Contingency Plan

The contingency plan for hazmat management is divided into two parts: initiation of the site plan and evacuation. Initiation of the site plan begins after the specific offending agent has been identified and the surrounding environment has been assessed. Only after the substance has been identified can the risks to the public and the environment accurately be identified. First responders should be trained to recognize the potential for a hazmat incident and should establish a perimeter. The hazmat technicians are specifically trained in the use of personal protective equipment (PPE), establishing entry into a hazmat scene, victim rescue, and determining the type and extent of a hazmat emergency. A central command post should be used to coordinate the activities of the hazmat team with those of the emergency medical services personnel, firefighters, police officers, and other relevant personnel.

Coping with Hazmat Incidents

In dealing with a hazmat incident, two distinct processes occur simultaneously. First, the scene is secured, which involves containing the substance, extinguishing fires, and controlling other environmental hazards. The second process involves treatment, which begins with decontamination. The exact decontamination depends on the specific agent and route of exposure. In general, all decontamination should be performed before arrival in the emergency department. Individuals who are not exposed to the hazardous material are kept away from the scene to prevent subsequent exposure.

At the outset of any contamination event, the offending agent may not be known. Therefore first responders and those having direct contact with ill patients must wear appropriate PPE. Once the first responder is dressed appropriately, decontamination begins by removing the patient’s contaminated clothes. Dry (anhydrous) chemicals can be brushed off the patient’s skin, followed by copious irrigation with water delivered under low pressure. Ideally, the contaminated water will be contained on the scene for appropriate disposal. Liquid chemicals can be copiously irrigated directly. If decontamination was indicated and not performed on the scene, the patient should be decontaminated before entering the ED. The primary and secondary survey can occur simultaneously with decontamination.

Although the exact requirements for PPE among hospital personnel are somewhat controversial, at a minimum, all personnel involved with decontamination should wear chemical-resistant clothing with a hood, boots, eyewear, at least two layers of gloves, and some form of respiratory protection.

Hydrotherapy

Hydrotherapy involves the application of large amounts of water or saline to the affected skin. Gentle irrigation of a large volume of water under low pressure for a prolonged time dilutes the toxic agent and washes it out of the skin. High-pressure irrigation should not be used because it is possible to drive the chemical deeper into the skin. Furthermore, the use of high-pressure irrigation can result in splattering of the chemical into the eyes of the patient or rescuer.

Elemental metals (e.g., sodium) may produce profound exothermic reactions when combined with water. To minimize the exothermic reaction from such compounds, mineral oil is applied to the skin first, if it is immediately available. However, hydrotherapy should not be delayed while waiting for mineral oil. In addition, some have argued that phenol (carbolic acid) should not be irrigated with water owing to concern for enhanced skin penetration after exposure to water. However, the use of a substance that has both hydrophobic and hydrophilic properties (i.e., polyethylene glycol [PEG]) has not been proven to exhibit clear benefit over water alone; therefore hydrotherapy should not be delayed while waiting for PEG.² If PEG solution is used for decontamination, the molecular weight of the preferred solution should be 200 to 400 daltons, which is different from the molecular weight of the PEG solution used for colonoscopy preparations.

After exposure to strong alkalis, prolonged hydrotherapy is especially important to limit the severity of the injury. In experimental animal models, the pH of chemically burned skin does not approach a normal concentration unless continuous irrigation has been maintained for more than 1 hour, and the pH often does not return to normal for 12 hours despite hydrotherapy. In contrast, with hydrochloric acid skin burns, the pH usually returns to normal within 2 hours after initiation of hydrotherapy.³ The mechanism by which sodium hydroxide (NaOH) maintains an alkaline pH despite treatment is related to the byproducts of its chemical reaction to skin. Alkalis combine with proteins or fats in tissues to form soluble protein complexes or soaps. These complexes permit passage of hydroxyl ions deep into the tissue, limiting their contact with the water diluent on the skin surface. On the other hand, acids do not form complexes, and their free hydrogen ions are easily neutralized.

Water is the agent of choice for decontaminating dermal burns from either acidic or alkali substances. The deleterious effects of attempting to neutralize acid and alkali burns were first noted in experimental models in 1927. In nearly every instance, animals with either acid or alkali burns that underwent initial irrigation with water survived longer than animals treated with chemical neutralizers. The striking difference between the results of these two treatment methods is attributed to the additional trauma of the heat generated by the neutralization reaction superimposed on the existing burn. Although the same effect may occur when certain chemicals come in contact with water, large volumes of water tend to limit the exothermic reaction.

However, scientists are beginning to question the belief that neutralization of an alkaline burn of the skin with acid does indeed increase tissue damage because of the exothermic nature of acid-base reactions.⁴ Using an animal model with 5% topical acetic acid (i.e., household vinegar), researchers demonstrated that the application of acetic acid to alkaline burns resulted in rapid neutralization of the tissue and reduction of the tissue injury in comparison with water irrigation alone. However, these data are preliminary and limited, and therefore irrigation with water alone is acceptable.

Ocular Injury

Chemical burns to the eye require emergent management. Alkali burns are more common than acidic burns, and unilateral involvement is more common than bilateral involvement.⁵ Common causes include inadvertent handling of chemicals with resultant splash injury, exploding batteries, airbag deployment, and intentional assaults. Alkali burns can initially appear trivial, but because of an interaction with lipids in the corneal epithelial cells, a coagulative necrosis results, and deep penetration through the corneal stroma can ensue. The injury can occur rapidly; for example, anhydrous ammonia can penetrate into the anterior chamber in less than 1 minute, resulting in complete blindness.

Similar to cutaneous burns, ocular burns are classified into four grades, with grade IV being the most severe. Grade I and II burns are associated with hyperemia, conjunctival ecchymosis, and defects in the corneal epithelium. Grade III and IV burns are associated with deeper penetration and therefore are associated with mydriasis, a gray discoloration of the iris, and early cataract formation.

Grade II burns are differentiated from grade I burns by the hazy appearance of the cornea in the former. Blood vessel thrombosis in the anterior chamber occurs in both grade III and grade IV burns, and as a result, limbus ischemia occurs. The degree of ischemia differentiates grade III from grade IV burns: ischemia occurs in less than half of the limbus in grade III, whereas ischemia occurs in more than half of the limbus in grade IV. In addition, grade IV burns are associated with necrosis of the bulbar and tarsal conjunctiva and significant limbal ischemia.5,6

Hydrofluoric Acid

Hydrofluoric acid (HF) is an acidic aqueous solution made from the element fluorine. It is commonly used in the petroleum industry to manufacture high-octane gasoline. It is also commonly used in the production of microelectronics and for etching glass, removing rust, and cleaning cement and bricks. Absorption of HF can occur after exposure to the lung, skin, and eyes. In an 11-year review of all HF deaths reported to the Occupational Safety and Health Administration, four deaths resulted strictly from dermal exposure, and five deaths resulted from both inhalational and dermal exposure. Several of these deaths were associated with inadequate medical therapy, and all of the cases were associated with unsafe workplace practices.⁸ HF solutions with a concentration exceeding 50% will produce near immediate pain, whereas burns from more dilute concentrations can be delayed for hours.

HF is unique in its mechanism of action. Despite being an acid, it is capable of causing a liquefactive necrosis, similar to alkalis. However, the free fluoride ion is actually responsible for most of the damage associated with HF exposure. The free fluoride ion scavenges cations, such as calcium and magnesium, thereby resulting in systemic hypocalcemia and hypomagnesemia. In addition, free fluoride ions can inhibit sodium, potassium–ATPase (Na⁺,K⁺-ATPase) and the Krebs cycle. The combination of cellular destruction and inhibition of Na⁺,K⁺-ATPase can also result in hyperkalemia, a preterminal finding. As a result of the numerous electrolyte disturbances, QT prolongation, hypotension, and ventricular arrhythmias can occur. The severity of injury depends on the concentration of the substance and the duration of exposure.