Pseudomembranous Colitis

Pseudomembranous colitis is being encountered with increasing frequency as a nosocomial infection complicating antibiotic therapy. This potentially life-threatening disorder is caused by overgrowth of Clostridium difficile and the subsequent release of a cytotoxic enterotoxin, which causes ulceration of the colonic mucosa and the formation of 2-3 mm pseudomembranes consisting of fibrin, mucus, sloughed epithelial cells, and leukocytes. Mild cases may demonstrate only mucosal irregularity and nodularity, with small plaque formation that cannot be detected radi-ologically. In advanced cases, there is thickening of haus-tral folds, a shaggy wall contour, and mucosal plaques.

CT shows a pancolitis with mural thickening that may be irregular or polypoid and have a shaggy endoluminal contour. The wall thickening (Fig. 2), usually 1.6-1.8 cm, is a result of submucosal edema. Mucosal and serosal en-

Fig. 2. Pseudomembranous colitis. There is mural and haustral thickening of the colon associated with submucosal edema (white arrow, enhancing muscularis propria; black arrow, enhancing mucosa)

hancement are seen following intravenous contrast administration. The haustra are also thickened and edema-tous producing an 'accordion pattern', which is highly suggestive of pseudomembranous colitis. This pattern consists of contrast material trapped between thickened haustral folds that are aligned in a parallel fashion. This appearance can sometimes simulate deep ulcerations or fissures. Pericolic stranding, ascites, pleural effusions, and subcutaneous edema are other ancillary CT findings. Complications of untreated pseudomembranous colitis include toxic megacolon and intestinal perforation with subsequent peritonitis. CT is also useful for monitoring the response to medical therapy with oral vancomycin and metronidazole [4, 5].

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