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rarely available on a stat basis. A decrease in the cholinesterase activity of the red
blood cells is more specific for organophosphate inhibition than is the plasma
assay. Although plasma cholinesterase is depressed by liver injury from various
causes and a small percentage of the population has a genetically determined
deficiency of plasma cholinesterase activity, a depression of 25% or more is a
strong evidence of excessive organophosphate absorption. However, it is
important not to delay treatment until confirmation of plasma cholinesterase.
Note that children may also encounter acetylcholinesterase inhibitors if they
ingest an adult’s medication for Alzheimer or Parkinson disease (i.e.,
rivastigmine, donepezil, tacrine, and galantamine).
The management of a patient who has ingested organophosphates must always
include safeguards against exposure for the persons who treat the patient because
the organophosphates are readily absorbed through the skin and mucous
membranes. Patients who have been poisoned by the topical application of
organophosphates should immediately receive a thorough scrubbing with a soap
solution to prevent further absorption. In addition, all contaminated clothing must
be removed and stored in a plastic bag to protect emergency personnel.
After decontamination, antidotal therapy begins with the administration of
atropine sulfate given in a dose of 0.02 to 0.05 mg/kg IV (to a maximum of 3 mg)
to children and 2 to 5 mg for adolescents and adults. This dose should be doubled
every 5 minutes as needed to obtain and maintain full atropinization, and then an
infusion of 10% to 20% of the total loading dose/hour should be administered.
Atropinization is indicated by the clearing of bronchial secretions and rales.
Therapy is continued until all absorbed organophosphate has been metabolized
and may require more than 2,000 mg of atropine, via bolus dosing and/or
subsequent atropine infusion, over the course of a few hours to several days.
After atropinization has been instituted, severe poisonings should be treated with
the addition of pralidoxime. This drug is particularly useful in poisonings
characterized by profound weakness and muscle twitching. A dose of 25 to 50
mg/kg should be administered in 100 mL of saline by infusion over
approximately 30 minutes; adults may receive 1 to 2 g by IV. In life-threatening

situations, 50% of the initial pralidoxime dose may be infused over 2 minutes,
followed by the remainder of the dose over 30 minutes. After loading, a 1%
concentration may be infused continuously at the rate of 500 mg/hr in adolescents
and adults, or approximately 10 mg/kg/hr in children, and can be titrated to
clinical effect. Occasionally, patients may require more than 48 hours of therapy;
the end point should be persistent relief of neurologic and cholinergic signs.