April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Peripapillary Atrophy in Chronic Vogt-Koyanagi-Harada Disease
Author Affiliations & Notes
  • Pooja Bhat
    Department of Ophthalmology, Northwestern Memorial Hospital, Feinberg School of Medicine, Chicago, IL
  • Anjali Parekh
    Department of Ophthalmology, Northwestern Memorial Hospital, Feinberg School of Medicine, Chicago, IL
  • Lana M Rifkin
    Department of Ophthalmology, Northwestern Memorial Hospital, Feinberg School of Medicine, Chicago, IL
  • Debra A Goldstein
    Department of Ophthalmology, Northwestern Memorial Hospital, Feinberg School of Medicine, Chicago, IL
  • Footnotes
    Commercial Relationships Pooja Bhat, None; Anjali Parekh, None; Lana Rifkin, None; Debra Goldstein, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 5315. doi:https://doi.org/
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      Pooja Bhat, Anjali Parekh, Lana M Rifkin, Debra A Goldstein; Peripapillary Atrophy in Chronic Vogt-Koyanagi-Harada Disease. Invest. Ophthalmol. Vis. Sci. 2014;55(13):5315. doi: https://doi.org/.

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

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Abstract
 
Purpose
 

Vogt-Koyanagi-Harada disease (VKH) is characterized by granulomatous panuveitis, exudative retinal detachment, papillitis in the acute phase and sunset glow fundus, retinal pigment epithelial migration, and atrophic chorioretinal lesions during the chronic convalescent phase. The chronic phase may have peripapillary atrophy (PPA) and neuroretinal rim (NRR) thinning. Patients with VKH with greater choroidal thickness at presentation are at higher risk of developing PPA (1). Most patients with non-glaucomatous optic neuropathies do not exhibit NRR thinning, optic disc cupping and PPA except for arteritic- anterior ischemic optic neuropathy (A-AION) (2). The purpose of this study is to evaluate optic nerve head changes in chronic VKH compared to glaucomatous optic neuropathy.

 
Methods
 

Retrospective review of patients with chronic VKH, including demographics, NRR status and PPA as assessed by disc photos, and visual fields.

 
Results
 

30 eyes of 15 patients were included. Mean age was 45 years (15-70), 11 were female. 4 were Hispanic, 2 African American, and 9 Caucasian. 26 eyes revealed PPA. Of these 26 eyes, 15 had NRR loss. PPA was not greater in areas of rim thinning. Visual fields were available in 11 eyes with PPA. Only 5 had typical glaucomatous field loss corresponding to NRR loss. The other 6 had field changes inconsistent with NRR loss and cupping.

 
Conclusions
 

To date, NRR loss and PPA have been described only in glaucomatous optic neuropathies and in A-AION. In this study, 87% of eyes with chronic VKH exhibited PPA. Of these eyes, only 57% exhibited significant NRR loss and >50% of eyes with PPA had field changes that did not correspond to NRR loss. These findings are important, as optic neuropathy in VKH may be secondary to an inflammatory vascular event akin to A-AION, different from mechanical and vascular mechanisms postulated in the pathogenesis of glaucomatous optic neuropathy. References 1. Nakayama M, Keino H, Okada AA, Watanabe T, Taki W, Inoue M, Hirakata A Enhanced depth imaging optical coherence tomography of the choroid in Vogt-Koyanagi-Harada disease. Retina 2012 Nov-Dec;32 (10):2061-2069. 2. Hayreh SS, Jonas JB (2001) Optic disc morphology after arteritic anterior ischemic optic neuropathy. Ophthalmology 108 (9):1586-1594.

 
Keywords: 432 autoimmune disease • 627 optic disc • 557 inflammation  
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