Acute Mesenteric Ischemia

Updated: Apr 29, 2022
Author: Chat V Dang, MD; Chief Editor: John Geibel, MD, MSc, DSc, AGAF 


Practice Essentials

Acute mesenteric ischemia (AMI) is a syndrome caused by inadequate blood flow through the mesenteric vessels, resulting in ischemia and eventual gangrene of the bowel wall. Although relatively rare, it is a potentially life-threatening condition.

Broadly, AMI may be classified as either arterial or venous. AMI as arterial disease may be subdivided into nonocclusive mesenteric ischemia (NOMI) and occlusive mesenteric arterial ischemia (OMAI); OMAI may be further subdivided into acute mesenteric arterial embolism (AMAE) and acute mesenteric arterial thrombosis (AMAT). AMI as venous disease takes the form of mesenteric venous thrombosis (MVT). Thus, for practical purposes, AMI comprises four different primary clinical entities, as follows:

  • NOMI
  • AMAE
  • AMAT
  • MVT

The four types of AMI have somewhat different predisposing factors, clinical pictures, and prognoses. A secondary clinical entity of mesenteric ischemia occurs as a consequence of mechanical obstruction (eg, from internal hernia with strangulation, volvulus, or intussusception). Tumor compression, aortic dissection and postangiography thrombosis[1]  are other reported causes. Occasionally, blunt trauma may cause isolated dissection of the superior mesenteric artery (SMA) and lead to intestinal infarction.

Because the four types of AMI share similarities and a final common pathway (ie, bowel infarction and death, if not properly treated), they may usefully be discussed together.

In 1930, Cokkinis remarked, “Occlusion of the mesenteric vessels is apt to be regarded as one of those conditions of which the diagnosis is impossible, the prognosis hopeless, and the treatment almost useless.”[2] This quote indicates some of the extreme difficulties faced by physicians treating AMI. Symptoms are nonspecific initially, before evidence of peritonitis presents. Thus, diagnosis and treatment are often delayed until the disease is advanced.[3, 4]

Fortunately, since 1930, many advances (eg, in magnetic resonance imaging [MRI] and Doppler flowmetry[5] ) have been made that allow earlier diagnosis and treatment. Whereas the prognosis remains grave for patients in whom the diagnosis is delayed until bowel infarction has already occurred, patients who receive the appropriate treatment in a timely manner are much more likely to recover.[6]

Treatment options for acute thrombosis focus on surgical methods, which have changed little since the late 20th century. Some patients may be good candidates for percutaneous transluminal angioplasty with stenting.[7, 8, 9, 10, 11, 12] Some authors recommend a trial of thrombolytic therapy if patients can be treated within 8 hours of presentation and do not have signs of bowel necrosis or peritonitis.[13] If no evidence of improvement is noted within 4 hours, patients should undergo exploration.

Because of the high mortality and the difficulty of diagnosis, mesenteric ischemia poses a substantial legal risk. This risk can be reduced by a high degree of clinical suspicion, early and aggressive diagnostic imaging, and early surgical consultation with clear documentation of timing. One review of 180 consecutive malpractice claims found seven cases involving AMI, with allegations of failure to make a timely diagnosis in five, failure to administer anticoagulation in one, and failure to prevent NOMI in one.[14]

Guidelines for the management of AMI have been published by the World Society of Emergency Surgery (WSES).[15]


Mastery of the anatomy of the mesenteric vessels is the key to understanding and treating patients with mesenteric ischemia. However, the endless array of vascular variations can make this difficult.

The celiac axis, the SMA, and the inferior mesenteric artery (IMA) supply the foregut, midgut, and hindgut, respectively.[16] The celiac axis arises from the ventral surface of the aorta at the T12-L1 vertebral body. It courses anteroinferiorly before branching into the common hepatic, splenic, and left gastric arteries. The possible variations are too numerous to describe in this article.

The hepatic artery gives off the gastroduodenal artery, which branches further to the right gastroepiploic artery and the anterosuperior and posterosuperior pancreaticoduodenal arteries. The right gastroepiploic artery communicates with the left gastroepiploic artery, which is an immediate branch of the splenic artery. The anterosuperior and posterosuperior pancreaticoduodenal arteries communicate with the corresponding inferior branches from the SMA.

The splenic artery gives off the left gastroepiploic artery, as well as the dorsal pancreatic artery, which supplies the body and tail of the pancreas and communicates with the anterosuperior pancreaticoduodenal and gastroduodenal arteries and sometimes with the middle colic artery or SMA.

The left gastric artery, the third important branch of the celiac axis, communicates with the right gastric artery along the posterior aspect of the lesser curvature of the stomach. The celiac artery supplies most of the blood to the lower esophagus, stomach, duodenum, liver, pancreas, and spleen.

The SMA comes off the ventral aorta and supplies the midgut by giving off the inferior pancreaticoduodenal artery, middle colic, right colic, and jejunal and ileal branches.

The inferior pancreaticoduodenal artery gives rise to the corresponding anteroinferior and posteroinferior branches, which anastomose with their superior counterparts. This communication is an important connection that helps to maintain bowel perfusion in times of atherosclerosis of the mesenteric vessels. (For an illustration of a meandering artery, see the image below.)

Meandering artery (radiographic sign of preexistin Meandering artery (radiographic sign of preexisting bowel ischemia).

The ileocolic artery supplies the ileum, cecum, and ascending colon, whereas the middle colic supplies the transverse colon and communicates with the IMA. The right colic artery typically branches at the same level as the middle colic artery. The right and middle colic arteries provide an important supply of blood to the marginal artery of Drummond and give rise to the terminal vasa recta, which provide blood to the colon.

The IMA, the smallest mesenteric vessel, also comes off the anterior aorta. It supplies the distal transverse, descending, and sigmoid colon, as well as the rectum. Many communications to the SMA exist within the mesentery, and rectal branches offer communication between the visceral blood supply and the common supply. The “watershed area” near the splenic flexure was once believed more susceptible to ischemia secondary to poor arterial flow; however, it is now thought that the poor development of this area results in an increased propensity for ischemia.

The venous system, for the most part, parallels the arterial system. The superior mesenteric vein (SMV) is formed by the jejunal, ileal, ileocolic, right colic, and middle colic veins, which drain the small intestine, cecum, ascending colon, and transverse colon. The right gastroepiploic vein drains the stomach to the SMV, whereas the inferior pancreaticoduodenal vein drains the pancreas and duodenum.

The inferior mesenteric vein (IMV) drains the descending colon, the sigmoid colon, and the rectum through the left colic vein, the sigmoid branches, and the superior rectal vein, respectively. The IMV joins the splenic vein, which then joins the SMV to form the portal vein. The portal vein enters the liver.


Insufficient blood perfusion of the small bowel and colon may result from embolic or thrombotic arterial occlusion (AMAE or AMAT), thrombotic venous occlusion (ie, MVT), or nonocclusive processes such as vasospasm or low cardiac output (NOMI).[17, 18, 19] Embolic phenomena account for approximately 50% of all clinical cases, arterial thrombosis for about 25%, NOMI for roughly 20%, and MVT for fewer than 10%.

Rarely, isolated spontaneous dissections of the SMA have been reported.[20, 21, 22, 23] Whether the occlusion is arterial or venous, hemorrhagic infarction leading to perforation is the common pathologic pathway.

Injury severity is inversely proportional to the mesenteric blood flow and is influenced by the number of vessels involved, systemic mean blood pressure, duration of ischemia, and collateral circulation. The superior mesenteric vessels are involved more frequently than the inferior mesenteric vessels, with blockage of the latter often being silent because of better collateral circulation.

Damage to the affected bowel portion may range from reversible ischemia to transmural infarction with necrosis and perforation. The injury is complicated by reactive vasospasm in the SMA region after the initial occlusion. Arterial insufficiency causes tissue hypoxia, leading to initial bowel-wall spasm (see the image below). This leads to gut emptying by vomiting or diarrhea. Mucosal sloughing may cause bleeding into the gastrointestinal (GI) tract.

Radiograph showing bowel spasm (early sign of isch Radiograph showing bowel spasm (early sign of ischemia).

At this stage, little abdominal tenderness is present, producing the classic intense visceral pain that is disproportionate to physical examination findings.

As the ischemia persists, the mucosal barrier becomes disrupted, and bacteria, toxins, and vasoactive substances are released into the systemic circulation (see the image below). This can cause death from septic shock, cardiac failure, or multisystem organ failure before bowel necrosis actually occurs.

Pathologic findings 2 hours after bowel ischemia s Pathologic findings 2 hours after bowel ischemia starts.

As hypoxic damage worsens, the bowel wall becomes edematous and cyanotic. Fluid is released into the peritoneal cavity; this explains the serosanguineous fluid sometimes recovered by diagnostic peritoneal lavage. Bowel necrosis can occur in 8-12 hours from the onset of symptoms (see the image below). Transmural necrosis leads to peritoneal signs and heralds a much worse prognosis.

Microscopic findings 24 hours after ischemia start Microscopic findings 24 hours after ischemia starts.

Acute mesenteric arterial embolism

AMAE (ie, embolic AMI) is usually caused by an embolus of cardiac origin. Typical causes include mural thrombi after myocardial infarction, atrial thrombi associated with mitral stenosis and atrial fibrillation, vegetative endocarditis, mycotic aneurysm, and thrombi formed at the site of atheromatous plaques within the aorta or at the sites of vascular aortic prosthetic grafts interposed anywhere between the heart and the origin of the SMA.

Because the vascular occlusion is sudden, patients have not been able to develop a compensatory increase in collateral flow. As a result, they experience worse ischemia than patients with AMAT. Because of its small takeoff angle from the aorta and higher flow, the SMA is the visceral vessel most susceptible to emboli (see the image below); the IMA is less commonly affected.[24] Most often, emboli lodge about 6-8 cm beyond the arterial origin, at a narrowing near the emergence of the middle colic artery.

Complete aortic occlusion (Leriche syndrome) with Complete aortic occlusion (Leriche syndrome) with acute embolism of superior mesenteric artery.

The US Centers for Disease Control and Prevention (CDC) Injury Center reports a special form of mesenteric ischemia due to systemic air embolism in victims of high-energy blast injuries. These patients sustain severe primary blast injury to the lung, a condition referred to as blast lung.

Acute mesenteric arterial thrombosis

AMAT (ie, thrombotic AMI) is a late complication of preexisting visceral atherosclerosis. Symptoms typically do not develop until two of the three arteries (usually the celiac artery and the SMA) are stenosed or completely blocked.[25] Progressive worsening of the atherosclerotic stenosis before the acute occlusion allows time for development of additional collateral circulation.

A thrombus forms during a state of low flow, resulting in acute cessation of flow to the gut. Bloody stools develop as the more sensitive mucosa dies first. The bowel gradually becomes necrotic (see the image below); subsequently, bacterial overgrowth develops, and the resulting bowel perforation causes sepsis and finally death.

Gross specimen of dead bowel. Gross specimen of dead bowel.

Most patients with AMAT have atherosclerotic disease at other sites (eg, coronary artery disease [CAD], cerebrovascular accident or stroke, or peripheral arterial disease [PAD]). A drop in cardiac output resulting from myocardial infarction (MI) or congestive heart failure (CHF) may cause AMI in a patient with visceral atherosclerosis.

AMAT may also be a complication of arterial aneurysm or other vascular pathologies, such as dissection, trauma, and thromboangiitis obliterans. In inflammatory vascular disease, smaller vessels are affected. Thrombosis tends to occur at the origin of the SMA, causing widespread infarction. These patients frequently present with a history of chronic mesenteric ischemia in the form of intestinal angina before the emergency event.

Nonocclusive mesenteric ischemia

NOMI is precipitated by a severe reduction in mesenteric perfusion, with secondary arterial spasm from such causes as cardiac failure, septic shock, hypovolemia, or the use of potent vasopressors in critically ill patients.[18] Because bowel perfusion, like cerebral perfusion, is preserved in the setting of hypotension, NOMI represents a failure of autoregulation. Many vasoactive drugs (eg, digitalis, cocaine, diuretics, and vasopressin) may also cause regional vasoconstriction.[26] Gross pathologic arterial or venous occlusions are not observed.

Mesenteric venous thrombosis

MVT often (ie, >80% of the time) is the result of some processes that make the patient more likely to form a clot in the mesenteric circulation (ie, secondary MVT). Primary MVT occurs in the absence of any identifiable predisposing factor. MVT may also occur after ligation of the splenic vein for a splenectomy or ligation of the portal vein or the SMV as part of damage control surgery for severe penetrating abdominal injuries. Other associated causes include pancreatitis, sickle cell disease, and hypercoagulability caused by malignancy.

The mechanism responsible for ischemia in this setting is a massive influx of fluid into the bowel wall and lumen, which results in systemic hypovolemia and hemoconcentration. The consequent bowel edema and decreased outflow of blood secondary to venous thrombosis impede the inflow of arterial blood, and this leads to bowel ischemia. Although bowel ischemia is itself detrimental to the patient, it is the resulting multiple organ system failure that actually accounts for the high mortality.

MVT often affects a much younger population. Symptoms may be present longer than in more typical cases of AMI, sometimes for more than 30 days. Infarction from MVT is rarely observed with isolated SMV thrombosis, unless collateral flow in the peripheral arcades or vasa recta is compromised as well. Fluid sequestration and bowel wall edema are more pronounced than in arterial occlusion. The colon is usually spared because of better collateral circulation.

In a study of mortality factors in 31 patients with MVT, Abu-Daff et al determined that 30-day mortality in these patients was strongly linked to colonic involvement in ischemia and to short-bowel syndrome.[27] Lack of anticoagulation also may have been a factor. The 5-year mortality, according to the investigators, was primarily related to short-bowel syndrome.


Acute mesenteric arterial embolism

Causes of AMAE (embolic AMI) include the following[19] :

  • Cardiac emboli - Mural thrombus after MI, auricular thrombus associated with mitral stenosis and atrial fibrillation, or septic emboli from valvular endocarditis (less frequent)
  • Emboli from fragments of proximal aortic thrombus due to a ruptured atheromatous plaque
  • Atheromatous plaque dislodged by arterial catheterization or surgery (eg, aortic aneurysm resection)

Most emboli lodge in the SMA, just distal to the origin of the middle colic artery. Embolization is less often associated with ischemic disease than thrombosis and has a better survival rate when optimally treated.

Acute mesenteric arterial thrombosis

Causes of AMAT (thrombotic AMI) include the following:

  • Atherosclerotic vascular disease (most common)
  • Aortic aneurysm
  • Aortic dissection
  • Arteritis
  • Decreased cardiac output from MI or CHF (thrombotic AMI may cause acute decompensation)
  • Dehydration from any cause

Unlike embolic events, which generally occur in arterial branches and result in limited bowel ischemia, thrombosis typically occurs at the vessel’s origin, resulting in extensive bowel involvement.

Nonocclusive mesenteric ischemia

Causes of NOMI include the following:

  • Hypotension from CHF, MI, sepsis, aortic insufficiency, severe liver or renal disease, or recent major cardiac or abdominal surgery
  • Vasopressors
  • Ergotamines
  • Cocaine [28, 29]
  • Digitalis (it is unclear whether digitalis use causes NOMI or whether patients who develop NOMI are older and thus more likely to have been prescribed digitalis)

Case reports have documented celiac artery compression syndrome (CACS) as a cause of mesenteric ischemia through external compression of the celiac artery, usually by the median arcuate ligament or the celiac ganglion.[30, 31] Case reports have also described marathon runners who develop ischemic colitis after a marathon; in most instances, this resolves with supportive treatment.[32]

Mesenteric venous thrombosis

Causes of MVT include the following (>80% of patients with MVT are found to have predisposing conditions):

  • Hypercoagulability [33] from protein C and S deficiency, [34, 35] antithrombin III deficiency, dysfibrinogenemia, abnormal plasminogen, polycythemia vera (most common), thrombocytosis, sickle cell disease, factor V Leiden mutation, pregnancy, and oral contraceptive use [36, 37, 38]
  • Tumor causing venous compression or hypercoagulability (paraneoplastic syndrome)
  • Infection, usually intra-abdominal (eg, appendicitis, diverticulitis, or abscess)
  • Venous congestion from cirrhosis (portal hypertension)
  • Venous trauma from accidents or surgery, [39, 40, 41, 42, 43] especially portacaval surgery
  • Increased intra-abdominal pressure from pneumoperitoneum during laparoscopic surgery [39]
  • Pancreatitis
  • Decompression sickness


United States and international statistics

The overall prevalence of AMI is 0.1% of all hospital admissions; this figure may be expected to rise as the population ages. The exact prevalence of MVT is not known, because many cases are presumed to be limited in symptomatology and to resolve spontaneously. It is believed to account for approximately 10-15% of all cases of mesenteric ischemia and for 0.006% of hospital admissions. Venous thrombosis is found in approximately 0.001% of patients who undergo exploratory laparotomy.

Risk factors for AMI include atherosclerosis, arrhythmias, hypovolemia, CHF, recent MI, valvular disease, advanced age, and intra-abdominal malignancy.[44, 45, 46, 47] Mesenteric artery stenosis is found in 17.5% of independent elderly adults.[48] Approximately two thirds of patients are women.

Research indicates that inflammatory bowel disease (IBD) is another risk factor for mesenteric artery thrombosis.[49] In a review comparing 17,487 patients who had either Crohn disease or ulcerative colitis with 69,948 control subjects, the investigators detected a significantly higher risk of AMI in the patients with IBD.[45]

Outside the United States, reported rates of AMI are probably lower in countries with limited diagnostic capability or whose populations have a shorter life expectancy because AMI is primarily a disease of older individuals.

Age-, sex-, and race-related demographics

In large part because of the association with atherosclerosis,[50] AMI is commonly considered a disease of the older population, with the typical age of onset being older than 60 years. Nevertheless, younger people who have atrial fibrillation or risk factors for MVT, such as oral contraceptive use or hypercoagulable states (eg, those caused by protein C or S deficiency), may present with AMI.

No overall sex preference exists for AMI. Men might be at higher risk for occlusive arterial disease because they have a higher incidence of atherosclerosis. Conversely, women who are taking oral contraceptives or are pregnant are at higher risk for MVT.

No racial predilections are known for AMI. However, people of races with a higher rate of conditions leading to atherosclerosis, such as African American people, might be at higher risk.


Although survival rates for AMI have improved over the past four decades, the prognosis for patients with AMI of any type remains grave.[19] Over the past 15 years, the all-cause mortality from AMI has averaged 71% (range, 59-93%). Once bowel-wall infarction has occurred, mortality may be as high as 90%. Even with good treatment, as many as 50-80% of patients die. For those patients who do survive, the risk of rethrombosis is high, and lifestyle may be hindered by a lifetime of total parenteral nutrition as a remedy for short-gut syndrome.

Predictors of mortality have included older age, bandemia, hepatic and renal impairment, hyperamylasemia, metabolic acidosis, hypoxia, intramural pneumatosis, and sepsis.[51] Mortality is highest for AMAT,[52] followed by NOMI, AMAE, and MVT.[53]

Early and aggressive diagnosis and treatment have been shown to reduce mortality substantially if the diagnosis is made before the development of peritonitis.[54] It is essential to act early on clinical suspicion, rather than wait for the arrival of hard evidence. Survivors of extensive bowel resection face significant long-term morbidity because of the reduced intestinal mucosal surface available for absorption. However, with rapid treatment, mortality can be reduced considerably, and patients may be spared bowel resection.

A long-term follow-up study of 31 AMI patients who had surgery and survived the acute episode revealed 2- and 5-year survival rates of 70% and 50%.[55] Deaths were mainly related to cardiovascular comorbidity and malignant disease. With appropriate anticoagulation, only one patient died after a recurrent attack of AMAT.

Early recognition and treatment of NOMI has been shown to reduce mortality to 50-55%.

In a report from Madrid describing 21 patients with SMA embolus, intestinal viability was achieved in 100% of patients if the duration of symptoms was shorter than 12 hours, 56% if the duration was 12-24 hours, and only 18% if the duration was longer than 24 hours.[56] Another study found that even at hospital centers with angiography available 24 hours a day, mortality still was approximately 70%.[57]

MVT is associated with a 30-day mortality of 13-15%. Without anticoagulant therapy, mortality approaches 30%, with a 25% recurrence rate. The combination of anticoagulant therapy with surgery is associated with the lowest recurrence rate (~3-5%). Patients presenting with peritonitis and infarcted bowel have a prolonged and complicated course.

Patient Education

Patients who survive to discharge should be educated regarding short-bowel syndrome. They should also be instructed about the importance of taking warfarin or other discharge medications to prevent recurrence.




To an extent, all types of acute mesenteric ischemia (AMI) present similarly. However, there are some differences in clinical appearance for each type (see below), which may be diagnostically useful. The most important finding is pain that is disproportionate to physical examination findings. Typically, pain is moderate to severe, diffuse, nonlocalized, constant, and sometimes colicky.

Onset varies from type to type. Nausea and vomiting are found in 75% of affected patients. Anorexia and diarrhea progressing to obstipation are also common. Abdominal distention and gastrointestinal (GI) bleeding are the primary symptoms in as many as 25% of patients. Pain may be unresponsive to opioids. As the bowel becomes gangrenous, rectal bleeding and signs of sepsis (eg, tachycardia, tachypnea, hypotension, fever, and altered mental status) develop. A review of systems, looking for risk factors of AMI, should be performed.

If not properly and rapidly treated, AMI has a catastrophic outcome. Accordingly, it should be considered in any patient with abdominal pain disproportionate to physical findings, gut emptying in the form of vomiting or diarrhea, and the presence of risk factors, especially age older than 60 years.

Acute mesenteric arterial embolism

Of all the types of AMI, acute mesenteric arterial embolism (AMAE; ie, embolic AMI) typically has the most abrupt and painful presentation as a consequence of the rapid onset of occlusion and the inability to form additional collateral circulation. It has been described as abdominal apoplexy and is sometimes referred to as a “bowel attack.”

Often, vomiting and diarrhea (gut emptying) are observed. Patients are usually found to have a source of embolization. Because most emboli are of cardiac origin, patients often have atrial fibrillation or a recent myocardial infarction (MI) with mural thrombus. Infrequently, patients may report a history of valvular heart disease or a previous embolic episode.

Acute mesenteric arterial thrombosis

Acute mesenteric arterial thrombosis (AMAT; ie, thrombotic AMI) typically develops when an artery already partially blocked by atherosclerosis becomes completely occluded.

A patient with AMAT presents with severe abdominal pain. He or she may give a history of postprandial pain, typically occurring 10-20 minutes after eating and lasting as long as 1-3 hours (abdominal angina). The pain is diffuse, and the patient may report frank blood in the stool. Symptoms worsen over time.

Typically, these patients typically have a history of atherosclerotic disease at other sites, such as coronary artery disease (CAD), cerebrovascular disease, recent MI, peripheral artery disease (PAD; especially aortoiliac occlusive disease), or a history of aortic reconstruction. They may have a long history of smoking or uncontrolled diabetes mellitus. Weight loss, “food fear,” early satiety, and altered bowel habits may be present.

The precipitating event that initiates AMAT may be a sudden drop in cardiac output from acute MI or congestive heart failure (CHF) or a ruptured plaque. Dehydration from vomiting or diarrhea due to an unrelated illness may also precipitate AMAT. As a consequence of the massive shifts in fluid volume and the hypercoagulable state, patients in surgical intensive care are especially prone to developing arterial thrombosis.

Compared with patients who have AMAE, patients who have AMAT have undergone a more gradual progression of arterial occlusion and frequently have a better collateral supply. Their bowel viability is better preserved, which means that the presentation is often less severe than would be the case with AMAE. Symptoms tend to be less intense and of more gradual onset.

Nonocclusive mesenteric ischemia

Nonocclusive mesenteric ischemia (NOMI) occurs more frequently in older patients. Often, these elderly patients are already in an intensive care unit (ICU) with acute respiratory failure or severe hypotension from cardiogenic or septic shock, or else they are taking vasopressive drugs. Historically, many were taking digitalis (which is seldom prescribed nowadays in the United States).

Symptoms typically develop over several days, and patients may have experienced a prodrome consisting of malaise and vague abdominal discomfort. When infarction occurs, the clinical condition of the ICU patient deteriorates with no apparent reason. Patients may report increased pain associated with vomiting. They may become hypotensive and tachycardic, with loose bloody stool.

Mesenteric venous thrombosis

Mesenteric venous thrombosis (MVT) is often observed in a much younger patient population than other types of AMI are. MVT patients can present with an acute or subacute abdominal pain syndrome related to involvement of the small intestine rather than the colon.

The symptoms of MVT are frequently less dramatic than those of other types of AMI, with a more insidious onset. Diagnosis can be even more difficult than for other AMI types, in that MVT symptoms may have been present for weeks before being noticed or reported (27% have symptoms for >30 days). Typical symptoms of MVT may have been experienced for a prolonged period with gradual worsening (eg, vague abdominal discomfort evolving over 7-10 days).

Many patients have a history of one or more of risk factors for hypercoagulability. These include oral contraceptive use, congenital hypercoagulable states, deep vein thrombosis (DVT), pulmonary embolism (PE), liver disease, cancer, and portacaval surgery. Patients presenting with pancreatitis or signs of intra-abdominal infection should be considered predisposed to developing MVT.

Physical Examination

The different etiologies notwithstanding, physical examination findings are generally similar in patients with AMI. The characteristic feature of this syndrome is a relatively normal abdominal examination in the face of severe abdominal pain. The main distinction to be made with respect to physical findings is between early and late presentations.

Early in the course of AMI, in the absence of peritonitis, physical signs are few and nonspecific. Tenderness is minimal to nonexistent. The abdomen may be distended. Stool may be positive for blood.

Peritoneal signs develop late, when infarction with necrosis or perforation occurs. Tenderness becomes severe and may indicate the location of the infarcted bowel segment. A palpable tender mass may be present. Bowel sounds range from hyperactive to absent. Voluntary and involuntary guarding appears.

Fever, hypotension, tachycardia, tachypnea, and altered mental status are observed. Foul breath may be noted with bowel infarction, from the putrefaction of undigested alimentary material accumulated proximal to the pathologic site. Paracentesis may demonstrate bloody peritoneal fluid; however, this occurs after bowel infarction and therefore is a late sign.

Signs reflecting risk factors for AMI may be noted. Patients with AMAE may have atrial fibrillation or heart murmurs. Those with AMAT or NOMI may have an abdominal murmur or the scar from an abdominal aortic repair with or without reimplantation of the superior mesenteric artery (SMA). Those with MVT may have evidence of tumor, cirrhosis, DVT, or recent abdominal surgery.


The following are potential complications of AMI:

  • Bowel necrosis necessitating bowel resection
  • Sepsis and septic shock
  • Multiple organ dysfunction syndrome (MODS)
  • Death


Diagnostic Considerations

Because acute mesenteric ischemia (AMI) is a condition with an unclear initial presentation, a substantial morbidity, and a high mortality if not properly treated, a high index of clinical suspicion should be maintained. Computed tomography (CT) angiography (CTA) should be performed at an early stage if any suspicion of AMI exists, and subsequent treatment should be initiated as rapidly as possible. No patient in whom AMI is suspected should be discharged unless AMI can be ruled out.

A diagnosis of AMI should be considered in all elderly patients with abdominal pain, especially if the pain is disproportionate to physical examination findings. Patients with atrial fibrillation, cardiovascular disease, or peripheral vascular disease, especially those with recent myocardial infarction, are at higher risk.

A diagnosis of mesenteric venous thrombosis (MVT) is usually confirmed during laparotomy or autopsy. Only after other causes of a hypercoagulable state have been excluded can a patient be considered to have idiopathic venous thrombosis.

In addition to the conditions listed in the differential diagnosis, other problems to consider include the following:

  • Ovarian torsion
  • Volvulus of midgut
  • Splenic vein thrombosis
  • Crohn disease colitis
  • Ulcerative colitis
  • Perforated viscus
  • Hepatic disease

Differential Diagnoses



Approach Considerations

Various laboratory studies may be performed for suspected acute mesenteric ischemia (AMI), but in general, such studies will not establish the diagnosis. At most, they suggest the diagnosis; they do not exclude it.

If serious suspicion of AMI exists, the clinician should order diagnostic imaging studies (eg, plain radiography, classic angiography, computed tomography [CT] angiography [CTA], magnetic resonance angiography [MRA], or ultrasonography [US]) without waiting for laboratory results. Electrocardiography (ECG) and diagnostic peritoneal lavage (DPL) may also be considered.

A review of 180 consecutive malpractice claims at a Veterans Affairs Medical Center over a 12-year period ending in 1998 revealed seven cases involving AMI. Failure to make a timely diagnosis was alleged in five cases, and failure to administer anticoagulation was alleged in one. The remaining allegation was failure to prevent nonocclusive mesenteric ischemia (NOMI). Legal risk is reduced with early surgical consultation and the ordering of CT contrast (CTA) as soon as AMI is noted in the differential diagnosis. (See also Mesenteric Ischemia Imaging.)

Laboratory Studies

Laboratory findings in AMI are nonspecific and generally unreliable. No serum marker is sensitive or specific enough to establish or exclude the diagnosis of AMI. However, the following laboratory examinations should be ordered:

  • Prothrombin time (PT)
  • Activated partial thromboplastin time (aPTT)
  • International normalized ratio (INR)
  • Complete blood count (CBC), which may reveal leukocytosis (bandemia) or hemoconcentration
  • Chemistry studies that may show metabolic acidosis, increased amylase levels, or increased lactate dehydrogenase (LDH) levels

The CBC may be within the reference range initially, but the white blood cell (WBC) count eventually rises as the disease progresses. Leukocytosis, a leftward shift, or both are observed in more than 50% of cases. The hematocrit is elevated initially from hemoconcentration due to third-spacing, but it decreases with gastrointestinal (GI) bleeding.

Metabolic acidosis is observed late in the disease course, but this is a nonspecific finding. Amylase levels are moderately elevated in more than 50% of patients, but this is also nonspecific. Lactate is elevated late in the clinical course. levels that are persistently within the reference normal range strongly indicate a diagnosis other than AMI (sensitivity 90-96%, specificity 60-87%).[58, 59, 60] Phosphate levels were initially thought to be sensitive, but later studies showed a sensitivity of only 25-33%.

If a hypercoagulable state is suggested, additional laboratory studies, such as tests for protein C and S deficiencies and antithrombin III deficiency, may be ordered. Testing for abnormalities in lupus anticoagulant, anticardiolipin antibody, and platelet aggregation may be considered.

Several studies have found that serum D-dimer may be used as an early marker for AMI, though it appears to be insensitive.[61, 62, 63, 64] Additional clinical experience will be required to validate the role of D-dimer in the screening and diagnosis of AMI.

Plain Abdominal Radiography

Although plain abdominal films can yield a presumptive diagnosis in 20-30% of patients with AMI, they often appear normal in this setting and therefore should not be used to rule out AMI. However, plain abdominal films are warranted for excluding identifiable causes of abdominal pain, such as perforated viscus with free intraperitoneal air.

Positive findings on plain abdominal radiography are usually late and nonspecific and include ileus, small-bowel obstruction, edematous or thickened bowel walls, and paucity of gas in the intestines. More specific signs, such as pneumatosis intestinalis (ie, submucosal gas), thumbprinting of the bowel wall, and portal vein gas are late findings (see the images below). In a study of 23 cases of bowel infarction, 30% of the patients demonstrated focally edematous bowel wall (thumbprinting) or pneumatosis intestinalis.

Pneumatosis intestinalis (black stripes of air) in Pneumatosis intestinalis (black stripes of air) in advanced acute mesenteric ischemia (AMI) with gangrenous bowel.
Pneumatosis intestinalis, one of few radiographic Pneumatosis intestinalis, one of few radiographic findings in patients with mesenteric ischemia.
Gas in colon wall (typical of advanced ischemia). Gas in colon wall (typical of advanced ischemia).
Thumbprinting of bowel, characteristic of mesenter Thumbprinting of bowel, characteristic of mesenteric artery ischemia.
Ischemia stricture. Ischemia stricture.

Conventional Angiography

Angiography (see the image below) has been the criterion standard for diagnosis and preoperative planning in AMI. Various studies have reported sensitivities of 74-100% and a specificity of 100% for acute arterial occlusion.[54, 65, 66, 67, 68, 69, 70] Anteroposterior views demonstrate collateral pathways, whereas lateral projections show the origins of visceral branches. Currently, however, angiography is less and less resorted to in clinical practice.

Aortogram showing narrowing of superior mesenteric Aortogram showing narrowing of superior mesenteric artery.

Patients with embolization to the superior mesenteric artery (SMA)—that is, acute mesenteric arterial embolism (AMAE)—have an aortogram that demonstrates filling of the proximal SMA vessels to a sharp cutoff with no visualization of the distal vessels. Such an abrupt cutoff with the absence of collateral circulation is diagnostic, with nearly 100% sensitivity in acute embolic occlusion.[71]

Unlike patients with AMAE, those with acute mesenteric arterial thrombosis (AMAT) have well-developed collateral circulation as a consequence of long-standing, chronic ischemia. Thrombosis of the SMA generally appears as a more tapered occlusion near to or flush with the aortic origin of the vessel, resulting in an aortogram that fails to demonstrate any visualization of the SMA.

NOMI is characterized by narrowing of the origins of multiple SMA branches, alternating dilation and narrowing of the intestinal branches (ie, the “string of sausages” sign), spasm of the mesenteric arcades, and impaired filling of the intramural vessels.

Angiography has the added advantage of offering therapeutic as well as diagnostic options, including administration of intra-arterial thrombolytic agents for acute arterial thrombosis[72] and intra-arterial infusion of papaverine for all types of arterial ischemia.

The disadvantages of angiography are that it is highly invasive and unsuitable for critically ill patients; that it often is not readily available and may delay surgical management; and that nephrotoxicity may occur because of the effects of intravenous (IV) contrast on the kidneys. Angiography also has a relatively high false-negative rate in patients presenting early in the course of AMI.[73] Finally, arteriography can precipitate acute ischemia; thus, it is important to make sure that the patient is well hydrated.

Despite the disadvantages, if suspicion for AMI is high in an emergency setting, the treating physician should aggressively pursue conventional angiography if it is easily accessible. Prompt laparotomy is indicated if AMI is suspected but expeditious angiography is not available. If the case is not an emergency, it may be worthwhile to perform a dipyridamole-thallium scan to evaluate for coronary artery disease (CAD).

If mesenteric venous thrombosis (MVT) is strongly suspected, as in a patient with a history of hypercoagulability, angiography is considered a second-line study because of the high false-negative rate; abdominal CTA is preferable. Findings with angiography in MVT include thrombus in the superior mesenteric vein (SMV), reflux of contrast into the aorta, prolonged arterial phase with accumulation of contrast and thickened bowel walls, extravasation of contrast into bowel lumen, and filling defect in the portal vein or complete lack of venous phase.

CT and CTA

Contrast CT has proved very valuable for the assessment of mesenteric ischemia; current multiarray spiral scanners allow detailed examination of both the small bowel and the mesenteric vessels.[74, 75, 76] Multiple studies have cited sensitivities of 96-100% and specificities of 89-94%.

CT findings with a specificity greater than 95% for AMI include SMA or SMV thrombosis, intestinal pneumatosis, portal venous gas, lack of bowel-wall enhancement, and ischemia of other organs[77] ; less specific findings include distended bowel, absence of intestinal gas, thickened bowel wall, mesenteric or perienteric fat stranding, ascites, pneumoperitoneum, and air-fluid levels.[78, 79]  (See the images below.)

Mesenteric venous air (red arrows) and free intrap Mesenteric venous air (red arrows) and free intraperitoneal air (white arrow.) Mesenteric venous air is common finding in advanced acute mesenteric ischemia. Courtesy of Brandon Dessecker, MD, Melanie Nukula, MD, and Robert Marx, DO.
Pronounced portal venous air seen within liver (re Pronounced portal venous air seen within liver (red arrow), as well as free intraperitoneal air (white arrow) and pneumatosis intestinalis throughout bowel wall, which are classic findings for advanced acute mesenteric ischemia. Courtesy of Brandon Dessecker, MD, Melanie Nukula, MD, and Robert Marx, DO.

Bowel-wall edema (see the image below) is the most common finding, representing submucosal infiltration of fluid or hemorrhage into ischemic bowel. Arterial occlusion may show nonenhancement of the vessels. MVT usually shows a thrombus in the SMV or the portal vein.

CT scan (with contrast) of nonocclusive mesenteric CT scan (with contrast) of nonocclusive mesenteric ischemia with resulting bowel wall edema (arrows).

CTA has a sensitivity of 71-96% and a specificity of 92-94% for AMI. In current clinical practice, CTA is ordered much more frequently than classic angiography. CTA is noninvasive and readily available, and serial CT angiograms can be used to monitor patients treated nonsurgically with anticoagulation.

Abdominal CTA is considered by many to be the diagnostic test of choice if the index of suspicion for MVT is high and the patient is stable enough to undergo the procedure; sensitivities are greater than 90%.[80, 34, 81] CT findings include enlargement of the SMV or portal vein, a sharply defined vein wall with a rim of increased density, and low density (representing thrombus) within the vein (see the images below).[36]

CT scan demonstrating cavernous change of superior CT scan demonstrating cavernous change of superior mesenteric vein as consequence of venous thrombosis.
CT scan demonstrating thrombosis of superior mesen CT scan demonstrating thrombosis of superior mesenteric vein.
CT scan demonstrating thrombosis of portal vein. CT scan demonstrating thrombosis of portal vein.


Magnetic resonance imaging (MRI) and MRA yield findings similar to those of CT in AMI. MRA has a sensitivity of 100% and a specificity of 91%. It is particularly effective for evaluating MVT.

Despite its high sensitivity, MRI is not yet as practical as CT in the setting of suspected AMI, because of the cost and the time required for the examination. If these drawbacks can be eliminated or mitigated, rapid MRA may eventually supplant CTA.


Duplex US is highly specific (92-100%), but its sensitivity (70-89%) does not match that of angiography. It cannot detect clots beyond the proximal main vessels, nor can it be used to diagnose NOMI. US is considered a second-line study for AMI. It is often less useful in the presence of dilated loops of bowel.

In some studies, US appears to be as useful as CT if duplex scanning is performed for MVT at an early stage. It may show a thrombus or absent flow in the involved arteries or veins. Other possible findings include portal vein gas, biliary disease, free peritoneal fluid, thickened bowel wall, and intramural gas. Some researchers believe that duplex scans should be used as a first-line diagnostic tool in any patient thought to have MVT.

Echocardiography may confirm the source of embolization or show valvular pathology.

Other Tests

ECG may show myocardial infarction or atrial fibrillation.

Nasogastric tube decompression is diagnostically useful, both for helping to relieve distention and for facilitating evaluation for upper gastrointestinal bleeding.

DPL may recover the serosanguineous fluid associated with bowel infarction; with the availability of CTA or MRA, DPL is now very rarely (if ever) used when AMI is suspected.

Foley catheterization allows monitoring of urinary output as an indicator for minimal fluid resuscitation. Placement of a central line may be useful in hemodynamically unstable patients.



Approach Considerations

Recognition of acute mesenteric ischemia (AMI) before permanent tissue damage occurs is the best way of improving patient survival, and only angiography or exploratory surgery makes early diagnosis possible. Computed tomography (CT) angiography (CTA) and magnetic resonance angiography (MRA) have become the cornerstones of the modern diagnostic approach, allowing prompt laparotomy in patients with suspected AMI. A second-look procedure is indicated whenever bowel of questionable viability is not resected.

After initial medical or surgical stabilization, patients with AMI typically have a prolonged inpatient recovery time. This is especially true when resection of necrotic bowel is performed. Such patients may need to be kept on nil per os (NPO) status, and they may be maintained on parenteral nutrition for some time. If sepsis is evident, liver abscess should be actively sought. During the inpatient stay, every effort must be made to find and, if possible, treat any predisposing cause(s) of AMI.

Inpatient medications that may be used include the following:

  • Papaverine
  • Heparin/low-molecular-weight heparin (LMWH)
  • Warfarin
  • Broad-spectrum antibiotics and pain medications
  • Thrombolytics

Because timing is essential in preventing bowel necrosis with its attendant severe morbidity and mortality, patients should be transferred only if the primary hospital lacks adequate services for diagnosing and treating the patient. Patients should be optimally resuscitated before transfer. Appropriate services must be available at the receiving hospital.

In 2000, the American Gastroenterological Association (AGA) released recommended algorithms for the diagnosis and management of mesenteric ischemia (see the images below).[73] However, these recommendations were formulated before the availability of improved data from multidetector CT, as a result of which CT now plays a larger role in the diagnosis of mesenteric ischemia.

Diagnosis and treatment of intestinal ischemia (me Diagnosis and treatment of intestinal ischemia (mesenteric venous thrombosis and major nonembolic arterial occlusion). Solid lines indicate accepted management plan; dashed lines indicate alternate management plan. DVT=deep vein thrombosis; SMA=superior mesenteric artery. Adapted from Gastroenterology. 2000 May;118(5):954-68.
Diagnosis and treatment of intestinal ischemia (mi Diagnosis and treatment of intestinal ischemia (minor arterial occlusion or embolus, major embolus, and splanchnic vasoconstriction without occlusion). Solid lines indicate accepted management plan; dashed lines indicate alternate management plan. DVT=deep vein thrombosis; SMA=superior mesenteric artery. Adapted from Gastroenterology. 2000 May;118(5):954-68.
Management of colon ischemia. Solid lines indicate Management of colon ischemia. Solid lines indicate accepted management plan; dashed lines indicate alternative management plan. BE=barium enema; NPO—nil per os (nothing by mouth); PLC=protein-losing colopathy; IBD=inflammatory bowel disease. Adapted from Gastroenterology. 2000 May;118(5):954-68.

Treatment options depend on the etiology of intestinal ischemia, as well as on the hemodynamic stability of the patient and the experience/expertise of the treating staff. Generally speaking, nonocclusive AMI is treated medically, whereas occlusive AMI is correctable with surgery. Definitive treatment options include the following:

  • Acute mesenteric arterial embolism (AMAE) - Papaverine infusion, surgical embolectomy, and intra-arterial thrombolysis
  • Acute mesenteric arterial thrombosis (AMAT) - Papaverine infusion and arterial reconstruction, either through aortosuperior mesenteric arterial bypass grafting or through reimplantation of the superior mesenteric artery (SMA) into the aorta [82]
  • Nonocclusive mesenteric ischemia (NOMI) - Papaverine infusion [54, 65, 83]
  • Mesenteric venous thrombosis (MVT) - Anticoagulation with heparin or warfarin, either alone or in combination with surgery; immediate heparinization should be started even when surgical intervention is indicated [71, 38, 84, 66, 85, 34]

All cases of mesenteric ischemia with signs of peritonitis or possible bowel infarction,[86] regardless of etiology, generally warrant immediate surgical intervention for the resection of ischemic or necrotic intestines. Hemodynamic instability can also be an indication for surgery. Surgical treatment may be contraindicated if the risks from comorbid conditions preclude survival after general anesthesia. If the ischemia is thought to be caused by vasospasm, surgery is not indicated. Medical management with anticoagulants and intra-arterial vasodilators is appropriate.

Some experience with percutaneous endovascular interventions has been accumulated. In select cases, especially in isolated spontaneous dissection of the SMA, stent placement may be the preferred option.[87]

Aside from timely diagnosis and treatment of predisposing conditions, there are no known preventive measures for AMI. In the presence of a clinical syndrome suggesting chronic mesenteric insufficiency, color Doppler evaluation of the mesenteric vessels may help identify at-risk patients for further workup and determine which patients might need angioplasty.

Guidelines for the management of AMI have been published by the World Society of Emergency Surgery (WSES).[15]

Initial Resuscitation and Stabilization

Because patients with mesenteric ischemia are usually in a highly toxic state or rapidly progressing toward such a state, resuscitation is often necessary. Every effort should be made to improve patients’ cardiovascular status. Vasopressors should be avoided, because they worsen ischemia. Oxygen should be provided to maintain a saturation between 96-99%, via endotracheal intubation if necessary. Early intubation in unstable patients may improve oxygenation and allow more aggressive fluid resuscitation.

If hypovolemia is considered likely, intravenous (IV) fluid resuscitation is required. This is accomplished with isotonic sodium chloride solution, and blood products are provided as needed. Adequacy of resuscitation can be determined by means of urinary output, central venous pressure, or Swan-Ganz pressure monitoring. A nasogastric tube should be inserted, and any arrhythmia, congestive heart failure (CHF), or myocardial infarction (MI) should be treated.

All patients with possible bowel ischemia should be started on broad-spectrum antibiotics at an early stage to cover the possibility of bowel necrosis with contamination. Adequate pain control should be provided (eg, with parenteral opioid analgesics) while stable blood pressure is maintained.

Pharmacologic Therapy


Intra-arterial infusion of papaverine through the angiography catheter at the affected vessel is useful for all arterial forms of AMI. Papaverine is an opium derivative that functions as a phosphodiesterase inhibitor, which acts to relax vascular smooth muscle. It is usually infused directly into the SMA, thus improving intestinal blood flow.

An infusion of 30-60 mg/hr may be started after angiography, with the dosage subsequently adjusted on the basis of the clinical response. This should be continued for at least 24 hours. If the catheter slips into the aorta, significant hypotension can occur. It must be kept in mind that papaverine is incompatible with heparin.

Papaverine relieves reactive vasospasm in occluded arterial vessels and is the only treatment of NOMI other than resection of gangrenous bowel. In some patients with AMAE, intra-arterial papaverine has reversed the ischemia and averted operation. AMAT, however, cannot be cured medically; if vasospasm is observed on arteriography in a patient with AMAT, intra-arterial papaverine may be started to improve flow, but it will not be curative.


Thrombolytic agents infused through the angiography catheter can be life-saving for selected patients with AMAE. Bleeding is the main complication. Thrombolytic administration is risky and should only be undertaken if peritonitis or other signs of bowel necrosis are absent.

The infusion must be started within 8 hours of symptom onset. If symptoms do not improve within 4 hours or if peritonitis develops, the infusion should be stopped and surgical treatment instituted.

Thrombolytics have shown no benefit in AMAT. Lytic therapy with urokinase, streptokinase, or tissue plasminogen activator has been found to be beneficial in some cases of MVT.


Heparin anticoagulation is the main therapy for MVT. If no signs of bowel necrosis exist, the patient may not even need an operation. Heparin may increase the chance of bleeding complications. A possible avenue for randomized clinical trials is the use of enoxaparin or another LMWH as a potential substitute for heparin in the treatment of MVT.

Heparin is administered first as a bolus of 80 U/kg, not to exceed 5000 U, and then as an infusion at 18 U/kg/hr until full conversion to oral warfarin. Appropriate monitoring of anticoagulation through measurement of the activated partial thromboplastin time (aPTT) is mandatory.

Surgical Intervention

Before operative management of AMI, patients should be stabilized as described above (see Initial Resuscitation and Stabilization). If possible, they should undergo bowel preparation the night before surgery and take nothing by mouth after midnight the evening before surgery.

If the surgeon thinks a patient may require extensive resection and that lifelong hyperalimentation is likely to be the only option, this possibility should be thoughtfully discussed with the patient and the family to help guide the surgeon during the exploration. Such issues are best decided preoperatively, with educated input from the patient, rather than intraoperatively by the surgeon.

It is essential to determine the locations of viable and nonviable bowel during surgery. In patients with AMAT, laparotomy reveals that the entire small bowel and proximal colon are affected, reflecting a proximal obstruction. In patients with AMAE, however, the proximal jejunum is spared, reflecting a more distal obstruction. When extensive bowel involvement is noted, every effort must be made to retain every centimeter of viable bowel. If determining bowel viability is difficult, a second look may be required 24-48 hours later.

Evaluation of viability begins with direct visualization of the bowel. If the first part of the jejunum is not involved, an embolus may be present, and immediate embolectomy may be indicated. Peristalsis should be sought, and the color of the bowel should be observed (pink and healthy vs red and edematous; see the image below). After reconstitution of arterial flow, the viability of the bowel is reassessed. This reassessment is based on clinical findings, including the color of the bowel and the presence or absence of palpable pulses.

Gross specimen showing hemorrhagic dead bowel afte Gross specimen showing hemorrhagic dead bowel after resection from patient with acute mesenteric ischemia.

Intraoperative Doppler scans of the bowel can provide valuable information on the patency of the vessels. Differentiation of nonviable from viable bowel can be enhanced by intraoperative fluorescein administration. During laparotomy, 1 g of fluorescein is infused. Viable bowel fluoresces brightly under a Wood lamp, thus allowing the surgeon to better identify the segments that must be resected.

Because of fat absorption, fluorescein can be used only once. Most patients can benefit from a 24- to 48-hour second-look operation to assess the viability of the remaining bowel. Intraoperative fluorescein administration may be performed either at the primary operation or during the second-look operation.

A second-look laparotomy is the most reliable method of determining bowel viability. The decision to perform a second-look procedure is made during the initial exploration. If a second look is deemed necessary, the surgeon should not change his or her mind, regardless of the patient’s clinical progress.

Acute mesenteric arterial embolism

For AMAE (ie, embolic AMI), unless the involved bowel is clearly gangrenous, reperfusion should be attempted. The SMA is exposed and isolated below the mesocolon distal to the middle colic artery, and the location of the blockage is determined by palpation of pulses. Because most emboli are near the origin of the middle colic artery, the proximal SMA pulse should be noted in AMAE.

A transverse (or, according to some surgeons’ preference, longitudinal) arteriotomy is made proximal to the point of occlusion, and a balloon-tipped Fogarty catheter (size 3 or 4) is passed distally. The balloon is then inflated and the clot extracted. The arteriotomy can be closed primarily or vein-patched to prevent lumen compromise. If primary closure or patching is difficult, the patient may require an endarterectomy. A bypass may be required if embolectomy is unsuccessful.

After restoration of flow, the intestines are observed for 10-15 minutes to allow assessment of bowel viability. As noted (see above), this assessment can be enhanced by intraoperative duplex ultrasonography (US), fluorescein use, and palpation of pulses distal to the occlusion.

Other methods of reperfusion involve prosthetic bypass grafting or autogenous vein grafting.

Acute mesenteric arterial thrombosis

Surgical treatment of AMAT (ie, thrombotic AMI) involves exploratory laparotomy, followed by identification of the involved artery and bowel. Anticoagulation therapy with IV heparin, if not already started, should be initiated.

Emergency surgical revascularization is indicated. Simple thrombectomy is of little or no benefit, because most patients have clinically significant atherosclerosis at the time of the acute decompensation. Unlike patients with AMAE, patients with AMAT have a lesion at the origin of the SMA, and no SMA pulsation is detected at the origin.

If the gut is not gangrenous, revascularization may proceed. An antegrade aortomesenteric bypass is preferred. Bypass may also be done with a prosthetic graft. If bowel perforation is discovered on laparotomy, an autogenous saphenous vein graft should be used because of the decreased risk of infection. Transaortic endarterectomy is an alternative when no vein is suitable for harvesting or when a prosthetic graft is contraindicated (eg, with massive fecal contamination).[88, 89] After revascularization, the viability of the bowel is reassessed.

Endovascular therapies have been described, and some authors have tried thromboaspiration.[90] The criterion standard remains operative exploration to allow assessment of bowel viability.

Mesenteric venous thrombosis

For patients with severe MVT, exploratory laparotomy with assessment of bowel viability is indicated (see above). Anticoagulation therapy with IV heparin should be initiated immediately and continued intraoperatively. Definitive surgical treatment is required for patients with signs of bowel infarction or peritonitis.[91, 34] Treatment involves resecting the dead bowel segment(s) and reanastomosing the remaining bowel ends.

Direct venous surgery to remove the clot is usually unsuccessful and is best reserved for patients with portal vein or superior mesenteric vein (SMV) involvement. Thrombectomy has little use in MVT, because it can only be performed if the thrombus is fresh (ie, no more than 1-3 days old) and because the thrombosis is usually so widespread that all the thrombi cannot be removed completely. Mechanical transhepatic thrombectomy has been described in one patient.[92]

To minimize the amount of bowel loss, a second-look laparotomy should be seriously considered, especially in patients with significant bowel involvement. However, unlike patients with mesenteric arterial ischemia, patients with MVT generally do not require a second-look laparotomy unless progression of the disease is observed or suspected (typically ~40% of cases).

Reports of diagnostic laparoscopy in patients with venous thrombosis suggest that this modality may be of some utility in preventing fruitless laparotomies in MVT patients; however, the decreased mesenteric blood flow that occurs with laparoscopy may worsen bowel ischemia.

Patients with severe intestinal loss due to MVT may be considered for intestinal transplantation in specialized centers.

Angioplasty and stenting

Some experience with percutaneous endovascular interventions has been accumulated. A few patients who have atherosclerotic plaques at the origin of the SMA after thrombolysis are eligible for angioplasty. Angioplasty is technically difficult because of the anatomy of the SMA. Restenosis rates are in the range of 20-50%. Limited study findings indicate a definite role for angioplasty in the treatment of AMI. A case of successful transcutaneous catheter aspiration of an embolic clot from SMA has been reported.[93]

In select cases, especially in isolated spontaneous dissection of the SMA diagnosed before the onset of intestinal infarction, stent placement has been successful and may constitute the best therapeutic option.[20, 21, 22, 23, 87]

Postoperative Care

Postoperative care should include close monitoring of blood pressure and hemoglobin level to evaluate for sepsis or hemorrhage. Heparin anticoagulation should be continued postoperatively to reduce thrombotic events.[94]  Antibiotics should be continued postoperatively to prevent any septic events. Papaverine may be administered to reduce vasospasm.

A 12-lead electrocardiogram (ECG) should be obtained to evaluate for myocardial dysfunction. Echocardiography should be considered to identify any for valvular vegetations. A workup for a hypercoagulable state is required postoperatively if it was not done preoperatively. Postoperative ileus due to bowel reperfusion should be expected and appropriately managed.


Because patients with MVT are typically in a hypercoagulable state, the incidence of deep vein thrombosis (DVT) is increased. Proper anticoagulation and liberal use of sequential compression stockings can help prevent this postoperative complication.

Because of the high incidence of atherosclerosis in patients with AMI, it is not surprising that one of the most common postoperative complications is MI. Prevention of postoperative MI involves preoperatively identifying correctable coronary artery disease. A Swan-Ganz catheter may be used during the perioperative period to monitor fluid status and cardiac function. During the cross-clamping of the supraceliac aorta, the anesthesiologist can ensure myocardial protection and afterload reduction to maximize cardiac output.

Because patients become acutely hypovolemic, acute renal failure may occur in the immediate postoperative period. This complication can be prevented by keeping the patient well hydrated and administering mannitol before the aorta is cross-clamped.

Other possible complications include bleeding, infection, bowel infarction, prolonged ileus, and graft infection.


To prepare for surgery and to reduce oxygen demand on the ischemic bowel, patients must be on NPO status. No other specific dietary measures are mandatory.


Patients’ activities are dictated by their conditions. Bed rest to allow for monitoring and to reduce demand on cardiac output is balanced against ambulation to prevent DVT.


The following consultations should be considered in the setting of AMI:

  • Vascular surgeon - To evaluate the patient and to perform a revascularization procedure if required; this consultation should be obtained as soon as the diagnosis is considered
  • Interventional radiologist - To perform any needed angiographic drug infusions or angioplasty
  • Critical care specialist - To evaluate the patient for possible insertion of a Swan-Ganz catheter or admission to a critical care unit; patients with AMI are often hemodynamically unstable or highly likely to progress to instability

Long-Term Monitoring

Because of the high likelihood of concomitant vascular disease in the rest of the arterial tree, patients must be closely monitored. Cardiac and renal status should be determined at follow-up. Carotid duplex studies may be necessary if diffuse atherosclerotic disease is a strong possibility.

Outpatient medications include antiarrhythmics for patients with atrial fibrillation (AF) and warfarin for long-term treatment of patients with MVT or AF. Patients who have had MVT need warfarin therapy for at least 6 months or for life if a hypercoagulable state was discovered during treatment. Patients with AF should also be discharged on warfarin. Patients with other treatable predisposing conditions should be continued on appropriate therapy.

Periodic evaluation of coagulation status is required as well. To ensure proper anticoagulation, patients should have frequent visits for monitoring of the international normalized ratio (INR).

Patients who have had extensive small-bowel resection have severe diarrhea for a few weeks, but many appear to be able to compensate for the reduced bowel length after a few months. Thereafter, they may have one to three liquid bowel movements a day and may maintain or gain weight with oral intake. On the other hand, patients who have undergone total resection of the small intestine need lifelong IV hyperalimentation (ie, total parenteral nutrition).

A number of patients who recover from ileus secondary to intestinal ischemia may develop fibrosis of a segment of small bowel with intermittent partial obstruction.



Medication Summary

Drug types used in the treatment of acute mesenteric ischemia (AMI) include vasodilators, thrombolytics, anticoagulants, antibiotics, and analgesics. Therapeutic drugs (except for analgesics and prophylactic antibiotics) should be withheld until the type of AMI present has been determined by means of computed tomography (CT) or angiography.


Class Summary

Vasodilators dilate the mesenteric arterial system, thereby reversing reactive arterial vasospasms in AMI.


Papaverine is a benzylisoquinoline derivative that exerts a direct nonspecific relaxant effect on vascular, cardiac, and other smooth muscle. In the absence of peritoneal signs, it is the drug of choice for AMI of arterial origin if angiography indicates good distal perfusion. Papaverine is advocated for treatment of the widespread vasoconstriction that follows therapy for superior mesenteric artery (SMA) emboli by other modalities.


Class Summary

Thrombolytics are angiographically infused to lyse thrombi. They are used in selected patients with embolic AMI.

Alteplase, tissue plasminogen activator (Activase)

Alteplase is a synthetic tissue plasminogen activator (tPA) used to manage acute myocardial infarction (MI), ischemic stroke, and pulmonary embolism. Its use in AMI is controversial and potentially dangerous. Alteplase may be indicated in patients with acute mesenteric arterial embolism (AMAE; ie, embolic AMI) if no signs of peritonitis are present. The safety and efficacy of concomitant administration with aspirin and heparin during the first 24 hours after onset of symptoms have not been investigated.

Reteplase (Retavase)

Reteplase is a recombinant tPA that forms plasmin after facilitating cleavage of endogenous plasminogen. In clinical trials with acute MI, reteplase has been shown to be comparable to tPA in achieving TIMI (thrombolysis in MI risk score) 2 or 3 patency at 90 minutes. Heparin and aspirin usually are given concomitantly and afterward.

Tenecteplase (TNKase)

Tenecteplase is a modified version of alteplase (tPA) made by substituting 3 amino acids of alteplase. It can be given as a single bolus over a 5-second infusion, instead of over 90 minutes as with alteplase. Tenecteplase appears to cause less nonintracranial bleeding than alteplase does, but it poses a similar risk of intracranial bleeding and stroke. The dose should be based on the patient's weight. Because tenecteplase contains no antibacterial preservatives, it must be reconstituted immediately before use.


Class Summary

Anticoagulants are indicated for preventing further extension of thrombus in mesenteric venous thrombosis (MVT) or, after revascularization, in arterial occlusive AMI. In arterial occlusive AMI, whether anticoagulant therapy should be started immediately or after 48 hours when infarction is clearly absent is undetermined, because of the risk of gastrointestinal (GI) bleeding. Vitamin K antagonists (eg, warfarin) are used for maintenance therapy because they interfere with hepatic synthesis of vitamin K–dependent coagulation factors.


Heparin augments the activity of antithrombin III and prevents conversion of fibrinogen to fibrin. This drug does not actively lyse but is able to inhibit further thrombogenesis. It prevents reaccumulation of clot after spontaneous fibrinolysis.

Warfarin (Coumadin, Jantoven)

Patients with MVT should be switched from heparin to warfarin when possible. Warfarin should be continued for 6 months if no contraindication or identifiable hypercoagulable state exists and for life if a permanent hypercoagulable state exists. Warfarin is also indicated for preventing further embolization in patients with atrial fibrillation. It is used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. The dosage should be tailored to keep the international normalized ratio (INR) in the 2-3 range.


Class Summary

Antibiotics are administered to prevent or treat sepsis caused by breakdown of the mucosal barrier in bowel necrosis or perforation.

Clindamycin (Cleocin)

Clindamycin is a lincosamide used for treatment of serious skin and soft-tissue staphylococcal infections. It is also effective against aerobic and anaerobic streptococci (except enterococci). It inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Metronidazole (Flagyl, Metro)

Metronidazole is an imidazole ring–based antibiotic active against various anaerobic bacteria and protozoa. It is used in combination with other antimicrobial agents (except for Clostridium difficile enterocolitis).

Ticarcillin and clavulanate (Timentin)

Ticarcillin-clavulanate inhibits biosynthesis of cell wall mucopeptide and is effective during the stage of active growth. It consists of an antipseudomonal penicillin plus a beta-lactamase inhibitor and provides coverage against most gram-positive organisms, most gram-negative organisms, and most anaerobes.


Cefotetan is a second-generation cephalosporin indicated for infections caused by susceptible gram-positive cocci and gram-negative rods. The dose and route of administration depend on the condition of the patient, the severity of the infection, and the susceptibility of the causative organism.

Cefoxitin (Mefoxin)

Cefoxitin is a second-generation cephalosporin that is indicated for infections with gram-positive cocci and gram-negative rods. Infections caused by cephalosporin- or penicillin-resistant gram-negative bacteria may respond to cefoxitin.

Meropenem (Merrem)

Meropenem is a bactericidal broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis. It is effective against most gram-positive and gram-negative bacteria.


Class Summary

Analgesics are used to relieve pain caused by bowel ischemia.

Morphine (Duramorph, Avinza, Astramorph, Kadian)

Morphine is the drug of choice for analgesia because of its reliable and predictable effects, its safety profile, and the ease with which its effects can be reversed by giving naloxone. Various intravenous doses are used; these are commonly titrated until the desired effect is obtained.


Questions & Answers


What is acute mesenteric ischemia (AMI)?

What is the classification of acute mesenteric ischemia (AMI)?

How is acute mesenteric ischemia (AMI) diagnosed and treated?

How can the high mortality risk for acute mesenteric ischemia (AMI) be reduced?

What is the role of mesenteric vessel anatomy in the management of acute mesenteric ischemia (AMI)?

What is the celiac axis anatomy relevant to acute mesenteric ischemia (AMI)?

What is the hepatic artery anatomy relevant to acute mesenteric ischemia (AMI)?

What is the splenic artery anatomy relevant to acute mesenteric ischemia (AMI)?

What is the left gastric artery anatomy relevant to acute mesenteric ischemia (AMI)?

What is the superior mesenteric artery (SMA) anatomy relevant to acute mesenteric ischemia (AMI)?

What is the inferior pancreaticoduodenal artery anatomy relevant to acute mesenteric ischemia (AMI)?

What is the ileocolic artery anatomy relevant to acute mesenteric ischemia (AMI)?

What is the inferior mesenteric artery (IMA) anatomy relevant to acute mesenteric ischemia (AMI)?

What is the venous system anatomy of relevant to acute mesenteric ischemia (AMI)?

What is inferior mesenteric vein anatomy relevant to acute mesenteric ischemia (AMI)?

What is the pathophysiology of acute mesenteric ischemia (AMI)?

What is the pathophysiology of acute mesenteric arterial embolism (AMAE)?

What is the pathophysiology of acute mesenteric arterial thrombosis (AMAT)?

What is the pathophysiology of nonocclusive mesenteric ischemia (NOMI)?

What is the pathophysiology of mesenteric venous thrombosis (MVT)?

What causes acute mesenteric arterial embolism (AMAE)?

What causes acute mesenteric arterial thrombosis (AMAT)?

What causes nonocclusive mesenteric ischemia (NOMI)?

What causes mesenteric venous thrombosis (MVT)?

What is the prevalence of acute mesenteric ischemia (AMI) in the US?

Which patient groups are at highest risk for acute mesenteric ischemia (AMI)?

What is the prognosis of acute mesenteric ischemia (AMI)?

What the mortality risk factors in acute mesenteric ischemia (AMI)?

Which factors improve the prognosis of acute mesenteric ischemia (AMI)?

What is included in patient education about acute mesenteric ischemia (AMI)?


What are the signs and symptoms of acute mesenteric ischemia (AMI)?

Which history is characteristic of acute mesenteric arterial embolism (AMAE)?

Which history is characteristic of acute mesenteric arterial thrombosis (AMAT)?

Which history is characteristic of nonocclusive mesenteric ischemia (NOMI)?

Which history is characteristic of mesenteric venous thrombosis (MVT)?

Which physical findings characteristic of acute mesenteric ischemia (AMI)?

What are potential complications of acute mesenteric ischemia (AMI)?


When should a diagnosis of acute mesenteric ischemia (AMI) be considered?

How is mesenteric venous thrombosis (MVT) diagnosed?

Which conditions should be considered in the differential diagnoses of acute mesenteric ischemia (AMI)?

What are the differential diagnoses for Acute Mesenteric Ischemia?


How is acute mesenteric ischemia (AMI) diagnosed?

What is the role of lab findings in the diagnosis of acute mesenteric ischemia (AMI)?

Which complete blood count (CBC) results suggest acute mesenteric ischemia (AMI)?

Which chemistry panel results suggest acute mesenteric ischemia (AMI)?

How is a hypercoagulable state assessed in the evaluation of acute mesenteric ischemia (AMI)?

What is the role of serum D-dimer in the diagnosis of acute mesenteric ischemia (AMI)?

What is the role of abdominal radiography in the diagnosis of acute mesenteric ischemia (AMI)?

What is the role of angiography in the diagnosis and management of acute mesenteric ischemia (AMI)?

Which angiography findings are diagnostic of acute mesenteric arterial embolism (AMAE)?

Which angiography findings are characteristic of acute mesenteric arterial thrombosis (AMAT)?

Which angiography findings are characteristic of nonocclusive mesenteric ischemia (NOMI)?

What are the advantages and disadvantages of angiography in the diagnosis and management of acute mesenteric ischemia (AMI)?

What is the role of angiography in the evaluation of suspected mesenteric venous thrombosis (MVT)?

What is the role of contrast CT scanning in the evaluation of acute mesenteric ischemia (AMI)?

Which CT findings are characteristic of acute mesenteric ischemia (AMI)?

What is the most common CT finding for acute mesenteric ischemia (AMI)?

What are the advantages of computed tomography angiography (CTA) for evaluation and management of acute mesenteric ischemia (AMI)?

What is the role of abdominal computed tomography angiography (CTA) in the diagnosis of mesenteric venous thrombosis (MVT)?

What is the role of MRI and MRA in the diagnosis of acute mesenteric ischemia (AMI)?

What is the role of ultrasonography in the evaluation of acute mesenteric ischemia (AMI)?

Which diagnostic procedures may be performed in workup for acute mesenteric ischemia (AMI)?


How is permanent tissue damage prevented in acute mesenteric ischemia (AMI)?

What care is provided for inpatient recovery from acute mesenteric ischemia (AMI)?

When is transfer indicated for patients with acute mesenteric ischemia (AMI)?

What are the limitations of the American Gastroenterological Association (AGA) algorithms for the diagnosis and management of acute mesenteric ischemia (AMI)?

What are the definitive treatment options for acute mesenteric ischemia (AMI)?

When is immediate surgical intervention indicated for acute mesenteric ischemia (AMI)?

How is acute mesenteric ischemia (AMI) prevented?

What is the initial treatment for acute mesenteric ischemia (AMI)?

What is the role of papaverine in the treatment of acute mesenteric ischemia (AMI)?

What is the role of thrombolytic therapy in the treatment of acute mesenteric ischemia (AMI)?

What is the role of heparin in the treatment of acute mesenteric ischemia (AMI)?

How is laparotomy performed in the treatment of acute mesenteric ischemia (AMI)?

What is the role of Doppler scans in surgical intervention for acute mesenteric ischemia (AMI)?

What is the role of fluorescein in the surgical intervention for acute mesenteric ischemia (AMI)?

When is a second-look laparotomy indicated in the treatment of acute mesenteric ischemia (AMI)?

How is acute mesenteric arterial embolism (AMAE) surgically treated?

How is acute mesenteric arterial thrombosis (AMAT) surgically treated?

How is mesenteric venous thrombosis (MVT) surgically treated?

What is the role of angioplasty and stenting in the treatment of acute mesenteric ischemia (AMI)?

What is included in postoperative care for acute mesenteric ischemia (AMI)?

What are potential postoperative complications of acute mesenteric ischemia (AMI)?

What are dietary restrictions during the treatment of acute mesenteric ischemia (AMI)?

What are activity restrictions following treatment of acute mesenteric ischemia (AMI)?

Which specialist consultations should be considered for the management of acute mesenteric ischemia (AMI)?

What is included in the long-term monitoring for acute mesenteric ischemia (AMI)?


Which drug types are used in the treatment of acute mesenteric ischemia (AMI)?

Which medications in the drug class Analgesics are used in the treatment of Acute Mesenteric Ischemia?

Which medications in the drug class Antibiotics are used in the treatment of Acute Mesenteric Ischemia?

Which medications in the drug class Anticoagulants are used in the treatment of Acute Mesenteric Ischemia?

Which medications in the drug class Thrombolytics are used in the treatment of Acute Mesenteric Ischemia?

Which medications in the drug class Vasodilators are used in the treatment of Acute Mesenteric Ischemia?