Proliferative Vitreoretinopathy

Proliferative vitreoretinopathy (PVR) is a complex pathological process and the leading cause of failure in retinal detachment surgery. Characterized by the proliferation and migration of retinal pigment epithelial (RPE) cells, glial cells, and fibroblasts into the vitreous cavity and onto retinal surfaces, PVR results in the formation of fibrotic membranes. These membranes contract, exerting traction on the retina, which can lead to recurrent or tractional retinal detachment. PVR typically develops following rhegmatogenous retinal detachment, ocular trauma, or intraocular surgery, although it may also arise spontaneously in rare cases. The pathogenesis of PVR is multifactorial and involves a cascade of cellular and molecular events, including inflammation, cytokine release, extracellular matrix remodeling, and cell-mediated contraction. Risk factors include the extent and duration of retinal detachment, large or multiple retinal breaks, vitreous hemorrhage, and prior ocular surgeries. Clinically, PVR is graded based on the extent and location of the membranes, with the most severe forms involving full-thickness retinal folds and fixed retinal detachment. Management of PVR remains a significant challenge in vitreoretinal surgery. While pars plana vitrectomy combined with membrane peeling and tamponade agents such as silicone oil or gas remains the standard approach, recurrence is not uncommon. Pharmacologic adjuncts, including anti-proliferative and anti-inflammatory agents, are being investigated to improve outcomes. Prevention strategies, early detection, and advances in surgical techniques are crucial to minimizing vision loss associated with PVR. Ongoing research aims to better understand its molecular mechanisms and to develop more effective therapeutic interventions.