> Table of Contents > Carbon Monoxide Poisoning
Carbon Monoxide Poisoning
Viren Kaul, MD
Faruq Pradhan, MBBCh
Anthony W. Gray Jr., MD
image BASICS
  • Carbon monoxide (CO) is an odorless, tasteless, colorless gas that has the potential to cause sudden illness and even death if inhaled; it is a leading cause of poisoning death in the United States.
  • CO is 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, further impairing oxygen unloading from hemoglobin.
  • CO also binds to mitochondrial cytochrome oxidase, impairing adenosine triphosphate (ATP) production. It also binds to myoglobin thereby affecting muscle function.
  • System(s) affected: cardiovascular, pulmonary, musculoskeletal, nervous
Pregnancy Consideration
Tissue hypoxia affects the fetal tissue. CO poisoning may cause significant fetal abnormalities, depending on the developmental stage. CO has a greater affinity for, and longer half-life when bound to fetal hemoglobin. Therefore, a pregnant mother potentially may be unaffected while the fetus is affected.
  • ˜50,000 emergency department visits annually (1)
  • 235 CO exposure-related deaths were reported to U.S. poison centers between 2000 and 2009; however, this is likely an underestimation with closer 500 deaths occurring per year, on review of previous data. Unintentional poisoning is most common during winter months in cold climates, but can also occur in warm climates with use of generators, boats, and so forth.
  • Intentional CO poisoning is ˜10 times higher than unintentional poisonings.
  • Likely markedly underdiagnosed because vague symptoms do not prompt individuals to seek medical attention
  • CO is rapidly absorbed in lungs.
  • CO has ˜240 times the affinity for hemoglobin compared to oxygen.
  • 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, related to lipid peroxidation by toxic oxygen species generated by xanthine oxidase
  • The half-life of CO while the patient is breathing room air is ˜320 minutes, while breathing 100% oxygen via a tight-fitting, nonrebreathing face mask is ˜74 minutes, and with 100% hyperbaric oxygen is ˜30 minutes.
  • CO exposure also causes inflammation through separate pathways than those that cause cardiac and neurologic sequelae (2).
  • 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.
  • Alcohol use (3)
  • Smoke inhalation
  • Being in a closed or improperly ventilated space with a faulty furnace, stove, running engine, or any fuel-burning device
  • Cigarette smoking
  • Use of generators during power outages
  • Extremes of age
  • Predisposing cardiovascular disease, anemia, chronic respiratory conditions
  • Exposure to exhaust (for example, riding in the back of enclosed pickup trucks or swimming near a motor boat) in precatalytic converter era automobiles.
  • Employment in a coal mine, as an auto mechanic, paint stripper, or in the solvent industry
  • Increased endogenous production in patients with hemolytic anemia
  • 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.
  • 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.
  • Acute CO poisoning is suggested by history, physical exam, and an elevated COHb.
  • Chronic CO intoxication is difficult to diagnose.
  • The newest pulse CO-oximeters can screen for CO exposure using different wavelengths of light.
  • Older pulse oximeters do not differentiate carboxyhemoglobin from oxyhemoglobin, causing normal pulse oximeter readings in hypoxic patients.
  • A level >3% in a nonsmoker and >10% in a smoker confirms exposure, but the level does not correlate well with the severity of the acute illness or the long-term prognosis (2).
  • “Cherry red” appearance of the lips and skin (<1% cases)
  • Respiratory depression or tachypnea
  • Cyanosis
  • Visual-field defects, papilledema, or nystagmus
  • CNS depression or coma, ataxia, seizure
  • Tachycardia, hypotension, cardiac dysrhythmias, or even (cardiac) arrest
  • Cyanide toxicity
  • Viral syndromes
  • Methylene chloride (dichloromethane) inhalation or ingestion
  • Psychological disorders including major depressive disorder
  • Other causes of mental status changes:
    • Infections such as meningitis or encephalitis
    • Metabolic causes such as hypoglycemia
    • Drugs: alcohol (EtOH) intoxication, opiates, acetylsalicylic acid (ASA) overdose
    • Trauma
    • CNS lesions
Initial Tests (lab, imaging)
  • Measurement of COHb (may be low despite significant poisoning if patient had been treated with O2 or has been breathing room air for a significant period of time before the level is drawn).
  • ABG (looking for metabolic acidosis)
    • Blood PO2 (PaO2) tends to be normal as O2 dissolved in blood is not affected by CO.
  • Blood glucose
  • Chemistries
  • Anion gap = ([Na+] + [K+]) - ([Cl-] + [HCO3-]). HCO3 decreased reflecting metabolic acidosis; anion gap >16
  • Pregnancy test in all women of childbearing age
  • Toxicology screen
  • ECG in all patients
  • Hemoglobin/hematocrit
  • CK to evaluate rhabdomyolysis
  • Cardiac enzymes in:
    • ≥65 years
    • Patient with cardiac risk factors or anemia
    • Patients with symptoms suggestive of cardiac ischemia
  • Head CT/MRI scan is helpful to rule out other causes of neurologic decompensation. May also show infarction due to hypoxia/ischemia

Follow-Up Tests & Special Considerations
  • Think of CO poisoning in younger patients with chest pain or symptoms suggestive of ischemia.
  • Consider the diagnosis and inquire about exposure in afebrile patients with “flulike” symptoms, especially in the winter when flu and CO poisoning are both more common.
  • Look for clusters of patients (coworkers, family members, school children) with similar symptoms.
  • Patients with intentional poisoning require psychiatric evaluation when medically stable.
  • Prompt removal from the CO source
  • Supportive care as necessary
  • Intubation and mechanical ventilation may be necessary for severe intoxication, if patient is not able to protect airway, or has significant respiratory depression.
  • Contact Poison Control Center at 800-222-1222 (United States only).
Rapid reduction in tissue hypoxia with 100% oxygen via nonrebreathing reservoir face mask (4)[A] until COHb is normal (<3%) and patient is asymptomatic.
  • Hyperbaric oxygen has been somewhat controversial (4,5)[A]. Existing randomized trials do not establish whether the administration of hyperbaric oxygen to patients with CO poisoning reduces the incidence of adverse neurologic outcomes (5)[A].
  • Despite this, hyperbaric oxygen recommended for levels >25-30%, evidence of cardiac involvement, severe acidosis, LOC, neurologic impairment, abnormal neuropsychiatric testing, age >36 years (6)[C].
  • Hyperbaric oxygen has been shown to be safe in pregnant woman, but there have been no prospective studies of efficacy (4)[A]. International consensus favors it as part of a more aggressive role in treating pregnant women (6)[C].
  • If no improvement occurs in cardiovascular or neurologic function within 4 hours, transport the patient to the nearest facility with hyperbaric oxygen, regardless of distance.
Admission Criteria/Initial Stabilization
Patients whose symptoms do not improve after 4 to 5 hours of 100% O2 should be transported to the nearest facility with hyperbaric oxygen. Those who demonstrate ECG or laboratory evidence of severe poisoning, who have evidence of end-organ damage, who require hyperbaric treatment, or who have another medical or social cause of concern should be hospitalized.
Discharge Criteria
Patients with mild symptoms from accidental poisoning can be managed in the ED and safely discharged.
All patients treated for acute CO poisoning should be seen for clinical follow-up in 1 to 2 months after they are safely discharged (4). Patients should undergo neuropsychological testing if suspicion of cognitive impairment. Consider evaluation of family members or cohabitants.
Patient Monitoring
  • Measurement of carboxyhemoglobin levels
  • Arterial blood gases
  • Professional installation and maintenance of combustion devices: 1-800-638-2772; Consumer Products Safety Commission hotline
  • Some states require CO detector installation in homes, especially near bedrooms and potential sources.
  • Annual furnace inspections (7)[B]
Most survivors recover completely, with only a minority developing chronic neuropsychiatric impairment.
1. Hampson NB, Weaver LK. Carbon monoxide poisoning: a new incidence for an old disease. Undersea Hyperb Med. 2007;34(3):163-168.
2. Weaver LK. Clinical practice. Carbon monoxide poisoning. N Engl J Med. 2009;360(12):1217-1225.
3. Yoon SS, Macdonald SC, Parrish RG. Deaths from unintentional carbon monoxide poisoning and potential for prevention with carbon monoxide detectors. JAMA.1998;279(9):685-687.
4. Hampson NB, Piantadosi CA, Thom SR, et al. Practice recommendations in the diagnosis, management, and prevention of carbon monoxide poisoning. Am J Respir Crit Care Med. 2012;186(11):1095-1101.
5. Buckley NA, Juurlink DN, Isbister G, et al. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev. 2011;(4):CD002041. doi: 10.1002/14651858.CD002041.pub3.
6. Centers for Disease Control and Prevention. Carbon monoxide poisoning after a disaster. http://emergency.cdc.gov/disasters/carbonmonoxide.asp
7. Rupert DJ, Poehlman JA, Damon SA, et al. Risk and protective behaviours for residential carbon monoxide poisoning. Inj Prev. 2013;19(2):119-123.
Additional Reading
  • Centers for Disease Control and Prevention. Unintentional, non-fire-related, carbon monoxide exposures—United States, 2001-2003. MMWR Morb Mortal Wkly Rep. 2005;54(2):36-39.
  • Internet resources available at http://www.cpsc.gov, http://www.cdc.gov/co, and http://www.epa.gov/iaq/co.html.
  • Iqbal S, Clower JH, Hernandez SA, et al. A review of disaster-related carbon monoxide poisoning: surveillance, epidemiology, and opportunities for prevention. Am J Public Health. 2012;102(10):1957-1963.
  • Satran D, Henry CR, Adkinson C, et al. Cardiovascular manifestations of moderate to severe carbon monoxide poisoning. J Am Coll Cardiol. 2005;45(9):1513-1516.
  • World Health Organization. World directory of poison centres. http://www.who.int/gho/phe/chemical_safety/poisons_centres/en/index.html.
  • T58.91XA Toxic effect of carb monx from unsp source, acc, init
  • T58.8X1A Toxic effect of carb monx from oth source, accidental, init
  • T58.01XA Toxic effect of carb monx from mtr veh exhaust, acc, init
Clinical Pearls
  • The most appropriate intervention in the management of a CO-poisoned patient is a prompt removal from the source of CO and institution of 100% oxygen by high-flow face mask or endotracheal tube.
  • A pregnant woman may appear normal while her fetus is severely affected.
  • Consider CO poisoning in younger patients with chest pain or ischemia or in patients who present in clusters.
  • COHb levels do not correlate well with symptoms, severity of illness, or outcome, so manage the patient, not the level.