2. 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.

3. 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.

4. 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.

5. 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.

6. 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.

7. PEOPLE EXPOSED TO LOW OR MODERATE DOSES OF STRYCHNINE BY ANY ROUTE WILL HAVE THE FOLLOWING SIGNS OR SYMPTOMS: 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

8. 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

9. 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.

10. 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.

11. http://www.bt.cdc.gov/agent/strychni ne/basics/facts.asp

12. 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, PaO 2 9.5 kPa, PaCO 2 2.6 kPa, HCO 3 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, PaCO 2 5.35 kPa, PaO 2 13.4 kPa, HCO 3 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. http://ccforum.com/content/CC1549