[Acute neurotoxic organophosphate poisoning: insecticides and chemical weapons].

OBJECTIVE

To review clinical and therapeutic bases of an organophosphate poisoning, either with insecticide or nerve agent.

METHODS

References were obtained from computerized bibliographic research (Medline), from personal data (academic memoir, documents under approbation of the National Defense Office), from Internet's data.

RESULTS

Generally, organophosphate poisoning occurs during accidental exposure with agricultural insecticide or suicide. The effects of organophosphate compounds are due to the inhibition of the enzyme acetylcholinesterase. The intoxication symptoms can be divided into muscarine-like, nicotine-like effects, effects on the central nervous system and symptoms related to the dysfunction of the neuromuscular junction. The interest of biological acetylcholinesterase's measuring is minimal because it is weakly specific or sensitive. The immediate severity is due to hypoxia. Respiratory failure 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 decrease of acetylcholinesterases, or later neuropathies induced by a different mechanism. Beside the symptomatic measures, atropine is the specific anticholinergic treatment. When promptly used, oximes can regenerate cholinesterases. The attempted effects of the treatment are mouth dryness, pupilar dilatation and flushing of the skin. Nerve agents are lethal toxics which have a short onset time and produce severe neurological pathology. In a terrorist incident, it is as important to identify rapidly the toxic agent and provide emergency decontamination as to manage medical care. An effective response must be multidisciplinary, involving clinicians, toxicologists, Emergency Medical Service and public's health personnel.