Carbon monoxide toxicity: Difference between revisions

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==Background==
==Background==
*Colorless, odorless gas
*Colorless, odorless gas  
*Effects:
*Most toxic component in [[smoke inhalation]] and major contributor to fire-related deaths
**Hypoxia
**Can co-occur with [[Cyanide]] toxicity in industrial fires
***Binding affinity of Hb for CO (carboxyhemoglobin) is 200x that of O2
*Case fatality rate as high as 30%<ref>Nikkanen H, Skolnik A. Diagnosis and management of carbon monoxide poisoning in the emergency department. Emerg Med Practice 2011;13(2):1-14.</ref>
**Lactic acidosis
*Peak incidence in winter months for unintentional exposure
***CO inhibits oxidative phosphorylation
**Hypotension
***CO induces NO2 and guanylate cyclase release --> vasodilation release
*Half-Life
**Room air: ~5hrs
**100% O2: ~1hr
**HBO 2.5atm: 24min


===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 <ref>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.</ref>
*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)<ref>Hoffman RS, Nelson, LS, Goldfrank LR et al. Goldfrank's Toxicologic Emergencies, Eleventh Edition. McGraw-Hill Education / Medical; 2019.</ref>


*Most toxic component in smoke inhalation and major contributor to fire-related deaths
===Pathophysiology===
*Can co-occur with cyanide toxicity in industrial fires
*[[Hypoxia]]
**See [[Cyanide]]
**Binding affinity of hemoglobin for CO (carboxyhemoglobin) is 200x that of O2
*Sources
**Half-Life
**Automotive exhaust
***Room air: ~5hrs
**Propane-fueled heaters
***100% O2: ~1hr
**Wood or coal-burning heaters
***HBO 2.5atm: 24min
**Structure fires
*[[Lactic acidosis]]
**Gasoline-powered motors
**CO inhibits oxidative phosphorylation
**Natural gas-powered heaters
*[[Hypotension]]
*Peak incidence in winter months
**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==
[[File:CO toxicity symptoms (en).jpg|thumb|Clinical features of CO toxicity]]
''May range from "flu-like" symptoms to coma''
*CNS
**[[Headache]]
**Visual disturbances
**Confusion
**[[Ataxia]]
**[[Seizure]]
**[[Syncope]]
**[[Retinal hemorrhage]]
**Focal neurologic deficit
**Coma
*GI
**[[Vomiting]]
*Pulm
**Dyspnea/tachypnea
*Cardio
**[[Chest pain]]
**[[ECG]] changes/[[dysrhythmias]]
*Derm
**[[Bullous skin lesions]]
**Classic finding of cherry red oral mucosa is rarely seen in living patients
***More likely seen in > 25% COhemoglobin levels


The combination of relative hypoxia and hypotension can cause ischemia-reperfusion injury in cardiac myocytes, as well as neuronal tissue. The damaged endothelium will attract neutrophils and trigger an inflammatory cascade resulting in lipid peroxidation and, ultimately, neuronal cell death. This complex intracellular process explains many of the clinical effects of carbon monoxide.8 Rhabdomyolysis, acute myocardial infarction, and neuronal cell death are a result of this cellular toxicity. Cells in the basal ganglia are particularly sensitive to this neurotoxic effect, demonstrated by the globus pallidus lesions sometimes seen on cranial CT imaging.
===Expected CNS Function by COhemoglobin%===
{| {{table}}
| align="center" style="background:#f0f0f0;"|'''COhemoglobin'''
| align="center" style="background:#f0f0f0;"|'''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<ref>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.</ref>===
{| class="wikitable"
|-
! Symptom !! %
|-
| [[Headache]] || 85
|-
| [[Dizzy]] || 69
|-
| Fatigue || 67
|-
| [[Nausea]] or [[Vomiting]] || 52
|-
| Confusion || 37
|-
| LOC || 35
|-
| [[Dyspnea]] || 7
|}


===Delayed Neurological Sequela<ref>Nikkanen H, Skolnik A. Diagnosis and management of carbon monoxide poisoning in the emergency department. Emerg Med Practice 2011;13(2):1-14.</ref>===
*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


==Workup==
==Differential Diagnosis==
#VBG
''A "great mimicker" due to the presentation of poisoning being diverse and nonspecific''
##Co-oximetry analysis will provide carboxyhemoglobin level
*[[Viral syndrome]]
#Lactate
*[[Depression]]
#Chemistry
*Chronic fatigue syndrome
#Troponin
*[[Chest pain]]
#Total CK
*Other [[headache]]
#ECG
*[[ARDS]]
##May range from normal to STEMI
*[[Acute mountain sickness]]
###Few of the pts w/ AMI from CO have occlusive lesions in their arteries
*[[Lactic acidosis]]
#?Head CT
*[[Diabetic ketoacidosis]]
##May show b/l globus pallidus lesions in severe cases
*[[Meningitis]]
*[[Methemoglobinemia]]
*[[Opioid toxicity|Opioid]] or [[Ethanol toxicity|toxic alcohol poisoning]]
*[[Inhalation exposure]]


==Clinical Features==
===Further Considerations===
#May range from "flu-like" symptoms to coma
*[[Dichloromethane methylene chloride toxicity]]
#CNS
**Consider when level not decreasing as expected, or is increasing due to prolonged absorption through skin/respiratory tract.
##Headache
 
##Visual disturbances
{{Toxic gas exposure DDX}}
##Confusion
{{Burn DDX}}
##Ataxia
 
##Seizure
==Evaluation==
##Syncope
===Workup===
##Retinal hemorrhage
*[[VBG]] (ABGs are no longer considered necessary<ref>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.</ref> as venous and arterial COHg levels will be within ±2%<ref>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.</ref>)
##Focal neurologic deficit
**CO-oximetry analysis will provide carboxyhemoglobin level
#GI
**pH will be low secondary to metabolic acidosis caused by anaerobic metabolism and elevated lactate levels
##Vomiting
*Pulse CO-oximetry
#Pulm
**Special pulse CO-ox can accurately determine CO level<ref>Coulange M, et al. Reliability of new pulse CO-oximeter in victims of carbon monoxide poisoning. Undersea Hyperb Med. 2008; 35(2):107-111. </ref>
##Dyspnea/tachypnea
*Lactate (usually not significantly elevated, and if so should raise concern for cyanide toxicity) <ref> 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. </ref>
#Cardio
*Chemistry
##Chest pain
*[[Troponin]]
##ECG changes/dysrhythmias
*Total CK ([[rhabdomyolysis]])
#Derm
*[[Beta-HCG]]
##Bullous skin lesions
*[[ECG]]
##Classic finding of cherry red oral mucosa is rarely seen in living pts
**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<ref>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</ref>
 
===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


==Diagnosis==
==Management==
#Must have high clinical suspicion (esp in pts w/ coma, AMS, or anion gap acidosis)
===General Management===
##Comatose pt removed from fire should be assumed to have CO poisoning
*If smoke inhalation, good pulmonary toilet is very important
#Carboxyhemoglobin Level
*'''NEVER''' use steroids in smoke inhalation injury; intubate early if concern for obstructing edema
##Interpretation must take into account time since exposure and O2 tx
*O2 100% by NRB or ETT
##Normal value in non-smokers is ~1%, normal value in smokers may be up to 10%
**Provide O2 until COhemoglobin value <10%
##Symptoms and COHb levels do not always correlate well
**Early PEEP prevents progressive atelectasis and improves O2 diffusion
#Pulse oximetry is unreliable
**In general, COhemoglobin levels fall rapidly to < 10% within 30 min of 100% O2
##CoHb registers the same as O2Hb so will have artificially high SpO2
**Maintain 100% O2 for additional 2-3 hrs after < 10%, since anaerobic COmetabolism is occuring due to cytochrome oxidase poisoning<ref>MetroHealth Medical Center Burn ICU Handbook (Not a policy manual), Cleveland, OH</ref>
##O2 saturation gap reflects discordance of SpO2 by pulse oximeter vs by VBG
***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]]


==Treatment==
===[[Hyperbaric medicine|Hyperbaric Therapy (HBO)]]===
#O2 100% by NRB or ETT
*Decision to initiate HBO should be made in consultation with a hyperbaric specialist  
##Provide O2 until COHb value <10%
*There is controversy regarding benefit<ref>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1116883/pdf/1083.pdf</ref><ref>Juurlink, D. N., Isbister, G., Bennett, M. H. and Lavonas, E. J. (1996) ‘Hyperbaric oxygen for carbon monoxide poisoning’, Cochrane Database of Systematic Reviews</ref>
#Hyperbaric Therapy (HBO)
**Three HBO treatments within 24hrs shown to reduce risk of cognitive sequelae 6 weeks and 12 months after CO poisoning<ref>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</ref>
##Decision to initiate HBO should be made in consultation w/ hyperbaric specialist
**However, another study showed no benefit and suggested worse outcomes in HBO therapy<ref> 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</ref>
##Controversial who exactly benefits from tx
*Patient must be stable prior to transport since response to acute medical conditions while undergoing hyperbaric therapy in a chamber is difficult.
##Pt must be stable prior to transport
*'''Indications (generally accepted guidelines):''' <ref>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</ref>
##Indications (generally accepted guidelines):
**[[Syncope]]
###Syncope
**Confusion/[[altered mental status]]
###Confusion/AMS
**[[Seizure]]
###Seizure
**[[Coma]]
###Coma
**[[Focal neuro deficit]]
###Focal neuro deficit
**[[Pregnancy]] with COhemoglobin level >15%  
###Pregnancy w/ CoHb level >15%
***Fetal Hb tends to bind more CO
###Blood level >25%
**Blood level >25%  
###Acute myocardial ischemia
**[[Acute myocardial ischemia]]
**Prolonged CO exposure with minor clinical findings (“soaking”)<ref>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</ref>


==Disposition==
==Disposition==
#Minimal or no symptoms
===Minimal or no symptoms===
##Discharge
*Discharge
#Mildly symptomatic
**If discharging patient, may need to alert local fire/police services to evaluate home/work before they return. Check with your local branch.
##Headache, vomiting, elevated COHb level
**Patient's should not be discharged to an environment where they will become toxic again
##Discharge after 4hr obs and symptom resolution
 
#Severely symptomatic
===Mildly symptomatic===
##Ataxia, syncope, chest pain, neuro deficit, dyspnea, ECG changes, pregnant w/ COHb >15%
*[[Headache]], [[vomiting]], elevated COhemoglobin level  
##Admit; discuss with hyperbaric specialist
*Discharge after 4hr obs and symptom resolution and assurance that the discharge environment is safe
 
===Severely symptomatic===
*[[Ataxia]], [[syncope]], [[chest pain]], [[focal neuro deficit]], [[dyspnea]], [[ECG]] changes, pregnant with COhemoglobin >15%  
*Admit; discuss with hyperbaric specialist
 
==See Also==
*[[Toxidromes]]
*[[Burns]]
*[[Cyanide]]
*[[Methemoglobinemia]]
 
==External Links==
[https://www.acep.org/patient-care/clinical-policies/carbon-monoxide-poisoning/ ACEP Clinical Policy Statement on Carbon Monoxide Poisoining]


==Source==
==References==
Tintinalli
<references/>


[[Category:Tox]]
[[Category:Toxicology]]

Latest revision as of 16:59, 22 December 2023

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

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

ACEP Clinical Policy Statement on Carbon Monoxide Poisoining

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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