Hydrogenium peroxydatum Anhang
Hydrogen peroxide is an oxidising agent that is used in a number of
household products, including general-purpose disinfectants, chlorine-free bleaches,
fabric stain removers, contact lens disinfectants and hair dyes, and it is a
component of some tooth whitening products. In industry, the principal use of
hydrogen peroxide is as a bleaching agent in the manufacture of paper and pulp.
Hydrogen peroxide has been employed medicinally for wound irrigation and for
the sterilisation of ophthalmic and endoscopic instruments. Hydrogen peroxide
causes toxicity via three main mechanisms: corrosive damage, oxygen gas
formation and lipid peroxidation. Concentrated hydrogen peroxide is caustic and
exposure may result in local tissue damage. Ingestion of concentrated (>35%)
hydrogen peroxide can also result in the generation of substantial volumes of
oxygen.
Where the amount of oxygen evolved exceeds its maximum solubility in
blood, venous or arterial gas embolism may occur. The mechanism of CNS damage
is thought to
be arterial gas embolisation with subsequent brain infarction. Rapid
generation of oxygen in closed body cavities can also cause mechanical distension
and there is potential
for the rupture of the hollow viscus secondary to oxygen liberation. In
addition, intravascular foaming following absorption can seriously impede right
ventricular output and produce complete loss of cardiac output. Hydrogen peroxide
can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of
hydrogen peroxide may cause irritation of the gastrointestinal tract with
nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct
the respiratory tract or result in pulmonary aspiration. Painful gastric
distension and belching may be caused by the liberation of large volumes of
oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are
common following ingestion of concentrated solutions, and laryngospasm and
haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy,
confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea,
cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion.
Oxygen gas embolism may produce multiple cerebral infarctions. Although most
inhalational exposures cause little more than coughing and transient dyspnoea,
inhalation of highly concentrated solutions of hydrogen peroxide can cause
severe irritation and inflammation of mucous membranes, with coughing and
dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur
up to 24-72 hours post exposure. Severe toxicity has resulted from the use of
hydrogen peroxide solutions to irrigate wounds within closed body cavities or
under pressure as oxygen gas embolism has resulted. Inflammation, blistering
and severe skin damage may follow dermal contact. Ocular exposure to 3%
solutions may cause immediate stinging, irritation, lacrimation and blurred
vision, but severe injury is unlikely. Exposure to more concentrated hydrogen
peroxide solutions (>10%) may result in ulceration or perforation of the
cornea. Gut decontamination is not indicated following ingestion, due to the
rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If
gastric distension is painful, a gastric tube should be passed to release gas.
Early aggressive airway management is critical in patients who have ingested
concentrated hydrogen peroxide, as respiratory failure and arrest appear to be
the proximate cause of death. Endoscopy should be considered if there is
persistent vomiting, haematemesis, significant oral burns, severe abdominal
pain, dysphagia or stridor. Corticosteroids in high dosage have been
recommended if laryngeal and pulmonary oedema supervene, but their value is
unproven. Endotracheal intubation, or rarely, tracheostomy may be required for
life-threatening laryngeal oedema. Contaminated skin should be washed with
copious amounts of water. Skin lesions should be treated as thermal burns;
surgery may be required for deep burns. In the case of eye exposure, the
affected eye(s) shod eye(s) should be irrigated immediately and thoroughly with
water or 0.9% saline for at least 10-15 minutes. Instillation of a local anaesthetic
may reduce discomfort and assist more thorough decontamination.
Hydrogen peroxide is a clear, colourless, odourless oxidizing agent
found in concentrations ranging from 3% to 90%. Three per cent solutions are
used as common household disinfectants, and are therefore a common source of
accidental poisonings, especially in children. In one study (1) of more than
95,000 toxic exposures reported to a poison control centre over three years,
0.34% were due to hydrogen peroxide and of these, 60% occurred in children
younger than six years of age, and 85% occurred through ingestion. Fatalities
in both adults and children have been reported with ingestion of 35% hydrogen
peroxide (1,2). A concentration of 35% is technical grade or food grade
hydrogen peroxide, and can be purchased in many health food stores because it
is reputed to have multiple health benefits including being useful in the
treatment of HIV, cancer, chronic obstructive pulmonary disease and Alzheimer’s
dementia. Higher concentrations of up to 90% are used as rocket fuel.
Hydrogen peroxide is relatively unstable and will rapidly decompose,
through an exothermic reaction, into water and oxygen in the presence of
alkali, metals and the enzyme catalase, which is found in mucous membranes,
liver, kidney, red blood cells and bone marrow. There are three main mechanisms
of toxicity from hydrogen peroxide: caustic injury, oxygen gas formation and
lipid peroxidation.
Ingestion of 3% hydrogen peroxide usually results in only mild
gastritis, unless ingested in large quantities. Ingestion of more concentrated
forms including 35% hydrogen peroxide can produce severe gastrointestinal
erosion, ulceration and perforation. Hydrogen peroxide enteritis with 3%
solution can cause instant bubbling on the mucosal surface followed by a
whitening of the mucosa termed the ‘snow white’ sign. This phenomenon is
thought to be secondary to absorption of hydrogen peroxide into the epithelial
interstices and capillaries, and the subsequent blanching caused by formation
of microbubbles of molecular oxygen. Caustic injury can also occur in the
airway
if aspirated or inhaled, and can lead to subglottic stenosis and
laryngospasm requiring intubation and mechanical ventilation.
The volume of oxygen liberated from the decomposition of hydrogen
peroxide can be considerable, with 30 mL of 35% hydrogen peroxide yielding 3.5
L of oxygen.
This rapid release of oxygen can lead to hollow viscous perforation. If
the amount of oxygen exceeds the maximum solubility in blood, it may lead to
gas embolism particularly in the portal venous system, gastric wall and brain.
Gas embolism in the brain presents similar to ischemic stroke and has been
successfully treated with hyperbaric oxygen therapy.
Lipid peroxidation from ingested hydrogen peroxide can lead to direct
cytotoxic effects.
Despite the potential for severe injury from hydrogen peroxide, it has
been used extensively throughout medical history. 1% to 3% solutions were used
for wound irrigation and as rectal enemas, but gas embolism and rectal ulceration
limited its use. A dilute IV version of hydrogen peroxide was administered for
the treatment of AIDS, but resulted in hemolysis and eventually death. The use
of hydrogen peroxide as a natural remedy is generally based on the premise that
it is a concentrated source of potential oxygen. It is administered orally,
through IV injection and through inhalation, for conditions such as COPD to
help oxygenate the lung and in diabetes mellitus to improve glucose
utilization. Possible mechanisms of action include vasodilation, strengthening
the immune system and stimulating prostaglandin synthesis. 35% hydrogen
peroxide
is available from commercial health food stores, is typically stored in
a refrigerator or freezer to retard decomposition, and is diluted to achieve
the desired concentration. Despite the little evidence on its benefits and
well-documented accidental poisonings, there is continued use and availability
of hydrogen peroxide for such health applications.
Management of hydrogen peroxide exposures depends on the severity of
ingestion and includes airway management, frequent monitoring, and diagnosis
and therapy of associated complications. Due to the rapid decomposition, gut
decontamination is not required. In the present case, the immediate ingestion
of 500 mL of water following the hydrogen peroxide may have prevented more
serious oropharyngeal and esophageal injury. Both x-ray and computed tomography
are useful for ruling out viscous perforation and air embolism. Endoscopy
should be performed in all patients (except if perforation is suspected or the
patient is hemodynamically unstable) because signs and symptoms do not
consistently correlate with the extent of injury, making endoscopy the only
reliable method to assess for injury. Endoscopic assessment of injury severity
within 24 h can be used to risk stratify patients because the severity of
mucosal injury strongly correlates with the risk of death and systemic
complications. Strictures occur most frequently in the esophagus and generally
develop between six and 12 weeks. Consequently, routine follow-up endoscopy may
be indicated in patients with esophageal injury. One trial reported using IV
cimetidine when there was evidence of gastric erosions or ulcers, but none have
documented using proton pump inhibitors. In the present case, IV pantoprazole,
40 mg 2x daily, was used, and the patient had resolution of all abdominal pain
symptoms. For cerebral gas embolism, hyperbaric oxygen therapy has been used
successfully.
Most exposures to hydrogen peroxide are with the 3% solution of hydrogen
peroxide, which results in little or no morbidity. However, the storage and use
of 35% hydrogen peroxide for natural health benefits results in an emerging
source for more serious ingestions. 35% hydrogen peroxide can be lethal when
ingested, and needs to be treated with caution and stored appropriately. Public
awareness and regulation of the use of this substance is required.
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