Intoxication par la strychnine en 2011 : une menace toujours présente !

Strychnine Intoxication: A Case Report

“…The dose-dependent effects remain controverse. It is difficult to define a lethal dose as the published data are variable from one study to another, but it is possible to admit that it is situated between 30 -100 mg [3]. By competing with glycine for glycinergic receptors (prevents the entrance of chloride, in the cell, that is responsible for a hyperpolarization and therefore stabilizing the membrane potential, diminishing the neuron excitability), strychnine inhibits post-synaptic inhibition, leading to increased motor neuron activity [3].…”

“…It is difficult to define a lethal dose as the published data are variable from one study to another, but it is possible to admit that it is situated between 30 -100 mg [3]. By competing with glycine for glycinergic receptors (prevents the entrance of chloride, in the cell, that is responsible for a hyperpolarization and therefore stabilizing the membrane potential, diminishing the neuron excitability), strychnine inhibits post-synaptic inhibition, leading to increased motor neuron activity [3]. Classical manifestations may include a swift prodromal stage with anxiety, increased sense of awareness and hyperreflexia followed by a well documented clinical stage with nystagmus, risus sardonicus, trismus, intense generalized muscle contractions with preserved consciousness, tactile, auditory and visual stimuli hypersensitivity which may culminate in respiratory arrest and death within hours after ingestion due to contraction of the diaphragm, thoracic and abdominal muscles [5].…”

“…Since the clinical index of suspicion was very elevated regarding the possibility of strychnine intoxication, further attempts in confirming its presence were not pursued. Treatment is supportive and includes benzodiazepines like diazepam (reports of use of 1 mg/kg [1]), lorazepam and clonazepam, GABA receptor-acting anticonvulsants (it may counteract the strychnine effect at the postsynaptic membrane by its inhibitory effect in the motor neuron [3]), mostly phenobarbital and sodium valproate (no specific dosages are described in literature), neuromuscular blocking agents, like atracurium or vecuronium, if previous muscle contractions controlling attempts were not successful, oxygen and airway support, as well as prevention of hemodynamic and metabolic complications (see above) [2,3]. Gastric lavage and induced emesis must be carefully considered, given the risk of precipitating motor manifestations that can culminate in death it may be attempted after the control of muscle contractions.…”

“…Since it is a substance no longer commercialized and thus not present in our every day routine, it calls for an extremely suspicious mind to timely rise this clinical hypothesis. When typical clinical manifestations are recognized early, appropriate treatment can result in a good outcome [2,3].…”

“…In the European Union, where it had its use as a rodenticide, authorities have prohibited its sale in 2003 and recalled all supplies in 2006. Neverthe-less, rare intoxication (accidental or deliberated) reports due to strychnine continue to be published in medical literature, some with the patient being discharged alive [2,3]. Pharmacologically it is a competitive antagonist of glycine, an important inhibitory neurotransmitter in the ventral horns of the spinal cord, brainstem, and higher centers [4].…”