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Strychnine poisoning can be fatal to humans and other animals and can occur by inhalation, swallowing or absorption through eyes or mouth. It produces some of the most dramatic and painful symptoms of any known toxic reaction. For this reason, strychnine poisoning is often used in literature and film.
[edit] Presentation in humansTen to twenty minutes after exposure, the body's muscles begin to spasm, starting with the head and neck in the form of trismus and risus sardonicus. The spasms then spread to every muscle in the body, with nearly continuous convulsions, and get worse at the slightest stimulus. The convulsions progress, increasing in intensity and frequency until the backbone arches continually. Convulsions lead to lactic acidosis, hyperthermia and rhabdomyolysis. These are followed by postictal depression . Death comes from asphyxiation caused by paralysis of the neural pathways that control breathing, or by exhaustion from the convulsions. The subject dies within 2–3 hours after exposure. [edit] TreatmentThere is no specific antidote for strychnine. Treatment of strychnine poisoning involves an oral application of an activated charcoal infusion which serves to absorb any poison within the digestive tract that has not yet been absorbed into the blood. Anticonvulsants such as phenobarbital or diazepam are administered to control convulsions, along with muscle relaxants such as dantrolene to combat muscle rigidity.[1] If the patient survives past 24 hours, recovery is probable. The treatment for strychnine poisoning in the late 19th and early 20th centuries was to administer tannic acid which precipitates the strychnine as an insoluble tannate salt, and then to anaesthetise the patient with chloroform until the effects of the strychnine had worn off. [edit] Strychnine toxicity in animalsStrychnine poisoning in animals occurs usually from ingestion of baits designed for use against rodents (especially gophers and moles) and coyotes. Rodent baits are commonly available over-the-counter, but coyote baits are illegal in the United States. However, since 1990 in the United States most baits containing strychnine have been replaced with zinc phosphide baits.[2] The most common domestic animal to be affected is the dog, either through accidental ingestion or intentional poisoning. An approximate lethal dose for a dog is 0.75 mg per kg body weight.[3] For a 0.3% strychnine bait, five grams of bait could be enough to kill a 20 kilogram dog. The onset of symptoms is 10 to 120 minutes after ingestion.[3] Symptoms include seizures, a "sawhorse" stance, and opisthotonus (rigid extension of all four limbs). Death is usually secondary to respiratory paralysis. Treatment is by detoxification using activated charcoal, pentobarbital for the symptoms, and artificial respiration for apnea. In most western nations a special license is needed to use and possess strychnine for agricultural use. [edit] Notable strychnine poisonings
[edit] Fictional strychnine poisonings
[edit] References
[edit] External links
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