Editorial

Management of Acute Colonic Pseudo-Obstruction

Loren Laine, M.D.

N Engl J Med 1999; 341:192-193July 15, 1999DOI: 10.1056/NEJM199907153410309

Article

Acute colonic pseudo-obstruction, also called Ogilvie's syndrome, refers to marked dilation of the colon in the absence of mechanical obstruction. It generally develops in hospitalized patients over a period of days, and up to 95 percent of affected patients have an associated medical or surgical condition,1,2 such as trauma, recent surgery, or serious infection.

The chief criterion for the diagnosis is the diameter of the colon on abdominal radiographs. However, there is no consensus regarding the minimal diameter required for the diagnosis. Perhaps the most commonly used value is 9 cm, based on a frequently cited study from 1956, in which 19 surgically treated patients who had cecal perforation or “impending” cecal perforation due to colonic obstruction all had cecal diameters of at least 9 cm and only 3 of 100 control patients had such cecal diameters after cecal distention during a barium enema.3 The applicability of these data to acute colonic pseudo-obstruction is questionable.

The most clinically meaningful diagnostic criterion for acute colonic pseudo-obstruction should be the threshold diameter above which there is a risk of colonic perforation. In a review of 400 cases, perforation or ischemia was not seen when the diameter of the cecum was less than 12 cm.1 Other studies have also suggested that perforation is uncommon unless the diameter of the cecum is at least 12 cm.4 However, there is a broad overlap in cecal diameters between patients in whom acute colonic pseudo-obstruction resolves and those in whom perforation occurs. Thus, once the threshold diameter is reached in an individual patient, the actual extent of dilation does not appear to matter. Some have suggested that the duration of dilation may be a more important risk factor.5,6

Acute colonic pseudo-obstruction can lead to colonic perforation and death. In a 1997 review of published studies, Rex reported that the risk of perforation was approximately 3 percent.2 However, since this figure is largely based on retrospective case series, its generalizability is unclear and it may represent an overestimate. At best, we can conclude that perforation does occur in patients with acute colonic pseudo-obstruction, but that it is uncommon. Furthermore, although perforation appears to increase the risk of death, patients with acute colonic pseudo-obstruction may die of their underlying conditions, even when the pseudo-obstruction resolves without complications.

The initial management of acute colonic pseudo-obstruction is conservative: the underlying cause is treated if possible, metabolic disturbances are corrected, and medications that may decrease colonic motility (e.g., narcotics, anticholinergic agents, and calcium-channel antagonists) are stopped. Nasogastric suction, rectal tubes, and frequent changes in the patient's position are often used. If symptoms persist or worsen and if the colonic diameter increases or remains above a certain level (e.g., 12 cm), colonoscopy is generally performed. Colonoscopic decompression reduces the diameter of the cecum on abdominal radiographs in about 70 percent of patients.2 However, the condition will recur in 40 percent of these patients, requiring repeated colonoscopy.2 The risk of recurrence may be decreased by the placement of a drainage tube into the right side of the colon at the time of initial colonoscopy.7,8 Bedside colonoscopy of an unprepared bowel is technically difficult and not without risk: a number of cases of perforation have been reported in this setting.2

Surgery is generally recommended for patients with persistent or worsening acute colonic pseudo-obstruction despite colonoscopic decompression. However, surgery also carries a risk in patients with serious concurrent illnesses, even in the absence of perforation: the mortality rate was 26 percent in a review of 125 surgically treated patients who were found to have viable bowel at operation.1 Thus, in the absence of randomized trials, it is uncertain whether the benefit of colonoscopic or surgical therapy outweighs the risks in these patients. Some have questioned the need for early endoscopic or surgical treatment.9

In this issue of the Journal, Ponec et al.10 present the results of a randomized, double-blind, controlled trial of neostigmine for patients with acute colonic pseudo-obstruction. Ten of 11 patients who were treated with intravenous neostigmine had prompt passage of flatus or stool, with reduced abdominal distention (median time to response, four minutes), as compared with none of the 10 patients who received placebo injections. Significant decreases were also seen in abdominal circumference and colonic diameters on radiographs. All the patients had had no response to at least 24 hours of conservative treatment. Two of the 10 patients with an initial response had a recurrence and underwent colonoscopy, surgery, or both. All seven patients in the placebo group who were given open-label neostigmine also had an immediate clinical response, and none had a recurrence. Symptomatic bradycardia requiring atropine developed in two patients; other side effects included abdominal pain, excessive salivation, and vomiting. Two of the 18 patients who received neostigmine died of causes unrelated to acute colonic pseudo-obstruction or its treatment, reinforcing the fact that such patients often die of their underlying illness.

The response to neostigmine, which increases cholinergic activity, may shed light on the cause of acute colonic pseudo-obstruction. In 1948, Ogilvie suggested that sympathetic activity of the colon was interrupted, allowing unopposed sacral parasympathetic innervation.11 More recently, it has been proposed that the condition is due to sympathetic overactivity, parasympathetic suppression, or both. Hutchinson and Griffiths12 studied sequential treatment with guanethidine (an adrenergic inhibitor) and neostigmine and found that improvement occurred only after neostigmine was given. Two subsequent uncontrolled studies reported that intravenous neostigmine was effective in over 80 percent of patients.13,14 These studies support the theory that acute colonic pseudo-obstruction is due to decreased parasympathetic activity.

How should we integrate the findings of Ponec et al. and others into clinical practice? Acute colonic pseudo-obstruction should be diagnosed only when symptoms and signs of abdominal distention are present and when marked dilation of the cecum or right colon is seen radiographically without evidence of distal obstruction. Although a diameter of 9 cm may be used as a threshold for diagnosis, 12 cm may be a more appropriate measure in terms of concern about perforation. Conservative treatment should still be used initially. If the condition persists or worsens after 24 hours of conservative measures and if there are no contraindications, such as bradycardia, neostigmine should be given. The most common potentially serious side effect is bradycardia. Therefore, patients should be monitored and remain supine before and for some period after the infusion.

Because colonic perforation is uncommon and the risk of death is greatly influenced by the underlying illness, it seems unlikely that any trial could be large enough to address adequately the effects of neostigmine on these important clinical outcomes. Nonetheless, the findings of Ponec et al. suggest an important role for neostigmine, which may speed the resolution of acute colonic pseudo-obstruction and reduce the need for colonoscopy and surgery.

Loren Laine, M.D.
University of Southern California School of Medicine, Los Angeles, CA 90033

References

References

1. 1

   Vanek VW, Al-Salti M. Acute pseudo-obstruction of the colon (Ogilvie's syndrome): an analysis of 400 cases. Dis Colon Rectum 1986;29:203-210
   CrossRef | Web of Science | Medline

2. 2

   Rex DK. Colonoscopy and acute colonic pseudo-obstruction. Gastrointest Endosc Clin N Am 1997;7:499-508
   Medline

3. 3

   Lowman RM, Davis L. An evaluation of cecal size in impending perforation of the cecum. Surg Gynecol Obstet 1956;103:711-718
   Web of Science | Medline

4. 4

   Gierson ED, Storm FK, Shaw W, Coyne SK. Caecal rupture due to colonic ileus. Br J Surg 1975;62:383-386
   CrossRef | Web of Science | Medline

5. 5

   Johnson CD, Rice RP, Kelvin FM, Foster WL, Williford ME. The radiologic evaluation of gross cecal distension: emphasis on cecal ileus. AJR Am J Roentgenol 1985;145:1211-1217
   Web of Science | Medline

6. 6

   Baker DA, Morin ME, Tan A, Sue HK. Colonic ileus: indication for prompt decompression. JAMA 1979;241:2633-2634
   CrossRef | Web of Science | Medline

7. 7

   Harig JM, Fumo DE, Loo FD, et al. Treatment of acute nontoxic megacolon during colonoscopy: tube placement versus simple decompression. Gastrointest Endosc 1988;34:23-27
   CrossRef | Web of Science | Medline

8. 8

   Geller A, Petersen BT, Gostout CJ. Endoscopic decompression for acute colonic pseudo-obstruction. Gastrointest Endosc 1996;44:144-150
   CrossRef | Web of Science | Medline

9. 9

   Sloyer AF, Panella VS, Demas BE, et al. Ogilvie's syndrome: successful management without colonoscopy. Dig Dis Sci 1988;33:1391-1396
   CrossRef | Web of Science | Medline

10. 10

    Ponec RJ, Saunders MD, Kimmey MB. Neostigmine for the treatment of acute colonic pseudo-obstruction. N Engl J Med 1999;341:137-141
    Free Full Text | Web of Science | Medline

11. 11

    Ogilvie WH. Large-intestine colic due to sympathetic deprivation: a new clinical syndrome. BMJ 1948;2:671-673
    CrossRef | Web of Science | Medline

12. 12

    Hutchinson R, Griffiths C. Acute colonic pseudo-obstruction: a pharmacological approach. Ann R Coll Surg Engl 1992;74:364-367
    Web of Science | Medline

13. 13

    Stephenson BM, Morgan AR, Salaman JR, Wheeler MH. Ogilvie's syndrome: a new approach to an old problem. Dis Colon Rectum 1995;38:424-427
    CrossRef | Web of Science | Medline

14. 14

    Turegano-Fuentes F, Munoz-Jimenez F, Del Valle-Hernandez E, et al. Early resolution of Ogilvie's syndrome with intravenous neostigmine: a simple, effective treatment. Dis Colon Rectum 1997;40:1353-1357
    CrossRef | Web of Science | Medline

Citing Articles (16)

Citing Articles

1. 1

   Robert J. Ponec, Michael B. Kimmey. Acute Colonic Pseudo-obstruction. In: Clinical Gastrointestinal Endoscopy. Elsevier, 2012:297-304.
   

2. 2

   Chetana Vaishnavi. (2011) Clostridium difficile infection: clinical spectrum and approach to management. Indian Journal of Gastroenterology
   

3. 3

   Eamonn M.M. Quigley, Seamus O'Mahony, Zaid Heetun. (2011) Motility Disorders in the Patient with Neurologic Disease. Gastroenterology Clinics of North America 40:4, 741-764
   

4. 4

   Belén Moliner Renau, Francisco Raga Baixauli, Cristina Ruiz Aguilar, Lorena Camps Selva, Fernando Bonilla-Musoles. (2011) Síndrome de Ogilvie: una complicación poscesárea. Progresos de Obstetricia y Ginecología 54:10, 537-539
   

5. 5

   Rosemary Mander, Graeme D. Smith. (2010) A systematic review of medical diagnosis of Ogilvie's syndrome in childbearing. Midwifery 26:6, 573-578
   

6. 6

   Huseyin Ozkurt, Fikriye Yilmaz, Nagihan Bas, Halil Coskun, Muzaffer Basak. (2009) Acute colonic pseudo-obstruction (Ogilvie's syndrome): radiologic diagnosis and medical treatment with neostigmine. Report of 4 cases. The American Journal of Emergency Medicine 27:6, 757.e1-757.e4
   

7. 7

   W. Thomas Crow, Lilia Gorodinsky. (2009) Does osteopathic manipulative treatment (OMT) improves outcomes in patients who develop postoperative ileus: A retrospective chart review. International Journal of Osteopathic Medicine 12:1, 32-37
   

8. 8

   Mayank Shukla, Romina Barros, Venkata S Majjiga, Asit K Tripathy. (2007) Acute Colonic Pseudo-obstruction in a Pediatric Patient. Journal of Pediatric Gastroenterology and Nutrition 45:5, 600-602
   

9. 9

   J SANTOSSANCHEZ, L MARTINMARTIN, J GARCIAALONSO. (2007) Síndrome de Ogilvie. Presentación de un caso y revisión de la literatura médica. Revista Española de Geriatría y Gerontología 42:3, 188-191
   

10. 10

    Christine E. M. De Die-smulders, Frans G. I. Jennekens, Chris J. Hweler. Myotonic Dystrophy Type 1. In: Management of Genetic Syndromes. John Wiley & Sons, Inc., 2005.
    

11. 11

    M. Rubio, N. González, J. Luna, C. Escrich, E. Castro, A. Prades. (2004) Síndrome de Ogilvie poscesárea. Progresos de Obstetricia y Ginecología 47:1, 51-54
    

12. 12

    D.J. Penney, K.M. Hillman. (2001) Ogilvie's syndrome: the novel use of a continuous neostigmine infusion. Clinical Intensive Care 12:5-6, 237-239
    

13. 13

    M Rondeau, J.C Weber, I Nodot, D Storck. (2001) Pseudo-obstructions coliques aiguës en médecine interne : circonstances étiologiques et pronostic, à propos d’une étude rétrospective. La Revue de Médecine Interne 22:6, 536-541
    

14. 14

    Haim Paran, Daniel Silverberg, Ami Mayo, Ivan Schwartz, David Neufeld, Uri Freund. (2001) Reply. Journal of the American College of Surgeons 192:3, 423
    

15. 15

    S. Benlloch, F. Pérez-Aguilar, J. Ponce, J. Berenguer. (2001) Pseudoobstrucción colónica crónica secundaria a neurolépticos. Gastroenterología y Hepatología 24:10, 500-502
    

16. 16

    Eamonn MM Quigley. (2000) Acute intestinal pseudo-obstruction. Current Treatment Options in Gastroenterology 3:4, 273-285