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Potassium permangante

1. NAME
   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 Main brand names, main trade names
   1.6 Main manufacturers, main importers
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
3. PHYSICO-CHEMICAL PROPERTIES
   3.1 Origin of the substance
   3.2 Chemical structure
   3.3 Physical properties
      3.3.1 Colour
      3.3.2 State/Form
      3.3.3 Description
   3.4 Hazardous characteristics
4. USES
   4.1 Uses
      4.1.1 Uses
      4.1.2 Description
   4.2 High risk circumstance of poisoning
   4.3 Occupationally exposed populations
5. ROUTES OF EXPOSURE
   5.1 Oral
   5.2 Inhalation
   5.3 Dermal
   5.4 Eye
   5.5 Parenteral
   5.6 Other
6. KINETICS
   6.1 Absorption by route of exposure
   6.2 Distribution by route of exposure
   6.3 Biological half-life by route of exposure
   6.4 Metabolism
   6.5 Elimination and excretion
7. TOXICOLOGY
   7.1 Mode of action
   7.2 Toxicity
      7.2.1 Human data
         7.2.1.1 Adults
         7.2.1.2 Children
      7.2.2 Relevant animal data
      7.2.3 Relevant in vitro data
      7.2.4 Workplace standards
      7.2.5 Acceptable daily intake (ADI)
   7.3 Carcinogenicity
   7.4 Teratogenicity
   7.5 Mutagenicity
   7.6 Interactions
8. TOXICOLOGICAL 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 contact
      9.2.4 Eye Contact
      9.2.5 Parenteral Exposure
      9.2.6 Other
   9.3 Course, prognosis, cause of death
   9.4 Systematic description of clinical effects
      9.4.1 Cardiovascular
      9.4.2 Respiratory
      9.4.3 Neurological
         9.4.3.1 Central nervous system (CNS)
         9.4.3.2 Peripheral nervous system
         9.4.3.3 Autonomic nervous system
         9.4.3.4 Skeletal and smooth muscle
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary
         9.4.6.1 Renal
         9.4.6.2 Other
      9.4.7 Endocrine and reproductive systems
      9.4.8 Dermatological
      9.4.9 Eye, ear, nose, throat: local effects
      9.4.10 Haematological
      9.4.11 Immunological
      9.4.12 Metabolic
         9.4.12.1 Acid-base disturbances
         9.4.12.2 Fluid and electrolyte disturbances
         9.4.12.3 Others
      9.4.13 Allergic reactions
      9.4.14 Other clinical effects
      9.4.15 Special risks
   9.5 Other
   9.6 Summary
10. MANAGEMENT
   10.1 General principles
   10.2 Life supportive procedures and symptomatic/specific treatment
   10.3 Decontamination
   10.4 Enhanced Elimination
   10.5 Antidote treatment
      10.5.1 Adults
      10.5.2 Children
   10.6 Management discussion
11. ILLUSTRATIVE CASES
   11.1 Case reports from literature
12. Additional information
   12.1 Specific preventive measures
   12.2 Other
13. REFERENCES
14. AUTHOR(S), REVIEWER(S), ADDRESS(ES), DATE(S) (INCLUDING UPDATES)



    POTASSIUM PERMANGANATE

    International Programme on Chemical Safety
    Poisons Information Monograph 409
    Chemical

    This monograph contains the following sections: 1. Name; 2. Summary;
    9. Clinical effects; 10. Management.

    1.  NAME

        1.1  Substance

             Potassium Permanganate

        1.2  Group

             Inorganic Chemical

        1.3  Synonyms

             Condy's Crystals;
             Kalii Permanganas;
             Kalium Hypermanganicum;
             Kalium Permanganicum;
             Nadmanganian Potasu (Polish).

        1.4  Identification Numbers

             1.4.1  CAS number

                    7722-64-7

             1.4.2  Other Numbers

                    RTECS SD 6475000
                    UN NO: 1490
                    UN HAZARD CLASS: 5.1

        1.5  Main brand names, main trade names

        1.6  Main manufacturers, main importers

    2.  SUMMARY

        2.1  Main risks and target organs

             Potassium permanganate is an oxidising agent and the
             crystalline form or concentrated solutions are corrosive.
             Solutions of greater than 1:5000 strength may cause corrosive
             burns to the skin and mucous membranes.

        2.2  Summary of clinical effects

             Most ingestions of diluted solutions of potassium
             permanganate used as an antiseptic are benign, and mild
             irritation is self-limited.  Spontaneous emesis and diarrhoea
             may occur, especially after a large volume ingestion. 
             Exposure to concentrated solutions may cause corrosive burns
             on the skin and mucous membranes, and oropharyngeal,
             oesophageal, or gastric injury may occur resulting in
             ulceration, haemorrhage and perforation.  Late complications
             of upper gastrointestinal ulceration include oesophageal
             stricture and pyloric stenosis. Glottic oedema and
             respiratory obstruction have been reported following
             ingestion of a concentrated solution. Adult respiratory
             distress syndrome may occur. Renal and hepatic impairment
             have been reported and haematological involvement was also
             observed in severe cases (methaemoglobinaemia, haemolysis).
             Pancreatitis may develop. The causes of death are
             cardiovascular collapse and hypotensive shock due to massive
             gastrointestinal haemorrhage and respiratory obstruction.
             Chronic ingestion may result in neurological effects
             (parkinsonism) similar to manganism.

        2.3  Diagnosis

             Diagnosis is based on the history of exposure and the
             presence of mild gastrointestinal  upset or frank corrosive
             injury. Solutions of potassium permanganate are dark purple,
             and skin and mucous membranes are often characteristically
             stained.  Potassium permanganate tablets are radiopaque thus
             abdominal radiographs may assist with the diagnosis.

        2.4  First-aid measures and management principles

             Most ingestions of diluted solutions of potassium
             permanganate are benign, and mild irritation is self-limited.
             After ingestion of crystals, tablets or concentrated
             solutions, monitor the airway for swelling and intubate if
             necessary. Perform endoscopy (not advancing the endoscope
             beyond areas of severe esophageal burns) as soon as
             practicable for the assessment of burns. Do not induce emesis
             because of the risk of corrosive injury. Activated charcoal
             and cathartics are not effective and are contraindicated. For
             significant ingestions consideration may be given to
             aspirating stomach contents, however the risk of haemorrhage
             or gastrointestinal perforation could be further compromised
             by this procedure. If undertaken this should be performed
             cautiously through a thin, flexible naso-gastric tube.
             Irrigate the eyes and skin with copious amounts of tepid
             water. Ocular exposure to a concentrated solution of
             permanganate may require longer irrigation than exposure to a
             dilute solution. Remove contaminated clothing. 

    3.  PHYSICO-CHEMICAL PROPERTIES

        3.1  Origin of the substance
        3.2  Chemical structure
        3.3  Physical properties
             3.3.1  Colour
             3.3.2  State/Form
             3.3.3  Description
        3.4  Hazardous characteristics

    4.  USES

        4.1  Uses
             4.1.1  Uses
             4.1.2  Description
        4.2  High risk circumstance of poisoning
        4.3  Occupationally exposed populations

    5.  ROUTES OF EXPOSURE

        5.1  Oral
        5.2  Inhalation
        5.3  Dermal
        5.4  Eye
        5.5  Parenteral
        5.6  Other

    6.  KINETICS

        6.1  Absorption by route of exposure
        6.2  Distribution by route of exposure
        6.3  Biological half-life by route of exposure
        6.4  Metabolism
        6.5  Elimination and excretion

    7.  TOXICOLOGY

        7.1  Mode of action
        7.2  Toxicity
             7.2.1  Human data
                    7.2.1.1  Adults
                    7.2.1.2  Children
             7.2.2  Relevant animal data
             7.2.3  Relevant in vitro data
             7.2.4  Workplace standards
             7.2.5  Acceptable daily intake (ADI)
        7.3  Carcinogenicity
        7.4  Teratogenicity
        7.5  Mutagenicity
        7.6  Interactions

    8.  TOXICOLOGICAL 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

                    Most ingestions of diluted solutions of
                    potassium permanganate used as an antiseptic are
                    benign, and mild irritation is self-limited. 
                    Spontaneous emesis and diarrhoea may occur, especially
                    after a large volume ingestion.  Exposure to
                    concentrated solutions may cause corrosive burns on
                    the skin and mucous membranes, and oropharyngeal,
                    oesophageal, or gastric injury may occur.  Glottic
                    oedema has been reported following ingestion of a
                    concentrated solution (Olsen, 1994).  Permanganate may
                    also cause methaemoglobinemia due to its oxidising
                    properties (Mahomedy et al., 1975).

             9.1.2  Inhalation

                    No data available.

             9.1.3  Skin exposure

                    Exposure to concentrated solutions may cause
                    corrosive burns on the skin and mucous membranes. 
                    Solutions of potassium permanganate are dark purple,
                    and skin and mucous membranes are often
                    characteristically stained purple brown (Olsen
                    1994).

             9.1.4  Eye contact

                    Eye exposure can cause corneal and conjunctival
                    burns (Michaels & Zugsmith, 1973).

             9.1.5  Parenteral exposure

                    No data available

             9.1.6  Other

                    Vaginal exposure (used as an abortifacient) can
                    cause vaginal or cervical burns and erosions (Vago,
                    1969; Le Coz et al., 1968).

        9.2  Chronic poisoning

             9.2.1  Ingestion

                    Chronic ingestion may result in neurological
                    effects (parkinsonism) similar to manganism
                    (Holzgraefe et al., 1986).

             9.2.2  Inhalation

                    No data available.

             9.2.3  Skin contact

                    No data available.

             9.2.4  Eye Contact

                    No data available.

             9.2.5  Parenteral Exposure

                    No data available.

             9.2.6  Other

                    No data available.

        9.3  Course, prognosis, cause of death

             Acute life threatening, laryngeal oedema is the most
             immediate concern after the ingestion of potassium
             permanganate.  Ulceration of the mouth, oesophagus and, to a
             lesser extent, stomach can occur secondary to the caustic
             action of potassium permanganate. Late complications (several
             days post exposure) of upper gastrointestinal ulceration
             including oesophageal stricture and pyloric stenosis may
             occur.  Renal, hepatic and haematological
             (methaemoglobinaemia, haemolysis) involvement has been
             reported.  The causes of death are cardiovascular collapse
             and hypotensive shock due to massive gastrointestinal
             haemorrhage and respiratory obstruction (Middleton et al.,
             1990; Southwood et al., 1987).

        9.4  Systematic description of clinical effects

             9.4.1  Cardiovascular

                    Transient hypertension and tachycardia may
                    develop soon after ingestion. Profound hypotension and
                    circulatory collapse has been reported in severe cases
                    of ingestion  (Middleton et al., 1990; Ong et al.,
                    1997; Young et al., 1996).

             9.4.2  Respiratory

                    Upper airway burns and oedema and stridor have
                    been reported after ingestion of   permanganate (Ong
                    et al., 1997; Young et al., 1996; Southwood et al.,
                    1987).  Adult respiratory distress syndrome has also

                    been described following ingestion (Middleton et al.,
                    1990).

             9.4.3  Neurological

                    9.4.3.1  Central nervous system (CNS)

                             Impairment of the extrapyramidal
                             system: dysarthria, resting tremor,
                             shortening of gait (Holzgraefe et al.,
                             1986).

                    9.4.3.2  Peripheral nervous system

                             Paraesthesias and hypoesthesias have
                             been reported in a case of a 66-year-old man
                             who was mistakenly administered potassium
                             permanaganate (125 mL of an 8% solution) over
                             a period of 4 weeks (Holzgraefe et al.,
                             1986).

                    9.4.3.3  Autonomic nervous system

                             Increased sweating (Holzgraefe et al., 1986).

                    9.4.3.4  Skeletal and smooth muscle

                             Tremor and widespread muscle
                             fasiculations have been reported in a case
                             involving a 66-year-old male who was
                             mistakenly administered 10 g of potassium
                             permanganate over 4 weeks. Nine months post
                             exposure he had developed evidence of a
                             Parkinson syndrome (Holzgraefe et al.,
                             1986).

             9.4.4  Gastrointestinal

                    The gastrointestinal tract is invariably
                    damaged by the caustic action of potassium
                    permanganate. Spontaneous emesis and diarrhoea may
                    occur, especially after a large volume ingestion.
                    Ulceration, perforation and haemorrhage after
                    ingestion of crystals, or tablets, or concentrated
                    solutions occasionally occur. The mucous membrane is
                    brown-black stained which may mimic necrosis. Late
                    complications of upper gastrointestinal ulceration
                    include oesophageal stricture and pyloric stenosis
                    (Southwood et al., 1987; Middleton et al.,
                    1990).

             9.4.5  Hepatic

                    Abnormalities of liver function (elevated AST,
                    bilirubin) suggesting hepatocellular damage have been
                    reported following ingestion of permanganate
                    (Middleton et al., 1990).  In severe cases fulminant
                    hepatic failure and necrosis may occur (Ong et al.,
                    1997).

             9.4.6  Urinary

                    9.4.6.1  Renal

                             Acute renal failure has been
                             reported to occur several days after the
                             ingestion of   permanganate (Ong et al.,
                             1997; Young et al., 1996).

                    9.4.6.2  Other

                             Proteinuria was reported to develop
                             in a 68-year-old male who injected about 7 g
                             of an aqueous solution of potassium
                             permanganate into his intercostal space
                             (Lustig et al., 1982).

             9.4.7  Endocrine and reproductive systems

                    Hyperglycaemia and elevated serum amylase levels
                    has been reported in a patient who developed severe 
                    haemorrhagic pancreatitis after ingesting 20 grams of
                    permanganate (Middleton et al., 1990). Potassium 
                    Permanganate has been used as an abortifacient via the
                    oral route, causing fetal death (Kochhar et al., 1986)
                    or by direct application to the vagina which usually 
                    results in vaginal bleeding and perforation and not 
                    abortion (Verelli, 1965).

             9.4.8  Dermatological

                    Exposure to concentrated solutions may cause
                    corrosive burns on the skin. Solutions of potassium
                    permanganate are dark purple, and skin and mucous
                    membranes are often characteristically stained purple
                    brown (Olsen, 1994).

             9.4.9  Eye, ear, nose, throat: local effects

                    Decreased visual acuity, corneal clouding,
                    subconjunctival haemorrhages and brownish conjunctival
                    discolouration were described in a 22-year-old male
                    subject who sustained potassium permanganate burns to
                    his eyes (Michaels & Zugsmith, 1973).  Occasional
                    diplopia was reported in a chronic case of
                    permanganate administration (Holzgraefe et al.,
                    1986).

             9.4.10 Haematological

                    Methaemoglobinemia has been reported to occur
                    following the ingestion of large doses of potassium
                    permanganate due to its oxidising properties (Mahomedy
                    et al., 1975).  Disseminated intravascular coagulation
                    has been described following a large ingestion of
                    potassium permanganate (Young et al., 1996).

             9.4.11 Immunological

                    No data available

             9.4.12 Metabolic

                    9.4.12.1 Acid-base disturbances

                             No data available.

                    9.4.12.2 Fluid and electrolyte disturbances

                             No data available.

                    9.4.12.3 Others

                             No data available.

             9.4.13 Allergic reactions

                    No data available.

             9.4.14 Other clinical effects

                    No data available.

             9.4.15 Special risks

                    Potassium Permanganate has been used as an
                    abortifacient via the oral route, causing fetal death
                    (Kochhar et al., 1986) or by direct application to the
                    vagina which usually results in vaginal or cervical

                    burns and erosions, extensive bleeding, shock and not
                    abortion (Verelli, 1965).

        9.5  Other

             No data available.

        9.6  Summary

    10. MANAGEMENT

        10.1 General principles

             Treatment is symptomatic and supportive. There is no
             specific antidote. Most ingestions are benign, and mild
             irritation is self-limited and only clinical observation and
             symptomatic treatment are necessary. After ingestion of
             crystals, tablets or concentrated solutions, monitor the
             airway for swelling and intubate if necessary. Perform
             endoscopy (not advancing the endoscope beyond areas of severe
             oesophageal burns) as soon as practicable for the assessment
             of burns.  Do not induce emesis because of the risk of
             corrosive injury. For  significant ingestions consideration
             may be given to aspirating stomach contents, however the risk
             of haemorrhage or gastrointestinal perforation could be
             further compromised by this procedure. If undertaken this
             should be performed cautiously through a thin, flexible
             naso-gastric tube. Activated charcoal and cathartics are not
             effective and are contraindicated. (EAPCCT and AACT, 1997;
             Southwood et al., 1987; Olsen, 1994).
    
             Irrigate the eyes and skin with copious amounts of tepid
             water. Ocular exposure to a concentrated solution of
             permanganate may require longer irrigation than exposure to a
             dilute solution. Remove  contaminated clothing (Southwood et
             al., 1987; Olsen, 1994).

        10.2 Life supportive procedures and symptomatic/specific treatment

             After ingestion of concentrated solutions, monitor the
             airway for swelling and intubate or perform emergency
             tracheostomy if necessary.
    
             Support respiratory and cardiovascular function. Early
             oesophagoscopy should be performed to assess the severity of
             the burns, although these may be obscured by the brown-black
             discolouration of the mucous membrane, which may mimic
             necrosis. Care should be taken not to pass the endoscope
             beyond the first severe burn as perforation is a possibility.
             Monitor liver and renal function tests in cases of
             significant exposure. Monitor INR or PT and platelet counts
             in subjects with severe toxicity. Monitor arterial blood

             gases in patients with severe respiratory symptoms (Southwood
             et al., 1987; Olsen, 1994). Treat methaemoglobinaemia if it
             develops.

        10.3 Decontamination

             Do not induce emesis because of the risk of corrosive
             injury. Activated charcoal and cathartics are not effective
             and are contraindicated. For significant ingestions
             consideration may be given to aspirating stomach contents,
             however the risk of haemorrhage or gastrointestinal
             perforation could be further compromised by this procedure.
             If undertaken this should be performed cautiously through a
             thin, flexible naso-gastric tube (Southwood et al 1987, Olsen
             1994).
    
             Remove and discard contaminated clothing. Wash skin with
             copious amounts of water.
    
             Irrigate exposed eyes with copious amounts of water or
             saline. Irrigation should be continued until the eyes have
             been thoroughly examined for particulate matter and returned
             to neutrality.  Ocular exposure to a concentrated solution of
             permanganate may require longer irrigation than exposure to a
             dilute solution.

        10.4 Enhanced Elimination

             No data available

        10.5 Antidote treatment

             10.5.1 Adults

                    No antidote is available

             10.5.2 Children

                    No antidote is available

        10.6 Management discussion

             Corticosteroids are not indicated. In the past they
             were used in the hope of reducing the incidence of
             oesophageal scarring but have since proved ineffective.
             Moreover, steroids may be harmful in the patient with
             perforation by masking early signs of inflammation and
             inhibiting resistance to infection (Olsen, 1994).
    
             Antibiotics may be considered in the case of severe burns and
             is recommended for suspected secondary infection. The use of
             antibiotics for prophylaxis is controversial.
    

             Following ingestion of potassium permanganate the use of
             histamine II antagonists has been considered but efficacy has
             not been fully evaluated.
    
             N-acetylcysteine has been used in the treatment of potassium
             permanganate induced hepatotoxicity, but efficacy has not
             been established (Young et al., 1996).

    11. ILLUSTRATIVE CASES

        11.1 Case reports from literature

    12. Additional information

        12.1 Specific preventive measures

        12.2 Other

    13. REFERENCES

        EAPCCT and ACCT (1997)  Position statements on
        gastrointestinal decontamination. Clin Toxicol, 35(7)
    
        Holzgraefe M, Poser W, Kijewski H Beuche W (1986) Chronic enteral
        poisoning caused by potassium permanganate: a case report. J
        Toxicol Clin Toxicol, 24(3): 235-244
    
        Kochhar R, Das K, Mehta SK (1986) potassium permanganate induced
        oesophageal stricture. Human Toxicol, 5: 393-394
    
        Le Coz A, Mazerolles J and Delafargue M (1968) Attempt at abortion
        with potassium permanganate tablets. Bulletin de la Fédération des
        Sociétés de Gynécologie et d'Obstétrique de Langue Française,
        20(2): 190-191
    
        Lustig S, Pitlik SD & Rosenfeld JB (1982) Liver damage in acute
        self-induced hypermanganemia.  Arch Intern Med, 142(2): 
        405-406.
    
        Mahomedy MC, Mahomedy YH, Canham PA, Downing JW and Jeal DE (1975)
        Methaemoglobinaemia following treatment dispensed by witch
        doctors.  Two cases of potassium permanganate poisoning
        Anaesthesia, 30(2): 190-193
    
        Michaels DD & Zugsmith GS (1973) Potassium permanganate burn of
        the eye. Eye, Ear, Nose & Throat Monthly, 52(3): 42-43
    
        Middleton SJ, Jacyna M, McClaren D, Robinson R and Thomas HC
        (1990) Haemorrhagic pancreatitis - a cause of death in severe
        potassium permanganate poisoning. Postgrad Med J, 66: 657-658
    

        Ong KL, Tan TH & Cheung WL (1997) Potassium permanganate poisoning
        - a rare cause of fatal self poisoning. J Accid Emerg Med, 14(1):
        43-45
    
        Olsen KR (1999) Poisoning and Drug Overdose, 3rd edition, Appleton
        & Lange, Norwalk, Connecticut
    
        Southwood T, Lamb CM & Freeman J (1987) Ingestion of potassium
        permanganate crystals by a three-year-old boy.  Med J Aust, 146:
        639-640
    
        Vago O (1969) Toxic and caustic complications through use of
        so-called abortifacients. Zeitschrift fur Geburtshilfe und
        Perinatologie, 170(3): 272-277
    
        Verelli D (1965) Osservazioni e considerazioni sull'applicazione
        di compresse di permanganato in vagina a scopo abortivo. Quaderni
        di Clinica Ostetrica e Ginecologica, 20(11): 617-643
    
        Young RJ, Critchley JAJH, Young KK, Freebairn RC, Reynolds
        AP,Lolin YI (1996) Fatal acute hepatorenal failure following
        potassium permanganate ingestion. Human Exp Toxicol, 15(3):
        259-261

    14. AUTHOR(S), REVIEWER(S), ADDRESS(ES), DATE(S) (INCLUDING
        UPDATES)

        Authors:        Dr W.A. Temple
                        Dr N.A. Smith
                        National Toxicology Group
                        Dunedin
                        New Zealand
    
        Date:           August 1998
    
        Peer
        Review:         INTOX PIM E-mail Group 1
                        (members: Dr N. Besbelli, Dr D. Cobaugh, Dr
                        L. Fruchtengarten, Dr B. Groszek, Dr K.
                        Hartigan-Go, Dr M.O. Rambourg)
    


See Also:
        Potassium permangante (ICSC)