![]() Pralidoxime is an acetylcholinesterase enzyme re-activator. Unlike poisoning with carbamates, this interaction is irreversible. The serine site lies within the enzyme's active site and is attacked by the organophosphate molecule this leads to the phosphorylation of the serine site and the formation of a strong covalent bond inactivating the active site of the enzyme in the process. This enzyme has a serine site and an anionic site on its molecule. ![]() Īcetylcholinesterase enzyme is responsible for the hydrolysis of the neurotransmitter acetylcholine at the various muscarinic and nicotinic sites in the body and hence does not let it accumulate. ![]() The number of suicidal poisonings is almost double that, and the combined death toll exceeds 200,000. Annually, there are about a million reported cases of accidental organophosphate poisoning globally. Instances of over-the-counter availability of these compounds coupled with their well-known notoriety as potent poisons have led to a high incidence of suicides using organophosphate compounds in the general population as well. Lack of adequate education and protection also leads to a high incidence of accidental poisonings in this cohort. Thus, easy access and cheap cost make organophosphate pesticides a pathway for committing suicide this is especially rampant in primarily agriculture-based economies like that of many developing countries today. Poor yield, drought, debt, and extreme working hours often drive farmers into depression. Common pharmaceutical guidelines recommend refrigeration for compounded products such as this if not completely used within 28 days.Pralidoxime also has approval as an antidote for organophosphate-based pesticides. Today organophosphate-based pesticides are widely used in agriculture all over the world. Once all materials were available, the compounding of this preparation required about 1 hour to complete.Įxisting atropine stocks can be readily augmented by fortification with powdered atropine accurately and inexpensively. The product was pyrogen free and maintained its potency at refrigeration temperature for at least 8 weeks after preparation and at room temperature for 4 weeks. The amount of atropine initially present varied by less than +/-5%, within the range allowed by the US Pharmacopeia for the original product. An independent analysis of the resulting formulation was undertaken to assess its potency, absence of pyrogens, and stability. ![]() To facilitate the delivery of larger atropine doses, we developed a method of fortifying existing injectable atropine with bulk pharmaceutical-grade atropine powder to a concentration of 2 mg/mL, thereby increasing the amount available and facilitating its intramuscular administration. Moderately ill victims may not require an intravenous line for other care, and in the setting of overwhelmed resources, intramuscular administration is faster and easier to perform. Atropine that is commercially available comes supplied at concentrations of either 0.4 mg/mL or 1 mg/mL, thereby requiring intravenous administration because of the volume necessary to administer the commonly recommended initial dose of 2 to 6 mg. Antidote stocks at many hospitals are inadequate to meet this demand. This situation would require the prompt availability of a large amount of atropine to provide treatment. A large-scale exposure to a nerve agent or organophosphate insecticide might result in many victims presenting for care within a short period of time. Atropine is the preferred antidote for immediate management of toxicity associated with nerve agents or other cholinergic syndromes.
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