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
May range from "flu-like" symptoms to coma
- CNS
- Headache
- Visual disturbances
- Confusion
- Ataxia
- Seizure
- Syncope
- Retinal hemorrhage
- Focal neurologic deficit
- Coma
- GI
- 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
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
- Viral syndrome
- Depression
- Chronic fatigue syndrome
- Chest pain
- Other headache
- ARDS
- Acute mountain sickness
- Lactic acidosis
- Diabetic ketoacidosis
- Meningitis
- Methemoglobinemia
- Opioid or toxic alcohol poisoning
- Inhalation exposure
Further Considerations
- Dichloromethane methylene chloride toxicity
- Consider when level not decreasing as expected, or is increasing due to prolonged absorption through skin/respiratory tract.
Toxic gas exposure
- Carbon monoxide toxicity
- Chemical weapons
- Cyanide toxicity
- Hydrocarbon toxicity
- Hydrogen sulfide toxicity
- Inhalant abuse
- Methane toxicity
- Smoke inhalation injury
- Ethylene dibromide toxicity
Burns
- Smoke inhalation injury (airway compromise)
- Chemical injury
- Acrolein
- Hydrochloric acid
- Tuolene diisocyanate
- Nitrogen dioxide
- Systemic chemical injury
- Specific types of burns
- Associated toxicities
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
- May range from normal to STEMI (most common ST/T changes, then prolonged QT)
- 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]
- 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]
- Syncope
- Confusion/altered mental status
- Seizure
- Coma
- Focal neuro deficit
- Pregnancy with COhemoglobin level >15%
- Fetal Hb tends to bind more CO
- Blood level >25%
- Acute myocardial ischemia
- Prolonged CO exposure with minor clinical findings (“soaking”)[17]
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
- Ataxia, syncope, chest pain, focal neuro deficit, dyspnea, ECG changes, pregnant with COhemoglobin >15%
- Admit; discuss with hyperbaric specialist
See Also
External Links
ACEP Clinical Policy Statement on Carbon Monoxide Poisoining
References
- ↑ Nikkanen H, Skolnik A. Diagnosis and management of carbon monoxide poisoning in the emergency department. Emerg Med Practice 2011;13(2):1-14.
- ↑ 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.
- ↑ Hoffman RS, Nelson, LS, Goldfrank LR et al. Goldfrank's Toxicologic Emergencies, Eleventh Edition. McGraw-Hill Education / Medical; 2019.
- ↑ 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.
- ↑ Nikkanen H, Skolnik A. Diagnosis and management of carbon monoxide poisoning in the emergency department. Emerg Med Practice 2011;13(2):1-14.
- ↑ 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.
- ↑ 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.
- ↑ Coulange M, et al. Reliability of new pulse CO-oximeter in victims of carbon monoxide poisoning. Undersea Hyperb Med. 2008; 35(2):107-111.
- ↑ 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.
- ↑ 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
- ↑ MetroHealth Medical Center Burn ICU Handbook (Not a policy manual), Cleveland, OH
- ↑ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1116883/pdf/1083.pdf
- ↑ Juurlink, D. N., Isbister, G., Bennett, M. H. and Lavonas, E. J. (1996) ‘Hyperbaric oxygen for carbon monoxide poisoning’, Cochrane Database of Systematic Reviews
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ 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