Fulminant Colitis and Toxic Megacolon
Heba N. Iskandar
C. Prakash Gyawali
I. GENERAL PRINCIPLES
A. Definitions.
1. Fulminant colitis.
a. Fulminant colitis implies a serious progression of colonic mucosal inflammation, extending into the deeper layers of the colon.
b. Patients typically manifest severe bloody diarrhea, abdominal tenderness, and systemic toxicity.
2. Toxic megacolon.
a. In the face of fulminant colitis, colonic circular muscle paralysis can precipitate acute colonic dilatation or toxic megacolon, the term used to describe this entire sequence of events, which includes systemic toxicity.
b. Toxic megacolon is most commonly seen as a complication of ulcerative colitis or Clostridium difficile infection colitis. It can also occur with other inflammatory conditions (Crohn colitis, Behcet disease, and collagenous colitis) and other colonic infections (bacterial: Salmonella, Shigella, Campylobacter, Yersinia, Escherichia coli; parasitic: Entameba, Cryptosporidium; fungal: Aspergillosis; and viral: Cytomegalovirus [CMV] and rotavirus); ischemia, colonic lymphoma, obstructive colon cancer, volvulus, diverticulitis, Kaposi sarcoma, chemotherapy, and idiopathic colitis are other causes.
c. Factors associated with increased mortality include age older than 40 years, the presence of colonic perforation, and delay of surgery.
d. Early recognition and treatment of toxic megacolon can substantially lower mortality from as high as 50% (with colonic perforation) to <15%.
e. Other conditions that can cause colonic dilation without systemic toxicity include Hirschprung disease, chronic constipation, and intestinal pseudoobstruction.
II. DIAGNOSIS
A. Clinical presentation.
1. History.
a. Inflammatory colitis.
i. Toxic megacolon usually occurs in the background of extensive colitis associated with chronic inflammatory bowel disease, especially ulcerative colitis, and, less commonly, Crohn disease.
ii. Toxic megacolon typically occurs during a relapse of established ulcerative colitis; however, 25% to 40% of cases present during an initial attack. Perianal disease and extraintestinal manifestations (joint, eye, skin, and liver) can be clues to a new inflammatory bowel disease diagnosis.
iii. Progressive bloody diarrhea and crampy abdominal pain are typical symptoms. A paradoxical decrease in stool frequency with passage of bloody “membranes” is an ominous sign.
iv. Manipulation of the inflamed bowel with diagnostic examinations such as barium enema or colonoscopy, medications (including vigorous laxatives, antidiarrheals, anticholinergics), electrolyte imbalances, and pH disturbances can contribute to the development of the condition.
v. Corticosteroids can suppress signs of perforation and peritonitis, but whether these drugs can precipitate toxic megacolon is controversial.
b. Infectious colitis.
i. C. difficile infections have been the cause of increasing hospitalizations over the last decade, due to increased use of broad-spectrum antibiotics and development of more virulent C. difficile strains.
ii. Patients age 65 and older are at increased risk of C. difficile infection and a severe course, including toxic megacolon. Other risk factors for megacolon in C. difficile colitis are malignancy, chronic obstructive pulmonary disease, renal failure, antiperistaltic medications, and antibiotics, especially clindamycin.
iii. A history of antibiotic use, antidiarrheals, anticholinergics, opiates, health facility contact, or immunosuppression (human immunodeficiency virus [HIV], chemotherapy) should be noted.
iv. Travel to endemic areas may suggest Entameba infection.
v. Exposure to others with gastrointestinal infectious symptoms should be elicited.
2. Physical examination.
a. Systemic toxicity is heralded by fever and tachycardia and can progress to hypotension, confusion, agitation, or apathy.
b. Abdominal tenderness and distension, with decreased bowel sounds on auscultation, are common. Constipation and obstipation may be present.
c. Peritoneal signs indicate transmural inflammation or perforation, but they may be minimal or absent in elderly patients or in patients receiving corticosteroids.
B. Diagnostic tests.
1. Laboratory studies.
a. Laboratory tests should assess the degree of systemic toxicity, fluid and electrolyte deficits, pH disturbances, and the need for blood transfusion.
b. Leukocytosis with a significant left shift is common.