Ischemic colitis: a clinical review.

Abstract: Ischemic colitis is the most common form of intestinal ischemia. It manifests as a spectrum of injury from transient self-limited ischemia involving the mucosa and submucosa to acute fulminant ischemia with transmural infarction that may progress to necrosis and death. Although there are a variety of causes, the most common mechanism is an acute, self-limited compromise in intestinal blood flow. Patients typically have mild abdominal pain and tenderness over the involved segment of bowel. There is usually passage of blood mixed with stool, but hemodynamically significant bleeding is unusual. Although computed tomography may have suggestive findings, colonoscopy is the procedure of choice for diagnosis. Supportive care with intravenous fluids, optimization of hemodynamic status, avoidance of vasoconstrictive drugs, bowel rest, and empiric antibiotics will produce clinical improvement within 1 to 2 days in most patients. Twenty percent of patients will have development of peritonitis or may deteriorate despite conservative management and will require surgery.

Key Words: colon, hematochezia, intestinal ischemia

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Ischemic colitis is the most common form of intestinal ischemia, and accounts for 1 in 1,000 hospitalizations. (1) Although frequent in the elderly, younger patients may also be affected. Clinically, it manifests as a spectrum of injury from transient self-limited ischemia involving the mucosa and submucosa, carrying a good prognosis, to acute fulminant ischemia with transmural infarction, which may progress to necrosis and death. Colon ischemia was first described as caused by ligation of the inferior mesenteric artery during aortic reconstruction or colon resection but is now recognized to have many potential causes. (2,3) The diverse causes, variable clinical presentations, and severity makes the diagnosis and management of ischemic colitis a challenge.

Blood Supply of the Colon

An understanding of the blood supply to the colon is necessary when considering ischemic colitis. The colon is perfused by the superior mesenteric artery (SMA), the inferior mesenteric artery (IMA), and branches of the internal iliac arteries. (4-6) The SMA gives rise to the middle colic, right colic, and ileocolic arteries, which supply the right colon and the right half of the transverse colon. The IMA branches into the left colic, sigmoid, and superior rectal (hemorrhoidal) arteries, which supply the left half of the transverse colon to proximal rectum. The distal rectum is supplied by inferior and middle rectal (hemorrhoidal) arteries, which are branches of the internal iliac artery. (5) There is an extensive mesenteric collateral circulation that provides substantial protection from ischemic insults. The SMA and IMA communicate through the marginal artery of Drummond, which runs along the splenic flexure and the arc of Riolan. The marginal artery of Drummond is absent or underdeveloped in 5% of the population, placing the splenic flexure at particular risk of ischemia. If SMA or IMA is gradually occluded, the arc of Riolan or the central anastomotic artery may dilate to compensate and be termed the "meandering artery." (7) The IMA and the internal iliac arteries communicate through the superior and middle/inferior rectal (hemorrhoidal) arteries. (8) The dual blood supply of the rectum from the mesenteric and iliac arteries makes it resistant to ischemia.

Pathophysiology

Although the incidence of ischemic colitis is increased in the elderly and many with risk factors for vascular disease, an index lesion on angiography is unusual. When present, abnormalities may include narrowing of small vessels and tortuosity of the long colic arteries. (9) Rather than a specific vascular lesion, there appears to be an acute, self-limited compromise in intestinal blood flow, which is inadequate for meeting the metabolic demands of the colon. (10) Diffuse disease of small, segmental vessels probably renders the colon susceptible to ischemic insults in certain patients. The colon is also predisposed to ischemia by its relatively low blood flow compared with the rest of the gastrointestinal tract. (11-13)

Colonic perfusion is also affected by the functional motor activity of the colon and by patient straining from constipation. (12) Of note, chronic constipation was found in one study (14) to be strongly associated with ischemic colitis. Experimental distension has been found to increase intraluminal pressure, reduce total blood, and reduce the arteriovenous oxygen gradient in the colonic wall. (15) This probably is the mechanism for the rare occurrence of ischemic colitis during colonoscopy or barium enema. (16,17) The colonic microvasculature plexus is also less well developed and embedded in a relatively thicker wall compared with the small bowel. (13) The vasa recta (end-vessels that provide blood directly to the bowel wall) are smaller and less developed in the right colon compared with the left colon. (17) The vasa recta are particularly sensitive to vasospasm, and collateral blood flow at this level is sparse. (18) This may explain the susceptibility of the right colon to ischemia from low flow states. (1) The "watershed" areas of the colon (the splenic flexure and rectosigmoid junction) have more limited collateral networks and are also vulnerable to low flow states. (13,19,20) In a study of more than 1,000 cases, the left colon was involved in 75% of cases, with 23% involving the splenic flexure specifically. (21) The right colon was involved in only 8% of cases; however, its involvement has ranged from 12% to 47% in more recent series. (22-25)

Underlying Causes

There are numerous conditions that predispose patients to ischemic colitis (Table 1). The most common mechanism is hypotension from sepsis or impaired left ventricular function and hypovolemia from dehydration or hemorrhage producing a compromise in systemic perfusion and triggering a reflex mesenteric vasoconstriction. The colon is more susceptible to these insults than the remainder of the gastrointestinal tract for the reasons previously stated. A low flow state often precipitates colonic ischemia in the setting of preexisting mesenteric microvascular atherosclerosis; however, it may produce colonic ischemia by itself when mesenteric vasoconstriction is profound. The colon and particularly the "watershed areas" are susceptible to such insults as the result of the previously described characteristics. Numerous medications may produce colonic ischemia by a similar mechanism (Table 2). (26-31) The most common offenders are anti-hypertensive agents, diuretics, nonsteroidal anti-inflammatory drugs, digoxin, oral contraceptives, pseudoephedrine, cocaine, and alosetron. Strenuous physical activities, such as long distance running or bicycling, have been reported to lead to colonic ischemia, presumably by physiologic shunting caused by mesenteric vasoconstriction and intravascular volume depletion from dehydration. (32) Ischemic colitis was first described in relation to vascular surgeries and continues to be a potential complication of aortic or cardiac bypass surgery. Aortic surgery is associated with a 1% to 7% incidence of ischemic colitis, often caused by iatrogenic IMA ligation or intraoperative hypoperfusion in patients with chronic IMA occlusion, and usually affects the distal left colon. (33-36) Colonic ischemia after endovascular abdominal aortic aneurysm stenting has also been reported. (37) The incidence of colonic ischemia after cardiopulmonary bypass is under 0.2% but carries a high death risk (approximately 85%). (38) Rarely, colonic ischemia may be produced by intraoperative vascular trauma during colonic surgery. (39) Colonic obstruction from tumors, adhesions, volvulus, diverticulitis, or intestinal prolapse are infrequent causes of ischemic colitis. (40,41) Colonic ischemia after barium impaction has also been reported. (42) Inherited or acquired thrombophilias, including deficiencies of protein C and S, antithrombin III, and the anticardiolipin syndrome, have been found to occur in as many as 74% of patients with colonic ischemia, although causality has not been established. (43-46) Yet to be explained is why younger individuals with these disorders do not tend to become afflicted or why the recurrence rates of ischemic colitis are low.

Clinical Presentation

Most patients will present with the acute onset of a mild, crampy abdominal pain and tenderness over the affected bowel. An urge to defecate is common. Within 24 hours, there is usually passage of bright red or maroon blood, often mixed with stool. Blood loss is usually minimal, without hemodynamic compromise or the need for transfusion. (12,20) Hemodynamically significant bleeding should prompt consideration of other diagnoses such as diverticula or angioectasia. Anorexia, nausea, vomiting, or abdominal distension may be present as the result of an associated ileus. About 15% of patients will have peritoneal signs caused by transmural infarction and necrosis. (20) Although laboratory studies will be normal in mild cases, severe ischemia or necrosis may produce leukocytosis, metabolic acidosis, or an elevated lactate.

Diagnosis

The diagnosis of ischemic colitis depends on characteristic findings in the appropriate clinical setting. Although laboratory markers of ischemia such as serum lactate, lactate dehydrogenase, alkaline phophatase, and systemic acidosis may be present, they are uncommon in mild ischemia and not present in severe ischemia until late in the course. Plain abdominal radiographs are generally insensitive and nonspecific, but they are important to exclude other disorders. They often show generalized bowel distension and air-filled bowel loops. In one series, abnormal findings were present in 21% of patients and included thumbprinting, air-filled loops, colonic aperistalsis, mural thickening, and exhausted bowel. (47) Barium enema may show suggestive findings in up to 75% of patients with ischemic colitis. (48-50) Thumbprinting is the most common finding, but it is nonspecific and is present in many forms of infective or inflammatory colitis. (47) Other findings include longitudinal ulcers, eccentric mural deformity, sacculation, and transverse ridging. (48)

Colonoscopy has largely supplanted barium enema as the diagnostic modality of choice because of its higher sensitivity for detecting mucosal changes and the ability to obtain biopsy specimens if necessary. Barium enema also makes the later use of angiography or endoscopy more difficult because of residual contrast. Care should be taken to avoid overinflation or advancement of the colonoscope beyond the affected region to minimize the risk of bowel perforation. The findings at colonoscopy will depend on the stage and severity of ischemia. In the early stages of ischemia, petechial hemorrhages are interspersed with areas of pale, edematous mucosa. Later, segmental erythema, with or without ulcerations and bleeding, may be observed. The colon single-stripe sign, a single longitudinal ulcerated or inflamed colon strip, may characterize milder disease. (53) With more severe ischemia, the mucosa appears cyanotic, dusky, gray, or black. Pseudopolyps and pseudomembranes may be appreciated, as well. A chronic stage of ischemia characterized by stricture, decreased haustrations, and mucosal granularity may occur several weeks or months later. (54) There are no endoscopic findings that are specific for ischemia, thus the clinical setting must be considered. Findings that favor ischemic colitis rather than inflammatory bowel disease are segmental area of injury, abrupt transition between normal and affected mucosa, rectal sparing, and a rapid resolution of mucosal changes on serial colonoscopy. (55) A more limited examination with flexible sigmoidoscopy is appropriate in certain circumstances. For example, when colonic ischemia is suspected after aortic surgery or aortic aneurysm rupture, the left colon is almost always affected, and colonoscopy may be dangerous in such critically ill patients. (51,52) In most situations, colonoscopy is preferred because 30% to 40% of cases of ischemia occur proximal to the splenic flexure and will be missed with sigmoidoscopy. This is particularly important because ischemia isolated to the right colon may carry a worse prognosis. (56)

The histologic changes of ischemic colitis are nonspecific and include edema, distorted crypts, mucosal and submucosal hemorrhage, inflammatory infiltration, granulation tissue, intravascular platelet thrombi, and necrosis. (57) Patients with inflammatory bowel disease will usually have less crypt damage and more inflammation. (58) The presence of a hyalinized, hemorrhagic lamina propria and full-thickness mucosal necrosis may help to differentiate pseudomembranous colonic ischemia from Clostridium difficile colitis. (59)

Computed tomography is often used in the evaluation of patients with abdominal pain and may have suggestive findings in up to 89% of patients with ischemic colitis. (60) The most common finding is segmental circumferential wall thickening. Pneumatosis suggests transmural ischemia or infarction.

The major mesenteric vessels are usually patent in ischemic colitis and therefore angiography is usually not indicated. Exceptions are when acute mesenteric ischemia is being considered or during isolated right colon ischemia, which may occur from an occlusion of the ileocolic branch of the SMA.

An area of debate is the utility of searching for cardiac sources of embolization in patients with ischemic colitis. Although not routinely recommended by most authorities, a recent study found that electrocardiography, rhythmic Holter monitoring over 24 hours, and transthoracic echocardiography identified cardiac sources of embolism in 43% of ischemic colitis patients versus 23% of age- and sex-matched control subjects. (61) Conditions mandating anticoagulation, such as atrial fibrillation or dilated cardiomyopathy, were identified in 32% of case patients. Conditions requiring antiarrhythmic therapy were identified in 25% of case patients.

Treatment

Treatment of the patient is dictated by the severity of the ischemia. In the absence of colonic gangrene or perforation, supportive care is appropriate. Patients should be placed on bowel rest and given intravenous fluids to ensure adequate colonic perfusion. Optimization of cardiac function and oxygenation is important. Empiric broad-spectrum antibiotics are often administered in patients with moderate to severe colitis to minimize bacterial translocation and sepsis. Although there is a lack of prospective, clinical data on humans, this practice is generally justified because of the difficulty in predicting who will progress to gangrenous colitis. (62) A nasogastric tube should be placed if an ileus is present. A rectal tube may also be helpful if the colon is distended. In critically ill patients with uncertain hemodynamic status, Swan-Ganz catheterization may assist in guiding fluid status and cardiac function. Any medications that are associated with ischemia should be withheld (Table 2). Careful monitoring is necessary for signs of necrosis, such as persistent fever, leukocytosis, peritoneal irritation, or protracted pain or bleeding. Serial abdominal radiographs may be helpful if colonic distension or thumbprinting are present. Cathartics should be avoided because they may rarely precipitate colonic perforation. (20,54) Most patients with ischemic colitis will clinically improve within 24 to 48 hours, and endoscopic and radiologic abnormalities resolve within several weeks.

Approximately 20% of patients with ischemic colitis will require surgery because of peritonitis or clinical deterioration despite conservative management (Table 3). (19,22) At laparotomy, all affected bowel should be resected, and the mucosa of the specimen should be examined in the operating room to ensure normal surgical margins. (63) Questionably viable areas of colon are generally resected unless extensive areas of small and large bowel are affected, in which case these areas are left intact and a second-look operation is planned 12 to 24 hours later. (64) Primary anastomosis is usually not performed because of the risk of anastomotic leaks. (13) A colostomy is formed with the proximal colonic loop and the distal loop is either exteriorized as a mucous fistula or closed to form a Hartman pouch. (20) Despite resection, the mortality rates exceed 50% in those with infarcted bowel. (21,25,65)

Conclusions

Ischemic colitis occurs as the result of a compromise in intestinal blood flow that can produce a spectrum of injury from transient self-limited ischemia to fulminant ischemia or transmural infarction. Its diagnosis requires a high index of suspicion, and the clinician should consider the diagnosis in patients with acute abdominal pain and bloody stools. Although most patients improve within several days with supportive care, others will require laparotomy with bowel resection.

There are some experiences in life which should not be demanded twice
from any man, and one of them is listening to the Brahms Requiem.
--George Bernard Shaw

Table 1. Conditions that predispose to ischemic colitis

Cardiac failure or dysrhythmias
Shock (sepsis, hemorrhagic, hypovolemic)
Strenuous physical activities, ie long-distance running
Arterial thrombus
Cholesterol emboli
Inferior mesenteric artery thrombosis
Mechanical colonic obstruction
  Tumors
  Adhesions
  Volvulus
  Strangulated hernia
  Diverticulitis
  Intestinal prolapse
Hypercoagulable states
  Protein C and S deficiencies
  Antithrombin III deficiency
  Anticardiolipin syndrome
Vasculitis
  Systemic lupus erythematosus
  Polyarteritis nodosa
  Wegner granulomatosis
  Rheumatoid arthritis
  Takayasu arteritis
  Thromboangitis obliterans
Iatrogenic surgical/procedural causes
  Aneurysmectomy
  Aortic surgery
  Coronary artery bypass surgery
  Colonic surgery
  Colonoscopy
  Barium enema
  Gynecologic surgery
Sickle cell disease
Hemodialysis
Thrombotic thrombocytopenia purpura
Airplane flights
Intra-abdominal inflammatory diseases
Schistososmiasis
Aortic dissection
Ruptured ectopic pregnancy
Trauma

Table 2. Medications associated with ischemic colitis

Antihypertensive agents
Cocaine
Diuretics
Nonsteroidal anti-inflammatory agents
Digoxin
Estrogens
Oral contraceptives
Vasopressin
Pseudoephedrine
Alosetron
Danazol
Sumatriptans
Psychotropic drugs
Amphetamines

Table 3. Indications for surgery in ischemic colitis

Peritoneal signs (perforation, fulminant colitis, gangrene)
Persistant fever or sepsis
Persistent symptoms beyond 2-3 weeks
Symptomatic strictures
Chronic protein-losing colopathy

Accepted June 22, 2004.

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RELATED ARTICLE: Key Points

* The most common mechanism of ischemic colitis is an acute, self-limited compromise in intestinal blood, which is inadequate for meeting the metabolic demands of a region of the colon.

* Patients typically have abdominal pain and tenderness over the affected segment of bowel (usually the left colon) followed by the passage of blood mixed with stools.

* In contrast to small-bowel ischemia (mesenteric ischemia), a focal lesion on visceral angiography is unusual.

* Although computed tomography may have suggestive findings, colonoscopy is the diagnostic modality of choice and is safe when performed carefully.

* Most patients will respond to supportive care with intravenous fluids, optimization of hemodynamic status, avoidance of vasoconstrictive drugs, bowel rest, and empiric antibiotics within 1 to 2 days; however, 20% of patients will require surgery because of peritonitis or clinical deterioration.

Bryan T. Green, MD, and David A. Tendler, MD

From the Division of Gastroenterology, Duke University Medical Center, Durham, NC.

Reprint requests to Dr. Bryan T. Green, Digestive Diseases Group 103 Liner Drive, Greenwood, SC 29646. E-mail: [e-mail]