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Carbon Monoxide Poisoning, Pediatric

Basics

Description

- 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

- Moderate to severe CO intoxication - Confusion - Syncope - Weakness - Angina

- Contraindications - Concurrent illness or injury requiring ongoing acute care - Unvented pneumothorax - Lack of accessible hyperbaric oxygen chamber

- Death - Delayed neurologic sequelae, for example - Neurocognitive deficits - Personality changes - Parkinsonism

  • 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 air1-2 hours in 100% oxygen20 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 exhaustSmoke inhalation from house firesOil, gas, or kerosene space heaters or cooking stovesPortable electricity generators and construction equipmentFaulty 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 symptomsMild CO intoxicationMalaiseNauseaLight-headednessHeadacheVomitingModerate to severe CO intoxicationConfusionSyncopeWeaknessAngina

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

  • NeuroimagingNot 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 indicationsLoss of consciousnessSeizuresPregnancyPersistent neurologic symptomsCO concentration >25%
  • ContraindicationsConcurrent illness or injury requiring ongoing acute careUnvented pneumothoraxLack of accessible hyperbaric oxygen chamber
  • ComplicationsBarotitis mediaTympanic membrane ruptureClaustrophobic anxietySeizurePneumothorax

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 exampleNeurocognitive deficitsPersonality changesParkinsonism

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.