Levels of personal protective equipment

US regulatory agencies mandate the use of appropriate levels of PPE.

• Level A PPE is required for first responders and others working inside the hot zone, where vapor concentrations may be immediately dangerous to life and health. These suits are fully encapsulated, resistant to liquid and vapor chemical penetration, and include a self-contained breathing apparatus. Level A suits are also cumbersome, hot, and very difficult to wear for more than 30 minutes. There has been some move to mandate the use of level-A suits for hospital personnel. This is a hotly debated subject and as yet is unresolved. The use of level-A suits in hospital-based decontamination is probably not warranted.
• Level B PPE is required for hospital personnel involved in decontamination of unknown hazardous materials. These suits provide adequate protection against liquid and vapor chemicals when accompanied by a self-contained breathing apparatus or supplied air respirator.
• Level C PPE is used when chemical agents have been identified and are amenable to removal by an air-purifying respirator. This suit also provides some protection against penetration by chemical liquids and vapors.

Decontamination

• Decontamination is the physical process of removing residual chemicals from persons, equipment, and the environment. Residual hazardous chemicals on those who have been exposed directly are a source of ongoing exposure to those persons and pose a risk of secondary exposure to first responders and emergency care personnel. Immediate decontamination is a major treatment priority for those with CWA exposure.
• Initial decontamination involves removal from the contaminated environment, removal of all contaminated clothes and jewelry, and copious irrigation with water.
• Rinse exposed persons with a 0.5% hypochlorite solution, which chemically neutralizes most CWAs (eg, nerve agents, mustards). A 0.5% hypochlorite solution conveniently is prepared by mixing 1 part 5% hypochlorite (household bleach) with 9 parts water.
• Avoid hot water and vigorous scrubbing, as they may increase chemical absorption.
• Vapor exposure alone does not require decontamination. Fully decontaminate patients with unclear exposure histories. As well, if a nerve agent is suspected, decontamination should be performed as the patient may off-gas significant levels of the agent with the potential of further exposure to both him or her and responders.
• Ideally, decontaminate as close as possible to the site of exposure to minimize duration of exposure and prevent further spread. Hospitals receiving contaminated persons should establish an area outside the emergency department in which to perform decontamination before people and equipment are allowed in. Portable decontamination equipment with showers and run-off water collection systems are commercially available. All hospitals should have the capacity to safely decontaminate at least one person.

Supportive and specific therapy

Supportive therapy for victims of CWAs generally follows the universally accepted algorithm of first ensuring the adequacy of airway, breathing, and circulation, with one important exception. Severe nerve agent poisoning may require immediate administration of parenteral atropine. Many CWAs only can be treated supportively. Specific, well-established antidotes are available only for nerve agent and cyanide exposures. Since no laboratory tests are available to rapidly confirm exposure to CWAs, treatment is based on clinical

Mechanism of Action

The 5 nerve agents, tabun (GA), sarin (GB), soman (GD), cyclosarin (GF), and VX, have chemical structures similar to the common organophosphate pesticide malathion. Like organophosphate insecticides, these agents phosphorylate and inactivate acetylcholinesterase (AChE). Acetylcholine accumulates at nerve terminals, initially stimulating and then paralyzing cholinergic neurotransmission throughout the body.

Inhibition of AChE may not account for all of the toxic effects of nerve agents. These agents also are known to bind directly to nicotinic receptors and cardiac muscarinic receptors. They also antagonize gamma-aminobutyric acid (GABA) neurotransmission and stimulate glutamate N-methyl-d-aspartate (NMDA) receptors. These latter actions may partly mediate nerve agent–induced seizures and CNS neuropathology.

Physical Properties

Under temperate conditions, all nerve agents are volatile liquids. The most volatile agent, sarin, evaporates at approximately the same rate as water. The least volatile agent, VX, has the consistency of motor oil. This persistence and higher lipophilicity make VX 100-150 times more toxic than sarin when victims sustain dermal exposure. A 10-mg dose applied to the skin is lethal to 50% of unprotected individuals.

All nerve agents rapidly penetrate skin and clothing. Nerve agent vapors are heavier than air and tend to sink into low places (eg, trenches, basements).

Clinical Effects

Nerve agents produce muscarinic, nicotinic, and direct CNS toxicity with a wide variety of effects on the respiratory tract, cardiovascular system, CNS, gastrointestinal (GI) tract, muscles, and eyes. Onset and severity of clinical effects vary widely, since numerous variables determine predominant effects. Agent identity, dose (determined by concentration and duration of exposure), and type of exposure primarily determine nerve agent toxicity. Toxic effects result from dermal exposure to liquid and ocular and inhalation exposure to vapor.

Liquid exposure

Liquid agents easily penetrate skin and clothing. Onset of symptoms occurs from 30 minutes to 18 hours following dermal exposure.

Minimal liquid exposure (eg, a small droplet on the skin) may cause local sweating and muscle fasciculation, followed by nausea, vomiting, diarrhea, and generalized weakness. Even with decontamination, signs and symptoms may persist for hours.

In contrast, persons with severe liquid exposures may be briefly asymptomatic (1-30 min) but rapidly may suffer abrupt loss of consciousness, convulsions, generalized muscular fasciculation, flaccid paralysis, copious secretions (nose, mouth, lungs), bronchoconstriction, apnea, and death.

Vapor exposure

Vapor inhalation produces clinical toxicity within seconds to several minutes. Effects may be local or systemic. Exposure to even a small amount of vapor usually results in at least one of the following categories of complaints: (1) ocular (miosis, blurred vision, eye pain, conjunctival injection), (2) nasal (rhinorrhea), or (3) pulmonary (bronchoconstriction, bronchorrhea, dyspnea).

Exposure to a vapor concentration of 3.0 mg/m³ for 1 minute causes miosis and rhinorrhea. Inhalation of a high concentration of vapor results in loss of consciousness after only one breath, convulsions, respiratory arrest, and death. For example, breathing 10 mg /m³ of sarin vapor for only 10 minutes (100 mg/m³ for 1 min) causes death in approximately one half of exposed individuals. Severe vapor exposures also are characterized by generalized fasciculations, hypersecretions (mouth, lungs), and intense bronchoconstriction with respiratory compromise.

Date: 2015-01-12; view: 1036