Although blood loss from sustained hemorrhage may be the most common complication of the illness, toxic megacolon is an associated clinical entity that must not be missed.

Toxic megacolon develops in advanced cases of colitis when the disease process begins to extend through all layers of the colon. The result is a loss of muscular tone within the colon, with dilatation and localized peritonitis. If the colon continues to dilate without treatment, signs of toxicity will develop. Plain radiography of the abdomen demonstrates a long, continuous segment of air-filled colon greater than 6 cm in diameter (see Fig 7.7.-1). Loss of colonic haustra and "thumbprinting,"

representing bowel wall edema, may also be seen. The distended portion of the atonic colon can perforate, causing peritonitis and septicemia. Mortality from this complication is approximately 50 percent if perforation occurs but less than 10 percent if surgery is undertaken prior to perforation. 7

FIG. 77-1. Long, continuous colonic loop in toxic megacolon.

A patient with toxic megacolon appears severely ill; the abdomen is distended, tender, and tympanitic. Severe diarrhea (more than 10 bowel movements per day) is often seen. Fever, tachycardia, and signs of hypovolemia are typically part of the clinical picture. Leukocytosis, anemia, electrolyte disturbances, and hypoalbuminemia are the supporting laboratory data.

Some of the more prominent features of toxic megacolon, such as leukocytosis and peritonitis, can be masked in the patient taking corticosteroids. When such therapy is being administered, greater suspicion is required to make the diagnosis. Antidiarrheal agents, hypokalemia, narcotics, cathartics, pregnancy, enemas, and recent colonoscopy have been implicated as precipitating factors in toxic megacolon. Medical therapy with nasogastric suction, intravenous prednisolone 60 mg/day or hydrocortisone 300 mg/day, parenteral antibiotics active against coliforms and anaerobes (ampicillin and clindamycin), and intravenous fluids should be attempted as initial therapy and in preparing the patient for possible surgery. However, prolonged medical treatment of these patients increases mortality; therefore, early surgical consultation must be sought with the aim of performing a colectomy if clinical improvement is not noted in 24 to 48 h with medical treatment.

The fistulas that constitute a hallmark of Crohn's disease occur infrequently in cases of ulcerative colitis. Perirectal fistulas and abscesses are much more common in patients with Crohn's disease but may occur in up to 20 percent of patients with ulcerative colitis. 8 Massive gastrointestinal hemorrhage, obstruction secondary to stricture formation, and acute perforation are other complications of the disease.

There is a 10- to 30-fold increase in the development of carcinoma of the colon in patients with ulcerative colitis. Carcinoma of the colon is the cause of 5 to 15 percent of the deaths attributed to ulcerative colitis. The major risk factors for the development of carcinoma of the colon are extensive involvement and prolonged duration of the disease. The cumulative risk of cancer after 20 and 30 years is 5 to 10 and 12 to 20 percent, respectively. Additional factors that increase the risk of cancer in patients with ulcerative colitis include early onset of the disease and a family history of colon cancer. The availability of fiberoptic colonoscopy allows surveillance of ulcerative colitis patients with periodic colonoscopies and biopsies to detect the high-grade dysplasia thought to predict the development or association of colon cancer. In patients with pancolitis, such surveillance should start 8 to 10 years after the onset of the disease. 9

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