Cyanide

Cyanide (CN) 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. ARDS 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).12 Treat with oxygen, mechanical ventilation, 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 minutes. 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 to 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.13 Treatment with nitrites carries significant risk of hypotension and methemoglobinemia, which can further jeopardize tissue oxygen delivery.

Carbon Monoxide

Carbon monoxide (CO) 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.14 Symptoms of CO toxicity include confusion, stupor, coma, seizures, and myocardial infarction.15 CO levels are traditionally measured using a co-oximeter, 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 may be present despite normal PaO2 and SpO2 readings. Newer non-invasive CO-oximetry may allow for early diagnosis and better monitoring.16 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 minutes.17 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 Suppressants

Chemical fire suppressants are released in military vehicle fires. The most common is HFC227 (HFC-227EA, heptafluoropropane). It replaced bromotrifluoromethane (one of many “Halons”) in military vehicles.18 These “virgin Halons” were banned by the Environmental Protection Agency (EPA) in 1994.19 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.20,21 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.4 Hydrogen fluoride (HF) as a byproduct of combustion with standard fire suppression systems may cause severe inhalation injury. Exposure to HF may result in rapidly progressive or fatal respiratory failure despite minimal external evidence of injury. In human tissue, HF dissociates into the hydrogen and fluoride ions. Fluoride ions rapidly bind calcium, leading to fatal hypocalcemia induced cardiac dysrhythmias. Patients present typically with shortness of breath, cough, or hypoxia; there must be a high level of suspicion. The administration of nebulized calcium gluconate (1.5 ml of 10% Ca Gluconate in 4.5 ml water) every 4 hours may provide benefit. If the patient is hypocalcemic, intravenous calcium gluconate (1000 mg) or intravenous calcium chloride (1000 mg) through a central venous line) should be administered and repeated every 15 minutes until normalization of serum calcium for a minimum of 12 hours. In the absence of significant burns, consider steroids if symptoms do not improve. Bronchopneumonia can develop within the first week.