eMedicine Specialties > Gastroenterology > Intestine

Chronic Mesenteric Ischemia

Deron J Tessier, MD, Staff Surgeon, Kaiser Permanente Medical Center, Fontana, CA
Russell A Williams, MBBS, Program Director, Professor, Department of Surgery, University of California Medical Center at Irvine

Updated: Oct 10, 2006

Introduction

Background

Antonio Hodgson first described mesenteric ischemia (see Media file 1) in the latter part of the 15th century. During the middle of the 19th century, the medical profession became more interested in this condition. By the turn of the 20th century, many review articles and texts were produced describing the recent advances in both the characterization and treatment of mesenteric ischemia.

In 1901, Schnitzler described a patient with a long history of postprandial abdominal pain. He was found to have an atherosclerotic plaque with an overlying thrombus of the superior mesenteric artery. Schnitzler concluded that if a patient could develop pain in his or her lower extremities secondary to atherosclerosis, the assumption that a patient could present with postprandial pain due to narrowing of the mesenteric vessels would be reasonable.

By the middle of the 20th century, Dunphy hypothesized that mesenteric ischemia was a manifestation of visceral atherosclerosis. In 1958, Shaw and Maynard described the first thromboendarterectomy of the superior mesenteric artery for the treatment of both acute and chronic mesenteric ischemia.

Several other surgical procedures have since been attempted, ranging from reimplantation of the visceral branch into the adjacent aorta to using an autogenous vein graft. In 1972, Stoney and Wylie introduced transaortic visceral thromboendarterectomy and aortovisceral bypass, which have proven to be very effective techniques.

Pathophysiology

In more than 95% of patients, the cause of mesenteric ischemia is diffuse atherosclerotic disease, which decreases the flow of blood to the bowel. As the atherosclerotic disease progresses, symptoms worsen. Usually, all 3 major mesenteric arteries are occluded or narrowed.

The pathophysiologic mechanism by which ischemia produces pain is still not completely understood.

Frequency

United States

Chronic mesenteric ischemia is a rare diagnosis. No reports of the actual incidence have been published. Moawad searched 20 years of literature and found only 330 cases. Because many cases are not reported, the true prevalence could be much higher. Autopsy studies support this theory, with findings of stenosis in up to 30% of selected patients with a history of abdominal pain.

International

No differences in frequency are reported in various regions of the world.

Mortality/Morbidity

• Chronic mesenteric ischemia by itself does not represent an important cause of mortality.
• Complications, which include acute thrombosis or embolus, are significant causes of increased mortality and are the main reason to revascularize these patients.
• Patients with chronic mesenteric ischemia often present with malnutrition secondary to their fear of postprandial abdominal pain. These patients may have a prolonged hospital course due to their chronic malnourished state.

Sex

• Some studies show an increased prevalence in females compared with males, while other studies show equal distribution.

Age

• The average age at presentation is 60 years.

Clinical

History

• Patients typically present with a history of the following:
  • Weight loss
  • Postprandial pain, generally epigastric or periumbilical
  • Fear of eating
  • History of vascular disease involving other organs such as myocardial infarction (MI), cerebral vascular disease, or peripheral vascular disease
• Other nonspecific symptoms include the following:
  • Nausea
  • Vomiting
  • Diarrhea
  • Constipation
  • Flatulence

Physical

Upon physical examination, the following may be found:

• Signs of malnutrition
• Pain disproportionate to examination findings
  • Usually diffuse mild abdominal tenderness
  • No rebound or guarding
• Abdominal bruit
• Signs of peripheral vascular disease, such as carotid bruits, decreased pulses, and ischemic feet

Causes

Factors that predispose to atherosclerosis are associated with increased risk for chronic mesenteric ischemia. These include the following:

• Smoking
• Hypertension
• Diabetes mellitus
• Hypercholesterolemia (although patients may present with hypocholesterolemia because of their chronic malnourished state)

Differential Diagnoses

Other Problems to Be Considered

Small bowel obstruction

Workup

Laboratory Studies

• CBC count may demonstrate anemia, leukopenia, or lymphopenia secondary to chronic malnourishment.
• Chemistries may show electrolyte abnormalities from malnutrition, vomiting, or diarrhea.
• Urinalysis should be performed to rule out stones or infection.
• Liver function tests may show hypoalbuminemia from malnutrition.
• If a patient presents with steatorrhea, send stool fat for examination.
• Preoperative considerations include the following;
  • CBC count
  • Chemistries
  • Prothrombin time (PT)
  • Activated partial thromboplastin time (aPTT)
  • International normalized ratio (INR)

Imaging Studies

• Perform chest radiography to rule out pneumonia (see Media file 2).
• Perform dipyridamole-thallium scanning if coronary artery disease is a suspected comorbidity.
• Arteriography is the criterion standard and will show occlusion (see Media file 4) of 2 visceral branches of the aorta, with severe stenosis of the remaining visceral branch, usually the celiac or superior mesenteric artery. Look for a dilated meandering artery (see Media file 3), which indicates well-developed collateral flow.
• Mesenteric duplex ultrasonography is a noninvasive method of analyzing flow through the vessels. Unfortunately, intraperitoneal gas, respiratory movements, obesity, and any previous abdominal surgeries limit results.
• MRI is under investigation as a future diagnostic tool.
• Preoperative studies include the following:
  • Chest radiography
  • Dipyridamole-thallium scanning
  • Arteriography

Other Tests

• Perform ECG to rule out cardiac disease.

Histologic Findings

Transected mesenteric vessels show diffuse atherosclerosis. The histological findings from the bowel include atrophy of the tips of the villi, which leads to loss of the absorptive surface in the small bowel. The loss of the absorptive surface in conjunction with the patient's fear of eating results in the malnourished state commonly seen in persons with this condition.

Treatment

Medical Care

• Because of the high rate of thrombosis, medical management as a sole treatment is warranted only in patients whose risk with surgery outweighs the benefits.
• Some patients may find short-term relief with nitrate therapy; however, this treatment is not curative.
• Medical management includes anticoagulation therapy with warfarin.
• Once a diagnostic arteriogram is obtained and surgery is deemed appropriate, start intra-arterial papaverine to reduce the risk of arterial spasm.

Surgical Care

• After the diagnosis is made by arteriography, patients should undergo surgery because of the risk of continued weight loss, acute infarction, perforation, sepsis, and death.
• Stenting of visceral vessels has been reported with some success and may be an alternative to surgery. One study suggests that stenting may result in equivalent patency rates to that of surgical correction; however, symptomatic improvement may not be as good. Another study suggests that the long-term outcome may be equal to that of surgery.
• Preoperative considerations include the following:
  • Because of the long period of malnutrition, patients should receive parenteral nutrition prior to surgery.
  • Cross and match 2 units of blood.
• Prepare the patient's bowel the night prior to surgery, and arrange for the patient to ingest nothing by mouth past midnight.
• Obtain informed consent.
• To decrease the risk of vasospasm, intra-arterial papaverine may be started at the time of the angiogram.
• Surgical correction includes (1) transaortic endarterectomy of the celiac or superior mesenteric artery, (2) retrograde bypass from the external iliac artery, and (3) anterograde bypass, which provides the best orientation of the graft to the aorta. Mesenteric artery reimplantation has been performed but is not widely recommended because of the technical difficulties of the procedure.

Consultations

• Because of the high rate of coronary artery disease in these patients, consultation with a cardiologist is warranted to evaluate potential risks associated with surgery.

Diet

• Because chronic mesenteric ischemia is a complication of diffuse atherosclerosis of the arterial tree, these patients should maintain a low-fat diet, similar to that of patients with cardiac disease.
• Some patients report increased postprandial pain after eating large or fatty meals. Therefore, the diet should be appropriately altered to include small, multiple meals or low-fat meals.

Activity

• Encourage regular exercise, as in patients with cardiac disease.

Medication

Drugs used in chronic mesenteric ischemia include heparin and warfarin for anticoagulation and intra-arterial papaverine as a vasodilator.

Anticoagulants

Prevent an acute thrombotic/embolic event.

Warfarin (Coumadin)

Anticoagulant that interferes with epoxide reductase, preventing production of vitamin K–dependent factors II, VII, IX, X, and protein C and S. Because protein C and S are the first factors to be inhibited, a prothrombic effect occurs during initial few days after instituting warfarin. Start patients on heparin first and then switch to warfarin when the PT, aPTT, and INR are therapeutic. Duration of action is 2-5 d.

Dosing

Adult

5 mg/d PO initially for 2-4 d; adjust dose to desired PT/INR

Pediatric

0.05-0.34 mg/kg/d PO; adjust dose according to desired INR; infants may require doses at or near high end of this range

Interactions

Drugs that may decrease anticoagulant effects include griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin K, spironolactone, oral contraceptives, and sucralfate
Medications that may increase anticoagulant effects include oral antibiotics, phenylbutazone, salicylates, sulfonamides, chloral hydrate, clofibrate, diazoxide, anabolic steroids, ketoconazole, ethacrynic acid, miconazole, nalidixic acid, sulfonylureas, allopurinol, chloramphenicol, cimetidine, disulfiram, metronidazole, phenylbutazone, phenytoin, propoxyphene, sulfonamides, gemfibrozil, acetaminophen, and sulindac

Contraindications

Documented hypersensitivity, severe liver or kidney disease, open wounds or GI ulcers

Precautions

Pregnancy

X - Contraindicated in pregnancy

Precautions

Do not switch brands after achieving therapeutic response; caution in active tuberculosis or diabetes; patients with protein C or S deficiency are at risk of developing skin necrosis

Heparin

Sulfated mucopolysaccharide. Anticoagulant effect is related to ability to activate plasma antithrombin. Main role of heparin in these patients is to prevent thrombus propagation.

Dosing

Adult

80 U/kg loading dose IV followed by 18 U/kg/h; adjust dose to appropriate aPTT level

Pediatric

50 U/kg loading dose IV followed by 25 U/kg/h

Interactions

Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, ASA, dextran, dipyridamole, and hydroxychloroquine may increase heparin toxicity

Contraindications

Documented hypersensitivity; presence of active hemorrhage, potential hemorrhage, and hemorrhagic disorders; severe thrombocytopenia

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Some preparations contain benzyl alcohol as a preservative and, when used in large amounts, are associated with fetal toxicity (gasping syndrome); preservative-free heparin is recommended in neonates; heparin should be used with caution in patients in shock or with severe hypotension

Vasodilators

Used during arteriogram to decrease vasospasm in occluded arteries, with the objective of improving blood flow.

Papaverine (Genabid)

Benzylisoquinoline-derivative with direct nonspecific relaxant effect on vascular, cardiac, and other smooth muscle.

Dosing

Adult

30-60 mg/h IV

Pediatric

Not established

Interactions

May decrease effectiveness of levodopa

Contraindications

Documented hypersensitivity; complete AV heart block

Precautions

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in angina, recent MI, recent stroke glaucoma

Follow-up

Further Inpatient Care

• Postoperative care includes the following:
  • Ambulate early because of the high rate of postoperative ileus.
  • Monitor blood pressure to prevent hypotension, which can induce ischemia.

Further Outpatient Care

• Monitor the PT and INR.
• Routine visceral duplex ultrasonography is recommended every 4-6 months.

Complications

• The risk of MI is increased but can be reduced with the following steps:
  • Identify patients at risk preoperatively.
  • Place a Swan-Ganz catheter perioperatively.
  • Inform the anesthesiologist when cross-clamping the aorta, so that myocardial protective maneuvers are used.
• Acute renal failure can be prevented with the following steps:
  • Adequately hydrate the patient before and during surgery.
  • Administer mannitol before cross-clamping the aorta.
  • Monitor BUN and creatinine levels in the preoperative and postoperative periods.

Prognosis

• The mortality rate associated with visceral reconstruction is approximately 4-6%.
• A 2004 study from the Wake Forest School of Medicine found the following:
  • The symptom-free survival rate for hospital survivors is 57% at 70 months.
  • Primary and primary-assisted patency rates are 81% and 89%, respectively
  • Patients with acute-on-chronic mesenteric ischemia had significantly higher perioperative mortality rates (54% vs 10%) than those with chronic symptoms alone.

Patient Education

• For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center and Cholesterol Center. Also, see eMedicine's patient education articles Abdominal Pain in Adults and Coronary Heart Disease.

Miscellaneous

Medicolegal Pitfalls

• Failure to have a high enough index of suspicion for the disease is the major medical pitfall. Many emergency department physicians and surgeons overlook placing this diagnosis on their differential. This can be disastrous.
• Failure to treat the disorder as aggressively as it deserves is also a pitfall. Once the diagnosis is considered, a complete workup, including an angiogram, should be performed.

Multimedia

Media file 1: Angiogram of a patient with chronic mesenteric ischemia. Notice the diffuse occlusive disease.

Media file 2: Radiograph showing a tortuous, dilated, meandering artery.

Media file 3: Narrowing of the superior mesenteric artery.

Media file 4: Chronic aortic occlusion (Leriche syndrome) with acute embolic occlusion of the superior mesenteric artery.

References

1. Cappell MS. Intestinal (mesenteric) vasculopathy. I. Acute superior mesenteric arteriopathy and venopathy. Gastroenterol Clin North Am. Dec 1998;27(4):783-825, vi. [Medline].

2. Chahid T, Alfidja AT, Biard M, et al. Endovascular treatment of chronic mesenteric ischemia: results in 14 patients. Cardiovasc Intervent Radiol. Nov-Dec 2004;27(6):637-42. [Medline].

3. Chang JB, Stein TA. Mesenteric ischemia: acute and chronic. Ann Vasc Surg. May 2003;17(3):323-8. [Medline].

4. English WP, Pearce JD, Craven TE, et al. Chronic visceral ischemia: symptom-free survival after open surgical repair. Vasc Endovascular Surg. Nov-Dec 2004;38(6):493-503. [Medline].

5. Geroulakos G, Tober JC, Anderson L, Smead WL. Antegrade visceral revascularisation via a thoracoabdominal approach for chronic mesenteric ischaemia. Eur J Vasc Endovasc Surg. Jan 1999;17(1):56-9. [Medline].

6. Hung KH, Lee CT, Lam KK, et al. Ischemic bowel disease in chronic dialysis patients. Chang Keng I Hsueh Tsa Chih. Mar 1999;22(1):82-7. [Medline].

7. Kazmers A. Operative management of chronic mesenteric ischemia. Ann Vasc Surg. May 1998;12(3):299-308. [Medline].

8. Kihara TK, Blebea J, Anderson KM, et al. Risk factors and outcomes following revascularization for chronic mesenteric ischemia. Ann Vasc Surg. Jan 1999;13(1):37-44. [Medline].

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12. Schaefer PJ, Schaefer FK, Mueller-Huelsbeck S. Chronic mesenteric ischemia: stenting of mesenteric arteries. Abdom Imaging. Sep 6 2006.

13. Sharafuddin MJ, Olson CH, Sun S, et al. Endovascular treatment of celiac and mesenteric arteries stenoses: applications and results. J Vasc Surg. Oct 2003;38(4):692-8. [Medline].

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15. Silva JA, White CJ, Collins TJ. Endovascular therapy for chronic mesenteric ischemia. J Am Coll Cardiol. Mar 7 2006;47(5):944-50.

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Keywords

chronic visceral ischemia, postprandial abdominal pain, atherosclerotic plaque, thrombus, superior mesenteric artery, atherosclerosis, visceral atherosclerosis, thromboendarterectomy, malnutrition, malnourishment, coronary artery disease, CAD, transaortic visceral thromboendarterectomy, aortovisceral bypass

Contributor Information and Disclosures

Author

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.

Coauthor(s)

Russell A Williams, MBBS, Program Director, Professor, Department of Surgery, University of California Medical Center at Irvine
Russell A Williams, MBBS is a member of the following medical societies: American College of Surgeons, American Pancreatic Association, Association for Surgical Education, Association of VA Surgeons, Society for Surgery of the Alimentary Tract, Southern California Society of Gastroenterology, and Southwestern Surgical Congress
Disclosure: Nothing to disclose.

Medical Editor

Mounzer Al Al Samman, MD, Department of Internal Medicine, Division of Gastroenterology, Assistant Professor, Texas Tech University School of Medicine
Mounzer Al Al Samman, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, and American Gastroenterological Association
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

BS Anand, MD, Department of Internal Medicine, Division of Gastroenterology, Professor, Baylor University College of Medicine
BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Assistant Dean for Medical Curriculum, Associate Professor of Medicine, Division of General Internal Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous coauthor, Yale D Podnos, MD, MPH, to the development and writing of this article.

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