Anatomical and Functional Outcomes After Vitrectomy in Eyes With Tractional Diabetic Macular Edema

Diabetic retinopathy (DR) is one of the leading causes of vision loss worldwide [1]. In 2010, DR affected more than 93 million individuals worldwide, 28 million of whom experienced vision-threatening DR[2].

Diabetic macular edema (DME) is a common cause of visual loss in diabetic retinopathy (DR) and is a complication in any stages of DR including proliferative diabetic retinopathy (PDR)[3].

The terms vitreous traction maculopathy, vitreous induced diabetic macular edema and maculopathy due to posterior hyaloid traction are synonymous and describe a pattern of diabetic maculopathy which is characterized by: (1) The absence of complete posterior vitreous detachment; (2) An increased retinal thickness in the center of the macula, and (3) a characteristic reflex of the vitreoretinal interface[4]. there are multiple factors in the vitreomacular interface including ERM, taut posterior cortices, vitreoschisis, PVD, and adhesions [5]. Anomalous PVD generates antero-posterior and tangential traction forces at the vitreo-retinal interface that act upon the inner and outer retinal layers [6]. Until recently, the only treatment option available for VMA was vitrectomy[7].

Few studies have used the multifocal electroretinogram (mfERG) technique to investigate the effects of vitrectomy on macular visual function for DME [8]. Mf-ERG is an objective electrophysiologic technique that measures the electrical changes in the central retinal area. This technique accurately assess the electrophysiologic activity in multiple retinal areas, and gives us a topographic charting of retinal function [9] .