Toxic Megacolon 

  • Author: Deepika Devuni, MBBS; Chief Editor: Julian Katz, MD   more...
 
Updated: Jan 5, 2012
 

Background

Toxic megacolon is the clinical term for an acute toxic colitis with dilatation of the colon. The dilatation can be either total or segmental. A more contemporary term for toxic megacolon is simply toxic colitis, because patients may develop toxicity without megacolon. For the purposes of this article, the term toxic megacolon (toxic colitis) is used, but either toxicity or megacolon can occur exclusively of each other.[1]

The hallmarks of toxic megacolon (toxic colitis), a potentially lethal condition, are nonobstructive colonic dilatation larger than 6 cm and signs of systemic toxicity. Toxic megacolon (toxic colitis)was recognized by Marshak and Lester in 1950.[2] Jalan et al described the diagnostic criteria.[3] The first criterion is radiographic evidence of colonic dilatation. The second criterion is any 3 of the following: fever (>101.5°F), tachycardia (>120 beats/min), leukocytosis (>10.5 103/µL), or anemia. The third criterion is any 1 of the following: dehydration, altered mental status, electrolyte abnormality, or hypotension.

Toxic megacolon (toxic colitis) was first thought to be a complication of ulcerative colitis. In fact, toxic megacolon (toxic colitis) may complicate any number of colitides, including inflammatory, ischemic, infectious, radiation, and pseudomembranous.[4, 5] See the image below.

A 22-year-old man presented with abdominal pain, pA 22-year-old man presented with abdominal pain, passage of blood and mucus per rectum, abdominal distention, fever, and disorientation. Findings from sigmoidoscopy confirmed ulcerative colitis. Abdominal radiographs obtained 2 days apart show mucosal edema and worsening of the distention in the transverse colon. The patient's clinical condition deteriorated over the next 36 hours despite steroid and antibiotic therapy, and the patient had to undergo a total colectomy and ileostomy.

The incidence of toxic megacolon (toxic colitis) is expected to increase due to the rising prevalence of pseudomembranous colitis. Colonic dilatation may be present in other conditions, such as Hirschsprung disease, idiopathic megacolon/chronic constipation, and intestinal pseudo-obstruction (Ogilvie syndrome). However, these patients do not develop signs of systemic toxicity and, therefore, do not fall into the category of having toxic megacolon (toxic colitis). See the images below.

Gross pathology specimen from a case of pseudomembGross pathology specimen from a case of pseudomembranous colitis demonstrating characteristic yellowish plaques. Computed tomography scan from a patient with pseudComputed tomography scan from a patient with pseudomembranous colitis demonstrating the classic accordion sign.
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Pathophysiology

Although the precise pathophysiology of toxic megacolon (toxic colitis) is unproven, several factors may contribute to its development and precipitation. Signs and symptoms of acute colitis may be present for as long as 1 week before dilatation develops.

Often, triggering or predisposing factors can be identified. Although the risk of toxic megacolon (toxic colitis) increases with the severity of colitis, rapid tapering or abrupt discontinuation of medications such as steroids, sulfasalazine, and 5-aminosalicylic acid may precipitate toxemia and dilatation. Medications that negatively impact bowel motility also are implicated in the development of toxic megacolon. These include, but are not limited to, anticholinergics, antidepressants, loperamide, and opioids. Procedures such as barium enema or colonoscopy may cause distention, may impair blood supply, or may exacerbate a microperforation and cause subsequent toxemia. See the image below.

A 72-year-old woman presented with vomiting and abA 72-year-old woman presented with vomiting and abdominal distention. The supine (right) and erect (left) plain abdominal radiographs show gross dilatation of the colon with multiple air-fluid levels. On further questioning, the patient revealed that she was taking diuretics for hypertension. Blood biochemical tests revealed markedly lowered potassium levels. After potassium replacement therapy, the patient's pseudo-obstruction completely resolved.

In cases of uncomplicated colitis, the inflammatory response is confined to the mucosa. The microscopic hallmark of toxic megacolon (toxic colitis) is inflammation extending beyond the mucosa into the smooth-muscle layers and serosa. Myenteric plexus involvement is not consistent and probably does not contribute to dilatation.

As inflammation progresses into the smooth-muscle layers of the colon, nitric oxide appears to be involved in the pathogenesis of toxic megacolon (toxic colitis). Nitric oxide inhibits smooth-muscle tone and is generated by inflammatory cells such as neutrophils and macrophages in the inflamed portions of the colon. Studies performed by Mourelle et al have shown increased amounts of inducible nitric oxide synthetase in the muscularis propria of patients with toxic megacolon.[6, 7] Inflammation and upregulated nitric oxide synthetase are thought to increase local nitric oxide, which inhibits colonic smooth muscle and causes dilatation.[6, 7, 8]

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Epidemiology

Frequency

International

The incidence of toxic megacolon (toxic colitis) cited in the literature of depends on the etiology. The lifetime risk of toxic megacolon (toxic colitis) in ulcerative colitis has been estimated to be 1-2.5%. In one series of 1236 patients admitted to the hospital over a 19-year period, toxic megacolon was present in 6% of patients, specifically 10% of ulcerative colitis admissions and 2.3% of Crohn disease admissions.[9]

Toxic megacolon (toxic colitis) occurs in approximately 5% of severe attacks of ulcerative colitis. In pseudomembranous colitis, toxic megacolon is reported to occur in 0.4-3% of patients. This number is expected to increase in proportion to the increasing prevalence of pseudomembranous colitis. This increasing prevalence is felt to be due to increased use of broad-spectrum antibiotics.

Mortality/Morbidity

Mortality rates for toxic megacolon (toxic colitis) have improved substantially over the past few decades, from 20% in 1976 to 4-5% currently. The decrease is a result of earlier recognition, intensive medical management, early surgical consultation, and improved surgical technique and postoperative care.

Race

In the United States, Jewish people are more prone to ulcerative colitis than people who are not Jewish. In Israel, Ashkenazi Jewish people have a higher incidence of ulcerative colitis than Sephardic Jewish people. No data exist regarding race and the incidence of toxic megacolon (toxic colitis).

Sex

Regarding ulcerative colitis, most studies demonstrate that both sexes are affected equally. See the images below.

Plain abdominal radiograph from a patient with knoPlain abdominal radiograph from a patient with known ulcerative colitis who presented with an acute exacerbation of his symptoms. This image shows thumbprinting in the region of the splenic flexure of the colon. Increased postrectal space is a known feature of uIncreased postrectal space is a known feature of ulcerative colitis.

Age

Regarding ulcerative colitis, young adults (aged 20-40 y) primarily are affected, but this disease may present at any age. With toxic megacolon (toxic colitis), no predilection appears to exist for any particular age group. All ages may be affected. Many individuals present with toxic megacolon (toxic colitis) during their first flare. The mean duration of disease has been reported to be 3-5 years.

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Contributor Information and Disclosures
Author

Deepika Devuni, MBBS  Resident Physician, Department of Internal Medicine, University Of Connecticut

Disclosure: Nothing to disclose.

Coauthor(s)

Lisa M Rossi, MD  Fellow, Department of Gastroenterology-Hepatology, University of Connecticut School of Medicine

Disclosure: Nothing to disclose.

George Y Wu, MD, PhD  Professor, Department of Medicine, Director, Hepatology Section, Herman Lopata Chair in Hepatitis Research, University of Connecticut School of Medicine

George Y Wu, MD, PhD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, American Medical Association, American Society for Clinical Investigation, and Association of American Physicians

Disclosure: Springer Consulting fee Consulting; Gilead Consulting fee Review panel membership; Vertex Honoraria Speaking and teaching; Bristol-Myers Squibb Honoraria Speaking and teaching; Springer Royalty Review panel membership; Merck Honoraria Speaking and teaching

Jerome H Liu, MD  Staff Physician, Department of Surgery, University of California at Los Angeles Medical Center

Disclosure: Nothing to disclose.

Clifford Y Ko, MD, MS  Professor, Department of Surgery, University of California, Los Angeles, David Geffen School of Medicine

Clifford Y Ko, MD, MS is a member of the following medical societies: American College of Surgeons, American Medical Association, American Society of Colon and Rectal Surgeons, Association for Academic Surgery, California Medical Association, and New York Academy of Sciences

Disclosure: Nothing to disclose.

Specialty Editor Board

Terence David Lewis, MBBS, FRACP, FRCPC, FACP  Program Director, Internal Medicine Residency, & Assistant Chairman, Associate Professor, Department of Internal Medicine, Division of Gastroenterology, Loma Linda University Medical Center

Terence David Lewis, MBBS, FRACP, FRCPC, FACP is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, California Medical Association, Royal College of Physicians and Surgeons of Canada, and Sigma Xi

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

Douglas M Heuman, MD, FACP, FACG, AGAF  Chief of GI, Hepatology, and Nutrition at North Shore University Hospital/Long Island Jewish Medical Center; Professor, Department of Medicine, Hofstra North Shore-LIJ School of Medicine

Douglas M Heuman, MD, FACP, FACG, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, and American Gastroenterological Association

Disclosure: Novartis Grant/research funds Other; Bayer Grant/research funds Other; Otsuka Grant/research funds None; Bristol Myers Squibb Grant/research funds Other; Scynexis None None; Salix Grant/research funds Other; MannKind Other

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.

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A 22-year-old man presented with abdominal pain, passage of blood and mucus per rectum, abdominal distention, fever, and disorientation. Findings from sigmoidoscopy confirmed ulcerative colitis. Abdominal radiographs obtained 2 days apart show mucosal edema and worsening of the distention in the transverse colon. The patient's clinical condition deteriorated over the next 36 hours despite steroid and antibiotic therapy, and the patient had to undergo a total colectomy and ileostomy.
A 72-year-old woman presented with vomiting and abdominal distention. The supine (right) and erect (left) plain abdominal radiographs show gross dilatation of the colon with multiple air-fluid levels. On further questioning, the patient revealed that she was taking diuretics for hypertension. Blood biochemical tests revealed markedly lowered potassium levels. After potassium replacement therapy, the patient's pseudo-obstruction completely resolved.
Gross pathology specimen from a case of pseudomembranous colitis demonstrating characteristic yellowish plaques.
Computed tomography scan from a patient with pseudomembranous colitis demonstrating the classic accordion sign.
Plain abdominal radiograph from a patient with known ulcerative colitis who presented with an acute exacerbation of his symptoms. This image shows thumbprinting in the region of the splenic flexure of the colon.
Increased postrectal space is a known feature of ulcerative colitis.
 
 
 
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