Acute Mesenteric Ischemia

S. Lowell Kahn

Luke R. Wilkins

Alan H. Matsumoto

Acute mesenteric ischemia (AMI) is a therapeutic emergency, requiring prompt intervention to attain a favorable outcome (1,2,3). Despite modern diagnostic and interventional advancements, the mortality associated with AMI remains high, historically between 60% and 80% (4), with more recent reports yielding a range of 52% to 70% (5,6). However, the reported high mortality rates are likely confounded by the associated comorbidities in this patient population.

The critical nature of this entity warrants a high index of clinical suspicion, particularly in elderly patients with cardiovascular disease or embolic or thrombotic risk factors. Risk factors for AMI vary depending on the underlying etiology. Common risk factors for thromboembolic causes of AMI include older age, atherosclerosis, cardiac arrhythmias, dilated cardiomyopathies, severe cardiac valvular disease, recent myocardial infarction, hypercoagulability, and intra-abdominal malignancy (1). Risk factors for AMI attributable to venous thrombosis include dehydration, hypotension, portal hypertension, hypercoagulability, abdominal infection, abdominal malignancy, pancreatitis, trauma, and splenectomy (7). Predisposing factors associated with the development of nonocclusive AMI include a low flow state, prolonged hypotension, older age with cardiovascular disease, and medications such as vasopressors or digitalis.

The clinical presentation of AMI is classically described as acute, severe, periumbilical abdominal pain that is out of proportion to physical exam findings,
with up to 25% of patients manifesting peritoneal signs (8). The presence of peritoneal signs raises concern that the bowel ischemia has progressed to infarction. Anorexia, nausea, vomiting, diarrhea, and hematochezia are common. Unfortunately, the clinical manifestations of AMI overlap with other, more common clinical entities, such as bowel obstruction, pancreatitis, diverticulitis, and peritonitis. Therefore, the clinical presentation must be considered in the context of the clinical history and patient-specific risk factors, physical examination, and laboratory and radiographic findings.

Although grouped as a common disease process, AMI reflects a heterogeneous group of entities, which include occlusive and nonocclusive etiologies that involve the arterial or venous systems. Occlusive causes of AMI consist of superior mesenteric artery (SMA) embolus, SMA thrombosis, mesenteric venous thrombosis, and less common entities such as trauma, strangulated hernias, adhesions, intestinal obstruction, cholesterol emboli, and aortic dissection. Nonocclusive etiologies for AMI include mesenteric arterial vasoconstriction, also known as nonocclusive mesenteric ischemia (NOMI), which is usually precipitated by a hypotensive event and/or use of vasopressors. Despite resolution of the hypotension or discontinuation of the vasopressors, persistent mesenteric arterial vasoconstriction (diffuse vasospasm) persists, causing bowel hypoperfusion and intestinal ischemia. Other causes of NOMI include drugs (i.e., cocaine) and vasculitides. NOMI can also be seen in association with mesenteric venous thrombosis or distal to an SMA embolus.

Accurate diagnosis of the cause for AMI is essential because the presentation, management, and prognosis are influenced by the etiology. To illustrate this point, it is well known that AMI secondary to mesenteric vein thrombosis often has a relatively insidious onset, whereas a patient with an SMA embolus usually presents with an abrupt and distinct onset of symptoms. Treatment will radically differ in these two comparative examples as well.

Historically, surgery represented the mainstay of therapy for AMI, but the treatment algorithm is rapidly evolving into an “endovascular-first” approach at many institutions in an effort to improve patient outcomes (9). A recent paper showed that the use of endovascular therapy for AMI has more than doubled from 11.9% in 2005 to 30% in 2009 (9). There are potential benefits to an endovascular-first approach, including decreased morbidity and mortality, avoidance of general anesthesia and open surgery, more targeted and limited bowel resections, decreased times for revascularization, a reduced need for parenteral nutrition, shortened lengths of stay, and fewer postoperative complications (2,9,10,11). Table 9.1 summarizes the differences between the etiologies for AMI and their management (8,7,12). A treatment algorithm employed at our institutions is demonstrated in Figure 9.1.

Indications

1. Diagnosis of AMI and determination of etiology

a. Although angiography remains the gold standard in the diagnosis of AMI, its diagnostic role has largely been replaced by computed tomographic angiography (CTA) and magnetic resonance angiography (MRA) (13).

(1) CTA and MRA generate high-resolution two- and three-dimensional images of the mesenteric arterial and venous anatomy facilitating accurate diagnosis and treatment planning for occlusive AMI while also providing suggestive findings of NOMI.

(2) Secondary and associated findings of bowel ischemia seen with CTA and MRA

(a) Ileus and bowel distention

(b) Bowel wall thickening/thumbprinting

(d) Abnormal bowel wall enhancement

Table 9.1 Etiologies and Treatment of Acute Mesenteric Ischemia

Etiology	General	Imaging Features	Treatment
SMA embolus	40%-50% of cases Frequent association with cardiac disease (e.g., atrial fibrillation) Abrupt presentation with severe abdominal pain and diarrhea (hematochezia) 20% with simultaneous peripheral arterial embolus; 33% with history of prior embolic event	Filling defect outlined by contrast, convex meniscus, and location that is typically at least 3 cm beyond origin of SMA. Lack of collaterals Poor distal flow 15% found in proximal SMA; 50% found at middle colic artery bifurcation, 25% at the ileocolic branch, and 10% in the distal small bowel branches of the SMA Ileus, mucosal edema, bowel infarction	Endovascular therapy (direct intrathrombus infusion) may be considered first-line in cases with short occlusion, adequate distal collateral circulation, and no peritoneal signs or elevation of lactic acid. Intraoperative thrombectomy or thrombolytic therapy may be considered in a hybrid OR setting, if available. Papaverine administered when arterial vasoconstriction present Systemic anticoagulation
NOMI	10%-15% of cases Typically occurs in patients with a prior hypotensive event, even if resolved Associated with low cardiac output, hypovolemia, hypotension, and splanchnic vasoconstriction. Also affiliated with vasoactive drugs (e.g., cocaine, vasopressin, α-agonists, and digoxin) May be an insidious onset	Diffuse arterial vasospasm with segmental, sausage-like narrowing or diffuse narrowing of vessels commonly identified near branch points Delayed filling of distal arterial and intramural branches Delayed bowel wall staining and/or venous filling Improved flow at angiography after administration of 60 mg papaverine into the SMA. Ileus, mucosal edema, bowel infarction	Papaverine infusion directly into the SMA at 1 mg/min is the mainstay of therapy and is continued until the symptoms resolve (typically within 12-36 h). If peritoneal signs develop, surgery is indicated to explore for dead bowel while continuing papaverine infusion.
Acute SMA thrombosis	25% of cases Typically occurs in patients with underlying atherosclerotic lesions 50%-75% of patients with history of intestinal angina May have acute or chronic symptoms	Occlusive lesion commonly located 1-2 cm from the origin of the SMA Collateral vessels may be present suggesting underlying chronic occlusive disease. Ileus; mucosal edema; bowel infarction	With elevated lactic acid or peritoneal signs, surgery may be warranted with an aortomesenteric bypass and/or thromboendarterectomy. Alternatively, preoperative thrombectomy or thrombolysis may be considered with coordination of surgery in a hybrid setting. ± Preoperative papaverine (may not be feasible because of proximal nature of these lesions) Second-look operation 24-48 h later Postoperative vasodilators as warranted Endovascular management if no peritoneal signs or lactic acidosis May perform primary stenting ± filter wire ± lytics Because lesions often represent acute clot superimposed on underlying chronic lesion, thrombolytics may be administered prior to stenting to reduce the risk of distal embolization.
SMV thrombosis	Accounts for less than 5% of all acute mesenteric ischemia Predisposing factors include portal hypertension, abdominal inflammatory disease, oral contraceptives, prior surgery on the portal venous system, trauma, and hypercoagulable states. Mesenteric venous thrombosis causes mucosal edema leading to arterial hypoperfusion.	Intraluminal filling defect in the mesenteric veins with venous congestion and mucosal edema. Secondary arterial vasospasm and diminished perfusion Prolonged mucosal enhancement Lack of or delay in opacification of the mesenteric veins Prolonged opacification of venules or larger regional veins Ileus, mucosal edema, bowel infarction	Hydrate patient and correct predisposing factors. Anticoagulate If bowel infarction, surgery is warranted. Pre- and postoperative anticoagulation Intra-arterial (IA) papaverine if coexistent mesenteric arterial vasoconstriction If no peritoneal signs or lactic acidosis, endovascular options include transarterial, systemic, and direct transhepatic or transjugular access for intrathrombus thrombolysis, mechanical thrombectomy, angioplasty, and stent placement. Most patients can be managed conservatively with supportive care and anticoagulation.
Aortic dissection	5% of all cases of acute mesenteric ischemia High (90%) operative mortality in this cohort Mesenteric vasculature can be supplied from true or false lumen. Inadequate flow results when blood flow fails to meet the metabolic needs of the bowel.	Identification of true and false lumens with possible visualization of a dissection flap extending into the SMA or compromise of the lumen perfusing the SMA Ileus, mucosal edema, bowel infarction	Operative mortality is high. Endovascular— intravascular ultrasound (IVUS) helpful Endograft therapy to cover primary aortic fenestration Creation of de novo fenestrations to equalize pressures between the true and false lumens Use of stents in the SMA to tack down the dissection flap

FIGURE 9.1 • Treatment algorithm for acute mesenteric ischemia.

FIGURE 9.1 • (Continued)

(e) Visualization of infarctions in other organs suggesting embolic disease

(f) Small-caliber branches of the SMA with delayed venous filling and poor mucosal staining with contrast

(3) Availability and rapidity of CTA allows its use as an emergent modality.

b. Angiography has diagnostic utility in cases with equivocal findings by CTA or MRA or in patients in whom endovascular intervention is likely.

(1) Angiography may reduce contrast load and potential renal injury by bypassing the CTA examination in select patients.

(2) Angiography is usually now performed in anticipation of an endovascular treatment solution.

2. Treatment of AMI

a. For patients with acute bowel ischemia without evidence of bowel infarction or for patients that are poor surgical candidates, endovascular management alone is an acceptable therapeutic option (2,3,9,10,11).

b. Catheter-based techniques can provide a potential therapeutic role for AMI, regardless of the underlying etiology. However, the first-line choice of treatment varies depending on the underlying cause (see Table 9.1).

(1) Treatment options include vasodilator infusion, thrombolysis, and mechanical thrombectomy with or without use of a filter wire, angioplasty, and stenting.

c. Because of the high mortality associated with surgery (14), some authors advocate a broader use of endovascular therapy, both alone and in combination with surgery for AMI, including patients with evidence of bowel infarction (peritoneal signs and lactic acidosis) (2,9,10,11).

d. There is growing interest in hybrid operative and endovascular procedures of various forms. The broader use of hybrid operating and interventional suites allows endovascular revascularization in the same setting as surgical removal of bowel. Alternatively, in the case of difficult or failed antegrade endovascular revascularization, exposure of the mesenteric root with retrograde SMA revascularization has been described (15).

Contraindications

1. Renal insufficiency is a relative contraindication for contrast administration, thereby compromising the ability to perform a diagnostic CTA or an endovascular intervention. However, contrast-induced renal failure may be a less of a risk for a patient than delaying the diagnosis and treatment of a highly lethal disease.

2. Performance of a diagnostic CTA or endovascular intervention in a patient with a severe contrast allergy history is typically contraindicated. In patients in whom the diagnosis of AMI is highly suspected, the use of contrast premedication and general anesthesia may obviate the concerns about the contrast allergy risks. MRA may be an acceptable alternative diagnostic modality.

3. Evidence of bowel infarction may mandate emergent surgical exploration and resection of dead bowel. Use of an endovascular solution alone may not be appropriate. However, adjunctive endovascular therapy is known to improve surgical outcomes while also helping to minimize the amount of bowel resected (2,9). Catheter-based interventions also provide the opportunity to relieve mesenteric vasospasm by pre-, intra-, and/or postoperative catheterdirected IA infusion of papaverine.

4. Relative contraindications to angiography and an endovascular intervention include uncontrolled bacteremia and an uncorrectable bleeding diathesis.

5. Other contraindications will be guided by the specifics of the intended therapy:

a. Papaverine is contraindicated in patients with complete heart block and papaverine allergies. Other relative contraindications exist as well (Table 9.2).

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