eMedicine Specialties > General Surgery > Abdomen

Abdominal Angina

Author: Carol EH Scott-Conner, MD, PhD, Professor, Department of Surgery, University of Iowa College of Medicine
Coauthor(s): Beth Ballinger, MD, Assistant Professor, Department of Surgery, Section of Vascular Surgery, University of Iowa College of Medicine
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Updated: Sep 6, 2007

Introduction

Background

Although Schnitzler first described the clinical picture of postprandial clinical pain in 1901, 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.

Abdominal angina is a highly descriptive term for 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.

Pathophysiology

The most common cause of abdominal angina is atherosclerotic vascular disease. The occlusive process commonly involves the ostia and the proximal few centimeters of the mesenteric vessels. Aortoiliac occlusive disease frequently coexists and may be the cause of the ostial lesions.

The 3 arteries supplying the gut are the celiac, superior mesenteric, and inferior mesenteric (see Media files 1-2). 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 artery occlusion. 

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.

Frequency

International

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

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.

Clinical

History

• The hallmark of this condition is disabling midepigastric or central abdominal pain that develops 10-15 minutes after eating.
  • The pain gradually increases in intensity, reaches a plateau, and then slowly decreases in intensity several hours after eating.
  • Initially, this pain pattern develops only after large meals, but as the disease progresses, even small meals may be poorly tolerated.
• Some patients have associated motility disturbances such as diarrhea or constipation, bloating, or vomiting.
• The pain is poorly localized and described as cramplike or a dull ache. Occasionally, a patient may have constant or intermittent pain that occurs without a clear temporal relationship to eating.
• Soon, patients associate eating with pain and develop a characteristic fear of food (ie, sitophobia) or food-avoidance behavior. In several clinical series, reported weight loss averages 15-25 lb.
• The constellation of abdominal pain, weight loss, and an average age of 60 years commonly leads to a presumed diagnosis of malignancy and a protracted workup. Because none of the usual contrast studies or endoscopies performed in the course of a workup for malignancy are diagnostic, considerable delay in diagnosis typically results. In several series, the reported delay averages 16-18 months.
• If patients have multiple risk factors for atherosclerotic occlusive disease, a heightened clinical suspicion for this diagnosis shortens the typical delay in diagnosis.
• A history of peripheral vascular disease is common. As with other vasculopathies, individuals who smoke predominate in all series.
• Although diabetes occurs in all series, it is uncommon in patients with this syndrome (in contrast to most other vascular problems).
• Occasionally, a patient presents with a duodenal or gastric ulcer (which may be Helicobacter pylori negative) or with ischemic colitis.
• Ischemic pancreatitis also may occur and is associated with epigastric pain. Laboratory studies reveal mildly elevated amylase and lipase. Steatorrhea may be observed.

Physical

• Physical examination reveals stigmata of weight loss. The abdomen typically is scaphoid and soft, even during an episode of pain.
• In one series, approximately 10% of patients had positive test results for guaiac.
• Abdominal bruit is present in 60-90% of patients, but this is common in many elderly persons who are not affected by this syndrome.
• Signs of peripheral vascular disease, particularly aortoiliac occlusive disease, may be present.

Causes

• Smoking is an associated risk factor. In most series, approximately 75-80% of patients smoke.

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