Carbon Monoxide Poisoning

Carbon Monoxide Poisoning is a topic covered in the 5-Minute Clinical Consult.

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Basics

Description

  • Carbon monoxide (CO) is an odorless, tasteless, colorless gas produced during the incomplete combustion of carbon-based compounds. If inhaled, CO may cause nonspecific symptoms and is potentially fatal.
    • CO inhalation leads to displacement of oxygen from binding sites on hemoglobin to form carboxy hemoglobin (COHb).
    • The formation of COHb leads to tissue hypoxia from decreased oxygen carrying capacity and a left shift of the oxyhemoglobin dissociation curve.
    • CO binds to mitochondrial cytochrome oxidase, impairing adenosine triphosphate (ATP) production. It also binds to myoglobin, affecting muscle function.
  • System(s) affected: cardiovascular, pulmonary, musculoskeletal, nervous

Pregnancy Considerations
Tissue hypoxia due to CO poisoning may cause significant fetal abnormalities because CO has a stronger affinity and a longer half-life when bound to fetal hemoglobin. The fetus is therefore susceptible to adverse outcomes even if the mother is unaffected.

Epidemiology

Incidence

CO poisoning is the third leading cause of poisoning death in the United States.

  • Accounts for 50,000 ER visits annually (16 cases per 100,000 population); 1–3% are fatal.
  • Approximately 15,000 intentional poisoning occur per year, accounting for 2/3 reported deaths (10-fold higher than unintentional poisonings).
  • Vague symptoms may cause patients to not seek care, leading to underdiagnosis.

Etiology and Pathophysiology

  • CO is rapidly absorbed through the lungs, binding hemoglobin with 210 to 240 times the affinity of oxygen. This stabilizes hemoglobin in the relaxed high affinity state (R state), reducing oxygen-carrying capacity and delivery, leading to left shift of the oxyhemoglobin dissociation curve.
  • CO inactivates cytochrome oxidase. This leads to decreased ATP production, especially in tissues with high metabolic demands (brain, heart). The electron transport chain continues, generating superoxide radicals, leading to further damage.
  • Increased peroxynitrite production contributes to impaired mitochondrial function and hypoxia.
  • CO displaces NO from platelets, leading to platelet activation and aggregation. Oxidative stress, lipid peroxidation, and apoptosis are additional effects.
  • Proteases released from neutrophil degranulation interact with xanthine hydrogenase forming xanthine oxidase. This inhibits endogenous defense against oxidative stress.
  • Brain hypoxia leads to excitatory amino acid production and increased nitrite levels, resulting in further ischemia.
  • CO also promotes the release of NO which can lead to profound hypotension.

Risk Factors

  • Alcohol and tobacco use
  • Closed or improperly ventilated spaces
  • Fires and fire-related injuries
  • High-risk vocations: coal miners, auto mechanics, paint stripping, work in the solvent industry
  • Exposure to exhaust from motor vehicles, faulty furnaces, stoves, generator use (power outages and storms), and other fuel burning devices
  • If exposed, infants, elderly patients, and patients with comorbid conditions such as cardiovascular disease, anemia, and chronic respiratory conditions have increased risk for poor outcomes.
  • Increased endogenous CO production occurs in patients with hemolytic anemia.

General Prevention

  • Appropriate ventilation around fuel-burning devices
  • Installation of in-home CO monitors or alarms
  • Postexposure determination of CO source to limit future exposures and/or eliminate source
  • Public policy to ensure building code safety

Commonly Associated Conditions

  • CO and cyanide poisoning often occur simultaneously after smoke inhalation and have synergistic effects.
  • Intentional poisoning often occurs in the context of coingestion of other substances (~40%).
  • Up to 50–75% of fire-related injuries have a component of CO poisoning.

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