Phosgene: Difference between revisions

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''Not to be confused with [[phosgene oxime]] (CX)''
''Not to be confused with [[phosgene oxime]] (CX)''
==Background==
==Background==
[[File:Phosgene poster ww2.jpg|thumb]]
[[File:Phosgene poster ww2.jpg|thumb]]
* phosgene (COCl2) is a highly toxic, colorless gas or liquid
*Phosgene (carbonyl chloride), chemical formula COCl2, is a colorless gas (at low temperatures, can also exist as a liquid)
*Classified as a [[pulmonary chemical agent]]
*Classically described as having odor of freshly cut hay
* gained infamy in WWI - responsible for 85% of deaths due to chemical weapons
*Used as a chemical weapon, and accounted for 80% of deaths from poison gas in WWI<ref name="Hardison">Hardison LS, Wright E, Pizon AF. Phosgene Exposure: A Case of Accidental Industrial Exposure. Journal of Medical Toxicology. 2014;10(1):51-56. doi:10.1007/s13181-013-0319-6.</ref>
* pulmonary irritant
*Currently most frequently used in the industrial setting
* major complication is non-cardiogenic pulmonary edema
**Used in the manufacture of plastics, dyes, pharmaceuticals and pesticides<ref name="Gutch">Gutch M, Jain N, Agrawal A, Consul S. Acute accidental phosgene poisoning. BMJ Case Reports. 2012;2012:bcr1120115233. doi:10.1136/bcr.11.2011.5233</ref>
* used in chemical reactions - large scale exposures usually 2/2 industrial accidents
*Heavier than air → stays close to ground
** manufacturers of dyes, resins, coal tar, pesticides
*Denser than air, settles in low-lying places – trenches/basements
*Rapid olfactory fatigue can occur leading to prolonged exposure
*Exposure may be secondary to fire at textile factory/house, metalwork, or burning Freon


===Pathophysiology===
===Pathophysiology===
* acrylation reaction with amino, hydroxyl, and sulfhydryl goups
*Hydrolysis = phosgene reacts with water in the lungs to form hydrochloric acid
* membrane structural changes, protein denaturation, depletion of glutathione
**Likely not clinically significant<ref name="Hardison" />
* increased vascular permeability leads to noncardiogenic pulmonary edema
*Acylation = causes oxidative damage and depletes glutathione<ref name="Hardison" />
**Damages alveolar membrane, increases vascular permeability
**Leads to noncardiogenic pulmonary edema


==Clinical Features==
==Clinical Features==
* some people may note a smell of freshly cut hay or grass
*Due to lower water solubility than other irritant gases (e.g. Chlorine gas), phosgene causes less immediate irritation of the mucous membranes and therefore is able to penetrate to and damage the lower respiratory tract
* eye and throat symptoms may occur at very low concentrations
*Immediate effects (depends on concentration) - mucous membrane irritation, tachypnea, shallow breathing
* unpredictable latent phase
**At low concentrations, no immediate symptoms may be noted<ref name="Hardison" />
* development of noncardiogenic pulmonary edema
*Latent phase length is inversely proportional to inhaled dose<ref name="Gutch" />
*Symptoms may take 2-24 hours to develop
*Delayed effects (depends on total inhaled dose) - respiratory distress, cough, and finally pulmonary edema
 
**May take hours to develop
===Symptoms by Concentration===
*Low: mild cough, chest tightness, shortness of breath
*Moderate: Lacrimation
*High: Non-cardiogenic [[pulmonary edema]] within 2 to 6 hours after exposure with death within 24-48 hours


==Differential Diagnosis==
==Differential Diagnosis==
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==Evaluation==
==Evaluation==
* high index of suspicion, ask about work history/exposures
*No specific test for exposure - workup should be based on history and sypmtoms. Consider:
* no combination of labs/xrays can predict whether pt will develop pulmonary edema
**Laboratory studies (e.g. CBC, CMP, lactate)
* latent phase can be 30 min - 72hrs but significant exposures usually developed pulmonary symptoms within 24 hrs
**Chest X-ray
**ABG


==Management==
==Management==
* supportive care
*Supportive care is the mainstay of treatment (no specific antidote exists)
* with [[pulmonary edema]] patients may require [[intubation]] with high PEEP
*Use supplemental oxygen only as needed, and then at low concentrations to avoid reactive oxygen species formation<ref name="Hardison" />
* [[albuterol]] for bronchospasm
*If intubation required, use ARDS lung-protective strategies
* [[steroid]]s recommended but no solid evidence for efficacy
 
* no specific antidote exists
===Specific treatment options<ref name="Hardison" />===
''Note: Evidence is lacking, and generally based on case reports and expert opinion - consultation with local [[poison control]] is recommended''
*Corticosteroids
*N-acetylcysteine (IV or nebulized)
*NSAIDS (e.g. Ibuprofen, Colchicine)
*Terbutaline
*Nebulized albuterol


==Disposition==
==Disposition==
*Admit


==See Also==
==See Also==

Latest revision as of 01:59, 13 August 2018

Not to be confused with phosgene oxime (CX)

Background

Phosgene poster ww2.jpg
  • Phosgene (carbonyl chloride), chemical formula COCl2, is a colorless gas (at low temperatures, can also exist as a liquid)
  • Classically described as having odor of freshly cut hay
  • Used as a chemical weapon, and accounted for 80% of deaths from poison gas in WWI[1]
  • Currently most frequently used in the industrial setting
    • Used in the manufacture of plastics, dyes, pharmaceuticals and pesticides[2]
  • Heavier than air → stays close to ground

Pathophysiology

  • Hydrolysis = phosgene reacts with water in the lungs to form hydrochloric acid
    • Likely not clinically significant[1]
  • Acylation = causes oxidative damage and depletes glutathione[1]
    • Damages alveolar membrane, increases vascular permeability
    • Leads to noncardiogenic pulmonary edema

Clinical Features

  • Due to lower water solubility than other irritant gases (e.g. Chlorine gas), phosgene causes less immediate irritation of the mucous membranes and therefore is able to penetrate to and damage the lower respiratory tract
  • Immediate effects (depends on concentration) - mucous membrane irritation, tachypnea, shallow breathing
    • At low concentrations, no immediate symptoms may be noted[1]
  • Latent phase length is inversely proportional to inhaled dose[2]
  • Delayed effects (depends on total inhaled dose) - respiratory distress, cough, and finally pulmonary edema
    • May take hours to develop

Differential Diagnosis

Chemical weapons

Evaluation

  • No specific test for exposure - workup should be based on history and sypmtoms. Consider:
    • Laboratory studies (e.g. CBC, CMP, lactate)
    • Chest X-ray
    • ABG

Management

  • Supportive care is the mainstay of treatment (no specific antidote exists)
  • Use supplemental oxygen only as needed, and then at low concentrations to avoid reactive oxygen species formation[1]
  • If intubation required, use ARDS lung-protective strategies

Specific treatment options[1]

Note: Evidence is lacking, and generally based on case reports and expert opinion - consultation with local poison control is recommended

  • Corticosteroids
  • N-acetylcysteine (IV or nebulized)
  • NSAIDS (e.g. Ibuprofen, Colchicine)
  • Terbutaline
  • Nebulized albuterol

Disposition

  • Admit

See Also

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Hardison LS, Wright E, Pizon AF. Phosgene Exposure: A Case of Accidental Industrial Exposure. Journal of Medical Toxicology. 2014;10(1):51-56. doi:10.1007/s13181-013-0319-6.
  2. ↑ 2.0 2.1 Gutch M, Jain N, Agrawal A, Consul S. Acute accidental phosgene poisoning. BMJ Case Reports. 2012;2012:bcr1120115233. doi:10.1136/bcr.11.2011.5233
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