Atropine toxicity

To administer such large doses, the authors had to have the atropine solutions prepared in a more concentrated form. The new injectable ampoules contained 50 mg per cc instead of the usual 2 or 5mg. These megadoses of atropine, and the claim that the resulting coma and delirium could be reversed by 4 mg of a dmg known to be ineffective in treating atropine toxicity, might have caused their reports to be r arded as balderdash by some readers. 

Meanwhile, the reports by Forrer et al. inspired doctors Toyoji Wada, Shoji Horigome and Takashi Sakurada to try it out on patients at the Hirosaki University School of Medicine, Hirosaki. Using a similar protocol, they treated 51 cases between 1957 and 1960. The doctors gave patients an average of 30-50 mg by injection (up to a maximum dose of 220 mg) every other day for 3-7 weeks without cessation. They published, Clinical Experience of the So-Called Atropine Toxicity Therapy (Forrer) in 1960 in Toboku J. Exper. Med. 

Forrer GR Atropine toxicity in the treatment of schizophrenia Journal of the Michigan State Medical Society. 1950 49 184-185. 

Atropine toxicity is characterized by dry mouth, burning sensation in the mouth, rapid pulse, mydriasis, blurred vision, photophobia, dry and flushed skin, restlessness, and excitement. 

If atropine is used, clinicians must be aware of the signs and symptoms of atropine toxicity. A similar concern exists when 2% cycfopentolate is used in infents or children. If side effects occm optometrists should be prepared to manage them either through direct intervention or referral to other practitioners. 

Systemic reactions from the topical administration of scopolamine are quite similar to those of atropine. However, CNS toxicity appears to be more common with scopolamine than with atropine. In a series of several hundred patients whose pupils were dilated with 1% scopolamine, seven cases of confiisional psychosis were observed. The reactions included restlessness, confusion, hallucinations, incoherence, violence, amnesia, imcon-sciousness, spastic extremities, vomiting, and urinary incontinence. Others have reported similar acute psychotic reactions in children receiving from 0.6 to 1.8 mg of topically administered scopolamine. However, no deaths have been reported from topical ocular use of scopolamine.Treatment of toxic reactions is the same as that far atropine toxicity. 

Systemic Effects. Systemic cyclopentolate toxicity is dose related and evolves in a manner similar to atropine toxicity. Compared with atropine, however, cyclopentolate causes more CNS effects. 

Peripheral effects typical of atropine, such as flushing or dryness of the skin or mucous membranes, have not been observed with cyclopentolate in children or adults. Moreover, temperature, pulse, blood pressure, and respiration are generally not affected. Treatment of cyclopentolate toxicity is the same as that for atropine toxicity. Because toxic reactions occur more commonly with the 2% solution or with multiple instillations of the 1% solution, the smallest possible dose should be used. 

During acute administration of various compounds, the time for recovery varied with dose with low doses, Che peak effects of parenteral administration were seen in 0.5 h and lasted up to 6 h with high doses, the effects persisted for up to 24 h. With toxic doses, a return to baseline occurred in the second day after administration. Followup EEG data are limited, Che principal data being reports of atropine toxicity. In these studies, the few statements referring to EEG changes suggest that the effects disappear within a few days of the last exposure. 

Goldner (19) reported chat he had used Intramuscular doses of 5-50 mg of scopolamine In treating beneficially an unspecified number of mental patients, but then had switched to atropine because of its greater availability. Be reported on a group of 20 patients treated with atropine-toxicity therapy, 13 (65Z) of whom were considered to have benefited moderately or markedly. Goldner also gave a limited comparison of the results of electroconvulsive therapy (EOT) and of atropine-toxicity therapy, stating chat several patients who had not benefited from ECT improved on substitution of atropine-induced coma. 

Goldner, R.O. 1956 Experience of Use [of atropine toxicity therapy] in Private Practice. J. Nerv. Ment. 

Forrer, G.R. 1956 History [of atropine toxicity therapy] and Future Research. J. Merv. Ment. Dls. 124 256-259. 

Wada, T., Horlgome, S., Sakurada, T. 1960 Clinical Experience of the So-Called "Atropine Toxicity Therapy [Forrer]". Tohoku J. Exp. Med. 72 398-404. 

Goldner, R.O. 1956 Symposium on atropine toxicity therapy. Experience of use In private practice, J. nerv. ment Dls. 

Only six of 36 children who took overdoses of co-phenotrope had signs of atropine overdose (central nervous system excitement, hypertension, fever, flushed dry skin) (1). Opioid overdose (central nervous system and respiratory depression with miosis) predominated or occurred without any signs of atropine toxicity in 33 cases (92%). Diphenoxylate-induced hjrpoxia was the major problem and was associated with slow or fast respiration, hypotonia or rigidity, cardiac arrest, and in three cases cerebral edema and death. Respiratory depression recurred 13-24 hours after the ingestion in seven cases and was probably due to accumulation of difenoxine, an active metabolite of diphenoxylate. Recommended treatment is an intravenous bolus dose of naloxone, followed by a continuous intravenous infusion, prompt gastric lavage, repeated administration of activated charcoal, and close monitoring for 24 hours. 

Atropine toxicity resulting from the use of the eye-drops to dilate the pupil has been... 

Animals are at risk for anticholinergic poisoning from atropine. Toxicity is similar to that in humans. Gastrointestinal decontamination and supportive care should be employed. 

E. Toxicity A traditional mnemonic for atropine toxicity is Dry as a bone, red as a beet, mad as a hatter." This description reflects both predictable antimuscarinic effects and some unpredictable actions. 

J. H. E. Baker and J. R. Silver, Atropine toxicity in acute cervical spine injury, Paraplegia, 1984, 22, 379-382. 

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