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Arteriovenous sheathotomy for branch retinal vein occlusion
Published in A Peyman MD Gholam, A Meffert MD Stephen, D Conway MD FACS Mandi, Chiasson Trisha, Vitreoretinal Surgical Techniques, 2019
Rizwan A Cheema, Ewan A Fraser
The current standards for treatment of branch retinal vein occlusion were set by the Multicenter BRVO Study.3 However, it has been noted that macular grid laser photo-coagulation produces only a moderate improvement in vision (20/40 vision in treated eyes versus 20/70 in untreated eyes) and is less effective in eyes with poor vision at time of treatment. All eyes with extensive hemorrhage and poor foveal perfusion were excluded from the BRVO Study.
Case 13: Loss of Vision and a Maculopapular Rash
Published in Layne Kerry, Janice Rymer, 100 Diagnostic Dilemmas in Clinical Medicine, 2017
Central or branch retinal vein occlusion can be differentiated from retinal artery occlusion through fundoscopy. The disc appears very swollen with sites of haemorrhage and cotton wool spots.
Retina
Published in Fiona Rowe, Visual Fields via the Visual Pathway, 2016
Patients with central retinal vein occlusion present with a haemorrhagic fundus, dilation of the retinal veins, retinal oedema and variable amounts of ischaemia. Branch retinal vein occlusion is limited to the affected area.
A review of risk factors for retinal vein occlusions
Published in Expert Review of Cardiovascular Therapy, 2022
Marie Ørskov, Henrik Vorum, Torben Bjerregaard Larsen, Nanna Vestergaard, Gregory Y. H. Lip, Toke Bek, Flemming Skjøth
The pathogenic mechanism of retinal vein occlusion is not fully characterized. Various theories for both branch retinal vein occlusion and central retinal vein occlusion with both similarities and differences have been described. A similarity between some of the theories, is the contribution of atherosclerosis to the development of retinal vein occlusion [5,6]. The central retinal vein and the central retinal artery share the adventitial sheath within the lamina cribrosa. Similarly, the branch retinal veins and the branch retinal arteries share a common adventitial sheath at the arteriovenous crossings. Therefore, one theory is, that if the retinal arteries become stiff and rigid due to localized atherosclerosis, they can obstruct the retinal veins by compression [5,7–13]. This theory has been challenged by a study investigating the lumen of the occluded retinal vein, where no signs of compression of the vein was determined [14]. Another theory suggests that the veins of the retina are specifically exposed to thrombosis formation due to the gradient between the vascular pressure and the intraocular pressure. Changes in the pressure gradient may cause partial collapse of the vein either in a branch retinal vein or in the entrance to the eye in the central retinal vein, making it susceptible to thrombosis formation. Initiation of thrombosis formation could be caused by the closely passing retinal artery, either by turbulence or changes in the biochemical environment resulting from changes caused by systemic atherosclerosis [15–22].
Pattern of Retinal Vasculitis in an Egyptian Cohort
Published in Ocular Immunology and Inflammation, 2019
Eiman Abd El Latif, Ahmed Samir Montasser, Mouamen M. Seleet, Walid Mohamed Elzawahry, Mohamed Abdulbadiea Rashed, Hossameldeen Elbarbary, Karim Sabry, Mohamed Abdelmonagy Ibrahim, Hazem El Hennawi, Mohamed A. Zayed, Hazem W. Kandil, Omar M. Said
Patients with retinal vasculitis associated with Behçet’s disease constituted 14.6% of the whole cohort in our study. Male predominance was noted among patients with this disease (male: female was 71.1: 28.9), a finding that has been stated in a previous report from the same country.9 Branch retinal vein occlusion was present in about two thirds of the affected eyes in our study, and about one fourth of these eyes suffered its recurrence. In addition, 11 eyes of our Behçet’s disease patients had occlusion of the central retinal vein. The propensity of Behçet’s disease for occlusion of the retinal veins has been repeatedly reported.1,10,11 About 28% of the involved eyes showed the transient yellowish-white retinal infiltrates, previously described by Graham et al1, and we found a statistically significant association between the presence of these infiltrates and the diagnosis of Behçet’s disease.
Branch retinal vein occlusion following cataract surgery
Published in Clinical and Experimental Optometry, 2018
Silvio Polizzi, Francesco Barca, Tomaso Caporossi, Gianni Virgili, Stanislao Rizzo
Branch retinal vein occlusion is the second most frequent major retinal vascular disease after diabetic retinopathy.2010 Several risk factors, such as hypertension, hyperlipidaemia, increased body mass index, thrombophilic conditions, hyperviscosity, systemic diseases, renal dysfunction, medications and ocular conditions have been found to be associated with BRVO.2013 The occlusion usually occurs at an arteriovenous crossing, where the artery and vein share a common adventitial sheath. It was demonstrated that in almost all the eyes with BRVO, the artery is located anterior to the vein at the obstructed site. This suggests that arterial pathology can play a role in the onset of BRVO. Indeed, at the arteriovenous crossing, the narrowing of the vein caused by the relatively thick‐walled artery may induce haemodynamic changes, which in their turn may lead to endothelial damage and thrombus generation;1998 however, BRVO may also develop in the absence of venous narrowing at arteriovenous crossings. Jefferies, Clemett and Day1993 have found that at arteriovenous crossings, where the vein abruptly changes direction to pass under the artery, there is a focal thickening of the venous basement membrane, which may result in venous endothelial injury. Recently an additional pathogenetic mechanism for BRVO has been postulated. Fraenkl, Mozaffarieh and Flammer2010 hypothesised that atherosclerotic arteries and/or hypoxic tissues produce vasoconstrictive molecules, which may spread across to the neighbouring vein, inducing a local venous constriction.