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E4606. A Comprehensive Imaging Review of Stercoral Colitis: Complications, Pearls and Pitfalls
Authors
  1. Soumyadeep Ghosh; Massachusetts General Hospital
  2. Nabih Nakrour; Massachusetts General Hospital
  3. Priyanka Prajapati; Massachusetts General Hospital
  4. Debra Gervais; Massachusetts General Hospital
  5. Francis Scholz; Massachusetts General Hospital
  6. Avinash Kambadakone; Massachusetts General Hospital
  7. Mukesh Harisinghani; Massachusetts General Hospital
Background
Stercoral colitis is a form of ischemic colitis that develops when hard stool distends the lumen and exerts pressure on the veins in the wall, impeding venous outflow. The arteries are less susceptible to compression, continuing to pump blood in, causing mural edema. If unrelieved by enema or laxatives, stercoral ulcerations will develop in the swollen wall, and eventually, the colon will perforate. Stercoral colitis is most apparent (and prone to perforations) in the sigmoid colon because hard stool cannot be pushed around the curves of the sigmoid. The rectum is the second most common site but less frequently perforated. The cecum can occasionally perforate from being distended by a long segment of distal stool.

Educational Goals / Teaching Points
To illustrate the imaging findings of uncomplicated stercoral colitis. Consider the possibility of “Stool extrusion” in the appropriate clinical setting. Apprise the radiologist of the spectrum of associated complications. Pearls and pitfalls in diagnosing its mimics.

Key Anatomic/Physiologic Issues and Imaging Findings/Techniques
Fecal impaction leading to colonic obstruction is seen primarily in the elderly, commonly in nursing homes or in neurologically impaired young patients. There is a well-known association with drugs that prolong bowel transit, such as opiates, tricyclic antidepressants, and tranquilizers. A history of chronic constipation is inevitably found in approximately 60% of patients presenting with fecal impaction. The three most common locations for stercoral ulceration are the anterior high rectum, the rectosigmoid junction at the antimesenteric border, and the apex of the sigmoid colon. Most cases are described as occurring on the antimesenteric side of the bowel wall, plausibly explained by the fact that the bowel is vascularized from the mesenteric side and blood supply is relatively poor on the antimesenteric side, predisposing to ischemia. Although the diagnosis of fecal impaction is usually straightforward, several findings on CT should suggest associated stercoral colitis. In uncomplicated fecal impaction, the colon is distended, and the wall is thin. There is usually a focal colonic wall thickening in cases of stercoral ulceration, likely representing edema from the ischemia and ulceration. Associated peri colonic fat stranding in a colonic segment showing fecal impaction suggests colonic edema or ischemia. The presence of extraluminal air or an abscess indicates that perforation has already occurred.

Conclusion
Fecal impaction may cause ischemic pressure necrosis and, as a result, colonic perforation. In the appropriate clinical setting, the imaging findings that should help the radiologist maintain a low threshold for entertaining this diagnosis are the presence of fecal impaction, focal colonic wall thickening, and adjacent fat stranding. If the fecal impaction is not promptly treated, the condition can deteriorate, progressively resulting in colonic perforation, peritonitis, and death.