Source
• STRYCHNINE IS MADE FROM THE BERRIES OF
THE PLANT STRYCHNOS NUX VOMICA.
• THE PLANT IS FOUND IN SOUTHERN ASIA.
• STRYCHNINE BERRIES ARE FLESHY AND
ORANGE OR YELLOW AND ARE ONE AND A
HALF INCH IN DIAMETER.
What is it and how can
you take it?
• white, odorless, bitter crystalline powder
• can be taken by mouth, inhaled (breathed in),
or mixed in a solution and given intravenously
(injected directly into a vein)
• strong poison; only a small amount is needed
to produce severe effects in people.
Past and Present
•In the past, strychnine was available in a pill
form and was used to treat many human
ailments.
•Today, strychnine is used primarily as a
pesticide, particularly to kill rats.
•Uncommonly, strychnine is found mixed with
“street” drugs such as LSD, heroin, and cocaine.
Exposure
• FOLLOWING RELEASE OF STRYCHNINE INTO WATER,
YOU COULD BE EXPOSED BY DRINKING CONTAMINATED
WATER.
• FOLLOWING CONTAMINATION OF FOOD WITH
STRYCHNINE, YOU COULD BE EXPOSED BY EATING THE
CONTAMINATED FOOD.
• IT IS ALSO POSSIBLE TO ABSORB STRYCHNINE
THROUGH THE MEMBRANES IN THE NOSE, EYES, OR
MOUTH. FOR EXAMPLE, A PERSON COULD BE POISONED
BY INHALING STRYCHNINE POWDER THAT HAS BEEN
RELEASED IN THE AIR.
• STRYCHNINE COULD BE SMOKED OR SNORTED AS A
COMPONENT OF STREET DRUGS.
• POISONING HAS BEEN REPORTED FROM STRYCHNINE
GIVEN INTRAVENOUSLY AND THROUGH THE NOSE.
How it works…
• STRYCHNINE PREVENTS THE PROPER
OPERATION OF THE CHEMICAL THAT CONTROLS
NERVE SIGNALS TO THE MUSCLES. THE CHEMICAL
CONTROLLING NERVE SIGNALS WORKS LIKE THE
BODY’S “OFF SWITCH” FOR MUSCLES. WHEN THIS
“OFF SWITCH” DOES NOT WORK CORRECTLY,
MUSCLES THROUGHOUT THE BODY HAVE SEVERE,
PAINFUL SPASMS. EVEN THOUGH THE PERSON’S
CONSCIOUSNESS OR THINKING ARE NOT
AFFECTED AT FIRST (EXCEPT THAT THE PERSON IS
VERY EXCITABLE AND IN PAIN), EVENTUALLY THE
MUSCLES TIRE AND THE PERSON CAN’T BREATHE.
• PEOPLE EXPOSED TO LOW OR MODERATE DOSES
OF STRYCHNINE BY ANY ROUTE WILL HAVE THE
FOLLOWING SIGNS OR SYMPTOMS:
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AGITATION
APPREHENSION OR FEAR
ABILITY TO BE EASILY STARTLED
RESTLESSNESS
PAINFUL MUSCLE SPASMS POSSIBLY LEADING TO
FEVER AND TO KIDNEY AND LIVER INJURY
UNCONTROLLABLE ARCHING OF THE NECK AND
BACK
RIGID ARMS AND LEGS
JAW TIGHTNESS
MUSCLE PAIN AND SORENESS
DIFFICULTY BREATHING
DARK URINE
INITIAL CONSCIOUSNESS AND AWARENESS OF
SYMPTOMS
• PEOPLE EXPOSED TO HIGH DOSES OF
STRYCHNINE MAY HAVE THE FOLLOWING SIGNS
AND SYMPTOMS WITHIN THE FIRST 15 TO 30
MINUTES OF EXPOSURE:
• RESPIRATORY FAILURE (INABILITY TO BREATHE),
POSSIBLY LEADING TO DEATH
• BRAIN DEATH
long term effects
• IF THE PERSON SURVIVES THE TOXIC EFFECTS
OF STRYCHNINE POISONING, LONG-TERM
HEALTH EFFECTS ARE UNLIKELY. HOWEVER,
LONG-TERM EFFECTS MAY RESULT FROM
DAMAGE CAUSED BY THE POISONING (FOR
EXAMPLE, BRAIN DAMAGE FROM LOW
OXYGEN, KIDNEY FAILURE). PEOPLE SEVERELY
AFFECTED BY STRYCHNINE POISONING ARE
NOT LIKELY TO SURVIVE.
long term effects
• IF THE PERSON SURVIVES THE TOXIC EFFECTS
OF STRYCHNINE POISONING, LONG-TERM
HEALTH EFFECTS ARE UNLIKELY. HOWEVER,
LONG-TERM EFFECTS MAY RESULT FROM
DAMAGE CAUSED BY THE POISONING (FOR
EXAMPLE, BRAIN DAMAGE FROM LOW
OXYGEN, KIDNEY FAILURE). PEOPLE SEVERELY
AFFECTED BY STRYCHNINE POISONING ARE
NOT LIKELY TO SURVIVE.
http://www.bt.cdc.gov/agent/strychni
ne/basics/facts.asp
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CASE STUDY
A 42-year-old man with no significant past medical history presented approximately 1 hour
after ingestion of a bottle of wine together with some "white powder" from his garden shed
(this was later confirmed to be strychnine). He was able to walk in to the Emergency
Department, but he was agitated and ataxic, in keeping with his ethanol intake. Within a few
minutes of his arrival, his condition rapidly deteriorated and he developed a marked tremor
and muscular spasms and shortly after this had a respiratory and secondary cardiac arrest.
At this stage he was intubated and ventilated, and cardiac output returned after 5 minutes.
He was transferred to the intensive care unit (ICU) and the National Poisons Information
Service (London) was contacted for further advice on management.
He continued to have marked muscle spasms and so was paralysed with 0.1 mg/kg
pancuronium given intravenously. He was given 50 g activated charcoal via a nasogastric
tube. Postarrest, his blood pressure was 85/40 mmHg, heart rate 96 beats/min and
temperature 38.2°C. Arterial blood gases showed a severe metabolic acidosis (pH6.51, PaO2
9.5 kPa, PaCO2 2.6 kPa, HCO3 3.7 mmol/l, base excess [BE] -18) and he was given 3 mmol/kg
8.4% sodium bicarbonate; his metabolic acidosis improved over the next 8 hours (pH7.26,
PaCO2 5.35 kPa, PaO2 13.4 kPa, HCO3 18 mmol/l, BE -9). He remained hypotensive despite
fluid resuscitation and over the first 24 hours he required norepinephrine to maintain his
blood pressure (maximum dose 900 g/h). His temperature rose to 39.9°C on day2 but settled
after simple cooling measures and rehydration. His creatinine kinase peaked at 8218 IU/l,
(although there was no evidence of myoglobinuria) and his creatinine peaked at 194 mol/l
on day 2.
He was extubated on day3, initially with some persisting twitching and muscular spasms,
requiring boluses of midazolam and diazepam and an alfentanil infusion for analgesia. By
day5 he was asymptomatic and his renal function had returned to normal. He was
discharged from hospital on day10 after psychiatric assessment.
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