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• W2015352235 abstract "Since the beginning of the anti-VEGF era in ophthalmology, tears of the retinal pigment epithelium (RPE) in patients receiving intravitreal anti-VEGF treatment due to serous-vascularized pigment epithelium detachment (svPED) in age-related macular degeneration (AMD) have increasingly become an important issue in clinical practice. As a tear of the RPE usually comes along with a deleterious decrease in visual acuity, clinical signs predicting the event of an RPE tear are valuable and may guide the way to optimizing treatment strategies that minimize the risk of RPE tear development. So far, several prognostic markers for an impending RPE tear have been described such as PED lesion's height, hyper-reflective lines in near-infrared images and a small ratio of choroidal neovascularization (CNV) size to PED size (Chan et al. 2007, 2010; Clemens et al. 2014). Microrips of the RPE were firstly described as a leak at the edge of the RPE detachment with passage of fluorescein into the subretinal space (Ie et al. 1992). Later on, Sarraf et al. (2010) introduced a classification system of RPE tears and defined grade 1 as a thin defect at the margin of the PED with a subtle ring sign of hyperfluorescence in angiography as well as a microscopic RPE defect detectable in optical coherence tomography (OCT). We report a 78-year-old patient who presented with a decrease in visual acuity in his left eye for 1 week. A treatment-naive svPED due to AMD was diagnosed, and an anti-VEGF therapy with ranibizumab was initiated. Note the microrips visible in fundus autofluorescence (FAF) and OCT as well as the ring sign prior to treatment start. The maximum PED height was 750 μm, the CNV PED size ratio was 0.4. Hyper-reflective lines in near-infrared images were not present. One week after the first injection, a large tear of the RPE was detectable (Fig. 1). Ie et al. hypothesized that the mechanism leading to a microrip is based on hydrostatic forces alone. In contrast, the forces involved in the development of a conventional RPE tear are hydrostatic forces combined with tangential traction from a CNV membrane adherent to the undersurface of the RPE applying the maximum traction at the junction of the attached and detached RPE that represents the ‘locus minoris resistentiae.’ Looking at the pretear and post-tear architectural configuration of the svPED, multimodal imaging provides mechanistic insights into RPE tear development. Firstly, note that the localization of the microrip in our patient is in accordance with Ie's hypothesis as the microrip is not lying perpendicular to the CNV's contraction force as it is usually the case in conventional RPE tears. However, in this case, it is located parallel to the axis of CNV's contraction force, which makes it rather improbable that contraction forces cause the microrip. Secondly, the fact that the microrip is located parallel to the axis of CNV's contraction force results in lower tensile forces acting on the microrip, which may be the reason that the microrip had not further increased before injection. Nevertheless, microrips supposedly lower the threshold of RPE resistance and the increase in contraction after anti-VEGF therapy eventually results in the anatomic failure of the RPE. Thirdly, the localization of microrips detectable prior to tear development at the temporal edge of the lesion is identical to the edge of the RPE tear suggesting that microrips may be regarded as a predetermined tearing edge. Therefore, microrips must be regarded as a risk factor for the development of RPE tears similar to other risk factors as discussed above. A microrip should not be regarded as a prestage RPE tear or the beginning of a RPE tear. Much more likely, microrips and RPE tears represent two separate entities based on different etiologic mechanisms as postulated by Ie et al. This case shall encourage clinicians to look for microrips, in addition to the previously established RPE tear risk factors, prior to anti-VEGF therapy in patients with svPED and to perform a thorough examination including OCT and FAF after each injection in high-risk patients. If several RPE tear risk factors accumulate or single risk factors significantly grow during the course of anti-VEGF treatment, we suggest to pause injection therapy, to re-evaluate the svPED lesion 1–2 weeks later and to reinject if signs of CNV contraction have declined. Such an adapted regimen may lead to a safer anti-VEGF therapy with regard to RPE tear development in svPED patients at high risk. Notably, not all known risk factors are present in all cases prior to RPE tear development. A future prospective study stratifying the weight of each individual risk factor to quantify the risk of RPE tear development of individual patients seems promising. In conclusion, microrips in OCT and FAF and the angiographic ‘ring sign’, respectively, may be regarded as a potential risk factor for impending RPE tear development in patients under anti-VEGF treatment for svPED." @default.
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• W2015352235 title "Reading the signs: Microrips as a prognostic sign for impending RPE tear development" @default.
• W2015352235 doi "https://doi.org/10.1111/aos.12683" @default.
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