Ischemic colitis (also spelled ischaemic colitis) is a medical condition in which inflammation and injury of the large intestine result from inadequate blood supply (ischemia). Although uncommon in the general population, ischemic colitis occurs with greater frequency in the elderly, and is the most common form of bowel ischemia. Causes of reduced blood flow can include changes in the systemic circulation (e.g. low blood pressure) or local factors such as constriction of blood vessels or a blood clot. In most cases, no specific cause can be identified. Ischemic colitis is usually suspected on the basis of the clinical setting, physical examination, and laboratory test results; the diagnosis can be confirmed by endoscopy or by using sigmoid or endoscopic placement of a visible light spectroscopic catheter (see Diagnosis). Ischemic colitis can span a wide spectrum of severity; most patients are treated supportively and recover fully, while a minority with very severe ischemia may develop sepsis and become critically, sometimes fatally, ill. Patients with mild to moderate ischemic colitis are usually treated with IV fluids, analgesia, and bowel rest (that is, no food or water by mouth) until the symptoms resolve. Those with severe ischemia who develop complications such as sepsis, intestinal gangrene, or bowel perforation may require more aggressive interventions such as surgery and intensive care. Most patients make a full recovery; occasionally, after severe ischemia, patients may develop long-term complications such as a stricture or chronic colitis.
Signs and symptoms Three progressive phases of ischemic colitis have been described:
A hyperactive phase occurs first, in which the primary symptoms are severe abdominal pain and the passage of bloody stools. Many patients get better and do not progress beyond this phase. A paralytic phase can follow if ischemia continues; in this phase, the abdominal pain becomes more widespread, the belly becomes more tender to the touch, and bowel motility decreases, resulting in abdominal bloating, no further bloody stools, and absent bowel sounds on exam. Finally, a shock phase can develop as fluids start to leak through the damaged colon lining. This can result in shock and metabolic acidosis with dehydration, low blood pressure, rapid heart rate, and confusion. Patients who progress to this phase are often critically ill and require intensive care. Symptoms of ischemic colitis vary depending on the severity of the ischemia. The most common early signs of ischemic colitis include abdominal pain (often left-sided), with mild to moderate amounts of rectal bleeding. The sensitivity of findings among 73 patients were:
abdominal pain (78%) lower gastrointestinal tract bleeding (62%) diarrhea (38%) Fever higher than 38 °C (100.4 °F) (34%) Physical examination
abdominal pain (77%) abdominal tenderness (21%)
Causes Ischemic colitis is often classified according to the underlying cause. Non-occlusive ischemia develops because of low blood pressure or constriction of the vessels feeding the colon; occlusive ischemia indicates that a blood clot or other blockage has cut off blood flow to the colon.
Non-occlusive ischemia In hemodynamically unstable patients (i.e. shock) the mesenteric perfusion may be compromised. This condition is commonly asymptomatic, and usually only apparent through a systemic inflammatory response.
Occlusive ischemia Mostly the result of a thromboembolism. Commonly the embolism is caused by atrial fibrillation, valvular disease, myocardial infarction, or cardiomyopathy. In addition, ischemic colitis is a well-recognized complication of abdominal aortic aneurysm repair, when the origin of the inferior mesenteric artery is covered by the aortic graft. In a 1991 review concerning 2137 patients the accidental inferior mesenteric artery ligation was the most common cause (74%) of ischemic colitis. Thus, patients without adequate collateralization are at risk for ischemia of the descending and sigmoid colon. Bloody diarrhea and leukocytosis in the postoperative period are essentially diagnostic of ischemic colitis. The complication can be prevented through careful selection of subjects that may require replanting inferior mesenteric artery (IMA) and completing the pre surgical procedure information with an instrumental evaluation during surgical treatment.
Pathophysiology
Colonic blood supply
The colon receives blood from both the superior and inferior mesenteric arteries. The blood supply from these two major arteries overlaps, with abundant collateral circulation via the marginal artery of the colon. However, there are weak points, or "watershed" areas, at the borders of the territory supplied by each of these arteries, such as the splenic flexure and the rectosigmoid junction. These watershed areas are most vulnerable to ischemia when blood flow decreases, as they have the fewest vascular collaterals. The rectum receives blood from both the inferior mesenteric artery and the internal iliac artery; the rectum is rarely involved by colonic ischemia due to this dual blood supply.
Development of ischemia Under ordinary conditions, the colon receives between 10% and 35% of the total cardiac output. If blood flow to the colon drops by more than about 50%, ischemia will develop. The arteries feeding the colon are very sensitive to vasoconstrictors; presumably this is an evolutionary adaptation to shunt blood away from the bowel and to the heart and brain in times of stress. As a result, during periods of low blood pressure, the arteries feeding the colon clamp down vigorously; a similar process can result from vasoconstricting drugs such as ergotamine, cocaine, or vasopressors. This vasoconstriction can result in non-occlusive ischemic colitis.
Pathologic findings A range of pathologic findings are seen in ischemic colitis, corresponding to the spectrum of clinical severity. In its mildest form, mucosal and submucosal hemorrhage and edema are seen, possibly with mild necrosis or ulceration. With more severe ischemia, a pathologic picture resembling inflammatory bowel disease (i.e. chronic ulcerations, crypt abscesses and pseudopolyps) may be seen. In the most severe cases, transmural infarction with resulting perforation may be seen; after recovery, the muscularis propria may be replaced by fibrous tissue, resulting in a stricture. Following restoration of normal blood flow, reperfusion injury may also contribute to the damage to the colon.
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