Current Management of Retinal Vein Occlusion

Current Management of Retinal Vein Occlusion

Retinal vein occlusion is a common vascular event that may result in severe, permanent visual impairment. Persons of any age may be affected, but the majority of occlusions occur in people over the age of 50.1 Critical signs of retinal vein occlusion include dilated, tortuous retinal veins, intraretinal hemorrhages, cotton-wool spots, macular edema, and neovascularization. There are 2 primary types of retinal vein occlusion: central retinal vein occlusion (CRVO) and branch retinal vein occlusion (BRVO). The prevalence of BRVO and CRVO in the United States is 0.6% and 0.1%, respectively.2 This article will review current recommendations for management of BRVO and CRVO, as well as discuss emerging treatment strategies for these conditions.

Figure 1. Macular ischemia: a broken perifoveal capillary ring. 


A branch retinal vein occlusion is defined as a focal occlusion of a retinal vein at an arteriovenous crossing site. The occlusion is presumed to arise from turbulence induced in the retinal vein by arteriosclerotic changes in the overlying arteriole, leading to venous flow abnormalities, blood stagnation, and eventual occlusion.3

Significant visual-threatening complications from BRVO include macular edema and neovascularization. The Branch Retinal Occlusion Study (BVOS) was a multicenter, randomized, controlled study that created recommendations for the treatment of these complications using argon laser photocoagulation.4,5 This study still guides the current management of BRVO (Table 1).

Assessment of macular edema in a patient with a retinal vein occlusion should ideally include optical coherence tomography (OCT). This imaging modality is more sensitive than a fundus contact lens examination in detecting mild amounts of foveal edema (200­300 microns), and can provide valuable information on the status of the vitreoretinal interface, such as the presence of an epiretinal membrane or vitreomacular traction, that may influence treatment decisions.6,7,8 Equally significant, OCT can provide quantitative assessments of macular thickness following treatment.

The conventional treatment of perfused macular edema secondary to BRVO is macular grid photocoagulation as outlined in the BVOS. This study investigated patients with perfused macular edema (as noted on fluorescein angiography) of at least months duration and a visual acuity of 20/40 or worse. Important exclusion criteria included macular ischemia, diffuse macular hemorrhage, media opacities, and coexisting ocular disease. With a mean follow-up of 3 years, 65% of patients treated with a macular grid laser gained 2 or more lines of vision compared with 37% of the controls.

The management of ischemic macular edema secondary to BRVO is unclear. A broken perifoveal capillary ring or an area of nonperfusion within 1 disc diameter of the foveal center on fluorescein angiography9 is suggestive of macular ischemia (Figure 1). Observation may be a good option, especially in patients with visual acuity of 20/100 or better: one study found that 21 of 23 eyes (91%) with macular ischemia improved their visual acuity over 3 years.9

Scatter argon photocoagulation is indicated in patients with neovascularization associated with BRVO. Eyes with greater than 5-disc diameters of ischemia on fluorescein angiography must be observed closely in the first year as they have a 50% chance of developing neovascularization (Figure 2).5 Since many eyes with significant ischemia do not progress to neovascularization, the BVOS recommends that treatment should be withheld until definite evidence of neovascularization is present.

Figure 2. Branch retinal vein occlusion with capillary nonperfusion.

Investigational Treatments

There exists a significant group of patients who are not eligible for or fail to improve with conventional treatment as outlined by the BVOS. This underscores the importance of exploring alternative medical and surgical treatments for BRVO.

One promising therapy is intravitreal triamcinolone acetonide for macular edema.10 This treatment is currently being investigated in the Standard Care vs. Corticosteroid for Retinal Vein Occlusion Study (SCORE), discussed in the CRVO section.

Pars plana vitrectomy has been suggested as a treatment for macular edema after BRVO. The rational is to relieve tangential vitreous traction on the retina in eyes without a posterior vitreous detachment.11 One study showed improvement in macular edema and visual acuity after vitrectomy, but was limited by its small size and failure to define the type of macular edema. Furthermore, all patients in the study underwent simultaneous phacoemulsification, thus confounding the visual acuity results.

Another treatment option being explored is pars plana vitrectomy with arteriovenous sheathotomy. Initial studies have shown mixed results: macular edema often improves, but visual outcome has varied.12,13,14 The addition of internal limiting membrane peeling may add to the efficacy of this technique15,16. A comparison of eyes undergoing an arteriovenous sheathotomy to those only undergoing a vitrectomy with posterior hyaloid removal found that both groups performed equally in resolving macular edema, improving vision, and preventing neovascularization.17 Intraocular injection of tissue plasminogen activator in combination with sheathotomy has also been noted to improve visual results.18 Larger controlled clinical trials will be needed to evaluate the role of these surgical techniques in the management of patients with BRVO.

Figure 3. Central retinal vein occlusion.


Histopathologic data suggests that CRVO (Figure 3) arises from thrombosis of the central retinal vein in the vicinity of the lamina cribosa.19 Here the close juxtaposition of the artery and vein may lead to compression-induced changes in the vein, turbulence, endothelial cell damage, and eventual thrombosis.20,21 The location of the thrombus relative to the lamina cribosa may be related to the risk of ischemia; an occlusion posterior to the lamina may provide more venous collateral channels and hence improved perfusion.22

Significant, visually threatening complications from CRVO include macular edema and anterior segment neovascularization. Also, the fellow eye is at a 1% annual risk of incurring a CRVO and is at increased risk of developing glaucoma.23 Our current management of these complications has been guided by the Central Vein Occlusion Study (CVOS), a multicentered, randomized, controlled, clinical trial (Table 2).

There are 2 types of CRVO: perfused and ischemic. An ischemic CRVO is at significantly higher risk of developing anterior segment neovascularization and neovascular glaucoma. In addition, 30% of eyes with a perfused CRVO will become ischemic in 3 years. Thus, it is important to assess a patient's degree of retinal ischemia on initial and subsequent evaluations. The degree of retinal ischemia can be assessed on fluorescein angiography: the CVOS defined ischemia as the presence of 10-disc areas of nonperfusion.24 However, when fluorescein angiography is not feasible, a relative afferent papillary defect test and an electroretinogram test may provide additional prognostic information.25,26,27 It is likely that no single test can solely determine the risk of neovascularization. After CRVO an investigation for retinal ischemia must be tailored to the individual patient.

The anterior segment is the principle site for the development of neovascularization secondary to a CRVO.28 Disc and retinal neovascularization have been reported to occur in only 5.1% and 7.7% of eyes incurring CRVO, respectively.28 This underscores the importance of a regular, undilated examination of the patient's anterior segment. The development of 2 or more clock hours of iris or any angle neovascularization is an indication for scatter panretinal photocoagulation.29 The CVOS showed that treating these eyes with photocoagulation caused the regression of neovascularization within 1 month of treatment in the majority of cases. The CVOS did not recommend prophylactic treatment of eyes without anterior segment neovascularization.

Chronic macular edema after CRVO causes significant visual morbidity: 60% of eyes will have a visual acuity less than 20/125 after 3 years.30 Focal laser photocoagulation is not clinically beneficial in treating this macular edema.30,31 The CVOS showed that treatment did not preserve or improve visual acuity relative to controls, though it did improve macular edema.

Initial visual acuity may be the best prognostic indicator for final visual outcome after CRVO in patients 50 years of age and older. The CVOS--in which most of the patients were 50 years of age or older--showed that 65% of eyes with 20/40 vision or better maintained their vision while 80% of eyes with vision worse than 20/200 failed to improve.17 In contrast, a recent retrospective study has suggested that initial visual acuity was not a good predictor of final visual outcome in younger patients.32

Investigational Treatments

The limited treatment options for patients for CRVO have prompted interest in new medical and surgical interventions (Table 3).

Intravitreal triamcinolone has been advocated in the treatment of macular edema secondary to diabetes, uveitis, and Irvine-Gass syndrome. In patients with CRVO, several small studies have suggested that intravitreal triamcinolone may improve macular edema and visual acuity.33,34,35,36 This treatment modality may be more effective in eyes with nonishchemic CRVO.35 Important risks associated with intravitreal triamcinolone injections include secondary glaucoma, cataract progression, endophthalmitis, and retinal complications.37,38,39

These results have led to the multicentered, randomized, prospective, SCORE Study (URL: Presently under recruitment, the SCORE trial plans to enroll 630 patients with BRVO and 630 patients with CRVO and randomly assign them to treatment with varying concentrations of intravitreal triamcinolone versus standard care (macular grid laser for BRVO and observation for CRVO). The SCORE Study will also use optical coherence tomography to assess and follow macular edema. The primary outcome measure is the improvement of vision by 15 letters on an EDTRS chart at 12 months. Patients will be followed for 3 years.

Systemic anticoagulation and antiplatelet therapy have been investigated for the treatment of retinal vein occlusions. Although these agents generally have not been shown to improve visual outcome,40, 41 newer pharmaceuticals may play a role in the future. The use of ticlopidine in rabbits with laser-induced retinal vein occlusion suggested a possible prophylactic effect preventing thrombosis.42 An interventional, clinical trial examining retinal vein occlusion with particle-counting light scattering showed that ticlopidine and beraprost were able to reduce platelet aggregation in patients with CRVO as compared to controls who did not have a CRVO.43 The potential benefit of antiplatelet therapy needs to be further studied prior to its adoption in the treatment of retinal vein occlusion.

The use of systemic fibrinolytics to dissolve the thrombus in CRVO has been limited by systemic complications, including a fatal stroke in 1 study.44 An intravitreal injection of tissue plasminogen activator (tPA) may be a safer alternative to systemic treatment. An early study of 23 eyes demonstrated a doubling of the visual angle with treatment,45 but later studies were not able to reproduce this same visual benefit.46,47 It has been hypothesized that intravitreal tPA acts by diffusing through the internal limiting membrane into the central retinal vein, but histopathologic studies do not support this mechanism.48 In an attempt to deliver a high concentration of tPA to the site of occlusion, a pars plana vitrectomy with injection of tPA into a cannulated retinal vein has been proposed. One study demonstrated 3 lines of visual improvement in 50% of treated patients.49,50 A later study in dogs with pharmacologically induced CRVO treated with tPA via a cannulated retinal vein suggested improvement in retinal circulation after treatment and a low incidence of side effects.51 Further studies are needed to investigate the efficacy and safety of intraocular tPA in the management of patients with CRVO.

Antivascular endothelial growth factor (VEGF) therapy may play a role in the management of visual complications associated with retinal vein occlusion. Measurement of VEGF levels by anterior chamber sampling after retinal vein occlusion found a close temporal relationship between elevated VEGF levels and neovascularization.52 In animals with laser-induced retinal vein occlusions, the usage of anti-VEGF antibodies decreased the risk of iris neovascularization.53 Stemming from these initial studies, a clinical trial investigating the use of pegaptanib sodium (Macugen) in treating patients with CRVO is currently underway (URL:

Surgical treatments are also being developed in treatment for CRVO. One technique being investigated is radial optic neurotomy (RON). It has been hypothesized that CRVO is a neurovascular compressive syndrome with increased pressure in the scleral outlet.54 Radial optic neurotomy attempts to decompress this compartment syndrome by making an incision through the scleral ring and cribiform plate on the nasal portion of the optic nerve. A retrospective, nonrandomized, pilot study of 11 eyes with CRVO and poor vision, demonstrated mean visual improvement of 5 lines in 8 patients.54 A histopathologic study in healthy pig eyes undergoing RON did not support the purported mechanism of scleral outlet decompression as extensive fibrous tissue filled the neurotomy site within 1 week of surgery.55 Another study utilizing indocyanine green videoangiography, suggested that creation of chorioretinal anastomosis is responsible for the benefits noted in optic nerve neurotomy.56 The possible benefits of RON must be balanced against potential complications, such as vitreous hemorrhage, laceration of the central retinal vein or artery, retinal detachment, choriodal neovascuarization, visual field loss, and globe perforation.36,57,58 This technique remains controversial and needs to undergo further studies to determine efficacy and safety.


It is important to evaluate the patient with retinal vein occlusion for associated systemic disease because hypertension and diabetes mellitus are strongly associated with retinal vein occlusions in patients of all age groups.59-62 Other significant associations include peripheral vascular disease and elevated body mass index in patients over 50 years of age.60,61 Elevated levels of homocysteine has also been proposed as a possible risk factor for retinal vein occlusion and is treatable with vitamin supplementation.63-67

Based on these findings, patients with a retinal vein occlusion should be referred to a primary care physician for a comprehensive history and physical examination focusing on hypertension and diabetes. Additional testing should be tailored to the individual patient based on history and physical examination findings by the primary care physician. In patients under 50 years of age or in cases of bilateral CRVO, the above evaluation should also focus on assessment of risk factors for possible hypercoaguable disorders, vasculitis, collagen vascular disease, and myeloproliferative disease (Table 4).64 A hematologic consultation may be helpful in this respect. Routine laboratory testing for rare disorders is generally not indicated.21,40, 68


While the BVOS and CVOS have provided evidence-based management guidelines for retinal vein occlusion, these studies still leave a significant group of patients at risk for visual loss. Emerging medical and surgical treatments may provide new therapeutic options for patients with retinal vein occlusion.

Address correspondence to: Paul B. Greenberg, MD, Retinal Consultants, Inc., 690 Eddy Street, Providence, RI 02903, Telephone: (401) 274-5844, Fax: (401) 274-9462, E-mail:

Division of Ophthalmology, Brown Medical School / Rhode Island Hospital, Providence, RI and Retina Consultants, Providence, RI.

Neither Dr. Greenberg nor Dr. Gupta has financial interest in this information. Dr. Greenberg is a Principal Investigator in the SCORE Study.


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20. Hayreh SS. Classification of central retinal vein occlusion. Ophthalmology. 1983;90:458-474.

21. Bhagat N, et al. Central retinal vein occlusion: review of mangement. Eur J Ophthalmol. 1999;9:165-180.

22. Hayreh SS. Retinal vein occlusion. Indian J Ophthalmology. 1983;90:109-132.

23. Hayreh SS, et al. Intraocular pressure abnormalities associated with central and hemicentral retinal vein occlusion. Ophthalmology. 2004;111:133-141.

24. Central Vein Occlusion Study Group. Natural history and clinical management of central retinal vein occlusion. Arch Ophtath. 1997;115:486-491.

25. Hayreh SS, et al. Differentiation of ischemic from non-ischemic central retinal vein occlusion during the early acute phase. Graefes Arch Clin Exp Ophthalmol. 1991;228:201-217.

26. Larsson J, et al. Fluorescein angiography versus ERG for predicting the prognosis in central retinal vein occlusion. Acta Ophthalmol Scand. 1998;76:456-460.

27. Morell AJ, et al. Electroretinography as a prognostic indicator of neovascularization in CRVO. Eye. 1991;5:362-368.

28. Hayreh SS, et al. Ocular neovascularization with retinal vascular occlusion-III. Incidence of ocular neovascularization with retinal vein occlusion. Ophthalmology. 1983;90:488-506.

29. CVOS. A randomized clinical trial of early panretinal photocoagulation for ischemic central vein occlusion. The central vein occlusion study group N report. Ophthalmology. 1995;102:1434-1444.

30. CVOS group. Evaluation of grid pattern photocoagulation for macular edema in central vein occlusion. The central vein occlusion study group M report. Ophthalmology. 1995;102:1425-1433.

31. Gaudrie A, et al. Photocoagulation with the argon laser in cystoid macular edema in retinal venous occlusions. J Fr Optalmol. 1988;11:319-326.

32. Recchia FM, Carvalho-Recchia CA, Hassan TS. Clinical course of younger patients with central retinal vein occlusion. Arch Ophthal. 2004;122;317-321.

33. Greenberg, PB, et al. Intravitreal triamcinolone for refractory macular edema secondary to central retinal vein occlusion. BJO. 2002;86:247-249.

34. Park CH, Jaffe GJ, Fekrat S. Intravitreal triamcinolone acetonide in eyes with cystoid macular edema associated with central retinal vein occlusion. AJO. 2003;136:419-425.

35. Bashshur ZF, et al. Intravitreal triamcinolone for the management of macular edema due to nonischemic central retinal vein occlusion. Arch Ophthal. 2004;122:1137-1140.

36. Ip MS, et al. Intravitreal triamcinolone for the treatment of macular edema associated with central retinal vein occlusion. Arch Ophthal. 2004;122:1131-1136.

37. Kaushik S, et al. intractable glaucoma following intravitreal triamcinolone in central retinal vein occlusion. AJO. 2004;137:758-760

38. Mithen LM, et al. Intravitreal triamcinolone acetonide and intraocular pressure. AJO. 2004;138:740-743

39. Moshfeghi DM, et al. Acute endophthalmitis following intravitreal triamcinolone acetonide injection. AJO. 2003;136:791-796.

40. Hayreh SS. Hematologic abnormalities associated with various types of retinal vein occlusion. Graefe's Archive Clinical Experimental Ophthal. 2002;240:180-196.

41. Browning DJ, Fraser CM. Retinal vein occlusion in patients taking warfarin. Ophthalmology. 2004;111:1196-1200.

42. Arroyo JG, Dastgheib K, Hatchell DL. Antithrombotic effect of ticlopidine in an experimental model of retinal vein occlusion. Jpn J Ophthalmol. 2001;45:359-362.

43. Yomamoto T, et al. Comparative effect of antiplatelet therapy in retinal vein occlusion evaluated by the particle-counting method using light scattering. AJO. 2004;138:809-817.

44. Elman MJ. Thrombolytic therapy for central retinal vein occlusion: results of a pilot study. Trans Am Ophthalmol Soc. 1996;94:471-504

45. Lahey JM, Fong DS, Kearney J. Intravitreal tissue plasminogen activator for acute central retinal vein occlusion. Ophthalmic Surg Lasers. 1999;30:427-434

46. Elman MJ, Raden RZ, Carrigan A. Intravitreal injection of tissue plasminogen activiator for central retinal vein occlusion. Trans Am Ophthalmol Soc. 2001;99:219-221.

47. Ghazi, NG, et al. Intravitreal tissue plasminogen activator in the management of central retinal vein occlusion. Retina. 2003;23:780-784.

48. Kamei M, Misono K, Lewis H. A study of the ability of tissue plasminogen activator to diffuse into the subretinal space after intravitreal injection in rabbits. AJO. 1999;128:738-746.

49. Weiss JN. Treatment of central retinal vein occlusion by injection of tissue plasminogen activiator into a retinal vein. AJO. 1998;126:142-144.

50. Weiss JN, Bynoe LA. Injection of tissue plasminogen activator into a branch retinal vein in eyes with central retinal vein occlusion. Ophthalmology. 2001;108:2249-2257.

51. Tameesh MK, et al. Retinal vein cannulatin with prolonged infusion of tissue plasminogen activator for the treatment of experimental retinal vein occlusion in dogs. AJO. 2004;138:829-839.

52. Boyd SR, et al. Correlation of increased vascular endothelial growth factor with neovascularization and permeability in ischemic central retinal vein occlusion. Arch Ophthal. 2002; 120:1644-1650.

53. Adamis AP, et al. Inhibition of vascular endothelial growth factor prevents retinal ischemia-associated iris neovascularization in a non-human primate. Arch Ophthal. 1996;114:66-71.

54. Opremcak EM, et al. Radial optic neurotomy for central retinal vein occlusion: a retrospective pilot study of 11 consecutive cases. Retina. 2001;21:408415.

55. Czajka MP, et al. Radial optic neurotomy in the porcine eye without retinal vein occlusion. Arch Ophthal. 2004;122:1185-1189.

56. Nomoto H, et al. Evaluation of radial optic neurotomy for central retinal vein occlusion by indocyanine green videoangiography and image analysis. AJO. 2004:138:612-619.

57. Bakri SJ, Beer PM. Choroidal neovascularization after radial optic neurotomy for central retinal vein occlusion. Retina. 2004;24: 610-611.

58. Hayreh SS. Radial optic neurotomy for central retinal vein occlusion (correspondence). Retina. 2002;22:374-377.

59. Eye Disease Case-Control Study Group. Risk factors for central retinal vein occlusion. Arch Ophthal. 1996;114:545-554.

60. Hayreh SS, et al, Systemic Diseases Associated with various types of retinal vein occlusion. AJO. 2001;131:61-77.

61. Sperduto RD. Risk factors for hemiretinal vein occlusion: comparison with risk for central and branch retinal vein occlusion. Ophthalmology. 1998;105:765-771.

62. Elman MJ, et al. The risk for systemic vascular diseases and mortality in patients with central retinal vein occlusion. Ophthalmology. 1990;97:1543-1548.

63. Recchia, FM, Brown, GC. Systemic disorders associated with retinal vascular occlusion. Curr Opin Ophthalmol. 2000;11:462-467.

64. Prisco D, Marcucci, R. Retinal vein thrombosis: risk factors, pathogenesis, and therapeutic approach. Pathophysiol Haemost Thromb . 2002;32:308-311.

65. Wilmink AB, et al. Dietary folate and vitamin B6 are independent predictors of peripheral arterial occlusive disease. J of Vasc Surg. 2004;39:513-516.

66. Narin F. Plasma homocysteine and retinal artery occlusive disease: a case-control study. Ann Saudi Med. 2004;24:186-188.

67. Parodi MB, Creecchio LD. Hyperhomocysteinemia in central retinal vein occlusion in young adults. Seminars in Ophthalmology. 2003;18:154-159.

68. Lahey JM, et al. Laboratory evaluation of hypercoagulable states in patients with central retinal vein occlusion who are less than 56 years of age. Ophthalmology. 2002;109:126-131.


Table 3. Current Treatment Modalities for BRVO and CRVO

  • Scatter argon panretinal photocoagulation for neovascularization (CRVO/BRVO)

Focal grid argon laser for perfused macular edema (BRVO only)


  • Intravitreal triamcinolone acetonide
  • Vitrectomy
  • Arteriovenous sheathotomy
  • Radial optic neurotomy
  • Intravitreal tissue plasminogen activator injection
  • Vitrectomy with retinal vein cannulation and infusion of tissue plasminogen activator
  • Anti-VEGF antibodies


Table 4. Diseases Associated With Retinal Vein Occlusions

Vascular disease
  • Hypertension
  • Diabetes mellitus
  • Hypercholesteremia
  • Carotid artery insufficiency

External compression

  • Antecedent trauma
  • Orbital tumor
  • Thyroid ophthalmopathy
  • Orbital abcess

Blood Dyscrasias

  • Polycythemia vera
  • Lymphoma
  • Leukemia
  • Sickle cell disease


  • Multiple myeloma
  • Cryoglobulinemia
  • Macroglobulinemia


  • Sarcoidosis
  • Syphillis
  • Human Immunodeficiency Syndrome

Hypercoagulability (90)

  • Protein C deficiency
  • Protein S deficiency
  • Factor V Leiden mutation
  • Antithrombin III
  • Mutation in prothrombin gene (G2010A)
  • Antiphospholipid antibody syndrome
  • Homocystinuria


  • Diuretics
  • Oral contraceptives