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Organophosphate exposure can present with paralysis and weakness
from nicotinic effects, as well as muscarinic findings, of which the most
severe may be bradycardia, bronchorrhea, and bronchospasm.
Treatment for organophosphates includes decontamination and
antidotal therapy, including atropine (may require repeated and large
doses) and pralidoxime.
Long-acting vitamin K antagonists are commonly used as rodenticides
and can lead to severe, prolonged coagulopathy in large intentional
overdose; though in the setting of small unintentional ingestions,
children are unlikely to develop coagulopathy.
Organophosphates
Current Evidence. Organophosphates are lipid-soluble insecticides that are
commonly applied in sprayed dust or emulsion formulations. These compounds
are found in agricultural and home use, and they form the basis of “nerve gases”
in chemical warfare agents. Some of these chemicals are “systemic” insecticides,
meaning that they are taken up by the roots of the plants and translocated into
foliage, flowers, and/or fruits.
Compounds of this class can be absorbed by inhalation, ingestion, and skin
penetration. They irreversibly phosphorylate the enzyme acetylcholinesterase in
tissues, allowing acetylcholine accumulation at cholinergic junctions in
autonomic effector sites (causing muscarinic effects), in skeletal muscle or
autonomic ganglia (causing nicotinic effects), and in the CNS.
Clinical Considerations. The symptoms of acute poisoning usually develop during
the first 12 hours of contact. These include findings related to the CNS (dizziness,
headache, ataxia, convulsions, and coma); nicotinic signs, including sweating,
muscle twitching, tremors, weakness, and paralysis; and muscarinic signs
characterized by the SLUDGE mnemonic (including s alivation, l acrimation, u
rination, d efecation, GI cramping, and e mesis). In addition there may be miosis,
bradycardia, bronchorrhea, and wheezing; in severe cases, pulmonary edema
develops.
A history of exposure to organophosphates and the clinical manifestations

already discussed are the best clues to an organophosphate poisoning. A
depression of plasma or red blood cell cholinesterase activity provides the best
laboratory marker of excessive absorption of organophosphates, although it is