Abstract
Purpose: :
The study of retinal phototoxicity may have important implications for our understanding of diseases that involve damage to photoreceptors or the retinal pigment epithelium (RPE). Our knowledge of light exposures that damage the retina stems primarily from fundus photography and histological studies of human and animal tissue. Most studies have been limited to observations hours and days after light exposure, thus not considering healing effects. In this work we investigate the long-term impact of damaging light exposures on the photoreceptors and RPE in humans in vivo.
Methods: :
Three individuals who had experienced accidental exposures to high power lasers years earlier underwent complete ophthalmic examinations and fluorescence adaptive optics scanning laser ophthalmoscopy (FAOSLO). Clinical history including mechanism of injury and type of laser exposure was obtained. Clinical imaging included fundus photography, confocal scanning laser ophthalmoscopy (HRA, Heidelberg Engineering) and optical coherence tomography (Spectralis, Heidelberg Engineering and/or Cirrus, Zeiss Meditech). The affected retinal areas were imaged by FAOSLO with reflectance from photoreceptors (796Δ17 nm) and autofluorescence of lipofuscin in the RPE (excitation 561 nm, emission 624Δ40 nm).
Results: :
The photoreceptor mosaics in the regions of photodamage appear different in all three patients, likely as a result of different damage mechanisms. One patient, with a highly reflective lesion 27° superior to the optic disc, shows regions of reduced autofluorescence as well as an apparently intact photoreceptor mosaic. In the second patient, a foveal thermal lesion resulted in patchy loss of photoreceptors co-localised with RPE disruption. Reduced OCT signal confirms loss of photoreceptors including their Henle fibers. The third patient, who likely experienced mechanical damage from a pulsed laser and suffered complications including choroidal neovascularization, has subretinal fibrosis at the center of the exposed area with surrounding intact photoreceptors. The extent of RPE disruption covers a larger area than that of apparent photoreceptor loss.
Conclusions: :
Despite RPE disruption resulting from intense light exposures, healthy appearing photoreceptors can be identified at the site of injury years afterwards. Whether this is a consequence of healing mechanisms within the light exposed photoreceptors or a migration from neighboring, unaffected regions remains to be investigated.
Keywords: imaging/image analysis: non-clinical • lesion study • radiation damage: light/UV