Alkali burns to the eye constitute a leading cause of worldwide blindness. In recent case series, corneal transplantation revealed unexpected damage to the retina and optic nerve in chemically burned eyes. We investigated the physical, biochemical, and immunological components of retinal injury after alkali burn and explored a novel neuroprotective regimen suitable for prompt administration in emergency departments. Thus, in vivo pH, oxygen, and oxidation reduction measurements were performed in the anterior and posterior segment of mouse and rabbit eyes using implantable microsensors. Tissue inflammation was assessed by immunohistochemistry and flow cytometry. The experiments confirmed that the retinal damage is not mediated by direct effect of the alkali, which is effectively buffered by the anterior segment. Rather, pH, oxygen, and oxidation reduction changes were restricted to the cornea and the anterior chamber, where they caused profound uveal inflammation and release of proinflammatory cytokines. The latter rapidly diffuse to the posterior segment, triggering retinal damage. Tumor necrosis factor-α was identified as a key proinflammatory mediator of retinal ganglion cell death. Blockade, by either monoclonal antibody or tumor necrosis factor receptor gene knockout, reduced inflammation and retinal ganglion cell loss. Intraocular pressure elevation was not observed in experimental alkali burns. These findings illuminate the mechanism by which alkali burns cause retinal damage and may have importance in designing therapies for retinal protection.

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Wide field swept-source optical coherence tomography angiography (SS-OCTA) was compared with ultra wide field (UWF) fluorescein angiography (FA) for evaluating neovascularization (NV) before and after panretinal photocoagulation (PRP) in eyes with treatment-naive proliferative diabetic retinopathy (PDR). Design: Prospective, observational, consecutive case series Participants: Patients with treatment-naive PDR Methods: Patients were imaged using the SS-OCTA 12×12mm field of view (PLEX® Elite 9000; Carl Zeiss Meditec, Inc, Dublin, CA) at baseline and at 1 week, 1 month, and 3 months after PRP. Select eyes were imaged with five SS-OCTA 12×12mm scans to create posterior pole montages. UWF fundus photography and UWF FA were obtained at baseline and 3 months after PRP. Main Outcome Measures: NV visualized using wide field SS-OCTA and UWF FA Results: From January through May 2018, wide field SS-OCTA was performed on 20 eyes with treatment-naive PDR from 15 patients. The en face SS-OCTA 12×12mm vitreoretinal interface (VRI) slab images showed NV at baseline in 18 of 20 eyes (90%). Of the remaining 2 eyes, the posterior pole montage captured peripheral NV in one eye, and in the other eye, no evidence of NV was detected with either UWF FA or SS-OCTA. After PRP, both SS-OCTA and FA †