eMedicine Specialties > Gastroenterology > Colon

Megacolon, Toxic

Author: Deepika Devuni, MBBS, Resident Physician, Department of Internal Medicine, University Of Connecticut
Coauthor(s): Lisa M Rossi, MD, Fellow, Department of Gastroenterology-Hepatology, University of Connecticut School of Medicine; George Y Wu, MD, PhD, Professor, Department of Medicine, Director, Hepatology Section, Herman Lopata Chair in Hepatitis Research, University of Connecticut School of Medicine; Jerome H Liu, MD, Staff Physician, Department of Surgery, University of California at Los Angeles Medical Center; Clifford Y Ko, MD, MS, Assistant Professor, Department of Surgery, University of California at Los Angeles School of Medicine
Contributor Information and Disclosures

Updated: Apr 14, 2009

Introduction

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.

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 1950.1 Jalan et al described the diagnostic criteria.2 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.

A 22-year-old man presented with abdominal pain, ...

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.

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A 22-year-old man presented with abdominal pain, ...

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.


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).

Gross pathology specimen from a case of pseudomem...

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


Computed tomography scan from a patient with pseu...

Computed tomography scan from a patient with pseudomembranous colitis demonstrating the classic accordion sign.

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Computed tomography scan from a patient with pseu...

Computed tomography scan from a patient with pseudomembranous colitis demonstrating the classic accordion sign.


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.

A 72-year-old woman presented with vomiting and a...

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.

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A 72-year-old woman presented with vomiting and a...

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.


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.3,4 Inflammation and upregulated nitric oxide synthetase are thought to increase local nitric oxide, which inhibits colonic smooth muscle and causes dilatation.3,4,5

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.6

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.

Plain abdominal radiograph from a patient with kn...

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.

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Plain abdominal radiograph from a patient with kn...

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 ...

Increased postrectal space is a known feature of ulcerative colitis.

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Increased postrectal space is a known feature of ...

Increased 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.

Clinical

History

  • Patients with toxic megacolon (toxic colitis) typically have signs and symptoms of acute colitis that may be refractory to treatment. Common complaints include diarrhea, abdominal pain, rectal bleeding, tenesmus, vomiting, and fever. The patient may already have a diagnosis of inflammatory bowel disease (IBD) or another cause of colitis (see Causes). In some patients, toxic megacolon (toxic colitis) may be the initial presentation of inflammatory bowel disease.
  • A careful history may reveal recent travel, antibiotic use, chemotherapy, or immunosuppression. Patients are usually very ill, with the toxic definition including some or all of the following symptoms:
    • High fever
    • Abdominal pain and tenderness
    • Tachycardia
    • Dehydration
  • The diagnostic criteria developed by Jalan et al  may be helpful to guide the history of patient suspected of having toxic megacolon (toxic colitis). They are as follows7 :
    • Radiographic evidence of colonic dilatation (classic finding is > 6 cm in the transverse colon)
    • Three of the following – Fever (>101.5°F), tachycardia (>120 beats/min), leukocytosis (>10.5 x 10 3/ μ L), or anemia
    • One of the following – Dehydration, altered mental status, electrolyte abnormality, or hypotension

Physical

  • The vital signs in a patient with toxic megacolon (toxic colitis) generally reveal tachycardia and fever. If the condition is severe, the patient may be hypotensive or tachypneic.
  • In inflammatory colitides (ie, ulcerative colitis, Crohn colitis), physical findings may be minimal, because high-dose steroids are routinely used; however, the abdomen maybe distended, and bowel sounds are usually decreased.
  • With toxemia, patients may be obtunded.
  • The presence of an increased white blood cell (WBC) count also contributes to the diagnosis of toxic megacolon (toxic colitis). Although most investigators believe that the absence of a high white blood cell count makes defining the disease as toxic megacolon difficult, an abnormally low, or even a white blood cell count that is within normal limits, does not rule out toxic megacolon.
  • Peritoneal signs may indicate perforation. They include the following:
    • Rebound
    • Rigidity
    • Peritoneal irritation
  • The form of megacolon usually associated with ulcerative colitis is defined by a transverse colon that is 6 cm or more in diameter, with loss of haustration.
  • The signs of perforation may be masked by high-dose steroids, as in inflammatory bowel disease.

Causes

  • The classic etiologies of toxic megacolon (toxic colitis) include the following inflammatory causes:
    • Ulcerative colitis8
    • Crohn colitis
    • Pseudomembranous colitis
  • The many causes of infectious colitis, including the following, may lead to toxic megacolon (toxic colitis):
    • Salmonella species
    • Shigella species
    • Campylobacter species
    • Yersinia species
    • Clostridium difficile9
    • Entamoeba histolytica
    • Cytomegalovirus10
  • Toxic megacolon (toxic colitis) may also be caused by the following:
    • Radiation colitis
    • Ischemic colitis
    • Nonspecific colitis secondary to chemotherapy11
    • Rarely as a complication of collagenous colitis12

More on Megacolon, Toxic

Overview: Megacolon, Toxic
Differential Diagnoses & Workup: Megacolon, Toxic
Treatment & Medication: Megacolon, Toxic
Follow-up: Megacolon, Toxic
Multimedia: Megacolon, Toxic
References
Further Reading
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References

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  3. Mourelle M, Casellas F, Guarner F, et al. Induction of nitric oxide synthase in colonic smooth muscle from patients with toxic megacolon. Gastroenterology. Nov 1995;109(5):1497-502. [Medline].

  4. Mourelle M, Vilaseca J, Guarner F, Salas A, Malagelada JR. Toxic dilatation of colon in a rat model of colitis is linked to an inducible form of nitric oxide synthase. Am J Physiol. Mar 1996;270(3 pt 1):G425-30. [Medline].

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Further Reading

Related eMedicine Topics

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Keywords

toxic megacolon, megacolon, dilated toxic colitis, fulminant dilated colitis, colonic dilatation, colitides, Hirschsprung disease, ulcerative colitis, Crohn disease, amebic dysentery, clostridium enterocolitis, idiopathic megacolon, chronic constipation, intestinal pseudoobstruction, intestinal pseudo-obstruction, Ogilvie syndrome, acute toxic colitis

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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: Humana Press Consulting fee Consulting; Novartis Consulting fee Review panel membership

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, Assistant Professor, Department of Surgery, University of California at Los Angeles 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.

Medical Editor

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.

Pharmacy Editor

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

Managing Editor

Douglas M Heuman, MD, FACP, Director of Hepatology, McGuire Veterans Affairs Medical Center, Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine
Douglas M Heuman, MD, FACP 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: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, 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; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
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 and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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