Light-induced Retinal Injury Research Articles

Light-induced Photoreceptor Apoptosis in vivo is Caspase Independent and Mediated by Nitric Oxide

INTRODUCTION. Retinitis pigmentosa (RP) is a genetically diverse disease, characterized by the progressive degeneration of rod and cone photoreceptors. Photoreceptor loss in RP occurs via apoptosis, a mode of programmed cell death, which allows a cell to partake in its own demise. Apoptosis therefore represents a common final pathway in the pathology of RP. However, the molecular events regulating photoreceptor apoptosis in human cases and animal models of RP remain undefined. In this study, we delineate the molecular events occurring during photoreceptor apoptosis in the light-induced retinal injury model of RP. METHODS. Retinal light damage: Adult male balb-c mice were exposed to 2 hours of cool white fluorescent light at a luminescence level of 5000 lux. Intraperitoneal injections: Mice were injected intraperitoneally with 100mgkg -1 of N G -nitro-L-arginine methyl ester (L-NAME) in phosphate buffered saline (PBS), or D-NAME (an inactive isomer) in PBS as a control, 1hr before light exposure. Flow cytometry was employed to monitor intracellular calcium levels, generation of reactive oxygen species and mitochondrial membrane depolarisation in untreated animals and in those treated with L-NAME. Caspase-3 activation was assessed by western blot and with the use of the synthetic substrate AcDEVD-pNA. The possible involvement of other caspases was assessed by treatment of the animals with ZVAD.fmk subretinally.

SCLERAL FIXATED INTRAOCULAR LENSES: An Angiographic Study

We reviewed the results, complications, and fluorescein angiographic (FA) findings in eyes that had undergone transscleral fixation of posterior chamber intraocular lenses (IOLs). Posterior chamber IOL implantation with scleral fixation was performed on 18 patients. Three patients were aphakic, 14 had an intraoperative posterior capsule rupture during cataract surgery, and one was operated on for a retained lens nucleus and dislocated IOL in the vitreous. Follow-up examinations measured visual acuity, intraocular pressure, and IOL decentration and tilting. In 14 patients, iris and retinal FA were performed. No major complications were noted during the procedure. Mean best-corrected visual acuity was 20/70 preoperatively and 20/30 postoperatively after a mean follow-up of 9.8 months. Fourteen patients achieved a visual acuity of 20/40 or better. Macular epiretinal membranes were diagnosed after surgery in five eyes but only one eye showed significant distortion of the fovea (macular pucker). Iris FA revealed no major vascular abnormalities. Fluorescein angiography showed cystoid macular edema in six cases. Light-induced retinal lesions occurred in six eyes. Transscleral fixation of posterior chamber IOLs provided adequate visual acuity in most patients. Incomplete visual recovery after surgery may be related to the occurrence of macular edema and epiretinal membranes. Light-induced retinal injury was the major irreversible intraoperative complication.

Updating on intraoperative light-induced retinal injury.

We are presenting the state of knowledge concerning intraoperative light-induced retinal injury, considered to be a combination of photic retinopathy and retinal photocoagulation. It may arise from retinal light exposure to the operating microscope or to the fiberoptic endoilluminator. Ultraviolet and short-wavelength visible light are more dangerous than longer wavelength light. Many risk factors may facilitate the onset of this iatrogenic disease following surgery. Many aspects of the retinal damage are still poorly understood. Many mid light-induced retinal injuries probably remain undiagnosed in routine postoperative examination. Current appropriate light filters are not the definitive solution. Appropriate precautions should be taken during both anterior segment and vitreoretinal surgery.

Operating microscope light-induced retinal injury: Mechanisms,clinical manifestations, and preventive measures

Experimental and clinical evidence of light-induced retinal injuryassociated with the operating microscope is reviewed. The mechanism of photochemical injury is discussed, as well as the concept of reversible phototoxic insults. Factors that influence retinal recovery and measures that can be taken by the surgeon to reduce light exposure to the retina are also discussed.