Approximately 9% of eyes do not respond to PRP, and the new vessels fail to regress.278

The efÞcacy of PRP in preventing NVG is a topic of controversy with some maintaining 100% efÞcacy and others claiming no difference in rate of NVG compared to an unlasered control group.103,175 Because only 70% of cases of NVI and 83% of cases of NVA after CRVO progress to NVG, and because PRP reduces peripheral visual Þeld, some have argued against using PRP at onset of NVI.108

Although early case series and pilot trials of PRP suggested that treatment could prevent ASNV in ischemic CRVO leading some to advocate prophylactic PRP in ischemic CRVO, the CVOS refuted this idea.156,157,182,278 In the CVOS, patients receiving PRP prophylactically went on to develop ASNV at a statistically indistinguishable rate from patients not receiving PRP, but suffered from a lesser response to further PRP once NVI occurred than patients who received their initial treatment at the time that ASNV was detected. Therefore, the preferred management strategy is frequent follow-up after an acute CRVO with initiation of PRP once NVI or NVA is detected.278 Although the threshold for applying PRP in the CVOS was that two or more clock hours of NVI be present, many clinicians consider detection of any NVI sufÞcient to trigger this intervention. After PRP for ASNV, follow-up is needed in 2Ð4 weeks to be sure that ASNV is regressing and not advancing. If nonregression or advancement is found, further PRP may be needed.278 PRP in eyes with ischemic CRVO is associated with an increase in mid-peripheral retinal blood ßow, but not back to levels observed in normal control eyes.8 Macular retinal blood ßow is unaffected by PRP.8

Because not all cases of NVI after CRVO progress to NVG, and because PRP reduces the peripheral visual Þeld, some have argued against PRP for all cases of NVI after CRVO.72,167,217 This group advocates the application of PRP only after documentation of progression of NVI upon weekly undilated slit lamp and gonioscopic evaluation. Perhaps because of the clinical burden of so many visits, this approach to management has not been widely adopted.

PRP for ASNV is effective in causing regression in 37Ð77% of cases after CRVO.23,27,72 In

patients with regression of ASNV after PRP, aqueous VEGF concentrations fall below 550 pg/ ml.23 By comparison, the aqueous VEGF levels in eyes undergoing cataract surgery range from 5 to 96 pg/ml.23 Regression of ASNV after PRP takes from 5 to 50 weeks with a median time of 23 weeks.23 Increasing patient age and presence of POAG are factors associated with a reduced rate of response of ASNV to PRP.72 In one series of 29 consecutive cases of NVG following CRVO, 41% ended with no light perception; 3% were enucleated for painful, blind eyes; and 38% ended with blind but comfortable eyes.72

13.5.4Intravitreal Injection of Antivascular Endothelial Growth Factor Drugs for Intraocular Neovascularization

Intravitreal bevacizumab injections can cause temporary regression of ASNV, NVE, and NVD after RVO, but must be given repetitively.130 Intravitreal injection of anti-VEGF drugs can buy time for the application of PRP with its more sustained effects.4,17

In certain cases, despite PRP, retinal neovascularization persists, and recurrent vitreous hemorrhage occurs. Case reports of intravitreal bevacizumab injection causing regression of the neovascularization and cessation of vitreous hemorrhage at least for a short term have been reported.4

Some patients with CRVO are Þrst seen when they develop NVG. In these cases, combination methods with injection of anti-VEGF drugs, PRP, and subsequent trabeculectomy with mitomycin C or with a tube shunt can be effective. In one series of 17 eyes of 15 patients, regression of ASNV occurred in 82.4% of eyes.7

13.6 Economic Considerations

Treatments for ME associated with RVO on average produce VA outcomes superior to the natural history of the untreated condition. Whereas these

277

281

93

304

305

36

280

93

303

306

29

improvements are statistically signiÞcant, they are modest. Smiddy has deÞned a quantity called lines of vision saved as the difference of mean lines of vision gained in an index study proving efÞcacy of a treatment and the lines of vision lost (or gained) from the natural history control group, preferably obtained within the same study but sometimes obtained from a different natural history sample of patients.258 The lines of vision saved are a number that applies to 1 year of treatment. Similarly a cost of care Þgure can be calculated based on assumptions of frequency of examinations, intensity and types of ancillary tests obtained, and the costs of the treatments. From this the cost per line of vision saved (CLVS) can be calculated for the various treatments over the course of a year. Table 13.8 lists the results of such a calculation. For BRVO, the CLVS varies by a factor of 26. For CRVO, the cost per line saved per year varies by a factor of 11.258

13.7 Future Directions

For patients who are seen shortly after the onset of RVO, practical and effective treatments that lyse the underlying thrombosis without serious systemic hemorrhagic complications remain a goal, despite many failed attempts taking this approach.

Drugs that could reduce VEGF upregulation in response to retinal hypoxia would be

theoretically attractive and could reduce the burden of anti-VEGF drug injections.

As the understanding of the pathophysiology and biochemistry of RVO increases, new targets for therapy come to light. Examples include decursin, which prevents VEGF-mediated loss of tight junction proteins including ZO-1/-2 and occludin. Such a drug might prevent bloodÐretina barrier disruption.136

Antibodies targeting soluble VEGF receptor 2 and soluble ICAM-1 might beneÞt patients with BRVO and ME who fail to respond to anti-VEGF antibodies and fusion proteins.195

Inhibitors of VEGFR2/Src kinase prevent VEGF-mediated increase in vascular permeability and reduce retinal edema in experimental retinal ischemia. Finding a safe and effective molecule for human RVO based on this mechanism would be a novel approach.248

In animal models of BRVO, a peripheral zone of ischemic retina may undergo delayed apoptosis after acute BRVO analogous to the ischemic penumbra noted in acute brain ischemia. Caspase activation is a leading candidate as the mediator for this ischemic apoptosis, and caspase inhibitors such as Z-VAD decrease the amount of apoptosis in a miniature pig model of BRVO.66 Translation into a safe treatment for human RVO has not been accomplished yet.

A chance observation that ME associated with BRVO improved when a patient with rheumatoid arthritis received intravenous injections of inßiximab, an anti-tumor necrosis factor a antibody (TNF-a), or etanercept, a dimeric fusion

protein consisting of the extracellular domain of the TNF receptor II and the Fc region of human immunoglobulin, suggests that such agents may have a role in this condition.129 The treatment has biologic plausibility because TNF-a is known to disrupt the bloodÐretina barrier.170

Antisense oligodeoxynucleotides bind to the VEGF mRNA preventing translation. This form of therapy could potentially block both basal and induced VEGF production after RVO. Basal RPE production of VEGF has been hypothesized to be necessary for choriocapillaris maintenance, and VEGF blockade could conceivably harm this necessary function.249

13.8 Summary of Key Points

¥Understanding the mechanism of action of treatments for RVO and their side effects informs the choice of appropriate treatment and sequence of treatments when initial therapy produces a suboptimal response.

¥Injection therapy (e.g., anti-VEGF drugs) can be given immediately for BRVO with ME. Grid laser usually follows a 3 or more month period of observation as intraretinal hemorrhage clears and perfusion status becomes deÞned.

¥There are nonresponders to every treatment. Therefore, having multiple effective treatments is desirable.

¥Systemic therapy for RVO, including thrombolysis, anticoagulation, and treatment of hyperhomocysteinemia, has shown little promise and is rarely examined.

¥Isovolumic hemodilution has demonstrated efÞcacy in RVO with ME but is not used in the United States and less often used now in Europe than formerly. This probably reßects a small effect of IH relative to the time and expense involved, and the appearance of intravitreal injections of anti-VEGF drugs, which seem more effective.

¥The most important systemic medical treatment for RVO is detection and treatment of unsuspected or inadequately treated hypertension.

¥GL is modestly effective for BRVO with ME without ischemia.

¥Serial intravitreal injections of anti-VEGF drugs for BRVO with ME are markedly effective, but costly.

¥Serial intravitreal injections of anti-VEGF drugs for CRVO with ME are markedly effective, but costly.

¥Serial intravitreal injections of triamcinolone are not more effective for BRVO with ME than GL.

¥Serial intravitreal injections of triamcinolone are more effective for CRVO with ME than observation, but with side effects of universal cataract development or worsening in phakic patients and intraocular pressure elevation in a signiÞcant fraction of cases.

¥An intravitreal dexamethasone insert is effective for RVO with macular edema. Cataract development in phakic patients is common, as well as intraocular pressure elevation controllable with topical therapy.

¥Anti-VEGF therapy does not address the underlying problem in RVO, and reinjections are frequently needed.

¥Vitrectomy can reduce macular edema in RVO with ME, but less commonly improves visual acuity, perhaps because it tends to be used later in the course of RVO after less invasive therapies fail.

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