Carbon monoxide toxicity

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Carbon monoxide (CO) toxicity causes tissue hypoxia via multiple mechanisms and is most commonly due to exposure to house fires, wood-burning stoves, or motor vehicle exhaust fumes. Symptoms are variable and nonspecific and include nausea, headache, and fatigue. Importantly, pulse oximetry will often show a normal waveform because standard pulse oximeters are unable to differentiate between oxyhemoglobin and carboxyhemoglobin (COHb). CO toxicity should be suspected in any individual with a history of exposure and symptoms consistent with CO toxicity, and the diagnosis can be confirmed by an elevated COHb level on CO oximetry. Management consists of 100% supplemental oxygen and possibly hyperbaric oxygen. In addition, supportive care should be provided with a focus on airway management and oxygenation. Chronic CO poisoning may also occur when individuals are chronically exposed to low levels of CO; symptoms are nonspecific and treatment consists of eliminating the source of CO exposure.

See also poisoning.

• House fires, wood-burning stoves/gas heaters, motor vehicle exhaust, furnaces in enclosed and poorly ventilated spaces, extensive water pipe smoking ^[2]
• Often involves multiple individuals (e.g., family) during the winter
• Intentional poisoning (may be a method of self-harm or suicide attempt)

Multiple patients presenting with similar clinical features from a common location (e.g., a residence or workplace) should raise suspicion for CO exposure.

• Properties: colorless, odorless, and tasteless gas
• Pathophysiology
  • The affinity of hemoglobin for CO is ∼ 240 times stronger than for O₂ → formation of COHb (carboxyhemoglobin)
  • ↑ COHb causes tissue hypoxia via the following mechanisms:
    • Decreased oxygen-carrying capacity of hemoglobin
    • Shift in the O₂ dissociation curve to the left → ↑ affinity for O₂ → ↓ release of O₂ in tissue
    • Binding of CO to myoglobin → cardiac ischemia → decreased cardiac output
  • CO inhibits mitochondrial cytochrome c oxidase → defective oxidative phosphorylation → ↑ anaerobic metabolism with ↓ ATP production and hypoxia
  • CO inhibits cytochrome p450 in the brain → lipid peroxidation and leukocyte-mediated inflammatory damage → cerebral edema

The correlation between feature severity and COHb level is poor. ^{[3][4][5][6][7]}

• Nonspecific symptoms
  • Headache
  • Dizziness
  • Fatigue
  • Nausea/vomiting
• Neurotoxicity
  • Altered mental status (e.g., agitation, confusion, somnolence, memory loss)
  • Seizures
  • Loss of consciousness/coma
• Cardiorespiratory toxicity
  • Inhalation injury: associated with fire-related exposures
  • Chest pain
  • Shortness of breath
  • Shock
  • Respiratory failure
• Other classical signs
  • Cherry-red skin with bullous skin lesions: after exposure to high levels (rare and usually seen postmortem)
  • Fundoscopic findings: bright red retinal vessels, retinal hemorrhages, papilledema (indicative of cerebral edema)
  • Symptoms of concurrent cyanide poisoning: See cyanide.
• Standard pulse oximetry: normal-appearing or ↑ SpO₂ (as pulse oximeters cannot distinguish between COHb and oxyhemoglobin)
  • Portable pulse CO oximetry may show abnormal COHb ^[3]

Clinical features do not correlate well with the COHb level. ^[4][5][6]

SpO₂ is not useful when screening for CO poisoning! Oximeters cannot distinguish between COHb and oxyhemoglobin.

Diagnostic triad

Ideally, all three criteria should be present to confirm acute poisoning, but symptoms vary widely and the history of exposure is not always evident. ^[3]

• Any symptoms of CO poisoning (see “Clinical features”)
• Exposure to CO source (see “Etiology”)
• Abnormal COHb level on venous/arterial CO oximetry
  • > 3–4% in nonsmokers
  • > 10–15% in smokers

Start 100% oxygen immediately if clinical suspicion for CO poisoning is high! Diagnostic workup should not delay oxygen administration (see treatment).

Laboratory studies

• Blood gas (venous or arterial)
  • CO oximetry with spectrophotometry ^[8]
    • Gold standard for diagnosis
    • The COHb level is used to guide therapeutic decisions.
    • Also measures methemoglobin levels
  • PaO₂: usually appears normal
  • pH: Tissue hypoxia may lead to high anion-gap metabolic acidosis. ^[4]
• Other routine laboratory studies: serum lactate, BMP, pregnancy test

Additional studies

Screen for affected organs and toxic coingestions.

• Inhalation injury: airway examination (e.g., direct laryngoscopy) ^[9]
• Cardiac toxicity ^[6][7]
  • All patients: ECG and cardiac monitor for 4–6 hours
    • Findings may include signs of myocardial ischemia; and/or arrhythmias.
  • Select patients ; : cardiac enzymes and echocardiography
    • Findings may include increased troponin and/or cardiac hypomotility.
• Neurological toxicity: CT/MRI brain ; ^[6]
  • Indications
    • Symptomatic patients (e.g., altered mental status)
    • Unconscious patients
    • Signs of extrapyramidal syndrome (e.g., rigidity)
    • Retinal hemorrhage (good indicator of CNS toxicity)
  • Findings
    • The globus pallidus is commonly affected (unspecific findings, usually bilateral ).
    • White matter changes
    • Cerebral edema
• Toxic coingestions: If intentional poisoning is suspected, screen for other substances: e.g., acetaminophen, salicylates, alcohol (see acetaminophen toxicity and salicylate toxicity). ^[4]

The differential diagnoses listed here are not exhaustive.

Patients often arrive in critical condition or comatose, which requires an ABCDE approach. Oxygen therapy is considered first-line treatment. Local authorities (e.g., public health, poison control) should be notified early due to the environmental risk of CO. ^[4][6][7][9]

Oxygen therapy

• Administer 100% oxygen immediately via nonrebreather facemask.
• Treatment endpoints
  • Patient asymptomatic for at least 6 hours
  • COHb level normalizes (< 3–5%)

Hyperbaric oxygen (HBOT) ^[3][4]

• The benefits of hyperbaric oxygen have not been conclusively demonstrated.
• The following are considered relative indications:
  • COHb > 25%
  • Pregnant women with a COHb > 15%
  • Neurological manifestations (e.g., confusion, loss of consciousness, seizures, focal neurological deficits)
  • Acute myocardial ischemia
  • Severe acidosis (pH < 7.15)
  • Age > 35 years
  • Exposure ≥ 24 hours
  • Post-cardiac arrest ^[10]

Management of systemic involvement and supportive care ^[4]

• Secure airway: Consider early intubation in patients with inhalation injury or severely impaired mental status (see airway management).
• Evidence of cardiac toxicity (e.g., arrhythmias, ischemia): urgent cardiology consult, continuous cardiac rhythm monitoring
• Metabolic acidosis: ^[6]
  • Improve perfusion (e.g., fluids, oxygen).
  • Avoid sodium bicarbonate.
• Pulmonology and toxicology consultations.
• Suspicion of concomitant cyanide poisoning (see cyanide) ^[4][11]
  • Administer hydroxocobalamin .
  • Indications
    • House fire as the source of CO toxicity
    • pH < 7.2
    • Lactate ≥ 10 mmol/L
• Suspicion of intentional poisoning
  • Evaluate for suicidal ideation
  • Obtain a psychiatric consultation and consider involuntary psychiatric hold.

pH < 7.2, exposure to fire, loss of consciousness, higher COHb level, and need for endotracheal intubation are all associated with higher short-term mortality. ^[3]

Monitoring and level of care ^[3][9]

• Continuous telemetry
• Serial neurologic examination (i.e., GCS and pupillary reflexes)
• Serial COHb monitoring (e.g., every 6 hours)
• Indications for ICU admission
  • Inhalation injury requiring close monitoring or intubation
  • Cardiac ischemia
  • Cerebral edema: See ICP management.
  • Consider transfer to HBOT center.

• Administer 100% oxygen.
• Check for inhalation injury.
• Secure airway.
• Obtain CO oximetry and ECG.
• Inquire about the source of CO exposure and notify appropriate authorities. ^[12]
• Consult pulmonology/ICU and toxicology as needed.
• Consider hyperbaric oxygen therapy.
• Consider empiric treatment of cyanide poisoning with hydroxocobalamin. ^[11]
• Evaluate for suicidal ideation.
• Consider further toxicology screening.
• Consider repeat COHb measurement every 6 hours.

Pathophysiology ^[3]

• Exposure to prolonged low levels of CO
  • Chronic mild hypoxia → ↑ erythropoietin → erythrocytosis, polycythemia, ↑ hemoglobin
  • Chronic CNS effects: unclear mechanism (probably anoxia and ischemia)

Clinical features ^[7][13]

Symptoms are often non-specific.

• Chronic fatigue
• Neurologic symptoms
  • Cognitive impairment
  • Paresthesias
  • Vertigo
  • Headache
• Abdominal pain/diarrhea
• Recurrent infections
• Exacerbation of chronic illness (e.g., coronary artery disease)

Diagnostics ^[7][13]

• Very challenging and often missed
  • Patients typically present with long-term nonspecific complications.
  • COHb levels are often below the toxic threshold.
  • Environmental CO measurement is usually required to confirm chronic low-level exposure.
• Suspect in the following scenarios:
  • Multiple patients from the same location with similar nonspecific symptoms
  • Unexplained neurologic symptoms
  • Clinical features of CO poisoning with polycythemia
• Imaging (CT or MRI)
  • Usually part of the diagnostic workup of patients presenting with unclear neurologic symptoms
  • Findings are typically inconclusive (e.g., atrophy, unspecific hyperintensities) and do not confirm the diagnosis.
  • Useful to rule out differential diagnoses (e.g., dementia)

Management ^[7][13]

• Consists of removing the source of CO
• No specific treatment available
• If COHb levels are measurably high (which is uncommon), patients may benefit from acute management (e.g., 100% oxygen).

• Counsel patients on the proper use of CO-generating equipment (e.g., gas heaters).
• Recommend the installation of environmental CO detectors and alarms.
• Provide treatment and support for preexisting mental health disorders.