Carbon Monoxide Poisoning

• Leading cause of poisoning in US
• Common sources: Fuels, radiators, space heaters, grilling any burning carbon containing compound
• The product of incomplete combustion; occurs when there isn’t enough O2
• Methylene Chloride
  • Inhaled/ingested/absorbed through skin → converted to CO in liver
• Clearance
  • Level must be periodically checked to ensure that it is decreasing
  • 1/2-life on RA = 300 mins
  • 1/2-life on 100% O2 = 90 mins
  • 1/2-life on HBO 100% O2 = 30 mins

EFFECTS

• Binding of CO to Hgb → less able to delivery O2 to tissue
• Shifts oxyhgb dissociation curve to left → Hgb less likely to deliver oxygen to tissue
• Interferes with cell respiration by inhibiting oxidative phosphorylation in mitochondria → lipid peroxidation of neurons in frontal cortex and hippocamp → memory problems or mood issues → delayed neurologic sequelae
• Will also displace nitrous oxide from platelets → endothelial change → Plt-neutrophil aggregation at damaged site → O2 free radical production
• Most deleterious effects are from impaired delivery of oxygen to brain and heart
  • Direct effect of dissolved CO being delivered to tissue

• Symptoms
  • Tired, HA, dizziness, nausea, CP, angina, LOC, seizure in severe cases
  • Can be confused with flu like symptoms
  • Must have high suspicion
• Myocardial injury
  • In 1/3 of severe
  • EKG changes and elevated trops
    • May include STE
  • 24% mortality
• DNS (Delayed Neurologic Sequelae)
  • Observed in 40% of significant CO exposures
  • Onset range 3-240 days, typically in first 20 days post-exposure
  • Include dementia, amnesia, ataxia, tremor, paralysis
  • Associated with LOC
• DNPS (Delayed Neuropsychiatric Sequelae)
  • Memory, mood, concentration

• Pulse ox unreliable
  • Reading will be artificially high
  • Pulse ox can only detect oxy and deoxy hemoglobin and is unable to detect COHb
• Pulse co-oximeter readings and COHb levels not well studied
  • Useful only in detecting CO poisoning
• ABG/VBG
  • PO2 will be normal because dissolved O2 not affected in CO poisoning
  • O2 saturation calculated from PO2 and is therefore normal
• Carboxyhemoglobin level
  • Not predictive of DNS
  • PO2 usually normal because it measures O2 dissolved in blood and not Hgb-bound
  • EKG
    • Get trops if EKG changes or h/o CAD
  • NCHCT if AMS
    • May have globus pallidus infarction with acute intoxication
• CN
  • Patient may have concomitant CN poisoning if rescued from fires

• Initial
  • Remove patient from exposure
  • COHb removed only through competitive binding in pulmonary system
  • Start on 100% NRB
  • Intubate as clinically indicated
• HBO
  • Increases dissolved oxygen → ↑ PaO2 (20x)
  • Prevents brain lipid peroxidation (proven only in animal studies)
  • Controversy over its effectiveness in decreasing DNS
  • Indications
    • End-organ damage
      • Acidosis (pH <7.1)
      • Ischemic EKG changes
      • Persistent CP
      • AMS
    • Prolonged exposure (>24 hrs)
    • By COHb
      • Controversial
      • No well-studied limit
      • >25% generally used (assumed peak concentration)
      • >15% in pregnant women, children
  • Should be started within 6 hours
  • No proven benefit if started after 12 hours post-exposure

• Mild symptoms may be discharged
  • Observe for 4h
• Admit:
  • Persistent symptoms
  • EKG changes
  • Acidosis

REFERENCES

Clardy, Peter. “Carbon Monoxide Poisoning.” Up To Date. www.uptodate.com, 18 Aug. 2015. Web. 10 Dec. 2015. http://www.uptodate.com/contents/carbon-monoxide-poisoning

Takematsu, Mai. “Carbon Monoxide Poisoning.” 11 Nov. 2015. Presentation given at Jacobi Medical Center, Emergency Medicine Conference.

Tintinalli, Judith E., and J. Stephan. Stapczynski. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York: McGraw-Hill, 2011.

Weaver LK. Clinical practice. Carbon monoxide poisoning. N Engl J Med 2009;360:1217-25.