Proliferative diabetic vitreoretinopathy

Abstract

This chapter reviews the pathogenesis of proliferative diabetic vitreoretinopathy (PDVR) and presents recommendations for its clinical staging. Although numerous biochemical mediators may be responsible for the pathogenesis of PDVR, there is no consensus about the biochemical pathway(s) responsible for the progression of PDVR. Among the known and most studied mediators is vascular endothelial growth factor (VEGF) [18]. Since the thickened posterior vitreous cortex is one of the main components in proliferative diabetic retinopathy (PDR) causing the subsequent development of retinal proliferations, shrinkage of the diabetic posterior vitreous cortex leads to traction retinal detachment. Although several classifications are described in the literature, the classification suggested herein is important in the clinical assessment of disease severity, the communication about the disease state, and the evaluation of therapy. A new morphological classification of PDVR is presented which emphasizes the role of vitreous, hence the name PDVR. Moreover, this classification reliably predicts the surgical outcome in advanced stages of PDVR.