7.2 Central Retinal Vein Occlusion |
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optic nerve sheath meningioma, and chronic papilledema, can cause them.38 Once formed, retinochoroidal collaterals tend not go away, although rarely they do. Their diameters and location on the optic disc have been observed to change over years of follow-up.38,108
Anterior segment neovascularization (ASNV) develops in 16Ð70% of ischemic CRVOs.17,36,48,54,5
6,57,61,62,81,82,112,140,146 If ASNV is going to develop, it
usually does so in the Þrst 7 months with an average time of onset of 4 months.57,98 Retinal and disc neovascularizations are less common than ASNV after CRVO, for unknown reasons, and tend to develop later, with median time to occurrence of 12 months.57,98 In the population-based BDES, 18 eyes suffered incident CRVO during 15 years of follow-up. Of these, three (17%) had retinal neovascularization.72 Without treatment, most eyes developing ASNV after ischemic CRVO will develop neovascular glaucoma (see Chap. 11). The risk of neovascular glaucoma developing in
eyes with ischemic CRVO is 23Ð60% over 12Ð15 months.86 The risk in eyes that convert from nonischemic to ischemic CRVO is 33%.56
Four variables have been tested for ability to predict ASNV after CRVO Ð capillary dropout greater than 10 disc areas, initial Snellen visual acuity less than 20/200, implicit time on 30 Hz ßicker fusion electroretinogram greater than 37 ms, and presence or absence of optic disc edema.62 For development of neovascular complications, the presenting variable of highest prognostic import is implicit time on 30 Hz ßicker fusion electroretinogram greater than 37 ms (kappa = 0.69), followed by initial visual acuity less than 20/200 (kappa = 0.60), capillary dropout greater than 10 disc areas (kappa = 0.49), and absence of optic disc edema (kappa = 0.28).62 In another study, predictive factors for occurrence of anterior or posterior neovascularization were male gender (higher risk) and baseline visual acuity (worse confers higher risk).39
Why Are Optic Disc Collaterals Associated with Worse Initial and Final Visual Acuity After CRVO?
A plausible hypothesis for the noted observation, counter to common intuition, has been advanced by Hayreh.56 The severity of CRVO depends on location of the thrombus in the optic nerve. The more anterior the thrombus, the worse the CRVO. If a thrombus occurs more anteriorly in the optic nerve, there are fewer preexisting channels to allow the retinal venous drainage to bypass the clot. Therefore, the preexisting collaterals on the optic disc are the only ones available to serve in that capacity, and they become swollen and clinically obvious. In cases in which optic disc collaterals are not visible clinically, they are by inference present in an unseen location behind the lamina cribrosa. These are cases with more posteriorly located clots which are less severe, have more collaterals between clot and lamina for venous drainage, and have better presenting visual acuities.56
In the late stage, macular atrophic scarring and sheathing of retinal veins can develop (Fig. 7.21). Rarely, choroidal neovascularization can follow CRVO with chronic macular edema.32
7.2.2.1 Visual Acuity
The natural history of CRVO is guarded. After 3 years, 58% of eyes have visual acuity worse than
20/100. Less than 20% of eyes will gain greater than or equal to two lines of visual acuity.139
The visual prognosis depends most predictably on the initial visual acuity.140 The poorer the initial visual acuity, the worse the Þnal visual outcome.140 The prognostic importance of initial visual acuity is greatest when it is obtained within 30 days of the CRVO.140 In the CVOS, the majority of eyes stayed in the visual acuity category
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7 The Clinical Picture and Natural History of Retinal Vein Occlusions |
a |
b |
c |
d |
e
7.2 Central Retinal Vein Occlusion |
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185 |
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Table 7.4 Visual prognosis in central retinal vein occlusion by initial visual acuity |
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Initial VA; N |
Final VA ≥ 20/40 (%) |
Final VA 20/50Ð20/200 (%) |
Final VA < 20/200 (%) |
≥ 20/40; 209 |
65 |
25 |
10 |
20/50Ð20/200; 204 |
19 |
44 |
37 |
<20/200; 301 |
1 |
19 |
79 |
|
|
|
|
Data from CVOS140 |
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|
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Visual prognosis has also been stratiÞed by level of ischemia, but the results of such analyses are inconsistent. Quinlan and colleagues found no important difference between the outcomes of nonischemic and ischemic eyes in a retrospective study of 157 eyes with CRVO.112 On the other hand, when the ischemic status of CRVO was classiÞed using the strict Hayreh deÞnition, the prognosis for visual acuity varied starkly by class. The odds ratio for greater than or equal to three Snellen line improvement was 2.96 (95% CI 1.55Ð5.66) for nonischemic CRVO relative to ischemic CRVO.56 Others have agreed with Hayreh that the prognosis of ischemic CRVO is worse.45 In a meta-analysis of 53 studies including 3,271 eyes, the pooled mean change in visual acuity was −10 ETDRS letters from baseline to 6 months and −3 ETDRS letters from baseline to 12 months for nonischemic CRVOs.86 For ischemic CRVOs, the mean changes were −15 letters at 6 months and −35 letters at 12 months.86
More often, the controversy concerns whether the prognosis for visual acuity of nonischemic CRVO is good. One study reported that 50% of nonischemic CRVOs would end with visual acuity
worsened until in November 2000, the visual acuity was reduced to 20/30, and he had difÞculty at his job and driving. Note the venous dilation and new tortuosity (compare superotemporal vein at black arrow to the same site in (c)). (e) After laser chorioretinal anastomosis, with successful shunts inferotemporally (the turquoise arrow) and superonasally (not shown), the intraretinal hemorrhages and macular edema resolved. Note the more dilated veins distally than proximally (the black arrow), a sign of a successful shunt. The proximal inferotemporal branch retinal vein is attenuated in the absence of signiÞcant blood ßow (the yellow arrow). Development of a second-eye CRVO led to ascertainment of serum homocysteine which was elevated at 11.6 mmol/l (normal 9.0 mmol/l). He was placed on folate 800 mg/day. In 2008, he suffered a stroke and in 2010 required coronary artery stents for myocardial ischemia