EM@3AM – Carbon Monoxide Toxicity

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 49-year-old male with no PMHx presents to the emergency department for two days of headache, nausea without emesis, and fatigue. The patient reports his headache as gradual in onset, without associated vertigo, disequilibrium, slurred speech, visual deficits, or motor/sensory alterations. The male notes: “My whole house is sick…when we were huddled near the space heater to keep warm, the kids and I noticed that even the cat was puking.” Review of systems is otherwise negative.

Initial VS: BP 137/88, HR 81, T 98.9F Oral, RR 14, SpO2 98% on room air.

What’s the next step in your evaluation and treatment?

Answer: Carbon Monoxide Toxicity^1,2

• Epidemiology: In adults, 20% of cases occur in the occupational setting.¹ Toxicity is most frequently seen during the fall and winter months in cold climates => inhaling smoke from fires or utilizing gasoline-powered portable generators, space heaters, or stoves in poorly-ventilated areas.
• Presentation: Varies according to the severity and duration of exposure:
  • Mild to moderate exposure: headache, myalgias, nausea, dyspnea, difficulty concentrating, blurred vision.^1,2
  • Severe exposure: hypotension, arrhythmias, cardiac ischemia, pulmonary edema, ataxia, LOC, seizure, coma.^1,2
• Evaluation and Treatment:
  • Perform a thorough H&P:
    • Question the patient regarding the use of wood-burning stoves and space heaters, and the occurrence of similar symptoms in persons residing in a shared living environment.
    • Look for: VS abnormalities (tachycardia, tachypnea, hypotension), neurologic findings (Parkinsonian movement disorder, cognitive deficits, behavioral abnormalities (acute psychosis)²), pulmonary crackles or rhonchi (pulmonary edema).
      • Note: When assessing VS => Pulse oximetry is frequently within normal limits, offering an inaccurate representation of oxygen saturation:
    • Evaluation:
      • EKG => evaluate for arrhythmias and evidence of myocardial injury.
      • Labs
        • CoHb level (measured by CO-oximetry) => level > 3% in non-smokers or >10% in smokers indicates toxic exposure.^1,2
        • Troponin => myocardial injury.
        • CMP, CK, and lactate => CO poisoning may result in lactic acidosis and rhabdomyolysis.
        • CBC if concern for chronic exposure => polycythemia secondary to chronic hypoxia.
        • Hcg in females of child-bearing age => directs therapy.
      • Imaging:
        • CXR if concern for non-cardiogenic pulmonary edema.
        • Consider CT/MRI if neurologic findings (damage to the globus pallidus or deep white matter).^1,2
    •  Treatment:
      • Remove from site of exposure, ensure airway is intact, initiate continuous EKG monitoring, and begin oxygen therapy (in addition: all pregnant females require tocodynamometry):
        • Room air (21% FiO2) => CO half-life = 4-5 hours.
        • Mask or ETT (100% FiO2) => CO half-life = 60-90 minutes.
        • Hyperbaric oxygen therapy (100% FiO2) => CO half-life = 20-30 mins.
          • No consensus guidelines regarding indications. Consider for:
            • COHb > 25%, LOC, neurological signs/symptoms, cardiovascular compromise, severe metabolic acidosis.
            • Pregnant females with COHb > 20% or signs of fetal distress.
• Disposition:
  • Mild accidental poisoning with unremarkable exam, EKG, and laboratory studies => treat in ED and DC to home.
  • Moderate/severe poisoning or medical co-morbidities => admit.^1,2

• Pearls:
  • An ABG is not helpful in ruling out CO toxicity => utilizes measurements of oxygen dissolved in plasma (not affected by CO) to calculate the oxygen saturation of hemoglobin.^1,2
  • Question patients regarding occupation: painters may present with carbon monoxide toxicity => paint stripper (methylene chloride) is converted to CO through hepatic metabolism.
  • 4-14% of survivors of severe CO toxicity exhibit long-term neurologic sequelae.¹

References:

1. Aulakh S. Carbon Monoxide Poisoning. In Ferri’s Clinical Advisor 2017. Philadelphia, Saunders. 2017; 227-228.e1.
2. Nelson L, Hoffman R. Inhaled Toxins. In Rosen’s Emergency Medicine. Philadelphia, Saunders. 2014; 159:2036-2043.e1.

 For Additional Reading:

Carbon Monoxide Poisoning:

http://www.emdocs.net/carbon-monoxide-poisoning/

CO Toxicity: A Potentially Elusive Diagnosis:

CO Toxicity: A Potentially Elusive Diagnosis