Carbon monoxide toxicity

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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

References

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

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

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[2]

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

Delayed Neurological Sequela[3]

  • 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
  • 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

Burns

Evaluation

  • 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

Workup

  • VBG (ABGs are no longer considered necessary[4] as venous and arterial COHg levels will be within ±2%[5])
    • 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[6]
  • Lactate
  • Chemistry
  • Troponin
  • Total CK (rhabdomyolysis)
  • bHCG
  • 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[7]

Management

General Mangement

  • 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[8]
      • 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[9][10]
    • Three HBO treatments within 24hrs shown to reduce risk of cognitive sequelae 6 weeks and 12 months after CO poisoning[11]
    • However, another study showed no benefit and suggested worse outcomes in HBO therapy[12]
  • 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): [13]

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

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. 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.
  3. Nikkanen H, Skolnik A. Diagnosis and management of carbon monoxide poisoning in the emergency department. Emerg Med Practice 2011;13(2):1-14.
  4. 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.
  5. 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.
  6. Coulange M, et al. Reliability of new pulse CO-oximeter in victims of carbon monoxide poisoning. Undersea Hyperb Med. 2008; 35(2):107-111.
  7. 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
  8. MetroHealth Medical Center Burn ICU Handbook (Not a policy manual), Cleveland, OH
  9. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1116883/pdf/1083.pdf
  10. Juurlink, D. N., Isbister, G., Bennett, M. H. and Lavonas, E. J. (1996) ‘Hyperbaric oxygen for carbon monoxide poisoning’, Cochrane Database of Systematic Reviews
  11. 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
  12. Scheinkestel C. et al. Med J Aust 1999; 170 (5): 203-210. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial http://www.mja.com.au/journal/1999/170/5/hyperbaric-or-normobaric-oxygen-acute-carbon-monoxide-poisoning-randomised
  13. 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