Managing the Vitreomacular Interface

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1 Managing the Vitreomacular Interface A Guide to VMA, VMT, Holes and ERM Anna K. Bedwell, OD, FAAO Indiana University School of Optometry Please silence all mobile devices and remove items from chairs so others can sit. Unauthorized recording of this session is prohibited.

2 Disclosure Statement: Nothing to disclose

3 Vitreous Anatomy Composition = 98-99% water the rest = 2 main macromolecules: collagen, hyaluronic acid 3 parts: Central core Cortex dense collagen matrix 100 microns thick Posterior hyaloid Thin membrane between cortex and internal limiting membrane of the retina

4 Vitreous Aging At age 9 or 10, the human vitreous gel begins to liquefy Liquefaction: occurs as collagen aggregates into bundles causing pockets of liquid (lacunae) By age 40 the vitreous is 80% gel/20% liquid By age 80 the vitreous is 50% gel/50% liquid

5 Posterior Vitreous Detachment Detachment of the posterior cortex of the vitreous from the internal limiting membrane of the retina PVD occurs as vitreous liquefaction and vitreoretinal adherence Attachment Sites: Ora (strongest) Post lens capsule Optic disc Macula Vasculature (weakest)

6 Stages of PVD Perifoveal separation with vitreofoveal adhesion Complete vitreomacular separation Complete vitreoretinal interface separation except at the optic disc Complete PVD with Weiss ring

7 Start of PVD occurred in patients in their 20s which became more extensive with increased age PVD started in paramacular-peripheral region (rather than the traditionally thought perifoveal area)

8 Blame it on the Vitreous Anomalous PVD = gel liquefaction > vitreoretinal dehiscence Complications: Periphery breaks, detachment, WWP Vasculature I/R hemorrhages, vitreous hemorrhage, aggravate neovascularization Optic disc aggravate NVD, vitreo-papillary traction syndrome Macula contributes to DME and exudative AMD, vitreomacular interface disorders

9 Stalmans P. Retina. 2013

11 Vitreomacular Adhesion (VMA) Partial detachment of the vitreous in the perifoveal area without corresponding retinal abnormality (no change in retinal contour) Normal finding that occurs over the natural course of PVD Focal: 1500 um Broad: >1500 um

12 VMA Broad posterior hyaloid vitreous cortex Focal

13 1,950 eyes: 38% had VMA and 1% had VMT VMA most often found in age group Odds of VMA/VMT decreased by 7% with each year of age African Americans were less likely to have VMA/VMT than Caucasians Retina 2017

14 Vitreomacular Traction (VMT) Partial detachment of the vitreous in the perifoveal area with corresponding retinal abnormality (ie: change in retinal contour, distortion, pseudocyst formation) No full thickness interruption of layers Can cause retinal thickening, schisis, pseudocyst formation, vascular leakage on FA or CME Sxs (if present): blur, metamorphopsia, micropsia, photopsias Focal: 1500 um Broad: >1500 um

15 Focal VMT Pseudocyst Disruption of foveal contour

16 VMT Example Timeline 3/5/15 2/26/16

17 3/30/16 7/6/16 11/6/16

18 Broad VMT with ERM

19 En Face

20 Broad VMT with ERM

21 Is VMT to blame?...no

Management of VMA/VMT VMA no treatment necessary Asymptomatic VMT monitor for spontaneous resolution Timeline for spontaneous resolution unclear ~5-12% of VMT will

22 Management of VMA/VMT VMA no treatment necessary Asymptomatic VMT monitor for spontaneous resolution Timeline for spontaneous resolution unclear ~5-12% of VMT will progress on to FTMH Symptomatic VMT Refer to retina to consider ocriplasmin injection or PPV OR If minimally symptomatic, can monitor closely for spontaneous resolution.

23 Diabetics: Relationship to DM Retain VMA longer Develop PVD at a later age Traction may antagonize DME Nesmith, BL. Retina 2017

ERM tend to respond poorly Sadiq et al -> DME patients with (+)VMA

24 VMA/VMT and DME Diabetic Macular Edema (DME) Diabetic patients with VMA/VMT tend to have better response to anti- VEGF tx DME w/ ERM tend to respond poorly Sadiq et al -> DME patients with (+)VMA responded better to anti-vegf than those (-)VMA Sadiq Ophthalmology 2016

VMA/VMT and Neovascular AMD VMA or VMT can decrease the effectiveness of anti-vegf treatment in patients with neovascular AMD The unfavorable effect

25 VMA/VMT and Neovascular AMD VMA or VMT can decrease the effectiveness of anti-vegf treatment in patients with neovascular AMD The unfavorable effect decreased over the treatment period likely as VMA/VMT naturally released worse effect earlier in treatment, less so at 12 months out Xie P, et al. Br J Ophthalmol 2017

26 VMA/VMT and Macular Edema Macular Edema due to Retinal Vein Occlusion Singh et al. -> found no association between VRI status and treatment outcomes with anti-vegf agents for ME secondary to RVO Noted a trend that those with VMT had better reduction in central retinal thickness on OCT than other groups Which raises the question Does anti-vegf injection induce PVD? Singh, RP. Br J Ophthalmol 2017

27 PVD and Injections Could the injection itself regardless of contents induce PVD? Geck et al. (yes) Prospective study of 61 eyes receiving anti-vegf and had concurrent VMA 15/61 eyes (24.6%) developed a PVD Veloso et al. (no) Cohort study of 125 eyes with neovascular AMD and VMA All received at least 3 monthly anti-vegf injections (avg 8.3) 7/125 (5.6%) eyes developed PVD, all of which had focal VMA Geck U. Graefes Arch Clin Exp Ophthalmol 2013 Veloso CE. Ophthalmology 2015

28 Full Thickness Macular Holes Anatomic defect in the fovea with interruption of all neural retinal layers from ILM to RPE Hourglass shape +/- vitreous attachment Primary v. Secondary F>M Fellow eye at increased risk

29 Full Thickness Macular Hole Classification: Small: <250 um Medium: um Large: > 400 um Also note +/- VMT Rare for spontaneous closure 71% of small holes progress Treatment: Small: vitrectomy (almost 100% success), ocriplasmin injection (good) Medium: vitrectomy (>90% success), ocriplasmin injection (ok) Large: vitrectomy (high closure rates w/ ILM peel)

31 FTMH - small 192 microns

32 Analyze All B-scans

33 Macular Cube same patient

34 Impending Hole Macular hole in one eye Contralateral eye has VMT Increased risk for development of hole

35 FTMH OD Impending hole (VMT) OS

36 Lamellar Hole Partial thickness foveal defect with +/- : Irregular foveal contour Defect in the inner fovea I/R splitting (schisis) Intact photoreceptor layer* Mechanism: incomplete FTMH formation vs. traction from ERM Surgery is controversial

37 Lamellar Hole PIL intact

38 Lamellar Hole from ERM

39 Macular Pseudohole Clinical diagnosis only* Reddish, round lesion in the fovea on exam -> but no lamellar or FTMH on OCT ERM causes pseudohole appearance by distorting the foveal contour Squared off shape on OCT

40 Pseudohole

41 Pseudohole OD VMT OS

42 Myopic Foveoschesis Occurs in high myopes presumably from traction due to anomalous PVD Other factors: rigidity to ILM, posterior staphyloma, ERM Can also develop: lamellar hole, MH Tx for symptomatic patients is PPV +/- ILM peel, +/- gas tamponade

43 Myopic Foveoschesis Images courtesy of Dr. Mohammad Rafieetary

44 Treatment of VMT and Holes Jetrea (Ocriplasmin) Alpha-2 antiplasmin reducer Produces proteolytic activity against protein components within the vitreous body and vitreoretinal interface (laminin, fibronectin, collagen) FDA approved in 2012 as treatment for VMT Dosage mg

45 MIVI-Trust Microplasmin for Intravitreal Injection-Traction Release without Surgical Treatment VMA/VMT resolved in 26.5% (vs 10.1% placebo) and 40.6% (vs 10.6% placebo) of holes closed with ocriplasmin

46 OASIS Ocriplasmin for Treatment for Symptomatic VMA Including Macular Hole VMT release rate of 41.7%; MH closure rate 30% versus 15.4% placebo (not statistically significant) Did not show any additional safety concerns or events Khan, M.A. & Haller, J.A. Ophthalmol Ther 2016

47 Ocriplasmin Who are the best candidates for treatment? Under 65 No ERM Phakic Focal VMT (vs broad) Presence of small full thickness hole (>250 microns) Only macular holes with concurrent VMT should be considered for ocriplasmin

48 Adverse Effects Floaters Blurred vision/ VA Photopsia Dyschromatopsia ERG changes Outer retina OCT changes Retinal break Intraocular inflammation IOP Worsening FTMH Lens subluxation single case in premature infant

49 OCT changes post-injection: Ellipsoid layer (PIL) disruption Accumulation of SRF Ocriplasmin Correlates with decreased BCVA Generally fully resolve and vision improves Often associated with successful VMT release Khan, MA. Ophthalmol Ther 2016

50 ORBIT Ocriplasmin Research to Better Inform Treatment trial Simulated real world ocriplasmin tx 480 patients with symptomatic VMT across 91 sites VMT resolution was 45.8% at 1 month, rate of FTMH closure was 30.5% at 1 month Adverse drug reactions were reported by 30.6% of patients; 5.2% experienced a serious ADR

brilliant blue G (BBG)* *less toxic For larger/chronic macular holes

51 Treatment of VMT and Holes PPV, +/- ILM peel, gas bubble and positioning Staining dyes: indocyanine green (ICG) trypan blue (TB)* brilliant blue G (BBG)* *less toxic For larger/chronic macular holes may do an inverted ILM flap or ILM patch Inverted ILM flap Lai, Retina Today

52 Face Down Positioning? Face down positioning -> traditional standard of care 5 days to 1 week after surgery for idiopathic macular hole repair Trending now toward minimal face down time or even none at all Equally successful in closure rates and end BCVA

53 Alternative Treatment Pneumatic vitreolysis Induction of PVD via 0.3 ml 100% C 3 F 8 gas or 0.3 ml of 100% SF 6 Lower cost vs ocriplasmin or PPV Chan et al -> 0.3 ml 100% C 3 F 8 gas for VMT +/- small MH VMT released in 43/50 eyes (86.0%) 80% (28/35) of eyes with VMT only and 100%, all 15 small MHs MH closed in 10 of 15 eyes (66.7%) VMT released between 4 days - 9 weeks (avg 3 weeks)

Epiretinal Membrane (ERM) AKA: macular pucker, cellophane maculopathy Fibrocellular proliferation found at the vitreoretinal interface made of up vitreous cortex remnants and glial cells Generally

54 Epiretinal Membrane (ERM) AKA: macular pucker, cellophane maculopathy Fibrocellular proliferation found at the vitreoretinal interface made of up vitreous cortex remnants and glial cells Generally occurs after PVD Can cause macular traction which then can result in anatomical changes Occurs idiopathically or 2/2 proliferative retinopathies, inflammatory conditions, trauma, hx of RD Risk factors for idiopathic ERM: Age Diabetes Smoking Arteriolar narrowing Hypercholesterolemia

ERM Prevalence increases with age (>60) peak prevalence observed in 8 th decade (11.6-35.

55 ERM Prevalence increases with age (>60) peak prevalence observed in 8 th decade ( %) Sxs (if present): decreased VA, metamorphopsia, and central photopsia Surgical Tx: vitrectomy with ILM peel

56 ERM Theories behind pathogenesis PVD process causes microscopic breaks in the ILM Müeller cells to migrate to the inner retinal surface ERM V. anomalous PVD hyalocytes from the cortical vitreous remain on the ILM activated by various growth factors to result in cellular proliferation ERM

58 ERM with DR

61 PPV, ERM peel (+/- ILM peel) Surgery VA recovery at 2-3 months after ERM peeling, though can be 6-12 months before reaching BCVA Better prognosis for recovery when idiopathic Risk of ERM recurrence w/o simultaneous ILM peel

To Peel or Not to Peel Pros Removes a potential scaffold for regrowth -> no recurrence Without peel 50% of ERM tissues remain on the central fovea vs 2.

62 To Peel or Not to Peel Pros Removes a potential scaffold for regrowth -> no recurrence Without peel 50% of ERM tissues remain on the central fovea vs 2.5% with peel ILM is stiff, so removal helps return the retina to its normal architecture Cons More difficult procedure Unknown toxic effect of dyes End result BCVA is similar w/ or w/o peel

63 Take Home PVD process takes many years to develop Anomalous PVD can cause complication at many sites in the eye including the macula OCT imaging allows for better classification of the vitreomacular interface following the IVTS Classification System VMA VMT FTMH (small, medium or large)

64 Please remember to complete your session evaluations on the Academy.18 meeting app Tweet about this session using the official meeting hashtag #Academy18

Vitreomacular interface disorders. Ghanbari MD 1393:10:25

Vitreomacular interface disorders Ghanbari MD 1393:10:25 Human vitreous after dissection of the sclera, choroid, and retina. Lamellar structure of the posterior vitreous cortex (PVC) in the monkey. V =