Hydrogen Peroxide (H₂O₂) Poisoning

Sources & Concentrations

Mechanisms of Toxicity

1. Corrosive damage - Direct caustic injury to mucous membranes, skin, GI tract, and eyes. More pronounced with concentrated (>10%) solutions.
2. Oxygen gas formation - H₂O₂ is rapidly decomposed by tissue catalase to O₂ + H₂O.
   • 1 mL of 3% H₂O₂ releases ~10 mL of O₂
   • 120 mL of 35% H₂O₂ releases approximately 14 litres of O₂ (Adams & Victor's Neurology, 12th ed.)
   • When the volume of evolved O₂ exceeds blood solubility, venous/arterial gas embolism occurs
   • In enclosed spaces (gut, vasculature), this causes mechanical distension, viscus rupture risk, and impaired right ventricular output (cardiac arrest)
3. Lipid peroxidation - Direct cytotoxic effect on cell membranes

Routes of Exposure

• Ingestion - most common route for serious poisoning
• Inhalation - vapors from concentrated solutions
• Skin/eye contact - local corrosive injury
• Intravenous (rare, "alternative medicine" misuse) - extremely dangerous, directly causes fatal gas embolism (PMID 37624158)

Clinical Features

Ingestion

• Nausea, vomiting, haematemesis
• Foaming at the mouth (white foam - pathognomonic)
• Gastric distension, painful belching
• GI irritation, occasional erosions

• All of the above, plus:
• Oropharyngeal burns and mucosal blistering
• Laryngospasm, stridor, sub-epiglottic narrowing
• Sinus tachycardia, lethargy, confusion
• Haemorrhagic gastritis
• Dysphagia

• Rapid loss of consciousness
• Coma, convulsions
• Apnoea and cardiorespiratory arrest (within minutes)
• Gas embolism → multiple cerebral infarcts in parasagittal watershed areas
• Portal venous gas, pneumatosis intestinalis, viscus perforation

Inhalation

• Eye and throat irritation, lacrimation
• Coughing, dyspnoea (usually transient with dilute vapor)
• Concentrated vapor: severe mucosal inflammation, pulmonary oedema (may be delayed 24-72 hrs)
• Shock, coma, convulsions in severe cases

Eye / Skin Contact

• Erythema, burning, bleaching
• Dilute (<10%): usually reversible mild irritation
• Concentrated (>10%): corneal ulceration or perforation possible

Neurological (Gas Embolism)

• Multiple small cerebral infarcts in watershed/parasagittal areas
• Stroke-like presentation; most cases reversible but permanent deficits reported (PMID 39077285)
• Blindness reported with recovery after hyperbaric O₂ (PMID 40125300)

Diagnosis

• Clinical - characteristic white foam from mouth, GI symptoms, history of ingestion
• Bedside test for ingestion: add 1 drop of 15% titanium chloride to acidified mixture of gastric contents + ethyl ether → yellow-orange colour confirms H₂O₂
• CXR + AXR - mandatory if concentrated ingestion; look for intravascular gas, pneumoperitoneum, portal vein gas
• CT scan - more sensitive for gas embolism (cerebral infarcts, portal venous gas, pneumatosis)
• ABG + pulse oximetry - for inhalation exposure
• Labs: FBC, glucose, electrolytes (routine)
• Endoscopy - for persistent vomiting, haematemesis, oral burns, dysphagia, stridor, severe abdominal pain (NOT if perforation suspected or haemodynamically unstable)

Management

General Principles

• No antidote exists
• Enhanced elimination (emesis, charcoal, lavage) is NOT indicated - H₂O₂ decomposes too rapidly; emesis risks aspiration of foam/caustic material; charcoal does not bind H₂O₂
• If gastric distension is painful, pass a nasogastric tube to decompress and release gas

Airway

• Top priority - respiratory failure and arrest are the proximate cause of death
• Early intubation for: severe oropharyngeal burns, laryngospasm, stridor, altered consciousness
• High-dose corticosteroids may be considered if laryngeal or pulmonary oedema present

Skin / Eye Exposure

• Irrigate copiously with water for at least 15-20 minutes
• Remove contaminated clothing

Inhalation

• Remove from exposure, fresh air
• Observe 24-72 hrs for delayed pulmonary oedema

Gas Embolism

• Hyperbaric oxygen (HBO) - used for severe cases with CNS or cardiac gas embolism; no controlled trials but supported by case evidence (ATSDR; PMID 40125300)
• Aspiration of air via central venous line - may be attempted in patients in extremis
• Place patient in left lateral decubitus + Trendelenburg position to trap air in right ventricle and prevent arterial embolism

Hospitalisation

• Admit: symptomatic patients, concentrated ingestion (>10%), inhalation with chest symptoms
• Observe ≥4-6 hrs; if asymptomatic at 4-6 hrs, discharge with return precautions
• Chest symptoms (pain, tightness, cough) → observe 24-72 hrs for delayed pulmonary oedema

Summary Table