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==Background==
==Background==
Amiodarone is an antiarrhythmic agent commonly used to treat supraventricular and ventricular arrhythmias. This drug is an iodine- containing compound with a large volume of distribution that tends to accumulate in several organs, including the lungs.  Although the incidence of this complication has decreased with the use of lower doses of amiodarone, it can occur with any dose.
[[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===
*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==
*[[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==
{{Amiodarone adverse effects}}
{{Amiodarone adverse effects}}


[[Category:Pulm]][[Category:Cards]][[Category:Drugs]]
==Differential Diagnosis==
*[[Pneumonia]]
*[[CHF]]
*[[Pulmonary fibrosis]]
*[[Interstitial lung disease]]
 
==Evaluation==
[[File:Xray Amiodarone Lung toxicity.png|thumbnail]]
[[File:CT Amiodarone Lung Toxicity.png|thumbnail]]
*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==
*[[Amiodarone]]
 
==References==
<references/>
[[Category:Pulmonary]][[Category:Cardiology]][[Category:Pharmacology]]

Revisión actual - 20:12 24 abr 2024

Background

Lobes of the lung with related anatomy.
  • 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
    Amiodarone hyperpigmentation.jpg

Differential Diagnosis

Evaluation

Xray Amiodarone Lung toxicity.png
CT Amiodarone Lung Toxicity.png
  • 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

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

  1. ↑ Wolkove N, Baltzan M. Amiodarone pulmonary toxicity. Can Respir J. 2009;16(2):43-48.
  2. ↑ Martin WJ, Rosenow EC. Amiodarone pulmonary toxicity: Recognition and pathogenesis (Part 2). Chest 1988;93:1242-8.
  3. ↑ Jessurum GA, Crijns HJG. Amiodarone pulmonary toxicity. BMJ 1997;314:619-20.
  4. ↑ Dusman, RE, Stanton MS, Miles WM, Klein LS, Clinical features of amiodarone induced pulmonary toxicity. Circulation. 1990;82:51-59.
  5. ↑ Rosen's 8th Edition
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