Carbon monoxide toxicity: Difference between revisions
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==Background== | == Background == | ||
#Colorless, odorless gas | |||
#Most toxic component in smoke inhalation and major contributor to fire-related deaths | #Colorless, odorless gas | ||
##Can co-occur with [[Cyanide]] toxicity in industrial fires | #Most toxic component in smoke inhalation and major contributor to fire-related deaths | ||
#Sources | ##Can co-occur with [[Cyanide]] toxicity in industrial fires | ||
##Automotive exhaust | #Sources | ||
##Propane-fueled heaters | ##Automotive exhaust | ||
##Wood or coal-burning heaters | ##Propane-fueled heaters | ||
##Structure fires | ##Wood or coal-burning heaters | ||
##Gasoline-powered motors | ##Structure fires | ||
##Natural gas-powered heaters | ##Gasoline-powered motors | ||
##Natural gas-powered heaters | |||
#Peak incidence in winter months | #Peak incidence in winter months | ||
==Pathophysiology== | == Pathophysiology == | ||
#Hypoxia | |||
##Binding affinity of Hb for CO (carboxyhemoglobin) is 200x that of O2 | #Hypoxia | ||
##Half-Life | ##Binding affinity of Hb for CO (carboxyhemoglobin) is 200x that of O2 | ||
###Room air: ~5hrs | ##Half-Life | ||
###100% O2: ~1hr | ###Room air: ~5hrs | ||
###HBO 2.5atm: 24min | ###100% O2: ~1hr | ||
#Lactic acidosis | ###HBO 2.5atm: 24min | ||
##CO inhibits oxidative phosphorylation | #Lactic acidosis | ||
#Hypotension | ##CO inhibits oxidative phosphorylation | ||
##CO induces NO2 and guanylate cyclase release -- | #Hypotension | ||
##CO induces NO2 and guanylate cyclase release --> vasodilation release | |||
== Workup == | |||
#VBG | |||
#VBG | ##Co-oximetry analysis will provide carboxyhemoglobin level | ||
##Co-oximetry analysis will provide carboxyhemoglobin level | #Lactate | ||
#Lactate | #Chemistry | ||
#Chemistry | #Troponin | ||
#Troponin | #Total CK (rhabdo) | ||
#Total CK (rhabdo) | #ECG | ||
#ECG | ##May range from normal to STEMI (most common ST, then prolonged QT) | ||
##May range from normal to STEMI | ###Few of the pts w/ AMI from CO have occlusive lesions in their arteries | ||
###Few of the pts w/ AMI from CO have occlusive lesions in their arteries | #?Head CT | ||
#?Head CT | |||
##May show b/l globus pallidus lesions in severe cases | ##May show b/l globus pallidus lesions in severe cases | ||
==Clinical Features== | == Clinical Features == | ||
#May range from "flu-like" symptoms to coma | |||
#CNS | #May range from "flu-like" symptoms to coma | ||
##Headache | #CNS | ||
##Visual disturbances | ##Headache | ||
##Confusion | ##Visual disturbances | ||
##Ataxia | ##Confusion | ||
##Seizure | ##Ataxia | ||
##Syncope | ##Seizure | ||
##Retinal hemorrhage | ##Syncope | ||
##Focal neurologic deficit | ##Retinal hemorrhage | ||
#GI | ##Focal neurologic deficit | ||
##Vomiting | #GI | ||
#Pulm | ##Vomiting | ||
##Dyspnea/tachypnea | #Pulm | ||
#Cardio | ##Dyspnea/tachypnea | ||
##Chest pain | #Cardio | ||
##ECG changes/dysrhythmias | ##Chest pain | ||
#Derm | ##ECG changes/dysrhythmias | ||
##Bullous skin lesions | #Derm | ||
##Bullous skin lesions | |||
##Classic finding of cherry red oral mucosa is rarely seen in living pts | ##Classic finding of cherry red oral mucosa is rarely seen in living pts | ||
==Diagnosis== | == Diagnosis == | ||
#Must have high clinical suspicion (esp in pts w/ coma, AMS, or anion gap acidosis) | |||
##Comatose pt removed from fire should be assumed to have CO poisoning | #Must have high clinical suspicion (esp in pts w/ coma, AMS, or anion gap acidosis) | ||
#Carboxyhemoglobin Level | ##Comatose pt removed from fire should be assumed to have CO poisoning | ||
##Interpretation must take into account time since exposure and O2 tx | #Carboxyhemoglobin Level | ||
##Normal value in non-smokers is ~1%, normal value in smokers may be up to 10% | ##Interpretation must take into account time since exposure and O2 tx | ||
##Symptoms and COHb levels do not always correlate well | ##Normal value in non-smokers is ~1%, normal value in smokers may be up to 10% | ||
##Symptoms and COHb levels do not always correlate well | |||
#Pulse oximetry is unreliable | #Pulse oximetry is unreliable | ||
##CoHb registers the same as O2Hb so will have artificially high SpO2 | ##CoHb registers the same as O2Hb so will have artificially high SpO2 | ||
##O2 saturation gap reflects discordance of SpO2 by pulse oximeter vs by VBG | ##O2 saturation gap reflects discordance of SpO2 by pulse oximeter vs by VBG | ||
==Treatment== | == Treatment == | ||
#O2 100% by NRB or ETT | |||
##Provide O2 until COHb value | #O2 100% by NRB or ETT | ||
#Hyperbaric Therapy (HBO) | ##Provide O2 until COHb value <10% | ||
##Decision to initiate HBO should be made in consultation w/ hyperbaric specialist | #Hyperbaric Therapy (HBO) | ||
##Controversial who exactly benefits from tx | ##Decision to initiate HBO should be made in consultation w/ hyperbaric specialist | ||
##Pt must be stable prior to transport | ##Controversial who exactly benefits from tx | ||
##Indications (generally accepted guidelines): | ##Pt must be stable prior to transport | ||
###Syncope | ##Indications (generally accepted guidelines): | ||
###Confusion/AMS | ###Syncope | ||
###Seizure | ###Confusion/AMS | ||
###Coma | ###Seizure | ||
###Focal neuro deficit | ###Coma | ||
###Pregnancy w/ CoHb level | ###Focal neuro deficit | ||
###Blood level | ###Pregnancy w/ CoHb level >15% | ||
###Blood level >25% | |||
###Acute myocardial ischemia | ###Acute myocardial ischemia | ||
==Disposition== | == Disposition == | ||
#Minimal or no symptoms | |||
##Discharge | #Minimal or no symptoms | ||
#Mildly symptomatic | ##Discharge | ||
##Headache, vomiting, elevated COHb level | #Mildly symptomatic | ||
##Discharge after 4hr obs and symptom resolution | ##Headache, vomiting, elevated COHb level | ||
#Severely symptomatic | ##Discharge after 4hr obs and symptom resolution | ||
##Ataxia, syncope, chest pain, neuro deficit, dyspnea, ECG changes, pregnant w/ COHb | #Severely symptomatic | ||
##Ataxia, syncope, chest pain, neuro deficit, dyspnea, ECG changes, pregnant w/ COHb >15% | |||
##Admit; discuss with hyperbaric specialist | ##Admit; discuss with hyperbaric specialist | ||
==Source== | == Source == | ||
Tintinalli | |||
Tintinalli | |||
[[Category:Tox]] | [[Category:Tox]] | ||
Revision as of 23:35, 21 April 2012
Background
- Colorless, odorless gas
- Most toxic component in smoke inhalation and major contributor to fire-related deaths
- Can co-occur with Cyanide toxicity in industrial fires
- Sources
- Automotive exhaust
- Propane-fueled heaters
- Wood or coal-burning heaters
- Structure fires
- Gasoline-powered motors
- Natural gas-powered heaters
- Peak incidence in winter months
Pathophysiology
- Hypoxia
- Binding affinity of Hb for CO (carboxyhemoglobin) is 200x that of O2
- Half-Life
- Room air: ~5hrs
- 100% O2: ~1hr
- HBO 2.5atm: 24min
- Lactic acidosis
- CO inhibits oxidative phosphorylation
- Hypotension
- CO induces NO2 and guanylate cyclase release --> vasodilation release
Workup
- VBG
- Co-oximetry analysis will provide carboxyhemoglobin level
- Lactate
- Chemistry
- Troponin
- Total CK (rhabdo)
- ECG
- May range from normal to STEMI (most common ST, then prolonged QT)
- Few of the pts w/ AMI from CO have occlusive lesions in their arteries
- May range from normal to STEMI (most common ST, then prolonged QT)
- ?Head CT
- May show b/l globus pallidus lesions in severe cases
Clinical Features
- May range from "flu-like" symptoms to coma
- CNS
- Headache
- Visual disturbances
- Confusion
- Ataxia
- Seizure
- Syncope
- Retinal hemorrhage
- Focal neurologic deficit
- GI
- Vomiting
- Pulm
- Dyspnea/tachypnea
- Cardio
- Chest pain
- ECG changes/dysrhythmias
- Derm
- Bullous skin lesions
- Classic finding of cherry red oral mucosa is rarely seen in living pts
Diagnosis
- Must have high clinical suspicion (esp in pts w/ coma, AMS, or anion gap acidosis)
- Comatose pt removed from fire should be assumed to have CO poisoning
- Carboxyhemoglobin Level
- Interpretation must take into account time since exposure and O2 tx
- Normal value in non-smokers is ~1%, normal value in smokers may be up to 10%
- Symptoms and COHb levels do not always correlate well
- Pulse oximetry is unreliable
- CoHb registers the same as O2Hb so will have artificially high SpO2
- O2 saturation gap reflects discordance of SpO2 by pulse oximeter vs by VBG
Treatment
- O2 100% by NRB or ETT
- Provide O2 until COHb value <10%
- Hyperbaric Therapy (HBO)
- Decision to initiate HBO should be made in consultation w/ hyperbaric specialist
- Controversial who exactly benefits from tx
- Pt must be stable prior to transport
- Indications (generally accepted guidelines):
- Syncope
- Confusion/AMS
- Seizure
- Coma
- Focal neuro deficit
- Pregnancy w/ CoHb level >15%
- Blood level >25%
- Acute myocardial ischemia
Disposition
- Minimal or no symptoms
- Discharge
- Mildly symptomatic
- Headache, vomiting, elevated COHb level
- Discharge after 4hr obs and symptom resolution
- Severely symptomatic
- Ataxia, syncope, chest pain, neuro deficit, dyspnea, ECG changes, pregnant w/ COHb >15%
- Admit; discuss with hyperbaric specialist
Source
Tintinalli
