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:
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). 
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.
United States data
No large-scale studies have been performed to determine the prevalence or incidence of acute megacolon.
Race-, sex-, and age-related demographics
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. 
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. 
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.
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