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 three 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 three articles devoted to megacolon, and they are separated based on the three 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 contract when dilated.
Many pathophysiologic mechanisms have been proposed in an attempt to explain the altered motility seen in acute megacolon; these include the following:
Causes of acute megacolon include the following:
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, the 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.
The typical patient is an elderly person who is in the hospital, usually for an unrelated reason (eg, recovering postoperatively from surgery), and may or may not already be taking oral feeds.
Orthopedic surgery, cesarean delivery, and cardiovascular or lung surgery are procedures that commonly predispose to acute megacolon.
Acute megacolon can occur on the medical wards as frequently as on the surgical wards (eg, in patients with unrelated problems, such as pneumonia, sepsis, myocardial infarction, or stroke).
Systemic diseases that affect the neuromuscular component of the GI tract, such as amyloidosis, may first present with an acute episode of pseudo-obstruction.
Not having a history of similar episodes of abdominal distension in the past is common.
Colic-type pain may be present, but the absence of this pain does not imply a less severe condition.
Patients often will experience nausea and vomiting as well as constipation and obstipation.
Physical examination findings may include the following:
Laboratory studies are directed at establishing the etiology of the acute megacolon as well as determining the patient's fluid status, and they include the following.
Imaging studies are used to determine the severity, to exclude free intraperitoneal air (perforation) as well as other etiologies (eg, extrinsic compression), and to follow the clinical course.[4]
Plain x-ray films of the abdomen demonstrate the massive gaseous distention of the colon. Generally, the small bowel is not seen. Dilation of all segments of the colon support the diagnosis of pseudo-obstruction.
Other imaging studies, such as hypaque (water soluble radiopaque contrast material) enema, CT scanning, or MRI, may also be used to exclude obstruction.
Perform other tests only to rule out a mechanical obstruction. Depending on the setting, severity, and condition of the patient, these tests may include either a colonoscopic examination (which also may be therapeutic) or a water-soluble contrast enema. Colonoscopy is preferred because of its diagnostic and therapeutic potential.
Conservative management is preferred when the patient is clinically stable. Consider the following:
Use of a rectal tube
Decompression using a rectal tube may assist in the treatment only if the sigmoid colon is involved. When such tubes are used, anecdotal experience has demonstrated that frequent position changes for the patient may help improve decompression. Complications with these rectal tubes include tube obstruction and colonic/rectal ulceration.
Colonoscopic decompression
If the dilatation persists or worsens, colonoscopic decompression with or without placement of a tube in the right colon should be considered. Although the placement of a decompression tube per rectum is generally suggested, some experts believe that the tube often becomes obstructed with stool and ceases to work after a short time. Randomized controlled trials of the efficacy of colonoscopic decompression are lacking. The resolution of ileus, perforation, and mortality rates are similar between endoscopic and conservative management.
Neostigmine (adrenergic antagonist) has been demonstrated in noncontrolled and controlled studies to improve acute colonic megacolon. Whether a trial of neostigmine should be performed before or after colonoscopic decompression is unclear.
The major indication for its use is failure of conservative therapy after 72 hours. Failure of conservative therapy is generally defined by a cecal diameter of greater than 9 cm.
Contraindications include bradycardia, systolic blood pressure of less than 90 mm Hg, active bronchospasm, serum creatinine level of greater than 3 mg/dL, and evidence of bowel perforation.
Adverse events include abdominal cramping (17%), excessive salivation (13%), transient bradycardia (6%), diaphoresis (4%), and nausea and vomiting (4%). Based on expert opinion, a starting dose of 1 mg may reduce the likelihood of developing bradycardia.
Cardiac monitoring of patients during treatment with neostigmine is generally recommended, and atropine should be at the bedside.
A second dose of neostigmine should be considered if there is a partial or minimal response to the initial administration.
Of note, although neostigmine often induces clinical decompression, this decompression has not been shown to reduce perforation and mortality rates.
The urgency of management often depends on the size of the colon and the rate of change of the cecal diameter. Some experts believe that regardless of the criteria used for defining acute megacolon, the diameter of the cecum is the most important criterion because the cecum is generally the area that perforates. While the diameter at which the cecum perforates is variable, expert experience indicates that the cecum rarely perforates at a diameter of less than 12 cm.
Once relieved, close follow-up care, including physical examination and maintenance of a normal electrolyte balance, is important.
Avoid using agents that slow transit time, such as opiates and anticholinergics.
Most patients are in the hospital when acute pseudo-obstruction is diagnosed, and bowel rest should be instituted. Parenteral nutrition may be considered depending on the patient's nutritional status.
Because many of the cases of acute pseudo-obstruction occur postoperatively, the patients tend to be already at bed rest. Remembering to continue prophylaxis for deep venous thrombosis, per the individual physician's protocol, is important; however, if the patient is not severely ill, is not in severe pain, and is stable to ambulate, no reason exists for the patient to remain in bed.
In view of the high rate of recurrence of colonic dilation following medical and endoscopic therapies, other therapeutic modalities have been proposed.
Percutaneous cecostomy may successfully allow for colonic decompression, but complications with this procedure are high.
Surgical options include cecostomy, colostomy, or colectomy, although surgical therapies are associated with even poorer outcomes. A colectomy is indicated if perforation or colonic ischemia is present.[5]
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Clinical Context: Improves acute colonic megacolon; may increase cholinergic activity by reducing acetylcholine degradation.
Increase peristalsis and secretions in the intestine and relax the sphincter.