First Author: H.Gerding SWITZERLAND
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The blood-retina barrier is safeguarded by tight junctions between retinal pigment epithelium and endothelial cells of intraretinal vessels. A third element of the blood-retina barrier is located between the preliminary optic nerve and adjacent retinal and choroidal tissue. It is formed by differentiated glial cells connected by tight junctions, previously described as the tissues of Kuhnt and Jacoby. It was the aim of this project to analyze cases with peripapillary retinopathy presumably related to defects of this retinooptic barrier.
In this study a series of institutional cases collected in a single tertiary eye hospital was retrospectively analyzed.
Between June 2011 and March 2017 a series of patients was identified with sub- and/or intraretinal fluid accumulation that could neither be explained by retinal or choroidal vascular, inflammatory, or neoplastic diseases, nor by disturbances of the retinal vessel or RPE barriers. All cases underwent routine basic ophthalmological examination, additional SD-OCT analysis (including scanning of the optic nerve head and peripapillary retina), and, except few cases, scanning-laser fluoresceine angiography. Sub- and/or intraretinal fluid was classified as presumably accumulated secondary to a defect in the retino-optic barrier if 1. One of the above mentioned diseases could be excluded as potentially source of fluid deposition, 2. Fluid accumulation was anatomically related to the border between the optic nerve and adjacent retina, and 3. Fluorescein angiography indicated a defect in the retinooptic barrier.
Peripapillary retinopathies, partially extending to the retinal centre with sub- and/or intraretinal fluid accumulation according to the above mentioned criteria were found in 40 eyes of 29 patients (16 male, 13 male). The median age was 75.8 years (70 ± 12.5), range: 39.9 - 85.5 years). Fluid accumulation was present either in the subretinal space, Henle fibre layer (HFL), outer nuclear layer (ONL), inner nuclear layer (INL), ganglion cells layer (GCL), or a combination of these. 3 of 29 patients presented an optic disc pit with classical optic disc pit maculopathy. In these 3 eyes fluid accumulation disappeared after ppV and removal of peripapillary vitreous traction, in 1 patient with a delay of several years. Combined fluid accumulation in the whole patient series resembled in many aspects the typical pattern of bilaminar fluid deposition seen in cases of optic disc pit maculopathy. In many cases peripapillary or papillary vitreous traction could be identified by OCT examination. In addition it was remarkable that many optic nerve heads presented deep central, non-glaucomatous excavations resembling optic pits in OCTs without presenting as a typical optic disc pit. Several cases were found with neovasculararizations causing a defect of the barrier of Kuhnt.
A series of cases was identified in whom intraand/or subretinal fluid accumulation was probably caused by defects of the retinooptic barrier according to OCT and angiographic criteria. Peripapillary or marginal vitreous traction at the optic disc, neovascular disease, papilloretinal neovascularization and papillitis seem to be important causal factors for breakdown of the retinopapillary barrier. Many of the observe cases seem share structural and aetiological aspects of optic disc pit maculopathy.