To describe patterns of hypoautofluorescence in eyes with neovascular age-related macular degeneration occurring after subretinal hemorrhage.
This was a retrospective descriptive analysis of neovascular age-related macular degeneration eyes presenting with subretinal hemorrhage over the last 5 years that underwent serial multimodal imaging. A review of color fundus photographs, fundus autofluorescence, near-infrared reflectance, and optical coherence tomography was performed at baseline and all available follow-up visits to document the course and evolution of subretinal hemorrhage in these eyes.
Eleven eyes of 10 patients (9 female, 1 male; mean age: 84.1 years, range: 72–99 years) with a mean follow-up of 19.8 months (range: 3–68 months) were included. Color fundus photographs showed subretinal hemorrhage that resolved over a mean of 5.5 months. During and after hemorrhage resolution, all eyes showed hypoautofluorescence, which appeared distinct from that due to retinal pigment epithelium loss. Discrete multifocal punctate hyperpigmented lesions were observed in 90% of eyes and were markedly hypoautofluorescent, producing a speckled pattern on fundus autofluorescence.
Areas of hypoautofluorescence in the absence of retinal pigment epithelium atrophy, often with a speckled pattern, delineate areas of prior subretinal hemorrhage long after its resolution in patients with neovascular age-related macular degeneration. Potential mechanisms for the development of this pattern are proposed.
This study describes a pattern of speckled hypoautofluorescence without retinal pigment epithelium atrophy occurring in eyes with neovascular age-related macular degeneration after resolution of subretinal hemorrhage. We document the course and evolution of subretinal hemorrhage in treated age-related macular degeneration with multimodal imaging using color fundus photographs, fundus autofluorescence, near-infrared reflectance, and optical coherence tomography.
*Vitreous Retina Macula Consultants of New York, New York, New York;
†LuEsther T. Mertz Retinal Research Center, Manhattan Eye, Ear and Throat Hospital, New York, New York;
‡Department of Ophthalmology, Edward S Harkness Eye Institute, Columbia University College of Physicians and Surgeons, New York, New York;
§Department of Ophthalmology, New York University School of Medicine, New York, New York;
¶Unit of Macula, Oftalvist Clinic, Valencia, Spain;
**F.M. Kirby Center for Molecular Ophthalmology, Scheie Eye Institute, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania; and
††Department of Ophthalmology and Visual Sciences, University of Alabama at Birmingham, School of Medicine, Birmingham, Alabama.
Reprint requests: K. Bailey Freund, MD, Vitreous Retina Macula Consultants of New York, 460 Park Avenue, New York, NY 10022; e-mail: email@example.com
Supported by the LuEsther T. Mertz Retinal Research Center, Manhattan Eye, Ear, and Throat Hospital, New York, NY, the Macula Foundation Inc, New York, NY, NIH R01 EY015240 (J.L.D.), NIH R01 R01EY027948 (CAC), R01EY015520 (CAC) and institutional support to the Department of Ophthalmology at UAB from EyeSight Foundation of Alabama and Research to Prevent Blindness. The funding organizations had no role in the design or execution of this research.
R. Dolz-Marco receives research support from Alcon, Genentech, Heidelberg Engineering, Novartis, Hoffman LaRoche, and Thea. K. B. Freund is consultant for Optovue, Zeiss, Heidelberg Engineering, and Novartis; he receives research support from Hoffman LaRoche. C. A. Curcio receives research support from Hoffman LaRoche and Heidelberg Engineering. The remaining authors have no financial/conflicting interests to disclose.