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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