- Clinical science
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 
- 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
- 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:
- 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
- Nonspecific symptoms
- Cardiorespiratory toxicity
- Other classical signs
- Standard pulse oximetry: normal-appearing or ↑ SpO2 (as pulse oximeters cannot distinguish between COHb and oxyhemoglobin)
Clinical features do not correlate well with the COHb level. 
Ideally, all three criteria should be present to confirm acute poisoning, but symptoms vary widely and the history of exposure is not always evident. 
- 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).
- Blood gas (venous or arterial)
- Other routine laboratory studies: serum lactate, BMP, pregnancy test
Screen for affected organs and toxic coingestions.
- Inhalation injury: airway examination (e.g., direct laryngoscopy) 
- Cardiac toxicity 
Neurological toxicity: CT/MRI brain 
- Toxic coingestions: If intentional poisoning is suspected, screen for other substances: e.g., acetaminophen, salicylates, alcohol (see acetaminophen toxicity and salicylate toxicity). 
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. 
- Administer 100% oxygen immediately via nonrebreather facemask.
- Treatment endpoints
- Patient asymptomatic for at least 6 hours
- COHb level normalizes (< 3–5%)
Hyperbaric oxygen (HBOT) 
- The benefits of hyperbaric oxygen have not been conclusively demonstrated.
- The following are considered relative indications:
Management of systemic involvement and supportive care 
- 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: 
- Improve perfusion (e.g., fluids, oxygen).
- Avoid sodium bicarbonate.
- Pulmonology and toxicology consultations.
- Suspicion of concomitant cyanide poisoning (see cyanide) 
- Suspicion of intentional poisoning
- Evaluate for suicidal ideation
- Obtain a psychiatric consultation and consider involuntary psychiatric hold.
Monitoring and level of care 
- Continuous telemetry
- Serial neurologic examination (i.e., GCS and pupillary reflexes)
- Serial COHb monitoring (e.g., every 6 hours)
- Indications for ICU admission
- 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. 
- Consult pulmonology/ICU and toxicology as needed.
- Consider hyperbaric oxygen therapy.
- Consider empiric treatment of cyanide poisoning with hydroxocobalamin. 
- Evaluate for suicidal ideation.
- Consider further toxicology screening.
- Consider repeat COHb measurement every 6 hours.
- Exposure to prolonged low levels of CO
Clinical features 
Symptoms are often non-specific.
- Chronic fatigue
- Neurologic symptoms
- Abdominal pain/diarrhea
- Recurrent infections
- Exacerbation of chronic illness (e.g., coronary artery disease)
- 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:
- Imaging (CT or MRI)
- 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.