Ammonia Inhalation Injury

Ammonia is a colourless, pungent, highly water soluble alkaline gas that reacts with moisture on mucous membranes to form ammonium hydroxide, causing liquefactive necrosis of tissue and deep penetrating injury. Sources include agricultural fertiliser (anhydrous ammonia), refrigeration plants (cold storage, ice factories), manufacture of explosives and plastics, and household cleaners. Release from storage tanks, mixing of household cleaners, and agricultural injection accidents are the typical scenarios.

Because ammonia is highly soluble, it injures the eyes, nose, oropharynx and upper airway first; the lower airway is spared unless concentrations are high (over 2500 ppm) or exposure is prolonged in an enclosed space. Odour threshold is 5 ppm; 300 ppm is immediately dangerous to life; 5000 ppm is rapidly fatal. Frostbite also occurs from liquefied anhydrous ammonia. Long term sequelae include chronic obstructive airflow limitation, bronchiectasis and corneal opacities.

• Intense burning of eyes, nose, throat, lacrimation, blepharospasm, cough, sneezing.
• Hoarseness, stridor, aphonia, laryngeal and pharyngeal oedema, dysphagia and drooling.
• Wheeze, chest tightness, dyspnoea, haemoptysis, pulmonary oedema 6 to 24 hours later with high concentration.
• Skin: chemical burns, blistering, frostbite from liquefied gas.
• Eye: corneal ulceration, conjunctival ischaemia (white eye), perforation, cataract and glaucoma later.
• Red flags: stridor, voice change, facial burns, eyelid swelling, SpO2 falling, corneal opacity.

• Exposure history and clinical syndrome; no test confirms exposure in time to guide treatment.
• Pulse oximetry, arterial blood gas, and chest radiograph (normal early; infiltrates at 6 to 24 hours).
• Flexible laryngoscopy or bronchoscopy for upper airway oedema, mucosal ulceration and slough.
• Eye: measure surface pH with litmus paper or pH strip (normal 7.0 to 7.4) after irrigation, repeat until neutral; fluorescein staining, slit lamp for depth of injury; check for limbal ischaemia.
• Spirometry in survivors.
• Exclude other irritant gases (chlorine, hydrogen chloride), carbon monoxide co-exposure, and cardiogenic oedema.

• Move to fresh air; remove clothing; rescuers wear self-contained breathing apparatus.
• Eyes and skin: irrigate immediately with water or normal saline, at least 15 to 30 minutes, until pH is 7.0 to 7.4; use a Morgan lens or equivalent; 2 to 4 litres per eye in severe exposure. Do not neutralise with acid.
• Oxygen: humidified 100 percent initially, titrate to SpO2 94 percent or more.
• Airway: early intubation by the most experienced operator for stridor, voice change, or swelling; surgical airway equipment ready. Adrenaline 5 mL of 1 mg/mL nebulised for upper airway oedema; dexamethasone 8 to 10 mg intravenously once.
• Bronchospasm: salbutamol 5 mg nebulised every 20 minutes for 3 doses, then as needed, with ipratropium 500 micrograms nebulised every 6 hours.
• Eye care after irrigation: topical cycloplegic (cyclopentolate 1 percent 1 drop three times daily), topical chloramphenicol 0.5 percent 1 drop every 4 hours (or ofloxacin 0.3 percent 1 drop every 4 hours) for 7 days, preservative free lubricants, ophthalmology referral for corneal ulceration, ischaemic limbus or perforation; topical prednisolone 1 percent every 6 hours for the first 7 to 10 days only under ophthalmic supervision.
• Skin burns: treat as thermal burns, cool dressings; tetanus toxoid 0.5 mL intramuscularly if not immunised in the last 5 years.
• Pulmonary oedema or ARDS: lung protective ventilation with tidal volume 6 mL/kg predicted body weight and PEEP.
• Observe at least 6 hours; admit for any respiratory symptoms, abnormal radiograph, or eye injury.
• Follow up: spirometry at 4 to 6 weeks and at 3 months; ophthalmology review at 1 week and 1 month.
• Prevention: ventilation, leak detectors, gas masks, training, and safe storage of cleaning agents.