Retinal damage to light is produced by either breakdown of the intrinsic protective mechanisms of the eye and/or to the external high risk conditions.

The development and severity of damage depends upon

Anatomic protective mechanisms of eye.

Area of tissue involved.

Wavelength of light.

Duration of light exposure.

Total energy exposure.

 

Mechanism

The mechanism of damage is primarily photochemical. This may be potentiated by rise in tissue temperature. Increased chorioretinal pigmentation facilitates light absorption, which increases the background retinal temperature. Retinal defences are broken by supra-normal exposure to light. Retinal phototoxicity was originally believed to be a permanent damage, but some visual recovery has been seen.

The extent of retinal injury and its possible recovery depends upon factors such as

Area of exposed retina.

Location of damage.

Spectrum, intensity and duration of light exposure.

Susceptibility of host.

Emmetropia or hypermetropia due to effective focusing of light on retina.

Systemic photosensitising agents such as tetracycline and psoralen, may predispose to damage due to light.

 Diagnosis depends upon clinical history/symptoms, manifesting signs, and investigations.

Clinical signs

A small yellow spot with a grey margin may appear shortly after exposure in the foveolar or parafoveolar area. This disc shaped lesion is about 200?m in diameter which corresponds to retinal image of the sun. Mild cases may not show any lesion.

 

Histopathology

Acute solar lesion

Acute solar lesion shows injury to retinal pigment epithelium (RPE) with necrosis, irregular pigmentation, and detachment. Photoreceptors show minimal change only.

Weeks following acute damage

The yellow lesion is replaced by a permanent focal depression, with mottling of RPE or there may be lamellar hole. Vision may show some recovery, but scotoma and metamorphopsia may persist. Previous episodesof sun gazing show multiple areas of mottling in RPE.

 

Fluorescein angiography may appear normal or may show transmission defects. There may be leakage of fluorescein dye in acute cases.

Optical coherence tomography (OCT) shows disrupted reflectivity in outer retina, or fragmentation of highly reflective outer retina.

Amsler grid testing may delineate small central or paracentral scotoma.

Multifocal electroretinography (ERG) shows decrease in amplitude with normal latency of the recordings.

 

Differential diagnosis

• Welding-arc maculopathy.
• Light flash or arc, produced by high-voltage electrical short-circuiting.
• Other causes of lamellar depressions or holes like posterior vitreous detachment or trauma.
• Post-surgical photic retinopathy.
• Accidental laser exposure.

In management, there is no specific therapy for solar retinopathy.

Oral corticosteroids have been used in acute lesions, but a beneficial effect is not being demonstrated conclusively.

Further episodes of solar viewing should be avoided. Eclipse viewing should be avoided unless there is proper protective eyewear. Solar filters with high quality of filtration of absolute visible, ultraviolet, and infrared light are recommended for viewing of eclipse.

 

Prognosis

Prognosis is guarded. Some improvement often occurs. Part of the defect usually remains, and the visual scotoma may persist permanently.

 Many patients of solar retinopathy do not develop complications and return to normal vision with resolution of symptoms over weeks and months. Some patients may develop

·         Permanent diminution of vision.

·         Persistent metamorphopsia.

·         Scotoma.