Phosgene Inhalation Injury

Phosgene (carbonyl chloride, COCl2) is a colourless gas with a smell of freshly cut hay at low concentrations, used in the manufacture of plastics, polyurethane foams, pesticides and dyes, and generated when chlorinated solvents (dichloromethane, trichloroethylene, carbon tetrachloride) are heated or burned, for example in welding degreasing solvents or fires. It was a World War I chemical weapon.

Phosgene is poorly water soluble, so it causes little upper airway irritation and gives no warning. It reaches the alveoli, where it acylates proteins, lipids and amino groups, and hydrolyses to hydrochloric acid, damaging the blood gas barrier.

After a latent period of 2 to 24 hours (shorter with higher dose), non-cardiogenic pulmonary oedema develops.

The dose product (concentration times minutes) predicts outcome: 3 ppm is irritant, 25 ppm for 30 minutes is lethal. Mild exposure recovers completely; severe cases die of respiratory failure within 48 hours.

• At exposure: mild eye, nose and throat irritation, cough, chest tightness, nausea, headache; often minimal.
• Latent period: symptom free for 2 to 24 hours; shorter latency means worse prognosis (under 4 hours indicates severe exposure).
• Pulmonary oedema phase: progressive dyspnoea, cough with frothy sputum, cyanosis, tachypnoea, crackles, hypotension from intravascular volume depletion, haemoconcentration.
• Late: ARDS, secondary infection, bronchiolitis obliterans.
• Red flags: dyspnoea within 4 hours, frothy sputum, SpO2 below 92 percent, haemoconcentration.

• Exposure history, even if the patient feels well; identify solvent fires or chemical leaks.
• Baseline chest radiograph, repeated at 6 and 24 hours: early signs include Kerley lines, peribronchial cuffing, then bilateral alveolar opacities.
• Arterial blood gas: hypoxaemia, respiratory alkalosis followed by acidosis; PaO2/FiO2 ratio.
• Full blood count: haemoconcentration (haematocrit over 55 percent) and leucocytosis indicate severity.
• Spirometry: FEV1 and FVC reduction; baseline for follow up.
• No rapid laboratory test confirms phosgene; do not delay treatment.
• Exclude cardiogenic oedema, other irritant gases (chlorine, nitrogen dioxide, hydrogen chloride), carbon monoxide, and infection.

• Remove from the source and decontaminate (clothing removed; wash skin and flush eyes with water); rescuers use self-contained breathing apparatus.
• Absolute rest for at least 24 hours regardless of symptoms; exertion shortens the latent period and worsens oedema. Observe all exposed people for at least 24 hours when exposure was above the irritant threshold, and for 48 hours if exposure was heavy.
• Oxygen: humidified, titrated to SpO2 94 percent or more; CPAP 5 to 10 cmH2O or positive end expiratory pressure ventilation for pulmonary oedema.
• Bronchospasm: salbutamol 2.5 to 5 mg nebulised every 4 hours as needed.
• Corticosteroid: methylprednisolone 1 mg/kg intravenously once daily for 3 days at the first sign of exposure or oedema, then a short oral taper over 7 days; or inhaled beclometasone 1 mg (4 puffs of 250 micrograms) every 6 hours for 3 days started early. Treatment is directed at lowering inflammatory injury; evidence is from case series.
• Nebulised sodium bicarbonate 3.75 percent, 4 mL every 4 hours for 24 hours, may be used for lower airway irritation if SpO2 and airway protection permit.
• Pulmonary oedema or ARDS: intubation, lung protective ventilation with tidal volume 6 mL/kg predicted body weight, PEEP 8 to 12 cmH2O, plateau pressure 30 cmH2O or less; restrictive fluid approach once perfusion is restored, but correct intravascular depletion with 250 mL crystalloid boluses guided by perfusion.
• Antibiotics only for proven infection.
• Follow up: spirometry and chest radiograph at 4 weeks and 3 months; bronchiolitis obliterans if exertional dyspnoea persists (CT with expiratory images).
• Prevention: closed systems, gas monitors, no heating or welding near chlorinated solvents, and emergency plans.