Treatment of Carbon Monoxide Poisoning
Immediately administer 100% oxygen via non-rebreather mask (10-15 L/min) or endotracheal tube to all patients with suspected carbon monoxide poisoning, even before obtaining carboxyhemoglobin levels, and continue for at least 6 hours until COHb normalizes to <3% and symptoms resolve. 1, 2, 3
Immediate Management Algorithm
Step 1: Oxygen Administration (Do Not Delay)
- Start 100% normobaric oxygen immediately at the highest possible flow rate, preferably via non-rebreather mask 1, 2, 4
- Do not wait for laboratory confirmation of COHb levels before initiating oxygen therapy 1, 2
- Oxygen reduces COHb elimination half-life from 320 minutes on room air to approximately 74 minutes 1, 2
- Continue oxygen therapy for minimum 6 hours, or until COHb drops to approximately 3% AND patient becomes asymptomatic 2, 3, 4
- In pregnant patients, extend oxygen therapy duration due to slower fetal CO elimination 4
Step 2: Diagnostic Confirmation
- Obtain carboxyhemoglobin level via CO-oximetry on venous or arterial blood 1, 2
- Critical pitfall: Standard pulse oximetry is completely unreliable—it will show falsely normal SpO2 readings (>90%) even with COHb levels as high as 25% 1, 2
- Obtain 12-lead ECG and continuous cardiac monitoring for all patients with moderate to severe poisoning 2, 5
- Check arterial blood gas for metabolic acidosis and lactate levels 3
- Important caveat: COHb levels correlate poorly with symptoms or prognosis and may be normal if several hours have elapsed since exposure—do not use COHb levels alone to guide treatment intensity 2, 3, 6
Step 3: Assess for Concomitant Cyanide Poisoning
- If CO source is a house fire, suspect concomitant cyanide poisoning 7, 2, 3
- Consider empiric cyanide treatment with hydroxocobalamin if arterial pH <7.20 or plasma lactate >10 mmol/L 2, 3
- The American Heart Association recommends hydroxocobalamin as primary treatment for suspected cyanide poisoning in fire victims 7
Hyperbaric Oxygen Therapy (HBOT) Decision Algorithm
Indications for HBOT (Consider if ANY of the following present):
- Loss of consciousness during or after exposure 2, 3
- Neurological deficits (confusion, memory problems, focal findings) 2, 3
- Ischemic cardiac changes on ECG or elevated troponin 2, 3
- Significant metabolic acidosis 2, 3
- COHb level >25% 2, 3
- Pregnancy with ANY symptoms of CO poisoning (mandatory indication regardless of COHb level) 3, 4
- Persistent symptoms despite normobaric oxygen therapy 4
HBOT Protocol:
- Treatment at 2.5-3.0 atmospheres absolute pressure 2, 3
- Reduces COHb half-life to approximately 20 minutes 2, 3
- First session should ideally occur within 6 hours of exposure 3, 6, 4
- Up to three treatments may be given for persistently symptomatic patients 3
HBOT Controversy and Practical Considerations:
- Evidence for HBOT preventing delayed neurological sequelae remains controversial due to heterogeneous study designs 7, 6, 8
- The European Committee of Hyperbaric Medicine (2016) strongly recommends HBOT for patients with altered consciousness, neurological/cardiac/respiratory symptoms, or pregnant women (Grade B evidence) 7
- However, HBOT may be contraindicated in severe burn patients due to hemodynamic or respiratory instability 7
- For burn patients with CO poisoning, evaluate case-by-case considering patient stability, burn severity, and availability of specialized equipment 7, 3
Special Populations and Considerations
Patients with Pre-existing Heart or Lung Disease:
- These patients are at higher risk for cardiac complications even with relatively low COHb levels 2, 5
- CO causes direct myocardial injury through tissue hypoxia and cellular damage, not just reduced oxygen-carrying capacity 1, 2, 5
- Myocardial toxicity from CO exposure is associated with increased short-term and long-term mortality 5
- Consider CPAP or non-invasive ventilation for pulmonary edema resulting from CO-induced cardiac dysfunction 1
- Obtain troponin levels and cardiology consultation for patients with cardiac symptoms or ECG changes 3, 5
Pregnant Patients:
- Fetal hemoglobin has higher affinity for CO than maternal hemoglobin, placing the fetus at greater risk 1
- HBOT is indicated for ALL pregnant women with any symptoms of CO poisoning, regardless of COHb level 3, 4
- Extend normobaric oxygen therapy duration due to slower fetal CO elimination 4
Intentional Poisoning:
- Perform toxicology screening for coingestions (present in up to 44% of cases) 3
- Check blood alcohol levels if mental status changes are disproportionate 3
- Mandatory psychiatric follow-up required due to high risk of subsequent suicide 3
Follow-Up Care Requirements
Short-Term Follow-Up (1-2 months):
- All patients with accidental CO poisoning require clinical follow-up to assess for delayed neurological sequelae (DNS) 2, 3, 6
- DNS occurs in 12-68% of poisoned patients and includes memory disturbance, depression, anxiety, calculation difficulties, vestibular problems, motor dysfunction, and sleep disorders 2, 3
- Patients not recovered to baseline functioning should be referred for formal neuropsychological evaluation 3
Cardiac Follow-Up:
- Patients with evidence of cardiac damage require appropriate cardiology follow-up 3
- Long-term mortality is increased up to 3-fold compared to unexposed individuals, suggesting possible residual brain injury even in "recovered" patients 2
Critical Pitfalls to Avoid
- Do not rely on pulse oximetry—it cannot differentiate between oxyhemoglobin and carboxyhemoglobin 1, 2
- Do not delay oxygen therapy while waiting for laboratory confirmation 1, 2
- Do not use COHb levels alone to determine treatment intensity or predict outcomes 2, 3, 6
- Do not discharge without identifying and eliminating the CO source to prevent re-exposure 1, 3
- Do not overlook cardiac complications which can occur even with relatively low COHb levels 1, 2
- Do not withhold HBOT solely because a patient appears clinically well—consider high-risk features listed above 3
- Do not assume normal PaO2 rules out significant poisoning—PaO2 measures dissolved oxygen in plasma, which is unaffected by CO binding to hemoglobin 1