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Carbon Monoxide Poisoning

Basics

  • CO is odorless, tasteless, colorless gas from incomplete combustion of carbon-based fuels.
  • Binds hemoglobin with 210–240x affinity vs oxygen, forming carboxyhemoglobin (COHb), causing tissue hypoxia.
  • Also binds cytochrome oxidase, inhibiting ATP production, and myoglobin, reducing cardiac contractility.
  • Pregnancy: fetal hemoglobin binds CO with higher affinity and longer half-life; fetal hypoxia risk even if mother asymptomatic.

Epidemiology

  • 3rd leading cause of poisoning deaths in the US; 481 deaths in 2020.
  • 50,000 ER visits annually; 1-3% fatal.
  • Two-thirds of deaths from intentional poisoning; many exposures during winter.
  • Occupational risk: methylene chloride exposure in paint removers, solvents.

Etiology and Pathophysiology

  • Rapid pulmonary absorption; stabilizes hemoglobin in high-affinity state, shifting O2 dissociation curve left.
  • Inhibits mitochondrial cytochrome oxidase → decreased ATP, increased reactive oxygen species.
  • Activates platelets via NO displacement, causing aggregation, oxidative stress, hypotension.
  • Inflammatory cascade leads to delayed neurological damage.

Risk Factors

  • Alcohol and tobacco use
  • Severe COPD
  • Enclosed/poorly ventilated spaces
  • Fire exposure
  • High-risk occupations (coal miners, mechanics, paint/solvent workers)

General Prevention

  • Proper ventilation of fuel-burning devices
  • CO detectors in homes and workplaces
  • Public policy for building safety and occupational exposure limits

Commonly Associated Conditions

  • Cyanide poisoning (often co-exists in smoke inhalation)
  • Intentional poisoning often involves co-ingestions
  • Fire-related injuries often include CO poisoning

Diagnosis

Clinical Triad

  • Symptoms + history of exposure + elevated COHb (>5% nonsmokers, >10% smokers)

History

  • Symptoms: headache (91%), dizziness (77%), weakness (53%), confusion, nausea, vomiting, chest pain, dyspnea
  • Long-term exposure: chronic fatigue, memory issues, neuropathy, polycythemia
  • Delayed neurologic symptoms 2–40 days post-exposure in 1–47% of cases

Physical Exam

  • Altered mental status, confusion
  • Respiratory distress (tachypnea, cyanosis)
  • Tachycardia, hypotension, cardiac arrhythmias
  • Rare cherry-red skin color (<1%)
  • Signs of burns or inhalation injury if fire-related

Differential Diagnosis

  • Cyanide toxicity, methylene chloride poisoning
  • Viral illness, depression, meningitis, metabolic disturbances
  • Alcohol or other substance intoxication

Diagnostic Tests

  • Blood COHb by co-oximetry (gold standard)
  • ABG: normal PaO2, metabolic acidosis, elevated lactate indicates severity
  • ECG and cardiac enzymes in moderate/severe poisoning
  • Pregnancy test in women of childbearing age
  • Imaging (CT/MRI brain): may show bilateral globus pallidus lesions or white matter changes
  • Toxicology screen and CK for rhabdomyolysis in intentional cases

Treatment

General Measures

  • Immediate removal from CO source
  • 100% oxygen via nonrebreather mask until COHb <3% and symptoms resolve
  • Supportive care; intubation/ventilation if needed

Medications

  • High-flow nasal cannula oxygen if nonrebreather not tolerated
  • Treat associated cyanide poisoning and coingestions as appropriate

Second Line

  • Hyperbaric oxygen therapy (HBO2): decreases COHb half-life, may reduce long-term neuropsychiatric complications
  • Indications: COHb >25% (>20% in pregnancy), altered mental status, ischemia, severe acidosis, within 6 hours of exposure preferred
  • HBO2 availability limited; consult Undersea and Hyperbaric Medical Society or Divers Alert Network

Admission and Nursing Considerations

  • Admit patients with severe poisoning, end-organ damage, unstable vitals
  • ICU admission for unconscious or intubated patients
  • Discharge mild cases with resolved symptoms after ED observation

Ongoing Care

  • Follow-up 1-2 months post-discharge for neuropsychological assessment if indicated
  • Monitor COHb levels with arterial blood gases

Patient Education

  • CO detectors at home
  • Proper ventilation and maintenance of combustion devices
  • Avoid running engines indoors
  • CDC resources: https://www.cdc.gov/

Prognosis

  • Most patients recover completely
  • 12–68% may develop chronic neuropsychiatric impairment
  • Complications include myocardial ischemia, pulmonary injury, neurological deficits, behavioral changes

Complications

  • Cardiac: myocardial ischemia, arrhythmias
  • Pulmonary: inhalation injury, pulmonary edema, respiratory failure
  • Neurologic: encephalopathy, cognitive dysfunction, parkinsonism
  • Behavioral: mood disorders, irritability

Clinical Pearls

  • Maintain high suspicion in winter, fire exposure, grouped presentations
  • Pulse oximetry unreliable for CO diagnosis
  • Immediate 100% O2 essential; consider HBO2 when available and indicated

References

  1. Chenoweth JA, Albertson TE, Greer MR. Carbon monoxide poisoning. Crit Care Clin. 2021;37(3):657-672.
  2. Rose JJ, Wang L, Xu Q, et al. Carbon monoxide poisoning: pathogenesis, management, and future directions of therapy. Am J Respir Crit Care Med. 2017;195(5):596-606.
  3. Wolf SJ, Maloney GE, Shih RD, et al. Clinical policy: critical issues in evaluation and management of acute carbon monoxide poisoning. Ann Emerg Med. 2017;69(1):98-107.e6.
  4. Nañagas KA, Penfound SJ, Kao LW. Carbon monoxide toxicity. Emerg Med Clin North Am. 2022;40(2):283-312.
  5. Huang CC, Ho CH, Chen YC, et al. Hyperbaric oxygen therapy is associated with lower mortality in patients with carbon monoxide poisoning. Chest. 2017;152(5):943-953.