Ogilvie Syndrome: Diagnosis, Diet, and Treatment

Ogilvie syndrome, also known as acute colonic pseudo-obstruction (ACPO), is characterized by a sudden and unexplained paralysis of the colon. In this condition, the colon behaves as if it is blocked or obstructed, but there is no physical obstruction. The primary issue lies in the colon's motor system, which fails to move food along, leading to a buildup inside and subsequent dilation of the colon walls.

Understanding Ogilvie Syndrome

What is Ogilvie Syndrome?

Ogilvie syndrome is an acute condition characterized by a paralytic ileus of the colon which causes severe colonic dilation. It specifically affects the colon, typically starting at the cecum. The syndrome is uncommon and more complex than paralytic ileus.

How it Differs from Other Conditions

It is important to differentiate Ogilvie syndrome from other types of intestinal pseudo-obstruction and paralytic ileus:

  • Intestinal Pseudo-Obstruction: An umbrella term for any paralysis of the intestines not caused by a mechanical obstruction. Some individuals may experience chronic intestinal pseudo-obstruction due to chronic diseases or congenital conditions.
  • Paralytic Ileus: An acute type of intestinal pseudo-obstruction that commonly affects both intestines and often occurs after abdominal surgery. It usually resolves within a few days.

Who is Affected?

While Ogilvie syndrome can affect anyone, it is most prevalent among older adults with multiple underlying health conditions. Factors such as surgery, trauma, cardiovascular disease, or severe infection can trigger the syndrome. Additional risk factors include electrolyte imbalances, neurological diseases, and the use of multiple medications, all of which can impact the nervous system's control over colon muscle movements. About 1 in 1,000 hospital admissions report Ogilvie syndrome.

Causes and Risk Factors

In intestinal pseudo-obstruction, the intestine is unable to contract and push food, stool, and air through the digestive tract. The disorder most often affects the small intestine, but can also occur in the large intestine. The condition may start suddenly or be a chronic or long-term problem. It is most common in children and older people. The cause of the problem is often unknown.

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Several factors and conditions are known to increase the risk of developing Ogilvie syndrome:

  • Cerebral palsy or other brain or nervous system disorders.
  • Chronic kidney, lung, or heart disease.
  • Staying in bed for long periods of time (bedridden).
  • Taking drugs that slow intestinal movements.

The leading theory suggests that a lack of GI motility results from overstimulation of the sympathetic nervous system (SNS). Normally, the parasympathetic nervous system (PNS) decreases heart rate and blood pressure while increasing GI motility and colonic contraction, relaxing the anal sphincter. In Ogilvie’s syndrome, the PNS is suppressed, leading to excessive SNS stimulation, causing colonic inactivity, fluid and gas build-up, and massive dilation.

Symptoms and Diagnosis

Recognizing Symptoms

Patients with Ogilvie’s syndrome often complain of bloating, fullness, abdominal tenderness, and constipation. Some patients may experience a full or swollen belly along with mild abdominal pain. Severe pain and fever are not typical unless bowel ischemia or perforation has occurred. It’s important to note that bowel movements don't exclude acute colonic pseudo-obstruction. Up to 40% of patients may continue to pass flatus and feces.

Diagnostic Process

Diagnosis involves ruling out other potential causes of the symptoms, particularly mechanical large-bowel obstruction. Assessment of bowel sounds may lack diagnostic value as they can be hyperactive, hypoactive, normal, or absent. However, large amounts of gas trapped in the colon commonly produce tympanic sounds (hollow, drumlike reverberations) on abdominal percussion.

  • Abdominal X-rays: Crucial for diagnosis, typically showing massive dilation of the colon, especially in the ascending and transverse segments. Cecum >12 cm indicates significant risk of perforation. Review of old imaging may be useful to establish chronicity.
  • Contrast Studies: Water-soluble contrast enemas help rule out mechanical obstruction. Barium enemas should be avoided due to the risk of barium retention or leakage into the peritoneal cavity if perforation occurs.

Treatment Strategies

Initial Conservative Management

Initially, Ogilvie’s syndrome calls for conservative treatment. If the syndrome is suspected, a nasogastric (NG) tube attached to suction is typically ordered. A rectal tube may also be placed to decompress the distal colon.

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Colonoscopic Decompression

If symptoms persist after 48 to 72 hours of conservative management, a gastroenterologist may perform a colonoscopy to reconfirm the absence of mechanical obstruction and decompress the colon. A right-sided colonic decompression tube is often placed during colonoscopy to allow gas and fluid to evacuate the area most severely affected. Both the ASGE (American Society for Gastrointestinal Endoscopy) and the ESGE (European Society for Gastrointestinal Endoscopy) recommend endoscopic decompression for patients with cecal diameter >12 cm and symptoms persisting for >48-72 hours despite medical management. Colonoscopy of a dilated and unprepared colon increases the risk of perforation, which may occur in ~2% of procedures.

Pharmacological Interventions

  • Neostigmine: The most commonly used drug for Ogilvie’s syndrome, neostigmine allows acetylcholine to build up at the neuromuscular junction. It is administered intravenously, typically after the first 24 hours if conservative treatment hasn't relieved symptoms. The usual dosage is 2 mg IV by direct bolus over 3 to 5 minutes, followed by a continuous infusion at a rate of 0.4 mg/hour for 24 hours. Patients typically experience cramping and begin to pass flatus within 10 to 30 minutes after the bolus dose and evacuate stool in about 1 to 2 hours. Efficacy is >80%. Repeated dosing or a continuous infusion of neostigmine is strongly contraindicated. Consider a more conservative dose strategy (e.g., administer 1 mg, ensure that it is tolerated, then give another 1 mg for a cumulative dose of 2 mg).
    • Neostigmine Considerations: Neostigmine has the advantage that it usually works quickly and is effective. The traditional management of bradycardia is atropine, but atropine will inhibit the activity of neostigmine on the bowel. Some neostigmine is metabolized, but most is excreted unchanged in the urine. The half-life is extended in renal dysfunction. Bioavailability is incomplete and variable (10-20%). The half-life is typically 1-2 hours following oral administration, but may be prolonged in renal dysfunction.
  • Prucalopride: Prucalopride is a 5HT-4 agonist that increases colonic motility with off-label use for chronic intestinal pseudo-obstruction.
  • Pyridostigmine: Oral pyridostigmine has been used for colonic pseudo-obstruction. Scheduled pyridostigmine (e.g., 60 mg PO q6hrs) may be considered as an alternative to a neostigmine infusion, especially if a neostigmine infusion isn't logistically feasible. There isn't high-level evidence regarding the use of pyridostigmine in colonic pseudo-obstruction. Glycopyrrolate or hyoscyamine may be used to reduce secretions caused by pyridostigmine (e.g., 1 mg PO glycopyrrolate with each dose of physostigmine). Pyridostigmine can be given intravenously but at 1/30th the dose of oral medication.

Surgical Interventions

Cecostomy can be performed percutaneously under moderate sedation for patients who don’t respond to conservative measures. Surgery is reserved for patients with persistent, severe colonic distention (increasing the risk of colonic ischemia, perforation, and peritonitis) or when other management attempts fail. Surgical options include exploratory laparotomy with resection of the perforated bowel or partial colectomy. Some patients may need colonic resection with reanastomosis (removal and reconnection of a large-bowel portion).

Dietary Considerations

Special diets often do not work for Ogilvie syndrome. Colonic pseudo-obstruction will usually respond nicely to prompt administration of IV neostigmine. Treatment with osmotic laxatives will make this worse (e.g., polyethylene glycol or especially lactulose). Be careful of treating constipation blindly with an escalating regimen of laxatives.

Prognosis

Most cases of acute pseudo-obstruction improve within a few days with appropriate treatment. However, the perioperative mortality is enormous (~25%), so surgery is generally avoided if at all possible.

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