Acute respiratory failure on a low dose of amiodarone – is it an underdiagnosed and undertreated condition?

Meter, Mijo; Prusac, Ivana Kuzmić; Glavaš, Duška; Meter, Diana

doi:10.1016/j.rmcr.2021.101500

Cited by 5 publications

(3 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Amiodarone-induced interstitial lung damage includes varying forms of presentation, from mild to moderate/severe [ 40 ]. These include organizing pneumonia, interstitial pneumonitis or respiratory failure.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary Fibrosis Related to Amiodarone—Is It a Standard Pathophysiological Pattern? A Case-Based Literature Review

et al. 2022

View full text Add to dashboard Cite

Amiodarone hydrochloride is an antiarrhythmic drug, with proven efficacy in prevention and treatment of numerous arrhythmias, atrial fibrillation especially, or ventricular arrhythmias, with a long half-life (55–60 days). The increased risk of developing amiodarone-induced pulmonary fibrosis is directly related to the dose and the duration of the intake. Amiodarone-induced pulmonary toxicity is conditioned by dose, patient’s age, and pre-existent pulmonary pathologies. The pattern for drug-induced lung injury may vary in many forms, but the amiodarone can cause polymorphous injuries such as diffuse alveolar damage, chronical interstitial pneumonia, organizing pneumonia, pulmonary hemorrhage, lung nodules or pleural disease. The pathological mechanism of pulmonary injury induced by amiodarone consists of the accumulation of phospholipid complexes in histocytes and type II pneumocytes. Differential diagnosis of pulmonary fibrosis induced by amiodarone is made mainly with idiopathic pulmonary fibrosis, left ventricular failure or infectious disease. Before starting treatment with amiodarone, patients should be informed of potential adverse effects and any new respiratory symptoms should promptly be reported to their family physician or attending physician. The assessment carried out at the initiation of amiodarone treatment should include at least chest X-ray and respiratory function tests and extrapulmonary evaluation.

show abstract

Section: Discussionmentioning

confidence: 99%

Pulmonary Fibrosis Related to Amiodarone—Is It a Standard Pathophysiological Pattern? A Case-Based Literature Review

et al. 2022

View full text Add to dashboard Cite

show abstract

“…Even though the adverse effects of amiodarone are well-documented, physicians and patients do not often follow the guidelines for monitoring the therapy. For instance, the serum levels of amiodarone, which can be measured in specific medical centers and indicate toxicity if above 2.5 mg/L, are not regularly measured [14].…”

Section: Discussionmentioning

confidence: 99%

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

Scaramozzino¹,

Sapone²,

Plastina³

et al. 2023

Cureus

View full text Add to dashboard Cite

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.

show abstract

“…A nonspeci c in ammatory syndrome can also be highlighted, characterized by a mild leucocytosis, increased erythrocyte sedimentation rate and increased C-reactive protein (CRP) value, but these are nonspeci c and are associated with interstitial in ammation 13 . Amiodarone-induced interstitial lung damage includes varying forms of presentation, from mild to moderate/severe 14 . These include organizing pneumonia, interstitial pneumonitis, or respiratory failure.…”

Section: Clinical Case Presentationmentioning

confidence: 99%

Amiodarone induced lung toxicity: a radiological overview that simulating COVID19 infection disease

Scaramozzino,

Sapone,

Plastina

et al. 2023

View full text Add to dashboard Cite

Amiodarone-induced pulmonary toxicity (AIPT) is among the most serious adverse effects and is one of the leading causes of death associated with its use. It is a clinical pathology that is conditioned by dose, patient’s age, and pre-existent pulmonary pathologies. Those effects reach a plateau at a cumulative dose bigger than 150g. Patient’s comorbidities; oxygen therapy, invasive procedures or surgical interventions can trigger the pulmonary symptoms induced by amiodarone toxicity. The increased risk of developing amiodarone-induced pulmonary fibrosis is directly related to the dose and the duration of the intake. Despite significant advances in the understanding of AIPT, its aetiology and pathogenesis remain incompletely understood. The role of steroids in the management of pulmonary toxicity from amiodarone is debatable, however, most reports of improvement after amiodarone withdrawal di"er little from those in which concomitant steroid therapy was employed. Therefore, the addition of therapeutic doses of corticosteroids in amiodarone induced pneumopathy may be indicated. Typically, prednisone is started in doses of 40 to 60 mg/day orally and slowly reduced. Again, the pharmacodynamics of amiodarone dictate a treatment period of four to 12 months. The case report describes a patient with AIPT who after therapy with Prednisone at a dosage of 50mg/day by gradually scaling down the doses as reported in the above clinical studies, had a clinical, functional and CT radiological picture that was markedly improved with disappearance of most of the scattered ground glass areas and the previously reported thickening with associated bi-apical fibrotic outcomes.

show abstract

Acute respiratory failure on a low dose of amiodarone – is it an underdiagnosed and undertreated condition?

Cited by 5 publications

References 23 publications

Pulmonary Fibrosis Related to Amiodarone—Is It a Standard Pathophysiological Pattern? A Case-Based Literature Review

Pulmonary Fibrosis Related to Amiodarone—Is It a Standard Pathophysiological Pattern? A Case-Based Literature Review

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

Amiodarone induced lung toxicity: a radiological overview that simulating COVID19 infection disease

Contact Info

Product

Resources

About