Carbon monoxide toxicity

To see contributor disclosures related to this article, hover over this reference: ^[1]

Physicians may earn CME/MOC credit by reading information in this article to address a clinical question, and then completing a brief evaluation, in which they will identify their question and report the impact of any information learned on their clinical practice.

AMBOSS designates this Internet point-of-care activity for a maximum of 0.5 AMA PRA Category 1 Credit(s)™. Physicians should claim only credit commensurate with the extent of their participation in the activity.

For answers to questions about AMBOSS CME, including how to redeem CME/MOC credit, see "Tips and Links" at the bottom of this article.

Diagnostic approach

• ABCDE survey
• Targeted clinical evaluation
• Blood gas analysis with CO-oximetry
• CBC
• BMP
• Lactate
• Pregnancy test
• ECG
• Chest x-ray

Red flag features

• Signs of inhalation injury
• Respiratory failure
• Chest pain
• Altered mental status
• Seizures
• Serum pH < 7.15
• COHb > 25%
• Signs of cyanide poisoning

Management checklist

• Administer 100% oxygen via nonrebreather facemask.
• Manage the airway.
• Call local poison control center.
• Manage acute seizures.
• Consider hyperbaric oxygen therapy.
• Assess for concomitant cyanide poisoning.
• Monitor serial neurologic examinations and COHb levels.
• Consult psychiatry for intentional poisoning.

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.

• 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 veins, 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.

Manifestations of CO poisoning may be atypical in children (e.g., isolated seizure episode, isolated vomiting). ^[8]

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][9]
  • ≥ 2% in nonsmokers
  • ≥ 10% 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 ^[10]
    • 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) ^[11]
• Cardiac toxicity ^[6][7]
  • All patients:
    • ECG; and cardiac monitor for 4–6 hours : Findings may include signs of myocardial ischemia; and/or arrhythmias.
    • Chest x-ray: may show cardiogenic pulmonary edema ^[8][9]
  • 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][11]}

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][12]

• The benefits of hyperbaric oxygen have not been conclusively demonstrated. ^[8]
• 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 ^[13]
• HBOT is likely safe to use in children and may help prevent neurological sequelae of CO poisoning. ^[8][14]

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.
• Treat acute seizures (see “Management of acute seizures and status epilepticus”).
• Pulmonology and toxicology consultations.
• Suspicion of concomitant cyanide poisoning ^[4][15]
  • Administer antidotes for cyanide poisoning.
  • 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]

Pediatric patients require judicious fluid replacement therapy due to risk of development or worsening of cerebral edema from volume overload. ^[3][8][16]

Monitoring and level of care ^[3][11]

• 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.

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][17]

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][17]

• 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][17]

• 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.