Gloriosa superba L.
| 1. NAME |
| 1.1 Scientific name |
| 1.2 Family |
| 1.3 Common name(s) of the plant and synonyms |
| 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 |
| 4.1.1 Uses |
| 4.1.2 Description |
| 4.2 High risk circumstances |
| 4.3 High risk geographical areas |
| 5. ROUTES OF EXPOSURE |
| 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 and excretion |
| 7. TOXINOLOGY |
| 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 Relevant 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 |
| 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 Central nervous system (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 Other |
| 9.4.7 Endocrine and reproductive systems |
| 9.4.8 Dermatological |
| 9.4.9 Eye, ear, 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 Other |
| 10. MANAGEMENT |
| 10.1 General principles |
| 10.2 Life supportive procedures and symptomatic/specific treatment |
| 10.3 Decontamination |
| 10.4 Enhanced elimination |
| 10.5 Antidote/antitoxin treatment |
| 10.5.1 Adults |
| 10.5.2 Children |
| 10.6 Management discussion |
| 11. ILLUSTRATIVE CASES |
| 11.1 Case reports from literature |
| 12. ADDITIONAL INFORMATION |
| 12.1 Specific preventative measures |
| 12.2 Other |
| 13. REFERENCES |
| 14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES) |
GLORIOSA SUPERBA
International Programme on Chemical Safety
Poisons Information Monograph 245
Plant
1. NAME
1.1 Scientific name
Gloriosa superba L.
1.2 Family
Colchicaceae
1.3 Common name(s) of the plant and synonyms
Flame lily; glory lily
2. SUMMARY
2.1 Main risks and target organs
The toxins in G. superba have an inhibitory action on
cellular division resulting in diarrhoea, depressant action
on the bone marrow and alopecia.
2.2 Summary of clinical effects
Initial symptoms develop within two to six hours after
ingestion of tubers of G. superba. They are characterized
by numbness and tingling around the mouth, burning and
rawness of the throat, nausea, intense vomiting, abdominal
pain and bloody diarrhoea leading to dehydration. The other
important complications that follow may include: respiratory
depression, dyspnoea, shock, hypotension, marked leucopenia,
thrombocytopenia, coagulation disorders, oliguria,
haematuria, confusion, seizures, coma and ascending
polyneuropathy. Alopecia and dermatitis are the late
manifestations that develop about one to two weeks after
poisoning.
2.3 Diagnosis
Bio-medical analysis: daily full blood counts,
coagulation tests, serum electrolyte levels and urinalysis
are the important investigations to assess the clinical
condition.
Blood collection for colchicine dosage has to be kept in the
dark with anticoagulant.
2.4 First-aid measures and management principles
First aid measures:
If the patient is conscious and alert, induce vomiting by
tickling the back of the throat or by giving syrup of ipecac:
6 to 18 months - 10 mL, 18 months to 12 years - 15 mL)
followed by 1 to 2 glasses of water to induce vomiting.
Repeat after 15 minutes if no response. If ipecac is not
available or if the patient has not responded in 5 minutes
after the second dose or in an adult, carry out a stomach
wash out.
The patient should be admitted to a hospital immediately
with, if available, vomit and any remaining plant
material.
Management principles:
Carefully monitor the respiration. Ensure adequate airway.
Perform gastric lavage immediately.
Anticipate and treat hypotension with adequate intravenous
fluids and vasopressors. Blood transfusion will also be
helpful to support the circulation. Continuous cardiac
monitoring is useful. Correct dehydration and electrolyte
imbalance. Monitor renal function. Initial forced diuresis
enhances elimination of colchicine and should be performed
once dehydration and shock is corrected. Keep the patient
under observation.
2.5 Poisonous parts
All parts of the plant, especially the tubers, are
extremely poisonous.
2.6 Main toxins
Colchicine, an alkaloid, is responsible for the toxic
effect of G. superba. The species also contains another
alkaloid 'gloriosine'.
3. CHARACTERISTICS
3.1 Description of the plant
3.1.1 Special identification features
G. superba is a semi-woody herbaceous,
branching climber, reaching approximately 5 metres in
height. 1 to 4 stems arise from a single V-shaped
fleshy cylindrical tuber. The leaves are stalkless,
lance-shaped, alternate or opposite or in whorls of up
to 3; leaf size: 5 to 15 cm long by 4 to 5 cm wide
with parallel veins and tips ending in spiral tendrils
which are used for climbing. Large, showy, long-
stalked flowers are made up of 6 long reflexed petals
usually with wavy margins. Flower size: 6 to 10 cm
long by 1 to 2.5 cm wide. Flower colour: usually
very bright ranging from red with yellow margins to
very pale yellow forms with a mauve or purple stripe;
pale white forms also occur. Many additional colour
forms have arisen through cultivation. The fruit is
oblong, 6 to 12 cm by 2 to 2.5 cm and contains about
20 globose red seeds in each valve (Huxley, 1992;
Neuwinger, 1994; Burkill, 1995).
3.1.2 Habitat
The plant grows in sunny positions in free-
draining soil; it is very tolerant of nutrient-poor
soils. In warm tropical countries it occurs in
thickets, bushland, forest edges and cultivated areas
up to a height of 2530 metres above sea level. It is
widely grown as an ornamental in cool temperate
countries under glass or in conservatories (Neuwinger,
1994).
3.1.3 Distribution
A native of tropical Africa and is now found
growing naturally throughout much of tropical Asia
including: India, Sri Lanka, Malaysia, Burma
(Jayaweera, 1982); G. superba is also planted
outdoors in the southern United States. In cool
temperate countries it is treated as a greenhouse or
conservatory plant.
3.2 Poisonous parts of the plant
The entire plant, especially the tubers, are extremely
poisonous.
3.3 The toxin(s)
3.3.1 Name(s)
The toxic properties of the plant are
essentially due to the highly active alkaloid
colchicine.
Colchicine:
CAS number: 64-86-8
Molecular formula: C22H25NO6
Molecular weight: 399.44
Structural name: colchicine
Another important alkaloid called gloriosine is also
found in tubers (Gooneratne, 1966).
3.3.2 Description, chemical structure, stability
Colchicine occurs as pale yellow to greenish
yellow, odourless crystals or amorphous scales or
powder. It darkens on exposure to light.
3.3.3 Other physico-chemical characteristics
Melting point is 157°C
Solubility in water is about 1/20. It is freely soluble
in alcohol and chloroform (Windholz, 1983).
3.4 Other chemical contents of the plant
In addition to colchicine and gloriosine, G. superba
also contains other compounds such as 3-desmethyl colchicine,
beta-lumicolchicine, N-Formyldesacetyl-colchicine,
2-desmethyl colchicine, chelidonic acid and salicylic acid
(Duke, 1985).
4. USES/CIRCUMSTANCES OF POISONING
4.1 Uses
4.1.1 Uses
Miscellaneous pharmaceutical product
Other therapeutic preparation
4.1.2 Description
Different parts of the plant have a wide
variety of uses especially within traditional medicine
practised in tropical Africa and Asia. The tuber is
used traditionally for the treatment of bruises and
sprains, colic, chronic ulcers, haemorrhoids, cancer,
impotence, nocturnal seminal emissions, leprosy and
also for inducing labour pains and abortion. Because
of its similar pharmacological action, the plant is
sometimes used as an adulterant of aconite (Aconitum
sp.). The juice of the leaves is used to kill head
lice and also as an ingredient in arrow poisons. The
flowers are used in religious ceremonies. The tuber
has commonly been used as a suicidal agent among women
in rural areas and it has also been used for
homicide.
The tuber also claims antidotal properties to snake-
bite and in India it is commonly placed on window
sills to deter snakes. Many cultures believe the
species to have various magical properties. (Watt &
Breyer-Brandwijk, 1962; Neuwinger, 1994; Burkill,
1995).
4.2 High risk circumstances
In parts of tropical Africa and Asia the tubers of G.
superba may be mistakenly eaten in place of Sweet Potatoes
(Ipomoea batatas) since the former is a weed of farmland
and the tubers resemble those of Sweet Potatoes.
4.3 High risk geographical areas
The highest risk areas are likely to be throughout the
natural range of the species (i.e. tropical Africa and Asia,
including Sri Lanka). Accidental exposure to the plant may
also occur in cool temperate countries of the West where it
is grown as an ornamental.
5. ROUTES OF EXPOSURE
5.1 Oral
Ingestion of tubers or other parts either intentionally
or accidentally.
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
Colchicine is readily absorbed from the gastrointestinal
tract. Absorption may be modified by pH, contents in the
stomach and intestinal motility.
6.2 Distribution by route of exposure
Colchicine is actively taken up intracellularly.
Approximately 50% circulating colchicine is bound to plasma
proteins. The apparent volume of distribution exceeds total
body water (2.2 ± 0.8 1/kg) (Ellenhorn et al., 1996).
6.3 Biological half-life by route of exposure
Colchicine has an extremely short plasma half life of
about 20 minutes (Ellenhorn et al., 1996).
6.4 Metabolism
Colchicine is partially deacetylated in the liver
although as much as 20% may be excreted unchanged by the
kidneys.
Large amounts of both colchicine and its metabolites are
subjected to enterohepatic circulation (Ellenhorn et al.,
1996).
6.5 Elimination and excretion
Colchicine and its metabolites are excreted in urine and
faeces (Reynolds, 1982).
7. TOXINOLOGY
7.1 Mode of action
Colchicine affects cell membrane structure indirectly by
inhibiting the synthesis of membrane constituents (Craker &
Simson, 1986). It binds to tubulin (the structural proteins
of microtubules) preventing its polymerization into
microtubules. This antimiotic property disrupts the spindle
apparatus that separates chromosomes during metaphase. Cells
with high metabolic rates (e.g. intestinal epithelium, hair
follicles and bone marrow) are the most involved by the
arrest of mitosis. The variable effects of colchicine may
depend on its binding to the protein subunit of microtubules
with subsequent disruption of microtubule functions
(Ellenhorn et al., 1996). Colchicine also has an inhibitory
effect on various phosphatases (Craker & Simson, 1986).
Gloriosine also has an antimitotic effect (Gooneratne,
1966).
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
Nickolls (1965) has suggested that
the lethal dose of colchicine for man may be
about 60 mg although smaller amounts have
also caused death (Angunawela & Fernando,
1971). Gooneratne (1966) has reported a
patient who survived after ingestion of 350
mg of colchicine tuber.
7.2.1.2 Children
No data available.
7.2.2 Relevant animal data
LD50 of colchicine for rats was 5 mg/kg
(Dunuwille et al., 1968).
7.2.3 Relevant in vitro data
No relevant data.
7.3 Carcinogenicity
No data available.
7.4 Teratogenicity
G. superba tubers are used for abortion (Duke, 1985).
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
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.1.2 Urine
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.1.3 Other fluids
8.3.2 Arterial blood gas analyses
8.3.3 Haematological analyses
"Basic analyses"
"Dedicated analyses"
"Optional 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
Sample collection
Collection remaining plant material, vomit and gastric
contents for identification purposes.
Biomedical analysis
Full blood counts with bleeding time, clotting time and serum
electrolytes, blood urea and creatinine are essential
investigations.
Urine analysis could show haematuria, proteinuria or
haemoglobin casts.
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
Acute manifestations begin two to six hours
after ingestion and consist of burning pain in the
mouth and throat with thirst, followed by nausea,
intense vomiting, colicky abdominal pain and severe
diarrhoea with blood, leading to hypotension and
shock.
Delirium, loss of consciousness, convulsions,
respiratory distress, haematuria, oliguria, transient
leucocytosis followed by leucopenia, thrombocytopenia
with haemorrhages, anaemia, muscle weakness which may
progress to polyneuropathy are seen in the second or
third day. Alopecia occurs 1 to 2 weeks after
intoxication as a late manifestation in
survivors.
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
The commonest clinical presentation of poisoning is
severe gastroenteritis with nausea, vomiting, diarrhoea with
blood leading to dehydration, hypovolaemic, shock and acute
renal failure. Muscle weakness, hypoventilation, ascending
polyneuropathy, bone marrow depression and coagulation
disorders are the other features of poisoning.
Death in severe poisoning occurs due to shock or respiratory
failure although haemorrhagic or infective complications may
cause death after the first day.
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
Heart - there is no direct effect on the heart,
but fluid and electrolyte loss, often causes
hypovolaemic shock manifested by hypotension and
tachycardia.
9.4.2 Respiratory
Respiratory failure is thought to be due to the
paralysis of intercostal muscles rather than the
direct depression of the respiratory centre by
colchicine (Angunawela & Fernando, 1971).
The patient may be dyspnoeic and cyanotic.
9.4.3 Neurological
9.4.3.1 Central nervous system (CNS)
There is progressive paralysis of
the central nervous system and peripheral
nervous system (Wijesundere, 1986).
Confusion and delirium may develop either
secondary to poor cerebral perfusion or as a
result of direct cerebral toxicity (Ellenhorn
et al., 1996). It may also cause
convulsions, restlessness and coma.
9.4.3.2 Peripheral nervous system
Ascending polyneuropathy, weakness,
loss of deep tendon reflexes may be
described.
9.4.3.3 Autonomic nervous system
No data available.
9.4.3.4 Skeletal and smooth muscle
Colchicine could have a direct toxic
effect on skeletal muscles causing muscular
weakness. Rhabdomyolysis may occur with
significant increase in muscle enzymes and
myoglobinuria as a result of direct muscular
damage.
Muscle weakness that may persist for many
weeks may contribute to respiratory deficiency
(Ellenhorn et al., 1996).
9.4.4 Gastrointestinal
Gastroenteritis including nausea, vomiting and
diarrhoea with blood accompanied by colic and
tenesmus. Loss of fluids and electrolytes leads to
hypovolaemia.
Intestinal ileus may develop within the first few
several days and may persist up to a week (Ellenhorn
et al., 1996).
9.4.5 Hepatic
Colchicine may exert direct hepatic toxicity
with moderate cytolysis.
9.4.6 Urinary
9.4.6.1 Renal
Any direct toxic effect of the toxin
on kidney is not clear. Renal failure is
probably secondary to excess fluid loss or
hypovolaemia and is preceded by oliguria and
haematuria. Proteinuria could also occur
(Murray et al., 1983).
9.4.6.2 Other
No data available.
9.4.7 Endocrine and reproductive systems
Vaginal bleeding has been reported as a feature
of intoxication. Tubers are used as an abortifacient
in some countries.
9.4.8 Dermatological
Alopecia usually occurs one or two weeks after
the ingestion of G. superba. A case of generalized
depilation has also been reported (Gooneratne, 1966).
Desquamative dermatitis has been reported as another
dermatologic manifestation (Angunawela & Fernando,
1971). Both these conditions can be attributed to the
antimitotic activity of the colchicine and gloriosine.
9.4.9 Eye, ear, nose, throat: local effects
Subconjunctival haemorrhages have been observed
(Gooneratne, 1966).
Burning and rawness of the throat may be early
symptoms of toxicity.
9.4.10 Haematological
Colchicine has a depressant action on the bone
marrow which is characterized by a transient
leucocytosis followed by leucopenia.
It could also cause thrombocytopenia that may give
rise to various coagulation disorders resulting in
vaginal bleeding, conjunctival and gastrointestinal
haemorrhages.
Severe thrombocytopenia occurring within 6 hours of
poisoning has been documented (Saravanapavananthan,
1985). Anaemia may occur, mostly secondary to
haemorrhages.
9.4.11 Immunological
Patients are prone to infections as a result
of leucopenia.
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
Metabolic acidosis.
9.4.12.2 Fluid and electrolyte disturbances
There is an extensive fluid and
electrolyte loss due to intense vomiting and
diarrhoea or sometimes due to
haemorrhages.
Hypokalaemia, hypocalcaemia,
hypophosphataemia and hyponatraemia may
occur (Murray et al., 1983).
9.4.12.3 Others
Hypothermia could occur.
9.4.13 Allergic reactions
No data available.
9.4.14 Other clinical effects
No data available.
9.4.15 Special risks
Pregnancy: Data on effects of G. superba on
the foetus are not available. However, colchicine is
contraindicated in pregnancy. Down's syndrome and
spontaneous abortions have been reported.
9.5 Other
No data available.
10. MANAGEMENT
10.1 General principles
Hospitalize the patient immediately. Constant and
prolonged monitoring is essential. Ensure adequate
ventilation. Before instituting symptomatic and supportive
therapy remove the plant material from gastrointestinal tract
by emesis or gastric lavage without delay to minimize further
absorption. Give adequate intravenous fluids. Correct any
electrolyte imbalance. Maintain a fluid balance chart.
Specific measures should also be taken for the management of
shock. Cardiac monitoring is useful.
Early forced diuresis may be of value. Specific fragments
a) b) have been experimented on animals. No human data are
available.
10.2 Life supportive procedures and symptomatic/specific treatment
Observation and monitoring:
Monitor pulse, respiration and blood pressure.
Fluid and electrolytes replacement:
Give adequate oral fluids. If the patient is unable to take
oral fluids Ha 9 + 14.
Hypotension and shock:
Fluid loss may lead to hypovolaemic shock with hypotension:
Correct hypotension as required.
Ensure a clear airway, improve ventilation and give oxygen
(Ha 4 + 5 + 6).
Early haemodynamic monitoring is very helpful (Murray et al.,
1983).
Respiratory: If respiratory depression is present assisted
ventilation and oxygen may be necessary.
Renal failure: Renal failure with oliguria is a common
feature. Maintain an adequate urine output with plenty of
intravenous fluids. Established renal failure may require
peritoneal or haemodialysis.
Leucopenia: Fresh blood transfusions are necessary to
correct leucopenia.
Prophylactic antibiotic therapy is advisable if leucopenia is
present.
Coagulation disorders: If clotting time is abnormal, vitamin
K and fresh frozen plasma should be given. Haemorrhagic
manifestations should be treated with fresh blood
transfusions.
Hypothermia: This may be a poor prognostic sign. Adopt
measures to keep the patient warm.
10.3 Decontamination
If consciousness is not impaired AP4 + AP 5.7.8.
10.4 Enhanced elimination
Forced diuresis, if instituted early should be of
benefit by eliminating colchicine. Haemodialysis,
haemoperfusion and other relevant measures are of no value
because of large volume of distribution and limited renal
excretion of colchicine (Ellenhorn et al., 1996).
10.5 Antidote/antitoxin treatment
10.5.1 Adults
There is no specific antidote available, but
immunotherapy (fragments fab) is available for
clinical trial on humans in some countries
(France).
10.5.2 Children
There is no specific antidote available, but
immunotherapy (fragments fab) is available for
clinical trial on humans in some countries
(France).
10.6 Management discussion
No data available.
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
A non-fatal case of poisoning following ingestion of
boiled G. superba tubers has been described by Gooneratne
(1966):
A 21 year old married woman, who was said to have eaten about
124 g of tuber (total amount of colchicine about 350 mg),
developed gastrointestinal symptoms in 2 hours.
On admission, about 24 hours after ingestion, she was
unconscious and dehydrated. Her blood pressure was 95/70 mm
Hg, pulse rate was 122/minute and the respiratory rate was
18/minute. She developed acute renal failure, menorrhagia,
subconjunctival haemorrhage in the left eye and after 11
days, marked generalized alopecia. She eventually recovered
and two months later her scalp hair showed regrowth. Pubic
and axillary hair also showed regrowth, though the latter
remained very scanty.
Angunawela and Fernando (1971) reported another non-fatal
case of an 18 year old girl who had eaten raw tubers. Six
hours after ingestion she developed severe gastrointestinal
symptoms, vaginal bleeding, acute renal failure, rapidly
ascending polyneuropathy, respiratory distress, absence of
tendon and plantar reflexes, leucopenia, alopecia and
dermatitis. She fully recovered in four weeks.
12. ADDITIONAL INFORMATION
12.1 Specific preventative measures
Public information. Labelling cultivated plants for
domestic use.
12.2 Other
See Poisons Information Monograph on Colchicine.
13. REFERENCES
Angunawela RM and Fernando HA (1971) Acute ascending
polyneuropathy & dermatitis following poisoning by tubers of G.
Superba. Ceylon Medical Journal, 16: 233-235.
Burkill HM (1995) The useful plants of West Tropical Africa, 2nd
ed., vol. 3. Royal Botanic Gardens, Kew.
Craker LE and Simson JC (1986) Recent advances in horticulture &
pharmacology botany, vol I. Arizona, Oryx Press.
Duke JA (1985) Handbook of medicinal herbs. USA, CRC Press.
Dunuwille R, Balasubramanium K and Bible SW (1968) Toxic
principles of Gloriosa superba. Ceylon Journal of Medical Science,
17(2): 1-6.
Ellenhorn MJ, Schonwald S, Ordog G and Wasserberger J (1996)
Ellenhorn's Medical toxicology: diagnosis & treatment of human
poisoning, 2nd ed. Williams & Wilkins, Baltimore.
Gooneratne BWM (1966) Massive generalized alopecia after
poisoning by G. superba. Br Med J, 1: 1023-1024.
Huxley A ed-in-chief (1992) The Royal Horticultural Society
dictionary of gardening, vol 2. London, MacMillan Press.
Jayaweera DMA (1982) Medicinal plants used in Ceylon. Colombo,
National Science Council of Sri Lanka (part 3).
Kimberly PR (1983) Non steroidal anti-inflammatory agents and
colchicine. In: Haddad LM and Winchester JF eds (1983) Clinical
management of poisoning and drug overdose. Philadelphia.
Murray SS, Kramlinger KG, McMichan JC and Mohr DN (1983) Acute
toxicity after excessive ingestion of colchicine. Mayo Clin Proc,
58: 528-532.
Neuwinger HD (1994) African ethnobotany. Poisons and drugs.
Chemistry, pharmacology, toxicology. English translation by A
Porter. Weinheim, Chapman & Hall.
Reynolds JEF (1989) Martindale: the extra pharmacopoeia, 29th ed.
London, The Pharmaceutical Press.
Saravanapavananthan T (1985) Plant poisoning in Sri Lanka.
Jaffna Medical Journal, 20(1): 17-21.
Senanayake N and Karalliedde L (1986) Acute poisoning in Sri
Lanka; an overview. Ceylon Medical Journal, 31(2): 61-71.
Watt JM and Breyer-Brandwijk MG (1962) The medicinal and
poisonous plants of southern and eastern Africa. Edinburgh, E. &
S. Livingstone.
Wijesundere A (1986) Plant poisons. Ceylon Medical Journal,
31(2): 89-91.
Windholz M ed. (1983) The Merck Index: an encyclopedia of
chemicals, drugs and biologicals, 10th ed. Rahway, New Jersey,
Merck & Co., Inc.
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)
Authors: Dr Ravindra Fernando and Miss Deepthi Widyaratna
National Poisons Information Centre
General Hospital
Faculty of Medicine
Kinsey Road
Colombo 8
Sri Lanka
Tel: 94 1 694016/686143/691111 ext 306
Fax: 94 1 699231
Date: November 1989
Peer Review: Adelaide, Australia, April 1991
General edit and botanical review:
Christine Leon
Medical Toxicology Unit
Guy's & St Thomas Hospital Trust
c/o Royal Botanic Gardens, Kew
Richmond
Surrey
TW9 3AB
United Kingdom
Tel: +44 (0) 181 332 5702
Fax: +44 (0) 181 332 5768
e-mail: c.leon@rbgkew.org.uk
July 1997