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7.1 Branch Retinal Vein Occlusion

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Serous retinal detachment is more easily detected by OCT than clinically (Fig. 7.5).67,78,101, 103,130,133 SRD accompanies major BRVO (63%) more commonly than macular BRVO (21%).144 Most cases of serous retinal detachment also have cystoid macular edema.107,130,135 There is a syndrome of a midperipheral BRVO associated with serous retinal detachment of the macula in the absence of cystoid macular edema.135 A subretinal bloodÐßuid level may develop. In these cases, the serous retinal detachment resolves in a few months, but macular hard exudates and retinal pigment epithelial atrophy may result.135 The presence of serous retinal detachment has been associated with more ischemia, a paucity of collateral vessel formation, and a generally poorer visual prognosis.107

7.1.2.1 Visual Acuity

The visual acuity in acute BRVO can range from 20/20 to 20/400, but in general the loss of vision is less severe than with CRVO. In a populationbased study, 14% of patients had visual acuity less than or equal to 20/200.96 A weighted average of baseline visual acuities of 223 eyes with BRVO from four studies suggests that mean baseline visual acuity in BRVO is 20/80 (logMAR 0.59 ± SD0.30).22,41,106,117 Macular BRVOs have better baseline visual acuity than major BRVOs. In a series of 35 patients with macular BRVO, the average baseline visual acuity was 20/50 (logMAR 0.42 ± SD 0.13).106 Presenting visual acuity for superotemporal BRVOs is generally poorer than for inferotemporal BRVOs because macular edema and ischemia tend to be worse for superotemporal BRVOs.71 The loss of visual acuity from BRVO is worse the more proximal the occlusion is to the optic disc.7

7.1.3 Chronic Phase

7.1.3.1 Clinical Signs

Cotton wool spots and intraretinal hemorrhages eventually clear, the former within 6 months and the latter by 1 year.74,94 After a year or more, the retinal vein in the occluded region may develop

Fig. 7.6 Example of a branch retinal vein occlusion 2 years after initial presentation in a 52-year-old woman with hypertension. The black arrows show intraretinal collateral venules that span regions of ischemic retina that have a featureless appearance. The artery to the involved quadrant has become more sclerotic (the white arrow) than its counterpart supplying the superotemporal retinal quadrant (the blue arrow). The occluded inferotemporal branch retinal vein has become Þbrotic and sheathed (the green arrows). All the macular edema that was initially present has spontaneously resolved. The visual acuity was 20/50, and a superior altitudinal scotoma was present

Þbrotic sheathing (Fig. 7.6).25,103 The venous segment proximal to the occlusion may become Þbrotic.84 The arteries to the involved quadrant can show secondary changes such as sheathing and nonperfusion (Fig. 7.6).103

Once a branch retinal vein is occluded, preexisting collateral vessels that connect adjacent venous beds become distended and carry more blood ßow, tending to decrease the retinal venous pressure in the occluded segment (see Chap. 1). Collateral vessels after BRVO have been reported to occur in 60Ð92% of cases with a mean time to development of 6 months (range 3Ð24 months). They commonly occur within the retina (Fig. 7.4), but if the site of the BRVO is close to the optic disc, the collaterals may connect retinal to optic disc venules (Fig. 7.7).44,84 Collateral venules, unlike retinal and disc new vessels, do not leak on ßuorescein angiography (Fig. 7.8). As collaterals mature over 6Ð24 months and retinal venous pressure drops, vascular permeability can decrease, leading to spontaneous resolution of macular edema.25 In more severe cases, vascular permeability never recovers, and edema is chronically

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7 The Clinical Picture and Natural History of Retinal Vein Occlusions

Fig. 7.7 A 67-year-old man had a superotemporal branch retinal vein occlusion of the right eye. Macular edema was present reducing visual acuity to 30/32. The green arrow shows the site of the occlusion at an arteriovenous crossing. The black arrow shows collateral venules bypassing the thrombus

present.19 Remodeling of collateral vessels can occur with time. Young collaterals may be numerous, but of small caliber. Later, some may collapse leaving fewer, larger-bore collaterals to carry the venous blood around the damaged zone.25

Some eyes with macular BRVO do not have macular edema at baseline but develop it over follow-up. The best estimate for incidence of macular edema after BRVO in eyes free of it at baseline is 15% over 7.5 months based on a study of 20 eyes.130 Spontaneous resolution of macular edema in BRVO with macular edema at baseline is relatively common. Macular edema in BRVO as assessed by stereophotography and ßuorescein angiography spontaneously improved in 69% at 12 months and 80% over 24 months.106 Other studies report spontaneously resolved macular edema in 61Ð80% of eyes at unspeciÞed followup times.106,117,129 Spontaneous resolution is less commonly observed when OCT is the method of detection of macular edema. Only 17% of cases had resolution at 4.5 months follow-up in one study.130

In BRVO with macular edema but without ischemia, the macular edema spontaneously

resolves in approximately 30% of cases.22,130 Chronic CME occurs in 62Ð70% and hard lipid exudates in 41%, usually in eyes with secondary microaneurysms or other intraretinal microvascular abnormalities.22,94,130 Lipid exudation tends to be most prominent at the border of the affected and normal retina with lesser involvement on the peripheral side of the involved retina (Fig. 7.9).141 Occasionally, massive amounts of lipid exudation develop, a picture sometimes called adult CoatsÕ disease.80,126 Persistence of CME past 6 months is associated with more ischemic BRVOs.130 Retinal pigment epithelial metaplasia from chronic CME may develop.103 Macular hole and lamellar macular hole can be seen occasionally (Fig. 7.8).103

In cases with serous retinal detachment (SRD), spontaneous reabsorption occurs in a delayed manner over a range of 2Ð24 months, with a mean time to reabsorption of 15 months.107 Reabsorption of subretinal ßuid can be associated with subretinal Þbrosis and retinal pigment epithelial atrophy.107 For a group of 15 patients with SRD followed without treatment for 24 months, the mean baseline visual acuity was 20/160, and the mean 24-month visual acuity was 20/400.107 Larger area of BRVO and higher aqueous VEGF levels correlate with development of SRD.105

Other clinical signs in chronic BRVO include hard exudates (5%) (Fig. 7.9), capillary macroaneurysms (100to 250-m diameter, case reports), venous macroaneurysms (16Ð19%, case reports), epiretinal membranes (21%) (Fig. 7.10), subretinal scarring (9%), vitreous hemorrhage (5Ð7%) (Fig. 7.11), and tractional retinal breaks in the ischemic retina (case reports).25,27,84,114,121,122,125,137 Macroaneurysms may develop from capillaries, arteries, or veins.84 They are subclassiÞed by size into small (100Ð149 m), medium (150Ð249 m), and large (greater than 250 m). They may occur more commonly in BRVOs with more severe capillary nonperfusion.27

Retinal new vessels develop in 22Ð29% of cases of major BRVO and do not develop after macular BRVO.11,57,71,72,94 Retinal neovascularization typically occurs at the junction of nonperfused and perfused retina (see Fig. 2.20). New