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Includes organophosphates and carbamates
Inhibit the enzyme acetylcholinesterase and increase acetylcholine activity at nicotinic and muscarinic receptors and in the peripheral and central nervous systems
Most are absorbed through intact skin
Most chemical warfare "nerve agents" (such as GA [tabun], GB [sarin], GD [soman] and VX) are organophosphates
Profound skeletal muscle weakness, aggravated by excessive bronchial secretions and wheezing, may result in respiratory arrest and death
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Abdominal cramps
Diarrhea
Vomiting
Excessive salivation
Sweating
Seizures
Lacrimation
Constricted pupils
Wheezing
Bronchorrhea
Skeletal muscle fasciculations
Initial tachycardia may be followed by bradycardia
Symptoms may persist or recur for days, especially with highly lipid-soluble agents such as fenthion or dimethoate
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Suspected in patients who present with miosis, sweating, and diarrhea
Serum and red blood cell cholinesterase activity is usually at least 50% below baseline with severe intoxication
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Emergency and supportive care
For recent ingestions, consider gut decontamination by aspiration of the liquid using a nasogastric tube followed by administration of activated charcoal
If the agent is on the victim's skin or hair, wash with soap or shampoo and water
Care providers should avoid skin exposure by wearing gloves and waterproof aprons
Dilute hypochlorite solution (eg, household bleach diluted 1:10) is reported to help break down organophosphate pesticides and nerve agents on equipment or clothing
Administer atropine, 2 mg intravenously, and give repeated doses as needed (may need several hundred milligrams) to dry bronchial secretions and decrease wheezing
Administer pralidoxime, 1–2 g intravenously, as soon as possible, and give a continuous infusion (200–500 mg/h) as long as there is any evidence of acetylcholine excess
Pralidoxime (2-PAM, Protopam) is a specific antidote that reverses organophosphate binding to the cholinesterase enzyme; therefore, it should be effective at the neuromuscular junction as well as other nicotinic and muscarinic sites
Most likely to be clinically effective if started very soon after poisoning, to prevent permanent binding of the organophosphate to cholinesterase
However, clinical studies have yielded conflicting results regarding the effectiveness of pralidoxime in reducing mortality
Administer 1–2 g intravenously as a loading dose and begin a continuous infusion (200–500 mg/hour, titrated to clinical response)
Continue to give pralidoxime as long as there is any evidence of acetylcholine excess
Pralidoxime is of questionable benefit for carbamate poisoning because carbamates have only a transitory effect on the cholinesterase enzyme
Other, unproven therapies for organophosphate poisoning include magnesium, sodium bicarbonate, clonidine, and extracorporeal removal