for these probably ischemic eyes.34 A separate series of 11 cases of CRVO in patients of age 45 or younger, however, documented a poor visual prognosis in the ischemic group.9

Intraocular neovascularization of any type after CRVO in 67 younger patients followed for a mean of 29 months has been reported to occur in 18%, ASNV in 11%, posterior segment neovascularization (PSNV) in 9%, and NVG in 5%.30 In another study of 103 younger patients with CRVO followed for an average of 32 months, ASNV occurred in 19%, PSNV in 3%, and NVG in 8%.8 These percentages are generally lower than median percentages reported for case series without age constraints (see Chaps. 10 and 11; Table 11.4). Patients developing intraocular neovascularization had a similar profile of systemic associations compared to patients who did not.30

14.4Workup in the Younger Patient with Retinal Vein Occlusion

As for RVO in older patients, the available evidence suggests that in younger patients, investigating for unsuspected hypertension is worthwhile.23 Although some have recommended

a search for various associated laboratory abnormalities if no common vascular risk factors are present, the evidence to support the recommendation is poor.23 Because of the rarity of finding thrombophilia in a young patient without vascular risk factors and with no personal or family history of thrombosis or miscarriage, most would recommend no special laboratory workup (see Chap. 6).29,32

14.5 Summary of Key Points

•The cutoff point in the definition of “younger” varies from 40 to 60 in studies of RVO. Therefore, combining results across studies is problematic.

•Approximately 5% of BRVOs, 10% of HCRVOs, and 15% of CRVOs occur in patients of age 45 and younger.

•No thrombophilic associations are recognized in population-based samples of younger patients with BRVO or CRVO compared to control samples without RVO. Specific patients with RVO may have thrombophilia.

•There is no evidence that CRVO in younger patients has an inflammatory basis. Papillophlebitis and benign retinal vasculitis

25. Lonn LI, Hoyt WF. Papillophlebitis: a cause of protracted yet benign optic disc edema. Eye Ear Nose Throat Mon. 1966;45:62–8.

26.Magargal LE, Brown GC, Augsburger JJ, Parrish RK. Neovascular glaucoma following central retinal vein obstruction. Ophthalmology. 1981;88:1095–101.

27.Mcleod D. Central retinal vein obstruction with cilio-

retinal infarction. Eye. 2003;17:283.

28. Mitchell P, Smith W, Chang A. Prevalence and associations of retinal vein occlusion in Australia: the Blue Mountains Eye Study. Arch Ophthalmol. 1996; 114:1243–7.

29.Priluck I, Robertson D, Hollenhorst R. Long-term follow-up of occlusion of the central retinal vein in young adults. Am J Ophthalmol. 1980;90:190–202.

30.Recchia FM, Carvalho-Recchia CA, Hassan TS. Clinical course of younger patients with central retinal vein occlusion. Arch Ophthalmol. 2004;122:317–21.

31.Salomon O, Moisseiev J, Rosenberg N. Analysis of genetic polymorphisms related to thrombosis and other risk factors in patients with retinal vein occlusion. Blood Coagul Fibrinolysis. 1998;9:617–22.

32.Tourville E, Schachat AP. Plasma proteins-possible risk factors for retinal vascular occlusive disease. 2007;424–42

33.Vannas S, Raitta C. Anticoagulant treatment of retinal venous occlusion. Am J Ophthalmol. 1966;62:874–84.

34.Walters RF, Spalton DJ. Central retinal vein occlusion in people aged 40 years or less: a review of 17 patients. Br J Ophthalmol. 1990;74:30–5.

35.Weger M, Renner W, Steinbrugger I, Cichocki L, Temmel W, Stanger O, El Shabrawi Y, Lechner H, Schmut O, Haas A. Role of thrombophilic gene polymorphisms in branch retinal vein occlusion. Ophthalmology. 2005;112:1910–5.

The history of treatments for many diseases is often as notable for failures as for successes. For retinal vein occlusions (RVO), the list of failed therapies is particularly long. A review of the failures and an analysis of the reasons may be helpful for future attempts at devising more successful therapy than we currently have. Reasons for failure range widely: treatment is based on an erroneous conception of pathogenesis, too many complications relative to successes, and insufficient efficacy relative to cost. Some treatments have not been failures, but have not been adopted for other reasons. An example would be laser chorioretinal venous anastomosis (LCRVA) for nonischemic central retinal vein occlusion (CRVO). A randomized, controlled clinical trial has shown that LCRVA is efficacious compared to observation.39 Nevertheless, the treatment has not been adopted because other treatments (e.g., intravitreal injections (IVI) of antivascular endothelial growth factor (VEGF) drugs) have been perceived, although not proven in head-to-head comparison, to be better.6 These unadopted treatments are also covered here. Abbreviations commonly used in the discussion of failed and unadopted treatments for RVO are listed in Table 15.1. Each abbreviation is spelled out at its first occurrence.

Table 15.1 Abbreviations used in failed and unadopted treatments for retinal vein occlusions