INTRODUCTION — Acute mesenteric ischemia refers to the sudden onset of small intestinal hypoperfusion, which can be due to reduction or cessation of arterial inflow. Ischemia due to acute mesenteric arterial occlusion can be caused by embolic obstruction of the intestinal blood supply, most commonly to the superior mesenteric artery (SMA). Acute ischemia can also occur due to acute thrombotic obstruction, often in the setting of an already diseased mesenteric vessel (eg, atherosclerosis).

Acute mesenteric ischemia due to acute arterial obstruction involving the small intestine will be reviewed here. Colonic ischemia, chronic mesenteric ischemia, and other forms of mesenteric ischemia, including mesenteric venous occlusion and nonocclusive mesenteric ischemia, are reviewed elsewhere. (See "Mesenteric venous thrombosis in adults" and "Chronic mesenteric ischemia" and "Colonic ischemia" and "Nonocclusive mesenteric ischemia".)

MESENTERIC ANATOMY AND PHYSIOLOGY — The arterial anatomy of the intestinal circulation is given in the figures (figure 1 and figure 2 and picture 1). Ischemic injury to the intestine develops when there is insufficient delivery of oxygen and nutrients required for cellular metabolism. An overview of intestinal anatomy, normal intestinal vascular physiology, and the response to acute ischemia are discussed in detail elsewhere. (See "Overview of intestinal ischemia in adults", section on 'Intestinal vascular anatomy' and "Overview of intestinal ischemia in adults", section on 'Physiology and mechanisms of ischemia'.)

The intestine may be able to compensate to some extent because of increased oxygen extraction as well as the presence of collateral flow pathways (figure 3) [1]. The status of the collateral circulation is particularly important in determining the severity of symptoms [2]. Acute superior mesenteric arterial occlusion as with embolism, in the absence of preexisting stenosis, causes a greater reduction in blood flow compared with other causes of intestinal ischemia leading to bowel infarction (picture 2). This is due to the lack of collateralization in the presence of relatively normal arterial vasculature. By contrast, acute thrombosis of atherosclerotic lesions may have had the opportunity to develop collateral pathways to provide some degree of perfusion even in the setting of complete occlusion. Inciting factors such as dehydration or low cardiac output states can lead to acute thrombosis of even modest stenosis, causing typical signs and symptoms of acute mesenteric ischemia with no prior history. For some patients, progression from stenosis to occlusion can be asymptomatic due largely to a sufficient time course to develop these collaterals.

ETIOLOGY OF MESENTERIC ARTERIAL OCCLUSION — The two major causes of acute mesenteric arterial occlusion are mesenteric arterial embolism and mesenteric arterial thrombosis. In an autopsy study, the ratio of superior mesenteric embolus to thrombus ratio was 1.4:1 [3].

●Arterial embolism – Embolism to the mesenteric arteries, which may partially or completely occlude the arterial lumen, is most frequently due to dislodged thrombus from the left atrium, left ventricle, cardiac valves, or proximal aorta. Systemic embolization occurs in 22 to 50 percent of cases of infected endocarditis, with embolization to the viscera second only to cerebral embolism [4,5]. A history of prior embolization is common. In an autopsy series, 19 percent had an acute myocardial infarction, 48 percent had remnant cardiac thrombus, and 68 percent had synchronous embolus [3]. Emboli tend to lodge at points of normal anatomical narrowing, usually at a branching point of an artery. The large diameter and narrow takeoff angle of the superior mesenteric artery (SMA) make it anatomically most susceptible to embolism. The inferior mesenteric artery is rarely affected due to its small caliber [6]. The embolus usually lodges 3 to 10 cm distal to the origin of the SMA, in a tapered segment distal to the takeoff of the middle colic artery and sparing the first few jejunal branches, but approximately 15 percent of emboli lodge at the origin of the SMA [7]. The middle segment of the jejunum, which is most distant from the collateral circulation of the celiac and inferior mesenteric arteries, is most often involved in the ischemic process, whereas the proximal jejunum is usually spared. Jejunal sparing suggests embolic occlusion rather than acute-on-chronic occlusion of the SMA related to atherosclerotic disease as the underlying cause of acute mesenteric ischemia (picture 3). Concomitant arteriolar vasoconstriction usually occurs, further impairing intestinal blood flow and exacerbating the ischemia. (See "Atrial fibrillation in adults: Use of oral anticoagulants" and "Antithrombotic therapy for mechanical heart valves" and "Left ventricular thrombus after acute myocardial infarction", section on 'Prevention of embolic events' and "Thromboembolism from aortic plaque".)

●Arterial thrombosis – Arterial thrombosis occurs at areas of severe narrowing most typically due to atherosclerosis. However, mesenteric arterial thrombosis can also occur in the setting of arterial injury, infection, or in association with hypercoagulable states.

•Acute thrombosis of the mesenteric circulation often occurs as a superimposed phenomenon in patients with a history of chronic mesenteric ischemia from progressive stenosis due to atherosclerotic aortic plaque that involves the takeoff of the celiac axis and SMA, also referred to as acute-on-chronic ischemia. Therefore, thrombosis of the SMA or celiac axis usually occurs at the origin of the vessel, and involvement of at least two major mesenteric arteries is generally needed for the patient to have significant symptoms because of the development of the collateral circulation over time [8]. (See "Chronic mesenteric ischemia" and "Overview of infected (mycotic) arterial aneurysm", section on 'Visceral arteries'.)

•Mesenteric arterial thrombosis can also occur in the setting of vascular injury related to abdominal trauma, mesenteric dissection (spontaneous, related to instrumentation), hypercoagulability, and infection. Septic embolization from infected heart valves to the visceral arteries can cause mycotic aneurysm, which can also thrombose. Thrombosis of a previously placed mesenteric stent can also occur.

EPIDEMIOLOGY AND RISK FACTORS — Thromboembolic occlusion of the superior mesenteric artery is the most common cause of acute mesenteric ischemia. Acute mesenteric arterial occlusion accounts for 67 to 95 percent of cases of acute mesenteric ischemia [3,6,7,9-12].

Risk factors — Risk factors for acute mesenteric arterial occlusion include any process that increases the potential for embolism from the heart or proximal arterial vasculature or for arterial thrombosis. (See "Overview of intestinal ischemia in adults", section on 'Risk factors'.)

●The risk of embolism is increased in patients with cardiac arrhythmias, cardiac valvular disease, infective endocarditis, recent myocardial infarction, ventricular aneurysm, cardiac surgery, cardiopulmonary bypass, cardiogenic shock, intra-aortic balloon pump placement, aortic atherosclerosis, aortic aneurysm, and infection with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2 [13-17]). Although incidence is rare, following cardiac surgery (1 percent), mortality remains high (87 percent) [18,19].

●The risk of thrombotic occlusion is increased in patients with peripheral artery disease (with or without prior mesenteric stenting), advanced age, and low cardiac output states [7]. Traumatic injury can also lead to visceral artery thrombosis [20].

●Unlike mesenteric venous thrombosis, there does not appear to be a significant association between inherited coagulation defects and mesenteric arterial thrombosis [21,22]. However, acquired hypercoagulable states can contribute to arterial thrombosis. In patients with coronavirus disease 2019 (COVID-19), thrombotic mesenteric occlusion with atypical clinical features can occur suggesting mechanisms specific to COVID-19 [23-25]. In patients with COVID-19, we have adopted a strategy using thromboelastography (TEG) to identify those at risk and to anticoagulate accordingly [26] (See "COVID-19: Gastrointestinal symptoms and complications", section on 'Possible etiologies of COVID-related gastrointestinal complications'.)

●Less frequently, acute mesenteric ischemia may also be observed in the setting of an underlying vasculitis, most commonly polyarteritis nodosa. Vasculitis affects the small- and medium-diameter arteries and can lead to acute segmental intestinal infarction, but it may be difficult to determine if acute symptoms are due to arterial occlusion or spasm (ie, nonocclusive ischemia). Fibrous intimal thickening is typically seen histologically [27,28]. In most cases, stenoses and/or microaneurysms are detected on arteriography without obstruction of the main mesenteric arteries. (See "Nonocclusive mesenteric ischemia" and "Overview of gastrointestinal manifestations of vasculitis" and "Clinical manifestations and diagnosis of polyarteritis nodosa in adults".)

CLINICAL FEATURES — Early symptoms and clinical signs, including laboratory studies and plain radiographs, are nonspecific, but any patient with acute-onset abdominal pain, minimal findings on abdominal examination (classically described as pain out of proportion to the exam), and metabolic acidosis should be regarded as having intestinal ischemia until proven otherwise. Risk factors for arterial embolism or for atherosclerosis (smoking, hypertension, hyperlipidemia, diabetes) may be present (see 'Risk factors' above). Symptoms of chronic mesenteric ischemia such as pain with meals and weight loss may be noted on the history. Plain films and cross-sectional abdominal imaging do not exclude mesenteric ischemia but may identify complications related to mesenteric ischemia (eg, necrosis, perforation) and indicate the need for immediate abdominal exploration, while also helping to exclude other obvious causes of abdominal pain (eg, volvulus, small bowel obstruction) [29-40]. (See "Overview of intestinal ischemia in adults", section on 'Laboratory studies' and "Overview of intestinal ischemia in adults", section on 'Plain radiographs' and "Overview of intestinal ischemia in adults", section on 'Advanced abdominal imaging'.)

Routine laboratory evaluation for abdominal pathology is performed, including complete blood count, arterial blood gas, and lactate. Classically, patients have leukocytosis, acidosis, and elevated lactate; however, this occurs in a minority of patients. Normal laboratory findings do not exclude the diagnosis of acute mesenteric arterial occlusion. (See "Overview of intestinal ischemia in adults", section on 'Laboratory studies'.)

Specific clinical features that suggest mesenteric arterial embolism or mesenteric arterial thrombus as a cause of acute mesenteric ischemia are as follows:

●Mesenteric arterial embolism – The typical clinical triad of acute embolic occlusion in an older adult patient with atrial fibrillation (or other source for embolism) and severe abdominal pain out of proportion to the physical examination is present in one-third to one-half of patients. Bowel emptying, nausea, and vomiting are also common, but bloody bowel movements are less common, unless advanced ischemia is present. The patient may be subtherapeutic on previously prescribed antithrombotic therapy. A prior embolic event is present in approximately one-third of patients. It is particularly important in these patients to perform a complete vascular examination examining the carotid, upper extremity, and lower extremity pulses for evidence of reduced perfusion related to synchronous embolism [41]. Over 20 percent of acute mesenteric emboli are multiple.

For patients with a history of infective endocarditis, most emboli (cerebral most common, followed by visceral, then lower extremity) occur within the first two to four weeks of antimicrobial therapy and may be more common in patients with mitral valve involvement, larger vegetation size (largest are associated with streptococcus), staphylococcus independent of vegetation size, and increasing vegetation size while on treatment [4,5]. (See 'Risk factors' above and "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis".)

●Mesenteric arterial thrombosis – The typical patient with acute mesenteric thrombotic occlusion is a patient with risk factors for atherosclerosis and possibly known peripheral artery disease who may or may not have an established diagnosis of chronic mesenteric ischemia based upon symptoms of chronic postprandial abdominal pain, food aversion, and weight loss. However, in contrast to the classic description, one study noted that patients may not be cachectic, possibly due to earlier diagnosis or a relatively high proportion of patients who were overweight before the onset of symptoms. However, obtaining an antecedent history of chronic mesenteric ischemic symptoms may be helpful for differentiating thrombotic versus embolic occlusion and may potentially influence the choice of initial treatment [12,42]. (See 'Endovascular intervention' below and "Chronic mesenteric ischemia".)

Patients with COVID-19 related mesenteric arterial thrombosis are often critically ill and may not exhibit classic symptomatology (eg, severe abdominal pain or tenderness) [13,25,43]. (See "COVID-19: Gastrointestinal symptoms and complications", section on 'Mesenteric ischemia'.)

DIAGNOSIS — As with all forms of mesenteric ischemia, the diagnosis of acute mesenteric arterial occlusion depends upon a high level of clinical suspicion, particularly in patients with known risk factors for peripheral embolization (eg, atrial fibrillation, recent myocardial infarction, valvular disease) or a history of peripheral artery disease with or without a history of chronic abdominal pain. Rapid diagnosis is essential to prevent the catastrophic events associated with intestinal infarction [44]. (See "Overview of intestinal ischemia in adults", section on 'Diagnosis'.)

A definitive diagnosis of mesenteric arterial occlusion relies upon demonstrating the occlusion within the mesenteric arteries on imaging studies. High-resolution computed tomographic (CT) angiography is highly diagnostic for cases of acute mesenteric ischemia. In addition, based upon the appearance of vessels in the abdomen, it is possible to differentiate between embolic and thrombotic etiologies. Further information for operative planning, such as distal arterial reconstitution and choice of inflow vessel for surgical bypass, can also be obtained. In the setting of equivocal CT angiography findings, catheter-based angiography may be needed. For patients who present with advanced ischemia (bowel perforation and peritonitis) and hemodynamic instability, a diagnosis will necessarily be made in the operating room. (See 'Management' below.)

●Embolic mesenteric occlusion – Embolic occlusion often appears as an oval-shaped thrombus surrounded by contrast in a noncalcified arterial segment located in the middle and distal portion of the proximal superior mesenteric artery (SMA) (image 1 and image 2).

●Thrombotic mesenteric occlusion

•Thrombotic occlusion in association with atherosclerosis usually appears as thrombus superimposed on a heavily calcified occlusive lesion at the ostium of the SMA (image 3).

•Thrombotic occlusion in association with hypercoagulable states (eg, COVID-19) or associated with shock can have a variable distribution (picture 4).

In addition to determining the type of mesenteric arterial occlusion (ie, embolism or thrombus), CT angiography identifies the collateral circulation and potential sources of inflow and avoidable sites with extensive atherosclerotic lesions in cases that might require revascularization.

DIFFERENTIAL DIAGNOSIS — Acute mesenteric arterial occlusion needs to be differentiated from other causes of abdominal pain and from mesenteric ischemia due to nonocclusive mesenteric ischemia or mesenteric venous thrombosis. These distinctions are reviewed elsewhere. (See "Causes of abdominal pain in adults" and "Overview of intestinal ischemia in adults", section on 'Differential diagnosis'.)

MANAGEMENT — Initial medical management for all patients with acute mesenteric ischemia includes the following, which are discussed in detail separately (algorithm 1) (see "Overview of intestinal ischemia in adults", section on 'Initial management'):

●Nothing by mouth, nasogastric decompression.

●Fluid therapy to maintain adequate intravascular volume and visceral perfusion and monitored as normal urine output.

●Avoidance of vasopressors, which can exacerbate ischemia.

●Antithrombotic therapy consists of anticoagulation (unfractionated heparin, weight-based protocol or alternative agent if contraindicated) to limit thrombus propagation and help alleviate associated arteriolar vasoconstriction with or without antiplatelet therapy [45].

●Empiric broad-spectrum antibiotic therapy.

●Proton pump inhibitors [46].

●Supplemental oxygen [46].

Approach to treatment — Clinical evaluation and vascular imaging determine whether the patient is a candidate for vascular intervention and whether the occlusion is embolic or thrombotic (algorithm 2 and algorithm 3), which has a bearing on the type of intervention offered. The goal of vascular intervention is to restore intestinal blood flow as rapidly as possible. The specific treatment chosen depends upon the clinical status of the patient and the etiology and location of the occlusion. Optimal treatment may include open, endovascular, or a combined approach. The ability to offer an endovascular approach depends upon local resources and the availability of vascular specialists. A hybrid interventional suite/operating room may be the ideal setting to manage acute mesenteric arterial occlusion, but these are generally available only at large vascular centers. (See 'Diagnosis' above and 'Surgical versus endovascular intervention' below.)

●Some patients (eg, acute-on-chronic occlusion) who are hemodynamically stable and do not have clinical signs of advanced bowel ischemia and have evidence of good collateral blood flow on vascular imaging studies can be observed while anticoagulated. Antiplatelet therapy may be justified in this setting if the risk of progressive ischemia appears to be greater than the risk of bleeding [45,47]. The patient should have serial clinical assessment (laboratory, physical examination) with a low threshold to repeat abdominal imaging studies or, if abdominal symptoms progress, surgical or endovascular intervention. (See 'Surgical versus endovascular intervention' below.)

●A palliative approach may be the best option for poor-risk surgical candidates with extensive transmural infarction (eg, small bowel up to the midtransverse colon). Extensive bowel resection would be inappropriate for these patients and may also be inappropriate for a subset of patients who might otherwise be expected to tolerate the procedure but for whom lifelong parenteral nutrition would be unacceptable (picture 5). (See "Palliative care: The last hours and days of life".)

●Patients who are good-risk surgical candidates with indications for immediate laparotomy such as peritonitis or radiologic features of advanced bowel ischemia (free air, extensive pneumatosis) should be taken directly to the operating room for exploration. Resection of bowel should ideally be delayed until after mesenteric arterial revascularization can be performed to salvage as much bowel as possible; however, in practice, this sequence does not commonly occur. In situations where an individual with appropriate vascular expertise is not immediately available, resection of grossly necrotic or perforated bowel (leaving any questionable bowel) while awaiting intraoperative consultation is appropriate, or, alternatively, following resection, abdominal closure and transfer is also a reasonable option when required. (See 'Abdominal exploration/damage control' below.)

•The traditional treatment for mesenteric embolism is open surgical embolectomy, which, in addition to expeditiously clearing the thrombus, allows direct assessment of bowel viability. (See 'Embolectomy' below.)

•Open surgical treatment of mesenteric artery thrombosis is treated principally with mesenteric bypass. Thrombectomy alone is unlikely to offer a durable solution due to the presence of thrombogenic atherosclerotic plaques. Intraoperative retrograde superior mesenteric artery angioplasty and stenting is another option, particularly in the presence of gross contamination where bypass is more problematic. (See 'Mesenteric bypass' below.)

●Patients who are hemodynamically stable and who do NOT have clinical or radiologic signs of advanced intestinal ischemia may be candidates for a primary endovascular approach.

•Although we prefer open surgical thrombectomy for patients with acute embolism, percutaneous aspiration of the clot or catheter-directed thrombolytic therapy is another approach that has been used successfully with reasonable outcomes. (See 'Embolectomy' below and 'Pharmacomechanical thrombolysis' below.)

•For patients with acute mesenteric thrombosis, a primary endovascular approach is a reasonable option with close clinical monitoring. (See 'Mesenteric angioplasty/stenting' below.)

Surgical versus endovascular intervention — Reports indicate that endovascular intervention may be as effective as traditional surgical approaches in patients with acute mesenteric arterial occlusion [48-50]. This approach remains somewhat controversial as direct visualization of the bowel is not an option during percutaneous interventions. The long-term outcome after percutaneous treatment (eg, re-occlusion after thrombolysis, stent thrombosis) has not been well studied [10,49-56].

In a review from Sweden, there has been a steady increase in mesenteric revascularizations for acute mesenteric ischemia since 2004. In 2009, endovascular treatment surpassed open surgery [42]. The authors noted that this shift in treatment has not yet taken place in other countries [49]. No randomized trials are available to guide treatment, but there are several observational studies that have compared open versus endovascular revascularization for acute mesenteric ischemia [42,49,50,54,57-61].

●In the Swedish study, the 30-day mortality rate was similar after open versus endovascular surgery for embolic occlusions (37 versus 33 percent), whereas the mortality rate was significantly higher after open than endovascular treatment for thrombotic occlusions (56 versus 23 percent) [42]. Differences in disease severity may have existed between the treatment groups, but the authors speculated that it is possible that the endovascular approach is better for thrombotic occlusions in older adult and fragile patients.

●A retrospective review found no significant difference in mortality between open and endovascular approaches for patients treated over a 20-year period [49].

●In another single-center study, endovascular compared with open surgery led to significantly lower rates of mortality for patients with acute thrombotic occlusions [50].

●Several reviews showed a lower frequency of bowel resection and death rates with endovascular therapy for acute thrombotic occlusion [54,57,59-61]. The long-term survival at five years after endovascular treatment and open vascular surgery was 40 and 30 percent, respectively [59]. Independent risk factors for decreased long-term survival were short bowel syndrome and advanced age.

●In a series of 70 patients with acute mesenteric ischemia, 56 initially underwent endovascular treatment with a technical success rate of 84 percent. Immediate procedure (in-hospital) mortality was significantly lower for endovascular compared with open surgical treatment (36 versus 50 percent) [50].

●In a review of the American College of Surgeons (ACS) National Surgical Quality Improvement Program (NSQIP) database, a total of 439 patients with acute mesenteric ischemia underwent treatment using an open approach in 88.6 percent, a hybrid approach in 5.2 percent, and an endovascular approach in 6.2 percent [58]. Among the 27 patients in the endovascular group, 16 patients avoided subsequent laparotomy. There was a trend toward lower transfusion requirements and complications, in particular pneumonia and sepsis, in the minimally invasive groups.

ENDOVASCULAR INTERVENTION — Initial catheter-based arteriography and possible endovascular treatment can only be considered for patients who are hemodynamically stable and who do not have clinical signs of advanced ischemia (eg, radiographic, peritonitis) [10]. For those who undergo endovascular intervention, there should be a low threshold to terminate the procedure if problems arise or to convert to open surgical exploration if the patient's clinical condition deteriorates at any time.

Endovascular options for patients with mesenteric arterial occlusion include [62-74]:

●Pharmacologic or mechanical thrombectomy

●Balloon angioplasty, typically with arterial stent placement

An antegrade approach to the superior mesenteric artery (SMA) can be performed via femoral or brachial artery access. Brachial access may be preferred if there is a sharp downward angle between the aorta and the superior mesenteric artery or if the ostium of the SMA is calcified; each scenario would make the approach from the femoral artery very difficult. (See 'Mesenteric angioplasty/stenting' below.)

If an antegrade approach from the femoral or brachial artery fails, a retrograde approach through the exposed SMA at the time of laparotomy is another option. (See 'Mesenteric angioplasty/stenting' below.)

Pharmacomechanical thrombolysis — Pharmacomechanical thrombolysis should only be considered in patients who can undergo arteriography within eight hours of the onset of abdominal pain and who do not have clinical evidence of advanced ischemia or other contraindications to thrombolytic therapy.  

After gaining access, the SMA is cannulated and catheterized. To directly aspirate the thrombus, a series of wires and catheters are used to place a relatively stiff wire into the ileocolic branch of the SMA over which an introducer with a removable hub is placed proximal to the embolus in the SMA (typically a 7-Fr, 45-cm introducer [eg, Destination, Terumo]) [10]. Inside the introducer, a 6-Fr guiding catheter is introduced into the clot. The clot is then aspirated into the guiding catheter with a 20-mL syringe as the catheter is withdrawn over the wire. The hub of the introducer can be removed to clear any residual clots. Repeat arteriography is performed, and, if needed, repeated aspirations can be performed. An alternative to this method is an over-the-wire double lumen aspiration catheter (eg, Export), which may allow removal of smaller, more peripheral clots (image 4).

Catheter-directed thrombolysis is an alternative for cases of incomplete aspiration embolectomy or distal mesenteric embolization. In cases of incomplete aspiration embolectomy or distal embolization, local thrombolysis is a reasonable alternative in patients without peritonitis [62]. With the introducer placed in the proximal SMA, a 4-Fr end-hole catheter can be advanced up to the clot or a multiple sidehole catheter (holes over 10 cm) advanced through the clot. The catheter is secured at its exit site and a dressing applied to the access site. Low-dose heparin (500 units/hour) administered through the sheath prevents its thrombosis. Papaverine infusion should not be used concomitantly, as it can precipitate in the presence of heparin. Termination of the infusion and abdominal exploration are indicated for any patient who develops progressive symptoms or signs of ischemia. Provided the patient remains clinically stable, arteriography should be repeated within four hours, and if clot lysis is not demonstrated, the patient should be taken to the operating room for abdominal exploration. (See 'Surgery' below.)

A review of 20 case reports and seven small series using thrombolytic therapy for acute SMA occlusion reported angiographic resolution of the SMA occlusion in 43 out of 48 patients (90 percent) [63]. Most were treated with infusions of urokinase. The overall 30-day survival rate was 43 out of 48 patients (90 percent).

Mesenteric angioplasty/stenting — Mesenteric artery angioplasty/stenting can be performed in an antegrade fashion (device introduced via the aorta into the SMA) or retrograde (device introduced via the SMA distal to the obstruction) [52,75]. Open mesenteric stenting for acute mesenteric ischemia is discussed below. Antegrade stenting, which is more typically performed in the setting of chronic ischemia (or acute-on-chronic ischemia), is discussed separately. (See "Chronic mesenteric ischemia", section on 'Management'.)

Retrograde open mesenteric stenting — In selected patients, retrograde catheter-based mesenteric revascularization may be appropriate [50,70,76-78]. In settings where thrombectomy is unsuccessful in restoring arterial inflow and autogenous bypass conduit (saphenous vein, femoral [deep] vein) to perform surgical bypass is not available or cannot be expeditiously harvested, it may be possible to establish arterial inflow using retrograde catheterization of the superior mesenteric artery. If successful, this approach avoids the risk of contaminating a prosthetic vascular graft. With appropriate endovascular equipment and fluoroscopic imaging, the procedure is relatively straightforward, with reported results competitive with those of open surgical bypass.

SURGERY — Immediate surgery is indicated for patients with acute mesenteric ischemia with clinical symptoms or signs of advanced ischemia (eg, peritonitis, sepsis, pneumatosis intestinalis) [79].

Abdominal exploration/damage control — Laparotomy is indicated for patients with acute abdominal findings on exam indicating peritonitis. Laparotomy, rather than laparoscopy, may be safer and more expedient for evaluating the viscera in the face of grossly dilated bowel. The intestinal tract should be evaluated first for areas of impending or gross perforation; these areas should be immediately resected using a stapler to contain gross spillage. A general abdominal exploration should be performed, looking for obvious pathology or other signs of visceral embolization.

The extent and severity of intestinal ischemia, including the appearance of the abdominal contents (color, distention), peristalsis, arterial pulsations in the mesenteric arcades, and bleeding from cut surfaces, should be assessed. Although mesenteric arterial revascularization is preferably performed before bowel resection, areas of the small or large intestine that are clearly nonviable (ie, full-thickness ischemia with dilated, dark, paralyzed bowel (picture 6 and picture 4)) can be quickly resected using a damage control approach. Bowel of questionable viability that peristalses even a little should be left intact until after perfusion is restored, after which bowel viability should be reassessed. (See "Bowel resection techniques" and "Overview of damage control surgery and resuscitation in patients sustaining severe injury".)

Revascularization

Embolectomy — Open superior mesenteric artery (SMA) embolectomy remains a good option and should be performed in those with indications for open surgical intervention [80]. Mesenteric embolectomy is performed through a midline abdominal incision that allows full inspection of the bowel. The proximal superior mesenteric artery can be exposed at the root of the mesentery by retracting the transverse colon cephalad, mobilizing the distal duodenum, and palpating the SMA in the root of the mesentery (picture 7).

A transverse arteriotomy is made, through which 3-Fr or 4-Fr Fogarty embolectomy catheters can be introduced to extract the clot (picture 8). The catheters should be advanced distally as well as proximally. Absence of additional thrombus with multiple passes and restoration of pulsatile inflow confirms clearance of the artery. The vessel is flushed with heparin and the arteriotomy repaired primarily. If arterial inflow cannot be obtained, repeat mesenteric arteriography may be necessary. If inflow cannot be restored, bypass from the aorta or other location can be necessary. (See 'Mesenteric bypass' below.)

Mesenteric bypass — Revascularization of the SMA can be achieved in several ways [81-84]. Superior mesenteric artery bypass is the most practical method in the setting of acute mesenteric arterial occlusion. Other options include thromboendarterectomy and translocation; however, these techniques are less commonly used in the setting of acute mesenteric ischemia. Translocation (transection of the SMA distal to the occlusive lesion with reimplantation into the infrarenal aorta) is unlikely to be feasible in acute circumstances given the typically distal level of obstruction. For patients with chronic mesenteric ischemia (or possibly acute-on-chronic disease), thromboendarterectomy may be an option if disease is confined to the origin of the visceral vessels. (See "Chronic mesenteric ischemia", section on 'Management'.)

Mesenteric bypass constructs a graft from the chosen inflow vessel (eg, aorta, iliac artery) to a site distal to the occlusive lesion. Autologous reversed saphenous vein may be the preferred conduit, but polytetrafluoroethylene (PTFE) grafts reinforced with rings are a reasonable option for retrograde revascularizations to prevent kinking. However, in general, prosthetic reconstruction is discouraged in the acute setting, particularly in the face of abdominal contamination because of an increased high risk for graft infection. If native conduit is not available, angioplasty and stenting (antegrade or retrograde) may be a better option rather than placing a prosthetic graft within a contaminated field. (See 'Mesenteric angioplasty/stenting' above.)

●Antegrade bypass – The inflow is from the supraceliac aorta.

●Retrograde bypass – The inflow is from the infrarenal aorta or iliac arteries.

Mesenteric artery bypass has good long-term patency rates and high rates of symptom-free survival; however, perioperative mortality in the face of acute intestinal ischemia remains high [85]. (See 'Morbidity and mortality' below.)

For patients with advanced ischemia, it should be anticipated that revascularization may result in acidosis, hyperkalemia, and hemodynamic instability. Prior to reestablishing arterial flow, dialogue with anesthesia should cover this foreseeable occurrence. Appropriate pharmacologic preparation should be initiated in advance to avoid sudden collapse of an otherwise stable-appearing patient. If the reperfusion results in an undesirable physiologic response, arterial inflow can be temporarily halted to allow more time for physiologic correction.

Bowel and abdominal closure — Following open revascularization, the small bowel should be carefully reexamined for areas of irreversible ischemic injury, which may require resection. In one review of 83 patients requiring revascularization for acute mesenteric ischemia, 24 percent required resection of a median length of 43 cm of bowel [81]. The presence of Doppler signals over the serosal surface may be helpful in identifying potentially salvageable ischemic segments to be left in place for reevaluation at second-look operation; however, surgeon experience and visual inspection have been shown to be as accurate as other adjunctive diagnostic techniques in the intraoperative assessment of bowel viability. At the time of definitive abdominal closure, intravenous injection of fluorescein dye with inspection of the intestine illuminated via a Wood's lamp can assist in determining remaining bowel viability (picture 9). With increasing availability, intraoperative indocyanine green (ICG) angiography is being used as an acceptable bowel assessment adjunct in lieu of fluorescein dye [86]. Potential advantages include a shorter half-life, which allows for repeated use in less time, and decreased intestinal staining due to near-complete isolation in the intravascular space.

Restoration of bowel continuity can be performed during the index surgery for well-demarcated, clearly viable bowel segments. If bowel viability is in question or the patient is hemodynamically unstable, a damage control approach can be undertaken by resecting the nonviable segments and stapling the small bowel closed awaiting a second-look procedure to restore bowel continuity.

The abdominal wall is left open when repeat laparotomy is planned, which is particularly likely if there has been a significant interval of ischemia that leads to bowel edema with reperfusion. If closure is elected (eg, no necrotic bowel, minimal ischemic time), abdominal compartment pressures should be monitored. A planned "second-look" laparotomy is frequently needed to reassess and resect irreversibly ischemic bowel. (See 'Second-look laparotomy and abdominal wall closure' below.)

POSTPROCEDURE CARE AND FOLLOW-UP — Patients with acute mesenteric ischemia are often very ill post-intervention, requiring intensive care management and nutritional support. In one study, the mean length of hospital stay was 23 days [49].

Second-look laparotomy and abdominal wall closure — A second-look laparotomy is needed for most patients after mesenteric revascularization for acute mesenteric arterial occlusion to reevaluate the bowel 24 to 48 hours after the initial operation [57,84]. In a review of 93 patients undergoing arterial revascularization for mesenteric ischemia, 80 percent of patients underwent a second-look laparotomy, and among those patients, 28 percent had necrotic bowel requiring resection at the second operation [49]. (See "Management of the open abdomen in adults".)

If primary abdominal closure was elected (eg, no necrotic bowel, minimal ischemic time), abdominal compartment pressures should be monitored. (See "Abdominal compartment syndrome in adults", section on 'Measurement of intra-abdominal pressure'.)

Long-term medical management — Long-term management is aimed at the prevention of future embolic events, typically with the use of vitamin K antagonists or novel oral anticoagulants [45]. Patients who survive after acute mesenteric embolic occlusion need long-term medical treatment [45]. (See "Atrial fibrillation in adults: Use of oral anticoagulants".)

Following revascularization of thrombotic arterial occlusion due to atherosclerosis, medical management of peripheral artery disease includes antiplatelet therapy and statin therapy as part of a cardiovascular risk reduction strategy.

Stent surveillance — Patients who have a stent inserted in the mesenteric artery should have periodic surveillance either using duplex ultrasound or computed tomography (CT) angiography. There are few data to guide a specific surveillance interval. There are no data to guide follow-up surveillance following mesenteric stenting. We perform follow-up imaging at three months post-intervention, then every six months for up to two years, and annually thereafter provided there is no evidence for restenosis. For those with recurrent stenosis, reintervention may be needed to prevent stent occlusion, which may lead to recurrent symptoms.

MORBIDITY AND MORTALITY — Mortality from acute mesenteric ischemia remains high, with most series not showing appreciable improvement despite an aggressive treatment regardless of approach [44,46,47,49,53,84,87-93]. Time to diagnosis and treatment is paramount to survival for acute mesenteric ischemia patients. Advanced mesenteric ischemia (picture 2) requiring bowel resection is associated with a 15-fold increase in mortality, and overall mortality for mesenteric ischemia requiring surgical intervention exceeds 50 percent [3,91].

For open surgical approaches to revascularization, perioperative mortality in contemporary studies ranges between 31 and 62 percent [44,46,89-93]. In a series limited to patients undergoing intervention for acute mesenteric arterial occlusion, perioperative mortality (open and endovascular) was 22 percent, and complications occurred in 68 percent [49]. Perioperative mortality was similar for open and endovascular approaches. The causes of perioperative death included ongoing mesenteric ischemia with intra-abdominal sepsis and multiorgan failure, cardiac causes, hemorrhage, and termination of care. At one year, overall survival was 38 percent. On multivariate analysis, independent predictors of any or major postoperative complications were bowel resection at initial surgery (hazard ratio [HR] 17.14, 95% CI 2.00-147) and prior transient ischemic attack (TIA)/stroke (HR 9.99, 95% CI 1.86-53.7). On univariate analysis, acute-on-chronic mesenteric ischemia appeared protective for mortality.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Intestinal ischemia".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (see "Patient education: Ischemic bowel disease (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Acute mesenteric ischemia refers to the sudden onset of small intestinal hypoperfusion. Risk factors for acute mesenteric arterial occlusion include any process that increases the potential for embolism from the heart or proximal arterial vasculature or the risk for mesenteric arterial thrombosis. (See 'Introduction' above and 'Risk factors' above.)

•Embolism to the mesenteric arteries most commonly lodges 3 to 10 cm distal to the origin of the superior mesenteric artery (SMA) in a tapered segment distal to the takeoff of the middle colic artery.

•Thrombosis of the mesenteric arteries is often superimposed on a preexisting stenosis due to atherosclerotic plaque. Mesenteric arterial thrombosis can also occur in the setting of vascular injury related to abdominal trauma, mesenteric arterial dissection (spontaneous, related to instrumentation), a previously placed mesenteric stent, hypercoagulability, and infection.

●Early symptoms and clinical signs are nonspecific. Specific clinical features that suggest mesenteric arterial embolism or mesenteric arterial thrombus as a cause of acute mesenteric ischemia include: (See 'Clinical features' above.)

•For acute embolic occlusion, the typical triad is an older adult patient with atrial fibrillation (or other source for embolism) and severe abdominal pain out of proportion to the physical examination.

•For mesenteric thrombosis, the typical patient is a patient with atherosclerosis risk factors and known peripheral artery disease who may or may not have an established diagnosis of chronic mesenteric ischemia based upon symptoms of chronic postprandial abdominal pain, food aversion, and weight loss.

●A definitive diagnosis of mesenteric arterial occlusion relies upon demonstrating the occlusion within the mesenteric arteries on imaging studies. For patients who present with acute abdominal findings on exam indicative of bowel infarction and peritonitis, the diagnosis will necessarily be made in the operating room at the time of emergent exploratory laparotomy. Multidetector computed tomography (CT) angiography (without oral contrast) is the initial study of choice for evaluating hemodynamically stable patients with acute abdominal pain and clinical features suggestive of acute mesenteric ischemia. (See 'Diagnosis' above and "Overview of intestinal ischemia in adults", section on 'Diagnosis'.)

•Embolic occlusion appears as an oval-shaped thrombus surrounded by contrast in a noncalcified arterial segment located in the middle and distal portion of the proximal SMA.

•Thrombotic occlusion often appears as thrombus superimposed on a calcified occlusive lesion at the origin of the SMA. Thrombotic occlusion in association with hypercoagulable states or associated with shock can have a variable distribution.

●The goal of treatment for patients with acute mesenteric ischemia is to restore intestinal blood flow as rapidly as possible after initial management that includes systemic anticoagulation and empiric broad-spectrum antibiotic therapy, among others. Specific treatment depends upon the clinical status of the patient and the etiology and location of the occlusion. (See 'Management' above.)

•Patients who are good-risk surgical candidates with indications for immediate laparotomy should be taken directly to the operating room for exploration. Mesenteric arterial revascularization is preferably performed before bowel resection, but areas of the small or large intestine that are clearly nonviable can be quickly resected using a damage control approach. (See 'Surgery' above.)

-For mesenteric embolism, the traditional treatment is open surgical embolectomy. We prefer open surgical thrombectomy, but percutaneous aspiration of the clot and catheter-directed thrombolytic therapy are alternative approaches.

-For patients with mesenteric artery thrombosis, mesenteric bypass is the treatment of choice. Thrombectomy alone is unlikely to be durable. Intraoperative retrograde superior mesenteric artery angioplasty and stenting is another option, particularly in the presence of gross contamination where surgical bypass is more problematic.

•Some hemodynamically stable patients with acute-on-chronic mesenteric artery occlusion, who do not have clinical signs of advanced bowel ischemia, can be observed while maintained on systemic anticoagulation, provided there is evidence of good collateral blood flow on vascular imaging studies. The patient should have serial clinical assessment with a low threshold to repeat abdominal imaging studies or, if abdominal symptoms progress, surgical or endovascular intervention.

•Patients who are hemodynamically stable and who do not have clinical or radiologic signs of advanced intestinal ischemia may be candidates for a primary endovascular approach, which may include pharmacomechanical thrombectomy and balloon angioplasty (typically with arterial stent placement). For those who undergo endovascular intervention, there should be a low threshold to convert to open surgical exploration at any time if problems arise or the patient's clinical condition deteriorates. (See 'Surgical versus endovascular intervention' above.)

•A palliative approach may be the best option for poor-risk surgical candidates with extensive transmural infarction (eg, small bowel up to the midtransverse colon).

●For most patients after mesenteric revascularization, a second-look laparotomy 24 to 48 hours after the initial operation is needed to reevaluate the bowel. (See 'Second-look laparotomy and abdominal wall closure' above.)

●Long-term management is aimed at preventing future embolic events with anticoagulation, and cardiovascular risk reduction strategies in those with thrombotic arterial occlusion related to atherosclerosis. (See 'Long-term medical management' above.)

●Following mesenteric artery stenting, the patient should have periodic surveillance. We obtain follow-up imaging, either using duplex ultrasound or CT angiography, at three months post-intervention, then every six months for up to two years, and annually thereafter provided there is no evidence for restenosis. For those with recurrent stenosis, reintervention may be needed to prevent stent occlusion, which can lead to recurrent symptoms. (See 'Stent surveillance' above.)

●Mortality from acute mesenteric ischemia remains high, with most series not showing appreciable improvement despite an aggressive treatment regardless of approach. For open surgical approaches to revascularization, perioperative mortality ranges between 31 and 62 percent. The causes of perioperative death included ongoing mesenteric ischemia with intra-abdominal sepsis and multiorgan failure, cardiac causes, hemorrhage, and termination of care. (See 'Morbidity and mortality' above.)