Strychnine Poisoning

The clinical presentation stems from the deleterious effects of strychnine on the central nervous system (CNS). By reducing the activity of glycine, the main inhibitory neurotransmitter in the CNS, strychnine causes profound motor stimulation as early as 10-30 minutes after ingestion, which is considered to be the main mode of poison introduction into the human body, but rare cases have documented dermal exposure as a mode of poisoning [1] [2] [3]. Muscle spasms and agitation may be encountered early on, followed by characteristic spasms of flexors of the upper limbs and extensors of the lower limbs, opisthotonos and risus sardonicus - spasm of the facial muscles [1]. In addition to enhanced muscle activity, convulsions are a constitutive feature of strychnine poisoning, primarily in the form of generalized attacks [1] [2]. In virtually all cases, convulsions are provoked by sensory stimuli, as hyperacuity of hearing, vision, and tactile sensation are also consequences of poisoning [4]. It must be noted that the patient is awake and conscious at the time of convulsions and during the appearance of muscle spasms [2]. Moreover, hyperthermia, rhabdomyolysis, renal failure due to myoglobinuria, and severe metabolic acidosis can develop in the setting of prolonged spasms [2], but the most important complication is the respiratory failure [3]. Spasms of the muscles of the chest and diaphragm are the main cause of death, and the majority of patients suffer from fatal respiratory distress before even reaching the hospital [2] [3].

An immediate laboratory workup comprising serum lactate levels, arterial blood gasses (ABG), pH measurement, and renal function tests must be performed in patients who are admitted to the hospital with profound spasms and generalized convulsions, to initiate adequate therapeutic measures and to save the patient's life. The diagnosis of strychnine poisoning may be difficult to make, however, as poisoning by this substance is very rare, but details from patient history such as recent exposure to rodenticides or use of intravenous drugs (strychnine was shown to be added as an adulterant drug to cocaine, heroin, and amphetamines) may be helpful [2]. Interview with friends or family should be conducted to assess the mental state of the patient, like attempted suicide using strychnine is also an important mode of intoxication [1]. In patients with an undisclosed cause of symptoms, especially in the setting of a sudden death, a routine toxicology report and a meticulous post-mortem examination are necessary [5]. Identifying strychnine as the underlying cause of symptoms can be made by its quantitative evaluation in body fluids (blood and urine) and tissues. Gas chromatography (GC) is recommended, both anti-mortem and post-mortem [1] [3]. It is the main diagnostic tool, and two methods have been mentioned in literature - GC-flame ionization detection (GC-FID) and GC nitrogen-phosphorus detection (GC-NPD) [3]. Mass spectrometry is another laboratory procedure that could be performed for detection of strychnine [1] [3].

1. Rosano TG, Hubbard JD, Meola JM, Swift TA. Fatal strychnine poisoning: application of gas chromatography and tandem mass spectrometry. J Anal Toxicol. 2000;24(7):642-647.
2. Wood DM, Webster E, Martinez D, Dargan PI, Jones AL. Case report: Survival after deliberate strychnine self-poisoning, with toxicokinetic data. Crit Care. 2002;6(5):456-459.
3. Greene R, Meatherall R. Dermal exposure to strychnine. J Anal Toxicol. 2001;25(5):344-347.
4. Porter RS, Kaplan JL. Merck Manual of Diagnosis and Therapy. 19th Edition. Merck Sharp & Dohme Corp. Whitehouse Station, N.J; 2011.
5. Kodikara S. Strychnine in amoxicillin capsules: a means of homicide. J Forensic Leg Med. 2012;19(1):40-41.