Clostridium difficile Colitis

Published on 26/03/2015 by admin

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Last modified 26/03/2015

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146 Clostridium difficile Colitis

Antibiotic-associated colitis was recognized soon after antibiotics were introduced in the 1940s, but the cause was not known until 1978 with the original reports of the role of Clostridium difficile as the putative agent in nearly all cases of antibiotic-associated pseudomembranous colitis and 10% to 15% of those with uncomplicated antibiotic-associated diarrhea.1 Subsequent work has identified the pathophysiology, epidemiology, diagnostic methods, and treatment for this condition. The major challenges continue to be prevention and the management of patients with advanced disease, particularly those with ileus.

image Pathophysiology

There are six relevant issues:

2 Toxin production: C. difficile produces two toxins, designated toxin A and toxin B.5 Early studies implicated toxin A as the major cause of enteric toxin based on animal studies that showed florid colitis with injection of toxin A into bowel loops, but more recent studies establish that toxin B is critical for clinical expression.5 Most strains of C. difficile produce both toxins, but about 1% to 2% produce only toxin B.6
4 Epidemiology: C. difficile is relatively infrequent in ambulatory persons, but rates of colonization and disease are much higher as a result of exposure to the hospital environment.3 C. difficile now represents an important and potentially lethal nosocomial pathogen. Nursing homes are another setting in which there is clustering of vulnerable patients with high rates of antibiotic use where C. difficile may be endemic or epidemic.6 In the period 2001-2006, the NAP-1 strain emerged as an important epidemic agent of C. difficile in Canada, the United States, and Europe.4,6 This strain appears to be particularly virulent, with increased toxin production, mortality, treatment failure, and relapses.

image Clinical Signs and Symptoms

The typical presentation of Clostridium difficile infection (CDI) is watery diarrhea associated with cramps.2 Other common features are fecal leukocytes, endoscopy showing PMC or colitis, characteristic changes on computed tomography (CT) (thickened bowel restricted to the colon, often associated with ascites), fever, hypoalbuminemia, and leukocytosis, sometimes with a leukemoid reaction. Nearly all cases of CDI are associated with diarrhea, but occasional postoperative patients will not have this owing to ileus. The laboratory clue that best predicts this diagnosis and its severity is the white blood cell (WBC) count. The average is about 15,000 cells/mL, but it may be much higher with counts over 20,000 or even 50,000 cells/mL. This strongly supports the CDI diagnosis and predicts severe disease.8

image Treatment

Most important to treatment of CDI is discontinuing the implicated antibiotic. If there is a need for antibiotic treatment, select a drug that is unlikely to cause CDI (narrow-spectrum β-lactams, macrolides, aminoglycosides, antistaphylococcal drugs, tetracyclines; Table 146-2). The two favored drugs for treatment of CDI are metronidazole and vancomycin, both given by mouth.1,6,7 Metronidazole is often preferred because it is less expensive. Earlier studies showed it to work as well as vancomycin, but more recent trials show oral vancomycin is superior to metronidazole in seriously ill patients,8 defined as having a WBC over 15,000 cells/mL or elevated creatinine to 1.5 × baseline.6

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