In branch retinal vein occlusion (BRVO), abnormal arteriovenous crossing with vein compression, degenerative changes of the vessel wall and abnormal hematological factors constitute the primary mechanism of vessel occlusion. In general, BRVO has a good prognosis: 50-60% of eyes are reported to have a final visual acuity (VA) of 20/40 or better even without treatment. One important prognostic factor for final VA appears to be the initial VA. Grid laser photocoagulation is an established treatment for macular edema in a particular group of patients with BRVO, while promising results for this condition are shown by intravitreal application of steroids or new vascular endothelial growth factor inhibitors. Vitrectomy with or without arteriovenous sheathotomy combined with removal of the internal limiting membrane may improve vision in eyes with macular edema which are unresponsive to or ineligible for laser treatment.

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To cite this article: Rehak M, Wiedemann P. Retinal vein thrombosis: pathogenesis and management. J Thromb Haemost 2010; 8: 1886-94.Summary. Retinal vein occlusion (RVO) is the most common retinal vascular disease after diabetic retinopathy. Owing to its multifactorial nature, however, management of this condition remains a challenge. Of the two main types of RVO, branch retinal vein occlusion (BRVO) is more prevalent than central retinal vein occlusion (CRVO). Most patients develop the disease at an elderly age, and more than half of them have associated systemic disorders (e.g. hypertension, hyperlipidemia and/or diabetes mellitus). There is no evidence to suggest routine testing for heritable thrombophilias in patients with RVO. The main cause of the visual impairment is macular edema, while neovascularization of the retina and optic disc are the most serious complications leading to vitreous hemorrhage, retinal detachment and neovascular glaucoma. Macular grid laser photocoagulation is an effective treatment for macular edema in patients with BRVO and a visual acuity of 20/40 or less. Other treatment options for reducing the edema are intravitreal steroids, anti-VEGF drugs and vitrectomy. The recently introduced intravitreal application of steroids and anti-VEGF drugs may prove to be a better approach for improving visual acuity. Finally, scatter panretinal laserphotocoagulation can effectively treat neovascularization and its secondary complications.

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Ranibizumab PRN resulted in greater visual acuity (VA) gains in macular oedema following BRVO compared with single-dose dexamethasone over a 6-month study period, observed from month 3, when administered according to their European label. In clinical practice, retreatment with dexamethasone may be required prior to this point.

The aim of this study was to compare the efficacy and safety profile of XEN microstent implantation with trabeculectomy (TET) in a comparable group of open-angle glaucoma cases in a retrospective, monocentric, single-surgeon setting. Each treatment group consisted of 100 eyes of 100 patients. At regular follow-up visits during the first 12 months after surgery, the following assessments were conducted and compared: intraocular pressure (IOP), number of IOP-lowering medications applied, best-corrected visual acuity (BCVA) and visual field testing. In both groups mean IOP was significantly reduced (p < 0.001). Mean IOP dropped from 24.8 ± 7.8 to 14.8 ± 4.0 mmHg in the TET and from 24.5 ± 6.7 to 16.6 ± 4.8 mmHg in the XEN group. The number of active compounds in the prescribed medication dropped from 3.3 ± 1.2 to 1.3 ± 1.4 in the TET and from 3.0 ± 1.1 to 1.4 ± 1.5 in the XEN group. BCVA and mean defect of static automated perimetry did not show a change of statistical significance in either group. Complications were more frequent after TET (p = 0.005) while postoperative needling was more frequent in the XEN group (p = 0.021). TET and XEN led to a significant reduction of IOP and IOP-lowering medication, while BCVA and visual field indices remained mostly unaltered over a 12-month postsurgical follow-up.

BRVO results in a rapid transient increase in the expression of VEGF and a delayed increase in the expression of PEDF. The downregulation of Kir4.1 and aquaporins, the mislocation of Kir4.1 protein, and the osmotic swelling of Müller cells may contribute to the development of edema and neuronal degeneration.

In a real-world setting, eyes with DME considered refractory to anti-VEGF therapy after three monthly injections which were switched to DEX implant and had better visual and anatomical outcomes at 12 months than those that continued treatment with anti-VEGF therapy.