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Retinal vein occlusion (RVO) is a common vascular disorder with a prevalence of 0.7–1.56%.1,2 It occurs due to thrombosis of a retinal vein and is defined by the location of the obstruction (central, hemi or branch vein occlusion).3–5 Branch RVO (BRVO) occurs at arteriovenous crossing sites that share a common adventitia.5 Central retinal vein occlusion (CRVO) is thought to be caused by external compression of the central retinal artery, which shares a common fibrous sleeve with the vein.6
Visual handicap occurs due to macular oedema and neovascularisation, which are secondary to retinal ischaemia.7–11 A number of inflammatory chemokines are thought to be involved in these processes and are found in elevated concentrations in the aqueous humour. Interleukin 6 (IL-6), IL-8, monocyte chemoattractant protein-1 (MCP-1), IL1-α, vascular endothelial growth factor (VEGF) and platelet-derived growth factor AA (PDGF-AA) are found to be elevated in CRVO. There are mixed results in terms of their concentrations in BRVO.12,13
The pathogenesis of RVO is believed to follow the principles of Virchow's triad for thrombogenesis: vessel damage, stasis and hypercoagulability.14 Contributing factors include: atherosclerosis, inflammatory disease and hypercoagulable/thrombophilia states.15–17 A major risk factor for RVO is hypertension.18–22 Dyslipidaemia is also a prevalent finding.22 Associations have also been reported for diabetes mellitus,18–22 renal disease,23 cigarette smoking18,23 and thrombophilia.16–18,24–26 An additional ocular risk factor is glaucoma or elevated intraocular pressure (IOP), which may compromise retinal venous outflow.18 More than 90% of cases of RVO occur in the >50 age group.14 In patients >50 years of age a cardiovascular risk factor is usually present. In patients <50 years of age there is no obvious risk factor in up to 40% of cases.27,28