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    Carbon Monoxide Toxicity: Treatment

    Environmental Injuries / Exposures, Neurological, Toxicology

    Last Updated Oct 27, 2020
    Read Disclaimer


    • Carbon Monoxide (CO) is a colourless, odourless, tasteless gas formed from the incomplete combustion of hydrocarbons.
    • Sources include: house fires, heating systems, charcoal grills, and motor vehicles, especially in areas with poor ventilation.
    • Most common acute presentations are after intentional self-exposure or entrapment in a house fire. Chronic presentations due to ongoing household exposure are less common.
    • Every year, the Vancouver General Hospital Hyperbaric Unit treats around 40 cases of CO poisonings, and there are approximately 300 CO related deaths in Canada. CO Toxicity is the most common cause of fire-related death.
    • CO strongly binds to hemoglobin forming carboxyhemoglobin (COHb), which reduces oxygen carrying and delivering capacity leading to tissue hypoxia. It also binds to cytochromes directly, causing direct cellular damage, and initiates an inflammatory cascade that includes lipid peroxidation leading to both immediate and delayed neurologic damage.
    • Diagnosis can be difficult, as chronic exposures can present with vague or nonspecific symptoms and patients may not be aware of their exposure history.

    Recommended Treatment


    • Removal from environment, cardiac monitoring and attention to ABC’s.
    • 100% FiO2 should be delivered regardless of SpO2, as it reduces the t1/2 of CO in the blood from 5 hours on room air, to 1 hour on 100% FiO2, and alleviates tissue hypoxia. This can be delivered via high flow nasal cannula, nonrebreather mask, or CPAP or BiPAP with a good seal.
    • Consider and treat other conditions including cyanide poisoning, burns, or toxic coingestions.
    • In those with severe poisoning (COHb >25% or with significant neurologic dysfunction), other maneuvers to reduce end-organ oxygen utilization may be helpful, including avoidance of fever or hyperthermia, maintaining adequate cardiac output and ventilation, deep sedation, and transfusion for severe anemia.

    Improve long term outcomes:

    Hyperbaric Oxygen Therapy: HBOT further promotes carbon monoxide elimination, increases ATP production and reduces oxidative stress and inflammation, which may counter some of CO’s end-organ effects. Its role is to reduce long-term neuropsychiatric and cognitive sequelae. It does not decrease mortality or short term survival and is not a resuscitative procedure for the critically ill patient.

    Indications: any one of the following:

    • Evidence of End-organ damage (even with normal COHb level):
      • New neurologic symptoms, including focal neuro signs or altered mental status at any time.
      • Myocardial ischemia, dysrhythmias, syncope, or other cardiac involvement.
    • Persistent symptoms after treatment with high flow O2 for 4 hours.
    • COHb levels (regardless of symptoms) >25%, or >15% for pregnant women or children, at any time.


    • Patient condition: are they fit for the hyperbaric chamber?
      • Is this patient unstable, or do they have significant medical needs that require urgent management? If HBOT is initiated, they will be confined with a single nurse attendant for hours.
      • Will this patient be unable to cooperate? Will they pose a significant risk to themselves, or the healthcare workers with them? Consider especially for patients with an intentional exposure or severe anxiety. The hyperbaric chamber is a confined space that is unsafe to exit quickly and is not immediately accessible by security.
    • Time to chamber:
      • Local practice is to initiate therapy as soon as is feasible, within 24 hours of exposure. There is some evidence to support improved outcomes only in those treated within 6 hours. If transport within 24 hours is not possible, the potential benefit to the patient is minimal.
    • Some ENT disorders including aural barotrauma or sinusitis, or any contraindications to myringotomy, which is performed prophylactically prior to HBOT.
    • Untreated pneumothorax, or bowel obstruction, especially closed loop obstruction – both entrapped air spaces which may worsen upon compression and decompression.
    • Doxorubicin or Bieomycin chemotherapy within the last 3 months, due to risk of exacerbating cardiac or pulmonary toxicity.
    • An undocumented pacemaker, which may be a fire risk.
    • Reduced seizure threshold, including high fever, high dose steroids, or acetazolamide, as hyperoxia can further reduce the seizure threshold.

    Given that most of these indications and contraindications are relative, expert consultation is almost always reasonable. In BC, this is with the Vancouver General Hospital Hyperbaric Unit via the on-call physician, reachable by phone at (604) 875-4033 or pager (604) 875-5000.

    Criteria For Transfer To Another Facility

    • Transfer to another facility is typically indicated to facilitate HBOT, and should happen only after consultation with the Hyperbarics Unit at the destination facility (Vancouver General Hospital).

    Criteria for Observation and/or Hospital Admission:

    • For all symptomatic CO toxicity or those with documented high COHb levels, high flow normobaric O2 should be continued for 6-8 hours, or until the COHb level is within a normal range, i.e. 3% or less and the patient is completely symptom free. To facilitate this, a short stay admission may be indicated, sometimes in a step-down unit of the ED.
    • Pregnant patients should have high flow O2 for a minimum of 24 hours with a fetal assessment, as the elimination t1/2is prolonged in fetal blood, and maternal hypoxemia further exacerbates fetal hypoxia. Fetal mortality exceeds 50% in cases of severe CO poisoning. Consultation is warranted, and admission to hospital or inter-facility transfer may be required per their discretion.
    • Admission to hospital may also be indicated for psychiatric consultation, if the CO Poisoning was a part of a suicide attempt.

    Criteria For Safe Discharge Home

    After the above monitoring and high flow O2, a person with CO Toxicity may be appropriate for discharge if they have:

    • Repeat COHb levels within the normal range (3% or less).
    • No ongoing symptoms or evidence of end-organ damage.
    • No ongoing psychiatric concerns, or have been evaluated and cleared for discharge by a psychiatrist.

    All patients with CO exposure should be counselled on prevention of further exposure, including avoiding operating combustion engines, periodic furnace inspections, and proper ventilation around alternative heating and cooking sources and generators. The US CDC has a printable patient handout with more detailed advice at cdc.gov.

    Patients, and ideally their family or next of kin, should be counselled about the potential for delayed neuropsychiatric symptoms. These happen with a frequency of 12-50%, more in those who have lost consciousness or are older, and usually appear after 2-40 days. Symptoms might include focal deficits, seizures, cognitive apathy, memory deficits, or mood changes. Patients with even mild CO poisoning should be followed up in 1-2 months, as the extent of the deficits and rate of recovery are variable.

    Quality Of Evidence?


    The role of HBOT in the treatment of CO poisoning remains controversial. Physiologic data and some randomized trial data suggest a potential benefit, but a Cochrane review of 6 trials has not supported the use of HBOT for CO poisoning after multiple revisions since 2002. The most rigorous study design is considered to be the Weaver et al 2002 study, which was a positive trial and forms the foundation for the VGH HBU protocol. ACEP guidelines recommend HBOT with Level B evidence only.

    The role of HBOT in treating a pregnant patient or fetus with CO poisoning is not well studied. Pregnant patients have been excluded from all trials of HBOT for this indication.

    There also remains uncertainty about the incidence and nature of long term sequelae after CO poisoning and which prognostic factors might be important, including presentation severity, specific patient factors, or even inflammatory markers. It is also unclear whether anti-inflammatory therapy or the use of other neuroprotective interventions could improve outcomes; these are not yet standard of care.


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