Pulmonary Oxygen Toxicity

Pulmonary oxygen toxicity is lung injury caused by prolonged breathing of oxygen at raised partial pressure. It ranges from reversible tracheobronchitis to diffuse alveolar damage resembling acute respiratory distress syndrome.

Exposure. Daily hyperbaric oxygen therapy, saturation diving, oxygen rebreather use and mechanical ventilation with a high inspired fraction. Symptoms begin after about 6 to 12 hours at 1 atmosphere of pure oxygen, or sooner at greater pressure.

Exposure units. Pulmonary toxic dose is estimated as unit pulmonary toxic doses from time at a given partial pressure. A vital capacity fall of 2% needs about 615 units, and 10% about 1425 units.

Course. Early injury reverses over days after exposure ends. Advanced disease can progress to fibrosis.

Risk modifiers. Prior bleomycin or amiodarone, paraquat, chest radiation and high lung disease burden. Hypercapnia and exercise do not clearly alter the lung effect.

Pathophysiology.

Reactive oxygen species damage alveolar epithelial and endothelial cells, producing inflammation, increased permeability, and surfactant loss.

Exudative changes with hyaline membranes follow, then proliferation of type II cells and fibroblasts and, if exposure continues, fibrosis.

• Early: retrosternal discomfort worsened by deep breath, cough, throat irritation.
• Later: dyspnoea, chest tightness, reduced exercise tolerance and crackles.
• Severe: hypoxaemia and respiratory failure.
• Vital capacity falls before symptoms are severe.

Red flags.

• Worsening hypoxaemia despite high inspired oxygen.
• New bilateral infiltrates with falling compliance.

• Exposure history: partial pressure, fraction and duration.
• Vital capacity measurement before and after hyperbaric sessions: a fall of over 10% needs action.
• Chest radiograph: diffuse bilateral opacities; CT for ground glass change and fibrosis.
• Arterial gas for PaO2 to FiO2 ratio; exclude infection, heart failure, aspiration and embolism.

Differential diagnosis. Acute respiratory distress syndrome from other causes, pneumonia, cardiogenic pulmonary oedema, drug induced lung disease (bleomycin, amiodarone), aspiration, pulmonary embolism, hypersensitivity pneumonitis.

• Reduce the oxygen dose: lower the inspired fraction to the minimum that keeps saturation at 94 to 98% (88 to 92% when at risk of carbon dioxide retention), add air breaks, and reduce hyperbaric depth, duration or frequency.
• Stop hyperbaric sessions when vital capacity has fallen by over 10% or symptoms are present, and resume only after recovery.
• Paraquat poisoning: give oxygen only when saturation is under 90%, because oxygen worsens the injury.
• Supportive care: low tidal volume ventilation (6 mL/kg predicted body weight) with plateau pressure under 30 cmH2O for acute respiratory distress syndrome.
• Prednisolone has no proven benefit in early injury; for organising or fibrotic disease use 0.5 mg/kg orally once daily in the morning, maximum 40 mg daily, for 4 weeks, then taper over 8 to 12 weeks if there is clear benefit. Monitor glucose, blood pressure and infection; exclude infection first; caution in diabetes and peptic ulcer; no renal adjustment.

Monitoring. Vital capacity before and after each hyperbaric session for long courses; oxygenation and radiograph daily during acute injury; lung function at 3 months after significant injury.

Referral and escalation. Hyperbaric physician for regimen change; critical care for respiratory failure; respiratory physician for persistent restriction.