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 | |||
**Can co-occur with [[Cyanide]] toxicity in industrial fires | |||
*Peak incidence in winter months | |||
===Sources=== | |||
*Automotive exhaust | |||
*Propane-fueled heaters | |||
*Wood or coal-burning heaters | |||
*Structure fires | |||
*Gasoline-powered motors | |||
*Natural gas-powered heaters | |||
== Pathophysiology == | === 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 == | ||
*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 | |||
*?Head CT | |||
**May show b/l globus pallidus lesions in severe cases | |||
== Clinical Features == | == Clinical Features == | ||
*May range from "flu-like" symptoms to coma | |||
*CNS | |||
**[[Headache]] | |||
**Visual disturbances | |||
**Confusion | |||
**Ataxia | |||
**[[Seizure]] | |||
**[[Syncope]] | |||
**[[Retinal hemorrhage]] | |||
**Focal neurologic deficit | |||
*CNS as a function of COHb % | |||
**10-20% - confusion and agitation 2/2 mild hypoxia | |||
**20-30% - progressive obtundation and nausea | |||
**> 40% - almost always unconscious | |||
**> 60% - survival is very rare | |||
*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 | |||
***More likely seen in > 25% COHb levels | |||
== 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 | |||
*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 == | == Treatment == | ||
*If smoke inhalation, good pulmonary toilet is very important | |||
*'''NEVER''' use steroids in smoke inhalation injury; intubate early if concern for obstructing edema | |||
*O2 100% by NRB or ETT | |||
**Provide O2 until COHb value <10% | |||
**Early PEEP prevents progressive atelectasis and improves O2 diffusion | |||
**In general, COHb levels fall rapidly to < 10% within 30 min of 100% O2 | |||
**Maintain 100% O2 for additional 2-3 hrs after < 10%, since anaerobic metabolism is occuring due to cytochrome oxidase poisoning<ref>MetroHealth Medical Center Burn ICU Handbook (Not a policy manual), Cleveland, OH</ref> | |||
***Anaerobic metabolism universally seen with COHb > 40% | |||
***Monitor for return of aerobic metabolism with normal serum bicarbonate levels | |||
===Hyperbaric Therapy (HBO)=== | ===Hyperbaric Therapy (HBO)=== | ||
*Decision to initiate HBO should be made in consultation w/ hyperbaric specialist | |||
*Controversial Outcomes regarding benefit<ref>http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1116883/pdf/1083.pdf</ref> | |||
**Three HBO treatments within 24hrs reduced risk of cognitive sequelae 6 weeks and 12 months after CO poisoning<ref>Weaver, L. et al. Hyperbaric Oxygen For Acute Carbon Monoxide Poisoning. NEJM. 2002:347(14):1057 http://emed.wustl.edu/Portals/2/Answer%20Key%20PDF/2012/January2012/SecondYear.pdf</ref> | |||
**While an Australian study showed not benefit and suggested worse outcomes in HBO therapy<ref> Scheinkestel C. et al. Med J Aust 1999; 170 (5): 203-210. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial http://www.mja.com.au/journal/1999/170/5/hyperbaric-or-normobaric-oxygen-acute-carbon-monoxide-poisoning-randomised</ref> | |||
*Pt must be stable prior to transport since response to acute medical conditions while undergoing hyperbaric therapy in a chamber is difficult. | |||
*Indications (generally accepted guidelines): | |||
**Syncope | |||
**Confusion/AMS | |||
**Seizure | |||
**Coma | |||
**Focal neuro deficit | |||
**Pregnancy w/ CoHb level >15% | |||
**Blood level >25% | |||
**Acute myocardial ischemia | |||
== Disposition == | == 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 | |||
^Note: if discharging patient- may need to alert local fire/police services to evaluate home/work before they return. Check with your local branch. | |||
== Source == | == Source == | ||
Revision as of 21:25, 11 January 2015
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
- Peak incidence in winter months
Sources
- Automotive exhaust
- Propane-fueled heaters
- Wood or coal-burning heaters
- Structure fires
- Gasoline-powered motors
- Natural gas-powered heaters
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
- CNS as a function of COHb %
- 10-20% - confusion and agitation 2/2 mild hypoxia
- 20-30% - progressive obtundation and nausea
- > 40% - almost always unconscious
- > 60% - survival is very rare
- 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
- More likely seen in > 25% COHb levels
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
- If smoke inhalation, good pulmonary toilet is very important
- NEVER use steroids in smoke inhalation injury; intubate early if concern for obstructing edema
- O2 100% by NRB or ETT
- Provide O2 until COHb value <10%
- Early PEEP prevents progressive atelectasis and improves O2 diffusion
- In general, COHb levels fall rapidly to < 10% within 30 min of 100% O2
- Maintain 100% O2 for additional 2-3 hrs after < 10%, since anaerobic metabolism is occuring due to cytochrome oxidase poisoning[1]
- Anaerobic metabolism universally seen with COHb > 40%
- Monitor for return of aerobic metabolism with normal serum bicarbonate levels
Hyperbaric Therapy (HBO)
- Decision to initiate HBO should be made in consultation w/ hyperbaric specialist
- Controversial Outcomes regarding benefit[2]
- Pt must be stable prior to transport since response to acute medical conditions while undergoing hyperbaric therapy in a chamber is difficult.
- 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
^Note: if discharging patient- may need to alert local fire/police services to evaluate home/work before they return. Check with your local branch.
Source
- ↑ MetroHealth Medical Center Burn ICU Handbook (Not a policy manual), Cleveland, OH
- ↑ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1116883/pdf/1083.pdf
- ↑ Weaver, L. et al. Hyperbaric Oxygen For Acute Carbon Monoxide Poisoning. NEJM. 2002:347(14):1057 http://emed.wustl.edu/Portals/2/Answer%20Key%20PDF/2012/January2012/SecondYear.pdf
- ↑ Scheinkestel C. et al. Med J Aust 1999; 170 (5): 203-210. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial http://www.mja.com.au/journal/1999/170/5/hyperbaric-or-normobaric-oxygen-acute-carbon-monoxide-poisoning-randomised