Acute Megacolon
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Megacolon, like megarectum, is a descriptive term. Megacolon denotes dilatation of the colon that is not caused by a mechanical obstruction. While the definition of megacolon has varied in the literature, most use a cecum measurement of greater than 12 cm in diameter to define megacolon. Adding to this definition, because the diameter of the large intestine is different in different areas, measurements of greater than 6.5 cm for the rectosigmoid region and greater than 8 cm for the ascending colon may also be significant.
Megacolon may be divided into 3 categories by acuity of onset, as follows: (1) acute megacolon (pseudo-obstruction); (2) chronic megacolon, which includes congenital, acquired, and idiopathic causes; and (3) toxic megacolon.
The Gastroenterology section of the Medscape Drugs & Diseases journal contains 3 articles devoted to megacolon, and they are separated based on the 3 aforementioned categories (see also Differentials). This article is devoted to the acute development of megacolon.
Whether dilatation is a result of abnormal motility of the colon remains unresolved. Much basic science research has been performed in this area. It is well known that the colonic distensibility changes in the presence of luminal contents. For example, fatty acids infused into the cecum appear to reduce the volume of the proximal large bowel. Long-term opiate narcotic use (including diphenoxylate and loperamide) may lead to colonic dilatation and may limit the ability of the colon to constrict when dilated.
Many pathophysiologic mechanisms have been proposed in an attempt to explain the altered motility seen in acute megacolon; these include the following:
Reflex motor inhibition through splanchnic nerves in response to noxious stimuli
Excess sympathetic motor input (failure to contract)
Excess parasympathetic motor input (failure to relax)
Decreased parasympathetic motor input (failure to contract)
Excess stimulation of peripheral opioid receptors by endogenous or exogenous opioids (initially excess activation followed by prolonged inhibition)
Inhibition of nitric oxide release from inhibitory motor neurons
Causes of acute megacolon include the following:
Electrolyte abnormality
Metabolic abnormality, including hypothyroidism and hyperparathyroidism
Certain medications, including anticholinergics, antidiarrheals, opiates, digitalis, and certain antipsychotic drugs
Inflammatory bowel disease, including ulcerative colitis and Crohn colitis
Infections, including Clostridium difficile (pseudomembranous colitis), Trypanosoma cruzi (Chagas disease), and Entamoeba histolytica (amebic dysentery). [1]
Note that in any setting, a mechanical cause (eg, a tumor) and a toxic cause (eg, acute ulcerative colitis) must be ruled out first because the treatments are very different for these conditions.
No large-scale studies have been performed to determine the prevalence or incidence of acute megacolon.
Race and sex have not been documented to play a role in acute megacolon.
Most patients are middle-aged or older; however, the increased incidence seen in older populations is more likely a reflection of their medical and surgical comorbidities rather than age alone.
Prognosis is determined in part by the underlying cause of the megacolon, the presence of any comorbidities, and the development of complications.
The mortality rate associated with spontaneous perforation of nontoxic megacolon is 50%; however, most patients respond to treatment prior to the onset of this complication. [2]
The most severe complication is perforation with an associated mortality rate of approximately 50%. In a study by Vanek et al, perforation rates were 0% for cecal diameters of less than 12 cm, 7% for cecal diameters of 12-14 cm, and 23% for cecal diameters of greater than 14 cm. [3]
Mortality was also shown to increase with a delay of decompression therapy.
If surgical therapy is required, mortality increases based on age, comorbidities, and functional status.
Tan CB, Rajan D, Shah M, et al. Toxic megacolon from fulminant Clostridium difficile infection induced by topical silver sulphadiazine. BMJ Case Rep. 2012 Aug 8. 2012:[Medline].
Frasko R, Uchytil Z, Svab J, Vyborny J, Krska Z. [Treatment outcomes in patients with toxic megacolon]. Rozhl Chir. 2011 Jun. 90(6):339-42. [Medline].
Vanek VW, Al-Salti M. Acute pseudo-obstruction of the colon (Ogilvie’s syndrome). An analysis of 400 cases. Dis Colon Rectum. 1986 Mar. 29(3):203-10. [Medline].
Moulin V, Dellon P, Laurent O, Aubry S, Lubrano J, Delabrousse E. Toxic megacolon in patients with severe acute colitis: computed tomographic features. Clin Imaging. 2011 Nov. 35(6):431-6. [Medline].
Antonopoulos P, Almyroudi M, Kolonia V, Kouris S, Troumpoukis N, Economou N. Toxic megacolon and acute ischemia of the colon due to sigmoid stenosis related to diverticulitis. Case Rep Gastroenterol. 2013 Sep 11. 7(3):409-13. [Medline]. [Full Text].
Camilleri M. Acute and chronic pseudo-obstruction. Felman M, Friedman LS, Sleisenger MH, eds. Sleisenger & Fordtran’s Gastrointestinal and Liver Disease. 8th ed. Philadelphia, PA: Saunders Publishing; 2007. 2679-2702.
Fazel A, Verne GN. New solutions to an old problem: acute colonic pseudo-obstruction. J Clin Gastroenterol. 2005 Jan. 39(1):17-20. [Medline].
Geller A, Petersen BT, Gostout CJ. Endoscopic decompression for acute colonic pseudo-obstruction. Gastrointest Endosc. 1996 Aug. 44(2):144-50. [Medline].
Ponec RJ, Saunders MD, Kimmey MB. Neostigmine for the treatment of acute colonic pseudo-obstruction. N Engl J Med. 1999 Jul 15. 341(3):137-41. [Medline].
Saunders MD, Kimmey MB. Colonic pseudo-obstruction: the dilated colon in the ICU. Semin Gastrointest Dis. 2003 Jan. 14(1):20-7. [Medline].
Stephenson BM, Morgan AR, Salaman JR, Wheeler MH. Ogilvie’s syndrome: a new approach to an old problem. Dis Colon Rectum. 1995 Apr. 38(4):424-7. [Medline].
Turegano-Fuentes F, Munoz-Jimenez F, Del Valle-Hernandez E, et al. Early resolution of Ogilvie’s syndrome with intravenous neostigmine: a simple, effective treatment. Dis Colon Rectum. 1997 Nov. 40(11):1353-7. [Medline].
Khajehnoori M, Nagra S. Acute colonic pseudo-obstruction (Ogilvie’s syndrome) with caecal perforation after caesarean section. J Surg Case Rep. 2016 Aug 23. 2016(8):[Medline]. [Full Text].
Roberto M Gamarra, MD Consulting Gastroenterologist, Digestive Health Associates, PLC
Roberto M Gamarra, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, Crohn’s and Colitis Foundation of America
Disclosure: Nothing to disclose.
Ross A Heil, DO Fellow, Department of Gastroenterology, St John Providence Health System
Ross A Heil, DO is a member of the following medical societies: American College of Osteopathic Internists, American Medical Association, American Osteopathic Association
Disclosure: Nothing to disclose.
Michael H Piper, MD Clinical Assistant Professor, Department of Internal Medicine, Division of Gastroenterology, Wayne State University School of Medicine; Consulting Staff, Digestive Health Associates, PLC
Michael H Piper, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Gastroenterology, American College of Physicians, Michigan State Medical Society
Disclosure: Nothing to disclose.
David Manuel, MD Affiliate Faculty, Department of Medicine, Loyola University Health System; Gastroenterologist, Digestive Health Center
David Manuel, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, Crohn’s and Colitis Foundation of America
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: Received salary from Medscape for employment. for: Medscape.
Douglas M Heuman, MD, FACP, FACG, AGAF Chief of Hepatology, Hunter Holmes McGuire Department of Veterans Affairs Medical Center; Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University 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, American Gastroenterological Association
Disclosure: Received grant/research funds from Novartis for other; Received grant/research funds from Bayer for other; Received grant/research funds from Otsuka for none; Received grant/research funds from Bristol Myers Squibb for other; Received none from Scynexis for none; Received grant/research funds from Salix for other; Received grant/research funds from MannKind for other.
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, American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.
Terence David Lewis, MBBS, MBBS
Terence David Lewis, MBBS, MBBS 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, Sigma Xi
Disclosure: Nothing to disclose.
The authors and editors of Medscape Drugs & Diseases gratefully acknowledge the contributions of previous author, Clifford Y Ko, MD, MS, to the development and writing of this article.
Acute Megacolon
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