Branch Retinal Vein Occlusion Treatment & Management
- Author: Lihteh Wu, MD; Chief Editor: Hampton Roy, Sr, MD more...
Medical treatment of branch retinal vein occlusion (BRVO) is not effective. In the past, anticoagulants, fibrinolytic agents, clofibrate capsules (Atromid-S), and carbogen inhalation have been used but without success.
Hemodilution has been proposed as an alternative treatment of BRVO by lowering the hematocrit and plasma viscosity and by improving retinal perfusion. However, the true benefit of hemodilution has not been established because published reports have used combination therapy in the hemodilution group.
Intravitreal injection of triamcinolone has been used to treat macular edema of different etiologies because of its potent antipermeability and anti-inflammatory properties. A few cases of macular edema secondary to BRVO treated with an intravitreal triamcinolone injection have been reported. The exact dose remains unclear. Doses from 4 mg to 25 mg have been reported to be effective. Multiple doses appear to be needed.
In a retrospective uncontrolled case series of 92 eyes, intravitreal injection of 4 mg of triamcinolone improved the mean best corrected visual acuity by 2.5 lines at 12 months of follow-up. It is unclear how many eyes required re-injection since this series combined eyes with central and hemiretinal vein occlusion. Trans-Tenon’s retrobulbar injection of 20 mg of triamcinolone acetonide has been reported to be effective. Interestingly, it appears to be more effective in eyes with a posterior vitreous detachment.
Dexamethasone is a more potent corticosteroid than triamcinolone. Furthermore, intravitreal injections of dexamethasone achieves high intravitreal drug levels without any toxic effects. The main drawback of dexamethasone is its short intraocular half life of 3 hours. A biodegradable intravitreal 0.7 mg of dexamethasone implant (Ozurdex) has been designed and approved in patients with macular edema secondary to RVO.
Clinical experience has shown that the effect of a single intravitreal injection of the dexamethasone intravitreal implant lasts close to 4 months. It may be re-injected and one can expect a similar effect with the exception that the effect does not last as long as the initial injection.[21, 22]
Complications resulting from corticosteroid therapy include cataract formation, elevation of intraocular pressure, infectious endophthalmitis, noninfectious endophthalmitis, and retinal detachment. The Standard Care vs Corticosteroid for Retinal Vein Occlusion (SCORE) Study compared the effects of macular laser photocoagulations with 1 mg and 4 mg of intravitreal triamcinolone in eyes with macular edema secondary to BRVO. At 12 months of follow-up, the visual acuity was similar in the 3 groups. However, the rates of elevated intraocular pressure and cataract formation were much higher in the 4-mg triamcinolone group.[23, 24] Vascular endothelial growth factor (VEGF) is a potent inductor of vascular permeability and intraocular neovascularization. In humans, the aqueous levels of VEGF and interleukin 6 (IL-6) are correlated with the degree of retinal ischemia and the severity of macular edema in BRVO. Therefore, VEGF inhibition appears to be a promising treatment modality for macular edema.
Bevacizumab is a humanized recombinant monoclonal IgG antibody that binds and inhibits all VEGF isoforms. Several small retrospective and uncontrolled case series suggest that intravitreal bevacizumab at doses up to 2.5 mg are effective in improving visual acuity and reducing central macula thickness in eyes with macular edema secondary to BRVO. These results are often seen within 1 month of injection. However, most of the eyes will require additional injections to maintain the effects of bevacizumab.[25, 26, 27, 28] Other small, uncontrolled prospective studies have confirmed these initial observations.[29, 30, 31, 32, 33]
The optimum dosing and sequence for intravitreal bevacizumab in BRVO is still undetermined. The 2 most commonly used doses of bevacizumab evaluated were 1.25 mg and 2.5 mg. In a small comparative retrospective study, no differences with respect to central macular thickness, best corrected visual acuity, or total number of injections were observed between the 1.25 mg dose and the 2.5 mg dose.
In a small prospective case series, 21 eyes received 3 initial intravitreal injections of 1 mg of intravitreal bevacizumab at monthly intervals and were followed for 12 months. If macular edema persisted, the patient was retreated with up to 2.5 mg of bevacizumab.
In a small prospective pilot study, 1.25 mg of intravitreal bevacizumab was shown to reduce central macular thickness and improve visual acuity more efficiently than macular photocoagulation at 12 months of follow-up.
A recent meta-analysis of the effect of intravitreal bevacizumab on macular edema secondary to BRVO concluded that intravitreal bevacizumab was beneficial in terms of improving visual acuity and reducing macular edema.
A multicenter, prospective, phase III trial (BRAVO Study) comparing intravitreal ranibizumab and sham injections demonstrated the value of VEGF inhibition in eyes with macular edema secondary to BRVO. In this study, eyes were randomized to monthly sham injections, 0.3 mg of ranibizumab and 0.5 mg of ranibizumab, for the first 6 months. Eyes were eligible for rescue laser at month 3 if the hemorrhages had sufficiently cleared to allow safe treatment and if the visual acuity remained at 20/40 or less and the central macular thickness was 250 µm or less.
During months 6-12 of the study, eyes were injected as needed, and the sham group was offered 0.5 mg ranibizumab. Again at month 9, eyes that did not responding to intravitreal ranibizumab were allowed laser rescue. At 12 months, eyes gained an average of 12.1, 16.4, and 18.3 letters in the sham, 0.3 mg, and 0.5 mg groups, respectively. Similarly, central foveal thickness decreased with ranibizumab treatment. Sham eyes had gained 7.3 letters at 6 months and had an additional gain of 4.8 letters after intravitreal ranibizumab was instituted. This suggests that timing is important and eyes with macular edema secondary to BRVO should be offered VEGF inhibition upon diagnosis in order to achieve the best possible visual outcome.
During months 13 to 24 (HORIZON Trial), eyes were followed at least every 3 months and were re-injected with 0.5 mg of ranibizumab if macular edema was present. In addition, these eyes were eligible for rescue grid laser therapy if the visual acuity was less than 20/40 and macular edema was still present. A large percentage of eyes received grid macular laser rescue therapy during the first 12 months of the study in all the study arms. After 2 years of follow-up, the visual gains were maintained with continued VEGF suppression.
Thirty-four eyes enrolled in the BRAVO and HORIZON Trials were followed for an average of 49 months (RETAIN Study). Half of these eyes experienced edema resolution, which was defined as an absence of intraretinal fluid for 6 months or longer since the last injection. The mean number of injections in eyes without edema resolution during year 4 of follow-up was 3.2. In eyes with resolution of edema, the mean gain of BCVA was 25.9 letters compared with 17.1 letters in eyes with unresolved edema. This difference was not statistically significant. Close to 80% of eyes obtained a BCVA of 20/40 or greater, regardless of edema resolution.
A 2016 clinical trial, the BRIGHTER Study, has shown that an individualized visual acuity–based regimen of ranibizumab results in good visual acuity gains.
In October 2014, the indication for aflibercept was expanded to include branch retinal vein occlusion (BRVO). The expanded indication is based on the previously approved indication for macular edema following CRVO and the positive results from the double-masked, randomized, controlled phase 3 VIBRANT study of 181 patients with macular edema following BRVO. The VIBRANT study compared intravitreal aflibercept 2 mg once every 4 weeks with macular laser photocoagulation (control).
At 24 weeks, significantly more patients treated with aflibercept gained at least 15 letters in vision (3 lines on an eye chart) from baseline as measured on the early treatment diabetic retinopathy study (ETDRS) chart, the primary endpoint of the study, compared with patients who received control (53% vs 27%; P < 0.01). Patients treated with aflibercept achieved a 17-letter mean improvement over baseline in best-corrected visual acuity (BCVA) compared to a 6.9-letter mean improvement in patients who received control (P < 0.01), a key secondary endpoint.
Multiple clinical trials have shown that timing is an important prognostic factor in eyes with macular edema due to BRVO. In the past, time was given for spontaneous resolution and clearing of intraretinal hemorrhages to allow performance of a "good" fluorescein angiogram. The authors no longer recommend this waiting period. An OCT should be the first diagnostic test; and if macular edema is present, initiation of treatment should be strongly considered.[17, 20, 37]
Retinal nonperfusion is related to intravitreal VEGF levels. Progressive retinal nonperfusion may be responsible for loss of visual gains, particularly in eyes in which macular edema has not resolved and anti-VEGF injections are given sporadically. The authors from this study state that in eyes with macular edema secondary to RVO, the resolution of macular edema should not be the sole treatment objective. The prevention of worsening retinal nonperfusion should be a treatment objective as well. Periodic fluorescein angiograms, preferably wide-angle, should be performed to monitor perfusion status.[42, 43]
Branch retinal vein occlusions (BRVOs) have a relatively benign course. Nevertheless, certain complications that lead to visual loss may occur. These complications include macular edema and the sequelae from retinal neovascularization (eg, vitreous hemorrhage, tractional retinal detachment, neovascular glaucoma). Several surgical and laser techniques are available to deal with these situations.
Macular grid laser photocoagulation
Macular grid laser photocoagulation was mildly effective in the treatment of macular edema in a small prospective trial, the BVOS.
The current recommendation is to wait 3 months to see if the patient's vision spontaneously improves.
If no improvement occurs and if the hemorrhages have mostly cleared from the macular area, a fluorescein angiogram is obtained. If the angiogram shows leakage in the macular area that is responsible for the decrease in vision, treatment with a macular grid laser is recommended. After 3 years of follow-up care, 63% of laser treated eyes improved by 2 or more lines of vision compared with 36% of control eyes.
Despite macular photocoagulation, eyes gained on average 1.33 lines of vision with respect to baseline. At the 3-year follow-up, 40% of eyes had a visual acuity of less than 20/40 and 12% of eyes had a visual acuity of less than 20/200.
If the fluorescein angiogram reveals macular nonperfusion, laser therapy is not warranted, and observation is recommended. Finkelstein reported that eyes with macular nonperfusion have a good visual prognosis. In his series, the median visual acuity was 20/30.
Macular grid laser photocoagulation remains the criterion standard treatment of eyes with perfused macular edema secondary to BRVO.
The BVOS also demonstrated that scatter photocoagulation reduces the prevalence of neovascularization from 40% to 20%.
However, if all eyes with nonperfusion were treated, 60% of patients who would never develop neovascularization would be treated.
If only the eyes that develop neovascularization were treated, the events of vitreous hemorrhage would decrease from 60% to 30%.
Therefore, the recommendation is to wait until neovascularization actually develops before scatter photocoagulation is considered.
Laser-induced chorioretinal anastomosis
Bypass of the normal retinal venous drainage channels is attempted by creating a communication between the obstructed vessel and the choroid.
Problems with this technique are the lack of reliability in creating an anastomosis (most groups report a 30-50% success rate) and its complications. Complications from the procedure include tractional retinal detachment and vitreous hemorrhage.
Vitrectomy and arteriovenous decompression
Virtually all cases of BRVO occur at arteriovenous crossings.
Because arterial compression is believed to be the major cause of this condition, some have recommended lifting the artery from the underlying vein to relieve the compression.
Several small, uncontrolled series have shown good results in improving macular edema and macular perfusion. However, others have reported a lack of efficacy of this procedure. Planning of a multicenter controlled trial is currently underway.
Several surgeons have reported resolution of macular edema secondary to BRVO after vitrectomy with or without peeling of the internal limiting membrane.
Vitrectomy and posterior hyaloid separation improved the visual acuity in eyes with macular edema secondary to BRVO. The addition of intravitreal triamcinolone had no additional benefit.
A number of eyes may develop a transient postoperative increase in macular edema following vitrectomy. The edema resolves spontaneously and does not appear to have an effect on visual acuity.
Pars plana vitrectomy techniques with or without scleral buckling may be necessary in eyes with tractional and rhegmatogenous retinal detachments.
Consult a vitreoretinal specialist if complications arise.
In atypical cases where a thrombophilic condition is suspected, consultation with a hematologic specialist is recommended.
Pe’er J, Shweiki D, Itin A, Hemo I, Gnessin H, Keshet E. Hypoxiainduced expression of vascular endothelial growth factor by retinal cells is a common factor in neovascularizing ocular diseases. Lab Invest. 1995. 72:638-645.
Zhang SX, Wang JJ, Gao G, Parke K, Ma JX. Pigment epithelium-derived factor downregulates vascular endothelial growth factor (VEGF) expression and inhibits VEGF-VEGF receptor 2 binding in diabetic retinopathy. J Mol Endocrinol. 2006 Aug. 37(1):1-12. [Medline].
Rehak M, Hollborn M, Iandiev I, Pannicke T, Karl A, Wurm A, et al. Retinal gene expression and Müller cell responses after branch retinal vein occlusion in the rat. Invest Ophthalmol Vis Sci. 2009 May. 50(5):2359-67. [Medline].
Campochiaro PA, Hafiz G, Shah SM, Nguyen QD, Ying H, Do DV. Ranibizumab for macular edema due to retinal vein occlusions: implication of VEGF as a critical stimulator. Mol Ther. 2008 Apr. 16(4):791-9. [Medline].
Noma H, Funatsu H, Yamasaki M, et al. Pathogenesis of macular edema with branch retinal vein occlusion and intraocular levels of vascular endothelial growth factor and interleukin-6. Am J Ophthalmol. 2005 Aug. 140(2):256-61. [Medline].
Pfister M, Rothweiler F, Michaelis M, Cinatl J Jr, Schubert R, Koch FH. Correlation of inflammatory and proangiogenic cytokines from undiluted vitreous samples with spectral domain OCT scans, in untreated branch retinal vein occlusion. Clin Ophthalmol. 2013. 7:1061-7. [Medline].
Klein R, Moss SE, Meuer SM, Klein BE. The 15-year cumulative incidence of retinal vein occlusion: the Beaver Dam Eye Study. Arch Ophthalmol. 2008 Apr. 126(4):513-8. [Medline].
Cheung N, Klein R, Wang JJ, Cotch MF, Islam AF, Klein BE. Traditional and novel cardiovascular risk factors for retinal vein occlusion: the multiethnic study of atherosclerosis. Invest Ophthalmol Vis Sci. 2008 Oct. 49(10):4297-302. [Medline]. [Full Text].
Lim LL, Cheung N, Wang JJ, Islam FM, Mitchell P, Saw SM. Prevalence and risk factors of retinal vein occlusion in an Asian population. Br J Ophthalmol. 2008 Oct. 92(10):1316-9. [Medline].
Xu L, Liu WW, Wang YX, Yang H, Jonas JB. Retinal vein occlusions and mortality: the Beijing Eye Study. Am J Ophthalmol. 2007 Dec. 144(6):972-3. [Medline].
Rogers S, McIntosh RL, Cheung N, Lim L, Wang JJ, Mitchell P. The prevalence of retinal vein occlusion: pooled data from population studies from the United States, Europe, Asia, and Australia. Ophthalmology. 2010 Feb. 117(2):313-9.e1. [Medline].
Klein R, Klein BE, Moss SE, Meuer SM. The epidemiology of retinal vein occlusion: the Beaver Dam Eye Study. Trans Am Ophthalmol Soc. 2000. 98:133-41; discussion 141-3. [Medline].
Christoffersen N, Gade E, Knudsen L, Juel K, Larsen M. Mortality in patients with branch retinal vein occlusion. Ophthalmology. 2007 Jun. 114(6):1186-9. [Medline].
Risk factors for branch retinal vein occlusion. The Eye Disease Case-control Study Group. Am J Ophthalmol. 1993 Sep 15. 116(3):286-96. [Medline].
Parodi MB, DI Stefano G, Ravalico G. Grid laser treatment for exudative retinal detachment secondary to ischemic branch retinal vein occlusion. Retina. 2008. 28(1):97-102.
Steinbrugger I, Haas A, Maier R, Renner W, Mayer M, Werner C. Analysis of inflammation- and atherosclerosis-related gene polymorphisms in branch retinal vein occlusion. Mol Vis. 2009. 15:609-18. [Medline]. [Full Text].
Branch Vein Occlusion Study Group. Argon laser photocoagulation for macular edema in branch vein occlusion. The Branch Vein Occlusion Study Group. Am J Ophthalmol. 1984 Sep 15. 98(3):271-82. [Medline].
Roth DB, Cukras C, Radhakrishnan R, Feuer WJ, Yarian DL, Green SN. Intravitreal triamcinolone acetonide injections in the treatment of retinal vein occlusions. Ophthalmic Surg Lasers Imaging. 2008 Nov-Dec. 39(6):446-54. [Medline].
Kawaji T, Takano A, Inomata Y, Sagara N, Iwao K, Inatani M, et al. Trans-Tenon's retrobulbar triamcinolone acetonide injection for macular oedema related to branch retinal vein occlusion. Br J Ophthalmol. 2008 Jan. 92(1):81-3. [Medline].
Haller JA, Bandello F, Belfort R Jr, Blumenkranz MS, Gillies M, Heier J. Randomized, sham-controlled trial of dexamethasone intravitreal implant in patients with macular edema due to retinal vein occlusion. Ophthalmology. 2010 Jun. 117(6):1134-1146.e3. [Medline].
Joshi L, Yaganti S, Gemenetzi M, Lightman S, Lindfield D, Liolios V. Dexamethasone implants in retinal vein occlusion: 12-month clinical effectiveness using repeat injections as-needed. Br J Ophthalmol. 2013 Aug. 97(8):1040-4. [Medline].
Mayer WJ, Wolf A, Kernt M, Kook D, Kampik A, Ulbig M. Twelve-month experience with Ozurdex for the treatment of macular edema associated with retinal vein occlusion. Eye (Lond). 2013 Jul. 27(7):816-22. [Medline].
Scott IU, Blodi BA, Ip MS, Vanveldhuisen PC, Oden NL, Chan CK. SCORE Study Report 2: Interobserver agreement between investigator and reading center classification of retinal vein occlusion type. Ophthalmology. 2009 Apr. 116(4):756-61. [Medline]. [Full Text].
Scott IU, Ip MS, VanVeldhuisen PC, et al. A randomized trial comparing the efficacy and safety of intravitreal triamcinolone with standard care to treat vision loss associated with macular Edema secondary to branch retinal vein occlusion: the Standard Care vs Corticosteroid for Retinal Vein Occlusion (SCORE) study report 6. Arch Ophthalmol. 2009 Sep. 127(9):1115-28. [Medline]. [Full Text].
Abegg M, Tappeiner C, Wolf-Schnurrbusch U, Barthelmes D, Wolf S, Fleischhauer J. Treatment of branch retinal vein occlusion induced macular edema with bevacizumab. BMC Ophthalmol. 2008. 8:18. [Medline]. [Full Text].
Fish GE. Intravitreous bevacizumab in the treatment of macular edema from branch retinal vein occlusion and hemisphere retinal vein occlusion (an AOS thesis). Trans Am Ophthalmol Soc. 2008. 106:276-300. [Medline]. [Full Text].
Rabena MD, Pieramici DJ, Castellarin AA, Nasir MA, Avery RL. Intravitreal bevacizumab (Avastin) in the treatment of macular edema secondary to branch retinal vein occlusion. Retina. 2007 Apr-May. 27(4):419-25. [Medline].
Wu L, Arevalo JF, Roca JA, et al. Pan-American Collaborative Retina Study Group (PACORES). Comparison of two doses of intravitreal bevacizumab (Avastin) for treatment of macular edema secondary to branch retinal vein occlusion: results from the Pan-American Collaborative Retina Study Group at 6 months of follow-up. Retina. 2008. 28(2):9:212-21.
Schaal KB, Höh AE, Scheuerle A, Schütt F, Dithmar S. [Bevacizumab for the treatment of macular edema secondary to retinal vein occlusion]. Ophthalmologe. 2007 Apr. 104(4):285-9. [Medline].
Jaissle GB, Leitritz M, Gelisken F, Ziemssen F, Bartz-Schmidt KU, Szurman P. One-year results after intravitreal bevacizumab therapy for macular edema secondary to branch retinal vein occlusion. Graefes Arch Clin Exp Ophthalmol. 2009 Jan. 247(1):27-33. [Medline].
Prager F, Michels S, Kriechbaum K, Georgopoulos M, Funk M, Geitzenauer W. Intravitreal bevacizumab (Avastin) for macular oedema secondary to retinal vein occlusion: 12-month results of a prospective clinical trial. Br J Ophthalmol. 2009 Apr. 93(4):452-6. [Medline].
Kreutzer TC, Alge CS, Wolf AH, Kook D, Burger J, Strauss R. Intravitreal bevacizumab for the treatment of macular oedema secondary to branch retinal vein occlusion. Br J Ophthalmol. 2008 Mar. 92(3):351-5. [Medline].
Pai SA, Shetty R, Vijayan PB, Venkatasubramaniam G, Yadav NK, Shetty BK, et al. Clinical, anatomic, and electrophysiologic evaluation following intravitreal bevacizumab for macular edema in retinal vein occlusion. Am J Ophthalmol. 2007 Apr. 143(4):601-6. [Medline].
Wu Z, Sadda SR. Effects on the contralateral eye after intravitreal bevacizumab and ranibizumab injections: a case report. Ann Acad Med Singapore. 2008 Jul. 37(7):591-3. [Medline].
Russo V, Barone A, Conte E, Prascina F, Stella A, Noci ND. Bevacizumab compared with macular laser grid photocoagulation for cystoid macular edema in branch retinal vein occlusion. Retina. 2009 Apr. 29(4):511-5. [Medline].
Zhu D, Jin ZY, Tao Y, Jonas JB. Meta-analysis of the effect of intravitreal bevacizumab in branch retinal vein occlusion. J Ocul Pharmacol Ther. 2013 Jul-Aug. 29(6):523-9. [Medline].
Brown DM, Campochiaro PA, Bhisitkul RB, et al. Sustained Benefits from Ranibizumab for Macular Edema Following Branch Retinal Vein Occlusion: 12-Month Outcomes of a Phase III Study. Ophthalmology. 2011 Aug. 118(8):1594-602. [Medline].
Heier JS, Campochiaro PA, Yau L, Li Z, Saroj N, Rubio RG, et al. Ranibizumab for Macular Edema Due to Retinal Vein Occlusions: Long-term Follow-up in the HORIZON Trial. Ophthalmology. 2012 Apr. 119(4):802-9. [Medline].
Campochiaro PA, Sophie R, Pearlman J, Brown DM, Boyer DS, Heier JS. Long-term outcomes in patients with retinal vein occlusion treated with ranibizumab: the RETAIN study. Ophthalmology. 2014 Jan. 121(1):209-19. [Medline].
Tadayoni R, Waldstein SM, Boscia F, Gerding H, Pearce I, Priglinger S, et al. Individualized Stabilization Criteria-Driven Ranibizumab versus Laser in Branch Retinal Vein Occlusion: Six-Month Results of BRIGHTER. Ophthalmology. 2016 Mar 30. [Medline].
Clark WL, Boyer DS, Heier JS, Brown DM, Haller JA, Vitti R, et al. Intravitreal Aflibercept for Macular Edema Following Branch Retinal Vein Occlusion: 52-Week Results of the VIBRANT Study. Ophthalmology. 2016 Feb. 123 (2):330-6. [Medline].
Campochiaro PA, Bhisitkul RB, Shapiro H, Rubio RG. Vascular endothelial growth factor promotes progressive retinal nonperfusion in patients with retinal vein occlusion. Ophthalmology. 2013 Apr. 120(4):795-802. [Medline].
Sophie R, Hafiz G, Scott AW, Zimmer-Galler I, Nguyen QD, Ying H. Long-term outcomes in ranibizumab-treated patients with retinal vein occlusion; the role of progression of retinal nonperfusion. Am J Ophthalmol. 2013 Oct. 156(4):693-705. [Medline].
Finkelstein D. Ischemic macular edema. Recognition and favorable natural history in branch vein occlusion. Arch Ophthalmol. 1992 Oct. 110(10):1427-34. [Medline].
Uemura A, Yamamoto S, Sato E, Sugawara T, Mitamura Y, Mizunoya S. Vitrectomy alone versus vitrectomy with simultaneous intravitreal injection of triamcinolone for macular edema associated with branch retinal vein occlusion. Ophthalmic Surg Lasers Imaging. 2009 Jan-Feb. 40(1):6-12. [Medline].
Shimada H, Nakashizuka H, Hattori T, Mori R, Mizutani Y. Transient increase in macular edema following vitrectomy for retinal branch vein occlusion. Int Ophthalmol. 2009 Apr. 29(2):95-8. [Medline].
Hayreh SS, Zimmerman MB. Branch retinal vein occlusion: natural history of visual outcome. JAMA Ophthalmol. 2014 Jan. 132(1):13-22. [Medline].
Arnarsson A, Stefansson E. Laser treatment and the mechanism of edema reduction in branch retinal vein occlusion. Invest Ophthalmol Vis Sci. 2000 Mar. 41(3):877-9. [Medline].
Avila CP Jr, Bartsch DU, Bitner DG, et al. Retinal blood flow measurements in branch retinal vein occlusion using scanning laser Doppler flowmetry. Am J Ophthalmol. 1998 Nov. 126(5):683-90. [Medline].
Baglivo E, Dosso A, Pournaras C. Thrombus and branch retinal vein occlusion. Graefes Arch Clin Exp Ophthalmol. 1997 Jan. 235(1):10-3. [Medline].
Battaglia Parodi M, Saviano S, Ravalico G. Grid laser treatment in macular branch retinal vein occlusion. Graefes Arch Clin Exp Ophthalmol. 1999 Dec. 237(12):1024-7. [Medline].
Branch Vein Occlusion Study Group. Argon laser scatter photocoagulation for prevention of neovascularization and vitreous hemorrhage in branch vein occlusion. A randomized clinical trial. Branch Vein Occlusion Study Group. Arch Ophthalmol. 1986 Jan. 104(1):34-41. [Medline].
Cahill MT, Kaiser PK, Sears JE, Fekrat S. The effect of arteriovenous sheathotomy on cystoid macular oedema secondary to branch retinal vein occlusion. Br J Ophthalmol. 2003 Nov. 87(11):1329-32. [Medline].
Chen HC, Wiek J, Gupta A, Luckie A, Kohner EM. Effect of isovolaemic haemodilution on visual outcome in branch retinal vein occlusion. Br J Ophthalmol. 1998 Feb. 82(2):162-7. [Medline].
Chen SD, Lochhead J, Patel CK, Frith P. Intravitreal triamcinolone acetonide for ischaemic macular oedema caused by branch retinal vein occlusion. Br J Ophthalmol. 2004 Jan. 88(1):154-5. [Medline].
Christoffersen NL, Larsen M. Pathophysiology and hemodynamics of branch retinal vein occlusion. Ophthalmology. 1999 Nov. 106(11):2054-62. [Medline].
Duker JS, Brown GC. Anterior location of the crossing artery in branch retinal vein obstruction. Arch Ophthalmol. 1989 Jul. 107(7):998-1000. [Medline].
Fekrat S, Goldberg MF, Finkelstein D. Laser-induced chorioretinal venous anastomosis for nonischemic central or branch retinal vein occlusion. Arch Ophthalmol. 1998 Jan. 116(1):43-52. [Medline].
Frangieh GT, Green WR, Barraquer-Somers E, Finkelstein D. Histopathologic study of nine branch retinal vein occlusions. Arch Ophthalmol. 1982 Jul. 100(7):1132-40. [Medline].
Friberg TR. Serpiginous choroiditis with branch vein occlusion and bilateral periphlebitis. Case report. Arch Ophthalmol. 1988 May. 106(5):585-6. [Medline].
Funk M, Kriechbaum K, Prager F, Benesch T, Georgopoulos M, Zlabinger GJ. Intraocular concentrations of growth factors and cytokines in retinal vein occlusion and the effect of therapy with bevacizumab. Invest Ophthalmol Vis Sci. 2009 Mar. 50(3):1025-32. [Medline].
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 Aug. 24(4):530-40. [Medline].
Ho JD, Liou SW, Lin HC. Retinal vein occlusion and the risk of stroke development: a five-year follow-up study. Am J Ophthalmol. 2009 Feb. 147(2):283-290.e2. [Medline].
Ikuno Y, Ikeda T, Sato Y, Tano Y. Tractional retinal detachment after branch retinal vein occlusion. Influence of disc neovascularization on the outcome of vitreous surgery. Ophthalmology. 1998 Mar. 105(3):417-23. [Medline].
Ikuno Y, Tano Y, Lewis JM, Ikeda T, Sato Y. Retinal detachment after branch retinal vein occlusion: influence of the type of break on the outcome of vitreous surgery. Ophthalmology. 1997 Jan. 104(1):27-32. [Medline].
Jonas JB, Akkoyun I, Kamppeter B, Kreissig I, Degenring RF. Branch retinal vein occlusion treated by intravitreal triamcinolone acetonide. Eye (Lond). 2005 Jan. 19(1):65-71. [Medline].
Kir E, Saatci AO, Ozbek Z, Kaynak S, Ergin MH. Retinal breaks and rhegmatogenous retinal detachment in association with branch retinal vein occlusion. Ophthalmic Surg Lasers. 1999 Apr. 30(4):285-8. [Medline].
Kriechbaum K, Michels S, Prager F, et al. Intravitreal Avastin for macular oedema secondary to retinal vein occlusion: a prospective study.Br. J Ophthalmol. 2008. 92(4):518-522.
Kumar B, Yu DY, Morgan WH, Barry CJ, Constable IJ, McAllister IL. The distribution of angioarchitectural changes within the vicinity of the arteriovenous crossing in branch retinal vein occlusion. Ophthalmology. 1998 Mar. 105(3):424-7. [Medline].
Majji AB, Janarthanan M, Naduvilath TJ. Significance of refractive status in branch retinal vein occlusion. A case-control study. Retina. 1997. 17(3):200-4. [Medline].
Mandelcorn MS, Nrusimhadevara RK. Internal limiting membrane peeling for decompression of macular edema in retinal vein occlusion: a report of 14 cases. Retina. 2004 Jun. 24(3):348-55. [Medline].
Martin SC, Butcher A, Martin N, et al. Cardiovascular risk assessment in patients with retinal vein occlusion. Br J Ophthalmol. 2002 Jul. 86(7):774-6. [Medline].
Mason J 3rd, Feist R, White M Jr, Swanner J, McGwin G Jr, Emond T. Sheathotomy to decompress branch retinal vein occlusion: a matched control study. Ophthalmology. 2004 Mar. 111(3):540-5. [Medline].
McAllister IL, Yu DY, Vijayasekaran S, Barry C, Constable I. Induced chorioretinal venous anastomosis in experimental retinal branch vein occlusion. Br J Ophthalmol. 1992 Oct. 76(10):615-20. [Medline]. [Full Text].
McIntosh RL, Mohamed Q, Saw SM, Wong TY. Interventions for branch retinal vein occlusion: an evidence-based systematic review. Ophthalmology. 2007 May. 114(5):835-54. [Medline].
Mester U, Dillinger P. Vitrectomy with arteriovenous decompression and internal limiting membrane dissection in branch retinal vein occlusion. Retina. 2002 Dec. 22(6):740-6. [Medline].
Mikkila HO, Seppala IJ, Viljanen MK, Peltomaa MP, Karma A. The expanding clinical spectrum of ocular lyme borreliosis. Ophthalmology. 2000 Mar. 107(3):581-7. [Medline].
Mitchell P, Smith W, Chang A. Prevalence and associations of retinal vein occlusion in Australia. The Blue Mountains Eye Study. Arch Ophthalmol. 1996 Oct. 114(10):1243-7. [Medline].
Nakazato K, Watanabe H, Kawana K, Hiraoka T, Kiuchi T, Oshika T. Evaluation of arterial stiffness in patients with branch retinal vein occlusion. Ophthalmologica. 2005 Nov-Dec. 219(6):334-7. [Medline].
Ohara K, Okubo A, Sasaki H, Kamata K. Branch retinal vein occlusion in a child with ocular sarcoidosis. Am J Ophthalmol. 1995 Jun. 119(6):806-7. [Medline].
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):1-5. [Medline].
Orth DH, Patz A. Retinal branch vein occlusion. Surv Ophthalmol. 1978 May-Jun. 22(6):357-76. [Medline].
Osterloh MD, Charles S. Surgical decompression of branch retinal vein occlusions. Arch Ophthalmol. 1988 Oct. 106(10):1469-71. [Medline].
Ota M, Tsujikawa A, Murakami T, et al. Association between integrity of foveal photoreceptor layer and visual acutiy in branch retinal vein occlusion. Br J Ophthalmol. 2007. 91(12):1644-1649.
Pournaras CJ, Tsacopoulos M, Strommer K, Gilodi N, Leuenberger PM. Experimental retinal branch vein occlusion in miniature pigs induces local tissue hypoxia and vasoproliferative microangiopathy. Ophthalmology. 1990 Oct. 97(10):1321-8. [Medline].
Remky A, Arend O, Jung F, Kiesewetter H, Reim M, Wolf S. Haemorheology in patients with branch retinal vein occlusion with and without risk factors. Graefes Arch Clin Exp Ophthalmol. 1996 Aug. 234 Suppl 1:S8-12. [Medline].
Russell SR, Blodi CF, Folk JC. Vitrectomy for complicated retinal detachments secondary to branch retinal vein occlusions. Am J Ophthalmol. 1989 Jul 15. 108(1):6-9. [Medline].
Shah GK. Adventitial sheathotomy for treatment of macular edema associated with branch retinal vein occlusion. Curr Opin Ophthalmol. 2000 Jun. 11(3):171-4. [Medline].
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 Ophthalmol. 2000 Jan. 129(1):104-6. [Medline].
Simons BD, Brucker AJ. Branch retinal vein occlusion. Axial length and other risk factors. Retina. 1997. 17(3):191-5. [Medline].
Simsek S, Demirok A, Cinal A, Yasar T. Effect of sex in branch retinal vein occlusion. Eur J Ophthalmol. 1998 Jan-Mar. 8(1):48-51. [Medline].
Spaide RF, Lee JK, Klancnik JK Jr, Gross NE. Optical coherence tomography of branch retinal vein occlusion. Retina. 2003 Jun. 23(3):343-7. [Medline].
Staurenghi G, Lonati C, Aschero M, Orzalesi N. Arteriovenous crossing as a risk factor in branch retinal vein occlusion. Am J Ophthalmol. 1994 Feb 15. 117(2):211-3. [Medline].
Tameesh MK, Lakhanpal RR, Fujii GY, et al. Retinal vein cannulation with prolonged infusion of tissue plasminogen activator (t-PA) for the treatment of experimental retinal vein occlusion in dogs. Am J Ophthalmol. 2004 Nov. 138(5):829-39. [Medline].
Wakabayashi T, Okada AA, Morimura Y, et al. Trans-tenon retrobulbar triamcinolone infusion for chronic macular edema in central and branch retinal vein occlusion. Retina. 2004 Dec. 24(6):964-7. [Medline].
Yamamoto S, Saito W, Yagi F, Takeuchi S, Sato E, Mizunoya S. Vitrectomy with or without arteriovenous adventitial sheathotomy for macular edema associated with branch retinal vein occlusion. Am J Ophthalmol. 2004 Dec. 138(6):907-14. [Medline].
Zhao J, Sastry SM, Sperduto RD, Chew EY, Remaley NA. Arteriovenous crossing patterns in branch retinal vein occlusion. The Eye Disease Case-Control Study Group. Ophthalmology. 1993 Mar. 100(3):423-8. [Medline].