Poisoning due to organophosphate insecticides: Acute and chronic manifestations

Abstract

Three patients with organophosphate insecticide poisoning are described. The first patient with Diazinon ® poisoning and the second with parathion poisoning illustrate the acute manifestations, the criteria for diagnosis, and treatment with pralidoxime and atropine in organophosphate poisoning. The diagnosis of acute organophosphate poisoning is based on a history of exposure to organophosphates, manifestations including miosis and fasciculations, improvement following administration of pralidoxime and atropine (increased tolerance to atropine), and reduction in blood cholinesterase activity. Pralidoxime has been effective in management of many patients with poisoning by parathion and methyl parathion, and in a smaller number with poisoning by Diazinon, EPN, DFP, TEPP; probably Bidrin, carbophenthion, dichlorvos and dimethoate; and possibly mevinphos. The effectiveness of pralidoxime in the management of poisoning in man by malathion, methyl demeton, phosphamidone and azinphosmethyl has not been established. Pralidoxime is effective in reactivating organophosphate-inhibited cholinesterase at the cholinergic synapses, including the central nervous system. The third patient with polyneuropathy illustrates the possibility of persistent manifestations of organophosphate poisoning. He had been exposed as a chemist to organophosphates and their intermediates, which appear to be the cause of polyneuropathy. In animal experiments some organophosphates caused polyneuropathy. In man, polyneuropathy has been caused frequently by triorthocresyl phosphate and less often by mipafox, but rarely by commercially available organophosphate insecticides, and the cause-result relationship has not been established. The other main persistent effect of organophosphate poisoning has been central nervous system symptoms, which usually follow acute poisoning inconsistently and are mainly of emotional origin.