Carbon monoxide toxicity

Background

  • Colorless, odorless gas
  • Most toxic component in smoke inhalation and major contributor to fire-related deaths
    • Can co-occur with Cyanide toxicity in industrial fires
  • Case fatality rate as high as 30%[1]
  • Peak incidence in winter months for unintentional exposure

Sources

Formed from incomplete combustion of hydrocarbons

  • Automotive exhaust
  • Propane-fueled heaters
  • Wood or coal-burning heaters
  • Structure fires
  • Gasoline-powered motors
  • Natural gas-powered heaters
  • Waterpipe/Hookah [2]
  • Methylene chloride (a degreasing solvent found in most paint strippers) fume inhalation
    • Metabolized by the liver into carbon monoxide resulting in delayed toxicity (8 hours or longer)[3]

Pathophysiology

  • Hypoxia
    • Binding affinity of hemoglobin for CO (carboxyhemoglobin) is 200x that of O2
    • Half-Life
      • Room air: ~5hrs
      • 100% O2: ~1hr
      • HBO 2.5atm: 24min
  • Lactic acidosis
    • CO inhibits oxidative phosphorylation
  • Hypotension
    • CO induces NO2 and guanylate cyclase release → vasodilation release
    • CO binds to myoglobin and alters its function
  • CO damage at cellular level due to reactive oxygen species, lipid peroxidation, and cellular apoptosis
    • Occurs in CNS and leads to neurological sequela

Clinical Features

Clinical features of CO toxicity

May range from "flu-like" symptoms to coma

Expected CNS Function by COhemoglobin%

COhemoglobin Presentation
10-20% Confusion and agitation secondary to mild hypoxia
20-30% Progressive obtundation and nausea
>40% Almost always unconscious
>60% Survival is very rare

Symptoms By Frequency[4]

Symptom %
Headache 85
Dizzy 69
Fatigue 67
Nausea or Vomiting 52
Confusion 37
LOC 35
Dyspnea 7

Delayed Neurological Sequela[5]

  • Can occur days to weeks after apparent resolution of acute symptoms in up to 46% of patients. The globus pallidus is the most commonly affected area.
  • Persistent, disabling, or permanent
  • Cognitive sequelae lasting one month or more appear to occur in 25-50 percent of patients with loss of consciousness or CO levels > 25%.
  • Includes:
    • Cognitive effects
    • Motor disturbances
    • Ataxia
    • Neuropathies
    • Psychosis
    • Dementia

Differential Diagnosis

A "great mimicker" due to the presentation of poisoning being diverse and nonspecific

Further Considerations

Toxic gas exposure

Burns

Household, Environmental, and Occupational Toxins

Evaluation

Workup

  • VBG (ABGs are no longer considered necessary[6] as venous and arterial COHg levels will be within ±2%[7])
    • CO-oximetry analysis will provide carboxyhemoglobin level
    • pH will be low secondary to metabolic acidosis caused by anaerobic metabolism and elevated lactate levels
  • Pulse CO-oximetry
    • Special pulse CO-ox can accurately determine CO level[8]
  • Lactate (usually not significantly elevated, and if so should raise concern for cyanide toxicity) [9]
  • Chemistry
  • Troponin
  • Total CK (rhabdomyolysis)
  • Beta-HCG
  • ECG
    • May range from normal to STEMI (most common ST/T changes, then prolonged QT)
      • Few of the patients with AMI from CO have occlusive lesions in their arteries
  • Head CT
    • Identified radiographically within 12 hours of exposure
    • Bilateral hypodense lesions in the basal ganglia: globus pallidus, putamen, and caudate nuclei[10]

Diagnosis

  • Must have high clinical suspicion (esp in coma, altered mental status, or anion gap acidosis)
    • Comatose patients removed from fire should be assumed to have CO poisoning
  • Carboxyhemoglobin Level
    • Interpretation must take into account time since exposure and O2 treatment
    • Normal value in non-smokers is ~1%, normal value in smokers may be up to 10%
    • Symptoms and COhemoglobin levels do not always correlate well
  • Pulse oximetry is unreliable
    • COhemoglobin registers the same as O2hemoglobin so will have artificially high SpO2
    • O2 saturation gap reflects discordance of SpO2 by pulse oximeter vs by VBG

Management

General Management

  • If smoke inhalation, good pulmonary toilet is very important
  • NEVER use steroids in smoke inhalation injury; intubate early if concern for obstructing edema
  • O2 100% by NRB or ETT
    • Provide O2 until COhemoglobin value <10%
    • Early PEEP prevents progressive atelectasis and improves O2 diffusion
    • In general, COhemoglobin levels fall rapidly to < 10% within 30 min of 100% O2
    • Maintain 100% O2 for additional 2-3 hrs after < 10%, since anaerobic COmetabolism is occuring due to cytochrome oxidase poisoning[11]
      • Anaerobic metabolism universally seen with COhemoglobin > 40%
      • Monitor for return of aerobic metabolism with normal serum bicarbonate levels
  • Consider other combustion products such as Cyanide

Hyperbaric Therapy (HBO)

  • Decision to initiate HBO should be made in consultation with a hyperbaric specialist
  • There is controversy regarding benefit[12][13]
    • Three HBO treatments within 24hrs shown to reduce risk of cognitive sequelae 6 weeks and 12 months after CO poisoning[14]
    • However, another study showed no benefit and suggested worse outcomes in HBO therapy[15]
  • Patient must be stable prior to transport since response to acute medical conditions while undergoing hyperbaric therapy in a chamber is difficult.
  • Indications (generally accepted guidelines): [16]

Disposition

Minimal or no symptoms

  • Discharge
    • If discharging patient, may need to alert local fire/police services to evaluate home/work before they return. Check with your local branch.
    • Patient's should not be discharged to an environment where they will become toxic again

Mildly symptomatic

  • Headache, vomiting, elevated COhemoglobin level
  • Discharge after 4hr obs and symptom resolution and assurance that the discharge environment is safe

Severely symptomatic

See Also

External Links

References

  1. ↑ Nikkanen H, Skolnik A. Diagnosis and management of carbon monoxide poisoning in the emergency department. Emerg Med Practice 2011;13(2):1-14.
  2. ↑ Eichhorn, L., Michaelis, D., Kemmerer, M., Jüttner, B., & Tetzlaff, K. (2018). Carbon monoxide poisoning from waterpipe smoking: a retrospective cohort study. Clinical Toxicology , 56(4), 264–272.
  3. ↑ Hoffman RS, Nelson, LS, Goldfrank LR et al. Goldfrank's Toxicologic Emergencies, Eleventh Edition. McGraw-Hill Education / Medical; 2019.
  4. ↑ Lavonas EJ. Carbon monoxide poisoning. In: Shannon M, Borron S, Burns M, eds. Haddad and Winchester’s Clinical Management of Poisoning and Drug Overdose. Philadelphia, Pa: Elsevier; 2007:1297-1307.
  5. ↑ Nikkanen H, Skolnik A. Diagnosis and management of carbon monoxide poisoning in the emergency department. Emerg Med Practice 2011;13(2):1-14.
  6. ↑ Lopez DM, et al. Relationship between arterial, mixed venous, and internal jugular carboxyhemoglobin concentrations at low, medium, and high concentrations in a piglet model of carbon monoxide toxicity. Crit Care Med. 2000; 28(6):1998-2001.
  7. ↑ Touger M. et al. Relationship between venous and arterial carboxyhemoglobin levels in patients with suspected carbon monoxide poisoning. Ann Emerg Med 1995;33:105-109.
  8. ↑ Coulange M, et al. Reliability of new pulse CO-oximeter in victims of carbon monoxide poisoning. Undersea Hyperb Med. 2008; 35(2):107-111.
  9. ↑ Wardi G, Brice J, Correia M, Liu D, Self M, Tainter C. Demystifying Lactate in the Emergency Department. Ann Emerg Med. 2020 Feb;75(2):287-298. doi: 10.1016/j.annemergmed.2019.06.027. Epub 2019 Aug 29. Erratum in: Ann Emerg Med. 2020 Apr;75(4):557. PMID: 31474479.
  10. ↑ Lee, DC: Hydrocarbons, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 7. St. Louis, Mosby, Inc., 2010, (Ch) 156:p 2035-2038
  11. ↑ MetroHealth Medical Center Burn ICU Handbook (Not a policy manual), Cleveland, OH
  12. ↑ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1116883/pdf/1083.pdf
  13. ↑ Juurlink, D. N., Isbister, G., Bennett, M. H. and Lavonas, E. J. (1996) ‘Hyperbaric oxygen for carbon monoxide poisoning’, Cochrane Database of Systematic Reviews
  14. ↑ Weaver, L. et al. Hyperbaric Oxygen For Acute Carbon Monoxide Poisoning. NEJM. 2002:347(14):1057 http://emed.wustl.edu/Portals/2/Answer%20Key%20PDF/2012/January2012/SecondYear.pdf
  15. ↑ Scheinkestel C. et al. Med J Aust 1999; 170 (5): 203-210. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomized controlled clinical trial http://www.mja.com.au/journal/1999/170/5/hyperbaric-or-normobaric-oxygen-acute-carbon-monoxide-poisoning-randomised
  16. ↑ Practice Recommendations in the Diagnosis, Management and Prevention of Carbon Monoxide Poisoning. Hampson NB et al. Am J Respir Crit Care Med 2012 Oct 18
  17. ↑ Marx, John A., and Peter Rosen. Rosen's Emergency Medicine - Concepts and Clinical Practice E-Book: Edition 9. Philadelphia, PA: Elsevier/Saunders, 2017. Pg 2387
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