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)