AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

"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."¹

This quote indicates some of the extreme difficulties faced by physicians treating acute mesenteric ischemia (AMI). Symptoms are nonspecific initially, before evidence of peritonitis presents. Thus, diagnosis and treatment are often delayed until the disease is advanced. Fortunately, since this statement was written, many advances have been made that allow earlier diagnosis and treatment. While the prognosis is 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.

AMI is a syndrome in which inadequate blood flow through the mesenteric circulation causes ischemia and eventual gangrene of the bowel wall. The syndrome can be classified generally as arterial or venous disease. Arterial disease can be subdivided into nonocclusive mesenteric ischemia (NOMI) and occlusive mesenteric arterial ischemia (OMAI).

Practically, AMI is divided into 4 different primary clinical entities: acute mesenteric arterial embolus (AMAE), acute mesenteric arterial thrombosis (AMAT), NOMI, and mesenteric venous thrombosis (MVT). OMAI includes both AMAE and AMAT.

All 4 types of AMI have somewhat different predisposing factors, clinical pictures, and prognoses. A secondary clinical entity of mesenteric ischemia occurs because of mechanical obstruction, such as internal hernia with strangulation, volvulus, intussusception, tumor compression, and aortic dissection. Occasionally, blunt trauma may cause isolated dissection of the superior mesenteric artery and lead to intestinal infarction. Because all types of AMI share many similarities and a final common pathway (ie, bowel infarction and death, if not properly treated), they are discussed together.

History

Antonio Beniviene first described mesenteric ischemia in the 15th century. It became more intensely studied in the mid 19th century after case reports by Virchow and others. The first successful surgery to repair a case of AMI was performed by Elliot, who, in 1895, resected a gangrenous portion of bowel and reanastomosed the viable bowel.

In the early 20th century, advances were made in diagnostic modalities, heparin was introduced for use in MVT, and residual arterial spasm was recognized. In the 1950s, vascular surgical repair to restore blood flow to ischemic bowel before gangrene occurred was introduced. The first successful embolectomy without bowel resection was performed in 1957.

NOMI was first recognized as a subtype of AMI in the 1950s. MVT was found to compose a much smaller portion of AMI than was originally thought. By 1960, the combination of heparin administration and bowel resection, when required, became the standard treatment of MVT. Hypercoagulable states were identified as the apparent cause of most cases of MVT.

In the 1970s, the use of angiography to diagnose and evaluate AMI, as well as the introduction of intra-arterial papaverine infusion, significantly improved the prognosis of patients by allowing early diagnosis and by combating residual arterial spasm. The increasing use of ultrasound and CT scan since the 1980s has helped achieve earlier diagnosis.

Anatomy

Typically, the celiac artery (CA) supplies the foregut, hepatobiliary system, and spleen; the superior mesenteric artery (SMA) supplies the midgut (ie, small intestine and proximal mid colon); and the inferior mesenteric artery (IMA) supplies the hindgut (ie, distal colon and rectum), but multiple anatomic variants are observed. Venous drainage is through the superior mesenteric vein (SMV), which joins the portal vein.

AMI arises primarily from problems in the SMA circulation or its venous outflow. Collateral circulation from the CA and IMA may allow sufficient perfusion if flow in the SMA is reduced because of occlusion, low-flow state (NOMI), or venous occlusion. The inferior mesenteric artery seldom is the site of lodgment of an embolus. Only small emboli can enter this vessel because of its smaller lumen. When lodgment occurs, the embolus lodges at the site of division of the inferior mesenteric artery into the left colic, sigmoidal, and superior hemorrhoidal arteries. In such instances, collateral flow from the middle colic and middle hemorrhoidal arteries (through the vascular arcades of the inferior mesenteric artery distal to the embolus) may sustain the perfusion of the left colon.

Pathophysiology

Insufficient blood perfusion to the small bowel and colon may result from arterial occlusion by embolus or thrombosis (AMAE or AMAT), thrombosis of the venous system (MVT), or nonocclusive processes such as vasospasm or low cardiac output (NOMI). Embolic phenomena account for approximately 50% of all cases, arterial thrombosis for about 25%, NOMI for roughly 20%, and MVT for less than 10%. Rarely, isolated spontaneous dissections of the SMA have been reported.^{2, 3, 4, 5} Hemorrhagic infarction is the common pathologic pathway whether the occlusion is arterial or venous.

Injury severity is inversely proportional to the mesenteric blood flow and is influenced by the number of vessels involved, systemic mean 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. This leads to gut emptying by vomiting or diarrhea. Mucosal sloughing may cause bleeding into the gastrointestinal tract. At this stage, little abdominal tenderness is usually present, producing the classic intense visceral pain disproportionate to physical examination findings.

The mucosal barrier becomes disrupted as the ischemia persists, and bacteria, toxins, and vasoactive substances are released into the systemic circulation. This can cause death from septic shock, cardiac failure, or multisystem organ failure before bowel necrosis actually occurs. As hypoxic damage worsens, the bowel wall becomes edematous and cyanotic. Fluid is released into the peritoneal cavity, explaining the serosanguineous fluid sometimes recovered by diagnostic peritoneal lavage. Bowel necrosis can occur in 8-12 hours from the onset of symptoms. Transmural necrosis leads to peritoneal signs and heralds a much worse prognosis.

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 between the heart and the origin of the superior mesenteric artery. The vascular occlusion is sudden, so the patients have not developed a compensatory increase in collateral flow. As a result, they experience worse ischemia than patients with thrombotic AMI. The SMA is the visceral vessel most susceptible to emboli because of its small take-off angle from the aorta and higher flow. Most often, emboli lodge about 6-8 cm beyond the arterial origin, at a narrowing near the emergence of the middle colic artery.

According to the US Centers for Disease Control and Prevention Injury Center, a special form of mesenteric ischemia may result from systemic air embolism in those who sustain high-energy blast injuries. These patients sustain severe primary blast injury to the lung, a condition referred to as "blast lung."

Thrombotic AMI is a late complication of preexisting visceral atherosclerosis. Symptoms do not develop until 2 of the 3 arteries (usually the celiac and superior mesenteric arteries) are stenosed or completely blocked. Progressive worsening of the atherosclerotic stenosis before the acute occlusion allows time for development of additional collateral circulation.

Most patients with thrombotic AMI have atherosclerotic disease at other sites such as coronary artery disease, stroke, or peripheral arterial disease. A drop in cardiac output from myocardial infarction or congestive heart failure (CHF) may cause AMI in a patient with visceral atherosclerosis. Thrombotic AMI 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 emergent event.

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 patients in critical condition. Because bowel perfusion, similar to cerebral perfusion, is preserved in the setting of hypotension, NOMI represents a failure of autoregulation. Many vasoactive drugs may also cause regional vasoconstriction, such as digitalis, cocaine, diuretics, and vasopressin. Gross pathologic arterial or venous occlusions are not observed in patients with NOMI.

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. The list of causes for MVT is long and includes infection, usually from an intra-abdominal source; phlebitis or pylephlebitis (portal pyemia) secondary to inflammatory diseases of the bowel such as diverticulitis, appendicitis, and secondarily infected carcinoma of the bowel; hypercoagulable states such as those caused by polycythemia, oral contraceptives, or genetic abnormalities (protein C or S deficiency); mesenteric venous stasis from portal hypertension or mass effect of abdominal tumors; and direct trauma to the mesenteric veins from a surgical procedure.

MVT may also occur after ligation of the portal vein or the superior mesenteric vein as part of "damage-control surgery" for severe penetrating abdominal injuries. Other associated causes include pancreatitis, sickle cell disease, and hypercoagulability caused by malignancy.

MVT often affects a much younger population. Symptoms may be present longer than in the typical cases of AMI, sometimes exceeding 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. The chronic form of SMV thrombosis may manifest as esophageal varices bleeding.

Frequency

United States

The overall prevalence of AMI is 0.1% of all hospital admissions; this may be expected to rise as the population ages. The exact prevalence of MVT is unknown because many cases are presumed to be limited in symptomatology and to resolve spontaneously. In 1989, the incidence of diagnosed MVT was reported to be 2 per 100,000 admissions over 20 years at the Albert Einstein College of Medicine Montefiore Medical Center.

International

Rates of AMI have not been demonstrated to be significantly different outside the United States. However, because it is primarily a disease of older individuals, rates are probably lower in countries whose populations have a shorter life expectancy.

Mortality/Morbidity

Overall, the mortality rate in the last 15 years from all causes of AMI averages 71%, with a range of 59-93%. Once bowel wall infarction has occurred, the mortality rate is as high as 90%. Survivors of mesenteric resection face significant long-term morbidity because of the reduced intestinal mucosal surface available for absorption. In a report from Madrid of 21 patients with SMA embolus with little delay in initiating maximal treatment, intestinal viability was achieved in 100% of patients if the duration of symptoms was shorter than 12 hours, 56% if it was 12-24 hours, and only 18% if it was longer than 24 hours. Early recognition and treatment of NOMI has been shown to reduce the mortality rate to 50-55%. MVT has a 30-day mortality rate of 13-15%.

Race

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

Sex

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 on oral contraceptives or are pregnant are at higher risk of MVT.

Age

AMI is frequently considered a disease of people older than 50 years. Younger people with 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.

CLINICAL

Section 3 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
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History

All types of AMI have a similar presentation to some extent. Differences in clinical appearance for each type are discussed below. The most important finding is pain 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 distension and GI bleeding are the primary symptoms in up to 25% of patients. Pain may be unresponsive to narcotics. As the bowel becomes gangrenous, rectal bleeding and signs of sepsis (eg, tachycardia, tachypnea, hypotension, fever, altered mental status) develop. A review of systems, looking for risk factors of AMI, should be performed. This syndrome has a catastrophic outcome if not properly and rapidly treated. 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 50 years.

• Embolic acute mesenteric ischemia  
• • AMI from embolic causes typically has the most abrupt and painful presentation of all types. This is due to the rapid onset of occlusion and inability to form additional collateral circulation. It has been described as abdominal apoplexy.
  • 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 (with mural thrombus). Infrequently, patients may report a history of valvular heart disease or previous embolic episode.
• Thrombotic acute mesenteric ischemia
• • AMI caused by a thrombus, such as a myocardial infarction, typically happens when an artery already partially blocked by atherosclerosis becomes completely occluded.
  • Similarly to angina pectoris preceding a myocardial infarction, 20-50% of these patients have a history of abdominal angina. Abdominal angina is a syndrome of postprandial abdominal pain starting soon after eating and lasting for up to 3 hours. The digestion of food requires increased perfusion of the intestine, so the mechanism is similar to that of exercise-induced angina pectoris. Weight loss, "food fear," early satiety, and altered bowel habits may be present.
  • The precipitating event that initiates thrombotic AMI may be a sudden drop in cardiac output from myocardial infarction or CHF or a ruptured plaque. Dehydration from vomiting or diarrhea due to an unrelated illness may also precipitate thrombotic AMI. These patients have undergone a gradual progression of arterial occlusion and frequently have a better collateral supply. Bowel viability is better preserved, often leading to a less severe presentation than with embolic AMI. Symptoms tend to be less intense and of more gradual onset. As might be expected, these patients typically have a history of atherosclerotic disease at other sites, eg, coronary artery disease, cerebral arterial disease, peripheral artery disease (especially aortoiliac occlusive disease), or a history of aortic reconstruction.
• Nonocclusive mesenteric ischemia
• • Nonocclusive AMI occurs more frequently in older patients than other forms of AMI. These elderly patients are often already in an ICU setting with acute respiratory distress syndrome or severe hypotension from cardiogenic or septic shock, or they are taking vasopressive drugs. Most of these patients are taking digitalis.
  • Symptoms typically develop over several days, and patients may have had a prodrome of malaise and vague abdominal discomfort. When infarction occurs, the patients develop increased pain associated with vomiting. They may become hypotensive and tachycardic, with loose bloody stool.
• Mesenteric venous thrombosis
• • MVT is often observed in a much younger patient population than other types of AMI. 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 are frequently less dramatic. Diagnosis can be even more difficult, because symptoms may have been present for weeks (ie, 27% have symptoms for >30 d). Typical symptoms of AMI may have been experienced for a prolonged period with gradual worsening. The chronic form may manifest as esophageal varices bleeding.
  • Many patients have a history of one or more of the risk factors for hypercoagulability. These include oral contraceptive use, congenital hypercoagulable states, deep vein thrombosis (DVT), liver disease, tumor, or portocaval surgery.

Physical

Despite different etiology, physical examination findings in patients with AMI are similar. The main distinction is between early and late presentation. Early in the course of the disease, in the absence of peritonitis, physical signs are few and nonspecific. Tenderness is minimal to nonexistent. Stool may be guaiac positive. 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.

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

Causes

• Embolic acute mesenteric ischemia  
• • Cardiac emboli - Mural thrombus post–myocardial infarction, auricular thrombus associated with mitral stenosis and atrial fibrillation, 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
• Thrombotic acute mesenteric ischemia
• • Atherosclerotic vascular disease (most common)
  • Aortic aneurysm
  • Aortic dissection
  • Arteritis
  • Decreased cardiac output from myocardial infarction or CHF (Thrombotic AMI may cause acute decompensation.)
  • Dehydration from other causes
• Nonocclusive mesenteric ischemia
• • Hypotension from CHF, myocardial infarction, sepsis, aortic insufficiency, severe liver or renal disease, or recent major cardiac or abdominal surgery
  • Vasopressive drugs
  • Ergotamines
  • Cocaine
  • Digitalis (Whether digitalis use causes NOMI or patients who develop NOMI are older and are more likely to have been prescribed digitalis is unclear.)
• MVT: More than 80% of patients with MVT are found to have predisposing conditions.
• • Hypercoagulability from protein C and S deficiency, antithrombin III deficiency, dysfibrinogenemia, abnormal plasminogen, polycythemia vera (most common), thrombocytosis, sickle cell disease, factor V Leiden mutation, pregnancy, and oral contraceptive use
  • Tumor causing venous compression or hypercoagulability
  • Infection, usually intra-abdominal, such as appendicitis, diverticulitis, or abscess
  • Venous congestion from cirrhosis (portal hypertension)
  • Venous trauma from accidents or surgery, especially portocaval surgery
  • Pancreatitis
  • Decompression sickness

DIFFERENTIALS

Section 4 of 11  

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Other Problems to be Considered

Ovarian torsion
Small bowel obstruction
Volvulus of midgut
Splenic vein thrombosis

WORKUP

Section 5 of 11  

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• Follow-up
• Miscellaneous
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Lab Studies

• In general, laboratory studies are not helpful in diagnosing AMI. No serum marker is sensitive or specific enough to establish or exclude the diagnosis of AMI. Waiting for laboratory results should not delay radiographic studies if serious suspicion of AMI exists.
• CBC may be within the reference range initially, but the WBC count eventually rises as the disease progresses. Leukocytosis and/or leftward shift are observed in over 50% of cases. The hematocrit is elevated initially from hemoconcentration due to third spacing, but it decreases with GI bleeding.
• Amylase levels are moderately elevated in over 50% of patients, but this finding is nonspecific.
• Phosphate levels were initially thought to be sensitive, but later studies showed a sensitivity of only 25-33%.
• ABG: Metabolic acidosis is observed late in disease course, but this is a nonspecific finding.
• Lactate is elevated late in the clinical course. Levels that are persistently within the reference range strongly indicate a diagnosis other than AMI (sensitivity 96%, specificity 60%).
• D-dimer has been suggested to possibly be helpful based on one small clinical study reported in 2001 and on one experimental study in rats.⁶ Clinical experience is lacking to validate the role of D-dimer in the screening and diagnosis of AMI.

Imaging Studies

• Plain abdominal films  
• • Findings on plain films of the abdomen often are normal in the presence of AMI. However, plain films are warranted to exclude identifiable causes of abdominal pain, such as perforated viscus with free intraperitoneal air.
  • Positive findings are usually late and nonspecific and include ileus, small bowel obstruction, edematous/thickened bowel walls, and paucity of gas in the intestines. More specific signs, such as pneumatosis intestinalis, that is, submucosal gas (see Media file 1); thumbprinting of the bowel wall; and portal vein gas, are late findings. In one study of 23 cases of bowel infarction, 30% of the patients demonstrated focally edematous bowel wall (thumbprinting) and/or pneumatosis intestinalis.
• Computed tomography scan
• • CT scan helps to evaluate AMI and to exclude other causes of abdominal pain. CT angiography has a sensitivity of 71-96% and a specificity of 92-94%. Although still not considered the criterion standard compared with classic angiography, CT angiography is noninvasive, readily available, and the preferred modality for MVT (90% sensitivity).
  • CT scan may show pneumatosis intestinalis, portal vein gas, bowel wall and/or mesenteric edema, abnormal gas patterns, thumbprinting, streaking of mesentery, and solid organ infarction. Bowel wall edema is the most common finding on CT scan. It represents 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 portal vein.
  • Serial CT angiograms can be used to monitor patients treated nonsurgically with anticoagulation.
• Angiography
• • This is the criterion standard for diagnosis and presurgical planning and is often an important part of treatment. To promptly diagnose patients with true AMI, a low threshold for obtaining early angiography should be adopted for patients at risk. Sensitivity is reported to be 88% for AMI.
  • An embolus appears as a sharp cutoff of flow near the origin of the middle colic artery. Thrombus appears as a more tapered occlusion near the origin of the SMA. NOMI is characterized by narrowing of the origins of multiple SMA branches, alternating dilation and narrowing of the intestinal branches (ie, "string of sausages" sign), spasm of the mesenteric arcades, and impaired filling of the intramural vessels.
  • Angiography is actually a second-line study in patients with a strong suspicion of MVT because false-negative findings are common. Findings with MVT include thrombus in the 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.
• Ultrasonography
• • Duplex sonography studies are highly specific (92-100%) but not as sensitive (70-89%) compared to angiography. The examination cannot detect clots beyond the proximal main vessels nor can it be used to diagnose NOMI. Ultrasound is considered a second-line study for AMI. It is often less useful in the presence of dilated fluid-filled loops of bowel.
  • Some studies show usefulness similar to CT scanning if duplex scanning is performed for MVT. 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.
• Magnetic resonance imaging/magnetic resonance angiography
• • MRI and MRA provide findings similar to CT scan in AMI. Sensitivity of MRA is 100% and specificity is 91%. MRA is particularly effective for evaluating MVT.
  • The main drawbacks are the expense and the time required. In the future, rapid MRA may supplant angiography.
• Echocardiography findings may confirm the source of embolization or show valvular pathology.

Other Tests

• Intraoperative fluorescein administration: During laparotomy, 1 g of fluorescein is infused. Viable bowel fluoresces brightly under a Wood lamp. This allows the surgeon to better evaluate the segments that need resection. It may be performed at the primary operation or during a 24-hour second-look operation.
• ECG may show myocardial infarction or atrial fibrillation.

Procedures

• Nasogastric tube decompression helps relieve distension and allows evaluation for upper GI bleeding.
• Diagnostic peritoneal lavage may recover the serosanguineous fluid associated with bowel infarction; this is not a preferred study if AMI is suspected.
• Foley catheterization allows for monitoring of urinary output as an indicator for minimal fluid resuscitation.
• In patients with intestinal angina, percutaneous transluminal angioplasty and stenting of the celiac and/or mesenteric arteries have been reported with variable short- and long-term patency rates. A multi-institutional, randomized, controlled clinical trial is needed to define the optimal conditions for their application.

TREATMENT

Section 6 of 11  

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Medical Care

Make all efforts to improve patients' cardiovascular status. Avoid use of vasopressors because they worsen ischemia. Provide oxygen at 100% or by intubation if needed. Fluid resuscitation is accomplished with isotonic sodium chloride solution, and blood products are provided as needed. Adequacy of resuscitation can be monitored by urinary output, central venous pressure, or Swan-Ganz pressure monitoring. Insert a nasogastric tube, and optimize cardiac status by treating arrhythmia, CHF, or myocardial infarction. Start broad-spectrum antibiotics early. Provide pain control while maintaining stable blood pressure.

• Angiographically infused papaverine  
• • Papaverine infused through the angiogram catheter at the affected vessel is useful for all arterial forms of AMI. It relieves reactive vasospasm in occluded arterial vessels and is the only treatment of NOMI other than resection of gangrenous bowel.
  • Start an infusion of 30-60 mg/h after angiogram, and adjust the dose for clinical response. Continue this for at least 24 hours.
  • If the catheter slips into the aorta, significant hypotension can occur. Papaverine is incompatible with heparin.
• Angiographically infused thrombolytics  
• • Thrombolytics infused through the angiogram catheter can be a life-saving therapy for selected patients with embolic AMI.
  • Bleeding is the main complication. Thrombolytic administration is risky and should only be undertaken if peritonitis or other signs of bowel necrosis are absent. It must be started within 8 hours of symptom onset.
  • If symptoms do not improve within 4 hours or if peritonitis develops, stop the infusion and perform surgery.
• Angioplasty after thrombolysis
• • A very select group of 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 20-50%.
  • Limited study findings indicate a definite role for angioplasty in the treatment of AMI. A case of successful transcutaneous catheter aspiration of a SMA embolic clot was reported from the Czech Republic.
• Heparin for MVT
• • Heparin anticoagulation is the main treatment of MVT. If no signs of bowel necrosis exist, the patient may not even need an operation. Heparin may increase the chance of bleeding complications. An avenue of study for possible future clinical trials may be the use of enoxaparin (Lovenox) or other low molecular weight heparins as a potential substitute for heparin in the treatment of MVT.
  • Administer heparin as a bolus of 80 U/kg, not to exceed 5000 U, and then as an infusion at 18 U/kg/h until full conversion to oral warfarin. Appropriate monitoring of anticoagulation using activated partial thromboplastin time (aPTT) is mandatory.
• Percutaneous endovascular interventions
• • Experience with percutaneous endovascular interventions has been accumulated.
  • In select cases, especially in isolated spontaneous dissection of the SMA, stent placement may offer the best option.⁷

Surgical Care

Recognition of AMI before permanent tissue damage occurs is the best way to improve patient survival, and only angiography or exploratory surgery makes early diagnosis possible. Experience with CT and MR angiography is rapidly changing the therapeutic approach, allowing for prompt laparotomy in patients with suspected AMI when expeditious formal angiography is not available. A second-look procedure is indicated whenever bowel of questionable viability is not resected.

• Preoperative care: Stabilize patients using IV fluids, antibiotics covering the colonic flora, nasogastric tube decompression, and bladder catheterization, with heparin or papaverine administered as indicated. Blood should be available.
• Operative care: All types of AMI may require resection of necrotic bowel if signs of peritonitis develop. Differentiation of nonviable versus viable bowel can be enhanced by intraoperative fluorescein use. 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 for viability of the remaining bowel.  
• • Embolic AMI
  • • Unless the involved bowel is clearly gangrenous, an attempt at reperfusion is necessary. The SMA is isolated, and the location of the blockage is determined by palpation of pulses. Because most emboli are near the origin of the middle colic artery, note the proximal SMA pulse in embolic AMI.
    • A transverse 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 avoid lumen compromise. A bypass may be required if thrombectomy is unsuccessful.
    • Observe the intestines for 10-15 minutes after restoration of flow to assess viability of bowel. This can be enhanced by intraoperative duplex ultrasound, fluorescein use, and palpation of pulses distal to the occlusion.
  • Thrombotic AMI
  • • Emergency surgical revascularization is indicated. Simple thrombectomy has little or no benefit because most patients have clinically significant atherosclerosis at the time of the acute decompensation. Unlike patients with embolic AMI, these patients have a lesion at the origin of the SMA and no SMA pulsation is detected at the origin.
    • If the gut is not irreparably gangrenous, proceed with the revascularization procedure. An antegrade aortomesenteric bypass is the best technique. Transaortic endarterectomy is an alternative when no vein is suitable to harvest or a prosthetic graft is contraindicated (eg, massive fecal contamination). Endarterectomy is more time consuming than thrombectomy and bypass procedures.
    • Reevaluate bowel viability after revascularization and thrombectomy.
  • Mesenteric venous thrombosis
  • • As for any patient with AMI and signs of peritonitis, including diagnosed NOMI, exploratory laparotomy and resection of infarcted bowel is indicated.
    • Thrombectomy has little use in MVT because it can only be performed if the thrombus is fresh (ie, 1-3 d). In MTV, thrombectomy has little proven effectiveness because the thrombus is usually too widespread and all the thrombi cannot be removed completely.
  • Spontaneous dissection of the SMA: When diagnosed before the onset of intestinal infarction, percutaneous stent placement has been successful.^{2, 3, 4, 5}

Consultations

• Vascular surgery: Consult a vascular surgeon to evaluate the patient and to perform a revascularization procedure if required.
• Interventional radiology: Consult an interventional radiologist to perform any needed angiographic drug infusions or angioplasty.
• Critical care specialist: A critical care specialist should evaluate the patient for possible insertion of a Swan-Ganz catheter or admission to a critical care unit.

Diet

Patients must take nothing by mouth (NPO) in preparation for surgery and to reduce oxygen demand on the ischemic bowel.

Activity

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.

MEDICATION

Section 7 of 11  

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Withhold therapeutic drugs (except analgesics and prophylactic antibiotics) until CT scan or angiogram determination of AMI type.

Drug Category: Vasodilators

Dilate mesenteric arterial system, reversing reactive arterial vasospasms in AMI.

Drug Category: Thrombolytics

Angiographically infused to lyse thrombi in selected patients with embolic AMI.

Drug Category: Anticoagulants

Indicated to prevent further extension of thrombus in MVT or postrevascularization 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 GI bleeding. Oral anticoagulants are used for maintenance therapy. They interfere with hepatic synthesis of vitamin K–dependent coagulation factors.

Drug Category: Antibiotics

To prevent or treat sepsis caused by breakdown of mucosal barrier in bowel necrosis or perforation.

Drug Category: Analgesics

For relief of pain caused by bowel ischemia.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• After initial medical and/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 NPO, and they may be maintained on parenteral nutrition for some time. If sepsis is evident, liver abscess should be actively searched for. During the inpatient stay, every effort must be made to find and, if possible, treat any predisposing cause(s) of AMI.

Further Outpatient Care

• 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 1-3 liquid bowel movements a day, and maintain or gain weight with oral intake. On the other hand, patients who have had total small intestine resection need lifelong intravenous hyperalimentation (ie, total parenteral nutrition [TPN]).
• 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.
• 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 atrial fibrillation should also be discharged on warfarin.
• Patients with other treatable predisposing conditions should be continued on appropriate therapy.
• Patients should be appropriately monitored in an anticoagulation clinic.

In/Out Patient Meds

• Inpatient medications
• • Papaverine - For patients with arterial occlusive AMI or NOMI
  • Heparin - For patients with MVT or after revascularization
  • Warfarin - For long-term treatment of patients with MVT or atrial fibrillation
  • Broad-spectrum antibiotics and pain medications - For all patients
  • Thrombolytics - For selected patients with embolic AMI
• Outpatient medications
• • Antiarrhythmics - For patients with atrial fibrillation
  • Warfarin - For long-term treatment of patients with MVT or atrial fibrillation

Transfer

• 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 to diagnose and treat the patient. Patients should be optimally resuscitated before transfer. Appropriate services should be available at the receiving hospital.

Deterrence/Prevention

• No preventive measures are known for AMI other than timely diagnosis and treatment of predisposing conditions. In the presence of a clinical syndrome suggesting chronic mesenteric insufficiency, color Doppler evaluation of the mesenteric vessels may help select patients at risk for further workup and those who might need angioplasty.

Complications

• Bowel necrosis requiring bowel resection
• Septic shock
• Death

Prognosis

• The prognosis of AMI of any type is grave. Patients in whom the diagnosis is missed until infarction occurs have a mortality rate of 90%. Even with good treatment, up to 50-80% of patients die. Survivors of extensive bowel resection face lifelong disability. However, with rapid treatment, the mortality rate can be reduced considerably, and patients may be spared bowel resection. A long-term follow-up study of 31 patients who had surgery and survived the acute episode, revealed 2- and 5-year survival rates of 70% and 50%. Deaths were mainly related to cardiovascular comorbidity and malignant disease. With appropriate anticoagulation, only 1 patient died after a recurrent attack of arterial mesenteric thrombosis.

Patient Education

• Educate patients who survive to discharge about short-bowel syndrome.
• Educate surviving patients about the importance of taking warfarin or other discharge medications to prevent recurrence.
• For excellent patient education resources, visit eMedicine's Environmental Exposures and Injuries Center. Also, see eMedicine's patient education article The Bends - Decompression Syndromes.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• A review of 180 consecutive malpractice claims at a Veterans Affairs Medical Center in Virginia over a 12-year period ending in 1998 revealed 7 cases involving AMI. Failure to make a timely diagnosis was alleged in 5 cases, and failure to administer anticoagulation was alleged in 1 case. The remaining allegation was failure to prevent NOMI.
• Legal risk is reduced with early surgical consultation and the ordering of CT scan or angiography as soon as AMI is noted in the differential diagnosis.
• Because AMI is a condition with an unclear initial presentation, serious morbidity, and a high mortality rate without proper treatment, clinical suspicion should remain high. Obtain early angiography if any suspicion of AMI exists. 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.

Special Concerns

• Elderly patients: Consider a diagnosis of AMI 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 MI, are at higher risk.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Pneumatosis intestinalis in advanced acute mesenteric ischemia (AMI) with gangrenous bowel.
	View Full Size Image
Media type:  X-RAY

Media file 2:  CT scan (with contrast) of nonocclusive mesenteric ischemia with resulting bowel edema (arrows).
	View Full Size Image
Media type:  CT

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

1. Cokkinis AJ. Observations on the mesenteric circulation. J Anat. Jan 1930;64:200-205. [Medline].
2. Leung DA, Schneider E, Kubik-Huch R, Marincek B, Pfammatter T. Acute mesenteric ischemia caused by spontaneous isolated dissection of the superior mesenteric artery: treatment by percutaneous stent placement. Eur Radiol. 2000;10(12):1916-9. [Medline].
3. Miyamoto N, Sakurai Y, Hirokami M, Takahashi K, Nishimori H, Tsuji K, et al. Endovascular stent placement for isolated spontaneous dissection of the superior mesenteric artery: report of a case. Radiat Med. Nov 2005;23(7):520-4. [Medline].
4. Ko GJ, Han KJ, Han SG, Hwang SY, Choi CH, Gham CW, et al. [A case of spontaneous dissection of the superior mesenteric artery treated by percutaneous stent placement]. Korean J Gastroenterol. Feb 2006;47(2):168-72. [Medline].
5. Casella IB, Bosch MA, Sousa WO Jr. Isolated spontaneous dissection of the superior mesenteric artery treated by percutaneous stent placement: case report. J Vasc Surg. Jan 2008;47(1):197-200. [Medline].
6. Acosta S, Nilsson TK, Bjorck M. Preliminary study of D-dimer as a possible marker of acute bowel ischaemia. Br J Surg. Mar 2001;88(3):385-8. [Medline].
7. Herbert GS, Steele SR. Acute and chronic mesenteric ischemia. Surg Clin North Am. Oct 2007;87(5):1115-34, ix. [Medline].
8. Altinyollar H, Boyabatli M, Berberoglu U. D-dimer as a marker for early diagnosis of acute mesenteric ischemia. Thromb Res. 2006;117(4):463-7. [Medline].
9. Bassiouny HS. Nonocclusive mesenteric ischemia. Surg Clin North Am. Apr 1997;77(2):319-26. [Medline].
10. Boley SJ, Brandt LJ, Sammartano RJ. History of mesenteric ischemia. The evolution of a diagnosis and management. Surg Clin North Am. Apr 1997;77(2):275-88. [Medline].
11. Brandt LJ, Boley SJ. AGA technical review on intestinal ischemia. American Gastrointestinal Association. Gastroenterology. May 2000;118(5):954-68. [Medline].
12. Fink S, Chaudhuri TK, Davis HH. Acute mesenteric ischemia and malpractice claims. South Med J. Feb 2000;93(2):210-4. [Medline].
13. Hansen KJ, Deitch JS. Transaortic mesenteric endarterectomy. Surg Clin North Am. Apr 1997;77(2):397-407. [Medline].
14. Hassan HA, Raufman JP. Mesenteric venous thrombosis. South Med J. Jun 1999;92(6):558-62. [Medline].
15. Hladík P, Raupach J, Lojík M, Krajina A, Voboril Z, Jon B, et al. Treatment of acute mesenteric thrombosis/ischemia by transcatheter thromboaspiration. Surgery. Jan 2005;137(1):122-3. [Medline].
16. Kirkpatrick ID, Kroeker MA, Greenberg HM. Biphasic CT with mesenteric CT angiography in the evaluation of acute mesenteric ischemia: initial experience. Radiology. Oct 2003;229(1):91-8. [Medline].
17. Klempnauer J, Grothues F, Bektas H, Pichlmayr R. Long-term results after surgery for acute mesenteric ischemia. Surgery. Mar 1997;121(3):239-43. [Medline].
18. Kozuch PL, Brandt LJ. Review article: diagnosis and management of mesenteric ischaemia with an emphasis on pharmacotherapy.