Intestinal Pseudo-Obstruction

Updated: Jul 23, 2018
Author: Burt Cagir, MD, FACS; Chief Editor: John Geibel, MD, MSc, DSc, AGAF 



The term intestinal pseudo-obstruction denotes a syndrome characterized by a clinical picture suggestive of mechanical obstruction in the absence of any demonstrable evidence of such an obstruction in the intestine.[1] On the basis of the clinical presentation, pseudo-obstruction syndromes can be divided into acute and chronic forms. In acute colonic pseudo-obstruction (ACPO[2] ; also referred to as Ogilvie syndrome[3] ), the colon may become massively dilated; if it is not decompressed, the patient risks perforation, peritonitis, and death. The mortality rate can be as high as 40% when perforation occurs.

Every effort should be made to prevent ACPO in hospitalized and postoperative patients with serious concurrent medical and surgical conditions. Earlier mobilization and positioning of hospitalized patients has become an important preventive strategy in this regard. Furthermore, prevention of colonic distention through more aggressive use of bowel regimens for the prevention of obstipation is critically important in hospitalized patients, who are particularly susceptible to this clinical condition.

The development of new and effective pharmacologic agents for the treatment of ACPO would substantially reduce the need for surgical intervention, which is associated with considerable morbidity and mortality. It is to be hoped that such agents will become available in the future.

Because ACPO can recur, patients and families should be offered counseling about this disease process. They should be educated regarding the signs and symptoms of recurrent pseudo-obstruction and should be informed that recurrent abdominal distention warrants prompt medical attention.

Chronic colonic pseudo-obstruction (CCPO) also exists and should be distinguished from patients with ACPO. Criteria for CCPO include symptoms of recurrent bowel obstruction in the last 6 months, abdominal bloating and/or pain in the previous 3 months, evidence of bowel obstruction on radiographic imaging, and no evidence of anatomic/structural abnormality.[4]


The large intestine may be divided into the following parts:

  • Cecum

  • Ascending colon

  • Hepatic flexure

  • Transverse colon

  • Splenic flexure

  • Descending colon

  • Sigmoid colon

  • Rectum

The cecum is located in the right iliac fossa. In comparison with the descending colon, sigmoid colon, and rectum, the cecum and ascending colon are saccular, are larger in diameter, and have thinner walls.

The largest dilatations in ACPO patients usually develop in the cecum. According to Laplace’s law, the intraluminal pressure needed to stretch the wall of a hollow tube is inversely proportional to its diameter. Accordingly, the cecum, with its larger diameter, requires less 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 (including iatrogenic perforation during open or laparoscopic procedures) can occur.

The vagus nerve supplies the parasympathetic tone from the upper gastrointestinal (GI) tract to the splenic flexure, and the sacral parasympathetic nerves (S2 to S5) supply the left colon, sigmoid, and 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, whereas lumbar segments 1-3 supply the left colon.[5, 6]


The exact pathophysiology of intestinal pseudo-obstruction remains to be elucidated.[7] Current theories continue to suggest the idea of an imbalance in the autonomic nervous system. These theories focus on the increased sympathetic tone, the decreased parasympathetic tone, or a combination of both as the cause of intestinal pseudo-obstruction.[8, 9]

One theory, examined in a 1988 study by Lee et al, is that increased sympathetic tone to the colon results in the inhibition of colonic motility.[10] By using epidural anesthesia to block the splanchnic sympathetics, the authors successfully treated several patients whose ACPO did not respond to conservative management.[11] A subsequent report on the use of spinal anesthesia for the treatment of Ogilvie syndrome supported this hypothesis.[12]

Another theory regarding the etiology of intestinal pseudo-obstruction focuses on parasympathetic tone. According to this theory, the nature of the parasympathetic distribution (see Etiology) suggests that disruption of the sacral innervation may leave the distal colon atonic, thus resulting in a functional obstruction.[8, 11, 13, 14] This hypothesis is consistent with studies showing a transition between a dilated and collapsed bowel that is often at or near the splenic flexure.[15, 16]

Other investigators believe that the disorder is a result of a combination of increased sympathetic tone and decreased parasympathetic tone. In 1992, Hutchinson et al reported successfully treating 8 of 11 patients with colonic pseudo-obstruction by using the sympathetic adrenergic blocker guanethidine, followed by the cholinesterase inhibitor neostigmine.[17]

The pathophysiology of ACPO has been studied in Sprague-Dawley male rats.[18] Partial colonic obstruction was created by placing a medical-grade silicon ring that was 3 mm wide and 1-2 mm longer than the outer circumference of the rat colon. The sham control rats underwent the same procedure with immediate removal of the ring at the completion of the procedure. Accumulation of stool pellets created the partial colonic pseudo-obstruction in rats with silicon rings.

The investigators examined 3-cm long colonic segments that included both obstructed and nonobstructed portions and found that the expression of cyclooxygenase (COX)-2 mRNA was drastically increased in only the obstructed and distended colonic portions.[18] (Mechanical stretch in obstruction induces the marked expression of COX-2, and COX-2 plays an important role in suppression of smooth muscle contractility.) The upregulation of COX-2 started at 12 hours after the pseudo-obstruction and lasted about 7 days.

A more recent proposal regarding the mechanism underlying symptomatic chronic intestinal pseudo-obstruction (CIPO) suggests involvement of the transition zone (TZ) between the dilated and nondilated bowel loops, leading to proximal distention and smooth muscle hypertrophy.[7] Deficiency in myenteric ganglia and neuronal nitric oxide synthase positive cells, particularly affecting the TZ, could be an important contributing factor.[7]


The causes of ACPO are multifactorial. The 3 most common associations are the following:

  • Trauma (especially retroperitoneal)

  • Serious infection

  • Cardiac disease (especially myocardial infarction and congestive heart failure)

Other conditions commonly associated with colonic pseudo-obstruction are as follows:

  • Recent surgery (abdominal, urologic, gynecologic, orthopedic, cardiac, or neurologic)

  • Spinal cord injury

  • Old age

  • Neurologic disorders

  • Hypothyroidism

  • Electrolyte imbalances (hyponatremia ,hypokalemia ,hypocalcemia ,hypercalcemia , orhypomagnesemia )

  • Respiratory disorders

  • Renal insufficiency

  • Medications (eg, narcotics, tricyclic antidepressants, phenothiazines, antiparkinsonian drugs, and anesthetic agents)

  • Severe constipation[19]

The condition may also observed in patients with the following:

  • Intestinal hypoperistalsis syndrome

  • Megacystis megacolon

  • Amyloidosis

  • GI carcinoma

  • Guillain-Barré syndrome

  • Multiple myeloma

  • Alcohol abuse

  • Systemic lupus erythematosus (SLE) (rare)[20, 21, 22]

  • Systemic sclerosis (rare)[23]


United States statistics

In studies involving more than 13,000 orthopedic and burn patients, the prevalence of ACPO was 0.29%.[24, 25] The frequency in patients undergoing major orthopedic surgery may be higher, with reported rates of 0.65-1.3%.[26] The true incidence of this disorder remains largely unknown because of the possibility of spontaneous resolution.

ACPO generally develops in hospitalized patients and is associated with a variety of medical and surgical conditions. Studies have documented that as many as 95% of cases of ACPO are associated with medical or surgical conditions, with the rest being classified as idiopathic.[2, 27, 28] The most commonly associated conditions include trauma; pregnancy; cesarean delivery; severe infections; and cardiothoracic, pelvic, or orthopedic surgery.[29, 30, 31, 32]

International statistics

Because ACPO is a rare clinical condition internationally, it is difficult to gather solid epidemiologic studies, particularly in regard to frequency.

Age-related demographics

Although intestinal pseudo-obstruction may occur in younger patients, particularly those with underlying spinal cord disorders, it is generally a disease of elderly patients. In fact, the mean age of patients with ACPO appears to be increasing.

In 1986, Vanek et al reviewed more than 400 cases of colonic pseudo-obstruction occurring between 1970 and 1985 and reported a mean patient age of 56.5 years for females and 59.9 years for males.[16] In the late 1980s, other reports also found mean ages to fall into the sixth decade.[33, 34] Since then, several reports have documented a rise in the mean age of ACPO patients, with most now finding the mean age to fall into the seventh and eighth decades of life.[25, 32, 35, 36]

Sex- and race-related demographics

Unlike the age distribution, the male-to-female ratio has apparently remained constant over the years. In the view of some, no convincing data suggest that frequency differs significantly according to sex; however, some researchers suggest that intestinal pseudo-obstruction may have a male predominance, possibly in a ratio of 1.5:1 (or even as high as 4:1).[16, 33, 37, 38]

No data suggest that frequency differs according to race.


Generally, the overall medical status of patients with ACPO is poor. The prognosis in patients successfully treated for this disorder is directly related to the severity of the underlying medical or surgical conditions that placed the patient at risk for colonic pseudo-obstruction to begin with.

Because of these associated conditions, morbidity and mortality remain high. In 1993, Datta et al documented an annual death rate of 200 patients (most of them elderly and bedridden) in the United Kingdom.[39] Mortality has been documented to be 14% in medically treated patients and 30% in surgically treated patients.[16] However, with increased awareness, better diagnostic tools, and prompt management of this disorder, mortality is decreasing.

Intestinal pseudo-obstruction is a rare gastrointestinal complication in patients with systemic sclerosis, but it is associated with high inpatient mortality relative to other patients with systemic sclerosis and those with intestinal pseudo-obstruction from other causes.[23]

The most serious complication of colonic pseudo-obstruction is perforation of the cecum. The reported incidence of cecal perforation is 3-40%, and the associated mortality is 40-50%.[2, 14, 35] A cecal diameter greater than 14 cm, a delay in colonic decompression, and advanced age are all predictors of colonic perforation.

Neostigmine should be administered only in patients without any mechanical colonic obstruction. Colonic distention can recur and may necessitate multiple administrations of neostigmine. A single dose of neostigmine is effective for 1-2 hours. Neostigmine is effective in treating 85-90% of cases of ACPO. Recurrent or persistent colonic distention may cause ischemia and perforation.[40]




Intestinal pseudo-obstruction (also referred to as acute colonic pseudo-obstruction [ACPO] or Ogilvie syndrome) occurs most commonly in debilitated, hospitalized patients with multiple medical problems and is associated with various medical and surgical conditions.[14, 27, 28, 29, 30, 31, 32] Surgical patients begin developing symptoms, which are often insidious in onset, an average of 3-5 days postoperatively.[2, 16, 25] Whether this disorder is associated with either medical or surgical conditions, the presenting signs and symptoms are similar.

Presenting symptoms include the following:

  • Abdominal pain (80%)

  • Nausea and vomiting (80%)

  • Obstipation (40%); as many as 40% may have a recent history of flatus or passage of stool

  • Fever (37%)

Physical Examination

Physical findings may include the following:

  • Abdominal distention (90-100%)

  • Abdominal tenderness (64%)

  • Hypoactive, high pitched, or absent bowel sounds (60%); normal or hyperactive bowel sounds (40%)

  • Empty rectum on digital examination

Vanek et al documented the presence of abdominal distention in virtually all patients with colonic pseudo-obstruction.[16] A subsequent report by Grassi et al found that the most relevant clinical finding in Ogilvie syndrome is abdominal distention, which arises suddenly, has a progressive course, and may worsen.[41]

Abdominal tenderness is noted in patients with perforated or ischemic bowel and in patients with viable bowel. As a rule, no significant differences are noted in the symptoms of patients with ischemic or perforated bowel compared with patients with viable bowel, except for a higher incidence of fever.



Diagnostic Considerations

Ogilvie syndrome should be considered in all patients with significant abdominal distention. Colonic volvulus may manifest in a fashion similar to colonic pseudo-obstruction and therefore should be considered as well.

In addition to the conditions listed in the differential diagnosis, other problems to be considered include the following:

  • Peritonitis

  • Electrolyte disturbances

  • Adverse reaction to medication

Differential Diagnoses



Approach Considerations

Laboratory investigations generally are of little diagnostic value for intestinal pseudo-obstruction (also referred to as acute colonic pseudo-obstruction [ACPO] or Ogilvie syndrome]). The diagnosis is based largely on the clinical signs and symptoms, the natural history of the condition, and the findings from radiographic studies.[42]

Plain radiography is the most useful diagnostic tool in this setting. If plain radiography fails to confirm the diagnosis, a contrast enema may be used. Contrast enema should also be used in cases to rule out mechanical colonic obstruction. Although computed tomography (CT) is not required to establish a diagnosis, it may be helpful for excluding the presence of frank perforation, obstruction, and toxic megacolon.[43]

Colonoscopy may be helpful not only diagnostically but also therapeutically. This procedure can help exclude an obstructive process and decompress the colon.

Laboratory Studies

A complete blood count (CBC) is indicated. A finding of leukocytosis should raise concerns for possible impending or frank perforation. However, it should be kept in mind that leukocytosis is found in the presence of viable as well as ischemic bowel and is therefore nondiagnostic of intestinal pseudo-obstruction.[2, 14]

Mild electrolyte imbalances are often present and typically signify dehydration.[27] Hyponatremia and hypokalemia can be present and reflect a consequence of the pathologic condition, rather than its etiologic factor.[2, 8, 14, 25] Patients frequently exhibit prerenal azotemia or renal insufficiency.

A liver function profile may be helpful.

Plain Abdominal Radiography

Aside from physical examination, the most useful screening test for intestinal pseudo-obstruction is plain abdominal radiography.[41] Films show a dilated colon, with dilatation often extending from the cecum to the splenic flexure and occasionally to the rectum (see the images below). Serial films may be used to follow the clinical course and the response to treatment.

Abdominal radiographs confirm acute colonic pseudo Abdominal radiographs confirm acute colonic pseudo-obstruction after hip surgery. Note extensive, diffuse colonic dilation with no evidence of transition point.
Ogilvie syndrome. Ogilvie syndrome.

The most common finding is massive colonic dilatation involving the cecum and the ascending and transverse colon. Progressive colonic dilatation can lead to marked increases in cecal distention. By the Laplace law, the tensile strength of the colonic wall will be exceeded first in that portion of the colon that has the greatest diameter—namely, the cecum.[13] Thus, the cecum is the most common site of perforation in colonic pseudo-obstruction.[16, 27]

Although no agreement has been reached regarding the absolute cecal diameter that results in perforation, most investigators agree that the risk of perforation is markedly increased with cecal diameters in the range of 12-14 cm.[13, 14, 16, 33, 37] Therefore, frequent abdominal radiographs to assess the diameter of the cecum are useful in the management of these patients.

The transition between dilated and collapsed bowel is usually near the splenic flexure but can occasionally occur in the distal or sigmoid colon.[27, 37, 44]

Air-fluid levels are only occasionally observed; small bowel dilatation can occur, but this relies on the incompetency of the ileocecal valve.[2, 8, 14, 29, 45]

Other radiologic features include well-defined colonic septa, a smooth contour of the inner lumen, and preservation of haustral markings.[16, 37, 45, 46]

Differentiating colonic pseudo-obstruction from true obstruction is sometimes difficult. A 1995 study suggested using a prone lateral view of the rectum to help confirm the diagnosis.[47] Placing patients in the right lateral decubitus position for several minutes to allow gas to pass into the distal colon facilitated gaseous filling of the rectum when patients were positioned for a prone lateral view of the pelvis. This approach had a 75% success rate in excluding mechanical obstruction, and gaseous filling did not occur in any patients with mechanical obstruction.[47]

An abdominal CT scan is very helpful to confirm the diagnosis by excluding mechanical obstruction and toxic megacolon.

Contrast Enema

If the diagnosis cannot be confirmed by means of plain radiography or physical examination, a contrast enema may be used. Common enemas include barium and diatrizoate meglumine. Both of these contrast materials are contraindicated in the presence of perforation. Because of the risk of perforation, the contrast material should be introduced under low pressure. No air is required, and the examination may be terminated when the dilated colon is reached.

Diatrizoate meglumine has advantages over barium in that it is clear and water-soluble. In addition, it can be more easily washed away at the time of colonoscopy and can often be therapeutic because of its hyperosmolarity, which results in fluid shifts into the lumen and may subsequently increase colonic motility. Furthermore, it removes the risk of peritoneal contamination with barium if a perforation occurs or a laparotomy becomes necessary.[16, 30, 48, 49, 50]


Flexible colonoscopy can differentiate colonic pseudo-obstruction from mechanical colonic obstruction and can also serve a therapeutic function when colonic decompression is performed during diagnostic colonoscopy. If a mechanical condition is identified as the cause of colonic obstruction during the diagnostic procedure, biopsy of the colonic mass can also be accomplished via flexible colonoscopy. The procedure may be challenging to perform in many patients because of the difficulty of accomplishing adequate bowel preparation.



Approach Considerations

Diagnosis and management of intestinal pseudo-obstruction (also referred to as acute colonic pseudo-obstruction [ACPO] or Ogilvie syndrome) require that mechanical bowel obstruction be absolutely excluded.[51] To this end, it is important to ensure that colonic air is found in all colonic segments, including the rectosigmoid, before considering neostigmine therapy (see Pharmacologic Therapy).[52] If air is not demonstrable on abdominal films, a mechanical obstruction should be excluded by means of a contrast enema.

Therapy should be initiated in a timely fashion once the diagnosis is confirmed (see the image below). Initial management requires an evaluation for signs of bowel ischemia or perforation; if present, these problems must be addressed immediately. Treatment goals include relief of symptoms associated with gut dysmotility, as well as abdominal pain control and optimization of nutritional support.[53]

Treatment algorithm for intestinal pseudo-obstruct Treatment algorithm for intestinal pseudo-obstruction.

It is critical to address basic issues of supportive care before initiating specific medical therapy. Any reversible underlying medical condition (eg, respiratory failure, congestive heart failure [CHF], or systemic infection) should be treated aggressively. Fluids should be administered intravenously (IV) to correct any volume deficit. Any electrolyte imbalances should be corrected as well.

Nasogastric suction or decompression can be helpful; furthermore, rectal tube decompression can be therapeutic in some cases. Any medications that might precipitate or exacerbate the problem (eg, narcotics or anticholinergics) should be promptly discontinued.

Pharmacologic options include erythromycin, cisapride, and metoclopramide, as well as cholinesterase inhibitors (eg, neostigmine and pyridostigmine).

The combined use of a sympathetic blocker followed by a cholinesterase inhibitor (neostigmine) to treat motility disorders was first documented by Catchpole in 1969.[54] In 1992, building on this earlier work, Hutchinson et al documented improvement in 73% of patients with ACPO after administration of guanethidine (20 mg IV) followed by neostigmine (2.5 mg IV over 1 minute).[17] These results have been confirmed in other nonrandomized trials using only neostigmine.[36, 38, 55, 56]

Colonoscopic decompression is a useful method for removing air from the colon and thereby, it is hoped, reducing the risk of subsequent colonic perforation; however, this procedure may be difficult to perform because of poor colonic preparation in most patients.

Colonoscopy for ACPO is carried out without the use of oral laxatives or bowel preparation. Because narcotics inhibit colonic motility, sedation should be achieved with benzodiazepines alone. Also, since decompression at the level of the proximal hepatic flexure is normally adequate, cecal intubation is unnecessary. Colonoscopy is contraindicated in cases involving overt peritonitis or perforation; it is uncertain whether ischemia is an absolute contraindication for colonoscopic decompression.[57, 58]

Using a multicenter database in Korea, Lee and colleagues investigated the clinical characteristics of colonic pseudo-obstruction (CPO) and the factors associated with the response to medical treatment and found that younger age at the time of diagnosis, abdominal distention as a chief complaint, and greater cecal diameter were independently associated with poor responses to medical treatment.[59]

A small percentage of patients with ACPO may require surgical intervention. Contraindications to the surgical correction of intestinal pseudo-obstruction are based on the patient’s comorbidities and his or her ability to tolerate surgery.

Consultation with a gastroenterologist, a general surgeon, or both may be helpful. If the level of endoscopic or surgical expertise in the area does not allow timely patient management, consider transferring the patient to another facility.

In general, patients with ACPO 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 ACPO typically are not ambulatory.

In general, further outpatient care is dictated by the patient’s underlying medical condition(s). Outpatient care can usually be managed by the primary care physician. 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.

Supportive Care and Conservative Management

Once the diagnosis is confirmed, conservative management may be attempted. This includes no oral intake (nil per os [NPO]), nasogastric decompression, correction of fluid and electrolyte disorders, reduction or discontinuance of drugs that inhibit gastrointestinal motility, and treatment of infections.[9, 19, 37, 60] Incentive spirometry and intermittent positive-pressure breathing may aggravate colonic dilatation and should be avoided or discontinued if possible. Changing the patient’s position in bed may help mobilize intestinal gas.[9, 37, 61]

Other, less effective treatment measures include repeat enemas, rectal tubes, and rigid sigmoidoscopy.[14, 33, 45] Several studies have documented mean durations of conservative management ranging from 3 days to 6.5 days and have reported even longer periods if clinical signs of perforation were absent and cecal diameters were less than 9 cm.[2, 8, 32, 34, 35, 60]

The success rate with conservative management varies markedly, with some studies documenting rates as high as 96%.[34] An analysis of 1027 cases reported in the literature concluded that a nonoperative approach (including conservative measures and colonoscopic decompression as the initial therapy of choice) was associated with few complications and high efficacy.[62]

Other studies have documented much lower success rates, and this disparity may largely be caused by differences in patient selection, diagnostic criteria, study design, and potential bias toward therapeutic interventions among various studies.[2, 8, 32, 35] Despite the wide variations in reported success rates, a trial of conservative therapy is still warranted, provided that no clinical signs of peritonitis or increases in abdominal distention are present.

An important component of conservative medical therapy is maintenance of a bowel regimen to prevent constipation or obstipation and improve colonic motility. Low-volume cathartic agents, such as lactulose or low-dose polyethylene glycol (both of which are nonabsorbable, nonmetabolized osmotic agents), and daily bisacodyl suppositories to induce rectal emptying can facilitate treatment of ACPO and prevention of recurrences.[63]

If conservative therapy elicits no improvement or if the cecal diameter continues to increase, additional therapeutic options should be considered with a view to avoiding cecal perforation, which is associated with a higher mortality.[56, 64, 65]

Pharmacologic Therapy

Another therapeutic option is the use of pharmacologic agents to increase colonic motility. Several agents have been tried for this purpose, including erythromycin, cisapride, and metoclopramide; benefit has been demonstrated mostly in case reports.[16, 66, 67] Cholinesterase inhibitors, such as neostigmine, have also been evaluated for the treatment of ACPO.

The combined use of a sympathetic blocker followed by a cholinesterase inhibitor (neostigmine) to treat motility disorders was first documented by Catchpole in 1969.[54] In 1992, building on this earlier work, Hutchinson et al documented improvement in 73% of patients with ACPO after administration of guanethidine (20 mg IV) followed by neostigmine (2.5 mg IV over 1 minute).[17] These results have been confirmed in other nonrandomized trials using only neostigmine.[36, 38, 55, 56]

In 1999, Ponec et al conducted the first randomized controlled study using neostigmine.[68] The investigators randomly assigned 21 patients with ACPO to receive either 2 mg of neostigmine IV or placebo. Whereas 10 (91%) of the 11 patients who received neostigmine had prompt colonic decompression, none (0%) of the 10 patients who received placebo did. The median time to response was 4 minutes.

A subsequent systematic review of ACPO reported that the best-studied treatment was IV neostigmine, which leads to prompt colonic decompression in most patients after a single infusion.[69]

A common approach has been to consider colonoscopic decompression the active intervention of choice when neostigmine therapy fails or is contraindicated, with surgery reserved for cases of peritonitis or impending perforation. However, a 2012 report that retrospectively assessed 100 ACPO patients over a period of 10 years concluded that colonoscopy is superior to neostigmine and should be considered first-line therapy, though neostigmine remains useful in specific situations.[70]

Adverse effects of cholinesterase inhibitors include salivation, nausea, vomiting, abdominal pain, bradycardia, hypotension, and bronchospasm.[71] Patients should undergo cardiac monitoring, and atropine should be readily available during the administration of neostigmine. A slow infusion may carry a lower risk of bradycardic episodes than an IV bolus does.[72]

In a prospective placebo-controlled trial, neostigmine infusion was also found to resolve critical illness−related colonic ileus in intensive care unit (ICU) patients with multiple organ failure.[73] In this trial, neostigmine was administered via continuous IV infusion at a dosage of 0.4-0.8 mg/hr over 24 hours.

The use of neostigmine should not be contemplated unless mechanical large intestinal obstruction has been ruled out. Contraindications to neostigmine therapy include the following[55] :

  • Baseline heart rate lower than 60 beats/min

  • Systolic blood pressure lower than 90 mm Hg

  • Active bronchospasm necessitating medication

Neostigmine should not be used if a recently sealed-off colonic perforation is possible, because of the possibility that it may be unplugged by strong peristaltic contractions.[74] Neostigmine should be administered with atropine at the bedside; the patient should be kept supine in bed with continuous electrocardiographic monitoring and complete physician assessment every 15-30 minutes.

In a small study examining the effects of pyridostigmine on colonic motility disorders in 6 patients with slow-transit constipation and 7 with recurrent pseudo-obstruction of the bowel, O’Dea et al found some symptom improvement in all of the patients suffering from pseudo-obstruction, with few side effects occurring (though 2 patients later underwent surgery for recurrent symptoms).[75] However, pyridostigmine did not reduce symptoms in those patients with slow-transit constipation.

The search for new colokinetic agents for the treatment of lower-gut motor disorders has made available a number of drugs that may also be therapeutic options for intestinal pseudo-obstruction, including 5-hydroxytryptamine-4 receptor agonists and motilin receptor agonists.[71]

Several reports describe successful treatment with erythromycin, a motilinlike agent.

Cisapride, a partial 5HT4 receptor agonist, has also been used with some success, but it is no longer available in United States because of class III antiarrhythmic properties. Tegaserod may be active but has not been evaluated.

Methylnaltrexone, a peripherally acting opioid antagonist, has been reported to be effective in a patient on opioids following surgery, after initial decompression with neostigmine failed. Obviously, it should be evaluated on a larger scale, particularly in patients with Ogilvie syndrome associated with opioid use.

Colonoscopic Decompression

Yet another option for treatment of ACPO is colonoscopic decompression, first described in this setting by Kukora and Dent in 1977.[76] Since this first description, decompression of the colon with colonoscopy has been shown to be a safe and effective method for treating ACPO.[77] Several studies have documented success rates ranging from 77% to 86% with morbidities of only 0.2-2%.[16, 32, 46, 78] A retrospective review found it to be superior to neostigmine and suggested that it be considered first-line therapy.[70]

A retrospective review of 48 cases of Ogilvie syndrome found that of 45 patients who underwent 60 colonoscopic decompressions, 84% were successfully treated with colonoscopy, and 11% required surgery.[79] A single colonoscopy was successful in 64% of patients, and approximately one third of patients required serial colonoscopic decompressions. The average cecal diameter was greater in patients requiring serial colonoscopic decompressions.

High success rates notwithstanding, decompressive colonoscopy remains a technically difficult and demanding procedure as compared with elective diagnostic colonoscopy, requiring an average of 45-60 minutes to complete.[78] The main reasons for the relative difficulty of the procedure are as follows:

  • Because of the nature of the disease process, the colon cannot undergo a thorough bowel preparation; repeated gentle saline or tap water enemas can improve visibility but are not ideal[9, 76, 78]

  • Because of the risk of perforating an already dilated cecum, only minimal air insufflation may be used to dilate the distal colon

  • Because of the lack of thorough bowel preparation, the examiner’s ability to evaluate the colonic mucosa carefully for signs of ischemia is hindered; any sign of mucosal ischemia (eg, mucosal ulceration, submucosal hemorrhage, or friable mucosa with yellow exudates) indicates the need for urgent laparotomy[80, 81]

A study examining the effect of colonoscopy on cecal diameter (measured on supine radiographs) determined that colonoscopic decompression caused only a small decrease in cecal size in patients with ACPO.[82] Notably, dilation patters of the cecum and transverse colon were significantly correlated, providing additional support that the same pathophysiology affects these 2 segments of the colon.

Documented recurrence rates after colonoscopic decompression range from 18% to 65%.[9, 16, 35, 83] Improvements in these recurrence rates can be achieved by placing long indwelling decompression tubes, as was first described by Bernton et al in 1982.[80]

Since 1982, several authors have documented success with placing various decompression tubes in the proximal colon.[9, 84, 85] In 1988, Harig et al found that the recurrence rate was markedly lower in patients undergoing colonoscopic decompression with placement of an indwelling catheter (0%) than in those undergoing colonoscopic decompression alone (44%).[86] Unfortunately, colonic decompression tubes frequently become obstructed. An alternative to consider is serial colonoscopic decompression.

Colonoscopy to the cecum is unnecessary. Adequate decompression may be obtained by advancing the colonoscope as far as the transverse colon, though it is more likely to be achieved when the scope is passed into the ascending colon.[9, 33, 35, 60]

A retrospective study assessing the efficacy of diatrizoate meglumine enema for colonic decompression in patients with Ogilvie syndrome determined that it was successful in all but 2 patients who subsequently required surgery. It also helped rule out a mechanical cause of large bowel obstruction. These findings require validation in other studies before this approach can be recommended as therapy.[87]

A subsequent study evaluated the effect of polyethylene glycol (PEG) electrolyte-balanced solution on the relapse rate of the syndrome after initial resolution with neostigmine therapy or endoscopic decompression in 30 patients with a cecal diameter of 10 cm or greater.[88] Patients were randomly assigned to receive PEG (29.5 g) or placebo and monitored for 7 days.

Patients who received neostigmine as their initial therapeutic intervention (n=25) had an 88% success rate, and 8 patients underwent successful colonoscopic decompression.[88] Five (33%) patients from the placebo group had recurrent cecal dilation, compared with none in the PEG group. PEG therapy with also resulted in a significant increase in stool and flatus evacuations. This study documented that administration of PEG to patients with ACPO after initial resolution of colonic dilation may increase sustained response and prevent recurrence.

Surgical Intervention

Surgery is indicated when conservative medical management and colonoscopy fail or when clinical signs of ischemia, abdominal sepsis, or perforation are present.[2, 16, 89]  A case series from 2005 found that early recognition and prompt appropriate conservative therapy could lower morbidity and mortality and can reduce the number of cases requiring surgical intervention.[90] In this series, surgery was reserved for those cases in which the risk of cecal perforation represented an absolute indication for surgical intervention.

In cases of acute colonic dilatation without perforation or ischemia, tube cecostomy should be considered.[2, 14, 16, 27, 60, 91] This procedure can be performed via an open, a percutaneous, or a laparoscopic approach.[92] In some patients, this procedure is curative, and the tube may later be removed without the need for subsequent surgical intervention.

Although complications are rare in typical cases, tube cecostomy can be associated with significant complications in patients with a highly dilated cecum with thinned wall; in these circumstances, cecal or right colon resection is indicated.

Urgent laparotomy is indicated if signs and symptoms of ischemia or perforation are present or if colonoscopy confirms ischemia. The choice of procedure is dictated by the status of the cecum and ascending colon. If necrosis or ischemia is evident, the cecum should be resected. Whether to perform a primary anastomosis or a diversionary procedure depends on the presence of perforation and the extent of fecal contamination. The rest of the large bowel must be inspected to exclude remaining areas of ischemia, necrosis, or perforation.[2, 8, 14, 16, 35]

In a study assessing 25 patients who underwent surgery for constipation over a 9-year period, 19 (76%) of the 25 had features of colonic pseudo-obstruction with a distinct left colonic transitional zone, and 6 (24%) had uniform colonic dilatation without any transitional zone.[93] All 6 of the patients without a transitional zone and 17 of those with a transitional zone underwent total abdominal colectomy with ileorectal anastomosis.

Long-term follow-up (60 months) revealed no recurrences in patients with a transitional zone and 4 recurrences in patients without a transitional zone.[93] Therefore, total abdominal colectomy is recommended in patients with chronic constipation, colonic pseudo-obstruction, and a left colonic transitional zone.

A subtotal colectomy may be considered in some patients with perforation. A Spanish group has described a case in which an elderly patient with refractory chronic intestinal pseudo-obstruction was successfully treated with endoscopic-assisted colopexy and push percutaneous colostomy in the proximal transverse colon.[94]

In a patient who requires surgical intervention for ACPO, it is important to ensure that preoperative fluid resuscitation and optimization of cardiac status are initiated early. These measures facilitate accurate assessment of intestinal viability at the time of surgery and determination of the best operative procedure on the basis of the surgical findings. Because of the high rate of surgical site infection with emergency abdominal surgical procedures, IV antibiotics are administered before the surgical incision is made.

Fluid resuscitation for optimization of intestinal perfusion must be continued intraoperatively because extensive fluid losses can occur in patients with ACPO as a consequence of sequestration of intestinal fluid in the colon lumen and interstitial edema of the colonic wall. If colonic resection is necessary, decompression of the dilated colon can be accomplished, provided that care is taken to avoid causing peritoneal contamination. This should be done before the intestinal anastomosis is formed.

Patients with ACPO are at high risk for abdominal compartment syndrome as a result of visceral edema. If attempts at primary fascial closure are difficult at the completion of the operative procedure, temporary abdominal closure may be considered for prevention of abdominal compartment syndrome. Days later, when the visceral edema has resolved, a return to the operating room for primary fascial closure may be considered.

Postoperative care

All efforts to improve splanchnic perfusion should be continued in the postoperative period because the dilated colon is particularly susceptible to ischemic injury. Patients are maintained on NPO (nil per os, “nothing by mouth”) status with nasogastric tube decompression until colonic function returns.


Complications related to surgical treatment of ACPO include abdominal sepsis, anastomotic dehiscence, intestinal fistula, and abdominal compartment syndrome. Surgical site complications, including infection, fascial dehiscence, and incisional hernia, are also quite common.



Medication Summary

One therapeutic option for intestinal pseudo-obstruction (also referred to as acute colonic pseudo-obstruction [ACPO] or Ogilvie syndrome) is the use of pharmacologic agents (eg, erythromycin, cisapride, and metoclopramide) to increase colonic motility. Acetylcholinesterase inhibitors, such as neostigmine, have also been employed, alone or as part of combination regimens.

Acetylcholinesterase Inhibitors

Class Summary

Acetylcholinesterase inhibitors, such as neostigmine, have been evaluated for the treatment of ACPO. The combined use of a sympathetic blocker followed by a cholinesterase inhibitor (neostigmine) has also been employed to treat motility disorders. The utility of neostigmine in colonic pseudo-obstruction has been demonstrated. A small study examining the effects of pyridostigmine on colonic motility disorders found some symptomatic improvement, though not in patients with slow-transit constipation.

Neostigmine (Prostigmin)

Neostigmine inhibits destruction of acetylcholine by acetylcholinesterase, thereby facilitating transmission of impulses across the myoneural junction.

Laxatives, Osmotic

Class Summary

Osmotic laxatives can be helpful in some cases of intestinal pseudo-obstruction. Osmotic laxative 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.

Polyethylene glycol (GoLYTELY, NuLYTELY, Colyte, TriLyte)

Polyethylene glycol is a laxative with strong electrolyte and osmotic effects that has cathartic actions in the gastrointestinal tract.

Sodium Phosphates (Fleet Enema, OsmoPrep, Fleet Pedia-Lax Enema)

Sodium phosphates enema lubricates the bowel and softens the stool. It can be used as a retention enema. It draws water into the lumen of the gut, which, in turn, produces distention and promotes peristalsis and evacuation of the bowel.


Questions & Answers


What is intestinal pseudo-obstruction?

What is the anatomy relevant to intestinal pseudo-obstruction?

What is the pathophysiology of acute colonic pseudo-obstruction (ACPO)?

What is the pathophysiology of chronic intestinal pseudo-obstruction (CIPO)?

What causes intestinal pseudo-obstruction?

Which conditions are associated with intestinal pseudo-obstruction?

What is the prevalence of intestinal pseudo-obstruction in the US?

What is the global prevalence of intestinal pseudo-obstruction?

Which age groups have the highest prevalence of intestinal pseudo-obstruction?

What are the racial and sexual predilections of intestinal pseudo-obstruction?

What is the prognosis of intestinal pseudo-obstruction?


Which clinical history findings are characteristic of intestinal pseudo-obstruction?

What are the signs and symptoms of intestinal pseudo-obstruction?

Which physical findings are characteristic of intestinal pseudo-obstruction?


Which conditions should be included in the differential diagnoses of intestinal pseudo-obstruction?

What are the differential diagnoses for Intestinal Pseudo-Obstruction?


Which studies are included in the workup of intestinal pseudo-obstruction?

What is the role of lab testing in the workup of intestinal pseudo-obstruction?

What is the role of plain radiography in the workup of intestinal pseudo-obstruction?

How is intestinal pseudo-obstruction differentiated from mechanical obstruction?

What is the role of contrast enema in the workup of intestinal pseudo-obstruction?

What is the role of colonoscopy in the workup of intestinal pseudo-obstruction?


How is mechanical bowel obstruction excluded prior to treatment of intestinal pseudo-obstruction?

How is intestinal pseudo-obstruction treated?

What is included in conservative management for treatment of intestinal pseudo-obstruction?

What is the efficacy of conservative management for treatment of intestinal pseudo-obstruction?

How are constipation and obstipation prevented in intestinal pseudo-obstruction?

Which therapies should be considered for intestinal pseudo-obstruction if there is no improvement with conservative management?

What is the role of pharmacologic therapy in the treatment of intestinal pseudo-obstruction?

What is the efficacy of colonoscopy as a first- treatment of intestinal pseudo-obstruction?

What are possible adverse effects of neostigmine for treatment of intestinal pseudo-obstruction?

What are possible benefits of neostigmine for the treatment of intestinal pseudo-obstruction?

What are the contraindications to neostigmine therapy for intestinal pseudo-obstruction?

What is the efficacy of pharmacologic therapy in the treatment of intestinal pseudo-obstruction?

What is the role of colonoscopic decompression in the treatment of intestinal pseudo-obstruction?

What is the efficacy of colonoscopic decompression for the treatment of intestinal pseudo-obstruction?

What is the efficacy of diatrizoate meglumine enema for the treatment of intestinal pseudo-obstruction?

What is the efficacy of polyethylene glycol (PEG) for the treatment of intestinal pseudo-obstruction?

What is the role of surgery in the treatment of intestinal pseudo-obstruction?

What are studies regarding the efficacy of surgical intervention for treatment of intestinal pseudo-obstruction?

What is the role of fluid resuscitation in the surgical treatment of intestinal pseudo-obstruction?

How is abdominal compartment syndrome prevented in intestinal pseudo-obstruction?

What is included in the postoperative care following surgery for intestinal pseudo-obstruction?

What are the possible complications of intestinal pseudo-obstruction surgery?


Which medications are used in the treatment of intestinal pseudo-obstruction?

Which medications in the drug class Laxatives, Osmotic are used in the treatment of Intestinal Pseudo-Obstruction?

Which medications in the drug class Acetylcholinesterase Inhibitors are used in the treatment of Intestinal Pseudo-Obstruction?