• Clinical science
  • Clinician

Carbon monoxide toxicity

Summary

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

  • House fires, wood-burning stoves/gas heaters, motor vehicle exhaust, furnaces in enclosed and poorly ventilated spaces, extensive water pipe smoking [1]
  • 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

Clinical features

The correlation between feature severity and COHb level is poor. [2][3][4][5][6]

Clinical features do not correlate well with the COHb level. [3][4][5]

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

Diagnostics

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. [2]

  • 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

Additional studies

Screen for affected organs and toxic coingestions.

Management

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. [6][5][8][3]

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][2]

  • The benefits of hyperbaric oxygen have not been conclusively demonstrated.
  • The following are considered relative indications:

Management of systemic involvement and supportive care [3]

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. [2]

Monitoring and level of care [8][2]

Acute management checklist

Chronic carbon monoxide poisoning

Pathophysiology [2]

Clinical features [6][12]

Symptoms are often non-specific.

Diagnostics [6][12]

  • 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 [6][12]

  • 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

  • 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.
  • 1. von Rappard J, Schönenberger M, Bärlocher L. Carbon monoxide poisoning following use of a water pipe/hookah. Dtsch Arztebl Int. 2014; 111(40): pp. 674–679. doi: 10.3238/arztebl.2014.0674.
  • 2. Rose JJ, Wang L, Xu Q, et al. Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy. Am J Respir Crit Care Med. 2017; 195(5): pp. 596–606. doi: 10.1164/rccm.201606-1275ci.
  • 3. Hampson NB, Piantadosi CA, Thom SR, Weaver LK. Practice Recommendations in the Diagnosis, Management, and Prevention of Carbon Monoxide Poisoning. Am J Respir Crit Care Med. 2012; 186(11): pp. 1095–1101. doi: 10.1164/rccm.201207-1284ci.
  • 4. Hampson NB. Myth busting in carbon monoxide poisoning. Am J Emerg Med. 2016; 34(2): pp. 295–297. doi: 10.1016/j.ajem.2015.10.051.
  • 5. Prockop LD, Chichkova RI. Carbon monoxide intoxication: An updated review. J Neurol Sci. 2007; 262(1-2): pp. 122–130. doi: 10.1016/j.jns.2007.06.037.
  • 6. Weaver LK. Carbon Monoxide Poisoning. N Engl J Med. 2009; 360(12): pp. 1217–1225. doi: 10.1056/nejmcp0808891.
  • 7. Fazekas AS, Wewalka M, Zauner C, Funk G-C. Carboxyhemoglobin levels in medical intensive care patients: a retrospective, observational study. Critical Care. 2012; 16(1): p. R6. doi: 10.1186/cc11138.
  • 8. ISBI Practice Guidelines Committee, Ahuja RB, Gibran N, et al. ISBI Practice Guidelines for Burn Care. Burns. 2016; 42(5): pp. 953–1021. doi: 10.1016/j.burns.2016.05.013.
  • 9. Vanden Hoek TL, Morrison LJ, Shuster M, et al. Part 12: Cardiac Arrest in Special Situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010; 122(18_suppl_3): pp. S829–S861. doi: 10.1161/circulationaha.110.971069.
  • 10. Lawson-Smith P, Jansen EC, Hyldegaard O. Cyanide intoxication as part of smoke inhalation - a review on diagnosis and treatment from the emergency perspective. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine. 2011; 19(1): p. 14. doi: 10.1186/1757-7241-19-14.
  • 11. Hampson NB, Courtney TG, Holm JR. Diffusion of Carbon Monoxide Through Gypsum Wallboard. JAMA. 2013; 310(7): p. 745. doi: 10.1001/jama.2013.43127.
  • 12. Knobeloch L, Jackson R. Recognition of chronic carbon monoxide poisoning. WMJ. ; 98(6): pp. 26–9. pmid: 10605352.
last updated 06/30/2020
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