Chapter 115. Industrial Toxins and Cyanide

Hazardous chemicals are defined as agents capable of causing adverse health effects or physical danger (combustion or explosion) and are summarized in Table 115-1. Useful resources in managing patients exposed to industrial chemicals include material safety data sheets and local poison control centers. Special at risk groups include pregnant women (the medical focus should be on treating the mother first, with early obstetric consultation) and children.

Clinical Features

Inhaled toxins include gases, dusts, fumes, and aerosols and generally cause acute dyspnea, burning of the mucous membranes, cough, and bronchospasm. Common irritating gases include chorine, ammonia, hydrogen sulfide, and nitrogen dioxide. Some gases, particularly nitrogen dioxide, chlorine, and phosgene, can cause delayed pulmonary edema. Consider systemic toxicity from carbon monoxide and cyanide whenever there is a history of combustion. Some of the more common dangerous inhalations are described in Table 115-2.

Diagnosis and Differential

ED evaluation includes chest radiography and laboratory studies (arterial blood gas, carboxyhemoglobin, methemoglobin, and lactate) in selected cases. The role of early bronchoscopy is controversial.

Emergency Department Care and Disposition

1. Administer 100% oxygen, usually humidified, along with bronchodilators as needed. Have a low threshold for intubation because of the potential for pulmonary edema.

2. Prophylactic steroids and antibiotics are generally not indicated, though steroids may be considered for patients with underlying reactive airway disease and may also reduce the risk of delayed pulmonary edema from nitrogen dioxide inhalation.

Clinical Features

Cyanide exposure most commonly results from fires that involve synthetic materials, wool, or plastics, but may also be associated with vermicidals, precious metal reclamation, chemical laboratories, and Prunus seeds. Cyanide is highly toxic.

The initial clinical features of cyanide poisoning involve the cardiovascular and central nervous systems, with subsequent lactic acidosis causing dyspnea and ultimately coma, cardiovascular collapse, and death. The most common presentation is unexplained confusion, hyperventilation, hypotension, and/or bradycardia, especially when accompanied by unexplained metabolic acidosis. Table 115-3 lists the signs and symptoms of acute cyanide toxicity.

Diagnosis and Differential

Because delays in treatment can lead to death, cyanide poisoning is usually diagnosed clinically at the bedside. Blood cyanide levels are not rapidly available.

Emergency Department Care and Disposition

1. Administer 100% oxygen and secure the airway. Administer crystalloids and vasopressors for hypotension.

2. Consider decontamination with activated charcoal if the airway is stable and the patient presents within an hour of cyanide ingestion.

3. Antidotal therapy for adults is outlined in Table 115-4, while Table 115-5 summarizes the weight-based treatment of children. Administer empiric treatment prior to confirmatory tests in patients presenting with coma, cardiovascular collapse, and severe unexplained metabolic acidosis in the appropriate clinical setting (industrial fires or accidents, smoke inhalation). Patients with mild to moderate symptoms can be closely observed prior to treatment. Traditionally, sodium nitrite is given first to induce methemoglobin, which helps remove cyanide from cytochrome. This is followed by sodium thiosulfate, which enhances enzymatic formation of less toxic thiocyanate from cyanide. This agent is safer than nitrites, especially for victims of smoke inhalation or when the diagnosis is unclear.

4. Hydroxocobalamin is a newer antidote for cyanide. It is administered as 2 vials, each 2.5 grams reconstituted in 100 mL NS, given over 7.5 min (for a total dose of 5 grams over 15 min). This can be repeated within 15 min as clinically indicated. Although not approved for pediatric use, a dose of 70 milligrams/kilogram has been used. There may be added benefits if sodium thiosulfate is given concurrently, though it must be administered through a separate IV line.

Hydrogen sulfide is a colorless gas used in the petrochemical industry and can emanate from sewage or manure. Although it has a distinct “rotten egg” odor, this olfactory warning is lost with extended exposure and high concentrations. Hydrogen sulfide causes cellular asphyxia that leads to lactic acidosis. In high concentrations, rapid loss of consciousness, seizures, and death can occur after only a few breaths. Treat with 100% oxygen, followed by administration of sodium nitrite IV, as with cyanide poisoning. The resultant methemoglobin enhances formation of less toxic sulfmethemoglobin from sulfide.