Hydrogen peroxide
| 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 exposure |
| 9.2.4 Eye contact |
| 9.2.5 Parenteral exposure |
| 9.2.6 Other |
| 9.3 Course, prognosis, cause of death |
| 9.4 Systematic description of clinical effects |
| 9.4.1 Cardiovascular |
| 9.4.2 Respiratory |
| 9.4.3 Neurological |
| 9.4.3.1 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), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES) |
Hydrogen peroxide
International Programme on Chemical Safety
Poisons Information Monograph 946
Chemical
This Monograph contain the following sections
completed: 1, 2, 3, 4.1, 7.2, 9 & 10.
1. NAME
1.1 Substance
Hydrogen peroxide
1.2 Group
Oxygen and compounds
Peroxide
1.3 Synonyms
Albone; Albone 35;
Albone 35CG; Albone 50;
Albone 50CG; Albone 70;
Albone 70CG; Dihydrogen dioxide;
Hioxyl; Hydrogen dioxide;
Hydroperoxide; Inhibine;
Interox; Kastone; Oxydol;
Perhydrol; Perone;
Perone 30; Perone 35;
Perone 50; Perossido di idrogeno;
Peroxan; Peroxide;
Peroxyde d'hydrogene; Superoxol;
T-Stuff; Wasserstoffperoxid;
Waterstofperoxyde
1.4 Identification numbers
1.4.1 CAS number
7722-84-1
1.4.2 Other numbers
UN2014 (DOT)
UN2015 (DOT)
UN2984 (DOT)
NIOSH/rtecs: MX0900000
1.5 Main brand names, main trade names
1.6 Main manufacturers, main importers
2. SUMMARY
2.1 Main risks and target organs
The dissociation of hydrogen peroxide is a violent and
exothermic reaction. Ingestion results in gastrointestinal
irritation, the severity of which depends on the
concentration of the solution. There is also a risk of gas
embolism. A number of deaths have been reported in the
literature. In most cases the exposures were to concentrated
solutions of 30 to 40%.
Ingestion of the more concentrated solutions (>10%, but
particularly 30 to 40% and above) should be regarded as
serious because of the risk of more severe irritation. The
risk of gas embolism is probably also increased with the
concentrated solutions, although a large quantity of a dilute
solution may also produce embolism. Death may occur within
minutes of ingestion.
2.2 Summary of clinical effects
Ingestion: These effects may occur with solutions of
3% but usually only where a large quantity has been ingested,
effects are generally more severe if a concentrated solution
has been ingested.
Vomiting (the vomitus may be frothy due to the liberation of
oxygen - risk of aspiration), haematemesis, 'burningœ throat
and gastric distension (due to the release of oxygen).
Lethargy, coma, convulsions, shock, and respiratory arrest
have been reported. Gastrointestinal bleeding and burns to
the stomach and duodenum may occur. These are usually not
severe and resolve with symptomatic treatment.
Gas embolism has been reported in adults and children. In
severe cases ischaemic ECG changes and EMD (electromechanical
dissociation) may be observed because of embolisation of the
heart restricting blood flow.
Inhalation: Transient dyspnoea and cough, with concentrated
solutions there may be more severe irritation and
inflammation of the respiratory tract
Dermal: Irritant to the skin with paraesthesia, blistering
and whitening; solutions >10% may cause burns. Bleaching of
the skin usually resolved within a few hours.
Ocular: Irritation with a burning sensation, conjunctival
hyperaemia, lacrimation and severe pain which resolves within
a few hours. With more concentrated solutions effects may
take up to 24 hours to resolve. There are rare cases of
temporary cornal injury resulting from application of 3%
solution to the eye (on contact lenses) including punctuate
staining of the cornea, decreased vision, cornal opacity and
oedema.
Intravenous: vomiting, pain at injection site, ventricular
fibrillation, embolism of heart and lung tissue, haemolytic
anaemia, renal failure and death.
Rectal: rectal bleeding, nausea, distension and difficulty
urinating.
2.3 Diagnosis
Gastrointestinal (GI) irritation possibly accompanied by
vomiting of frothy material and gas embolism can help the
diagnosis if the exposure is not known. Whitening of the skin
and mucous membranes and pain may be signs of exposure.
2.4 First aid measures and management principles
Ingestion: Gastric decontamination is not worthwhile
for ingestion of hydrogen peroxide due to its rapid
dissociation. Asymptomatic patients who have ingested only a
small quantity of low concentrated solutions (3 to 6%)
probably do not require treatment. Any patient with
haematemesis, abdominal discomfort, persistent vomiting,
central nervous system (CNS) or respiratory effects must be
admitted.
Treatment is supportive. If gastric distension is severe a
fine bore gastric tube may be passed to aid the release of
gas. Endoscopy should be considered in patients with
haematemesis or persistent vomiting or if the solution was
>10%.
Patients with severe clinical effects require abdominal and
chest X-rays. The Trendelenburg positioning (head down,
elevated foot of bed) should be avoided since this may trap
air in the apex of the right ventricle and cause obstruction
of the blood flow. Monitor the ECG in severe cases.
Ventilation may be required in patient with severe
respiratory effects.
Hyperbaric oxygen therapy has been suggested for patients
with evidence of cerebral embolism due to hydrogen
peroxide.
Inhalation: remove from exposure; supportive care should be
given.
Dermal: irrigate thoroughly with saline or water and treat
symptomatically.
Ocular: irrigate thoroughly with running water or saline
for 15 minutes. Refer to an ophthalmologist.
Intravenous: monitor ECG and check renal function. Perform
X-rays.
Rectal: give supportive care; parenteral (then oral)
steroids may be of benefit. Sigmoidoscopy is recommended to
determine the extent of the injury.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
3.2 Chemical structure
Chemical formula: H2O2
Molecular mass: 34
3.3 Physical properties
3.3.1 Colour
Colourless
3.3.2 State/Form
Liquid
3.3.3 Description
Hydrogen peroxide is an odourless liquid with a
bitter taste; it is an oxidising agent which in the
presence of organic matter or if permitted to become
alkaline vigorously decomposes to oxygen and water.
The strength of a solution may be described as a
percentage or volume, where 1% hydrogen peroxide
releases 3.3 volumes of oxygen during decomposition.
Thus, a 3% solution is equivalent to 10 volume and a
6% solution to 20 volume, etc.
Boiling point: 115 to 157°C
Melting point: <50°C
Relative density (water = 1): 1.3
Solubility in water: Miscible
Vapour pressure, kPa at 30°C: 0.7
Relative vapour density (air = 1): 1.2
Relative density of the vapour/air-mixture at 20°C
(air = 1): 1.06
3.4 Hazardous characteristics
Hydrogen peroxide decomposes on warming producing oxygen
which increases fire hazard. The substance is a strong
oxidant and reacts violently with combustible and reducing
materials causing fire and explosion hazard particularly in
the presence of metals. Hydrogen peroxide attacks many
organic substances, e.g. textile and paper.
4. USES
4.1 Uses
4.1.1 Uses
4.1.2 Description
Hydrogen peroxide is used as a 6% solution for
bleaching hair and some disinfectant solutions for
contact lenses contain 3% hydrogen peroxide. Chlorine
free bleaches contain 6% hydrogen peroxide. Some newer
fabric stain removers/bleaches contain 5 to 15%
hydrogen peroxide. Industrial strengths of hydrogen
peroxide are manufactured up to 90%. They are used
mainly as bleaching and oxidising agents. Solutions
of 90% are used as rocket fuel.
Hydrogen peroxide (35%) is also sold as a health aid
for so-called 'hyperoxygenation therapy' for
everything from arthritis to AIDS and cancer. It is
kept refrigerated, diluted for use, and taken
regularly (Leikin et al., 1993).
4.2 High risk circumstance of poisoning
4.3 Occupationally exposed populations
5. ROUTES OF EXPOSURE
5.1 Oral
Common route of exposure.
5.2 Inhalation
Hydrogen peroxide can be inhaled.
5.3 Dermal
Hydrogen peroxide is irritant to the skin.
5.4 Eye
Ocular exposure results in irritation with a burning
sensation.
5.5 Parenteral
Intravenous injection of hydrogen peroxide has been reported.
5.6 Other
Rectal exposure is possible.
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
The dissociation of hydrogen
peroxide is a violent and exothermic
reaction. Ingestion results in
gastrointestinal irritation, the severity of
which depends on the concentration of the
solution. There is also a risk of gas
embolism. A number of deaths have been
reported in the literature. In most cases
the exposures were to concentrated solutions
of 30 to 40%.
Ingestion of the more concentrated solutions
(>10%, but particularly 30 to 40% and above)
should be regarded as serious because of the
risk of more severe irritation. The risk of
gas embolism is probably also increased with
the concentrated solutions, although a large
quantity of a dilute solution may also
produce embolism (Cina et al., 1994). Death
may occur within minutes of ingestion
(Dickson and Caravati, 1994).
Most cases of ingestion of hydrogen peroxide
result in only mild effects. Of 270 cases of
hydrogen peroxide ingestion in one study only
24% required medical referral (Dickson and
Caravati, 1994).
Cerebral infarction, believed to have
resulted from gas embolisation of the
cerebral vasculature, has been reported in an
84 year old man who took 30 ml of 35%
hydrogen peroxide diluted in 100 to 300 mL of
water (Sherman et al., 1994). Multiple brain
embolism occurred in a 63 year old who
ingested 120mL of 35% solution. He recovered
(Ijichi et al., 1997).
Fatal doses:
Ingestion:
Ingestion of 240 mL of 35% hydrogen peroxide
in a 49 year old female caused death in 78
hours later (Litovitz et al., 1995).
Intravenous:
0.8mL of a 35% solution diluted in 200mL
normal saline (0.14% of hydrogen peroxide)
once daily for 5 days in a 50 year old male
(Leikin et al., 1993).
2mL (strength unknown) in a dialysis catheter
caused abdominal pain, hypertension, collapse
and coma within 1 hour. She made some
improvement with hyperbaric oxygen by the 8th
day, then had a cardiac arrest and
convulsions. She recovered in the following
week and then had another cardiac arrest and
died 19 days post-injection (Litovitz et al.,
1997).
7.2.1.2 Children
Fatal doses:
Ingestion:
225 mL of 3% in a 16 month old, he was found
dead 10 hours later (Cina et al., 1994).
About 100 to 170 mL of 35% in a 2 year old,
taken off life-support 4 days later with
hypoxic encephalopathy (Christensen et al.,
1992).
Intravenous:
100mL of 3% hydrogen peroxide in a 7 month
old child (Lubec et al., 1996).
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
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.1.2 Urine
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.1.3 Other fluids
8.3.2 Arterial blood gas analyses
8.3.3 Haematological analyses
"Basic analyses"
"Dedicated analyses"
"Optional 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
These effects may occur with solutions of 3%
but usually only where a large quantity has been
ingested, effects are generally more severe if a
concentrated solution has been ingested.
Vomiting (the vomitus may be frothy due to the
liberation of oxygen - risk of aspiration),
haematemesis, 'burningœ throat and gastric distension
(due to the release of oxygen). Lethargy, coma,
convulsions, shock, and respiratory arrest have been
reported (Giberson et al., 1989). Gastrointestinal
bleeding and burns to the stomach and duodenum may
occur. These are usually not severe and resolve with
symptomatic treatment.
Gas embolism has been reported in adults (Luu et al.,
1992) and children (Cina et al., 1994; Christensen et
al., 1992; Litovitz et al., 1991; Rackoff and Merton,
1990). In severe cases ischaemic ECG changes and EMD
(electromechanical dissociation) may be observed
because of embolisation of the heart restricting blood
flow (Christensen et al., 1992).
Cerebral infarction, believed to have resulted from
gas embolisation of the cerebral vasculature, has been
reported in an 84 year old man who took 30 mL of 35%
hydrogen peroxide diluted in 100 to 300 mL of water
(Sherman et al., 1994). Multiple brain embolism
occurred in a 63 year old who ingested 120mL of 35%
solution. He recovered (Ijichi et al., 1997).
9.1.2 Inhalation
Transient dyspnoea and cough, with concentrated
solutions there may be more severe irritation and
inflammation of the respiratory tract.
9.1.3 Skin exposure
Irritant to the skin with paraesthesia,
blistering and whitening; solutions >10% may cause
burns. Bleaching of the skin usually resolved within
a few hours.
9.1.4 Eye contact
Irritation with a burning sensation,
conjunctival hyperaemia, lacrimation and severe pain
which resolves within a few hours, with more
concentrated solutions effects may take up to 24 hours
to resolve. There are rare cases of temporary cornal
injury resulting from application of 3% solution to
the eye (on contact lenses) including punctuate
staining of the cornea, decreased vision, cornal
opacity and oedema. Historically 1 to 3% solutions
were applied to the eye as an antibacterial agent.
9.1.5 Parenteral exposure
Intravenous: vomiting, pain at injection site,
ventricular fibrillation, embolism of heart and lung
tissue, haemolytic anaemia, renal failure and death.
9.1.6 Other
Rectal: rectal bleeding, nausea, distension and
difficulty urinating (Dickson and Caravati, 1994).
9.2 Chronic poisoning
9.2.1 Ingestion
9.2.2 Inhalation
9.2.3 Skin exposure
9.2.4 Eye contact
9.2.5 Parenteral exposure
9.2.6 Other
9.3 Course, prognosis, cause of death
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
9.4.2 Respiratory
9.4.3 Neurological
9.4.3.1 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
Ingestion: Gastric decontamination is not worthwhile
for ingestion of hydrogen peroxide due to its rapid
dissociation. Asymptomatic patients who have ingested only a
small quantity of low concentrated solutions (3-6%) probably
do not require treatment. Any patient with haematemesis,
abdominal discomfort, persistent vomiting, central nervous
system (CNS) or respiratory effects must be admitted.
Treatment is supportive, if gastric distension is severe a
fine bore gastric tube may be passed to aid the release of
gas. Endoscopy should be considered in patients with
haematemesis or persistent vomiting or if the solution was
>10%.
Patients with severe clinical effects require abdominal and
chest X-rays. The Trendelenburg positioning (head down,
elevated foot of bed) should be avoided since this may trap
air in the apex of the right ventricle and cause obstruction
of the blood flow (Henry et al., 1996). Monitor the ECG in
severe cases. Ventilation may be required in patient with
severe respiratory effects.
Hyperbaric oxygen therapy has been suggested for patients
with evidence of cerebral embolism due to hydrogen peroxide
(Sherman et al., 1994).
Inhalation: remove from exposure, supportive care
Dermal: Irrigate thoroughly with saline or water and treat
symptomatically.
Ocular: Irrigate thoroughly with running water or saline
for 15 minutes. Refer to an ophthalmologist.
Intravenous: monitor ECG and check renal function.
Perform X-rays.
Rectal: supportive care, parenteral (then oral) steroids
may be of benefit. Sigmoidoscopy is recommended to determine
the extent of the injury (Dickson and Caravati, 1994).
10.2 Life supportive procedures and symptomatic/specific treatment
See section 10.1
10.3 Decontamination
Gastric decontamination is not worthwhile for ingestion
of hydrogen peroxide due to its rapid dissociation.
10.4 Enhanced elimination
See section 10.1
10.5 Antidote treatment
10.5.1 Adults
No antidote available.
10.5.2 Children
No antidote available.
10.6 Management discussion
See section 10.1
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
12. Additional information
12.1 Specific preventive measures
12.2 Other
13. REFERENCES
Christensen DW, Faught WE, Black RE, Woodward GA and Timmons
OD. (1992) Fatal oxygen embolization after hydrogen peroxide
ingestion. Crit Care Med 20 (4):543-544
Cina SJ, Downs JCU and Conradi SE. (1994) Hydrogen peroxide: a
source of lethal oxygen embolism. Case report and review of the
literature. Am J Forensic Med Pathol 15 (1):44-50
Dickson KF and Caravati EM. (1994) Hydrogen peroxide - 325
exposures reported to a regional poisons control center. Clin
Toxicol 32 (6):705-714
Giberson TP, Kern JD, Pettigrew DW 3d, Eaves CC Jr & Haynes JF Jr
(1989) Near-fatal hydrogen peroxide ingestion. 18(7): 778-779.
Henry MC, Wheeler J, Mofensen HC, Caraccio TR, Marsh M, Comer GM,
Singer AJ. (1996) Hydrogen peroxide 3% exposure. Clin Toxicol 34
(3): 323-327
Ijichi I, Itoh T, Sakai R, Nakaji K, Miyauchi T, Takahashi R,
Kadosaka S, Hirata M, Yoneda S, Kajita Y, Fujita Y (1997) Multiple
brain embolism after ingestion of concentrated hydrogen peroxide.
Neurology 48 (1): 277-79
Leikin J, Sing K and Woods K (1993) Fatality from intravenous use
of hydrogen peroxide for home 'superoxygenation therapyœ
(abstract). Vet Hum Toxicol 35 (4):342
Litovitz Tl, Bailey Km, Schmitz BF, Holm KC & Klein-Schwartz W
(1991) 1990 Annual report of the AAPCC National Data Collection
System. Am J Emerg Med 9(5):461-509
Litovitz TL, Felberg L, Soloway RA, Ford M, Geller R. (1995) 1994
Annual Report of the AAPCC toxic exposure surveillence system. Am
J Emerg Med 13 (5):551-597
Litovitz TL, Smilkstein M, Felberg L, Klein-Schwartz W, Berlin R
and Morgan JL. (1997) 1996 Annual Report of the AAPCC toxic
exposure surveillence system. Am J Emerg Med 15 (5):447-500
Lubec B, Hayn M, Denk W and Bauer G (1996) Brain lipid
peroxidation and hydroxyradical attack following the intravenous
infusion of hydrogen peroxide in an infant. Free Rad Biol Med 21
(2):219-223
Luu TA, Kelley MT, Strauch JA & Avradopoulos K (1992) Portal vein
embolism from hydrogen peroxide ingestion. Ann Emerg med 21(11):
1391-1393
Rackoff Wr & Merton DF (1990) Gas embolism after ingestion of
hydrogen peroxide. Pediatrics 85(4): 593-594
Sherman SJ, Boyer LV and Sibley WA (1994) Cerebral infarction
immediately after ingestion of hydrogen peroxide. Stroke
25:1065-1067
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)
Author: Medical Toxicology Unit,
Guyœs and St Thomasœ Trust
Avonley Road, London SE14 5ER, UK
Date: December, 1997
Review: As for author. 1997
Peer review: INTOX meeting, March 1998, London, UK
(Members of group: Drs G. Allridge, L.
Lubomovir, R. Turk, C. Alonso, S. de Ben, K.
Hartigan-Go, N. Bates)
Editor: Dr M.Ruse (September, 1998)