Amiodarone Pulmonary Toxicity Research Articles

L-Carnitine Ameliorates Amiodarone-Mediated Alveolar Damage: Oxidative Stress Parameters, Inflammatory Markers, Histological and Ultrastructural Insights

The aim of this study was to assess L-carnitine’s effects on adult male rats’ lung damage brought on by amiodarone, which is a potent antiarrhythmic with limited clinical efficacy due to potentially life-threatening amiodarone-induced lung damage. Because of the resemblance among the structural abnormalities in rats’ lungs that follows amiodarone medication and pulmonary toxicity in human beings, this animal model may be an appropriate example for this disease entity. Amiodarone produced pulmonary toxicity in twenty-four healthy male albino rats (150–180 g) over a period of 6 weeks. Four groups of six rats each were established: control, sham, amiodarone, and L-carnitine plus amiodarone. Histological, ultrastructural, oxidative stress, and inflammatory markers were determined during a 6-week exposure experiment. Amiodarone-induced lung damage in rats may be brought on due to oxidative stress producing significant pulmonary cytotoxicity, as evidenced by the disruption of the mitochondrial structure, severe fibrosis, and inflammatory response of the lung tissue. Lungs already exposed to such harmful effects may be partially protected by the antioxidant L-carnitine. Biochemical markers of lung damage brought on by amiodarone include lung tissue levels of the enzyme’s catalase, superoxide dismutase, and reduced glutathione. The levels of lipid peroxides in lung tissue measured as malondialdehyde increased significantly upon exposure to amiodarone. In addition, the levels of tumor necrosis factor alpha were significantly elevated in response to amiodarone. The effect of L-carnitine on amiodarone-induced pulmonary toxicity was studied in rats. It is interesting to note that the intake of L-carnitine in rats treated with amiodarone partially restored the biochemical and histopathological alterations brought on by amiodarone to their original levels. Tumor necrosis factor alpha levels were significantly reduced upon L-carnitine exposure. These results suggest that L-carnitine can be used to treat amiodarone-induced pulmonary dysfunction.

AMIODARONE-INDUCED PNEUMOTOXICITY AT LOWER DOSES THAN EXPECTED

TYPE: Late Breaking Abstract TOPIC: Lung Pathology PURPOSE: To determine if doses of amiodarone lower than 400 mg per day can result in increased risk of lung injury, such as pneumonitis or pulmonary fibrosis. METHODS: We used TriNetX, a federated, global research network that provides access to anonymized medical record information from more than 75 million patients in 55 large healthcare organizations. We created four patient cohorts consisting of patients on 100, 200, and 400 mg of amiodarone per day, as well as a control group not taking amiodarone. Patients with a history of lung disease were excluded. The 4 cohorts were evaluated for the endpoints of pneumonitis (ICD-10 code J84), and for the subset of pulmonary fibrosis (ICD-10 code J84.10). RESULTS: We found that at a low dose of 100 mg of amiodarone, risk of pneumonitis increased almost 4-fold (2.163% vs 0.554%), and the risk of pulmonary fibrosis was 2.2-fold increased (0.801% vs 0.355%). Doses of 100 vs 200 mg had comparable pneumonitis but at 200 mg the fibrosis risk increased significantly. See Fig. 1. Figure 1. Rates of pneumonitis and fibrosis at different amiodarone doses CONCLUSIONS: Amiodarone-associated pneumonitis and pulmonary fibrosis occur in a dose-dependent fashion, but doses of 100 and 200 mg had similar overall risk. All three amiodarone cohorts had significant risk elevation compared to the control group. CLINICAL IMPLICATIONS: The use of amiodarone at any dose can be associated with significant pulmonary toxicity compared to patients that are not taking it. Practitioners should be aware of these risks and properly inform and monitor patients who receive amiodarone treatment. DISCLOSURE: Nothing to declare. KEYWORD: Amiodarone pulmonary toxicity

A multicenter retrospective cohort study on predicting the risk for amiodarone pulmonary toxicity

BackgroundAmiodarone is one of the most commonly used anti-arrhythmic agents. Amiodarone pulmonary toxicity is a potentially fatal adverse effect associated with amiodarone use. Previous studies on the epidemiology and risk factors for amiodarone pulmonary toxicity showed diverse results.MethodsA multicenter retrospective cohort study was conducted to identify clinic-epidemiologic markers associated with amiodarone pulmonary toxicity for development of a prediction rule. Patients taking amiodarone who were managed in 3 centres in Hong Kong from 2005 to 2015 were included in this study. Penalized logistic regression was used to model the outcome as it is rare.ResultsA total of 34 cases with amiodarone pulmonary toxicity were identified among 1786 patients taking amiodarone for at least 90 days from 2005 to 2015. The incidence of amiodarone pulmonary toxicity was estimated to be 1.9%. The risk factors for amiodarone pulmonary toxicity included advanced age (OR 1.047, 95% CI 1.010–1.085, p = 0.013), ventricular arrhythmia (OR 2.703, 95% CI 1.053–6.935, p = 0.039), underlying lung disease (OR 2.511, 95% CI 1.146–5.501, p = 0.021) and cumulative dose of amiodarone (OR 4.762, 95% CI 1.310–17.309 p = 0.018).ConclusionsThe incidence of amiodarone pulmonary toxicity in Chinese patients in Hong Kong is estimated to be 1.9% in this study. Age, underlying lung disease, ventricular arrhythmia and cumulative dose of amiodarone are associated with the development of amiodarone pulmonary toxicity. A prediction rule was developed to inform the risk of developing amiodarone pulmonary toxicity.

ACUTE AMIODARONE TOXICITY PRESENTING AS A LUNG MASS

TOPIC: Imaging TYPE: Medical Student/Resident Case Reports INTRODUCTION: We present a very uncommon case of lung mass developed within a month of starting amiodarone in an elderly male. CASE PRESENTATION: An 82-year-old male with a past medical history of end-stage renal disease on hemodialysis, congestive heart failure, diabetes mellitus, coronary artery disease, atrial fibrillation on amiodarone (200mg/day started a month ago) presented with dry cough and altered mental status for one day. On exam, he appeared tachypneic and drowsy with mild bibasilar lungs crackles. Laboratory findings included WBCs 4.8 K/UL, procalcitonin 0.3 ng/ML with sterile blood, urine, and respiratory cultures. Chest x-ray showed a new right upper lobe opacity with persistent bilateral lower lobes congestion (figure 1a). Computerized tomography (CT) of the chest showed dense, irregular soft tissue mass with high attenuation at the right apex and adjacent smaller spiculated nodules compatible with the deposition of amiodarone (figure 1b). Pulmonary and cardiology services advised stopping amiodarone with no further intervention. Bronchoscopy and biopsy were not done due to poor cardiac function. He was discharged to a nursing home after a significant improvement in his symptoms. On follow up after a year, patient had complete resolution of the symptoms. DISCUSSION: Amiodarone is a widely used iodinated antiarrhythmic agent with significant side effects due to its deposition in various organs including lungs (4-17%). Organ toxicity may occur from direct cytotoxicity or T-cell mediated hypersensitivity reaction. Though there is no safe dose, amiodarone associated pulmonary toxicity is mostly suspected in patients taking a daily dose of 400 mg for more than 2 months or any dose for more than 2 years [1,2]. Life-threatening and irreversible pulmonary toxicity is frequently associated with older age, longer duration of treatment, high dosage, and pre-existing lung disease. Diagnosis is made after the exclusion of other causes in patients presenting with nonproductive cough and/or dyspnea, new chest imaging findings, biopsy showing lipid-laden foamy macrophages. Once identified, significant improvement is noted with the withdrawal of the drug. Several patterns of lung inflammation including interstitial or organizing pneumonia, pleural effusion, nodule, or mass-like lesions are evident [3]. High density (> 80 Hounsfield units) lung nodules due to iodinated-amiodarone accumulation are appreciated more on high-resolution chest CT with typical findings frequently in the upper lobes as seen in our case [3]. The mainstay of treatment includes discontinuation of the drug with or without oral steroids. Patient education, regular follow up with chest imaging and use of lowest effective doses are key in reducing its adverse effects [3]. CONCLUSIONS: Given the condition is reversible and curable; the author wants to highlight the importance of early diagnosis of the case for a favorable prognosis. REFERENCE #1: Jessurun GA, Crijns HJ. Amiodarone pulmonary toxicity. BMJ. 1997;314(7081):619-620. doi:10.1136/bmj.314.7081.619 REFERENCE #2: Schwaiblmair, M., Berghaus, T., Haeckel, T. et al. Amiodarone-induced pulmonary toxicity: an under-recognized and severe adverse effect?. Clin Res Cardiol 99, 693–700 (2010). https://doi.org/10.1007/s00392-010-0181-3 REFERENCE #3: Jarand J, Lee A, Leigh R. Amiodaronoma: an unusual form of amiodarone-induced pulmonary toxicity. CMAJ. 2007;176(10):1411-1413. doi:10.1503/cmaj.061102 DISCLOSURES: No relevant relationships by Kabu Chawla, source=Web Response No relevant relationships by Resha Khanal, source=Web Response No relevant relationships by Sharad Oli, source=Web Response No relevant relationships by Shital Oli, source=Web Response No relevant relationships by Shaurya Sharma, source=Web Response

Amiodarone-induced organizing pneumonia mimicking COVID-19: a case report

BackgroundDifferential diagnosis of interstitial lung diseases (ILDs) during the COVID-19 pandemic is difficult, due to similarities in clinical and radiological presentation between COVID-19 and other ILDs on the one hand, and frequent false-negative swab results on the other. We describe a rare form of interstitial and organizing pneumonia resembling COVID-19, emphasizing some key aspects to focus on to get the right diagnosis and treat the patient properly.Case presentationA 76-year-old man presented with short breath and dry cough in the midst of the COVID-19 outbreak. He showed bilateral crackles and interstitial-alveolar opacities on X-ray, corresponding on computed tomography (CT) to extensive consolidations with air bronchograms, surrounded by ground glass opacities (GGO). Although his throat-and-nasopharyngeal swab tested negative, the picture was overall compatible with COVID-19. On the other hand, he showed subacute, rather than hyperacute, clinical onset; few and stable parenchymal consolidations, rather than patchy and rapidly evolving GGO; pleural and pericardial thickening, pleural effusion, and lymph node enlargement, usually absent in COVID-19; and peripheral eosinophilia, rather than lymphopenia, suggestive of hypersensitivity. In the past year, he had been taking amiodarone for a history of ventricular ectopic beats. CT scans, in fact, highlighted hyperattenuation areas suggestive of amiodarone pulmonary accumulation and toxicity. Bronchoalveolar lavage fluid (BALF) investigation confirmed the absence of coronavirus genome in the lower respiratory tract; conversely, high numbers of foamy macrophages, eosinophils, and cytotoxic T lymphocytes with low CD4/CD8 T-cell ratio were detected, confirming the hypothesis of amiodarone-induced cryptogenic organizing pneumonia. Timely discontinuation of amiodarone and initiation of steroid therapy led to resolution of respiratory symptoms, systemic inflammation, and radiographic opacities.ConclusionsA comprehensive analysis of medical and pharmacological history, clinical onset, radiologic details, and peripheral and BALF cellularity, is required for a correct differential diagnosis and management of ILDs in the COVID-19 era.

Acute Lung Injury Associated With Perioperative Amiodarone Therapy—Navigating the Challenges in Diagnosis and Management

AMIODARONE IS an antiarrhythmic that commonly is indicated in the cardiothoracic surgical intensive care unit for the management of atrial fibrillation. 1 Boons J Van Biesen S Fivez T et al. Mechanisms, prevention and treatment of atrial fibrillation after cardiac surgery: A narrative review [epub ahead of print]. J Cardiothorac Vasc Anesth. 2021; (Accessed June 14th 2021)https://doi.org/10.1053/j.jvca.2020.11.030 Abstract Full Text Full Text PDF PubMed Scopus (2) Google Scholar ,2 Zimetbaum P. Antiarrhythmic drug therapy for atrial fibrillation. Circulation. 2012; 125: 381-389 Crossref PubMed Scopus (153) Google Scholar Acute lung injury associated with amiodarone exposure is a rare but life-threatening syndrome that may complicate perioperative management. 3 Feduska ET Thoma BN Torjman MC et al. Acute amiodarone pulmonary toxicity. J Cardiothorac Vasc Anesth. 2021; 35: 1485-1494 Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar This case conference presents a complex clinical scenario that included acute pulmonary toxicity in the setting of amiodarone therapy for atrial fibrillation. The subsequent expert commentaries explore the diagnostic and management options for this pharmacologic complication in light of the recent literature.

THE ENIGMATIC CASE OF RECURRENT VENTILATORY DEPENDENT RESPIRATORY FAILURE

SESSION TITLE: Medical Student/Resident Lung Pathology SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Amiodarone, one of the most frequently prescribed antiarrhythmic medications in the United States, is associated with serious side effects including amiodarone-induced pulmonary toxicity (APT). One needs high suspicion to diagnose APT as the presentation can be misdiagnosed as pneumonia and heart failure. CASE PRESENTATION: A 74-year-old Caucasian female presented to the emergency department with progressively worsening shortness of breath and dry cough. She had a past medical history of left ventricular diastolic dysfunction, atrial fibrillation (on amiodarone 200mg/day), rheumatoid arthritis (RA), and 2 prior episodes of ventilatory dependent respiratory failure. On examination, the patient was hypoxemic on room air and had bibasilar lung crackles. BNP was elevated and Chest x-ray showed vascular congestion and perihilar infiltrates. The patient was placed on BiPAP for respiratory support and admitted to CCU for acute hypoxic respiratory failure secondary to CHF exacerbation. Diuretics did not improve the patient's condition and subsequent infectious workup was negative. CT chest showed patchy air-space consolidation and ground-glass opacities. Upon further interrogation, it was found that she was started on amiodarone 4 years back and multiple intubations for respiratory failure reported within the previous 2 years which responded to steroids. Amiodarone-induced pulmonary toxicity was diagnosed based on surgical lung biopsy revealing vacuolated foamy macrophages in alveolar pneumocytes, bronchial epithelial cells, and endothelial cells with diffuse interstitial pneumonitis and fibrosis. Amiodarone was discontinued and steroids were started at 1 mg/kg with a slow taper. The patient was subsequently extubated. DISCUSSION: Though APT can occur at any time after treatment is initiated, patients on a daily dose of 400 mg for >2 months or 200 mg daily for >2 years are at high risk. The reported incidence rate varies from 1.6 to 15% for daily doses of 400mg or less. The risk factors include > 60 years, high levels of des-ethyl metabolite, pre-existing lung disease, history of cardiothoracic surgery, use of iodinated contrast media, and/or use of high oxygen mixtures. Pathophysiology is direct cytotoxicity due to reactive oxygen species and the angiotensin enzyme system activation. In this patient, the diagnosis was delayed because the respiratory decompensation was attributed to heart failure. Despite adequate diuresis with central venous pressure of 6 cm H20 and negative infectious workup, her respiratory symptoms did not resolve. We were able to pinpoint the culprit behind her respiratory failure with a surgical lung biopsy and a history of amiodarone exposure. CONCLUSIONS: Strong index of suspicion for APT is necessary for prompt diagnosis in patients receiving amiodarone and presenting with respiratory symptoms. Reference #1: Schwaiblmair M, Berghaus T, Haeckel T, Wagner T, Von Scheidt W. Amiodarone-induced pulmonary toxicity: an under-recognizedand severe adverse effects?.Clin Res Cardiol 2010; 99:693–700 Reference #2: Kitaichi M. Differential diagnosis of bronchiolitis obliterans organizing pneumonia. Chest 1992; 102 (suppl.):44S-49S Reference #3: Marchlinski FE, Gansler TS, Waxman HL, Josephson ME. Amiodarone pulmonary toxicity. Ann Intern Med 1982; 97: 839-845. DISCLOSURES: No relevant relationships by Kristin Fless, source=Web Response No relevant relationships by Mashrutee Maharaul, source=Web Response No relevant relationships by SHREY SHAH, source=Web Response No relevant relationships by ARCHANA SREEKANTAN NAIR, source=Web Response

A CRAZY CAUSE OF CRAZY PAVING: AN UNUSUAL CASE OF AMIODARONE INDUCED LUNG TOXICITY

SESSION TITLE: Tuesday Fellows Case Report Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/22/2019 01:00 PM - 02:00 PM INTRODUCTION: Amiodarone induced pulmonary toxicity is a well described entity that can present with an array of histopathologic and radiologic findings. The exact incidence of amiodarone pulmonary toxicity is estimated to between 1-10% of patients [1]. Radiologic findings vary and can include ground glass opacities, interlobular septal thickening, pulmonary nodules, reticulation, fibrosis and honeycombing [2]. Isolated unilateral findings of amiodarone pulmonary toxicity, as described in the case below, is far less common and not well described. CASE PRESENTATION: A 78 year old man with non-ischemic cardiomyopathy and atrial fibrillation on amiodarone, presented with dyspnea on exertion and a non-productive cough. He was afebrile and hemodynamically stable but was hypoxemic with an oxygen saturation of 80% on ambient air. His chest X-ray at the time showed diffuse reticular opacifications on the right side. A follow up CT of the chest showed extensive interlobular septal thickening and ground glass opacities in a “Crazy Paving” pattern on the right side only. On physical examination, the patient had bilateral lower extremity pitting edema and an elevated NT-ProBnp of 6660. Given constellation of clinical and radiologic findings, there was suspicion for cardiogenic pulmonary edema and the patient was treated with diuresis. Despite maintenance of negative fluid balance, the patient had increasing oxygen requirements and did not improve clinically. His radiologic findings had persisted as well, and a decision was made to pursue a surgical lung biopsy. Pathology of the biopsy showed acute organizing process as well as lipid laden or “foamy” macrophages. A diagnosis of unilateral amiodarone lung toxicity was made. The patient was started on glucocorticoids, amiodarone was discontinued and the patients clinical status improved. DISCUSSION: This case highlights a unique presentation of amiodarone induced pulmonary toxicity in that the findings on CT were quite significant but only found unilaterally. The pathology findings, in particular the foamy macrophages, are consistent with the diagnosis of pulmonary toxicity from amiodarone 3. This highlights the importance of recognizing amiodarone induced lung toxicity as prompt cessation of the drug and if indicated steroid therapy can result in significant clinical improvement CONCLUSIONS: Although less common, unilateral amiodarone pulmonary toxicity can occur. If the clinical timeline, symptoms, and radiologic features are otherwise consistent, consideration should be given to amiodarone induced pulmonary toxicity even with unilateral findings. Reference #1: Jackevicius CA, Tom A, Essebag V, et al. Population-level incidence and risk factors for pulmonary toxicity associated with amiodarone. Am J Cardiol. 2011;108(5):705-710. https://doi.org/10.1016/j.amjcard.2011.04.024 Reference #2: Wolkove N, Baltzan M. Amiodarone pulmonary toxicity. Can Respir J. 2009;16(2):43-48. https://doi.org/10.1155/2009/282540 Reference #3: Schwaiblmair M, Berghaus T, Haeckel T, Wagner T, von Scheidt W. Amiodarone-induced pulmonary toxicity: an under-recognized and severe adverse effect? Clin Res Cardiol Off J Ger Card Soc. 2010;99(11):693-700. https://doi.org/10.1007/s00392-010-0181-3 DISCLOSURES: No relevant relationships by Erica Altschul, source=Web Response No relevant relationships by Nader Ishak Gabra, source=Web Response No relevant relationships by Oki Ishikawa, source=Web Response No relevant relationships by Omar Mahmoud, source=Web Response No relevant relationships by Bushra Mina, source=Web Response No relevant relationships by Maly Oron, source=Web Response No relevant relationships by Varun Shah, source=Web Response

Toxicidad pulmonar por amiodarona: no todo es insuficiencia cardiaca

Toxicidad pulmonar por amiodarona: no todo es insuficiencia cardiaca

UNUSUAL PRESENTATION OF AMIODARONE PULMONARY TOXICITY (APT) WITH MULTIPLE LUNG NODULES

SESSION TITLE: Diffuse Lung Disease 2 SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 pm - 02:15 pm INTRODUCTION: The incidence of amiodarone-induced pulmonary toxicity (APT) is 5%-15%. Diffuse interstitial infiltrate is the most common radiographic finding associated with APT. Fewer than 10 cases of multiple pulmonary nodules due to APT have been reported in the literature. We report a case of APT presenting as bilateral multiple pulmonary nodules. CASE PRESENTATION: A 59-year-old female presented to the pulmonary clinic for evaluation of multiple pulmonary nodules found incidentally on cardiac MRI. Patient’s complaints consisted of progressive DOE, persistent dry cough without any constitutional symptoms. A dedicated chest CT revealed multiple, various sized, bilateral pulmonary nodules. The nodules were predominantly in the lower lung zones. Her PMHx was significant for HFpEF, PAF on chronic amiodarone, and papillary thyroid cancer s/p left thyroidectomy one year ago. Given the history of malignancy and a high suspicion for metastatic disease, the patient was sent for VATS. Diagnostic lung wedge biopsies revealed an intense lymphoplasmacytic interstitial infiltrate and alveoli filled with macrophages with fine vacuolization on histopathologic examination. In some nodules, there were minor foci of organizing pneumonia. There was no evidence of granulomas or metastatic thyroid tumor. The finding was suggestive of inflammatory process most consistent with amiodarone toxicity. DISCUSSION: The clinical presentation of APT varies from non-productive cough, dyspnea on exertion to acute respiratory failure. Typically, pulmonary toxicity of amiodarone consists of diffuse alveolar damage, organizing pneumonia, hypersensitivity pneumonitis, and irreversible pulmonary fibrosis. Multiple lung nodules due to APT has been reported but rare in the literature. Nodular pulmonary disease is thought to be an inflammatory response to drug-induced phospholipid accumulation in the alveolar cells. Therefore, the lung nodules due to APT may be reversible and has a favorable outcome by discontinuing the drug. The use of corticosteroid also has been shown to be helpful. The diagnosis of APT is challenging due to the complex nature of clinical and radiographic findings. CONCLUSIONS: In summary, APT presenting with diffuse nodular pulmonary disease is rare; however, clinicians must be aware of the variability of clinical and radiographic finding of APT. APT should be considered in patients taking amiodarone present with new pulmonary nodules radiographically. Reference #1: 1. Morell, EB et al., 2005. Multiple pulmonary noduels and amiodarone. KL-6 as a new diagnostic tool. Rev Esp Cardiol 58(4):447-449 Reference #2: 2. Rodriguez-Garcia, JL et al., 2001. Pulmonary mass and multiple lung nodules mimicking a lung neoplasm as amiodarone-induced toxicity. Eur J Intern Med 12(4):372-376 Reference #3: 3. Wolkove, N et al., 2009. Amiodarone pulmonary toxicity. Can Respir J 16(2):43-48 DISCLOSURES: No relevant relationships by Michael Ayers, source=Web Response No relevant relationships by Debabrata Bandyopadhyay, source=Web Response No relevant relationships by Anna Kyu Chen, source=Web Response No relevant relationships by Md Islam, source=Web Response No relevant relationships by Matthew Stanton, source=Web Response

A Reason of Delayed Weaning in Critical Care: Amiodarone Pulmonary Toxicity

Amiodaron yogun bakimda sikca kullanilan bir antiaritmiktir ve ozellikle ventrikuler aritmilerin tedavisinde kullanilir. Ama bilinmelidir ki kimyasal yapisindan dolayi ilac dokularda birikebilir ve kardiyak, oftalmik, pulmoner ve norolojik yan etkiler olusturabilir. Amiodaron pulmoner toksisitesi (APT) ilacin hayati tehtit eden yan etkilerinden biridir ve solunum yetmezligi seklinde karsimiza cikabilir. Hastalik toraks bilgisayarli tomografisinde pnomonitis, buzlu cam opasiteleri, fibrosis bulgularini verir. Dispne ve oksuruk en sik gorulen belirtilerdir. Ancak tipki bizim olgumuzda oldugu gibi, entube ve mekanik ventilasyon uygulanan bir hastada APT’nin yarattigi solunum yetmezligi karsimiza sadece gecikmis ventilatorden ayrilma olarak cikabilir. En onemlisi hizli tani ve erken baslanan tedavi hastalarin mortalitesini azaltan en onemli faktorlerdir.

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

Introduction: Amiodarone pulmonary toxicity (APt) can be a diagnostic challenge to clinicians as it has no pathognomonic clinical, laboratory, radiological or histological features. It can potentially be fatal particularly in high risk patients. Amiodarone pulmonary toxicity is dose dependent, however, low dosages have also been reported to cause severe pulmonary disease. therefore, it should be considered in every patient with respiratory distress and on current or recent amiodarone therapy. case report: We report a case of APt with fatal outcome in a 49-year-old female taking the recommended doses of amiodarone with history of atrial fibrillation, rheumatic heart disease and pulmonary hypertension. Our patient was taking amiodarone for three years. she presented with severe respiratory distress necessitating endotracheal intubation. Despite treatment with systemic corticosteroids and broad spectrum antimicrobials, patient died in intensive care unit (IcU) after one month of admission. Amiodarone pulmonary toxicity is usually dosedependent, however, our patient was taking safe

Amiodarone Pulmonary Toxicity: A Case Report and Review of the Literature

Amiodarone, a common and efficacious antiarrhythmic agent, carries with it an array of serious side effects, most notably, amiodarone induced pulmonary toxicity, or APT. Patients typically present with dyspnea, and chest X-rays will show interstitial infiltrates. In severe cases, toxicity can lead to fibrosis and even respiratory failure. In this report, such effects are demonstrated based on the case of an 85 year old female who presented with multiple hospital admissions for multilobar pulmonary infiltrates and acute hypoxic respiratory failure, which did not respond to antibiotic therapy. She had, at the time of admission, been on amiodarone for over 2 years. The patient’s amiodarone was discontinued, and she was started on prednisone. The patient displayed a significant clinical and radiographic improvement within 4 weeks. In patients with pulmonary infiltrates of unclear etiology who are on amiodarone, APT should be considered in the differential diagnosis. At this time, no specific diagnostic test for APT exists, and therefore clinical management must rely on a combination of clues gleaned from the medical history, diagnostic imaging, and a systematic exclusion of other differential diagnoses. A high index of suspicion is required to make the diagnosis of amiodarone pulmonary toxicity.

Medical image of the week: acute amiodarone pulmonary toxicity

Medical image of the week: acute amiodarone pulmonary toxicity

NATURAL HISTORY OF PULMONARY FUNCTION IN PATIENTS MONITORED FOR RISK OF AMIODARONE PULMONARY TOXICITY

NATURAL HISTORY OF PULMONARY FUNCTION IN PATIENTS MONITORED FOR RISK OF AMIODARONE PULMONARY TOXICITY

Amiodarone pulmonary toxicity: a report on two cases

Amiodarone pulmonary toxicity: a report on two cases

Amiodarone pulmonary toxicity: a report on two cases

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.

Acute Amiodarone Pulmonary Toxicity after Drug Holiday: A Case Report and Review of the Literature.

Amiodarone is reported to cause a wide continuum of serious clinical effects. It is often challenging to detect Amiodarone-induced pulmonary toxicity (AIPT). Typically, the diagnosis is made based on the clinical settings and may be supported by histopathology results, if available. We describe a 57-year-old patient who developed severe rapidly progressive respiratory failure secondary to AIPT with acute bilateral infiltrates and nodular opacities on chest imaging. Interestingly, Amiodarone was discontinued 3 weeks prior to his presentation. He had normal cardiac filling pressures confirmed by echocardiography. To our knowledge, this is the first case of isolated acute lung injury induced by Amiodarone, three weeks after therapy cessation, with adequate clinical improvement after supportive management and high dose steroid therapy.

Acute Amiodarone Pulmonary Toxicity Following Lung Resection

Amiodarone is one of the most frequently prescribed antiarrhythmic agents. Despite its widespread use, it is associated with systemic side effects. Pulmonary toxicity, the most severe adverse effect of amiodarone, has usually been described in the context of chronic amiodarone use. We report a case of an 80-year-old male presenting acutely following right upper lung lobe resection for stage 1b adenocarcinoma. He developed atrial fibrillation on postoperative day four and received 12.5 g of amiodarone within a 12 day period. On presentation, he had new bilateral lung opacities and a 35% absolute decline in the predicted diffusion capacity for carbon monoxide. Pulmonary embolism was ruled out on chest computed tomography. Amiodarone was discontinued and prednisone was initiated. Despite initial improvement, he suffered from multiple hypoxemic episodes until his death in the fourth month. In a subset of patients undergoing thoracic surgery who are intubated and require high levels of oxygen, the risk of amiodarone lung toxicity increases and patients may present acutely.

Amiodarone and its Pulmonal Toxicity

Amiodarone is an antiarrhythmic agent commonly used to treat supraventricular and ventricular arrhythmias. The drug prevents the recurrence of life-threatening ventricular arrhythmias and produces a modest reduction of sudden deaths in high-risk patients. This drug is an iodine-containing compound that tends to accumulate in several organs, including the lungs. It has been associated with a variety of adverse events. Of these events, the most serious is amiodarone pulmonary toxicity. Although the incidence of this complication has decreased with the use of lower doses of amiodarone, it can occur with any dose. Because amiodarone is widely used, all clinicians should be vigilant of this possibility. Pulmonary toxicity usually manifests as an acute or subacute pneumonitis, typically with diffuse infiltrates on chest x-ray and high-resolution computed tomography. Other, more localized, forms of pulmonary toxicity may occur, including pleural disease, migratory infiltrates, and single or multiple nodules. With early detection, the prognosis is good. Most patients diagnosed promptly respond well to the withdrawal of amiodarone and the administration of corticosteroids, which are usually given for four to 12 months. It is important that physicians be familiar with amiodarone treatment guidelines and follow published recommendations for the monitoring of pulmonary as well as extrapulmonary adverse effects.