eMedicine Specialties > Gastroenterology > Intestine

Intestinal Pseudo-obstruction, Surgical Treatment: Treatment

Author: Burt Cagir, MD, FACS, Assistant Professor of Surgery, State University of New York, Upstate Medical Center; Consulting Staff, Director of Surgical Research, Robert Packer Hospital; Associate Program Director, Department of Surgery, Guthrie Clinic
Coauthor(s): Lena M Napolitano, MD, FACS, FCCP, FCCM, Professor of Surgery, University of Michigan School of Medicine; Chief, Surgical Critical Care, Program Director, Surgical Critical Care Fellowship, Associate Chair, Department of Surgery, University of Michigan Health System; James Dunne, MD, Clinical Instructor, Department of Surgery, Trauma/Critical Care, University of Maryland Medical Center
Contributor Information and Disclosures

Updated: May 1, 2008

Treatment

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

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.

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References
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Further Reading

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Keywords

intestinal pseudoobstruction, colonic pseudo-obstruction, Ogilvie's syndrome, Ogilvie syndrome, large intestinal obstruction, large bowel obstruction, cecal perforation, abdominal distention, abdominal sepsis, anastomotic dehiscence, intestinal fistula, abdominal compartment syndrome

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Contributor Information and Disclosures

Author

Burt Cagir, MD, FACS, Assistant Professor of Surgery, State University of New York, Upstate Medical Center; Consulting Staff, Director of Surgical Research, Robert Packer Hospital; Associate Program Director, Department of Surgery, Guthrie Clinic
Burt Cagir, MD, FACS is a member of the following medical societies: American College of Surgeons, American Medical Association, and Society for Surgery of the Alimentary Tract
Disclosure: Nothing to disclose.

Coauthor(s)

Lena M Napolitano, MD, FACS, FCCP, FCCM, Professor of Surgery, University of Michigan School of Medicine; Chief, Surgical Critical Care, Program Director, Surgical Critical Care Fellowship, Associate Chair, Department of Surgery, University of Michigan Health System
Lena M Napolitano, MD, FACS, FCCP, FCCM is a member of the following medical societies: Alpha Omega Alpha, American Association for the Surgery of Trauma, American College of Chest Physicians, American College of Critical Care Medicine, American College of Physicians, American College of Surgeons, American Medical Association, American Society for Parenteral and Enteral Nutrition, Association for Academic Surgery, Association of VA Surgeons, Association of Women Surgeons, California Professional Society on the Abuse of Children, Eastern Association for the Surgery of Trauma, Phi Beta Kappa, Shock Society, Society of Critical Care Medicine, and Society of University Surgeons
Disclosure: Nothing to disclose.

James Dunne, MD, Clinical Instructor, Department of Surgery, Trauma/Critical Care, University of Maryland Medical Center
James Dunne, MD is a member of the following medical societies: Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Medical Editor

George Y Wu, MD, PhD, Professor, Department of Medicine, Director, Hepatology Section, Herman Lopata Chair in Hepatitis Research, University of Connecticut School of Medicine
George Y Wu, MD, PhD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, American Medical Association, American Society for Clinical Investigation, and Association of American Physicians
Disclosure: Humana Press Consulting fee Consulting; Novartis Consulting fee Review panel membership

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

James L Achord, MD, Professor Emeritus, Department of Medicine, Division of Digestive Diseases, University of Mississippi School of Medicine
James L Achord, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, Mississippi State Medical Association, New York Academy of Sciences, Sigma Xi, and Southern Medical Association
Disclosure: Nothing to disclose.

CME Editor

Paolo Zamboni, MD, Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy
Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York Academy of Sciences
Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, DSc, MA, Vice Chairman, Professor, Department of Surgery, Section of Gastrointestinal Medicine and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New Haven Hospital
John Geibel, MD, DSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, and Society for Surgery of the Alimentary Tract
Disclosure: AMGEN Royalty Other

 
 
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