Oxygen Toxicity

Oxygen toxicity is injury from breathing oxygen at raised partial pressure. It affects the central nervous system (seizures), lungs (tracheobronchitis and diffuse injury), eyes and, in neonates, the developing retina. Risk depends on partial pressure and duration.

Settings. Diving with enriched air or oxygen, hyperbaric treatment, oxygen rebreathers, prolonged high fraction oxygen therapy in hospital, and neonatal intensive care.

Thresholds. Central nervous system toxicity occurs with partial pressures over about 1.4 atmospheres, mainly in diving. Pulmonary toxicity follows exposures over about 0.5 atmospheres for many hours, such as an inspired fraction over 0.6 for over 48 hours at sea level.

Other effects. Reversible myopia and cataract after repeated hyperbaric exposure, absorption atelectasis, and retinopathy of prematurity in preterm infants.

Risk modifiers. Exercise, immersion, carbon dioxide retention, cold, fatigue, caffeine and steroids increase central nervous system risk. Bleomycin, amiodarone and paraquat increase lung risk.

Pathophysiology.

Excess oxygen generates reactive oxygen species that overwhelm antioxidant defences. They injure lipids, proteins and DNA and cause neuronal hyperexcitability through effects on GABA and glutamate.

Lung injury follows endothelial and epithelial damage and inflammation, and retinal vessels constrict in the immature retina and later proliferate abnormally.

• Central nervous system: twitching, nausea, dizziness, visual and hearing change, irritability, then tonic clonic seizure.
• Pulmonary: retrosternal burning, cough, dyspnoea and reduced vital capacity.
• Ocular: myopic shift over weeks; neonatal retinal changes.

Red flags.

• Seizure or loss of consciousness during a hyperbaric exposure or dive.
• Progressive hypoxaemia or new infiltrates on a high inspired oxygen fraction.

• Clinical, from exposure history and the timing of onset.
• Record partial pressure and duration of exposure.
• Spirometry showing reduced vital capacity after hyperbaric or prolonged oxygen exposure; chest radiograph or CT for infiltrates.
• Eye examination after repeated hyperbaric exposure or in preterm infants.
• Exclude other causes: infection, heart failure, drug toxicity, embolism and other seizure causes.

Differential diagnosis. Pulmonary infection, acute respiratory distress syndrome from other causes, heart failure, drug induced lung injury, hypoglycaemia and other seizure causes, decompression sickness.

• Reduce the inspired oxygen partial pressure at once. In a chamber, remove the mask and breathe air or a lower oxygen mix.
• Hospital oxygen therapy: titrate to saturation 94 to 98%, or 88 to 92% with risk of carbon dioxide retention. Keep the inspired fraction under 0.6 where possible.
• Seizure: protect the airway, do not restrain, and give lorazepam 4 mg intravenously over 2 minutes only if it persists beyond 5 minutes. Repeat once after 10 minutes. Maximum 8 mg. Monitor breathing and blood pressure; caution in respiratory depression and hepatic impairment; no renal adjustment.
• Hyperbaric sessions: use air breaks (for example 5 minutes of air after each 20 to 25 minutes of oxygen) and limit session depth and duration.
• Supportive care for pulmonary injury, with ventilation strategies that limit pressure and volume.
• Neonates: titrate oxygen to the lowest effective saturation and arrange retinal screening.

Monitoring. Symptoms and vital capacity after hyperbaric courses; eye review after prolonged courses; oximetry during oxygen therapy.

Referral and escalation. Diving or hyperbaric physician for any seizure; critical care for respiratory failure; ophthalmology for visual change; neonatology for retinopathy screening.