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Intestinal Pseudo-Obstruction Treatment & Management

  • Author: Burt Cagir, MD, FACS; Chief Editor: John Geibel, MD, DSc, MSc, MA  more...
 
Updated: Dec 28, 2015
 

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.

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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]

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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.

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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.

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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

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.

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Contributor Information and Disclosures
Author

Burt Cagir, MD, FACS Clinical Professor of Surgery, The Commonwealth Medical College; Attending Surgeon, Assistant Program Director, Robert Packer Hospital; Attending Surgeon, Corning Hospital

Burt Cagir, MD, FACS is a member of the following medical societies: American College of Surgeons, American Medical Association, 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 is a member of the following medical societies: Alpha Omega Alpha, American Society for Parenteral and Enteral Nutrition, California Professional Society on the Abuse of Children, Eastern Association for the Surgery of Trauma, Association of Women Surgeons, 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, Association for Academic Surgery, Association of VA Surgeons, Phi Beta Kappa, Shock Society, Society of Critical Care Medicine, Society of University Surgeons

Disclosure: Nothing to disclose.

Prospere Remy, MD Assistant Professor of Medicine, Albert Einstein College of Medicine; Attending Physician, Department of Internal Medicine, Bronx-Lebanon Hospital Center

Prospere Remy, MD is a member of the following medical societies: American College of Physicians, American Society for Gastrointestinal Endoscopy

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.

Chief Editor

John Geibel, MD, DSc, MSc, MA Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, Surgical Research, Department of Surgery, Yale-New Haven Hospital; American Gastroenterological Association Fellow

John Geibel, MD, DSc, MSc, 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, Society for Surgery of the Alimentary Tract

Disclosure: Received royalty from AMGEN for consulting; Received ownership interest from Ardelyx for consulting.

Acknowledgements

Steven Lee Carpenter, MD, FACP, AGAF, FASGE Academic Chair, Associate Professor of Medicine, Department of Internal Medicine, Internal Medicine Program Director, Mercer University School of Medicine; Senior Partner, The Center for Digestive and Liver Health, The Endoscopy Center

Steven Lee Carpenter, MD, FACP, AGAF, FASGE is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Douglas M Heuman, MD, FACP, FACG, AGAF Chief of GI, Hepatology, and Nutrition at North Shore University Hospital/Long Island Jewish Medical Center; Professor, Department of Medicine, Hofstra North Shore-LIJ School of Medicine

Douglas M Heuman, MD, FACP, FACG, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, and American Gastroenterological Association

Disclosure: Novartis Grant/research funds Other; Bayer Grant/research funds Other; Otsuka Grant/research funds None; Bristol Myers Squibb Grant/research funds Other; Scynexis None None; Salix Grant/research funds Other; MannKind Other

Bjorn Holmstrom, MD Assistant Professor, Department of Internal Medicine, University of South Florida

Bjorn Holmstrom, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Medical Association, Medical Association of Georgia, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Julian Katz, MD Clinical Professor of Medicine, Drexel University College of Medicine

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law, Medicine & Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Kavitha Kumbum, MD Associate Program Director and Attending Physician, Gastroenterology Fellowship Program, Division of Gastroenterology, Bronx Lebanon Hospital Center, Albert Einstein College of Medicine

Kavitha Kumbum, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, and New York Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Prospere Remy, MD Assistant Professor of Medicine, Albert Einstein College of Medicine; Attending Physician, Department of Internal Medicine, Bronx-Lebanon Hospital Center

Prospere Remy, MD is a member of the following medical societies: American College of Physicians and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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: Springer Consulting fee Consulting; Gilead Consulting fee Review panel membership; Gilead Honoraria Speaking and teaching; Bristol-Myers Squibb Honoraria Speaking and teaching; Springer Royalty Review panel membership

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