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

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

Pathophysiology

  • Hypoxia
    • Binding affinity of Hb 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 per oxidation, and cellular apoptosis
    • Occurs in CNS and leads to neurological sequela

Clinical Features

Clinical features of CO toxicity

Expected CNS Function by COHb%

  • 10-20% - confusion and agitation 2/2 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

Diagnosis

  • Must have high clinical suspicion (esp in pts w/ coma, AMS, or anion gap acidosis)
    • Comatose pt removed from fire should be assumed to have CO poisoning
  • Carboxyhemoglobin Level
    • Interpretation must take into account time since exposure and O2 tx
    • Normal value in non-smokers is ~1%, normal value in smokers may be up to 10%
    • Symptoms and COHb levels do not always correlate well
  • Pulse oximetry is unreliable
    • CoHb registers the same as O2Hb 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 (rhabdo)
  • hCG
  • ECG
    • May range from normal to STEMI (most common ST/T changes, then prolonged QT)
      • Few of the pts w/ 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

  • 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 COHb value <10%
    • Early PEEP prevents progressive atelectasis and improves O2 diffusion
    • In general, COHb 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 COHb > 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 w/ hyperbaric specialist
  • Controversial outcomes regarding benefit[9]
    • Three HBO treatments within 24hrs reduced risk of cognitive sequelae 6 weeks and 12 months after CO poisoning[10]
    • While an Australian study showed not benefit and suggested worse outcomes in HBO therapy[11]
  • Pt 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): [12]

Disposition

†If discharging patient- may need to alert local fire/police services to evaluate home/work before they return. Check with your local branch.

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. ↑ 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
  11. ↑ 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
  12. ↑ 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
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