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47 year old female with history of flashes of light OD
Digital Journal of Ophthalmology 2005
Volume 11, Number 6
January 9, 2005
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Rishi Singh, M.D. | Massachusetts Eye and Ear Infirmary
Donald D'Amico, M.D. | Massachusetts Eye and Ear Infirmary
Diagnosis and Discussion
Proliferative vitreoretinopathy (PVR) is a non-neoplastic intraocular growth resulting from an excessive inflammatory reaction after a retinal break. On a microscopic level, PVR consists of dense glial membranes with complex layered architectures and focal glial ‘pegs’ extending to the inner retina from the membranes (1). It occurs in 5-10% of all rhegmatogenous retinal detachments (2), and in case of penetrating ocular trauma and retinal translocation surgery, the incidence of PVR increases to 25% and 18-23% respectively (3,4). While the causes of PVR have not been elucidated, certain risk factors for the development of this condition have been identified by multivariate analysis. These risk factors include aphakia, long duration of retinal detachment, vitreous hemorrhage, choroidal detachment, presence of preoperative PVR, larger size of detachment, use of silicone oil, high vitreous protein level, and the use of extensive cryotherapy during retinal detachment repair (5,6,7).
Visual outcome in PVR has been historically poor after repair. Many studies such as the Silicone Oil Study group have reported 11-25% of patients overall will have 20/100 or better vision (8,9). It is hypothesized that poor visual outcome after PVR repair may be due to irreversible photoreceptor loss or misaligment, epiretinal and subretinal pathology such as RPE scarring and multilayering, toxicity to intraocular agents such as silicone oil, or optic neuropathy (3).
The current management of PVR is largely surgical. The Silicone Oil Study group evaluated the outcomes of vitreoretinal surgery for retinal detachment with PVR and compared long-acting gas or silicone oil as the intraocular tamponade. In this prospective, randomized, multicentered surgical trial, it was found that silicone oil and perfluoropropane gas were equal in most respects for the management of retinal detachments with PVR (8).
Many studies have investigated the use of adjuvant therapies for fighting PVR. These agents have typically targeted the proliferation of cell types known to be involved in PVR, the production and subsequent traction of the extracellular matrix proteins, retinal deposition of fibrin for the scaffolding of membrane formation, or growth factors found in PVR development. One of the first agents used was Daunorubicin infused at the time of vitrectomy. This randomized study found a significant decrease in reoperations after one year of treatment. However, retinal reattachment rates were only marginally improved, and there was no statistically significant difference in visual acuity between the two groups (10).
Current trials in Europe have examined 5-flourouracial (5-FU) and low molecular weight heparin (LMWH) in combination to reduce PVR formation. These studies showed significant reduction in both the incidence of postoperative PVR and in the re-operation rate. Again, visual outcomes in this study were not statistically different between adjuvant and placebo groups (11). Other promising agents currently under investigation include intravitreal injections of corticosteriods and retinoic acid (12,13).