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Spartium junceum L.

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
       Spartium junceum L.
     1.2 Family
       Leguminosae (sub-family Faboideae, Papilionoideae)
     1.3 Common name(s)
       Gayomba (Spain)
       Giesta (Portugal, Brazil)
       Ginesta (Spain)
       Ginestera (Spain)
       Retama (Uruguay)
       Retama Amarilla (Uruguay)
       Retama de olor (Spain)
       Spanish broom (USA)
       Weaver's broom (USA)
    2. SUMMARY
     2.1 Main risks and target organs
       Convulsions are the main risk, and may be followed by muscle 
       paralysis and coma. Target organ: Central nervous system
     2.2 Summary of clinical effects
       Symptoms develop within one hour. Mild irritation of the oral 
       mucosa and salivation are followed by violent vomiting, 
       sometimes with blood. Confusion and delirium may occur. Tonic-
       clonic convulsions, muscle paralysis and coma occur in severe 
       cases.
     2.3 Diagnosis
       Clinical features: violent vomiting; confusion; tonic-clonic 
       convulsions; muscle paralysis.
       
       Pharmacological diagnosis: not relevant.
       
       Laboratory analysis: specimen of the plant for botanical 
       identification; blood samples for blood gases, electrolytes, 
       muscle enzyme levels to detect possible rhabdomyolysis; and 
       urinalysis to detect possible myoglobinuria.
     2.4 First-aid measures and management principles
       Vomiting is an early symptom, therefore supportive treatment 
       should not be delayed by decontamination measures. Fluid and 
       electrolytes balance should be maintained and respiratory 
       support provided if necessary. Convulsions should be treated 
       with intravenous diazepam or rapid-acting barbiturates.
     2.5 Poisonous parts
       The whole plant, especially the seeds.
     2.6 Main toxins
       Sparteine and cytisine
    3. CHARACTERISTICS
     3.1 Description of the plant
       3.1.1 Special identification features
             Two to three meters high shrub with junk- shaped 
             branches. An untidy, stiff, rush-like bush. The leaves 
             are deciduous, alternate, oblanceolate to linear, blue-
             green, and scarce. The fragrant flowers are yellow, 
             growing in terminal racemes, blooming in spring time. 
             The fruits are flat, 6 to 8 cm long, hairless pods, 
             green changing to black when they mature, with 10 to 16 

             seeds each (Bianchini, 1981; Pronczuk & Laborde, 1988) 
             (see Figure 1).
             
             Figure 1  -  Spartium junceum (Font Quer 1979)
       3.1.2 Habitat
             Spartium junceum usually grows at the sides of country 
             roads in areas exposed to sunlight (Bianchini, 1981; 
             Pronczuk, 1988). In  the Mediterranean, it also occurs 
             on dry slopes and dry woods. General species are 
             cultivated.
       3.1.3 Distribution
             Native to mediterranean Europe, now widely planted and 
             naturalized to parts of the world with mediterranean 
             climate (Millspaugh, 1974).
     3.2 Poisonous parts of the plant
       The whole plant is toxic, especially the seeds.
     3.3 The toxin(s)
       3.3.1 Name(s)
             Sparteine, cytisine.
       3.3.2 Description, chemical structure, stability
             Sparteine and cytisine are quinolizidine alkaloids (see 
             figure 2) (Frohne-Pfänder, 1983).
             
             Sparteine : CAS 90-39-1 (Martindale, 1989)
             
             Cytisine:1,2,3,4,5,6-hexahydro-1,5-methano-8H-pyrido
             [1,2-a][1,5] diazocin-8-one (C11H14N2O).
             
             CAS: 485-35-8
             
             Freely soluble in water, alcohol and chloroform 
             (Martindale, 1982).
             
             Figure 2  -  Chemical formula of Cytisine and Sparteine 
             (Frohne-Pfänder, 1983)
       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
       The fibres are used in Europe for cordage and the 
       manufacture of gunny-sacks. The flowers yield a yellow 
       dye (Millspaugh, 1974).
     4.2 High risk circumstances
       Children playing with the seeds.
     4.3 High risk geographical areas
       No data available.
    5. ROUTES OF ENTRY
     5.1 Oral
       Accidental or intentional ingestion of portions of the plant.
     5.2 Inhalation
       No data available.
     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
       The peripheral effects of sparteine are similar to those of 
       nicotine, and it exerts quinidine-like effects on the heart. 
       It reduces the sensitivity and conductivity of cardiac muscle 
       and has been used in the treatment of cardiac arrhythmias.  
       Small doses stimulate and large doses paralyse autonomic 
       ganglia.  Peripherally, it has a fairly strong curare-like 
       action, arresting respiration by paralysing the phrenic nerve 
       (Martindale, 1989).
       
       The principal actions of cytisine are similar to those of 
       nicotine; however, its ganglion-stimulating activity is more 
       marked than its ganglion-blocking activity (Fronhe-Pfänder, 
       1983). Cytisine is also found in laburnum and some  other 
       leguminous plants.
     7.2 Toxicity
       7.2.1 Human data
             7.2.1.1 Adults
                     No data available.
             7.2.1.2 Children
                     No data available.
       7.2.2 Animal data
             11 kg of the plant is reportedly necessary to poison a 
             horse (Garner, 1970).
       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
             Poisoning usually occurs after ingestion of seed or 
             other parts of the plant.  Symptoms appear within an 
             hour of ingestion and include mild irritation of the 
             mouth and throat, salivation and vomiting.  Vomiting can 
             be violent and sometimes bloody. Abdominal pain and 
             diarrhea sometimes occur. Signs of CNS toxicity include 
             dilated pupils, headache, delirium, mental confusion; in 
             more severe cases, these are associated with tremor, 
             tonic-clonic convulsions followed by muscle paralysis, 
             and coma (Arena, 1981; Pronczuk, 1988).
       9.1.2 Inhalation
             No data available.

       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
       Early vomiting achieves a rapid, spontaneous gastric 
       decontanimation and indicates good prognosis is likely (Arena, 
       1981; Pronczuk, 1988). Possible complications include 
       rhabdomyolysis and myoglobinemia. Death occurs from 
       respiratory failure due to central nervous system depression 
       and muscle paralysis.
     9.4 Systematic description of clinical effects
       9.4.1 Cardiovascular
             Tachycardia is likely (Martindale, 1982).
       9.4.2 Respiratory
             Respiratory failure is the cause of death.
       9.4.3 Neurological
             9.4.3.1 CNS
                     Headache, mental confusion and delirium may be 
                     followed by tremor, tonic-clonic convulsions and 
                     coma.
             9.4.3.2 Peripheral nervous system
                     Peripheral paralysis may occur in the final 
                     stages of severe poisoning.
             9.4.3.3 Autonomic nervous system
                     Since cytisine exhibits nicotine-like effects, 
                     dizziness, sweating and faintness may occur.
             9.4.3.4 Skeletal and smooth muscle
                     Nicotinic effects may be anticipated. Muscle 
                     paralysis may occur due to a curare-like action; 
                     rhabdomyolysis may also occur.
       9.4.4 Gastrointestinal
             Vomiting is the first and principal gastrointestinal 
             symptom. Salivation is common, and abdominal pain and 
             diarrhoea sometimes occur.
       9.4.5 Hepatic
             No data available.
       9.4.6 Urinary
             9.4.6.1 Renal

                     Myoglobinuria may develop due to rhabdomyolysis.
             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
                       Acidosis
              9.4.12.2 Fluid and electrolyte disturbances
                       Vomiting may lead to dehydration and  
                       hypokalemia.
              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
         Management is mainly supportive and should be aimed at 
         preventing dehydration and electrolyte disturbances, and 
         controlling convulsions. Respiratory assistance may be 
         necessary. Symptomatic treatment should not be delayed by 
         decontamination measures.  (In case of rhabdomyolysis, refer 
         to the reevant protocol for the management of 
         myoglobinuria.)
      10.2 Relevant laboratory analyses and other investigations
         10.2.1 Sample collection
                Specimen of the plant for botanical identification.  
                Blood and urine samples for biomedical analyses.
         10.2.2 Biomedical analysis
                Serum electrolytes and acid-base balance if 
                necessary. Creatine phosphokinase in blood. 
                Urinalysis.
         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 and electrolyte replacement may be indicated. 
         Convulsions should be managed by establishing a clear airway,
          providing oxygenation and administering intravenous 
         diazepam or a rapid-acting barbiturate.  Acid base balance 

         must be maintained.  Urine output must be monitored and 
         adequate excretion must be maintained.
      10.4 Decontamination
         Because of the rapid onset of toxicity, gastric 
         decontamination should be performed in asymptomatic patients 
         by gastric lavage followed by activated charcoal (see 10.7).
      10.5 Elimination
         No specific elimination procedures are indicated.
      10.6 Antidote/antitoxin treatment
         10.6.1 Adults
                No antidote available.
         10.6.2 Children
                No antidote available.
      10.7 Management discussion
         Gastric lavage could be controversial since convulsions may 
         develop.
    11. ILLUSTRATIVE CASES
      11.1 Case reports from literature
         No data available.
      11.2 Internally extracted data on cases
         The PCC of Montevideo (1988) has received 8 consultations 
         about children who ingested an unknown amount of Spartium 
         junceum seeds. All developed vomiting prior to admission 
         (within two hours) with mild abdominal pain.
         
         Spontaneous vomiting was monitored and allowed to proceed 
         with administration of intravenous fluids. Symptoms resolved 
         over 24 hours.
      11.3 Internal cases
         To be added by the PCC using the monograph.
    12. ADDITIONAL INFORMATION
      12.1 Availability of antidotes/antitoxins
         None
      12.2 Specific preventive measures
         Take special care of children playing nearby Spartium 
         junceum.
      12.3 Other
    13. REFERENCES
      13.1 Clinical and toxicological
         Arena JM (1981)  Plants that poison.  Emergency Medicine, 
         June, 15: 22-57.
         
         Font Quer P. (1979)  Plantas Medicinales.  Editorial Labor 
         S.A. Barcelona. pp. 355.
         
         Frohne D, Pfänder H (1983)  Poisonous Plants.   Wolfe 
         Publishing. Sttugart,  pp 123 and 131.
         
         Garner L (1970)  Toxicologia Veterinaria. Plantas Venenosas. 
         3th Ed. Editorial Acribia. España, pp 365.
         
         Martindale (1982)  Cytisine.  The Extra Pharmacopeia. 28th 
         Ed. The Pharmaceutical Press. London, pp 1700.
         
         Martindale (1989)  Sparteine Sulphate.  The Extra 
         Pharmacopoeia. 29th Ed. The Pharmaceutical Press. London, pp 1618.

         
         Millspaugh CF (1974)  American Medicinal Plants.  General 
         Publishing Co. Toronto.
         
         Pronczuk J, Laborde A (1988)  Plantas Silvestres y de 
         cultivo. Universidad de la Republica.
         
         Riesgo de intoxicación para el hombre (1988)  Universidad de 
         la República Oriental del Uruguay, Montevideo, pp 77.
      13.2 Botanical
         Bianchini F & Carrara Pantano A (1981)  Guía de plantas y 
         flores.  Ed. Grijalbo, 5° ed., pp 117.
    14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE 
    ADDRESS(ES)
    Author:   Dr A. Laborde
              CIAT - piso 7°
              Hospital de Clínicas
              Av Italia s/n
              Montevideo
              Uruguay
    
              Tel: 598-2-470300
              Fax: 598-2-602088
    
         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)