Respiratory tract

Nerve agents act on the upper respiratory tract to produce profuse watery nasal discharge, hypersalivation, and weakness of the tongue and pharynx muscles. Laryngeal muscles are paralyzed, resulting in stridor. In the lower respiratory tract, nerve agents produce copious bronchial secretions and intense bronchoconstriction. If untreated, the combination of hypersecretion, bronchoconstriction, respiratory muscle paralysis, and CNS depression rapidly progresses to respiratory failure and death. Nerve agents depress the central respiratory drive directly. Thus, early death following large vapor exposure likely results from primary respiratory arrest, not from neuromuscular blockade, bronchorrhea, or bronchoconstriction.

Cardiovascular system

The cardiovascular effects of nerve agents vary and depend on the balance between their nicotinic receptor–potentiating effects at autonomic ganglia and their muscarinic receptor–potentiating effects at parasympathetic postganglionic fibers that innervate the heart.

Sinus tachydysrhythmias with or without hypertension (sympathetic tone predomination) or bradydysrhythmias with or without variable atrioventricular blockade and hypotension (parasympathetic tone predomination) may occur.

Superimposed hypoxia may produce tachycardia or precipitate ventricular tachydysrhythmias.

Nerve agent–induced prolonged QT and torsades de pointes have been described in animals.

In victims of the Tokyo sarin gas attack, sinus tachycardia and hypertension were common cardiovascular abnormalities, while sinus bradycardia was uncommon.

Central nervous system

Nerve agents produce a variety of neurologic signs and symptoms by acting on cholinergic receptors throughout the CNS. The most important clinical signs of neurotoxicity are a rapidly decreasing level of consciousness (sometimes within seconds of exposure) and generalized seizures. Symptoms such as headache, vertigo, paresthesias, anxiety, insomnia, depression, and emotional lability also have been reported.

Musculoskeletal system

Nerve agents initially stimulate and then paralyze neurotransmission at the neuromuscular junction. With minimal exposure, exposed persons may complain of vague weakness or difficulty walking. More significant exposures resemble the clinical effects that result from succinylcholine, with initial fasciculations followed by flaccid paralysis and apnea.

Ocular

Nerve agent liquid or vapor readily penetrates the conjunctiva and exerts direct muscarinic parasympathetic effects. This results in constriction of the iris (miosis, blurred and dim vision, headache), constriction of the ciliary muscle (pain, nausea, vomiting), and stimulation of the lacrimal glands (tearing, redness). Although miosis is the most consistent clinical finding after vapor exposure to nerve agents (occurred in 99% of persons exposed in Tokyo sarin attack), it may be absent or delayed in dermal exposure. Duration of miosis varies according to the extent of ocular exposure (up to 45 d).

Laboratory Tests

Routine toxicology testing does not identify nerve agents in serum or urine. Measurements of red blood cell (RBC) or plasma cholinesterase activity have been used as an index of the severity of nerve agent toxicity, but this approach is not always reliable. The reference range of RBC cholinesterase activity may vary widely, and mild exposures may be difficult to interpret without baseline measurement. In addition, RBC cholinesterase activity may not correlate with the severity of signs and symptoms following vapor exposure.

In the Tokyo subway sarin attack, 27% of patients with clinical manifestations of moderate poisoning had plasma cholinesterase activity in the normal range. Moreover, different organophosphates variably inhibit RBC and plasma cholinesterase. For example, in mild-to-moderate exposures to sarin or VX, RBC cholinesterase activity is decreased to a much greater extent than plasma cholinesterase activity.

Since plasma cholinesterase is produced by the liver, its activity also may be depressed in certain conditions (eg, liver disease, pregnancy, infections) or with certain drugs (eg, oral contraceptives). Conversely, a 20-25% reduction in RBC cholinesterase activity tends to correlate with severe clinical toxicity and, despite the exception noted above, activity of both enzymes approaches zero in most severely poisoned victims. Nevertheless, treatment decisions should be clinically based. Never withhold treatment from a symptomatic patient

Personal Protective Equipment

First responders are at serious risk of exposure within the contaminated environment (hot zone), either from direct contact with persistent liquid or from inhaling residual vapors. First responders and subsequent emergency care providers outside the hot zone are at risk from handling persons contaminated with liquid nerve agent (through both dermal and inhalation exposure).

Conversely, victims exposed to nerve agent vapor pose little risk to emergency care providers outside the hot zone; residual agent is not present and off-gassing may occur but rarely in significant amounts. In the Tokyo sarin attack, approximately 90% of exposed persons reported to medical facilities by private or public transportation without notable contamination of others. Additionally, secondary injury to hospital staff was minimal and did not necessitate specific treatment.

Unless a clear history of vapor exposure only is obtained, emergency medical personnel should assume that liquid contamination is present and wear PPE. For most nerve agent exposures, first responders require level A PPE inside the hot zone, and hospital personnel involved in decontamination should wear level B PPE.

Decontamination

Decontamination should proceed as described in General Considerations. Decontaminate with a triple wash, including initial irrigation with tepid water followed by 0.5% hypochlorite solution or soap and water (alkaline solutions also neutralize nerve agent) and repeated thorough water rinsing. In survivors, the amount of residual liquid contaminant is likely to be small, because victims with larger exposures probably will die before they reach the hospital. Other than removing clothing and jewelry, decontamination is unnecessary for victims of vapor nerve agent exposure.

Date: 2015-01-12; view: 816