Amiodarone pulmonary toxicity: Difference between revisions
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==Background== | ==Background== | ||
[[Amiodarone]] is an antiarrhythmic agent commonly used to treat supraventricular and ventricular arrhythmias | *[[Amiodarone]] is an antiarrhythmic agent commonly used to treat [[SVT|supraventricular]] and ventricular [[arrhythmias]] | ||
*Iodine-containing compound with large volume of distribution | |||
*Tends to accumulate in several organs, including lungs | |||
*Can occur with any dose, though incidence has decreased with use of lower doses<ref>Wolkove N, Baltzan M. Amiodarone pulmonary toxicity. Can Respir J. 2009;16(2):43-48.</ref> | |||
*Long half life of amiodarone--> effects can persist long after discontinuation | |||
===Pathophysiology=== | ===Pathophysiology=== | ||
[[File:Xray Amiodarone Lung toxicity.png|thumbnail]][[File:CT Amiodarone Lung Toxicity.png|thumbnail]] | [[File:Xray Amiodarone Lung toxicity.png|thumbnail]][[File:CT Amiodarone Lung Toxicity.png|thumbnail]] | ||
Amiodarone and | *Amiodarone and metabolites damage lungs<ref>Martin WJ, Rosenow EC. Amiodarone pulmonary toxicity: Recognition and pathogenesis (Part 2). Chest 1988;93:1242-8.</ref>: | ||
**Directly by cytotoxic effect, production of toxic O2 radicals<ref>Jessurum GA, Crijns HJG. Amiodarone pulmonary toxicity. BMJ 1997;314:619-20.</ref> | |||
**Indirectly via immunological reaction | |||
==Clinical Features== | ==Clinical Features== | ||
*Dyspnea, particularly with exertion | *[[Dyspnea]], particularly with exertion | ||
*Cough | *[[Cough]] | ||
*Low grade fever | *Low grade [[fever]] | ||
*Less common features include: nausea, generalized fatigue, weight loss, pleuritic chest pain <ref>Dusman, RE, Stanton MS, Miles WM, Klein LS, Clinical features of amiodarone induced pulmonary toxicity. Circulation. 1990;82:51-59.</ref> | *Less common features include: nausea, generalized fatigue, weight loss, pleuritic chest pain <ref>Dusman, RE, Stanton MS, Miles WM, Klein LS, Clinical features of amiodarone induced pulmonary toxicity. Circulation. 1990;82:51-59.</ref> | ||
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==Evaluation== | ==Evaluation== | ||
*Often clinical diagnosis based on history of amiodarone use, presence of ground glass opacities on CT, and exclusion of alternate diagnoses (such as pneumonia) | |||
*CT chest: | |||
**Ground glass opacities with interstitial or alveolar inflitrations and lung nodules | |||
*Ground glass opacities with interstitial or alveolar inflitrations and lung nodules | **Pleural thickening and pleural effusions | ||
*Pleural thickening and pleural effusions | |||
==Management== | ==Management== | ||
* | *Discontinue amiodarone | ||
* | *[[Steroids]] | ||
==Disposition== | ==Disposition== | ||
Revision as of 16:53, 19 September 2019
Background
- Amiodarone is an antiarrhythmic agent commonly used to treat supraventricular and ventricular arrhythmias
- Iodine-containing compound with large volume of distribution
- Tends to accumulate in several organs, including lungs
- Can occur with any dose, though incidence has decreased with use of lower doses[1]
- Long half life of amiodarone--> effects can persist long after discontinuation
Pathophysiology
- Amiodarone and metabolites damage lungs[2]:
- Directly by cytotoxic effect, production of toxic O2 radicals[3]
- Indirectly via immunological reaction
Clinical Features
- Dyspnea, particularly with exertion
- Cough
- Low grade fever
- Less common features include: nausea, generalized fatigue, weight loss, pleuritic chest pain [4]
Differential Diagnosis
Amiodarone Adverse effects
Amiodarone Adverse Effects
- Bradycardia
- Hypotension with older solvent-based formulation. Uncommon with newer aqueous formulation.
- Prolonged QT
- Thyrotoxicosis[5]
- Between 5-20% of patients treated with amiodarone have thyrotoxicosis (higher in areas of iodine deficiency)
- Iodine-induced hyperthyroidism
- It is thought that the iodine load may unmask hyperthyroidism in patients with multinodular goiter and subclinical Graves’ disease
- Drug-induced destructive thyroiditis
- More commonly, the cytotoxic effects of amiodarone destroy thyroid cells, resulting in a release of preformed hormone.
- Amiodarone pulmonary toxicity
- Hyperpigmentation rash
Evaluation
- Often clinical diagnosis based on history of amiodarone use, presence of ground glass opacities on CT, and exclusion of alternate diagnoses (such as pneumonia)
- CT chest:
- Ground glass opacities with interstitial or alveolar inflitrations and lung nodules
- Pleural thickening and pleural effusions
Management
- Discontinue amiodarone
- Steroids
Disposition
- Admit the patient for rule out of an infectious etiology.
- Consult with the patient's pulmonologist or cardiologist for recommendations on stopping the amiodarone
See Also
References
- ↑ Wolkove N, Baltzan M. Amiodarone pulmonary toxicity. Can Respir J. 2009;16(2):43-48.
- ↑ Martin WJ, Rosenow EC. Amiodarone pulmonary toxicity: Recognition and pathogenesis (Part 2). Chest 1988;93:1242-8.
- ↑ Jessurum GA, Crijns HJG. Amiodarone pulmonary toxicity. BMJ 1997;314:619-20.
- ↑ Dusman, RE, Stanton MS, Miles WM, Klein LS, Clinical features of amiodarone induced pulmonary toxicity. Circulation. 1990;82:51-59.
- ↑ Rosen's 8th Edition