Article Date: 1/1/2005

PEER REVIEWED
The Evolving Treatment Paradigm for Eyes With Branch Retinal Vein Occlusion
SHARON FEKRAT, MD, JONATHAN ETTER

Ten years ago, treatment options for eyes with retinal vein occlusion were limited. For eyes with a branch retinal vein occlusion (BRVO), either observation or grid-pattern laser photocoagulation per the Branch Vein Occlusion Study (BVOS) was recommended.1 In 2005, the treatment paradigm has expanded.

TREATMENT OPTIONS FOR BRANCH RETINAL VEIN OCCLUSION

Vision loss in eyes with BRVO is caused by 1 or more of the following: perfused or nonischemic macular edema, nonperfused or ischemic macular edema (Figure 1), foveal hemorrhage, foveal retinal pigment epithelial (RPE) changes from chronic macular edema, vitreous hemorrhage, and/or traction retinal detachment. The majority of novel treatment options are aimed at reducing the macular edema, whether perfused or nonperfused, in order to restore visual acuity with or without a simultaneous attempt to hasten resolution of the associated intraretinal hemorrhage. Arteriovenous sheathotomy is the only method that attempts to achieve this by actually restoring the impaired venous outflow.

NATURAL HISTORY
Perfused Macular Edema

The natural history of perfused macular edema in eyes with BRVO has not been well documented. Of 35 untreated eyes in the BVOS at 3 years, all had a BRVO for 3­18 months prior to study entry. It is not possible to obtain adequate natural history information from such small numbers with such variable durations of BRVO prior to study entry.1 Moreover, no patient was entered into the BVOS until 3 months after the occlusion because of a clinical impression that spontaneous improvement often occurred during that period. The change in visual acuity and natural history in untreated eyes with BRVO from onset until 3 months cannot be extracted from the BVOS.

In a 1999 report by Parodi and colleagues, all 99 eyes with a macular BRVO of less than 2 weeks duration upon study entry, and a 3 month observation period upon study entry, had statistically significant spontaneous improvement in mean logMAR (logarithm of the inverse of the Snellen fraction) visual acuity values at 3 months compared with baseline.4 However, only macular BRVO, a subgroup of BRVO in which the occlusion is limited to a small vessel draining a sector of the macular region, was evaluated. (Figure 2) Thus, the improvement in mean acuity is not surprising since a smaller area of involved retina is more likely to be efficiently drained by surrounding collateral channels. In larger and more commonly observed BRVO, the visual acuity may not similarly improve within the first 3 months after the onset of symptoms.

Unfortunately, there is little natural history data about the early course of BRVO to help guide management and timing of intervention.

Nonperfused Macular Edema

There is currently no recommended treatment for eyes with nonperfused macular edema because of BRVO.

In a retrospective study, Finkelstein found that in 23 BRVO eyes seen between 1975 and 1989 with macular capillary nonperfusion and macular edema, there was a greater likelihood of spontaneous improvement without grid-pattern laser photocoagulation treatment when compared to 7 similarly untreated cases of perfused macular edema.5 In that study, 91% of BRVO eyes with nonperfused macular edema improved without treatment compared with 29% with perfused macular edema. The time to best visual acuity ranged from 3­64 months (median, 14 months). Median initial visual acuity was 20/80 and median final visual acuity was 20/30. Although this retrospective report with nonstandardized visual acuity measurements is interesting, the numbers are too small to be convincing.

In contrast to Finkelstein's findings, other studies have evaluated the natural history for visual acuity in untreated eyes with BRVO and macular nonperfusion and have suggested a worsened visual acuity outcome in these cases.6,7 Clemett and colleagues noted that 34 untreated eyes with perfused macular edema on high-quality angiography had a significantly better prognosis than 21 untreated eyes with nonperfused macular edema.6 Shilling and Jones evaluated 2 groups of eyes with BRVO.7 One group consisted of 22 eyes with a BRVO of 3 months duration or less and nonperfused macular edema, 13 eyes that received grid-pattern laser treatment to areas of angiographic capillary leakage at 3 months and 9 eyes that did not. Treated eyes did not have significantly better visual acuity than untreated eyes at both the 1- and 2-year follow-up visits. The second group consisted of 25 eyes with a BRVO greater than 1 year in duration, 15 eyes which received grid-pattern laser photocoagulation treatment and 10 that did not. Similar to the other group, treated eyes did not have significantly better visual acuity than untreated eyes. Within the treated and untreated groups, those with perfused macular edema had a significantly better visual prognosis than those with macular nonperfusion.7

MEDICAL INTERVENTION

Currently, there is no known benefit of using systemic anticoagulants in BRVO. The use of systemic anticoagulation may result in adverse effects, such as increased intraretinal hemorrhage and systemic bleeding sequelae, and thus is contraindicated.2 The utility of troxerutin in BRVO has been investigated, but awaits more formal evaluation with a large-scale trial.3

Figure 1. Ischemic branch retinal vein occlusion.

Grid-pattern Laser Photocoagulation

The BVOS evaluated grid-pattern laser photocoagulation for the treatment of macular edema.1 Based on the BVOS data, grid-pattern laser photocoagulation has been recommended for eyes with a BRVO of 3­18 months duration if visual acuity is 20/40 or worse and if fluorescein angiography documents macular edema without foveal hemorrhage as the cause of visual loss. It is important to realize that the eyes in the BVOS were not rigorously divided into categories of macular perfusion (ie, perfused versus nonperfused macular edema) because the fluorescein angiograms generally were not of high enough quality to provide differentiation.5 However, patients with "distinct" areas of capillary nonperfusion in the macula were excluded. Although the BVOS is the largest randomized trial evaluating laser treatment of macular edema, only 139 patients were enrolled in the macular edema arm, 71 treated and 68 not treated; the reported 3-year data were only in 78 eyes, 43 treated and 35 not treated.1 These small numbers and lack of precise angiographic differentiation of macular edema make the results more difficult to interpret.

The BVOS demonstrated a benefit of grid-pattern laser photocoagulation treatment for macular edema from BRVO that met the criteria defined above.1 At 3 years, 65% of 43 treated individuals gained at least 2 lines of vision vs. 37% of the 35 eyes in the untreated, control group. A higher percentage of treated patients had a visual acuity of 20/40 or better at 3 years (60% vs. 34%). The mean number of lines of vision gained was 1.33 in the treated and 0.23 in the control group at 3 years. While the improved outcome of treated eyes was statistically significant, it offers little hope to those with poor acuity. A 1.33 line improvement in a patient with 20/100 or worse visual acuity does not provide vision that meets the legal driving limit in that eye in most states. These results indicate that the natural course of this retinal vascular disease is relatively static at 3 years with only an average 0.23 line improvement in untreated eyes. Since eyes with foveal hemorrhage or macular nonperfusion were excluded from the BVOS, there is no currently recommended treatment for these subgroups.

In a small, retrospective, uncontrolled study, 11 of 12 eyes with macular edema from BRVO had improved visual acuity after grid-pattern laser photocoagulation treatment administered per the BVOS guidelines, and all of the 12 eyes had improvement or disappearance of the macular edema.8 Visual acuity measurements were not standardized or masked. The angiographic type of macular edema was not mentioned nor was concurrent foveal edema or hemorrhage noted.

Other studies have suggested that grid-pattern laser photocoagulation may not be effective in improving visual acuity in eyes with BRVO.4,7,9-10 Parodi and colleagues prospectively studied 99 eyes with a macular BRVO and equivalent numbers of both nonischemic and ischemic macular edema in all groups.4 Eyes were randomized to observation or laser treatment (early at 3 months or later at 6­18 months). No statistically significant difference between the treated and control groups with regard to reduction of angiographic leakage or visual acuity was found. Similarly, Shilling and Jones demonstrated that eyes receiving grid-pattern laser photocoagulation treatment did not have significantly better vision than untreated eyes, even though the macular edema decreased in treated eyes.7 Finally, Barbazetto and Schmidt-Erfurth evaluated functional defects in BRVO before and after grid-pattern laser photocoagulation treatment per the BVOS using scanning laser perimetry.10 Of 39 treated eyes with BRVO, the central scotoma remained unchanged or encroached on foveal fixation in 67% of eyes. In addition, the total scotoma size increased in 50% of eyes after laser treatment. Treated eyes had worse mean visual acuity 3 months after laser treatment compared to untreated eyes, although the numbers were small.

Although the BVOS showed a benefit of laser photocoagulation in perfused macular edema, the numbers in the BVOS were small, the improvement in visual acuity minimal, and because of conflicting data regarding grid-pattern laser photocoagulation treatment, it is important to re-evaluate conventional laser treatment per the BVOS, as well as evaluate novel treatments to lessen macular edema in eyes with BRVO.

Intravitreal Triamcinolone Acetonide

Intravitreal triamcinolone (Kenalog, Bristol-Myers Squibb) has been documented to lead to resolution of macular edema in eyes with BRVO with improved visual acuity. However, its effect is transient, and its use may lead to steroid-induced cataract formation as well as steroid-induced intraocular pressure elevation. There is currently a multicenter, randomized, clinical trial study in progress called The Standard of Care vs. Corticosteroid for Retinal Vein Occlusion (SCORE) Study.11 The SCORE study will randomize eyes with macular edema secondary to BRVO into 3 treatment groups. One group will receive the standard of care (observation or grid-pattern laser photocoagulation per the BVOS criteria), a second group will receive
4 mg of intravitreal triamcinolone, and a third group will receive 1 mg of intravitreal triamcinolone. In total, these groups will be followed for 36 months. The primary efficacy will be measured by an improvement of 15 or more letters in visual acuity at the 12-month visit. The SCORE study will evaluate the safety profile of triamcinolone by monitoring cataract formation, intraocular pressure changes, and injection-related events such as endophthalmitis, vitreous hemorrhage, and retinal detachment. The results of this important study are awaited by many.

Pegaptanib Sodium Injection (Macugen)

Pegaptanib sodium injection is a pegylated aptamer that selectively inhibits vascular endothelial growth factor (VEGF) 165. Its ability to reduce macular edema in eyes with central retinal vein occlusion (CRVO) is currently under study and it may subsequently be evaluated in eyes with BRVO. Pegaptanib sodium itself is associated with few adverse effects; however, the intravitreal injection may rarely result in endophthalmitis or retinal detachment.

SURGICAL INTERVENTION
Sustained Drug Release Devices

Intraocular devices that provide sustained release of medication have application in several posterior segment diseases. Proposed advantages include constant drug levels and duration of treatment tailored to the appropriate disease.12 Two such devices, the fluocinolone acetonide implant (Retisert) and dexamethasone implant (Posurdex), have been used to treat diabetic macular edema, and Retisert is currently being evaluated in eyes with retinal vein occlusion.

Retisert is nonbiodegradable and is secured intraocularly with scleral suture. The device contains a total of 0.5 mg fluocinolone and is designed to release 0.5 mcg per day for 3 years. Adverse effects, such as increased intraocular pressure and cataract progression, present in increased frequency in eyes with diabetic edema that received the implant. Most patients with elevated intraocular pressure (IOP) were satisfactorily treated with drops. Eight patients required trabeculectomy. The study is ongoing.

Figure 2. Macular branch retinal vein occlusion.

Vitrectomy With Vitreomacular Separation

Removal of the posterior hyaloid during vitrectomy surgery may contribute to resolution of cystoid macular edema in eyes with BRVO. Recent data suggest that a detached posterior hyaloid may be beneficial for eyes with macular edema from BRVO. Studies by Avunduk and associates and Takahashi and coworkers demonstrated that eyes with BRVO and ophthalmoscopic separation of the vitreous from the macula had a significantly lower rate of macular edema.13,14 Takahashi and associates further suggested that the status of the vitreomacular interface might affect macular edema associated with BRVO. Of 58 eyes that were retrospectively studied, the incidence of macular edema was significantly lower in eyes with vitreomacular separation (41%) than vitreomacular attachment (93%).14 However, eyes with vitreomacular separation may still have cystoid macular edema.14 In these cases, the remaining vitreous gel, although detached from the retinal surface, may prevent access of oxygenated aqueous to the deprived inner retinal surface.19 Vitrectomy in eyes with vitreomacular separation and macular edema may allow access of oxygenated aqueous to the inner retina, thereby improving macular edema, decreasing retinal nonperfusion, decreasing the risk of neovascularization, and improving visual acuity.19 Conversely, Trempe and colleagues reported no significant correlation between the status of the hyaloid (separated in only 8 of 28 eyes with macular edema) and the development of macular edema despite acknowledging that the vitreous may have influenced the evolution of BRVO in 50 eyes with BRVO when compared to age-matched controls.15 The number of eyes in this study was too small for definitive conclusions.

An increased risk of BRVO formation is present in eyes with decreased axial length and hyperopia.16-18 This may be due in part to the higher likelihood of vitreomacular attachment in these shorter eyes. Perhaps attached hyaloid may compress a susceptible arteriovenous crossing, resulting in BRVO formation in addition to or irrespective of the adventitial sheath. It is interesting to note that the development of a BRVO has not been reported anywhere in the literature in a vitrectomized eye nor has such a case been described by colleagues indirectly implying that the vitreous itself may play a role in the development of a BRVO and perhaps the associated macular edema. Those eyes with vitreomacular separation may be less likely to have macular edema and perhaps less likely to even develop a BRVO.

Stefansson and colleagues demonstrated that inducing a BRVO in nonvitrectomized feline eyes resulted in retinal hypoxia, while inducing a BRVO in vitrectomized eyes produced no change in the retinal oxygen tension.19 It may be that in vitrectomized eyes with BRVO, the normally oxygenated aqueous may then gain access to and bathe the inner retina, thereby providing oxygen to the deprived inner retinal tissue.19 In 7 human eyes with BRVO and no posterior vitreous detachment, Kurimoto and coworkers reported that pars plana vitrectomy with intraoperative posterior hyaloid separation/removal improved visual acuity and decreased macular edema, both angiographically and by retinal thickness analysis in 7 eyes 1 month postoperatively.20 In another series of 16 eyes with nonperfused macular edema from BRVO, vitrectomy with intraoperative detachment and removal of the hyaloid resulted in improved visual acuity in 12 of 16 eyes (75%) and no change in the remaining 4 eyes.21 Moreover, in these eyes there was new vessel and collateral vessel growth into previously nonperfused areas postoperatively.21

These studies suggest that vitrectomy and posterior hyaloid separation/removal from the macular region alone can decrease macular edema and improve visual acuity, as well as lessen and perhaps improve retinal nonperfusion, thus decreasing neovascular complications. The potential added benefit of concurrent removal of the internal limiting membrane in these eyes with or without the assistance of indocyanine green (ICG) is unknown.

Vitrectomy With Arteriovenous Sheathotomy

Pars plana vitrectomy and posterior hyaloid separation/removal with sectioning of the adventitial sheath (sheathotomy) at the etiologic arteriovenous crossing has been performed as a treatment for BRVO. Published studies have demonstrated that vitrectomy with sheathotomy can result in retinal reperfusion, decreased macular edema, and visual improvement.22-28

Osterloh and Charles reported significant visual improvement after sheathotomy in a 54-year-old woman with a 3-week history of a BRVO.24 The perfusion status of the vein occlusion and macular edema was not mentioned. Preoperatively, the visual acuity was 20/200, and this gradually improved to 20/40 by 3 months and 20/25 by 8 months postoperatively. No changes were noted in the caliber of the affected vein intraoperatively. There was no mention of the posterior hyaloid status. At 8 months, the intraretinal hemorrhage had reabsorbed, which may have occurred due to the natural history alone. Macular edema remained.

In a prospective, nonrandomized series, Opremcak and Bruce reported equal or improved visual acuity in 12 of 15 patients (80%).22 Ten (67%) patients had improved postoperative visual acuities, with a mean gain of 4 lines. Three patients had a mean decline in acuity of 2 lines. Visual acuity examiners in this small series were not masked to treatment, potentially biasing the results. All had marked resolution of intraretinal hemorrhage and edema over a mean follow-up of 5 months. However, 46% of these 15 eyes had macular nonperfusion,22 the natural history of which may be favorable.5 The duration of visual symptoms ranged from 1­12 months, with a mean of 3.3 months. It is possible that the intraoperative removal of an attached hyaloid is necessary to relieve any mechanical pressure from the hyaloid on the etiologic arteriovenous crossing, to remove any traction exerted on the macula,29 to remove the reservoir for molecules that may increase capillary permeability, and to improve inner retinal oxygenation as aqueous bathes the inner retinal surface.30

In a retrospective, uncontrolled series, Shah and colleagues reported 4 of 5 eyes with visual improvement after sheathotomy.26 All 5 eyes had a preoperative visual acuity of 20/200 or worse. The status of the posterior hyaloid was not mentioned. In 4 of 5 eyes, the visual acuity improved to 20/30­20/70 over a mean follow-up of 6.5 years.26

In a prospective, nonrandomized study of 50 patients, Opremcak and Bruce reported equal or improved visual acuity in 92% of patients.23 Visual acuity improved in 38 of 50 eyes (76%) with a mean of 4.5 lines of acuity gained. Visual recovery was not related to perfusion status.

In a retrospective, case-control study of 24 eyes, Lee and colleagues compared visual acuity outcomes in persons with BRVO who underwent arteriovenous sheathotomy or grid-pattern laser photocoagulation treatment.27 Five of 14 (36%) eyes that underwent sheathotomy surgery and 6 of 14 (43%) eyes that underwent grid-pattern laser photocoagulation treatment improved 2 or more lines (P=1.00) at a mean follow-up of 7.8 months. There was progression of nuclear sclerotic cataract in 50% of those eyes that underwent sheathotomy and this was not observed in the eyes that received laser treatment. The cataract progression may have lessened any beneficial effect on visual acuity.

In a prospective, uncontrolled study, Mester and Dillinger reported improved visual acuity in all 12 eyes following sheathotomy, and 25% of eyes gained more than 4 lines in the few weeks postoperatively.25 The perfusion status of the BRVO was not disclosed.

Cahill and colleagues noted that in the majority of cases, despite an improvement in macular edema following sheathotomy, there was no improvement in visual acuity.28 Visual improvement following sheathotomy surgery may not be the direct result of intervention. The visual acuity may have improved because of natural history, or perhaps the visual improvement was the direct result of the vitrectomy alone and not the sheathotomy portion of the procedure. Moreover, if indeed a thrombus had formed in the branch vein at the etiologic arteriovenous crossing,31,32 sectioning the adventitial sheath may not lead to improvement in venous outflow because the thrombus may have already organized. Relieving the obstruction may not remove the organized thrombus, rendering the sheathotomy portion of the surgery ineffective in some cases. Thus, if arteriovenous sheathotomy is to be effective in eyes with an organized thrombus at the crossing, the procedure may have to be performed early in the course of the BRVO for a chance at visual improvement. Which eyes form an organized thrombus and which do not cannot currently be predicted preoperatively.

Some have added an injection of recombinant tissue plasminogen activator (r-tPA) following sheathotomy to achieve additional fibrinolysis. A recent study by Garcia-Arumi and colleagues demonstrated that sheathotomy with subsequent r-tPA injection at the venous occlusion site resulted in a 40% postoperative reduction macular thickness in 31 of 40 patients. Visual acuity also increased by 3 or more lines in 70% of treated eyes.33

Overall, vitrectomy with arteriovenous sheathotomy is being performed less commonly than it had been in the past.

The best treatment option for eyes with BRVO is currently unknown and the treatment paradigm is continually evolving. In another 10 years, our approach to BRVO will likely be altogether different.

Address correspondence to: Sharon Fekrat, MD, Associate Professor, Vitreoretinal Surgery Department, Duke University Eye Center, Box 3802, DUMC, Durham, NC 27710, Telephone: (919) 681-0341, Fax: (919) 681-6474, E-mail: fekra001@mc.duke.edu.

 

REFERENCES

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4. Parodi BM, Saviano S, Ravalico G. Grid laser treatment in macular branch reti nal vein occlusion. Graefes Arch Clin Exp Ophthalmol. 1999;237:1024-1027.

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8. Arnarsson A, Steffansson E. Laser treatment and the mechanism of edema reduction in branch retinal vein occlusion. Invest Ophthalmol Vis Sci. 2000;41:877-879.

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10. Barbazetto IA, Schmidt-Erfurth UM. Evaluation of functional defects in branch retinal vein occlusion before and after laser treatment with scanning laser perimetry. Ophthalmology. 2000;107:1089-1098.

11. National Eye Institute. The Standard Care vs. Corticosteroid for Retinal Vein Occlusion (SCORE) Study: two randomized trials to compare the efficacy and safety of intravitreal injection(s) of triamcinolone acetonide with standard care to treat macular edema. Available at: http://www.nei.nih.gov/neitrials/viewstudyweb.aspx?id=99. Accessed on December 7, 2005.

12. Jaffe GJ. Intraocular sustained drug delivery for retinal diseases. Available at: http://www.retinalphysician.com/article.aspx?article=100040. Accessed on December 9, 2004.

13. Avunduk AM, Cetinkaya K, Kapicioglu Z, Kaya C. The effect of posterior vitreous detachment on the prognosis of branch retinal vein occlusion. Acta Ophthalmol Scand. 1997;75:441-442.

14. Takahashi MK, Hikichi T, Akiba J, Yoshida A, Trempe CL. Role of the vitreous and macular edema in branch retinal vein occlusion. Ophthalmic Surg Lasers. 1997:28:294-299.

15. Trempe CL, Takahashi M, Topilow HW. Vitreous changes in retinal branch vein occlusion. Ophthalmology. 1981;88:681-687.

16. Timmerman EA, de Lavalette VR, van den Brom HB. Axial length as a risk factor to branch retinal vein occlusion. Retina. 1997:17:196-199

17. Majji AB, Janarthanan M, Naduvilath TJ. Significance of refractive status in branch retinal vein occlusion. A case-control study. Retina. 1997;17:200­204.

18. Bandello F, Tavola A, Pierro L, Modorati G, Azzolini C, Brancato R. Axial length and refraction in retinal vein occlusions. Ophthalmologica. 1998;212:133-135.

19. Stefansson E, Novack RL, Hatchell DL. Vitrectomy prevents retinal hypoxia in branch retinal vein occlusion. Invest Ophthalmol Vis Sci. 1990;31:284-289.

20. Kurimoto M, Takagi H, Suzuma K, et al. Vitrectomy for macular edema secondary to retinal vein occlusion: evaluation by retinal thickness analyzer. Jpn J Ophthalmol. 1999;53:717-720.

21. Ando, N. Vitrectomy for ischemic maculopathy associated with retinal vein occlusion. Vail Vitrectomy Meeting; Vail, CO; March 13­15, 2000.

22. Opremcak EM, Bruce RA. Surgical decompression of branch retinal vein occlusion via arteriovenous crossing sheathotomy: a prospective review of 15 cases. Retina. 1999;19:1-5.

23. Opremcak EM, Bruce RA. AV Crossing Sheathotomy for BRVO (RVS-BRVO). Invest Ophthalmolo Vis Sci. 2001;42:S718.

24. Osterloh MD, Charles S. Surgical decompression of branch retinal vein occlusions. Arch Ophthalmol. 1988;106:1569-1571.

25. Mester U, Dillinger P. Vitrectomy with decompression in branch retinal vein occlusion. XXIInd Meeting of the Club Jules Gonin. Taormina, Italy; September 2­6, 2000; abstract 25:51.

26. Shah GK, Sharma S, Fineman MS, Federman J, Brown MM, Brown GC. Arteriovenous adventitial sheathotomy for the treatment of macular edema associated with branch retinal vein occlusion. Am J Ophthalmo.l 2000;129:104-106.

27. Lee W-H, Thompson JT, Sjaarda RN. Visual acuity results in arteriovenous sheathotomy versus grid laser photocoagulation in branch retinal vein occlusion. Invest Ophthalmolo Vis Sci. 2001;42:S718.

28. Cahill MT, Kaiser PK, Sears JE, Fekrat S. The effect of arteriovenous sheathotomy on cystoid macular edema secondary to branch retinal vein occlusion. Br J Ophthalmol. 2003;87:1329-1332.

29. Sebag J, Balazs EA. Pathogenesis of cystoid macular edema: an anatomic consideration of vitreoretinal adhesions. Surv Ophthalmol. 1984;28:493-498.

30. Stefansson E, Novack RL, Hatchell DL. Vitrectomy prevents retinal hypoxia in branch retinal vein occlusion. Invest Ophthalmol Vis Sci. 1990;31:284-289.

31. Frangieh GT, Green WR, Barraquer-Somers E, Finkelstein D. Histopathologic study of nine branch retinal vein occlusions. Arch Ophthalmol. 1982;100:1132-1140.

32. Kumar B, Yu DY, Morgan WH, Barry CJ, Constable IH, McAllister IL. The distribution of angioarchitectural changes within the vicinity of the arteriovenous crossing in branch retinal vein occlusion. Ophthalmology. 1998;105:424-427.

33. Garcia Arumi J, Martinez Castillo V, Boixadera A, Blasco H, Corcostegui B. Management of macular edema in branch retinal vein occlusion with sheathotomy and recombinant tissue plasminogen activator. Retina. 2004;24:530-540.

 

NEXT ISSUE

In the March/April issue of Retinal Physician, Dr. Fekrat will address emerging treatments for central retinal vein occlusion.

From Vitreoretinal Surgery Department, Duke University Eye Center, Durham, NC. Dr. Fekrat has no financial interest in this information.

 



Retinal Physician, Issue: January 2005