Abdominal Angina 

  • Author: Faisal Aziz, MD; Chief Editor: John Geibel, MD, DSc, MA   more...
 
Updated: Jan 6, 2012
 

Background

Abdominal angina is defined as the postprandial pain that occurs in individuals with sufficient mesenteric vascular occlusive disease such that blood flow cannot increase enough to meet visceral demands. The mechanism is believed to be similar to the angina pectoris that occurs in individuals with coronary artery disease or the intermittent claudication that accompanies peripheral vascular disease, as depicted in the image below.

The superior mesenteric artery and inferior mesentThe superior mesenteric artery and inferior mesenteric artery share collateral circulation near the splenic flexure of the colon. When dilated, this vessel is termed the meandering mesenteric artery. As seen on an angiogram, this is a sign of chronic mesenteric ischemia. The pancreaticoduodenal arcades are collateral patThe pancreaticoduodenal arcades are collateral pathways between the celiac artery and the superior mesenteric artery.

Although Schnitzler first described the clinical picture of postprandial clinical pain in 1901, description of the syndrome of postprandial abdominal angina generally is attributed to Baccelli or Goodman (1918). In 1936, Dunphy recognized that this syndrome was a precursor of fatal intestinal necrosis; however, not until 1957 did Mikkelsen propose surgical treatment of occlusive mesenteric vascular disease. Shaw and Maynard reported the first transarterial thromboendarterectomy of the superior mesenteric artery (SMA) in 1958, followed in rapid succession by Mikkelsen and Zarro in 1959. Numerous technical refinements followed.

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Pathophysiology

Intestinal ischemia results from the mismatch of oxygen supply to and oxygen consumption by the gastrointestinal tract owing to reduced blood flow. The decreased blood flow results from narrowing of the mesenteric vessels, which can be can be secondary to a thrombus or embolus. The most common cause of abdominal angina is atherosclerotic vascular disease. The occlusive process commonly involves the ostia and a few proximal centimeters of the mesenteric vessels. Aortoiliac occlusive disease frequently coexists and may be the cause of the ostial lesions.[1]

The 3 arteries supplying the gut are the celiac, superior mesenteric, and inferior mesenteric, as shown below. Unless significant stenoses or actual occlusion of 2 of the 3 vessels is present, efficient collateral circulation between the celiac and superior mesenteric arteries (ie, the pancreaticoduodenal arcades) and the superior and inferior mesenteric arteries (ie, the meandering mesenteric artery) ensures that blood flow to the gut generally is adequate. The internal iliac arteries also may be an important source of collateral hindgut and midgut perfusion in the presence of inferior mesenteric arterial occlusion.

The superior mesenteric artery and inferior mesentThe superior mesenteric artery and inferior mesenteric artery share collateral circulation near the splenic flexure of the colon. When dilated, this vessel is termed the meandering mesenteric artery. As seen on an angiogram, this is a sign of chronic mesenteric ischemia. The pancreaticoduodenal arcades are collateral patThe pancreaticoduodenal arcades are collateral pathways between the celiac artery and the superior mesenteric artery.

SMA occlusion almost invariably is observed in patients with symptomatic occlusive mesenteric ischemia. Theories suggest that, because the SMA provides vascularity to the foregut, midgut, and hindgut, collaterals cannot sufficiently compensate for occlusion of this central artery.

Within 15 minutes of eating, duplex Doppler studies can show increased blood flow in the celiac and superior mesenteric vessels in healthy volunteers. Patients with abdominal angina are unable to sufficiently increase flow in the mesenteric vessels, and ischemic pain results. Affected individuals learn to associate food with pain, and thus, they develop a fear of eating. Weight loss may be significant.

Median arcuate ligament syndrome is thought to be a syndrome of abdominal pain caused by compression of the celiac trunk by the median arcuate ligament and, perhaps, by dense encasement by periarterial neural tissue. Described in 1965 by Dunbar and colleagues, compression of the celiac artery is thought to cause intimal fibrosis that leads to luminal stenosis and impaired splanchnic blood flow. This would result in symptoms similar to those of atherosclerotic mesenteric ischemia, which nearly always is caused by at least 2 major visceral artery occlusive lesions. In patients with median arcuate ligament syndrome, symptoms may be a result of compression of a single visceral artery in the absence of adequate collaterals; mesenteric steal or neurogenic mechanisms also have been proposed as causes. Symptoms have been reported to be provoked by exercise in isolated cases.

Definitive corroboration of any of these explanations is lacking, hence the controversial nature of the condition. Further discussion of this topic exceeds the scope of this article, but interested readers may refer to related references in the bibliography.

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Epidemiology

Frequency

International

The syndrome is extremely rare, and the true incidence is unknown.

Mortality/Morbidity

Despite advances in surgery, the mortality rate associated with acute mesenteric ischemia ranges from 60-95%. [2]

Race

No data are available regarding the relative incidence among different races.

Sex

In contrast to the usual male predilection of atherosclerotic vascular disease, in most series, females outnumber males by approximately 3 to 1.

Age

The mean age of affected individuals is slightly older than 60 years. Median arcuate ligament syndrome (see Pathophysiology above) has been reported in young individuals.

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Contributor Information and Disclosures
Author

Faisal Aziz, MD  Assistant Professor of Surgery, Divsion of Vascular and Endovascular Surgery, Department of Surgery, Pennsylvania State University College of Medicine

Faisal Aziz, MD is a member of the following medical societies: American College of Surgeons and American Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Anthony J Comerota, MD, FACS, FRACS(HON), FACC  Director of Jobst Vascular Institute, Program Director of General Vascular Surgery Residency, Toledo Hospital; Director of Jobst (ProMedica) Vascular Laboratories; Adjunct Professor of Surgery, Department of Surgery, University of Michigan Medical School

Anthony J Comerota, MD, FACS, FRACS(HON), FACC is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Chest Physicians, American College of Surgeons, American Heart Association, American Stroke Association, American Surgical Association, American Venous Forum, Association for Academic Surgery, Eastern Vascular Society, Society for Clinical Vascular Surgery, Society for Vascular Surgery, and Society of University Surgeons

Disclosure: BMS Honoraria Speaking and teaching; BMS Consulting fee Consulting; BMS Grant/research funds None; Covidien Honoraria Speaking and teaching; Covidien Consulting fee Consulting; Otsuka Honoraria Speaking and teaching; Sanofi/Aventis Speaking and teaching; Sanofi/Aventis Consulting fee Consulting; Sanofi/Aventis Grant/research funds None; Servier Honoraria Speaking and teaching

Specialty Editor Board

Marc D Basson, MD, PhD, MBA, FACS  Professor, Chair, Department of Surgery, Assistant Dean for Faculty Development in Research, Michigan State University College of Human Medicine

Marc D Basson, MD, PhD, MBA, FACS is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Gastroenterological Association, Phi Beta Kappa, and Sigma Xi

Disclosure: Nothing to disclose.

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

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

Paolo Zamboni, MD  Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy

Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York Academy of Sciences

Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, DSc, 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

John Geibel, MD, DSc, 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, and Society for Surgery of the Alimentary Tract

Disclosure: AMGEN Royalty Consulting; ARdelyx Ownership interest Board membership

Additional Contributors

We wish to thank Carol EH Scott-Conner, MD, PhD, and Beth Ballinger, MD, for their previous contributions to this article.

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The superior mesenteric artery and inferior mesenteric artery share collateral circulation near the splenic flexure of the colon. When dilated, this vessel is termed the meandering mesenteric artery. As seen on an angiogram, this is a sign of chronic mesenteric ischemia.
The pancreaticoduodenal arcades are collateral pathways between the celiac artery and the superior mesenteric artery.
A lateral aortogram shows abrupt cutoffs at the origin of the visceral vessels and a tapered occlusion of the distal aorta. Because these vessels originate from the anterior surface of the aorta, stenoses and occlusions are not observed clearly on standard anteroposterior views.
This arteriogram illustrates a meandering mesenteric artery. The appearance of a meandering mesenteric artery such as this one supports the diagnosis of chronic mesenteric ischemia.
The celiac artery is exposed at its origin in preparation for antegrade bypass.
The superior mesenteric artery and several branches are exposed for antegrade bypass.
This photo shows an antegrade bypass from the aorta to the superior mesenteric artery and the celiac artery (superior mesenteric artery anastomosis is shown) using a Dacron graft.
This operative photograph shows a completed retrograde bypass to the superior mesenteric artery using ePTFE graft material. Photograph courtesy of Jamal Hoballah, MD, University of Iowa College of Medicine.
This diagram shows the possible incision for a trapdoor aortotomy. Plaque at the orifices of the visceral vessels is removed after the trapdoor incision is lifted. When a satisfactory endarterectomy has been achieved, the trapdoor is sutured shut.
This completion duplex ultrasonographic study shows excellent flow at the distal anastomosis.
Upper gastrointestinal series (barium swallow) shows an ulcer.
 
 
 
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