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{{SK}} Colon enlargement; colonic enlargement; colon dilatation; colonic dilatation; dilatation of colon; dilatation of large intestine; enlargement of colon; enlargement of large intestine
{{SK}} Colon enlargement; colonic enlargement; colon dilatation; colonic dilatation; dilatation of colon; dilatation of large intestine; enlargement of colon; enlargement of large intestine


==Overview==
==[[Megacolon overview|Overview]]==
'''Megacolon''' is an abnormal dilatation of the [[colon (anatomy)|colon]] (a part of the large [[intestine]]s) that is not caused by mechanical obstruction. The dilatation is often accompanied by a [[paralysis]] of the [[peristalsis|peristaltic]] movements of the bowel, resulting in chronic [[constipation]]. In more extreme cases, the feces consolidate into hard masses inside the colon, called [[fecaloma]]s (literally, ''fecal tumor''), which require [[surgery]] to be removed.


A human colon is considered abnormally enlarged if it has a diameter greater than 12 cm in the [[cecum]], greater than 6.5 cm in the [[rectum|rectosigmoid]] region and greater than 8 cm for the ascending colon [http://www.emedicine.com/med/topic1417.htm]
==[[Megacolon historical perspective|Historical Perspective]]==


A megacolon can be either [[Acute (medical)|acute]] or [[chronic (medicine)|chronic]]. It can also be classified according to [[etiology]].
==[[Megacolon classification|Classification]]==


==Etiology==
==[[Megacolon pathophysiology|Pathophysiology]]==


* [[Congenital]] or aganglionic megacolon
==[[Megacolon causes|Causes]]==
* Acquired megacolon, of which there are several possible etiologies:
** [[Idiopathic]] megacolon
** [[Toxic megacolon]]
** Megacolon secondary to [[infection]]
** Other neurologic, systemic and metabolic diseases


===Aganglionic megacolon===
==[[Megacolon differential diagnosis|Differentiating Megacolon from other Diseases]]==
Also called [[Hirschsprung's disease]], it is a [[congenital]] disorder of the colon in which [[nerve cell]]s of the myoenteric or [[Auerbach's plexus]] in its walls, also known as ganglion cells, are absent. It is a rare disorder (1:5 000), with prevalence among males being four times that of females. Hirschsprung’s disease develops in the [[fetus]] during the early stages of [[pregnancy]]. The exact [[Genetics|genetic]] cause remains unsolved, although in familial cases (in which families have multiple affected patients), it seems to exhibit [[autosomal dominant]] transmission, with a [[gene]] called RET, in [[chromosome]] 10, being dominant. Other 7 seven genes seem to be implicated, however. If untreated, the patient can develop [[enterocolitis]].


===Toxic megacolon===
==[[Megacolon epidemiology and demographics|Epidemiology and Demographics]]==
{{main|Toxic megacolon}}
Toxic megacolon is mainly seen in [[ulcerative colitis]] and [[pseudomembranous colitis]], two chronic [[inflammation]]s of the colon. Its mechanism is incompletely understood. It is probably due to an excessive production of [[nitric oxide]], at least in ulcerative colitis. The prevalence is about the same for both sexes.


===Megacolon in Chagas disease===
==[[Megacolon risk factors|Risk Factors]]==
In Central and South America, the most common incidence of chronic megacolon is that observed in ca. 20% of patients affected with [[Chagas disease]], caused by [[Trypanosoma cruzi]], a flagellate [[Protozoa|protozoan]] transmitted by the feces of an hematophagous insect, the assassin bugs, or by contamination through [[blood transfusion]] or [[pregnancy]]. There are several theories on how megacolon (and also megaesophagus) develops in Chagas disease. The  Austrian-Brazilian [[physician]] and [[pathologist]] [[Fritz Köberle]] was the first to propose a coherent hypothesis based on the documented destruction of the Auerbach's plexus in the walls of the intestinal tracts of Chagas patients, the so-called ''neurogenic hypothesis''. In this, the destruction of the [[autonomic nervous system]] innervation of the colon leads to a loss of the normal [[smooth muscle]] tone of the wall and subsequent gradual dilation. His research proved that, by extensively quantifying the number of neurons of the autonomic nervous system in the Auerbach's plexus, that: 1) they were strongly reduced all over the digestive tract; 2) that megacolon appeared only when there was a reduction of over 80% of the number of neurons 3) these pathologies appeared as a result of the disruption of the neurally integrated control of [[peristalsis]] (muscular annular contraction) in those parts where a strong force is necessary to impel the luminal [[Bolus (digestion)|bolus]] of [[feces]]; and 4) Idiopathic megacolon and Chagas megacolon appear to have the same etiology, namely the degeneration of the Auerbach's myoenteric plexus.


Why ''T. cruzi'' causes the destruction, however, remains to be elucidated: there are evidences for the presence of specific [[neurotoxin]]s as well as a disordely [[immune system]] reaction.
==[[Megacolon screening|Screening]]==


==Signs and symptoms==
==[[Megacolon natural history, complications and prognosis|Natural History, Complications and Prognosis]]==
External signs and symptoms are [[constipation]] of very long duration, abdominal [[bloating]], abdominal tenderness and [[Tympanites|tympany]], [[abdominal pain]], [[palpation]] of hard fecal masses and, in toxic megacolon, [[fever]], low blood [[potassium]], [[tachycardia]] and [[Shock (medical)|shock]]. Stercorary ulcers are sometimes observed in chronic megacolon, which may lead to perforation of the intestinal wall in ca. 3% of the cases, leading to [[sepsis]] and risk of death.


==Diagnosis==
==Diagnosis==
[[Diagnosis]] is achieved mainly by plain and contrasted [[radiography|radiographical]] and [[ultrasound]] imaging. Colonic marker transit studies are useful to distinguish colonic inertia from functional outlet obstruction etiologies. In this test, the patient swallows a water soluble bolus of radio-opaque contrast and films are obtained 1, 3 and 5 hours later. Patients with colonic inertia show the marker spread the large intestines, while patients with outlet obstruction exhibit show accumulations of markers in some places. A [[colonoscopy]] can also be used to rule out mechanical obstructive causes. Anorectal manometry may help to differentiate acquired from congenital forms. Rectal biopsy is recommended to make a final diagnosis of Hirschsprung disease.
[[Megacolon history and symptoms|History and Symptoms]] | [[Megacolon physical examination|Physical Examination]] | [[Megacolon laboratory findings|Laboratory Findings]] | [[Megacolon CT|CT]] | [[Megacolon MRI|MRI]] | [[Megacolon other imaging findings|Other Imaging Findings]] | [[Megacolon other diagnostic studies|Other Diagnostic Studies]]


==Treatment==
==Treatment==
Possible treatments include:
[[Megacolon medical therapy|Medical Therapy]] | [[Megacolon surgery|Surgery]] | [[Megacolon cost-effectiveness of therapy|Cost-effectiveness of therapy]] | [[Megacolon future or investigational therapies|Future or Investigational Therapies]]
* In stable cases, use of [[laxative]]s and bulking agents, as well as modifications in [[diet (nutrition)|diet]] and stool habits are effective.
* [[Corticosteroid]]s and other anti-inflammatory medication is used in toxic megacolon.
* Desimpaction of feces and decompression using anorectal and nasogastric tubes.
* When megacolon worsens and the conservative measures fail to restore transit, [[surgery]] may be necessary.


There are several surgical approaches to treat megacolon, such as a total abdominal [[colectomy]] (removal of the entire colon) with ileorectal [[anastomosis]] (ligation of the remaining ileus and rectum segments), or a total [[proctocolectomy]] (removal of colon, sigmoid and rectum) followed by [[ileostomy]] or followed by ileoanal anastomosis.


==See also==
 
 
==Related Chapters==
* [[Chagas disease]]
* [[Chagas disease]]
* [[Carlos Chagas]]
* [[Carlos Chagas]]
* [[Toxic megacolon]]
* [[Toxic megacolon]]
* [[Hirschsprung's disease]]
* [[Hirschsprung's disease]]
==References==
* Koeberle, F. Enteromegaly and cardiomegaly in Chagas disease. ''Gut''. 1963 Dec;41:399-405.
* Porter NH: Megacolon: A physiological study. ''Proc R Soc Med'' 1961; 54: 1043.
* Stabile G, Kamm MA, Hawley PR: Colectomy for idiopathic megarectum and megacolon. ''Gut'' 1991 Dec; 32(12): 1538-40 [PMID 1773963]


==External links==
==External links==
* [http://healthlink.mcw.edu/article/930605447.html Hirschsprung's disease].
* [http://cchs-dl.slis.ua.edu/clinical/gastroenterology/lower/colonicdiseases/megacolon.html Megacolon resources]
* [http://www.nlm.nih.gov/medlineplus/ency/article/000248.htm Toxic megacolon]. National Institutes of Health.
* [http://www.nlm.nih.gov/medlineplus/ency/article/000248.htm Toxic megacolon]. National Institutes of Health.



Revision as of 16:59, 5 September 2012

Megacolon
ICD-10 K59.3
ICD-9 564.7
DiseasesDB 32198
MeSH D008531

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Synonyms and keywords: Colon enlargement; colonic enlargement; colon dilatation; colonic dilatation; dilatation of colon; dilatation of large intestine; enlargement of colon; enlargement of large intestine

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Megacolon from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | CT | MRI | Other Imaging Findings | Other Diagnostic Studies

Treatment

Medical Therapy | Surgery | Cost-effectiveness of therapy | Future or Investigational Therapies



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