Acute Colonic Pseudo-Obstruction (Ogilvie’s Syndrome)
- Jason D. Ferreira, M.D.
Basic Information
Definition
Ogilvie’s syndrome is characterized by acute massive dilation of the cecum and right colon, with occasional extension to the rectum, in the absence of any mechanical obstruction. Oftentimes, acute colonic pseudo-obstruction occurs after surgery, and it can also be seen in patients with significant underlying medical illnesses. Cecal diameter on abdominal radiographs greater than 12 cm is considered to be the threshold where spontaneous perforation becomes more likely. Medications such as opioids and anticholinergics also contribute to the development of this condition.
Synonyms
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Ogilvie’s syndrome
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ACPO
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Acute megacolon
ICD-10CM CODES | |
K56.6 | Other and unspecified intestinal obstruction |
Epidemiology & Demographics
Incidence
Unknown
Peak Incidence
Unknown
Prevalence
Unknown
Predominant Sex and Age
Although recent data is lacking, data from a retrospective study in 1986 suggested a male predominance with average age of onset in the 6th decade. In general, prevalence is thought to increase with age, although affected females tend to be younger because of the association of acute colonic pseudo-obstruction with obstetric complications.
Genetics
None
Risk Factors
Elderly patients seem to be at greatest risk. Other risk factors include significant underlying medical illness, sepsis, electrolyte abnormalities, recent cardiac events, certain medications (opioids, anticholinergics, phenothiazines, benzodiazepines, calcium channel blockers, chemotherapeutic agents, and antiparkinsonian agents), and postoperative patients (Box E1).
BOX E1Clinical Factors Predisposing to Ogilvie’s Syndrome or Acute Colonic Pseudo-Obstruction
Cardiovascular
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Heart failure, stroke
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Gut ischemia
Critical illness
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Severe sepsis
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Acute pancreatitis
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Shock or hypoxemia
Postoperative state or trauma
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Intestinal manipulation
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Peritonitis
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Immobility and dehydration
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Vertebral, pelvic or hip fracture/surgery
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Retroperitoneal hematoma
Metabolic factors
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Hypokalemia and hyperglycemia
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Hypothyroidism, diabetes mellitus
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Liver or renal failure
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Amyloidosis
Drugs
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α-Adrenergic agonists, dopamine
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Clonidine and dexmedetomidine
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Opioids
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Anticholinergics, calcium channel antagonists
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Antipsychotics
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Antidepressants
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High-dose phosphodiesterase inhibitors
Gastrointestinal infections
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Cytomegalovirus, herpes zoster
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Tuberculosis
Neurologic
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Transection of the spinal cord
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Low spinal cord disease
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Parkinson’s disease
Obstetric
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Caesarean section
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Normal delivery
From Vincent JL, Abraham E, Moore FA, Kochanek PM, Fink MP: Textbook of critical care, ed 6, Philadelphia, 2011, Saunders.
Physical Findings & Clinical Presentation
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Acute abdominal distention and crampy abdominal pain are the most common symptoms associated with Ogilvie’s syndrome. The distention can be so severe that it may lead to labored breathing. Nausea, vomiting, obstipation, constipation, and, paradoxically, diarrhea, can also be seen but are not consistently present. It has been estimated that 40% to 50% of patients continue to pass flatus.
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Physical exam is significant for massive abdominal distention that is tympanic to percussion and varying degrees of abdominal pain or discomfort are also present. Hypoactive or hyperactive bowel sounds are often described. Peritoneal signs are often absent early on but their presence is concerning for imminent perforation.
Etiology
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Colonic motor and secretory functions are mediated by the autonomic nervous system with the ascending colon receiving parasympathetic innervation from the medulla oblongata via the vagus nerve, which increases gut motility, and sympathetic innervation from the spinal cord, which decreases motility. It is thought that parasympathetic dysfunction is the main driving force that leads to Ogilvie’s syndrome but the exact mechanism is unknown.
Diagnosis
Differential Diagnosis
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Mechanical obstruction
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Volvulus
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Intussusception
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Ileus
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Toxic megacolon
Workup
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History should be focused on the perceived progression of distention and timing of most recent flatus or bowel movement as well as determining any predisposing factors such as recent surgery, severe illness, and recent medication changes. Physical examination should focus on assessing the degree of abdominal distention and percussion to evaluate for tympanic sounds, which is a hallmark of Ogilvie’s syndrome. Serial abdominal exams should be performed to ensure no peritoneal signs such a rebound, guarding, or rigidity that would suggest impending or frank perforation.
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Laboratory evaluation should center on metabolic abnormalities as well as lactic acidosis and leukocytosis, which can both be used as a barometer of the severity of the patient’s underlying illness as well as a marker for impending perforation.
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Imaging of the abdomen with plain radiograph is important for tracking degree of distention.
Laboratory Tests
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Metabolic abnormalities such as hypocalcemia, hypomagnesemia, and hypokalemia are commonly present and should be corrected accordingly.
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Leukocytosis as well as lactic acidosis for markers of underlying disease and impending perforation.
Imaging Studies
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Plain and upright abdominal radiographs (Fig. E1) are important to establish degree of colonic distention, which often involves the cecum but can also extend to the splenic flexure or rectum. Haustral markings are usually normal.
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CT scan or enema-enhanced radiograph is imperative to confirm the diagnosis and rule out underlying mechanical obstruction.
Treatment
The goals of treatment are to decompress the colon in order to relieve the patient’s abdominal discomfort and also mitigate the risk of developing intestinal ischemia or frank perforation. Fig. E2 illustrates an algorithm for the treatment of acute colonic pseudo-obstruction.
Nonpharmacologic Therapy
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Supportive care with plain radiographs every 12-24 hr, serial abdominal exams, elimination of potential precipitants (medications, treatment of underlying medical illness), correction of electrolyte abnormalities, restricting PO intake, gastric decompression with NG tube to intermittent suction, rectal decompression with rectal tube attached to gravity, IV fluids, encouraging ambulation if possible, and alternating the patient in bed between right and left lateral decubitus as well as prone positioning with hips elevated are all appropriate nonpharmacologic approaches that can be made initially in the absence of colonic distention >12 cm or significant abdominal pain.
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Colonoscopic decompression with or without placement of a decompression tube is often the next step in management although use of this technique remains controversial as some studies indicate that the majority of patients spontaneously resolve within 48 hr. The risk of complication with colonoscopy in this setting is 3%, with a quoted death rate of 1%. Other studies suggest a success rate of 69% to 90% with colonoscopic decompression.
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Colonoscopic decompression is indicated when supportive measures fail, there is clinical deterioration, or colonic diameter is between 11 and 13 cm. Placement of a decompression tube at the time of colonoscopy is thought to reduce the need for repeat colonoscopic decompression, which is required in about 40% of cases, but no trials have been done to compare rates of repeat decompression with and without decompression tube placement.
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Alternative minimally invasive options which are usually reserved for failed colonoscopic decompression include percutaneous tube cecostomy performed under radiologic guidance and percutaneous endoscopic colostomy, which are both techniques that grant percutaneous access to the colon for both decompression and irrigation to promote transit.
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Surgical management is reserved for those who have failed minimally invasive approaches or for patients with peritonitis or perforation. Surgical cecostomy tube or right hemicolectomy can be performed in the absence of perforation whereas ileostomy, colectomy, and Hartmann procedure can be performed in patients who have perforated or who have significant ischemia.
Acute General Rx
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Neostigmine is an IV anticholinesterase inhibitor that induces rapid colonic decompression in 80% to 100% of appropriate candidates with a median response rate of 4 minutes at a starting dose of 2 mg, but requires close cardiovascular monitoring at the time of its administration and has several contraindications. Dose adjustments are required in chronic kidney disease and caution should be used in patients who have bradyarrhythmias, recent myocardial infarction, beta-blocker use, and asthma. Atropine should be made available at bedside and administration of glycopyrrolate, an anticholinergic agent, should be considered to decrease the risk of bradycardia and bronchoconstriction.
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Methylnaltrexone, a peripherally acting opiate receptor antagonist, can also be considered in cases thought to be precipitated by opioids but little data supports its use at this time.
Chronic Rx
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None
Complementary and Alternative Medicine
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None
Disposition
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Close inpatient monitoring is indicated until there is return of spontaneous bowel function and resolution of abdominal distention.
Referral
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Ogilvie’s syndrome is best managed in a team approach involving both surgeons and gastroenterologists. Administration of neostigmine in proper candidates or decompressive colonoscopy should be pursued in patients with absence of peritoneal signs. If there is evidence of perforation, surgical management is indicated.
Pearls & Considerations
Comments
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Maximal supportive care should be initiated for up to 48 hr barring any significant abdominal pain or massive distention >12 cm on imaging.
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Administration of neostigmine is suggested in appropriate candidates.
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Colonic decompression should be attempted with or without decompression tube placement in patients who fail neostigmine or those who have contraindications to its use.
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Minimally invasive fluoroscopic, endoscopic, or surgical approaches are rarely needed. Surgery is reserved for patients who show signs of perforation.
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Oral laxatives should be discontinued with diagnosis but should be restarted once decompression is achieved.
Prevention
Box E2 describes some prevention strategies for Ogilvie’s syndrome in the critically ill.
BOX E2Strategies to Prevent Ogilvie’s Syndrome in the Critically Ill
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Early resuscitation of the circulation
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Minimizing prolonged infusion of high doses of α-adrenergic drugs
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Minimizing the use of dopamine
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Minimizing the prolonged use of opioids
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Use of thoracic epidural anesthesia
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Minimally invasive or laparoscopic surgery
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Selective decontamination of the digestive tract
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Avoiding antibiotics that disrupt growth of anaerobic fecal bacteria
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Early oral or enteral feeding
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Avoidance of proton pump inhibitors
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Early mobilization and ambulation
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Promoting timely defecation with
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Oral polyethylene glycol from day 3
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Intravenous neostigmine from day 5
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From Vincent JL, Abraham E, Moore FA, Kochanek PM, Fink MP: Textbook of critical care, ed 6, Philadelphia, 2011, Saunders.
Suggested Readings
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Acute and chronic pseudo-obstruction: a current update. : ANZ J Surg. 85:709–714 2015 25943300
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Acute colonic pseudoobstruction. : Clin Colon Rectal Surg. 28:112–117 2015 26034408
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Neostigmine for acute colonic pseudo-obstruction: a meta-analysis. : Ann Med Surg (Lond). 3:60–64 2014 25568788
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Clinical practice guidelines for colon volvulus and acute colonic pseudo-obstruction. : Dis Colon Rectum. 59:589–600 2016 27270510