Carbon Monoxide Poisoning

Clinical assessment

High index of suspicion based on history of potential exposure (ask specifically about heating sources, fires, generators, car exhaust, indoor charcoal use). Compatible symptoms (esp. headache, dizziness, nausea, confusion, collapse). Multiple individuals affected from the same environment strongly suggests CO poisoning. Important: Do NOT rely on standard pulse oximetry (SpO2) - it is falsely reassuringly normal or high because it cannot differentiate oxyhemoglobin from carboxyhemoglobin (COHb).

Investigations

• Carboxyhemoglobin (COHb) Level: Measured by CO-oximetry on an arterial or venous blood gas sample. Confirms exposure. Levels: <5% normal non-smokers, <10% smokers; >10-15% significant exposure; >25% severe; >50% often fatal. Note: COHb level correlates poorly with clinical severity and does not predict delayed sequelae. Treat based on history and clinical presentation, not just the number.
• Electrocardiogram (ECG): Essential to check for myocardial ischemia, injury, or arrhythmias.
• Blood Glucose: Check routinely.
• Consider: Arterial Blood Gas (ABG) - may show metabolic acidosis (lactic acidosis from tissue hypoxia). Cardiac enzymes (Troponin) if chest pain/ECG changes. Creatine Kinase (CK) for rhabdomyolysis. Chest X-ray (for smoke inhalation injury, aspiration, pulmonary edema). CT Head if persistent coma, focal neurological deficits, or seizures.
• Lactate level: May be elevated due to tissue hypoxia.

Diagnostic criteria

History of potential CO exposure + Compatible clinical symptoms + Elevated COHb level (if measured). However, a normal COHb level obtained late after removal from exposure does not rule out significant poisoning.

Non-pharmacological management

• Immediate removal from the source of exposure to fresh air. Ensure rescuer safety.
• Stabilization: ABCDE approach.
• Airway & Breathing: Secure airway if patient is comatose or has respiratory distress (intubation may be needed).
• Oxygen Therapy: Administer 100% High-Flow Oxygen via a tight-fitting non-rebreather mask IMMEDIATELY to ALL suspected cases. This is the cornerstone of treatment. It significantly shortens the half-life of COHb (from ~4-5 hours on room air to ~60-90 minutes on 100% O2). Continue 100% O2 until patient is asymptomatic AND COHb level is low (<5-10%, if measurable).
• Hyperbaric Oxygen (HBO) Therapy: Involves breathing 100% oxygen at increased atmospheric pressure (e.g., 2.5-3 ATA). Further shortens COHb half-life (~20-30 mins) and may reduce risk of delayed neurological sequelae. Consider for severe poisoning: Coma, seizures, transient loss of consciousness, cardiovascular instability (hypotension, arrhythmias, ischemia), persistent neurological deficits (confusion, focal signs), COHb level >25-40% (controversial threshold), OR Pregnant patient with COHb >15-20% or fetal distress. Requires transfer to a specialized facility (Referral essential). Decision often based on clinical severity more than COHb level.
• Supportive Care: Treat seizures (benzodiazepines), arrhythmias (ACLS), hypotension (IV fluids, vasopressors if needed), pulmonary edema, rhabdomyolysis.

Pharmacological treatment

• No specific antidote other than oxygen.
• Medications are used for supportive care: IV fluids, vasopressors, antiarrhythmics, anticonvulsants as needed.

Monitoring

Continuous cardiac monitoring (ECG). Monitor vital signs (HR, BP, RR, Temp). Monitor neurological status closely (GCS, focal signs). Monitor respiratory status and oxygenation (ABG may be needed). Serial COHb levels (if available) to guide duration of oxygen therapy. Assess for development of complications (rhabdomyolysis, renal failure, pulmonary edema). Follow up for delayed neurological sequelae.