The adverse effects of sun viewing have been known for centuries, with the earliest documentation of visual damage reported in the 17th century.1 Although most described cases of solar retinopathy resulted from eclipse viewing, solar retinopathy has also been reported after sun gazing in the setting of religious events, ritualistic practices, psychiatric illnesses, and the consumption of hallucinogens.1 Multimodal imaging (MMI) of acute solar retinopathy has been recently described by Wu et al.2 To our knowledge, however, long-term follow-up with MMI has not been reported. We present MMI analysis of a patient with solar retinopathy followed in our clinic for a decade to enhance our understanding of the disease course.
A 48-year-old black male with hypertension, anxiety, and schizophrenia presented with chronic bilateral central scotomas. He had a history of recreational sungazing while outdoors practicing martial arts and boating. Best-corrected visual acuity (BCVA) was 20/20-1 in the right eye (OD) and 20/40 in the left eye (OS), with a normal anterior segment examination. Funduscopic examination revealed a blunted foveal reflex OD (Figure 1a), and a small yellow-white foveal lesion OS (Figure 1b). On spectral-domain optical coherence tomography (SD-OCT), there was subfoveal loss of the ellipsoid zone (EZ) and interdigitation zone (IZ) bilaterally (Figures 2a and 2b). Foveal retinal pigment epithelium (RPE) thinning and choroidal hypertransmission were present OS (Figure 2b). Fluorescein angiography (FA) showed hyperfluorescent foveal window defects bilaterally (Figures 3a–3d).
Fundus photos at presentation showing a blunted foveal reflex in the right eye (a) and a circular, yellow-white lesion in the fovea of the left eye (b). Fundus photos 10 years after presentation show yellow, well-circumscribed lesions in the right (c) and left eyes (d), more prominent in the latter.
Spectral-domain optical coherence tomography (SD-OCT) at presentation showing loss of the ellipsoid zone (EZ) and interdigitation zone (IZ) in the right (a) and left eyes (b). There is attenuation of the retinal pigment epithelium (RPE)/Bruch's membrane complex in the left eye demonstrated by the choroidal hypertransmission (b). SD-OCT photos 10 years after presentation showing mild progression of EZ and IZ loss in the right eye (c) and stable loss of the EZ and IZ in the left eye (d). There is progressive thinning of the RPE/Bruch's membrane complex in the right eye with choroidal hypertransmission at the fovea (c). The RPE in the left eye has undergone hyperplasia, causing a shadowing effect on the choroid (d).
Early (a) and late-phase (b) fluorescein angiography (FA) at presentation (top row) of right eye and early (c) and late-phase (d) FA of the left eye demonstrates an early window defect in both eyes due to loss of outer retinal layers, without leakage or staining. Ten years after presentation (bottom row), early (e) and late-phase (f) FA of the right eye and early (g) and late-phase (h) FA of the left eye demonstrate a persistent window defect, with a focal point of subfoveal hypofluorescence corresponding to the RPE hyperplasia in the left eye (g and h). Transit time is shown in minutes.
After a decade of monitoring without intervention, the patient reported progressive bilateral glare attributed to posterior subcapsular cataracts. Interval posterior changes on MMI included enlargement of the yellow foveal lesions on funduscopy bilaterally (Figures 1c and 1d) and slight widening of the cavitary lesions on SD-OCT (Figures 2c and 2d). There was mild attenuation of the RPE with choroidal hypertransmission OD (Figure 2c). Subfoveal RPE hyperplasia developed OS (Figure 2d), with corresponding subfoveal hypofluorescence on FA (Figures 3g and 3h) and punctate hyperautofluorescence on fundus autofluorescence (Figure 5b). En face OCT angiography (OCTA) showed relatively symmetric foveal avascular zones and slight vessel tortuosity bilaterally (Figures 4a and 4c). Structural en face OCT showed central hyporeflectivity in both eyes (Figures 4b and 4d). On dense B-scan OCTA, the superficial capillary plexus and deep vascular complex were normal (Figures 4e and 4f). Microperimetry revealed bilateral decreased central sensitivity and eccentric fixation OS (Figure 6). Though counseled on prognosis given his chronic solar retinopathy, the patient elected to have cataract surgery in both eyes. Surgery improved glare symptoms, but not BCVA.
Full retina color depth encoded en face optical coherence tomography angiography (OCTA) shows relatively symmetric foveal avascular zones and slight vessel tortuosity in the right (a) and left (c) eyes. Structural en face OCT demonstrates loss of reflectivity in the right eye (b) and left eye (d), with central reflectivity in the left eye corresponding to retinal pigment epithelium hyperplasia. Ten-degree dense B-scan OCTA images show high-resolution structure of the right (e) and left (f) eyes, with OCTA signal overlaid in yellow showing a normal superficial capillary plexus and deep vascular complex. There is slight hypertransmission of signal in the fovea of the right eye (e) due to retinal pigment epithelium (RPE) thinning and blockage of signal in the fovea of the left eye (f) due to RPE hyperplasia.
Fundus autofluorescence showing mild foveal hypoautofluorescence in the right eye (a) and central, focal, hyperautofluorescence surrounded by a diffuse rim of hypoautofluorescence in the left eye (b).
Microperimetry demonstrated decreased central sensitivity in the right (a) and left (b) eyes with eccentric fixation in the left eye (b).
In this case report, we have utilized multimodal imaging across a span of 10 years to demonstrate the natural history of solar retinopathy. In our patient, the outer retinal changes remained remarkably stable, with only mild widening of the EZ and IZ defects over 10 years. Although en face imaging of the EZ was not available 10 years prior, this imaging modality provides a sensitive measure of the area of EZ loss that can be followed over time. Contrary to the stability of the EZ, the RPE OD showed progressive attenuation with choroidal hypertransmission, and there was early RPE thinning followed by RPE hyperplasia OS. Despite some loss of outer retinal tissue and RPE remodeling, the patient maintained stable vision.
Solar retinopathy results from photochemical damage to the outer retina caused mainly by light in the 400 nm to 500 nm wavelength range, with most damage occurring at 441 nm.3–5 Photochemical damage to the photoreceptors and RPE is primarily driven by free radical formation and oxidative damage.6 A histopathological study of an eye with acute solar retinopathy revealed widespread organelle swelling, nuclear changes, and cellular membrane changes in the foveal and parafoveal photoreceptors (rods greater than cones) and the RPE.7 The first OCT images of acute solar retinopathy to be reported were taken within 48 hours of exposure and demonstrated hyperreflectivity of all foveal retinal layers.8 Chen et al.9 found that the most common OCT finding in acute solar retinopathy is photoreceptor layer disruption, followed by external limiting membrane and RPE layer defects. Patients who presented with photoreceptor layer disruption had poorer presenting BCVA.9
Nevertheless, most patients with acute solar retinopathy generally have a good visual prognosis with full or almost full recovery of visual acuity (VA) within months following the initial insult.1,6,10,11 A study of 34 patients (51 eyes) presenting within a week of observing a partial solar eclipse found that 42 eyes had a VA of 20/25 or better at up to 18 months of monitoring.11 Additionally, in a field study of 329 Nepali patients (420 eyes) clinically diagnosed with solar retinopathy, 81% of eyes had BCVA 20/40 or better, and of the 44 eyes re-examined 1 to 3 years later, BCVA remained 20/40 or better in 91% of them.10 The potential for such good visual recovery may be attributable to the resilience of cones from photochemical damage, which, in the histopathological study by Hope-Ross et al.,7 did not demonstrate nuclear pyknosis to the same degree as rods.
A subset of patients, presumably with more severe photochemical damage, have chronic poor VA and/or central scotomas and metamorphopsia.11 No temporal links between acute findings and chronic appearance have been established. Moreover, features of chronic solar retinopathy itself have been less extensively documented. As in acute solar retinopathy, patients with chronic solar retinopathy and disruption of the EZ have been reported to have poorer VA.12–14 A modest association between the foveal thickness and BCVA in chronic solar retinopathy has also been noted.14–16
In our case study of solar retinopathy followed for a decade, the patient's SD-OCT showed persistent loss of photoreceptor layers with RPE involvement in both eyes. Over time, one eye demonstrated progressive RPE attenuation with corresponding OCT signal hypertransmission to the choroid. The second eye demonstrated RPE remodeling with hyperplasia. It is conceivable that when the level of photochemical damage is severe enough to involve the RPE, recovery is unlikely and progressive RPE remodeling may occur. Nonetheless, the EZ layer changes remained remarkably stable, which likely accounts for preservation of VA in the long-term.
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- Wu CY, Jansen ME, Andrade J, et al. Acute solar retinopathy imaged with adaptive optics, optical coherence tomography angiography, and en face optical coherence tomography. JAMA Ophthalmol. 2018;136(1):82–85. doi:10.1001/jamaophthalmol.2017.5517 [CrossRef]
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