Poison treatment organophosphates

Sidell, F.R. (1974). Soman and sarin clinical manifestation and treatment of accidental poisoning by organophosphates. Clin. Toxicol. 7 1-17. 

Fig. 5-4. This man was accidentally exposed to an unknown amount of nerve agent vapor. The series of photographs shows his eyes gradually recovering their ability to dilate. All photographs were taken with an electronic flash (which is too fast for the pupil to react) after the subject had been sitting in a totally dark room for 2 minutes. These photographs were taken (from top to bottom) at 3, 6, 13, 20, 41, and 62 days after the exposure. Subsequent photographs indicate that the eyes did not respond fully to darkness for 9 weeks maximal dilation was reached on day 62 after the exposure. Reprinted with permission from Sidell FR. Soman and sarin Clinical manifestations and treatment of accidental poisoning by organophosphates. Clin Toxicol. 1974 7 11.

Schomig, A., Richardt, G., Kurz, T., 1995. Sympatho-adrenergic activation of the ischemic myocardium and its arrhythmogenic impact. Herz 20,169-186. SideU, F.R., 1974. Soman and sarin clinical manifestations and treatment of accidental poisoning by organophosphates. Clin. Toxicol. 7,1—17. 

Jokanovic, M., 2010. Medical treatment of poisoning with organophosphates and carbamates. In Satoh, Tetsuo, Gupta, Ramesh (Eds.), Anticholinesterase Pesticides Metabolism, Neurotoxidty and Epidemiology John Wiley Sons, Hoboken, New Jersey, pp. 583-597. (Chapter 42). 

F. R. Sidell, Soman and Sarin - Clinical Manifestations and Treatment of Accidental-Poisoning by Organophosphates, Clin. Toxicol, 1974, 7, 1-17. 

Lotti M, Becker CE. 1982. Treatment of acute organophosphate poisoning Evidence of a direct effect on central nervous system by 2-PAM (pyridine-2-aldoxime methyl chloride). J Toxicol Clin Toxicol 19 121-127. 

Irreversible anticholinesterases include the organophosphorus inhibitors and ambenonium, which irreversibly phosphorylate the esteratic site. Such drugs have few clinical uses but have been developed as insecticides and nerve gases. Besides blocking the muscarinic receptors with atropine sulphate in an attempt to reduce the toxic effects that result from an accumulation of acetylcholine, the only specific treatment for organopho-sphate poisoning would appear to be the administration of 2-pyridine aldoxime methiodide, which increases the rate of dissociation of the organophosphate from the esteratic site on the enzyme surface. 

Malathion is an organophosphate cholinesterase inhibitor. Up to 8% of the topically applied dose may be absorbed. Malathion is used as a treatment for head lice, body lice and scabies. It effectively kills both the eggs and the adult lice. Malathion is an insecticide of relatively low human toxicity. However if malathion is used in an indoor environment, as it breaks down into malaoxon, it can be seriously and chronically poisonous. The safety of malathion in pregnancy and in lactating women and in children has not been established. 

Davies, D.R., Green, A.L., and Willey, G.L. 2-Hydroxy-iminomethyl-N-methylpyridlnium methanesulphonate and atropine in the treatment of severe organophosphate poisoning. Br. J. Pharmacol. Chemother. 14 5-8, 1959. 

Bajgar J (2004) Organophosphates/nerve agent poisoning mechanism of action, diagnosis, prophylaxis, and treatment. Adv Clin Chem 38 151-216... 

---