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Sci-Tech Dictionary: megacolon (′meg·ə′kō·lən) (medicine) Hypertrophy and

dilation of the colon associated with

prolonged constipation.
Dental Dictionary: megacolon

An abnormal dilation of the colon that may be congenital, toxic, or acquired.Veterinary
Dictionary: megacolon Dilatation and hypertrophy of the colon. • • acquired m. — colonic enlargement associated with chronic constipation, but with normal ganglion cell innervation. Most common in dogs and cats, the usual causes are dietary factors, lack of exercise, prostatic enlargement, anal disease and neurological deficits. aganglionic m. — due to congenital absence of myenteric ganglion cells and abnormal motor activity in a distal segment of the large bowel. There is continuous spasm in the aganglionic segment that causes a stenosis, and a massive distention of the normal proximal colon develops secondarily. The disease in humans is called Hirschsprung's disease and a similar, but not identical, condition occurs in piebald mice and Overo horses. Congenital megacolon may occur in dogs and cats, but acquired disease is much more common. Called also congenital megacolon. congenital m. — see aganglionic megacolon (above). idiopathic m. — recurrent episodes of constipation in aging cats over a long period of time is believed to lead to the progressive development of a dilated colon. inherited m. — is presumed in fattening pigs in which there is abdominal distention and wasting without rectal stricture. psychogenic m. — seen in cats and dogs that will not defecate indoors. Prolonged fecal retention causes loss of the defecation reflex, especially in aged patients.

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Wikipedia: megacolon

Megacolon is an abnormal dilatation of the colon (a part of the large intestines) that is not caused by mechanical obstruction. The dilatation is often accompanied by a paralysis of the peristaltic movements of the bowel, resulting in chronic constipation. In more extreme cases, the feces consolidate into hard masses inside the colon, called fecalomas (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 rectosigmoid region and greater than 8 cm for the ascending colon [1]A megacolon can be either acute or chronic. It can also be classified according to etiology.
Etiology Congenital or aganglionic megacolon Acquired megacolon, of which there are several possible etiologies: o o o o Idiopathic megacolon Toxic megacolon Megacolon secondary to infection Other neurologic, systemic and metabolic diseases

Aganglionic megacolon

Also called Hirschsprung's disease, it is a congenital disorder of the colon in which nerve cells 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 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

Main article: Toxic megacolon Toxic megacolon is mainly seen in ulcerative colitis and pseudomembranous colitis, two chronic inflammations 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 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 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 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 neurotoxins as well as a disordely immune system reaction. Signs and symptoms External signs and symptoms are constipation of very long duration, abdominal bloating, abdominal tenderness and tympany, abdominal pain, palpation of hard fecal masses and, in toxic megacolon, fever, low blood potassium, tachycardia and 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 is achieved mainly by plain and contrasted 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 throughout 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. Treatment Possible treatments include: • • • • In stable cases, use of laxatives and bulking agents, as well as modifications in diet and stool habits are effective. Corticosteroids 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.

Hirschsprung’s Disease (Congenital Megacolon, Colonic Aganglionosis) En Español (Spanish Version) Definition Hirschsprung's disease is a rare congenital disorder—affecting about 1 in 5,000 US newborns— that results in an obstruction of the bowel. This prevents normal bowel movements. It usually occurs as an isolated finding but can also be part of a syndrome. Causes Hirschsprung's disease is caused by the absence of certain nerve cells, called ganglia, in the wall of the bowel. Normally, these nerve cells help relax the bowel wall to allow fecal matter to move through the colon. However, in children with Hirschsprung's disease, the colon stays contracted, and bowel contents build up before the obstruction. The condition usually affects the last 1-2 feet of the colon that ends with the rectum. Hirschsprung's Disease

© 2008 Nucleus Medical Art, Inc. The absence of ganglia is due to a genetic defect. In some cases, HD is hereditary, which means parents could pass it to their children. This can happen even if the parents don't have HD. If you have one child with HD, you could have more children with the disease. Talk to your doctor about the risk and consider genetic counseling. Risk Factors A risk factor is something that increases your chance of getting a disease or condition. Risk factors for Hirschsprung's disease include:    Family members with the disease More common in males May be associated with other congenital defects

Symptoms Hirschsprung's disease is usually diagnosed in infancy, but can also be diagnosed later. Symptoms can differ with age.  In newborns: Failure to pass meconium within the first 48 hours of life (Meconium is a dark sticky substance that is the first bowel movement.)  Vomiting after eating  Abdominal distention In young children:  Severe constipation  Diarrhea  Anemia  Growth delay In teenagers: 

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Severe constipation for most of their lives Anemia

Diagnosis Most cases of Hirschsprung's disease are diagnosed in infancy, although some may not be diagnosed until adolescence or early adulthood. Tests for diagnosis may include:    Barium enema —injection of fluid into the rectum that makes the colon show up on an x-ray so the doctor can see abnormal areas in the colon Biopsy —removal of a sample of bowel tissue to check for ganglia (or the absence of ganglia) Anorectal manometry—measurement of the pressures of the internal and external sphincter with a rectal balloon

Treatment The primary treatment for Hirschsprung's disease is surgery to remove the affected portion of the colon. There are three potential phases to the surgery, but all three phases may not be needed. Your doctor will discuss the best methods for you or your child's condition. The three phases are:    Colostomy—This involves surgically creating an opening into the colon, which is brought to the abdominal surface. Stool contents are excreted through this opening and into a bag. Pull-through operation—The affected area of the colon is removed, then the healthy colon is brought down to the rectum and joined to the rectal wall. Closure of the colostomy—The colostomy opening is closed, and bowel function gradually returns to normal.

Outcome Symptoms are eliminated in 90% of children after surgical treatment. A better outcome is associated with early treatment, and shorter bowel segment involvement. Complications Complications may include:    Perforation of the intestine Enterocolitis Short gut syndrome

Prevention There are no guidelines for the prevention of Hirschsprung's disease.