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Thevetia peruviana

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
       Thevetia peruviana (pers).  K Shum
     1.2 Family
       Apocynaceae
     1.3 Common name(s)
       Be still Tree
       Digoxin
       Lucky Nut
       Nerium oleander
       Yellow Oleander
    2. SUMMARY
     2.1 Main risks and target organs
       The main toxic effects of glycosides found in Thevetia 
       peruviana are  related to its digitalis-like action on the 
       heart and severe  gastrointestinal irritation. 
     2.2 Summary of clinical effects
       The common presenting symptoms are: numbness, burning of the 
       mouth,  nausea, vomiting, abdominal pain and diarrhoea.  Other 
       features seen are:   drowsiness, coma, occasional convulsions, 
       and cardiac arrhythmias. Death is  due to ventricular 
       fibrillation.
     2.3 Diagnosis
       Diagnosis depends on the patient's history and the clinical  
       presentation.
       
       Cardiac glycosides can be investigated in the blood by 
       competitive  immunoassay.  The serum potassium concentration 
       should be monitored.   Electrocardiography, frequent serum 
       electrolytes (especially potassium concentration), and renal 
       function tests  are essential investigations.  Remnants of 
       seeds, vomitus or gastric  aspirate should be collected for 
       identification purposes.
     2.4 First-aid measures and management principles
       Admit the patient to a hospital.  Treatment should aim at a) 
       gut  contamination by emesis or lavage if the ingestion is 
       recent; b) correction  of electrolyte imbalance; c) correction 
       of severe bradycardia with atropine  or electrical pacing and 
       correction of ventricular dysrrhythmias; and d)  
       administration of digoxin Fab antibodies if available.
     2.5 Poisonous parts
       All parts of the plant, particularly the seeds are poisonous 
       owing to  the presence of cardiac glycosides or cardiac toxins 
       which act directly on  the heart.  Ingestion of these plant 
       parts could lead to death.  The whole  plant exudes in a milky 
       juice which is very poisonous.
     2.6 Main toxins
       Thevetin A, Thevetin B and Peruvoside.
    3. CHARACTERISTICS
     3.1 Description of the plant
       3.1.1 Special identification features
             It is a small ornamental tree which grows to about 10 to 
             15  feet high.  The leaves are spirally arranged, linear 
             and about 13  to 15 cm in length.  Flowers are bright 
             yellow and funnel-shaped  with 5 petals spirally 

             twisted.  The fruits are somewhat globular,  slightly 
             fleshy and have a diameter of 4 to 5 cm.  The fruits,  
             which are green in colour, become black on ripening.  
             Each fruit  contains a nut which is longitudinally and 
             transversely divided.   All parts of the plant contain 
             the milky juice.
       3.1.2 Habitat
             Grown as an ornamental tree in gardens.
       3.1.3 Distribution
             This plant is native of Central & South America, but now 
             frequently grown throughout the tropical and sub-
             tropical regions.
     3.2 Poisonous parts of the plant
       All parts of the plant are poisonous, especially the kernels 
       of the  fruit. 
       
       The absorption of the equivalent of two Thevetia peruviana 
       leaves may be  sufficient to kill a 12.5 kg child (Ellenhorn 
       and Barceloux, 1988).
     3.3 The toxin(s)
       3.3.1 Name(s)
             Cardiac glycosides, Thevetin A & B, Thevetoxin, 
             Peruvoside,  Ruvoside and Nerifolin are found in  T. 
             Peruviana (Arnold et al.,  1935).
       3.3.2 Description, chemical structure, stability
             Thevetin A = C42H64O19; MW = 872.93;
             
                  CAS number: 37933-66-7
             
             Thevetin B = C42H66O18; MW = 858.95;
             
                  CAS number: 11005-70-2
             
             Peruvoside = C42H44O9; MW = 548.65; 
             
                  CAS number: 1182-87-8
             
             Peruvoside is freely soluble in methanol and ethanol and 
             sparingly  soluble in chloroform acetone (Merck Index, 
             1976).
       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 plant is widely grown as an ornamental tree to adorn 
       gardens and at  religious sites for offerings.
       
       The cardiac glycoside peruvoside from yellow oleander is 
       used medicinally  for treatment of cardiac insufficiency,
       (Frohne & Pfander, 1983).  However,  it has been found 
       that the margin between the therapeutic and the toxic 
       dose is too small for thevetin to be therapeutically 
       useful (Watt &  Breyer-Bradwijk, 1962).
     4.2 High risk circumstances

       Children have easy access to this plant in gardens or  
       hedgerows, and they may play with and taste the bright yellow 
       flowers and the conspicuous green fruit.
       
       The kernel of the seeds is used in suicide attempts, 
       particularly by young people and especially in northern parts 
       of Sri Lanka.  Sometimes it is taken with alcoholic drinks 
       (Shaw and Pearn, 1979).
     4.3 High risk geographical areas
       This plant is a native of Central and South America, but is 
       now frequently grown in parks and gardens in tropical and 
       subtropical areas.
    5. ROUTES OF ENTRY
     5.1 Oral
       Accidental ingestion of the seeds by children may cause 
       poisoning.   Suicidal ingestion is also common in some areas.  
     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
       Thevetin is easily absorbed from the gastrointestinal tract.
     6.2 Distribution by route of exposure
       Thevetin glycosides occur in higher concentrations in heart 
       muscle than  in blood (Ellenhorn and Barceloux, 1988).
     6.3 Biological half-life by route of exposure
       Thevetin probably has a shorter half-life than digoxin and a 
       lower risk  of accumulation in the body (Arnold et al., 1935).
     6.4 Metabolism
       No data available.
     6.5 Elimination by route of exposure
       No human data available.
    7. TOXICOLOGY/TOXINOLOGY/PHARMACOLOGY
     7.1 Mode of action
       Cardiac glycosides exert a digoxin-like effect by inhibiting 
       the  sodium-potassium adenosine-triphosphatase (ATP) enzyme 
       systems.  The  increased intracellular sodium concentration 
       and the increased serum potassium concentration produce 
       negative chronotropic  and positive inotropic effect (Shaw and 
       Pearn, 1979).  The resulting toxic  syndrome resembles 
       digitalis poisoning with marked hyperkalaemia, conduction 
       abnormalities and  ventricular arrhythmias (Ellenhorn and 
       Barceloux, 1988).
     7.2 Toxicity
       7.2.1 Human data
             7.2.1.1 Adults
                     The kernels of about 10 fruits may be fatal  
                     (Saravanapavananthan, 1985). 
             7.2.1.2 Children

                     The kernel of one fruit may be fatal  
                     (Saravanapavananthan, 1985).
       7.2.2 Animal data
             Cattle grazing on grass under Thevetia peruviana trees 
             are  known to have died (Saravanapavananthan 1985) and 
             nuts are lethal  to chickens (Arnold et al., 1935).
       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
       Pre-medication with digoxin or other cardiac glycosides 
       increases the  severity of poisoning.  The interaction between 
       digoxin and quinidine  (increasing digoxin levels) may also 
       occur with Thevetia glycosides. 
    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
             Thevetia peruviana poisoning closely resembles digitalis 
              poisoning, with gastrointestinal and cardiac symptoms.
             
             Local irritation of mucous membranes and mouth is 
             followed by  nausea, vomiting and giddiness within 
             hours.  Other clinical  features are: severe diarrhoea, 
             abdominal pain, dilated pupils and  occasionally 
             convulsions.  Cardiovascular manifestations range from 
             sinus bradycardia with sino-atrial-block, first and 
             second degree heart block, junctional rhythms, A-V block,
              atrial and ventricular ectopic beats, and ventricular 
             fibrillation.
       9.1.2 Inhalation
             No data available.
       9.1.3 Skin exposure
             Burning sensation of the skin due to the sap.
       9.1.4 Eye contact
             Severe eye irritation caused by the sap is possible.
       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, diarrhoea, vomiting, abdominal pain and 
       sinus  bradycardia are early features.  Hyperkalaemia, 
       conduction block and  ventricular ectopics indicate serious 
       toxicity (Ellenhorn & Barceloux,  1988).
       
       
       Indicators of a poor prognosis include multiple and varying 
       cardiac rhythms  occur, with sinoatrial and atrio-ventricular 

       blocks in combination with ventricular excitability, ST 
       depression over 2.5 mm and response to atropine 
       (Saravanapavananthan &  Ganeshmoorthy, 1986).
       
       Conduction block and sinus bradycardia may persist for 5 days 
       after  ingestion.  Patients usually recover from these if no 
       underlying  cardiovascular pathology exist (Ellenhorn & 
       Barceloux, 1988).
       
       The usual cause of death is ventricular fibrillation.
     9.4 Systematic description of clinical effects
       9.4.1 Cardiovascular
             The main actions of thevetin and other cardiac 
             glycosides  are on the heart.  In mammalian heart, low 
             doses of thevetin have a stimulant action, and large  
             doses depress and stop ventricular contraction (Arnold 
             et al.,  1935).
             
             ECG changes include: sinus bradycardia, inversion of T 
             waves, P-R prolongation, A-V dissociation, ventricular 
             tachycardia and ultimately ventricular fibrillation, 
             which is the usual cause of death.
       9.4.2 Respiratory
             Thevetin has little, if any, direct effect on 
             respiration  (Watt and Breyer-Branwijk, 1962).
       9.4.3 Neurological
             9.4.3.1 CNS
                     Mydriasis, drowsiness, coma, and occasionally  
                     convulsions.
             9.4.3.2 Peripheral nervous system
                     Paraesthesia and weakness have been reported 
                     even  in the early phase. (Ellenhorn & Barceloux,
                      1988).
             9.4.3.3 Autonomic nervous system
                     Pupils may be dilated (Duke, 1987) and excessive 
                      salivation has been reported (Ellenhorn & 
                     Barceloux,  1988).
             9.4.3.4 Skeletal and smooth muscle
                     Thevetin has a direct stimulant action on the  
                     smooth muscles of the intestine bladder, uterus 
                     and blood  vessel walls (Watt & Breyer-Branwijk, 
                     1962).
                     
                     
                     Skeletal muscle hypertonia has also been 
                     reported  (Ellenhorn & Barceloux).
       9.4.4 Gastrointestinal
             Nausea, intense vomiting and diarrhoea.
       9.4.5 Hepatic
             No data available.
       9.4.6 Urinary
             9.4.6.1 Renal
                     Acute renal failure may occur secondary to  
                     cardiogenic shock.
             9.4.6.2 Others
                     No data available.

       9.4.7 Endocrine and reproductive systems
             The seed is used as an abortifacient in Bengal and  
             neighbouring provinces (Watt & Breyer-Bradwijk, 1962).
       9.4.8 Dermatological
             Irritant to skin.
       9.4.9 Eye, ears, nose, throat:  local effects
             Burning sensation and dryness of throat could occur.
       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
                       Circulatory collapse could cause metabolic  
                       acidosis.
              9.4.12.2 Fluid and electrolyte disturbances
                       Gastrointestinal fluid loss often leads to  
                       dehydration and hypovolaemic shock.  Hyperkalaemia 
                       is seen in severe poisoning.
              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
              Pregnancy: No data available
              Breast feeding: No data available
              Enzyme deficiencies: No data available
     9.5 Others
       No data available.
     9.6 Summary
    10. MANAGEMENT
      10.1 General principles
         Admit the patient to a hospital immediately.  In severe 
         poisoning,  admit to an Intensive Care Unit for immediate 
         cardiac monitoring.  Treatment  usually depends on the 
         severity of poisoning and includes: immediate gastric  
         decontamination, and correction of arrhythmias and 
         electrolyte disturbance.
         
         Frequent electrocardiograms or continuous cardiac monitoring 
         are necessary.  Check electrolytes regularly, particularly 
         serum potassium levels.
      10.2 Relevant laboratory analyses and other investigations
         10.2.1 Sample collection
                Remaining parts of the ingested plant  (fruit, flower,
                 branches with leaves) and gastric contents are 
                useful for botanical  identification. Plant portions 
                found in vomitus should be stored in  a plastic bag 
                for the laboratory.
         10.2.2 Biomedical analysis
                ECG is valuable for diagnosis, prognosis and 
                treatment, and  shows changes similar to those
                produced by digitalis glycosides.  
                

                In moderate to severe poisoning check serum 
                electrolytes  (especially serum potassium),and
                monitor renal function. Arterial blood gases should 
                be determined.
         10.2.3 Toxicological/toxinological analysis
                Digoxin immunoassay can be used to detect Thevetin  
                poisoning.
         10.2.4 Other investigations
      10.3 Life supportive procedures and symptomatic treatment
         Prolonged repeated ECG monitoring is required in serious 
         cases.
         
         Ensure adequate airway and ventilation.
         
         Give adequate oral or IV fluids and correct any electrolyte 
         imbalance.  If  serum potassium level exceeds 6 mmol/l give 
         50 ml of 50% glucose and  initially 10 units of soluble 
         insulin IV.
         
         Treatment is determined by the presence of cardiotoxicity. 
         Bradycardia may require atropine or electrical pacing.  
         Ventricular arrhythmias may be be  controled with lidocaine 
         or, less appropriately, phenytoin.  
         
         Phenytoin should be infused slowly IV (at a rate no greater 
         than 50  mg/minute) until dysrrhythmias are controlled, to a 
         maximum total dose of  1000 mg (adult). 
         
         Lidocaine may be administered as 1 mg/kg IV bolus, followed 
         by continuous  infusion of 1 to 4 mg/minute (adult).
         
         Treatment of hyperkalemia should aim at lowering the serum 
         potassium level,  with insulin, glucose, NaHCO3 and ion-
         exchange resins.  Hemoperfusion may be considered in severe 
         cases.  Calcium chloride is contraindicated (Goldfrank,  
         1986).
      10.4 Decontamination
         If consciousness is not impaired, induce emesis or perform 
         gastric  lavage.
         
         After emesis or gastric lavage, give oral activated charcoal,
         which is highly effective in adsorbing plant toxins.
      10.5 Elimination
         Forced diuresis, dialysis and haemoperfusion are not helpful 
         in the elimination of cardiac glycosides.
      10.6 Antidote/antitoxin treatment
         10.6.1 Adults
                Digoxin-specific Fab antibody fragments, have been 
                used  successfully in an adult patient intoxicated 
                with Nerium Oleander  (Shamaik, 1988).  The same may 
                apply to Thevetia poisoning.
         10.6.2 Children
                No data available.  (see above)
      10.7 Management discussion
         The use of digoxin specific Fab fragments deserves further 
         evaluation.

    11. ILLUSTRATIVE CASES
      11.1 Case reports from literature
         Children: In South West Africa two children were poisoned 
         after eating  the kernel of a seed; one died six hours later 
         (Watt & Breyer-Brandwijk,  1962).
         
         A presumed case of fatal Thevetia poisoning was observed by 
         Ansford & Morris  (1981), in a 3 year-old child who had 
         played near a yellow oleander tree and  was taken to 
         hospital.  The child showed characteristic symptoms and the 
         presence of cardiac  glycoside was detected by radio-
         immunoassay of heart muscle.
         
         Analysis of 170 cases due to yellow Oleander (T. peruviana) 
         seed poisoning  admitted to the Teaching Hospital, Jaffna 
         between January 1983 and December  1985 over a 3-year period 
         showed the following: 
         
         The number of seeds ingested varied from 0.5 - 20 (mean 
         3.5). Patients were  admitted between 15 minutes and 38 
         hours after ingestion (mean 7.2 hours).
         
         The common presenting symptoms were: vomiting (68%), 
         giddiness (36%) and diarrhoea (22%).  Other symptoms 
         included abdominal pain (6%), numbness of mouth and tongue 
         (4.%) and palpitations (3%).  13% of the patients remained  
         asymptomatic.  ECG changes were recognized in 62% of the 
         cases which  included first degree, second degree and 
         variable A-V blocks.
         
         Bradycardia was seen in  50% of the patients.  Only 35% of 
         the cases showed  flattening or inversion of T waves.  ST 
         depression was seen in 24% of the  cases whcih was sometimes 
         deep and "saucer" shaped.  Ventricular and atrial ectopic 
         beats were seen in 7 and 3% of the cases respectively.  
         Seven patients died (Saravanapavananthan & Ganeshmoorthey 
         1986).
      11.2 Internally extracted data on cases
         (In preparation)
      11.3 Internal cases
    12. ADDITIONAL INFORMATION
      12.1 Availability of antidotes/antitoxins
         Fab antibody fragments may be used, if available.
      12.2 Specific preventive measures
      12.3 Other
         The cardiac glycoside peruvoside, from yellow oleander, has 
         been used  medicinally for cardiac insufficiency (Frohne and 
         Pfander, 1983).
         
         It has been found that the  margin between the therapeutic 
         and the toxic  limit is too small for thevetin to prove a 
         useful therapeutic agent (Warr & Breyer-Brandwijk, 1962).
    13. REFERENCES
      13.1 Clinical and toxicological
         Ansford AJ & Morris H (1981).  Fatal Oleander Poisoning. 
         Medical J.  Australia, 1: 360-361.   

         
         Arnold HL, Middleton WS, & Chen KK (1935).  The action of 
         Thevetin, a cardiac glycoside and its clinical application.  
         American J. Med. Sci,  189-193.
         
         Duke JA (1987) ed. Handbook of Medicinal Herbs.  USA, CRC 
         Press, Inc.
         
         Ellenhorn MJ & Barceloux DG (1988).  1st ed. Medical 
         Toxicology - Diagnosis  and treatment of Human poisoning, 
         New York, Elsevier Science Publishing  Company Inc. 1252-
         1255.
         
         Frohne D & Pfander HJ (1983).   Ed. A Colour Atlas of 
         Poisonous Plants,  Germany, Wolfe Publishing Ltd., 47.
         
         Lampe KF & McCann MA (1985).  Ed. AMA Handbook of Poisonous 
         and Injurious  Plants, Chicago, Illinois American Medical 
         Association, 169.
         
         Merck Index (1976).  Ed. Windholz M, Merck & Co., USA.
         
         Saravanapavananthan N & Ganeshmoorthy J (1986).  Yellow 
         oleander poisoning - a study of 170 cases.  Proceedings of 
         the 2nd Indo-Pacific Congress on Legal Medicine & Forensic 
         Sciences, 49. (Abstract).
         
         Saravanapavananthan T. (1985).  Plant poisoning in Sri 
         Lanka. Jaffna Medical  Journal, 20(1): 17-21.
         
         Shaw D & Pearn J (1979).  Oleander Poisoning. Medical 
         Journal of Australia,  2: 267-269.
         
         Watt JM & Breyer-Brandwijk MG (1962).   ed. The Medicinal & 
         Poisonous Plants  of Southern & Eastern Africa.  Edinburgh & 
         London, E & S Livingstone Ltd,  107-109.
      13.2 Botanical
    14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE 
    ADDRESS(ES)
    Author:   Dr Ravindra Fernando and Miss Deepthi Widyaratna
              National Poison Information Centre
              General Hospital
              Colombo 8
              Sri Lanka
    
              Tel:
              Fax:
    
    Date:     October 1989
    
    Reviewer: Dr J. Pronczuk
              CIAT 7 piso
              Hospital de Clinicas
              Av. Italia s/n
              Montevideo
              Uruguay

    
              Tel: 598-2-470300
              Fax: 598-2-470300
    
    Date:     March 1990
    
    Peer review:   London, March 1990



    See Also:
       Toxicological Abbreviations