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Vascular occlusion of a retinal artery or vein is a common cause of retinal vascular pathology with potential life-changing complications.1 ,2 Retinal vein occlusion (RVO) may differentiate itself from retinal artery occlusion (RAO) in terms of its aetiology and pathology, but both contribute to sight loss or even blindness.
The pathogenesis of RAO is generally accepted to be directly related to atherosclerotic thromboembolism (80%) and cardiac embolism, rarely vasculitis, or thrombophilic states. Importantly, the pathogenesis of RAO and strokes or arterial thromboembolism has many similarities. Indeed, retinal emboli are commonly associated with hypertension, atrial fibrillation, coronary heart disease, increased plasma lipoprotein, and smoking,3 thus we are dealing with a systemic condition, not something simply isolated to the eye.
In contrast, the pathogenesis of RVO has more diverse precipitating factors of ocular or systemic causes. The central retinal artery and central retinal vein share a common adventitial sheath and are naturally compressed when crossing through the lamina cribrosa behind the eye. Increased intra-ocular pressure, deformation of the lamina, and compression by an atherosclerotic central retinal artery are suggested mechanisms of central retinal vein obstruction (CRVO). Hypercoagulable states, thrombophilia or vasculitis become more important in younger patients.1
With regard of branch retinal vein obstruction (BRVO), venous flow is usually interrupted at a retinal arteriovenous crossing site as a retinal artery crosses over a retinal vein. Systemic vascular risk factors of …
Contributors The editorial was jointly written by all authors
Competing Interest None.
Provenance and peer review Commissioned; externally peer reviewed.