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Pseudomembranous Colitis, Surgical Treatment

Author: Said Fadi Yassin, MD, Assistant Professor of Surgery, Department of Cardiothoracic Surgery, University of New Mexico School of Medicine
Contributor Information and Disclosures

Updated: Apr 7, 2009

Introduction

Pseudomembranous colitis is an inflammatory disease of the colon. (See image below and Image 1.) It has changed in the last 100 years from a fatal disease caused by a postoperative event to, in the era of antibiotics, a commonly occurring complication of antibiotic use that may lead to serious morbidity but that usually is treated easily.

  • In the late 1800s, prior to the availability of antibiotics, Finney reported the first case of pseudomembranous colitis, calling it "diphtheritic colitis."1
  • Hall and O'Toole first described Clostridium difficile in 1935.2
  • C difficile was first implicated as a causative factor in pseudomembranous colitis in the 1970s.
Colonic pseudomembranes of pseudomembranous colit...

Colonic pseudomembranes of pseudomembranous colitis. Photographs courtesy of Eric M. Osgard, MD.

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Colonic pseudomembranes of pseudomembranous colit...

Colonic pseudomembranes of pseudomembranous colitis. Photographs courtesy of Eric M. Osgard, MD.


Problem

Pseudomembranous colitis is an acute inflammatory disease of the colon that in mild cases may appear as minimal inflammation or edema of the colonic mucosa. In more severe cases, the mucosa often is covered with loosely adherent nodular or diffuse exudates. These raised exudative plaques are 2-5 mm in size. Coalescence of these plaques generates an endoscopic appearance of yellowish pseudomembranes lining the colonic mucosa. (See images below and Images 2-4.)

Endoscopic visualization of pseudomembranous coli...

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

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Endoscopic visualization of pseudomembranous coli...

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


Gross pathology specimen from a case of pseudomem...

Gross pathology specimen from a case of pseudomembranous colitis revealing characteristic yellowish plaques.

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Gross pathology specimen from a case of pseudomem...

Gross pathology specimen from a case of pseudomembranous colitis revealing characteristic yellowish plaques.


Gross pathology specimen from a case of pseudomem...

Gross pathology specimen from a case of pseudomembranous colitis, again demonstrating characteristic yellowish plaques.

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Gross pathology specimen from a case of pseudomem...

Gross pathology specimen from a case of pseudomembranous colitis, again demonstrating characteristic yellowish plaques.


Frequency

Incidence of antibiotic-associated diarrhea varies from 5-39% depending on the antibiotic type. Pseudomembranous colitis complicates 10% of the cases of antibiotic-associated diarrhea. C difficile is found in the stool of 15-25% of asymptomatic, antibiotic-treated, hospitalized adults. Similar numbers were found in debilitated patients and in patients who received 1 dose of prophylactic antibiotics before surgical procedure.

C difficile is an unusual component of healthy bowel flora. It is found in 3-5% of healthy adults; however, as many as 50% of infants and children harbor the bacteria and its toxins. Pseudomembranous colitis is a surprisingly rare disease in infants and young children—a population recognized as frequent asymptomatic colonizers. The low incidence of colitis in the pediatric population is attributed to the strength of the immune system. Antibodies to C difficile frequently are detected in infected young patients.

Twenty-five percent of human C difficile isolates are nontoxigenic. C difficile colitis is the fourth most common nosocomial disease reported to the Centers for Disease Control and Prevention. C difficile is one of the most frequently isolated enteric pathogens, second only to Campylobacter jejuni.3

High-risk populations4 include elderly people, patients in the intensive care unit (ICU), people with uremia, people with burns, people undergoing abdominal surgery, women undergoing cesarean delivery, and patients with cancer. One suggestion is that these patients do not have greater susceptibility to the disease but are at heightened risk of nosocomial infection. C difficile can be transmitted nosocomially, via the hands of personnel or by contaminated objects. It can survive in spore form for as long as 5 months on hospital floors.

For prevention, use antibiotics prudently. Wash hands and use examination gloves routinely. Clean potentially contaminated surfaces. Use glutaraldehyde disinfection of instruments that come into contact with gastrointestinal secretions. Enteric isolation of patients at risk is recommended. Treatment of asymptomatic carriers is not recommended, because treatment may prolong carriage, which usually resolves spontaneously.

Etiology

  • Pseudomembranous colitis usually is associated with antibiotic use, which may alter the balance of normal gut flora and allow overgrowth of certain organisms.5
  • C difficile, a gram-positive, spore-forming, anaerobic bacillus, is isolated in almost all of these cases.
  • Clindamycin, lincomycin, ampicillin, and cephalosporin have been implicated in most of the reported cases, but any antimicrobial agent (including antifungal, antiviral, and metronidazole) could incite the disease, regardless of the amount administered or the route of administration.
  • Rare cases have been related to Staphylococcus aureus, Salmonella species, Clostridium perfringens, Yersinia species, Shigella species, Campylobacter species, cytomegalovirus, Entamoeba histolytica, and Listeria species.
  • Conditions other than antimicrobial administration could predispose to C difficile pseudomembranous colitis. Such conditions include bowel ischemia, recent bowel surgery, uremia, dietary change, change in bowel motility, malnutrition, chemotherapy, shock, and Hirschsprung disease.

Pathophysiology

The antibiotic-induced change in the balance of normal gut flora allows overgrowth of C difficile.5 Colitis results from the bacterial production of large amount of toxins. The most important toxins are toxin A (enterotoxin) and toxin B (cytotoxin). One theory explains the variable severity of clinical disease through differential production rates of one or the other toxin by selected bacterial isolates. Most experts, however, believe that these variations are due to host factors.

The toxins bind to the mucosa, attack the membranes and the microfilaments of the mucosal cells, and subsequently result in cytoplasmic contraction, hemorrhage, inflammation, cellular necrosis, and protein loss. They also interfere with mucosal protein synthesis, stimulate granulocyte chemotaxis, and increase capillary permeability, intestinal myoelectric responses, and peristalsis. Intestinal tissue invasion by C difficile has been reported in fatal cases of pseudomembranous colitis in pediatric patients with hematologic malignancy.

Presentation

  • Symptoms of pseudomembranous colitis may not begin until a few weeks after discontinuation of the antibiotic.
  • Symptoms range from loose stool in the mildest cases to toxic megacolon (fever, nausea, vomiting, and ileus)6 and colonic perforation (rigid abdomen and rebound tenderness) in the most severe cases.
  • Symptoms include the following:
    • Profuse, watery or mucoid, green, foul-smelling, liquid stool may contain small amounts of blood.
    • Cramping abdominal pain may occur.
    • The patient's temperature may reach 103-105°F.
    • Extraintestinal manifestations of oligoarthritis and iridocyclitis are extremely rare.
  • One day to 6 weeks may elapse between starting the antibiotic and the beginning of the clinical symptoms. In most cases, however, symptoms begin 3-9 days after starting the antibiotics.
  • In some cases (5-19%), the disease is localized to the cecum and the proximal colon. These patients may present with acute abdomen and localized rebound tenderness in the right lower quadrant but no diarrhea. When facing such a clinical presentation, considering this diagnosis and confirming it with stool studies (stool cytology results might be negative for C difficile toxins) and computed tomography (CT) scanning may help avoid unnecessary surgery.
  • C difficile colitis should be suspected in infants and children with Hirschsprung disease when it is complicated by enterocolitis. These cases require special attention, because they often are associated with high risk.
  • Refractory C difficile colitis can be defined as disease that is unresponsive to vancomycin and/or metronidazole. Fulminant C difficile colitis can be defined as disease that progresses rapidly to cause systemic manifestation, including hypotension, renal failure, and anasarca. In practice, these 2 forms often overlap; their management is challenging and their incidence is rising. Abdominal distension and tenderness may be present and diarrhea may be absent or minimal due to ileus, which may obscure the diagnosis. Subtotal colectomy can be lifesaving, but the optimal timing is difficult to establish. Early surgical consultation when fulminant or refractory disease is suspected is highly recomended.7

Differential diagnosis

  • Staphylococcal enterocolitis and typhlitis - These are diseases that were more prevalent before the advent of new antibiotics that caused an etiologic shift favoring the emergence of C difficile. Currently, these entities are observed in patients receiving chemotherapy, who may present with clinical symptoms similar to those of C difficile colitis. These diagnoses should be suspected when gram-positive cocci are identified on Gram stain of stool smear with negative results for C difficile tests and when the terminal ileum is involved in the disease.
  • Human immunodeficiency virus (HIV) - This virus can cause a similar inflammatory process.
  • Acute exacerbation of Crohn's disease and ulcerative colitis - Pseudomembranous colitis could be a superimposed infection in these chronic patients. In cases of acute symptoms that do not respond to standard therapy, investigation and therapy for C difficile should be considered, especially when a history of antibiotics exposure is present.
  • Chemical colitis - This can occur after chemotherapy and gold exposure.
  • Ischemic colitis
  • Other types of bacterial colitis - Colitis may be caused by Campylobacter species, C perfringens, Salmonella species, Shigella species, Escherichia coli, and Yersinia species.

Indications

Pseudomembranous colitis usually is associated with antibiotic use. In mild or moderate cases, supportive therapy alone is sufficient. This includes discontinuing or changing the offending antibiotics, avoiding narcotics and antidiarrheal agents, maintaining fluid and electrolyte intake, and employing enteric isolation. In fulminant or intractable cases, hospitalization for IV hydration will be necessary. Two thirds of patients with toxic megacolon require surgical intervention.6

Relevant Anatomy

Pseudomembranous colitis is an inflammatory disease of the colon. In some cases (5-19%), the disease will be localized to the cecum and the proximal colon.

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References
Further Reading
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Keywords

pseudomembranous colitis , colitis, Clostridium, Clostridium difficile, C difficile, Clostridium difficile colitis, toxic megacolon, antibiotic side effects, antibiotic diarrhea, antibiotics diarrhea, C difficile colitis, antibiotic colitis, antibiotic-associated colitis

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Contributor Information and Disclosures

Author

Said Fadi Yassin, MD, Assistant Professor of Surgery, Department of Cardiothoracic Surgery, University of New Mexico School of Medicine
Said Fadi Yassin, MD is a member of the following medical societies: Society of Thoracic Surgeons
Disclosure: Nothing to disclose.

Medical Editor

H Scott Bjerke, MD, FACS, Clinical Associate Professor, Department of Surgery, Indiana University School of Medicine, Medical Director of Trauma Services, Methodist Hospital, Clarian Health Partners, Inc
H Scott Bjerke, MD, FACS is a member of the following medical societies: American Association for the History of Medicine, American Association for the Surgery of Trauma, American College of Surgeons, Association for Academic Surgery, Eastern Association for the Surgery of Trauma, Midwest Surgical Association, National Association of EMS Physicians, Pan-Pacific Surgical Association, Royal Society of Medicine, Southwestern Surgical Congress, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Amy L Friedman, MD, Professor of Surgery, Director of Transplantation, State University of New York Upstate Medical University College of Medicine, Syracuse
Amy L Friedman, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, American Medical Women's Association, American Society for Artificial Internal Organs, American Society of Transplant Surgeons, American Society of Transplantation, Association for Academic Surgery, Association of Women Surgeons, International College of Surgeons, International Liver Transplantation Society, New York Academy of Sciences, Pennsylvania Medical Society, Philadelphia County Medical Society, Society of Critical Care Medicine, and Transplantation Society
Disclosure: Nothing to disclose.

CME Editor

Paolo Zamboni, MD, Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy
Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York Academy of Sciences
Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, DSc, MA, Vice Chairman, Professor, Department of Surgery, Section of Gastrointestinal Medicine and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New Haven Hospital
John Geibel, MD, DSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, and Society for Surgery of the Alimentary Tract
Disclosure: AMGEN Royalty Other

 
 
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