Chlorine Gas Inhalation Injury

Chlorine is a yellow green gas denser than air, with a pungent odour. It reacts with water in mucous membranes to form hydrochloric and hypochlorous acids, producing oxidant injury and liquefactive necrosis of the airway epithelium. Exposure arises from swimming pool maintenance accidents, mixing bleach with acid or ammonia containing cleaners, water treatment plant leaks, industrial release and transport accidents, and chemical attack.

Injury depends on concentration and duration: 1 to 3 parts per million causes mucosal irritation, 15 to 20 ppm causes airway oedema and lower respiratory injury, 430 ppm is lethal within 30 minutes, and 1000 ppm kills within minutes. The water solubility of chlorine is intermediate, so it damages both upper and lower airways. Most survivors recover completely, but a minority develop reactive airways dysfunction syndrome or bronchiolitis obliterans.

• Immediate burning of eyes, nose and throat, lacrimation, cough, choking, chest tightness.
• Dyspnoea, wheeze, stridor, hoarseness, laryngeal oedema.
• Haemoptysis, chest pain, nausea and vomiting.
• Non-cardiogenic pulmonary oedema within 2 to 24 hours with crackles and hypoxaemia.
• Skin and eye burns, corneal injury.
• Severe cases: respiratory failure, hypotension, metabolic acidosis, seizures.
• Red flags: stridor, SpO2 below 92 percent, pink frothy sputum, facial burns.

• Clinical diagnosis based on exposure history and irritant syndrome; concentration estimates are seldom available.
• Pulse oximetry and arterial blood gas for hypoxaemia and acidosis.
• Chest radiograph: normal early; bilateral infiltrates and pulmonary oedema appear after 2 to 12 hours.
• Spirometry: obstructive pattern (FEV1 below 80 percent) in survivors; peak flow tracking.
• Laryngoscopy or bronchoscopy for upper airway oedema, mucosal sloughing.
• Fluorescein eye examination for corneal injury; eye pH after irrigation.
• Exclude other irritant gases (ammonia, phosgene, nitrogen dioxide), asthma exacerbation, cardiogenic pulmonary oedema, and infection.

• Remove from source into fresh air, take off contaminated clothing (this removes most of the residual gas), wash skin with copious water, irrigate eyes with 1 to 2 litres of normal saline until pH is 7.0 to 7.4.
• Rescuers need self-contained breathing apparatus.
• Oxygen: humidified, titrate to SpO2 94 percent or more; continuous positive airway pressure or non-invasive ventilation for early pulmonary oedema.
• Bronchospasm: salbutamol 5 mg nebulised every 20 minutes for 3 doses, then every 1 to 4 hours as needed; add ipratropium 500 micrograms nebulised every 6 hours.
• Nebulised sodium bicarbonate 3.75 percent, 4 mL every 4 hours for 24 hours, can be given for lower airway irritation if available; avoid in patients with unprotected airway.
• Stridor or laryngeal oedema: adrenaline 1 mg/mL, 5 mL nebulised (undiluted), and early intubation when the voice is changing or the airway is narrowing. Dexamethasone 8 to 10 mg intravenously once; inhaled budesonide 800 micrograms every 12 hours for 5 days is used for airway inflammation.
• Pulmonary oedema or ARDS: lung protective ventilation (tidal volume 6 mL/kg predicted body weight, PEEP 8 to 12 cmH2O), conservative fluid strategy.
• Antibiotics only for confirmed infection; avoid routine prophylaxis.
• Observation: at least 6 hours for mild exposure, and 24 hours if any chest symptoms or abnormal radiograph.
• Follow up: spirometry at 4 to 6 weeks and 3 months; persistent symptoms may signal reactive airways dysfunction syndrome or bronchiolitis obliterans (inhaled budesonide formoterol 200/6 micrograms 2 puffs twice daily, review CT).
• Prevention: never mix bleach with acid or ammonia products, store pool chemicals separately, ventilated plant rooms, and emergency plans.