Solar retinopathy (SR) is a photic maculopathy caused by sunlight. It occurs in individuals with mental disorders or those who stare at the sun for religious reasons, as well as from improper use of filters during solar eclipse observation. The concentration of intense light energy on the fovea causes phototoxic retinal damage, also known as “eclipse retinopathy.” 1)
Causes are diverse. 1)
Recovery often occurs naturally within 3 to 6 months after onset, but some cases may result in permanent visual impairment.1) Younger individuals are more susceptible than older adults because their lenses have higher light transmittance and their pupils are larger.
Even a few seconds of exposure without a protective filter can cause phototoxic damage if focused ultraviolet and visible light reaches the fovea. On a clear day, even a one-second gaze can cause damage. It is essential to use solar eclipse glasses certified to ISO 12312-2.2)
Symptoms appear within hours to days after light exposure.1)2) In photochemical damage, there may be no immediate abnormality, with subjective symptoms appearing several days later.
In cases of strong sunlight exposure at high altitudes, multiple individuals may develop symptoms simultaneously, and increased ultraviolet radiation was involved in the etiology. 4)
OCT is the most important examination for the diagnosis and follow-up of solar retinopathy. 1)2) In the early stage of injury, a yellow spot approximately 160 μm in diameter is seen at the fovea, which often disappears within 1–2 weeks. OCT findings change depending on the disease stage.
Acute Phase
Disruption or loss of the ellipsoid zone (IS/OS junction): Observed directly beneath the fovea. The most characteristic finding.
Hyperreflective lesions: Small lesions in the outer nuclear layer to photoreceptor layer.
Thinning of the outer retinal layers: Reflects structural changes around the fovea.
Recovery Phase
Partial regeneration of the ellipsoid zone: The disrupted area shrinks over weeks to months.
Reduction or resolution of hyperreflective lesions: Reflects the repair process of the outer layers.
Residual subtle changes: Visual impairment persists in cases where complete resolution does not occur.
Chronic Phase
Foveal cystoid changes or pseudocysts: Permanent changes observed in some cases.
Verhoeff membrane (IZ layer) destruction: Specific to certain phototoxic patterns. 1)
Full-thickness defect: Final stage of severe damage. Poor visual prognosis.
Microperimetry can quantitatively evaluate foveal function. In a case of bilateral solar retinopathy in a photographer, the size of the central scotoma and reduced residual sensitivity were recorded. 2)
Depending on the direction of direct light and the use of protective equipment, it can be either unilateral or bilateral. Bilateral onset has been reported in photographers exposed to sunlight. 2)
The wavelength, intensity, and exposure conditions of light differ depending on the cause of solar retinopathy. 1)
Risk Factors
Young age and clear lens: Young people have higher lens transparency and larger pupil diameter, allowing more light energy to reach the retina.
High-altitude activities: The higher the altitude, the lower the atmospheric shielding of ultraviolet light. 4)
Dilated pupil: Sudden exposure to light from a dark place, direct sun gazing after using dilating eye drops.
Social media and peer pressure: Young people are led by friends to stare at the sun for long periods. 2)
Protective Factors
Cataract (lens opacity): The cloudy lens absorbs and scatters ultraviolet and visible light, reducing the amount reaching the retina.
High myopia and refractive errors: In general, the focus of sunlight may be shifted away from the retina.
Wearing ISO-certified filters: Eclipse viewing glasses with ISO 12312-2 certification provide appropriate light blocking. 2)
In diagnosis, obtaining a history of sun gazing is most important. Weather is a key factor; even a one-second gaze on a clear day can cause damage. The following points should be confirmed.
OCT is the most important test for diagnosing solar retinopathy. 1) It can evaluate changes in the outer layers (ellipsoid zone, outer nuclear layer, photoreceptor layer) with high resolution. It is useful for staging, visual prognosis prediction, and follow-up.
A comparison of diseases that require differentiation from solar retinopathy is shown below.
| Disease | Main cause | OCT findings |
|---|---|---|
| Solar retinopathy | Sunlight or strong light source | IS/OS disruption, hyperreflective lesion |
| Laser retinopathy | Laser pointer, etc. | Outer layer destruction, scar formation |
| Welder’s retinopathy | Welding arc ultraviolet light | Similar to solar retinopathy |
A detailed history of exposure is essential for differential diagnosis. Other conditions to consider include retinal artery occlusion (similar to cherry-red spot), traumatic maculopathy, macular degeneration, perifoveal telangiectasia (MacTel), acute macular neuroretinopathy (AMN), and perifoveal acute middle maculopathy (PAMM).2)
There is no effective treatment for solar retinopathy. Most cases recover spontaneously.
In a case of bilateral solar retinopathy in a photographer, visual acuity improved 3 months after photography without appropriate protective filters. 2) The spontaneous recovery rate is reported to be 50–83%. 2)
The main treatment options and their evaluations are shown below.
| Treatment | Evaluation | Notes |
|---|---|---|
| Observation | First-line | Most recover spontaneously within 3–6 months |
| Systemic steroids | Uncertain, with risks | Efficacy unknown. Risk of inducing CSCR. 2)3) |
| Antioxidants (vitamin C, E, etc.) | Theoretical only | In vitro studies show damage suppression, but effect after injury is unknown. 1) |
If a permanent central scotoma remains, the use of low vision aids and eccentric fixation training may be beneficial.
In many cases, vision improves naturally over 3 to 6 months. Recovery rates are reported to be 50–83%, but severe phototoxicity or delayed presentation may result in permanent visual impairment. 2)
The damage mechanism of solar retinopathy consists mainly of two pathways: photochemical damage and photothermal damage. 2)
A characteristic of photochemical damage is that there are no fundus abnormalities immediately after injury, but subjective symptoms and macular degeneration appear several days later.
If the light is intense, such as when directly viewing the southern summer sky for a short time, thermal conversion in the retina causes immediate coagulation damage. In the case of thermal effects, subjective symptoms and a coagulation spot in the macula are observed immediately after injury.
In mild to moderate damage, if the photoreceptor nuclei (outer nuclear layer) are preserved, regeneration of the outer segments is possible.5)
In the case of mobile device reflection light reported by Marticorena et al. (2022), partial recovery of outer segments was observed after phototoxic damage with preserved photoreceptor nuclei.5)
When severe damage, cystoid changes, or full-thickness defects occur, tissue regeneration is limited, leading to permanent visual impairment. The degree of damage varies from cases with no fundus abnormalities to those with chorioretinal atrophy.
Multimodal evaluation combining OCT, fundus autofluorescence, mfERG, and microperimetry is being studied as a biomarker for disease staging and visual prognosis prediction. 1)2) In particular, the correlation between the extent of ellipsoid zone damage and residual visual acuity is being investigated. 1)
Retinal damage caused by sunlight focused through smartphone camera lenses was first reported worldwide in 2022. 5) With the widespread use of mobile devices, the risk of accidental exposure is increasing, especially among young people and during outdoor activities. The need for preventive education addressing this new form of exposure has been proposed. 5)
Based on the mechanism of ROS-mediated photochemical damage, the therapeutic potential of antioxidants (vitamin C, E, lutein) and neuroprotective agents is being theoretically considered. In vitro studies have reported that antioxidants such as vitamin C suppress damage, but the effect of taking them after injury is unknown, and evidence demonstrating clinical efficacy is currently insufficient. 1)
Research on antioxidant therapy and neuroprotective therapy for photochemical damage is progressing, and early intervention after onset is considered important. Currently, there is no established treatment, and prevention is the most important measure. 1)
