Clostridium difficile colitis, also known as pseudomembranous colitis, is a common cause of antibiotic-associated diarrhea, and increasingly encountered in sick hospitalised patients. If undiagnosed and untreated, it continues to have high mortality. It may be classified as a form of infectious colitis.
C. difficile infection is usually preceded by antibiotic use or chemotherapy and is therefore usually encountered in unwell, hospitalised patients with significant comorbidity.
Typically, patients present with diarrhea, fever, raised white cell count, and abdominal pain with distension.
Clostridium difficile is a gram-positive anaerobic bacterium which is not a normal bowel commensal, but rather colonizes the bowel after the normal colonic biology has been disrupted. This is typically due to antibiotic use or chemotherapy within 6 weeks of presentation 1. C. difficile produces two toxins (A and B) which have both cytotoxic and enterotoxic effects on the bowel. Clinical manifestation is thought to be predominantly due to toxin B 4.
An exudate composed of fibrin, white cells and cellular debris forms a pseudomembrane on the mucosa of the colon, which is characteristic 1. Definitive diagnosis is made by isolating C. difficile toxin in the stool sample.
Early in the disease, few findings may be evident on abdominal radiographs. Bowel dilatation, mural thickening and thumbprinting (due to thickening of the haustral folds) are seen later. Eventually, in untreated or fulminant cases, appearances will be those of toxic megacolon 3, with subsequent perforation and free intraperitoneal gas.
The most common feature is a pronounced increase in wall thickness of the involved segment of colon, usually the rectosigmoid region, with variable, continuous proximal extension. The mucosa will often be discontinuous and seemingly redundant, representing the mucosal ulceration and presence of pseudo-membranous debris, retrospectively. Luminal collapse is also sometimes observed. If interrogated with Doppler, the bowel wall will demonstrate preserved vascularity. The haustral folds will be present, and may be unusually thick and conspicuous. Free fluid is typically found between bowel loops, and typically assumes a complex, heterogeneously echoic appearance 9.
Barium studies demonstrate the same findings as plain radiography. Additionally, the pseudomembrane may be visible on double contrast studies. The role of barium enema has significantly reduced in its use for the diagnosis of this entity due to the availability of CT and the risk of perforation 2.
Findings include 2:
- bowel wall thickening (most common)
- accordion sign
- shaggy mucosal outline
- pericolic stranding: is present but minimal as it is mainly a mucosal disease
- peritoneal free fluid (ascites) is seen in up to 40% of cases 8
- although typically the whole colon is involved, the right colon and transverse colon may be affected in isolation in up to 5% of cases 2
- rectal involvement in the vast majority of cases (90-95%) 2
Treatment and prognosis
Treatment involves supportive therapy (fluid and electrolyte replacement) and eradication of C. difficile with antibiotics (usually vancomycin or metronidazole) 5.
A novel treatment option is that of fecal transplant, whereby 'healthy' fecal matter is either administered via nasogastric tube or directly into the colon, after having been donated by a family member 5.
Untreated pseudomembranous colitis carries a high mortality from the sequelae of toxic megacolon and perforation.
Other causes of toxic megacolon and colitis include:
- neutropenic colitis
- inflammatory bowel disease
- ischemic colitis
- radiation-induced colitis
- colonic lymphoma: also causes thumbprinting
If there is a history of bone marrow transplantation and the bowel involvement is not limited to the colon, consider:
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