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Omar Saeed, MC, USN, Joint Trauma System, 3698 Chambers Pass, Joint Base San Antonio, Fort Sam Houston, TX Search for other works by this author on: Nathan L Boyer, MC, USA,Joint Trauma System, 3698 Chambers Pass, Joint Base San Antonio, Fort Sam Houston, TX Search for other works by this author on: Jeremy C Pamplin, MC, USA,Jeremy C Pamplin, MC, USA Joint Trauma System, 3698 Chambers Pass, Joint Base San Antonio, Fort Sam Houston, TX Search for other works by this author on: Ian R Driscoll, MC, USA,Joint Trauma System, 3698 Chambers Pass, Joint Base San Antonio, Fort Sam Houston, TX Search for other works by this author on: Jeff DellaVolpe, USAF, MC,Jeff DellaVolpe, USAF, MC Joint Trauma System, 3698 Chambers Pass, Joint Base San Antonio, Fort Sam Houston, TX Search for other works by this author on: Jeremy Cannon, USAFR, MC,Joint Trauma System, 3698 Chambers Pass, Joint Base San Antonio, Fort Sam Houston, TX Search for other works by this author on: Leopoldo C Cancio, MC, USALeopoldo C Cancio, MC, USA Joint Trauma System, 3698 Chambers Pass, Joint Base San Antonio, Fort Sam Houston, TX Search for other works by this author on: Received: 21 November 2016 Published: 05 September 2018
Close Navbar Search Filter Microsite Search Term Search AbstractToxic industrial chemicals include chlorine, phosgene, hydrogen sulfide, and ammonia have variable effects on the respiratory tract, and maybe seen alone or in combination, secondary to inhalation injury. Other considerations include the effects of cyanide, carbon monoxide, and fire suppressants. This Clinical Practice Guideline (CPG) will provide the reader with a brief overview of these important topics and general management strategies for each as well as for inhalation injury. Chlorine, phosgene, hydrogen sulfide, and ammonia are either of intermediate or high water solubility leading to immediate reactions with mucous membranes of the face, throat, and lungs and rapid symptoms onset after exposure. The exception to rapid symptom onset is phosgene which may take up to a day to develop severe acute respiratory distress syndrome. Management of these patients includes early airway management, lung-protective ventilator strategies, aggressive pulmonary toilet, and avoidance of volume overload. INTRODUCTIONPatients with both burn and inhalation injury have significantly increased morbidity and mortality compared with those with burn injury alone.1 The current CPG is intended to review relevant information in the care of patients with inhalation injury and more specifically toxic industrial chemicals. Also included is a brief overview of the management strategies for these patients. We intend to inform caregivers with the goal of reducing some of the complications of inhalation injury. GOALThere are multiple toxic industrial chemicals that act on the respiratory tract. This CPG reviews the most common toxic industrial chemicals which lead to pulmonary injury. More information is available from the Center for Disease Control and Prevention, http://www.bt.cdc.gov/agent/agentlistchem-category.asp, and the Textbook of Military Medicine, http://www.bordeninstitute.army.mil/published_volumes/biological_warfare/biological.html. GENERAL SMOKE INHALATION INJURYSmoke inhalation injury occurs from several agents. Thermal injury and chemical injury are the primary initial toxicities. Chemical injury occurs from several materials of combustion and pyrolysis.2 Highly water soluble irritants such as acrolein, sulfur dioxide, hydrogen chloride and ammonia, and intermediate water soluble irritants such as chlorine and isocyanates are produced. Poorly water soluble irritants are oxides of nitrogen and phosgene. Simple asphyxiants which displace oxygen include carbon dioxide and methane, and chemical asphyxiants which inhibit mitochondrial activity and reduce hemoglobin carrying capacity include carbon monoxide, cyanide, and hydrogen sulfide. Treatment is generally supportive, some require antidotes. Most critically ill patients require unique ventilation techniques used for acute respiratory distress syndrome (ARDS). TOXIC INDUSTRIAL CHEMICAL INHALATIONAL INJURYIn general, the treatment of ARDS secondary to toxic industrial chemicals is similar to that for smoke inhalation injury. The care is supportive with a focus on:
Patients requiring mechanical ventilation (MV) secondary to toxic industrial chemical 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)Chlorine 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. If the patient develops pulmonary toxicity, it may worsen over days. Treatment is primarily skin decontamination, supplemental oxygen, beta agonists, and ARDS ventilatory techniques.3 Inhaled corticosteroids (e.g., fluticasone) improved secondary outcomes in severely toxic animal models.4 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.5 Prone positioning MV maybe effective.6 Nebulized bicarbonate has not reliably improved outcomes.3,5,7,8 Phosgene (CARBONYL CHLORIDE, COCl2)Phosgene 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). The primary symptom is delayed ARDS (up to a day after exposure), which can be very severe. 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)Hydrogen sulfide 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 seizures, myocardial ischemia, keratoconjunctivitis, and upper airway and pulmonary injury. Treat with skin irrigation, supplemental oxygen, removal from exposure, intravenous sodium nitrite (300 mg), and supportive care.2 Inhalation of sodium nitrite is associated with methemoglobinemia and hypotension. Infuse it over 5–7 min. Ammonia (NH3)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, ARDS ventilatory techniques, and supportive care.3 OTHER COMMON CHEMICAL TOXINS RELATED TO INHALATIONAL EXPOSURESCyanide (CN)Cyanide is released in structural and vehicle fires and in occupational settings of chemical or synthetic material combustion. It is used in manufacturing of pesticides and synthetic materials, metal extraction, and in chemical laboratories. Cyanide inhibits mitochondrial cytochrome oxidase thereby halting cellular respiration and aerobic metabolism. Early or mild effects are mostly neurologic (dizziness, headache, nausea, and anxiety). Late or severe effects are coma, seizure, respiratory depression, hypotension, and tachycardia. Acute lung injury and pulmonary edema can occur in severe cases. Coma precedes apnea, and then hypotension develops. The triad of severe toxicity is hypotension, altered mental status, and lactic acidosis (commonly > 8 mmol/L).9 Treat with oxygen, MV, and rapid administration of an antidote. Hydroxocobalamin, the most commonly available antidote (sold as Cyanokit), binds to CN to form cyanocobalamin, which is nontoxic and excreted in the urine. The standard dose of 5 g is infused intravenously over 15 min. A second dose of 5 g can be administered in patients with severe toxicity or poor clinical response. It is generally regarded as safe. Red discoloration of the skin and urine is common which may interfere with colorimetric assays. Hydroxocobalamin has been compared with sodium nitrite (300 mg) and sodium thiosulfate (12.5 g), prior treatment options, and was found to be superior with less toxicity and the latter two therapies are now not recommended for severe cyanide toxicity.10 Treatment with nitrites carries significant risk of hypotension and methemoglobinemia, which can further jeopardize tissue oxygen delivery. Carbon Monoxide (CO)Carbon monoxide is released from the combustion of carbon containing compounds with combustion engines and cooking stoves in enclosed spaces. CO has a high affinity for hemoglobin and displaces oxygen when present. This displacement of oxygen ultimately leads to decreased oxygen delivery at the tissue and mitochondrial level.11 Symptoms of CO toxicity include confusion, stupor, coma, seizures, and myocardial infarction.12 CO levels are traditionally measured using a cooximeter, in a blood gas lab; however, this testing may not always be available and a high index of suspicion must be present as elevated CO maybe present despite normal PaO2 and SpO2 readings. Newer non-invasive CO-oximetry may allow for early diagnosis and better monitoring.13 Treatment of CO poisoning involves producing 100% oxygen, shortening the half-life of CO binding to hemoglobin to about 45 minutes. Hyperbaric oxygen therapy (HBO) has been used to reduce the half-life to about 20 min.14 Logistical factors have limited the utilization of HBO and a systematic review found that not enough evidence exists at this point to determine definitively whether HBO reduces adverse neurologic outcomes after CO poisoning. Fire SuppressantsChemical fire suppressants are released in military vehicle fires. The most common is HFC227 (HFC-227EA, heptafluoropropane) which replaced bromotrifluoromethane (one of many “Halons”) in military vehicles.15 These “virgin Halons” were banned by the EPA in 1994.16 HFC227 is inert, a simple asphyxiant, and no cases of combustion related toxicity have been published or reported to the EPA or Occupational Safety and Health Administration.17,18 HFC227 can convert to hydrogen fluoride in small amounts during a fire, and, treatment is supportive, similar to other chemical exposures resulting in inhalation injury.3 Hydrogen fluoride as a byproduct of combustion with standard fire suppression systems may cause severe inhalation injury. Exposure to hydrogen fluoride may result in rapidly progressive or fatal respiratory failure despite minimal external evidence of injury. Patients present typically with shortness of breath, cough, or hypoxia; there must be a high level of suspicion. Treatment is supportive. If hypocalcemia is present, administer nebulized calcium gluconate (1.5 mL of 10% Ca Gluconate in 4.5 mL water) every 4 hours until normalization of serum calcium. In the absence of significant burns, consider steroids if symptoms do not improve. Bronchopneumonia can develop within the first week. Refer to the full JTS CPG at https://jts.amedd.army.mil/index.cfm/PI_CPGs/cpgs for further details and specifics on the treatment of suspected inhalation injury and chemical exposure. CONCLUSIONInhalation of smoke and toxic chemicals is a risk on the battlefield and increases morbidity and mortality. Rapid identification and mitigation of supportive care is key. REFERENCES1
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Which of the following is one of the most common inhaled poisons associated with fire suppression?
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