the patient had ME at the time of her acute BRVO, but when seen for the first time, no ME was present. The case illustrates that capillary nonperfusion can extend beyond the drainage area of the blocked vein. The reason is unclear, but one hypothesis is that the elevated levels of VEGF over the nonperfused retina have the adverse effect of decreasing capillary perfusion of the border zone. This case illustrates the importance of regular long-term follow-up of patients with ischemic BRVO.2 Retinal neovascularization did not develop until more than 3 years after the BRVO occurred. With timely recognition and application of sector panretinal laser photocoagulation, the patient probably could have been spared the need to undergo vitrectomy surgery.

16.9Case 16.9: Nonischemic Central Retinal Vein Occlusion with Secondary Branch Retinal Artery Occlusion

A 78-year-old woman with hypertension and a history of previous coronary artery disease and stroke developed a sudden scotoma of the left eye (Fig. 16.10). She was found to have a nonischemic CRVO with a concomitant branch retinal artery occlusion. The VA was 20/20. During follow-up of 17 months, the CRVO resolved, but the scotoma from the branch retinal artery occlusion remained. VA has remained 20/20 in this eye.

16.9.1 Discussion

At first, this case suggests cilioretinal arteriolar insufficiency in the setting of a nonischemic CRVO, a well-known clinical scenario.17,18 However, close inspection shows that it is not. The involved artery is a branch retinal artery, not a cilioretinal arteriole. This situation has been described rarely before.19,22 In this case, there was a true infarction of the ischemic, whitened retina, which is often not the case with cilioretinal arteriolar insufficiency in CRVO (see Chap. 7).21 A new dense scotoma was evident on the visual field (Fig. 16.10d). Thinning of the inner retina (Fig. 16.10f) occurred as infarcted cells atrophied. Hemodynamic blockade of retinal arterial flow after CRVO can occur at several levels. Cilioretinal arteriolar insufficiency and infarction is the most common, but a similar mechanism can cause branch retinal arterial infarction, as in this case, or even central retinal arterial insufficiency, as in the cases shown in Chap. 2 (Fig. 2.24) and Chap. 14 (Fig. 14.2).

16.10Case 16.10: Nonischemic Central Retinal Vein Occlusion with Macular Edema or Asymmetric Diabetic Retinopathy with Diabetic Macular Edema?

A 47-year-old man with an 18-year history of type 1 diabetes was seen with acute blurred vision of the right eye. VA was 20/20 bilaterally

Fig. 16.10 Fundus images from a 78-year-old woman with a nonischemic CRVO and concomitant branch retinal artery occlusion. (a) Monochromatic fundus photograph showing intraretinal hemorrhages in all quadrants as well as dilated veins. A region of ischemic retinal whitening is present around a branch retinal arteriole (the green arrow). (b) Frame from the early-phase FA showing that the arteriole is a branch retinal arteriole and not a cilioretinal arteriole. It connects to a larger branch retinal artery (follow the green arrows). (c) Frame from the arte- riovenous-phase FA. (d) Two 24–2 visual fields are shown.

The first was obtained on 4/12/2006 and shows a suggestion of a superior Bjerrum scotoma. The second one was obtained on 7/26/2010 at the time of the fundus photographs. A new scotoma that corresponds to the location of the ischemic retinal whitening is present (the red oval). (e) SD-OCT line scan at the time of the initial visit shows hyperreflectivity of the inner retina in the ischemic region (the yellow arrow). (f) Follow-up SD-OCT line scan 6 weeks later shows thinning (yellow arrow) of the inner retina and resolution of the hyperreflectivity

but he complained of subjective blurring of the right eye. The appearance of the fundi is shown in Fig. 16.11. How would you manage this case?

a

c

16.10.1 Discussion

The concomitant effects of diabetic retinopathy and CRVO have been considered in previous case

b

d