Acute Colonic Pseudo Obstruction (Ogilvie Syndrome)  

What is Ogilvie syndrome? 

Acute Colonic Pseudo Obstruction presents with signs, symptoms, and radiologic findings suggestive of obstruction without a mechanical source.

It is most often seen in hospitalized patients with other underlying medical conditions found to have marked colonic air on abdominal radiograph.

DEFINITION

Acute Colonic Pseudo Obstruction Ogilvie 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 also can be seen in patients with significant underlying medical illnesses. Cecal diameter on abdominal radiographs greater than 12 cm is considered the threshold where spontaneous perforation becomes more likely. ¹ Medications such as opioids and anticholinergics also contribute to the development of this condition.

SYNONYMS

Ogilvie syndrome

ACPO

Acute megacolonView full size

ICD-10CM CODE
K56.6	Other and unspecified intestinal obstruction

EPIDEMIOLOGY & DEMOGRAPHICS

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 sixth 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. ²

Peak Incidence

Unknown.

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 ² ( Box E1 and Table E1 ).

BOX E1

Clinical Factors Predisposing to Ogilvie Syndrome or Acute Colonic Pseudo-Obstruction

From Vincent JL et al: Textbook of critical care, ed 6, Philadelphia, 2011, Saunders .

Cardiovascular

• •Heart failure, stroke
• •Gut ischemia

Critical illness

• •Severe sepsis
• •Acute pancreatitis
• •Shock or hypoxemia

Postoperative state or trauma

• •Intestinal manipulation
• •Peritonitis
• •Immobility and dehydration
• •Vertebral, pelvic or hip fracture/surgery
• •Retroperitoneal hematoma

Metabolic factors

• •Hypokalemia and hyperglycemia
• •Hypothyroidism, diabetes mellitus
• •Liver or renal failure
• •Amyloidosis

Drugs

• •α-Adrenergic agonists, dopamine
• •Clonidine and dexmedetomidine
• •Opioids
• •Anticholinergics, calcium channel antagonists
• •Antipsychotics
• •Antidepressants
• •High-dose phosphodiesterase inhibitors

Gastrointestinal infections

• •Cytomegalovirus, herpes zoster
• •Tuberculosis

Neurologic

• •Transection of the spinal cord
• •Low spinal cord disease
• •Parkinson disease

Obstetric

• •Caesarean section
• •Normal delivery

Table

TABLE E1

Conditions Associated With Pseudo-Obstruction

From Townsend CM et al: Sabiston textbook of surgery, ed 21, St Louis 2022, Elsevier.

Category	Risk Factors
Postsurgical	Following major orthopedic and/or spinal surgery, solid organ transplants, cardiac procedures
Neurologic disease	Parkinson disease, Alzheimer disease, stroke, spinal cord injury
Cardiac	Congestive heart failure, myocardial infarction
Pulmonary	Chronic obstructive pulmonary disease
Trauma	Major trauma, shock, burns
Metabolic	Diabetes mellitus, renal failure, electrolyte disturbances
Infectious	Cytomegalovirus, varicella-zoster virus
Obstetric/gynecologic	Caesarean section, normal and instrumental delivery
Miscellaneous	Lupus, scleroderma
Drugs	Opiates, chemotherapy, anti-Parkinson drugs, anticholinergics, antipsychotic drugs, clonidine

Genetics

None

PHYSICAL FINDINGS & CLINICAL PRESENTATION

• •Acute abdominal distention and crampy abdominal pain are the most common symptoms associated with Ogilvie 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. ¹
• •Physical examination 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. ¹

ETIOLOGY

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 syndrome, but the exact mechanism is unknown. ¹

DIFFERENTIAL DIAGNOSIS

• •Mechanical obstruction
• •Volvulus
• •Intussusception
• •Ileus
• •Toxic megacolon

How is this condition diagnosed?

• •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 syndrome. Serial abdominal examinations should be performed to ensure no peritoneal signs such as rebound, guarding, or rigidity that would suggest impending or frank perforation.
• •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.
• •Imaging of the abdomen with plain radiograph is important for tracking degree of distention. ¹

LABORATORY TESTS

• •Metabolic abnormalities such as hypocalcemia, hypomagnesemia, and hypokalemia are commonly present and should be corrected accordingly.
• •Leukocytosis as well as lactic acidosis are markers of underlying disease and impending perforation. ¹

IMAGING STUDIES

• •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. ¹
• •CT scan ( Fig. E2 ) or enema-enhanced radiograph is imperative to confirm the diagnosis and rule out underlying mechanical obstruction.

TREATMENT

How is Ogilvie syndrome treated? 

The vast majority of patients improve with bowel rest and removal of narcotics; however, colonic decompression is indicated in the presence of pain or significant distention (more than 12 cm). Intravenous neostigmine as a prokinetic agent has a high success rate (greater than 80%–90% in some small series), although cardiac risk must be assessed prior to administration. Tube cecostomy can be considered in moribund patients.

Treatments include managing the underlying medical issues, colonoscopic decompression, and neostigmine.

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. E3 illustrates an algorithm for the treatment of acute colonic pseudo-obstruction.

NONPHARMACOLOGIC THERAPY

• •Supportive care with plain radiographs every 12 to 24 h, serial abdominal examinations, elimination of potential precipitants (medications, treatment of underlying medical illness), correction of electrolyte abnormalities, restricting PO intake, gastric decompression with nasogastric 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. ³
• •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 h. 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. ⁴
• •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. ⁴
• •Alternative minimally invasive options that 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. ³
• •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. ³

Acute General Treatment

• •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 min 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. ³
• •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 Treatment

None

DISPOSITION

• •Close inpatient monitoring is indicated until there is return of spontaneous bowel function and resolution of abdominal distention.

COMPLEMENTARY & ALTERNATIVE MEDICINE

None

Referral

Ogilvie 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

• •Maximal supportive care should be initiated for up to 48 h barring any significant abdominal pain or massive distention >12 cm on imaging.
• •Administration of neostigmine is suggested in appropriate candidates.
• •Colonic decompression should be attempted with or without decompression tube placement in patients who fail neostigmine or those who have contraindications to its use.
• •Minimally invasive fluoroscopic, endoscopic, or surgical approaches are rarely needed.
• •Surgery is reserved for patients who show signs of perforation.
• •Oral laxatives should be discontinued with diagnosis but should be restarted once decompression is achieved.

PREVENTION

Box E2 describes some prevention strategies for Ogilvie syndrome in the critically ill.

BOX E2

Strategies to Prevent Ogilvie Syndrome in the Critically Ill

From Vincent JL et al: Textbook of critical care, ed 6, Philadelphia, 2011, Saunders.

• •Early resuscitation of the circulation
• •Minimizing prolonged infusion of high doses of α-adrenergic drugs
• •Minimizing the use of dopamine
• •Minimizing the prolonged use of opioids
• •Use of thoracic epidural anesthesia
• •Minimally invasive or laparoscopic surgery
• •Selective decontamination of the digestive tract
• •Avoiding antibiotics that disrupt growth of anaerobic fecal bacteria
• •Early oral or enteral feeding
• •Avoidance of proton pump inhibitors
• •Early mobilization and ambulation
• •Promoting timely defecation with:
  • 1.Oral polyethylene glycol from day 3
  • 2.Intravenous neostigmine from day 5

REFERENCES

1.Underhill J., et al.: Acute colonic pseudo-obstruction and volvulus: pathophysiology, evaluation, and treatment . Clin Colon Rectal Surg 2021; 34 (4): pp. 242-250.

2.Caroselli C., et al.: Acute colonic pseudo-obstruction: a syndrome due to many causes . Intern Emerg Med 2019; 16 (1): pp. 161-165.

3.Alavi K., et al.: The American Society of Colon and Rectal Surgeons clinical practice guidelines for the management of colonic volvulus and acute colonic pseudo-obstruction . Dis Colon Rectum 2021; 64 (9): pp. 1046-1057.

4.Naveed M., et al.: American Society for Gastrointestinal Endoscopy Guideline on the role of endoscopy in the management of acute colonic pseudo-obstruction and colonic volvulus . Gastrointest Endosc 2020; 91: pp. 228-235.