Branch and central retinal vein occlusion

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Wilfred Lee
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Second most common retinal vasclar disorder1 with age (n=3654)2 Estimated worldwide projection: 16 million people affected in at least one eye3 ~520 new cases annally per million poplation3 10-year

1 Second most common retinal vasclar disorder1 with age (n=3654)2 Estimated worldwide projection: 16 million people affected in at least one eye3 ~520 new cases annally per million poplation3 10-year incidence of 1.6% in people aged 49 years4 5 Prevalence (%) Retinal vein occlsionprevalence (RVO) of RVO varies < Years >80 Vision loss sbstantially affects qality of life Of 325 people with visal loss of 20/40 or worse in >1 eye, the average person with 20/40 vision in the better eye was willing to trade 2 of 10 years of life in retrn for perfect vision5 1. Shahid et al. Br J Ophthalmol 2006; 90: ; 2. Mitchell et al. Arch Ophthalmol 1996; 114: (figre Copyright 1996 American Medical Association. All rights reserved); 3. Rogers et al. Ophthalmology 2010; 117: ; 4. Cgatti et al. Arch Ophthalmol 2006; 124: ; 5. Brown. Trans Am Ophthalmol Soc 1999; 97: Branch and central retinal vein occlsion CRVO Cotton wool spots 70% of RVO are branch retinal vein occlsions (); the remainder are central retinal vein occlsions (CRVO)1 Retinal hemorrhages Optic disc, hyperemiaedema, venos dilatation, and tortosity Oedema Oedema Retinal thickening Retinal Retinal thickening thickening 1. Mitchell et al. Arch Ophthalmol 1996; 114: ; 2. Rogers et al. Ophthalmology 2010; 117: ; 3 Wong et al. N Engl J Med. 2010; 363: CRVO fnds photograph from Wong et al. Clinical practice: retinal-vein occlsion. Copyright 2010 Massachsetts Medical Society. Reprinted with permission from Massachsetts Medical Society. fnds photograph reprodced with permission from Dr Tim Hillson.

Pathogenesis of RVO Occlsion occrs at the arteriovenos intersection major branch

cribrosa or the adjacent retrolaminar region CRVO Ischaemic (non-perfsed) occlsion is

areas of capillary non-perfsion (florescein angiography) 1 1.

fnds photograph (top) reprodced with permission from Dr Tim Hillson; CRVO fnds

2 Pathogenesis of RVO Occlsion occrs at the arteriovenos intersection major branch retinal vein, or maclar venle Non-ischaemic (perfsed) occlsion is distal to the lamina cribrosa or the adjacent retrolaminar region CRVO Ischaemic (non-perfsed) occlsion is in the region of the lamina cribrosa (or immediately posterior) defined by >10 disc areas of capillary non-perfsion (florescein angiography) 1 1. Central Vein Occlsion Stdy Grop. Arch Ophthalmol 1993; 111: fnds photograph (top) reprodced with permission from Dr Tim Hillson; CRVO fnds photographs (middle and bottom) reprodced from Morley and Heier. Chapter In Yanoff and Dker: Ophthalmology. 3rd ed, Copyright Elsevier 2008.

Clinical featres of RVO Sdden, painless, nilateral loss of vision Not always perceived by patient Degree of vision loss dependent on retinal involvement and retinal perfsion stats Simlated vision

3 Clinical featres of RVO Sdden, painless, nilateral loss of vision Not always perceived by patient Degree of vision loss dependent on retinal involvement and retinal perfsion stats Simlated vision Simlated CRVO vision CRVO Inferotemporal or nasal often asymptomatic 1 VA at time of presentation is a strong predictor of prognosis for vision 2 Vision prognosis worse in CRVO than, particlarly when nonperfsed 3 VA, visal acity 1. Shirodkhar et al. Br J Hosp Med 2012; 73: 20-23; 2. Central Vein Occlsion Stdy Grop. Arch Ophthalmol 1993; 111: ; 3. McIntosh. Ophthalmology 2010; 117:

4 Risk factors for RVO Strongest risk factor for Age 1 Hypertension 3-6 Glacoma 2 Cardiovasclar disease 1 Hyperviscosity 1 Renal disease 7 Additional risk factors for CRVO 1.Shahid et al. Br J Ophthalmol 2006; 90: ; 2. Mitchell et al. Arch Ophthalmol 1996; 114: ; 3. Rath et al. Ophthalmology 1992; 99: ; 4. Hayreh et al. Am J Ophthalmol 2001; 131: 61-77; 5. Elman et al. Ophthalmology 1990; 97: ; 6. Wong et al. Ophthalmology 2005;

formation and retinal atrophy neovasclarisation3 Oedema Retinal thickening Neovasclar glacoma neovasclar glacoma 1. Aiello et al.

5 What happens if we don t treat? Retinal ischaemia preglates VEGF prodction1 High VEGF levels stimlate2 capillary leakage leading to maclar oedema lamellar hole formation epiretinal membrane formation and retinal atrophy neovasclarisation3 Oedema Retinal thickening Neovasclar glacoma neovasclar glacoma 1. Aiello et al. N Engl J Med 1994; 331; ; 2. Boyd et al. Arch Ophthalmol 2002; 120: ; 3. Wong et al. N Engl J Med 2010; 363: Optical coherence tomography image from Wong et al. Clinical practice: retinal-vein occlsion. Copyright 2010 Massachsetts Medical Society. Reprinted with permission from Massachsetts Medical Society.

6 At initial presentation Review VA RAPD Baseline IOPs :?disc morphology Co-existing pathology : CATARACT, diabetes, hypertension, glacoma sspect Ishaemic? Poor VA RAPD Retina Prognosis? Ischemic Other pathology Glacoma

7 Frther evalation Fnds floroscein angiography -ischemia? -role for laser? OCT imaging Even patients with maclar ischemia improved with -patient edcation - follow-p anti-vegf injections {Crystal trial data 2015} Cataract srgery and RVO Patient edcation as to case of visal loss Consider changes to pre-op and post-op drop regimen Treat retinal pathology first Consider intravitreal therapy at time of srgery Carefl mangement of IOP Changes to follow p regimen

8 Tailoring treatment in RVO The advent of anti-vegf therapy represents a significant advancement BRAVO and CRUISE: stdy designvisal impairment de to ME secondary to 1 Visal impairment de to ME secondary to CRVO 2 28-day screening period 1:1:1 randomisation 28-day screening period 1:1:1 randomisation Monthly treatment period PRN treatment period Sham (n=132) Monthly monitoring and PRN b treatment Resce laser at Month 9 if eligible a 0.3 mg (n=134) Monthly treatment (Day 0, Months 1, 2, 3, 4, 5) Resce laser at Month 3 if eligible a 0.3 mg (n=131) Sham (n=130) 0.3 mg (n=132) Monthly monitoring and PRN treatment b 0.3 mg (n=130) Monthly treatment (Day 0, Months 1, 2, 3, 4, 5) Month 6 primary endpoint Month 12 secondary endpoint ahaemorrhages cleared sfficiently to allow laser AND VA is 20/40 Snellen eqivalent or worse or CRT 250 μm AND BCVA increased by <5 letters or CRT decreased by <50 µm compared with visit 3 months prior to crrent visit; b treated if BCVA is 20/40 or worse or mean CRT 250 μm. BCVA, best-corrected visal acity; CRT, central retinal thickness; ME, maclar oedema; PRN, pro re nata. 1. Campochiaro et al. Ophthalmology 2010; 117: ; 2. Brown et al. Ophthalmology 2010; 117: Figres adapted/reprinted from Campochiaro et al. Ranibizmab for maclar oedema following branch retinal vein occlsion: six-month primary end point reslts of a phase III stdy.ophthalmology 2010; 117: and Brown et al. Ranibizmab for maclar oedema following central retinal vein occlsion: six-month primary end point reslts of a phase III stdy. Ophthalmology 2010; 117: , Copyright 2010, with permission from Elsevier.

9 Mean BCVA change from baseline (ETDRS letters SE) BRAVO: mean change in Primary endpoint BCVA over time * +16.4* Sham (n=132) Sham / ranibizmab a (n=115) Ranibizmab 0.3 mg (n=134) Ranibizmab (n=131) 0 0 Day Month Day 0-Month 5: monthly treatment Months 6-11: PRN treatment Sham Ranibizmab 0.3 mg Ranibizmab Mean (SD) no. of injections 5.5 (1.1) 5.7 (0.9) 5.7 (0.9) Sham / ranibizmab a Ranibizmab 0.3 mg Ranibizmab Mean (SD) no. of injections 3.6 (2.1) 2.8 (2.1) 2.7 (2.2) asham patients received ranibizmab, PRN treatment from Month 6 to 11. *p<0.01 vs sham / ranibizmab ; p< vs sham (pairwise ANOVA). Randomised patients, LOCF (last observation carried forward). ANOVA, analysis of variance; BCVA, best-corrected visal acity; ETDRS, Early Treatment Diabetic Retinopathy Stdy; PRN, pro re nata; SD, standard deviation; SE, standard error. 1. Brown et al. Ophthalmology 2011; 118: Figre reprinted from Brown et al. Sstained benefits from ranibizmab for maclar oedema following branch retinal vein occlsion: 12-month otcomes of a phase III stdy. Ophthalmology 2011; 118: , Copyright 2011, with permission from Elsevier. Tailoring treatment in RVO Redcing treatment brden: how many injections is enogh to maintain stable visal vision? What is the most appropriate therapy combination for my patient? (retinal laser, anti-vegf, steroid) How do we improve otcomes in ischaemic occlsions?

10 HORIZON cohort 2 5 (Phase III; completed) Maclar oedema secondary to and CRVO 2-year extension stdy: ranibizmab, mlticenter PRN dosing reslted in sstained BCVA & OCT improvement in first 12 months Qarterly monitoring visits or more freqently patients received fewer injections dring first year BRIGHTER 6 Maclar oedema secondary to 24-month stdy: PRN ranibizmab alone or with adjnctive laser ranibizmab with adjnctive laser is non-inferior to ranibizmab monotherapy wrt to mean average BCVA change from baseline ranibizmab with adjnctive laser redces the nmber of ranibizmab retreatments CRYSTAL 7 Maclar oedema secondary to CRVO 24-month stdy: 3 x monthly injections then PRN ranibizmab Maintenance of BCVA Some cases of improvement despite maclar ischemia at baseline, branch retinal vein occlsion; CRVO, central retinal vein occlsion; PRN, pro re nata; RVO, retinal vein occlsion. 1. Brown et al. Ophthalmology 2011; 117: ; 2. Campochiaro et al. Ophthalmology 2010; 117: ; 3. Brown et al. Ophthalmology 2010; 117: ; 4. Campochiaro et al. Ophthalmology 2011; 118: ;

Comparison of BRVO and CRVO management

Comparison of BRVO and CRVO management Francesco Bandello, MD, FEBO Department of Ophthalmology University Vita-Salute Scientific Institute San Raffaele Milan, Italy 1 Financial Disclosure Advisory Board