Aconitum napellus spp.
| 1. NAME |
| 1.1 Scientific name |
| 1.2 Family |
| 1.3 Common name(s) |
| 2. SUMMARY |
| 2.1 Main risks and target organs |
| 2.2 Summary of clinical effects |
| 2.3 Diagnosis |
| 2.4 First-aid measures and management principles |
| 2.5 Poisonous parts |
| 2.6 Main toxins |
| 3. CHARACTERISTICS |
| 3.1 Description of the plant |
| 3.1.1 Special identification features |
| 3.1.2 Habitat |
| 3.1.3 Distribution |
| 3.2 Poisonous parts of the plant |
| 3.3 The toxin(s) |
| 3.3.1 Name(s) |
| 3.3.2 Description, chemical structure, stability |
| 3.3.3 Other physico-chemical characteristics |
| 3.4 Other chemical contents of the plant |
| 4. USES/CIRCUMSTANCES OF POISONING |
| 4.1 Uses |
| 4.2 High risk circumstances |
| 4.3 High risk geographical areas |
| 5. ROUTES OF ENTRY |
| 5.1 Oral |
| 5.2 Inhalation |
| 5.3 Dermal |
| 5.4 Eye |
| 5.5 Parenteral |
| 5.6 Others |
| 6. KINETICS |
| 6.1 Absorption by route of exposure |
| 6.2 Distribution by route of exposure |
| 6.3 Biological half-life by route of exposure |
| 6.4 Metabolism |
| 6.5 Elimination by route of exposure |
| 7. TOXICOLOGY/TOXINOLOGY/PHARMACOLOGY |
| 7.1 Mode of action |
| 7.2 Toxicity |
| 7.2.1 Human data |
| 7.2.1.1 Adults |
| 7.2.1.2 Children |
| 7.2.2 Animal data |
| 7.2.3 Relevant in vitro data |
| 7.3 Carcinogenicity |
| 7.4 Teratogenicity |
| 7.5 Mutagenicity |
| 7.6 Interactions |
| 8. TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS |
| 8.1 Material sampling plan |
| 8.1.1 Sampling and specimen collection |
| 8.1.1.1 Toxicological analyses |
| 8.1.1.2 Biomedical analyses |
| 8.1.1.3 Arterial blood gas analysis |
| 8.1.1.4 Haematological analyses |
| 8.1.1.5 Other (unspecified) analyses |
| 8.1.2 Storage of laboratory samples and specimens |
| 8.1.2.1 Toxicological analyses |
| 8.1.2.2 Biomedical analyses |
| 8.1.2.3 Arterial blood gas analysis |
| 8.1.2.4 Haematological analyses |
| 8.1.2.5 Other (unspecified) analyses |
| 8.1.3 Transport of laboratory samples and specimens |
| 8.1.3.1 Toxicological analyses |
| 8.1.3.2 Biomedical analyses |
| 8.1.3.3 Arterial blood gas analysis |
| 8.1.3.4 Haematological analyses |
| 8.1.3.5 Other (unspecified) analyses |
| 8.2 Toxicological Analyses and Their Interpretation |
| 8.2.1 Tests on toxic ingredient(s) of material |
| 8.2.1.1 Simple Qualitative Test(s) |
| 8.2.1.2 Advanced Qualitative Confirmation Test(s) |
| 8.2.1.3 Simple Quantitative Method(s) |
| 8.2.1.4 Advanced Quantitative Method(s) |
| 8.2.2 Tests for biological specimens |
| 8.2.2.1 Simple Qualitative Test(s) |
| 8.2.2.2 Advanced Qualitative Confirmation Test(s) |
| 8.2.2.3 Simple Quantitative Method(s) |
| 8.2.2.4 Advanced Quantitative Method(s) |
| 8.2.2.5 Other Dedicated Method(s) |
| 8.2.3 Interpretation of toxicological analyses |
| 8.3 Biomedical investigations and their interpretation |
| 8.3.1 Biochemical analysis |
| 8.3.1.1 Blood, plasma or serum |
| 8.3.1.2 Urine |
| 8.3.1.3 Other fluids |
| 8.3.2 Arterial blood gas analyses |
| 8.3.3 Haematological analyses |
| 8.3.4 Interpretation of biomedical investigations |
| 8.4 Other biomedical (diagnostic) investigations and their interpretation |
| 8.5 Overall Interpretation of all toxicological analyses and toxicological investigations |
| 8.6 References |
| 9. CLINICAL EFFECTS |
| 9.1 Acute poisoning |
| 9.1.1 Ingestion |
| 9.1.2 Inhalation |
| 9.1.3 Skin exposure |
| 9.1.4 Eye contact |
| 9.1.5 Parenteral exposure |
| 9.1.6 Other |
| 9.2 Chronic poisoning |
| 9.2.1 Ingestion |
| 9.2.2 Inhalation |
| 9.2.3 Skin exposure |
| 9.2.4 Eye contact |
| 9.2.5 Parenteral exposure |
| 9.2.6 Other |
| 9.3 Course, prognosis, cause of death |
| 9.4 Systematic description of clinical effects |
| 9.4.1 Cardiovascular |
| 9.4.2 Respiratory |
| 9.4.3 Neurological |
| 9.4.3.1 CNS |
| 9.4.3.2 Peripheral nervous system |
| 9.4.3.3 Autonomic nervous system |
| 9.4.3.4 Skeletal and smooth muscle |
| 9.4.4 Gastrointestinal |
| 9.4.5 Hepatic |
| 9.4.6 Urinary |
| 9.4.6.1 Renal |
| 9.4.6.2 Others |
| 9.4.7 Endocrine and reproductive systems |
| 9.4.8 Dermatological |
| 9.4.9 Eye, ears, nose, throat: local effects |
| 9.4.10 Haematological |
| 9.4.11 Immunological |
| 9.4.12 Metabolic |
| 9.4.12.1 Acid base disturbances |
| 9.4.12.2 Fluid and electrolyte disturbances |
| 9.4.12.3 Others |
| 9.4.13 Allergic reactions |
| 9.4.14 Other clinical effects |
| 9.4.15 Special risks |
| 9.5 Others |
| 9.6 Summary |
| 10. MANAGEMENT |
| 10.1 General principles |
| 10.2 Relevant laboratory analyses and other investigations |
| 10.2.1 Sample collection |
| 10.2.2 Biomedical analysis |
| 10.2.3 Toxicological/toxinological analysis |
| 10.2.4 Other investigations |
| 10.3 Life supportive procedures and symptomatic treatment |
| 10.4 Decontamination |
| 10.5 Elimination |
| 10.6 Antidote/antitoxin treatment |
| 10.6.1 Adults |
| 10.6.2 Children |
| 10.7 Management discussion |
| 11. ILLUSTRATIVE CASES |
| 11.1 Case reports from literature |
| 11.2 Internally extracted data on cases |
| 11.3 Internal cases |
| 12. ADDITIONAL INFORMATION |
| 12.1 Availability of antidotes/antitoxins |
| 12.2 Specific preventive measures |
| 12.3 Other |
| 13. REFERENCES |
| 13.1 Clinical and toxicological |
| 13.2 Botanical |
| 14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES) |
POISONOUS PLANTS
1. NAME
1.1 Scientific name
Aconitum napellus spp.
1.2 Family
Leguminosae
1.3 Common name(s)
Aconite "feroz" (Argentina, Uruguay)
Aconite "maralobo" (Argentina)
Aconite "saludable" (Argentina)
Aconite (Spain, Argentina, Uruguay)
Aconite (USA, UK)
Aconite de flor grande (Argentina, Uruguay)
Aconite napelo (Spain)
Aconitum carmichaelii
Aconitum columbiatum Nutt
Aconitum japonicum
Aconitum napellus L.
Aconitum pyramidale Mill (Dewit, 1962)
Aconitum reclinatum Gray (white flowers)
Aconitum uncinatum (blue flowers)
Aconitysat
Anapello (Italy)
Anapelo (Spain, Argentina, Uruguay)
Capilla de mono (Argentina)
Delfinium (USA), Delphinium (UK)
Espora (Brazil)
Espora-de-jardin (Brazil)
Esporiaha-de-jardin (Brazil) (Schvartsman, S. 1979)
Haba de lobo (Argentina)
Kurt (Turkey)
Larkspur (USA, UK)
Monkshood (USA, UK)
Raiz del diablo (Argentina)
Staggerweed (USA, UK) (Hardin, 1974)
Wolfsbane (USA, UK)
2. SUMMARY
2.1 Main risks and target organs
The main target organs are the cardiovascular and central
nervous systems (bulbar paralysis), and also the
gastrointestinal tract.
The main risks are cardiovascular collapse and ventricular
arrythmias, as well as vomiting and diarrhoea leading to
dehydration and hypotension. Respiratory paralysis and
convulsions may occur.
2.2 Summary of clinical effects
The first symptoms of poisoning appear rapidly: numbness and
tingling of the mouth and tongue, followed within hours by
salivation, nausea, vomiting, and diarrhoea. Convulsions and
changes in the sensorium may occur.
Severe poisoning is characterized by cardiac effects:
conduction abnormalities, with sinus bradycardia,
supraventricular tachycardia, ventricular tachycardia and
torsade de pointe. Although the cardiotoxic effects usually
occur within the first 24 hours of poisoning, ECG
abnormalities may persist for several days. Minor cases of
poisoning may resolve in 24 to 48 hours, but the neurological
effects (especially generalized weakness) may persist for
weeks.
Disorders of the thermal regulation centre may occur.
Intoxication may first cause excitement and then paralysis of
the bulbar centre. A characteristic symptom is the
paraesthesia that can spread over the entire body. Loss of
consciousness and dysarthria may occur.
2.3 Diagnosis
The diagnosis is made from history of exposure and clinical
features: tingling and burning sensation of mouth and throat,
excessive salivation, gastroenteritis, cardiac dysrhythmias,
convulsions and respiratory failure.
Aconitine and other alkaloids can be identified in gastric
contents or in the plant (e.g. by thin layer chromatography)
but laboratory methods are very seldom used for diagnostic
purposes.
Analysis of blood gases and electrolytes and
electrocardiographic monitoring are helpful in the diagnosis
in assessing the severity of poisoning and follow-up of
patients.
Identification of a sample of the plant by a specialist is
indicated.
2.4 First-aid measures and management principles
Since all parts of the Aconitum plant contain aconitine,
reducing absorption by usual measures (induction of emesis by
syrup of ipecac, lavage, charcoal, cathartics) is advised in
patients who ingest toxic amounts of the plant.
Toxicity is difficult to predict because of the variability in
the alkaloid content of different plants; observation for
several hours is therefore appropriate. Symptomatic patients
should be hospitalized for 24 hrs and cardiac monitoring
should always be indicated.
Cardiac defibrillation and antiarrhythmic therapy may be
required for cardiac dysrhythmias. Patients should be
monitored.
Fluid, electrolyte and acid-base imbalance should be corrected,
but hypokalaemia should not be corrected with administration
of potassium salts.
Give oxygen and assist respiration in case of respiratory
depression.
Prevent hypothermia. Raise the body temperature slowly with
physical methods and avoiding burns to the patients.
2.5 Poisonous parts
All parts of the plant contain aconitines; particularly high
concentrations occur in the roots.
2.6 Main toxins
Aconitine, mesaconitine, jesaconitine.
3. CHARACTERISTICS
3.1 Description of the plant
3.1.1 Special identification features
Aconite is a perennial herb with ascending or slightly
descending stems.
The flowers appear in terminal racemes or panides.
Their colour ranges from white to deep purple-blue, the
upper part resembles a hood.
Fruit: three to five follicles.
Root: a dark brown conical tuber with adventitious
roots; in general there is a main root and an accessory
root. A cross section shows two distinct portions: the
cortical (greyish white) and the medulla (white)
separated by a garlanded line (the cambium) that
simulates a star with five to seven branches.
3.1.2 Habitat
Aconite is found in various regions, from hill tops to
forests. It grows best in moist and dimly lit areas.
The word "Aconite" is derived from Acona city, which is
part of Eraclea country (Britinia, in Asia Minor). It
is believed that the plant originated in Acona.
"Aconite" also come from the word Greek "Acona", which
means rock, because the plant grows at the foot of
mountains (Benigni et al., 1971).
3.1.3 Distribution
Aconium reclinatum Gray (white flowers) and Aconitum
uncinatum (blue flowers) are found in the mountains of
Georgia and north ward to Ohio and New York, in shadowy
woods, on slopes, and along creeks.
Aconitum columbiatum Nutt is a found in the high
mountains and moist meadows of western Canada an
southward to California and New Mexico.
Aconitum napellus L. is found in Europe only, but is
often grown in gardens in North and South America.
3.2 Poisonous parts of the plant
Aconite and other alkaloids are found in all parts of the
plant. These alkaloids are found in the roots (0.97 to 1.23%)
and in the leaves (0.18 to 0.21%). Ingestion of 2 to 4 grams
of the roots can cause severe poisoning, but chewing the
leaves does not seem to cause symptoms.
3.3 The toxin(s)
3.3.1 Name(s)
Aconitines
3.3.2 Description, chemical structure, stability
Aconites have different alkaloids combined with aconitic
acid. According to Soler and Batlle (1974), Aconitum
napellus L. contains the following:
aconitine (acetylbenzoylaconine, C33H47NO11);
picroaconitine (benzoylaconitine); isoaconitine;
benzaconitine; aconine; neopelline; eoline; napelline;
mesaconitine; ipaconitine.
Two substances are obtained by hydrolysis: aconine and
acetic acid, or benzoic acid and veratric acid.
It is possible to identify groups of alkaloids according
to the acid pH produced by hydrolysis:
a) Aconitine groups (acetylbenzoylaconine),
represented by Aconitine and Neopelline
b) Pseudoaconitine or acetylveratroylaconine groups,
including pseudoaconitine and bikaconitine.
"Aconitines" are usually referred to in the plural. The
aconitines of the Japanese species are more toxic than
other species (Japaconitines A and B and Jesaconitine);
although they have the same pharmacological effects,
they are more potent.
The level of alkaloids range from 0.2 to 1.3% depending
on their geographic region and on the part of the plant.
3.3.3 Other physico-chemical characteristics
No data available.
3.4 Other chemical contents of the plant
Aconitum roots also contain catecholamine alkaloids,
quaternary ammonium compounds, isoquinolines and other
compounds.
4. USES/CIRCUMSTANCES OF POISONING
4.1 Uses
In folk medicine, infusions or tinctures are used as
sedatives and as antineuralgics for trigeminal, sciatic,
rheumatic pains and for pain due to gout, toothache and
headache.
When taken by mouth, aconite acts as a mild diaphoretic.
When applied to the skin, it causes a tingling
sensation followed by numbness. Aconite liniments were
once used extensively to treat neuralgia, sciatica and
rheumatism. Aconite is a component of a number of multi-
ingredient preparations (Reynolds, 1993).
Some aconite preparations are used in homeopathic
medicine. Aconitum species are used as anti-
inflammatory agents in traditional Chinese medicine: A.
carmichaeli ("chauanwu") and A. kusnezoffii ("caowu")
(Chan et al., 1993).
Aconite root was used in the past as a homicidal weapon.
4.2 High risk circumstances
Aconite can be extremely dangerous if swallowed, because its
potency may vary and there is no significant difference
between the therapeutic and toxic amounts of aconite.
Aconite can be eaten as it may easily be mistaken for
horseradish, celery, or turnips, and inadvertently used in
salads.
Cutaneous absorption may occur after prolonged contact of the
skin with aconite leaves (Lampe & Fagerstrom, 1968).
4.3 High risk geographical areas
Toxicity varies according to climatic conditions though no
specific data are available.
5. ROUTES OF ENTRY
5.1 Oral
Parts of the plant can be accidentally or intentionally
ingested. In traditional medicine, infusions, granules and
tinctures are made from different parts of the plant.
5.2 Inhalation
Not relevant.
5.3 Dermal
Aconitine can be absorbed through the skin and may cause
severe poisoning. Liniments containing aconite should never
be used on wounds or abraded skin (Reynolds, 1982). Aconite
is seldom used for its local counter-irritant properties.
5.4 Eye
No data available.
5.5 Parenteral
No data available.
5.6 Others
No data available.
6. KINETICS
6.1 Absorption by route of exposure
Absorption from the gastrointestinal tract is rapid. Alkaloids
can be absorbed after prolonged skin contact with aconite
leaves (Lampe and Fagerstrom, 1968).
6.2 Distribution by route of exposure
After the ingestion or infusion of any part of the plant, the
alkaloids are present in the blood and reach the target organs
(heart and brain) within 30 minutes.
6.3 Biological half-life by route of exposure
No data available.
6.4 Metabolism
Aconite is rapidly metabolized by the liver in less than 24 h.
6.5 Elimination by route of exposure
Excretion of the alkaloids and metabolites occurs mainly
through the urine and faeces.
7. TOXICOLOGY/TOXINOLOGY/PHARMACOLOGY
7.1 Mode of action
Aconite alkaloids modify cell membrane to sodium and potassium
ions, inhibiting repolarisation (Jouglard et al, 1977).
Aconite alkaloids activate the sodium channel and have
widespread effects on the excitable membranes of cardiac,
neural and muscle tissue. Nausea, vomiting and generalised
paraesthesia are due to parasympathetic activation and sensory
nerve ending stimulation. Muscarinic activation causes
hypotension and bradyarrhythmias. Enhancement of a
transmembrane inward sodium current during the plateau phase
of the action potential prolongs repolarisation in cardiac
myocytes and induces afterdepolarisations with triggered
automaticity (Tai et al, 1992).
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
Toxicity is common at the doses of aconitine
used therapeutically, although there is wide
variation between individuals. The lethal dose
for adults is about 5 mg; the most severe
cardiac rhythm disturbances occur at a dose of 2
mg. If the patient survives this dose, the
symptoms usually resolve within 24 hours (Ory,
1968).
Poisoning resulting only from aconite tincture
is rare.
Severe poisoning has been reported after
ingestion of as little as 0.2 mg aconitine, or
consumption of decoctions prepared with 6 g of
cured Aconitum rootstocks (Tai et al., 1992).
7.2.1.2 Children
No data available.
7.2.2 Animal data
No data available.
7.2.3 Relevant in vitro data
No data available.
7.3 Carcinogenicity
No data available.
7.4 Teratogenicity
No data available.
7.5 Mutagenicity
No data available.
7.6 Interactions
No data available.
8. TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
8.1.1.2 Biomedical analyses
8.1.1.3 Arterial blood gas analysis
8.1.1.4 Haematological analyses
8.1.1.5 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
8.1.2.1 Toxicological analyses
8.1.2.2 Biomedical analyses
8.1.2.3 Arterial blood gas analysis
8.1.2.4 Haematological analyses
8.1.2.5 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
8.1.3.1 Toxicological analyses
8.1.3.2 Biomedical analyses
8.1.3.3 Arterial blood gas analysis
8.1.3.4 Haematological analyses
8.1.3.5 Other (unspecified) analyses
8.2 Toxicological Analyses and Their Interpretation
8.2.1 Tests on toxic ingredient(s) of material
8.2.1.1 Simple Qualitative Test(s)
8.2.1.2 Advanced Qualitative Confirmation Test(s)
8.2.1.3 Simple Quantitative Method(s)
8.2.1.4 Advanced Quantitative Method(s)
8.2.2 Tests for biological specimens
8.2.2.1 Simple Qualitative Test(s)
8.2.2.2 Advanced Qualitative Confirmation Test(s)
8.2.2.3 Simple Quantitative Method(s)
8.2.2.4 Advanced Quantitative Method(s)
8.2.2.5 Other Dedicated Method(s)
8.2.3 Interpretation of toxicological analyses
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemical analysis
8.3.1.1 Blood, plasma or serum
8.3.1.2 Urine
8.3.1.3 Other fluids
8.3.2 Arterial blood gas analyses
8.3.3 Haematological analyses
8.3.4 Interpretation of biomedical investigations
8.4 Other biomedical (diagnostic) investigations and their
interpretation
8.5 Overall Interpretation of all toxicological analyses and
toxicological investigations
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
Soon after ingestion (one to two hours), aconite causes
a tingling and burning sensation on the lips, tongue,
mouth, and throat, which is followed by numbness and
constriction of the throat. Gastrointestinal
disturbances are usual.
Generalized weakness, convulsions and cardiac
dysrhythmias may develop in the next few hours.
9.1.2 Inhalation
No data available.
9.1.3 Skin exposure
Cutaneous absorption may occur (Lampe & Fagerstrom,
1968). Sufficient aconitine may be absorbed through the
skin to cause serious poisoning (Reynolds, 1993).
9.1.4 Eye contact
No data available.
9.1.5 Parenteral exposure
No data available.
9.1.6 Other
No data available.
9.2 Chronic poisoning
9.2.1 Ingestion
No data available.
9.2.2 Inhalation
No data available.
9.2.3 Skin exposure
No data available.
9.2.4 Eye contact
No data available.
9.2.5 Parenteral exposure
No data available.
9.2.6 Other
No data available.
9.3 Course, prognosis, cause of death
The course of poisoning is rapid. Symptoms appear almost
immediately after ingestion of the tincture but may be delayed
for up to one hour when only parts of the plant are ingested.
When lethal doses have been ingested, death usually occurs
within six hours.
If the patient survives for 24 hours the prognosis is good
because the alkaloids are metabolised and eliminated rapidly.
Death may occur from cardiac dysrhythmias and cardiac arrest
and from respiratory depression (secondary to paralysis of the
respiratory centre). In fatal cases, death usually occur
within 6 hr, although in severe poisoning it may be
instantaneous (Reynolds, 1993).
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
Serious aconitine poisoning is characterized by
hypotension, palpitations, shock, delay in myocardial
conduction and dysrhythmia beginning within 6 hr of
ingestion. Sinus bradycardia with first degree
atrioventricular block, supraventricular tachycardia
multiple premature ventricular contractions,
bidirectional tachycardia, bundle branch block,
junctional escape rhythms, ventricular tachycardia and
torsade de pointes have been reported. Serious
ventricular dysrhythmias occur within 24 hours of
ingestion and ST-T wave abnormalities and delayed
conduction may persist for several days (Ellenhorn,
1988; Tai et al., 1992).
9.4.2 Respiratory
Respiration is progressively depressed by the effect of
aconitine on the bulbar respiratory centre.
Fatal acute pulmonary oedema may occur.
9.4.3 Neurological
9.4.3.1 CNS
Consciousness, speech, and senses may be
affected. Generalized excitement and seizures
can occur before paralysis of the bulbar centre.
There may be lack of coordination. Changes in
sensorium result from secondary causes rather
than direct CNS depression.
Convulsions may occur up to 5 hr after
ingestion. At toxic doses, the alkaloids impair
thermoregulation and cause hypothermia.
9.4.3.2 Peripheral nervous system
Doses used therapeutically may cause excitement,
followed by paralysing effects on the trigeminal
nerve. Larger doses also cause initial
paraesthesia followed by anaesthesia of the
facial nerves. Excitement and then paralysis of
the motor nerves can also occur later.
Tingling of the tongue, mouth, and skin,
followed by numbness and anaesthesia, are
characteristic signs of aconitine poisoning.
9.4.3.3 Autonomic nervous system
Excessive salivation is a characteristic sign of
poisoning. The skin becomes cold, clammy, sweaty,
and pale. Initial bradycardia is due to vagal
stimulation.
9.4.3.4 Skeletal and smooth muscle
Muscular weakness and cramps may occur.
9.4.4 Gastrointestinal
Soon after ingestion aconite causes a tingling, burning
sensation on the lips, tongue, mouth, and throat, which
is followed by numbness and constriction of the throat.
Nausea, vomiting, diarrhoea, and excessive salivation
may occur.
9.4.5 Hepatic
Hepatic impairment (but no other data) was reported in
one patient (Tai et al., 1992).
9.4.6 Urinary
9.4.6.1 Renal
Renal failure has been reported after ingestion
of aconite leaves mistakenly used in salads.
9.4.6.2 Others
No data available.
9.4.7 Endocrine and reproductive systems
No data available.
9.4.8 Dermatological
When applied to the skin, aconite causes a tingling
sensation and then numbness (Reynolds, 1982).
9.4.9 Eye, ears, nose, throat: local effects
Eyes - Blurring of vision occurs. Initial miosis is
followed by mydriasis.
Throat - There is a feeling of constriction in the
throat.
9.4.10 Haematological
No data available.
9.4.11 Immunological
No data available.
9.4.12 Metabolic
9.4.12.1 Acid base disturbances
Respiratory alkalosis and metabolic andor
respiratory acidosis have been reported (Tai
et al., 1992).
9.4.12.2 Fluid and electrolyte disturbances
Hypokalaemia or hyperkalaemia may occur.
9.4.12.3 Others
No data available.
9.4.13 Allergic reactions
No data available.
9.4.14 Other clinical effects
No data available.
9.4.15 Special risks
It is not known whether aconite alkaloids exert
significant effects on the fetus or whether significant
concentrations are found in breast milk.
9.5 Others
No data available.
9.6 Summary
10. MANAGEMENT
10.1 General principles
Symptomatic patients should always be admitted to hospital
for observation and cardiac monitoring (Ellenhorn, 1988).
Since all parts of the aconitum plant contain aconitine,
reducing gastric absorption by the usual measures (emesis
with syrup of ipecac, gastric lavage, charcoal, cathartics)
is advisable in those patients who ingest more than a small
quantity of the plant.
No single antiarrhythmic drug was uniformly effective for
arrhythmias. Amiodarone, flecainide, mexiletine,
procainamide and phenytoin have been clinically successful
in suppressing ventricular dysrhythmia due to aconite
poisoning (Tai et al., 1992; Sherf, 1960). Administration
of potassium and _-blocking agents is contraindicated.
The skin should be decontaminated if necessary. Body
temperature should be monitored and controlled if necessary.
The likelihood of toxicity is difficult to predict because
of the variability in the alkaloid content of the plant; a 2
to 4 hr observation period is appropriate (Ellenhorn, 1988).
10.2 Relevant laboratory analyses and other investigations
10.2.1 Sample collection
Collect the aspirated gastric contents to identify
which part of the plant were ingested and to confirm
the presence of aconitine (by gas chromatography,
rarely used in practice).
The plant should be obtained for botanical identification.
Collect samples of blood and urine for analyses.
10.2.2 Biomedical analysis
Serum electrolytes and blood gas analysis, and ECG
are important for assessing the severity of
poisoning.
Serum creatine kinase level should also be determined
(may be elevated).
10.2.3 Toxicological/toxinological analysis
Identify the aconitines (this is not usually
performed in practice).
10.2.4 Other investigations
No data available.
10.3 Life supportive procedures and symptomatic treatment
Make a proper assessment of airway, breathing, circulation
and neurological status of the patient. Symptomatic
patients should be hospitalized for 24 hours. Monitor
cardiac function (Ellenhorn, 1988).
Maintain a clear airway. Aspirate respiratory secretions.
Perform endotracheal intubation if the patient is comatose
or convulsing. Administer oxygen. If necessary, support
ventilation using appropriate mechanical device.
Symptomatic patients should receive an IV line. Equipment
for cardiac defibrillation should be available. Correct
electrolyte disturbances and hypotension with IV fluids.
Do not give potassium for hypokalaemia. Administer IV
glucose only.
Control body temperature. The patient should be kept warm
and if hypothermia occurs the body temperature must be
raised gradually.
Control cardiac dysrhythmias. No single antiarrhythmic drug
is uniformly effective. Repeated direct current
cardioversion, and drugs such as lignocaine, amiodarone,
bretylium, flecainide, mexiletine and procainamide have been
used (Tai et al, 1992).
Procainamide (2 g in 250 ml glucose 5%) could be
administered intravenously (rate of 5 ml/minute) until sinus
rhythm is recovered, up to a total dose of 1 g. Phenytoin
(25 to 50 mg/minute IV to a total dose of 250 mg) has also
been used clinically and experimentally to suppress
ventricular dysrhythmia resulting from aconite poisoning
(Sherf, 1960).
N.B. Contraindications: Administration of potassium and _-
blocking agents is contraindicated.
10.4 Decontamination
Since all parts of the Aconitum contain aconitine, reducing
gastric absorption by usual measures (emesis with syrup of
ipecac, gastric lavage, activated charcoal, cathartics) is
advisable in those patients who ingest more than a small
quantity of the plant (Ellenhorn, 1988).
If the patient is obtunded, convulsing or comatose, or if
the poison involved may induce these conditions rapidly,
insert an oro- or a naso-gastric tube and lavage after
endotracheal intubation.
Wash the skin with soap and copious amounts of water if skin
contamination is present.
10.5 Elimination
No data available.
10.6 Antidote/antitoxin treatment
10.6.1 Adults
No antidote is available.
10.6.2 Children
No antidote is available.
10.7 Management discussion
An injection of 0.1% procaine was reportedly successful in
treating cardiac arrhythmia in one patient but no
experimental data are available (Lampe, 1986).
Symptomatic and supportive treatment should never be
postponed because of decontamination procedures.
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
Eight cases were reported due to adverse effects of
traditional herbal medicines containing the roots of
Aconitum species. They had mild to moderate intoxication:
nausea, vomiting, paraesthesias or numbness in the mouth and
extremities, hypotension and ventricular extrasystoles (Chan
et al., 1993).
Merchan (Ory, 1968) reported three patients who ingested 7
to 10 ml tincture (equal to about 4 mg of alkaloids).
Lampe and Fagerstrom (1968) reported a case of cutaneous
absorption resulting from prolonged skin contact with
aconite leaves.
Lampe (1986) treated one case of aconite poisoning
successfully with procaine.
One patient died and another developed cardiac dysrhythmias
following ingestion of a herbal preparation believed to be
containing aconite (Kelly, 1990).
Two cases of aconite poisoning following ingestion of herbal
preparations have been reported. A 30-year-old man died in
spite of cardiopulmonary resuscitation for five hours and 40
minutes, cardiopulmonary bypass for two hours and 47 minutes,
and insertion of a transvenous pacing electrode (Fatovich,
1991).
Severe poisoning after ingesting herbal medicine with
aconite was reported in 17 patients who developed
tachyarrhythmias. Two patients died (Tai et al., 1992).
11.2 Internally extracted data on cases
To be added by the poisons centre.
11.3 Internal cases
To be added by the poisons centre.
12. ADDITIONAL INFORMATION
12.1 Availability of antidotes/antitoxins
No antidote is available.
12.2 Specific preventive measures
As aconitine and its related alkaloids may be highly toxic,
herbal medicines with these substances should not be used in
therapy. Strict surveillance and control of herbal
preparations which may contain aconite is recommended.
12.3 Other
No data available.
13. REFERENCES
13.1 Clinical and toxicological
Benigni R, Capra C & Cattorini PE (1971) Pianti medicinali,
Quimica, Farmacologia e Terapia. 2 vol. Iverni e Della
Beffa, Milan.
Chan TY, Tomlinson B, Critchley JA (1993) Acontine
poisoning following the ingestion of Chinese herbal
medicines: a report of eight cases. Aust NZ J Med, 23(3):
268-271.
Chan TY, Tomlinson B, Chan WW, Yeung VT, Tse LK (1993) A
case of acute aconitine poisoning caused by chuanwu and
caowu. J Top Med Hyg, 96(1): 62-63.
Dewit H (1963) Les plantes du monde. Hachette ed., Paris,
Vol. I, II et III.
Ellenhorn MJ & Barceloux DG (1988) Elsevier Science
Publishing Company, Inc. New York, pp 1242-1243.
Fatovich DM (1991) Aconite: A Lethal Chinese Herb. Annals
of Emergency Medicine, 21: 309-311.
Hardin JN & Arena JM (1974) Human poisoning from native and
cultivated plants. 2nd Ed. Duke University Press, Durham,
North Carolina.
Kelly SP (1990) Aconite poisoning. Med J Australia, 153:
499.
Lampe KF (1986) Toxic effects of plants toxins. Toxicology,
3rd Ed., Macmillan Publishing Co., 762.
Lampe KF & Fagerstrom R (1986) Plant toxicity and
dermatitis. A manual for physicians. William & Wilkins Co.
Ed. Baltimore, 231.
Jouglard J, Arditti J, Brun A, Poyen D, Richardot-Prieur R,
Regli P (1977) Intoxication d'origine veg_tal. Encyclop_die
M_dico-chirurgicale, Paris 16065 A10 - 2.
Ory J (1968) L'intoxication par l'aconit et l'aconitine.
Th_se, Paris, pp 333.
Schvartsman S (1979) Plantas venenosas. Savier, Sao Paulo,
Brazil.
Soler & Batlle E (1947) Medicamenta. Editorial Labor,
Buenos Aires.
Sherf D, Blumenfeld S, Taner D (1969) The effect of
diphenylhydantoin (Dilantin R)) sodium on atrial flutter and
fibrillation provoked by focal application of aconite and
delphinine, Am Heart J, 60: 936-947.
Reynolds JEF (1982) Martindale, The Extra Pharmacopoeia.
Pharmaceutical Press, London, pp 1330.
Reynolds JEF (1993) Martindale, The Extra Pharmacopoeia.
Pharmaceutical Press, London, pp 1674.
Tai Y, But PP, Young K, Lau C (1992) Cardiotoxicity after
accidental herb-induced aconite poisoning. Lancet,
340(8830): 1254-1256.
13.2 Botanical
No data available.
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)
Authors: Dr Héctor Armando MOSTO and Dr J. Higa de Landoni
Jefa Seccion Toxicologia
Hospital de Clinicas "Jose de San Martin"
Facultad de Medicina
Universidad de Buenos Aires
Cordoba 2351
Buenos Aires
Argentina
Tel: 54-1-9621280
Fax: 54-1-3318605
Date: May 1990
Peer Review: Adelaide, Australia, April 1991
Update: Dr R. Fernando
Date: July 1993
Reviewed: IPCS, May 1994