Amiodarone-Induced Pulmonary Toxicity (original) (raw)

Amiodarone pulmonary toxicity: a report on two cases

The Southwest Respiratory and Critical Care Chronicles, 2015

Amiodarone is an iodine-containing antiarrhythmic drug commonly used for the treatment of ventricular and supraventricular arrhythmias. Amiodarone toxicity has several clinical presentations and affects multiple organs. One well-known serious side effect of amiodarone is pulmonary toxicity which can be acute, sub-acute, or chronic. Amiodarone pulmonary toxicity may present a diagnostic dilemma, particularly when clinical suspicion of pulmonary infection is high. Here we report two cases of amiodarone lung toxicity that were diagnosed in an early stage and improved after the discontinuation of amiodarone.

Amiodarone-induced pulmonary toxicity (APT): A low dose fatal adverse event

International Journal of Case Reports and Images, 2016

International Journal of Case Reports and Images (IJCRI) is an international, peer reviewed, monthly, open access, online journal, publishing high-quality, articles in all areas of basic medical sciences and clinical specialties. Aim of IJCRI is to encourage the publication of new information by providing a platform for reporting of unique, unusual and rare cases which enhance understanding of disease process, its diagnosis, management and clinico-pathologic correlations. IJCRI publishes Review Articles, Case Series, Case Reports, Case in Images, Clinical Images and Letters to Editor.

Amiodarone-induced pulmonary toxicity: an under-recognized and severe adverse effect?

Clinical Research in Cardiology, 2010

Several forms of pulmonary disease occur among patients treated with amiodarone, i.e. chronic interstitial pneumonitis, organizing pneumonia, ARDS, a solitary pulmonary mass of fibrosis. The prevalence is estimated to be about 5%. Two major hypotheses of amiodarone-induced pulmonary injury include direct cytotoxicity and a hypersensitivity reaction. Given the frequency and potential severity of amiodarone-induced pulmonary toxicity, early detection is desirable. Unfortunately, there are no adequate predictors of pulmonary toxicity due to amiodarone. Patients who should benefit from amiodarone should be carefully selected and the lowest effective dosage of amiodarone should be taken. Amiodarone-induced pulmonary toxicity is a diagnosis of exclusion. Pulmonary evaluation with chest X-ray and pulmonary function testing, including diffusion capacity for carbon monoxide is recommended when amiodarone is started. A documented decline in the diffusing capacity of greater than 20% is useful in suggesting the need for closer monitoring or for further diagnostic testing. Although the optimal frequency of follow-up has not been determined, most cases of amiodarone-induced lung injury develop during the first 2 years of treatment and disease onset usually is slow. Pulmonary function tests and imaging may be performed every 3-6 months, depending on the presumed individual risk. Treatment of amiodarone pulmonary toxicity consists primarily of stopping amiodarone. Corticosteroid therapy can be life-saving for severe cases and for patients with less severe disease in whom withdrawal of amiodarone is not desirable. Due to its accumulation in fatty tissues and long elimination half-life, pulmonary toxicity may initially progress despite drug discontinuation and may recur after steroid withdrawal. The prognosis of amiodarone lung disease is generally favourable.

Amiodarone-Induced Pulmonary Toxicity—A Fatal Case Report and Literature Review

Cardiovascular Drugs and Therapy, 2013

Amiodarone is a widely used and very potent antiarrhythmic substance. Among its adverse effects, pulmonary toxicity is the most dangerous without a causal treatment option. Due to a very long half-life, accumulation can only be prevented by strict adherence to certain dosage patterns. In this review, we outline different safe and proven dosing schemes of amiodarone and compare the incidence and description of pulmonary toxicity. Reason for this is a case of fatal pulmonary toxicity due to a subacute iatrogenic overdosing of amiodarone in a 74-year-old male patient with known severe coronary artery disease, congestive heart failure and ectopic atrial tachycardia with reduced function of kidneys and liver but without preexisting lung disease. Within 30 days, the patient received 32.2 g of amiodarone instead of 15.6 g as planned. Despite early corticosteroid treatment after fast exclusion of all other differential diagnoses, the patient died another month later in our intensive care unit from respiratory failure due to bipulmonal pneumonitis.

Amiodarone induced lung disease

Archive of Clinical Cases

Amiodarone, a primarily class III antiarrhythmic drug is one of the most commonly used drug in atrial fibrillation. A possible rare side effect of amiodarone treatment is to develop a diffuse parenchymal lung disorder - amiodarone pulmonary toxicity (APT). There is no pathognomonic finding to diagnose APT. A 64-year-old patient with multiple comorbidities presented in our hospital with worsening a five-month history of grade 3 mMRC dyspnea, wheezing, frequent nonproductive cough, fatigue. She has a medical history of atrial fibrillation in treatment with amiodarone 400mg/day for 2 years. Her oxygen saturation was 90% on room air, chest radiography showed disseminated lung irregular opacities with a tendency to confluence in right and left lung and chest computed tomography scan showed asymmetric centrilobular nodules and asymmetrical areas of dense ground glass opacity with few consolidation. Amiodarone pulmonary toxicity was suspected, the drug was stopped and treatment with methyl...

Amiodarone induced pulmonary toxicity: An unusual response to steroids

2012

Background: Amiodarone, class III anti-arrhythmic was originally introduced to treat angina pectoris, was later approved by FDA in 1985 for the treatment of ventricular arrhythmias. Despite its anti-arrhythmic properties, amiodarone is associated with side effects such as thyroid dysfunction, corneal deposits, bluish skin discoloration, neuropathy and pulmonary toxicity. Amiodarone induced pulmonary toxicity (AIPT) is one of the most serious side effect thus limiting its use.

Pulmonary complications after long term amiodarone treatment

Thorax, 1992

BACKGROUND: Amiodarone hydrochloride is an antiarrhythmic agent useful in arrhythmias refractory to standard therapy. Although interstitial pneumonitis is known to be its most serious side effect, several aspects of amiodarone lung toxicity are still controversial. METHODS: Pulmonary side effects were examined in a sample of 61 symptomless patients (mean (SD) age 55 (7) years) who had had long term treatment

Pulmonary Toxicity in Patients Receiving Low-Dose Amiodarone*

Chest, 2003

asthma." A CT scan revealed and located the airway narrowings, preventing delay of the diagnosis. Management with self-expandable stents has kept the proximal airways patent. Without the stenting technology, the outcome of this patient's case would be unpredictable and could be less than satisfactory.

Management of Hyperacute Amiodarone-induced Pulmonary Toxicity

Journal of Cardio-Vascular-Thoracic Anaesthesia and Intensive Care Society

One of the major complications of amiodarone therapy is acute pulmonary toxicity (APT). Patients tend to have amiodarone-induced toxicity after Coronary Artery Bypass Surgery (CABG). For this reason, priority should be given to the treatment of this fatal complication. Acute pulmonary toxicity due to amiodarone is a treatable phenomenon if diagnosed at an early stage, for this reason, meticulous follow-up and suspicion are of great importance. We presented the treatment of a 72-year-old male who underwent 4-vessel coronary artery bypass grafting surgery but developed amiodarone-induced pulmonary toxicity immediately after amiodarone infusion.