Erythroxylum coca Lam
| 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
Erythroxylum Coca Lam
1.2 Family
Erythroxylaceae
1.3 Common name(s)
Coca Brazil
Coca France
Coca shrub England
Cuca Peru
Epadu Brazil
Hayo Brazil, Venezuela, some indigenous tribes of the Andes
Huaunuco Coca Bolivia
Ipadu Brazil
Spadic Colombia
Ypadu Brazil
2. SUMMARY
2.1 Main risks and target organs
The leaves of E. Coca are used as a stimulant in Western South
America. For centuries the indians of Peru and Bolivia have
chewed coca leaves, often mixed with ashes of plants or
limestone. This is the most common manner of use but the
chewing of the powdered plant, the smoking, or the swallowing
in various infusions are also practised (Morch, 1963).
Chewing the leaves releases the alkaloid cocaine in contact
with the saliva. The chewing habit (named "coqueio") induces
a mild stimulation, enabling the user to withstand strenuous
work, walking, hunger, or thirst.
The contact with the mucous membranes of mouth and stomach
produces local anaesthesia. The psychological and
physiological effects are lighter than the administration of
pure extracted alkaloid cocaine. The hazards of this pattern
of use are considerably diminished.
Other effects are related to the potentiation of responses of
sympathetically innervated organs to catecholamines, and to
sympathetic nerve stimulation causing tachycardia and
mydriasis (Goodman & Gilman, 1985).
According to the amount of cocaine ingested by the habitual
users of coca chewing - 60 grams of leaves a day - (Phillips,
1980) the various effects include mainly local anaesthesia,
slight euphoria and diminishing of fatigue.
The greatest hazard is addiction. For many centuries the
populations of the Andes region have used coca leaves as part
of the social and religious habits. Changing the pattern of
use to the administration of pure cocaine is another permanent
risk.
The target organs are the central nervous system, and the
cardiovascular system.
2.2 Summary of clinical effects
Chewing coca leaves rarely induces acute effects but chronic
effects are often observed.
The manifestations of acute poisoning are dose-related and are
well understood from the description of the clinical effects
induced by ingestion of the pure alkaloid:
Acute poisoning - With small amounts, cocaine users
experience euphoria, restlessness, excitability. There is a
lessened sense of fatigue, and increased capacity for muscular
work. Later, hallucinations, tachycardia, dilated pupils,
arterial hypertension and abdominal pain develop. The
stimulation is followed by depression of the nervous system.
Irregular respiration, convulsions, coma, and circulatory
failure are observed.
Chronic poisoning - Impaired sensibility of mucous membranes
of mouth; the irritating and vasoconstricting properties may
cause ulceration of the mucous membranes; weight loss; altered
character; hallucinations and mental deterioration have been
described.
2.3 Diagnosis
An initial excitatory phase produces euphoria and
restlessness; this is followed by hallucinations and
tachycardia. Later, CNS depression occurs, with
abnormal respiration, coma and circulatory failure;
convulsions may also occur.
Remnants of leaves, vomitus or gastric aspirate should be
collected in clean bottles for identification purposes.
2.4 First-aid measures and management principles
First-Aid Measures:
Remove any leaves present in the mouth. Wash the mouth
thoroughly with water or a saline solution. Induce vomiting
by giving syrup of ipecac.
Dose of syrup of ipecac (this should be taken with a glass of
water and may be repeated after 20 minutes if necessary).
Children: 6 to 18 months 10 ml
18 months to 12 years 15 ml
Adults: 30 ml
Do not induce vomiting if consciousness is impaired or if fits
occur.
Management principles
The treatment of acute overdose is basically symptomatic and
supportive. Ensure patient's airway and ventilation.
Supportive measures include: oxygen, artificial respiration,
intravenous fluids with vasopressors (dopamine) and control of
agitation and seizures with intravenous diazepam.
2.5 Poisonous parts
The leaves are the poisonous parts of the plant. Description
of the leaves: Lively green, or greenish brown and clear brown,
smooth, slightly glossy, opaque, oval and more or less
tapering at the extremities. They are 1.5 - 3 cm wide, and
2.5 to 11 cm long. Characteristically, the leaves have an
areolate portion bounded by two longitudinal curved lines one
on each side of the midrib, and more evident on the under face
of the leaf.
When chewed they have a pleasant, pungent taste. Dried leaves
are uncurled, deep green on the upper surface, grey-green on
the lower, and have a strong tea-like odour (Morch, 1963; Cruz,
1982 Hoehne, 1978).
2.6 Main toxins
Cocaine (methylbenzoylecgonine) is one of at least 12
alkaloids extracted from the leaves of E. coca. All have
ecgonine as common constituent.
Some other alkaloid are: cinnamylcocaine, hygrine,
tropococaine, truxillines, isotropylcocaine, cocaicine.
3. CHARACTERISTICS
3.1 Description of the plant
3.1.1 Special identification features
The wild coca shrub often grows to a height of 3 to 5.5
m (12 to 18 feet). The cultivated plant is usually kept
to 6 meters. Diameter of the stem is about 16
centimetres. The plant is very hardy and its roots can
penetrate 2 to 3 m into the soil. The reddish branches
are straight, alternate. The stem has a whitish bark.
The leaves are lively green, or greenish brown, and
clear brown, smooth, slightly glossy, opaque, oval or
elliptical, and more or less tapering at the
extremities. The leaves are 1.5 to 3 cm wide, and .5 to
11 cm long. A special characteristic of the leaf is an
areolate portion bounded by two longitudinal curved
lines one on each side of the midrib, and more evident
on the under face. The taste is bitter and faintly
aromatic. Dried leaves are uncurled, deep green on the
upper surface, grey-green on the lower, and have a
strong tea-like odour. The flowers are succeeded by red
berries. These fruits are drupaceous, oblong, measuring
around 1 cm; these produce only one seed (monospermous).
The main characteristic of the plant is the perennial
renewal of the branches, after cutting, in a geometrical
progression (Morch, 1963; Cruz, 1982).
3.1.2 Habitat
The wild coca shrubs develop well in tropical humid
climates, preferably zones such as clearings in forests,
or on the wet side of mountains. Wild species are
commonly found in altitudes of 300 to 2000 m.
Cultivated plants can thrive in different climatic
conditions.
3.1.3 Distribution
Erythroxylum coca grows throughout the tropical regions
in the Eastern Peruvian Andes, mainly Peru, Ecuador and
Bolivia. It also grows in Colombia, Chile, and in the
Brazil Amazon region, and to a lesser extent in Mexico,
and the West Indies. It is cultivated in Indonesia.
3.2 Poisonous parts of the plant
The leaves are the poisonous parts of the plant.
3.3 The toxin(s)
3.3.1 Name(s)
The alkaloid cocaine (methylbenzoylecgonine) is the
active principle obtained from the leaves of E. coca.
It is one of at least 12 alkaloids extracted from the
leaves. All toxins have ecgonine as common constituent.
Cocaine is synthetically obtained from ecgonine. Other
toxins are cinnamylcocaine, truxillococaine,
isotropylcocaine, cocaicine, tropococaine (Merck Index,
1983; Reynolds, 1989).
3.3.2 Description, chemical structure, stability
Cocaine is methybenzoylecgonine.
CAS number: 50-36-2
Molecular weight: 303.4
Structural formula: C17H24N04
Colourless odourless crystals, or white crystalline
powder, with a numbing taste. It is slightly volatile.
Stability: Melting point from 96 °C to 98 °C. Should
be protected from light (Reynolds, 1989).
3.3.3 Other physico-chemical characteristics
Cocaine is soluble in water, alcohol, arachis oil,
castor oil, chloroform, ether, liquid or soft paraffin,
oleic acid. Practically insoluble in glycerol. The
saturated solution in water is alkaline to
phenolphthalein. Only a mild degree of heat is used to
prepare oily solutions (Reynolds, 1989).
3.4 Other chemical contents of the plant
In addition the leaves contain:-
Dextrin and sugars
Starch
Protein
Crude fibre
Volatile oils.
Nutritional analysis shows that 100 g of leaves contain 305
calories (Phillips & Wynne, 1980).
4. USES/CIRCUMSTANCES OF POISONING
4.1 Uses
The tradition of chewing of coca leaves is deeply fixed
among the Andes Indians, farmers and miners, who use it
to arouse physical energy, and to fight against pain,
hunger and thirst.
Some countries in South America, for example, Peru and
Bolivia, have legal plantations of coca shrub, to supply
this local and traditional use.
From the leaves the alkaloid cocaine is extracted, for
limited medical use as an ophthalmic anaesthetic.
One of the reported uses of the coca leaves is as an
ingredient in the composition of soft drinks, cocaine
being previously removed.
The most important use of cocaine is an illegal one, as
defined by all countries and the United Nations. The
free base, the paste and cocaine are extracted from coca
leaves. "Crack" is a potent smokable form of cocaine.
The illicit use of cocaine has increased dramatically
because of its accelerated use among all social classes
(Ellenhorn, 1988).
4.2 High risk circumstances
poisoning may occur in association with the traditional
chewing of leaves in some well-defined geographical areas, and
due to ingestion by children who chew or swallow the leaves.
The use of infusions is a minor risk for poisoning, because
the concentration of the alkaloid is very low.
This monograph will not discuss the use of the alkaloid
cocaine. Readers are referred to Cocaine.
4.3 High risk geographical areas
Especially the regions of the Andes (Peru, Bolivia, Ecuador,
Columbia, Chile) and the Amazon region of Brazil.
5. ROUTES OF ENTRY
5.1 Oral
Ingestion is commonly by chewing, sucking or swallowing the
leaves entire or in powdered form. Leaves can also be
ingested in the form of infusion: 'coca tea' is very popular
in the Andes.
5.2 Inhalation
Smoking the leaves is not a current practice. Although pure
leaves can be used as cigars, the concentration of alkaloids
is very low. This use is different from making cigars with
the basic paste.
5.3 Dermal
Folk medicine uses leaves or infusions as topical treatment of
burns or skin diseases.
5.4 Eye
Infusions are used in traditional medicine.
5.5 Parenteral
Not described.
5.6 Others
Not described.
6. KINETICS
6.1 Absorption by route of exposure
When coca leaves are chewed there is absorption from the
mucous membranes of the mouth and from the gastrointestinal
tract. The exact sites of absorption (stomach or duodenum)
are not known. Systemic absorption is 30 to 40% after oral
doses (Grabowski, 1984).
The extent of absorption after smoking the leaves is unknown
though the absorption of smoked cocaine and crack has been
extensively studied.
6.2 Distribution by route of exposure
Distribution occurs throughout the tissues of the body.
Cocaine easily diffuses across the blood-brain barrier. The
significance of enterohepatic circulation is still undefined
(Gosselin, 1984). The volume of distribution of cocaine is
1.2 to 1.9 L/kg (Ellenhorn, 1988).
6.3 Biological half-life by route of exposure
6.4 Metabolism
Cocaine is rapidly and extensively metabolized by the liver
although absorption from the mucous membranes of the mouth
avoids some presystemic hepatic metabolism. Enzyme esterases,
specifically the plasma cholinesterase, play an important
role in the metabolism of cocaine and the activity of
cholinesterase can vary greatly between individuals.
Cocaine is hydrolysed to water soluble metabolites. The major
products of metabolism are ecgonine methyl ester (32 to 49%)
and benzoylecgonine (29 to 45%). The latter may be hydrolysed
nonenzymatically. Other metabolites, including hydroxycocaine,
methylecgonidine, and norcaine, have been identified
(Gillenhorn, 1988).
6.5 Elimination by route of exposure
The metabolites are excreted in urine, and can be identified
up to 48 hours after oral ingestion (Noji & Kelen, 1989).
After metabolism, 1 to 9 % of cocaine is excreted unchanged in
the urine (Gosselin, 1984).
7. TOXICOLOGY/TOXINOLOGY/PHARMACOLOGY
7.1 Mode of action
The main effects of cocaine result from sympathetic
stimulation. Cocaine inhibits the reuptake of catecholamines,
particularly norepinephrine (noradrenaline) and dopamine, at
the nerve terminal. The effects of sympathetic
neurotransmitters are therefore enhanced due to the
persistence of catecholamines in the synaptic cleft.
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
There is considerable individual variation in
the susceptibility to cocaine. The toxicity of
cocaine may be lower if it is ingested orally by
chewing coca leaves (Grabowski, 1984). The
lethal oral dose of the alkaloid is 1,200 mg for
adults (Noji & Kelen, 1989), but it has been
reported that chronic users consume 5 to 10
g/day.
The leaves of the South American plants contain
0.5% to 1% of the alkaloid cocaine.
Coca leave chewers may use 20 to 80 g of leaves
per day. This corresponds to an ingestion of
0.16 to 0.64 mg/day of the alkaloid. The lethal
dose is not achieved by chewing the leaves.
7.2.1.2 Children
Data on oral absorption and toxicity of cocaine
after chewing of leaves in children are not
available.
7.2.2 Animal data
Estimates of oral acute LD50 in animals are not
available. The approximate LD50 in the rabbit is: 15
mg/kg IV; 50 mg/kg intranasally (Gosselin, 1984)
The LD50 IV in the rat is 17.5 mg/kg (Merck Index,
1983).
7.2.3 Relevant in vitro data
In vitro, cocaine is hydrolysed by human hepatic and
plasma esterase to ecgonine methyl ester. Treated the
same way, norcocaine yields norecgonine methyl ester
(Reynolds, 1989).
7.3 Carcinogenicity
No data available.
7.4 Teratogenicity
The evidence from animal studies is conflicting (Ellenhorn,
1988).
Congenital malformations are more common among children born
to mothers who abuse cocaine (Reynolds, 1989).
7.5 Mutagenicity
Not available.
7.6 Interactions
Patients with esterase deficiencies may develop severe
reactions (Ellenhorn, 1988). Interactions are possible with
methyldopa, tricyclic antidepressants, monoamine oxidase
inhibitors, chlorpromazine, reserpine, guanethidine,
adrenaline, and alpha- and beta-adrenoreceptor blocking agents
(Reynolds, 1989).
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
Full blood count
8.3.1.2 Urine
Urinalysis to detect red and white blood cells;
and glucose, protein.
8.3.1.3 Other fluids
8.3.2 Arterial blood gas analyses
Arterial p02 and pCO2 and acid-base balance.
8.3.3 Haematological analyses
Serum electrolytes, blood urea nitrogen, creatinine,
glucose, phosphorus, bilirubin, serum glutamic-
oxaloacetic transaminase, and serum glutamic-pyruvic
transaminase.
8.3.4 Interpretation of biomedical investigations
ECG.
8.4 Other biomedical (diagnostic) investigations and their
interpretation
8.5 Overall Interpretation of all toxicological analyses and
toxicological investigations
Oral doses of 2 mg/kg produce an average peak plasma
concentration of 0.21 mg/l in one hour. After ingestion of
cocaine filled condoms ('body-packing'), the serum cocaine
level in one patient was 2 mg/l. Postmortem cocaine blood
levels range from 0.1 to 2.11 mg/l and blood concentrations
are highest in patients who die after oral ingestion
(Ellenhorn, 1988).
Blood: Leukocytosis commonly occurs after large doses of
cocaine (Ellenhorn, 1988).
Urine: Red blood cells in urine; electrolytes, blood urea
nitrogen, and glucose show changes after large doses of
cocaine (Ellenhorn, 1988). Glucose and protein are increased.
Severe overdoses cause hypoxaemia and hypercarbia due to
respiratory depression and seizures. Acid-base abnormalities
follow hypoxaemia (Ellenhorn, 1988).
The most frequent ECG changes are tachycardia and ventricular
arrhythmias (Noji & Kelen, 1989).
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
The onset of action after ingestion is 2 to 5 minutes.
Clinical features include: restlessness, excitability,
hallucinations, mydriasis, chills, abdominal pain,
vomiting, numbness and muscular spasms.
9.1.2 Inhalation
Acute poisoning after inhalation of the smoking of
leaves has not been reported.
9.1.3 Skin exposure
Not relevant.
9.1.4 Eye contact
Not relevant.
9.1.5 Parenteral exposure
Not described.
9.1.6 Other
Not described.
9.2 Chronic poisoning
9.2.1 Ingestion
Chronic ingestion or chewing of the leaves may produce
some specific clinical features, including physical
exhaustion, weight loss, impaired sensitivity of mouth
mucous membranes, pallor, tremors, hallucinations,
mental deterioration and altered personality.
9.2.2 Inhalation
Effects in chronic smokers of leaves have not been
reported.
9.2.3 Skin exposure
Not described.
9.2.4 Eye contact
Not described.
9.2.5 Parenteral exposure
Not described.
9.2.6 Other
Not described.
9.3 Course, prognosis, cause of death
The course of cocaine poisoning has 3 phases: an early phase
of stimulation, a second phase of late stimulation and a third
phase of depression.
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
Acute: Tachycardia.
Chronic: Arrhythmias.
9.4.2 Respiratory
Acute: Tachypnoea.
9.4.3 Neurological
9.4.3.1 CNS
Acute: Euphoria, headache, vertigo, tremor,
restlessness, hyperreflexia.
Chronic: Hallucinations, mental deterioration.
9.4.3.2 Peripheral nervous system
Local application of cocaine blocks nerve
conduction.
9.4.3.3 Autonomic nervous system
Mydriasis and cycloplegia.
9.4.3.4 Skeletal and smooth muscle
Muscular tremor and hyperactivity. Increased
contraction of intestinal smooth muscles.
9.4.4 Gastrointestinal
Acute: Nausea, vomiting, diarrhoea, abdominal cramps.
9.4.5 Hepatic
Hepatoxicity is not a well recognized complication
(Ellenhorn, 1988).
9.4.6 Urinary
9.4.6.1 Renal
Haematuria.
9.4.6.2 Others
Not available.
9.4.7 Endocrine and reproductive systems
Not available.
9.4.8 Dermatological
Not relevant.
9.4.9 Eye, ears, nose, throat: local effects
Acute: Mydriasis by local action. Anaesthesia and
vasoconstriction of mucous membranes.
Chronic: Sneezing and coryza-like symptoms.
9.4.10 Haematological
Acute: Leukocytosis after large doses.
9.4.11 Immunological
Not described.
9.4.12 Metabolic
9.4.12.1 Acid base disturbances
Acid base disturbances occur after hypoxemia.
9.4.12.2 Fluid and electrolyte disturbances
Vomiting and diarrhoea may result in loss of
fluids.
9.4.12.3 Others
Higher temperature is observed due to
vasoconstriction that reduces the amount of
heat loss.
9.4.13 Allergic reactions
Not described.
9.4.14 Other clinical effects
Chronic: Psychiatric complications of addiction:
dysphoric agitation, acute psychoses.
9.4.15 Special risks
There is evidence that the risk of congenital
malformations is increased in mothers who abuse
cocaine; perinatal mortality is also greater (Ellenhorn,
1988).
During pregnancy there is a decrease of cholinesterase
activity which increases cocaine toxicity (Grabowski,
1984). Cocaine is excreted breast milk.
9.5 Others
Not relevant.
9.6 Summary
10. MANAGEMENT
10.1 General principles
Supporting symptomatic treatment. Remove any leaves present
in the mouth. Wash the mouth with water or saline.
Ingested leaves should be removed from the stomach by
gastric lavage or emesis.
10.2 Relevant laboratory analyses and other investigations
10.2.1 Sample collection
(In preparation).
10.2.2 Biomedical analysis
As indicated. Choline esterase blood levels.
10.2.3 Toxicological/toxinological analysis
(In preparation)
10.2.4 Other investigations
10.3 Life supportive procedures and symptomatic treatment
Monitor pulse, respiration, and blood pressure. Maintain a
fluid balance chart.
Respiration: assess ventilation and establish an adequate
airway. Correct anoxia by mechanical ventilation and oxygen.
Convulsions: Diazepam 10 mg (0.1 to 0.3 mg/kg) IV mg for an
adult.
10.4 Decontamination
Remove any leaves present in the mouth. Wash the mouth
thoroughly with water or a saline solution. If convulsions
are not imminent, induce vomiting or perform gastric lavage.
Gastric lavage may be performed if emesis fails, bearing in
mind the risk of imminent convulsions.
Activated charcoal is indicated.
10.5 Elimination
Due to its very short half-life and large volume of
distribution, measures to enhance the elimination of cocaine
are not indicated.
10.6 Antidote/antitoxin treatment
10.6.1 Adults
10.6.2 Children
10.7 Management discussion
Management is mainly symptomatic. There are few case
reports of ingestion of leaves or the consequences of
chewing the leaves. Scientific papers refer primarily to the
use of the pure alkaloid.
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
Zapata Ortiz (1952) describes the chronic use of E. coca
among the Andean miners:
"Although it is true that the chewing of coca leaf
diminishes fatigue and by exerting a stimulating effect may
increase the output of work within the short period of a
particular experiment, the result in no way shows that coca
addicts are capable of doing more work and achieving a
greater output over the protracted period required for their
customary tasks and much less that they have a greater
capacity for work than persons who do not consume coca and
who receive proper nourishment".
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
Know the botanical name of the house and yard plants or
trees.
Teach children never to put leaves, stems, bark, seeds, nuts,
or berries from any plant into their mouths.
Keep poisonous house plants out of the reach of all
children.
Never eat a wild plant unless you are sure of its identity.
Do not assume that plant is safe because birds or animals
eat it.
Cooking seldom do not destroy active principles of the
plant.
Do not smoke plant materials.
12.3 Other
13. REFERENCES
13.1 Clinical and toxicological
Dreisbach RH, Robertson WO (1987). Handbook of poisoning;
prevention, diagnosis, and treatment. 12th ed Norwalk:
Appleton & Lange, p. 589.
Ellenhorn MJ, Braceloux DG (1988). Medical Toxicology:
Diagnosis and treatment of human poisoning. New York:
Elsevier, p. 1512.
Gillam AG, Goodman LS, Rall TW, Murad F, eds. Goodman and
Gilman's The Pharmacological Basis of Therapeutics. 7th.ed.
New York, Toronto, London: Macmillan, 1985. p. 1839.
Gosselin RE, Smith RP, Hodge HC (1984). Clinical toxicology
of commercial products. 5th Ed. Baltimore: Williams &
Wilkins.
Grabowski J (1984). Cocaine; Pharmacology, effects, and
treatment of abuse. Washington: National Institute on Drug
Abuse. (NIDA Research Monograph, 50).
Merck Index (1983). An encyclopedia of chemicals, drugs
and biologicals. 10th ed. Rahway: Merck, p. 10000.
Noji EK, Kelen GD (1989). Manual of toxicological
emergencies. Chicago, London, Boca Raton: Year Blood Medical
Publishers, p. 850.
Phillips JL, Wynne RW (1980). Cocaine - the mystique and
the reality. New York: Avon Bloods, p. 318.
Reynolds JEF (ed). Martindale, The Extra Pharmacopoeia. 29th
Ed. London: Pharceutical Press, 1989. p. 1896.
Zapata-Ortiz V (1952). The problems of the chewing of the
coca leaf in Peru. Bulletin of Narcotics: 26-33.
13.2 Botanical
Cruz Gl (1982). Dicionario de plantas uteis do Brazil. 2nd
Ed Rio de Janeiro: Civilizaçåo Brasileria, p. 599. (in
Portuguese).
Hoehne FC (1978). Plantas e substancias vegetais toxicos e
medicinais. Reimpressao, Sao Paulo, (1st Ed. 1939) (in
Portuguese).
Morch ET (1963). Cocaine. In: Encyclopedia Britannica,
vol.5. chicago, London, Toronto, Geneva: William Benton
Publisher, p. 993-4.
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)
Authors: M.S.C. de Medeiros and A. Furtado Rahde
Rua Riachuelo 677 ap 201
90010 Porto Alegre
Brazil
Tel: 55-512 275419
Fax: 55-512 391564/246563
Telex: 051 2077 FUOC BR
Date: September 1989
Peer Review: Strasbourg, France, April 1990