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Strychnine poisoning

Kavita M Babu, MD
Section Editor
Stephen J Traub, MD
Deputy Editor
Jonathan Grayzel, MD, FAAEM


Strychnine, an alkaloid derived from seeds of the tree Strychnos nux vomica, was first used as a rodenticide in Germany in the early 16th century. By the early 1900s, strychnine became widely available in cathartic pills, and caused a significant number of fatalities from suicidal and unintentional ingestions in the United States. In the early 1900s, strychnine toxicity was a major cause of toxicologic death in children [1,2]. The number of strychnine exposures in the United States has fallen significantly since its elimination from nonprescription preparations in 1962 [1].

Although rare, most strychnine poisonings today result from the adulteration of street drugs (eg, cocaine, heroin), as well as from small amounts found in herbal medications and homeopathic remedies [3]. Rarely, cases of poisoning occur in which a strychnine-containing rodenticide is implicated [4-6].

This topic review will discuss the basic pharmacology, clinical presentation, and management of strychnine poisoning. Discussions of the general approach to the management of poisoned patients and detailed management of other toxins are found elsewhere. (See "General approach to drug poisoning in adults".)


The seeds of Strychnos nux vomica contain 1.1 to 1.4 percent of strychnine and brucine, another toxic alkaloid [7]. Commercial rodenticide preparations typically contain between 0.3 to 5.0 percent strychnine [2,8]. Strychnine is typically formulated as a relatively odorless and tasteless white powder [4]. While brucine (2,3-dimethoxystrychnine) is the lesser alkaloid, lethal ingestion of brucine alone has been reported [9].

Lethal doses of strychnine are generally accepted as 1 to 2 mg/kg [10], although death has been reported at lower doses, and survival has been documented with significantly higher doses [11].

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Literature review current through: Nov 2017. | This topic last updated: Dec 12, 2016.
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