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| {{Infobox_Disease | | | {{Infobox_Disease | |
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| {{SI}} | | {{Megacolon}} |
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| {{CMG}} | | {{CMG}} |
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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 |
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| | ==[[Megacolon overview|Overview]]== |
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| ==Overview== | | ==[[Megacolon historical perspective|Historical Perspective]]== |
| '''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.
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| 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 classification|Classification]]== |
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| A megacolon can be either [[Acute (medical)|acute]] or [[chronic (medicine)|chronic]]. It can also be classified according to [[etiology]].
| | ==[[Megacolon pathophysiology|Pathophysiology]]== |
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| ==Etiology== | | ==[[Megacolon causes|Causes]]== |
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| * [[Congenital]] or aganglionic megacolon
| | ==[[Megacolon differential diagnosis|Differentiating Megacolon from other Diseases]]== |
| * Acquired megacolon, of which there are several possible etiologies:
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| ** [[Idiopathic]] megacolon
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| ** [[Toxic megacolon]]
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| ** Megacolon secondary to [[infection]]
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| ** Other neurologic, systemic and metabolic diseases
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| ===Aganglionic megacolon=== | | ==[[Megacolon epidemiology and demographics|Epidemiology and Demographics]]== |
| 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]].
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| ===Toxic megacolon=== | | ==[[Megacolon risk factors|Risk Factors]]== |
| {{main|Toxic megacolon}}
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| 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.
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| ===Megacolon in Chagas disease=== | | ==[[Megacolon screening|Screening]]== |
| 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.
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| 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 natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
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| ==Signs and symptoms==
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| 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.
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| ==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 x ray|X Ray]] | [[Megacolon CT|CT]] | [[Megacolon MRI|MRI]] | [[Megacolon echocardiography or ultrasound|Echocardiography or Ultrasound]] | [[Megacolon other imaging findings|Other Imaging Findings]] | [[Megacolon other diagnostic studies|Other Diagnostic Studies]] |
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| ==Treatment== | | ==Treatment== |
| Possible treatments include:
| | [[Megacolon medical therapy|Medical Therapy]] | [[Megacolon surgery|Surgery]] | [[Megacolon primary prevention|Primary Prevention]] | [[Megacolon secondary prevention|Secondary Prevention]] | [[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.
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| * [[Corticosteroid]]s and other anti-inflammatory medication is used in toxic megacolon.
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| * Desimpaction of feces and decompression using anorectal and nasogastric tubes.
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| * When megacolon worsens and the conservative measures fail to restore transit, [[surgery]] may be necessary.
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| 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.
| | ==Case Studies== |
| | [[Megacolon case study one|Case #1]] |
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| ==See also== | | ==Related Chapters== |
| * [[Chagas disease]] | | * [[Chagas disease]] |
| * [[Carlos Chagas]] | | * [[Carlos Chagas]] |
| * [[Toxic megacolon]] | | * [[Toxic megacolon]] |
| * [[Hirschsprung's disease]] | | * [[Hirschsprung's disease]] |
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| ==References==
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| * Koeberle, F. Enteromegaly and cardiomegaly in Chagas disease. ''Gut''. 1963 Dec;41:399-405.
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| * Porter NH: Megacolon: A physiological study. ''Proc R Soc Med'' 1961; 54: 1043.
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| * Stabile G, Kamm MA, Hawley PR: Colectomy for idiopathic megarectum and megacolon. ''Gut'' 1991 Dec; 32(12): 1538-40 [PMID 1773963]
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| ==External links== | | ==External links== |
| * [http://healthlink.mcw.edu/article/930605447.html Hirschsprung's disease].
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| * [http://cchs-dl.slis.ua.edu/clinical/gastroenterology/lower/colonicdiseases/megacolon.html Megacolon resources]
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| * [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. |
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| [[Category:Gastroenterology]] | | [[Category:Gastroenterology]] |
| [[Category:Needs patient information]] | | [[Category:Needs patient information]] |
| [[Category:Mature chapter]]
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| [[de:Megacolon]] | | [[de:Megacolon]] |