Pathogenesis of Retinal Vein Occlusion

Abstract

Retinal vein occlusion (RVO) has multiple pathogenetic mechanism that including local anatomical susceptibility, degenerative changes of the vessel wall and abnormal hematological abnormalities. All of these mechanisms could contribute to develop vascular obstruction. Anatomic features of arteriovenous crossings and common adventitial sheath shared by artery and vein could cause turbulent flow. Turbulence in vessel flow promotes endothelial phenotypic changes that cause endothelial f-actin expression increase. Intercellular adhesions and endothelial functions are affected by high f-actin levels. Damaged arteries and hypoxic tissues express endothelin-1 (ET-1). Endothelin-1 can diffuse from the neighboring veins and stimulate venous vasoconstriction. Vasoconstiriction of veins lead to an increase in pressure. High blood viscosity is another important factor in pathogenesis of RVO. Pathogenesis of RVO is very complex and these factors can lead to a vicious cycle of worsening the other factor.