Description

• Carbon monoxide (CO) is a leading cause of poisoning death in the US (1). CO is an odorless, tasteless, colorless gas produced by combustion of carbon-containing compounds (wood, charcoal, oil, gas):
  • CO inhalation leads to displacement of oxygen from binding sites on hemoglobin.
  • Detrimental effects are related to tissue hypoxia from decreased oxygen content and a shift of the oxyhemoglobin dissociation curve to the left.
  • CO also binds to mitochondrial cytochrome oxidase, impairing adenosine triphosphate (ATP) production, and to myoglobin, affecting muscle function.
• System(s) affected: Cardiovascular; Musculoskeletal; Nervous

Pregnancy Considerations
Tissue hypoxia includes the fetus. CO poisoning may cause significant fetal abnormalities, depending on the developmental stage. Adult hemoglobin holds oxygen less tightly than does fetal hemoglobin. Therefore, a pregnant mother potentially may be unaffected while the fetus is affected.

Epidemiology

• Roughly 40,000 emergency department visits annually (2)
• 5,000–6,000 deaths annually in the US
• Unintentional CO poisoning likely causes 450 deaths annually.
• Intentional CO poisoning is ~10 times higher.
• Unintended poisoning is most common during winter months in cold climates, but can also occur in warm climates with use of generators, boats, etc.
• Likely markedly underdiagnosed because of vague symptoms.

Risk Factors

• Smoke inhalation
• Being in a closed or improperly ventilated space with a faulty furnace or stove or running engine or any fuel-burning device.
• Cigarette smoking
• Extremes of age (3)
• Cardiovascular disease, anemia, chronic respiratory conditions (3)
• Exposure to exhaust (riding in the back of enclosed pickup trucks or swimming near a motor boat)
• Employment in a coal mine, as an auto mechanic, paint stripper, or in the solvent industry

General Prevention

• Appropriate ventilation, especially where there are fuel-burning devices
• Use of CO monitors
• Public education
• Determining the mechanism of exposure is critical in cases of accidental poisoning in order to limit future risk.
• Victims must not be discharged back to a contaminated environment.

Pathophysiology

• CO is rapidly absorbed in lungs.
• CO has ~220 times the affinity for hemoglobin that oxygen has.
• CO binds to hemoglobin to form carboxyhemoglobin (COHb), resulting in impaired oxygen-carrying capacity, utilization, and delivery:
  • Leftward shift of the oxyhemoglobin dissociation curve occurs.
  • CO interferes with peripheral oxygen utilization by inactivating cytochrome oxidase.
• Delayed neurologic sequelae, probably due to lipid peroxidation by toxic oxygen species generated by xanthine oxidase.
• The half-life of CO while the patient is breathing room air is ~300 minutes, while breathing 100% oxygen via a tight-fitting, nonrebreathing face mask is ~60 minutes, and with 100% hyperbaric oxygen is ~20 minutes.
• CO exposure also causes inflammation through separate pathways than those that cause cardiac and neurologic sequalae (4).

Etiology

• CO inhalation
• Inhaled or ingested methylene chloride (from paint remover [dichloromethane]) is metabolized to CO by the liver, causing CO toxicity in the absence of ambient CO.

Commonly Associated Conditions

• CO and cyanide poisoning can occur simultaneously following smoke inhalation (synergistic effect).
• Consider CO poisoning in a burn victim who has been in an enclosed space.