Clinical Photic Retinopathy: Mechanisms, Manifestations, and Misperceptions

Abstract

This chapter presents an analysis of photic retinopathy's mechanisms, manifestations, and misperceptions. Photic retinopathy is also known as retinal phototoxicity. It causes acute retinal damage in solar or welder's maculopathy and in operating microscope or endoilluminator injury. Retinal phototoxicity occurs when intraretinal photochemical reactions from intense light exposure transiently overwhelm retinal defensive and repair systems. Experimental studies in primates and rodents have identified photosensitizer-mediated and photopigment-mediated phototoxicities, respectively. Phototoxicity is a useful biomarker in experimental studies of retinal pathophysiology. Photosensitizer-mediated phototoxicity is the probable cause of clinical photic retinopathy. Potent intraretinal photosensitizers include lipofuscin and all-trans-retinal. The action spectra of human retinal phototoxicity and lipofuscin are similar. Ultraviolet (UV) radiation is more hazardous than violet light, which in turn is more hazardous than blue or longer wavelength optical radiation. Children and young adults are at greatest risk for retinal phototoxicity because of their clear ocular media and crystalline lens transmission of UV-B radiation around 320 nm which ends by 30 years of age. Phototoxicity occurs at retinal temperature increases too low for photocoagulation, but it can be enhanced by elevated retinal temperature at high retinal irradiances and/or accompanied by concurrent photothermal damage. The term "chronic" photic retinopathy is misused in the clinical literature to describe the long-term pathophysiologic sequelae of an acute injury rather than a continuing photochemical damage process. Solar and welder's maculopathies are examples of foveomacular retinitis, a clinical syndrome that can be caused also by mechanical trauma, inflammation, or drug abuse. Foveomacular retinitis is classified as secondary or primary (idiopathic) depending upon whether its cause is known or unknown, respectively. Optical coherence tomography (OCT) and OCT angiography (OCTA) are valuable for identifying photic retinopathy, characterizing its severity, and differentiating it from photocoagulation. Acute solar and welding arc injuries can have normal or full-thickness foveolar hyperreflectance. OCTA imaging may show choriocapillaris abnormalities. Weeks to months after an injury, structural OCT commonly documents a localized zone of outer retinal foveolar hyporeflectance documenting photoreceptor loss. The interdependence of the retinal photoreceptor, retinal pigment epithelium, and choriocapillaris layers obfuscates clinical identification of the initial site(s) of phototoxic damage. The risk of photic retinopathy can be eliminated or reduced by using protective filters for solar observation or welding arc exposure and minimizing the duration and intensity of surgical illumination. There is no scientific evidence that fundus cameras, ophthalmoscopes, or video displays cause retinal phototoxicity in normal use. Blue light-dependent retinal ganglion circadian photoreception is largely responsible for cataract surgery's nonvisual health benefits including improved cognition, increased longevity, and decreased depression. Photic retinopathy from environmental light exposure is not a proven risk factor for age-related macular degeneration. Blue-blocking intraocular lenses reduce blue light-dependent scotopic and circadian photoreception but provide the equivalent phototoxicity protection of only a 28-year-old crystalline lens.