💨 Carbon Monoxide Poisoning
Carbon monoxide (CO) is an odourless, colourless, tasteless gas produced by incomplete combustion of carbon-containing fuels. It is the leading cause of poisoning death worldwide — known as the "silent killer."
CO is undetectable by human senses — no smell, no colour, no taste. Victims may have no warning before incapacitation.
Sources of CO
Common Sources
- Faulty gas heaters, boilers, cookers
- Petrol/diesel generators (indoors or poorly ventilated)
- Car exhaust in enclosed space (deliberate self-harm)
- Wood/charcoal fires in enclosed spaces
- Industrial processes (metal smelting, chemical production)
- House fires (smoke inhalation)
Pathophysiology
- CO binds to haemoglobin with 200–250× greater affinity than O₂
- Forms carboxyhaemoglobin (COHb) → reduces O₂ carrying capacity
- Causes leftward shift of O₂-Hb dissociation curve → reduced O₂ offloading to tissues
- Binds to cytochrome oxidase → inhibits cellular respiration (histotoxic hypoxia)
- Binds to cardiac myoglobin → myocardial dysfunction
Critical Diagnostic Point — Pulse Oximetry
Standard pulse oximetry CANNOT detect CO poisoning.
The pulse oximeter reads COHb as oxyhaemoglobin — SpO₂ appears NORMAL (98–99%) even when CO is critically elevated. A patient can be severely poisoned with apparently normal SpO₂.
Diagnosis requires: CO-oximetry (co-oximeter ABG) measuring actual COHb level.
🌡️ Clinical Features
Symptoms by COHb Level
| COHb Level | Symptoms |
|---|
| 0–3% | Normal (non-smokers); smokers may have 5–10% baseline |
| 10–20% | Headache (frontal), mild dyspnoea on exertion, nausea — may be mistaken for flu/migraine |
| 20–40% | Severe headache, confusion, visual disturbance, tachycardia, ataxia, chest pain |
| 40–60% | Seizures, syncope, profound confusion, severe cardiovascular compromise |
| >60% | Coma, cardiovascular collapse, death |
Classic Presentation
- Multiple people from same household/workplace presenting simultaneously with same symptoms = CO poisoning until proven otherwise
- Symptoms worse indoors, better when outside (fresh air = lower COHb)
- Household pets dying or acting strangely = early warning
- "Cherry red" skin — classically described but RARE in practice; usually seen in severe poisoning or post-mortem
Complications
Cardiac Complications
- Arrhythmias (AF, VT) — myocardial CO binding
- ST elevation/depression — myocardial ischaemia
- Troponin rise
- Cardiac arrest
Neurological Complications
- Delayed neurological syndrome (DNS): cognitive impairment, personality change, parkinsonism developing days–weeks after apparent recovery
- Cerebral oedema in severe poisoning
- Seizures
- Peripheral neuropathy
Delayed Neurological Syndrome (DNS): Occurs in 10–30% of significant CO poisoning — neuropsychiatric symptoms appearing 2–40 days after apparent recovery. Risk factors: high COHb on presentation, loss of consciousness, age >36. Hyperbaric oxygen may reduce DNS risk.
💊 Treatment of CO Poisoning
Step 1: Remove from Source + Resuscitation
- Remove patient from CO environment (ensure rescuer safety — wear SCBA if confined space)
- ABCDE assessment
- ECG — assess for cardiac arrhythmias
- IV access and bloods: FBC, U&E, lactate, troponin, glucose
- ABG with CO-oximetry — confirm COHb level
Step 2: 100% Oxygen — First-Line Treatment
High-flow 100% oxygen via tight-fitting non-rebreather mask (15 L/min) is the mainstay of treatment.
Why it works: Breathing 100% O₂ reduces CO half-life (t½) dramatically:
• Room air: CO half-life ~5 hours
• 100% O₂ at atmospheric pressure: CO half-life ~60–90 minutes
• Hyperbaric O₂ (2.5 ATM): CO half-life ~20–30 minutes
Continue until COHb <5% AND symptoms resolved.
Step 3: Hyperbaric Oxygen (HBO) — Indications
Indications for Hyperbaric Oxygen Therapy:
- COHb ≥25% (some guidelines ≥20%)
- Loss of consciousness (any duration)
- Neurological signs (confusion, seizures, focal deficit)
- Cardiac arrhythmia or ischaemia (ECG changes, troponin elevation)
- Pregnancy — any significant CO exposure (foetal Hb has even higher CO affinity)
- Severe metabolic acidosis
HBO at 2.5–3.0 atmospheres (ATM) — patient breathes 100% O₂ in hyperbaric chamber
Special Considerations
- Pregnancy: Foetal COHb 10–15% higher than maternal. Treat with 100% O₂ for 3× longer than non-pregnant. HBO more readily indicated.
- Cyanide co-poisoning: House fires produce both CO AND cyanide from burning plastics/synthetics. Consider IV hydroxocobalamin (Cyanokit) for house fire victims with cardiovascular collapse.
- Cardiac monitoring: ECG and troponin — CO causes myocardial injury; arrhythmias require treatment
- Seizures: IV benzodiazepines; high-dose O₂ continued
Nursing Considerations
- Ensure mask fits TIGHTLY — any air entrainment reduces FiO₂ and slows CO elimination
- Standard pulse oximetry unreliable — use ABG CO-oximetry to monitor COHb levels
- Neurological observations: GCS, confusion assessment, every 30–60 minutes
- Advise not to return home until source found and fixed
- Report cluster cases to public health (common source = carbon monoxide incident)
- Delayed neurological syndrome: follow-up cognitive assessment at 1 month