to cause systemic effects, whereas a fatal dose (still smaller than a pinhead) may lead to sudden collapse, convulsions, paralysis, apnea, and death after a latent period of only 10 to 30 minutes Because absorption from inhalation is fast and complete, patients who have inhaled nerve-agent vapor typically not deteriorate once they are removed from exposure However, the latency conferred by the time needed for the nerve agent to traverse the epidermis means that symptoms may arise (gradually or, with a high dose, suddenly) and progress minutes to hours after exposure and even after successful decontamination of the surface of the skin Vapor-exposed patients typically exhibit either gradual or sudden-onset local effects such as miosis, lacrimation, rhinorrhea, hypersalivation, bronchoconstriction, and bronchorrhea followed or accompanied by, if the dose or duration of exposure is high enough, systemic effects involving the GI tract, skeletal muscles, and the CNS Patients exposed via the skin may also exhibit local effects (diaphoresis and fasciculations) and then systemic effects either gradually or all at once, but after a delay With high doses, collapse, apnea, and death from bolus delivery to the circulation may be so rapid that miosis and other peripheral muscarinic effects may not have time to develop Management The diagnosis of traditional nerve-agent poisoning is primarily by clinical recognition of acute signs and symptoms and by observing the response to antidotal therapy Routine toxicologic studies not identify OP compounds or their metabolites in blood or urine, and the ability to measure acetylcholinesterase is not widely available Although presumptive antidotal therapy for symptomatic patients is indicated, treatment is not needed for exposed asymptomatic patients These patients, however, should be carefully observed if there is any possibility of concomitant exposure to liquid nerve agent As discussed previously, in this setting immediate decontamination is an urgent medical intervention, since it can decrease the internal dose of the agent The drugs of choice to treat nerve-agent toxicity are atropine for its antimuscarinic effects and pralidoxime (also called 2PAM), which serves to reactivate acetylcholinesterase Atropine treats bronchospasm and increased bronchial secretions, bradycardia, and GI effects and may lessen seizure activity However, atropine will not improve skeletal muscle paralysis Atropine is dosed initially at 0.05 mg/kg, with a minimum dose of 0.1 mg and a maximum of mg ( Table 132.4 ) It should be given in repeat doses until secretions decrease and airway resistance lessens; a typical total dose of atropine for an adult nerve-agent victim is 20 to 30 mg, as opposed to over 20,000 mg that may be needed in an adult exposed to an OP pesticide (there is at least one known case of a pediatric pesticide poisoning that required a total of 5,000