NOMI leads to the following. Correction of underlying shock plus minimization of vasopressors plus consider catheter dissected vasodilation. Thrombotic AMI leads to low suspicion for bowel necrosis and high suspicion for bowel necrosis. Embolic AMI leads to low suspicion for bowel necrosis and high suspicion for bowel necrosis. Anticoagulation leads to low suspicion for bowel necrosis which leads to close monitoring for bowel necrosis and high suspicion for bowel necrosis which leads to laparotomy with bowel resection as indicated. Correction of underlying shock plus minimization of vasopressors plus consider catheter dissected vasodilation leads to low suspicion for bowel necrosis which leads to close monitoring for bowel necrosis and high suspicion for bowel necrosis which leads to laparotomy with bowel resection as indicated. Under Thrombotic AMI, if there is low suspicion for bowel necrosis then consider endovascular revascularization, followed by close monitoring for bowel necrosis. If there is a high suspicion of bowel necrosis, consider endovascular revascularization followed by bowel resection as indicated. Under embolic AMI, if there is low suspicion for bowel necrosis then consider endovascular revascularization, followed by close monitoring for bowel necrosis. If there is a high suspicion of bowel necrosis, consider SMA embolectomy or consider endovascular revascularization followed by bowel resection as indicated."
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TABLE 37-1
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TABLE 37-1

Embolic

Thrombotic

NOMI

MVT

Depiction

image

image

image

image

~ % of AMI cases

40%–50%4

20%–35%4

5%–15%4

5%–15%4

Description

Embolic arterial occlusion

Acute arterial thrombosis usually on preexisting severe atherosclerotic disease

Low cardiac output associated with diffuse mesenteric vasoconstriction

Venous thrombosis causing venous engorgement and in turn impaired arterial inflow

Anatomy

Most frequently affects SMA due to oblique origin. Most emboli lodge distal to middle colic artery.5 This can lead to characteristic sparing of the first portion of small intestine and ascending colon.

Most frequently affect SMA origin, causing ischemia from midduodenum to splenic flexure. Collaterals can delay bowel infarction until critical. Stenosis/occlusion of vessel or collateral.

Paradoxical splanchnic vasoconstriction usually affects distribution of SMA. NOMI has a propensity to affect water shed areas.

Thrombi usually originate in venous arcades and propagates to SMV, ± to the portal vein. This causes bowel wall edema, sloughing, and hemorrhage, as well as ascites on imaging.

Risk factors

Most emboli are cardiac origin: Afib/aflutter, low EF (CHF, cardiomyopathy) recent MI, ventricular aneurysm, or proximal arterial source (cardiac valvular disease, endocarditis), proximal aneurysm, aortic mural thrombi, recent catheter-based angiogram.

History of chronic mesenteric ischemia (in about 20%), complication of mesenteric revascularization (stent occlusion, stent migration, distal embolization, vessel perforation/dissection), and PAD (27%).

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