Amiodarone-Induced Lung Toxicity: A Case Initially Not Correctly Framed

Abstract

Amiodarone-induced pulmonary toxicity (AIPT) is one of the most serious adverse effects of amiodarone and is one of the leading causes of death associated with its use. The onset of AIPT depends on dosage, patient's age, and pre-existing pulmonary pathologies; typically, the adverse effects stop progressing when a cumulative dose higher than 150 mg is reached. The risk of developing amiodarone-induced pulmonary fibrosis is directly related to the dosage and duration of administration. In this case report, the effect of a prolonged overdose of amiodarone taken at doses of 200 mg/day for two years is reported, with symptoms and instrumental evidence of respiratory pathology induced by amiodarone drug toxicity. Comorbidities, oxygen therapy, invasive procedures, and surgical interventions can trigger pulmonary symptoms. Despite significant advances in understanding AIPT, its etiology and pathogenesis remain poorly understood. The role of steroids in the treatment of AIPT is still under debate as most reports of improvement after amiodarone withdrawal differ little from those in which concomitant steroid therapy was used. In clinical practice, therapeutic doses of corticosteroids may be indicated for patients with AIPT; usually, a starting dose of prednisone from 40 to 60 mg daily, which is then gradually reduced, is prescribed. The pharmacodynamics of amiodarone determines a treatment period of four to 12 months.The patient with AIPT in this case report, who markedly improved after treatment with prednisone at a starting dose of 50 mg/day, which was then gradually tapered. At the end of the therapy, the computed tomography (CT) scan revealed the disappearance of most of the scattered ground-glass opacities and of the thickening indicating bi-apical pulmonary fibrosis.The case report is unique because: 1) Bronchoalveolar lavage (BAL)/transbronchial biopsy was not used for diagnosis.2) The case was framed based on the patient's laboratory and clinical data.3) The pathology is normally prevalent in men rather than women.

Too Little, Too Late: A Case of a Swift Fatal Culmination of Amiodarone Induced Pulmonary Toxicity in an Adult Male

“…Furthermore, despite the quick discontinuation of amiodarone and the use of intravenous pulsed methylprednisolone at high doses, it did not provide any rapid therapeutic relief or positive response as suggested commonly in literature. 4,10,15,16 These factors have all contributed to the rapidity and severity of APT in this patient. Though not previously highlighted in literature for the cut off for reversible versus non-reversible drug induced interstitial lung disease, it could be considered that this patient's APT may very well have been past that of a reversible stage.…”

“… 3 , 8 With the right starting dosage of prednisolone, patients with APT may achieve partial or complete resolution of their amiodarone induced pulmonary damage. 15 , 16 It is essential to note that after cessation of amiodarone, there could be a duration of worsening symptoms due to its long half-life. 10 Conversely, all patients starting therapy on long term oral amiodarone should receive baseline testing of a CXR, lung function test, liver function test along with thyroid function tests – this should be followed up in regular intervals.…”