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Strychnine is an alkaloid derived from the seeds of the tree Strychnos nux-vomica. It is odorless and colorless, with a bitter taste. Brucine, a similar but weaker alkaloid, comes from the same seeds. At one time, strychnine was an ingredient in a variety of over-the-counter tonics and laxatives, and it was used in the treatment of cardiac arrest and snake envenomation, and as an analeptic. Although strychnine is no longer found in pharmaceuticals; it is still available as a pesticide and rodenticide. It is also sometimes found as an adulterant in illicit drugs (eg, cocaine, heroin).

  1. Mechanism of toxicity

    1. Strychnine competitively antagonizes glycine, an inhibitory neurotransmitter released by postsynaptic inhibitory neurons in the spinal cord. Strychnine binds to the chloride ion channel, causing increased neuronal excitability and exaggerated reflex arcs. This results in generalized seizure-like contraction of skeletal muscles. Simultaneous contraction of opposing flexor and extensor muscles causes severe muscle injury, with rhabdomyolysis, myoglobinuria, and, in some cases, acute renal failure.

    2. Pharmacokinetics. Strychnine is absorbed rapidly after ingestion or nasal inhalation and distributed rapidly into the tissues. It has low plasma protein binding and a large volume of distribution (Vd estimated at 13 L/kg in one case report). Strychnine is metabolized by the hepatic cytochrome P-450 microsome system to a major metabolite, strychnine N-oxide, by first-order kinetics. Elimination is predominantly extrarenal, with an elimination half-life of about 10–16 hours (see also Table II–61).

  2. Toxic dose. A toxic threshold dose is difficult to establish. The potentially fatal dose is approximately 50–100 mg (1 mg/kg), although death was reported in an adult who had ingested 16 mg. Signs of toxicity can occur rapidly, and because management decisions should be based on clinical findings rather than the reported amount ingested, any dose of strychnine should be considered potentially life-threatening.

  3. Clinical presentation. Signs and symptoms usually develop within 15–30 minutes of ingestion and may last up to 12 to 24 hours.

    1. Muscular stiffness and painful cramps precede generalized muscle contractions, extensor muscle spasms, and opisthotonus. The face may be drawn into a forced grimace (risus sardonicus, “sardonic grin”). Muscle contractions are intermittent and easily triggered by emotional, auditory, or minimal physical stimuli. Repeated and prolonged muscle contractions often result in hypoxia, hypoventilation, hyperthermia, rhabdomyolysis, myoglobinuria, and renal failure.

    2. Muscle spasms may resemble the tonic phase of a grand mal seizure, but strychnine does not cause true convulsions, as its target area is the spinal cord, not the brain. The patient is usually awake and painfully aware of the contractions, described as “conscious seizures.” Profound metabolic acidosis from increased lactic acid production is common.

    3. Victims may also experience hyperacusis, hyperalgesia, and increased visual stimulation. Sudden noises or other sensory input may trigger muscle contractions. Rarely, anterior tibial compartment syndrome can be seen.

    4. Death usually is caused by respiratory arrest that results from intense contraction of the respiratory muscles. Death may also be secondary to hyperthermia or rhabdomyolysis and renal failure.

  4. Diagnosis is based on a history ...

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