ANTICHOLINERGIC POISONING: TREATMENT WITH PHYSOSTIGMINE

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Abstract
The increased incidence of poisoning by overdoses of commonly used drugs with anticholinergic properties (Table I) and the general lack of knowledge concerning a specific treatment for these poisons warrants a summary of the problem at this time. Some plants containing anticholinergic alkaloids are also included in this group as they may also be taken intentionally or accidentally. Drugs with anticholinergic properties primanly antagonize acetylcholine competitively at the neuroreceptor site. Cardiac muscle, exocrine glands, and smooth muscle are most markedly affected.1 Action of the inhibitors is overcome by increasing the level of acetylcholine naturally generated in the body through inhibiting the enzyme (choline esterase) which normally prevents accumulation of excess acetylcholine. It does this by hydrolyzing that compound to inactive acetic acid and choline. Agents which inhibit this enzyme, so that acetylcholine accumulates at the neuroreceptor sites, are called anticholine esterases. Physostigmine, one of the anticholine esterases which is a tertiary amine, crosses into the central nervous system and can reverse both central and peripheral anticholinergic actions2. Neostigmine and pyridostigmine are also anticholine esterases but they are quaternary amines and are capable of acting only outside the central nervous system because of solubility and ionization characteristics. The anticholinergic syndrome has both central and peripheral signs and symptoms. Central toxic effects include anxiety, delirium, disorientation, hallucinations, hyperactivity, and seizures.2 Severe poisoning may produce coma, medullary paralysis, and death. Peripheral taxicity is characterized by tachycardia, hyperpyrexia, mydriasis, vasodilatation, urinary retention, diminution of gastrointestinal motility, decrease of secretion in salivary and sweat glands, and loss of secretions in the pharynx, bronchi, and nasal passages.

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