AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Background

Megacolon, like megarectum, is a descriptive term. Megacolon denotes dilatation of the colon that is not caused by 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 eMedicine 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.

Pathophysiology

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 to attempt to explain the altered motility seen in acute megacolon and 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

Frequency

United States

No large-scale studies have been performed to determine the prevalence or incidence of acute megacolon.

Mortality/Morbidity

The mortality rate associated with spontaneous perforation of nontoxic megacolon is 50%; however, most patients respond to treatment prior to this complication.

Race

Race has not been documented to play a role in acute megacolon.

Sex

Sex has not been documented to play a role in acute megacolon.

Age

Most patients are middle-aged or older; however, the increased incidence seen in older populations is more likely reflexion of their medical and surgical comorbidities than age alone.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

History

• 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 a diet.
• Orthopedic surgery, cesarean delivery, and cardiovascular or lung surgery are surgeries 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

• The vital signs can all be normal.
• Depending on the duration of the megacolon and the fluid status, the patient may become tachycardic.
• With distension of the abdomen pushing on the lungs, the patient also may develop tachypnea. In this regard, the lung fields may be decreased.
• The abdominal examination generally reveals a distended abdomen, which may or may not be tense. Serial measurement of abdominal girth is routinely unreliable.
• Bowel sounds vary from absent to diminished to high-pitched, mimicking mechanical obstruction.
• Tympany invariably is present.
• Digital rectal examination should generally be performed to exclude fecal impaction.

Causes

• Causes of acute megacolon include the following:  
• • Electrolyte abnormality
  • 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.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Other Problems to be Considered

Intestinal/colonic obstruction (eg, malignancy, volvulus, intussusception, fecal impaction, rectal prolapse, foreign body)

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Lab Studies

Laboratory studies are directed at establishing the etiology of the acute megacolon as well as determining the patient's fluid status.

• Complete blood count
• Electrolytes (including calcium, magnesium, and phosphorus)
• BUN and creatinine
• Thyroid studies
• Stool studies (including leukocytes, ova and parasites, and C difficile toxin assay)
• Blood cultures

Imaging Studies

Imaging studies are used to determine severity, to exclude free intraperitoneal air (perforation) as well as other etiologies (eg, extrinsic compression), and to follow clinical course. 

• 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 enema, CT, or MRI, may also be used to exclude obstruction.

Procedures

• 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.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Medical Care

• Conservative management is preferred when the patient is clinically stable.  
• • The underlying cause is treated, if possible, such as correction of any electrolyte/metabolic abnormalities and removal of medications that may decrease colonic motility (eg, narcotics, anticholinergic agents, calcium channel antagonists).
  • Oral feeding should be discontinued, and intravenous fluids should be initiated.
  • If nausea and vomiting are present, nasogastric decompression should be initiated.
• 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.
• 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 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 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.
• 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.
• 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 one uses for defining acute megacolon, the diameter of the cecum is the most important criterion because the cecum is generally the area that may be perforated. 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.

Surgical Care

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 remain 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.

Diet

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 nutritional status.

Activity

Because many of the cases of acute pseudo-obstruction occur postoperatively, patients tend to be 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.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Drug Category: Cholinergic agents

Increase peristalsis and secretions in the intestine and relax the sphincter.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Further Inpatient Care

• Once relieved, close follow-up care, including physical examination and maintenance of a normal electrolyte balance, is important.

Further Outpatient Care

In/Out Patient Meds

• Avoiding agents that slow transit time, such as opiates and anticholinergics, is advisable.

Complications

• 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.¹
• 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.

Prognosis

Prognosis is determined in part by the underlying cause of the megacolon, any comorbidities, and the development of complications.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Medical/Legal Pitfalls

• Failure to diagnose megacolon may result in mortality associated with spontaneous perforation of nontoxic megacolon.

ACKNOWLEDGMENTS

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Clifford Y Ko, MD, MS, to the development and writing of this article.

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

1. Vanek VW, Al-Salti M. Acute pseudo-obstruction of the colon (Ogilvie's syndrome). An analysis of 400 cases. Dis Colon Rectum. Mar 1986;29(3):203-10. [Medline].
2. Camilleri M. Acute and chronic pseudo-obstruction. In: Felman M, Friedman LS, Sleisenger MH. Sleisenger & Fordtran's Gastrointestinal and Liver Disease. 8^th ed. Philadelphia, PA: Saunders Publishing; 2007:2679-2702.
3. Fazel A, Verne GN. New solutions to an old problem: acute colonic pseudo-obstruction. J Clin Gastroenterol. Jan 2005;39(1):17-20. [Medline].
4. Geller A, Petersen BT, Gostout CJ. Endoscopic decompression for acute colonic pseudo-obstruction. Gastrointest Endosc. Aug 1996;44(2):144-50. [Medline].
5. Ponec RJ, Saunders MD, Kimmey MB. Neostigmine for the treatment of acute colonic pseudo-obstruction. N Engl J Med. Jul 15 1999;341(3):137-41. [Medline].
6. Saunders MD, Kimmey MB. Colonic pseudo-obstruction: the dilated colon in the ICU. Semin Gastrointest Dis. Jan 2003;14(1):20-7. [Medline].
7. Stephenson BM, Morgan AR, Salaman JR, Wheeler MH. Ogilvie's syndrome: a new approach to an old problem. Dis Colon Rectum. Apr 1995;38(4):424-7. [Medline].
8. Turegano-Fuentes F, Munoz-Jimenez F, Del Valle-Hernandez E, Perez-Díaz D, Calvo-Serrano M, De Tomas J, et al. Early resolution of Ogilvie's syndrome with intravenous neostigmine: a simple, effective treatment. Dis Colon Rectum. Nov 1997;40(11):1353-7. [Medline].

Article Last Updated: Apr 16, 2008