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Death is usually secondary to respiratory paralysis. Symptoms include seizures, a " sawhorse" stance, and opisthotonus (rigid extension of all four limbs). The onset of symptoms is 10 to 120 minutes after ingestion. The most common domestic animal to be affected is the dog, either through accidental ingestion or intentional poisoning. However, since 1990 in the United States most baits containing strychnine have been replaced with zinc phosphide baits. Rodent baits are commonly available over-the-counter, but coyote baits are illegal in the United States. Strychnine poisoning in animals occurs usually from ingestion of baits designed for use against rodents (especially gophers and moles) and coyotes. The concentrations in blood or urine of those with symptoms are often in the 1–30 mg/L range. Strychnine is easily quantitated in body fluids and tissues using instrumental methods in order to confirm a diagnosis of poisoning in hospitalized victims or to assist in the forensic investigation of a case of fatal overdosage. 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.ĭetection in biological specimens If the patient survives past 24 hours, recovery is probable. Anticonvulsants such as phenobarbital or diazepam are administered to control convulsions, along with muscle relaxants such as dantrolene to combat muscle rigidity. "The convulsions are often triggered by stimuli – when your body senses something, neurons want to fire, and if they aren’t controlled seizures occur – so patients are generally kept in quiet, dark rooms." 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. There is no specific antidote for strychnine. No unpleasant symptoms, no headache, &c., but a desire " toīe on the move " and a slight feeling of stiffness in the jaw. Judge, I took the same quantity of bromide, potassiumĪnd chloral– and a little time after I lost consciousness andįell into a " profound sleep," awaking in the morning with There was no opisthotonos, only a slight stiffnessĪt the back of the neck. I felt better, but my lower limbs were as cold as ice, and the calf muscles kept tense and were Off." I did not call for medical aid, as I thought that the symptoms wereĭeclining. My whole body was in a cold sweat, with anginousĪttacks in the precordial region, and a feeling of "going bromide of potassium and 10 gr.Ĭhloral-put them in a tumbler with some water, and drank Had no confidence or courage to weigh them, so I guessed (fortunately) the bromide of potassium and the chloral. Off the bed and scrambled to a case in my room and got out I then knew something serious was developing, so I crawled Turned my head flashes of light kept darting across my eyes.
My toes drew up under my feet, and as I moved or I lay on the bed and the calf muscles began to stiffen and Great uneasiness and restlessness, and I felt a desire to walkĪbout and do something rather than sit still and read. Muscles " and a peculiar metallic taste in the mouth. It, towards the evening, I felt a tightness in the "facial Solution (B.P.) with the same quantity of dilute phosphoric acid Three years ago I was reading for an examination,Īnd feeling "run down". One medical student in 1896 described the experience in a letter to the Lancet:
The subject usually dies within 2–3 hours after exposure. Death comes from asphyxiation caused by paralysis of the neural pathways that control breathing, or by exhaustion from the convulsions. These are followed by postictal depression. Convulsions lead to lactic acidosis, hyperthermia and rhabdomyolysis. The convulsions progress, increasing in intensity and frequency until the backbone arches continually. The spasms then spread to every muscle in the body, with nearly continuous convulsions, and get worse at the slightest stimulus. Ten 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.