Carbon Monoxide Poisoning Medical Slides

Present the critical teaching point: standard pulse oximetry reads falsely normal in CO poisoning because it cannot distinguish COHb from oxyhemoglobin (both absorb light at similar wavelengths at 660 nm). A patient with lethal COHb of 40% may display SpO2 of 99%. Diagnosis requires CO-oximetry (available on most arterial blood gas analyzers, also measurable on venous blood). Newer pulse CO-oximeters (RAD-57) can noninvasively screen for COHb but have limited accuracy. Key point: in any patient with altered mental status, headache, or syncope — especially in winter or with multiple affected household members — obtain COHb level regardless of SpO2.

Present the Weaver 2002 trial (NEJM): three HBO sessions within 24 hours reduced cognitive sequelae from 46% to 25% at 6 weeks (NNT=5). Commonly cited indications (not universally agreed upon): COHb >25% (>15% if pregnant), loss of consciousness, neurological symptoms, cardiac ischemia, significant metabolic acidosis, and COHb >15% with ongoing symptoms despite normobaric O2. HBO reduces COHb half-life to 23 minutes (vs 90 min on 100% O2). Practical limitations: HBO availability (limited centers), transport time vs benefit, contraindications (untreated pneumothorax).

Present DNS (delayed neuropsychiatric sequelae): occurs in 10-30% of moderate-severe CO poisoning, typically manifesting 2-40 days after initial recovery ("lucid interval"). Symptoms: cognitive impairment (memory, concentration), personality changes, parkinsonism, dementia, incontinence. MRI findings: bilateral globus pallidus necrosis and periventricular white matter demyelination. Risk factors: prolonged exposure, loss of consciousness, age >36, COHb >25%. Prognosis: 50-75% improve over 1 year. The primary rationale for HBO therapy is DNS prevention. Follow-up neuropsychiatric testing at 4-6 weeks is recommended for all significant exposures.