Carbon monoxide toxicity: Difference between revisions

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== Disposition ==
== Disposition ==
*Minimal or no symptoms  
*Minimal or no symptoms  
**Discharge  
**Discharge^
*Mildly symptomatic  
*Mildly symptomatic  
**Headache, vomiting, elevated COHb level  
**Headache, vomiting, elevated COHb level  
**Discharge after 4hr obs and symptom resolution  
**Discharge after 4hr obs and symptom resolution^
*Severely symptomatic  
*Severely symptomatic  
**Ataxia, syncope, chest pain, neuro deficit, dyspnea, ECG changes, pregnant w/ COHb >15%  
**Ataxia, syncope, chest pain, neuro deficit, dyspnea, ECG changes, pregnant w/ COHb >15%  
**Admit; discuss with hyperbaric specialist
**Admit; discuss with hyperbaric specialist


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


== Source ==
== Source ==

Revision as of 21:27, 11 January 2015

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
  • Peak incidence in winter months

Sources

  • 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

Workup

  • VBG
    • Co-oximetry analysis will provide carboxyhemoglobin level
  • Lactate
  • Chemistry
  • Troponin
  • Total CK (rhabdo)
  • ECG
    • May range from normal to STEMI (most common ST, then prolonged QT)
      • Few of the pts w/ AMI from CO have occlusive lesions in their arteries
  • ?Head CT
    • May show b/l globus pallidus lesions in severe cases

Clinical Features

  • May range from "flu-like" symptoms to coma
  • CNS
  • CNS as a function of 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
  • 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 pts
      • More likely seen in > 25% COHb levels

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

Treatment

  • 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 metabolism is occuring due to cytochrome oxidase poisoning[1]
      • Anaerobic metabolism universally seen with COHb > 40%
      • Monitor for return of aerobic metabolism with normal serum bicarbonate levels

Hyperbaric Therapy (HBO)

  • Decision to initiate HBO should be made in consultation w/ hyperbaric specialist
  • Controversial Outcomes regarding benefit[2]
    • Three HBO treatments within 24hrs reduced risk of cognitive sequelae 6 weeks and 12 months after CO poisoning[3]
    • While an Australian study showed not benefit and suggested worse outcomes in HBO therapy[4]
  • 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):
    • Syncope
    • Confusion/AMS
    • Seizure
    • Coma
    • Focal neuro deficit
    • Pregnancy w/ CoHb level >15%
    • Blood level >25%
    • Acute myocardial ischemia

Disposition

  • Minimal or no symptoms
    • Discharge^
  • Mildly symptomatic
    • Headache, vomiting, elevated COHb level
    • Discharge after 4hr obs and symptom resolution^
  • Severely symptomatic
    • Ataxia, syncope, chest pain, neuro deficit, dyspnea, ECG changes, pregnant w/ COHb >15%
    • Admit; discuss with hyperbaric specialist

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

Source

  1. ↑ MetroHealth Medical Center Burn ICU Handbook (Not a policy manual), Cleveland, OH
  2. ↑ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1116883/pdf/1083.pdf
  3. ↑ 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
  4. ↑ 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
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