POISONOUS PLANTS
    1. NAME
     1.1 Scientific name
       Wisteria sinensis (Sims) Sweet Wisteria floribunda (Willd) DC
     1.2 Family
       Leguminosae (Fabaceae)
     1.3 Common name(s)
       Chinese Kidney Bean (UK)
       Chinese Wisteria (UK) (W. sinensis)
       Glicina (Uruguay, Spain)
       Japanese Wisteria (UK) (W. floribunda)
       Kidney Bean Tree (USA)
       Wistaria (USA)
       Wisteria (USA)
    2. SUMMARY
     2.1 Main risks and target organs
       Hypovolemic shock because of fluid loss.  Target organ is the 
       gastrointestinal tract.
     2.2 Summary of clinical effects
       Nausea, vomiting and abdominal pain.  Diarrhoea is uncommon.
     2.3 Diagnosis
       Clinical features: mainly gastrointestinal.
       
       Pharmacological diagnosis: not relevant.
       
       Laboratory analysis: specimen of the plant for botanical 
       identification;  samples for electrolytes.
     2.4 First-aid measures and management principles
       In asymptomatic patients decontamination measures should be  
       performed.  In case of symptomatic patients fluid replacement 
       should be instituted if  indicated.  Antiemetics can be 
       useful.
     2.5 Poisonous parts
       All parts of the plant are toxic.
     2.6 Main toxins
       An uncharacterized glycoside, wisterine and a lectin.
    3. CHARACTERISTICS
     3.1 Description of the plant
       3.1.1 Special identification features
             Wisteria is a woody liane that can reach a height of 20 
             m,  characterized by pendent racemes of light blue-
             violet, sweetpea-like, scented flowers. It flowers in  
             springtime, and often again in the late summer.  There 
             are  varieties of pink and white flowers.  The fruit are 
             pods (oblong  and velvety) that persist through winter.  
             The leaves are  alternates, caducae, imparipinnate.  
             Leaflets are lanceolate, and  petiolate, with between 11 
             and 19 leaflets about 3-4 cm in length  (Bianchini, 
             1981; Lampe, 1985; Frohne, 1983).
       3.1.2 Habitat
             Usually cultivated as ornamental covering walls, 
             balconies  and bowers.  Native to China, Japan and 
             Southern USA.
       3.1.3 Distribution
             Originally from China and Japan, Wisteria was brought 
             into  Europe in 1816 (Bianchini, 1981).  Wisterias are 

             hardy in the north  but are most common in the south-
             eastern USA, as far west as Texas  (Lampe, 1985).  It is 
             widely cultivated in temperate Europe.
     3.2 Poisonous parts of the plant
       All  parts of  this  plant  are  toxic.  Statements  in  the 
       literature  that the flowers  are nontoxic are in error (Lampe,
        1985).
     3.3 The toxin(s)
       3.3.1 Name(s)
             Wisterine; and an undefined lectin.
       3.3.2 Description, chemical structure, stability
             An uncharacterized glycoside, wisterine.  The plant also 
             contains lectins, whose structures and haemagglutinating or
             mitogenic effects have recently been studied (Frhone-Pfander,
             1983;  Lampe, 1985).
       3.3.3 Other physico-chemical characteristics
             No data available.
     3.4 Other chemical contents of the plant
       No data available.
    4. USES/CIRCUMSTANCES OF POISONING
     4.1 Uses
       4.1.1 Uses
       4.1.2 Description
             Cultivated as ornamental.  There are no medicinal uses.
     4.2 High risk circumstances
       Children playing with parts of the plant.
     4.3 High risk geographical areas
       No data available.
    5. ROUTES OF ENTRY
     5.1 Oral
       Accidental or suicidal ingestion of portions of the plant.
     5.2 Inhalation
       Not relevant.
     5.3 Dermal
       No data available.
     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
       No data available.
     6.2 Distribution by route of exposure
       No data available.
     6.3 Biological half-life by route of exposure
       No data available.
     6.4 Metabolism
       No data available.
     6.5 Elimination by route of exposure
       No data available.
    7. TOXICOLOGY/TOXINOLOGY/PHARMACOLOGY
     7.1 Mode of action
       No data available.
     7.2 Toxicity

       7.2.1 Human data
             7.2.1.1 Adults
                     No data available.
             7.2.1.2 Children
                     It has been reported that two seeds are enough 
                     to  cause a severe intoxication in a child 
                     (Faravel-Carrigues,  1978).
       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
             Acid-base balance.
       8.3.3 Haematological analyses
             Full blood count.
       8.3.4 Interpretation of biomedical investigations
     8.4 Other biomedical (diagnostic) investigations and their 
       interpretation
       Hyponatremia, hypokalemia and hemoconcentration can be found.
     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
             Poisoning usually occurs after ingestion of seeds or 
             other  parts of the plants.  Symptoms can appear up to 
             24 hours after  ingestion and include nausea, abdominal 
             pain and repeated vomiting.
             
             Diarrhea is mild or absent; vomiting is sometimes bloody 
             or bilious  (Hardin-Arena, 1974; Pronczuk & Laborde, 
             1988; Dreisbach, 1987).  Ingestion of massive amounts 
             (from chewing the bark) have been  associated with fluid 
             loss sufficient to cause hypovolemic shock  (Lampe, 
             1985).
       9.1.2 Inhalation
             Not relevant.
       9.1.3 Skin exposure
             No data available.
       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
       In severe poisoning, the acute effects are followed by 
       hemodynamic and  electrolyte disturbances (Hardin-Arena, 
       1974).  Ingestion of massive amounts (from chewing the bark)  
       have been associated with fluid loss sufficient to cause 
       hypovolemic shock  (Lampe, 1985). Death is due to hypovolemic 
       shock. 

     9.4 Systematic description of clinical effects
       9.4.1 Cardiovascular
             In acute poisoning, hypotension may precede hemodynamic  
             shock.  Severe gastroenteritis may contribute to fluid 
             and electrolyte losses and therefore to the  
             cardiovascular effects.
       9.4.2 Respiratory
             No data available.
       9.4.3 Neurological
             9.4.3.1 CNS
                     No data available.
             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
                     No data available.
       9.4.4 Gastrointestinal
             Usually transient but intense abdominal pain, nausea and 
             vomiting which may be bloody or bilious vomiting.  Usually 
             they are transitory (Pronczuk & Laborde, 1988). 
             Diarrhoea sometimes occurs.
       9.4.5 Hepatic
             No data available.
       9.4.6 Urinary
             9.4.6.1 Renal
                     No data available.
             9.4.6.2 Others
                     No data available.
       9.4.7 Endocrine and reproductive systems
             No data available.
       9.4.8 Dermatological
             No data available.
       9.4.9 Eye, ears, nose, throat:  local effects
             No data available.
       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
                       Metabolic alkalosis may occur.
              9.4.12.2 Fluid and electrolyte disturbances
                       Because of the gastrointestinal loss of fluids 
                        and electrolytes, hypokalemia or hyponatremia 
                       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
              No data available.
     9.5 Others
       No data available.

     9.6 Summary
    10. MANAGEMENT
      10.1 General principles
         In symptomatic patients, the aim of treatment is to maintain 
         fluid and  electrolyte balance.  Antiemetic treatment is 
         useful.  Fluid replacement may  be indicated (Lampe, 1985).  
         
         
         If the patient is asymptomatic, decontamination measures are 
         indicated with  gastric lavage or emesis, followed by 
         activated charcoal (Dreisbach, 1987).   Patients usually 
         become asymptomatic within 24 hours (Lampe, 1985).
      10.2 Relevant laboratory analyses and other investigations
         10.2.1 Sample collection
                Specimen of the plant for botanical identification.
                Blood samples for biomedical analyses (see section 
                8.3.1).
         10.2.2 Biomedical analysis
                Electrolytes, full blood count and acid-base balance 
                if  necessary.
         10.2.3 Toxicological/toxinological analysis
                No data available.
         10.2.4 Other investigations
                No data available.
      10.3 Life supportive procedures and symptomatic treatment
         Fluid replacement and antiemetics if necessary.
      10.4 Decontamination
         Empty the stomach by inducing vomiting or performing gastric 
         lavage if  the patient's clinical condition allows it and if 
         timing is appropriate.   Give activated charcoal.
      10.5 Elimination
         No specific elimination procedures are indicated.
      10.6 Antidote/antitoxin treatment
         10.6.1 Adults
                None
         10.6.2 Children
                None
      10.7 Management discussion
    11. ILLUSTRATIVE CASES
      11.1 Case reports from literature
         No data available
      11.2 Internally extracted data on cases
         One incident has been reported by the Poison Control Centre 
         of Montevideo (Hospital de Clinicas, Uruguay, 1988). Four 
         children between five  and ten years old were playing with
         the plant and ate an unknown number of seeds.
         
         They were admitted and remained asymptomatic for 20 hours. 
         They then  developed abdominal pain and vomiting, and two 
         became dehydrated.  Treatment  was based on fluid 
         replacement and recovery was complete (Pronczuk & Laborde,  
         1988).
      11.3 Internal cases
    12. ADDITIONAL INFORMATION
      12.1 Availability of antidotes/antitoxins
         No data available.

      12.2 Specific preventive measures
         Take special care of children playing near this plant.
      12.3 Other
         No data available.
    13. REFERENCES
      13.1 Clinical and toxicological
         Dreisbach RH & Robertson WO (1987)  Handbook of poisoning. 
         12th ed. Appleton-Lange.  Norwalk, Connecticut.
         
         Faravel-Carrigues JC, Castaig Y, et al. (1978) Bordeaux Med. 28.
         
         Frohne D & Pfander H (1984)  Poisonous Plants Ed. Wolfe.
         
         Hardin JW & Arena JM (1974) Human poisoning from native and 
         cultivated plants. Duke University Press, 2nd ed.  Kingsport,
          Tennessee.
         
         Lampe KF & McCann MA (1985)  AMA Handbook of Poisonous and 
         Injurious Plants,  AMA Chicago Illinois.
         
         Pronczuk J & Laborde A (1988) Plantas Silvestres y de 
         Cultivo.
      13.2 Botanical
         Bianchini F & Carrara Pantano A (1981)  Guía de Plantas y 
         Flores, Ed.  Grijalbo 5° ed. pg. 184.
    14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE 
    ADDRESS(ES)
    Author:   Dr J. Mallet
              CIAT
              Hospital de Clinicas - Piso 7
              Av. Italia s/n
              Montevideo 
              Uruguay 
              Tel: 598-2-470300
              Fax: 598-2-470300
    
    Date:     June, 1991
    
    Peer review:   Singapore, November 1991
                   (Members: K. Hartigan-Go, A. Laborde, C. Leon,
                   L. Matainaho, W. Temple)
    
    Update peer review:  London, United Kingdom, February 1994
                         (Members: C. Alonzo, A. Furtado Rahde,
                         O. Kasilo, Z. Petrochenko, J. Trestrail,
                         N. Maramba, J. Szajewski, E. Wickstrom,
                         X. Zhang)

    See Also:
       Toxicological Abbreviations