eMedicine Specialties > Emergency Medicine > Cardiovascular

Mesenteric Ischemia

Author: Daniel K Nishijima, MD, Staff Physician, Department of Emergency Medicine, University of California Davis Medical Center
Coauthor(s): Mark Su, MD, FACEP, FACMT, Consulting Staff and Director of Fellowship in Medical Toxicology, Department of Emergency Medicine, North Shore University Hospital; Consulting Staff, North Shore University Hospital
Contributor Information and Disclosures

Updated: Apr 8, 2009

Introduction

Background

Mesenteric ischemia is a relatively rare disorder seen in the emergency department (ED); however, it is an important diagnosis to make because of its high mortality rate. Vague and nonspecific clinical findings and limitations of diagnostic studies make the diagnosis a significant challenge. Moreover, delays in diagnosis lead to increased mortality rates. Despite recent advances in diagnosis and treatment, mortality rates continue to remain high.

Pneumatosis intestinalis is one of the few radiog...

Pneumatosis intestinalis is one of the few radiographic findings in patients with mesenteric ischemia.

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Pneumatosis intestinalis is one of the few radiog...

Pneumatosis intestinalis is one of the few radiographic findings in patients with mesenteric ischemia.


Pathophysiology

Mesenteric ischemia is caused by decreased intestinal blood flow that can be caused by a number of mechanisms. Decreased intestinal blood flow results in ischemia and subsequent reperfusion damage at the cellular level that may progress to the development of mucosal injury, tissue necrosis, and metabolic acidosis.

The blood supply to the intestine is derived predominantly from 3 major gastrointestinal arteries that arise from the abdominal aorta: the celiac axis, the superior mesenteric artery (SMA), and the inferior mesenteric artery (IMA). The intestine has significant collateral circulation at all levels that allows for some protection from ischemia and is able to compensate for approximately a 75% acute reduction in mesenteric blood flow for up to 12 hours, without substantial injury.1

The pathophysiology of intestinal ischemia can be divided into arterial and venous etiologies and acute and chronic ischemia. The vast majority of cases are secondary to arterial causes. All diseases and conditions that affect arteries, including atherosclerosis, arteritis, aneurysms, arterial infections, dissections, arterial emboli, and thrombosis, are reported to occur in the intestinal arteries.2

Acute mesenteric ischemia (AMI) can be further divided into embolic, thrombotic, or nonocclusive causes.3

  • Arterial embolism
    • Arterial embolism accounts for approximately one third of acute cases of acute mesenteric ischemia.
    • Emboli to the mesenteric arteries are usually from a dislodged cardiac thrombus.
    • The superior mesenteric artery (SMA) is most commonly affected, whereas the inferior mesenteric artery (IMA) is rarely affected due to its small caliber.4
  • Arterial thrombosis
    • Arterial thrombosis accounts for approximately one third of acute cases of acute mesenteric ischemia.
    • It is usually due to acute worsening of ischemia in patients who have preexisting atherosclerosis of the mesenteric arteries.
    • Thrombosis often involves at least 2 of the major splanchnic vessels.5
  • Nonocclusive etiology
    • Nonocclusive etiology accounts for approximately one third of acute cases of acute mesenteric ischemia.
    • The primary mechanism is severe and prolonged intestinal vasoconstriction.
    • The most common setting is severe systemic illness with systemic shock usually secondary to reduced cardiac output.2
    • Intestinal vasospasm has also been seen to occur in cocaine ingestion6,7 , ergot poisoning8 , digoxin use, and with alpha-adrenergic agonists.
    • A small proportion of cases are from venous thrombosis, seen mostly in patients with hypercoagulable states.
    • Venous thrombosis of the visceral vessels may precipitate an acute ischemic event as compromised venous return leads to interstitial swelling of the bowel wall, with subsequent impedance of arterial flow and eventual tissue necrosis.3

Chronic mesenteric ischemia (CMI) usually results from long-standing atherosclerotic disease of 2 or more mesenteric vessels.9 Other nonatheromatous causes of chronic mesenteric ischemia include the vasculitides such as Takayasu arteritis. Symptoms are caused by the gradual reduction in blood flow to the intestine that occurs during eating since total blood flow to the intestine can increase by 15% during meals.10  Another rare cause of chronic mesenteric ischemia is due to celiac artery compression syndrome (CACS), which entails external compression of the celiac artery by the median arcuate ligament or the celiac ganglion.11

Frequency

United States

Acute mesenteric ischemia (AMI) is involved in up to 0.1% of all hospital admissions, although this number is likely to rise as the population ages.

Mortality/Morbidity

  • Mortality rates are high and range from 60-100% depending on the source of obstruction.3 Early and aggressive diagnosis and treatment has been shown to significantly decrease the mortality rate if the diagnosis is made prior to the development of peritonitis.12
  • One report of 21 patients with superior mesenteric artery (SMA) embolus, intestinal viability was achieved in 100% of patients before diagnosis if the duration of symptoms was less than 12 hours, in 56% if it was between 12 and 24 hours, and in only 18% if symptoms were more than 24 hours in duration.13
  • Another study found that, even at hospital centers with angiography available 24 hours, mortality rates still were approximately 70%.14

Sex

No sex predilection exists.

Age

Mesenteric ischemia is generally a disease of the older population, with the typical age of onset being older than 60 years; however, with risk factors and other predisposing factors, it may be seen in younger patients.

Clinical

History

  • The clinical presentation is largely dependent on the underlying etiology, with acute mesenteric ischemia (AMI) and chronic mesenteric ischemia (CMI) presenting very differently.
  • The classic picture of a patient with acute mesenteric ischemia involves severe abdominal pain with a paucity of significant abdominal findings in patients with significant underlying risk factors.
  • Because the pathologic process is ischemia, the pain is initially visceral in nature and generally poorly localized.
  • Acute pain may occur if an embolus is the cause, but it is essential to remember that a gradual onset of pain is more common in the overall spectrum of mesenteric ischemia.
  • The pain is usually severe and may occasionally be refractory to opioid analgesics.
  • Prior episodes of a similar pain, often related to meals (intestinal angina), may be reported.
  • Abdominal pain may be absent in 15-25% of cases; associated GI symptoms are common and caution must be taken to not be misled.
  • Nausea and vomiting are frequent, and diarrhea may occur in as many as 50% of patients with mesenteric ischemia.
  • The classic triad of superior mesenteric artery (SMA) embolism includes GI emptying, abdominal pain, and underlying cardiac disease.
  • Chronic mesenteric ischemia typically causes postprandial abdominal pain and weight loss that results in chronic dull pain as the obstructive process worsens.
  • Patients with chronic mesenteric ischemia may also report sitophobia (fear of eating).

Physical

  • The sine qua non of mesenteric ischemia is a relatively normal abdominal examination in the face of severe abdominal pain.
  • Advanced ischemia may be signified by increasing abdominal distention, ileus, frank peritonitis, and shock.
  • Theoretically, before the onset of significant mucosal injury, blood in the GI tract should be absent early in the disease process.
  • Melena or hematochezia occurs in 15% of cases, and occult blood is detected in approximately 50% of patients.12

Causes

  • Acute arterial embolus: Embolic lesions are usually secondary to conditions that predispose the patient to embolus formation such as atrial fibrillation, ventricular aneurysm, and valvular disease.3
  • Acute arterial thrombosis
    • Acute arterial thrombosis usually occurs following a superimposed insult in patients with preexisting atherosclerosis.
    • Other causes include aortic aneurysm, aortic dissection, and arteritis.
  • Nonocclusive ischemia
    • The causes of nonocclusive mesenteric ischemia include all of the causes of splanchnic vasoconstriction including hypovolemia, cardiac shock, sepsis, alpha-agonism, ergots, cocaine, and digitalis.
    • Case reports exist of marathon runners developing ischemic colitis following a marathon that resolved in most runners with supportive treatment.15
  • Mesenteric venous thrombosis
    • Approximately 75% of patients with mesenteric venous thrombosis have an underlying hypercoagulable state16 or other risk factors including portal hypertension, intra-abdominal sepsis, cirrhosis, pancreatitis, malignancy, and trauma.
    • Oral contraceptive use accounts for 9-18% of the episodes of mesenteric venous thrombosis in young women.17,18,19
  • Mechanical compression: Case reports have documented the etiology of celiac artery compression syndrome (CACS) as a cause of mesenteric ischemia due to external compression of the celiac artery usually by the median arcuate ligament or the celiac ganglion.11,20

More on Mesenteric Ischemia

Overview: Mesenteric Ischemia
Differential Diagnoses & Workup: Mesenteric Ischemia
Treatment & Medication: Mesenteric Ischemia
Follow-up: Mesenteric Ischemia
Multimedia: Mesenteric Ischemia
References
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Further Reading

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Keywords

acute mesenteric ischemia, AMI, chronic mesenteric ischemia, CMI, interruption of blood flow to small intestine, arterial mesenteric ischemia, venous mesenteric ischemia, superior mesenteric artery occlusion, nonocclusive infarction, inferior mesenteric artery occlusion, mesenteric venous thrombosis, arteritis

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Contributor Information and Disclosures

Author

Daniel K Nishijima, MD, Staff Physician, Department of Emergency Medicine, University of California Davis Medical Center
Daniel K Nishijima, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Mark Su, MD, FACEP, FACMT, Consulting Staff and Director of Fellowship in Medical Toxicology, Department of Emergency Medicine, North Shore University Hospital; Consulting Staff, North Shore University Hospital
Mark Su, MD, 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, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

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 and National Association of EMS Physicians
Disclosure: Intellicare Salary Management position; South Middlesex EMS Consortium Salary Management position

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

David FM Brown, MD, Assistant Professor, Department of Medicine, Division of Emergency Medicine, Harvard Medical School; Associate-Chief, Attending Physician, 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: Schering  Honoraria Speaking and teaching

 
 
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