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Phosgene - Prehospital Management

Acute Management Overview

Agent Identification

  • Phosgene is colorless, fuming liquid below 47°F (8.2°C) and a colorless, nonflammable gas above 47°F with a suffocating odor like new mown hay. The odor threshold for phosgene is significantly higher than current inhalation exposure limits. Thus, odor provides insufficient warning of hazardous concentrations.
  • Responders should obtain assistance in identifying the chemical(s) from container shapes, placards, labels, shipping papers, and analytical tests. General information on these identification technicques is located in Emergency Response Guidebook.
  • Identification Tools - CHEMM-IST, WISER, Phosgene Chemical Properties
  • Devices - Chemical Agent Detector C2 Kit (liquid and vapor), M256A1 chemical agent detector kit (liquid and vapor), M18A3, M90 chemical agent detectors (vapor), Draeger CDS Kit (vapor and aerosol)
  • A comprehensive source for the selection of chemical identification equipment is the Guide for the Selection of Chemical Detection Equipment for Emergency First Responders, Guide 100-06, January 2007, 3rd Edition published by the Department of Homeland Security to assist with this process.

Rescuer Protection

Phosgene Specific Triage

  • Immediate irritant effects such as conjunctivitis, rhinitis, pharyngitis, bronchitis, lacrimation, blepharospasm conjunctival hyperemia, and upper respiratory tract irritation may occur after exposure to concentrations of 3 to 5 ppm.
  • Severe pulmonary toxicity may develop after exposure to higher concentrations or following exposures for longer periods of time.
  • A phosgene casualty who develops respiratory distress within 4 hours of exposure has probably inhaled an LD50 dose and is at severe risk if not properly supported.
  • Signs and symptoms of toxicity may be delayed, although rare, for 24 to 72 hours and include choking, chest tightness, cough, severe dyspnea, production of foaming bloody sputum, and pulmonary edema. Non-respiratory symptoms include nausea and anxiety. Cardiac failure has occasionally occurred as a complication of severe pulmonary edema. Concentration-response guidelines include:
  • Victims with inhalation doses of < 25 ppm/min and without clinical signs and symptoms require no immediate medical attention. Exposure to a cumulative dose of 50 ppm x minutes may cause pulmonary edema; a dose of 150 ppm x min will probably cause pulmonary edema and a dose of 300 ppm x min is likely to be fatal.
  • Brief exposure to 500 ppm or greater may be rapidly fatal. Prolonged exposure to low concentrations (e.g. 3 ppm for 170 min) can also be fatal. Exposure to concentrations less than 3 ppm may not be immediately accompanied by irritant symptoms; delayed effects usually occur within 24 hrs of exposure.
  • Victims with unknown phosgene exposure must be closely observed.

Decontamination

  • Victims exposed only to phosgene gas that have no evidence of skin or eye irritation may be transferred immediately to the Support Zone as they do not pose substantial risks of secondary contamination to personnel outside the Hot/Warm Zones.
  • Victims whose clothing or skin is contaminated with liquid phosgene (ambient temperature below 47°F) can secondarily contaminate response personnel through direct contact or off-gassing vapor and will require decontamination.
  • Link to prehospital management section

Route of Exposure

  • Inhalation - Inhalation is the major route of phosgene exposure. Phosgene's effects as a respiratory irritant can be mild and delayed, which may result in a lack of immediate avoidance leading to exposure for prolonged periods. Phosgene is heavier than air and may cause asphyxiation due to oxygen displacement in poorly ventilated, low-lying, or enclosed spaces.
  • Skin/Eye Contact - When phosgene gas contacts moist or wet skin, it may cause irritation and erythema. High airborne concentrations can also cause corneal inflammation and opacification. Direct contact with liquid phosgene under pressure can cause frostbite as well as severe irritation and corrosive effects.
  • Ingestion - Ingestion of phosgene is unlikely because it is a gas at room temperature.

Clinical Signs and Symptoms

  • Inhaling low concentrations may cause no signs or symptoms initially, or cause symptoms that are secondary to mild irritation of the eyes and throat - some coughing, choking, feeling of tightness in the chest, nausea and occasional vomiting, headache, and lacrimation.
  • Respiratory - after an asymptomatic period for 30 minutes to 48 hours, in those developing severe pulmonary damage, a progressive pulmonary edema ensues with increasing work of breathing and subsequent hypoxia.
  • Cardiovascular - circulatory collapse secondary to severe pulmonary edema.
  • Dermal - phosgene can cause skin irritation and with sufficient concentration can cause, burning pain, inflammation, and blisters. Liquefied phosgene can cause frostbite injury.
  • Ocular - high vapor concentration can cause tearing and blood in the eye. Contact with liquid phosgene may result in clouding of the cornea and delayed perforation.
  • Link to Toxic Syndromes
  • Link to Primary and Secondary Survey

Differential Diagnosis

  • Since phosgene is a respiratory tract irritant, but has unique toxicological concerns due to the latency for onset of pulmonary edema, differentiating it from the typical presentation of symptoms from other common chemical irritants is an important consideration.
  • Phosgene is distinguished by its smell in high concentrations and delayed onset of pulmonary edema.
  • Chlorine has a characteristic odor even in low concentrations, immediate onset of respiratory distress, bronchospasm, eye, skin, and upper airway irritation.
  • Riot agents cause an acute onset of burning sensation in the eyes and upper airway without progression of symptoms with ongoing exposures.
  • Nerve agents induce watery secretions as well as respiratory distress, but have a host of other symptoms, such as miosis, seizures, rapidity of onset, that can distinguish them from pulmonary agents.
  • The respiratory toxicity of vesicants (i.e. Mustard Gas) is usually delayed, but affects the central rather than the peripheral airway. Vesicant toxicity severe enough to cause dyspnea typically causes airway necrosis often with upper airway obstruction.
  • Link to Chemical Hazards Emergency Medical Management Intelligent Syndromes Tool (CHEMM-IST)

Treatment

Acute Patient Care Guidelines References