The eye has several mechanisms to protect itself against light damage, including pupil constriction, light absorption by melanin in the RPE, and the presence of antioxidants, such as lutein and zeaxanthin, in the macula. Light injures the retina by 3 basic mechanisms: (1) mechanical, (2) thermal, and (3) photochemical. Mechanical injury occurs when the power of the absorbed light is high enough to form gas or water vapor or to produce acoustic shock waves that mechanically disrupt retinal tissues. The absorbed energy may be enough to strip electrons from molecules in the target tissue, producing a collection of ions and electrons referred to as plasma. For example, a Q-switched Nd:YAG laser produces its therapeutic effect through mechanical light damage and uses this effect to disrupt a cloudy posterior capsule behind an intraocular lens.
Thermal injury occurs when excessive light absorption by the RPE and surrounding structures causes local elevation of the tissue temperature, leading to coagulation, inflammation, and scarring of the RPE and the surrounding neurosensory retina and choroid. A therapeutic application of thermal light injury is the retinal burn caused by laser photocoagulation. See Chapter 19 for discussion of photocoagulation.
Photochemical injury results from biochemical reactions that cause retinal tissue destruction without elevation of temperature. It is the result of the transfer of light energy to a molecule; the excess energy initiates reactions that cause tissue damage. Damaging reactions can include oxidation, photoisomerization, photochemical cleavage, and electrocyclic reactions. Such changes occur primarily at the level of the outer segments of the photoreceptors, which are more sensitive than the inner segments. Examples of photo-chemical injury are solar retinopathy and photic retinopathy that occurs after excessive exposure to illumination from an operating microscope.
Mainster MA, Turner PL. Photic retinal injuries: mechanisms, hazards, and prevention. In: Schachat AP, Wilkinson CP, Hinton DR, Sadda SR, Wiedemann P, eds. Ryan’s Retina. Vol 2. 6th ed. Philadelphia: Elsevier/Saunders; 2018:chap 93.
Solar retinopathy, also known as foveomacular retinitis, eclipse retinopathy, or solar retinitis, is a thermally enhanced photochemical retinal injury caused by direct or indirect gazing at the sun; it may also occur after viewing a solar eclipse without proper protection. The extent of the damage depends on the duration and intensity of the exposure. Younger patients with clearer lenses are at a higher risk of solar retinopathy. Symptoms include decreased vision, central scotomas, dyschromatopsia, metamorphopsia, micropsia, and frontal or temporal headache within hours of exposure. Visual acuity is typically reduced to 20/25–20/100 but may be worse depending on the degree of exposure. Most patients recover within 3–6 months, with visual acuity returning to the level of 20/20–20/40, but there may be residual metamorphopsia and paracentral scotomas. Typical findings include a central opacified area of the fovea acutely and depigmentation after the acute changes resolve (Fig 18-9). No known beneficial treatment exists, and therefore prevention through education is critically important.
Figure 18-9 Solar retinopathy. The fundus photos show central foveal hypopigmentation. On OCT imaging, outer retinal cavitation in the fovea is typically seen.
(Courtesy of David Sarraf, MD.)
Comander J, Gardiner M, Loewenstein J. High-resolution optical coherence tomography findings in solar maculopathy and the differential diagnosis of outer retinal holes. Am J Ophthalmol. 2011;152(3):413–419.e6.
Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.