II. Epidemiology
- Emergency Department visits per year: 50,000 in U.S.
- Leading cause of toxin related death in United States
- Accidental or Intentional (Suicide) deaths per year: 5000
III. Sources: Carbon Monoxide
- Gas powered engine
- Car with faulty exhaust system
- Passengers riding in back of a pickup truck
- Swimmers at back of a houseboat
- Propane fueled forklifts
- Ice skating rink Zamboni
- Indoor tractor pulls
- Home
- Indoor Heaters (most common cause)
- Furnace
- Home water heaters
- Gas heaters
- Pool heaters
- Kerosene heaters
- Indoor Flames
- Wood stoves
- Indoor charcoal fires
- Sterno fuel
- Tobacco smoke
- Tobacco Smokers
- Carboxyhemoglobin levels may reach 6-10%
- Hookah Smokers
- Carboxyhemoglobin levels may reach 15-20%
- Nonsmokers exposed to passive smoke
- Cigarette tip 2.5 fold greater CO than inhaled
- Tobacco Smokers
- Indoor Heaters (most common cause)
- Industrial or Occupational
- Fire fighters
- Steel foundry
- Pulp paper mill
- Formaldehyde and coke producing plants
- Methylene Chloride
- Found in paint strippers and industrial solvents
- Transdermal exposure or inhalational (esp. in poorly ventilated areas)
- Cytochrome P450 2E1 (CYP2E1) oxidizes methylene chloride to formyl chloride, which is metabolized to CO
- Carbomyl bromide (another industrial chemical) may also cause similar effects
- Fire
- Building or structure fire
- Wilderness fire
-
Suicide Attempt
- Closed garage with car Running
- Ingestion of formic acid and sulfuric acid (sulphuric acid)
- Combination yields Carbon Monoxide
- Strong acid fumes may also result in Burn Injury and lung injury
- Swadron and Nordt (2022) EM:Rap 22(6): 5-7
IV. Pathophysiology
- Carbon Monoxide Properties (no warning features that gas is present until symptoms develop)
- Colorless
- Odorless
- Non-irritating gas
- Small molecule that crosses through some barriers into closed spaces (e.g. drywall)
- Exposures leading to Toxicity
- Carbon Monoxide Toxicity occurs at Ambient levels >200-500 parts per million
- More severe illness occurs with longer exposure times
- Carbon Monoxide inhalation
- Carbon Monoxide has a high affinity for Hemoglobin (>200-250 times higher affinity than oxygen)
- In the tissues, Carbon Monoxide binds myoglobin
- Displaces Oxygen and produces Carboxyhemoglobin (COHb)
- Impairs oxygen off-loading from Hemoglobin And oxygen tissue delivery
- Shifts oxygen dissociation curve left with poor delivery of any residual oxygen to tissues
- Functional Anemia is however not responsible for Carbon Monoxide's lethal effects
- Carbon Monoxide has a high affinity for Hemoglobin (>200-250 times higher affinity than oxygen)
- Direct neurotoxic effects of Carbon Monoxide
- Mechanisms of Carbon Monoxide neurotoxicity
- Mitochondrial dysfunction
- Binds cytochrome oxidase (Complex 4)
- Displaces nitric oxide
- Nitric oxide levels increase and result in CNS micovascular effects
- Mitochondrial dysfunction
- Inflammatory cascade (responsible for neurologic toxicity)
- White Blood Cell response
- Glutamic Acid (inflammatory)
- Free radicals
- Neurotoxicity effects
- Basal Ganglia (Parkinsonism)
- Occiput (occipital blindness)
- Frontal cortex (personality change)
- Mechanisms of Carbon Monoxide neurotoxicity
- Other toxicity
- Indirect Sodium channel activation
V. History
- Multiple persons (e.g. family, coworkers, pets) in the same environment with similar symptoms
VI. Symptoms
- Dull, frontal, constant Headache (88%)
- Dizziness (83%)
- Nausea (75%)
- Drowsiness (75%)
- Dry Mouth (44%)
- Syncope
- Hypotension
- Chest Pain
- Shortness of Breath
- Blurred Vision
- Myalgias
- Carbon Monoxide also binds myoglobin
VII. Signs
- Precautions
- Do NOT rely on Oxygen Saturations (not accurate see below)
- Do NOT use Co-Oximetry devices (inaccurate; used to measure total Hemoglobin, not Carboxyhemoglobin)
- Cherry-red skin and mucosa
- Late or post-mortem finding
- Bounding Pulse
- Hypertension
- Neurologic
- Muscular Fasciculations
- Stertorous breathing
- Dilated pupils
- Convulsions
- Altered Mental State to coma
VIII. Findings: Carboxyhemoglobin level
-
Carboxyhemoglobin: 10%
- Frontal Headache
- Carboxyhemoglobin: 20%
- Carboxyhemoglobin: 30%
-
Carboxyhemoglobin: 40%
- Confusion
- Syncope
- Carboxyhemoglobin: 50%
- Carboxyhemoglobin: 60%
-
Carboxyhemoglobin: 70%
- Death
IX. Pharmacokinetics
- Elimination Half-Life (via ventilation): 4 hours
- Half-Life decreases to 1-2 hours with 100% Supplemental Oxygen
X. Labs
- Blood grossly appears abnormal red color
- Venous Blood Gas
-
Carboxyhemoglobin
- Normal background Carboxyhemoglobin is 2-3%
-
Carboxyhemoglobin elevated >25% is significant and associated with toxicity
- See above for findings related to Carboxyhemoglobin levels
- Complete Blood Count
- Lactic Acid
- Serum Troponin
- Creatine Phosphokinase (CPK)
- bHCG (Pregnancy Test in women of child-bearing age)
XI. Precautions
-
Oxygen Saturation (Pulse Oximeter) data is inaccurate
- Does not distinguish Carboxyhemoglobin from oxygenated Hemoglobin
- Drywall does not deter Carbon Monoxide
- Carbon Monoxide diffuses across drywall and may permeate separated rooms in multi-tenant housing
- Consider concurrent Cyanide toxicity in structure fires
- Smoke Inhalation and Lactic Acid >8 suggests cyanide Poisoning
- Especially with Altered Level of Consciousness
- Start oxygen while awaiting lab testing results if higher level of suspicion
- Start 100% oxygen via non-rebreather
- Hyperglycemia is a Neurotoxin and worsens outcomes
XII. Management: Mild Poisoning
- Criteria
- Carboxyhemoglobin <30%
- No Neurologic or Cardiovascular Impairment
- Management
- Oxygen 100% Non-Rebreathing Mask
- Continue until Carboxyhemoglobin <5%
- Carbon Monoxide decreases 50% in 6 hours on room air
- Carbon Monoxide decreases 50% in 60 minutes on Non-Rebreather Mask
- Carbon Monoxide decreases 50% in 30 minutes on 100% oxygen while intubated
- Continuous Positive Airway Pressure (CPAP) with oxygen lowers Carbon Monoxide faster than oxygen alone
- Hyperbaric Oxygen Indications
- See Hyperbaric Oxygen below
- Carboxyhemoglobin >25% and associated factors (cardiac or neurologic findings, age >36 years old)
- Consider in Pregnancy
- Other measures
- Consider Dexamethasone 10 mg daily for 3 days
- Admission criteria
- All patients with Carboxyhemoglobin >25%
- Abnormal cardiac exam or lab markers
- Underlying heart disease
- Persistent neurologic symptoms
- Oxygen 100% Non-Rebreathing Mask
XIII. Management: Moderate Poisoning
- Criteria
- Carboxyhemoglobin: 30-40%
- No Neurologic Impairment
- Management
- Oxygen 100% Non-Rebreathing Mask
- Continue until Carboxyhemoglobin <5% (see above)
- Admission to telemetry (cardiovascular monitor)
- Other measures
- Consider Dexamethasone 10 mg daily for 3 days
- Consider hyperbaric oxygen (see below)
- Cerebellar signs
- Focal neurologic deficit
- Persistent severe Headache
- Loss of consciousness, Seizure or coma
- Glasgow Coma Scale (GCS) <15
- Age >36 years old
- Prolonged Carbon Monoxide exposure
- Venous Blood Gas
- Determine acid-base status
- Oxygen 100% Non-Rebreathing Mask
XIV. Management: Severe Poisoning
- Criteria
- Carboxyhemoglobin: >40%
- Neurologic Impairment
- Management
- Oxygen 100% Non-Rebreathing Mask
- Continue until Carboxyhemoglobin <5% (see above)
- Admission to telemetry (cardiovascular monitor)
- Endotracheal Intubation may be required due to severe Hypoxemia
- Venous Blood Gas
- Follow acid-base status
- Other measures
- Consider Dexamethasone 10 mg daily for 3 days
- Extracorporeal Membrane Oxygenation (VA-ECMO)
- Indicated in refractory cardiovascular collapse
- Hyperbaric oxygen (see below)
- Ideally performed within 6 hours of presentation
- Chamber immediately available OR
- No improvement in 4 hours
- Cardiovascular status
- Neurologic status
- Oxygen 100% Non-Rebreathing Mask
XV. Management: Hyperbaric oxygen chamber
- Mechanism
- Carbon Monoxide decreases 50% in 20-30 minutes on hyperbaric oxygen at 2.8 atm
- Allows oxygen to dissolve in blood at a much greater extent (beyond Hemoglobin binding)
- Decreases inflammatory cascade
- Decreases reperfusion injury
- Efficacy
- Decreases risk of delayed neuropsychiatric effects
- Reduces risk of personality change, Parkinsonism, cognitive effects
- Better short-term and long-term cognitive outcome
- Weaver (2002) N Engl J Med 347:1057-67 [PubMed]
- Rose (2018) Crit Care Med 46(7): e649-55 [PubMed]
- Decreases risk of delayed neuropsychiatric effects
- Indications
- Carboxyhemoglobin: >40%
- Carboxyhemoglobin: >25-30% and associated factors
- Neurologic Impairment or Altered Mental Status
- Transient or prolonged loss of consciousness
- Severe acidosis
- Cardiac involvement
- Abnormal neuropsychiatric findings
- Age >36 years old
- Carboxyhemoglobin: <15%
- Consider hyperbaric oxygen for pregnant patients
XVI. Complications
- Hypoxic Encephalopathy
- Delayed Neurological Sequelae or Delayed Neuropsychiatric Syndrome (DNS or D/PNS)
- Risk Factors
- Age >36 years
- Exposure for >24 hours
- Syncope
- Increased Lactic Acid level
- CT Brain white matter hypodense Subcortical Regions (including at Globus Pallidus)
- Appearance within 1 day of exposure is associated with poor prognosis
- Findings
- Cognitive effects may persist for weeks to months or even permanently (up to 15-40% of cases)
- Reduced risk with hyperbaric oxygen therapy (see above)
- Parkinsonism
- Occipital blindness
- Personality change
- Cognitive effects may persist for weeks to months or even permanently (up to 15-40% of cases)
- Coronary ischemia or myocadial infarction
- Increased risk of Coronary Artery Disease
XVII. Prevention
XVIII. Resources
- Consumer Products Safety Commission
XIX. References
- Carroll (2025) Crit Dec Emerg Med 39(11): 36
- Kinker and Glauser (2021) Crit Dec Emerg Med 35(9): 19-27
- Moayedi and Swaminathan in Herbert (2016) EM:Rap 16(7): 13-14
- Nordt and Shoenberger in Herbert (2019) EM:Rap 19(1): 4-6
- Reisdorf (1996) in Tintinelli (1996)
- (1995) MMWR Morb Mortal Wkly Rep 44:765-7 [PubMed]