Vascular disorders of the gastrointestinal tract typically present as abdominal pain or bleeding, or both. Several of the disorders that cause bleeding, such as ischemic colitis, angiodysplastic lesions, and vascular-enteric fistulas. Mesenteric vascular insufficiency. The clinical spectrum of mesenteric vascular insufficiency is broad, ranging from transient postprandial «abdominal angina» to severe abdominal pain caused by acute occlusion of a mesenteric vessel. Some patients with mild symptomatic vascular insufficiency are otherwise well, whereas acute occlusion of a mesenteric artery can be catastrophic.
Occlusion of a mesenteric vessel by a thrombus or an embolus is dramatic, and the pathogenesis is easy to understand. However, nonocclusive mesenteric vascular disease also is recognized and may affect a larger number of patients than the occlusive type does. The latter includes transient ischemia due to inadequate perfusion under some circumstances, such as the high demand for mesenteric blood flow after eating, resulting in «intestinal angina,» or the reduction in blood flow during an episode of heart failure or a cardiac arrhythmia, resulting in bleeding and abdominal pain. Vascular disorders of the bowel are more common in older people, and as the elderly population increases, these disorders are becoming more prevalent.
The stomach and intestines are supplied by three unpaired arteries: the celiac axis, the superior mesenteric artery, and the inferior mesenteric artery. The gut receives nearly 30% of the resting cardiac output through these three splanchnic arteries. Small vessels, called arteriae rectae, derive from the terminal branches of the intestinal arcade in the small intestine and from the marginal artery in the colon and penetrate the muscle layer of the gut to form a rich submucosal plexus. In the small intestine, arterioles arise from the submucosal plexus to supply each villus. A central arteriole runs the length of each villus and branches at the tip to form a capillary network, which is drained by venules that parallel the central arteriole.
Oxygen diffuses directly from the arterial to the venous side along the villus, thus creating a countercurrent mechanism that diminishes the oxygen concentration at the tip of the villus. This shunt is accentuated by low-flow states. It also may explain why small-intestinal ischemia is first manifested by destruction of the villous tips and consequently by breakdown of the barrier to bacteria, which predisposes the mucosa to bacterial invasion. In the colon, arterioles and venules also lie in close approximation, creating a similar predisposition to ischemia at the mucosal surface.
Occlusive vascular disease
Occlusion of the celiac axis, superior mesenteric artery, or inferior mesenteric artery, or their branches, can result from thrombosis or embolus, resulting in acute intestinal ischemia. A dissecting aortic aneurysm also can occlude one or more mesenteric vessels. If collateral circulation is inadequate, the bowel becomes ischemic and the patient experiences severe abdominal pain. The most common cause of arterial thrombosis is ordinary atherosclerotic vascular disease. Emboli may accompany acute myocardial infarction, ventricular aneurysm, atrial fibrillation, valvular heart disease, or bacterial endocarditis.
Occlusion of a splanchnic artery by thrombosis or embolus causes acute abdominal pain. Initially, the pain may be colicky, but as transmural infarction and peritonitis develop, the pain becomes constant and more severe. Tachycardia, hypotension, fever, elevated white cell count, and bleeding ensue. A careful examination should be done to evaluate for abdominal aortic aneurysm, abdominal bruits, and changes in peripheral pulses.
The differential diagnosis includes most causes of abdominal pain, including dissecting aortic aneurysm, bowel obstruction, perforation of a viscus, acute cholecystitis, appendicitis, diverticulitis, peptic ulcer disease, pancreatitis, and pancreatic carcinoma. Patients with a dissecting aortic aneurysm may have severe abdominal pain radiating to the back. During the dissection, occlusion of the mesenteric vessels also may occur. Bowel obstruction and perforation of a viscus are acute events that may be confused with mesenteric vascular thrombosis or embolus. Inflammatory conditions, such as cholecystitis, appendicitis, and diverticulitis, often have localizing signs but may be difficult to distinguish from ischemic bowel disease that is accompanied by fever and elevated white blood cell counts. The signs and symptoms of peptic ulcer disease, pancreatitis, and pancreatic cancer usually are less acute than those of mesenteric vascular disease.
Patients in whom acute ischemic bowel disease is suspected should have a complete blood count and differential white cell count and levels of serum amylase and electrolytes. The white cell count and amylase level may be increased in intestinal ischemia, but the latter usually is not elevated more than five times above normal level. Higher levels of serum amylase are more typical of acute pancreatitis. A urinalysis also should be performed. A metabolic acidosis may develop as ischemia worsens.
Plain films of the abdomen may show distended loops of bowel with air-fluid levels. Bowel loops may be separated by edema and blood within the bowel wall. Barium-contrast studies are not indicated during the initial evaluation and treatment of patients with acute ischemic bowel disease. The diagnosis is confirmed by angiography, although in some instances, when the clinical course is rapid and perforation is suspected, immediate surgery is indicated.
The initial treatment of thrombotic or embolic infarction of the bowel consists of nasogastric suction, intravenous fluid and electrolyte replacement, blood transfusions as indicated, broad-spectrum antibiotics, and, if necessary, vasopressors. Definitive treatment is surgical resection of the infarcted bowel.
Nonocclusive Vascular Disease
Angiodysplasias are ecstatic, vascular lesions within the submucosa consisting of arterial, venous, and capillary elements. They may be found throughout the gastrointestinal tract but occur most frequently in the cecum and ascending colon. Angiodysplasias are clinically important because they are a cause of acute and chronic gastrointestinal bleeding, particularly in elderly patients. Most angiodysplasias are thought to develop as a consequence of normal aging. Aortic stenosis occurs in up to 15% of patients with bleeding angiodysplasias, but pathogenic association is uncertain. In some patients, angiodysplastic lesions may occur throughout the gastrointestinal tract as part of the hereditary disorder known as Osler-Weber-Rendu disease. In this disease, telangiectatic lesions also are found on the skin, in the nail beds, and in the mucosa of the mouth and nasopharynx.
Angiodysplasias cause no symptoms until they bleed. In patients who ultimately are diagnosed as having bled from an angiodysplasia, therefore, the only common history is that of gastrointestinal bleeding. The usual presentation is one of acute lower gastrointestinal bleeding. Often a cause of bleeding is not found or the bleeding is attributed to another common, coexisting disorder, such as peptic disease or diverticulosis. Patients may experience several bleeding episodes, sometimes over a period of months, before the correct diagnosis is made.
The two methods of diagnosing angiodysplasias are colonoscopy and angiography.
An angiodysplastic lesion appears as a submucosal red blush resembling a spider angioma of the skin. To optimize the chance of visualizing the lesion by colonoscopy, however, the bowel must be free of blood and debris, which may not be possible during acute bleeding.
The lesions may be identified angiographically by the following findings:
- An early-filling vein.
- A vascular tuft of dilated vessels.
- A slowly emptying vein.
The traditional treatment of a bleeding angiodysplasia has been to resect the segment of bowel that contains the lesion, usually the ascending colon. Up to 30% of patients so treated bleed again, either from a new angiodysplastic lesion or from a lesion that was not resected. An alternative to surgical resection is colonoscopic electrocoagulation if the lesions can be identified by colonoscopy.
An unusual cause of gastrointestinal bleeding is a fistula between a vascular structure and the gastrointestinal tract. Most commonly, the fistula develops between an aortic graft and the third portion of the duodenum months to years after an aortic aneurysm repair. Fistulas also may develop between an unresected aneurysm and the bowel. Less common sites are the sigmoid colon, the cecum, and the esophagus. Fistulas between aneurysms of the aorta or smaller vessels and virtually every portion of the gastrointestinal tract have been reported.
Patients with vascular-enteric fistulas typically have massive hematemesis or hematochezia. A history of an aneurysm or aneurysm repair raises the likelihood. A «herald bleed» is characteristic: Most patients with vascular-enteric fistulas stop bleeding after the initial dramatic hemorrhage, only to rebleed within hours or days.
Diagnostic studies and treatment.
Upper gastrointestinal endoscopy is useful chiefly in excluding another bleeding lesion but usually does not identify the fistula. Angiography rarely identifies the fistula. Barium studies are not recommended due to the risk of severe bleeding but also are not likely to identify the fistula. Computed tomography of the abdomen may show a leaking aneurysm or fistula and therefore is helpful in making the decision to operate. A high index of suspicion for a vascular-enteric fistula in a patient with an aortic aneurysm or a history of an aneurysmectomy is worth more than diagnostic studies because immediate surgery usually is indicated after nondiagnostic upper gastrointestinal endoscopy is performed.