Ogilvie Syndrome Medical Slides
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Generate Ogilvie Syndrome DeckWhy teach Ogilvie Syndrome?
Ogilvie syndrome (acute colonic pseudo-obstruction, ACPO) is characterized by massive colonic dilation without mechanical obstruction, typically occurring in hospitalized patients with severe medical or surgical comorbidities. Cecal diameter >12 cm on plain radiograph is associated with increasing perforation risk (3-15%), and perforation carries mortality exceeding 40%. Neostigmine, an acetylcholinesterase inhibitor, was validated by the landmark Ponec 1999 RCT and remains the first-line pharmacological treatment, achieving decompression in 80-90% of patients.
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Ogilvie Syndrome Presentation FAQ
How should the neostigmine protocol be presented in Ogilvie syndrome teaching?
Present the Ponec 1999 RCT evidence: neostigmine 2 mg IV produced colonic decompression in 91% of patients vs 0% with placebo. Protocol: patient in monitored setting (ICU or telemetry), continuous cardiac monitoring, atropine 0.5-1 mg at bedside, IV access established. Administer neostigmine 2 mg IV over 3-5 minutes. Expected response: abdominal cramping and passage of flatus/stool within 3-30 minutes. Monitor for bradycardia (most common side effect — occurs in 10-30%, treated with atropine if symptomatic). Contraindications: mechanical obstruction (must be excluded first), bradycardia <60, active bronchospasm, recent MI. May repeat once at 3-4 hours if initial dose unsuccessful. Success rate 80-90% with 1-2 doses.
What cecal perforation risk factors should be highlighted?
Present the risk assessment: cecal diameter is the primary predictor — <12 cm: low risk, 12-14 cm: moderate risk (3-8%), >14 cm: high risk (>15% perforation rate). Duration of dilation matters: >6 days of dilation increases perforation risk independent of diameter (Laplace law — wall tension increases with diameter AND duration of distension). Other risk factors: cecal ischemia (assess on CT — pneumatosis, portal venous gas), delay in treatment >6 days, and failed conservative/pharmacological management. Key teaching point: the 12 cm threshold is a guideline, not an absolute — clinical context matters. A patient with cecal diameter 10 cm that is increasing despite conservative management may need intervention, while a patient at 13 cm that is decreasing may be observed.
How should the management algorithm be structured from conservative to surgical?
Present the stepwise escalation: Step 1 (Conservative, 24-48 hours): NPO, NGT decompression, rectal tube, discontinue opioids/anticholinergics, correct electrolytes (K+ >4.0, Mg2+ >2.0), ambulate if possible, position changes (knee-chest, prone). Step 2 (Pharmacological): neostigmine 2 mg IV if no response to conservative measures within 24-48 hours OR cecal diameter >12 cm. Step 3 (Endoscopic): colonoscopic decompression for neostigmine failure — advance to hepatic flexure, aspirate gas, place decompression tube. Success 60-90% but recurrence in 20-40%. Step 4 (Surgical): cecostomy (percutaneous or surgical tube cecostomy) for recurrent pseudo-obstruction after failed medical/endoscopic management. Colectomy reserved for: perforation, ischemia/necrosis, or inability to control with less invasive means.
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