Overview of Strychnine Poisoning

Strychnine is ionized in an acidic pH and then rapidly and completely absorbed in the small intestine. It is metabolized in the liver by microsomal enzymes. The highest concentrations of strychnine are found in the blood, liver, and kidneys. Strychnine and its metabolites are excreted in the urine. Depending on the quantity ingested and treatment measures taken, most of the toxic dose is eliminated within 24–48 hr.

Strychnine inhibits competitively and reversibly the inhibitory neurotransmitter glycine at postsynaptic neuronal sites in the spinal cord and medulla. This results in unchecked reflex stimulation of motor neurons affecting all the striated muscles. Because the extensor muscles are relatively more powerful than the flexor muscles, they predominate to produce generalized rigidity and tonic-clonic seizures. Death results from anoxia and exhaustion.

The onset of strychnine poisoning is fast. After oral exposure, clinical signs may appear within 30–60 min. Presence of food in the stomach can delay onset. Early signs, which may often be overlooked, consist of apprehension, nervousness, tenseness, and stiffness. Vomiting is possible but uncommon. Severe tetanic seizures may appear spontaneously or may be initiated by stimuli such as touch, sound, or a sudden bright light. An extreme and overpowering extensor rigidity causes the animal to assume a “sawhorse” stance. Hyperthermia (104°–106°F [40°–41°C]) due to stiffness and seizures is often present in dogs. The tetanic convulsions may last from a few seconds to ~1 min. Respiration may stop momentarily. Intermittent periods of relaxation are seen during convulsions but become less frequent as the clinical course progresses. The mucous membranes become cyanotic and the pupils dilated. Frequency of the seizures increases, and death eventually occurs from exhaustion or asphyxiation during seizures. If untreated, the entire syndrome may last only 1–2 hr. There are no characteristic necropsy lesions. Sometimes, because of prolonged convulsions before death, agonal hemorrhages of heart and lungs and cyanotic congestion from anoxia may be seen. Animals dying from strychnine poisoning have rapid rigor mortis.

Tentative diagnosis of strychnine poisoning is usually based on history of exposure and clinical signs. Recovery of strychnine alkaloid from the stomach contents, vomitus, liver, kidneys, or urine should be considered diagnostic. Sometimes, urine may not have a detectable amount of strychnine present if analyzed 1–2 days after exposure; therefore, multiple samples should be collected and analyzed. Occasionally, poisoned animals may show presence of undigested grain-laced red or green strychnine bait in the stomach.

Strychnine poisoning can be confused with poisonings by several other seizurigenic substances such as metaldehyde; tremorgenic mycotoxins (penitrem a); organochlorine, organophosphate, or carbamate insecticides; fluoroacetate (1080); zinc phosphide; nicotine; 4-aminopyridine; caffeine; or human medications (tricyclic antidepressants, 5-fluorouracil, metronidazole, isoniazid). Acute, massive hepatic necrosis (hepatic encephalopathy) can also produce clinical signs that resemble those of strychnine poisoning.

Strychnine poisoning is an emergency, and treatment should be instituted quickly. Treatment should be aimed at decontamination, control of seizures, prevention of asphyxiation, and supportive care. Seizures should be controlled, and symptomatic animals stabilized before decontamination is attempted.

Decontamination consists of removal of gastric contents by inducing emesis or gastric lavage, and binding of remaining bait in the GI tract with activated charcoal. Because of the rapid onset of clinical signs, emesis may be of limited value in most cases. If exposure is recent and no clinical signs are present, emesis should be induced with 3% hydrogen peroxide (small animals and pigs) at 1–2 mL/kg, PO, maximum 3 tbsp, repeated once after 30 min if vomiting has not occurred; apomorphine (dogs only) at 0.03 mg/kg, IV, or 0.04 mg/kg, IM; or xylazine (dogs or cats) at 0.5–1 mg/kg, IV or IM. If emesis cannot be induced, gastric lavage should be performed with tepid water. Animals already seizuring should be anesthetized first (with pentobarbital), and an endotracheal tube passed before gastric lavage. After emesis or gastric lavage, activated charcoal should be administered at 2–3 g/kg in small animals and 0.5–1 g/kg in large animals with a cathartic such as magnesium sulfate at 250 mg/kg, PO, or sorbitol at 1–3 mL/kg, PO.

Seizures should be controlled in small animals with pentobarbital, IV to effect, repeated as necessary. Muscle relaxants such as methocarbamol at 100–200 mg/kg, IV, also work well; they should be repeated as needed with a maximal dose of 330 mg/kg/day. In large animals, chloral hydrate or xylazine can be used to control seizures. Other medications such as glyceryl guaiacolate (5%, 110 mg/kg), diazepam, and xylazine have been used in dogs to control seizures with variable success. Propofol (3–6 mg/kg, IV, or 0.1–0.6 mg/kg/min as a constant-rate IV infusion) can also be tried to control seizures in dogs or cats. Isoflurane inhalation anesthesia can be used in small animals if preceding measures to control seizures do not work.

Severely affected dogs should be intubated, and artificial respiration provided. Acidification of urine with ammonium chloride (100 mg/kg, bid, PO) may be useful for ion trapping and urinary excretion of the alkaloid. IV fluids should be administered to force diuresis and maintain normal kidney function. Hyperthermia treatment (fans, cool bath) should be given if necessary. Acid-base balance should be monitored and corrected as needed. Most clinical cases may require 1–3 days of treatment.