Organophosphate poisoning/intoxication

A classification of organophosphate poisoning has been proposed by Tafuri and Roberts (1987) modified from Namba et al. (1971). Clinical signs and symptoms of intoxication may occur when serum cholinesterase levels drop to below 50% of the normal value. Mild poisoning, with the patient still ambulatory, may occur when serum cholinesterase levels are 20-50% of normal moderate poisoning with inability to walk with levels 10-20% of normal and severe poisoning with respiratory distress and unconsciousness with serum cholinesterase levels <10% of normal. 

Tarbah FA, Kardel B. Pier S, Temme O, Daldrup T. Acute poisoning with phosphamidon determination of dimethyl phosphate (DMP) as a stable metabolite in a case of organophosphate insecticide intoxication. J Anal Toxicol 2004 28 198-203. 

Guillan-Barre syndrome, organophosphate poisoning, myasthenia gravis, magnesium intoxication, tick paralysis, atropine poisoning. 

Due to the lack of gas masks and other protective clothes and gear, the total number of victims poisoned with sarin in Matsumoto who needed professional help (600) included not only residents, but also members of the rescue team and health care professionals. Seven out of 58 residents admitted to the hospitals died. A physician from the duty ambulance vehicle and seven rescuers out of the 95 engaged, had mild symptoms of organophosphate intoxication [13],... 

Phenylcarbonyl- and cyclohexylcarbonyl-substituted bispiridinium oximes known as HGG- and BDB-oximes were developed as experimental antidotes against poisonings with highly toxic organophosphates [23, 32], Analogical studies of recovery of MNT after intoxication with soman have been carried out (Table 5) [13]. 

A. Oximes are used to treat poisoning caused by cholinesterase inhibitor insecticides and nerve agents, ie, organophosphates, mixtures of organophospho-ms and carbamate insecticides, or pure carbamate insecticide intoxication with nicotinic-associated symptoms. Because of its low toxicity, possible ineffectiveness if treatment is delayed until after the cholinesterase enzyme has aged, ability to reverse nicotinic as well as muscarinic effects, and ability to reduce atropine requirements, pralidoxime should be used early and empirically for suspected cholinesterase inhibitor poisoning. 

Inhibition of AChE is irreversible, preventing the substrat (ACh) from reacting with the esterase site. Consequently, accumulation of ACh results in all symptoms of acetylcholine poisoning caused by organophosphates (Santos et al. 2007). Symptoms of intoxication appear after approximately 50 % of the AChE is inhibited and the typical effects are agitation, muscle weakness, muscle fasciculations, hypersalivation and sweat. Severe poisonings may cause respiratory failure, unconsciousness, confusion, convulsions and/or death (Sogorb and Vilanova 2002 Duysen et al. 2012). 

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