AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

The term intestinal pseudo-obstruction is used to indicate 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 Based on clinical presentation, pseudo-obstruction syndromes can be divided into acute and chronic forms. Acute colonic pseudo-obstruction is a clinical condition that appears with symptoms, signs, and radiological findings similar to those of acute large bowel obstruction, without any apparent mechanical cause.²

In 1948, Sir Heneage Ogilvie described 2 cases of massive colonic dilatation without any mechanical obstruction. Despite a normal barium enema finding, both patients underwent an exploratory laparotomy for persistent symptoms. Both were found to have malignant infiltration in the region of the celiac axis and semilunar ganglion without evidence of a mechanical obstruction. Ogilvie concluded that the symptoms were caused by an imbalance in the autonomic nerve supply to the colon, with an emphasis on what he called "sympathetic deprivation."³

Problem

Intestinal pseudo-obstruction, acute colonic pseudo-obstruction, and Ogilvie syndrome are defined as the symptoms, signs, and radiological appearance of acute large intestinal obstruction unrelated to any mechanical cause.

Frequency

Studies involving more than 13,000 orthopedic and burn patients documented the prevalence of acute colonic pseudo-obstruction to be 0.29%.^{4, 5} The incidence in patients undergoing major orthopedic surgery may be higher, with reported rates of 0.65-1.3%.⁶ The true incidence of this disorder remains largely unknown because of the possibility of spontaneous resolution.

Acute colonic pseudo-obstruction generally develops in hospitalized patients and is associated with a variety of medical and surgical conditions. Studies have documented that up to 95% of the cases of acute colonic pseudo-obstruction are associated with medical or surgical conditions, with the rest being classified as idiopathic.^{7, 2, 8} The most commonly associated conditions include trauma, pregnancy, cesarean delivery, severe infections, and cardiothoracic, pelvic, or orthopedic surgery.^{9, 10, 11, 12}

The mean age of patients with acute colonic pseudo-obstruction appears to be increasing. In 1986, Vanek et al reviewed more than 400 cases of colonic pseudo-obstruction occurring between 1970-1985 and documented the mean age of patients to be 56.5 years for females and 59.9 years for males.¹³ In the late 1980s, other reports also documented the mean age to be in the sixth decade.^{14, 15} Several reports have since documented an increase in the mean age of patients with acute colonic pseudo-obstruction. Most reports now indicate the mean age to be in the seventh and eighth decades of life.^{16, 5, 17, 12} 

Unlike age, the male-to-female ratio (1.5-4:1) has apparently remained constant over the years. ^{14, 13, 18, 19}

Mortality/Morbidity: Because of the associated medical and surgical conditions, the morbidity and mortality rates associated with colonic pseudo-obstruction remain high. In 1993, Datta and colleagues documented an annual death rate in the United Kingdom of 200 patients per year; most of these deaths occurred in elderly bedridden patients.²⁰ The mortality rate in medically treated patients has been documented to be 14%; in surgically treated patients, 30%.¹³ 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 rate is 40-50%.

Pathophysiology

Since Ogilvie's original description of the syndrome, the exact pathophysiology remains unknown. Current theories continue to suggest the idea of an imbalance in the autonomic nervous system. In contrast to Ogilvie's original proposal, these theories focus on the increased sympathetic tone, the decreased parasympathetic tone, or a combination of both as the cause for colonic pseudo-obstruction.^{21, 22} One theory, supported by Lee and colleagues' 1988 study, relies on the fact that increased sympathetic tone to the colon results in the inhibition of colonic motility.²³ By using epidural anesthesia to block the splanchnic sympathetics, these authors successfully treated several patients whose acute colonic pseudo-obstructions did not respond to conservative management.²⁴ A more recent report on the use of spinal anesthesia for the treatment of Ogilvie syndrome also supports this hypothesis.²⁵

Another theory regarding the etiology of intestinal pseudo-obstruction focuses on the parasympathetic tone. The vagus nerve supplies the parasympathetic innervations for the upper gastrointestinal tract down to the splenic flexure of the colon. From this point, the parasympathetic innervation is via the lumbar nerves from the spinal segments S2 to S4. Given the parasympathetic distribution, one theory hypothesizes that if the sacral innervation becomes disrupted, the distal colon may be left atonic, thus resulting in a functional obstruction.^{26, 21, 27, 24} This theory is in agreement with studies showing a transition between a dilated and collapsed bowel that is often at or near the splenic flexure.^{28, 13}

Other investigators believe that the disorder is a result of a combination of increased sympathetic 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.²⁹

Clinical

Acute colonic pseudo-obstruction occurs most commonly in debilitated, hospitalized patients and is associated with a wide variety of medical and surgical conditions.^{7, 9, 10, 11, 8, 12} Surgical patients begin developing symptoms, which are often insidious in onset, an average of 3-5 days after their operative procedure.^{13, 5, 2} Whether this disorder is associated with either medical or surgical conditions, the presenting signs and symptoms are similar.

Vanek et al documented the presence of abdominal distention in virtually all patients with colonic pseudo-obstruction.¹³ A more recent report documented that the most relevant clinical finding in Ogilvie syndrome is abdominal distention, which arises suddenly, has a progressive course, and may worsen.³⁰ Most patients had abdominal pain, nausea, vomiting, and constipation. Diarrhea and the passage of small amounts of flatus were also present in a number of patients. The most dramatic physical finding was massive abdominal distention. Fever was present in 37% of patients. Abnormal bowel sounds (ie, high-pitched, hyperactive, hypoactive) were present in 88% of patients; 12% had no detectable bowel sounds.

Abdominal tenderness was noted in patients with perforated or ischemic bowel and in patients with viable bowel. No significant differences were noted in the symptoms of patients with ischemic or perforated bowel compared with patients with viable bowel except for a higher incidence of fever (78% vs 31%). Digital examination revealed an empty rectum.^{13, 27}

INDICATIONS

Section 3 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

See Treatment.

RELEVANT ANATOMY

Section 4 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

The large intestine consists of the cecum, ascending colon, hepatic flexure, transverse colon, splenic flexure, descending colon, sigmoid colon, and rectum. The cecum is located in the iliac fossa.  The cecum and ascending colon are saccular, are larger in diameter, and have thinner wall properties when they are compared to the descending colon, sigmoid colon, and rectum. Therefore, one should be extremely careful in avoiding iatrogenic perforation of the cecum and ascending colon while manipulating in the operating room for laparoscopic or open cecostomy and segmental colectomy.

CONTRAINDICATIONS

Section 5 of 12  

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• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Contraindications to the surgical correction of intestinal pseudo-obstruction are based on the patient's comorbidities and his or her ability to tolerate surgery.

WORKUP

Section 6 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Lab Studies

• Laboratory investigations are of little diagnostic value. Mild electrolyte imbalances are often present and typically signify dehydration.⁷
• Hyponatremia and hypokalemia can be present and reflect a consequence of the pathologic condition, rather than its etiologic factor.^{21, 27, 5, 2}
• Leukocytosis can also be present, but it is found in the presence of viable as well as ischemic bowel and is therefore nondiagnostic.^{27, 2}

Imaging Studies

• Plain abdominal radiography  
• • Except for physical examination, the most useful screening test is plain abdominal radiography.³⁰
  • 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. Consequently, the cecum is the most common site of perforation in colonic pseudo-obstruction.^{7, 13}
  • • This observation is based on the Laplace law, which states that the pressure required to stretch the walls of a hollow viscus decreases in inverse proportion to the radius of curvature of the viscus.
    • Accordingly, the tensile strength of the colonic wall is first exceeded in that portion of the colon that has the greatest diameter, that is, the cecum.²⁶
  • 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.^{26, 14, 13, 27, 18} 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.^{7, 31, 18}
  • Air fluid levels are only occasionally observed; small bowel dilatation can occur, but this relies on the incompetency of the ileocecal valve.^{21, 9, 32, 27, 2}
  • Other radiologic features include well-defined colonic septa, a smooth contour of the inner lumen, and preservation of haustral markings.^{32, 33, 13, 18}
  • Differentiating colonic pseudo-obstruction from true mechanical colonic obstruction can sometimes be difficult.
  • • Low's 1995 study suggests using a prone lateral view of the rectum to aid in confirming the diagnosis.³⁴
    • Low recommends placing the patient in the right lateral decubitus position for several minutes to allow passage of gas into the distal colon.³⁴ This maneuver facilitates the gaseous filling of the rectum when the patient is positioned for a prone lateral view of the pelvis.
    • Low documented a 75% success rate in excluding mechanical obstruction and reported that gaseous filling of the rectum did not occur in any patient with a mechanical obstruction.³⁴

Other Tests

• Contrast enema  
• • If the diagnosis cannot be confirmed by plain radiography or physical examination, a contrast enema may be used. Common enemas include either barium or diatrizoate meglumine (Gastrografin), but 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 several advantages over barium because it is clear and water-soluble. Diatrizoate meglumine 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. Furthermore, it removes the risk of peritoneal contamination with barium if a perforation occurs or a laparotomy becomes necessary.^{35, 10, 36, 37, 13}

Diagnostic Procedures

• Flexible colonoscopy can differentiate colonic pseudo-obstruction from mechanical colonic obstruction and can also serve as a therapeutic procedure with colonic decompression performed during the diagnostic colonoscopy procedure. If a mechanical etiology of colonic obstruction is identified as the causative factor during the diagnostic procedure, biopsy of the colonic mass can also be accomplished via flexible colonoscopy.
  

TREATMENT

Section 7 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Medical therapy

Conservative management

Once the diagnosis has been confirmed, a conservative management approach may be attempted. This includes no oral intake, nasogastric decompression, correction of fluid and electrolyte disorders, reduction or discontinuation of drugs that inhibit gastrointestinal motility, and treatment of infections.^{22, 18, 38, 39} In addition, 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 aid in mobilizing intestinal gas.^{40, 22, 18}

Other, less effective treatment measures include repeat enemas, rectal tubes, and rigid sigmoidoscopy.^{32, 14, 27} Several studies have documented durations of conservative management ranging from a mean of 3-6.5 days and have reported even longer periods if clinical signs of perforation were absent and cecal diameters were less than 9 cm.^{21, 15, 16, 2, 38, 12} The success rate with conservative management varies markedly, with documented success rates up to 96%.¹⁵ In an analysis of 1027 cases reported in the literature, it was documented that a nonoperative approach (including conservative measures and colonoscopic decompression as the initial therapy of choice) was associated with few complications and high efficacy.⁴¹

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.^{21, 16, 2, 12}

Despite these differences in success rates, a trial of conservative therapy is still warranted provided no clinical signs of peritonitis or increases in abdominal distention are present. An important component of conservative medical therapy includes maintenance of a bowel regimen to prevent constipation/obstipation and improve colonic motility. Low-volume cathartic agents, such as lactulose or low-dose polyethylene glycol (both nonabsorbable, nonmetabolized osmotic agents), and daily bisacodyl suppositories to induce rectal emptying can aid in the treatment and prevention of recurrence of acute colonic pseudo-obstruction.⁴²

If conservative therapy elicits no improvement, or if the cecal diameter continues to increase, consider additional therapeutic options in order to avoid cecal perforation, which has a higher mortality rate.^{43, 44, 45}

Pharmacologic agents

One option includes the use of pharmacologic agents to increase colonic motility. Several agents have been tried, including erythromycin, cisapride, and metoclopramide, with benefit demonstrated mostly in case reports.^{13, 46, 47} Interest has also focused on cholinesterase inhibitors, such as neostigmine, for the treatment of acute colonic pseudo-obstruction.

Catchpole was the first to document the combined use of a sympathetic blocker followed by a cholinesterase inhibitor (neostigmine) to treat motility disorders.⁴⁸ Based on this work, Hutchinson and colleagues' 1992 study documented improvement in 73% of patients with acute colonic pseudo-obstruction following administration of guanethidine (20 mg IV) followed by neostigmine (2.5 mg IV over 1 min).²⁹ These results have been confirmed in other nonrandomized trials using only neostigmine.^{49, 44, 17, 19}

Ponce et al conducted the first randomized controlled study using neostigmine in 1999.⁵⁰ They randomized 21 patients with acute colonic pseudo-obstruction to receive either 2 mg of neostigmine IV or placebo. Ten (91%) of 11 patients who received neostigmine had prompt colonic decompression, in contrast to 0 (0%) of 10 patients who received placebo (P <.001). The median time to response was 4 minutes.

A more recent systematic review of acute colonic pseudo-obstruction reported that the best-studied treatment is intravenous neostigmine, which leads to prompt colon decompression in most patients after a single infusion. In patients failing or with contraindications to neostigmine, colonoscopic decompression is the active intervention of choice. Surgery is reserved for those with peritonitis or impending perforation.⁵¹ See Media file 2.

Adverse effects of cholinesterase inhibitors include salivation, nausea, vomiting, abdominal pain, bradycardia, hypotension, and bronchospasm.⁵² 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 compared with an intravenous bolus.⁵³ Neostigmine infusion has also been documented to resolve critical illness-related colonic ileus in intensive care patients with multiple organ failure in a prospective placebo-controlled trial. The dose of neostigmine used was continuous intravenous administration of neostigmine at 0.4-0.8 mg/h over 24 hours.⁵⁴

Neostigmine should not be contemplated in patients unless mechanical large intestinal obstruction has been ruled out. Contraindications to neostigmine include patients with baseline heart rates of less than 60 beats per minute (bpm), systolic blood pressure of less than 90 mm Hg, and active bronchospasm requiring medication.⁴⁹ Do not use neostigmine if a recently sealed-off colonic perforation is possible secondary to the possibility of being unplugged by strong peristaltic contractions.⁵⁵

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 Ogilvie syndrome. Among these agents, the potential of 5-hydroxytryptamine-4 receptor agonists and motilin receptor agonists are promising.⁵²

Colonoscopy

Another option for treatment of acute colonic pseudo-obstruction is with colonoscopy. Successful colonoscopic decompression for acute colonic pseudo-obstruction was first described in 1977 by Kukora and Dent in 5 of 6 patients.⁵⁶ Since then, decompression of the colon with colonoscopy has been documented to be a safe and effective method of treatment for acute colonic pseudo-obstruction.⁵⁷ Several studies have documented success rates for decompressive colonoscopy ranging from 77-86% and low morbidity rates of 0.2-2%.^{58, 33, 13, 12}

A retrospective review of 48 cases of Ogilvie syndrome documented that 45 patients required 60 colonoscopic decompressions, 84% were successfully treated using colonoscopy, and 11% required surgery. Single colonoscopy was successful in 64% of patients, and approximately one third of patients required serial colonoscopic decompressions. Average cecal diameter was larger in patients requiring serial colonoscopic decompressions.⁵⁹

Despite these success rates, decompressive colonoscopy remains a technically difficult and demanding procedure compared with elective diagnostic colonoscopy and requires 45-60 minutes (on average) to complete.⁵⁸ Note that the colon cannot undergo a thorough bowel preparation because of the nature of the disease process. Repeated gentle saline or tap water enemas can improve visibility but are not ideal.^{56, 58, 22}

Also note that only minimal air insufflation may be used to dilate the distal colon secondary to the risk of perforating an already dilated cecum. Finally, the ability to carefully evaluate the colonic mucosa for signs of ischemia is hindered owing to the lack of thorough bowel preparation. Any signs of mucosal ischemia (eg, mucosal ulceration, submucosal hemorrhage, friable mucosa with yellow exudates) indicate the need for urgent laparotomy.^{60, 61}

The effect of colonoscopy on the cecal diameter (measured on supine radiographs) was examined, and it was determined that colonoscopic decompression only causes a small decrease in the cecal size in patients with acute colonic pseudo-obstruction (2+/-3.4 cm at 4 hours and -2.2+/-3.3 cm 1 day after decompression). Interestingly, dilation patters of the cecum and transverse colon were significantly correlated, providing additional support that the same pathophysiology affects these two segments of the colon.⁶²

Documented recurrence rates following colonoscopic decompression range from 18-65%.^{13, 63, 22, 16} Improvement in these recurrence rates can be accomplished with placement of long-indwelling decompression tubes. Colonoscopic placement of a decompression tube was first described by Bernton et al in 1982.⁶⁰ Since then, several authors have documented success with placement of various types of decompression tubes in the proximal colon.^{64, 65, 22} For example, in 1988, Harig et al documented a marked reduction in the recurrence rate of patients with colonoscopic decompression and placement of an indwelling catheter in contrast to those that received colonoscopic decompression alone (0 [0%] of 11 vs 4 [44%] of 9).⁶⁶

Colonic decompression tubes frequently become obstructed, however, and another alternative to consider is serial colonoscopic decompression. Colonoscopy to the cecum is unnecessary. Adequate decompression may be obtained by reaching the transverse colon, though adequate decompression is more likely when the colonoscope is passed into the ascending colon.^{14, 22, 16, 38}

A retrospective study assessed the efficacy of Cystografin enema for colonic decompression in patients with Ogilvie syndrome (n=18) and determined that it was successful in all but 2 patients that subsequently required surgery. This also assisted in ruling out a mechanical cause of large bowel obstruction. This will require validation in other studies before it can be recommended as therapy.⁶⁷

More recently, a study evaluated the effect of polyethylene glycol electrolyte (PEG) balanced solution on the relapse rate of the syndrome after initial resolution with neostigmine or endoscopic decompression in 30 patients with a cecal diameter of greater than or equal to 10 cm, which resolved conservatively. Patients were then randomized to receive PEG (29.5 g) or placebo and monitored for 7 days. Patients who had received neostigmine as their initial therapeutic intervention (n=25) had an 88% success rate, and 8 patients underwent successful colonoscopic decompression. Five (33%) patients from the placebo group had recurrent cecal dilation compared with no patients in the PEG group (p=0.04). Therapy with PEG also resulted in a significant increase in stool and flatus evacuations. This study documented that the administration of PEG in patients with Ogilvie syndrome after initial resolution of colonic dilation may increase the sustained response rate and may prevent recurrence of the syndrome.⁶⁸

Surgical therapy

Surgery is indicated when a failure of conservative medical management and colonoscopy occurs or when clinical signs of ischemia, abdominal sepsis, or perforation are present.^{13, 2} A more recent case series documented that early recognition and prompt appropriate conservative therapy can reduce the morbidity and mortality of this syndrome and can decrease the number of cases that require surgical intervention. In this series, surgical therapy was reserved only for those cases in which the risk of perforation of the cecum represented an absolute indication for surgical intervention.⁶⁹

In cases of acute colonic dilatation without perforation or ischemia, tube cecostomy should be considered because successful decompression can be obtained with few complications.^{7, 13, 27, 2, 38, 70} Tube cecostomy can be performed by an open, percutaneous, or laparoscopic approach.⁷¹ Tube cecostomy, however, can be associated with significant complications in patients with a very dilated cecum with thinned wall; in these circumstances, cecal or right colon resection is indicated (see Media file 2). 

An urgent laparotomy is indicated if signs and symptoms of colonic ischemia or perforation are present or if colonoscopy confirms ischemia. The choice of procedure is then dictated by the status of the cecum and the ascending colon. Resect the cecum if necrosis or ischemia is evident. Whether to perform a primary anastomosis or a diversionary procedure depends on the presence of perforation and the extent of fecal contamination. The remaining large bowel must be inspected to exclude any remaining areas of ischemia, necrosis, or perforation.^{21, 13, 27, 16, 2}

Preoperative details

In a patient who requires surgical intervention for acute colonic pseudo-obstruction, 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 based on the surgical findings. Perioperative intravenous antibiotics are administered before making the surgical incision because of the high rate of surgical site infection with emergent abdominal surgical procedures.

Intraoperative details

Continued fluid resuscitation for optimization of intestinal perfusion is necessary because extensive fluid losses can occur in patients with acute colonic pseudo-obstruction owing to 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 care is taken to avoid causing peritoneal contamination. Accomplish this prior to formation of the intestinal anastomosis.

Patients with acute colonic pseudo-obstruction are at high risk for abdominal compartment syndrome because of visceral edema. If attempts at primary fascial closure are difficult at the completion of the operative procedure, consider temporary abdominal closure for prevention of abdominal compartment syndrome. A return to the operating room for primary fascial closure can then be reconsidered days later, when the visceral edema has resolved.

Postoperative details

Continue all attempts to improve splanchnic perfusion in the postoperative period because the dilated colon is particularly susceptible to ischemic injury. Patients are maintained NPO (non per os, ie, nothing by mouth) with nasogastric tube decompression until colonic function returns.

Follow-up

Acute colonic pseudo-obstruction can recur; therefore, counsel patients and families about this disease process.

COMPLICATIONS

Section 8 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Complications related to surgical treatment for acute colonic pseudo-obstruction 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.

OUTCOME AND PROGNOSIS

Section 9 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Colonic distension can recur and may require 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 Ogilvie syndrome. Recurrent or persistent colonic distension may cause ischemia and perforation.⁷² 

Surgery for the treatment of colonic pseudo-obstruction has a 30% mortality rate, whereas conservative management has a 14% rate. If cecal perforation occurs, the rate can be up to 50%.^{13, 27, 16, 2}

A cecal diameter of greater than 14 cm, a delay in colonic decompression, and advanced age are predictors of colonic perforation.

FUTURE AND CONTROVERSIES

Section 10 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

All attempts should focus on prevention of acute colonic pseudo-obstruction in the hospitalized and postsurgical patient. Earlier mobilization and positioning of hospitalized patients has become an important preventive strategy in this regard. Furthermore, prevention of colonic distention by the 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 pharmacological agents for the treatment of acute colonic pseudo-obstruction would allow a substantial decrease in the need for surgical intervention, which is associated with considerable morbidity and mortality, and the authors hope that these agents will become available in the future.

MULTIMEDIA

Section 11 of 12  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

Media file 1:  Abdominal radiographs confirm acute colonic pseudo-obstruction after hip surgery. Note extensive, diffuse colonic dilation with no evidence of a transition point.
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Media type:  X-RAY

Media file 2:  Treatment algorithm.
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Media type:  Chart

REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• Multimedia
• References

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3. Olgilvie H. Large-intestine colic due to sympathetic deprivation. BMJ. 1948;2:671-673.
4. Kadesky K, Purdue GF, Hunt JL. Acute pseudo-obstruction in critically ill patients with burns. J Burn Care Rehabil. Mar-Apr 1995;16(2 Pt 1):132-5. [Medline].
5. Clarke HD, Berry DJ, Larson DR. Acute pseudo-obstruction of the colon as a postoperative complication of hip arthroplasty. J Bone Joint Surg Am. Nov 1997;79(11):1642-7. [Medline].
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12. Tenofsky PL, Beamer L, Smith RS. Ogilvie syndrome as a postoperative complication. Arch Surg. Jun 2000;135(6):682-6; discussion 686-7. [Medline].
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15. Sloyer AF, Panella VS, Demas BE, Shike M, Lightdale CJ, Winawer SJ, et al. Ogilvie's syndrome. Successful management without colonoscopy. Dig Dis Sci. Nov 1988;33(11):1391-6. [Medline].
16. Geller A, Petersen BT, Gostout CJ. Endoscopic decompression for acute colonic pseudo-obstruction. Gastrointest Endosc. Aug 1996;44(2):144-50. [Medline].
17. Paran H, Silverberg D, Mayo A, Shwartz I, Neufeld D, Freund U. Treatment of acute colonic pseudo-obstruction with neostigmine. J Am Coll Surg. Mar 2000;190(3):315-8. [Medline].
18. Marinella MA. Acute colonic pseudo-obstruction complicated by cecal perforation in a patient with Parkinson's disease. South Med J. Oct 1997;90(10):1023-6. [Medline].
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Article Last Updated: May 1, 2008