1.1 Substance
   1.2 Group
   1.3 Synonyms
   1.4 Identification numbers
      1.4.1 CAS number
      1.4.2 Other numbers
   1.5 Brand names,Trade names
   1.6 Manufacturers, Importers
   1.7 Presentation/formulation
   2.1 Main risks and target organs
   2.2 Summary of clinical effects
   2.3 Diagnosis
   2.4 First aid measures and management principles
   3.1 Origin of the substance
   3.2 Chemical structure
   3.3 Physical properties
      3.3.1 Properties of the substance Colour State/Form Description
      3.3.2 Properties of the locally available formulation
   3.4 Other characteristics
      3.4.1 Shelf-life of the substance
      3.4.2 Shelf-life of the locally available formulations
      3.4.3 Storage conditions
      3.4.4 Bioavailability
      3.4.5 Specific properties and composition
   4.1 Indication
      4.1.1 Indications
      4.1.2 Description
   4.2 Therapeutic dosage
      4.2.1 Adults
      4.2.2 Children
   4.3 Contraindications
   5.1 Oral
   5.2 Inhalation
   5.3 Dermal
   5.4 Eye
   5.5 Parenteral
   5.6 Other
   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
   7.1 Mode of action
      7.1.1 Toxicodynamics
      7.1.2 Pharmacodynamics
   7.2 Toxicity
      7.2.1 Human data Adults 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
   7.7 Main adverse effects
   8.1 Sample
      8.1.1 Collection
      8.1.2 Storage
      8.1.3 Transport
   8.2 Toxicological analytical methods
      8.2.1 Test for active ingredient
      8.2.2 Test for biological sample
   8.3 Other laboratory analyses
      8.3.1 Haematological investigations
      8.3.2 Biochemical investigations
      8.3.3 Arterial blood gas analysis
      8.3.4 Other relevant biomedical analyses
   8.4 Interpretation
   8.5 References
   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 Central nervous system Peripheral nervous system Autonomic nervous system Skeletal and smooth muscles
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary Renal Other
      9.4.7 Endocrine and reproductive system
      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 Acid-base disturbances Fluid and electrolyte disturbances Others
      9.4.13 Allergic reactions
      9.4.14 Other clinical effects
      9.4.15 Special risks
   9.5 Other
   10.1 General principles
   10.2 Relevant laboratory analyses
      10.2.1 Sample collection
      10.2.2 Biomedical analysis
      10.2.3 Toxicological analysis
      10.2.4 Other investigations
   10.3 Life supportive procedures and symptomatic/specific treatment
   10.4 Decontamination
   10.5 Elimination
   10.6 Antidote treatment
      10.6.1 Adults
      10.6.2 Children
   10.7 Management discussion
   11.1 Case reports from literature
   11.2 Internally extracted data on cases
   11.3 Internal cases
   12.1 Availability of antidotes
   12.2 Specific preventive measures
   12.3 Other
    1. NAME

       1.1 Substance 

           Dimercaprol (INN)


       1.2 Group

           ATC classification index

           All other therapeutic products (V03)/Antidotes (V03B)

           (WHO, 1992]

       1.3 Synonyms

           British Anti-Lewisite

           (Budavari, 1989)

       1.4 Identification numbers

           1.4.1 CAS number


           1.4.2 Other numbers

       1.5 Brand names,Trade names

           BAL, Dimercaprol, Sulfactin (Germany), 
           (To be completed by each Centre using local data)
       1.6 Manufacturers, Importers

           Boots (UK) 
           Hynson, Westcott & Dunning, Inc. (UK)
           Société l'Arguenon (France).

           (To be completed by each Centre using local data)

       1.7 Presentation/formulation

           Ampoules (2 ml) containing 50 mg/ml (100 mg/ampoule) (BAL-
           Boots) (Dimercaprol 5% solution in peanut oil and 10% benzyl 

           Ampoules (3 ml) containing 100 mg/ml (300 mg/ampoule) (BAL-
           Hynson, Westcott & Dunning, Inc.) (Dimercaprol 10% solution 
           in peanut oil and 10% benzyl benzoate) 
           Ampoules (2 ml) containing 100 mg/ml (200 mg/ampoule) (BAL-
           Société l'Arguenon)(Dimercaprol 10% solution in peanut oil 
           with butacaine 1 mg). 
           (To be completed by each Centre using local data)

    2. SUMMARY

       2.1 Main risks and target organs

           The main risks are hypertension, tachycardia, cardiovascular 
           collapse, convulsions, excitation, hyperglycaemia, and 

           Special care should be taken in cases of oliguria, 
           hypertension, and impaired hepatic function, when the 
           antidote has to be administered. 

           The target organs are the kidneys, the cardiovascular and the 
           central nervous systems. 

           Adverse reactions have been reported in 50% of patients who 
           were given more than 5 mg/kg IM. 

       2.2 Summary of clinical effects

           The clinical effects are nausea, vomiting, headache, burning 
           sensation in the lips, throat, mouth, and eyes; lacrimation 
           and salivation; sweating, rhinorrhea, and burning sensation 
           of the penis; a feeling of constriction or pain in the throat 
           or chest, muscle pains and spasms, and tingling of the skin 
           of the hands; hypertension and tachycardia; abdominal pain, 
           anxiety, nervousness and weakness; urticaria and 

           Clinical effects peak 30 minutes after injection and subside 
           in a few hours. 

           Pain and sterile abscesses can occur at the injection site.

           Irritation of the skin and mucous membranes can be observed 
           after local contact. 

       2.3 Diagnosis

           Clinical diagnosis would be difficult in deliberate overdose, 
           but could be more readily made if poisoning was iatrogenic. 

           Determination of dimercaprol levels, heavy metal complexes 
           and dimercaprol metabolites in the urine may be done but is 
           not used in practice. 

       2.4 First aid measures and management principles

           Interrupt parenteral administration by lowering the dosage or 
           increasing the time between doses. 

           Anti-histaminics may possibly alleviate some of the adverse 

           Strict clinical observation and monitoring of blood pressure 
           and diuresis. 

           Note:  Dimercaprol should be given with caution in 
           hypertensive patients and in patients who have renal and 
           hepatic dysfunction. 


       3.1 Origin of the substance

           Dimercaprol is a therapeutic synthetic substance developed 
           during World War II as an antidote against the vesicant 
           arsenic war gases (Lewisite). 

           The first experiments were based on the fact that arsenic 
           products react with SH radicals.  Of all the compounds 
           originally tested, BAL was the most effective and the least 
           toxic.  The intrinsic toxicity of BAL later led to the 
           development of its water soluble and less toxic derivatives 
           dimercaptosuccinic acid (DMSA) and dimercaptopropanesulfonic 
           acid (DMPS) (see 10.7). 

           Dimercaprol is prepared by the bromination of allyl alcohol 
           to glycerol di-bromine-hydrine followed by reaction with 
           sodium hydrosulfide under pressure.  It can also be prepared 
           by hydrogenizing hydroxide propylene trisulfide (Budavari, 

       3.2 Chemical structure

           Structural formula

           Molecular formula

           Molecular weight


           Structural names


           2-3-dimercapto-1-propanol (IUPAC) 


           (Budavari, 1989)

       3.3 Physical properties

           3.3.1 Properties of the substance


                         Clear, colourless, or slightly yellow




                         Alliaceous, pungent odour of mercaptan.

                         Dimercaprol may be turbid or may contain small 
                         amount of flocculated material. This material, 
                         which develops during sterilization, is not an 
                         indication of deterioration. 

                         Water solubility is 1 in 20.  The solution is 
                         not stable in water so arachis or peanut oil is 
                         used in pharmaceutical preparations.  
                         Solubility in vegetable oils is 1 in 18 
                         (Reynolds, 1982). 

                         Dimercaprol is miscible with alcohol, benzyl, 
                         benzoate, ether, methyl alcohol, and many other 
                         organic solvents. 

                         A saturated solution water has a pH 5 to 6.5. 

                          Relative density    1.239 to 1.259 (BP)
                                             1.242 to 1.244 (USP)
                         (Reynolds, 1989)

           3.3.2 Properties of the locally available formulation

                 To be completed by each Centre using local data.

       3.4 Other characteristics

           3.4.1 Shelf-life of the substance

                 No data available.

           3.4.2 Shelf-life of the locally available formulations 

                 To be completed by each Centre using local data

           3.4.3 Storage conditions

                 Stability in light  

                 Dimercaprol must be protected from the light.  The 
                 addition of benzyl benzoate increases its stability 
                 (and solubility). 

                 Thermal stability

                 Dimercaprol must be stored at between 2 and 10 °C in 
                 small vials that are hermetically sealed and completely 
                 filled (Reynolds, 1989). 

           3.4.4 Bioavailability

                 To be completed by each Centre using local data

           3.4.5 Specific properties and composition

                 Dimercaprol is prepared in vegetable oil (peanut or 
                 arachis oil) and stabilized with benzyl benzoate 
                 (Reynolds, 1982). 

                 (To be completed by each Centre using local data)

    4. USES

       4.1 Indication

           4.1.1 Indications

                 In most recent studies of the use of dimercaprol it has 
                 been compared to its water-soluble analogues DMPS and 
                 DMSA.  These studies suggest dimercaprol should never 
                 be the first drug of choice in any form of poisoning 
                 due to metals or metalloids.  This statement is based 
                 on the better efficacy and lower toxicity of the newer 
                 antidotes referred above. The intrinsic toxicity or 
                 dimercaprol is significant and should always be 
                 considered whenever there might be an indication for 
                 its use. 

                 However, in some countries dimercaprol may remain more 
                 readily available than DMPS and DMSA for some years, 

                 and this being the case, dimercaprol may be found 
                 useful in the treatment of poisonings due to: 

                 -      arsenic (organic & inorganic)
                 -      gold
                 -      inorganic mercury.

                 It should be noted that in none of these types of 
                 poisoning is the indication for the use of dimercaprol 
                 clearcut (even if DMSA/DMPS are not available). 

                 The recommendation for the use of dimercaprol in 
                 inorganic arsenic poisoning is based on documented 
                 reduced mortality, and significantly decreased arsenic 
                 content of body tissues, in animal studies. Increased 
                 urinary excretion has been documented in at least one 
                 human case, but other clinical data are not conclusive. 
                 However, animal data uniformly shows that dimercaprol 
                 treatment is associated with increased brain content of 
                 arsenic and its value as an antidote has therefore been 

                 In organic arsenic poisonings, where data is mainly 
                 from lewisite exposure, dimercaprol appears to remove 
                 arsenic from the body and significantly lower lethality 
                 without increasing the brain content of arsenic. 
                 Clinical data are, however, non-conclusive. 

                 The recommendation for the use of dimercaprol in gold 
                 intoxication is based mainly on toxicokinetic data from 
                 the one case studied by Lalanne (1980). No other 
                 clinical reports provide conclusive data. A reduced 
                 mortality has not been reported in animal studies, only 
                 an increase in urinary gold excretion. 

                 The recommendation for the use of dimercaprol in 
                 poisoning due to inorganic mercury salts is based on 
                 reduced mortality and reduced nephrotoxicity in animal 
                 studies. However, an effect of mortality was not 
                 observed when the antidote was administered more than 
                 one hour after mercury exposure. Though clinical 
                 reports have tended to be favourable, they are not 

                 The use of dimercaprol (in conjunction with CaNa2EDTA) 
                 in lead poisoning is considered controversial and is 
                 therefore not recommended.

                 (IPCS dimercaprol antidote monograph, 1994)
                 No efficacy has been documented for poisonings due to 
                 silver (argyria), thallium, tellurium, vanadium, 
                 chromium, cobalt, copper, nickel, zinc, antimony, tin, 
                 titanium, beryllium, magnesium, manganese, tungsten, 
                 and organic compounds of mercury and lead. 

                 Dimercaprol is more effective when given soon after 
                 toxic exposure because it is more effective in 
                 preventing inhibition of sulfhydryl enzymes than in 
                 reactivating them (Gilman et al., 1985). 
           4.1.2 Description

                 Not applicable
       4.2 Therapeutic dosage

           4.2.1 Adults

                 Dimercaprol should always be administered as soon as 
                 possible by deep intramuscular injection (never 
                 intravenous nor subcutaneous), and rotating sites.  The 
                 generally recommended doses are similar for arsenic, 
                 gold and inorganic mercury poisoning: 

                  Mild cases   

                 2.5 mg/kg every 4 hours on the lst day
                 2.5 mg/kg every 6 hours on the 2nd day
                 2.5 mg/kg every 12 hours on the 3rd day
                 2.5 mg/kg every 24 hours for 10 days (or until clinical

                  Severe cases

                 3to 4 mg/kg every 4 hours on the first 2 days
                 3to 4 mg/kg every 6 hours on the 3rd day
                 3to 4 mg/kg every 12 hours for 10 days
                 (doses of 5 mg/kg can be employed in the most severe 

                 (IPCS dimercaprol antidote monograph, 1994)

           4.2.2 Children

                 Dimercaprol is well tolerated by children.  The dosage 
                 should be calculated according to body weight, using 
                 the same unit-dose per kilogram of body weight as for 
                 adults under similar clinical conditions. 

       4.3 Contraindications

           Dimercaprol cannot be used in poisonings due to iron, 
           cadmium, tellurium, selenium, vanadium, and uranium.  It is 
           also contraindicated in poisonings due to elemental mercury 
           vapour, because it can further increase the metal in the 
           brain (Berlin & Ullberg, 1963). 

           Dimercaprol should not be given in case of acute renal 
           failure (anuria) or extensive hepatic insufficiency (Cameron 

           et al., 1947), and should be used with special care in 
           hypertensive patients. 

           Note:  Dimercaprol is not effective in massive, severe 
           poisonings because its antidotal effect is surpassed by the 
           toxicity of the toxic metal. 

           If given 7 days after arsenic exposure, it has little or no 
           effect on the subsequent course of the neuropathy (Heymann et 
           al., 1956). 


       5.1 Oral

           Dimercaprol is given only by intramuscular injection -
           ingestion is only accidental or intentional. 

       5.2 Inhalation


       5.3 Dermal

           Skin absorption is possible and occurs with a rate of 3 
           µmol/cm2/h in rats and humans (Young, 1946; Simpson & Young, 
           1950).  Dimercaprol can be applied to the skin to heal local 
           effects caused by arsenic vesicant substances (Stocken & 
           Thompson, 1946). 

       5.4 Eye

           No data available.

       5.5 Parenteral

           Dimercaprol is usually administered by the parenteral route. 
           Because of its viscosity and lipid vehicle, a deep 
           intramuscular injection must be given.  This will prevent fat 
           emboli that may occur with intravenous injections, the slow 
           and irregular absorption, and sterile abscesses that can 
           occur with intravenous  and subcutaneous injections. 

       5.6 Other

           No data available.


       6.1 Absorption by route of exposure

           Peak concentrations in blood are obtained in about 30 to 60 
           minutes after intrasmuscular injection of dimercaprol (Gilman 
           et al., 1985). 

           It is readily absorbed through the skin after topical 
           application.  Percutaneous absorption in rats and humans 
           equals 3 millimol (124 mg)/cm2 per hour (Tamboline et al., 

       6.2 Distribution by route of exposure

           Because it is a lipophilic drug, dimercaprol penetrates 
           rapidly the intracellular spaces.  The highest concentrations 
           are found in the liver, kidneys, brain and small intestine 
           (Simpson & Young, 1950). 

           Due to its lipophilic characteristic, the complexes formed 
           with mercury and other metals may be redistributed into 
           sensitive cells in the brain following dimercaprol treatment 
           (Aaseth, 1983). 

       6.3 Biological half-life by route of exposure

           Biological half-life is short and metabolic degradation and 
           renal excretion are complete within 6 to 24 hours according 
           to animal studies (Catsch & Harmuth-Hoene, 1976). 

       6.4 Metabolism

           The metabolic contribution to its elimination is not clear. 
           The renal excretion is most often cited as its major 
           elimination route but there appears to be a significant 
           contribution from its conjugation with glucuronic acid. 

           The dimercaprol not fixed to the heavy metal is the fraction 
           that may be rapidly metabolized to inactive products, some of 
           which are glucuronide-conjugated.  

           Dimercaprol is not metabolically inert, and it can be broken 
           down to inactive and toxic metabolites (Tamboline & Matheson, 

       6.5 Elimination and excretion 

           The major portion of the drug is the fraction that may be 
           excreted rapidly in the urine, and part of it is eliminated 
           in the faeces (via bile). The dimercaprol-metal complexes 
           dissociate rapidly in the body, especially in an acid 
           internal medium; alkalinization of the urine may prevent this 
           dissociation and protect the kidneys from metal and BAL 
           nephrotoxicity (Reynolds 1982).  If the BAL-metal complex is 
           oxidized, the metal is released and can exert its toxic 
           effect again; therefore, the dosage of dimercaprol must be 
           high enough to assure the excess of free BAL in body fluids 
           until the metal is completely excreted. 


       7.1 Mode of action

           7.1.1 Toxicodynamics

                 The toxicity of BAL is due mainly to its effects on the 
                 kidneys, liver, and the cardiovascular and central 
                 nervous systems (CNS).  The mechanisms are not clearly 
                 understood, but may be explained in part by the 
                 inactivation of metal-containing enzymes, and also by 
                 increased capillary permeability. 

           7.1.2 Pharmacodynamics

                 Dimercaprol is a dithiol chelating agent, with an 
                 affinity for the "sulfur-seeking" metals, such as 
                 mercury and arsenic. 

                 It forms heterocyclic ring complexes with some heavy 
                 metals, preventing or reversing the binding of metallic 
                 cations to body ligands, such as the essential 
                 sulfhydryl-containing enzymes. 

                 Its application is based on its high affinity for the 
                 toxic metal, relatively low toxicity, minimal 
                 interactions with the essential biological molecules, 
                 penetration into the tissue deposits of the metal, 
                 minimal metabolism, and rapid elimination of the 
                 chelated metal (Aaseth, 1983).  The toxic metal cation 
                 accepts free electron pairs furnished by electron-donor 
                 groups (sulfur) from the chelator. 

                 Dimercaprol has to be used in a dosage high enough to 
                 have an antidotal effect, but it is limited by its own 
                 toxicity (Aaseth, 1983).  When the affinity of the 
                 toxic metal for Dimercaprol is greater than for the 
                 enzymes, the "chelate" is formed.  This new compound, a 
                 mercaptide, has a certain stability and can be rapidly 
                 excreted in the urine, thus preventing the noxious 
                 effect of some metals. 

       7.2 Toxicity

           7.2.1 Human data


                         The highest therapeutic dose recommended is 5 
                         mg/kg, repeated every 4 h initially.  At this 
                         dosage, 50% of patients develop side-effects 
                         (Gilman et al., 1985) and if the dose exceeds 5 
                         mg/kg, most patients will have toxic effects.  
                         Doses under 5 mg/kg are well tolerated, and 
                         side-effects, if they occur, are usually 
                         transient, and disappear in a few hours. 


                         In a report by Bismuth et al. (1987), 2  
                         children who received a dosage of about 20 
                         mg/kg developed seizures and toxic effects, but 
                         their clinical course was favourable. 

           7.2.2 Relevant animal data

                 In studies in rabbits and rats, the LD50 was 0.6 to 
                 1 mmol/kg of SC injection and death occurred within the 
                 first 4 hours. 

                 The LD50 in rabbits and rats was in the range of 0.6 -
                 1.0 mmol/kg by IM, IP or SC absorption (Fitzhugh et al. 
                 1946; Catsch & Harmuth-Hoene, 1976; Zvirblis & Ellin, 

                 In another study (Sandmeyer, 1981), the LD50 in rats
                 after IM injection was 105 mg/kg.

                 In animals, a lethal dose of dithiols causes 
                 convulsions and severe spasm of the abdominal muscles 
                 shortly before death occurs.  After injection of 
                 sublethal amounts of dimercaprol, the animals become 
                 apathetic and develop lacrimation, oedema of the 
                 conjunctiva, blepharospasm, salivation, and vomiting.  
                 With increasing doses, they develop ataxia, analgesia, 
                 tachypnea, and hyper-excitability.  Nystagmus and 
                 muscle tremor develop, and tonic and clonic convulsions 
                 occur at the final stages.  Death occurs during coma 
                 (Durlacher et al., 1946; Modell et al., 1946; Waters 
                 and Stock, 1945). 

                 The most important systemic acute toxic effect of 
                 dimercaprol, according to Catsch & Harmuth-Hoene 
                 (1976), is cardiovascular depression as judged by a  
                 fall in systemic and pulmonary artery pressure 
                 following intravenous injection in cats (Chenoweth, 

           7.2.3 Relevant in vitro data

                 No relevant data.

       7.3 Carcinogenicity

           No data available.

       7.4 Teratogenicity

           Dimercaprol may be teratogenic in mice (see Section 9.4.15).

       7.5 Mutagenicity

           No data available.

       7.6 Interactions

           Iron therapy should be given 24 hours or more after the last 
           dose of dimercaprol.  It should never be given at the same 
           time as dimercaprol. 

           Dimercaprol forms toxic complexes with iron, cadmium, 
           selenium, and uranium. 

           Dimercaprol decreases insulin effectiveness by reducing
           disulfide bridges (Catsch & Harmuth-Hoene, 1976).

       7.7 Main adverse effects

           About 50% of patients who receive high therapeutic doses 
           (4 to 5mg/kg) have minor reactions: nausea, vomiting, 
           fatigue, restlessness, apprehension, headache, burning 
           sensation of the mouth, throat, and eyes, lacrimation, 
           blepharospasm, salivation, tingling of extremities, a feeling 
           of constriction in the chest muscle, diffuse pain and muscle 
           spasm, hypertension (systolic and diastolic) and tachycardia. 

           Large doses may cause convulsions and coma. 

           There may be pain at the injection site.

           Dimercaprol gives the breath an odour of mercaptan.

           Haemolytic anaemia was reported in individuals with a G6PD 
           deficiency (Janakiraman et al., 1978; Reynolds, 1982). 

           Dimercaprol is less toxic in patients who have heavy-metal 
           poisoning than in patients who are not poisoned.  The adverse 
           effects are less severe in case of heavy metal poisoning, 
           presumably because the antidote bound to the metal does not 
           show its side-effects (Gilman et al., 1985). 

       8.1 Sample

           8.1.1 Collection
           8.1.2 Storage
           8.1.3 Transport

       8.2 Toxicological analytical methods

           8.2.1 Test for active ingredient
           8.2.2 Test for biological sample
       8.3 Other laboratory analyses

           8.3.1 Haematological investigations
           8.3.2 Biochemical investigations
           8.3.3 Arterial blood gas analysis
           8.3.4 Other relevant biomedical analyses
       8.4 Interpretation
       8.5 References


       9.1 Acute poisoning

           9.1.1 Ingestion

                 No data available.

           9.1.2 Inhalation

                 No data available.

           9.1.3 Skin exposure

                 Dimercaprol is irritating to the skin and mucous 
                 membranes.  Studies in humans show that when undiluted 
                 dimercaprol is applied to contaminated skin, a 
                 scarlatina-like oedematous rash or erythema develops, 
                 accompanied by severe tingling, slight lacrimation, and 
                 conjunctival irritation.  These symptoms disappear 
                 within 4 to 6 h (Stocken & Thompson, 1946).  "Repeated-
                 insult" of the skin with 10% dimercaprol can cause 
                 extreme sensitization (Reynolds, 1982). 

           9.1.4 Eye contact

                 Dimercaprol may cause eye irritation.

           9.1.5 Parenteral exposure

                 Dimercaprol may cause many adverse and toxic effects 
                 that are usually dose-dependent and reversible.  The 
                 most common side-effects due to parenteral 
                 administration are on the kidneys, the cardiovascular 
                 and central nervous system, and metabolism, besides the 
                 usual local pain at site of injection. 

                 Minor reactions that occur with doses of 4 to 5 mg/kg 
                 are: nausea, vomiting, headache, burning sensation of 

                 the lips, throat, mouth, and eyes, lacrimation and 
                 salivation, rhinorrhoea, urticaria, a feeling of 
                 constriction or pain in the throat or chest, muscle 
                 pains and spasms, tingling of the skin of the hands, 
                 systolic and diastolic hypertension and tachycardia, 
                 burning sensation in the penis, sweating, abdominal 
                 pain and anxiety, nervousness, or weakness. 

                 These effects usually peak within 30 to 60 min after 
                 injection and subside in 1 hour, or when administering 
                 low doses. Administration of ephedrine or an 
                 antihistamine may prevent or relieve many of the mild 

                 Dimercaprol has a strong odour and gives the breath an 
                 unpleasant mercaptan-like odour. 

                 Painful, sterile or purulent abscesses may occur at the 
                 injection site, particularly if the drug is not given 
                 by IM injection. Children treated with BAL often 
                 develop hyperpyrexia after the second dosage that lasts 
                 until the end of the treatment.  This side-effect can 
                 be alleviated by increasing the time between 
                 injections.  Repeated high doses lead to a severe 
                 clinical state characterized by cardiovascular 
                 collapse, convulsions, and further coma, acidosis with 
                 hyperlactataemia, accompanied by hyperglycaemia that is 
                 followed by hypoglycaemia. 

           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

                 After repeated local applications in animals, a 
                 sensitization dermatitis may develop (Peters et al. 

           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

           Since dimercaprol is rapidly metabolized and eliminated, the 
           clinical course is brief.  If the most serious complications 
           do not occur, the prognosis is good, although it also depends 
           on the patient's previous pathology. 

           The major causes of death are usually related to the cause of 
           poisoning.  But Dimercaprol could cause convulsions and coma; 
           irreversible cardiovascular collapse; acidosis and 
           hydroelectrolytic disturbances, renal failure; and secondary 
           consequences of hypertension such as brain injury or cardiac 

       9.4 Systematic description of clinical effects
           9.4.1 Cardiovascular

                 Only acute effects have been described, such as 
                 hypertension and tachycardia (Reynolds, 1989). 

           9.4.2 Respiratory

                 The respiratory system is affected only secondarily 
                 (e.g., acute pulmonary oedema after cardiac failure).  
                 Dimercaprol very often causes a feeling of constriction 
                 or pain in the chest. 

           9.4.3 Neurological

        Central nervous system

                         Headache, anxiety, nervousness, weakness, 
                         convulsions, and coma. (Only acute effects have 
                         been described). 

        Peripheral nervous system

                         Muscle pains and spasms, tingling of 
                         extremities. (Only acute effects have been 

        Autonomic nervous system

                         Sweating, trembling, salivation, hypertension, 
                         and other effects can be attributed to the 
                         autonomic nervous system. (Only acute effects 
                         have been described). 
        Skeletal and smooth muscles

                         Muscle pain and cramps.

           9.4.4 Gastrointestinal

                 Nausea and vomiting.

           9.4.5 Hepatic

                 Dimercaprol is contraindicated in patients with 
                 impaired hepatic function (except those with jaundice 
                 due to arsenic poisoning). 

                 Chronic effects in the animals are fatty degeneration 
                 of the liver and impairment of liver function. 

           9.4.6 Urinary


                         If acute renal failure develops during 
                         dimercaprol therapy, the drug should be 
                         discontinued or used with care because serum 
                         concentrations of dimercaprol may reach toxic 
                         levels and impair normal elimination. 


                         No data available.

           9.4.7 Endocrine and reproductive system

                 BAL interferes with the normal accumulation of iodine 
                 by the thyroid and may decrease iodine-131 thyroidal 
                 uptake (Gilman et al., 1985). 

                 BAL decreases insulin's effectiveness by reducing
                 disulfide bridges.

           9.4.8 Dermatological

                 Acute dermatological effects may occur after parenteral 
                 or topical application. 

                 Urticaria is the most common symptom that occurs after 
                 parenteral administration.  Skin application may 
                 produce a scarlatina-like, oedematous rash or erythema. 

                 Chronic effect:  If BAL is frequently applied to the 
                 skin, extreme sensitization may develop. 

           9.4.9 Eye, ear, nose, throat: local effects

                 Parenteral or topical administration may cause: 
                 lacrimation and conjunctival irritation, burning 
                 sensation of the throat, mouth, and eyes, rhinorrhea, a 
                 feeling of constriction or pain in the throat. 

           9.4.10 Haematological

                  Acute effects

                  Children may have a transient reduction in 
                  polymorphonuclear leucocytes. 

                  Dimercaprol can cause haemolytic anaemia in people who 
                  have glucose-phosphate dehydrogenase deficiency. 

                  Chronic effects

                  In animals, chronic parenteral administration 
                  increases the white blood cell count by 30%. 

           9.4.11 Immunological

                  No data available.

           9.4.12 Metabolic

         Acid-base disturbances

                           Dimercaprol may cause metabolic acidosis with 
                           hyperlactacidaemia and hyperglycaemia, which 
                           is followed by hypoglycaemia and glycosuria.  
                           The mechanism by which BAL increases blood 
                           glucose is not fully understood, but since 
                           the hyperglycaemia does not occur in 
                           adrenalectomized animals, it may be 
                           attributed to a release of adrenalin from the 
                           adrenal medulla. 

         Fluid and electrolyte disturbances

                           Disturbances in fluids and electrolytes may 

                           No data available.

           9.4.13 Allergic reactions

                  May be observed.

           9.4.14 Other clinical effects

                  No data available.
           9.4.15 Special risks


                  In studies in mice, there were malformations of the 
                  skeletal system, growth retardation, and increased 
                  embryo mortality. 

                  However, a woman with Wilson's disease was treated 
                  with dimercaprol during two pregnancies and had normal 
                  infants (Reynolds, 1982). 

       9.5 Other

           No data available.


        10.1 General principles

             There is no specific treatment, but symptomatic measures 
             can be taken to improve the clinical course. 

        10.2 Relevant laboratory analyses

             10.2.1 Sample collection

                    Blood and urine for routine clinical analysis.

             10.2.2 Biomedical analysis

                    Patients who have overdosed should be studied.  
                    Tests for the following abnormalities should be 

                    Metabolic effects: hyperglycaemia, glycosuria, 
                    hyperlactataemia, pH, electrolytes, etc. 

                    Serum creatinine, uric acid, urinalysis.


                    Other routine studies, as required.

             10.2.3 Toxicological analysis

                    "Dimercaprol-metal" complexes can be measured in the 
                    urine (but are not usually indicated in clinical 

             10.2.4 Other investigations

                    As required by patient's clinical condition.

        10.3 Life supportive procedures and symptomatic/specific 

             Stop dimercaprol immediately if adverse reactions are 

             Convulsions should be treated as usual with benzodiazepines 
             and barbiturates. 

             If cardiovascular collapse develops, give fluids according 
             to the patient's hydroelectrolytic balance.  Dopamine can 
             be used, if necessary. 

             Bicarbonate solution is useful, not only to correct 
             acidosis but also to increase renal elimination of BAL-
             metal complexes, (in preventing their dissociation and 
             decreasing their toxicity) (Reynolds, 1989). 

             If interruption of the chelating treatment is not possible, 
             treatment should be re-installed with lower doses or 
             increasing the time intervals between doses. 

        10.4 Decontamination

             If there has been dermal exposure, wash the skin with a 
             non-irritating soap and water.  If the eyes have been 
             exposed, irrigate them with tap water.  If ingested give 
             activated charcoal. 
        10.5 Elimination

             No special measures should be taken unless there are signs 
             of renal failure.  The use of intravenous bicarbonated 
             fluids, under clinical and biochemical control, is 
             recommended (Reynolds, 1989) 

        10.6 Antidote treatment

             No antidotal treatment is available.

             10.6.1 Adults


             10.6.2 Children


        10.7 Management discussion

             Even though dimercaprol is still recommended as the drug of 

             choice in poisoning due to arsenic and several other heavy 
             metals, it appears that much evidence is now available 
             showing that DMSA (dimercapto-succinic acid) and DMPS 
             (dimercaptopropane sulphonate) are more efficient and 
             significantly less toxic than BAL. (Aaseth, 1987). 

             It is suggested that the formation of lipophilic heavy 
             metal-BAL complexes may lead to redistribution of these 
             metals to the central nervous system and to increased 
             toxicity. (Aaseth, 1987). 


        11.1 Case reports from literature

             Bismuth et al. (1987) reported two children who had 
             received doses above 20 mg/kg. They developed hypertension, 
             seizures, and coma, but completely recovered in less than 1 

             Janakiraman et al. (1978) reported the occurrence of 
             haemolysis during dimercaprol chelation therapy for high 
             lead blood levels in two children who had glucose-6-
             phosphate-de-hydrogenase deficiency. 

             Epidemiological, clinical, and laboratory features in 41 
             patients with arsenic neuropathy were analyzed and the 
             effects of BAL therapy were reviewed.  BAL administered 7 
             or more days after arsenic exposure had little effect on 
             the subsequent course of the neuropathy (Heymann et al. 
             Freeman & Couch (1978) reported prolonged arsenic 
             encephalopathy in a 51-year-old woman. She improved after 5 
             weeks of BAL chelation therapy in hospital. 

        11.2 Internally extracted data on cases

             According to the experience of CIAT (Poisons Control 
             Centre, Montevideo, Uruguay), when Dimercaprol is given in 
             large doses adverse effects occur.  They consist of 
             uneasiness, chest constriction and dyspnea, itching of 
             skin, peri-oral paresthesia, and hypertension.  The patient 
             becomes very anxious and sometimes even excited. 

             Large doses have been given under two circumstances: 
             firstly, when samples of out-dated Dimercaprol had to be 
             used and a higher dosage was thought to be required; 
             secondly, in cases where patients falsely reported the 
             ingestion of massive amounts of arsenic.  The outcome of 
             Dimercaprol overdoses has always been favourable in our 
             experience.  But massive arsenic poisoning does not respond 
             to chelating therapy with Dimercaprol in our experience. 

        11.3 Internal cases

             To be completed by each Centre using local data.


        12.1 Availability of antidotes


        12.2 Specific preventive measures

             Dimercaprol should be administered by deep intramuscular 

             It should be administered carefully and under strict 
             clinical control in patients with hypertension, hepatic or 
             renal impairment, and G6PD deficiency. 

        12.3 Other


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        Berlin M & Ullberg S (1963)  Increased uptake of mercury in 
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        Budavari S ed. (1989) The Merck index, an encyclopedia of 
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        Chenoweth MB, Modell W & Riker WF (1946)  Pharmacology of 
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        Pharmac Exp Ther, 87(Supplement): 6-22. 

        Durlacher SH, Bunting H, Harrison HE, Ordway NK & Albrink WS 
        (1946)  The toxicological action of 2,3-dimercaptopropanol (BAL)  
        J Pharmac Exp Ther, 87(Supplement): 28-32. 

        Fitzhugh OG, Woodard G, Braun HA, Lusky LM & Calvery HO (1946)  
        The toxicities of compounds related to 2,3-dimercaptopropanol 
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        Pharmac Exp Ther, 87(Supplement): 23-27. 

        Freeman JW & Couch JR (1978)  Prolonged encephalopathy with 
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        Gilman AG, Goodman LS, Rall T, & Murad R eds. (1985)  Goodman 
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        neuropathy caused by arsenical intoxication.  N Eng J Med, 254: 

        Janakiraman N, Seeler RA, Royal JE & Chen MF (1978) Hemolysis 
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        deficient children.Clin Pediat, 17: 485 -487. 

        Lalanne H (1980) Hepatite secondaire a un surdosage par les sels 
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        Peters et al. (1947)  The use of British Anti-lewisite 
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        Reynolds JEF ed. (1982) Martindale, the extra pharmacopoeia, 
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        Simpson SD & Young L (1950) Biochemical studies of toxic agents. 
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        Tamboline B, Matheson, AT & Zbarsky SH (1955).  Radioactive 
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        Waters LL & Stock C (1945)  BAL (anti-Lewisite).  Science, 102: 

        WHO (1992) International nonproprietary names (INN) for 
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        WHO (1992) Anatomical Therapeutic Chemical (ATC) classification 
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        Author  Dr R Peyraube
                CIAT  piso° 7
                Hospital de Clinicas
                Av Italia s/n

                Tel     598-2-808300/470300
                Fax     598-2-470300

       Date     June 1988

       Reviewer Dr D Jacobsen
                Medical Department
                Ulleval Hospital
                0407 Oslo 4

                Tel     47-2-119100/1191359

                Fax     47-2-119181

       Date     August 1990

       Peer     Strasbourg, France, April 1990

    See Also:
       Toxicological Abbreviations