Carbon Monoxide Poisoning

Carbon monoxide (CO) is an odorless, colorless, tasteless, nonirritating gas formed by hydrocarbon combustion (e.g., fires, car exhaust, gas heaters). Carbon monoxide has a higher affinity to hemoglobin than oxygen, forming carboxyhemoglobin (COHb). Increased levels of COHb lead to tissue hypoxia and brain damage. Symptoms of CO poisoning include headache, nausea, weakness, chest pain, shortness of breath, seizures, coma, and even death. Oxygen therapy is key to the management of CO poisoning.

Last update:

Table of Contents

Share this concept:

Share on facebook
Share on twitter
Share on linkedin
Share on reddit
Share on email
Share on whatsapp

Etiology

  • Fire-related smoke inhalation:
    • Most common cause of carbon monoxide (CO) poisoning
    • CO poisoning is the most common cause of fire-related death in the United States.
  • Other sources of CO include the following, especially in poorly ventilated areas:
    • Gas-powered generators within homes
    • Clogged vents from home heating
    • Wood-burning stoves
    • Motor vehicle exhaust (may be associated with a suicide attempt)
    • Extensive water pipe or hookah smoking
  • Most common in the winter months due to increased use of heating devices
  • Multiple members of the household are usually affected and may present with similar symptoms.

Pathophysiology

  • CO has an affinity for hemoglobin that is approximately 240 times greater than oxygen, causing a displacement of oxygen from hemoglobin in the lungs
  • CO binds to hemoglobin, forming carboxyhemoglobin (COHb) and causing a configurational change in the hemoglobin that prevents oxygen from being released in the peripheral tissues.
  • Causes a leftward shift in the oxygen-hemoglobin curve
  • Inhibits oxidative phosphorylation at the mitochondrial level, leading to anaerobic respiration and cell death
  • CO also binds to cardiac myoglobin, leading to myocardial depression, hypotension, and arrhythmias.
  • CO induces re-oxygenation injury and the formation of oxygen free radicals in the nervous system.

Clinical Presentation

The symptoms of CO poisoning are varied and nonspecific.

The severity of the clinical presentation of CO poisoning depends on the amount of CO in the inhaled air, the duration of the exposure, and the general state of health of the affected individual.

Mildly to moderately intoxicated individuals

  • Headache (the most common presenting symptom)
  • Malaise
  • Nausea/vomiting
  • Dizziness
  • Impaired judgment and difficulty concentrating
  • Confusion
  • Shortness of breath

Severely intoxicated individuals

  • Neurologic symptoms:
    • Seizures
    • Syncope
    • Altered mental status
    • Loss of consciousness and/or coma
  • Cardiovascular symptoms:
    • Chest pain and shortness of breath (due to myocardial infarction)
    • Palpitations and arrhythmias
    • Hypotension
  • Respiratory symptoms:
    • Shortness of breath
    • Pulmonary edema
    • Respiratory failure
    • Concomitant airway injuries due to smoke inhalation (in cases of house fires)
  • Delayed neuropsychiatric syndrome: presents in 30% of patients, usually within the first 30 days but sometimes up to 240 days after exposure
    • Dementia
    • Personality changes
    • Cognitive and learning difficulties
    • Psychosis
    • Movement disorders (e.g., parkinsonism, paralysis, chorea)

Diagnosis and Management

Diagnosis

  • Clinical suspicion is a key factor in establishing a diagnosis of CO poisoning. 
  • The wide variety and nonspecificity of the symptoms make misdiagnosis very common, especially in the absence of evident exposure. 
  • A history of CO exposure is essential, but not always evident: Due to the lack of odor, color, and taste of the gas, individuals may not be aware of their exposure.
  • Work-up: 
    • Arterial blood gases show elevated levels of carboxyhemoglobin (> 3% in nonsmokers, > 10% in smokers).
    • Pulse oximetry is not useful and may appear normal because it cannot differentiate between COHb and oxyhemoglobin.
    • Electrocardiogram (ECG) and/or cardiac enzymes to rule out myocardial ischemia
    • Airway examination to assess for smoke inhalation injury

Management

  • Initial treatment with high-flow 100% oxygen: Oxygen therapy should begin immediately if clinical suspicion is high.
  • Consider hyperbaric oxygen in the following conditions:
    • Failed initial treatment
    • CO level > 25% with no clinical findings
    • CO level > 15% in pregnant patients with fetal distress
    • Loss of consciousness
    • Seizure
    • Severe metabolic acidosis (pH < 7.1)  
    • Evidence of end-organ ischemia (e.g., ECG changes, chest pain, altered mental status) 
  • Consider intubation and mechanical ventilation for severely impaired patients.

Differential Diagnosis

  • Respiratory failure: results when there is inadequate oxygenation of blood or inadequate ventilation/elimination of CO2 or both. May be an acute condition that develops over hours or a chronic condition that takes months to years to develop. Management involves treating the underlying cause, oxygen administration, and, if necessary, mechanical ventilation.
  • Cyanide poisoning: Hydrogen cyanide (HCN) is a colorless, extremely poisonous, and flammable liquid used in multiple industries and products, including rubber, plastic, and household paints. Lethal complications of cyanide poisoning occur in closed-space fires when plastics burn. Exposure is via inhalation, dermal, or intestinal. Symptoms develop within seconds to minutes and involve cardiovascular, respiratory, and neurological changes. Management includes sodium thiosulfate, nitrites, and hydroxocobalamin.
  • Acute respiratory distress syndrome (ARDS): a severe inflammatory reaction of the lungs that is characterized by the presence of pulmonary infiltrates due to alveolar fluid accumulation. Systemic inflammatory response syndrome and sepsis are the major causes of ARDS. The main finding is respiratory failure. Chest X-ray usually shows diffuse bilateral lung infiltrates (“butterfly opacity”). 
  • Alcohol toxicity: Alcoholism is a level of alcohol consumption that exceeds the sociocultural standard. The condition is marked by mental and physical addiction with an irresistible desire for alcohol and tolerance of the drug. Severe alcohol intoxication presents as nausea, vomiting, problems speaking and articulating, amnesia, delirium, lethargy, respiratory depression, seizures, coma, and even death.
  • Meningitis: an infection of the meninges, the protective membranes around the brain, most often caused by Streptococcus pneumoniae or Haemophilus influenzae. Presents with fever, stiff neck, and headache. Diagnosis is by lumbar puncture for cerebrospinal (CSF) evaluation. Treatment consists of the rapid administration of antibiotics.
  • Opioid toxicity: Opioids are central nervous system depressants used medically as a potent analgesic and commonly abused due to their euphoric effect. Features of opioid intoxication include drowsiness, respiratory depression, and pinpoint pupils, which can be managed by naloxone. Patients may develop withdrawal symptoms (yawning, lacrimation, runny nose, piloerection, stomach cramps) that can be managed by methadone or buprenorphine. 

References

  1. Clardy, P.F., Manaker, S., & Perry, H. Carbon monoxide poisoning. UpToDate. Retrieved January 24, 2021, from
    https://www.uptodate.com/contents/carbon-monoxide-poisoning
  2. O’Malley, G.F. & O’Malley, R. (2020). Carbon Monoxide Poisoning. MSD Manuals. https://www.msdmanuals.com/professional/injuries-poisoning/poisoning/carbon-monoxide-poisoning
  3. Rose, J. J., Wang, L., Xu, Q., McTiernan, C. F., Shiva, S., Tejero, J., & Gladwin, M. T. (2017). Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy. American journal of respiratory and critical care medicine, 195(5), 596–606. https://doi.org/10.1164/rccm.201606-1275CI
  4. Wu, P. E., & Juurlink, D. N. (2014). Carbon monoxide poisoning. CMAJ : Canadian Medical Association journal = journal de l’Association medicale canadienne, 186(8), 611. https://doi.org/10.1503/cmaj.130972
  5. Gozubuyuk, A. A., Dag, H., Kacar, A., Karakurt, Y., & Arica, V. (2017). Epidemiology, pathophysiology, clinical evaluation, and treatment of carbon monoxide poisoning in child, infant, and fetus. Northern clinics of Istanbul, 4(1), 100–107. https://doi.org/10.14744/nci.2017.49368

Study on the Go

Lecturio Medical complements your studies with evidence-based learning strategies, video lectures, quiz questions, and more – all combined in one easy-to-use resource.

Learn even more with Lecturio:

Complement your med school studies with Lecturio’s all-in-one study companion, delivered with evidence-based learning strategies.

🍪 Lecturio is using cookies to improve your user experience. By continuing use of our service you agree upon our Data Privacy Statement.

Details