Carbon monoxide toxicity: Difference between revisions

No edit summary
No edit summary
Line 1: Line 1:
==Background==
==Background==
*Colorless, odorless gas
#Colorless, odorless gas
*Effects:
#Most toxic component in smoke inhalation and major contributor to fire-related deaths
**Hypoxia
##Can co-occur with [[Cyanide]] toxicity in industrial fires
***Binding affinity of Hb for CO (carboxyhemoglobin) is 200x that of O2
#Sources
**Lactic acidosis
##Automotive exhaust
***CO inhibits oxidative phosphorylation
##Propane-fueled heaters
**Hypotension
##Wood or coal-burning heaters
***CO induces NO2 and guanylate cyclase release --> vasodilation release
##Structure fires
*Half-Life
##Gasoline-powered motors
**Room air: ~5hrs
##Natural gas-powered heaters
**100% O2: ~1hr
#Peak incidence in winter months
**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.
 


==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==
==Workup==
Line 37: Line 30:
#Chemistry
#Chemistry
#Troponin
#Troponin
#Total CK
#Total CK (rhabdo)
#ECG
#ECG
##May range from normal to STEMI
##May range from normal to STEMI

Revision as of 01:25, 22 September 2011

Background

  1. Colorless, odorless gas
  2. Most toxic component in smoke inhalation and major contributor to fire-related deaths
    1. Can co-occur with Cyanide toxicity in industrial fires
  3. Sources
    1. Automotive exhaust
    2. Propane-fueled heaters
    3. Wood or coal-burning heaters
    4. Structure fires
    5. Gasoline-powered motors
    6. Natural gas-powered heaters
  4. Peak incidence in winter months

Pathophysiology

  1. Hypoxia
    1. Binding affinity of Hb for CO (carboxyhemoglobin) is 200x that of O2
    2. Half-Life
      1. Room air: ~5hrs
      2. 100% O2: ~1hr
      3. HBO 2.5atm: 24min
  2. Lactic acidosis
    1. CO inhibits oxidative phosphorylation
  3. Hypotension
    1. CO induces NO2 and guanylate cyclase release --> vasodilation release

Workup

  1. VBG
    1. Co-oximetry analysis will provide carboxyhemoglobin level
  2. Lactate
  3. Chemistry
  4. Troponin
  5. Total CK (rhabdo)
  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=5817"