Author Affiliations: Section of Ophthalmology and Visual Science, University of Chicago Pritzker School of Medicine (Drs Afshar, Hariprasad, and Sheth) and Department of Ophthalmology, Northwestern University Feinberg School of Medicine (Dr Jampol), Chicago, and Division of Ophthalmology, NorthShore University HealthSystem, Glenview (Dr Sheth), Illinois.
West Nile virus (WNV) appeared in the United States in 1999; ocular sequela have been documented since 2003.1- 3 Associated chorioretinitis, ischemic vasculitis, retinal hemorrhages, and choroidal neovascularization have all been reported.3- 5
A 66-year-old man residing in a northern suburb of Chicago, Illinois, had increasing fatigue, severe headaches, confusion, and fevers for 4 days. Enzyme-linked immunosorbent assay of his cerebrospinal fluid was positive for WNV-specific IgM. The patient received supportive therapy for 2 weeks.
Two weeks after discharge, the patient had profound vision loss in his right eye. Visual acuity was counting fingers at 3 ft OD (no improvement with pinhole) and 20/20 OS with correction. Anterior segment examination showed a posterior subcapsular cataract in the right eye. Fundus examination showed absence of vitreous cells in each eye. In the right eye, vasculitis, intraretinal hemorrhages, and areas of nonperfusion were seen (Figure 1A and B). In the left eye, linear streaks of chorioretinal scarring were seen, with no vasculitis or retinal hemorrhages (Figure 1D and E). Fluorescein angiography confirmed areas of nonperfusion in the right macula (Figure 1C) and linear streaklike hyperfluorescent scars along the arcades of the left eye (Figure 1F). Spectral-domain optical coherence tomography (OCT) showed a central thickness of 415 μm OD (Figure 2A); findings from OCT of the left eye were unremarkable.
Figure 1. Fundus photograph (A), red-free photograph (B), and fluorescein angiogram (C) of the right eye and fundus photograph (D), red-free photograph (E), and fluorescein angiogram (F) of the left eye at the initial visit.
Figure 2. Spectral-domain optical coherence tomographic images of the right eye at the initial visit (A), 2 weeks after the initial visit (B), and 7 months after the initial visit (C). T indicates temporal; N, nasal; S, superior; and I, inferior.
On routine eye examination for type 2 diabetes 5 months prior to hospitalization, visual acuity was 20/40 OD and 20/20 OS. There was no diabetic retinopathy, and diabetes was controlled with metformin hydrochloride (the hemoglobin A1c level was 6.8% of total hemoglobin 6 months prior to hospitalization [to convert to proportion of total hemoglobin, multiply by 0.01]). Visual acuity of 20/40 OD was attributed to the mild cataract.
The macular edema was treated with topical nepafenac in the right eye, 4 times daily. The patient returned 2 weeks later; OCT showed worsening macular edema with a thickness of 502 μm centrally (Figure 2B). Bevacizumab (1.25 mg) was injected intravitreously into the right eye. Two weeks later, visual acuity had improved to 20/150 OD and the OCT central thickness was 346 μm. During the next 2 months, macular edema in the right eye remained stable on clinical examination and OCT; the patient underwent cataract extraction with a monofocal intraocular lens implant.
At the last follow-up, 7 months after the initial hospitalization, visual acuity was 20/80 OD and 20/20 OS. On dilated retinal examination, vascular sheathing was seen along the right superior arcade; macular edema and hemorrhage in the right eye had resolved. The left eye showed old, inactive pigmented streaks of chorioretinal scarring along the arcades. Spectral-domain OCT showed the right macula to have a normal thickness of 301 μm centrally (Figure 2C).
To our knowledge, this is the first case of WNV chorioretinitis with macular edema and the first use of intravitreous bevacizumab to treat it. Despite the patient's history of diabetes, the patient had no diabetic retinopathy on funduscopic examination 5 months prior to acquiring WNV. The course of WNV infection, onset of visual symptoms, and detection of macular edema strongly suggest that the macular edema was the result of increased vascular permeability from WNV chorioretinitis and retinal vasculitis. Diabetes likely predisposes patients with WNV to occlusive vasculitis in the brain and retina,3 and diabetes has been implicated as an independent risk factor in WNV-related death.6 While the macular edema may have regressed on its own, the prompt resolution of the macular edema and improvement in visual acuity that followed shortly after use of bevacizumab suggest a potential use for the drug in this condition that warrants further investigation.
Correspondence: Dr Sheth, NorthShore University Eye Center, 2050 Pfingsten Rd, Ste 280, Glenview, IL 60026 (firstname.lastname@example.org).
Author Contributions: Dr Sheth had full access to all of the data in the study and takes responsibility for the integrity of the data and accuracy of the data analysis.
Financial Disclosure: Dr Hariprasad has been a consultant for Alcon, Allergan, Genentech, Bayer, OD-OS, Optos, and Regeneron.
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