Updated: Jul 30, 2008
Ogilvie syndrome, or acute colonic pseudo-obstruction (ACPO), is a clinical disorder with the signs, symptoms, and radiographic appearance of an acute large bowel obstruction with no evidence of distal colonic obstruction. The colon may become massively dilated; if not decompressed, the patient risks perforation, peritonitis, and death.
In 1948, Ogilvie described 2 patients with metastatic cancer and retroperitoneal spread to the celiac plexus. The patients also had signs and symptoms of colonic obstruction but with no evidence of organic obstruction to the intestinal flow. Ogilvie hypothesized that the etiology of their conditions was an imbalance in the autonomic nervous system with sympathetic deprivation to the colon, leading to unopposed parasympathetic tone and regional contraction, with resulting functional obstruction.
In 1958, Dudley et al used the term pseudo-obstruction to describe the clinical appearance of a mechanical obstruction with no evidence of organic disease during laparotomy.
The pathophysiology of Ogilvie syndrome is not clearly understood. Research into the neurophysiology of the colon reveals that Ogilvie's hypothesis was close to the proposed current understanding. The parasympathetic nervous system promotes gut motility. The vagus nerve supplies the parasympathetic tone from the upper GI tract to the splenic flexure, and the sacral parasympathetic nerves (S2 to S5) supply the left colon and the rectum. Sympathetic stimuli result in the inhibition of bowel motility and the contraction of sphincters. The lower 6 thoracic segments supply the sympathetic tone to the right colon, while lumbar segments 1-3 supply the left colon.
An imbalance in the autonomic innervation appears to lead to a functional bowel obstruction, as supported by pharmacologic and spinal blockade studies, metabolic abnormalities, and retroperitoneal trauma. Unlike Ogilvie's hypothesis, some current evidence suggests that an interruption of the sacral parasympathetic nerves occurs, leading to an adynamic distal colon that is similar to Hirschsprung disease, except with normal ganglion cells observable on autopsy. Other research supports the belief that the sympathetic tone increases in these patients, who are usually very ill, leading to inhibition of colonic motility.
The cecum is the usual site of the largest dilatation in patients with Ogilvie syndrome and, thus, is more prone to the risk of perforation. The Laplace law indicates that the intraluminal pressure needed to stretch the wall of a hollow tube is inversely proportional to its diameter. The cecum, with its larger diameter, requires the smallest amount of pressure to increase in size and in wall tension. As the wall tension of the colon increases, ischemia with longitudinal splitting of the serosa, herniation of the mucosa, and perforation can occur.
The frequency has not been established.
This rare clinical condition makes it difficult to gather solid epidemiological studies, particularly in regard to its frequency.
Mortality rates of 15-50% have been reported; however, with increased awareness, better diagnostic tools, and prompt management of this disorder, mortality rates have decreased. The risk of perforation is higher with a larger cecal diameter. Generally, the overall medical status of patients with Ogilvie syndrome is poor. The prognosis in patients successfully treated for this disorder is directly related to the severity of the co-occurring medical conditions.
No data suggest a different frequency according to race.
No convincing data suggest a different frequency according to sex; however, some researchers suggest that this illness may have a slight male predominance, possibly by a ratio of 1.5:1.
Ogilvie syndrome is generally a disease of elderly patients, usually older than 60 years; however, this disorder may occur in younger patients, particularly those with underlying spinal cord disorders.
Patients with Ogilvie syndrome present with abdominal distention and generally have obstipation. Up to 40% may have a recent history of flatus or passage of stool. Presenting symptoms are as follows:
Ogilvie syndrome usually occurs in a setting of a recent serious medical illness or surgical procedure. The 3 most common associations are trauma, infection, and cardiac disease, especially myocardial infarction and congestive heart failure.
| Acute Mesenteric Ischemia | Hirschsprung Disease |
| Chronic Mesenteric Ischemia | Intestinal Perforation |
| Colon Cancer, Adenocarcinoma | Megacolon, Acute |
| Colonic Obstruction | Megacolon, Chronic |
| Constipation | Megacolon, Toxic |
| Diverticulitis | Pseudomembranous Colitis |
Colonic volvulus may manifest in a fashion similar to colonic pseudo-obstruction. The following conditions should also be considered:
Diagnosis and management of colonic pseudo-obstruction require that mechanical bowel obstruction be completely excluded. Initial management requires an evaluation for signs of bowel ischemia or perforation; if present, these problems must be addressed immediately.
A small percentage of patients with Ogilvie syndrome may require surgical intervention.
In general, patients with Ogilvie syndrome are not allowed to have anything by mouth until the disorder is reversed.
If the patient is able, ambulation can have beneficial aspects on colonic motility patterns. However, patients with acute Ogilvie syndrome typically are not ambulatory.
Prior to medical therapy, a mechanical bowel obstruction must be excluded. Ensure that colonic air is found in all colonic segments, including the rectosigmoid, prior to consideration of neostigmine therapy. If air is not demonstrable on abdominal films, a mechanical obstruction should be excluded via contrast enema.
Ponec et al demonstrated the utility of neostigmine in colonic pseudo-obstruction.1
Inhibits destruction of acetylcholine by acetylcholinesterase, which facilitates transmission of impulses across myoneural junction.
1-2 mg IV/SC; may repeat in 3 h if needed
Not established
Atropine antagonizes muscarinic effects of neostigmine; effects of neuromuscular agents are increased; other agents that cause bradycardia, including beta-blockers and calcium channel blockers, should not be coadministered
Documented hypersensitivity; GI or GU obstruction; baseline heart rate <60 bpm or systolic blood pressure <90 mm Hg; sick sinus syndrome or history of second- or third-degree A-V block without a pacemaker; active bronchospasm requiring medication
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in renal failure, epilepsy, asthma, bradycardia, hyperthyroidism, cardiac arrhythmias, or peptic ulcer; anticholinesterase insensitivity can develop for brief or prolonged periods; patients with renal impairment may have an increased or prolonged response after administration; monitor carefully for bradycardia (should be on a heart monitor during administration); keep atropine (0.6-1.2 mg IV) on hand as an antidote for muscarinic adverse effects
Can be helpful in some circumstances. This therapy may cleanse the colon and gently enhance colonic motility, thereby correcting the underlying problem. The cleansing effect may also make subsequent attempts at colonoscopic decompression easier.
Laxative with strong electrolyte and osmotic effects that has cathartic actions in GI tract.
1 adult enema PR
Not established
Reduces effectiveness and absorption of oral medications
Documented hypersensitivity, colitis, megacolon, bowel perforation, gastric retention, GI obstruction
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in ulcerative colitis and hot loop polypectomy
Lubricates the bowel and softens the stool. Can be used as a retention enema.
1 adult enema PR
Not established
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in leukemia or thrombocytopenia
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Ogilvie syndrome, Ogilvie's syndrome, acute colonic pseudo-obstruction, ACPO, colonic pseudoobstruction, bowel obstruction, colonic obstruction, acute large bowel obstruction, colonic perforation, intestinal perforation, peritonitis, nontoxic megacolon, bowel motility, adynamic distal colon, Hirschsprung disease, abdominal distention, obstipation, cecal perforation, cecostomy, colonoscopy, colonoscopic decompression, colectomy
Prospere Remy, MD, Assistant Professor of Medicine, Albert Einstein College of Medicine; Attending Physician, Department of Internal Medicine, Bronx-Lebanon Hospital Center
Prospere Remy, MD is a member of the following medical societies: American College of Physicians and American Society for Gastrointestinal Endoscopy
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Kavita Kumbum, MD, Fellow, Division of Gastroenterology, Bronx Lebanon Hospital Center, Albert Einstein College of Medicine
Kavita Kumbum, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
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Steven Carpenter, MD, Chair, Program Director, Department of Internal Medicine, Memorial Health University Medical Center
Steven Carpenter, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
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Bjorn Holmstrom, MD, Assistant Professor, Department of Internal Medicine, University of South Florida
Bjorn Holmstrom, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Medical Association, Medical Association of Georgia, and Phi Beta Kappa
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Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
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Douglas M Heuman, MD, FACP, Director of Hepatology, McGuire Veterans Affairs Medical Center, Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine
Douglas M Heuman, MD, FACP is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, and American Gastroenterological Association
Disclosure: Nothing to disclose.
Alex J Mechaber, MD, FACP, Assistant Dean for Medical Curriculum, Associate Professor of Medicine, Division of General Internal Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
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Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
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