Introduction
Branch retinal vein occlusion (BRVO) is a retinal vascular disorder seen most frequently in the elderly population (median age of 66 years). The Beaver Dam Eye Study reported that the prevalence and 5-year incidence of BRVO were both 0.6%.1 Significant risk factors for BRVO include arterial hypertension and cardiovascular disease. The condition is usually unilateral, though up to 7% of patients will eventually develop bilateral disease. Visual loss commonly occurs from macular edema or vitreous hemorrhage secondary to disc or retinal neovascularization.
Pathophysiology
Histopathological studies have demonstrated that BRVO arises from thrombus formation at sites of arteriovenous crossing where arteries and veins share a common adventitial sheath. The arteries cross over the veins in more than 90% of cases of BRVO. Progressive arteriosclerosis may lead to arteriolar rigidity, secondary turbulence in venous blood flow, endothelial cell damage, and venous thrombosis. This results in ischemia and a blood-retina barrier breakdown in the area drained by the vein.
Clinical Presentation
In the acute phase of BRVO, retinal hemorrhages and cotton-wool spots are seen distal to the arteriovenous crossing and in the area of the retina drained by the obstructed vein. If the temporal veins are involved, there may also be macular thickening which usually presents as cystoid macular edema (CME). The degree of obstruction determines the severity of the clinical presentation. Widespread retinal hemorrhage may obscure the site of venous obstruction and preclude the use of fluorescein angiography. In the chronic phase, 9 to 12 months after occurrence, of BRVO, the retinal hemorrhages have typically been reabsorbed, leaving the retinal vascular abnormalities in the involved segment more apparent. These include venous collaterals (which may cross the horizontal raphe), retinal capillary telangiectasis, capillary nonperfusion, and CME.
Complications
The two primary vision-threatening complications of BRVO are neovascularization and macular edema. In BRVO, disc and retinal neovascularization develop in 12% and 24% of eyes, respectively. The presence of ischemia is a requirement. In the Branch Vein Occlusion Study (BVOS), 50% of eyes with BRVO and 5 disc diameters or more of capillary nonperfusion develop neovascularization (Table).2,3 Retinal neovascularization usually develops within 1 year. The BVOS also demonstrated that 50% of eyes with retinal neovascularization develop vitreous hemorrhage. Tractional retinal detachment and, rarely, anterior segment neovascularization and neovascular glaucoma can also occur.
When high quality fluorescein angiography can be obtained, macular edema from a BRVO can be classified as perfused or nonperfused. In perfused macular edema, there is an intact perifoveal capillary ring made up of dilated capillaries that often encircle the macula. These dilated vessels leak fluorescein in the later phases, usually in a petalloid pattern. Ischemic macular edema can be identified on fluorescein angiography by a broken perifoveal capillary ring; distinct areas of capillary nonperfusion within 1 disc diameter of the foveal center are also of diagnostic significance in this respect. In contrast to perfused cases, ischemic macular edema does not typically leak on fluorescein angiography, even when cystoid changes are present on clinical examination.
Distinguishing between these two types of macular edema has prognostic significance. If not widespread, eyes with ischemic macular edema may have a better natural history than those with perfused macular edema. A pilot study reported that 91% of eyes with ischemic macular edema experienced improved visual acuity compared to less than one-third of perfused cases. Similarly, the BVOS showed that only one-third of untreated eyes with perfused macular edema had improvement in baseline visual acuity (see below).2,3
Management
The BVOS recommended that eyes with BRVO and neovascularization undergo scatter panretinal photocoagulation (PRP), as this lowers the risk of developing a vitreous hemorrhage by 50%. The study also showed that PRP lowers the risk of neovascularization in eyes with 5 disc diameters or more of nonperfusion. However, PRP is not recommended in this instance. Because 50% of eyes with ischemia will not develop neovascularization, the laser therapy would treat twice as many people as necessary.2,3
The BVOS also demonstrated the efficacy of grid laser treatment for eyes with perfused macular edema for more than 3 months’ duration and 20/40 or less visual acuity: 65% of eyes with perfused macular edema gained two more lines of visual acuity versus 37% of controls. The mean final visual acuity at 3 years was 20/70 for the treated group and 20/45 for the control group.2,3
Eyes with ischemic macular edema should be followed conservatively as the majority will gain an improvement in visual acuity (median time: 14 months). Similarly, eyes with areas of both ischemic and nonischemic macular edema should be observed for 6 to 12 months to allow the ischemia to resolve before considering grid laser treatment.
Several small studies have suggested that pars plana vitrectomy with adventitial sheathotomy may be of benefit to selected eyes with BRVO. Larger controlled studies will be necessary to define the role of this procedure in the management of BRVO.
References
- Klein R, Klein B, Moss SE, Meuer SM. The epidemiology of retinal vein occlusion: The Beaver Dam Eye Study. Trans Am Ophthalmol Soc. 2001;98:133-141.
- Branch Vein Occlusion Study Group. Argon laser photocoagulation for macular edema in branch vein occlusion. Am J Ophthalmol. 1984;98:271-282.
- Branch Vein Occlusion Study Group. Argon laser scatter photocoagulation for prevention of neovascularization and vitreous hemorrhage in branch vein occlusion: A randomized clinical trial. Arch Ophthalmol. 1986;104:34-41.
Bibliography
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Finkelstein D. Ischemic macular edema: Recognition and favorable natural history in branch vein occlusion. Arch Ophthalmol. 1992;110:1427-1434.
Hayreh SS, Rojas P, Podhajsky P, Montague P, Woolson RF. Ocular neovascularization with retinal vascular occlusion—III: Incidence of ocular neovascularization with retinal vein occlusion. Ophthalmology. 198;90:488.
Hayreh SS, Zimmerman MB, Poldajsky P. Incidence of various types of retinal vein occlusion and their recurrence and demographic characteristics. Am J Ophthalmol. 1994;117(4):49-441.
Hayreh SS, Zimmernam B, McCarthy MJ, Podhajsky P. Systemic diseases associated with various types of retinal vein occlusion. Am J Ophthalmol. 2001;131:61-77.