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


History
A 47 year-old woman presented with complaints of bright flashes of light, decreased vision, and pain OD for one week. Her past ocular history was significant for cataract surgery three years prior and intraocular lens exchange two years ago. She presented to her primary ophthalmologist one year prior with similar symptoms. At that time, her visual acuity OD was 20/200 and dilated fundoscopic examination revealed a temporal macula off retinal detachment. The patient underwent scleral buckling, endolaser photocoagulation, and SF6 gas exchange. Her retina was attached up to five months prior to current presentation when she developed an inferior retinal detachment. She subsequently underwent IOL removal, repeat vitrectomy, and silicone oil tamponade.

Examination
Visual Acuity - Hand motions OD, 20/25 OS
Pupils - surgically dilated OD pupil, unable to determine if there is an afferent defect.
Intraocular pressures: 8 mm Hg OD, 18 mm Hg OS
Lens - aphakic
Dilated fundoscopic examination:
Silicone oil with total retinal detachment with multiple breaks, retinal and submacular fibrosis (Figures 1 and 2).

Fundus Picture 1
 Initial fundus examination

Fundus pic 2
 Initial peripheral fundus exam

Treatment
The patient underwent pars plana vitrectomy, epiretinal membrane peeling, relaxing retinotomy, air/fluid exchange, argon endolaser, and silicone oil exchange (see videos).

Initial exam.
 Requires Windows Media Player to view.

Membrane removal.

Retinotomy.

Endolaser.

Final appearance.

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).

References
1. Charteris DG. Sethi CS. Lewis GP. Fisher SK. Proliferative vitreoretinopathy-developments in adjunctive treatment and retinal pathology. Eye. 2002; 16(4):369-74.
2. The Retina Society Terminology Committee. The classification of retinal detachment with proliferative vitreoretinopathy. Ophthalmology 1983; 90: 121-125.
3. Cardillo JA. Stout JT. LaBree L. Azen SP. Omphroy L. Cui JZ. Kimura H. Hinton DR. Ryan SJ. Post-traumatic proliferative vitreoretinopathy. The epidemiologic profile, onset, risk factors, and visual outcome. Ophthalmology 1997; 104(7):1166-73.
4. Claes C, Bartz-Schmidt K, Eckardt C. Advanced Vitreoretinal Course, Antwerp, Belgium Mar. 16-8 2001.
5. Kon CH. Asaria RH. Occleston NL. Khaw PT. Aylward GW. Risk factors for proliferative vitreoretinopathy after primary vitrectomy: a prospective study. British Journal of Ophthalmology. 2000; 84(5):506-1.
6. Bonnet M. Guenoun S. Surgical risk factors for severe postoperative proliferative vitreoretinopathy (PVR) in retinal detachment with grade B PVR. Graefes Archive for Clinical & Experimental Ophthalmology. 1995; 233(12):789-91.
7. Nagasaki H. Shinagawa K. Mochizuki M. Risk factors for proliferative vitreoretinopathy. Progress in Retinal & Eye Research. 1998; 17(1):77-98.
8. Abrams GW. Azen SP. McCuen BW 2nd. Flynn HW Jr. Lai MY. Ryan SJ. Vitrectomy with silicone oil or long-acting gas in eyes with severe proliferative vitreoretinopathy: results of additional and long-term follow-up. Silicone Study report 11. Archives of Ophthalmology. 1997; 115(3):335-44.
9, Lewis H, Aaberg TM, Abrams GW. Cause of failure after initial vitreoretinal surgery for severe proliferative vitreoretinopathy. Am J Ophthalmol 1991; 111: 8-14.
10. Wiedemann P. Hilgers RD. Bauer P. Heimann K. Adjunctive daunorubicin in the treatment of proliferative vitreoretinopathy: results of a multicenter clinical trial. Daunomycin Study Group. American Journal of Ophthalmology. Oct; 126(4):550-9.
11. Asaria RH. Kon CH. Bunce C. Charteris DG. Wong D. Khaw PT. Aylward GW. Adjuvant 5-fluorouracil and heparin prevents proliferative vitreoretinopathy : Results from a randomized, double-blind, controlled clinical trial. Ophthalmology. 2001. 108(7):1179-83.
12. Jonas JB. Hayler JK. Panda-Jonas S. Intravitreal injection of crystalline cortisone as adjunctive treatment of proliferative vitreoretinopathy. British Journal of Ophthalmology. 2000; 84(9):1064-7.
13. Takahashi M. Refojo MF. Nakagawa M. Veloso A Jr. Leong FL. Antiproliferative effect of retinoic acid in 1% sodium hyaluronate in an animal model of PVR. Current Eye Research. 1997; 16(7):703-9.