Introduction
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 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.
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.
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.
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 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.
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.
Mortality/Morbidity
Despite advances in surgery, the mortality rate associated with acute mesenteric ischemia ranges from 60-95%. 1
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 classic description of intestinal angina is abdominal pain that is out of proportion with physical examination.
- 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.
More on Abdominal Angina |
 Overview: Abdominal Angina |
| Differential Diagnoses & Workup: Abdominal Angina |
| Treatment & Medication: Abdominal Angina |
| Follow-up: Abdominal Angina |
| Multimedia: Abdominal Angina |
| References |
| Further Reading |
| Next Page » |
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Further Reading
Clinical guidelines:
ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease). American College of Cardiology Foundation - Medical Specialty Society
American Heart Association - Professional Association
Society for Cardiovascular Angiography and Interventions - Medical Specialty Society
Society for Vascular Medicine and Biology - Medical Specialty Society
Society for Vascular Surgery - Medical Specialty Society
Society of Interventional Radiology - Medical Specialty Society. 2005. 191 pages. NGC:004740
Clinical trials:
Biomagnetic Signals of Intestinal Ischemia
Biomagnetic Signals of Intestinal Ischemia II (SQUID)
Keywords
abdominal angina, mesenteric ischemia, arteriotomy, superior mesenteric artery, celiac artery, intestinal angina, acute mesenteric ischemia, inferior mesenteric artery, postprandial abdominal angina, occlusive mesenteric vascular disease, postprandial pain, symptomatic occlusive mesenteric ischemia, central abdominal pain
