Toxin
Carbon Monoxide Poisoning
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Carbon Monoxide Poisoning
, Carbon Monoxide
See Also
Smoke Inhalation
Carboxyhemoglobin
Epidemiology
Emergency Department visits per year: 50,000 in U.S.
Leading cause of toxin related death in United States
Accidental or Intentional (
Suicide
) deaths per year: 5000
Sources
Carbon Monoxide
Gas powered engine
Car with faulty exhaust system
Passengers riding in back of a pickup truck
Swimmers at back of a houseboat
Propane fueled forklifts
Ice skating rink Zamboni
Indoor tractor pulls
Home
Indoor Heaters (most common cause)
Furnace
Home water heaters
Gas heaters
Pool heaters
Kerosene heaters
Indoor Flames
Wood stoves
Indoor charcoal fires
Sterno fuel
Tobacco
smoke
Tobacco
Smokers
Carboxyhemoglobin
levels may reach 6-10%
Hookah Smokers
Carboxyhemoglobin
levels may reach 15-20%
Nonsmokers exposed to passive smoke
Cigarette
tip 2.5 fold greater CO than inhaled
Industrial or Occupational
Steel foundry
Pulp paper mill
Formaldehyde and coke producing plants
Fire fighters
Fire
Building or structure fire
Wilderness fire
Suicide
Attempt
Closed garage with car
Running
Ingestion of formic acid and sulfuric acid (sulphuric acid)
Combination yields Carbon Monoxide
Strong acid fumes may also result in
Burn Injury
and lung injury
Swadron and Nordt (2022) EM:Rap 22(6): 5-7
Pathophysiology
Carbon Monoxide Properties (no warning features that gas is present until symptoms develop)
Colorless
Odorless
Non-irritating gas
Small molecule that crosses through some barriers into closed spaces (e.g. drywall)
Exposures leading to Toxicity
Carbon Monoxide toxicity occurs at
Ambien
t levels >200-500 parts per million
More severe illness occurs with longer exposure times
Carbon Monoxide inhalation
Carbon Monoxide has a high affinity for
Hemoglobin
(>200-250 times higher affinity than oxygen)
Displaces Oxygen and produces
Carboxyhemoglobin
Shifts oxygen dissociation curve left with poor delivery of any residual oxygen to tissues
Functional
Anemia
is however not responsible for Carbon Monoxide's lethal effects
Direct toxin effects of Carbon Monoxide
Sodium
channel activation
Nitric oxide levels increase
Neurotoxic
Basal Ganglia
(
Parkinsonism
)
Occiput (occipital blindness)
Frontal cortex (personality change)
Inflammatory cascade (responsible for neurologic toxicity)
White Blood Cell
response
Glutamic Acid
(inflammatory)
Free radicals
History
Multiple persons (e.g. family, coworkers, pets) in the same environment with similar symptoms
Symptoms
Headache
(88%)
Dizziness
(83%)
Nausea
(75%)
Drowsiness (75%)
Dry Mouth
(44%)
Syncope
Chest Pain
Shortness of Breath
Myalgias
Carbon Monoxide also binds myoglobin
Signs
Cherry-red skin and mucosa
Late or post-mortem finding
Bounding Pulse
Hypertension
Muscular
Fasciculation
s
Stertor
ous breathing
Dilated pupils
Convulsion
s
Altered Mental State
to coma
Do not rely on
Oxygen Saturation
s (not accurate see below)
Findings
Carboxyhemoglobin
level
Carboxyhemoglobin
: 10%
Frontal
Headache
Carboxyhemoglobin
: 20%
Throbbing
Headache
Dyspnea
on exertion
Severe
Hypoxemia
requiring intubation may occur at this level
Carboxyhemoglobin
: 30%
Impaired judgment
Nausea
or
Vomiting
Dizziness
Visual disturbance
Fatigue
Carboxyhemoglobin
: 40%
Confusion
Syncope
Carboxyhemoglobin
: 50%
Coma
Seizure
s
Carboxyhemoglobin
: 60%
Hypotension
Respiratory Failure
Carboxyhemoglobin
: 70%
Death
Labs
Blood grossly appears abnormal red color
Venous Blood Gas
Carboxyhemoglobin
Normal background
Carboxyhemoglobin
is 2-3%
Carboxyhemoglobin
elevated >25% is significant and associated with toxicity
See above for findings related to
Carboxyhemoglobin
levels
Complete Blood Count
Leukocytosis
Precautions
Oxygen Saturation
(
Pulse Oximeter
) data is inaccurate
Does not distinguish
Carboxyhemoglobin
from oxygenated
Hemoglobin
Drywall does not deter Carbon Monoxide
Carbon Monoxide diffuses across drywall and may permeate separated rooms in multi-tenant housing
Consider concurrent
Cyanide
toxicity in structure fires
Smoke Inhalation
and
Lactic Acid
>8 suggests cyanide
Poisoning
Especially with
Altered Level of Consciousness
Start oxygen while awaiting lab testing results if higher level of suspicion
Start 100% oxygen via non-rebreather
Hyperglycemia
is a
Neurotoxin
and worsens outcomes
Consider
Insulin
for
Glucose
>300 mg/dl
Management
Mild
Poisoning
Criteria
Carboxyhemoglobin
<30%
No Neurologic or Cardiovascular
Impairment
Management
Oxygen 100%
Non-Rebreathing Mask
Continue until
Carboxyhemoglobin
<5%
Carbon Monoxide decreases 50% in 6 hours on room air
Carbon Monoxide decreases 50% in 60 minutes on
Non-Rebreather Mask
Carbon Monoxide decreases 50% in 30 minutes on 100% oxygen while intubated
Continuous Positive Airway Pressure (
CPAP
) with oxygen lowers Carbon Monoxide faster than oxygen alone
Bal (2020) Eur J Emerg Med 27(3):217-22 +PMID:31815874 [PubMed]
Hyperbaric Oxygen Indications
See Hyperbaric Oxygen below
Carboxyhemoglobin
>25% and associated factors (cardiac or neurologic findings, age >36 years old)
Consider in Pregnancy
Admission criteria
All patients with
Carboxyhemoglobin
>25%
Underlying heart disease
Management
Moderate
Poisoning
Criteria
Carboxyhemoglobin
: 30-40%
No Neurologic
Impairment
Management
Oxygen 100%
Non-Rebreathing Mask
Continue until
Carboxyhemoglobin
<5% (see above)
Admission to telemetry (cardiovascular monitor)
Consider hyperbaric oxygen (see below)
Cerebellar signs
Focal neurologic deficit
Persistent severe
Headache
Loss of consciousness,
Seizure
or coma
Glasgow Coma Scale
(GCS) <15
Age >36 years old
Prolonged Carbon Monoxide exposure
Venous Blood Gas
Determine acid-base status
Management
Severe
Poisoning
Criteria
Carboxyhemoglobin
: >40%
Neurologic
Impairment
Management
Oxygen 100%
Non-Rebreathing Mask
Continue until
Carboxyhemoglobin
<5% (see above)
Admission to telemetry (cardiovascular monitor)
Endotracheal Intubation
may be required due to severe
Hypoxemia
Venous Blood Gas
Follow acid-base status
Extracorporeal Membrane Oxygenation
(
VA-ECMO
)
Indicated in refractory cardiovascular collapse
Hyperbaric oxygen (see below)
Ideally performed within 6 hours of presentation
Chamber immediately available OR
No improvement in 4 hours
Cardiovascular status
Neurologic status
Management
Hyperbaric oxygen chamber
Mechanism
Carbon Monoxide decreases 50% in 20-30 minutes on hyperbaric oxygen at 2.8 atm
Allows oxygen to dissolve in blood at a much greater extent (beyond
Hemoglobin
binding)
Decreases inflammatory cascade
Decreases reperfusion injury
Efficacy
Decreases risk of delayed neuropsychiatric effects
Reduces risk of personality change,
Parkinsonism
, cognitive effects
Better short-term and long-term cognitive outcome
Weaver (2002) N Engl J Med 347:1057-67 [PubMed]
Rose (2018) Crit Care Med 46(7): e649-55 [PubMed]
Indications
Carboxyhemoglobin
: >40%
Carboxyhemoglobin
: >25-30% and associated factors
Neurologic
Impairment
Transient or prolonged loss of consciousness
Severe acidosis
Cardiac involvement
Abnormal neuropsychiatric findings
Age >36 years old
Carboxyhemoglobin
: <25%
Consider hyperbaric oxygen for pregnant patients
Complications
Hypoxic Encephalopathy
Cognitive effects may persist for weeks to months or even permanently (up to 15-40% of cases)
Reduced risk with hyperbaric oxygen therapy (see above)
Parkinsonism
Occipital blindness
Personality change
Coronary ischemia or myocadial infarction
Increased risk of
Coronary Artery Disease
Henry (2006) JAMA 295(4): 398-402 [PubMed]
Prevention
Adequate Ventilation
Carbon Monoxide detectors
Alarm sounds when
Ambien
t Carbon Monoxide levels are >50 parts per million
Carbon Monoxide toxicity occurs at
Ambien
t levels >200-500 parts per million
Resources
Consumer Products Safety Commission
http://www.cpsc.gov/en/safety-education/safety-education-centers/carbon-monoxide-information-center/
References
Kinker and Glauser (2021) Crit Dec Emerg Med 35(9): 19-27
Moayedi and Swaminathan in Herbert (2016) EM:Rap 16(7): 13-14
Nordt and Shoenberger in Herbert (2019) EM:Rap 19(1): 4-6
Reisdorf (1996) in Tintinelli (1996)
(1995) MMWR Morb Mortal Wkly Rep 44:765-7 [PubMed]
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