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