Solar retinopathy (SR) is a photic maculopathy caused by sunlight. It can occur not only in people with mental illness or in those who stare at the sun for religious reasons, but also from improper use of equipment when observing a solar eclipse. Concentration of intense light energy on the fovea causes phototoxic retinal damage, and it is also called eclipse retinopathy.1)
The causes are varied.1)
Spontaneous recovery often occurs within 3 to 6 months after onset, but some cases leave permanent vision loss.1) Younger people are more likely to be affected than older people because the lens transmits more light and the pupil is larger.
Even for a few seconds without a protective filter, focused ultraviolet and visible light can reach the fovea and cause phototoxic injury. On a clear day, even about 1 second of staring can cause damage. It is essential to use eclipse glasses certified to ISO 12312-2.2)
Symptoms appear within several hours to a few days after exposure to light.1)2) In photochemical injury, there may be no abnormality immediately after the injury, and symptoms may appear days later.
In cases with strong sunlight exposure at high altitude, several people developed symptoms at the same time, and the increased amount of ultraviolet light was involved in the cause.4)
OCT is the most important test for diagnosing and following solar retinopathy.1)2) In the early stage after injury, a yellow spot about 160 μm in diameter may be seen at the fovea, and it often disappears within 1 to 2 weeks. OCT findings change depending on the stage of the disease.
Acute phase
Disruption or loss of the ellipsoid zone (IS/OS junction): Seen directly beneath the fovea. This is the most characteristic finding.
Hyperreflective lesion: A small lesion seen 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 several weeks to several months.
Reduction and disappearance of hyperreflective lesions: Reflects the repair process in the outer layers.
Persistent subtle changes: In cases where the changes do not disappear completely, vision impairment continues.
Chronic phase
Foveal cyst-like change / pseudocyst: A lasting change seen in some cases.
Destruction of the Verhoeff membrane (IZ layer): Specific to certain phototoxic patterns.1)
Full-thickness defect (full-size defect): The final appearance in severe cases. Poor visual prognosis.
Microperimetry can quantitatively assess foveal function. In a photographer’s bilateral solar retinopathy case, the size of the central scotoma and the drop in residual sensitivity were recorded.2)
Depending on how directly the light hits and whether protective eyewear was used, it can be unilateral or bilateral. Bilateral onset has been reported in photographers exposed to sunlight.2)
For each cause of solar retinopathy, the light’s wavelength, intensity, and exposure circumstances differ.1)
Risk factors
Young age and a clear lens: because young people have a higher lens transmittance and larger pupils, more light energy reaches the retina.
Activities at high altitude: the higher the altitude, the less the atmosphere shields against ultraviolet rays.4)
Dilated pupils: sudden exposure after coming out of a dark place, or looking at the sun after using a pupil-dilating medicine.
Social media and peer pressure: young people stare at the sun for long periods because of encouragement from their peers.2)
Protective factors
Cataracts (lens opacity): the cloudy lens absorbs and scatters ultraviolet and visible light, reducing the amount that reaches the retina.
High myopia and refractive errors: In general, the focus of sunlight may be shifted away from the retinal plane.
ISO-certified filters: Eclipse glasses certified to ISO 12312-2 provide proper shading.2)
In diagnosis, asking about a history of solar viewing is the most important one. Weather is an important factor; even a one-second stare on a clear day can cause damage. Check the following items.
OCT is the most important test in diagnosing solar retinopathy. 1) It can evaluate changes in the outer layers (ellipsoid zone, outer nuclear layer, photoreceptor layer) at high resolution. It is useful for staging, predicting visual prognosis, and follow-up.
A comparison of diseases that need to be differentiated from solar retinopathy is shown below.
| Disease | Main cause | OCT findings |
|---|---|---|
| solar retinopathy | sunlight / intense light source | IS/OS disruption, hyperreflective lesion |
| laser retinopathy | laser pointers, etc. | outer layer damage, scar formation |
| welder’s retinopathy | ultraviolet light from welding arc | similar to solar retinopathy |
A detailed exposure history is essential for the differential diagnosis. Retinal artery occlusion (similar to cherry-red spot), traumatic maculopathy, macular degeneration, paracentral macular telangiectasia (MacTel), acute macular neuroretinopathy (AMN), and paracentral acute middle maculopathy (PAMM) should also be considered in the differential.2)
There is no effective treatment for solar retinopathy. Many cases recover on their own.
In a photographer with bilateral solar retinopathy, visual acuity improved 3 months after taking photos without an appropriate protective filter. 2) The spontaneous recovery rate has been reported to be 50–83%. 2)
The main treatment options and their evaluations are shown below.
| Treatment | Assessment | Notes |
|---|---|---|
| Observation | First-line | Most recover spontaneously in 3–6 months |
| Systemic steroid therapy | Uncertain; risk present | Effect is unclear. Risk of inducing CSCR2)3) |
| Antioxidants (such as vitamins C and E) | Theoretical rationale only | In vitro studies have reported inhibition of damage, but the effect of taking it after injury is unclear1) |
If a permanent central scotoma remains, using low-vision aids and training in eccentric fixation may be helpful.
In many cases, vision improves over 3 to 6 months on its own. Recovery rates of 50 to 83% have been reported, but severe phototoxicity or delayed medical attention can leave lasting vision loss.2)
The mechanism of injury in solar retinopathy mainly involves two pathways: photochemical injury and photothermal injury.2)
With photochemical injury, the fundus is normal immediately after injury, and symptoms and macular degeneration appear a few days later.
If the light is intense enough, such as when looking directly at the midsummer southern sky for a short time, heat conversion in the retina causes immediate coagulative damage. In thermal injury, symptoms and a coagulation spot in the macula are seen immediately after injury.
In mild to moderate injury, if the photoreceptor nuclei (outer nuclear layer) are preserved, the outer segments can regenerate.5)
In the mobile-device reflected-light cases reported by Marticorena et al. (2022), partial recovery of the outer segments was observed after phototoxic injury with preservation of the photoreceptor nuclei.5)
When injury is severe and progresses to cystic change or full-thickness loss, tissue regeneration is limited and can lead to permanent visual impairment. Damage ranges from no fundus abnormalities to residual chorioretinal atrophy.
Multimodal assessment 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 relationship between the extent of ellipsoid zone damage and remaining visual acuity is being examined.1)
Retinal injury from sunlight focused through a smartphone camera lens was reported for the first time in the world in 2022.5) As mobile devices become more widespread, the risk of accidental exposure is increasing, especially in young people and during outdoor activities. The need for preventive education tailored to 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, vitamin E, lutein) and neuroprotective drugs is being considered in theory. In vitro, antioxidants such as vitamin C have been reported to reduce damage, but the effect of taking them after injury is unclear, and evidence showing clinical effectiveness is currently insufficient.1)
Research on antioxidant therapy and neuroprotective therapy for photochemical damage is progressing, and early intervention after onset is thought to be important. At present, there is no established treatment, and prevention is the most important measure.1)
