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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: Civilizašňo 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



    See Also:
       Toxicological Abbreviations