Carbon Monoxide Poisoning

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

To view the entire topic, please or .

Medicine Central™ is a quick-consult mobile and web resource that includes diagnosis, treatment, medications, and follow-up information on over 700 diseases and disorders, providing fast answers—anytime, anywhere. Explore these free sample topics:

-- The first section of this topic is shown below --

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).
  • Results in approximately 1,200 to 1,600 deaths a year in the United States due to fire- and non–fire-related poisoning.
  • Vague symptoms may cause patients to not seek care, leading to underdiagnosis.

Prevalence
  • More prevalent during the winter months in areas with colder climate
  • Occupational exposure to methylene chloride, an industrial solvent that is a component of paint remover, can also lead to CO poisoning.

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.
  • Mitochondrial dysfunction and hypoxia leads to myocardial stunning and injury.
  • 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 initiates an inflammatory cascade that can lead to oxidative degradation of nervous system lipids and delayed neurologic damage.
  • CO also promotes the release of NO which can lead to profound hypotension.

Risk Factors

  • Alcohol and tobacco use
  • Patients with severe COPD regardless of current tobacco smoke exposure
  • 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, eliminate source, and initiate treatment
  • Public policy to ensure building code safety
  • Limiting occupational exposures for those who work with automobiles, paint, solvents, or mines

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.

-- To view the remaining sections of this topic, please or --

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).
  • Results in approximately 1,200 to 1,600 deaths a year in the United States due to fire- and non–fire-related poisoning.
  • Vague symptoms may cause patients to not seek care, leading to underdiagnosis.

Prevalence
  • More prevalent during the winter months in areas with colder climate
  • Occupational exposure to methylene chloride, an industrial solvent that is a component of paint remover, can also lead to CO poisoning.

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.
  • Mitochondrial dysfunction and hypoxia leads to myocardial stunning and injury.
  • 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 initiates an inflammatory cascade that can lead to oxidative degradation of nervous system lipids and delayed neurologic damage.
  • CO also promotes the release of NO which can lead to profound hypotension.

Risk Factors

  • Alcohol and tobacco use
  • Patients with severe COPD regardless of current tobacco smoke exposure
  • 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, eliminate source, and initiate treatment
  • Public policy to ensure building code safety
  • Limiting occupational exposures for those who work with automobiles, paint, solvents, or mines

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.

There's more to see -- the rest of this entry is available only to subscribers.