Key Points
- To report a rare case of rapid-onset amiodarone-induced pulmonary toxicity occurring after a low loading dose in a post-thoracic surgery patient.
- Clinical and diagnostic evaluation of a 58-year-old female who developed acute respiratory failure following lung lobe resection and subsequent amiodarone administration for post-operative atrial fibrillation (N=1).
- Assessment via chest computed tomography (CT), tracheal secretion cytology, and systemic inflammatory markers including C-reactive protein and procalcitonin.
- Treatment intervention involving immediate cessation of amiodarone and administration of systemic glucocorticoids (prednisolone 50 mg/day for five days).
- The patient developed severe respiratory failure meeting acute respiratory distress syndrome criteria four days after amiodarone initiation, presenting with bilateral infiltrates and foam cells in tracheal secretions without infectious pathogens.
- Laboratory findings revealed marked leukocytosis and elevated C-reactive protein in the absence of elevated procalcitonin.
- Glucocorticoid therapy combined with amiodarone withdrawal led to rapid clinical improvement, successful ventilator weaning within five days, and complete radiological resolution of pulmonary infiltrates on follow-up CT.
Structured PICO
PPopulation1 58-year-old woman who underwent thoracic surgery with lobe resection and developed post-operative atrial fibrillation with hemodynamic instability.
IInterventionAmiodarone therapy (low loading dose) followed by withdrawal and initiation of prednisolone 50 mg/d for 5 days upon toxicity.
OOutcomeDevelopment and resolution of amiodarone-induced pulmonary toxicity (APT)safety
Amiodarone can cause rapid-onset pulmonary toxicity even at low loading doses after thoracic surgery, requiring prompt recognition, drug withdrawal, and glucocorticoid therapy.