Intestinal ischemia produces a spectrum of diseases affecting the gastrointestinal tract. These syndromes, which can be acute or chronic, can affect the upper abdominal viscera, as well as the small intestine, colon, and rectum. They account for significant morbidity and mortality and continue to be the subject of clinical and laboratory investigation. The most common form of intestinal ischemia is ischemic colitis, accounting for 50% to 60% of all cases, with an incidence of 4.5 to 44 cases per 100,000 patients per year. The pathophysiologic changes associated with ischemic disease of the colon are related to numerous factors. In certain circumstances, these factors are known and may be corrected, but more often they are unknown, and treatment is based on symptoms.
Cases of colonic gangrene were first described in the late nineteenth and early twentieth centuries, but it was not until the 1960s that the pathophysiology of ischemic colitis was appreciated. In 1963, Boley described noniatrogenic, spontaneous colon ischemia in five patients. In 1966, Martson coined the term colonic ischemia , or ischemic colitis , when he described 16 cases of spontaneous colonic ischemia. Usually no major vessel occlusion occurs, and often the original insult precipitating the ischemic event cannot be established. Many advances in the diagnosis and treatment of patients with colonic ischemia have been made since it was originally described by Boley and colleagues, and it is clear that the outcome depends on numerous factors, including the severity, extent, and rapidity of the ischemic insult, as well as the therapy provided. Increased awareness of this disease and knowledge regarding appropriate treatment are fundamental for its successful management.
Etiology and Pathogenesis
Causes of colonic ischemia ( Table 66-1 ) can be classified as either occlusive or nonocclusive. Frequently, a cause is not easily identified. Spontaneous episodes of ischemic colitis are by far the most common form of the disease and generally are viewed as localized forms of nonocclusive ischemia. Colonic blood flow is decreased by a variety of local and systemic physical and biochemical factors, through intensive vasoconstriction and arteriovenous shunting within the mesenteric circulation and bowel wall. Furthermore, obstruction or diffuse vasospasm involving the major arterial supply of the large intestine can result in severe ischemia to extensive regions of the colon or rectum.
|Aortic balloon pump |
|Small vessel disease ||Atherosclerosis |
Paclitaxel and carboplatin
|Surgical||Cardiopulmonary bypass |
Colectomy + IMA ligation
|Long distance running |
|Venous Obstruction||Hypercoagulable state |
Sickle cell disease
|Colonic Obstruction||Volvulus |
Patients with ischemic colitis tend to have several risk factors for vascular disease, including age greater than 65 years, cardiac arrhythmias, and thrombophilia. Antiphospholipid antibodies and factor V Leiden mutations are more frequently noted in patients with ischemic colitis. Increased risk of colonic ischemia is also seen in patients with irritable bowel syndrome (threefold higher), chronic obstructive pulmonary disease (two- to fourfold higher), constipation (even higher in persons who use laxatives), hypertension, diabetes, and renal failure. Trauma, thrombosis, or immobilization of the mesenteric arteries can cause occlusion of the blood supply to the colon, although such instances are rare. Several medications have been implicated in the occurrence of colonic ischemia. Colonic obstruction related to tumor, adhesions, diverticular disease, volvulus, or fecal impaction also may be responsible. In most cases, however, no precipitating cause or event can be identified.
Colonic ischemia in younger patients is usually related to medications and drugs, intensive exertion, vasculitis, and sickle cell disease. For unknown reasons, the right colon is frequently involved.
Several factors predispose the colon to ischemia. The splanchnic circulation receives 10% to 35% of the cardiac output, but the colon has less blood flow per 100 g of tissue than does any other part of the gastrointestinal tract. The colon also frequently relies on a collateral arterial circulation. Another factor predisposing the colon to ischemic insult is the decrease in blood flow that accompanies the functional motor activity of the colon. During hypotension, the colon does not autoregulate well compared with the remainder of the gastrointestinal tract, and oxygen supply quickly reaches a critically low level, resulting in ischemia. The initial insult to the colon is usually seen in the mucosa and subsequently extends to the submucosa and muscularis. This mucosal change is most evident at the antimesenteric border of the colon. With impairment of the blood flow to the colon, mucosal injury will develop within 20 to 60 minutes, whereas transmural infarction can take up to 8 to 16 hours to develop. Unfortunately, re-establishment of blood flow is associated with reperfusion injury because of the formation of reactive oxygen species, which cause peroxidation of lipids in the cell membranes and, ultimately, cell necrosis.
Clinically, the two principal forms of ischemic colitis noted are a gangrenous and a nongangrenous type. Nongangrenous ischemia can be a transient reversible form or a chronic form ( Fig. 66-1 ). The severity of the ischemia determines the depth of the tissue damage, with transmural necrosis noted in gangrenous colitis and mucosal or submucosal involvement noted in the nongangrenous form, which accounts for 80% to 85% of cases. In the 15% to 20% of cases of gangrenous colitis, surgical resection of the involved colonic segment is required. Gangrenous ischemic colitis is associated with a mortality of up to 50%.
The transient reversible form of nongangrenous ischemic colitis is characterized by edema, submucosal hemorrhage, and partial mucosal necrosis. A complete structural and functional recovery usually occurs within 1 to 2 weeks with no long-term sequelae. If the ischemia extends to the muscularis propria, the damaged muscularis is replaced by fibrous tissue over a period of weeks to months, sometimes resulting in a stricture. These strictures may be symptomatic. Chronic damage in the form of persistent segmental colitis and stricturing occurs in 20% to 25% and 10% to 15% of patients, respectively.
Ischemic colitis may involve any portion of the colon and rectum, although the splenic flexure, descending colon, and sigmoid are most commonly affected, accounting for 75% of all cases. Certain causes have a propensity to affect specific areas of the bowel. Ischemia resulting from systemic low-flow states usually involves the right colon, most commonly its retroperitoneal surface. Localized, nonocclusive ischemia classically involves watershed areas of the colon such as the splenic flexure (Griffith’s point) and the junction of the sigmoid and rectum (Sudek’s point). The right colon is involved in approximately 10% of the cases, and right colon ischemia may be a manifestation of midgut ischemia resulting from an embolus or thrombus in the superior mesenteric artery, because the midgut includes this part of the colon. Ischemic proctosigmoiditis is a rare event (discussed in a subsequent section).
Ischemic colitis presents with acute onset of abdominal pain and cramping that often is localized to the lower abdomen and frequently to the left side. An acute urge to defecate as a result of reactive muscle spasm often accompanies the pain. Hematochezia may develop within 24 hours; blood loss is usually mild, but “red currant jelly” stools may be present. Occasionally patients present with painless diarrhea with or without hematochezia. Other symptoms include diarrhea (68%), abdominal distention (63%), and nausea/vomiting (38%).
Abdominal examination is significant for mild tenderness that usually corresponds to the site of ischemia, along with mild distention. A low-grade fever may accompany the pain. Rectal examination reveals either fresh blood or heme-positive stool. Moderate leukocytosis with a left shift is often seen. Peritoneal signs such as rebound and guarding are more suggestive of late transmural ischemia, and these patients usually have other signs of systemic inflammatory response syndrome. Once patients with full-thickness gangrene experience a perforation through the dead bowel, signs and symptoms of a catastrophic abdominal event occur, including sepsis and shock.
Ischemic colitis is not limited to elderly persons. Colonic ischemia may affect younger people, for whom the causes include vasculitis, medication-induced reactions, coagulopathies, sickle cell disease, long-distance running, and cocaine abuse. Because they have fewer comorbidities, these patients usually tolerate both surgery and ischemia well.
Chronic ischemic colitis can present with distention and obstipation as a result of ischemic strictures in the affected segment of intestine.