Hydrogen peroxide

Hydrogen Peroxide is an oxidising agent used widely in domestic and industrial products. It causes damage by three main mechanisms: direct corrosive injury, oxygen gas formation and lipid peroxidation. One tox email circulated during my clinical attachment of a patient who ingested hydrogen peroxide, seemed fine and then boarded a plane to develop the “bends” from oxygen formation and improve some what during landing.

Toxic Mechanism:

Hydrogen peroxide is corrosive and exposure causes local tissue damage. Metabolism of hydrogen peroxide will liberate large quantities of oxygen. Once solubility in the blood is at maximum oxygen will precipitate in the venous and arterial circulation to form gas emboli. If oxygen forms i na hollow viscus under tension then perforation is possible. If foaming occurs in the left ventricle then cardiac output can be severely impeded. Lipid per oxidation causes direct cytotoxic effects.


  • Hydrogen peroxide is rapidly absorbed.
  • Rapidly metabolised – predominantly by red cells to yield oxygen and water.
  • 35 ml of 35% hydrogen peroxide liberates 3.5L of oxygen at a standard pressure and temperature.


  • Airway compromise: Intubate and ventilate especially if signs of laryngeal oedema (stridor, dysphonia, throat pain, horseless or respiratory distress).
  • High flow oxygen to all patients
  • Hyperbaric oxygen maybe required to all those with symptoms of cerebral gas embolism
  • Hypotension: Usually responds to fluid administration, noradrenaline is second line therapy [0.15mg/kg in 50ml D5W at 1-10ml/hr (0.05 – 0.5 mcg/kg/min)], other vasopressors may be used.

Risk Assessment

  • Ingestion of small volumes (<30 ml) of 3% hydrogen peroxide causes only mild GI irritation.
  • >10% ingestions can cause potentially life-threatening corrosive injury to the airway, GI tract and propagate life-threatening gas emboli. If exposed to the cornea it can cause permanent injury.
  • Children: minor exposures to solutions 3% of less are unlikely to cause significant injury. Any higher concentration or if they have symptoms warrants hospital evaluation.
  • Clinical features:
    • Ingestion: ranges from the symptoms associated with GI irritation (nausea, vomiting, haematemasis, foaming at the mouth) to upper airway distress (oral burns, laryngospasm, stridor, cyanosis and respiratory arrest) to severe toxicity form the 10% solutions (tachycardia, confusion, coma, seizures, cardiac arrest and death).
    • Features of gas emboli include; hemiplegia, altered GCS, blindness, focal motor or sensory signs, multifocal neurological deficit or cardiac arrhythmias.
    • Inhalation: Coughing and transient dyspnoea. If high concentrations are inhaled it is possible to develop severe respiratory distress, coma, seizures and pulmonary oedema.
    • Dermal: Localised listening or even skin necrosis can occur. Subcutaneous emphysema is even possible.
    • Ocular: Stinging, irritation, lacrimation and blurred vision. Subepithelial corneal and conjunctival bubbles may be seen. Corneal ulceration and perforation are possible with higher concentrations of hydrogen peroxide.

Supportive Care

  • Analgesia


  • Screening: 12 lead ECG, BSL, Paracetamol level
  • Specific:
    • EUC, FBC and acid-base status
    • Chest and abdominal X-ray to demonstrate perforation or gas embolism
    • Cerebral CT or MRI is indicated in anyone developing CNS effects to determine if there is a cerebral gas embolism or infarction.
    • Upper GI endoscopy is considered if there are symptoms suggestive of corrosion (persistent vomiting, haematemasis, oral burns, abdominal pain, dysphagia, stridor or the patient has ingested >10% concentration solutions).


  • Exposed skin should be washed
  • Cornea if exposed require irrigation for at least 15 minutes.

Enhanced Elimination

  • Not clinically useful.


  • None available.


  • Minor unintentional expose to 3% solutions in either children or adults does not require evaluation unless persistent symptoms develop.
  • Any ingestion or inhalation of >10% solution or someone with ongoing symptoms requires close observation and monitoring, likely HDU or ICU
  • Any evidence of corrosive injury to the airway or GI tract require definitive treatment.
  • Patients with evidence of gas emboli should be referred for consideration for hyperbaric oxygen.
  • Patients with corneal injury should be referred to ophthalmology after irrigation.


  • Moon JM, Chun BJ, Min YI. Haemorrhagic gastritis and gas embolism after ingestion of 3% hydrogen peroxide. Journal of Emergency Medicine 2006; 30(4):403-406.
  • Papfragkou S, Gasparyam A, Batista R et al. Treatment of portal venous gas embolism with hyperbaric oxygen after accidental ingestion of hydrogen peroxide: a case report and review of the literature. Journal of Emergency Medicine 2009; in press
  • Watt BE, Proudfoot AT, Vale JA. Hydrogen peroxide poisoning. Toxicological Reviews 2004; 23:51-57.
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Dr Neil Long BMBS FACEM FRCEM FRCPC. Emergency Physician at Kelowna hospital, British Columbia. Loves the misery of alpine climbing and working in austere environments (namely tertiary trauma centres). Supporter of FOAMed, lifelong education and trying to find that elusive peak performance.

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