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 | [[File:Lung and diaphragm.jpg|thumb|Lobes of the lung with related anatomy.]] | ||
*[[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=== | ||
*Amiodarone and metabolites damage lungs:<ref>Martin WJ, Rosenow EC. Amiodarone pulmonary toxicity: Recognition and pathogenesis (Part 2). Chest 1988;93:1242-8.</ref> | |||
Amiodarone and | **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== | |||
*[[Dyspnea]], particularly with exertion | |||
*[[Cough]] | |||
*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> | |||
{{Amiodarone adverse effects}} | |||
==Differential Diagnosis== | ==Differential Diagnosis== | ||
| Line 11: | Line 25: | ||
*[[Pulmonary fibrosis]] | *[[Pulmonary fibrosis]] | ||
*[[Interstitial lung disease]] | *[[Interstitial lung disease]] | ||
== | ==Evaluation== | ||
[[File:Xray Amiodarone Lung toxicity.png|thumbnail]] | |||
[[File:CT Amiodarone Lung Toxicity.png|thumbnail]] | |||
*Ground glass opacities with interstitial or alveolar inflitrations and lung nodules | *Often clinical diagnosis based on history of amiodarone use, presence of ground glass opacities on CT, and exclusion of alternate diagnoses (such as pneumonia) | ||
*Pleural thickening and pleural effusions | *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. | *Admit the patient for rule out of an infectious etiology. | ||
*Consult with the patient's pulmonologist or cardiologist for recommendations on stopping the amiodarone | *Consult with the patient's pulmonologist or cardiologist for recommendations on stopping the amiodarone | ||
==See Also== | |||
*[[Amiodarone]] | |||
==References== | ==References== | ||
<references/> | <references/> | ||
[[Category: | [[Category:Pulmonary]][[Category:Cardiology]][[Category:Pharmacology]] | ||
Latest revision as of 20:12, 24 April 2024
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]
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
Differential Diagnosis
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