reports in which venous congestion preceded the asymmetric development of ME.7 Venous backpressure is transmitted directly to retinal capillaries and will worsen a tendency toward ME. In diabetic retinopathy, decreased autoregulation of retinal vessels may compromise the ability of the retinal arterioles to constrict as local metabolic conditions dictate. Thus, degrees of severity of CRVO that would cause no edema in nondiabetic patients may cause ME in an eye with diabetic retinopathy.7 In this case, the venous dilation of the right eye and marked asymmetry in number of intraretinal hemorrhages suggested that a nonischemic CRVO was superimposed on a backdrop of mild nonproliferative diabetic retinopathy (as reflected in the right eye). Although the VA was still 20/20, the patient complained and was intolerant of observation as a management option.

The distinction whether this was diabetic ME or CRVO with ME had more than academic interest because focal laser was the standard treatment for the former, but was known to be ineffective in the latter.6 An IVBI was given, which resolved the ME and the symptoms temporarily. Over the ensuing 4 years, the ME kept recurring as the antiVEGF drug level in the eye declined. The patient received 10 IVBIs or intravitreal ranibizumab injections to treat recurrent ME. The VA varied from 20/40 to 20/200 over this interval, depending on the amount of ME. The left eye, meanwhile,

developed no worse diabetic retinopathy and remained 20/20.

16.11 Summary of Key Points

•In a case of CRVO, it is advisable to look at the pattern of veins on the optic disc to discern if the case represents two simultaneous HCRVOs or a CRVO. If the case represents the former, the ischemic status of each HCRVO needs to be assessed independently as the status may differ between the two.

•In a patient of age 60 or older with vascular risk factors, a history of blurred vision, and few fundus clues, consider the diagnosis of an old macular BRVO. OCT and FA may show evidence not seen clinically.

•RVOs need continued long-term follow-up as NVE, NVD, and NVI can occur years later.

•The natural history of nonischemic CRVO with ME is highly variable. Enough cases spontaneously resolve that all purported treatments need to be tested in a randomized controlled clinical trial against the contemporary standard therapy (in 2012, serial IVIs of anti-VEGF drugs).

•Acute nonischemic RVOs need more frequent follow-up in the first 6 months as they can convert to nonischemic RVOs.

Fig. 16.11 Fundus images of a 47-year-old man with mild nonproliferative diabetic retinopathy and a superimposed nonischemic CRVO with ME of the right eye. (a) Fundus photograph of the right eye showing dilated veins and many intraretinal hemorrhages, especially in the temporal macula. (b) Fundus photograph of the left eye showing minimal diabetic retinopathy. The black arrows denote

two microaneurysms. Compare the retinal vein denoted by the blue arrow in (b) to the more tortuous and dilated vein denoted by the green arrow in (a). (c) False-color time domain OCT maps and line scans at baseline showing ME temporally in the right eye. (d) False-color time domain OCT maps and line scans 1 month after IVBI showing resolution of ME

•Although RVO is not a risk factor for NAION, the two conditions share risk factors. Therefore, it is not uncommon to have both conditions occur in the same patient.

•Although the IOS and CRVO both cause intraretinal hemorrhages in all four quadrants, they can be distinguished. Arterial perfusion is tenuous in IOS, but not in CRVO. Optic disc edema is common in CRVO, but never occurs in IOS.

•Retinal artery occlusions of all types can occur after CRVO by a mechanism of hemodynamic blockade. Cilioretinal arteriolar insufficiency occurs not commonly by this mechanism. Branch and central retinal artery insufficiency and occlusion after CRVO are much rarer, but can also occur without invoking an embolic, second etiology.

References

1. Branch Vein Occlusion Study Group. Argon laser scatter photocoagulation for prevention of neovascularization and vitreous hemorrhage in branch vein occlusion. Arch Ophthalmol. 1986;104:34–41.

2. Browning DJ. Optic nerve disease in diabetes mellitus. In: Diabetic retinopathy: evidence based management. New York: Springer; 2010. p. 357–68.

3.Browning DJ, Antoszyk AN. Laser chorioretinal venous anastomosis for nonischemic central retinal

vein occlusion. Ophthalmology. 1996;105:670–9. 4. Fuller JJ, Mason III JO, White Jr MF, McGwin Jr G,

Emond TL, Feist RM. Retinochoroidal collateral veins protect against anterior segment neovascularization after central retinal vein occlusion. Arch Ophthalmol. 2003;121:332–6.

5.Giuffre G, Palumbo C, Ranadazzo-Papa G. Optociliary veins and central retinal vein occlusion. Br J Ophthalmol. 1993;77:774–7.

6. Hansen LL, Danisevskis P, Arntz HR, Hovener G, Wiederholt M. A randomized prospective study on treatment of central retinal vein occlusion by isovolaemic haemodilution and photocoagulation. Br J Ophthalmol. 1985;69:108–16.

7.Hayreh SS. So-called “central retinal vein occlusion”

II:venous stasis retinopathy. Ophthalmologica. 1976;172:14–37.

8. Hayreh SS. Retinal vein occlusion. Indian J Ophthalmol. 1994;42:109–32.

9.Hayreh SS, Hayreh MS. Hemi-central retinal vein occlusion: pathogenesis, clinical features, and natural history. Arch Ophthalmol. 1980;98:1600–9.

10.Hayreh SS, Podhajsky PA, Zimmerman B. Ipsilateral recurrence of nonarteritic anterior ischemic optic neuropathy. Am J Ophthalmol. 2001;132:734–42.

11.Hayreh SS, Podhajsky PA, Zimmerman MB. Natural history of visual outcome in central retinal vein occlusion. Ophthalmology. 2011;118:119–33.

12.Hayreh SS, Zimmerman MB. Nonarteritic anterior ischemic optic neuropathy: clinical characteristics in diabetic patients versus nondiabetic patients. Ophthalmology. 2008;115:1818–25.

13.Kearns TP. Differential diagnosis of central retinal vein obstruction. Ophthalmology. 1983;90:475–80.

14.Laatikainen L, Kohner EM. Fluorescein angiography and its prognostic significance in central retinal vein occlusion. Br J Ophthalmol. 1976;60:411–8.

15.Levin LA, Danesh-Meyer HV. Hypothesis: a venous etiology for nonarteritic anterior ischemic optic neuropathy. Arch Ophthalmol. 2008;126:1582–5.

16.McAllister IL, Constable IJ. Laser-induced chorioretinal venous anastomosis for treatment of nonischemic central retinal vein occlusion. Arch Ophthalmol. 1995;113:456–62.

17.Mcleod D. Cilio-retinal arterial circulation in central retinal vein occlusion. Br J Ophthalmol. 1975;59: 486–92.

18.Mcleod D, Ring CP. Cilio-retinal infarction after retinal vein occlusion. Br J Ophthalmol. 1976;60: 419–27.

19.Rosenbaum PS, Srinivasan S, Zelefsky JR, Mayers M, Moradi IE. Branch retinal artery occlusion and nonischemic central retinal vein occlusion due to hyperhomocysteinemia in a 14-year-old child. J Pediatr Ophthalmol Strabismus. 2010;47:E1–4.

20. Russo V, Barone A, Conte E, Prascina F, Stella A, Noci ND. Bevacizumab compared with macular laser grid photocoagulation for cystoid ME in branch retinal vein occlusion. Retina. 2009;29:511–5.

21. Schatz H, Fong ACO, McDonald HR, et al. Cilioretinal artery occlusion in young adults with central retinal vein occlusion. Ophthalmology. 1991;98:594–601.

22.Singh AJ. Branch retinal artery obstruction with simultaneous central retinal vein occlusion. Eye. 2001;15:225–7.

23.Takahashi K, Muraoka K, Kishi S, Shimizu K. Formation of retinochoroidal collaterals in central retinal vein occlusion. Am J Ophthalmol. 1998;126: 91–9.

24.The Branch Vein Occlusion Study Group. Argon laser photocoagulation for macular edema in branch vein occlusion. Am J Ophthalmol. 1984;98:271–81.

25.The Central Vein Occlusion Study Group. Baseline and early natural history report. Arch Ophthalmol. 1993;111:1087–95.

26.The Central Vein Occlusion Study Group. Natural

history and clinical management of central retinal vein occlusion. Arch Ophthalmol. 1997;115:486–91.

27. The Central Vein Occlusion Study Group N Report. A randomized clinical trial of early panretinal photocoagulation for ischemic central vein occlusion. Ophthalmology. 1995;102:1434–44.

28.The Score Study Research Group. A randomized trial comparing the efficacy and safety of intravitreal triamcinolone with observation to treat vision loss associated with macular edema secondary to central retinal vein occlusion. Arch Ophthalmol. 2009;127:1101–14.

29.The SCORE Study Research Group. A randomized trial comparing the efficacy and safety of intravitreal triamcinolone with standard care to treat vision loss associated with macular edema secondary to branch

retinal vein occlusion: the Standard Care vs Corticosteroid for Retinal Vein Occlusion (SCORE) study report 6. Arch Ophthalmol. 2009;127:1115–28.

30. Wallow IHL, Danis RP, Bindley C, Neider M. Cystoid macular degeneration in experimental BRVO. Ophthalmology. 1988;95:1371–9.

31.Williamson TH, O’Donnell A. Intravitreal triamcinolone acetonide for cystoid macular edema in nonischemic central retinal vein occlusion. Am J Ophthalmol. 2005;139:860–6.