Figure. Progression of an acquired vitelliform lesion (AVL) to a full-thickness macular hole. A, Color photograph of the right eye at the initial visit showing an AVL. B, Corresponding fundus autofluorescence image showing hyperautofluorescence of the AVL. C, Color photograph of the right eye 15 months following the initial visit, showing resolution of the AVL and the appearance of a macular hole. D, Corresponding fundus autofluorescence image showing hypoautofluorescence of the regressed AVL. Eye-tracked spectral-domain optical coherence tomography of the right eye at the initial visit with vitelliform material in the subretinal space and focal thickening of the retinal pigment epithelium (arrow) as shown in previous studies1 (E) and at 5 months (F), 9 months (G), 11 months (H), and 15 months (I) following the initial visit, showing the evolution of the AVL (E) to foveal atrophy (G) and ultimately to a full-thickness macular hole. Visual acuity was 20/50 at the initial visit (E), 20/60 in follow-up (F-H), and 20/80 when the macular hole appeared (I).
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Goldberg N, Freund KB. Progression of an Acquired Vitelliform Lesion to a Full-Thickness Macular Hole Documented by Eye-Tracked Spectral-Domain Optical Coherence Tomography. Arch Ophthalmol. 2012;130(9):1221–1223. doi:10.1001/archophthalmol.2012.407
Author Affiliations: Vitreous Retina Macula Consultants of New York (Drs Goldberg and Freund) and Department of Ophthalmology, New York University Medical Center (Dr Freund), New York.
Vitelliform lesions (VLs), classically seen in young patients in autosomal dominant Best disease, are also seen as acquired lesions in entities such as adult-onset foveomacular vitelliform dystrophy, cuticular drusen, and central serous chorioretinopathy. These lesions appear as round yellowish deposits of material exhibiting hyperautofluorescence with fundus autofluorescence imaging. Spectral-domain optical coherence tomography (SD-OCT) shows hyperreflective material in the subretinal space, often with focal thickening at the level of the retinal pigment epithelium.1 The natural course of these lesions is often a gradual reduction in lesion size with fragmentation and resorption of the vitelliform material and eventual photoreceptor disruption and atrophy with accompanying hypoautofluorescence.2 A few studies have shown the development of a macular hole (MH) in eyes with VLs due to Best disease or adult-onset foveomacular vitelliform dystrophy.3,4 Herein, we report the first case to our knowledge showing with eye-tracked SD-OCT the evolution of an acquired VL (AVL) to a full-thickness MH in the absence of vitreomacular traction or an epiretinal membrane.
A 69-year-old man, with no significant ophthalmic or family history, reported progressive distortion in both eyes. Visual acuity was 20/50 OD and 20/40 OS. Slitlamp examination revealed mild cataracts. Funduscopic examination showed bilateral AVLs that were hyperautofluorescent on fundus autofluorescence imaging. A posterior vitreous detachment was noted. The SD-OCT findings confirmed the presence of vitelliform material in the subretinal space, without vitreomacular traction or an epiretinal membrane (Figure).
Over the following 11 months, the AVL in the right eye was noted to decrease in size, with new retinal pigment epithelial changes and progressive foveal atrophy noted on SD-OCT. Visual acuity was 20/60 at that time. Fifteen months following the initial visit, visual acuity was 20/80 OD and a full-thickness MH was noted (Figure).
First described in association with adult-onset foveomacular vitelliform dystrophy,5 AVLs have been the subject of several studies using multimodal imaging to define the location and morphology of these lesions. The material composing the VL has been shown to occupy the space between the external limiting membrane and retinal pigment epithelium and is believed to represent unphagocytized photoreceptor outer segments and pigmented cells laden with melanin and melanolipofuscin granules. The chronic separation of photoreceptors from the retinal pigment epithelium is the presumed mechanism for progressive outer retinal atrophy and the accompanying gradual decline in visual acuity. Formation of MHs has been reported in eyes with VLs and is thought to result from progressive retinal thinning rather than vitreofoveal traction related to posterior vitreous detachment formation, which accounts for the majority of MHs.1,6 With the enhanced resolution and eye-tracking ability of SD-OCT, the natural course of the AVL to foveal atrophy and ultimately to a full-thickness MH can be documented.
Correspondence: Dr Freund, Vitreous Retina Macula Consultants of New York, 460 Park Ave, Fifth Floor, New York, NY 10022 (firstname.lastname@example.org).
Financial Disclosure: None reported.
Funding/Support: This work was supported by the Macula Foundation, Inc, New York, New York.