eMedicine Specialties > Gastroenterology > Intestine

Intestinal Pseudo-obstruction, Surgical 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

Introduction

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

Presentation

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

See Treatment.

Relevant Anatomy

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

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

More on Intestinal Pseudo-obstruction, Surgical Treatment

Overview: Intestinal Pseudo-obstruction, Surgical Treatment
Workup: Intestinal Pseudo-obstruction, Surgical Treatment
Treatment: Intestinal Pseudo-obstruction, Surgical Treatment
Follow-up: Intestinal Pseudo-obstruction, Surgical Treatment
Multimedia: Intestinal Pseudo-obstruction, Surgical Treatment
References
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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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