Amiodarone Induced Lung Toxicity Summary
Who?
• 5% of patients
• Dose ≥ 400 mg per day
How? Possible mechanisms:
• Direct cytotoxic lung injury
• Indirect hypersensitivity/immunologic reaction
• Amiodarone half life: 45 days in fatty tissue
Presentation?
• Acutely (hours to days after surgery or angiography)
• Chronically (months to years after starting amiodarone treatment)
• Can rarely present with eosinophilic pneumonia, organizing pneumonia, ARDS, DAH, solitary and multiple pulmonary nodules and masses, and exudative pleural effusions
• Acute toxicity (e.g., acute respiratory distress syndrome) is rare but is associated with high mortality (up to 50%).
• Chronic toxicity (e.g., chronic interstitial pneumonitis, organizing pneumonia) is more common and presents gradually with symptoms including:
1. Non-productive cough
2. Dyspnea
3. Fever
4. Pleuritic chest pain
5. Fatigue and/or weight loss
6. Mortality has been reported as up to 10% in some studies
Characteristic finding is accumulation of lipid-laden 'foamy' macrophages in alveolar spaces.
• Patchy or diffuse infiltrates
• Ground glass opacities
• Reticular + Nodular opacities; traction bronchiectasis
• Most commonly: Interstitial pneumonitis
Diagnosis:
• Exclude other causes like:
- Heart failure
- Infectious pneumonia
- Pulmonary embolism
- Malignancy
- Exclusion of other ILDs
• Presence of foamy macrophages in the BAL
• Improvement in symptoms and radiographic manifestations following withdrawal of amiodarone (with or without glucocorticoid therapy)
• 20% ↓ in DLCO & new ground glass or reticular opacities on chest radiograph and confirmatory findings on HRCT is highly suggestive but not diagnostic of amiodarone-induced pulmonary toxicity.
Labs:
• Nonspecific leukocytosis
• ↑ LDH
• ↑ ESR, CRP
BAL:
• Lymphocytosis
• Neutrophilia
• Eosinophilia
• Normal BAL cellular counts
• Foamy macrophages
Treatment:
• Stopping amiodarone
• Symptomatic patients: Corticosteroids
Prognosis:
• Favorable in case of most common presentation: Interstitial pneumonitis
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