Objective: To review clinical and therapeutic bases of an organophosphate p
oisoning, either with insecticide or nerve agent.
Data sources: References were obtained from computerized bibliographic rese
arch (Medline(R)), from personal data (academic memoir, documents under app
robation of the National Defense Office), from Internet's data.
Data synthesis: Generally, organophosphate poisoning occurs during accident
al exposure with agricultural insecticide or suicide. The effects of organo
phosphate compounds are due to the inhibition of the enzyme acetylcholinest
erase. The intoxication symptoms can be divided into muscarine-like, nicoti
ne-like effects, effects on the central nervous system and symptoms related
to the dysfunction of the neuromuscular junction. The interest of biologic
al acetylcholinesterase's measuring is minimal because it is weakly specifi
c or sensitive. The immediate severity is due to hypoxia. Respiratory failu
re results from the lack of central drive inflated with excessive bronchial
secretions, bronchospasm and respiratory muscles paralysis. The secondary
complications are early myopathies whose gravity is correlated with the dec
rease of acetylcholinesterases, or later neuropathies induced by a differen
t mechanism. Beside the symptomatic mesures, atropine is the specific antic
holinergic treatment. When promptly used, oximes can regenerate cholinester
ases. The attempted effects of the treatment are mouth dryness, pupilar dil
atation and flushing of the skin. Nerve agents are lethal toxics which have
a short onset time and produce severe neurological pathology. In a terrori
st incident, it is as important to identify rapidly the toxic agent and pro
vide emergency decontamination as to manage medical care. An effective resp
onse must be multidisciplinary, involving clinicians, toxicologists, Emerge
ncy Medical Service and public's health personnel. (C) 2000 Editions scient
ifiques et medicales Elsevier SAS.