Amiodarone induced optic neuropathy

Nagra, Parveen K.; Foroozan, Rod; Savino, Peter J.; Castillo, I.G.; Sergott, Robert C.

doi:10.1136/bjo.87.4.420

Cited by 51 publications

(28 citation statements)

References 11 publications

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“…19 Optic disc oedema was present in 85% of cases. Optic nerve swelling tends to persist for several months 18,20 and resolves more slowly than the 2-to 6-week period seen in typical nonarteritic anterior ischaemic optic neuropathy (NAION). The disc oedema may persist even after discontinuing amiodarone, since its half-life is up to 100 days.…”

Section: Clinical Manifestationsmentioning

confidence: 99%

“…18 Nagra et al suggested that with discontinuing amiodarone, slow resolution of optic disc swelling occurs and visual function improves in some patients. 20 Passman et al have reviewed 296 cases with AAON. They found that following amiodarone discontinuation, 58% of patients had improved visual acuity, 21% were unchanged, and 21% had further visual impairment.…”

Section: Treatmentmentioning

confidence: 99%

“…For an optic neuropathy patient with following clinical characteristics, we should consider the diagnosis of AAON: (1) a clear history of taking amiodarone, (2) insidious onset, (3) slow progression, (4) bilateral visual loss, (5) protracted disc swelling. 18,20 Moreover, if the patients didn't have a small crowded optic disc (disc at risk) classically seen in NAION, clinicians should be vigilant for the possibility of AAON. 25 Amiodaone-associated optic neuropathy (AAON) and non-arteritic anterior ischaemic optic neuropathy (NAION) Despite the obscure causal relationship, we still try to differentiate clinically between AAON and NAION in each individual case, since the treatment and visual outcome may differ for these two entities.…”

Section: Differential Diagnosismentioning

confidence: 99%

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Amiodarone-Associated Optic Neuropathy: Clinical Review

Wang

Cheng

2016

Neuro-Ophthalmology

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Amiodarone, an antiarrhythmic agent, has been associated with visual loss secondary to optic neuropathy. The reported mean duration of amiodarone use before visual loss is about 9 months. Patients receiving amiodarone have a 2-fold increased risk of developing optic neuropathy, especially in males and possibly in patients with longer duration of treatment. Amiodarone-associated optic neuropathy is characterised by an insidious onset, slow progression, bilateral simultaneous visual loss, and protracted disc swelling. After discontinuing amiodarone use, visual acuity and visual field deficits tend to improve or stabilise in most patients, with about 20% of the patients getting worse. ARTICLE HISTORY

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Section: Clinical Manifestationsmentioning

confidence: 99%

Section: Treatmentmentioning

confidence: 99%

Section: Differential Diagnosismentioning

confidence: 99%

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Amiodarone-Associated Optic Neuropathy: Clinical Review

Wang

Cheng

2016

Neuro-Ophthalmology

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“…There were apparently degenerated nerve fibers distributed among the apparently normal ones. This could explain the findings of Nagra et al (2003) who described visual field defects as a result of AD-induced optic neuropathy.…”

Section: Discussionmentioning

confidence: 71%

“…The widespread use of this drug has increased after approval by the American Heart Association for its use in advanced cardiac life support protocols (Nagra et al, 2003). Amiodarone is considered the most effective anti-arrhythmic drug and is widely prescribed (Zimetbaum, 2007).…”

Section: Introductionmentioning

confidence: 99%

Can L-Carnitine Protect Against Amiodarone-Induced Optic Neuropathy in Rabbits?

Mostafa

EL–Shafei

2011

The Egyptian Journal of Anatomy

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Background: Amiodarone (AD), the most effective anti-arrhythmic drug, has been reported to cause optic neuropathy, which may result in permanent visual loss. Aim of the work: The current study aimed to clarify the effect of amiodarone administration on the structure of optic nerve and to evaluate the role of L-Carnitine (LC) in protection against such effect. Materials and Methods: This study was carried out on 20 male rabbits divided into five equal groups (four rabbits each). Group I (control group) received no treatment. Group II received saline. Group III received LC. Group IV received AD. Group V received both LC and AD. Animals of treated Groups (II-V) received daily dose for four weeks, then animals of all groups were sacrificed one day after the last dose. Their optic nerves were subjected to light microscopic, electron microscopic and morphometric studies. Results: After AD administration, there was a significant decrease in the number of total and apparently normal nerve fibers while the apparently degenerated ones were increased. There were areas of thickened perineurium. The myelin sheath showed areas of loss of lamellar pattern, splitting or thickening. Many axons appeared with areas of shrinkage and separation from the myelin sheath. The axoplasm of some fibers looked with inclusion bodies or with disrupted organelles. The astrocytes, oligodendrocytes and microglia cells were increased in number. Some oligodendrocytes appeared degenerated. Some oligodendrocytes and astrocytes looked with swollen mitochondria with disrupted cristae. Concomitant administration of LC with AD has minimized the AD-induced effects on the optic nerve. Conclusion: It is concluded that AD administration caused several degenerative effects in the optic nerve. These degenerative effects were greatly ameliorated by concomitant administration of LC. Thus, it is recommended to use LC with AD for treatment of cardiac arrhythmias.

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