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Summary![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
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.
Etiology![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
- 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.
Pathophysiology![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
- Properties: colorless, odorless, and tasteless gas
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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
Clinical features![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
The correlation between feature severity and COHb level is poor. [3][4][5][6][7]
- Nonspecific symptoms
-
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.
Diagnostics![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
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]
-
CO oximetry with spectrophotometry [8]
- 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.
- All patients: ECG and cardiac monitor for 4–6 hours
-
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
- Indications
- Toxic coingestions: If intentional poisoning is suspected, screen for other substances: e.g., acetaminophen, salicylates, alcohol (see acetaminophen toxicity and salicylate toxicity). [4]
Differential diagnoses![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
Carbon monoxide poisoning vs. cyanide poisoning | ||
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Carbon monoxide poisoning | Cyanide poisoning | |
Etiology |
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Change in oxygen-myoglobin dissociation curve |
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Clinical features |
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Laboratory measurements |
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CT/MRI brain |
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Management |
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The differential diagnoses listed here are not exhaustive.
Management![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
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
- 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.
Acute management checklist![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
- 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.
Chronic carbon monoxide poisoning![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
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)
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).
Prevention![toggle arrow icon](https://manus-media.amboss.com/icons/chevron_up.svg)
- 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.