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Vitreoretina Editorial The Vitreoretinal Interface in Retinal Vein Occlusions – A Clue for Surgery? Simon Brunner Ophthalmologist, Department of Ophthalmology, The Rudolph Foundation Hospital, Vienna, Austria Abstract Retinal vein occlusions are still one of the leading retinal vasculopathies with a strong impact on the quality of life. Despite the success in symptomatic treatment with anti-vascular endothelial growth factor (VEGF) medication, no real causal therapy has been developed so far. As most of the pathogenetic changes have been observed in the vitreoretinal interface, actual therapeutic strategies are being focused on this area. Modern surgical techniques may help to release vitreovascular traction, stop cytokine activation and improve retinal oxygenation. Keywords Retinal vein occlusions, central retinal vein occlusion, branch retinal vein occlusion, vitreoretinal interface, vitreoretinal surgery, vitrectomy surgery Disclosure: Simon Brunner has nothing to disclose in relation to this article. There were no publication fees associated with this article. Open Access: This article is published under the Creative Commons Attribution Noncommercial License, which permits any non-commercial use, distribution, adaptation and reproduction provided the original author(s) and source are given appropriate credit. Received: 23 November 2015 Published Online: 21 December 2015 Citation: European Ophthalmology, 2015;9(2):138–40 Correspondence: Simon Brunner, The Rudolph Foundation Hospital, Department for Ophthalmology, Juchgasse 25, A-1030 Vienna, Austria; E: [email protected] Retinal vein occlusions (RVO) affect over 16 million people worldwide, with 2.5 million affected by central retinal vein occlusions (CRVO) and 13.9 million affected by branch retinal vein occlusions (BRVO). 1 RVO are still the second leading retinal vasculopathy after diabetic retinopathy and the fifth leading cause of monocular blindness. 2 Up to 15  % of patients are younger than 50 years, pointing to a strong impact on quality of life as well as on economic burden, especially for patients affected by CRVO. 3,4 Current evidence suggests two main unquestionable principles of therapy: first, the reduction of macular oedema (MO), venostasis and extravasation of cytokines and other blood components by multiple administrations of intravitreal anti-angiogenetic medication (IVAM, such as vascular endothelial growth factor [VEGF]-inhibitors) in the short- and mid-term; and, second, the recognition and treatment of cardiovascular risk factors, especially for CRVO patients, in the long term. 5,6 Unfortunately, no real causal therapy for RVO has been developed so far. However, most of the pathogenetic changes following RVO are observed in a region called the vitreoretinal interface (VRI): extravasation of cytokines, growth factors and other blood components, secondary inflammatory processes and the breakdown of the blood–retina barrier. Anatomically, the VRI consists of the posterior vitreous cortex, the inner limiting membrane (ILM) and an intervening extracellular matrix. 7 Consequently, several new surgical strategies targeting the VRI have been developed to overcome the need for repeated intravitreal injections over months and years, and to optimally reduce the risk of late local or systemic complications. 138 Anatomic Role of the Vitreoretinal Interface It has been observed that the ILM is much thinner in the regions close to the retinal vasculature. Moreover, a strong adhesion of vitreous with blood vessels does exist with a tendency for traction, vascular leakage, neovascularisation (NV) and haemorrhage. 8,9 In a prospective case-control study, vitreovascular traction at the occlusion site was significantly associated with BRVO. 10 Similarly, other studies showed a higher incidence for MO or NVs in eyes with vitreomacular adhesions after BRVO or CRVO, respectively. 11,12 Therefore an attached posterior vitreous cortex with or without traction may play a pathogenetic role in RVO. In fact, the induction of a posterior vitreous detachment (PVD) with or without plasmin seems to protect against retinal or optic disc NV in severe CRVO, 11 increases vitreal oxygen levels via microplasm 13 and may improve acuity and reduced MO in BRVO. 14 Pars-plana vitrectomy alone can also improve acuity and/or MO in RVO by removing blood components, vitreomacular traction and the scaffold for later NV 15,16 (see Figure 1). Vitrectomy may be combined with ILM peeling with significant anatomic and functional improvements. 17 Further additional tools include radial optic neurotomy (RON) at the level of the lamina cribrosa in CRVO (see Figure 2) or adventitial sheathotomy at the arteriovenous crossing site in BRVO. Whereas RON has proved a significantly better anatomical and functional outcome in several randomised trials, 18,19 adventitial sheathotomy showed only a small, if any, benefit – if compared with standard vitrectomy or IVAM therapy. 20,21 RON seems also to protect patients from anterior NV; however, this technique is more invasive and risky than routine vitrectomy procedure. 22 TOU C H ME D ICA L ME D IA