Devarsh Joshi

Introduction

Solar retinopathy is an uncommon macular injury caused by excessive light exposure. It is most often associated with direct sungazing or unsafe viewing of a solar eclipse, although similar retinal injury can occur after other intense photic exposures. It may also be referred to as solar maculopathy, eclipse retinopathy or photic retinopathy, depending on the clinical context (1,2).

Although rare, it remains a relevant condition for clinicians to recognise. Patients may present with new central visual symptoms after looking at the sun, often with few external signs of eye disease. The eye may appear quiet, and pain is usually absent. This can make the diagnosis easy to miss unless the history is explored carefully (2).

The condition is particularly important because there is no proven treatment that reliably reverses the retinal injury once it has occurred (2,3). Prevention, early recognition and clear counselling therefore remain central to management.

Pathophysiology

The macula is vulnerable to solar injury because the eye focuses light onto the fovea. The resulting damage is thought to be mainly photochemical, although photothermal mechanisms may also contribute depending on the intensity and duration of exposure (2). The outer retina is most affected, particularly the photoreceptors and retinal pigment epithelium, which explains why patients usually notice central visual disturbance rather than a more generalised loss of vision (2).

A common misconception is that discomfort will act as a warning sign. In reality, the retina does not produce pain in the same way as the ocular surface. During an eclipse, the reduced brightness may also create a false sense of safety, encouraging longer viewing than would normally be tolerated (3).

Solar retinopathy is not limited to eclipses. Similar photic injuries have been described after direct sungazing, sunbathing, welding arc exposure, laser pointer exposure and other intense light exposures (1,2). Eclipse-related cases are one of the more recognisable settings, as several patients may present after the same public event.

Clinical Presentation

Patients usually present with painless central visual disturbance. Symptoms may begin within hours, although some patients present later when they notice difficulty reading, driving or focusing on fine detail. Symptoms can include blurred central vision, a central or paracentral scotoma, metamorphopsia, photophobia, reduced contrast sensitivity or altered colour perception (2).

Visual acuity can vary from near normal to significantly reduced. This is clinically important because a patient may still read reasonably well on a Snellen chart while describing a persistent central defect or distortion. Amsler grid testing can therefore be useful, particularly when symptoms are subtle but clearly central.

Fundus findings may be mild. In the acute phase, there may be a small yellow-white foveal lesion, reduced foveal reflex or subtle retinal pigment epithelial change (2). In some patients, the fundus may appear almost normal early on. A normal-looking fundus should therefore not exclude solar retinopathy when the history is suggestive.

Diagnosis and Imaging

Diagnosis is usually clinical, based on a compatible history of light exposure and new central visual symptoms. Useful history points include the timing of symptom onset, whether the patient looked directly at the sun, whether eclipse glasses or filters were used, whether binoculars or cameras were involved, and whether symptoms are unilateral or bilateral.

Optical coherence tomography is the most useful investigation. OCT may show focal disruption of the outer retinal layers, including the ellipsoid zone, interdigitation zone and photoreceptor outer segments (2,5). In chronic cases, a small outer retinal defect or persistent foveal abnormality may be seen (2,5). These findings can support the diagnosis, document the extent of injury and help explain the symptoms to the patient.

Fluorescein angiography is less consistently useful. In one comparative series, OCT was better than fluorescein angiography at demonstrating the structural outer retinal changes seen in solar retinopathy (5). OCT angiography and other advanced imaging techniques may provide additional detail in selected cases, but they are not required for every patient (6).

Important differential diagnoses include acute macular neuroretinopathy, paracentral acute middle maculopathy, central serous chorioretinopathy, early macular hole, toxic maculopathy, inherited macular disease and inflammatory or infective macular pathology (2). In practice, the history is often the most important clue.

Management and Prognosis

There is no proven treatment for solar retinopathy. Management is usually conservative, with reassurance, observation and follow-up (2,3). The immediate priority is to confirm the likely diagnosis, exclude alternative macular pathology and provide clear counselling.

Steroids have been used in some reported cases, usually because of a possible inflammatory component to photic injury. However, the evidence for benefit is limited and inconsistent (2,3). They should therefore not be considered routine treatment.

Follow-up should include more than visual acuity alone. Patients should also be asked about persistent scotoma, distortion, reading difficulty and reduced contrast sensitivity. Repeat OCT may be useful if symptoms continue, particularly to assess whether the outer retinal changes are improving or stable (2,8).

Many patients improve over weeks to months (2,4). In the UK national study after the 1999 eclipse, there were no reported cases of persistent visual loss or symptoms at six months among those with available outcome data (4). However, solar retinopathy should not be dismissed as harmless. Other studies have reported persistent symptoms, including central scotomas and incomplete visual recovery, particularly where OCT shows ongoing outer retinal disruption (2,7,8).

Patients should therefore be counselled that visual acuity often improves, but subtle central scotomas or distortion may persist. This distinction is important, as Snellen acuity alone may not fully reflect the patient’s visual experience.

Prevention and Clinical Relevance

Prevention is the most important aspect of solar retinopathy. Patients should be advised never to look directly at the sun without appropriate certified solar viewing protection. Ordinary sunglasses, smoked glass, phone screens, cameras, binoculars and telescopes without correct solar filters are not safe substitutes (3).

Clinicians should consider solar retinopathy in patients with new central visual symptoms after sun exposure, even when the eye appears externally normal. OCT is useful where available, particularly when fundus findings are subtle (2,5).

Conclusion

Solar retinopathy is an uncommon but important cause of central visual disturbance after unsafe light exposure. It is best known after eclipse viewing, but similar injury can occur after other intense photic exposures. Diagnosis relies on careful history-taking, clinical assessment and OCT evidence of outer retinal disruption. As there is no proven treatment, prevention, recognition and realistic counselling remain central.

References

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2. Jourieh M. Solar retinopathy: A literature review. Oman J Ophthalmol. 2024;17(2):173–180. doi:10.4103/ojo.ojo_248_23.
3. Bressler NM. Safely viewing a solar eclipse. JAMA Ophthalmol. 2024;142(4):377. doi:10.1001/jamaophthalmol.2024.0401.
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6. Wu CY, Jansen ME, Andrade J, Chui TYP, Do AT, Rosen RB, 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.
7. Wong SCK, Eke T, Ziakas NG. Eclipse burns: a prospective study of solar retinopathy following the 1999 solar eclipse. Lancet. 2001;357(9251):199–200. doi:10.1016/S0140-6736(00)03597-2.
8. Stephenson KAJ, Stephenson GR, Forristal MT, Moran S, O’Donoghue E. Long-term anatomical and functional findings of solar maculopathy. Ir J Med Sci. 2024;193(1):435–441. doi:10.1007/s11845-023-03434-2.