Patients requiring MV secondary to toxic industrial chemicals inhalation, in particular chlorine, are at a higher risk of developing ventilator-associated pneumonia and should be monitored closely. The treatments in this CPG are primarily based on animal experiments. Evidence for clinical use in humans is limited.
Chlorine (Cl2) (Appendix A) is used commonly in industry. It is a commonly found in industrial and transportation accidents and are sometimes used in weapons such as improvised explosive devices. Chlorine dissolves in water to form hydrochloric and hypochlorous acids.
Chlorine has intermediate water solubility. Just after exposure the patient develops mucosal irritation (tearing, skin burning, drooling), but after large or sustained exposure the patient may develop cough, shortness of breath, and chest pain due to alveolar injury. Except for in cases of large exposure, upper airway symptoms proceed lower airway symptoms. If the patient develops pulmonary toxicity, it may worsen over days.
Treatment is primarily skin decontamination, supplemental oxygen as necessary, beta agonists and ARDS ventilatory techniques.4 Inhaled corticosteroids (e.g., fluticasone) improved secondary outcomes in severely toxic animal models.5 Clinical data on the efficacy of corticosteroids after human exposure to lung-damaging agents are inconclusive as the number of well-structured controlled studies is small and the indications for administration of corticosteroids are unclear.6 Prone positioning mechanical ventilation may be effective.7 Nebulized bicarbonate has not reliably improved outcomes.4,6,8,9
Phosgene (Carbonyl chloride, COCl2) has a sweet, pleasant smell of mown hay. It is poorly water soluble, not noxious and does not prompt escape from the location by the victim. It was used in WWI as a chemical weapon. It is produced from the combustion of chlorinated hydrocarbons (welding, fires) and from synthesis of solvents (degreasers, cleaners). Phosgene is a respiratory irritant. Immediate effects may include coughing, burning sensation in throat and eyes, lacrimation, blurred vision, dyspnea, nausea and vomiting, and or cutaneous injury. High-dose inhalation may cause onset of pulmonary edema within 2-6 hours. High concentrations may produce a severe cough with laryngospasm that results in sudden death; this possibly could be due to phosgene hydrolysis, which releases free hydrochloric acid at the level of the larynx. On the other hand, delayed-onset pulmonary edema as late as 48 hours after exposure is also possible. Thus, patients should be monitored for that length of time after exposure.10 The mechanism of toxicity is release of hydrochloric acid and reactive oxygen species and free radicals in the lung epithelial layers. Decontamination is typically not needed once the patient leaves the exposure. Treat with observation, supplemental oxygen, and ARDS ventilation techniques.
Hydrogen sulfide (H2S) smells like rotten eggs and is a chemical irritant. Exposures occur in waste management, petroleum, natural gas industries, and asphalt and rubber factories. The gas acts like cyanide and inhibits cytochrome oxidase, preventing mitochondrial oxygen use and cellular respiration. At lower doses, H2S causes skin and mucous membrane irritation. At high concentrations, it produces a “knockdown” effect, a sudden loss of consciousness. At these concentrations it can produce seizure, myocardial ischemia, keratoconjunctivitis, and upper airway and pulmonary injury. The vast majority of patients will have died prior to receiving medical care or will make a full recovery immediately after removal from the exposure. In those patients who do not immediately recover after removal from the exposure, treat with supplemental oxygen and intravenous hydroxocobalamin (5 g) or intravenous sodium nitrite (300 mg), and supportive care.2 Inhalation of sodium nitrite is associated with methemoglobinemia and hypotension. Infuse it over 5-7 minutes.
Ammonia (NH3) is a common industrial and household chemical used as a fertilizer, refrigerant, cleaning agent. NH3 has a pungent odor. It is also used in plastic and explosive synthesis. NH3 is transported under pressure in liquid form at sub-zero temperatures. It reacts with water upon release, to form ammonium hydroxide (NH4OH), a strong base, which produces mucosal irritation (tearing, skin irritation, eye pain and burns), severe upper airway irritation, and alkali skin burns. High concentrations or prolonged exposure duration (patient unconscious in a closed room) can produce tracheobronchial and pulmonary inflammation. It can produce respiratory failure within 2-5 minutes of exposure. Treat with skin and eye irrigation, alkali burn skin care, supplemental oxygen as necessary, ARDS ventilatory techniques, and supportive care.4 Proper eye care, particularly copious irrigation, is essential immediately after the exposure. The eye is often the forgotten organ in a patient with an acute irritant gas exposure.11