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 but 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.[1] 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. See the image below.
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Ogilvie syndrome.
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.[2, 3]
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.
This rare clinical condition makes it difficult to gather solid epidemiological studies, particularly in regard to its frequency.
Mortality/Morbidity
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.
Race
No data suggest a different frequency according to race.
Sex
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.
Age
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.
CBC count: Leukocytosis should raise concerns for possible impending or frank perforation.
Electrolytes: Disorders of potassium, sodium, calcium, and magnesium may be the underlying cause of the problem. Patients with colonic pseudo-obstruction are commonly dehydrated and frequently exhibit prerenal azotemia or renal insufficiency.
This is the most useful diagnostic tool for this disorder. Plain and upright abdominal films show a dilated colon, often from the cecum to the splenic flexure and occasionally to the rectum. Haustral markings remain normal. Serial films may be used to follow the clinical course and the response to treatment.
Specific attention to the diameter of the colon is important. If the colonic diameter exceeds 10 cm, decompression of the colon must be considered and expedited. In addition to cecal diameter, the duration of distension also appears to be an important factor in perforation risk, with the risk lowest in patients who undergo decompression within less than 4 days of onset.
CT scan
While a CT scan is not required to establish a diagnosis, it may be helpful in excluding the presence of frank perforation, obstruction, and toxic megacolon.[4]
Gastrografin is water-soluble and has a high osmolarity; therefore, this contrast medium tends to cause a fluid shift into the colon and may subsequently increase colonic motility. A Gastrografin enema may be both diagnostic and therapeutic for this disorder.
Barium enema
Given the nature of pseudo-obstruction, air should not be instilled into the colon if this procedure is performed.
Diagnosis and management of colonic pseudo-obstruction require that mechanical bowel obstruction be completely excluded.[5] Initial management requires an evaluation for signs of bowel ischemia or perforation; if present, these problems must be addressed immediately.
Addressing basic issues of supportive care prior to initiating specific medical therapy is critical. Aggressively treat any reversible underlying medical condition (eg, respiratory failure, congestive heart failure [CHF], systemic infection). Administer intravenous fluids to correct any volume deficit. Correct electrolyte imbalances.
Nasogastric suction or decompression can be helpful; furthermore, rectal tube decompression can be therapeutic in some cases.
Promptly discontinue any medications that might precipitate or exacerbate this problem (eg, narcotics, anticholinergics).
Colonoscopic decompression is a very useful method to remove air from the colon and, hopefully, to reduce the risk of subsequent colonic perforation; however, this procedure may be difficult to perform because of poor colonic preparation in most patients. Colonoscopy is successful in reducing colonic air in 70-85% of patients.
Decompression may be facilitated by placement of a decompression tube.
Passage of the endoscope to the hepatic flexure is usually sufficient to decompress the cecum.
If a decompression tube is placed, flush the tube every 2-4 hours with enough saline to maintain patency.
The main risk of decompressive colonoscopy is perforation. Maintain great care to avoid excessive air insufflation during endoscope insertion.
The risk of perforation is probably higher in patients with significant colonic ischemia.
Although colonoscopic decompression is usually successful, cecal distention often recurs. The literature indicates recurrence rates of 22-41%.
A small percentage of patients with Ogilvie syndrome may require surgical intervention.
Tube cecostomy
This procedure allows for colonic venting in patients with Ogilvie syndrome. In some patients, this procedure is curative, and the tube may later be removed without the need for subsequent surgical intervention.
Reserve cecostomy for patients with impending cecal perforation.
Generally, a cecostomy is performed via open technique.
Percutaneous cecostomy may also be performed via CT guidance.
A laparoscopically assisted cecostomy using T-bars to anchor the cecum to the anterior abdominal wall is another acceptable intervention.
Subtotal colectomy
In patients with subsequent perforation, a subtotal colectomy may be required.
Generally, patients with perforation require temporary diversion, with plans for a second operation to establish bowel continuity at a later date.
Potential complications include abscess formation, ileus, and bleeding.
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.[6] 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.[7]
In a small study examining the effects of pyridostigmine on colonic motility disorders, O'Dea et al investigated treatment outcomes in 6 patients with slow-transit constipation and 7 patients with recurrent pseudo-obstruction of the bowel.[8] The authors found some symptom improvement in all of the patients suffering from pseudo-obstruction, with few side effects occurring (although 2 patients later underwent surgery for recurrent symptoms). However, pyridostigmine did not reduce symptoms in those patients with slow-transit constipation.
These agents 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.
Treatment of the underlying medical condition: As previously mentioned, colonic pseudo-obstruction is usually precipitated by an important underlying condition. Appropriately replace electrolytes and promptly manage infections with adequate antimicrobial therapy.
If the patient shows a tendency toward colonic inertia, outpatient treatment is necessary. Osmotic laxatives and fiber can be useful to provide adequate stool frequency.
If endoscopic or surgical expertise in the area does not allow for patient management in a timely manner, consider transferring the patient to another facility.
If the colon is not decompressed before it reaches critical diameter, the patient is at risk for colonic perforation. Once again, this complication may be prevented by timely diagnosis and management of the problems at hand.
Prospere Remy, MD, Assistant Professor of Medicine, Albert Einstein College of Medicine; Attending Physician, Department of Internal Medicine, Bronx-Lebanon Hospital Center
Disclosure: Nothing to disclose.
Coauthor(s)
Bjorn Holmstrom, MD, Assistant Professor, Department of Internal Medicine, University of South Florida
Disclosure: Nothing to disclose.
Kavitha Kumbum, MD, Associate Program Director and Attending Physician, Gastroenterology Fellowship Program, Division of Gastroenterology, Bronx Lebanon Hospital Center, Albert Einstein College of Medicine
Disclosure: Nothing to disclose.
Steven Lee Carpenter, MD, FACP, AGAF, FASGE, Academic Chair, Associate Professor of Medicine, Department of Internal Medicine, Internal Medicine Program Director, Mercer University School of Medicine; Senior Partner, The Center for Digestive and Liver Health, The Endoscopy Center
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Douglas M Heuman, MD, FACP, FACG, AGAF, Chief of GI, Hepatology, and Nutrition at North Shore University Hospital/Long Island Jewish Medical Center; Professor, Department of Medicine, Hofstra North Shore-LIJ School of Medicine
Alex J Mechaber, MD, FACP, Senior Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Disclosure: Nothing to disclose.
Chief Editor
Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine
Disclosure: Nothing to disclose.
References
Ogilvie WH. Large intestine colic due to sympathetic deprivation: a new clinical syndrome. BMJ. 1948;2:671-3.
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