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 (8). 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.