Clostridium Difficile Colitis Follow-up

  • Author: Faten N Aberra, MD; Chief Editor: Julian Katz, MD   more...
 
Updated: Feb 8, 2012
 

Further Inpatient Care

  • The development of dehydration, electrolyte disturbances, and worsening clinical condition may necessitate inpatient management.
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Deterrence/Prevention

C difficile is now recognized as a major nosocomial pathogen, and universal precautions should be implemented. The following guidelines are recommended when dealing with patients with C difficile colitis:

  • Use disposable gloves, laboratory coats, and proper washing techniques.
  • Educate the medical and nursing staff regarding the disease and its epidemiology.
  • The mode of hospital transmission is unclear, but spores survive on inanimate objects. Therefore, close attention to cleanliness and disinfective measures are important.
  • Isolation of patients who are infected is recommended but is often impractical at most hospitals.
  • More aggressive control measures, such as treatment of asymptomatic carriers, might be considered in a severe epidemic.

The most important preventive measure is judicious use of antimicrobial agents.

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Complications

  • Fulminant colitis is a rare form of C difficile infection, occurring in only 3% of patients but accounting for most of the serious complications. These include toxic megacolon, colonic perforation, and death. Surgical intervention may be required. Sailhamer et al conducted a retrospective review of nearly 4800 records of 4796 C difficile colitis patients, of which 199 (4.1%) had fulminant C difficile colitis, as defined by the need for colectomy or admission to the intensive care unit for C difficile colitis.[6] The inhospital mortality rate for fulminant C difficile colitis was 34.7%.The investigators determined independent predictors of mortality included: (1) age 70 years or older, (2) severe leukocytosis or leukopenia or bandemia, and (3)cardiorespiratory failure. The presence of all 3 factors resulted in a 57.1% mortality rate; in the absence of all 3, the mortality rate was 0%.[6] Sailhamer concluded that despite awareness and treatment of fulminant C difficile colitis, this condition remains highly lethal. Thus, reliable predictors of mortality should be used to prompt aggressive surgical intervention.[6] To determine the long-term survival rate, rate of gastrointestinal continuity restoration, and rate of recurrence following an attack of fulminant C difficile colitis, Miller et al searched a pathological database for patients with this condition, defined as those who had a bout of C difficile colitis and whose disease required surgical intervention after failing medical therapy.[7] Of 49 patients who fit the criteria, the investigators found a 30-day mortality rate of 57% (28/49), with an in-hospital mortality rate of 49%. However, the 5-year survival rate for the long-term survival group was poor (38%) (16.3% for all patients). Twenty percent of patients had restored gastrointestinal continuity. One case of recurrence C difficile colitis was reported.
  • Toxic megacolon is diagnosed clinically in a patient with signs and symptoms of severe toxicity, the presence of a tender abdomen, and a dilated colon on plain radiograph of the abdomen.
  • Colonic perforation is usually accompanied by abdominal rigidity, involuntary guarding, rebound tenderness, and absent bowel sounds. Free air may be revealed on abdominal radiographs. Any suspicion of perforation in this setting should prompt immediate surgical consultation.
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Prognosis

  • Most patients with C difficile colitis recover, even without specific therapy. However, persistent diarrhea may be debilitating and can last for several weeks.
  • By using oral metronidazole or vancomycin, response rates greater than 95% are obtained, with symptomatic improvement in as little as 2-3 days and complete resolution in 7-10 days.
  • Approximately 20-27% of patients treated for a first episode of C difficile colitis relapse following successful therapy. Relapse is manifested by return of symptoms, usually occurring within a week of completing treatment.
  • Patients who relapse once are at an even greater risk of further relapses. The relapse rate for those with 2 or more relapses is 65%.
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Contributor Information and Disclosures
Author

Faten N Aberra, MD  Assistant Professor, Department of Medicine, Division of Gastroenterology, University of Pennsylvania School of Medicine

Faten N Aberra, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, Crohns and Colitis Foundation of America, and Sigma Xi

Disclosure: Nothing to disclose.

Coauthor(s)

Craig A Gronczewski, MD  Clinical Assistant Professor, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey; Consulting Staff, Princeton Medical Center; Consulting Staff, Robert Wood Johnson University Hospital

Craig A Gronczewski, MD is a member of the following medical societies: Alpha Omega Alpha and American College of Emergency Physicians

Disclosure: Nothing to disclose.

Jonathan P Katz, MD  Assistant Professor of Medicine, Department of Medicine, University of Pennsylvania School of Medicine

Jonathan P Katz, MD is a member of the following medical societies: American Gastroenterological Association and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Specialty Editor Board

Waqar A Qureshi, MD  Associate Professor of Medicine, Chief of Endoscopy, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine and Veterans Affairs Medical Center

Waqar A Qureshi, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

BS Anand, MD  Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Alex J Mechaber, MD, FACP  Senior Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine

Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD  Clinical Professor of Medicine, Drexel University College of Medicine

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law, Medicine & Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

References
  1. FDA Drug Safety Communication: Clostridium difficile-associated diarrhea can be associated with stomach acid drugs known as proton pump inhibitors (PPIs). US Food and Drug Administration. Available at http://www.fda.gov/Drugs/DrugSafety/ucm290510.htm. Accessed February 8, 2012.

  2. Bauer MP, Notermans DW, van Benthem BH, et al. Clostridium difficile infection in Europe: a hospital-based survey. Lancet. Jan 1 2011;377(9759):63-73. [Medline].

  3. Nylund CM, Goudie A, Garza JM, Fairbrother G, Cohen MB. Clostridium difficile infection in hospitalized children in the United States. Arch Pediatr Adolesc Med. May 2011;165(5):451-7. [Medline].

  4. Guerrero DM, Chou C, Jury LA, et al. Clinical and infection control implications of Clostridium difficile infection with negative enzyme immunoassay for toxin. Clin Infect Dis. Aug 1 2011;53(3):287-90. [Medline].

  5. Louie TJ, Miller MA, Mullane KM, et al. Fidaxomicin versus vancomycin for Clostridium difficile infection. N Engl J Med. Feb 3 2011;364(5):422-31. [Medline].

  6. Sailhamer EA, Carson K, Chang Y, et al. Fulminant Clostridium difficile colitis: patterns of care and predictors of mortality. Arch Surg. May 2009;144(5):433-9; discussion 439-40. [Medline].

  7. Miller AT, Tabrizian P, Greenstein AJ, et al. Long-term follow-up of patients with fulminant Clostridium difficile colitis. J Gastrointest Surg. May 2009;13(5):956-9. [Medline].

  8. Bartlett JG. Pseudomembranous enterocolitis and antibiotic-associated colitis. In: Feldman M, Scharschmidt BF, Sleisenger MH, eds. Sleisenger and Fordtran's Gastrointestinal and Liver Disease. 6th ed. Philadelphia, Pa:. WB Saunders Co;1998:1633-1647.

  9. Cleary RK. Clostridium difficile-associated diarrhea and colitis: clinical manifestations, diagnosis, and treatment. Dis Colon Rectum. Nov 1998;41(11):1435-49. [Medline].

  10. Fekety R. Guidelines for the diagnosis and management of Clostridium difficile- associated diarrhea and colitis. American College of Gastroenterology, Practice Parameters Committee. Am J Gastroenterol. May 1997;92(5):739-50. [Medline].

  11. Gilbert DN, Moellering RC, Sande MA. The Sanford Guide to Antimicrobial Therapy. 13th ed. Hyde Park, Vt:. Antimicrobial Therapy;2000:12.

  12. Johnson S, Gerding DN. Clostridium difficile--associated diarrhea. Clin Infect Dis. May 1998;26(5):1027-34; quiz 1035-6. [Medline].

  13. Jones EM, Kirkpatrick BL, Feeney R. Hospital-acquired Clostridium difficile diarrhoea. Lancet. Apr 19 1997;349(9059):1176-7. [Medline].

  14. Kelly CP, LaMont JT. Clostridium difficile infection. Annu Rev Med. 1998;49:375-90. [Medline].

  15. Kelly CP, LaMont JT. Clostridium difficile--more difficult than ever. N Engl J Med. Oct 30 2008;359(18):1932-40. [Medline].

  16. Kelly CP, Pothoulakis C, LaMont JT. Clostridium difficile colitis. N Engl J Med. Jan 27 1994;330(4):257-62. [Medline].

  17. Lyerly DM, Wilkins TD. Clostridium difficile. Infections of the Gastrointestinal Tract. 1995;867-891.

  18. McDonald CL, Gerding DN, Johnson S,. "Clostridium difficile: Changing Diagnosis, Epidemiology, and Treatment" The content of this virtual lecture is derived from a satellite symposium presented on April 7, 2008, during the 18th Annual SHEA Scientific Meeting. Available at http://www.rmei.com/CDI010/.

  19. McFarland LV, Mulligan ME, Kwok RY. Nosocomial acquisition of Clostridium difficile infection. N Engl J Med. Jan 26 1989;320(4):204-10. [Medline].

  20. Schneeweiss S, Korzenik J, Solomon DH, et al. Infliximab and other immunomodulating drugs in patients with inflammatory bowel disease and the risk of serious bacterial infections. Aliment Pharmacol Ther. Aug 2009;30(3):253-64. [Medline].

  21. Sonnenberg A. Similar geographic variations of mortality and hospitalization associated with IBD and Clostridium difficile colitis. Inflamm Bowel Dis. Jul 27 2009;epub ahead of print. [Medline].

  22. Starr J. Clostridium difficile associated diarrhoea: diagnosis and treatment. BMJ. Sep 3 2005;331(7515):498-501. [Medline].

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Endoscopic visualization of pseudomembranous colitis, a characteristic manifestation of full-blown Clostridium difficile colitis. Classic pseudomembranes are visible as raised yellow plaques ranging from 2-10 mm in diameter and scattered over the colorectal mucosa. Courtesy of Gregory Ginsberg, MD, University of Pennsylvania.
 
 
 
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