May 2004
Volume 45, Issue 13
ARVO Annual Meeting Abstract  |   May 2004
The Clinical Spectrum of Amiodarone Induced Optic Neuropathy
Author Affiliations & Notes
  • L.N. Johnson
    Mason Eye Institute, Univ of Missouri–Columbia, Columbia, MO
  • G.B. Krohel
    Ophthalmology, Albany Medical Center, Troy, NY
  • E.R. Thomas
    Mason Eye Institute, Univ of Missouri–Columbia, Columbia, MO
  • Footnotes
    Commercial Relationships  L.N. Johnson, None; G.B. Krohel, None; E.R. Thomas, None.
  • Footnotes
    Support  Research to Prevent Blindness, Inc.
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 1613. doi:
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      L.N. Johnson, G.B. Krohel, E.R. Thomas; The Clinical Spectrum of Amiodarone Induced Optic Neuropathy . Invest. Ophthalmol. Vis. Sci. 2004;45(13):1613.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose:To describe the clinical spectrum of amiodarone–induced optic neuropathy, since early recognition of this disorder is important as permanent visual loss can occur. Methods:Observational cases series involving two neuro–ophthalmology clinical practices and Medline literature review of patients with optic neuropathy in association with amiodarone use. Main outcome measure is an assessment of the clinical presentations and outcomes of patients with amiodarone–induced optic neuropathy. Results:Of 55 cases, the median time interval for onset of amiodarone–induced optic neuropathy was 4 months after initiating amiodarone; 88% of cases occurred within 12 months. Seven (13%) patients were asymptomatic. Thirty–two (58%) patients reported unilateral visual loss, yet 56% of these patients had simultaneous bilateral optic nerve involvement. Twenty–two (40%) patients presented with sudden visual loss, and 26 (47%) had insidious loss of vision. Visual acuity at presentation ranged from 20/15 to light perception;10 (18%) patients had legal blindness with visual acuity of 20/200 or worse. Visual field loss was present in 91% of cases. Color vision loss was present in 8 (40%) of 20 cases. Optic disc edema was present in 85% of cases, while 8 (15%) patients had retrobulbar optic neuropathy, without evidence of disc edema. Optic disc edema resolved over a median time of 3 months. Five patients had raised intracranial pressure on lumbar puncture. Conclusions:Amiodarone–induced optic neuropathy can be classified into 5 distinct forms: insidious–onset (43%); acute–onset (28%); retrobulbar (13%), raised intracranial pressure (8%), and delayed–progressive onset (8%) subtypes. Most cases of optic neuropathy commenced within 12 months of initiating amiodarone, and over 10% of patients have no symptoms at the onset. In contrast to visual acuity, visual field loss generally is permanent, despite cessation of amiodarone. Early detection and discontinuation of amiodarone could affect visual prognosis.

Keywords: neuro–ophthalmology: optic nerve • visual impairment: neuro–ophthalmological disease • clinical (human) or epidemiologic studies: outcomes/complications 

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