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Acute Mesenteric Ischemia Clinical Presentation

  • Author: Chat V Dang, MD; Chief Editor: John Geibel, MD, DSc, MSc, MA  more...
Updated: Dec 16, 2015


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 myocardial infarction (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 mesenteric venous thrombosis.


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
Contributor Information and Disclosures

Chat V Dang, MD Clinical Professor of Emergency Medicine, Charles Drew University of Medicine and Science; Clinical Professor, Department of Medicine, University of California, Los Angeles, David Geffen School of Medicine

Disclosure: Nothing to disclose.


Mark Su, MD, MPH, FACEP, FACMT Consulting Staff and Director of Fellowship in Medical Toxicology, Department of Emergency Medicine, North Shore University Hospital

Mark Su, MD, MPH, FACEP, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Daniel K Nishijima, MD, MAS Assistant Professor of Emergency Medicine, Associate Research Director, Department of Emergency Medicine, University of California, Davis, School of Medicine

Daniel K Nishijima, MD, MAS is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, DSc, MSc, MA Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, Surgical Research, Department of Surgery, Yale-New Haven Hospital; American Gastroenterological Association Fellow

John Geibel, MD, DSc, MSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, Society for Surgery of the Alimentary Tract

Disclosure: Received royalty from AMGEN for consulting; Received ownership interest from Ardelyx for consulting.


David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: lippincott Royalty textbook royalty; wiley Royalty textbook royalty

Burt Cagir, MD, FACS Assistant Professor of Surgery, State University of New York Upstate Medical University; Consulting Staff, Director of Surgical Research, Robert Packer Hospital; Associate Program Director, Department of Surgery, Guthrie Clinic

Burt Cagir, MD, FACS is a member of the following medical societies: American College of Surgeons, American Medical Association, Association of Program Directors in Surgery, and Society for Surgery of the Alimentary Tract

Disclosure: Nothing to disclose.

Brian James Daley, MD, MBA, FACS, FCCP, CNSC Professor and Program Director, Department of Surgery, Chief, Division of Trauma and Critical Care, University of Tennessee Health Science Center College of Medicine

Brian James Daley, MD, MBA, FACS, FCCP, CNSC is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Chest Physicians, American College of Surgeons, American Medical Association, Association for Academic Surgery, Association for Surgical Education, Eastern Association for the Surgery of Trauma, Shock Society, Society of Critical Care Medicine, Southeastern Surgical Congress, Southern Surgical Association, andTennessee Medical Association

Disclosure: Nothing to disclose.

Michael A Grosso, MD Consulting Staff, Department of Cardiothoracic Surgery, St Francis Hospital

Michael A Grosso, MD is a member of the following medical societies: American College of Surgeons, Society of Thoracic Surgeons, and Society of University Surgeons

Disclosure: Nothing to disclose.

Chandler Long, MD Resident Physician, Department of Surgery, University of Tennessee Medical Center-Knoxville

Disclosure: Nothing to disclose.

Ashis Mandal, MD Professor, Department of Surgery, Drew University of Medicine and Science and UCLA College of Medicine

Disclosure: Nothing to disclose.

Robert M McNamara, MD, FAAEM Chair and Professor, Department of Emergency Medicine, Temple University School of Medicine

Robert M McNamara, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Association, Pennsylvania Medical Society, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David L Morris, MD, PhD, FRACS Professor, Department of Surgery, St George Hospital, University of New South Wales, Australia

David L Morris, MD, PhD, FRACS is a member of the following medical societies: British Society of Gastroenterology

Disclosure: RFA Medical None Director; MRC Biotec None Director

Yale D Podnos, MD, MPH Consulting Surgeon, Department of Surgery, City of Hope National Medical Center

Disclosure: Nothing to disclose.

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; Royalty Other

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Deron J Tessier, MD Staff Surgeon, Kaiser Permanente Medical Center, Fontana, CA

Deron J Tessier, MD is a member of the following medical societies: American College of Surgeons and American Medical Association

Disclosure: Nothing to disclose.

Jeff Wade, MD Resident Physician, Department of Emergency Medicine, Long Beach Community Hospital, Greater El Monte Medical Center

Disclosure: Nothing to disclose.

Russell A Williams, MBBS Program Director, Professor, Department of Surgery, University of California Medical Center at Irvine

Disclosure: Nothing to disclose.

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Pneumatosis intestinalis (black stripes of air) in advanced acute mesenteric ischemia (AMI) with gangrenous bowel.
CT scan (with contrast) of nonocclusive mesenteric ischemia with resulting bowel wall edema (arrows).
Aortogram showing narrowing of superior mesenteric artery.
Radiograph showing bowel spasm (early sign of ischemia).
Gas in colon wall (typical of advanced ischemia).
Ischemia stricture.
Thumbprinting of bowel, characteristic of mesenteric artery ischemia.
Pathologic findings 2 hours after bowel ischemia starts.
Microscopic findings 24 hours after ischemia starts.
Gross specimen showing hemorrhagic dead bowel after resection from patient with acute mesenteric ischemia.
Pneumatosis intestinalis, one of few radiographic findings in patients with mesenteric ischemia.
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 (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 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.
Complete aortic occlusion (Leriche syndrome) with acute embolism of superior mesenteric artery.
Gross specimen of dead bowel.
Meandering artery (radiographic sign of preexisting bowel ischemia).
CT scan demonstrating thrombosis of superior mesenteric vein.
CT scan demonstrating thrombosis of portal vein.
CT scan demonstrating cavernous change of superior mesenteric vein as consequence of venous thrombosis.
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