Carbon monoxide toxicity: Difference between revisions
No edit summary
Line 1: Line 1:
==Background==
==Background==
*can co-occur with HCN (cyanide) toxicity in certain fires like industrial fires
*Colorless, odorless gas
**treat HCN with Sodium thiosulfate 12.5grams
*Effects:
*multiple pts from same building/car
**Hypoxia
*winter months
***Binding affinity of Hb for CO (carboxyhemoglobin) is 200x that of O2
**Lactic acidosis
***CO inhibits oxidative phosphorylation
**Hypotension
***CO induces NO2 and guanylate cyclase release --> vasodilation release
*Half-Life
**Room air: ~5hrs
**100% O2: ~1hr
**HBO 2.5atm: 24min
 
 
*Most toxic component in smoke inhalation and major contributor to fire-related deaths
*Can co-occur with cyanide toxicity in industrial fires
**See [[Cyanide]]
*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
 
 
The combination of relative hypoxia and hypotension can cause ischemia-reperfusion injury in cardiac myocytes, as well as neuronal tissue. The damaged endothelium will attract neutrophils and trigger an inflammatory cascade resulting in lipid peroxidation and, ultimately, neuronal cell death. This complex intracellular process explains many of the clinical effects of carbon monoxide.8 Rhabdomyolysis, acute myocardial infarction, and neuronal cell death are a result of this cellular toxicity. Cells in the basal ganglia are particularly sensitive to this neurotoxic effect, demonstrated by the globus pallidus lesions sometimes seen on cranial CT imaging.
 


===Half-Life===
*decreases from 5 hrs to 1 hr with 100% FiO2,
**to 20 min 2.5 atm HBO.


==Workup==
==Workup==
#VBG
##Co-oximetry analysis will provide carboxyhemoglobin level
#Lactate
#Chemistry
#Troponin
#Total CK
#ECG
#ECG
#CXR
##May range from normal to STEMI
#CT Head
###Few of the pts w/ AMI from CO have occlusive lesions in their arteries
#Pregnancy test
#?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==
==Diagnosis==
# Symptoms generally depend on CO level (i.e. carboxyhemoglobin)
#Must have high clinical suspicion (esp in pts w/ coma, AMS, or anion gap acidosis)
##20-40%
##Comatose pt removed from fire should be assumed to have CO poisoning
###CNS SX first... Dizziness, Headache, weakness, n/v, disturbed judgment, confusion, decreased visual acuity (Often misdiagnosed as 'Flu', 'viral syndrome.)
#Carboxyhemoglobin Level
##40-60%:
##Interpretation must take into account time since exposure and O2 tx
###CP, DOE, Tachycardia, tachypnea, ataxia, syncope, seizures
##Normal value in non-smokers is ~1%, normal value in smokers may be up to 10%
##>60%
##Symptoms and COHb levels do not always correlate well
###arrhythmias, hypotension, coma, death
#Pulse oximetry is unreliable
# To get CO level, ABG with carboxyhemoglobin level (this needs to be specifically requested; done by co-oximetry)
##CoHb registers the same as O2Hb so will have artificially high SpO2
##Pulse Ox usually NORMAL.
##O2 saturation gap reflects discordance of SpO2 by pulse oximeter vs by VBG
##Need co-oximetry. Oxygen Sat gap, SpO2-SaO2 increases as COHb increases.
##mortality usually due to ventricular arrhythmias.


==Treatment==
==Treatment==
# Treat with 100% oxygen by tight-fitting mask or endotracheal tube
#O2 100% by NRB or ETT
# Measure CO level q2-4 hours until <10%
##Provide O2 until COHb value <10%
##smokers... COHb level up to 10%
#Hyperbaric Therapy (HBO)
##<5% is normal
##Decision to initiate HBO should be made in consultation w/ hyperbaric specialist
##levels not predictive of outcome
##Controversial who exactly benefits from tx
##lactate more useful for inferring tissue hypoxia
##Pt must be stable prior to transport
 
##Indications (generally accepted guidelines):
==Hyperbaric Tx^==
###Syncope
===Indications===
###Confusion/AMS
#sz, coma, focal deficit
###Seizure
#COHb > 25%
###Coma
#COHb > 15% in pregnancy (fetal Hb has greater affinity for CO, and nml intrauterine Mt Everest makes CO poisoning very toxic to fetus)
###Focal neuro deficit
#myocardial ischemia, arrhythmias
###Pregnancy w/ CoHb level >15%
###Blood level >25%
###Acute myocardial ischemia


^Hyperbaric treatment is of contraversial utility (3 days of 100% FiO2 may be equivalent to hyperbaric)
==Disposition==
==Disposition==
===Admit===
#Minimal or no symptoms
#all symptomatic CO poisonings
##Discharge
#all > 20%
#Mildly symptomatic
 
##Headache, vomiting, elevated COHb level
Gas company and Fire Dept will test home/work environments.
##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==
==Source==
Tibbles, PM et al. NEJM. Hyperbaric oxygen Rx. 1996.
Tintinalli
 
Scheinkestel, C. Med J Aust. 1999. 170: 2203-2210.


[[Category:Pulm]]
[[Category:Tox]]
[[Category:Tox]]

Revision as of 01:21, 22 September 2011

Background

  • Colorless, odorless gas
  • Effects:
    • Hypoxia
      • Binding affinity of Hb for CO (carboxyhemoglobin) is 200x that of O2
    • Lactic acidosis
      • CO inhibits oxidative phosphorylation
    • Hypotension
      • CO induces NO2 and guanylate cyclase release --> vasodilation release
  • Half-Life
    • Room air: ~5hrs
    • 100% O2: ~1hr
    • HBO 2.5atm: 24min


  • 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


The combination of relative hypoxia and hypotension can cause ischemia-reperfusion injury in cardiac myocytes, as well as neuronal tissue. The damaged endothelium will attract neutrophils and trigger an inflammatory cascade resulting in lipid peroxidation and, ultimately, neuronal cell death. This complex intracellular process explains many of the clinical effects of carbon monoxide.8 Rhabdomyolysis, acute myocardial infarction, and neuronal cell death are a result of this cellular toxicity. Cells in the basal ganglia are particularly sensitive to this neurotoxic effect, demonstrated by the globus pallidus lesions sometimes seen on cranial CT imaging.


Workup

  1. VBG
    1. Co-oximetry analysis will provide carboxyhemoglobin level
  2. Lactate
  3. Chemistry
  4. Troponin
  5. Total CK
  6. ECG
    1. May range from normal to STEMI
      1. Few of the pts w/ AMI from CO have occlusive lesions in their arteries
  7. ?Head CT
    1. May show b/l globus pallidus lesions in severe cases

Clinical Features

  1. May range from "flu-like" symptoms to coma
  2. CNS
    1. Headache
    2. Visual disturbances
    3. Confusion
    4. Ataxia
    5. Seizure
    6. Syncope
    7. Retinal hemorrhage
    8. Focal neurologic deficit
  3. GI
    1. Vomiting
  4. Pulm
    1. Dyspnea/tachypnea
  5. Cardio
    1. Chest pain
    2. ECG changes/dysrhythmias
  6. Derm
    1. Bullous skin lesions
    2. Classic finding of cherry red oral mucosa is rarely seen in living pts

Diagnosis

  1. Must have high clinical suspicion (esp in pts w/ coma, AMS, or anion gap acidosis)
    1. Comatose pt removed from fire should be assumed to have CO poisoning
  2. Carboxyhemoglobin Level
    1. Interpretation must take into account time since exposure and O2 tx
    2. Normal value in non-smokers is ~1%, normal value in smokers may be up to 10%
    3. Symptoms and COHb levels do not always correlate well
  3. Pulse oximetry is unreliable
    1. CoHb registers the same as O2Hb so will have artificially high SpO2
    2. O2 saturation gap reflects discordance of SpO2 by pulse oximeter vs by VBG

Treatment

  1. O2 100% by NRB or ETT
    1. Provide O2 until COHb value <10%
  2. Hyperbaric Therapy (HBO)
    1. Decision to initiate HBO should be made in consultation w/ hyperbaric specialist
    2. Controversial who exactly benefits from tx
    3. Pt must be stable prior to transport
    4. Indications (generally accepted guidelines):
      1. Syncope
      2. Confusion/AMS
      3. Seizure
      4. Coma
      5. Focal neuro deficit
      6. Pregnancy w/ CoHb level >15%
      7. Blood level >25%
      8. Acute myocardial ischemia

Disposition

  1. Minimal or no symptoms
    1. Discharge
  2. Mildly symptomatic
    1. Headache, vomiting, elevated COHb level
    2. Discharge after 4hr obs and symptom resolution
  3. Severely symptomatic
    1. Ataxia, syncope, chest pain, neuro deficit, dyspnea, ECG changes, pregnant w/ COHb >15%
    2. Admit; discuss with hyperbaric specialist

Source

Tintinalli

Retrieved from "https://www.wikem.org/w/index.php?title=Carbon_monoxide_toxicity&oldid=5816"