Mechanisms involved in vein occlusion related macular edema

Abstract

AbstractPurpose To describe the pathophysiological processes involved in vein occlusion related macular edema.Methods Review of the experimental and clinical published data explaining the pathophysiological mechanisms involved in vein occlusion related macular edema.Results Venous stasis lead to internal blood‐retinal barrier breakdown, extravasation of blood vessel content and finally to macular edema. Tissular hypoxia of the internal retinal layers develops secondary to arterial blood flow decrease, followed by Na+/K+ ATPase pump dysfunction, intracellular edema, and neuronal cell death by necrosis and apoptosis. Many vasopermeability factors will be subsequently released, as inflammatory mediators and VEGF. The rationale for clinical treatment of macular edema is based on the understanding and the inhibition of these pathophysiological mechanisms. On the medical side, nonsteroidal anti‐inflammatory drugs inhibit the production of prostaglandins and leukotrienes, and modulate fluid movement coupled to chloride movement. Corticosteroids block cyclooxygenase and interleukin, downregulate VEGF and decrease the phosphorylation of occludin, thereby increasing the tightness of the blood‐retinal barrier. Anti‐VEGF agents restore occludin proteins in the blood‐retinal barrier and reduce protein kinase C activation.Conclusion New advances in understanding the mechanisms involved vein occlusion related macular edema lead to development of new therapeutical strategies which have to be confirmed by clinical randomized trials.