Colonic Pseudo-Obstruction (Ogilvie Syndrome)

Acute colonic dilation in the absence of a mechanical obstruction. First described by Sir William Heneage Ogilvie in 1948. Content below is from a textbook reference chapter (Sabiston Ch52 - Diverticular Disease, Obstruction & Pseudo-Obstruction), not primary literature.

Epidemiology and pathophysiology

Rare (~100/100,000 admissions). Hypothesized mechanism: dysregulation of colonic autonomic innervation, with relative sympathetic-over-parasympathetic excess, disrupted colonic reflex arcs, plus contributions from chronic disease and medications.

Classic setting: elderly, multiple comorbidities, following an acute illness (often hospitalization, medical or surgical).

Common associated conditions:

Category	Examples
Postsurgical	Major orthopedic/spinal surgery, solid organ transplant, cardiac procedures
Neurologic	Parkinson disease, Alzheimer disease, stroke, spinal cord injury
Cardiac	CHF, myocardial infarction
Pulmonary	COPD
Trauma	Major trauma, shock, burns
Metabolic	Diabetes, renal failure, electrolyte disturbances
Infectious	CMV, VZV
Obstetric/gynecologic	Cesarean section, normal and instrumental delivery
Miscellaneous	Lupus, scleroderma
Drugs	Opiates, chemotherapy, anti-Parkinson drugs, anticholinergics, antipsychotics, clonidine

Presentation and diagnosis

Distension, pain, nausea/vomiting; obstipation common, though some patients have diarrhea from hypersecretion. Decreased/absent bowel sounds, or high-pitched tinkling sounds. Systemic toxicity or peritoneal signs are uncommon and should raise suspicion for ischemia/perforation.

• Plain film: cecum/right colon typically most dilated (can reach 10–12 cm); dilation and gas extending all the way to the rectum favors pseudo-obstruction over a mechanical obstruction (which usually shows a gas paucity distal to the obstruction point).
• Water-soluble contrast enema can reliably distinguish mechanical obstruction from pseudo-obstruction; CT is now typically used as the standard confirmatory test, also assessing for ischemia/impending perforation.
• Red flags for ischemia/perforation: abdominal tenderness, leukocytosis, fever, cecal diameter

  12 cm.

• Differential: mechanical obstruction, toxic megacolon (C. difficile or other causes).

Management (escalating by severity)

1. Supportive care — for cecal diameter <12 cm without ischemia/toxicity: NPO, correct electrolytes, stop contributing medications (opiates, anticholinergics, neuroleptics, antihistamines, clonidine), NG tube/rectal tube for decompression, ambulation, prone/knee-chest positioning to aid flatus passage. Avoid osmotic/stimulant laxatives (worsen dilation). Serial exams and abdominal films to monitor.
2. Neostigmine — acetylcholinesterase inhibitor, 2–2.5 mg IV bolus over 3–5 minutes in a monitored setting with atropine available. Success (flatus/bowel movement) 60–94%; recurrence in up to 31%. Contraindicated in mechanical obstruction and in ischemia/perforation; caution in asthma/COPD, bradycardia, recent ACS, renal failure. Common side effects: vomiting, cramping, salivation, bradycardia.
3. Colonoscopic decompression — for neostigmine failure, contraindication, or unresponsiveness. Advance to the right colon with minimal insufflation, place a decompression tube. Initial success 61–95%, sustained success 70–90%; perforation rate 1–3%.
4. Surgery — for patients who fail conservative measures or show toxicity/ischemia/perforation. Tube cecostomy or cecostomy if the colon is viable (high success rate); resection (usually with a diverting stoma) if ischemic or perforated.

Ischemia/perforation occurs in an estimated 3–15% of cases and carries ~50% mortality when it does — the rationale for the escalating, time-sensitive protocol above.

Open items / gaps

• No primary trial data in the wiki yet on neostigmine dosing/protocols or comparative effectiveness vs. colonoscopic decompression as first-line.
• ASCRS Clinical Practice Guidelines are referenced by the textbook as the fuller resource on this topic — not yet ingested directly.