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The development of macular edema (ME) followed by BRVO has been hypothesized to be caused by fluid flux from vessels to tissue according to Starling's law,47,48 which is based on the breakdown of the blood-retinal barrier (BRB) as a result of damage to the tight junctions of capillary endothelial cells,49vitreoretinal adhesion,50 and secretion into the vitreous of vasopermeability factors produced in the retina.51,52 Observations by Noma et al.52 suggest that in patients with BRVO, vascular occlusion induces the expression of vascular endothelial growth factor (VEGF) and Interleukin-6 (IL-6), resulting in BRB breakdown and increased vascular permeability