Strychnine
Strychnine
1. NAME
1.1 Substance
Strychnine
1.2 Group
Alkaloid, Stimulant of the central nervous system
1.3 Synonyms
Strychnidin-10-one
Estricnina (Portuguese and Spanish)
Stricnina (Italian)
Strychnin(German)
Strychnine (English and French)
1.4 Identification numbers
1.4.1 CAS
57-24-9
1.4.2 Other numbers
NIOSH WL 2275000
SIC/CODES 2834; 2833
CEC 614-003-00-5.
1.5 Brand names/trade names
Certox
Dog-Button
Dolco Mouse Ceral
Kwik-kill
Mole Death
Mouse Nots
Mouse-Rid
Mouse-Tox
Pied Piper Mouse Seed
Quaker Button
Ro-Dex
Sanaseed
(Note: In Portugal, rodenticides do not contain strychnine).
1.6 Manufacturers and importers
To be completed by each centre.
(Note: In Portugal, pesticides do not contain strychnine).
2. SUMMARY
2.1 Main risks and target organs
Strychnine is a potent convulsant. It causes increased
reflex excitability in the spinal cord that results in a loss
of the normal inhibition of spread of motor cell stimulation,
so that all muscles contract simultaneously.
Strychnine is also dangerous when heated as it emits highly
toxic fumes.
2.2 Summary of clinical effects
The symptoms usually appear within 15 to 30 min after
exposure.
The initial symptoms are tightness and twitching of the
muscles, agitation, and hyperreflexia.
Convulsions and hyperreactivity to stimuli are characteristic
of strychnine poisoning. The patient is conscious and has
intense pain.
The body arches backwards in hyperextension (opisthotonus).
The facial muscles contract producing a characteristic
expression known as "risus sardonicus".
Complications are lactic acidosis, rhabdomyolysis, and acute
renal failure.
The convulsions may recur repeatedly and each episode is
followed by a period of relaxation.
Death is caused by asphyxia or medullary paralysis.
Cumulative toxicity from strychnine has not been
reported.
The prognosis for strychnine poisoning is good if the
patient's condition can be maintained over the first 6 to 12
hours.
2.3 Diagnosis
Diagnosis is based on a history of ingestion (or illicit
intravenous drug abuse) and the development of muscular
stiffness and generalised muscular contractions easily
triggered by eternal stimuli, accompanied by hypothermia,
lactic acidosis and rhabdomyolysis.
Strychnine can be measured chemically but there is no time to
perform this procedure before treatment. Strychnine is found
in the urine, the blood, and the gastric fluid.
Serum glutamic oxaloacetic transaminase (SGOT) and creatine
phosphokinase (CPK) are elevated in serum. Also lactate
dehydrogenases (LDH) levels are raised.
Measure acidosis and serum potassium.
2.4 First-aid measures and management principles
Therapy should be symptomatic and supportive.
Prevent any secondary sensory input.
Prevent or control convulsions with:--
- diazepam
- phenytoin
- phenobarbital.
Gastric aspirations and lavage may be done after the seizures
are controlled.
Give activated charcoal with a cathartic.
Strychnine poisoning is rare. It is caused by the accidental
ingestion of tonic and cathartic pills. Since they are
brightly coloured and sugarcoated, they are attractive to
children.
The ingestion of strychnine bait causes accidental
poisonings, particularly in children who are attracted by the
similarity of the bait to peanuts. Its use as a pesticide is
a source of suicidal and homicidal poisonings, but these
cases are rare.
The ingestion of the whole plant, mainly the seeds of
Strychnos nux vomica or Strychnos ignatii, can cause
poisoning because these plants contain strychnine.
Symptoms usually appear within 15 to 30 minutes after
exposure.
Convulsions and hyperreactivity to stimuli are characteristic
of strychnine poisoning. The patient is conscious throughout
the episode and has intense pain.
Death is caused by asphyxia.
The prognosis for strychnine poisoning is good if the patient
can be supported over the first 6 to 12 hours.
First-aid measures:-
- Therapy should be symptomatic and supportive.
- Prevent any secondary sensory input.
- Prevent or control convulsions with:
- diazepam
- phenytoin
- phenobarbital.
- Gastric aspiration and lavage may be used after the
seizures are controlled.
- Give activated charcoal with a cathartic.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
Natural.
Strychnine is an alkaloid obtained from the seeds of
Strychnos or Loganiaceae:
Strychnos nux vomica Linnaeus
Strychnos ignatii.
3.2 Chemical structure
(Windholz, 1983; Sax, 1988).
Molecular formula: C21H22N2O2
Molecular weight: 334,40
C 75,42%
H 6,63%
N 8,38%
O 9,57%
Structural formula:
3.3 Physical properties
3.3.1 Colour
Translucent or white
3.3.2 State/form
Crystals or crystalline powder
3.3.3 Description
Boiling point: 270°C to 280°C with decomposition
Melting point: 268°C to 290°C depending on speed of
heating
Odour: odourless
Taste: a very bitter metallic taste
pH of saturated solution: 9.5
Specific gravity: 1.36 at 20 °C referred to water at
4°C
Solubility: 1 g dissolves in:
6400 mL water
3100 mL boiling water
150 mL alcohol
35 mL chloroform
180 mL benzene
200 mL toluene
260 mL methanol
320 mL glycerol
220 mL amyl alcohol
very slightly soluble in ether.
(Sax, 1988; Windholz, 1983)
3.4 Other characteristics
Products of combustion: highly toxic
Environmental risk, air pollution: high
Explosiveness: Stable
(Sax, 1988; Hayes, 1982; Reynolds, 1982).
4. USES/HIGH RISK CIRCUMSTANCES OF POISONING
4.1 Uses
4.1.1 Uses
4.1.2 Description
Pesticide:
Strychnine and its salts are used for killing birds,
rodents, moles, and predatory animals, and for
trapping fur-bearing animals.
Pharmaceutical:
Strychnine is an unjustifiable component of
traditional tonics and cathartic pills.
Properties have been attributed to the drug that it
does not possess or that it exhibits only when
administered in toxic doses.
However, preliminary experiments suggest that
judicious treatment with strychnine may modify the
neurological deterioration that occurs in infants who
have "nonketotic hyperglycinemia" (Goodman & Gilman,
1985). Improvement in severe forms of this condition
is limited and transient (Sankaran et al.,
1982).
4.2 High-risk circumstances of poisoning
Strychnine poisoning is rare. It is caused by the
accidental ingestion of tonic and cathartic pills which are
brightly coloured and sugarcoated and thus attractive to
children (Arena & Drew, 1986).
The ingestion of strychnine bait causes accidental poisoning,
particularly in children who are attracted by the similarity
of the bait to peanuts. Its use as a pesticide is a source
of suicidal and homicidal poisonings, but these cases are
rare.
The ingestion of the whole plant, mainly the seeds of
Strychnos nux vomica or Strychnos ignatii can cause poisoning
because these plants contain strychnine. Strychnol nux
vomica contains 1.1 to 1.4% and Strychnos ignatii 2 to 3%
(Poisindex, 1989a).
The accidental ingestion or sniffing of strychnine when it is
used to adulterate cocaine, heroin, LSD, and other street
drugs, has caused poisoning (O'Callaghan et al., 1982).
Strychnine emits toxic vapours when heated to
decomposition.
4.3 Occupationally exposed population
The professions in which there may be exposure to
strychnine are:
pharmaceuticals
agriculture
industry.
Personal safety precautions: (protect skin with clothing to
avoid contact and use) self-contained breathing apparatus
(Sax, 1988).
5. ROUTES OF ENTRY
5.1 Oral
Ingestion of pills and pesticides with strychnine and
also plants of Strychnos or Loganiaceae species.
Strychnine is quickly absorbed from the gastrointestinal
tract, mainly from the intestine.
5.2 Inhalation
When strychnine is sniffed or is smoked with adulterated
marijuana, it is quickly absorbed from the mucous
membranes.
5.3 Dermal
Skin allergen.
5.4 Eye
Unknown.
5.5 Parenteral
Strychnine is rapidly absorbed from parenteral sites of
injection. If subcutaneously injected, the site of the
injection may affect the beginning of action (Sax,
1988).
5.6 Others
Unknown.
6. KINETICS
6.1 Absorption by route of exposure
Strychnine is rapidly absorbed from the gastrointestinal
tract, nasal passages, or from parenteral injection sites.
Symptoms begin within 15 to 30 minutes, occasionally after a
delay of 1 hour. If it is taken by mouth, the time of action
depends on whether the stomach is empty or full, and on the
type of food that is eaten.
6.2 Distribution by route of exposure
Strychnine travels in both plasma and erythrocytes, and
rapidly leaves the bloodstream. Approximately 50% can enter
the tissues in 5 minutes (Reynolds, 1982).
In a fatal poisoning, there were concentrations in the bile,
the liver, and stomach wall (Perper, 1985).
6.3 Biological half-life by route of exposure
Half-life=10 hours.
Strychnine concentrations were measured in a patient who
attempted suicide. The half-life of 10 hours suggested that
normal hepatic function can efficiently degrade strychnine
even when the quantity ingested is high enough to cause
severe poisoning. The elimination constant (Kel=0.07 h-1)
indicates that 7% of the strychnine in the serum at any one
moment would be eliminated in 1 hour (Edmunds et al.,
1986).
6.4 Metabolism
Strychnine is readily metabolized, mainly by enzymes of
hepatic microsomes. The rate of destruction is such that
approximately two lethal doses can be given over 24 hours
without cumulative effects (Goodman & Gilman, 1985).
6.5 Elimination
A few minutes after ingestion, strychnine is excreted
unchanged in the urine, and accounts for about 5% of a
sublethal dose given over 6 hours (Boyd et al., 1983).
Approximately 10 to 20% of the dose will be excreted
unchanged in the urine 24 hours later. The percentage
excreted decreases with the increasing dose. Of the amount
excreted by the kidneys, about 70% is excreted in the first 6
hours, and almost 90% in the first 24 hours (Weiss & Hatcher,
1922). Excretion is almost complete in 48 to 72 hours
(Cooper, 1974).
7. TOXICOLOGY
7.1 Mode of action
Strychnine causes excitation of all parts of the central
nervous system, It increases the level of neuronal
excitability by interfering with inhibitory influences on the
motor neurons. The site of action of strychnine is the
postsynaptic membrane. The convulsant action of the
substance is due to interference with the postsynaptic
inhibition that is mediated by glycine. Glycine is an
inhibitory transmitter to motor neurons and interneurons in
the spinal cord. Strychnine acts as a selective competitive
antagonist to block the inhibitory effects of glycine at the
glycine receptors. Studies indicate that strychnine and
glycine interact with the same receptor complex, although
probably at different sites (Goodman & Gilman, 1985).
7.2 Toxicity
7.2.1 Human data
The maximum exposure limit is approximately
0.15 mg/m3.
There is one report of one case on ingestion of 3.75 g
that was not fatal (Poisindex, 1989b).
7.2.1.1 Adults
The lethal dose for adults varies.
The minimal oral human lethal dose ranges
from 30 to 120 mg. When given intravenously
or subcutaneously, the lethal dose is
significantly lower.
7.2.1.2 Children
The lethal dose in children may be
as low as 15 mg (Goodman & Gilman,
1985).
7.2.2 Animal data
oral-rat LD50: 16 mg/kg
intraperitoneal-rat LD50: 2500 µg/kg
subcutaneous-rat LD50: 1200 µg/kg
intravenous-rat LD50: 960 µg/kg
oral-mouse LD50: 2 mg/kg
intraperitoneal-mouse LD50: 980 µg/kg
subcutaneous-mouse LD50: 474 µg/kg
intravenous-mouse LD50: 410 µg/kg
oral-dog LDLo: 1100 µg/kg
subcutaneous-dog LdLo: 350 µg/kg
intravenous-dog LDLo: 250 µg/kg
oral-cat LDLo: 750 µg/kg
subcutaneous-cat LDLo: 750 µg/kg
intravenous-cat LDLo: 330 µg/kg
oral-rabbit LDLo: 600 µg/kg
subcutaneous-rabbit LDLo: 700 µg/kg
intravenous-rabbit LDLo: 350 µg/kg
oral-pigeon LD50: 21 mg/kg
subcutaneous-pigeon LDLo: 1 mg/kg
subcutaneous-chicken LDLo: 3 mg/kg
oral-duck LD50: 3 mg/kg
subcutaneous-duck LDLo: 1 mg/kg
subcutaneous-frog LDLo: 35 µg/kg
(NIOSH, 1983-84 Supplement)
7.2.3 In vitro data
Strychnine has been studied extensively. The
convulsions caused by strychnine have a characteristic
motor pattern which is determined by the most powerful
muscles acting as a given joint. In most laboratory
animals, convulsions are characterized by tonic
extension of the body and limbs. Typical strychnine
convulsions also occur in spinal animals. Thus, the
effects of strychnine are often attributed to a spinal
locus of action, although other parts of the CNS are
also excited by doses that produce the characteristic
motor manifestations in a spinal animal (Goodman &
Gilman, 1985).
7.2.4 Workplace standards
Occupational exposure limits:
TLV: ppm; 0.15 mg/m3 (as TWA)
(IIPCS & CEC, 1990)
7.2.5 Acceptable daily intake (ADI)
The maximum permissible atmospheric
concentration of strychnine is 150 œg per m3
(Reynolds, 1982).
7.3 Carcinogenicity
No data available.
7.4 Teratogenicity
Ims-rat TDLo: 500 µg/kg /5D preg (Sax, 1988).
7.5 Mutagenicity
No data available.
7.6 Interactions
No data available.
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
Symptoms appear in 15 minutes to 1 hour after
ingestion causing violent generalized
convulsions.
9.1.2 Inhalation
After sniffing, toxic symptoms of poisoning
appear in 30 minutes and are the same as the symptoms
that appear after ingestion.
9.1.3 Skin exposure
Strychnine may be an allergen that is caused by
direct skin exposure (Sax, 1988).
9.1.4 Eye contact
Not described.
9.1.5 Parenteral exposure
Symptoms are the same as after ingestion (see
Section 9.1.1).
9.1.6 Other
No data available.
9.2 Chronic poisoning by:
Chronic poisoning is not known (Cooper, 1974) and
significant cumulative toxicity is not recognized (Gosselin
et al., 1984).
9.2.1 Ingestion
Not described.
9.2.2 Inhalation
Not described.
9.2.3 Skin exposure
Strychnine may be a chronic dermatological
allergen, but systemic effects are not known (Sax,
1988).
9.2.4 Eye contact
Not described.
9.2.5 Parenteral exposure
Not described.
9.2.6 Other
No data available.
9.3 Course, prognosis, cause of death
Seizures are the major side effects of strychnine
poisoning.
Sometimes there are prodromal symptoms e.g., stiffness of
facial and neck muscles and hyperreflexia.
The patient is hyperexcited, and even a very small stimulus
can precipitate violent convulsions.
These convulsions are very painful because of the strong
contractions of the muscles; the patient may even cry. He is
fully conscious and lucid until anoxia supervenes.
Convulsions may occur frequently with intermittent periods of
depression. The frequency and severity of the convulsions
are increased by sensory stimulation.
If the patient survives 6 to 12 hours the prognosis is good
(Boyd et al., 1983).
If the convulsions are not treated, the patient may die with
in 1 to 3 hours after a fatal dose. Death is usually due to
asphyxia from respiratory arrest during or between
convulsions.
9.4 Systemic description of clinical effects
9.4.1 Cardiovascular
The pulse may be difficult to detect, and there
may be tachycardia and hypertension.
9.4.2 Respiratory
The diaphragm, chest, and abdominal muscles are
in a sustained spasm and breathing becomes difficult.
Hypoxia and cyanosis occur followed by death.
9.4.3 Neurological
9.4.3.1 Central nervous system
Seizures are the major symptoms of
strychnine poisoning and are caused by
excitation of all parts of the CNS.
The onset of symptoms may occur with a
prodromal syndrome that includes: tonic
twitching of the face and neck muscles,
muscular cramps in the legs, preceded by
restlessness, apprehension, and heightened
acuity of perception (hearing, vision,
feeling) and hyperreflexia. However, the
initial symptoms may be only generalized
violent convulsions. These convulsions can
begin suddenly after any minor sensory
stimulus and last from 50 seconds to 2
minutes. Initially, the convulsions are
clonic but are soon followed by tonic
contractions similar to convulsions due to
tetanus.
The patient remains conscious and has intense
pain. After the convulsions, all the muscles
relax and sometimes the patient falls asleep
from exhaustion. Hyperexcitability recurs
suddenly after 10 to 15 minutes.
Repeated convulsions (1 to 10) are common
before recovery or death. In severe
untreated poisoning, each convulsion lasts
longer than the previous one, and the
intervals between them are shorter.
9.4.3.2 Peripheral nervous system
No data available.
9.4.3.3 Autonomic nervous system
No data available.
9.4.3.4 Skeletal and smooth muscle
After strychnine poisoning, all
voluntary muscles contract simultaneously,
although there is no direct effect on
skeletal muscles. The increase in muscle
tone is caused by the central action of the
drug (Goodman & Gilman, 1985). The major
effects are caused by the action of the most
powerful muscle on the joint.
During the convulsions, the patient shows
hypertonicity of the muscles beginning by
thrismus, risus sardonicus, and cramps of the
arms and legs, that are soon followed by
opisthotonus.
Respiratory muscles - diaphragm, thoracic,
and abdominal, also contract. Respiration
ceases, and the patient may die.
Repeated convulsions with muscular spasms are
very painful. They are succeeded by the
relaxation of all muscles.
Rhabdomyolysis associated with myoglobinuria,
and also elevation of serum glutamic
oxaloacetic transaminase (SGOT), lactate
dehydrogenases (LDH), and creatine
phosphokinase (CPK), may occur after the
intense muscular contractions.
9.4.4 Gastrointestinal
Vomiting may occur (Gosselin et al., 1984).
Small quantities of strychnine have an extremely
bitter taste and cause reflex gastric secretion
(Gossel & Bricker, 1984).
9.4.5 Hepatic
No data available.
9.4.6 Urinary
9.4.6.1 Renal
Rhabdomyolysis and myoglobinuria
have been reported and renal damage may occur
from precipitation of myoglobin in the renal
tubules (Conn, 1988).
9.4.6.2 Others
The urine may have a green colour
because commercial preparations of strychnine
that are used as rodenticides contain
methylene-blue (Bismuth et al.,
1987).
9.4.7 Endocrine and reproductive systems
No data available.
9.4.8 Dermatological
Strychnine may be a skin allergen if there is
direct or chronic skin exposure.
9.4.9 Eyes, ears, nose, throat: local effects
The eyes protrude and the pupils dilate. One
case of mystagmus was reported: bilateral horizontal
pendular nystagmus that was not responsive to diazepam
ceased spontaneously (Blain et al., 1982).
The throat may be dry (Hayes, 1982).
9.4.10 Haematological
Leukocytosis may also occur (Poisindex, 1989b)
9.4.11 Immunological
No data available.
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
Lactic acidosis: seizures and
muscular spasms may cause hyperthermia and
lactic acidosis.
9.4.12.2 Fluid and electrolyte disturbances
Hyperkalaemia and dehydration can
occur after several convulsions (Gosselin et
al., 1984).
9.4.13 Allergic reactions
Strychnine may be an allergen if there is
direct or chronic contact with the skin (Sax,
1988).
9.4.14 Other clinical effects
During the remissions, cold perspiration
covers the skin (Gosselin et al., 1984), and the
patient may be thirsty.
9.4.15 Special risks, pregnancy, breast feeding, enzyme
deficiencies
There may be elevations of serum glutamic
oxaloacetic transaminase (SGOT), lactate
dehydrogenases (LDH), and creatine phosphokinase (CPK)
(Poisindex, 1989b).
9.5 Others
No data available.
10. MANAGEMENT
10.1 General principles
Treatment of strychnine poisoning is symptomatic and
supportive.
Since strychnine is rapidly absorbed from the
gastrointestinal tract and may cause convulsions with 15 to
60 minutes, the main object of therapy is to prevent or
control convulsions and asphyxia.
Emesis is not contraindicated.
10.2 Relevant laboratory analyses and other investigations
10.2.1 Sample collection
Take samples of blood, urine, and gastric
fluid for biomedical analysis, and a sample of the
product for identification.
10.2.2 Biomedical analysis
The drug can be detected in the urine, blood,
gastric aspirate, and other organs by colorimetry or
ultraviolet spectrophotometry, but gas-liquid
chromatograph with a flame ionization detector is more
accurate.
Blood levels do not indicate the need for therapy or
the extent of the treatment.
The following biomedical investigations should be
carried out
- lactic acidosis
- hyperkalaemia
- elevation of creatine phosphokinase, serum
glutamic oxaloacetic transaminase, lactate
dehydrogenases, and leukocytosis.
10.2.3 Toxicological analysis
No data available.
10.3 Life-supportive procedures and symptomatic treatment
Reduce all sensory stimulation to a minimum by keeping
the intoxicated patient in a warm, quiet, and darkened
room.
Protect the patient from self-inflicted injury.
Support respiratory and cardiovascular functions and
administer:
Diazepam IV Adult: 5 to 10 mg initially over one minute.
If convulsions continue give further 10 mg
over one minute.
Children: the dose is 0.5 mg/kg..
If an intravenous line is not available, diazepam may be
given rectally.
If convulsions cannot be controlled with diazepam or if they
recur, administer phenobarbitone or phenytoin.
Phenobarbitone Adult: 10 to 15 mg/kg slowly administered
intravenously upto a total dose of 30
mg/kg.
Child: 10 to 15 mg/kg at a rate of 25 to 50
mg/min.
Phenytoin IV Adult: 15 to 20 mg/kg (in 0.9% normal
saline) not to exceed 50 mg/kg.
Child: 15 mg/kg at a rate of 0.5 to 1.5
mg/kg per min is recommended.
For seizures that do not respond to previous treatments,
general anaesthesia including neuromuscular blocking agents,
such as tubocurarine or suxamethonium chloride should be
used, with assisted respiration using oxygen.
Tubocurarine chloride is usually administered by intravenous
injection over 1 to 1.5 minutes. For infants or other
patients in whom a suitable vein is not accessible, the drug
may be administered intramuscularly in the same dosage as the
intravenous drug. The usual initial dose is 75 to 150 µg/kg
body weight, with subsequent doses as required.
Suxamethonium chloride is usually administered
intravernously, but may also be given intramuscularly. The
usual single dose of suxamethonium chloride for an adult is
20 to 100 mg intravenously. Doses may be repeated if
necessary with little danger of cumulative effect.
The recommended dose for children is 1 to 2 mg/kg
intravenously.
When administered intramuscularly, the dose for adults and
children is up to 2.5 mg/kg body weight to a maximum total of
150 mg (Reynolds, 1982).
10.4 Decontamination
Administer activated charcoal alone or with cathartic.
Emesis or gastric lavage is not recommended because they may
cause convulsions.
When convulsions and hyperactivity are completely controlled,
gastric lavage can be performed safely.
Activated charcoal: Administer aqueous charcoal
alone or mixed with saline
cathartic or sorbitol.
Adult: 60 to 100 g
Child: 30 to 60 g (Borges,
1986)
Cathartics:
Saline cathartics:
Magnesium or sodium sulfate:
Adult: 30 g per dose
Child: 250 mg/kg per dose
Sorbitol: Adult: 1 to 2 g/kg per dose to a maximum of
150 g per dose
Child: (over 1 yr old): 1 to 1.5 g/kg per
dose as a 35% solution to a maximum of 50 g
per dose. Monitor fluid and electrolyte
status, especially in children (Abrantes &
Marques Penha, 1986).
10.5 Elimination
Forced acid diuresis seems to enhance urinary excretion
but should be avoided if rhabdomyolysis and associated
myoglobinuria are present since an acidic urine may
precipitate myoglobin in the renal tubules and cause renal
insufficiency.
There are not enough data available to assess the efficacy of
peritoneal dialysis after strychnine intoxication.
10.6 Antidote
There is no antidote.
10.7 Management discussion
There are no major controversies or alternatives
regarding patient management. Treatment is designed to
prevent convulsions and to protect medullary asters from
excessive stimulation and from anoxia (Gosselin et al.,
1984).
11. ILLUSTRATIVE CASES
11.1 Case reports from the literature
A 1-year-old child swallowed Easton's syrup tablets
prescribed for her mother and became distressed within 30
minutes. She convulsed 30 minutes later and was sent to
hospital where her stomach was washed out. Convulsions
became continuous and the infant was given intramuscular
paraldehyde for opisthotonos. Cardiac arrest was reversed
and she was given desferrioxamine and intravenous sodium
bicarbonate and noradrenaline. Despite external cardiac
massage and intermittent positive-pressure respiration, she
died approximately 3 to 3.5 hours after the accident. From
examination of the viscera, it was estimated that she had
swallowed iron 2.94 g and strychnine 16 mg, with 0.79 g of
quinine (Stannard, 1969).
A 13-month old child ate Easton's syrup tablet and cried and
became rigid 15 minutes later. In hospital, he had a
convulsion and respiratory arrest that required mouth-to-
mouth assisted respiration and external cardiac massage. He
continued to have repeated fits and intermittent respiratory
arrest and was given endotracheal intubation and oxygen
therapy. Facial grimacing and opisthotonos persisted.
Muscular relaxation occurred immediately after an intravenous
injection of 2.5 mg diazepam. Gastric lavage was performed
with sodium bicarbonate solution 45 minutes after the
accident, and desferrioxamine mesylate was given to
counteract possible iron intoxication from the Easton's
formula. Convulsions were completely controlled with
diazepam and the endotrachael tube was removed 6 hours later
(Jackson et al., 1971).
A 50-year-old man took an unknown quantity of strychnine that
he used to control skunks on his bee farm. He was admitted
to hospital with generalized convulsions and in extreme pain.
When he was given diazepam 10 mg intravenously the seizures
stopped in less than 1 minutes and gastric lavage was
performed. Diazepam 10 mg every 6 hours intramuscularly
stopped the spasms (Harden & Griggs, 1971).
A 42-year-old man ingested an unknown quantity of strychnine
in a suicide attempt. On arrival at hospital, he complained
of severe muscle cramps and within 5 minutes developed
convulsions and respiratory arrest. He was immediately given
succinyl choline intravenously, and was then intubated and
ventilated mechanically. He had a cardiac arrest, and
although external cardiac massage was successful, he remained
unconscious for 72 hours. He was given bicarbonate but
developed a mixed respiratory and metabolic acidosis; with
mechanical ventilation, the acidosis improved considerably.
During this period, he was sedated and was given muscle
relaxants. He developed a severe chest infection and from
days 8 to 18 required a further period on the ventilator.
Two hours after the poisoning, gastric lavage was performed
with 10 g activated charcoal and 2 litres water. Forty-eight
hours after admission, there was biochemical evidence of
rhabdomyolysis, and renal failure occurred. Peritoneal
dialysis was begun, but due to technical problems, the
treatment was changed to intermittent haemodialysis. Renal
function was fully recovered. After discharge at 8 weeks, he
returned to work, but serial psychometric testing showed
residual impairment of short- and medium-term memory
(Edmunds, 1986).
12. ADDITIONAL INFORMATION
12.1 Availability of antidotes
There is no specific antidote.
12.2 Prevention of poisoning
There is no justification for use of strychnine as
bitter and analeptic.
Do not use strychnine as a pesticide.
Strychnine should be kept out of the reach of children and
irresponsible people.
For safe use of the pesticides, follow instructions
carefully.
Wear skin protection (rubber gloves and synthetic clothing)
and self-contained breathing apparatus wherever the product
is manufactured, packaged, or stored.
12.3 Other
No data available.
13. REFERENCES
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E (1982). Unusual strychnine poisoning and its treatment - report
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encephalopathy in a neonate: treatment with intravenous strychnine
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material. Report, 8(1): 78-83.
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14. AUTHORS, DATE
A. Borges, J. Abrantes, MT. Teixeira, P. Parada
Centro de Informmacao Antivenenos
Instituto Nacional de Emergênca Médica
Rua Infante D. Pedro 8
1700 Lisbon
Portugal
Tel: 73 05 03
Telex: 13 304 SNALP P
Telefax: 77 34 74
March 1989
Reviewer: A.F. Rahde
Poison Control Centre
Rua Riachuelo 677
Apartado 201
90010 Porto Alegre
Brazil
Tel: 55-512-275419
Telex: 051-2077 FUOC BR
Telefax: 55-512-391564
May 1989.
Peer Review: Hamilton, May 1989
London, March 1990
Editor: M.Ruse
Finalised: IPCS, April 1997.