Basics
Description
- Carbon monoxide (CO) is an odorless gas produced via incomplete combustion of carbonaceous fuels.
- CO poisoning occurs when carboxyhemoglobin and CO accumulation leads to impaired physiologic function.
Epidemiology
CO poisoning is a leading cause of death by poisoning within the United States.
Incidence
- More than 13,000 CO exposures were reported to the American Association of Poison Control Centers in 2011, with ~1/3 of such exposures occurring in children.
- Seasonal cold weather and other natural disaster events lead to increases in incidence of exposure.
General Prevention
- Furnaces should receive regular maintenance by skilled technicians.
- Automobiles, gas-powered machinery, and nonelectrical space heaters should only be used with proper ventilation.
- CO detectors should be installed within living spaces.
Pathophysiology
- On inhalation, some CO binds to hemoglobin to form carboxyhemoglobin.
- Carboxyhemoglobin does not carry oxygen.
- Carboxyhemoglobin produces an allosteric leftward shift of the oxyhemoglobin dissociation curve.
- Carboxyhemoglobin elimination half-life
- ~4 hours in room air
- 1-2 hours in 100% oxygen
- 20 minutes in 100% oxygen at 3 atmospheres
- CO interacts with cellular proteins, leading to impaired mitochondrial function.
- CO is a source of oxidative stress and poisoning may begin a cascade of inflammatory vasculitis within the CNS and heart.
Etiology
- Common sources of CO exposure include the following:
- Automobile or boat exhaust
- Smoke inhalation from house fires
- Oil, gas, or kerosene space heaters or cooking stoves
- Portable electricity generators and construction equipment
- Faulty home furnaces
- The solvent methylene chloride is metabolized to CO by the liver after ingestion, inhalation, or dermal absorption.
- CO is a component of cigarette smoke and environmental air pollution.
- CO is a naturally occurring by-product of the heme biosynthesis pathway.
Commonly Associated Conditions
Victims of house fires may suffer from thermal injury and/or cyanide poisoning.
Diagnosis
Many emergency medical services crews carry CO detectors.
History
- Health of family members?
- CO is an environmental gas that often sickens multiple household members.
- Use of furnace or space heaters?
- May suggest source of exposure
- Time of exposure?
- Carboxyhemoglobin levels must be interpreted with consideration to their timing.
- Duration of exposure?
- Toxicity is related to both magnitude and duration of exposure.
- Loss of consciousness?
- Syncope appears to be the best clinical predictor of delayed neurologic sequelae.
- Signs and symptoms
- Mild CO intoxication
- Malaise
- Nausea
- Light-headedness
- Headache
- Vomiting
- Moderate to severe CO intoxication
- Confusion
- Syncope
- Weakness
- Angina
Physical Exam
- Soot on nasal mucosa: suggests possibility of thermal pulmonary injury
- Hypotension: suggests severe CO poisoning
- Cherry red skin: This classic sign is mostly a postmortem finding.
Diagnostic Tests & Interpretation
Lab
- CO-oximetry: allows quantitation of carboxyhemoglobin
- Arterial blood gas: allows accurate assessment of oxygenation
- Hemoglobin quantitation: The percentage of carboxyhemoglobin concentration must be considered in relation to the total hemoglobin.
- Serum bicarbonate: A wide anion gap metabolic acidosis suggests the accumulation of lactate, which may result from severe CO poisoning or concomitant cyanide poisoning.
- Creatine kinase: CO poisoning victims are susceptible to rhabdomyolysis.
- Troponin: CO poisoning may lead to myocardial injury.
- ECG: Hypoxemia and metabolic poisoning may lead to cardiac ischemia.
- Transcutaneous carboxyhemoglobin measurement devices are now marketed.
Imaging
- Neuroimaging
- Not routinely helpful in acute management
- Globus pallidus and subcortical white matter changes may be seen after severe or chronic CO poisoning.
Alert
Pitfalls
- Pulse oximetry frequently overestimates the percentage of oxyhemoglobin.
- Smokers may have carboxyhemoglobin levels up to 10%.
- Hemolysis, or the presence of fetal hemoglobin, may lead to mild elevation of carboxyhemoglobin.
- In-hospital carboxyhemoglobin levels are not good at predicting risk of delayed neurologic sequelae.
Differential Diagnosis
- Influenza
- Gastroenteritis
- Vasomotor syncope
- Asphyxia
- Stroke
Treatment
General Measures
- Recognize CO exposure.
- Remove patient from source of CO.
Initial Stabilization
Administer 100% oxygen at least until patient is asymptomatic and carboxyhemoglobin level is <5-10%.
Additional Therapies
- Consider hyperbaric oxygen treatment referral to prevent delayed neurologic sequelae.
- Relative indications
- Loss of consciousness
- Seizures
- Pregnancy
- Persistent neurologic symptoms
- CO concentration >25%
- Contraindications
- Concurrent illness or injury requiring ongoing acute care
- Unvented pneumothorax
- Lack of accessible hyperbaric oxygen chamber
- Complications
- Barotitis media
- Tympanic membrane rupture
- Claustrophobic anxiety
- Seizure
- Pneumothorax
Alert
Pitfalls
- Failure to differentiate CO poisoning from winter viral illness
- Syncope may be hard to discern in young infants.
- Undue delay in hyperbaric oxygen therapy, which is most effective in first 6 hours after exposure
Issues for Referral
- Neuropsychological testing may benefit individuals with perceived neurocognitive deficits.
- Cardiac evaluation for those with myocardial ischemia
Inpatient Considerations
Admission Criteria
- Perceived merit of hyperbaric oxygen therapy
- Persistent neurologic symptoms
- Evidence of myocardial ischemia
- Associated injuries that merit hospitalization
Discharge Criteria
- Conclusion of hyperbaric therapy
- Stable cardiovascular and neurologic systems after elimination of excess carboxyhemoglobin
Ongoing Care
Follow-up Recommendations
Delayed neurologic sequelae may develop 2-40 days after exposure.
Prognosis
- Acute mortality appears to be caused by carboxymyoglobin formation and ischemic ventricular dysrhythmia.
- Patients stable on presentation to medical care have a good prognosis for recovery.
- Delayed neurologic sequelae may manifest in as many as 10-40% of patients after a CO-mediated syncopal episode.
Complications
- Death
- Delayed neurologic sequelae, for example
- Neurocognitive deficits
- Personality changes
- Parkinsonism
Additional Reading
- Baum CR. What's new in pediatric carbon monoxide poisoning? Clin Pediatr Emerg Med. 2008;9:43-46.
- Teksam O, Gumus P, Bayrakci B, et al. Acute cardiac effects of carbon monoxide poisoning in children. Eur J Emerg Med. 2010;17(4):192-196. [View Abstract]
- Weaver LK. Clinical practice. Carbon monoxide poisoning. N Engl J Med. 2009;360(12):1217-1225. [View Abstract]
Codes
ICD09
- 986 Toxic effect of carbon monoxide
ICD10
- 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
- T58.11XA Toxic effect of carb monx from utility gas, acc, init
SNOMED
- 17383000 Toxic effect of carbon monoxide (disorder)
- 95874006 carbon monoxide poisoning from fire (disorder)
- 95872005 Carbon monoxide poisoning from motor vehicle exhaust
- 95873000 carbon monoxide poisoning from faulty furnace AND/OR heater (disorder)
FAQ
- Q: At what carboxyhemoglobin level should hyperbaric oxygen therapy be recommended?
- A: In practice, most dissociation of carboxyhemoglobin occurs with administration of normal-pressure oxygen before hyperbaric therapy can be administered.
- The advocated value of hyperbaric oxygen is to limit cerebral ischemic reperfusion injury in an effort to ameliorate delayed neurologic sequelae.
- Carboxyhemoglobin levels may not directly correlate in this risk stratification, and the occurrence of syncope or seizure may be used as a surrogate marker.
- Currently, patients with CO concentrations >25% may be considered as potential candidates for hyperbaric oxygen.
- Q: In a household, which family member is at greatest risk of CO poisoning?
- A: Smaller and younger children have greater minute ventilation rates and may attain higher carboxyhemoglobin concentrations at a given exposure level.
- It is possible that developing brain tissue is more susceptible to the deleterious effects of CO poisoning.