Managing PVR in the Era of Small Gauge Surgery

Abstract

Proliferative vitreoretinopathy (PVR) is the leading cause of failed rhegmatogenous retinal detachment (RRD) surgery. Based upon the presence of clinical features and due to associated underlying risk factors, it is classified into various grades based upon its severity and extent of involvement. Despite excellent skills, flawless techniques, and high-end technology applied in the management of RRD, PVR still occurs in 5–10% of cases. Due to the advancements in wide angle viewing systems, advance vitrectomy machines and fluidics, early identification, use of long-term heavy silicon oil tamponades, high-speed cutters, small-gauge vitrectomies, use of perfluorocarbon liquid (PFCL), and small-gauge forceps and scissors, the success rate in the management of PVR has increased leading to improved anatomical outcomes. However, functional outcomes do not correlate well with improved anatomical outcomes. Various complications occur after RRD repair that are responsible for re-retinal detachment and recurrence of PVR. This article highlights causes, risk factors, classification, grading, diagnosis, and approach to management of PVR and post-PVR surgery complications.

Outcomes and predictors of vitrectomy and silicone oil tamponade in retinal detachments complicated by proliferative vitreoretinopathy

“…R hegmatogenous retinal detachments (RRD) are managed with a variety of methods and the success rate for primary repair is over 80% [1][2][3] . The major cause of failure in retinal detachment repair is proliferative vitreoretinopathy (PVR) [4][5] . The key factor triggering PVR development seems to be partial dedifferentiation, migration, and proliferation of retinal pigment epithelial (RPE) cells, resulting in the formation of fibrocellular membrane [5][6][7] .…”

“…The major cause of failure in retinal detachment repair is proliferative vitreoretinopathy (PVR) [4][5] . The key factor triggering PVR development seems to be partial dedifferentiation, migration, and proliferation of retinal pigment epithelial (RPE) cells, resulting in the formation of fibrocellular membrane [5][6][7] . The formation of these membranes may lead to traction on both surfaces of the retina and cause fixed retinal folds, new retinal breaks and re-opening of treated breaks.…”

Pirfenidone: A Promising Drug in Ocular Therapeutics

“…[17] Additionally, X. Liu et al reported a decrease in cystic fibrosis transmembrane conductance regulator (CFTR), E-cadherin, matrix metalloproteinase (MMP), and fibronectin levels attributed to pirfenidone. [40] Based on the literature findings it could be [22] (B) corneal wound, [23] (C) microbial keratitis, [24] (D) corneal fibrosis, [25] (E) acute angle closure glaucoma, [26] (F) ocular inflammation, [27] (G) proliferative vitreoretinopathy, [28] and (H) strabismus surgery. [29] [The figures were reproduced with appropriate copyright permissions obtained from the respective publishers.…”

N6-Methyladenosine-Modification-Related Ophthalmic Diseases and Potential Therapeutic Strategies

“…Broadly Proliferative vitreoretinopathy (PVR) can be divided into two groups, one is a long-standing preexisting rhegmatogenous retinal detachment (RRD) and the other is PVRs that occur after initial surgery in patients with RRDs. These events trigger a complex pathogenic mechanism by bringing RPE cells into the vitreous cavity, leading to membrane formation and ultimately to PVR complications [89]. EMT is considered a key pathological mechanism of PVR, and TGF-β is a pivotal growth factor known to induce EMT of RPE cells [90].…”